Koster-Rasmussen R.,Copenhagen University |
Koster-Rasmussen R.,University of Southern Denmark |
Permin C.A.,Copenhagen University |
Siersma V.,Copenhagen University |
And 7 more authors.
Objective: To examine the impact of smoking cessation on body weight compared with normal long-term weight development. Methods: Of 1970 adults (20-69 years) in a rural town in Denmark invited to take part in the study in 1998-2000, 1374 (70%) participated. After 9 years, 1121 participated in the follow-up study. Weight changes were compared using multivariable regression models. Results: The mean baseline weight of never-smokers was 76.4 kg (SD 16.0). The adjusted weight of smokers and ex-smokers differed by - 4.2 kg (95% CI: - 5.9, - 2.6), and - 0.7 kg (95% CI: - 2.5, 1.1), respectively. The adjusted weight gain rate (kg/year) of never-smokers, smokers, and ex-smokers was 0.213, 0.127, and 0.105, respectively. The absolute post cessation weight gain (PCWG) was 5.0 kg (SD 7.0), and the adjusted PCWG was 2.8. kg (95% CI: 1.7, 3.9) compared with never-smokers, and 3.5. kg (95% CI: 2.3, 4.8) compared with smokers. The follow-up weight did not differ between quitters and never-smokers (0.1 kg; 95% CI: - 2.4, 2.6). Conclusion: Smokers weigh less than never-smokers. By quitting, they gain weight and end up weighing the same as comparable never-smokers. Weight gain rates differ by smoking status. Consequently, PCWG depends on the length of follow-up. Our graphical model indicates that smoking cessation results in a return to normal weight development. © 2015 Elsevier Inc. Source
Deelen J.,Leiden University |
Beekman M.,Leiden University |
Uh H.-W.,Leiden University |
Broer L.,Leiden University |
And 104 more authors.
Human Molecular Genetics
The genetic contribution to the variation in human lifespan is ~25%. Despite the large number of identified disease-susceptibility loci, it is not known which loci influence population mortality. We performed a genome-wide association meta-analysis of 7729 long-lived individuals of European descent (≥85 years) and 16 121 younger controls (<65 years) followed by replication in an additional set of 13 060 long-lived individuals and 61 156 controls. In addition, we performed a subset analysis in cases aged ≥90 years. We observed genomewide significant association with longevity, as reflected by survival to ages beyond 90 years, at a novel locus, rs2149954, on chromosome 5q33.3 (OR =1.10, P = 1.74 × 10-8). We also confirmed association of rs4420638 on chromosome 19q13.32 (OR =0.72, P = 3.40 × 10-36), representing the TOMM40/APOE/APOC1 locus. In a prospective meta-analysis (n = 34 103), the minor allele of rs2149954 (T) on chromosome 5q33.3 associates with increased survival (HR = 0.95, P = 0.003). This allele has previously been reported to associate with low blood pressure in middle age. Interestingly, the minor allele (T) associates with decreased cardiovascular mortality risk, independent of blood pressure.We report on the first GWAS-identified longevity locus on chromosome 5q33.3 influencing survival in the general European population. The minor allele of this locus associates with low blood pressure in middle age, although the contribution of this allele to survival may be less dependent on blood pressure. Hence, the pleiotropic mechanisms by which this intragenic variation contributes to lifespan regulation have to be elucidated. © The Author 2014. Published by Oxford University Press. All rights reserved. Source