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This study tested interactions among puberty-related genetic risk, prenatal substance use, harsh discipline, and pubertal timing for the severity and directionality (i.e., differentiation) of externalizing and internalizing problems and adolescent substance use. This is a companion paper to Marceau et al. (2021) which examined the same influences in developmental cascade models. Data were from the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort (n = 4504 White boys, n = 4287 White girls assessed from the prenatal period through 18.5 years). We hypothesized generally that later predictors would strengthen the influence of puberty-related genetic risk, prenatal substance use exposure, and pubertal risk on psychopathology and substance use (two-way interactions), and that later predictors would strengthen the interactions of earlier influences on psychopathology and substance use (three-way interactions). Interactions were sparse. Although all fourteen interactions showed that later influences can exacerbate or trigger the effects of earlier ones, they often were not in the expected direction. The most robust moderator was parental discipline, and differing and synergistic effects of biological and socially-relevant aspects of puberty were found. In all, the influences examined here operate more robustly in developmental cascades than in interaction with each other for the development of psychopathology and transitions to substance use.
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Poder Familiar , Transtornos Relacionados ao Uso de Substâncias , Masculino , Criança , Feminino , Gravidez , Humanos , Adolescente , Estudos Longitudinais , Puberdade/genética , Transtornos Relacionados ao Uso de Substâncias/genética , PaisRESUMO
The present study examined the intergenerational transmission of internalizing and externalizing symptom severity, which indexes comorbidity, and symptom directionality, which indicates differentiation toward externalizing versus internalizing problems. Data are from 854 male and female, same-sex adult twin pairs born between 1926 and 1971 (32-60 years old, M = 44.9 years, SD = 4.9 years) from the Twin and Offspring Study in Sweden and their adolescent offspring (11-22 years old, M = 15.7 years, SD = 2.4 years, 52% female). Children-of-twins models revealed additive (9%) and dominant (45%) genetic and nonshared environmental (47%) influences on twins' symptom severity, and additive genetic (39%) and nonshared environmental (61%) influences on twins' symptom directionality. Both comorbid problems and preponderance of symptoms of a particular - internalizing versus externalizing - spectrum were correlated across parent and child generations, although associations were modest especially for directionality (i.e., transmission of specific symptom type). By interpreting findings alongside a recent study of adolescent twins, we demonstrate that the intergenerational transmission of symptom severity and symptom directionality are both unlikely to be attributable to genetic transmission, are both likely to be influenced by direct phenotypic transmission and/or nonpassive rGE, and the intergenerational transmission of symptom severity is also likely to be influenced by passive rGE.
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This research examines maternal smoking during pregnancy and risk for poorer executive function in siblings discordant for exposure. Data (N = 173 families) were drawn from the Missouri Mothers and Their Children study, a sample, identified using birth records (years 1998-2005), in which mothers changed smoking behavior between two pregnancies (Child 1 [older sibling]: M age = 12.99; Child 2 [younger sibling]: M age = 10.19). A sibling comparison approach was used, providing a robust test for the association between maternal smoking during pregnancy and different aspects of executive function in early-mid adolescence. Results suggested within-family (i.e., potentially causal) associations between maternal smoking during pregnancy and one working memory task (visual working memory) and one response inhibition task (color-word interference), with increased exposure associated with decreased performance. Maternal smoking during pregnancy was not associated with stop-signal reaction time, cognitive flexibility/set-shifting, or auditory working memory. Initial within-family associations between maternal smoking during pregnancy and visual working memory as well as color-word interference were fully attenuated in a model including child and familial covariates. These findings indicate that exposure to maternal smoking during pregnancy may be associated with poorer performance on some, but not all skills assessed; however, familial transmission of risk for low executive function appears more important.
