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1.
Hum Mol Genet ; 2019 Sep 13.
Artigo em Inglês | MEDLINE | ID: mdl-31518406

RESUMO

Humans are social animals that experience intense suffering when they perceive a lack of social connection. Modern societies are experiencing an epidemic of loneliness. While the experience of loneliness is universally human, some people report experiencing greater loneliness than others. Loneliness is more strongly associated with mortality than obesity, emphasizing the need to understand the nature of the relationship between loneliness and health. While it is intuitive that circumstantial factors such as marital status and age influence loneliness, there is also compelling evidence of a genetic predisposition towards loneliness. To better understand the genetic architecture of loneliness and its relationship with associated outcomes, we extended the genome-wide association study (GWAS) meta-analysis of loneliness to 511 280 subjects, and detect 19 significant genetic variants from 16 loci, including four novel loci, as well as 58 significantly associated genes. We investigated the genetic overlap with a wide range of physical and mental health traits by computing genetic correlations and by building loneliness polygenic scores in an independent sample of 18 498 individuals with electronic health record data to conduct a PheWAS with. A genetic predisposition towards loneliness was associated with cardiovascular, psychiatric, and metabolic disorders, and triglycerides and high-density lipoproteins. Mendelian randomization analyses showed evidence of a causal, increasing, effect of both BMI and body fat on loneliness. Our results provide a framework for future studies of the genetic basis of loneliness and its relationship to mental and physical health.

2.
Br J Psychiatry ; : 1-7, 2019 Sep 17.
Artigo em Inglês | MEDLINE | ID: mdl-31526406

RESUMO

BACKGROUND: There is increasing evidence that smoking is a risk factor for severe mental illness, including bipolar disorder. Conversely, patients with bipolar disorder might smoke more (often) as a result of the psychiatric disorder. AIMS: We conducted a bidirectional Mendelian randomisation (MR) study to investigate the direction and evidence for a causal nature of the relationship between smoking and bipolar disorder. METHOD: We used publicly available summary statistics from genome-wide association studies on bipolar disorder, smoking initiation, smoking heaviness, smoking cessation and lifetime smoking (i.e. a compound measure of heaviness, duration and cessation). We applied analytical methods with different, orthogonal assumptions to triangulate results, including inverse-variance weighted (IVW), MR-Egger, MR-Egger SIMEX, weighted-median, weighted-mode and Steiger-filtered analyses. RESULTS: Across different methods of MR, consistent evidence was found for a positive effect of smoking on the odds of bipolar disorder (smoking initiation ORIVW = 1.46, 95% CI 1.28-1.66, P = 1.44 × 10-8, lifetime smoking ORIVW = 1.72, 95% CI 1.29-2.28, P = 1.8 × 10-4). The MR analyses of the effect of liability to bipolar disorder on smoking provided no clear evidence of a strong causal effect (smoking heaviness betaIVW = 0.028, 95% CI 0.003-0.053, P = 2.9 × 10-2). CONCLUSIONS: These findings suggest that smoking initiation and lifetime smoking are likely to be a causal risk factor for developing bipolar disorder. We found some evidence that liability to bipolar disorder increased smoking heaviness. Given that smoking is a modifiable risk factor, these findings further support investment into smoking prevention and treatment in order to reduce mental health problems in future generations. DECLARATION OF INTEREST: W.v.d.B received fees in the past 3 years from Indivior, C&A Pharma, Opiant and Angelini. G.M.G. is a National Institute for Health Research (NIHR) Emeritus Senior Investigator, holds shares in P1vital and has served as consultant, advisor or CME speaker in the past 3 years for Allergan, Angelini, Compass Pathways, MSD, Lundbeck (/Otsuka and /Takeda), Medscape, Minervra, P1Vital, Pfizer, Sage, Servier, Shire and Sun Pharma.

3.
Nat Neurosci ; 22(7): 1196, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31168101

RESUMO

Several occurrences of the word 'schizophrenia' have been re-worded as 'liability to schizophrenia' or 'schizophrenia risk', including in the title, which should have been "GWAS of lifetime cannabis use reveals new risk loci, genetic overlap with psychiatric traits, and a causal effect of schizophrenia liability," as well as in Supplementary Figures 1-10 and Supplementary Tables 7-10, to more accurately reflect the findings of the work.

