Obese Military?

I came across some articles on obesity and the military (see below). Metabolic syndrome, obesity being one part of it, is on the rise in the military and in the population in general, along with much else such as autoimmune and mood disorders.

Weight issues are not an issue of mere exercise, as I discovered in aging. The weight began accruing in my thirties and continued into my forties. I’ve always been active and so, in response, I became even more active. I had long done aerobic exercise multiple times a week, often long jogs and sometimes carrying extra weight. Weightlifting was added to my regimen these past few years. Still, the body fat wouldn’t budge. Besides, the worst rates of obesity are found among the young and so aging is not the issue, as further demonstrated by age-related diseases (e.g., what was once called adult onset diabetes) hitting hard at younger and younger ages.

Why is that? Some of it is basic biological changes in aging, of course — still, that couldn’t explain it all since it is happening in all age groups. I had improved my diet over time, but admittedly I was still eating a fair amount of carbs and sugar, even if no where near the amount the average American gets. In the wider population, the consumption of carbohydrates and added sugars has drastically increased over time, specifically as dietary percentage of red meat and saturated fat has gone down while dietary percentage of vegetables and vegetable oils has been on the rise. There are other complex factors that could be mentioned, but I’ll keep it simple.

The point is that the American population, in and outside of the military, are in compliance with official dietary recommendations. The military is even able to enforce a high-carb, low-fat diet on military personnel since they have few other choices when food is prepared for them, and it is specifically during deployment that military personnel have the worst diet-related health decline. There is no greater opportunity than the military for gathering highly-controlled dietary data, as the only other segment with more controlled diets are those locked away in institutions. Also, the military enforces a rigid exercise program, and those who join are those who self-selected for this lifestyle and then had to meet high standards to be accepted. Yet military personnel apparently are getting fatter and fatter.

The amount of carbohydrates we’re talking about here is not insignificant. The USDA recommends 50-60% of the diet to consist of carbohydrates with an emphasis on grains, most of those simple starchy carbs. Even adding some fiber back into processed foods doesn’t really make them any healthier. Grains alone brings up a whole mess of other issues besides gluten (e.g., grains block absorption of certain key nutrients) — it’s long been known that the best way of fattening animals is with grains.

To put in context how distorted is our diet, a recent study compared a high-carb and a low-carb diet where the latter consisted of 40% carbs. If that is what goes for low-carb these days, no wonder we are such a sickly population. Most traditional societies rarely get such high levels of carbs and what they do get usually comes from sources that are fibrous and nutrient-dense. Look at hunter-gatherers — 40% carbs would be at the extreme high end with many groups only getting 22% carbs. As a concrete example, compared to potato chips or a baked potato, chewing on a fibrous wild tuber is a laborious process because of how tough it is, only gaining slightly more calories than you’d be expending for all the effort.

For further perspective, a study published this month implemented a ketogenic diet (Richard A. LaFountain et al, Extended Ketogenic Diet and Physical Training Intervention in Military Personnel). That by itself isn’t noteworthy, as ketosis has been scientifically studied for about a century. What is significant is that it was the first time that such a diet done was done with military personnel. If you’re familiar with this area of research, the results were predictable which is to say they were typical. Military personnel aren’t essentially any different than other demographics. We all evolved from the same ancestors with the same metabolic system.

The results were positive as expected. Health improved in all ways measured. Body fat, in particular, was lost — relevant because the subjects were overweight. Benefits were seen in other aspects of what is called metabolic syndrome, such as better insulin sensitivity. All of this was accomplished while physical fitness was maintained, an important factor for the military. Going by what we know, if anything, physical fitness would improve over time; but that would require a longer term study to determine.

Ketosis is how I and millions of others have lost weight, even among those who don’t know what ketosis is. Anyone who has ever restricted their diet in any way, including fasting, likely has experienced extended periods of ketosis with no conscious intention being required — ketosis simply happens when carbs and sugar are restricted, and even commercial diets like Weight Watchers are quite restrictive along these lines. Other ketogenic gains often are experienced in relation to hunger, cravings, mood, energy, stamina, alertness, and focus. The point here, though, was weight loss and once again it was a glorious success.

That such studies are finally being done involving the military indicates that, after a century of research, government officials are maybe finally coming around to taking ketosis seriously. It’s understandable why drug companies and doctors have been resistant, since there is no profit in a healthy sustainable diet, but profit isn’t a concern for the military or shouldn’t be, although military contractors who provide the food might disagree (high-carb food is cheaper to provide because of high-yield crops subsidized for a half century by the government). If the USDA won’t change its guidelines, maybe the military should develop its own. A military filled with those of less than optimal health is a national security threat.

As for the rest of us, maybe it’s time we look to the studies and make informed decisions for ourselves. Not many doctors know about this kind of research. And if anything, doctors have a misinformed fear about ketosis because of confusion with diabetic ketoacidosis. Doctors aren’t exactly the most knowledgeable group when it comes to nutrition, as many have noted. And the government is too tied up with agricultural and food corporations. Any positive changes will have to come from the bottom up. These changes are already happening in a growing movement in support of alternative diets such as ketogenic low-carb, which is maybe what brought it to the attention of some military officials.

Government will eventually come around out of necessity. A global superpower can’t maintain itself in the long run with a malnourished and obese population. The healthcare costs and lost sick days alone could cripple society — even now most of the healthcare costs go to a few preventable diseases like diabetes. I’m willing to bet that when the next world war is fought the soldiers will be eating low-carb, high-fat rations made with nutrient-dense ingredients. Not doing so would risk having an inferior military. For-profit ideology only goes so far when the stakes are high.

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Is U.S. Nutrition Policy Making the Military (and Recruits) too Fat to Fight?
from Nutrition Coalition

This year, for the first time since 2005, the Army fell short of its recruitment goal, according to the recent report, “Unhealthy and Unprepared,” by The Council for a Strong America, a group of retired generals and admirals. Obesity was largely to blame. Some 71% of young people between the ages of 17 and 24 fail to qualify for military service, says the report. These alarming numbers raise the disturbing question of whether the U.S. will be able to continue the luxury of maintaining an all-volunteer army in the future.

Another recent study, this one by the Rand Corporation found that some two-thirds of the nation’s active military personnel are overweight or obese. Topping the scale is the Army, with 69.4% of its personnel overweight or obese. But even the trimmest military branch – the Marine Corps – isn’t much better, at 60.9%. These numbers may be misleading, since “obesity” is defined by BMI (body mass index), which does not distinguish between whether extra pounds come fat or muscle—the latter being more likely to be the case in the military. Still, rates of 60-69% are disturbingly high. Since these folks are following the military’s exercise program, we certainly can’t blame them for shirking on physical activity.

It seems, in fact, that the U.S. military diet actually worsens health, according to an Army publication six years ago. Chanel S. Weaver of the U.S. Army Public Health Command wrote, “Even those Soldiers who are actually fit enough to deploy can face challenges in maintaining a healthy weight while serving in the deployed environment.”

In the article, Dr. Theresa Jackson, a public health scientist at the U.S. Army Public Health Command, states, “Literature suggests that fitness decreases and fat mass increases during deployments.” This is an astonishing fact: fitness declines in the military, despite mandated regular exercise.

This paradox could be explained by the growing understanding that exercise plays a relatively minor role in weight loss. “You can’t exercise your way out of a bad diet,” is the new common catchphrase among experts. Instead, the principal factor driving obesity, as the data increasingly show, is poor nutrition.

A look at the Army’s nutrition guidelines shows that they emphasize low-fat, high-carbohydrate foods. The Army recommends eating “…high protein, low-fat items such as: fish, beans, whole wheat pasta, egg whites, skim or 1 percent milk, and low-fat yogurt” while avoiding “items such as: fried items, high fat meats, egg yolks, and whole milk.” This guidance comes from the U.S. Dietary Guidelines for Americans (DGA), a policy that has been co-issued by USDA and US-HHS since 1980. The military essentially downloads these guidelines and serves food in mess halls to reflect DGA recommendations.

Ironically, this reliance on the U.S. Guidelines could well be the very reason for the military’s obesity problems. This diet tells the entire U.S. population to eat 50-60% of their calories as carbohydrates, principally grains, and just as a high-grain diet fattens cattle, a large body of government-funded science shows that a high-carbohydrate diet, for most people, is inimical to sustainable weight loss.

The argument that Americans don’t follow the guidelines is not supported by the best available government data on this subject—which demonstrates widespread adherence to the Dietary Guidelines.

New military study: “Remarkable” results among soldiers on a ketogenic diet
by Anne Mullens and Bret Scher

Those on the ketogenic diet lost an average of 17 pounds (7.5 kg), 5 percent of their overall body fat, 44 percent of their visceral fat, and had their insulin sensitivity improve by 48 per cent. There was no change in the participants on the mixed diet. Training results in physical strength, agility, and endurance in both groups were similar.

The researchers noted:

The most striking result was consistent loss of body mass, fat mass, visceral fat, and enhanced insulin sensitivity in virtually all the ketogenic diet subjects despite no limitations on caloric intake. Physical performance was maintained…. These results are highly relevant considering the obesity problem affecting all branches of the military.

[…] Although neither group counted calories, the ketogenic diet group naturally reduced their caloric intake while eating to satiety.

The most noteworthy response was a spontaneous reduction in energy intake, resulting in a uniformly greater weight loss for all ketogenic diet participants.

The military should lead the U.S. fight against obesity
by Steve Barrons

That advice, driven by the government’s Dietary Guidelines for Americans, has largely stuck to the familiar low-fat, high-carbohydrate diet that calls on us to cut meat, butter and cheese. Yet in recent years, the science has evolved, and it has become increasingly clear to people like me that fats aren’t the enemy. Indeed, as I ate more fat and reduced my intake of sugars and other carbohydrates like grains, I lost weight and became healthier.

Experiences like mine are now backed by a fast-growing body of science, showing carbohydrate restriction to be effective for fighting obesity and diabetes while improving most heart-disease risk factors.

For many, it’s hard to get past the basic assumption that the fat on your plate becomes the fat in your body. But the truth is that it’s excessive carbohydrates that turn into body fat — completely contrary to what Americans have long been told.

So why hasn’t the government’s dietary advice caught up to the science? According to a rigorous investigation in The BMJ on the dietary guidelines, the experts appointed to review the scientific evidence relied on weak scientific standards in their report and failed to review the most recent science on a number of topics, including optimal intakes for carbohydrates, saturated fat and salt. Most critically, the report relied heavily on observational studies in which researchers follow test groups over long periods of time. But even the best epidemiological studies, according to the BMJ, “suffer from a fundamental limitation. At best they can show only association, not causation. Epidemiological data can be used to suggest hypotheses but not to prove them.” This is science 101.

The U.S. military serves more than 150 million meals per year to its personnel, and when those meals are based on a government-advised, high-carbohydrate diet, our troops have a harder time staying trim and healthy. The Army’s own website warns people to stay away from high-fat meats, egg yolks and whole milk and advises “eating less fatty food for better overall health,” while encouraging a diet that includes pasta and bread. Making matters worse, service members usually have fewer options for avoiding these nutritional mistakes, especially on deployments when they often can’t cook their own meals. 

Fasting, Calorie Restriction, and Ketosis

What we eat obviously affects gut health such as the microbiome and through that, along with other mechanisms, it affects the rest of our body, the brain included (by way of permeability, immune system, vagus nerve, substances like glutamate and propionate, and much else). About general health, I might add that foods eaten in what combination (e.g., red meat and grains) is also an issue. Opposite of what you eat impacting neurocognition and mental health, not eating (i.e., fasting, whether intermittent or extended) or else caloric restriction and carbohydrate reduction, ketogenic or otherwise, alters it in other ways.

