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Diet is a component in the etiology of the two major causes of death in the United States, namely, cardiovascular disease and cancer. During the last decade, various organizations have suggested that we alter the "typical" American diet in order to decrease the incidence of these diseases even though both diseases are indisputably of multiple etiology. An implication behind these recommendations is that individuals will increase their longevity by changing their diets. The burden of proof falls on those proposing changes to the diet that such alterations will be safe and effective. In spite of our often indicted diet, mortality from heart disease and stroke continue to fall and deaths from diet-related cancers are static or dropping. Longevity in the U.S. is exceeded by only five countries, whose populations consume a diet similar to ours in four, and that in the fifth is approaching ours. While low-fat high-fiber diets probably have some beneficial effect vis-a-vis chronic diseases, it is likely that other risk factors contribute more to the total risk of disease. Therefore, it is illogical to expect dietary manipulation to offset significantly other concurrent risks such as heredity, tobacco use, hypertension, and obesity. Individuals who are at high risk for specific diseases should modify their diets to minimize this particular risk factor. Most Americans can safely reduce their intake of total calories, fat, sugar, and salt. Although this can be achieved most readily on a population basis by following a form of "prudent" diet, it is premature to promise medical benefits to individuals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The Western diet: an examination of its relationship with chronic disease. 302 70

Based on psycho-physiological, clinical and epidemiological studies, essential arterial hypertension is considered to be a consequence of an inadequate 'person-environment fit', objectively, subjectively or both. Besides genetic predisposition, salt intake, obesity and physical inactivity, psychological factors--among them 'hyper-reactivity' of the sympathetic nervous system, predisposing behaviour patterns and stressful life-events--should be taken into account in reaching a better understanding of the causes, prediction and prevention of hypertension. It was demonstrated that a maladaptation in various functional systems, even to minor psycho-emotional stress, is an important pathogenetic link between environment, objectively defined stressors and blood pressure regulation from the earliest phases of the disease. Implications for further research and behavioural interventions, together with other lifestyle-related factors, are discussed for improving the population-based health care in cardiovascular disease in the G.D.R.
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PMID:Life stress and hypertension. 303 55

In adults of Western societies the positive relationship between blood pressure and body weight has often been demonstrated, both cross-sectionally and longitudinally. This correlation is even stronger in children and early adulthood. In most studies in children, the association between age and blood pressure disappears after controlling for weight. Association must be differentiated from causation. It has however been shown in several intervention studies that treatment of obesity by weight loss decreases blood pressure substantially both in hypertensive and normotensive subjects. Although combining results from several intervention trials is difficult this is the only practical way to get an overall estimate of the hypotensive response to be expected from weight reduction. In the randomised controlled intervention studies, conducted in obese hypertensive patients and reviewed in the present meta-analysis, a decrease in body weight by 1 kg resulted in a reduction of systolic and diastolic pressure by 1.2 and 1.0 mmHg, respectively. Blood pressure generally decreased before normal weight was achieved and remained reduced as long as there was no marked regain in body weight. Although a decrease in salt intake during dieting may contribute to the blood pressure lowering effect of weight reduction, also other mechanisms, such as a reduction in plasma renin activity and a decrease in sympathetic tone may also be involved.
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PMID:The relationship between body weight and blood pressure. 307 38

