Reproductive history and risk of colorectal cancer in postmenopausal women.

Abstract

3618 Background: Estrogen/progestin hormone therapy (HT) use has been associated with a low risk of colorectal cancer. Endogenous estrogen levels, in contrast, have been reported to have a positive relationship with incidence of colorectal cancer in recent studies. An important surrogate measure of estrogen exposure, which has been associated with estrogen-related cancers such as breast cancer, is reproductive history. Therefore, we were interested in studying the relationship of reproductive history with incident colorectal cancer. Methods: We prospectively analyzed the association between reproductive factors and development of colorectal cancer. Subjects were postmenopausal women enrolled in the NIH-AARP Diet and Health Study, a cohort of 566,402 individuals (age 50-71) who completed a baseline questionnaire on demographics and lifestyle factors. Hazard ratios (HR) and 95% confidence intervals (95% CI) for the association of age at menarche, age at first child's birth, and age at menopause, as well as total parity and oral contraceptive use, were assessed using multivariate Cox models. Covariates included current age, body mass index (BMI), alcohol consumption, smoking, race, family history of colorectal cancer, physical activity, education, HT use, and diabetes. Results: During a median of 8.2 years of follow-up, 2,305 postmenopausal women were diagnosed with colorectal cancer. Compared with women who underwent menopause at < 40 years of age, menopause after 55 years of age was associated with an increased risk of colorectal cancer (HR = 1.45, 95%CI: 1.21-1.74; p-trend = 0.003). Among leaner women (BMI ≤ 25 Kg/M2), increasing parity was inversely related with colorectal cancer incidence; p-trend = 0.04), while later age at first child's birth (≥ 30 compared with ≤ 19 years) was associated with an increased risk of colorectal cancer (HR = 1.56, 95%CI: 1.13-2.14; p-trend, 0.02). Conclusions: These data support a role for sex hormones in colorectal tumorigenesis and suggest that higher endogenous estrogen exposure may increase risk of colorectal cancer. No significant financial relationships to disclose.