Literature Review PDF

Preview

Summary

I received 86% for this literature review which was worth 40% overall. The average mark for this assignment was 62%....

Description

Running head: AUD Literature Review

Literature Review of Factors Contributing to Alcohol Use Disorder Sabeena Manalis Student ID: 218512316 Deakin University Word count: 1647

1!

AUD Literature Review

2!

Literature Review of Factors Contributing to Alcohol Use Disorder Alcohol use disorder (AUD) is a debilitating chronic condition characterised by compulsive alcohol use, cravings, drinking excessively, frequent episodes of intoxication despite adverse consequences, clinically significant distress and impairment, withdrawal symptoms and a high tolerance for alcohol (Grant et al. 2015, 2016; Tawa, Hall & Lohoff 2016). According to the World Health Organization (2014), 3.3 million deaths were attributed to alcohol misuse in 2012 (Sudhinaraset et al. 2016). Prevalence rates in Australia are around 17.6% for men and 10.4% for women (Grant et al. 2016). Due to the severity of the potential consequences linked to alcohol use disorders such as disease, disability and death and the poorly understood underlying pathophysiology of AUD it is important to evaluate the contributing biological, psychological and social factors to determine the most efficacious treatment options (Sudhinaraset et al 2006; Tawa 2016). This review aims to critically evaluate how each factor plays a role in the maintenance and aetiology of AUD and explore whether a unidimensional or integrative explanation and approach is most effective. Biological Factor Family, twin, and adoption studies have shown that heritability of certain genes is a biological factor which accounts for approximately 50% of the risk for developing AUD (Hicks et al. 2004, 2007; Kendler et al. 2011; Tawa 2016; Verhulst, Neale & Kendler 2015). Researchers have attempted to pinpoint precise genes linked to AUD however, conclusive results are scarce due to the complex combination of genes involved. The strongest associations with AUD have been identified in the alcohol metabolising genes, alcoholdehydrogenase (ADH) and aldehyde

AUD Literature Review

3!

dehydrogenase (ALDH) (Bierut et al. 2012; Choi et al. 2005; Edenberg 2007; Gelernter et al. 2014). Ethanol is first oxidized to acetaldehyde by ADH and then further oxidized to acetate by ALDH. Both enzymes occur in multiple forms that are encoded by different genes which have coding variants (i.e., alleles) in the ADH1B, ADH1C and ALDH2 genes (Edenberg 2007). Which ADH or ALDH alleles a person carries may influence his or her level of alcohol consumption due to the physiological effects of alcohol use. For example, particular ADH1B and ADH1C alleles encode overly active ADH enzymes, resulting in a faster ethanol to acetaldehyde conversion rate (Edenberg et al. 2006; Lee et al. 2006). Individuals with isoforms of ADH that oxidize ethanol more rapidly and/or ALDH that oxidize acetaldehyde at a slower rate are at a significantly reduced risk of becoming alcohol dependent due to the adverse physiological effects that result from the toxic acetaldehyde accumulation (Choi et al. 2005; Edenberg et al. 2006). These unpleasant symptoms include nausea, overheating, mood swings, flushing syndrome and tachycardia (Brooks et al. 2009; Edenberg et al. 2006). Reversely, If a person is predisposed to metabolise alcohol in a way that is pleasurable and activates the reward pathway they may be more likely to develop AUD (Norden-Krichmar et al. 2014). A limitation of current research is population bias, ADH1B and ALDh2 coding variants are mostly found in East Asian populations and there is limited evidence into the genes encoding other ADH enzymes which increase the risk of alcohol dependance in other populations (Chen et al. 2005; Edenberg et al. 2006). Risk for developing AUD is modulated by many different genes and there is no singular genetic factor that can be designated as a cause (Han et al. 2005; Lee et al. 2006). Moreover, the gene-environment interaction significantly increases susceptibility so

AUD Literature Review

4!

