impulse control

The psychic change as continual behavioural change?

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) and that the 12 steps are a program of action!

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.”

The question is whether this spiritual change is the result of behavioural change?

As I was told when I came into recovery that if I did not change my actions, and how I acted in this world, my actions would take me back to where my actions had taken me before – back to drinking.

This is the cornerstone of AA recovery; thinking, feeling differently about the world as the result of acting differently in the world, as 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 act.

In line with this thinking, it is we that need to change, not the world.

According to one study (1) which examined whether personality traits were modified during prolonged abstinence in recovering alcoholics, two 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 obtained a high “neuroticism” score (emotions, stress), associated with a low “agreeableness” score (relationship to others).

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).

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.

 

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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”

If we want to to recover from addiction we have to change how we behave.  We have to start by following a recovery program of action. 

No by thinking about it, or emoting about it but by doing it!

Action is the magic word.

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.

 

How Mindfulness could help Recovery?

Mindfulness training modifies cognitive, affective, and physiological mechanisms implicated in alcohol dependence.

Posted on May 7, 2015 | Leave a comment

Yesterday we looked a how low heart rate variability in alcoholics (active and in recovery) may influence self, emotion and stress regulation, and have a limited effect on impulsivity, and result in a “locked in” attention to alcohol-related cues, all of which have obvious consequences for relapse.

Here we cite and use excerpts from an article by Eric Garland et al (1) which addresses the effects of mindfulness  meditation on those with alcohol dependence.

Although Garland suggest mindfulness could be an alternative to other treatment and recovery programs, I suggest that it can be used most effectively with other treatment and recovery programs, e.g. with step 11 of 12 step programs.

I believe the consequence of emotion dysregulation  over many years of addiction leaves behind numerous unprocessed emotions which have not been consigned to long term memory and as a result float around the mind as resentments, shame and guilt based memories etc.

Emotion dysregulation has not allowed us to consigned them properly to the past (the so-called wreckage of the past) or long term memory and only an intensive process of emotional processing these e.g. via step 4 or 5 or via an alternative stock taking of our pasts seems to resolve this problem.

I know from my previous experience of intensive meditation involving various 10 day intensive courses and meditating on a very regular basis, before realising I am an alcoholic, would always result in relapse via the distress of the past being resurgent in my mind.

Some method of addressing all of these past behaviours, which invariably have hurt someone, need to be addressed and processed, even making amends to those hurt by our previous behaviours,  before we profoundly ease the distress of the past and help facilitate a greater recovery and more effective meditation practice.

Anyway, that’s my vies, on with the article…

“When attention is fixated on visual or olfactory alcohol cues, alcohol dependent individuals exhibit significant psychophysiological reactivity (Carter & Tiffany 1999). In turn, this alcohol cue-reactivity may lead to increased craving, which can trigger alcohol consumption as a means of reducing distress. Many persons recovering from alcohol use disorders attempt to suppress cravings, which, paradoxically, can serve to increase intrusive, automatic alcohol-related cognitions (Palfai, Monti, Colby, & Rohsenow 1997), dysphoria, and autonomic arousal (Wenzlaff & Wegner 2000). Indeed, among alcohol dependent persons, thought suppression is negatively correlated with vagally-mediated heart rate variability (Ingjaldsson, Laberg, & Thayer 2003), a putative index of emotion regulation and parasympathetic inhibition of stress reactions (Thayer & Lane 2000).

As thoughts of drinking intensify and are coupled with psychobiological distress, the impulse to consume alcohol as a form of palliative coping may overcome depleted self-regulation strength (Muraven, Collins, & Nienhaus 2002; Muraven & Shmueli 2006) leading to relapse. The attempt to avoid distress or allay its impact through compulsive alcohol consumption results in negative reinforcement conditioning that may perpetuate this cycle by further sensitizing the brain to future stressful encounters via allostatic dysregulation of neuroendocrine systems (Koob 2003). Components of this risk chain may be especially malleable to targeted behavioral therapies.

