Podcast: Demystifying Mast Cell Activation Syndrome

Demystifying Mast Cell Activation Syndrome with Nathalie Niddam

Could you imagine a condition that affects virtually every organ, eludes the standard diagnostic criteria, and causes multi-system inflammation? Meet the perplexing world of mast cell activation syndrome (MCAS). MCAS is an elusive condition that affects many, yet remains largely misunderstood. MCAS is a syndrome that triggers multi-system inflammation, and due to its diverse range of symptoms, it often eludes typical diagnostic processes. It has a profound impact on both the body and mind. Mast cells are integral to our innate immune system, playing a crucial role in safeguarding us against foreign invaders, allergens, and environmental toxins. However, potential triggers of mast cell hyperactivity can range from environmental toxins to mold.

Today I’m with Dr. Bruce Hoffman and we dissect this complex condition and delve into the critical role of mast cells in our immune system. Learn how mast cells, our body’s fierce protectors against toxins, might turn hyperactive due to triggers like environmental toxins, heavy metals, or mold, launching a cell danger response that could send your body into a protective shutdown. The conversation takes a deeper turn as we explore the intersection of physical and mental health. Focusing on those battling MCAS and early developmental trauma, Dr. Hoffman shares invaluable self-regulation strategies and lends insight into the significance of neurofeedback and building a window of tolerance.

Dr. Hoffman is board-certified and has a fellowship in anti-aging medicine as well as a Master’s degree in clinical nutrition. He is also a certified functional medicine practitioner. In addition to his clinical training, Dr. Hoffman has studied with many of the leading mind-body and spiritual healers of our times, including Deepak Chopra, Paul Lowe, Osho, Ramesh Balsekar, and Jon Kabat-Zinn. He has shared the stage with Dr. Deepak Chopra, Dr. John F. Demartini, and he continues to spread his inspiring vision of healing and wellness with audiences and patients around the world.

Thank you to our sponsors for making this episode possible:

Mitopure: Use code NAT10 for 10% your order at https://www.timelinenutrition.com/shop/nutrition

LMNT: Use Drinklmnt.com/NAT to get 8 free single serves with any order to try different flavors.

Profound Health: Use code longevity15 to save 15% off your first order at https://profound-health.com/

Find more from Nathalie:

YouTube: https://www.youtube.com/channel/UCmholC48MqRC50UffIZOMOQ
Facebook Group: https://www.facebook.com/groups/biohackingsuperhumanperformance
Instagram: https://www.instagram.com/nathalieniddam/
Website: www.NatNiddam.com
Join Nat’s Membership Community: https://www.natniddam.com/bsp-community
Work with Nat: Book Your 20 Minute Optimization Consult: https://calendly.com/nniddam/intro-call?month=2021-08

Find more from Dr. Bruce Hoffman:

Website: https://hoffmancentre.com/

What we discuss:

(0:03:00) – Understanding Mast Cell Activation Syndrome

(0:15:27) – Treating Physical and Mental Health Impacts

(0:23:09) – Understanding and Healing Unconscious Dynamics

(0:38:05) – Treatment and Management of Histamine Intolerance

(0:45:12) – Building Resilience and Shifting Healthcare Paradigms

(0:57:19) – New Health Curriculum for Transformation

Key takeaways:

Mast Cell Activation Syndrome (MCAS) is a condition where mast cells, a component of our immune system, become hyperactive and trigger inflammation across multiple systems in the body. This can result in a wide range of symptoms and can be difficult to diagnose. Potential triggers of this hyperactivity can include environmental toxins, mold, and certain foods.

Physical and mental health are interconnected when it comes to MCAS. Individuals with this syndrome may have early developmental trauma which can exacerbate symptoms. Learning self-regulation techniques, such as neurofeedback, can be beneficial for managing stress and promoting balance in

Full Transcript

This transcript was automatically generated, please excuse any errors.


Welcome to the biohacking superhuman performance podcast. My name is Natalie Niddam. I’m a nutritionist and human potential and epigenetic coach. And I created this podcast to bring you the latest ways to take control of your health and longevity. We cover it all, from new technology to ancestral health practices, personalized interventions, and a very special interest of mine: peptides. Enjoy the show.


Hey, folks, welcome back to the show. Today’s episode is going to be amazing. It’s a topic I’ve been wanting to explore forever, and a doctor I’ve wanted to have on the show for even longer. His name is Dr. Bruce Hoffman. And we’re going to talk about mast cell activation syndrome, cellular membrane stability and everything associated with it. But before we do that, I do want to thank one of our sponsors, who is Mito pure from timeline nutrition, so metal pure. If you haven’t been listening to this podcast for too long, you might not know is the first product to offer a precise dose of your lithium a that supports my toppity and increases cellular energy. So why is this important? Well, mitochondria become damaged and dysfunctional over time, which leads to the production of harmful byproducts and the disruption of normal cellular function. This is a huge issue. My toffee G ultimately helps in maintaining healthy mitochondria by eliminating these damaged ones, which allows for the proper functioning of cells and overall cellular health. It also encourages the body to make new mitochondria. So optimizing your cellular health is crucial for maintaining healthy tissues, organs and systems in your body. So not just it might appear has been shown clinically to improve performance in muscle. But it’s also been shown to improve immune function, brain function, heart function, it is amazing. Well, I mean, frankly, mitochondria are critical to every single system. So might appear from timeline nutrition gives you three ways to get your daily dose of 500 milligrams of your lithium a, there’s a delicious vanilla protein powder that combines muscle building protein with the cellular energy of myopia. There’s also a berry or a ginger powder that easily mixes into smoothies or just about any drink. I love it in my yogurt in the morning, sometimes if I have yogurt, and for my as part of my breakfast. And finally they have these amazing soft gels that you can use for travel, I would recommend that you consider the starter pack because that lets you try all three forms of myopia so you can figure out which one is your favorite. So timelines offering 10% off your first order of myopia, all you have to do is go to timeline nutrition.com, forward slash net 10 and use code net 10 to get 10% off your order. All right, now let’s talk a little bit more about the episode. So imagine a condition that affects virtually every organ eludes the standard diagnostic criteria. And this is where people get gaslit all the time, and causes multi system inflammation. Meet the perplexing world of mast cell activation syndrome, otherwise known as M. Cass. Today I’m joined by Dr. Bruce Hoffman to discuss this complex condition and explore the critical role of mast cells in our immune system. Mast cells are a body’s first line of defense against foreign invaders, allergen and environmental toxins. However, they can become hyperactive in response to triggers like environmental toxins, heavy metals, mold, and even early developmental trauma. And we talked about that in the episode. This can ultimately lead to a cell danger response, which essentially sends the body into protective shutdown. And if this is you, you might be that person that seems to react everything. Dr. Hoffman is amazing. He’s just the kindest, most knowledgeable, unbelievable guy. He’s board certified has a fellowship in anti aging medicine, as well as a master’s degree in clinical nutrition is also a certified Functional Medicine Practitioner. In addition to his clinical training, Dr. Hoffman has studied with many of the leading mind body and spiritual healers of our times including people like Deepak Chopra, Paulo, our show, Ramesh balsa car, and Jon Kabat Zinn, who wrote the book, Why zebras don’t get ulcers. Rate, great book that highly recommend you read that Dr. Hoffman specializes in complex medical conditions. And he is the medical director of the Hoffman center of integrative medicine in Alberta, in Canada in Calgary and Alberta and Canada. And so to learn more about Dr. Hoffman or to reach out to him if you think that you might want to talk to him about something that’s going on in your world, you just need to go to the Hoffman Hoffman center.com. We’ll put that in the show notes. And that’s H O F F ma N center C E N T R e.com.


harm. And that’s the website and you can find out about all the amazing things that they do there. Okay, before we jump into the episode, I have one more sponsor I need we need to thank and then we’re going to rock on. So one shot you about element and an electrolyte drink that I am obsessed with.


I dump a single packet into my one and a half liter water bottle. Now this is important because if you put it in too little water, it’s gonna be too concentrated so one and a half liter bottle, and I sip on it throughout the day. And not only does it help me drink more water because it tastes amazing, but it also ensures that my electrolyte levels are always balanced. And these this balance ensures that you regulate fluid balance and helps with digestion circulation temperature regulation helps to maintain the body’s pH balance, which is ultimately vital for enzyme activity and biochemical reactions, as well as optimizing nerve and muscle function element contains a science backed electrolyte ratio with 1000 milligrams of sodium, 200 milligrams of potassium, and 60 milligrams of magnesium with no junk, no sugar, no coloring, no artificial ingredients. No gluten, no fillers. Bottom line, no BS. So right now element is offering my listeners a free sample pack with any purchase. That’s eight single serving packets free with any element order. And this is an amazing way to try all eight flavors or share element with a salty friend like I just did last night. So get yours at drink element.com forward slash net. Now element has no E’s in it. So drink lm n t.com forward slash net. And this deal is only available through my links. So you’ve got to go there. Now one last thing I will say about these guys is they offer a no questions asked refund policy, you get to try it totally risk free. If you don’t like it, just share what’s left with a salty friend, and they will give you your money back with no questions asked, you literally have nothing to lose. So thank you. Thank you. Thank you. Thank you guys for being here. Thank you for listening to the podcast, please make sure that you share it with your friends in your network if you get value from it. And of course, if you’re feeling inspired, leave us a review. And that’s it. Let’s get in. Let’s get into it with Dr. Bruce Hoffman. Hey, folks, just a quick reminder that all of the information presented in this podcast is for informational purposes only. No medical advice, no diagnosing no treatments suggested here. Before you try anything that you hear about or learn about here. Make sure that you check with your medical provider. Dr. Bruce Hoffman, welcome to the show. It’s a pleasure to have you here today. Thank you very much. Yeah, so we are gathered here today we’re going to, we’re going to explore let’s say the universe or the world of M casts, I mean, there’s many other things I know you could talk to speak to, but m Cass being mast cell activation syndrome, which is, you know, in good company with one of the most vexing kind of health issues that people deal with. And I think in part because it’s not well understood, it’s very disruptive to people who suffer with it. And it’s tough to get a diagnosis. And even if you get a diagnosis, it’s really hard to figure out how to stabilize those little mast cells. So I thought maybe we could start with explaining to people what the heck a mast cell is and why we even need them because, you know, that’s just get rid of the buggers if they’re overactive.


A huge mistake, but you know, yeah, we just die a lot quicker. Exactly. You wouldn’t suffer but maybe one but okay, well, let’s talk about mast cells and what they do. Sure, so you know what, my cells are part of the innate immune system, and they provide protection against invading toxins. So they send out their bad white 1% of your white cells. So they’re not a huge component, but they are all the surfaces of your tissue, they in your eyes, your skin, your GI tract, your lungs, and they they send out up to 1000 mediators of inflammatory substances in order to protect you from further toxic load. That In so doing, they create a huge sort of multi symptom multi system array of symptomatology, and in every single organ system of the body. If you look at Dr. Efrain is one of the pioneers in this work. If you look at his sort of, there’s a chapter he hasn’t one of his books, he lists all the organs and all the symptoms as every single symptom in the book really, in every single organ can be potentially a mast cell activation issue. Wow patients you present with mast cell activation. You know, they go from pillar to post from specialist to specialist trying to find out why they don’t feel well with waxing and waning symptoms over a lifetime usually, and they never get diagnosed. They never get appropriately diagnosed. Because it’s not just allergy it’s inflammation with or without allergy.


So you can have inflammation and not be have the IGE allergy typical symptomatology, like rhinitis, or asthma or urticaria, or any of the IGE to allergy types and things that you can be massively inflamed from muscle activation, and have various symptoms that just evade normal diagnostic criteria. Right? Yeah. So someone tell if they have inflammation, just inflammation, or if their inflammation is linked back to their mast cells.


Suspicion really, you know, you’re just people who present with my cell activations, and they’ve been, you know, I’ve been sick for as long as I can remember, I had allergies as a child, I’ve been intolerant. I’ve got an unexplained anxiety and insomnia, that one go away. And they just have got exam or skin rashes that won’t respond. I got poor wound healing abilities, I got cross and nodules on my skin that seemed to grow cherry angiomas that seem to come and go, because my cells release growth factors that create little skin growths and skin tags and angiomas. So this is multitude are present multitude


ways of presenting, and if you don’t really have a high index of suspicion, you can often miss the diagnosis. Wow, okay, what’s the react to all the supplements? They react to all the foods?


This? I mean, I’ve spoken to people who can’t take a supplement like they can we get them in our group, you know, like they, they’re like, I can’t take any supplements. I’m down to four foods. I don’t know what to do anymore. So a patient today for foods can’t take anything. Like, what is that? That’s insane.


It’s insane. So what do we think? Is there any theory about what causes these mast cells to go haywire? Like? I mean, this is clearly not, you know, this is clearly not normal. This is not the way that they’re intended to work. Like, it’s almost like an autoimmune thing, right? It’s an immune system gone into overdrive. So what might drive what do we think might be driving myself into the state of hyper vigilance or hyperactivity? Well, we live in a world that is somewhat


overwhelming in terms of its capacity to


invade our defenses, we really have no idea how


vulnerable we are to food, mental, environmental, toxins, and how our body is just struggling to survive and keep abreast of this incoming wave of toxicity. And it’s really overwhelming. And it’s not hyperbole. It’s not conspiracy theory. It’s real. Ya know, we just wanted just at this moment in our evolution to put up with all the microplastics and heavy metals and insecticides and pesticides, and EMFs and mental stresses and buses that demand things of us. And, you know, it’s endless, the toxic load, and my cells are trying to keep up. And they trying to just protect you from going into this inflammatory response that that then shuts down your body in the so called Cell danger response.


Well, if you look at the Porges, autonomic polyvagal theory, that dorsal vagal response, where you shut yourself down to withdraw you from life, so you don’t keep exposing yourself to the things that are incoming.


Yeah, it’s like the first infantry men in the on the battleground trying to say, hey, you know, I’m going to protect you, and make sure you don’t die. But in the meantime, we can wreak havoc with your organ system shutting it down.


Out of life, stop doing it. Yeah.


Question by the Kandra. We’re going to produce a fatigue state so you can’t get up and keep doing what you’ve been doing.


That’s how it works. And then Robert Navarro cell danger response is absolutely clinically relevant. If all those people are watching, listening, if they don’t aren’t familiar with Robert Nivas theory of the cell danger response, I would highly recommend they get up to speed immediately on, on his work, which has been going on for 10 years now. Which he has carefully put together through multiple research papers, saying that you know, in the mitochondria, the first the canaries in the coal mine, you got these cells, you got 70 trillion cells. Inside each cell. We’ve got, you know, 100 to 2000 mitochondria, mitochondria,


drive the ATP


We produce like 70 kilograms of ATP a day is like ATP is is it?


Is it and mitochondria, they the most sensitive to this whole incoming onslaught. And as soon as they detect an overload of stresses, they change the outer membrane, they change their phospholipid structure, they change the voltage, and they literally undergo autophagy and die. And they take with them.


And my cell activation is one of the ways in which mitochondria get destroyed micelle, the mediators of inflammation


and they get all the factors, you know, the chemicals, the metals and the mold. Okay, so let’s so so let’s talk about those all of those triggers, right. So I mean, you’ve named now you know, so there’s, there’s the environmental toxins. So there’s the mold, there’s the heavy metals, there’s the pollutants in the air, there’s non native EMFs that you mentioned, as well, which some people seem to be more sensitive to than others, but anybody who thinks they’re not being affected by them, I used to be one of those people. I used to be like, Ah, I’m immune to EMFs until I was presenting at an event that happened to be in the middle of a field in Kentucky, where you couldn’t so much get a cell phone respond like a cell phone signal in this place. And my aura ring kept working because I, you know, I just wore it, but it was, The nights were so cold, and it was rainy and uncomfortable. And my HRV scores were off the charts. Yeah. And I was like, and it was it was the first time I probably the first time I’d been away from from the soup that we live in. And I was just like, wow, that’s nuts. Like you don’t know that you’re, you don’t know your body’s responding something to something because sometimes because it’s become your new normal like this is just how you are. Yeah, interestingly, my cell activation works EMFs trigger my cells to create these inflammatory mediators, which open up the ionic receptors in the cell membrane, which increase intracellular calcium, which increases intracellular glutamate, which is neuro excitatory Neuro Stimulator. So my cell EMF stimulate my cell activation. That’s how they work. Wow. That’s how they wreak havoc. Interestingly, just on that point, I recently went to South Africa, where they have load shedding. They have what? Load Shedding every hours, they shut off electricity to certain parts of the country. Oh,


yeah. So in Cape Town, and every two or three hours, electricity goes up dead.


And interestingly, the people around me with EMF sensitivity were having the time of their life, they felt so relaxed. So the whole country is in crisis, because you can’t get electricity. But the people with EMF will say, this is heaven. I want to move here. Thank God, that’s hilarious. It’s crazy and hilarious. Okay, so what do we do? So what do we do? So I mean, look, EMFs is the big knock, right? Because you cannot remove yourself from EMF. And so is it possible and I’m sorry, I’m just literally asking you this. We’ve we’ve mentioned all these different toxins? Is it possible that by reducing other toxins in the body by reducing that overall toxin load, we can help to rebuild some resilience so that the EMFs aren’t as dramatic?


Yes and no. So people who are electromagnetic hypersensitive will always tend to be you know, electromagnetic sensitive, but you can definitely lower the threshold. So, I mean, if I look at the major stressors for my cell activation, number one that trumps it, early developmental trauma, interesting. Yeah. Trump’s at 100% of the time, due to the dysregulated HPA axis, the hypothalamic pituitary adrenal cortisol, adrenaline, noradrenaline axis, those individuals are very susceptible to mast cell activation. And that pathway has been well worked out by high cortisol, adrenaline triggers Maesa release. So early developmental trauma with ongoing stresses, mental stresses, number two would be mold. Mold is a massive trigger of muscle activation.


And then number three is food. I histaminergic, high inflammatory foods. Those are the top three in my well, then we go look for all the rest of metals, the chemicals, the infections and everything else.


BIOSIS the microbiome triggers? Yeah, yeah, it always comes down to those same things. Okay. So it you know, it is crazy, right? It’s, it’s, we’re, as I interviewed different people, we’re talking about different issues. So often it just comes right back to all these things and the, the early developmental those aces as people call it aces


that early developmental trauma is so again, it’s under reported, it’s even under acknowledged, I think by individuals themselves, right? It’s, it’s gaining momentum. I mean, I don’t think you can take a good medical history without doing an a score. Even though the a score, isn’t it, there’s much more to it. The thing that we look for mostly is interrupted bonds with a mother. Interesting. When there’s interrupted bonds with the mother, the HPA axis is usually quite dysregulated. And that systems in trouble. And you know, and it’s all unconscious dynamics, if you don’t do a Family Constellation, where you look into the unconscious dynamics, and entanglements of family systems, you won’t know that it’s that potent of an issue, then you look at heart rate variability and see if they tweaked in the sympathetic dominance. And then you look at q e g, is looking at brainwaves to see if they have dysregulation between the different delta theta, alpha and beta brainwaves. And you can tell this, these systems that are so dysregulated, and we do stress assessments looking for


physical stress based on mental triggers. And the first thing I do with every muscle activation patient is look at these parameters. And suggest and insist that they learn self regulation as a primary strategy before they even address the rest of it. If these individuals aren’t self regulating, and having the capacity to move between sympathetic and parasympathetic as you heal in that coherent zone between the two, they permanently in fight flight or collapse. Don’t even begin your work with the rest of it. It gets them to self regulate. Yeah, over and over and over every day, like working your biceps, morning, night, every hour. It takes nine months to a year to shift the neuroplasticity modules in the brain and to shift the default mode network that creates your sense of self is lot of work. Nobody wants to do it. Yeah.


No, no, everybody wants what Wait, wait, surely there’s a drug or a supplement I could take that would be so much easier than breathing, or this coherent business. So what are the two? You’re laughing? I know, I know, I know, listen, we all want the easy answer. And and sometimes humans, it’s actually is an easy answer. It just takes time and work and an application. So what have you found to be the best tools? And I’m sure it varies from person to person. Because I mean, I even find, you know, you’re, we’re all in a world where we’re in a sympathetic state. So even without M casts we’re trying to teach we’re trying to help people to figure out how they’re going to get themselves out of this constantly activated state. And I’ve found that what works for one doesn’t resonate for the other very, very individualized. Yeah, yes. So how we start with this is we start with even good ol Heart Math and wave training, love heart match, we use that we use that. Then we use neuro biofeedback we use neurofeedback, we use that five different six different strategies of Neurofeedback mind left brain tap all sorts of things. Yeah, then we do vagal tone strengthening with Razia Max and other devices. And if that’s not helpful, we then refer to as E practitioners to do somatic work to assist people in building a window of tolerance, whereby they can stay somewhat stabilized in the world of, you know, incoming stresses and they don’t just integrate and D granulate. Much. It’s the first sign of something that they can’t handle, you know, that is the core of treating myself in my world, in the world I work with, if that isn’t enough, and usually it is enough to begin the process of then building back up. But that’s where we begin is self regulation, neuro biofeedback. Building a window of tolerance, building self regulation, coherence so that they’re not so disintegrate, they don’t just, they don’t


fall apart as easily. It can be a lot of work, you know, it can be a lot of work. Well, I mean, in the case, I mean, when you’re talking about early developmental trauma, you’re talking about broken bond disrupted bonds with mom when they were babies, like we’re talking about deep deep work here like are this isn’t just, you know, I’m gonna I’m gonna learn how to do a box breath and everything’s gonna be great. I mean, box breath might be helpful, but this is I mean, this is this is so interesting, right? Because it takes a physiological condition into the realm of, of mental health. It’s interesting thing, Natalie is that you know, we have this Cartesian body


Mighty body mind split, which we know is not true. But the body mind is one thing, there is no separation, there’s not there isn’t a body and a mind is, is one phenomena. And those two are equal. Yeah. So whatever your internal dialogue is, from your early development for all inherited family trauma, you can act out your


inherited trauma, early developmental trauma, if you don’t try and create some conscious insight into what actually happened, and what you’ve inherited, and what’s not yours to act out, you can’t begin the process of downregulation because I work in these layers and levels of healing from you know, the so called self was or soul down to mind and ego down to emotion down to brain and energetics down to biology and structure down to toxicology and the external environment. If you don’t heal at the higher levels, which trickled down to biology, you can’t go at biology now because all of this is impeding the you know, it’s impeding the flow of electrons


on right, like they’re, the body’s hanging on to stuff and it won’t let go. Unconscious dynamics of entanglement can ruin your life. And you won’t even know it because it’s before memory was developed at the age of three or four. Yeah, but you need somebody who’s skilled in how to interpret family systems inherited trauma and early developmental trauma and apply it to physiology and practice. It’s just it’s it needs you need to somebody a very well trained in that who can really lead you through that and put you into a practical approach how to manage it. Yeah. So But now everybody that that’s that present with them cast doesn’t necessarily have that early childhood trauma. And yeah, but But you but you’re going in position is most if not all, people still have some degree of of self regulation issue in the parasympathetic nervous system. Almost always Yeah. which then translates into the gut through the vagus nerve of course, so they get cut this motility and all sorts of dysautonomia is of the vagal tone. Then they get you know, you have these pent these triads and Pentair symptoms go together. We’ve got the muscle activation pots, hypermobility people,




There’s a triad, you see them a lot together. Then you get the Pentel where you get this autonomia and you get autoimmune disease. That’s the pintech. So that adds on to the first three. Yeah, they’re all they will go around like a you know, like a water in a sort of drain, they swirl around each other, and the one precedes the other, then they just sort of feed of each other. And the phenotype that presents often females aged 15 to 45 is a very common phenotype of people presenting in that way. But we’ll have a mobile much more my so much more artsy. Not a Potts, a lot of disorder. Yeah. So but with EDS, it’s which is Ehlers Danlos Syndrome, for those of you listening who don’t know what EDS is, that’s a genetic condition, is it not?


There’s different subcategories of Ehlers Danlos, peros danlos, sort of hyper mobile type three, there’s no genetics, particular genetics that drive it. There’s just a predisposition to it. But there are genetic, Ehlers Danlos conditions of course, yeah. Well, these people who just don’t make collagen, or they don’t make it efficiently, or they don’t make enough or they don’t make a certain type. I mean, I have, I have a friend. You know, I didn’t know anything about EDS. And I mean, this is a woman who literally had to have all of the teeth pulled out of her mouth because they were just breaking like she, you know, her body wasn’t forming the connective tissue


to hang on to them. Like it’s, it’s pretty intense, at its most extreme, is just, you know, people draw you dizzy when you stand up. That’s my patients, you know, do you get nausea and vomiting and without any real cause? And that’s the Potts sort of symptom, then you do the 10 minute


standing test looking at blood pressures and pulses. And then the other one is you just do on Zoom to do the Buyten score, you know, can you build your thumb on? Yeah, can you bend your finger back? Let me look at your elbow. It takes 30 seconds. Yeah. And it’s got hyper mobile, they got parts and then my cell symptoms or every, you know, they just inflamed and allergic and Urticaria and angioedema and allergy symptoms and runny nose, runny eyes, seasonal allergies, joint pain. So for these people, still we start with the autonomic regulation, and then there’s little programs now both


Around the DNR s and the copter and this and that, but I don’t find them deep enough, quite frankly.


You don’t? Interesting. Well, I guess especially if there’s ace, I mean, if there’s early childhood trauma, they’re not they’re not going to go there. Because implies it’s sort of like it’s sort of a, an intellectual imposition over an unconscious dynamic.


And you can’t you need to, you need to make unconscious dynamics conscious, right? You only heal through consciousness, you don’t heal by just slapping things on people.


Yeah, take this take that do this go. Yeah. Well, I actually it adds more stress to the system it to some degree. And what do you know, you can’t change a negative thought by thinking of positive thought that doesn’t work? Well, not, not at that point, you can’t.


The unconscious dynamic needs to be looked at, understood and transformed.


So you need consciousness to grapple with some of these entities.


Okay, so step one, is identifying that indeed, a person is dealing with M casts, which presents I mean, I think the people with the worst cases of M casts know at this point, they have a constellation of symptoms that are inexplicable and unresolved, they, they don’t respond to anything, right, or they respond badly to things they should respond well to. So once, once we’ve hopefully gotten to a point where we’ve gotten, we’ve helped them to regulate their nervous system, because nobody’s going to do it for them, right? Like this is really helping in the individual tap into their own ability to self regulate, understand the unconscious dynamics, and self regulate, and know why they self regulating, if you don’t explain the reason, if you don’t provide salience, you are doing these exercises for this reason, because you want to end up over here. But you now over here, to get you this way. It’s like going to the gym, you have to practice and you have to get feedback. And you have to check in with your provider to see if you’re making progress with self regulation. You don’t just say, Oh, you need to meditate and do box breathing. No, it’s great relevance, and you link it, and you measure it, and you see progress that’s has to be sort of supervised and with feedback. Well, you’re rewiring the brain, right? And you’re essentially trying to overcome the dominance of your inner Darth Vader, who’s basically saying, dude, I’m just trying to keep you alive, you don’t understand.


And that’s the toughest one to rewire. Because it’s the it’s the big bully that hides behind. I’m just trying to keep you alive, you just don’t know what’s good for you.


And, and, you know, we have our default mode network, which creates our sense of self, we have our internal dialogue, we have our defense structures, we have all these things in place, that often keep us from knowing what the hidden dynamics are.


We have very sophisticated entities, with lots of slippery sort of corners, you know,


it’s not linear, it’s not, you know, we trained in n squared d squared, medicine, name of disease, name of drugs, single organ, single, single drag. It is completely without merit. When you come to complex illness when you’re trying to do whole person healing. It has the cupboard is bare, there is nothing to offer. Mm hmm. Well, which is what happens to these people, right? They’re desperate. I mean, I see them in my Facebook community, by the time they they show up there. They’ve tried everything. They’ve been everywhere. They’ve been told that they’re crazy half the time off 90% of the time, put on an SSRI and refer to the psychiatrist. Yeah. Which is, which is almost the answer, but not quite.


I mean, you know, we’re there, at least we’re going to the head, but we’re not we’re not doing it with the right intention. You also named mold, high histamine foods. These are things that can probably that I’m guessing you’re addressing while you’re helping this person to do this work, right? Because take a history of mold exposure, which is almost always in every case there. Although mold is too big, you know, it’s hidden. It’s everywhere. It’s everywhere. So you got it. There’s different ways to measure mold illness, and there’s simple quick ways which everybody falls into the trap. They do a urine mycotoxin test to say I got moldy on this. No, that’s not my that’s not chronic inflammatory response syndrome, which is a mold inflammatory condition. You’ve got urine mycotoxin. That doesn’t mean you got SIRs says is the real diagnosis you’ve got that says that you got to take a history. You got to fail the visual contrast test, you got to look at the cytokines. You’ve got to look at the IG


I’ll test for the intracellular mold species and the mycotoxins. Yes, you can do a urine mycotoxin test. But that is not diagnostic. It’s just indicative of a possibility. You got to do Ermias or hurts me twos in the home, you got to measure mold spores. There’s a lot to faking a diagnosis of chronic inflammatory response syndrome, which, by the way, is closely linked to myself. I was gonna say like, they’re, they’re kind of frickin crack the two of them, right? Because you’re, they, they feed, they feed off each other molds, a terrible trigger of miso, terrible trigger, is and it’s ubiquitous. It’s it’s, it’s everywhere. And it doesn’t mean mold in this home, it could be the mold that you were in three homes ago, that’s still in your system that hasn’t been bound up and excreted. So are there people that are more susceptible to that kind of thing? Yes. Yeah. I know, genetically, there’s genes that show that you might be like some people just their body can’t clear it somehow. Yeah, Shoemaker, Richard Shoemaker developed all that genetics around mold toxicity and inability to clear mold.


So there is a genetic basis, because only 25% of the populations are so called mold sensitive. I don’t think that big is correct. I think it’s much more well, there’s probably other genes somewhere that we just don’t, you know, there’s so much we don’t know, in genetics, but the spouse of a mold patient will go What’s wrong with you, I don’t see mold. I don’t feel mold. I’m fine, what’s wrong with you. But then the poor wife is 25% the husband’s part of the 75% they don’t crash with mold. But you know, the child or the wife’s on the floor with mold exposure. And it doesn’t make any sense because it’s a hidden toxin most of the time, for sure. When you go scratching and then you find it behind the drywall, you find it in the dishwasher, you find it behind the washing machine in the washing machine in Sangamon Bobby


in the lift up the toilet along the you know, the all that.


But you smell I mean, I smell mold. I will walk into a place and smell it and my husband will be like, I don’t know what you’re talking about. I’m like everybody smells it but


they trained dogs to smell for it. Like that dog.


I smell mold and I taste rancid oils. Other people are like, I don’t understand why you don’t like this. I’m like, Dude, this peanut butter or almond butter is rancid and they look at me like I’m crazy. And I look at them like I’m so sorry for you that your taste buds are dead.


Yeah, that’s


yeah. You could smell Molins musty for sure. Yeah, some people.


So do binders help?


In a situation like that? Oh, absolutely. They do. But the common error again, once again, there’s many errors that get made in this holistic functional world of ours. People get you know, they go down the mall. Oh god mold. Well, mold may be one of your triggers. But let’s look for everything else as well. Most the big trigger and if you do have more than you do have inflammation from mold and you have chronic inflammatory response syndrome for mold and your mitochondria undergoing cell death because of mold. Then you do have to a remove yourself, clean up the remediation and you use binders but what is taught is you use colas. tyramine is one of the primary binders because thymine is highly absorbent of all the fats and oils. So if you don’t check the fatty acid status, and you just go throw collars tyramine as a binder, that person is going to crash in front of your eyes. Yeah, yeah, for sure. And that’s, I mean, then the cause it’s funny, I have a box of it sitting there. And I haven’t touched it because I just kind of it’s one of those ones where I’m like, I’m not so sure it’s worth the downside. I’d rather take a whole lot of other stuff and I don’t know depends what what mycotoxin use secreting with a color style I mean, there’s going to be a benefit effective so you really have to do that testing to figure out what is at play here. It’s best for the awkward toxins, you know, but But what I do is I do the body by a Kennedy Krieger fatty acid test and that measures all your omega sixes or your omega threes or your omega nines, it measures your D myelination of your of your fatty acids. And you can see if your total lipid con count is below minus 30 Don’t touch call this dummy you got to crash that mission Interesting. Okay, I use the body by a fatty acid test is my one of my primary tests that I use. Oh no, I didn’t realize they had one I just there’s another company that does an omega fatty acid test but I don’t know if it says detailed that that one but you know what don’t even it’s not it’s not it’s gonna tell you tell you the only test was doing is the Kennedy Krieger test. And it measures all these fatty


He asked his body by I have developed software to interpret nice software from body but it’s not the test. The test is Kennedy Krieger. Okay, so there’s a research based lipid panel. Okay, Kennedy Krieger. Yeah, and it’s the only one worth doing. But you’ve got to put it through the body by software. Because they they give you a nice one page handout, the Omega six omega threes lipids, do this do that. It’s the software that really orientates you to the test. Hey guys quick interruption to the episode to let you in on a huge announcement. And to thank our final sponsor, a final sponsor is profound health, and they are purveyors of oral bio regulator peptides. And that’s the actual extracts of tissues, glands and organs of animals in capsules, so contains the bio regulator peptide, plus all those cofactors. And we use by regulators to help the body to regenerate at a cellular level. All of these different tissues and organs. If you want to learn more about our regular peptides, you can definitely go to the profound dash health.com website and learn more there or you can go back earlier this summer, I recorded a podcast on bio regulator basics that you might find interesting. They also have other amazing anti aging supplements, as well as synthetic bio regulators that are bioavailable just by little drops under the tongue. Now, on your first order, you will get to save 15% Off with discount code longevity 15 All right. So once again, that’s profound dash health.com. And now let’s get back to the episode. Well listen, the test is not worth the paper it’s on, if you don’t know what to do with it.


Like literally, there’s no point doing it unless you’re gonna you’re getting a roadmap with it. So or somebody who knows how to interpret it. So okay, so we we measure those, and then the high histamine foods so that this now looks like the low hanging fruit. This is the easy stuff compared to dealing with your early childhood trauma that may or may not have happened from the time you were in the womb, and then dealing with mold, which, you know, remediation is an ugly, ugly thing. Because half the time it doesn’t work like once, once mold is in that and and you know, it’s like mold is probably one of the most well adapted organisms on the face of the planet. Like it’s insidious. So let’s say we’re kind of doing what we can for the mold getting away from the high histamine foods becomes the next thing and these are the people who tell you you know you say to them what listen have some bone broth or have protein shake and they’re like,


like they go into like crisis.


Bone broth, no fermented foods, they just like crush a person overnight. And leftovers are a disaster for these folks. And I live on leftovers, but I mean like to them. Leftovers is it just is not okay. You can freeze your food and then eat it the next day, but don’t leave it in the fridge overnight. Yeah. Though, some people get away with it for 12 hours. But the very severe people they know they can’t do that, you know, so we do, but we I do paleo, autoimmune, low histamine, then adding the oxalates. And you know, the FODMAPs if they have those issues, but it’s usually paleo autoimmune, low histamine, high fat.


Right, usually replace the lipids along with reduce removing the inflammatory foods. So replacing the lipids is a big deal. And this is the body bio stuff. This is restoring the cellular membrane integrity. So let’s talk about that a little bit what those lipids are. Yeah, yeah. So I do I do the body bio fatty acid test. I do the ITL butter Conrail test that test measures phosphate title choline, and phosphate tidal ethyl Alameen. The ethyl LME is on the inner membrane of the mitochondria where your electron transport chain takes place


measures the body voltage.


So if those phosphor titled choline, Phosphatidyl ethanolamine, body volume all affected, you know, you’ve got to replace with phospholipids, then the body by a fatty acid test measures the Omega sixes, and all the Omega threes and the myelinated fats and the mega anions and the saturated fats and measures all of it. So between that and the IGF mitochondrial test, I determine what needs to be done to repair mitochondria and move people out of the cell danger response which takes three to six months to do. It’s long. It’s a long project. Yeah, but that’s but there’s a path to it. Right? And I think by the time people come to you three to six months doesn’t sound so bad when they’ve been suffering for years. I’m sure. So, so high fat so you’re saying hi, high fat have the right fat


kind of diet, you’ve got to analyze what they’re deficient in.


And then you got to replace that particular fat. So we have all these kinds of oils that have different


structures that repeat, like primrose oil for, you know, DGI, we’ve got different oils for different deficiencies. Interesting. So you just very choose your fat replacement accordingly. That’s amazing. So you’re literally kind of going at it like really like rebuilding that cellular membrane to help him to regain function. And so do you. Do you see people actually start to stabilize at some point? I mean, it sounds amazing, right? Like, no, no, it must be. It must be for these people where they wake up one morning and all of a sudden, they may not itch, or they don’t have a rash, or they get better when the test starts improving, they feel better. And they repair their cell membranes. They repair the mitochondria. They stabilize the mast cells, usually with diet and lifestyle stabilizers, which we haven’t discussed. And then they stabilize the autonomic nervous system and amygdala so they’re not so twitchy and so reactive all the time.


Yeah, so you got all the things going. So let’s talk about those mast cell stabilizer stabilizers you said, right?


So we use this nutraceuticals. And there’s you know, we use the hiss Dao enzyme, which we measure there’s tests from Precision labs, measures Dao.


There’s a Doa enzyme you can get from any genetic profile as well to see if you have and


then we look at the h&m T gene to see if you break down histamine appropriately. We look at methylation because most of method lot of methylation goes towards making phospholipids and breaking down histamine intracellularly. But what we do is we use Dao for the gut Dao, you use quercetin and associated nutrients, including vitamin C, there’s many others.


black cumin seed and Nigella sativa and luteolin for nutraceuticals vitamins, yeah, we use those. But I usually go straight to pharmaceuticals, I go straight, and I get them all compounded. Because if you go over the counter, you get all the excipients and dyers, which just make you worse, not better. But yeah, you’re talking about the most sensitive people on the planet here. So those things would destroy them. For sure. I usually start with h1 blocker. I use the h1 like levers tourism when you have to dose it twice a day, not once a day, even though it says 24 hours, not 24 hours. And if you don’t dose it twice a day, you get breakthrough history in flares. So we use h1 blocker, we use h2 blockers. And we use first generation h1 blockers at night called key Titan and keep our different own stabilizers. My sauce at NAB is also anti histamine, so you get nighttime coverage while you’re sleeping.


And then we go on to cromolyn a lot of the time. Chroma is like quercetin, it’s a mast cell stabilizer particularly for those people with food sensitivities and food reactions. And then we go on to monta, Lucasta singular, which is for the asthma, the leukotrienes. And then there’s a whole host of other pharmaceuticals you can use if you need to, but generally speaking, we get most of the work done doing that. But you know, a lot of these very sick people, I can’t take anything, I can’t do anything. And they can’t and you’ve got to bring I have to have to come to patients move to Calgary to be stabilized. We have to get them in a neutral environment. Some of our patients have developed mold free EMF free homes where people stay.


And then they stay for three to six months. And then they get IV muscle intravenous stabilization to begin with, while they’re learning self regulation. Then we add the oral supplements and my soft stabilizers while they got IV coverage.


And we’re building a window of tolerance building self regulation, lowering the amygdala building up the fats, they all speak to the nutritionist Justin Stanger, who gets them on a paleo autoimmune, low histamine high fat diet, if tolerated sometimes some people need more carbs. A lot of people need more protein as well. Yeah, but it’s all done through a chronometer, we do the eight day chronometer, we do the freestyle libera blood sugar measurements. So we get everything regulated and try and get that system to stabilize and move them through the cell danger response which is anyway as I said, from six months to a year sometimes. Wow.


And so do people. Then after this six months to a year work is done


Do they then just go on their merry way and have a perfectly normal histamine meself stable life? Or are these people often? You know, it’s a it’s an ongoing journey. Let’s say it’s an ongoing


relationship with your body and mind. And yes, they move through the cell, they’re no longer in cell danger response. They’re not shut down.


Functional, they’re back at work, they’re off disability, they, you know, they can live a life, their brain fog is lifted, they got the concentrating, they can focus, they can have energy.


And but then they always have to be hyper vigilant for being smart. They go on holiday, they go into a moldy hotel room, they go eat buffet dressed mean, yeah. Well, the more moldy hotels are the worst and you can’t screen for those. You know, the Airbnb site does not, there’s no sniff test.


People crash all the time from those sort of exposures, you know, so they always sensitive and vulnerable, but they get super educated and, you know, not to the point of neurosis, that they’re just gonna say hyper vigilant, hypervigilant, is a bit of a of a, it’s a trigger word, right? Because we just spent all this time saying they have to wait, you know, you’re helping them to retrain themselves not to be in constant sympathetic mode. So it’s conscious hyper vigilance.


They know they walk into a hotel room and it smells musty. It’s best they probably leave. Yeah. Whereas before they try and stick it out and try and please, the spouse or something, you know? Yeah. Yeah. No, they just put their foot down, honey, I’m out of here. I don’t care what we lose our deposit. I don’t care. Yeah, yeah. Because they know, well, and by then probably their spouse or their partner knows, you know, saying that you’re trying to fight this is just impossible, it’s a world of hurt, right? You’re just you’re gonna be dealing with a partner who’s unhappy and miserable, and it is not going to be a romantic holiday, it’s just not going to happen.


We always try and make sure that the value systems of both partners are equally aligned, and that the spouse comes to the educational trainings and sessions so that they get an understanding. Because it’s very, you know, if you have an avoidant spouse, and an anxious, you know, they have different attachment styles it can lead to a disaster can lead to managers breaking up? Well, for sure, and especially in a world where, you know, a lot of a lot of this type of patient gets told by the conventional medical system, that it’s all in their head. And you know, what you said earlier, you know, go see a psychiatrist, get out of your head, and you’re gonna be fine. This is and you know, and then if you have an unsympathetic or, or a spouse who doesn’t get it, it’s a family. That’s unsupportive. Yeah, exactly, it’s gonna make the problem worse, it’s gonna make you feel worse, it’s like, it’s just going to exacerbate the situation. So you know, to bring in the partner or family member or someone as a support person who can actually get their heads around understanding what’s going on.


Not to mention, allowing the person to feel safe with someone to help co regulators sort of their creators, limbic resonance and CO regulation, which is extremely important in the beginning phases of treatment anyway, you know, while people are getting back on their feet, I mean, I can’t tell you how many people just end up crying in my office, because they say, Thank God, you know, finally, this makes sense. Yeah, I’m not crazy. You know, I can’t bear the rejection by all the help prepare, whoever is trying to do the best, but it’s just not in consensual reality. The full scope of this condition hasn’t really reached the academic institutions where it’s not taught and, and used. It’s still in its infancy. So it’s a new way of looking at things. Yeah, it is. And it’s, and do you think, do you think it was around 4050 years ago or really what you’re talking about? It’s the human body was not built to deal with this kind of crap. And it’s just awesome to be exposed. There’s no question it’s an escalating condition that’s gotten worse decade to decade. Yeah. Wow.


Okay, well, let’s think on that for a minute ladies and gentlemen, and let’s pull out our self regulating devices our brain taps and new comms and whatnots are since it’s an Apollo’s I mean there’s you know, like I mean, I’m sure you see them right the number of devices that are out there right now, and nevermind people with M casts just Joe Blow walking down the street. We know that if we can help people to get out of this constant state of of activation hanging on you know, an activation I mean, if nothing else, it shuts down our immune system. It shifts to th one th


You balance goes through the roof. Yeah, yeah. No, we live in very challenging times. And we can’t take our, you know, we can’t take resilience for granted anymore, let alone all the political changes and all the cultural adjustments and let’s, let’s not, let’s forget this stuff go. Yeah, no, we can’t even go there. No. And I mean, you know, at this stage of the game, I think people are left in one of two camps, you’ve got the camp, that’s like taking up arms and saying, you know, we have to do something about this, and they’re taking it on. And, you know, we need definitely, we need people taking on whatever system is broken and trying to fix it. And then you get other people who are just kind of like keeping their heads down and going, you know, I’m just gonna keep doing what I’m doing over here and hope it goes away. But even for that person, and for both camps, the idea of self regulation, the idea of building it, and what you said it perfectly building resilience in your system, so that you can deal with, with the the incoming all the time, and it doesn’t directly affect you. And building sanctuaries, you know, finding a space that, you know, when you sleep at night, you know, bombarded by your router that you know, the amplifier that’s under your pillow, or, you know, the dirty electricity from your switch, we send building biologists into every patient’s home to measure electrical fields, magnetic fields, radio frequencies, and dirty electricity, because people with my cell activation, which by the way,


electromagnetic fields amplify mold exposure dramatically. Yeah, they have to create sanctuaries, they have to eat impeccably, they have to sleep and you know, they had to create, often they have to create Faraday cages with silver nets, and, and they have to turn off the electricity to the beds, bedside lights and turn off the routers or have kill switches to their routers. And it’s not neurotic. It’s just makes sense. Smart. It’s just smart. I mean, having it you know, we’re I’m moving into, like, I live in a very old house. And so we’re, you know, I’ve been kicking and screaming because my husband decided, you know, almost unilaterally, we’re downsizing. We’re leaving this house. And I’m like, No, I like my house, I don’t want to go. And meanwhile, I’m sitting here thinking, and if he listens to this episode, he’s going to come over, and he’s going to be seriously, you said that. And, and, but we’re moving into a home that was built 16 years ago. And these, I now I’m gonna have a lot more options in terms of what I can and cannot do in this, like in this house. We’re lucky to have electricity in that house, there will be a breaker that’s associated with the room. But I can tell that it’s not a smart home was rigged up to me. It’s not. No, it’s not. It’s not that. I mean, and you know, it’s interesting, right? Smart Homes, electric vehicles.


All of this, like somebody who I think we went, Oh, yeah, we went in to get buy a dishwasher and a washing machine and a dryer. And they’re like, Oh, guess what, you can get these smart electronics, and you can program it from the car. And I’m like, why would I even want to do that? Like, why would I want to bring more of this into my life? I don’t need to tell my dishwasher to turn on when I’m in the car. I can turn it on when I get home. That’s what buttons are.


I do believe that we will evolutionary adjust to the incoming toxic load and develop some resilience in our genetic machinery.


I like that line of thinking, Yeah, I don’t think we’re doomed to sort of be extinct because of the incoming toxic load. I mean, even yes, we’ve had periods of extinction. But there’s a sort of, you know, that whenever we support whenever we challenge, there’s always an adjustment that we make, and we develop genetic mutations. Unfortunately, it is, you know, the strong survive and the weak guy really does amount to that, in the end, the ones who have resilience, good gene pools, you know, they stay healthy, and they they survive better longer. But we do have to adjust a whole new mental healthcare model of well being as opposed to disease can rise to the host shifting consciousness and an awareness of environmental toxins and all these things. It will come it’ll come. Yeah, no, I agree with you. And I do think that there’ll be and your I’ve heard it from a couple of people, this whole idea of, you know, eventually nonnative EMFs acting as a hormetic stressor, as long as you’re not one of these electrically sensitive people. If we have healthier membranes, if we’re eating better foods, if we’re, you know, if we’re taking care of all those other things, and limit the toxins, all those toxins, whether it’s stress or EMF or food


and just give ourselves more buffer, human beings have value systems, you know, we have relationships we have


have social connections, we have health and well being. We have mental health education, we have careers, and we have the making of money. And then we have our spiritual calling what we meant to do, we have to raise health as a very dominant value across the board. We cannot take your absence of disease. Forget about that’s not health. No, yeah, we know that. So when you know, people come and see me for wellness, medicine, you open the hood, and they just rife with all sorts of metabolic imbalances, you know.


So yeah, so we’ve got to emphasize healthcare. And we emphasize food and emphasize nutrition and stress response and sleep and exercise and flexibility and movement, that must become the new model that we will work towards the disease care model has had its day. And we don’t want it to go away, because we still want a day when we get diseases. But we’ve got to replace it with a whole new paradigm that’s has equal clout and validity and consensual reality. And it’s not, you know, oh, those hippies over there, they know, this is real, this, we’ve got to raise health as a value system and make it stand alongside disease care. Well, and I think to do that, effectively, it has to it even has to be taught in schools, like it needs to be woven through the very fabric, like little kids, like a man, you know, like I’ve and I know this one, I’ve worked with families as a nutritionist, and when the little kids get on board, and they are like the Secret Service, these kids are relentless. Like when you get them on side, nobody gets destroyed. And they’re awesome. But they have to be empowered and taught and, and given the tools. And the next wave was, you know, this whole Surgeon General of the United States issued some thing two days ago saying the exposure to social media electromagnetics is definitely impeding children’s mental health and well being. It’s, you know, it’s gaining momentum, because lobbyists are fighting against all of it. So it’s a very, it’s a big struggle,


maybe a century to evolve into a new paradigm. But yeah, it will eventually get there. Yeah. And it comes down to the individuals, right. I think different parents, it’s up to parents to make, make different choices for their kids not buy them a cell phone when therefore. And you know, those things, but it’s going to be a process and but there’s hope, right? I mean, that’s the good news. And the good news is that, you know, for people with M casts,


there’s a sense of desperation until they come across people like you, doctors, like you who, you know, it’s not like you have all the answers, but you sure have figured out a bunch of it, and you can help them to get to a place a better place. Yeah, absolutely. Yeah. This patient I saw this morning had no clue she had pots, not only she had pots, she has a misoperation for foods and reacting to angioedema, urticaria reactionary said, Are you dizzy when you stand up? Yes, I think I have pots. As I was told some time ago, I had pots. She did a blood pressure she had like pots, like the worst case I’ve seen in a long time. And she just started putting more salt in water in her diet, and she’s feeling 50% Better, just one little thing. Now pots isn’t well recognized. Either. We don’t use that, well. 10. There you go. For a tilt table, you don’t need a tilt table test. You just do 10 minutes of your blood pressure lying down. You lie down for three minutes, take your blood pressure pulse stand up for one minute. Take it again with the Omron you know, three minutes, five minutes, 10 minute. If your pulse rate goes up over 30 beats per minute over there 10 minutes, or over 120 At any given time. You got Putz? Really? Yeah, oh, if your systolic blood pressure drops more than 20 You’ve got orthostatic hypotension. If you don’t treat that you won’t fix your muscle activation.