those who inherit genetic mutations which predispose them to AUD are at a significantly higher risk of developing the disorder if affected by social and/or psychological factors as well (Edenberg et al. 2006). Psychological Factor A psychological factor in AUD is self-efficacy in controlling alcohol consumption (Bandura, 1977). The level of confidence one has about their ability to abstain from drinking (refusal self-efficacy) has emerged as a strong predictor of the development and maintenance of AUD (Connor et al. 2011; Ilgen et al. 2006; Moos & Moos 2006; Romo et al. 2009). Comorbid mental disorders are common for people with AUD so negative moods and a lack of coping skills can increase cravings and undermine refusal self-efficacy (Cooney et al. 2007; Watkins et al. 2006). The physiological and emotional response to withdrawal also make it more difficult to stay in control and recall relevant successes to motivate refusal self efficacy (Connor & Feeney 2011; Moos et al. 2006). Refusal self-efficacy is also undermined by high alcohol expectancies which are the perceived rewards of drinking alcohol (Gullo et al. 2010). People with an AUD tend to have exaggerated positive expectancies and memory bias for rewarding experiences which lowers their motivation to control their intake (Connor et al. 2011; Young et al. 2006). The beliefs one has about alcohol consumption may be initially formed through social factors such as vicarious learning from family members long before consuming alcohol (Palmer et al., 2009). Some studies have failed to find associations between self-efficacy and treatment outcome (Wong et al. 2004). It is unclear whether increased refusal self-efficacy causes behaviour change or if it is an epiphenomenon resulting from behaviour change (Bates et al.,

AUD Literature Review

5!

2006; Ilgen et al. 2006; Moos et al. 2006). Future research should test whether specific treatments increase self-efficacy while control treatments do not and that self-efficacy mediates treatment effects. Social Factor Family influence is recognised as an important social factor in the maintenance and aetiology of AUD (Chartier, Thomas & Kendler 2016; Mares et al. 2011; Sudhinaraset et al 2016). Children who have a parent with AUD are at an increased risk of developing the disorder themselves (Palmer et al., 2009; Varvil-Weld et al. 2014). There is mixed literature on whether family influence is associated with AUD due to genetic factors or social learning factors. In a social context, direct cultural transmission indicates that disorders are passed down to children through social learning or modeling (White et al. 2006; Sudhinaraset et al 2016). Family is a significant social context which impacts the decision to use alcohol and early exposure to AUD and addiction normalises maladaptive coping strategies which increases the risk of developing dangerous drinking patterns later in life (Johnston et al., 2008; Trucco et al. 2014). Positive family norms around alcohol may also reinforce psychological factors like refusal self-efficacy and be responsible for an early age of drinking onset which has been found to be a significant factor in AUD (Connor et al. 2011; Ewing et al. 2015; Hingson, Heeren & Winter 2006) There is controversy regarding the explanation for the link between familial alcoholism and AUD. Some twin-family designs and adoption studies reject the claim of social learning factors due to evidence suggesting AUD is transmitted through genetic factors only and other studies have found no evidence at all for genetic heritability (Verhulst et al. 2015).

AUD Literature Review

6!

Future research should consider the methodological limitations in current research due to the complexity of controlling other variables which may be responsible for the AUD vulnerability parents pass on to their off-spring (Knopik et al. 2004; Mares et al. 2011). Comorbid psychiatric disorders, parenting behaviour and discipline style, age of onset, parental monitoring, and adverse childhood events impact psychological risk factors which may be a predictor of AUD (Hingson et al. 2006; Mares et al. 2011; White et al. 2006). Integration of factors It is evident from the literature reviewed that a multidimensional interaction between biological, psychological and social factors account for the aetiology and maintenance of AUD. The evidence suggests that individuals who are at highest risk of developing AUD are those who are affected by a combination of factors rather than just one biological, psychological or social factor. Alcohol metabolising genes, refusal self-efficacy and family influence reinforces an integrative model in the way they interact with each other in AUD symptomatology. Individuals who inherit protective alleles often have high refusal self-efficacy and are significantly less likely to be influenced by family social contexts which encourage alcohol use due to the unpleasant physiological response of alcohol consumption (Choi et al. 2005; Edenberg et al. 2006). Likewise, learned behaviours, beliefs and attitudes affect how genes are expressed so genetically predisposed individuals who are also raised in an environment where drinking is acceptable and/or valued are at a substantially higher risk of developing AUD compared to those who are influenced by only a social or biological factor (Brooks et al. 2009; Edenberg et al. 2006). Conversely, genetically predisposed individuals who are raised in an environment which

