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

Alcoholics Anonymous and Reduced Impulsivity: A Novel Mechanism of Change

Impulsivity or lack of behaviour inhibition, especially when distressed, is one psychological mechanisms which is implicated in all addictive behaviour from substance addiction to behaviour addiction.

It is, in my view, linked to the impaired emotion processing as I have elucidated upon in various blogs on this site.

This impulsivity is present for example in those vulnerable to later alcoholism, i.e. sons and daughters of alcoholic parents or children  from a family that has a relatively high or concentrated density of alcoholics in the family history, right through to old timers, people who have decades of recovery from alcoholism.

It is an ever present and as a result part of a pathomechanism of alcoholism, that is it is fundamental to driving alcoholism to it’s chronic endpoint.

It partly drives addiction via it’s impact on decision making – research shows people of varying addictive behaviours choose now over later, even if it is a smaller short term gain over a greater long term gain. We seem to react to relieve a distress signal in the brain rather than in response to considering and evaluating the long term consequences of a decision or act.

No doubt this improves in recovery as it has with me. Nonetheless, this tendency for rash action with limited consideration of long term consequence is clearly a part of the addictive profile. Not only do we choose now over then, we appear to have an intolerance of uncertainty, which means we have difficulties coping with uncertain outcomes. In other words we struggle with things in the future particularly if they are worrying or concerning things, like a day in court etc. The future can continually intrude into the present. A thought becomes a near certain action, again similar to the though-action fusion of obsessive compulsive disorder. It is as if the thought and possible future action are almost fused, as if they are happening in unison.

Although simple, less worrying events can also make me struggle with leaving the future to the future instead of endless and fruitlessly ruminating about it in the now. In early recovery  especially I found that I had real difficulty dealing with the uncertainty of future events and always thought they would turn out bad. It is akin to catastrophic thinking.

If a thought of a drink entered into my head it was so distressing, almost as if I was being dragged by some invisible magnet to the nearest bar. It was horrendous. Fortunately I created my own thought action fusion to oppose this.

Any time I felt this distressing lure of the bar like some unavoidable siren call of alcohol I would turn that thought into the action of ringing my sponsor. This is why sponsees should ring sponsors about whatever, whenever in order to habitualize these responses to counteract the automatic responses of the addicted brain.

I think it is again based on an inherent emotion dysregulation. Obsessive thoughts are linked to emotion dysregulation.

My emotions can still sometimes control me and not the other way around.

Apparently we need to recruit the frontal part of the brain to regulate these emotions and this is the area most damaged by chronic alcohol consumption.

As a result we find it difficult to recruit this brain area which not only helps regulate emotion but is instrumental in making reflective, evaluative decisions about future, more long term consequence. As a result addicts of all types appear to use a “bottom up” sub-cortical part of the brain centred on the amgydala region to make responses to decisions instead of a “top down” more cortical part of the brain to make evaluative decisions.

We thus react, and rashly act to relieve the distress of undifferentiated emotions, the result of unprocessed emotion rather than using processed emotions to recruit the more cortical parts of the brain.

Who would have though emotions were so instrumental in us making decisions? Two parts of the brain that hold emotions in check so that they can be used to serve goal directed behaviour are the orbitofrontal cortex and the ventromedial prefrontal cortex.



These areas also keep amgydaloid responding in check. Unfortunately these two areas are impaired in alcoholics and other addictive behaviours so their influence on and regulation of the amgydala is also impaired.

This means the sub cortical areas of the amgydala and related regions are over active and prompt not a goal directed response to decision making but a “fight or flight” response to alleviate distress and not facilitate goal directed behaviour.



Sorry for so much detail. I have read so much about medication recently which does this or that to reduce craving or to control  drinking but what about the underlying conditions of alcoholism and addictive behaviour? These are rarely mentioned or considered at all.


We always in recovery have to deal with alcoholism not just it’s symptomatic manifestation of that which is chronic alcohol consumption. This is a relatively simple point and observation that somehow alludes academics, researchers and so-called commentators on this fascinating subject.

Anyway that is some background to this study which demonstrates that long term AA membership can reduce this impulsivity and perhaps adds validity to the above arguments that improved behaviour inhibition and reducing impulsivity is a very possible mechanism of change brought about by AA membership and the 12 step recovery program.

It shows how we can learn about a pathology from the recovery from it!

