An Account of Berridge and Robinsons Incentive-Sensitisation Theory of Addiction
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In modern society, many people are facing addiction or know someone fighting addiction. Whether it be a drug, gambling or eating addiction, the effects are widespread and impact society. In England alone, between 2014/2015 257,476 people are addicted to Opiates and 182,828 to Crack Cocaine (Hay, Swinthenbank, & dos Santos, 2014/2015). ‘Addiction is the repeated involvement with a substance or activity, despite the substantial harm it now causes, because that involvement was (and may continue to be) pleasurable and/or valuable’ (Misra, Amy, Galen, & Horvath, 2013). The impacts of addiction are innumerable on the individual and wider society. Drug addicts are twice as likely to acquire a mood or anxiety disorder compared to the rest of the population (NIDA, 2017). This affects their quality of life by heightening their levels of distress. Furthermore, addicts are likely to turn to crime to finance their addictions or due to their drug-fuelled state. Resultantly, this affects the victims on an emotional and/or economic way. There are many credible theories that delve into the explanations for addiction. In this essay, I will focus on the incentive-sensitisation theory of addiction (Berridge & Robinson, 2016) specifically drug addiction. Firstly, I will examine the main basis of the theory. I will then move on to relevant supporting research. Finally, I will evaluate how the theory can apply to psychopathological disorders. I will close this essay with a discussion on how the areas I’ve researched pose further questions that are yet to be answered.
The incentive-sensitisation theory of addiction is about the neurological differences between ‘liking’ and ‘wanting’. Despite our familiarity with these words, we often use them synonymously even though there is a distinct difference between the two. Berridge and Robinson looked into the neurological differences and into forms of ‘wanting’ such as incentive salience. Incentive Salience is a type of wanting that is less focused on a cognitive goal – it is triggered by vivid image cues and other stimuli that represent something that may appear desirable to an individual. An example could be a recovering alcoholic seeing people drinking at a pub with their friends. This stimulus would trigger a ‘want’ for alcohol due to the desirable imagery presented. This is incentive salience as the ‘want’ is triggered by reward cues. (Hickey & Peelen, 2015). Recovering addicts have a want to recover – a cognitive goal. Yet presentation of drug-related stimuli can trigger a ‘want’ for the drug despite not actually wanting to experience the primary and secondary effects of the drug. This is the difference between wanting and ‘wanting’ (incentive salience). Drugs such as cocaine, heroin and amphetamine can ‘sensitise’ our brain dopamine systems. (Robinson & Becker, 1986/06). A variety of neurotransmitters can be affected by mesolimbic sensitisation. The mesolimbic system is made up of pathways which release the neurotransmitter dopamine and it is located in the centre of our brain. (Ikemoto, 2010). The main function of this system is the cognitive process of motivation which fuels incentive salience. The system is known as the “reward system” (Salamone & Correa, 2012). Dopamine sensitisation occurs after repeated exposure to a drug resulting in an increased effect of the drug on the individual. ‘Liking’ is not expected to increase with sensitisation – in fact, it can decrease. This is thought to be because ‘liking’ is mediated by smaller and more fragile neural systems. Addicts may ‘want’ a drug without liking the effects of the drug whether it’s down to the physiological, social or other undesirable impacts they can have. Not liking the drug is often motivation to abstain along with the cognitive goal (want) to quit. When ‘wanting’ increases in the presence of cues, ‘wanting’ then acts on the dopamine system because of previous mesolimbic sensitisation (Robinson & Berridge, 1993).
