vulnerability

Is the Impulsive Behaviour that Precedes Addiction Hardwired into the Brain?

Posted on by alcoholicsguide

In various blogs we have forwarded the idea that emotional and stress dysregulation are that the heart of addiction and alcoholism and are also possible present in those at risk to these disorders.

Essentially we suggest that the behavioural endpoint of addictive behaviours, the distress based impulsivity (negative urgency) seen in alcoholics and addicts which shapes decision making may be the consequence of chronic neurotoxic activity (as the consequence of chronic alcohol and drug use)  on brain areas which have a pre-existing impairments or vulnerability such as brain regions involved in emotional regulation, processing, inhibition and stress and reward response.

Here we cite an article (1) which looks at some of these brain regions, specifically those involved in emotional regulation and impulsivity and considers whether these deficits may be “hardwired” into the brain in terms of white and grey matter impairments.

 

Brain areas actively developing during adolescence include the prefrontal cortex, limbic system areas, and white matter myelin ( electrically insulating material that forms a layer, the myelin sheath – the yellow insulation below), usually around only the axon of a neuron. It is essential for the proper functioning of the nervous system.)

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These areas serving cognitive, behavioral, and emotional regulation may be particularly vulnerable to adverse alcohol effects.

Alternatively, deficits or developmental delays in these structures and their functions may underlie liability to accelerated alcohol use trajectories in adolescence.

The prefrontal cortex, limbic brain regions, white matter ( composed of bundles of myelinated nerve cell axons which connect various grey matter areas (the locations of nerve cell bodies) of the brain to each other (see below – grey on outside, white inside) and carry nerve impulses between neurons. Myelin acts as an insulator, increasing the speed of transmission of all nerve signals, and reward circuits undergo active development during adolescence (Chambers et al., 2003; Spear, 2000).

 

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These structures and their functions, involving behavioral, emotional and cognitive regulation, may be particularly vulnerable to the adverse effects of alcohol exposure during adolescence.

Delays or deficits in the development of neural substrates necessary for these psychological regulation abilities to fully develop may be termed neurodevelopmental dysmaturation.

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Psychological Dysregulation

The development of accelerated alcohol involvement in adolescence is not an isolated phenomenon, but is typically presaged by persistent behavioral characteristics including attentional deficits, conduct problems, and irritability (Chassin et al., 1999; Clark et al., 1997a, 2005; Tapert et al., 2002).

Two main psychological factors have been identified: (1) Behavioral Undercontrol, comprised of conduct disorder symptoms and personality characteristics including aggression and diminished constraint, and (2) Negative Emotionality, comprised of depression, anxiety and stress reactivity variables (Martin et al., 2000).

These two factors were significantly correlated. These correlated characteristics have been hypothesized to comprise the early phenotypic manifestations of a core liability for SUDs (Tarter et al., 1999).

The proposed construct manifested by these psychopathologic features has been termed psychological dysregulation (Clark and Winters, 2002). Psychological dysregulation is a deficiency in the ability to regulate attention, emotions and behavior in response to environmental challenges. Psychological regulation is thus the ability to modulate prepotent responses in order to optimize reward opportunities. The skills involved in psychological regulation include executive cognitive functioning (ECF), behavioral inhibition and emotional management.

Deficiencies in psychological regulation may be the result of delays or persistent deficits in the acquisition of behavioral, emotional, and cognitive regulation skills.

Adolescents at risk for developing SUDs exhibit deficits in psychological regulation. Childhood psychological dysregulation, or neurobehaviour disinhibition, correlates with parental substance use disorders (SUDs) and prospectively predicts adolescent alcohol and other substance use as well as related disorders (Clark et al., 2005; Tarter et al., 2003).

The psychological dysregulation dimension integrates several psycho patholological dimensions heretofore considered distinct, including affective disorders and SUDS themselves (Krueger et al., 2002).

