Alzheimer’s Disease and How Not to Get It

I’m often asked my opinion about a diet or a disease is. Who cares what my or anyone else’s opinion is? All we should care about is what the science says. What does the best available balance of evidence published in the peer-reviewed medical literature have to say right now?

Welcome to the NutritionFacts Podcast – I’m your host Dr. Michael Greger.

I know so many people – who have been diagnosed with Alzheimer’s disease – the most common cause of dementia. And I bet you do too. In fact – more than 6 million people in the U.S. have it. So, how do we avoid becoming one of those statistics? That’s the main thrust of my forthcoming book “How Not to Age.” But in the meanwhile, here are some little-known risk factors in this our 300th podcast episode.

Although there is a growing list of Alzheimer’s disease susceptibility genes, even if you put them all altogether, they account for less than half of all Alzheimer’s cases. The single most compelling piece of data on the potential control we have over the disease is the fact that if you have identical twins, with the exact same genes, even if one gets Alzheimer’s, the other usually does not. So, we have to think about all the other contributing factors beyond just genetics.
In my video on pesticides and cancer, I talked about this study. There’s a list of chlorinated pesticides, including DDE (a metabolite of DDT), that are classified by the EPA as probable human carcinogens. But in the study, blood levels of DDE and others were associated not with increased cancer mortality, but increased risk of other-cause mortality. This led researchers to speculate it may be due to an associated increased risk of diabetes or dementia. I’ve talked previously about the diabetes link. What about dementia? One study: “Elevated Serum Pesticide Levels and Risk for Alzheimer Disease.”
A research team at Rutgers found significantly higher blood levels of DDE in Alzheimer’s disease patients compared to controls, and autopsy studies show blood levels are a good proxy for brain levels. Those with the highest levels were at about four times the odds of being demented with Alzheimer’s. And in a petri dish, DDE increases amyloid precursor protein levels in human brain cells, providing a potential mechanism.
Put all these studies together, and there does indeed seem to be a link, consistent with data showing about a doubling of risk for developing dementia among those acutely pesticide poisoned. Among U.S. elders, DDT and its breakdown product DDE are also associated with increased risk of cognitive decline in general.
DDT was extensively used in the United States from the 1940s through the 1960s. At its peak, we were churning out 180 million pounds a year. And it’s still in our bodies to this day, contaminating the bloodstreams of more than 90 percent of Americans, and DDE, the pesticide linked to quadrupling the odds of Alzheimer’s, were at the highest levels.
It’s still in our bodies because it’s still in the food supply. In my last video on the topic, I noted that the levels of DDT, DDE, and other banned pesticides and pollutants were much lower in the breast milk from a vegetarian mother compared to breast milk of her non-vegetarian sister. And the largest difference was noted for DDE, which was four times lower in the vegetarian sister.
These toxins build up in the food chain; so, it makes sense that the most contaminated foods are meat, fish, and dairy products. There are 5 to 10 times higher levels in meat, eggs, fish, and dairy than what they found in plant foods. And unfortunately, cooking doesn’t destroy pollutants like DDE—in fact, it may make them even more concentrated. And this is for a pesticide that may increase the risk of Alzheimer’s disease as much as if you carried the so-called Alzheimer’s gene APOE e4.

In our next story, we look at the role of meat in Alzheimer’s disease.