Indeed when one looks back at one’s step 4 and 5 how many times was this distress based impulsivity the real reason for “stepping on the toes of others” and for their retaliation?

Were we not partly dominated by the world because we could not keep ourselves in check? Didn’t all our decisions get us to AA because they were inherently based on a decision making weakness? Isn’t this why it is always useful to have a sponsor, someone to discuss possible decisions with?

Weren’t we out of control, regardless of alcohol or substance or behaviour addiction? Isn’t this at the heart of our unmanageability?

I think we can all see how we still are effected by a tendency not to think things through and to act rashly.

The trouble it has caused is quite staggeringly really?

Again we cite a study (1) which has Rudolf H. Moos as a co-author. Moos has authored and co-authored a numbered of fine papers on the effectiveness of AA and is a rationale beacon in a sea of sometimes quite controversial and ignorant studies on AA, and alcoholism in general.


Reduced impulsivity is a novel, yet plausible, mechanism of change associated with the salutary effects of Alcoholics Anonymous (AA). Here, we review our work on links between AA attendance and reduced impulsivity using a 16-year prospective study of men and women with alcohol use disorders (AUD) who were initially untreated for their drinking problems. Across the study period, there were significant mean-level decreases in impulsivity, and longer AA duration was associated with reductions in impulsivity…

Among individuals with alcohol use disorders (AUD), Alcoholics Anonymous (AA) is linked to improved functioning across a number of domains [1, 2]. As the evidence for the effectiveness of AA has accumulated, so too have efforts to identify the mechanisms of change associated with participation in this mutual-help group [3]. To our knowledge, however, there have been no efforts to examine links between AA and reductions in impulsivity-a dimension of personality marked by deficits in self-control and self-regulation, and tendencies to take risks and respond to stimuli with minimal forethought.

In this article, we discuss the conceptual rationale for reduced impulsivity as a mechanism of change associated with AA, review our research on links between AA and reduced impulsivity, and discuss potential implications of the findings for future research on AA and, more broadly, interventions for individuals with AUD.

Impulsivity and related traits of disinhibition are core risk factors for AUD [5, 6]. In cross-sectional research, impulsivity is typically higher among individuals in AUD treatment than among those in the general population [7] and, in prospective studies, impulse control deficits tend to predate the onset of drinking problems [811]

Although traditionally viewed as static variables, contemporary research has revealed that traits such as impulsivity can change over time [17]. For example, traits related to impulsivity exhibit significant mean- and individual-level decreases over the lifespan [18], as do symptoms of personality disorders that include impulsivity as an essential feature [21, 22]. Moreover, entry into social roles that press for increased responsibility and self-control predict decreases in impulsivity [16, 23, 24]. Hence, individual levels of impulsivity can be modified by systematic changes in one’s life circumstances [25].

Substance use-focused mutual-help groups may promote such changes, given that they seek to bolster self-efficacy and coping skills aimed at controlling substance use, encourage members to be more structured in their daily lives, and target deficits in self-regulation [26]. Such “active ingredients” may curb the immediate self-gratification characteristic of disinhibition and provide the conceptual grounds to expect that AA participation can press for a reduction in impulsive inclinations.

…the idea of reduced impulsivity as a mechanism of change…it is consistent with contemporary definitions of recovery from substance use disorders that emphasize improved citizenship and global health [31], AA’s vision of recovery as a broad transformation of character [32], and efforts to explore individual differences in emotional and behavioral functioning as potential mechanisms of change (e.g., negative affect [33,34]).

Several findings are notable from our research on associations between AA attendance and reduced impulsivity. First, consistent with the idea of impulsivity as a dynamic construct [18, 19], mean-levels of impulsivity decreased significantly in our AUD sample. Second, consistent with the notion that impulsivity can be modified by contextual factors [25], individuals who participated in AA longer tended to show larger decreases in impulsivity across all assessment intervals.


Blonigen, D. M., Timko, C., & Moos, R. H. (2013). Alcoholics anonymous and reduced impulsivity: a novel mechanism of change. Substance abuse, 34(1), 4-12.

Childhood Maltreatment and later Alcoholism/Addiction

One old timer I know often says two things that I often take issue with – 1. there are as many alcoholisms as alcoholics and that 2. we all come to AA in different boats but end up in the same dock.

