Lecture: 11th Annual CHNC, Mild Cognitive Impairment

Since 2000, deaths from heart disease have decreased by 14%, while deaths from Alzheimer’s disease have increased by 89%. Alzheimer’s disease is the third-leading cause of death in the USA. There is a major distinction between just memory loss and a wider range of cognitive abilities and decline.

In this lecture, Dr. Hoffman discusses how to differentiate between mild symptoms of cognitive decline versus those of advancing Alzheimer’s dementia. Only 5% of all incidents of Alzheimer’s disease are considered genetic in origin; the rest are caused by lifestyle factors over which we can exert significant control.

Dr. Hoffman also talks about the different subtypes of Alzheimer’s disease, many of the 150 potential risk factors for their development and the lifestyle, nutritional, hormonal and medication interventions that can make a marked difference in patient outcomes.

Mild Cognitive Impairment 11th Annual CHNC Part 1

Dr Bruce Hoffman

Mild Cognitive Impairment 11th Annual CHNC Part 2

Dr Bruce Hoffman


Dr. Bruce Hoffman:

And so, I look at the broader model, the seven levels of healing, I look upstream, I look at the family system. Epigenetically, you don’t escape the fate of your forefathers. Whatever fate your forefathers went through, you don’t escape it, you epigenetically manifest their experiences and if they have unresolved experiences, traumas, murders, deaths, you do not escape the effects. It has been studied extensively, many studies now, mainstream research, this is not esoteric research, with children that have been born since the world trade centres went down- higher incidence of PTSD even though they weren’t there. These events were just epigenetically transmitted.  

We know through cognitive behavior therapy that if you don’t change the way you interpret reality, you can release a whole storm of inflammatory and toxic neurochemistry which then influences your cellular expression of micro RNA, which then influences metabolic cellular outcomes; so your very thoughts, every single thought you think, 60,000 thoughts a day depending on how you bias those thoughts, determines physiological outcomes. That’s what CBT is all about. Those of you know about CBT- (cognitive behavioral therapy) – is all about changing the way you interpret reality, based on a new world view or interpretation. We have a saying in this work that we don’t heal until we actually have a new image, a new way of interpretation, a new way of looking at the world, a new story. Also, we don’t heal until we align ourselves in an accepting if not loving way with our mothers and fathers, and our ancestors. Those of you who hate your mothers and fathers. Those of you who cut off from your mothers and fathers. Those of you who judge your mothers and fathers for not having given you enough. You need to maybe open that up and look a bit closer because you are half your mother and you are half your father. How are you going to heal and cut off half your lifeforce? You can’t do it.  I tell my kids, when they need new partners, I say to them, here’s your screening tool, the one question to ask the person in front of you to whom you are potentially attracted to, “how are you with your mother and father”? Just ask the question. If they tell you that they hate their mother and father, and that they never want to see them again, run like hell. It’s not going to go well. And I tell you that’s a very reliable indicator for how people are in the world. So we use a much larger, larger model to view and interpret people’s health.

Just by way of some definitions. Dementia is when cognition fails, but Alzheimer’s is characterized by particular findings that you find in the brain. The tangles, and the amyloid plaque that defines Alzheimer’s and although it starts with memory loss, it very soon ends up in the inability to formulate language, and then socialize, and then eventually end up in the with the reptilian brain expression where you barely function. You can eat, you can sleep, but your whole orientation to the world outside of you is shut down. 

There are different types of dementia. Alzheimer’s is the most common, but there are other types. Neurologists are extraordinarily good diagnosticians. So, if anybody has a dementing process, or cognitive decline, you really do want to see your neurologist because they have the ability to really discern the subtleties of different types of dementia, and what differentiates Alzheimer’s disease from other forms of dementia. As I said there is the APOE4 gene- if you have the APOE  3/3 gene, you have a 9% risk of Alzheimer’s. If you have the 3/4 gene you have a 30% three times increased risk, and if you have the 4/4 gene you have a 50-90% risk potential for developing Alzheimer’s disease as you age if you don’t do something to change the inputs. There is a website https://www.apoe4.info/wp/ for carriers of these genes because the people who run this website are aware now of how profound this gene is. This website is dedicated to informing individuals with the gene and what can be done to down-regulate the potentially negative outcomes of disease expression. 

I’m going to skip some of the basics because I know I’m going to run out of time but here’s the hallmark of Alzheimer’s, these tau tangles which are in the neurofibrillary and the amyloid plaque. This creates an inflammatory response which shuts down neuronal synaptic communication, which kills neurons so as your synapses die from these tangles, neurons die. Your brain atrophies and dementia can ensue, and if you had to look at what in at the most minute level- what’s really going on in Alzheimer’s disease. It has everything to do with the interplay between trophic factors and blastic factors, growth factors and destructive factors that influence one particular protein called the amyloid precursor protein. This is where amyloid plaque comes from, it comes from this protein. It’s a subset of it and you have what are called molecular scissors, or proteases that come along and they snip through this amyloid precursor protein. If it makes one snip, you get the anti-Alzheimer’s outcome. If it makes four snips, you get the pro Alzheimer’s outcome, so the entire Bredesen protocol is everything to do with how you influence these molecular scissors to favorably produce the two pieces of amyloid precursor protein, as opposed to the four. That’s what it is, what you can do to drive support for neurons, as opposed to destruction of neurons by influencing these molecular switches. That’s it at the molecular level anyway. 

So, we don’t go progress straight to Alzheimer’s disease. Before Alzheimer’s occurs, there’s a subjective cognitive decline that can occur, for people 10-15 years before where people may say “I’m just off my game, I’m not as smart as I used to be now.” Normal aging produces this, our brains slow down but if you are going down the dementing routes- if you’re going down the Alzheimer’s route, you may start in a preclinical way. Some of your tests may be already positive before you actually pick it up. It’s subjective decline. Then you actually start to get mild cognitive decline where you actually objectively starting to register negatively with specific testing. I can’t tell you how many people come to my office who are running corporations, CEOs, with mild cognitive decline. Their biochemistry, their markers of cognition, they fail, but they’re still operational but they’ve got objective signs of decline. After that is when you lose tasks of daily living and you start to go down the dementing path. There is a difference between dementia and normal aging with statements like “I forgot my keys.” People with just normal aging usually remember where they parked. They can retrace their movements and realize, “Ah that’s where I left them.” So, these are some differences, but it’s a bit of a fuzzy line in the beginning. As I said those of you on the right side of your biological drives when your brains speed is still travelling at 300 milliseconds. You still got a good brain speed, so you’re not so concerned about this but I’m personally on the other side of that curve and I’m very concerned about things like this. That’s why I started the brain treatment centre, not only to help patients. I had a selfish interest; I want to keep my brain moving at 300 milliseconds for as long as I can. Okay so this is the difference. Everything has to do with brain speed. Our brains move at 300 milliseconds per second. After age 20, and every decade thereafter, 10 milliseconds are lost just through normal aging. That’s profound, you know when your brain speed slows down you literally slow down. When your brain slows down, neurons and synapses die and there may be a bad outcome if you don’t do something about it. There’s a separation, a gap, between thinking a thought and executing the thought, by doing. 

There’s many reasons why people’s brains slow down or are exacerbated by lifestyle issues that don’t lead to necessarily dementing Alzheimer’s illness. The aging is the number one cause of brain slowing down but then you may have strokes and stress. People also drink far too much, it’s a neurotoxin they get addicted to. Certain things, prescription medications, can have profound effects. I mean you have no idea how many statins are given out like candy. Some of them cross the blood-brain barrier and shut down cholesterol metabolism. Cholesterol is a building block of brain neurons and myelin. You have got to think before people start taking these drugs. Some people come into the office and we suggest they go through something called the Cognoscopy. Everybody at age 50 gets a free colonoscopy, free under health care. Now, in terms of the future, start spreading the word, ask you friends, ask your parents, mom have you undergone a cognoscopy? A cognoscopy is a brain evaluation. Now your mother will say no because it doesn’t exist in the healthcare system. We can plant the seed; we can start thinking about it. It will happen because as I said in the beginning, try living one day without a functional brain. You know, it’s awful.

At the clinic we do questionnaires. Any of you recognize this MoCA (Montreal Cognitive Assessment)? You recognize it? Do you remember Donald Trump 2 months ago flashed this test and said “I’m brilliant, I’m a genius.” No, I’m serious he did pass the most elementary of cognition testing called the MoCA- and this is a five-minute test. He got 30 out of 30 apparently, but people with dementia they fail it. If you know anybody with a score less than 19, you’re on the wrong side of your MoCA. Your MoCA score for the average Alzheimer’s patient is around 16, 16.2. If the score is 19 to 22 those people with dementia will, if they can’t you now- they can’t take care of the daily tasks of living.  That’s a serious pattern. People with a mild cognitive impairment they have a MoCA score between 22 to 25. People who passed had a score of 26 or up. If you want to be in that range, I suggest that you get your brains assessed even if you do this online. It takes five minutes. We also have at our center the computerized CNS vital signs tool which is a computerized measurement of cognition. With this slide you can see this is one of our Alzheimer’s patients. They can’t perform the tasks of executive functioning which the frontal lobe performs. What we take for granted they completely failed as opposed to somebody with a relatively normal executive functioning. You see how the brain atrophies and the brain atrophy starts in this part of the brain called the medial temporal cortex; that’s the hippocampus. The hippocampus is where we lay down new memories. It has limited capacity but we lay down our new memories in the hippocampus and as the dementing process spreads, it reduces the hippocampal neurogenesis and the nerves start to die but then it’s spread throughout the brain and this is a typical brain with Alzheimer’s. It really is shrunk, it’s quite remarkable, when you see it on MRI and there’s many imaging techniques which are used, MRIs, FDG-PET scans, amyloid PET scans, there’s all kinds of diagnostic tests. We’ve recently introduced in Canada software called the NeuroQuant MRI and this has to be privately ordered. You can’t get this from healthcare, I’ve asked, they won’t do it. But this NeuroQuant MRI actually measures objectively the size of each different area of your brain and compares you to a normative database of particularly the hippocampus and the frontal cortex. These are the two parts that go first, they shrink and we can objectively measure and compare these to other people’s brains. A normal MRI doesn’t do this. Here you can see the hippocampus is reduced. We also do QEEGs, and we can see the brain slowing down, that’s a slowed brainwave that we measure through a QEEG. 

Then we get to Dr. Bresden’s six subtypes of Alzheimer’s disease. Here we really have to understand the different six subtypes to learn how to work them up and how to treat them. If we don’t understand them according to this model, we can’t treat themand so the subtypes are: 

A) Inflammation. Here inflammation is at the root cause of the Alzheimer’s expression, Here, all these inflammatory markers get expressed in APOE4 subtypes. Inflammation is the most important risk factor for that subtype. Here you can see the hippocampus atrophied. We then have to seek out all the causes of that inflammation and all of you know the following triggers very well. Food, gut health, leaky gut, this is at the basis of this inflammatory subtype. We look at the causes of leaky gut, these are all lifestyle issues and we can actually measure how leaky your gut is and how leaky your brain is. You can actually measure now with specific labs the leakiness of your barrier functions and you can measure gut ecology and look at inflammatory factors. You can measure and look at zonulin – the protein that causes leakiness and histamine that makes it worse and then you can actually measure the protein in the lipopolysaccharide coating of bacteria that leak across the gut and cause bacterial endotoxemia and an inflammatory response. These are called LPS lipopolysaccharides. This is the root of many inflammatory brain disorders. Look at all the diseases that get expressed when lipopolysaccharides get expressed.

