Flux Health Forum

Alzheimer’s and Diabetes: cause or effect?

Alzheimer’s and Diabetes: Cause or Effect?

Alzheimer’s is often called “diabetes type 3” because there appears to be a correlation between the two disorders.

After first identifying amyloid β plaques and tau tangles in the brain of a deceased patient in the early 1900’s, Alois Alzheimer was careful to not infer that these structures had caused the dementia in the patient. Unfortunately, most of the research until recently (at least by drug companies) has been aimed at finding ways to reverse the accumulation, or at least stop the spread of these structures. While drugs have been developed that can successfully accomplish that task, it appears that Dr. Alzheimer was right—even when plaques and tangles are decreased in Alzheimer’s patients, cognitive decline continues.

Such distinctive, distinguishing structures seem like such a good place to start when addressing a cure to the disease, so where to next? Recent research has begun exploring other avenues including comorbidities to Alzheimer’s disease. This has proved much more successful, particularly with regards to Type 2 Diabetes (Janson et al. 2004 reported that 81% of Alzheimer’s patients have either Type 2 Diabetes or “Impaired Fasting Glucose”). Treating AD patients with diabetes drugs has proved successful, so clearly there is a link between AD and insulin. One current hypothesis is that insulin acts as a growth factor in the brain—Talbot et al. 2012 found that even in non-diabetic AD patients, insulin was no longer effective as a growth factor. Furthermore, the use of diabetes drugs has also shown to be successful in treating other neurodegenerative conditions such as Parkinson’s Disease and even mTBI/concussions (reviewed in Hölscher 2018). The strong link between AD and insulin sensitivity has led many researchers to refer to AD as “diabetes Type 3”.

What we learned about the role of insulin in brain health with the Brain Gauge

The pancreas is not the only place that produces insulin; erratic productivity of insulin in the brain could play a leading role in many disorders. Most textbooks and online references will point you to the pancreas as the body’s site of insulin production. Increase glucose in the system and your pancreas starts producing/releasing insulin into the blood stream. That has been the standard doctrine for decades. However, in 2014, a paper reported that neurogliaform (NGF) cells produce insulin in the brain (Molnar et al, 2014). There have been many papers since that time confirming this, and many of these papers point to the brain playing a role in insulin regulation. In fact, insulin can be found to be at 10-100 times higher levels in the brain than in the bloodstream. That in itself is pretty good evidence that the brain has different needs from the rest of the body and that it has a mind of its own when it comes to regulating what it needs (pun intended).

What does this have to do with the Brain Gauge? At the time of the discovery of the NGF cell’s insulin producing capability, we had been involved in research in several different neurological disorders that yielded some interesting results. Namely, some individuals with chronic pain, autism and chronic TBI had the common characteristic of having lower than normal feed-forward inhibition (how that measure is obtained is described here: https://downloads.corticalmetrics.com/pub/favorov_role_2017.pdf), and we were working on a hypothesis that feed-forward inhibition was modulated by the NGF cells, and that this was GABAb mediated (as opposed to GABAA; GABAA vs. GABABwill be discussed in another post). Our finding that feed-forward inhibition was lower than normal in these populations was consistent with the idea that the NGF cells were hypo-active. Could we test a population in which NGF cells were hyper-active? If we could do that, then we could validate that this particular measure of feed-forward inhibition was sensitive to NGF cell activity. If insulin production is low in diabetics, then it was a good bet that the brain’s insulin production would be higher than normal. This idea is simply based on the brain’s ability to take care of itself, such as it does with the diving reflex (other parts of the body shut down when oxygen is low in order to maintain brain function). Increasing activity in the NGF cells would have the effect of increasing insulin in the brain to counter-act the reduced levels of insulin in the blood stream, but increasing the activity of the NGF cell would also increase feedforward inhibition. The results from the study of early stage diabetics (who did not have peripheral neuropathy) was that feedforward inhibition was much greater than normal (as opposed to the other neurological disorders we had studied that were lower than normal – see graph). There are many cognitive deficits that have been documented to be co-morbid with diabetes type 2, and above normal feed-forward inhibition is consistent with that.

Feed-forward inhibition metrics. Note that autism and chronic pain is below average normative value; diabetics are well above normative value.

