Staving off Alzheimer’s has many schools of thought


Do you remember what I wrote about Alzheimer’s last month. I’m fuzzy about it, too. Here’s a restatement.


A cross section of healthy brain, left, is compared to a brain afflicted with severe Alzheimer's disease.

More than a century ago Alois Alzheimer described misshapen proteins, or peptides, in the brains of patients with dementia. Studies seem to confirm an association, but not necessarily cause and effect. Treatments to clear these proteins from the brain have produced disappointing results. While we wait for clarification, what might help?

1 Can we fight deterioration with activity? Academic achievement and maintaining social contacts are among activities that seem to sustain functioning levels, in the presence of brain damage. One explanation is that there is value in building cognitive reserve. Many studies support that idea, including one reported March 2003 in Archives of Neurology. It showed that maintaining intellectual interest, improved functional capacity despite worse changes in PET scans.

My comment: Keep reading my column, books, whatever. Keep involved in society. There are potential arguments about cause and effect, but the weight of available data supports the idea of staying mentally and physically active.

2 The concept that fasting at least twice a week seemed goofy to me, but it got ink in the U-B on Nov. 15, 2013. What’s that about? We don’t really know.

The U-B article includes a blast from a university dean who said, “There will be some buzz, and then the diet will go away, never to be heard from again.”

On the plus side, there are supportive studies, including a report in May 2010 that showed alternate-day fasting in rats also offered cardiovascular protection and improved glycemic control. This and similar research imply a beneficial role connected with the metabolic syndrome.

My comment: It warrants study in humans. Until then, we should assume that the outcome might show it offers no benefit, or a negative outcome.

3 Have you tried the Mediterranean diet? Did it make you smarter? If you want the bottom line, evidence supports the conclusion that people who follow the diet live longer, have less heart disease and probably decrease dementia risks substantially.

It’s not clear why. The degree of adherence to the diet plays a role. Following it over a lifetime may be more significant than late adoption, but I can’t conclude that with certainty.

Extra-virgin olive oil has components called phenols. They perform potentially important functions, resulting from anti-inflammatory, antimicrobial and antioxidant capacities. The oil is polyunsaturated, believed to be the healthy form.

Recommendations, if you choose this diet, include making fresh vegetables the center of meals; limiting red meats to a couple times a month and using fish or poultry a few times a week; using olive oil to dip bread, make salads and to cook; staying physically active; and eating meals with family or friends, mainly at home.

If you want to go a bit deeper, realize that epidemiologic studies are hard to interpret. Observations of increased longevity were reported in Greek villages in the mid-1990s. These villagers’ diets were, more or less, like what I’ve described but their life styles were very different.

Subsequent investigations have been made in France and the U.S. Not everyone agrees, but there is a pattern that supports my observations.

I must add I am also impressed by the importance of keeping sugar levels as low as you can. Don’t finish that healthy meal with pie and ice cream, except, sometimes.

Want more? Check the writings of Catherine Feart and check out the Mayo Clinic food pyramid for the Mediterranean Diet.

4 A recent Los Angeles Times article the U-B ran shows a correlation between beta-amyloid and cholesterol levels. The risk of over-interpreting correlation as causation can lead to bad choices. It is possible, for example, that some factor causes both, but neither is related. It is even possible that the beta-amyloid and tangles that Alzheimer described are markers of a disease, but not the cause.

That would mean getting rid of plaques and tangles wouldn’t cure or curtail dementia. In the parlance of a younger generation than I, “I’m Just sayin’.” I don’t have the answer, but I urge you to keep asking questions. That’s one of the ways to keep the old brain churning

5 Brain inflammation may play a role in the disease, but studies on anti-inflammatory drugs suggest they might have a preventive effect but also increase progression once the disease is established.

6 I could turn this subject into another book, but I don’t have time to promote the ones I’ve written.

I’ll end with the new studies in this January’s New England Journal of Medicine. Investigators used two antibodies to break up plaques of beta-amyloid. They tested subjects for clinical improvement. Although they apparently interrupted plaque growth, moderately severe patients didn’t improve and patients with mild disease gave a only hint of an effect. No subset met the criteria for success.

A new study is redesigning the approach to treat only mildly involved patients.

The current working concept of Alzheimer’s is that factors associated with aging produce an increase in beta-amyloid plaques. These promote fibrillary tangles and result in the death of neurons and brain shrinkage.

Answers may come out of that model or a different one that somebody is working on.

Dr. Larry Mulkerin is a retired clinical professor and oncologist who lives in Walla Walla. A former U.S. Army Green Berets medical officer with experience in the Middle East, he also is the author of “The Ayatollah’s Suitcase,” a novel available at and other online book retailers. He can be reached at


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