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      Prospective Study of Nutritional Factors, Blood Pressure, and Hypertension Among US Women

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          Abstract

          We examined prospectively the relation of nutritional factors with hypertension and blood pressure levels among 41,541 predominantly white US female nurses, aged 38 to 63 years, who completed a detailed semiquantitative food frequency questionnaire in 1984 and were without diagnosed hypertension, cancer, or cardiovascular disease. During 4 years of follow-up, from 1984 to 1988, 2,526 women reported a diagnosis of hypertension. Age, relative weight, and alcohol consumption were the strongest predictors for the development of hypertension. Dietary calcium, magnesium, potassium, and fiber were not significantly associated with risk of hypertension, after adjusting for age, body mass index, alcohol, and energy intake. Among women who did not report hypertension during the follow-up period, calcium, magnesium, potassium, and fiber were each significantly inversely associated with self-reported systolic and diastolic pressures, after adjusting for age, body mass index, alcohol consumption, and energy intake. When the four nutrients were added simultaneously to the regression model, only fiber and magnesium intakes retained significant inverse associations with systolic and diastolic pressures. In analyses of food groups, intakes of fruit and vegetables were inversely associated with systolic and diastolic pressures, and intakes of cereals and meat were directly associated with systolic pressure. These results support hypotheses that age, body weight, and alcohol consumption are strong determinants of risk of hypertension in middle-aged women. They are compatible with the possibilities that magnesium and fiber as well as a diet richer in fruits and vegetables may reduce blood pressure levels.

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          Most cited references32

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          The Effects of Nonpharmacologic Interventions on Blood Pressure of Persons With High Normal Levels

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            By how much does dietary salt reduction lower blood pressure? III--Analysis of data from trials of salt reduction.

            To determine whether the reduction in blood pressure achieved in trials of dietary salt reduction is quantitatively consistent with estimates derived from blood pressure and sodium intake in different populations, and, if so, to estimate the impact of reducing dietary salt on mortality from stroke and ischaemic heart disease. Analysis of the results of 68 crossover trials and 10 randomised controlled trials of dietary salt reduction. Comparison of observed reductions in systolic blood pressure for each trial with predicted values calculated from between population analysis. In the 45 trials in which salt reduction lasted four weeks or less the observed reductions in blood pressure were less than those predicted, with the difference between observed and predicted reductions being greatest in the trials of shortest duration. In the 33 trials lasting five weeks or longer the predicted reductions in individual trials closely matched a wide range of observed reductions. This applied for all age groups and for people with both high and normal levels of blood pressure. In people aged 50-59 years a reduction in daily sodium intake of 50 mmol (about 3 g of salt), attainable by moderate dietary salt reduction would, after a few weeks, lower systolic blood pressure by an average of 5 mm Hg, and by 7 mm Hg in those with high blood pressure (170 mm Hg); diastolic blood pressure would be lowered by about half as much. It is estimated that such a reduction in salt intake by a whole Western population would reduce the incidence of stroke by 22% and of ischaemic heart disease by 16% [corrected]. The results from the trials support the estimates from the observational data in the accompanying two papers. The effect of universal moderate dietary salt reduction on mortality from stroke and ischaemic heart disease would be substantial--larger, indeed, than could be achieved by fully implementing recommended policy for treating high blood pressure with drugs. However, reduction also in the amount of salt added to processed foods would lower blood pressure by at least twice as much and prevent some 75,000 [corrected] deaths a year in Britain as well as much disability.
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              Dietary fat and the risk of breast cancer.

              Dietary fat has been suggested as a risk factor for breast cancer in women, but the available data on humans are sparse and inconsistent. In 1980, 89,538 U.S. registered nurses who were 34 to 59 years of age and had no history of cancer completed a previously validated dietary questionnaire designed to measure individual consumption of total fat, saturated fat, linoleic acid, and cholesterol, as well as other nutrients. In a subsample of 173 participants studied in detail, those in the highest quintile of fat intake consumed a mean of 44 percent of calories from fat, as compared with 32 percent for those in the lowest quintile. During four years of follow-up, 601 cases of breast cancer were diagnosed among the 89,538 nurses in the study. After adjustment for known determinants in multivariate analyses, the relative risk of breast cancer among women in the highest quintile of calorie-adjusted total fat intake, as compared with women in the lowest quintile, was 0.82 (95 percent confidence limits, 0.64 and 1.05). The corresponding relative risks were 0.84 (confidence limits, 0.66 and 1.08) for saturated fat, 0.88 (0.69 and 1.12) for linoleic acid, and 0.91 (0.70 and 1.18) for cholesterol intake. Similar results were found for both postmenopausal and premenopausal women. These data are based on a limited period of follow-up and do not exclude a possible influence of fat intake before adulthood or at levels lower than 30 percent of calories. They suggest, however, that a moderate reduction in fat intake by adult women is unlikely to result in a substantial reduction in the incidence of breast cancer.
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                Author and article information

                Journal
                Hypertension
                Hypertension
                Ovid Technologies (Wolters Kluwer Health)
                0194-911X
                1524-4563
                May 1996
                May 1996
                : 27
                : 5
                : 1065-1072
                Affiliations
                [1 ]From the Channing Laboratory (C.H., W.W., F.S., B.R., M.S.) and Division of Preventive Medicine (C.H., J.M.), Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Mass; Department of Nutrition (A.A., W.W., F.S.) and Department of Epidemiology (A.A., W.W., M.S.), Harvard School of Public Health, Boston, Mass; and Department of Epidemiology and Biostatistics, Erasmus University School of Medicine, Rotterdam, Netherlands (J.W.).
                Article
                10.1161/01.HYP.27.5.1065
                8621198
                45a49bc3-1ae6-40ed-afa2-1991b02db3c5
                © 1996
                History

                Molecular medicine,Neurosciences
                Molecular medicine, Neurosciences

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