Inability to make fine-grained distinctions regarding negative emotions prompts impulsivity.

When I first came into recovery I was assigned a task which has gone on to shape much of my thinking about my alcoholism and addiction. I was prompted by my wife to sit with my emotions, that is, to sit in one place beside my wife and not suddenly get up and go elsewhere to avoid whatever emotional state consumed me, terrified me.

I have to say it was the bizarre experience. In my drinking any negative emotions would prime my thoughts towards alcohol and any increased intensity of such thoughts would practically have me skipping to the nearest drinking establishment.

Ever since I was a child, emotions were something to be avoided, tamed or feared. They were destructive, counterproductive things which somehow weakened you.

Now I was being asked to do something I had never accomplished in over thirty years. To sit with, not run from, whatever emotions starting to arise in my mind. As the first undifferentiated blobs of emotions arose I was struck my how I could not recognise them or say with any conviction what emotions they were exactly. In this undifferentiated state they felt like waves of feeling, like possessions, like being haunting by mute poltergeists!

The urge to flee these unpleasant feeling states was overwhelming. I asked my wife for help “what was happening to me!?” “What are these feeling things?”

My wife calmly said they are simply feelings, you are experiencing emotions in their entirety. It was horrible. How the hell had I not done this before, sat with my emotions instead to constantly escaping them somehow?

In fact, I am willing to say that I knew next to nothing about emotions when I arrive in recovery. These is why they have come to fascinate me and inspired my research into affective and clinical/psychiatric neuroscience.

How is it that a grown man got to this stage, to the stage where all his undifferentiated emotions propelled him into movement away from them?

The answer to this question may have been demonstrated in this study (1).



“Affective functioning plays a prominent role in several etiological models of substance use (e.g., Kassel et al., 2010; McCarthy, Curtin, Piper, & Baker, 2010; Simons, Wills, & Neal, in press). These models suggest that individuals with poor affect regulation show a diminished capacity to handle intense emotion states and often rely upon maladaptive coping strategies, such as substance or alcohol use, to manage their emotions (Lavallo, 2007; Spence & Courbasson, 2012).

One factor related to emotion regulation is emotion differentiation. Emotion differentiation is the ability to make fine grained distinctions between similarly valenced emotion states (Feldman Barrett, 2004). Individuals differ greatly in their ability to differentiate their affective experiences. Some tend to describe their emotional experiences in more global terms, such as feeling “good” or feeling “bad” and find it difficult to make more subtle distinctions, while others make these nuanced differentiations easily. These differences have been shown to impact the ability to regulate emotions and consequential behaviors (Feldman Barrett, Gross, Conner Christensen, & Benvenuto, 2001; Tugade, Fredrickson, & Feldman Barrett, 2004). In support of this, emotional differentiation has been shown to moderate associations between negative emotion and alcohol consumption (Kashdan, Ferssizidis, Collins, & Muraven, 2010).

This research suggests that the inability to differentiate emotion may foster maladaptive behavior when emotionally aroused.

Hence, it is possible that the inability to differentiate emotions may
be related to urgency, defined as rash action in response to intense emotion. Along these lines, research on alexithymia, a construct related to deficits in identifying and describing emotions, shows that these deficits are positively associated with urgency, with urgency often fully mediating the relationship between alexithymia and problematic outcomes, including alcohol consequences (Gaher, Hofman, Simons, & Hunsaker, 2013; Shishido, Gaher, & Simons, 2013).

Moreover, alexithymia has been shown to mediate the relationship between childhood maltreatment (Gaher, Arens, & Shishido, 2013) as well as trauma history
(Gaher, Hofman, et al., 2013) and urgency, suggesting that deficits in
emotional understanding may underlie urgent responding.

The findings of this study (1) showed that negative emotion differentiation was associated with both negative urgency and alcohol which suggests that the inability to make fine-grained distinctions regarding the experience of negative emotions contributes to behavioral disinhibition when in a state of high emotional arousal.


1. Emery, N. N., Simons, J. S., Clarke, J. C., & Gaher, R. M. (2014). Emotion Differentiation and Alcohol-Related Problems: The Mediating Role of Urgency.Addictive Behaviors.


“I don’t know how I feel, therefore I act!”

One of my pet hates in experimental study is researchers suggesting that one can generalise findings from a non-clinical group of participants in a particular study to a clinical  group, not in the study. For example, most studies in Psychology and in Neuroscience are conducted on very well informed, healthy undergraduate Psychology students with the suggestion that the findings will also be seen in a clinical groups such as alcoholics or addicts. That the findings have ecological validity, they will also be observed in the reality of addicts in real everyday life.

Obviously this is very controversial. How can you one really say that brain processes in a perfectly healthy undergraduate psychology student are similar to those suffering from a mental disorder such as addiction?

It is clear that the behavioural responses of someone with an addictive disorder will be different to those with a perfectly healthy adaptive brain and adaptive behavioural choices. The point of addiction, is that individuals with an addictive disorder often make maladaptive choices and make poor decisions as many brain processes and mechanisms have become chronically impaired. They tend to choose now over then, be very emotional reactive, use “fight or flight” responding to situations rather than reflective, evaluative, goal-directed, action-outcome type of thinking…the list goes on and on, believe me!