Neurobiological Basis of Psychological Dysregulation

The functions subsumed under the construct of psychological dysregulation are thought to be served by the prefrontal cortex (Koechlin and Summerfield, 2007). The capabilities that comprise psychological regulation improve during adolescence (Levin et al., 1991; Welsh et al., 1991). The ongoing development of the prefrontal cortex has been hypothesized to be the primary neurobiological foundation for the advancement of these abilities (Happaney et al., 2004; Spear, 2000). Developmental abnormalities in the frontal cortex have been found in children and adolescents with behavioral problems reflecting psychological dysregulation (Rubia et al., 2000; Spear, 2000).

Diffusion tensor imaging (DTI) studies  indicated that white matter organization increases from early childhood to young adulthood (Klingberg et al., 1999; Nagy et al., 2004; Schmithorst et al., 2002; Zhang et al., 2005).White matter development may underlie advancing executive functioning. The prefrontal cortex is a brain region undergoing relatively late gray matter pruning, and volumes of gray matter appear to decrease over adolescence (Gogtay et al., 2004; Lenroot and Giedd, 2006; Sowell et al., 2001, 2004). Unlike grey matter volume, white matter volume appears to increase during adolescence, particularly in the prefrontal area (Ashtari et al., 2007;Barnea-Goraly et al., 2005; Lenroot and Giedd, 2006).

 

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White Matter Development and Alcohol Exposure

Selective white matter loss has been reported among adults with Alcohol Use Disorders (AUDs) (Carlen et al., 1978, 1986) and with fMRI (Agartz et al., 2003), and postmortem specimens (Krill et al., 1997).  Compared with controls, adolescents with AUDs have been found to have smaller prefrontal white matter volumes (DeBellis et al., 2005). Prefrontal grey and white matter volumes were compared in adolescents with AUDs. Compared with control subjects, subjects with AUDs had significantly smaller prefrontal white matter volumes.Marijuana use has also been found to be associated with smaller white matter volumes in adolescents (Medina et al., 2007b). While these volumetric findings suggest problematic frontal development among adolescents with AUD, the emergence of neuroimaging techniques developed to examine white matter organization may prove to be more specifically relevant to understanding the effects of alcohol on neurodevelopmental maturation.

Changes in gene expression may be involved in alteration of white matter structure in AUDs.  In a postmortem study, myelin-related genes were found to be down-regulated in the AUD group (Lewohl et al., 2000).

While evidence has been presented that alcohol consumption may disrupt white matter organization, the possibility remains that delayed or diminished white matter organization may presage alcohol involvement and constitute a risk factor for AUDs. Immaturity of white matter development and the related deficits in the functional integration of brain areas may in part explain individual differences in psychological regulation during adolescence. For example, disruptive behavior disorders in childhood, particularly conduct disorder, have been found to predict accelerated trajectories of alcohol use, cannabis use, and substance-related problems in adolescence (Clark et al., 1999).

Limbic System Development and Alcohol Exposure

The limbic system is central to the processing of affective stimuli, the successful formation of new memories, and the implementation of related responses. Limbic system structures, including the hippocampus and amygdala, may be susceptible to alcohol-induced dysmaturation.

Smaller hippocampal volumes have been reported in adults with AUDs compared with control adults (Sullivan et al., 1995). As hippocampal development progresses in adolescence (Gogtay et al., 2006), this brain area may be particularly susceptible to the adverse effects of alcohol involvement during this developmental period.

DeBellis et al. (2000) compared the hippocampal volumes of 12 adolescents and young adults with adolescent-onset AUD to those of 24 control subjects. Both left and right hippocampi were significantly smaller in AUD subjects compared to the volumes in controls. Specifically, left hippocampal volumes were smaller in teens with AUD than demographically similar controls, and youth with greater severity of AUD had the smallest left hippocampal volumes (Medina et al., 2007a; Nagel et al., 2005).

The amygdala may also be important for understanding the neurodevelopmental effects of alcohol exposure. The amygdala, along with ventral striatum, has been hypothesized to be involved in reward mechanisms and thereby critical for understanding alcohol use trajectories (Koob, 1999). Amygdala volumes have been found to be relatively smaller in high-risk older adolescents and adults with SUDs compared to that in control subjects (Hill et al., 2001; Makris et al., 2004). Lack of correlation with use levels has led to the suggestion that this may be a predisposing characteristics rather than a substance effect.

