Why we need to be more accurate in diagnosing co-morbidity.

In this blog we have repeatedly queried whether the co-occurrence of so-called co-morbidities with substance use disorders (SUDs) is as high as reported in many studies (1).

In a blog from yesterday Are most co-morbidities really substance-induced disorders?  that diagnosis is often flawed in many studies and that the so-called diagnosis of co-morbidity is not borne out long term with many presumed co-morbid disorders disappearing in time.

In an recurring example given, the author uses the high prevalence of so-called comorbidity with mood disorders to illustrate how alcoholics and addicts appear to have a similar range of mood disorders as that of a normal population sample, i.e. as normally in society, around 15%.

This is in keeping with our ancedotal evidence of attending numerous AA meetings over a number of years has shown that in the vast majority of individuals the symptoms of a supposedly co-morbid disorder such as General Anxiety Disorder (GAD) or major depression (MD) appear to dissipate after some weeks.

This either means that there 12 step program of recovery outlined in mutual support groups like AA can provide profound therapeutic effect on other disorders (which they very well may do) or that the co-morbidities highlighted in many studies is greatly exaggerated.

This exaggeration has two major consequences. The study of and research into SUDs is hampered by relegating affective dimensions to that of co-morbidity while not exploring the specific emotional dysregulation at the heart of SUDs ( in particular dyscontrol over subcortical/amgydaloid emotional responding appears at the heart of most of these psychopathologies so they have common neural substrates and mechanisms but they may not manifest in the same behavioural responses – in other words there may be common emotional dysregulatory mechanisms but different pathomechanisms)

Burden of Addiction Graph


That is not to say that co-occuring disorders can not exaggerate the trajectory of a SUDs as disorders such as post traumatic stress disorders may, for example, add to distress based responding and may also require further and more specific treatment in addition to that for a SUD.

Also research needs to not only to predict behaviour e.g. in the case of addiction, relapse, but also to help prevent conditions arising. Thus it is imperative that research more fully informs prevention and intervention in children and adolescents at risk from later SUDs.

Thus the specific aspects of emotional dysregulation specific to a SUD such as, for example, a tendency to act rashly or impulsively under distress may be addressed by considering whether this is also the function of emotional processing deficits which mean emotions are “avoided” rather than processed by cortical areas, resulting in more reactive sub-cortical responding which has consequence for a decision making profile which is more based on alleviating this distress state, this unpleasant feeling state, than it does the recruiting via effective emotional processing and regulation of more cortical areas of the brain. All of which has ramifications for a more accurate study of the aetiology of addiction per se and it’s prevention.

For example, teaching at risk children how to identify, label, and verbalise their emotions at an early age will help them learn how to process and regulation them; to then use these feeling states to guide goal-directed adaptive behaviour rather than and  recruiting more subcortical emotive-motor parts of the brain to flee these distress states resulting in more reactive  decision making and emotional management. It would also help with reducing the effect that initial alcohol use has on adolescents as  emotional dysregulation potentiates reward, so distress/stress make the rewarding effects of drugs and alcohol heightened. It may also mean heart rate variability is also higher so that the smoothing, calming effects of alcohol are not as exaggerated. It would help put some neural brakes on increasingly out of control behaviour.

It would help tackle the premorbid distress at the heart of vulnerability to later addiction at its source, its manifestation as emotional reactivity.

It would return us to a theoretical conception of addicts as suffering human beings not neurobiological machines, which can be tweeked by this neurochemical or that!

This leads me onto the second short point. If we relegate the anxiety, impulsivity mood  and affective dimensions of a SUD to co-morbidity we limit our understanding of the overlapping and interlinked roles of emotional processing and regulation deficits on reward processing for example.

There is a tendency in some researchers to see addiction purely in terms of neurbiological processes, usually dopaminergic, equating addiction to the effects that a drug or alcohol has on the neurobiology and neuro-anatomy of the brain, and not to see how these deficits may not be simply drug induced but also linked to stress dysregulation which itself is linked profound and pre-existing impairments in emotion processing and regulation.

A chronic addict is emotionally distressed most of the time, who do dopaminergic models explain this emotional response or the fact that most relapse is stress or emotional distress based and prompted.

