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Description
The present study utilized longitudinal data from a high-risk community sample (n=254, 52.8% female, 47.2% children of alcoholics, 74% non-Hispanic Caucasian) to test questions concerning the effects of genetic risk, parental knowledge, and peer substance use on emerging adult substance use disorders (SUDs). Specifically, this study examined whether parental knowledge and peer substance use mediated the effects of parent alcohol use disorder (AUD) and genetic risk for behavioral undercontrol on SUD. The current study also examined whether genetic risk moderated effects of parental knowledge and peer substance use on risk for SUD. Finally, this study examined these questions over and above a genetic "control" which explained a large proportion of variance in the outcome, thereby providing a stricter test of environmental influences.
Analyses were performed in a path analysis framework. To test these research questions, the current study employed two polygenic risk scores. The first, a theory-based score, was formed using single-nucleotide polymorphisms (SNPs) from receptor systems implicated in the amplification of positive effects in the presence of new/exciting stimuli and/or pleasure derived from using substances. The second, an empirically-based score, was formed using a data-driven approach that explained a large amount of variance in SUDs. Together, these scores allowed the present study to test explanations for the relations among parent AUD, parental knowledge, peer substance use, and SUDs.
Results of the current study found that having parents with less knowledge or an AUD conferred greater risk for SUDs, but only for those at higher genetic risk for behavioral undercontrol. The current study replicated research findings suggesting that peer substance use mediated the effect of parental AUD on SUD. However, it adds to this literature by suggesting that some mechanism other than increased behavioral undercontrol explains relations among parental AUD, peer substance use, and emerging adult SUD. Taken together, these findings indicate that children of parents with AUDs comprise a particularly risky group, although likelihood of SUD within this group is not uniform. These findings also suggest that some of the most important environmental risk factors for SUDs exert effects that vary across level of genetic propensity.
Analyses were performed in a path analysis framework. To test these research questions, the current study employed two polygenic risk scores. The first, a theory-based score, was formed using single-nucleotide polymorphisms (SNPs) from receptor systems implicated in the amplification of positive effects in the presence of new/exciting stimuli and/or pleasure derived from using substances. The second, an empirically-based score, was formed using a data-driven approach that explained a large amount of variance in SUDs. Together, these scores allowed the present study to test explanations for the relations among parent AUD, parental knowledge, peer substance use, and SUDs.
Results of the current study found that having parents with less knowledge or an AUD conferred greater risk for SUDs, but only for those at higher genetic risk for behavioral undercontrol. The current study replicated research findings suggesting that peer substance use mediated the effect of parental AUD on SUD. However, it adds to this literature by suggesting that some mechanism other than increased behavioral undercontrol explains relations among parental AUD, peer substance use, and emerging adult SUD. Taken together, these findings indicate that children of parents with AUDs comprise a particularly risky group, although likelihood of SUD within this group is not uniform. These findings also suggest that some of the most important environmental risk factors for SUDs exert effects that vary across level of genetic propensity.
ContributorsBountress, Kaitlin (Author) / Chassin, Laurie (Thesis advisor) / Crnic, Keith (Committee member) / Lemery-Chalfant, Kathryn (Committee member) / MacKinnon, David (Committee member) / Arizona State University (Publisher)
Created2015
Description
Prior research has established associations between sleep duration and body mass index (BMI) scores and risk for obesity in middle childhood, but it is less clear whether other objectively- and subjectively-measured sleep indicators may be associated with BMI scores, weight status (e.g., obesity), and other estimates of weight and body fat such as waist circumference (WC) and percent body fat. Empirical studies have also demonstrated independent associations between broad self-regulation and sleep indicators and BMI scores, but no study to date has tested these factors in a model together and the extent to which associations between normative sleep problems, weight indicators, and effortful control (EC) may be explained by shared genetic or environmental influences. Data from a large longitudinal study of twins was used to test phenotypic associations between sleep problems at eight years and weight indicators at nine years, including whether EC at eight years moderates these associations. Additionally, multiple quantitative behavior genetic models were used to estimate unique and shared genetic and environmental covariances among normative sleep problems, weight indicators, and EC at eight years of age and whether additive genetic influence on weight in middle childhood differs by child weight status group. Phenotypic findings showed that greater sleep duration at eight years predicted greater decreases BMI at nine years of age for children with low levels of EC at eight years. Greater sleep midpoint variability at eight years predicted greater increases in percent body fat from eight to nine years of age for children with low EC at eight years. Behavior genetic findings showed greater environmental influences on parent-reported sleep duration and quality, as well as objective sleep midpoint variability. Similarly, associations between parent-reported sleep duration and sleep midpoint variability and other sleep indicators and EC were primarily accounted for by shared environmental factors. In contrast, there was high additive genetic influence on objective sleep quantity and quality, all weight indicators, and EC. Many of the associations between sleep indicators, sleep and weight indicators, and among weight indicators were entirely accounted for by shared additive genetic factors, suggesting that common, underlying sets of genes explain these relations.