Although feed-forward inhibition is a measure that only researchers are currently obtaining with the Brain Gauge, increases and decreases in that metric parallel degradation in other measures that are more commonly collected with the Brain Gauge. For example, the average data for the diabetics that had the higher than normal feed-forward inhibition metric was significantly worse for several scores. Compare the chart on the left (healthy controls) with the chart on the right (early stage diabetics).

Current working hypothesis

As mentioned above, there is quite a bit of literature linking insulin deficiencies with Alzheimer’s (it is even referenced by many as “diabetes type 3”) and diabetes type 2 has been linked with Alzheimer’s epidemiologically. Why would not enough insulin contribute to the degenerative process that is observed in AD? If our working hypothesis is correct, then the tendency to have lower than normal insulin in the blood stream causes the NGF cells to become hyper-active, which causes an imbalance in excitation and inhibition. This imbalance – which also could result in a feedback loop from the brain to that would lower pancreatic insulin production. Lower levels of blood insulin would in turn lead to more insulin production in the brain, which would further exacerbate the condition. The hyperactivity in insulin production would lead to hyperactivity in feed-forward inhibition, which would basically disrupt a cascade of events that culminates in degenerative processes in the brain. The diabetes drugs that improve degenerative disorders break the cycle of the out-of-control feedback loop. While this working hypothesis description is pretty over-simplified (lots of details left out!), the big picture appears to hold up in the literature. You can read more about some of the details here (Favorov et al 2017; all our publications can be found at www.corticalmetrics.com/publications).

One question that is worth asking is – does the degenerative process of AD initiate the degenerative process of diabetes, does diabetes lead to AD, or is it a little bit of both? In our opinion, all three options are viable, but it depends on the initial conditions of physical and mental health, environment and genetics. We will continue to investigate and keep you up to date in future posts.


Janson J, Laedtke T, Parisi JE, O’Brien P, Petersen RC, Butler PC. Increased risk of type 2 diabetes in Alzheimer disease. Diabetes. 2004 Feb 1;53(2):474-81.

Hölscher C. Novel dual GLP-1/GIP receptor agonists show neuroprotective effects in Alzheimer’s and Parkinson’s disease models. Neuropharmacology. 2018 Jan 31.

Molnár G, Faragó N, Kocsis Á et al (2014) GABAergic neurogliaform cells represent local sources of insulin in the cerebral cortex. J Neurosci 34(4):1133-1137.

Talbot K, Wang H-Y, Kazi H, et al. Demonstrated brain insulin resistance in Alzheimer’s disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline. The Journal of Clinical Investigation . 2012;122(4):1316-1338. doi:10.1172/JCI59903.

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Im not an expert, so bear with me. I know that Alzheimers and Diabetes are issues i have the latter and have family medical history that make me sure i will get the former later on. Id like to try and prevent these. Where do i place the coils. I need to know how to use to treat so that i dont end up progressing worse. This information seems IRRELEVANT, so im glad we will have experts here to help answer. Lets focus on how to get better and the pemf. Looking forward to learning how i can place the coils to prevent.

@Bob is this a pemf forum

The short answer to your question, unfortunately, is that I don’t know where to place to coils to prevent Alzheimer’s. What we are looking into in terms of the research is how the inflammatory process leads to deficits in the central nervous system and how to measure those deficits. For example, if you look at the post on treating TBI with PEMF, the Brain Gauge was helpful in determining whether or not the coils had an effect and whether or not they were in the optimal location. Our plan is to continue to conduct research to eventually help give guidance to these questions, but there is generally not a one-size-fits-all answer. Iteratively measuring the process (in my opinion, using the Brain Gauge is one way to do just that) and adjusting the parameters of whatever you are doing (diet, exercise, PEMF coil settings, PEMF coil placement) is the only way to determine what works for each individual.

hope that helps.