Or the effects of maltreatment or abusive childhoods, or economic deprivation or deviant peers. Observing addiction as a inherited emotional regulation and processing deficit, exaggerated by sometimes dysfunctional  parenting  (especially if the parents are also addicts and alcoholics) and persistent stress allows us to observe how genes in certain individuals are influenced by environment and manifest in behavioural undercontrol, emotion lability and reactivity and impaired, impulsive decision making in those at risk from later addiction. It may be important to study what is impaired before the neurotoxic effects of chronic drug and alcohol use profoundly aggravate these “pre-morbid”  impairments.

To conclude, there is “overlap of the biological substrates and the neurophysiology of addictive processes and psychiatric symptoms associated with addiction”

Pani et al suggest the “inclusion of specific mood, anxiety, and impulse-control dimensions in the psychopathology of addictive processes.”

We suggest these can be accommodated under the umbrella of emotional regulation and processing deficits as the above and additional deficits seen in alcoholics and addicts are more satisfactorily covered by this nosology.

We agree with Pani et al, that “addiction reaches beyond the mere result of drug-elicited effects on the brain and cannot be peremptorily equated only with the use of drugs despite the adverse consequences produced.”

We infer that emotional dysregulation is at the “very core of both the origins and clinical manifestations of addiction and should be incorporated into the nosology of the same, emphasising how addiction is a relapsing chronic condition in which psychiatric manifestations play a crucial role.”

We agree that “addictionology cannot be severed from its psychopathological connotations, in view of the undeniable presence of symptoms, of their manifest contribution to the way addicted patients feel and behave, and to the role they play in maintaining the continued use of substances.”


Pani, P. P., Maremmani, I., Trogu, E., Gessa, G. L., Ruiz, P., & Akiskal, H. S. (2010). Delineating the psychic structure of substance abuse and addictions: Should anxiety, mood and impulse-control dysregulation be included?. Journal of affective disorders, 122(3), 185-197.

Are most co-morbidities really substance-induced disorders?

Are most co-morbidities really substance-induced disorders?

a Guest Blog from Inside the Alcoholic Brain

In this blog we re-emphasize the need for accurate diagnosis of co-morbidity with a substance use disorder. It appears form the article cited here (1) that diagnosis is often flawed in many studies and that the so-called diagnosis of co-morbidity is not borne out long term with many presumed co-morbid disorders disappearing in time.

Most diagnoses in medicine are based on a combination of symptoms, their time-course and a threshold beyond which the syndrome is felt to be clinically relevant [1].

No single indicator is likely to be sufficient to establish a diagnosis because these are rarely unique to one syndrome.

Potential problems with the diagnostic process increase almost exponentially when substance use disorders  (SUDs) and psychiatric syndromes occur together.

First, combinations of SUDs and psychiatric disorders may represent two or more independent conditions, each of which is likely to run the distinct clinical course relatively unique to that disorder. Here, both conditions must be treated comprehensively.

Secondly, the first disorder could influence the development of the second condition in a such manner that the additional disorder  then runs an independent course. For example, the frequent use of high doses of substance could unmask a latent predisposition toward a psychiatric disorder.

Similarly, a psychiatric disorder (e.g. mania) could increase the risk for heavy use of substances, an SUD that might continue even when the pre-existing psychiatric condition is treated or remits.

A third relationship could be seen if the second condition developed through an effort of the patient to diminish problems associated with the first
syndrome. Here, for example, a person might escalate the use of substances and develop an SUD in an attempt to alleviate feelings of depression, or to decrease side-effects of psychiatric medications. Here, while the substance
use disorders might become a long-term problem, the excessive use of alcohol or an illicit drug might disappear when the pre-existing clinical syndrome is addressed appropriately.

This review focuses the high prevalence of psychiatric comorbidities
seen in individuals with SUDs and syndromes which may be
temporary psychiatric conditions.  The distinction between the types of comorbidities, each of which are likely to operate in some patients, has
important implications [8,9]. The etiologies may be different  (a factor of importance for research), as these “substance-induced disorders” are likely to have distinct clinical courses and responses to treatment.



Different definitions of comorbidity
Comorbidity has been defined in a variety of ways. Some studies place an emphasis on ‘pure psychiatric diagnoses’, defined as a psychiatric condition observed in the absence of any other major diagnosis during the same year.

Multiple diagnoses have been placed into a primary versus secondary
approach where the first condition to develop is labeled as ‘primary’.

The independent versus substance-induced distinction  is an extension of the primary/secondary approach.
It was developed in recognition that a psychiatric syndrome (e.g. a major depressive episode) might also be identified during periods of abstinence.

Problems with making a diagnosis – One major  issue is whether the diagnosis
is required to be associated with great distress or impairment  or if a simple endorsement of the symptoms by a respondent is enough to make a diagnosis.

