A recent study reported an increased risk of non-insulin dependent diabetes (type II) among reproductive age women who retrospectively reported long or irregular menstrual cycles during ages 18-22 years.  We examined the association between menstrual patterns and diabetes history in 668 white, college-educated women who prospectively recorded menstrual cycle data throughout their reproductive years and subsequently completed a self-administered health history questionnaire.  Cycle length and variability and bleeding duration were calculated for ages 22 , 23 27, 28 32, and 33 37 years.  The analysis included 35,418 person-years of follow-up and 49 cases of diabetes; age at diagnosis ranged from 35-76 (median 63) years.  There was no association between diabetes risk and age at menarche, mean cycle length, cycle variability, or frequency of long cycles (42 days) at any age.  Longer bleeding periods during the later years were associated with an increased risk of diabetes.  The age-, body mass-, and physical activity- adjusted risk ratio was 1.4 (95% confidence interval 1.0 1.8), per day increase in bleeding duration for menses during ages 28 32.  These results do not support the association of long or irregular menstrual cycles with post-menopausal diabetes incidence, but do suggest a possible protective association of short bleeding duration with subsequent onset of diabetes.  Potential mechanisms underlying this association are not known.  We analyzed data from 4 case-control studies pertaining to ovarian cancer risk in relation to pregnancy history: 628 cases and 3432 controls, ages 18-79, were included.  Pregnancy recency, as measured by years since last pregnancy, was associated with increased ovarian cancer risk, with odds ratios of 1.4, 1.4, 1.8, and 2.1 for 10-14, 15-19, 20-24, and 25 years compared to 0-9 years (trend test p = 0.004), respectively.  Apoptosis is an important means through which cells which have sustained DNA damage can be eliminated, and recent studies indicate that the progestin component in oral contraceptives induces apoptosis in the ovarian epithelium and that progesterone induces apoptosis in ovarian carcinoma cell lines.  These observations suggest that the protective effect resulting from recent time since last pregnancy observed in our study may be due to apoptosis in the ovarian epithelium mediated by higher progestin levels that occur during pregnancy.  A later (more recent) pregnancy would thus be more likely to eliminate a larger accumulation of damaged cells than an earlier pregnancy. -  diabetes, ovarian cancer, pregnancy, menarche, menopause, mensturation, menstrual cycle length, risk factors, epidemiology - Human Subjects & Human Subjects: Interview, Questionaires, or Surveys Only