So if i buy the brain gauge and use it with the pemf i can prevent the alzheimers. Ive been able to utilize powers of crystal energies and pemf to target treatments and have had so much success with cancer, prostate, diabetes, migraines, food allergies, complete acl tear. I am open to anything that can help to prevent what i think will be the inevitable alzheimers. With the gauge will it be swomething that i can use while also treating with pemf. If i already have the coils on my head will i also be able to put the brain gauge on my head will there be room.


well, no. This forum is not just for PEMF. People are free to discuss other modalities that they think would be helpful. In this case, Mark is discussing a related technology we developed (Brain Gauge) that gives direct insight into cognitive functioning. The precise cause and course of AD (and many others) remains unclear. The potential involvement of insulin is quite important, and shows a link between the two conditions (AD and T2D). This is a matter under scientific study. All of the technology we have used is still experimental, but we are trying to make it accessible to people. Scientific study in most of these related areas is just not yet well developed enough, there is simply not enough information, so we try to also present scientific context and a summary of what little information is available. Some people find it quite helpful, others do not. If you don’t find it helpful, don’t read it.

In the case of T2D, my personal belief is that much of the problem is related to feeding patterns. Basically, I think people are eating too frequently, not necessarily too much, and this impacts insulin levels and insulin resistance. From what I have read, much of T2D may benefit from regular fasting, which will allow insulin levels to cycle down periodically. Frequent small meals prevent this cycling. Fasting promotes it, This is the basis of keto diets, and I personally believe there is a lot of truth to it. Scientific evidence is mounting that this may be the case, but strong disagreement remains, and powerful forces with pro-consumption biases are at play.

Mark’s point (one of many) is that if the brain also produces insulin, a little-known fact but it is true, then the brain must be involved in insulin regulation as well. If this regulation extends to pancreatic production, the brain-insulin link becomes very evident, and problems with insulin sensitivity and over-production may involve as-yet unelucidated feedback mechanisms in the brain. Mark has been trying to sort this out for quite some time. But the scientific research in this area is woefully inadequate, the forces at play are highly biased, and it may be that T2D is related to AD by this poorly understood mechanism. Bottom line IMHO: T2D is likely a problem of feeding patterns, and is not likely to respond to PEMF, AD may be related to this mechanism and may respond better to fasting than to PEMF. The answers are not simple and clear.

BTW, the Brain Gauge does not go on your head. It applies tactile signals to your fingers. The Brain Gauge gives you quantitative insight into cortical function, the same way a blood pressure test gives you insight into cardiovascular health, or how a thermometer tells you about general health. But a thermometer does not treat or cure anything. It has to be used properly to guide treatment, not as a cure.

My personal experience supports your view that “grazing” keeps glucose and insulin levels high, and keeps the glucose set point high.

I’ve reduced by fasting glucose level from above 100 to below 90 by cutting down my carbohydrate intake and cutting out snacks. I’m on a modified ketogenic diet with about 50 to 60 grams of net carbs a day. I also have breakfast 13 or more hours after the previous night’s dinner.
My 96 year old mother doesn’t want to reduce her carb intake, so her fasting glucose level was consistently about 106 to 112. When she cut out snacks, her glucose level dropped to about 95 to 97. The snacks were not high carb snacks but high protein, moderate carb snacks.

Dr. Jason Fung is the leading advocate of intermittent fasting, and has impressive results.

Getting my glucose level below 90 was my target since I read Deep Nutrition by Dr. Cate Shanahan. Then when I read Dr. Dale Bredesen’s book, The End of Alzheimer’s, I was set on getting my fasting glucose below 90, which is also his recommended cutoff level.

Dr. Bredesen has reversed cognitive decline, including Alzheimer’s, in many patients. He has identified 30-some factors that put the brain in a self-reinforcing cycle of increasing amyloid and destroying synapses. High glucose and insulin is one factor. He says insulin resistance is “arguably the single most important metabolic contributor to Alzheimer’s disease development and progression.” (p.177)

Dr. Bredesen says there are three types of Alzheimer’s due to: 1) inflammation, 2) lack of nutrients and hormones that support the brain, and 3) toxins. I am certainly not an expert, but it does seem that PEMF would be most useful with the type of disease caused by inflammation. In this type 1 disease, the hippocampus loses volume but most other brain regions don’t, at least in the early stages. Maybe targeting the hippocampus with the coils would be helpful. His discussion of inflammation-caused Alzheimer’s begins on page 100 of his book.

That is a very coherent and helpful response. I agree entirely with you. I also follow Jason Fung and have read and studied his book very closely. Fasting has taken me off the dreaded “pre-diabetes” list (my PCP is confused by this), my mind is clearer, and I feel a lot better. Fasting also seems to reduce my pain, which is evidently tied to diet somehow.

