scholarly journals Testing the causal effects between subjective wellbeing and physical health using Mendelian randomisation

2018 ◽  
Author(s):  
Robyn E Wootton ◽  
Rebecca B Lawn ◽  
Louise A C Millard ◽  
Neil M Davies ◽  
Amy E Taylor ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Physical Health ◽  
Subjective Wellbeing ◽  
Ldl Cholesterol ◽  
Causal Effect ◽  
Hdl Cholesterol ◽  
Mendelian Randomisation ◽  
Artery Disease

AbstractObjectivesTo investigate whether the association between subjective wellbeing (subjective happiness and life satisfaction) and physical health is causal.DesignWe conducted two-sample bidirectional Mendelian randomisation between subjective wellbeing and six measures of physical health: coronary artery disease, myocardial infarction, total cholesterol, HDL cholesterol, LDL cholesterol and body mass index (BMI).ParticipantsWe used summary data from four large genome-wide association study consortia: CARDIoGRAMplusC4D for coronary artery disease and myocardial infarction; the Global Lipids Genetics Consortium for cholesterol measures; the Genetic Investigation of Anthropometric Traits consortium for BMI; and the Social Science Genetics Association Consortium for subjective wellbeing. A replication analysis was conducted using 337,112 individuals from the UK Biobank (54% female, mean age =56.87, SD=8.00 years at recruitment).Main outcome measuresCoronary artery disease, myocardial infarction, total cholesterol, HDL cholesterol, LDL cholesterol, BMI and subjective wellbeing.ResultsThere was evidence of a causal effect of BMI on subjective wellbeing such that each 1 kg/m2 increase in BMI caused a 0.045 (95%CI 0.006 to 0.084, p=0.023) SD reduction in subjective wellbeing. Replication analyses provided strong evidence of an effect of BMI on satisfaction with health (β=0.034 (95% CI: −0.042 to −0.026) unit decrease in health satisfaction per SD increase in BMI, p<2-16). There was no clear evidence of a causal effect between subjective wellbeing and the other physical health measures in either direction.ConclusionsOur results suggest that a higher BMI lowers subjective wellbeing. Our replication analysis confirmed this finding, suggesting the effect in middle-age is driven by satisfaction with health. BMI is a modifiable determinant and therefore, our study provides further motivation to tackle the obesity epidemic because of the knock-on effects of higher BMI on subjective wellbeing.

scholarly journals Modifiable Factors for Coronary Artery Disease, Myocardial Infarction, and Stroke: A Mendelian Randomisation Analysis (P15-006-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Tao Huang
Keyword(s):  
Risk Factors ◽  
Myocardial Infarction ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Pulse Pressure ◽  
Causal Effect ◽  
Mendelian Randomisation ◽  
Carotid Artery Plaque ◽  
Modifiable Factors ◽  
Artery Disease

Abstract Objectives We aimed to examine the causal associations of potentially risk factors, including lifestyle/dietary, cardiometabolic, and inflammatory factors, with risks of coronary artery disease (CAD), myocardial infarction (MI), and stroke. Methods We used single nucleotide polymorphisms (SNPs) associated with risk factors as instrumental variables to test the causal effect of risk factors on cardiovascular diseases using summary-level data from consortia. Results A total of 53 potentially risk factors were included. A Bonferroni corrected threshold of P = 0.00094 was considered to be significant. Genetically predicted higher BMI (odds ratio: 1.43, confidence interval: 1.26 to1.63 per 1 kg/m2, P = 7.64 × 10−8), smoking initiation (1.62, 1.42 to1.85 per year, P = 2.72 × 10−12), vitamin E (3.22, 1.81 to 4.63, P = 1.33 × 10−6). sIL-6R (1.63, 1.22 to 2.05, P = 0.0002), LDL (1.60, 1.46 to 1.75, P = 8.78 × 10−23), TC (1.48, 1.34 to 1.64, P = 1.14 × 10−13), TG (1.27, 1.13 to 1.43, P = 7.32 × 10−5), SBP (1.03, 1.02 to 1.05, P = 6.8 × 10−5), asthma (1.07, 1.05 to 1.09, P = 3.94 × 10−12), T2DM (1.12, 1.08 to 1.17, P = 4.37 × 10−8) were associated with higher risk of CAD; whilst, genetically predicted education (0.64, 0.55 to 0.75 per year, P = 2.68 × 10−8), and HDL (0.84, 0.76 to 0.92, P = 0.0003) were associated with lower risk of CAD. Similar results were observed for MI. In addition, atrial firillation (1.24, 1.18 to 1.30 P = 2.75 × 10−17), carotid artery plaque (1.24, 1.10 to 1.41, P = 0.0006), asthma (1.04 to 1.02, 1.06, P = 6.81 × 10−5), and T2DM (1.09, 1.04 to 1.14, P = 0.0002) were associated with higher risk of stroke per unit increase in log odds. We further observed suggestive associations of morning person, iron, fasting glucose, insulin, HbA1c, uric acid, and pulse pressure with CAD and suggestive associations of education, intelligence, Hcy, HDL, and pulse pressure with stroke. Conclusions Our results identified several modifiable factors as treatment targets for prevention of CAD, MI, or stroke. Funding Sources None. Supporting Tables, Images and/or Graphs

