Measuring the “Psychic” Change

Prolonged Abstinence and Changes in Alcoholic Personality?

When I came into AA I remember hearing the words “the need for a psychic change” which was the product of a spiritual awakening (as the result of doing the 12 steps).

The big Book of Alcoholics Anonymous clearly states this need “The great fact is just this, and nothing less: That we have had deep and effective spiritual experiences* which have revolutionised our whole attitude toward life, towards our fellows and toward God’s universe.”

This is the cornerstone of AA recovery; thinking, feeling and acting differently about the world to when we were active drinkers. Otherwise one does the same things and ends up in the same places, doing the same things, namely drinking. It is a behavioural revolution; a sea change in how we perceive and act.

In line with this thinking, we came across this French study which measured via questionnaire the very same changes that occur in recovery. The French study uses different term for alcoholics and recovery but is saying the same things – it is we that need to change, not the world.

This study aimed to examine whether personality traits were modified during prolonged abstinence in recovering alcoholics. Groups of both recovering and recently detoxified alcoholics were asked via questionnaire to see if they differed significantly from each other in three personality domains: neuroticism, agreeableness and conscientiousness The recovering alcoholics were pooled from self help groups and treatment centres and the other group, the recently detoxified drinkers were pooled from various clinics throughout France.

Patients with alcohol problems who were administered the NEO PI-R had previously obtained a high “neuroticism” score (emotions, stress), associated with a low “agreeableness” score (relationship to others; Loukas et al., 2000). In the same vein, low “conscientiousness” scores (determination) were reported in patients who had abstained from alcohol for short periods (6 months to 1 year; Coëffec, Romo, & Strika, 2009)

In this study, recently detoxified drinkers scored high on neuroticism. They experienced difficulty in adjusting to events, a dimension which is associated with emotional instability (stress, uncontrolled impulses, irrational ideas, negative affect). Socially, they tend to isolate themselves and to withdraw from social relationships.

This also ties in with what the Big book also says “We were having trouble with personal relationships, we couldn’t control our emotional natures, we were prey to misery and depression, we couldn’t make a living, we had a feeling of uselessness, we were unhappy, we couldn’t seem to be of real help to other people-“

In contrast, regarding neuroticism, they found that recovering persons did not necessarily focus on negative issues. They were not shy in the presence of others and remained in control of their emotions, thus handling frustrations better (thereby enhancing their ability to remain abstinent).

Regarding agreeableness (which ties back into social relationships), the researchers also found that recovering persons cared for, and were interested in, others (altruism). Instead, recently detoxified drinkers’ low self-esteem and narcissism prevented them from enjoying interpersonal exchanges, and led them to withdraw from social relationships.

Finally, regarding conscientiousness, they observed that, over time, recovering persons became more social, enjoyed higher self-esteem (Costa, McCrae, & Dye, 1991), cared for and were interested in others, and wished to help them. They were able to perform tasks without being distracted, and carefully considered their actions before carrying them out; their determination remained strong regardless of the level of challenge, and their actions are guided by ethical values. Instead, recently detoxified drinkers lacked confidence, rushed into action, proved unreliable and unstable. As a result, lacking sufficient motivation, they experienced difficulty in achieving their objectives.

Recovering persons seemed less nervous, less angry, less depressed, less impulsive and less vulnerable than recently detoxified drinkers. Their level of competence, sense of duty, self-discipline and ability to think before acting increased with time.

The authors of the study concluded that “these results are quite encouraging for alcoholic patients, who may aspire to greater quality of life through long-term abstinence”.

However, in spite of marked differences between groups, their results did not provide clear evidence of personality changes. While significant behaviour differences between the two groups were revealed, they were more akin to long-term improvements in behavourial adequacy to events than to actual personality changes.

This fits in with the self help group ethos of a change in perception and in “taking action” to resolve issues. In fact, 12 steps groups such as AA are often referred to as utilising a “program of action” in recovering from alcoholism and addiction and in altering attitudes to the world and how they act in it.

The authors also noted the potential for stabilization over time by overcoming previous behaviour weaknesses, i.e. in responding to the world. Hence, this process is ”one of better adequacy of behaviour responses to reality and its changing parameters.”

In fact, treatment-induced behaviour changes showed a decrease in neuroticism and an increase in traits related to responsibility and conscientiousness.

In line with our various blogs which have explained alcoholism in terms of an emotional regulation and processing disorder, as the Big Book says ““We were having trouble with personal relationships, we couldn’t control our emotional natures” the authors here concluded that “rational management of emotions appears to be the single key factor of lasting abstinence”

References

Boulze, I., Launay, M., & Nalpas, B. (2014). Prolonged Abstinence and Changes in Alcoholic Personality: A NEO PI-R Study. Psychology, 2014.

Alcoholics Anonymous. (2001). Alcoholics Anonymous, 4th Edition. New York: A.A. World Services.

What makes some children of alcoholics vulnerable, and some resilient?

I come from a family of four siblings, two of whom are alcoholic and two who are not. I have often wondered why this is the case? Why is it the case that certain children of alcoholic parents will grow up to become alcoholics and why some will not? What is it that makes certain children vulnerable to alcoholism and other children, from the very same family, protected. What do these children have that protects them from later alcoholism?

This is especially important to know in terms of prevention strategies to help children at risk.

Obviously environment has an impact on vulnerability but does an inherited protectiveness help prevent this sometimes dysfunctional and abusive childhood environment of alcoholic parenting from having the same impact as those children who have inherited a genetic vulnerability?

Throughout our blogs has been a thread suggesting alcoholics, and children of alcoholics, may have difficulties in processing and regulating emotions. Is this the vulnerability, is there a difference in affective/emotional circuitry in the brain?

