How a Multi-Level Approach to Medicine Can Augment a Cancer Patient’s Treatment

How a Multi-Level Approach to Medicine Can Augment a Cancer Patient’s Treatment

Contrary to mainstream rhetoric, the treatment and prevention of cancer in patients is much more layered than a simple diagnosis and chemo, for example. Things such as past trauma, mold exposure, allergies, and metal toxicity exposure can truly impact how one recovers and even how one reacts to chemo. 

Watch the full video as Dr. Hoffman dives into some of the complexities of a multi-level approach to treatment of cancer in patients. 

Watch the Video

How a Multi-Level Approach to Medicine Can Augment a Cancer Patient’s Treatment

Reference Links

Transcript

Hi everybody. I received an email today from a colleague who is posting his case history on a cancer patient. He detailed the specific oncology issues that had arisen, his approach, and what he believed to be the correct treatment. I was thinking as I was reading this report from an integrative medicine physician about how far integrated medicine, medicine that incorporates many different layers and levels and dimensions of a personal experience, has come. This patient was managed impeccably by her oncologists. Insights were derived from post oncology or peri oncology type issues. When I read through the presentation of my colleague, I was struck by how we can bring so many more diagnostic and therapeutic features to the patient’s experience. When we consider the layers and levels that any individual person brings to the consultation, the history given by my colleague on this patient just touched on a few issues and could have been further expanded upon. I’d like to expand upon the history to provide a road map of how the seven levels, or the seven stages, to health and transformation can be incorporated when thinking of strictly biologically-based medicine.

In his history, he mentioned that this patient had breast cancer. She was treated with chemo and radiation and developed side effects. He went on to mention a few things, such as that she was sensitive, that she had experienced early developmental trauma, that she was a poet and artist, and that she had post chemo fatigue. He also happened to mention that she had a supportive framework, a loving husband, and was very involved in her own patient advocacy. In addition to everything else that he was bringing to the table, he wanted to treat her mast cell activation syndrome. He was looking for further triggers as to why she was still fatigued and anxious, things such as mold exposures or possible Lyme disease. 

In looking through this history, things came to my mind. Whenever there’s a history of early trauma, you have to look upstream to ancestral Inheritance. We know now that individuals carry the experiences of their forefathers. This is well researched and well studied and is now being incorporated into clinical medicine. Whatever the ancestors, particularly the mother, father, and grandparents had emotionally experienced gets epigenetically transferred into the proteomics and metabolomics. This is the cellular expression of that patient’s life that can’t be ignored. Secondly, when a person is born into a dramatic scenario, when they have interrupted bonds between them and their mothers, particularly their mothers in the first ten, twenty even thirty years, there’s a price that’s paid. Particularly if the patient isn’t entrained with the mother’s right prefrontal cortex in an empathic entrainment, one sense of self that inhibits early anxiety and stress or fear doesn’t develop a robust mechanism or the ability to inhibit should anxiety and stressful events arise in the future. So in early developmental trauma, when the child’s developing brain doesn’t entrain with the mother’s development, the mother’s external prefrontal cortex and just a side note, the mother may not have a very robust right prefrontal cortex either, but the child pays a price. They pay a price of potentially a fragile sense of self or even a very undeveloped sense of self and an inability to self regulate.

This is very obviously seen when you do NeuroQuant MRIs or qEEGs. You can see these fingerprints on the qEEG and on the NeuroQuant MRI in the form of increased amygdala size and increased thalamus size. The evidence is there. On a qEEG you can see heightened amplitude of the beta brainwaves, what’s called the anterior cingulate area, and you can see diminished alpha brain waves. You can see these fingerprints of biographical data on biomedical equipment. It’s important to know that. So if somebody has cancer and he’s had a very bad chemo experience with many symptoms post chemo, one does look upstream to any possible inherited trauma from the ancestral realm. One looks at early developmental trauma because all of these get affected through what’s called the HPA axis, the hypothalamic pituitary adrenal axis, in the form of a heightened stress response. The height and stress response can create permeability of gut membranes, mitochondrial membranes, and blood-brain barrier membranes, leading to a flood of potential autoimmune disease and/or inflammatory compounds. So it’s important to take that particular history to look at the brain through a NeuroQuant MRI and to look at the qEEG to see if there are any fingerprints and then therapeutically to assist that individual in self-regulation through various techniques, whether they be inside therapy, m-wave training, vehicle tone stimulators. I always recommend that people get an insight into the underlying dynamics, not just downregulate the biochemical or physiological pathway. 

When there’s early trauma and when there’s early developmental trauma we usually suggest family constellation therapy insight or family constellation workshop to look at the unconscious dynamics of that inheritance. For early developmental trauma, again we use family constellation therapy but sometimes we have to be more advanced. In those cases instead of doing a technique like DNRS, which just downregulates the expression of the anxiety that’s being felt, you need to do more advanced psychological techniques like ISDP. This looks at the defenses the individual developed as a child who wasn’t safe in their environment. They’ve developed the provisional self in order to cope with the slings and arrows of modern life, or just their early life.  So you’ve got to look at the family system that’s inherited, look at early developmental trauma, and the defenses that were developed by that person. Then you’ve got to look at the ego strength and structure of that individual to see if they have a robust sense of self. This determines if they can cope with sometimes what’s required of them to get their physiology and their health back online.

So with oncology and cancer, yes we can give chemo, we do radiation. We do those plus all the natural therapies but if you don’t look further upstream to all these potential mediators that keep a person somewhat off kilter, you don’t complete your healing interrogation and your diagnostic interrogation. So it’s very important to shine your light upstream to look at these potential inherited issues. We know from clinical experience that when you heal at a deeper level, the downstream metabolites and the downstream effects are profound. The body tends to express those consequences of the new images and the new insights and the new narratives in a more cohesive fashion. We say in this work that nobody truly heals until they have a new image or a new narrative or a new story to tell about their past and their present. This is vitally true to understand people who present with extreme complex multi-system illness. It’s never only at level two,which is the physical level. You can do all the most sophisticated functional medicine workups, you can give them every supplement in the book, you can send them to wherever you want to detoxify, or you can do bioidentical hormone therapy. But it doesn’t land in a robust place if that sense of self is fragile, if the ability to self-regulate is poor, if the defenses of the individual are too fortified and won’t allow you in. If a child has had an early experience that keeps them from trusting parental figures, do you think they’re going to trust medical authorities? Unlikely since we’re just external representations of parental figures. No healing occurs without a deep sense of trust. This is deeply profound. I’ve been called out over the years for not taking this seriously and developing an empathic trusting relationship with the patient because if that’s not established you might as well give up the rest of it. It’s not going to occur. Patients will resist your efforts to help them if there’s not an empathic relatedness between you and them whereby you understand their dynamics, you understand the fortifications of the psyche that prevent healing from occurring, and you relate subtly to what they’re asking you to do. Sometimes it takes time to establish a therapeutic alliance and a trusting relationship. If you bulldoze your way in and try to tell somebody what to do who has high resistance, something called projection of will, which means they’re asking you to fix them without any advocacy of their own, you’re in a precarious position and success is very limited.

So in this particular case I was struck by the fact that:

A) she had early trauma 

B) she had heightened anxiety

C) she had post chemo fatigue

And the whole world of post chemo fatigue of course has lots to do with mitochondrial dysfunction. In traditional medicine we’re not taught anything about mitochondrial dysfunction unless it’s a genetically inherited mitochondrial disease. Even in functional medicine you know mitochondrial dysfunction is paid lip service and people are given you know coenzyme q10, carnitine, lipoic acid, vitamin C, magnesium, and so on. But through the work of Robert Naviaux and the cell danger response we know that the mitochondria also need to be approached with a certain elegance, a certain sophistication, a certain patience because you can’t coax a mitochondria back to health by just throwing everything in the kitchen sink at it, hoping it’s going to recover. You have to understand the timelines and the movement through what they call the cell danger response, where there’s an inflammatory response and the mitochondria shut down

to protect the host. Then there’s moving through a healing response, which takes time. Our bone marrow turns over every four months and the mitochondria too have their own timeline, their own seasons so to speak. If you’re interested in the subject I’d suggest you read anything by Robert Naviaux. 

So this patient needed chemo, she had post radiation, post chemo fatigue, she was highly anxious, and wasn’t sleeping but she also had resources and she had some insight into her case. With these issues in mind it’s always important to expand our diagnostic and therapeutic base and try and bring everything to the table, to assist that person moving through their present symptomatology of anxiety fatigue and gut issues. This particular individual had gut issues. You have to do a full functional medicine workup with food sensitivities, gut permeability, hormonal HPA axis assessment, and methylation micelle detoxification. That’s just a given, a basement workup. I was struck by how far we’ve come in the understanding of illness and the fact that illness isn’t something that just requires a therapeutic drug. That concept of n squared, d squared, name of disease, name of drug, is so far advanced. We’ve come so far over the last thirty years in this understanding. Unfortunately the healthcare systems that exist are still very mechanistically based, disease based, which is fine. But when it comes to a true transformative healing experience, all layers, all levels, and interpersonal relatedness with trust are now available to us. It behooves us as therapists and medical personnel and healers if you wish to use that word. We have to do our own work and we have to know how to navigate the nuances and subtleties and levels and layers of a person’s experience and how to read the hidden signs. How to access unconscious dynamics and how to make conscious that which is being asked to be made conscious. Symptoms are often in a person’s life in order to bring to consciousness that which is hidden. It’s been said before that all sickness is homesickness. Even though this could be considered a sort of glib metaphor, especially when somebody’s suffering severely.  It’s been my experience that if you really lean into that possibility, the full potential of the person’s self-expression can be realized through a sensitive, insightful and broad palette of diagnostic and therapeutic insights. So these were my musings on a Sunday afternoon and I just wanted to share those with you. Thank You.

A Discussion About Mold and Mold Exposure with Dr. Bruce Hoffman

A Discussion About Mold and Mold Exposure with Dr. Bruce Hoffman

We discuss how mold and mold exposure can be a trigger for Chronic Inflammatory Response Syndrome (CIRS), and Mast Cell Activation Syndrome (MCAS). We discuss ways to investigate and determine if you have been exposed to mold and what you should do if you suspect mold exposure is affecting your overall health.

To learn more about mold treatment, prevention, and recommendations, visit the Mold Illness section of our Hoffman Centre website.

Watch the Video

A Discussion About Mold and Mold Exposure with Dr. Bruce Hoffman

Reference Links

Transcript

I wanted to talk a bit about mold and mold exposure as a potential cause for chronic ill health. Mold is ubiquitous and, without question, many people are suffering from the effects of mold. Mold triggers Mast Cell Activation Syndrome (MCAS), and many people are suffering from that, which is why I feel that it has to be part of a differential diagnosis for chronic ill health.  

It’s shocking how many people have mold exposure as a trigger and as an ongoing mediator, keeping them in an inflamed state resulting in Chronic Inflammatory Response Syndrome or CIRS. There is a 34-page article on my website describing the diagnosis and treatment of mold illness or CIRS.  

I would recommend the following steps to people who feel they have mold exposure.

Do the CIRS questionnaire found on page 9 of the aforementioned article. You can see if you fulfill the criteria for the potential diagnosis of mold illness. Some of those symptoms are not just for mold illness. Some are more psychiatric based questions that can arise from mold. So, the questionnaire itself isn’t enough but it’s a good start. If you have more than eight symptoms in more than six of the subtypes on the questionnaire, consider mold as a potential differential diagnosis.

The second thing you can do is a visual contrast test. This too can be googled. Dr. Shoemaker’s website has access to a computerized VCS test. Take the test and if you fail it, consider mold as a potential illness or reason for feeling unwell.

Then, of course, the most important consideration is exposure. If you know that you’ve got a basement full of mold or your bathroom or your bedroom has mold on the windows from condensation, you have to consider that in your differential.

Not everybody gets sick from mold. Some people simply get allergy type symptoms,  but some people get true inflammatory response illness (CIRS). It’s been estimated that only 25% of people will have significant illness from mold. However, in my experience it’s more than that. People often downplay how important mold and the mycotoxins produced by mold are in influencing your health. 

So, what is important? Your exposure and your history. Is what you are exposed to visible mold? If it’s not visible, it could be hidden and so you often have to do your own homework and call in a mold inspector to look for the potential sources of mold. So, what can you do to potentially identify a problem? Look up at your pot lights. Is there a brown ring around your pot lights? Do you have buckled baseboards? Do you have black mold on your window frames? Is there mold in the grout in your shower? Do you have a front-end loading washing machine that smells musty? Does your house smell musty? Is there any potential mold in your air-conditioning system? Do you have a food composter in your kitchen? Because a lot of mold grows there. If you aren’t sure, it’s important that you call in a mold inspector, someone who will do a visual inspection and is armed with specific tools such as an infrared camera. Someone who is able to actually measure the dryness or wetness of drywall and put a small hole through drywall if you suspect mold or moisture behind the wall. The inspector will begin the examination of your home in the attic, looking at the insulation and at the condensation potential. Is your upstairs attic vented? A lot of the homes that we built in the Calgary building boom in 2009-2010, including my own by the way, didn’t have venting.  Condensation and wetness were ubiquitous and many people didn’t discover the mold until many years later, so get a good visual inspection. Find somebody to come in and inspect from the attic to the basement, someone who goes inside and outside and looks in multiple areas. If you go online, you’ll see how to do a visual inspection and a lot of it you can do yourself.   

Then you want somebody to do what’s called an ERMI test, which is a mold spore count. You want to do it either through a vacuum collecting dust from carpets or a swiffer cloth collecting dust off the floors. We recommend living rooms and bedrooms first. Some people do it in the basements although it’s not often recommended because a lot of basements are moldy. In my personal experience it’s important to know if your basement is moldy because through your furnace you’ll be pulling in mold through the furnace and pushing it throughout the house. Molds have also traveled from the basement through convection currents when your home heats up and so if the basement is a source, you want to know exactly how bad it is.  

Once you’ve done the visual inspection, once you’ve done ERMI testing looking for mold spores, once you’ve found mold (or not), the next step in the diagnosis is to do what we call the cytokine testing. Those aren’t done in Canadian labs, so we have to send them out. We call them the Shoemaker panel and we measure things like C4a, TGF Beta-1, MMP-9, VEGF, MSH and we do a nasal swab for something called MARCoNS, a coagulase negative staph. Basically, it’s a staph that lives in your nasal passages. It doesn’t produce overt nasal symptoms but can have significant cognitive effects and mitochondrial effects on your symptoms. So, we do those inflammatory markers.  