In other words, they tend to act in a very different way to healthy undergraduate studies!

I do not have a problem with using undergraduate studies but please do not attempt to generalise findings to a clinical group, or in other words, a group suffering a psychiatric disorder. It is like saying that a study observed in healthy 19-20 year olds could also be said to exist or occur in middle aged schizophrenics? Most rational people would view this as quite peculiar, to say the least. So why do this very same thing with those suffering another mental disorder, called addiction?



So why do it at all, use students as participants? Well the study I refer to in this blog shows why using a student sample may have utility. If nothing else this sampling of students provides a control group – that is a group that can act as a “healthy” group compared to a later study  which has used a clinical group as participants. This way we can compare results to observe differences in both sample groups and this can highlight fundamental differences (and sometimes similarities) in healthy and clinical groups and may help highlight specific difficulties which may need to be considered in treating these clinical groups.

Also, and importantly for our overall discussion, through many of our blogs thus far,  regarding the role of emotional processing deficits in impulsivity and decision making deficits in addiction, this type of study can look at “proof of concept” which can then be studied in clinical groups such as those with addictive disorders.

But one must also have the proviso that generalising to this clinical group is not without it’s pitfalls. Just because a certain behavioral manifestation is seen in one healthy group, which has also been seen in a more severe from in a clinical  group , it does not follow that this severity is simple down to using a substance more chronically.

Severity may also be a function of genetic expression within a specific type of environment, e.g. a genetic vulnerability in an “at risk” son of an alcoholic reared in a emotionally abusive background may be a main reason for certain behavioural manifestation rather than simply chronic substance use. Altered stress systems may represent in a similar manner to the chronic toxic effects of chronic drug use but not actually be driven by the same mechanisms or underlying processes.

Regardless on these many sensible caveats, it is still possible to look at certain psychological  traits and relate them to certain behaviours before testing whether these are also observed in a clinical  group such as those with addictive disorders.

The study we refer to here (1) used a large sample of 429 undergraduate students and examined the nature of the relationship between alexithymia and impulsivity.  “Alexithymia is a multifaceted personality construct that is characterized by difficulty identifying and describing feelings  (Taylor, 2000). Alexithymia is associated with a range of disorders, many of which are associated with poor impulse control (Parker, Wood, Bond, & Shaughnessy, 2005; Thorberg, Young, Sullivan, & Lyvers, 2009).
The development of emotional awareness and skills to express feelings are strongly linked to cognitive development because humans use language to identify and express their feelings. According to Taylor, Bagby, and Parker (1997), all individuals have emotions (i.e., neurophysiological arousal), but how we feel the emotions differ
based on our subjective cognitive understanding and experiences.
Without adequate words to describe various neurophysiological stimuli, we cannot feel (identify and describe) them accurately and precisely, and thus we have difficulties regulating our behaviors that follow the emotions (Lane & Schwartz, 1987; Taylor et al., 1997).
The emotional awareness theory presented by Lane and Schwartz (1987) has provided some explanations for the development of alexithymia (Taylor, 2000; Taylor et al., 1997). According to this theory, individuals with alexithymia are considered to be on the first two levels of emotional awareness (i.e., sensorimotor reflexive and sensorimotor enactive) as their abilities to cognitively identify
various feelings precisely by recognizing specific physiological signs of emotions are not yet fully developed (Taylor et al., 1997).
Perhaps, lack of cognitive representations for neurophysiological stimuli may make individuals with alexithymia distressed…and thus they may use alcohol to alleviate their discomfort (Kauhanen et al., 1992; Thorberg et al., 2009; Uzun, 2003)… impulsive individuals tend to rely on reflexive affective (emotional) processes rather than on reflective cognitive processes, to lead their behaviors (Lieberman, 2007; Metcalfe & Mischel, 1999)… impulsivity and alexithymia research emphasize the necessity of using reflective and sophisticated cognitive processes in order to
better regulate emotions and behaviors (Carlson, 2007; Cyders & Smith, 2008)… it is plausible that alexithymia and impulsivity are related under a higher order structure, namely neuroticism, and thus they robustly predict behaviors associated with emotion dysregulation.

This study demonstrated that individuals with alexithymia are more likely to act impulsively when experiencing heightened negative affect…and thus engage in more drinking or experience more negative consequences after drinking.



These results support the use of treatment models that emphasize awareness of feelings and psychological mindfulness as these treatment approaches help clients learn to identify and acknowledge their feelings first, in order to learn how to better regulate them. The results indicate that deficits in the cognitive representation of emotional experience may contribute to impulsive action when emotionally aroused. The current findings may help explain why alexithymia has been identified
as a risk factor for many psychological problems that involve emotional and behavioral regulation deficits, including substance use related disorders (Kauhanen et al., 1992; Troisi et al., 1997).”