Atherosclerosis and hypertension are, by far, the most common cardiovascular diseases affecting women, and both are influenced by diet. Atherosclerosis occurs more commonly in men than women; generally women are 10 to 15 years older than men when symptoms develop. The prevalence of hypertension is about equal in the two sexes, particularly in middle aged and older persons. These cardiovascular diseases are major causes of death and disability in this country. Atherosclerosis results in myocardial infarction, thrombotic strokes, and claudication. Hypertension, when severe, damages small blood vessels, causing kidney failure, hemorrhage, strokes, and heart failure; when the condition is mild to moderate, it produces atherosclerosis. Nutritional factors are of primary importance in both atherosclerosis and hypertension. Risk factors for atherosclerosis related to nutrition are hypercholesterolemia, hyperglycemia-diabetes, and for hypertension, obesity, high salt intake, and excessive use of alcohol. Of all these risk factors, obesity seems to be the most important because it is strongly linked to hypertension and diabetes. Dietary intake of saturated fat is a potent factor in determining the blood cholesterol level, and reducing intake often decreases the level, thus lessening the risk of atherosclerotic complications. Although high salt intake and excessive alcohol use produce hypertension in susceptible people, less is known about the frequency of this adverse effect than is known about obesity.
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PMID:Nutrition and cardiovascular diseases of women. 312 Feb 15

An elderly Belgian population group anno 1986 consisting of 53 men and 110 women above the age of 75 years with a mean age of 80 and 81 years, respectively, is characterized by relative obesity and low diastolic blood pressure, both in men and women. The SBP/DBP ratio is 1.91 in men and 1.88 in women. HDL-cholesterol levels are relatively high in men. Women still have slightly higher HDL-cholesterol levels than men, the difference between women and men being 3.4 mg/dl. In both sexes HDL-cholesterol correlates negatively with body weight. The 24-hour urinary sodium/potassium ratio is 2.9 in men and 2.5 in women. Factors significantly related to diastolic blood pressure in a multiple regression analysis included being on a low-salt diet, the level of 24-hour urinary potassium excretion and of 24-hour urinary creatinine excretion in men, and body weight, heart rate and the level of 24-hour urinary calcium excretion in women. It may be concluded that significant differences exist between the distribution of cardiovascular risk factors in older compared to middle-aged subjects.
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PMID:Cardiovascular risk factor distribution above the age of 75 years in a Belgian community. 320 30

Body mass index, alcohol and salt consumption, and parental history of hypertension were examined as possible predictors of the development of essential hypertension in 1,031 persons, ages 30-49 years at entry, with documented normotension followed by documented hypertension after a mean interval of 6 years. In a comparison with 1,031 matched persistently normotensive persons initial body mass index and percentage increase in body mass index were each predictive of hypertension. Consumption of three or more alcoholic drinks a day at baseline was also predictive, more so if this level of intake persisted than if it diminished. Heavy salt intake as crudely estimated at baseline by one question was also associated with the development of hypertension. Parental history of hypertension was also predictive, more so for hypertension in the mother than for hypertension in the father, and the association was apparent only in female subjects. These characteristics at baseline showed independent associations with subsequent hypertension in multivariate analysis. When follow-up data were included in the multivariate analysis, alcohol consumption at the hypertensive examination was much more strongly related than at the baseline examination, suggesting a short-term effect, and heavy salt consumption was no longer predictive, possibly because of a marked loss of subjects due to missing follow-up data. This large study confirms longitudinally the importance of obesity, weight gain during adulthood, alcohol, family history, and, to some extent, salt as predictive and possibly causal factors for essential hypertension.
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PMID:Precursors of essential hypertension: body weight, alcohol and salt use, and parental history of hypertension. 321 72

Body constituents (cellular and extracellular mass, fat, extracellular fluid) were examined by means of K-40 whole-body radiometry in male essential hypertension patients with normal body weight and alimentary obesity. Second-stage essential hypertension was associated with a reduction of body cell mass, its relative parameters in particular. This fall was even more pronounced in patients with alimentary obesity. Apparently, increased proportion of fat in relation to body cell mass, which is more active metabolically, alters water-salt balance and, consequently, arterial blood pressure.
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PMID:[Body constitution of patients of different somatotypes with hypertension]. 324 60

