4.7 Article

Sarcopenia, sarcopenic obesity and inflammation: Results from the 1999-2004 National Health and Nutrition Examination Survey

Journal

CLINICAL NUTRITION
Volume 35, Issue 6, Pages 1472-1483

Publisher

CHURCHILL LIVINGSTONE
DOI: 10.1016/j.clnu.2016.03.028

Keywords

Obesity; Sarcopenia; Insulin resistance; Inflammation

Funding

  1. Health Resources Service's Administration [UB4HP19206-01-00]
  2. Junior Faculty Career Development Award
  3. Department of Medicine, Dartmouth-Hitchcock Medical Center
  4. Dartmouth Centers for Health and Aging
  5. National Institute of Mental Health [K12 HS0217695, T32 MH073553, R01 MH078052, R01 MH089811, R24 MH102794 CDC U48DP005018]
  6. Dartmouth Health Promotion and Disease Prevention Research Center from the Centers for Disease Control and Prevention [U48DP005018]

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Background: The Foundation for the National Institutes of Health Sarcopenia Project validated cutpoints for appendicular lean mass (ALM) to identify individuals at risk for functional impairment. Recognizing possible underlying mechanisms between adipose tissue and muscle, we sought to apply the recent definitions and determine the relationship with markers of glucose homeostasis and inflammation in individuals with sarcopenia and sarcopenic obesity. Methods: The National Health and Nutrition Examination Surveys 1999-2004 were used to identify 4984 adults aged >= 60 years with DEXA measures. Sarcopenia was defined using ALM (men<19.75 kg, women<15.02 kg) and ALM adjusted for body mass index (BMI; men<0.789 kg/m(2), women<0.512 kg/m(2)). Sarcopenic obesity was defined as subjects fulfilling the criteria for sarcopenia and obesity by body fat (men >= 25%, women >= 35%). We assessed the association between ALM and ALM:BMI with inflammatory and markers of glucose homeostasis, both as continuous variables but also classifying as having sarcopenic obesity or not after adjusting for confounding variables including pro-inflammatory chronic diseases such as diabetes and cancer. Results: Mean age was 71.1 years (56.5%) females. Prevalence of sarcopenia and sarcopenic obesity were (ALM definition: 29.9 and 24.4%; ALM:BMI definition: 23.0 and 22.7%). There were significant associations with ALM and In C-reactive protein (beta = 0.0287; p = 0.001), fibrinogen (beta = 0.519; p < 0.001), and HOMA-IR (beta = 0.359; p < 0.001). Using ALM:BMI, significant associations were observed with in CRP beta = -2.58; p = 0.001), fibrinogen (beta = -124.2; p < 0.001), and HOMA-IR (beta = -6.63; p < 0.001). Sarcopenic obesity using the ALM:BMI definition demonstrated significant associations with CRP (beta = 0.422; p < 0.001), fibrinogen (beta = 22.5; p < 0.001), but not HOMA-IR (beta = 1.19; p = 0.13). Strong associations with seen with increased levels of fibrinogen and CRP with sarcopenic obesity (ALM:BMI definition) that persisted after adjusting for diabetes and cancer. Conclusions: Biologically plausible associations exist between ALM:BMI and inflammation and HOMA-IR that were not observed when using ALM alone. Future study should validate each of these definitions to prevent disparate results from being determined. (C) 2016 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism. All rights reserved.

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