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• Highlights
• Introduction
• Biologic and Medical Causes
• Cultural and Emotional Causes
• Risk Factors
• Complications
• Weight Loss and Maintenance
• Weight Management
• Medications
• Other Treatments
• Resources
• References

Weight control and diet

Description

An in-depth report on losing and managing weight safely for health benefits.

Alternative Names

Dieting; Obesity; Weight loss

Biologic and Medical Causes

Obesity results when a person consumes more calories than energy. Several different factors may influence weight gain.

About 90% of people who lose weight through dieting gain every pound back regardless of their weight-loss method.

Some evidence suggests that every person has an inherited weight range that varies by only about 10% either up or down from some set point. For instance, a man whose "genetically-determined" weight is 200 pounds would tend to swing from 180 to 220 pounds. He would be unlikely to lose or gain more than this.

Genetic factors that influence fat metabolism and regulate the hormones and proteins that control appetite may play some part in 70 - 80% of obesity cases.

The Biologic Pathway to Appetite

Appetite is determined by processes that occur both in the brain and gastrointestinal tract. Eating patterns are controlled by areas in the hypothalamus and pituitary glands. The body produces a number of molecules that stimulate or suppress appetite. In some cases, the following factors may produce imbalances in this process:

• Insulin. Insulin is a hormone that helps change blood sugar (glucose) into energy. During digestion, carbohydrates from our diet break down into different types of sugar molecules (including glucose). Proteins from ones diet break down into smaller molecules called amino acids . Immediately after eating, blood glucose levels rise. This triggers the release of insulin, which pours into the bloodstream. Insulin pushes the glucose and amino acids into cells and muscles. Insulin and other hormones determine which nutrients will be burned for energy or stored for future use. The inability to use insulin efficiently (insulin resistance) has been associated with both obesity and diabetes.
• Leptin . Leptin is a hormone that is released by fat cells. Some think this hormone may also be released by cells in the stomach. Leptin appears to play an important role in insulin resistance and fat storage in the body, but its role in obesity is unclear. The most likely scenario is that  leptin levels rise as more fat is stored in the cells. This increase curbs appetite. Falling levels of leptin make you feel hungry. In people who have genetically lower levels of leptin, however, the brain may be tricked into thinking that it is always starving because there is no leptin to suppress appetite. This can lead to gain weight.
• Resistin. Resistin is a hormone produced by fat cells that makes the body resistant to insulin activity. Some experts believe it may help explain the role of obesity in diabetes type 2.
• Intestinal Chemicals.  Ghrelin is a chemical produced in the stomach. It appears to be important in triggering the desire to eat. Peptide YY3–36 (PYY) is a substance secreted in the intestines after a meal. The level of PYY is proportionate to the number of calories a person eats. PYY tells the brain that you feel full. Deficiencies in these substances may contribute to some cases of obesity. Researchers are hoping that blocking ghrelin or infusing PYY may be possible therapies for obesity.
• Other Chemicals. Many brain chemicals are being studied for their role in appetite stimulation and weight gain. Among them are neuropeptide Y, melanocortins, agouti-related protein, and melanocyte stimulating hormone. Pain-relieving chemicals called endorphins may be critical in reducing appetite and regulating energy use. Cholecystokinin, a hormone released in the upper intestine that stimulates digestive juices, may work to control meal size.

Specific Genetic Factors

Genetics may directly contribute to severe obesity in people with family histories of the problem. Genetic factors such as slow metabolisms may also make people more prone to being overweight. At least seven genetic mutations have been associated with specific and uncommon cases of severe obesity. Some are outlined below.

• HOB1 (human obesity 1) is a gene that is linked to a high BMI in women.
• Leptin gene variants have been linked to leptin deficiencies and obesity.
• Melanocortin-4 receptor is a gene that helps turn off the urge to eat. It may not work properly in those with a family history of obesity.
• Researchers have also identified a mutation in a gene for a protein called proopiomelanocortin, which results in a syndrome of obesity, red hair, and deficiencies in stress hormones.
• About 5% of severely obese people have mutations that over respond to agouti-related protein.

Genetics also determine the number of fat cells a person has. Some people are simply born with more. It should be noted that even when genetic factors are present, a person can still control their diet.

The Thrifty Gene. Some experts think the existence of a so-called "thrifty" gene regulates hormonal fluctuations to accommodate seasonal changes. Theoretically, it works in the following manner:

• In certain populations, hormones are released during seasons when food supplies have traditionally been low. This leads to insulin resistance and increased fat storage.
• The process is reversed in seasons when food is readily available.
• Because modern industrialization has made high carbohydrate and fatty foods available all year long, the gene no longer serves a useful function. Fat, originally stored for famine situations, is not used.

Such a theory could explain the high incidence of type 2 diabetes and obesity found in Pima tribes and other Native American tribes with nomadic histories and Western dietary habits. In the past, the traditional low-fat high-fiber foods (corn, lima beans, white and yellow teparies, mesquite, and acorns) of the Pima people may have protected them from obesity and type 2 diabetes. But today, they now have a high incidence of such disease.

Although genetic abnormalities may make it harder or easier to lose weight, the prevalence of obesity has dramatically increased over the past two decades, and genes cannot have changed within that short amount of time. Human metabolism evolved so that it could conserve energy and store fat during times of famine. Most cases of obesity now occur in people with normal body function who live in industrialized nations where food is overly plentiful.

Medical or Physical Causes of Obesity

A number of medical conditions may contribute to being overweight, but rarely are they a primary cause of obesity.

• Hypothyroidism is sometimes associated with weight gain. But, patients with an underactive thyroid generally show only a moderate weight increase of five to 10 pounds.
• Very rare genetic disorders, including Froehlich's syndrome in boys, Laurence-Moon-Biedl, and the Prader-Willi syndromes, cause obesity.
• Abnormalities or injury to the hypothalamus gland can cause hypothalamic obesity.
• Cushing's disease is a rare condition caused by high levels of steroid hormones. It results in obesity, a moon-shaped face, and muscle wasting.
• Obesity is also linked to polycystic ovarian syndrome, a hormonal disorder in women.

Effects of Certain Medications

Some prescription medications contribute to weight gain, usually by increasing appetite. Such drugs include the following:

• Corticosteroids
• Female hormone treatments, including some oral contraceptives (usually temporary) and certain progestins (such as Megestrol) used to treat cancer
• Antidepressants and anti-psychotic drugs, including lithium and valproate
• Insulin and insulin-stimulating drugs used to treat diabetes often leads to weight gain, a particularly unfortunate conflict of interest for obese individuals with type 2 diabetes

You should not stop taking any medications without your doctor's knowledge.

• Review Date: 3/29/2006
• Reviewed By: Harvey Simon, MD, Editor-in-Chief, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital

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