By our seventies, 1 in 5 of us will suffer from cognitive impairment, and within five years, half will progress to dementia, in a progression from cognitive impairment without dementia, 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, even interventions just to control risk factors could prevent millions of cases. So, an immense effort has been spent on identifying risk factors for Alzheimer’s, and developing treatments to reduce them.

In 1990, a small study of 22 Alzheimer’s patients reported they had high concentrations of something called 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. So, “Is it possible?” he asked, that homocysteine could cause brain damage even in people without genetic defects?

Well, now 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 may double our risk. In the Framingham Study, they estimated that as many as 1 in 6 Alzheimer’s cases may be attributable to elevated homocysteine in the blood–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 homocysteine and cognitive decline, dementia, or Alzheimer’s disease, a causal role–a cause-and-effect role–can be confirmed only 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–actually seeing what’s happening to the brain.

And 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 brain slowly atrophies, but the shrinking is much accelerated in patients suffering from Alzheimer’s disease. An intermittent rate of shrinkage is found in people with mild cognitive impairment. The thinking is that maybe if we could slow the rate of brain loss, we could slow the conversion to Alzheimer’s disease. So, they tried giving people B vitamins for two years and they 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 sevenfold, the brain atrophy in the regions specifically vulnerable to the Alzheimer’s disease process. Here’s the amount of brain atrophy over two years in the placebo group; here’s the amount of loss in the B vitamin group. Less brain loss.

Now the beneficial effect of B vitamins was confined to those with high homocysteine, indicating a relative deficiency in one of those three vitamins. So, wouldn’t it be better to not get deficient in the first place? Most people get enough B12 and B6, but the reason these folks were stuck up at a homocysteine of 11 is that they probably weren’t getting enough folate, which is found predominantly in beans and greens. 96% of Americans don’t even make the minimum recommended amount of dark green leafy vegetables, the same pitiful number who don’t eat the minimum recommendation for beans.

In fact, if you put people on a healthy diet, a plant-based diet, you can drop their homocysteine levels 20% in just one week–up from around 11 down to 9. The fact that they showed significant homocysteine lowering without any pills, without supplements–even at one week–suggests that multiple mechanisms may have been at work. They 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 our colon by our friendly gut bacteria. It also could be from the decreased methionine intake; that’s where homocysteine comes from. Homocysteine is a breakdown product of methionine, which comes mostly from animal protein. And so, if you give someone bacon and eggs for breakfast, then a steak for dinner, you can get these 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 up at 11, but vegetarians at nearly 14, and vegans at 16. Why? They’re getting more fiber and folate, but they’re not getting enough vitamin B12. Most vegans can be classified as being likely to suffer from hyperhomocysteinaemia–too much homocysteine in the blood–because most vegans in this study were not supplementing with vitamin B12, or eating vitamin B12-fortified foods, which is critical for anyone eating a plant-based diet. But if you take vegans and give them B12, their homocysteine can drop down below 5. Why not just down to 11? The reason the meat-eaters were stuck up at 11 is probably because they weren’t getting enough folate. But 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.

To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video. This is just an approximation of the audio contributed by Katie Schloer.

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