Co-morbidity between alcohol, tobacco and cannabis use: reply to David Fergusson

No abstract

Patterns of co-morbidity between alcohol use and other substance use in the Australian population

The present study describes patterns of co-morbidity between alcohol use and other substance use problems in the Australian population using data from the 1997 National Survey of Mental Health and Well-Being. Multiple regression analyses examined whether the observed associations between alcohol and other drug use disorders were explained by other variables, including demographic characteristics and neuroticism. We also assessed whether the presence of co-morbid substance use disorders affected treatment seeking for a mental health problem. Alcohol use was related strongly to the use of other substances. Those who did not report alcohol use within the past 12 months were less likely to report using tobacco, cannabis, sedatives, stimulants or opiates. Higher rates again were observed among those with alcohol use disorders: half (51%) of those who were alcohol-dependent were regular tobacco smokers, one-third had used cannabis (32%); 15% reported other drug use; 15% met criteria for a cannabis use disorder and 7% met criteria for another drug use disorder. These associations were not accounted for by the demographic and other variables considered here. Co-morbid substance use disorders (sedatives, stimulants or opioids) predicted a high likelihood of seeking treatment for a mental health problem among alcohol-dependent people.

Does the tendency to act impulsively underlie binge eating and alcohol use problems? An empirical investigation

The co-occurrence of problem drinking and binge eating and purging has been well documented. However, there has been relatively little investigation of etiological models that may influence the development of this co-occurrence. This study tests the hypotheses that impulsivity is heightened in eating disordered women compared with controls, and that women with comorbid bulimia and alcohol use disorders show higher impulsivity than bulimic-only women. The Impulsivity scale, BIS/BAS scales, State Anxiety Inventory, and a behavioural measure of reward responsiveness (CARROT) were administered to 22 women with bulimia, 23 women with comorbid bulimia and alcohol abuse/dependence, and 21 control women. As hypothesised, eating disordered women scored higher than controls on several self-report measures of impulsivity and sorted cards faster during a financially rewarded trial on the behavioural task. Also, as predicted, comorbid women scored higher than bulimic women on the Impulsivity scale. These findings suggest that individual differences in impulsiveness and a tendency to approach rewarding stimuli may contribute to developing these disorders. (C) 2003 Elsevier Ltd. All rights reserved.

Methadone maintenance therapy for opioid dependence - A guide to appropriate use

Opioid dependence is a chronic, relapsing condition that is associated with significant morbidity and mortality. Methadone maintenance therapy involves the provision of a controlled supply of an orally administered opioid, thereby stabilising the opioid-dependent patient. Research studies have shown that methadone maintenance reduces illicit opioid use, opioid-related crime, premature mortality and the risk of HIV infection. It is most effective when prescribed at an adequate dosage (usually 60 to 100 mg/day) and when long term maintenance on methadone is the goal of treatment rather than detoxification from all drugs including methadone. Successful long term methadone maintenance is more likely when it takes place within the context of a well established therapeutic relationship and when the medical, social and psychological needs of patients are met either through direct assistance or referral.

The role of legal coercion in the treatment of offenders with alcohol and heroin problems

This article discusses the ethical justification for and reviews the American evidence on the effectiveness of; treatment for alcohol and heroin dependence that is provided under legal coercion to offenders whose alcohol and drug dependence has contributed to the commission of the offence with which they have been charged or convicted. The article focuses on legally coerced treatment for drink-driving offenders and heroin-dependent property offenders. it outlines the various arguments that have been made for providing such treatment under legal coercion, namely. the over-representation of alcohol and drug dependent persons in prison populations; the contributory causal role of alcohol and other drug problems in the offences that lead to their imprisonment; the high rates of relapse to drug use and criminal involvement after incarceration; the desirability of keeping injecting heroin users out of prisons as a way of reducing the transmission of infectious diseases such as HIV and hepatitis; and the putatively greater cost-effectiveness of treatment compared with incarceration. The ethical objections to legally coerced drug treatment are briefly discussed before the evidence on the effectiveness of legally coerced treatment for alcohol and other drug dependence is reviewed. The evidence, which is primarily from the USA, gives qualified support for some forms of legally coerced drug treatment provided that these programs are well resourced, carefully implemented, and their performance is monitored to ensure that they provide a humane and effective alternative to imprisonment. Expectations about what these programs can achieve also need to be realistic.

