There is little doubt that heredity has a role to play in determining weight, but how large a part is still being debated. There is considerable evidence for a genetic predisposition to obesity. Identical twins are twice as likely to have a similar height-to-weight ratio, or Body Mass Index (BMI), then are non-identical twins. Studies show a relationship between the BMI of adult adoptees and their biological parents, but there is no correlation with their adoptive parents.
Genetic factors recently there has been much excitement about the discovery of a genetic fault in some mice that causes obesity. The genetic fault means that the mice do not produce enough of a protein called leptin which appears to help control weight. A similar gene has been identified in humans but the theory is complicated by the fact that obese people have more leptin in their blood than thin people. This suggests that in humans the leptin being produced is not working effectively, whereas in obese mice insufficient leptin is produced.
This protein could be the previously unknown factor released from fat identified in the Lipostat Theory. Although human trials of leptin have already begun, even if they are successful, it will be many years before this leads to a new treatment for obesity.
Moreover, there is probably no single gene that causes obesity in humans. Rather, a combination of genes is involved which makes identification much more difficult and makes it unlikely that anyone's treatment will help everyone.
One of the discoveries made recently is that the nourishment a fetus receives may affect that person's health in later life. Professor David Barker and his team in Southampton in the early 1990s studied birth records, such as birth weight and length, of a group of people born in Herefordshire from 1911 onwards. They were able to trace these people as adults and record their state of health, or discover their cause of death. The results showed that babies who are born at full term but are lighter than expected, have more health problems later on in life. One theory for this is that the mother's poor diet may cause a decrease in the number of cells formed in the pancreas, thus putting the baby at risk later of diabetes. The baby may also adapt to its poor diet by becoming very efficient at storing nutrients, and later in life, this may lead to a greater risk of diabetes and heart disease. An increased risk of obesity might also result, although this has not yet been shown Not all studies, however, show the same effect. There is probably an interplay between genetic susceptibility to disease, the baby's environment in the womb, and other events later in life that together determine the likelihood of chronic illnesses. Rehan Riaz Merchant about lifestyle and weight