Abstract
Background and aims: Cardiovascular disease (CVD) is among the leading causes of morbidity and mortality worldwide. Traditional risk factors predict 75-80% of an individual's risk of incident CVD. However, the role of early life experiences in future disease risk is gaining attention. The Barker hypothesis proposes fetal origins of adult disease, with consistent evidence demonstrating the deleterious consequences of birth weight outside the normal range. In this study, we investigate the role of birth weight in CVD risk prediction. Methods and results: The Women's Health Initiative (WHI) represents a large national cohort of post-menopausal women with 63,815 participants included in this analysis. Univariable proportional hazards regression analyses evaluated the association of 4 self-reported birth weight categories against 3 CVD outcome definitions, which included indicators of coronary heart disease, ischemic stroke, coronary revascularization, carotid artery disease and peripheral arterial disease. The role of birth weight was also evaluated for prediction of CVD events in the presence of traditional risk factors using 3 existing CVD risk prediction equations: one body mass index (BMI)-based and two laboratory-based models. Low birth weight (LBW) (<6 lbs.) was significantly associated with all CVD outcome definitions in univariable analyses (HR = 1.086, p = 0.009). LBW was a significant covariate in the BMI-based model (HR = 1.128, p < 0.0001) but not in the lipid-based models. Conclusion: LBW (<6 lbs.) is independently associated with CVD outcomes in the WHI cohort. This finding supports the role of the prenatal and postnatal environment in contributing to the development of adult chronic disease.
Original language | English (US) |
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Pages (from-to) | 239-245 |
Number of pages | 7 |
Journal | Nutrition, Metabolism and Cardiovascular Diseases |
Volume | 26 |
Issue number | 3 |
DOIs | |
State | Published - Mar 1 2016 |
Funding
This work was supported by a K99/R00 grant from the National Institute of Child Health and Human Development [ R00 HD-065786 ]. We would like to acknowledge the WHI Program Office, specifically Jacques Rossouw, Shari Ludlam, Dale Burwen, Joan McGowan, Leslie Ford, and Nancy Geller ( National Heart, Lung, and Blood Institute , Bethesda, Maryland). Also individuals at the WHI Clinical Coordinating Center Garnet Anderson, Ross Prentice, Andrea LaCroix, and Charles Kooperberg ( Fred Hutchinson Cancer Research Center , Seattle, WA). Investigators and Academic Centers contributing to WHI science include: JoAnn E. Manson ( Brigham and Women's Hospital , Harvard Medical School , Boston, MA); Barbara V. Howard (MedStar Health Research Institute/Howard University, Washington, DC); Marcia L. Stefanick (Stanford Prevention Research Center, Stanford, CA); Rebecca Jackson (The Ohio State University , Columbus, OH); Cynthia A. Thomson (University of Arizona, Tucson/Phoenix, AZ); Jean Wactawski-Wende (University at Buffalo, Buffalo, NY); Marian Limacher (University of Florida, Gainesville/Jacksonville, FL); Robert Wallace (University of Iowa, Iowa City/Davenport, IA); Lewis Kuller (University of Pittsburgh, Pittsburgh, PA); Sally Shumaker ( Wake Forest University School of Medicine, Winston–Salem, NC). The WHI programs is funded by the National Heart, Lung, and Blood Institute , National Institutes of Health , U.S. Department of Health and Human Services through contracts, HHSN268201100046C , HHSN268201100001C , HHSN268201100002C , HHSN268201100003C , HHSN268201100004C . We would like to acknowledge the WHI Program Office, specifically Jacques Rossouw, Shari Ludlam, Dale Burwen, Joan McGowan, Leslie Ford, and Nancy Geller (National Heart, Lung, and Blood Institute, Bethesda, Maryland). Also individuals at the WHI Clinical Coordinating Center Garnet Anderson, Ross Prentice, Andrea LaCroix, and Charles Kooperberg (Fred Hutchinson Cancer Research Center, Seattle, WA). Investigators and Academic Centers contributing to WHI science include: JoAnn E. Manson (Brigham and Women''s Hospital, Harvard Medical School, Boston, MA); Barbara V. Howard (MedStar Health Research Institute/Howard University, Washington, DC); Marcia L. Stefanick (Stanford Prevention Research Center, Stanford, CA); Rebecca Jackson (The Ohio State University, Columbus, OH); Cynthia A. Thomson (University of Arizona, Tucson/Phoenix, AZ); Jean Wactawski-Wende (University at Buffalo, Buffalo, NY); Marian Limacher (University of Florida, Gainesville/Jacksonville, FL); Robert Wallace (University of Iowa, Iowa City/Davenport, IA); Lewis Kuller (University of Pittsburgh, Pittsburgh, PA); Sally Shumaker (Wake Forest University School of Medicine, Winston–Salem, NC). The WHI programs is funded by the National Heart, Lung, and Blood Institute, National Institutes of Health, U.S. Department of Health and Human Services through contracts, HHSN268201100046C, HHSN268201100001C, HHSN268201100002C, HHSN268201100003C, HHSN268201100004C. This work was supported by a K99/R00 grant from the National Institute of Child Health and Human Development [R00 HD-065786].
Keywords
- Barker hypothesis
- Life course epidemiology
- Metabolic syndrome
- Proportional hazards model
- Risk prediction
- Self-reported birth weight
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Nutrition and Dietetics
- Medicine (miscellaneous)
- Endocrinology, Diabetes and Metabolism