So pots comes right up front and center. And is that because it sends a stress signal to the nervous system like shits about to go bad? And therefore that puts you in that fight or flight? Like it drives anxiety? Virtually right? Anxiety it drives it’s better if you don’t perfuse your mitochondria and you or your brain because then there’d be that Yeah.


You get hypoxia hypovolemia you feel awful.


And they walk around sort of dizzy and can’t stand up and feeling faint and palpitations and pots is ubiquitous, especially amongst that phenotype I mentioned. Yeah, yeah.


Okay, well, we’ve covered a lot of ground sir


Yeah, it’s, I love what I do. And it’s very pleasant when you finally can help a person put some foot on the ground and stabilize the imbalances and provide insight that my colleagues in traditional medicine, having come from medical school, we just don’t learn this, you know, postgraduate exposure and interests of mine. That’s why I know it, but I was gonna say what sent you down this path? Like, how did you get here? Because, uh, you’re, you’re classically trained MD, like, you’re you went to med school.


I was interested in as a young boy and what? How did people become the most evolved? They could possibly be? So I was always curious from a very young age. What does it take to become self? actualized?


Young age? All right. You’ve been around a few for a while. Okay. I read your um, and I read about individuation self. And then I got exposed to Indian, you know, philosophies and things. So when I became an MD, I was like, these people are presented with all these senses. But who are they really? And who do they wish to become? So then I started to just just examine everything that could possibly help a person self actualizing become who they meant to be. And that led to every single, you know, ology in the book, I got to go study everything I still study. I just came back last night from Ozone conference learning.


Yeah, ozone is a very interesting, very interesting area, especially when you’re trying to, you know, reduce toxic load and a person and treat mitochondrial issues. Yeah, yeah. Yeah, I have that podcast, and you have to


stay curious. You just stay, you know, close to the end, you listen to your patients? Yeah. Well, I mean, you know, you said one thing earlier that not a lot of I mean, that, you know, in the conventional system, there’s no space allowed for this anymore. And it’s that whole, taking down medical history with the patient. And, and, and that can that takes time. But the person taking the history has to be exposed to a very wide range, there has to be a new curriculum of, of healer, who gets exposed to a very wide range of ologies and sciences and methodologies. So that when they sitting in front of a patient, they can go up and down layers and levels of healing, not just work with biochemistry and mechanistic medicine. They know if there’s inherited trauma, if there’s early defense structures, if there’s, you know, they can tell just by taking the history, that the diagnostic pellet has to be very broad. Yeah, don’t be trained in n squared d squared medical school only, they have to be curious about the human condition. Yeah. And they have a curriculum that’s exposes them to some of the core tenants of the of what it takes to diagnose and treat a complex patient. Maybe your next job, she needs to be like starting a new med school or some kind. I’ve written my book is the new curriculum I’ve written again, you have, yeah, I should have that book published. Well, when it’s published.


Okay, at some point, you’re just gonna have to put your pen down and send it off to the publisher. And you can always do a version two, or an addendum.


But as I sit down on a Friday night to start a chapter for revision, and then I get, you know, a new podcast to listen to or something. Yeah, no, yeah, yeah. Okay, you know what, you’re just gonna have to give us what you got. And then you can always just give us more.


For an idea, no, I’ve written this book, the new curriculum, seven stages to health and transformation, a new medical curriculum. And that is the title of the book. It’s based on the layers and levels of healing, and how you need to amplify your diagnostic and therapeutic template. And I do wish to eventually have people fill in all the gaps of all the layers and levels that are created, and then create a new curriculum for a new healer, or a new a new way of approaching complex illness. Yeah, well, I think that’s brilliant. You just, you know, the way to get the ball rolling, though, is to put that book out.


I’ve done small versions of it. All right, whatever.


chapter by chapter, if you have to whatever.


All right. Well, Dr. Hoffman, I thank you so much for today. Is there anything else that you’d like to leave the audience with? I mean, you’ve you’ve dropped a lot of wisdom on us, but yeah, anything else? I just, I just, you know, I don’t know if there’s anything else to say but don’t. If you’ve read for patients, or anybody who’s hearing if you don’t be tempted to find the latest diagnosis, the mole the heavy metal, just be careful of that. It’s usually that plus 50 other things. That’s number one. Number two, you your body is the final resting place.


Not only of your own experiences, but your ancestral experience as well. So it may not have started with you, which is the title of one of my friends bookmark Walden, who did family work. So it may not be what you think it is. And there may be a complexity that you haven’t even imagined. And don’t lose hope, because you will find the heat up. If you stay curious and you stay open, you will eventually, hopefully, meet up with somebody who can assist you on your transition path, you know.


And so in the meantime, you may have to deal with an you know, somebody who’s got a little piece of the puzzle, hopefully, over time, you can expand and meet people who got a bigger piece of the puzzle, who can see the whole you and institute a whole person healing, not just parts are not just SIBO, or not just Lyme, you know, you really, really need to have a very broad diagnostic palate, when we’re sitting in front of a person and listening listening to what they’re trying to tell you. Yeah, yeah. Well, I actually interviewed a practitioner last year. And she said, you know, almost without fail, the patient has the answer. Did you have the lucky. They know, like, they know everything changed when or things have never been the same since or they it’s just the taking the time to like, in her case that you know, she had one patient, she wasn’t getting anywhere with her. She went back to her pages and pages and pages of notes and came across this one thing and said, Oh, I missed that goes back, talk to the patient. And boom, it turned out to be a turning point for for the practitioner and for the patient. And patients are very educated. Now. They all have a Google and whatnot. And they will come in and say oh, have you thought of this? Have you thought of that? What about this? And nine times out of 10 day in suggestions are completely spot on. Interesting. Interesting. Body, right. Oh, I gotta talk today. I have a salt supplement for parts that I hadn’t heard of. So I go look it up quick. Yeah, he was right. Is that is a better option. The one I was using. There you go. And there’s people making stuff all the time. Right. So there’s always something new.


All right. Well, Dr. Hoffman, where can people find you Ben? When Calgary, Calgary. So Hoffman center. Your website is Hoffman center.com.


Oh, come on.


I think if you Google happened center, it comes up. The title is Hopkins Center for functional and integrative medicine, but I don’t think you have to put that in. It’s just open center. Okay. Perfect.


in Calgary, Alberta. This is in Canada, folks. No, this is not a US doctor with this is one of our own in Canada. Very proud of him. So thank you so much for your time and for sharing and we’re looking forward to the book when you decide to share it with the rest of us. Get it out for sure. Thanks. Thank you. Thank you. Okay, bye bye. Thanks so much for joining me on this episode of The biohacking superhuman performance podcast. If you enjoyed the show, please remember to leave us a five star review on iTunes, because that’s what helps us to be heard and to be seen. If you’d like to connect with me directly. Or if you’d like to leave any comments or if you have any questions about this episode, please reach out to me directly through my website, Matt agnitum.com. And of course, if you’re not already a member of the biohacking to superhuman performance community on Facebook, that’s where you’ll find me every day. It’s a short application, just answered a couple of questions and you’re in and interfacing with other amazing biohackers thanks again, and we’ll look forward to seeing you on the next episode.

Postural Orthostatic Tachycardia Syndrome (POTS) Part I

Postural Orthostatic Tachycardia Syndrome (POTS) Part I

Many people suffer from what is termed dysautonomia. This is an umbrella term used to describe any disease or malfunctioning of the autonomic nervous system. Our nervous systems are comprised of different parts:

  • a central nervous system (CNS),
  • a peripheral nervous system (PNS)
  • an autonomic nervous system (ANS).
Nervous system diagram

The autonomic nervous system is the part of the system that’s responsible for master regulation of organ function and thus the control of the bodily functions that aren’t consciously directed, such as breathing, the heartbeat, temperature regulation, and the digestive processes.

Dysautonomia is a full body condition, affecting the malfunctioning of many or all of the organs under the body’s control. Due to multiorgan system involvement, patients often present with numerous, seemingly unrelated, maladies. Dysautonomia has this feature in common with MCAS. Patients are often consulting a variety of doctors, each specializing in a different organ system, none of whom view the symptom presentation as a whole-body system involvement.

Dysautonomia is quite common and can include conditions such as vasovagal syncope, sinus tachycardia, orthostatic hypotension, diabetic autonomic neuropathy, neurocardiogenic syncope (NCS), mitral valve prolapse dysautonomia, and postural orthostatic tachycardia syndrome (POTS), the subject of today’s essay.

Simply put, POTS is the body’s inability to make the necessary adjustments to counteract gravity when standing up.

Dysautonomia is often associated with other disease processes such as Lyme disease, primary biliary cirrhosis, multiple system atrophy (Shy-Drager syndrome), Ehlers-Danlos syndrome, and Marfan syndrome.

POTS isn’t a rare condition but often isn’t considered, understood, or accurately diagnosed by primary healthcare providers. Most doctors don’t routinely think about it or test for the condition in their offices. A missed diagnosis of POTS (as well as that of orthostatic hypotension) can have devastating consequences for an individual’s health issues and prospects of recovery. In fact, my experience is that without recognition and adequate treatment of this condition, very little can be achieved regarding recovery for those suffering from complex, chronic health issues, where POTS is frequently a dominant co-morbid condition that’s notoriously underdiagnosed. This condition is often accompanied by a high degree of functional disability, appearing under the radar and masquerading as many other health conditions, most commonly referred to as psychosomatic, a cruel diagnosis to assign to a person that has very real biological and physiological imbalances.

POTS was first described in the 1860s and initially named Civil War Syndrome and Effort Syndrome, among other names.[i] It was also often called neurasthenia. Prevalence is estimated to be at around 0.3 percent of the U.S. population, affecting around three million people. However, within the population with chronic, complex illness that present themselves at my clinic, the prevalence is much higher, approaching ten to twenty percent. The condition is most often diagnosed in younger females, with onset occurring between fifteen and forty-five years of age.[ii]

POTS is a complex condition that can drastically affect the day-to-day lives of those that suffer from it. POTS is a type of orthostatic intolerance, which means that it gets worse when people who have the condition are standing, or when they move from a lying or sitting position to a standing position.

The two broad classifications for POTS are for those individuals who have the condition all the time (non-positional), and those who have it only with positional changes.[iii]  

One of the main characteristics of the condition is that the main focus is on the sympathetic nervous system activation, which characterizes the disorder.[iv] In emergency rooms and primary care clinics, it’s one of the most common presentations of syncope and pre-syncope. This refers to the patient feeling faint, but not quite passing out.

POTS is often described as a clinical syndrome consisting of multiple heterogeneous disorders. In addition, there are several possible underlying pathophysiological processes underlying the condition, including partial sympathetic neuropathy, hyperadrenergic state, hypovolemia, mast cell activation, deconditioning, and immune-mediated.[v] Many clinical features may overlap, making it difficult to categorize exactly what aspects are activated at any particular time. The good news is that although POTS may be extremely unpleasant to live with, limiting many activities associated with daily living, POTS isn’t associated with mortality. Patients can make significant symptomatic improvements over time, once the condition has been diagnosed and treated appropriately.

In addition to POTS, there are other conditions of orthostatic intolerance, like orthostatic hypotension. These conditions are also frequently seen with other ‘invisible’ conditions, such as Ehlers-Danlos syndrome, chronic fatigue syndrome, migraine, fibromyalgia, autoimmune disorders, irritable bowel syndrome (IBS), food allergies, and mast cell activation syndrome (MCAS). Please see my other articles related to MCAS.

In this two-part series, I’ll be discussing the etiology of POTS, how it manifests in most people, the common comorbid conditions it’s often seen with, and how to diagnose and treat the condition.

In this first part you’ll learn:

  • What POTS is and its signs, symptoms, and complications
  • The difference between POTS, orthostatic hypotension, and sinus tachycardia syndrome
  • How POTS often manifests alongside other conditions, like MCAS and CFS
  • What we currently understand about the cause of POTS
  • How POTS is diagnosed

What is POTS?

As I already mentioned, POTS is a type of orthostatic intolerance. This means that it gets worse when people with the condition are in a standing position or when they get up from a lying or seated position.

With POTS, the heart rate increases rapidly when standing, by at least an additional thirty beats per minute compared to sitting, or up to 120 beats per minute within ten minutes. Tachycardia is the medical term for an increased heart rate.[vi]

The strict criteria for making the diagnosis are as follows:

  • Symptoms must be for greater than or equal to six months in the absence of offending medication (SNRIs) and a thorough workup must be undertaken to exclude other conditions that can mimic POTS, such as Addison’s Disease, vasovagal syncope, physical deconditioning
  • Heart rate increase within ten minutes of standing that’s greater than or equal to thirty beats per minute for adults older than eighteen, sustained; greater than or equal to forty beats per minute for adolescents, aged eighteen or younger; or  greater than 120 beats per minute after eight minutes of standing
  • No orthostatic hypotension, featuring a drop in blood pressure of 20 mm Hg systolic or 10 mm Hg diastolic within five minutes of standing
  • Symptoms such as presyncope, dizziness, lightheadedness, palpitations, tremor, or nausea, any of which are exacerbated with standing and relieved when recumbent
  • No other overt causes of orthostatic symptoms or tachycardia can be identified, including panic attacks, pain, exercise, caffeine consumption, medication effects, anemia, dehydration, hyperthyroidism
  • Resolution or improvement of signs or symptoms with assuming a lying  or seated position
  • Standing plasma norepinephrine greater than or equal to 600 pg/ml (greater than or equal to 3.5 nM)

The pathophysiology pf POTS is complex but it appears to revolve around three central mechanisms:

  • A predilection for hypovolemia or low blood volume
  • Partial autonomic neuropathy, causing damage to the autonomic nervous system
  • A hyperadrenergic state, in which the stress neurotransmitters adrenaline and noradrenaline increase [vii]

For a diagnosis of POTS to be made, the increased pulse rate must be sustained for longer than ten minutes, sometimes noted to be increased for up to thirty minutes. Many people will have a transient increase in pulse rate within forty-five seconds of standing, but it isn’t sustained and is often associated with a transient drop of blood pressure, which indicates a variant of orthostatic hypotension. Many patients with POTS will also have orthostatic hypotension, especially if associated with hypovolemia. However, if the increased pulse rate is less than thirty beats from baseline and is only associated with a drop in blood pressure, then this isn’t considered to constitute a diagnosis of POTS. Furthermore, in order to consider a diagnosis of POTS, the symptoms must be chronic in nature. Many people will experience transient POTS-like symptoms such as with a viral infection, which often resolve in a few days. Sometimes POTS may even be accompanied by a small rise in systolic blood pressure.   

Tachycardia is thought to occur because of the pooling of blood below the heart. In response to this pooling, the body releases norepinephrine and epinephrine in order to constrict the peripheral blood vessels and send blood pumping throughout the body again. However, in POTS and other orthostatic conditions, the vessels don’t respond properly to this increase of epinephrine and norepinephrine, so the blood vessels don’t constrict and blood remains pooled below the heart.

However, in POTS specifically, the heart still has a normal reaction to the norepinephrine and epinephrine, although the peripheral vessels don’t constrict appropriately and so the heartbeat quickens.[viii] Patients with POTS will often have high upright levels of plasma norepinephrine, reflecting sympathetic nervous system activation. In addition, some patients may have a dramatic response to eating food, whereby they can experience debilitating fatigue postprandial. This occurs because in the process of digesting a meal, a large amount of blood is diverted away from other areas of the body to the gastrointestinal tract, depriving the brain and the peripheral mitochondria of blood flow and hence energy, in order to run the rest of the individual’s physiology.  

There are four types of POTS:[ix]

Neuropathic/vagal tone dysfunction

This type of POTS may be caused by nerve damage that interferes with the blood vessels’ ability to constrict, as well as resulting from poor parasympathetic vagal tone and low levels of the neurotransmitter acetylcholine.

Hyperadrenergic/sympathetic fight/flight overdrive

This is POTS that’s associated with high levels of sympathetic nervous system overdrive and the production of adrenaline and norepinephrine.


This type of POTS occurs as a result of low blood volume. This has often been found to be associated with physical deconditioning.[x] It can also be associated with significant upright GI symptoms.


This type of POTS is caused by another disease, like diabetes or Lyme disease.

It’s also important to note that POTS doesn’t usually occur as a result of any physical malformations of the blood vessels or heart, but rather as a result of functional abnormalities.

POTS is most commonly seen in women between the ages of fifteen and forty-five years old, mostly during child bearing years, and is thought to be widely prevalent. However, the exact statistics regarding the prevalence of the condition in the United States and Canada aren’t known because it’s likely that many people with POTS are misdiagnosed or undiagnosed.[xi] A family history is reported in thirteen percent of patients.[xii]

Signs and symptoms

Some of the signs and symptoms of POTS include:[xiii]

  • Increased heart rate when standing, particularly after ten minutes
  • Lightheadedness, dizziness, or vertigo caused by a lack of blood flow to the brain as blood pools in the lower portion of the body. This can lead to nausea, vomiting, and even fainting.
  • Excessive fatigue after standing or light activity, which may be extreme
  • Exercise intolerance and/or post exertional fatigue
  • Diminished concentration and brain ‘fog’ or mental clouding
  • Noticeable heart palpitations or forceful heartbeats
  • Headaches
  • Sleep disturbances
  • Feelings of anxiety and panic, but ones that aren’t mentally induced. This is a very important distinction to be aware of.
  • Shortness of breath and chest pains
  • Unsteadiness, shakiness, or tremulousness
  • Clammy skin
  • Facial flushing and acid reflux
  • Dark, red-blue discolorations of the lower extremities that are cold to the touch, known as acrocyanosis. This feature is seen in up to fifty percent of patients.[xiv]
  • The vast majority of POTS patients, greater than or equal to ninety percent, have at least one gastrointestinal symptom, with the most common being nausea, abdominal pain, and bloating.[xv] Nausea and vomiting may represent the more common upright GI symptom of POTS and may improve altogether in the supine position.[xvi]

These symptoms don’t typically occur when a person is sitting or lying down, but they can be triggered by standing, exercise, stressful events, or warm environments. Approximately a quarter of blood volume resides in the chest when in the supine position. Upon standing and due to the effects of gravity, there’s an immediate shift of 500 to 1000 ml of blood from the chest cavity to the vessels in the lower extremities, buttocks, and lower abdomen. This leads to impaired venous blood return to the heart, with a resultant drop in blood pressure. There’s also a ten to twenty-five percent shift of plasma volume out of the vasculature and into the interstitial tissue.

When you stand up, gravity causes blood flow to be pulled downwards. For someone with poor parasympathetic vagus nerve injury with low acetylcholine production, this shift decreases venous return to the heart. This in turn results in a transient decrease in both arterial pressure and cardiac filling, reduced blood flow to the head, and an increased pooling of blood in the lower part of the body.

One of the consequences of blood pooling in the venous system is that it struggles to fill the heart. If the system fails to do this, the heart tries to compensate by increasing its heart rate to keep up the cardiac output. However, it usually still fails because if the blood isn’t there to fill the heart, the cardiac output is still going to drop, no matter how fast the heart goes.

In a healthy person, the autonomic nervous system compensates for these hemodynamic changes by stimulating the sympathetic (fight/flight) nervous system to release adrenaline to vasoconstrict the peripheral blood vessels, speed up the heart rate, and suppress the parasympathetic (rest/digest) nervous system. This facilitates an increased return of blood flow to the heart to counteract the initial decline in blood pressure. If the dynamics are working properly, these compensatory changes result in negligible changes in systolic and diastolic blood pressures with a normal ten to twenty beats per minute increase in the pulse rate when standing and a 5 mm Hg increase in diastolic blood pressure.

However, as with POTS, if there are any abnormalities of the autonomic nervous system’s regulation of these hemodynamics, a resultant fall in blood pressure can occur, as well as the increased pulse rate as seen in POTS. 

The body then tries to compensate for that as best it can by revving up the sympathetic nervous system, secreting a significant amount of adrenaline and noradrenaline. The consequence of these adrenaline surges is a lot of anxiety, a racing heart, heart palpitations, and insomnia. These are the consequences of compensatory sympathetic overdrive.

As already mentioned, POTS symptoms may also be triggered after eating. This is because blood flow is redirected to the digestive tract, or if a person with POTS isn’t drinking enough fluid or getting enough salt in their diet.[xvii]

GI motility abnormalities appear to be a significant driver of POTS symptoms in both the orthostatic and the non-positional types of the condition. Many studies using combined 24-hour antroduodenal manometry (ADM), the study of stomach and small bowel motility, and TILT (TTT) table testing, have proven this association.[xviii] Even among patients whose gastric motility studies were normal at baseline, sixty-eight percent became abnormal during the TTT. Gastrointestinal symptoms of nausea/vomiting and abdominal pain were reproduced in eighty-nine percent of subjects during TTT. Vomiting was significantly more frequent in those with delayed gastric emptying, which is defined as greater than or equal to a ten percent retention of food in the stomach at four hours post ingestion. 

Interestingly, women with POTS often report that they feel better than ever when they’re pregnant. This is because there’s a natural increase in blood volume during pregnancy, which helps to ease their symptoms. However, women who aren’t pregnant may experience a worsening of their POTS symptoms when their menstrual cycle begins.[xix]

Symptoms may also be worsened by dehydration, exercise, alcohol intake, heat exposure, asthma, allergies, endometriosis and pelvic congestion syndrome in women, migraines, depression, anxiety, concussions, and sinusitis. However, there are many other conditions that aren’t listed here that may make the symptoms of POTS worse.[xx]


POTS may seem like a minor issue if you’ve never dealt with it before, but that’s actually far from the reality faced by those suffering from POTS. The condition can be profoundly impactful, severely interrupting the lives of people with POTS. Consider how your life would change if you couldn’t stand for more than ten minutes or spend any amount of time in hot weather. There would be no waiting in line, no walking your dog or walking around the block, no shopping, and no sports. Even attempting to take a vacation would be a significant challenge. Or what if merely eating a meal was enough to leave you fatigued for the rest of the day?[xxi]

For people with severe POTS, their quality of life can be seriously affected. In fact, some physicians have compared the level of disability accompanying POTS to that of chronic obstructive pulmonary disease (COPD), an obstructive airway disease that limits breathing and can deprive the body of oxygen. Additionally, some researchers have surmised that the quality of life of people with severe POTS is approximately the same as the quality of life of people with kidney failure who are on dialysis.[xxii]

POTS and other conditions

POTS and other conditions are often seen together in patients. Because POTS isn’t a disease itself, it doesn’t typically develop in the absence of any other diseases, conditions, or health factors. There’s always a causal factor, be it genetics, another condition or disease, or an illness or injury trigger.

POTS compared to orthostatic hypotension and sinus tachycardia syndrome

POTS isn’t the only orthostatic intolerance condition. Orthostatic hypotension and sinus tachycardia syndrome, while similar to POTS, are different conditions. Although these conditions are similar to POTS, with similar signs and symptoms, they’re not identical.

Orthostatic hypotension is characterized by a decline in blood pressure of more than 20 m (systolic) /10 (diastolic) mmHg while standing rather than an increase in heart rate.[xxiii] This condition usually results from autonomic failure and the changes are often far greater than those mentioned above, resulting in a temporarily loss of consciousness soon after standing.

Sinus tachycardia syndrome is when your body sends out electrical impulses that cause your heart to beat faster, typically at rest, but without cause. It’s normal for your body to send out these impulses in response to exercise, stress, or fever, but abnormal for these electrical signals to occur in the absence of these external triggers.[xxiv]

POTS and mast cell activation syndrome (MCAS)

In some people, POTS and mast cell activation syndrome are seen together. This is fairly common for people with hyperadrenergic POTS. These patients often exhibit severe flushing or redness during standing, along with an increased heart rate, diarrhea, abdominal cramping, and nausea.

Mast cells are a type of white cell representing one percent of the total white cell count. They’re found in all vascularized tissue throughout the body at the junction point of the host and the external environment at points of entry of a toxin or antigen. They’re particularly represented in the mucosal and the epithelial cells, such as those in the respiratory tract, the skin, and in the GI tract, particularly in the duodenum. These cells are involved in defending the host from incoming toxins of any kind.

MCAS is an abnormal activation of the mast cells, which when activated on mast cell receptors by triggers, of which there are many, degranulate and release into the extracellular matrix potent mediators of inflammation, anticoagulation, and vasodilatation such as histamine and tryptase, heparin, proteases, enzymes, prostaglandins, eicosanoids, cytokines, growth factors, and reactive oxygen species, otherwise known as ‘free radicals’. In many cases where histamine is involved, it can cause a response similar to an allergic reaction. In severe cases, people with MCAS are considered to be ‘allergic to everything’. Mast cells seem to degranulate more severely when a patient is upright with hypotension and tachycardia.[xxv]

In addition to all the standard POTS symptoms, those with MCAS may also have gastrointestinal symptoms. The following paragraph explains how MCAS can result in GI symptoms, skin reactions, hives, and angioedema, often seen as accompanying conditions with those suffering from POTS.

When the gastrointestinal tract is exposed to an antigen, its response is to increase fluid secretion, increase smooth muscle contraction, and increase peristalsis. Proteins derived from different plants and animals can act as antigens and activate the immune system in vulnerable subjects. The antigen (peptide) permeates through the epithelial layer of the mucosa of the gut and binds to IgE on mucosal mast cells. These peptides are presented to Th2 cells, and if there is an IgE antibody against the peptide present, it will cause activation of the mast cell resulting in an immune response. This causes mast cells to degranulate and release a variety of inflammatory mediators. These mediators increase vascular permeability, causing edema in the gut epithelium and smooth muscle contraction, which lead to vomiting and diarrhea. This type of reaction can occur in response to peptides found in certain medications. Food allergens can also cause skin reactions. Uptake from the gastrointestinal tract can introduce antigens into the blood, which are transported throughout the body where they bind to IgE on mast cells in the connective tissue in the deep layers of the skin. This results in urticarial reaction and angioedema. [xxvi]

Researchers are still studying how exactly POTS and MCAS interact with one another, along with whether one causes the other or if they might occur side-by-side in response to some other type of trigger, such as mitochondrial dysfunction. It’s been speculated that chronic exposure to prostaglandins and histamines affect the connective tissue and vasculature in the GI tract, resulting in conditions such as chronic constipation. Whenever a patient is seen with chronic GI symptoms, POTS, and MCAS, it’s imperative that the pathologist restain the GI tract biopsy specimens for CD 117 cells, which is a sure way to quantify the number of mast cells seen per high-power field in the biopsy specimen. If more than twenty mast cells are seen in a specimen stained in this way, it’s a clear indication that the person is suffering from MCAS. My blogs on MCAS provide a more detailed explanation regarding this. It has been referenced that an estimated nine percent of POTS patients have MCAS,[xxvii] although in my clinical experience it’s more like fifty percent. Avoiding certain food and gut bacterial antigen triggers can have a dramatic effect on reducing these symptoms. Please see the recent paper published by Dr. Afrin, with myself and others as co-authors, on the Consensus-2 criteria for the diagnosis of MCAS, entitled Diagnosis of mast cell activation syndrome: a global “consensus-2”[xxviii]

Formal diagnosis of MCAS requires fulfilling the major criteria, which is having characteristics of mast cell activation symptoms in two or more systems, along with one minor criteria.[xxix] Minor criteria include have more than twenty mast cells per high-powered field using the CD 117 immunohistochemical staining from a specimen collected from the second part of the duodenum, having an elevated number of mast cells mediators in the blood or urine, or document of improvement of symptoms with mast cell stabilizers.[xxx]

Other conditions often seen with POTS

In addition to MCAS, several other conditions may be present with POTS.

Chronic fatigue syndrome

POTS can lead to extreme fatigue, and people with POTS report poorer quality of sleep. CFS is commonly noted alongside POTS for these reasons. In fact, people who have been diagnosed with CFS and people who have been diagnosed with POTS tend to have similar symptoms when standing, leading some researchers to conclude that CFS may be part of the clinical presentation of POTS.[xxxi]

Ehlers-Danlos syndrome

Ehlers-Danlos syndromes are a group of inheritable connective tissue disorders characterized by joint hypermobility, skin hyperextensibility and tissue fragility with an incidence of 1 in 500. [xxxii] Joint Hypermobility Syndrome (JHS), synonymous with Ehlers-Danlos Hypermobile Type, formerly Type III (hEDS III), is the most commonly seen subset involving hypermobility of the musculoskeletal system and is associated with abnormal collagen formation and autonomic nervous systems abnormalities. Please see the paper entitled Neurovisceral phenotypes in the expression of psychiatric symptoms[xxxiii]for a table outlining the criteria for making diagnosis of JHS/EDSIII.

People with EDS often have symptoms of orthostatic intolerance, including POTS. Their symptoms can also be exacerbated by physical activity, eating, standing, and warm environments. According to one study, eighteen to twenty-five percent of POTS patients also meet the criteria for an EDS diagnosis, EDS-type III, characterized by hypermobility, is the most common condition that’s associated with POTS. The vast majority of hEDS patients also have gastrointestinal symptoms and if seen together with POTS, these symptoms are amplified. GI conditions such as irritable bowel syndrome (IBS), functional constipation, and GERD are prevalent in forty-eight, thirty-six, and seventy-eight percent respectively.[xxxiv]

There are various theories regarding why hEDS and the manifestation of GI symptoms, ranging from connective tissue abnormalities, lead to laxity increase in the GI tract with resultant mechanical dysfunction and altered motility. In addition, it’s known that neuronal development in the enteric nervous system is dependent on normal collagen formation.

Patients with concomitant POTS and hEDS were younger in age and had a higher prevalence of chronic fatigue syndrome, fibromyalgia, and depression. Symptoms such as functional dyspepsia, chronic nausea and vomiting syndrome, functional heartburn, dysphagia, fecal incontinence, and levator ani syndrome were all higher in the hEDS-POTS cohort.[xxxv]

Other conditions that have been associated with joint hypermobility include ADHD, anxiety, asthma, carpal tunnel syndrome, chiari malformation type I, chronic fatigue syndrome, chronic regional pain syndromes, Crohns disease, hiatus hernia, mitral valve prolapse, migraine, headaches, pelvic organ prolapse, rectal evacuatory dysfunction, and urinary stress incontinence.[xxxvi]

Median Arcuate Ligament syndrome (MALS). Median arcuate ligament syndrome (MALS) occurs when the arc-shaped band of tissue in the chest area, known as the median arcuate ligament, presses on the artery that sends blood to the upper abdomen. The artery is called the celiac artery. MALS can cause stomach pain in some people.[xxxvii]

Vasovagal syncope is a disorder characterized by sudden, sharp declines in blood pressure that lead to fainting episodes. Although POTS is primarily characterized by heart rate increases, people with POTS may also have vasovagal syncope or orthostatic hypotension, which can also lead to fainting.[xxxviii]

Fibromyalgia is a condition that’s characterized by muscle pain of an unknown cause. Like CFS, it’s commonly seen in people with orthostatic intolerance conditions, like POTS. Researchers theorize that POTS with fibromyalgia may be caused by neuroinflammation, which can occur after a triggering event like a viral infection.[xxxix]

Other conditions include migraine headaches, celiac disease and/or gluten sensitivity, gastroesophageal disease, and peptic ulcer disease. An ever-increasing number of COVID-19 patients are also now seen to have symptoms suggestive of POTS[xl]

Recently, a group of physicians have observed a strong relationship between Hypermobile Ehlers-Danlos Syndrome, Postural Orthostatic Tachycardia, and Mast Cell Activation syndrome, naming this as the triad of conditions. If further autoimmune conditions and gastric motility issues were noted, this has been referred to as a pentad of conditions. Dr Andrew Maxwell has an excellent PowerPoint describing these associated conditions.

Causes of POTS

POTS isn’t a disease itself, but rather a cluster of symptoms. It can be caused by any manner of other conditions, and may even be caused by genetics or trauma. Here are some of the many potential causes of POTS:[xli]

  • Genetic factors
  • Infection (most common) or other infectious illnesses – seen after Epstein-Barr virus, influenza and Borrelia burgdorferi infections[xlii]
  • Physical trauma
  • Autoimmune disorders, such as Type 1 diabetes
  • Surgery
  • Pregnancy
  • Exposure to chemicals
  • Degenerative neurological conditions, such as Parkinson’s disease and Multiple Systems Atrophy (MSA)
  • Concussion or traumatic brain injuries
  • Cervical spine deformities, such as cervical spine stenosis or Chiari malformation
  • Vitamin B1 deficiency, known as beriberi, which is a treatable form of the condition

Some of the known diagnoses that may cause secondary POTS include heavy metal toxicity, amyloidosis, Sjogren syndrome, sarcoidosis, and lupus. Alcohol abuse may also increase a person’s risk of POTS, as well as a history of chemotherapy use.

Unfortunately, there’s still a great deal that we don’t understand about the pathophysiology of POTS and exactly what causes it.


POTS is diagnosed by taking a thorough history, using a POTS questionnaire such as the Self-Report Orthostatic Grading Scale,[xliii] and by performing a physical examination during which orthostatic vital signs are recorded. POTS is often associated with hypermobility syndromes, so an examination using the Beighton Score is essential.

Specific diagnostic tests include a standing test or a tilt-table test with a 12 lead ECG.[xliv]

Standing Test

With a standing test, the patient lies down for a few minutes before their pulse and blood pressure are recorded with an electronic device, such as the Omron blood pressure machine. They then stand up and while not holding onto anything, and without talking or moving too much, their pulse and blood pressure are recorded at one, three, five, and ten minute intervals. Since POTS may be influenced by diurnal variations, with the morning being the most sensitive time of day, it may increase diagnostic accuracy if the readings are taken in the morning.

Tilt-table Test

A tilt-table test is considered to be the gold standard test for confirming the diagnosis. During this test, the patient is strapped standing up to a table and connected to monitoring equipment, which checks their vital signs at regular intervals. The patient rests while standing up for twenty minutes, before the table is then tilted to seventy degrees. Blood pressure and heart rate are monitored continuously and recorded at two, five, and ten minute intervals. The patient is kept in an upright position for forty minutes or until they faint.

The test is considered positive if the diagnostic criteria are met. Keeping the patient still on the table prevents fidgeting or any compensatory movements to which the patient may have grown accustomed to help ease their symptoms. Keeping them still enables the full magnitude of the patient’s symptoms to be assessed. The tilt-table test is most commonly used for people who experience frequent fainting episodes.

Each of these tests are brief when assessing POTS, taking only about ten to fifteen minutes. However, if other orthostatic syndromes are a possibility, these tests may take significantly longer. In the case of orthostatic hypotension, tests may take up to forty-five minutes.

People with POTS may also experience minor increases in blood pressure when standing. In addition, they will often have elevated blood levels of norepinephrine.[xlv]


There’s much more to POTS than meets the eye. It’s a complex condition characterized by an increased heart rate while standing, but it’s also associated with a number of other conditions and disorders. These include mast cell activation syndrome, chronic fatigue syndrome, Ehrler-Danlos syndrome, and fibromyalgia.

In this first part, we reviewed the definition of POTS, along with signs and symptoms, complications, associated conditions, and how to diagnose POTS. In Part Two, we’ll be reviewing how POTS is treated. It’s a multi-faceted treatment that may include diet changes, specialized compression clothing, strict exercise routines, pharmaceuticals, or indeed all of these.

In the meantime, please reach out to my office if you suspect POTS or if you need help managing your POTS. There’s no need to suffer in silence.

Please watch Dr. Andy Maxwell’s presentation.

[i] Fedorowski A. Postural orthostatic tachycardia syndrome: clinical presentation, aetiology and management. J Internal Med.2019: 285(4):352-366

[ii] Fedorowski A. Postural orthostatic tachycardia syndrome: clinical presentation, aetiology and management. J Internal Med.2019: 285(4):352-366

[iii] Tu Y. Abell T, Raj S, Mar P. Mechanisms and management of gastrointestinal symptoms in postural orthostatic tachycardia syndrome Neurogastroenterology & Motility 2020: \00e14031.

[iv] Raj S. The Postural Tachycardia Syndrome (POTS): Pathophysiology, Diagnosis and Management. Indian Pacing Electrophys J 2006 April-Jun; 6 (2): 84-99.

[v] Arnold A, Ng J, Raj S., Postural tachycardia syndrome – Diagnosis, physiology, and prognosis. Autonomic Neuroscience: Basic and Clinical 215 (2018) 3-11

[vi] Rowe P. General information brochure on orthostatic intolerance and its treatment. March 2014. Accessed March 2021. https://www.dysautonomiainternational.org/pdf/RoweOIsummary.pdf

[vii] Mar Pl, Raj SR. Postural orthostatic tachycardia syndrome: mechanisms and new therapies. Annu Rec\v Med. 2020; 71: 235-248

[viii] Rowe P. General information brochure on orthostatic intolerance and its treatment. March 2014. Accessed March 2021. https://www.dysautonomiainternational.org/pdf/RoweOIsummary.pdf

[ix] Johns Hopkins Medicine. Postural orthostatic tachycardia syndrome (POTS). N.d. Accessed March 2021. https://www.hopkinsmedicine.org/health/conditions-and-diseases/postural-orthostatic-tachycardia-syndrome-pots

[x] Ibid.

[xi] Cedars Sinai. Postural orthostatic tachycardia syndrome (POTS). N.d. Accessed March 2021. https://www.cedars-sinai.org/health-library/diseases-and-conditions/p/postural-orthostatic-tachycardia-syndrome-pots.html

[xii] Ibid pg. 4

[xiii] Rowe P. General information brochure on orthostatic intolerance and its treatment. March 2014. Accessed March 2021. https://www.dysautonomiainternational.org/pdf/RoweOIsummary.pdf

[xiv] Ibid pg. 4

[xv] DiBlaise JK, Harris LA, Goodman B. Postural Tachycardia Syndrome (POTS) and the GI Tract: a primer for the gastroenterologist. Am J Gastroenterol. 2028;113(10):1458-1467

[xvi] Tu Y. Abell T, Raj S, Mar P. Mechanisms and management of gastrointestinal symptoms in postural orthostatic tachycardia syndrome Neurogastroenterology & Motility 2020: \00e14031.

[xvii] Rowe P. General information brochure on orthostatic intolerance and its treatment. March 2014. Accessed March 2021. https://www.dysautonomiainternational.org/pdf/RoweOIsummary.pdf

[xviii] Moak JP. Fabian RR, Clarke LC et al. Antroduodenal manometry is abnormal in children presenting with orthostatic intolerance and gastrointestinal symptoms. J Pediatric Gastroenterol Nutr. 2016:63 (3):329-335

[xix] Rowe P. General information brochure on orthostatic intolerance and its treatment. March 2014. Accessed March 2021. https://www.dysautonomiainternational.org/pdf/RoweOIsummary.pdf

[xx] Cedars Sinai. Postural orthostatic tachycardia syndrome (POTS). N.d. Accessed March 2021. https://www.cedars-sinai.org/health-library/diseases-and-conditions/p/postural-orthostatic-tachycardia-syndrome-pots.html

[xxi] Dysautonomia International. Postural orthostatic tachycardia syndrome. N.d. Accessed March 2021. http://www.dysautonomiainternational.org/page.php?ID=30

[xxii] Dysautonomia International. Postural orthostatic tachycardia syndrome. N.d. Accessed March 2021. http://www.dysautonomiainternational.org/page.php?ID=30

[xxiii] Arnold AC, Raj SR. Orthostatic Hypotension: A Practical Approach to Investigation and Management. Can J Cardiol. 2017;33(12):1725-1728. doi:10.1016/j.cjca.2017.05.007

[xxiv] Garland EM, Celedonio JE, Raj SR. Postural Tachycardia Syndrome: Beyond Orthostatic Intolerance. Curr Neurol Neurosci Rep. 2015;15(9):60. doi:10.1007/s11910-015-0583-8

[xxv] Tu Y. Abell T, Raj S, Mar P. Mechanisms and management of gastrointestinal symptoms in postural orthostatic tachycardia syndrome Neurogastroenterology & Motility 2020: \00e14031

[xxvi] https://www.frontiersin.org/articles/10.3389/fimmu.2015.00620/full

[xxvii] Shaw BH, Stiles LE, Bourne K, et al. The face of postural tachycardia syndrome- insights from a large cross-sectional community-based survey. J Intern Med. 2019; 286 (4): 438-448

[xxviii] https://www.degruyter.com/document/doi/10.1515/dx-2020-0005/html

[xxix] Tu Y. Abell T, Raj S, Mar P. Mechanisms and management of gastrointestinal symptoms in postural orthostatic tachycardia syndrome Neurogastroenterology & Motility 2020: \00e14031

[xxx] Weinstock LB, Pace LA,Rezaie A, Afrin LB, Molderings GJ. Mast cell activation syndrome: a primer for the gastroenterologist. Dig Dis Sci.2020

[xxxi] Garland EM, Celedonio JE, Raj SR. Postural Tachycardia Syndrome: Beyond Orthostatic Intolerance. Curr Neurol Neurosci Rep. 2015;15(9):60. doi:10.1007/s11910-015-0583-8

[xxxii] Tu Y. Abell T, Raj S, Mar P. Mechanisms and management of gastrointestinal symptoms in postural orthostatic tachycardia syndrome Neurogastroenterology & Motility 2020: \00e14031

[xxxiii] Eccles J, et al. Neurovisceral phenotypes in the expression of psychiatric symptoms. Frontiers in Neuroscience Feb 2025 Volume 9 Article 4 pg 1

[xxxiv] Ibid.

[xxxv] Ibid.

[xxxvi] bid.

[xxxvii] https://www.mayoclinic.org/diseases-conditions/median-arcuate-ligament-syndrome-mals/symptoms-causes/syc-20505001

[xxxviii] Garland EM, Celedonio JE, Raj SR. Postural Tachycardia Syndrome: Beyond Orthostatic Intolerance. Curr Neurol Neurosci Rep. 2015;15(9):60. doi:10.1007/s11910-015-0583-8

[xxxix] Staud R. Autonomic dysfunction in fibromyalgia syndrome: postural orthostatic tachycardia. Curr Rheumatol Rep. 2008;10(6):463-466. doi:10.1007/s11926-008-0076-8

[xl] Blitshteyn S. Whitelaw S. Postural orthostatic tachycardia syndrome (POTS) and other autonomic disorders after Covid

-19 infections: a case series of 20 patients. Immunologic Research 30th March 2021

[xli] Rowe P. General information brochure on orthostatic intolerance and its treatment. March 2014. Accessed March 2021. https://www.dysautonomiainternational.org/pdf/RoweOIsummary.pdf

[xlii] Eccles J, et al. Neurovisceral phenotypes in the expression of psychiatric symptoms. Frontiers in Neuroscience Feb 2025 Volume 9 Article 4 pg 1

[xliii] Self-Report Orthostatic Grading Scale Mayo Clin. Proc. 2005; 80 (3): 330-334

[xliv] Rowe P. General information brochure on orthostatic intolerance and its treatment. March 2014. Accessed March 2021. https://www.dysautonomiainternational.org/pdf/RoweOIsummary.pdf

[xlv] Raj SR. The Postural Tachycardia Syndrome (POTS): pathophysiology, diagnosis & management. Indian Pacing Electrophysiol J. 2006;6(2):84-99. Published 2006 Apr 1.

Gas Stove Controversy

Gas Stove Controversy

A recent controversy has emerged over the use of the gas stoves.  Gas stoves are present in roughly 1/3 of United States homes and it has been observed that there may be an increased risk of asthma in children and other respiratory health risks linked to indoor air pollution from these appliances. A study published in the Journal of Environmental Science and Technology in October 2022, found that gas stoves can emit low levels of methane, carbon monoxide, formaldehyde and benzene.  Two further lung irritant substances emitted from gas stoves are nitrogen dioxide and tiny airborne particles known as PM2.5 – both of which are lung irritants. Cooking of any kind produces some pollutants that are harmful if not properly handled. Applying heat to food produces particles — tiny particles (PM10, or particulate matter 10 micrometers in diameter), tinier particles (PM2.5, or 2.5 micrometers in diameter), and even tinier “ultrafine” particles (100 nanometers in diameter) — that can exacerbate respiratory problems.[i]

For a more in depth analysis of all of the indoor pollutants and the levels at which they produce health effects please see this VOX news article written by David Roberts.

In a further study published December in the International Journal of Environmental Research and Public Health, postulated that more than 12% of current childhood asthma cases in the U.S. can be linked to the use of gas stoves.

The controversy is made worse by the fact that these low levels can emit even when the stove is not in use. Given that people in the U.S. spend on average roughly 90 percent of their time indoors. With Covid -19, the average time spent indoors may be much higher.[ii] 

Thus, we do most of our breathing inside but very little attention or regulation standards govern indoor air quality. Outdoor air is the subject of massive legal and regulatory legal wranglings going back decades. The six common air pollutants covered by the U.S. Clean Air Act — ground-level ozone, particulate matter, carbon monoxide, lead, sulfur dioxide (SO2), and nitrogen dioxide (NO2) — have fallen an average of 74 percent since the Act was passed in 1970.

This is  a good thing, because a growing body of research suggests that those pollutants are even more harmful to humans, at lower exposures, than previously believed.

But the more ominous news is that the Environmental Protection Agency (EPA) warns that “studies of human exposure to air pollutants indicate that indoor levels of pollutants may be two to five times — and occasionally more than 100 times — higher than outdoor levels.”

Despite those risks, there are no federal standards or guidelines governing indoor pollution. A patchwork of state and local standards in the U.S. protects consumers, inadequately.[iii]

According to a David Roberts, four research and advocacy groups — the Rocky Mountain Institute, Mothers Out Front, Physicians for Social Responsibility, and the Sierra Club — released a literature review, assessing two decades worth of peer-reviewed studies. They find that “gas stoves may be exposing tens of millions of people to levels of air pollution in their homes that would be illegal outdoors under national air quality standards.” Like most issues involving health and environmental toxicants, the pro- lobbying groups, in this case the natural gas companies, have fought long and hard to fend off any regulatory standards being applied. 

The controversy of a gas cooking health hazards began almost 50 years ago when researchers in England and Scotland showed that 5000 children were linked to a positive correlation between gas cooking and asthma symptoms. Since then, a slew of new studies has been published.  

Use of a high-efficiency range hood that extracts indoor air contaminants and carries them outside appears to be of benefit. Opening windows may be of help and using a HEPA air filter ( which, if it extracts particles below 0.3 microns, will be of help in removing mold particles as well)  may also be of use. 

Environmentalists believe that switching to electric induction cooking is an important climate step. this is furthered by the awareness that there are cooking benefits to electric stoves- they allow you to cook faster.  Chefs have commented that making the switch to induction may help increase production and improved employee mental health because the kitchens are not as hot as when using gas stoves. 

It has been postulated by certain media outlets that U.S. federal regulators are considering a ban on gas stoves but the U.S. Consumer Product Safety Commission (CPSC) has commented that it is still figuring out the best way to tackle this issue. The CPSC are considering all approaches to regulation and has commented that any action would be a very lengthy process, implying that there are no eminent policy changes in the near future. It appears that the most likely move will be that, instead of having people physically remove gas stoves, the CPSC will require that new products comply with its regulations. This would mean that new homes be built with electric stoves or high-efficiency exhaust vents.[iv]

However, a very sensible article was written in Medscape by F. Perry Wilson Jan 24 2023[v] titled “The Gas Stove Debate Hinges on One Bad Word”. Here he points out the difference between association and causation. He makes the point, through deductive reasoning and math, that if all gas stoves were to be removed, there would very likely not be a reduction in the amount of asthma systems in children by 12%. The word “attributable” is the key word in his argument, bringing into focus the age-old conundrum of “association (or correlation), in studies, does not imply causation.”   There are a host of other factors that may be playing a role in the gas -stove/asthma debate, such as the economics and living conditions of those with gas stoves versus those without. There are multiple causes of asthma.

As always, an open mind is required when drawing conclusions about many studies that are published these days. There are too many factors that come into play when attempting to make up one’s mind about conclusions reached such as these. See my blog on evidence-based studies for further insights to the limitations of certain publications here.

[i] https://www.vox.com/energy-and-environment/2020/5/7/21247602/gas-stove-cooking-indoor-air-pollution-health-risks

[ii] Ibid

[iii] Ibid

[iv] Time Magazine Jan 30th 2023.

[v] The Gas Stove Debate Hinges on One Bad Word (medscape.com)

Electrosmog: The Expert Guide to the Effects of EMFs on the Body

Effects of EMFs on the Body

The damage electromagnetic fields (EMFs) can inflict on the human body is very real, and health organizations are only slowly realizing the extent of the problem. After all, electromagnetic and radiofrequency fields are everywhere these days, including in the office, at home, in the car, and wherever we take our cell phones. As a doctor, it’s so important to be aware of the symptoms caused by electromagnetic sensitivity, and what action can be taken to counteract the disease.

An electromagnetic field comprises energy created from electrical and magnetic energy emitted by electronic devices. The electrical current running through a device creates the magnetic field, and the electrical field is generated by the difference in voltage.

The planets and the solar system all have electromagnetic fields, as does the human body. Electromagnetic fields are a fact of life. However, due to advances in technology over the past thirty years, we’re now exposed to man-made EMFs on a daily basis for long periods from multiple sources. This is something that only happened occasionally in the past.