What is behind the dramatic increase in dementia in Japan over recent decades? Maybe it’s rising obesity rates or the “increases in cholesterol, saturated fat, and iron from increases in [meat and other] animal products.” Overall, calories went up just about 10% in Japan, whereas animal fat and meat consumption rose 500%, about 10 times the rise in sugary junk. Now, during this timespan, rice consumption went down, but the thinking is that rather than white rice somehow being protective, maybe they were eating something worse instead. It’s like when you find fish consumption is correlated with less disease, you wonder if it’s because they’re eating that rather than some worse meat.
If you look across multiple countries, you see a similar pattern, with “[t]he most important dietary link to [Alzheimer’s appearing] to be meat consumption, with eggs and high-fat dairy also [maybe] contributing.” There appears to be a really tight correlation between Alzheimer’s and per capita meat supply. And, then, studies within countries uncover similar findings, with Alzheimer’s and cognitive decline associated with meaty, sweety, fatty diets, whereas most plant foods were associated with risk reduction.
This could be for a variety of reasons. Animal products tend to have more copper, mercury, lead, and cadmium, and no folate but contain saturated fat and cholesterol, and pro-inflammatory advanced glycation end products, so many mechanisms that dietary modification may be our best bet for reducing risk of Alzheimer’s disease. But, how do we know it’s cause and effect? The evidence that meat consumption is causally linked to Alzheimer’s disease, well, there’s the strength of the association, the consistency across different types of studies, the fact that the dietary changes preceded the risk of dementia, the dose response—more meat linked to more risk—a bunch of plausible mechanisms. We know that “[m]eat is…a risk factor for other chronic diseases,” but there’s never been randomized controlled trials to put it to the test.
When you read reviews of the damaging effects of high-fat diets to the brain and cognition, “a number of factors are proposed to [account for the] high-fat diet-induced damage to the brain…[—] oxidative stress, insulin resistance, inflammation, and changes to [blood vessels and the integrity of the blood-brain barrier].” But, these are based mostly on studies of rodents. Yes, high fat diets can cause energy dysfunction in the brain, based on fancy MRI techniques.
With CT scans, you can follow this “intracranial artery stenosis”—this brain-artery clogging—over time, and follow the “progression from mild cognitive impairment to Alzheimer’s disease.” Those who only had low-grade stenosis were pretty stable over time in terms of their cognitive function and ability to dress themselves and other activities of daily living, whereas those with more clogging started slipping over the years, and those who started out with the most brain atherosclerosis rapidly went downhill, and were twice as likely to progress to full-blown Alzheimer’s.
“Chronic consumption of standard Western diets [rich in saturated fat] and cholesterol [may] compromise [our] cerebrovascular integrity” and compromise the blood vessels in our brain. So, of course, drugs are recommended—“pharmacological modulation” of diet-induced dysfunction—but why not just try to eat healthier in the first place?

Finally today – we look at reducing glycotoxin intake to ward off Alzheimer’s.

Each of us has six billion miles of DNA. How does our body keep it from getting all tangled up? There are special proteins called histones, which act like spools, with DNA as the thread. Enzymes called sirtuins wrap the DNA around the histone spools, and in doing so, silence whatever genes were in that stretch of DNA–hence their name SIRtuins, which stands for silencing information regulator.
Although they were discovered only about a decade ago, the study of sirtuins has become one of the most promising areas of biomedicine, since they appear to be involved in promoting healthy aging and longevity. Suppression of this key host defense is considered a central feature of Alzheimer’s disease.
Autopsies of Alzheimer’s victims reveal that loss of sirtuin enzyme activity is closely associated with the accumulation of plaques and tangles in the brain that are characteristic of Alzheimer’s disease. Sirtuins appear to activate pathways that steer the brain away from the formation of plaque and tangled proteins. Because a decrease in sirtuin activity can clearly have deleterious effects on nerve health, they’re trying to come up with drugs to increase sirtuin activity–but why not just prevent its suppression in the first place?
Glycotoxins in our food suppress sirtuin activity, these so-called advanced glycation end products, or AGEs. Our modern diet includes excessive AGE’s, which can be neurotoxic. High levels in the blood may predict cognitive decline over time.
If you measure the urine levels of glycotoxins flowing through the bodies of older adults, those with the highest levels went on to suffer the greatest cognitive decline over the subsequent nine years.
As we age, our brain literally shrinks. In our 60s and 70s, we lose an average of five cubic centimeters of total brain tissue volume every year, but some lose more than others. Brain atrophy may be reduced in very healthy individuals. And a few people don’t lose any brain at all. Normally, we lose about 2% of brain volume every year, but that’s just the average. Although the average brain loss for folks in their 70s and 80s was 2.1%, some lost more, some lost less, and some men and women lost none at all over a period of four years.
Researchers in Australia provided the first evidence linking AGEs with this kind of cerebral brain loss. So, limiting one’s consumption of these compounds may end up having significant public health benefits.
Because sirtuin deficiency is both preventable and reversible by dietary AGE reduction, a therapeutic strategy that includes eating less AGEs may offer a new strategy to combat the epidemic of Alzheimer’s.
Some of these glycotoxins are produced internally, particularly in diabetics, but anyone can get them from smoking and eating–particularly foods high in fat and protein.
In a previous video, I listed the 15 foods most contaminated with glycotoxins–mostly chicken, but also pork, beef, and fish–which may help explain why those who eat the most meat may have triple the risk of getting dementia, compared to long-time vegetarians.
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