Then you look at food sensitivities. There are many different ways to look at food sensitivities. Many people come and see me and they have done one IgG test. That’s not it, you have to look at different immunological pathways to look at food expression. One test at our local private lab for IgG foods is not how you work up food sensitivity. You must learn about the other methodologies because they are extremely relevant. One may be positive may be negative in the next test. We also do a whole ton of work around gluten. Gluten as you know, nobody processes gluten well, even if you have or don’t have celiac disease. Even if you have or don’t have gluten sensitivity, nobody has the enzymes to break down the gluten molecule. Nobody. Dr. Fasano the great gluten researcher has said this for 10 years. You get a leaky gut from gluten, now those of you without the bad genes can repair it within hours. But every time you have gluten, you have a leaky gut- quick repair- ok. We measure the gluten molecule in all of its subsets with specialized labs and we measure antibodies to cross-reactive foods. Gluten cross-reacts with different foods. How many of you like coffee? How many of you like coffee and are gluten sensitive? How many of you knew (instant) coffee performs molecular mimicry and ignites the same pathways as gluten may? Just a thought. A particularly horrible thought. And then we can measure antibodies to specific tissue. We can measure antibodies against all of our organs and particularly we can actually measure immune systems attacking of core neurological structures, synapses, tubulins, myelin. You can see how under attack your brain is when you start doing these tests. 

Dentistry. How many of you lump dentistry and health together? How many of you lump dentistry and medicine together? It’s a separated discipline in present ways it is practiced. We can’t work up an Alzheimer’s patient without doing an extensive dental work-up. I do a panorex x-ray and a 3D cone beam CT, looking for periodontal disease, root canals, mercury fillings, dissimilar metals, implants, cavitations. There’s a whole slew of potential toxicity existing in the mouth. Multiple studies show the link between periodontal disease and the risk of Alzheimer’s disease. We do peridontal workups.

B). The second subtype is the glycotoxic, the type that causes too much sugar. Sugar as you all know is a potent, potent toxin. It should be a classified substance. 300 years ago, it was sought after like cocaine is today, people would seek it out because they knew how it made you feel- temporarily. Our bodies can’t cope with more than 15 grams of sugar a day. What is in one  sugar soda contain -4200 grams of sugar (not diet). We can’t cope with this huge input of sugar, I mean I know you know formulas but this is the second subtype that causes neurological causes, dementing processes.

C) And then we get the atrophic type, the atrophic type is the type that as the brain ages, it loses neurotropic support, vitamin D, zinc, estrogen, testosterone, pregnenolone, DHEA, all of it gets withdrawn as we age. If there’s one thing in my practice that I enjoy the most, is to see a postmenopausal woman who’s not dementing but she has cognitive decline, go back onto bioidentical hormones and they are so happy. Three months later they come in and the first thing they’ll say, I can’t believe it, I’ve got my brain back. Why? Estrogen is a neurotropic, neuroblastic hormone. It improves synaptic connections and improves dopamine; it changes cognition dramatically. This is the second type. 

D) The third subtype is the subtype that is toxic. This is a subtype of Alzheimer’s, it’s a different presentation of Alzheimer’s. It’s usually in younger people, it’s not so much influenced by the APOE4 gene and they usually present with a lot of frontal lobe symptoms as opposed to the typical hippocampal memory loss. But they do get- the first sign of somebody who’s got a toxic sort of brain is somebody who can’t multitask anymore. They used to do five things and now they can’t, they just have to delegate and that’s one of the first symptoms and we have a whole new world of work being done by Ritchie Shoemaker and others on the chronic inflammatory response syndrome. This is where the innate immune system is upregulated due to mold and Lyme and it causes this very specific profile of inflammation through the innate immune system which affects the brain and effects all the neuro peptides in the brain which regulate leaky gut which regulate hormones which regulate oxygen delivery to mitochondria. This is a whole subset of work that’s going on not in mainstream medicine, you won’t see it, you won’t find it, it’s not there but it’s in the research literature and we do certain things in our clinic to try and find out. We do questionnaires of that particular type, type three chronic inflammatory response. We look at the visual contrast test to see if people fail this test and we do spore counts and mold counts in their homes. Then we look at metals, heavy metals is a big cause and pesticides and air pollution and Lyme disease. How many people will have heard about Lyme disease epidemic, it doesn’t exist in Alberta right? Yeah. My entire day- do day-to-day, week-to-week- is made up by mold and Lyme, toxic people. They travel, they get it from other sources and we believe now the literature’s quite clear that Lyme disease may be transmitted by other factors, and there’s literature here in Calgary by Maureen Middleveen, that it may be sexually transmitted as well. This hasn’t been published in peer-reviewed journals but the literature is out there making those suggestions. With Lyme disease we find the pathogen inside the brains of people with Alzheimer’s disease. We find herpes simplex 1, the good old cold sore as a big cause. There is also a link between pesticides and Alzheimer’s. Glyphosate. How many of you eat organic food? Even organic food is riddled with glyphosate because of cross-contamination. It’s everywhere. Glyphosate is highly toxic to many core organs. It causes gut permeability; it shuts down neuronal pathways. 

E) Then the vascular subtype is with people with hypertension and atherosclerosis which decreases oxygen supply to the brain causing Alzheimer’s decline. 

F) And then we get the traumatic subtyppe; the brain injured people; I mean look at these statistics. Not all head trauma patients will develop Alzheimer’s, but there is 2.3 times increase incidence in mild or moderate traumatic brain injury. 4.5 increase in severe brain trauma. There are no studies linking mild brain injury to Alzheimer’s disease, but three or more concussions -a fivefold higher incidence for memory loss and cognitive impairment.

I’m out of time. Well there’s a whole slew of lab tests you can do to sort of think through this problem. You won’t get it under health care, you won’t get it from your family doctor, in fact you’ll get dismissed so it’s up to you to educate yourself. Dr. Bredesen’s book The End of Alzheimer’s is fabulous, I suggest you read it and you start working through your own cognoscopies, how you can work yourself up to see if you’re at risk and then therapeutically there’s at least 36 things you can do to down regulate cognitive decline and/or Alzheimer’s of which- guess what’s number one? Nutrition. 

One last word, ketogenic diets seems to trump every other diet when to comes to changing brain outcomes. Combine that with good sleep, exercise, stress reduction, you’ve got the four pillars of turning down mild cognitive decline of potential dementia, and then you can look at all the other factors with influence outcomes and just teach yourself because nobody out there is going to teach it to you and you definitely won’t get it from your medical doctors. So thank you very much. Thank you.

Judith Cobb:

Thank you, Dr. Hoffman, that was amazing. If you have questions please come and use the mic, we have about 8 minutes for questions, and at 9:30 you might get cut off right in the middle because we’ll be live streaming with Toronto, so questions?


Just a quick one, I know vitamin D is a really controversial item right now and is limited in information especially with auto-immunity, so what do you recommend for dosing, food versus supplements in the grocery list this summer?

Dr. Bruce Hoffman:

So, those are the  foods that contain vitamin D, this is how you can calculate your vitamin D needs, but I can tell you it’s not that accurate. Every Calgarian that I’ve ever seen who’s not on vitamin D supplements is vitamin D deficient, everyone. But you can’t tell them how much to take because everybody has a variation in the amount they need, depending on A) The VDR gene receptors which is from the 23andme gene test. because the people with a VDR plus plus gene need a lot more vitamin D. The state of the small intestines is where you absorb vitamin D and many people have very disrupted small intestines, and they have SIBO and small bowel SIFO with fungal overgrowth and they don’t absorb the D vitamin and you need the D vitamin and you need a lot of oil. In fact, Vit D – this is a fat-soluble vitamin. I can’t tell you how many people are fatty acid deficient, the majority of people by far. Everybody’s taking omega-3s, that’s epidemic right now, everybody comes in taking fish oil- fish oil isn’t it. It’s got benefits but you need your omega-3, your sixes, your nines, your mono and saturate fats; your saturates in order to absorb vitamin D and vitamin A and vitamin E which are fat soluble. So, to answer that question is complex but patients hate me, they always ask me questions and I say “I’m not sure, it’s complex”, they go “give me an answer”. Then I will do a ten minute explanation, and they go “oh I see”. So that’s the kind of complexity that this requires to answer that question.


For people in our industry, it’s really hard for us to help with stuff like this especially now that Alberta does not test vitamin D, so how do you recommend we help people that do come to us with these issues when we can’t convince them to their doctor to get tested for this?

Dr. Bruce Hoffman:

So, it’s a great question. First of all, you can get vitamin D tested just so you know, there’s a trick. Yes, the trick you got to have a friendly GP who’s going to lie and say you’ve got celiac disease or malabsorption syndrome or osteoporosis. They need to sign a form, if they sign the form you can get it done, but I can tell you from my experience, none of them will, but if you have a good relationship with them and you can prove to them that there’s a need, they will do it for you. If you put a circle where it shouldn’t be and you don’t cross the box where it should be, you’ll be rejected. It’s that weird, that’s firstly. Secondly you can get vitamin D from private labs so people have to spend out of pocket. 

This notion of having Canadian healthcare pay for your functional medicine and wellbeing, please give it up, it’s not going to happen. You have to have health as an extremely high value and you have to invest in your health with your own after-tax dollars because they won’t let you deduct it in order to maximize your health outcomes. Please don’t think that Alberta health care is going to do this for you and I don’t think they should by the way. People always feel almost shattered when I say that. The disease based system,  we already pay exorbitant taxes to fund the free health care and they do a good job of you know, when we have a heart attack and go to the emergency and we get 5-star treatment and intensive care. Don’t try and muddy the waters asking that system which treats tertiary disease, to start doing preventative medicine overnight. I think it will creep in overtime but if you want them to do functional medicine and preventive medicine and start to fund what you do your taxes will be 95%. It can’t happen, so please be responsible, get rid of an adolescent fantasy that health care should take care of all this, it won’t and I don’t think it can afford to. You have to have health as a high value, you have to invest in yourself, you have to educate yourself,  you have to become your own patient advocate and you have to do what it takes to get you where you need to go.


Hello, outside of MRIs, EEGs, CAT scans and others in our regular system, how do you feel about the spec imaging, neurospec imaging?

Dr. Bruce Hoffman:

Neurospec imaging? It’s not- it’s generalized but it’s not specific. You can see signs and symptoms, you can see certain images like you know the ring of fire, Daniel Amen’s. It’s not specific but it is done. PET scans, more accurate and some of the more advanced PET scans are more accurate. Neurospec is sort of a secondary test, I wouldn’t use it as a primary test unless you got free access.


Hi, I just saw on a slide that you said with inflammation it had to do with Pitta and Ayurveda and what the relationship was there?

Dr. Bruce Hoffman:

Are you familiar with the Ayurveda? So, I evaded talking about doshas- doshas are constellations of elements, vata is air and space, pitta is fire. What is inflammation? Fire, too much fire.


So, someone with Pitta is more susceptible to Alzheimer’s?

Dr. Bruce Hoffman:

I don’t know if that’s statistically true, but theoretically of the subtype one, inflammation, I would say, I would posit a guess, I don’t think studies have been done- now Bredesen knows a bit about Ayurveda.  I was astonished that he did, so I would think they may be something to that, there may be literature on that  that but I can’t say for sure, but it makes sense. Pita is the hardest to treat by the way. 