Essentially this study on undergraduates has observed similar findings as seen in addicted individuals but this does mean the findings generalise. It means that there is theoretical utility in further exploring this link between emotional processing deficit, alexithymia, the psychological trait of impulsivity and the behavioural manifestation of chronic addiction. Finally it may also be possible by scrutinizing results to identify key differences between these two samples which may aid treatment, intervention and even prevention. We have often mentioned that prevention may in the future involve the identification of emotional processing and regulation deficits in “at risk” children and helping them process emotions more adaptively and effectively.

Addiction seems even more tragic if one considers addiction as the consequence of processes that could possible be rectified or improved in early childhood. Emotional dysregulation heightens the effects of drugs and alcohol also and sets up a viscous cycle of use that often leads to chronic addiction.

It may be the source or rather the heart of the problem.  Prevention would then need to act at the heart of this disorder.



Shishido, H., Gaher, R. M., & Simons, J. S. (2013). I don’t know how I feel, therefore I act: alexithymia, urgency, and alcohol problems. Addictive behaviors, 38(4), 2014-2017.

Feeding Distress-based action.

Even as I a child I had difficulties controlling my impulses and my behaviours, “I was into everything”. I did not use much forethought in decisions making and would generally react and always be after something that I wanted desperately that very moment. Now in fact!

I believe I had sugar addiction, and chocolate and playing, and girl chasing addictive behaviours way before I ever got near alcohol in my early teens, with a six month, and quite disastrous period of poker machine gambling in between. And of course you couldn’t get me off the “Space Invader” machine.  I just couldn’t get enough of anything, ever. Always wanted more, more and some more. My mother would call for me to come home in the darkening hours of evening. I had to be scraped off the playing fields in order to come home. Exhausted.

So why this constant overdoing of everything!!?

Why couldn’t I stop once in a while, ponder the consequences of my decisions, employ some, goal-directed, action-outcome type of thinking?

Following on for our very recent blog which described the neural mechanisms implicated in negative urgency we now look at at an article which attempts to  bring together some of our most consuming research interests by attempting to explain whether there is  a  link between emotional processing deficits (alexithymia)  negative urgency and dysregulated behaviours.

This study (1) looked at whether whether negative urgency (distress-based impulsivity)  would be the link in relationship between alexithymia and dysregulated behaviors.

Dysregulated behaviors have been defined as behaviors that are difficult to control, and often  result in functional impairment for the affected individual (Selby & Joiner, 2009).

An inability to understand affective and physiological experiences inherent in alexithymia might prompt individuals to engage in maladaptive behaviors in an effort to regulate emotions. One type of behavior linked to alexithymia is binge eating. Wheeler and colleagues (2005) found that alexithymia was positively correlated with binge eating in a sample of females.

Carano and colleagues (2006) found that alexithymia was positively correlated with the severity of binge eating behaviors. Additionally, Speranza and colleagues (2007) found that alexithymia predicted eating disorder treatment outcome in a three year prospective study meaning high levels of alexithymia can interfere with treatment response even more than the actual severity of the presenting problem.



Taylor and colleagues (1990) found that 50% of substance dependent males admitted to a drug and alcohol rehabilitation program were characterized as alexithymic. Similarly, Haviland and colleagues (1988) found that approximately 50% of individuals diagnosed as alcohol dependent were characterized as alexithymic. These numbers are significantly greater than the reported prevalence of alexithymia in the general population, which has been estimated to fall between 10 and 15% (Rybakowski et al., 1988; Parker et al., 1989), and suggests that alcohol and drug abuse is another example of a maladaptive behavior that may be used to modulate negative affective states when one is incapable of doing so in an adaptive way.

Loas and colleagues (1997) conducted a one year follow-up on individuals admitted to a psychiatric facility for alcohol treatment. Results suggested that individuals who remained abstinent from alcohol use one year post-treatment had
significantly lower scores on alexithymia measures.

“Why does the lack of understanding and expression of emotions have such a powerful influence over dysregulated behaviors?” 

Why  do individuals with high levels of alexithymia who experience negative affect seem to engage in dysregulated behaviors so frequently, while other individuals may simply cry, ruminate, or develop vegetative symptoms of depression?

Is negative urgency (Whiteside & Lynam, 2001; Cyders, Smith, Spillane, Fischer, Annus, & Peterson, 2007) the mechanism through which these behaviors are developed  and sustained?     It may be that the relationship between alexithymia and behavior is explained by a tendency on the part of individuals with high levels of alexithymia to act rashly in an attempt to immediately reduce psychological and physiological sensations associated with negative affect (negative mood, negative emotions, anxiety etc).

Negative urgency could be thought the  mechanism that drives dysregulated behaviors in individuals who experience difficulty recognizing and expressing their emotions.  


The authors (1) concluded that when faced with negative affect, many individuals are able to recognize and process their emotions adaptively. However, if people are not able to identify or describe their emotions (the very definition of alexithymia), our results suggest that this confusing affective experience may be quite upsetting (or unpleasant) and could lead to negative urgency, or a tendency to act rashly when they experience any type of negative affect.