5.
Nicotine Tob Res ; 2018 Oct 26.
Artigo em Inglês | MEDLINE | ID: mdl-30365022

RESUMO

Introduction: Cigarette smokers are at increased risk of poor sleep behaviours. However, it is largely unknown whether these associations are due to shared (genetic) risk factors and/or causal effects (which may be bi-directional). Methods: We obtained summary-level data of genome-wide association studies of smoking (smoking initiation (n=74,035), cigarettes per day (n=38,181) and smoking cessation (n=41,278)) and sleep behaviours (sleep duration and chronotype, or 'morningness') (n=128,266) and insomnia (n=113,006)). Using LD score regression, we calculated genetic correlations between smoking and sleep behaviours. To investigate causal effects, we employed Mendelian randomization (MR), both with summary-level data and individual level data (n=333,581 UK Biobank participants). For MR with summary-level data, individual genetic variants were combined with inverse-variance weighted meta-analysis, weighted median regression, MR-RAPS (Robust Adjusted Profile Score) and MR Egger methods. Results: We found negative genetic correlations between smoking initiation and sleep duration (rg=-0.14, 95% CI=-0.26 to -0.01) and smoking cessation and chronotype (rg=-0.18, -0.31 to -0.06), and positive genetic correlations between smoking initiation and insomnia (rg=0.27, 0.06 to 0.49) and cigarettes per day and insomnia (rg=0.15, 0.01 to 0.28). MR provided strong evidence that smoking more cigarettes causally decreases the odds of being a morning person, and weak evidence that insomnia causally increases smoking heaviness and decreases smoking cessation odds. Conclusions: Smoking and sleep behaviours show moderate genetic correlation. Heavier smoking seems to causally affect circadian rhythm and there is some indication that insomnia increases smoking heaviness and hampers cessation. Our findings point to sleep as a potentially interesting smoking treatment target. Implications: Using LD score regression we found evidence that smoking and different sleep behaviours (sleep duration, chronotype ('morningness') and insomnia) are moderately genetically correlated - genetic variants associated with less or poorer sleep also increased the odds of smoking (more heavily). Mendelian randomization analyses suggested that heavier smoking causally affects circadian rhythm (decreasing the odds of being a morning person) and there was some indication that insomnia increases smoking heaviness and hampers smoking cessation. Our findings indicate a complex, bi-directional relationship between smoking and sleep behaviours and point to sleep as a potentially interesting smoking treatment target.

6.
Nat Neurosci ; 21(9): 1161-1170, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-30150663

RESUMO

Cannabis use is a heritable trait that has been associated with adverse mental health outcomes. In the largest genome-wide association study (GWAS) for lifetime cannabis use to date (N = 184,765), we identified eight genome-wide significant independent single nucleotide polymorphisms in six regions. All measured genetic variants combined explained 11% of the variance. Gene-based tests revealed 35 significant genes in 16 regions, and S-PrediXcan analyses showed that 21 genes had different expression levels for cannabis users versus nonusers. The strongest finding across the different analyses was CADM2, which has been associated with substance use and risk-taking. Significant genetic correlations were found with 14 of 25 tested substance use and mental health-related traits, including smoking, alcohol use, schizophrenia and risk-taking. Mendelian randomization analysis showed evidence for a causal positive influence of schizophrenia risk on cannabis use. Overall, our study provides new insights into the etiology of cannabis use and its relation with mental health.

