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2015 - SRCD Biennial Meeting Pages: unavailable || Words: 204 words || 
1. Su, Jinni. and Supple, Andrew. "Predicting Alcohol Use Trajectories from Adolescence to Young Adulthood: Gene-Gene Interaction and Gene-Environment Interaction" Paper presented at the annual meeting of the SRCD Biennial Meeting, Pennsylvania Convention Center and the Philadelphia Marriott Downtown Hotel, Philadelphia, PA, Mar 19, 2015 <Not Available>. 2019-11-14 <>
Publication Type: Individual Poster
Review Method: Peer Reviewed
Abstract: Alcohol use is prevalent among adolescents and adults. Although typically initiated during adolescence, individuals follow different trajectories of alcohol use over time. Those who start drinking early in adolescence and continue drinking over time are at higher risk for adverse psychosocial outcomes including alcohol dependence (e.g., Flory, Lynam, Milich, Leukefeld, & Clayton, 2004). As such, it is important to understand the etiology of alcohol use trajectories. The goal of this study was to examine alcohol use trajectories from adolescence to young adulthood, and to examine whether the dopamine D4 receptor gene (i.e., DRD4) and the serotonin transporter gene (i.e., 5-HTTLPR) independently and interactively predict alcohol use trajectories; whether parental support and childhood maltreatment interact with the genes in predicting alcohol use trajectories.
The sample for this study included 20,745 individuals who participated in the National Longitudinal Study of Adolescent Health, a nationally representative sample of adolescents who were in Grade 7th through Grade 12th in the year of 1995 (n = 20,745). Participants were followed up in 1996 (n = 14,738), 2000 (15,197), and 2008 (n = 15,701). Alcohol use was measured by two items (i.e., the number of days drank alcohol, and number of drinks each time, in the past 12 months) at four waves. Parental support was measured at Wave I, with participants responding to five items regarding how loving, supportive, and caring their parents were. Childhood maltreatment was a retrospective measure at Wave III, a dichotomized indicator of whether participants experienced neglect, physical abuse, or sexual abuse during their childhood. DRD4 and 5-HTTLPR were genotyped using buccal cell DNA extracted from saliva samples collected at Wave IV. 50.5% of the participants were female. 3,525(17%) of the participants were Hispanic, 10,829 (47.8%) were non-Hispanic White, 4,599 (22.2%) were African American, 181 (0.9%) were Native American, 1,406 (6.8%) were Asian, and 213 (1%) reported “other race”.
Growth mixture modeling (GMM) was conducted in Mplus 7.0 to identify trajectories of alcohol use over time. 1,006 (4.8%) of the participants had never used alcohol (i.e., abstainers) and thus they were excluded from the GMM analysis. GMM specifying quadratic growth and different number of classes were evaluated and the optimal model was determined based on model fit indices, entropy, and interpretability of classes. Results suggested that a three-class model fit best, identifying three distinct trajectories of use among alcohol users (Figure 1). Multinomial logistic regression was then conducted to predict membership of alcohol use trajectory (abstainers were the reference group) from DRD4, 5-HTTLPR, parental support, and childhood maltreatment, controlling for age, gender, and race/ethnicity. Results (Table 1) indicated that parental support was associated with lower likelihood of being in any alcohol use trajectory, whereas childhood maltreatment was associated with higher risk of being in any alcohol use trajectory, relative to being in the abstainers group. There were no main effects of the DRD4 and 5-HTTLPR genes; however, results indicated significant gene-gene (Figure 2) and gene-environment interactions (Figure 3) in predicting alcohol use trajectories over time. Implications of these findings will be discussed.

2013 - ARNOVA Annual Conference Words: 97 words || 
2. Konrath, Sara. "Good Genes Don’t Need Good Deeds: Oxytocin Receptor Genes, Prosociality, and Mortality" Paper presented at the annual meeting of the ARNOVA Annual Conference, Marriott Hartford Downtown, Hartford, CT, Nov 21, 2013 <Not Available>. 2019-11-14 <>
Publication Type: Conference Paper/Unpublished Manuscript
Review Method: Peer Reviewed
Abstract: This study finds that non-volunteers, self-oriented ones, and people who described themselves as low in caring traits all have a higher mortality risk 7 years later. However, this depends on the type of genes people have. Prior research has found that one variant of the oxytocin receptor gene (G/G) predicts more prosocial behavior and lower stress regulation than other variants (with A alleles). In the current study, people with the “prosocial” variant were buffered from the negative effects of low prosociality. In other words, they did not need to be “good” to have lower mortality risks.

