Thesis (M.A. (Criminology)) -- University of Limpopo, 2017 / Binge drinking, crime and victimisation are increasingly being recognised as problems on university and college campuses. Binge drinking is a pattern of drinking that can lead to anti-social behaviour among students. This can lead to a number of negative individual and social effects such as crime and victimisation. The key concepts, binge drinking, crime and victimisation during bashes are defined in relation to the Lifestyle Exposure Theory and Routine Activities Theory. This is done within the concepts of the theories and in particular motivated offenders, suitable targets, in the absence of a capable guardian. The aim of the study was to describe binge drinking and its resultant criminological outcomes during bashes at the University of Limpopo. A qualitative design was used in this study. The sampling method that was used to select the participants was nonprobability sampling and specifically snowball sampling. Data was collected until the saturation point, where no new information occurred. To analyse the data, thematic content analysis was used.

Master of Science / Department of Psychology / Laura A. Brannon / Self-monitoring was examined as a moderator of the effectiveness of persuasive messages for reducing college student binge drinking. Low self-monitors tend to be influenced by their personal values and attitudes, while high self-monitors tend to be influenced by the behavior of those around them. Via a website simulation, college students were presented with one of three types of anti-binge drinking messages: a self-schema message, which highlighted how responsible drinking is consistent with the message recipient’s personal values and attitudes; a social norms message, which explained that most college students drink less than one might think they do; or a control message, which stated in general terms that people can experience a variety of problems from binge drinking. Overall intended drinking behavior in the self-schema message condition was almost identical to that of the social norms message condition, both of which were lower than drinking intentions in the control message condition. When presented with a self-schema matched message, low self-monitors intended to drink less alcohol than did high self-monitors, but these means were not significantly different. However, high self-monitors intended to drink significantly less than did low self-monitors when presented with a social norms message. The results suggest that self-schema matched messages may be effective at reducing binge drinking for most students, and that social norms messages may be equally as effective but only for high self-monitors.

Excessive ethanol consumption, characteristic of alcohol use disorders (AUDs), is associated with widespread neurodegeneration and cognitive and behavioral impairments that may contribute to the chronic and relapsing nature of alcoholism. Therefore, identifying novel targets that can afford neuroprotection will undoubtedly aid current treatment strategies for AUDs. The cannabinoids have been shown to provide neuroprotection in a variety of preclinical models of neurodegeneration; however minimal data is available regarding the use of cannabinoid-based pharmacotherapies for treating ethanol-induced neurodegeneration. Therefore, the current dissertation examined the overarching hypothesis: the cannabinoids are a therapeutic strategy to afford neuroprotection in the context of ethanol-induced neurodegeneration. Importantly, this overarching hypothesis was approached with translational considerations in mind. Specifically, the use of many cannabinoids in the clinic is hindered due to multiple unfavorable pharmacokinetic/pharmacodynamic profiles, including high first pass metabolism and untoward psychoactivity. Therefore, the studies herein were designed to circumvent these PK/PD obstacles. The first set of studies examined whether transdermal delivery of the phytocannabinoid, cannabidiol (CBD), could attenuate binge ethanol induced neurodegeneration. Transdermal CBD afforded neuroprotection in the entorhinal cortex and neuroprotection was similar in magnitude as intraperitoneal administration. The second set of studies found that binge ethanol treatment transiently down-regulated the main CNS cannabinoid receptor, CB1R. Interestingly, these changes were not accompanied by alterations in one of the major endogenous ligands, anandamide (AEA), or other related n-acylethanolamides (NAEs). The latter finding is in contrast to other literature reports demonstrating that endocannabinoid content is substantially elevated in response to a CNS insult. Nevertheless, studies were carried out to determine if administration of the AEA and NAE catabolism inhibitor, URB597, could attenuate binge ethanol induced neurodegeneration. URB597 failed to produce neuroprotection in the entorhinal cortex and dentate gyrus of the hippocampus. However, additional studies found that URB597 failed to elevate AEA in the entorhinal cortex, and in general the biological activity of URB597 was impaired by ethanol exposure. Therefore, with further drug discovery/development efforts, it may be feasible to optimize such treatment strategies. In conclusion, the studies within the current dissertation demonstrated the feasibility of using some cannabinoid-based agents to prevent ethanol-induced neurodegeneration.

