Ninety percent of menstruating women experience some kind of premenstrual symptoms during the luteal phase of the menstrual cycle, with 20-30% experiencing moderate to severe symptoms. With an even more severe collection of symptoms, is premenstrual dysphoric disorder (PMDD). 3-8% of menstruating women report symptoms severe enough to be considered suffering from PMDD. Yet another designation, premenstrual magnification (PMM), is used to describe women who are symptomatic the entire cycle but have a premenstrual exacerbation of a diagnosed psychiatric, medical, or gynecological condition.
With a large number of wide-ranging symptoms and the difficulty involved in making a diagnosis, it is not surprising that the various theories advanced to explain premenstrual syndrome (PMS) have yet to been proven. One problem is that PMS is a diagnosis of exclusion, meaning there could be a variety of poorly understood conditions responsible for these symptoms. Several theories attribute PMS to fluctuations in sex hormones and neurotransmitters. The observation that symptoms disappear when a women has a menstrual cycle during which she does not ovulate and a corpus luteum is not formed, led to the theory that sex steroids, estrogen and progesterone, produced by the corpus luteum are responsible. In addition, the neurotransmitters serotonin and gamma amino butyric acid (GABA) have been implicated in various pathways. The list of other hormones and their modes of action that are suspected to be involved is long and confusing, making it no wonder that there is still no known etiology.
One distinctly different hypothesis is that PMS is due to a broad set of persistent infectious illnesses that are exacerbated by cyclic changes in immunosuppression due to the fluctuating levels of progesterone and estrogen. In general, there have been studies looking at two major categories of causation- genetic and environmental and have found moderate correlations at the best. Infectious causation has been overlooked for the most part, with almost no empirical support in published literature. I don’t think this means there is no value to the theory, simply that it is a very hard one to test. One very convincing article by Doyle et. al explains how this possibility of infectious causation is integrated with the cyclic changes in hormone levels that have been observed and are generally thought to be involved in PMS.