AUD Literature Review

7!

offers family support, bonding, and parental monitoring may significantly reduce AUD vulnerability (White et al. 2006; Ramirez et al. 2012). The causes and maintaining factors of AUD are complex often with a presence of comorbid mental health disorders therefore, most patients will benefit from multilevel interventions incorporating families, neuropharmaceuticals and psychological therapies. Specifically, Disulfiram is a medication option which acts as deterrent to drinking by inducing the negative side-effects of acetaldehyde accumulation (Edenberg et al. 2006). CBT and mindfulness-based methods may increase refusal self-efficacy to reduce intake to safe drinking levels and help to distinguish maladaptive behaviours learned in the family social context (Carroll & Kiluk 2017; Onken et al. 2013). Conclusion This literature review aimed to evaluate the biological, psychological and social factors which contribute to the maintenance and aetiology of AUD and explore whether a unidimensional or integrative approach is most effective. Evidence for three factors and how they interact with each other were outlined as well as limitations and gaps in the literature. The factors discussed suggest a clear multi-dimensional approach in the maintenance and aetiology of AUD due to the importance of all three factors and the influence each one has on the other. Considering the seriousness of AUD and the risks the disorder has on the individual and society, an integrative model which considers all three factors is imperative to effectively prevent and treat AUD.

AUD Literature Review

8! References

Bandura, A, Freeman, WH & Lightsey, R 1999, ‘Self-Efficacy: The Exercise of Control’, Journal of Cognitive Psychotherapy, vol. 13, no. 2, pp. 158–166.

Bierut, LJ, Goate, AM, Breslau, N, Johnson, EO, Bertelsen, S, Fox, L, Agrawal, A, Bucholz, KK, Grucza, R, Hesselbrock, V, Kramer, J, Kuperman, S, Nurnberger, J, Porjesz, B, Saccone, NL, Schuckit, M, Tischfield, J, Wang, JC, Foroud, T, Rice, JP & Edenberg, HJ 2011, ‘ADH1B is associated with alcohol dependence and alcohol consumption in populations of European and African ancestry’, Molecular Psychiatry, vol. 17, no. 4, pp. 445–450.

Brooks, PJ, Enoch, M-A, Goldman, D, Li, T-K & Yokoyama, A 2009, ‘The Alcohol Flushing Response: An Unrecognized Risk Factor for Esophageal Cancer from Alcohol Consumption’, PLoS Medicine, vol. 6, no. 3, p. e1000050.

Carroll, KM & Kiluk, BD 2017, ‘Cognitive behavioral interventions for alcohol and drug use disorders: Through the stage model and back again.’, Psychology of Addictive Behaviors, vol. 31, no. 8, pp. 847–861.

Connor, JP, George, SM, Gullo, MJ, Kelly, AB & Young, RM 2011, ‘A Prospective Study of Alcohol Expectancies and Self-Efficacy as Predictors of Young Adolescent Alcohol Misuse’, Alcohol and Alcoholism, vol. 46, no. 2, pp. 161–169.

AUD Literature Review

9!

Cooney, NL, Litt, MD, Cooney, JL, Pilkey, DT, Steinburg, HR & Oncken, CA 2007, ‘Alcohol and tobacco cessation in alcohol-dependent smokers: Analysis of real-time reports.’, Psychology of Addictive Behaviors, vol. 21, no. 3, pp. 277–286.

Chen, H-J, Tian, H & Edenberg, HJ 2005, ‘Natural haplotypes in the regulatory sequences affect human alcohol dehydrogenase 1C (ADH1C) gene expression’, Human Mutation, vol. 25, no. 2, pp. 150–155.

Choi, I-G, Son, H-G, Yang, B-H, Kim, SH, Lee, J-S, Chai, Y-G, Son, BK, Kee, BS, Park, BL, Kim, LH, Choi, YH & Shin, HD 2005, ‘Scanning of genetic effects of alcohol metabolism gene (ADH1BandADH1C) polymorphisms on the risk of alcoholism’, Human Mutation, vol. 26, no. 3, pp. 224–234.