Electromagnetic pollution map in 2004

These two maps show the increase in electromagnetic pollution from 2004 (above) until 2022 (below) with a corresponding increase in 5G cell antenna, satellites, cell phone antennas, smart meters, smart appliances, and wearable smart devices.

Electromagnetic pollution map in 2022

The human body generates its own electromagnetic fields in relation to the heart, brain, and nervous system, so it isn’t that far-fetched to imagine that man-made EMFs can disrupt the health of sensitive individuals.

As many modern electronic devices can emit different frequencies of EMFs simultaneously, as practitioners we must take combined exposures into consideration when treating our patients.

Is Electrosmog Harming Our Health?

Electromagnetic fields, sometimes known as electrosmog, can have a severe impact on human health. While there’s considerable skepticism about the types of health effects caused by EMFs, there’s evidence that long-term exposure can contribute to diseases such as some forms of cancer, multiple sclerosis, and Alzheimer’s.

Electromagnetic hypersensitivity infographic

Much of the focus in legislation and guidelines regarding EMF exposure relates to excessive thermal effects, meaning the increased temperatures caused by absorption of electromagnetic energy. However, a rise in temperature isn’t the only way electromagnetic fields can affect the human body. This is largely unreported by political organizations and in the press. EMF regulations remain largely unchanged to reflect EMF dangers, but the tide is turning.

Recent guidelines on EMF exposure across the world include:

  • The International Agency for Research on Cancer (IARC) recognized low-frequency magnetic fields as a possible cause of cancer in humans in 2002, making the same ruling on radio frequency radiation in 2011.
  • The European Environment Agency has compared EMFs to other environmental carcinogens such as tobacco, benzene, and asbestos.
  • The American Academy of Environmental Medicine (AAEN) drew attention to EMF exposure in 2012, urging doctors to reconsider electromagnetic exposure as an underlying cause of illness.
  • In Belgium, the government banned the advertising of mobile phones to children under the age of seven in 2014. The specific absorption rate (SAR) of mobile phones also has to be published and all cell phone packaging must feature warnings that advise users to use a headset and minimize their exposure.
  • In 2015, France decided to ban Wi-Fi in nurseries for children under the age of three. The government also mandated that at schools for children under the age of eleven, Wi-Fi should only be used when specifically needed for lessons.
  • In September 2015, following the Paris Appeal Congress, the scientific committee published an international declaration, calling upon international and national organizations to recognize both electromagnetic hypersensitivity and multiple chemical sensitivity as diseases.

While government bodies and organizations are beginning to pay attention, we now need to be aware of the specific health risks related to electromagnetic fields.

Evidence of harm caused by EMFs

Electromagnetic fields can cause the following health conditions:

  • EMFs have been known to cause breast cancer, along with brain tumors, and leukemia, particularly in young children. An existing condition of leukemia can actually be made worse by EMFs, while brain tumors are linked to cell phone use.
  • EMFs can increase the prevalence of Alzheimer’s disease and other neurological defects, as well as worsen cognitive function. Radio frequency EMFs, such as those emitted by cell phones, can also affect the blood-brain barrier.
  • The risks of infertility and stillbirthare increased for women living near a power line.
  • Infertility in mencan be caused by proximity to a power line or by simply keeping a cell phone in a front pocket or attached to a belt.
  • Increased blood pressure and cardiovascular strain.
  • Damage to DNA and gene expression.
  • In terms of depression, EMFs can alter a patient’s mood by activating his or her voltage-gated calcium channels, creating an imbalance of neurotransmitters and neuroendocrine hormones.
  • EMFs can lead to the alteration of plasma membranes in cells. The activation of voltage-gated calcium channels also alters the structure of the membrane surrounding the cell, which may affect cell membrane permeability.
  • The correlation between EMF exposure and amyotrophic lateral sclerosis (ALS) suggests that a confused immune system response and increased glutamate levels caused by EMF exposure may instigate ALS in susceptible individuals.
  • EMFs are linked to increased blood sugar levels in diabetics and pre-diabetics. Dirty electricity can impede diabetics’ progress in managing their disease, potentially leading to them needing to use more insulin.
  • Neurodevelopmental and neurobehavioral changes such as memory loss, learning difficulties, and attention and behavioral problems have been reported in numerous studies and are manifested in autism and attention-deficit hyperactivity disorders, where both epigenetic and genetic (DNA) damage are likely contributors. [iii]

For patients with electromagnetic hypersensitivity and mast cell activation syndrome (MCAS), any exposure to EMFs causes a systematic change in their body, leading to long-term illness. Researchers first noted skin-specific reactions, including skin and mucosa signs of itching and redness, flushing, pain, papules, and pustules in patients who were exposed to electronic screens and mobile phones in studies conducted back in the 1980s. They also noted symptoms in the same patients that were triggered in the heart and central nervous system. Further research in the early 2000s regarding electrical hypersensitivity noted headaches in about 85 per cent of cell phone users, with a significant number of subjects also reporting fatigue, dizziness, nausea, itching, redness, burning, and cognitive symptoms.

EMFs activate mast cells and increase histamine release, increasing the intracellular uptake of calcium across cell membranes.

In Sweden, Olle Johannson is leading the way with research into the effects of EMFs on mast cell physiology. Johannson describes a phenomenon called electromagnetic-hypersensitivity (EHS), where certain patients experience reactions to the full-body penetration of electrical and magnetic fields in their environment. Specifically, patient labeling of ‘environmental illness’ or ‘multiple chemical sensitivity’ are the strongest predictors of electro-hypersensitivity to EMFs. Whenever a patient presents with symptoms suggestive of mast cell activation syndrome, I immediately enquire about their exposures to electrical fields, magnetic fields, radiofrequency fields, and dirty electricity then have them answer the EMF sensitivity questionnaire.

All of these diseases and changes in the body are serious, but let’s focus on electromagnetic hypersensitivity, as this is an extremely modern disease that can often be mistaken for other conditions.

What is electromagnetic sensitivity?

Electromagnetic sensitivity, also known as electromagnetic hypersensitivity (EHS), is a physical intolerance to electromagnetic fields generated by power lines and power stations, electronic radio signals, and/or Wi-Fi. One patient with electromagnetic sensitivity may be more sensitive than another. Electromagnetic hypersensitivity exists on a spectrum dependent on individual susceptibility and the strength and duration of the EMF exposure. Individuals with this condition may have symptoms occurring from exposure to EMF radiation even below recommended reference levels and, when completely isolated from these fields, have complete remission of their symptoms. Although there’s still skepticism regarding the diagnosis of electromagnetic sensitivity, there are plenty of studies indicating that the condition exists. In modern society, it’s harder than ever to avoid electromagnetic fields. In fact, the sheer density of overlapping electromagnetic fields and radiation fields means that doctors are likely to be seeing increasing numbers of patients exhibiting the same symptoms.

When patients experience symptoms suggestive of EHS, this cluster of chronic inflammatory disorders still lacks validated pathogenic mechanisms, diagnostic biomarkers, and management guidelines. Many individuals get marginalized by their traditionally trained healthcare providers as having a psychogenic or somatization disorder. However, the research is continuing to advance and has provided several plausible mechanisms that explain how EMFs cause electromagnetic sensitivity, including:

Of course, these issues are often interconnected. When a patient’s body is out of balance, many reactions can happen simultaneously.

EMF Exposure Symptoms

For a medical practitioner, one of the most fascinating aspects of the illness caused by electronic magnetic fields is that the symptoms seem so familiar. Our patients present with symptoms very similar to those found in patients with long-term chronic illness, particularly autoimmune disorders. In fact, many patients struggling with EMF exposure may have been misdiagnosed as suffering from chronic fatigue syndrome or multiple chemical sensitivity. Many patients have neurological symptoms such as numbness and tingling in various body parts suggestive of multiple sclerosis, but when an MRI is performed, the characteristic white matter lesions of multiple sclerosis are not evident

Electromagnetic hypersensitivity exposure symptoms are characterized by a broad range of nonspecific multiorgan symptoms suggestive of both acute and chronic inflammatory processes, involving skin, nervous system, respiratory, cardiovascular, musculoskeletal, and gastrointestinal systems. These symptoms may include:

Not all symptoms are present at the same time. In addition, these symptoms can vary from one patient to another, as an individual’s genetics, state of health, and exposure to other environmental or immune stressors influence how EMF manifests in the body. In most cases, these symptoms are self-reported and there’s an absence of organ-specific pathological signs except skin manifestations, which are the most common.

Additional symptoms experienced by patients living near a cell phone tower include:

  • Visual disruptions
  • Hearing disruptions
  • Loss of appetite
  • Difficulty moving with loss of balance
  • Vertigo
  • General discomfort

Some patients may react to an EMF source over time, whereas others are so frequently affected by acute exposure that the symptoms and cause are easy to miss. I can’t stress enough how crucial it is to ask the right questions as part of a routine doctor visit, ensuring that no stone is left unturned. It’s important to note that some patients only react to specific sources of EMFs, such as smart meters or cell phones.

It’s also advisable to keep EMFs in mind when examining patients who don’t exhibit classic electromagnetic hypersensitivity symptoms. The new man-made pollution of EMFs hasn’t been studied in detail in terms of its adverse effects on the human body. There’s certainly an argument to consider the effects EMFs could have on non-sensitive individuals, increasing their levels of biological stress at a cellular level. If you’re treating a patient who’s sensitive to heavy metals, chemicals, perfumes, fragrances, and other toxins, it’s worthwhile to educate him or her on how to reduce EMF exposure.In fact, we could all benefit from reducing our exposure to electromagnetic fields wherever possible. Even though not all of us are sensitive, EMFs do increase our chances of developing symptoms and diseases related to increasing levels of oxidative, free radical damage to vital cells of our body.

Symptoms experienced by people in the vicinity of cellular phone base station

In addition, keep in mind that other medical conditions may be linked to electromagnetic sensitivity, often meaning that your patient is suffering from a total toxin overload or immune dysfunction, with electromagnetic exposure being the “straw that breaks the camel’s back”, so to speak.

These conditions include:

  • Gastrointestinal problems
  • PTSD
  • Mast cell activation syndrome (MCAS)
  • Neurodegenerative disease, including Parkinson’s, Alzheimer’s, Huntington’s, and ALS
  • Liver disease
  • Food allergies
  • Chronic Fatigue Syndrome (CFS)
  • Autoimmune diseases, including lupus, Hashimoto’s, rheumatoid arthritis, and thyroid dysfunction
  • Allergic skin reactions, such as eczema
  • MTHFR genetic mutation
  • Lyme disease
  • Asthma, Diabetes, and Autism

You’ll have to connect the dots between your patient’s different ailments, because your patient often won’t be able to do so.

Sources of Electromagnetic exposure

Man-made electromagnetic fields can be loosely sorted into two types, namely power-based and wireless-based. Electricity EMFs are generated by any appliance or machine operating on alternating current (AC) power. Radiofrequency EMFs, also known as microwave frequency EMFs, are generated by communication devices and the cell tower network.

Frequency and wavelength infographic

Sources of electrical electromagnetic fields (electricity)

Sources in the home are from such things as home appliances and lighting, including:

  • Microwave ovens
  • Computers
  • Washers and dryers
  • Radios
  • Magnetic induction stove tops
  • Video game consoles
  • Energy efficient HVAC systems
  • Air conditioning systems
  • Portable heating systems
  • Portable fans
  • Air filtration systems
  • CPAP machines
  • Electric beds
  • Portable air conditioning systems
  • Grounding or earthing pads plugged into the third prong of an electrical outlet
  • Compact fluorescent bulbs
  • Other fluorescent lighting
  • Bedside lamps
  • Televisions
  • Aquariums
  • Hot tub, pool, and pond pumps

Places where the electricity enters the home are also sources, such as:

  • The electrical main panel
  • The sub-panels in your home
  • Photovoltaic (solar) panels
  • Improperly wired electrical cables within the walls

Other sources include:

  • Smart Home systems
  • Hybrid cars, with some models having high EMF levels, making it important to check the technical specifications before buying
  • Electric car chargers
  • Neighbors with photovoltaic (solar) panels

Sources at school and work include fluorescent lighting, especially compact fluorescent bulbs, as well as proximity to a variety of devices, such as:

  • Slide projectors
  • Overhead projectors
  • The main body of computers on the floor
  • Any power chargers, power strips, or where a large number of wires are plugged in
  • Computers, printers, or any appliances that plug into the electrical wall plugs
  • Separate hard drives
  • Copiers and fax machines
  • Electrical main panels, sub-panels, or switchgear rooms
  • Large electrical systems, such as electric motors, generators, and electric cables
  • Power tools, drills, welding tools, and induction motors, including sewing machines

 Public sources include proximity to:

  • Power lines (above and underground)
  • Transmission lines (above and underground)
  • Transformers
  • Pad-mounted ground transformers, such as the big green boxes labeled ‘high voltage’ that sit outside buildings
  • Electrical substations
  • Wind farms/solar power plants

Other public sources include:

  • Electrical transportation systems, such as trains and light rail
  • Electric and hybrid cars, with exposure varying widely
  • Broadband over power lines (BPL)

BPL is a relatively new technology that uses the existing electrical power grid to transmit a radio frequency signal for internet access. BPL runs through all buildings with electrical wiring, exposing occupants to constant radio frequency, even if they aren’t signed up for the service.

Sources of radio frequency electromagnetic fields (wireless)

Sources in the home include:

  • Routers
  • Cell phones
  • Cordless phones
  • Phone base stations
  • Pagers
  • Microwave ovens
  • Bluetooth
  • Nextel phones
  • IDEN phones, which constantly emit a strong radio frequency signal
  • Smart thermostats, smoke detectors, TVs, fridges, microwaves, stoves, washer/dryers, lighting/automation systems
  • Smart watches, fitness trackers
  • Wireless air purifiers/fans
  • Smart TVs

Wireless sources include:

  • Networks
  • Laptops
  • PDAs
  • Tablets
  • Virtual assistant hubs
  • Smart speakers
  • Wireless baby monitors
  • Any other wireless device
  • Smart energy meters
  • CPAP machines

Sources at school and work include wireless networks, phones, computers, and cell towers or antennae such as:

  • Cell phones
  • Pagers
  • Cordless phones
  • Phone base stations
  • Bluetooth
  • Laptops
  • PDAs
  • Synchronized clocks
  • Alarm/security systems and school lockdown systems
  • Tablets
  • Wireless microphones
  • Bluetooth peripherals, such as mice, keyboards, and printers
  • Cell towers or antennae that are on-site or adjacent to the site
  • Antennae on buildings next door or on the building above, which can radiate in the direction of a nearby building with glass windows, since the glass reflects the radio frequency toward the building.

Public sources include:

  • Cell towers and cellular antennae
  • Wireless networks from local businesses and retail spaces
  • Wi-Fi hotspots and municipal systems
  • WiMAX
  • Broadcast towers (AM/FM/ digital TV)
  • Radar from a nearby airports or military bases
  • Electronic article surveillance systems (EAS) in the security gates that resemble flat white panels near store entrances
  • Radio frequency identification and metal detector systems found in airports, stores, libraries, and hospitals

Faced with a list like the one above, many of your patients may feel that avoiding EMFs is impossible. However, there are ways to minimize exposure if your patient is struggling with electromagnetic sensitivity.

Diagnosing electromagnetic sensitivity

When diagnosing electromagnetic sensitivity, it’s crucial to rule out other illnesses, understanding that this illness can make other environmental and immune conditions worse. However, if your patient believes that they’re struggling with EMF exposure, it’s likely to be true. There are a number of ways to diagnose electromagnetic sensitivity.


The first way is to complete a questionnaire and have it reviewed by a healthcare professional well-versed in the diagnosis of EHS. Please be forewarned that there won’t be many healthcare practitioners who will be vaguely interested, never mind well informed on this issue. However, it’s relevant to note that the International Classification of Diseases ICD-10 includes codes for RFR and other forms of non-ionizing radiation.

Take a full history of health problems and EMF exposure, using a functional medicine timeline:

  • Ask the usual questions regarding past illnesses and exposure to environmental issues.          Assess the time and place regarding the appearance of symptoms, but also ask about chemical trauma, such as exposure to heavy metals, chlorinated hydrocarbons, and DDT pesticides.
  • In addition, ask about electrical trauma, such as electrocution, being struck by lightning, or multiple shocks.
  • Investigate any biotrauma in the form of parasites, fungal infections, or viral infections.
  • Consider any past physical trauma to the central nervous system, such as spinal problems, accidents, or whiplash.
  • Make sure that your questions also cover any autoimmune disorders.
  • Examining your patient from a systemic perspective is key.

Ensure that you ask the patient the following questions:

  • Do you own a cell phone?
  • Do you use your cell phone for talking, keeping it next to your ear or using speakerphone, or for texting?
  • Do you switch it off at night?
  • If you own a cell phone, for how many hours do you use it in an average day?
  • Where is your Wi-Fi router located and how close do you sit/sleep next to it?
  • How many Wi-Fi networks does your device detect in your home?
  • Are you in a condominium where you can detect all of your neighbor’s router Wi-Fi signals?
  • Have you had a smart meter installed in your home recently?
  • Do you have cordless phones and a cordless base station close to you, particularly at night when you sleep?
  • Do you own an electric or hybrid car?
  • Have you had a solar panel installed in your home recently?
  • Has a new cell tower been installed near your home lately?

Look for the health issues listed above, but also watch for blood pressure problems, increased risk of infections, lack of coordination, urinary urgency, tinnitus, and a sensation of pressure in the head and ears.

The severity of electromagnetic sensitivity depends on the person and the type of exposure. Full body EMF exposure may create flu-like symptoms, whereas cell phone use may cause a slight headache.

Order tests and examine the patient

Begin with basic tests, including blood pressure and resting heart rate tests with an electronic device in the morning, while still in bed. Omron devices are quite adequate for this purpose. These levels may need to be monitored by the patient, possibly several times a day in different locations. Encourage patients to keep a journal of their symptoms and how they feel over the course of the week.

Have them do the ten-minute blood pressure and pulse test. Advise them to lie down for five minutes then take their blood pressure and pulse. They should then stand up and at one minute, three minutes, five minutes, and ten minutes they need to repeat the blood pressure and pulse readings without moving or talking. They need to note the difference between their highest and lowest pulse rates, as well as the difference between the highest and lowest systolic and diastolic blood pressures. Advise them that they should be concerned if their pulse rate changes more than thirty beats over this ten-minute time period and their systolic blood pressure falls more than twenty points. 

Hoffman Centre electrosensitivity chart

Blood work may include:

  • ACTH and am cortisol
  • Bilirubin and liver enzymes
  • Blood count and differential blood count
  • Creatinine
  • High-sensitivity c-reactive protein (hs-CRP)
  • Electrolytes
  • Fasting blood glucose
  • Ferritin
  • Glutathione peroxidase (GPX)
  • Reduced glutathione (GSHL)
  • Glutathione S-transferase (GST)
  • Cholesterol (LDL, HDL, triglycerides)
  • 8-hydroxydeoxyguanosine- for DNA oxidation (rusting or degradation/inflammation)
  • Lipid peroxidase – for lipid peroxidation ( “rusting or degradation/inflammation”)
  • Malondialdehyde (MDA)
  • Nitrotyrosine and peroxynitrate
  • Prolactin
  • Selenium, whole blood
  • Zinc, whole blood
  • Coenzyme Q10
  • Magnesium, whole blood
  • Vitamin D3
  • Vitamin E
  • Testosterone
  • Immune cytokine factors: Interferon-gamma, interleukin-10, interleukin-17, interleukin-6, interleukin-8, Nuclear factor kappa b
  • Folate profile using FIGLU or the folate panel with Health Diagnostics laboratory
  • Methyl malonic acid – intracellular B 12
  • TSH, Free T3 and free T4 and thyroid antibodies
  • Tumor necrosis factor (Alpha, TNF-alpha)
  • Histamine and diamine oxidase (DAO)
  • MCAS markers – see my article on MCAS and blood work
  • Interleukin-1
  • Intracellular ATP
  • Intracellular glutathione, glutathione transferase, glutathione peroxidase, superoxide dismutase, n-acetyl cysteine, Vitamin E, Coenzyme Q10, Vitamin D, measurements of antioxidant activity
  • Vitamin B6
  • Folate profile using FIGLU or the folate panel with Health Diagnostics laboratory
  • Homocysteine – an indirect measure of adequate methylation, required for histamine degradation

Second-morning urine test to assess urinary catecholamines

  • Adrenaline
  • Dopamine
  • Noradrenaline
  • Noradrenaline/adrenaline ratio
  • Serotonin

24-hour urine test

  • Melatonin sulfate
  • Urinary cortisol, cortione, DHEA
  • Saliva test for 4-point cortisol  
  • Test at 8 am, 12 noon, 6 pm, and 10 pm

Also consider the following:

  • 24-hour blood pressure monitor
  • 24-hour ECG heart rhythm diagnosis
  • 24-hour heart rate variability (HRV), ruling out autonomous nervous system diagnosis
  • Sleep EEG at home to indicate if sleep is disturbed

Urine test

  • Provocation Heavy Metal test, depending on patient’s history, focusing in particular on mercury, lead, arsenic, aluminum, and cadmium
  • Kryptopyrroles

When treating a family, it’s worth checking out individual susceptibility to electromagnetic sensitivity.

Most of the studies to date on EHS have been animal-based, but a human case-controlled study, published in 2014, Metabolic and Genetic Screening of Electromagnetic Hypersensitive Subjects as a Feasible Tool for Diagnostics and Intervention[i] demonstrated that sensitive individuals may have shared organic determinants of impaired detoxification of common physic-chemical stressors, altered cell membrane integrity, pro-inflammatory cytokine markers, and depleted antioxidant defenses.

The following drug metabolizing enzyme-gene polymorphisms and cell markers were studied and were shown to have altered functions in sensitive individuals:

  • glutathione peroxidase,
  • catalase
  • superoxide dismutase
  • catechol-O-methyltransferase
  • Coenzyme Q10 oxidation increased rates
  • Vitamin E
  • Depletion of polyunsaturated fatty acids
  • CYP 2C19 variants
  • GSTT variants. Glutathione S-transferase (GST) is a family of important drug-metabolizing enzymes, conjugating endogenous and exogenous compounds. Genetic polymorphisms result in the inter-individual variability of GST activity in humans. In particular, human GSTT1 and GSTT2 null alleles are associated with toxicity and various cancers derived from chemicals. [ii]

Measure EMF exposure

It’s best to liaise with a building biologist who can visit the patient’s home or workplace and carry out the necessary checks for the different types of EMF exposures that are derived from electrical and wireless sources. Crucially, a building biologist can assess your patient’s current sleeping arrangements in relation to electronics located close to the head and trunk of the body. A professional building biologist can provide suggestions regarding how to reduce the EMF exposure as part of the measurement report.

For a building biologist in Calgary, contact Mitch Marchand of EMF Aware at 1-403-264-2970

For a building biologist in your area, contact the Building Biology

Limit EMF exposure and provide a diagnosis

Advice on how to limit EMF exposure is included in the section below. Diagnosis of your individual patient depends upon careful monitoring of the times, places, and circumstances of possible EMF exposure, as well as the changing or intensity of symptoms over time. The report from the building biologist can help you determine whether EMF exposure is likely to be the culprit. However, other potential causes need to be excluded before you reach a diagnosis of electromagnetic hypersensitivity or EMF-related health problems.


Although the main focus should be on minimizing EMF exposure, it’s also beneficial for your patient if you work together to strengthen their immune systems, improve antioxidant defenses, reduce their total body burden of associated toxins, improve diet with macro and micronutrient adjustments, help them to sleep and reduce stress. After all, everything’s connected.

Focus on things such as:

  • Counteracting any other environmental pollutants in the body, which may bring about illness due to mold, allergies, food allergies, or an immune system reaction to toxins
  • Instigating a detox program to neutralize any heavy metals found as a result of the patient’s blood test
  • Reducing oxidative or peroxynitrate stress through diet, healthy sleep, and exercise
  • Easing any forms of gastrointestinal upset, such as food intolerance or leaky gut
  • Treating inflammation and poor mitochondrial function through diet and vitamin supplements
  • Encouraging patients to drink more water

A lifestyle or health coach may be able to help with these aspects of the patient’s recovery.

How to Combat Health Effects of EMFs and Limit EMF Exposure

Many of your patients may feel frustrated with the diagnosis of electromagnetic sensitivity because of the nature of modern life and the reality of working all day in an office or with other industrial machinery. Yet it’s important to stress to them that it’s possible to counteract their symptoms with careful behaviors.

The most important piece of advice you can give to any patient suffering from electromagnetic sensitivity is to move if they live near a power line and transformer, since these are such a powerful source of EMFs.

Close proximity to the following places can also be problematic for patients with electromagnetic sensitivity:

  • Radio or digital TV broadcast stations
  • Cell phone towers
  • Police stations
  • Fire stations
  • Hospitals
  • Airports
  • Military bases
  • Solar parks
  • Wind turbines
  • Electrical substations
Symptoms experienced by people in the vicinity of cellular phone base station infographic

Cell phone towers emit microwave radiation and can have a directional beam, but some emit in all directions. A broadcast station is problematic when it’s closer than 1.24 miles (2 km) and a direct line of sight usually leads to greater exposures. Proximity to emergency service facilities is a risk because the personnel use terrestrial trunked radio (TETRA) to communicate. Airports and military bases use radar and shortwave radio communications, in addition to other harmful technologies.

Ideally, your patient should consult a building biologist to learn more about the specific EMFs that may be radiating from inside their home, but may also be occuring externally.

Here are some general guidelines for your patients to follow after their diagnosis.

In the home

  • Use a landline phone with a cord for your regular telephone, particularly for lengthy calls
  • Avoid wearing a cell phone or PDA while the device is on, as the battery-switching EMF emissions are excessively high, along with the RF emissions
  • Avoid using a cordless or cell phone while pregnant or while carrying an infant or toddler
  • Avoid DECT or IDEN cordless phones, since the base is always on and transmitting and these phones emit a large, continuous source of RF compared to other cordless phones
  • Stop using smartwatches (Apple) or fitness trackers such as Fitbit
  • Keep printers turned off and unplugged from the wall socket, unless needed
  • Reduce use of video game consoles or remove them entirely when not in use, disconnecting them from the wall
  • Be aware that digital media players emit EMFs unless unplugged from the wall
  • Smart TVs need to be unplugged as they constantly emit RF, although older models may have the option to turn off Wi-Fi or Bluetooth. For an excellent guide on different types of TVs and their emissions, visit https://emfacademy.com/do-tvs-emit-radiation-complete-guide/
  • Avoid using wireless virtual assistants such as Amazon Echo and Alexa, Google Home, or any wireless Bluetooth sound system
  • Energy efficient HVAC systems or other air conditioning systems may emit dirty electricity, so have this measured by the building biologist
  • Remember that home alarm systems can emit microwave radiation and many alarm systems have a wireless capability
  • Avoid using wireless baby monitors, or at least place them more than ten feet from a crib or bed
  • Use a battery-powered clock by the bed and sleep with your head at least six feet from electrical sources
  • In the bedroom, your body needs to be at least three feet from electrical sources
  • Remove any metal slats and frames in beds and cribs and remove mattresses containing bedsprings, replacing them with a memory foam mattress
  • Don’t use electric blankets
  • At night, the bedroom needs to be electronic-free, so remove all computers, laptops, cell phones, or cordless phones and don’t charge devices in the bedroom
  • Exposure to EMF before bedtime can interfere with melatonin production and the sleep cycle
  • Don’t install a smart meter or any smart appliances in the home
  • Wear turquoise or blue-blocker glasses for two hours before bed, as these induce melatonin production and reset the suprachiasmic nucleus, which is the master controller of your circadian clock.
  • Avoid using a laptop on your lap, as the wireless card gives out a strong emission similar to a cell phone and it’s better to have the laptop on a table
  • Replace Wi-Fi-enabled devices such as thermostats, fire alarms, doorbells, and cameras
  • An electric vehicle charging station should be assessed by a building biologist
  • Remove the microwave oven from the home
  • Portable heating systems, fans, CPAP machines, and portable AC systems all need to be kept at arm’s length or further.

It’ is advisable that everyone limit their cell phone and cordless calls by frequency and duration. Children should never use cordless phones or cell phones at all, as the level of radiation penetration into the brain far exceeds that experienced by adults.[iv] 

How mobile phone radiation penetrates the brain graphic

If there’s a need to use a cordless phone or cell phone, use a wired headset. These types of headsets are best, but any type of cord that creates distance between a person’s head and the phone is helpful. Alternatively, use the speakerphone. Avoid using Bluetooth headsets at all costs, as these generate RFs. While it’s harder than ever for patients to avoid using wireless laptops and wireless routers these days, if possible, your patient should use a computer that’s plugged into a cable modem via LAN (Ethernet cable). Stress the importance of having a non-wireless router, as unfortunately most routers default to wireless even when the Wi-Fi isn’t being used. It’s also impossible to determine if the router is transmitting wirelessly.

In addition to the recommendations above regarding bedrooms, hire a building biologist to determine which circuits to turn off at night. An electrician can then install a cut-off switch so that when you turn off your lights at night in the bedroom, this also turns off all the electrical supply to the room. If a cut-off switch isn’t installed, all electrical devices in the bedroom must be unplugged from the wall socket every night.

A Christmas light timer can be employed to turn off all Wi-Fi access at night, although using wired internet through ethernet at home is the best option. If your use of Wi-Fi is unavoidable, only plug the router in when the Wi-Fi is in use and unplug the router during sleeping hours. Beacon signal, power output, and number of radios enabled can be configured to reduce the amount of exposure from wireless access points. Install the wireless access points as far as possible from occupied space, such as your desk, and never have the wireless access points located in a child’s bedroom. You must also always work at least ten feet away from where the Wi-Fi signal is generated.

Compact fluorescent bulbs may be better for the environment, but they can emit dirty power. To protect your health, switch to LED or incandescent light bulbs and remove any dimmer switches from the home. However, keep in mind that LED light bulbs can still be a concern, as they’re known to disturb melatonin production and affect sleep patterns.

Although also recommended as being good for the environment, solar panels can emit dirty electricity if they use a particular type of inverter to convert the electricity that’s generated. If a neighbor uses a solar panel, EMF can permeate the neighborhood. You should also ask your immediate neighbors to turn off their Wi-Fi routers at night and when not in use. When you see several different wireless networks available on your device, it’s important to remember that each individual signal is a RF stressor and can potentially interfere with your health.

All personal wireless devices, such as cell phones, tablets, or laptops, need to be kept one foot away from a person’s body. Keep your laptop on the table, use speakerphone or wired headphones when talking on the phone, and use airplane mode when carrying a cell phone in your pocket. In addition, ensure that you’re ten feet away from these devices when they’re charging. Bluetooth should also be turned off unless it’s in use.

As EMS increases sensitivity to other environmental toxins, it’s also important to ensure that the home is free of pollutants such as mold, toxins, and common household chemicals. Get a quality air purifier with a HEPA filter and keep it at least a foot away from you. Doctors, please note that you should follow protocol to ensure that your patient isn’t dealing with a secondary sensitivity.

While driving and out in public

  • Don’t use a cell phone inside the car, on staircases, or in elevators, as the cell phone increases its EMF emissions up to 10,000-fold, even when locked away or on standby
  • If it’s necessary to make phone calls inside the car while driving, get a built-in, hands-free car phone jack and have the antenna hook up outside the car
  • Hybrid electric cars can increase sensitivity for some individuals
  • Modern cars often include Bluetooth systems and Wi-Fi hotspots, which need to be turned off
  • Avoid staying in hotels that have Wi-Fi hotspots or at airports, if you want to sleep well
  • Avoid cafes and restaurants that have wireless hotspots, particularly if children are with you
  • Avoid making multiple trips through the security gates in stores, and don’t let children play between their panels or linger near them
  • Avoid non-crucial medical procedures during pregnancy, such as MRIs and extra ultrasounds, to avoid unnecessarily exposing your baby to strong electromagnetic fields

Don’t use cell phones in the car as it can be immediately dangerous, but also ramp up exposure to EMFs. In particular, avoid using cell phones when children are present, as RF levels can be incredibly high in the back seat while a phone is used in the front of the car. Turn off cell phones in the car and avoid returning or taking calls while driving, retrieving messages when you arrive at a safe spot. In addition, don’t use Bluetooth for hands-free, as this is also a source of EMFs. Try to select a cell phone with a low specific absorption rate or SAR value. Choose the lowest where possible, which you can learn more about with this handy guide.

At work and at school

  • Try to restrict your child’s exposure to Wi-Fi in school by encouraging staff to change school policy. See Techsafeschools.org for more information.
  • Work at least ten feet from the Wi-Fi source, but ideally use an ethernet cable at work
  • Watch out for extension cords or power bars underneath desks and close to feet

Most of the precautions recommended for the home can also be used at work or school, although there may be some resistance from bosses, coworkers, teachers, and the school district authorities. However, there’s no reason to use Wi-Fi in the classroom if it’s not pertinent to the lesson.

Although it may be tempting to provide all these guidelines at once, many patients may feel overwhelmed by all the things they’re advised to remember. Introduce the guidelines gradually where possible, perhaps focusing on those related to the bedroom and the home to begin with, alongside those regarding personal and portable electronic devices. Remind your patients that this is a process, and that it takes time to improve electrosmog symptoms.

EMF Protection in the Home

There are several forms of EMF protection your patient can employ to minimize their exposure to electromagnetic fields. These include:

  • Installing a cut-off switch in the bedroom, which minimizes your patient’s EMF exposure at night and improves sleep significantly
  • Installing GS filters, which filter out the most dangerous levels of dirty electricity in the home. Only do this after having a building biologist check your home for wiring errors and current over your water lines.
  • Painting inside or outside the house using RF-screening paint. which blocks most cell phone Wi-Fi and TETRA signals
  • Lining windows with RF-reducing window film
  • Using a RF-shielding canopy, which resemble mosquito nets and are easy to install, over the bed at night. These are very effective for those living in apartments and condos.
  • Investing in meters that check magnetic field levels and RF levels
  • Hardwire computer workspace where computers, laptops, and tablets are located
  • Unplug WIFI printers, smart TVs, streaming media devices, such as Apple TV, Roku, or Chrome Cast, when not in use

As healthcare professionals, we need to be aware of man-made pollutants, particularly those that have been introduced without any consideration of the health risks. Cell phones, Wi-Fi hotspots, and electrical devices seem to be everywhere these days, and the number of patients with electromagnetic sensitivity is bound to increase over time. You’re uniquely qualified to advise patients on how to minimize their vulnerability to EMFs. Ultimately, EMF exposure is avoidable but with your help, your patients can see a real improvement in their health.

This is a summary of 4425 peer review EMF studies showing biological effects downloaded from the ORSAA database. Oceania Radiofrequency Scientific Advisory Association (ORSAA) is a not-for-profit organization composed of scientists and professionals from various academic disciplines who are investigating the scientific research that relates to the effects of artificial electromagnetic radiation (EMR) on humans, animals, and the environment. As the name indicates, ORSAA has a special focus on radiofrequency electromagnetic radiation (RF-EMR) that includes high frequency microwaves widely used for wireless communication and surveillance technologies. However, ORSAA’s interest in biological effects research extends to extremely low frequency (ELF) fields such as those utilized for domestic electrification or power frequencies.


[i] Sage C., Burgio E., Electromagnetic Fields, Pulsed Radiofrequency Radiation, and Epigenetics: How Wireless Technologies May Affect Childhood Development. Child Development, XXX 2017, Vol 00, No 0, pages 1-8 

[ii] Mchiara De Luca et al., Metabolic and Genetic Screening of Electromagnetic Hypersensitive Subjects as a Feasible Tool for Diagnostics and Intervention Mediators of Inflammation Vol 201 Article ID 924184

[iii] https://pubmed.ncbi.nlm.nih.gov/30169019/

[iv] https://ehtrust.org/research-on-childrens-vulnerability-to-cell-phone-radio-frequency-radiation/

Practical Tips on Exercise and Diet

Practical Tips for exercise and diet


Hire a personal trainer to start you off with your new lifestyle.

Find exercises that you enjoy, wherever possible.

Workout on a daily basis. Remember, it’s a choice of lifestyle not a temporary solution to an immediate health issue.

Hydrate before you work out, with salt, water, and electrolytes. Drink half your body weight in pounds in ounces. For example, if you weigh 200 pounds, drink 100 ounces or 3 litres. If you’re educated regarding the deuterium-depleted water controversy, the proponents of this approach wouldn’t agree on consuming this amount of water that isn’t deuterium-depleted.

In addition, check your bioimpedance to assess your total body water content, as well as your intracellular and extracellular fluid content.

Salt is essential, especially if you have Postural Orthostatic Tachycardia Syndrome
(POTS). Use salt that’s rich in mineral diversity, such as New Earth Organics, Crucial 4 Icelandic Flake Salt, or Redman’s Real Salt. Salt prevents muscle cramps and headaches, increases cardiac output, improves endurance, and replaces some of the electrolytes that have been lost.

Aim for cardio three times per week and high-intensity interval training three times per week.

Walk for between thirty and sixty minutes per day. If you’re a dog owner, maintaining your pet’s exercise routine can really help!

Lift weights between three and five times per week, for approximately thirty to forty-five minutes per day.

To gain muscle mass, use heavier weights in your routines. For toning of existing muscle, do less weight, but more reps.

Don’t be consistently sleep deprived, since this increases your caloric intake the next day by as much as 440 calories.

Turn your bedroom into a sleep sanctuary. Enhance sleep by wearing glasses that block blue light after 6 pm. Limit your screen time with devices such as TVs or IPads, unplug your router, and turn off your cell phone.

Find the best sleep aids from any number of combinations, from materials such as melatonin, glycine, magnesium, inositol, Gaba, or CBD. There are many different possibilities.

Define your top values in life in a hierarchal fashion by asking yourself the questions
“what do I spend most of my time doing, what do I spend my money on, what do I talk about the most, what do my surroundings demonstrate what I love the most, how do I spend my energy and what energizes me the most, what do I think about the most, what inspires me the most?”

Most people have their highest values within one or two of the following seven areas.

  • Career enhancement
  • Knowledge and education
  • Health and well-being
  • Relationships and family
  • Financial well-being
  • Spiritual goals
  • Social enhancement

Then compile a list of the top twenty benefits of daily exercise to your top one or two values columns.

If you can link all the benefits of exercise and a good meal plan to your highest values, it will be much easier for you to continue this change in lifestyle. i.e., ask yourself “by going to the gym and eating correctly every day, how will I be even more successful at what I most enjoy doing and what I love the most?”

You have to set your priorities and values, get up early to work out, link exercise and diet to your highest values, jettison low priority activities, such as endless Netflix and Instagram engagement, be honest with yourself, and don’t entertain a fantasy of achieving huge gains without significant effort. Nobody is going to do this for you and there’s no one to blame if you don’t achieve your intended results. This begins and ends with you and your effort.

Protein and food in general

Hire a nutritionist that’s highly skilled in providing an eight-day diet analysis using a cronometer in order to estimate where you may be macro or micronutrient deficient or over-fed, protein deficient, and whether you’re metabolically optimized.

In addition, ensure that your nutritionist is skilled in providing an anti-inflammatory approach and is knowledgeable regarding all the various food reaction subtypes. The list these days is rather long, but includes histamine, oxalates, salicylates, lectins, fodmaps, and sulfates, for example. For the most part, using a traditionally trained dietician following Canada’s Food Guide won’t help you to achieve the subtlety that’s often needed to attain your nutritional health goals.

Be quite prepared to analyze, through functional medicine laboratories, how metabolically repleted you are, the health of your cell membranes, and how functional your mitochondria and peroxisomes are in their specialized task of making both ATP and adequate fats for cell function. The biomarkers found in traditional laboratories are far from adequate when it comes down to analyzing these subtle variations.

Eat organic, whole, and nutritious food all of the time.

Don’t eat or snack after you slow down your activities for the day. Have supper no later than 6 pm and don’t snack at night. If you do, the calories contained in those snacks will immediately be deposited into storage, meaning into fat tissue.

Avoid snacking during the day, unless it’s part of your nutritional plan and you have hypoglycemic tendencies. If you’ve excluded sleep apnoea as the cause, use a Freestyle Libre blood glucose monitor if you suspect low blood sugars. This is particularly important if you wake up in the middle of the night with some or all of the following symptoms:

  • Fast heartbeat
  • Shaking
  • Sweating
  • Nervousness or anxiety
  • Irritability or confusion
  • Dizziness
  • Hunger

Stop eating processed or packaged food.

Eat between 1 and 1.25 grams of protein per pound of lean body weight. This helps with hunger and weight loss.

A minimum of 30 to 50 grams of protein per meal is recommended, which means a minimum of six ounces of chicken, fish, or red meat. That’s for breakfast, lunch, and supper combined. In addition to essential fats, this will get you off the carbohydrate and sugar rollercoaster.

Substitute with a good quality animal protein powder, such as Designs for Health PurePaleo beef protein. Don’t substitute with a rice or pea protein, primarily due to contamination with heavy metals, glyphosate, and issues with histamine.

A lack of protein, as well as good quality essential fats, is the main reason why you lose muscle mass as you age. This also influences overeating and feeling hungry at the end of the day.

Eliminate all junk food and nutritiously-deficient food from your pantry and from your fridge. Don’t hesitate and simply throw it out!

Starting the day with a high carbohydrate and sugar-laden meal will spike your insulin and blood sugar levels and these will never quite settle down throughout the day. It won’t make any difference how ‘organic’ the meal is supposed to be, or if it was bought at a health food store. You’ll be playing catch-up all day, with feelings of hunger and cravings. Eating a protein-dense meal in the morning, after you’ve woken in a catabolic state, will help to regulate your blood sugar levels for twenty-four hours and prevent any further breakdown of muscle tissue for energy requirements.

Eat consciously. Food transformation to energy and information requires the cooperation of the vagus nerve, which is the main parasympathetic nerve in the body. Parasympathetic dominance enhances rest, relaxation, healing, and digestion.

  • Eat in a quiet, settled, and comfortable environment.
  • Never eat when you’re upset.
  • Always sit down to eat.
  • Eat only when you feel hungry.
  • Minimize the consumption of ice-cold foods and beverages.
  • Finish chewing and swallowing what’s in your mouth before taking another bite.
  • Eat more slowly and at a comfortable pace, always remaining conscious of the process.
  • Listen to your appetite, by digesting the previous meal before starting the next one.
  • Don’t overeat, always leaving a third of your stomach empty to aid digestion.
  • Eat freshly prepared foods. Lightly-cooked foods are preferable to raw or over-cooked food..
  • Sit quietly for a few minutes after finishing your meal. Focus your attention on the sensations in your body.
  • Go for a short walk after your meals to aid your digestion.


Read my blogs on Intermittent Fasting Part One and Part Two

Read my blog on the Ketogenic Diet

Read my blog on the Qualities of a Successful Patient

Read The Obesity Code and The Diabetes Code by Jason Fung

Read The Obesity Fix by James DiNicolantonio

Contact the Hoffman Centre for a consultation at www.hoffmancentre.com or Justine Stenger for a nutritional workup.

How Chronic Illness Requires Multi-Layers of Healing

How Chronic Illness Requires Multi-Layers of Healing

In this talk with Judy Cho, Board Certified Holistic Nutritionist and Functional Nutritional Therapy Practitioner, we talk about how to get to the root cause of illness, omega-6’s, histamine, Lyme disease, and much more.

This transcript was automatically generated, please excuse any errors.

Hey guys, it’s Judy from nutrition with Judy.

Thanks for joining me today. While you’re here, please make sure to like, and subscribe. If you’re listening to this on podcast, please make sure to leave a review as this allows my content to get in front of more people. And thank you for that. My name is Judy Cho and I’m board certified in holistic nutrition.

I focus on root cause healing, and oftentimes I start with the carni cures meat, only elimination diet. Okay, so today I had the pleasure of sitting down with Dr. Bruce Hoffman, Dr. Bruce Hoffman focuses on so many things, and he really tries to get people that are suffering with chronic illness to root cause healing and truly heal people to a place that they could have a better life.

As you listen to this conversation, you’ll see that it gets very complex. There are layers of healing and he is not somebody that will sugar coat things in a sense. You just need to do this and therefore you will heal or you need to do that, or you need to take this magic pill. It’s not like that for him.

And he’s just very real in terms of chronic illness is difficult. Chronic illness can cost a lot. Um, it can take a lot of effort and time and energy, but. The point is that he says that there is hope and that you can heal, but there are certain things that you just need to go through and it takes time and diligence and the fortitude to want to heal.

Sometimes it’s working on our mental health and working on traumas from our past or even limbic system retraining and focusing our brains to not be as heightened in a immune response or a fight or flight. And it could even be deeper than that. And working on somatic retraining, I will put a lot of the stuff in the show notes, but this is a very important conversation, especially if you’re dealing with chronic illness, you’ve been to so many different doctors, you’ve done so many different modalities, tried different diets and nothing is fully working to get you better.

I talk a lot about SIRS as I spoke with Dr. Eric Dorner, and we continued from that conversation to talk about little nuances about some of the medication, as well as how it. Combines with limbic system retraining and other things. What I want you to really get out of this conversation is to understand that healing is very comprehensive, but if you want it enough, and if you try enough and you do these things, that there is a way to get to root cause healing.

I know that sometimes it may seem like our lot in life where illness is just prevalent, but it may sometimes be that we need to focus on healing our past traumas, as well as even the way that we are viewing the world. As Dr. Hoffman brought up, we often think about 60,000 thoughts in one day. How many of those thoughts are actually making you sicker or an unwell or in a negative state, that’s then bringing that into your life instead of healing and the belief that you can actually heal.

So while this conversation, isn’t the easiest, I think it’s the most real and most open and genuine that you will find in terms of really trying to heal chronic illness so that you can have a better chance at optimal health. Dr. Bruce Hoffman is board certified and he has a fellowship in anti-aging medicine, as well as a master’s degree in clinical nutrition.

He’s a certified functional medicine practitioner and in his clinical training, Dr. Hoffman has also studied with many of the leading mind, body and spiritual healers of our times, including Deepak Chopra, Paul OSHA Rames Baskar and John Katz. Dr. Hoffman was born and educated in South Africa and obtained his medical degree from the university of Cape town.

As you’ll see in our interview, Dr. Hoffman is a lifelong learner. He is always wanting to learn and grow and learn from other practitioners and just provide the best level of care to get people to healing with his patients. I’ve met many functional doctors and naturopaths and integrative doctors that really tried to consider the body as a whole, but Dr.

Hoffman truly takes it to a whole different level. And that was one reason why I wanted to interview him because I felt that he can provide more answers for some of the hardest cases that we may find in the Carver community. Let’s get right into the interview. Hi, Dr. Bruce Hoffman. I am so excited to have you on my channel.

I heard a lecture of yours and I was enamored because you were able to consider all different illnesses and understand that the body is really one body and how so many things are affected. And you talked about how chronic. Is just more than one thing and how everything is connected. So, um, I really wanted to have you on my channel.

I think so many people will benefit from your knowledge. I loved also that you knew about the carni diet. So that was a bigger plus to me. But if you can introduce yourself. Oh sure. So I am a south African trained MD, um, graduated from the university of Cape dun where the first heart transplant was done. And, uh, moved to Canada in 86 and first was a rural physician. And then. Started to be influenced and started to investigate all forms of healing. Um, having been originally exposed to Eastern philosophies and religions as a, as a teenager by my high school teacher, Roger. And so when I found myself a medical school, and then when I started to become a family physician, I started.

Visit some of the ancient heating practices that are investigated as a teenager and some of the philosophies. And then all of a sudden fell across Larry DSY and Deepak Chopra and all the leaders in the field and went and met them and studied with them. And then just kept expanding my diagnostic paradigm and therapeutic paradigm wider and wider to incorporate as many levels and layers of the human experience as I could, and then fell into Ken Wilber’s integral theory of everything.

And once you start, and once you start looking at external and internal and, and individual and cultural, and you just start looking at all the determinants of illness, you end up with a very large roadmap, if you will. And I eventually ended up taking the, um, ive. Roadmap of the, the, the Ko, the bodies that people seem to have.

So if you look at the ancient tic text, they say, we’re not just a physical body where we a physical body, that’s constantly in exchange with the external environment. So we always exchanging atoms, you know, right. As Deepak lights to say, we’ve got, you know, a million atoms of Atel Jesus Christ and Hitler, you know, , we’re constantly exchanging information.

So, so the first level of the, of the paradigm I use is the external world of air and, and water and earth. And that incorporates all the toxicology because we in touch with that. And it, it interfaces with our second level, which is our physicality, our biochemistry, and our structure. And that’s what we do in traditional medicine and functional medicine chiropractic and, and.

All the therapies that to do with structure and, and biochemistry. And then the third level is to, you know, to do with the, um, energetic, the electromagnetic fields, as we’ve learned from Cal, uh, from Albert PA and, and others that are light emits from our body in a coherent form from DNA. So DNA S squeezes light and it emits, and there’s a standing wave around us, which is either coherent or incoherent.

And it also resonates with human resonance, which is the sort of resonance of the earth. But then you got all the manmade fields that are interposed deployment now, and then you have this dysregulation of that are own innate. Coherent electromagnetic fields and that’s correlated with the brain and the autonomic nervous system.

So I have a brain treatment center where I do Q EEGs and we do heart rate, variability studies and stress response testing. And that’s the sort of the brain and the autonomic nervous system is the, is the sort of gateway between our internal experiences and our external world. It all eventually comes through the brain.