High alexithymia individuals appear to be highly motivated to alleviate negative affect, regardless of the consequences. It may be that the emotional confusion inherent in alexithymia prompts individuals high on negative urgency to engage in dysregulated behaviors, by acting out either
against themselves or others.


As we mentioned in our previous blog  emotional processing deficits are common in addiction and in other dysregualted behaviours and these deficits may not recruit the goal-directed parts of the brain. They do not guide action or choices effectively. As a result they manifest in perhaps crude, undifferentiated or processed forms as distress signals instead and recruit more limbic, motoric regions of the brain.  Hence they are not used to anticipate future, long term consequence.

We disagree that it is not simply negative affect that prompts negative urgency but rather the chronic stress dsyregulation underpinning the manifestation of negative affect.

We are simply adding that as addiction becomes more chronic, so does stress and emotional distress and this appears to lead to a distress-based “fight or flight” responding to decision making. Addicts increasing appear to recruit sub-cortical or limbic areas in decision making and this is prevalent in abstinence as in active using. It is the consequence of chronic emotional and stress dysregulation.

References for this blog

Fink, E. L., Anestis, M. D., Selby, E. A., & Joiner, T. E. (2010). Negative urgency fully mediates the relationship between alexithymia and dysregulated behaviours. Personality and Mental Health, 4(4), 284-293.

Do alcoholics drive through life with Faulty Brakes!

There has been a lot of debate in the last thirty – forty years about genetic inheritance – with at least half of children of alcoholic families at risk for later alcoholism. What is less known is what exactly is inherited in our genes? What marks us out for later alcoholism? Prior to drinking are there aspects of our behaviour, personality or emotional responding that marks us out compared to so-called normal healthy types.

Recently research has looked at brain systems which overlap in decision making such as cognitive control over impulsive behaviour and also emotional processing. Children from alcoholics seem to have difficulties with both these overlapping circuits in the brain – they are not only impulsive but also do not seem to process emotions in the same way their “health” peers do. Research has also begun  to show that emotional processing is indeed important to making decisions, as is the ability to inhibit impulsive responses.

It seems  young alcoholics in the making, are not using our emotions  to make decisions and  are also prone to being impulsive. This difficulty with making decisions must shape all other future decisions ?

Youth for families with a history of alcoholism (FH+) are more likely to engage in early adolescent alcohol use (1), they may be more prone to experience the neurotoxic effects of alcohol use during adolescence.


Heavy alcohol use during adolescence is related to poorer neuropsychological functioning, including response inhibition (2), working memory (3-5), and decision-making (6).

Neuroimaging studies have shown that alcohol abusing teens have atypical grey matter volume in the PFC (7,8), and subcortical structures, such as the hippocampus (9,10) OFC and the amgydala.

Further, they have reduced integrity of white matter pathways, in both long-range connections between frontal and parietal brain regions as well as in pathways connecting subcortical and higher-order brain areas (11,12).

FMRI studies have found reduced BOLD response in adolescent alcohol abusers
in brain regions important affective decision-making (13).

The raging debate in research has been to whether these deficits are a consequence of heavy alcohol use or if genetic and environmental factors, such as family history of alcoholism, may contribute.

Risk Factor for Alcohol Use Disorders (AUDs): Family History of Alcoholism

The observation that alcoholism runs in families has long been documented
(14-16). Over the past few decades, adoption (17,18) and twin (19)
studies have suggested that there is an increased likelihood of individuals with a family history of alcoholism to develop the disorder themselves (20, 21).

These studies indicate that familial alcoholism is one of the most robust predictors of the development of an AUD during one’s lifetime. Furthermore, this risk factor appears to be stable over time, since it also predicts the chronicity of alcohol dependence at multiple time points (22).
This indicates that higher familial density is often associated with greater
risk (23), with genetic vulnerability accounting for about 30-50% of
individual risk (24-26).


One of the best characterized findings in individuals with familial alcoholism are greater impulsivity and difficulties in response inhibition which are commonly seen in this population (27,28), and FH+ individuals are less able to delay reward gratification compared with their peers (29).

Emotional processing and its relationship with executive control has received much less
attention in FH+ individuals.

Alcohol Use Disorders and Emotional Processing

Emotion Recognition and Affective Processing – Research suggests that alcohol use disorder (AUDs)  are associated with deficits in emotion recognition
(30-33), which may be related to atypical brain structure and functioning observed in the
limbic system among alcoholics (34-37).

Alcoholics not only tend to overestimate the intensity of emotions seen in faces  but they also make more negative emotional attributions and often confuse one emotion for another, such as mislabeling disgust as anger or contempt (32). Additionally, these deficits seem to be specific to alcoholism, since alcoholics, both recently abstinent and long-term abstinent, perform poorer on emotion recognition tasks than individuals with other drug abuse history (38). Alcoholics have also been shown to have slower reaction time when recognizing emotions (39).
Furthermore, poorer accuracy on emotion recognition tasks in alcoholics does not improve across the duration of the task, even though better performance is seen over time with other drug abusers (38).