We cite a very interesting article here Affective circuitry and risk for alcoholism in late adolescence: Differences in frontostriatal responses between vulnerable and resilient children of alcoholic parents

in setting out an argument that children of alcoholics who are at greater risk of later alcoholism may have inherited impairments in brain neural circuitry which is responsible for affective/emotional processing.

Children of alcoholics (COAs) are at elevated risk for alcohol use disorders (AUD), yet not all COAs will develop AUD. One aim of this study was to identify neural activation mechanisms that may mark protection or vulnerability to AUD in COAs.

Some differences between alcohol abusers and control samples may precede alcoholism onset and thus constitute markers of precursive risk. After all, behavioral and affective markers early in life can predict later alcoholism (Caspi et al., 1996; Mayzer et al., 2001). Thus, it is reasonable to hypothesize that pre-alcoholic differences in the functioning of relevant neural systems will be related to risk for alcoholism.

In hoping to identify neural activation mechanisms that may mark protection or vulnerability to AUD in children of alcoholic fathers, the guiding conceptual framework was that the functioning of affective and behavioral regulation networks in the brain may serve as such mechanisms.

Consistent with that framework, the resilient and vulnerable groups were distinguished from one another by remarkably consistent inverse or opposite patterns of activation in the brain in response to the processing of emotional stimuli and which were most apparent with regard to negative affective stimuli and the vulnerable group.

These results suggest separate pathways of risk and resilience in the COA’s. First, the COA group that was not prone to early problem drinking (the resilient group) had more activation of the orbital frontal gyrus (OFG) than controls in response particularly to negative affect stimuli, but also to some extent in response to positive affect stimuli. The OFG is involved in the monitoring and evaluation of the affective value of stimuli, allowing for appropriate behavioral responses (Kringelbach and Rolls, 2004; Rolls, 2004).

The resilient group also had increased left insula activation to negative words. The insula is involved in evaluating internally generated emotions and the monitoring of ongoing internal emotional state (Phan et al., 2002).

The present findings, then, are consistent with the hypothesis that resilient youth have enhanced monitoring of emotionally arousing stimuli, even compared to typically developing youth. Yet, in an important nuance, they did not suppress the emotional experience.

They were prepared to modify behavioral response while maintaining affective response to these stimuli. This pattern of response in resilient youth may represent increased flexibility in emotional and social behavior. These youth may be exhibiting precisely an ability to delay external response to arousing stimuli, while internally processing those stimuli. In short, this may be a “reflective” pattern of approach to the world.

It is not difficult to speculate how this pattern might protect these at risk youth from substance misuse: they are able to respond to the emotional stimuli, but demonstrate enhanced monitoring that may allow for the inhibition of inappropriate responding, buying time for flexible response options based on well-processed information.

Interestingly, the vulnerable group displayed no differences from the control group in emotional monitoring and behavioral regulation systems (OFG and insula), suggesting that weakness in that system is not a risk factor. Rather, they demonstrated over-activation of DMPFC and an atypical under-activation of key emotion processing regions (particularly extended amygdala and ventral striatum). This pattern was more notable in regard to negative affect, it was also observed to a lesser extent with positive affect.

All of this may be consistent with a reactive approach to the world, in which affect is not fully processed.

Supporting this interpretation, neuroimaging studies have consistently shown the involvement of the DMPFC with conscious self-monitoring of emotional responses (Beauregard et al., 2001; Kuchinke et al., 2006; Levesque et al., 2003; Levesque et al., 2004; Phan et al., 2005). For example, during the voluntary suppression of negative affect in healthy adults, activation in the dorsal medial and lateral prefrontal cortex increased and that in the nucleus accumbens and extended amygdala decreased (Phan et al., 2005). It has been suggested that emotional information is conveyed from limbic regions to the prefrontal cortex allowing conscious, voluntary emotional self-regulation (Levesque et al., 2003; Levesque et al., 2004).

Therefore, one interpretation of the present findings is that the vulnerable youth were recruiting an emotional control system that was suppressing emotional response.

References

Heitzeg, M. M., Nigg, J. T., Yau, W. Y. W., Zubieta, J. K., & Zucker, R. A. (2008). Affective circuitry and risk for alcoholism in late adolescence: differences in frontostriatal responses between vulnerable and resilient children of alcoholic parents. Alcoholism: Clinical and Experimental Research, 32(3), 414-426.

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).

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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!

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.

binge_drink404_675458c

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.

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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

Abusive Childhoods Increase Risk of Later Alcoholism

Sitting in AA meetings over a number of years I have been struck by the amount of stories I have heard about fellow AAs having had abusive childhoods and have always wondered how much this sort of maltreatment in childhood contributes to later alcoholism.

In my research I have found that child maltreatment has been frequently identified in the life histories of adolescents and adults in treatment for substance use disorders, as well as in epidemiological studies of risk factors for substance use and abuse.

Ample evidence exists for higher rates of substance abuse and dependence among maltreated individuals (1) so much so that alcoholism and addiction for many represent a developmental cascade.

In clinical samples undergoing treatment for substance use disorders, between one third and two thirds evince child abuse and neglect histories (2-7).

In a survey in The USA, of over 100,000 youth in 6th though 12th grade, Harrison, Fulkerson, and Beebe (1997) found that those reporting either physical or sexual abuse in childhood were from 2 to 4 times more likely to be using drugs than those not reporting abuse; the rates were even higher for youth reporting multiple forms of child maltreatment (8).

Similar findings (9,10) have been reported by Rodgers et al. (2004) and Moran, Vuchinich, and Hall (2004). Among youth with Child Protective Services documenting maltreatment, Kelly, Thornberry, and Smith (1999) reported one-third higher risk for drug use among those with an abuse history(11).

In a large epidemiological study, Fergusson, Boden, and Horwood (2008) showed physical abuse and particularly sexual abuse to be related to illicit drug use, as well as abuse and dependence (12).

