Do dietary lectins cause disease?

I’m lifting this wholesale from the NCBI site because it’s one of the more reliable articles on lectins and as it dates back to 1999, it seems to be mostly off the radar. My emphasis added.

In 1988 a hospital launched a “healthy eating day” in its staff canteen at lunchtime. One dish contained red kidney beans, and 31 portions were served. At 3 pm one of the customers, a surgical registrar, vomited in theatre. Over the next four hours 10 more customers suffered profuse vomiting, some with diarrhoea. All had recovered by next day. No pathogens were isolated from the food, but the beans contained an abnormally high concentration of the lectin phytohaemagglutinin. Lectins are carbohydrate binding proteins present in most plants, especially seeds and tubers like cereals, potatoes, and beans. Until recently their main use was as histology and blood transfusion reagents, but in the past two decades we have realised that many lectins are (a) toxic, inflammatory, or both; (b) resistant to cooking and digestive enzymes; and (c) present in much of our food. It is thus no surprise that they sometimes cause “food poisoning.” But the really disturbing finding came with the discovery in 1989 that some food lectins get past the gut wall and deposit themselves in distant organs. So do they cause real life diseases?This is no academic question because diet is one part of the environment that is manipulable and because lectins have excellent antidotes, at least in vitro. Because of their precise carbohydrate specificities, lectins can be blocked by simple sugars and oligosaccharides. Wheat lectin, for example, is blocked by the sugar N-acetyl glucosamine and its polymers. These natural compounds are potentially exploitable as drugs should lectin induced diseases be identified.

Wheat gliadin, which causes coeliac disease, contains a lectin like substance that binds to human intestinal mucosa, and this has been debated as the “coeliac disease toxin” for over 20 years. But coeliac disease is already managed by gluten avoidance, so nothing would change were the lectin hypothesis proved. On the other hand, wheat lectin also binds to glomerular capillary walls, mesangial cells, and tubules of human kidney and (in rodents) binds IgA and induces IgA mesangial deposits. This suggests that in humans IgA nephropathy might be caused or aggravated by wheat lectin; indeed a trial of gluten avoidance in children with this disease reported reduced proteinuria and immune complex levels.

Of particular interest is the implication for autoimmune diseases. Lectins stimulate class II HLA antigens on cells that do not normally display them, such as pancreatic islet and thyroid cells. The islet cell determinant to which cytotoxic autoantibodies bind in insulin dependent diabetes mellitus is the disaccharide N-acetyl lactosamine, which must bind tomato lectin if present and probably also the lectins of wheat, potato, and peanuts. This would result in islet cells expressing both class II HLA antigens and foreign antigen together—a sitting duck for autoimmune attack. Certain foods (wheat, soya) are indeed diabetogenic in genetically susceptible mice. Insulin dependent diabetes therefore is another potential lectin disease and could possibly be prevented by prophylactic oligosaccharides.

Another suspect lectin disease is rheumatoid arthritis. The normal human IgG molecule possesses carbohydrate side chains, which terminate with galactose. In rheumatoid arthritis much of the galactose is missing, so that the subterminal sugar—N-acetyl glucosamine—is exposed instead. These deficient IgG molecules feature strongly in the circulating immune complexes that cause fever and symptoms. In diet responsive rheumatoid arthritis one of the commonest trigger foods is wheat, and wheat lectin is specific for N-acetyl glucosamine—the sugar that is normally hidden but exposed in rheumatoid arthritis. This suggests that N-acetyl glucosamine oligomers such as chitotetraose (derived from the chitin that forms crustacean shells) might be an effective treatment for diet associated rheumatoid arthritis. Interestingly, the health food trade has already siezed on N-acetyl glucosamine as an antiarthritic supplement.

Among the effects observed in the small intestine of lectin fed rodents is stripping away of the mucous coat to expose naked mucosa and overgrowth of the mucosa by abnormal bacteria and protozoa. Lectins also cause discharge of histamine from gastric mast cells, which stimulates acid secretion. So the three main pathogenic factors for peptic ulcer—acid stimulation, failure of the mucous defence layer, and abnormal bacterial proliferation (Helicobacter pylori) are all theoretically linked to lectins. If true, blocking these effects by oligosaccharides would represent an attractive and more physiological treatment for peptic ulcer than suppressing stomach acid. The mucus stripping effect of lectins also offers an explanation for the anecdotal finding of many allergists that a “stone age diet,” which eliminates most starchy foods and therefore most lectins, protects against common upper respiratory viral infections: without lectins in the throat the nasopharyngeal mucus lining would be more effective as a barrier to viruses.