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INTRODUCTION: Dynamic relations between genetic, hormone, and pre- and postnatal environments are theorized as critically important for adolescent substance use but are rarely tested in multifactorial models. This study assessed the impact of interactions of genetic risk and cortisol reactivity with prenatal and parenting influences on both any and frequency of adolescent substance use. METHODS: Data are from the TRacking Adolescents' Individual Lives Survey (TRAILS), a prospective longitudinal, multi-rater study of 2,230 Dutch adolescents. Genetic risk was assessed via 3 substance-specific polygenic scores. Mothers retrospectively reported prenatal risk when adolescents were 11 years old. Adolescents rated their parents' warmth and hostility at age 11. Salivary cortisol reactivity was measured in response to a social stress task at age 16. Adolescents' self-reported cigarette, alcohol, and cannabis use frequency at age 16. RESULTS: A multivariate hurdle regression model showed that polygenic risk for smoking, alcohol, and cannabis predicted any use of each substance, respectively, but predicted more frequent use only for smoking. Blunted cortisol reactivity predicted any use and more frequent use for all 3 outcomes. There were 2 interactions: blunted cortisol reactivity exacerbated the association of polygenic risk with any smoking and the association of prenatal risk with any alcohol use. CONCLUSION: Polygenic risk seems of importance for early use but less so for frequency of use, whereas blunted cortisol reactivity was correlated with both. Blunted cortisol reactivity may also catalyze early risks for substance use, though to a limited degree. Gene-environment interactions play no role in the context of this multifactorial model.
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Hidrocortisona , Transtornos Relacionados ao Uso de Substâncias , Adolescente , Criança , Feminino , Humanos , Estudos Longitudinais , Poder Familiar , Gravidez , Estudos Prospectivos , Estudos Retrospectivos , Transtornos Relacionados ao Uso de Substâncias/epidemiologia , Transtornos Relacionados ao Uso de Substâncias/genéticaRESUMO
Maternal smoking during pregnancy is associated with an ensemble of neurodevelopmental consequences in children and therefore constitutes a pressing public health concern. Adding to this burden, contemporary epidemiological and especially animal model research suggests that grandmaternal smoking is similarly associated with neurodevelopmental abnormalities in grandchildren, indicative of intergenerational transmission of the neurodevelopmental impacts of maternal smoking. Probing the mechanistic bases of neurodevelopmental anomalies in the children of maternal smokers and the intergenerational transmission thereof, emerging research intimates that epigenetic changes, namely DNA methylome perturbations, are key factors. Altogether, these findings warrant future research to fully elucidate the etiology of neurodevelopmental impairments in the children and grandchildren of maternal smokers and underscore the clear potential thereof to benefit public health by informing the development and implementation of preventative measures, prophylactics, and treatments. To this end, the present review aims to encapsulate the burgeoning evidence linking maternal smoking to intergenerational epigenetic inheritance of neurodevelopmental abnormalities, to identify the strengths and weaknesses thereof, and to highlight areas of emphasis for future human and animal model research therein.
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Metilação de DNA , Epigênese Genética , Epigenoma , Transtornos do Neurodesenvolvimento/genética , Nicotina/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal/genética , Fumar/efeitos adversos , Feminino , Humanos , Herança Materna , GravidezRESUMO
The current study leveraged the Avon Longitudinal Study of Parents and Children (ALSPAC) cohort (n = 4504 White boys, n = 4287 White girls assessed from the prenatal period through 18.5 years of age) to test a developmental cascade from genetic and prenatal substance use through pubertal timing and parenting to the severity of (regardless of type) and directionality (i.e., differentiation) of externalizing and internalizing problems to adolescent substance use. Limited associations of early pubertal timing with substance use outcomes were only observable via symptom directionality, differently for girls and boys. For boys, more severe exposure to prenatal substance use influenced adolescent substance use progression via differentiation towards relatively more pure externalizing problems, but in girls the associations were largely direct. Severity and especially directionality (i.e., differentiation towards relatively more pure externalizing problems) were key intermediaries in developmental cascades from parental harsh discipline with substance use progressions for girls and boys.