It also appears that extreme economic deprivation characterizes many maltreating families who are residing in impoverished areas with substantial neighborhood disorganization and ample availability of drugs in the community(13).

Hawkins, Catalano, and Miller’s (1992) highlighted poor and inconsistent family management practices, high family conflict, and poor bonding to family as risks for adolescent substance abuse, and these factors also are characteristic of the dysfunction in maltreating families in which abuse and neglect occur.

These features are consistent with the progression of developmental failures exhibited by maltreated children (14).

Consequently, compromised adaptation in the social and academic arena contributes to association with deviant peers, who escalate the access to and modeling of substance abuse, contributing to early onset of drug use.

For many the propensity for later alcoholism and drug addiction are determined in part by genetic inheritance but all genetic transmission also relies on environmental conditions.

It would appear that abusive childhoods and emotional deprivation provide fertile grounds.

References

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

2. Bayatpour M, Wells RD, Holford S. Physical and sexual abuse as predictors of substance abuse and suicide among pregnant teenagers. Journal of Adolescent Health. 1992;13:128–132.

3. Cavaiola AA, Schiff M. Behavioral sequelae of physical and/or sexual abuse in adolescents. Child Abuse & Neglect.1988;12:181–188.

4. Dembo R, Dertke M, Borders S, Washburn M, Schmeidler J. The relationship between physical abuse, sexual abuse and tobacco, alcohol, and illicit drug use among youths in a juvenile detention center. International Journal of the Addictions.1988;23:351–378

5. Edwall GE, Hoffman NG, Harrison PA. Psychological correlates of sexual abuse in adolescent girls in chemical dependency.Journal of Adolescent Chemical Dependency. 1989;1:53–68.

6. Pribor EF, Dinwiddie SH. Psychiatric correlates of incest in childhood. American Journal of Psychiatry. 1992;149:52–56.

7. Schaefer MR, Sobieragi K, Hollyfield RL. Prevalence of child physical abuse in adult male veteran alcoholics. Child Abuse & Neglect. 1988;12:141–150.

8. Harrison PA, Fulkerson JA, Beebe TJ. Multiple substance use among adolescent physical and sexual abuse victims. Child Abuse & Neglect. 1997;21:529–539.

9. Harrison PA, Fulkerson JA, Beebe TJ. Multiple substance use among adolescent physical and sexual abuse victims. Child Abuse & Neglect. 1997;21:529–539.

10. Moran PB, Vuchinich S, Hall NK. Associations between types of maltreatment and substance use during adolescence. Child Abuse & Neglect. 2004;28:565–574.

11. Kelly BT, Thornberry TP, Smith CA. In the wake of child maltreatment. Washington, DC: Office of Juvenile Justice and Delinquency Prevention; 1997. pp. 1–15.

12. Fergusson DM, Boden JM, Horwood LJ. Exposure to childhood sexual and physical abuse and adjustment in early adulthood.Child Abuse & Neglect. 2008;32:607–619.

13. Hawkins JD, Catalano RF, Miller JY. Risk and protective factors for alcohol and other drug problems in adolescence and early adulthood: Implications for substance abuse prevention. Psychological Bulletin.1992;112:64–105.

14. Cicchetti D, Valentino K. An ecological transactional perspective on child maltreatment: Failure of the average expectable environment and its influence upon child development. In: Cicchetti D, Cohen DJ, editors. Developmental psychopathology: Vol. 3. Risk, disorder, and adaptation. 2nd ed. New York: Wiley; 2006. pp. 129–201

The earlier you start drinking the greater the chance of being alcoholic

Early Onset to Begin Drinking

It is a very common theme in AA meetings and other 12 step groups about how young alcoholics started drinking. I always wondered if this had an effect on later alcoholism, although I know many alcoholics who started drinking much later in life. Looking at the research below it seems that the age a person started drinking can predict later problems with alcohol. Interestingly “disinhibited” behaviour, such as impulsiveness and not being able to “stop oneself” from engaging in certain behaviours also have a bearing on later alcohol problems, as does adverse childhood experiences and the amount of alcoholism in the family.

The age of onset to begin regular drinking is an important predictor of age of first alcohol problem and subsequent alcohol dependence (1,2), as well as greater severity and persistence of problems with illicit drugs (3).

For individuals that initiated drinking prior to age 14 years, the likelihood of adult alcohol dependence was 40%, four times more likely than individuals who began drinking at 20 years or older (2) . It was also reported that individuals that drank before age 14 years were more than twice as likely to become alcohol dependent than those trying alcohol after age 16 years (4).

A number of factors such as early adverse childhood experiences (5,6) and familial density of alcoholism (7,8), predict earlier age of drinking onset.

Earlier onset of drinking also appears to be related to the presence of behaviors often characterized as “disinhibited”.There is also abundant evidence that behavioral under-control is an important determinant of later development of substance use disorders (SUD) (9,10). Behavioral under-control observed as early as 3 years is predictive of alcohol-related problems at 21 years (11), and in adolescents mediates the relationship between family history of alcoholism and young adult SUDs (12)

References

1. Hawkins JD, Graham JW, Maguin E, Abbott R, Hill KG, Catalano RF. Exploring the effects of age of alcohol use initiation and psychosocial risk factors on subsequent alcohol misuse.Journal of Studies Alcohol. 1997;58(3):280–290.[PMC free article]

2. Grant BF, Dawson DA. Age at onset of alcohol use and its association with DSM-IV alcohol abuse and dependence: results from the National Longitudinal Alcohol Epidemiologic Survey.Journal of Substance Abuse. 1997;9:103–110.

3. Kandel DB, Yamaguchi K, Chen K. Stages of progression in drug involvement from adolescence to adulthood: further evidence for the gateway theory. Journal of Studies Alcohol.1992;53(5):447–457.