Fasting, for example, increases the level of neurotransmitters such as serotonin, dopamine, and norepinephrine while temporarily reducing the brains release and use of them; plus, serotonin and its precursor tryptophan are made more available to the brain. So, it allows your reserves of neurotransmitters to rebuild to higher levels. That is partly why a ketogenic diet, along with the brains efficient use of ketones, shows improvements in behavior, learning, memory, acuity, focus, vigilance, and mood (such as sense of well-being and sometimes euphoria); with specific benefits, to take a couple of examples, in cerebral blood flow and prefrontal-cortex-related cognitive functions (mental flexibility and set shifting); while also promoting stress resistance, inflammation reduction, weight loss, and metabolism, and while decreasing free radical damage, blood pressure, heart rate, and glucose levels. Many of these are similar benefits as seen with strenuous exercise.

We know so much about this because the ketogenic diet is the only diet that has been specifically and primarily studied in terms of neurological diseases, going back to early 20th century research on epileptic seizures and autism, was shown effective for other conditions later in the century (e.g., V. A. Angelillo et al, Effects of low and high carbohydrate feedings in ambulatory patients with chronic obstructive pulmonary disease and chronic hypercapnia), and more recently with positive results seen in numerous other conditions (Dr. Terry Wahl’s work on multiple sclerosis, Dr. Dale Bredesen’s work on Alzheimer’s, etc). By the way, the direction of causality can also go the other way around, from brain to gut: “Studies also suggest that overwhelming systemic stress and inflammation—such as that induced via severe burn injury—can also produce characteristic acute changes in the gut microbiota within just one day of the sustained insult [15].” (Rasnik K. Singh et al, Influence of diet on the gut microbiome and implications for human health). And see:

“Various afferent or efferent pathways are involved in the MGB axis. Antibiotics, environmental and infectious agents, intestinal neurotransmitters/neuromodulators, sensory vagal fibers, cytokines, essential metabolites, all convey information about the intestinal state to the CNS. Conversely, the HPA axis, the CNS regulatory areas of satiety and neuropeptides released from sensory nerve fibers affect the gut microbiota composition directly or through nutrient availability. Such interactions appear to influence the pathogenesis of a number of disorders in which inflammation is implicated such as mood disorder, autism-spectrum disorders (ASDs), attention-deficit hypersensitivity disorder (ADHD), multiple sclerosis (MS) and obesity.” (Anastasia I. Petra et al, Gut-Microbiota-Brain Axis and Its Effect on Neuropsychiatric Disorders With Suspected Immune Dysregulation)

There are many other positive effects. Fasting reduces the risk of neurocognitive diseases: Parkinson’s, Alzheimer’s, etc. And it increases the protein BDNF (brain-derived neurotrophic factor) that helps grow neuronal connections. Results include increased growth of nerve cells from stem cells (as stem cells are brought out of their dormant state) and increased number of mitochondria in cells (mitochondria are the energy factories), the former related to the ability of neurons to develop and maintain connections between each other. An extended fast will result in autophagy (cellular housekeeping), the complete replacement of your immune cells and clearing out damaged cells which improves the functioning of your entire body (it used to be thought to not to occur in the brain but we now know it does) — all interventions known to prolong youthful health, lessen and delay diseases of aging (diabetes, cancer, cardiovascular disease, etc), and extend lifespan in lab animals involve autophagy (James H. Catterson et al, Short-Term, Intermittent Fasting Induces Long-Lasting Gut Health and TOR-Independent Lifespan Extension). Even calorie restriction has no effect when autophagy is blocked (Fight Aging!, Autophagy Required For Calorie Restriction Benefits?). It cleans out the system, gives the body a rest from its normal functioning, and redirects energy toward healing and rebuilding.

As a non-human example, consider hibernation for bears. A study was done comparing bears with a natural diet (fruits, nuts, insects, and small mammals) and those that ate human garbage (i.e., high-carb processed foods). “A research team tracked 30 black bears near Durango, Colo., between 2011 and 2015, paying close attention to their eating and hibernation habits. The researchers found that bears who foraged on human food hibernated less during the winters — sometimes, by as much as 50 days — than bears who ate a natural diet. The researchers aren’t sure why human food is causing bears to spend less time in their dens. But they say shorter hibernation periods are accelerating bears’ rates of cellular aging” (Megan Schmidt, Human Food Might Be Making Bears Age Faster). As with humans who don’t follow fasting or a ketogenic diet, bears who hibernate less don’t live as long. Maybe a high-carb diet messes with hibernation similarly to how it messes with ketosis.

Even intermittent fasting shows many of these benefits. Of course, you can do dramatic changes to the body without fasting at all, if you’re on a ketogenic diet (though one could call it a carb fast since it is extremely low carb) or severe caloric restriction (by the way, caloric restriction has been an area of much mixed results and hence confusion — see two pieces by Peter Attia: Calorie restriction: Part I – an introduction & Part IIA – monkey studies; does intermittent fasting and ketosis mimic caloric restriction or the other way around?). I’d add a caveat: On any form of dietary limitation or strict regimen, results vary depending on specifics of test subjects and other factors: how restricted and for how long, micronutrient and macronutrient content of diet, fat-adaptation and metabolic flexibility, etc; humans, by the way, are designed for food variety and so it is hard to know the consequences of modern diet that often remains unchanged, season to season, year to year (Rachel Feltman, The Gut’s Microbiome Changes Rapidly with Diet). There is a vast difference between someone on a high-carb diet doing an occasional fast and someone on a ketogenic diet doing regular intermittent fasting. Even within a single factor such as a high-carb diet, there is little similarity between the average American eating processed foods and a vegetarian monk eating restricted calories. As another example, autophagy can take several days of fasting to be fully achieved; but how quickly this happens depends on the starting conditions such as how many carbs eaten beforehand and how much glucose in the blood and glycogen stores in the muscles, both of which need to be used up before ketosis begins.

Metabolic flexibility, closely related to fat-adaptation, requires flexibility of the microbiome. Research has found that certain hunter-gatherers have microbiomes that completely switch from season to season and so the gut somehow manages to maintain some kind of memory of previous states of microbial balance which allows them to be re-established as needed. This is seen more dramatically with the Inuit who eat an extremely low-carb diet, but they seasonally eat relatively larger amounts of plant matter such as seaweed and they temporarily have digestive issues until the needed microbes take hold again. Are these microbes dormant in the system or systematically reintroduced? In either case, the process is unknown, as far as I know. What we are clear about is how dramatically diet affects the microbiome, whatever the precise mechanisms.

For example, a ketogenic diet modulates the levels of the microbes Akkermansia muciniphila, Lactobacillus, and Desulfovibrio (Lucille M. Yanckello, Diet Alters Gut Microbiome and Improves Brain Functions). It is the microbes that mediate the influence on both epileptic seizures and autism, such that Akkermansia is decreased in the former and increased in the latter, that is to say the ketogenic diet helps the gut regain balance no matter which direction the imabalance is. In the case of epileptic seizures, Akkermansia spurs the growth of Parabacteroides which alters neurotransmission by elevating the GABA/glutamate ratio (there is glutamate again): “the hippocampus of the microbe-protected mice had increased levels of the neurotransmitter GABA, which silences neurons, relative to glutamate, which activates them” (Carolyn Beans, Mouse microbiome findings offer insights into why a high-fat, low-carb diet helps epileptic children), but no such effect was found in germ-free mice, that is to say with no microbiome (similar results were found in human studies: Y. Zhang, Altered gut microbiome composition in children with refractory epilepsy after ketogenic diet). Besides reducing seizures, “GABA is a neurotransmitter that calms the body. Higher GABA to glutamate ratios has been shown to alleviate depression, reduce anxiety levels, lessen insomnia, reduce the severity of PMS symptoms, increase growth hormone, improve focus, and reduce systemic inflammation” (MTHFR Support, Can Eating A Ketogenic Diet Change Our Microbiome?). To throw out the other interesting mechanism, consider Desulfovibrio. Ketosis reduces its numbers and that is a good thing since it causes leakiness of the gut barrier, and what causes leakiness in one part of the body can cause it elsewhere as well such as the brain barrier. Autoimmune responses and inflammation can follow. This is why ketosis has been found beneficial for preventing and treating neurodegenerative conditions like Alzheimer’s (plus, ketones are a useful alternative fuel for Alzheimer’s since their brain cells begin starving to death for loss of the capacity to use glucose as a fuel).

All of this involves the factors that increase and reduce inflammation: “KD also increased the relative abundance of putatively beneficial gut microbiota (Akkermansia muciniphila and Lactobacillus), and reduced that of putatively pro-inflammatory taxa (Desulfovibrio and Turicibacter).” (David Ma et al, Ketogenic diet enhances neurovascular function with altered gut microbiome in young healthy mice). Besides the microbiome itself, this has immense impact on leakiness and autoimmune conditions, with this allowing inflammation to show up in numerous areas of the body, including the brain of course. Inflammation is found in conditions such as depression and schizophrenia. Even without knowing this mechanism, much earlier research has long established that ketosis reduces inflammation.

It’s hard to know what this means, though. Hunter-gatherers tend to have much more diverse microbiomes, as compared to industrialized people. Yet the ketogenic diet that helps induce microbial balance simultaneously reduces diversity. So, diversity isn’t always a good thing, with another example being small intestinal bacterial overgrowth (SIBO). What matters is which microbes one has in abundance and in relation which microbes one lacks or has limitedly. And what determines that isn’t limited to diet in the simple sense of what foods we eat or don’t eat but the whole pattern involved. Also, keep in mind that in a society like ours most of the population is in varying states of gut dysbiosis. First eliminating the harmful microbes is most important before the body can heal and rebalance. That is indicated by a study on multiple sclerosis that found, after the subjects had an initial reduction in the microbiome, “They started to recover at week 12 and exceeded significantly the baseline values after 23–24 weeks on the ketogenic diet” (Alexander Swidsinski et al, Reduced Mass and Diversity of the Colonic Microbiome in Patients with Multiple Sclerosis and Their Improvement with Ketogenic Diet). As always, it’s complex. But the body knows what to do when you give it the tools its evolutionarily-adapted to.

In any case, all of the methods described can show a wide range of benefits and improvements in physical and mental health. They are potentially recommended for almost anyone who is in a healthy state or in some cases of disease, although as always seek medical advice before beginning any major dietary change, especially anyone with an eating disorder or malnourishment (admittedly, almost all people on a modern industrialized diet are to some degree malnourished, especially Americans, although most not to a degree of being immediately life-threatening). Proceed with caution. But you are free to take your life in your hands by taking responsibility for your own health through experimentation in finding out what happens (my preferred methodology), in which case the best case scenario is that you might gain benefit at no professional medical cost and the worst case scenario is that you might die (not that I’ve heard of anyone dying from a typical version of a diet involving fasting, ketosis, and such; you’re way more likely to die from the standard American diet; but individual health conditions aren’t necessarily predictable based on the experience of others, even the vast majority of others). Still, you’re going to die eventually, no matter what you do. I wish you well, until that time.

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Let me clarify one point of widespread confusion. Talk of ‘diets’, especially of the variety I’ve discussed here, are often thought of in terms of restriction and that word does come up quite a bit. I’m guilty of talking this way even in this post, as it is about impossible to avoid such language considering it is used in the scientific and medical literature. So, there is an implication of deprivation, of self-control and self-denial, as if we must struggle and suffer to be healthy. That couldn’t be further from the truth.