Chronic ethanol exposure results in neuroadaptations that drive the progression of an alcohol use disorder (AUD). One such driving force is alcohol-induced neurodegeneration. Neuroinflammation has been proposed as a mechanism underlying this damage. Although neuroinflammation is a physiological response to damage, overactivation of its pathways can lead to neurodegeneration. A hallmark indicator of neuroinflammation is microglial activation, but microglial activation is a heterogeneous continuum of phenotypes that can promote or inhibit neuroinflammation. Furthermore acute microglial activation is necessary to restore homeostasis, but prolonged activation can exacerbate damage. The diversity of microglia makes both the level and timecourse of activation vital to understanding their role in damage and/or recovery. The current set of experiments examines the effects of ethanol on microglia within the hippocampus and entorhinal cortex in a binge model of alcohol-induced neurodegeneration. In the first set of experiments, the phenotype of microglia activation was assessed using Raivich’s 5-stages of activation that separates pro- and anti-inflammatory forms of microglia. Morphological and functional assessments suggest that ethanol does not elicit classical microglial activation but instead induces partially activated microglia. In the second set of experiments, the earliest signs of microglial activation were determined to understand the initiation of microglial activation. Experiments indicated that activation occurred subsequent to previous evidence of neuronal damage; however, activation was accompanied by a loss of microglia and the discovery of dystrophic microglia. The final set of experiments examined whether alcohol-induced partial activation of microglia would show a differential response with further alcohol exposure. Experiments showed that animals previously exposed to ethanol showed a greater response to a second ethanol insult. Overall, these studies suggest that although alcohol may initially interrupt the normal microglia response, during abstinence from ethanol a partial activation phenotype appears that may contribute to recovery. Once activated, however, data suggest that these microglia are primed and upon subsequent exposure show an increased response. This heterogeneous microglial response with respect to time does not necessarily reflect a neuroinflammatory response that would be neurodegenerative but does imply that chronic ethanol consumption affects the normal neuroimmune system.

BACKGROUND: Various human and animal studies suggest that peak alcohol exposure during a binge episode, rather than total alcohol exposure, may determine fetal development. Research about the impact of binge drinking on birth outcomes is sparse and inconclusive. Data from the Born in Bradford cohort study were used to explore the impact of binge drinking on birth outcomes. METHODS: Interview-administered questionnaire data about the lifestyle and social characteristics of 10 851 pregnancies were linked to maternity and birth data. The impact of self-reported binge drinking (5 units: 40 g of pure alcohol) on two birth outcomes (small for gestational age (SGA) and preterm birth (<37 weeks)) was assessed using multivariate logistic regression models, while adjusting for confounders. RESULTS: The percentage of women classified as binge drinkers fell from 24.5% before pregnancy to 9% during the first trimester and 3.1% during the second trimester. There was a significant association between SGA birth and binge drinking (all categories combined; OR 1.68, 95% CI 1.15 to 2.47, p=0.01). No association was observed between moderate drinking and either birth outcome, or between binge drinking and preterm birth. CONCLUSIONS: Binge drinking during the second trimester of pregnancy was associated with an increased risk of SGA birth. No association was found between any level of alcohol consumption and premature birth. This work supports previous research showing no association between SGA and low-alcohol exposure but adds to evidence of a dose-response relationship with significant risks observed at binge drinking levels.

The reasons why people may periodically resort to binge eating behavior have long been a focus of study, and the reasons are elusive and varied. For people troubled by poor sleep and living with chronic stress, binge eating may be an attempt by the brain's glucose-depleted executive processing center to both regulate (i.e., increase) glucose levels and induce restorative sleep. Recovery resulting from restorative sleep may lead to a reduction in perceived stress, improved mood, and increased willpower, reducing the likelihood of another binge episode in close temporal proximity to the sleep-induced recovery. A repetitive cycle may ensue when stress inevitably again disturbs sleep, lowering mood, reducing willpower, and heightening sensitivity to stigma and stress. The purpose of the research described here is to synthesize recent findings from three diverse fields of scientific inquiry to predict factors that influence episodes of binge eating. Combining studies of sleep and sleep disorders, stress and stigma research, and recent work on self-regulatory capacity, I attempt to show how poor sleep ultimately leads to binge eating. A seven-day study consisted of three parts: an initial set of baseline questionnaire and physiological measures; collection of objective sleep quality data using an electronic motion logger; and an online daily diary in which participants completed measures of self-regulatory capacity and reported details about their sleep, stress levels, experiences with stigma, mood, and eating events. The data partially supported a path model where sleep quality, stress, mood, and self-regulation affected binge eating behavior.

