Impulsivity is an Independent Predictor of 15-Year Mortality Risk among Individuals Seeking Help for Alcohol-Related Problems

In yesterday’s blog we looked at how AA membership and the 12 step program of recovery helped reduce impulsivity in recovering alcoholics.

We mentioned also that impulsivity was present as a pathomechanism of alcoholism from vulnerability in “at risk” children from families, were there was a history of alcoholism, right the way through to recovering alcoholics in long term recovery (i.e. many years of recovery).

We cited and used excerpts from a study written by the same authors as the study we cite now (1).

This study shows and highlights how, if untreated, by recovery programs such as AA’s 12 steps, that “trait” impulsivity can lead to increased mortality in alcoholics.

This study interestingly shows there is a difference from “state-like” impulsivity in early recovery when recovering people are still distressed and “trait-like” which is after Year 1 of recovery when some of the severity of withdrawal from alcohol has long since abated and some recovery tools have been learnt.

The fact that this impulsivity continues to contribute to relapse and mortality may suggest it is a trait state in alcoholics and possibly a vulnerability to later alcoholism also.

In effect, it illustrates the role impulsivity plays as a pathomechanism in alcoholism, i.e. it is a psychological mechanism that drives addiction and alcoholism forward to it’s chronic endpoint.

Again research shows us how we can learn about a pathology from the recovery from it!


impulse control.preview



Although past research has found impulsivity to be a significant predictor of mortality, no studies have tested this association in samples of individuals with alcohol-related problems or examined moderation of this effect via socio-contextual processes. The current study addressed these issues in a mixed-gender sample of individuals seeking help for alcohol-related problems.


…higher impulsivity at baseline was associated with an increased risk of mortality from Years 1 to 16; higher impulsivity at Year 1 was associated with an increased risk of mortality from Years 1 to 16, and remained significant when accounting for the severity of alcohol use, as well as physical health problems, emotional discharge coping, and interpersonal stress and support at Year 1. In addition, the association between Year 1 impulsivity and 15-year mortality risk was moderated by interpersonal support at Year 1, such that individuals high on impulsivity had a lower mortality risk when peer/friend support was high than when it was low.


The findings highlight impulsivity as a robust and independent predictor of mortality.


…personality traits related to impulsivity (e.g., low conscientiousness) have been identified as significant predictors of poor health-related outcomes including mortality (Bogg and Roberts, 2004; Roberts et al., 2007). Although there is a well-established association between disinhibitory traits and alcohol use disorders (AUDs) (Labouvie and McGee, 1986; McGue et al., 1999;Sher et al., 2000), to our knowledge, no studies have tested these traits as predictors of mortality among individuals with alcohol-related problems or examined moderation of this effect via socio-contextual processes.

Predictors of Mortality Risk among Individuals with Alcohol Use Disorders

Relative to the general population, individuals with AUDs are more likely to die prematurely (Finney et al., 1999; Johnson et al., 2005; Valliant, 1996). Accordingly, several longitudinal studies have aimed to identify the most salient risk factors for mortality in this population (for a review, see Liskow et al., 2000)

…more reliance on avoidance coping, less social support, and more stress from interpersonal relationships increase the risk of mortality among individuals with AUDs (Finney and Moos, 1992; Holahan et al., 2010; Mertens et al., 1996; Moos et al., 1990).

Impulsivity and Risk for Mortality: Relevance for Individuals with Alcohol Use Disorders

Despite the litany of variables that have been examined as predictors of mortality among individuals with AUDs, tests of the significance of individual differences in personality are noticeably absent from this literature. In the clinical and health psychology literatures, however, personality traits have long been identified as possible risk factors for mortality (Friedman and Rosenman, 1959), with low conscientiousness emerging as one of the most consistent, trait-based predictors of poor health and reduced longevity (Kern and Friedman, 2008; Roberts et al., 2007). Conscientiousness is a broad domain of personality reflecting individual differences in the propensity to control one’s impulses, be planful, and adhere to socially-prescribed norms (John et al., 2008).

(previously) no studies in this literature have tested impulsivity as an independent predictor of mortality in a sample of individuals with alcohol-related problems. This is a surprising omission, given that impulsivity is a well-established risk factor for alcohol misuse (Elkins et al., 2006; McGue et al., 1999; Sher et al., 2000) and therefore may be an especially potent predictor of mortality among individuals with AUDs. Furthermore, the role of impulsivity as an independent predictor of mortality risk among individuals with AUDs is relevant from the standpoint of the stage of the alcohol recovery process.