Once you are fat-adapted and have metabolic flexibility, you are less restricted than you were before, in that you can eat more carbs and sugars for a time and then more easily return back to ketosis, as is a common seasonal pattern for hunter-gatherers. And once you no longer are driven by food cravings and addictions, you’ll have a happier and healthier relationship to food — eating when genuinely hungry and going without for periods without irritation or weakness, as also is common among hunter-gatherers.

This is simply a return to the state in which most humans have existed for most of our historical and evolutionary past. It’s not restriction or deprivation, much less malnourishment. It’s normalcy or should be. But we need to remember what normalcy looks and feels like: “People around the world suffer from starvation and malnutrition, and it is not only because they lack food and nutrients. Instead they suffer from immature microbiomes, which can severely impact health” (AMI, The effects of fasting and starvation on the microbiome). Gut health is inseparable from the rest, and these diets heal and rebalance the gut.

We need to redefine what health means, in a society where sickness has become the norm.

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Here is a good discussion that is relevant here, even though the author never discusses ketosis anywhere in his book. He is pointing out that calorie intake and energy usage is approximately the same for urbanized humans as for hunter-gatherers. Yet the former have higher rates of obesity and the latter don’t. As many have noted, not all calories are the same and so calories-in/calories-out is a myth. This data makes more sense once you understand how profoundly different the body functions under ketogenic and non-ketogenic states.

100 Million Years of Food
by Stephen Le
pp.166 -168

At this point, a reader might conclude that the root of modern food-related ailments like obesity and diabetes lies in people eating a lot more food, due to the miracle of nitrogen fixation, and doing a lot less physical activity, due to the miracle of combustion engines and private vehicles. However, it turns out that neither of these common beliefs is supported by the evidence.

First, the food intake myth. The daily energy consumed through food in contemporary industrialized nations runs from about 2,300 kcal (kilocalories) among Japanese men and 1,800 kcal among Japanese women to 2,600 kcal among American men and 1,900 kcal among American women. 21 What is surprising is that the average daily caloric intake of these overweight industrialized societies is about the same as among hunter-gatherer groups, with some hunter-gatherer groups below and others above the calories consumed of industrialized nations. 22 Although hunter-gatherers ate about as much as we do today, they faced much greater variability in their food supply. In northern Australia, among the Anbarra, the daily energy intake dropped to 1,600 kcal during the rainy season and peaked at 2,500 kcal during the dry season. The calorie consumption of the Hiwi in the rainforests of Venezuela bounced between 1,400 and 2,800 kilocalories, depending on the season (plant foods were most plentiful at the end of the wet season). Thus, if any major pattern emerges in terms of caloric intake, it is that our hunter-gatherer ancestors lived on a dramatically varying diet, which swung between feast and famine according to the season and other hazards of fortune.

Another surprising finding concerns physical activity. Although it is commonly believed that people in hunter-gatherer societies expended much more energy than people in industrialized societies today, the evidence so far does not support this assumption. One common measure of physical activity level (PAL) expresses the total energy used in one day as a multiple of a person’s metabolic rate. For example, a PAL of 1 means that a person uses only his/her metabolic energy, i.e., the energy expended by breathing, thinking, digesting, etc. A PAL of 2 means that a person uses twice as much energy as his or her base metabolic rate. PAL allows us to adjust for the fact that people have varying levels of metabolism; a person who has a high metabolic rate can burn up a lot of energy by just sitting in one place compared to a person with low metabolism, so a good measure of physical activity needs to compensate for differences in metabolism. To determine the amount of energy used in a day, the best measure involves giving a person a drink of water that has been “tagged” with isotopes of hydrogen and oxygen. Measurement of these two tags in samples of saliva, urine, or blood allows measurement of exhaled carbon dioxide and hence the degree of respiration from metabolic processes.

Using tagged water, the average PAL among foragers was found to be 1.78 for men and 1.72 for women. Among industrialized contemporary societies with a high human development index (which measures income, literacy, and so on), the PAL of men was 1.79 for men and 1.71 for women. 23 In other words, the energy expenditure of overweight contemporary industrialized societies is roughly the same as that of lean hunter-gatherer societies once metabolism is taken into account; or to put it another way, the cause of obesity is unlikely to be lack of exercise, because people in industrialized societies today use about the same amount of energy as people in hunter-gatherer societies. 24

This finding has important implications for understanding obesity. All of us living in industrialized societies are aware of the stigma associated with obesity, and perhaps the longer-term health consequences of diabetes, high blood pressure, gout, and cancers associated with being overweight. Since food intake and energy expenditure levels today are roughly the same as during ancestral times (using the lifestyles of modern hunter-gatherers as a reasonable model for our ancestors’ lifestyles), why are obesity and diabetes so prevalent among industrialized societies and virtually nonexistent among our ancestors?

The first argument might be an objection that obesity has in fact been with us since the days of our earliest ancestors, so nothing has changed. It has been suggested that figurines of markedly obese women, found in Europe and dating to thirty thousand years ago, are proof that obesity existed at that time. However, no hunter-gatherer or small-scale horticultural group has ever manifested signs of obesity, despite having caloric intake and energy expenditure (adjusted for metabolism) within the range of contemporary industrialized populations. Thus the prehistoric statuettes may be representative of idealized feminine beauty, just as Barbie dolls and Japanese anime characters with huge eyes and exaggerated busts are fantasies more revealing of their creators than of real women.

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Genius Foods:
Become Smarter, Happier, and More Productive While Protecting Your Brain for Life
by Max Lugavere

Baby Fat Isn’t Just Cute—It’s a Battery

Have you seen a baby lately? I’m talking about a newborn, fresh out of the womb. They’re fat. And cute. But mostly fat. Packed with stored energy prior to birth in the third trimester, the fatness of human babies is unprecedented in the mammal world. While the newborns of most mammal species average 2 to 3 percent of birth weight as body fat, humans are born with a body fat percentage of nearly 15, surpassing the fatness of even newborn seals. Why is this so? Because humans are born half-baked.

When a healthy human baby emerges from the womb, she is born physically helpless ad with an underdeveloped brain. Unlike most animals at birth, a newborn human is not equipped with a full catalogue of instincts preinstalled. It is estimated that if a human were to be born at a similar stage of cognitive development to a newborn chimp, gestation would be at least double the length (that doesn’t sound fun—am I right ladies?). By being born “prematurely,” human brains complete their development not in the womb, but in the real world, with open eyes and open ears—this is probably why we’re so social and smart! And it is during this period for rapid brain growth, what some refer to as the “fourth trimester,” that our fast serves as an important ketone reservoir for the brain, which can account for nearly 90 percent of the newborn’s metabolism. Now you know: baby fat isn’t just there for pinching. It’s there for the brain.

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Mitochondria and the Future of Medicine:
The Key to Understanding Disease, Chronic Illness, Aging, and Life Itself
by Lee Know

Ketogenic Diets and Calorie Restriction

Ketone bodies, herein also referred to simply as ketones , are three water-soluble compounds that are produced as by-products when fatty acids are broken down for energy in the liver. These ketones can be used as a source of energy themselves, especially in the heart and brain, where they are a vital source of energy during periods of fasting.

The three endogenous ketones produced by the body are acetone , acetoacetic acid , and beta-hydroxybutyric acid (which is the only one that’s not technically a ketone, chemically speaking). They can be converted to acetyl-CoA, which then enters the TCA cycle to produce energy.

Fatty acids are so dense in energy, and the heart is one of the most energy-intensive organs, so under normal physiologic conditions, it preferentially uses fatty acids as its fuel source. However, under ketotic conditions, the heart can effectively utilize ketone bodies for energy.

The brain is also extremely energy-intensive, and usually relies on glucose for its energy. However, when glucose is in short supply, it gets a portion of its energy from ketone bodies (e.g., during fasting, strenuous exercise, low-carbohydrate, ketogenic diet, and in neonates). While most other tissues have alternate fuel sources (besides ketone bodies) when blood glucose is low, the brain does not. For the brain, this is when ketones become essential. After three days of low blood glucose, the brain gets 25 percent of its energy from ketone bodies. After about four days, this jumps to 70 percent!

In normal healthy individuals, there is a constant production of ketone bodies by the liver and utilization by other tissues. Their excretion in urine is normally very low and undetectable by routine urine tests. However, as blood glucose falls, the synthesis of ketones increases, and when it exceeds the rate of utilization, their blood concentration increases, followed by increased excretion in urine. This state is commonly referred to as ketosis , and the sweet, fruity smell of acetone in the breath is a common feature of ketosis.

Historically, this sweet smell was linked to diabetes and ketones were first discovered in the urine of diabetic patients in the mid-nineteenth century. For almost fifty years thereafter, they were thought to be abnormal and undesirable by-products of incomplete fat oxidation.

In the early twentieth century, however, they were recognized as normal circulating metabolites produced by the liver and readily utilized by the body’s tissues. In the 1920s, a drastic “hyperketogenic” diet was found to be remarkably effective for treating drug-resistant epilepsy in children. In 1967, circulating ketones were discovered to replace glucose as the brain’s major fuel during prolonged fasting. Until then, the adult human brain was thought to be entirely dependent upon glucose.

During the 1990s, diet-induced hyperketonemia (commonly called nutritional ketosis ) was found to be therapeutically effective for treating several rare genetic disorders involving impaired glucose utilization by nerve cells. Now, growing evidence suggests that mitochondrial dysfunction and reduced bioenergetic efficiency occur in brains of patients with Parkinson’s disease and Alzheimer’s disease. Since ketones are efficiently used by brain mitochondria for ATP generation and might also help protect vulnerable neurons from free-radical damage, ketogenic diets are being evaluated for their ability to benefit patients with Parkinson’s and Alzheimer’s diseases, and various other neurodegenerative disorders (with some cases reporting remarkable success).

There are various ways to induce ketosis, some easier than others. The best way is to use one of the various ketogenic diets (e.g., classic, modified Atkins, MCT or coconut oil, low-glycemic index diet), but calorie restriction is also proving its ability to achieve the same end results when carbohydrates are limited.

Features of Caloric Restriction

There are a number of important pieces to caloric restriction. First, and the most obvious, is that caloric intake is most critical. Typically, calories are restricted to about 40 percent of what a person would consume if food intake was unrestricted. For mice and rats, calorie restriction to this degree results in very different physical characteristics (size and body composition) than those of their control-fed counterparts. Regarding life extension, even smaller levels of caloric restriction (a reduction of only 10–20 percent of unrestricted calorie intake) produce longer-lived animals and disease-prevention effects.

In April of 2014, a twenty-five-year longitudinal study on rhesus monkeys showed positive results. The benefit of this study was that it was a long-term study done in primates—human’s closest relatives—and confirms positive data we previously saw from yeasts, insects, and rodents. The research team reported that monkeys in the control group (allowed to eat as much as they wanted) had a 2.9-fold increased risk of disease (e.g., diabetes) and a 3-fold increased risk of premature death, compared to calorie-restricted monkeys (that consumed a diet with 30 percent less calories).

If other data from studies on yeast, insects, and rodents can be confirmed in primates, it would indicate that calorie restriction could extend life span by up to 60 percent, making a human life span of 130–150 years a real possibility without fancy technology or supplements or medications. The clear inverse relationship between energy intake and longevity links its mechanism to mitochondria—energy metabolism and free-radical production.

Second, simply restricting the intake of fat, protein, or carbohydrates without overall calorie reduction does not increase the maximum life span of rodents. It’s the calories that count, not necessarily the type of calories (with the exception of those trying to reach ketosis, where type of calorie does count).