9.
J Sleep Res ; 27(5): e12695, 2018 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-29682839

RESUMO

Observationally, higher caffeine consumption is associated with poorer sleep and insomnia. We investigated whether these associations are a result of shared genetic risk factors and/or (possibly bidirectional) causal effects. Summary-level data were available from genome-wide association studies on caffeine intake (n = 91 462), plasma caffeine and caffeine metabolic rate (n = 9876), sleep duration and chronotype (being a "morning" versus an "evening" person) (n = 128 266), and insomnia complaints (n = 113 006). First, genetic correlations were calculated, reflecting the extent to which genetic variants influencing caffeine consumption and those influencing sleep overlap. Next, causal effects were estimated with bidirectional, two-sample Mendelian randomization. This approach utilizes the genetic variants most robustly associated with an exposure variable as an "instrument" to test causal effects. Estimates from individual variants were combined using inverse-variance weighted meta-analysis, weighted median regression and MR-Egger regression. We found no clear evidence for a genetic correlation between caffeine intake and sleep duration (rg = 0.000, p = .998), chronotype (rg = 0.086, p = .192) or insomnia complaints (rg = -0.034, p = .700). For plasma caffeine and caffeine metabolic rate, genetic correlations could not be calculated because of the small sample size. Mendelian randomization did not support causal effects of caffeine intake on sleep, or vice versa. There was weak evidence that higher plasma caffeine levels causally decrease the odds of being a morning person. Although caffeine may acutely affect sleep when taken shortly before bedtime, our findings suggest that a sustained pattern of high caffeine consumption is more likely to be associated with poorer sleep through shared environmental factors. Future research should identify such environments, which could aid the development of interventions to improve sleep.

10.
J Epidemiol Community Health ; 72(8): 708-710, 2018 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-29666151

RESUMO

BACKGROUND: Body mass index (BMI) is correlated negatively with subjective well-being and positively with depressive symptoms. Whether these associations reflect causal effects is unclear. METHODS: We examined bidirectional, causal effects between BMI and mental health with Mendelian randomisation using summary-level data from published genome-wide association studies (BMI: n=339 224; subjective well-being: n=204 966; depressive symptoms: n=161 460). Genetic variants robustly related to the exposure variable acted as instrumental variable to estimate causal effects. We combined estimates of individual genetic variants with inverse-variance weighted meta-analysis, weighted median regression and MR-Egger regression. RESULTS: There was evidence for a causal, increasing effect of BMI on depressive symptoms and suggestive evidence for a decreasing effect of BMI on subjective well-being. We found no evidence for causality in the other direction. CONCLUSION: This study provides support for a higher BMI causing poorer mental health. Further research should corroborate these findings and explore mechanisms underlying this potential causality.

11.
Addiction ; 113(7): 1333-1338, 2018 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-29334416

RESUMO

BACKGROUND AND AIMS: Epidemiological studies consistently show co-occurrence of use of different addictive substances. Whether these associations are causal or due to overlapping underlying influences remains an important question in addiction research. Methodological advances have made it possible to use published genetic associations to infer causal relationships between phenotypes. In this exploratory study, we used Mendelian randomization (MR) to examine the causality of well-established associations between nicotine, alcohol, caffeine and cannabis use. METHODS: Two-sample MR was employed to estimate bidirectional causal effects between four addictive substances: nicotine (smoking initiation and cigarettes smoked per day), caffeine (cups of coffee per day), alcohol (units per week) and cannabis (initiation). Based on existing genome-wide association results we selected genetic variants associated with the exposure measure as an instrument to estimate causal effects. Where possible we applied sensitivity analyses (MR-Egger and weighted median) more robust to horizontal pleiotropy. RESULTS: Most MR tests did not reveal causal associations. There was some weak evidence for a causal positive effect of genetically instrumented alcohol use on smoking initiation and of cigarettes per day on caffeine use, but these were not supported by the sensitivity analyses. There was also some suggestive evidence for a positive effect of alcohol use on caffeine use (only with MR-Egger) and smoking initiation on cannabis initiation (only with weighted median). None of the suggestive causal associations survived corrections for multiple testing. CONCLUSIONS: Two-sample Mendelian randomization analyses found little evidence for causal relationships between nicotine, alcohol, caffeine and cannabis use.