A similar problem can occur if the criteria did not include the need for some problems to have occurred repeatedly (an issue relevant to many of the criterion items for SUDs), or did not determine if the items clustered together during the relevant period. Studies also vary regarding their emphasis on syndromes occurring in the last year versus during the life-time. Differences across studies on any one of these items are likely to have a large impact on the results regarding the incidence, time course, and optimal treatment of comorbidities.
An additional and very important research issue relates to the types of interviewers employed and their level of supervision.  Many  studies
require large numbers of non-clinician interviewers who can have difficulty interpreting the relevance of some complaints (e.g. mania), and demonstrate problems determining whether the symptoms were relatively mild and transitory (e.g. for some simple phobias) versus those relevant to a diagnosis. The need for so many interviewers also means that the problems reported by subjects are less likely to be reviewed by clinicians.

Other problems reflect the approach used to deal with what appear to be multiple diagnoses in the same person. This occurs, for example, when a subject endorses depressive symptoms, reports panic attacks and describes discomfort in social situations. In some studies these are listed as three separate diagnoses, but others establish a hierarchy, searching for one overarching diagnosis (e.g. major depression) that might explain the other complaints (e.g. temporary panic attacks and feelings of social discomfort).

Unless closely supervised lay interviewers may have difficulties distinguishing periods of situational excitement or substance-related irritability from mania?  Epidemiological interviewer-based instruments might exaggerate the rates of psychiatric disorders and SUDs by reporting conditions that might not meet a full and clinically relevant
syndrome. These interviews might not be optimal for exploring more complex questions such as comorbid conditions, especially with regard to substance-induced disorders.

No one study or single group of subjects can give the ‘true answer’ regarding the prevalence and patterns of psychiatric and SUDs.

The timing of the evaluation is also important. For example, rates of comorbid psychiatric syndromes are likely to be temporarily elevated if substance-dependent subjects are interviewed during intoxication, withdrawal or the first several weeks of abstinence. These are times of highest prevalence of substance-induced disorders.

It is also important to gather additional sources of data about subjects whenever possible. These include clinician reviews of all available information on a patient using additional informants (e.g. a spouse).

These can be key in determine  whether, for example, depressive symptoms reported in a follow-up were truly independent of substance use.


Evidence supporting substance-induced mood disorders

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Temporary depressive symptoms have been reported in the context of intoxication or withdrawal for nicotine, cannabinoids, opioids, hallucinogens and other drugs of abuse.

Interviews with clinician review of diagnoses have documented that >40% of alcoholics have ever fulfilled criteria for major depressive-like syndromes, with almost 70% of these being substance-induced disorders. However, a large national epidemiological study using the AUDADIS diagnostic  and lay interviewers without clinical supervision reported high rates of depression in alcoholics, but noted that few were substance-induced. These divergent results probably reflect different methods across studies as described above.

Additional support for the relevance of substance induced mood disorders comes from prospective studies that suggest that heavy drinking at time 1 is likely to predict depressive symptoms at time 2. A 6-year follow up of 176 subjects reported that drinking predicted an increased number of subsequent transitions from functioning well to periods of depression (perhaps reflecting substance-induced mood disorders), while individuals with prior (but not currently active) alcoholism had no increased number of transitions to depression over time.

Another prospective study reported that heavier drinking during month 2 predicted depressive symptoms during month 3

In addition, 3- and 12-month follow-ups of almost 200 alcoholics
revealed that only those who had returned to drinking were likely to demonstrate depressions.  Finally, a follow-up of young subjects found no relationship between earlier heavy drinking and later AUDs, unless the individuals continued heavy drinking.

Prospective studies of populations at high risk for depression or alcoholism also generally support the existence of substance-induced mood disorders.

Results also indicate that independent major depressions tend to run a true course, and are not usually associated with later alcoholism unless, perhaps, there are alcohol-dependent relatives as well.

Some studies have  noted no increased risk for alcohol use disorders (AUDs) in children of depressed individuals. One study, an evaluation of ∼1000 16–25-year-old subjects in New Zealand, showed  earlier drinking patterns were predictors of alcohol-related outcomes but not of depressive disorders.

A prospective evaluation of two generations of 453 families of alcoholics and controls noted that an orders, but not independent major depressive episodes
alcoholic relative predicted higher rates of alcohol use disorders, but not independent major depressive episodes

When substance-induced mood disorders are identified, they are likely to disappear soon after abstinence, a situation not seen with independent depressive episodes.

