Eating Disorders based on a Body “Feeling State” Confusion?

Here we look at emotion processing deficits in eating disorders and whether the extent of these difficulties can predict treatment outcome three years later.  This would demonstrate the ongoing role of emotion processing, as conceptualised as alexithymia, plays an ongoing role in the pathomechanism driving eating disorders.

This article also had a very good description of the somatic/emotional confusion which creates that unpleasant feeling state we have referred to before which appears to end in compulsive reactive behaviour rather than goal-directed, adaptive, evaluative, action-outcome thinking.

As we have shared before this is due to emotions not be labelled and used as guides to recruit goal directed parts of the brain but rather in their emotionally undifferentiated state they appear to compel us to react rather than consider our long term actions and their consequences.

“Several cross-sectional studies have reported high levels of alexithymia in populations with eating disorders.

However, only few studies, fraught with multiple methodological biases, have assessed the prognostic value of alexithymic features in these disorders. The aim of this study (1) was to investigate the long-term prognostic value of alexithymic features in a sample of patients with eating disorders.

The Difficulty  Identifying Feelings factor of the Toronto Alexithymia Scale (TAS-20), often used to assess levels of alexithymia, emerged as a significant
predictor of treatment outcome. In other words, the results  of this study indicated that difficulty in identifying feelings can act as a negative prognostic ( meaning predictive of something in the future)   factor of the long-term outcome of patients with eating disorders.

eating_disorder_by_ttonny-d2yezty (1)


The authors of this study also suggested that professionals should carefully monitor emotional identification and expression in patients with eating disorders and develop specific strategies to encourage labeling and sharing of emotions.

The identification of variables that predict treatment outcome in patients with eating disorders is critical if we are to increase the degree of sophistication with which we treat eating disorders…Among the several psychological features that have been proposed to predict treatment outcome in patients with eating disorders, alexithymia has attracted special interest.
Alexithymia is a personality construct characterized (partly) by a difficulty in identifying and describing feelings.

Several arguments, namely, factor analyses and longitudinal studies, have supported the view that alexithymia is a stable personality trait rather than a state-dependent phenomenon linked to depression or to clinical status [3,4].

Several studies have reported high levels of alexithymia in patients with eating disorders, especially in individuals with anorexia nervosa [5–8]. There are several reasons to believe that this construct could play a major role in the illness course of eating disorders: due to their cognitive limitations in emotion regulation, alexithymic individuals with eating disorders may resort to
maladaptive self-stimulatory behaviors such as starving, bingeing, or drug misuse to self-regulate disruptive emotions.

The results of our study indicate that one of the facets of the alexithymia construct, the difficulty in identifying feelings, is a negative prognostic factor for the long-term outcome of patients with eating disorders. Patients with the
greatest difficulties at identifying emotions at baseline are more often symptomatic at follow-up and show a less favorable clinical improvement.

There are several ways in which alexithymia can affect the clinical outcome of eating disorders: via the negative influence it exerts on the clinical expression of the disorders and on the response to therapeutic interventions.

First, the difficulty in identifying feelings may reduce the capacity of patients with eating disorders to adapt to stressful situations [28]. Such situations generate an emotional overflow that alexithymic subjects apprehend less by emotional and cognitive features than by their associated somatic indexes[29]. This uncertainty between feelings and bodily sensations reminds us of the interoceptive (a sensitivity to stimuli originating inside of the body) confusion proposed by Hilde Bruch [30,31].

Luminet et al. [32] have experimentally observed a dissociation of the components of the emotional response of alexithymic subjects (a physiological hyperreactivity to emotional stimuli associated to a deficit at the level of the cognitive experience), which illustrate the functioning of patients with eating disorders.

Faced with the physiological arousal induced by emotional demands, these patients may show poor adaptive strategies. They may resort to restricted patterns of repetitive and automated behaviors, such as the hyperactivity of anorexic individuals or the binges/purge cycles of bulimic  subjects, which temporarily relieve their feeling of discomfort and restore their inner equilibrium [33,34] but generate, in the long term, a positive reinforcement of the eating disorder. 

Second, alexithymia may be related to a chronic course of eating disorders by its relationship with other pathological behaviors, especially with addictive disorders. We have shown in previous studies that alexithymia is associated
with addictive behaviors in patients with bulimia [35].

Patients with eating disorders may resort to addictive behaviors to relieve the anxious and depressive feelings elicited by their negative perceptions of themselves [36].”

Thus to conclude, eating disorders appear to have the same emotion processing and regulation deficits as other addictive behaviours, particularly emotional differentiation, a difficulty in knowing exactly what one is feeling.

Interestingly eating disorders seem also to be driven by the same negative self perception we have seen in other addictive disorders.


1.  Speranza, M., Loas, G., Wallier, J., & Corcos, M. (2007). Predictive value of alexithymia in patients with eating disorders: A 3-year prospective study.Journal of psychosomatic research, 63(4), 365-371.


“Eating our Words!?” – Emotion-Processing Deficits in Eating Disorders

In eating disorder patients, an impairment of emotional processing is clinically supposed. As quoted by Bruch (1985), anorexic patients not only show impaired differentiation between hunger and satiety, but they can hardly differentiate their physical sensations from their intimate emotions, which they often cannot describe. Bulimic patients often respond to stress with a bulimic crisis and vomiting, but they can hardly correlate their crisis with any emotional stimulus (Davis, Marsh, 1986).

Several studies suggest that alexithymia is a predominant factor in eating disorder.

Emotional awareness was defined by Lane and Schwartz in the late 1980s as the capacity of an individual to describe his or her own feelings and another person’s emotional experience (Lane & Schwartz, 1987). Lane and Schwartz  conceptualised emotional awareness as a cognitive process undergoing various structural transformations along a cognitive-developmental sequence (1987,
p. 134).