The original research conducted by Berridge and Robinson investigated liking in rats by minimising their levels of brain dopamine. Dopamine levels were reduced by a surgical procedure known as a neurochemical lesion. It was hypothesised that the reduction of dopamine would reduce levels of liking. They measured this via the facial expressions and actions the rats presented when they were administered a sweet (sucrose) or bitter (quinine) solution. They observed this by having each rat in a chamber with a transparent floor. Cameras were placed underneath facing upwards to pick up on the rats’ reactions. The footage could be viewed to a precise degree. Behavioural categories based on research by Grill and Norgren (1978) determined if the reactions to the solutions would be classed as aversive, hedonic or neutral. Examples of actions that were deemed aversive were chin rubs, face washing and locomotion. Hedonic actions and expressions were paw licks and rhythmic tongue protrusions. If the rat alternated between face washing and paw licking with less than a 1-second transition that sequence would be classed as a neutral reaction. Results showed that despite the rats being depleted of nearly all dopamine in their brain, their reactions to the solutions did not change. They were still able to distinguish between the two. This unexpected finding pushed the researchers to take a different stance. They followed a path of looking at how mesolimbic dopamine systems mediate ‘wanting’, not ‘liking’. (Berridge, Venier, & Robinson, 1989)
Mesolimbic brain responses in drug addicts when viewing drug cues are heightened compared to those who are not addicts (Childress, et al., 2008). This is evidence for hyper-reactivity of the dopamine system. A laboratory study investigated how heroin abusers respond to drug-related cues. The study was conducted with 22 male abstinent heroin abusers and 20 healthy males. The study had two conditions. The first condition was to push a lever as a response to a neutral image such as a vehicle and to pull the lever to a heroin-related stimulus (e.g. an image of a needle). The actions were reversed in the second condition. Pushing the lever was considered as an avoidance response whereas the response of pulling was considered an approach response. The actions of the participants were observed to see if their responses aligned with their past addiction. It was found that in comparison to the control group of healthy males, the abstinent heroin abusers had a quicker reaction time when pulling the lever as a response to heroin-related pictures and they took longer to push the lever in response to heroin-related stimuli. This shows that their responses were relevant to their past addiction as the hesitation to relate heroin to an ‘avoidance’ behaviour is representative of their ‘want’ for heroin. Yet it should be recognised that having being drawn towards heroin-related stimuli is indirect in comparison to actually taking the drug. (Zhou, Li, & Zhang, 2011) This links in with the incentive-sensitisation model as those who have experienced being chronic drug users now see either drugs or drug-related cues as a strong incentive (Berridge & Robinson, 2016). Despite the task in Zhou’s study requiring a simple push or pull action, it highlights how addiction can affect your levels of compulsion; a factor highlighted in the incentive sensitisation theory. This is especially significant in relevance to the risk of relapse in individuals who experience compulsions around drug cues.
Due to the developed understanding of how the ‘Incentive- Sensitisation’ theory functions, concepts can be applied to psychopathological disorders such as schizophrenia. Excessive or insufficient levels of dopamine can contribute to the development of schizophrenic symptoms – this is known as the Dopamine Hypothesis (Seeman, et al., 2005). Focusing on mesolimbic pathways in addiction has meant that we can understand how schizophrenics react to reward incentives. Anti-psychotics that are prescribed to patients usually work on the dopamine system to reduce psychosis-like symptoms. These findings suggest that the prescribed doses of the anti-psychotics should be adapted to the dopamine levels of the individual in order to prevent the risk of psychosis or related symptoms (Heinz & Schlagenhauf, 2010).
In conclusion, the theory has high credibility due to the multitude of studies looking into the accuracy of the claims. However, I would argue that there are multitudinous theories that explain addiction on other levels such as genetic predispositions or sociodemographics. Research in this area found a vulnerability to nicotine addiction varied depending on ‘age; gender; ethnicity and acculturation; living arrangements, family size and structure; parental socioeconomic status (SES); spending money and employment status; and rural/urban residence’ (Tyas & Pederson LL, 1998). Due to this, I believe that this theory may not have the explanatory power for all cases of addiction but it does ground our knowledge on a neurochemical level. As discussed in this essay, there are other studies (e.g Zhou) that support the premise of the theory showing that it has reliability yet Zhou’s study cannot be directly paralleled to actually taking heroin. Robinson and Berridge’s rat study also has generalisability issues as humans have further developed emotional cognition than rats. This is a limitation as we cannot assume that because the rats didn’t show any changes from depleted dopamine that humans would have the same result. Due to our uncertainty of how far the claims go, it is very important that research is still ongoing. Modern-day neuroimaging has advanced to such a degree that we may be able to get closer to these answers in the not too distant future. However, the theory should be commended for the impact it has had on recovery models for addicts and those who are abstaining as well as understanding psychopathological illnesses from a different perspective.