The Causal Effects of Place on Health and Longevity.
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ABSTRACT:
SUBMITTER: Deryugina T
PROVIDER: S-EPMC10512696 | biostudies-literature | 2021
REPOSITORIES: biostudies-literature
Publications
The Causal Effects of Place on Health and Longevity.
Deryugina Tatyana T Molitor David D
The journal of economic perspectives : a journal of the American Economic Association 20210101 4
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Project description:Parents with better-educated children are healthier and live longer, but whether there is a causal effect of children's education on their parents' health and longevity is unclear. First, we demonstrate an association between adults' offspring education and parental mortality in the 1958 British birth cohort study, which remains substantial-about two additional years of life-even when comparing parents with similar socioeconomic status. Second, we use the 1972 educational reform in England and Wales, which increased the minimum school leaving age from 15 to 16 years, to identify the presence of a causal effect of children's education on parental health and longevity using census-linked data from the Office for National Statistics Longitudinal Study. Results reveal that children's education has no causal effects on a wide range of parental mortality and health outcomes. We interpret these findings discussing the role of universal health care and education for socioeconomic inequality in Great Britain.
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Project description:Growing evidence suggests that exposure to fine particulate matter (PM2.5) may reduce life expectancy; however, the causal pathways of PM2.5 exposure affecting life expectancy remain unknown. Here, we assess the causal effects of genetically predicted PM2.5 concentration on common chronic diseases and longevity using a Mendelian randomization (MR) statistical framework based on large-scale genome-wide association studies (GWAS) (>400,000 participants). After adjusting for other types of air pollution and smoking, we find significant causal relationships between PM2.5 concentration and angina pectoris, hypercholesterolaemia and hypothyroidism, but no causal relationship with longevity. Mediation analysis shows that although the association between PM2.5 concentration and longevity is not significant, PM2.5 exposure indirectly affects longevity via diastolic blood pressure (DBP), hypertension, angina pectoris, hypercholesterolaemia and Alzheimer's disease, with a mediated proportion of 31.5, 70.9, 2.5, 100, and 24.7%, respectively. Our findings indicate that public health policies to control air pollution may help improve life expectancy.
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Project description:Although high-protein diets continue to be popular for weight loss and type 2 diabetes, evidence suggests that worsening renal function may occur in individuals with-and perhaps without-impaired kidney function. High dietary protein intake can cause intraglomerular hypertension, which may result in kidney hyperfiltration, glomerular injury, and proteinuria. It is possible that long-term high protein intake may lead to de novo CKD. The quality of dietary protein may also play a role in kidney health. Compared with protein from plant sources, animal protein has been associated with an increased risk of ESKD in several observational studies, including the Singapore Chinese Health Study. Potential mediators of kidney damage from animal protein include dietary acid load, phosphate content, gut microbiome dysbiosis, and resultant inflammation. In light of such findings, adopting current dietary approaches that include a high proportion of protein for weight reduction or glycemic control should be considered with care in those at high risk for kidney disease. Given the possibility of residual confounding within some observational studies and the conflicting evidence from previous trials, long-term studies including those with large sample sizes are warranted to better ascertain the effects of high protein intake on kidney health.
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Project description:BackgroundThis work delves into the relationship between cardiovascular health (CVH) and aging. Previous studies have shown an association of ideal CVH with a slower aging rate, measured by epigenetic age acceleration (EAA). However, the causal relationship between CVH and EAA has remained unexplored.Methods and resultsWe performed genome-wide association studies (GWAS) on the (12-point) CVH score and its components using the Taiwan Biobank data, in which weighted genetic risk scores were treated as instrumental variables. Subsequently, we conducted a one-sample Mendelian Randomization (MR) analysis with the two-stage least-squares method on 2383 participants to examine the causal relationship between the (12-point) CVH score and EAA. As a result, we observed a significant causal effect of the CVH score on GrimAge acceleration (GrimEAA) (β [SE]: - 0.993 [0.363] year; p = 0.0063) and DNA methylation-based plasminogen activator inhibitor-1 (DNAmPAI-1) (β [SE]: - 0.294 [0.099] standard deviation (sd) of DNAmPAI-1; p = 0.0030). Digging individual CVH components in depth, the ideal total cholesterol score (0 [poor], 1 [intermediate], or 2 [ideal]) was causally associated with DNAmPAI-1 (β [SE]: - 0.452 [0.150] sd of DNAmPAI-1; false discovery rate [FDR] q = 0.0102). The ideal body mass index (BMI) score was causally associated with GrimEAA (β [SE]: - 2.382 [0.952] years; FDR q = 0.0498) and DunedinPACE (β [SE]: - 0.097 [0.030]; FDR q = 0.0044). We also performed a two-sample MR analysis using the summary statistics from European GWAS. We observed that the (12-point) CVH score exhibits a significant causal effect on Horvath's intrinsic epigenetic age acceleration (β [SE]: - 0.389 [0.186] years; p = 0.036) and GrimEAA (β [SE]: - 0.526 [0.244] years; p = 0.031). Furthermore, we detected causal effects of BMI (β [SE]: 0.599 [0.081] years; q = 2.91E-12), never smoking (β [SE]: - 2.981 [0.524] years; q = 1.63E-7), walking (β [SE]: - 4.313 [1.236] years; q = 0.004), and dried fruit intake (β [SE]: - 1.523 [0.504] years; q = 0.013) on GrimEAA in the European population.ConclusionsOur research confirms the causal link between maintaining an ideal CVH and epigenetic age. It provides a tangible pathway for individuals to improve their health and potentially slow aging.
