The researchers found that while equol production did not appear to impact levels of amyloid-beta deposited within the brain, it was associated with reduced white matter lesion volumes. Sekikawa’s team also discovered that high levels of isoflavones—soy nutrients that are metabolized into equol—had no effect on levels of white matter lesions or amyloid-beta when equol wasn’t produced.

According to Sekikawa, the ability to produce equol from soy isoflavones may be the key to unlocking protective health benefits from a soy-rich diet, and his team has previously shown that equol production is associated with a lower risk of heart disease. As heart disease is strongly associated with cognitive decline and dementia, equol production could help protect the aging brain as well as the heart.

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A metabolite produced following consumption of dietary soy may decrease a key risk factor for dementia—with the help of the right bacteria, according to a new discovery led by researchers at the University of Pittsburgh Graduate School of Public Health.

Their study, published today in the journal Alzheimer’s & Dementia: Translational Research & Clinical Interventions, reports that elderly Japanese men and women who produce equol—a metabolite of dietary soy created by certain types of gut bacteria—display lower levels of white matter lesions within the brain.

Our immune system’s capacity to mount a well-regulated defense against foreign substances, including toxins, weakens with age and makes vaccines less effective in people over age 65. At the same time, research has shown that immunotherapy targeting neurotoxic forms of the peptide amyloid beta (oligomeric Aβ) may halt the progression of Alzheimer’s disease, the most common age-related neurodegenerative disease.

A team led by Chuanhai Cao, Ph.D., of the University of South Florida Health (USF Health), has focused on overcoming, in those with impaired immunity, excess inflammation and other complications that interfere with development of a therapeutic Alzheimer’s vaccine.

Now, a preclinical study by Dr. Cao and colleagues indicates that an antigen-presenting dendritic vaccine with a specific antibody response to oligomeric Aβ may be safer and offer clinical benefit in treating Alzheimer’s disease. The vaccine, called E22W42 DC, uses immune cells known as dendritic cells (DC) loaded with a modified Aβ peptide as the antigen.

Here’s my latest post!

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Sleep changes during aging may impact Alzheimer’s disease risk, and with the goal of minimizing that risk, can sleep, in particular, levels of deep sleep, be optimized?

If Dr. Ken Berry actually meant to say that you need to eat saturated fat for your nerves and brain, he flunks Biochem 101. First of all, your body can make all the saturated fat you need out of carbs and proteins. You don’t need to eat ANY saturated fat. Second, the most common fatty acid in your brain is the polyunsaturated fatty acid (PUFA) called DHA, which you DO need to eat, because you can’t make it from non-fats (you need to eat it or EPA in things like seafood, or at least the precursor omega-3 PUFA called ALA in cold-climate plants.) Ironically enough, ALA is common in Canola oil, which Dr. Berry deprecates, but not in the tropical plant oils that he likes. More on that later.

A diet with a lot of saturated fat is NOT the best for the heart. The American Heart Association continues to recommend low saturated fat diets (with the missing sat-fat replaced by mono and polyunsaturated fat, not by carbohydrates) because the evidence from animal and human trials and even properly controlled epidemiology, shows these the best diets (see reference below—an extensive review of meta analyses [1]). Examples are the DASH hypertension diet and the closely-related Mediterranean diet (which has lots of olive oil for monounsaturated fatty acid, and seafood for DHA). If Dr. Berry thinks he has something better than the Mediterranean diet for longevity, what is his direct evidence?

Saturated fat, of course, is used by the body to make cholesterol (you don’t need to eat any cholesterol for this reason), and it does raise cholesterol levels and it does increase atherosclerosis in nearly every controlled prospective experimental model in animals and humans. This is the gold standard of evidence in medicine.

One can go only so far with epidemiology, because occasionally when one bad thing (saturated fat) is heavily replaced for calories by another bad thing (certain carbohydrates) one detects no epidemiologic effect from changing just the first thing.

That happens with various high and low saturated fat diets around the world enough to make saturated fat look benign as a single input variable. It is not. Rather, what these studies really show is that replacing butter with sugar or high glycemic carbs gives you a diet equally bad for the arteries. One cannot see how bad that is, until one compares these with low-carbohydrate, low-saturated-fat diets, which are less common, but better. The double-negative tradeoff of carbs and saturated fats (where carbs are a statistical “confounder”) is one of those occasional cruel misdirectional things that happen with imperfectly controlled past-observations, but (again) it’s why biomedical knowledge consists of more than just epidemiology.