Genetic Influences on Body Weight
How many overweight or obese individuals have developed their condition as a result of a major deficiency in one gene? How many are overweight or obese as a consequence of a strong genetic predisposition determined by DNA sequence variation at several genes? How many have only a slight genetic predisposition but have gained large amounts of body weight because they have poor nutritional habits and a sedentary lifestyle? How many do not have any genetic susceptibility but have nonetheless become overweight or obese? We cannot yet answer these questions, but in recent years, genetic epidemiology and molecular genetic studies have begun to generate data that allow us to formulate these questions in more relevant terms and to sketch some answers. This chapter examines the genetic epidemiology of the obesity epidemic. The molecular genetic issues are addressed in Chapter 5.
C. B. Davenport, from the Carnegie Institute, described in 1923 the first comprehensive attempt to understand the role of inheritance in human body mass for stature. Among his findings were that normal-weight parents sometimes have obese adult offspring, and that obese parents frequently have normal-weight adult descendants. In the aggregate, however, his study demonstrated that body mass index (BMI) values were more similar among family members than among unrelated persons.
Except for some rare Mendelian disorders, the vast majority of obese patients do not exhibit a clear pattern of Mendelian inheritance. Despite many studies on the familial aggregation and heritability of the obesity phenotypes, there is no unanimity among researchers regarding the importance of genetic factors.
Heritability is the fraction of the population variation in a trait (e.g., BMI) that can be explained by genetic transmission. It has been considered in a large number of twin, adoption, and family studies. The results depend on sampling strategy, sample size, and