The brain sort of records everything that our internal dialogue, our 60,000 thoughts a day, right? Our values, our perceptions are all run through the system. And we know that our thoughts and beliefs influence our biochemistry and our immunology and I sell receptors. So the fourth level. The emotional body.

So trauma plays a big role in that, as we know, and this is very real, uh, people with early developmental trauma attachment disorders, either neglect, trauma, or abuse, trauma, or disorganized attachment, they have much higher, um, negative sort of health outcomes. And they have a much more difficulty in self-regulation and self-regulation in the parasympathetic state is, is the healing state.

And if these, and if these individuals with, you know, early separation from mother or early neglect trauma, if they don’t develop a sense of self, they don’t have a ability to self regulate. And that sets these so-called HPA access in this heightened state of, of hyper vigilance and inability to self regulate, which then shuts down the VA tone and so forth and so on.

So that’s fourth level is the emotional level. And then the fifth is the ego based. The part of our, our reality that sort of gets us through life. Mm-hmm , you know, ego based. Um, ability to negotiate the slings and errors of life is based on the resilience or the fragility of our ego self, which is very much the first half of life drivers.

You know, we are driven in the first half of life by the ego to be a, you know, find safety with mother and father, find connection with other, and then find our way in the professional world, which is the three stages of development of the brain. You know, the reptilian brain, the limbic brain, the prefrontal cortex.

We are driven to develop that, you know, neurodevelopmentally so that in our thirties, we’ve now got a nice prefrontal cortex that can inhibit any fears or any, uh, trust issues we have from early developmental support or not. Uh, so that’s all to do with. With the fifth level, which is the, which is the egos, the ego drives and our defenses, when life gets to difficult, we develop defenses against certain things, right?

And people have very, sometimes very rigid defenses or very fragile defenses and are often not open or susceptible to the healing movement. They just, they defended against any further intrusion into their sacred innocence. You know, they’ll protect you. And so you’ll launch into a, a mold diagnosis you’ll launch into.

Marcel and Liam and whatever you want. You’ll be working at level two with toxicology and physicality. But if that person’s unconscious belief system is shutting out and defending them against any sensitivity or any vulnerability you can work until, you know, the cows come home. You’re not gonna penetrate that, that system, that person.

And you’ve gotta be subtly aware of defense structures, internal dialogue value systems. You’ve gotta know those subtleties, I think in order to best help that person. Because if a person’s sitting in front of you and they don’t trust you, you can work till you can run test all accounts. Come on.

Nothing’s gonna shift in that system. Well, the sixth level is the soul. Um, second half of life, the authentic self that we often leave behind in the first half of life pursuits. You know, we go out and find safety and companionship and educate and. Safety. And we slay the dragons, the drives, the, the Freudian drives, right?

You know, the bitterness drives the Adlerian drives to power, but Carl Yung came along and said, the real drive is to know yourself. And that only sort of starts the surface in the, in the second half of life, when all the machinations and twisting of your psyche to get your needs met in the first half of life, you leave your authentic self behind in order to get seen and met and, and to get educated.

But then in the second half of life, you gotta go and reclaim all the parts you left behind.  right. In order to get where you are going. So that’s soul driven and the soul is. Personal and collective, uh, and families, the family soul. We now know from early, you know, family in constellation work that is initiated by ber Heminger and, uh, and, and taught by others, including mark Warland, who does fantastic work in this area that we, when we born, we not only get exposed to our parental influences, which have a, the whole set of determinants in the fourth level, but we also inherit, um, epigenetically, right?

The experiences and emotions of our ancestors. And so you’ve gotta like diagnose and treat ancestral inheritance of early experiences. And that’s another whole subset that we look at. And in union psychotherapy, we look at the individual soul. What is, what, what is the most authentic and instinctual. Core of this human being that’s sitting in front of you.

What is being asked to manifest? Because symptoms, as I’ve said in other webinars, symptoms are not, they don’t fall out of the sky. You know, they, they teleological, they have meaning and intent and sometimes symptoms, whatever silent in the system in, in your psyche will often show up as some form of illness or tragedy or bankruptcy or betrayal or whatever you want.

And symptoms are like that. They they’re often pointing to that, which is unseen in your evolution. So if you lose symptoms, it’s just things to get rid of, you know, suppress the mild cell, press the, my cell response.  um, as opposed to why the, my cells active is it because the child was never safe with mother.

So she, they developed my cell activation as a means to, to keep people at a distance with the skin rashes and the eczema IM not worthy of being touched. So I will keep my defenses. So sometimes that can be teleological in that. And if you don’t ask that question, you often miss the boat. And then the seventh level is everything beyond the ego-based pursuits.

You know, we in the infinite universe, the evidence for our insignificance is rather overwhelming and, uh, And so sometimes we have to sort of give up our hubris and arrogance and, and know that in the vast scheme of things, just give thanks because we really don’t know what’s going on. You know, there’s something, there’s some divine intelligence that’s manifesting that we need to be humbled to.

You know, I, I love that. And so I’m sure the people that are listening it’s it makes sense. A lot of what you said, it’s, it’s really everything. That we have experienced, but it’s also a lot of what we don’t know. And, and it includes the brain. It includes mindset. It, it could include religion and even just ancestrally a lot of the things as well.

The question becomes then, I mean, we, or Western medicine is all about, like you said, it’s you have a symptom. It’s how do you alleviate that symptom? And most of the people listening to this and watching this know that that’s not good enough, right. We need to figure out why do I have pain so that I don’t have to take that anti-inflammatory medication.

But beyond that, then we go to naturopaths and functional doctors and they say, it’s an autoimmune or it’s thyroid related. And again, it’s treating a certain thing without considering all of the things that you just mentioned. Yeah. So if we are, for example, struggling with chronic fatigue, how do we start?

Like where, where do we journey and how do we start getting to root? Cause because most people that are consuming this information, understand, we do need to get to root cause, but it gets confusing. Do I need to treat the limbic system first, do I need to get out of the environment? That’s um, I’m struggling with mold, you know, where do I start?

Because I really just wanna heal and I don’t wanna waste my money in this journey, but from everything you’ve said, it’s it’s complex. Objection. It’s complicated. So I, I can only tell you what I do. I don’t know if this is correct. I don’t, you know, it just works most of the time with P I’m sitting in my office here, and three feet for me is where patients sit or six feet and I take history.

So I, you know, I have a methodology of doing that. So I have a 70 page questionnaire and I ask, and I read everything on that. And I take the history from that. And my question is like, is set up so I can quickly go through what I do is ask, first of all, what are your top symptoms? And I write them all done, and I go through fatigue, cognition, sleep dentistry, and then all the systems.

And then I look at hormonal issues of male, female diet, um, psychological development, uh, family systems, uh, spiritual practices. So I grow through all of those and I, I. Try and do it as quickly as I can. It takes two to two and a half hours to take a history. And then what, but the thing is to attune to all the UN unsaid cues, you gotta, you gotta, you gotta limbically relate with the individual in front of you and you gotta look for hidden cues and symptoms.

Cause it’s not just knowledge, you know, it’s, it’s, it’s limbic resonance. It’s it’s you can’t only use your thinking function. You gotta use your feeling function as well. If you look at the Myers Briggs type and so you take this history, you feel into it, but you also use left brain didactic reasoning.

And then once you’ve taken a history across all the layers and levels, you then. Diagnostically work out where, what do I need in order to help fill in the gaps of knowledge that this patient, uh, needs in order to diagnose potential. As we use the words antied mediators and triggers. And then I usually set out a whole series of labs, but I can tell you what I use more often than not.

Um, I almost always do a Q EEG. I look at the different speeds of the brain, the Delta theater. Alpha and beta brain waves. And I look to see if they’re amplified or depressed and the ratios between them. I look at the autonomic nervous system through heart rate variability. I do bio Imped studies, looking at fat muscle fluid content.

Um, look at the phase angle to see if the cell membranes intact. Then we always do never forget this piece. Always, always like if there’s one thing I’m passionate about is this one always do the NASA lean test, the 10 minute lying and standing test. Oh, okay. Because I tell you 20% of people are pots.

Right. Get really busy and, and you won’t treat anybody with, unless you get the pots under control. There’s no one. Yeah, yeah, yeah. So do the lean, you know, do that test. My staff are trained to do it on everybody and we train patients to do it at home.
And so many pots. Yeah. I also do a neuroco MRI. We looking at different parts of the brain.

Uh, we pixelate different frontal lobe. You know, temporal lobes, looking at the coordinate nuclear gray matter white matter, and looking at the amygdala, cuz you’ll see a amygdala hypertrophy from traumatized people who are highly stressed and anxious and also look at the thalamus. Cause the thalamus is richly innovated with my cells, this rich with my, and, and so we look at these different parameters, then I do all the sort of functional I do standard labs, everything I could possibly get my hands on that hasn’t been done before.

And you’ll often find all sorts of things, you know, find. Thyroid antibodies that nobody’s looked at before, or you’ll find, you know, tssh levels that are sort of suboptimal with a low T3, which if you just tweak that things improve, you’ll find prolactinomas, you’ll find, you know, pituitary, micro, OMAS, you know, you’ll find these things.

If you really keep your diagnostic net quite wide, I always do a Panex dental x-ray and then get a 3d coin beam and get a dental opinion on everybody. If somebody’s had a head injury, I always get a nuclear chiropractic assessment of C1 C two. And if there’s any suggestion of creating a cervical instability, I send people off to that group of people who specialize in that like Dr.
Boies and others. And then on the functional side, I do food sensitivities, not just I G G, but I G G IgE. IG, and I do the lymphocyte sensitivity test as well. Oh wow. And I look at the trends in it. I don’t look at one. People come with the, I G four test isn’t it’s hopeless, you know, so I look at all of those.

I do many stool tests. I do the GI maps. Mm-hmm  I do the Genova tool test. I do the dun wit precision lab Lin, his D AO, um, histamine levels and the lip polysaccharide I do that. I do the intro lab test. If I suspect any gluten issues looking not only for the, the genes, but looking for. Uh, tissue trans determinates antibodies and fecal fat mal absorption.
I also do, um, CIBO testing on half my patients. Cause most of them huge majority, if they have a history of bloating, uh, Sibos always a role, but there’s, CIBO, there’s C nav, quite the term. LIBO large bowel bacteria, Leto, the words we use, you gotta treat them all. And then you look at Vaal time, the whole motility issue, and that’s through heart rate variability and specific devices we used.

Then I look at the, I use the ion panel. I know some people use the, uh, neutro valve, but I, the ion panel I can read in 15 seconds and look at amino acids, minerals, antioxidants, steady acids, but for fatty acids, I mostly look at the Kennedy Krieger body bio fatty acid panel for am omega three, six distribution saturate a fat distribution, the ratios between minimal and look to see if the lipid content of the cell membrane is high or low.

Because if the lipid content is low, like minus 25 minus 30, and you go put people on binders for mold, you’re gonna crash that patient like instantly. And so I look at that. I look at fats, uh, we look at the organ, the oats, the part of the ion panel. I do oats testing. I do the great. It’s heavy metals and the microtoxin test, but I I’m really moving away from the microtoxin testing because there’s so much bad medicine being practiced at that test.

It’s it’s I think it’s, uh, I think Richie Shoemaker for all of his, you know, he’s, he’s, he’s got some certain opinions about. Things. And one of the opinions he has is on the microtoxin test, not being indicative of SARS, chronic inflammatory response syndrome. And on that, he’s incredibly correct. You cannot go and diagnose mold illness based on a urine microtoxin testing.

Don’t even begin to tell me, you can, you know, you can’t and it’s it’s bad medicine and I wish it would stop, you know? Yeah. I learned that too, because essentially if you’re healthy, you will be able to remove microtoxins from even your diet, um, in a urine test. So you can’t differentiate between a healthy person that’s releasing versus somebody that’s really poisoned from it.

And so you need more markers than that. What’s interesting is I’ll find some SIRS clients that will then take the microtoxin test and they’re not releasing any because I think they’re unwell. And so that part of it is interesting, but you’re right. The test itself is not enough, but well, they they’ve done testing with healthy controls and the healthy controls have the same microtoxins in urine cause they had corn and uh, pizza the night before.

Right. You know, if I was your patient and I didn’t have all the funds to do all that testing, is there a baseline you can start with with, based on my symptoms, maybe running some of the lab tests? Maybe not all of those, because that’s a lot. Well, I haven’t finished yet.  let me tell you the, let me tell you the test that I really rely on now.

Okay. That’s the IGL test out of Germany that. Has changed my practice, cuz that measures the ducts that sit on DNA, affecting DNA transcription, and you can find mold and mercury and aluminum and glyphosate affecting how messenger RNA is transcribed. It also tells you about cell membrane voltage. It tells you about mitochondrial numbers cuz when you have what’s called a cell danger response.

Mitochondria undergo oage die and you can measure how many mitochondria there are, and you can see it’s low or not. You can see if the cell membrane voltage is low, you can then look at superoxide DYS glut levels. You can look at phosphide choline, phosphide ethyl, OME, the outer inner membrane of the cell.

And you can see how depleted they are. You look at cardio lipins and whether that enzyme is making cardio Lipin. And on and on and on. It’s just a fantastic test. It also tells you about, it gives you a lymphocyte sensitivity test to mold, fungal elements and metabolites. So you can see if mold is sitting on the DNA or whether there’s fungal metabolites or fungal SPOs in the bloodstream to which the lymphocytes are sensitive.

So I find that very helpful. Now you’ll often find people with a microtoxin test in the urine that’s negative, but when you go and look at the DNA, there’s mold micro mold for sitting on the DNA affecting, you know, um, transcription wow. Of messenger RNA. And that person is often, far sicker than the one who’s got microtoxins in the urine is excluding them.

Right? So you in answer your question, what tests you run and how do I do it? Well, I’ve got to the stage in my career where they, everybody who comes to see me now, it appears has done lots of these things, you know, but never. Never enough. And so I say, look, here’s what I need. Here’s the tests. I also do Cyrex antibody testing.

I do the neural Zuma antibodies to brain. You know, I do all the almond lab mold, Lyme testing, and iGen X. If I have to. So I say, here’s what I need to complete your diagnostic profile. And my staff then send it to them. And then it’s their decision with their budgetary restrictions. I try not to interfere with that.

Cuz some people have funds. Some people don’t, if they don’t have funds, I then try and adjust my practice accordingly, but then you’ve gotta adjust their expectations as well, because they’ll always come with you and say, oh, I’ve got, I’ve got mold on this. Look at my microtoxin test. And then you take a two hour history and they’ve got 50 other determinants of being unwell.
Right? So then you give them the diagnostic roadmap to give them the, what you believe I believe is the insight into that. But then they on, you know, they’re they don’t have funding. So then you try and work with what you can, but you’ve got to taper your expectation and they’ve gotta taper theirs. And that’s a tricky relationship with people, you know?

They’ve been traumatized because if they don’t trust what you’re saying, they’re gonna project all they distrust onto you and then they’re going, you know, they’re gonna, it’s tricky. It’s a tricky relationship working with ill people. Not always, but it can be. Yes. Yes. So let’s, let’s talk about an example of sir, somebody that has the genetic haplotype, they’re all the blood markers that Dr. Shoemaker brings up, like the MMP nine TGF beta one, Ms. They’re all low or they’re all high. And the weight they’re all low, right? SOH is low. The other markers are extremely high and their environment isn’t the greatest because they don’t have the funds to really fix the environment. But then, then I meet people that are limbic system retraining specialists, and they talk about how they.

Force their body to rewire their brain and, and be able to get better, even in an environment where their army score isn’t the best. So, you know, you talked about all these layers of health. Yeah. How do we know that if we were to just pull the layer of trying to manage the brain and how it reacts to stress?

Like what if that will just heal some of the other areas, even if in tests they’re off tricky, tricky dynamics  so if you take the history there’s water exposure. Yes. You do the army testing. There’s positive, you know, all hurts me too above 10, and they got all the bad ones and the, the symptom questionnaire they’ve got, you know, 25 symptoms in 13, 12 clusters, and they fail a visual contrast test.

And then you do the Shoemaker markers and the TGF B is 10,000, the C four H 20,000. Ms. H is five, you know, and. The person is highly reactive to the mold that they’re exposed to. I don’t believe that you can only do DRS or Gupta’s retraining program and treat them with that methodology. I think that methodology is important when the amygdala gets sensitized.

And is hyper reactive to the incoming biotoxins, but I do think you’ve gotta work biologically to downregulate the innate immune system while addressing the amygdala hyperactivity at the same time. And often you’ve gotta work sooner logistically. Yes, but there’s even a deeper layer that the DNRs and crypto training program often don’t get to the hidden defenses of the individual who’s hyper reacted because they’re protecting their, the last vest of their innocence, which never got traumatized.

And they are so defended against anything. That’s could be perceived as toxic that they can’t downregulate the amygdala because the trust is not there and they can’t trust anything. And that’s when you need to go into internal psychotherapeutic work. Uh, and you can’t just work with dynamic neuro retraining or cook program.

You have to address the defenses of the individual. So it’s tricky, but it can be negotiated. And some of my patients with the amygdala sensitivity, they just think of mold and they react that they do. It’s a real reaction. It’s not, they’re just so sensitive. And you look at the neuro quite, and then amygdalas in the 98 percentile it’s hypertrophy is big.

It’s two standard deviations than everybody, and then their colleagues and their age match controls. So then you’ve gotta, you gotta do all sorts of neuro bio, all the whole things around neuroplasticity and cell membrane, integrity and fatty acid manipulation. And it’s complex. That’s interesting because that’s kind of what I’m coming down to.

So just to give you a background, I specialize in the carnivore diet because I believe it’s the ultimate elimination diet in terms of just getting food off the table as a culprit of your illness, and then we can work on everything else. And so there’s a handful of people, including myself that have healed a lot.

In terms of illness, mental illness through a meat, only diet. But as I worked with more people in more complicated cases that the food doesn’t fix everything. So they get a lot better, but not enough that they feel better. And so they start working with me and I started noticing there were people that had this serves and I fell into shoemaker’s work.

We started testing some of the markers and they had the genetic type. They had all the markers we just mentioned. And, and so they started some of the coolest tyramine. They did some of the excess fish oils and it wasn’t enough. And my guess is like, you mentioned that, um, Kennedy test, they would’ve probably had really low markers and you not touch tyramine unless, you know, the lipid content it’s fatal mistake.

Second fatal mistake. First is treating a person with, with a microtoxin test is having mold illness. Second is throwing tyin at they prematurely. Sorry, carry on. Yeah. Yes, yes. And so, well, that test is not part of the NA the original protocol. And so, no, no, no. I, I actually learned it from you and it made so much sense of, well, this is a bio acid reducer, which also was known to reduce your cholesterol.

And if you cannot take in fatty acids, you might not have the wherewithal to even take the colony remain. And so the, the phospholipid flush the, and the fatty. That all made sense, but this and cholesterol, cholesterol forms is structured in your cell membrane and is a precursor to all your hormones. You don’t wanna block cholesterol to the point of extinction.

You want a cholesterol to be sort of highish normal, not yes, yes. You wanna block Cho. And I think that’s where carnivore is so powerful that if somebody has been eating carnivore with a high fat diet and their cholesterol markers are high, they’re more prepared to take tyramine yes. Than the average person that’s eating a low fat diet.

Exactly. The don’t get me started on the vegan diet and I’m gonna get everybody’s kinda scream at me on social media. No, no. Well, my community is not plant based. Um, I actually got sick on a plant-based diet, so, but yeah, I was, I was the head of the vegetarian society for 17 years, so I’m familiar with it.

OK. But my experience, you don’t get people well on a vegan diet, if they’re in a chronic ill health multisystem, multis symptom, complex illness mode, it’s just not gonna happen. Right. Right. And I, and I fully agree with that. And so. Happened was some of the people as they got diagnosed with SIRS, they started going into the excess research of what do I need to do now.
I need to be super mindful of every building I go into and, you know, that fight or flight mode, just really high gear of stress and, um, just being in their illness all day long. And I think those people then using the, the limbic system retraining. So it seems like it’s a lot of these modalities together that can actually heal people more than a lot of them together.

Yes. Most of those people, and I say this generically and somewhat, I hope it doesn’t come off as sort of prejudicial, but a lot of those people with the limb. Hyperactivity have trauma. Oh no, I believe that too. And they can’t there’s no, there’s no re they can’t self regulate. There’s no window of tolerance.

And I send them to somatic experiencing trauma therapists. I don’t, they do good DS, but they often need to do body based body up therapy, where they need to actually learn how to tolerate more and develop a window of tolerance. Um, uh, that I use se practitioners a lot somatically. I refer to that. I’ll have to look into that.

That’s fascinating. Yeah. Just check that one out because it’s, uh, it’s a, it’s the game changer. Yeah. When DNRs fails and Gupta fails, think trauma think early thinks se uh, body base, you know, be off on cult’s book. The body keeps the score. Mm-hmm  yes. That’s real stuff, you know? Okay. And it’s, if you look at Robert Navo cell danger response, you look at PGES body vagal, uh, dorsal, Vago, shutdown, response, those people.

Autonomic nervous system shut down. Mitochondria are shut down. They’re in an inflammatory response. So is part of, uh, Robert NEAU cell danger response, number one. Okay. That makes sense. And they shut down and they don’t have a capacity to self regulate. It’s not happening cuz they, they, their whole system is in a state of freeze, not fight flight that’s, you know, beyond they’re beyond that.

Yeah. And they, and se practitioners know that stuff backwards and they can help you negotiate that territory. Yeah. And PGE developed a sat and sound protocol, which is a series of, of sounds and music and patients with severe trauma reduce up and sound. This is the feedback I’ve got. It found. It sounded.

My mother’s soothing voice had finally spoken and got through to me.  wow. Is that, that, what does the mother’s soothing voice do to a child? The child in trains with the mother’s voice and tone, the right prefrontal cortex of the mother resonates with the child’s right. Prefrontal cortex. They entrain with each other.

Over 30 years, the child looks away, looks away. Self-regulate looks to the mother. Mother’s still there. Mother still loves me, challenged me a bit, you know, support challenge. Over 30 years of neurodevelopment, the child learns to trust the environment, learns to trust safety, learns limbic resonance. They learn to self regulate their system.

If there’s been early trauma, doesn’t work self, a sense of self doesn’t develop the sense of self trust. And self-regulation, isn’t there safe and sound recreates that which is missing the mother’s voice. That’s hard like Clinton, like Clinton in the mother’s eye mother just has to have be 30% present, apparently to have a reasonable child upbringing.

oh wow. You be a perfect mother. You just felt be present about 30% of the time and you gotta support and challenge that child and give it appropriate sort of boundaries to work in and, and create a sense of trust and safety. So would you recommend then for a lot of the people that are dealing with chronic illness, chronic fatigue, let’s say they don’t have a lot of funds, but some of that trauma work and, um, the somatic, as you were talking about doing that can be very beneficial with, in tandem with someone like yourself that can also support improve, provide care.

It’s so difficult here, Judy I’m so used to working with a very broad diagnostic. Okay. That I, I can say yes, but, and you know, yes. What else is going on?  right. Is the theater brainwave feed standard deviations higher than the peer group. And if so, that person doesn’t do well. They in a disassociate in, in pathy.

Okay. So they may not be able to do safe and sound work, you know? Okay. Yeah. Yeah. I know. There’s always nuance and I, I totally understand that fully. I wanted to shift topics a little bit. I know that you, on your Instagram page, you share a lot about M a histamine responses. Yeah. Yeah. Can you share a little bit about in the carnivore community?

For example, a lot of people will remove certain foods and then they try to reintroduce it. It could even be salmon for example. And they say that they have more mass cell activation and more histamine responses eating the carni way. I don’t know if it’s because part of the reason is that they’ve removed the food for a while and now as they’re introducing it, they’re just a, um, reacting.

And maybe it just takes a little bit of reintroduction, but what are your thoughts? Well, histamine, you. Breakdown product OFTA Dean right rights more there. And where’s, HETA Dean found more in salmon. Right. So, you know, um, if they’ve got my cell activation and I, you, if you go and do an ion panel, you’ll see histidine there.

Oh, okay. And all my, my cell patients have high Heine levels. You see it all the time. And so if you’re introducing salmon in particular, if it’s not flash frozen on the boat. Sure, sure. Aged one of the worst triggers of myself that, and. You know, and all the fermented foods that are so popular now I know.

So, so you gotta be careful with that one. You gotta, you know, beef, if it’s, you know, a lot of beef is old too, they let it, the it, the, yeah, the it, and so of course, you know, that’s a, something duck for myel activation, but that’s where you gotta do the precision done Woody test and see what the DAOs doing and see what the histamine levels and the Lin levels, and then ready prepare them, you know, use your umbrellas or your, his Dao in huge amounts, 30 minutes along with chromosome.

You know, if you suspect you’re gonna react to meat or, or any food for that matter. And then you use all your myself, I’m very aggressive with myself. Like, cuz I use. Okay. I use pharmaceuticals and nutraceuticals, but I, I, I happen to use pharmaceuticals more than nutraceuticals because I find they get the job done quicker.

And I do intravenous myself blockade for the very sensitive people, the ones that just wiped out, they can’t function. They can’t leave their hospice. They’re reactor really. They they’re down to three foods. Right. So we, we bring them. Look for parts first, look for hypermobility. Number two, then treat them with intravenous ma cell Benadryl ol Aban.

We use I IV Avan, which is a Maal blocker. Unden Thero for some of the nausea and GI symptoms. Get them stabilized then onto pharmaceuticals. Then maybe nutraceuticals. I work that way around. I know lots of people work nutraceutical, but I, I just because I’m an MD, but you’ve gotta use them without excipient or diets.

You’ve gotta get compounded pharmaceuticals. Sure. So what is the root cause of this? M a right. So it’s obviously there’s a hypersensitivity to histamines. Not everyone has that same reaction. I mean, some of it is maybe they have gut permeability, but something triggered the M a to occur. Like, what is the root cause of why are people getting diagnosed with M a S and it, sometimes it just happens in their thirties and forties, but what is causing it?

And so Aron Lawrence Aron, who I work with. Okay. And part of his little group we wrote, he wrote the paper, which we co-authored on the consensus two statement of what is my cell activation, how to diagnose it. There are genetics to it. There’s not the same genetics that are there with systemic master psychosis.

So my cell activation syndrome is just an overactivity of my cells. Systemic mass cytosis, as you know, is increased numbers of milestones. So in, in my cell activation syndrome, you’ve got twitchy, my cells and my cells sit in all the surfaces of a body to protect you from incoming, toxic load and internal mental stresses.

LA Ron’s Han believes that the mental, uh, trigger of myel activation is more powerful than the physiological triggers. So what you have is, you know, these vigilant cells sitting there ready to pounce, whenever something comes in that shouldn’t be coming in and they send out thousand mediators of inflammation.

Right. Of which we measure 10 histamine is one of them and histamine. Yeah. So you’ve got these, my cells sitting on all the RFS in your nose, um, your GI tract, particularly richly innovated in the judum all the way through to the anus in the skin, in the brain, in the. Cardiac tissue and lungs in particular.

And they send out a thousand mediators of inflammation, histamine being one of them. Right, right. One out of a thousand. And they send out these in these signalings to try and dampen the incoming, toxic load. So they protect it. But they’re overreactive.
Why? Because. Look around you. We’re inundated all day long with, you know, toxins or triggers.

Biotoxins chemicals, metals, insecticides, pesticides, EMFs. Oh my don’t have you started on the EMF story, terrible trigger of muscle cell activation in a subset of patients. So those with the electromagnetic hypersensitivity syndrome, just to, for your, for your, um, clients don’t work without a building biologist, looking at the EMF exposures of your patients, ask them about it.

The same is don’t work without a biological dentist looking at the bite and the root canals and the capitations and the metals and the alloys and everything else. So the reason why the, my cells are so active is because our toxic load is so active. It’s so huge.

And so you get, there’s a genetic predisposition to some people.

For my cell activation syndrome. Mm-hmm  but it’s a toxic load. That’s exceeded like capacity to self-regulate once again. And so they’re just throwing out, you know, Ava trying, trying to keep the lid on a massive inflammatory response, but they trigger my cells, trigger oxidative stress. They trigger peroxide nitrate.

What does Pery nitrate do? It rips through your outer membrane and your inner cell membrane phosphocoline phosphine gets to your DNA, your mitochondrial DNA, mitochondrial DNA unravels goes outside the cell with ATP. Wow. Outside the cell. They become pro-inflammatory and they, then they call purines, they then trigger my cell activation to trigger Parx nitrate.
And all of a sudden you’re stuck in an inflammatory response you can’t get out of. So that’s the cell danger response, which is so beautifully described by Robert paver. Again, for your audience, please don’t go far without knowing his work backwards and forwards. Yeah, sure. And I’ll put that in the show notes.

Yeah. So then do you think if people get out of the toxic soup and they change their environment, work on some of the trauma, you know, and I’m saying it so simply I know it’s not that simple, but that we can actually reverse some of the M C. So that our bodies are not reacting as much. Oh, absolutely. Yes, absolutely.

Okay. I’ve had people, you know, they do the MQ symptom questionnaire, which is the IFM standard questionnaire for toxicity. All the symptoms score 180, 1 90 for add up all their symptoms, normals 20 or less. They come in a year later, they scores down at 20. Yeah. Now people get better. Now the ones who don’t get better are the highly traumatized individuals who with personality disorders, they are trickier to work with, you know, borderline and, and people with severe mental health issues like anxiety.

Sure. OCD, OCD is a big one. Yeah. They often don’t get better until they use it. S Sri or some form of control of the, uh, hacker activity of the system. How much do you think diet plays a role outta curiosity? A hundred percent, but is not the only thing. Diet is everything. Of course, diet in general, a hundred percent diet with M C.

99%. It’s big. You know, it is big now Lawrence Aron doesn’t believe diet is as big as some of us do in the functional world. But those of us who work in the functional world, I mean, there’s no way you’re gonna treat a severe mass cell person. Who’s eating eggs and drinking kombucha and you know’s drinking wine every night.

It’s not gonna happen. There’s no way. So you have them on lower histamine foods. Then I work with Justin Sanger and nutritionist, chef Revis, a cookbook together, and we do paleo autoimmune, low histamine, ketogenic, maybe FODMAPs, maybe isolates, maybe Oates. We do. We have to know all the diets. Yes. And that makes sense.

We know, we have to know how to juggle them. And we’ve developed a two page cheat sheet with every food color coded. So, you know, onions, it’s got a color code for oxalates orates or Fatma. So a food may have four colors on it because it’s got four different potential effects in the body and to try and work that out.

You’ve. Look at your food testing, you gotta take your history because the food testing doesn’t tell you about my cell necessarily, but you’ll see trends showing up quite a lot. You’ll see pineapples in there, Kiwis in there, Candis in there. A lot of the beans are in there. A lot of the beans are always in there.

That’s fascinating. Yeah. And so you just look at trends and you gotta think it through and you look at their diet and, and you eventually work out what to do. But I think the mildly ketogenic, paleo autoimmune low histamine is where, uh, we sort of trend towards to restore the cell membrane, integrity and repair mitochondria.

Yeah. And that’s where I love the carnivore diet. I mean, obviously I have my biases, but so I know that there are foods in the carnivore diet that are high histamine, but if you were to remove those, so let’s say the eggs, let’s say some of the fish, but if you were to focus on mostly meat based and then, um, I mean, it’s so similar to the paleo.
It’s just, I think I, I forget if the autoimmune paleo contains nuts. I don’t think it does, but maybe it does. Um, well, you take out all nuts in nap pale or two. I, I include three, three of the non mini nuts sometimes just in the beginning, Brazil, Nu pine. And I always forget the third one. Is it Macada okay.

Okay. There’s three nuts. That aren’t many. Okay. How funny? So people are really, I got no foods. We always use those to begin with. And then when you see, yeah. Oh, sure, sure. So you do it like a trickle down effect. Okay. Does that make sense? But I take out all grains, all legumes, all nitrates, all dairy, all fermented foods, all alcohol.

Oh, uh, you know, we take them out, right? We start from scratch meat, fish, chicken, stir fries, salads with oils and fats, the oils, and the fats are the piece that people do not do properly. I agree.  and, and that’s why if you stick, stick to mostly carnivore, you’re not eating seed oil. So then it becomes so so much.

I know it’s a lot more restrictive than at least giving them. Those three nuts, but in general, if you do a meat only, it becomes easier because it’s really easy to figure out which ones, um, you just focus on meats and then you’re not eating seed oil. So you’re just sticking to the lad or the, um, the sewed and other types of fat.
And, and then you may just have to have a list of what foods in the animal based world that are higher in histamines, and you may just have to reduce those. And it becomes a lot more simple when these people are trying to do so many different things.
And that’s where I personally like the Carver diet, um, especially as an elimination diet first, and then as they heal, they can introduce other foods.

So I think, I think it makes a lot of sense is another player on the, on the market these days is, uh, Gooden, ours work with plasmin. Okay. And he does a test called the prodrome scan where he measures all the, all the plasman and DHA and okay. Hospital co. So now I’m learning to work with that test, the, um, Kennedy KRE of fatty acid and the IGL mitochondria and our, all our work is to repair some membranes mm-hmm  and to work with the right fats to, to, uh, improve, um, neuronal tissue, uh, white matter, and to create a anti-inflammatory effect through DHA and so forth and so on.

But majority of people that come and see me are a omega six depleted. They all, none of them are doing all, uh, vegetable based oils and all of them are onco and they officially interesting. It’s completely suppressed the omega six side and the omega six side, the line lake acid is the raw material for phosphide choline.

That’s so fascinating. So a lot of people in my community are so scared of omega sixes because of the line lake acid that’s causing. Oh, obesity. No, no, no, no. So can you explain a little bit, so these people are, have been on a diet and they’re they’ve, they’re now becoming deficient in omega six, omega sixes.

Ole linolenic RONIC, it’s all wiped out. They minus minus a hundred on the, a omega six profile on the Kennedy Krieger test. And that’s the precursors to a lot of your phosphide co, which is the major fat that’s made from methylation that helps run outer and inner cell membranes go figure. And so the reason why they don’t use the vegetable oils is because most of them are toxic and they ran it and they got deodorizers in them.

Yes. Hide smell of the rans body bios fuit co I think is, you know, uh, is a fantastic omega six precursor. If you deficient in it, I would take the body bio balanced oil, which is ad. Oh, okay. Okay. I’m aware of that one. Yes. Yeah. And, and it’s, it’s, it’s prepared in a very clean, you know, cold press for okay.

Yeah. Very clean, no oxidation. And if you lower it in a lake, that’s what we plug in. Mm. Um, Justine St again, the nutritionist I work with, she, she consults on the plasman PLA the prodrome and the body bio fatty acid, and works people together with those nutritionally and supplementally. Yeah. It’s, it’s amazing that.

We hear certain context of certain nutrition and wellness, and then people take it to a lump to an extreme, and then they become deficient in omega sixes. And, and I started seeing that a little bit in my, um, I, I do a basic omega three, six test and people were starting to get more omega three rich because they were afraid of the omega sixes.

And now people are standing to get deficient because of all the polyunsaturated fatty acids that can cause obesity or insulin resistance. And also because of the fear of these seed oils. And, and now we’re becoming super more it’s either that we don’t have any fats or that we’re becoming more omega three rich, and we’ becoming deficient.

And I didn’t even think about the PPH ti choline. And that makes sense because I do recommend PPH ti choline, but without thinking about the omega six and the pre, because six often the omega the little lake is the, you. Pho often made from saturated that could be made from saturated. Fat was Lu lake is one of the major contributors towards fus curly.
Right? And so is the methylation panel, the folic acid, B12 zinc, magnesium ATP, that whole, uh, Sammy, that whole methylation panel, 70% of methylation and methol transfer is all to do with making phosphate. Possible is rules, you know? Right, right. And creatine, I mean the, the methylation cycle is big on creatine too.

So, you know, one marker in the service protocol is that our Ms. Sh is low and the goal is to increase thath so that our brain is not atrophying. And you know, a lot of the protocol says that the way that you increase sh is eventually you go through the whole Shoemaker protocol. Yeah. But you take V I P yeah.

But when I was doing some re research, the pituitary is what produces the UMH or melanocyte stimulating hormone. And some of it gets activated by UV rays. So couldn’t, we, some of us go outside every day. And get more UV rays and maybe it’s not enough, but could it actually increase some of theh? I don’t know the answer to that.

I do know looking, you know, at the sunrise and sunset has a tremendous effect on the duty function. Okay. Me production. But with Ms. Being low, most people with serves of low MSA, like sometimes super low. Right. And, and you’ve gotta all the up upstream, you know, inflammatory cytokines have to be downregulated.

And then you’ve gotta look for marks because the, you know, the nasal staff is what suppresses the MSA. Right. So you gotta treat the marks first. Treat the marks don’t regulate all the up, you know, all the steps, get them out of the toxic thing out the toxic building. And some people are now using peptides to help treat the Ms.
Stage or me. Yeah. Peptide. But again that you see that’s an N squared D squared thought process. Yes. Yes. Name of medicine. Name of symptom. Name of drug. Yes, it’s true. It’s not like that. You’ve gotta look systemically. How do I remove everything? That’s suppressing Ms. H right. And then how does Ms. H naturally start to find its way back up?

Yeah. And your patients, do you ever see them fully heal and their markers all normalize over time? If they follow the no, no, absolutely. Oh yes. Oh yes. Oh yeah. And, and white matter lesions in the brain disappear. How much do you think the environment needs to be pristine? Because that’s the biggest thing I get the hangup is it’s nearly impossible to have an environment that’s has zero mold.

So it depends on the level of the amygdala sensitization to that patient and the level of trauma and the level of trust it’s it’s algorithmically complex. So some people who. They are say HLA positive, but they’ve got good ego strength and have resilience. They can tolerate a lot more than somebody who’s, you know, in VEIC terms, vital imbalance.

Sure. Fatty active deficient, sympathetic dominance, or in polyvagal shut down. They can’t tolerate a lot. And so they just look at our building and if they just catch a whiff of a, of a nasty smell, they are in a full, you know, flare surge reaction. Yeah. It’s so individual, you never know. That’s so fascinating.

And that makes a lot of sense. When I think about my individual clients, how certain people are a lot more resilient, even though they have the haplo type and then other ones, just the fact that they have a split second, where they feel finally I have an answer, but then the split second later is, oh no, I have this haplo type.

And then they start reacting. So it is interesting, but because you see says. You can often not be exposed to mold, but serves in and of itself is the disease that you now have. Right? You have a chronically active, innate immune system that is now your problem. Yeah. And you may not be living in a moldy environment, but you haven’t gone through the steps of reduction of the, of the biotoxin that originally was there that triggered the whole surge response in the first base.

Right. Right. And that’s what nivo called the cell danger response. You stuck in the cell danger response and Robert nivo brilliantly said, we need things. He called the word emesis. You need to input therapeutic signaling to change the. The cell danger response. You can’t just hope to get better. One day, you’ve actually gotta do things.

You know, what are some of the examples that he, um, that Robert Novo recommends to improve the cell danger response? Well, he’s a researcher and he used the drug serum, which is a, uh, an old drug that you can’t get. Oh, okay. And serum blocked the receptors for the, um, DNA fragments and ATP fragments for triggering this whole self danger response.

Oh, okay. Okay. But he also did all the work on what are the biological changes on the self danger response and what is the one that is most consistent, fast choline? Vaso. Choline is big. That is so crazy because I do, I have been adding that before people even consider tyramine. So maybe do some of the omega threes.

I, I did see that balance of the omega 6 36. And I wasn’t sure if I was gonna use that one, but, and then I thought of the PPH title calling for the membranes, but it’s so fascinating. I’ll definitely have to look more into his research. Many people overdo the DHA component of omega three S yes or the EPA.

Now the I don’t, this is right Dr. Good’s research. I’m not sort of up on it as much as I should be. Okay. But I do know that alpha little Lennic. And EPA, uh, signaling molecules and they don’t do much for the whole equation. It’s a DHA that does everything. Okay. So here’s a Smogen DHA specific plasma Mogen, but you can overdose on DHA as well.

Right? So everybody who comes in with this amigo, you know, three, six index that’s off the chart for a MEUs sticks, the end danger of being very deficient in some of the essential fats to regulate cell membrane and mitochondrial functioning. So I wouldn’t go off those simple tests. I would, I would look at Kennedy Krieger or the, uh, fatty acid test.

Okay. No, no. Even the, even the ion panel, fatty acid is not robust enough. Sometimes it even contradicts the Kennedy credo and that’s fascinating. Okay. Okay. No, good to. A question about the IME test. So, um, I had a client that took a, you know, like a, I think it’s just a air sample from a person that normally, you know, sells homes and they do the mole testing.

And then I told him that he should pro and so his house came out clean, and then he did the IIE test and his number was maybe in the twenties. And I told him that you have high mold and that the other test is not really accurate. The first mold inspector came back and showed a link to the EPA saying that IMI tests are not supposed to be used.

Yeah. Yeah. What are your thoughts of the testing? So the answer to that question, you know, the one you, the person you want to read, who’s done so much work is Richie Shoemaker. Okay. He’s already dissected this issue backwards and forwards. Okay. And he did a series of, uh, articles in the tons and letter, which we just Google it.

One to five on mold and he discusses that question in detail. Okay. And so the world out organization has come out saying that the air sampling test is irrelevant. Uh, it’s worth us and meaningless because a you’ve gotta circulate air through. First of all, a lot of the toxins aren’t in the air, they’re on the ground.

Secondly, the particulate size of the, of the, the spores or the microtoxins are lower than 0.3 microns. And they pass through the, they pass through the replace. They don’t pick them up. And so, and, and thirdly, like STAs, the most damaging of all of them is on the floor. It’s not in the air. There’s this whole in the Shoemaker group anyway, this whole.

Sort of don’t they don’t use air sampling. It’s not used they, right. You see. And he says, do not even somebody comes at you with the air sample, throw them at your hearts, but it’s the industry standard. I know that’s and the lawyers and the insurance companies, that’s what they use. So, and army test was not supposed to be used clinically, but I can tell you now that I hurts me to test with the added Acton SIS and other components.

That’s what, I don’t even look at air sampling. I just wanted to clarify for the audience. I mean, there are people that’s, what we are known for is the air sampling. But if you have anyone that’s struggling with mold illness, the recommend the IEN and the SME. So I, it hurts me too. And looking at the aspergillus for, and the other thing is doesn’t differentiate the, the Asper species.
You don’t know if it’s for or Pallo. It doesn’t look for Olevia it’s it’s not good. Okay. Okay. Good to know. Yeah. There are some people that struggle with Lyme and Lyme is they say it’s really, really hard to detect that it’s really hard to figure out the co-infections people will do the Western blot and it doesn’t always, uh, show that you have it.

There’s like the other, the galaxy. And I forget the I Genix one, I think. But do you recommend a certain test that people can figure out if they have Lyme? No. And I, and I, I, it is just such a again, I mean, I, I think one word that’s coming on mouth repeatedly. It’s complex. And I hate to say that, but it’s complex.

I know you’ve gotta get a history from a patient. Okay. Not necessarily the tick bite and the MI, you know, the, the erythema rash and the weak followed by flulike illness. If you get that history. Okay. That’s great. But many people don’t have that history, you know? Okay. Yes. And so you’ve gotta do a history.

Then I do, I do questionnaires. I do the NCE questionnaire by Horowitz and I do the can lime questionnaire revised, which is from the Canadian Limus associate can lime.comal.org or something. And then I added Boris’s questionnaire and I made my own, okay. So I do Horovitz my own. I take a history and if I’m suspecting tickborne infection and co-infection, I then run T-cell testing or through Armon labs in Germany, and I run iGen X, full iGen X immuno block testing.

And if I suspect, and I’m looking there for IgM, I G G PCR, um, and I’m looking for RNA fragmentation, and I’m looking for all the.
Added lime biomarkers that have recently come up with relapsing fever and MIMO and things like that. So I do all of those iGen X, Y Armin lab, El spots. I don’t do the tick Plex plus much with Armin because I get what I need on the, um, agen X.

And then I run galaxy labs for . And then I sit with the awareness that many people will have negative labs and still have tickborne illness. And that’s the sort of current teaching. Amongs one of the PI all the pioneers in lime world, which is vilified by the, uh, I S D a association. There’s no such thing as chronic ly, right?

The test, you know, the testing’s irrelevant. It’s a, it’s a mess. It’s a minefield. And what I do know is that many people come in with a, you know, an I G G I X Lyme test. On one of the bands and say, I got lime. It’s like coming with a microtoxin test and say,
I’ve got first, that’s a perilous mistake to make.

Okay. You gotta really, you gotta have your wits about you from a, for a number of reasons. A if you, the diagnostic testing is expensive. Yes. B patients love to find single point causation. If they say you’ve got lime, you’re gonna send them down a rabbit hole of two to four years of whatever treatment you choose.

Sure. And C you are going to be vilified by your traditional colleagues.

If you’re not surefooted on this one. And most of our medical boards will take your license away. Wow. If you, oh yeah. If you start dabbling in this field, so it depends on your resilience to withstand the whole onslaught of the lime world. Now there’s people out there who do lime beautifully and who are experts like Horovitz and.

Steve Harris and others, you know, mm-hmm  and I recommend you probably go to the, the most prominent, most qualified, loud, you know, most outspoken expert in the field and go treated by them, but to be treated by an inexperienced naturopath or has been to one eyelids course and has one test, I be careful.
Yeah. It’s a perilous path. Um, okay. Yeah. As we’re closing, if people are, you know, have tried many different diets and they’re just not getting fully better and you know, standard care is really not been doing. Good for them. And diet helps somewhat, but not enough. And they’re just feeling chronic fatigue.

Where, where should they start? Like what should they do to maybe incrementally start getting better? Should they save up money to work with somebody? I mean, what are your thoughts? So a person who’s. Changed their diet, but still chronically fatigued. Yeah. I guess mostly fatigue. Maybe they’re still struggling with hypothyroid and they’re, I guess maybe we don’t take talk about the hypothyroid because maybe they have to balance their medication, but somebody that’s just still not fully feeling well.

And I guess the main symptoms would be chronic fatigue, maybe some brain fog. But just generally unwell, Julia, I hate to sort of be the bearer bad news, but you gotta do all layers, all levels. You gotta take your history. That’s fair. You know, if so, so let’s look at one of the variables. Yeah. A person may be uninspired.
They’re living a life. They’re not living their values system. They’re living their fathers. And they’re go to get up and go to work every day, not inspired and not being called from above, if you will, by that, which is speaks to them and evokes their creative spirit. Yes. And, but they got a positive microtoxin and a Mo or whatever test you want, and then you start taking the history and you realize.

Is this person, what do they have to get up to every day? What, what in sport calls I get up every day and do what I do. Cause I love to do what I do. What’s calling them from above to get up and do what they love to do. Why? Because the particular activating system in the brain is designed to shut you down when you’re not doing what you inspired to do.
Mm. So their fatigue, maybe just the fact that they’re not living their value system, they’re living their fathers, or they don’t even know what their value system is. They don’t even know who they are. They’ve got no self inside. They’re not inside. They don’t know why they get up every day. They’ve got nothing that calls them from above.

So yeah, you can go and do the mold in the diet. But they have no reason to get up every morning. And there’s a lot of patients like that, you know, and you have to start appealing to that aspect of them. Look at their value system and see what’s inspired them. And some of them, you know, patient, how many patients have you had chronic fatigue, sick unwell.
You work beautifully for two years. You go through every single test in the book, you do everything right. No better. And then you go. And you find out they go away and a year later they come back and they fine. What happened to you? I left my husband. I left my job and I fell in love. How much of, how many of us work in that?

You know, we ask about that, but you don’t know. Until the person has changed some of their experiences as to what role those played in their life. You may have hinted it, but until they, they get insight until they change, some of their determinants healing is must. We know so little, you know, We know so little, uh, and sometimes it takes, sometimes it takes, if you will, an act of God, it takes, I don’t mean that in a religious sense, but there’s some movement that sort of enters their field that pulls them into a new experience.

And all of a sudden they shift and they buy chemistry shifts and the molecular signaling shift shows, then they, they feel inspired and life’s meaningful. Again. I don’t know the answer to that question. No, I, I think that’s good. I mean, for me, I struggled with mental health and depression, anxiety. I didn’t like my job.

It was a very well paying job. I traveled the world. Everyone loved the kind of work I did in that sense. But at the core of me, I hated what I was doing. It wasn’t fun. I didn’t enjoy it. Um, and, and I struggled with depression and so I changed the diet and that helped me a lot, but it was really when I.

Found my purpose and yeah. Um, and God had something to do with it too. Yeah. And all of that together has healed me a lot.
So now I no longer share that. It’s just the diet because it diet helped me a lot, but it was like you said, it’s all the layers and I will always have something to work on in that whole sphere of things that you mentioned.
But I think acknowledging that because a lot of my clients will say I have stress it’s, um, that’s normal. This is just the life we live in nowadays. I think it’s making us more sick than we realize. Yeah. There’s a term in the integrated field called the allostatic load, you know? Yes. The incoming load versus the resilience and often that’s, you know, and people are often, people are so habituated to living in the world in a certain way.

They don’t know any other way. And so they think that’s their norm. Right. But then they go on holiday. They fall in love, they have another experience and all of a sudden they go. That wasn’t harmonious or coherent with my values. Now I can see. And only in retrospect, can they look back and see, or they leave a difficult relationship?

You know, sometimes people through Mayas, Bri typology or through attachment styles or VEIC styles, they just oil and water, but they try out of the goodness of their heart to make it work. And it’s, but it’s the allostatic load of that relationship is push them out of homeostasis and then something happens and that relationship breaks.