4. Sartor CE, Lynskey MT, Heath AC, Jacob T, True W. The role of childhood risk factors in initiation of alcohol use and progression to alcohol dependence. Addiction.2007;102(2):216–225.

5. Rothman EF, Edwards EM, Heeren T, Hingson RW. Adverse childhood experiences predict earlier age of drinking onset: results from a representative US sample of current or former drinkers. Pediatrics. 2008;122(2):e298–e304.

6. Waldrop AE, Ana EJ, Saladin ME, McRae AL, Brady KT. Differences in early onset alcohol use and heavy drinking among persons with childhood and adulthood trauma. American Journal on Addictions. 2007;16(6):439–442.

7. Hill SY, Yuan H. Familial density of alcoholism and onset of adolescent drinking. Journal of Studies on Alcohol.1999;60(1):7–17.

8. Hill SY, Shen S, Lowers L, Locke J. Factors predicting the onset of adolescent drinking in families at high risk for developing alcoholism. Biological Psychiatry. 2000a;48(4):265–275.

9. Stice E, Barrera M, Jr., Chassin L. Prospective differential prediction of adolescent alcohol use and problem use:examining the mechanisms of effect. Journal of Abnormal Psychology.1998;107(4):616–628

10. Zucker RA. Anticipating problem alcohol use developmentally from childhood into middle adulthood: what have we learned?Addiction. 2008;103(Suppl 1):100–108. [PMC free article]

11. Caspi A, Moffitt TE, Newman DL, Silva PA. Behavioral observations at age 3 years predict adult psychiatric disorders. Longitudinal evidence from a birth cohort. Archives of General Psychiatry. 1996;53(11):1033–1039.

12. King KM, Chassin L. Mediating and moderated effects of adolescent behavioral undercontrol and parenting in the prediction of drug use disorders in emerging adulthood.Psychology of Addictive Behaviors. 2004;18(3):239–249.

Explaining that “warm glow” of the first drink!?

The first drink does it!?

Some structural and functional differences in affective circuitry in the brain have been found in adolescents at risk of alcoholism compared to controls, and may precede alcoholism onset and thus constitute markers of risk.

Thus, it is reasonable to hypothesize that pre-alcoholic differences in the functioning of relevant neural systems will be related to risk for alcoholism.

One aspect of the at risk argument that struck a chord was how difficulties in the regulation of stress in the offspring of alcoholics has a pronounced affect on how alcohol effects them.

This we believe may partly explain that rosy or golden glow of the first drink, which appears to often alter the perception of at risk alcoholics to such a profound effect, especially compared to those not at risk to later alcoholism.

We know that dopamine rises in relation to the “rewarding” properties of drugs and alcohol, rising in a more pronounced way in drugs such as cocaine than in alcohol so perhaps alcohol does something else to alcoholics than to non-alcoholics, perhaps it effects something other than dopamine or natural opioids or other neurochemicals in the brain, perhaps it hits us via our hearts and in reducing heightened stress levels?

For example in terms of inherent stress regulation, offspring of alcoholics tend to have higher baseline heart rates (1,2) and show increased cardiovascular reactivity to aversive stimuli (3-6).

In simple terms those at risk have inherent difficulties in stress regulation, react more than those not at risk, studies have shown that cortisol (stress chemical) response to psychosocial stress is significantly increased in offspring with a family history of alcoholism compared to those with no family history of alcoholism (7,8)

Interestingly, this stress dysregulation may potentiate (heighten) the rewarding properties of alcohol as we have also seen in emotion dysregulation. Alcohol appears to not only be rewarding but is doubly so in that it provides a release from stress also.

In fact, offspring from families with alcoholics may be hypersensitive to the effects of alcohol on cardiovascular activity (3,5,9,10)

Alcohol may serve to dampen heart rate and electrodermal reactivity to stress more in young adults with a family history of alcoholism than in offspring without a family history.

Slowing of heart rate may be associated with increased perception of relaxation making alcohol more rewarding to high risk offspring.

In offspring of alcohol dependent individuals, ethanol (alcohol) consumption results in significantly lower stress chemicals like adrenocorticotropic hormone (ACTH) and cortisol levels compared to control subjects and these are predictive of future alcoholism (11).

Initial alcohol use may have a double whammy effect on alcoholics, possibly right from the first drink. It may be the reason some alcoholics say they were alcoholic from their first drink, that the drink could do for them what they could not do for themselves.

Alcohol may involve a profound a release from self, a self prone to stress difficulties and more susceptible to the releasing, stress reducing properties of alcohol.

References

1. Harden PW, Pihl RO. Cognitive function, cardiovascular reactivity, and behavior in boys at high risk for alcoholism.Journal of Abnormal Psychology. 1995;104(1):94–103.

2. Hill SY. Absence of paternal sociopathy in the etiology of severe alcoholism: is there a type III alcoholism? Journal of Studies Alcohol. 1992;53(2):161–169.

3. Finn PR, Pihl RO. Risk for alcoholism: a comparison between two different groups of sons of alcoholics on cardiovascular reactivity and sensitivity to alcohol. Alcoholism, Clinical and Experimental Research. 1988;12(6):742–747.

4. Finn PR, Zeitouni NC, Pihl RO. Effects of alcohol on psychophysiological hyperreactivity to nonaversive and aversive stimuli in men at high risk for alcoholism. Journal of Abnormal Psychology. 1990;99(1):79–85.

5. Peterson JB, Pihl RO, Séguin JR, Finn PR, Stewart SH. Heart-rate reactivity and alcohol consumption among sons of male alcoholics and sons of non-alcoholics. Journal of Psychiatry & Neuroscience. 1993;18(4):190–198. [PMC free article]

6. Stewart SH, Finn PR, Pihl RO. The effects of alcohol on the cardiovascular stress response in men at high risk for alcoholism: a dose response study. Journal of Studies on Alcohol. 1992;53(5):499–506.

