Metabolic syndrome and mammographic density: The Study of Women's Health Across the Nation


  • Clinical Centers: University of Michigan, Ann Arbor, MI: MaryFran Sowers, Principal Investigator (PI); Massachusetts General Hospital, Boston, MA: Joel Finkelstein, PI, 1999 to present and Robert Neer, PI, 1994–1999; Rush University, Rush University Medical Center, Chicago, IL: Howard Kravitz, PI, 2009 to present and Lynda Powell, PI, 1994–2009; University of California, Davis/Kaiser, CA: Ellen Gold, PI; University of California, Los Angeles, CA: Gail Greendale, PI; Albert Einstein College of Medicine, Bronx, NY: Rachel Wildman, PI, 2010 and Nanette Santoro, PI 2004–2010; University of Medicine and Dentistry-New Jersey Medical School, Newark, NJ: Gerson Weiss, PI 1994–2004; and the University of Pittsburgh, Pittsburgh, PA: Karen Matthews, PI. NIH Program Office: National Institute on Aging, Bethesda, MD: Sherry Sherman, 1994 to present and Marcia Ory, 1994–2001; National Institute of Nursing Research, Bethesda, MD: Program Officer. Central Laboratory: University of Michigan, Ann Arbor, MI: Daniel McConnell; (Central Ligand Assay Satellite Services). Coordinating Center: University of Pittsburgh, Pittsburgh, PA: Kim Sutton-Tyrrell, PI, 2001 to present; New England Research Institutes, Watertown, MA: Sonja McKinlay, PI, 1995–2001. Steering Committee: Susan Johnson, Current Chair; Chris Gallagher, Former Chair.


The metabolic syndrome (MetS) is associated with an increase in breast cancer risk. In our study, we evaluated whether the MetS was associated with an increase in percent mammographic density (MD), a breast cancer risk factor. We used linear regression and mixed models to examine the cross-sectional and longitudinal associations of the MetS and components of the MetS to percent MD in 790 premenopausal and early perimenopausal women enrolled in the Study of Women's Health Across the Nation (SWAN). In cross-sectional analyses adjusted for body mass index (BMI), modest inverse associations were observed between percent MD and the MetS [β = −2.5, standard error (SE) = 1.9, p = 0.19], abdominal adiposity (β = −4.8, SE = 1.9, p = 0.01) and raised glucose (β = −3.7, SE = 2.4, p = 0.12). In longitudinal models adjusted for covariates including age and BMI, abdominal adiposity (β = 0.34, SE = 0.17, p = 0.05) was significantly positively associated with slower annual decline in percent MD with time. In conclusion, our results do not support the hypothesis that the MetS increases breast cancer risk via a mechanism reflected by an increase in percent MD.