Alzheimer’s Disease: Recent News About the Influence of Omega-3 Oils, Phosphatidylserine, B-Vitamins and Green Tea Extract.
Article by Don Goldberg
Recent News About the Influence of Omega-3 Oils, Phosphatidylserine, B-Vitamins and Green Tea Extract.
The role of diet, nutritional supplements and herbs on the prevention and treatment of Alzheimer’s disease is, as expected, controversial. Agents that appeared promising in early research sometimes fail to meet that promise after additional testing. Sometimes, we have to rely on common sense, as rigid, scientifically designed experimental data is unavailable, or unlikely to be forthcoming. There is nothing wrong with common sense, by the way. If a nutrient offers promise, and that promise has a logical, scientific basis, why not avail ourselves of its potential benefit--especially if there is little downside to doing so. And finally, certain foods and supplements continue to pass both tests. They make sense, and they continue to look promissing in the laboratory.
We will start off with some comments about two supplements in this category from the Alzheimer’s Association, alz.org.
Omega-3 fatty acids
Omega-3s are a type of polyunsaturated fatty acid (PUFA). Research has linked certain types of omega-3s to a reduced risk of heart disease and stroke.
The U.S. Food and Drug Administration (FDA) permits supplements and foods to display labels with “a qualified health claim” for two omega-3s called docosahexaneoic acid (DHA) and eicosapentaenoic acid (EPA). The labels may state, “Supportive but not conclusive research shows that consumption of EPA and DHA omega-3 fatty acids may reduce the risk of coronary heart disease,” and then list the amount of DHA or EPA in the product. The FDA recommends taking no more than a combined total of 3 grams of DHA or EPA a day, with no more than 2 grams from supplements.
Research has also linked high intake of omega-3s to a possible reduction in risk of dementia or cognitive decline. The chief omega-3 in the brain is DHA, which is found in the fatty membranes that surround nerve cells, especially at the microscopic junctions where cells connect to one another.
Theories about why omega-3s might influence dementia risk include their benefit for the heart and blood vessels; anti-inflammatory effects; and support and protection of nerve cell membranes.
Two studies reported at the 2009 Alzheimer's Association International Conference on Alzheimer's Disease (AAICAD) found mixed results for the possible benefits of DHA:
The first study was a large federally funded clinical trial conducted by the Alzheimer's Disease Cooperative Study (ADCS). In the ADCS study, participants with mild to moderate Alzheimer's disease taking 2 grams of DHA daily fared no better overall than those who took a placebo (inactive, lookalike treatment). The data indicated a "signal" (preliminary but not conclusive evidence) that participants without the APOE-e4 Alzheimer's risk gene might have experienced a slight benefit. More research is needed to confirm whether that preliminary signal is valid. Results of this study also appeared in the Nov. 3, 2010, issue of the Journal of the American Medical Association.
The second study—Memory Improvement with DHA (MIDAS)—enrolled older adults with normal age-related cognitive decline. Those who took 900 milligrams of DHA daily scored slightly better on a computerized memory test than those receiving the placebo. MIDAS was conducted by Martek Biosciences, the manufacturer of the DHA used in both studies.
Experts agree that more research is needed, and there is not yet sufficient evidence to recommend DHA or any other omega-3 fatty acids to treat or prevent Alzheimer's disease.
Phosphatidylserine (pronounced FOS-fuh-TIE-dil-sair-een) is a kind of lipid, or fat, that is the primary component of the membranes that surround nerve cells. In Alzheimer’s disease and similar disorders, nerve cells degenerate for reasons that are not yet understood. The theory behind treatment with phosphatidylserine is its use may shore up the cell membrane and possibly protect cells from degenerating.
The first clinical trials with phosphatidylserine were conducted with a form derived from the brain cells of cows. Some of these trials had promising results. However, most trials were with small samples of participants.
This line of investigation came to an end in the 1990s over concerns about mad cow disease (bovine spongiform encephalopathy), a fatal brain disorder believed to be caused by consuming foods or other products from affected cattle. Supplements containing phosphatidylserine are now derived from soy extracts. The FDA permits supplements containing very high-quality soy-derived phosphatidylserine to display a "qualified health claim" stating that "Very limited and preliminary scientific research suggests that phosphatidylserine may reduce the risk of dementia in the elderly. FDA concludes that there is little scientific evidence supporting this claim." . . .Experts agree that more research is needed, and do not currently recommend use of phosphatidylserine.
It is important to note that the above information, as mentioned previously, is from an organization (alz.org) that is very critical of “alternative treatments.” They say the following in the introduction to their review of various “alternative treatments:” “. . .Claims about the safety and effectiveness of these products, however, are based largely on testimonials, tradition and a rather small body of scientific research.”
That is ok. It never hurts to hear what the “other guys” have to say. They only say good things very grudgingly. So when they cannot find very much negative to say about a supplement, one has to take it as being very close to a recommendation. I consider their comments on omega-3 oils and phosphatidylserine as about as close to endorsements as they can come.