Recent advances have been very controversial regarding the use of urinary mycotoxin testing. In the original workup by Dr. Shoemaker didn’t believe that urea mycotoxin testing had any role to play in the diagnosis of mold illness. He has personally moved on to transcriptomic testing for definitive diagnosis but many other clinicians do urine mycotoxin testing to determine if there are any toxic mycotoxins of mold in the urine.  This is used quite extensively by the breakaway group that doesn’t adhere strictly to the Shoemaker protocol. There are two schools, which are the Shoemaker purists and then the group that has broken away. Like any good movement, there are always two camps, we can’t get away from that. Support and challenge exists throughout nature, exists throughout medicine, exists throughout clinical diagnosis and treatment.   

So, if you have a symptom profile that was suggested by the questionnaire, if you have a positive VCS test, if you have any signs of mold in your home, if the testing for mold spores in your home is positive, if your urine mycotoxin tests are positive and your Shoemaker labs are very positive, it’s highly likely that mold is playing a role in your illness. You need to find a practitioner who knows how to treat it. The treatment is extensive, requires lots of steps, and has to be followed in a specific sequence otherwise you can overload the detox pathways and get into increased symptom expression and feeling worse, not better.

A Discussion About Lyme Disease with Dr. Bruce Hoffman

A Discussion About Lyme Disease with Dr. Bruce Hoffman

The diagnosis and care of a patient with Lyme Disease is multifaceted and can be approached from more than one angle. It likely goes without saying that mainstream medicine is taking a much different approach than those in the functional and integrative space. 

In this video, I discuss the importance of looking at the larger history of said patient and how lab testing plays a role in proper diagnosis of Lyme Disease. 

If you are looking for answers regarding your situation, please contact our office today for more information. 

Watch the Video

A Discussion About Lyme Disease, with Dr. Bruce Hoffman

Reference Links

https://hoffmancentre.com/podcast-understanding-symptoms-and-treating-the-whole-person/

Transcript

Good afternoon everybody. I just finished an interview with the CBC (Canadian Broadcasting Corporation) and they wanted to talk about Lyme disease in Canada. We had a good, 20-minute chat that will probably be aired on some CBC broadcast in the fall. 

I was struck by one of the issues that often arises in my practice when I’m asked to treat complex multi-system, multi-symptom patients. They often come in and say, “I’ve got Lyme disease can you help me?” or “I’ve seen five doctors, naturopaths, et cetera, but I’m not better”.  

One of the biggest frustrations has been people believing that there’s one single trigger for their presentation of symptoms. They have one or two positive antibodies on their lab test, are told that’s a positive Lyme marker, and then are told by their medical provider that they should be on a full treatment program. I think that it’s medical malpractice to jump into the diagnosis and treatment of Lyme disease without a considered approach. 

We do know that there are two schools of thought in the standard of Lyme diagnosis. There are the traditional infectious disease specialists, who have very strict criteria for the diagnosis of Lyme disease, rightfully or wrongfully. Then there is a more broad approach to the understanding, diagnosis, and treatment of Lyme disease, which is purported and put forth by a group called ILADS, to which I happen to belong. 

The two schools of thought do not see eye to eye and that continual friction places the patient in the middle, trying to work out what is the best approach. 

Often patients get a diagnosis of Lyme disease from a provider they’ve seen based on the US test. They then get sent by their family doctor to an infectious disease specialist who reads them the riot act and lets them know that the tests are recording too many false positives, that they are irrelevant, that the lab is just trying to make money, or that the labs aren’t standardized. This battle goes back and forth, causes frustration for everyone, and the poor patient sits in the middle, trying to make sense of it all. 

Our aim is to talk about the differences between the two approaches, address the specifics as to why one group is vehemently certain of their position and the other group contests that position and has their own set of criteria for diagnosing and treating, which, based on the data, can’t be invalidated and has to be taken into account.

So here’s my take on patients who believe Lyme may be a trigger without a thorough health history. Lyme disease and co-infections are based on a very thorough clinical history.

I’m not going to go into the specifics of that clinical history, but the doctor or healthcare professional interviewing you must spend a lot of time taking a very specific history as to what symptoms you’re presenting and how you came to this diagnosis.

Just walking in with a positive lab test, whether it be US based or even Canadian based, isn’t good enough. Although with the Canadian test, if it’s positive, there’s a strong likelihood that Lyme disease is playing a role.

The Canadian test has very strict criteria for false positives and negatives, so if you have a positive test in the Canadian lab, it’s very likely that Lyme is an issue. So, I suggest that your practitioner takes a very thorough history and starts to use certain criteria to make the diagnosis.

One, is there history of a visit to an endemic area? Secondly, is there a history of tick bites?  Third, is there history of rashes? The problem is that many times, in fact most times, that history isn’t obtained. But if the history is there, that guides you in a certain direction. Those questions must be asked. Then a full list of symptoms must be taken, to try and differentiate whether your symptoms are specific to Lyme and related co-infections or whether they cross over with other conflicting or added potential causes for illness.

For instance, we know that in Lyme disease patients, after the first thirty days, the disease is characterized particularly in the later stages by migratory polyarthritis, which is joint pain or muscle pain that goes from joint to joint or muscle to muscle. These sorts of symptoms are very diagnostic. There are other things that cause this, but in the context of exposure to tick-borne illness, if those symptoms exist, you want to dig deeper.   

So migratory polyarthritis or muscle pain, those are very big symptoms for Lyme disease. Now for the co-infections, you want to ask very specific things. Do you have night sweats? Do you have day sweats? These occurrences are very specific for Babesia symptomatology. Do you have shortness of breath or “air hunger”? Do your symptoms come and go? Are there a lot of emotionally based symptoms, particularly anxiety as this has been associated with Babesia. You want to ask these very specific things.

Bartonella tends to be more peripheral so you tend to get a lot of pain syndromes such as Neuritis, which is pain in the peripheral nerves. Painful soles of the feet, particularly when you get out of bed in the morning. This is why the history is so important.

Lyme disease is now considered to be a clinical diagnosis based on history and physical examination, not based on a positive lab test. Why? Because you do get false positives and depending on which tests you run, the interpretation of results is highly complex. Unfortunately, due to cost we have the Canadian tests, which are elementary and introductory at best. 

Infectious disease specialists will say that they’re good enough, however, I disagree. When you want to look further and beyond you do have to look at more advanced testing which is, unfortunately, cost prohibitive. Most people can’t afford what’s really needed. I do try and get as many tests as I can across the spectrum of different testing types, including B-cell antibody testing, T-cell testing, PCR testing, plasma testing, and FISH testing. The more tests you can get, and the more that you correlate those tests with the clinical diagnosis in the symptom profile picture, the more you can hone in on the diagnosis of potential Lyme disease.

In Canada, Lyme disease is rising at a very alarming rate due to the migration of ticks and songbirds to the North. There was a study done showing that there are 32 million South American ticks brought north by South American birds every year. That’s a pretty alarming statistic. We know that songbirds are migrating to the North due to global warming and spreading their tick-borne load further and further North, hence the rise in tick-borne illness in Canada.

So, be cautious. Don’t jump to a diagnosis of Lyme disease because you have a positive test. Make sure that you have a very thorough history taken and make sure that the person who’s interviewing you has experience in the diagnosis and in interpreting lab data. The more lab data you have, the better.

Don’t rush ahead and treat yourself for Lyme disease without due caution. It can lead you into the wrong direction and make your immune system and your gut microbiome quite compromised if you treat inappropriately with some of the drugs out there that are available. Just a word of caution. This was covered in a podcast that you can listen to here.

Inflammatory Bowel Disease – Crohn’s Disease and Ulcerative Colitis, Part 1

Inflammatory Bowel Disease – Crohn’s Disease and Ulcerative Colitis

In anticipation of the upcoming Crohn’s and Colitis Summit, I want to share more about inflammatory bowel disease, Crohn’s disease, and ulcerative colitis. This two-part series will be a deep-dive into the root cause of inflammatory bowel disease, along with a comprehensive look at lifestyle changes and functional therapies that may provide relief. This free summit, hosted by Ravi Jandhyala and Mallika Allu of Gut Heal Protocol, will be held September 21st-27th. I will be speaking at the summit, and I encourage you to sign up if you or a loved one has Crohn’s disease or ulcerative colitis.

Inflammatory bowel disease (IBD) comprises a number of different medical conditions. The most significant of these are Crohn’s disease (CD) and ulcerative colitis (UC). These are chronic, immunologically mediated diseases with periods of relapse and remission, in addition to marked variations in mucosal inflammation from near normal in remission to severe ulceration in relapse.

UC affects only the colon with superficial inflammation, whereas CD affects the entire gastrointestinal tract and leads to transmural inflammation, strictures, fistulas, and abscess formation. 

The etiology of IBD is complex, but intricate dynamic interactions between the intestinal microbiome, host genetics, and external environmental factors all play an interrelated role in the development of IBD and its subsequent outcomes. 

The key mechanisms underlying the pathogenesis of these diseases are a genetically susceptible host exposed to external environmental factors, affecting gut microbiome and commensal flora. This results in a dysregulated immune response to different aspects of the gut microflora and increased intestinal permeability.

In this article, you will learn:

  • The etiology (root causes) of IBD, CD, and UC,
  • How the intestinal microbiome and your body’s immune response lead to IBD,
  • And the risk factors that may make you more susceptible to developing CD or UC, or having more severe flare-ups.

In Part 2, I will discuss our current strategies for diagnosing and treating CD and UC.

What causes IBD?


The health of the intestinal microbiome plays a key role in the pathogenesis of CD and UC. In particular, this is related to dysbiosis and reduced diversity of the gut microbiome. It also relates to protective bacteria subpopulations, such as Firmicutes, and an increased representation of potentially pathogenic bacteria, such as enteroinvasive Escherichia coli in subsets of ileal CD. In these conditions, species richness decreases, although some species seem to overgrow and increase in number. 

Both CD and UC are defined by an abnormal immune response, in which the immune system mistakes benign or beneficial cells and bacteria for harmful foreign substances. When this happens, the immune system, through a process known as molecular mimicry, can damage the gastrointestinal tract and produce symptoms of IBD.  UC is primarily a T-helper 2 (Th2) immune cell response, while CD is primarily T-helper 1 (Th1) cell mediated. 

Starting at birth, the cumulative effects of different environmental exposures, combined with a predetermined genetic susceptibility, is thought to cause IBD. It appears that continuous exposure to the collective effect of dynamic environmental factors, referred to as ‘exposome’ by Christopher Wild, affects the incidence of IBD.  Infancy and early childhood influence the formation of the immune system, whereas adult exposures to environmental factors alter established pathways.

Western lifestyles also seem to play a role, indicated by higher number of cases of IBD in Europe and the USA. The condition affects 1.5 million US citizens and 2.2 million people in Europe. There has been a significant increase in the last five years that’s consistent across several distinct ethnic groups and geographic locations. This increase parallels the Westernization or industrialization of an area’s lifestyle

Immigrants moving from low risk to high risk areas tend to assume the qualities of the high-risk areas within a generation or two. In their new location, the risks are much higher than in their low-risk country of origin. There has also been an increase in the number of cases in developing countries in Asia, Eastern Europe, and Northern Africa, as their lifestyles and living environments change. Onset of IBD in young adulthood is characterized by a relapsing and remitting course with frequent hospitalizations or surgery.

  1. Is irritable bowel syndrome a type of IBD?

Irritable Bowel Syndrome (IBS) is considered non-inflammatory and a syndrome, or a group of symptoms, rather than a specific disease. Symptoms of IBS typically include chronic abdominal pain, diarrhea, constipation, or alternating bouts of both of these. People with IBS are also more likely to have other functional disorders such as fibromyalgia and chronic fatigue syndrome (CFS). IBS doesn’t produce the destructive inflammation found in IBD, so it may be considered a less serious condition. However, it can still cause chronic discomfort and affect quality of life. Research suggests that IBS can be caused by stress and the manner in which the brain and gut interact.

Risk factors of IBD


Well known risk factors for IBD include:

  1. Cigarette smoking: reduced risk of UC, increased risk of CD
  2. Appendectomy: reduced risk 
  3. Western diet: increased risk
  4. Stress: increased risk 
  5. Depression: increased risk 
  6. Low vitamin D levels: increased risk
  7. Estrogen replacement therapy: increased risk of UC
  8. Left-handedness: increased risk
  9. Mycobacterium paratuberculosis infection: increased risk of CD

Breast-feeding, appendectomy, and smoking, surprisingly, are all associated with reduced risk of UC. 

The effects of some of the risk factors outlined above appear to differ between CD and UC. Despite shared genetic and immunologic mechanisms, distinct pathways of pathogenesis exist.

There’s a substantial body of research that’s available regarding risk factors, but limited evidence for the treatment of these environmental triggers to modify disease outcomes or prevent relapse. There have only been a few controlled clinical trials for modification of risk factors resulting in an improvement in patient outcomes.

Risk loci, or specific gene locations within your chromosomes that appear to alter IBD risk, highlight several key pathways in pathogenesis. These include the following:

  • Innate immunity
  • Adaptive immune responses
  • Abnormal glycosaminoglycan (GAG) content of the mucosa
  • Maintenance of intestinal barrier function with increased intestinal permeability
  • Pathogen sensing 
  • Endoplasmic reticulum stress
  • Response to oxidative stress
  • Decreased oxidation of short chain fatty acids  
  • Increased inflammatory mediators 
  • Increased sulfide production
  • Decreased methylation
  1. Genetics

Everyone is born with a certain genetic susceptibility to IBD. Following exposure to a Western lifestyle, diet, and certain environmental triggers, a specific threshold is reached and IBD may develop. This explains the low concordance rate in twins, suggesting that genetic influence, while important, is only one piece of the IBD puzzle. The exposome, or the total coherent effect of all environmental factors from birth to death, plays the determining role.  

A positive family history of IBD is the most important risk factor for the development of the condition. Whole genome scans have found susceptibility genes for UC on chromosomes 1 and 4. A concordance rate of 19 percent for UC and 50 percent for CD in monozygotic twins has also been established. 

Genetics have shown 204 distinct genetic risk loci for IBD, with the majority of risk alleles being shared between both diseases. However, 37 CD-specific and 27 UC-specific loci have been identified. Known loci account for only a third of the risk for either disease. 

  1. Childhood exposures

Breast-feeding appears to confer a protective effect on both UC (1.8-fold) and CD (2.2-fold), in keeping with known protective effects for other immune-mediated diseases such as eczema and asthma, allergic rhinitis, and type 1 diabetes. This is thought to be due to protective maternal antibodies and the induction of immune tolerance to specific food antigens and gut microbes.

