Obesity
An excess in body fat—typically 20% above desired body weight and a body mass index (BMI) of 30 or greater—is considered obese. Morbid obesity is defined as a BMI greater than 40, or weight more than 100 pounds greater than the patient’s ideal body weight.
Weight gain occurs when more energy is consumed than spent, and the excess is stored in the fat cells of the adipose tissue. The amount of fat stored in the body reflects the number and size of the fat cells. The number of fat cells increases most rapidly during late childhood and early puberty; therefore, prevention of obesity is critical during these years.
Obesity develops when fat cells increase in number or size—or, most often, in both. Hyperplastic obesity is an increase in the number of fat cells. Hypertrophic obesity is an increase in the size of the fat cells. In weight loss, fat cells diminish in size, but the number of fat cells remains the same.
Despite widespread preoccupation with body image and weight loss, the prevalence of obesity continues to increase in the United States; more than 50% of Americans are overweight. The incidence of obesity is increasing among American children as well as adults; 1 in 5 American children are overweight. Complications arising from obesity are the second-leading cause of preventable death.
Causes
Obesity has many interrelated causes, including genetics, environment, culture, metabolism behavior, and psychological influences. Caloric intake that exceeds energy expenditure is considered to be the primary cause of obesity. However, studies indicate that genetics plays a role in determining susceptibility to obesity because inherited factors may influence nutritional intake, attitudes toward food, activity levels, and metabolic rates.
Researchers have identified an obesity gene, ob, which is found in fat cells. The gene contains code for leptin, a protein with hormonal properties. Leptin acts on the hypothalamus by suppressing appetite and increasing energy use. Changes in energy use reflect changes in basal metabolism and may result in increased physical activity. Serum leptin levels often correlate with body fat—a high percentage of body fat is accompanied by a high level of leptin. Obese individuals typically have high leptin levels. Research has uncovered some mechanisms for the regulation of leptin, but research continues in this area.
High-fat fast foods constitute a significant environmental factor in the development of obesity because they’re pervasively advertised, readily available, and low in cost. Technologies that decrease or eliminate the need for physical activity lead to decreased energy consumption, which in turn contributes to weight gain. Socioeconomic status, psychological factors, abnormal absorption of nutrients, impaired actions of the GI tract and growth hormones, and hypothalamic dysfunctions of the hunger and satiety centers have also been implicated in the development of obesity.
Complications
Obesity can result in the development of chronic health conditions, such as diabetes,
metabolic syndrome, hypertension, cardiovascular disease, renal disorders, psychological disorders, sleep apnea, osteoarthritis, cancer, gallbladder disease, and respiratory disorders. Patients who are obese are at greater risk for complications during pregnancy and surgery, and for premature death. (See Understanding metabolic syndrome.)
metabolic syndrome, hypertension, cardiovascular disease, renal disorders, psychological disorders, sleep apnea, osteoarthritis, cancer, gallbladder disease, and respiratory disorders. Patients who are obese are at greater risk for complications during pregnancy and surgery, and for premature death. (See Understanding metabolic syndrome.)
Understanding metabolic syndrome
Metabolic syndrome—also called syndrome X, insulin resistance syndrome, dysmetabolic syndrome, and multiple metabolic syndrome—is a cluster of conditions characterized by abdominal obesity, high blood glucose (type 2 diabetes mellitus), insulin resistance, high blood cholesterol and triglycerides, and high blood pressure. More than 22% of people in the United States meet three or more of the criteria for metabolic syndrome, increasing their risk of heart disease, stroke, and death due to myocardial infarction. Metabolic syndrome was first defined in the Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults on May 15, 2001. The disorder commonly goes unrecognized.
In the normal process of digestion, food is broken down in the intestines into basic components. One such component, glucose, provides energy for cellular activity. Insulin, a hormone secreted in the pancreas, guides excess glucose into storage cells for future use.
In metabolic syndrome, glucose doesn’t respond to insulin’s attempt to guide it into storage cells. Excess insulin is released to overcome this resistance; the excess results in damage to the lining of the arteries, promotion of fat storage deposits, and prevention of fat breakdown. This series of events can lead to diabetes, blood clots, and coronary artery problems.
Abdominal obesity is a strong predictor of metabolic syndrome because intra-abdominal fat tends to be more resistant to insulin than fat in other areas of the body. Insulin-resistant fat increases the release of free fatty acid into the portal system, leading to increased apolipoprotein B, increased low-density lipoprotein (LDL), decreased high-density lipoprotein (HDL), and increased triglycerides. As a result, the risk of cardiovascular disease is increased.
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