65 percent of America’s adults are overweight and 31 percent of adults are obese and at risk for chronic diseases


Obesity and Hypertension



Many but not all studies suggest that abdominal adiposity or “beer gut” is more closely associated with high blood pressure rather than overall obesity.  Obese individuals with elevated intra-abdominal (visceral) fat demonstrate a clustering of coronary heart disease risk factors (i.e., the Metabolic Syndrome). Heretofore, medical researchers believed the accumulation of visceral fat is the central feature of this syndrome. However, recent evidence favors a role for ectopic or inappropriate fat storage as a cause of the metabolic syndrome. In this regard, both the accumulation of visceral fat and ectopic fat storage in a number of tissues and organs may be important in the cause and consequences of obesity hypertension.

A Comprehensive Review

Two researchers have provided an overview of cause, process, and treatment of obesity hypertension. Their focus was on the current state of knowledge of this condition in humans, particularly with the potential role of abdominal obesity. This Invited Review, entitled “Obesity and Hypertension: Two Epidemics or One?,” was authored by Kevin P. Davy from Department of Human Nutrition, Foods and Exercise, Virginia Polytechnic Institute and State University, Blacksburg, VA; and John E. Hall, with the Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS.  Their discussion appears in the May 2004 edition of the American Journal of Physiology-Regulatory, Integrative, and Comparative Physiology. The journal is one of 14 published each month by the American Physiological Society (APS) (www.the-aps.org).

Highlights of this comprehensive review of existing literature and research regarding the association between hypertension and obesity are:

1.  Not all obese individuals are hypertensive by clinical standards.   Weight gain is almost invariably associated with an increased BP.  The increase in BP is closely related to the magnitude of weight gain, and even moderate weight gain is associated with an increased risk of developing hypertension. However, there is considerable inter-individual variability in the BP response to weight gain and not all obese individuals become hypertensive, at least by the standard of 140/90 mmHg. In addition, weight loss is associated with a reduction in BP in many normotensive obese individuals. Therefore, BP is higher in obese humans than would be achieved at a lower level of excessive fat cells.

The reasons for the inter-individual variability in the BP response to weight gain remain unclear, but genetic factors may contribute. In addition, inter-individual variability in visceral fat accumulation with weight gain may also play a role. It is important to emphasize that any elevation in BP above optimal levels (approximately120/80 mmHg) will increase an individual’s risk of developing cardiovascular diseases. In turn, reductions in BP from above optimal levels should confer a health benefit.

2.  Blood circulation alterations are linked to obesity hypertension.   Animal studies indicate cardiac output and blood flow to fatty tissue and several other regions (e.g., heart, kidney, muscle, gut) are increased with weight gain. In humans, this also appears to be the case. Cardiac output is elevated at rest and parallels the increase in resting oxygen consumption, whereas systemic vascular resistance is similar or reduced in obese compared with non-obese individuals. 

There is some evidence that abdominal obesity is associated with altered blood circulation adjustments to weight gain. Specifically, individuals with an excess accumulation of abdominal fat demonstrate lower levels of cardiac output and higher peripheral resistance compared with individuals with lower body or subcutaneous obesity.

3.  Organ damage can result from obesity hypertensionElevated blood pressure due to obesity can cause long-term damage to the body’s vital organs and functions.  This damage can occur to the:

            Heart: Cardiac filling pressures are elevated in obese humans, due in part to an increase in ventricular stiffness in the face of an expanded blood volume. Diastolic dysfunction is evident early in obesity and characterized by impaired ventricular filling dynamics and relaxation. There may also be systolic dysfunction and an enlarged heart with prolonged obesity. Obesity and hypertension worsen the degree of left ventricular hypertrophy in a synergistic manner, and this translates into a greater risk of congestive heart failure.  Weight loss improves systolic and diastolic function and reduces left ventricular mass.  The severity, duration, and type (visceral vs. subcutaneous) of obesity also appear to be important determinants of the cardiac dysfunction and left ventricular hypertrophy observed in obese individuals. The degree of cardiac dysfunction and left ventricular hypertrophy appears to be more closely associated with the enlarged abdomen than total body obesity.

            Vasculature (blood vessels): The endothelium, a layer of flat cells lining especially blood and lymphatic vessels and the heart, plays an important role in cardiovascular homeostasis by modulating vascular tone, inhibiting monocyte and platelet adhesion, and maintaining fibrinolytic balance. In obesity, the endothelium is exposed to mechanical forces and other cardiovascular risk factors that can alter vascular structure and function. There is increasing evidence that obesity in humans is associated with peripheral and coronary endothelial dysfunction.

