Individuals exposed to alcohol in utero have reduced cortical grey matter volumes. However, the underlying determinants of these reductions have not been investigated exclusively in alcohol-related neurodevelopmental disorder (ARND). Using magnetic resonance imaging scans from 121 participants (57 ARND and 64 controls) aged 8 to 16 years, cortical morphology was analyzed. Results revealed the ARND group had reduced cortical grey matter volumes, but did not differ from controls in cortical thickness. Rather, the cortical abnormalities reflected reductions in global surface area, local surface area reductions in the right occipital-temporal area and right superior temporal gyrus, as well as reduced gyrification. A significant interaction between sex and group was observed, with females showing greater reductions than males in cortical volume and surface area. Results suggest that ARND is characterized by global reductions in cortical surface area and gyrification and females are more vulnerable than males to the teratogenic effects of alcohol.

Individuals exposed to alcohol in utero have reduced cortical grey matter volumes. However, the underlying determinants of these reductions have not been investigated exclusively in alcohol-related neurodevelopmental disorder (ARND). Using magnetic resonance imaging scans from 121 participants (57 ARND and 64 controls) aged 8 to 16 years, cortical morphology was analyzed. Results revealed the ARND group had reduced cortical grey matter volumes, but did not differ from controls in cortical thickness. Rather, the cortical abnormalities reflected reductions in global surface area, local surface area reductions in the right occipital-temporal area and right superior temporal gyrus, as well as reduced gyrification. A significant interaction between sex and group was observed, with females showing greater reductions than males in cortical volume and surface area. Results suggest that ARND is characterized by global reductions in cortical surface area and gyrification and females are more vulnerable than males to the teratogenic effects of alcohol.

This study examined the independent and interactive effects of acute alcohol consumption, perceived alcohol consumption of a female confederate, and distal alcohol expectancies of intoxicated women, on sexual aggression. Participants were a diverse community sample (54% African-American) of heterosexual males (N = 156) between 21 and 35 years of age who were recruited to complete the study with a male friend and an ostensibly single, heterosexual female who reported a strong dislike of sexual content in the media. Sexual aggression was measured utilizing a well-validated laboratory paradigm in which participants viewed a sexually explicit or non-sexually explicit video clip as part of a contrived media rating task and made individual choices of which video clip to show the female confederate. Sexual aggression was operationalized as selection of the sexually explicit video, as opposed to the non-sexually explicit video. Results demonstrated that acute alcohol consumption, perceived female alcohol consumption, and distal alcohol expectancies of women’s vulnerability to sexual coercion and sexual drive while intoxicated, were not significantly related to sexual aggression utilizing the current paradigm. Post-hoc analyses revealed that the primary predictor variables were significantly related to participants’ perceived distress of a female confederate following an act of sexual aggression. Discussion focused on understanding what factors may have been relevant in understanding why the primary predictor variables were not significantly related to sexual aggression utilizing the current paradigm. Finally, clinical implications were explored in addressing a lack of perceived distress in potential female victims by individuals who endorsed higher levels of distal alcohol expectancies of intoxicated women’s vulnerability to sexual coercion and what potential interventions be utilized clinically.

The present dissertation aims at analysing the effects of recent alcohol policy changes. The traditional strict policy in Sweden had focused on high pricing and limited availability to control levels of alcohol consumed and thus alcohol-related harms. However, increased travellers’ allowances meant larger availability of cheaper alcohol when importing from Denmark and Germany, which are the countries from which Swedes obtain most of their private imports; the tax decrease in Denmark further decreased the price. As the economic literature links demand to price of a commodity and the early (smaller) quota changes had resulted in higher consumption in southern Sweden, it was expected that these latest changes would mean higher consumption and more alcohol-related problems in this area in particular. Some groups were additionally expected to be more affected than others. The present compilation thesis comprises four related articles and an introductory chapter that ties them together. Article I focuses on private imports in relation to quota changes 2002 – 2004 and relate this to purchase at the alcohol monopoly stores. Self-reported consumption and alcohol-related problems are studied in Article II and IV. In Article III, register data on alcohol-related harms, i.e. hospitalizations and police-recorded crimes, are analysed. The results of the dissertation were puzzling, since there was no large increase in consumption or alcohol-related problems in the south, but increases in the north during the period. However, private imports and cases of hospitalization due to alcohol poisoning were found to have increased in the south. Thus, the results imply that these policy changes had an effect on private imports, but that this effect was not large enough to increase total consumption as well. Additionally, increased alcohol poisoning cases implied that there had been an impact among high consumers. The increases found in consumption and problems in the north may instead have other explanations. / <p>At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 2: In press. Paper 2: Submitted. Paper 3: Submitted.</p>