Polysubstance abusing adults, the majority of whom were alcohol abusers, showed emotion recognition deficits on angry, disgusted, fearful, and sad faces (40). Based on the evidence of emotion recognition deficits in alcoholics, it is necessary to determine whether similar difficulties are present in FH+ youth that could be disruptive to emotional functioning and may contribute to the ultimately higher prevalence of alcohol abuse in this population.

Ultimately we may be observing here external emotional processing difficulties in the same manner we observed “internal” emotional processing difficulties in those with alexithymia, the reduced ability to “read” internal emotions of which a majority of alcoholics appear to suffer.

In summary, alcoholics and children of alcoholic families appear to have both external, i.e. recognition of other people’s emotions as well as their own and these may relate to immature development of brain regions which govern emotional, processing, recognition and regulation, which appears to contribute greatly to the initiation and progression of alcohol abuse.


In addition to emotional processing deficits, alcoholics have various structural
and functional abnormalities in affective processing brain regions. Studies of the limbic system have found reduced volume in subcortical structures, including the amygdala, thalamus, ventral striatum, and hippocampus among adult alcoholics (41,42). Alcoholics with smaller amygdalar volumes, are more likely to continue drinking after six months of abstinence (37).

Marinkovic et al. (2009) alcoholics exhibited both amygdalar and hippocampal hypoactivity during face encoding, and when recognizing deeply encoded faces, alcoholics had significantly reduced amygdalar activity to positive and negative emotional expressions compared with controls (35). These results help explain findings in behavioral studies of alcoholics that have found considerable evidence for emotion recognition deficits in this population.

Furthermore, during emotion identification, alcoholics showed comparable
performance to controls, but had reduced brain response in the affective division of the
anterior cingulate cortex (ACC) to disgust and sadness, with this lack of affective response to aversive stimuli believed to underlie disinhibitory traits in AUDs (36).

There is also evidence to suggest that non-alcohol abusing FHP individuals
share similar deficits in affective systems to alcohol abusers, including reduced
amygdalar volume, less amygdalar activity in response to emotional stimuli, and high
rates of internalizing symptoms such as anxiety and depression (37; 45-47).

Furthermore, research examining the relationship between emotional
processing and cognition has found that poor inhibition in individuals with co-morbid
substance and alcohol abuse is associated with atypical arousal in response to affective images (48), and affective measures in FH+ alcoholics also relate to deficits in executive functioning, e.g impulsivity (47).

This suggests that familial history of AUDs may put individuals at greater risk for problems with emotional processing and associated disruptions in executive functioning (47), which could, in turn, increase risk for alcohol abuse (49).

As we suggested previously, in relation to decision making profiles, in those at risk, those with alexithymia and also with cocaine addicts, decision making often involves more emotion expressive-motor areas of the brain like the caudate nucleus which is more of a “feel it-do it” type of reaction to decision making or a emotionally impaired or distress-based impulsivity. If there is a difficulty  processing emotions, these emotions can not be used as a signal to guide adaptive, optimal decisions. Decisions appear more compulsive and short term.

It may be this tendency to act now, rather than later,  that defines the vulnerability in FH+ children. It is like driving through life with faulty brakes on decision making, which sets up a chain of maladaptive choices such as alcohol abuse which then damages these affective based decision making regions of the brain even more, with increasing  deleterious consequences as the addiction cycle progresses until the endpoint of addiction of very limited choice of behaviour as emotional distress acts eventually as a stimulus response to alcohol use.  Emotional processing usurped by compulsive responding.



Main reference – Cservenka, A., Fair, D. A., & Nagel, B. J. (2014). Emotional Processing and Brain Activity in Youth at High Risk for Alcoholism. Alcoholism: Clinical and Experimental Research.

1.  Dawson, D.A., 2000. The link between family history and early onset alcoholism: earlier initiation of drinking or more rapid development of dependence? J Stud Alcohol 61, 637-646.

2. Ferrett, H.L., Cuzen, N.L., Thomas, K.G., Carey, P.D., Stein, D.J., Finn, P.R., Tapert, S.F., Fein, G., 2011. Characterization of South African adolescents with alcohol use disorders but without psychiatric or polysubstance comorbidity. Alcohol Clin Exp Res 35, 1705-1715.

3. Brown, S.A., Tapert, S.F., 2004. Adolescence and the trajectory of alcohol use: basic to clinical studies. Ann N Y Acad Sci 1021, 234-244.

4.   Brown, S.A., Tapert, S.F., Granholm, E., Delis, D.C., 2000. Neurocognitive functioning of adolescents: effects of protracted alcohol use. Alcohol Clin Exp Res 24, 164-171.

5.   Squeglia, L.M., Schweinsburg, A.D., Pulido, C., Tapert, S.F., 2011. Adolescent binge drinking linked to abnormal spatial working memory brain activation: differential gender effects. Alcohol Clin Exp Res 35, 1831-1841.

6. Johnson, C.A., Xiao, L., Palmer, P., Sun, P., Wang, Q., Wei, Y., Jia, Y., Grenard, J.L.,  Stacy, A.W., Bechara, A., 2008. Affective decision-making deficits, linked to a dysfunctional ventromedial prefrontal cortex, revealed in 10th grade Chinese adolescent binge drinkers. Neuropsychologia 46, 714-726.

