scholarly journals Is there a causal relationship between executive function and liability to mental health and substance use? A Mendelian randomisation approach

2022 ◽  
Author(s):  
Sabrina M.I Burton ◽  
Hannah M Sallis ◽  
Alexander S Hatoum ◽  
Marcus R Munafo ◽  
Zoe E Reed
Keyword(s):  
Mental Health ◽  
Substance Use ◽  
Executive Function ◽  
Alcohol Consumption ◽  
Causal Relationship ◽  
Causal Effect ◽  
Smoking Initiation ◽  
Mendelian Randomisation ◽  
P Value ◽  
Causal Relationships

Background: Executive function consists of several cognitive control processes that are able to regulate lower level processes. Poorer performance in tasks designed to test executive function is associated with a range of psychopathologies such as schizophrenia, major depressive disorder (MDD) and anxiety, as well as with smoking and alcohol consumption. Despite these well-documented associations, whether they reflect causal relationships, and if so in what direction, remains unclear. We aimed to establish whether there is a causal relationship between a latent factor for performance on multiple executive function tasks - which we refer to as common executive function (cEF) - and liability to schizophrenia, MDD, anxiety, smoking initiation, alcohol consumption, alcohol dependence and cannabis use disorder (CUD), and the directionality of any relationship observed. Methods: We used a two-sample bidirectional Mendelian randomisation (MR) approach using genome-wide association study (GWAS) summary data from large cohorts (N=17,310 to 848,460) to examine whether causal relationships exist, and if so in which direction. Results: We found evidence of a causal effect of increased cEF on reduced schizophrenia liability (IVW: OR=0.10; 95% CI 0.05 to 0.19; p-value=3.43x10-12), reduced MDD liability (IVW: OR=0.52; 95% CI 0.38 to 0.72; p-value=5.23x10-05), decreased drinks per week (IVW: β=-0.06; 95% CI -0.10 to -0.02; p-value=0.003), and reduced CUD liability (IVW: OR=0.27; 95% CI 0.12 to 0.61; p-value=1.58x10-03). We also found evidence of a causal effect of increased schizophrenia liability on decreased cEF (IVW: β=-0.04; 95% CI -0.04 to -0.03; p-value=3.25x10-27), as well as smoking initiation on decreased cEF (IVW: β=-0.06; 95%CI -0.09 to -0.03; p-value=6.11x10-05). Conclusion: Our results indicate a potential bidirectional causal relationship between a latent factor measure of executive function (cEF) and schizophrenia liability, a possible causal effect of increased cEF on reduced MDD liability, CUD liability, and alcohol consumption, and a possible causal effect of smoking initiation on decreased cEF. These results suggest that executive function should be considered as a potential risk factor for some mental health and substance use outcomes, and may also be impacted by mental health (particularly schizophrenia). Further studies are required to improve our understanding of the underlying mechanisms of these effects, but our results suggest that executive function may be a promising intervention target. These results may therefore inform the prioritisation of experimental medicine studies (e.g., of executive function interventions), for both mental health and substance use outcomes, to improve the likelihood of successful translation.

scholarly journals Evidence for Causal Effects of Smoking Initiation and Alcohol Consumption on Substance Use Outcomes

2021 ◽  
Author(s):  
Zoe E. Reed ◽  
Robyn E. Wootton ◽  
Marcus R. Munafò
Keyword(s):  
Substance Use ◽  
Risk Factor ◽  
Alcohol Consumption ◽  
Opioid Dependence ◽  
Smoking Initiation ◽  
Cannabis Use ◽  
Causal Effects ◽  
P Value ◽  
Gateway Hypothesis ◽  
Shared Risk