ContributorsBreitenstein, Reagan Styles (Author) / Doane, Leah D. (Thesis advisor) / Lemery-Chalfant, Kathryn (Committee member) / Perez La Mar, Marisol (Committee member) / Grimm, Kevin (Committee member) / Arizona State University (Publisher)
Created2019
Description
Brave Bears was a Barrett creative project that operated under local non-profit organizations, Amanda Hope Rainbow Angels and Arizona Women’s Recovery Center. Amanda Hope Rainbow Angels provides support and education for children fighting cancer and their families. Arizona Women’s Recovery Center provides rehabilitation programs for women fighting substance abuse and housing for the women and their children. The Brave Bears Project was focused on helping children in these situations cope with the trauma they are experiencing. The children received a teddy bear, which is a transitional object. In addition, a clay pendant with the word, “brave” pressed into it was tied around the bear’s neck with a ribbon. A poem of explanation and encouragement was also included.<br/><br/>The teddy bear provided comfort to children experiencing emotionally distressing situations as they receive treatment for their illness or as their mom undergoes rehabilitation. This can be in the form of holding the teddy bear when they feel frightened, anxious, lonely or depressed. The “brave” pendant and poem seek to encourage them and acknowledge their trauma and ability to persevere.
ContributorsRichards, Emma Joy (Author) / Lopez, Kristina (Thesis director) / Safyer, Paige (Committee member) / College of Health Solutions (Contributor) / Barrett, The Honors College (Contributor)
Created2021-05
Description
Sufficient sleep in childhood is fundamental to proper development as well as preventing behavioral or emotional complications later in adulthood (Gregory & Sadeh, 2012; Bruni, 2010). Sleep is controlled by a 24-hour cycle of hormonal regulation termed the circadian rhythm, which is controlled by different environmental inputs such as light (Reppert & Weaver, 2002). Previous research has also demonstrated that light exposure at night can delay the night phase production of specific hormones that promote sleep (Zeitzer, Dijk, Kronauer, Brown, & Czeisler, 2004; Chang, Aeschbach, Duffy, & Czeisler, 2015), which in turn delays sleep onset. Such studies involving the effects that light may have on sleep have focused on adult subjects, however, and it is important to explore this idea in childhood to promote proper development. The first aim of this study was to examine the effects of light exposure in the hour before bedtime on different measures of sleep in middle childhood. The second aim was to determine the genetic and environmental contributions to light exposure and sleep. A diverse sample of 490 twin children was assessed at 8 years of age. Twins followed a week long protocol in which they wore actigraph watches that collected data on both light and sleep. Zero-order correlations with subsequent multilevel regression analyses showed that any light exposure in the hour before bedtime was significantly positively associated with sleep onset latency. Twin intraclass correlations indicated no heritability for light exposure, but did indicate some heritability ranging from 7-66% for the sleep indicators. Overall, these findings regarding the impacts of sleep in childhood build upon an area of research that has only been explored in adulthood. These impacts of light on sleep in childhood suggest that possible interventions ought to be explored for implementation to minimize the long-term effects of altered sleeping patterns in childhood.
ContributorsScheel, Sydney Elise (Author) / Lemery-Chalfant, Kathryn (Thesis director) / Clifford, Sierra (Committee member) / School of Molecular Sciences (Contributor) / School of International Letters and Cultures (Contributor) / Barrett, The Honors College (Contributor)
Created2019-05