Antibiotic exposure is associated with an increased risk of adult and pediatric-onset IBD. Exposure during infancy or early childhood is associated with the greatest increase in risk. Use of antibiotics between the ages of five and sixteen, through the effect on the microbiome, appears to increase the incidence 1.6-fold. If antibiotics are used in the first year of life, the risk of CD increases 5.3-fold. 

The strongest risk increase is linked to the use of broad-spectrum penicillin (3.1-fold), pen V (2.9-fold), then cephalosporin (1.9-fold).

It’s been hypothesized that by altering the gut microbiome composition, pathogenic bacteria colonize while the normal process of tolerance, which is crucial for immune development, is disrupted. This leads to an aberrant response of the host immune system to its microflora.

On the other hand, early childhood Helicobacter pylori infection is associated with a decreased risk of CD of 1.7-fold and UC of 1.3-fold. H. pylori increases Fox-3, the transcription factor of T-regulatory cells, which down-regulates the inflammatory response. 

  1. Hygiene

A high hygiene level increases the risk of IBD. Living in an urban environment increases risk by 1.2-fold.

Having a smaller number of siblings increases risk 2.6-fold. The more siblings you have, the lower your risk for IBD.

Sharing a bedroom decreases risk of UC by 2.1-fold and CD by 2.3-fold, while a hot water tap in the home increases the risk of CD by 5-fold.

Animal contact decreases risk of UC and CD, with similar effects seen regarding asthma and eczema.

The implication is that the more hygiene measures employed, the fewer helminths (worms and parasites) you’re exposed to, and therefore less induction of dendritic cells maturation and ability to drive the T-cell immune system occurs. This results in decreased protection against autoimmunity. 

In simpler terms, “germophobes” may be at an increased risk of developing IBD.

  1. Autism

There have been several reports of a link between autism spectrum disorder (ASD) and chronic gastrointestinal (GI) symptoms. Endoscopy trials have demonstrated a higher prevalence of nonspecific colitis, lymphoid hyperplasia, and focally enhanced gastritis in people with ASD compared with controls. Postulated mechanisms include aberrant immune responses to some dietary proteins, abnormal intestinal permeability, and unfavourable gut microflora. 

Wakefield et al conducted one of the earliest studies investigating gastrointestinal anomalies in autistic children in 1998. In this study, twelve children with regressive developmental disorders, nine of whom were autistic, were all reported to have abnormal colonoscopies. The most consistent finding was lymphoid nodular hyperplasia (LNH), which was present in nine of the twelve children. This mild to moderate colitis was deemed nonspecific on the basis of not fulfilling criteria for either Crohn’s disease or ulcerative colitis.

Criticism regarding the ‘normalcy’ of LNH in children prompted Wakefield, et al. to perform ileocolonoscopies in 60 children with regressive developmental disorders and compare them with 37 developmentally normal controls. In this trial, ileal LNH was present in 93 percent of affected children in comparison to 14.3 percent of controls (P<0.001). Chronic colitis was detected in 88% of affected children compared with 4.5% of controls. 

Torrente et al. compared the gastric biopsies of 25 autistic children with those of ten normal controls, ten CD patients, and ten children with H. pylori infection. Eleven of the 25 autistic children had a focally enhanced gastritis, while two had mild diffuse gastritis. Immunohistochemistry results demonstrated the pattern of lymphocyte infiltration was most similar to Crohn’s disease, with the exception of a striking predominance of CD8-positive over CD4-positive cells and a marked increase in intra-epithelial lymphocytes. Another highly specific finding among autistic children was a dense, sub-epithelial basement membrane immunoglobulin G deposition, which was absent in the other subgroups.

ASD patients and their caregivers often report improvement in the patient’s condition after following elimination diets. Improvements occur not only in the GI symptoms, but also in behavioural and cognitive problems such as hyperactivity, communication skills, and attentiveness. Interestingly, 36% of children with ASD have a history of cow’s milk and/or soy protein intolerance in infancy. In addition, while studies haven’t indicated an increased incidence of Celiac disease in these individuals, parents have often reported an improvement in their child’s behavioural disturbances when following a gluten-free diet. These benefits haven’t been seen consistently in randomized trials, although a Cochrane review did report a significant reduction in autistic traits on a gluten-free, casein-free diet.

One hypothesis is that ASD may be accompanied by aberrant innate immune responses to dietary proteins, leading to GI inflammation and aggravation of behavioural problems. One study, measuring pro-inflammatory cytokines in response to common dietary proteins, showed a greater than two standard deviations (SD) excess in tumour necrosis factor-alpha and interferon-gamma production in response to gluten and cow’s milk protein among ASD children, when compared with controls. 

A subsequent study confirmed a higher prevalence of elevated tumour necrosis factor-alpha and interleukin-12 production with beta-lactoglobin and alpha-lactoglobin, but not casein, in autistic children and children with non-allergic food hypersensitivity, compared with normal controls. 

Another theory suggests that abnormal intestinal permeability in children with ASD causes them to absorb fragments of incompletely broken-down peptides such as gluten or casein, which cross the blood-brain barrier and act as endogenous opioids. 

The gut microflora has also been targeted as a potential player. There have been anecdotal reports of the onset of autism following broad-spectrum antibiotics, suggesting that disruption of the indigenous flora may lead to colonization by neurotoxin-producing bacteria. Autistic children have been shown to have higher counts and more species of Clostridia than controls matched by age or gender. A small prospective trial demonstrated a significant but transient improvement in autistic features following a course of vancomycin (antibiotic) therapy, with relapses presumed to occur because of persistent spores that proliferate upon discontinuing the medication.

  1. Yeast

The ratios of yeasts in the gut, such as Saccharomyces cerevisiae and Candida albicans, may be significantly altered by IBD. Normally, yeasts and fungi account for less than 0.1% of the total microbiota population. However, there is often a decreased population of S. cerevisiae and increased populations of C. albicans and other Candida yeasts in the guts of people with IBD.

Antibiotic use can result in fungal overgrowth, especially of the Candida yeasts, which may then compete with the bacteria in the gut for survival and growth. This fungal overgrowth can make the host more susceptible to mold illness, paving the way for an immune response that may invoke chronic inflammation, autoimmunity, or IBD.

It appears also that certain components of the cell walls of fungi can trigger immune responses, which may add to the overall exposomeXI.

  1. Gut microbiome

Recent studies have highlighted the association between the gut microbiome and the pathogenesis of IBD. 

Reduced biodiversity of the gut microbiome is apparent even at the onset of diagnosis, before treatment is initiated. CD, especially ileal CD, has been associated with increased frequency of pathogenic bacteria such as enteroinvasive E. coli. There can also be a reduction in the frequency of anti-inflammatory bacterial subgroups, particularly Faecalibacterium prausnitzii. Giving strains of this specific bacteria has resulted in improved outcomes and amelioration of colitis in animal models.

By the time someone reaches adulthood, the immune system has matured and lifestyle factors become more apparent as choices are increased. Adult exposures seem to be involved in changing the already developed immune system. Several environmental factors have been identified as playing a role in IBD development independent of stage of life, previous development of acute bacterial gastroenteritis, geographical location, and vitamin D. 

Bacterial gastroenteritis as a result of Clostridium difficile, Campylobacter, and/or Salmonella infections can increase risk of IBD. The risk of developing IBD increases significantly after bacterial gastroenteritis, especially within the first year. The largest effect is seen with CD, for which there is a 2.9-fold increase, rather than the 2.1-fold for UC. This may be explained by the increase in interleukin-6 (IL6), blockage of T-reg cells, and the activation of self-reactive T-cells, leading to a chronic inflammatory response.

  1. Mycobacterium avium infection

M. avium subspecies paratuberculosis (MAP) infection rates are higher in CD, although a causative link hasn’t been established. Meta-analysis has shown a 7-fold increase in CD in MAP infections, but the timing of this infection couldn’t be ascertained to be a cause of CD and is perhaps merely a bystander. 

  1. Tap water

Drinking tap water lowers the risk of CD 2-fold. It’s been proposed that this might be due to harmless microorganisms triggering regulatory T-cells.  

  1. Flying

Individuals have an increased risk of disease flare following high-altitude flights or after travelling more than 2,000 metres above sea level. Mild hypoxia leads to an increase in IL6 and C-reactive protein (CRP), which are markers of inflammation.

  1. Obesity

An American cohort study showed a 2.5-fold increase in CD in obese women with a body mass index (BMI) greater than 30 kg/m2. 

  1. Smoking 

Smoking confers a 2-fold increase in risk of CD, which is somewhat lessened when stopping smoking, although the pathogenic mechanism remains unknown. 

Smoking is associated with a more aggressive form of CD, more surgery, and an earlier risk of recurrence and re-operation following a bowel resection. Stopping smoking prior to the diagnosis can result in a reduced likelihood of progressing to complicated disease behaviour or the need for surgery. Smoking cessation is also associated with a reduced rate of relapse regarding CD.

With UC, current but not former smokers appear to have some protection, with half the risk of UC in current smokers compared to individuals that have never smoked. Smoking confers a 1.7-fold reduction in risk for UC. 

For former smokers, the risk for both UC and for CD increases by the same amount.

For patients with UC, smoking leads to a more benign disease course with fewer flares, a reduced need for steroids, and lower colectomy rates. Smoking cessation increases the risk, with the effect lasting for up to ten years after quitting smoking. This suggests that smoking only defers the development of UC. Quitting smoking is also associated with flare-ups.

Passive, or second-hand, smoking has a weaker beneficial effect. The mechanism of this different effect between CD and UC is unknown, but is thought to be influenced by the constituents of cigarette smoke having different effects on oxidative stress in mononuclear cells.

Smoking is known to affect the immune system through both cellular and humeral pathways by transforming the synthesis of pro-inflammatory cytokines, altering gut permeability, reducing smooth muscle tone and contractility due to nitrous oxide, and effecting changes in the gut microflora. 

There’s also an interaction between smoking and genetic variants in the CYP2A6/EGLN 2 locus and glutathione transferase enzymes (GSTP1) and risk of CD and UC. Snips in these genes showed significantly different outcomes. 

  1. Appendectomy

There are divergent effects between UC and CD following appendectomy.

When performed before the age of twenty, there’s an increased risk of UC with no effect or only a slightly increased risk of CD. The mechanisms remain unclear, and appendectomy may result in intestinal microbiome alteration with a protective effect on UC. The microbiome composition in the appendix also appears to confer protective effects against UC

  1. Diet 

The role of diet has been problematic to determine. This is due to difficulty in tracking it through the course of a lifetime, different recall between controls and cases, and potential restrictions on diet choices pre-diagnosis based on the nature of the disease. 

Increased fibre of approximately 24 grams was associated with a significant reduction in risk of CD but not UC.   This was related to fruit fibre and not that of vegetables, including cruciferous ones. No association was found between fibre from cereals, whole grains, or legumes. 

Fibre may confer epithelial integrity and reduce translocation of potentially pathogenic bacteria such as enterovirus E. Coli, which may play a role in CD. Fibre activates the aryl hydrocarbon receptor (AhR) expressed in intestinal lymphocytes, which offers protection against environmental antigens.  

A diet high in long-chain n-3 polyunsaturated fatty acids (PUFA) was associated with a reduced risk of UC. CD had no modifiable fat intake risk factors for CD. One large study found omega-3 supplements had no beneficial effects, while a high intake of animal protein revealed a potential association with IBD. Sugar and a high-carbohydrate diet are associated with an increased risk of IBD, while fruits and vegetables seem to have a protective effect.

Alteration of diet can trigger flares in many different types of disease. High fat diets result in expansion of specific bacterial subpopulations that are associated with a pro-inflammatory response, particularly diets high in meats, as well as polyunsaturated omega-6 fats (like those found in industrial seed oils such as soybean oil, corn oil, and canola oil).XVI Elemental diets show improved outcomes in CD, whereas partial and complete enteral nutrition show effects superior to placebo but lower than steroids. 

Elimination diets, such as the specific carbohydrate diet, lectin-free diet, autoimmune paleo, and Whole30, are of particular interest as well, but there is still a lack of strong evidence regarding their efficacy for IBD treatment.

Childhood diet and antibiotic exposure is an important determinant of microbiome composition. Breastfeeding appears to reduce UC risk, but it doesn’t appear that formula-feeding necessarily increases UC risk. Researchers have found that the gut microbiome of both breastfed and formula-fed children changes significantly after the introduction of foods. Therefore, the first foods a child receives (other than breastmilk or formula), and the foods they eat throughout their early childhood, may profoundly affect their gut microbiota composition and affect their IBD risk level.

  1. Glyphosate

Glyphosate is the world’s most widely produced herbicide. It’s the primary toxic chemical in Roundup™ and many other herbicides. As a broad-spectrum herbicide, glyphosate is present in more than 700 different products and used in industries such as agriculture and forestry, and even in the home. 

Glyphosate was introduced in the 1970s to kill weeds by targeting the enzymes that produce the amino acids tyrosine, tryptophan, and phenylalanine. However, the enzymes of many bacteria are susceptible to inhibition by this chemical, so it can also alter the gut flora of many animals. 

Usage of glyphosate significantly increased after the introduction of genetically modified (GMO), glyphosate-resistant crops that grow well despite the presence of this chemical in the soil. In addition, the toxicity of the surfactant polyoxyethyleneamine (POEA), which is commonly mixed with glyphosate, is greater than the toxicity of glyphosate alone. 

In addition, Enlist Duo™, a herbicide product containing a 2,4-dichlorophenoxyacetic acid (2,4-D) salt and glyphosate, was approved for use in Canada and the United States in 2014. This was for use on GMO soybeans and maize, both of which were designed to be resistant to both 2,4-D and glyphosate. 2,4-D has many toxic effects of its own. 

Research has shown that glyphosate disrupts the microbiome in the intestine, causing a decrease in the ratio of beneficial to harmful bacteria. Highly pathogenic bacteria such as Salmonella entritidis, Salmonella gallinarum, Salmonella typhimurium, Clostridium perfringens, and Clostridium botulinum are highly resistant to glyphosate. Unfortunately, however, most beneficial bacteria such as Enterococcus faecalis, Enterococcus faecium, Bacillus badius, Bifidobacterium adolescentis, and Lactobacillus ssp. were found to be moderately to highly susceptible. 

The relationship between the microbiome of the intestine and overall human health is still unclear.

 However, current research indicates that disruption of the microbiome could lead to conditions such as metabolic disorder, diabetes, depression, autism, cardiovascular disease, and autoimmune diseases such as IBD. 