And I think the insulin-brain-AD link is becoming pretty clear.

I am trying to fast every-other day. I find that I need more than 13 hours overnight. I am experimenting with alternate day fasting, and I only take a tablespoon of MCT once during the day during the carb-to-keto shift, where I find some difficulty at the 13 to 16 hour fasting point. Thereafter, my head clears and I feel very much better.

Protein can spike insulin, so beware of that. When I fast, I try to cut out everything, but only take a tiny bit of MCT when needed, once, to get my brain metabolism over the hump and into keto metabolism. It works for me so well, I can’t believe it is just my imagination.

I plan to stay clear of the pre-diabetes list for the rest of my life, and avoid AD with fasting too. And of course there is evidence fasting may help prevent some types of cancer.

I would say to the extent PEMF helps with any of these, it is likely to be greatly enhanced by adjunctive use with regular fasting. My 2c.

Regarding protein, yes, it can raise insulin and can be turned into glucose, but my belief is that many people do not get enough protein, and most people do not get enough healthy fats. I see lots of older people having trouble walking and likely having sarcopenia, the age-related loss of muscle mass and function. It is reversible to a large extent with adequate protein intake and resistance exercises. The recommended amount of protein by sarcopenia experts is 0.54 grams per pound of ideal body weight. This is more than America’s RDA, but is in line with Norway’s RDA.

I am straying a bit from the topic of glucose, insulin, and AD, but I’d like to suggest looking at AD and other diseases by looking at the overall health of the cell and its ability to heal itself. I think PEMF stimulates the self-healing capability, and the healthier the cells, the more effective PEMF can be. IMO, the best measure of cellular health is the phase angle. It is measure obtained through Bioelectrical Impedance Analysis. The phase angle has been described by different people as:

  • a measure of your biological age
  • a fundamental indicator of good or poor health
  • an indicator of cellular health and integrity
  • a fancy name for cell membrane health
  • a measure of intracellular hydration
  • a measure of mitochondrial health
  • a measure of nutritional status
  • a prognosticator of survival and recovery of patients with severe illnesses

Cell membranes are on average 50% protein and 50% fat. Weak cell membranes can’t hold water in the cell and can’t control the flow of water and nutrients into the cell and waste out of the cell. Those functions also require adequate electrolytes and healthy mitochondria.

Regarding brain health, a healthy brain is more than 70% water. As we age, the amount of water in all our cells goes down and our phase angle goes down. Newborn babies are about 75% water by weight, adults average 60% water, while the elderly are about 50% water or less. With age, we lose our vitality and ability to heal, and become susceptible to diseases like cancer and AD.

There’s a lot of factors to maintaining health as we age. We need balance to adequately address all those factors. I’m an advocate of getting adequate protein and fats to maintain muscle mass and cell membrane integrity, while still controlling glucose and insulin levels. I might mention that the 42-year old NFL quarterback who is still playing at an elite level, Tom Brady, is a strong advocate of hydration and electrolytes. He drinks electrolyte water all day.

Its interesting… protein intake can spike insulin, but clearly I respond to it very differently than I do to carbs. Of course the glycemic indices are very different, but I think it is more than just that. Based on my individual feeling about my response, a bit of protein during a fast is probably a good thing. At least in my opinion.

Sarcopenia is dreadful, and is not frequently enough part of the discussion. To combat this loss, I try to get adequate protein as well, a bit challenging when fasting. My strategy is to try to enter a fasted state after a ketogenic meal, and later break the fast with a high protein meal. Overall, this makes me feel the best.

Bioimpedance is an interesting topic. I don’t think its potential has been fully explored. I dabbled with it a bit when I was in graduate school 35 years ago as a potential way to analyze blood content. Other work had been done before, of course, but at the time it seemed to me there was still a lot of unexplored territory.

At the time I was thinking at thinking about potential biological research uses of impedance spectra. Impedance will of course change with frequency, and I do not think it is linear with amplitude (current), but I think a phase spectral analysis of the tissues being sampled could give significant information on the content and structure of tissues, as you suggest. But analysis of the spectra is complex, literally.

