Twin Research and Human Genetics

Articles

Genetics of Body Mass Stability and Risk for Chronic Disease: A 28-Year Longitudinal Study

Carol E. Franza1 c1, Michael D. Granta2, Kristen C. Jacobsona3, William S. Kremena4, Seth A. Eisena5, Hong Xiana6, James Romeisa7, Heather Thompson-Brennera8 and Michael J. Lyonsa9

a1 Department of Psychiatry, University of California San Diego, La Jolla, California, United States of America. cfranz@ucsd.edu

a2 Department of Psychology, Boston University, Boston, Massachusetts, United States of America.

a3 Division of Psychiatry, University of Chicago, Chicago, Illinois, United States of America.

a4 Department of Psychiatry, University of California San Diego, La Jolla, California, United States of America; Center for Behavioral Genomics, University of California San Diego, California, United States of America.

a5 Department of Internal Medicine, Washington University, St Louis, Missouri, United States of America; Research Service, St. Louis VA Medical Center, St Louis, Missouri, United States of America; Medical Service, St. Louis VA Medical Center, St Louis, Missouri, United States of America; Department of Psychiatry, Washington University School of Medicine, St Louis, Missouri, United States of America.

a6 Department of Internal Medicine, Washington University, St Louis, Missouri, United States of America.

a7 Research Service, St. Louis VA Medical Center, St Louis, Missouri, United States of America; Department of Psychiatry, Washington University School of Medicine, St Louis, Missouri, United States of America; Department of Health Management and Policy, School of Public Health, St. Louis University, St. Louis Missouri, United States of America.

a8 Department of Psychology, Boston University, Boston, Massachusetts, United States of America.

a9 Department of Psychology, Boston University, Boston, Massachusetts, United States of America.

Abstract

We examined the contributions of genetic and environmental factors to body mass index (BMI) over approximately 28 years. Participants were 693 male, predominantly middle-class, twins (355 monozygotic, 338 dizygotic) from the Vietnam Era Twin Registry. The phenotypic correlation between age 20 and age 48 BMI was 0.52; the genetic correlation was 0.60. Most of the remaining variance at both times was accounted for by nonshared environmental factors. Since genetic factors are not perfectly correlated, this indicates that other genes affect BMI at one or both time points, leaving room for further exploration of the genetics of body mass stability. Mean BMI increased significantly from 22.7 (normal) to 27.8 (overweight). Overweight BMI at age 20 predicted midlife adult onset diabetes (adjusted odds ratio = 4.62, 95% CI 1.91 to 11.18), but not hypertension. Depending on one's vantage point, the results indicate elements of both stability and change in BMI. Very similar phenotypic and genetic correlations were observed over a similar time period in a WW II twin sample, but without the substantial mean increase in BMI. It seems unlikely that different genes influence BMI in the two cohorts. Therefore, we argue that nonshared environmental factors are probably primarily responsible for the secular increase in midlife BMI. Our results also provide prospective evidence that early excess BMI may have serious long-term health consequences, and that this risk is not limited to minorities or adults of lower socioeconomic status.

(Received February 01 2007)

(Accepted May 28 2007)

Correspondence:

c1 Address for correspondence: Carol E. Franz, University of California San Diego, Department of Psychiatry, 9500 Gilman Drive, MC 0738, La Jolla, CA 92093.

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