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

Published on June 11, 2004 at 10:37 PM · No Comments

Government and private sector health experts now estimate that 65 percent of America’s adults are overweight and 31 percent of adults are obese and at risk for chronic diseases such as diabetes and hypertension. The link between obesity and hypertension is well known, but the exact nature of the association between the two disorders remains unclear. 

Obesity and Hypertension

With the significant rise in obesity in this last decade comes a corresponding increase in the prevalence of hypertension.  Almost 29 percent of the population is hypertensive (having a blood pressure (BP) greater than 140/90 mmHg or using hypertensive medications).  The relationship between obesity and BP appears to be linear and exists throughout the non-obese range. But the strength of the association of obesity with hypertension varies among different racial and ethnic groups. Generally, risk estimates suggest that approximately 75 and 65 percent of the cases of hypertension in men and women, respectively, are directly attributable to an overweight condition and obesity.

It is important to recognize that long-duration obesity does not appear necessary to elevate BP, as demonstrated by obesity in children without a condition of hypertension. Therefore, rather than a special case, obesity hypertension should be considered the most common form of hypertension due to unknown reasons.

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.

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