That’s a major area of potential study, and a quick glance at the scientific literature suggests to me that people continue to dabble with the concept for probing cell cultures: cell number, density, motility, etc. It is a major area for research I think. I have not stayed current with it.

To really study PEMF, what we need is a very reliable, easily measured biomarker. One of the biggest obstacles to PEMF research is the lack of readily obtained biological response signals. I know these are reported all the time, but when you look closely, they tend to be impractical for one reason or another. I’ll think about the possibility of using a bioimpedance measurement as a possible biomarker for PEMF. I am not sure it will go anywhere, but I like to think about these sorts of things…

I find collagen peptides helpful as a protein supplement, especially for bones and cartilage and skin. Collagen is not a complete protein, but it is the most abundant protein in the body.

I am not at all familiar with biological response signals to PEMF. If they have been frequently reported, could you recommend a few references? I would guess that there would be process markers and outcome markers. For process markers, wouldn’t you need to hypothesize about the mechanism? For example, for inflammation, PEMF might activate the nrf2 pathway. What are the markers of that? increased superoxide dismutase, glutathione and catalase? Common outcome markers of reduced inflammation are lower C-reactive protein and higher albumin/globulin ratio. Lab work required; not as easily obtained as BIA measurement.

I would hypothesize that the phase angle, as crude a measure as it is, could predict who will not be helped by PEMF. Those with a low phase angle would need to improve their basic cellular health before PEMF could be effective. Maybe that is not correct, but there are many studies showing the phase angle predictive of survival and recovery from different diseases and injuries. There is something there with the phase angle and the ability to maintain health…

Wow, Mark, thank you so much for posting this.

I will have to read it about 100 times because it is so packed full of information, but I will read it that often.

I have to reconcile it with what I have been learning from the various Whole Food Plant Based sources and I had also watched a theory by Big Pharma, which clumped it with stroke and Parkinson’s.

Dr. Greger does the fact that most of them have seriously clogged arteries upon autopsy theory.

Diabetes from the Whole Food Plant Based is more lowering the saturated fats enough to turn the pancreas back on, and it seems pretty effective for T2D, but you are talking the brain and I have to learn how insulin works in the brain.

A lot of people get off insulin by doing Whole Food Plant Based and others by doing Keto. I went Whole Food Plant Based and reversed neuropathy and horizontal nail ridges and vision problems really quickly. My brother went Keto, but he still is pre-Diabetes so far. He isn’t adding in intermittent fasting and from my understanding Keto is about the fact that fat doesn’t spike blood sugar and Whole Food Plant Based is about getting the fat out of the pancreas and most of the time in T2D the pancreas simply starts working normally again in a few weeks. I watched a documentary where everybody, except for one T1D got off all of their meds in a week.

But that doesn’t say whether it would work for brain insulin. It does work for normalizing A1C quickly.

The Brain Gage results with Diabetics testing differently than things like Autism and TBI is very interesting.

I listened to Bredesen last year at the Food Revolution Summit. He was one of the speakers. I believe there was also a speaker who was using Whole Food Plant Based for it.

I liked Bredesen’s list of 30-something things which can contribute to it. When he spoke, I am pretty sure he said that he had gotten the list up to 60-something things. I am waiting for the newest study by Dr. Ornish. Dr. Ornish has reversed heart disease and cancer and had telomeres grow longer on his diet and he said that all he could say was that there was a positive result.

I know that WFPB tends to be excellent at actually healing T2 Diabetes at the root cause, and is excellent at lowering inflammation.

Your mother could probably lower her glucose from the WFPB direction if she wants carbs. It is a different mechanism. If she is T2 Diabetes.

I read things from both perspectives Whole Food Plant Based and Keto and they seem opposite, but they aren’t. They have different mechanisms.

I am allergic to meat and to get rid of Diabetes, I had to get rid of animal products, fat and oil and refined carbs and sugar (and by sugar, I don’t mean carbs. I mean sugar and refined carbs - flour and white pasta)

It worked. But it is like taking the same pack of cards, which Dr. Fung uses and playing Poker versus Cribbage. You have to stay within the rules of the one you are working with.

