Narcissism and Devaluing Others: An Exploration of Impaired Control Over Drinking as a Mediating Mechanism of Alcohol-Related Problems.

Devaluing or diminishing the worth of others is how many individuals destroy their relationships, such as by drinking beyond limits at inappropriate times and letting others down. Impaired control over drinking (IC) reflects consuming alcohol beyond predetermined limits. This investigation sought to determine whether facets of vulnerable narcissism (e.g., entitlement-rage, hiding-the-self, contingent-self-esteem, and devaluing) or narcissistic grandiosity (e.g. grandiose-fantasy, self-sacrificing-for-self-enhancement, and exploitativeness) were directly related to IC and indirectly related to drinking outcomes. We examined a path model of 759 university student drinkers. Our results show that while grandiose-fantasy (i.e., desire for special recognition) was negatively linked to IC, devaluing was positively linked to IC. In addition, men scored higher on exploitativeness (i.e., interpersonally manipulative for personal gain) than women. We conducted mediational analysis with asymmetric confidence intervals and a bias-corrected bootstrap technique. Mediational tests showed that higher levels of grandiose-fantasy were indirectly related to fewer alcohol-related problems through less IC and less heavy-episodic drinking. In contrast, higher levels of devaluing were indirectly related to more alcohol-related problems through more IC and heavy-episodic-drinking. Our results suggest that targeting thought processes in which people with Alcohol Use Disorders (AUDs) are actively devaluing others may be a good target for therapeutic intervention.

Some factors involved in alcohol consumption of first-year undergraduates.

Three studies were conducted with samples of first-year undergraduates in order to assess relationships among college drinking, adjustment, recent life-changing events, interpersonal factors, self-control, and perceived risk. Significant correlations were found between alcohol use and life-change, but not between alcohol use and college adjustment. In addition, several significant findings linked alcohol use to social factors. Responses to open-ended interview questions suggest that self-control and risk may play a role in students' decisions regarding consumption, after initial experience with alcohol use. Non-social factors, namely stressful events, appear to play a role in consumption behavior; however, students more frequently report on social factors as motivating their decisions regarding alcohol intake.

A comprehensive analysis of cytokine-induced and nuclear factor-kappa B-dependent genes in primary rat pancreatic beta-cells.

Type 1 diabetes mellitus results from an autoimmune destruction of pancreatic beta-cells. Cytokines, such as interleukin-1 beta and interferon-gamma, are putative mediators of immune-induced beta-cell death and, under in vitro conditions, cause beta-cell apoptosis. We have recently shown that interleukin-1 beta + interferon-gamma modifies the expression of >200 genes in beta-cells. Several of these genes are putative targets for the transcription factor nuclear factor-kappa B (NF-kappa B), and in subsequent experiments we showed that NF-kappa B activation is mostly pro-apoptotic in beta-cells. To identify cytokine-induced and NF-kappa B-regulated genes in primary rat beta-cells, we presently combined two experimental approaches: 1) blocking of NF-kappa B activation in cytokine-exposed beta-cells by a recombinant adenovirus (AdI kappa B((SA)2)) containing an inhibitor of NF-kappa B alpha (I kappa Bac) super-repressor (S32A/S36A) and 2) study of gene expression by microarray analysis. We identified 66 cytokine-modified and NF-kappa B-regulated genes in beta-cells. Cytokine-induced NF-kappa B activation decreased Pdx-1 and increased c-Myc expression. This, together with NF-kappa B-dependent inhibition of Glut-2, pro-hormone convertase-1, and Isl-1 expression, probably contributes to the loss of differentiated beta-cell functions. NF-kappa B also regulates several genes encoding for chemokines and cytokines in beta-cells. The present data suggest that NF-kappa B is a key "switch regulator" of transcription factors and gene networks controlling cytokine-induced beta-cell dysfunction and death.

Identification of novel cytokine-induced genes in pancreatic beta-cells by high-density oligonucleotide arrays.

Type 1 diabetes is an autoimmune disease resulting from the selective destruction of insulin-producing beta-cells. Cytokines may contribute to pancreatic beta-cell death in type 1 diabetes. beta-cell exposure to interleukin (IL)-1beta induces functional impairment, whereas beta-cell culture for 6-9 days in the presence of IL-1beta and interferon (INF)-gamma leads to apoptosis. To clarify the mechanisms involved in these effects of cytokines, we studied the general pattern of cytokine-induced gene expression in beta-cells. Primary rat beta-cells were fluorescence-activated cell sorter-purified and exposed for 6 or 24 h to control condition, IL-1beta + INF-gamma, or IL-1beta alone (24 h only). Gene expression profile was analyzed in duplicate by oligonucleotide arrays. Nearly 3,000 transcripts were detected in controls and cytokine-treated beta-cells. Of these, 96 and 147 displayed changes in expression after 6 and 24 h, respectively, of exposure to IL-1beta + INF-gamma, whereas 105 transcripts were modified after a 24-h exposure to IL-1beta. The cytokine-responsive genes were clustered according to their biological functions. The major clusters observed were metabolism, signal transduction, transcription factors, protein synthesis/ processing, hormones, and related receptors. These modifications in gene expression may explain some of the cytokine effects in beta-cells, such as decreased protein biosynthesis and insulin release. In addition, there was induction of diverse cytokines and chemokines; this suggests that beta-cells may contribute to mononuclear cell homing during insulitis. Several of the cytokine-induced genes are potentially regulated by the transcription factor NF-kappaB. Clarification of the function of the identified cytokine-induced gene patterns may unveil some of the mechanisms involved in beta-cell damage and repair in type 1 diabetes.