Three new articles appeared in various Journals of the American Medical Association (JAMA) this week that suggest Vitamins D and E can prevent or reduced the severity of cognitive diseases or declines.
Here are the press releases on the studies. If you follow the citations for each press release, you should be able to view the abstracts - full articles are limited to media (me) and subscribers.
Low Vitamin D Levels Associated With Cognitive DeclineCHICAGO—Older adults with low levels of vitamin D appear more likely to experience declines in thinking, learning and memory over a six-year period, according to a report in the July 12 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.
An estimated 40 percent to 100 percent of older adults in the United States and Europe are deficient in vitamin D, according to background information in the article. This deficiency has been linked to fractures, various chronic diseases and death. Vitamin D may help prevent the degeneration of brain tissue by having a role in formation of nervous tissue, maintaining levels of calcium in the body, or clearing of beta-amyloid, the substance that forms the brain plaques and tangles associated with Alzheimer's disease.
David J. Llewellyn, Ph.D., of University of Exeter, England, and colleagues assessed blood levels of vitamin D in 858 adults who were age 65 or older when the study began in 1998. Participants completed interviews and medical examinations and provided blood samples. At the beginning of the study and again after three and six years, they repeated three tests of cognitive function—one assessing overall cognition, one focusing on attention and one that places greater emphasis on executive function, or the ability to plan, organize and prioritize.
Participants who were severely deficient in vitamin D (having blood levels of 25-hydroxyvitamin D of less than 25 nanomoles per liter) were 60 percent more likely to have substantial cognitive decline in general over the six-year period and 31 percent more likely to experience declines on the test measuring executive function than those with sufficient vitamin D levels. "The association remained significant after adjustment for a wide range of potential confounders and when analyses were restricted to elderly subjects who were non-demented at baseline," the authors write. However, no significant association was seen for the test measuring attention.
"If future prospective studies and randomized controlled trials confirm that vitamin D deficiency is causally related to cognitive decline, then this would open up important new possibilities for treatment and prevention," the authors conclude.
(Arch Intern Med. 2010;170[13]:1135-1141).
Editor's Note: Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.
Editorial: Randomized Controlled Trials Needed to Examine Vitamin D's Role"Vitamin D has been known for many years to play a critical role in skeletal health, such that very low levels of this hormone (less than 20 nanomoles per liter) can cause osteomalacia, a disorder of impaired bone mineralization," write Andrew Grey, M.D., and Mark Bolland, M.B.Ch.B., Ph.D., of University of Auckland, New Zealand, in an accompanying editorial. "More recently, observational studies have reported inverse associations between levels of serum 25-hydroxyvitamin D, the metabolite that best reflects overall vitamin D status, and the risk of a wide range of disease, including cancer, vascular disease, infectious conditions, autoimmune diseases, osteoporosis, type 2 diabetes mellitus and obesity."
"The results of these observational studies have prompted calls for widespread treatment of individuals with low levels of vitamin D and the establishment of public health programs aimed at raising the population levels of vitamin D to 'healthy' values," the authors write.
"It is now time to test the various hypotheses generated by observational studies of vitamin D, including that of Llewellyn et al, in adequately designed and conducted randomized controlled trials," they conclude. "Very importantly, such trials will also provide an opportunity to systematically assess potential harms of vitamin D supplementation, an issue that has been largely overlooked or dismissed. We should invest in trials that provide the best possible evidence on the benefits and risks of vitamin D before we invest in costly, difficult and potentially unrewarding interventional strategies."
(Arch Intern Med. 2010;170[13]:1099-1100).
Editor's Note: This work received funding from the Health Research Council of New Zealand. Please see the article for additional information, including author contributions and affiliations, financial disclosures, funding and support, etc.
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Eating Foods Rich in Vitamin E Associated With Lower Dementia RiskCHICAGO—Consuming more vitamin E through the diet appears to be associated with a lower risk of dementia and Alzheimer's disease, according to a report in the July issue of Archives of Neurology, one of the JAMA/Archives journals.
Oxidative stress—damage to the cells from oxygen exposure—is thought to play a role in the development of Alzheimer's disease, according to background information in the article. Experimental data suggest that antioxidants, nutrients that help repair this damage, may protect against the degeneration of nervous system cells. "Although clinical trials have shown no benefit of antioxidant supplements for Alzheimer's disease, the wider variety of antioxidants in food sources is not well studied relative to dementia risk; a few studies, with varying lengths of follow-up, have yielded inconsistent results," the authors write.
Elizabeth E. Devore, Sc.D., of Erasmus Medical Center, Rotterdam, the Netherlands, and colleagues assessed 5,395 participants 55 years and older who did not have dementia between 1990 and 1993. Participants underwent a home interview and two clinical examinations at the beginning of the study, and provided dietary information through a two-step process involving a meal-based checklist and a food questionnaire.
The researchers focused on four antioxidants: vitamin E, vitamin C, beta carotene and flavonoids. The major food sources of vitamin E were margarine, sunflower oil, butter, cooking fat, soybean oil and mayonnaise; vitamin C came mainly from oranges, kiwi, grapefruit juice, grapefruit, cauliflower, red bell peppers and red cabbage; beta carotene, from carrots, spinach, vegetable soup, endive and tomato; and flavonoids from tea, onions, apples and carrots.
