There is little doubt that disordered gonadotropin economy plays a central role in the pathophysiology of PCOD. However, the nature of the mechanism(s) responsible for altered gonadotropin release remains somewhat controversial. Most importantly, it is difficult to unequivocally determine at this time whether or not the disordered release of gonadotropins is due to a primary central nervous system (for example, hypothalamic) disorder as opposed to constituting a secondary phenomenon reflecting abnormal modulation of gonadotropin release by peripheral glandular input (for example, sex steroids). Regardless of the exact mechanism(s) at play, it is clear that both gonadotropin pulse frequency and amplitude are involved. These alterations combine to produce an overall increase in LH secretion. This hyperactivity, coupled with the apparent secretion of highly bioactive LH molecule(s), is undoubtedly responsible for the intense stimulation of the ovarian androgen-producing cells. It remains to be determined whether this latter phenomenon is consequential to abnormal gonadotropin release or whether it merely represents an epiphenomenon. In contrast, the central role of estrogens in modulating gonadotropin release appears highly likely. However, whether this effect is merely exerted at the level of the pituitary or possibly involves modulation at higher regulatory centers remains the subject of future investigation.