7. De Bellis, M.D., Narasimhan, A., Thatcher, D.L., Keshavan, M.S., Soloff, P., Clark, D.B.,  2005. Prefrontal cortex, thalamus, and cerebellar volumes in adolescents and young adults with adolescent-onset alcohol use disorders and comorbid mental disorders. Alcohol Clin Exp Res 29, 1590-1600.

8.  Medina, K.L., McQueeny, T., Nagel, B.J., Hanson, K.L., Schweinsburg, A.D., Tapert, S.F., 2008. Prefrontal cortex volumes in adolescents with alcohol use disorders: unique gender effects. Alcohol Clin Exp Res 32, 386-394.

9.  De Bellis, M.D., Clark, D.B., Beers, S.R., Soloff, P.H., Boring, A.M., Hall, J., Kersh, A., Keshavan, M.S., 2000. Hippocampal volume in adolescent-onset alcohol use disorders. Am J Psychiatry 157, 737-744.

10.  Nagel, B.J., Schweinsburg, A.D., Phan, V., Tapert, S.F., 2005. Reduced hippocampal volume among adolescents with alcohol use disorders without psychiatric comorbidity. Psychiatry Res 139, 181-190.

11.  Bava, S., Jacobus, J., Thayer, R.E., Tapert, S.F., 2013. Longitudinal changes in white matter integrity among adolescent substance users. Alcohol Clin Exp Res 37 Suppl 1, E181-189.

12.   McQueeny, T., Schweinsburg, B.C., Schweinsburg, A.D., Jacobus, J., Bava, S., Frank, L.R., Tapert, S.F., 2009. Altered white matter integrity in adolescent binge drinkers. Alcohol Clin Exp Res 33, 1278-1285.

13. Xiao, L., Bechara, A., Gong, Q., Huang, X., Li, X., Xue, G., Wong, S., Lu, Z.L., Palmer, P., Wei, Y., Jia, Y., Johnson, C.A., 2012. Abnormal Affective Decision Making Revealed in Adolescent Binge Drinkers Using a Functional Magnetic Resonance Imaging Study. Psychol Addict Behav.

14. Cotton, N.S., 1979. The familial incidence of alcoholism: a review. J Stud Alcohol 40, 89-116.

15. Goodwin, D.W., 1979. Alcoholism and heredity. A review and hypothesis. Arch Gen Psychiatry 36, 57-61.

16.  Schuckit, M.A., 1985. Genetics and the risk for alcoholism. Jama 254, 2614-2617

17. Bohman, M., 1978. Some genetic aspects of alcoholism and criminality. A population of adoptees. Arch Gen Psychiatry 35, 269-276.

18. Cloninger, C.R., Bohman, M., Sigvardsson, S., 1981. Inheritance of alcohol abuse. Cross-fostering analysis of adopted men. Arch Gen Psychiatry 38, 861-868.

19. Merikangas, K.R., Stolar, M., Stevens, D.E., Goulet, J., Preisig, M.A., Fenton, B., Zhang, H., O’Malley, S.S., Rounsaville, B.J., 1998. Familial transmission of substance use disorders. Arch Gen Psychiatry 55, 973-979

20. Finn, P.R., Kleinman, I., Pihl, R.O., 1990. The lifetime prevalence of psychopathology in men with multigenerational family histories of alcoholism. J Nerv Ment Dis 178, 500-504.

21. Goodwin, D.W., 1985. Alcoholism and genetics. The sins of the fathers. Arch Gen Psychiatry 42, 171-174.

22. Hasin, D., Paykin, A., Endicott, J., 2001. Course of DSM-IV alcohol dependence in a community sample: effects of parental history and binge drinking. Alcohol Clin Exp Res 25, 411-414.

23. Hill, S.Y., Yuan, H., 1999. Familial density of alcoholism and onset of adolescent drinking. J Stud Alcohol 60, 7-17.

24.   Heath, A.C., Bucholz, K.K., Madden, P.A., Dinwiddie, S.H., Slutske, W.S., Bierut, L.J., Statham, D.J., Dunne, M.P., Whitfield, J.B., Martin, N.G., 1997. Genetic and environmental contributions to alcohol dependence risk in a national twin sample: consistency of findings in women and men. Psychol Med 27, 1381-1396.

25. Kaprio, J., Koskenvuo, M., Langinvainio, H., Romanov, K., Sarna, S., Rose, R.J., 1987. Genetic influences on use and abuse of alcohol: a study of 5638 adult Finnish twin brothers. Alcohol Clin Exp Res 11, 349-356.

26.  Knopik, V.S., Heath, A.C., Madden, P.A., Bucholz, K.K., Slutske, W.S., Nelson, E.C., Statham, D., Whitfield, J.B., Martin, N.G., 2004. Genetic effects on alcohol dependence risk: re-evaluating the importance of psychiatric and other heritable risk factors. Psychol Med 34, 1519-1530.

