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- All Subjects: psychology
- Genre: Doctoral Dissertation
- Creators: Lemery-Chalfant, Kathryn
Description
Fibromyalgia (FM) is a chronic musculoskeletal disorder characterized by widespread pain, fatigue, and a variety of other comorbid physiological and psychological characteristics, including a deficit of positive affect. Recently, the focus of research on the pathophysiology of FM has considered the role of a number of genomic variants. In the current manuscript, case-control analyses did not support the hypothesis that FM patients would differ from other chronic pain groups in catechol-O-methyltransferase (COMT) and mu-opioid receptor (OPRM1) genotype. However, evidence is provided in support of the hypothesis that functional single nucleotide polymorphisms on the COMT and OPRM1 genes would be associated with risk and resilience, respectively, in a dual processing model of pain-related positive affective regulation in FM. Forty-six female patients with a physician-confirmed diagnosis of FM completed an electronic diary that included once-daily assessments of positive affect and soft tissue pain. Multilevel modeling yielded a significant gene X environment interaction, such that individuals with met/met genotype on COMT experienced a greater decline in positive affect as daily pain increased than did either val/met or val/val individuals. A gene X environment interaction for OPRM1 also emerged, indicating that individuals with at least one asp allele were more resilient to elevations in daily pain than those homozygous for the asn allele. In sum, the findings offer researchers ample reason to further investigate the contribution of the catecholamine and opioid systems, and their associated genomic variants, to the still poorly understood experience of FM.
ContributorsFinan, Patrick Hamilton (Author) / Zautra, Alex (Thesis advisor) / Davis, Mary (Committee member) / Lemery-Chalfant, Kathryn (Committee member) / Presson, Clark (Committee member) / Arizona State University (Publisher)
Created2011
Description
Externalizing behaviors are pervasive, widespread, and disruptive across a multitude of settings and developmental contexts. While the conventional diathesis-stress model typically measures the disordered end of the spectrum, studies that span the range of behavior, from externalizing to competence behaviors, are necessary to see the full picture. To that end, this study examined the additive and nonadditive relations of a dimension of parenting (ranging from warm to rejecting), and variants in dopamine, vasopressin, and neuropeptide-y receptor genes on externalizing/competence in a large sample of predominantly Caucasian twin children in toddlerhood, middle childhood, and early adolescence. Variants within each gene were hypothesized to increase biological susceptibility to both negative and positive environments. Consistent with prediction, warmth related to lower externalizing/higher competence at all ages. Earlier levels of externalizing/competence washed out the effect of parental warmth on future externalizing/competence with the exception of father warmth in toddlerhood marginally predicting change in externalizing/competence from toddlerhood to middle childhood. Warmth was a significant moderator of the heritability of behavior in middle childhood and early adolescence such that behavior was less heritable (mother report) and more heritable (father report) in low warmth environments. Interactions with warmth and the dopamine and vasopressin genes in middle childhood and early adolescence emphasize the moderational role gene variants play in relations between the rearing environment and child behavior. For dopamine, the long variant related to increased sensitivity to parent warmth such that the children displayed more externalizing behaviors when exposed to rejection but they also displayed more competence behaviors when exposed to high warmth. Vasopressin moderation was only present under conditions of parental warmth, not rejection. Interactions with neuropeptide-y and warmth were not significant. The picture that emerges is one of gene-environment interplay, wherein the influence of both parenting and child genotype each depend on the level of the other. As genetic research moves forward, gene variants previously implicated as conferring risk for disorder should be reexamined in conjunction with salient aspects of the environment on the full range of the behavioral outcome of interest.
ContributorsO'Brien, T. Caitlin (Author) / Lemery-Chalfant, Kathryn (Thesis advisor) / Eisenberg, Nancy (Committee member) / Enders, Craig (Committee member) / Nagoshi, Craig (Committee member) / Arizona State University (Publisher)
Created2011
Description
In rehabilitation settings, activity limitation can be a significant barrier to recovery. This study sought to examine the effects of state and trait level benefit finding, positive affect, and catastrophizing on activity limitation among individuals with a physician-confirmed diagnosis of either Osteoarthritis (OA), Fibromyalgia (FM), or a dual diagnosis of OA/FM. Participants (106 OA, 53 FM, and 101 OA/FM) who had no diagnosed autoimmune disorder, a pain rating above 20 on a 0-100 scale, and no involvement in litigation regarding their condition were recruited in the Phoenix metropolitan area for inclusion in the current study. After initial questionnaires were completed, participants were trained to complete daily diaries on a laptop computer and instructed to do so a half an hour before bed each night for 30 days. In each diary, participants rated their average daily pain, benefit finding, positive affect, catastrophizing, and activity limitation. A single item, "I thought about some of the good things that have come from living with my pain" was used to examine the broader construct of benefit finding. It was hypothesized that state and trait level benefit finding would have a direct relation with activity limitation and a partially mediated relationship, through positive affect. Multilevel modeling with SAS PROC MIXED revealed that benefit finding was not directly related to activity limitation. Increases in benefit finding were associated, however, with decreases in activity limitation through a significant mediated relationship with positive affect. Individuals who benefit find had a higher level of positive affect which was associated with decreased activity limitation. A suppression effect involving pain and benefit finding at the trait level was also found. Pain appeared to increase the predictive validity of the relation of benefit finding to activity limitation. These findings have important implications for rehabilitation psychologists and should embolden clinicians to encourage patients to increase positive affect by employing active approach-oriented coping strategies like benefit finding to reduce activity limitation.
