PubMed · 9731878
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L A Roberts. 1998. Cesarean section.. https://doi.org/10.1016/s0002-9378(98)70410-7
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CONTEXT: Whether menopausal hormone replacement therapy using a combined estrogen-progestin regimen increases risk of breast cancer beyond that associated with estrogen alone is unknown. OBJECTIVE: To determine whether increases in risk associated with the estrogen-progestin regimen are greater than those associated with estrogen alone. DESIGN: Cohort study of follow-up data for 1980-1995 from the Breast Cancer Detection Demonstration Project, a nationwide breast cancer screening program. SETTING: Twenty-nine screening centers throughout the United States. PARTICIPANTS: A total of 46355 postmenopausal women (mean age at start of follow-up, 58 years). MAIN OUTCOME MEASURE: Incident breast cancers by recency, duration, and type of hormone use. RESULTS: During follow-up, 2082 cases of breast cancer were identified. Increases in risk with estrogen only and estrogen-progestin only were restricted to use within the previous 4 years (relative risk [RR], 1.2 [95% confidence interval [CI], 1.0-1.4] and 1.4 [95% CI, 1.1-1.8], respectively); the relative risk increased by 0.01 (95% CI, 0.002-0.03) with each year of estrogen-only use and by 0.08 (95% CI, 0.02-0.16) with each year of estrogen-progestin-only use among recent users, after adjustment for mammographic screening, age at menopause, body mass index (BMI), education, and age. The P value associated with the test of homogeneity of these estimates was .02. Among women with a BMI of 24.4 kg/m2 or less, increases in RR with each year of estrogen-only use and estrogen-progestin-only use among recent users were 0.03 (95% CI, 0.01-0.06) and 0.12 (95% CI, 0.02-0.25), respectively. These associations were evident for the majority of invasive tumors with ductal histology and regardless of extent of invasive disease. Risk in heavier women did not increase with use of estrogen only or estrogen-progestin only. CONCLUSION: Our data suggest that the estrogen-progestin regimen increases breast cancer risk beyond that associated with estrogen alone.
BACKGROUND: A twofold or greater risk of neural tube defect (NTD)-affected pregnancy has been associated with prepregnant obesity, where obesity was defined as body mass index (BMI) of >29 kg/m(2). Risks have been more elevated for spina bifida than for anencephaly. METHODS: We investigated whether finer phenotypic classifications of spina bifida, in combination with other factors, were associated with a BMI of >29 kg/m(2). Data were derived from a case-control study of fetuses and infants with NTDs among 1989-1991 California births. Interviews were conducted with mothers of 277 spina bifida cases and 517 nonmalformed controls. RESULTS: Women with a BMI of >29 kg/m(2) compared with those </=29 kg/m(2) revealed an odds ratio (OR) of 2.2 (95% confidence interval [95% CI] = 1.4-3. 3) for spina bifida in their infants and fetuses. Elevated risks were observed for each spina bifida subphenotype, and risks varied by subphenotype: open spina bifida, OR = 2.0 (1.2-3.1); closed (skin-covered), 3.3 (1.4-7.5); isolated, 2.2 (1.4-3.4); nonisolated, 1.9 (0.9-4.2); high, 4.5 (2.1-9.6); low, 1.9 (1.2-2.9); open/isolated/high, 7.1 (2.8-18.1); and open/isolated/low, 1.8 (1. 1-3.1). Risks were higher among female infants/fetuses and foreign-born Latinas, and for some phenotypes the risks were quite large, e.g., OR = 8.3 (2.9-23.6) for "closed" spina bifida among female infants/fetuses whose mothers were >29 kg/m(2) compared with males whose mothers were </=29 kg/m(2). Maternal periconceptional vitamin use was not observed to influence risk as greatly across phenotypes. CONCLUSIONS: The observed pathogenetic heterogeneity of prepregnant obesity and spina bifida risks suggests that there are likely to be several biologic mechanisms underlying the association.