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Research by the neuroscientist Aya Altoni.

Alcohol Addiction

Introduction

Definitions of addiction in the late 19th and early 20th centuries were broad as addiction was described by imbalances within the central nervous system that lead to aberrant behaviour (Meyer, 1996). In the mid to late 20th century, definitions of addiction became more detailed, and included the nature of being highly habituated to a behaviour such that avoidance of that behaviour led to discomfort, and that this discomfort preoccupied the individual in other areas of their life (Alexander and Schweighofer, 1988; Levine, 1978). However, truly objective definitions of addiction are difficult and definitions still vary, particularly between research disciplines (Foddy and Savulescu, 2010a; Nordenfelt, 2010).

The biological explanation of addiction has relied heavily on animal models to draw on observations regarding the neurobiological changes, particularly relating to substance abuse of addictive drugs. As technology has advanced, imaging techniques and a greater understanding of neurochemistry has provided a solid foundation for a biological origin for addiction to substances. However, despite great strides in this area, it is unclear whether addiction is part of normal desire, or originates from a unique part of the brain (Foddy and Savulescu, 2010b). Further, whilst the biological model is useful in understanding substance addiction, its use in non-substance addiction such as gambling and social media addiction is more questionable.

Psychological models of addiction include aspects that are behavioural, cognitive or psychodynamic, and are perhaps more suited to understanding non-substance addiction. Of the psychological models, the behavioural model suggests that addiction is caused by certain learned behaviours (American Psychiatric Association, 2013: Pp461-481), but in many cases the line between a normal healthy behaviour and addiction of these behaviours is not clear (Kardefelt‐Winther et al., 2017). Whilst gambling is the only medically recognised behavioural addiction (Petry, Zajac and Ginley, 2018), other behavioural addictions such as video game addiction are increasingly being recognised and investigated by researchers (Kuss, 2013).

Investigating addiction from a purely biological or psychological viewpoint can be problematic because it could be argued that it is not possible to fully separate these approaches. This is particularly true for addiction to substances. For example, alcohol addiction can be viewed as a disease process and therefore relating to biology, but also contain behavioural aspects. Therefore this essay will describe and critically discuss alcohol addiction from the perspective of the biological and behavioural perspective and highlight the overlapping nature of these approaches, as well as the impact this has on treatment. It will be argued that whilst these approaches are distinct, they can never fully be separated and as such are complementary rather than oppositional in nature.

2. Alcohol Addiction Substance addiction is one area of addiction research that has been extensively studied (Zou et al., 2017). According to the DSM-5 (American Psychology Society, 2013) substances that can cause addiction include alcohol, caffeine, cannabis, hallucinogens, inhalants, opioids, sedatives, hypnotics, stimulants and tobacco. The pharmacological pathways for each substance are different, but research suggests that the reason for addiction may be the stimulation of the brain’s reward pathways (McHugh and Kneeland, 2019). Of these substances, addiction to alcohol is an area of interest in biology and psychology, because it is relatively common, hugely damaging and not fully understood. For example, one study estimated the prevalence of alcohol addition in the United Kingdom to be 11.9 % for men and 2.9 % for women (Singleton et al., 2003) with the cost of alcohol problems as high as 18 billion pounds per annum in England and Wales (Leontaridi, 2003). It has been suggested that current changes to the way alcohol is consumed, with a ‘more is better’ attitude, has created a significant public health crisis (Sheron, 2004).

2.1. The biological disease model of alcohol addiction The biological model of alcoholism viewing alcohol addiction as a disease was first proposed by Jellinek (1960) and since this time revisions have been developed further based on advances in molecular biology (Ferraguti, Pascale and Lucarelli, 2015). The contemporary view of the biological disease model is that the development of alcoholism is observably unitary in nature and as such one is either an alcoholic or is not an alcoholic. Another concept in the biological disease model is that sufferers have a high or low sensitivity to grain alcohol, creating a pathology that determines their reaction to consumption (Addolorato et al., 2005). This sensitivity manifests itself whenever alcohol is consumed. Because there exists a pathology, the individual is not responsible for their action towards alcohol, and the addiction is not something that can easily be controlled by behavioural changes. In this regard the alcohol sensitivity is permanent and untreatable, and this means that an alcoholic will always remain an alcoholic, even if they never drink again. This model therefore determines that moderation is not possible and that total abstinence of alcohol is a necessity.

Evidence for the biological disease model has come from molecular biology (Crabbe and Harris, 2013). Rats showing alcoholic preferences (P-rats) have been bred and are now used as a basis for this model (McBride et al., 2014). The foundation for much of this work was performed in the later part of the twentieth century, where in a series of experiments, it was demonstrated that the offspring of alcohol addicted rats have a much higher propensity to become addicted to alcohol themselves, thus evidencing a genetic “disease factor”. This heritable component can be increased through selective breeding (Meisch and George, 1988). Experiments such as those by Waller et al. (1984) controlled for the taste of alcohol by intragastrically administering the alcohol, suggesting that researchers were concerned about eliminating behavioural factors.

A genetic component for alcohol addiction appears to be present in humans, with 46 % of male siblings of alcohol addicted individuals becoming addicted themselves, whereas with female siblings the number is only 5 % (Fialkov, 1985). In addition, up to 50 % of male offspring of alcohol addicts become addicted themselves, yet only 3 to 8 % of female offspring share this fate (Stabenau, 1988). Twin studies have found that there is a significantly higher concordance in the rates of alcohol addiction in monozygotic rather than dizygotic male twins, and that male concordance rates amongst twins were three times higher compared to females twins (Pickens et al., 1991).

