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Lewis Landsberg, Wednesday, May 14, 4:00 PM-6:00 PM-Hypertension in the Obese Patient: Pathogenic Mechanisms, Cardiovascular Risk, and Treatment: Introduction: hypertension in the obese patient: pathogenic mechanisms, cardiovascular risk and treatment: , American Journal of Hypertension, Volume 16, Issue S1, May 2003, Page 266A, https://doi.org/10.1016/S0895-7061(03)00800-8
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Abstract
The worldwide increase in obesity has led to a number of adverse health consequences including hypertension, coronary artery disease, and type 2 diabetes. This symposium will consider obesity and hypertension, focusing on pathogenesis, cardiovascular risk, and management.
Projections indicate that the prevalence of obesity in the United States may approach 50% by 2030. What is the cause of this remarkable increase in obesity? Clearly dietary excess and physical inactivity are critically important. But people differ significantly in their capacity to resist weight gain. Some individuals gain weight incrementally in the face of increased caloric intake while others dissipate the caloric load by increasing their metabolic rate, a phenomenon known as dietary thermogenesis. An efficient metabolism that does not waste ingested calories is one component of what has been called a “thrifty metabolic trait”; the other component involves sensitivity to the action of insulin on glucose uptake. Resistance to this action of insulin fosters utilization of non-glucose substrates by muscle while preserving glucose for use in the brain, a tissue that requires glucose, but not insulin, for normal function. Both components of this “thrifty” trait would prolong survival during periods of famine, and would therefore be favored by evolutionary pressures. In the face of a plentiful food supply, however, the thrifty trait predisposes to obesity and type 2 diabetes. Since most of the untoward consequences of obesity occur in postreproductive life, selective pressures against the thrifty trait would be minimal.
The hypertension of obesity involves insulin and leptin, both of which stimulate the sympathetic nervous system as a compensatory mechanism recruited to stabilize body weight. Body fat distribution also contributes to the complications of obesity. Adipocytes within the abdomen produce angiotensinogen, suggesting that enhanced angiotensin-2 production may contribute to elevated blood pressure.
