Risk factors and biomarkers of low lung function in early adulthood in the Lifelines study

Author(s):  
Núria Olvera Ocaña ◽  
Àlvar Agustí ◽  
Sandra Casas ◽  
Judith M. Vonk ◽  
Tamara Garcia ◽  
...  
2020 ◽  
pp. 2001600
Author(s):  
Vânia Rocha ◽  
Sílvia Fraga ◽  
Carla Moreira ◽  
Cristian Carmeli ◽  
Alexandra Lenoir ◽  
...  

BackgroundLung function is an important predictor of health and a marker of physical functioning at older ages. This study aimed to quantify the years of lung function lost according to disadvantaged socioeconomic conditions across life-course.MethodsThis multicohort study used harmonised individual-level data from six European cohorts with information on life-course socioeconomic disadvantage and lung function assessed by FEV1 and FVC. 70496 participants (51% women) aged 18–93 years were included. Socioeconomic disadvantage was measured in early life (low paternal occupational position), early adulthood (low educational level), and adulthood (low occupational position). Risk factors for poor lung function (e.g., smoking, obesity, sedentary behaviour, cardiovascular and respiratory diseases) were included as potential mediators. The years of lung function lost due to socioeconomic disadvantage were computed at each life stage.ResultsSocioeconomic disadvantage during life-course was associated with a lower FEV1. By age 45, individuals experiencing disadvantaged socioeconomic conditions had lost 4 to 5 years of healthy lung function versus their more advantaged counterparts (low educational level: −4.36 [95% CI −7.33; −2.37] for men and −5.14 [−10.32; −2.71] for women; low occupational position: −5.62 [−7.98; −4.90] for men and −4.32 [−13.31; −2.27] for women), after accounting for the risk factors for lung function. By ages 65 and 85, the years lung function lost due to socioeconomic disadvantage decreased by 2 to 4 years, depending on the socioeconomic indicator. Sensitivity analysis using FVC yielded similar results to those using FEV1.ConclusionLife-course socioeconomic disadvantage is associated with lower lung function and predicts a significant number of years of lung function loss in adulthood and older ages.


2021 ◽  
pp. 1-14
Author(s):  
Thao Ha ◽  
Mark J. Van Ryzin ◽  
Kit K. Elam

Abstract Previous studies have established that individual characteristics such as violent behavior, substance use, and high-risk sexual behavior, as well as negative relationships with parents and friends, are all risk factors for intimate partner violence (IPV). In this longitudinal prospective study, we investigated whether violent behavior, substance use, and high-risk sexual behavior in early adulthood (ages 22–23 years) mediated the link between family conflict and coercive relationship talk with friends in adolescence (ages 16–17 years) and dyadic IPV in adulthood (ages 28–30 years). A total of 998 individuals participated in multimethod assessments, including observations of interactions with parents and friends. Data from multiple reporters were used for variables of interest including court records, parental and self-reports of violence, self-reports of high-sexual-risk behaviors and substance use, and self- and romantic partner-reports of IPV. Longitudinal mediation analyses showed that violent behavior during early adulthood mediated the link between coercive relationship talk with friends in adolescence and dyadic IPV in adulthood. No other mediation paths were found and there was no evidence of gender differences. Results are discussed with attention to the interpersonal socialization processes by which IPV emerges relative to individual risk factors.


Author(s):  
Sara M. Mensink‐Bout ◽  
Susana Santos ◽  
Johan C. de Jongste ◽  
Vincent W.V. Jaddoe ◽  
Liesbeth Duijts

2021 ◽  
Vol 8 (1) ◽  
pp. e000759
Author(s):  
Daniel Higbee ◽  
Raquel Granell ◽  
Esther Walton ◽  
Roxanna Korologou-Linden ◽  
George Davey Smith ◽  
...  

