The Diet We Were Designed to Eat

There are three broad theories about evolution and food. One is that humans have become adapted to grains and other products of the agricultural revolution over the last 10,000 years. Two is the paleo view “that 10,000 years is a blink of an evolutionary eye, and that humans are adapted to paleolithic diets with a lot of lean meat,” but why stop there? The third theory is that the last 200,000 years “is a minute of the evolutionary year” when we were mostly Stone Age humans and represents just the last 1 percent of the roughly 20 million years we’ve been evolving since our common great ape ancestor. So, What Is the “Natural” Human Diet?

During our truly formative years, which one might say was the first 90 percent of our existence, our nutritional requirements reflected an ancestral past in which we ate mostly leaves, flowers, and fruits, with some bugs thrown in, thanks to wormy apples, to get our vitamin B12. “For this reason, another approach that might improve our understanding of the best dietary practices for modern humans is to focus attention not on the past but rather on the here and now; that is, on study of the foods eaten by the closest living relatives of modern humans,” given the bulk of our ancestral diets and “the lack of evidence supporting any notable diet-related changes in human nutrient requirements, metabolism, or digestive physiology” compared to our fellow great apes.

This could explain why fruits and vegetables are not only good for us but are vital to our survival. Indeed, we’re one of the few species so adapted to a plant-based diet that we could actually die from not eating fruits and vegetables, from the vitamin C-deficiency disease, scurvy. Most other animals simply make their own vitamin C, but why would our body waste all that effort when we evolved hanging out in the trees just eating fruits and veggies all day long?

Presumably, it’s not a coincidence that the few other mammals unable to synthesize their own vitamin C—including guinea pigs, some bunny rabbits, and fruit bats—are all, like us great apes, strongly herbivorous. Even during the Stone Age, data from rehydrated human fossilized feces tell us we may have been getting up to ten times more vitamin C and ten times more dietary fiber than we get today. The question is: Are these incredibly high-nutrient intakes simply an unavoidable by-product of eating whole, plant foods all the time, or might they actually be serving some important function, like antioxidant defense?

Plants create antioxidants to defend their own structures against free radicals. The human body must defend itself against the same types of pro-oxidants, so we too have evolved an array of amazing antioxidant enzymes, which are effective but not infallible. Free radicals can breach our defenses and cause damage that accumulates with age, leading to a variety of disease-causing and ultimately fatal changes. This is where plants may come in: “Plant-based, antioxidant-rich foods traditionally formed the major part of the human diet,” so we didn’t have to evolve that great of an antioxidant system. We could just let the plants in our diet pull some of the weight, like giving us vitamin C so we don’t have to be bothered to make it ourselves. Using plants as a crutch may well have relieved the pressure for further evolutionary development of our own defenses. That is we’ve become dependent on getting lots of plant foods in our diet, and when we don’t, we may suffer adverse health consequences.

Even during the Stone Age, this may not have been a problem. Only in recent history did we start giving up on whole plant foods. Even modern-day paleo and low-carb followers may be eating more vegetables than those on standard Western diets. There’s a perception that low-carbers are chowing down on the three Bs—beef, bacon, and butter—but that’s only a small minority. What they are eating more of is salad. Indeed, according to an online low-carb community, the number one thing they said they were eating more of was vegetables. Great! The problem isn’t people wanting to cut their carb intake by swapping junk food for vegetables. The concern is the shift to animal-sourced foods. “Greater adherence to [a low-carb diet] high in animal sources of fat and protein was associated with higher all-cause and cardiovascular mortality post-MI,” or after a heart attack, meaning they cut their lives short.

If there’s one takeaway from our studies of ancestral diets, perhaps it’s that “diets based largely on plant foods promote health and longevity.”


For more on the paleo and low carb diets, see:

If you were fascinated by how we can take advantage of plant defense mechanisms, check out my videos Appropriating Plant Defenses and Xenohormesis: What Doesn’t Kill Plants May Make Us Stronger.

How many antioxidants should we shoot for? See:

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Reversing Massive Obesity With Diet

Dr. Walter Kempner introduced the first comprehensive dietary program to treat chronic kidney disease and, in doing so, also revolutionized the treatment of other disorders, including obesity. Kempner was Professor Emeritus of Medicine at Duke, where he came up with the so-called rice diet, which basically consisted of rice, sugar, fruit, and fruit juices, was extremely low in sodium and fat, and included no animal fat, no cholesterol, and no animal protein. The sugar was added as a source of calories so people wouldn’t lose too much weight. But some people need to lose weight, so he started treating obese patients with a lower calorie version of the diet, which I discuss in my Can Morbid Obesity Be Reversed Through Diet? video.