Reasons are given why calcium, obesity and genetics cannot be considered primary factors in the etiology of essential hypertension. This leaves the major protagonists as salt and neuroendocrine responses to the emotions aroused by the social environment. Most essential hypertension is renin dependent and associated with the physiological changes induced by arousal of the defence response. The psychosocial stimulation associated with this arousal induces an increase in salt appetite. This makes the salt consumption of society a measure of the social stress to which it is exposed. Primitive people whose blood pressure remains normal throughout their lives may lack modern societies' physically protective achievements but their religiously prescribed social solidarity may protect them from psychosocial stress. Our chronic suppression of awareness of emotional arousal together with loss of the ritualized support of affiliative behavior may result in repressed emotional responses which find somatic expression in diseases such as essential hypertension. Hypertensiologist George Pickering proposed that the primitive's ritual and taboo (the equivalent in our society might be the Alcoholic's Anonymous belief in a 'Higher Power') protect them from much anger and despair. He gave this precedence over salt as the primary factor in essential hypertension. New evidence supports this. Despite a high salt diet the blood pressure of socially adjusted rodents remains normal throughout their lifespan. On the other hand, the hypertension that develops when they are psychosocially stimulated is not abated by a low salt diet. In humans, the blood pressure of cloistered, secluded Italian nuns on a high salt diet has remained normal for 20 years while that of nearby village women has risen at a startling 2 mmHg/annum during the same period. On the other hand, in rapidly changing Malawi mature adult, rural and urban blood pressures are rising fast despite a low salt intake. Thus the evidence today argues that the most important factor in the etiology of essential hypertension is not salt but psychosocial stimulation.
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PMID:Stress, salt and hypertension. 327 18

We conclude that the following may explain the rise in blood pressure with obesity and the subsequent fall in blood pressure (Fig. 2): (1) An increase in calories, protein, or carbohydrate leads to an increase in plasma catecholamines, sympathetic nervous system activity, and insulin secretion. (2) These factors, in turn, lead to increased renal sodium retention and stimulation of the renin-aldosterone system which, in turn, leads to: (3) An increased cardiac output with an inability to appropriately adjust the peripheral resistance to maintain normotension with resultant hypertension. Conversely, the fall in blood pressure with weight reduction can be explained by (Fig. 3): (1) A decrease in calorie, carbohydrate, or protein intake which leads to: (2) A decrease in circulating plasma catecholamines, sympathetic nervous system activity, and insulin secretion which results in: (3) A natriuresis and decrease in the renin-aldosterone system, which causes a decrease in circulating blood volume and in cardiac output. This, in turn, lowers blood pressure towards normal. The unanswered question still remains: why do some obese patients become hypertensive and others remain normotensive? Perhaps there are weight-sensitive individuals and weight-resistant individuals just as there appear to be salt-sensitive and salt-resistant hypertensive patients. Perhaps the answer is genetic. These questions also remain to be answered.
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PMID:Mechanisms of hypertension in obesity. 332 17

One hundred nine 19-year-old female students were surveyed as to academic test marks; salt detection and recognition thresholds; serum cholesterol, serum uric acid, serum cortisol, and other biochemical indices in serum; urinary sodium/creatinine and potassium/creatinine, as well as number of complaints based on the Cornell Medical Index (CMI) and personality based on the Yatabe-Guilford (Y-G) test. The salt recognition threshold showed a high negative correlation with serum uric acid concentration and a slight correlation with CMI complaint number, academic test marks, blood pressure, obesity, and serum cholesterol. The subjects with high salt thresholds had relatively passive personalities. Cholesterol, uric acid, hemoglobin, ferritin, and glucose levels in the serum were higher in the group with higher academic marks. These students also had fewer complaints and more of them were type B individuals based on the Y-G test. They also seemed to be under greater stress. In regression analysis, the partial regression coefficient between academic test marks and serum cholesterol was 60 percent higher than that between academic test marks and serum uric acid. Students who lived on campus had 24.8 milligrams per deciliter (15.7 percent) more serum cholesterol and 3.8 micrograms per deciliter (37.7 percent) more serum cortisol than those who commuted from home.
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PMID:An epidemiologic study on the correlation between salt threshold, academic test marks, biochemical data, number of complaints, and personality in women college students. 345 2


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