I looked seriously at Dr. Fung and intermittent fasting, but ended up closer to Dr. Longo saying to stick to 12 to 13 hours between dinner and breakfast. I chose that because I wasn’t sure what to make of the recent animal study where certain types of intermittent fasting actually caused insulin resistance. It is in PubMed. I think it also made animals prone to fatty liver in one study though I think it was after they went off and I think that would depend on what they ate when they went off.

I can vouch for Fiji water to remove aluminum or silica pills probably work.

I watched Dr. Greger’s video where he showed how blocked the arteries were in autopsy of Alzheimer’s patients and I know that is part of it.

I also do think the drug company said that at a basic level Parkinson’s, Alzheimer’s and strokes are all brain damage at varying levels and that simply increasing oxygen and blood flow to those parts of the brain can often already have the dormant parts function better. ICES and a nasal light like Vie light seriously improve circulation.

I was spooked by the animal study about alternate day fasting increasing insulin resistance.

I do highly see the value with 13 hours because of the Alzheimer’s studies and because of the breast cancer study where women were less likely to get it back if they waited 13 hours between dinner and breakfast.

You though are in a special category because intermittent fasting increases brain plasticity.

I wasn’t willing to risk insulin resistance, but if I ever had cancer or a verified stroke, I would be water fasting for at least a week. My dog is still alive almost a year after being given a 100% death sentence. I listened to Dr. Longo and Dr. Fung and Dr. Seyfried who all come from combining fasting with keto and Dr. Goldhamer who combines water fasting with Whole Food Plant Based.

It make sense that you are craving intermittent fasting. Your brain wants all the plasticity it can get.

That is the whole problem, and a catch-22: we don’t have reliable, practical biomarkers and we don’t have a really viable, testable hypothesis for elucidating the fundamental, underlying biophysical mechanisms of PEMF. There have been many attempts, but these fall short for one reason or another.

But if we had one of the above, it would point directly at the other.

I also agree with what your statement implies: the potential effects of PEMF are acting at least in part at a system level, and receptivity to it depends on perturbations to the system. Based on my experiments and observations, it is very difficult to see effects of PEMF on isolated cells. It is possible, but difficult. We did this when I was consulting for NASA in the late 1990’s. But we don’t have a simple, reliable system-level model.

Discussion of metabolism and diet is squarely outside my areas of expertise. I have not studied these formally for decades, so the only information I have is the same information everyone else has readily available. But I do read and think about these all the time, and I do have a first-hand insight into how science and medical research actually work (and sometimes fail to work).

I would be very skeptical of any single-paper findings. Surprising or otherwise ostensibly controversial findings need to be replicated several times, by different researchers, in different locations, before taken as “scientific gospel”.

This pervasive problem with medical research is described very well in the book
“Rigor Mortis: How Sloppy Science Creates Worthless Cures, Crushes Hope, and Wastes Billions”, by Richard Harris, an NPR Health and Medicine reporter.

I suggest everyone read this book before combing through the scientific literature to find any stand-alone gems. This book gives a very clear and coherent description of the most important problem with and limitations of modern medical research. This is only part of the problem, but it is a very important part indeed.

I mention this because of your concern over the findings in one paper on animals that developed insulin resistance while fasting. Unless that paper can be repeated, I would only consider it an interesting and important finding that needs to be replicated before further action, not as a guideline for dietary planning.

Another problem is that the animal type in the study may have been entirely inappropriate for modeling human metabolism. For example, mice may be excellent models for some types of studies (such as fundamental molecular mechanisms), but can be very inaccurate and misleading for other studies that relate to human health. And in particular, rodents and humans have very different metabolic needs. And I do not know that any study of humans during fasting has shown similar results; quite the opposite so far as I know.

The main impression I get is that, for HUMANS, most forms of fasting are quite beneficial, appear to be safe, and no effects such as insulin resistance seem to have emerged as a repeatable outcome. If that were shown in humans, it would certainly make the headlines, and so far as I know, it has not.

IMHO, this is an example of the inappropriate application of animal models in medical research, resulting in misleading and inaccurate extrapolation to human health. But I could be wrong, it would not be the first time.