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Poder Familiar , Transtornos Relacionados ao Uso de Substâncias , Adolescente , Criança , Estudos de Coortes , Feminino , Humanos , Estudos Longitudinais , Masculino , Pais , Gravidez , Transtornos Relacionados ao Uso de Substâncias/genéticaRESUMO
INTRODUCTION: Heritability estimates of nicotine dependence (ND) range from 40% to 70%, but discovery GWAS of ND are underpowered and have limited predictive utility. In this work, we leverage genetically correlated traits and diseases to increase the accuracy of polygenic risk prediction. METHODS: We employed a multi-trait model using summary statistic-based best linear unbiased predictors (SBLUP) of genetic correlates of DSM-IV diagnosis of ND in 6394 individuals of European Ancestry (prevalence = 45.3%, %female = 46.8%, µâage = 40.08 [s.d. = 10.43]) and 3061 individuals from a nationally-representative sample with Fagerström Test for Nicotine Dependence symptom count (FTND; 51.32% female, mean age = 28.9 [s.d. = 1.70]). Polygenic predictors were derived from GWASs known to be phenotypically and genetically correlated with ND (i.e., Cigarettes per Day [CPD], the Alcohol Use Disorders Identification Test [AUDIT-Consumption and AUDIT-Problems], Neuroticism, Depression, Schizophrenia, Educational Attainment, Body Mass Index [BMI], and Self-Perceived Risk-Taking); including Height as a negative control. Analyses controlled for age, gender, study site, and the first 10 ancestral principal components. RESULTS: The multi-trait model accounted for 3.6% of the total trait variance in DSM-IV ND. Educational Attainment (ß = -0.125; 95% CI: [-0.149,-0.101]), CPD (0.071 [0.047,0.095]), and Self-Perceived Risk-Taking (0.051 [0.026,0.075]) were the most robust predictors. PGS effects on FTND were limited. CONCLUSIONS: Risk for ND is not only polygenic, but also pleiotropic. Polygenic effects on ND that are accessible by these traits are limited in size and act additively to explain risk. IMPLICATIONS: These findings enhance our understanding of inherited genetic factors for nicotine dependence. The data show that genome-wide association study (GWAS) findings across pre- and comorbid conditions of smoking are differentially associated with nicotine dependence and that when combined explain significantly more trait variance. These findings underscore the utility of multivariate approaches to understand the validity of polygenic scores for nicotine dependence, especially as the power of GWAS of broadly-defined smoking behaviors increases. Realizing the potential of GWAS to inform complex smoking behaviors will require similar theory-driven models that reflect the myriad of mechanisms that drive individual differences.
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Alcoolismo , Tabagismo , Adulto , Feminino , Estudo de Associação Genômica Ampla , Humanos , Masculino , Herança Multifatorial/genética , Fumar , Tabagismo/diagnóstico , Tabagismo/epidemiologia , Tabagismo/genéticaRESUMO
Theoretical models of attention-deficit/hyperactivity disorder implicate neurocognitive dysfunction, yet neurocognitive functioning covers a range of abilities that may not all be linked with inattention. This study (a) investigated the single nucleotide polymorphism (SNP) heritability (h2SNP) of inattention and aspects of neurocognitive efficiency (memory, social cognition, executive function, and complex cognition) based on additive genome-wide effects; (b) examined if there were shared genetic effects among inattention and each aspect of neurocognitive efficiency; and (c) conducted an exploratory genome-wide association study to identify genetic regions associated with inattention. The sample included 3,563 participants of the Philadelphia Neurodevelopmental Cohort, a general population sample aged 8-21 years who completed the Penn Neurocognitive Battery. Data on inattention was obtained with the Kiddie Schedule of Affective Disorders (adapted). Genomic relatedness matrix restricted maximum likelihood was implemented in genome-wide complex trait analysis. Analyses revealed significant h2SNP for inattention (20%, SE = 0.08), social cognition (13%, SE = 0.08), memory (17%, SE = 0.08), executive function (25%, SE = 0.08), and complex cognition (24%, SE = 0.08). There was a positive genetic correlation (0.67, SE = 0.37) and a negative residual covariance (-0.23, SE = 0.06) between inattention and social cognition. No SNPs reached genome-wide significance for inattention. Results suggest specificity in genetic overlap among inattention and different aspects of neurocognitive efficiency.