RationaleLarge retrospective case-control studies have reported an association between chronic obstructive pulmonary disease (COPD), reduced lung function and an increased risk of Alzheimer’s disease. However, it remains unclear if these diseases are causally linked, or due to shared risk factors. Conventional observational epidemiology suffers from unmeasured confounding and reverse causation. Additional analyses addressing causality are required.ObjectivesTo examine a causal relationship between COPD, lung function and Alzheimer’s disease.MethodsUsing two-sample Mendelian randomisation, we used single nucleotide polymorphisms (SNPs) identified in a genome wide association study (GWAS) for lung function as instrumental variables (exposure). Additionally, we used SNPs discovered in a GWAS for COPD in those with moderate to very severe obstruction. The effect of these SNPs on Alzheimer’s disease (outcome) was taken from a GWAS based on a sample of 24 807 patients and 55 058 controls.ResultsWe found minimal evidence for an effect of either lung function (OR: 1.02 per SD; 95% CI 0.91 to 1.13; p value 0.68) or liability for COPD on Alzheimer’s disease (OR: 0.97 per SD; 95% CI 0.92 to 1.03; p value 0.40).ConclusionNeither reduced lung function nor liability COPD are likely to be causally associated with an increased risk of Alzheimer’s, any observed association is likely due to unmeasured confounding. Scientific attention and health prevention policy may be better focused on overlapping risk factors, rather than attempts to reduce risk of Alzheimer’s disease by targeting impaired lung function or COPD directly.


2020 ◽  
Vol 16 (S6) ◽  
Author(s):  
Rachel Peterson ◽  
Kristen M. George ◽  
Paola Gilsanz ◽  
Elizabeth Rose Mayeda ◽  
M. Maria Glymour ◽  
...  

Author(s):  
Alicia Abellan ◽  
Raquel Garcia ◽  
Céline Roda ◽  
Mireia Gascón ◽  
Judith Garcia-Aymerich ◽  
...  

2018 ◽  
Vol 48 (4) ◽  
pp. 546-559 ◽  
Author(s):  
Thomas W. Wojciechowski

This study seeks to examine heterogeneity in developmental patterns of ecstasy use during adolescence and early adulthood among juvenile offenders and identify risk factors predicting development. Group-based trajectory modeling was utilized to elucidate heterogeneity in developmental patterns of ecstasy use. Multinomial logistic regression was utilized to identify covariates that affected the risk of assignment to groups elucidated in the trajectory model. A five-group model was found to best fit the ecstasy use data. Baseline measures of deviant peer association, self-control, other drug use, and race were identified as important risk factors predicting patterns of development. Risk of ecstasy use may be greatest for some juvenile offenders during critical periods of the life course and some social and personal characteristics that may elevate risk. Stability that is characteristic of self-control may be highly relevant for predicting persistent ecstasy use during adolescence and early adulthood.


2021 ◽  
Author(s):  
Daniel Hui ◽  
Christopher S. Thom ◽  
Kimberly Lorenz ◽  
Scott M. Damrauer ◽  
Themistocles L. Assimes ◽  
...  

An inverse correlation between stature and risk of coronary artery disease (CAD) has been observed in several epidemiologic studies, and recent Mendelian randomization (MR) experiments have suggested evidence that this association may be causal. However, the extent to which the effect estimated by MR can be explained by established cardiovascular risk factors is unclear, with a recent report suggesting that lung function traits could fully explain the height-CAD effect. To clarify this relationship, we utilized the largest set of genetic instruments for human stature to date, comprising >2,000 genetic variants for height and CAD. In univariable analysis, we confirmed that a one standard deviation decrease in height (~6.5 cm) was associated with a 12.0% increase in the risk of CAD, consistent with previous reports. In multivariable analysis accounting for effects from up to 12 established risk factors, we observed a >3-fold attenuation in the causal effect of height on CAD susceptibility (3.7%, p = 2.1x10-2). We observed minimal effects of lung function traits on CAD risk in our analyses, indicating that these traits are unlikely to explain the residual association between height and CAD risk. In sum, these results suggest that height does not add meaningful clinical impact on CAD risk prediction beyond established risk factors.


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