US researchers suggest there is an underlying mechanism that affects both cancer and low LDL (so-called "bad") cholesterol, because they found low LDL cholesterol in people with no history of taking drugs to lower their cholesterol precedes cancer risk by decades. Lead investigator Dr Paul Michael Lavigne, of Tufts Medical Center in Boston, presented the findings, which are based on new data from the Framingham Heart Study (FHS) offspring cohort, at the American College of Cardiology's 61st Annual Scientific Session in Chicago on Sunday. The benefits of using cholesterol-lowering drugs to prevent heart disease are well established. However, studies of these drugs have suggested there could be a link between low levels of low-density lipoprotein cholesterol (LDL-C) and cancer risk. Still, what is not clear from those studies, is whether the link is because of the drugs, or in spite of them.
By analyzing the hundreds of metabolic products present in the liver, researchers with the UC Irvine Center for Epigenetics & Metabolism have discovered that circadian rhythms - our own body clock - greatly control the production of such key building blocks as amino acids, carbohydrates and lipids. They identified more than 600 liver-originated metabolites, which are the chemical substances created by metabolism that sustain and promote cell health and growth. Approximately 60 percent of these metabolites were found to be dependent on the endogenous circadian clock - many more than expected, as only about 15 percent of the body's genes are regulated by it. Circadian rhythms over 24 hours govern fundamental biological and physiological processes in almost all organisms. They anticipate environmental changes and adapt certain bodily functions to the appropriate time of day.
A 12-week treatment of the fermented soy germ-based nutritional supplement containing S-equol significantly lowered hemoglobin A1c (HbA1c), LDL cholesterol and improved vascular stiffness, all factors that occur as part of metabolic syndrome, according to a first-of-its-kind peer-reviewed study reported in a poster at the Women's Health 2012 annual meeting. "This study is the first to provide evidence that a daily supplement of soy-based S-equol favorably change metabolic syndrome risk factors, particularly in women. Because not all individuals have the ability to produce S-equol naturally after eating soy, the study results are very interesting and warrant examination in future studies, " said Belinda H. Jenks, Ph.D., coauthor of the study and director of Scientific Affairs & Nutrition Education at Pharmavite LLC, an U.
A nutrient found in the dark meat of poultry may provide protection against coronary heart disease (CHD) in women with high cholesterol, according to a study by researchers at NYU Langone Medical Center. The study, published online in the European Journal of Nutrition, evaluated the effects of taurine, a naturally-occurring nutrient found in the dark meat of turkey and chicken, as well as in some fish and shellfish, on CHD. It revealed that higher taurine intake was associated with significantly lower CHD risk among women with high total cholesterol levels. The same association was not seen in women with low cholesterol levels, however. There is very little information available about taurine, said principal investigator Yu Chen, PhD, MPH, associate professor of epidemiology at NYU School of Medicine, part of NYU Langone Medical Center.
A New Genre Of Anti-Cholesterol Medicines Could Result From Lessons Learned In 800-Million Drug Flop
Mindful of lessons from a failed heart drug that cost $800 million to develop, drug companies are taking another shot at new medications that boost levels of so-called "good cholesterol, " which removes cholesterol from the body. A report on how three new versions of medications in the same family as the failed torcetrapib appears in the current edition of Chemical & Engineering News, the newsmagazine of the American Chemical Society, the world's largest scientific society. In the cover story, C&EN Associate Editor Carmen Drahl explains that the drug maker Pfizer abruptly stopped development of its newest heart medicine in 2006, when clinical trials showed it was increasing patients' risk of death. Torcetrapib then was a high-profile potential new medication that blocked a substance called cholesteryl ester transfer protein (CETP) in a way expected to increase blood levels of HDL-cholesterol, high-density lipoprotein cholesterol.