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Transtorno do Deficit de Atenção com Hiperatividade , Polimorfismo de Nucleotídeo Único , Adolescente , Adulto , Transtorno do Deficit de Atenção com Hiperatividade/genética , Criança , Cognição , Predisposição Genética para Doença , Estudo de Associação Genômica Ampla , Humanos , Adulto JovemRESUMO
The genetic architecture of neurodevelopmental disorders is largely polygenic, non-specific, and pleiotropic. This complex genetic architecture makes the search for specific etiological mechanisms that contribute to neurodevelopmental risk more challenging. Monogenic disorders provide an opportunity to focus in on how well-articulated signaling pathways contribute to risk for neurodevelopmental outcomes. This paper will focus on neurofibromatosis type 1 (NF1), a rare monogenic disorder that is associated with varied neurodevelopmental outcomes. Specifically, this paper will provide a brief overview of NF1 and its phenotypic associations with autism spectrum disorder, attention-deficit/hyperactivity disorder, and specific learning disorders, describe how variation within the NF1 gene increases risk for neurodevelopmental disorders via altered Ras signaling, and provide future directions for NF1 research to help elucidate the genetic architecture of neurodevelopmental disorders in the general population.
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Transtornos do Neurodesenvolvimento/genética , Neurofibromatose 1/genética , Proteínas ras/genética , Transtorno do Deficit de Atenção com Hiperatividade/genética , Transtorno do Espectro Autista/genética , Humanos , Deficiências da Aprendizagem/genética , Neurofibromatose 1/epidemiologia , Neurofibromatose 1/metabolismo , Proteínas ras/metabolismoRESUMO
INTRODUCTION: Maternal smoking during pregnancy (SDP) is associated with disruptive behavior. However, there is debate whether the SDP-disruptive behavior association is a potentially causal pathway or rather a spurious effect confounded by shared genetic and environmental factors. AIMS AND METHODS: The Missouri Mothers and Their Children Study is a sibling comparison study that includes families (n = 173) selected for sibling pairs (aged 7-16 years) discordant for SDP. Critically, the sibling comparison design is used to disentangle the effects of SDP from familial confounds on disruptive behavior. An SDP severity score was created for each child using a combination of SDP indicators (timing, duration, and amount of SDP). Multiple informants (parents and teachers) reported on disruptive behavior (i.e., DSM-IV semi-structured interview, the Child Behavior Checklist, and Teacher Report Form). RESULTS: The variability in disruptive behavior was primarily a function of within-family differences (66%-100%). Consistent with prior genetically informed approaches, the SDP-disruptive behavior association was primarily explained by familial confounds (genetic and environmental). However, when using a multi-rater approach (parents and teachers), results suggest a potentially causal effect of SDP on disruptive behavior (b = 0.09, SE = 0.04, p = 0.03). The potentially causal effect of SDP remained significant in sensitivity analyses. DISCUSSION: These findings suggest that familial confounding likely plays a complex role in the SDP-disruptive behavior association when examining both parent and teacher reports of behavior. Importantly, the current study highlights the importance of multiple raters, reflecting a more comprehensive measure of complex behaviors (e.g., disruptive behavior) to examine the teratogenic effects of SDP. IMPLICATIONS: Our study provides additional evidence that controlling for genetic and family factors is essential when examining the effect of SDP on later behavioral problems, as it explains a portion of the association between SDP and later behavioral problems. However, we found a significant association between SDP and disruptive behavior when using a multi-rater approach that capitalizes on both parent and teacher report, suggesting that parent and teacher ratings capture a unique perspective that is important to consider when examining SDP-behavior associations.
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Mães/psicologia , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Comportamento Problema , Irmãos/psicologia , Fumar/efeitos adversos , Adolescente , Criança , Manual Diagnóstico e Estatístico de Transtornos Mentais , Feminino , Humanos , Masculino , Missouri/epidemiologia , GravidezRESUMO
This study used polygenic scoring (PGS) to test whether puberty-related genes were correlated with depressive symptoms, and whether there were indirect effects through pubertal maturation. The sample included 8,795 adolescents from the Avon Longitudinal Study of Parents and Children (measures of puberty drawn ages 8-17 years; of depressive symptoms at age 16.5 years). The PGS (derived from a genome-wide meta-analysis of later age at menarche) predicted boys' and girls' later pubertal timing, boys' slower gonadal development, and girls' faster breast development. Earlier perceived breast development timing predicted more depressive symptoms in girls. Findings support shared genetic underpinnings for boys' and girls' puberty, contributing to multiple pubertal phenotypes with differences in how these genetic variants affect boys' and girls' development.