One such intervention, mindfulness training, which originates from Buddhist traditions but has been co-opted by Western clinicians, has recently gained prominence in the psychological and medical literatures for its salutary effects on stress-related biobehavioral conditions (Baer & Krietemeyer 2006; Ludwig & Kabat-Zinn 2008). Mindfulness involves self-regulation of a metacognitive form of attention: a nonreactive, non-evaluative monitoring of moment-by-moment cognition, emotion, perception, and physiological state without fixation on thoughts of past or future (Garland 2007). A growing body of research suggests that mindfulness affects implicit cognition and attentional processes (e.g., Jha, Krompinger, & Baime 2007; Lutz, Slagter, Dunne, & Davidson 2008; Wenk-Sormaz 2005) as well as heart rate variability indices of parasympathetic regulation (Tang et al. 2009).

 

Mindfulness treatments may enhance clinical outcomes in substance-abusing populations.

Bowen et al. (2007) found that mindfulness training of incarcerated inmates reduced post-release substance use, substance-related problems, and psychiatric symptoms to a greater extent than standard chemical dependency services offered at the prison. Other pilot studies of mindfulness-based interventions with substance abusers have found significant reductions in distress, negative affect, stress-related biomarkers, and substance use (Marcus, Fine, & Kouzekanani 2001; Marcus et al. 2003;Zgierska et al. 2008).

To that end, a randomized, controlled design was used to compare the therapeutic effects of a mindfulness-oriented recovery enhancement (MORE) intervention to those of an evidence-based alcohol dependence support group (ASG).

We hypothesized that, relative to ASG, MORE would result in significantly greaterdecreases in perceived stress, impaired alcohol response inhibition, craving for alcohol, psychiatric symptoms, and thought suppression and significantly greater increases in mindfulness and in heart rate variability (HRV) recovery from stress-primed alcohol cues.

 

MINDFULNESS TRAINING REDUCES STRESS AND THOUGHT SUPPRESSION

Among recovering alcohol-dependent individuals, mindfulness training appears to be a potentially effective stress reduction technique. MORE reduced perceived stress to a greater extent than did ASG, which is noteworthy given that social support reduces stress reactivity and buffers deleterious effects of stressful life events (Christenfeld & Gerin 2000). The stress reduction effects of mindfulness training among nonclinical populations are well known in the literature (Grossman, Niemann, Schmidt, & Walach 2004), but it is notable that significant effects were obtained in a sample of clinically-disordered, alcohol-dependent adults with extensive trauma histories who may be more vulnerable to stress-precipitated relapse due to allostatic dysregulation of neural stress circuitry (Valdez & Koob 2004).

Like stress, thought suppression significantly decreased over the course of ten weeks of mindfulness training. In turn, decreases in thought suppression among MORE participants were significantly correlated with decreases in impaired alcohol response inhibition, raising the possibility that participants who improved their ability to regulate drinking urges may have done so via reductions in thought suppression.

In the context of alcohol dependence, thought suppression seems to enhance the conscious awareness of alcohol-related cognitions and affective reactions. MORE, with its emphasis on nonjudgmental, metacognitive awareness of present-moment experience, appeared to counter this deleterious cognitive strategy and therefore may have prevented post-suppression rebound effects from exacerbating negative affect and intrusive alcohol-related cognitions that can promote relapse.

CONCLUSION

In sum, the unwitting attempts of recovering alcohol dependent persons to suppress appetitive cognitive-emotional reactions towards alcohol may obscure these responses from consciousness only to perpetuate and intensify them within the cognitive unconscious. In the domain of unconscious mental life, automatic processes run smoothly and efficiently uninhibited by volitional control (Kihlstrom 1987). Hence, by shunting appetitive reactions into the unconscious, the alcohol dependent individual may increase the very appetitive response towards alcohol he or she is trying to suppress and exacerbate psychophysiological reactivity to alcohol cues. Mindfulness training may serve to undo this process, making unconscious responses conscious. Thus, practice of mindfulness may promote the recovery of alcohol dependent persons through: a) deautomatization of alcohol use action schema, resulting in diminished attentional bias towards subliminal alcohol cues and increased craving as a result of disrupted automaticity; and b) decreased thought suppression resulting in increased awareness of alcohol urges over time, increased HRV recovery from alcohol cue-exposure, and improved ability to inhibit appetitive responses.