ContributorsKinderdietz, Jeffrey Scott (Author) / Zautra, Alex (Thesis advisor) / Davis, Mary (Committee member) / Barrera, Manuel (Committee member) / Okun, Morris (Committee member) / Arizona State University (Publisher)
Created2012
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
The purpose of this study was to examine whether maternal personality (i.e., Agreeableness and Conscientiousness) predicted maternal positive parenting (i.e., warmth/sensitivity and structure), and whether maternal parenting predicted children's regulation and sympathy and/or prosocial behavior. Additionally, the mediated effect of maternal warmth/sensitivity on the relation between maternal Agreeableness and children's regulation and the mediated effect of maternal structure on the relation between maternal Agreeableness and children's observed sympathy/prosocial behavior were investigated. Maternal personality was measured when children (N = 256 at Time 1) were 18 months old; maternal parenting was assessed when children were 18, 30, and 42 months old; children's regulation and sympathy/prosocial behavior (observed and reported) were assessed when children were 30, 42, and 54 months old. Mothers reported on their personality; maternal warmth/sensitivity was observed; maternal structure was observed and mothers also reported on their use of reasoning; mothers and caregivers rated children's regulation (i.e., effortful control [EC]) and regulation was also observed; mothers and fathers rated children's prosocial behavior; sympathy and prosocial behavior were also observed. In a path analysis, Conscientiousness did not significantly predict maternal warmth/sensitivity or structure at 30 months, whereas Agreeableness marginally predicted maternal warmth/sensitivity at 30 months and significantly predicted maternal structure at 30 months. Maternal warmth/sensitivity at 18 months significantly predicted 30-month EC, and 30-month maternal warmth/sensitivity significantly predicted 42-month EC. Maternal structure at 30 months significantly predicted 42-month observed sympathy/prosocial behavior. Maternal warmth/sensitivity at 42 months significantly predicted 54-month observed sympathy/prosocial behavior and marginally predicted 54-month reported prosocial behavior. Maternal structure and EC did not significantly predict reported prosocial behavior across any time point. EC did not significantly predict observed sympathy/prosocial behavior across any time point and maternal warmth/sensitivity at 18 and 30 months did not predict observed or reported sympathy/prosocial behavior at 30 or 42 months, respectively. Maternal Agreeableness directly predicted 30-month reported prosocial behavior and additional paths suggested possible bidirectional relations between maternal warmth/sensitivity and structure. Mediation analyses were pursued for two indirect relations; however, neither mediated effect was significant. Additional results are presented, and findings (as well as lack thereof) are discussed in terms of extant literature.
ContributorsEdwards, Alison (Author) / Eisenberg, Nancy (Thesis advisor) / Spinrad, Tracy L. (Thesis advisor) / Lemery-Chalfant, Kathryn (Committee member) / Bradley, Robert A. (Committee member) / Arizona State University (Publisher)
Created2015
Description
Research on attachment in adults began by assuming parallels from attachment as a behavioral system for using relationships to balance the tradeoff between safety and exploration in infants, to the same tradeoff function in adults. Perhaps more pressing, for adults, are the novel social tradeoffs adults face when deciding how to invest resources between themselves and their close relationship partners. The current study investigated the role of the attachment system in navigating two such tradeoffs, in a sample of ASU undergraduates. In one tradeoff condition, participants had the option of working on puzzles to earn either themselves or their closest friend a monetary reward. In the second tradeoff condition, participants worked to earn monetary rewards for a close or new friend. Analyses showed no evidence of attachment avoidance predicting prioritizing redistributing money to a close friend in either condition. While there was no effect of anxiety on prioritizing one’s close friend over one’s self, there was a marginal effect in both prioritizing one’s close friend over a new friend when redistributing money and starting on the close friend’s word search first. Although attachment style largely did not predict earning or redistributing monetary rewards in these two relationship tradeoffs, implications for how these results fit within the broader theoretical perspective are discussed.