12.
Nicotine Tob Res ; 20(7): 836-842, 2018 Jun 07.
Artigo em Inglês | MEDLINE | ID: mdl-28575460

RESUMO

Introduction: Classical twin studies show that smoking is heritable. To determine if shared family environment plays a role in addition to genetic factors, and if they interact (G×E), we use a children-of-twins design. In a second sample, we measure genetic influence with polygenic risk scores (PRS) and environmental influence with a question on exposure to smoking during childhood. Methods: Data on smoking initiation were available for 723 children of 712 twins from the Netherlands Twin Register (64.9% female, median birth year 1985). Children were grouped in ascending order of risk, based on smoking status and zygosity of their twin-parent and his/her co-twin: never smoking twin-parent with a never smoking co-twin; never smoking twin-parent with a smoking dizygotic co-twin; never smoking twin-parent with a smoking monozygotic co-twin; and smoking twin-parent with a smoking or never smoking co-twin. For 4072 participants from the Netherlands Twin Register (67.3% female, median birth year 1973), PRS for smoking were computed and smoking initiation, smoking heaviness, and exposure to smoking during childhood were available. Results: Patterns of smoking initiation in the four group children-of-twins design suggested shared familial influences in addition to genetic factors. PRS for ever smoking were associated with smoking initiation in all individuals. PRS for smoking heaviness were associated with smoking heaviness in individuals exposed to smoking during childhood, but not in non-exposed individuals. Conclusions: Shared family environment influences smoking, over and above genetic factors. Genetic risk of smoking heaviness was only important for individuals exposed to smoking during childhood, versus those not exposed (G×E). Implications: This study adds to the very few existing children-of-twins (CoT) studies on smoking and combines a CoT design with a second research design that utilizes polygenic risk scores and data on exposure to smoking during childhood. The results show that shared family environment affects smoking behavior over and above genetic factors. There was also evidence for gene-environment interaction (G×E) such that genetic risk of heavy versus light smoking was only important for individuals who were also exposed to (second-hand) smoking during childhood. Together, these findings give additional incentive to recommending parents not to expose their children to cigarette smoking.

13.
Drug Alcohol Depend ; 183: 7-12, 2018 02 01.
Artigo em Inglês | MEDLINE | ID: mdl-29220643

RESUMO

BACKGROUND: Genetic and environmental factors contribute about equally to alcohol-related phenotypes in adulthood. In the present study, we examined whether more stress at home or low satisfaction with life might be associated with heavier drinking or more alcohol-related problems in individuals with a high genetic susceptibility to alcohol use. METHODS: Information on polygenic scores and drinking behavior was available in 6705 adults (65% female; 18-83 years) registered with the Netherlands Twin Register. Polygenic risk scores (PRSs) were constructed for all subjects based on the summary statistics of a large genome-wide association meta-analysis on alcohol consumption (grams per day). Outcome measures were quantity of alcohol consumption and alcohol-related problems assessed with the Alcohol Use Disorders Identification Test (AUDIT). Stress at home and life satisfaction were moderating variables whose significance was tested by Generalized Estimating Equation analyses taking familial relatedness, age and sex into account. RESULTS: PRSs for alcohol were significantly associated with quantity of alcohol consumption and alcohol-related problems in the past year (R2=0.11% and 0.10% respectively). Participants who reported to have experienced more stress in the past year and lower life satisfaction, scored higher on alcohol-related problems (R2=0.27% and 0.29 respectively), but not on alcohol consumption. Stress and life satisfaction did not moderate the association between PRSs and the alcohol outcome measures. CONCLUSIONS: There were significant main effects of polygenic scores and of stress and life satisfaction on drinking behavior, but there was no support for PRS-by-stress or PRS-by-life satisfaction interactions on alcohol consumption and alcohol-related problems.


Assuntos
Consumo de Bebidas Alcoólicas/genética , Alcoolismo/genética , Herança Multifatorial/genética , Satisfação Pessoal , Estresse Psicológico/psicologia , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Alcoolismo/complicações , Feminino , Interação Gene-Ambiente , Estudo de Associação Genômica Ampla , Humanos , Masculino , Pessoa de Meia-Idade , Países Baixos , Fenótipo , Fatores de Risco , Estresse Psicológico/complicações , Adulto Jovem
15.
Eur J Epidemiol ; 33(3): 323-334, 2018 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-29260431