Thanks to having a wife in Al Anon I have had the benefit of her insight and from other al-anons who state how remarkably similar we alcoholics are in our behaviour, particularly in dealing/coping with distress and stress, our emotional reactivity and at times immaturity (or so-called defects of character), I disagree that we are so different in our addictive behaviours.

All addictive behaviours from alcoholism, substance addiction, eating disorders to hypersexual disorder seem to be based on an inherent problem with emotion and stress dysregulation.

I believe I have a distress based condition. It results in what appear to be distress based reactions such as perfectionism, distress intolerance and frustration intolerance, normally exemplified in my shouting at my PC when it doesn’t work quickly enough or crashes!

I also believe I have distress based impulsivity, I want that thing, whatever it is, NOW. That anything!

In fact I have noticed when I want something, anything, I end up pathological wanting it in no time at all! It seems then like I NEED it. I too think this is based on distress and heighten stress reactivity.

In fact it is through this pathological wanting that my so-called defects of character that my examples  of emotional dysregulation appear.

If I can’t get what I want, all range of negative emotions spill forth such as intolerance, impatience, arrogance, pride, shame, selfishness etc .  They only appear when I want something and you are getting in the way of me having it!!

So there is a link between my motivation (which is dysregulated due to the effects of chronic stress which turns simple wanting into something more akin to “needing”) and my subsequent emotional dysregulation.

So where does this distress come from? Is it purely the effects of chronic stress dysregulation caused by years of neuro toxic brain damage or does it go back further, into childhood?

I do not think we all have separate alcoholisms, I feel we have remarkably similar reactions to life and these centre on an inherent difficulty regulating stress and emotion.

I also believe we have come to recovery in similar boats. In fact the majority of us have come to recovery in a remarkable similar boat so much so that it would resemble a gigantic ship rather than a boat. That boat is the ship of childhood maltreatment.

Child maltreatment has been frequently identified in the life histories of adolescents and adults in treatment for substance use disorders, as well as in epidemiological studies of risk factors for substance use and abuse.

 Child Maltreatment

One study (1) suggests there is ample evidence exists for higher rates of substance abuse and dependence among maltreated individuals.

In clinical samples undergoing treatment for substance use disorders, between one third and two thirds evince child abuse and neglect histories (Dembo, Dertke, Borders, Washburn, & Schmeidler, 1988Edwall, Hoffman, & Harrison, 1989Pribor & DiWiddie, 1992Schaefer, Sobieragi, & Hollyfield, 1988).

In the US a survey of over 100,000 youth in 6th though 12th grade, Harrison, Fulkerson, and Beebe (1997) Harrison, Fulkerson, and Beebe (1997) found that those reporting either physical or sexual abuse in childhood were from 2 to 4 times more likely to be using drugs than those not reporting abuse; the rates were even higher for youth reporting multiple forms of child maltreatment. Similar findings have been reported by Rodgers et al. (2004) and Moran, Vuchinich, and Hall (2004).

Among youth with Child Protective Services documented maltreatment, Kelly, Thornberry, and Smith (1999) reported one-third higher risk for drug use among those with an abuse history. In a large epidemiological study, Fergusson, Boden, and Horwood (2008) have shown physical abuse and particularly sexual abuse to be related to illicit drug use, as well as abuse and dependence.

Another Study (2) study would suggest the figures are much higher –   data were collected on 178 patients–101 in the United States and 77 in Australia–in treatment for drug/alcohol addiction. The purpose of the study was to determine the degree to which a correlation exists between child abuse/neglect and the later onset of drug/alcohol addiction patterns in the abuse victims. The questionnaire explored such issues as family intactness, parental violence/abuse/neglect, parental drug abuse, sibling relationships and personal physical/sexual abuse histories, including incest and rape. The study determined that 84% of the sample reported a history of child abuse/neglect.

A third study (1) stated that, using the Childhood Trauma Questionnaire-Short Form (CTQ-SF; Bernstein & Fink, 1998; Bernstein et al., 2003) to assess childhood maltreatment in a community sample of active drug users, Medrano, Hatch, Zule, and Desmond (2002) found that 53% of women and 23% of men were sexually abused, 53% of women and 43% of men were physically abused, 58% of women and 39% of men were emotionally abused, 52% of women and 50% of men were physically neglected, and 65% of women and 52% of men were emotionally neglected.