But if we all eat lectins, why don’t we all get insulin dependent diabetes, rheumatoid arthritis, IgA nephropathy, and peptic ulcers? Partly because of biological variation in the glycoconjugates that coat our cells and partly because these are protected behind a fine screen of sialic acid molecules, attached to the glycoprotein tips. We should be safe. But the sialic acid molecules can be stripped off by the enzyme neuraminidase, present in several micro-organisms such as influenzaviruses and streptococci. This may explain why diabetes and rheumatoid arthritis tend to occur as sequelae of infections. This facilitation of lectins by micro-organisms throws a new light on post-infectious diseases and makes the folklore cure of fasting during a fever seem sensible.

Alternative medicine popularisers are already publishing articles about dietary lectins, often with more enthusiasm than caution, so patients are starting to ask about them and doctors need to be armed with facts. The same comment applies to entrepreneurs at the opposite end of the commercial spectrum. Many lectins are powerful allergens, and prohevein, the principal allergen of rubber latex, is one. It has been engineered into transgenic tomatoes for its fungistatic properties, so we can expect an outbreak of tomato allergy in the near future among latex sensitive individuals. Dr Arpad Pusztai lost his job for publicising concerns of this type (20 February, p 483).


Side Effects of Low Carb Diets: TSH, LDL, Dry Eyes

Here are a few things to watch out for that I learned the hard way.

Low carb diets can cause:

(1) Dry Eyes – [more].

Tears, saliva, and mucus of the sinuses, airways, and gastrointestinal tract are all comprised substantially of glycoproteins called mucins. Mucins are primarily composed of sugar; they typically have a number of large sugar chains bound to a protein backbone. If, for whatever reason, mucin production were halted for lack of glucose, we would have no tears, no saliva and no gastrointestinal or airway mucus.

(2) High LDL – which you may or may not consider a problem [more]

(3) High TSH – which may be a good thing [more]

“Reduced thyroid levels (TSH levels above 5), for a lean individual following a low-carb diet, may be normal and healthy!”

More side effects here.

BMJ support criticism of Industry backed Statin Research

Sir Rory Collins is an advocate for statins claiming it is safe and effective in healthy patients. His research has shown that they benefit practically everyone and have virtually no side-effects. His opinion is based on “secret data” has not been made available for inspection. And, yes, his research is funded by the companies supplying those drugs including Pfizer and Merck Sharp & Dohme.

Lipitor“The research centre that Sir Rory heads – the Cholesterol Treatment Trialists (CTT) in Oxford – holds the biggest collection of statin data in the world, but no one outside the organisation has been able to study it for 20 years.”

Two authors have written papers attacking his work (Abramson Oct 2013 | Malhotra October 2013). These were published in the British Medical Journal. Sir Collins took offense and has been demanding that the BMJ retract the papers.

The BMJ suggested Sir Collins write a rebuttal which is the normal way these things get duked out in peer reviewed journals. But instead, he sent replies by letter marked “Not For Publication” – a move which doesn’t exactly encourage open dialogue.

A committee was then set up by the BMJ to consider Sir Collin’s request to have the opposing papers withdrawn. Not only did this body reject his demands but has instead issued a report which criticizes how he has been dealing with data (Statin Papers Stand, Aug 1).

Although statin use is widely prescribed, the jury is still out on whether they are effective and worth the cost of side effects.

“Yet here we are 20 years on and there is widespread agreement that we still don’t really know how effective they are at preventing heart attacks in healthy people – the group who get by far the most statin prescriptions – or what the true side-effect rate is. Part of the problem is the drug companies’ well-known habit of fiddling of statistics, hiding of unfavourable results, selecting trial subjects most likely to produce favourable results and so on.”


Birds of a feather, toxic together

If chicken is a regular part of your diet, that might mean that arsenic is too… along with a number of other ingredients not listed in the fine print.

If you are buying mass produced chicken, then it is a good idea to find out what the chicken you are eating, has been eating…

What’s in chicken meal?