Thus, we sought to examine the impulsivity-mortality link at baseline and one year after participants had initiated help-seeking for their alcohol use problems. At baseline, participants were in a state of distress due to their problematic alcohol use, whereas at Year 1 most participants had obtained help for their alcohol-related problems and reduced their drinking (Finney and Moos, 1995).

Given prior research on acute clinical states and self-report assessments of personality (e.g., Brown et al., 1991; Peselow et al., 1994;Reich et al., 1987), we hypothesized that individuals’ self-reports of impulsivity at Year 1 would be less a reflection of their alcohol problems – and therefore more likely to be independently linked to mortality risk – than their reports at baseline, which may be more closely associated with concurrent alcohol use and problems (i.e., state effects).


…impulsivity at baseline was a significant predictor of mortality risk from Years 1 to 16; however, this effect was accounted for by the severity of alcohol use at baseline. In contrast, impulsivity at Year 1 was associated with an increased risk of mortality over the subsequent 15 years…

In addition, a significant interaction was observed between impulsivity and peer/friend support at Year 1, which suggested that, among individuals high on impulsivity, the mortality risk may be reduced for those high on support from peers/friends. Collectively, these findings highlight impulsivity as an independent risk factor for mortality in AUD samples…

…It is also conceivable that, given participants were in a state of crisis at baseline, their reports of their impulsive tendencies at that time partly captured “state” effects (e.g., psychiatric distress from concurrent substance use; withdrawal symptoms) and therefore were less an indication of their typical or “characterological” pattern of impulsivity, independent of alcohol use. However, at Year 1, most participants had reduced their drinking and were not in a state of crisis; thus, their reports at that time may have been a better reflection of their “trait-like” pattern of impulsivity, which in turn may be a more robust independent predictor of long-term outcomes such as mortality. Accordingly, future studies that seek to test impulsivity as an independent predictor of mortality among individuals with AUDs should consider the stage of the alcohol recovery process.

Moderation of the Impulsivity-Mortality Link via the Social Context

The results of the moderator analyses suggest that the effects of impulsivity on mortality may become manifest through interactions between traits and socio-contextual process (Friedman, 2000). That is, the dire effects of impulsivity on risk for mortality may not reach fruition for individuals who are able to maintain a strong peer support network. Conceivably, by virtue of their strong bond with a high-risk individual, such peers may have sufficient leverage to discourage expression of the individual’s impulsive tendencies and encourage consideration of the long-term consequences of his/her actions.

Such a perspective is consistent with evidence from the AUD treatment-outcome literature that social support networks are a key mechanism by which Alcoholics Anonymous (AA) and other psychosocial treatments can improve long-term drinking-related outcomes (Humphreys and Noke, 1997; Kaskutas et al., 2002).

Furthermore, from the standpoint of treatment, the present findings suggest that interventions for AUDs may benefit from an ecological perspective that considers the contexts in which dispositional tendencies, such as impulsivity, become expressed in individuals’ everyday lives. Notably, based on prior work with this sample, longer duration in AA and alcohol treatment was associated with a decline in impulsivity (Blonigen et al., 2009). In combination with the present findings, it appears that formal and informal help for AUDs may include “active ingredients” that can help curtail expression of impulsive tendencies (e.g., social integration, peer bonding; Moos, 2007,2008) and buffer the otherwise deleterious impact of such tendencies on health and longevity.


1. Blonigen, D. M., Timko, C., Moos, B. S., & Moos, R. H. (2011). Impulsivity is an Independent Predictor of 15-Year Mortality Risk among Individuals Seeking Help for Alcohol-Related Problems. Alcoholism, Clinical and Experimental Research, 35(11), 2082–2092. doi:10.1111/j.1530-0277.2011.01560.x

What recovers in Recovery? – Cognitive Control over emotions?