RESUMO

Alternative tobacco products are increasing in popularity. An important question is whether their use is associated with or even leads to conventional smoking, but large-scale (European) studies are scarce. In two cohorts of Dutch adolescents (Cohort I n = 6819, mean age = 13.8 SD = 1.1, 48.2% female; Cohort II n = 2758, mean age = 17.3 SD = 1.8, 61.3% female), we investigated use of electronic (e)-cigarettes with nicotine, e-cigarettes without nicotine and waterpipe. Generalized estimating equation modelling was conducted with ever conventional smoking as the dependent variable (0 = no, 1 = yes) and ever alternative tobacco use as the independent variable, correcting for clustering within schools, age, sex and education in both cohorts. In a subsample (n = 2100), the association between alternative tobacco use at baseline and conventional smoking 6 months later was tested, taking into account smoking propensity (based on personality, susceptibility to peer pressure and smoking intentions). Ever use prevalence was 13.7% for e-cigarettes with nicotine, 29.4% for e-cigarettes without nicotine and 22.1% for waterpipe in Cohort I and 12.3, 27.6 and 45.3% respectively in Cohort II. Ever smokers had tried alternative tobacco products more often than never smokers. Among never-smoking adolescents at baseline, alternative tobacco use predicted ever smoking 6 months later (e-cigarettes with nicotine OR 11.90 95% CI 3.36-42.11; e-cigarettes without nicotine OR 5.36 95% CI 2.73-10.52; waterpipe OR 5.36 95% CI 2.78-10.31). This association was strongest for adolescents with a low baseline risk of smoking. Experimenting with alternative tobacco products is common among Dutch youth. Alternative tobacco use predicts (future) smoking, especially among adolescents with a low smoking propensity.

16.
Int J Epidemiol ; 46(6): 1958-1967, 2017 12 01.
Artigo em Inglês | MEDLINE | ID: mdl-29025033

RESUMO

Background: There is evidence for a positive relationship between cigarette and coffee consumption in smokers. Cigarette smoke increases metabolism of caffeine, so this may represent a causal effect of smoking on caffeine intake. Methods: We performed Mendelian randomization analyses in the UK Biobank (N = 114 029), the Norwegian HUNT study (N = 56 664) and the Copenhagen General Population Study (CGPS) (N = 78 650). We used the rs16969968 genetic variant as a proxy for smoking heaviness in all studies and rs4410790 and rs2472297 as proxies for coffee consumption in UK Biobank and CGPS. Analyses were conducted using linear regression and meta-analysed across studies. Results: Each additional cigarette per day consumed by current smokers was associated with higher coffee consumption (0.10 cups per day, 95% CI: 0.03, 0.17). There was weak evidence for an increase in tea consumption per additional cigarette smoked per day (0.04 cups per day, 95% CI: -0.002, 0.07). There was strong evidence that each additional copy of the minor allele of rs16969968 (which increases daily cigarette consumption) in current smokers was associated with higher coffee consumption (0.16 cups per day, 95% CI: 0.11, 0.20), but only weak evidence for an association with tea consumption (0.04 cups per day, 95% CI: -0.01, 0.09). There was no clear evidence that rs16969968 was associated with coffee or tea consumption in never or former smokers or that the coffee-related variants were associated with cigarette consumption. Conclusions: Higher cigarette consumption causally increases coffee intake. This is consistent with faster metabolism of caffeine by smokers, but could also reflect a behavioural effect of smoking on coffee drinking.


Assuntos
Cafeína/administração & dosagem , Fumar Cigarros/epidemiologia , Fumar Cigarros/genética , Café , Comportamento de Ingestão de Líquido , Adulto , Idoso , Idoso de 80 Anos ou mais , Alelos , Dinamarca/epidemiologia , Feminino , Humanos , Modelos Lineares , Masculino , Análise da Randomização Mendeliana , Metanálise como Assunto , Pessoa de Meia-Idade , Noruega/epidemiologia , Fatores de Risco , Índice de Gravidade de Doença , Reino Unido/epidemiologia , Adulto Jovem
17.
Appetite ; 118: 97-105, 2017 11 01.
Artigo em Inglês | MEDLINE | ID: mdl-28826746

