Exercise as a Therapeutic Modality for Obesity

Pathology of Obesity

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Obesity may account for over 300,000 deaths a year, almost as many deaths as from cigarette smoking (1). According to the U.S. National Center for Health Statistics surveys, nearly 50% of adult women report that they are dieting to lose weight. Even more surprising, 60 to 75% of teen-aged girls in the U.S. reported that they are dieting to lose weight (2).

Aside from physical activity, treatments for obesity have involved dietary, psychological, pharmacological, surgical approaches. Dietary intervention is considered to be the most crucial therapeutic modality. Dietary methods have included low calorie diets, dietary fat reduction, and more recently, low carbohydrate diets. Dietary fat reduction was commonly recommended for the mildly and moderately obese. More recent studies have demonstrated the efficiency and safety of low carbohydrate diets. See Protein and Weight Loss and Macronutrient Ration Studies. Ironically, high protein, low carbohydrate diets were once not generally accepted by the scientific community and were considered dangerous by many so called authorities.

Low calorie diets, either medically supervised, commercially packaged, or as seen with many fad diets, possess many undesirable consequences. These disadvantages include an adaptive decrease in energy expenditure, reduced resting metabolic rate, decrease muscle mass, reduced norepinephrine induced thermogenesis, decreased fat cell lipolysis, decreased glycogen stores, and a sequential Yo-yo phenomenon. The reduction in resting metabolic rate has been attributed to a reduction of body mass. Interestingly, a decrease in resting metabolic rate is not seen when body weight is expressed as "Calories per kilogram" (3). An initial dramatic decrease in body weight, commonly seen with calorie restrictive diets, can be attributed to water weight loss directly related to depleted glycogen stores in the muscles in liver.

Risk factors and the clinical status of an individual must also be considered when interpreting the body composition data. For example, consider a middle age man with a body composition of approximately 16%. This value is considered well within normal range by most authorities yet a reduction of body composition may be warranted when accompanied by hypercholesterolimia or hypertension. In this case we know that even a modest weight loss in even non-obese people often can reduce particular risk factors. On the other hand, a man with an estimated body composition of 22% and no risk factors may not have to be strongly encouraged to lose body fat (4).

Exercise professionals sometimes erroneously ignore the principle of variability when interpreting body composition measurements. Humans vary greatly on any anthropometric, and body composition is no exception. Exercise professionals must take into account the wide range of normal values (4). The number and size of the adipose cells varies among individuals. Even the different fat deposits have varying size, number, and mobilization rates (5).

Comparable mortality risks throughout a wide range of body composition values illustrate leaner body composition values are not necessarily healthier. The relationship between body composition and mortality is relatively flat throughout a wide range of body compositions (2). Obesity is considered a medical condition that causes significant morbidity and decreased life expectancy (1). Only at the upper extremes of the body composition distribution, health risk increases significantly. Significant risk of health begin at a BMI of about 27.3 kg/m2 for women and 27.3 kg/m2 for men (2). In men and women, obesity is related to body mass index, abdominal circumference, and total skinfold thickness. In men only, obesity is also related to abdominal/hip circumference ratio (6).

Body mass index, as an expression of fatness, is positively related to excess mortality. More specifically, obesity is associated with non-insulin-dependent diabetes mellitus, hypertension, hyperlipidemia, osteoarthritis, psoriasis, respiratory insufficiency (including sleep apnea), gallstones, and biliary tract disease (7).

Although obesity is frequently associated with atherogenic factors such as diabetes, hypertension, and hyperlipedemia, a direct relationship between obesity and cardiovascular disease is debated by some authorities (8). Obesity increases blood volume and cardiac output while increasing left ventricular work and heart weight. Hypertrophy of the ventricles, particularly the left ventricle, seems to increase in proportion to the degree of obesity. Conversely, left ventricle hypertrophy may contribute to left ventricle failure (9).

Hyperlipidemia is another risk factor associated with obesity. Obese individuals commonly have elevated serum triglyceride levels and depressed levels of high density lipoprotein cholesterol (HDL-C) (10). The amount of subcutaneous fat has been found to have a significant association with HDL cholesterol in serum. Interestingly, this association had been found to be independent of overall obesity (11).

Insulin resistance seems to be a common finding in the obese (12). It has been proposed that chronic hyperinsulinemia is largely responsible for hunger, cravings and weight gain observed in many obese. This has been attributed to the frequent failures of diet and behavioral modification programs. Epidemiological evidence and animal experimentation support the role of chronic hyperinsulinemia as a major factor in obesity. Chronic hyperinsulinemia changes normal metabolic balances and favors anabolic metabolism; promotes carbohydrate cravings; fosters insulin resistance which further promotes anabolic metabolism; and insulin resistance in turn exacerbates chronic hyperinsulinemia. This cycle maintains excess fat and can override attempts of dietary and behavioral intervention. A program focused on dietary reduction of chronic hyperinsulinemia coupled with appropriate exercise and behavior modification has been recommended to permanently bring down cravings, hunger and body weight (13).

Weight reduction can effectively lower the risk of atherogenesis, restore health, increase life expectancy, and reduce the complications associated with obesity (8). The condition of obesity is a multifactorial in origin, with genetic, metabolic, biobehavioral, and psychosocial factors contributing to an alteration of energy balance control (7). Body fat is reduced when a chronic negative caloric balance exists. Both an increase in caloric expenditure through exercise and a decrease in caloric intake is usually recommended to accomplish this goal. Since it is known that one pound of fat is equivalent to approximately 3500 Calories of energy (4), it may be possible to estimated short term fat loss through a mathematical model.

Sheer weight loss may be challenging to predict since weight loss can vary dependent upon the method of caloric imbalance. For example, fasting and extreme caloric restriction diets can markedly decrease lean body weight and body hydration. In contrast, exercise can induce a negative caloric balance which decreases fat or increases muscle mass in varying magnitudes and proportion. Total caloric expenditure may be affected by other factor such as meal distribution, food sources of calories, absolute caloric intake and basal metabolic rate (4).


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