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      Duration of Reproductive Life Span, Age at Menarche, and Age at Menopause Are Associated With Risk of Cardiovascular Disease in Women

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          Abstract

          Background

          Although the timing of menarche and menopause may be associated with cardiovascular disease (CVD), the entire reproductive life span has not been considered comprehensively as risk for CVD. We investigate the associations of reproductive life span duration and ages at menarche and menopause, induced by natural means or surgical bilateral oophorectomy, with incident CVD in women.

          Methods and Results

          Prospective cohort study of 73 814 Nurses' Health Study following participants without CVD, defined as incident coronary heart disease or stroke, from 1980 through 2012. Duration of reproductive life span was generated by subtracting age at menarche from age at menopause. A shorter reproductive life span was associated with a higher risk of incident CVD after multivariable adjustment (relative risk, 1.32 [95% confidence interval, 1.16–1.49] comparing duration <30 with ≥42 years; P trend<0.0001). Early age at menopause was associated with higher multivariable‐adjusted CVD risk (1.32 [1.16–1.51] comparing age <40 with 50 to <55 years; P trend<0.0001), with excess risk for both natural and surgical menopause. Compared with women with menarche at 13 years, the multivariable‐adjusted CVD risk for early menarche at ≤10 years was 1.22 (1.09–1.36). The association between reproductive life span and CVD remained significant in sensitivity analyses excluding women who experienced extreme early age at menarche or who used hormone therapy.

          Conclusions

          A shorter duration of reproductive life span is associated with a higher risk of CVD, which is likely driven by the timing of menopause induced either naturally or surgically. Extremely early age at menarche is also associated with a higher risk of CVD.

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          Most cited references 26

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          Postmenopausal status and early menopause as independent risk factors for cardiovascular disease: a meta-analysis.

          Loss of ovarian function and subsequent deficiency of endogenous estrogens is suggested to enhance cardiovascular disease risk and related death after menopause. The aim was to obtain valid estimates of the cardiovascular disease risk associated with postmenopausal status and early menopause. A literature search of observational studies was performed using PubMed and EMBASE (1966 to May 1, 2004). Eighteen studies on postmenopausal status and age at menopause in relation to cardiovascular disease were selected. Six studies investigated menopausal status, nine studies investigated menopausal age, and three studied both. General variance-based methods were used to pool relative risk estimates and corresponding 95% confidence intervals. Stratification was performed for study design, type of menopause, outcome, and adjustment for age and smoking. The pooled relative risk estimate for postmenopausal versus premenopausal status and cardiovascular disease was 1.36 (95% CI, 1.15-1.60). In the stratified analysis, the pooled effect was 0.96 (95% CI, 0.77-1.21) after controlling for age and smoking. The pooled effect of bilateral oophorectomy on cardiovascular disease was 2.62 (95% CI, 2.05-3.35). For early menopause and cardiovascular disease, with the menopausal age category containing 50 years as a reference, the pooled relative risk estimate was 1.25 (95% CI, 1.15-1.35). In the stratified analysis, the pooled effect was 1.38 (95% CI, 1.21-1.58) after controlling for age and smoking. The pooled effect of bilateral oophorectomy on cardiovascular disease was 4.55 (95% CI, 2.56-8.01). Overall, there was no convincing relationship between postmenopausal status and cardiovascular disease. However, there was a modest effect of early menopause on cardiovascular disease. The effect was more pronounced for women with an artificial menopause than for women with a natural menopause.
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            Are changes in cardiovascular disease risk factors in midlife women due to chronological aging or to the menopausal transition?

            This prospective study examined whether changes in traditional and novel coronary heart disease (CHD) risk factors are greater within a year of the final menstrual period (FMP), relative to changes that occur before or after that interval, in a multiethnic cohort. Understanding the influence of menopause on CHD risk remains elusive and has been evaluated primarily in Caucasian samples. SWAN (Study of Women's Health Across the Nation) is a prospective study of the menopausal transition in 3,302 minority (African American, Hispanic, Japanese, or Chinese) and Caucasian women. After 10 annual examinations, 1,054 women had achieved an FMP not due to surgery and without hormone therapy use before FMP. Measured CHD risk factors included lipids and lipoproteins, glucose, insulin, blood pressure, fibrinogen, and C-reactive protein. We assessed which of 2 models provided a better fit with the observed risk factor changes over time in relation to the FMP: a linear model, consistent with chronological aging, or a piecewise linear model, consistent with ovarian aging. Only total cholesterol, low-density lipoprotein cholesterol, and apolipoprotein B demonstrated substantial increases within the 1-year interval before and after the FMP, consistent with menopause-induced changes. This pattern was similar across ethnic groups. The other risk factors were consistent with a linear model, indicative of chronological aging. Women experience a unique increase in lipids at the time of the FMP. Monitoring lipids in perimenopausal women should enhance primary prevention of CHD.
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              Validity of self-reported waist and hip circumferences in men and women.