  1. Celiac disease, IBD, and the glyphosate connection

Researchers have found that people with Celiac disease are about 10 times as likely as a control group to have IBD. Conversely, the prevalence of Celiac disease in IBD appears to be comparable with that indicated in controls.

Celiac disease, and more generally, gluten intolerance, is a growing problem worldwide. It’s particularly serious in North America and Europe, where an estimated 5% of the population now suffers from this condition. It’s a multi-factorial disease associated with numerous nutritional deficiencies, as well as reproductive issues and an increased risk of thyroid disease, kidney failure, and cancer. 

It has been proposed by researchers Samsel and Seneff that glyphosate is the most important causal factor in this epidemic. Fish exposed to glyphosate develop digestive problems that are reminiscent of Celiac disease. The condition is associated with imbalances in gut bacteria that can be fully explained by the known effects of glyphosate on these particular types of bacteria. 

Characteristics of celiac disease point to impairment in many cytochrome P450 (CYP450) enzymes, which are involved with detoxifying environmental toxins, activating vitamin D3, catabolizing vitamin A, and maintaining bile acid production and sulfate supplies to the gut. Glyphosate is known to inhibit CYP450 enzymes. 

Deficiencies in iron, cobalt, molybdenum, copper, and other rare metals associated with Celiac disease can also be attributed to glyphosate’s strong ability to chelate these elements. Deficiencies in tryptophan, tyrosine, methionine, and selenomethionine associated with Celiac disease also match glyphosate’s known depletion of these amino acids. 

Celiac disease patients have an increased risk of developing non-Hodgkin’s lymphoma, which has also been implicated in glyphosate exposure. Reproductive issues associated with Celiac disease, such as infertility, miscarriages, and birth defects, can similarly be linked to glyphosate. 

Glyphosate residues in wheat and other crops have been increasing recently due to the growing practice of crop desiccation just prior to the harvest. The practice of ‘ripening’ sugar cane with glyphosate may also explain the recent surge in cases of kidney failure among agricultural workers in Central America. 

  1. Mast Cell Activation Syndrome (MCAS)

As early as 1980, Dvorak and colleagues reported that mast cells were markedly increased in the ileum of patients with CD. In 1990, Nolte et al. showed the same findings in patients with UC. There were increased numbers of mast cells with associated degranulation products of histamine and tryptase, along with associated increases in cytokines and leukotrienes IL-16. TNF-alpha and substance P have also been found in the mucosa of patients with IBD, particularly when stained with the CD 117 stain. 

According to the latest literature research conducted by Dr. Lawrence Afrin, one of the key researchers in MCAS, mast cells release at least 1,000 mediators of inflammation. This includes, but isn’t limited, to histamine, proteoglycans (heparin and chondroitin sulfate), proteases (tryptase, chymase and carboxypeptidase), eicosanoids, and platelet activating factor (PAF).

Activation of mast cells leads to the release of the eicosanoid arachidonic acid from the phospholipids on the cell membrane. This 20-carbon fatty acid is then rapidly oxidised, along either the cyclooxygenase pathway to form prostaglandin D2 (PGD2) or the lipoxygenase pathway to form leukotriene C4 (LTC4). Histamine triggers the histamine H1 receptor and tryptase, the protease-activated receptor 2 (PAR2).

Therapies aimed at down-regulation of mast cell activity may be important in the treatment of IBD. 

Mast cell cytokines constitute a third category in that they may be both preformed and newly synthesized. These include IL-4, IL-5, IL-6 and TNF-alpha in the nasal mucosa and bronchi, as well as IL-1B, IL-3, IL-8, IL-9, IL-10, IL-13, IL-16, IL-18, IL-25, granulocyte -macrophage colony stimulating factor (GM-CSF), and stem cell factor macrophage chemotactic peptide (MCP)-1, MCP-3, and MCP-4. 

Many factors are known to activate mast cells, and their activation is a crucial step involving pathophysiological changes. These factors include antigens, anti-IgE, substance P, VIP, C5a, C3a, somatostatin, morphine, very low-density lipoprotein, stem cell factor, tryptase, and eosinophil cationic protein, all of which are known to activate mast cells. 

It should be noted that mechanisms of mast cell activation differ with different classes of triggers.

  1. Nutrient deficiencies 

UC patients were found to have lower levels of vitamin A, vitamin E, and carotenoids than those in  controls. This implies that certain nutrient deficiencies may either play a role in the development of UC, or, conversely, are a complication of UC. 

  1. Vitamin D

Vitamin D intake is inversely associated with UC risk, meaning that higher vitamin D intake is linked to a lower UC risk.  Additionally, higher blood levels of vitamin D are associated with reduced risk of CD.

 Patients who increased their blood vitamin D levels had a 1.9-fold protective effect for CD, but not for UC. They also had a lower risk of surgery compared to those who remained vitamin D deficient. Low vitamin D levels are also associated with a higher rate of colon cancer and C. difficile infections.

Vitamin D administration may reduce the risk of IBD relapses. Vitamin D is also known to play a role in the regulation of the innate immune system by activating the TH1 lymphocytes and monocytes. This causes the inflammatory response to be down-regulated. 

  1. Weather and latitude

Incidence of IBD is higher in northern latitudes where people have reduced exposure to ultraviolet (UV) light. The Women’s Health Initiative (WHI) study noted a lower risk for both UC and CD in women in southern latitudes (1.6-fold for UC) compared to those at higher latitudes. Living in southern latitudes appears to be protective, likely due to increased UV light and subsequently higher vitamin D levels.

Warm summers have a protective effect for UC and possibly for CD as well. This is also the case for other inflammatory diseases such as multiple sclerosis (MS), rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE). This is thought to be due to an increase in microbial diversity, which in turn confers benefit.

  1. Psychological behaviours

IBD has long been associated with neuroticism, dependency, anxiety, and perfectionism. Recent well-designed studies have confirmed that adverse life events, chronic stress, and depression increase the likelihood of relapse in patients with quiescent (dormant) IBD.

The evolving science of psychoneuroimmunology has outlined the mechanisms by which the nervous system can affect immune function at both the systemic and gut mucosal levels. These mechanisms are thought to be due to changes in the hypothalamic-pituitary-adrenal (HPA) axis and alterations in the bacterial mucosal barrier. These occur via mucosal mast cells and mediators, such as corticotrophin releasing factor (CRF). 

To maintain homeostasis, a living organism must constantly adapt at a mental, emotional, molecular, cellular, physiological, and environmental level. Stress is defined as a threat to an organism’s homeostasis. The function of the stress response is to maintain homeostasis through behavioural and biological or physiological adaptations. The stress response involves the complex integration between a series of interconnected regions within the brain. These are the hypothalamus, the amygdala, and the hippocampus. This hub receives inputs from viscera and somatic afferents and from higher cortical structures, including the internal dialogue and mental perceptions of the patient. This in turn, affects the neuroendocrine stress response via two interconnected effector pathways, namely the HPA axis and the autonomic nervous system (ANS).  

Stress stimulates the release of CRF from the hypothalamus, causing the release of adrenocorticotrophic hormone (ACTH) from the anterior pituitary. This in turn causes the release of cortisol from the adrenal cortex. Stress also activates the descending neural pathways from the hypothalamus to pontomedullary nuclei, which control the autonomic nervous system response. Stimulation of the sympathetic nervous system (fight/flight) causes the release of adrenaline and noradrenaline from the adrenal medulla. This is in addition to supplying the entire gut directly. The parasympathetic vagus nerve and sacral nerves provide parasympathetic input to the upper gut and to the distal colon and rectum. 

The gut has its own nervous supply called the enteric nervous system (ENS), which is innervated by both sympathetic and parasympathetic fibres. This network has been termed the gut-brain axis. The ENS contains 100 million neurons and regulates the motility, the exocrine and endocrine functions, and the microcirculation of the gut. These axes (HPA, ANS, ENS) can then interact directly with the immune system. Psychoneuroimmunology is the study of how behavioural factors and CNS function can influence the immune system, and hence inflammation, at both systemic and local tissue levels.

Nerve fibres of the ANS form close effector junctions with lymphocytes and macrophages in lymph glands, bone marrow, the thymus, the spleen, and mucosa associated lymph tissue. These nerve fibres also release a number of chemicals called neurotransmitters, such as catecholamines, vasoactive intestinal peptides, angiotensin II, neurotensin, somatostatin, and substance P. These are capable of affecting lymphocytes, macrophages, neutrophils, and other inflammatory cells at the neuro-immune cell junction. Lymphocytes and other inflammatory cells also carry receptors for the hormones and neuropeptides of the HPA axis, such as growth hormone, ACTH, corticosteroids, and CRF. 

At high concentrations, cortisol has an immunosuppressive effect, increasing the release of anti-inflammatory proteins and IL-10. Transcription of inflammatory signalling molecules such as IL-6, IL-1, and TNF-α are reduced through transcription factors AP-1 and nuclear factor kappa beta. At lower doses, cortisol has an immune stimulating effect.

Similarly, adrenaline and noradrenaline have mixed effects at different doses on immunity and inflammation. Adrenaline causes an increase in serum IL-6, an increase in lipopolysaccharide (LPS) induced IL-8 and IL-10, and an increase in cytotoxic (cell-killing) T-cells and natural killer (NK) cells.

Chronic sustained stress due to adverse life events, such as bereavement, divorce, and depression, have been shown to reduce the numbers of cluster of differentiation 8 (CD8, a glycoprotein) lymphocytes, NK cells, and macrophages in the blood. However, in addition to immunosuppression, chronic stress with reduced heart rate variability, which is a sign of increased sympathetic tone, has been shown to increase inflammation, showing raised CRP.  

Acute stress causes stimulation of the sympathetic nervous system with a rise in adrenaline and noradrenaline, followed a little later by a rise in cortisol. This leads to an acute episode of immune enhancement with an increase in inflammatory cytokines that are known to be associated with flares of IBD. This includes a rise in cytotoxic CD8 T lymphocytes and NK cells and an increase in their cytolytic activity, in addition to platelet activation and thrombin generation, producing effects of microcirculation ischemia causing thrombosis and microinfarction. This effect is lowered with beta blockers rather than aspirin, suggesting that a stress response or sympathetic activation is at the root of it. 

Psycho-social stressors have long been associated with triggers. Recent and remote stress is associated with an increased incidence of IBD, with recent stress being more significant. When questioned, patients indicated that stress was the trigger for 70% of their flares. Depression feelings were associated with a 2.4-fold increased risk of CD, but not UC. Depression, anxiety, and stress are also associated with increased rates of relapse and surgery for IBD.

The inflammatory response to stress through elevation of IL-6 levels can be changed in mice by administrating antibiotics, suggesting antibiotics exerts their effects through changes in the gut microbiota.

Using medications to treat these conditions appears to have variable effects. People referred for therapy following increased stress due to the diagnosis have reduced rates of relapse, outpatient attendance, and use of steroids or other medications for IBD. 

In summary, stress can play a significant role in immune system dysfunction leading to an inflammatory response, which may trigger new-onset IBD or a flare of existing disease.

  1. Sleep

Both increased and reduced amounts of sleep have been associated with negative health outcomes. Reduced sleep quality was associated with an increased risk of relapse at six months post-remission in CD, supporting an association between poor sleep and gut inflammation. Sleep disturbances in IBD may lead to a 2-fold increase of disease flare. Sleep deprivation also leads to activation of the immune cascade.

  1. Nonsteroidal anti-inflammatory drugs

The use of nonsteroidal anti-inflammatory drugs (NSAIDS) for fifteen days per month increases the risk of UC 1.9-fold and CD 1.6-fold. These figures are increased by greater weekly dosage, and a higher frequency or longer duration of use. NSAIDS lead to inhibition of cyclooxygenase (COX), resulting in a decrease in protective prostaglandins in the gut mucosa, increasing gut permeability. 

  1. Oral contraceptives

Current use of oral contraceptives (OCP) leads to 1.3-fold increased risk of UC. The risk of developing CD with current use of OCP is increased by 1.5-fold. 

  1. Post -menopausal HRT

Post menopausal HRT increases the risk of UC by 1.7-fold, but not CD. It’s been proposed that estrogen modulates gut inflammation by acting on estrogen receptors that are found on gastrointestinal epithelial and immune cells. 

UC is a Th2 mediated illness, and estrogen promotes Th2 cytokines. The same holds true for other Th2 mediated diseases, such as RA and SLE. However, this is not the case with CD, which is a Th1 mediated illness. 

A prospective cohort study (the Women’s Health Study) followed 108,844 postmenopausal American women, with a median age of 54, without a prior history of CD or UC in 1976. The risk of UC appeared to increase with longer duration of hormone use and decrease depending on the time since discontinuation. There was no difference in risk according to the type of hormone therapy used, such as estrogen as opposed to estrogen and progestin. No association was noted between the current use of hormones and the risk of CD. The effect of hormones on the risk of UC and CD was also not modified by age, BMI, or smoking.

  1. Ambient air pollution

On the whole, air pollution exposure wasn’t associated with the incidence of IBD. However, residential exposure to sulfur dioxide and nitrous dioxide gases found in industrialized regions may increase the risk of early-onset UC and CD respectively. 

Living in regions with high sulfur dioxide emissions before the age of 25 increases the chances of UC 2-fold. A high nitrogen dioxide exposure before the age of 23 increases the chance of CD 2.3-fold. Total pollutant emissions correlate significantly with an increased risk of hospitalization in established IBD. Pollutants may also be absorbed and incite the inflammatory process that’s characteristic of IBD.

  1. Physical activity

Researchers have found that women engaging in active physical activity have a 44% reduction in CD risk compared with sedentary women. Physical activity was not associated with risk of UC.

The absolute risk of UC and CD among women in the highest fifth of physical activity levels was at just 8 and 6 events per 100,000 person years. This compares to 11 and 16 events per 100,000 person years among women in the lowest fifth of physical activity. 

Age, smoking, BMI, and cohort didn’t significantly modify the association between physical activity and the risk of UC or CD in these findings. The pathway appears to be mediated through the autophagy (clearing out or recycling of damaged cells) pathway or cell senescence (cell aging).

Summary

There’s a rich body of research showing potential environmental risk factors for the development of IBD. However, there aren’t many high-quality studies showing that environmental changes may have a large effect on disease outcomes. For a large number of possible environmental factors, meta-analyses are not yet available.

Many novel factors are identified by large cohort or case-control studies, but are yet to be reproduced by and validated by independent research groups. Consequently, the level of evidence is somewhat low and caution should be exercised when drawing firm conclusions or making recommendations.

