Obesity

                                                   

                                                                                             

            Obesity is defined qualitatively as the storage of excess fat in the body, particularly under the skin and around certain internal organs.  Excessive body fat is stored in adipocytes.  An adipocyte (fat cell) is a cell containing a glistening oil droplet composed almost entirely of neutral fat (triglycerides).  The droplet occupies most of the cell's volume, compressing the nucleus to one side.  Mature adipocytes are among the largest cells in the body.  Although they can take up and release fat, becoming plumper or more wrinkled respectively, they are fully specialized for fat storage and are unable to divide.

            Obesity, which is considered to be is the number one nutritional problem in the United States (Reed, 1980), usually results from a positive energy balance and not having a well-balanced, nutritional diet.  Obesity often begins early in childhood as evidenced by the fact that 30-60% of American children are considered to be obese.  The San Jose Mercury News (November 13, 1992) reported that children's metabolism rates drop 40% faster while they are watching television than it does while they are merely sleeping.  Interestingly, as little as 2.5 hours of television per day impacts their metabolic rate enough to produce weight gain.  Childhood obesity often has long-term consequences as obese children are three times more likely to be obese adults than normal weight children.  Alarmingly, both childhood obesity and adult obesity appear to be on a continual rise in the United States (Nieman, 1993; Weight Watchers:  We weigh a bit more, 1978).

            Many authorities use total body weight as an indicator of obesity,  but obesity is not quite the same as being overweight.  It is generally agreed that obesity exists when percent body fat is greater than 25% in males and 30% in females (Body composition:  A round table, 1986).  By this definition it is possible to be obese without being overweight.  Conversely, athletes may be overweight for their height because of muscular development, without being obese.

            In terms of percent body fat, optimal health exists when body fat ranges from 10-25% in males and 18-30% in females, although optimal fitness ranges may be slightly lower in both genders (Body composition:  A round table, 1986).  The existing gender differences in percent body fat are due to differences in essential or minimal body fat levels, which are approximately 4% in males and 8-12% in females (Body composition:  A round table, 1986).  The gender differences in essential body fat levels are primarily due to differences in secondary sexual characteristics occurring at the onset of puberty.   

Kinds of Obesity

            The two general types of obesity are: (1) childhood (juvenile) onset obesity, or hyperplastic obesity; and (2) adult (maturity) onset obesity, or hypertrophic obesity.  Childhood (juvenile) onset obesity, or hyperplastic obesity, is characterized by an increase in both the total number and size of adipocytes (fat cells) prior to early adulthood (McArdle et al., 1991; Oscai, 1973).  Hyperplastic obesity often has a carryover into adulthood as reductions in fat weight during adulthood is due to a decrease in fat cell size with minimal changes, if any, in the number of fat cells (McArdle et al., 1991; Oscai, 1973).  Further, research indicates that massive obesity is related more to a person having a greater number of fat cells than to having larger fat cells (McArdle,1991; Oscai, 1973).  When children and adolescents become obese, they are creating new adipocytes as well as enlarging existing adipocytes.  When children and adolescents lose fat weight, there appears to be a decrease in the number of fat cells as well as a shrinkage in adipocyte size, which may have far

reaching implications in terms of preventing the development of severe obesity (Oscai, 1973).

            Adult (maturity) onset obesity, or hypertrophic obesity, is characterized by an increase in the size of existing adipocytes without an increase in the number of adipocytes (McArdle, 1993).  When adults become obese, they are enlarging or increasing the size of existing adipocytes rather than creating new adipocytes.  When adults lose weight, there is a shrinkage in adipocyte size with no change in the number of adipocytes.

            Since childhood (juvenile) onset obesity potentially has a strong carryover to adulthood, overweight children have a greater likelihood of being overweight adults than normal weight children.  Consequently, overweight children may have a more difficult time maintaining ideal body weight throughout life because of the greater number of adipocytes than normal weight children.  Further, research suggests that overweight adults who have a greater number of adipocytes may have a more difficult time losing excess body fat than similar overweight adults who have fewer adipocytes (Bray, 1990).

Causes of Obesity

            Obesity often results from the interaction of many factors including a long-term, positive caloric balance, genetics, environmental factors and social influences as well as gender and racial differences.  Whereas as only 5% of the obesity in the United States is attributable to metabolic disorders, 95% is attributable to regulatory factors (Reed, 1980). 

            Behavioral causes underlying regulatory causes of obesity include (1) excess caloric consumption due to the easy availability of food, (2) association of food with emotional responses, (3) social and cultural pressures of food consumption, (4) body image and self-perception, (5) eating patterns, (6) food packaging and marketing, and (7) lack of daily physical activity (Reed, 1980).  The increase in body fat associated with aging appears primarily to be a function of the decline in physical activity, as the excessive weight gain throughout life often closely parallels a reduction in physical activity rather than an increase in caloric intake.

            Recent research argues rather convincingly that biochemical differences due to genetics appear to underlie many of the regulatory as well as metabolic causes of obesity (Powers & Scott, 1990) and hence, genetics may be the most important factor in the development of obesity. Although overweight individuals are generally observed to be less physically active, it is difficult to conclusively establish that overweight individuals actually eat more, on the average, than normal weight individuals.  Therefore, the primary etiology of obesity may have a strong genetic basis.

             

Consequences of Obesity

            Obesity per se is not only considered a medical problem, it causes or contributes to many other serious medical problems such as those listed below (Fox et al., 1993; Garfinkel & Coscina, 1990; Reed, 1980; McArdle et al., 1991).

 

1.      Diabetes mellitus (impaired carbohydrate metabolism).           

2.      Hypertension (high blood pressure).        

3.      Cardiovascular diseases.                           

4.      Stroke.                                                            

5.      Respiratory ailments.                                   

6.      Elevated blood lipid (cholesterol and triglyceride) levels.

7.      Kidney disease and gall bladder disease (e.g., gall stones).

8.      Surgical risk.                                     

9.      Pregnancy problems.

10.    Lower resistance to infections.

11.    Several endocrine disorders.

12.    Mechanical difficulties (e.g., damage to weight bearing joints).

13.    Decreased longevity.

14.    Social discrimination and psychological and emotional problems.

            Cardiovascular disease is the number one cause of death in the United States (McArdle, 1991).  Most medical authorities are convinced that obesity is an independent and powerful heart disease risk factor that may be equal to that of smoking, elevated blood lipids, diabetes mellitus, and hypertension (Body composition:  A round table, 1986; McArdle et al., 1991). 

            In the longitudinal Framingham Study, for every 10% increase in body

weight, systolic blood pressure increased by 6.5 mmHg, serum cholesterol

increased by 12.5 mg/dl, and blood glucose increased indicating impaired carbohydrate metabolism (Kannel, 1976).  On the other hand,  reduction in excess body weight resulted in equivalent reductions in these medical abnormalities (Kannel, 1976).  Hence, reductions in excess body weight and fat can substantially reduce the risk of many life-threatening diseases.