This chapter has reviewed the evidence for obesity being characterized by distinct patterns of hormonal changes related to both the degree of obesity and the distribution of fat tissue. Many of these changes are also seen in subjects with Cushing's and polycystic ovary syndromes, in particular hyperinsulinaemia, alterations in adrenocortical activity and sex steroid secretion and binding. Animal models of obesity provide evidence to suggest the possibility of a primary abnormality of hypothalamic-pituitary function as a basis to corpulence and this cannot be excluded in the human situation. Nevertheless, abdominal distribution of adiposity plays a significant role in establishing a vicious cycle of metabolic events which may perpetuate both the obese state and PCOS. It is of interest that the additive genetic effect for total body fat is about 25% whereas the heritability of subcutaneous truncal-abdominal fat is about 30-35%, and may possibly be higher (Bouchard et al, 1993). Upper body obesity is characterized by large adipose cells with higher LPL activity, elevated basal and stimulated lipolysis but a low antilipolytic effect of insulin. The results from preliminary investigations of potential candidate genes suggest a possible genetic basis to hyperinsulinaemia/insulin resistance found in upper body obesity but further studies of greater numbers are required for confirmation. It is hoped that the findings from such molecular studies will shed additional light on both the genetic background to obesity and the complex hormonal alterations seen at the tissue level. This should provide the confirmation of a unifying theory for the causal factors associated with obesity and related conditions.