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The Ketogenic Diet – The Secret to Neuroprotection

Ever taken a trip to the grocery store only to forget why you went there in the first place? Or perhaps you have difficulty concentrating on something you usually enjoy, like reading a book. In either of these cases, you usually don’t feel as if your brain is working normally.

  • Maybe you’ve lost confidence in your mental abilities.mol
  • Maybe your doctor has dismissed your brain fog as a consequence of aging.
  • Maybe you’ve struggled with chronic migraines or cluster headaches for what feels like forever.
  • Maybe you’re apprehensive regarding a future that involves living with neurodegenerative disease.

Sound familiar?

Well, I’m here to tell you not to lose hope. There are ways in which conventional Western medicine is letting us all down. The idea of losing cognitive functions, your memory becoming poorer, or even not being able to recognize the faces of your family, is all pretty scary. Every 65 seconds a patient in the US develops Alzheimer’s disease and there’s no magic pill that cures it.

Fortunately, there’s another way.

As a functional and integrative doctor, I find the issue of cognitive decline to be on my mind regularly. My patients are concerned that they won’t be able to work, socialize, or enjoy hobbies for much longer. They even worry that they’ll have to give up on life.

However, I’m able to help them treat their neurodegenerative progression from the inside. By adopting the ketogenic diet for neurodegenerative diseases, you can change your life and turn back the clock. Dr. Dale Bredesen’s extensive research and treatments have shown that the effects of Alzheimer’s disease can be reversed with simple lifestyle changes. A modified version of the ketogenic diet is the backbone of Dr. Bredesen’s protocol and the science behind this is truly incredible.

The History of the Ketogenic Diet

While the ketogenic diet is currently very popular due to its fast and effective results related to weight loss, the diet actually started out as a medical therapy in the 1920s. Doctors saw that fasting was beneficial regarding controlling seizures in epileptic children, but restricting food was not a sustainable solution in the long term.

The doctors reasoned that when you fast, your levels of glucose and insulin drop and ketone bodies appear in your blood and urine. Ketone bodies indicate fat breakdown, so the doctors realized that a high-fat diet could build up levels of ketones that were sufficient enough to mimic the benefits of fasting, thus reducing their young patients’ seizures. Epileptic children who were prescribed the ketogenic diet did indeed stop seizing. However, the ketogenic diet never became a popularized form of therapy for epilepsy once anticonvulsant drugs were fully researched and then put into production.

The therapeutic effects of the ketogenic diet were only really rediscovered towards the end of the twentieth century. Many parents of epileptic children that were frustrated with the severe side effects of anticonvulsant drugs, and worried about the impact of seizures on their child’s cognitive abilities, did their research and decided that inducing ketosis was something that they’d like to try.

While the ketogenic diet isn’t the first option that medical practitioners explore when treating children with epilepsy, it has garnered more interest in the medical community as new and exciting applications have been discovered and research is increasingly being undertaken into the neuroprotective characteristics of the diet.

It’s important to realize that ketosis isn’t an unusual state for human beings. Infants are naturally in ketosis much of the time, since breast milk is high in medium chain triglycerides or MCT. We are naturally in ketosis during sleep, fasting and exercise as the body and brain have become accustomed to metabolic flexibility, shifting between glucose and ketones as fuel sources when the need arises. As human beings become more sedentary and accustomed to eating three meals a day with snacks, often well into the night, these diurnal and seasonal changes became a thing of the past.

What Neurological Disorders Does the Keto Diet Help Treat?

Following the ketogenic diet is often a game changer for patients suffering from:

  • Parkinson’s disease – Keto improved the condition of patients in a small study.
  • Traumatic brain injury – There has been success in an animal study, with potential for human application.
  • Epilepsy, Stroke, Migraine – All three conditions share similar characteristics, migraine patients are at an additional risk for stroke, and patients often deal with epilepsy and migraine together. Migraines and epilepsy share similar symptoms and often epilepsy medications are used to treat chronic migraines off-label. As the ketogenic diet has reduced the number of seizures for epileptics, chronic migraine patients have also experienced longer gaps between migraine attacks.
  • Chronic cluster headaches (CCH) – There has also been success for chronic cluster headache sufferers, suggesting that the anti-inflammatory nature of the ketogenic diet is particularly healing for CCH patients.
  • Autism – A ketogenic diet has had some success in reducing some symptoms of autism. One of the leading contributors of autism may be mitochondrial dysfunction and the ketogenic diet improves mitochondrial function.
  • Brain tumors – Many cancer patients have seen success with the ketogenic diet slowing down their tumor growth as several types of tumors require glucose and a very high carbohydrate diet. However, the ketogenic diet is not a one-size-fits-all remedy for cancer. Studies are ongoing.
  • Trigeminal Neuralgia – A study shows promise of relief for sufferers of this severe form of facial pain after adopting the keto diet.
  • Multiple Sclerosis – Research is ongoing, but there does seem to be potential for the keto diet to protect neurons from further damage.
  • Alzheimer’s disease – The ketogenic diet benefits Alzheimer’s disease patients because it combats insulin resistance, inflammation, gluten sensitivity, obesity, and leaky gut.

You’ll learn more about each of these subjects below.

The ketogenic lifestyle is also a fantastic solution for healthy individuals who wish to avoid neurodegenerative disease or cognitive dysfunction. The only good way to ensure better health when you’re older is to take action today. Even if you have the APOE4 gene, meaning that you’re more susceptible to developing Alzheimer’s, or have a formal diagnosis, you can benefit from the ketogenic diet. It’s never too late to start.

Neuroprotective and Disease-Modifying Effects of the Ketogenic Diet

There are a number of ways in which following a ketogenic diet can protect your brain and even reverse neurodegenerative disease. By severely restricting your carbohydrate intake, reducing protein, exercising regularly, and increasing your consumption of good fats, you encourage your body to look for an alternative energy source to sugars and carbohydrates. If you eat to a calorie deficit, your body begins breaking down fat stores and inducing a state known as ketosis. The brain prefers ketones to glucose as they cross the blood-brain barrier much easier since they don’t rely on transport proteins. They also produce less in the way of free radicals or oxidative damage, the key biochemical process underlying most forms of chronic disease including neuroinflammation and neurodegeneration. However, if you’re eating to maintain your existing weight, the fat is supplied purely through your diet.

The Power of the Humble Ketone

Most of your body can use the fat stores or dietary fat to power your cells. However, your brain and the central nervous system can’t access this energy in the same way. As a result, your liver breaks down the fatty acids and a by-product of this chemical process are ketones. These are your body’s alternative energy source.

Ketones are made up of acetone, acetoacetate, and beta-hydroxybutyrate.

Ketone bodies are capable of crossing the blood-brain barrier and are the only source of energy the brain can use that can replace glucose made from carbohydrates. As such, ketones can fuel up to 75% of the energy needed by your brain. The other 25% or more of your energy continues to be fueled by glucose, but it’s glucose that’s made by your body from the few carbs that you do eat and also by your protein sources.

Ketones are an amazing form of energy for your body and have a host of benefits for your metabolism and health.

Concentrating on neuroprotection, here’s a list of ketosis brain benefits:

  • Ketones are water-soluble and cross the blood-brain barrier in proportion to your blood levels. Consequently, they can compensate for an existing neurological disorder where there’s a regional brain glucose deficiency. It’s been observed that studies show reduction in glucose utilization in the Alzheimer regions of the brain in the temporal and frontal lobes long before cognition declines. This is due to insulin resistance, a concept that’s well described a little later.
  • When the cells of your body, and specifically those of your brain, convert ketones into adenosine triphosphate (ATP) via the mitochondria, ATP generation is markedly improved in mitochondria that are fed ketones. The keto diet improves the efficiency of your brain cells.
  • Ketones inhibit reproduction of the HDAC enzymes, which protect and repair the neurons that make up your double-stranded DNA. Ketones therefore have a powerful role to play in epigenetics and future research may potentially shed light on how they protect your brain.
  • The beta-hydroxybutyrate in ketones suppresses your NLRP3 inflammasome, reducing inflammation in your body. The mechanism is pivotal in the development of Alzheimer’s disease and related brain tissue damage. In animal studies, beta-hydroxybutyrate was found to suppress oxidative stress, protecting the integrity of the DNA and overall health.

What Is Insulin Resistance and Why Is It a Problem?

Normally, the insulin hormone is produced by the pancreas. Insulin joins your bloodstream to regulate the amount of glucose in your blood. In a healthy individual, when the insulin detects too much glucose in your blood, it signals muscles, tissues, and your liver to absorb the glucose.

The glucose is then converted into ATP, ready to be used as cellular energy or broken down by your liver. The levels of glucose in your bloodstream need to be controlled because they can be toxic at high levels.

When you have insulin resistance, which is often a precursor to diabetes, your body ignores or resists the insulin signal to absorb glucose. The levels of glucose build up and your pancreas creates more and more insulin in order to trigger glucose regulation.

Obviously, any condition that may lead to diabetes is a concern, but insulin resistance also has an impact on your neurological health. Sugar is a known inflammatory and inflammation can disrupt the careful balance of your blood-brain barrier.

More crucially, insulin is a signaller that aids neural cell survival. If there are high levels of insulin in your bloodstream, the amount of insulin should be reduced and your body needs several enzymes to break it down.

One enzyme called insulin-degrading enzyme (IDE) can break down insulin. However, if it’s responsible for working on an overabundance of insulin, the enzyme can’t be used to degrade amyloid beta. Amyloid beta in the brain contributes to Alzheimer’s disease.

However, if you increase your insulin sensitivity, it’s possible to reduce your chances of developing Alzheimer’s disease. Ketones also modulate your neurons by reducing glutamate toxicity and inhibiting gamma-aminobutyric acidergic (GABAergic) effects, limiting seizures if you’re epileptic.

The Mind-Gut Connection

In integrative and functional medicine approaches, it’s understood just how important the health of the gut is in relation to achieving optimal overall health. Understanding the connection between your brain and your gut microbiome is crucial to maximizing the neuroprotective conditions of the ketogenic diet. Sugar causes inflammation and can trigger conditions such as leaky gut. Eating whole foods and reducing your carbohydrates and processed food intake helps to heal your gut. Improving your gut microbiome actually improves your cognitive abilities as well

Keto Helps You Sleep Deeply

A lower-carb diet, such as the ketogenic diet, may help reduce your symptoms of sleep apnea or other sleep airway disorders. Quality of sleep and deep REM sleep are crucial for keeping your brain healthy.

An airway sleeping disorder usually results in your brain not receiving enough oxygen at night. The effect of a lack of oxygen is that your brain can’t fall into a deeper sleep and your brain is unable to perform certain neuroprotective tasks, such as autophagy where old cell components are recycled.

The recent discovery of the glymphatic system in the brain is of great interest to researchers examining neurodegenerative diseases. The glymphatic system only works while you’re asleep and removes excess fluid and waste products from the brain and spinal column tissues. Amyloid beta proteins are a form of waste in the brain that the glymphatic system deals with. Links have been established between these proteins, your cholesterol levels, and the lymphatic system in regard to neurodegenerative diseases.

The glymphatic system also delivers central building block nutrients, some of which are used in improving your cognitive functions. Unfortunately, with sleep apnoea your body is unable to undertake these functions, leading to neurodegeneration.