Thus, overall continued abstinence in alcoholics is likely to be associated with a decrease in depressive symptoms.

For example, follow-up of alcoholics with substance-induced mood disorders reported that the proportion with marked depressive symptoms decreased from 42% to 6% with 1 month of abstinence [67]. A separate study of unmedicated male alcoholics documented that, for those with induced depressions, an average Hamilton Depressive score of 16 after 1 week of abstinence decreased to a score of six after 4 weeks dry, while similar
decreases are not seen for subjects initially identified as having independent major mood disorders.

Similarly, in another investigation the proportion of alcoholics with major depressive-like symptoms decreased from 67% to 13% over a month, without antidepressant treatment,  findings supported by several other clinical
observations.  In addition, 85% of those with alcohol-induced mood disorders ran the course predicted regarding the temporary nature of the symptoms.

A tendency toward diminution or disappearance of depressive symptoms
with abstinence has also been reported for patient in care for  stimulant or opioid dependence.

To summarise, it appears that  substance-induced disturbances are more likely than independent disorders to diminish and disappear with time alone.

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While the acute phase of withdrawal from alcohol lasts 4 days or so, this is likely to be followed by a protracted abstinence syndrome that can last several months or more . Here, while the alcoholic is not depressed all day every day (i.e. does not fulfill criteria for a major depressive episode), they are likely to experience insomnia, problems concentrating and irritability that improve with increasing time of abstinence.

These are not, however, independent major depressive episodes. It is also worth noting that as many as 15% of any group of individuals (including alcoholics) are likely to show major depressive episodes as a reflection of the usual prevalence of these mood disorders.

Therefore, in summary, most studies document substantial proportions of alcoholics and stimulant-dependent subjects have substance-induced conditions.

The symptoms of most substance induced conditions resemble closely those of the relevant independent psychiatric disorders. However, 85% or more of substance-induced syndromes improve rapidly with abstinence,  distinct from what would be expected with, for example, independent schizophrenia
and major depressive episodes.



Schuckit, M. A. (2006). Comorbidity between substance use disorders and psychiatric conditions. Addiction, 101(s1), 76-88.

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

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.)


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).




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).





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.



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.


Measuring the so-called “Alcoholic Personality”.

Measuring the So-called “Alcoholic Personality”?

Guest Blog

by Paul Henry

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

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

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

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

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

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

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

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

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

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



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

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

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

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

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

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

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

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

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


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

Why a spiritual solution?

The Alcoholics Guide to Alcoholism

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…

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Are Alcoholics Emotionally Immature?

Concerted attempts have been made to relate personality factors to alcohol dependence.

In fact, for many years, research attempted to define the so-called alcoholic personality. Attempts to do so have dwindled in recent years.

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

Although the obvious emotional immaturity often seen in alcoholics seems to cover a number of the more recent findings on bio-psychologcal aspects a alcoholism.

For example, if we partly defined emotional immaturity as containing some of the following, then we appear to be covering a number of much researched and demonstrated aspects of alcoholism. Do these then not come under an umbrella term of emotional immaturity? This list was complied by Psych Central

Dimensions of Emotional maturity

  1. The ability to modulate emotional responses.  Addicts tend to have an all or nothing emotional response.  When they respond they become overly emotional and take a longer time to return to baseline.  They are easily flooded with emotion to the point of impairing functioning.
  1. The ability to tolerate frustration.  Addicts tend to respond to frustrating situations as disasters rather than having any perspective.
  1. The ability to delay gratification.  Emotionally immature people have trouble planning and working toward goals.  The ability to give up immediate gratification is necessary for anyone to go about life in a successful way.
  1. The ability to control impulses.  The mature self has the ability to see that feeling the urge to do something is not the same as doing it.  The recovering addict has a level of control over his or her behavior and can put boundaries around what is inappropriate to say or do.
  1. The ability to be reliable and accountable.  Addicts are often self centered and not good at dealing with the everyday requirements of life like being on time, fulfilling obligations and telling the truth.  As they gain emotional maturity they gain the ability to get out of themselves and think about the impact of their actions on others and on their own lives as well.




According to a list drawn up by alcoholrehab.com

If people are emotionally immature, they may exhibit some of the following symptoms:

* Such individuals will often find it hard to deal with the normal challenges of life. When they are faced with problems they feel unable to cope. They may have developed a psychological state known as learned helplessness.