 In recent blogs we have called for an increase in research into the neurobiology of recovery to add to the extensive research already published on the neurobiology of the addiction cycle.
There has been extensive research into the neurobiology of addiction, most of this has focused on reward and motivation networks of the brain.  In effect this suggests there is a pathological wanting in addicts, an excessive motivation towards drug taking over all other rewarding activities.
This view does not fully consider that this pathological wanting is in itself a product of dysregulated stress systems in the brain, many the product of neglect, abuse and maltreatment in childhood. These stress factors are also reflective of the role of emotional distress in the addiction cycle . This distress is we feel a product of the emotion processing and regulation deficits commonly seen in all addictive behaviours such as alcohol and substance addiction, eating and gambling disorders and sex addiction etc (and often reflective of childhood maltreatment).
In fact , this emotion processing and  regulation deficit is also apparent in certain children of alcoholics and may be a vulnerability to later alcoholism as these children demonstrate a deficit in impulsivity (common to alcoholics and addicts) and a decision making profile based on choosing now over later (short term gains based) and which recruits more subcortical and motor expressive (compulsive) parts of the brain rather than cortical and reflective/evaluative parts of the brain.
This means they make decisions to alleviate the distress of decisions (as undifferentiated emotions appear to be distressing) not via evaluative processes). This has obvious consequence for decision making over a life span.
This emotion dysregulation is also seen in active addicts and alcoholics and at the endpoint of addiction there is a fairly complete reliance of this compulsive decision making profile, which begs the question, does the decision making deficits seen in at risk children simply get worse in the addiction cycle via the neuro toxic effects of substance abuse?
This emotion (and stress) dysregulation also potentiates reward (makes things more rewarding) so alcohol is seen as more stimulating than for non risk children. This vulnerability may lead to the need  to regulate, especially negative, emotions ( and low self esteem ) via the stimulating and highly rewarding effects of alcohol make perpetuate the addiction cycle to it’s chronic endpoint where chronic emotional distress acts as a compulsive stimulus to the responding of chronic alcohol and drug use.
This emotion dysregulation also seems to play a huge part in relapse – so it begs the question does this emotion regulation improve in time via recovery, particularly long term recovery?
In the next two blogs we look at how the emotion regulation areas of the brain become reinforced, strengthened by the process of recovery or in other words we appear to develop the brain capacity for controlling and regulating our emotions more adaptively and this reduces the stress/distress which often prompts relapse.
Personally, I can wholeheartedly say, that the one main aspect I have developed in my recovery has been the awareness and skills in regulating/controlling emotions. Via recovery I have learnt to identify, label, describe by verbalising and sharing with others how I feel. This processes and regulates the emotions that used to cause me so much distress.
I have also developed a more acute awareness of the the emotional expression and needs of yours. These were previously aspects of my life which were completely lacking and frustrating/confusing as a result.
By emotionally engaging in with the world, by becoming more emotionally literate, I can converse with the world in a way that was previously beyond my capabilities.
The research we look at in the next two blogs asks the question – is cognitive control over emotions, lacking in active addiction, one of the main brain functions that improve in recovery?
A core aspect of alcohol dependence is poor regulation of behavior and emotion.
Alcohol dependent individuals show an inability to manage the appropriate experience and expression of emotion (e.g., extremes in emotional responsiveness to social situations, negative affect, mood swings) (1,2). Dysfunctional emotion regulation has been considered a primary trigger for relapse (1,3) and has been associated with prefrontal dysfunction.
While current alcohol dependence is associated with exaggerated bottom-up (sub-cortical) and compromised top-down (prefrontal cortex) neural network functioning, there is evidence suggesting that abstinent individuals may have overcome these dysfunctional patterns of network functioning (4) .
Neuro-imaging studies showing chronic alcohol abuse to be associated with stress neuroadaptations in the medial prefrontal and anterior cingulate regions of the brain (5 ), which are strongly implicated in the self-regulation of emotion and behavioral self-control (6).
One study (2) looking at how emotional dysregulation related to relapse, showed compared with social drinkers, alcohol-dependent patients reported significant differences in emotional awareness and impulse control during week 1 of treatment. Significant improvements in awareness and clarity of emotion were observed following 5 weeks of protracted abstinence.
Another study (7) which did not look specifically at emotional regulation but rather on the recovering of prefrontal areas of the brain known to be involved also in the inhibition of  impulsive behaviour and emotional regulation showed that differences between the short- and long-abstinence groups in the patterns of functional recruitment suggest different cognitive control demands at different stages in abstinence.

In one study, the long-term abstinent group (n=9) had not consumed cocaine for on average 69 weeks, the short-term abstinent (SA) group (n=9) had an average 0f 2.4 weeks.