And all of a sudden the life force gets released and the patient’s back on track, but they were, they were just pushing against an aesthetic load that they weren’t conscious of until they somehow they got out of it for an act of guard or whatever, and then out and they look back and they go, oh my goodness, how did I persevere for so long?

It’s a lot to think about. And I love, I love it because I’ve just found so many of my clients that this is the way to heal is they have to touch everything in their life and it’s not easy. And people want the magic pill to fix everything. Whether it’s the diet, a supplement, a medication, a test. But I think from our conversation, it’s probably a difficult one to listen to because it’s not that simple, but if people really want to get to a level of healing that they can reach, um, It’s really looking into a lot of these layers that you so eloquently have brought up.

So thank you for that. Yeah. Layers, layers, and levels. Yeah. In the, in the roadmap thingy that I do here, which I haven’t published yet because I it’s in my book, but it’s, you know, each level is experience and anatomical conceptual designation as related science, a diagnostic method and the treatment method.

So it all layers. There’s sort of a template of possibilities and many people go to the wrong level. You know, they go, they go and see an acupuncturist when they should be seeing an oncologist or they go and see a shaman when they should be going to see a chiropractor. So there’s different layers and different levels.

So try and educate as to what layer, what level, when and how to integrate. All the possibilities. Well, thank you so much for your time. You, if so I know you’re in Canada. And so this was my struggle is I always need to find a service practitioner to work with my people that have the markers that need to start going through this journey, but you’re in Canada.
So one, how does that work with insurance? If people are in America, is your clinic open for new patients? So I, I do see new patients, but with the us patients, I act as an educator and guide an advocate because we, you know, we. Sort of practice across state lines, so to speak so I can suggest and guide, uh, but they have to have a primary care provider that will implement suggestions and, uh, advice.

And then do you normally have somebody in the states that you recommend? I recommend people go to the ICI website. I S E a I and find a practitioner in the area that has the most experience. Yeah. And so where can people find you your clinic? Um, in Calgary, Alberta, and, um, I have a website, that’s got a lot of my blogs where I write about all these things.
And that’s the Hoffman center.com center is T R E not the American ER . And then I think my staff may have sent you my Instagram thingy and yes, I’ll, I’ll put it in the show notes. I know. Yeah, I know you’re busy. Okay. No, no, no. I understand. I have read. Several of your blogs and you are so well versed and comprehensive, and I, I was totally drawn to you because of that.

So thank you for all your work. No pleasure. I’m glad you, uh, were able to make use of some of the late night research.  yes, no, I get that. Trust me. Um, so I will put all your information in the show notes. I’m excited to just see people really take a look at their illness and, um, take it to another level and look at the different layer.
And I would, I’d like to say thank you to all the, you know, the saying that’s cliche, but the standing on the shoulders of others, but Deri Khar Neil, Nathan, Richie, Shoemaker, Larry Doy, Deepak, all of these people that, you know, you just, you make your way. In relationship to all that they’ve done before you.

So we are not isolated in that way. And, uh, it’s good to say thank you to all your teachers and, you know, gratitude for what we can pass on and integrate and make new, you know, constantly reinventing the diagnostic and therapeutic. Uh, platform, you know? Yes. The goal is always the people and trying to get people better.

And if we can fine tune someone’s work, that’s absolutely the goal is because we want people to heal. So, yeah. And, and, and, and advice just stay related to your patients, you know, through limbic resonance, just, you know, the masks I done away with that, you know, The eyes, the tone of voice, the, the connection, um, that’s where trust gets established and that’s the, the hidden alchemy of healing, you know, that makes sense.

I love it. I believe it . Well, thank you so much. All right. Thank you, Judy. I was chatting to you. Okay guys, I know that this interview is not the most rainbows in unicorns in terms of healing. It may be a long journey, but always have hope that you can heal. Sometimes it takes a lot more extra work than the average person that may eat a meat only elimination diet, but you can still heal.

And there’s a lot that you can do, even with all the. Nuances and depends. And it’s complex from Dr. Hoffman. He says that diet is a hundred percent. Part of the equation. Carnivore is a perfect diet to do while you’re trying to heal all these other levels and modalities in your life that you need to focus on.

It’s never really about the carbs. It’s never really about the POAs. It’s never really about those other things. Oftentimes the illness is far deeper than that in our conversation. One thing that was really fascinating was that Dr. Hoffman brings up how a lot of his patients after having learned a lot about the damaging seed oils and the toxins in canola oil and soybean oil are now actually showing up that they’re really deficient in omega sixes.

He talks about how we need. Some of these essential omega six, such as linoleic acid and the other omega six is to even produce fossil tidal choline. We may be hurting ourselves by trying to reduce our omega six to the point of illness. It’s just something to consider. I know there’s a lot of advocates that are so against omega six to the point that we are just focusing on omega threes, but it is in balance and we are required for both for optimal health.

It’s just something to consider. If you are removing all levels of omega six in your. I hope that this conversation really makes you think and figure out what you need to do to help you get to root cause healing. Make sure to eat a lot of meat, take care of your bodies because it is the only place you have to live.

I will talk to you later. Bye guys.

Addressing Mold Illness in the Complex Patient

Addressing Mold Illness

This transcript was automatically generated, please excuse any errors.

Dr. Hoffman

Well welcome everybody. Today I’m going to be talking about complex patients and in the setting of mold illness, but I want you to know that this isn’t going to be about how to diagnose mold illness, sirs, and the steps A, B, C, D, E, F, G, which you can get, and I’ve listed some of the fabulous sites that are out there that you can go to to reference some of the logistics of how to diagnose mold illness and what to do about it every step of the way. This is more of just about what I, as a physician who treats complex illness, find when people present to me with a diagnosis or suspicion of having mold illness as a trigger for the complex symptomatology. And what I found problematic and difficult sometimes to negotiate when trying to understand where the mold may fit into the complex scenario. So these are some websites that you can go to Dr. Andrew hymens YouTube videos on SIRs are fabulous. Richie Shoemaker has been teaching mold illness for a very long time. The ici website has got some amazing people that belong to that group and present on mold all the time. They have an annual conference coming up soon. And then many of you may know Neil Nathan and his approach, real time lab have lots of information. And Dr. Dennis is an EMT surgeon who does a lot of work on sinus colonization of mold and performance surgery and treats mold illness as a occupant of hollow spaces. So those are some references for you.

But here’s the scenario. A patient presents at your office, this is what I see. This is what I see all day, every day. I’ve seen patients this week already with this type of presentation. patient presents, they say I have mold illness. So I suspect mold is playing a role in my symptomatology. And they’ve got many symptoms. You know, as we all know, when dealing with chronically ill people, they fatigue, they got body pain, they got brain fog, mood disorders, got GI tract is always involved, immune systems always involved, they feel inflamed, they hurt, they saw, they ache, and they very symptomatic. And they’ve often been that way for a very long time and have seen every specialist in the book and seen many times many naturopaths, chiropractors, you name it. They’ve been there. And then they show up with a host of lab tests and specialist letters and special investigations.

And now I once but to sort of sift through this and try and make sense of it and see where does mold fit into this complexity. So this is a common thing I get patients say I’ve got mold illness, and they’ve seen everybody. They’ve tried everything, and they always want to get onto Colas tyramine. I don’t know why. It’s a very common presentation. Can I get a colostomy today? Can you prescribe it for me, and I’ll show you as this presentation progresses, that this is probably the very last thing that you want to be doing. So the most common way people are presenting now is with a mold urine test. And they think that from this urine test of the mycotoxin, which is a toxic byproduct of mold, that they could have mold illness, and this is one of the biggest mistakes ever made. In my clinical career when it comes to dealing with complex patients and etiology of disease processes. This test cannot determine whether you have mold illness or not. And I hope my presentation will enunciate why I say that.

So where do we begin? So I’m not going to go straight into SIRs or mold illness right away. I’m going to just give you some background to how I sort of orient myself to these complex patients. You know, where do we practically begin? When we know in systems biology that everything’s connected to everything else? Everything’s embedded in deep chains and networks and systems and we are very tempted as physicians or clinicians to plunge into the typical n square D square approach to medicine, name of disease, name of drug, and this sort of prescribing an allopathic way, something to help relieve the patient’s symptomatology.

But over the years, I’ve developed a system of trying to work through complexity. And I adapted the eidetic model of the cultures or bodies, these different layers or levels to our reality model somewhat on a bit antic literature. It is very training that I’ve done in the past and also German biological medicine as developed by Dr. Dietrich Klinghardt. So I’ve sort of melded all these models together. And I look at the person presenting in front of me having different layers and levels of of their, to their reality.

So the first level is the environment. Outside, we can’t just do an exchange with our environment. So we all the toxicology issues come into play. Level two is the biochemistry and the structure, the physicality of our being. Level three is the energetics the sort of biophotons that radiate from us squeeze DNA, and the interaction with our nervous systems and brains. Stage four has everything to do with our emotional body and how we’ve been seen or not seen in our early developmental years, and what our attachment disorders may or may not be, and how we’ve oriented ourselves to the world in terms of developing a window of tolerance for self regulation in the midst of complexity and challenge. Level five is the the ego, the the operational sense of self that gets us through life. And that has our value systems, our defenses, our beliefs, or morals or values. And there’s a lot that goes on at that level.

And then level six is the so called Soul the most authentic part of yourself, that part of you, which is calling union, psychology the daemon. It’s your true authentic self that sort of, sort of holds yourself together consciously or unconsciously, it’s usually only accessible in the second half of life, I’m afraid to say. And I don’t mean that flippantly, it just seems to be that as we progress through life, the first 30 years or ego based, we driven to become something. And so we have these drives that that force us to be seen by our parents to be seen by our peers, to find a mate to procreate to educate and create some stability and safety in the world. But the second half of life is all to do with authenticity. Who are we really, and how much of our true self that we leave behind in this in this search for authenticity, or in the search for gaining something in the world and procreating the species.

And then the last level is that which is above and beyond and has nothing to do with our individual reality, which we call God or the grand organized design. And some people are very connected to that aspect of their non-local reality and other people aren’t. And it plays a role in diagnosis and therapeutics. So this is the model I use. When a person sits in front of me, can I use a practically very practically. And it looks like this on a map. Where we this is what it looks like when I when my book eventually comes out, this will be there. But this so these are the seven stages of reality and all the experiences anatomical designation sciences, diagnostic methods and treatment methods. And so here we have a lady to make it more practical and less easy to Tarek, a woman may present say, in her 50s with mold illness. And she’s got all these complex, additive diagnostics. That when you go through the layers and levels, they sort of show up. At the first level. Yes, she’s been exposed to mold. She’s lived in a moldy environment for 10 years and it’s deadly well since. But she also has other toxic exposures, mercury from fillings. organophosphates because she like lives next to a farmer’s field. She got a lot of dental issues, she’s lived in tick, bite country, and so forth and so on. You’ll see a lot of these different in functional medicine we call them antecedents, mediators and triggers of illness. Level two or two you know, we all know about food, gut, brain immune system issues, level three auditor electromagnetics and, and brain function, level four all about early trauma and inherited trauma from ancestors, level five or to do with ego strengths, personality disorders or mood disorders, and then level, that’s level five, and then level six, inherited family trauma, meaning and purpose in life.

Some people have no idea why they get up every day. And so people without that drive to, towards what we call a strange attractor, people get driven, there’s a biological urge to become something. And some people feel very disconnected from that, and that has vast diagnostic and therapeutic implications. And then at level seven, this woman had no connection to anything outside of her own reality. And so these sort of these, this sort of presentation becomes very palpable, very practical. I had a patient just last week, and she came to see me with severe muscle activation syndrome and reacting to foods she had, she was eating like three foods, she was breastfeeding her 15 month old son, who was also had very little to eat. Because everything was rejected.

He vomited continuously, she could only hold on a few foods. And this person was never sleeping through the night. She lived in a moldy home food was an obvious trigger as well electromagnetic fields, which as you’ll see are huge triggers of my cell activation and the so called Cell danger response, which we’ll get to in a minute. In a bit upon deep inquiry, it was apparent that she’d had a tumultuous upbringing with with lots of trauma, and interrupted bonds with the parents, their parents got divorced when she was three. And she spent the next two decades going to court and having to choose sides between her wearing parents. And she had allergies from a very young age.

And then I was just talking to her and I said, Oh, you know, I think we’re going to have to use a tighter, firmer h1, first generation h1 blocker for your son at night to help him with his micelle quietening. And to help him sleep. But she said to me, I just Google that in my chat group, and I heard that it’s gonna induce rage in children. So immediately, her fear based brain her amygdala was on high alert, she was already rejecting a potent life transforming treatment. Ketotifen is amazing when it works. And she had no trust in any allopathic intervention, she already had rejected it. And this you will see, when children had Don’t be unseen, and don’t have limbic resonance with parents, they often have, they’re not able to self regulate, and inhibit, they fear or they fight flight responses. And so they see everything as a threat. And they often have these very distorted relationships with their parents and projected onto therapists, doctors naturopaths, because our profession is very paternalistic, to put it mildly, in that we direct and tell people what to do. And so we act as authority figures. And if this person from a very young age has not been regulated appropriately by the parental influences, and there’s a lot of confusion and inability to self regulate, she will project her fear onto you as a parental figure. And she won’t be able to take anything in. So no matter if she has mold illness or anything else, it doesn’t matter what the diagnoses are, if no trust is established, and if no limbic resonance is established with her as a client, and no stable ability to self regulate is established, you will never get anywhere, no matter what the illness, you have to start at a much deeper level to try and really see that patient and understand the defense’s and understand the trauma before we drop into western or alternative functional medicine diagnostics.

So that’s one of the clinical pearls I would like to introduce when dealing with complex patients when they come in with a urine mycotoxin panel and say can we use code and stymied take a deep take a big step backwards we you know, we familiar with ranch rushing in and going you know, we take functional medicine, even a western medicine diagnosis and then we we want to treat it in diagnosis and then treat it but use a much larger or wider lens when you’re sitting in In front of these people and really start to see who this person is that’s sitting in front of you, what story is wanting to be told through this presentation? And where do you have to really start relating to this person? How many layers and levels are at play? Do they trust you?

Now, obviously, trust is a huge issue. And nobody’s going to trust you on their first visit, they’re going to not trust you on their first visit. So trust is earned. But if they were never seen by their mothers or their fathers, they won’t trust you. And so you can’t come on all strongly occupying the hero archetype and say, you know, I know what’s going on. And I’ll just, let’s do this and that, you have to really enter into the field and create the limbic resonance with them, and hear them and listen to them. They are dying to be heard and seen. So please don’t make that fundamental error of imposing all your knowledge on them. Right out the gate, really, really hear what they say. And these people, as you all know, have been to so many places and just got a sliver of information and not being able to do anything with it. Because in systems biology, there’s nobody practicing systems biology work. It’s all compartmentalized into silos, and square d squared, kind of organ systems.

Very few people are doing complex workups and treating them in a complex way. And again, be aware of the projection of unresolved early issues, the relationship to parents, because this is recreated in the clinical encounter, you will very often be the object of unresolved parental complexes. The other concept that becomes very important is to understand Robert Nivas work on the cell danger response. And also Steven Porges, his work with the polyvagal dorsal response, people who have been sick for a long time, their mitochondria are stuck, they are stuck in CD one or CD two roads famous responses, and they just can’t get out of it. They stuck. Even though the initial trigger may be gone, they stay stuck in this shutdown response. And in this collapsed response, and that’s a whole nother skill set to try and recognize if they in this shutdown cell danger response or if they you know, polyvagal, dorsal shut down, withdrawal from the world. And then you’ve also got to ask yourself, are they cognitively capable? And do they have enough ego strength to really take on the complex workup and treatment protocols? 

So we do all sorts of things to try and help us we do heart rate variability, you can see this person is highly in high sympathetic dominance with parasympathetics in the Negative Zone, you can see her Moca score was 2323 out of 30 is not good, there are some you know, memory issues and the hippocampal decline in this person. And then we redid the CNS vital signs computerized executive functioning test, she was in the low average too low to very low functioning capacity. This is not normal for a young, you know, 50 year old person. And then we did the Toba which is a method of ability to concentrate and stay focused and fail this one miserably. And then looked at a Qt T and saw that she had very high the CETA brainwave which is a slowed brainwave, which occurs as a result often of toxic and capital apathy.

Oxidative stress and toxicity generally came from head injuries as well. And that was associated with very high beta brainwaves with joy, anxiety brainwaves. Often this whole part of the brain is lit up like a Christmas tree due to early trauma, which which shows up in brain to E G’s. And then if you look here at the Alpha brainwave this alpha brainwave, here is the brainwave that chills, people are to calms them down, and that’s deficient. That’s one to two standard deviations below normal. So this person’s in fight flight. Her brain is slowed. So she’s cognitively impaired and she can’t regulate her. Her her her physiology, her autonomic nervous system, she’s really, you know, very ill and very depressed and very anxious and can’t sleep and fatigue and so forth and so on. So without these additive insights, you know, if somebody just walks in the room and they go mold illness put me on Curtis datamine and you don’t have some background data at the sort of higher levels of functioning.

You can really run into a lot of trouble and to, I don’t want to say harm, but really not be of much help. In the autonomic nervous system, we meant to self regulate and have coherence between the sympathetic and parasympathetic nervous systems. But many of our patients are in this fight flight, or even hyper freeze where they are actually frozen, they just they shut down. This is poisonous polyvagal theory, dorsal vagal, shut down. They, they they freeze, they withdrawn, they dissociate, they really sick and they stack you can’t get out of it. So, so learn to recognize these states. What you will then want to do is help them build a window of tolerance. And this is a slow process, they often have to refer to particular practitioners like Somatic Experiencing practitioners and others. We do a lot of work with neuro biofeedback as well as refer to Somatic 

Experiencing people and help these patients, you know, develop some capacity, some resilience, before they either hyper aroused or hyper arousal was completely shut down. Many of our patients they, you know, they are not thriving, they’re not incoherence, they’re not solving, self regulating. They are in crisis, they struggle, I can’t keep this up, I can’t survive, really learn to know these people and also learn how to diagnose and how to enter into a therapeutic relationship with them because you can’t go touch them mold, or their micelle or their life, you cannot go near those diagnoses, until this person has developed some resilience or some capacity to self regulate. So that’s the first sort of big insight. We’ve got three brains, as you know, the the reptilian brain, the mammalian brain and the human neocortex. It’s the it’s the neocortex, the executive function that learns to inhibit the fears of the amygdala, and the fight flight from early trauma and lack of trust. But many people’s prefrontal cortices are very damaged from mold exposure, and they can’t inhibit the impulses in their peers and they stay constantly upregulated. So the second sort of Pitfall, if you will, I don’t like after I wrote this, I thought, using the word pitfalls, pretty negative, but I hope you don’t take exception to this. It’s not implying it’s a pitfall, but it’s a sort of, it could be a stumbling block in your therapeutic encounter.

You’ve also got to know yourself a little bit. And you got to be attuned to your own blind spots, your unconscious complexes, your defenses, and where your knowledge begins and ends and don’t try and occupy the hero archetype and just be all knowing and impose everything without really relating to the individual. Are you present? Are you related? Are you resonant? Are you tuned? Your whole thing with these masks, you know, Porsche has has developed this polyvagal theory of social engagement. The ventral vagus is all to do with our tone of voice and eyes and facial muscles. And here we are walking. Two years we’ve all been unrelated and dissociated from each other for the last, it’s I think there’s significant consequences and, and a lot of parents notice, hence wanting to remove masks and things. So that’s another whole saga. 

But there is a there’s a physiological price we pay when we don’t establish trust, by by looking at somebody in the eyes and looking at the gaze and, and seeing the smile and hearing the tone in the voice because those are the unconscious signals we used to attune to others missing for the last two years. The other thing I asked you is, symptoms aren’t, they don’t fall out of the sky. You’ll those of you who are more experienced know that symptoms often point to somewhere in the system of this individual where unconscious dynamics need to be made conscious. I take symptoms as highly highly teleological they have they have they have meaning and often teach my patients to actually go quiet and go into their symptoms and ask their symptoms. What is it I’m not seeing? And sort of like a conscious meditation if you will, and you’ll be shocked at how many patients will come back with saying you know, I did that and I heard something my dream showed me something some synchronistic activity showed up and guided me through the process.

So don’t take symptoms. There’s objective, like we learned, let’s call a symptom that has to be destroyed and gotten rid of No, you vote lean into your center, what is it, trying to tell you that you’re not making a conscious symptoms are often pointing to what is silent or hidden in a system, or highly defended against so, so use symptoms teleologically again, are you acting as a authority figure upon which your patient projects all the rage? You know, if you look at the stages of emotion, anxiety isn’t an emotion, it’s a defense against emotion. But beneath that comes sadness and depression, anger and rage, murderous rage. So people are often highly defended against feeling things they don’t want to feel because those things are so awful, or were awful. So they will suppress a lot of the emotional self. And then because it’s so uncomfortable projected on you because it was projected onto the parent that they couldn’t engage with for various reason.

Again, what stage of life are your patients in first half first, second half and what defenses are active in you and them when you when you find when you find yourself becoming dogmatic and insistent know that you probably in a defense, you you’re activating your own core complexes. And it’s very difficult sometimes to not become self righteous and sort of have that patriarchal approach. We trained to have that approach, forged. As we’re learning more about trauma and empathy. Many of us have done you know, our work on this and know that that patriarchal attitude doesn’t really get you very far. You wanted in an era when you have a heart attack, you want to patriarchal person takes control and does exactly what they need to do to save your life. But in a therapeutic encounter, it can be disastrous. So, again, establish who is in front of you established your body felt sensations or the way you feel in your own body in front of this person? Are you in limbic resonance with them? Or are you completely disconnected? Know when people are shut down, know when they struggling to even show up with appointment? Know what the ego strengths and cognitive abilities, if they’ve got low motor scores, and they’re not going to be able to take on your program, you’re going to have to make some decisions on how best to approach that.

Person personality disorders are which they are out there borderline personalities, narcissist, and those people are difficult, be careful and know your way around them. Because those are the three that threaten to be lentiginous they often aren’t. It’s just a threat that they can be they can take up a lot of your time. But do your very best to create a trusting relationship? Not? Not? You know, it’s not it’s a genuine relationship. It’s not a false sense of camaraderie or anything. It’s a genuine sense of getting to know this person and what’s really what’s it like for them? You know, what’s the internal dialogue? We have 60,000 thoughts a day? What’s What’s the content of that thought process? Is it despair? Is it rage, often, you know, because it’s hidden behind the fences, and then help them to self regulate and create windows of tolerance. To to coin a phrase from Somatic Experiencing world and learn about neuroplasticity and neuro modulation, how the brain changes it states, there’s a lovely video of a guy who learns to ride a bicycle. And when he turns right, bicycle goes left. And he took him. It’s like a party trick. He goes on stage and asked everyone to come up, nobody can do it. And he took eight months to learn how to change is fun when you turn right.

The bicycle went left and he learned how to ride this backwards bicycle but to him eight months to do it. And the same is with your brain and your neuroplasticity and your defenses and your psyche. You can’t just shift a person’s consciousness overnight. And you’ve got to really almost juice that relationship into being through multiple modalities of information and salience and education and empathy and referring out to the right people. So I mean, I’m not trying to make this complicated, but just be a healer first and not a doctor. You know, just just the healing archetype is very different from the from the doctor argue To become a very good doctor know your western based diagnosis and treatment protocols, but also approach it from an empathic point of view. And a related point of view and know that any change is going to be particularly with these complex people is not overnight. It takes time, and learn all the ways to treat this neuro plasticity and vagal tone. And many of you know all these modalities, but I just listed some of them. And then know about the cell danger response. It’s an incredibly important concept to take into account.

It’s the concept that Robert Novo has developed over the years of research, which basically says that, when you’re, you know, you’ve got 30 trillion cells. And each cell is surrounded by a cell membrane inside of which there’s been 100 to 2000. Mitochondria, also surrounded by membranes with an electrical charge of approximately 170 millivolts. And the mitochondria are the canaries in the coal mine are the first thing to detect oxidative damage or any incoming stress. And as the incoming toxins come in, the the voltage on the cell membrane changes. And then that launches a whole host of metabolic changes, which leads to mitochondrial autophagy, which leads to the intracellular contents of the mitochondria going outside the cell, which creates another whole pro inflammatory response, and then the body stays in the so called Cell danger response never being unstuck, because the triggers are never addressed, and the metabolic machinery is never addressed. And so learning the cell danger response, I think, has become a very therapeutically, almost essential, We fortunately have some labs now, that can show us some of this before it was just in the research phase. But now, we have labs that can show us how to note if somebody is in the cell danger response. And we have therapeutics that give assist body by being probably the main one that I know of anyway, to help repair cell membranes, and how the outer leaflet the inner leaflet, how to get rid of very long chain fats that are produced by toxic load.

By using beauty rates and taxes and things. We’ll get to that a bit later. The important thing I know this is a mold talk I’m getting. But the mold exposure initiates a cell danger response. If you’d see the CDR one, and that is initiated by chronic activation of the innate immune system, and that can stay stuck in the cell danger response. Long after the initial signal has passed, people can just stay there and not shift. Now Robert Navarro has incredibly listed a number of different scenarios like the cell danger response, one cell danger response to cell danger response, three different conditions that are in different phases of the so called Cell danger response. So he’s reframed this, as I said, the pathogenesis of chronic illness in this way as a biological systems response that maintains disease, rather than focusing only on the triggers or triggers that initiated the original injury. We want to run a chain and cheat mode, but what’s happened to the metabolism of the organism? How can we identify and treat that and that’s where cell membrane medicine in the body byproducts have a fantastic role to play?

Yeah, so that’s just some more graphs of the cell danger response. And he’s also came up with this incredible insight that you know, we’re always rushing in, in functional medicine to look at oxidative stress and antioxidant defenses. And this is the teeter totter. But he’s positive the theory that you know, and oxidative reactive oxygen species are released by the mitochondria to protect the cells from further damage in a dysfunctional cellular response, and it continues to be activated despite the neutralization of the threat and these reactive oxygen species act, dysfunctional, damaging healthy cells, and he says he had contrary to long held beliefs about the etiology of these diseases. This D redefines reactive oxygen species activity in the context as a defense mechanism and oxidative shield. Therefore reducing reactive oxygen species would not necessarily address the root cause of disease, which actually lies within the destruction of the mitochondria and they have normal cell danger metabolism. Many practitioners were rushing to quench free radicals. I know I did still do for various reasons, with antioxidants, but this can actually cause further harm, as these free radicals may be providing a protective response very important to keep that in. Here’s the oxidative stress markers we often measure.

These are the antioxidants we often use. Common. The another pitfall that we encounter when we rushed into diagnose mold illness, is we we don’t consider a background understanding of other possible differential diagnosis. I use a lot of questioners, this is the MS Q questionnaire, which you’re all familiar with, I believe from AFM. I really have found it essential to know about methylation. And I like to look at methylation through the eyes of William Walsh’s work that he he’s is still teaching right now. On is the old Carl Pfeiffer work with over and under methylation, zinc copper issues and crypto Pio issues. He’s done a fabulous job of initiating the whole methylation complexity. And we need to sort of know that when we addressing mold illness, whether the person’s under over methylator, whether they have cooked up piles, and that they they have copper overload or cryptic barrels.

And then we have to sort of know this methylation panel backwards, because if you see here, here’s the stressors and total toxic load of environmental toxicity level one in my model and stage one more is there more than juicers, peroxy, nitrate peroxy, nitrate being the or it’s also called no or No, which is sort of the nature of free radicals that initiates the destruction of the mitochondria. And we can measure peroxy nitrite. There it is right there. If you do a methylation panel, from a company called Health diagnostics, it measures the peroxy nitrate there we can see how high it is and how much damage is caused into the mitochondria and whether the mitochondrial contents are being released from the cell along with ATP and when that’s released, that then triggers the micelles that they perpetuate this ongoing cell danger response that goes round and round in circles.

So we do have to know our methylation pathways. In red all the bad guys or pro oxidant issues and in blue are all the sort of good guys good to find catalase superoxide, dismutase. We don’t want to go rushing in with all antioxidants, when we don’t understand the cell danger machinery and we don’t understand all the triggers that are initiating the cell dangerous buttons. But we do want to use them where we need to Lyme disease which is which is a biotoxin illness in the same camp as mold illness. Very important to differentiate between biotoxin illness and chemical toxicity. Explain that in a minute. I use a lot of questionnaires I use Dr harvesters, MC lime questionnaire, and I’ve made up my own sort of conglomerate of many other question is that the basis of the kanlaon questionnaire, this is an alternative activist, patient advocacy group in Canada called kanlaon. And I’ve used the equation added some things to I found the use of question is very helpful. And then you’ve got to know your mast cell activation issues, because most of these patients with illness can’t tolerate a lot of things.

And if you don’t down regulate and put a lid on my cell activation before you begin your therapeutics, this patient will never get better, just like if you don’t help them self regulate and go from sympathetic to parasympathetic, which is the healing state. You can’t you know, if you don’t help them and assist them in that process, and if you don’t help them damp and myself, my cells are a consequence of the cell danger response. They don’t have cause just like people walk in and say, Oh, I have mold. They also walk in and say oh, because I’ve written many blogs on myself. They will say, Oh, I’ve got my cell activation syndrome, and I’ll go really okay. What are the triggers? Then then starts the whole diagnostic complexity where the triggers of my selector, so my cell activation is a consequence of an upregulated oxidative stress pathways and it’s our task to find out all the triggers we have which there are many, in my cells being they release 1000 mediators of inflammation, which damage the mitochondria, as do mold toxins. If you don’t understand my cell activation, know how to dampen it.

That’s another patient you can’t treat because they can’t take anything. If you give them 10 supplements as a one sometimes forget about it, they won’t be able to handle, they will, you know, they’ll have all kinds of reactions, and you’ll get lots of phone calls. This is the paper Lawrence app. And one of the main researchers put out on on the consensus of my cell activation, which is different from there’s different ways to diagnose myself. And this is a paper a whole bunch of us, co authored with him, but he was the main author. It’s a good paper, it’s on my website, if you want to read it. Know About pots, POTS is extremely important. Postural Orthostatic Tachycardia Syndrome, if you don’t, if you’ve missed pots, that patient will never feel better. Learn about it, learn how to treat it. And always have somebody in your office do blood pressures, that 10 minute blood pressure test.

You get them to lie down, you take the pulse rate and blood pressure, get them to stay in that one minute, three minute, five minute 10 minutes pulse systolic diastolic blood pressure, and then you work out the difference between the two. If they’re stuck if they post rate increases by 30 beats per minute. That’s parts by definition. And this is this simple little test. This is as good as doing a talk table. And many people will come in with the pulse rate differential 4050 beats per minute, that person’s not diffusing their brain. They’re not confusing their periphery. They’re not confusing the mitochondria. They are sick, and they know they sick but nobody’s done the 10 Minute blood pressure test. So when I learned about it about 10 years ago, I now I won’t see a patient before this is done by my staff before they come in the door. And if I’m doing a zoom consult, they have to go by a blood pressure cap and do this. The question is do you get dizzy when you stand up? 50% of my patients with mold illness or myself illness? Say yes. You have to learn to differentiate between parts orthostatic hypotension and idiopathic Tachycardia Syndrome. That that’s another whole subset of issues know about hypermobility and Ehlers Danlos.

These patients are very different are very difficult sometimes to treat because they so loosey goosey and they got so much muscle activation and their collagen fibers I’m tired and so they got leaky guts and leaky brain barriers and they really can be in quite a lot of distress. And no Dr. Andrew Maxwell cardiologist has put together that triads and paint ads, people who have my cell activation pots and Ehlers Danlos, plus dysautonomia, plus autoimmunity. These are groups of patients that you’ll get to, you’ll get to see them over and over again. And if you go on his website, he’s done some beautiful PowerPoint presentations on this complexity of how to put these things together. Never work with a patient without knowing their dental history. The the lower jaw the job, the trigeminal nerve goes back into the brainstem. So toxins in the lower jaw affect the brain in a dramatic way, just like the vagus nerve in the gut goes back up into the brain. And the sinuses affect the brain tremendous way you can colonize hollow spaces with mold and Candida.

I think 80 to 90% of all chronic sinusitis is yeast or mold related. So you got to know this area of the body. A good panorex X ray or 3d Cone Beam or getting somebody to interpret it for you, a biological dentist who knows what to do can help you tremendously. Root canals cavitations these are all issues that you’ll learn about as you get more deeper into complexity. Know about sleep. This is you know everybody knows the sleep issue. You you don’t you know you don’t restore If you don’t go into deep sleep, you don’t restore a lot of your circadian rhythms and your detoxification through your glymphatic ‘s, this doesn’t, things don’t go very well if you don’t get enough sleep every night.

So I know how to assess the patient and know how to take a sleep apnea history and I refer probably 95% of my patients now to sleep clinics for sleep studies, 90 to 90 and then also know every diet in the book you got to be very clued up on your diets because everybody’s got something else going on. From carnivore to low oxalate to. It’s everywhere and low mode, Candida. Justin who works with me as a nutritionist health coach, and also is very connected to the body by a team. We use a mixture of paleo, Paleo autoimmune, low histamine and membrane stabilizing. Those are that sort of scenarios where we get our most benefit. When we start treating patients, we often have to do low FODMAPs, low oxalates. And most patients now seem to do better on a ketogenic approach. But some people are really sick. We go, we haven’t do carnivore diets for a month or two.

Now we get two more. Sorry, they took a little bit, but the topic was more and complexity. So I address the complexity part first, now we get into more. So this is a pitfall not understanding chronic inflammatory response syndrome. If you look at the immune system, here, we’ve got two new parts, the adaptive and the innate immune system. The innate immune system is the primitive, not too intelligent by the immune system. And it’s the first thing to go into action when any threat approaches. But the innate immune system hands off to the more sophisticated adaptive immune system to T cells, by the use of antigen presenting cells, when the antigen presenting cells of the innate immune system detected danger, they envelop little epitopes little DNA fragments and present them to the adaptive immune system to the T cell, which then triggers the B cells to create antibodies and memory cells. Now, this is this is SIRs or chronic inflammatory response syndrome. It’s a chronic, chronic more than six months inflammatory response, where people get sick and remain sick and don’t know why. And what happens is people with this condition often have a poor transfer of the innate to the nt body part of the immune system.

They have an inability to hand off to the adaptive immune system to call in the troops to put out the fires of inflammation, so they stay stuck in a chronic innate inflammatory response. They don’t create a transfer, they don’t create an anti inflammatory response. And this has been shown by Richie Shoemaker and others to be dependent on the nine gene sequence on chromosome six was houses the so called HLA set of genes, of which he believes about 22% of the population have this gene set. Now this, this theory of the HLA origin of innate immune activation has been contested by a number of practitioners who’ve sort of broken away from shoemakers original research. But I I’ve sort of returned to it recently, because when people have this set of genes is HLA a set of genes. I do think there’s something to be said by the fact that it is those set of people with those gene issues that don’t get out of the innate immune activation, they just don’t have an ability to turn off the inflammatory response.

And I do think there’s something to it, although as I said, it has been highly contested by other people as not being reproducible in terms of research. Once you stay in a chronic inflammatory response being triggered by mold exposures or any biotoxin, whether it be Lyme disease, secretario, or any, any biologically active substance. If this immune threat increases, you can’t turn it off. You’re constantly making inflammatory genes and proteins that circulate, they go to the liver, the biliary tract go emulsified by bile. Many people have Kali cystectomy. They don’t make bile, and it’s dumped into the GI tract. Then it either go out through the store, that’s your where people use their binders. And that’s where they want to call the stymy to bind the toxins or remove them, or it’s reabsorbed through the entropy circulation. And this goes round and round around in circles, you just can’t turn it off, you keep recycling toxins.

So what turns on this in the heat system is a biotoxin, an organism or a fragment of an organism? tick borne illnesses do it, some pathogens do it or multiple pathogens to turn on the innate immune system. This is not a chemical, it’s not a plastic. It’s not a heavy metal. It’s not an organic type. It’s not glyphosate. This is a biotoxin that turns on. It’s an organism this is important to realize. So pitfall number four, you confuse SIRs with chemical heavy metal toxicity. A biotoxin is not a toxin, as we learned, many people think this is a toxic problem, and they go rushing into detoxify without really understanding the biochemistry underneath it. So this is a chronic, persistent, innate inflammatory response induced by biotoxin. And these biotoxins can be mold. buildings contain over 30 Different inflammatory foods, many of which are bio toxins like actinomyces, etc. It’s mycoplasmas. They are not just mold, there’s many other inflammatory diseases can cause all kinds of trouble, really secretaria for stereo, and these people, they can’t turn off this innate inflammation due to these HLA gene problems. So it’s a genetic is genetically influenced, epigenetics turn on but genetically stays on, you won’t get these patients better by detoxifying them.

You won’t get them better by doing chelation therapy. So last thing you want to be doing, even though they may have a heavy metal burden that has to be addressed at some stage, you’ve got to address this chronic persistent innate immune system activation first, but you’ve got to measure it first before you can address it. So another problem that people often make is confusing mold allergy with SIRs are many of the mold remediation specialists, they end a lot of the even even practitioners risk virologists make this problem that patients will go see them with, say, I have sirs and they said no you don’t you’re IGE antibody to mold is negative, complete. The two ends of the spectrum serves as a chronic innate immune activation. mold allergy is an IGE antibody induced response to an allergen like mold. This shows up on an IGE test, which I do all the time. Very different from innate immune activation. If you’re allergic to mold, your immune system is overly sensitive to specific spores and treats them as an allergen. Ige is often upregulated. But the markers of serves the innate immune system, they’re not touched, and there’s no downstream damage to hormones and other parts of the body that occur with innate immune activation. And so the pitfall here is not fully grasping the subtleties of the SIRs diagnosis and the treatment options. Often, you’ve got to you got to ask yourself when you start treating and do these patients fit the SIRs criteria, and I’ll show you how to determine that in a minute.

There’s a patient for further criteria for a tick borne illness notoriously difficult to diagnose. Lab diagnostics are not reliable by any means. That the person get bitten by tick, turn on the HLA genes and then get exposed to mold very common. Are they still being exposed to mold or is it historical exposure? Often the disease the chronic disease, the ill health of the person, it’s the chronic inflammation itself. It’s not the mold of a lamp. It’s the fact that these HLA genes are turned on in a system which is just running with recirculation of the biotoxin nobody’s addressed it. Nobody knows what’s going on. And so there’s a lot of complexity involved in making the diagnosis and then how to treat it, which is on the other side of the slide, which I’ll get to. So how do we make a diagnosis for mold toxicity, or biotoxin illness? First of all, symptomatically. It’s a multiple unexplained multi system non responsive symptoms across many organs or regions of the body. And this question is that we use to determine that there must be a past or present history of exposure to a water damage building. You’ve got to exclude other diagnoses like putts, although they often coexist. And your mold score count the DNA probe for mold spores must pass a certain threshold the either it mustn’t be more than two, or the five molds that are pathogenic Aspergillus Penicillium IDs Aspergillus vesicular, ketone, yum, Stacie, vitalism Alinea together and there’s a scorecard they must be greater than 10 to 15.

These questions here and these diagnostic assumptions, they help you make the diagnosis. And then in order to assist you go over to the proteomics to the labs that help assist you in establishing, you’ve got to have three out of six do you have this HLA set of genes, this is a relative risk of susceptibility. Some people get sick from mold and they don’t have the HLA genes. Dr. Shoemaker said the prognosis is much better. But those of us who sort of broke away the ICI people that Neil Nathan people, we have found people with the so called dreaded gene that Dr. Shoemaker has spoken about get quite well. And we found people without that gene stay sick. So it’s not as cut and dried and as linear as one things. And then the next thing we need to measure are the direct and indirect markers of innate immune dysregulation. And sitting at the center of that is melanocytes stimulating hormone. This is a brain hormone that gets damaged by the innate immune system upregulation of cytokines that then cross the blood brain barrier and damage melanocytes stimulating hormone in the anterior pituitary. And that’s a neuro regulatory neuropeptide that is very much suppressed when the brain is on fire, which is in mold illness, and it starts to drop, and when it starts to drop, all sorts of things go haywire. I’ll enunciate those in a minute.

Another test is C four a, it’s an alternative pathway of complement activation, it’s an expression of huge inflammation. MMP nine is a is a molecule that gets expressed whenever there’s breakage in in blood band barriers, it it causes endothelial disruption and allows like the lime bags and the mold toxins and mycotoxins to penetrate your tissues, anti diuretic hormone and osmolality, which get affected by mold. These are people who pee a lot. They drop their blood pressure because they don’t concentrate the urine because they don’t retain salt. That’s where you get your pots. And they appear they pee a lot. And often those are the people who, when they touched door handles, I get shots quite frequently because of all the sodium that gets excreted because they don’t have that antidiuretic hormone. And then often when Msh drops, you get dysregulation of the ACTH and cortisol pathways with lack of loss of feedback, which is very closely related to the hippocampus in the brain. Cortisol originally goes up saturates the hippocampus, the hippocampus degrades, shrinks, and then you get hyper adrenal states. Now people come and say, Oh, but I’ve been diagnosed with low adrenals. Low adrenals are a consequence of chronic inflammation. They not a diagnosis. So if anybody says I got low adrenals No, there’s more going on. It’s a down regulation of the HPA Axis due to chronic ill health. It’s not a diagnosis, just like my cell activation is not a diagnosis. It’s a consequence of incoming toxicity not being regulated through the cell danger response and getting you out of being stuck. So these are the tests. Now this is the fabulous.

You must know this diagram to understand biotoxin illness and those of you who’ve dealt with mold or SIRs know this pathway backwards, and it sort of summarizes everything, if you will. Here’s the bio toxins in HLA systems trouble person 22 to 25% of the population affecting and inducing inflammation cytokines, those cytokines then have an inflammatory effect on the hypothalamus. And they down regulate leptin, leptin receptors called Dark. These are people who get heavier and heavier and heavier because they can’t regulate appetite. Not it doesn’t happen all the time, but it does happen occasionally. But most importantly, it reduces melanocytes stimulating hormone. This is the main neuropeptide, that when that goes haywire, the consequences are traumatic sleep gets affected, pain gets affected, and melanocytes stimulating hormone controls. Guess what? intestinal permeability, here’s your famous leaky gut or intestinal permeable gut, which is at the root of many chronic diseases is often because the melanocytes stimulating hormone has been suppressed due to a biotoxin load, that then creates a permeability issue. That also when your Msh is suppressed, it allows for the growth of resistant staph in the nose, which releases the toxin which goes up and affects the brain. And then here, it affects the antidiuretic hormone it affects is the sex hormones, you get decreased libido, and you go into premature menopause.

And here’s the cortisol and ACTH. And hear you get all these hormonal consequences to biotoxin illness, as opposed to the other 75 80% of people they have, they don’t, they don’t have the HLA gene, and they just get rid of toxins and they you know, husband of a spouse will go what are you complaining about I’m fine. And not understanding the genetic, multi heterogeneity of the gene process. They they, they just, they have an antigen presenting cell that sends it to the B cell. And a B cell mounts an anti inflammatory response. And that’s the end of it, they don’t get sick. But in 25% of the genetically predisposed, this is the scenario that’s installed for them. And all these cytokines are released. And you get all these immune system dysregulation, downregulated T reg cells and shifting of the th one th two axes, you also get hypoxia because of VEGF, another hormone. And oxygen isn’t delivered for the mitochondria to make use of to make ATP. And these are the people who can’t take a deep breath and often do well on oxygen supplementation. These you can really affect your hypoxia of your cellular tissue. Here’s the I mentioned this already. Another pitfall is not understanding other conditions, parts myself, hypermobility, etc, we’ve gone over that. And another pitfall is not using this questionnaire, I encourage you to fill out this questionnaire and get your patients all of them to fill it in.

If they come on this questionnaire, they’ve got 27 symptoms in 13 clusters. And they don’t pass the visual contrast test that Asians got says until proven otherwise. Very helpful. I had a patient this morning, who had this folded patient presented with a head injury. And this was form and no history of mold exposure. So no history of modern exposures. So this questionnaire of four, which is anything less than eight is considered a pass. I didn’t go down the mold pathway. I didn’t ask him. I asked him as a mold on the windows and things but there wasn’t so mold wasn’t an issue with him. But this question helped this questionnaire helped me. Now, you cannot, you cannot tell what the exposure is based on the surface questionnaire, all you can say is that if you have more than eight, you look here, the symptom clusters. If you have more than eight of these clusters symptoms in eight of these clusters, the probability of having SIRs goes up quite substantially and if you have the HLA set of genes, this confounds the diagnostic probability. And if you don’t pass the visual contrast test, or the visual contrast test this is a test that Dr. Shoemaker and Dr. Hudnall in 1997 they, they show that if you’re exposed to by a toxic illness, the neurological functioning of the optic nerve, from the retina to the cortex, you aren’t able to discriminate between shades of colors. And the more the by toxic load, the less the discrimination. And you want to pass a seven C and 60, you want this whole bottom part of the chart to be the tick mark. If you’ve got this all filled in the probability of having SIRs with a positive questionnaire, symptom cluster greater than age 98.5%, shown in multiple studies, first one in 2005.

So just by doing that, taking a history of knowledge pleasure. And doing this, you right there, you being launched into the probability of mold exposures being part of a differential diagnosis. And people. I do this a lot. And when people are being treated, I follow this. And you’ll see these bars clearing beautifully, and the patient feels better than they know. A few people 10% will pass the visual contrast but still show signs of inflammation. And some people have very good visual acuity. Professional baseball players apparently can have sirs and pass the test because they’re so used to having visual acuity. And some other occupational exposures can cause you to fail the visual acuity but generally speaking, it’s a very good test. And that can be done online at surviving mo.com $15 I believe. And then another pitfall is not doing some of the additional lab tests. Now encourage you to study with shoemakers group, or read up on this, I’m not going to go into all the different tests that we do in order to substantiate and gray the severity of the illness. But there’s certain ones that are very important. The Urmi test, which is a measure mold spores in the house essential marchands is a measure of the infected bacteria in your nose that that releases neurotoxin.

And then see for a TGF beta, I run these tests on most of my patients, if not all of them. And then the one at the bottom where it will do quite a lot is the neuro quant MRI, the neuro quant MRI pixelate the brain so that you can put the different areas of the brain the temporal lobes the frontal lobes, the gray matter, the white matter, you can put it into algorithms based on age match controls. And you can see if the brain swollen or atrophied and you get specific findings in mold illness of deterioration in some of the basal ganglia nuclear and inflammation of white matter. So I do neuro cleanse, and probably 80 to 90% of my chronically ill complex patients just to see the state of the brain as it’s been exposed to mold or head injuries. People with a lot of early trauma have a enlarged Amygdala on an MRI two to three standard deviations above normal because they’re always in a fear and fight flight response. You’ll see that all the time. 

And that correlates with a beta brainwave being upregulated on the QE G, people with muscle activation syndrome will have very high thickened thalamus is because the thalamus is richly innovated with micelles, and those with head injuries will have asymmetry of between the two sides of the of the brain with the ventricles being different. It’s important to look at these things. If you if you need to know if that brains on fire or not, which you do need to know. One big pitfall is not looking through the lens of standard medicine and through functional medicine. And these are the list of you’re probably quite familiar with this list. I run many or most of these tests all the time on everybody. There’s a stupid thing which you’ve been exposed to that you can’t manage what you can’t measure. And it’s true. We try and do it because everybody, you know, nobody can afford the test. And that’s a given. It’s just a given that you’ve got to try and establish a practice whereby you are comfortable with the amount of labs you’re running, to give you insight to help the level of patients that you see. If you seen somebody just for hormones or leaky gut, then that’s fine. But if you see complex, sick people, we’ve been sick for 1020 years and we’ve got binders this thick and Mayo Clinic console.

You cannot run your practice by doing a few tests just I don’t encourage you to do that. So you have to find the ways and means to spread your diagnostics quite far and wide. Now some people have, who do you know, trickling hearts muscle testing protocols find that they can cut their costs by doing muscle testing, which is, if you skilled at it, I believe it has significant validity and I studied it for 10 years with Dieter, I prefer to work left brain with labs. But the drawback is the cost. People have been sick enough will often shift their value systems to find the means to pay for what they need in order to get better. And you really do need a broad diagnostic brush to bring a lot of this complexity together. You cannot do a stool test and treat these people do you know VCs and the urine mycotoxin test and hope to to help somebody it’s just impossible in my experience anyway. And so here’s some of the labs and all the links that I found helpful but again, that’s subject for another election.

And here’s the biggest bugbear I have is using the urine mycotoxin test is proof of diagnosis answers. I know neon Nathan and the real time people believe that this is enough. But I I think I think that’s too simplistic. Why? Because many healthy controls have lots of mycotoxin in the urine. So just because you’ve got mycotoxins in your urine doesn’t mean you’ve got mold illness. foods contain mycotoxins. You don’t know if you had mycotoxins in your urine, whether they were three years ago, one year ago last night what you had oatmeal for breakfast. And you don’t know if you’re good or poor excreta. I much prefer the next test which is coming up soon as the AGL test which actually measures cellular toxicity, whereby mold mycotoxins get attached to DNA and mitochondrial membranes, and they affect the translation of genes. And you may be a terribly terrible excreta of mycotoxins have a negative test. But if you do the ideal cell test, you’ll see that these micro toxins are sitting right on the DNA affecting translation of proteins and fats.

That’s a much sicker patient, often with neurodegenerative type diseases than somebody who’s got some mycotoxins in the urine. So please don’t make the mistake of just doing this test and diagnosing mold illness. And now that this, these tests have become popular, I see it, it’s everywhere. And I get this test all the time. And I get told I’ve got mold illness based on this one test. It’s not you can’t diagnose mold on this on this test. I hope I’m not sounding you know, the negative on this test, but I think it has to be. I think it has to be the truth has to be told on this one. If you join the ICI group, they debate this test back and forth in the States. It’s a fabulous dialogue to be part of, because Richie shoemakers work originally when he put this all together, he was most indignant that people were using this test and he made us made as those of us who pass these exams, write essays or why this test was so useful.

