RESUMEN
Executive functions (EFs) and intelligence (IQ) are phenotypically correlated. In twin studies, latent variables for EFs and IQ display moderate to high heritability estimates; however, they show variable genetic correlations in twin studies spanning childhood to middle age. We analyzed data from over 11,000 children (9- to 10-year-olds, including 749 twin pairs) in the Adolescent Brain Cognitive Development (ABCD) Study to examine the phenotypic and genetic relations between EFs and IQ in childhood. We identified two EF factors-Common EF and Updating-Specific-which were both related to IQ (rs = 0.64-0.81). Common EF and IQ were heritable (53%-67%), and their genetic correlation (rG = 0.86) was not significantly different than 1. These results suggest that EFs and IQ are phenotypically but not genetically separable in middle childhood, meaning that this phenotypic separability may be influenced by environmental factors.
Asunto(s)
Función Ejecutiva , Inteligencia , Adolescente , Encéfalo , Niño , Cognición , Humanos , Inteligencia/genética , Persona de Mediana Edad , Gemelos/genéticaRESUMEN
In a technology-driven society, screens are being used more than ever. The high rate of electronic media use among children and adolescents begs the question: is screen time harming our youth? The current study draws from a nationwide sample of 11,875 participants in the United States, aged 9 to 10 years, from the Adolescent Brain Cognitive Development Study (ABCD Study®). We investigate relationships between screen time and mental health, behavioral problems, academic performance, sleep habits, and peer relationships by conducting a series of correlation and regression analyses, controlling for SES and race/ethnicity. We find that more screen time is moderately associated with worse mental health, increased behavioral problems, decreased academic performance, and poorer sleep, but heightened quality of peer relationships. However, effect sizes associated with screen time and the various outcomes were modest; SES was more strongly associated with each outcome measure. Our analyses do not establish causality and the small effect sizes observed suggest that increased screen time is unlikely to be directly harmful to 9-and-10-year-old children.
Asunto(s)
Rendimiento Académico/psicología , Salud del Adolescente , Ansiedad/epidemiología , Trastorno por Déficit de Atención con Hiperactividad/epidemiología , Salud Infantil , Depresión/epidemiología , Salud Mental , Problema de Conducta/psicología , Tiempo de Pantalla , Adolescente , Atención , Niño , Cognición , Estudios de Seguimiento , Humanos , Relaciones Interpersonales , Estudios Longitudinales , Autoinforme , Sueño , Estados Unidos/epidemiología , Adulto JovenRESUMEN
BACKGROUND: It is unclear whether cannabis use causes cognitive decline; several studies show an association between cannabis use and cognitive decline, but quasi-experimental twin studies have found little support for a causal effect. Here, we evaluate the association of cannabis use with general cognitive ability and executive functions (EFs) while controlling for genetic and shared environmental confounds in a longitudinal twin study. METHODS: We first examined the phenotypic associations between cannabis initiation, frequency, and use disorder with cognitive abilities, while also controlling for pre-use general cognitive ability and other substance involvement. We tested the concurrent association between the cannabis use variables and cognitive abilities in late adolescence and young adulthood and the longitudinal association between cannabis use variables during adolescence and young adulthood cognitive abilities. Next, we used multilevel models to test whether these relations reflect between- and/or within-twin pair associations. RESULTS: Phenotypically, cannabis use was related to poorer cognitive functioning, although most associations were negligible after accounting for other substance use. Nevertheless, there were few significant within-family twin-specific associations, except that age 17 cannabis frequency was associated with worse age 23 Common EF and general cognitive ability. CONCLUSIONS: We found little support for a potential causal effect of cannabis use on cognition, consistent with previous twin studies. Results suggest that cannabis use may not cause decline in cognitive ability among a normative sample of cannabis users.
