The psychobiology of premenstrual dysphoria: the role of prolactin

(1) The evidence for a role of prolactin in the premenstrual syndrome is discussed in this review. (2) The timing of the onset and offset of both physical and psychological dysphoric symptoms corresponds with the luteal elevation and menstrual decrease of serum prolactin levels. (3) Women with premenstrual symptoms have been shown to have high prolactin levels throughout the menstrual cycle and especially in the premenstruum. (4) Suppression of prolactin secretion with bromocriptine is reported to be effective in preventing both physical and psychological premenstrual symptoms. (5) The mode of action of bromocriptine requires further study to exclude possible direct central nervous system effects of the drug, independent of its prolactin-suppressing action. (6) Indirect evidence for a role of prolactin in the premenstrual syndrome comes from (a) the actions of prolactin in causing renal retention of water, sodium and potassium; (b) the interactions of prolactin with lithium (which is reported to relieve premenstrual symptoms in some patients); some of the other reported treatments also may suppress prolactin secretion or antagonize its peripheral effects. (7) Prolactin may interact with the ovarian hormones to cause specific types of dysphoric symptoms. High prolactin levels associated with low estrogen levels may cause depressive symptoms. High prolactin levels associated with low progesterone levels may cause symptoms of anxiety or irritable hostility. (8) Interactions of prolactin with the ovarian hormones may also help to account for some related clinical states—mid-cycle mood elevations, elation in late pregnancy, postpartum depression and dysphoric menopausal symptoms.