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      Early life adversity and health-risk behaviors: proposed psychological and neural mechanisms : Early life adversity and health-risk behaviors

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          Abstract

          <p class="first" id="P1">Early life adversity (ELA) is associated with poorer health in adulthood, an association explained, at least in part, by increased engagement in health-risk behaviors (HRBs). In this review, we make the case that ELA influences brain development in ways that increase the likelihood of engaging in HRBs. We argue that ELA alters neural circuitry underpinning cognitive control as well as emotional processing, including networks involved in processing threat and reward. These neural changes are associated psychologically and behaviorally with heightened emotional reactivity, blunted reward responsivity, poorer emotion regulation, and greater delay discounting. We then demonstrate that these adaptations to ELA are associated with an increased risk of smoking cigarettes, drinking alcohol, and eating high-fat, high-sugar foods. Furthermore, we explore how HRBs affect the brain in ways that reinforce addiction and further explain clustering of HRBs. </p><p id="P2">Early life adversity (ELA) involves exposure to environmental circumstances during childhood or adolescence that are likely to require significant psychological, behavioral, or neurobiological adaptation by an average child. It is associated with poorer health in adulthood, an association explained, at least in part, by increased engagement in health-risk behaviors (HRBs). In this review, we make the case that ELA influences brain development in ways that increase the likelihood of engaging in HRBs. </p>

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          Most cited references138

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          Separate neural systems value immediate and delayed monetary rewards.

          When humans are offered the choice between rewards available at different points in time, the relative values of the options are discounted according to their expected delays until delivery. Using functional magnetic resonance imaging, we examined the neural correlates of time discounting while subjects made a series of choices between monetary reward options that varied by delay to delivery. We demonstrate that two separate systems are involved in such decisions. Parts of the limbic system associated with the midbrain dopamine system, including paralimbic cortex, are preferentially activated by decisions involving immediately available rewards. In contrast, regions of the lateral prefrontal cortex and posterior parietal cortex are engaged uniformly by intertemporal choices irrespective of delay. Furthermore, the relative engagement of the two systems is directly associated with subjects' choices, with greater relative fronto-parietal activity when subjects choose longer term options.
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            Childhood abuse, neglect, and household dysfunction and the risk of illicit drug use: the adverse childhood experiences study.

            Illicit drug use is identified in Healthy People 2010 as a leading health indicator because it is associated with multiple deleterious health outcomes, such as sexually transmitted diseases, human immunodeficiency virus, viral hepatitis, and numerous social problems among adolescents and adults. Improved understanding of the influence of stressful or traumatic childhood experiences on initiation and development of drug abuse is needed. We examined the relationship between illicit drug use and 10 categories of adverse childhood experiences (ACEs) and total number of ACEs (ACE score). A retrospective cohort study of 8613 adults who attended a primary care clinic in California completed a survey about childhood abuse, neglect, and household dysfunction; illicit drug use; and other health-related issues. The main outcomes measured were self-reported use of illicit drugs, including initiation during 3 age categories: or=19 years); lifetime use for each of 4 birth cohorts dating back to 1900; drug use problems; drug addiction; and parenteral drug use. Each ACE increased the likelihood for early initiation 2- to 4-fold. The ACE score had a strong graded relationship to initiation of drug use in all 3 age categories as well as to drug use problems, drug addiction, and parenteral drug use. Compared with people with 0 ACEs, people with >or=5 ACEs were 7- to 10-fold more likely to report illicit drug use problems, addiction to illicit drugs, and parenteral drug use. The attributable risk fractions as a result of ACEs for each of these illicit drug use problems were 56%, 64%, and 67%, respectively. For each of the 4 birth cohorts examined, the ACE score also had a strong graded relationship to lifetime drug use. The ACE score had a strong graded relationship to the risk of drug initiation from early adolescence into adulthood and to problems with drug use, drug addiction, and parenteral use. The persistent graded relationship between the ACE score and initiation of drug use for 4 successive birth cohorts dating back to 1900 suggests that the effects of adverse childhood experiences transcend secular changes such as increased availability of drugs, social attitudes toward drugs, and recent massive expenditures and public information campaigns to prevent drug use. Because ACEs seem to account for one half to two third of serious problems with drug use, progress in meeting the national goals for reducing drug use will necessitate serious attention to these types of common, stressful, and disturbing childhood experiences by pediatric practice.
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              Cumulative risk and child development.

              Childhood multiple risk factor exposure exceeds the adverse developmental impacts of singular exposures. Multiple risk factor exposure may also explain why sociodemographic variables (e.g., poverty) can have adverse consequences. Most research on multiple risk factor exposure has relied upon cumulative risk (CR) as the measure of multiple risk. CR is constructed by dichotomizing each risk factor exposure (0 = no risk; 1 = risk) and then summing the dichotomous scores. Despite its widespread use in developmental psychology and elsewhere, CR has several shortcomings: Risk is designated arbitrarily; data on risk intensity are lost; and the index is additive, precluding the possibility of statistical interactions between risk factors. On the other hand, theoretically more compelling multiple risk metrics prove untenable because of low statistical power, extreme higher order interaction terms, low robustness, and collinearity among risk factors. CR multiple risk metrics are parsimonious, are statistically sensitive even with small samples, and make no assumptions about the relative strengths of multiple risk factors or their collinearity. CR also fits well with underlying theoretical models (e.g., Bronfenbrenner's, 1979, bioecological model; McEwen's, 1998, allostasis model of chronic stress; and Ellis, Figueredo, Brumbach, & Schlomer's, 2009, developmental evolutionary theory) concerning why multiple risk factor exposure is more harmful than singular risk exposure. We review the child CR literature, comparing CR to alternative multiple risk measurement models. We also discuss strengths and weaknesses of developmental CR research, offering analytic and theoretical suggestions to strengthen this growing area of scholarship. Finally, we highlight intervention and policy implications of CR and child development research and theory. © 2013 American Psychological Association
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                Author and article information

                Journal
                Annals of the New York Academy of Sciences
                Ann. N.Y. Acad. Sci.
                Wiley
                00778923
                September 2018
                September 2018
                July 16 2018
                : 1428
                : 1
                : 151-169
                Affiliations
                [1 ]Basic Biobehavioral and Psychological Sciences Branch, Behavioral Research Program; National Cancer Institute, National Institutes of Health; Bethesda Maryland
                [2 ]Department of Psychology; University of Washington; Seattle Washington
                Article
                10.1111/nyas.13928
                6158062
                30011075
                6778a382-dcf9-4786-8029-7c8177f5dbb2
                © 2018

                http://doi.wiley.com/10.1002/tdm_license_1.1

                http://onlinelibrary.wiley.com/termsAndConditions#vor

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