However, the behavioural aspects of alcohol addiction are represented within genders also, as female drinking problems have increased in recent decades as culture has normalised drinking patterns between the genders such that it is socially acceptable for women to drink greater quantities of alcohol (Goodwin, 1991). Further, behaviours can be learned from genetically related individuals, and so although evidence does show a genetic component to the biological disease model, its contribution may have been overestimated in some studies of humans (Bell et al., 2006). It is also questionable as to whether specially bred rats which are often administered alcohol intragastrically are representative of human alcoholics. Further, the biological disease model is complicated by the presence of alcoholism as a comorbidity to other disorders, including in psychiatric patients (Mueser, Drake and Wallach, 1998).

2.2. The behavioural model of alcohol addiction Behavioural aspects to alcohol addiction predates biological aspects, with the moral model being established by theological underpinnings of the church and the Holy Roman Empire (Cook, 2006: Pp 127-135). The early moral model suggests that alcoholics suffer from a lack of self control over their consumption of alcohol, and this results in excessive alcohol intakes (Cook, 2006; p 153). This lack of control was considered a character deficit, and as a result alcoholics were punished for their indiscretions and sin, and treatment for an addiction was not considered. Externalisation of the moral model also suggests that perceived moral judgement by others also modifies the behaviours of the alcoholic, for example by attempting to hide their addiction (Carmona‐Perera et al., 2014). However, the moral model has perhaps become outdated as more is understood about the behaviour of the alcoholic (Cook, 2006), particularly with relation to the lack of treatment options it presents. Objective studies regarding treating alcoholics via punishment protocols are absent from the contemporary literature, but recidivism in the criminal justice system has been shown to be lower with treatment compared to punishment for drink driving offences in alcoholics, suggesting that punishment does not deter detrimental behaviours associated with drinking (Taxman and Piquero, 1998).

The contemporary behavioural model contrasts with the biological disease model because it assumes that alcohol intakes fall into a range from zero to excessive amounts, and that this intake can be modified under different circumstances. Therefore alcohol addiction is not unitary as suggested by the biological disease model, but rather behaviours towards alcoholism develop over time and can be modified and reversed, which creates a larger range of treatment options compared to the biological disease model. Another of the main assumptions made by the behavioural model is that for those that consume any alcohol, the experience is positively reinforcing and that this reinforcement is governed by the same principles that govern other positively reinforcing behaviour. This reinforcing behaviour causes alcoholism to be a learned but abnormal behaviour, and because of this the behaviour pattern can be unlearned and therefore altered by the appropriate reinforcement contingencies, which allows the individual to move back down the alcohol range to more appropriate levels of intake. Therefore total abstinence, as determined by the biological disease model, is not a prerequisite of successful treatment.

Critics of the behavioural model often claim that alcohol consumption is evidently not positively reinforcing, and that this assumption is therefore false. However, one of the overlooked aspects of the behaviour model is that immediate consequences that are positively reinforcing are much stronger than those that are delayed. Therefore whilst excessive alcohol intake is damaging in the long term, it is the short term intake that provides the behavioural modification due to its short-term reinforcing pattern. For the alcoholic, the detrimental effects of drinking such as damage to the liver and a hangover, are outweighed by the perceived beneficial effects of positive reinforcement in the short term such as increased sociability, euphoria and anxiolysis. Further, as alcoholism develops, there is an increased requirement for alcohol to reduce the anxiety and withdrawal that is created from abstinence, and this further increases the positive reinforcement in the short-term. In addition, tolerance to the effects of the alcohol also decreases some of the long-term negative effects, which maintains the balance of consumption towards the beneficial short-term positive reinforcement.

2.3. Treatment of alcohol addiction Whilst the behavioural model may have its roots in psychology, the model does not preclude the possibility that aspects of the model are defined biologically and in their regard the behavioural model may overlap considerably with the disease model of alcoholism. For example, it is entirely possible that the behavioural model has a genetic component to it, with certain polymorphisms increasing the risk of developing certain behaviours that increase the positive reinforcing aspects of drinking alcohol, whilst affecting the way the individual responds to treatment (Thome et al., 2000). Further, the behavioural aspects of alcoholism is animal models investigating the disease model have been fairly well established (Bell et al., 2006). The biological aspects of addiction are further increased in complexity by the relatively new field of epigenetics, which covers the interactions of genes with the environment. Epigenetic interactions make behavioural aspects of addition able to directly influence biological aspects through expression of particular genes, and as such the two components interact to such a degree that they are inseparable. The acceptance of such an interaction between genes and environment suggests that treatments for alcoholism must consider both the psychological and biological approaches and that by excluding one or the other, treatments options will be at a high risk of failure. Contemporary treatment protocols take this multi-discipline approach and use evidence-based protocols based on biological and psychological approaches (Campbell, Lawrence and Perry, 2018).

3. Conclusion Addiction involves a heightened focus on a particular substance or behaviour. Further, addiction will consume other areas of the individual’s life and absence will cause discomfort. The biological disease model of alcohol addiction identifies a particular pathology and the sufferer is either an alcoholic or is healthy. The behavioural model of alcohol addiction understands the addiction as a more gradual process, and understands alcohol addiction as a learned pattern which deviates from normality. Effective treatments for alcohol addiction must rely on accurate models in order to provide effective treatments, and treatments must consider the disease of alcoholism within the context of the body and the mind because evidence suggests that both components play a role in the development of alcoholism. The increase in holistic treatments seen for alcohol addiction in recent decades suggests that clinicians that treat alcohol addiction understand the importance of both psychology and biology in alcohol addiction.