ContributorsYee, Claire (Author) / Shiota, Michelle N. (Thesis advisor) / Kenrick, Douglas T. (Committee member) / Lemery-Chalfant, Kathryn (Committee member) / Luecken, Linda J. (Committee member) / Arizona State University (Publisher)
Created2018
Description
Cognitive reappraisal, or redefining the meaning of a stressful circumstance, is useful in regulating emotional responses to acute stressors and may be mobilized to up- or down- regulate the stressors’ emotional salience. A conceptually-related but more targeted emotion regulation strategy to that offered by cognitive reappraisal, termed positive cognitive shift, was examined in the current study. Positive cognitive shift (“PCS”) is defined as a point of cognitive transformation during a chronic, stressful situation that alters the meaning and emotional salience of the situation for the individual. Key aspects of the PCS that differentiate it from the broader reappraisal construct are that it 1) is relevant to responses to chronic (versus acute) aversive events, 2) is deployed when there is a mismatch between coping and stressors, and 3) involves insight together with redefinition in meaning of the situation generating stress. The current study used qualitative and quantitative analyses to 1) examine whether PCS is an observable, reliable, and valid experience in response to a stressful event that occurred in the past year, and 2) test whether PCS moderates the relations between the number of past-year stressful life circumstances and subsequent emotional well-being and functional health. A community sample of 175 middle-aged individuals were interviewed regarded a past chronic stressor and completed questionnaires regarding number of past year stressors and health outcomes. Theory-based coding of interviews was conducted to derive reliable scores for PCS, and findings indicated that PCS was evident in 37.7 % of participant responses. Furthermore, PCS scores were related positively to openness, personal growth from one’s most difficult lifetime event, and affect intensity-calm, in line with predictions. Also in line with prediction, PCS moderated the relations between number of past-year life events and health outcomes, such that the deleterious relations between past year stressful events and cognitive functioning, wellbeing, positive affect, and negative affect were weaker among individuals higher versus lower in PCS. Of note, PCS moderation effects diminished as the number of stressful events increased.
ContributorsRivers, Crystal (Author) / Davis, Mary (Thesis advisor) / Luecken, Linda (Committee member) / Infurna, Frank (Committee member) / Robinson Kurpius, Sharon (Committee member) / Arizona State University (Publisher)
Created2018
Description
The current study utilized data from two longitudinal samples to test mechanisms in the relation between a polygenic risk score indexing serotonin functioning and alcohol use in adolescence. Specifically, this study tested whether individuals with lower levels of serotonin functioning as indexed by a polygenic risk score were vulnerable to poorer self-regulation, and whether poorer self-regulation subsequently predicted the divergent outcomes of depressive symptoms and aggressive/antisocial behaviors. This study then examined whether depressive symptoms and aggressive/antisocial behaviors conferred risk for later alcohol use in adolescence, and whether polygenic risk and effortful control had direct effects on alcohol use that were not mediated through problem behaviors. Finally, the study examined the potential moderating role of gender in these pathways to alcohol use.
Structural equation modeling was used to test hypotheses. Results from an independent genome-wide association study of 5-hydroxyindoleacetic acid in the cerebrospinal fluid were used to create serotonin (5-HT) polygenic risk scores, wherein higher scores reflected lower levels of 5-HT functioning. Data from three time points were drawn from each sample, and all paths were prospective. Findings suggested that 5-HT polygenic risk did not predict self-regulatory constructs. However, 5-HT polygenic risk did predict the divergent outcomes of depression and aggression/antisociality, such that higher levels of 5-HT polygenic risk predicted greater levels of depression and aggression/antisociality. Results most clearly supported adolescents’ aggression/antisociality as a mechanism in the relation between 5-HT polygenic risk and later alcohol use. Deficits in self-regulation also predicted depression and aggression/antisociality, and indirectly predicted alcohol use through aggression/antisociality. These pathways to alcohol use might be the most salient for boys with low levels of socioeconomic status.
Results are novel contributions to the literature. The previously observed association between serotonin functioning and alcohol use might be due, in part, to the fact that individuals with lower levels of serotonin functioning are predisposed towards developing earlier aggression/antisociality. Results did not support the hypothesis that serotonin functioning predisposes individuals to deficits in self-regulatory abilities. Findings extend previous research by suggesting that serotonin functioning and self-regulation might be transdiagnostic risk factors for many types of psychopathology.
Structural equation modeling was used to test hypotheses. Results from an independent genome-wide association study of 5-hydroxyindoleacetic acid in the cerebrospinal fluid were used to create serotonin (5-HT) polygenic risk scores, wherein higher scores reflected lower levels of 5-HT functioning. Data from three time points were drawn from each sample, and all paths were prospective. Findings suggested that 5-HT polygenic risk did not predict self-regulatory constructs. However, 5-HT polygenic risk did predict the divergent outcomes of depression and aggression/antisociality, such that higher levels of 5-HT polygenic risk predicted greater levels of depression and aggression/antisociality. Results most clearly supported adolescents’ aggression/antisociality as a mechanism in the relation between 5-HT polygenic risk and later alcohol use. Deficits in self-regulation also predicted depression and aggression/antisociality, and indirectly predicted alcohol use through aggression/antisociality. These pathways to alcohol use might be the most salient for boys with low levels of socioeconomic status.