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Project description:BackgroundObservational studies have suggested that paternal longevity is associated with reduced risks of cardiovascular diseases, yet the causal association remains to be determined.ObjectivesTo investigate whether Mendelian randomization (MR) results support a causal role of paternal longevity for risks of cardiovascular diseases.MethodsGenetic variants associated with paternal longevity and cardiovascular diseases were obtained from public genome-wide association study data. We used inverse variance weighted MR under a random-effects model to provide causal estimates between paternal longevity and cardiovascular diseases.ResultsPaternal longevity was associated with decreased risks of coronary heart disease (odds ratio (OR): 0.08; 95% confidence interval (CI): 0.02-0.37; p = 0.001) and peripheral artery disease (OR: 0.15; 95% CI: 0.03-0.65; p = 0.011). No significant differences were observed in hypertension, atrial fibrillation, heart failure, transient ischemic attack, ischemic stroke, or cardiac death. The weighted median method revealed consistent results between genetically instrumented paternal longevity and decreased risk of coronary heart disease and peripheral artery disease. No significant differences were observed in the MR-Egger results. Multivariable MR consistently indicated causal associations between paternal longevity and decreased cardiovascular diseases. The leave-one-out analysis suggested that the causal associations were not affected by individual single-nucleotide polymorphisms. The intercept of the MR-Egger estimator and funnel plot revealed no indication of horizontal pleiotropic effects.ConclusionsOur MR analyses supported a causal role of paternal longevity for decreased risks of coronary heart disease and peripheral artery disease, which highlighted the need for better monitoring and intervention of cardiovascular diseases in populations with premature paternal death.
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Project description:Current methods of cost effectiveness analysis implicitly assume zero spillovers among social ties. This can underestimate the benefits of health interventions and misallocate resources toward interventions with lower comprehensive effects. We discuss the implications of social spillovers for program evaluation and document the first evidence of causal spillovers of health behaviors between spouses by leveraging experimental data from the Lung Health Study (smoking) and COMBINE Study (drinking). We find large decreases in spousal substance use from treatments with a therapy component, which reduces the incremental cost effectiveness ratios of some treatments by 12 to 18 percent.
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Project description:BackgroundGut microbiome plays a significant role in longevity, and dysbiosis is indeed one of the hallmarks of aging. However, the causal relationship between gut microbiota and human longevity or aging remains elusive.MethodsOur study assessed the causal relationships between gut microbiome and longevity using Mendelian Randomization (MR). Summary statistics for the gut microbiome were obtained from four genome-wide association study (GWAS) meta-analysis of the MiBioGen consortium (N = 18,340), Dutch Microbiome Project (N = 7738), German individuals (N = 8956), and Finland individuals (N = 5959). Summary statistics for Longevity were obtained from Five GWAS meta-analysis, including Human healthspan (N = 300,447), Longevity (N = 36,745), Lifespans (N = 1,012,240), Parental longevity (N = 389,166), and Frailty (one of the primary aging-linked physiological hallmarks, N = 175,226).ResultsOur findings reveal several noteworthy associations, including a negative correlation between Bacteroides massiliensis and longevity, whereas the genus Subdoligranulum and Alistipes, as well as species Alistipes senegalensis and Alistipes shahii, exhibited positive associations with specific longevity traits. Moreover, the microbial pathway of coenzyme A biosynthesis I, pyruvate fermentation to acetate and lactate II, and pentose phosphate pathway exhibited positive associations with two or more traits linked to longevity. Conversely, the TCA cycle VIII (helicobacter) pathway consistently demonstrated a negative correlation with lifespan and parental longevity.ConclusionsOur findings of this MR study indicated many significant associations between gut microbiome and longevity. These microbial taxa and pathways may potentially play a protective role in promoting longevity or have a suppressive effect on lifespan.
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