A ction must be taken to prevent cardiovascular disease in women and men before signs and symptoms of the disease appear or a myocardial infarction or stroke is experienced. Prevention is critical because 40% of all coronary events in women are fatal, 67% of all sudden deaths in women occur in those without a history of coronary heart disease,1 and stroke is one of the leading causes of severe disability among women. Much is known about the risk factors for cardiovascular disease in women, but much less is known about the effect modification of these risk factors has on the reduction of risk in women. However, given the knowledge available, much can be done to prevent or control risk factors in women.Prevention of morbidity and death from cardiovascular diseases must start in the young. Although healthy living habits should begin in childhood, this report focuses on cardiovascular diseases among postmenopausal women entering the coronary heart diseaseand stroke-prone years. The discussion is extended to younger women where applicable: for example, in the sections on oral contraceptives and prevention and control of risk factors.Because of the growing number of older women in the population and those at risk for cardiovascular disease, the diagnosis and treatment of heart disease, stroke, and peripheral arterial disease are vital.General Considerations Cardiovascular diseases, especially coronary heart disease and cerebrovascular disease, are the leading causes of death in women in the United States and claim more black women's and white women's lives than do cancer, accidents, and diabetes combined.2Each year more than 236 000 women die of a heart attack, and more than 87 000 women die of a stroke. The age-adjusted death rates from diseases of the heart in women are four times higher in white women and six times higher in black women than the death rates for breast cancer. From 1980 to 1989 there was a 27% decline in age-adjusted death rates from coronary heart disease and a 65% decline in death rates "Cardiovascular Disease in Women" was approved by the Science Advisory from cerebrovascular diseases from 1960 to 1989 among white women. In black women there was a 22% and 68% decline, respectively. Despite these substantial declines in mortality, coronary heart disease and stroke still rank first and third as the causes of death for middle-aged and older women, with substantially higher rates in black women. With each decade of life, the rate of death from coronary heart disease increases threefold to fivefold. By the ages of 75 to 84, the death rate in white women is more than 1290 per 100 000 population and in black women it is more than 1300 per 100 000 population.2 Cardiovascular diseases are also a leading cause of disability in women.3 Estimates of the percentage of women with ischemic heart disease who were disabled by their illness in 1980 ranged from 36% in women aged 55 to 64 to 55% in women aged 75 and older. Women who survive a stroke fare even worse: 62% of female stroke survivors aged 55 to 64 had so...
Shrimp is very low in total fat, yet it has a high cholesterol content. Although shrimp is a popular food in the American diet, many people avoid it because of its high cholesterol content. The objective of this study was to test the effect of the addition of cholesterol from shrimp to a low-fat baseline diet as well as to compare the effect of an equal amount of dietary cholesterol derived from shrimp or egg on the plasma lipoprotein pattern of normolipidemic subjects. In a randomized crossover trial, a diet containing 300 g shrimp/d, which supplied 590 mg dietary cholesterol/d, significantly increased low-density-lipoprotein (LDL) cholesterol by 7.1% (P = 0.014) and high-density-lipoprotein (HDL) cholesterol by 12.1% (P = 0.0001) when compared with a baseline diet matched for fat content but containing only 107 mg cholesterol/d. However, because the percentage increase in LDL cholesterol was less than for HDL cholesterol, the shrimp diet did not worsen the ratio of total cholesterol to HDL cholesterol or the ratio of LDL to HDL cholesterol. Moreover, shrimp consumption decreased triacylglycerol (triglyceride) concentrations by 13% (P = 0.004). The diet containing two large eggs per day with 581 mg dietary cholesterol/d also raised LDL- and HDL-cholesterol concentrations compared with baseline, but the percentage increase in LDL cholesterol (10.2%, P = 0.0001) was more than for HDL cholesterol (7.6%, P = 0.004) and there was a trend toward worse lipoprotein ratios. In a comparison of the two high-cholesterol diets, the shrimp diet produced significantly lower ratios of total to HDL cholesterol and lower ratios of LDL to HDL cholesterol than the egg diet as well as lower triacylglycerol concentrations. We conclude that moderate shrimp consumption in normolipidemic subjects will not adversely affect the overall lipoprotein profile and can be included in "heart healthy" nutritional guidelines.
al, for the Finnish Diabetes Prevention Study Group. Prevention of type 2 diabetes by changes in lifestyle among subjects with impaired glucose tolerance.
To compare their relative absorption and effect on platelet function, concentrated fish oil and tuna were given to 10 subjects in a randomized crossover study. Although plasma enrichment of eicosapentaenoic acid (EPA) from either preparation was similar, relative absorption of EPA from tuna was significantly greater than that from fish oil (46.6 +/- 3.0 mg.L-1.g EPA-1 from tuna compared with 16 +/- 1.0 mg.L-1.g EPA-1 from fish oil, P less than 0.001). Relative absorption of docosahexaenoic acid (DHA) was equivalent (54.0 +/- 9.0 mg.L-1.g DHA-1 from tuna, 56 +/- 9.0 mg.L-1.g DHA-1 from fish oil, NS). Platelet aggregation in response to the endoperoxide analog U46619 was significantly diminished after either preparation but aggregation in response to other agonists, bleeding time, and membrane n-3 (omega-3) fatty acid content were not changed. Thus, n-3 fatty acids are well absorbed after one dose of either tuna or fish oil but EPA absorption appears to be more efficient from tuna. Additionally, a single dose of n-3 fatty acids decreases platelet aggregation by a mechanism not requiring incorporation into platelet membranes.
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