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).