Genetic versus environmental influences on disease: perspectives from obesity in particular populations

Publisher Summary This chapter reviews the genetic versus environmental influences on disease. Information on disease risks from obesity, possibly the most common of all deviations from the norm, is often conflicting, but there is persuasive evidence of a significant association with maturity-onset diabetes, premature myocardial infarction and hypertension, gallbladder disease, gout, cancer of the uterus, and possibly fatal cancer of the prostate. Obesity clearly occurs in all ethnic groups as do most, if not all, these diseases. There is a growing literature on its familiarity and attempts at defining truly genetic components. This chapter presents a perspective, in the context of race or ethnicity, of how genes may interact with, rather than be an alternative to, environmental stimuli in promoting a chronic disorder. Variety of conventional strategies has been employed to determine the role of genetic variation in obesity. Each has its strengths and limitations. The approaches include the correspondence in weight between monozygous versus dizygous twins, and the correlation in weight between foster children and their adoptive and biological parents, and traditional family investigations. An enzymic defect exists in the obese mouse, a common animal model for obesity in man. There is a loss of thyroid-induced sodium- and potassium-dependent ATP, and the homozygous obese mouse has reduced levels of sodium–potassium ATPase. This observation prompted to look for evidence of reduced energy use in the cells of obese persons since ATP is the principal energy currency of the body.