Third, calorie restriction has been shown to be effective in disease prevention and longevity in diverse species. Although most caloric restriction studies have been conducted on small mammals like rats or mice, caloric restriction also extends life span in single-celled protozoans, water fleas, fruit flies, spiders, and fish. It’s the only method of life extension that consistently achieves similar results across various species.

Fourth, these calorie-restricted animals stay “biologically younger” longer. Experimental mice and rats extended their youth and delayed (even prevented) most major diseases (e.g., cancers, cardiovascular diseases). About 90 percent of the age-related illnesses studied remained in a “younger” state for a longer period in calorie-restricted animals. Calorie restriction also greatly delayed cancers (including breast, colon, prostate, lymphoma), renal diseases, diabetes, hypertension, hyperlipidemia, lupus, and autoimmune hemolytic anemia, and a number of others.

Fifth, calorie restriction does not need to be started in early age to reap its benefits. Initiating it in middle-aged animals also slowed aging (this is good news for humans, because middle age is when most of us begin to think about our own health and longevity).

Of course, the benefits of calorie restriction relate back to mitochondria. Fewer calories mean less “fuel” (as electrons) entering the ETC, and a corresponding reduction in free radicals. As you know by now, that’s a good thing.

Health Benefits

As just discussed, new research is showing that judicious calorie restriction and ketogenic diets (while preserving optimal nutritional intake) might slow down the normal aging process and, in turn, boost cardiovascular, brain, and cellular health. But how? We can theorize that the restriction results in fewer free radicals, but one step in confirming a theory is finding its mechanism.

In particular, researchers have identified the beneficial role of beta-hydroxybutyric acid (the one ketone body that’s not actually a ketone). It is produced by a low-calorie diet and might be the key to the reduced risk of age-related diseases seen with calorie restriction. Over the years, studies have found that restricting calories slows aging and increases longevity, but the mechanism behind this remained elusive. New studies are showing that beta-hydroxybutyric acid can block a class of enzymes, called histone deacetylases , which would otherwise promote free-radical damage.

While additional studies need to be conducted, it is known that those following calorie-restricted or ketogenic diets have lower blood pressure, heart rate, and glucose levels than the general population. More recently, there has been a lot of excitement around intermittent fasting as an abbreviated method of achieving the same end results.

However, self-prescribing a calorie-restricted or ketogenic diet is not recommended unless you’ve done a lot of research on the topic and know what to do. If not done properly, these diets can potentially increase mental and physical stress on the body. Health status should be improving, not declining, as a result of these types of diets, and when not done properly, these diets could lead to malnutrition and starvation. Health care practitioners also need to properly differentiate a patient who is in a deficiency state of anorexia or bulimia versus someone in a healthy state of ketosis or caloric restriction.

I’ll add a final word of caution: While ketogenic diets can be indispensable tools in treating certain diseases, their use in the presence of mitochondrial disease—at this point—is controversial and depends on the individual’s specific mitochondrial disease. In some cases, a ketogenic diet can help; in others it can be deleterious. So, of all the therapies listed in this book, the one for which I recommend specific expertise in its application is this diet, and only after a proper diagnosis.

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Grain Brain:
The Surprising Truth about Wheat, Carbs, and Sugar–Your Brain’s Silent Killers

by David Perlmutter

Caloric Restriction

Another epigenetic factor that turns on the gene for BDNF production is calorie restriction. Extensive studies have clearly demonstrated that when animals are on a reduced-calorie diet (typically reduced by around 30 percent), their brain production of BDNF shoots up and they show dramatic improvements in memory and other cognitive functions. But it’s one thing to read experimental research studies involving rats in a controlled environment and quite another to make recommendations to people based upon animal research. Fortunately, we finally have ample human studies demonstrating the powerful effect of reducing caloric intake on brain function, and many of these studies have been published in our most well-respected medical journals. 13

In January 2009, for example, the Proceedings of the National Academy of Science published a study in which German researchers compared two groups of elderly individuals—one that reduced their calories by 30 percent and another that was allowed to eat whatever they wanted. The researchers were interested in whether changes could be measured between the two groups’ memory function. At the conclusion of the three-month study, those who were free to eat without restriction experienced a small but clearly defined decline in memory function, while memory function in the group on the reduced-calorie diet actually increased, and significantly so. Knowing that current pharmaceutical approaches to brain health are very limited, the authors concluded, “The present findings may help to develop new prevention and treatment strategies for maintaining cognitive health into old age.” 14

Further evidence supporting the role of calorie restriction in strengthening the brain and providing more resistance to degenerative disease comes from Dr. Mark P. Mattson, chief of the Laboratory of Neurosciences at the National Institute on Aging (NIA). He reported:

Epidemiological data suggest that individuals with a low calorie intake may have a reduced risk of stroke and neurodegenerative disorders. There is a strong correlation between per capita food consumption and risk for Alzheimer’s disease and stroke. Data from population-based case control studies showed that individuals with the lowest daily calorie intakes had the lowest risk of Alzheimer’s disease and Parkinson’s disease. 15

Mattson was referring to a population-based longitudinal prospective study of Nigerian families, in which some members moved to the United States. Many people believe that Alzheimer’s disease is something you “get” from your DNA, but this particular study told a different story. It was shown that the incidence of Alzheimer’s disease among Nigerian immigrants living in the United States was increased compared to their relatives who remained in Nigeria. Genetically, the Nigerians who moved to America were the same as their relatives who remained in Nigeria. 16 All that changed was their environment—specifically, their caloric intake. The research clearly focused on the detrimental effects that a higher caloric consumption has on brain health. In a 2016 study published in Johns Hopkins Health Review, Mattson again emphasized the value of caloric restriction in warding off neurodegenerative diseases while at the same time improving memory and mood. 17 One way to do that is through intermittent fasting, which we’ll fully explore in chapter 7 . Another way, obviously, is to trim back your daily consumption.

If the prospect of reducing your calorie intake by 30 percent seems daunting, consider the following: On average, we consume 23 percent more calories a day than we did in 1970. 18 Based on data from the Food and Agriculture Organization of the United Nations, the average American adult consumes more than 3,600 calories daily. 19 Most would consider “normal” calorie consumption to be around 2,000 calories daily for women and 2,500 for men (with higher requirements depending on level of activity/exercise). A 30 percent cut of calories from an average of 3,600 per day equals 1,080 calories.

We owe a lot of our increased calorie consumption to sugar. Remember, the average American consumes roughly 163 grams (652 calories) of refined sugars a day—reflecting upward of a 30 percent hike in just the last three decades. 20 And of that amount, about 76 grams (302 calories) are from high-fructose corn syrup. So focusing on just reducing sugar intake may go a long way toward achieving a meaningful reduction in calorie intake, and this would obviously help with weight loss. Indeed, obesity is associated with reduced levels of BDNF, as is elevation of blood sugar. Remember, too, that increasing BDNF provides the added benefit of actually reducing appetite. I call that a double bonus.

But if the figures above still aren’t enough to motivate you toward a diet destined to help your brain, in many respects, the same pathway that turns on BDNF production can be activated by intermittent fasting (which, again, I’ll detail in chapter 7 ).

The beneficial effects in treating neurologic conditions using caloric restriction actually aren’t news for modern science, though; they have been recognized since antiquity. Calorie restriction was the first effective treatment in medical history for epileptic seizures. But now we know how and why it’s so effective: It confers neuroprotection, increases the growth of new brain cells, and allows existing neural networks to expand their sphere of influence (i.e., neuroplasticity).

While low caloric intake is well documented in relation to promoting longevity in a variety of species—including roundworms, rodents, and monkeys—research has also demonstrated that lower caloric intake is associated with a decreased incidence of Alzheimer’s and Parkinson’s disease. And the mechanisms by which we think this happens are via improved mitochondrial function and controlling gene expression.

Consuming fewer calories decreases the generation of free radicals while at the same time enhancing energy production from the mitochondria, the tiny organelles in our cells that generate chemical energy in the form of ATP (adenosine triphosphate). Mitochondria have their own DNA, and we know now that they play a key role in degenerative diseases such as Alzheimer’s and cancer. Caloric restriction also has a dramatic effect on reducing apoptosis, the process by which cells undergo self-destruction. Apoptosis happens when genetic mechanisms within cells are turned on that culminate in the death of that cell. While it may seem puzzling at first as to why this should be looked upon as a positive event, apoptosis is a critical cellular function for life as we know it. Pre-programmed cell death is a normal and vital part of all living tissues, but a balance must be struck between effective and destructive apoptosis. In addition, caloric restriction triggers a decrease in inflammatory factors and an increase in neuroprotective factors, specifically BDNF. It also has been demonstrated to increase the body’s natural antioxidant defenses by boosting enzymes and molecules that are important in quenching excessive free radicals.

In 2008, Dr. Veronica Araya of the University of Chile in Santiago reported on a study she performed during which she placed overweight and obese subjects on a three-month calorie-restricted diet, with a total reduction of 25 percent of calories. 21 She and her colleagues measured an exceptional increase in BDNF production, which led to notable reductions in appetite. It’s also been shown that the opposite occurs: BDNF production is decreased in animals on a diet high in sugar. 22 Findings like this have since been replicated.

One of the most well-studied molecules associated with caloric restriction and the growth of new brain cells is sirtuin-1 (SIRT1), an enzyme that regulates gene expression. In monkeys, increased SIRT1 activation enhances an enzyme that degrades amyloid—the starch-like protein whose accumulation is the hallmark of diseases like Alzheimer’s. 23 In addition, SIRT1 activation changes certain receptors on cells, leading to reactions that have the overall effect of reducing inflammation. Perhaps most important, activation of the sirtuin pathway by caloric restriction enhances BDNF. BDNF not only increases the number of brain cells, but also enhances their differentiation into functional neurons (again, because of caloric restriction). For this reason, we say that BDNF enhances learning and memory. 24

The Benefits of a Ketogenic Diet

While caloric restriction is able to activate these diverse pathways, which are not only protective of the brain but enhance the growth of new neuronal networks, the same pathway can be activated by the consumption of special fats called ketones. By far the most important fat for brain energy utilization is beta-hydroxybutyrate (beta-HBA), and we’ll explore this unique fat in more detail in the next chapter. This is why the so-called ketogenic diet has been a treatment for epilepsy since the early 1920s and is now being reevaluated as a therapeutic option in the treatment of Parkinson’s disease, Alzheimer’s disease, ALS, depression, and even cancer and autism. 25 It’s also showing promise for weight loss and ending type 2 diabetes. In mice models, the diet rescues hippocampal memory deficits, and extends healthy lifespan.

Google the term “ketogenic diet” and well over a million results pop up. Between 2015 and 2017, Google searches for the term “keto” increased ninefold. But the studies demonstrating a ketogenic diet’s power date back further. In one 2005 study, for example, Parkinson’s patients actually had a notable improvement in symptoms that rivaled medications and even brain surgery after being on a ketogenic diet for just twenty-eight days. 26 Specifically, consuming ketogenic fats (i.e., medium-chain triglycerides, or MCT oil) has been shown to impart significant improvement in cognitive function in Alzheimer’s patients. 27 Coconut oil, from which we derive MCTs, is a rich source of an important precursor molecule for beta-hydroxybutyrate and is a helpful approach to treating Alzheimer’s disease. 28 A ketogenic diet has also been shown to reduce amyloid in the brain, 29 and it increases glutathione, the body’s natural brain-protective antioxidant, in the hippocampus. 30 What’s more, it stimulates the growth of mitochondria and thus increases metabolic efficiency. 31

Dominic D’Agostino is a researcher in neuroscience, molecular pharmacology, and physiology at the University of South Florida. He has written extensively on the benefits of a ketogenic diet, and in my Empowering Neurologist interview with him he stated: “Research shows that ketones are powerful energy substrates for the brain and protect the brain by enhancing antioxidant defenses while suppressing inflammation. No doubt, this is why nutritional ketosis is something pharmaceutical companies are aggressively trying to replicate.” I have also done a lot of homework in understanding the brain benefits of ketosis—a metabolic state whereby the body burns fat for energy and creates ketones in the process. Put simply, your body is in a state of ketosis when it’s creating ketones for fuel instead of relying on glucose. And the brain loves it.