Demmel, R, Nicolai, J & Jenko, DM 2006, ‘Self-Efficacy and Alcohol Relapse: Concurrent Validity of Confidence Measures, Self-Other Discrepancies, and Prediction of Treatment Outcome’, Journal of Studies on Alcohol, vol. 67, no. 4, pp. 637–641.

Edenberg, HJ & Foroud, T 2006, ‘The genetics of alcoholism: identifying specific genes through family studies’, Addiction Biology, vol. 11, no. 3–4, pp. 386–396.

Ewing, BA, Osilla, KC, Pedersen, ER, Hunter, SB, Miles, JNV & D’Amico, EJ 2015, ‘Longitudinal family effects on substance use among an at-risk adolescent sample’,

AUD Literature Review

10 !

Addictive Behaviors, vol. 41, pp. 185–191, viewed 27 November 2019, .

Grant BF, Saha TD, Ruan WJ 2016, Epidemiology of DSM-5 drug use disorder: results from the National Epidemiologic Survey on Alcohol and Related Conditions-III. JAMA Psychiatry 73:39–47.

Grant, BF, Goldstein, RB, Saha, TD, Chou, SP, Jung, J, Zhang, H, Pickering, RP, Ruan, WJ, Smith, SM, Huang, B & Hasin, DS 2015, ‘Epidemiology of DSM-5Alcohol Use Disorder’, JAMA Psychiatry, vol. 72, no. 8, p. 757.

Gullo, MJ, Dawe, S, Kambouropoulos, N, Staiger, PK & Jackson, CJ 2010, ‘Alcohol Expectancies and Drinking Refusal Self-Efficacy Mediate the Association of Impulsivity With Alcohol Misuse’, Alcoholism: Clinical and Experimental Research

Haller, M, Handley, E, Chassin, L & Bountress, K 2010, ‘Developmental cascades: Linking adolescent substance use, affiliation with substance use promoting peers, and academic achievement to adult substance use disorders’, Development and Psychopathology, vol. 22, no. 04, pp. 899–916.

Han, Y, Oota, H, Osier, MV, Pakstis, AJ, Speed, WC, Odunsi, A, Okonofua, F, Kajuna, SLB, Karoma, NJ, Kungulilo, S, Grigorenko, E, Zhukova, OV, Bonne-Tamir, B, Lu, R-B,

AUD Literature Review

!11

Parnas, J, Hicks, BM, Blonigen, DM, Kramer, MD, Krueger, RF, Patrick, CJ, Iacono, WG & McGue, M 2007, ‘Gender differences and developmental change in externalizing disorders from late adolescence to early adulthood: A longitudinal twin study.’, Journal of Abnormal Psychology, vol. 116, no. 3, pp. 433–447.

Hicks, BM, Krueger, RF, Iacono, WG, McGue, M & Patrick, CJ 2004, ‘Family Transmission and Heritability of Externalizing Disorders’, Archives of General Psychiatry, vol. 61, no. 9, p. 922.

Hingson, RW, Heeren, T & Winter, MR 2006, ‘Age at drinking onset and alcohol dependence: age at onset, duration, and severity’, Archives of pediatrics & adolescent medicine, vol. 160, United States, no. 7, pp. 739–46, viewed 24 January 2019, .

Ilgen, M, Tiet, Q, Finney, J & Moos, RH 2006, ‘Self-Efficacy, Therapeutic Alliance, and Alcohol-Use Disorder Treatment Outcomes’, Journal of Studies on Alcohol, vol. 67, no. 3, pp. 465–472.

Johnston, LD, O’Malley, PM & Bachman, JG 2003, ‘Monitoring the Future: National Results on Adolescent Drug Use: Overview of Key Findings’, Focus, vol. 1, no. 2, pp. 213–234.

AUD Literature Review

12 !

Kendler, KS, Gardner, C & Dick, DM 2010, ‘Predicting alcohol consumption in adolescence from alcohol-specific and general externalizing genetic risk factors, key environmental exposures and their interaction’, Psychological Medicine, vol. 41, no. 7, pp. 1507–1516.

