Time filter

Source Type

Michels K.B.,Obstetrics and Gynecology Epidemiology Center
Obstetrics and Gynecology | Year: 2010

Objective: To estimate the association between maternal pregnancy-related hypertension and offspring hypertension later in life in a birth cohort from New England. Methods: Covariate and exposure data were collected between 1959 and 1966 through the Collaborative Perinatal Project. Follow-up information was obtained through the New England Family Study between 2001 and 2004, when study participants were between 34 and 44 years old. The study population consisted of 1,556 individuals. Participants who reported having hypertension diagnosed at least once were considered to have hypertension. Logistic regression was used to estimate the association between maternal pregnancy-related hypertension and offspring hypertension later in life. Results were adjusted for sex, maternal race, maternal body mass index, maternal socioeconomic status, maternal diabetes, and twin pregnancy. Results: Maternal pregnancy-related hypertension was associated with an increased risk of being prescribed antihypertensives compared with never having hypertension diagnosed (from 8.8% to 17.4%; adjusted odds ratio 1.88, 95% confidence interval 1.00-3.55). The association was not attenuated after adjustment for birth weight or preterm delivery. After excluding offspring of women who reported hypertension during pregnancy only, this association increased to an adjusted odds ratio of 1.97 (95% confidence interval 1.04-3.72). Conclusion: In a birth cohort from New England, maternal pregnancy-related hypertension was associated with hypertension in offspring later in life. © 2010 by The American College of Obstetricians and Gynecologists. Published by Lippincott Williams and Wilkins.

Harris H.R.,Harvard University | Harris H.R.,Obstetrics and Gynecology Epidemiology Center | Willett W.C.,Harvard University | Terry K.L.,Harvard University | And 3 more authors.
Journal of the National Cancer Institute | Year: 2011

Body mass index is inversely associated with risk of premenopausal breast cancer, but the underlying mechanisms for this association are poorly understood. Abdominal adiposity is associated with metabolic and hormonal changes, many of which have been associated with the risk of premenopausal breast cancer. We investigated the association between body fat distribution, assessed in 1993 by self-reported waist circumference, hip circumference, and waist to hip ratio, and the incidence of premenopausal breast cancer in the Nurses' Health Study II. Cox proportional hazards regression models were used to calculate hazard ratios and 95% confidence intervals (CIs). Statistical tests were two-sided. During 426164 person-years of follow-up from 1993 to 2005, 620 cases of breast cancer were diagnosed among 45799 women. Hormone receptor status information was available for 84% of the breast cancers. The age-standardized incidence rates of breast cancer were 131 per 100000 person-years among those in the lowest quintile of waist circumference and 136 per 100000 person-years among those in the highest quintile. No statistically significant associations were found between waist circumference, hip circumference, or the waist to hip ratio and risk of breast cancer. However, each of the three body fat distribution measures was statistically significantly associated with greater incidence of estrogen receptor (ER)-negative breast cancer. The multivariable-adjusted hazard ratios of ER-negative breast cancer for the highest vs the lowest quintile of each body fat distribution measure were 2.75 (95% CI = 1.15 to 6.54; Ptrend =. 05) for waist circumference, 2.40 (95% CI = 0.95 to 6.08; Ptrend =. 26) for hip circumference, and 1.95 (95% CI = 1.10 to 3.46; Ptrend =. 01) for waist to hip ratio. Our findings suggest that body fat distribution does not play an important role in the overall incidence of premenopausal breast cancer but is associated with an increased risk for ER-negative breast cancer. © 2011 The Author.

Xue F.,Obstetrics and Gynecology Epidemiology Center | Xue F.,Harvard University | Willett W.C.,Channing Laboratory | Willett W.C.,Harvard University | And 7 more authors.
Archives of Internal Medicine | Year: 2011

Background: Tobacco smoke contains carcinogens, which may increase the risk of breast cancer (BC). Conversely, cigarette smoking also has antiestrogenic effects, which may reduce the risk of BC. The association between smoking and BC remains controversial. Methods: Prospective cohort study of 111 140 participants of the Nurses' Health Study from 1976 to 2006 for active smoking and 36 017 women from 1982 to 2006 for passive smoking. Results: During 3 005 863 person-years of follow-up, 8772 incident cases of invasive BC were reported. After adjustment for potential confounders, the hazard ratio (HR) of BC was 1.06% (95% confidence interval [CI], 1.01%-1.10%) for ever smokers relative to never smokers. Breast cancer incidence was associated with a higher quantity of current (P for trend = .02) and past (P for trend = .003) smoking, younger age at smoking initiation (P for trend = .01), longer duration of smoking (P for trend = .01), and more pack-years of smoking (P for trend = .005). Premenopausal smokingwas associated with a slightly higher incidence of BC (HR,1.11; 95% CI, 1.07-1.15 for every increase of 20 pack-years), especially smoking before first birth (1.18; 1.10-1.27 for every increase of 20 pack-years). Conversely, the direction of the association between postmenopausal smoking and BC was inverse (0.93; 0.85-1.02 for every increase of 20 pack-years). Passive smoking in childhood or adulthood was not associated with BC risk. Conclusion: Active smoking, especially smoking before the first birth, may be associated with a modest increase in the risk of BC. ©2011 American Medical Association. All rights reserved.

Loading Obstetrics and Gynecology Epidemiology Center collaborators
Loading Obstetrics and Gynecology Epidemiology Center collaborators