While science typically has looked at the liver as the main source of ketone production in human physiology, it is now recognized that the brain can also produce ketones in special cells called astrocytes. These ketone bodies are profoundly neuroprotective. They decrease free radical production in the brain, increase mitochondrial biogenesis, and stimulate production of brain-related antioxidants. Furthermore, ketones block the apoptotic pathway that would otherwise lead to self-destruction of brain cells.

Unfortunately, ketones have gotten a bad rap. I remember in my internship being awakened by a nurse to treat a patient in “diabetic ketoacidosis.” Physicians, medical students, and interns become fearful when challenged by a patient in such a state, and with good reason. It happens in insulin-dependent type 1 diabetics when not enough insulin is available to metabolize glucose for fuel. The body turns to fat, which produces these ketones in dangerously high quantities that become toxic as they accumulate in the blood. At the same time, there is a profound loss of bicarbonate, and this leads to significant lowering of the pH (acidosis). Typically, as a result, patients lose a lot of water due to their elevated blood sugars, and a medical emergency develops.

This condition is exceedingly rare, and again, it occurs in type 1 diabetics who fail to regulate their insulin levels. Our normal physiology has evolved to handle some level of ketones in the blood; in fact, we are fairly unique in this ability among our comrades in the animal kingdom, possibly because of our large brain-to-body weight ratio and the high energy requirements of our brain. At rest, 20 percent of our oxygen consumption is used by the brain, which represents only 2 percent of the human body. In evolutionary terms, the ability to use ketones as fuel when blood sugar was exhausted and liver glycogen was no longer available (during starvation) became mandatory if we were to survive and continue hunting and gathering. Ketosis proved to be a critical step in human evolution, allowing us to persevere during times of food scarcity. To quote Gary Taubes, “In fact, we can define this mild ketosis as the normal state of human metabolism when we’re not eating the carbohydrates that didn’t exist in our diets for 99.9 percent of human history. As such, ketosis is arguably not just a natural condition but even a particularly healthful one.” 32

There is a relationship between ketosis and calorie restriction, and the two can pack a powerful punch in terms of enhancing brain health. When you restrict calories (and carbs in particular) while upping fat intake, you trigger ketosis and increase levels of ketones in the blood. In 2012, when researchers at the University of Cincinnati randomly assigned twenty-three older adults with mild cognitive impairment to either a high-carbohydrate or very low-carbohydrate diet for six weeks, they documented remarkable changes in the low-carb group. 33 They observed not only improved verbal memory performance but also reductions in weight, waist circumference, fasting glucose, and fasting insulin. Now here’s the important point: “Ketone levels were positively correlated with memory performance.”

German researchers back in 2009 demonstrated in fifty healthy, normal to overweight elderly individuals that when calories were restricted along with a 20 percent increase in dietary fat, there was a measurable increase in verbal memory scores. 34 Another small study, yes, but their findings were published in the respected Proceedings of the National Academy of Sciences and spurred further research like that of the 2012 experiment. These individuals, compared to those who did not restrict calories, demonstrated improvements in their insulin levels and decline in their C-reactive protein, the infamous marker of inflammation. As expected, the most pronounced improvements were in people who adhered the most to the dietary challenge.

Research and interest in ketosis have exploded in recent years and will continue. The key to achieving ketosis, as we’ll see later in detail, is to severely cut carbs and increase dietary fat. It’s that simple. You have to be carb restricted if you want to reach this brain-blissful state.

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Power Up Your Brain
by David Perlmutter and Alberto Villoldo

Your Brain’s Evolutionary Advantage

One of the most important features distinguishing humans from all other mammals is the size of our brain in proportion to the rest of our body. while it is certainly true that other mammals have larger brains, scientists recognize that larger animals must have larger brains simply to control their larger bodies. An elephant, for example, has a brain that weighs 7,500 grams, far larger than our 1,400-gram brain. So making comparisons about “brain power” or intelligence just based on brain size is obviously futile, Again, it’s the ratio of the brain size to total body size that attracts scientist’s interests when considering the brain’s functional capacity. An elephant’s brain represents 1/550 of its body weight, while the human brain weighs 1/40 of the total body weight. So our brain represents 2.5 percent of our total body weight as opposed to the large-brained elephant whose brain is just 0.18 percent of its total body weight.

But even more important than the fact that we are blessed with a lot of brain matter is the intriguing fact that, gram for gram, the human brain consumes a disproportionately huge amount of energy. While only representing 2.5 percent of our total body weight, the human brain consumes an incredible 22 percent of our body’s energy expenditure when at rest. this represents about 350 percent more energy consumption in relation to body weight compared with other anthropoids like gorillas, orangutans, and chimpanzees.

So it takes a lot of dietary calories to keep the human brain functioning. Fortunately, the very fact that we’ve developed such a large and powerful brain has provided us with the skills and intelligence to maintain adequate sustenance during times of scarcity and to make provisions for needed food supplies in the future. Indeed, the ability to conceive of and plan for the future is highly dependent upon the evolution not only of brain size but other unique aspects of the human brain.

It is a colorful image to conceptualize early Homo sapiens migrating across and arid plain and competing for survival among animals with smaller brains yet bigger claws and greater speed. But our earliest ancestors had one other powerful advantage compared to even our closest primate relatives. The human brain has developed a unique biochemical pathway that proves hugely advantageous during times of food scarcity. Unlike other mammals, our brain is able to utilize an alternative source of calories during times of starvation. Typically, we supply our brain with glucose form our daily food consumption. We continue to supply our brains with a steady stream of glucose (blood sugar) between meals by breaking down glycogen, a storage form of glucose primarily found in the liver and muscles.

But relying on glycogen stores provides only short-term availability of glucose. as glycogen stores are depleted, our metabolism shifts and we are actually able to create new molecules of glucose, a process aptly termed gluconeogenesis. this process involves the construction of new glucose molecules from amino acids harvested form the breakdown of protein primarily found in muscle. While gluconeogenesis adds needed glucose to the system, it does so at the cost of muscle breakdown, something less than favorable for a starving hunter-gatherer.

But human physiology offers one more pathway to provide vital fuel to the demanding brain during times of scarcity. When food is unavailable, after about three days the liver begins to use body fat to create chemicals called ketones. One ketone in particular, beta hydroxybutyrate (beta-HBA), actually serves as a highly efficient fuel source for the brain, allowing humans to function cognitively for extended periods during food scarcity.

Our unique ability to power our brains using this alternative fuel source helps reduce our dependence on gluconeogensis and therefore spares amino acids and the muscles they build and maintain. Reducing muscle breakdown provides obvious advantages for the hungry Homo sapiens in search of food. It is this unique ability to utilize beta-HBA as a brain fuel that sets us apart from our nearest animal relatives and has allowed humans to remain cognitively engaged and, therefore, more likely to survive the famines ever-present in our history.

This metabolic pathway, unique to Homo sapiens, may actually serve as an explanation for one of the most hotly debated questions in anthropology: what caused the disappearance of our Neanderthal relatives? Clearly, when it comes to brains, size does matter. Why then, with a brain some 20 percent larger than our own, did Neanderthals suddenly disappear in just a few thousand years between 40,000 and 30,000 years ago? the party line among scientists remains fixated on the notion that the demise of Neanderthals was a consequence of their hebetude, or mental lethargy. The neurobiologist William Calvin described Neanderthals in his book, A Brain for All Seasons: “Their way of life subjected them to more bone fractures; they seldom survived until forty years of age; and while making tools similar to [those of] overlapping species, there was little [of the] inventiveness that characterizes behaviorally modern Homo sapiens.”

While it is convenient and almost dogmatic to accept that Neanderthals were “wiped out” by clever Homo sapiens, many scientists now believe that food scarcity may have played a more prominent role in their disappearance. Perhaps the simple fact that Neanderthals, lacking the biochemical pathway to utilize beta-HBA as a fuel source for brain metabolism, lacked the “mental endurance” to persevere. Relying on gluconeogenesis to power their brains would have led to more rapid breakdown of muscle tissue, ultimately compromising their ability to stalk prey or migrate to areas where plant food sources were more readily available. their extinction may not have played out in direct combat with Homo sapiens but rather manifested as a consequence of a simple biochemical inadequacy.

Our ability to utilize beta-HBA as a brain fuel is far more important than simply a protective legacy of our hunter-gatherer heritage. George F. Cahill of Harvard Medical School stated, “Recent studies have shown that beta-hydroxybutyrate, the principle ‘ketone’ is not just a fuel, but a ‘superfuel’ more efficiently producing ATP energy than glucose. . . . It has also protected neuronal cells in tissue culture against exposure to toxins associated with Alzheimer’s or Parkinson’s.”

Indeed, well beyond serving as a brain superfuel, Dr. Cahill and other researchers have determined that beta-HBA has other profoundly positive effects on brain health and function. Essentially, beta-HBA is thought to mediate many of the positive effects of calorie reduction and fasting on the brain, including improved antioxidant function, increased mitochondrial energy production with an increased in mitochondrial energy production with an increase in mitochondrial population, increased cellular survival, and increased levels of BDNF leading to enhanced growth of new brain cells (neurogenesis).

Fasting

Earlier, we explored the need to reduce caloric intake in order to increase BDNF as a means to stimulate the growth of new brain cells as well as to enhance the function of existing neurons. The idea of substantially reducing daily calorie intake will not appeal to many people despite the fact that it is a powerful approach to brain enhancement as well as overall health.

Interestingly, however, many people find the idea of intermittent fasting to be more appealing. Fasting is defined here as a complete abstinence from food for a defined period of time at regular intervals—our fasting program permits the drinking of water. Research demonstrates that many of the same health-providing and brain-enhancing genetic pathways activated by calorie reduction are similarly engaged by fasting—even for relatively short periods of time. Fasting actually speaks to your DNA, directing your genes to produce an astounding array of brain-enhancement factors.

Not only does fasting turn on the genetic machinery for the production of BDNF, but it also powers up the Nrf2 pathway, leading to enhanced detoxification, reduced inflammation, and increased production of brain-protective antioxidants. Fasting causes the brain to shift away from using glucose as a fuel to a metabolism that consumes ketones. When the brain metabolizes ketones for fuel, even the process of apoptosis is reduced, while mitochondrial genes turn their attention to mitochondrial replication. In this way, fasting shifts the brain’s basic metabolism and specifically targets the DNA of mitochondria, thus enhancing energy production and paving the way for better brain function and clarity . . .

