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Gentics+Wrong foods= Heart Disease

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A recent study completed in the US would seem to indicate that Six in every 100 Americans carry gene variants that greatly increase their succeptibility to heart disease. But eating the correct foods and avoiding the wrong ones can virtually eliminates this risk.

A recent study completed in the US would seem to indicate that Six in every 100 Americans carry gene variants that greatly increase their succeptibility to heart disease. But eating the correct foods and avoiding the wrong ones can virtually eliminates this risk. The heart-disease gene types, variant forms of a normal gene,are more common among blacks, Asians, Pacific Islanders, and other racial or ethnic groups, than among Hispanics and non-Hispanic whites. But some people of all races seem to be carriers of the gene variants.How bad are these gene variants we speak of? They pose a greater risk of heart disease, based on thickening of arteries, than smoking, and nearly as great a risk as diabetes. A diet high in arachidonic acid, mostly found in meat fats, increases the bad effects of the inherited gene forms. But a diet which is high in fish oils, such as those found in salmon, tuna, and mackerel. can effectively void these effects. “These findings suggest that the [heart-protective] effects of [oils] derived from fish might be more prominent in (or perhaps limited to) persons with [the gene variants],” write Raffaele De Caterina, MD, PhD, and Antonella Zampolli, PhD, of Italy’s National Research Council. Their commentary — and the study itself — appears in the Jan. 1, 2004, issue of The New England Journal of Medicine. The Origins of Heart Disease:The findings come from a groundbreaking study that pulls back the covers shrouding the mysterious origins of heart disease. James H. Dwyer, PhD, and colleagues at the University of Southern California and UCLA knew that mice lacking the 5-lipoxygenase gene were nearly immune to atherosclerosis, or hardening of the arteries. To find out whether this gene was important in human disease, they analyzed a racially diverse group of 470 healthy, middle-aged men and women. They found that 6% of these people had a variant form of the gene. Apparently, these gene variants increased a person’s 5-lipoxygenase activity. That’s bad, as it turns out. Theoretically, increased 5-lipoxygenase activity would cause cells of the immune system to accumulate inside artery walls. As they accumulated, they cause inflammation and promote the accumulation of cholesterol molecules in the artery wall. Over time, the buildup of artery-clogging plaque leads to heart disease. And that’s what seems to happen. People with the gene variants had much thicker artery walls than those with normal forms of the 5-lipoxygenase gene. Thicker artery walls is a marker for cardiovascular disease. Nutrition and Genetics go hand in hand:But Dwyer’s team didn’t stop there. 5-lipoxygenase is an enzyme that breaks down fats — particularly arachidonic acid, which comes mainly from fatty red meat — into substances that cause inflammation. They reasoned that the more arachidonic acid a person with the gene variant ate, the more signs of heart disease they’d find. And that, too, proved true. People with the gene variant were particularly sensitive to the heart-clogging effects of a diet high in arachidonic acid. But there was good news, too. People with the gene variant were also particularly sensitive to the healthy effects of diets high in fish oils. Those who ate the most of these oils were able to blunt the effects of their genetic tendency toward heart disease. “These findings could lead to new dietary and targeted molecular approaches to the prevention and treatment of cardiovascular disease according to genotype, particularly in populations of non-European descent,” Dwyer and colleagues suggest. (Sources: Dwyer, J. The New England Journal of Medicine, Jan. 1, 2004; vol 350: pp 29-37. De Caterina, R. and Zampolli, A. The New England Journal of Medicine, Jan. 1, 2004; vol 350: pp 4-7., WEBMD, Jan 2004)


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Posted On: 9 January, 2004
Modified On: 3 December, 2013

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