They struggle to develop meaningful relationships with other people. They may appear too needy or a bit overbearing.
* Those people who are emotionally immature will tend to have a pessimistic outlook on life. They may see the future as a threatening and hostile place.
* This type of person will usually have low self-esteem. This means that they do not value themselves highly so will be willing to accept very little in life as being all they deserve.
* They find it almost impossible to live in the present moment. They are either reliving the past or worrying about the future.
* They can easily lose their temper at the slightest provocation. When they are dealing with uncomfortable emotions they will tend to take things out on other people.

* People who are emotionally immature can have unrealistically high expectations. This means that they are frequently disappointed. Such and individual can have impossibly high expectations for other people yet low expectations for themselves.
* Such individuals can suffer from severe mood swings. This instability of mood can make life a bit uncomfortable.
* If people are emotionally immature, they find it much harder to control their own behavior.

Recognize any of these symptoms?

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We were completely like this before doing the 12 steps.

We, however, do not think that anyone, alcoholics or otherwise choose to behave in this emotional immature way.

We have already looked at the emotional distress accompanies alcoholism and addiction, and will be examining more in the months ahead and it is difficult not to see the above emotional immaturity as all being products of a distress state.

In the course of addiction the alcoholic in particular grows in emotional distress as the stress and emotional dysregulation associated with addiction increases.

This means the brain “collapses” from more cortical, goal-directed (and emotionally regulated) areas of the brain to more sub-cortical areas which are more automatic, unthinking and compulsive.

Emotional distress activates these areas of habit-like compulsive behaviour, acting as a stimulus response, distress the stimulus and compulsive (unthinking)  responding as the response.

This is like a distress based or “fight or flight” reality or a heightened emotional state or “emergency” state. It seems to us that alcoholics live in this region more than cortical regions. They are primed to go off!

They then have a tendency to either run away from situations or to fight “everybody and everything”, to be intolerant of uncertainty, to catastrophize, to be fear-based people to be over reactive, hypervigilant, perfectionist etc These are all distress based states.

Are aspects of the  apparent emotional immaturity mentioned above not also not  a surface manifestation of these deep subcortical processes?

It is this state of heightened uncertainty and fear that whittles away at the alcoholic psyche. This amount of stress/distress promotes implicit, do, memory, over explicit, reflective, evaluative, memory. Distress makes one act without much thought of consequence, it makes one choose short term over greater long term gain, it makes one want to act impulsively or compulsively to alleviate distress. It is this distress that is in charge of action and emotional behaviour. It calls the shots.  A state of emergency has been called in the brain of the alcoholic.

I know it is widely shared at AA meetings that we got stuck in the emotional age of our first drink, in the early teens and never developed our emotional selves or capacity to regulate and process emotions. We are not sure this is completely true as the stress that accompanies alcoholism, as alcohol is literally classified as a pharmacological stressor,  not only causes chronic stress dysregulation but also the emotional dysregulation which accompanies this. It is emotional parts of the brain and the cortical areas that are supposed to keep them in check that are most impaired via chronic alcoholism.

Dr. Stephanie Brown (2) has explored these developmental changes in cognition, which lead to “alcoholic thinking.” She states that these changes refer “not only to rationalization, denial and frame of mind, but also to character traits that frequently accompany drinking. These include grandiosity, omnipotence and low frustration tolerance.” (3) These traits appear to be directly associated with the addictive process rather than with the individual’s personality prior to establishing this abusive cycle.

As alcohol becomes more dominant, the need to deny these changes becomes greater. It appears that there is an interaction between physiological changes and psychological defenses which creates emotional immaturity, self-centeredness and irresponsibility. Alcoholism becomes a thought disorder as well as an addiction to alcohol.

This is the consequence we believe of prefrontal atrophy and subcortical hypertrophy caused by chronic alcohol consumption, a constant injection a pharmacological stressor into the brain, wrecking the ability to maturely deliberate and instead rely on “I want it now!”  type of thinking.

We firmly believe this progression is to a state of constant distress signal in the brain and a cortical hyperarousal.

The alcoholic may not be emotionally distressed all the time but his brain is never satisfied, it constantly needs more, it finds only transient balance, via allostasis, it never finds true balance, i.e. homeostasis. it is always seeking, never reaching satiety, never completely at rest. This is emotionally exhausting.

It may represent, on superficial observation to some, the “emotional immaturity, self-centeredness and irresponsibility” (4) but is it really this simple, seeing these as the primary defenses and interpersonal style typical of normal development in the first three years of life or to characterize the addictive part of self as a “two-year-old child”?

