Adult height and lung function as markers of life course exposures: Associations with risk factors and cause-specific mortality

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.

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Race and crime: The contribution of individual, familial, and neighborhood level risk factors to life-course-persistent offending

PsycEXTRA Dataset ◽

10.1037/e552582012-022 ◽

2002 ◽

Author(s):

Alex R. Piquero ◽

Terrie E. Moffitt ◽

Brian Lawton

Keyword(s):

Risk Factors ◽

Life Course ◽

Race And Crime ◽

Life Course Persistent ◽

Persistent Offending ◽

Neighborhood Level

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Cardio‐metabolic risk factors during childhood in relation to lung function and asthma

Pediatric Allergy and Immunology ◽

10.1111/pai.13509 ◽

2021 ◽

Author(s):

Sara M. Mensink‐Bout ◽

Susana Santos ◽

Johan C. de Jongste ◽

Vincent W.V. Jaddoe ◽

Liesbeth Duijts

Keyword(s):

Risk Factors ◽

Lung Function ◽

Metabolic Risk Factors ◽

Metabolic Risk

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RISK FACTORS OF INCREASING LUNG FUNCTION DECLINE IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE: A REAL-WORLD ANALYSIS

Respirology ◽

10.1111/resp.13207_425 ◽

2017 ◽

Vol 22 ◽

pp. 248-248

Keyword(s):

Risk Factors ◽

Chronic Obstructive Pulmonary Disease ◽

Lung Function ◽

Pulmonary Disease ◽

Real World ◽

Chronic Obstructive ◽

Lung Function Decline ◽

Obstructive Pulmonary Disease

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Examining the possible causal relationship between lung function, COPD and Alzheimer’s disease: a Mendelian randomisation study

BMJ Open Respiratory Research ◽

10.1136/bmjresp-2020-000759 ◽

2021 ◽

Vol 8 (1) ◽

pp. e000759

Author(s):

Daniel Higbee ◽

Raquel Granell ◽

Esther Walton ◽

Roxanna Korologou-Linden ◽

George Davey Smith ◽

...

Keyword(s):

Risk Factors ◽

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Lung Function ◽

Causal Relationship ◽

Mendelian Randomisation ◽

P Value ◽

Unmeasured Confounding ◽

Increased Risk ◽

Shared Risk

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.

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Newborn DNA-methylation, childhood lung function, and the risks of asthma and COPD across the life course

European Respiratory Journal ◽

10.1183/13993003.01795-2018 ◽

2019 ◽

Vol 53 (4) ◽

pp. 1801795 ◽

Cited By ~ 17

Author(s):

Herman T. den Dekker ◽

Kimberley Burrows ◽

Janine F. Felix ◽

Lucas A. Salas ◽

Ivana Nedeljkovic ◽

...

Keyword(s):

Gene Expression ◽

Lung Function ◽

Life Course ◽

Cord Blood ◽

Childhood Asthma ◽

Respiratory Health ◽

Forced Expiratory Volume ◽

Chronic Obstructive ◽

Obstructive Pulmonary Disease ◽

The Life Course

RationaleWe aimed to identify differentially methylated regions (DMRs) in cord blood DNA associated with childhood lung function, asthma and chronic obstructive pulmonary disease (COPD) across the life course.MethodsWe meta-analysed epigenome-wide data of 1688 children from five cohorts to identify cord blood DMRs and their annotated genes, in relation to forced expiratory volume in 1 s (FEV1), FEV1/forced vital capacity (FVC) ratio and forced expiratory flow at 75% of FVC at ages 7–13 years. Identified DMRs were explored for associations with childhood asthma, adult lung function and COPD, gene expression and involvement in biological processes.ResultsWe identified 59 DMRs associated with childhood lung function, of which 18 were associated with childhood asthma and nine with COPD in adulthood. Genes annotated to the top 10 identified DMRs were HOXA5, PAOX, LINC00602, ABCA7, PER3, CLCA1, VENTX, NUDT12, PTPRN2 and TCL1A. Differential gene expression in blood was observed for 32 DMRs in childhood and 18 in adulthood. Genes related with 16 identified DMRs were associated with respiratory developmental or pathogenic pathways.InterpretationOur findings suggest that the epigenetic status of the newborn affects respiratory health and disease across the life course.

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