Genetic factors that include thousands of different genes contribute to 40 to 70 percent of obesity. Obesity, according to the Obesity Medicine Association, is not a personal choice. It is a complex interplay of genetics, environment, and other factors. The Obesity Medicine Association regards obesity as a medical disease that occurs when a person’s body accumulates and stores excessive body fat.

But as in most genetic-related ailments, possessing such genes only predisposes the individual towards the emergence of that ailment; it is not a definitive outcome of these genes. Epigenetics is responsible for the increased susceptibility of an individual to obesity. External exposures during critical development periods can alter the profile of epigenetic marks and result in obesity. (Herrera et al., 2011)

There are critical periods in people’s lives when there is an increased risk for the onset of obesity. These periods are the prenatal stage, at ages 5 to 6 years, called the age of adiposity rebound, and adolescence. (Dietz, 1994) Prevention of obesity starts in childhood. Lower birth weight seems to be associated with later risk for central obesity. It confers increased cardiovascular risk, which is probably occurring through changes in the hormone systems. (Oken et al., 2003)

Pregnancy and the immediate period post-childhood are also when mothers are likely to become obese. Post-childbirth lifestyle behavior has an impact on weight gain. Spending extended periods watching television leaves little time for mothers to walk, leading to weight gain. (Oken et al., 2007)

Data for the BMI of Americans between the ages of 50 to 60 shows a gradual increase, while a decline in body weight and BMI occurs in the age group between 70 and 80. (IOM, 1995) Several studies have noted that body fat increases with age, and muscle loss occurs, even after controlling body weight changes and physical activity. (Baumgartner et al., 1995) Skeletal body mass declines from the 3rd decade of life onwards. (Dutta et al., 1995) The rates of decline are higher in women after menopause. (Aloia et al., 1991)

While genetics play a role in determining a person’s susceptibility to obesity, the same is responsible for this condition are still not fully understood.

Here are a few examples of genetics and the development of obesity:

  1. Leptin resistance: Leptin is a hormone that regulates hunger and metabolism. A genetic variation that leads to a reduced sensitivity to leptin has been linked to obesity.
  2. Insulin resistance: Some people may have a genetic predisposition to insulin resistance, which can lead to obesity and type 2 diabetes.
  3. Melanocortin-4 receptor (MC4R) gene: The MC4R gene regulates appetite and metabolism. Mutations in this gene have been linked to obesity.
  4. FTO gene: The FTO (fat mass and obesity-associated) gene has been strongly linked to obesity. This gene regulates energy balance and controls food intake and energy expenditure.
  5. Adrenergic receptors: The adrenergic receptors are involved in regulating metabolism. A genetic variation in these receptors has been linked to obesity.


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