Brain Recovery Following Alcohol Use Disorders

Since the early promulgation of addiction as a brain disease, I have warned that such a model could increase rather than decrease addiction-related stigma if not also accompanied by a parallel understanding of the neurobiology of addiction recovery (See HERE and HERE). To that end, I joined several colleagues in calling for a recovery research agenda that includes a focus on the degree to which brain functioning is restored during the recovery process (See HERE and HERE). In the intervening years, significant research has illuminated such healing processes and their implications for recovery management. The most significant of this work has been done on alcohol use disorders. The extent to which these findings are applicable to other substance use disorders remains unclear.

Alcohol use disorders (AUDs) are associated with significant cognitive impairment, though not all individuals with an AUD experience such impairment and the degree of impairment can vary widely depending on AUD severity and duration, number of detoxification episodes, and age. Such impairments span several areas related to functional health: attention, memory, problem-solving (e.g., choice generation, choice analysis), impulse control, risk-taking, self-perception, social cue perception, and capacity for empathy. These impairments can pose significant obstacles to recovery and constitute part of the debris of addiction that extends well into the recovery process. Scientific studies to date on changes in AUD-related cognitive impairment following recovery initiation and maintenance reveal four main findings:

Many dimensions of brain functioning improve following recovery initiation, many quite quickly.
Even where full healing does not occur, the brain may achieve “compensatory mechanisms” that enhance cognitive and social functioning.

AUD-related cognitive deficits often progressively remit with duration of recovery stability, particularly among those with 5+ years of sobriety.

Some individuals with AUD experience persistent deficits in cognitive and emotional processing and ability to identify and respond to high-risk social situations—factors that increase risks of strained family and social relationships in sobriety as well as risks for resumed alcohol use and AUD recurrence.

So what are the implications of such findings? I would suggest the following, pending new research on these effects and how they may be reversed.

*Cognitive deficits may limit the degree to which people initiating recovery can acquire and retain information about substance use disorders during the early months of recovery—a finding with significant implications for therapies that rely on a baseline of cognitive functioning, e.g., cognitive behavioral therapy and models of psychosocial education.

*Findings to date add value to condensing and conveying complex ideas into slogans and simple behavioral prescriptions as well as the value of repeated booster sessions and literature to reinforce recovery-supportive information.

*Findings to date suggest the potential value of extended healing sanctuaries (e.g., recovery mutual aid societies, recovery residences, recovery-conducive educational or work environments) that can provide a scaffolding of sustained recovery support while brain healing is progressing and risk of addiction recurrence is at its greatest.

*There is a critical need for research on medical interventions and rehabilitation strategies that can accelerate brain healing within addiction recovery.

If the “hijacked brain” is to be an effective meme or metaphor for conveying the etiology of addiction, then we as a society have a responsibility to also convey four things:

1) whether repossession of a hijacked brain is possible (e, g., it is)

2) when one can expect such repossession to occur (e.g., quickly and progressively for most),

3) how such repossession can be accelerated (yet to be discovered, but I suspect it will be a combination of sustained sobriety, nutrition and dietary supplements, medications, and rehabilitation regimes to enhance cognitive skills), and

4) what does one do in the interim to enhance social functioning and quality of life (e.g., seek recovery-safe space, take steps to enhance global health, develop mechanisms to compensate for limitations, and, where available, seek specialized resources to enhance cognitive rehabilitation).

These findings confirm what Crews and colleagues suggested in their early review of neurobiological healing in alcoholism recovery:

“Improved brain functioning [in recovery] probably arises from neural repair as well as reorganization of brain structural networks and functional strategies. These changes in neuroanatomy, chemistry, and neuropsychology probably contribute to successful recovery from [alcohol] dependence.” (Crews, et al, 2005)

Reference: Crews, F. T., Buckley, T., Dodd, P. R., Ende, G. et al, (2005). Alcoholic neurobiology: changes in dependence and recovery. Alcoholism: Clinical and Experimental Research, 29(8), 1504-1513.

Sources: There is a full recovery research bibliography that includes citations on studies related to brain recovery, but many of these are highly technical.  A recommended single resource for brain recovery in alcohol use disorder is the following: Le Berre, A-P., Fama, R., Sullican, E. V. (2017). Executive functions, memory, and social cognitive deficits and recovery in chronic alcoholism: A critical review to inform future research. Alcoholism: Clinical and Experimental Research, 41(8), 1432-1443.

William (“Bill”) White
Emeritus Senior Research Consultant at Chestnut Health System
Recovery Historian

Read all of Bill White’s Blog Posts on his website here www.williamwhitepapers.com

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Phil Rutherford

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