Lane and Schwartz focused on a way to measure the level of emotional awareness an individual has reached. For these authors, the degree of structural organization of emotional awareness is reflected by the verbal material individuals provide to describe their emotional experience. They pinpoint that emotional experience does not require language to be conscious, but that language helps to structure and
establish concepts, and therefore increases the ability to discriminate between differentiated emotional states.

From this point of view, Lane, Quinlan, Schwartz, Walker, and Zeitlan (1990) elaborated the Levels of Emotional Awareness Scale (LEAS), which is aimed at evaluating an individual’s capacity to describe not only his or her own emotional experience but also the emotional states of others. The scoring of this instrument is based on the analysis of the verbal contents the individual provides in response to a series of 20 short stories depicting a variety of emotional situations. The discriminant validity of this instrument has confirmed that the level of emotional awareness is independent of depression and anxiety (Bydlowski et al., 2002;
Lane et al., 1990).


Alexithymia was considered by Lane and Schwartz  as corresponding to the lower end of the emotional awareness continuum, that is, the preconceptual level of emotion organization and regulation within their hierarchical model. Indeed, alexithymia can be viewed as a deficit in the cognitive processes involved in the representation of emotional internal and external experiences, characterized by the
persistence of cognitive-affective modalities of the first levels of development, below the concrete operational level (where emotions are experienced somatically).




This study (1) in accordance with their initial hypothesis, demonstrated that patients suffering  from eating disorders showed evidence of an emotion-processing deficit independent of affective disorders, such as anxiety and depression.

In the current study, individuals with an eating disorder were characterized by a global emotion processing deficit, with impaired ability to identify their own emotions, as well as an impairment in judging others’ emotional experience.

In our study, anorexic patients had a significantly lower level of emotional awareness than bulimic patients, Our results are in line with those
of Smith, Amner, Johnsson, and Franck (1997), who showed a marked tendency of these patients to develop alternative strategies to avoid empathizing.
These strategies are not limited to the restricted use of emotional words. According to the authors, eating disorder patients have good verbal skills, but
cannot use them adequately to describe their emotional experience, indicating a pronounced in capacity for emotional understanding.

The current report is also consistent with clinical descriptions of the types of affective difficulties characteristic of anorexics and bulimics. Indeed, some authors consider the deficits in the processing of the subjective experience and the perception of oneself as the most fundamental difficulties of this type of disorder (Corcos, 2000; De Groot & Rodin,
1994; Jeammet, 1997).

These subjects seem to have a limited access to their emotional life and/or feel easily dominated and overwhelmed by their emotions  (Bruch, 1962). Thus, the ability to take into account one’s own emotions is diminished in individuals  with eating disorders, probably because body sensations cannot be related to affects, or because the perception of undifferentiated body impulses prevents understanding of how affects are elaborated. Lacking knowledge of their own emotions, these individuals are not able to represent another person’s emotional experience.

Because the capacity to differentiate one’s own and others’ emotions in a given context is associated with the ability to tolerate and manage a large number of emotional states, emotions that are not integrated remain global and undifferentiated, which leads to an incapacity to use affects to guide the selection of an adapted behavior (Krystal, 1974),

These emotion-processing deficits induce intense, often uncontrolled, affective reactions. The food related behavioral problems of anorexic and bulimic
patients have been conceptualized as a consequence of the incapacity to control distressing emotions through psychic processes (Taylor, 1997a).

Abnormal eating behaviors would thus represents a way of discharging negative affects.

With the demonstration of increased secretion of cerebral b-endorphin in patients with anorexia nervosa perhaps eating disorders should, therefore, be regarded as addictive behaviours, whose purpose is to control the subject’s affective inner turmoil (Jeammet-1997).

The finding that neither level of emotional awareness scores nor alexithymia scores were correlated with the duration of illness suggests that emotional internal life impoverishment is not due to the severity of the disorder. One may wonder whether this deficit predates the occurrence of the disease, potentially favoring the development of eating disorders. This hypothesis is in line with the point of view of some authors who consider alexithymia to be a predisposing factor in addictive behaviours (Taylor, 1997a, 1997b).


1. Bydlowski, S., Corcos, M., Jeammet, P., Paterniti, S., Berthoz, S., Laurier, C., Chambry, J. and Consoli, S. M. (2005), Emotion-processing deficits in eating disorders. Int. J. Eat. Disord., 37: 321–329.


Different addictive behaviours all centre on the same inherent difficulties.

by alcoholicsguide


Commonalities across all addictive disorders. 