2015 - American Society of Criminology – 71st Annual Meeting Words: 130 words || 
3. Wells, Jessica., Armstrong, Todd., Boisvert, Danielle. and Lewis, Richard. "Stress, Genes, and Generalizability Across Gender: Direct and Interactive Effects of Candidate Genes and Life Stress on Antisocial Behavior" Paper presented at the annual meeting of the American Society of Criminology – 71st Annual Meeting, Washington Hilton, Washington, DC, <Not Available>. 2019-11-14 <>
Publication Type: Individual Paper
Abstract: Criminologists have long noted the gendered nature of crime rates wherein males offend at significantly higher rates than females. While the polygenic threshold model has suggested that females offend less because they have a higher threshold of risk that leads to antisocial behavior, interesting research has emerged pointing to variation in how genetic polymorphisms associated with antisocial behavior vary across sexes. Further, as genes do not operate in isolation of the environment, varying effects of environmental stressors across gender are beginning to emerge. The proposed study seeks to extend the current literature in GxE interaction studies by examining not only sex-specific contributions of widely studied genetic polymorphisms but also by examining how these polymorphisms interact with both distal and proximal stressor in each sex to explain variation in antisocial behavior.

2010 - 4S Annual Meeting - Abstract and Session Submissions Words: 483 words || 
4. Lappe, Martine. "Extension, Connection, and “Enriched Risk” in Research on Gene-Environment Interactions and Autism" Paper presented at the annual meeting of the 4S Annual Meeting - Abstract and Session Submissions, Komaba I Campus, University of Tokyo, Tokyo, Japan, <Not Available>. 2019-11-14 <>
Publication Type: Abstract
Abstract: Within the United States, diagnosed cases of autism spectrum disorders (ASD) have risen from 4-5 in 10,000 in 1966 (Lotter 1966) to 1 in 110 today (CDC 2009), shifting autism from a rare condition to a common diagnosis. This rise in prevalence has become the site of considerable debate in recent years, raising questions about the role of changing diagnostic criteria (Croen et al., 2002; Hertz-Picciotto and Delwiche 2009), increased awareness, and the salience of environmental factors in causing autism (Daniels 2006; Szpir 2006; Schechter and Grether 2008).

The unknown source of this rise in cases has placed questions of cause at the center of political, social, and scientific discourses surrounding autism. In an attempt to address these questions, researchers have started to explore the role of gene-environment interactions in the etiology and pathogenesis of autism. This research posits an interaction between environmental factors – such as toxic chemicals, pesticides, and viral or infectious agents – and genetic biomarkers of susceptibility (Hertz-Picciotto et al. 2006).

In this paper I first provide background on the emergence of autism epidemiology in the United States. This brief history traces the role of parents of children with autism, government agencies, and the technological and disciplinary shifts within epidemiology in the emergence of gene-environment interaction research on autism today. Within this section, I discuss the ways in which concerns about specific environmental exposures have been extended to encompass the study of gene-environment interactions in autism more broadly.

Second, through analysis of documentary materials, research observations, and interviews conducted with autism scientists and participating families I discuss the practices – and social and scientific dimensions – of several prospective "enriched risk" cohort studies. These epidemiological studies follow mothers who have a biological child diagnosed with autism through a subsequent pregnancy, gathering information about the pre-natal and post-partum genetic and environmental factors that may contribute to the development of autism.

I argue that the emergence and practice of “enriched risk” cohort studies are assembling new relationships among bodies, environments, autism risk, and diagnosis. Through webs of disciplinary and parent expertise, bodies, exposures, and histories are drawn together and interrogated in ways that are simultaneously extending questions surrounding autism’s cause(s) into the womb, out to the world, and through generations.

While families are enrolled in these studies to identify both external and biological risk factors for autism, they also interrogate their own personal histories, homes, and behaviors, all the while monitoring their pregnancies and newborn children in relation to new assemblages of (partial and possible) risk knowledge (Kaufman 2010). This paper will discuss the implications of this research for our understandings of the connections between bodies, environments, histories, and (possible) futures, as well as extensions of risk inward, outward, and through time. In particular, I draw on the work of Adele Clarke, Michelle Murphy, Rayna Rapp, and Nikolas Rose to consider the scientific, technological, and gendered dimensions of this phenomenon.

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