Neuroendocrine Dysfunction

Although most OCD investigations concentrate on hormonal aberrations as secondary rather than primary to the disorder, case reports and anecdotal experience suggest that hormonal dysfunction and OCD may be etiologically related (Swedo, 1989). OCD symptoms often begin during early puberty, and some female patients experience an increase in obsessive thoughts and rituals immediately before their menses. Other hints at an influence of gonadal steroid on obsessive-compulsive symptomatology include the increased frequency of OCD during the postpartum period (Rasmussen and Eisen, 1992) and reports of successful antiandrogen therapy for obsessive-compulsive symptoms (Casas et al., 1986). In the latter study, 5 out of 5 patients with OCD experienced a remission in their symptoms following treatment with cyproterone acetate, a potent antiandrogen. At the NIMH, two boys (ages 8 and 15) and a 14-year-old girl were treated with spironolactone, a peripheral antiandrogen (particularly antitestosterone) agent, and testolactone, a peripheral antiestrogen medication. All experienced a temporary reduction of obsessions and compulsions but relapsed within 3 to 4 months (Salzberg and Swedo, 1992).

Leckman and colleagues (1994) have suggested that oxytocin abnormalities may be involved in OCD. The investigators cite oxytocin-mediated mating behaviors in animals as a possible model for some OCD symptoms (Leckman and Mayes, 1999) and found abnormal concentrations of cerebrospinal fluid (CSF) oxytocin among a small group of children with OCD and tic disorders. In a larger group of 43 children and adolescents studied at the NIMH, CSF oxytocin levels were not significantly correlated with OCD severity but were correlated with depressive symptoms (Swedo et al., 1992). Interestingly, arginine vasopressin (AVP) concentrations decreased following treatment with clomipramine (Altemus et al., 1994), although baseline concentrations had shown a negative correlation with symptom severity (Swedo et al., 1992). In adult patients with OCD, significantly increased CSF AVP concentrations at baseline were found, and it was noted that patients secreted significantly more AVP into plasma in response to hypertonic saline than did controls (Altemus et al., 1992). The latter results are in keeping with Barton's (1987) observations of OCD among patients with diabetes insipidus, a disorder with elevated central AVP concentrations.

At present, there is not sufficient evidence to implicate hormonal dysfunction as a direct cause of OCD. However, some intriguing data build a circumstantial case for an association between OCD and growth hormone abnormalities, perhaps through the serotonergic system. In the epidemiological study of OCD among high school students, described earlier, males with OCD were noted to be smaller and lighter than the community of normal controls (Flament et al., 1988). This was also shown to be true of males with other anxiety disorders (Hamburger et al., 1989). There were no reductions in the height or weight of the adolescent girls with OCD. The small size of the OCD males could be due to an effective lack of growth hormone, or to a delay in the pubertal growth spurt, although, of course, no causality is demonstrated by the relationship. To address the issue of causality, future research might employ direct assays, hormonal challenges, or therapeutic interventions.

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