There are those, and some in treatment centres, who maintain that addiction is addiction is addiction. I have not always been convinced by this, mainly because I see differences in temperament and personality among different types of addicts (i.e alcoholics often appear different to heroin addicts in my mind) but these supposed and perhaps superficial distinctions may be masking inherent similarities or commonalities in the aetiology of all addictive disorders. There seems to be commonalities in particular between alcoholics, sex addicts, gambling addicts and those with eating disorders.  This commonality may also help explain “cross addiction” – the tendency to become addicted to various things, whether substances or behaviours.
I personally have become” addicted” in very short periods of time to chocolate and many other substances and behaviours, such as constantly having to watch my workaholic behaviour. By addicted I mean I have quickly suffered addictive behaviour symptoms such as excessive consumption, pathological craving, physiological withdrawals from the substance or behaviour and the gamut of negative emotions surrounding my shame and despair  at these obsessive compulsive behaviours. I can’t take it or leave in relation to many things in my life. Period!
There seems to a “manic hamster on the treadmill” mechanism in me that gets ignited by my engaging in what appears to be the most innocuous behaviour. Suddenly, whatever it is, leads me to want more, more, MORE of it!
I have an addicted brain and a recovering mind. 
What is this intrinsic mechanism in my brain? What trips the switch towards addictive behaviour? This is the heart of the question.
How does the brain tumble towards unbridled wanting. What leads our brain to suddenly say I NEED THIS! rather than simply wanting it?
Why does the most simple behavioural decision suddenly seem life or death, urgent, most necessary? Why a such a sudden recruitment of this emergency state? For us it is due to the limbic and subcortical areas, the “fight or flight” areas of the brain being recruited to make the most simple decision urgent. Even the most simple decisions seem to involve feeling about our very survival. As we have blogged about before in “Why a “Spiritual Solution” to a Neurobiological Disease?” survival becomes the domain of these emergency parts of the brain so we do everything like there is no tomorrow, It is everything or nothing NOW. We need these things. Our survival regions have become extreme and constantly react, not act.
Our very survival has become habitually and compulsive governed as if our brains are constantly under siege.
These commonalities centre on the fundamental role we believe emotional processing and regulation deficits have in these various types of addictive disorder. It may be these deficits that are present in all addictive behaviours and  it may suggest that they are fundamental mechanisms in driving addictive behaviours forward.
In a previous blog we showed how these areas of emotional dysfunction may even be inherited in many, so it is tempting to conclude that the vulnerability, or some of the major vulnerabilities that addicts and those with addictive behaviours inherit are the impaired ability to process and regulate emotions which leads to fundamental decision making difficulties and distress-based impulslivity (as the lack of processing emotions represents as distress signals act to relief these states not guide reflective decision making) which combine to shape the rest of their lives.
The encouraging aspect is that at an affective-cognitive level it may be possible to target these deficits in children at risk via prevention programs.
It illustrates what addicts of various types have said about their illness, however, that they suffer from an emotional disease.
The solution may be prevention and/or intervention to shore up these difficulties which is primarily what various treatments do without explicitly saying so. We first need to state categorically this is what we think drives addictive behaviours and then use complementary therapeutic strategies to specifically address these vulnerabilities.
We have to relearn emotions, how to identity, label, verbalise, process and subsequently regulate our emotions so that we become less impulsively driven and ultimately make better decisions in our lives.

We have in previous blogs discussed how substance addiction seems to have emotional processing and regulation deficits at the heart of their manifestation and act as pathomechanisms in propelling these disorders to eventual  chronicity.

In the next series of blogs we will be discussing whether fundamental emotional processing and regulation deficits are common to (or intrinsic to the aetiology of) other addictive disorders too).

First up, we discuss emotional (or otherwise known in research as affective) dysregulation in those with Hypersexual Disorder or more commonly know to lay persons as sexual addiction.

Hypersexual Disorder – the proposed diagnostic criteria that were given consideration for the Diagnostic and Statistical Manual of Mental Disorder Fifth Edition (DSM-5) characterize hypersexual disorder (HD) (1) which is commonly known as sexual addiction.

This study (1) states that HD is a phenomenon involving repetitive and intense preoccupation with sexual fantasies, urges, and behaviors, leading to adverse consequences and clinically significant distress or impairment in social, occupational, or other important areas of functioning(Bancroft, 2008; Kafka, 2010; Kaplan & Krueger, 2010; Marshall & Briken, 2010; Reid, Garos, & Fong, 2012).

Patients seeking help for HD typically experience multiple unsuccessful attempts to control or diminish the amount of time spent engaging in sexual fantasies, urges, and behaviors in response to dysphoric mood states or stressful life events (Kafka, 2010).

Personality characteristics such as proneness to boredom (Chaney
& Blalock, 2006), impulsivity and shame (Reid, Garos, & Carpenter, 2011), interpersonal sensitivity, alexithymia, loneliness, and low self-esteem also have been observed in association with hypersexual behavior (Reid, Dhuffar, Parhami, & Fong, 2012; Reid, Stein, et al., 2011; Reid, Carpenter, Spackman, & Willes, 2008). Collectively, these  characteristics create significant challenges for hypersexual patients.

The importance of finding effective treatments for HD cannot be underestimated given the gravity of its consequences (Reid, Garos, et al., 2012): Hypersexual patients are at increased risk for loss of employment, legal problems, social isolation, higher rates of divorce (Reid & Woolley, 2006; Reid, Carpenter, Draper, & Manning, 2010; Zapf, Greiner, & Carroll, 2008), and sexually transmitted infections (Coleman et al., 2010; Dodge, Reece, Cole, & Sandfort, 2004; Rinehart & McCabe, 1997, 1998).

This study found (1) significant associations between unpleasant emotions, impulsivity, stress proneness, and hypersexuality replicating findings
noted in other studies (Reid et al., 2008; Reid, 2010). The findings in this study also offer some support for the DSM-5 proposed classification criteria for HD (Kafka, 2010). Specifically, stress and emotional dysregulation have been hypothesized as precipitating and perpetuating risk factors for hypersexuality, and, accordingly,  correlations to reflect this relationship, were consistent with findings of this study (1).

Another study (2) looked at  investigating alexithymia, emotional instability, and vulnerability to stress proneness among individual seeking help for hypersexual behavior. Findings (2) provide evidence for the hypothesis thatindividuals who manifest symptoms of hypersexual behavior are more likely to experience deficits in affect regulation and negative affect (including
alexithymia,  depression, and vulnerability to stress).


An increasing number of individuals are seeking help for hypersexual behavior related to a constellation of symptoms that reflect difficulties in regulating sexual thoughts, feelings, and behaviors.

This study’s (2) conceptualization of this phenomenon keys onbehavior dysregulation as manifest through exaggerated frequency and focus on sexual behavior (from sexual activity with partners, to use of pornography, sexual fantasy, or other erotic stimuli, to excessive masturbation).

Hypersexual behavior may include a sense of being out of control or a history of failed attempts at increased control, and it encompasses elements common to other psychiatric dysfunctions, such as impaired functioning in aspects of daily living, subjective distress, and deficits in coping strategies for addressing uncomfortable affective experiences (e.g., anxiety reduction), usually because of over reliance on sexual behavior as a means of affective regulation and relief. Many patients presenting with hypersexual behavior also report incongruence between their values and beliefs and their sexual behavior.