Interacting brain areas are involved in reward processing (McClure et al., 2004), motivation (Chambers et al., 2003), and decision-making (Verdejo-Garcia et al., 2006).  The interactions between the prefrontal cortex and subcortical areas, including the amygdala and nucleus accumbens, constitute the neurocircuitry involved in reward responding. In the affective component of reward responding, the amygdala appears to be a network node involved in reactivity to emotional stimuli (Hariri et al., 2006; Schwartz et al., 2003). An understanding of the adolescent development of neural circuits underlying reward processing and decision making is central to considering the role of these systems in the development of alcohol involvement.

Impulsivity, defined as acting without forethought, progressively decreases from childhood into adulthood. This change has been thought to occur as a result of neuromaturation in the prefrontal cortex (Casey et al., 2005).

The generation of behaviors optimizing long-term reward opportunities often involves behavioral inhibition. The activation of prefrontal cortical areas during response inhibition tasks has been found to increase from childhood through adolescence, a change corresponding to the development of abilities to suppress prepotent behaviors (Luna and Sweeney, 2004; Luna et al., 2004). The ability to select an optimally adaptive behavioral response while suppressing a predominant or prepotent response with problematic consequences defines impulse control and is fundamental to psychological regulation skills. Improved abilities in response inhibition and related prefrontal activation during adolescence are thought to involve maturation of functional connectivity subserved by ongoing myelination.

Adolescents with psychopathology predictive of SUDs, similar to adults with alcohol dependence, have difficulty with behavioral inhibition during laboratory tasks (Bjork et al., 2004a; Dougherty et al., 2003; Schweinsburg et al., 2004). Furthermore, adolescents with histories of substantial marijuana use, compared with control adolescents, showed more activation in frontal cortical areas during behavioral inhibition tasks (Tapert et al., 2007). More activitation suggests greater effort was required by the marijuana using group.

 

References

1.  Clark, D. B., Thatcher, D. L., & Tapert, S. F. (2008). Alcohol, psychological dysregulation, and adolescent brain development. Alcoholism: Clinical and Experimental Research, 32(3), 375-385.

 

Understanding Emotional Processing Deficits in Addiction – Guest Blog

Posted on by alcoholicsguide

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).

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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 neurosciences, 32(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 medicine, 7(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 Behaviors, 37(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 medicine, 7(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.Psychopharmacology, 183(2), 171-180.

Do alcoholics drive through life with Faulty Brakes!

Posted on by alcoholicsguide

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.

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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.

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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.

 

References

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.

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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.

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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.

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At Risk Adolescents have Emotional Dysregulation?

Posted on by alcoholicsguide

Following up from our previous blog on the abnormalities in the ventromedial prefrontal cortex  (vmPFC) in alcoholics,  brain regions which govern emotional regulation, we came across another study which appears to show that adolescents at increased risk for later alcohol use disorders (AUDs) may also be showing an emotion regulation difficulty.

This emotional regulation difficulty may be a biomarker for later alcoholism, which is in keeping with our previous proposals that an emotional processing and regulation difficulty or disorder underpins the aetiolgy of of alcoholism. In order words it is part of the pathomechanism – or the mechanism by which a pathological condition occurs- of later alcoholism.

 

 ventromedial-prefrontal-cortex

 

The area in this study, the vmPFC,   showed relatively increased cerebral blood flow (CBF) in bilateral amygdala and vmPFC and relatively decreased CBF in bilateral insula, right dorsal anterior cingulate cortex (ACC) and occipital lobe cuneus of high-risk adolescents. This suggests that adolescents at relatively high-risk for AUD exhibit altered patterns of resting CBF in distributed corticolimbic regions supporting emotional behaviors.

The authors’ hypothesized that the relatively increased amygdala and ventromedial prefrontal CBF may contribute to increased emotional reactivity and sensitivity to environmental stressors in these individuals while diminished insula/occipital cuneus and dorsal anterior cingulate cortex (ACC) CBF may lead to poor integration of visceral and sensory changes accompanying such emotional stress responses and top-down regulation of amygdala reactivity.

