HYPOTHESIS These observations have led to a new hypothesis for the etiology of PCOS; genetic variation resulting in hyperandrogenemia leads to many of the reproductive and metabolic features of PCOS later in life. We will directly test the hypothesis that there is an excess androgen production in female offspring of women with PCOS. Further, we will test whether A8(+) female offspring have more profound changes in these parameters (increased androgen and/or decreased insulin levels in fetal life and in infancy) compared to A8(-) female offspring.