Results are novel contributions to the literature. The previously observed association between serotonin functioning and alcohol use might be due, in part, to the fact that individuals with lower levels of serotonin functioning are predisposed towards developing earlier aggression/antisociality. Results did not support the hypothesis that serotonin functioning predisposes individuals to deficits in self-regulatory abilities. Findings extend previous research by suggesting that serotonin functioning and self-regulation might be transdiagnostic risk factors for many types of psychopathology.
ContributorsWang, Frances Lynn (Author) / Chassin, Laurie (Thesis advisor) / Eisenberg, Nancy (Committee member) / Lemery-Chalfant, Kathryn (Committee member) / MacKinnon, David (Committee member) / Arizona State University (Publisher)
Created2017
Description
The present study utilized longitudinal data from a high-risk community sample (n= 377; 166 trauma-exposed; 54% males; 52% children of alcoholics; 73% non-Hispanic/Latino Caucasian; 22% Hispanic/Latino; 5% other ethnicity) to test a series of hypotheses that may help explain the risk pathways that link traumatic stress, posttraumatic stress disorder (PTSD) symptomatology, and problematic alcohol and drug use. Specifically, this study examined whether pre-trauma substance use problems increase risk for trauma exposure (the high-risk hypothesis) or PTSD symptoms (the susceptibility hypothesis), whether PTSD symptoms increase risk for later alcohol/drug problems (the self-medication hypothesis), and whether the association between PTSD symptoms and alcohol/drug problems is due to shared risk factors (the shared vulnerability hypothesis). This study also examined the roles of gender and ethnicity in these pathways. A series of logistic and negative binomial regressions were performed in a path analysis framework. A composite pre-trauma family adversity variable was formed from measures of family conflict, family life stress, parental alcoholism, and other parent psychopathology. Results provided the strongest support for the self-medication hypothesis, such that PTSD symptoms predicted higher levels of later alcohol and drug problems among non-Hispanic/Latino Caucasian participants, over and above the influences of pre-trauma family adversity, pre-trauma substance use problems, trauma exposure, and demographic variables. Results partially supported the high-risk hypothesis, such that adolescent substance use problems had a marginally significant unique effect on risk for assaultive violence exposure but not on overall risk for trauma exposure. There was no support for the susceptibility hypothesis, as pre-trauma adolescent substance use problems did not significantly influence risk for PTSD diagnosis/symptoms over and above the influence of pre-trauma family adversity. Finally, there was little support for the shared vulnerability hypothesis. Neither trauma exposure nor preexisting family adversity accounted for the link between PTSD symptoms and later substance use problems. These results add to a growing body of literature in support of the self-medication hypothesis. Findings extend previous research by showing that PTSD symptoms may influence the development of alcohol and drug problems over and above the influence of trauma exposure itself, preexisting family risk factors, and baseline levels of substance use.
ContributorsHaller, Moira (Author) / Chassin, Laurie (Thesis advisor) / Davis, Mary (Committee member) / Pina, Armando (Committee member) / Tein, Jenn-Yun (Committee member) / Arizona State University (Publisher)
Created2014
Description
Excessive drinking in adolescence is a public health issue with major consequences on both an individual and societal level. Elucidating genetic and environmental influences could be particularly informative for prevention efforts. One potential source of genetic influence is sensitivity to environmental influences. It was hypothesized that parent knowledge would interact with genetic sensitivity to the environment to indirectly reduce risk for alcohol problems through less adolescent rule breaking behavior. Participants (N=316) provided genetic data and reported their rule breaking behavior and past year frequency of heavy drinking, and participants’ custodial parents reported their perceived knowledge of their child’s activities. A novel index of genetic sensitivity to environmental influence was created using published methylation quantitative trait locus data from the frontal lobe. Study hypotheses were mostly not supported. The study results likely reflect the poor distribution of study variables and the limitations of the current study’s sensitivity gene score. The current study underscored the importance of adhering to methodological rigor and explored alternate conceptualizations and methods that future research could use to elucidate the role of inherited to sensitivity to environmental influences in adolescent drinking.
ContributorsPandika, Danielle Mutiara (Author) / Chassin, Laurie (Thesis advisor) / Elam, Kit (Committee member) / Lemery-Chalfant, Kathryn (Committee member) / Edwards, Michael (Committee member) / Arizona State University (Publisher)
Created2020