This study, used the definition of Reid and Woolley (2006) was used
to operationalize hypersexual behavior as: difficulty in regulating (e.g., diminishing or inhibiting) sexual thoughts, feelings, or behavior to the extent that negative consequences are experienced by self or others. The behavior causes significant levels of personal or interpersonal distress and may include activities that are incongruent with personal values, beliefs, or desired goals.The behavior may function as a maladaptive coping mechanism (e.g., used to avoid emotional pain or used as a tension-reduction activity)…. (p. 220)

“It may be that such persons possess deficits in affective regulation similar to those encompassed by the constructs of alexithymia and neuroticism. . It
is plausible that such deficits would influence exaggerated sexual behavior
in some persons (e.g., in the absence of other coping strategies for successful affective monitoring and regulation, the stress-reduction aspects of sexual behavior as a substitute may be powerfully reinforced).

Adams and Robinson (2001), as well as others (e.g., Schwartz & Masters,
1994; Wilson, 2000), have theoretically postulated thathypersexuality represents a compensatory behavior that attempts to alleviate symptom distress associated with problems of affect regulation. A similar theory among individuals with eating disorders was advanced by Heatherton and Baumeister (1991), who argued that motivation for binge eating emerged as an attempt to escape from negative appraisals associated with self-awareness and unpleasant mood states triggered by stressful events.
It can be reasonably argued that sexual activity provides a mood-altering experience enabling individuals to disassociate from uncomfortable, awkward, or unpleasant emotions (Quayle, Vaughan, & Taylor, 2006).

The power of sexual experience to shield one from negative emotions, then, probably arises from sexual arousal’s inherent ability to create intense focus on the competing state of pleasurable arousal, as well as the release of tension associated with orgasm. Furthermore, some individuals may find that fantasizing about sexual activity provides a greater distraction than partnered activity because it encourages—and maybe even requires— disconnect from relationships with their inherent problems, challenges, and complexities.

One plausible way to understand hypersexuality is seeing behaviors associated with reward, distraction, or soothing—such as overeating, exaggerated focus on somatic complaints, substance abuse, or hypersexuality—as being particularly likely in those for whom emotional distancing has high priority. This need for emotional distance can arise from increased stress proneness, negative affective states, emotional pain associated with unresolved trauma, or the inability to develop and form secure attachment bonds.

Our clinical impressions of patients displaying hypersexuality, as defined above, are consistent with those of other researchers who have suggested that alexithymic individuals seek tension reduction from uncomfortable or unpleasant emotions (Keltikangas-Jarvinen, 1982; Kroner & Forth,
1995; Zimmermann, Rossier, de Stadelhofen, & Gaillard, 2005), thereby contributing to their eating disorders (Corcos et al., 2000; Larsen, van Strien, & Eisinga, 2006), substance abuse (Haviland, Hendryx, Shaw, & Henry, 1994),
and the like. Our rationale for suggesting associations of stress vulnerability, emotional instability, and alexithymia with hypersexual behavior also stems, in part, from our own observations of poor affect regulation and deficits in stress management among these patients.

Research supports some associations between alexithymia and stress. For instance, high, as compared to low, alexithymic individuals show different cardiovascular response to stress (e.g., Linden, Lenz, & Stossel, 1996).

The findings  support our hypothesis that alexithymia, emotional instability,
and vulnerability to stress are associated with the severity of hypersexual
behavior. More specifically, it appears that patients who present with more
profound levels of hypersexual behavior are more depressed, alexithymic,
and prone to stress.

These findings are consistent with our theoretical conceptualization of
emotional instability among individuals with hypersexual behavior. Our clinical impressions suggest this population struggles with uncomfortable, awkward, or unpleasant affective states, and in fact, these data indicate that they also experience the prevalence of such emotions in greater proportions than those found in normal populations.

images (34)

Many of the subjects in the present study displayed emotional deficits and a paucity of emotional awareness. Queries about feelings in therapy would often elicit a response such as “I don’t know” or “I’m not feeling anything.” – otherwise know as emotional differentiation and discussed recently in another blog. 

Our clinical impressions of hypersexual patients suggest that many of
these individuals habitually entertain negative self-appraisals that are likely
influenced by attention bias which seeks evidence in daily experiences to
confirm irrational beliefs (I’m unlovable, worthless, etc.). Additionally, many
of these patients devote time to maintaining facades and implementing strategies of impression management that may further disconnect them from their authentic self, including their genuine emotions. Patients desperately desire external validation by others and privilege such adulation while marginalizing subjective positive perceptions about the self. Unable to control and predict the reactions of others, patients vacillate along a continuum of emotional instability. Negative appraisals by others become threats to their sense of self-worth, and such criticisms often result in disavowing aspects of the self. Specifically, the patients disconnect from undesirable emotional states.

The function of sexual activity in these instances is stress reduction and escape from or avoidance of uncomfortable and unpleasant affective experiences attributable to difficulties in their interpersonal relationships and other challenges in daily living.



1.  Reid, R. C., Bramen, J. E., Anderson, A., & Cohen, M. S. (2014). Mindfulness, emotional dysregulation, impulsivity, and stress proneness among hypersexual patients. Journal of clinical psychology, 70(4), 313-321.

2.  Reid, R. C., Carpenter, B. N., Spackman, M., & Willes, D. L. (2008). Alexithymia, emotional instability, and vulnerability to stress proneness in patients seeking help for hypersexual behavior. Journal of Sex & Marital Therapy, 34(2), 133-149.

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.




“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.

They can fuck you up, your mum and dad.

They fuck you up, your mum and dad.
    They may not mean to, but they do.
They fill you with the faults they had
    And add some extra, just for you.

Phillip Larkin – This Be The Verse

Looking back on my own childhood it is easier now to observe the fertile ground from which my genetic seeds of alcoholism started to flourish. I have long maintained that growing up in a dysfunctional family environment did not create my alcoholism but certainly did not help. A family environment were emotional expression was limited and veered between sentimentality and  outright anger.

It is difficult to see how I learnt the essential adaptive skills of emotional regulation then; how to identify, label and express emotions freely without sanction, verbally, and non-verbally. For me emotions where something you cut off, experientially avoided, resisted. The more you did not let them get to you the tougher you were mentally somehow. Emotions were strangely dangerous things almost.

Emotions, having them, made you weak! People who indulged in them were weak.

I also grew up with a father who was a boxer and alcoholic (abstinent, thank God, via the local Church) who insisted emotions had to tolerated like a man, like some tough  hombre in a 1950s Western. I had a host of uncles and a Grandad who agreed and they all set out to toughen me up. I even had boxing matches with cousins at various homes to show how I was progressing!

When I started drinking I found that this tough guy routine was greatly enhanced. Alcohol made me bullet proof. I drank and grew up to manhood in one go. Or so I thought – I didn’t realise that I stayed at that emotionally  impaired 14 years old for nearly three decades later.

The worst effect on my emotional regulation  skills was my relationship with my mother who struggled with valium abuse most of her adult life. This meant she was emotionally distant a lot of the time. Wose than that, she mixed mawkishness with being cold as a stone. It was an insecure attachment.  You were never sure, emotionally, where you were at with her. It made me insecure, anxious and eventually very very angry. Cold blue angry.

But did this also have an effect on my ability to processing emotions. How could maternal emotional deprivation have an effect on my emotional processing skills? Andd how could this emotional processing difficulty affect the amount I craved alcohol??

I recently came across this article (1) which looked at this very question.  I refer widely from it here.

Attachment theory is a widely used framework for understanding emotion regulation as well as alexithymia, and this perspective has also been applied to understand alcohol use disorders. One hypothesized function of attachment is the interpersonal regulation of affective experiences (Shaver & Mikulincer, 2007; Sroufe, 1977).

One hypothesized function of attachment is the interpersonal regulation of affective experiences (Shaver & Mikulincer, 2007; Sroufe, 1977). In the development of alexithymia, attachment theories stress the importance of significant others in childhood (Krystal & Krystal, 1988; Nemiah, 1977; Taylor et al., 1997). Evidence suggests that alexithymia is related to dysfunctional parenting (Thorberg, Young, Sullivan & Lyvers, in press).

Insecure attachment is associated with alexithymia and both harmful drinking and alcohol-dependence (Cooper, Shaver, & Collins, 1998; De Rick & Vanheule, 2006; Thorberg & Lyvers, 2006; Thorberg, Young, Sullivan, Lyvers, Connor & Feeney, 2009). In addition, alcohol abuse has been hypothesized to be a consequence of alexithymia (Taylor, Bagby, & Parker, 1997).

Research on alexithymia (1) has found significant positive associations between alexithymia, difficulties identifying feelings, difficulties describing feelings and alcohol problems (Thorberg, Young, Sullivan, & Lyvers, 2009; Thorberg, Young, Sullivan, Lyvers, Connor & Feeney, 2010). Individuals with alcohol-dependence and alexithymia report more severe alcohol problems compared to those with alcohol-dependence alone (Sakuraba, Kubo, Komoda, & Yamana, 2005; Uzun, Ates, Cansever, & Ozsahin, 2003). They also have poorer treatment outcomes (Loas, Fremaux, Otmani, Lecercle, & Delahousse, 1997; Ziolkowski, Gruss, & Rybakowski, 1995).

Individuals may use alcohol to escape feelings of rejection and establish a “secure attachment base” (Hofler & Kooyman, 1996), given alcohol’s stress and anxiety reducing effects.

In this study (1)  results highlight the importance of alexithymia and difficulties identifying and describing feelings as related to preoccupation, obsessions and compulsive behaviors regarding drinking in those with alcohol-dependence. Or in more simple terms between alexithymia and craving.  In this study 32.4% of this alcohol dependent groups were alexithymic. This is less than previously reported prevalence rates of 45-67% (Thorberg et al., 2009).

In this study (1)  alcohol-dependence severity, alexithymia and insecure attachment were associated with more intrusive and interfering cognitions, ideas and impulses about alcohol, including an impaired ability to control these thoughts and impulses. This cognitively based “craving” as measured by the Obsessive Compulsive Drinking Scale (OCDS; Anton, Moak, & Latham, 1995), which is designed to assess obsessive thoughts and compulsive behavior toward drinking.

Hence there was a demonstrated relationships between alexithymia, craving, anxious attachment and alcohol problems in an alcohol-dependent sample. Higher levels of alexithymia led to a stronger desire for alcohol that was partially explained by an underlying mechanism, anxious attachment. One possible reason for this  it may reflect an impairment in affect regulation.

Findings of the RAAS-Anxiety scale measured insecure attachment as related to a current or previous relationship, these findings may suggest that worries about being rejected, not cared for or unloved lead to an increased craving for alcohol.

One explanation for this mediational relationship may perhaps be that increased relationship stress is associated with a fear of intimacy and anxious attachment that leads to increased craving and perhaps a stronger attachment to alcohol. In other words, the alexithymia of insecure attachment may cause a stress dysregulation which prompts craving particularly as craving is a consequence of dysregulated stress systems. Stress dysregulations is also implicated in increased or more chronic alexithymia as suggested by George Koob in various articles. This has also been observed in other studies – this relationships of negative affect (anxiety, negative mood and emotion) with both alexithymia and craving (Sinha & Li, 2007).

To summarise, the results of this study support important relationships between alexithymia, difficulties identifying and describing feelings in relation to alcohol craving. These relationships extend to significantly higher levels of obsessive thoughts and compulsive behaviors in relation to alcohol use and alcoholism severity amongst individuals with combined alexithymia and alcohol-dependence, compared with alcohol-dependence alone. This study identified anxious attachment as a potentially important mechanism, in the relationship between alexithymia and alcohol craving.

References De Rick, A., Vanheule, S., & Verhaeghe, P. (2009). Alcohol addiction and the attachment system: an empirical study of attachment style, alexithymia, and psychiatric disorders in alcoholic inpatients. Substance use & misuse,44(1), 99-114.

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.

Measuring the so-called “Alcoholic Personality”.

Measuring the So-called “Alcoholic Personality”?

Guest Blog

by Paul Henry

We recently came across an article which satisified some of our curiosity with regards to two important theoretical and research considerations in relation to both the accurate definition of  the so-called “addictive or alcoholic personality “, which has falling out of fashion in terms of recent research but which still intrigues some researchers, while also addressing, in passing, an issue of so-called co-morbidity which is reported to be high in alcoholics, particularly generalized anxiety disorder (GAD).

We have written in the past about co-morbidities and whether the prevalence of co-occurring conditions or psychiatric disorders such as GAD are as prevalent as many researchers suggest.

We will discuss difficulties with measuring co-morbidities in later blogs. The study we cite here appears to be reporting that  so-called anxiety reported here in this participant pool of alcoholic dependent people were  transient. This tallies with our own ancedotal evidence of anxiety disappearing as recovery proceeds or in the words of this study “high state anxiety unlike those with anxiety neurosis, who have a high trait anxiety. This indicates that anxiety in alcohol-dependent individuals is transitory, varies in intensity and fluctuates over time, and can be easily modified.”

This type of finding outlines difficulties in diagnosing GAD in alcoholics and supports the idea that anxiety is transient. In fact we suggest that the symptoms of anxiety often expressed in alcoholics may be the result of escalating chronic stress and emotional dysregulation in the addiction cycle and which appears to lessen or disappear in recovery or be provoked by situations.

Potential alcoholics tend to be emotionally immature, expect a great deal of the world, require an inordinate amount of praise and appreciation, react to failure with marked feelings of hurt and inferiority, have a low frustration tolerance, and feel inadequate and unsure of their abilities to fulfil expected male or female roles.1

This study (1) found significantly higher scores on extroversion which indicates that alcohol-dependent subjects are characterized by traits such as being more assertive, dominant, sociable, carefree and venturesome as compared to non-dependent people. This finding is in agreement with that of Mathew and Baby13

Alcohol-dependent patients also obtained significantly higher scores on the neuroticism dimension. This indicates that they are significantly more emotional, frequently anxious and/or depressed, moody and tense. Similar results were reported in earlier studies.12,15

Among the personality traits studied in alcohol-dependent individuals, antisocial personality has been looked into most often.1 In this study alcohol-dependent subjects obtained significantly higher scores which is in agreement with the findings of Neeliyara et al.16 A longitudinal study of men older than 40 years also revealed that antisocial behaviour in adolescence is the sole individual predictor of alcoholism.17  However, it must be pointed out here that the high Pd scores in alcohol-dependent patients indicate a transitory state, which may be amenable to change with treatment. Our finding that alcohol-dependent patients showed disturbances in the depression, mania, schizophrenia, psychopathic deviance and anxiety scales is consistent with previous research that the emotional disturbance in people with substance abuse is broad-based, variable and non-specific.18

Alcohol-dependent individuals also obtained significantly higher trait and state anxiety scores.  These findings support those of a few earlier studies.14,16

This aspect may be aetiologically significant in alcohol dependence. Anxiety has been suggested to be an important factor in the initial development and subsequent maintenance of alcohol abuse and dependence. Some patients use alcohol as a medication for the treatment of anxiety. Unfortunately, an accurate diagnosis of anxiety disorders is difficult to make, since current anxiety symptoms may be secondary to alcohol withdrawal rather than reflecting underlying anxiety disorders.19 The findings of this study also reveal that alcohol-dependent individuals are different from those with anxiety neurosis, since they have a high state anxiety unlike those with anxiety neurosis, who have a high trait anxiety. This indicates that anxiety in alcohol-dependent individuals is transitory, varies in intensity and fluctuates over time, and can be easily modified.



One of the sources of anxiety is a low level of self-esteem, fear of disapproval from significant people, loss of position, prestige, stature or self-esteem.16 Thus, these findings also support our finding that alcoholics have low self-esteem.

Patients with alcohol dependence experience significantly more stressful life events in the past year and over their lifetime. These findings are in line with previous reports.13,14,20.

Men who are lifelong abstainers experience fewer life events than problem drinkers. Alcoholics may offset stress-induced emotional distress by resorting to drink which, in turn, might lead to a further increase in negative life events.

A person’s self-structure is an important aspect of his personality. A healthy personality is manifested when an individual has a positive attitude towards him/herself. Studies in this area have shown that psychiatric patients have unhealthy self-structures by way of poor self-concept. In this view, alcohol-dependent individuals suffer from lowered feelings of self-esteem, pervasive feelings of inferiority and powerlessness, coupled with unusually strong inhibitions against the expression of hostile or aggressive impulses. In the present study, alcohol-dependent individuals had significantly lower self-esteem as compared with normal subjects. This finding is in agreement with that of Neeliyara et al.16 This indicates that alcohol-dependent individuals have less positive self-feelings and more feelings of alienation and isolation.

Higher numbers of alcohol-dependent subjects were identified to have alexithymia. This finding is congruent with earlier work.15,21 

In recently sober alcoholics the alexithymic cognitive dimension—an inability to identify feelings and to distinguish them from bodily sensations—is related to depressive symptoms and suicidal ideation.

Finally this study concluded that alcohol-dependent individuals show significantly high neuroticism, extroversion, anxiety, depression, psychopathic deviation and significantly low self-esteem as compared to normal control subjects. Significantly more alcoholics were found to be alexithymic.

So what does this study tell us? It is useful in illustrating the transient nature of some co-called co-morbid disorders such as GAD. It more importantly does highlight   certain personality characteristics which we believe, based on extensive ancedotal evidence of a number of years in recovery, are relevant and pertinent to alcohol-dependent people. In fact in recovery, new comers to recovery are often warned against the very variables highlighted here such as not isolating from others in recovery.