Ketogenic Basics: Macronutrients and Keeping Track

Macronutrients are another term for the basic food groups:

  • Protein
  • Fat
  • Carbohydrates

Both the standard American diet and calorie restrictive low-fat diet are heavily slanted toward the consumption of carbohydrates. In the ketogenic diet, the values are flipped on their head. On the keto diet, you aim for a high-fat intake, medium to low amounts of protein, and low levels of carbohydrates. A good rule of thumb is to not eat foods with a glycemic index of more than 35. Here is a link to a food glycemic index database that should be useful.

The original ketogenic diet for epileptic children focused on a 4:1 ratio, or four parts fat to one part carbohydrates and protein. However, this is at the extreme end of the ketogenic diet and is usually too difficult to attempt at home.

Generally, you should aim for your intake to be:

  • 60-75% fat
  • 15-35% protein
  • 5-10% of carbohydrates, although the lower the carbohydrates, the better.

Use a quality online ketogenic calculator to adjust your macros. This one has options for eating to maintain weight, lose weight, or gain weight.

To track whether your body is in the state of ketosis that’s creating ketones and using them as your body’s main source of energy, it’s advisable that you invest in a good ketone and glucose meter. By using it, you can keep an eye on what foods your body responds to after a meal. Tracking your ketones through beta-hydroxybutyrate levels in your blood is the most accurate way to keep tabs on whether you’re in ketosis. Unfortunately, ketone breathalyzers or keto sticks aren’t accurate enough to be reliable.

Ketogenic Neuroprotective Basics: The Diet


Although an outsider may think the mainstream version of the ketogenic diet is mostly made up of bacon, the focus is actually on plant-based foods to promote the diet’s neuroprotective benefits. While it’s true that many vegetables contain high amounts of carbohydrates, these are usually tempered by fiber and the resistant starches that are found in complex carbohydrates.

Your body has a harder time breaking down complex carbohydrates, so they don’t raise your glycemic index so sharply. Simple carbohydrates, on the other hand, are sugars or carbohydrates that break down easily into glucose.

Here’s a guide to vegetables and fruit on a neuroprotective ketogenic food plan:

Eat frequently:

The majority of the diet should consist of organic, non-GMO, seasonal, local, colorful, deeply pigmented non-starchy vegetables with a limited amount of starchy vegetables.

Cruciferous vegetables – These contain sulfur, an important building block for production of amino acids, especially glutathione, which is the main brain antioxidant. These types of vegetables are ideally consumed after being lightly sautéed at medium heat or lightly steamed.

  • Alliums (onion family -shallots, garlic, leeks)
  • Brassicas (cabbage, broccoli, Brussel sprouts, bok choy, cauliflower)

Leafy green vegetables – These are at the top of the list for the ketogenic diet. They contain high levels of nutrients beneficial to your brain health, such as vitamins, minerals, polyphenols, carotenoids.

  • Spinach (caution if histaminic and high oxalates)
  • Kale (caution if high oxalates
  • Lettuce

Mushrooms – These contain sulfur and beta-D-glucan, which may help the reversal of cognitive decline through immune enhancing effects. There are many varieties, including Portobello, shitake, reishi, oyster, and white button mushrooms. Add them to sauces, stews, and for flavour when cooking other vegetables.

Resistant starches – The good bacteria in your gut microbiome can feast on resistant starches and fibre and they excrete short-chain fatty acids crucial for your wellbeing.

  • Rutabagas
  • Parsnips
  • Sweet potatoes
  • Green bananas

Herbs and spices – These contain antiviral and antimicrobial properties and are an essential part of a ketogenic diet. This extensive list includes ginger, turmeric, basil, bay leave, chives, cilantro cinnamon, coriander, cumin, lavender, marjoram, mint, oregano, parsley, rosemary, saffron, sage, thyme and more. Herbs and spices have been widely studied to determine their medicinal properties.

Nuts and Seeds – These are rich in vital brain protective nutrients and contain excellent sources of fat, protein, vitamins, minerals, and fibre. These should be raw, fresh, organic, and soaked if possible, thus reducing lectins and phytates. Use dry, roasted nuts where possible if you’re unable to roast them yourself. Roast at low temperatures (77-104 degrees C) while frequently turning the nuts during the process. Nuts that have already been roasted in added oils are usually rancid and oxidized, increasing the risk of inflammation. All nuts and seeds should be stored in the freezer or refrigerator to retain maximum freshness.

Eat sometimes:

Starchy vegetables

  • White potatoes (caution if high histaminic and sensitive to nightshades and not usually advised)
  • Corn (not the best food due to it being high glycemic, moldy, or GMO, amongst other issues)
  • Squash

Nightshades – These inflammatory vegetables contain solanine, a toxin that plants produce to deter animals from eating them. Solanine can stimulate the acetylcholine neurotransmitter in your brain and nervous system. For most people, this is of no concern, but for a patient facing early-onset Alzheimer’s disease, an imbalance in neurotransmitters can complicate matters.

  • Peppers (caution if high histaminic and pain syndromes)
  • Tomatoes (caution if high histaminic and pain syndromes)
  • Eggplant (caution if high histaminic and pain syndromes)

Legumes – Eat these with caution as legumes can raise glucose levels in the blood and shouldn’t be eaten in the early weeks of adopting the ketogenic diet. Depending on the severity of your insulin resistance, you may not be able to eat them.

  • Peas
  • Beans

Fruits – Small berries contain polyphenol compounds that can play a role in reducing cognitive decline:

  • Wild berries such as blueberries have been extensively studied for their antioxidant effects on brain health
  • Avocado is high in fibre, nutrients and beneficial fats
  • Olives
  • Lemons and limes (caution if high histaminic)


You may find it easy to go overboard with animal-based protein when beginning the ketogenic diet, but it’s crucial to calculate your daily allowance of protein. It’s advisable to employ the one gram of protein for each kg of your weight equation. For example, if you weigh 80kg you can consume up to 80g of protein per day.

Eating protein to excess ensures that some protein is converted to glucose, increasing the levels of insulin in your bloodstream. Think of your controlled amount of protein in the same way as when your ancestors would share a part of the communal hunting kill, only eating a small part of the animal. The rest of the time it was possible to get enough protein through plant-based food sources and this remains true today.

As much as possible, ensure that the protein you eat is organic, grass fed, grass finished, hormone and antibiotic free, and that the animals are not subjected to the stresses and toxins of concentrated feeding operations. To prevent muscle wasting, ensure weight training and weight bearing exercises are incorporated into your routine.

On a neuroprotective ketogenic diet, vegetarians need to get their protein from vegetables, nuts, seeds, tempeh, and beans. However, these are often incomplete proteins and vegetarians will need to supplement with omega-3’s, vitamin B’s, Vitamin D, and choline.

Eat frequently:

Oily fish – These are rich in Omega-3 and Omega-6 and both are excellent for brain health. Farmed fish or shrimp should be avoided. The least contaminated fish, which are smaller and don’t live as long, are known as the SMASH fish.

  • Salmon – The least contaminated are wild Alaskan and sock-eye
  • Mackerel – Fish from the United States and Canada is low in mercury, whereas King and Spanish mackerel are high in mercury
  • Anchovies
  • Sardines – Canned sardines are high in histamine and Pacific sardines are the best.
  • Herring

Free range eggs – These are full of protein and good fats, especially choline, which is a key nutrient for acetylcholine, the main neurotransmitter for memory. However, eggs can trigger a histamine response so caution may be warranted. A list of foods high in histamine and possible substitutes may be found here.

Eat sometimes:

  • Grass-fed beef – This is an acceptable occasional treat, but it’s incredibly easy to go over your protein allowance with a good steak.
  • Free-range chicken – While fantastic as part of a salad this shouldn’t be the main focus of the meal.
  • Meats are generally considered as a condiment, not as a main course.

Avoid eating:

Processed meats often contain hidden sugars, histamine, wheat, gluten, and other inflammatory ingredients.

  • Salami
  • Chorizo
  • Shaped ham
  • Bologna

Fish containing high levels of mercury, since this is known to cause cognitive decline.

  • Tuna
  • Shark
  • Swordfish

Dairy can be highly inflammatory as the lectin in dairy can irritate the gut, so dairy should be avoided as much as possible.

  • Milk
  • Cheese
  • Cream
  • Yoghurt

Alcohol is a known neurotoxicant and solvent and should be avoided, especially if you have the APOE4 gene. Alcohol will slow down fat loss in those patients that use the ketogenic diet for weight loss reasons. Many alcohol drinks such as beer, wine, cocktails, mixers, and flavoured liquors contain carbohydrates. Alcohol is ethanol, which is easily broken down into sugar.

Peanuts are a legume known to be moldy and inflammatory. If you’ve been exposed to mold, download my mold exposure guide here.


Although the ketogenic diet is high in fat, not all fats are created equally. Developing an awareness of the different varieties of fat and what foods are good sources of fat ensures that you’ll find it easier to maintain the neuroprotective ketogenic diet in the long term.

Eat frequently:

Monounsaturated fatty acids (MFUA)

  • Avocados, avocado oil
  • Olives, extra virgin olive oil
  • Nuts and seeds, although be careful of walnuts, pecans and peanuts if high histaminic. Many nuts are also moldy
  • Walnuts have been associated with brain health but must be eaten raw. Macadamias are similarly highly desirable for maintaining brain health

Polyunsaturated fatty acids (PUFA) that include Omega-3 and Omega-6.

  • Seed oils such as walnut oil, macadamia oil, or sesame oil
  • Cod liver oil
  • Algae
  • Chia seeds
  • Fish, nuts, and seeds

Saturated fatty acids (SFA)

  • Animal fats are great for this but can be highly reactive in histaminic patients
  • Butter from grass-fed goats, sheep, or A2 cows, although in small amounts as dairy this is an inflammatory
  • Coconut oil
  • MCT oil
  • Free range eggs

Cocoa butter and nuts

  • The fat in chocolate comes from cocoa butter and is made up of equal amounts of oleic acid, a heart-healthy monounsaturated fat also found in olive oil, stearic and palmitic acids, which are forms of saturated fat.
  • They also contain flavanols and have four times the antioxidant properties of dark chocolate.
  • Dark chocolate (over 86%), also has brain health properties.

Avoid eating:

Trans fats and synthetic hydrogenated fats result in raised low-density lipoprotein (LDL) cholesterol levels. High levels of LDL cholesterol can occur at the onset of Alzheimer’s disease in middle age.

  • Avoid all seed, grain, bean and partially hydrogenated oils such as soy, corn, canola, peanut, sunflower oil, safflower (usually adulterated with oleic acid mix), cottonseed, and palm kernel.
  • Avoid all foods processed with trans fats such as crackers, cookies, cakes, chips, microwave popcorn, frozen dinners, pizza, creamers, margarine, cool whip, and fast food.

Testing for fats

With regards to fatty acid intake, it’s best not to engage in a guessing game regarding which fats you need in what ratios. It’s advisable to conduct the Kennedy Krieger fatty acids analysis through a company called Body Bio. In this way, your exact fatty acid dietary deficiencies and excesses can be measured and managed effectively through the correct ratios of biologically active fats, either through food, cooking, or supplementation. Phosphatidyl choline is an essential fat for cardiovascular, mitochondrial, and cognitive health and the levels are best measured before embarking on an extensive therapeutic fatty acid regime.