He published an analysis of 106 patients who each lost at least 100 pounds. Why 106? Kempner simply picked the last 100 people who lost more than 100 pounds, and, by the time he finished reviewing their charts, 6 more had joined the so-called century club. Average weight loss among them was 141 pounds. “This study demonstrates that massively obese persons can achieve marked weight reduction, even normalization of weight, without hospitalization, surgery, or pharmacologic intervention…[O]ne important fact to be gained from this study is that, despite the misconception to the contrary, massive obesity is not an uncorrectable malady. Weight loss can be achieved, massive obesity can be corrected, and it can be done without drastic intervention.”

Well, Kempner’s rice diet is pretty drastic, so definitely don’t try this at home. In fact, the rice diet is dangerous. It’s so restrictive that it may cause serious electrolyte imbalances, unless the patient is carefully medically supervised with frequent blood and urine lab testing. Dangerous? Says who? Said the world’s number-one advocate for the rice diet: Dr. Kempner himself.

The best, safe approximation of the diet, meaning low in sodium and without fat, protein, or cholesterol from animals, would be a vitamin B12-fortified diet centered around whole, unprocessed plant foods. However, even a medically supervised rice diet could be considered un-drastic compared to procedures like getting one’s internal organs stapled or rearranged, wiring someone’s jaws shut, or even undergoing brain surgery.

Attempts have been made to destroy the parts of the brain associated with the sensation of hunger, by irradiation or going in through the skull and burning them out. “It shows how ineffective most simpler forms of treatment are that anyone should think it reasonable to produce irreversible intracranial lesions in very obese patients.” The surgeons defended these procedures, however, explaining that their “justification in attempting the operation is, of course, the very poor results of conventional therapy in gross obesity, and the dark prognosis, mental and physical, of the uncorrected condition.” In reply, a critic countered, “Such strong feelings [about how dark the prognosis is] run the risk of being conveyed to the patient, to the effect of masking the operative dangers and steam-rolling the patient’s approval.” The surgeon replied, “If any ‘steamrolling’ is taking place, it comes rather from obese patients who sometimes threaten suicide unless they are accepted for experimental surgical treatment.”

As of 2013, the American Medical Association officially declared obesity a disease, by identifying the enormous humanitarian impact of obesity as requiring the medical care and attention of other diseases. Yet the way we treat diseases these days involves drugs and surgery. Anti-obesity drugs have been pulled from the market again and again after they started killing people—an unrelenting fall of the pharmacological treatment of obesity.

The same has happened with obesity surgeries. The procedure Kempner wrote about was discontinued because of the complication of causing irreversible cirrhosis of the liver. Current procedures include various reconfigurations of the digestive tract. Complications of surgery appear to occur in about 20 percent of patients, and nearly one in ten of which may be death. In one of the largest studies, 1.9 percent of patients died within a month of the surgery. “Even if surgery proves sustainably effective, the need to rely on the rearrangement of [our] anatomy as an alternative to better use of feet and forks [that is, diet and exercise] seems a societal travesty.”


For more on Kempner and his rice diet, see my videos:

Learn more on the surgical approach in Reversing Diabetes with Surgery and Stomach Stapling Kids.

And, for more on weight, see:

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

The 3 Vitamins that Prevent Brain Loss

By our seventies, one in five of us will suffer from cognitive impairment. Within five years, half of those cognitively impaired will progress to dementia and death. The earlier we can slow or stop this process, the better.

Although an effective treatment for Alzheimer’s disease is unavailable, interventions just to control risk factors could prevent millions of cases. An immense effort has been spent on identifying such risk factors for Alzheimer’s and developing treatments to reduce them.

In 1990, a small study of 22 Alzheimer’s patients reported high concentrations of homocysteine in their blood. The homocysteine story goes back to 1969 when a Harvard pathologist reported two cases of children, one dating back to 1933, whose brains had turned to mush. They both suffered from extremely rare genetic mutations that led to abnormally high levels of homocysteine in their bodies. Is it possible, he asked, that homocysteine could cause brain damage even in people without genetic defects?