Accordingly, mindfulness training may be a tractable means of promoting enduring behavior change. Although brief motivational interventions may be highly effective at impelling the desire towards sobriety, participants of such motivational enhancement therapies remain prone to eventual relapse; indeed, relapse is often a part of the recovery process. As such, interventions that consolidate short-term treatment gains into broader lifestyle change are of major significance to the addictions treatment field. During the gradual practice of mindfulness, one learns to work with negative emotions in a metacognitive context, resulting in nonreactivity to difficult mental contents and improved self-regulation in the face of stressors. The developmental process of cultivating and embedding mindfulness principles into all aspects of one’s life may solidify gains made in prior treatment and provide an effective, long-term approach to coping with stress-precipitated relapse.

Despite evidence suggesting that stress appraisal and attentional biases are key components of alcohol dependence, the form of addictions treatment most available to poor and marginalized persons, social support groups, does not target these pathogenic mechanisms directly. In contrast, practice of mindfulness may attenuate stress reactivity and thought suppression while disrupting addictive automaticity, resulting in increased awareness of craving and greater ability to cope with and recover from alcohol urges in stressful contexts. Hence, mindfulness training may hold promise as an alternative, targeted treatment for stress-precipitated alcohol dependence among vulnerable members of society.”

Equally mindfulness meditation may be used alongside other treatment regimes. For example, it can be used in a daily manner as part of step 11 in the 12 step program. It is also used as part of DBT, for example.

I think that there are ideas out there, is so-called different treatment regimes, which can simply compliment each other. Whatever works, works.

I personally meditate using both  Christian and Buddhist meditation techniques.

Sometimes appreciating the therapeutic strengths of different treatment philosophies and practice can augment one’s own main treatment and recovery program.

References

1.  Garland, E. L., Gaylord, S. A., Boettiger, C. A., & Howard, M. O. (2010). Mindfulness training modifies cognitive, affective, and physiological mechanisms implicated in alcohol dependence: results of a randomized controlled pilot trial. Journal of psychoactive drugs, 42(2), 177-192.

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The terror of “Locked In” Attention!

I remember when I was in the first days, weeks and months of early recovery I used to give myself such a hard time when my attention was drawn to some alcohol-related cue, like someone drinking ,or finding it difficult not dealing with some  reminder of people places and things from my alcohol abusing past; finding that I found it nigh on impossible dragging my attention away from these and related memories associated with my drinking past.

It was as if I was entranced by it, in some of tunnel vision. It used to scare the life out of me.

I rarely found these thoughts appetitive but if I dwelt on these thoughts or trained my attention on cues I would find that the adverse, fearful things would turn to more desire based physiological reactions like salivating and so on.

I took these to mean that I actually wanted to drink and not stay sober. My sponsor at the time said two things which helped – a. I have an alcoholic brain that wants to drink period, 2. cues from my past may always have this effect on me. Accept it, don’t fight it.

That was what I had been doing in fact. Fighting it, these cues reminders and their automatically occurring intrusive thoughts about the past. It is in fighting these thoughts that they proliferate and then become “craving”.

Years later after much research I found that all alcoholics seem to have an attentional bias towards alcohol-related cues which leads to a cue reactivity.

Originally I thought this meant that I simply wanted to drink but found out that in  any manifestation of urge to drink (which is slightly different from a craving which requires an affective response on the part of the alcoholic in order to become a craving similar to mental obsession of the Big Book ) there is a stress reponse like the hear beat quickening, differences in galvanic skin conductance, increased saliva production etc .

Thus this cue reactivty seems to involve not only appetitive or desire states, i.e. it activates the reward system in the brain to motivate one to drink but also contains a stress based reactivity.

Any so-called “craving” state also manifests as either an anxiety state in simple cue reactivity e.g. the sight of alcohol or in negative emotions such as fear, anger and sadness in terms of a stress based craving.

Together, i.e. a cue based reactivity in the face stress/distress leads to a greater urge to drink than by either alone. By reacting to these one is increasing the stress/distress.

