Kristine Marceau1, Leslie A Brick2, Joëlle A Pasman3, Valerie S Knopik1, Sijmen A Reijneveld4. 1. Department of Human Development and Family Studies, Purdue University, West Lafayette, Indiana, USA. 2. Department of Psychiatry and Human Behavior, Alpert Medical School at Brown University, Providence, Rhode Island, USA. 3. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden. 4. Department of Health Sciences, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Abstract
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.
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.
Authors: Kristine Marceau; Emily Rolan; Leslie D Leve; Jody M Ganiban; David Reiss; Daniel S Shaw; Misaki N Natsuaki; Helen L Egger; Jenae M Neiderhiser Journal: Dev Psychol Date: 2019-03-07
Authors: Merlijne Jaspers; Gea de Meer; Frank C Verhulst; Johan Ormel; Sijmen A Reijneveld Journal: J Clin Epidemiol Date: 2009-08-13 Impact factor: 6.437
Authors: Carolyn Y Fang; Brian L Egleston; Kathleen M Brown; John V Lavigne; Victor J Stevens; Bruce A Barton; Donald W Chandler; Joanne F Dorgan Journal: J Adolesc Health Date: 2009-02-24 Impact factor: 5.012
Authors: Esther M C Bouma; Harriëtte Riese; Johan Ormel; Frank C Verhulst; Albertine J Oldehinkel Journal: Psychoneuroendocrinology Date: 2009-02-04 Impact factor: 4.905