LDL-cholesterol and HDL-cholesterol concentrations decrease during the day

2002 ◽  
Vol 39 (3) ◽  
pp. 241-249 ◽  
Author(s):  
Takashi Miida ◽  
Yuichi Nakamura ◽  
Toru Mezaki ◽  
Osamu Hanyu ◽  
Seitaro Maruyama ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Coronary Arteries ◽  
Ldl Cholesterol ◽  
Hdl Cholesterol ◽  
Normal Coronary Arteries ◽  
The Mean ◽  
Baseline Levels ◽  
Artery Disease ◽  
Homogeneous Assays

Background Homogenous assays for LDL-cholesterol (LDL-C) and HDL-cholesterol (HDL-C) are highly accurate, with little interference from triglyceride. Using these methods, we measured postprandial LDL-C and HDL-C. Earlier studies suggested a postprandial decrease in LDL-C. Methods To elucidate whether LDL-C and HDL-C decrease significantly during the day, we determined daily profiles of LDL-C and HDL-C using homogeneous assays in subjects with normal coronary arteries (N; n = 10), and subjects with coronary artery disease (CAD; n = 23). Results In both groups, LDL-C and HDL-C were significantly lower from after breakfast until midnight than they were before breakfast. The next morning, they returned to baseline levels. The mean reduction in LDL-C was 0·09--0·13 mmol/L in N and 0·05--0·20 mmol/L in CAD, while that in HDL-C was 0·02--0·06 mmol/L in N and 0·00--0·05 mmol/L in CAD. Conclusion LDL-C and HDL-C decrease significantly over the course of the day.

scholarly journals ADHD genetic liability and physical health outcomes - A two-sample Mendelian randomization study

2019 ◽  
Author(s):  
Beate Leppert ◽  
Lucy Riglin ◽  
Christina Dardani ◽  
Ajay Thapar ◽  
James R Staley ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Childhood Obesity ◽  
Health Outcomes ◽  
Physical Health ◽  
Mendelian Randomization ◽  
Causal Effect ◽  
Genetic Liability ◽  
Physical Health Outcomes ◽  
Artery Disease

AbstractObjectiveAttention-deficit/hyperactivity disorder (ADHD) has been associated with a broad range of physical health problems, including cardiometabolic, neurological and immunological conditions. Determining whether ADHD plays a causal role in these associations is of great importance for treatment and prevention but also because comorbid health problems further increase the serious social and economic impacts of ADHD on individuals and their families.MethodsWe used a two-sample Mendelian randomization (MR) approach to examine the causal relationships between genetic liability for ADHD and previously implicated physical health conditions. 11 genetic variants associated with ADHD were obtained from the latest summary statistics. Consistent effects obtained from IVW, weighted median and MR Egger methods were taken forward for sensitivity analysis, including bidirectional MR and multivariable MR (MVMR).ResultsWe found evidence of a causal effect of genetic liability for ADHD on childhood obesity (OR:1.29 (95% CI:1.02,1.63)) and coronary artery disease (CAD) (OR:1.11 (95% CI:1.03,1.19)) with consistent results across different MR approaches. There was further evidence for a bidirectional relationship between genetic liability for ADHD and childhood obesity. The effect of genetic liability for ADHD on CAD was independent of smoking heaviness but was attenuated when simultaneously controlling for childhood obesity. There was little evidence for a causal effect on other cardiometabolic, immunological, neurological disorders and lung cancer.ConclusionOur findings strengthen the argument for early treatment and support for children with ADHD and their families and especially promoting physical activity and providing them with dietary advice to reduce future risk for developing CAD.Key MessageEpidemiological studies have reported observational associations between ADHD and adult onset physical health outcomes.Mendelian Randomization can be used to assess causal associations for ADHD on health outcomes that would traditionally require long term follow-up and may suffer confoundingWe found that genetic liability for ADHD was associated with coronary artery disease and there was evidence for a bidirectional association between genetic liability for ADHD and childhood obesityMultivariable mendelian randomization suggests that the link between genetic liability and coronary artery disease might partially act through childhood obesity but was independent of smoking heavinessThere was little evidence of a causal of ADHD on other cardiometabolic and immunological diseases.

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