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Depressão/genética , Herança Multifatorial/genética , Puberdade/genética , Adolescente , Desenvolvimento do Adolescente , Fatores Etários , Criança , Feminino , Humanos , Estudos Longitudinais , Masculino , Polimorfismo de Nucleotídeo Único , Puberdade/psicologia , Caracteres SexuaisRESUMO
Cortisol reactivity is a frequently studied biomarker of substance use, though infrequently examined in adolescence. However, past research provides evidence that multiple developmental influences, including genetics and both prenatal and postnatal environmental influences, contribute both to cortisol reactivity and adolescent substance use. The aim of this study was to assess the impact of these earlier developmental influences on cortisol reactivity to a social stress challenge and adolescent substance use (smoking, alcohol, and marijuana use frequency assessed at age 16 years), using data from the TRacking Adolescents' Individual Lives Survey (TRAILS; N= 2230 adolescents, 51% female). Developmental pathways included polygenic risk, prenatal stress, warm parenting (age 11), and internalizing and externalizing problems (intercepts and change from 11-16 years). Cortisol reactivity was associated with smoking but not alcohol or marijuana use. Externalizing problems were the stronger predictor of adolescent substance use, but internalizing problems also had an important role. Prenatal stress and middle childhood parenting operated via middle childhood externalizing problems, and parenting also operated via trajectories of growth of externalizing problems in predicting adolescent substance use outcomes. Further, there were protective effects of internalizing problems for alcohol and marijuana use in the context of a more comprehensive model. These developmental influences did not attenuate the association of cortisol reactivity and smoking. These findings suggest a need to understand the broader developmental context regarding the impact of internalizing pathways to substance use, and that it is unlikely that cortisol reactivity and smoking are associated solely because of common developmental influences.
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Comportamento do Adolescente/psicologia , Hidrocortisona/metabolismo , Estresse Psicológico/metabolismo , Transtornos Relacionados ao Uso de Substâncias/metabolismo , Adolescente , Mecanismos de Defesa , Feminino , Humanos , Masculino , Abuso de Maconha , Fumar Maconha/metabolismo , Fumar/metabolismoRESUMO
Alcohol dependence (AD) affects individuals from all racial/ethnic groups, and previous research suggests that there is considerable variation in AD risk between and among various ancestrally defined groups in the United States. Although the reasons for these differences are likely due in part to contributions of complex sociocultural factors, limited research has attempted to examine whether similar genetic variation plays a role across ancestral groups. Using a pooled sample of individuals of African and European ancestry (AA/EA) obtained through data shared within the Database for Genotypes and Phenotypes, we estimated the extent to which additive genetic similarity for AD between AA and EAs using common single nucleotide polymorphisms overlapped across the two populations. AD was represented as a factor score by using Diagnostic and Statistical Manual dependence criteria, and genetic data were imputed by using the 1000 Genomes Reference Panel. Analyses revealed a significant single nucleotide polymorphism-based heritability of 17 percent (SE = 5) in EAs and 24 percent (SE = 15) in AAs. Further, a significant genetic correlation of 0.77 (SE = 0.46) suggests that the allelic architecture influencing the AD factor for EAs and AAs is largely similar across the two populations. Analyses indicated that investigating the genetic underpinnings of alcohol dependence in different ethnic groups may serve to highlight core etiological factors common to both groups and unique etiological factors specific to each ethnic group.
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Alcoolismo/genética , População Negra/genética , População Branca/genética , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , Alcoolismo/etnologia , Feminino , Variação Genética , Humanos , Masculino , Pessoa de Meia-Idade , Adulto JovemRESUMO
Background: Polymorphisms in cannabinoid receptor type 1 (encoded by CNR1) and fatty acid amide hydrolase (encoded by FAAH) have been associated with cannabis dependence, but it remains unknown whether variation within these genes influences cannabis' acute effects on affect. Objective: Conduct a secondary data analysis study to determine whether previously observed acute effects of tetrahydrocannabinol (THC) on mood was dependent upon variation in CNR1 and FAAH. Methods: A balanced placebo design was used crossing marijuana administration (i.e., 0% THC vs. 2.8% THC) with stimulus expectancy. Participants (N = 118; 64% male) provided DNA and completed the Profile of Mood States questionnaire prior to and after smoking. Haplotypes were constructed from genotyped single nucleotide polymorphisms for CNR1 (rs1049353 and rs806368) and FAAH (rs4141964, rs324420, and rs11576941); rs2023239 (CNR1) and rs6703669 (FAAH) were not part of a phased haplotype block. Analyses tested both main and interaction effects for genotype across CNR1 and FAAH, and drug, and expectancy effects. Results: THC increased levels of POMS Tension-Anxiety and Confusion-Bewilderment over and above the effects of variation in CNR1 and FAAH. Significant drug X genotype/haplotype and expectancy X genotype/haplotype interaction effects were observed for some but not all mood states [e.g., 'C' allele carriers of rs2023239 who received THC had higher levels of Anger-Hostility (ß= 0.29 (0.12), p= .02) compared to those who received placebo]. Conclusion: These preliminary findings suggest individual differences in mood states after using marijuana depend on genetic variation. Such information might be useful in understanding either motivation for use of marijuana and/or risk for associated behaviors.
