Moderation Kills

What if we don’t want just low risk for a heart attack, but no risk? One great stumbling block has been that government and national health organizations appear to have taken the patronizing view that the public can’t handle the truth and would rather the science be watered down.

However, as Dr. Esselstyn wrote in the Cleveland Clinic Journal of Medicine, in regard to cholesterol lowering, moderation kills. “Even if all Americans kept their total cholesterol below 200 mg/dL, as recommended by the American Heart Association, millions would develop coronary artery disease.” Strong evidence shows we need to keep our total cholesterol under 150 mg/dL in order to stem the American epidemic of coronary artery disease, our number-one killer. What kind of evidence? In many cultures, coronary artery disease is practically unheard of when total serum cholesterol levels are under 150 mg/dL. In the United States, the famous Framingham Heart Study demonstrated that few of those with levels below 150 mg/dL developed heart disease, and none died from it.

In my video Everything in Moderation? Even Heart Disease? you can see the data from a 26-year follow-up of the Framingham Heart Study comparing the cholesterol levels of people who get heart attacks and the cholesterol levels of those who don’t. The study suggests that because we now know that 35% of heart attacks occur in people with total cholesterol levels of 150-200 mg/dL, a target level of only 200 mg/dL guarantees that millions of U.S. citizens will die from coronary artery disease.

Dr. Esselstyn states, “We cannot continue to have public and private organizations on the forefront of health leadership recommend to the public a dietary plan that guarantees that millions will perish from the very disease the guidelines were supposed to prevent. With its lack of fiber and antioxidants, and its emphasis on animal protein, fat, and extreme free-radical production, the US diet is largely responsible for our bitter harvest of [chronic] diseases….” He continues, “If the coronary artery disease epidemic is seen as a raging fire, and cholesterol and fats as the fuels, the AHA [American Heart Association] has merely recommended cutting the flow of fuel. The only tenable solution is to cut off the fuel supply altogether—by reducing cholesterol levels to those proven to prevent coronary artery disease.”

It’s worth closely examining the Framingham data. At first, it seems those who get heart disease and those who don’t have very similar cholesterol levels, but that’s only at “normal” levels. To get an Optimal Cholesterol Level, one has to eat an exceedingly healthy diet. It’s worth it, though, since we’re not just talking life and death with heart disease, but life and the number-one cause of death.


What’s so bad about having high cholesterol? Well, it’s not only involved in the formation of atherosclerotic plaque, as I discuss in my video, Cholesterol Crystals May Tear Through Our Artery Lining. What about fluffy versus dense cholesterol? I cover that in Does Cholesterol Size Matter?. But can’t you just take cholesterol-lowering statin drugs? I encourage you to see The Actual Benefit of Diet vs. Drugs. When should we start monitoring cholesterol? As it turns out, Heart Disease May Start in the Womb.

For more on this concept of being at normal risk and dying from all the normal diseases, watch my video, When Low Risk Means High Risk. I continue questioning the patronizing paternalism of authorities in Optimal Diet: Just Give It To Me Straight, Doc. Finally, check out my latest heart disease overview, How Not to Die from Heart Disease.

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: