Summary 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 4,984 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 homestasis, 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.
To determine whether leptin is related to all-cause and cardiovascular (CV) mortality in older adults.
Participants 60 years and older with plasma leptin level measurements from the National Health ...and Nutrition Examination Survey III (1988-1994) and mortality data linked to the National Death Index were included. We created sex-specific tertiles of leptin (men: 4.2-7.7 μg/L; women: 11.5-21.4 μg/L) to identify the effect of leptin on all-cause and CV mortality. We also determined whether leptin predicted mortality in patients with obesity. We classified obesity using 4 possible definitions: body mass index 30 kg/m(2) or greater; body fat 25% or more in men and 35% or more in women; waist circumference 102 cm or greater in men and 88 cm or greater in women; and waist-hip ratio 0.85 or higher in women and 0.95 or higher in men. Sex-specific proportional hazard models were used to assess the effect of leptin on all-cause and CV mortality.
Of 1794 participants, 51.6% were women; the mean age was 70.3±0.4 years, and the follow-up period was 12.5 years with 994 deaths (469 were CV deaths). All-cause mortality in the highest leptin tertile was significant neither in men (hazard ratio HR, 1.23; 95% CI, 0.93-1.63) nor in women (HR, 0.97; 95% CI, 0.68-1.40). CV mortality was the highest in the highest leptin tertile in men (HR, 1.69; 95% CI, 1.06-2.70) but not in women (HR, 1.21; 95% CI, 0.73-1.98). Evaluating the effect of leptin in subgroups of different obesity definitions, we found that high leptin levels as predict CV mortality in men as measured by waist circumference or body fat.
Elevated leptin level is predictive of CV mortality only in men. Leptin may provide additional mortality discrimination in obese men.
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