There is increasing evidence that obesity is associated with an increase in central arterial stiffness, and weight loss reduces arterial stiffness. Furthermore, arterial stiffness appears to be more closely associated with abdominal visceral fat than whole body measures of adiposity. The mechanisms responsible for arterial stiffening in obese humans are unclear, but endothelial dysfunction, elevated advanced glycation end products, and collagen cross-linking may play a role. 

Two of the most common causes of chronic renal (kidney) failure, diabetes and hypertension, are closely associated with obesity. Other metabolic factors including hyperlipidemia and hyperglycemia may contribute to alterations in kidney structure and function in obesity. However, it is unclear whether the alterations in kidney structure and function are more severe in visceral obesity.

4.  There are several potential mechanisms linking obesity with hypertensionThere are several potential mechanisms that could mediate the sodium retention and hypertension associated with obesity, including sympathetic nervous system activation, renin-angiotensin-aldosterone system activation, and compression of the kidney. 

5. A potential association between obesity hypertension and obstructive sleep apnea.  Obesity is an important risk factor for obstructive sleep apnea but obstructive sleep apnea may be more closely associated with the enlarged abdomen than overall body obesity.  Obstructive sleep apnea has been linked to hypertension in both clinical and epidemiological studies. As such, obstructive sleep apnea may be an important mechanism linking obesity and hypertension in some individuals.

6. Non-pharmacological treatments for obesity hypertensionRecommendations for using a non-pharmacological approach to treat obesity hypertension include: 

            Weight loss: Weight loss is considered the most effective non-pharmacological therapy for lowering BP in obese hypertensives. There is a dose-response relation between the degree of weight loss and the reduction in BP that is independent of sodium intake. Even modest weight loss of 5–10 percent of body weight is associated with clinically significant reductions in BP.

            Regular physical activity: The incidence of hypertension is highest in obese sedentary and lowest in lean physically active individuals. Physically active individuals have a lower risk of hypertension compared with their sedentary counterparts. Importantly, the risk of hypertension associated with weight gain also appears to be lower in physically active individuals. As such, regular physical activity is recommended for individuals with elevated BP.

            Sodium restriction: Sodium restriction reduces BP, albeit modestly, in obese individuals. However, additional research has reported that moderate sodium restriction resulted in dramatic reduction in BP in obese postmenopausal women.

7.  Pharmacological therapy of obesity hypertensionThere are currently no specific recommendations for the pharmacological treatment of obesity hypertension, although some have suggested that the selection of therapy should be based on etiology of the disorder. As such, pharmacological blockade of the sympathetic nervous system activation and renin-angiotensin-aldosterone system are logical choices for intervention.

8.  Pharmacological treatment of obesity may be a logical approach for lowering BP.  If obesity is an underlying cause of essential hypertension, as appears to be the case, then pharmacological treatment of obesity may be a logical approach for lowering BP in obese individuals. However, only two drugs, sibutramine and orlistat, have been approved for long-term use in weight loss and weight management. The modest efficacy of both drugs in short-term weight loss and long-term weight maintenance has been documented in randomized controlled trials but attrition rates are high. 

9.  Prevention of obesity hypertension.  The average weight gain of the population in the United States is estimated to be approximately two pounds per year and weight gain is almost invariably associated with an increase in BP. Accordingly, preventing weight gain should be a primary goal for reducing hypertension.  Regular physical activity and reduced dietary fat intake reduce weight gain in normal weight people and weight regain after weight loss in obese individuals. The authors suggest that increasing the amount of regular physical activity and reducing energy intake by an amount equal to 100 kcal/day could prevent weight gain in most of the population. This could be achieved by relatively small lifestyle changes such as adding 15 minutes of walking each day and reducing portion sizes by a few bites per meal.


The continuing problem of weight gain and obesity in the United States shows no sign of abating.  With obesity a major cause of hypertension, rising BP, and associated illnesses, there is growing support that sympathetic nervous system activation and renin-angiotensin-aldosterone system activation have an important role in the cause of obesity hypertension.

Today’s experts also believe that the enlarged abdomen, resulting from visceral fat, has a role in the activation of these systems, thereby increasing the risk for the development of hypertension. The abnormal deposition of fat may also contribute to the BP raising effect of weight gain and the accompanying cardiac, vascular, and renal dysfunction.

This comprehensive review reveals that there is much we do know about the association between high blood pressure and obesity.  But the most effective treatment for obesity hypertension remains the tried and true method that leads to weight loss and other lifestyle modification.


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