Saturated fats and cardiovascular risk

People with the ApoE4 gene need to be cautious when using increased amounts of saturated fats, as these are known to raise LDL particle number and APOB, a lipoprotein associated with increased cardiovascular disease. Although the increased saturated fats may increase cognitive health, in the long term it may lead to increased cardiovascular risk factors that are not beneficial. Therefore, it is advised that one monitors one’s cardiovascular risk factors including but not limited to APOB, oxidised LDL, LDL particle number and size, and HDL particle number and size. Increased saturated fats are known to lower triglycerides, increase HDL, and shift LDL particle size from the smaller dangerous particle size to the more advantageous larger ‘fluffy’ type, which is known to be cardioprotective.

Cooking Methods

The way you cook your food is almost as important as the food you choose to eat. Many everyday methods of cooking food can result in advanced glycation end products (AGE). These glycotoxins are produced when there’s a reaction between protein or fat and sugars, so AGEs can instigate inflammation and are bad news for brain health.

Methods to use:

  • Vegetables prepared raw
  • Steaming
  • Boiling
  • Marinating in lemon, lime, or vinegar (caution if histaminic)

 Methods to avoid:

  • Roasting
  • Broiling
  • Frying
  • Grilling

Fats to cook with:

  • Choose oils with a high smoking point, such as avocado, coconut, ghee, and animal fat

Foods to Avoid and Why


Grains are dense in carbohydrates, contain lectins that are known to be associated with ‘leaky gut’, phytates, and enzyme inhibitors. Gluten is a known inflammatory agent, especially when it provokes an autoimmune inflammatory response to brain proteins such as myelin and tubulin. Foods to avoid include:

  • Wheat
  • Barley
  • Oats
  • Corn
  • Rye
  • Soy
  • Flour
  • Bread
  • Polenta
  • Pasta
  • Tortilla wraps
  • Noodles
  • Rice
  • Nachos
  • Popcorn
  • Crackers


Dairy foods are inflammatory particularly as the dairy cows in the United States are A1 cows that produce a protein similar to lectin. A2 cows do not contain these lectins. Furthermore, casein and whey, the two milk proteins, are frequently cross-reactive with gluten.


The glycemic index is too high with these types of foods:

  • Agave
  • Alcohol
  • Cane sugar
  • Candy
  • Cookies
  • Cake
  • Dessert
  • Fries
  • Fruit juices
  • High fructose corn syrup
  • Honey
  • Ice cream
  • Maple syrup
  • Pastries
  • Pizza
  • Potato chips
  • Soda
  • Anything containing sugar

  • Microwave dinners
  • Convenience food
  • Anything out of a packet


  • Melon
  • Pineapple
  • Yellow bananas
  • Grapes
  • Cherries
  • Apricots
  • Mango

Food Intolerances and allergies – All patients that are using the ketogenic diet for cognitive health should be extensively tested for food sensitivities, gut ecology and permeability, leaky blood brain, and antibodies to brain proteins (detected using Cyrex labs 2, 10x, 12 and 20).

Different Ketogenic Diets 


This diet is typically recommended for most people and is very effective. The diet focuses on high consumption of:

  • Healthy fats (70% of your diet)
  • Moderate protein (25% of your diet)
  • Very little carbohydrates (5% of your diet)

Keep in mind that there’s no set limit to the fat because energy requirements vary from person to person, depending on their daily physical activities. The majority of your calories still need to come from fats and you still need to limit your consumption of carbohydrates and protein for your diet to become a standard ketogenic one.


This is generally geared towards fitness enthusiasts. In this approach, you eat the entirety of your allocated carbohydrates for the day in one meal, around 30 to 60 minutes before engaging in exercise.

With this diet the idea is to use the energy provided by the carbohydrates effectively before it disrupts ketosis. You eat carbs that are easily digestible with a high glycemic index to avoid upsetting your stomach. When you’re done exercising, increase your intake of protein to help with muscle recovery then continue consuming your fats afterward.


This one is generally focused more on athletes and body builders

Cycling between a normal ketogenic diet, followed by a set number of days of high carbohydrate consumption, also known as “carbo-loading”

The diet takes advantage of the carbohydrates to replenish the glycogen lost from your muscles during athletic activity or working out. This usually consists of five days of SKD, followed by two days of carb-loading. During the ketogenic cycle, carbohydrate consumption is around 50 grams, but when you reach the carb-loading cycle, the amount jumps to 450-600 grams.

This method isn’t recommended for people that don’t have a high rate of physical activity.


This method is a variant of SKD, in which you increase the ratio of protein consumption to 10% and reduce your healthy fat consumption by 10%. In a study involving obese men that tried this method, researchers noted that it helped reduce their hunger and lowered their food intake significantly, resulting in weight loss.

If you’re overweight or obese, this diet may help you initially, before you can transition to SKD after you normalize your weight.


As mentioned earlier, ketogenic diet can be an effective weapon against cancer. For this method to be effective, you need to be on a restricted ketogenic diet. By restricting your carbohydrate and calorie intake, your body loses glycogen and starts producing the ketones that your healthy cells can use as energy. Cancer cells are unable to use these ketones and starve to death.

Meal Examples

1st Meal

  • 4 to 5 cups of organic vegetables
  • Some limited starchy vegetables, such as sweet potato
  • One or two pasteurized eggs, lightly cooked or poached
  • Olive oil, MCT oil, or ghee as a dip for the vegetables
  • Use of spices, herbs, and sea salt for flavouring

2nd Meal

  • Organic, seasonal vegetables, either as a salad or lightly steamed
  • Small serving of fish or chicken
  • Healthy fats such as avocado, olives, nuts or seeds, and/or olive oil
  • Seasonings such as herbs, spices, and sea salt

Snack example

  • Coconut yoghurt or coconut milk kefir
  • Blueberries
  • Walnuts, almonds, or macadamias
  • Cocoa nibs
  • Coconut flakes
  • Stevia

Shake example

  • 2 tablespoons of Body Bio phosphatidyl choline
  • 1 tablespoon of Body Bio balanced oil
  • 1 tablespoon of MCT oil
  • 1 scoop of amino acid powder
  • Lions mane, turmeric, and /or mushroom powder
  • Stevia and vanilla to add flavour

Please note that the above ratios would be determined based on a fatty acid test

Neuroprotective Keto: Fasting and Exercising

Fasting and exercising aren’t optional when undergoing the ketogenic diet for neuroprotection. The good news is that neither has to be conducted to the extreme on order to get results.

Fasting is an effective way to stimulate ketogenesis, the process that produces ketones. Fasting also enables autophagy, as discussed above in the section about sleeping. Autophagy is an advantageous function that removes damaged proteins from the brain, protecting it from a dangerous build-up. Fasting has also been shown to have a number of other health benefits, including improved cardiovascular health, reduced cancer risk, increasing longevity (by increasing the sirtuin gene) and repairing damaged DNA.

Here are the easiest ways to incorporate fasting into your daily routine, without feeling like you’re missing out or that you’re going to be hungry:

  • Fast between the end of your dinner and your breakfast the next day. Aim for twelve hours without snacking. Individuals with the APOE4 gene may need to increase the fasting state for sixteen hours.
  • Make sure you eat your evening meal early so that you have a minimum of three to four hours between your evening meal and going to sleep.
  • Your body’s calorie burning clock is most effective in the morning and least effective at night. You don’t need food for energy at night so by eating less at that time you induce a fat burning state that helps prepare your body for detoxification and repair.
  • Water, black tea, or coffee are all allowed during the fast, particularly in the early morning. Stevia may be used as a sweetener

Remember that once you are fully in ketosis you won’t experience hunger pangs in the same way. In fact, you may be able to go even longer between meals.

Exercise is crucial for neuroprotection as it helps reduce insulin resistance, aids ketosis, and reduces stress. A combination of aerobic exercise and weight training can improve your sleep at night via vascular function in your brain and protect the hippocampus, which can often shrink in those suffering with Alzheimer’s disease. Start slowly and build your way up to a full program of activity.

Individuals with insulin resistance may have a harder time inducing ketosis and may suffer from carbohydrate cravings. Ask your doctor to measure your insulin, fasting glucose, and hemoglobin A1c levels. HbA1c is a measurement of your average glucose levels over three months. Using high dose medium chain triglyceride fats (MCT) or coconut fats assists in helping you overcome sugar cravings and glycotoxicity. One has to increase these fats slowly and use fat digesting enzymes containing lipase and emulsification aids such as ox-bile to initially assist in the increased fat load. Another way to combat the initial sugar cravings is to increase fats in your diet such as nuts and seeds, avocado, or non-starchy vegetables cooked in ghee, coconut, or avocado oil.

Neuroprotective Keto: Supplementation

As mentioned above in the section about the mind-gut connection, your brain and gut have a special relationship. In order to achieve neuroprotection, it’s necessary to heal your gut by encouraging your good bacteria to take charge. The best way to improve your gut microbiome is to take probiotics and prebiotics.

Probiotics contain the good bacteria that are able to take carbohydrates and convert them into lactic acid, which suppresses your bad bacteria. Probiotic should be used with caution if histaminic but include:

  • Kombucha
  • Miso
  • Pickled vegetables
  • Yogurt (unsweetened)
  • Kefir from coconut
  • Kimchi
  • Sauerkraut
  • Tempeh

Prebiotics comprise food that’s indigestible for you, but it can be digested in your colon by your good bacteria. The bacteria break probiotics down into materials that aid the maintenance of your gut. Many of the resistant starches and fibrous plants listed above count as prebiotics.

Here are a few further examples of prebiotic supplements:

  • Organic psyllium seed husks
  • Plantain
  • Green banana starch
  • Inulin
  • Acacia fibre

When you begin the ketogenic diet it takes a few days to achieve ketosis. In the meantime, you may experience some side effects, often referred to as ‘keto-flu’ by some people. With this condition, patients often experience:

  • Feeling run down
  • Brain fog
  • Headaches
  • Fatigue
  • Abdominal pain
  • Constipation
  • Diarrhea
  • Poor mood
  • Muscle cramps

All of these symptoms are perfectly normal, considering that you’re detoxing from sugar, training your body to run off ketones, and often experiencing the loss of electrolytes and dehydration. However, there are ways to combat this as follows:

  • Caffeine dehydrates you so you need to drink plenty of water to reduce dehydration symptoms, such as fatigue or headaches.
  • While iodized table salt is usually considered something that’s best avoided, increasing your intake of high mineral sea salt improves your water retention and replenishes your salt levels.
  • Supplement with magnesium in liquid form and foods rich in potassium, such as avocado, nuts, mushrooms, leafy salads, and bone broth.

You’ll discover that following the ketogenic diet is extremely rewarding because you’ll begin to feel some benefits within weeks. However, it may take at least six months to begin to feel the full advantages when attempting to reverse cognitive decline. The ketogenic diet tweaked to improve neuroprotection is a powerful tool in your quest for optimal health. Too often we treat the symptoms of disease when we could have headed off the condition years or decades earlier. Your body is amazing and can reverse the impact of poor diet, stress, and sometimes even genetics if you make the necessary changes.

What do you have to lose? Schedule an appointment at the Hoffman Centre For Integrative and Functional Medicine and get started with the ketogenic diet today.