However, individuals with a genetic susceptibility can be cognisant of environmental factors and do their best to lower or delay their genetic expression, as their exposure threshold may not be reached. Being aware of which environmental factors are involved in developmental phases as well as along the course of the disease to increase flares and development of complications, gives the treating physician and patient as advocate the opportunity to make the necessary adjustments along the patient’s timeline.

 This has the effect of lowering the risk of disease expression with a more personalized treatment plan.

In Part 2, I will be reviewing the lab tests that are used to diagnose CD and UC, along with lifestyle changes and treatment options that are often successfully employed in IBD care.

In the meantime, I encourage you to join me at the Crohn’s & Colitis Summit from September 21st-27th, or to contact my office if you are seeking functional and integrative care for your IBD. 

Podcast: Understanding Symptoms and Treating the Whole Person

Looking at Lyme

I was recently interviewed by Sarah Cormode for an episode of Looking at Lyme, an educational podcast created by the Canadian Lyme Disease Foundation, where I highlight the importance of taking an in-depth patient history to understand and document symptoms.

I also discuss several approaches to treating Lyme disease and explain why such a variety of symptoms amongst patients with Lyme disease exists.

Take a listen below.

Diagnosis of Mast Cell Activation Syndrome – A Global Consensus 2

Diagnosis of Mast Cell Activation Syndrome - A Global Consensus

Please take a look at this newly published peer-reviewed article by Dr. Lawrence Afrin of which I was a co-author, on the revised criteria for the diagnosis of mast cell activation syndrome (MCAS):

Diagnosis of mast cell activation syndrome: a global “consensus-2”

One of the most common difficulties patients seem to face after they have been to our clinic and given a diagnosis of mast cell activation syndrome is when they return to their GP’s or specialists with a description of this syndrome. Traditional medicine is well-schooled in the diagnosis of systemic mastocytosis, a condition characterized by an increased number of mast cells as opposed to MCAS which is a diagnosis arrived at due to the increased activity of mast cells (and not an increase in the actual numbers).

Systemic mastocytosis is most often diagnosed by using a biomarker called tryptase, whereas the diagnosis of MCAS has much broader diagnostic criteria as this article will outline.

For a much more in-depth description of MCAS, please see my treatment page and the following articles:

  1. Treating Mast Cell Activation Syndrome (MCAS)
  2. Mast Cell Activation Syndrome: When You Immune System Runs Rampant
  3. Natural Treatments For Mast Cell Activation Syndrome
  4. Your Ultimate Guide to the Low-Histamine Diet

COVID-19 Testing: What You Need To Know

As I learn more about COVID-19 and share that information with you, my community, I’m increasingly asked about testing. Time is moving on and it’s clear that one of the limitations regarding the management of this global pandemic has been testing, or more specifically the lack of testing. There are still so many questions about how widespread SARS-CoV-2 (the virus that causes COVID-19 disease) is here in Alberta, Canada, and across the globe. We know that many people carry and spread the virus without showing any symptoms or just display very mild ones, but how many people are we talking about? 

As we enter the next phase of pandemic management, as people begin to enter communities again, testing will play a key role.1 It’s incredibly important to know who’s been exposed as well as who hasn’t and therefore may still be at risk. More widespread testing will help to keep those most vulnerable, including those with pre-existing conditions safe. 

While there’s undoubtedly still a lot to learn, in this article I’ll distill for you what I know and believe, as of now. I’ll cover:

  • Some background on testing, including understanding the timeline of COVID-19 infections
  • Types of testing, including viral RNA and antibody 
  • What test results mean
  • Test accuracy
  • Next steps for testing

Background on testing: The viral timeline 

To understand testing it’s helpful to understand the timeline of COVID-19 infection. This image was compiled by the Institute for Functional Medicine and provides a helpful visual.2 It’s important to note that this timeline is based on the data that has been collected so far, and some of it hasn’t been peer-reviewed and published yet. 

As you can see, the first thing that can be detected after exposure and with the onset of symptoms is the virus itself. This is depicted by the red and purple lines in the graph. 

After the initial infection, the body begins to mount an immune response and develop antibodies. This is depicted by the orange, blue, and green lines. 

Most of the testing that’s been done so far, mainly in hospitals, has been conducted when people are symptomatic. It’s also important to note that the time between when someone’s exposed to the virus and when they begin showing symptoms is widely variable. Some will show symptoms two days later and others may not show symptoms for three weeks. Others will show no symptoms at all, or only mild ones, yet still be spreading the virus during the first couple weeks of infection.

Time Course for testing after Exposure to SARS-CoV-2
Source:  https://p.widencdn.net/n3trkt/IFM_Sars_Graph_v3

Types of testing

There are two main types of testing, namely viral and antibody. Both have their place in the timeline of events. 

The Viral RNA tests look for an active viral infection. They test for the presence of RNA (ribonucleic acid) from SARS-CoV-2. The test will be positive for someone with a current or very recent infection.3 This test can be undertaken using several methods of collection.

  • Nasopharyngeal swab – This goes into the nose about three or four inches. 
  • Oropharyngeal swab – This down the throat and is similar to a test for strep throat. 
  • Sputum – This is the thick mucus produced by the lungs during an infection. If this can be collected from a person’s coughing, it can be tested. 
  • Saliva – Saliva collection for this test works best after a cough.
  • Stool – Viral RNA can be detected in the stool after an infection.4

A positive test result doesn’t necessarily mean that you’re contagious and are ‘shedding’ the virus. In order to verify that, we’d need to culture your sample in a laboratory. However, there are issues with safety and containing the virus in a laboratory setting, so this type of testing is mostly only done in a research environment at the moment. 

Therefore, we’ll assume that a positive test means you’re contagious and that you need to quarantine for two weeks in order to protect others. It also means that you should watch for symptoms and seek medical care if needed. You can read about treatment options, including herbs and nutrients, here. Tracking positive testing is also important from a public health perspective, in order to trace the spread of the virus.  

Viral RNA testing is going to be most accurate around four to six days after symptoms appear, since this is the peak of the viral RNA production.4 If you wait too long to be tested, you might get a negative Viral RNA test, even though you were infected. This is why this testing has a high false negative rate. You need to get the timing right. If you have a negative test, but a known exposure, you’ll still need to take precautions and may need to be tested again. 

The second type of test that’s helpful is an antibody test. This is a blood test that studies your immune response to the viral exposure. Essentially, it’s looking to determine if you were exposed to SARS-CoV-2 in the past and may be particularly helpful for mild or asymptomatic cases.5 The best time to take the test is about seven days after symptoms resolve or a minimum of fifteen to twenty-one days after exposure. 

There are two main antibodies that current testing is looking at.

  • IgM – This non-specific antibody is produced as the immune system is figuring out exactly what it’s dealing with. If you look at the chart above, you’ll see that IgM rises and then fades away as more specific antibodies (IgG) are produced. 
  • IgG – This more specific antibody takes a little time to develop and then stays high for a period of time.6

This pattern that we’re seeing with SARS-CoV-2 antibodies is typical of what we see with other viruses. 

A positive test suggests that you’ve been infected and that your body mounted an immune response to the infection, whether you had severe symptoms, mild ones, or no symptoms at all. Timing matters here as well. If you test IgG antibodies too early, you might miss them because they take some time, possibly around three weeks, to develop. False positive tests are also possible as some of the tests are detecting previous exposures to other coronaviruses, such as the ones that cause the common cold.4

A negative test might mean that you still need to take precautions to prevent exposure, especially if you’re at higher risk for severe COVID-19. Because of the timeline, it’s important to note that a negative antibody test does not rule out current infection. 

As you can see, the testing is quite nuanced, which is why connecting with your healthcare team for guidance is so important. 

Understanding test accuracy

Naturally, we want a test to be accurate, to be both sensitive and specific. This will limit false positive and false negative results. 

When it comes to accuracy, sensitivity refers to how likely a test is to pick up a positive result in those that have definitely been infected, known as true positives. It’s those that have been exposed to the virus that test positive. Specificity refers to individuals that haven’t been infected by the virus that test negative, which are referred to as true negatives.7. In a perfect world we always want a test to be 100 percent sensitive and 100 percent specific, but this isn’t the case when it comes to coronavirus testing. It can also be similar for many other antibody tests. The poor test results for Lyme disease detection are a good example of this.

We’ve already seen that there are cases of false positives and negatives based on timing and other factors. For example, with a viral RNA test, the nose swab can be really unpleasant so it’s possible that an error can occur as a result of not going deep enough to collect the appropriate sample. Alternatively, there might be low sensitivity because the test picks up antibodies to another coronavirus that are connected to a previous coronavirus infection.4

You might also hear the terms positive predictive value (PPV) and negative predictive value (NPV) in discussion regarding test accuracy. These take into account sensitivity and specificity in terms of the infection rates in a specific population.7 Of course, we need more testing to determine what rates are in each area. This article in Scientific American provides a useful guideline to the testing.

If I have the antibodies, am I immune? 

A conservative answer to this question is that we don’t know for sure. Because this virus is new, we don’t know if everyone that’s exposed develops antibodies, if those antibodies truly mean immunity, and if so for how long.4

However, it’s likely that this virus acts like other viruses that we know more about. For example, for a coronavirus that causes a common cold, you get the cold, develop antibodies, and those antibodies protect you for a while. For something more severe than a cold, such as chicken pox, you can develop immunity for a lifetime. 

You may have heard stories of those that tested positive, negative, and then tested positive again sometime later. However, this is more likely to be an issue with testing methods and timing more than a case of the immune system not creating immunity.  

That being said, I do think that having positive antibodies will be a tool that’s used to help open society up and allow individuals to return to daily life with more confidence.  

Should I get tested?

While I do think that widespread testing is important for both the individual and society, the availability of testing is still quite limited. 

There are many laboratories working to address the issues of access. These include functional testing laboratories, that are frequently used by myself and my colleagues, which are now coming to the market with tests. I have some colleagues that prefer one test over another and others that are waiting for the testing to become more accurate before widely applying it to their patient population. Another factor is that testing through private laboratories is quite expensive. At some point the cost will come down and testing will become more widely available. 

In Canada, we only have access to the provincial laboratory services, whereby they’ll perform PCR testing and antibody testing provided the correct criteria are met. If a private test is requested, we’re able to use certain US-based laboratories. Diagnostic Solutions Laboratory ships their COVID test kits to Canada. They have three test options, which are nasal swab, antibody and stool. 

A German laboratory called Euroimmun AG introduced a test with 100 percent specificity, thus eliminating the chance of a false positive. It’s been approved in the USA. A full list of all the tests approved for diagnostic purposes in all countries is included here at the Center for Health Security website. The Mayo Clinic has also launched an antibody assay with a specificity of 99.3 percent when tested against normal serum. Approximately three percent of serum is IgG positive less than seven days post-symptom onset, 35 percent are IgG positive in samples collected between eight and fourteen days after symptom onset, and 100 percent are IgG positive after fourteen days of symptom onset.

We’ve learned a lot so far about SARS-CoV-2 and COVID-19, but still have plenty that we need to understand. I’ll be keeping a pulse on the new research as it becomes available and will continue these important discussions with my colleagues in order to keep you updated regarding the very latest information. My understanding of this virus is that it’s evolving day by day and although testing is relatively new, it’s still extremely important. 

As we navigate this next wave of outbreak management, testing will be key in order to understand who has active infections, who’s already been exposed, and who may still be at risk. Testing will help us to understand how the virus is spreading, answer important questions about immunity, and ultimately to save lives. My sense is that until the antibody testing can approach a specificity that’s close to 100 percent, it may be worthwhile to wait it out.  

Please don’t hesitate to reach out for support as needed. My team and I are always here for you during this challenging time. 

References: 

  1. Patel R, Babady E, Theel ES, et al. Report from the American Society for Microbiology COVID-19 International Summit, 23 March 2020: Value of Diagnostic Testing for SARS-CoV-2/COVID-19. mBio. 2020;11(2):e00722-20. Published 2020 Mar 26. Full text: https://mbio.asm.org/content/11/2/e00722-20 
  2. The Institute for Functional Medicine. The Functional Medicine Approach to COVID-19: Primer on SARS-CoV-2 Testing. https://www.ifm.org/news-insights/functional-medicine-approach-covid-19-primer-sars-cov-2-testing/ 
  3. Wölfel R, Corman VM, Guggemos W, et al. Virological assessment of hospitalized patients with COVID-2019 [published online ahead of print, 2020 Apr 1]. Nature. 2020;10.1038/s41586-020-2196-x. Abstract: https://pubmed.ncbi.nlm.nih.gov/32235945
  4. The Institute for Functional Medicine. The Functional Medicine Approach to COVID-19: Primer on SARS-CoV-2 Testing Webinar. Hosted by Dr. Patrick Hanaway with Dr. Helen Messier. April 28, 2020. 
  5. Guo L, Ren L, Yang S, et al. Profiling Early Humoral Response to Diagnose Novel Coronavirus Disease (COVID-19) [published online ahead of print, 2020 Mar 21]. Clin Infect Dis. 2020;ciaa310. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7184472/ 
  6. He-wei Jiang, Yang Li, Hai-nan Zhang, Wei Wang, Dong Men, Xiao Yang, Huan Qi, Jie Zhou, Sheng-ce Tao. Global profiling of SARS-CoV-2 specific IgG/ IgM responses of convalescents using a proteome microarray. Preprint article: https://www.medrxiv.org/content/10.1101/2020.03.20.20039495v1 
  7. Abdul Ghaaliq Lalkhen, MB ChB FRCA, Anthony McCluskey, BSc MB ChB FRCA, Clinical tests: sensitivity and specificity, Continuing Education in Anaesthesia Critical Care & Pain, Volume 8, Issue 6, December 2008, Pages 221–223, Full text: https://academic.oup.com/bjaed/article/8/6/221/406440 

A Positive Outlook During the COVID-19 Outbreak

The vast majority of the world’s population that has access to any source of media outlets is currently under the collective fear-driven news cycles of an upcoming apocalypse due to the emergence and spread of the coronavirus, COVID-19.  As I write this, a CCN alert flashed across my screen stating that there were 3,000 cases of coronavirus in the United States with 62 deaths. This number was updated six hours later to 3,155 cases. No doubt by this evening, this number will be adjusted upwards, a trend that will probably increase for the foreseeable future, the exact end-point being entirely unknown.

While all due caution is absolutely imperative and all medical guidance should be strictly followed, as I stated in my other pieces regarding coronavirus, parts one and two, I couldn’t help but reflect on what appears to be an innate tendency of all living systems to trigger homeostatic mechanisms that force self-correction whenever one side of its expression become too polarized to either extreme. It appears that evolution itself has to adjust course in light of new information by self-correcting evolutionary realignments.