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Amidoidrolases/genética , Abuso de Maconha/psicologia , Fumar Maconha/psicologia , Receptor CB1 de Canabinoide/genética , Afeto/efeitos dos fármacos , Dronabinol/farmacologia , Feminino , Genótipo , Haplótipos , Humanos , Masculino , Abuso de Maconha/genética , Fumar Maconha/genética , Polimorfismo de Nucleotídeo ÚnicoRESUMO
Learning to respond optimally under a broad array of environmental conditions is a critical brain function that requires engaging the cognitive systems that are optimal for solving the task at hand. Serotonin is implicated in learning and decision-making, but the specific functions of serotonin in system-level cognitive control remain unclear. Across 3 studies, we examined the influence of a polymorphism within the promoter region of the serotonin transporter gene (5-HTTLPR polymorphism in SLC6A4) on participants' ability to engage the task appropriate cognitive system when the reflexive (Experiments 1 and 2) or the reflective (Experiment 3) system was optimal. Critically, we utilized a learning task for which all aspects remain fixed with only the nature of the optimal cognitive processing system varying across experiments. Using large community samples, Experiments 1 and 2 (screened for psychiatric diagnosis) found that 5-HTTLPR S/LG allele homozygotes, with putatively lower serotonin transport functionality, outperformed LA allele homozygotes in a reflexive-optimal learning task. Experiment 3 used a large community sample, also screened for psychiatric diagnosis, and found that 5-HTTLPR LA homozygotes, with putatively higher serotonin transport functionality, outperformed S/LG allele homozygotes in a reflective-optimal learning task.
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Aprendizagem/fisiologia , Proteínas da Membrana Plasmática de Transporte de Serotonina/genética , Alelos , Cognição/fisiologia , Tomada de Decisões , Feminino , Frequência do Gene , Genótipo , Humanos , Curva de Aprendizado , Masculino , Neostriado/fisiologia , Polimorfismo Genético , Córtex Pré-Frontal/fisiologia , Desempenho Psicomotor , Serotonina/fisiologia , Adulto JovemRESUMO
Children exposed to maternal smoking during pregnancy (MSDP) exhibit difficulties in executive function (EF) from infancy through adolescence. Due to the developmental significance of EF as a predictor of adaptive functioning throughout the life span, the MSDP-EF relation has clear public health implications. In this paper, we provide a comprehensive review of the literature on the relationship between MSDP and offspring EF across development; consider brain-based assessments, animal models, and genetically informed studies in an effort to elucidate plausible pathways of effects; discuss implications for prevention and intervention; and make calls to action for future research.
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Função Executiva/fisiologia , Efeitos Tardios da Exposição Pré-Natal/psicologia , Fumar/efeitos adversos , Criança , Feminino , Humanos , Masculino , GravidezRESUMO
Impulsivity and sensation seeking have been linked to hazardous drinking, increased sexual risk behaviors, and lower treatment adherence among persons living with HIV (PLH). The dopamine active transporter1 (DAT1or SLC6A3) gene has been linked to impulsivity and sensation seeking in several populations but has not been investigated among populations of PLH. This study used data from 201 PLH who report a recent history of heavy episodic drinking. Results indicate that DAT1*10R vs DAT1*9R genotype was related to higher propensity for risk taking (standardized difference score (d) = 0.30 [95% CI: 0.02;0.59]), more hazardous drinking (d = 0.35 [0.05;0.64]), and more condomless sex (rate ratio (RR)= 2.35[1.94; 2.85]), but were counter-intuitively associated with fewer sexual partners (RR = 0.65[0.43;0.91]) and possibly better treatment adherence (d = 0.32 [-0.01;0.65]). Results are consistent with the suggested associations between DAT1 and risk-taking behavior. The counter-intuitive finding for partner selection and treatment adherence may be evidence of additional factors that place PLH at risk for engaging in hazardous drinking as well as relationship difficulties and problems with treatment adherence (e.g., depressive symptoms, avoidant coping, trauma history). Caution is required when using a single gene variant as a marker of complex behaviors and these findings need to be replicated using larger samples and additional variants.
