Secretion of the anterior pituitary hormone prolactin can be significantly increased by antipsychotic drugs, leading to a range of adverse effects in patients with schizophrenia. However, there is evidence from a variety of studies that prolactin may also be related to symptom profile and treatment response in these patients, and recent work has identified variations in prolactin secretion even in drug-free patients. In this paper, a selective review of all relevant studies pertaining to prolactin and schizophrenia, including challenge and provocation studies, is presented. The implications of this work are discussed critically. A tentative model, which synthesizes these findings and argues for a significant role for prolactin in the development of schizophrenia, is outlined. 1. Introduction Prolactin is a polypeptide hormone secreted by the anterior pituitary gland. Prolactin has multiple functions, including lactation and maternal-infant bonding, in mammals. Recent work has found it to be relevant to parental and sexual behaviour in humans [1, 2] as well. Various factors, including gender, sexual activity, childbirth, stress, smoking, and drugs, can affect the release of prolactin [3, 4]. The production of prolactin is inhibited by dopamine release in the hypothalamo-pituitary circuit and can be increased by blocking type 2 (D2) dopamine receptors. Most available antipsychotic drugs can therefore cause elevations in prolactin secretion. This increase is associated with a variety of adverse effects: lack of libido and erectile dysfunction in men [5], amenorrhoea and galactorrhoea in women [6], acceleration of osteoporosis in women [7], weight gain [8], and—potentially—an increased risk of cancer, particularly breast cancer in women [9]. The association of prolactin with male sexual dysfunction is complex and has been challenged by some authors [10] but is supported by research showing that antipsychotics which cause greater elevations in prolactin also have more marked sexual adverse effects [11]. Besides this, a variety of studies over the past four decades have examined other facets of the relationship between prolactin and schizophrenia and call for a reappraisal of this relationship. In this paper, the author highlights the important findings pertaining to prolactin and schizophrenia, excluding the literature on drug-induced hyperprolactinemia which has been extensively reviewed elsewhere. The author also proposes a model that may explain these findings. In the discussion that follows, the term “prolactin levels” refers to plasma prolactin, unless
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