AbstractBackground and AimsThe ‘gateway’ hypothesis proposes that initial use of drugs such as tobacco and alcohol can lead to subsequent more problematic drug use. However, it is unclear whether true casual pathways exist, or whether there is instead a shared underlying risk factor. We used bidirectional Mendelian Randomisation (MR) to test these two competing hypotheses.MethodsWe conducted two-sample MR analyses, using genome-wide association data for smoking initiation, alcoholic drinks per week, cannabis use and dependence, cocaine and opioid dependence. We used several MR methods that rely on different assumptions: inverse-variance weighted (IVW), MR-Egger, weighted median, simple mode and weighted mode. Consistent results across these methods would support stronger inference.ResultsWe found evidence of causal effects from smoking initiation to increased drinks per week (IVW: β=0.06; 95% CI 0.03 to 0.09; p-value=9.44×10-06), cannabis use (IVW: OR=1.34; 95% CI 1.24 to 1.44; p-value=1.95×10-14), and cannabis dependence (IVW: OR=1.68; 95% CI 1.12 to 2.51; p-value=0.01). We also found evidence of an effect of cannabis use on increased likelihood of smoking initiation (IVW: OR=1.39; 95% CI=1.08 to 1.80; p-value=0.01). We did not find evidence of an effect of drinks per week on substance use outcomes, except for weak evidence of an effect on cannabis use. We also found evidence of an effect of opioid dependence on increased drinks per week (IVW: β=0.002; 95% CI=0.0005 to 0.003; p-value=8.61×10-03).ConclusionsOverall, we found evidence suggesting a causal pathway from smoking initiation to alcohol consumption, and both cannabis use and dependence, which may support the gateway hypothesis. However, we also found causal effects of cannabis use on smoking initiation, and opioid dependence on alcohol consumption, which suggests the existence of a shared risk factor. Further research should explore whether this is the case, and in particular the nature of any shared risk factors.

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

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.

scholarly journals Causal Association Between Heart Failure and Alzheimer’s Disease: A Two-Sample Bidirectional Mendelian Randomization Study

2022 ◽  
Vol 12 ◽  
Author(s):  
Chenglin Duan ◽  
Jingjing Shi ◽  
Guozhen Yuan ◽  
Xintian Shou ◽  
Ting Chen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Sensitivity Analysis ◽  
Causal Relationship ◽  
Observational Studies ◽  
Mendelian Randomization ◽  
Causal Effect ◽  
Causal Relationships ◽  
Simple Mode

Background: Traditional observational studies have demonstrated an association between heart failure and Alzheimer’s disease. The strengths of observational studies lie in their speed of implementation, cost, and applicability to rare diseases. However, observational studies have several limitations, such as uncontrollable confounders. Therefore, we employed Mendelian randomization of genetic variants to evaluate the causal relationships existing between AD and HF, which can avoid these limitations.Materials and Methods: A two-sample bidirectional MR analysis was employed. All datasets were results from the UK’s Medical Research Council Integrative Epidemiology Unit genome-wide association study database, and we conducted a series of control steps to select the most suitable single-nucleotide polymorphisms for MR analysis, for which five primary methods are offered. We reversed the functions of exposure and outcomes to explore the causal direction of HF and AD. Sensitivity analysis was used to conduct several tests to avoid heterogeneity and pleiotropic bias in the MR results.Results: Our MR studies did not support a meaningful causal relationship between AD on HF (MR-Egger, p = 0.634 > 0.05; weighted median (WM), p = 0.337 > 0.05; inverse variance weighted (IVW), p = 0.471 > 0.05; simple mode, p = 0.454 > 0.05; weighted mode, p = 0.401 > 0.05). At the same time, we did not find a significant causal relationship between HF and AD with four of the methods (MR-Egger, p = 0.195 > 0.05; IVW, p = 0.0879 > 0.05; simple mode, p = 0.170 > 0.05; weighted mode, p = 0.110 > 0.05), but the WM method indicated a significant effect of HF on AD (p = 0.025 < 0.05). Because the statistical powers of IVW and MR-Egger are more than that of WM, we think that there is no causal effect of HF on AD. Sensitivity analysis and horizontal pleiotropy were not detected in the MR analysis.Conclusion: Our results did not provide significant evidence indicating any causal relationships between HF and AD in the European population. Therefore, more large-scale datasets or datasets related to similar factors are expected for further MR analysis.

scholarly journals Potential influence of socioeconomic status on genetic correlations between alcohol consumption measures and mental health