Here we are in the 21st century, and homocysteine is considered “a strong, independent risk factor for the development of dementia and Alzheimer’s disease.” Having a blood level over 14 (µmol/L) may double our risk. In the Framingham Study, researchers estimate that as many as one in six Alzheimer’s cases may be attributable to elevated homocysteine in the blood, which is now thought to play a role in brain damage and cognitive and memory decline. Our body can detoxify homocysteine, though, using three vitamins: folate, vitamin B12, and vitamin B6. So why don’t we put them to the test? No matter how many studies find an association between high homocysteinea and cognitive decline, dementia, or Alzheimer’s disease, a cause-and-effect role can only be confirmed by interventional studies.

Initially, the results were disappointing. Vitamin supplementation did not seem to work, but the studies were tracking neuropsychological assessments, which are more subjective compared to structural neuroimaging—that is, actually seeing what’s happening to the brain. A double-blind randomized controlled trial found that homocysteine-lowering by B vitamins can slow the rate of accelerated brain atrophy in people with mild cognitive impairment. As we age, our brains slowly atrophy, but the shrinking is much accelerated in patients suffering from Alzheimer’s disease. An intermediate rate of shrinkage is found in people with mild cognitive impairment. The thinking is if we could slow the rate of brain loss, we may be able to slow the conversion to Alzheimer’s disease. Researchers tried giving people B vitamins for two years and found it markedly slowed the rate of brain shrinkage. The rate of atrophy in those with high homocysteine levels was cut in half. A simple, safe treatment can slow the accelerated rate of brain loss.

A follow-up study went further by demonstrating that B-vitamin treatment reduces, by as much as seven-fold, the brain atrophy in the regions specifically vulnerable to the Alzheimer’s disease process. You can see the amount of brain atrophy over a two-year period in the placebo group versus the B-vitamin group in my Preventing Brain Loss with B Vitamins? video.

The beneficial effect of B vitamins was confined to those with high homocysteine, indicating a relative deficiency in one of those three vitamins. Wouldn’t it be better to not become deficient in the first place? Most people get enough B12 and B6. The reason these folks were stuck at a homocysteine of 11 µmoles per liter is that they probably weren’t getting enough folate, which is found concentrated in beans and greens. Ninety-six percent of Americans don’t even make the minimum recommended amount of dark green leafy vegetables, which is the same pitiful number who don’t eat the minimum recommendation for beans.

If we put people on a healthy diet—a plant-based diet—we can drop their homocysteine levels by 20% in just one week, from around 11 mmoles per liter down to 9 mmoles per liter. The fact that they showed rapid and significant homocysteine lowering without any pills or supplements implies that multiple mechanisms may have been at work. The researchers suggest it may be because of the fiber. Every gram of daily fiber consumption may increase folate levels in the blood nearly 2%, perhaps by boosting vitamin production in the colon by all our friendly gut bacteria. It also could be from the decreased methionine intake.

Methionine is where homocysteine comes from. Homocysteine is a breakdown product of methionine, which comes mostly from animal protein. If we give someone bacon and eggs for breakfast and a steak for dinner, we can get spikes of homocysteine levels in the blood. Thus, decreased methionine intake on a plant-based diet may be another factor contributing to lower, safer homocysteine levels.

The irony is that those who eat plant-based diets long-term, not just at a health spa for a week, have terrible homocysteine levels. Meat-eaters are up at 11 µmoles per liter, but vegetarians at nearly 14 µmoles per liter and vegans at 16 µmoles per liter. Why? The vegetarians and vegans were getting more fiber and folate, but not enough vitamin B12. Most vegans were at risk for suffering from hyperhomocysteinaemia (too much homocysteine in the blood) because most vegans in the study were not supplementing with vitamin B12 or eating vitamin B12-fortified foods, which is critical for anyone eating a plant-based diet. If you take vegans and give them B12, their homocysteine levels can drop down below 5. Why not down to just 11? The reason meat-eaters were stuck up at 11 is presumably because they weren’t getting enough folate. Once vegans got enough B12, they could finally fully exploit the benefits of their plant-based diets and come out with the lowest levels of all.

This is very similar to the findings in my video Vitamin B12 Necessary for Arterial Health.

For more details on ensuring a regular reliable source of vitamin B12:

There are more benefits to lowering your methionine intake. Check out Methionine Restriction as a Life Extension Strategy and Starving Cancer with Methionine Restriction.

For more on brain health in general, see these videos:

In health,

Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live, year-in-review presentations: