Importantly it has been claimed that addiction is not just a passing disease

Importantly it has been claimed that addiction is not

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Importantly, it has been claimed that addiction is not just a passing disease like the flu, but a chronic disease like diabetes and chronic hypertension (Leshner 1997 ). Hence, the BDMA not only states that there are brain changes which occur as one gets addicted (true), but also that these brain changes are chronic and cause relapse. In its strong form this statement is obviously untrue, as pointed out both with epidemiological and historical data (Heyman 2009 ) and with case-histories of severely addicted people who successfully quit (Lewis 2015 ). However, this falsifies the strong BDMA (one black swan is enough to falsify the statement that all swans are white), but does not mean a lighter form of the BDMA is not true: addiction severity is a continuum and for severe cases the BDMA may hold true (Berridge 2017 ; Fenton and Wiers 2017 ). However, it would then have to be shown that: 1. There are neural changes specifically related to severity of addiction; 252 N. HEATHER ET AL.
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2. These changes do not reverse with prolonged abstinence; 3. These changes increase the risk of relapse after a period of abstinence. At present, none of these claims has been proven beyond dispute. First, many studies have compared brains of addicted people with controls, but any difference could be a risk-marker rather than a consequence; there are no con- vincing longitudinal studies yet available (Schulte et al. 2014 ), but this could change in the future with large pro- spective neuroimaging studies on the way (Imagen, ABCD) 1 . The second claim also remains to be proven and, while there are indications of lack of recovery in some functions, there is evidence of recovery in others (Lewis 2017 ; Schulte et al. 2014 ). The third claim is likely to be true: a sensitised reward response, strong stress-reactivity, combined with lack of control are likely to contribute to relapse, as do other neurocognitive correlates of addiction such as lack of insight (Goldstein et al. 2009 ), and reduced ability of voluntary choice (Fenton and Wiers 2017 ; Wiers et al. 2016 ). In add- ition, there can be collateral damage strongly related to the addiction (e.g. Korsakoff s syndrome) which may contribute to relapse (Fenton and Wiers 2016). However, the causal role of these changes with respect to relapse remains to be established beyond doubt. (There is some evidence for a pre- dictive value of cue reactivity (Schacht et al. 2012 ), but cer- tainly not strong enough at this moment to support BDMA rather than alternative accounts.) In conclusion, the BDMA consists of a number of hypotheses that could be tested for different addictions. It appears premature at best to describe it as the current state of knowledge. Concluding remarks It is clear from the six summaries presented above that there are a range of views on what is wrong with the BDMA, both from a strictly scientific perspective and from a consider- ation of its consequences for the avoidance and reduction of harm due to addiction. Some find that some forms of what is known as addiction are not usefully thought of as brain disease, some that addiction is not just
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