2019 ◽  
Vol 50 (3) ◽  
pp. 484-498 ◽  
Author(s):  
Andries T. Marees ◽  
Dirk J. A. Smit ◽  
Jue-Sheng Ong ◽  
Stuart MacGregor ◽  
Jiyuan An ◽  
...  
Keyword(s):  
Mental Health ◽  
Substance Use ◽  
Alcohol Consumption ◽  
Genetic Correlations ◽  
High Alcohol ◽  
Genetic Associations ◽  
Potential Influence ◽  
High Alcohol Consumption ◽  
Genome Wide ◽  
Consumption Frequency

AbstractBackground. Frequency and quantity of alcohol consumption are metrics commonly used to measure alcohol consumption behaviors. Epidemiological studies indicate that these alcohol consumption measures are differentially associated with (mental) health outcomes and socioeconomic status (SES). The current study aims to elucidate to what extent genetic risk factors are shared between frequency and quantity of alcohol consumption, and how these alcohol consumption measures are genetically associated with four broad phenotypic categories: (i) SES; (ii) substance use disorders; (iii) other psychiatric disorders; and (iv) psychological/personality traits.Methods. Genome-Wide Association analyses were conducted to test genetic associations with alcohol consumption frequency (N = 438 308) and alcohol consumption quantity (N = 307 098 regular alcohol drinkers) within UK Biobank. For the other phenotypes, we used genome-wide association studies summary statistics. Genetic correlations (rg) between the alcohol measures and other phenotypes were estimated using LD score regression.Results. We found a substantial genetic correlation between the frequency and quantity of alcohol consumption (rg = 0.52). Nevertheless, both measures consistently showed opposite genetic correlations with SES traits, and many substance use, psychiatric, and psychological/personality traits. High alcohol consumption frequency was genetically associated with high SES and low risk of substance use disorders and other psychiatric disorders, whereas the opposite applies for high alcohol consumption quantity.Conclusions. Although the frequency and quantity of alcohol consumption show substantial genetic overlap, they consistently show opposite patterns of genetic associations with SES-related phenotypes. Future studies should carefully consider the potential influence of SES on the shared genetic etiology between alcohol and adverse (mental) health outcomes.

scholarly journals Evidence for causal effects of lifetime smoking on risk for depression and schizophrenia: a Mendelian randomisation study

2019 ◽  
Vol 50 (14) ◽  
pp. 2435-2443 ◽  
Author(s):  
Robyn E. Wootton ◽  
Rebecca C. Richmond ◽  
Bobby G. Stuijfzand ◽  
Rebecca B. Lawn ◽  
Hannah M. Sallis ◽  
...  
Keyword(s):  
Causal Effect ◽  
Association Studies ◽  
Smoking Initiation ◽  
Smoking Behaviour ◽  
Positive Control ◽  
Mendelian Randomisation ◽  
Genome Wide Association Studies ◽  
Weak Evidence ◽  
Smoking Duration ◽  
The Uk

AbstractBackgroundSmoking prevalence is higher amongst individuals with schizophrenia and depression compared with the general population. Mendelian randomisation (MR) can examine whether this association is causal using genetic variants identified in genome-wide association studies (GWAS).MethodsWe conducted two-sample MR to explore the bi-directional effects of smoking on schizophrenia and depression. For smoking behaviour, we used (1) smoking initiation GWAS from the GSCAN consortium and (2) we conducted our own GWAS of lifetime smoking behaviour (which captures smoking duration, heaviness and cessation) in a sample of 462690 individuals from the UK Biobank. We validated this instrument using positive control outcomes (e.g. lung cancer). For schizophrenia and depression we used GWAS from the PGC consortium.ResultsThere was strong evidence to suggest smoking is a risk factor for both schizophrenia (odds ratio (OR) 2.27, 95% confidence interval (CI) 1.67–3.08, p < 0.001) and depression (OR 1.99, 95% CI 1.71–2.32, p < 0.001). Results were consistent across both lifetime smoking and smoking initiation. We found some evidence that genetic liability to depression increases smoking (β = 0.091, 95% CI 0.027–0.155, p = 0.005) but evidence was mixed for schizophrenia (β = 0.022, 95% CI 0.005–0.038, p = 0.009) with very weak evidence for an effect on smoking initiation.ConclusionsThese findings suggest that the association between smoking, schizophrenia and depression is due, at least in part, to a causal effect of smoking, providing further evidence for the detrimental consequences of smoking on mental health.

