The Vitamin D Pandemic and its Health Consequences\nPresented by Michael Holick, PhD, MD, Professor of medicine, physiology and biophysics and director of the General Clinical Research Center at Boston University Medical Center\nKeynote address at the opening ceremony of the 34th European Symposium on Calcified Tissues, Copenhagen 5 May, 2007\n
Researchers at the University of California, Berkeley, have identified a gene that plays a critical regulatory role in the process of converting dietary carbohydrates to fat. In a new study, they disabled this gene in mice, which consequently had lower levels of body fat than their normal counterparts, despite being fed the equivalent of an all-you-can-eat pasta buffet.
The authors of the study, to be published in the March 20 issue of the journal Cell, say the gene, called DNA-PK, could potentially play a role in the prevention of obesity related to the over-consumption of high-carbohydrate foods, such as pasta, rice, soda and sugary snacks.
It turns out that statins inhibit not only the liver from making cholesterol but may also block the brain from making cholesterol. That's a serious consequence, according to Yeon-Kyun Shin, a biophysics professor in the department of biochemistry, biophysics and molecular biology at Iowa State, because cholesterol is vital for healthy and optimum brain function. "If you deprive cholesterol from the brain, then you directly affect the machinery that triggers the release of neurotransmitters. Neurotransmitters affect the data-processing and memory functions. In other words, how smart you are and how well you remember things," said Dr. Shin in a statement to the media.
A heat-stable extract of white button mushrooms (Agaricus bisporus) with potential chemopreventive and immunomodulating activities. Phytochemicals, such as polysaccharides and especially beta-D-glucans found in the white button mushroom extract, bind to and inhibit the activity of aromatase, an enzyme responsible for the conversion of androgens to estrogens and which is often upregulated in breast cancer cells. The consequent decrease in estrogen production may result in the suppression of estrogen-dependent cellular proliferation. In addition, this extract may promote dendritic cell (DC) maturation, increase interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) production, and may enhance natural killer (NK) cell activity, thus amplifying both innate and T cell-mediated immune responses against cancer cells. Check for active clinical trials or closed clinical trials using this agent.