172 research outputs found

    Addiction in context

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    The dissertation provides a comprehensive exploration of the interplay between social and cultural factors in substance use, specifically focusing on alcohol use disorder (AUD) and cannabis use disorder (CUD). It begins by introducing the concept of social plasticity, which posits that adolescents' susceptibility to AUD is influenced by their heightened sensitivity to their social environment, but this sensitivity increases the potential for recovery in the transition to adulthood.A series of studies delves into how social cues impact alcohol craving and consumption. One study using functional magnetic resonance imaging (fMRI) investigated social alcohol cue reactivity and its relationship to social drinking behavior, revealing increased craving but no significant change in brain activity in response to alcohol cues. Another fMRI study compared social processes in alcohol cue reactivity between adults and adolescents, showing age-related differences in how social attunement affects drinking behavior. Shifting focus to cannabis, this dissertation discusses how cultural factors, including norms, legal policies, and attitudes, influence cannabis use and processes underlying CUD. The research presented examined various facets of cannabis use, including how cannabinoid concentrations in hair correlate with self-reported use, the effects of cannabis and cigarette co-use on brain reactivity, and cross-cultural differences in CUD between Amsterdam and Texas. Furthermore, the evidence for the relationship between cannabis use, CUD, and mood disorders is reviewed, suggesting a bidirectional relationship, with cannabis use potentially preceding the onset of bipolar disorder and contributing to the development and worse prognosis of mood disorders and mood disorders leading to more cannabis use

    Risk factors and prevention in the offspring of parents with an affective disorder: associations between neuroendocrine function, the caregiving environment, and child emotional and behavioural problems

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    The offspring of parents with an affective disorder (OAD) are at high risk of developing mental disorders. This thesis examines the influence of hypothalamic-pituitary-adrenal (HPA) axis functioning and the caregiving environment on the transmission and prevention of psychopathology in the OAD. First, meta-analytic procedures were used to quantitatively summarize studies comparing diurnal cortisol levels in the natural environment in the OAD to control offspring. Relative to controls, the OAD had higher mean levels of cortisol at different timepoints throughout the day (Hedges’ g = .21). These findings suggest that changes in HPA function may predate the onset of a full-blown affective disorder (AD). In the second study, data from a longitudinal study of offspring of parents with bipolar disorder (OBD) was used to study the relations between HPA axis functioning, the caregiving environment, and offspring psychopathology. As expected, the OBD who developed an AD had a higher cortisol awakening response (CAR) than OBD who did not have an AD (Cohen’s d = 0.423) and controls (Cohen’s d = 0.468). Serial mediation analyses revealed that family structure in childhood and the CAR in offspring mediated the relationship between risk status (having a parent with bipolar disorder) and offspring internalizing symptoms 12 years later (CI [.01, .66]). The last study aimed to evaluate the efficacy of the Reducing Unwanted Stress in the Home program using a quasi-experimental design with an assessment-only control group. Assessments were conducted at pre- and post-intervention, and at a three- and six-month follow-up. Multilevel modelling revealed reduced externalizing symptoms in the OBD and enhanced family organization immediately post-intervention. The gains in organization remained at the six-month follow-up, while reductions in family conflict became apparent. Mediation analyses indicated treatment induced changes in organization, but not other aspects of the family environment, were associated with reduced externalizing problems in the OBD at the six-month follow-up. Taken together, HPA abnormalities may represent a biomarker of risk among the OAD which may be shaped, at least in part, by specific, early experiences in the caregiving environment. These findings highlight the need for targeted, developmentally-informed treatments to offset adverse outcomes in the OAD

    Examining the relation between individual differences in early memory and adulthood anxiety across species

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    Mental illnesses that emerge early in life are associated with greater comorbidity, treatment resistance, and financial cost than those that emerge later in life. Because anxiety disorders are some of the earliest emerging mental illnesses, there is interest in identifying early predictors of anxiety so that interventions can be administered to “at-risk” individuals. Rodent work has previously shown that accelerated development of long-term fear memory retention predicts heightened learned/unlearned fear in adulthood. In this thesis, I took a cross-species approach to better understand the relation between individual differences in early memory and adulthood fear/anxiety. In rats, I found that neither sex nor early life adversity exposure moderate the strength of the relation between fear memory expression during infancy and learned/unlearned fear in adulthood (Chapter 2). I also found evidence suggesting that a rat’s social environment is critically involved in the relation between fear memory retention during infancy and learned/unlearned fear in adulthood. Specifically, rats that received lower levels of maternal care (i.e., licking) during the first postnatal week expressed stronger fear memory later in infancy (Chapter 3). Post-weaning, rats housed with cagemates that exhibited poorer fear memory retention during infancy had greater expression of fibroblast growth factor-2 (a biomarker of reduced vulnerability to fear/anxiety) in adulthood (Chapter 4). The average fear memory retention of a rat’s cagemates also moderated the strength of the association between the “target” rat’s fear memory retention during infancy and learned/unlearned fear in adulthood (Chapter 5). Finally, I examined whether accelerated memory maturation is similarly associated with heightened adulthood anxiety in humans. Specifically, I examined whether adults that report being younger at the time of their earliest memory report higher current anxiety (Chapter 6). Counter to predictions, reporting an older age at the time of one’s earliest memory was associated with greater anxiety. This relation was partially mediated by self-reported attachment to one’s parents during childhood. Taken together, these studies suggest that, across species, individual differences in early memory are associated with adulthood fear/anxiety (although the direction of the relation may differ across species), and that social relationships act as critical moderators and/or mediators of this relation

    Examining allostatic load as a biological mechanism linking childhood adversity and pediatric pain

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    Despite a strong literature base relating childhood adversity to pain, the biological mechanisms underlying these associations remain unclear. Theoretical and preliminary empirical evidence supports allostatic load as a potential biological mechanism, though prior studies investigating associations between childhood adversity and elevated allostatic load and/or between elevated allostatic load and poorer pain outcomes have primarily focused on adult populations and individual allostatic load indicators rather than a comprehensive index. Thus, the current study built upon prior literature by testing longitudinal relationships between childhood adversity and multiple biological indicators spanning across physiological systems (i.e., comprehensive allostatic load index) and pediatric pain outcomes (i.e., pain intensity and pain-related disability) within the nationally representative sample of early adolescents from the ABCD study. Allostatic load index was hypothesized as a mediator explaining the relationship between childhood adversity and poor pediatric pain outcomes (i.e., pain intensity and pain-related disability). The current study found childhood adversity in year 1 was significantly related to increased pain intensity and pain related disability in year 2, but not in year 3. Allostatic load did not significantly mediate the relationship between childhood adversity and pediatric pain outcomes. Future research should explore other biological mechanisms (e.g., epigenetic mechanisms) that may link childhood adversity to pediatric pain-related outcomes. Future research investigating allostatic load within a pediatric population should also consider the influence of key developmental stages (e.g., middle childhood, adolescence) to inform the selection of biological indicators as well as consider the type, duration and timing of adversity
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