Introduction: Recent studies suggested that sarcopenia may be a significant comorbidity of diabetes mellitus (DM). Nonetheless, studies with nationally representative data are scarce, and the changing trend of sarcopenia prevalence over time is largely unknown. Therefore, we aimed to estimate and compare the prevalence of sarcopenia in diabetic and nondiabetic US older population, and to explore the potential predictors of sarcopenia as well as the trend of sarcopenia prevalent in the past decades. Methods: Data were retrieved from the National Health and Nutrition Examination Survey (NHANES). Sarcopenia and DM were defined according to corresponding diagnosis criteria. Weighted prevalence was calculated and compared between diabetic and nondiabetic participants. The differences among age and ethnicity groups were explored. Results: A total of 6,381 US adults (>50 years) were involved. The overall prevalence of sarcopenia was 17.8% for US elders, and the prevalence was higher (27.9% vs. 15.7%) in those with diabetes ones than those without. Stepwise regression revealed that sarcopenia was significantly associated with DM (adjusted odds ratio = 1.37, 95% CI: 1.08–1.22; p < 0.05) after controlling for potential confounders including gender, age, ethnicity, educational level, BMI, and muscle strengthening activity. A slight fluctuation but overall increasing trend of sarcopenia prevalence was observed among diabetic elders, while no obvious changing trend was observed in their counterparts in recent decades. Conclusion: Diabetic US older adults face significantly higher risk of sarcopenia when compared with their nondiabetic counterparts. Gender, age, ethnicity, educational level, and obesity were important influencing factors of sarcopenia development.

Background: Recently, several observational studies reported that smoking is associated with shortened leucocyte telomere length (LTL), which has been considered as a marker of tissue self-repair capability, regeneration and aging. However, patterns of tobacco consumption and cessation varied, whether concrete smoking status and quantity are the causes for shortened LTL remains unknown. Method: Genetic summary statistics of smoking status (current smoker, never smoking, previous smoker), smoking quantity (pack years of cigarette consumption) as well as LTL were sourced from the UK Biobank. Two-sample mendelian randomization (MR) method was adopted, while allele harmonization and clumping were performed in advance. MR estimates of inverse variance weighted method were obtained, and R 4.2.2 was used for all analyses. Results: There were 472,174 eligible European ancestry participants, and 113 instrumental SNPs regarding smoking status (current: 15 SNPs; never: 78 SNPs; previous: 20 SNPs) as well as 11 SNPs regarding pack years of cigarette smoking included. For the relationships, current smoking status was statistical significantly associated with shorter LTL (r=-0.27, p=0.013), whereas never smoking was positively associated with LTL (r=0.21, p<0.0001). Former cigarette smoking failed to reach significance though a negative trend presented (r=-0.15, p=0.221). In terms of consumption quantity, larger pack years was significantly linked to shorter LTL (r=-0.08, p=0.008). Conclusion: This MR study supports a causal effect of smoking on risk of shortened LTL. Smoking may inhibit tissue repair and regeneration while quitting may considerably decrease related risk.