But then people left his group because some of the things that he said couldn’t be correlated with other evidence. And then those who left his group started to use this test and just use this test for diagnosis. And so the field is in its infancy, just bear with it. I’m sure over time, things will shake out in the wash you know. Many foods contain mycotoxins so one of the things we do you know, people outs and corn and peanuts, I mean, it’s full of market toxins. So these are everyday foods that people eat. So people do get put onto a low mold diet and sup to some benefit. But it’s, it’s really, you know, if you got my cell activation, you got to be on low histamine diet. I find that people got mold illness going on low mold diet isn’t isn’t the therapeutic input that makes the big difference.

Now, here we are back to the cell danger response and membrane medicine. See when these toxins come in which mold is one of the causes oxidative damage, they they destroy the cell membrane, and the sum of these toxins attached to the DNA. And this causes poor translation of messenger RNA into the ribosomes. And then often the cell due to this ongoing toxic insult, undergoes autophagy due to the DNA and the ATP go outside the cell becoming pro inflammatory, inducing my cell activation with 1000 mediators of inflammation and further destroying the cell. And this is this perpetuation of the cell danger response. And so, here we have a lot of research showing how mycotoxins which are the byproducts of mold spores affect the mitochondria, causing the cell danger response has been published. Here’s some of the publications and these mycotoxins disrupt the the Krebs cycle and the electron transport chain and many, many different sites. This is all being published. So we know mold damages, ATP production and citric acid and mitochondria. There’s many papers published presenting that by the way, there’s a very good presentation on the GPL Great Plains laboratory website by Kurt Warner, on mycotoxins and mitochondria.

It’s worth watching I got the slide from him. Sorry to say I didn’t obtain permission. But I do know him and I will seek permission when time permits but I’m acknowledging that I got the slide from him. And he got the slide from a publication. So mitochondria are these micro toxins they affect the mitochondria in many different pathways in this Krebs cycle, they you know, we have our macronutrients that have to be eaten, shut fats, for instance, shuttled through by carnitine into the mitochondria across the cell membrane, and all these mighty micronutrients that activate these enzymes that then activate NID, NADH, that then go through the electron transport chain on the inner membrane of the mitochondria that make your ATP here, and these mycotoxins disrupt these pathways in multiple sites, they are crud toxin A affects ATP production inhibits ATP production. Many studies done on this now. So here’s this test, which is sort of revolutionized the way I practice medicine the last five years is a German based test and you can actually measure it can measure mold, fungal species and mold, fungal metabolites, by measures measuring lymphocyte sensitivity to these mold toxins. And you can see here that all at the level of the genome and the mitochondrial membrane, you can get mold. You can get your lymphocytes being high, react highly reactive to mold species and to the mycotoxins. And this is this test is what I rely on now. Apart from doing my traditional shoemakers sort of workup, I look here to see if this person is has mold still in their system. I only saw two patients this morning. Because of preparing for the lecture and get everything set up. One of the patients was from Switzerland, chronic fatigue syndrome, 10 years, supposed to mold in Lyme disease. And she was here in Calgary in December doing very well in Calgary home. Normal. We’ve done me tests looking for mold spores. She went back to Switzerland.

And I got this test, which she had done a week after leaving Switzerland and she had dramatic levels of mycotoxins that had gone from her previous one we did two years ago. The levels jump from 1500 to 500 600. And I just looked at this and I said so and so you’ve you’ve been exposed to mold, you are highly mold, toxic. And she said I knew it. This house I’m living in in Switzerland, there’s mold everywhere. I’ve tried to clean it up and it keeps reappearing. It’s in my shower. It’s on my window. I said, and she was told she was in bed 90% of the time. That’s and she moved back to Switzerland two years, two months ago. She’s her levels of mold are gone up five times. So this test showed me at the level of a mitochondrial DNA. She had mold lymphocyte sensitivity, and she clinically confirmed it. She said, I know I’ve tried to clean it. I said you try to clean it, don’t go near it. So get out of that house right away. I can’t say very well. And then we had a big discussion about what to do because many of these people are chronically ill for prolonged periods. The innate immune systems go round and round around in circles and they stand exposed and they often it’s the home that’s causing them to be sick, or it’s the quality They took from the home or is the couch they took from the home or something that they took from a home.

And they just go around in circles and never get better until the cycle is broken. This test also allows us to measure ATP production to see how blocked it is. And here’s the beauty of the test. It also measures mitochondrial numbers so you can see if mitochondria undergoing destruction and is less numbers than they should be. It also can tell us whether it’s the mitochondria, mitochondria are expressing abnormal proteins and lipids, very long chain fats. And it can tell us about some of the mineral deficiencies that are contributing towards the cell membrane voltage being affected. Here’s the ATP blocking active sites 21% You don’t want that block more than 14%. And here you can see that the DNA which gets released when the mitochondria undergoing destruction is at a level of 17. It shouldn’t be more than nine. So they their DNA is outside the cell triggering micelle and further oxidative damage. And here you can see after a toxin you can see one of the mycotoxins from Aspergillus is sitting on cardio lipid and actually the the enzyme that makes the inner membrane of of your, of your cell in your mitochondria. 

There’s a toxin sitting on on that enzyme affecting cardio lipid. And there’s your phospho title fo Alameen, which is found in the body by PC, low, the inner membrane along which the electron transport chain occurs. And there’s your plasma title choline, which is the external membrane. And this Melange, the height you can see that the fats, the lipids in the body are oxidized, deficient, and the cellular machinery that making the lipids is impaired. That enzyme also requires manganese to work that the manganese deficient. That’s why you use the body by minerals and electrolytes. So mineral sessions. And here on the DNA you’ve got sitting on the DNA, formaldehyde, and there’s aflatoxin, there is a micro toxin from mold affecting translation of messenger RNA sitting on the DNA. This is huge, you know, this is serious business. This is not lightweight testing.

This is serious. And when people it’s going to affect the metabolic machinery of the cell, and it’s going to put people into chronic ill health that gets a stain unless it’s dealt with. This person also had zinc deficiency was incorporations. Zinc is the largest role to play. Regulating DNA destruction, and immune function. And then you can also see here, I can’t see the slides so small that’s the same same one sorry. Keep repeating this. Here, you can also look at your antioxidant states glutathione. You can see that it’s low in the bloodstream, here superoxide dismutase, the good guy that is sis glutathione and putting up peroxy nitrate. Here you can see conatins low so shuttling your fat into the cell to active cellular energy is low. Here’s the mast cell membrane, the cell membrane of 159, the voltage of your cell is low. This is dramatic because the electron transport chain depends on the cell voltage being normal, and that’s low. This gets affected by mineral deficiency, intracellular calcium, intracellular calcium triggering the NMDA receptors and causing the excited toxicity and magnesium there, which is found in your minerals. Magnesium is a calcium channel blocker.

This person was highly exposed to electromagnetic fields, which induce high levels of intracellular calcium and mast cell activation, the cell membrane was depleted that phospholipids were depleted this this cell is in a lot of trouble. He has a heavy metal test, you can see the telephoning, which binds to heavy metals is high because it’s working overtime, binding to barium. And when the telethon is running around mopping of metals, it drops off zinc and you become zinc depleted. And here NID vitamin d3 which is central for the electron transport chain is depleted. That’s why everybody is now on to nitrogen and other NADH or energy supplements. And then another beauty of this testing is we can look at the cell membranes and we can see the deficiencies and excesses, we can tell what the saturated fats are doing this is not now the AGL test. This is the the test we do the Kennedy Krieger looking at lipid membranes, we call it the body by a red soul lipid membrane test. We can look at saturated fats and Omega sixes, look at total lipid content.

Now look at this total lipid content. The total lipid content of this person is completely negative. And I can’t tell you how many people come in. And they get put on colas, tyramine and crash. Because Patricia Kane, who initiated this therapy many years ago, made the statement I don’t know where she got it from. But she said that if your lipid content is less than minus 25, and you use curl to stymie, you’re going to crash that person’s lipid membranes and create tremendous damage to the mitochondria. And I believe that statement is true, because I’ve seen it. I’ve seen I’m treating a patient right now with an ALS condition and that that’s his total lipid profile. And he did have mold and he was put on polystyrene, and he’s much worse right now. So we had to repeat this lipid content. It is omega sixes up to scratch, saturated fats structural bets, we can also test by the myelinating, making making white matter. And we can also see how many abnormal oxidized bad renegade fats are being made. Here’s where your butyrate and your tadka come into play, because those help get rid of these very long chain fats. And as you get healthier and healthier, these go down and down. So this, this IGR test in the body via red cell membrane tests are extremely helpful. And this is where the whole membrane medicine comes into place. And we start to repeat cell membranes, sweep toxins off the DNA and repair as much as we can.

With various therapies, of which body via products take a central role, I can’t say enough about how I’ve benefited and how the patients have benefited by repeating outer inner membranes using peterites and tadka. Replacing minerals, just you know, I’ve developed a shake, which I’m sure tastes awful, but very competent is very beneficial. And to sell membranes, Justin has the job of making it taste pleasant by using the only thing that we use is coconut milk and, and blueberries because everything else most of our patients have my cell activation behind us much else that we put into the shake, you know, PC and body bio balance and electrolytes and minerals and glutathione and superoxide, dismutase and resveratrol. So we make a shake of it. And we use blueberries and chopped vegetables for poly phenols. And most people find this very nourishing if if they can get past the medicinal quality of it. So here’s another pitfall we’re nearing the end, so we’ll be done pretty soon. pitfall is using color styling, inappropriately, not only the synthetic color styling, which is full of aspartame. But if your lipid membranes are very low, using polystyrene will rarely crash a patient very quickly, so it’s not appropriate to use color stymie right out of the gate.

Just very quickly. Other pitfalls using the wrong test as sampling is absolute. No, no. The settle plates are worthless. tapeless, okay. But the real test is the Urmi test, which I’ll show you in a second. Another big mistake people make is I have a new home it doesn’t have mold. I live in Arizona, it’s not wet and damn. new constructions are often the worst. I had a new condo, which was put up in the boom they didn’t put events in a flat roof and I had mold in three floors, condensing down the sides. No visible mold does not mean the building is safe. No musty smell does not mean it does not have mold, or crawl spaces and basements usually have mold. ductwork is often contaminated. And this is the Urmi test where you measure dust spores by either swip upright or vacuum cleaner and you quantify that according to specific algorithms. People call in mold inspectors and they don’t do a thorough visual inspection. You’ve got to go from the attic to the basement and outside and have a look. And he has some of the questions you want to ask. If somebody comes in waves a sample meter and walks out and says you don’t have mold, run for the hills.

Look at baseboards, pull out dishwashers go up into the attic. Do you have a front end loader washing machine? Is there condensation? Did they use a water moisture meter, you know the day to do thermal imaging looking for wetness behind dry walls. Here’s some fabulous references for people who do good work, shall see acres with a whole bunch of web videos on YouTube about how she’s an architect you have mold on us. She’s very thorough, and patients report doing her series is very helpful. So, in summary, mold illness is ubiquitous. It’s everywhere. It involves genomics. transcriptomics. Proteomics involves abnormal regulation of micelles hormones, mitochondria, autonomic nervous system. These conditions are everywhere. Look around, you’ll find them. They’re ubiquitous. There’s just a summary of some of the pitfalls. Here’s some papers and links to articles I’ve written on mold. Things you can find. And that’s my details. And that’s it for me. Am I doing 68 minutes? I’m sorry.

Thank you so much. Dr. Ruffin, can you just click on can you make me the host again, so that I can go over some of these questions. I’m trying to turn on my video, but it doesn’t look like I’m able to unless you give me permission. What do I do you go to the top of your video, there’s three little circles. If you just click on that those three little circles it should show up to make me the host. If not, it’s okay. I’m I can say off camera as well.

Doesn’t say it says pause recording stop recording raise hand.

Okay, okay. We’ll just leave it as is I’ll go over there’s quite a few questions. So do you have a few more minutes to answer your question? Okay. So the first question is from Christy. And she just was asking what the German test costs? You can answer that one or I can choose?

No, it depends on how many panels you choose. So they range in price. If you just go to the Igel website, and you ask them for to send the cost the the extensive panel that I do, it’s 1000 or two euros. But you could do subsets of it to get what you want to look at. And then you go

in there they are. That lab is expensive. I mean, I think I just ran it in last year. And I think it was close to $2,000. Canadian for whatever panel I did. So it’s not an inexpensive lab, that’s for sure.

But remember that is many in when that’s not one panel that’s like 10 panels. So you can if you want to just know your first blood lipids, you can just do that little panel. But if you want to do a complex mitochondrial workup, then it’s going to cost a lot more.

So the question is what is the next question is what is the difference between ErmI and Emma testing?

The Emma testing measures mycotoxins and spores, whereas the Ermias just pause. I don’t do any testing because I just historically have stayed with micro metrics. I do use other lab for actinomyces. I haven’t run many Emma tests. I don’t think the tests been validated. And so I just stick with what’s been validated by the think by the FDA. Let me test

Okay, thank you. And then Shelley. Shelley Wilson, who we love. Thanks Dr. Hoffman to Justine excellent presentation. We adore you, Shelly. Um, okay. And then Chris, you had another question is Well, what is the extensive

sorry, surely didn’t ask me a bone crushing question.

So, if you have a question I’m Christy I will find out if you can. So she just asked what is the extensive one called the IG L so if you email me I will find out from the girls at the front desk and and I’ll let you know I don’t think I don’t know that. I’m right now and I don’t think Dr. would know that offense either. Okay, um, now in the chat there was lots of questions I’m going to have to go back. Um, do you have an MRI and the neuro quant software at the clinic?

No, you’ve got to get me the neuro quant is quite complicated because you’ve got to, you’ve got to get the MRI company to do specific settings on the MRI to read the neuro quant the neuro con software, but that requires certain settings on the MRI. So you’ve got to buy the software from neuro quant, you’ve got to get your MRI company to be willing to use the settings on the different Siemens devices. And once they change the settings you can read neuro quant but it’s two parts to it. So it took us two years to get neuro quant in Calgary. I tried to get it through healthcare, but they wouldn’t do it. So a private company doesn’t. Because they wouldn’t do it because it requires changing settings and they don’t want to do that.

Okay, Allison just asked where she can find the recipe to the shakes, or recipe for the shake. So Allison, you can send me an email as well. I’m happy to send you Dr. Hoffman’s template, if you can just make sure that you give him credit

for our upcoming book. No, we’ll give it

Yeah, that’s true. We’re doing a cookbook that should be out in a few months. And the recipe will be there’ll be plenty of recipes in there. When working on cell membrane, what daily oral PC dose Do you work patients up to?

It’s a It’s depends on so many things. If you’ve got a very high micelle population, they can’t tolerate much of anything. If you’ve got a robust population, they are often much more able to tolerate higher doses, but they often need assistance with lipase and bile Oxbo. That’s a tadka. And we use a product called Beta plus. And it had Kali cystectomy is that’s another whole puppy sub population of people who can’t tolerate high fats. But it say all those confounding variables are taken out, we always start them slow, like half a teaspoon. And then we work up to you know, I don’t really go more than two tablespoons a day of both of them. The body by a balance we use a lot on food, not in the shake, because it’s pleasant, you know after you’ve cooked it and cook it up. But put it on stir fries and salads. And the PC goes into the shake because some people just eat it off the spoon, but it goes on the shake quite nicely. But I don’t usually use more than two tablespoons. But keep in mind, I tracked labs, I tracked the red cell membrane tests and attract the AGL test. And also there’s another variable there. I’ll think of it in a second. I forget what it was, but there’s another variable to it.

Okay, in addition to body bio products, would you recommend adding an all encompassing Mito booster supplement like mitochondria and RG from designs for health? You can

well, so a lot of the supplements that boost mitochondrial function oh, here’s what I wanted to say before I get back to the question. Our OPC helps strip the cell membrane, or helps repair the cell membrane because it’s got the three phospholipids versatile ever elevate hospitality knows at all. Whereas IVP PC which I use a lot of help strip the DNA of the acts of the toxins. And that’s a general rule. So I do IV password title choline with phosphine or butyrate and glutathione. And I do aro PC and body by a balance for different purposes. There is some crossover, but there is a different therapeutic reason for each of them. Just I just wanted to emphasize that point. And then sorry, what was the question

is so there’s so many questions there. Oh, the other one was on mitochondrial support?

Yes. So much. So using the micronutrients that support the mitochondria, I find is false thinking. You can do it. But you want to sit back and look at that cell and see what state it’s in. Look at the state of the individual look at the state of the food gut brain axis. And you can’t just start stimulating enzyme pathways without first repairing cell membranes and look Looking at the toxicology of cell membranes and the viability of the electron, the voltage of the cell membrane, whether there’s deficient numbers on line. So I don’t go use a lot of mitochondrial traditional support, until I’ve helped repair the cell membrane. improvement in the AGL. And lipid testing, I tend to, I do use carnitine and 210. And nada, I do use them. But if you go use those without preparing the cellular toxicology and the soul structure, it’s a it’s a, it’s a losing battle. You won’t get anywhere.

Yeah, and that’s something that I’ve seen too, which was what really what drew me to membrane medicine because without, I mean, you’re really just throwing things that people do first don’t repair the self.

Find remove as many incoming stresses, and then balance the cell by much and modulating the homeostatic mechanisms, the allostatic load, you know, you’ve got to sort of work this whole system.

But there are specific nutrients like B one, b two and B three will support that front end of the mitochondria and carnitine. And then the electron transport chain is supported by Coenzyme Q 10. NAC. Creatine is helpful.


Okay, let’s see here. I think I’ve covered all of them. Is anybody? Did I miss a question? Oh, if someone has recovered from mold toxicity, is it helpful to use the LPC long term? I will say? I will say yes. But now let you answer.

You know, I’ve measured igvault, postmitotic, choline and fllo mean, I’ve never seen levels outside of the range. So people stay on it. We’ve constantly under salt. So as a lipid bilayer is are very much susceptible to oxidative damage. So I think a daily intake of phospholipids is crucial to maintain cellular health.

And then I think it was a question about cosmologists in here too. We do use cosmologists have you? So yeah, we have definitely heard of plasma halogens? Um, regard? Have you heard of plasma ologists with regard to membrane lipids? If so, can you comment on any overlap between plasma telogen deficiency and sirs?

So I’m assuming of Doctor good enough. I’m learning his plasminogen I take them. But as you know, a doctor good enough. He’s a biochemist with a lot of knowledge and where players margins fit in. That’s another whole level of complexity. I’m just starting to get my head around. Justine actually knows a lot more about origins than I do, because she has studied with him recently. But it is definitely appears very exciting. And I think plasma legends will be playing a huge role. In the future, just like peptides came up and exosomes. These things have the, you know, the waves of fashion, but I think plasma origins are going to be a big deal.

Well, and I’ll just quickly comment to that too. So with plasma halogens are a subtype of phospho lipids, so about 20 to 30% of the brain is made up of plasma halogens, so it’s third so they’re made by the ProxySG. They’re endogenous, and you can’t consume anything that’s going to help to support plasma telogen levels. And with SIRs with that chronic inflammatory condition you burn through a lot of those plasma halogens because they’re a very potent antioxidant. So you’re, you’re gonna want to support with plasma halogens likely if you have sirs, the other issue too is with that chronic inflammation you are going to have compromised paroxysmal functioning. So your proxy isms are not going to be making adequate amounts of plasma halogens and then what they are making is getting used up as antioxidants.

Good enough as a test now to measure all of those which we’ve just started to use.

Okay, um What would you recommend to move a patient into dorsal Oh, when we have it an H bot? I don’t know if you talks about H button the lecture by H bot recommended after stabled with mast cell. Do you recommend hyperbaric oxygen?

I think hyperbaric oxygen has a very definite role to play. But I never use it in the front of any protocol. I often use it as a cleanup down the line. Particular In traumatic brain injured patients, so I never use it in the front end, I usually wait one or one one and a half years before I start recommending age parts.

And I think we have all the questions. Let me just go through one more time. If anybody has something like pressing that I did not ask, you can raise your hand. Oh, sorry. Okay, the dorsal are your questions about please see the q&a. Okay. Oh, my gosh, there’s lots.

You don’t want person in the dorsal vagal shutdown response. That’s when they are compromised. The withdrawn they depress the stack. So everything we spoke about today is attempting to shift the dorsal vagal structure into more window of tolerance, self regulation between sympathetic, parasympathetic. And there’s a complexity to it. I did, there was a slide that says what to do. If you go back to that slide, I listed about 20 different therapies vagal tone exercises Somatic Experiencing safe and sound protocols. resi Max, there’s a whole list of them. But if a patient has undergone trauma, and they’re in PTSD type response that requires sophisticated therapeutic encounters, referred to professionals who work with trauma, because that’s very hard to shift if there’s an underlying traumatic etiology to the dorsal vagal shutdown.

Okay, and then we have a few questions about Oh, where did it go? Snowy? You had two questions. One was, okay, how to get patients to tolerate oral PC when they have resistant? dysbiosis?

Chris? You, resistant dysbiosis? I, I just keep working with the dysbiosis until something ships? This that’s a very big discussion. But yes, you’re right. People can’t handle anything coming into the GI tract when it’s severely dysregulated. So you have to go through the whole gut fiber or whatever methodologies you use treats CBOs and levers and CFOs. And there’s a complexity to it. So those people who are in sympathetic dominance with poor vagal tone will have massive dysbiosis. I work around the issue and try and find out what’s what is the problem? Do they have lower last days with low lipase? Are they not making bile? I get gallbladder motility studies. So there’s a lot of complexity to it. It’s difficult to answer that.

And then this question, I laughed when I read this, I shouldn’t I shouldn’t have laughed, but I did. Because I’m excited to hear your answer. The initial part of your discussion, what is the best way to build the patience and love for patients with limbic disorders, especially when you’re seeing many of them and they drain you and your staff tremendously?

This is the million dollar question. How do you stay regulated when your whole world around you is dysregulated? Well, here’s my answer to that. I’m in my I’m in my 60s, I mean 65. So the longer you live, the more resilient you become. So that’s that’s to my advantage. You also learn to know your defenses and as soon as your palms start sweating, you know you’re in trouble and your defenses are up and you’re in a complex. You delegate you delegate low priority items to other people and hopefully you find good people to help you manage the complexity of managing complex patients. And then I find having policies and procedures and systems that hopefully get followed with lots of sort of patient education helps somewhat dampen the chaos get again shoo, which you can never fight, you know, get rid of because any patient any clinic with treating complex patients has a one or two borderlines there At least five or six severely traumatized people with PTSD, myself everywhere you look. And so you will get complexity. And if you love what you do if you just get up every morning enjoying and loving what you do that itself is a buffer against some of the, the stresses that hit you on a daily basis. So there were other things you can do as you can read about in the self help books, but that’s been my experience. It’s just my age has helped me become more resilient, great stuff. Most of the times when you lose a good staff member, chaos ensues and then just loving what you do. If you love in what you do is a high priority. You You can withstand some of the slings and arrows that come your way.

Okay, who do you have run the neuro quant for you? I’m looking to access the test software here in Calgary in Canada.

The only neuro quant in Canada is in Calgary, you have to fly here or you have to go to the neuro quant company and ask them to find the nearest neuro quant in your vicinity. Have you in the US? There is one in Seattle as well I believe so my patients go to Seattle or come to Calgary? I don’t know if there’s anyone close. They may have they may have one in Toronto or Vancouver by now but I much I don’t know that.

Okay, I think we have finished all the questions. Um, let me just double check one more time. There was a comment about oral PVC is worse because it can cause translocation of LPs into the blood and then raise inflammation significantly. I was curious to hear your comment on that because I have never seen that.

I think theoretically that’s true. And I’ve been I haven’t seen I haven’t seen LPs. Well the only test I have for LPS is the Dunwoody one. And I haven’t seen any of the LPS IgG IgM. IGA is getting worse in ever since I’ve run the test, which is the last 10 years. So I can’t vouch for that it probably from an academic perspective, we know how high fat low carb diets increase oxidative damage for LPS, but I haven’t seen it clinically.

Okay, thank you. Thank you all for joining us, right or I’m staying with us right to the end. And thank you again so much for the really really informative, lovely presentation. We’re really grateful that you were able to do this for us today.

Thank you very much. Bye now.

A Holistic Approach to Complex and Chronic Illness

Holistic Approach to Chronic Illness

In this podcast with Dr. Trevor Campbell, we discuss how an added comprehensive, holistic approach using social, psycho-spiritual, family dynamics and generational issues can be used to treat complex and chronic disease. Early childhood trauma of any kind as well as neglect can enormously impact the pathogenesis of disease as well as the course of recovery. This approach is foundational to my 7 Stages to Health and Transformation Model (TM), a fundamental approach to  integrative medicine. Please scroll down to listen to the podcast.

Learn More Here

Could SARS-CoV-2 Spike Protein Be Responsible for Long-COVID Syndrome?

long covid


SARS-CoV-2 infects cells via its spike protein binding to its surface receptor on target cells and results in acute symptoms involving especially the lungs known as COVID-19. However, increasing evidence indicates that many patients develop a chronic condition char-acterized by fatigue and neuropsychiatric symptoms, termed long-COVID. Most of the vaccines produced so far for COVID-19 direct mammalian cells via either mRNA or an adenovirus vector to express the spike protein, or administer recombinant spike protein, which is recognized by the immune system leading to the production of neutralizing antibodies. Recent publications provide new findings that may help decipher the pathogenesis of long-COVID. One paper reported perivascular inflammation in brains of deceased patients with COVID-19, while others showed that the spike protein could damage the endothelium in an animal model, that it could disrupt an in vitro model of the blood-brain barrier (BBB), and that it can cross the BBB resulting in perivascular inflammation. Moreover, the spike protein appears to share antigenic epitopes with human molecular chaperons resulting in autoimmunity and can activate toll-like receptors (TLRs), leading to release of inflammatory cytokines. Moreover, some antibodies produced against the spike protein may not be neutralizing, but may change its conformation rendering it more likely to bind to its receptor. As a result, one wonders whether the spike protein entering the brain or being expressed by brain cells could activate microglia, alone or together with inflammatory cytokines, since protective antibodies could not cross the BBB, leading to neuro-inflammation and contributing to long-COVID. Hence, there is urgent need to better understand the neurotoxic effects of the spike protein and to consider possible interventions to mitigate spike protein-related detrimental effects to the brain, possibly via use of small natural molecules, especially the flavonoids luteolin and quercetin.


The SARS-CoV-2 infects cells by first binding to its surface receptor, angiotensin converting enzyme 2 (ACE2), via its corona spike protein [1]. The S protein is trimeric and cata-lyzed fusion between the viral and host cell membrane; his “prefusion” trimer has three receptor-binding domains (RBD), while the post fusion structure expresses N-linked glycans that may serve to protect against immune responses [2]. Infection then leads to a complex immune response that involves the release of a “storm” [3, 4] of pro-inflam-matory cytokines [3–11], especially IL-6 [12–15] and IL-1β [16, 17] leading to the development of COVID-19 [3, 18]. Most infected patients develop antibodies against the spike protein, but immune protection against SARS-CoV-2 may involve more than neutralizing antibodies [19]. A prospective study of more than 3,000 healthy mem-bers of the US Marines Corps concluded that those sero-positive could still be infected but had only 20% the risk of subsequent re-infection as compared to those who were seronegative [20]. It is not known if individuals who get re-infected do not mount sufficient neutralizing antibodies or lack some other aspect of antiviral immunity. New data from immunized individuals indicate that the rate of re-infection varies depending on the type of vaccine used [21]. There is emerging evidence of reduced neutralization of some SARS-CoV-2 variants [22].


Some of the damaging effects of SARS-CoV-2, especially in the brain, may be due to direct action of the Spike protein, acting alone or in conjunction with other mediators such as inflammatory cytokines, on target cells.

Long‑COVID Syndrome

It is now recognized that many patients infected with SARS-CoV-2 develop a post-acute syndrome a few months after the initial infection known as “post-acute COVID” [23] or “long-COVID” [23–26]. Long-COVID occurs in 30–50% of COVID patients [23, 27–30] and is charac-terized by multisystem symptoms, primarily persistent fatigue and cognitive impairment [31] that varied consid-erably among patients [32] and were more common with increasing age and female sex [29]. These persistent symp-toms should not be confused or misinterpreted as persis-tent infection that has been reported in immunocompro-mised hosts [33]. Nevertheless, patients with long-COVID have not recovered even by 7 months post infection and continue to suffer mostly from systemic and neurological symptoms [34].

Long-COVID is particularly associated with neurologi-cal [35–43], neurodegenerative [38, 44, 45], psychiatric [46–52], and cognitive [47–57] problems, especially brain fog [23, 25, 26, 46, 58–62]. In fact, over 90% of patients who were initially hospitalized for COVID-19 and had neuro-logical symptoms had significantly worse outcome 6 months later [63]. Even though some of the mental fatigue experi-enced by long-haulers may be due to the perceived stress [64], the extent of this disability is unlike any other medical condition known.

In spite of early impressions that long-COVID may develop only in those patients who were hospitalized and intubated, increasing evidence indicates that long-COVID can develop regardless of the severity of the original symptoms [61, 65] and has been considered the “next health disaster” in the USA [66]. So far the duration of long-COVID symptoms is not known, but recent data indicate that it may depend on antigen per-sistence [67] and a sustained specific immune responses to SARS-CoV-2 [68].
The neurologic effects of COVID-19 may be due to SARS-CoV-2 entering the brain, but the pathways of such

neurotropism are still unclear [69, 70]. One possibility is that the virus crosses or damages the blood-brain bar-rier (BBB) [71], accompanied by basement membrane disruption, in K18-hACE2 transgenic mice infected with SARS-CoV-2 [72]. Similar findings were reported independently, and it was also shown that the virus was detected in human cortical neurons [73]. In another study, a fragment specific to SARS-CoV-2 was amplified from cultures of a brain specimen from a deceased patient with COVID-19, and associated pathology showed neuronal necrosis and glial cell hyperplasia [74]. Alternatively, the virus could enter from the nose by crossing the neural-mucosal interface of the olfactory nerve [75] and enter the brain via the olfactory nerve tract [76]. Viral entry into the brain via gustatory-olfactory trigeminal path-way eventually compromising the BBB was recently reported in deer mice infected with SARS-CoV-2 [77]. It is interesting that single-cell RNA sequencing showed that ACE2 was not expressed by olfactory sensory or bulb neurons but instead was expressed by olfactory epi-thelium and pericytes [78].

The effect of SARS-CoV-2 to the brain is also not well understood. One paper showed the presence of megakaryocytes in cortical capillaries that could lead to brain ischemia [79] and subsequent cerebrovascu-lar events [80–82]. In the autopsy report of an infant who died with COVID-19, there was evidence of corti-cal atrophy and severe neuronal loss, and findings were restricted to capillaries of the choroid plexus [83]. A recent paper did not document any molecular traces of SARS-CoV-2 in the brains of deceased patients with COVID-19, but detected choroid plexus perturbations associated with pathologic morphological changes in the microglia [84]. In addition to the evidence discussed above of neuronal damage due to SARS-CoV-2, a paper reported that the virus can enter a 3D human brain orga-noid and preferentially targets neurons resulting in their death [85]. Such pathology may be explained by the expression of the ACE2 receptor by human glial cells and neurons [86], exacerbated through the activation of the complement and kinin systems [87].

Increasing evidence indicates the involvement of neuro-inflammation [71, 88, 89] that may damage brain blood vessels [90, 91], as well as brain cells [88, 92, 93], pos-sibly via activation of microglia [94, 95] and mast cells [96]. In fact, long-COVID could be considered a state of “brain autoimmunity” [22].

In summary, the effect of SARS-CoV-2 to the brain could be direct via invasion or indirect effect via damaging endothelial cells and pericytes or via activation of neuroimmune responses as has been invoked for neurologic complications following HIV [97].

Direct Effects of Spike Protein

An alternative explanation of the CNS effect of SARS-CoV-2 may be due to direct effects of the spike protein. The spike protein is made up of the S1 subunit containing a receptor-binding domain (RBD) that attaches to ACE2 and the S2 subunit containing a transmembrane anchor that mediates fusion of viral and host cell membranes [1]. Most infected patients develop antibodies that neutral-ize the spike protein to various extents. A recent paper reported that blood of patients infected with SARS-CoV-2 contained, in addition to antibodies against the RBD that were protective, also antibodies against the N-terminal domain (NTD) of the spike protein that induced the open conformation of the RBD enhancing its binding ability and infectivity in vitro using cultured cells [98]. A more recent study of molecular modeling using an antibody from a symptomatic COVID-19 patient concluded that there was higher NTD binding with the delta variant resulting in antibody-dependent enhancement (ADE) [99]. Such inter-actions, where antibodies can neutralize one serotype but are less potent at neutralizing another, are known to increase the chances of ADE to the new serotype [100]. Even though ADE remains controversial, a recent paper reported that virus-mimicking anti-idiotype antibodies present after infection or after vaccination may potentially explain long-COVD symptoms [101]. These findings may potentially explain why those vaccinated against the origi-nal Wuhan SARS-CoV-2 strain and then exposed to the Delta variant may still get infected. Al alternative or addi-tional explanation may be the fact that immunity to vac-cines has been reported to decrease over time [102, 103]

It is not yet known if the spike protein is released extracellularly after the SARS-CoV-2 infects its target cells. Given the absence of infection of the brain dis-cussed above, the neuropathologic findings may be due to the SARS-C0V-2 spike protein. Indirect evidence of its presence within the CNS may be the detection of anti-SARS-CoV-2 antibodies in the CSF of two children who died with COVID-10 and had subacute neuropsychiatric symptoms [104], even though such antibodies may had crossed a disrupted BBB. Free spike protein could have a number of direct pathologic actions on different cell types (Fig. 1A). These include direct stimulation of peripheral nerves [105] and stimulation of release of pro-inflam-matory and vasoactive mediators [106, 107], especially platelet-activating factor (PAF) [108, 109].

A number of papers have reported direct pathologic effect of the spike protein by itself (without being part of the coronavirus). One paper reported that the spike pro-tein could damage the endothelium in an animal model [110], while another paper showed that recombinant S1 RBD can damage mouse brain endothelial cells in vitro by inducing degradation of endothelial junction proteins, thus affecting endothelial barrier function [111]. A recent paper reported rapid internalization of S1 RBD and of the spike RBD active trimer by cultured human brain microvascular endothelial cells, followed by increased permeability of transferrin and dextran, as well as mitochondrial damage [112]. Another recent paper using a 3D-BBB microflu-idic model showed that S1 upregulated ACE2 expression and triggered RhoA activation, a key molecule regulating endothelial cytoskeleton [113]. Yet, another paper reported that spike-transfected human epithelial cells showed increased senescence-associated secretory and inflamma-tory proteins [114].

Two other papers reported that the spike protein could disrupt the barrier function in an in  vitro model of the blood-brain barrier (BBB) [115] and that the S1 protein can actually cross the BBB and enter the brain in mice 116. Using transgenic mice expressing the human sigma protein, it was shown that intranasal infection with SARS-CoV-2 rapidly induced ischemic-like reactivity in brain pericytes and the S protein reached the brain of the mice [117].

In addition to direct damage, the spike protein appears to share antigenic epitopes with human molecular chaperons resulting in autoimmunity against endothelial cells [118]. Moreover, a recent paper showed that spike epitopes could form heterodimeric complexes with selected human glial proteins [119]. Interestingly, it was shown that three recom-binant sigma protein peptides exhibited molecular interac-tions with acetylcholinesterase and antioxidant enzymes both in silico and in tad poles in vivo [120].

Interestingly, symptoms experienced by long-COVID patients, especially cognitive dysfunction [121–123], are similar [106] to those present in patients with mast cell activation syndrome (MCAS) [124, 125], in whom mast cells can be stimulated by environmental and stress trig-gers [126], including viruses [127] such as SARS-CoV-2 [107, 128]. Mast cells are located perivascularly in close proximity to neurons, especially in the hypothalamus [129, 130], where functional mast cell-neuron interactions have been documented [130, 131]. Mast cells also interact with microglia [132] leading to their activation [133] and neuro-inflammation [134].

SARS-CoV-2 binding may not be limited to the ACE2 receptor. New evidence indicates that the spike protein also binds to heparan sulfate (HS) molecules expressed on the surface of target cells, with mutant variants having higher binding affinity to HS [135]. This binding may be due to the fact that the SARS-CoV-2 spike protein contains four more positively charged and five fewer negatively charged residues than SARS-CoV, thus increasing the binding affin-ity of SARS-CoV-2 for HS [136]. Apparently, binding to HS allows the virus to reach the ACE2 receptor, and the RBD portion of the spike protein can engage both HS and ACE2 without dissociation of one or the other ligand [137]. The S1 subunit can also bind to the surface glycoprotein neuropilin-1 (NRP-1), thus increasing infectivity, but also dysregulating angiogenesis, immune responses, and neu-ronal development [138, 139]. Different coronavirus variants have evolved more efficient electrostatic interactions to allow them to bind to the ACE2 receptor [140]. SARS-CoV-2 also appears to become “pre-activated” by the proprotein con-vertase furin, thus bypassing the target cell proteases for entry [141].

Long Covid diagram

Fig. 1. A Diagrammatic representation of how SARS-CoV-2 spike protein can stimulate different cell types and collectively contribute to the pathogenesis of long-COVID. B Diagrammatic representation of how SARS-CoV-2 can cross the blood-brain barrier (BBB) through endothelial cell gaps or how free spike protein can dam-age the integrity of the BBB and enter the brain.

SARS-CoV-2 can do additional damage by activating toll-like receptors (TLRs), especially TLR2, leading to secretion of pro-inflammatory cytokines independent of viral entry [142, 143]. Such immune-mediating molecules could contribute to neurologic symptoms [144] as a result of or in addition to the action of the spike protein. Moreover, activating TLR4 increases expression of ACE2 [145] further enhancing viral infectivity in an autocrine loop. Activation of TLRs may not only involve activation of inflammasomes [146], but also activation of the mammalian target of rapamycin (mTOR) complex [147, 148], which is invoked in the pathogenesis of many neuropsychiatric diseases 149. Increased levels of a number of pro-inflammatory cytokines have been detected in the CSF of COVID-19 patients [150], especially IL-6 [150, 151]. In fact, use of an anti-IL-6 antibody or IL-6 receptor antibody reduced neuronal injury in a mouse model, accompanied by inflammation and neuronal death unrelated to hypoxia [152]. Integration of serum levels of IL-6 and heparin-binding protein were shown to have significant predictive value for severity of COVID-19 [153].

Spike protein diagram

Fig. 2. Diagrammatic representation of how SARS-CoV-2 spike protein can stimulate endothelial cells, mast cells, microglial cells, and neurons first by binding to the ACE2 receptor costimulated by binding to heparin sulfate, and then acted upon by a serine protease before entering the nucleus. SARS-CoV-2 can also stimulate Toll-like receptors (TLRs) and lead to the synthesis and release of pro-inflammatory cytokines via activation of the inflammasomes and or mTOR. The diagram also shows the targets of the inhibitory actions of luteolin, methoxyluteolin, and quercetin (green line), which may be used to prevent or treat the development of long-COVID.

A recent paper reported cloning and expressing 26 of the 29 proteins encoded by the SARS-CoV-2 genome and showed most proteins, especially non-structural protein (NSP) 2, 5, and 7, induced significant changes in endothe-lial permeability [154]. These findings imply that SARS-CoV2-associated proteins other than the spike protein may contribute to pathologic effects on their own, sequentially or synergistically with the structural sigma protein.

Lastly, a recent paper analyzed human fetal expression of six different S protein “interactors” and showed weak expression of ACE2 and TMPRSS2, but high expression of furin with peak expression 12–26 weeks post concep-tion; moreover, using publically available single-cell RNA sequencing datasets, it was shown that these interactors showed higher co-expression with neurons [155]. This find-ing indicates that the spike protein can adversely affect the developing brain and potentially lead to neurologic com-plications in neonates of infected mothers [156], including autism spectrum disorder [157].


A major unaddressed issue, especially with respect to the pathogenesis of long-COVID, is whether the spike protein that enters the brain or is expressed in neurons and glial cells can activate microglia directly or via stimulation of mast cells leading to neuro-inflammation [158]. This pathogenetic process would go on unhindered in the absence of any neutralizing antibodies since they do not cross the BBB, thus contributing to the pathogenesis of long-COVID. Moreover, such spike protein-induced neurocognitive damage could be worse in vulnerable populations like those with minimal cognitive impairment [159] or others suffering from traumatic brain injury [160].

There are presently no biologics that can block SARS-CoV-2 binding to its receptor(s). Certain biologics aimed at blocking IL-6 [161] or IL-1 [162] have been reported to improve clinical status of patients with COVID-19 However, a meta-analysis of clinical trials using IL-6 antagonists as an add-on to usual care did not reduce the risk of stroke [163], and a recent double-blind, randomized placebo-controlled study showed no benefit of an Il-6 blocker [164]. This conclusion may not be surprising as these humanized antibodies are not likely to cross the BBB unless it has already been disrupted. It is interesting that a main source of IL-6 is the mast cells [165–167], which have been reported to secrete it after stimulation with IL-1 [168] and acute stress [169]. Moreover, IL-6 can be constitutively released from human mast cells bearing the D816V-KIT mutation [170] and act on mast cell in an autocrine fashion to stimulate their proliferation [171].

This manuscript does not attempt to review and discuss all possible drugs, biologics, or natural molecules that could interfere with SARS-CoC-2 binding and its effects on tar-get cells. Rather, it focuses on certain natural molecules for

which there is sufficient basic and clinical evidence sup-porting their possible usefulness, both in prevention and treatment, especially in long-COVID. A number of recent reviews have discussed the potential use of natural molecules in that capacity [172–174]. Some simulation and in vitro studies have reported the potential benefit of small mole-cules found in Ginkgo biloba, such as the flavonoid quercetin discussed later. For instance, extracts from Ginkgo biloba leaves were identified as potential inhibitors of SARS-CoV-23CL(pro) using large-scale screening [175]. Another Ginkgo biloba extract was reported to block TNFα-induced reactive oxygen species from human aortic endothelial cells [176]. The Ginkgo biloba extract EGb 761 was beneficial in generalized anxiety disorder [177] and dementia [178], actions that may be useful for the neuropsychiatric aspects of long-COVID. Ginkgolic acid (GA) was shown to inhibit the fusion and synthesis of viral proteins [179]. Other stud-ies have shown that green tea catechins could be useful in COVID-19 [180, 181], especially against entry of SARS-CoV-2 [182]. The broccoli extract sulforaphane inhibited expression of IL-6 and IL-8 induced by the SARS-CoV-2 spike protein in bronchial epithelial cells [183].

Certain natural flavonoids [184] have been proposed as prophylaxis or treatment against COVID-19 [185–189]. Such flavonoids are found in green plants and seeds and possess potent anti-oxidant, anti-inflammatory, and cyto-protective properties [184]. However, their consumption as part of the diet does not provide sufficient systemic levels. However, there are a number of sources of pharmaceutical-grade purity (>98%) using different biomasses such as Cit-rus limon, Cynara cardunculus (artichoke), oregano, and Saphora japonicum.

In particular, a number of studies using in silico approaches identified the flavonol quercetin and the struc-turally related flavone luteolin as a potential strong block-ers of RBD [190–192]. Luteolin and some of its methylated analogues have a number of beneficial actions with respect to long-COVID: broad antiviral properties [193–195], inhi-bition of coronavirus entry [127, 196, 197], and inhibition of the serine protease required for spike protein process-ing [198, 199]. Furthermore, luteolin inhibits activation of both microglia [200–203] and mast cells [204, 205] via inhibition of signaling pathways involving the inflamma-some [206, 207] and mTOR (Fig. 2) in both mast cells [205] and microglia [203]. The novel luteolin structural analogue tetramethoxyluteolin (methoxyluteolin) is an even more potent inhibitor than luteolin [203–206].

With respect to long-COVID especially, luteolin could prevent neuro-inflammation [208–211], is neuroprotective [208, 210, 212, 213], and reduces cognitive dysfunction [214–218], especially brain fog [58, 60, 62].

Quercetin has been discussed in a few recent studies [219, 220], including an open-label clinical study showing good tolerability and benefit [221]. A double-blind, placebo-con-trolled, randomized study using a liposomal preparation of luteolin (PureLut) in long-COVID patients is underway. Combining quercetin with luteolin may provide additional benefits, especially when formulated in olive pomace oil (FibroProtek) that increases oral absorption, that is otherwise quite limited (<10%) [222]. Moreover, olive pomace oil provides additional antiviral [223] and anti-inflammatory [224]. Such liposomal preparations are available [222] and have been successfully used in pilot clinical trials [225] and reduced neuropsychiatric symptoms and associated serum IL-6 levels [226].


Further studies are urgently needed to address the neu-ropathogenesis of SARS-CoV-2 infection [227, 228] or the long-term effects of COVID-19 especially in the brain [229]. COVID vaccines have been enormously helpful [230–232], but there have been reports of rare neurological complica-tions including Guillain-Barre syndrome and Bell’s palsy [233]. These may be related to the recent finding that the spike protein expressed in response to mRNA vaccines was detected in the circulation as early as 1 day post vac-cination and became undetectable by day 14 [234]. Hence, we should try to limit or prevent spike-related detrimental effects especially to the brain and their potential contribution to the development of long-COVID.

Author Contribution: Single author

Availability of Data and Materials: Not applicable


Ethics Approval: Not applicable

Consent to Participate: Not applicable

Consent for Publication: Not applicable

Competing Interests: The author is Scientific Director of Algonot LLC that develops flavonoid-containing dietary supplements.