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Insights into human evolution from ancient and contemporary microbiome studies
by Stephanie L Schnorr, Krithivasan Sankaranarayanan, Cecil M Lewis, Jr, and Christina Warinner

Brain growth, development, and behavior

The human brain is our defining species trait, and its developmental underpinnings are key foci of evolutionary genetics research. Recent research on brain development and social interaction in both humans and animal models has revealed that microbes exert a major impact on cognitive function and behavioral patterns []. For example, a growing consensus recognizes that cognitive and behavioral pathogenesis are often co-expressed with functional bowel disorders []. This hints at a shared communication or effector pathway between the brain and gut, termed the gutbrain-axis (GBA). The enteric environment is considered a third arm of the autonomic nervous system [], and gut microbes produce more than 90% of the body’s serotonin (5-hydroxytryptamine or 5-HT) []. Factors critical to learning and plasticity such as serotonin, γ-aminobutryic acid (GABA), short chain fatty acids (SCFAs), and brain derived neurotrophic factor (BDNF), which train amygdalin and hippocampal reactivity, can be mediated through gut-brain chemical signals that cross-activate bacterial and host receptors []. Probiotic treatment is associated with positive neurological changes in the brain such as increased BDNF, altered expression of GABA receptors, increased circulating glutathione, and a reduction in inflammatory markers. This implicates the gut microbiome in early emotional training as well as in affecting long-term cognitive plasticity.

Critically, gut microbiota can modulate synthesis of metabolites affecting gene expression for myelin production in the prefrontal cortex (PFC), presumably influencing the oligodendrocyte transcriptome []. Prosocial and risk associated behavior in probiotic treated mice, a mild analog for novelty-seeking and risk-seeking behaviors in humans, suggests a potential corollary between entrenched behavioral phenotypes and catecholamines (serotonin and dopamine) produced by the gut microbiota []. Evolutionary acceleration of the human PFC metabolome divergence from chimpanzees, particularly the dopaminergic synapse [], reifies the notion that an exaggerated risk-reward complex characterizes human cognitive differentiation, which is facilitated by microbiome derived bioactive compounds. Therefore, quintessentially human behavioral phenotypes in stress, anxiety, and novelty-seeking is additionally reinforced by microbial production of neuroactive compounds. As neurological research expands to include the microbiome, it is increasingly clear that host–microbe interactions have likely played an important role in human brain evolution and development [].

Ancient human microbiomes
by Christina Warinner, Camilla Speller, Matthew J. Collins, and Cecil M. Lewis, Jr

Need for paleomicrobiology data

Although considerable effort has been invested in characterizing healthy gut and oral microbiomes, recent investigations of rural, non-Western populations () have raised questions about whether the microbiota we currently define as normal have been shaped by recent influences of modern Western diet, hygiene, antibiotic exposure, and lifestyle (). The process of industrialization has dramatically reduced our direct interaction with natural environments and fundamentally altered our relationship with food and food production. Situated at the entry point of our food, and the locus of food digestion, the human oral and gut microbiomes have evolved under conditions of regular exposure to a diverse range of environmental and zoonotic microbes that are no longer present in today’s globalized food chain. Additionally, the foods themselves have changed from the wild natural products consumed by our hunter-gatherer ancestors to today’s urban supermarkets stocked with an abundance of highly processed Western foodstuffs containing artificially enriched levels of sugar, oil, and salt, not to mention antimicrobial preservatives, petroleum-based colorants, and numerous other artificial ingredients. This dietary shift has altered selection pressure on our microbiomes. For example, under the ‘ecological plaque hypothesis’, diseases such as dental caries and periodontal disease are described as oral ecological catastrophes of cultural and lifestyle choices ().

Although it is now clear that the human microbiome plays a critical role in making us human, in keeping us healthy, and in making us sick, we know remarkably little about the diversity, variation, and evolution of the human microbiome both today and in the past. Instead, we are left with many questions: When and how did our bacterial communities become distinctly human? And what does this mean for our microbiomes today and in the future? How do we acquire and transmit microbiomes and to what degree is this affected by our cultural practices and built environments? How have modern Western diets, hygiene practices, and antibiotic exposure impacted ‘normal’ microbiome function? Are we still in mutualistic symbiosis with our microbiomes, or are the so-called ‘diseases of civilization’ – heart disease, obesity, type II diabetes, asthma, allergies, osteoporosis – evidence that our microbiomes are out of ecological balance and teetering on dysbiosis ()? At an even more fundamental level, who are the members of the human microbiome, how did they come to inhabit us, and how long have they been there? Who is ‘our microbial self’ ()?

Studies of remote and indigenous communities () and crowdsourcing projects such as the American Gut (www.americangut.org), the Earth Microbiome Project (www.earthmicrobiome.org), and uBiome (www.uBiome.com) are attempting to characterize modern microbiomes across a range of contemporary environments. Nevertheless, even the most extensive sampling of modern microbiota will provide limited insight into Pre-Industrial microbiomes. By contrast, the direct investigation of ancient microbiomes from discrete locations and time points in the past would provide a unique view into the coevolution of microbes and hosts, host microbial ecology, and changing human health states through time. […]

Diet also plays a role in shaping the composition of oral microbiomes, most notably by the action of dietary sugar in promoting the growth of cariogenic bacteria such as lactobacilli and S. mutans (). Two recent papers have proposed that cariogenic bacteria, such as S. mutans, were absent in pre-Neolithic human populations, possibly indicating low carbohydrate diets (), while evolutionary genomic analyses of S. mutans suggest an expansion in this species approximately 10,000 years, coinciding with the onset of agriculture (). […]

Ancient microbiome research provides an additional pathway to understanding human biology that cannot be achieved by studies of extant individuals and related species alone. Although reconstructing the ancestral microbiome by studying our ancestors directly is not without challenges (), this approach provides a more direct picture of human-microbe coevolution. Likewise, ancient microbiome sources may reveal to what extent bacteria commonly considered ‘pathogenic’ in the modern world (for example, H. pylori) were endemic indigenous organisms in pre-Industrial microbiomes ().

The three paths to reconstructing the ancestral microbiomes are also complimentary. For example, analysis of the gut microbiome from extant, rural peoples in Africa and South America have revealed the presence of a common, potentially commensal, spirochete belonging to the genus Treponema (). Such spirochetes have also been detected in extant hunter-gatherers (), and in 1,000-year-old human coprolites from Mexico (), but they are essentially absent from healthy urban populations, and they have not been reported in the gut microbiome of chimpanzees (). These multiple lines of evidence suggest that this poorly understood spirochete is a member of the ancestral human microbiome, yet not necessarily the broader primate microbiome. Future coprolite research may be able to answer the question of how long this microbe has co-associated with humans, and what niche it fills.

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Ketogenic Diet and Neurocognitive Health
Spartan Diet
The Agricultural Mind
Malnourished Americans

Neuroscientist Shows What Fasting Does To Your Brain & Why Big Pharma Won’t Study It
by Arjun Walia

Does Fasting Make You Smarter?
by Derek Beres

Fasting Cleans the Brain
by P. D. Mangan

How Fasting Heals Your Brain
by Adriana Ayales

Effect of Intermittent Fasting on Brain Neurotransmitters, Neutrophils Phagocytic Activity, and Histopathological Finding in Some Organs in Rats
by Sherif M. Shawky, Anis M. Zaid, Sahar H. Orabi, Khaled M. Shoghy, and Wafaa A. Hassan

The Effects of Fasting During Ramadan on the Concentration of Serotonin, Dopamine, Brain-Derived Neurotrophic Factor and Nerve Growth Factor
by Abdolhossein Bastani, Sadegh Rajabi, and Fatemeh Kianimarkani

Gut microbiome, SCFAs, mood disorders, ketogenic diet and seizures
by Jonathan Miller

Study: Ketogenic diet appears to prevent cognitive decline in mice
by University of Kentucky

Low-carb Diet Alleviates Inherited Form of Intellectual Disability in Mice
by Johns Hopkins Medicine

Ketogenic Diet Protects Against Alzheimer’s Disease by Keeping Your Brain Healthy and Youthful
by Joseph Mercola

The Gut Microbiota Mediates the Anti-Seizure Effects of the Ketogenic Diet.
by C. A. Olson

Is the Keto Diet Bad for the Microbiome?
by David Jockers

Does a Ketogenic Diet Change Our Microbiome?
by Christie Rice

Can Health Issues Be Solved By Dietary Changes Altering the Microbiome?
by Russ Schierling

Some Benefits of Intermittent Fasting are Mediated by the Gut Microbiome
by Fight Aging!

RHR: Is High Fat Healthy for the Gut Microbiota?
by Chris Kresser

A Comprehensive List of Low Carb Research
by Sarah Hallberg

Randomised Controlled Trials Comparing Low-Carb Diets Of Less Than 130g Carbohydrate Per Day To Low-Fat Diets Of Less Than 35% Fat Of Total Calories
from Public Health Collaboration

The Agricultural Mind

Let me make an argument about individualism, rigid egoic boundaries, and hence Jaynesian consciousness. But I’ll come at it from a less typical angle. I’ve been reading much about diet, nutrition, and health. There are significant links between what we eat and so much else: gut health, hormonal regulation, immune system, and neurocognitive functioning. There are multiple pathways, one of which is direct, connecting the gut and the brain. The gut is sometimes called the second brain, but in evolutionary terms it is the first brain. To demonstrate one example of a connection, many are beginning to refer to Alzheimer’s as type 3 diabetes, and dietary interventions have reversed symptoms in clinical studies. Also, microbes and parasites have been shown to influence our neurocognition and psychology, even altering personality traits and behavior (e.g., toxoplasma gondii).

One possibility to consider is the role of exorphins that are addictive and can be blocked in the same way as opioids. Exorphin, in fact, means external morphine-like substance, in the way that endorphin means indwelling morphine-like substance. Exorphins are found in milk and wheat. Milk, in particular, stands out. Even though exorphins are found in other foods, it’s been argued that they are insignificant because they theoretically can’t pass through the gut barrier, much less the blood-brain barrier. Yet exorphins have been measured elsewhere in the human body. One explanation is gut permeability that can be caused by many factors such as stress but also by milk. The purpose of milk is to get nutrients into the calf and this is done by widening the space in gut surface to allow more nutrients through the protective barrier. Exorphins get in as well and create a pleasurable experience to motivate the calf to drink more. Along with exorphins, grains and dairy also contain dopaminergic peptides, and dopamine is the other major addictive substance. It feels good to consume dairy as with wheat, whether you’re a calf or a human, and so one wants more.

Addiction, of food or drugs or anything else, is a powerful force. And it is complex in what it affects, not only physiologically and psychologically but also on a social level. Johann Hari offers a great analysis in Chasing the Scream. He makes the case that addiction is largely about isolation and that the addict is the ultimate individual. It stands out to me that addiction and addictive substances have increased over civilization. Growing of poppies, sugar, etc came later on in civilization, as did the production of beer and wine (by the way, alcohol releases endorphins, sugar causes a serotonin high, and both activate the hedonic pathway). Also, grain and dairy were slow to catch on, as a large part of the diet. Until recent centuries, most populations remained dependent on animal foods, including wild game. Americans, for example, ate large amounts of meat, butter, and lard from the colonial era through the 19th century. In 1900, Americans on average were only getting 10% of carbs as part of their diet and sugar was minimal.

Another factor to consider is that low-carb diets can alter how the body and brain functions. That is even more true if combined with intermittent fasting and restricted eating times that would have been more common in the past. Taken together, earlier humans would have spent more time in ketosis (fat-burning mode, as opposed to glucose-burning) which dramatically affects human biology. The further one goes back in history the greater amount of time people probably spent in ketosis. One difference with ketosis is cravings and food addictions disappear. It’s a non-addictive or maybe even anti-addictive state of mind. Many hunter-gatherer tribes can go days without eating and it doesn’t appear to bother them, and that is typical of ketosis. This was also observed of Mongol warriors who could ride and fight for days on end without tiring or needing to stop for food. What is also different about hunter-gatherers and similar traditional societies is how communal they are or were and how more expansive their identities in belonging to a group. Anthropological research shows how hunter-gatherers often have a sense of personal space that extends into the environment around them. What if that isn’t merely cultural but something to do with how their bodies and brains operate? Maybe diet even plays a role. Hold that thought for a moment.