27. Acheson, A., Richard, D.M., Mathias, C.W., Dougherty, D.M., 2011a. Adults with a family history of alcohol related problems are more impulsive on measures of response initiation and response inhibition. Drug Alcohol Depend 117, 198-203.

28.  Saunders, B., Farag, N., Vincent, A.S., Collins, F.L., Jr., Sorocco, K.H., Lovallo, W.R., 2008. Impulsive errors on a Go-NoGo reaction time task: disinhibitory traits in relation to a family history of alcoholism. Alcohol Clin Exp Res 32, 888-894.

29.  Acheson, A., Vincent, A.S., Sorocco, K.H., Lovallo, W.R., 2011b. Greater discounting of delayed rewards in young adults with family histories of alcohol and drug use disorders: studies from the Oklahoma family health patterns project. Alcohol Clin Exp Res 35, 1607-1613.

30. Foisy, M.L., Kornreich, C., Petiau, C., Parez, A., Hanak, C., Verbanck, P., Pelc, I., Philippot, P., 2007b. Impaired emotional facial expression recognition in alcoholics: are these deficits specific to emotional cues? Psychiatry Res 150, 33-41.

31.  Foisy, M.L., Philippot, P., Verbanck, P., Pelc, I., van der Straten, G., Kornreich, C., 2005. Emotional facial expression decoding impairment in persons dependent on multiple substances: impact of a history of alcohol dependence. J Stud Alcohol 66, 673-681.

32.  Philippot, P., Kornreich, C., Blairy, S., Baert, I., Den Dulk, A., Le Bon, O., Streel, E., Hess, U., Pelc, I., Verbanck, P., 1999. Alcoholics’ deficits in the decoding of emotional facial expression. Alcohol Clin Exp Res 23, 1031-1038.

33.  Townshend, J.M., Duka, T., 2003. Mixed emotions: alcoholics’ impairments in the recognition of specific emotional facial expressions. Neuropsychologia 41, 773-782.

34.  Gilman, J.M., Hommer, D.W., 2008. Modulation of brain response to emotional images by alcohol cues in alcohol-dependent patients. Addict Biol 13, 423-434.

35. Marinkovic, K., Oscar-Berman, M., Urban, T., O’Reilly, C.E., Howard, J.A., Sawyer, K., Harris, G.J., 2009. Alcoholism and dampened temporal limbic activation to emotional faces. Alcohol Clin Exp Res 33, 1880-1892.

36.  Salloum, J.B., Ramchandani, V.A., Bodurka, J., Rawlings, R., Momenan, R., George, D., Hommer, D.W., 2007. Blunted rostral anterior cingulate response during a simplified decoding task of negative emotional facial expressions in alcoholic patients. Alcohol Clin Exp Res 31, 1490-1504.

37.  Wrase, J., Makris, N., Braus, D.F., Mann, K., Smolka, M.N., Kennedy, D.N., Caviness, V.S., Hodge, S.M., Tang, L., Albaugh, M., Ziegler, D.A., Davis, O.C., Kissling, C., Schumann, G., Breiter, H.C., Heinz, A., 2008. Amygdala volume associated with alcohol abuse relapse and craving. Am J Psychiatry 165, 1179-1184.

38.  Kornreich, C., Foisy, M.L., Philippot, P., Dan, B., Tecco, J., Noel, X., Hess, U., Pelc, I., Verbanck, P., 2003. Impaired emotional facial expression recognition in alcoholics, opiate dependence subjects, methadone maintained subjects and mixed alcohol-opiate antecedents subjects compared with normal controls. Psychiatry Res 119, 251-260.

39.  Maurage, P., Campanella, S., Philippot, P., Martin, S., de Timary, P., 2008. Face processing in chronic alcoholism: a specific deficit for emotional features. Alcohol Clin Exp Res 32, 600-606.

40.  Fernandez-Serrano, M.J., Perez-Garcia, M., Schmidt Rio-Valle, J., Verdejo-Garcia, A., 2010. Neuropsychological consequences of alcohol and drug abuse on different components of executive functions. J Psychopharmacol 24, 1317-1332.

41.  Durazzo, T.C., Tosun, D., Buckley, S., Gazdzinski, S., Mon, A., Fryer, S.L., Meyerhoff, D.J., 2011. Cortical thickness, surface area, and volume of the brain reward system in alcohol dependence: relationships to relapse and extended abstinence. Alcohol Clin Exp Res 35, 1187-1200.

42.   Makris, N., Oscar-Berman, M., Jaffin, S.K., Hodge, S.M., Kennedy, D.N., Caviness, V.S., Marinkovic, K., Breiter, H.C., Gasic, G.P., Harris, G.J., 2008. Decreased volume of the brain reward system in alcoholism. Biol Psychiatry 64, 192-202.

43.   Benegal, V., Antony, G., Venkatasubramanian, G., Jayakumar, P.N., 2007. Gray matter volume abnormalities and externalizing symptoms in subjects at high risk for alcohol dependence. Addict Biol 12, 122-132.