  • Farmers mostly don’t know as meal formulas are proprietary.
  • Most chicken feed contains drugs (including antibiotics) which help the chickens to grow quickly and to minimize risk of infection.
  • Because these drugs are administered through food, the dose given is not precise.
  • Legal restrictions on how feed is used preclude direct testing of feed ingredients.
  • However scientists are able to test the feathers of chickens, which, like human hair, accumulate the chemicals and drugs in their diet.

What the studies show
Studies of chicken feather meal and chickens have revealed the following substances in the chicken diet:

  • arsenicRosarxone and Histostat are arsenic-based drugs given to kill parasites, accelerate growth and give meat a pink colour; the carcinogenic arsenic residue of this drug is found in chicken livers and feather meal
  • fluorophinolones – this is a class of antibiotics which is illegal for use in poultry because they can breed antibiotic resistance in humans
  • caffeine – this is given to keep the bird awake so that they will eat more
  • paracetamol – a common pain killer, for anxiety
  • diphenhydramine – a kind of antihistamine, also for anxiety
  • prozac – some samples from China included this antidepressant which, if you were a Chinese chicken, was probably welcome relief.

So why do I care what they find in chicken feathers?
Chicken feathers get fed back to chickens. Yes. They are turned into meal and fed back to chickens raised for meat. In this way toxins which accumulate in feathers may get into the food of chickens destined for human consumption.

To minimize exposure to these toxins, at a minimum, avoid chicken livers from non-organic birds. If chicken is a large part of your diet you may want to supplement with other meats or organic sources. Or maybe just cut back on meat altogether.

Note that there are no known incidents of toxicity from exposure to these substances through chicken meat. However there is a recognized potential for the development of drug resistant infections from continued exposure to antibiotics. Multi-drug resistant “superbugs” are on the rise and kill hundreds of thousands of people every year.

a verterinary drug that contains arsenic

No Coconut does NOT have Cholesterol.

Cholesterol is an animal product. Plants do not contain cholesterol except in trace amounts. This includes coconut.

But my doctor said coconut is high in cholesterol and I must avoid it to reduce my risk of heart disease.

It is possible he is misinformed or you misunderstood. Coconut is high in saturated fat. Saturated fat is not the same thing as cholesterol.

Saturated fat, along with cholesterol, is frequently blamed for heart disease. Yes coconut is high in saturated fat. It even has more of the stuff than butter.

Fatty Acid Composition of Various Oils:

But let’s unpack that. The saturated fat in coconut oil is NOT the same as in animal fat (not that you should be running in fear from animal fat, but that’s another story).

Most of the saturated fat in coconut oil is in the form of medium-chain fatty acids which do not circulate in the bloodstream like other fats do, but rather are directly channeled to the liver where they are immediately converted into energy, thus avoiding fat buildups.

Note also that almost 50% of the fatty acid content of coconut oil is lauric acid which is a main component of human breast milk. Another 7% of the fatty acids are capric acid which stimulates anti-viral activity in the body.

If coconut is so great, why did my doctor say to avoid it?

Coconuts have fallen victim to bad science which was helped along by the marketing efforts of competing products (in particular the soy oil and corn oil campaigns pushing the idea that coconut was healthy and their hydrogenated oils were).

Once upon a time, some very questionable research by a Dr. Ancel Keys was published which suggested that there was a correlation between saturated fat and heart disease. Watch this video for the background on how the data was cherry picked:

Keys was able to convince a sizable part of the US public that replacing saturated fat with unsaturated fat would reduce blood cholesterol and the incidence of coronary heart disease. Once this became widely accepted (despite protestations from many members of the scientific community) foods high in saturated fat got put on the blacklist including coconut and eggs.

It is increasingly accepted today that this advice was wrong and that these foods have been part of a healthy human diet for thousands of years. However beliefs die hard and old school doctors are unlikely to contravene the old prescriptions.

Coconut oil is, in fact, good for you. It has factors which strengthen the immune system and may even confer neurological benefits which may slow or prevent the onset of Alzheimer’s.