Thus we see our model in a snapshot even in adolescents potentially.  The emotional processing deficits we have discussed previously implicate the insula and ACC, as there appears to be a difficulty in alcoholics in reading emotional or somatic signals/states and integrating these signals into the identifying, labelling and processing of emotions. Equally there appears to be a hyperactivty in the vmPFC and amgydala as with alcoholics which implies emotional dysregulation, a hyper reactive emotional response and a tendency perhaps to a more “fight or flight” response, distress based impulsivity and short termist decision making, wanting it NOW rather than later.

 

References Lin, A. L., Glahn, D. C., Hariri, A. R., & Williamson, D. E. (2008). Basal Perfusion in Adolescents at Risk for Alcohol Use Disorders. In Proc. Intl. Soc. Mag. Reson. Med (Vol. 16, p. 60).

Alcoholics as secret overachievers!

Posted on by alcoholicsguide

A recent article suggests that  some people may have a genetic predisposition to alcoholism. Dr Alexander Niculescu  and his team, identified 11 “risk” genes (1) that can predict which people are more at prone to becoming alcoholic. For those with a family history of alcoholism, the danger is even greater. All of this can be detected with a simple genetic test.

“Having a family history already suggests that there is a genetic risk that’s being transmitted. Those people should not expose themselves to temptation and drink even small amounts, as they are more prone to go down a slippery slope of higher amounts of alcohol and full-blown alcoholism,” Dr Niculescu said.

Dr Niculescu said these gene variants also have a lot to do with drive and compulsions, which can be used for positive things like professional achievement. “What we are discovering at the biological level is that there is this physiological robustness and drive that goes hand in hand with predisposition or compulsion to alcoholism and if you manage to avoid getting sucked into alcoholism and just use your biological endowments and drive for other things, you might be an overachiever in other areas.”

In the conclusion to the article it states that  it is likely at its core a disease of an exogenous agent (alcohol) modulating different mind domains/dimensions (anxiety, mood and cognition) precipitated by environmental stress on a background of genetic vulnerability (2).

In simple language, this is what we have been suggesting in this blog. Alcohol acts on underlying mechanisms  relating to anxiety, mood, cognition, which we view under the umbrella term of emotional regulation and processing deficits.

It also shows how genetic vulnerability may overlap with other psychiatric disorders, overlap does not mean the same as.

 

 

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The oft cited co-morbidities which supposedly co-occur alongside alcoholism are in fact not co-morbidity in our view  but intrinsic to the condition. Although this argument and article at least acknowledges there is a growing debate about what constitutes co-morbidity and pathology in alcoholism.

For us alcoholism is these so-called “co-morbidities” mixed with the deleterious effects of chronic alcohol on these deficits and which are commonly exacerbated pre-morbidity or before the actual start of alcohol use by traumatising or distressing early childhood experiences which have been known to result in both stress and emotional dysregulation which in turns leads to a heightening of the rewarding effect of alcohol (or drugs) as stress chemicals increase dopamine in reward networks such as the nucleus accumbens. Alcoholics find a “solution” to their emotional difficulties in the the heightened, calming effects of alcohol and eventually find in the course of time and chronic use that they cannot do without it.

For us genetically, this research is showing what manifestly, in terms of emotional and behavioural problems, is being shown by cognitve, affective and clinical neuroscience.

It also explains why so many recovering alcoholics surprise us and themselves, especially those underachievers at school of which I am one, with their vigour, intelligence and achievements in recovery once they have climbed out of their own personal hell of active alcoholism.

It also explains how they physically survived ordeals which would have killed most. 

References

Levey, D. F., Le-Niculescu, H., Frank, J., Ayalew, M., Jain, N., Kirlin, B., … & Niculescu, A. B. (2014). Genetic risk prediction and neurobiological understanding of alcoholism. Translational psychiatry, 4(5), e391.

Niculescu AB 3rd, Schork NJ, Salomon DR. Mindscape: a convergent perspective on life, mind, consciousness and happiness. J Affect Disord2010; 123: 1–8. |