Obesity and Heredity

Type and Genes In some animal species, the shape and size of the individual's body is largely determined by the shape and size of its parents' bodies. Many scientists have explored the role of heredity in determining human body shapes. Some researchers argue that obesity has a strong genetic determinant (it tends to run in families). They cite statistics showing that 80 percent of children having two obese parents are also obese. But why is this the case? Can you really blame your parents for your problems with weight? • Twin Studies Studies of identical twins who were separated at birth and raised in different environments have provided us with some of the most conclusive evidence to date that obesity may be an inherited trait. Whether raised in family environments with fat or thin family members, twins with obese natural parents tend to be obese in later life. According to another study, sets of identical twins who were separated and raised in different families and who ate widely different diets still grew up to weigh about the same. So, if you are overweight, you cannot blame it all on your parents for overfeeding you as a child. These studies contain the strongest evidence yet that the genes a person inherits are the major factor determining overweight, leanness, or average weight. Although the exact mechanics remain unknown, it is believed that genes set metabolic rates, influencing how the body handles calories. Some experts believe that this genetic tendency may contribute as much as 25 to 40 percent of the reason for being overweight. • Specific Obesity Genes? In the past decade, more and more research has pointed to the existence of a special "fat gene." The most promising candidate is the Db gene (for obesity), which is believed to disrupt the body's "I've had enough to eat" signaling system and may prompt individuals to keep eating past the point of being comfortably full. Research on Pima Indians, who have an estimated 75 percent obesity rate and nine in ten who are overweight, seems to point to an Ob gene that is a "thrifty gene." It is theorized that because their ancestors had to struggle through centuries of famine, their ancestor's basal metabolic rates slowed, allowing them to store precious fat for survival. They may have passed these genes on to their children, explaining the lower metabolic rates found in Pimas today and their greater propensity for obesity. Scientists have found that they can manipulate mice genes and construct an Ob gene that will invariably lead to fatness in mice and to the development of diabetes II. Many suspect a human counterpart to this gene, but an actual gene formation has yet to be found. In addition, the (Beta)-3 adrenergic-receptor gene has been identified and found in human beings and mice. When mutated, it is thought to impede the body's ability to bum fat. Although the 1994 discovery of the Ob gene has provided fertile ground for speculation, researchers have since further refined their theories to focus on a protein that the Ob gene may produce, known as Leptin, and a new leptin receptor in the brain. According to these studies, leptin is the chemical that signals the brain when you are full and need to stop eating. Although obese people have adequate amounts of leptin and working leptin receptors, they do not seem to work properly, much like with the diabetic who has adequate insulin but is not able to utilize it properly. Another group of scientists appear to have isolated a more direct route to appetite suppression, a protein called GLP-l, which is known to slow down the passage of food through the intestines to allow the absorption of nutrients. When scientists injected GLP-l into the brains of hungry rats, the rats stopped eating immediately. Are leptin and GLP-l key factors in appetite suppression? It is speculated that leptin and GLP-l might play complementary roles in weight control.