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September 2003

What's Hot Archive

September 29, 2003

Aspirin reduces the incidence of first heart attack by nearly one-third

The September 22 2003 of the journal Archives of Internal Medicine published the results of a meta-analysis of five major clinical trials which confirmed that aspirin plays an important role in heart attack prevention. The investigation was led by Charles H Hennekens MD of the University of Miami School of Medicine, who was the first to prove aspirin’s role in preventing a first heart attack in the Physician’s Health Study, which included 22,071 participants and was published in the New England Journal of Medicine in 1988. At that time the Cardio-Renal Drugs Advisory Committee recommended that the US Food and Drug Administration grant approval to professional labeling of aspirin to prevent a first heart attack. But because the British Doctors Trial (the only other study of this kind which included 5,139 participants) did not reveal benefits, the FDA failed to act on the recommendation.

Since that time three more trials concerning aspirin’s primary prevention benefits have been published. The current study analyzed data from 55,580 randomized participants and found a 32 percent reduction in heart attack and a 15 percent combined reduction in the risk of heart attack, stroke and vascular death associated with aspirin use. Dr Hennekens summarized, “The individual trials and their meta-analysis support the AHA [American Heart Association] and USPSTF [U.S. Preventive Services Task Force] guidelines, which note that the benefits of long-term aspirin use are likely to outweigh any risks for these individuals. The more widespread and appropriate use of aspirin in primary prevention could avoid hundreds of thousands of first heart attacks and important vascular events each year in the U.S. Yet despite the clearly demonstrated cardioprotective benefits of aspirin, this medication remains alarmingly underutilized among survivors of prior events, those having a heart attack and apparently healthy men and women, whose 10-year risk is 10 percent or more. “

—D Dye


September 17, 2003

Antioxidants for osteoporosis

A study published in the September 2003 issue of The Journal of Clinical Investigation proposed a new theory of how estrogen loss causes osteoporosis by concluding that a deficiency of the hormone lowers thiol antioxidants in osteoclasts (the cells that promote bone absorption), which increases their activity.

The researchers, from St George’s Hospital Medical School in London, removed the ovaries of several groups of female rats and mice while performing sham operations on control groups. After three weeks the rodents were given a dose of 17-alpha-estradiol, 17 beta-estradiol, or an inert substance and femoral bone marrow levels of glutathione and thioredoxin, the major thiol antioxidants, were measured. Removal of the ovaries and its consequent reduction of estradiol levels was associated with a decrease in both glutathione and thioredoxin, but animals who were administered beta-estradiol had levels restored to those of the animals whose ovaries were intact. In a second experiment, mice had their ovaries removed or received a sham ovariectomy, and were injected daily with 2 micromoles per kilogram body weight vitamin C or 100 milligram per kilogram N-acetyl-cysteine for 14 days. When the femurs of the mice were examined, ovariectomized mice who did not receive the antioxidant nutrients experienced bone loss, but NAC and vitamin C prevented this in mice who received either nutrient. And in an in-vitro experiment, NAC prevented the formation of osteoclasts, while the administration of an agent that depletes thiol antioxidants induced bone loss.

The results of these experiments suggest that the mechanism of estrogen deficiency in bone loss is that of lowering thiol antioxidants in osteoclasts which sensitizes them to signals that promote bone resorption. The authors write that bone loss is a consequence of not only estrogen deficiency but of other situations in which reactive oxygen species are involved, such as aging and inflammation.

—D Dye


September 15, 2003

Young ovaries give mice longer lives

In a study echoing early attempts at rejuvenation by transplanting the testicles of young animals into humans, researchers at the University of California, Davis have found that transplanting the ovaries of young mice into older females led to a significant extension of lifespan in the recipients. The researchers believe this is the first time it has been demonstrated that ovarian function plays a direct role in how mammals age.

Pioneering longevity researcher Cynthia Kenyon, of the University of California, San Francisco, stated, "This is a very interesting study, and it will stimulate a hunt for mammalian longevity hormones or signals produced by the reproductive system."

The study, which was published in the June 2003 issue of the journal Aging Cell, involved mice who had their ovaries removed at 3 weeks of age, who received transplanted ovaries from two month old mice at the age of 5, 8 or 11 months. The researchers found a 40 percent increase in lifespan at 11 months of age in the transplanted animals compared to mice of the same age who did not have the surgery, and a 60 percent increase compared to mice who had their ovaries removed but did not receive young ovaries. The equivalency in human terms would be a 50 year old woman with a life expectancy of 98 years of age rather than the current 80.

"Interwoven with existing data from earlier studies, these findings underscore the important role the reproductive organs play in modulating aging and longevity in mammals," stated lead investigator Professor James Carey of UC Davis entomology department. "They also underscore the need to revisit the relationship of longevity to indicators of reproductive aging in women, including the age when menopause begins, childbearing ability at later ages and childlessness," he said.

—D Dye


September 12, 2003

B vitamin supplements lower peripheral arterial disease risk in men

The September 2003 Journal of Nutrition published the results of a study conducted by Harvard researchers that found an inverse relationship between the use of B vitamin supplements, particularly folic acid, and the incidence of peripheral arterial disease (PAD). Peripheral arterial disease is a potentially fatal condition involving atherosclerosis in the noncoronary arteries, which restricts blood flow. Because elevated homocysteine levels have been associated with coronary heart disease and peripheral arterial disease, the researchers sought to determine if increased levels of B vitamins, which are known to lower homocysteine, are related to a lower incidence of PAD.

The study included 46,036 male health professionals enrolled in the Health Professionals Follow-up study, who were free of peripheral arterial disease, coronary heart disease, stroke and diabetes at the study's onset. Information concerning diet and supplement use was provided by questionnaires that were completed by all participants.

During the twelve year follow up period, 308 subjects developed peripheral arterial disease. It was found that for each 400 microgram per day increment of folate there was a decrease of 21 percent in the risk of developing PAD. Men in the top 20 percent of folate intake from diet and supplements had approximately two thirds the risk of developing peripheral arterial disease than men in the bottom 20 percent. Folate from food alone was not associated with a decrease in PAD risk. Men who took supplements containing folate had a 32 percent lower risk of PAD than those who did not take supplemental folate. There were also weaker associations between recent intake of vitamin B6 and vitamin B12 and a reduction in peripheral arterial disease incidence.

Although homocysteine reduction may be the mechanism of action for folate or other B vitamins against cardiovascular disease, the vitamins could also prevent the disease by quenching free radicals and improving endothelial dysfunction.

—D Dye

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