To the alcoholic brain having a drink or the desire to drink is the brain suggesting to us as alcoholics that this is the best way to attain transient homeostasis from an allostatic state of distress because this is how we used to balance the effects of emotional distress when we were drinking. We experience distress and automatically had thoughts about drinking. Thus alcoholism is a distress-based condition. We think it is us wanting the drink but it is the distress prompting the wanting of the drink!!

The distress does the drinking for us, itgets us out of our seats and down the street to the bar, it gets us on the bar stool….We may think it is our actions as we use rationalisng and justifying schemata afterwards to justify behaviour that had, in fact, been automatic or compulsive, compulsive meaning to relieve a distress state.

As a schema, which is implicit, i.e. it is automatically prompted and activated by distress also. We are not even in charge of this. We feel and think that we are in control over behaviour bit this is not the case as self control has become so impaired and limited it is distress doing the action and the subsequent rationalising.

The compusive part of the brain, the dorsal striatum, is the only part of the brain that requires us to make a post hoc rationalisation of why we did an action that was essentially automatic and compulsive.

We have become passengers in our own lives. Distress is now doing the driving.

So the brain thinks it is simply telling us the best way to survive this distress or in other words to regulate this distress. Thus it is an incredibly impaired way to regulate stress and emotional distress.

I want to further explain how some of this is linked to low heart rate variability. If we have low HRV we find it difficult inhibiting automatic responses and in changing behaviour. We become behaviourally rigid, and locked into attending to things like cues when we don’t really want to.

This is often the result of distress reducing the ability of the heart rate variability to inform and change our responses.

I cite and use excerpts form one of my favourite articles again by co-authored by Julian Thayer (1).

 

“The recovering alcoholic must face the difficulty of having his or her ambition to remain abstinent challenged in various situations in which memories about the pleasurable effects of alcohol are activated and the striving for abstinence no longer seems meaningful (Anton 1999; Marlatt and Gordon 1985). The odds for successful coping with such temptations are related to numerous factors, such as one’s subjective affective state and the ability to shift one’s focus from the automatic impulse to drink toward a cognitive reconstruction of the situation (Palfai et al 1997b; Tiffany 1990). Despite the importance of  attentional flexibility in effectively modulating such “highrisk” situations, research on the topic is scarce.

Thayer and Lane (2000) suggested that the interplay between positive (excitatory) and negative (inhibitory) feedback circuits in the nervous system (NS) allows for flexible and adaptive behavior across a wide range of situations. The uniqueness of this model lies with its emphasis on the importance of inhibitory processes in effective modulation of affective experience. In short, these researchers propose that the defects in neurovisceral regulation of affective experience seen in various psychiatric conditions (e.g., anxiety disorders) may be better explained by faulty inhibitory function in the NS than by unitary arousal models.

Tonic heart rate variability (HRV) may be a physiologic indicator of such inhibitory processes (Friedman and Thayer 1998a; Porges 1995). Heart rate variability refers to the complex beat-to-beat variation in heart rate produced by the interplay of sympathetic and parasympathetic (vagal) neural activity at the sinus node of the heart.

Importantly, heart rate (HR) is under tonic inhibitory control via the vagus nerve (Levy 1990). These neural connections to the heart are linked to brain structures involved in goal-directed behavior and adaptability (Thayer and Lane 2000). Compelling evidence now exists to show that high levels of HRV are related to cognitive flexibility (Johnsen et al 2003), modulation of affect and emotion (see Bazhenova 1995, cited in Porges 1995), and increased impulse control (Allen et al 2000; Porges et al 1996).

The hypothesis that reduced HRV is related to defective affective and emotional regulation has been supported in recent research in which reduced HRV was present in clinical disorders such as generalized anxiety disorder (Thayer et al 1996), panic disorder (Friedman and Thayer 1998b), posttraumatic stress disorder (Cohen et al 1997) several scientific arguments suggest that impaired inhibitory function may play a role in chronic alcohol abuse.

