Obesity is a major driver of hypertension, and while weight loss reduces blood pressure, there is currently no evidence that any specific class of antihypertensive agents is superior for obese patients.
The prevalence of obesity, including childhood obesity, is increasing worldwide. Weight gain is associated with increases in arterial pressure, and it has been estimated that 60-70% of hypertension in adults is attributable to adiposity. Centrally located body fat, associated with insulin resistance and dyslipidemia, is a more potent determinant of blood pressure elevation than peripheral body fat. Obesity-related hypertension may be a distinct hypertensive phenotype with distinct genetic determinants. Mechanisms of obesity-related hypertension include insulin resistance, sodium retention, increased sympathetic nervous system activity, activation of renin-angiotensin-aldosterone, and altered vascular function. In overweight individuals, weight loss results in a reduction of blood pressure, however, this effect may be attenuated in the long term. An increasing number of community-based programs (including school programs and worksite programs) are being developed for the prevention and treatment of obesity. Assessment and treatment of the obese hypertensive patient should address overall cardiovascular disease (CVD) risk. There are no compelling clinical trial data to indicate that any one class of antihypertensive agents is superior to others, and in general the principles of pharmacotherapy for obese hypertensive patients are not different from nonobese patients. Future research directions might include: (i) development of effective, culturally sensitive strategies for the prevention and treatment of obesity; (ii) clinical trials to identify the most effective drug therapies for reducing CVD in obese, hypertensive patients; (iii) continued search for the genetic determinants of the obese, hypertensive phenotype.
Theodore A. Kotchen (Thu,) studied this question.