Asunto(s)
Cognición/efectos de los fármacos , Disfunción Cognitiva/inducido químicamente , Uso de la Marihuana/psicología , Gemelos/psicología , Adolescente , Adulto , Función Ejecutiva/efectos de los fármacos , Femenino , Humanos , Estudios Longitudinales , Masculino , Uso de la Marihuana/genética , Ensayos Clínicos Controlados no Aleatorios como Asunto , Fenotipo , Gemelos/genética , Adulto JovenRESUMEN
BACKGROUND/OBJECTIVES: Although childhood attention deficit hyperactivity disorder (ADHD) has been previously associated with concurrent and later obesity in adulthood, the etiology of this association remains unclear. The objective of this study is to determine the shared genetic effects of ADHD symptoms and BMI in a large sample of sibling pairs, consider how these shared effects may vary over time, and examine potential sex differences. SUBJECT/METHODS: Sibling pair data were obtained from the National Longitudinal Study of Adolescent to Adult Health (Add Health); childhood ADHD symptoms were reported retrospectively during young adulthood, while three prospective measurements of BMI were available from young adulthood to later adulthood. Cholesky decomposition models were fit to this data using Mx and maximum-likelihood estimation. The twin and sibling sample for these analyses included: 221 monozygotic (MZ) pairs (92 male-male, 139 female-female), 228 dizygotic (DZ) pairs (123 male-male, 105 female-female), 471 full-sibling (FS) pairs (289 male-male, 182 female-female), 106 male-female DZ twin pairs, and 234 male-female FS pairs. RESULTS: The magnitude of the association between childhood ADHD symptoms and BMI changed over time and by sex. The etiological relationship between childhood ADHD symptoms and the three prospective measurements of BMI differed for males and females, such that unique or non-shared environmental influences contributed to the relationship within males and genetic factors contributed to the relationship within females. Specifically, among females, genetic influences on childhood ADHD symptoms were partially shared with those effecting BMI and increased from adolescence to later adulthood (genetic correlation = 0.20 (95% CI: 0.07-0.36) in adolescence and 0.24 (95% CI: 0.10, 0.41) in adulthood). CONCLUSION: Genetic influences on ADHD symptoms in childhood are partially shared with those effecting obesity. However, future research is needed to determine why this association is limited to females.
Asunto(s)
Trastorno por Déficit de Atención con Hiperactividad/genética , Índice de Masa Corporal , Predisposición Genética a la Enfermedad/genética , Obesidad/genética , Adolescente , Desarrollo del Adolescente , Trastorno por Déficit de Atención con Hiperactividad/epidemiología , Trastorno por Déficit de Atención con Hiperactividad/fisiopatología , Femenino , Interacción Gen-Ambiente , Humanos , Estudios Longitudinales , Masculino , Obesidad/epidemiología , Obesidad/fisiopatología , Distribución por Sexo , Gemelos Dicigóticos , Gemelos MonocigóticosRESUMEN
Simple sequence repeats (SSRs) are one of the earliest available forms of genetic variation available for analysis and have been utilized in studies of neurological, behavioral, and health phenotypes. Although findings from these studies have been suggestive, their interpretation has been complicated by a variety of factors including, among others, limited power due to small sample sizes. The current report details the availability, diversity, and allele and genotype frequencies of six commonly examined SSRs in the ethnically diverse, population-based National Longitudinal Study of Adolescent Health. A total of 106,743 genotypes were generated across 15,140 participants that included four microsatellites and two di-nucleotide repeats in three dopamine genes (DAT1, DRD4, DRD5), the serotonin transporter, and monoamine oxidase A. Allele and genotype frequencies showed a complex pattern and differed significantly between populations. For both di-nucleotide repeats we observed a greater allelic diversity than previously reported. The availability of these six SSRs in a large, ethnically diverse sample with extensive environmental measures assessed longitudinally offers a unique resource for researchers interested in health and behavior.