Ultimately, however, we believe that the personality characteristics mentioned in this study come under a wider definitional umbrella of emotional regulation and processing deficits which manifest as these personality characteristics and explain not only these characteristics but also the sometimes situationally specific trait anxieties and perhaps other co-morbidities.


1. Chaudhury, S.K. Das, B. Ukil,  Psychological assessment of alcoholism in males Indian J Psychiatry. 2006 Apr-Jun; 48(2): 114–117. doi: 10.4103/0019-5545.31602

Understanding Emotional Processing Deficits in Addiction – Guest Blog

Understanding Emotional Processing Deficits in Addiction

by alcoholicsguide

We recently blogged on how alcoholics, and children of alcoholics, have difficulty with recognizing and differentiating external signs of emotions such as facial emotional expressions, now we will consider increasing evidence that alcoholics have difficulties with identifying and differentiating internal emotional states also.

Both these areas of research point to real difficulties in alcoholics in relation to the processing of emotion.

As we shall explain below, this deficit in emotional processing has real consequence for decision making capabilities and this has an important role to play in the initiation and maintenance of substance abuse and eventual addiction.

Alexythymia and Addiction

Effective emotion regulation skills include the ability to be aware of emotions, identify and label emotions, correctly interpret emotion-related bodily sensations, and accept and tolerate negative emotions (2,3).

Alexithymia is characterized by difficulties identifying, differentiating and expressing feelings. The prevalence rate of alexithymia in alcohol use disorders is between 45 to 67% (4,5)

Finn, Martin and Pihl (1987) investigated the presence of alexithymia among males at varying levels of genetic risk for alcoholism. They found that the high risk for alcoholism group was more likely to be alexithymic than the moderate and low genetic risk groups (6).

Higher scores on alexithymia were associated poorer emotion regulation skills, fewer percent days abstinent, greater alcohol dependence severity (7). Some studies have emphasized a right hemisphere deficit in alexithymia [8,9] based on the hypothesis that right hemisphere plays a more important role in emotion processing than the left [10, 11].

Dysfunction of the anterior cingulate cortex has been frequently argued, e.g., [12], and others have focused on neural substrates, such as the amygdala, insula, and orbitofrontal cortex (see the review in [13]). All different components of the the emotional regulation  network.

These models may interact with each other and also map onto the brain region morphological vulnerability mentioned as being prevalent in alcoholics.

Magnetic resonance imaging and post-mortem neuropathological studies of alcoholics indicate that the greatest cortical loss occurs in the frontal lobes, with concurrent thinning of the corpus callosum. Additional damage has been documented for the amygdala and hippocampus, as well as in the white matter of the cerebellum. All of the critical areas of alcoholism-related brain damage are important for normal emotional functioning (14) .

One might speculate that thinning of the corpus collosum may render alcoholics less able to inhibit negative affect in right hemisphere circuits.

Alcoholics are thus vulnerable to thinning of the corpus collosum and perhaps even to emotional processing difficulties (15 ). The inability to identify and describe affective and physiological experiences is itself associated with the elevated negative affect (16) commonly seen in alcoholics, even in recovery (17.

Thus, this unpleasant experience might prompt individuals to engage in maladaptive behaviors, such as excessive alcohol consumption, in an effort to regulate emotions, or, more specifically, cope with negative emotional states (18 )

One neuroimaging study (19) looked at and compared  various models of alexithymia showing people with alexithymia showed reduced activation in the dorsal ACC and right anterior insula (AI), and suggested individuals who exhibit impaired recognition of their own emotional states may be due to a dysfunction of the ACC-AI network, given these regions’ important role in self-awareness. These studies suggest alexithymics may not be able to use feelings to guide their behaviour appropriately.

The Iowa gambling task (IGT) was developed to assess decision-making processes based on emotion-guided evaluation. When alexithymics perform the IGT, they fail to learn an advantageous decision-making strategy and show reduced activity in the medial prefrontal cortex, a key area for successful performance of the IGT, and increased activity in the caudate, a region associated with impulsive choice (20).

ep neg

The neural machinery in alexithymia is therefore activated more on the physiologic, motor-expressive level, similar to the study on children of alcoholics and thus may represent a vulnerability.

The function of the caudate is to regulate or control impulsivity and disinhibition. Individuals with alexithymia may work on the IGT impulsively rather than by using emotion-based signals. This IGT study suggests that individuals with alexithymia may be unable to use feelings to guide their behavior appropriately.

Alexithymic individuals thus may be unable to use emotion for flexible cognitive regulation. Thus, there may be dysfunction in the interaction of the aspects of the emotional response system in alexithymia with greater activation in the caudate (basal ganglia) and less activation in the mPFC in alexithymics during the IGT.

Thus alexithymics show weak responses in structures necessary for the representation of emotion used in conscious cognition and stronger responses at levels focused on action. This ties in with the blog on an emotional disease? and also  so how is your decision making? which suggested that alcoholics do not use emotion to guide decision making and rely on more motor, or automatic/compulsive parts of the brain to make decisions.

Consequently, alexithymics experience inflexible cognitive regulation, owing to impairment of the emotion guiding system. These dysregulated physiological responses over many years may result in untoward health effects such as drug addiction.

To illustrate this, one study demonstrated that patients with cocaine dependence had higher alexithymia scores compared with healthy control subjects (21).

In a study of 46 inpatients with alcohol abuse or dependence, the total TAS (Toronto Alexithymia Scale) score was significantly higher among those who relapsed after discharge than among those who did not, even when depressive symptoms were taken into account(4)

Cocaine-dependent patients also failed to activate the anterior cingulate and other paralimbic regions during stress imagery, suggesting dysregulation of control under emotional distress in these patients (22).