Research Involving Human Participants and/or Animals: Not applicable

Informed Consent: Not applicable


  1. Tai W, He L, Zhang X et al (2020) Characterization of the receptor-binding domain (RBD) of 2019 novel coronavirus: implication for development of RBD protein as a viral attachment inhibitor and vaccine. Cell Mol Immunol 17(6):613–620Cai Y, Zhang J, Xiao T et al (2020) Distinct conformational states of SARS-CoV-2 spike protein. Science 369(6511):1586–1592
  2. Canna SW, Cron RQ (2020) Highways to hell: mechanism-based management of cytokine storm syndromes. J Allergy Clin Immu-nol 146(5):949–959
  3. Giamarellos-Bourboulis EJ, Netea MG, Rovina N et al (2020) Complex immune dysregulation in COVID-19 patients with severe respiratory failure. Cell Host Microbe 27(6):992–1000
  4. Ye Q, Wang B, Mao J (2020) The pathogenesis and treatment of the ‘cytokine storm’ in COVID-19. J Inf Secur 80(6):607–613
  5. Chen G, Wu D, Guo W et al (2020) Clinical and immunological features of severe and moderate coronavirus disease 2019. J Clin Invest 130(5):2620–2629
  6. Conti P, Ronconi G, Caraffa A et al (2020) Induction of pro-inflammatory cytokines (IL-1 and IL-6) and lung inflammation by coronavirus-19 (COVI-19 or SARS-CoV-2): anti-inflamma-tory strategies. J Biol Regul Homeost Agents 34(2):327–331
  7. Tang Y, Liu J, Zhang D, Xu Z, Ji J, Wen C (2020) Cytokine storm in COVID-19: the current evidence and treatment strate-gies. Front Immunol 11:1708
  8. Paces J, Strizova Z, Smrz D, Cerny J (2020) COVID-19 and the immune system. Physiol Res 69(3):379–388
  9. Ragab D, Salah EH, Taeimah M, Khattab R, Salem R (2020) The COVID-19 cytokine storm; what we know so far. Front Immunol 11:1446
  10. Brodin P (2021) Immune determinants of COVID-19 disease presentation and severity. Nat Med 27(1):28–33
  11. Herold T, Jurinovic V, Arnreich C et al (2020) Elevated levels of IL-6 and CRP predict the need for mechanical ventilation in COVID-19. J Allergy Clin Immunol 146(1):128–136
  12. Han H, Ma Q, Li C et al (2020) Profiling serum cytokines in COVID-19 patients reveals IL-6 and IL-10 are disease severity predictors. Emerg Microbes Infect 9(1):1123–1130
  13. Mazzoni A, Salvati L, Maggi L et al (2020) Impaired immune cell cytotoxicity in severe COVID-19 is IL-6 dependent. J Clin Invest 130(9):4694–4703
  14. Liu F, Li L, Xu M et al (2020) Prognostic value of interleukin-6, C- reactive protein, and procalcitonin in patients with COVID-19. J Clin Virol 127:104370
  15. Copaescu A, Smibert O, Gibson A, Phillips EJ, Trubiano JA (2020) The role of IL-6 and other mediators in the cytokine storm associated with SARS-CoV-2 infection. J Allergy Clin Immunol 146(3):518–534
  16. Conti P, Caraffa A, Gallenga CE et al (2020) Coronavirus-19 (SARS-CoV-2) induces acute severe lung inflammation via IL-1 causing cytokine storm in COVID-19: a promising inhibitory strategy. J Biol Regul Homeost Agents 34(6):1971–1975
  17. Moore JB, June CH (2020) Cytokine release syndrome in severe COVID-19. Science 368(6490):473–474
  18. Sadarangani M, Marchant A, Kollmann TR (2021) Immunologi-cal mechanisms of vaccine-induced protection against COVID-19 in humans. Nat Rev Immunol 21(8):475–484
  19. Letizia AG, Ge Y, Vangeti S et al (2021) SARS-CoV-2 seroposi-tivity and subsequent infection risk in healthy young adults: a prospective cohort study. Lancet Respir Med 9(7):712–720
  20. Puranik A, Lenehan PJ, Silvert E et al. Comparison of two highly-effective mRNA vaccines for COVID-19 during periods of Alpha and Delta variant prevalence. medRxiv 2021.
  21. Harvey WT, Carabelli AM, Jackson B et al (2021) SARS-CoV-2 variants, spike mutations and immune escape. Nat Rev Microbiol 19(7):409–424
  22. Nalbandian A, Sehgal K, Gupta A et  al (2021) Post-acute COVID-19 syndrome. Nat Med 27(4):601–615
  23. Baig AM. (2020) Chronic COVID syndrome: need for an appro-priate medical terminology for long-COVID and COVID long-haulers. J Med Virol.
  24. Higgins V, Sohaei D, Diamandis EP, Prassas I. (2020) COVID-19: from an acute to chronic disease? Potential long-term health consequences. Crit Rev Clin Lab Sci 1-23.
  25. Huang C, Huang L, Wang Y et al (2021) 6-month consequences of COVID-19 in patients discharged from hospital: a cohort study. Lancet 397(10270):220–232
  26. Moreno-Perez O, Merino E, Leon-Ramirez JM et al (2021) Post-acute COVID-19 syndrome. Incidence and risk factors: a Medi-terranean cohort study. J Inf Secur 82(3):378–383
  27. Montagne A, Nation DA, Sagare AP et al (2020) APOE4 leads to blood-brain barrier dysfunction predicting cognitive decline. Nature 581(7806):71–76
  28. Sudre CH, Murray B, Varsavsky T et al (2021) Attributes and predictors of long COVID. Nat Med 27(4):626–631
  29. Dennis A, Wamil M, Alberts J et al (2021) Multiorgan impair-ment in low-risk individuals with post-COVID-19 syndrome: a prospective, community-based study. BMJ Open 11(3):e048391
  30. de Erausquin GA, Snyder H, Carrillo M, Hosseini AA, Brugha TS, Seshadri S (2021) The chronic neuropsychiatric sequelae of COVID-19: the need for a prospective study of viral impact on brain functioning. Alzheimers Dement 17(6):1056–1065
  31. Deer RR, Rock MA, Vasilevsky N et al (2021) Characterizing long COVID: deep phenotype of a complex condition. EBio-Medicine 74:103722
  32. Choi B, Choudhary MC, Regan J et al (2020) Persistence and evolution of SARS-CoV-2 in an immunocompromised host. N Engl J Med 383(23):2291–2293
  33. Davis HE, Assaf GS, McCorkell L et al (2021) Characterizing long COVID in an international cohort: 7 months of symptoms and their impact. EClinicalMedicine 38:101019
  34. Helms J, Kremer S, Merdji H et al (2020) Neurologic features in severe SARS-CoV-2 infection. N Engl J Med 382(23):2268–2270
  35. Fotuhi M, Mian A, Meysami S, Raji CA (2020) Neurobiology of COVID-19. J Alzheimers Dis 76(1):3–19
  36. Najjar S, Najjar A, Chong DJ et al (2020) Central nervous system complications associated with SARS-CoV-2 infection: integra-tive concepts of pathophysiology and case reports. J Neuroin-flammation 17(1):231
  37. Singh AK, Bhushan B, Maurya A, Mishra G, Singh SK, Awasthi R (2020) Novel coronavirus disease 2019 (COVID-19) and neu-rodegenerative disorders. Dermatol Ther 33(4):e13591
  38. Liotta EM, Batra A, Clark JR et al (2020) Frequent neurologic manifestations and encephalopathy-associated morbidity in Covid-19 patients. Ann Clin Transl Neurol 7(11):2221–2230
  39. Koralnik IJ, Tyler KL (2020) COVID-19: a global threat to the nervous system. Ann Neurol 88(1):1–11
  40. Nepal G, Rehrig JH, Shrestha GS et al (2020) Neurological manifestations of COVID-19: a systematic review. Crit Care 24(1):421
  41. Favas TT, Dev P, Chaurasia RN et al (2020) Neurological mani-festations of COVID-19: a systematic review and meta-analysis of proportions. Neurol Sci 41(12):3437–3470
  42. Nazari S, Azari JA, Mirmoeeni S et al (2021) Central nerv-ous system manifestations in COVID-19 patients: a systematic review and meta-analysis. Brain Behav 11:e02025
  43. Kempuraj D, Selvakumar GP, Ahmed ME et al (2020) COVID-19, mast cells, cytokine storm, psychological stress, and neuro-inflammation. Neuroscientist 26(5-6):402–414
  44. Levin SN, Venkatesh S, Nelson KE et al (2021) Manifestations and impact of the COVID-19 pandemic in neuroinflammatory diseases. Ann Clin Transl Neurol 8(4):918–928
  45. Baig AM (2020) Deleterious outcomes in long-hauler COVID-19: the effects of SARS-CoV-2 on the CNS in chronic COVID syndrome. ACS Chem Neurosci 11(24):4017–4020
  46. Ongur D, Perlis R, Goff D (2020) Psychiatry and COVID-19. JAMA 324(12):1149–1150
  47. Vindegaard N, Benros ME (2020) COVID-19 pandemic and mental health consequences: systematic review of the current evidence. Brain Behav Immun 89:531–542
  48. Pfefferbaum B, North CS (2020) Mental health and the Covid-19 pandemic. N Engl J Med 383(6):510–512
  49. Xiang YT, Yang Y, Li W et al (2020) Timely mental health care for the 2019 novel coronavirus outbreak is urgently needed. Lan-cet Psychiatry 7(3):228–229
  50. Gordon JA, Borja SE (2020) The COVID-19 pandemic: set-ting the mental health research agenda. Biol Psychiatry 88(2):130–131
  51. Taquet M, Luciano S, Geddes JR, Harrison PJ (2021) Bidirec-tional associations between COVID-19 and psychiatric disorder: retrospective cohort studies of 62 354 COVID-19 cases in the USA. Lancet Psychiatry 8(2):130–140
  52. Schirinzi T, Landi D, Liguori C (2020) COVID-19: dealing with a potential risk factor for chronic neurological disorders. J Neurol
  53. Steardo L Jr, Steardo L, Verkhratsky A (2020) Psychiatric face of COVID-19. Transl Psychiatry 10(1):261
  54. Shader RI (2020) COVID-19 and depression. Clin Ther 42(6):962–963
  55. Smith CM, Komisar JR, Mourad A, Kincaid BR (2020) COVID-
  56. 19- associated brief psychotic disorder. BMJ Case Rep 13(8)
  57. Druss BG (2020) Addressing the COVID-19 pandemic in populations with serious mental illness. JAMA Psychiatry 77(9):891–892
  58. Theoharides TC, Cholevas C, Polyzoidis K, Politis A (2021) Long-COVID syndrome-associated brain fog and chemofog: luteolin to the rescue. Biofactors 47(2):232–241
  59. Graham EL, Clark JR, Orban ZS et al (2021) Persistent neu-rologic symptoms and cognitive dysfunction in non-hospi-talized Covid-19 “long haulers”. Ann Clin Transl Neurol 8(5):1073–1085
  60. Stefano GB, Buttiker P, Weissenberger S, Martin A, Ptacek R, Kream RM (2021) Editorial: The pathogenesis of long-term neu-ropsychiatric COVID-19 and the role of microglia, mitochondria, and persistent neuroinflammation: a hypothesis. Med Sci Monit 27:e933015
  61. Bell ML, Catalfamo CJ, Farland LV et al (2021) Post-acute sequelae of COVID-19 in a non-hospitalized cohort: results from the Arizona CoVHORT. PLoS One 16(8):e0254347
  62. Hugon J, Msika EF, Queneau M, Farid K, Paquet C (2021) Long COVID: cognitive complaints (brain fog) and dysfunction of the cingulate cortex. J Neurol Jun 18:1–3
  63. Frontera JA, Yang D, Lewis A et al (2021) A prospective study of long-term outcomes among hospitalized COVID-19 patients with and without neurological complications. J Neurol Sci 426:117486
  64. Podlesek A, Komidar L, Kavcic V (2021) The relationship between perceived stress and subjective cognitive decline dur-ing the COVID-19 epidemic. Front Psychol 12:647971
  65. Townsend L, Dyer AH, Jones K et al (2020) Persistent fatigue following SARS-CoV-2 infection is common and independent of severity of initial infection. PLoS One 15(11):e0240784
  66. Phillips S, Williams MA (2021) Confronting our next national health disaster – long-haul Covid. N Engl J Med 385(7):577–579
  67. Gaebler C, Wang Z, Lorenzi JCC et al (2021) Evolution of anti-body immunity to SARS-CoV-2. Nature 591(7851):639–644
  68. Files JK, Sarkar S, Fram TR et al (2021) Duration of post-COVID-19 symptoms is associated with sustained SARS-CoV-
  69. 2- specific immune responses. JCI. Insight 6(15)
  70. McQuaid C, Brady M, Deane R (2021) SARS-CoV-2: is there neuroinvasion? Fluids Barriers CNS 18(1):32
  71. Veleri S (2021) Neurotropism of SARS-CoV-2 and neurological diseases of the central nervous system in COVID-19 patients. Exp Brain Res
  72. Welcome MO, Mastorakis NE (2021) Neuropathophysiology of coronavirus disease 2019: neuroinflammation and blood brain barrier disruption are critical pathophysiological processes that contribute to the clinical symptoms of SARS-CoV-2 infection. Inflammopharmacology 29(4):939–963
  73. Zhang L, Zhou L, Bao L et al (2021) SARS-CoV-2 crosses the blood-brain barrier accompanied with basement membrane dis-ruption without tight junctions alteration. Signal Transduct Tar-get Ther 6(1):337
  74. Song E, Zhang C, Israelow B et al (2021) Neuroinvasion of SARS-CoV-2 in human and mouse brain. J Exp Med 218(3)
  75. Xu J, Zhong S, Liu J et al (2005) Detection of severe acute res-piratory syndrome coronavirus in the brain: potential role of the chemokine mig in pathogenesis. Clin Infect Dis 41(8):1089–1096
  76. Meinhardt J, Radke J, Dittmayer C et  al (2021) Olfactory transmucosal SARS-CoV-2 invasion as a port of central nerv-ous system entry in individuals with COVID-19. Nat Neurosci 24(2):168–175
  77. Jiao L, Yang Y, Yu W et al (2021) The olfactory route is a poten-tial way for SARS-CoV-2 to invade the central nervous system of rhesus monkeys. Signal Transduct Target Ther 6(1):169
  78. Fagre A, Lewis J, Eckley M et al (2021) SARS-CoV-2 infec-tion, neuropathogenesis and transmission among deer mice: implications for spillback to New World rodents. PLoS Pathog 17(5):e1009585
  79. Brann DH, Tsukahara T, Weinreb C et al (2020) Non-neuronal expression of SARS-CoV-2 entry genes in the olfactory system suggests mechanisms underlying COVID-19-associated anosmia. Sci Adv 6(31)
  80. Nauen DW, Hooper JE, Stewart CM, Solomon IH (2021) Assess-ing brain capillaries in coronavirus disease 2019. JAMA Neurol 78(6):760–762
  81. Tsivgoulis G, Palaiodimou L, Zand R et al (2020) COVID-19 and cerebrovascular diseases: a comprehensive overview. Ther Adv Neurol Disord 13:1756286420978004
  82. Bass DI, Meyer RM, Barros G et al (2021) The impact of the COVID-19 pandemic on cerebrovascular disease. Semin Vasc Surg 34(2):20–27
  83. Dhamoon MS, Thaler A, Gururangan K et al (2021) Acute cere-brovascular events with COVID-19 infection. Stroke 52(1):48–56
  84. Gomes I, Karmirian K, Oliveira JT et al (2021) SARS-CoV-2 infection of the central nervous system in a 14-month-old child: a case report of a complete autopsy. Lancet Reg Health Am 2:100046
  85. Yang AC, Kern F, Losada PM et al (2021) Dysregulation of brain and choroid plexus cell types in severe COVID-19. Nature 595(7868):565–571
  86. Ramani A, Muller L, Ostermann PN et  al (2020) SARS-CoV-2 targets neurons of 3D human brain organoids. EMBO J 39(20):e106230
  87. Baig AM, Khaleeq A, Ali U, Syeda H (2020) Evidence of the COVID-19 virus targeting the CNS: tissue distribution, host-virus interaction, and proposed neurotropic mechanisms. ACS Chem Neurosci 11(7):995–998
  88. Savitt AG, Manimala S, White T et al (2021) SARS-CoV-2 exac-erbates COVID-19 pathology through activation of the comple-ment and kinin systems. Front Immunol 12:767347
  89. Karnik M, Beeraka NM, Uthaiah CA et al (2021) A review on SARS-CoV-2-induced neuroinflammation, neurodevelopmental complications, and recent updates on the vaccine development. Mol Neurobiol 5:1–29
  90. Liberman AC, Trias E, da Silva CL et al (2018) Neuroimmune and inflammatory signals in complex disorders of the central nervous system. Neuroimmunomodulation 25(5-6):246–270
  91. Lee MH, Perl DP, Nair G et al (2021) Microvascular injury in the brains of patients with Covid-19. N Engl J Med 384(5):481–483
  92. Magro CM, Mulvey J, Kubiak J et al (2021) Severe COVID-19: a multifaceted viral vasculopathy syndrome. Ann Diagn Pathol 50:151645
  93. Bodnar B, Patel K, Ho W, Luo JJ, Hu W (2021) Cellular mecha-nisms underlying neurological/neuropsychiatric manifestations of COVID-19. J Med Virol 93(4):1983–1998
  94. Ng JH, Sun A, Je HS, Tan EK. (2021) Unravelling pathophysiol-ogy of neurological and psychiatric complications of COVID-19 using brain organoids. Neuroscientist 10738584211015136.
  95. Tremblay ME, Madore C, Bordeleau M, Tian L, Verkhratsky A (2020) Neuropathobiology of COVID-19: the role for glia. Front Cell Neurosci 14:592214
  96. McMahon CL, Staples H, Gazi M, Carrion R, Hsieh J (2021) SARS-CoV-2 targets glial cells in human cortical organoids. Stem Cell Rep 16(5):1156–1164
  97. Theoharides TC (1990) Mast cells: the immune gate to the brain. Life Sci 46:607–617
  98. Al-Harthi L, Campbell E, Schneider JA, Bennett DA (2021) What HIV in the brain can teach us about SARS-CoV-2 neuro-logical complications? AIDS Res Hum Retrovir 37(4):255–265
  99. Liu Y, Soh WT, Kishikawa JI et al (2021) An infectivity-enhanc-ing site on the SARS-CoV-2 spike protein targeted by antibodies. Cell 9(7):712–720
  100. Yahi N, Chahinian H, Fantini J. (2021) Infection-enhancing anti-SARS-CoV-2 antibodies recognize both the original Wuhan/D614G strain and Delta variants. A potential risk for mass vac-cination? J Infect.
  101. Wan Y, Shang J, Sun S et al (2020) Molecular mechanism for antibody-dependent enhancement of coronavirus entry. J Virol 94(5):e02015–e02019
  102. Murphy WJ, Longo DL. (2021) A possible role for anti-idiotype antibodies in SARS-CoV-2 infection and vaccination. N Engl J Med.
  103. Levin EG, Lustig Y, Cohen C et al. (2021) Waning immune humoral response to BNT162b2 Covid-19 vaccine over 6 months. N Engl J Med.
  104. Goldberg Y, Mandel M, Bar-On YM et al. (2021) Waning immu-nity after the BNT162b2 vaccine in Israel. N Engl J Med.
  105. Bartley CM, Johns C, Ngo TT et al. (2021) Anti-SARS-CoV-2 and autoantibody profiles in the cerebrospinal fluid of 3 teenaged patients with COVID-19 and subacute neuropsychiatric symp-toms. JAMA Neurol.
  106. Moosavi F, Hosseini R, Saso L, Firuzi O (2016) Modulation of neurotrophic signaling pathways by polyphenols. Drug Des Devel Ther 10:23–42
  107. Theoharides TC, Conti P (2020) COVID-19 and multisystem inflammatory syndrome, or is it mast cell activation syndrome?J Biol Regul Homeost Agents 34(5):1633–1636
  108. Theoharides TC (2020) Potential association of mast cells with COVID-19. Ann Allergy Asthma Immunol 126(3):217–218
  109. Theoharides TC, Antonopoulou S, Demopoulos CA (2020) Coro-navirus 2019, microthromboses, and platelet activating factor. Clin Ther 42(10):1850–1852
  110. Demopoulos C, Antonopoulou S, Theoharides TC (2020) COVID-19, microthromboses, inflammation, and platelet acti-vating factor. Biofactors 46(6):927–933
  111. Lei Y, Zhang J, Schiavon CR et al (2021) SARS-CoV-2 spike protein impairs endothelial function via downregulation of ACE
  112. Circ Res 128(9):1323–1326
  113. Raghavan S, Kenchappa DB, Leo MD (2021) SARS-CoV-2 spike protein induces degradation of junctional proteins that maintain endothelial barrier integrity. Front Cardiovasc Med 8:687783
  114. Kim ES, Jeon MT, Kim KS, Lee S, Kim S, Kim DG (2021) Spike proteins of SARS-CoV-2 induce pathological changes in molecu-lar delivery and metabolic function in the brain endothelial cells. Viruses 13(10):2021
  115. DeOre BJ, Tran KA, Andrews AM, Ramirez SH, Galie PA.(2021) SARS-CoV-2 spike protein disrupts blood-brain barrier integrity via rhoa activation. J Neuroimmune Pharmacol.
  116. Meyer K, Patra T, Vijayamahantesh RR (2021) SARS-CoV-2 spike protein induces paracrine senescence and leukocyte adhe-sion in endothelial cells. J Virol 95(17):e0079421
  117. Buzhdygan TP, DeOre BJ, Baldwin-Leclair A et al (2020) The SARS-CoV-2 spike protein alters barrier function in 2D static and 3D microfluidic in-vitro models of the human blood-brain barrier. Neurobiol Dis 146:105131
  118. Rhea EM, Logsdon AF, Hansen KM et al (2021) The S1 protein of SARS-CoV-2 crosses the blood-brain barrier in mice. Nat Neurosci 24(3):368–378
  119. Khaddaj-Mallat R, Aldib N, Bernard M et al (2021) SARS-CoV-2 deregulates the vascular and immune functions of brain pericytes via Spike protein. Neurobiol Dis 161:105561
  120. Paladino L, Vitale AM, Caruso BC et al (2020) The role of molecular chaperones in virus infection and implications for understanding and treating COVID-19. J Clin Med 9(11):3518
  121. Dasgupta S, Bandyopadhyay M (2021) Molecular docking of SARS-COV-2 spike epitope sequences identifies heterodimeric peptide-protein complex formation with human Zo-1, TLR8 and brain specific glial proteins. Med Hypotheses 157:110706
  122. Charlie-Silva I, Araujo APC, Guimaraes ATB et al (2021) Toxi-cological insights of spike fragments SARS-CoV-2 by expo-sure environment: a threat to aquatic health? J Hazard Mater 419:126463
  123. Zhang X, Dong H, Li N et al (2016) Activated brain mast cells contribute to postoperative cognitive dysfunction by evoking microglia activation and neuronal apoptosis. J Neuroinflamma-tion 13(1):127
  124. Moura DS, Sultan S, Georgin-Lavialle S et al (2012) Evidence for cognitive impairment in mastocytosis: prevalence, features and correlations to depression. PLoS One 7(6):e39468
  125. Afrin LB, Pohlau D, Raithel M et al (2015) Mast cell activation disease: an underappreciated cause of neurologic and psychiatric symptoms and diseases. Brain Behav Immun 50:314–321
  126. Akin C, Valent P, Metcalfe DD (2010) Mast cell activation syn-drome: proposed diagnostic criteria. J Allergy Clin Immunol 126(6):1099–1104
  127. Theoharides TC, Tsilioni I, Ren H (2019) Recent advances in our understanding of mast cell activation – or should it be mast cell mediator disorders? Expert Rev Clin Immunol 15(6):639–656
  128. Theoharides TC, Valent P, Akin C (2015) Mast cells, mastocy-tosis, and related disorders. N Engl J Med 373(2):163–172
  129. Marshall JS, Portales-Cervantes L, Leong E (2019) Mast cell responses to viruses and pathogen products. Int J Mol Sci 20(17):4241
  130. Motta Junior JDS, Miggiolaro AFRD, Nagashima S et al (2020) Mast cells in alveolar septa of COVID-19 patients: a pathogenic pathway that may link interstitial edema to immunothrombosis. Front Immunol 11:574862
  131. Theoharides TC, Konstantinidou A (2007) Corticotropin-releasing hormone and the blood-brain-barrier. Front Biosci 12:1615–1628
  132. Rozniecki JJ, Dimitriadou V, Lambracht-Hall M, Pang X, Theo-harides TC (1999) Morphological and functional demonstration of rat dura mast cell-neuron interactions in vitro and in vivo. Brain Res 849:1–15
  133. Dimitriadou V, Rouleau A, Trung Tuong MD et al (1997) Func-tional relationships between sensory nerve fibers and mast cells of dura mater in normal and inflammatory conditions. Neurosci-ence 77:829–839
  134. Hendriksen E, van BD, Oosting RS, Redegeld FA. (2017) Mast cells in neuroinflammation and brain disorders. Neurosci Biobe-hav Rev 79:119–133
  135. Zhang X, Wang Y, Dong H, Xu Y, Zhang S (2016) Induction of microglial activation by mediators released from mast cells. Cell Physiol Biochem 38(4):1520–1531
  136. Skaper SD, Facci L, Zusso M, Giusti P (2017) Neuroinflam-mation, mast cells, and glia: dangerous liaisons. Neuroscientist 23(5):478–498
  137. Yue J, Jin W, Yang H et al (2021) Heparan Sulfate facilitates spike protein-mediated SARS-CoV-2 host cell invasion and con-tributes to increased infection of SARS-CoV-2 G614 mutant and in lung cancer. Front Mol Biosci 8:649575
  138. Hassanzadeh K, Perez PH, Dragotto J et al (2020) Considerations around the SARS-CoV-2 spike protein with particular attention to COVID-19 brain infection and neurological symptoms. ACS Chem Neurosci 11(15):2361–2369
  139. Liu L, Chopra P, Li X et al (2021) Heparan sulfate proteo-glycans as attachment factor for SARS-CoV-2. ACS Cent Sci 7(6):1009–1018
  140. Gudowska-Sawczuk M, Mroczko B (2021) The role of neuro-pilin-1 (NRP-1) in SARS-CoV-2 infection: review. J Clin Med 10(13):2772
  141. Sarabipour S, Mac GF (2021) Targeting neuropilins as a viable SARS-CoV-2 treatment. FEBS J
  142. Xie Y, Karki CB, Du D et al (2020) Spike proteins of SARS-CoV and SARS-CoV-2 utilize different mechanisms to bind with human ACE2. Front Mol Biosci 7:591873
  143. Shang J, Wan Y, Luo C et al (2020) Cell entry mechanisms of SARS-CoV-2. Proc Natl Acad Sci U S A 117(21):11727–11734
  144. Onofrio L, Caraglia M, Facchini G, Margherita V, Placido S, Buonerba C (2020) Toll-like receptors and COVID-19: a two-faced story with an exciting ending. Future Sci OA 6(8):FSO605
  145. Sariol A, Perlman S (2021) SARS-CoV-2 takes its toll. Nat Immunol 22(7):801–802
  146. Singh H, Singh A, Khan AA, Gupta V (2021) Immune mediating molecules and pathogenesis of COVID-19-associated neurologi-cal disease. Microb Pathog 158:105023
  147. Aboudounya MM, Heads RJ (2021) COVID-19 and toll-like receptor 4 (TLR4): SARS-CoV-2 may bind and activate TLR4 to increase ACE2 expression, facilitating entry and causing hyper-inflammation. Mediat Inflamm 2021:8874339
  148. Yi YS, Yun M (2021) Editorial of Special Issue “Regulatory roles of inflammasomes in human diseases”. Int J Mol Sci 22(6):3008
  149. Maiese K (2020) The mechanistic target of rapamycin (mTOR): novel considerations as an antiviral treatment. Curr Neurovasc Res 17(3):332–337
  150. Zheng Y, Li R, Liu S (2020) Immunoregulation with mTOR inhibitors to prevent COVID-19 severity: a novel intervention strategy beyond vaccines and specific antiviral medicines. J Med Virol 92(9):1495–1500
  151. Ryskalin L, Limanaqi F, Frati A, Busceti CL, Fornai F (2018) mTOR-related brain dysfunctions in neuropsychiatric disorders. Int J Mol Sci 19(8)
  152. Espindola OM, Gomes YCP, Brandao CO et al (2021) Inflam-matory cytokine patterns associated with neurological diseases in coronavirus disease 2019. Ann Neurol 89(5):1041–1045
  153. Oka Y, Ueda A, Nakagawa T et al (2021) SARS-CoV-2-re-lated progressive brain white matter lesion associated with an increased cerebrospinal fluid level of IL-6. Intern Med 60(19):3167–3170
  154. Sparrow NA, Anwar F, Covarrubias AE et al (2021) IL-6 inhibi-tion reduces neuronal injury in a murine model of ventilator-induced lung injury. Am J Respir Cell Mol Biol 65(4):403–412
  155. Saridaki M, Metallidis S, Grigoropoulou S et al (2021) Integra-tion of heparin-binding protein and interleukin-6 in the early prediction of respiratory failure and mortality in pneumonia by SARS-CoV-2 (COVID-19). Eur J Clin Microbiol Infect Dis 40(7):1405–1412
  156. Rauti R, Shahoha M, Leichtmann-Bardoogo Y et  al (2021) Effect of SARS-CoV-2 proteins on vascular permeability. Elife 10:e69314
  157. Varma P, Lybrand ZR, Antopia MC, Hsieh J (2020) Novel targets of SARS-CoV-2 spike protein in human fetal brain development suggest early pregnancy vulnerability. Front Neurosci 14:614680
  158. Vivanti AJ, Vauloup-Fellous C, Prevot S et al (2020) Transpla-cental transmission of SARS-CoV-2 infection. Nat Commun 11(1):3572
  159. Theoharides TC (2021) Ways to address perinatal mast cell activation and focal brain inflammation, including response to SARS-CoV-2, in autism spectrum disorder. J Pers Med 11(9):860
  160. Theoharides TC, Tsilioni I, Bawazeer M (2019) Mast cells, neu-roinflammation and pain in fibromyalgia syndrome. Front Cell Neurosci 13:353
  161. Rahman MA, Islam K, Rahman S, Alamin M (2021) Neurobio-chemical cross-talk between COVID-19 and Alzheimer’s disease. Mol Neurobiol 58(3):1017–1023
  162. Kempuraj D, Ahmed ME, Selvakumar GP et al (2019) Brain injury-mediated neuroinflammatory response and Alzheimer’s disease. Neuroscientist 26(2):134–155
  163. (2021) WHO recommends life-saving interleukin-6 receptor blockers for COVID-19 and urges producers to join efforts to rapidly increase access. Saudi Med J 42(8):923
  164. Kyriazopoulou E, Poulakou G, Milionis H et al (2021) Early treatment of COVID-19 with anakinra guided by soluble uroki-nase plasminogen receptor plasma levels: a double-blind, rand-omized controlled phase 3 trial. Nat Med 27(10):1752–1760
  165. Sagris D, Florentin M, Tasoudis P et al (2021) Immunomod-ulation and reduction of thromboembolic risk in hospitalized COVID-19 patients: systematic review and meta-analysis of randomized trials. J Clin Med 10(22):5366
  166. Rosas IO, Brau N, Waters M et al (2021) Tocilizumab in hospi-talized patients with severe Covid-19 pneumonia. N Engl J Med 384(16):1503–1516
  167. Theoharides TC, Boucher W, Spear K (2002) Serum interleu-kin-6 reflects disease severity and osteoporosis in mastocytosis patients. Int Arch Allergy Immunol 128:344–350
  168. Brockow K, Akin C, Huber M, Metcalfe DD (2005) IL-6 lev-els predict disease variant and extent of organ involvement in patients with mastocytosis. Clin Immunol 115(2):216–223
  169. Mayado A, Teodosio C, Garcia-Montero AC et  al (2015) Increased IL6 plasma levels in indolent systemic mastocytosis patients are associated with high risk of disease progression. Leukemia 30(1):124–130
  170. Kandere-Grzybowska K, Letourneau R, Kempuraj D et al (2003) IL-1 induces vesicular secretion of IL-6 without degranulation from human mast cells. J Immunol 171(9):4830–4836
  171. Huang M, Pang X, Karalis K, Theoharides TC (2003) Stress-induced interleukin-6 release in mice is mast cell-dependent and more pronounced in Apolipoprotein E knockout mice. Cardio-vasc Res 59(1):241–249
  172. Tobio A, Alfonso A, Botana LM (2015) C-kit mutations deter-mine dasatinib mechanism of action in HMC-1 neoplastic mast cells: dasatinib differently regulates PKCdelta translocation in HMC-1(560) and HMC-1(560,816) cell lines. Immunopharmacol Immunotoxicol 37(4):380–387
  173. Desai A, Jung MY, Olivera A et al (2016) IL-6 promotes an increase in human mast cell numbers and reactivity through sup-pression of suppressor of cytokine signaling 3. J Allergy Clin Immunol 137(6):1863–1871
  174. Peter AE, Sandeep BV, Rao BG, Kalpana VL (2020) Calming the storm: natural immunosuppressants as adjuvants to target the cytokine storm in COVID-19. Front Pharmacol 11:583777
  175. Nouadi B, Ezaouine A, El MM, Blaghen M, Bennis F, Cheg-dani F (2021) Prediction of anti-COVID 19 therapeutic power of medicinal moroccan plants using molecular docking. Bioinform Biol Insights 15:11779322211009199
  176. Alesci A, Aragona M, Cicero N, Lauriano ER. (2021) Can nutra-ceuticals assist treatment and improve covid-19 symptoms? Nat Prod Res 1-20.
  177. Xiong Y, Zhu GH, Wang HN et al (2021) Discovery of naturally occurring inhibitors against SARS-CoV-2 3CL(pro) from Ginkgo biloba leaves via large-scale screening. Fitoterapia 152:104909
  178. Chen JS, Chen YH, Huang PH et al (2012) Ginkgo biloba extract reduces high-glucose-induced endothelial adhesion by inhibiting the redox-dependent interleukin-6 pathways. Cardiovasc Diabetol 11:49
  179. Woelk H, Arnoldt KH, Kieser M, Hoerr R (2007) Ginkgo biloba special extract EGb 761 in generalized anxiety disorder and adjustment disorder with anxious mood: a randomized, double-blind, placebo-controlled trial. J Psychiatr Res 41(6):472–480
  180. Gauthier S, Schlaefke S (2014) Efficacy and tolerability of Ginkgo biloba extract EGb 761(R) in dementia: a systematic review and meta-analysis of randomized placebo-controlled tri-als. Clin Interv Aging 9:2065–2077
  181. Ibrahim MA, Ramadan HH, Mohammed RN (2021) Evidence that Ginkgo biloba could use in the influenza and coronavi-rus COVID-19 infections. J Basic Clin Physiol Pharmacol 32(3):131–143
  182. Jimenez-Avalos G, Vargas-Ruiz AP, Gado-Pease NE et al (2021) Comprehensive virtual screening of 4.8 k flavonoids reveals novel insights into allosteric inhibition of SARS-CoV-2 M(PRO). Sci Rep 11(1):15452
  183. Wang YQ, Li QS, Zheng XQ, Lu JL, Liang YR (2021) Antiviral effects of green tea EGCG and its potential application against COVID-19. Molecules 26(13):3962
  184. Mhatre S, Gurav N, Shah M, Patravale V (2021) Entry-inhibitory role of catechins against SARS-CoV-2 and its UK variant. Com-put Biol Med 135:104560
  185. Gasparello J, D’Aversa E, Papi C et al (2021) Sulforaphane inhib-its the expression of interleukin-6 and interleukin-8 induced in bronchial epithelial IB3-1 cells by exposure to the SARS-CoV-2 Spike protein. Phytomedicine 87:153583
  186. Middleton E Jr, Kandaswami C, Theoharides TC (2000) The effects of plant flavonoids on mammalian cells: implications for inflammation, heart disease, and cancer. Pharmacol Rev 52(4):673–751
  187. Theoharides TC (2020) COVID-19, pulmonary mast cells, cytokine storms, and beneficial actions of luteolin. Biofactors 46(3):306–308
  188. Richman S, Morris MC, Broderick G, Craddock TJA, Klimas NG, Fletcher MA (2019) Pharmaceutical interventions in chronic fatigue syndrome: a literature-based commentary. Clin Ther 41(5):798–805
  189. Goris T, Perez-Valero A, Martinez I et al (2021) Repositioning microbial biotechnology against COVID-19: the case of micro-bial production of flavonoids. Microb Biotechnol 14(1):94–110
  190. Gour A, Manhas D, Bag S, Gorain B, Nandi U (2021) Flavo-noids as potential phytotherapeutics to combat cytokine storm in SARS-CoV-2. Phytother Res 35(8):4258–4283
  191. Alzaabi MM, Hamdy R, Ashmawy NS et al. (2021) Flavonoids are promising safe therapy against COVID-19. Phytochem Rev 1- 22.
  192. Kumar B, Zaidi S, Haque S et al. (2020) In silico studies reveal antiviral effects of traditional Indian spices on COVID-19. Curr Pharm Des
  193. Ali AM, Kunugi H (2021) Propolis, bee honey, and their com-ponents protect against coronavirus disease 2019 (COVID-19): a review of in silico, in vitro, and clinical studies. Molecules 26(5):1232
  194. Stalin A, Lin D, Senthamarai KB et al. (2021) An in-silico approach to identify the potential hot spots in SARS-CoV-2 spike RBD to block the interaction with ACE2 receptor. J Biomol Struct Dyn 1-16.
  195. Xu L, Su W, Jin J et  al (2014) Identification of luteolin as enterovirus 71 and coxsackievirus A16 inhibitors through reporter viruses and cell viability-based screening. Viruses 6(7):2778–2795
  196. Fan W, Qian S, Qian P, Li X (2016) Antiviral activity of luteolin against Japanese encephalitis virus. Virus Res 220:112–116
  197. Yan H, Ma L, Wang H et al (2019) Luteolin decreases the yield of influenza A virus in vitro by interfering with the coat protein I complex expression. J Nat Med 73(3):487–496
  198. Russo M, Moccia S, Spagnuolo C, Tedesco I, Russo GL (2020) Roles of flavonoids against coronavirus infection. Chem Biol Interact 328:109211
  199. Derosa G, Maffioli P, D’Angelo A, Di PF (2020) A role for quercetin in coronavirus disease 2019 (COVID-19). Phytother Res 35(3):1230–1236
  200. Jo S, Kim S, Shin DH, Kim MS (2020) Inhibition of SARS-CoV 3CL protease by flavonoids. J Enzyme Inhib Med Chem 35(1):145–151
  201. Xue G, Gong L, Yuan C et  al (2017) A structural mecha-nism of flavonoids in inhibiting serine proteases. Food Funct 8(7):2437–2443
  202. Rezai-Zadeh K, Ehrhart J, Bai Y et al (2008) Apigenin and luteolin modulate microglial activation via inhibition of STAT1-induced CD40 expression. J Neuroinflammation 5:41
  203. Jang S, Kelley KW, Johnson RW (2008) Luteolin reduces IL-6 production in microglia by inhibiting JNK phosphorylation and activation of AP-1. Proc Natl Acad Sci U S A 105(21):7534–7539
  204. Burton MD, Rytych JL, Amin R, Johnson RW (2016) Dietary luteolin reduces proinflammatory microglia in the brain of senes-cent mice. Rejuvenation Res 19(4):286–292
  205. Patel AB, Tsilioni I, Leeman SE, Theoharides TC (2016) Neu-rotensin stimulates sortilin and mTOR in human microglia inhibitable by methoxyluteolin, a potential therapeutic target for autism. Proc Natl Acad Sci U S A 113:E7049–E7058
  206. Weng Z, Patel AB, Panagiotidou S, Theoharides TC (2015) The novel flavone tetramethoxyluteolin is a potent inhibitor of human mast cells. J Allergy Clin Immunol 135(4):1044–1052
  207. Patel AB, Theoharides TC (2017) Methoxyluteolin inhibits neuropeptide-stimulated proinflammatory mediator release via mTOR activation from human mast cells. J Pharmacol Exp Ther 361(3):462–471
  208. Taracanova A, Tsilioni I, Conti P, Norwitz ER, Leeman SE, Theoharides TC (2018) Substance P and IL-33 administered together stimulate a marked secretion of IL-1beta from human mast cells, inhibited by methoxyluteolin. Proc Natl Acad Sci U S A 115(40):E9381–E9390
  209. Lee MN, Lee Y, Wu D, Pae M (2021) Luteolin inhibits NLRP3 inflammasome activation via blocking ASC oligomerization. J Nutr Biochem 92:108614
  210. Ashaari Z, Hadjzadeh MA, Hassanzadeh G et al (2018) The flavone luteolin improves central nervous system disorders by different mechanisms: a review. J Mol Neurosci 65(4):491–506
  211. Calis Z, Mogulkoc R, Baltaci AK (2020) The roles of flavonols/flavonoids in neurodegeneration and neuroinflammation. Mini-Rev Med Chem 20(15):1475–1488
  212. Kempuraj D, Thangavel R, Kempuraj DD et al (2020) Neuro-protective effects of flavone luteolin in neuroinflammation and neurotrauma. Biofactors 47(2):190–197
  213. Theoharides TC, Conti P, Economu M (2014) Brain inflamma-tion, neuropsychiatric disorders, and immunoendocrine effects of luteolin. J Clin Psychopharmacol 34(2):187–189
  214. Dajas F, Rivera-Megret F, Blasina F et al (2003) Neuroprotection by flavonoids. Braz J Med Biol Res 36(12):1613–1620
  215. Lin TY, Lu CW, Wang SJ (2016) Luteolin protects the hippocam-pus against neuron impairments induced by kainic acid in rats. NeuroToxicol 55:48–57
  216. Rezai-Zadeh K, Douglas SR, Bai Y et al (2009) Flavonoid-medi-ated presenilin-1 phosphorylation reduces Alzheimer’s disease beta-amyloid production. J Cell Mol Med 13(3):574–588
  217. Theoharides TC, Stewart JM, Hatziagelaki E, Kolaitis G (2015) Brain “fog,” inflammation and obesity: key aspects of 2 neu-ropsychiatric disorders improved by luteolin. Front Neurosci 9:225
  218. Yao ZH, Yao XL, Zhang Y, Zhang SF, Hu JC (2018) Luteolin could improve cognitive dysfunction by inhibiting neuroinflam-mation. Neurochem Res 43(4):806–820
  219. Gratton G, Weaver SR, Burley CV et al (2020) Dietary flavanols improve cerebral cortical oxygenation and cognition in healthy adults. Sci Rep 10(1):19409
  220. Devi SA, Chamoli A (2020) Polyphenols as an effective thera-peutic intervention against cognitive decline during normal and pathological brain aging. Adv Exp Med Biol 1260:159–174
  221. Manjunath SH, Thimmulappa RK. (2021) Antiviral, immu-nomodulatory, and anticoagulant effects of quercetin and its derivatives: potential role in prevention and management of COVID-19. J Pharm Anal.
  222. Simsek Y, Baran SS, Aslim B (2021) In silico identification of SARS-CoV-2 cell entry inhibitors from selected natural antivi-rals. J Mol Graph Model 109:108038
  223. Di PF, Derosa G, Maffioli P et al (2021) Possible therapeutic effects of adjuvant quercetin supplementation against early-stage COVID-19 infection: a prospective, randomized, controlled, and open-label study. Int J Gen Med 14:2359–2366
  224. Theoharides TC (2020) Luteolin supplements: all that glitters is not gold. Biofactors 47(2):242–244
  225. Hartvig P, Larsson BS, Lindberg BS et al (1986) Influence of monoamine oxidase inhibitors and a dopamine uptake blocker on the distribution of 11C-N-methyl-4-phenyl-1,2,3,6-tetrahy-dropyridine, 11C-MPTP, in the head of the rhesus monkey. Acta Neurol Scand 74(1):10–16
  226. Serreli G, Deiana M (2020) Extra virgin olive oil polyphenols: modulation of cellular pathways related to oxidant species and inflammation in aging. Cells 9(2):478
  227. Taliou A, Zintzaras E, Lykouras L, Francis K (2013) An open-label pilot study of a formulation containing the anti-inflamma-tory flavonoid luteolin and its effects on behavior in children with autism spectrum disorders. Clin Ther 35(5):592–602
  228. Tsilioni I, Taliou A, Francis K, Theoharides TC (2015) Children with autism spectrum disorders, who improved with a luteolin containing dietary formulation, show reduced serum levels of TNF and IL-6. Transl Psychiatry 5:e647
  229. Khan S, Gomes J (2020) Neuropathogenesis of SARS-CoV-2 infection. Elife 9:e59136
  230. Farhadian SF, Seilhean D, Spudich S (2021) Neuropatho-genesis of acute coronavirus disease 2019. Curr Opin Neurol 34(3):417–422
  231. Ellul MA, Benjamin L, Singh B et al (2020) Neurological asso-ciations of COVID-19. Lancet Neurol 19(9):767–783
  232. Dai L, Gao GF (2021) Viral targets for vaccines against COVID-
  233. Nat Rev Immunol 21(2):73–82
  234. Theoharides TC, Lauritano D, Ronconi G, Calvisi V, Conti P (2021) Antibodies for COVID-19 – which, when and how long?J Biol Regul Homeost Agents 35(2):417–422
  235. Escobedo RA, Singh DK, Kaushal D (2021) Understanding COVID-19: from dysregulated immunity to vaccination status quo. Front Immunol 12:765349
  236. Kneussl MP, Richardson JB (1978) Alpha-adrenergic receptors in human and canine tracheal and bronchial smooth muscle. J Appl Physiol Respir Environ Exerc Physiol 45(2):307–311
  237. Ogata AF, Cheng CA, Desjardins M et al. (2021) Circulating SARS-CoV-2 vaccine antigen detected in the plasma of mRNA-1273 vaccine recipients. Clin Infect Dis.

Publisher’s Note: Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Male Andropause – Hormonal & Neurotransmitter Imbalances in Midlife

Male Andropause

Men do not usually present at the doctor’s office requesting an assessment for andropause, or “male menopause.” The more common scenario is a fifty-year-old executive, slightly overweight, appearing exhausted and irritable, reluctantly showing up in the doctor’s office for a consultation.  It was his wife, enquiring into her menopausal status the week before, who had mentioned to the doctor, “You know, I think my husband should have a check-up. He hasn’t been himself lately. He is grumpy. He lies down on the sofa any chance he can get. He complains of vague aches and pains, and I can’t remember the last time we had sex!” 

Upon closer enquiry, it appears that his symptoms were slower and more insidious in onset than his wife’s but, nevertheless, just as dramatic in their consequences. Men traditionally tend to have a more stoic and fatalistic approach to encroaching signs and symptoms, but as hormone depletion typically affects a man’s sexual performance first, this is often what propels him to seek medical attention.  The danger of ignoring all the other signs and symptoms of declining hormones is that andropause is not necessarily a benign process. It is often accompanied by profound physiological and mental changes that, over the long term, can have a significant effect on silent disease processes. According to Dr Jerald Bain, testosterone is much more than just a male sex hormone. It is an important contributor to the robust metabolic functioning of multiple bodily systems.[1] Men with low testosterone die earlier than those with normal levels.[2] Andropause can thus be considered a lethal disease. There is a 41 % decrease in the chance of dying with a testosterone level of 20 nmol/l compared to 12 nmol/l (average level 12-35 nmol/l).[3] For this reason, it is imperative that male andropause enters into consensual reality as forcefully and as well publicized as female menopause, lest we have a whole generation of men developing life threatening disease that may have been prevented with much earlier interventions.

[1] Bain J.The many faces of testosterone Clin Interv Aging. 2007; 2(4):567-76

[2] Shores MM et al, Low serum testosterone and mortality in male veterans. Arch Intern Med. 2006 Aug 14-28; 166 (15):1660-5

[3] Ibid.

It has been estimated that among men more than 45-50 years old, the prevalence of low testosterone is at least 20-30 %.[1] Some of the more common and somewhat insidious presenting features of andropause include:

Loss of drive or competitive edge in business,

  • Various aches and pains in muscles and joints,
  • Loss of memory, a decreasing level of fitness,
  • Endurance and effectiveness in workouts,
  • Loss of muscle mass and increased abdominal obesity,[2]
  • Fatigue,
  • Depression,
  • Negative mood,[3]
  • Irritability
  • Most importantly, decreased libido and erection frequency, endurance, and strength, as well as unsatisfying orgasms.  Sex on a nightly basis turns into sex on a weekly basis as the desire and ability to perform decrease, while general fatigue increases.  Increasing loss of graying hair seems to be the final insult to an already distressing situation. However, this is just the tip of the iceberg. In addition, there may be many other subtle clues as to a declining sense of wellbeing. (See table 1) 

[1] Goepp J, Life Extension June 2010 pg 84

[2] Harman SM, et al, Longtitudinal effects of aging on serum total and free testosterone levels in healthy men. J Clin Endocrin Metab, 2001 Feb;86 (2):724-31

[3] Zitzmann M. Testosterone and the brain. Aging Male. 2006 Dec; 9 (4):567-76


  • Headache
  • Tinnitus (ringing in the ears)
  • Aging facial appearance with increased wrinkles
  • Quickly out of breath with physical activity
  • Unexplained numbness and tingling
  • Constipation
  • Hypochondriasis
  • Lack of interest in sports
  • Disturbed sleep with less than eight hours of uninterrupted sleep as trips to the bathroom increase due to prostate swelling as well a slower levels of melatonin
  • Hot flushes and sweating spells (mostly head and upper chest)
  • Prostate infections
  • Reduction in ejaculate
  • Gynecomastia (Fat accumulation in the breasts)
  • Longitudinal lines on nails
  • Hemorrhoids
  • Cellulite
  • Loss of hair on legs, especially the external sides
  • Nervousness and irritability
  • Poor concentration
  • Poor memory
  • Voice developing a higher anxious tone
  • Messy clothing (due to the depressive tendency and lack of the desire to be sexually attractive)
  • Becoming shorter in height, dry, thin (atrophic) skin
  • Dry glans penis (tip of penis)
  • Small, flaccid, atrophied penis
  • Peyronie’s disease (skew penis)
  • Lax testicles with reduction in size
  • Male pattern baldness (androgenic alopecia)
  • Dry eyes
  • Decreased axillary and pubic hair

If some of these symptoms and signs start to appear in your life or in the lives of your 40–50-year-old male loved ones, be very suspicious of the insidious onset of what has been termed male andropause.

What Is Male Menopause (also known as Viropause or Andropause)?

Male menopause is generally recognized as a gradual shift in hormonal, physiological and chemical changes that occur in all men between the ages of 40 and 45, although it can occur as low as 35 and as late as 65. [1] The term “hormone” is derived from the Greek word, hormo, which means to set in motion. This is precisely what hormones do. Hormones are involved in almost every biological process, including sexual reproduction, growth, metabolism, and immune function. They stimulate, regulate, and control the function of various tissues and organs and are manufactured by specialized groups of cells within structures called glands.

[1] Jed Diamond Male Menopause Sourcebook INC. Naperville, IL 1998, 1v

These glands, including the hypothalamus, pituitary, thyroid, adrenals, ovaries, and testes, release various hormones into the body as needed. The hormones that decline as a man age are Testosterone, Growth Hormone, Melatonin, DHEA, Progesterone, Pregnenolone and Oxytocin. (See table 2)   Hormone levels that usually go up with andropause are estrogen (the female sex hormone), insulin (the hormone responsible for sugar metabolism and the metabolic syndrome) and the stress hormone, cortisol. Testosterone, the main hormone responsible for andropause,[1] seems to peak in a man at approximately 30 years of age and then begins its gradual decline.[2]

[1] Rosick E.Male Menopause. Life Extension. Oct 2003,  pg 65

[2] Anawalt BD, Merriam G|R. Neuroendocrine aging in men. Endo and Met Clinics 2001 Sep; 30 (3): 647-69


  • Testosterone.
  • Growth hormone
  • Melatonin
  • DHEA
  • Pregnenolone
  • Progesterone
  • Thyroid hormone
  • Oxytocin
  • Dopamine
  • Acetylcholine
  • Gaba
  • Serotonin

The changes experienced by men during andropause can affect every aspect of a man’s life. These changes create not only serious, life-threatening health effects, but often they are harbingers of a deeper social and spiritual transition.  These changes signal the beginning of the end of the first part of a man’s life and herald in a new phase of his evolution, whereby the male may reexamine his life by asking sometimes frightening and often liberating questions.[1] If this transition is well managed medically, it may turn out to be the most productive and purposeful time of a man’s life.

