The Framingham Heart Study, a famous study for 44 years, estimated that excess body weight (including overweight and obesity), accounted for approximately 26 percent of cases of hypertension in men and 28 percent in women.
Technically, obesity is defined as the abnormal accumulation of ≥20% of body fat, over the individual's ideal body weight. The latter constitutes the maximal healthful value for an individual that is calculated based chiefly on the height, age, build and degree of muscular development.
Obesity and in particular central obesity have been consistently associated with hypertension and increased cardiovascular risk. Based on population studies, risk estimates indicate that at least two-thirds of the prevalence of hypertension can be directly attributed to obesity.
Obesity might lead to hypertension and cardiovascular disease by activating the renin–angiotensin–aldosterone system, by increasing sympathetic activity, by promoting insulin resistance and leptin resistance, by increased procoagulatory activity and by endothelial dysfunction. Further mechanisms include increased renal sodium reabsorption, causing a shift to the right of the pressure–natriuresis relationship and resulting in volume expansion.
High dietary content in fat and carbohydrate has been suggested to acutely stimulate peripheral α1 and β-adrenergic receptors thereby leading to the elevation of sympathetic activity and hypertension.
Overweight can cause hypertension