Dr. Stasha Gominak Discusses Sleep and Vitamin D

This lecture will knock your socks off…
(Notes below)


Writings by Dr. Gominak


  • We heal during sleep
  • Improving sleep quality heals many different conditions
  • It’s ability to heal exceeds the ability of most medicines
  • Growth hormone is released while you sleep
  • Body pain is associated with poor sleep
  • REM sleep is particularly important for healing
  • Sleep disorders have increased significantly since the onset of electric lighting
  • When sleep goes bad, we stop repairing out genetic weaknesses and injuries
  • Sleep shores up genetic weakness.
  • If you have a sleep disorder but don’t have the migraine gene, you won’t get migraines… something else will go wrong.
  • In her practice, every person who tested positive for poor sleep had low vitamin D levels.
  • Vitamin D is made by an interaction between sunlight and the cholesterol in your skin
  • When you reduce cholesterol levels – like with statins – you reduce your body’s ability to make vitamin D naturally.
  • When you add vitamin D to a skin cancer cell in a petri dish, it stops reproducing inappropriately.
  • Many inflammatory connections have vitamin D receptors including bone marrow components, all blood cells and platelets.
  • You still have to get the sleep better to make the effects of dosing with D obvious
  • Rats have a unique property of being able to use D2 from their diet therefore they do not need sunlight and can live nocturnally.
  • Humans, on the other hand, cannot process D2 (it can be toxic) and need sunlight or D3. Doctors still give out D2 for bone disease because of studies with rats.
  • Vitamin D is not a vitamin: it is a hormone.
    • Vitamin: My cell needs this chemical. I can’t make it. Therefore I need to get it from my environment.
    • Hormone: My body makes it. It is not in the environment.
  • Low Vitamin D associate with health issues in multiple areas of the body: metabolic syndrome, atherosclerosis, visceral adiposity, hypertension, hyperglycemia, diabetes, leg swelling.
  • Hypothesis: we’ve made statins in response to high cholesterol which is caused by vitamin D deficiency.
  • Hospitals are set up for the doctors convenience: we wake up our patients to do an x-ray, to take blood, to bathe them. It’s ridiculous: they are at the lowest ebb of their physical strength when they need sleep most and we are interrupting it. We need to protect their sleep.
  • What the right level to have normal sleep?
  • Humans can make 20,000 IU on our skin in 1-6 hours depending on our skin color.
  • People who are genetically made to live at the equator (dark skin) take a much longer time to make Vitamin D.
  • The daily recommended dose varies GREATLY depending on your genetics, where you live, the time of year and your lifestyle. The FDA dosage recommendation should be ignored.
  • Furthermore you cannot depend on the amount of Vitamin D in the pills because of poor regulation. What is stated on the label is often unreliable.
  • Too much Vitamin D IS toxic. The symptoms vary because the first problem is disturbed sleep and that can cascade to a very wide variety of problems.
  • D25 OH test optimum blood level is about 60-80 ng/ml.
  • MS is a vitamin D deficiency disorder
  • You need to take D3. D2 is NOT the same. D2 is toxic. Do not take it.
  • Co-factors: vitamins you may need to take with D3:
    • B12
    • Iron (IF there is a deficiency)
    • Magnesium
  • You have to be very careful with self-dosing. This is a hormone. If you get it wrong, it will screw you up.
  • Monitor you levels. Monitor you sleep.
  • Having correct D levels will not matter if your sleep is constantly interrupted for other reasons. It’s ultimately the sleep that confers health.

Sleep Apnea is associated with:

  • high blood pressure
  • heart disease
  • diabetes
  • stroke
  • obesity
  • daytime sleepiness
  • memory problems
  • depression
  • headache
  • fibromyalgia
  • fatigue

She frequently refers to a CPAP mask which is a device which delivers “Continuous positive airway pressure”.

Chocolate Covered Lard

OK so I don’t usually post recipes but… I came across this ridiculous recipes for chocolate covered lard… on a Russian website no less!

And given how hard it is to find ways to get fat into your diet when you are low carbing, and given that it marries bacon and chocolate which I personally believe are a match made in heaven (and have been RIDICULED for it)… well you get the idea. Here goes.

Chopping Board
Mold for final product (you may need to be a bit creative here)
Bain marie (metal bowl over a pot of steaming water)

Salted lard (pork fat) 300 grams
Dark Chocolate 150 grams
Butter 40 grams
Crushed nuts 50 grams
Ginger powder 1/3 tsp
Allspice 1/2 tsp
Cardamom 1/4 tsp
Nutmeg 1 pinch
Ground red pepper to taste

1. Grind fat in blender.
2. Place on chopping board and form into a square 5mm high.
3. Place board with lard in freezer for 1-2 hours until solid.
4. Melt the chocolate and butter over a bain marie .
5. Add in all the spices and mix well.
6. Remove frozen lard from freezer and cut into thin strips.
7. Place lard in molds and sprinkle with nuts.
8. Cover with chocolate.
9. Return to freezer for another 1 or until chocolate is solid.