This transition for men has been hotly debated for some time as to whether or not it was a real or imagined phenomenon. While the female menopause is often abrupt and life changing, signaling within a few months the change from her reproductive years to post reproductive reality, the male transition is often more gradual and not defined by reproductive incapacity.  Many people have long believed that levels decline as a natural consequence of advancing age, and thus there is nothing we can or should do about them.[2] Dr Morgentaler, associate professor at Harvard Medical School and author of  Testosterone for Life (McGraw Hill, 2008), explains, “That’s like telling a middle-aged person that since vision typically deteriorates with age, there’s no point in prescribing glasses- or that we shouldn’t treat atherosclerosis to prevent heart attacks, because it too is an age-related phenomenon. It just doesn’t make sense!” [3]

If one compares the physiological changes between men and women during this period of transition, there are striking similarities. For both sexes, as their hormones undergo this transition, body fat increases; well-being decreases; and sexual function decreases. Incidences of cardiovascular disease (heart attacks, hypertension, high cholesterol), type 2 diabetes, depression, obesity, Alzheimer’s and osteoporosis increase. Muscle wasting increases, and both prostate and breast cancer increase (as both cancers arise from similar embryological tissue).

[1] Hollis J. The MiddlePassage. From Misery to Meaning in Midlife. Inner City Books Toronto Canada 1993 pg 7

[2] Goep J..Testosterone Therapy for Life. Life Extension June 2010 pg 83

[3] Ibid, pg 84

Testosterone – Basic Physiology

Testosterone – Basic Physiology

Testosterone plays an essential role in the development of the normal male and in the maintenance of many male characteristics, including muscle mass and strength, bone mass, libido, potency, and sperm production.  Testosterone is also important in synthesizing proteins. It affects many metabolic activities such as the production of blood cells in the bone marrow, formation of bone, lipid and carbohydrate metabolism, and growth of the prostate gland. Testosterone production begins in the part of the brain known as the hypothalamus, which secretes gonadotropin-releasing hormone (GnRH). This hormone then signals the pituitary gland to make either follicular-stimulating hormone (FSH) or luteinizing hormone (LH). FSH helps to stimulate the testes to produce sperm, while LH stimulates the production of testosterone via the Leydig cells of the testes. Like the declining levels of eggs in a woman’s ovary as she ages, it has been estimated that men are born with 700 million Leydig cells and begin to lose six million of these cells yearly after his twentieth birthday. [1]

After testosterone is released from the testes, some testosterone is tightly bound to sex hormone binding globulin (SHBG) as well as loosely bound to albumin, a protein. Together, these are measured in the blood stream as total testosterone. Free testosterone is unbound to sex hormone binding globulin or albumin, and it is this hormone which exerts its powerful anabolic effects on the body (approx. 2-3% of testosterone). Bioavailable testosterone is also measurable – it is the sum of the unbound and the loosely bound portion to albumin. It is believed that the bioavailable measurement is the most accurate for assessing the amount of the most active hormone exerting its effect on the tissues.

As men grow older, not only do their bodies produce less testosterone, but the levels of another hormone called sex binding hormone globulin (SHBG) begin to increase. Levels of this hormone increase due to the aging process, increased alcohol use, increased obesity and estrogen levels, and decreased growth hormone and progesterone levels. As SHBG increases, bioavailable or free testosterone levels plummet.

As we age, testosterone is furthermore converted via an enzyme called 5-alpha reductase into dihydrotestosterone (DHT), a hormone responsible not only for aspects of a man’s libido but also most importantly, for hair distribution, heralding in the usually most unwelcome signs of male pattern baldness. Testosterone can also be converted via an enzyme called aromatase to estrogen, a vital hormone in men for bone health and cognitive wellbeing. [2] Too much estrogen production in men, a common event seen in obesity as well as seen more frequently in injectable testosterone replacement therapy.  This excess of estrogen increases a male’s risk of breast and prostate cancer.

[1] Morales A,Tenover JL. Androgen deficiency in the aging male. Urological Clinics North America 2002: 29 (4); 975- 82

[2] Nelson LR, Bulun SE. Estrogen production and action. Journal of Amer Acad Derm 2001 Sep; 45 (3): 116-24.

Lab Testing for Testosterone

When measuring testosterone levels, it is best to ask your doctor for total testosterone, free as well as bioavailable testosterone. One can measure levels in the serum and the saliva as well as through 24-hour urine collection. The benefit of saliva testing is that it is the only way to measure whether one has therapeutic levels of testosterone once transdermal creams have been initiated. It is absolutely useless to assess serum levels to measure the efficacy of transdermal creams or patches because it will require toxic doses of the transdermal creams to raise the serum levels to therapeutic serum levels. The reason for this is that, when applied transdermally, testosterone stays in the serum for a total of three seconds before being sequestered into the tissues where it exerts its effect. In order to raise serum levels, the tissue levels have to be super-saturated before the excess spills back into the serum. By this time, toxic tissue levels have been achieved. However, if testosterone is given via intramuscular injection, then serum levels are the standard way of measuring therapeutic efficacy.

The average range of male total testosterone levels and one that is considered “normal” by the US based FDA is between 12.15-35.76 nmol/l. However, no single number should be used as an absolute level. It is a man’s symptoms combined with his serum levels that should guide therapy. If a man’s symptoms are consistent with low testosterone and his serum levels are at the low range of normal, that man deserves a trial of testosterone therapy.

Once testosterone therapy is begun, it is advised to test the following blood levels every 3 to 6 months in the first year and then twice a year thereafter: Hemoglobin, hematocrit, total, free and bioavailable testosterone, estrogen, progesterone, pregnenolone, dihydrotestosterone as well as PSA. Blood testing should be accompanied by a yearly digital rectal examination (DRE).

Testosterone declines with age

Testosterone declines with age

Free testosterone declines at a rate of 1% per yr. or 10% per decade.[1] As our total testosterone levels only range from approx. 12-35 nmol/l, (extremely small amounts), one can deduce that, in 20 years, significant inroads may be made into one’s total testosterone stores.  In various studies, testosterone measures correlated with strength, bone mineral density, body composition and fat mass. [2] As our levels decrease, so do these parameters of health. [3] Half of healthy men between the ages of 50 to 70 will have a bioavailable testosterone level below the lowest level seen in healthy men who are 20 to 40 years of age. [4]

One of the reasons why men are not diagnosed as being hormone deficient is that the levels of the hormones that appear on standard lab tests are age adjusted for an aging population with an anticipated reduction in hormone levels. In anti-aging medicine, we aim to restore hormone levels to a healthy youthful range of a healthy 25–35-year-old.

[1] Decreased bioavailable testosterone in aging normal and impotent men. Nankin HR et al. J Clin.Endocrinol Metab. 1986 Dec; 63(6):1418-20.

[2] Measures of Bioavailable Serum Testosterone and Estradiol and Their Relationships with Muscle Strength, Bone Density, and Body Composition in Elderly Men.  Annewieke W et al. The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 9 3276-3282, 2000

[3] Morley J. Longitudinal changes in testosterone, luteinizing hormone, and follicle-stimulating hormone in healthy older men. Metabolism 1997 Apr;46(4):410-3

[4] Korenman SG, Morley JE, Mooradian AD, et al. 1990 Secondary hypogonadism in older men: its relationship to impotence. J Clin Endocrinol Metab. 71:963–969.

With declining levels of free testosterone as we age, the following health effects have been well documented

Cardiovascular Disease:

Man with cardiovascular disease

Men with coronary artery disease had significantly lower levels of total testosterone as well as free and bioavailable testosterone than the men in the control group. [1] Furthermore, exercise-induced myocardial ischemia (reduced blood flow to the heart) improved with the use of testosterone, showing significant improvements in pain perception with no negative alterations in cholesterol levels or blood clotting capacity. [2] This effect is thought to be due to a direct coronary artery relaxing effect. [3] The many cardiac benefits of adequate levels of testosterone include assisting in the heart beating stronger, widening the coronary artery lumen, increasing blood supply to the heart, reducing serum cholesterol, minimizing atherosclerosis, reducing hypertension by vasodilatation, and making blood more fluid by increasing fibrinolytic (breaking down of clots) activity and thus reducing blood clots. Of note, very high doses of testosterone may suppress the protective high-density cholesterol whereas low levels of testosterone are associated with increased levels of total cholesterol.  As cardiovascular disease is by far the leading cause of death in the aging population in developed countries, [4] it behooves our health practitioners to be extremely diligent in measuring and managing this highly preventable risk factor.

[1] English K et al. Men with coronary artery disease have lower levels of androgens than men with normal coronary  ngiograms.  Eur Heart J 2000 Jun;21(11):890-4

[2] English KM et al.Low-dose transdermal testosterone therapy improves angina threshold in men with chronic stable angina: Circulation 2000 Oct 17;102(16):1906-11

[3] Rosano GM et al. Acute anti-ischemic effect of testosterone in men with coronary artery disease. Circulation 1999 Apr 6;99(13):1666-70

[4]  World Health Organization (2004). “Annex Table 2: Deaths by cause, sex and mortality stratum in WHO regions, estimates for 2002” (pdf). The world health report 2004 – changing history. http://www.who.int/entity/whr/2004/annex/topic/en/annex_2_en.pdf.

Memory and cognitive function:

Multiple studies have proven that men with optimal testosterone levels as they age have fewer symptoms of senility compared to men with lower levels of testosterone. Testosterone supplementation increases working memory in men. [1]  It has also been shown to improve visual and verbal memory and visuospatial functioning as well as reduce the rate of decline in visual memory.[2] Testosterone levels correlate with cognitive function; as testosterone levels are replaced to therapeutic levels, memory and cognition improved accordingly.[3]

[1] Janowsky J et al.Sex steroids modify working memory.J Cogn Neurosci 2000 May;12(3):407-14

[2] Moffat SD, et al. Longitudinal assessment of free testosterone concentration predicts memory performance and cognitive status in elderly men. J Clin Endocrinol Metab 2002 Nov; 87 (11): 5001-7

[3] Alexander GM, Swerdloff RS, Wang C, et al. Androgen-behavior correlations in hypogonadal men and eugonadal men. II. Cognitive abilities. Hormones and Behavior 1998; 33(2):85-94


Numerous studies have shown testosterone replacement therapy is effective when psychiatric drugs do not work in with men with depression. [1] In this study, testosterone therapy improved both natural and spontaneous erections as well as mood.[2] Low testosterone was shown to be associated with fatigue, and testosterone therapy produces a sense of wellbeing.[3] Men with low levels of testosterone are more prone to depression [4]as well as dramatic mood swings. [5]

[1] Cooper MA.  Testosterone Replacement Therapy for Anxiety Am J Psychiatry 157:1884, November 2000

[2] Burris A et al. A long-term, prospective study of the physiologic and behavioral effects of hormone replacement in untreated hypogonadal men. J Androl 1992 Jul-Aug;13(4):297-304

[3] Margolese HC et al. The male menopause and mood: testosterone decline and depression in the aging male–is there a link? J Geriatr Psychiatry Neurol 2000 Summer;13(2):93-101

[4] Pope HG, Jr et al, Testosterone gel supplementation for men with refractory depression: a randomized, placebo controlled trial. Am J Psychiatry, 2003 Jan: 160 (1): 105-11

[5] Goep J. Testosterone Therapy for Life. Life Extension June 2010 pg 86

Mortality Risk:

Testosterone deficiency can be seen as a lethal disease as individuals who had the lowest levels of testosterone had the greatest mortality rates. In this study, during an average 11.8-year follow-up, 538 deaths occurred.Men whose total testosterone levels were in the lowest quartilewere 40% more likely to die than thosewith higher levels, independent of age, adiposity, and lifestyle.[1]

[1] Gail A.  Low serum testosterone and mortality in older men. J of Clin Endocrin and Metab. Vol. 93, No. 1, 68-75

Alzheimer’s disease:

Testosterone replacement therapy prevents the production of beta amyloid precursor protein in men,[1] thus reducing the risk for Alzheimer’s disease. In established Alzheimer’s disease, treatment with testosterone improved the patient’s cognition over 1 year, whereas the control group deteriorated. [2]

[1] Gouras GK et al. Testosterone reduces neuronal secretion of Alzheimer’s beta-amyloid peptides Proc Natl Acad Sci U S A 2000 Feb 1; 97(3):1202-5.

[2] Tan RS. A pilot study on the effects of testosterone in hypogonadal aging male patients with Alzheimer’s disease. Aging male. 2003 Mar 6 (1): 13-7

Strength and Muscle Mass:

Man's arm flexing

Testosterone is a major predictor of skeletal mass, synergistic with growth hormone. In this same study, significantly improved strength was demonstrated with testosterone use even without exercise. [1]There was a more marked improvement when exercise was added to the program. With the increase in muscle mass, increased performances were noted in muscle power, strength, and endurance, with a resultant improvement in physical function, athletic performance and overall improved health related outcomes. [2]

[1] Bhasin S. The dose-dependent effects of testosterone on sexual function and on muscle mass and function. Mayo Clin Proc. 2000 Jan;75 Suppl: 70-5

[2] Ibid.


A study of 403 healthy men aged 73-94 years proved that muscle strength and bone mass were at optimal levels in men with the highest levels of free testosterone. [1] This led the researchers to conclude that “a number of clinical problems present in older men may be related to testosterone deficiency, including reduced muscle mass, changes in body composition and loss of bone mass density.” Furthermore, using testosterone has been demonstrated to increase the bone mass of the lumbar spine in elderly men.[2]

[1] Van Den Beld AW, et al. Measures of bioavailable serum testosterone and estradiol and their relationships with muscle strength, bone density and body composition in elderly men. J Clin Endocrinol Metab 32000 Sep; 85 (9): 3276-82

[2] Snyder PJ et al. Effects of testosterone treatment on bone mineral density in men over the 65 years old. J Clin Endo Metab 1999; 84:1966-72

Diabetes and Metabolic Syndrome:

Testosterone therapy has been shown to reduce LDL cholesterol, blood sugar, glycated hemoglobin (a marker of long-term blood sugar control) and insulin resistance.

Testosterone replacement therapy

Most men choose to use bioidentical testosterone replacement therapy when they realize that many of their symptoms may be due to low levels of this hormone. The most obvious symptom that is desirous of being restored is loss of peak sexual functioning. Numerous studies now show the benefit of testosterone replacement in improving both libido and erection capability. [1] [2] [3]  The preferred route of administration is via a transdermal cream, applied to the skin or to the anal mucosal tissue. Anecdotal evidence suggests that some of the transdermal cream be applied to the glans (head) penis if erection strength is a dominant symptom. Some men prefer to have a weekly injection or to apply a hormone patch. Other routes of administration are via a subcutaneous pellet insertion under the skin every three months or via oral administration. The oral route is never used when replacing low levels due to significant potential for liver toxicity. There are also testosterone gels commercially available. A long-lasting injectable form of testosterone called testosterone undecanoate may soon be available. It lasts for 2.5 months. 

[1] Morley JE, et al. Effects of testosterone replacement therapy in old hypogonadal males: a preliminary study. J Am Geriatr Soc 1993 Feb; 41 (2): 149-52

[2] Hajjar RR et al. Outcomes of long-term testosterone replacement therapy in older hypogonadal males. J Clin Endocrinol Metab 1997 Nov; 82 (11): 3793-96

[3] Wang C, et al. Transdermal testosterone gel improves sexual function, mood, muscle strength and body composition parameters in hypogonadal males. J Clin Endocrin Metab 2000 Aug;85(8): 2839-53

Natural ways to raise testosterone:

If applying a cream or injections are not your preferred methods of treatment, there are some natural ways to improve testosterone function although, the truth be told, they are nowhere near as effective as getting a repeated dose of the real thing!

Testosterone supplements
  • Diets low in protein in elderly men (40-70 years old) may lead to elevated SHBG levels and decreased testosterone bioavailability.[1]  Eat a well-balanced diet, rich in protein and full of fresh organically grown fruit and vegetables so as to avoid estrogen producing chemicals. The estrogen mimicking chemical HPTE, a metabolite of a commonly used pesticide methoxychlor, causes a decrease in testosterone production from the Leydig cells.[2] Avoid plastic bottles, laundry detergent and other cosmetics which are man-made mimics of estrogen.
  • Increase cruciferous vegetable intake (cabbage, cauliflower, zucchini, brussel sprouts), or take DIM (di-indole methane). These foods and/or supplements help reduce the so-called bad estrogens (16-alpha-hydroxyestrones) and increase the “good” estrogens (2–hydroxyestrones), thus reducing prostate and breast cancer risk.[3]
  • Increase soy intake (fermented non-GMO varieties) as well as increase one’s levels of omega three fatty acids. Soy appears to inhibit the aromatase enzyme thus lowering estrogen levels.[4] Essential fatty acids, found in non-mercury containing fish and supplements, decrease levels of SHBG thus making more free testosterone available.
  • Engage in daily exercise and keep one’s weight as trim as possible. Strength training in middle aged men (44-48) causes an increase in free testosterone levels.[5]
  • The mushroom extract Cordyceps has been shown to increase sexual vitality in both men and women, particularly increasing male sexual performance. It appears to have a direct effect on the sexual center of the brain and the sex organs.[6]
  • Take Tribulus – 500 mg three times per day. Tribulus is a natural herb known for its testosterone raising properties in many different cultures. It is not a hormone but appears to exert its effect by raising the levels of LH, the hormone that stimulates testosterone production.
  • Take Zinc -30 mg three times per day. This mineral is involved in multiple aspects of a male’s sexuality, including testosterone production, sperm formation and sperm motility and is commonly used in male infertility.  In one study, with the use of 60 mg of zinc, sperm counts rose from eight to twenty million.[7] Supplementation of this mineral may become very important for some men as it has been estimated that with every ejaculate, 0.5 mg of zinc is lost!
  • Take Vit A- 50,000 IU a day for one month, then reduce the dose to 25,000 IU of a mycelized Vit A.
  • Take Boron – 3 mg daily.
  • Take Vitex agnus -1200 mg twice daily – this herb also stimulates the pituitary to make more LH.
  • Sweating in an infrared sauna increases testosterone and nitric oxide synthase (dilating the vessels to the penis, similar in effect to Viagra) by 1400 % and more than over 30 saunas have been shown to reduce toxic burden by two thirds.
  • The amino acid arginine, taken an hour before intercourse, has a milder but similar effect as Viagra. Use 2 grams twice daily or 4 -6 grams 1 hour before intercourse.
  • Use propionyl and acetyl L carnitine- 1 gram of each twice a day. [8] In this study, the carnitine group had a better response than the group given testosterone 160 mg a week. It has been shown that carnitine can be used successfully in prostate cancer patients so as to restore sexual potency after a surgical nerve block. Carnitine and Viagra together seem to be the best combination.
  • Lipoic acid 500 mg daily improves cognitive function as well as increasing libido.
  • Eat enough calories and follow a Paleolithic diet.
  • Use a mixed amino acid supplement or protein drink.
  • Avoid alcohol, vinegar, caffeinated drinks, sugar, sweets, soft drinks, cookies, breads, milk, tobacco, and marijuana.
  • Avoid tight underwear and reduce weight.
  • Avoid chronic stress and strenuous physical activities i.e., triathlon training.
  • Reduce the use of anti-hypertensive beta -blockers as they reduce testosterone levels.

[1] Longscope C, et al. Diet and SHBG. J CLin Endocrinol Metab 2000 Jan; 85(1):293-96.

[2] Kuipper GG, et al. Interaction of estrogenic chemicals and phytoestrogens with estrogen receptor beta. Endocrinology 1998 Oct; 139(10:4252-63)

[3] Muti p et al. Urinary estrogen metabolites and prostate cancer; a case-control study in the united States. Cancer causes Control 2002 Dec ; 13 (10):947-55

[4] Nagata C, et al. Inverse association of soy product intake with serum androgen and estrogen concentrations in Japanese men. Nutr Cancer 2000; 36(1): 14-18

[5] Izquierdo M, et al. Effects of strength training on muscle power and serum hormones in middle-aged men. J App Physiol 2001; 90(40 1497-1507

[6] Zhu J et al, Cordymax: A scientific product review. Pharmanex Phytoscience Review Series. 1997

[7] Netter A, et al. Effects of zinc administration on seminal zinc and fertility of oligospermic males. Ind J Phys

 Pharm 1987 Jan-Mar:31 (1) 30-34

[8] Cavallini G.Urology. 2004;63:641-646

If the serum free testosterone is low but the total testosterone is normal:

  • Pygeum – 3- 4 caps daily or
  • Urtica Dioscorea – 3 caps 2 times a day

If low testosterone with low LH- i.e., the pituitary is the problem:

  • Human Chorionic Gonadotropin (HCG) – 200-500 IU daily. If this is not helpful within 4 weeks, it won’t help, and one needs to stop
  • Vitex agnus – 1200 mg twice daily
vial from testosterone test

It is important to realize that testosterone replacement therapy can take many months before symptom improvement is realized. Restoration to normal sexual functioning may take as long as six months. It is advised to go slow and measure levels from time to time (remember to use saliva if using transdermal creams and serum levels if using injectable testosterone). Measure total, free and bioavailable levels of testosterone. In addition, measure levels of hemoglobin, estrogen, and prostate specific antigen (PSA), a biomarker for prostate cancer risk. DHEA, cortisol, pregnenolone and DHT should also be measured. Maintenance of a sugar and starch-free, as well as relatively alcohol-free, diet is recommended for maximum effect. Apply the hormone to large, hairless skin surfaces with high levels of penetration such as the forehead or inner thigh. Use a cream with a high concentration of testosterone and avoid areas of the skin with increased amounts of fat as fat tissue will have increased levels of aromatase and will easily convert the testosterone to unwanted levels of estrogen. Some individuals apply the cream to anal tissue to achieve a higher level of penetration.

Contraindications for testosterone therapy

An absolute contraindication is active breast or prostate cancer. A relative contraindication is active prostate infections or obstruction of urinary flow due to an enlarged prostate. Testosterone-replacement therapy has been associated with exacerbations of sleep apnea or with the development of sleep apnea in men treated with higher doses of testosterone who have other identifiable risk factors for sleep apnea.[1]

[1] Schneider BK, Pickett CK, Zwillich CW,et al. Influence of testosterone on breathing during sleep. J Appl Physiol 1986;61: 618-23.

Is testosterone therapy safe?

One of the most common questions asked of anti-aging physicians is, “Does testosterone replacement therapy cause cancer “? It appears that, at present, only about 5% of men with low testosterone levels are being treated.[1] It appears that it is the fear of getting prostate cancer that prevents a more proactive approach. Upon review of the relevant literature, the evidence is absolutely conclusive. Testosterone replacement therapy in physiological doses DOES NOT increase the risk of either benign prostatic hypertrophy (swollen prostate gland) or prostatic cancer.[2] In one study, not only was there no correlation between testosterone and increased levels of prostate specific antigen (a prostate cancer biomarker), prostatic volume, percent of positive cancer biopsies, biopsy Gleason score[3] or clinical staging of prostate cancer, [4] it was shown that, on the contrary, low free testosterone correlated with positive prostatic cancer biopsies and with a higher Gleason score (more serious staging of cancer). In another study, intramuscular testosterone injections at a dose of 100 mg, 250 mg or 500 mg a week (these last two doses are considered excessive and will exceed normal physiological levels) showed increased levels of serum testosterone with no change in either prostate volume or serum prostate specific antigen.

The Journal of the National Cancer Institute reviewed the work of dozens of world class researchers in the Endogenous Hormones, Prostate Cancer Collaborative Group who pooled all their data. Eighteen prospective studies that included 3,886 men with prostate cancer and 6,438 control subjects[5] concluded that serum concentrations of sex hormones were not associated with the risk of prostate cancer.

Another study showed that levels of dihydrotestosterone and testosterone were in fact lower than the controls in men with prostate cancer. In fact, with more advanced prostate cancer tumors, the same low levels of dihydrotestosterone held true.[6] It appears that it is not testosterone that is the culprit in the induction of prostate cancer, but that it is more closely linked to levels of estrogen in males, along with a poor western based diet.[7] An article in the World Journal of Urology summarized the current understanding by stating: “Estrogenic stimulation through estrogen receptor alpha in a milieu of decreasing androgens (testosterone, DHT and DHEA), contributes significantly to the genesis of benign prostatic hyperplasia, prostate dysplasia and prostate cancer.” [8]

Most interestingly, many experts are beginning to provide testosterone replacement therapy to men who have had prostate cancer, [9] an approach that was considered strict heresy just a few years ago. This approach is not, however, considered a mainstream approach as many oncologists and urologists are still concerned that testosterone therapy may increase the risk of cancer recurrence. [10]

[1] Rhoden El. Morgentaler A.  Risks of testosterone-replacement therapy and recommendations for monitoring. N Engl J Med. 2004 Jan 29; 350(5):482-92

[2] Morley JE. Testosterone replacement and the physiologic aspects of aging in men. Mayo Clin Proc. 2000 Jan; 75 Suppl: S83-7.

[3] Gleason score refers to the microscopic appearance of prostatic cancer which together with other parameters, is incorporated into a strategy of prostate cancer staging which predicts prognosis and helps guide therapy. Cancers with a higher Gleason score are more aggressive and have a worse prognosis

[4] Hoffman MA.Is low serum free testosterone a marker for high grade prostate cancer?J Urol 2000 Mar;163(3):824-7

[5] Roddam Aw et al. Endogenous sex hormones and prostate cancer: a collaborative analysis of 18 prospective studies. J Natl Cancer Inst. 2008 Feb 6; 100 (3): 170-83

[6] Gustafsson et al.  Dihydrotestosterone and testosterone levels in men screened for prostate cancer: a study of a randomized population. Br J Urol 1996 Mar;77(3):433-40

[7] Coffey DS. Similarities of prostate and breast cancer: Evolution, diet, and estrogens. Urology 2001 Apr;57(4 Suppl 1):31-8

[8] Steiner Ms, Raghow S. Antiestrogens and selective estrogen receptor modulators reduce prostate cancer risk. World J Urol 2003 may; 21 (1): 31-67

[9] Morgentaler A. Testosterone therapy for men at risk for or with a history of prostate cancer. Curr Treat Options Oncol. 2006 Sep;7(5):363-9

[10] Goep J. Testosterone Therapy for Life. Life Extension June 2010 pg 89.

Man standing on dock looking out at lake

The other hormones involved in Andropause

Andropause is primarily due to decreasing levels of testosterone, but many other hormones and neurotransmitters may be similarly affected.


DHEA is a steroid hormone secreted by the adrenal glands, gonads, brain and skin in both men and women, which also declines with advancing age. By the time we are 70-80 years of age, peak levels of DHEA are only 10-20 % of those in young adults. [1]As DHEA is the dominant and most abundant steroid hormone in the body and the precursor of all other sex steroid hormones, DHEA has extraordinary restorative effects on multiple aspects of one’s functioning. Low levels of DHEA are associated with aging and most diseases of aging. Specifically, a deficiency of DHEA has been found to correlate negatively with immune dysfunction, inflammation, greater risks of certain cancers, heart disease in men and osteoporosis.[2]

[1] Genazzani Ad, et al. Might DHEA be considered a beneficial replacement therapy in the elderly? Drugs Aging. 2007; 24(3):173-85

[2] Greenwell I. Life Extension. August 2001; pg25.

DHEA and Cardiovascular Disease

Studies have shown that the dramatic age-related drop in DHEA levels is accompanied by an equally dramatic rise in cardiovascular disease.  The mechanism of action is that it appears DHEA is incorporated into both high- and low-density cholesterol, protecting it from oxidation. As we age, the cholesterol-bound levels of DHEA become infinitesimal, thus the cholesterol molecules are much more susceptible to oxidation than in younger individuals. 

In the Massachusett’s Male Aging Study, following 1700 men between the ages of 40 and 70 for 9 years, authors found that men in the lowest quartile of serum DHEA at baseline were 60% more likely to develop ischemic heart disease than controls.  Low serum levels of DHEA were also a significant predictor.

In a study done at the University of Wroclaw, Poland, it was found that DHEA decreased the level of serum lipid peroxides in rabbits fed a normal diet but not in rabbits with induced severe hypercholesterolemia. DHEA was able to increase the activity of the platelet superoxide dismutase (SOD), a crucial antioxidant enzyme.  This increase in superoxide dismutase’s activity may partly explain DHEA’s antioxidant effects.[1]

[1] Bednarek-Tupikowska G et al. Influence of DHEA on platelet aggregation, superoxide dismutase activity and serum lipid peroxide concentration in rabbits with induced hypercholesterolemia. Med Sci Monit 2000; 6:40-45.

DHEA and Brain Health

It is well known that cortisol, the hormone resulting from chronic prolonged stress has harmful effects on the brain.[1]  DHEA, due to its action in suppressing cortisol, appears to protect the brain from these damaging effects. Furthermore, a Canadian study found that rats implanted with a high dose of DHEA showed significantly less hippocampus (an area of the brain associated with memory) damage after stroke was experimentally induced. There were 60% injured neurons (brain cells) as compared to 88% in the control group.[2] [3]

[1] Canning MO et al. Opposing effects of DHEA and dexamethasone on the generation of monocyte-derived dendritic cells. Eur J Endocrinol 2000; 143:685-95.

[2] Aragno M et al. Oxidative derangement in rat synaptosomes induced by hyperglycemia: restorative effect of DHEA treatment. Biochem Pharmacol 2000; 60:389-95.

[3] Aragno M et al. DHEA prevents oxidative injury induced by transient ischemia/reperfusion in the brain of diabetic rats. Diabetes 2000; 40:1924-31.

DHEA and Infection/Immune Health

DHEA has also been shown to not only enhance the immune response but also fight infection.  Several studies have confirmed its usefulness in combating bacterial, parasitic, and viral infections including HIV. DHEA has been shown to lower the levels of IL-6, a proinflammatory cytokine (a chemical messenger used by the immune system). [1] Furthermore, it lowers the production of another inflammatory cytokine, tumor necrosis factor alpha (TNF Alpha).  As we age, both of these levels rise, which indicates immune dysfunction and an increasing inflammatory state.  The ability to lower the levels of these inflammatory mediators may be an important part of the neuroprotective mechanism of DHEA.[2] Thus, the decline in DHEA levels is closely tied to immunosenescence.[3]  It can thus be shown that maintaining youthful levels of DHEA means less chronic inflammation.  It has been shown repeatedly that many of the diseases of aging, i.e., heart disease, Alzheimer’s, certain cancers, diabetes, osteoporosis are all linked to the inflammatory process. It thus becomes imperative to maintain youthful levels of DHEA so that we harbor less inflammation as we age.

[1] Greenwell I. Life Extension. August 2001; 26.

[2] Cardounel A et al. DHEA protects hippocampal neurons against neurotoxin-induced cell death: mechanism of action. Proc Soc Exp Biol Medicine 1999; 222:145-49.

[3] Greenwell I. Life Extension. August 2001; 26.

DHEA and Sexuality

DHEA’s role in sexual physiology of both men and women is that of a mood modulator. [1] One study showed that supplementing with 50 mg of DHEA every night for six months in both males and females, aged 40-70, improved energy levels, quality of sleep, mood, and the ability to handle stress.[2] In another study of men with advanced age (90-103), those who had the highest levels of DHEA had the highest levels of normal daily activities. [3]

The average dose for men is 25 to 100 mg and for women, anywhere from 1 to 25 mg.  Testing blood levels for optimal levels is indicated. Too much DHEA in women will cause either acne or increased hair growth. This can be avoided by using a form of DHEA called 7-Keto-DHEA.

[1] Cameron Dr, Braunstein GD. The use of dehydroepiandrosterone therapy in clinical practice. Treat Endocrinol. 2005; 4 (2): 95-114

[2] Morales AJ, et al. Effects of replacement doses of DHEA in men and women of advanced age. J Clin  Endo Metab 1994 Jan; 78(6):1360-67

[3] Ravaglia G, et al. The relationship between DHEA-S to endocrine metabolic parameters and functional status in the oldest-old. J Clin Endo Metab 1996; 81(3):1173-78

Natural ways to raise DHEA

Man tying his shoes about to start exercising


A low-calorie ketogenic diet using less than 40 gm of carbohydrates per day (8:57) in rheumatoid arthritis patients resulted in a 34% rise in DHEA within a week. [1] In primates, calorie restriction has indeed been found to preserve higher DHEA levels indicating a slower rate of aging.  Fasting has also been shown to raise DHEA levels in men and women.  Anorexic and bulimic individuals likewise show higher serum DHEA.[2]

Exercise and meditation:

Exercise and meditation have been shown to raise DHEA in some individuals.[3]

Drum Circles:

Participation in drum circles[4] has also been shown to increase DHEA confirming the hypothesis that stress reduction in general boosts DHEA production probably through a shift of adrenal steroidogenesis from cortisol to DHEA.[5]

[1] Cutolo M. Sex hormone adjuvant therapy in rheumatoid arthritis. Rheum Dis Clin North Am 2000; 26: 881-95

[2] Montelone P et al. Plasma levels of Neuroactive steroids are increased in untreated women with anorexia nervosa or bulimia nervosa. Psychosom Medicine 2001: 63: 62-8

[3] Boudou P. et al. Effects of a single bout of exercise and exercise training on steroid levels in middle-aged type 2 diabetic men: relationship to abdominal adipose tissue distribution and metabolic status. Diebetes Metab 2000; 26:450-57.

[4] Bittman BB et al. Composite effects of group drumming music therapy on modulation of neuroendocrine-immune parameters in normal subjects. Alternative Ther Health Medicine 2001; 7:38-47.

[5] Greenwell I. Life Extension. August 2001; 27.


Growth hormone (GH) deficiency in aging males can have a dramatic effect on one’s sense of well being. GH is considered the master hormone with multiple protective roles. It is growth hormone which is responsible for our major growth spurt during puberty, without which we would all be dwarves.[1] In adulthood, GH maintains skin, muscle, and bone health. With a deficiency of this hormone, signs of aging are quickly accelerated.

Skin wrinkles and sags; fat soon replaces muscle. Growth hormone also helps maintain and repair the health of various organs, including the heart, lungs, liver kidneys joints, nerves as well as the brain. As growth hormone activates the calming, regenerative parasympathetic nervous system, a deficiency may result in increased tension, anxiety, depression, and an increasing inability to cope with stress.  From the age of thirty onwards, growth hormone levels decline fairly rapidly, about 1-3 % per year. This loss is quickly accelerated in the presence of obesity. The most efficient way to replace growth hormone is through subcutaneous daily injection, similar to a diabetic insulin injection. Some companies make precursor amino acid preparations (arginine, lysine, glutamine, and ornithine) which have a variable effect on raising GH. Most anti-aging doctors will not treat GH in the first year of restoring optimal hormone levels as a protein rich diet, adequate sleep, and exercise program, and replacing testosterone, progesterone, melatonin, and thyroid levels, may increase GH levels by as much as 20-30 %. (See table 3)   

[1] Hertoghe T. The Hormone Handbook . International Medical Publications. U.K. pg 54


  • Take Amino acid supplement
  • Exercise daily
  • Replace all deficient hormones
  • Eat a protein rich diet
  • Avoid alcohol, sugar, sweets, breads, and pasta
  • Reduce weight
  • Avoid milk products
  • Avoid sleep deprivation
  • Avoid prolonged stress.


The subject of progesterone replacement therapy in men was well covered in this magazine, Edition 3, 2010.[1] Men typically produce between 1.5 to 3 mg per day, and as men age, progesterone levels fall exponentially. From a biochemical point of view, progesterone is used in the production of cortisol (the stress hormone). Thus, if a man leads a particularly stressful life, it is highly likely he will have depleted levels of progesterone. Progesterone is vital in keeping the higher levels of estrogen in aging men in check and thus minimizing the risk of heart attacks, prostate enlargement, and prostate cancer.  A typical dose of progesterone may lower estradiol levels by up to 30 %. [2] Progesterone also lowers DHT, thus preventing or attenuating male pattern baldness.[3] Progesterone also blocks aldosterone receptors, thereby reducing excessive fluid retention and possibly high blood pressure caused by increased aldosterone production[4]. (See table 4)


  • Eat a diet rich in protein and cholesterol, a precursor of progesterone synthesis
  • Manage stress daily with stress reduction techniques
  • Herbs and nutraceuticals such as Rhodiola, Siberian Ginseng, and Liquorice root extract, Vitamins B 5 and C, and Ashwagandha

[1] Arthur D, Wessels M. Men and the forgotten hormone. Health Intelligence, 2010 Edition 3, pg 20

[2] Hertoghe T. The Hormone Handbook. International Medical Publications. U.K. pg 246

[3] Ibid.

[4] Ibid, pg 247


Melatonin is another hormone that declines with advancing age. Symptoms suggestive of melatonin deficiency include a superficial, agitated sleep with many anxious thoughts, easy waking during the night, difficulty falling asleep and falling back asleep once awake, poor dream or dream recall, anxiety especially at night, depression (especially seasonal affective disorder) excessive emotionality and irritability, and restless leg syndrome with increased muscle spasms. Intestinal spasms or cramps may also dominate. A positive result of melatonin is the so-called regenerative or anabolic effect that it has on the parasympathetic nervous system, the part of our autonomic nervous system that is involved in rest and relaxation.   Melatonin has a positive effect on the parasympathetic nervous system, that part of our

autonomic nervous system that is involved in rest, relaxation- a so-called regenerative or anabolic effect. Without adequate levels of melatonin, the sympathetic nervous system dominates, leading to a heightened fight/flight response with an overall degenerative or catabolic effect.[1] Melatonin may improve sexual performance, enhancing serenity and relaxation after sex. [2]

Human and animal studies have linked a melatonin deficiency to hypertension, coronary artery disease, cardiac arrhythmias, obesity, diabetes, osteoporosis, lowered immunity with recurrent infections, breast and prostate cancer, and neurological diseases such as Parkinson’s and Alzheimer’s disease. The antioxidant effect of melatonin is responsible for its positive effect in cancer patients.  Some labs now offer a 24-hour saliva melatonin assay.

Treatment involves the use of either an oral or sublingual dosing. It is best to use the sublingual dosing for immediate, sleep-inducing effect, while using the oral route is best to assist in maintaining a restful sleep. Melatonin is best utilized when given in conjunction with vitamin B6 and serotonin precursors such as tryptophan or 5-hydroxytryptophan, which in the presence of the B6, convert to melatonin. High levels of melatonin may suppress cortisol, so use with caution if one desires an active immune system to suppress inflammation. Low levels of cortisol can produce many undesirable side effects, not the least of which is fatigue, headaches and low blood pressure. There are natural ways to raise melatonin. (See Table 5)


  • Increase morning daylight (a sunlamp may be used)
  • Make the room pitch black at night, use an eye mask
  • Avoid alcohol and caffeinated drinks,
  • Avoid stressful activities
  • Avoid electromagnetic exposures at night such as cell phones, electrical clocks and radios
  • Wear turquoise colored glasses 30 minutes before bed.

Some asthmatics may react negatively to melatonin as one study showed possible increased inflammation with nocturnal asthmatic exacerbations.[1]

[1] Sutherland E, et al Elevated serum melatonin is associated with the nocturnal worsening of asthma. Jour Allergy Clin Immunol 2003; 112: 513-17

[1] Ibid, pg 47

[2] Drago F, Busa L. Acute low doses of melatonin restore full sexual activity in impotent male rats. Brain Res 2000 Sep 29;878 (1-2):98-104


Pregnenolone is the forerunner of many of our major hormones. It is made from cholesterol and, once made, results in a series of metabolic reactions that lead to the production of other sex hormones such as DHEA, testosterone, estradiol, progesterone, cortisol and aldosterone. [1] In addition to functioning as a hormone, it also functions as a neurotransmitter in specific areas of the brain responsible for memory. Pregnenolone regulates the flow of calcium ions through the cell membrane, and calcium ion exchange determines how memory is encoded by neurons. In addition, pregnenolone increases the neurotransmitter acetylcholine, the neurotransmitter responsible for memory, as well as increasing neurogenesis in the hippocampus, the main part of the brain that stores memory.[2] The most common complaints of individuals with pregnenolone deficiency include memory loss and arthritic pains as well as dry skin and fatigue.  Replacement doses are typically 30 mg twice a day for memory loss.  In addition, one may choose to use other cognitive enhancing nutraceuticals such as:

  • Acetyl-L -Carnitine
  • Vinpocetine
  • Phosphatidyl Serine, combined with omega three fatty acids
  • Phosphatidyl choline
  • DMAE
  • G6PC
  • Huperizine 
  • Vitamin D
  • Blueberries

[1] Hertoghe T. The Hormone Handbook . International Medical Publications. U.K. pg 144

[2] Schumacher M. Neurosteroids in the Hippocampus: Neuronal Plasticity and memory. Stress 1997 Oct; 2 (1): 65-78

Stressed man


Oxytocin, a hormone known to improve social bonding, is secreted from the posterior lobe of the pituitary gland. In women with newborn babies, it starts to flow in abundance at the first attachment of the baby to the nipple and aids in mother-child bonding.  According to researcher Dr Joan Borysenko, author of A Woman’s Book of Life, oxytocin helps a woman to become totally infatuated with her newborn, doting on every movement and every look.[1] Men and women both have endogenous levels of oxytocin naturally created by the body — it likely helps them fall in love, spurs parenting instincts and makes orgasms, well, more orgasmic. [2] It might also help women be so adept at reading social cues.

Researchers in the Journal of Neuroscience, after giving men oxytocin through a nasal mist, write “emotional empathy responses in men were raised to levels similar to those found in untreated women.” Not only were the men more affected by emotional scenes, but they also were better at learning tasks that required social cues. The effects didn’t last long though. The men needed another squirt two hours later. Oxytocin is presently being used by a few select practitioners to mainly enhance sexual arousal and bonding in men.

[1] Diamond J. Male Menopause. Sourcebooks, Inc. Naperville, IL 1998 pg. 211


In order for a man to feel at his best, there are multiple, interconnected physiological systems that need optimization to achieve this effect. For healthy sexual functioning this requires not only adequate hormone levels but also requires a healthy vascular system as well as psychological health. The “molecules of emotion” that link a man’s subjective sense of wellbeing to his biochemical pathways are called neurotransmitters and have a dramatic role to play in optimizing mood, sleep, pain, attention, relaxation as well as sexual function.   Sexuality in humans can be broken down into four components: desire, arousal, orgasm, and resolution. Each phase is governed by a corresponding neurotransmitter as well as a contributing hormone.[1]

[1] Bravermann E. Life Extension October 2008 pg 77


Dopamine is a neurotransmitter that we all seek out in abundance. It is involved in creating pleasure and a sense of joyful exuberance. Most people with any type of addiction, be it food, sex, drugs, alcohol, or thrill seeking, is self-medicating in order to raise their levels of dopamine. Low levels of dopamine result in loss of desire for sex as well as reduced arousal, interest, and energy for sex.[1] Dopamine levels can be raised by using the antidepressant Wellbutrin, the prescription drug L-dopa as well as naturally with tyrosine, phenylalanine, macuna bean extracts, gingko biloba and guarana.

[1] Ben Z, Tessler R, Cohen L et al, Polymorphisms in the dopamine D4 receptor gene ( DRD4) contribute to individual differences in human sexual behavior, desire, arousal and sexual function. Mol Psychiatry. 2006 Aug; 11 (8): 782-6


Acetylcholine is the main neurotransmitter involved in arousal and has significant effects on cognitive function, especially memory attention and creativity.[1] [2] A loss of acetylcholine particularly effects sexual arousal[3] as well as regulating internal moisture.[4]  Lower moisture levels can adversely affect semen volume in men.  The supplements used to boost acetylcholine naturally are Huperizine, acetyl- l- carnitine, phosphatidylserine, glycerophosphocholine and ginkgo biloba.

[1] Braverman ER. Younger you: unlock the hidden power of your brain to look and feel 15 years younger. New York, NY: McGraw-Hill; 2007.

[2] Amenta F, Tayebati SK. Pathways of acetylcholine synthesis, transport and release as targets for treatment of adult-onset cognitive dysfunction. Curr Med Chem. 2008;15(5):488-98.

[3] Andersson KE. Neurotransmitters: central and peripheral mechanisms. Int J Impot Res. 2000 Oct;12 Suppl 4:S26-33.

[4] Braverman ER. Younger you: unlock the hidden power of your brain to look and feel 15 years younger. New York, NY: McGraw-Hill; 2007.


Gaba is the main inhibitory neurotransmitter that downregulates anxiety in chronically distressed individuals.  Chronic anxiety often leads to loss of sexual interest and sexual dysfunction in men, particularly with loss of erections.  Gaba has been shown to be responsible for enhancing orgasms.  When Gaba becomes depleted, it is difficult to relax and let go of fear, anxiety, and negative thoughts, thus inhibiting orgasms. Gaba enhancing compounds also increase dopamine which, therefore, enhances sexual satisfaction.  Supplements which increase gaba are taurine, glycine, inositol and gaba itself.  A medical drug called Gabapentin has a similar effect.


Serotonin is one of our most powerful neurotransmitters and is responsible for modulating sleep, pain, mood, and gastrointestinal function.[1]  Low serotonin levels can result in negative thinking, a lack of joy and decreased feelings of intimacy.  Serotonin may also play a role in premature ejaculation, a condition which affects 20-30% of men.[2].  The commonly prescribed SSRI drugs, Paxil or Prozac, delay serotonin’s re-uptake into nerve cells and may increase ejaculatory control and delay ejaculation in men with premature ejaculation.[3]  Supplements which are helpful to raise serotonin are tryptophan and 5-hydroxytryptophan which readily cross the blood-brain barrier to exert their effect.  Other supplements that are needed to increase serotonin are magnesium and vitamin B6.

[1] Mohammad-Zadeh LF, Moses L, Gwaltney-Brant SM. Serotonin: a review. J Vet Pharmacol Ther. 2008 Jun;31(3):187-99.

[2] Ali ME, Abdel-Hafez HZ, Mahran AM, et al. Erectile dysfunction in chronic renal failure patients undergoing hemodialysis in Egypt. Int J Impot Res. 2005 Mar;17(2):180-5.

[3] Arafa M, Shamloul R. A randomized study examining the effect of 3 SSRI on premature ejaculation using a validated questionnaire.  Ther Clin Risk Manag. 2007 Aug;3(4):527-31.


Although a male andropause workup is not yet standard practice amongst primary care physicians, Dr Morgentaler,[1] believes that within 5-10 years, “individuals will know their testosterone levels just like they know their cholesterol and PSA levels today.” [2]  If all men (and their loved ones) were aware of a treatment that not only improved one’s sex drive, mental focus and energy levels but also reduced their risk of the number one killer, heart disease and associated metabolic syndrome, reduced the risk of all age related diseases while also having the potential to increase the quality of one’s life while increasing longevity, it is highly likely that this treatment would be the number one subject on everyone’s lips at the next cocktail party and/or braaivleis!

Furthermore, as a man approaches this phase of his life, it is time to take stock of multiple factors that may be preventing him from living at his maximum potential. This article has focused on only a small percentage of possible factors (hormones and neurotransmitters) that may be preventing him from living at the full capacity of his genetic potential. Other factors are infinite in their scope and include issues such as environmental toxicities, mold and chronic infectious exposures, dental cavitation, and root canal toxicity, nutritional deficiencies, structural imbalances, unresolved emotional conflicts and deep-seated toxic belief systems, family systems that block a healing resolution as well as a lack of a deep relationship to something other than one’s sole ego-based activities.

Our present generation tends to believe that, if something is not feeling quite right, it must be only a physical reason that is causing this sense of malaise. We run to doctors to get a traditional allopathic diagnosis and breathe a huge sigh of relief if there is no definable disease process. We also demand of our doctors that they provide a simple, drug-based solution that is effective almost immediately, does not take any time out of our busy schedules, requires very little effort by us and preferably is at very low cost, lest it interfere with our holiday trip to Majorca or our cosmetic surgery bill.  My answer is, “try showing up one day in your life without your brain or your body. “The fact that health concerns are seldom the number one priority in terms of individual’s value systems is a matter for grave concern in this emergent toxic, nutritionally depleted and stressed world we find ourselves in.

Our bodies and our minds are our greatest assets and must not be taken for granted! Our health and wellness should be guarded on a daily basis with the utmost dedication and the discipline to act wisely in a preventative manner, decades before disease manifests itself. Dr Myron Wentz, owner of the Usana line of nutraceuticals, makes the following profound comment, “Most of us spend our lives working hard to save enough money to enjoy the golden years, only to discover that we are going to have to spend a great deal of money and effort to regain the health we sacrificed in our harried pursuit of material comfort. Many of us think of health care after the fact, as a high-tech cure or series of treatments from a private practitioner or government agency, funded by insurance. We seldom view it as an individual responsibility.” [3]

In order to move away from this adolescent fantasy of someone else who is going to “fix us”, we have to become part of the solution. We all need to raise health as a dominant value in our lives, or at least define our highest values (it may be running a business or a large family) and link our health practices to this value. We need to ask ourselves, “how by staying fit and healthy  and working within a wellness, preventative model of health care, will I be even more effective at what I love to do?”

Every day we should devote time, energy, and money to the preservation of our greatest assets, our minds, and our bodies, and develop a heath team to assist us in this process. After all, the best way to avoid disease is to maintain health, not to get a disease and then treat it. Ask yourself “where do I fit on the health/illness continuum?” Are you experiencing a high level of wellness with education, discipline, regular assessments, and functional medicine[4] (not disease based) lab testing, or are you in the illness mode, experiencing signs, symptoms, and continued disabilities? It is my suggestion that if this is the case, that you act immediately as you may be heading down a slippery slope towards full blown illness, or at worst, a premature death.

[1] Morgentaler A. Testosterone for Life  McGraw Hill, 2008

[2] Goep J. Testosterone therapy for Life. Life Extension June 2010 pg 86

[3] Wentz M. “Invisible Miracles”. Rosarito Beach, Baja California:Medicis, S.C.;2002

[4] Functional Medicine looks at optimizing biochemical pathways so that maximum efficiency is attained in key systems i.e. liver detoxification, food sensitivities and gut health, immune balance and inflammation, nutrition, neurotransmitter and hormonal harmonization, structural alignment and mind/body health. This is not standard allopathic practice.

Moustache drawing