John A Batsis1, Todd A Mackenzie2, Jonathan D Jones3, Francisco Lopez-Jimenez4, Stephen J Bartels5. 1. Section of General Internal Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, NH, United States; Geisel School of Medicine at Dartmouth and The Dartmouth Institute for Health Policy & Clinical Practice, Lebanon, NH, United States; Dartmouth Centers for Health and Aging, Dartmouth College, Hanover, NH, United States; Health Promotion Research Center at Dartmouth, Lebanon, NH, United States; Dartmouth Weight & Wellness Center, Lebanon, NH, United States. Electronic address: john.batsis@gmail.com. 2. Geisel School of Medicine at Dartmouth and The Dartmouth Institute for Health Policy & Clinical Practice, Lebanon, NH, United States. 3. Geisel School of Medicine at Dartmouth and The Dartmouth Institute for Health Policy & Clinical Practice, Lebanon, NH, United States; Section of Rheumatology, Dartmouth-Hitchcock Medical Center, Lebanon, NH, United States. 4. Division of Cardiovascular Disease, Department of Medicine, Mayo Clinic, Rochester, MN, United States. 5. Geisel School of Medicine at Dartmouth and The Dartmouth Institute for Health Policy & Clinical Practice, Lebanon, NH, United States; Dartmouth Centers for Health and Aging, Dartmouth College, Hanover, NH, United States; Health Promotion Research Center at Dartmouth, Lebanon, NH, United States.
Abstract
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/m2, women<0.512 kg/m2). 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 ln C-reactive protein (β = 0.0287; p = 0.001), fibrinogen (β = 0.519; p < 0.001), and HOMA-IR (β = 0.359; p < 0.001). Using ALM:BMI, significant associations were observed with ln CRP (β = -2.58; p = 0.001), fibrinogen (β = -124.2; p < 0.001), and HOMA-IR (β = -6.63; p < 0.001). Sarcopenic obesity using the ALM:BMI definition demonstrated significant associations with CRP (β = 0.422; p < 0.001), fibrinogen (β = 22.5; p < 0.001), but not HOMA-IR (β = 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.
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/m2, women<0.512 kg/m2). 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 ln C-reactive protein (β = 0.0287; p = 0.001), fibrinogen (β = 0.519; p < 0.001), and HOMA-IR (β = 0.359; p < 0.001). Using ALM:BMI, significant associations were observed with ln CRP (β = -2.58; p = 0.001), fibrinogen (β = -124.2; p < 0.001), and HOMA-IR (β = -6.63; p < 0.001). Sarcopenic obesity using the ALM:BMI definition demonstrated significant associations with CRP (β = 0.422; p < 0.001), fibrinogen (β = 22.5; p < 0.001), but not HOMA-IR (β = 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.
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