Premenstrual distress is now widely recognized to be a major social and health problem, with epidemiological surveys estimating that 95% of women experience physical and psychological changes premenstrually. Up to 40% experience moderate distress, categorized by clinicians and researchers as Premenstrual Syndrome (PMS) and 11–13% experience severe distress and disruption to their lives, categorized as Premenstrual Dysphoric Disorder (PMDD) (Steiner & Born, 2000). However, ever since discussions of premenstrual distress first appeared contemporaneously in the medical and psychoanalytic literature in 1931, this has been a research field dogged by controversy and disagreement.
Initially described as ‘premenstrual tension’, and attributed to either hormonal imbalances (Frank, 1931), or to intrapsychic conflict exacerbated by women's social role (Horney, 1931), it was renamed ‘Premenstrual Syndrome’ in 1953, ‘Late Luteal Phase Dysphoric disorder in the DSM III-R and ‘Premenstrual Dysphoric Disorder’ in the DSM-IV. Regardless of the diagnostic classification adopted, the divide between biomedical and psychological explanations continues to this day, with a range of competing theories associating PMS with a single causal factor. Biological theories of PMS can be divided into six categories: gonadal steroids and gonadoptrophins; neurovegetive signs (sleep, appetite changes); neuroendocrine factors; serotonin and other neurotransmitters; β-endorphin; and other potential substrates (including prostaglandins, vitamins, electrolytes and CO2) (Parry, 1994, p.47). The psychosocial theories include: personality; cognitions associated with femininity and menstruation; the influence of stress and life events; and propensity for psychological illness (Walker, 1997).