Abstract

Numerous gender differences have been noted in schizophrenia, although the illness is equally common in both sexes. It has been suggested that these differences reflect prenatal organizational effects and subsequent activational effects of sex hormones (Seeman and Lang ! 990). One activational effect may be a protective influence of estrogens via their reduction of dopamine iDA) neurotransmission (Seeman 1982). Several observations can be explained via this mechanism (for review see Seeman and Lang 1990). For example, premenopausal women experience less severe expression of the illness and their psychotic symptoms respond to lower neuroleptic doses. Furthermore, fluctuations in estrogen levels correlate with schizophrenic ep;.sodes: relapse is relatively uncommon during pregr.ancy when estrogens levels are high; in contrast, vulnerability increases postpartum and after menopause--both are times of decreased estrogen. Exogenous estrogens may also help reduce schizophrenic symptomatology in women, especially recurrent exacerbations related to the menstrual cycle (for review see Felthous and Robinson 1981). Evidence from animal studies suggests that the protective effects of estrogens may relate to down-regulation of central nervous system (CNS) DA-D2 receptor sensitivity (Hafner et al 1991). Cor, sistent with this is the report that the rat's anterior pituitary contains fewer D2 receptors during the proestrus phase of its estrous cycle, when plasma estrogen is elevated (Pasqualini et al 1984; Pazos et al 1985). Reports that psychosis can exacerbate perimenstrually also implicate influences of sex hormones; however, specific menstrual phase as well as diagnosis (e.g., undetermined, mania, schizophrenia) varied both between and within studies (Brockingon et al 1988; Dennerstein et al 1983; Gerada and Reveley 1988; Glick and Stewarl 1980; Felthous and Robinson 1981).

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