44.  Glahn, D.C., Lovallo, W.R., Fox, P.T., 2007. Reduced amygdala activation in young adults at high risk of alcoholism: studies from the Oklahoma family health patterns project. Biol Psychiatry 61, 1306-1309.

45.   Hill, S.Y., De Bellis, M.D., Keshavan, M.S., Lowers, L., Shen, S., Hall, J., Pitts, T., 2001. Right amygdala volume in adolescent and young adult offspring from families at high risk for developing alcoholism. Biol Psychiatry 49, 894-905.

46.  Oscar-Berman, M., Bowirrat, A., 2005. Genetic influences in emotional dysfunction and alcoholism-related brain damage. Neuropsychiatr Dis Treat 1, 211-229.

47.  Sinha, R., Parsons, O.A., Glenn, S.W., 1989. Drinking variables, affective measures and neuropsychological performance: familial alcoholism and gender correlates. Alcohol 6, 77-85

48.  Verdejo-Garcia, A., Bechara, A., Recknor, E.C., Perez-Garcia, M., 2006. Executive dysfunction in substance dependent individuals during drug use and abstinence: an examination of the behavioral, cognitive and emotional correlates of addiction. J Int Neuropsychol Soc 12, 405-415.

49.  Fox, H.C., Hong, K.A., Sinha, R., 2008. Difficulties in emotion regulation and impulse control in recently abstinent alcoholics compared with social drinkers. Addict Behav 33, 388-394


Intolerance of Uncertainty

Like many recovering alcoholics I know I have a real problem with “Not projecting into the future” but staying in the moment or even the day. Why is this? When I “project” or even consider a near future event I can feel distressed by it. I want to do something about it now! Not later.

The future seems to be urgently now.

I have long researched why this is? I seem to become overwhelmed at times by future tense and it is not even due to future events being that distressing in themselves. I just have this constant need to act now rather than later. I have an urgency or a negative urgency or in other words a  distress based impulsivity which prompts a desire to act now, make a decision now rather than later. I call this a compulsion to act  because a distress state compels me to make a decision to act now.

As I have mentioned in previous blogs, alcoholics appear to have a bias in decision making towards choose the short term solution over a long term one, even though the long term solution will yield greater gains. There are various  theories on why this is so. Sometimes it appears like a “fight or flight” response!

My theory is that I am very poor at tolerating uncertainty and what is the future but uncertain. I have  an “unconscious” negative bias about the future, linked at times to a tendency to then catastrophize.

This intolerance of uncertainty is seen in other disorders, such as anxiety, obsessive-compulsive and post traumatic stress disorders as well as in eating disorders but it is rarely researched in alcoholism.

I believe when confronted with a decision about the future I often make a decision to relieve a distress which manifests as an unpleasant feeling state which compels me, via a stimulus response to act now. Distress is the stimulus, acting now is the response.

I am not saying that I have to be in a negative frame of mind for this to occur. It is simply a decision making bias I have when left to my own devices.   It is the reason I speak to others when making important decisions in life because the need to relief distress can show in the mind as a good idea when it is often on reflection not such a great idea.

This is due to distress being a stress-fuelled experience and excessive stress reduces the awareness of future consequence of a decision. It seems like a good idea at the time because it relieves distress. To the brain this is a good idea.  It is a automatic response of the dorsal striatum, an implicit memory (procedural) system, that requires one to retrospectively rationalise and justify the automatic responding of this area of the brain, it justifies a previous action in other words, thus a decision is represented in the mind as a good idea, what was most urgently required!

These rationalisations and justifications through time can become automatic schemas and are automatically activated following a compulsive response. Some of us are probably familiar with these schemas being a big part of our alcohol and drug use. As we needed to use, we had automatic addiction schemas following shortly after our decisions to head to the pub or to score some drugs or even to propel some decisions, as the consequence of distress states. It is these habitual response, based on distress states which bias decisions making to acting now, even in recovery.

I came across an article (1) which looked at this intolerance of uncertainty in relation to decision making and came up with similar conclusions to the above. “high IU (intolerance of uncertainty) predicted shorter wait times and more frequent selection of the immediate, less valuable (and riskier) reward. We take this tendency as evidence that IU was associated with an aversion to waiting in a state of uncertainty. One might argue that choices for the more immediate, less valuable reward might reflect an aversion to waiting per se…, the delay associated with the more valuable reward in the
current study appears to have magnified the unpleasant affective responses to uncertainty… delay is provoking unpleasant affective responses, choices for the smaller, immediate reward can be seen as avoidance of distress.” Decisions are thus like an “escape route” and more based on emotional avoidance.  “That is, the affective consequences of uncertainty may play a more central role in determining behavior than uncertainty itself…decision  making tendencies among those high in IU may be maintained through negative reinforcement…to  reduce or eliminate affectively unpleasant circumstances that accompany waiting in uncertainty.”

These “unpleasant affective responses” are distress based and lead to a negative urgency to act now.


1. Luhmann, C. C., Ishida, K., & Hajcak, G. (2011). Intolerance of uncertainty and decisions about delayed, probabilistic rewards. Behavior therapy42(3), 378-386.