According to research by Douaud et al. published in the Proceedings of the National Academy of Sciences, a new study is suggesting that a high dose of B vitamins could stop the onset of Alzheimer’s by preventing shrinkage of the medial temporal lobe, the area of the brain that defines the disease.
What does that mean? They found that this part of the brain shrank slower in people with mild cognitive impairment when they took B Vitamins.
To reach these conclusions, the researcher gave 156 elderly people with mild cognitive impairment, the stage before dementia or Alzheimer’s, a combination of vitamin B12 (500 mcg), B6 (20 mg) and folic acid or placebo pills over a two year period.
As you might realize, this is not a typical B-Complex formulation, but, instead, is a limited selection of B-vitamins designed to affect homocysteine levels.
The 80 subjects receiving B Vitamins showed significantly less brain degeneration than the placebo group.
Lead researcher David Smith of Oxford University said: "In those with high homocysteine levels, the specific areas of the brain associated with Alzheimer's, disease shrank eight times more slowly in those taking B vitamins than in those on the placebo.”
“This is strongly indicative that the B vitamins may be substantially slowing down, or even potentially arresting, the disease process in those with early stage cognitive decline.”
“This is the first treatment that has been shown to potentially arrest Alzheimer’s related brain shrinkage.”
Previous research has shown that raised levels of plasma total homocysteine (tHcy) are associated with cognitive impairment, Alzheimer's Disease, or vascular dementia.
The present study concluded that B-vitamin treatment could lower mean plasma tHcy levels by 29%.
Smith said: "This makes the need for early screening for the first signs of cognitive decline from the age of 50…vitally important, backed up by homocysteine testing and potential B vitamin treatment.
“Our study shows that those with a homocysteine level above 10mcmol/l, which is about half of all people over age 65, potentially may benefit with reduced brain shrinkage by taking high dose B6, B12 and folic acid, but this should be done under medical supervision.”
(Reference: Proceedings of the National Academy Sciences (In Press) ‘Preventing Alzheimer's disease-related gray matter atrophy by B vitamin treatment’ Authors: Douaud, G., et al.)
Green tea EGCG may help prevent plaque formation in Alzheimer's disease
The last study we will discuss in this article is also promising. It appears that extracts from green tea may block the formation of beta-amyloid plaques that have been linked to the onset of Alzheimer's disease and other neurodegenerative conditions, according to new laboratory data.
The study, published in the Proceedings of the National Academy of Sciences, reports that green tea extract, and in particular the powerful polyphenol epigallocatechin-3-gallate (EGCG) prevented the formation of potentially dangerous beta-amyloid aggregates and broke down existing aggregate structures in proteins that contained metals - specifically copper, iron and zinc.
The aggregation of these proteins, called metal-associated amyloids, is associated with Alzheimer's disease and other neurodegenerative conditions, explained the research team behind the study.
"A lot of people are very excited about this molecule," said Dr Mi Hee Lim from the University of Michigan, USA - who noted that EGCG and other flavonoids in natural products have long been established as powerful antioxidants.
Facts About Green Tea
The majority of science on tea has looked at green tea, with benefits reported for reducing the risk of Alzheimer's and certain cancers, improving cardiovascular and oral health, as well as aiding in weight management.
Green tea contains between 30 and 40% of water-extractable polyphenols, while black tea (green tea that has been oxidized by fermentation) contains between 3 and 10%. Oolong tea is semi-fermented tea and is somewhere between green and black tea. The four primary polyphenols found in fresh tealeaves are epigallocatechin gallate (EGCG), epigallocatechin, epicatechin gallate, and epicatechin.
However, Lim explained that while many researchers are investigating small molecules such as EGCG and their effect on metal-associated amyloid plaques, most of them are looking from a limited perspective.
"We used a multidisciplinary approach," said Lim, who led the new study.
"This is the first example of structure-centric, multidisciplinary investigations by three principal investigators with three different areas of expertise," she explained, noting that the research team behind the work included chemists, biochemists and biophysicists.
"We believe you have to have a lot of approaches working together, because the brain is very complex," she said, explaining that the current PNAS findings are a starting point.
Lim said her team's next step is to try and 'tweak' EGCG and then test its ability to interfere with plaque formation in fruit flies.
"We want to modify them for the brain, specifically to interfere with the plaques associated with Alzheimer's," she said.
(Source: Proceedings of the National Academy of Sciences, Published online ahead of print, oi:10.1073/pnas.1220326110
"Insights into antiamyloidogenic properties of the green tea extract (-)-epigallocatechin-3-gallate toward metal-associated amyloid-ß species" Authors: Suk-Joon Hyung, Alaina S. DeToma, Jeffrey R. Brender, Sanghyun Lee, et al. Reported in William Reed Business Media SAS.)
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