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  33. http://www.pnas.org/content/108/7/3017
  34. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2821835/
  35. Mercola A Beginner’s Guide to the Ketogenic Diet: An Effective Way of Optimizing Your Health
  36. https://www.apollohealthco.com/dr-bredesen/ Dr Bredesen’s ReCODE Report Nutritional Guidelines Ketoflex 12/3
  37. https://bodybio.com/
  38. Organic Creamed Coconut – www.earthschoice.ca
  39. Quality Nuts and Seeds  – www.ranchovignola.com and https://nuts.com/nuts/pili
  40. Quality Olive Oil – www.rawelements.ca
  41. Nut pods unsweetened coffee creamer – www.naturamarket.ca
  42. MCT emulsified coffee creamer – www.onnit.com
  43. Exogenous ketone powder – www.perfectketo.com (salted chocolate caramel flavor is best)
  44. Ketone and glucose meter – www.keto-mojo.com
  45. Humanly raised Certified organic beef, pork, turkey, chicken, and eggs https://www.sunworksfarm.com/certified-organic-beef/     (Bush Lane Organics/ Community Natural Foods/ Amaranth Whole Foods/ Planet Organics-chicken & eggs mainly, other meats can be ordered). Also TK Ranch meats at https://tkranch.com/

Reversing Alzheimer’s and Preventing Cognitive Decline: Seven Steps You Can Take Today

Alzheimer’s disease is a devastating condition for both patients and their families. Unfortunately, Alzheimer’s disease (AD) is also on the rise globally. Effective treatment of AD has been of growing concern within the medical community because its prevalence continues to spread. The fact of the matter is that Alzheimer’s treatment demands a different approach.

While our treatments of many other chronic diseases ( heart disease, diabetes, cancer) have improved over the years, effective Alzheimer’s treatments continue to remain incomplete and disappointing.

Alzheimer’s disease not only impacts patients’ health, but it is physically, emotionally, and financially taxing on their families as well. It is estimated that AD will directly impact over 15% of the US population, meaning its indirect effect on families and caretakers is widespread and includes hundreds of millions of people.

Unfortunately, as a society, we have come to view cognitive decline, a precursor to Alzheimer’s disease, as an accepted sign of aging.

However, this is a myth that needs to be immediately dispelled. The types of cognitive decline associated with AD are NOT normal signs of aging.

Still, there is good news when it comes to Alzheimer’s disease. New methods have shown promise in completely stopping and even reversing cognitive decline in patients.

Let’s look more deeply into these methods and uncover ways you can help yourself or your loved ones who are suffering from this devastating disease.

Today, there is more hope than ever before for those touched by Alzheimer’s.

Alzheimer’s Reaches Epidemic Proportions

According to the World Alzheimer Report 2016, approximately 47 million people globally live with dementia, and estimates for 2050 are projected to be more than 131 million. In fact, Alzheimer’s disease (AD) is now considered the third leading cause of death in the United States, just behind cardiovascular disease and cancer.

Women are at the heart of this epidemic. About 65% of all those who develop AD are women, and 60% of all caretakers of those affected by AD are women. Women are now more likely to develop AD than breast cancer. Many believe this is because women live longer than men, but this reasoning still does not explain or justify why this condition is on the rise. Of significance is that only 5% of Alzheimer’s cases are familial, i.e., having a genetic basis that causes early onset Alzheimer’s. The rest are caused by lifestyle factors that are influenced by many variables over which patients have a significant degree of choice and control.

Nonetheless, the question remains: Why is Alzheimer’s worsening, and what can be changed in how we approach the treatment of such a deadly and heartbreaking disease?

Other treatments of chronic illnesses such as cardiovascular disease, HIV, and cancer have improved because of the combination therapies that have been applied, and yet a majority of AD treatment has been focused primarily on monotherapeutic drug treatments. It is a startling fact that neurodegenerative diseases have not benefitted as other diseases have from advances in modern medicine. Only through tackling a disease like Alzheimer’s with multiple therapies can we find a successful approach to reducing the growing global impact it is having on our society.

Research has found that AD involves extensive networks of molecular interactions, which means the disease demands a network-based, multi-system treatment approach. The key issue in understanding Alzheimer’s is that it is not a single disease; the different biochemical imbalances involved require different treatments. There is no single drug that will cure Alzheimer’s, and nor will there ever be one. Present Alzheimer’s drug treatments make only slight differences to symptoms but do little to address disease progression.

At the forefront of this functional medicine approach to AD is Dr. Dale Bredesen and his team from the Buck Institute for Research on Aging. Through careful examination of the pathogenesis of Alzheimer’s, Dr. Bredesen and his team have found promising results. They have developed a multiple modality approach to achieving what they call metabolic enhancement for neurodegeneration (MEND), now referred to as Reversal of Cognitive Decline or ReCODE.

Through the approach Dr. Bredesen has developed, patients have been able to dramatically improve cognitive function, achieve reversal of symptoms, and in some cases, return to work. The ReCODE program includes lifestyle interventions, therapeutic diets, and targeted nutrients.

Before we dive into Dr. Bredesen’s program, it is important that we understand the pathogenesis of AD and its six subtypes. Let’s take a closer look at this disease, how it presents itself, how it develops, and what can be done to prevent it.

The Development of Alzheimer’s

The reason a multifaceted approach is needed for the treatment of Alzheimer’s is because its cause is not due to any single factor. Many metabolic processes are at play. In fact, there are six different subtypes of AD, distinguished by the different metabolic abnormalities that underlie the root causes of each form of this condition.

An individual usually develops Alzheimer’s disease after the age of 65. Symptoms begin showing as general memory loss and eventually progress to further impact daily life. The 10 warning signs and symptoms of Alzheimer’s disease versus normal signs of aging are listed below.

Alzheimer’s disease Symptoms Signs of Normal Aging
Memory loss that disrupts daily life, especially forgetting newly learned information Forgetting newly learned information such as appointments or names but being able to recall them later
Having difficulty solving everyday problems such as paying billsMaking occasional errors but none that are significant or out of the ordinary
Struggling to complete familiar tasks such as driving home or to workNeeding help setting up new equipment or electronics
Losing track of dates, seasons, or timeTemporarily forgetting the day but having the ability to recall it later
Difficulty judging distance, spatial relationships, and contrastWorsening vision caused by cataracts
Trouble recalling words for things, following conversations, and speakingOccasionally having difficulty finding the preferred word while not forgetting names of items
Misplacing items and not being able to retrace stepsBeing able to remember steps to find misplaced items
Poor judgement or decision-making; inability to multitask Occasionally making poor decisions, but  rarely with major negative consequences
Social withdrawalPreferring to socialize a bit less
Changes in personality and moodBecoming irritated when things are not done a particular and preferred way.

Click here for an Alzheimer’s Questionnaire.

Signs and symptoms of AD are not normal signs of aging. If you or someone you love is experiencing any of these symptoms, it is important to make an appointment with your functional medicine doctor as soon as possible because AD worsens over time.

AD is a progressive disease and although there is no cure, Dr. Bredesen’s protocol has been able to slow and reverse cognitive decline. Remember, the earlier AD is caught, the easier it is to successfully treat the condition.

Once a person has noticeable symptoms, they are in the later stages of cognitive decline. AD has an initial “silent phase,” where brain degeneration is occurring but these changes are not detectable using objective tests. Patients may, however, notice slight memory and cognitive changes. See the image below.

Alzheimer’s disease (and dementia) does not begin suddenly.

Before AD develops, there is a noticeable slow decline in mental health. It has been estimated that the pathophysiology of the disease exists for approximately 20 years before any diagnosis is made. This means that many individuals have the beginnings of the disease without actually realizing it.

Preclinical begins with a subtle loss of neurons and a subjective sense of the brain’s mental processes not being as sharp as they once were.

Mild Cognitive Impairment is said to be present when a noticeable decline in mental functioning is noticed by others, and objective cognitive testing (performed simply by doing a mini-mental exam, computerized cognitive testing such as the CNS Vital Signs test, or a more sophisticated workup by a neuro-psychologist) is decreased. Activities of daily living have not yet been affected.

Dementia is said to occur when cognitive decline is sufficient to interfere with daily life. Objective testing such as PET scans and Neuroquant MRIs will show distinct patterns of brain changes such as cortical and hippocampal atrophy, reduced glucose uptake, and amyloid-beta-production.

Temporal Progression of Cognitive Impairment

What exactly is Alzheimer’s disease?

Simply put, Alzheimer’s has been observed to occur when the genes associated with the disease cause brain cells to become suicidal. The question that Dr. Bredesen asked was, “What are the fundamental processes and mechanisms that drive these genes to turn on and cause brain cells to die?”

Based on numerous studies, we now know that AD results from an imbalance in the destruction of neurons and synapses and the building up and maintenance of synapses and neurons. It has been observed that a molecule known as amyloid-beta accumulates in higher than normal concentrations in the brain, which causes the synapses, along with the neurons essential for memory, to die.

Where does amyloid-beta come from? It is derived from the amyloid precursor protein (APP), of which amyloid-beta is but a small portion. The APP, once produced by neurons, is cut by molecular scissors called proteases, which can cut at any of the three spots along the APP or at one distinct site. If the APP is cut at three particular sites, the four peptides produced from this action underlie the process of the synaptic loss and neuronal death that characterize AD. If, however, the APP is cut at just a single site, the two peptides that result cause just the opposite to occur; synaptic connections are maintained and neuron growth is nourished. These two peptides are referred to as the anti-Alzheimer’s peptides. See image below.

Alternative processing of, and signaling by, APP

Thus, the APP appears to act as a molecular switch that mediates plasticity-related processes. In summary, in order to reduce your risk of AD, you have to maintain all the necessary lifestyle practices and therapies that induce the two brain-affirming, anti-AD peptides and reduce all the factors that induce the production of the four pro-AD-inducing peptides. How exactly to achieve this, forms the basis of Dr. Bredesen’s ReCODE program.

AD is similar to other chronic illnesses in that there is an age-associated imbalance between the building up of cells that mediate neural plasticity and the destruction of cells. In AD, this occurs at the level of neuronal synapses, called synaptoblastic (building up of synapses), as opposed to synaptoclastic (destruction of synapses) activity. These intricate processes happen over time, in reinforcing cycles.

Six Subtypes of Alzheimer’s disease

Understanding the different Alzheimer’s subtypes is also critical for creating the best treatment plan for each patient.

There are numerous metabolic processes involved in contributing to AD, with six different subtypes that have been identified by Dr. Bredesen. These six subtypes are based on three papers by Dr. Bredesen: The first paper, in 2014, describes the initial contributions to his protocol (first called MEND), the second paper in 2016 outlines 10 case studies, and the third paper, also in 2016, describes neurodegeneration due to biotoxin exposure.

These subtypes are not widely used in diagnostic workups and clinical protocols at this time, but understanding the differences is essential to creating a comprehensive treatment plan. The six subtypes of Alzheimer’s disease are as follows:

Subtype 1 (inflammatory or “hot”) Alzheimer’s: Patients with this form of AD have predominantly inflammatory symptoms. These proinflammatory factors include cytokines, chemokines, acute-phase reactants, and other inflammation-causing mediators.

Patients with subtype 1 AD also have increased levels of c-reactive protein, high interleukin-6, and a low albumin-to-globulin ratio. The microglia and activated astroglia (brain structures) are also inflamed.