Substance abusers, in addition to having higher rates of childhood maltreatment than members of the general population, have been found to have levels of psychological distress that increase with increasing severity of all types of childhood maltreatment (Medrano et al., 2002). This association is important considering that stress increases an individual’s vulnerability to addiction and addiction relapse (Goeders, 2003; Sinha, 2001;Wills & Hirky, 1996).

There is also evidence that the way in which people cope with stress is related to substance use. For example, researchers have found that greater use of avoidance stress-coping strategies (i.e., disengaging from investing effort to cope with a problem) is related to a greater likelihood of drug use initiation, higher levels of ongoing drug use, and a greater probability of relapse, whereas greater use of active stress-coping strategies (i.e., taking steps to deal with a problem) most consistently functions to protect individuals from substance use initiation and relapse (Wagner, Myers, & McIninch, 1999; Wills & Hirky, 1996).

Childhood maltreatment may influence substance use behavior through its effect on stress and coping. There is emerging evidence that childhood maltreatment may negatively affect the maturation of self-regulatory systems that enable an individual to modulate and tolerate aversive emotional states (Cicchetti & Toth, 2005; Hein, Cohen, & Campbell, 2005). Childhood maltreatment may disrupt neurobiological development and elevate subjective stress by biologically altering the brain’s response to stress (Bugental, 2004;DeBellis, 2002; Heim & Nemeroff, 2001; Heim et al., 2000; Sinha, 2005; Wills & Hirky, 1996). Childhood maltreatment may also affect an individual’s characteristic style of coping with stress so that he or she may be more likely to rely upon maladaptive strategies, such as avoidance of problems, wishful thinking, and social withdrawal, rather than active strategies, such as seeking information and advice from others (Bal, Crombez, Van Oost, & Debourdeaudhuij, 2003; Futa, Nash, Hansen, & Garbin, 2003; Krause, Mendelson, & Lynch, 2003; Leitenberg, Gibson, & Novy, 2004; Thabet, Tischler, & Vostanis, 2004).

Elevated stress and maladaptive coping related to childhood maltreatment may translate to greater substance use behavior by making the coping motives of substance use appear more attractive (Wills & Hirky, 1996). Indeed, substance users commonly report using psychoactive substances such as alcohol, cannabis, and cocaine to cope with stress and regulate affect (Boys, Marsden, & Strang, 2001)

Most cocaine dependent inpatients reported multiple types of childhood maltreatment, and only 15% reported no maltreatment at all, (similar figures to study 2).

“Our findings suggest that the severity of overall childhood maltreatment experienced by recently abstinent cocaine dependent adults has a significant relationship with perceived stress and avoidance coping in adulthood.

Our findings suggest that having a more severe childhood maltreatment history may result in a greater sensitivity to stress…basic coping skills training may not be adequate in decreasing distress and avoidant coping in order to decrease substance use and relapse. Additional interventions that focus on stress tolerance, altering appraisals of stress, stress desensitization, and affect and emotion regulation skills may be of particular benefit to patients with childhood maltreatment histories.

The fact that childhood maltreatment is a preventable phenomenon that occurs early in life and affects psychological functioning well into adulthood makes our findings relevant to clinical practice with children as well. Early identification and treatment of maltreated children may help prevent stress sensitivity or the development of a less adaptive style of coping. Assessment of coping ability and the implementation of coping skills and stress tolerance training may also be indicated for maltreated children in an effort to increase their coping efficacy and decrease their vulnerability to stress later in life.”

I may have been in recovery for a number of years now but coping with stress/distress is still central to my recovery. Dealing with the effects of childhood maltreatment not only via negative self esteem and self schema but in the real sense of coping with every day stress/distress, mainly prompted in my interpersonal relationships (other people!) and with my PC!



1. Rogosch, F. A., Oshri, A., & Cicchetti, D. (2010). From child maltreatment to adolescent cannabis abuse and dependence: A developmental cascade model.Development and psychopathology, 22(04), 883-897.

2. Cohen, F. S., & Densen-Gerber, J. (1982). A study of the relationship between child abuse and drug addiction in 178 patients: Preliminary results. Child Abuse & Neglect, 6(4), 383-387.

3.  Hyman, S. M., Paliwal, P., & Sinha, R. (2007). Childhood maltreatment, perceived stress, and stress-related coping in recently abstinent cocaine dependent adults. Psychology of Addictive Behaviors, 21(2), 233.