              Recent epidemiologic evidence indicates an association between fat distribution and many diseases. To assess the validity of circumference measurements obtained by self-report, the authors analyzed data from 123 men aged 40-75 years and 140 women aged 41-65 years, drawn from two large ongoing prospective studies. On mailed questionnaires, subjects were asked to measure and record their weight and waist and hip circumferences. These data were compared with standardized measurements taken approximately six months apart by technicians who visited participants at their homes. Crude Pearson correlations between self-reported waist circumferences and the average of two technician-measured waist circumferences were 0.95 for men and 0.89 for women. Similar correlations for hip measurements were 0.88 for men and 0.84 for women, and for waist-to-hip ratios, 0.69 for men and 0.70 for women. After adjusting for age and body mass index (kg/m2), correlations for waist-to-hip ratios were 0.55 for men and 0.58 for women. Correlations became stronger after correcting for random within-person variability from daily or seasonal fluctuations. Self-reported and measured weights were highly correlated: 0.97 for men and 0.97 for women. Self-reported waist, hip, and weight measurements appear reasonably valid. The moderate degree of measurement error for the ratio of self-reported waist and hip circumferences, however, implies that previously reported associations based on self-report of these measures may have been appreciably underestimated.
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                Author and article information

                Contributors
                sylvia.ley@channing.harvard.edu
                krexrode@bwh.harvard.edu
                Journal
                J Am Heart Assoc
                J Am Heart Assoc
                10.1002/(ISSN)2047-9980
                JAH3
                ahaoa
                Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
                John Wiley and Sons Inc. (Hoboken )
                2047-9980
                02 November 2017
                November 2017
                : 6
                : 11 ( doiID: 10.1002/jah3.2017.6.issue-11 )
                Affiliations
                [ 1 ] Department of Nutrition Harvard T.H. Chan School of Public Health Boston MA
                [ 2 ] Channing Division of Network Medicine Department of Medicine Brigham and Women's Hospital and Harvard Medical School Boston MA
                [ 3 ] Division of Preventive Medicine Department of Medicine Brigham and Women's Hospital and Harvard Medical School Boston MA
                [ 4 ] Division of Women's Health Department of Medicine Brigham and Women's Hospital Boston MA
                [ 5 ] Department of Epidemiology Harvard T.H. Chan School of Public Health Boston MA
                [ 6 ] Department of Biostatistics Harvard T.H. Chan School of Public Health Boston MA
                Author notes
                [* ] Correspondence to: Kathryn M. Rexrode, MD, MPH, Brigham and Women's Hospital; Harvard Medical School; Division of Women's Health, Department of Medicine, Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115. E‐mail: krexrode@ 123456bwh.harvard.edu and Sylvia H. Ley, PhD, RD, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School; Department of Nutrition, Harvard T.H. Chan School of Public Health, 665 Huntington Ave, Boston, MA 02115. E‐mail: sylvia.ley@ 123456channing.harvard.edu
                Article
                JAH32718
                10.1161/JAHA.117.006713
                5721766
                29097389
                © 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

                This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                Page count
                Figures: 0, Tables: 5, Pages: 16, Words: 8534
                Product
                Funding
                Funded by: NIH
                Award ID: UM1 CA186107
                Award ID: UM1 CA87969
                Award ID: R01 HL034594
                Award ID: and R01 HL088521
                Categories
                Original Research
                Original Research
                Epidemiology
                Custom metadata
                2.0
                jah32718
                November 2017
                Converter:WILEY_ML3GV2_TO_NLMPMC version:5.2.6 mode:remove_FC converted:21.11.2017

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