First, alcoholics have repeatedly been shown to have problems shifting attention and directing their attention away from task-irrelevant information (Johnsen et al 1994; Setter et al 1994; Stormark et al 2000). Second, frontal areas of the brain are most affected by the acute and chronic effects of alcohol, and these structures are of crucial importance in inhibitory functioning and self-control (Lyvers 2000). Third, acute effects of alcohol ingestion result in reductions in HRV, implying that chronic alcohol ingestion may result in a long-lasting impairment of the vagal modulation of HR (Reed et al 1999; Weise et al 1986)

Fourth, severely dependent alcoholics show a sustained phasic HR acceleration when processing alcohol information, indicating defective vagal modulation of cardiac function (Stormark et al 1998). Tonic HRV has similarly been found to be a useful measure of physiologic activity in challenging situations (Thayer and Lane 2000). Appropriate modulation of HRV (increases, decreases, or no change) depends on the type of challenge and the characteristics of individuals as they interact with specific contextual manipulation (Friedman and Thayer 1998a; Hughes and Stoney 2000; Porges et al 1996; Thayer et al 1996).

For example, during attention demanding tasks, healthy individuals show appropriate reductions in HRV (Porges 1995). In general, high tonic levels of HRV allow for the flexible deployment of organism resources to meet environmental challenges. With respect to attention, it is suggested that high levels of HRV reflect flexible attentional focus, whereas low HRV is related to “locked in attention” (Porges et al 1996). Moreover, increased tonic vagal activity is related to adaptive development and lack of behavioral and emotional problems (Hughes and Stoney 2000; Porges et al 1996).

Furthermore, it has been demonstrated that increases in vagal activity during challenging tasks discriminates between individuals who have experienced traumatic events and managed to recover from them and those who still suffer from chronic symptoms of posttraumatic stress (Sahr et al 2001). Such increases in vagal activity during challenging tasks are particularly interesting because studies on alcohol abusers have found increases in HRV after exposure to alcohol-related cues (Jansma et al 2000; Rajan et al 1998).

One could speculate that such enhanced vagal activity could be a sign of compensatory coping aimed at taming automatic drinking related processes (Larimer et al 1999). Such an interpretation is in agreement with cognitive theories predicting that alcoholics and other drug users do not simply respond passively to exposure to drug-related cues, but, on the contrary, in such situations conscious processes are invoked, inhibiting execution of drug-related cognition (Tiffany 1990, 1995). If this explanation is correct, alcoholics who have more effective coping resources should show stronger increases in vagal activity during such challenging exposure than alcoholics who express greater difficulty in resisting drinking-related impulses.

Also  general differences in HRV between alcoholics and nonalcoholics are interesting indicators of defective inhibitory functioning, a measure of rigid thought-control strategies and lack of cognitive control should be an important indicator of defective inhibitory function and “positive feedback loops” reflected as low HRV (Wegner and Zanakos 1994).

Linking these measures to the physiologic index of HRV makes a stronger case for attributing reduced vagal tone (HRV) to a defective regulatory mechanism resulting in unpleasant affective states and maladaptive coping with psychologic stressors

The main results of our study may be summed as follows. First, as expected, alcoholic participants had lower HRV compared with the nonalcoholic control group. Second, the imaginary alcohol exposure increased HRV in the alcoholic participants. Third, across the groups, an inverse association was found between HRV and negative mood and a positive association between positive mood and HRV. Fourth, HRV was negatively correlated with compulsive drinking during the imaginary alcohol exposure in the alcoholic participants. Fifth, within the alcoholic group, HRV was negatively associated with chronic thought suppression (WBSI).

Generally, these findings are in agreement with the neurovisceral integration model and the polyvagal theory that suggests HRV is a marker of the level of cognitive, behavioral, and emotional regulatory abilities (Thayer and Lane 2000).

The fact that the alcoholic group had generally lower tonic HRV compared with the nonalcoholic control group indicates that such reduced HRV may also be a factor in alcohol abuse; however, such group differences in HRV provide only indirect support for the theory that low HRV in alcoholics may be related to impaired inhibitory mechanisms

Because HRV is related to activity in frontal brain areas involved in cognition and impulse control (Thayer and Lane 2000), we speculated that tonic HRV would be an index of nonautomatic inhibitory processes aimed at suppressing and controlling automatic drug-related cognitions. To test this hypothesis more directly, the association between HRV and problems with controlling drinking-related impulses were studied.

