An elevated level of male hormones in your body can lead to infertility, excessive facial or body hair, hair thinning, acne and other problems associated with PCOS. The male hormone we mostly hear about is testosterone. However, the real culprit is dihydrotestosterone, or DHT. DHT is the biologically active form of testosterone. DHT is formed when testosterone interacts with an enzyme called 5-alpha-reductase.A recent study at the University of Birmingham in the UK showed that both overweight and normal-weight women with PCOS had higher 5-alpha-reductase activity than women who did not have PCOS.In other words, if you have polycystic ovary syndrome, it appears you also have a tendency for higher 5-alpha-reducase activity, when in turn makes it easier for you to convert testosterone into the undesirable DHT. The excessive levels of DHT in turn create some of the distressing symptoms of PCOS such as hair loss or facial and body hair growth.You can suppress 5-alpha-reductase activity with supplements or pharmaceuticals.One example of a supplement is saw palmetto extract, which inhibits 5-alpha-reductase. It is extracted from the berry of a small palm tree. The fruit of this palm have been part of the diet of natives of the south-eastern U.S. for hundreds of years. Saw palmetto extract does not have the side effects that pharmaceuticals may have.Pharmaceuticals commonly used to inhibit 5-alpha-reductase include spironolactone (Aldactone), and finasteride (Propecia, Proscar).Increased 5{alpha}-reductase activity and adrenocortical drive in women with polycystic ovary syndrome.Vassiliadi DA, Barber TM, Hughes BA, McCarthy MI, Wass JA, Franks S, Nightingale P, Tomlinson JW, Arlt W, Stewart PM.Centre for Endocrinology, Diabetes and Metabolism, University of BirminghamContext: Polycystic Ovary Syndrome (PCOS) is characterized by hyperandrogenism, anovulation and susceptibility to the metabolic syndrome. Altered peripheral cortisol metabolism has been reported in PCOS but also in simple obesity. Objective: To describe cortisol metabolism and metabolic characteristics of a large PCOS cohort and to delineate the effect of obesity by comparison to BMI-matched controls. Design: Observational, cross-sectional study. Setting: Outpatient clinics of two secondary/tertiary care centres Patients or Other Participants: 178 PCOS patients fulfilling Rotterdam criteria and 100 BMI-matched controls. Intervention: 24-h urine collection for steroid metabolite excretion, fasting blood samples followed by an OGTT. Main Outcome Measures: Urinary steroid metabolites including glucocorticoids and androgens and the ratios reflecting enzymatic activities involved in peripheral cortisol and androgen metabolism, 5alpha-reductase and 11beta-hydroxysteroid dehydrogenase type 1 and 2. Circulating levels of glucose, insulin, DHEA, DHEAS and testosterone, calculation of HOMA. Results: Total androgen metabolites were higher in PCOS compared to BMI-matched controls (4105+/-2047 vs. 2532+/-1610 microg/24h for the non-obese, 5547+/-2911 vs. 2468+/-1794 microg/24hr for the obese, both p < 0.001). Total glucocorticoid metabolites were higher in obese PCOS vs. controls (10786+/-3852 vs. 8834+/-4487microg/24hr, p=0.001). 5alpha-reductase activity correlated with BMI, insulin levels and HOMA. Both obese and non-obese PCOS patients had higher 5alpha-reductase activity than controls (all p<0.05). 11beta-hydroxysteroid dehydrogenase activities did not differ between PCOS and controls. Conclusions: PCOS is associated with enhanced androgen and cortisol metabolite excretion and increased 5alpha-reductase activity that cannot be explained by obesity alone. Increased adrenal corticosteroid production represents an important pathogenic pathway in PCOS.J Clin Endocrinol Metab. 2009 Jun 30.PMID: 19567518