7. Uhart M, Oswald L, McCaul ME, Chong R, Wand GS. Hormonal responses to psychological stress and family history of alcoholism. Neuropsychopharmacology. 2006;31(10):2255–2263.

8. Zimmermann U, Spring K, Kunz-Ebrecht SR, Uhr M, Wittchen HU, Holsboer F. Effect of ethanol on hypothalamicpituitary-adrenal system response to psychosocial stress in sons of alcohol-dependent fathers. Neuropsychopharmacology.2004;29(6):1156–1165.

9. Schuckit MA. Low level of response to alcohol as a predictor of future alcoholism. American Journal of Psychiatry.1994;151(2):184–189.

10. Schuckit MA, Tsuang JW, Anthenelli RM, Tipp JE, Nurnberger JI., Jr. Alcohol challenges in young men from alcoholic pedigrees and control families: a report from the COGA project. Journal of Studies on Alcohol. 1996;57(4):368–377.

11. Schuckit MA, Smith TL. Assessing the risk for alcoholism among sons of alcoholics. Journal of Studies on Alcohol.1997;58(2):141–145.

Why erase addiction memories when they can help others?

According to one UK newspaper The Independent, dated the 9th July 2014 “Substance abusers could have their memories of drug addiction wiped in a bid to stop them using illegal narcotics, an award-winning neuroscientist has said.

According to new research by Cambridge University’s Professor Barry Everitt: disrupting the memory pathways of drug users could weaken powerful “compel” cravings, reduce “drug seeking behaviour” and open a new field of addiction therapy.

Professor Everitt told this week’s Federation of European Neuroscience Societies (FENS) how his research in rodents had found that targeting “memory plasticity” in rats was able to reduce the impact of maladaptive drug memories.

He added that this knowledge could offer a radical new method of treatment of drug addiction in humans, where researchers have already established that the path to addiction operates by shifting behavioural control from one area of the brain to another. This process sees drug use go from a voluntary act to a goal directed one, before finally becoming an compulsive act.

It was this process that Professor Everitt’s research is trying to “prevent” by targeting “maladaptive drug-related memories” to “prevent them from triggering drug-taking and replaces”.

In humans this could potentially be done by blocking brain chemicals.

“It’s the emotional intrusiveness of drug and fear memoirs that can be diminished, rather than an individual’s episodic memory that they did in the past take drugs or had a traumatic experience,” he told The Independent. “Conscious remembering is intact after consolidation blockade, but the emotional arousal [that] leads to drug seeking or distressing feelings of fear that are diminished.”

His research group discovered that when drug memories are reactivated by retrieval in the brain, they enter a pliable and unstable state. By putting rats in this state Professor Everitt was able to prevent memory reconsolidation by blocking brain chemicals or inactivating key genes.

In one study, the team diminished drug seeking behaviours by obstructing a brain chemical receptor linked to learning and memory, thus erasing memories, while in another study it found they could weaken drug use memories by altering a particular gene in the amygdala, a brain area processing emotional memory.

“Of course, inactivating genes in the brain is not feasible in humans,” the professor told FENS. “So we’re directing our research to better identify the underlying brain mechanisms of memory reconsolidation.”

He added: “We specifically examined how we could target these maladaptive drug-related memories, and prevent them from triggering drug-taking and relapse.”

So to recap, this new treatment is based on altering genes in rats!

There is no need to actually wipe an alcoholics’ addiction memories.

In fact it may be very counter productive to recovery from alcoholism. One 80 year old and hyper ecologically valid experiment into the mnemonics of “treating addiction memories” has shown that by honestly looking at the consequences of one’s actions as the result of one’s alcoholic drinking that the positive associations of previous drinking were reappraised in light of the damage done to oneself, one’s loved ones and family and society at large.

Addiction memories via this profound reappraisal were then more accurately processed in long term explicit memory. Implicit schematic memory was also altered fro a self schema in which one is a drinking alcoholic to one in which one is a recovering alcoholic.

So-called positive associations in long term episodic and explicit memory were, when labile via recall, then challenged and replaced by more accurate negative associations in long term memory – no memories needed to be erased just reappraised more accurately.

This type of ongoing experiment is happening on a daily basis at an AA meeting near you.

AA groups have found that memories need not be erased, with possible deleterious knock on effects on fear processing and amgydaloid performance, but rather memories simply need to be faced up to, and via honesty appraisal reprocessed more adaptively in long term memory.

This also means alcoholics in recovery can use their addiction memories in not only clearing away the wreckage of the past, repairing broken relationships with loved ones and society as a whole by making amends to those involved in this wreckage and also put the memories of the past to excellent therapeutic use by using it to help others with similar memory difficulties.

In fact even academic researchers have found and have demonstrated that abstinent, treatment seeking individuals also have a different cognitive or/and memory bias to active alcoholics. This has been illustrated in findings that the greater “accessibility” for positive vs. negative alcohol- associations in heavy vs. light drinkers was not found to be generalized to alcoholics in treatment vs. social drinkers (2). Rather, there was a trend for treated inpatients, motivated to attain abstinence, to show greater availability and accessibility for negative alcohol-related information.

This is how to use memories of addiction to the best possible use, instead of erasing them, wiping them our and hoping for the best, memories of our addiction can be used to great purpose in helping others. Also “addiction memory” is often activated by those who have not come to terms with their alcoholism and still want to drink. Unless some one has come to terms with their alcoholism little can be done, by erasing memories or otherwise. These are sticking plasters on a gaping wound. They will be replaced with other “addiction memory” as there an underlying condition to alcoholism ( we believe it to be emotional regulation and processing deficits) and it is this that drives this fear-based condition called alcoholism, memories are the result of this malady. Address the underlying conditions and the rest takes care of itself.

