Treatment of Hypertension in Obesity

1

What is the epidemiology of obesity and hypertension?

Overweight and obesity are defined as abnormal or excessive fat accumulation that may impair health (World Health Organization). Body mass index (BMI) is the simplest way to classify overweight (BMI between 25 and 29.9 kg/m ² ) and obesity (BMI > 30 kg/m ² ) in adults.

Worldwide obesity has nearly tripled since 1975, and almost a third of the world’s adult population are overweight and obese today. Unfortunately, children and adolescents aged 5 to 19 can also become overweight or obese. In 2016, 18% of this population was classified as being either overweight or obese.

The prevalence of obesity is greater in women than men and increases with age.

In the United States, 39.8% of the adult population are obese. Hispanics (47%) and non-Hispanic Blacks (46.8%) have the highest age-adjusted prevalence of obesity, followed by non-Hispanic Whites (37.9%) and non-Hispanic Asians (12.7%).

Obesity is a risk factor for developing hypertension and cardiorenal and metabolic disorders. The Framingham Heart Study suggests that 78% of primary hypertension in men and 65% in women can be attributed to excess weight gain. Central obesity is a better predictor than subcutaneous fat for the development of obesity, and duration of obesity also has a negative impact on blood pressure (BP) levels.

2

How does obesity cause and/or aggravate hypertension?

The pathophysiological mechanisms involved in obesity-related hypertension are complex and have not been fully elucidated. Adipose tissue, particularly with excess visceral fat, serves as an endocrine organ producing multiple hormones and cytokines, which increase the risk of developing hypertension and cardiovascular disease. Obesity is accompanied by increases in macrophages and other immune cells in adipose tissue, in part because of tissue remodeling in response to adipocyte apoptosis. These immune cells secrete proinflammatory cytokines, which contribute to insulin resistance, sympathetic activation, and vascular remodeling.

Compression of the kidney by surrounding adipose tissue may also contribute to relative ischemia, renin-angiotensin activation, increased sodium reabsorption, and hypertension. Obesity also is often accompanied by an increase in pharyngeal soft tissues, which can contribute to the respiratory events observed in obstructive sleep apnea (OSA). Once present, this common sleep-disordered breathing (especially moderate and severe OSA) amplifies sympathetic activation, aldosterone production, inflammation, and oxidative stress observed in obesity. These contributions provide additional indirect mechanisms by which obesity may promote hypertension.

3

What is the impact of the nonpharmacologic (and nonsurgical) intervention to obesity treatment over hypertension?

Lifestyle modifications can significantly decrease BP in patients with hypertension. Proven nonpharmacologic interventions for obesity that also improve hypertension control include physical activity (especially aerobic exercises), which reduces BP by approximately 5 to 8 mm Hg. Weight loss strategies including caloric restriction may be expected to reduce BP by 1 mm Hg for every 1 kg reduction in body weight. Most evidence on weight loss is based on short-term follow-up, and a high rate of recidivism over a longer timeframe negatively impacts the effects of lifestyle modifications on hypertension control in clinical practice.