Asunto(s)
Predisposición Genética a la Enfermedad/genética , Variación Genética/genética , Genotipo , Adolescente , Etnicidad/genética , Femenino , Humanos , Estudios Longitudinales , Masculino , Repeticiones de Minisatélite/genéticaRESUMEN
BACKGROUND: Limited current information on the epidemiology of lifetime alcohol and cannabis use disorders in the United States is available. AIMS: To present detailed information about the prevalence and sociodemographic correlates of lifetime alcohol and cannabis use disorders rates in the United States. To examine gender differences in hazard ratios for the onset of alcohol and cannabis dependence. METHODS: Participants in Wave IV of the National Longitudinal Study of Adolescent Health (N=15,500, age range: 24-32) were interviewed between 2008 and 2009. Participants who exceeded screening thresholds were queried about lifetime DSM-IV alcohol and marijuana abuse and dependence symptoms. Age of substance dependence onset was queried. RESULTS: Lifetime rates of alcohol abuse and dependence were 11.8 and 13.2%. Lifetime rates of cannabis abuse and dependence were 3.9 and 8.3%. Lifetime alcohol and cannabis dependence onset peaks were 23 and 20. Correlates of lifetime alcohol abuse included being male (OR 1.4), African-American (OR 0.7), income in the 2nd or 3rd quartile (OR 0.7 and 0.6). Correlates of lifetime alcohol dependence were: being male (OR 1.8), African-American (OR 0.5), and never being married (OR 1.5), and regions outside of the west (Midwest OR 0.7, South OR 0.6, Northeast OR 0.6). Correlates of cannabis abuse and dependence were being male (OR 1.8 and 1.4). CONCLUSIONS: Lifetime alcohol and cannabis use disorders are highly prevalent in the US population. Men are at higher risk for alcohol and cannabis use disorders. Alcohol use disorders demonstrated specific sociodemographic correlates while marijuana use disorders did not.
Asunto(s)
Alcoholismo/epidemiología , Abuso de Marihuana/epidemiología , Adolescente , Conducta del Adolescente , Adulto , Escolaridad , Etnicidad , Femenino , Humanos , Estudios Longitudinales , Masculino , Prevalencia , Factores Socioeconómicos , Estados Unidos/epidemiología , Adulto JovenRESUMEN
BACKGROUND: Maltreatment by an adult or caregiver during childhood is a prevalent and important predictor of antisocial behaviors in adulthood. A functional promoter polymorphism in the monoamine oxidase A (MAOA) gene has been implicated as a moderating factor in the relationship between childhood maltreatment and antisocial behaviors. Although there have been numerous attempts at replicating this observation, results remain inconclusive. METHODS: We examined this gene-environment interaction hypothesis in a sample of 3356 white and 960 black men (aged 24-34) participating in the National Longitudinal Study of Adolescent Health. RESULTS: Primary analysis indicated that childhood maltreatment was a significant risk factor for later behaviors that violate rules and the rights of others (p < .05), there were no main effects of MAOA genotype, and MAOA genotype was not a significant moderator of the relationship between maltreatment and antisocial behaviors in our white sample. Post hoc analyses identified a similar pattern of results among our black sample in which maltreatment was not a significant predictor of antisocial behavior. Post hoc analyses also revealed a main effect of MAOA genotype on having a disposition toward violence in both samples and for violent convictions among our black sample. None of these post hoc findings, however, survived correction for multiple testing (p > .05). Power analyses indicated that these results were not due to insufficient statistical power. CONCLUSIONS: We could not confirm the hypothesis that MAOA genotype moderates the relationship between childhood maltreatment and adult antisocial behaviors.
Asunto(s)
Trastorno de Personalidad Antisocial , Maltrato a los Niños/psicología , Interacción Gen-Ambiente , Predisposición Genética a la Enfermedad/genética , Monoaminooxidasa/genética , Adulto , Negro o Afroamericano , Trastorno de Personalidad Antisocial/etnología , Trastorno de Personalidad Antisocial/etiología , Trastorno de Personalidad Antisocial/genética , Niño , Genotipo , Humanos , Masculino , Población BlancaRESUMEN
Multiple studies have provided evidence for genetic associations between single nucleotide polymorphisms (SNPs) located on the CHRNA5/A3/B4 gene cluster and various phenotypes related to Nicotine Dependence (Greenbaum et al. 2009). Only a few studies have investigated other substances of abuse. The current study has two aims, (1) to extend previous findings by focusing on associations between the CHRNA5/A3/B4 gene cluster and age of initiation of several different substances, and (2) to investigate heterogeneity in age of initiation across the different substances. All analyses were conducted with a subset of the Add Health study with available genetic data. The first aim was met by modeling onset of tobacco, alcohol, cannabis, inhalants, and other substance use using survival mixture analysis (SMA). Ten SNPs in CHRNA5/A3/B4 were used to predict phenotypic differences in the risk of onset, and differences between users and non-users. The survival models aim at investigating differences in the risk of initiation across the 5-18 age range for each phenotype separately. Significant or marginally significant genetic effects were found for all phenotypes. The genetic effects were mainly related to the risk of initiation and to a lesser extent to discriminating between users and non-users. To address the second goal, the survival analyses were complemented by a latent class analysis that modeled all phenotypes jointly. One of the ten SNPs was found to predict differences between the early and late onset classes. Taken together, our study provides evidence for a general role of the CHRNA5/A3/B4 gene cluster in substance use initiation that is not limited to nicotine and alcohol.
