Obesity-Induced Hypertension: Heavy on the Accelerator.

Hypertension is the most important cause of morbidity and mortality worldwide, with 182 million disability‐adjusted life years and 10.4 million deaths annually.1 In the Framingham population, the fraction of hypertension attributable to excess fat was 56% in women and 73% in men.2 Approximately two thirds of US adults have become overweight and more than one third are obese.3 This epidemic increasingly affects developing societies (including China). The body mass index (BMI) has increased globally by 20% in just 10 years, and elevated BMI is now the fourth leading cause of morbidity and mortality.1 In this issue of the Journal of the American Heart Association (JAHA), Zhang et al examine both the level of BMI and the change in BMI in young Chinese adults who underwent repeated measurements of BMI and blood pressure and who were followed an average of 5.5 years.4 (Measures of central adiposity were not obtained, but BMI is similar to those measures in predicting hypertension.5) As expected, the level of BMI was an important risk factor for incident hypertension. However, individuals with a sharp increase in BMI had a relative risk for new‐onset hypertension that was many times the risk in those with a low‐stable trajectory. The crucial period for incident hypertension associated with the sharply increasing trajectory was in those 20 to 30 years of age, a relationship that was independent of achieved BMI level. Before 30 years of age, the rate of increase in BMI was found to be a better predictor of hypertension than BMI level. The relationship between the sharply increasing trajectory in BMI and new‐onset hypertension persisted after adjustment for baseline BMI, baseline systolic blood pressure, and other risk factors: hazard ratio 12.3 (95% CIs 8.1 and 18.9). However, salt consumption was not measured and is correlated with both obesity and hypertension.6 Exercise reduces blood pressure independently of reductions in body weight and is also a potential confounder.7 Because of increased upper arm circumference and a conical shape, accurate measurement of blood pressure in obese individuals may be challenging.8 However, the high upper and lower 95% confidence limits make it virtually impossible to explain the results on the basis of unmeasured parameters. Nonetheless, it would be valuable to repeat such a study with measurements of salt consumption and exercise and to examine these relationships in other populations. Endothelial dysfunction and arterial stiffness precede hypertension in animals and humans.9, 10 However, arterial stiffness has been shown to be reversible.11, 12, 13 This suggests that there are mechanisms for adapting to stressors such as obesity (Figure). Obesity promotes the activity of factors (SOCS3 and PTP1B) that appear to counter the obesity‐induced increase in sympathetic tone. The obesity‐induced increase in leptin suppresses appetite through the arcuate nucleus in the hypothalamus and may lead to weight loss.14 Open in a separate window Figure 1 Counterbalancing effects* on blood pressure from SOCS3, PTP1B, weight loss, and nitric oxide, adapted from Hall et al14 with permission. Copyright ©2015, Wolters Kluwer Health, Inc. Obesity and increased sympathetic activity both activate the RAAS, which fosters hypertension. Nitric oxide mitigates the pro‐hypertensive effects of RAAS by reducing RAAS activation and by buffering the angiotensin II‐induced peripheral vasoconstriction. PTP1B indicates protein tyrosine phosphatase 1B; RAAS, renin–angiotensin–aldosterone system; SOCS3, suppressor of cytokine signaling 3.16