Effects of alcohol consumption on indices of iron stores and of iron stores on alcohol intake markers

Background: Alcohol increases body iron stores. Alcohol and iron may increase oxidative stress and the risk of alcohol-related liver disease. The relationship between low or safe levels of alcohol use and indices of body iron stores, and the factors that affect the alcohol-iron relationship, have not been fully characterized. Other aspects of the biological response to alcohol use have been reported to depend on iron status. Methods: We have measured serum iron, transferrin, and ferritin as indices of iron stores in 3375 adult twin subjects recruited through the Australian Twin Registry. Information on alcohol use and dependence and smoking was obtained from questionnaires and interviews. Results: Serum iron and ferritin increased progressively across classes of alcohol intake. The effects of beer consumption were greater than those of wine or spirits. Ferritin concentration was significantly higher in subjects who had ever been alcohol dependent. There was no evidence of interactions between HFE genotype or body mass index and alcohol. Alcohol intake-adjusted carbohydrate-deficient transferrin was increased in women in the lowest quartile of ferritin results, whereas adjusted gamma -glutamyltransferase, aspartate aminotransferase, and alanine aminotransferase values were increased in subjects with high ferritin. Conclusions: Alcohol intake at low level increases ferritin and, by inference, body iron stores. This may be either beneficial or harmful, depending on circumstances. The response of biological markers of alcohol intake can be affected by body iron stores; this has implications for test sensitivity and specificity and for variation in biological responses to alcohol use.

Ethanol-related adaptive changes and physical dependence in rats after exposure to ethanol

Adaptive changes that occur after chronic exposure to ethanol are an important component in the development of physical dependence. We have focused our research on ethanol-induced changes in the expression of several genes that may be important in adaptation. In this article, we describe adaptive changes at the level of the N-methyl-D-aspartate receptor, in the protein expression and activity of the Egr transcription factors, and in the expression of a novel gene of unknown function. (C) 2001 Elsevier Science Inc. All rights reserved.

CDT, GGT, and AST as markers of alcohol use: The WHO/ISBRA Collaborative Project

Background: Estimates of the performance of carbohydrate deficient transferrin (CDT) and gamma glutamyltransferase (GGT) as markers of alcohol consumption have varied widely. Studies have differed in design and subject characteristics. The WHO/ISBRA Collaborative Study allows assessment and comparison of CDT, GGT, and aspartate aminotransferase (AST) as markers of drinking in a large, well-characterized, multicenter sample. Methods: A total of 1863 subjects were recruited from five countries (Australia, Brazil, Canada, Finland, and Japan). Recruitment was stratified by alcohol use, age, and sex. Demographic characteristics, alcohol consumption, and presence of ICD-10 dependence were recorded using an interview schedule based on the AUDADIS, CDT was assayed using CDTect(TM) and GGT and AST by standard methods. Statistical techniques included receiver operating characteristic (ROC) analysis. Multiple regression was used to measure the impact of factors other than alcohol on test performance. Results: CDT and GGT had comparable performance on ROC analysis, with AST performing slightly less well. CDT was a slightly but significantly better marker of high-risk consumption in men. All were more effective for detection of high-risk rather than intermediate-risk drinking. CDT and GGT levels were influenced by body mass index, sex, age, and smoking status. Conclusions: CDT was little better than GGT in detecting high- or intermediate-risk alcohol consumption in this large, multicenter, predominantly community-based sample. As the two tests are relatively independent of each other, their combination is likely to provide better performance than either test alone, Test interpretation should take account sex, age. and body mass index.

Gene Expression in Brain: A Window on Ethanol Dependence, Neuroadaptation, and Preference

This article represents the proceedings of a symposium at the 2002 joint RSA/ISBRA Conference in San Francisco, California. The organizer was Paula L. Hoffman and the co-chairs were Paula L. Hoffman and Michael Miles. The presentations were (1) Introduction and overview of the use of DNA microarrays, by Michael Miles; (2) DNA microarray analysis of gene expression in brains of P and NP rats, by Howard J. Edenberg; (3) Gene expression patterns in brain regions of AA and ANA rats, by Wolfgang Sommer; (4) Patterns of gene expression in brains of selected lines of mice that differ in ethanol tolerance, by Boris Tabakoff; (5) Gene expression profiling related to initial sensitivity and tolerance in gamma-protein kinase C mutants, by Jeanne Wehner; and (6) Gene expression patterns in human alcoholic brain: from microarrays to protein profiles, by Joanne Lewohl.