There is also an antagonism between the sirtuinT1 enzyme (anti-inflammatory) and NFkB (the nuclear factor k-light-chain enhancer of activated B cells [proinflammatory]); when NFkB inflammation is activated and SirT1 is suppressed, it can alter gene transcription and turn on gamma-secretase and beta-secretase. Gamma-secretase cleaves to the APP and contributes to synaptoclastic destructive processes within the brain.

The inflammation in subtype 1 primarily involves the innate immune system, and usually (but not always), there is systemic inflammation. Onset of this subtype typically occurs in an individual’s 70s or later.

Subtype 1.5 (glycotoxic or “sweet”) Alzheimer’s: This subtype is the in-between of subtypes 1 and 2 because it involves both inflammatory perpetrators and atrophic processes. Glucose regulation is impaired, resulting in insulin resistance and inflammation due to hyperglycemia (increased blood glucose). This glucose dysfunction also disrupts hormone-signaling and trophic factors (molecules that allow neurons to maintain and create neighboring connections).

Subtype 2 (atrophic, non-inflammatory, or “cold”) Alzheimer’s: Patients with subtype 2 AD have atrophic symptoms, meaning there is degeneration and dysfunction of neurological functions due to the insufficiency of certain nutritional and metabolic factors. Even though this underlying cause is different from inflammation, it still results in the same disease.

Similar to subtype 1, subtype 2 causes the APP to create amyloid plaques. Subtype 2 AD is associated with declining trophic factors, such as nerve growth, brain-derived neurotrophic factors (BDNF), testosterone, estradiol, vitamin D, thyroid hormone function, and insulin levels.

All of these declining trophic factors cause your brain to stop synaptogenesis (creation of new synapses), which is why learning new things becomes more difficult and worsens over time.

Subtype 3 (toxic or “vile”) Alzheimer’s: Subtype 3 is caused by toxin exposures, most commonly inhaled toxins (such as mold mycotoxins), and is sometimes called inhalational Alzheimer’s disease (IAD). One 2014 study showed fungal proteins in the brains of Alzheimer’s patients, and another study in 2015 showed fungal infections in the brains of Alzheimer’s patients. Fungal DNA and proteins were detected in the brain tissue from AD patients, but not in controls. Fungal particles could also be detected in the neurons of the same AD patients. Herpes simplex type 1 (HSV-1) and chlamydia pneumoniae have also been associated with amyloid protein production in AD.

Many patients with subtype 3 AD have markers of chronic inflammatory response syndrome (CIRS) but do not fit the official criteria for a CIRS diagnosis. Dr. Bredesen says that those with IAD will have lab results similar to those of CIRS patients, but their symptoms are mostly Alzheimer’s-like dementia.

Typically, patients with this form of AD have high levels of the complement component C4a and the transforming growth factor beta-1 (TGF-b1), both of which are specific inflammatory cytokines, as well as high levels of matrix metallopeptidase 9 (MMP9), an enzyme involved in the cell membrane penetration of inflammation. Patients also have decreased levels of the melanocyte-stimulating hormone (MSH), the vascular endothelial growth factor (VEGF), and the antidiuretic hormone (ADH). Usually, there are other abnormalities present such as high levels of cortisol and low levels of the adrenocorticotropic hormone (ACTH) and the antidiuretic hormone (ADH).

Symptoms of subtype 3 AD are similar to those of the other subtypes in that they include memory loss and difficulty with word recall; however, patients may also report having a metallic taste in their mouth and an increased sensitivity to smell. These patients rarely have the respiratory complaints, chronic fatigue, muscle pain, or other symptoms usually associated with CIRS.

Subtype 4 (vascular) Alzheimer’s: Alzheimer’s development in subtype 4 patients is a protective response to vascular insufficiency and results in a triggered amyloid response.

Subtype 5 (traumatic) Alzheimer’s: This subtype is characterized by head trauma, and these patients typically have significant personality changes. Not all head trauma patients will develop AD. One major study showed an 2.3 times increased risk of developing AD in older adults with a history of moderate traumatic brain injury than seniors with no history of head injury. Those with a history of severe traumatic brain injury had a 4.5 times greater risk of developing AD. Traumatic brain injury changes brain chemistry by inducing beta-amyloid and tau proteins, the hallmark proteins linked to AD. Traumatic brain injury may be more likely to cause dementia in individuals who have either one or two of the APOE-e4 genes. There are no studies linking mild brain injury or concussion to the development of AD.

Genetics and Alzheimer’s Disease

It is important to note subtypes 1, 1.5, and 2 are all associated with the ApoE4 gene mutation. Although 95% of all Alzheimer’s cases are not caused by genetics, genetic testing is essential to determine if there is a propensity for these forms of Alzheimer’s. In fact, what is called familial Alzheimer’s is very rare, appears to be clustered in families, and presents earlier in life. That said, two-thirds of AD patients carry one or two copies of the ApoE4 gene.

Individuals who are ApoE4-positive with one copy of the gene (approximately 75 million Americans) have a 30% lifetime risk of developing AD. Those with two copies of the gene (approximately 7 million Americans) face a 50% lifetime risk of developing AD.

Interestingly, scientists have found that while the ApoE4 gene increases the risk of subtypes 1 and 2, it decreases a person’s risk for developing subtype 3. This is believed to be due to the protective nature of ApoE4, which can fight off the microbes that cause subtype 3 AD. Ultimately, ApoE4 is thought to be an advantage in your youth but can contribute to chronic illnesses as you age.

You can be tested for ApoE4 with your functional medicine doctor. This is a good idea because if you have the ApoE4 gene mutation, there are certain measures you can take to decrease the chances of developing Alzheimer’s. The website www.apoE4.info is an excellent resource for individuals with one or two copies of this gene.

One fascinating behavior a person with the ApoE4 gene can implement in order to favorably influence the outcome is 12-hour fasting. The ApoE4 gene helps you survive famine, and so it makes sense that intermittent fasting can help those with the gene avoid Alzheimer’s. The ApoE4 allows your body to use fat more efficiently and go longer without eating. This means if you find out through testing you have this gene, fasting can be used as a tool to have your body switch to burning ketones for energy over glucose, which is believed to aid in preventing AD.

Even if you do have the APoE4 gene, you can still prevent Alzheimer’s disease from developing, but you have to be proactive, educate yourself, and implement as many of the lifestyle factors as you possibly can. Let’s look at how to do that.

What Do All Forms of Alzheimer’s Disease Have in Common?

There are 36 mechanisms that Dr. Bredesen has identified as contributing to Alzheimer’s, but mitochondrial dysfunction is at the core of all of these.

Your mitochondria are the powerhouses of your cells, creating the energy molecules (ATP) every cell of your body needs to function. Additionally, free radicals (damaging molecules produced as byproducts of normal metabolism but enhanced by toxic exposures, genetic detoxification, and nutritional deficiencies) tend to be created in your mitochondria. When you have a higher incidence of free radicals in your cells, your mitochondria suffer damage and cannot produce adequate amounts of ATP, resulting particularly in neuronal cell death.

Through his research, Dr. Bredesen found that the APP makes amyloid in response to your cells being under attack by free radicals and toxic substances. Your body’s trophic support may also be decreased. Together, both low trophic factors and increased amyloid levels contribute to cognitive decline.

The complexity behind the pathogenesis of Alzheimer’s disease is why a comprehensive, multivariable approach is necessary. With that in mind, Dr. Bredesen’s recommendations include addressing these 36 mechanisms:

  • Increasing mitochondrial function; mitochondria produce ATP, the necessary chemical responsible for the energy needed for nerve growth, health, and maintenance.
  • Increasing mitochondrial protection
  • Decreasing beta-amyloid production, the main component of amyloid plaques found in Alzheimer’s
  • Increasing beta-amyloid degradation
  • Decreasing beta-amyloid oligomerization, i.e., the creation of longer molecules of beta-amyloid
  • Increasing the brain-derived nerve factor (BDNF), a neuropeptide with growth effects on neurons
  • Increasing the nerve-growth factor (NGF), a neuropeptide involved in the growth and maintenance of neurons
  • Increasing the granulocyte-stimulating factor (G-CSF), a growth factor that has neuroprotective effects and that increases neuronal growth
  • Increasing the activity-dependent neuroprotective protein (ADNP), a protein essential to brain health and cognitive function
  • Decreasing p-tau; neurofibrillary tangles are aggregates of hyperphosphorylated tau proteins, which are primary markers of Alzheimer’s disease.
  • Decreasing homocysteine, a proinflammatory protein
  • Building synapses
  • Increasing beta-amyloid breakdown
  • Increasing the albumin/globulin (A/G) ratio, indicative of inflammatory AD
  • Decreasing inflammation
  • Inhibiting NF-kB, a protein complex that controls inflammatory cytokines
  • Increasing glutathione (GSH), a major antioxidant
  • Increasing antioxidants, which decrease neuroinflammation
  • Decreasing iron, a pro-inflammatory mineral
  • Increasing cerebral blood flow
  • Increasing acetylcholine, a neurotransmitter involved in memory
  • Increasing alpha-seven nicotinic acetylcholine receptors (α7), a critical link between neurodegeneration and AD
  • Increasing amyloid-beta transport
  • Increasing amyloid beta clearance
  • Decreasing the ApoE4 effect; this gene determines increased risk for AD, with the 4/4 gene having the highest risk
  • Increasing gamma-aminobutyric acid (GABA), a calming and neuroprotective neurotransmitter that downregulates glutamate, an excitatory neurotransmitter
  • Decreasing N-methyl-D-aspartate receptor activity (NMDA), a receptor that regulates the activity of glutamate, an important neurotransmitter in the brain involved in learning and memory
  • Optimizing hormones, especially estradiol, progesterone, testosterone, DHEA, and thyroid
  • Increasing vitamin D
  • Decreasing the pro-form of the neuron growth factor (pro-NGF), a protein expressed at higher levels in brains of AD patients
  • Decreasing caspase-6, the activity of which is associated with increased risk of AD
  • Decreasing the N-terminal fragment of the beta-amyloid precursor protein (N-APP)
  • Enhance detoxification
  • Increasing vascularization
  • Increase telomere length
  • Reduce toxic metals

Dr. Bredesen explains that these are like holes in a roof, which need to be individually addressed in order for a full recovery to be made.

It is important to realize that AD is a protective response to three major metabolic and toxic disturbances:

  1. Inflammation- be it infectious (viruses) or sterile (modified inflammatory proteins)
  2. The withdrawal of trophic support (e.g. nerve growth factor, estradiol, testosterone, vitamin D etc.)
  3. Exposure to toxins such as mercury, aluminum, mold mycotoxins.

Dr. Bredesen has identified a number of factors that induce the APP receptor to go in the right direction of trophic or building synapses and neuronal health. The APP responds to dozens of molecules that assist brain health and anti-Alzheimer’s protection. Our brains have 100 billion neurons, and each neuron has approximately 10,000 connections, called synapses. Synapses are critical for cognitive functioning, memory storage, decision-making, and neurotransmitter communication. One’s brain has nearly one quadrillion energy-demanding synapses to power and run efficiently with energy-producing raw materials. In short, the APP has to constantly assess if the incoming data is shifting the lever in the direction of neuronal building or in the direction of neuronal destruction.

The sum total of the way one lives one’s life minute-to-minute affects this highly complex algorithm shift in either one of two directions—towards brain protection and maintenance, or towards brain inflammation, destruction, and reduced neuronal death. It really does come down to choice. AD begins with the loss of function of the synapses, the loss of the synapses themselves, and eventually, the loss of brain cells themselves, leading to brain shrinkage that is visible on MRI scans.