This paper seeks to understand how college health organizations use social media to communicate alcohol-related issues with its audiences, specifically universities that are recognized as “party schools” and “sober schools”. Existing literature, social networking trends, and a content analysis are applied to two communication models – the Theory of Planned Behavior and the Uses and Gratification Model – to identify how organizations can leverage social media to influence students’ behavior. The qualitative data collection will be used to provide social media communication recommendations for the University of Texas’ health service organization – Healthy Horns. These recommendations will be applied to the general healthcare field as well as the advertising industry. / text

Doctor of Philosophy (PhD) / Proteomics is rapidly achieving recognition as a complimentary and perhaps superior approach to examine global changes in protein abundance in complex biological systems and the value of these techniques in neuropsychiatry is beginning to be acknowledged. Characterizing the brain’s regional proteomes provides a foundation for the detection of proteins that may be involved in disease-related processes. Firstly, optimal conditions were achieved for the application of two dimensional-gel electrophoresis (2D-GE)-based proteomics with postmortem human brain tissue. These optimized techniques were then applied to soluble fractions of adjacent grey and white matter of a single cytoarchitecturally defined area (Brodmann area 9; BA9) and of two adjacent regions of frontal white matter (BA9 and CC body) from healthy individuals. These normative proteomic comparisons highlighted the importance of correct tissue sampling, i.e. proper separation of regional white matter, as heterogeneity in the respective proteomes was demonstrated. Furthermore, they stressed the necessity for future molecular brain mapping studies. The main focus of this thesis however, was to examine the proteomes of brain regions specifically vulnerable to alcohol-induced damage underlying cognitive dysfunction. Alcoholic patients commonly experience mild to severe cognitive decline. It is postulated that cognitive dysfunction is caused by an alcohol-induced region selective brain damage, particularly to the prefrontal cortex. The cerebellum is increasingly recognized for its role in various aspects of cognition and alcohol–induced damage to the cerebellar vermis could indirectly affect neurocognitive functions attributed to the frontal lobe. We used a 2D-GE-based proteomics approach to compare protein abundance profiles of BA9 grey and white matter and the cerebellar vermis from human alcoholics (neurologically uncomplicated and alcoholics complicated with liver cirrhosis) and healthy control brains. Among the protein level changes observed are disturbances in the levels of a number of thiamine-dependent enzymes. A derangement in energy metabolism perhaps related to thiamine deficiency seems to be important in all regions analysed, even where there are no clinical or pathological findings of Wernicke-Korsakoff Syndrome. Evidence of oxidative changes was also seen in all regions and effects of liver dysfunction in the vermis found. However, overall, these results highlight the complexity of this disease process in that a number of different proteins from different cellular pathways appear to be affected. By identifying changes in protein abundance levels in the prefrontal grey and white matter and the cerebellar vermis, hypotheses may draw upon more mechanistic explanations as to how chronic ethanol consumption causes the structural and functional alterations associated with alcohol-related brain damage. Furthermore, by comparing these results, we may be able to isolate disturbances in molecular pathways specific to the brain damage caused by alcohol, severe liver dysfunction and thiamine deficiency.

Diss. (sammanfattning) Stockholm : Karol. inst., 2002. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2003. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2004. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2006. / Härtill 5 uppsatser.