RESUMO

The prevalence of overweight and obesity is increasing, due to, among other factors, increased availability of highly palatable food (food high in fat, salt and/or sugar). It has been proposed that certain foods and/or eating behaviours may be addictive, to a degree comparable to substances of abuse. The Yale Food Addiction Scale (YFAS) measures 'food addiction' by translating the diagnostic criteria for substance use disorder to eating behaviour. So far, only a few studies have examined the prevalence of food addiction in children with the YFAS for children (YFAS-C). Large-scale studies, especially among adolescents, are lacking. Adolescence is of particular interest because it is a period wherein unhealthy eating behaviours or addictive tendencies are likely to develop. The current study examines the prevalence of food addiction using the YFAS-C in a large group of Dutch adolescents (N = 2653) aged 14-21 years. With Generalized Estimation Equation (GEE) analysis we tested the relationship between food addiction symptoms and smoking, cannabis use, alcohol use, and sugar intake through drinks, while controlling for gender, age, educational level and weight class. In the total sample 2.6% met the criteria for a food addiction 'diagnosis', and the average symptom count was 1.0 (SD = 1.3, range 0-7). Symptoms of food addiction were positively associated with smoking, alcohol use, cannabis use and sugar intake. We propose that future studies focus on possible genetic/(neuro)biological mechanisms involved in both food addiction and substance use and that longitudinal designs are needed to examine possible causal pathways.


Assuntos
Dependência de Alimentos/epidemiologia , Transtornos Relacionados ao Uso de Substâncias/epidemiologia , Adolescente , Peso Corporal , Açúcares da Dieta/administração & dosagem , Ingestão de Alimentos , Feminino , Seguimentos , Dependência de Alimentos/complicações , Comportamentos Relacionados com a Saúde , Humanos , Masculino , Países Baixos/epidemiologia , Prevalência , Fatores Socioeconômicos , Transtornos Relacionados ao Uso de Substâncias/complicações , Inquéritos e Questionários , Adulto Jovem
18.
Drug Alcohol Depend ; 178: 66-69, 2017 09 01.
Artigo em Inglês | MEDLINE | ID: mdl-28641132

RESUMO

BACKGROUND: Ecstasy is a widely used psychoactive drug that users often take because they experience positive effects such as increased euphoria, sociability, elevated mood, and heightened sensations. Ecstasy use is not harmless and several immediate and long term side effects have been identified. Lifetime ecstasy use is likely to be partly influenced by genetic factors, but no twin study has determined the heritability. Here, we apply a classical twin design to a large sample of twins and siblings to estimate the heritability of lifetime ecstasy use. METHODS: The sample comprised 8500 twins and siblings aged between 18 and 45 years from 5402 families registered at the Netherlands Twin Registry. In 2013-2014 participants filled out a questionnaire including a question whether they had ever used ecstasy. We used the classical twin design to partition the individual differences in liability to ecstasy use into that due to genetic, shared environmental, and residual components. RESULTS: Overall, 10.4% of the sample had used ecstasy during their lifetime, with a somewhat higher prevalence in males than females. Twin modelling indicated that individual differences in liability to lifetime ecstasy use are for 74% due to genetic differences between individuals, whereas shared environmental and residual factors explain a small proportion of its liability (5% and 21%, respectively). Although heritability estimates appeared to be higher for females than males, this difference was not significant. CONCLUSIONS: Lifetime ecstasy use is a highly heritable trait, which indicates that some people are genetically more vulnerable to start using ecstasy than others.


Assuntos
N-Metil-3,4-Metilenodioxianfetamina/química , Psicotrópicos/farmacologia , Gêmeos Dizigóticos/genética , Gêmeos Monozigóticos/genética , Gêmeos/genética , Meio Ambiente , Feminino , Humanos , Masculino , Países Baixos , Prevalência , Psicotrópicos/química , Sistema de Registros , Irmãos , Inquéritos e Questionários
19.
Addict Biol ; 22(4): 1090-1102, 2017 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-27027469