scholarly journals Hubungan antara Perilaku Merokok Anggota Rumah Tangga dengan Perilaku Merokok Remaja di Indonesia

2020 ◽  
Vol 23 (2) ◽  
pp. 80-88
Author(s):  
Olwin Nainggolan ◽  
Ika Dharmayanti ◽  
A Yudi Kristanto
Keyword(s):  
Alcohol Consumption ◽  
Service Providers ◽  
Economic Status ◽  
Smoking Behavior ◽  
Secondary Data ◽  
Smoking Initiation ◽  
Adolescent Smoking ◽  
P Value ◽  
Consumption Behavior ◽  
Confounding Variables

This study aimed to know the association and risk levels of household other members and adolescent smoking behaviors in Indonesia. As confounding variables of study involving Alcohol Consumption Behavior, Lived Area, and Social-Economics Status Variables. A study hypothesis declared that there was a signifi cant correlation between smoking behavior of household other members as a smoker with the smoking behavior of 15 to 18 years old after being controlled by other variables. Furthermore, this study using a Basic Health Research Secondary Data of 2018 aged 15 until 18 years and a multivariable analyzed uses logistic regression. The results showed a signifi cant correlation (p-value 0,000) between Household Other Members as a Smoker with smoking behavior of 15 to 18 years old after being controlled by confounding variables with OR 1,449 (95% CI 1,346-1,56-0). Smoker Variable not as a Head of Household was signifi cantly correlated (p-value 0,007) with OR 2,002 (95% CI 1,211-3,377), Alcohol Consumption Behavior was signifi cantly correlated (P-value 0,000) with OR 20,602 (95% CI 17,611-24,101), Lived Area with OR 1,129 (95% CI 1,051-1,212), also Social Economic Status with OR 1,098 (95%CI 1,024-1,178). An Alcohol Consumption Behavior Variable was the most dominant variable in determining Adolescent Smoking Behavior. We should focalize on areas identity is driven by health service providers, stakeholders, and policymakers. Accordingly, formulate awareness programs and education, particularly adolescents, to eliminate smoking initiation.  Abstrak Penelitian ini bertujuan untuk mengetahui hubungan dan besaran risiko perilaku merokok anggota rumah tangga lain dengan perilaku merokok remaja berusia 15 sampai dengan 18 tahun di Indonesia. Variable perancu pada penelitian ini meliputi perilaku konsumsi alkohol, wilayah tempat tinggal, serta status sosial ekonomi responden. Hipotesis penelitian ini adalah ada hubungan yang bermakna antara perilaku merokok anggota rumah tangga lain sebagai perokok, dengan perilaku merokok remaja usia 15 sampai dengan 18 tahun setelah dikontrol oleh variabel lain. Penelitian ini menggunakan data sekunder Riset Kesehatan Dasar (Riskesdas) tahun 2018 dengan rentang usia 15-18 tahun dan data di analisis secara multivariabel menggunakan regresi logistik. Hasil penelitian diperoleh bahwa terdapat hubungan yang bermakna (p value 0,000) antara anggota rumah tangga lain sebagai perokok dengan dengan perilaku merokok pada remaja usia 15 sampai dengan 18 tahun setelah dikontrol oleh variabel perancu dengan OR 1,449 (95% CI 1,346-1,56-0). Variabel perokok bukan sebagai kepala rumah tangga berhubungan bermakna (p value 0,007) dengan OR 2,002 (95% CI 1,2113,377), perilaku minum alkohol berhubungan bermakna (p value 0,000) dengan OR 20,602 (95% CI 17,611-24,101), wilayah tempat tinggal responden dengan OR 1,129 (95% CI 1,051-1,212), serta status sosial ekonomi dengan OR 1,098 (95%CI 1,024-1,178). Variabel perilaku minum alkohol adalah variabel yang paling besar pengaruhnya terhadap perilaku merokok pada remaja. Perlu fokus identifi kasi area oleh penyedia layanan kesehatan serta para stake holder pembuat kebijakan dalam merumuskan program kesadaran dan pendidikan khususnya pada remaja untuk eliminasi inisiasi merokok.