Isn’t it more apt to say instead of  a “two-year-old wounded part of self begins to “drive the bus” and create havoc for all concerned” to say chronic stress manifest  as emotional distress “driving the bus”?

Thus a valid question remains for us and we ask it to our normies or earthling friends (i.e. non-alcoholics), wouldn’t you act in a childish if you were this distressed most of the time, having to rely on impaired emotional regulation and processing parts of the brain?



In fact, to all those normies or earthlings who are reading this blog, how well do you think or consider others when in a state of persistent and daily distress? In this heightened anxiety how good is your action outcome memory, goal-directed planning and awareness of future consequence?

Are you ever moody, emotionally volatile and over reactive in this state of high anxiety? Hyper sensitive? Ever strike out unthinkingly at others although you had not intended to? Leading to guilt and shame, and remorse and self pity which can in the fullest of time lead to depression? This is called a transient emotional dysregulation, distress leading to an emotional cascade. This is the brain of an alcoholic all the time. It can lead to dejection and relapse.

In this sate of nauseating anxiety, how well do you consider the consequence, negative or otherwise, or your fear-based decision making?  Do you choose the short term answer in these anxiety-filled moments just to simply relieve this distress this unpleasant feeling of doom? So do alcoholics!

It is not enough to call the alcoholic emotional immature or stuck in the “terrible twos”, although let’s face it the evidence for it is compelling at times!! Let’s instead understand the reasons for it. Would you like to be in a state of distress most of the time? It’s not a whole lot of fun!

The 12 steps help solve these issues, there is a solution to emotional immaturity – it leads to emotional maturity or emotional sobriety which is blogged about here also.

The next time the alcoholic is your life acts in an immature way don’t ask them why they are acting that way, ask them how they feel. instead. Get them to identify, label and process their feelings  by verbalizing them.

When the anxious amgydala has quelled and  it’s feverish responding quietened,  get them to an AA meeting where many tens of thousands of alcoholics are doing the same, “sharing”, processing their emotions by talking about them and how they really feel.



Not running away from them or intellectualizing about them, not fighting them. Simply saying in words how they feel.

It is a miracle awakening for us in recovery, the emotional regulation normies and earthlings take for granted.

The age of miracles is amongst us and it starts by opening your mouth, asking for help, getting help and getting real about what you are really feeling.

It is through sharing our deepest feelings that we start to mature and grow up.





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

2. Brown S. (1985). Treating the Alcoholic: A Developmental Model of Recovery. New York: John Wiley & Sons, Spring.

3. Brown, S. (1988). Treating Adult Children of Alcoholics: A Developmental Perspective. New York: John Wiley and Sons.

4. http://www.cairforyou.com/alchoholdrugs/alcoholcharacter.htm


Processing Emotions by verbalising them!?

The Therapeutic Benefits of “Sharing”

In early recovery I did not have a clue what emotions I was experiencing. I was not able to identify, label or process them. As a result of his failure to process emotions I seemed to be constantly distressed and and, as we seen in previous blogs, this distress leads to a distress-based impulsivity and a negative urgency to either engage in “fight or flight” behaviour, i.e. running away from fearful situations or ignoring the Big Book of AA’s recommendation not to fight anybody or anything.

The only way I could handle these troublesome and frightening emotions was by talking about them to my sponsor or my wife or other people in recovery.

In recent years it has become evident to that what I have been doing all these years have been using a technique of verbalising my emotions to actually process them. I now believe this is a fundamental part of my recovery and that I sometimes need to verbalise my emotions in order to process them. How does this work?

I recently came across an article (1) which might shed some light on this process.

Putting feelings into words (affect labeling) has long been thought to help manage negative emotional experiences. Affect labeling or naming emotions diminishes the response of the amygdala and other limbic regions to negative emotional images.  A  brain imaging study by UCLA psychologists reveals why verbalizing our feelings makes our sadness, anger and pain less intense.

When people see a photograph of an angry or fearful face,they have increased activity in a region of the brain called the amygdala, which serves as an alarm to activate a cascade of biological systems (including stress chemicals) to protect the body in times of danger. Scientists see a robust amygdala response even when they show such emotional photographs subliminally, so fast a person can’t even see them.

But does seeing an angry face and simply calling it an angry face change our brain response? The answer is yes, according to Matthew D.Lieberman, UCLA associate professor of psychology.

