Gordon E. Barnes

A structural equation model of the effect of poverty and unemployment on alcohol abuse.

The short- and long-term effects of poverty and unemployment on alcohol abuse are investigated using structural equation modelling (SEM) to better understand the observed conflicting relationships among them. We studied 795 community residents who provided complete data in both 1989 and 1991 in the Winnipeg Health and Drinking Survey (WHDS), with equal representation of males and females. Results indicate that (a) increased poverty causes increased alcohol use and alcohol problems, and (b) recent unemployment decreases alcohol use while longer unemployment increases it. It is concluded that the effect of unemployment on alcohol abuse changes direction with time and, thus, both cross-sectional and longitudinal data are required to assess any meaningful relationship between them.

Personality characteristics of smokers and ex-smokers

Abstract The present paper examines the relationship between personality and smoking status in a random sample of 1257 adults. A broad sample of personality constructs were assessed to cover the major dimensions of personality. These included the EPQ, MMPI MacAndrew and Ego Strength scales, the Vando augmenter-reducer scale, the trait subscale of the STAI and the Rosenberg self-esteem scale. Factor analysis suggested that trait anxiety, neuroticism, self-esteem and ego strength could be grouped into a construct analogous to Esysencks notion of neuroticism. Extraversion, augmenting-reducing, and the MacAndrew scale were grouped into a construct called extraversion. Results showed that smokers were the most extraverted group. Gender differences in the relation between smoking and neuroticism were found. Male smokers were much more neurotic than non-smokers and men who quit smoking, whereas there were no group differences in neuroticism for women. Both male and female smokers were high on psychoticism.

Individual differences in substance dependence: at the intersection of brain, behaviour and cognition.

Recent theories of drug dependence propose that the transition from occasional recreational substance use to harmful use and dependence results from the impact of disrupted midbrain dopamine signals for reinforcement learning on frontal brain areas that implement cognitive control and decision‐making. We investigated this hypothesis in humans using electrophysiological and behavioral measures believed to assay the integrity of midbrain dopamine system and its neural targets. Our investigation revealed two groups of dependent individuals, one characterized by disrupted dopamine‐dependent reward learning and the other by disrupted error learning associated with depression‐proneness. These results highlight important neurobiological and behavioral differences between two classes of dependent users that can inform the development of individually tailored treatment programs.

Prevalence and Predictors of “Heavy” Marijuana Use in a Canadian Youth Sample

In this investigation, secondary analyses were performed on an extensive database for 473 biological and 128 adoptive families. These data, which were gathered as part of the Vancouver Family Survey, were used to examine the prevalence and predictors of “heavy” marijuana use in a Canadian youth sample aged 14–25. Results in this study showed that 12.6% of the sample reported using marijuana once a week or more. These respondents were categorized as “heavy” marijuana users. Higher levels of life problems were associated with this use pattern. Results from a series of regression analyses suggested that the family, personality, and peer domains all contributed significantly in predicting “heavy” marijuana use. Fathers alcoholism and peer illicit drug use had direct relationships with heavy marijuana use in this final model. A possible mediated pathway was also suggested with the Addiction Prone Personality influencing use through its relationship with heavier peer drug use.

Reward sensitivity of acc as an intermediate phenotype between drd4-521t and substance misuse

The development and expression of the midbrain dopamine system is determined in part by genetic factors that vary across individuals such that dopamine-related genes are partly responsible for addiction vulnerability. However, a complete account of how dopamine-related genes predispose individuals to drug addiction remains to be developed. Adopting an intermediate phenotype approach, we investigated whether reward-related electrophysiological activity of ACC—a cortical region said to utilize dopamine reward signals to learn the value of extended, context-specific sequences of goal-directed behaviors—mediates the influence of multiple dopamine-related functional polymorphisms over substance use. We used structural equation modeling to examine whether two related electrophysiological phenomena associated with the control and reinforcement learning functions of ACC—theta power and the reward positivity—mediated the relationship between the degree of substance misuse and genetic polymorphisms that regulate dopamine processing in frontal cortex. Substance use data were collected from 812 undergraduate students. One hundred ninety-six returned on a subsequent day to participate in an electrophysiological experiment and to provide saliva samples for DNA analysis. We found that these electrophysiological signals mediated a relationship between the DRD4-521T dopamine receptor genotype and substance misuse. Our results provide a theoretical framework that bridges the gap between genes and behavior in drug addiction and illustrate how future interventions might be individually tailored for specific genetic and neurocognitive profiles.

Drinking pattern as a predictor of cardiovascular harm: A longitudinal study using alternative drinking pattern measures

Background: This study compared measures of drinking pattern at baseline, and subsequent cardiovascular harm in a longitudinal study. Method: In Winnipeg, Manitoba, Canada, a community sample of 1154 adult men and women was interviewed at baseline in 1990 and 1991, then followed with all‐cause surveillance. Cox proportional hazards regressions were used to assess the “time to event” for morbidity or mortality from coronary heart disease (CHD), hypertension, or other cardiovascular disease. Surveillance was through a 10‐year series of documented physician visits, hospital discharges and deaths, classified by diagnosis. Drinking pattern was defined as either ⩾8 drinks (80–120 g of alcohol or more) at a sitting in the past 12 months, a report of feeling the effects, or ⩾5 usual drinks/day. Results: There were 104 individuals with CHD events in the data. When ⩾8 drinks at a sitting was the predictor, there were significant hazards for CHD among both men and women [hazard ratio (HR) = 2.32 and 1.07; p = 0.004 and 0.04], and marginally significant hazards for hypertension among men (HR = 1.40; p = 0.08). When feeling the effects or ⩾5 usual drinks/day were the predictors, there were no significant hazards of drinking pattern. Conclusion: Eight or more drinks was a stronger predictor of cardiovascular harm in these data than were feeling the effects or ⩾5 usual drinks.

Exploring the boundary between health protective and hazardous drinking in a community cohort

We sought to identify a level of alcohol consumption representing the boundary between health protective and hazardous drinking. The Winnipeg Health and Drinking Survey began in 1990-91 (n = 1257). Seven years later, a third wave of interviews (n = 785) expanded questions on heavy episodic drinking (HED) and assessed the consumption of > or = 3, > or = 5, > or = 8, and > or = 12 drinks at a sitting for each of wine, beer and liquor (equivalent to about 40 g, 65 g, 105 g and 155 g of ethanol). Cox proportional hazards models were based on seven years of illness and mortality data following the Wave 3 interview, and were stratified by gender and HED definition. For HED of > or = 40 g, > or = 65 g, > or = 105 g, or > or = 155 g per occasion, the hazard ratios for morbidity and mortality from all causes were 1.06, 1.09, 1.17, and 1.16 respectively in women, and 1.00, 0.98, 1.02, and 1.02 in men. Most of these hazard ratios were significant in women, whereas none was significant in men. This study did not provide support for a definition of HED that could divide protective from hazardous alcohol consumption.