When one is young, the ratio between neuronal growth and destruction is equally balanced between the two. As we age, the destructive (clastic) part of the process tends to dominate over the building (blastic) part of brain preservation. We must decide to do all we can do to downregulate any of the factors that induce inflammation and further clastic activity and upregulate anything we can that induces growth, blastic activity, and hence, neuronal plasticity.

The realization that multiple factors induce brain growth as well as brain destruction will explain why the single drug model of AD treatment has not borne any fruit. There is no single drug that can ever address the complexity of all the metabolic factors that contribute to brain health maintenance and optimization. Dr. Bredesen’s analogy is that of a roof with 36 holes in it. A roofer called in to fix only one hole where the rain is pouring in will never be able to stem the flood of water pouring in through the other 35 holes no matter how well he patches the one hole.

Robert M Cardiff, MD, Commissioner of the Food and Drugs Administration (FDA) concurs with this observation:

“Multimodal therapy approaches that combine interventions aimed at different aspects of disease are emerging as potential-and perhaps essential-ways to enhance clinical outcomes for patients with psychiatric and neurological disorders. Indeed, for most chronic diseases, multiple pathways are involved simultaneously, making it unlikely that a single treatment will prove sufficiently effective.”

From these insights it is important to realize that we do not get Alzheimer’s for no reason. There are many possible reasons and the doctors of the future will be trained to investigate and look for many if not most of these factors identified to date.

Dr. Bredesen’s ReCODE program aims to achieve the following:

  1. Optimize metabolic parameters to the maximum, not just simply normalize them.
  2. Address as many of the causative network components as necessary with the understanding that combination effects will be additive and cumulative and will create an effect that is more than the sum of the many single therapies.
  3. The more that patients are able to achieve in terms of their therapeutic input, the more likely it is that a certain threshold will be reached that will tip them over from a pathogenic process to a therapeutic benefit. This implies that a combination of therapies will be more than the sum of individual parts.
  4. A personalized approach is needed with a prioritization of therapeutic inputs, which needs to be computerized and analyzed according to the laboratory values affecting the plasticity networks.
  5. Repetitive application of therapeutics is necessary to optimize outcomes over time.
  6. The goal of therapy is to use a physiological approach with as much of an upstream causative approach that can possibly be implemented.

A Therapeutic System was developed by Dr. Bredesen

Therapeutic System (adapted from Bredesen, 2014 and cited by Ash, 2015)

The critical role of several factors in Alzheimer’s disease necessitates several therapeutic interventions. The required interventions seek to:

  • reduce inflammation
  • address autoimmunity
  • minimize insulin resistance
  • decrease amyloid-beta (Aβ)
  • reduce excess cortisol and the corticotropin-releasing factor (CRF).

In so doing:

  • the hypothalamic adrenal axis is supported
  • antioxidant function is optimized
  • blood glucose is balanced
  • acetylcholine synthesis is supported.

Interventions identified by Bredesen (2014) to achieve these aims include:

  • Diet optimization to minimize simple CHO, inflammation, and insulin resistance: Simple CHO, inflammation, and insulin resistance are minimized by providing patients with a choice of several low-glycemic, low-inflammatory, and low-grain diets.
  • Autophagy and ketogenesis enhancement: Autophagy and ketogenesis are enhanced by having the patient fast for 12 hours each night (including at least three hours before bedtime), thereby reducing insulin and Aβ levels.
  • Stress reduction: Stress is reduced by having the patient engage in personalized stress reduction activities (e.g., yoga, meditation, music, etc.) that target the stress axis, reduce cortisol, and equilibrate the CRF.
  • Sleep optimization: Sleep is optimized by having the patient follow a sleep regimen, including eight hours of sleep per night, the use of 0.5 mg melatonin and/or 500 mg of tryptophan if awakening, in addition to ruling out possible sleep apnea.
  • Exercise regimen: Patients are provided with an exercise regimen, including 30–60 minutes of physical exercise 4–6 days per week.
  • Brain training and stimulation: Patients are provided with BrainHQ or related brain-training software programs.
  • Homocysteine optimization: Homocysteine is optimized to <7 using methylcobalamin (Me-B12), methylfolate (MTHF), pyridoxal-5-phosphate (P5P), and, if necessary, trimethylglycine (TMG). Optimization of serum B12: Serum B12 is optimized to >500 using methylcobalamin (Me-B12).
  • Lowering c-reactive protein: Due to the critical role of inflammation in Alzheimer’s disease, c-reactive protein is lowered to <1 through the use of optimized hygiene and an anti-inflammatory diet that includes curcumin and fish oil (DHA/EPA).
  • Insulin optimization: Due to the role of inflammation in Alzheimer’s disease and the relationship it shares with type II diabetes, insulin levels are optimized to <7 (fasting) and hemoglobin A1c (HbA1c) to <5.5 through the use of an anti-inflammatory diet.
  • Hormone optimization: Hormones are optimized, including free T3, free T4, the thyroid-stimulating hormone (TSH), pregnenolone, progesterone, estradiol, testosterone, cortisol, and dehydroepiandrostenedione (DHEA).
  • Restoration and optimization of gastrointestinal health: Gastrointestinal health is restored, repaired, and optimized, including the use of prebiotics, probiotics, and avoidance of inflammation and autoimmunity.
  • Reduction of a-beta Levels: A-beta (Aβ) levels are reduced using curcumin and ashwagandha (an Ayurvedic adaptogenic herb).
  • Cognitive enhancement: Cognitive enhancement is achieved through the use of bacopa monniera (an Ayurvedic herb known for its cognitive enhancing properties) and magnesium threonate (MgT).
  • Optimization of vitamin D3: Vitamin D3 (25-OH-D3) levels are optimized to 50–100 ng/ml (US levels), using vitamins D3 and K2.
  • Nerve-growth factor optimization: The nerve-growth factor is increased using h. erinaceus or acetyl-l-carnitine.
  • Provision of synaptic structural components: Provide synaptic structural components using citicoline and docosahexaenoic acid (DHA).
  • Optimization of antioxidants: Optimize antioxidants using mixed tocopherols and tocotrienols, selenium (Se), blueberries, n-acetyl-cysteine (NAC), ascorbate, and a-lipoic acid.
  • Optimization of the zinc:copper (zn:cu) ratio: Optimize the zn:cu ratio based on values obtained.
  • Ensure nocturnal oxygenation: Ensure nocturnal oxygenation through treating or ruling out sleep apnea.
  • Optimize mitochondrial function: Optimize mitochondrial function through optimizing CoQ or ubiquinol, a-lipoic acid, pyrroloquinoline quinone (PQQ), n-acetylcysteine (NAC), N-acetyl-L-carnitine (ALCAR), selenium (Se), zinc (Zn), resveratrol, ascorbate, and thiamine.
  • Increase focus: Increase focus using pantothenic acid as required for acetylcholine synthesis.
  • Increase SirT1 function: Increase SirT1 function using resveratrol.
  • Exclude heavy metal toxicity: Evaluate mercury (Hg), lead (Pb), and cadmium (Cd) to confirm or exclude heavy metal toxicity; chelate if indicated to address the effects of heavy metals on the central nervous system.
  • Increase medium-chain triglyceride (MCT) oil effects: Use coconut oil or Axona.

According to Dr. Bredesen’s research and discussions, the effects of various targeted therapies may be additive, multiplicative, accumulative, and synergistic.

A functional medicine approach is the most effective way to implement these approaches.

7 Things You Can Do to Prevent Cognitive Decline Right Now

Here are some things you can do right now to work on your own personal cognitive health, using similar principles to those found in the Bredesen ReCODE Protocol.

1. You Must Get Quality Sleep

Getting seven to eight hours of quality sleep each night is critical to promoting cognitive function because during sleep is when your body removes metabolic waste from your body.

If you have sleep apnea, you must address it. Your brain is starved of oxygen when you have sleep apnea, and it directly impacts your cognitive abilities. Ask your doctor to refer you for a sleep study.

2. Implement Overnight Fasts

By putting your body in an overnight fast (12 hours at least), you induce ketogenesis (you also need a low-sugar and low-carb intake to promote this). When your body is in ketogenesis, your insulin levels are lowered. Additionally, amyloid-beta levels are reduced, which are a main contributor to the amyloid plaques found in Alzheimer’s patients. A low-sugar and low-carb diet makes overnight fasting surprisingly easy.

3. Reduce Carb and Sugar Intake

Diets with few carbs and little to no sugars are the best for reducing inflammation in the body, and they reduce your chances of developing insulin resistance. Additionally, low-sugar and low-carb diets have been linked to a decreased risk of developing Alzheimer’s disease.

4. Reduce Your Toxic Load

Reducing toxin exposure gives every bodily system a better chance at functioning properly, and your mitochondria and metabolic systems are no exception.

You can reduce your toxic load through having good air and water filters in your home. Additionally, avoid toxin-containing items such as:

  • Non-stick and aluminum pans
  • Harmful personal care products (you can check your items against the EWG Database)
  • Harsh cleaning products (opt for natural solutions)
  • Paints with volatile organic compounds (VOCs)
  • Metal dental fillings
  • Fish high in heavy metals
  • Plastics with BPA
  • Charred and fried meat (high-lipid peroxidation)

Remember, if your lab results are coming back similar to those of a CIRS patient, yet you are not having typical symptoms of CIRS, check for signs of Alzheimer’s and other indicators of toxin exposure due to building damage from mold and water (inflammagen exposures).

5. Add These Supplements

Dietary changes are at the heart of the Bredesen Protocol, and by adding certain supplements, you can protect your brain. Consider the following supplements because each has shown to promote healthy brain function.

  • Vitamin B12—methylcobalamin
  • Vitamin C – must be taken twice daily as it is water soluble and is excreted quickly
  • Vitamin E—mixed tocopherols
  • Turmeric—a lipophilic form is best
  • Vitamin D—measure your 25 OH Vitamin D levels to achieve the optimal dosage for you
  • DHA (found in fish and fish oil supplements)
  • Citicoline
  • Probiotics

6. Exercise Every Day

Having an exercise routine has been unequivocally linked to a reduction in cognitive decline. Studies have found that even a walk each day significantly slows the decline of Alzheimer patients.

I encourage you to get up and move at least once a day. Even a quick 15-minute high-intensity interval workout has been shown to be as effective as an hour-long workout.

7. Reduce Stress

Stress causes high levels of cortisol and CRF, which are both linked to Alzheimer’s. Add stress-reducing habits to your day. These can include quick meditations, yoga, listening to calming music, or taking walks.

Reversing Cognitive Decline Is Within Reach

We are living in an exciting time when it comes to Alzheimer’s treatments. Through a comprehensive approach to this illness, we may be able to slow down and even reverse most cases of Alzheimer’s.

While the Bredesen Protocol works to reverse cognitive decline, we can take the same science and apply it to our lives today to prevent Alzheimer’s from developing in the first place. We can even take these concepts one step further and optimize brain health to improve function overall.

Share this article with someone you know who would benefit from hearing about this monumental approach to a devastating disease. The future of Alzheimer’s treatment is bright.

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The End of Alzheimer’s. Dale Bredesen  Avery – An Imprint of Penguin Random House 375 Hudson Street New York, New York 10014, 2017