We know from history that disasters are often followed by tremendous gains and achievements. The extreme horrors of World War II were followed by an extraordinary period of increased economic, social, and political global growth and relatedness, rather than nationalism, which was unprecedented in history. It was the same with 9/11. Immediately following those events, murder rates plummeted, and kindness and appreciation were unleashed upon civil servants, hospitals, demolition crews, and emergency medical services. Out of control real estate, airline, and hotel prices were corrected, and there was increased dedication to global causes. The list is much more extensive but undoubtedly real, when previous issues and statistics were assessed through this lens. 

One of the greatest and most well remembered political speeches of all time was delivered at the first inauguration by Franklin D. Roosevelt as the 32nd President of the United States. At that time, the nation was at the peak of the Great Depression and the speech was heard by tens of millions of American citizens.  

“So, first of all, let me assert my firm belief that the only thing we have to fear is...fear itself — nameless, unreasoning, unjustified terror which paralyzes needed efforts to convert retreat into advance. In every dark hour of our national life a leadership of frankness and of vigor has met with that understanding and support of the people themselves, which is essential to victory. And I am convinced that you will again give that support to leadership in these critical days.”

He went on to say, “There is no unsolvable problem if we face it wisely and courageously. There are many ways in which it can be helped, but it can never be helped merely by talking about it. We must act and act quickly.”

So, while we’re currently in the grip of the downward, fear-driven spiral that’s mostly emphasizing the potential catastrophic consequences that may or may not result from CoVID-19, how can we best compensate for those fears and reflect on the potential upside of this situation? And most importantly, what can we do to mitigate this fear-driven spiral into ennui, inaction and a potential sense of hopelessness?

What follows are some compensatory ideas that are in no way meant to downplay or minimize the suffering that many people have gone through or are about to go through. However, if we’re to embrace the homeostatic principles that there are no crises without blessings and we don’t live in a one-sided world where there are only losses without gains. So, let’s examine a few potential consequences that might arise from this present situation. 

  1. Global warming. The global warming crisis seemed to be almost impossible to reign in, despite the most well-meaning attempts by a subset of global political and environmental leaders. With all kinds of global travel grinding to a halt, it’s inevitable that at least a pause to the upward tend of global warming, primarily due to the carbon footprint induced by travel, will be inevitable. When climate change experts examine this effect in months or years to come, maybe their statistics can be used to convince others of the need for a more sustained and ambitious action regarding this omnipresent threat.
  2. Exotic animal trade. China stopped the trade in wild animals for the purpose of consumption such as dogs, rodents, yaks, snakes, porcupines, and bats when the link between animals and the coronaviruses was discussed. Officials from the Chinese Center for Disease Control and Prevention said they isolated the virus taken from a seafood and wildlife market in Wuhan believed to be the source of the outbreak. The coronavirus that caused the 2003 SARS outbreak was traced to the civet cat, a wild animal considered a delicacy in parts of South China. The civet is used in the popular dragon tiger phoenix soup, which is believed by locals to help with arthritis, stimulate poor blood flow, and revive decreased libido. The movement of humans toward recognizing animals as sentient beings may be assisted, a movement initiated and kept alive by the PETA president and founder Ingrid Newkirk and written about in her best selling book, Animalkind.   
  3. Consumerism. Our western culture is an extroverted and consumer driven one. Perhaps by sitting at home for extended periods, with the stores, at least at present, bare of many types of consumer goods, we can reflect on our impulse to seek emotional consolation outside of ourselves by buying new items that we may not need. I do realize that the beast of online shopping may be unleashed but here’s hoping that the online stores may not be able transport unnecessary consumer goods due to the transport channels being slowed down. 
  4. Possibility of increased relatedness. A series of recent posts by Rebecca Arendell Franks, who along with her husband and child has now been on forced quarantine in China for over 50 days, is quite illuminating. She said that, “Our family life has never been better. Usually, one weekend is long enough before I’m ready to send each of us back to school or work. But for SEVEN weeks, we’ve been home together with very little outside influences or distraction, forced to reconnect with one another, learn how to communicate better, give each other space, slow down our pace, and be a stronger family than ever before. I encourage you to read the link regarding this at the end of this article. 
  5. Nature emerging from the technological and human encroachment upon its domain. It’s been observed in Wuhan that the sound of birds singing has been heard for the first time in a long time since the crisis began. In Wuhan, Rebecca Arendell Franks commented, “Right now, I hear birds outside my window (on the 25th floor). I used to think there weren’t really birds in Wuhan, because you rarely saw them and never heard them. I now know they were just muted and crowded out by the traffic and people. All day long now I hear birds singing. It stops me in my tracks to hear the sound of their wings.”
  6. Learning new technologies for virtual relatedness. How does ZOOM actually work and can I teach my grandfather to hook up? 
  7. Learning to cook. Maybe we can now, instead of ordering food in or going out to a restaurant, learn to cook for ourselves and make that tasty, healthy recipe that we’ve always been meaning to get around to. 
  8. Examination of our national leader’s skill set in crisis management. 
  9. Exercise. Finally, the Peloton bike or treadmill can be put to good use!
  10. Non-drug based medicine. Examination and renewed interest, along with a certain amount of respect given, of alternative methods for treating symptoms of coronavirus, and indeed other viral related illnesses such as the three studies currently underway in China on the use of IV vitamin C for the treatment of corona related pneumonia. See blog posts part one and two for further details. 
  11. Lifestyle factors. An awareness of how lifestyle factors such as diet, exercise, sleep, and stress play an extraordinary role in immune efficiency.
  12. Business awareness. Small business will become aware of cash flow issues, staffing needs, and unemployment issues.
  13. US Federal Reserve slashing interest rates. Maybe now is the time where one can afford the mortgage on a new home that seemed out of reach a few years before. Or maybe people with fixed student loan payments can borrow money at a lower rate to pay those off. 
  14. Learning to connect with others non-locally. There’s a common misconception that in order to benefit from the full experience of another human being we have to be in their physical presence. Yet if we truly love someone and see both sides, the dark and the light, of their being, we can sit quietly, hold them in our hearts, and send deep love and appreciation to them for being in our lives. It helps if we have an understanding of the Einstein-Podolsky- Rosenberg paradox (EPR paradox) in quantum physics that showed that if one particle had ever been in contact with another particle, if they were separated across the full expanse of the universe in space and time, they’d be eternally intertwined or entangled. Einstein called it “spooky action at a distance.”  

(Please note this is a very simplistic explanation for quite a complex issue.)  

A few more quick possibilities:

  1. Increased revenues for the medical device industry.
  2. Increased revenues for the supplement industry.
  3. Increased connection to neighbours to assist with grocery runs.
  4. Appreciation for the media and their updates.
  5. Appreciation for our doctors, nurses, and miscellaneous healthcare workers and politicians for rising to the occasion and setting minute by minute guidelines
  6. Appreciation for mobile device apps, Google, Facebook, Instagram, and Twitter for keeping us informed.
  7. Appreciation and understanding of our own vulnerability.
  8.  Resetting of values and personal reflection on what is truly meaningful, including a reorganization of values and priorities.  

So, as we step back, reassessing our priorities both personally and collectively, these are a few thoughts I’ve had in these troubling and somewhat frightening times. If Nobel Prize winning chemist Ilya Prigogine is to be believed, even insentient material systems have an inherent drive to self-organization. When physical systems get pushed too “far from equilibrium” they escape this chaos by leaping into higher level states of organized order, referred to as “order out of chaos”. My challenge to all of you is, what inherent dynamic force may be at play in your life, driving you toward greater and greater wholeness, complexity, and consciousness in the midst of these very challenging times? What thoughts of this nature have come to your mind in these times?

While you contemplate these deeper thoughts, stay safe, follow your governmental and health directive guidelines, and do what you need to do to get through these times. We must attempt to move beyond the greatest fear, which is that of fear itself. 

See part one and two for specific coronavirus updates and treatment suggestions. 

Preventive and Treatment Strategies for COVID-19: Part 2

Part 1 of this series can be found here

Keep Fighting Fit

It’s only common sense to keep our bodies as healthy as we can to help us to fight off all kinds of illnesses. Obviously, we’re always going to encounter germs in our daily lives but keeping our immune systems in good condition is an excellent defense strategy. 

Follow these steps: 

  • Get enough sleep, ideally seven or eight hours each night. 
  • Try to reduce stress where you can in your life. 
  • Make sure you’re on a diet that contains plenty of plant-based antioxidants, minerals and vitamins and eat healthy food to keep your body and immune system in good shape. 
  • Make sure that you always get enough exercise whenever you can to keep everything in working order. 
  • Stop consuming all sugar
  • Stop smoking or vaping immediately. 

Wear Mask Protection

Get some N95 facemasks before supplies are gone. 

  • An N95 respirator is a respiratory protective device designed to achieve a very close facial fit and very efficient filtration of airborne particles.
  • The ‘N95’ designation means that when subjected to careful testing, the respirator blocks at least 95% of very small (0.3 micron) test particles. If properly fitted, the filtration capabilities of N95 respirators exceed those of facemasks. However, even a properly fitted N95 respirator doesn’t completely eliminate the risk of illness or death.

N95 respirators aren’t designed for children or people with facial hair. Because a proper fit cannot be achieved on children and people with facial hair, the N95 respirator may not provide full protection.

A full list of FDA approved respirators is provided below. These might already be out of stock everywhere but put orders in regardless of the backorder. 

  • 3M™ Particulate Respirator 8612F
  • Pasture Tm F550G Respirator
  • Pasture Tm A520G Respirator

Wear Eye Protection

Transmission through the eye is a common vector for the aerosolized virus. One of the common transmissions is touching public items then touching your face and transmitting it through the eye. Frequent hand washing and excellent hygiene are paramount.

Drug treatments

General

It’s important to be aware that there are at present no antiviral treatments that are effective for the treatment of Covid-19. There are currently no vaccines available for SARS-CoV-2. The present treatment approach is for supportive care and symptom management only. If people become severely ill, vital organ function support is necessary, usually in a hospital or ICU setting. 

Here’s a link to the number of drugs that as of February 2020 were being studied for the treatment of Covid 19.

The CDC also has a site discussing antiviral medications for the flu here

Chloroquine Phosphate

A Chinese multicenter collaboration group suggested this malaria drug might be useful for the treatment of Covid-19 pneumonia. In another recently published paper, the use of hydroxychloroquine, 400 mg twice daily followed by a maintenance dose of 200mg twice daily for four days, was found to be more potent than chloroquine to inhibit SARS-CoV2. Hydroxychloroquine was also shown to have fewer side effects than chloroquine while still addressing the inflammatory cytokine storm induced by the virus. 

The recommended dose of chloroquine phosphate was 500mg twice daily for ten days. 

Alinia (Nitazoxanide)

This drug is traditionally is used as an antiparasitic and has been studied for the treatment of Middle East Respiratory Syndrome (MERS) coronavirus. This drug has been shown, in test tube studies at least, to have activity against MERS-CoV and other coronaviruses. Further studies are being undertaken to determine its true efficacy. The recommended dose was 1000mg twice daily for 10 days.

HIV Drug - Kaletra (lopinavir-ritonavir)

A 62-year-old man who became Spain’s first coronavirus patient is believed to have made a full recovery after being treated with an HIV drug called Kaletra or lopinavir-ritonavir. Miguel Ángel Benítez was admitted to the Virgen del Rocio Hospital in Seville, where he received an antiretroviral drug, which has been used to treat HIV and AIDS for over ten years. The drug was combined with interferon beta, which is a protein that prevents cells from becoming infected and is administered to multiple sclerosis patients. Santiago Moreno, head of infectious diseases at the Ramón y Cajal hospital in Madrid, said that the “SARS-CoV-2 protease is very similar to that of HIV,” using a name that sometimes refers to the novel coronavirus.

Mast Cell Activation Syndrome (MCAS

In this February 2020 article it was discussed that “Coronavirus infection (regardless of the various types of corona virus) is primarily attacked by immune cells including mast cells (MCs), which are located in the submucosa of the respiratory tract and in the nasal cavity and represent a barrier of protection against microorganisms. Virus activate MCs which release early inflammatory chemical compounds including histamine and protease; while late activation provokes the generation of pro-inflammatory IL-1 family members including IL-1 and IL-33.” The article proposes for the first time that inflammation by coronavirus may be inhibited by anti-inflammatory cytokines belonging to the IL-1 family members. 

It may be that individuals with MCAS are at higher risk for developing the serious consequences of this infection and thus may benefit from much stricter control of the mast cell activation syndrome if infected. Nebulized cromolyn and/or glutathione or n-acetyl cysteine (NAC) and/or IV Benadryl may be extremely helpful in these conditions.

Alternative Remedies

In addition to the previous suggestions, there are a number of natural substances and supplements that can be of help in lowering your risk of becoming infected with the current coronavirus. Many of these approaches are not specific treatments for the coronavirus but have been studied and referenced in the literature as having antiviral effects.

Vitamin C

It’s common knowledge that vitamin C is good for us but there have been clinical trials in China regarding the intravenous use of vitamin C to help treat patients suffering from Covid-19. A dose of between 100 and 200 mg/kg body weight (this is equal to quite a low dose of between 7.5 and 15 grams for a 180 lb person) was given to patients intravenously for three consecutive days and was very effective. There are currently three clinical trials sponsored by the Chinese government studying vitamin C. Dr. Tom Levy and Dr. Jeanne Drisko from the integrative U.S. medical community are involved in the Chinese studies. Dr. Richard Cheng MD PhD, who has been studying IV vitamin C, is suggesting the use of oral vitamin C.  The one study can be found at the clinicaltrial.gov website. High dose vitamin C at 20 grams has been used in ICUs for some time in an attempt to reduce mortality from septic shock, in one study from 40% to 4%. However, most hospitals refuse to administer IV vitamin C for viral infections since it’s not considered standard of care. It’s quite likely that these Chinese studies will place high dose IV vitamin C therapy for viral infections a part of mainstream treatment in the future.   

In the United States, doctors who have pioneered vitamin and mineral therapies have also been studying the effects of intravenous vitamin C, with a February 2020 paper being published. “Early Large Dose Intravenous Vitamin C is the Treatment of Choice for 2019-nCov Infected Pneumonia” recommends this for the treatment for pneumonia resulting from the virus. 

