How the Brain Recovers in Abstinence and Recovery

If addiction is characterized by loss of control over the use of substances and behaviour and a severely diminished self control or volitional control over behaviour is recovery the regaining over control over behaviours?

 

This study (1)  looked at the recovery of grey matter (and brain function in cocaine addicts (CD).  This study used a brain imaging technique called voxel based morphometry (VBM) to assess how local grey matter (GM) volume varies with years of drug use and length of abstinence in a cross-sectional study of cocaine users (presently or formerly inpatients or outpatients at treatment centres) with various durations of abstinence (1–102 weeks) and years of use (0.3–24 years).

“Extensive evidence indicates that current and recently abstinent cocaine abusers compared to drug-naïve controls have decreased grey matter in regions such as the anterior cingulate, lateral prefrontal and insular cortex. Relatively little is known, however, about the persistence of these deficits in long-term abstinence despite the implications this has for recovery and relapse.

Lower grey matter volume associated with years of use was observed for several regions including anterior cingulate, inferior frontal gyrus and insular cortex. Conversely, higher grey matter volumes associated with abstinence duration were seen in regions that included the anterior and posterior cingulate, insular, right ventral and left dorsal prefrontal cortex. Grey matter volumes in cocaine dependent individuals crossed those of drug-naïve controls after 35 weeks of abstinence, with greater than normal volumes in users with longer abstinence.

The asymmetry between the regions showing alterations with extended years of use and prolonged abstinence suggest that recovery involves distinct neurobiological processes rather than being a reversal of disease-related changes. Specifically, the results suggest that regions critical to behavioral control may be important to prolonged, successful, abstinence.

Findings suggest a cumulative effect of cocaine use wherein the longer the period of substance use the lower the grey matter volume [22]. That these effects were observed in abstinent users is consistent with prior reports of GM deficits in alcoholism that last from 6–9 months to more than a year or, in some reports, up to at least 6 years following abstinence [42][44].

Similarly, decreased GM as a function of years of use of heroin [6], [45], [46] and cocaine [15] have previously been reported. in regions important to emotional regulation…given that emotional reactivity has been implicated as a factor modulating vulnerability to drug abuse [49], this may have been a preexisting factor that served to increase the likelihood of the development and prolongation of drug abuse.

If addiction can be characterized as a loss of self-directed volitional control [22], abstinence and its maintenance may be characterized by a reassertion of these aspects of executive function [24]

Current cocaine users demonstrate reduced GM in brain regions critical to executive function, such as the anterior cingulate, lateral prefrontal, orbitofrontal and insular cortices [6][11]. In contrast, the group of abstinent CD users reported here show elevations in GM as a function of abstinence duration that exceeds control levels after 36 weeks, on average, of abstinence. One possible explanation for this is that abstinence may require reassertion of cognitive control and behavior monitoring that is diminished during current cocaine dependence [11], [50], [51].

 

We, and others, have previously hypothesized that drug abusers may develop increased cerebellar activity to compensate for reduced prefrontal activity in tasks demanding elevated levels of cognitive control [52], [53] and that this may play a role in maintaining abstinence [24]. Reassertion of behavioral control may produce a practice-related expansion [54] in GM regions such as the anterior insula, anterior cingulate, cerebellum, and dorsolateral prefrontal cortex and is consistent with our previous reports of elevated activity levels, compared to controls, in long-term abstinent substance users [24], [55].

 

It should be noted that we also observed regions displaying increased GM with abstinence in bilateral cingulate gyri that did not overlap with those showing decreased GM with years of use. This suggests that the brain is capable of compensating in response to changes in demands, such as the maintenance of abstinence [54], [76].”

It would have been interesting to correlate the findings of this type of research with more information on the treatment undertaken, e.g. was it a 12 step facilitation treatment, to assess the nature of this behaviour-based neuro-plasticity. We need more research into translating the elements of “how it works” into the areas of the brain to observe where it works. In other words how do new attitudes and behaviours shape the brain literally. How does the brain recover volume, connectivity, functionality via behavioural change?

The brain areas which regain volume are implicated also in emotion regulation. It is interesting that the authors point to a possibility that the decreased brain volume in certain areas regulating emotion may also be a pre-existing condition, or in other words, a vulnerability to later addiction risk.

It may be that in recovery some of us learn to master or at least attempt to manage and control emotions in a way we could not previously.

For us this is an essential part of the pathomechanism of addictive  behaviours,  this emotion processing and regulation deficit; a deficit we learn to overcome in recovery. An unmanageability that we learn to manage in recovery.

In our next blog we will look at how these emotional factors drive the addiction cycle to it’s chronic endpoint.

We will look at how emotional dysregulation around forgiveness has contributed to a need to continually distance ourselves chemically from the incidents that needed our forgiveness. It will also look at how forgiveness itself is a emotional regulation strategy in itself, just like “letting go” is. We learn so many emotion regulation strategies in recovery and these appear essential to long term recovery.

References

1. Connolly, C. G., Bell, R. P., Foxe, J. J., & Garavan, H. (2013). Dissociated Grey Matter Changes with Prolonged Addiction and Extended Abstinence in Cocaine Users. PLoS ONE, 8(3), e59645. doi:10.1371/journal.pone.0059645

 

 

Recovery – a need for change?

A need for change?

Addiction is a chronic condition but is treated as if it was an acute disorder. Treatment has become disconnected from the longer processes of recovery. Hence is there a need to redesign “treatment” to address the reality that recovery is a long process, not something that can be treated in weeks or months? Should there be a greater focus on interpersonal and family relationships, especially as they are demonstrated to be a major reason for relapse.

Toward a new Recovery Paradigm?

What do we know about this thing called recovery?

First we have to define recovery, so let’s start with “What is recovery?”  Do we need to move from a pathology and treatment paradigm to a recovery paradigm? Although it is feasible that these paradigms could be interlinking? Or at least considered more than at present.

At present we focus almost exclusively on what is wrong with addicts not how they get better via recovery and the ways in which they get better too? We need more research to evaluate the processes in recovery, the different types of recovery, we need research into the success of recovery, i.e. how many people actually recover, the durability of recovery etc.

We need to clearly say where we are headed and what we can hope for by coming into recovery!

We could fill libraries with what we know about the neurobiology of addiction but barely a library shelf with what we know about recovery from addiction.

 What exactly do we know about the neurobiology of recovery?

In recovery are there any ways recovering persons can help with altering vulnerabilities, such as developing the verbalising of emotion, to help with emotion processing and regulation which we know have a aetiological influence of the risk of later addiction?

In short can we affect the epigenetics of addiction (how genes are expressed in environments) by recovery? Can we reduce the stress that potentiates dopamine and reward and acts as a vulnerability to adolescent drinking which in itself is linked to later alcoholism? Can we counter the child maltreatment and insecure attachment that propels addiction?

So many questions remain unanswered. Can the people who suffer addiction, in recovery, be the most potent agents in actually affect vulnerability to later addiction? Can certain, seemingly unavoidable eventualities be addressed and changed?

Can our recoveries help our at risk children? Can we modify the effects of genetic inheritance? Is it inevitable that addiction occurs, can it not be “treated” in early childhood. Can we intervene to disrupt or alter the course of addiction?

This is the research question of the next decade?