|Volume 6 Issue 160 Published - 14:00 UTC 08:00 EST 8-Jun-2004 Next Update - 14:00 UTC 08:00 EST 9-Jun-2004||Editor: Susan K. Boyer, RN
© Vidyya., Inc.
All rights reserved.
Obesity and hypertension: Two epidemics or one?
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 hypertension. Elevated blood pressure due to obesity can cause long-term damage to the body's vital organs and functions. This damage can occur to the:
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 hypertension. There 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 hypertension. Recommendations for using a non-pharmacological approach to treat obesity hypertension include:
7. Pharmacological therapy of obesity hypertension. There 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.
Source: Invited Review, 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).