One more thing I would like to say about fasting, just my opinion, but it makes sense to me: I think human metabolism and the many cycles and states driven by the feeding cycle in humans should be viewed in the context of human evolution. I don’t think human metabolism is optimized to have a beneficial response only when a precise eating pattern is followed. Precise feeding patterns that you see in the scientific literature are a necessary expedient for research. But it is wrong to think that people evolved to eat precise amounts of macronutrients at precise intervals. I think that metabolic agility arises from variations in feeding/fasting intervals, and therefore I do not follow strict patterns.

I base this on my own self-experimentation. It is really just common sense and I think everyone observes this. I have observed it by monitoring my own metabolic shifting during IF using a Ketonix meter and strips (they correlate well for me).

Any given pattern of feeding/IF that induces a shift to ketones for me will get better and faster over time. This is a general metabolic agility that also works when I use very different patterns of feeding/IF: the shift to a keto metabolism gets more efficient with time and fasting cycles, even for very different feeding patterns. I view fasting as a form of exercise for my metabolism. So, I think it is valuable to vary the pattern of fasting, just as it is valuable to vary any other form of exercise. And this is precisely what I do, and it seems to work well for me.


Yes, I totally agree with you about animal studies not being good representations of human studies and I also totally agree about the science creating worthless cures and definitely wasting billions.

Even with brain problems, that became obvious the very first time I researched anything. I do look at the data from both sides and I do look at the various communities and what they are succeeding at and I also do self-experimentation.

I have reversed thing after thing after thing with WFPB and the list keeps getting longer. I don’t live in Ketosis. I do visit there sometimes.

I find that WFPB suits me better with the food allergies I have had and they are reversing things like people no longer needing heart transplants and people reverse neuropathy in 3 days and get off insulin in a week and reverse retinopathy in 9 weeks or that one might be months.

I know that my brain has improved so much and that my vision improved and that I got rid of cancer symptoms (which I didn’t verify as cancer, though cancer is strong in my family. My mother and grandparents died from it younger than I am now and my brother has already had it.)

I guess I just wasn’t willing to even risk messing up my metabolism or risk insulin resistance or the fatty liver (I think was another, but that was on going off of it.) Those things are more in question marks on my list and I do have a question mark list.

You obviously feel more comfortable and it may well be that I just am not someone who ever studied science and it is already a big deal for me to have read thousands of PubMed articles all in scientific language with the brain problems that I had.

Not complaining. I am where I am comfortable. Slowly moving down a list.

The question section is at the bottom of my list and longer intermittent fasting would be there.

Okay, leader Mark, I found the articles on the Corticalmetrics and read the HSV-1 / Lysine and Alzheimer’s theory and looked at PubMed articles about it and I pondered that I am doing vegan and I did look up the vegan foods with lysine and then, I went to Dr. Greger and found Wakame studies on HSV-1.

I am going to try BOTH.

I am thinking the Lysine one is that I would have to lower Arginine or can I just eat foods with Lysine? Some of the vegan foods seem to have both, so if I don’t have to drop Arginine, that would be easier.

according dr. Delgado, the studies for protein needs were done with rats a long time ago, and rats are natural carnivores, so their protein needs are not relevant to humans who are anatomically herbivores. This is supposedly a known fact and Dr. Delgado explains it in detail . He goes on to show that protein requirements for humans are very low. In fact protein is actually recycled in our system.

Okay, I was back to reading studies on PEMF and the brain and you talked about the question of reaching certain areas of the brain.

This article, from Dr. Pawluk referenced a study where they wanted to treat the Hippocampus, but weren’t sure they could reach, so they treated the Parietal lobe.

I bought my C5 and my deep coils because of that comment and this will be my first time treating the Parietal Lobe. Do the deep coils get me closer to the HIppocampus? Or is that really out of reach?

I have been reading so many excellent studies that I am going to want another C5 eventually. Laughing. Studies are fun for me. But they are only fun if you get to try them out for yourself.

There are some which I saw and know that I probably got rid of hunger using the TMS function. I was trying to break the emotional response to food, but I do not have hunger. Whole Food Plant Based uses Calorie Density teachings to get rid of hunger because vegetables take up so much room in the stomach and the stretch receptors shut off hunger, but I also used PEMF so now I don’t know which one did it, but it is a nice side effect anyway. In all fairness, people don’t get food cravings when they are eating things like broccoli and cauliflower, etc. So it might not be either, but it worked, whatever “it” is.