It is not brain regions which are the problem either such as activation of the amgydala, it is how this sometimes errant and overactive brain region in alcoholics is tamed via the serenity found in the AA program of recovery.

The compel parts of the brain, Everitt mentions, are activated by emotional distress, so treat the distress not the symptom of it. He also confuses implicit, automatic memory, with explicit, conscious memory. Either way they are both activated by stress/distress, and are thus both emotional memories. Again treat the emotional dysregulation, the primary problem not the secondary manifestation of the problem.

As I mentioned above, there has been an ongoing experiment into recovery from alcoholism going on for nearly 80 years now, there is a lab in most areas of town.

It would benefit the world and science, in particular, if neuroscientists would pop in for a coffee and check our our findings.

References

2. McCusker CG Cognitive biases and addiction: an evolution in theory and method. Addiction 2001;96:47–56.

Spiritus contra spiritum.

Explaining the Spiritual Thirst

In this blog we copy from an article that we have come across recently in which very respective neuroscientists, in their introduction, give a good insight into the spirituality of recovery (1). One day we believe science will come to accept that these so-called spiritual practices are actually essential to recovery from addiction and alcoholism, and possibly a host of other psychiatric disorders by helping to unite the fragmented self.

” One commenter Jerome Dollard says, “Spirituality is a lot like health. We all have health; we may have good health or poor health, but it‘s something we can’t avoid having. The same is true of spirituality: every human being is a spiritual being. The question is not whether we ‘have spirituality’ but whether the spirituality we have is a negative one that leads to isolation and self-destruction or one that is more positive and life-giving”

Addiction has been understood in terms of a spiritual craving for wholeness, freedom, and transformation. It is not by coincidence that the Latin root of “addict” connotes the idea of a willing slave, or one who has become enslaved by so many acts of willing devotion.

Once the pursuit of the special release from self, the self-transcendence, which comes with using a particular substance or activity, becomes the organizing principle of the person’s life, the hedonic habit takes on a life of its own. What initially promised freedom from the bondage of self or freedom to become someone else turns out to be a “rapacious creditor” bleeding the borrower of “all self-sufficiency and will to resist its demands” .

The “habit” becomes obsession and eventually fragments the person until his or her will to resist is rendered impotent, or powerless. The admission of this powerlessness is an intensely personal event, which functions as the first step toward actual freedom.

From this phenomenological interpretation of addiction, we can begin to see how it is linked to spirituality. This insight was captured well by the psychiatrist Carl Jung in his letter to Bill Wilson: “You see, Alcohol in Latin is ‘spiritus’ and you use the same word for the highest religious experience as well as for the most depraving poison. The helpful formula therefore is: spiritus contra spiritum.”

In other words, the highest form of religious experience counters the most depraving poison – high spirit against low spirit.

In his Varieties of Religious Experiences, the philosopher William James related a similar insight about this interaction in the opposite direction: “The only radical remedy I know of for dipsomania (another name for alcoholism) is relgiomania.”

These insights have been validated more recently by neuroscientist Patrick McNamara. In his book, The Neuroscience of Religious Experience, McNamara makes the convincing argument that religion may have evolved in the first place to facilitate the process of unifying the fractured human person by means of a spiritual experience. The same spiritual craving for wholeness, self-integration, and freedom that motivates the use and abuse of a variety of substances and activities is also that which frequently motivates people’s involvement in religious and spiritual communities.

From this phenomenological interpretation of addiction, we can begin to see how it is linked to spirituality.

Evidence of McNamara’s insight can potentially be observed among the contemporary movement of mutual-help fellowships, such as AA and their Twelve Step Program. According to their preamble, “AA is a fellowship of men and women who share their experience, strength, and hope with each other to help other alcoholics achieve sobriety.” To be organized around the purpose of achieving recovery and helping others is certainly a crucial piece in transforming an individual’s purpose and meaning.

Another one of the reasons for the success of the AA fellowship in facilitating these transformative experiences is their emphasis on its members telling stories about “what they were like, what happened, and what they are like now.”

The continued practice of telling such stories not only serves to remind the storyteller of the despair and anguish associated with using alcohol, but also to remind them of how far they have come. It functions to facilitate a sort of deductive reasoning, where what exists today appears to have required what preceded it.

Therefore, gratitude is a frequent theme in these stories. Telling these stories also requires learning to look at oneself, and especially one’s relationship with alcohol, differently. It is a major piece in transforming that way of seeing oneself in the world that extends into a way of being.

The twelve steps are also about cultivating an expanded consciousness through a reinterpretation of one’s own actions and reactions towards the people, places, and things around him or her.

The morality emphasized in these steps encourages personal responsibility for one’s actions, consideration of other people’s cares and concerns, and thus, a kind of fitness in terms of the person’s conscience. They are a systematic method of actualizing the spiritual awakening that have consistently been exhorted by many of the world’s great religions.”

Well said.

References

1. Blum, K., Thompson, B., Oscar-Berman, M., Giordano, J., & Braverman, E. (2013). Genospirituality: Our Beliefs, Our Genomes, and Addictions. J Addict Res Ther, 4(162), 2.

Why a spiritual solution?

In the first in a series of blogs we discuss the topic of why does the solution to one’s alcoholism and addiction require a spiritual recovery.

This is a much asked question within academic research, although the health benefits of meditation are well known and life styles incorporating religious affiliation are known to increase health and span of life.