Variation: add bacon bits and/or chili in place of the nuts.

Obesity and Food Palatability

Great talk by Steven Guyenet on the hypothesis that increased food palatability is an important factor in growing rates of obesity.

There is no doubt that increased calorie consumption is a proximate cause of increased levels of obesity. But that is not very useful information. The question is WHY are we eating so much more?

Guyenet provides details from a number of studies which suggest that food palatability is driving our consumption of calorie dense processed foods.

  • Study found that rats ignored their rat show in favor of human “cafeteria” junk food diet and gained weight rapidly. Such tasty human food far exceeded any other rat chow diets in producing weight gains – Sclafani & Springer, 1976
  • Overweight patients who were free to consume as many calories as they wanted from a bland diet consistently lost weight without reporting hunger despite, at times, consuming less than 300 calories per day. Lean patients on the same diet maintained their body weight. “This machine-feeding regimen was nearly as close as one can get to a diet with no rewarding properties whatsoever.” – New York Academy of Sciences, 1965
  • These findings were replicated in a similar study in which “subjects reduced their calorie intake voluntarily and were always in good spirits” while consuming a bland diet. – Michel Cabanac, 1976

Guyenet has more detailed write-ups on these studies here.

Factors involved in the reward value of a diet:

  • calorie density
  • fat
  • starch
  • sugar
  • absense of bitterness
  • free glutamate (MSG)
  • textures (crunchy, soft, liquid(
  • variety
  • certain aromas
  • consistency of flavour

The last point is worth noting: the more we can depend on a food tasting the same, the more we are likely to crave it for the certainty of the food reward. Think McDonalds.

He went on to compare two weight-loss diet studies, one low carb and another low fat, and showed that loss was comparable regardless of the preponderance of these two macronutrients. It suggests that, perhaps, whether you remove fat or carbohydrates, the common factor is a reduction in food palatability.

He also gave examples of a two native peoples who, despite having diets with widely different macronutrient contents, were both extremely lean:

  • Kung San of Botswana: consumed mostly nuts, starchy tubers, fruit, assorted leaves, insects and, less often, large and small game. At times up to 58% of their diet came from a single food (Mongongo nuts). “Somewhat monotonous”. Overall their diet was 60% fat, 25% carbs, 15% protein.
  • The people of Tukisenta, Papua New Guinea: Sweet potato accounted for 90% of food consumed. The rest included taro, sugarcane, pandanus, insects and, rarely during festivals, pork. Overall their diet was 95% carbs, 2% fat, 3% protein.

It seems that the low fat versus low carb wars may be a red herring.

So what has happened to our own tribe? Americans have changed where they eat, and therefor what they eat, quite significantly over the past 100 years with the presence of fast food really taking off since the late 60’s.

Guyenet points out that this graph understates the magnitude of the change in diet as much of the food now being consumed at home is also processed.

His next graph illustrated the massive increase in sugar consumption, another marker of this processed food intake:

A similar trend is seen in the consumption of fresh versus processed potatoes:

So what’s the bottom line? Return to simple food.

“Food that is professionally engineered to maximize palatability and reward value is uniquely fattening. The solution is to avoid it.”

The first step is to eliminate comfort aka “maximum reward” foods:

  • Candy
  • Chocolate
  • Ice cream
  • Potato/corn chips
  • Cookies/cakes
  • Fast food
  • Pizza

If that thought is painful, he proposes a strategy for easing into a healthier diet. Each step requires increased effort so get comfortable with a stage before moving on to the next one:

  1. Eat three of fewer meals per day, but no snacks
  2. Cook food at home from simple ingredients
  3. Restrict palatability/reward factors that were absent in the ancestral environment
  4. Eat a few staple foods consistently, with no flavorings added

This sounds quite daunting but he claims that simple food becomes more satisfying after a 1-2 week period of withdrawal. He doesn’t actually say withdrawal but as you look at this list, you can feel the monkey on your back and he does NOT want off.

It’s a sensible plan. Should definitely work. Requires effort.
Isn’t there a pill I can take instead???