Over an average of 9.6 years of follow-up, 465 participants developed dementia; 365 of those were diagnosed with Alzheimer's disease. After adjusting for other potentially related factors, the one-third of individuals who consumed the most vitamin E (a median or midpoint of 18.5 milligrams per day) were 25 percent less likely to develop dementia than the one-third of participants who consumed the least (a median of 9 milligrams per day). Dietary intake levels of vitamin C, beta carotene and flavonoids were not associated with dementia risk. Results were similar when only the participants diagnosed with Alzheimer's disease were assessed.
"The brain is a site of high metabolic activity, which makes it vulnerable to oxidative damage, and slow accumulation of such damage over a lifetime may contribute to the development of dementia," the authors write. "In particular, when beta-amyloid (a hallmark of pathologic Alzheimer's disease) accumulates in the brain, an inflammatory response is likely evoked that produces nitric oxide radicals and downstream neurodegenerative effects. Vitamin E is a powerful fat-soluble antioxidant that may help to inhibit the pathogenesis of dementia."
Future studies are needed to evaluate dietary intake of antioxidants and dietary risks, including different points at which consuming more antioxidants might reduce risk, the authors conclude.
(Arch Neurol. 2010;67[7]:819-825).
Editor's Note: This study was supported in part by a grant from the Netherlands Organization for Scientific Research (Dr. Breteler) and by a training grant from the National Institutes of Health and by a U.S. Fulbright Fellowship to the Netherlands (Dr. Devore). Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.
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Vitamin D Levels Associated With Parkinson's Disease RiskCHICAGO—Individuals with higher levels of vitamin D appear to have a reduced risk of developing Parkinson's disease, according to a report in the July issue of Archives of Neurology, one of the JAMA/Archives journals.
Vitamin D is known to play a role in bone health and may also be linked to cancer, heart disease and type 2 diabetes, according to background information in the article. "Recently, chronically inadequate vitamin D intake was proposed to play a significant role in the pathogenesis of Parkinson's disease," the authors write. "According to the suggested biological mechanism, Parkinson's disease may be caused by a continuously inadequate vitamin D status leading to a chronic loss of dopaminergic neurons in the brain."
Paul Knekt, D.P.H., and colleagues at the National Institute for Health and Welfare, Helsinki, Finland, studied 3,173 Finnish men and women age 50 to 79 who did not have Parkinson's disease at the beginning of the study, in 1978 to 1980. Participants completed questionnaires and interviews about socioeconomic and health background, underwent baseline examinations and provided blood samples for vitamin D analysis.
Over a 29-year follow-up, through 2007, 50 of the participants developed Parkinson's disease. After adjusting for potentially related factors, including physical activity and body mass index, individuals in the highest quartile (one-fourth of the study population) of serum vitamin D levels had a 67 percent lower risk of developing Parkinson's disease than those in the lowest quartile of vitamin D levels.
"Despite the overall low vitamin D levels in the study population, a dose-response relationship was found," the authors write. "This study was carried out in Finland, an area with restricted sunlight exposure, and is thus based on a population with a continuously low vitamin D status. Accordingly, the mean [average] serum vitamin D level in the present population was about 50 percent of the suggested optimal level (75 to 80 nanomoles per liter). Our findings are thus consistent with the hypothesis that chronic inadequacy of vitamin D is a risk factor for Parkinson's disease."
The exact mechanisms by which vitamin D levels may affect Parkinson's disease risk are unknown, but the nutrient has been shown to exert a protective effect on the brain through antioxidant activities, regulation of calcium levels, detoxification, modulation of the immune system and enhanced conduction of electricity through neurons, the authors note.
"In intervention trials focusing on effects of vitamin D supplements, the incidence of Parkinson disease merits follow up," they conclude.
(Arch Neurol. 2010;67[7]:808-811).
Editor's Note: This work was supported by a National Institutes of Health grant. Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.
Editorial: Findings Add to Research on Neurological Effects of Vitamin D"The study by Knekt et al in this issue of the Archives is the first longitudinal analysis of vitamin D status as a risk of incident Parkinson's disease and examines a cohort of more than 3,000 participants from the Mini-Finland Health Survey," writes Marian Leslie Evatt, M.D., M.S., of Emory University, Atlanta, in an accompanying editorial.
"A growing body of basic research lends plausibility to a role for adequate vitamin D status protecting against development of Parkinson's disease," Dr. Evatt writes. "Knekt and colleagues' study provides the first promising human data to suggest that inadequate vitamin D status is associated with the risk of developing Parkinson's disease, but further work is needed in both basic and clinical arenas to elucidate the exact role, mechanisms and optimum concentration of vitamin D in Parkinson's disease."
"With the animal data showing a U-shaped curve for neuroprotective effects of vitamin D, it seems prudent to confirm the findings presented in this issue and investigate whether the apparent dose-response relationship observed in the current study maintains its slope, levels off or becomes negative with higher 25-hydroxyvitamin D concentrations. In the interim, data from interventional studies of fractures and falls appear to justify optimizing vitamin D levels to greater than 30 to 40 nanograms per milliliter."
(Arch Neurol. 2010;67[7]:795-797).
Editor's Note: Please see the article for additional information, including author contributions and affiliations, financial disclosures, funding and support, etc.
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