Asunto(s)
Genotipo , Proteínas del Tejido Nervioso/genética , Fenotipo , Receptores Nicotínicos/genética , Trastornos Relacionados con Sustancias/genética , Adolescente , Edad de Inicio , Trastornos Relacionados con Alcohol/genética , Femenino , Predisposición Genética a la Enfermedad , Humanos , Abuso de Inhalantes/genética , Masculino , Abuso de Marihuana/genética , Familia de Multigenes , Polimorfismo de Nucleótido Simple , Análisis de Supervivencia , Tabaquismo/genéticaRESUMEN
AIM: To examine individual differences in positive and negative subjective experiences to initial cigarette use. DESIGN: Retrospective self-reports of initial subjective experiences were examined to estimate the genetic and environmental influences and the extent of their covariation across different effects. PARTICIPANTS: Data was drawn from 2482 young adult same-and opposite sex twins- and siblings participating in the National Longitudinal Study of Adolescent Health. MEASUREMENT: Subjective experiences were retrospectively collected using the Early Smoking Experience (ESE) questionnaire. FINDINGS: Positive experiences evidenced moderate heritable contributions (40%, 95% CI: 0.22 to 0.56), as did an overall hedonic measure (34%, 95% CI: 0.22 to 0.46) and dizziness (34%, 95% CI: 0.15 to 0.52). Negative experiences evidenced small heritable contributions (13%, 95% CI: 0.00 to 0.36). Individual specific environmental influences were strong and accounted for the remaining proportion of observed variation in these experiences. Multivariate genetic modeling identified a moderately heritable underlying factor (37%, 95% CI: 0.22 to 0.52) that influenced the covariation of diverse subjective experiences and loaded most heavily on dizziness. Positive experiences also evidence residual genetic influences that were uncorrelated with other subjective experiences. CONCLUSIONS: How a person experiences their initial few cigarettes is due to both heritable contributions and environmental experiences unique to the person. The covariation of diverse subjective experiences appears to be due to a heritable latent sensitivity to the chemicals contained in an average cigarette and is best indexed by dizziness.
Asunto(s)
Mareo/etiología , Predisposición Genética a la Enfermedad , Modelos Genéticos , Fumar/genética , Adolescente , Adulto , Interpretación Estadística de Datos , Mareo/epidemiología , Mareo/genética , Femenino , Humanos , Masculino , Placer , Estudios Retrospectivos , Sensación , Hermanos , Fumar/efectos adversos , Fumar/epidemiología , Gemelos , Adulto JovenRESUMEN
It is often assumed that childhood maltreatment causes conduct problems via an environmentally mediated process. However, the association may be due alternatively to either a nonpassive gene-environment correlation, in which parents react to children's genetically-influenced conduct problems by maltreating them, or a passive gene-environment correlation, in which parents' tendency to engage in maltreatment and children's conduct problems are both influenced by a hereditary vulnerability to antisocial behavior (i.e. genetic mediation). The present study estimated the contribution of these processes to the association between maltreatment and conduct problems. Bivariate behavior genetic analyses were conducted on approximately 1,650 twin and sibling pairs drawn from a large longitudinal study of adolescent health (Add Health). The correlation between maltreatment and conduct problems was small; much of the association between maltreatment and conduct problems was due to a nonpassive gene-environment correlation. Results were more consistent with the hypothesis that parents respond to children's genetically-influenced conduct problems by maltreating them than the hypothesis that maltreatment causes conduct problems.
