ABSTRACT
The relationship between the luteal phase of the menstrual cycle and symptom development in premenstrual dysphoric disorder/premenstrual syndrome (PMDD/ PMS) is self-evident. Symptoms starts after ovulation and then increase in parallel with the rise in serum progesterone during the luteal phase. The symptom severity reaches a peak during the last five premenstrual days or the first day of menstruation. Thereafter, the symptoms decline and disappear 3-4 days after the onset of menstrual bleeding. During the postmenstrual phase there is a period of well-being, closely following estrogen production, to the estradiol peak. This suggests that there is a symptom-provoking factor produced by the corpus luteum of the ovary.1 This is further supported by the fact that in anovulatory cycles, spontaneous or induced, when a corpus luteum is not formed, no symptom cyclicity occurs.2-4
Further evidence that progesterone and progestogens induce negative mood symptoms similar to those in PMDD/PMS is seen in postmenopausal women receiving estrogen/progesterone hormone therapy.5-7 As discussed above, there are strong indications that steroids from the corpus luteum are the symptom-provoking factor in the central nervous system (CNS). But the classical hormonal receptor for progesterone seems not to be involved in the pathophysiology of PMS/PMDD; treatment with the progesterone receptor antagonist
mifepristone (RU-486) fails to reduce the physical or behavioral manifestations of PMS.8