A recommended minimum oral daily dose of vitamin C is 2,000mg. Twice daily dosing is recommended due to the water-soluble nature of vitamin C and the fact that it’s quickly metabolized. If one wants a liposomal formulation, certain brands do provide this option or you can make your own by adding https://klinghardtinstitute.com/one or two teaspoons of Body Bio PC (phosphatidyl choline) to 2 grams of powdered vitamin C and stirring it vigorously. Divide your dose and take twice daily. Watch for diarrhea if your dose is excessive.

Vitamin D

This is also very important. It’s recommended that we have a minimum of 2,000 IU and a maximum of 10,000 IU per day. The usual daily dosage for vitamin D is 1000 IU per 25 pounds of body weight. It’s best to get vitamin D levels measured and to have serum levels in Canada between 150 and 200 nmol/l. People tend to have lower vitamin D levels in the fall and winter months due to fewer hours of sunlight. However, our bodies need vitamin D to support our immune system so we need to make sure that we’re getting enough of this vital ingredient. All the cells in our bodies have receptor sites but only two types are in every cell. These are thyroid hormone receptor sites, which are responsible for metabolism, and vitamin D receptor sides. This gives you some idea of the importance of vitamin D in maintaining our overall health and wellbeing. Research indicates that vitamin D may even be more effective than the flu vaccine when it comes to flu prevention. Consequently, it’s a good idea to include vitamin D in the fight against Covid-19.

It has been reported by many clinicians that high doses vitamin D of 50,000 IU over three days is highly effective in treating acute viral infections. This dosing is contraindicated in any person with lymphoid malignancies and in any patient with granulomatous diseases such as sarcoidosis, where high calcium levels are an issue. Also, a relative contraindication is pregnancy. This is by no means an approved treatment for Covid 19.   

Zinc 

This has been shown to be effective in fighting infections and also supports the immune system. Zinc can help to prevent coronavirus and other viruses multiplying in the throat and nasopharynx, which is the space above the soft palate at the back of the nose connecting the nose to the mouth and allowing us to breathe through our nose. When you begin to exhibit symptoms of the illness zinc capsules can be taken several times a day. The recommended dose for zinc is between 40 and 50mg per day.

Silver 

This has also has some antibacterial and anti-viral properties. If you use an official product such as Argentyn 23 you have a clear idea of how much silver you are putting into your body and don’t run the risk of taking too much. If you have viral symptoms, the recommended dosage is one teaspoon seven times per day. However, this is only a short-term solution as there are side effects such as skin discoloration if silver is used for too long.

Andrographis 

This herb has been used in traditional Chinese medicine and Ayurveda for a long time. It’s been shown that the herb’s compounds have anti-inflammatory, antiviral, and antioxidant benefits. The herb boosts the immune system and is often employed to fight cold and flu symptoms. As a result it does have a role to play in treating the latest version of coronavirus, at least in the short term. One capsule twice a day is the recommended dose of the herbal supplement if you exhibit symptoms of the virus. There are a number of referenced articles that demonstrate its effectiveness against the influenza virus, particularly with regards to respiratory symptoms. Lyme patients with active disease may have a Herxheimer reaction as it increases lymphocyte proliferation and interleukin -2. 

Elderberry

Another natural short-term solution if you have typical flu symptoms, such as a cough, sneezing, and a runny nose, is elderberry extract taken up to six times a day. Elderberries come from the European elder tree, which is not the same as the American Elder, Elderflower, or Dwarf Elder. People believe the extract helps with the common cold, influenza, boosts the immune system, and reduces inflammation.

Calendula

Is also known as marigold and has been used as a medicinal herb for a very long time. The plant’s extracts have antiviral, antigenotoxic, and anti-inflammatory properties that can be used to treat some of the symptoms of Covid-19. 

Taraxasterol 

Also known as dandelion, this can also be used as an anti-inflammatory supplement. Dandelion also has antioxidant properties and some studies indicate that it has antiviral benefits and is good for our immune system. 

Propolis 

This is known to be a potent antiviral, particularly in animal models infected with corona virus. Dr. Ramzi Asfour, an infectious disease physician, suggests Beekeeper’s Natural propolis spray. Propolis increases cellular immune responses and has antiviral properties. Propolis can also be dispensed in a vaporizer (available from Ki Science) and has been shown to neutralize circulating mycotoxins in the air. 

CAUTION: Propolis is not to be taken if you have a Honey or Bee allergy.

Scutellaria

Most commonly known as skullcap, this is another flowering plant with medicinal qualities. It has been used to treat conditions such as respiratory infections and inflammation and have antibacterial, antiviral, and antioxidant properties. 

Artemisia annua

Also referred to as sweet wormwood this has been used in traditional medicine for some time and has been employed in medicines to treat malaria. There are some indications that the plant may also be used to treat some coronavirus symptoms, particularly the SARS related coronavirus.

Dr. Klinghardt, in his extremely informative PowerPoint presentation, has recommended placing calendula, licorice, scutalaria, andrographis, artemisia, and dandelion tinctures, calculated for their weekly dose, in a blender with 100mls of clean water and 14 grams of vitamin C powder. Add two tablespoons of liquid Body Bio PC phosphatidyl choline and blend for a few minutes. Put this mixture in a glass and keep in the fridge. Each day, drink one seventh of the dose.

Beyond Balance Herb Tinctures- IMN-V-III

This product contains 19 different herbs with antiviral and immune modulating effects, including licorice, skullcap, dandelion, and rosemary.

Peptides

Some patients have access to peptides with immunomodulating effects. I recently returned from a peptide conference in Los Angeles and the following peptides were suggested for their antiviral and immune modulatory effects.         

  • Thymosin alpha 1 - This is the most recommended peptide for immune stimulation. This should be used as a treatment adjuvant and a prophylactic and can help with many conditions beyond viral illness. The recommended daily dose in 450mcg.
  • Thymosin beta 4 - Natural killer cells are essential for defense against tumors and virus-infected cells. The cells are activated in by ONF-Gamma. This is activated by IL-18, which TB4 upregulates. Therefore, TB4 has ben studied for many Immune related diseases. Caution is warranted with cancer patients as it can increase the growth of cancers.
  • LL 37 (cathelicidin) - This peptide has broad spectrum antiviral/microbial, fungal effects. Peptides such as LL 37 are key components of innate defenses against infection, with both microbial and host defense modulatory functions. In addition to their well documented bactericidal potential, CHDP have more recently been shown to have antiviral properties. LL 37 has ben shown to be highly effective in preventing viral attachment to cells. It’s been used in several virus studies and has been anecdotally reported to work well with respiratory tract viruses.
  • Pentosan polysulfate - Polysulfates are highly potent and selective inhibitors of the in vitro replication of HIV and other enveloped viruses such as coronavirus. The anti-viral activity of polysulfates is a result of their shielding of the positively charged sites in the V3 loop of the viral envelope glycoprotein gpl120, which inhibits viral entry into cells and allows for immune clearance. The usual dose is 2mg/kg.
  • Selank - This is a variant of the immune molecule tufstin and has potent antiviral properties in addition to its neurological effects. The antiviral characteristics of Selank were evaluated both in vitro and in vivo against the influenza virus strain H3N2 and H5N1 and the type 1 and 2 Herpes virus. It was revealed that Selank might have a prophylactic effect during influenza infection and a therapeutic effect during a herpes virus infection. It could also be helpful with Covid-19.

The Hoffman Centre Programs for cold and flu treatment

We have developed a number of potential programs for acute cold and flu treatment. While the details aren’t specific to coronavirus many of the recommendations are applicable to dealing with virus that commonly infect us in the winter months. These recommendations are in no way a substitute for quick and rapid communication with your healthcare providers and the guidelines as issued via websites (like this one), previously mentioned at the beginning of this article.

Any treatment that you decide to undertake should start at the first onset of symptoms. The following instructions are to be followed for the duration of symptoms unless otherwise stated. 

Immediately stop consuming any sugar, since this paralyzes your white blood cells, the body’s first defense against illness. Make sure you also get plenty of sleep, at least between 7.5 and 8.5 hours per night. Hot apple cider vinegar baths twice a day will help to speed up the progression of the cold and reduce your fever, potentially halving the amount of time you may have symptoms. Add two cups of apple cider vinegar to a full bath of hot water and soak for twenty minutes, remembering to fully submerge your body. If the illness has affected the chest, you can steam water over the stove, add eucalyptus drops, and breathe in the vapor for some relief from your symptoms.

Please note that this treatment program is not to be undertaken if you are pregnant or breastfeeding.

Adult Dosage (age 16 and up)

Oscillococcinum is the first supplement to take at the first sign of a cold or flu. This works better for flu like symptoms (not cold symptoms) and you simply need to follow the directions on the package.

  • Vitamin D - 50,000 IU for three days. Contraindication to use of high dose vitamin D is lymphoid malignancies, pregnancy, and granulomatous diseases such as sarcoidosis
  • Mycelized vitamin A - 100,000 IU for three days. Contraindicated in pregnancy. 
  • Vitamin C - 1 to 2g two to three times daily (titrate dose upward to bowel tolerance)
  • Astragalus Tincture - 1 dropper three times daily
  • Echinamide Anti-Cold tincture - 2ml three times daily
  • Probiomax probiotic - 1 capsule two times daily 
  • Saccharomyces Boulardii - 2 capsules twice daily
  • Garlic/allicin - 2 capsules three times daily after meals. Open the capsule in 6oz of water and let sit for two minutes before drinking.
  • Argentyn 23 colloidal silver  - 1 teaspoon three times daily in water
  • Andrographis - 2 dropperfuls twice daily in water
  • Transfer Factor Multi Immune - 2 capsules twice daily
  • DHEA - 50mg per day for two to three days will boost the immune system and fight infection. Note that this is for adults only.
  • For muscle aches take arnica and/or magnesium malate - 2 caps three times daily
  • Add anti-viral supplements such as olive leaf extract - 2 capsules three times daily, oil of oregano (brand name ADP) 2 capsules three times per day and lysine 500mg 2 capsules three times daily

IV Treatment for 3 days

  • IV vitamin C - 15 to 35g once per day. Check for G6PG enzyme deficiency first
  • Alternatively - IV Hydrogen Peroxide, once per day

Child Dosage (2 years and older)

    • Mycelized vitamin A – 10,000 IU for three days
    • Vitamin D - 10,000 IU for three days
    • Vitamin C - Between 250 and 500mg three times daily (to bowel tolerance)
    • Echinamide Anti-Cold - Between an third and a half a dropper three times daily 
    • Probiomax probiotic  - Half a capsule twice daily
    • Saccharomyces Boulardii - Half to a full capsule twice daily
    • Garlic - Half to a full capsule twice daily after meals. Open capsule in 6oz of water and let sit for two minutes before drinking. Note that it is difficult to get a child to take this.
    • Argentyn 23 colloidal silver - Half a teaspoon three times daily in water
    • Transfer Factor Multi Immune - 2 capsules daily

Maintenance and Prevention 

Remember to stop consuming any sugar immediately, since sugar paralyzes your white blood cells, which provide your body’s first defense against sickness. Make sure you get at least 7.5 to 8.5 hours of sleep each night as well. This treatment program is not for women that are pregnant or breastfeeding.

Throat Infection

  • Zinc - 30 to 50mg lozenges. The topical antimicrobial effect can be important in infections of the throat.
  • Biocidin throat spray - 2 sprays three to five times daily
  • Propolis throat spray – 5 sprays three times daily
  • Argentyn 23 throat spray- 3 sprays three times per day
  • See your doctor for a throat swab to exclude strep throat and/or mononucleosis

CAUTION: Propolis is not to be taken if you have a Honey or Bee allergy.

Nasal Irrigation

Use a Neti Pot, particular with upper respiratory infection, for three days. 

  • Place one dropper full of Nasya wash into your Neti Pot with warm water and a heaping quarter teaspoon of pure non-ionized Neti Pot Salt. 
  • Stir until salt is dissolved. 
  • Add three drops of Echinacea Anti Cold and Core Phyto Lavage to the solution. Use this to perform the nasal wash as directed by the Neti Pot instructions on the bottle.

Air Spray

  • Add a quarter teaspoon of salt to the bottom of an empty spray bottle. 
  • Add five drops of Thieves, an essential oil by Young Living, on top of the salt as this will help to dissipate it, 
  • Fill bottle with warm water. 

Now you now have an air spray that will assist in lowering counts of viruses, bacteria, and molds in the air. 

  • Spray your home, office, and other areas a couple of times a day. 
  • You can also put Thieves drops into your palms and cup your hands over your face then inhale five or six times. 
  • This will prevent you from contracting a sinus or lung infection, especially during long distance flights.

Dr. Alex Vasquez Recommendations

Dr. Alex Vasquez is an internationally recognized author, presenter, and teacher, particularly with regards to immune related disorders. He earned three doctorate degrees from fully accredited universities in the United States and has worked in various clinical facilities ranging from private boutique clinics to inpatient hospital settings. Dr. Vasquez has published 120 books, articles, letters and editorials in various magazines and peer-reviewed medical journals, including British Medical Journal, Journal of the American Medical Association, Nature Reviews Rheumatology, and Annals of the New York Academy of Sciences.

What follows are his recommendations for viral infections and are not meant to be specific treatments for any infections, particularly coronavirus. I’ve included these references for those curious patients who are always checking out protocols online.  

Antiviral

  • Powdered Glycyrrhiza Glabra - 1.5g BID for a maximum of four weeks. Works as a tea. This is a great expectorant but avoid in heart failure patients, monitor BP and potassium
  • Zinc - Between 20 and 50mg a day
  • Selenium – 400 to 600 ug per day
  • Iodoral Iodine/Iodide - 12.5mg a day for two weeks
  • Melissa officialis - Dose variable depending on formulation
  • Carica papaya leaf extract
  • Grape seed extract (see Biotics Research Bio-Cyanidins below)

Viral Anti-replication

  • SAMe - 400mg TID plus Betaine TMG 3g BID for one week
  • Methyl-Folate - 1.6mg od for one to two weeks
  • Alpha Lipoic Acid - 300 to 400mg TID plus Thiamine 100mg (or B Complex High Potency)
  • NAC - 600mg BID to TID between meals

Immunonutrition

  • Paleo-Mediterranean Diet with no refined carbohydrates 
  • Protectamin Whey Protein - 45g a day for immune dipeptides, if dairy tolerant
  • L-Glutamine powder - 9g TID between meals 
  • Vitamin A - 100,000 IU load for three to five days, then 25,000 to 50,000 IU for two weeks (not during pregnancy)
  • Vitamin D3 - 100,000 to 300,000 IU load for one dose, then 10,000 IU for ten days to increase endogenous antimicrobial peptides
  • Nordic Naturals Arctic Cod Liver Oil without vitamin D - One teaspoon TID with meals
  • Selenium - 600-800mcg/d plus 800 IU vitamin E per day
  • Melatonin - 20mg qHS
  • Ubiquinol CoQ10 - 300mg od to protect the mitochondria
  • Biotics Research KappArest - Three capsules BID as NFKB hijacked by viruses for replication
  • Biotics Research Bio-Cyanidins - One tablet BID (contains marine pine bark and grape seed extract)
  • Biotics Research UltraVir-X - One capsule TID (Red-rooted sage, Boneset, Actratylodes, Sweet Violet, Wheat Grass, Bupleurum, Astralagus, Bee Propolis, Maitake, Black Walnut, Hesperidin, Rutin)
  • Biotics Research POA-Phytolens (Cats’ Claw, Lens esculenta extract) - One capsule TID
  • Consider broad spectrum multi such as Metagenics PhytoMulti at two tablets per day (adjust dosage of Zinc and Selenium above)

CAUTION: Propolis is not to be taken if you have a Honey or Bee allergy.