Asunto(s)
Trastornos de la Conducta Infantil/diagnóstico , Trastornos de la Conducta Infantil/genética , Adolescente , Adulto , Niño , Maltrato a los Niños , Ambiente , Femenino , Humanos , Estudios Longitudinales , Masculino , Modelos Genéticos , Negociación , Proyectos de Investigación , Estudios Retrospectivos , HermanosRESUMEN
Theory and empirical evidence suggest that children's genetically influenced characteristics help to shape the environments they experience, including the parenting they 'receive'. The extent of these genetically-mediated child effects on childhood maltreatment is not well known. The present study estimates the magnitude of genetically mediated child effects on maltreatment in 3,297 twins and siblings who were part of a large nationally representative sample of adolescents (ADD health). Participants in early adulthood retrospectively reported their experiences of physical and sexual maltreatment and neglect. Results are consistent with small genetically-mediated child effects on physical maltreatment and neglect, and none on sexual maltreatment, and all three forms of maltreatment are influenced mainly by idiosyncratic individual circumstances.
Asunto(s)
Trastorno de Personalidad Antisocial/genética , Déficit de la Atención y Trastornos de Conducta Disruptiva/genética , Abuso Sexual Infantil/psicología , Maltrato a los Niños/psicología , Trastorno de la Conducta/genética , Responsabilidad Parental/psicología , Medio Social , Adolescente , Agresión/psicología , Análisis de Varianza , Trastorno de Personalidad Antisocial/psicología , Déficit de la Atención y Trastornos de Conducta Disruptiva/psicología , Niño , Trastorno de la Conducta/psicología , Epistasis Genética/genética , Femenino , Humanos , Masculino , Modelos Genéticos , Modelos Psicológicos , Relaciones Padres-Hijo , Determinación de la Personalidad , Factores Sexuales , Gemelos Dicigóticos/genética , Gemelos Dicigóticos/psicología , Gemelos Monocigóticos/genética , Gemelos Monocigóticos/psicología , Adulto JovenRESUMEN
BACKGROUND: One potential site of convergence of the nicotine and alcohol actions is the family of the neuronal nicotinic acetylcholine receptors. Our study examines the genetic association between variations in the genomic region containing the CHRNA5, A3, and B4 gene cluster (A5A3B4) and several phenotypes of alcohol and tobacco use in an ethnically diverse young adult sample. Significant results were then replicated in a separate adult population-representative sample. METHODS: In a selected sample, nine single nucleotide polymorphisms (SNPs) were tested for association with various nicotine and alcohol phenotypes, including age of initiation and measures of frequency, quantity, and subjective responses to the substances. Analysis was conducted with the statistical genetics program WHAP in the full sample (1075 subjects) including ethnicities as covariates and within each ethnic group sub-sample. Replication of the significant results in a separate population-based sample was carried out with the PBAT statistical genetics program. RESULTS: Two linked SNPs (rs8023462 and rs1948) located in a conserved region of the A5A3B4 gene cluster significantly predicted early age of initiation for tobacco with a hazard ratio (HR) of 1.35 (95% confidence interval [CI]1.08-1.70) for the CC genotype of rs8023462 and a HR of 1.29 (95% CI 1.01-1.63) for the TT genotype of rs1948 [corrected]. These findings were then replicated in a separate population-representative sample, showing rs1948 and rs8023462 to be associated with age of initiation for both tobacco and alcohol use (p < .01 and p < .001). CONCLUSIONS: Variations in A5A3B4 genes might influence behaviors that promote early age of experimentation with drugs.
