scholarly journals Addiction as a brain disease revised: why it still matters, and the need for consilience

Author(s):  
Markus Heilig ◽  
James MacKillop ◽  
Diana Martinez ◽  
Jürgen Rehm ◽  
Lorenzo Leggio ◽  
...  

AbstractThe view that substance addiction is a brain disease, although widely accepted in the neuroscience community, has become subject to acerbic criticism in recent years. These criticisms state that the brain disease view is deterministic, fails to account for heterogeneity in remission and recovery, places too much emphasis on a compulsive dimension of addiction, and that a specific neural signature of addiction has not been identified. We acknowledge that some of these criticisms have merit, but assert that the foundational premise that addiction has a neurobiological basis is fundamentally sound. We also emphasize that denying that addiction is a brain disease is a harmful standpoint since it contributes to reducing access to healthcare and treatment, the consequences of which are catastrophic. Here, we therefore address these criticisms, and in doing so provide a contemporary update of the brain disease view of addiction. We provide arguments to support this view, discuss why apparently spontaneous remission does not negate it, and how seemingly compulsive behaviors can co-exist with the sensitivity to alternative reinforcement in addiction. Most importantly, we argue that the brain is the biological substrate from which both addiction and the capacity for behavior change arise, arguing for an intensified neuroscientific study of recovery. More broadly, we propose that these disagreements reveal the need for multidisciplinary research that integrates neuroscientific, behavioral, clinical, and sociocultural perspectives.

Neuroethics ◽  
2019 ◽  
Vol 13 (3) ◽  
pp. 311-324 ◽  
Author(s):  
Anna E. Goldberg

AbstractSubstance addiction affects millions of individuals worldwide and yet there is no consensus regarding its conceptualisation. Recent neuroscientific developments fuel the view that addiction can be classified as a brain disease, whereas a different body of scholars disagrees by claiming that addictive behaviour is a choice. These two models, the Brain Disease Model and the Choice Model, seem to oppose each other directly. This article contends the belief that the two models in the addiction debate are polar opposites. It shows that it is not the large amount of addiction research in itself what sets the models apart, but rather their extrapolated conclusions. Moreover, some of the most fiercely debated aspects - for instance, whether or not addiction should be classified as a disease or disorder - are irrelevant for the conceptualisation of addiction. Instead, the real disagreement is shown to revolve around capacities. Discussing addiction-related capacities, especially regarding impaired control, rather than the assumed juxtaposition of the two models can be considered the true addiction debate. More insight into the extent to which the capacities of the addicted individual were affected would be highly useful in various other areas, especially legal responsibility.


2020 ◽  
Vol 3 (1) ◽  
pp. 51-53
Author(s):  
Rano Azizova ◽  
◽  
Umida Shamsiyeva ◽  
Mirzohid Turabbayev ◽  
Begzod Jorayev ◽  
...  

Traumatic brain disease (TBHD) is a pathological process triggered by the damaging effect of mechanical energy on the brain and is characterized — with a variety of clinical forms — by the unity of etiology, pathogenetic and sanogenetic mechanisms of development and outcomes.


2019 ◽  
Author(s):  
Faisal Mushtaq ◽  
Samuel D. McDougle ◽  
Matt P. Craddock ◽  
Darius E. Parvin ◽  
Jack Brookes ◽  
...  

AbstractLosing a point playing tennis may result from poor shot selection or poor stroke execution. To explore how the brain responds to these different types of errors, we examined EEG signatures of feedback-related processing while participants performed a simple decision-making task. In Experiment 1, we used a task in which unrewarded outcomes were framed as selection errors, similar to how feedback information is treated in most studies. Consistent with previous work, EEG differences between rewarded and unrewarded trials in the medial frontal negativity (MFN) correlated with behavioral adjustment. In Experiment 2, the task was modified such that unrewarded outcomes could arise from either poor execution or selection. For selection errors, the results replicated that observed in Experiment 1. However, unrewarded outcomes attributed to poor execution produced larger amplitude MFN, alongside an attenuation in activity preceding this component and a subsequent enhanced error positivity (Pe) response in posterior sites. In terms of behavioral correlates, only the degree of the early attenuation and amplitude of the Pe correlated with behavioral adjustment following execution errors relative to reward; the amplitude of the MFN did not correlate with behavioral changes related to execution errors. These results indicate the existence of distinct neural correlates of selection and execution error processing and are consistent with the hypothesis that execution errors can modulate action selection evaluation. More generally, they provide insight into how the brain responds to different classes of error that determine future action.Significance StatementTo learn from mistakes, we must resolve whether decisions that fail to produce rewards are due to poorly selected action plans or badly executed movements. EEG data were obtained to identify and compare the physiological correlates of selection and execution errors, and how these are related to behavioral changes. A neural signature associated with reinforcement learning, a medial frontal negative (MFN) ERP deflection, correlated with behavioral adjustment after selection errors relative to reward outcomes, but not motor execution errors. In contrast, activity preceding and following the MFN response correlated with behavioral adjustment after execution errors relative to reward. These results provide novel insight into how the brain responds to different classes of error that determine future action.


Author(s):  
Regina Moro

This chapter explores common issues relevant to addiction that school counselors encounter in their work. Prevalence rates are introduced that provide a context for counselors to understand how common the issue is, whether it is use amongst children/adolescents or in the households the students reside. The brain disease model is explained along with common substances of addiction as well as a discussion of behavioral addictions. Direct and indirect services focused on addiction issues in the schools. Resources for further learning are included at the end of the chapter.


Author(s):  
Helen Keane ◽  
David Moore ◽  
Suzanne Fraser

Author(s):  
David J. Nutt ◽  
Liam J. Nestor

Many of the same behavioural and brain disturbances observed in addiction are also seen in obesity and binge-eating disorder. This suggests that there are shared neural substrates between substance addiction and compulsive food consumption. Food intake and appetite are regulated by numerous appetite hormones that exert their effects through brain systems involved in reward sensitivity, stress, impulsivity, and compulsivity. There is now emerging evidence that appetite hormones (e.g. ghrelin, glucagon-like peptide-1, orexin) can modulate addictive behaviours (e.g. craving) and the intake of alcohol and drugs. Therefore, there is an emerging shift into a new field of testing drugs that affect appetite hormones and their receptors in the brain, and their use in regulating the brain mechanisms that lead to relapse in addiction disorders.


2016 ◽  
Vol 374 (4) ◽  
pp. 363-371 ◽  
Author(s):  
Nora D. Volkow ◽  
George F. Koob ◽  
A. Thomas McLellan

2006 ◽  
Vol 18 (2) ◽  
pp. 132-138 ◽  
Author(s):  
Martin Hasselblatt ◽  
Hannelore Ehrenreich ◽  
Anna-Leena Sir??n
Keyword(s):  

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