The current investigation used qualitative methodology to examine adolescent girls’ perceptions of control over their eating, as well as triggers, and consequences of binge and related eating behaviors. Focus groups were completed with 19 adolescent girls (aged 13-17, 58% African American, 41% White) who endorsed the behaviors. Responses to focus group questions were qualitatively analyzed using a grounded theory approach and constant comparison coding. Results reflected a fundamental lack of awareness of the loss of control (LOC) eating behaviors. Yet, the data did reflect a central theme of the need to affirm independence and autonomy through eating behaviors via three distinct pathways; asserting physical, emotional, and relational control with food. Each strategy produces different positive and negative consequences regarding emotions and physical sensations. This study suggests that adolescent need for autonomy interacts with a sense of feeling out of control of one’s external environment and insufficient coping mechanisms may increase susceptibility to maladaptive eating behaviors.

Binge eating is a pervasive disordered eating behavior associated with numerous psychological and physical comorbidities. Preliminary research indicates that emotion regulation difficulties, behavioral impulsivity, and executive dysfunction may contribute to the onset and/or maintenance of these behaviors. However, few studies have utilized neuropsychological measures to examine this link, and the assessment of behavioral and cognitive emotion regulation strategies are limited in scope. The purpose of the current study was to gain a deeper understanding of the emotional, behavioral and cognitive processes associated with binge eating behavior. Greater clarity regarding how these factors relate to binge eating is critical to the development of effective treatment and prevention efforts. To address these aims, the current study examined the executive functioning, depression, behavioral impulsivity, distress tolerance, and emotion regulation strategies of 50 women engaging in weekly binge eating in the absence of compensatory behaviors; their outcomes were compared to 66 women with no history of binge eating. Hierarchical regression analyses revealed that groups did not significantly differ in executive functioning after controlling for depression, state anxiety, body mass, psychopharmaceutical use, and general intelligence; nonetheless, correlation analyses suggest that, among the binge eating group, individuals endorsing more frequent binge eating might have greater difficulties thinking flexibly or shifting attention. Secondary analyses indicated that individuals who binge eat are more depressed, are more likely to engage in impulsive behavior (but only when distressed), have more difficulties tolerating distress, are more likely to engage in rumination, self-blame, and catastrophizing, and less likely to focus on the positive. Although the current study is unable to determine whether these cognitive, emotional, and behavioral factors precede or follow binge eating episodes, outcomes have clinical implications. Specifically, programs focused on the prevention and treatment of binge eating should help individuals learn to better identify and tolerate difficult affective states and to utilize more adaptive means of coping. Outcomes also provide important directions for future research, including longitudinal designs to better understand the temporal associations of the current study’s variables, as well as suggestions to broaden and standardize neuropsychological assessment and scoring procedures to facilitate comparisons across studies.

Both eating disorders and smoking are significant problems for Black and White college women. Additionally, these two negative health behaviors frequently co-occur. This study aimed to investigate the relationship between these health behaviors using a multivariate model. Two models, one for full and one for partial mediation, were tested using Structural Equation Modeling. The Model for full mediation tested whether the relationship among general distress and smoking are fully mediated by body dissatisfaction, restraint, and binge eating. The model for partial mediation hypothesized that the relationships among general distress, and smoking are mediated by body dissatisfaction, restraint, and binge eating. Results indicated that there was not a significant difference between the full and partial model and therefore, the full model was retained as it is more parsimonious. In addition, a test of model invariance was conducted on the full mediation model to test form potential differences in Black and Whites. It was found that the structural model is invariant across these two groups. Results of this study may have important implications for future research as well as for treatment and preventative interventions.

This study examined how attentional sub-processes contribute to binge-eating. Dense-array EEG and a version of the canonical attentional blink task were used to ascertain the neural correlates underlying the attentional sub-processes that comprise the Posner model of attention (alerting, orienting, and executive control) and how attentional activation differs for binge-eaters vs. non-binge eaters. Furthermore, we examined a number of the event-related potentials (ERP), including P2 activation, which has been linked with orientating of attention, and N2 activation which has been linked with attentional conflict. We found decreased P2 activation for binge-eaters, in the negative condition, for incorrect target 2 (T2) detection trials. We also found more N2 activation for binge-eaters than non-binge eaters, in negative trials when T2 was not detected. This pattern of results suggest that binge-eaters showed deficiencies in allocating attention to stimuli that followed negative images; this attention deficiency may be a key factor for binge-eating behavior.