My thoughts:

What I find interesting about his theory is how it somewhat overlaps but clashes with Seth Robert’s theory behind the Shangri-La diet. The diet involves taking a small serving of flavorless calories 1-2 times per day and that this on its own seems to cause the body to change its body fat set point. Food palatability IS a factor but you don’t have to completely eliminate modern foods from your diet. Roberts does not know how this works or what the mechanism is but many people claim to have successfully lost weight this way without any other changes to their diet or activity levels.

Is it possible that Guyenet is describing a much more arduous route to reach the same Shangri-La brain hack so to speak? The question is to what extent those people who claimed to have lost weight on the Shangri-La diet have continued to eat junk food. Maybe they spontaneously lost interest in junk food due to this protocol. Perhaps the actual hack of Shangri-La is to change one’s preference for highly palatable foods.

Certainly the Shangri-La route seems much easier. But try downing 100 calories of light olive oil and you will certainly question whether it is healthier, regardless of how easy it goes down.

Guyenet’s advice is undoubtedly no-nonsense and will work. But it may require massive changes to how you meet and socialise over food. It is likely that most people could adjust to the dietary changes required here. But in the long run, how many can maintain the social changes eating an ancestral diet may require? I doubt there are many.

So yes there are still no shortcuts. And maybe that’s the point. We have all the answers, just not ones we like.

Anti-Inflammatory Diet

So who needs a so-called “Anti-inflammatory diet”? Well just about anyone who is not genetically adapted to a modern diet… meaning everyone. Inflammation is your body’s response to you giving it stuff it is not adapted to.

A wide range of modern health problems start as elevated levels of inflammation.

In a nutshell, an anti-inflammatory diet is this:

  • Take Vitamin D
  • Eat Low carb – avoid grains
  • Avoid vegetable oils — only olive oil is safe (trans fats are dangerous), butter is better
  • Consume Fish oil
  • Eliminate High fructose corn syrup
  • Eat Saturated Fats — safer than polyunsaturated fats, major source of calories
  • Eat Fermented foods — boost your good bacteria


It all sounds vaguely familiar…
Bottom line: no more bread… but you are welcome to enjoy a steak with butter!


Alzheimer’s treated with Ketones

I saw a touching documentary on Alzheimers recently but it freaked me out a bit because my dad is in the advanced stages of Alzheimers and I wondered, is this my fate?

I’ve long heard that Alzheimer’s is referred to as Type-III diabetes. So the obvious question was, had anyone done research on the impact of a ketogenic diet for arresting or delaying the disease? The answer sadly, is no, not really.

But if you are happy to be swayed by anecdotal evidence (I often am) then this story from 2008 is full of hope:

In this account, Dr. Mary Newport supplemented her husbands diet with coconut oil (a medium chain triglyceride) to increase ketones in circulation.

There was no carbohydrate restriction. In fact many of you will cringe to see pictures of coconut oil added to every grain imaginable (she usually stirs it into his oatmeal). The dose given was 2 tablespoons of pure coconut oil daily (non-hydrogenated).

In just 24 hours his severe Alzheimer’s showed improvement and this continued for several months. He literally “rolled back the clock” as shown by the amazing improvement in his ability to draw a clock face (a standard test for Alzheimer’s).

She has written a book on her experience but to save time and money, just check out this 4 page case study she wrote.

Here is a similar story of using coconut oil to treat Alzheimers. In this case, intervention was a lot sooner and appears to have been completely effective in stopping progression of the disease (although they do not appear to have independently verified his condition):


Peter at Hyperlipid looked at Dr. Newport’s story when it first came out and made this interesting comment:

One of the first posts I ever put up on Hyperlipid was the use of the full blown ketogenic diet for the partial reversal of Parkinsons Disease. As far as I can see Alzheimers Disease, Parkinsons Disease and ALS are all essentially the same disease, but the genetics of your glutamate receptor subtypes or quirks of your glutamate processing enzymes determine which you get. They’re excitotoxin diseases, and Russell Blaylock has the most self consistent hypothesis of their generation that I’ve come across.

For me all this means that I need to hunt down a good source of coconut oil pronto. If Alzheimer’s is in the cards I may notice nothing for another 20 years, but likely the seeds of it are taking hold now.

I have had a hard time sticking to a low carb diet over the long terms and have indulged in regular carb-filled relapses. So it seems that, as a minimum, I should start taking coconut oil as a potential prophylactic against brain rot…