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------------------------------------------------------------------------ Low Caloric Intake May Prolong Life ------------------------------------------------------------------------ NEW YORK, Oct 01 (Reuters) -- In a review article in this week's issue of The New England Journal of Medicine, leading researchers point to a growing body of scientific evidence that favors limiting calorie intake for a longer, healthier life. In addition to extending longevity in many animals, studies show caloric restriction slows age-related deficits in behavior, learning, immune response, gene expression, and DNA repair, according to Dr. Richard Weindruch, professor of medicine at the University of Wisconsin, and researcher at the Geriatric Research, Education, and Clinical Center at Middleton Veterans Hospital in Madison. Weindruch was the first to show that even starting rodents on a controlled calorically restricted diet in mid-life produced longer-lived, healthier animals. "Several lines of evidence suggest that caloric intake influences the rate of aging and the onset of associated diseases in animals and, possibly, humans," the researcher states. Since the 1930s, researchers have observed that laboratory rats live longer and have fewer age-associated diseases when their caloric intake is restricted by 30% to 60%. Weindruch cites one of the newer lines of evidence that focuses on the cellular effect of oxidative stress -- damage caused by molecular substances known as free radicals, which arise as energy is generated within cells. "It's now appreciated that levels of free radicals in cells determine a broad spectrum of normal activity, such as which genes are transcribed or how the cells send signals within cells and between cells," he explains. As the number of free radicals increases, organs -- such as the brain and heart -- become particularly susceptible to damage from oxidative stress. "We think that free-radical involvement in aging is probably going to be more significant in cells having limited repair capacities -- such as neurons (in the brain), skeletal muscle, and heart muscle cells," Weindruch says. He and co-author, Dr. Rajindar Sohal of Southern Methodist University in Dallas, Texas, say a rapidly expanding body of data implicates oxidative stress in the development of Parkinson's disease, Alzheimer's disease, heart failure, and other geriatric problems, such as frailty. "I really think that these 'postmitotic' cells are extremely important potential targets for oxidative damage accruing in aging related to these very stubborn geriatric conditions," Weindruch says. According to Weindruch, evidence suggests that caloric restriction may lead to a reduction in oxidative stress. He cites experiments in laboratory rats in which oxidative damage to DNA in brain, heart, and skeletal muscle tissues was halted by caloric restriction. He also cites a study in mice in which caloric restriction retarded the severity of oxidative damage in regions of the brain associated with cognitive (learning) and motor functions. Weindruch says other findings in mice with systemic lupus, hypertension, breast cancer, and type-II diabetes show caloric restriction is associated with increased longevity, "and the diseases occur much later, if at all." If caloric restriction is found to have the same benefits in humans as in animals, might people be persuaded to reduce their caloric intake by 30% for an extended period? Weindruch acknowledges that many people would probably find it difficult to do that. However, he says some individuals might be "extremely motivated" to try -- "For example, people from cancer-prone families or with a family history of early-onset degenerative diseases associated with aging might be suitable candidates for long-term dietary restriction." SOURCE: The New England Journal of Medicine (1997;337(14):986-994) Copyright 1997 Reuters Limited. http://www.reutershealth.com/news/rhdn/199710/1997100108.html ------------------------------------------------------------------------