Instead, cocaine-dependent patients demonstrated greater craving-related activation in the dorsal striatum, a region that has been implicated in reward processing and obsessive–compulsive behaviours. The greater activation associated with alexithymia in men in the right putamen during stress is broadly consistent with earlier studies implicating the striatum in emotional motor responses.

This also corresponds to  the study of  children of alcoholics show significantly more activation in the left dorsal anterior cingulate cortex and left caudate nucleus a region associated with impulsive choice, illustrating perhaps in children of alcoholics a bias in brain decision-making systems as an underlying  elevated risk for alcoholism.

We have also suggested previously a ‘compulsive’ emotional  habit bias in endpoint addiction which reflects a stiumulus response or automatic behaviour in the face of emotional distress, which then influences an automatic decision making profile. This may be the effect of chronic drug use impacting on an inherited emotional expressive-motor decision making vulnerability seen in children of alcoholics.

In simple terms, these vulnerable individuals may recruit more automatic rather than goal-directed areas of the brain when making decisions. This would result in impulsive/compulsive decisions which do not fully consider consequences, negative or otherwise, of their decisions and resultant actions. This decision making profile would then have obvious consequences in terms of a propensity to addiction.


References (to be finished)

1. Naqvi, N. H., & Bechara, A. (2009). The hidden island of addiction: the insula.Trends in neurosciences32(1), 56-67.

2. Berking M, Margraf M, Ebert D, Wupperman P, Hogmann SG, Junghanns K. Deficits in emotion-regulation skills predict alcohol use during and after cognitive-behavioral therapy for alcohol dependence. Journal of Consulting and Clinical Psychology. 2011;79:307–318

3. Gratz KL, Roemer L. Multidimensional assessment of emotion regulation and dysregulation: Development, factor structure, and initial validation of the Difficulties in Emotion Regulation Scale. Journal of Psychopathology and Behavioral Assessment.2004;26:41–54

4. Loas G, Fremaux D, Otmani O, Lecercle C, Delahousse J. Is alexithymia a negative factor for maintaining abstinence? A follow-up study. Comprehensive Psychiatry. 1997;38:296–299.

5. Ziolkowski M, Gruss T, Rybakowski JK. Does alexithymia in male alcoholics constitute a negative factor for maintaining abstinence. Psychotherapy and psychosomatics. 1995;63:169–173.

6.  Finn PR, Martin J, Pihl RO. Alexithymia in males at high genetic risk for alcoholism.Psychotherapy and Psychosomatics.1987;47:18–21

7.  Moriguchi, Y., & Komaki, G. (2013). Neuroimaging studies of alexithymia: physical, affective, and social perspectives. BioPsychoSocial medicine7(1), 8.

8. Miller L. Is alexithymia a disconnection syndrome? A neuropsychological perspective. Int J Psychiatry Med. 1986;7:199–209. doi: 10.2190/DAE0-EWPX-R7D6-LFNY.

9. Sifneos PE. Alexithymia and its relationship to hemispheric specialization, affect, and creativity.Psychiatr Clin North Am. 1988;7:287–292.

10. Buchanan DC, Waterhouse GJ, West SC Jr. A proposed neurophysiological basis of alexithymia. Psychother Psychosom. 1980;7:248–255. doi: 10.1159/000287465.

11. Shipko S. Further reflections on psychosomatic theory. Alexithymia and interhemispheric specialization. Psychotherapy and psychosomatics.

12. Lane RD, Reiman EM, Axelrod B, Yun LS, Holmes A, Schwartz GE. Neural correlates of levels of emotional awareness Evidence of an interaction between emotion and attention in the anterior cingulate cortex. J cognitive neuroscience. 1998;7:525–535. doi: 10.1162/089892998562924.

13. Wingbermühle E, Theunissen H, Verhoeven WMA, Kessels RPC, Egger JIM. The neurocognition of alexithymia: evidence from neuropsychological and neuroimaging studies.Acta Neuropsychiatrica. 2012;7:67–80. doi: 10.1111/j.1601-5215.2011.00613.x.

14. Oscar-Berman, M., & Bowirrat, A. (2005). Genetic influences in emotional dysfunction and alcoholism-related brain damage.

15. Sperling W, Frank H, Martus P, et al. The concept of abnormal hemispheric organization in addiction research. Alcohol Alcohol.2000;35:394–9.

16.  Connelly M, Denney DR. Regulation of emotions during experimental stress in alexithymia. Journal of Psychosomatic Research. 2007;62:649–656

17. Stasiewicz, P. R., Bradizza, C. M., Gudleski, G. D., Coffey, S. F., Schlauch, R. C., Bailey, S. T., … & Gulliver, S. B. (2012). The relationship of alexithymia to emotional dysregulation within an alcohol dependent treatment sample.Addictive Behaviors37(4), 469-476.

18.  Thorberg FA, Young RM, Sullivan KA, Lyvers M, Hurst CP, Connor JP, Feeney GFX. Alexithymia in alcohol dependent patients is partially mediated by alcohol expectancy. Drug and Alcohol Dependence. 2011;116:238–241

19. Moriguchi, Y., & Komaki, G. (2013). Neuroimaging studies of alexithymia: physical, affective, and social perspectives. BioPsychoSocial medicine7(1), 8.

20.  Kano M, Fukudo S. The alexithymic brain: the neural pathways linking alexithymia to physical disorders. BioPsychoSocial medicine. 2013;7:1. doi: 10.1186/1751-0759-7-1.

21.  Li, C. S. R., & Sinha, R. (2006). Alexithymia and stress-induced brain activation in cocaine-dependent men and women. Journal of psychiatry & neuroscience,31(2).

22.  Sinha, R., Lacadie, C., Skudlarski, P., Fulbright, R. K., Rounsaville, B. J., Kosten, T. R., & Wexler, B. E. (2005). Neural activity associated with stress-induced cocaine craving: a functional magnetic resonance imaging study.Psychopharmacology183(2), 171-180.

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