scholarly journals Does smoking cause lower educational attainment and general cognitive ability? Triangulation of causal evidence using multiple study designs

2020 ◽  
pp. 1-9
Author(s):  
Suzanne H. Gage ◽  
Hannah M. Sallis ◽  
Glenda Lassi ◽  
Robyn E. Wootton ◽  
Claire Mokrysz ◽  
...  
Keyword(s):  
Educational Attainment ◽  
Cognitive Ability ◽  
Fluid Intelligence ◽  
Causal Effect ◽  
Smoking Initiation ◽  
Sensitivity Analyses ◽  
Mendelian Randomisation ◽  
General Cognitive Ability ◽  
Inverse Variance ◽  
Lower Educational Attainment

Abstract Background Observational studies have found associations between smoking and both poorer cognitive ability and lower educational attainment; however, evaluating causality is challenging. We used two complementary methods to explore this. Methods We conducted observational analyses of up to 12 004 participants in a cohort study (Study One) and Mendelian randomisation (MR) analyses using summary and cohort data (Study Two). Outcome measures were cognitive ability at age 15 and educational attainment at age 16 (Study One), and educational attainment and fluid intelligence (Study Two). Results Study One: heaviness of smoking at age 15 was associated with lower cognitive ability at age 15 and lower educational attainment at age 16. Adjustment for potential confounders partially attenuated findings (e.g. fully adjusted cognitive ability β −0.736, 95% CI −1.238 to −0.233, p = 0.004; fully adjusted educational attainment β −1.254, 95% CI −1.597 to −0.911, p < 0.001). Study Two: MR indicated that both smoking initiation and lifetime smoking predict lower educational attainment (e.g. smoking initiation to educational attainment inverse-variance weighted MR β −0.197, 95% CI −0.223 to −0.171, p = 1.78 × 10−49). Educational attainment results were robust to sensitivity analyses, while analyses of general cognitive ability were less so. Conclusion We find some evidence of a causal effect of smoking on lower educational attainment, but not cognitive ability. Triangulation of evidence across observational and MR methods is a strength, but the genetic variants associated with smoking initiation may be pleiotropic, suggesting caution in interpreting these results. The nature of this pleiotropy warrants further study.

scholarly journals Tendency towards being a “Morning person” increases risk of Parkinson’s disease: evidence from Mendelian randomisation

2018 ◽  
Author(s):  
AJ Noyce ◽  
DA Kia ◽  
K Heilbron ◽  
JEC Jepson ◽  
G Hemani ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Circadian Rhythm ◽  
Causal Relationship ◽  
Odds Ratio ◽  
Causal Effect ◽  
Coffee Consumption ◽  
Sensitivity Analyses ◽  
Mendelian Randomisation ◽  
Effect Estimate