RESUMO

Smoking and caffeine consumption show a strong positive correlation, but the mechanism underlying this association is unclear. Explanations include shared genetic/environmental factors or causal effects. This study employed three methods to investigate the association between smoking and caffeine. First, bivariate genetic models were applied to data of 10 368 twins from the Netherlands Twin Register in order to estimate genetic and environmental correlations between smoking and caffeine use. Second, from the summary statistics of meta-analyses of genome-wide association studies on smoking and caffeine, the genetic correlation was calculated by LD-score regression. Third, causal effects were tested using Mendelian randomization analysis in 6605 Netherlands Twin Register participants and 5714 women from the Avon Longitudinal Study of Parents and Children. Through twin modelling, a genetic correlation of r0.47 and an environmental correlation of r0.30 were estimated between current smoking (yes/no) and coffee use (high/low). Between current smoking and total caffeine use, this was r0.44 and r0.00, respectively. LD-score regression also indicated sizeable genetic correlations between smoking and coffee use (r0.44 between smoking heaviness and cups of coffee per day, r0.28 between smoking initiation and coffee use and r0.25 between smoking persistence and coffee use). Consistent with the relatively high genetic correlations and lower environmental correlations, Mendelian randomization provided no evidence for causal effects of smoking on caffeine or vice versa. Genetic factors thus explain most of the association between smoking and caffeine consumption. These findings suggest that quitting smoking may be more difficult for heavy caffeine consumers, given their genetic susceptibility.


Assuntos
Cafeína/administração & dosagem , Estimulantes do Sistema Nervoso Central/administração & dosagem , Estudo de Associação Genômica Ampla/estatística & dados numéricos , Fumar/epidemiologia , Adulto , Feminino , Humanos , Estudos Longitudinais , Masculino , Países Baixos/epidemiologia , Sistema de Registros/estatística & dados numéricos , Fatores de Risco , Fumar/genética , Inquéritos e Questionários , Gêmeos/genética , Gêmeos/estatística & dados numéricos
20.
Am J Clin Nutr ; 104(4): 1144-1150, 2016 10.
Artigo em Inglês | MEDLINE | ID: mdl-27581476

RESUMO

BACKGROUND: High sugar consumption contributes to the rising prevalence of obesity. Sugar can have rewarding effects that are similar to, but less strong than, the effects of addictive substances. People who consume large amounts of sugar also tend to use more addictive substances, but it is unclear whether this is due to shared genetic or environmental risk factors. OBJECTIVE: We examined whether there are genetic influences on the consumption of sugar-containing drinks and whether genetic factors can explain the association with substance use. DESIGN: The frequency of consumption of sugar-containing drinks (e.g., cola, soft drinks, and energy drinks) and addictive substances (nicotine, caffeine, alcohol, cannabis, and illicit drugs) was obtained for 8586 twins who were registered at the Netherlands Twin Register (women: 68.7%; mean ± SD age: 33.5 ± 15.3 y). Participants were categorized as high or low sugar consumers (>1 compared with ≤1 SD above daily consumption in grams) and as high or low substance users (≥2 compared with <2 substances). Through bivariate genetic modeling, genetic and environmental influences on sugar consumption, substance use, and their association were estimated. RESULTS: Genetic factors explained 48% of the variation in high sugar consumption, whereas unique environmental factors explained 52%. For high substance use, these values were 62% and 38%, respectively. There was a moderate phenotypic association between high sugar consumption and high substance use (r = 0.2), which was explained by genetic factors (59%) and unique environmental factors (41%). CONCLUSIONS: The positive association between high sugar consumption and high substance use was partly due to unique environmental factors (e.g., social situations). Genetic factors were also of influence, suggesting that neuronal circuits underlying the development of addiction and obesity are related. Further research is needed to identify genes that influence sugar consumption and those that overlap with substance use.


Assuntos
Comportamento Aditivo/genética , Bebidas , Sacarose na Dieta/administração & dosagem , Comportamento Alimentar , Fenótipo , Transtornos Relacionados ao Uso de Substâncias/genética , Gêmeos/genética , Adolescente , Adulto , Dieta , Meio Ambiente , Feminino , Humanos , Masculino , Recompensa , Gêmeos Dizigóticos/genética , Gêmeos Monozigóticos/genética , Adulto Jovem
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