Treatment and Vaccines

  • There is no vaccine currently available to combat the current coronavirus outbreak. 
  • The best advice is to protect yourself in some of the ways outlined above and avoid contact with infected individuals or locations where you might encounter potential carriers of the virus. 
  • There’s no specific antiviral treatment that’s recommended for patients with the Covid-19 virus. 
  • Those infected should receive the medical treatment required to deal with their symptoms, including care of vital organs in the most severe cases. 

In Conclusion

  • While we still don’t know everything about the current Covid-19 virus, common sense and taking precautions and preventative measures will be a great help. 
  • The feeling in the medical community is that the virus is likely to become less aggressive and less dangerous over time, as many viruses do, although this is far from certain. 
  • Many viruses adapt, mutate, and continue to live with us everyday. Time will tell if the latest threat will follow the same pattern in the coming weeks and months.

As a final note, in the current circumstances, if you’re suffering from what you’d describe as symptom similar to flu such as a cough, fever, chills, or an aching feeling in the body, please don’t visit the office. If you have an appointment we can do a phone consultation instead or even connect via zoom online. Staying at home will allow you the opportunity to recover and also reduce the likelihood that you’ll pass on the virus to others.

Resources

 https://www.cdc.gov/coronavirus/2019-ncov/about/prevention.html?CDC_AA_refVal=https%3A%2F%2Fwww.cdc.gov%2Fcoronavirus%2F2019-ncov%2Fabout%2Fprevention-treatment.html
 Courtesy of Tailor Made Pharmacy  
https://www.cdc.gov/coronavirus/2019-ncov/about/prevention-treatment.html 
 Expert consensus on chloroquine phosphate for the treatment of novel coronavirus pneumonia. Zhonghua Jie He He Hu Xi Za ZHi 2020 Feb 20. 43:E019
https://www.ncbi.nlm.nih.gov/pubmed/32150618
 https://www.sciencedirect.com/science/article/pii/S1876034116300181
https://nypost.com/2020/03/05/coronavirus-patient-in-spain-reportedly-recovers-after-being-treated-with-hiv-drug/
https://www.ncbi.nlm.nih.gov/pubmed/32013309/
https://clinicaltrials.gov/ct2/show/NCT04264533
 http://orthomolecular.org/resources/omns/v16n11.shtml
 Epidemic Influenza and Vit D. https://www.ncbi.nlm.nih.gov/pubmed/16959053
 https://www.argentyn23.com/
 https://link.springer.com/article/10.1007/s00705-016-3166-3
 Biol Pharm Bull. 2009 Aug; 32 (8) : 1385-91
https://www.webmd.com/vitamins/ai/ingredientmono-434/elderberry
 http://insajournal.in/insaojs/index.php/proceedings/article/view/305
https://www.ncbi.nlm.nih.gov/pubmed/28480383
 Ferreira L, Effect of the ethanolic extract from green propolis on production of antibodies after immunization against canine parvovirus (CPV) and canine coronavirus (CCOV). Brazilian Journal of Veterinary Research and Animal Science 49.2 (2012):116-121. http://www.revistas.usp.br/bjvras/article/view/40267
Dr Horowitz newsletter 
 https://kiscience.com/product/propolair-propolis-diffuser-therapy-model/
 https://www.sciencedirect.com/science/article/pii/S2211383520302999
http://www.hdbiosciences.com/Download/Identification%20of%20natural%20compounds%20with%20antiviral%20activities%20against%20SARS-associated%20coronavirus.pdf
 Antiviral Research 67, No 1 (2005): 18-23
 https://klinghardtinstitute.com/
 Courtesy of Tailor Made Pharmacy.
 https://www.inflammationmastery.com/

What You Need to Know About COVID-19: Part 1

Every day brings a new update about the spread of coronavirus. There are more cases all around the world every day and naturally people are very concerned. There’s certainly not a shortage of stories in the media but is the virus as dangerous as it’s being portrayed? And is the hysteria that’s being generated potentially more damaging than the threat posed by the virus?

In Canada, you can get the very latest updates courtesy of the federal government, including the current situation in different parts of the country, the risk to Canadians, how the government is monitoring the virus, travel advice, and the symptoms, treatment, and risk factors here.

A similar range of information is available for Alberta residents here. For those of you in the U.S. you can access pertinent information here

Mass panic is certainly not going to help the situation but neither will complacency. Despite the fear being whipped up on social media and in the traditional media reports, it’s perfectly natural to be anxious about this situation. This outbreak isn’t to be casually dismissed as it is very serious and everyone needs to accept that and not be in denial. We all need to work together to get through this. We may not know everything about the coronavirus yet and vaccines, treatment and indeed cures are still some way off, but we need to determine strategies that are going to work to protect ourselves and prevent the spread of the virus. So what exactly is coronavirus?

The Virus

Coronavirus is an illness that mostly affects our respiratory system. Doctors are still learning about the virus but it is thought to primarily be airborne, which means that it can be spread from one person to another. When a person coughs or sneezes they produce what are known as respiratory droplets. These can be breathed in by other people that are nearby or left on your hands if you touch your face after coughing or sneezing. In China, the fact that the illness seems to be mainly transmitted to family members, healthcare workers and others in close contact with an infected person strongly indicates the transfer of the virus is by respiratory droplets. The droplets can also remain on objects that have been touched, such as door handles, keyboard, elevator buttons, and many other everyday items. The virus can then spread if a person comes into contact with a surface that’s been contaminated. 

It has been suggested by recent studies that asymptomatic patients are also able to transmit the infection. This means that isolation might not be as effective a weapon against the virus as was previously thought. Researchers followed viral expression through infection through throat and nasal throat swabs in a small select group of patients. The researchers discovered that there were increases in viral loads at the point when the patients became asymptomatic. Doctors in Wuhan, China, studied 425 patients that had the virus. Many of the earliest cases were linked to direct exposure to live animal and seafood markets. However, later cases were unconnected to the animal markets, reinforcing the theory that the virus is transmitted between humans. 

There are believed to be many different types of coronavirus but only 7 of them can cause disease in humans. Some of the coronaviruses that usually affect animals are also able to infect people. The diseases Severe Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome (MERS) are also caused by coronaviruses that moved to people from animals. Like MERS and SARS, COVID-19 is believed to have originated in bats. Before the illness was brought under control in 2003, SARS infected more than 8,000 people and almost 800 died. 2,465 cases of MERS have been reported since 2012 and 850 people have died. The mortality rate for SARS was around 10%, whereas for MERS the mortality rate is around 34.5%.

The coronavirus that is currently in the news is called SARS-COV-2 (formerly called 2019-nCOV). The disease that it causes has been called Coronavirus disease 2019 (Covid-19). Once someone has the virus, the symptoms can be very mild but for some people they can be very serious and endanger life. Although we’re still learning about COVID-19 it does seem to be milder in its effects than SARS or MERS, with only a 2% mortality rate. Initially, the World Health Organization (WHO) reported that the worst severe cases in China were mostly in adults over 40 years old with significant comorbidities. This means that the patient has more than one chronic medical condition. The illness also seemed to affect more men than women, although this could change as the outbreak continues. As of March 12, 2020, COVID-19 had been confirmed in more than 128,343 people, mostly in China. To date 68,324 people have recovered from the infection. By this date, the virus had caused more than 4,720 deaths and has spread to more and more countries. These websites have information on the global situation that is updated regularly. Keep in mind that an estimated 291,000 to 646,000 people die worldwide from flu every year.

Symptoms of Coronavirus

A person that has Covid-19 might not show any symptoms at all for between 2 and 12.5 days, with the average time being 5.2 days. This one can easily pass it on to others without even knowing that they are infected in the early stages. The average time from infection to symptoms appears to be 12.5 days. The pandemic worldwide appears to be doubling every 7 days and every infected person appears to infect an average of 2.2 others.

Symptoms can include:

  • Fever
  • Cough
  • Breathing difficulties and shortness of breath.

While some of the symptoms are similar to colds and flu that people suffer from throughout the year, there are important differences. With the common cold we suffer from a runny nose and there is sputum or phlegm. This is the mixture of mucus and saliva that we cough up from our lungs when we get sick. With the coronavirus there’s a dry cough but no runny nose. This may occur in a small percentage of patients (4%) but it’s thought this is because they already have some form of flu or cold symptoms.

If nasal congestion does occur with this virus, it is usually very severe. If there is an associated sore throat, it can last for three or four days. The virus might then move to the trachea and lungs, resulting in pneumonia that can last for five or six days. Breathing difficulties and a high fever are also likely at this stage of the illness. People infected might have one or more other symptoms including headaches, muscle pain and stiffness, fatigue, loss of appetite, chills and sweats, a rash, dizziness, stomach upsets, or nausea. Numbers do vary but around 90-98% of people have a fever, 80% a dry cough, and 30% have trouble breathing and extreme fatigue. Acute respiratory distress syndrome developed in about 29 % of patients infected. Even though pneumonia is involved, 80% percent of these cases are mild and the person doesn’t need to go to a hospital. About 15 % had severe infection and 5 % were critical. The Chinese CDC analysis of 44,672 patients reported that the fatality rate on healthy people with no reported comorbid conditions was 0.9%.  

In general, children, younger people, and young adults seem to get mild versions of the illness. Those at the highest risk are people aged 70 to 75 or older that have existing medical conditions such as cardiac problems or pulmonary issues such as emphysema. The virus is also more likely to affect people with weakened immune systems, kidney disease, diabetes, hepatitis B, and cancer.

Protecting Yourself

There are a number of ways that you can protect yourself from being infected by the Covid-19 virus. Many of these are things should be part of our daily routines to prevent the spread of germs and keep our bodies healthy.

  • Washing your hands regularly throughout the day with soap and warm water for at least 20 seconds each time will help to keep infection at bay. 
  • All surfaces of the hands need to be cleaned, front and back, between the fingers and under the nails. You can use an alcohol-based non-toxic hand sanitizer (60% alcohol-based) if there’s no soap and water available. However, always use soap and water rather than hand sanitizer whenever possible. 
  • Always wash your hands before eating and touching your face. This is something you may have heard quite often recently, but infection can be spread via the nose, mouth, or eyes if your hands aren’t clean. Admittedly, the virus can only survive on your hands for between and ten minutes but although that may not seem long you could touch another part of your body in that time and spread the virus. 
  • Things that are frequently touched in the home, workplace or other locations must be regularly cleaned and disinfected with wipes or cleaning sprays. The virus can survive for up to twelve hours if it falls onto a metal surface. On fabric it lives for between six and twelve hours but regular laundry detergent will destroy the virus.
  • Gargling can work to protect your throat from the virus. You can use a standard solution from the drugstore but really one made from salt in warm water is all you really need. 
  • It’s also a good idea to drink plenty of warm liquids such as tea rather than cold drinks, either with or without ice. 
  • Some people have also found bee propolis mouth spray to work well. Propolis is a substance created by bees to protect their hives against bacteria. As a spray it helps to relieve a sore throat or other mouth issues and strengthens the immune systems. It also encourages antioxidants in our bodies. Antioxidants are molecules that neutralize free radicals, which are unstable molecules cause cell damage. CAUTION: Propolis is not to be taken if you have a Honey or Bee allergy.
  • If you’re showing no symptoms and remain healthy, avoid contact with others that are sick since the virus is considered to be airborne and spreads very quickly. It’s believed that the virus can travel between six and eight feet when it’s airborne. 
  • If you are sick with the virus, avoid contact with other so that you don’t help the virus to spread. Stay away from work or school and isolate yourself at home until you can recover. 
  • If you’re coughing and sneezing, try not to do this into your hands but into the crook of your arm or use a tissue to cover your nose and mouth and ensure that tissues are safely disposed of in the garbage. 
  • If you’re sick and have no choice but to go outside your home, wear a mask that covers your nose and mouth. This will stop you from infecting others while you’re out. However, bear in mind that if you don’t already have the virus a mask this will not protect you from catching the virus from an infected person that isn’t wearing a mask.

To Follow: PREVENTIVE STRATEGIES AND TREATMENT SUGGESTIONS 

Resources

https://www/medscape.com/viewarticle/924268.
https://www.nejm.org/doi/10.1056/NEJMc2001737
https://www.nejm.org/doi/full/10.1056/NEJMoa2001316
https://www.youtube.com/channel/UCMONnSecl445zOPy7-KXJKw?utm_source=Klinghardt+Institute+Newsletter&utm_campaign=72be1085f0-EMAIL_CAMPAIGN_2020_03_09_05_16_COPY_01&utm_medium=email&utm_term=0_e85a79fc40-72be1085f0-154835213&mc_cid=72be1085f0&mc_eid=980e013edf 
 https://www.medscape.com/viewarticle/924268.
https://www.arcgis.com/apps/opsdashboard/index.html#/bda7594740fd40299423467b48e9ecf6
 https://www.cdc.gov/coronavirus/2019-ncov/locations-confirmed-cases.html
http://cdc.gov/media/releases/2017p1213-flu-death-estimate.html
Li Q, Guan X, Wu P, et al. Early Transmission Dynamics in Wuhan, China of Novel Coronavirus-infected Pneumonia. N Engl. J Med. 2020 Jan 29 
 https://www.cdc.gov/coronavirus/2019-ncov/about/symptoms.html
 https://www.cdc.gov/coronavirus/2019-ncov/about/prevention.html?CDC_AA_refVal=https%3A%2F%2Fwww.cdc.gov%2Fcoronavirus%2F2019-ncov%2Fabout%2Fprevention-treatment.html