Research Study Abstract

Sedentary Time and Cardio-Metabolic Biomarkers in US Adults: NHANES 2003–06

  • Published on January 11, 2011

Aims Prolonged sedentary time is ubiquitous in developed economies and is associated with an adverse cardio-metabolic risk profile and premature mortality. This study examined the associations of objectively assessed sedentary time and breaks (interruptions) in sedentary time with continuous cardio-metabolic and inflammatory risk biomarkers, and whether these associations varied by sex, age, and/or race/ethnicity.

Methods and Results Cross-sectional analyses with 4757 participants (≥ 20 years) from the 2003/04 and 2005/06 US National Health and Nutrition Examination Survey (NHANES). An Actigraph accelerometer was used to derive sedentary time [< 100 counts per minute (cpm)] and breaks in sedentary time. Independent of potential confounders, including moderate-to-vigorous exercise, detrimental linear associations (P for trends < 0.05) of sedentary time with waist circumference, HDL-cholesterol, C-reactive protein, triglycerides, insulin, HOMA-%B, and HOMA-%S were observed. Independent of potential confounders and sedentary time, breaks were beneficially associated with waist circumference and C-reactive protein (P for trends <0.05). There was limited evidence of meaningful differences in associations with biomarkers by age, sex, or race/ethnicity. Notable exceptions were sex-differences in the associations of sedentary time and breaks with HDL-cholesterol, and race/ethnicity differences in the association of sedentary time with waist circumference with associations detrimental in non-Hispanic whites, null in Mexican Americans, and beneficial in non-Hispanic blacks.

Conclusion These are the first population-representative findings on the deleterious associations of prolonged sedentary time with cardio-metabolic and inflammatory biomarkers. The findings suggest that clinical communications and preventive health messages on reducing and breaking up sedentary time may be beneficial for cardiovascular disease risk.


  • Genevieve N. Healy 1,2
  • Charles E. Matthews 3
  • David W. Dunstan 1,2
  • Elisabeth A.H. Winkler 1
  • Neville Owen 1,2


  • 1

    Cancer Prevention Research Centre, School of Population Health, The University of Queensland, Herston Rd, Herston, QLD 4006, Australia

  • 2

    Baker IDI Heart and Diabetes Institute, PO Box 6492, St Kilda Road Central, Victoria 8008, Melbourne, Australia

  • 3

    Division of Cancer Epidemiology and Genetics, Nutritional Epidemiology Branch, National Cancer Institute, 6120 Executive Boulevard, MSC 7242, Bethesda, MD 20892-7335, USA


Eur Heart J (2011) 32 (5): 590-597. doi: 10.1093/eurheartj/ehq451


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