It is abundantly clear that a number of subtle abnormalities in hypothalamic function are associated with human obesity. Some hormonal abnormalities-the diminished growth hormone responses, for example-are critically dependent on increased caloric intake and are quickly reversible with weight loss. Others, such as the blunted prolactin response to acute hypoglycemia, may persist in the reduced-obese state. Still others (e. g. , the blunted ACTH responses to insulin­ induced hypoglycemia) may, in some patients, first appear in the reduced-obese state. It remains uncertain whether any of these abnormalities is ever antecedent to the presence of obesity. Obviously, it is difficult to plan experiments in which the amounts of stored triglyceride, the level of caloric intake, and the state or his­ tory of obesity can all be individually evaluated. The issue is made even more complex by the fact that there may be subgroups of obese in whom hypothalamic function may be abnormal, whereas many obese may have nearly normal hypo­ thalamic function. It should be remembered that for years clinicians and investigators, working with available research tools, have ruled out pituitary or hypothalamic abnor­ malities as a cause of human obesity. These tools have oftentimes been no more sophisticated than skull roentgenograms and samples of excreted steroid hormones in 24-hr urine. The advent of radioimmunoassays for peptide hormones and the availability of synthetic releasing hormones have offered possibilities of studying hypothalamic function undreamed of just a few years ago.