I guess people are curious as to how the spirit changes matter or material being when it should perhaps be rephrased to how does application of the ephemral mind affect neuroplasticity of the brain. Or in other words how does behaviour linked to a particular faith/belief system alter the functions and structure of the brain. We have discussed these points in two blogs previously and will do so again in later blogs. Here I just want to highlight in a short summary why spiritual practice helps alcoholics and addicts with with regulating themselves especially when the areas of their brains which govern self regulation have been taken over by the action of drugs and alcohol, so that they have very limited control over their own selves and their own behaviour.

This seems to be at the heart of addiction and alcoholism, this increasingly limited self control over addictive behaviors. In addressing this need for a spiritual solution we also hope to address choice versus limited control arguments. As we will see, the addicted or alcoholic brain is usurped to such a profound extent by effects of drugs and alcohol and this brain acts so frequently without conscious awareness of the negative consequences of these actions that it is appears undoubtedly the case that addicts and alcoholics have profoundly diminished control over their choices of behaviour.

This is especially pertinent in chronic addicts and alcoholics were the thrill is long gone so why would they continue doing something which has little reward other than because they are compelled to.

In addiction, vital regions of the brain and processes essential to adaptive survival of the species become hijacked or usurped or “taken over” by the combination of the effects of alcohol or drugs or addictive compulsive behaviours (acting as pharmacological stressors) on pre-existing impairment in certain parts and functions of the brain. The actions of drugs and alcohol lead to a hyperactive stress system which enhances the rewarding aspects of drugs and alcohol in initial use, especially in those with maladaptive stress response such as individuals who have altered stress systems in the brain due to abusive childhood experiences (1-3).

In the second abusing phase, stress interacts with various neurotransmitters especially dopamine to drive this abusive cycle. In this phase of the addiction cycle stress heightens attention towards cues and creates an heightened attentional bias towards drugs and alcohol (4,5). Stress chemicals also increase activation of “addiction memory” (6,7). Thus there is multi-network usurping of function in the brain as the addiction cycle progresses (8). Recruited of attention, reward and memory networks are enhanced by the effects of stress chemicals.

Stress also enhances the rewarding effects of alcohol and drugs so makes us want them more (9). Enjoy them more. These are the so-called “good times” some of us look back on, in our euphoric recall.

In the final endpoint phase of addiction, stress incorporates more compulsive parts of the brain, partly by the stimulus response of emotional distress which automatically activates a compulsive response to approach drug and alcohol use while in distress, which is a common reality for chronic addicts and alcoholics.

Thus stress chemicals acting on mainly dopamine circuits in the brain and other neurotransmitters eventually take over control of the brain in terms of the control of behaviour (8).

In usurping “survival” or self regulation networks in the brain, control over behaviour “implodes” or collapses inwards, from control over behaviour moving inwards from the action outcome, or goal directed, conscious prefrontal cortex to the unconscious automatic, motoric, subcortical parts of the brain (10).

This greatly limits one’s conscious self control over one’s own behaviour if one is addicted or chronically alcoholic. Control of behaviour appears to have becomes a function of hyperactive stress systems in the brain and their manifestation as emotional distress (11,12).

This emotional distress constantly activates a “flight or flight” response in the brain and this means behaviour is carried out without reflection or without explicit knowledge of consequences, usually negative in the case of addiction (13,14).

The alcoholic or addicted brain becomes a reactionary brain not a forward thinking, considering of all possible options type of brain. The addict or alcoholic becomes driven by his brain and to a great extent a passenger in his own reality. Automatic survival networks act or react continually as if the addicted brain is on a constant state of emergency, constantly under threat.

There is a profoundly reduced conscious cognitive control over behaviour. This heighted, excessive and chronic stress and distress cuts off explicit memory of previous negative consequences of our past drinking and drug use and recruits implicit memory systems which are mainly habitual and procedural, they are “do” or “act” without conscious deliberation systems of the brain (14) .

It is as if our alcoholic or addicted brains are doing the thinking for us. Or not as the case may be. Alcoholics are on automatic pilot, fuelled by distress. This neuroscientific explanation fits almost perfectly with the description of alcoholism in the Big Book of Alcoholics Anonymous, “The fact is that most alcoholics…have lost choice in drink. Our so-called will power becomes practically nonexistent. We are unable , at certain times, to bring into our consciousness with sufficient force the memory of the suffering and humiliation of even a week or month ago. We are without defense against the first drink”

The” suffering and humiliation” are now called “negative consequences” in current definitions of addiction…”continued use despite negative consequences”. (15)

We “cannot bring into our consciousness with sufficient force the memory” because this is an explicit memory cut off by the effects of excessive stress which “offlines” the prefrontal cortex and hippocampal memory in favour of unconscious habitual, implicit or procedural memory (14,16). The memory of drinking not the memory of the “ situations surrounding this drinking”. How is this not a disorder that has placed us “ beyond human aid” and beyond our own human aid” ?

The “unable at certain times” are possibly times of great distress or emotional dysregulation and they leave the alcoholic and addict vulnerable to relapse.

“Once more: The alcoholic, at certain times, has no effective mental defence against the first drink.”

“His defence must come from a Higher Power”

In later blogs we will discuss, in terms of the brain, why we need to recruit parts of the brain, via selfless behaviours, which activate areas outside those implicated in self regulation.

The cited power greater than ourselves in AA meetings, for example, often follows an experiential trajectory – first it is the first person an alcoholic asks for help whether a family member, loved one or a G.P. – this often leads to an AA meeting or a treatment centre – then they are presented with other alcoholics who suffer from the same disorder – in AA parlance this is the first, and for many alcoholics in recovery, their only experience or attempt to find G.O.D. – this Group. of. Drunks. is like all that preceded it, a power greater than ourselves, regardless on whether we attain a spiritual connection with God after that.