Do emotional processing problems run in the family?

Throughout our blogs so far we have looked at who the vulnerability to later alcoholism is transmitted genetic via family members.

The task for science is answering the question – “What exactly is inherited in this vulnerability?”

Again via various blogs we have looked at certain vulnerabilities that we believe contribute to the aetiology of alcoholism (and possible other addictive disorders). These relate to specific emotional processing and regulation problems which we feel not only make alcohol more rewarding for various reasons but also seem to create a decision making profile whereby the inability to properly use emotions to guide decisions making, via not properly recruiting the goal-directed, reflective and evaluative areas of the brain – areas of the prefrontal cortex – and instead recruiting, reactionary, sub-cortical parts of the brain such as the amgydala and dorsal striatum in decision making, to relieve emotional unpleasantness rather than guide adaptive behaviour.

This may be a fundamental difference between those vulnerable to later alcoholism and those who are not, even those in the same family.

If there is a fundamental deficit in decision making this will have numerous knock on effects  obviously and right from the beginning of alcohol use.

So is this borne out in studies? Do studies suggest emotional processing deficits are linked to a family  history of alcoholism. In other words, is this emotional processing deficit, which may lead to later alcoholism, inherited?

One study in particular (1), high alexithymic (50%) patients suffering alcohol use disorders (AUDs)  were more likely to have fathers with alcohol problems…

” Sifneos first described the notion of alexithymia in 1973 [1] as the inability to express emotions or feelings. Alexithymia is mostly seen as a personality construct characterized as a deficit in the ability to cognitively process and regulate emotions [2]. Whereas the prevalence of alexithymia in population-based studies varies between 8% and 15% [3], rates of up to 67% have been reported in patients with alcohol use disorders (AUD) [4] and up to 50% in patients with other substance use disorders (SUD) [5] and [6].

Based on genetic and familial influence, a higher percentage of alexithymia is expected in parents and other family members of alexithymic patients. As alexithymia and alcohol use disorders are related, this could be a reason for more alcohol problems in the relatives of alexithymic patients [4] and [15]. However, in alexithymic patients with SUD or AUD, other genetic, environmental or familial mechanisms could of course have an important role in the alcohol problems of their relatives [19].

As part of an often shared environmental or familial mechanism, problems with alcohol in parents could result in neglecting their child’s emotional states, leading to emotional self-regulation deficits, such as alexithymia. The latter has been shown in a recent meta-analysis on parental bonding and alexithymia [20].

In line with this, a disturbed family functioning has been found to relate to the development of alexithymic characteristics [21]. Similar finding was observed for a history of neglect or sexual abuse, regardless of whether it occurred within the family [22], [23] and [24].

We found that high alexithymic SUD-patients were more likely to have fathers or both fathers and mothers  with alcohol problems compared to low alexithymic SUD-patients. Next, we found that especially paternal family history of alcoholsim (FHA) relates to the degree of alexithymia, independent of disturbed family functioning. The high degree of alexithymia in our abstinent SUD sample is consistent with previous reports [4],[10] and [34]The relationship between alexithymia and these symptoms suggests that the high baseline alexithymia score can at least partially be interpreted as a state phenomenon [4] and [34].




de Haan, H. A., Joosten, E. A., de Haan, L., Schellekens, A. F., Buitelaar, J. K., van der Palen, J., & De Jong, C. A. (2013). A family history of alcoholism relates to alexithymia in substance use disorder patients. Comprehensive psychiatry, 54(7), 911-917.




Thinking You Are Bullet Proof might just Kill You.

Alcohol seemed to fortify me, make me stronger limbed, heroic, thrusting and invincible. With alcohol in me I communed with the Gods.

The blood seemed to flow around my body better, muscles seemed to get enhanced. I was less inhibited, funnier, nicer, more humane, better company. I looked on the world and it’s troubles with a kinder, gladder heart. People sought me out for advice. I was often sage-like. Especially compared to the insecure, disconnected from people, sober me.

People would comment on how transformed I became with the drink, nicer, more trusting, more human, more warmed up and less distant.

Alcohol was my first profound spiritual awakening –  alcohol brought about a profound alteration in how I felt and thought about the world and it’s people. How I acted towards them.  It made me connect with humanity, become a part of, not separate.  It made me exhale and go “phew”.  My wife said the main reason I gave for drinking when I was in the midst of chronic alcoholism was to escape from myself – not to get drunk but to escape the unbearable lightness of being ME.