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Consumo de Bebidas Alcoólicas/psicologia , Proteínas da Membrana Plasmática de Transporte de Dopamina/genética , Infecções por HIV/genética , Adesão à Medicação , Assunção de Riscos , Comportamento Sexual , Adulto , Consumo de Bebidas Alcoólicas/genética , Consumo de Bebidas Alcoólicas/metabolismo , Estudos Transversais , Feminino , Marcadores Genéticos , Infecções por HIV/diagnóstico , Humanos , Masculino , Pessoa de Meia-Idade , Parceiros SexuaisRESUMO
We introduce and discuss a special issue on prenatal factors in genetics research, that includes 14 papers ranging from studies on chorionicity, smoking during pregnancy, and more general prenatal risks to papers about theory, methods and measurement. There are two review papers, one focused on chorioncity and the second on pre- and perinatal ischemia-hypoxia, that help to frame the state of research in these areas with a focus on the relevance across multiple fields of study. Taken together, these papers clearly demonstrate the importance of considering prenatal environment influences on functioning in offspring across the lifespan while also underscoring the importance of using genetically informed designs as a means to clarify causality.
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Genética Comportamental , Feminino , Humanos , Gravidez , FumarRESUMO
We document the growth in published papers on behavioral genetics for 5-year intervals from 1960 through 2014. We used 1861 papers published in Behavior Genetics to train our search strategy which, when applied to Ovid PsychINFO, selected more than 45,000 publications. Five trends stand out: (1) the number of behavioral genetic publications has grown enormously; nearly 20,000 papers were published in 2010-2014. (2) The number of human quantitative genetic (QG) publications (e.g., twin and adoption studies) has steadily increased with more than 3000 papers published in 2010-2014. (3) The number of human molecular genetic (MG) publications increased substantially from about 2000 in 2000-2004 to 5000 in 2005-2009 to 9000 in 2010-2014. (4) Nonhuman publications yielded similar trends. (5) Although there has been exponential growth in MG publications, both human and nonhuman QG publications continue to grow. A searchable resource of this corpus of behavioral genetic papers is freely available online at http://www.teds.ac.uk/public_datasets.html and will be updated annually.
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Genética Comportamental/tendências , Publicações/tendências , Animais , Bases de Dados como Assunto , HumanosRESUMO
When examining the effects of prenatal exposure to maternal smoking during pregnancy (MSDP) on later offspring substance use, it is critical to consider familial environments confounded with MSDP. The purpose of this study was to examine the effect of MSDP on offspring's initial reactions to cigarettes and alcohol, which are indicators of future substance-use related problems. We tested these effects using two propensity score approaches (1) by controlling for confounding using the MSDP propensity score and (2) examining effects of MSDP across the MSDP risk distribution by grouping individuals into quantiles based on their MSDP propensity score. This study used data from 829 unrelated mothers with a reported lifetime history of smoking to determine the propensity for smoking only during their first trimester (MSDP-E) or throughout their entire pregnancy (MSDP-T). Propensity score analyses focused on the offspring (N = 1616 female twins) of a large subset of these mothers. We examined the effects of levels of MSDP-E/T on offspring initial reactions to their first experiences with alcohol and cigarettes, across the distribution of liability for MSDP-E/T. MSDP-E/T emerged as significant predictors of offspring reactions to alcohol and cigarettes, but the effects were confounded by the familial liability for MSDP. Further, the unique MSDP effects that emerged were not uniform across the MSDP familial risk distribution. Our findings underscore the importance of properly accounting for correlated familial risk factors when examining the effects of MSDP on substance related outcomes.