A sizable minority in AA remain agnostic or atheist. This does not mean they have not performed essentially “spiritual” acts such as asking for help, accepting powerless over their life at that present moment. These are all acts of humility of accepting one needs help from beyond oneself. They also attend meetings where no one is in charge apart from God as He may express Himself in our group conscience.

Our first sponsors (mentors) in AA are also a power beyond ourselves as are their sponsors and their sponsors and the people in all their lives who advise and support. From the moment one has wholeheartedly accepted the need for help, one has accepted that help will come from a power greater than themselves. It is a humbling and I believe spiritual act. A new breath filling one’s life.

All these people are already doing something for us which we could not do ourselves, they are helping us recruit the prefrontal cortex and explicit memories of the disasters alcohol or drug addiction has wrought on our lives – they move, eventually, activity in the brain from the unthinking dorsal striatal to the reasoning prefrontal cortex, helped also by sharing our stories in meetings. They give us a new recovery alcoholic self schema to replace the former drinking alcoholic self schema and stores it in implicit memory.

These people helps us change positive memory association of alcohol with negative associations. They overturn old ideas about the good times with a deep awareness of how bad these so-called good times were. The attentional bias is avoided or is rarely activated as the distress and stress are greatly reduced so as not to activate it.

We find recovery rewarding in the way we formerly (but not latterly) found drinking. In fact we find recovery better than drinking even at it’s best. The worst day in recovery seems much better than the worst day in drinking. We learn how to regulate our emotions so as to avoid prolonged bouts of distress, we ring our sponsors when such moments arise, talk to a loved one.

Again an external prefrontal cortex helps us climb out of the sub-cortical “fear” areas of the dorsal striatum and the anxious amgydala. The solution is in the prefrontal cortex, in it’s control over emotions, in it’s clear appraisal of our past, in it’s activation of negative, realistic memories of the past and in avoiding the people, places and things which remind us of drinking.

The prefrontal cortex becomes more in charge rather than our illness doing the thinking. The prefrontal also gets strengthened by us sharing our experience strength and hope at meetings, it uses a recovery narrative to reconcile the drinking self with the recovering self, making us whole, it embeds in our mind the truth of the progressive nature of this illness. It helps us see what it was like, what happened and what it is today. It gives us the tools to help others.

In the follow up blog to this we will further explore how this works – this spiritual solution.

References

1. Cleck, J. N., & Blendy, J. A. (2008). Making a bad thing worse: adverse effects of stress on drug addiction. The Journal of clinical investigation, 118(2), 454.

2. Koob, G. F., & LeMoal, M. (2001). Drug addiction, dysregulation of reward, and allostasis. Neuropsychopharmacology, 24, 97–129.

3. Sinha, R. (2008). Chronic stress, drug abuse, and vulnerability to addiction. Annals of the New York Academy of Sciences, 1141, 105–130

4. Peciña, S., Schulkin, J., & Berridge, K. C. (2006). Nucleus accumbens corticotropin-releasing factor increases cue-triggered motivation for sucrose reward: paradoxical positive incentive effects in stress? BMC biology, 4(1), 8.

5. Ventura, R., Latagliata, E. C., Morrone, C., La Mela, I., & Puglisi-Allegra, S. (2008). Prefrontal norepinephrine determines attribution of “high” motivational salience. PLoS One, 3(8), e3044

6. Hyman, S. E. (2007). Addiction: a disease of learning and memory. Focus, 5 (2), 220.

7. Adinoff , B. (2004) Neurobiologic processes in drug reward and addiction, Harvard Review of Psychiatry

8. Duncan E, Boshoven W, Harenski K, Fiallos A, Tracy H, Jovanovic T, et al (2007) An fMRI study of the interaction of stress and cocaine cues on cocaine craving in cocaine-dependent men. The American Journal on Addictions, 16: 174–182

9. Berridge, K. C., Ho, C. Y., Richard, J. M., & DiFeliceantonio, A. G. (2010). The tempted brain eats: pleasure and desire circuits in obesity and eating disorders.Brain research, 1350, 43-64.

10. Everitt, B. J., & Robbins, T. W. (2005). Neural systems of reinforcement for drug addiction: From actions to habits to compulsion. Nature Neuroscience, 8, 1481–1489

11. Sinha, R., Lacadie, C., Sludlarski, 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, 171–180.

12. Goodman, J., Leong, K. C., & Packard, M. G. (2012). Emotional modulation of multiple memory systems: implications for the neurobiology of post-traumatic stress disorder.

13. Schwabe, L., Tegenthoff, M., Höffken, O., & Wolf, O. T. (2010). Concurrent glucocorticoid and noradrenergic activity shifts instrumental behavior from goal-directed to habitual control. Journal of Neuroscience, 20, 8190–8196.

14. Schwabe, L., Dickinson, A., & Wolf, O. T. (2011). Stress, habits, and drug addiction: a psychoneuroendocrinological perspective. Experimental and clinical psychopharmacology, 19(1), 53.

15. American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders (Fifth ed.). Arlington, VA: American Psychiatric Publishing. pp. 5–25.

16. Arnsten, A. F. (2009). Stress signalling pathways that impair prefrontal cortex structure and function. Nature Reviews Neuroscience, 10(6), 410-422.

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The Alcoholics Guide to Alcoholism

Blogging The Language of the Heart

Month: July 2014

Measuring the “Psychic” Change

What makes some children of alcoholics vulnerable, and some resilient?

Understanding Emotional Processing Deficits in Addiction – Guest Blog

Understanding Emotional Processing Deficits in Addiction

Do alcoholics drive through life with Faulty Brakes!

Abusive Childhoods Increase Risk of Later Alcoholism

The earlier you start drinking the greater the chance of being alcoholic

Explaining that “warm glow” of the first drink!?

Why erase addiction memories when they can help others?

Spiritus contra spiritum.

Why a spiritual solution?