“When you attach the word ‘angry,’ you see a decreased response in the amygdala,” said Lieberman, lead author of the study. The study showed that while the amygdala was less active when an individual labeled the feeling, another region of the brain was more active: the right ventrolateral prefrontal cortex.

This region is located behind the forehead and eyes and has been associated with thinking in words about emotional experiences. It has also been implicated in inhibiting behavior and processing emotions.

“What we’re suggesting is when you start thinking in words about your emotions —labeling emotions — that might be part of what the right ventrolateral region is responsible for,” Lieberman said.

If a newcomer to recovery one is sad or angry or resentful , getting them person to talk or write may many have benefits.

In Lieberman’s study  participant’s viewed images of individuals making different emotional expressions. Below the picture of the face they either saw two words, such as “angry” and “fearful” and chose which emotion described the face, or they saw two names,such as “Harry” and “Sally,” and chose the gender-appropriate name that matched the face.

“When you attach the word ‘angry,’ you see a decreased response in the amygdala,” Lieberman said. “When you attach the name ‘Harry,’you don’t see the reduction in the amygdala response.

“When you put feelings into words, you’re activating this prefrontal region and seeing a reduced response in the amygdala,” he said. “In the same way you hit the brake when you’re driving when you see a yellow light,when you put feelings into words, you seem to be hitting the brakes on your emotional responses.”

As a result, an individual may feel less angry or less sad.

“This is ancient wisdom,” Lieberman said.

Putting our feelings into words helps us heal better and if we can get newcomers to talk about them, that  will make them feel better. They will experience part of the “solution” right way and be encouraged to come back for more.

So putting feelings into words helps with not only regulating and modulating the intensity of emotions, but helps with processing them, reduces distress and distress based impulsivity and shows there is a solution to unruly negative  emotions.

In my experience this process has been a fundamental part of how it works!



Lieberman, M. D., Eisenberger, N. I., Crockett, M. J., Tom, S. M., Pfeifer, J. H., & Way, B. M. (2007). Putting feelings into words affect labeling disrupts amygdala activity in response to affective stimuli. Psychological Science, 18(5), 421-428.



AA helps to reduce Impulsivity


One constant in studies on addiction and in alcoholism, in particular is the  fundamental role played by impulsivity in these disorders. It is seen to be present in early use but appears to be more distress based (i.e. more negative urgency based) as the addiction cycle becomes more chronic. This impulsivity has obvious consequences for propelling these disorders via impulsive behaviours and decision making difficulties.

Thus it then follows that any treatment of these addictive disorders must have treatment of impulsivity at the core as it appears to a fundamental pathomechanism.


Here, we review a study that on links  AA attendance and reduced impulsivity using a 16-year prospective study of men and women, who were initially untreated for their drinking problems. Across the study period, there were significant l decreases in impulsivity, and longer AA duration was associated with reductions in impulsivity.

Alcoholics Anonymous (AA) is linked to improved functioning across a number of domains [2,3]. As the evidence for the effectiveness of AA has accumulated, so too have efforts to identify the mechanisms of change associated with participation in this mutual-help group [4].

This study concluded that help-seeking and exposure to the “active ingredients” of various types of help (i.e., AA principles/practices, sponsors), which, in turn, leads to improvements in reduced impulsivity.

Impulsivity is typically higher among individuals in AUD treatment than among those in the general population [5] and, impulse control deficits tend to predate the onset of drinking problems [6-9].

Contemporary research has revealed that traits such as impulsivity can change over time [10]. Mutual-help groups like AA may promote such changes, given that they seek to bolster self-efficacy and coping skills aimed at controlling substance use, encourage members to be more structured in their daily lives, and target deficits in self-regulation [11].


impulse control.preview


Such “active ingredients” may curb the immediate self-gratification characteristic of disinhibition and provide the conceptual grounds to expect that AA participation can press for a reduction in impulsive inclinations. In turn, given the range of outcomes related to impulsivity (e.g., legal, alcohol-related, and psychosocial problems), decreases in impulsivity may account for part of the association between AA participation and improvements in these outcomes.

AA’s vision of recovery as a broad transformation of character [12], and  explores individual differences in emotional and behavioural functioning as potential mechanisms of change (13,14).

Such groups encourage members to be more structured and goal-directed, which may translate into greater efforts to delay gratification of one’s impulses and  to improve clients’ general coping skills (e.g., reduce avoidance coping).

