Brain Nutrition Facts » Journal Articles

Dietary Pattern Protective for Alzheimer Disease

Dr. Jain, M.D. — Wed, 21 Jul 2010 04:25:22 +0000

Recent research has uncovered a dietary pattern associated with reduced risk of Alzheimer disease. The traditional approach to studying the association of foods with illnesses is to take one or two foods or nutrients, and determine whether they are individually associated with the condition. The same group at Columbia University in New York that showed that the Mediterranean diet (consisting of a high intake of fish, legumes, vegetables, cereals, fruits, mostly olive oil for fat, a low to moderate amount of regular alcohol consumption, and low intake of dairy products, meat, and saturated fatty acids) protected against Alzheimer disease, conducted a new analysis trying to understand how dietary patterns that might be more relevant to multiethnic populations influenced Alzheimer disease risk. They found that a diet that was low in intake of high-fat dairy products, butter, red and organ meat, and high in dark and green leafy vegetables, cruciferous vegetables (cabbage, brussel sprouts, bok choy, etc.), tomatoes, poultry, fish, fruits and nuts, and salad dressing was associated with a lower risk of Alzheimer disease. Specifically, people who consumed this diet had about a 40% lower chance of developing Alzheimer disease. If you could cut your risk of Alzheimer almost in half by adhering to a healthier diet, wouldn’t you do it? The data suggests that this is a good possibility. Check it out for yourself!

Curcumin Shows Potential in Treating Depression:

Dr. Willison M.D. Ph.D. — Tue, 10 Nov 2009 02:45:42 +0000

Previous research has suggested that eating a diet containing curcumin, an active ingredient in turmeric, may prevent memory loss in older populations. Now, there is growing interest in the possible anti-depressant effects of curcumin. In a recent review by a group of authors from India, several plausible mechanisms are presented for how curcumin may help treat depression. For example, curcumin has been shown to be an inhibitor of the monoamine oxidase enzymes, MAO-A and MAO-B, which in turn causes an increase in the levels of certain neurotransmitters in the brain. A large family of powerful, well studied prescription medications owes their anti-depressant effects to a similar inhibition of these enzymes. Curcumin has also been shown to modulate norepinephrine, dopamine, and serotonin levels in the brain, to promote the generation of new neurons, and to reduce markers of inflammation which are all possible reasons behind its anti-depressant effects. Increasingly more evidence points to turmeric, and therefore curcumin, as potentially powerful agents for the treatment of various mental illnesses.

Future posts will examine the scientific evidence behind these claims.

Could Chronic Fatigue Syndrome be Caused by a Virus?

Dr. Jain, M.D. — Tue, 20 Oct 2009 15:40:46 +0000

A report was recently published in one of the most prestigious scientific journals that a virus called “xenotropic murine leukemia virus related virus” was recently found to infect 67% of white blood cells of chronic fatigue syndrome patients, but only ~4% of normal individuals (Lombardi et al., Science, Oct. 2009). This finding was covered in the New York Times, Wall Street Journal, and several other major publications, as it seemed to provide an answer to the conundrum of chronic fatigue syndrome, which did not have a known cause. If a virus caused chronic fatigue syndrome, it could potentially be treated with anti-viral medications, much like is done with HIV.

But how well was the study done? A close review of the figures showed several inconsistencies. It appeared that there was actually evidence of a viral protein DNA in several of the “normal” controls, that was not counted in the final results. One of the experiments in which they tried to show that the virus produced an infection in a new cell did not seem to show the positive conclusions they derived. Additionally, there were typos and unclear descriptions of methodology, raising questions about how well the work was done. There were other worrying signs. After the paper was published, the senior author said that there was evidence of viral infection in 95% of patients, a much larger percentage than reported in the actual paper. Given the seemingly arbitrary way in which some of the experiments were called “positive” and others “negative”, this claim is hard to believe, and it is possible that the increased numbers reflect poor methodology that yields false positive results.

Despite all of these uncertainties, the question for a chronic fatigue syndrome patient, many of whom have suffered for years, is, “Could this possibly be helpful for me?” If, for example, XMRV were actually a causative agent in chronic fatigue syndrome, and a patient tested positive for the virus, an anti-viral medication might theoretically be able to decrease viral replication and thus improve symptoms. However, there are serious side-effects to anti-viral medications that make their utilization potentially dangerous, and any such usage would be “off-label”, opening up physicians who prescribed them for chronic fatigue syndrome to a wide range of lawsuits. As the benefit is unclear, there is cause for caution, for both patients and physicians. Additionally, as the detection method for the virus is not yet standardized, it is possible that the laboratory doing the testing might do so sloppily, and provide a positive result when the patient is actually negative, or vice versa.

At this stage, there is both promise and peril in the testing of XMRV. The true impact of the discovery of XMRV in chronic fatigue syndrome will not be known until many more studies – of independent authorship from the original group — are completed.