ADH genotype does not modify the effects of alcohol on high-density lipoprotein

Background: Alcohol consumption has beneficial effects on mortality which are mainly due to reduction in cardiovascular disease. These are believed to be due, at least in part, to the increase in plasma high-density lipoprotein (HDL) which is associated with alcohol consumption. It has been proposed that ADH3 genotype modifies the relationships between alcohol intake and cardiovascular disease by altering the HDL response to alcohol. The aim of this paper was to test for effects of ADH2 and ADH3 genotypes on the response of HDL components to habitual alcohol consumption. Methods: Adult male and female subjects were genotyped for ADH2 and ADH3; and plasma HDL cholesterol, apolipoprotein A-I, and apolipoprotein A-II were measured. Nine hundred one subjects had both ADH2 and ADH3 genotypes and HDL cholesterol results, while 753 had both genotypes and all three lipid results. The effect of alcohol intake on the three measured HDL components, and a factor score derived from them, was estimated for each of the ADH2 and ADH3 genotype groups. Results: All the measured components of HDL increased with increasing alcohol consumption over the range of intakes studied, 0-4 drinks per day. There were no significant interactions between alcohol consumption and ADH2 or ADH3 genotypes. Conclusions: The concept that alcohol dehydrogenase genotype and alcohol metabolic rate modify the effects of alcohol on plasma HDL concentration is not supported by our results.

The contribution of research to Australian policy responses to heroin dependence 1990-2001: a personal retrospection

Periodic public concern about heroin use has been a major driver of Australian drug policy in the four decades since heroin use was first reported. The number of heroin-dependent people in Australia has increased from several hundreds in the late 1960s to around 100000 by the end of the 1990s. In this paper I do the following: (1) describe collaborative research on heroin dependence that was undertaken between 1991 and 2001 by researchers at the National Drug and Alcohol Research Centre: (2) discuss the contribution that this research may have made to the formulation of policies towards the treatment of heroin dependence during a period when the policy debate crystallized around the issue of whether or not Australia should conduct a controlled trial of heroin prescription; and (3) reflect on the relationships between research and policy-making in the addictions field, specifically on the roles of investigator-initiated and commissioned research, the interface between researchers, funders and policymakers: and the need to be realistic about the likely impact of research on policy and practice.

The complexity of drinking: Interactions between the cognitive and behavioural determinants of alcohol consumption

This study expanded the earlier work conducted by this laboratory ( Hasking, P.A. and Oei, T.P.S. (2002a) . The differential role of alcohol expectancies, drinking refusal self-efficacy and coping resources in predicting alcohol consumption in community and clinical samples. Addiction Research and Theory , 10 , 465-494), by examining the independent and interactive effects of avoidant coping strategies, positive and negative expectancies and self-efficacy, in predicting volume and frequency of alcohol consumption in a sample of community drinkers. Differential relationships were found between the variables when predicting the two consumption measures. Specifically, while self-efficacy, seeking social support for emotional reasons and using drugs or alcohol to cope were independently related to both volume and frequency of drinking, complex interactions with positive and negative alcohol expectancies were also found. These interactions are discussed in terms of the cognitive and behavioural mechanisms thought to underlie drinking behaviour.

Maternal alcohol use disorder and offspring ADHD: disentangling genetic and environmental effects using a children-of-twins design

Background. Children of alcoholics are significantly more likely to experience high-risk environmental exposures, including prenatal substance exposure, and are more likely to exhibit externalizing problems [e.g. attention deficit hyperactivity disorder (ADHD)]. While there is evidence that genetic influences and prenatal nicotine and/or alcohol exposure play separate roles in determining risk of ADHD, little has been done on determining the joint roles that genetic risk associated with maternal alcohol use disorder (AUD) and prenatal risk factors play in determining risk of ADHD. Method. Using a children-of-twins design, diagnostic telephone interview data from high-risk families (female monozygotic and dizygotic twins concordant or discordant for AUD as parents) and control families targeted from a large Australian twin cohort were analyzed using logistic regression models. Results. Offspring of twins with a history of AUD, as well as offspring of non-AUD monozygotic twins whose co-twin had AUD, were significantly more likely to exhibit ADHD than offspring of controls. This pattern is consistent with a genetic explanation for the association between maternal AUD and increased offspring risk of ADHD. Adjustment for prenatal smoking, which remained significantly predictive, did not remove the significant genetic association between maternal AUD and offspring ADHD. Conclusions. While maternal smoking during pregnancy probably contributes to the association between maternal AUD and offspring ADHD risk, the evidence for a significant genetic correlation suggests: (i) pleiotropic genetic effects, with some genes that influence risk of AUD also influencing vulnerability to ADHD; or (ii) ADHD is a direct risk-factor for AUD.