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Biomedical subjects

L Landsberg

Publications and source records attributed to L Landsberg.

148 records · Page 9Linked to original sources
PubMedDate not supplied

Weight reduction and obesity.

Obesity and hypertension are intimately linked. Weight loss lowers blood pressure and improves the blood pressure response to sodium restriction and antihypertensive medications. In addition to the effects of energy restriction, diets rich in fruits and vegetables (and hence potassium) and rich in low fat dairy products (and hence rich in calcium and magnesium), high in fiber, and low in saturated fat also lower blood pressure independent of sodium and energy content. These dietary modifications, along with weight loss are beneficial in patients only mildly overweight and, because of beneficial effects on other cardiac risk factors should be part of the therapeutic regimen in all obese hypertensive patients.

Blood Pressure↗
PubMedDate not supplied

Insulin resistance and hypertension.

Insulin resistance, a common accompaniment of essential hypertension, increases cardiovascular risk both directly, and via its adverse effect on other cardiovascular risk factors. Decreasing insulin resistance by lifestyle modification including diet, weight loss, and physical exercise is an important component of therapy in all patients. With the exception of thiazide diuretics as monotherapy, the currently utilized classes of agent appear equally effective in lowering blood pressure in insulin resistant patients. Currently utilized agents do, however, differ substantially in their effect on insulin resistance and associated risk factors. Agents that diminish insulin resistance may have a rationale in treating insulin resistant patients with hypertension although a decisive recommendation about class of agent in this group of patients must await several prospective large scale trials currently underway. Lower intervention thresholds and lower therapeutic goals would appear to apply to hypertensive patients with insulin resistance especially in the presence of impaired glucose tolerance or overt diabetes mellitus.

Blood Pressure↗
PubMedDate not supplied

Obesity, metabolism, and hypertension.

The relationship between obesity and hypertension is complex and poorly understood. A developing body of information suggests that metabolic factors related to the obese state are importantly involved. The pertinent observations include: (1) Diet influences sympathetic nervous system activity. Fasting suppresses, while carbohydrate and fat feeding stimulate, sympathetic activity. (2) Dietary-induced changes in sympathetic activity contribute to the changes in metabolic rate that accompany changes in dietary intake. (3) Insulin-mediated glucose metabolism in the hypothalamus provides a link between dietary intake and sympathetic nervous system activity. And (4) hyperinsulinemia, a consequence of insulin resistance in the obese, is associated with hypertension. These observations have suggested the following hypothesis. Hyperinsulinemia results in sympathetic stimulation which drives thermogenic mechanisms, thereby increasing metabolic rate. The net result is a restoration of energy balance at the expense of hyperinsulinemia and increased sympathetic activity. Hypertension is thus the unfortunate consequence of hyperinsulinemia, which increases renal sodium reabsorption, and sympathetic stimulation of the heart, kidney, and vasculature. The data on which this hypothesis is constructed are reviewed and the implications discussed.

Humans↗