Given that impulsivity is a risk factor for a host of problematic behaviors and outcomes beyond drinking-e.g., criminality [15], drug abuse [16], reckless driving and sexual practices [17],  lower quality of interpersonal relationships [18], and poor health [19] this reduced impulsivty is beneficial in other aspects too.

Notably, this effect was buffered by a higher quality of social support-a probable active ingredient of AA. Thus, the impact of reducing impulsivity may be widespread across a range of outcomes that are critical for long-term sobriety.


Our main caveat on this study is that it does not distinguish between different types of impulsivity and does not mention negative urgency (or distress-based impulsivity) which is more commonly seen is this sample group.

AA’s “active ingredients” may reduce distress, via a new found emotional regulation gained via the steps and use of a sponsor (acting as an external prefrontal cortex to help us inhibit our impulsive and distress based responses)  which in turns reduces our tendency to impulsive decision making and behaviour.


It would have been interesting in this study to have also measure how emotional dysregulation changed in the time span of 16 years (using the DERS scale) and to have used a different impulsivity scale i.e. used the UPPS-P scale which would both have helped more specificallylook  at the interaction of how emotional regulation and impulse control changed over the 16 year period.




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

2. Humphreys, K. Circles of recovery: Self-help organizations for addictions. Cambridge Univ Pr; 2004.

3.. Tonigan JS, Toscova R, Miller WR. Meta-analysis of the literature on Alcoholics Anonymous: Sample and study characteristics moderate findings. Journal of Studies on Alcohol. 1995

4. Kelly JF, Magill M, Stout RL. How do people recover from alcohol dependence? A systematic review of the research on mechanisms of behavior change in Alcoholics Anonymous. Addiction Research & Theory. 2009; 17(3):236–259.

5. Conway KP, et al. Personality, drug of choice, and comorbid psychopathology among substance abusers. Drug and alcohol dependence. 2002; 65(3):225–234. [PubMed: 11841894]

6. Caspi A, et al. Behavioral observations at age 3 years predict adult psychiatric disorders: Longitudinal evidence from a birth cohort. Archives of General Psychiatry. 1996; 53(11):1033. [PubMed: 8911226]

7. Cloninger CR, Sigvardsson S, Bohman M. Childhood personality predicts alcohol abuse in young adults. Alcoholism: Clinical and Experimental Research. 1988; 12(4):494–505.

8. Elkins IJ, et al. Personality traits and the development of nicotine, alcohol, and illicit drug disorders: Prospective links from adolescence to young adulthood. Journal of abnormal psychology. 2006; 115(1):26. [PubMed: 16492093]

9. Sher KJ, Bartholow BD, Wood MD. Personality and substance use disorders: A prospective study. Journal of Consulting and Clinical Psychology. 2000; 68(5):818. [PubMed: 11068968]

10. Caspi A, Roberts BW, Shiner RL. Personality development: Stability and change. Annual Review of Psychology. 2005; 56:453–484

11. Moos RH. Active ingredients of substance use focused self help groups. Addiction. 2008; 103(3):387–396. [PubMed: 18269361]

12. White WL. Commentary on Kelly et al. (2010): Alcoholics Anonymous, alcoholism recovery, global health and quality of life. Addiction. 2010; 205:637–638. [PubMed: 20403015]

13. Kelly JF, et al. Mechanisms of behavior change in alcoholics anonymous: does Alcoholics Anonymous lead to better alcohol use outcomes by reducing depression symptoms? Addiction. 105(4):626–636. [PubMed: 20102345]

14. KELLY JF, et al. Negative Affect, Relapse, and Alcoholics Anonymous (AA): Does AA Work by Reducing Anger? Journal of studies on alcohol and drugs.

15. Krueger RF, et al. Personality traits are linked to crime among men and women: Evidence from a birth cohort. Journal of abnormal psychology. 1994; 103(2):328. [PubMed: 8040502]

16. McGue M, Slutske W, Iacono WG. Personality and substance use disorders: II. Alcoholism versus drug use disorders. Journal of Consulting and Clinical Psychology. 1999; 67(3):394. [PubMed: 10369060]

17. Caspi A, et al. Personality differences predict health-risk behaviors in young adulthood: Evidence from a longitudinal study. Journal of Personality and Social Psychology. 1997; 73(5):1052. [PubMed: 9364760]

18. Ozer DJ, Benet-Martinez V. Personality and the prediction of consequential outcomes. Annu. Rev. Psychol. 2006; 57:401–421. [PubMed: 16318601]

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