Asunto(s)
Alcoholismo/genética , Predisposición Genética a la Enfermedad , Familia de Multigenes , Polimorfismo de Nucleótido Simple/genética , Receptores Nicotínicos/genética , Tabaquismo/genética , Adolescente , Adulto , Edad de Inicio , Etnicidad , Femenino , Frecuencia de los Genes , Genotipo , Humanos , Masculino , Proteínas del Tejido Nervioso , Modelos de Riesgos ProporcionalesRESUMEN
BACKGROUND: While college attendance has been shown to be associated with increased drinking behaviors, there are no studies to our knowledge that have examined whether college attendance moderates genetic influences for drinking. We first tested for changes in alcohol consumption in adolescents who did and did not subsequently attend college, and then tested for variation of the genetic and environmental determinants of drinking in these 2 groups. METHODS: Participants eligible for this study were selected from 2 samples from the National Longitudinal Study of Adolescent Health (Add Health), a national probability sample (n=7,083) and a sample of sibling pairs (n=855 pairs). Participants were assessed for measures of drinking behaviors as adolescents (wave I) and reinterviewed at 1 (wave II) and 6 years (wave III) following the initial survey. Changes in binge drinking and average quantity of alcohol consumed in the past year were estimated among 4 groups (2-year college students, 4-year college students, college withdrawers, noncollege participants) in sequential cohorts which spanned the ages of 13 to 24 across the 3 Add Health waves. Gene by environment interactions were then tested at wave III using biometrical models in the genetically informative pairs. RESULTS: Participants who did not attend college reported more binge drinking and consumed greater quantities of alcohol as adolescents than participants who subsequently attended college. However, the college students not only surpassed their noncollege peers in alcohol use as young adults, but also exhibited a greater genetic influence on quantity of alcohol consumed per drinking episode. CONCLUSIONS: Exposure to a college environment acts as an environmental moderator, supporting the hypothesis that the magnitude of genetic influence on certain aspects of alcohol consumption is greater in environments where drinking behaviors are more likely to be promoted.
Asunto(s)
Consumo de Bebidas Alcohólicas/genética , Universidades/estadística & datos numéricos , Adolescente , Consumo de Bebidas Alcohólicas/epidemiología , Femenino , Humanos , Estudios Longitudinales , MasculinoRESUMEN
AIM: To examine variation in nicotine dependence scores and covariation between different dependence symptoms. DESIGN: A 12-year, nationally representative, probability-based survey of adolescent health-related behaviors and their outcomes during young adulthood in the United States. The genetic contribution to nicotine dependence was evaluated in the sibling-pairs sample of the US National Longitudinal Study of Adolescent Health. MEASUREMENTS: Nicotine dependence (ND) was assessed using the Fagerström Test for Nicotine Dependence (FTND) and Heaviness of Smoking Index (HSI) in 1154 young adults, between the ages of 18 and 25 years, who were from twin, full sibling and half-sibling pairs. FINDINGS: Dependence in this sample was common and varied in degree. Total HSI scores evidenced moderate to large heritable contributions (61%, 95% confidence interval (CI): 0.46-0.72), as did the quantity of cigarettes smoked (52%, 95% CI: 0.39-0.63) and urgency to smoke (55%, 95% CI: 0.38-0.68). Multivariate modeling identified a highly heritable underlying factor (76%, 95% CI: 0.56-0.91) that influenced the covariation of dependence symptoms and loaded most heavily on how soon after waking a smoker uses his or her first cigarette. The quantity of cigarettes smoked per day also evidenced residual genetic influences that were not common to other dependence-related behaviors. CONCLUSIONS: In this sample of young adults from the general population, both genes and individual-specific environments are important etiological factors in ND. The urgency to smoke, as measured by the time to first cigarette, may be the most informative measure on the FTND for genetic studies of nicotine dependence.