Relative to controls, abstinent cocaine abusers have been shown to have reduced metabolism in left anterior cingulate cortex (ACC) and right dorsolateral prefrontal cortex (DLPFC), and greater activation in right ACC.
In this study  the abstinent groups of cocaine addicts showed more elevated activity in the DLPFC ; a finding that has also been observed in abstinent marijuana users (8).
The elevation of frontal activity also appears to undergo a shift from the left to right hemisphere over the course of abstinence.  The right is used more in processing (labelling/identifying) of emotion.
Furthermore, the left inferior frontal gyrus (IFG) has recently been shown to be important for response inhibition (9) and in a task similar to that described here, older adults have been shown to rely more on left PFC (10). Activity observed in these regions is therefore likely to be response inhibition related.
The reliance of the SA group on this region suggests that early in abstinence users may adopt an alternative cognitive strategy in that they may recruit the LIFG in a manner akin to children and older adults to achieve behavioral results similar to the other groups.
In longer,  prolonged abstinence a pattern topographically typical of normal, healthy controls may emerge.
In short-term abstinence there was an increased inhibition-related dorsolateral and inferior frontal activity indicative of the need for increased inhibitory control over behaviour,  while long-term abstinence showed increased error-related ACC activity indicative of heightened behavioral monitoring.
The results suggest that the improvements in prefrontal systems that underlie cognitive control functions may be an important characteristic of successful long-term abstinence.
Another study (11) noted the loss of grey matter 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 (12 -14).
It has been suggested cocaine abuse blunts responses in regions important to emotional regulation (15)
Given that emotional reactivity has been implicated as a factor in vulnerability to drug abuse (16)  this may be a preexisting factor that  increased the likelihood of the development and prolonging of drug abuse
If addiction can be characterized as a loss of self-directed volitional control (17),  then abstinence (recovery) and its maintenance may be characterized by a reassertion of these aspects of executive function (18)  as cocaine use has been shown to reduce grey matter in brain regions critical to executive function, such as the anterior cingulate, lateral prefrontal, orbitofrontal and insular cortices (19-24) .
The group of abstinent cocaine addicts (11) reported here show elevations in  (increased) grey matter in abstinence exceeded those of the healthy control in this study 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.
Reassertion of behavioral control may produce a expansion (25)  in grey matter  in regions such as the anterior insula, anterior cingulate, cerebellum, and dorsolateral prefrontal cortex .
All brain regions implicated in the processing and regulating of emotion. 
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19.  Liu X, Matochik JA, Cadet JL, London ED (1998) Smaller volume of prefrontal lobe in polysubstance abusers: a magnetic resonance imaging study. Neuropsychopharmacol 18: 243–252 doi:10.1016/S0893-133X(97)00143-7.
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Recovery: can you feel “Better than Well!”?

Degrees of Recovery?

Better than Well – I love this concept and reality and relate to it myself. This is a reality for many recovery people who feel they had an amplified recovery or in simple terms, people who got better than well!

This people did not simply have the pathology of addiction extracted from their lives. These people did not only go on to recover but went on to live incredibly rich lives in terms of the quality of their lives and the service to their communities.

These are people who talk about addiction and recovery as a blessing! These are individuals who suggest that what they achieved after recovery was not in spite of their recovery but because of the strength they drew out from their addiction recovery.

Their fulfillment of life was greater perhaps than if they had never been addicted and suffered from addiction. Their recovery from addiction gave them a meaning that they may not have had, if they had not been addicts.

I believe I am 25% smarter in recovery (can be proved in terms of exam grades), I understand people now in recovery, I am a more empathetic human being in recovery. My life is immeasurably better than it was before. I have a contentment unknown to me previously. A peace of mind I thought impossible.

My roots grasp a new soil! I feel like I have been reborn.

This kinda fits in also with Bill White’s description of recovery as a method of transcending the self or “getting out of self”. This idea and reality relates to various previous blogs on why we need to live “outside” self regulation” systems of the brain as these appear to have been hijacked by the effects of drug and behavioural addiction.

One way of doing this is by using our self in a different way, to use self to serve others. This way we can use our stories to help others in recovery and improve our own self regulation as it strengthens areas of the brain like the ventromedial pre frontal cortex used in self referential information and emotional regulation.

We can get reward not from drugs or behaviour but by helping others which supplants the depleted dopamine, natural opioids, oxytocin of increased attachment and bonding and the serotonin of well being. It improves our orbitofrontal cortex as we become more empathetic, begin to become emotional literate, reading emotional expression in other’s faces.  It reduces stress and distress. Lowers glutamate and increases GABA. We become less fearful and more serene.

Helping others helps us so profoundly.  It changes the neurobiology and hence neuroplasticity of our brains.

The video ends with a brief look at the “hot flash” spiritual awakening of recovery a la Bill Wilson and  the slower more incremental or “educational” variety of spiritual awakening. For me, spiritual awakening can mean emotional catharsis, sometimes so dramatic that it immediately changes how we think and feel about the world and our place in it or the more experiential, where our views and attitudes to the world gradually change. Each leads to the same goal of long term recovery. The latter being, by far, the most common.


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?