Sexual Function and Gonadal Hormones in Patients Taking Antipsychotic Treatment for Schizophrenia or Schizoaffective Disorder

Oliver D. Howes, M.R.C.Psych.; Michael J. Wheeler, M.R.C.P.; Lyn S. Pilowsky, Ph.D.; Sabine Landau, Ph.D.; Robin M. Murray, D.Sc.; and Shubulade Smith, M.R.C.Psych.

Objective: To determine rates of sexual dysfunction and hypogonadism and establish the relationship between gonadal hormone levels and sexual function in patients taking antipsychotic treatment for schizophrenia or schizoaffective disorder.

Method: We studied 103 patients with schizophrenia or schizoaffective disorder (mean age = 46.2 (SD = 12.9) years; 51.5% male) from October 2003 through March 2005. Sexual function was assessed using the Sexual Functioning Questionnaire (SFQ) and compared with (1) normal controls (N = 62; mean age = 36.1 (SD = 9.6) years; 55% male) recruited from primary care attendees and (2) sexually dysfunctional controls recruited from a local sexual dysfunction clinic (N = 57; mean age = 39.1 (SD = 10.7) years; 79% male). Prolactin, sex hormone-binding globulin, testosterone, estradiol, progesterone, follicle-stimulating hormone, and luteinizing hormone levels; psychopathology; and side effects were measured.

Results: Mean (SD) total SFQ scores were significantly greater in patients (women = 9.9 [5.3]; men = 7.8 [4.9]) compared with normal controls (women = 4.1 [2.9]; men = 4.09 [2.95]), and similar to the scores of sexual dysfunction clinic attendees (women = 7.2 [2.9]; men = 9.9 [4.5]). The odds ratios of patients having sexual dysfunction compared with normal controls were 15.2 for women and 3.7 for men. Hypogonadism was common (in premenopausal women, 79% showed hypoestrogenism and 92% showed low progesterone levels, and 28% of men showed hypotestosteronism). There was no association between total SFQ scores and prolactin or gonadal hormone levels.

Conclusion: Patients receiving treatment for schizophrenia or schizoaffective disorder show high rates of sexual dysfunction and hypogonadism. Sexual functioning was not related to prolactin or gonadal hormone levels.

(J Clin Psychiatry 2007;68:361-367)

Received Feb. 28, 2006; accepted Aug. 4, 2006. From the Institute of Psychiatry (Drs. Howes, Pilowsky, Murray, and Smith); the Department of Chemical Pathology, St. Thomas' Hospital (Dr. Wheeler); and the Department of Biostatistics, the Institute of Psychiatry (Dr. Landau) London, United Kingdom.

Funded by an investigator-led charitable research grant from AstraZeneca, London, United Kingdom.

This study has not been previously presented or published.

Dr. Murray's department has received his lecture fees and research grants from most major pharmaceutical companies; Dr. Murray has received grant/research support from Eli Lilly; has received honoraria from Eli Lilly, Janssen, and AstraZeneca; and serves on the speakers or advisory boards for Bristol-Myers Squibb and GlaxoSmithKline. Dr. Smith has received grant/research support from AstraZeneca; has received honoraria from Bristol-Myers Squibb, Otsuka, and Eli Lilly; and serves on the speakers or advisory boards for Eli Lilly and AstraZeneca. Drs. Howes, Wheeler, Pilowsky, and Landau report no other financial relationships relevant to this article.

Corresponding author and reprints: Oliver D. Howes, M.R.C.Psych., Institute of Psychiatry, Box 67, De Crespigny Park, London, SE5 8AF, U.K. (e-mail: O.Howes@iop.kcl.ac.uk).