Now go back to the two staples of the modern diet, grains and dairy. Besides exorphins and dopaminergic substances, they also have high levels of glutamate, as part of gluten and casein respectively. Dr. Katherine Reid is a biochemist whose daughter was diagnosed with autism and it was severe. She went into research mode and experimented with supplementation and then diet. Many things seemed to help, but the greatest result came from restriction of glutamate, a difficult challenge as it is a common food additive. This requires going on a largely whole foods diet, that is to say eliminating processed foods. But when dealing with a serious issue, it is worth the effort. Dr. Reid’s daughter showed immense improvement to such a degree that she was kicked out of the special needs school. After being on this diet for a while, she socialized and communicated normally like any other child, something she was previously incapable of. Keep in mind that glutamate is necessary as a foundational neurotransmitter in modulating communication between the gut and brain. But typically we only get small amounts of it, as opposed to the large doses found in the modern diet.

Glutamate is also implicated in schizophrenia: “The most intriguing evidence came when the researchers gave germ-free mice fecal transplants from the schizophrenic patients. They found that “the mice behaved in a way that is reminiscent of the behavior of people with schizophrenia,” said ,Julio Licinio, who co-led the new work with Wong, his research partner and spouse. Mice given fecal transplants from healthy controls behaved normally. “The brains of the animals given microbes from patients with schizophrenia also showed changes in glutamate, a neurotransmitter that is thought to be dysregulated in schizophrenia,” he added. The discovery shows how altering the gut can influence an animals behavior” (Roni Dengler, Researchers Find Further Evidence That Schizophrenia is Connected to Our Guts; reporting on Peng Zheng et al, The gut microbiome from patients with schizophrenia modulates the glutamate-glutamine-GABA cycle and schizophrenia-relevant behaviors in mice, Science Advances journal). And glutamate is involved in other conditions as well, such as in relation to GABA: “But how do microbes in the gut affect [epileptic] seizures that occur in the brain? Researchers found that the microbe-mediated effects of the Ketogenic Diet decreased levels of enzymes required to produce the excitatory neurotransmitter glutamate. In turn, this increased the relative abundance of the inhibitory neurotransmitter GABA. Taken together, these results show that the microbe-mediated effects of the Ketogenic Diet have a direct effect on neural activity, further strengthening support for the emerging concept of the ‘gut-brain’ axis.” (Jason Bush, Important Ketogenic Diet Benefit is Dependent on the Gut Microbiome). Glutamate is one neurotransmitter among many that can be affected in a similar manner; e.g., serotonin is also produced in the gut.

That reminds me of propionate, a short chain fatty acid. It is another substance normally taken in at a low level. Certain foods, including grains and dairy, contain it. The problem is that, as a useful preservative, it has been generously added to the food supply. Research on rodents shows injecting them with propionate causes autistic-like behaviors. And other rodent studies show how this stunts learning ability and causes repetitive behavior (both related to the autistic demand for the familiar), as too much propionate entrenches mental patterns through the mechanism that gut microbes use to communicate to the brain how to return to a needed food source. Autistics, along with cravings for propionate-containing foods, tend to have larger populations of a particular gut microbe that produces propionate. In killing microbes, this might be why antibiotics can help with autism. But in the case of depression, it is associated instead with the lack of certain microbes that produce butyrate, another important substance that also is found in certain foods (Mireia Valles-Colomer et al, The neuroactive potential of the human gut microbiota in quality of life and depression). Depending on the specific gut dysbiosis, diverse neurocognitive conditions can result. And in affecting the microbiome, changes in autism can be achieved through a ketogenic diet, reducing the microbiome (similar to an antibiotic) — this presumably takes care of the problematic microbes and readjusts the gut from dysbiosis to a healthier balance.

As with proprionate, exorphins injected into rats will likewise elicit autistic-like behaviors. By two different pathways, the body produces exorphins and proprionate from the consumption of grains and dairy, the former from the breakdown of proteins and the latter produced by gut bacteria in the breakdown of some grains and refined carbohydrates (combined with the proprionate used as a food additive; added to other foods as well and also, at least in rodents, artificial sweeteners increase propionate levels). This is part of the explanation for why many autistics have responded well to low-carb ketosis, specifically paleo diets that restrict both wheat and dairy, but ketones themselves play a role in using the same transporters as propionate and so block their buildup in cells and, of course, ketones offer a different energy source for cells as a replacement for glucose which alters how cells function, specifically neurocognitive functioning and its attendant psychological effects.

What stands out to me about autism is how isolating it is. The repetitive behavior and focus on objects resonates with extreme addiction. Both conditions block normal human relating and create an obsessive mindset that, in the most most extreme forms, blocks out all else. I wonder if all of us moderns are simply expressing milder varieties of this biological and neurological phenomenon. And this might be the underpinning of our hyper-individualistic society, with the earliest precursors showing up in the Axial Age following what Julian Jaynes hypothesized as the breakdown of the much more other-oriented bicameral mind. What if our egoic individuality is the result of our food system, as part of the civilizational project of mass agriculture?

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Mongolian Diet and Fasting

For anyone who is curious to learn more, the original point of interest for me was a quote by Jack Weatherford in his book Genghis Khan and the Making of the Modern World: “The Chinese noted with surprise and disgust the ability of the Mongol warriors to survive on little food and water for long periods; according to one, the entire army could camp without a single puff of smoke since they needed no fires to cook. Compared to the Jurched soldiers, the Mongols were much healthier and stronger. The Mongols consumed a steady diet of meat, milk, yogurt, and other diary products, and they fought men who lived on gruel made from various grains. The grain diet of the peasant warriors stunted their bones, rotted their teeth, and left them weak and prone to disease. In contrast, the poorest Mongol soldier ate mostly protein, thereby giving him strong teeth and bones. Unlike the Jurched soldiers, who were dependent on a heavy carbohydrate diet, the Mongols could more easily go a day or two without food.” By the way, that biography was written by an anthropologist who lived among and studied the Mongols for years. It is about the historical Mongols, but filtered through the direct experience of still existing Mongol people who have maintained a traditional diet and lifestyle longer than most other populations. It isn’t only that their diet was ketogenic because of being low-carb but also because it involved fasting.

From Mongolia Volume 1 The Tangut Country, and the Solitudes of Northernin (1876), Nikolaĭ Mikhaĭlovich Przhevalʹskiĭ writes in the second note on p. 65 under the section Calendar and Year-Cycle: “On the New Year’s Day, or White Feast of the Mongols, see ‘Marco Polo’, 2nd ed. i. p. 376-378, and ii. p. 543. The monthly fetival days, properly for the Lamas days of fasting and worship, seem to differ locally. See note in same work, i. p. 224, and on the Year-cycle, i. p. 435.” This is alluded to in another text, in describing that such things as fasting were the norm of that time: “It is well known that both medieval European and traditional Mongolian cultures emphasized the importance of eating and drinking. In premodern societies these activities played a much more significant role in social intercourse as well as in religious rituals (e.g., in sacrificing and fasting) than nowadays” (Antti Ruotsala, Europeans and Mongols in the middle of the thirteenth century, 2001). A science journalist trained in biology, Dyna Rochmyaningsih, also mentions this: “As a spiritual practice, fasting has been employed by many religious groups since ancient times. Historically, ancient Egyptians, Greeks, Babylonians, and Mongolians believed that fasting was a healthy ritual that could detoxify the body and purify the mind” (Fasting and the Human Mind).

Mongol shamans and priests fasted, no different than in so many other religions, but so did other Mongols — more from Przhevalʹskiĭ’s 1876 account showing the standard feast and fast cycle of many traditional ketogenic diets: “The gluttony of this people exceeds all description. A Mongol will eat more than ten pounds of meat at one sitting, but some have been known to devour an average-sized sheep in twenty-four hours! On a journey, when provisions are economized, a leg of mutton is the ordinary daily ration for one man, and although he can live for days without food, yet, when once he gets it, he will eat enough for seven” (see more quoted material in Diet of Mongolia). Fasting was also noted of earlier Mongols, such as Genghis Khan: “In the spring of 2011, Jenghis Khan summoned his fighting forces […] For three days he fasted, neither eating nor drinking, but holding converse with the gods. On the fourth day the Khakan emerged from his tent and announced to the exultant multitude that Heaven had bestowed on him the boon of victory” (Michael Prawdin, The Mongol Empire, 1967). Even before he became Khan, this was his practice as was common among the Mongols, such that it became a communal ritual for the warriors:

“When he was still known as Temujin, without tribe and seeking to retake his kidnapped wife, Genghis Khan went to Burkhan Khaldun to pray. He stripped off his weapons, belt, and hat – the symbols of a man’s power and stature – and bowed to the sun, sky, and mountain, first offering thanks for their constancy and for the people and circumstances that sustained his life. Then, he prayed and fasted, contemplating his situation and formulating a strategy. It was only after days in prayer that he descended from the mountain with a clear purpose and plan that would result in his first victory in battle. When he was elected Khan of Khans, he again retreated into the mountains to seek blessing and guidance. Before every campaign against neighboring tribes and kingdoms, he would spend days in Burhkhan Khandun, fasting and praying. By then, the people of his tribe had joined in on his ritual at the foot of the mountain, waiting his return” (Dr. Hyun Jin Preston Moon, Genghis Khan and His Personal Standard of Leadership).

As an interesting side note, the Mongol population have been studied to some extent in one area of relevance. In Down’s Anomaly (1976), Smith et al writes that, “The initial decrease in the fasting blood sugar was greater than that usually considered normal and the return to fasting blood sugar level was slow. The results suggested increased sensitivity to insulin. Benda reported the initial drop in fating blood sugar to be normal but the absolute blood sugar level after 2 hours was lower for mongols than for controls.” That is probably the result of a traditional low-carb diet that had been maintained continuously since before history. For some further context, I noticed some discusion about the Mongolian keto diet (Reddit, r/keto, TIL that Ghenghis Khan and his Mongol Army ate a mostly keto based diet, consisting of lots of milk and cheese. The Mongols were specially adapted genetically to digest the lactase in milk and this made them easier to feed.) that was inspired by the scientific documentary “The Evolution of Us” (presently available on Netflix and elsewhere).

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3/30/19 – An additional comment: I briefly mentioned sugar, that it causes a serotonin high and activates the hedonic pathway. I also noted that it was late in civilization when sources of sugar were cultivated and, I could add, even later when sugar became cheap enough to be common. Even into the 1800s, sugar was minimal and still often considered more as medicine than food.

To extend this thought, it isn’t only sugar in general but specific forms of it. Fructose, in particular, has become widespread because of United States government subsidizing corn agriculture which has created a greater corn yield that humans can consume. So, what doesn’t get fed to animals or turned into ethanol, mostly is made into high fructose corn syrup and then added into almost every processed food and beverage imaginable.

Fructose is not like other sugars. This was important for early hominid survival and so shaped human evolution. It might have played a role in fasting and feasting. In 100 Million Years of Food, Stephen Le writes that, “Many hypotheses regarding the function of uric acid have been proposed. One suggestion is that uric acid helped our primate ancestors store fat, particularly after eating fruit. It’s true that consumption of fructose induces production of uric acid, and uric acid accentuates the fat-accumulating effects of fructose. Our ancestors, when they stumbled on fruiting trees, could gorge until their fat stores were pleasantly plump and then survive for a few weeks until the next bounty of fruit was available” (p. 42).