The second, and most vital and absolutely necessary profound spiritual awakening I had was when I came into recovery via the 12 steps. Then I found a program that also enabled let me go “phew” and also connected me to my fellow human beings. With much less damage and tragedy wrought!

Don’t get me wrong I wasn’t some shy kid, fidgeting in the corner.  I was not. I was not all there, a character, wired to the moon some would say. I was extrovert, but I was also insecure, uncertain, distrusting of people. Sure I was someone who appeared to get  on with people but in a manipulative way. People worried me so I have a whole bundle of strategies to keep them happy, at arms reach. This included my family.

I was also less than whole when sober. Not properly filled in, felt like I was missing something or was protecting some indescribable weakness or deficit in me, although I was never sure want this was, this undefined sense of lacking. Always attending to, protecting some invisible psychic wound.

When drinking I underwent some transformation of spirit. I connected better with my fellow human beings. I became someone I liked more than the sober me. Other people seemed to like the sober me less also and much preferred the company of the wisecracking, fun seeking drinking me.

The drinking me was a shinier, more colourful me, expansive, inclusive, connecting, less manipulative. The sober me was greyer, more insular, cut off and suspicious of people.

When I drank I could drink a lot and rarely had the negative impairments to speech, gait and behaviour that I saw frequently in friends and others.

Alcohol did not make me drowsy or make me want to hug my friends and family. It made me slap people on the back, high five. It was not a sedative it was a major stimulant and much more. A wonderful cocktail of effects. For me it is the most brilliantly designed concoction of effect, and I have tried quite a few other drugs in my time.

In fact it wasn’t a drug to me so much as a homecoming to myself.

If you could mix cocaine with opium in liquid form then that was what  alcohol was me. Not only did it give me a warm glow of absolute well being, in a way no other drug has – although opium was pretty good at that! – it also made me feel that I could conquer the world, that everything was possible. It made me dream big dreams, plan my next imaginary offensive.




Alcohol made me more me! Seemed to make me work better. I became more the  me I wanted to be, that is before  the magic began to dissipate in later years until the point in the end of drinking the alcohol had not affect but to calm the delirium tremens or stave off that imminent alcoholic fit, or momentarily quietened the auditory and visual hallucinations, before reigniting and refuelling them again. Alcoholism gives you many heavenly feelings as it drags you to hell!

The thrill was long gone by this stage. So why did alcohol have this effect. Is it only alcoholics that get this euphoric alive and kicking reaction to alcohol? And for years I got away with the physiological withdrawals and hangovers too. Alcohol made me feel bullet proof, it made me stronger. Invincible, like my internal organs were steam powered and made of metal. That I was beyond human.

In this response to alcohol, in this lack of impairing effects of alcohol, in this thinking I was invincible, that the drink was my greatest ally may well have lain the seeds of my eventually destruction. In this combination of impulsive seeking and stimulative effects of alcohol was an alcohol fuelled propulsion into eventual chronic alcoholism and compulsive addictive behaviours. Alcoholism would never be something I ever had to consider because I was good, very good, at drinking!!


We cite and quote directly from a very interesting article on how a family history of alcoholism contributes to impulsivity, the one psychological domain that turns up repeatedly and is supported in studies of alcoholics, addicts and those at risk genetically from these addictive disorders. Impulsivity from an early age is one variable that appears central to later addictive disorders.

“A family history of alcoholism (FHA) doubles the risk of alcohol dependence (Nurnberger et al., 2004). Beyond the risk for alcohol use disorders, familial alcoholism is also significantly associated with impulsive and externalizing behaviors (Marmorstein et al., 2009)–behaviors thought to be relevant to drinking initiation, escalation, and treatment relapse (Perry & Carroll, 2008).



Impulsive behavior is associated with both alcohol use disorders and a family history of alcoholism (FHA). One operational definition of impulsive behavior is the stop signal task (SST), which measures the time needed to stop a ballistic hand movement.

Stop signal reaction time (SSRT) is distinct from delay discounting, which measures impulsive devaluing of reward as a function of time, the motor impulsiveness assessed by SSRT represents the speed  (or slowness) with which an individual can accommodate an environmental demand to halt a behavior. Using the stop signal task (SST) to quantify SSRT, Nigg et al. (2004) found that alcohol-naïve adolescent offspring of alcoholic fathers had slower SSRTs than children from control families, and that SSRT predicted aggregate future alcohol and drug problems (Nigg et al., 2006).