Asunto(s)
Fumar/genética , Tabaquismo/genética , Adolescente , Adulto , Femenino , Humanos , Masculino , Fumar/epidemiología , Tabaquismo/epidemiología , Estados Unidos/epidemiologíaRESUMEN
OBJECTIVE: Cannabis is the most frequently abused illicit substance among adolescents and young adults. Genetic risk factors account for part of the variation in the development of cannabis dependence symptoms; however, no linkage studies have been performed for cannabis dependence symptoms. This study aimed to identify such loci. METHOD: Three hundred and twenty-four sibling pairs from 192 families were assessed for cannabis dependence symptoms. Probands (13-19 years of age) were recruited from consecutive admissions to substance abuse treatment facilities. The siblings of the probands ranged in age from 12 to 25 years. A community-based sample of 4843 adolescents and young adults was utilized to define an age- and sex-corrected index of cannabis dependence vulnerability. DSM-IV cannabis dependence symptoms were assessed in youth and their family members with the Composite International Diagnostic Instrument-Substance Abuse Module. Siblings and parents were genotyped for 374 microsatellite markers distributed across the 22 autosomes (average inter-marker distance=9.2cM). Cannabis dependence symptoms were analyzed using Merlin-regress, a regression-based method that is robust to sample selection. RESULTS: Evidence for suggestive linkage was found on chromosome 3q21 near marker D3S1267 (LOD=2.61), and on chromosome 9q34 near marker D9S1826 (LOD=2.57). CONCLUSIONS: This is the first reported linkage study of cannabis dependence symptoms. Other reports of linkage regions for illicit substance dependence have been reported near 3q21, suggesting that this region may contain a quantitative trait loci influencing cannabis dependence and other substance use disorders.
Asunto(s)
Cromosomas Humanos Par 3/genética , Cromosomas Humanos Par 9/genética , Ligamiento Genético/genética , Genoma , Abuso de Marihuana/genética , Adolescente , Trastorno de Personalidad Antisocial/genética , Enfermedades en Gemelos/genética , Femenino , Marcadores Genéticos/genética , Genotipo , Humanos , Masculino , Repeticiones de Microsatélite , Análisis de RegresiónRESUMEN
BACKGROUND: While it has been demonstrated that smoking cigarettes in adolescence increases the likelihood of progressing to marijuana use, few studies have considered the reverse scenario in which early use of cannabis leads to greater tobacco smoking. METHODS: Participants (n=5963), who had never smoked cigarettes daily by wave I of the National Longitudinal Study of Adolescent Health, were followed 6 years (waves I-III) from adolescence into young adulthood. Measures of marijuana use (lifetime use, monthly use, age at first use), as assessed at wave I within 12-16 (n=3712) and 17-21 (n=2251) year-olds, were separately modeled as predictors of three tobacco-related outcomes: (1) age at onset of daily cigarette smoking, (2) lifetime nicotine dependence, (3) current nicotine dependence. RESULTS: In the older cohort (17-21-year-olds at wave I), lifetime (>10 times) and past-month marijuana use at wave I were predictive of an earlier initiation into daily cigarette smoking and a greater likelihood of developing nicotine dependence by wave III. Furthermore, age at first use of cannabis was negatively associated with risk of nicotine dependence in the older, but not younger cohort. CONCLUSION: After controlling for baseline measures of tobacco smoking and other demographic risk factors, the use of marijuana in adolescence was modestly associated with daily cigarette smoking and nicotine dependence in young adulthood.
Asunto(s)
Abuso de Marihuana/complicaciones , Tabaquismo/epidemiología , Adolescente , Adulto , Edad de Inicio , Niño , Femenino , Humanos , Estudios Longitudinales , Masculino , Nicotina , Grupos Raciales , Instituciones Académicas , Estados Unidos/epidemiologíaRESUMEN
OBJECTIVE: This study examines the familial transmission of alcohol abuse and dependence to adolescents. METHOD: Male adolescents recruited from a treatment program for substance problems, matched controls, and all available biological parents and siblings were assessed with a structured psychiatric interview assessing Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, based diagnoses of alcohol abuse and alcohol dependence. A total of 2,612 individuals from 911 families were interviewed. Structural equation modeling estimated tetrachoric correlations among family members, the proportion of variance in abuse and dependence attributable to parent-offspring transmission, and the effects of assortative mating and horizontal transmission among siblings. RESULTS: Tetrachoric correlations among siblings and parent-offspring ranged from .19 to .34 for abuse and dependence. Mother-father correlations were .14 and .37 for abuse and dependence, respectively. Modeling of familial transmission showed that 33% of the variance in abuse and 56% of the variance in dependence was accounted for by factors transmitted from parents. The effects of assortative mating could not be dropped from the abuse model without significant loss of model fit but could be dropped from the dependence model. Horizontal transmission among siblings could be dropped from both models without significant loss of fit. CONCLUSIONS: These results suggest that aggregation of alcohol abuse and alcohol dependence in families of male probands is significantly influenced by parental transmission of risk but is not reliably influenced by horizontal sibling effects such as sibling interactions or cohort effects. Spousal resemblance was found to be an important source of familial aggregation for alcohol abuse but not alcohol dependence.
