Zunehmen nach dem Rauchstopp: Ab wie viel Kilo es für Ihre Fitness im Alter zählt

<h4>Introduction</h4>Smoking cessation is important for healthy ageing, but accompanying weight change may influence subsequent functional vulnerability. We examined whether attained cessation duration and weight change across the observed cessation interval distinguished later frailty risk and frailty-index progression.<h4>Methods</h4>This longitudinal secondary analysis included 27020 Health and Retirement Study participants with self-reported smoking and body-weight data, and valid consecutive frailty assessments who were non-frail at risk-set entry during 1998-2020. Smoking status, body weight, and covariates were assessed biennially by structured interviews. Time-varying Cox models estimated incident frailty (frailty index ≥0.25), mixed-effects models assessed annual frailty-index change, and restricted cubic splines evaluated continuous associations.<h4>Results</h4>Over a median follow-up of 8.1 years, 10641 incident frailty cases occurred during 250439.9 person-years. Compared with current smokers, quitters before baseline had lower frailty risk (hazard ratio, HR=0.79; 95% CI: 0.75-0.84), whereas follow-up quitters overall did not (HR=0.98; 95% CI: 0.90-1.07). In the duration spline, HRs at 0, 7, and 10 years of attained cessation duration were 1.14 (95% CI: 1.01-1.28), 0.79 (95% CI: 0.67-0.93), and 0.73 (95% CI: 0.60-0.89), respectively. Among follow-up quitters, >10.0 kg versus 0.1-5.0 kg weight gain was associated with higher risk (HR=1.94; 95% CI: 1.44-2.61); stand

<h4>Background</h4>Electrocardiographic left ventricular hypertrophy is a known risk factor for cardiovascular morbidity and mortality. Although smoking cessation has general cardiovascular benefits, its impact on left ventricular hypertrophy regression remains unclear.<h4>Objective</h4>To investigate whether smoking cessation is associated with regression of electrocardiographic left ventricular hypertrophy.<h4>Methods</h4>We analyzed data from 752 non-hypertensive participants (695 males; mean age, 47.8 ± 9.2 years) who underwent annual health checkups. Left ventricular hypertrophy was defined using the Sokolow-Lyon criteria (SV1 + RV5 > 3.5 mV). Measurements were compared between baseline and 6 years after smoking cessation. Multivariable logistic regression analysis was used to identify predictors of left ventricular hypertrophy progression.<h4>Results</h4>After 6 years, the average left ventricular voltage decreased significantly (2.47 → 2.41 mV, p < 0.0001), and the prevalence of left ventricular hypertrophy declined from 8.4% to 6.5%. This regression occurred despite increases in body weight (65.7 → 68.1 kg, p < 0.0001) and systolic blood pressure (112.8 → 122.0 mmHg, p < 0.0001). Left ventricular hypertrophy regression was observed in both participants who received antihypertensive medication and in those who did not. Multivariable analysis identified antihypertensive medication as an independent predictor of electrocardiographic LVH regression.<h4>Conclusions</h4>Smo

Smoking cessation is a major public health goal, yet concerns about post-cessation weight gain remain a significant barrier for many smokers. The metabolic and behavioral changes following nicotine withdrawal frequently lead to increased caloric intake and reduced energy expenditure, potentially triggering relapse. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), originally developed for type 2 diabetes and later approved for weight management, have recently been investigated as a potential strategy to address both nicotine dependence and weight control. Emerging evidence from preclinical studies and limited clinical trials suggests that GLP-1 RAs may reduce nicotine cravings and intake by modulating central reward pathways while simultaneously curbing appetite and supporting weight loss. This dual mechanism may improve quit success rates and mitigate the psychological burden of post-cessation weight gain. However, the current human evidence base is limited, with small sample sizes, short follow-up periods, and reliance on preliminary data. While the pharmacological profile and cardiometabolic benefits of GLP-1 RAs make them a promising candidate for adjunctive use in smoking cessation, more rigorous randomized controlled trials are required to confirm efficacy, evaluate safety, and establish clinical guidelines. This narrative review synthesizes existing evidence to highlight both the potential and the current uncertainties surrounding GLP-1 RAs as dual-target pharmaco