Twenty two family history positive (FHP; age = 22.7 years, SD= 1.9) and 18 family history negative (FHN; age = 23.7, SD= 1.8) subjects performed the SST in fMRI in two randomized visits: once during intravenous infusion of alcohol. The results showed FHP being less sensitive to alcohol’s effects.

Beyond its potential as a reflection of baseline behavioral impulsiveness, SSRT and inhibition success (but not choice reaction time) are worsened by alcohol intoxication (e.g., De Wit et al., 2000; Fillmore & Vogel-Sprott, 1999).

Thus, as inhibitory control worsens during intoxication, so does ad lib alcohol consumption (Weafer & Fillmore, 2008), speaking to a potential mechanism in the loss of control of drinking.

The principal finding from this experiment (1) was a significant interaction between alcohol exposure and those with family history of alcoholism (FHA) in right prefrontal BOLD activation during motor inhibition. During clamped alcohol infusion, however, this right frontal activation in FHN was significantly reduced, while in FHP activation remained essentially unchanged. Those subjects with a smaller right prefrontal BOLD response during behavioral inhibition (FHN) also tended to need more time (had a longer SSRT) to successfully inhibit their behavioral responses so SSRT may have been lengthened by alcohol infusion.

While we found only an insignificantly smaller difference in frontal responses to correct stop signal responses in FHP subjects, which is consistent with data on another task measuring impulsivity, the Go/No-Go, of Schweinsburg, et al. (2004), which showed only FHN subjects’ activation frontal activation was significantly reduced by alcohol.

Schuckit et al. (1980) first proposed that individuals with FHA are less sensitive to alcohol’s effects. A recent meta-analysis (Quinn & Fromme, 2011) found that, when compared to lower drinkers, heavier drinkers are more sensitive to alcohol’s stimulant effects, and less sensitive to alcohol’s sedative effects.

The data form this study (1)  the data are generally consistent with the concept that FHP subjects are less susceptible to (in this case, the adverse cognitive) effects of alcohol exposure in a brain region that plays an important role in behavioral inhibition.

…a resistance to the cognitively impairing effects of intoxication may carry its own risks, as subjects may perceive a reduced vulnerability to alcohol’s punishing consequences— or in this case the adverse effects in brain systems regulating behavioral control. Thus, the combination of an increased sensitivity to reward and a tolerance to alcohol’s cognitively impairing effects could represent a mechanism of increased risk of progression to heavier drinking, in particular by creating expectancies in drinkers that they can increase their consumption without adverse consequences to their behavior (Vogel-Sprott & Sdao-Jarvie, 1989).”

So to summarise, solely from our own perspective, it may not be the effect of alcohol that prompts  impulsive, loss of control drinking observed in alcohol dependent individuals but impulsivity that prompts drinking behaviour initially and with an apparent lack of cognitive impairment as the result of drinking then leading some individuals to thinking they can “handle the drink” and it negative psychological effects and consequences when, over time and chronic use, it may be progressively contributing to an increased impulsive behaviour to the point where this impulsivity becomes  compulsivity.

It may be that in thinking they are “in control” of drinking and it’s consequences that this paradoxically gives rise to loss of control in drinking via an increased compulsivity but much more on this another time!


1. Kareken, D. A., Dzemidzic, M., Wetherill, L., Eiler II, W., Oberlin, B. G., Harezlak, J., … & O’Connor, S. J. (2013). Family history of alcoholism interacts with alcohol to affect brain regions involved in behavioral inhibition.Psychopharmacology, 228(2), 335-345.


How does the First Drink really get you Drunk?

In treatment circles, I have constantly heard the refrain “one is not enough and two is too many!” and “the first drink gets you drunk” which points to a difficulty certain people have with stopping once they start drinking; a “loss of control” over drinking.

It is as if drinking gives you a thirst rather than taking it away. Many thousands of recovering alcoholics will tell you about this phenomenon – how they had only intended to have a couple but then lost a weekend to drinking instead.

It is an essential question to get to the bottom of, why do certain people not have the ability  or have a reduced ability to stop once they start.