AbstractBackgroundCircadian rhythm may play a role in neurodegenerative diseases such as Parkinson’s disease (PD). Chronotype is the behavioural manifestation of circadian rhythm and Mendelian randomisation (MR) involves the use of genetic variants to explore causal effects of exposures on outcomes. This study aimed to explore a causal relationship between chronotype and coffee consumption on risk of PD.MethodsTwo-sample MR was undertaken using publicly available GWAS data. Associations between genetic instrumental variables (IV) and “morning person” (one extreme of chronotype) were obtained from the personal genetics company 23andMe, Inc., and UK Biobank, and consisted of the per-allele odds ratio of being a “morning person” for 15 independent variants. The per-allele difference in log-odds of PD for each variant was estimated from a recent meta-analysis. The inverse variance weight method was used to estimate an odds ratio (OR) for the effect of being a “morning person” on PD. Additional MR methods were used to check for bias in the IVW estimate, arising through violation of MR assumptions. The results were compared to analyses employing a genetic instrument of coffee consumption, because coffee consumption has been previously inversely linked to PD.FindingsBeing a “morning person” was causally linked with risk of PD (OR 1⋅27; 95% confidence interval 1⋅06-1⋅51; p=0⋅012). Sensitivity analyses did not suggest that invalid instruments were biasing the effect estimate and there was no evidence for a reverse causal relationship between liability for PD and chronotype. There was no robust evidence for a causal effect of high coffee consumption using IV analysis, but the effect was imprecisely estimated (OR 1⋅12; 95% CI 0⋅89-1⋅42; p=0⋅22).InterpretationWe observed causal evidence to support the notion that being a “morning person”, a phenotype driven by the circadian clock, is associated with a higher risk of PD. Further work on the mechanisms is warranted and may lead to novel therapeutic targets.FundingNo specific funding source.

scholarly journals Genetic and Causal Relationship Between Coffee Intake and Cardiometabolic Risks: Cross-Phenotype Association And Mendelian Randomization Analysis

2020 ◽  
Author(s):  
Xinpei Wang ◽  
Jinzhu Jia ◽  
Tao Huang
Keyword(s):  
Genetic Structure ◽  
Genetic Correlation ◽  
Causal Relationship ◽  
Mendelian Randomization ◽  
Causal Effect ◽  
P Value ◽  
Coffee Intake ◽  
Randomization Analysis ◽  
Cardiometabolic Traits ◽  
Shared Genetic

Abstract Background: Many epidemiological studies have shown that there is a significant association between coffee intake and cardiometabolic diseases, which may be due to the common genetic structure or causal relationship. Methods: We used linkage disequilibrium score regression analysis to calculate the genetic correlation between coffee intake and 23 cardiometabolic traits (diseases), and then used cross-phenotype association analysis to identify the shared genetic loci for the trait pairs with significant genetic correlation. Besides, a bi-directional Mendelian Randomization analysis was used to explore the causal relationship between coffee intake and 23 cardiometabolic traits (diseases).Results: Coffee intake has a significant genetic correlation (after Bonferroni correction) with body mass index (BMI) (Rg = 0.3713, P-value = 4.13ⅹ10-64), body fat percentage (BF%) (Rg = 0.2810, P-value = 1.81ⅹ10-13), type 2 diabetes (T2D) (unadjusted for BMI) (Rg = 0.1189, P-value = 8.80ⅹ10-6), heart failure (HF) (Rg = 0.2626, P-value = 6.00ⅹ10-9), atrial fibrillation (AF) (Rg = 0.1007, P-value = 4.30ⅹ10-5). There are 203, 18, 86, 13, 38 independent shared loci between coffee intake and BMI, BF%, T2D, HF, AF, respectively, among which 22, 2, 23, 4,13 loci do not achieve genome-wide significance in single trait GWAS. Coffee intake has significant causal effect on BMI (b = 0.0717, P-value = 2.33ⅹ10-5), T2D (unadjusted for BMI, OR = 1.27, P-value = 1.46ⅹ10-7), and intracerebral haemorrhage (ICH) (all types ICH: OR = 1.86, P-value = 3.37ⅹ10-4; deep ICH: OR = 2.12, P-value = 2.93ⅹ10-4 ). And BMI (b = 0.3694, P-value=3.64ⅹ10-154), BF% (b = 0.5500, P-value = 1.68ⅹ10-4), T2D (adjusted for BMI, b = -0.0252, P-value = 4.83ⅹ10-6) and triglycerides (TG) (b = -0.1209, P-value = 4.56ⅹ10-15) have significant causal effect on coffee intake.Conclusions: Our study identified the shared genetic structure and causal relationship between coffee intake and several cardiometabolic traits (diseases), providing a new insight into the mechanism of coffee intake and cardiometabolic traits (diseases).

Sign in / Sign up

Export Citation Format

Share Document