Asunto(s)
Alcoholismo/epidemiología , Alcoholismo/genética , Hijo de Padres Discapacitados/estadística & datos numéricos , Padre/estadística & datos numéricos , Madres/estadística & datos numéricos , Adolescente , Adulto , Niño , Femenino , Humanos , Masculino , Persona de Mediana Edad , Prevalencia , HermanosRESUMEN
: We examined three components of the "gateway theory" in relation to marijuana use: (1) whether adolescent marijuana use predicts young adult drug use, (2) whether this association persists when controlling for similar family background, (3) whether common genetic or environmental factors contribute to the association. The three components were tested in adolescents from the National Longitudinal Study of Adolescent Health assessed twice during adolescence and then re-interviewed 5 years later. Component 1 was tested in 18,286 subjects, component 2 in sibling pairs (n=360) discordant for marijuana use, and component 3 in a genetically informative sub-sample (n=4846). Marijuana use was defined as any use during adolescence, and drug use was defined as self-reported past year use of other illicit drugs besides marijuana. Marijuana users were twice as likely to use illicit drugs as young adults than non-users. Shared environmental factors mediated much of the relationship between adolescent marijuana use and young adult drug use. The association remained, however, even when controlling for familial environmental and other measured factors.
Asunto(s)
Drogas Ilícitas , Abuso de Marihuana/epidemiología , Trastornos Relacionados con Sustancias/epidemiología , Adolescente , Adulto , Colorado , Intervalos de Confianza , Humanos , Estudios Longitudinales , Abuso de Marihuana/clasificación , Abuso de Marihuana/complicaciones , Trastornos Relacionados con Sustancias/clasificación , Trastornos Relacionados con Sustancias/complicacionesRESUMEN
Associations between smoking behavior and polymorphisms in the dopaminergic genes (DAT1 and DRD2) were tested by using within- and between-family measures of allelic transmission in 2,448 young adults from the National Longitudinal Study of Adolescent Health. The 9-repeat allele of the dopamine transporter gene polymorphism (DAT1) was inversely associated with smoking in samples that included all subjects and only those who had initiated smoking, accounting for approximately 1% of the variance. Never smokers and current nonsmokers had an excess transmission of the 9-repeat allele compared with regular smokers, suggesting a protective effect of the 9-repeat allele, which is hypothesized to alter synaptic dopamine levels.
Asunto(s)
Polimorfismo Genético , Receptores de Dopamina D1/genética , Receptores de Dopamina D2/genética , Fumar/epidemiología , Adolescente , Adulto , Mejilla/microbiología , Femenino , Humanos , Entrevistas como Asunto , Estudios Longitudinales , Masculino , Hermanos , Fumar/genética , Estados UnidosRESUMEN
Although a number of studies have shown that various measures of religiosity are inversely correlated with smoking behavior, none of these studies have used genetically informative samples to test for a gene-environment interaction between the determinants of smoking initiation and religiosity. We tested the moderating effects of three measures of religiosity (religious affiliation, organizational religious activity, and self-rated religiousness) on the genetic and environmental determinants of smoking initiation in 237 monozygotic twin pairs, 315 dizygotic twin pairs, 779 full-sibling pairs, and 233 half-sibling pairs in young adults surveyed from the third wave of the National Longitudinal Study of Adolescent Health. Primary analyses incorporated all sibling pairs, irrespective of whether they were concordant or discordant for the environmental moderator, in models designed to account for the confounding effects of a gene-environment correlation. High levels of self-rated religiousness attenuated the additive genetic component for smoking initiation and were associated with a lower prevalence of smoking initiation. Although all three measures of religiosity were associated with lower rates of smoking initiation, only self-rated religiousness moderated genetic influences on the liability for smoking.