In research published in the July edition of the Journal of Epidemiology and Community Health, the York team led by Dr Simon Gilbody, concluded that there was a link between depression and low folate levels, following a review of 11 previous studies involving 15,315 participants.
Last month, the Food Standards Agency recommended to UK Health Ministers the introduction of mandatory fortification of either bread or flour with folic acid to prevent neural tube defects, which can result in miscarriage, neonatal death or lifelong disability. The York study suggests that the measure may also help in the fight against depression.
Dr Gilbody said: Our study is unique in that for the first time all the relevant evidence in this controversial area has been brought together. Although the research does not prove that low folate causes depression, we can now be sure that the two are linked. Interestingly, there is also some trial evidence that suggests folic acid supplements can benefit people with depression. We recommend that large trials should be carried out to further test this suggestion.
Recent research from the same team published in the American Journal of Epidemiology has also proved that people with depression commonly have a gene that means that they process folate less efficiently. Folate is linked to the production of some of the feel good ™ chemicals in the brain, such as serotonin. The identification of this gene provides a plausible explanation as to why folic acid supplements may help people with depression.
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These changes contributed to the ability of these mice to fend off weight gain despite a high-fat diet and lack of exercise. Together these results suggest that a CD38 deficiency has a protective effect against high-fat, diet-induced obesity, Dr. Chini says.
Dr. Chini and colleagues also examined the effects of resveratrol in mice. Resveratrol is a naturally occurring substance found in some plants such as mulberries, peanuts and red grapes used to make wine. It has been marketed as a drug that mimics the effects of moderate exercise without the physical act of exercising and also as a longevity drug, despite the lack of evidence that resveratrol is safe and effective in humans.
Mice with CD38 were treated with 30 milligrams (mg) of resveratrol per day. And, to determine the effects of the SIRT genes on obesity, mice without CD38 received the same dose of sirtinol, a drug that shuts down the SIRT genes.
Researchers found that mice with CD38 that were treated with resveratrol for two weeks were protected from high-fat, diet-induced obesity. By contrast, the protective effect against high-fat, diet-induced obesity in the absence of CD38 in mice was invalidated by sirtinol. Mice without CD38 that were treated with sirtinol gained a statistically significant amount of weight when compared with mice without the gene who were not treated with sirtinol.
This data supports the novel notion that CD38 modulates high-fat, diet-induced obesity by a SIRT- dependent mechanism.
Together these results identify a novel pathway regulating body weight and clearly show that CD38 is a nearly obligatory component of the cellular cascade that led to diet-induced obesity, the authors write.
The authors say the study's results are promising and should be explored in follow-up studies that will focus on the quality of life and longevity in mice.
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