Consistent with this hypothesis, the compulsive subscale of the OCDS was found to be inversely associated with HRV in the alcohol-exposure condition, thus suggesting that HRV may be an indirect indicator of the level of impulse control associated with drinking. These findings are therefore consistent with Stormark et al (1998), who found that sustained HR acceleration (lack of vagal inhibition) when processing alcohol-related information was related to compulsive drinking and “locked-in attention.”

Post hoc analysis further suggested that alcoholics who expressed a relatively high ability to resist impulses to drink (OCDS) had the clearest increase in HRV under the alcohol exposure this study suggests that alcoholics may actively inhibit or compensate for their involuntary attraction to alcohol-related information by activation of higher nonautomatic cognitive processes (Tiffany 1995). Such conscious avoidance has previously been demonstrated in studies on attentional processes in alcoholics (Stormark et al 1997) and by the fact that frontal brain structures involved in inhibition and control of affective information are often highly activated in the processing of alcohol related cues (Anton 1999). Furthermore, this interpretation is in agreement with other studies suggesting that high HRV during challenging tasks is associated with recovery from acute stress disorders (Sahr et al 2001).

Several studies have indicated that low HRV is associated with impaired cognitive control and perseverative thinking (Thayer and Lane 2002). Consistent with these reports a negative association was found between HRV and chronic thought suppression. The WBSI assesses efforts to eliminate thoughts from awareness while experiencing frequent intrusions of such “forbidden” thoughts and thus represents an interesting and well-validated measure of ineffective thought control (Wegner and Zanakos 1994). Thought suppression has been found to be an especially counterproductive strategy for coping with urges and craving (Palfai et al 1997a, 1997b) and may even play a causal role in maintaining various clinical disorders (Wenzlaff and Wegner 2000).

To our knowledge, this is the first time a link between physiologic indicators of a lack of cognitive flexibility (low HRV) and chronic thought suppression has been demonstrated.

Thayer and Friedman (2002) have reviewed evidence indicating that there is an association between vagally mediated HRV and the inhibitory role of the prefrontal cortex. Consistent with Thayer and Lane (2000), this study suggests that impaired inhibitory processes are significantly related to ineffective thought control.

The fact that this association between HRV and WBSI was only found in the alcoholics may be related to the fact that only this clinical group shows signs of such faulty thought control.

Wegner and Zanakos (1994) suggested that thought suppression is particularly ineffective when the strategic resources involved in intentional suppression are inhibited or blocked (Wegner 1994). Consistent with this hypothesis, our findings show that those reporting high scores on WBSI show signs of impaired inhibitory functioning as indexed by low vagally mediated HRV.”

This excellent article fro me is also alluding to the fact that those with increased HRV was related to successfully related to regulating negative emotion,  stress/distress and affect, not just the thoughts that these affective states gave rise to .

Thus any strategies that help with improving  the ability to increase HRV will likely have positive results in coping with cue associated materials.

We look at one of these therapeutic strategies next…that of mindfulness meditation.

 

References

1. Ingjaldsson, J. T., Laberg, J. C., & Thayer, J. F. (2003). Reduced heart rate variability in chronic alcohol abuse: relationship with negative mood, chronic thought suppression, and compulsive drinking. Biological Psychiatry, 54(12), 1427-1436.

 

 

 

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.)

400px-Neuron_Hand-tuned.svg

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

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

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

 

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

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

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Psychological Dysregulation

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

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

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

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

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

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

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

Neurobiological Basis of Psychological Dysregulation

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

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

 

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White Matter Development and Alcohol Exposure

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

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

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

Limbic System Development and Alcohol Exposure

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

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

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

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

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

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

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

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

 

References

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

 

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.

 

References

 

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]

19. Bogg T, Roberts BW. Conscientiousness and Health-Related Behaviors: A Meta-Analysis of the Leading Behavioral Contributors to Mortality. Psychological Bulletin. 2004; 130(6):887. [PubMed: 15535742]

 

 

 

 

 

 

 

 

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.

 

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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.

 

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.

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

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

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

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

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

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

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

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

 

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

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

Alcohol Use Disorders and Emotional Processing

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

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

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

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

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

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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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