I came across an article from a few years back which addressed this issue (1) .

In those with a family history of alcoholism,  drinking alcohol affects how the brain responds to an alcohol cue – in other words these individuals appear to want more compared to controls when they see alcohol cues. So drinking alcohol heightens a wanting for alcohol  rather than causing a  feeling of having had enough (not wanting). 

Although a family history of alcoholism is the strongest risk factor for developing alcohol dependence, there are few studies of the association between familial alcoholism and the human brain’s reward system activity. This study used a functional magnetic resonance imaging (fMRI) to determine how family history affects the brain’s response to subjects’ preferred alcoholic drink odors (AO).

A family history of alcoholism doubles the odds of developing alcoholism (Hasin et al., 1997; Nurnberger et al., 2004). While environmental influences exert considerable influence in early adolescence, twin studies show an increasingly larger genetic influence by age 18 (Dick, Rose, & Kaprio, 2006), with a family history of alcoholism being a significant factor in the transition from abusive to dependent drinking (Hasin, Paykin, & Endicott, 2001).

While a number of studies have examined the human cerebral response to alcohol-related cues, particularly in alcoholics (e.g., Bragulat et al., 2008; Filbey et al., 2008b;Kareken et al., 2004; Myrick et al., 2008; Tapert et al., 2004;Wrase et al., 2007), very little research shows how familial alcoholism affects the brain response to alcohol-related cues— particularly in at-risk individuals who have yet to become dependent.



Animal research suggests that selective breeding for alcohol preference might affect the heavily dopaminergic mesocorticolimbic reward system. For example, rodents selectively bred to prefer alcohol have reduced dopamine in the striatum (see Murphy et al., 2002; Strother et al., 2005) and medial prefrontal cortex (Engleman et al., 2006), but greater striatal dopaminergic responses to alcohol itself (Bustamante et al., 2008; also see Smith & Weiss, 1999;Weiss et al., 1993). In at least one case, alcohol-preferring rats (compared to Wistar rats) showed a greater dopaminergic response in the ventral striatum during alcohol anticipation (Katner, Kerr, & Weiss, 1996). In non-abusive drinkers without a family history of alcoholism there is greater striatal dopamine receptor availability (Volkow et al., 2006), suggesting a potential protective factor.

Family history affects the brain’s response to alcohol’s olfactory (smell) cues in non-dependent, at-risk heavy drinkers and this study  sought to determine how acute alcohol exposure affects the reward system’s response to alcohol’s conditioned cues by using intravenous (IV) alcohol infusion— a method that prescribes a constant level of brain alcohol throughout functional imaging and avoids the highly variable time courses of breath alcohol concentrations that accompany oral consumption (O’Connor et al., 1998; Plawecki et al., 2007;Ramachandi et al., 2004; Ramchandani et al., 1999).

So in effect alcohol was infused rather than simply drunk.

The researchers hypothesized that a family history of alcoholism would be associated with stronger responses to alcoholic drink aromas in the mesocorticolimbic reward system, and that a low-level of steady-state brain exposure to alcohol would potentiate these stimulus-induced responses (Bragulat et al., 2008). Such a potentiation could reflect a possible substrate for priming, when alcohol exposure increases desire to drink (De WitDe Wit, 2000).

In this study (1) fourteen non-dependent heavy drinkers (HD) who were family history positive (FHP) participated, as did 12 HD who were family history negative (FHN). Subjects were imaged under both alcohol intoxication and placebo.

In this study alcohol intoxication dampened this “cued” response in the HD-FHP but potentiated (heightened)  it in the HD-FHN.

This suggests that a family history of alcoholism and brain exposure to alcohol interact in heavy drinkers to differentially affect how the brain responds to alcohol cues.

In conclusion, frontal regions thought to process reward value may respond differently to alcohol’s classically conditioned cues in subjects with a family history of alcoholism. While alcohol appears to dampen medial frontal responses to alcohol cues in HD-FHP, it may enhance it in HD-FHN. Genetic background may therefore determine when, and under what circumstances, cues activate the reward network


Kareken, D. A., Bragulat, V., Dzemidzic, M., Cox, C., Talavage, T., Davidson, D., & O’Connor, S. J. (2010). Family history of alcoholism mediates the frontal response to alcoholic drink odors and alcohol in at-risk drinkers. Neuroimage,50(1), 267-276.