Knopkin, VS, Heath, AC, Madden, PAF, Bucholz, KK, Slutske, WS, Nelson, EC, Statham, D, Whitefield, JB & Martin, NG 2004, ‘Genetic effects on alcohol dependence risk: reevaluating the importance of psychiatric and other heritable risk factors’, Psychological Medicine, vol. 34, no. 8, pp. 1519–1530.

Lee, S-L, Chau, G-Y, Yao, C-T, Wu, C-W & Yin, S-J 2006, ‘Functional Assessment of Human Alcohol Dehydrogenase Family in Ethanol Metabolism: Significance of First-Pass Metabolism’, Alcoholism: Clinical and Experimental Research, vol. 30, no. 7, pp. 1132– 1142.

Mares, SHW, van der Vorst, H, Engels, RCME & Lichtwarck-Aschoff, A 2011, ‘Parental alcohol use, alcohol-related problems, and alcohol-specific attitudes, alcohol-specific communication, and adolescent excessive alcohol use and alcohol-related problems: An indirect path model’, Addictive Behaviors, vol. 36, no. 3, pp. 209–216.

McD. Young, R, Connor, JP & Feeney, GFX 2011, ‘Alcohol expectancy changes over a 12-week cognitive–behavioral therapy program are predictive of treatment success’, Journal of Substance Abuse Treatment, vol. 40, no. 1, pp. 18–25.

AUD Literature Review

13 !

Moos, RH & Moos, BS 2006, ‘Rates and predictors of relapse after natural and treated remission from alcohol use disorders’, Addiction, vol. 101, no. 2, pp. 212–222.

Norden-Krichmar, TM, Gizer, IR, Wilhelmsen, KC, Schork, NJ & Ehlers, CL 2014, ‘Protective variant associated with alcohol dependence in a Mexican American cohort’, BMC Medical Genetics, vol. 15, no. 1.

Onken, LS, Carroll, KM, Shoham, V, Cuthbert, BN & Riddle, M 2013, ‘Reenvisioning Clinical Science’, Clinical Psychological Science, vol. 2, no. 1, pp. 22–34.

Palmer, RHC, Young, SE, Hopfer, CJ, Corley, RP, Stallings, MC, Crowley, TJ & Hewitt, JK 2009, ‘Developmental epidemiology of drug use and abuse in adolescence and young adulthood: Evidence of generalized risk’, Drug and Alcohol Dependence, vol. 102, no. 1– 3, pp. 78–87.

Ramirez, R, Hinman, A, Sterling, S, Weisner, C & Campbell, C 2012, ‘Peer Influences on Adolescent Alcohol and Other Drug Use Outcomes’, Journal of Nursing Scholarship, vol. 44, no. 1, pp. 36–44.

Romo, L, Strat, YL, Aubry, C, Marquez, S, Houdeyer, K, Batel, P, Adès, J & Gorwood, P 2009, ‘The Role of Brief Motivational Intervention on Self-Efficacy and Abstinence in a Cohort

AUD Literature Review

14 !

of Patients with Alcohol Dependence’, The International Journal of Psychiatry in Medicine, vol. 39, no. 3, pp. 313–323.

Schulz, LO, Kidd, JR & Kidd, KK 2005, ‘Considerable Haplotype Diversity within the 23kb Encompassing the ADH7 Gene’, Alcoholism: Clinical and Experimental Research, vol. 29, no. 12, pp. 2091–2100.

Trucco, EM, Colder, CR, Wieczorek, WF, Lengua, LJ & Hawk, LW 2014, ‘Early adolescent alcohol use in context: How neighborhoods, parents, and peers impact youth’, Development and Psychopathology, vol. 26, no. 2, pp. 425–436.

Varvil-Weld, L, Turrisi, R, Hospital, MM, Mallett, KA & Bámaca-Colbert, MY 2014, ‘Maternal and peer influences on drinking among Latino college students’, Addictive Behaviors, vol. 39, no. 1, pp. 246–252.

Watkins, JA, Howard-Barr, EM, Moore, MJ & Werch, CC 2006, ‘The mediating role of adolescent self-efficacy in the relationship between parental practices and adolescent alcohol use’, Jour...