That makes sense to me, but he goes on to argue against this possible explanation. “The problem with this theory is that it does not explain why only primates have this peculiar trait of triggering fat storage via uric acid. After all, bears, squirrels, and other mammals store fat without using uric acid as a trigger.” This is where Le’s knowledge is lacking for he never discusses ketosis that has been centrally important for humans unlike other animals. If uric acid increases fat production, that would be helpful for fattening up for the next starvation period when the body returned to ketosis. So, it would be a regular switching back and forth between formation of uric acid that stores fat and formation of ketones that burns fat.

That is fine and dandy under natural conditions. Excess fructose, however, is a whole other matter. It has been strongly associated with metabolic syndrome. One pathway of causation is that increased production of uric acid. This can lead to gout but other things as well. It’s a mixed bag. “While it’s true that higher levels of uric acid have been found to protect against brain damage from Alzheimer’s, Parkinson’s, and multiple sclerosis, high uric acid unfortunately increases the risk of brain stroke and poor brain function” (p. 43).

The potential side effects of uric acid overdose are related to other problems I’ve discussed in relation to the agricultural mind. “A recent study also observed that high uric acid levels are associated with greater excitement-seeking and impulsivity, which the researchers noted may be linked to attention deficit hyperactivity disorder (ADHD)” (p. 43). The problems of sugar go far beyond mere physical disease. It’s one more factor in the drastic transformation of the human mind.

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4/2/19 – More info: There are certain animal fats, the omega-3 fatty acids EPA and DHA, that are essential to human health. These were abundant in the hunter-gatherer diet. But over the history of agriculture, they have become less common.

This is associated with psychiatric disorders and general neurocognitive problems, including those already mentioned above in the post. Agriculture and industrialization have replaced these healthy oils with overly processed oils that are high in linoleic acid (LA), an omega-6 fatty acids. LA interferes with the body’s use of omega-3 fatty acids.

The Brain Needs Animal Fat
by Georgia Ede

Ketogenic Diet and Neurocognitive Health

Below is a passage from Ketotarian by Will Cole. It can be read in Chapter 1, titled “the ketogenic diet (for better and worse)”. The specific passage is to be found on pp. 34-38 in printed book (first edition) or pp. 28-31 in the Google ebook. I share it here because it is a great up-to-date summary of the value of the ketogenic diet. It is the low-carb diet pushed to its furthest extent where you burn fat instead of sugar, that is to say the body prioritizes and more efficiently uses ketones in place of glucose.

The brain, in particular, prefers ketones. That is why I decided to share a passage specifically on neurological health, as diet and nutrition isn’t the first thing most people think of in terms of what often gets framed as mental health, typically treated with psychiatric medications. But considering the severely limited efficacy of entire classes of such drugs (e.g., antidepressives), maybe it’s time for a new paradigm for treatment.

The basic advantage to ketosis is that, until modernity, most humans for most of human evolution (and going back into hominid evolution) were largely dependent on a high-fat diet for normal functioning. This is indicated by how the body more efficiently uses ketones than glucose. What the body does with carbs and sugar, though, is to either to use it right away or store it as fat. This is why hunter-gatherers would, when possible, carb-load right before winter in order to fatten themselves up. We have taken this knowledge in using carbs to fatten up animals before the slaughter.

Besides fattening up for winter in northern climes, hunter-gatherers focus most of their diet on fats and oils, in that when available they choose to eat far more fats and oils than they eat meat or vegetables. They do most of their hunting during the season when animals are the fattest and, if they aren’t simply doing a mass slaughter, they specifically target the fattest individual animals. After the kill, they often throw the lean meat to the dogs or mix it with fat for later use (e.g., pemmican).

This is why, prior to agriculture, ketosis was the biological and dietary norm. Even farmers until recent history were largely dependent in supplementing their diet with hunting and gathering. Up until the 20th century, most Americans ate more meat than bread, while intake of vegetables and fruits was minor and mostly seasonal. The meat most Americans, including city-dwellers, were eating was wild game because of the abundance in nearby wilderness areas; and, going by cookbooks of the time, fats and oils were at the center of the diet.

Anyway, simply in reading the following passage, you will not only become more well informed on this topic than average American but, sadly, also the average American doctor. This isn’t the kind of info that is emphasized in medical schools, despite it being fairly well researched at this point (see appended section of the author’s notes). “A study in the International Journal of Adolescent Medicine and Health assessed the basic nutrition and health knowledge of medical school graduates entering a pediatric residency program and found that, on average, they answered only 52 percent of eighteen questions correctly,” as referenced by Dr. Cole. He concluded that, “In short, most mainstream doctors would fail nutrition” (see previous post).

Knowledge is a good thing. And so here is some knowledge.

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NEUROLOGICAL IMPROVEMENTS

Around 25 percent of your body’s cholesterol is found in your brain, (19) and remember, your brain is composed of 60 percent fat. (20) Think about that. Over half of your brain is fat! What we have been traditionally taught when it comes to “low-fat is best” ends up depriving your brain of the very thing it is made of. It’s not a coincidence that many of the potential side effects associated with statins—cholesterol-lowering drugs—are brain problems and memory loss. (21)

Your gut and brain actually form from the same fetal tissue in the womb and continue their special bond throughout your entire life through the gut-brain axis and the vagus nerve. Ninety-five percent of your happy neurotransmitter serotonin is produced and stored in your gut, so you can’t argue that your gut doesn’t influence the health of your brain. (22) The gut is known as the “second brain” in the medical literature, and a whole area of research known as the cytokine model of cognitive function is dedicated to examining how chronic inflammation and poor gut health can directly influence brain health. (23)

Chronic inflammation leads to not only increased gut permeability but blood-brain barrier destruction as well. When this protection is compromised, your immune system ends up working in overdrive, leading to brain inflammation. (24) Inflammation can decrease the firing rate of neurons in the frontal lobe of the brain in people with depression. (25) Because of this, antidepressants can be ineffective since they aren’t addressing the problem. And this same inflammatory oxidative stress in the hypothalamic cells of the brain is one potential factor of brain fog. (26)

Exciting emerging science is showing that a ketogenic diet can be more powerful than some of the strongest medications for brain-related problems such as autism, attention deficit/hyperactivity disorder (ADHD), bipolar disorder, schizophrenia, anxiety, and depression. (27) Through a ketogenic diet, we can not only calm brain-gut inflammation but also improve the gut microbiome. (28)

Ketones are also extremely beneficial because they can cross the blood-brain barrier and provide powerful fuel to your brain, providing mental clarity and improved mood. Their ability to cross the blood-brain barrier paired with their natural anti-inflammatory qualities provides incredible healing properties when it comes to improving traumatic brain injury (TBI) as well as neurodegenerative diseases. (29)

Medium-chain triglycerides (MCTs), found in coconuts (a healthy fat option in the Ketotarian diet), increase beta-hydroxybutyrate and are proven to enhance memory function in people with Alzheimer’s disease (30) as well as protect against neurodegeneration in people with Parkinson’s disease. (31) Diets rich in polyunsaturated fats, wild-caught fish specifically, are associated with a 60 percent decrease in Alzheimer’s disease. (32) Another study of people with Parkinson’s disease also found that the severity of their condition improved 43 percent after just one month of eating a ketogenic diet. (33) Studies have also shown that a ketogenic diet improves autism symptoms. (34) Contrast that with high-carb diets, which have been shown to increase the risk of Alzheimer’s disease and other neurodegenerative conditions. (35)

TBI or traumatic brain injury is another neurological area that can be helped through a ketogenic diet. When a person sustains a TBI, it can result in impaired glucose metabolism and inflammation, both of which are stabilized through a healthy high-fat ketogenic diet. (36)

Ketosis also increases the brain-derived-neurotrophic factor (BDNF), which protects existing neurons and encourages the growth of new neurons—another neurological benefit. (37)

In its earliest phases, modern ketogenic diet research was focused on treating epilepsy. (38) Children with epilepsy who ate this way were more alert, were more well behaved, and had more enhanced cognitive function than those who were treated with medication. (39) This is due to increased mitochondrial function, reduced oxidative stress, and increased gamma-aminobutyric acid (GABA) levels, which in turn helps reduce seizures. These mechanisms can also provide benefits for people with brain fog, anxiety, and depression. (40)

METABOLIC HEALTH

Burning ketones rather than glucose helps maintain balanced blood sugar levels, making the ketogenic way of eating particularly beneficial for people with metabolic disorders, diabetes, and weight-loss resistance.

Insulin resistance, the negative hormonal shift in metabolism that we mentioned earlier, is at the core of blood sugar problems and ends up wreaking havoc on the body, eventually leading to heart disease, weight gain, and diabetes. As we have seen, healthy fats are a stronger form of energy than glucose. The ketogenic diet lowers insulin levels and reduces inflammation as well as improving insulin receptor site sensitivity, which helps the body function the way it was designed. Early trial reports have shown that type 2 diabetes symptoms can be reversed in just ten weeks on the ketogenic diet! (41)

Fascinating research has been done correlating blood sugar levels and Alzheimer’s disease. In fact, so much so that the condition is now being referred to by some experts as type 3 diabetes . With higher blood sugar and increased insulin resistance comes more degeneration in the hippocampus, your brain’s memory center. (42) It’s because of this that people with type 1 and 2 diabetes have a higher risk of developing Alzheimer’s disease. This is another reason to get blood sugar levels balanced and have our brain burn ketones instead.

Notes:

* * *

I came across something interesting on the Ketogenic Forum, a discussion of a video. It’s about reporting on the ketogenic diet from Dateline almost a quarter century ago, back when I was a senior in high school. So, not only has the ketogenic diet been known in the medical literature for about a century but has even shown up in mainstream reporting for decades. Yet, ketogenic-oriented and related low-carb diets such as the paleo diet get called fad diets, and the low-carb diet has been well known for even longer, going back to the 19th century.

The Dateline show was about the ketosis used as treatment for serious medical conditions. But even though it was a well known treatment for epilepsy, doctors apparently still weren’t commonly recommending it. In fact, the keto diet wasn’t even mentioned as an option by a national expert, instead focusing on endless drugs and even surgery. After doing his own research for his son’s seizures, the father discovered the keto diet in the medical literature. The doctor was asked why he didn’t recommend it for the child’s seizures when it was known to have the highest efficacy rate. The doctor essentially had no answer other than to say that there were more drugs he could try, even as he admitted that no drug comes close in comparison.

As one commenter put it, “Seems like even back then the Dr’s knew drugs would always trump diet even though the success rate of the keto diet was 50-70%. No drugs at the time could even come close to that. And the one doctor still insisted they should try even more drugs to help Charlie even after Keto. Ugh!” Everyone knows the diet works. It’s been proven beyond all doubt. But there is a simple problem. There is no profit to be made from an easy and effective non-pharmaceutical solution.

This doctor knew there was a better possibility to offer the family and chose not to mention it. The consequences to his medical malfeasance is the kid may have ended up with permanent brain damage from seizures and from the side effects of medications. The father was shocked and angry. You’d think cases like this would have woken up the medical community, right? Well, you’d be wrong if you thought so. Yet quarter of a century later, most doctors continue to act clueless that these kinds of diets can help numerous health conditions. It’s not a lack of information being available, as many of these doctors knew about it even back then. But it simply doesn’t fit into the conventional medicine nor within the big drug and big insurance framework.

Here is the video: