emotional regulation

How it (Mindfulness) Works? (Part 3)

“Mindfulness Training Ameliorates Addiction by Targeting Neurocognitive Mechanisms

In the third part of this excellent review paper  (1) we look at the empirical evidence is presented suggesting that MBIs ameliorate addiction by enhancing cognitive regulation of a number of key processes.

EMOTION REGULATION

When individuals are unable to marshal effective problem-solving to resolve a stressor, lack of a favorable resolution may lead to deployment of emotion regulation efforts to manage the emotional distress elicited by the stressful circumstance. Neuroimaging research has provided evidence for a reciprocal, dual-system neural network model of emotion regulation comprised of a dorsal brain system (e.g., dlPFC, dACC, parietal cortex) subserving top-down cognitive control, and a ventral brain system (e.g., amygdala, striatum) subserving bottom-up emotional impulses (133–135). Top-down engagement of proactive cognitive control mechanisms regulates negative affect and attenuates the effects of emotional interference on cognition (135–138), and is associated with increased activation of PFC which in turn attenuates amygdala activation (139, 140). Research suggests that dysregulated emotional reactions occur when the reciprocal balance between the relative activation of bottom-up and top-down neural circuits becomes tipped in favor of bottom-up processes (141). A number of studies suggest that mindfulness training may counter this imbalance and augment emotion regulation [for reviews, see Ref. (78, 142)] by restructuring neural function in favor of context-dependent top-down control processes. For example, Goldin and Gross (143) demonstrated that individuals with elevated negative affect at baseline who later received mindfulness training exhibited increased emotion regulatory capacity coupled with greater recruitment of attentional control resources and reduced amygdala activation during exposure to negative, self-relevant stimuli. Thus, by enhancing top-down cognitive control over emotional responses in a context-dependent fashion, MBIs may reduce drug use precipitated by negative affective states.

Importantly, MBIs provide training in cultivating a state of mindful awareness and acceptance of the extant emotional response as a precondition for emotion regulation. While acceptance of aversive mental experience may itself result in reduced negative affect (144), mindfulness training may also exert downstream facilitative effects on cognitive regulation of emotion following the acute state of mindfulness. For instance, mindfulness training may promote cognitive reappraisal, the process by which the meaning of a stressful or adverse event is re-construed so as to reduce its negative emotional impact (125). One theoretical model posits a multi-stage process of mindful emotion regulation (1, 145). According to this model, during an adverse experience mindfulness practitioners first disengage from initial negative appraisals into the metacognitive state of mindfulness in which cognitions and emotions are viewed and accepted as transitory mental events without inherent veridicality. Subsequently, the scope of attention broadens to encompass a larger set of previously unattended information from which new situational appraisals may be generated. By accessing this enlarged set of contextual data, present circumstances may be reappraised in an adaptive fashion that promotes positive affect and behavioral activation. For instance, a newly abstinent alcohol dependent individual might reappraise an affront by a former “drinking buddy” as evidence of their need to build new, sober relationships. In support of this model, recent studies indicate that mindfulness during meditation predicts enhanced cognitive reappraisal (146), which in turn mediates the association of mindfulness and reduced substance craving (147). This context-dependent use of prefrontal regulatory strategy represents a “middle way” between hypo- and hyper-activation of cognitive control resources, thereby preventing resource depletion and untoward rebound effects.

Speculatively, this “mindful reappraisal” process may involve spreading activation in a number of brain networks. Generating the state of mindfulness in the midst of a negative affective state may activate the ACC and dlPFC (148, 149), which could facilitate metacognitive monitoring of emotional reactivity, foster attentional disengagement from negative appraisals, and regulate limbic activation. In so doing, the acute state of mindfulness may attenuate activation in brain areas that subserve self-referential, linguistic processing during emotional experience (e.g., mPFC) while promoting interoceptive recovery from negative appraisals by increasing activation in the insula (113). Metacognitive disengagement from the initial negative appraisal may result in non-elaborative attention to somatosensory information, thereby facilitating the set shifting process of cognitive reappraisal, as brain activations shift from posterior to anterior regions of cortex centered on the node of the OFC. During this process emotional interference is attenuated while alternate appraisals are retrieved from memory and evaluated for goodness-of-fit to situational parameters and demands (150).

The effects of mindfulness-centered regulation of negative emotion might be measured with a standard emotion regulation paradigm [c.f. (137)], in which participants are instructed to use reappraisal to reduce negative affect in response to exposure to aversive visual stimuli [e.g., images from the International Affective Picture System; (151)]. In this task paradigm, mindfulness practitioners may exhibit enhanced reappraisal efficacy, as evidenced by reduced self-reported and psychophysiological responses to aversive stimuli on reappraise relative to attend trials. In that regard, a study employing ERP analysis found that when compared to controls, meditators exhibited significantly greater reappraisal efficacy as evidenced by significantly larger attenuation of brain activity during reappraisal of stressful stimuli in centro-parietal regions subserving attentional and emotional processing (152).

STRESS REACTIVITY

In addition to pro-regulatory effects on emotion, mindfulness training may facilitate neurocognitive regulation of the effects of stress on the autonomic nervous system. As addicts in treatment develop dispositional mindfulness through mindfulness training, they may be more able to engage prefrontal cortical modulation of the sympathetic “fight-or-flight” response via parasympathetic nervous system activation of the “vagal brake,” resulting in increased HRV and heart-rate deceleration in the face of stress or addictive cues (153, 154). Thus, increasing dispositional mindfulness may be reflective of greater neurovisceral integration and flexibility in the central autonomic network (67). This network is comprised of neuroanatomic and functional linkages between central (e.g., PFC and ACC) and autonomic (e.g., vagus nerve) nervous system structures which coordinate the self-regulation of attention, cognition, and emotion while exerting regulatory influences over perturbations to visceral homeostasis (155), such as those that might be evoked in abstinent substance dependent individuals exposed to stressful and/or substance-related stimuli. Mindful individuals may have greater capacity for contextually appropriate engagement and subsequent disengagement of neurocognitive resources in response to the presence and absence of stress and drug-cues. Such autonomic flexibility (156) engendered through mindfulness training may help persons in recovery from addiction adapt to situational demands without succumbing to a stress-precipitated relapse.

This hypothesis is consistent with evidence of the effects of mindfulness on neural function in dlPFC and ACC (149, 157), key structures involved in central autonomic regulation of HRV via downstream influences on the amygdala and hypothalamus (158, 159). Congruent with such findings, MBIs increase parasympathetically mediated HRV to an even greater extent than relaxation therapy (160,161), and decreases sympathetically mediated indices of stress (8), including blood pressure (162), heart rate (163), skin conductance responses (161), and muscle tension (164). These effects of mindfulness-centered regulation on autonomic function may result in improved ability to manage substance cue-reactivity. In support of this hypothesis, a Mindfulness-Oriented Recovery Enhancement intervention for alcohol dependence increased HRV recovery from stress and alcohol cue-reactivity (7). Congruent with this finding, relative to their less mindful counterparts, alcohol dependent individuals with higher levels of dispositional mindfulness exhibited greater attentional disengagement from alcohol cues which predicted the extent to which their HRV recovered from alcohol cue-exposure levels (67). Lastly, persons participating a mindfulness-based smoking cessation intervention who exhibited increased HRV during mindfulness meditation smoked fewer cigarettes following treatment than those who exhibited decreased HRV (165). Thus, addicts who develop dispositional mindfulness through participation in MBIs may become better able to regulate appetitive responses by virtue of enhanced neurocognitive control over autonomic reactivity to stress and substance cues.

The effects of MBIs on cognitive regulation of autonomic cue-reactivity might be measured with a stress-primed cue-reactivity paradigm, in which participants are first exposed to a laboratory stress induction [e.g., aversive IAPS images, c.f. (7); or the TSST, c.f. (132)], then exposed to substance-related cues (either in vivo, imaginally, or images of alcohol or drugs), and finally asked to use mindfulness skills to downregulate the resultant state of autonomic arousal.

References

1. Garland, E. L., Froeliger, B., & Howard, M. O. (2013). Mindfulness  training targets neurocognitive mechanisms of addiction at the attention-appraisal-emotion interface. Frontiers in psychiatry, 4.

Neural mechanisms of mindfulness meditation

Mindfulness is simply paying attention to thoughts, emotions, and body sensations in a non-judgmental manner.Meditation is a platform used to achieve mindfulness. This practice originated from the idea of mindfulness in Buddhism and has been widely promoted by Jon Kabat-Zinn.

Components of mindfulness meditation

Although several components for mindfulness meditation have been proposed, four components have found to be common among most: attention regulation, body awareness, emotion regulation, and change in perspective on the self.[1] All of the components described above are connected to each other.

Attention regulation

Attention regulation is the task of focusing attention on an object, acknowledging any distractions, and then returning your focus back to the object. Some evidence for mechanisms responsible for attention regulation during mindfulness meditation are shown below.

  • Mindfulness meditators showed greater activation of rostral anterior cingulate cortex (ACC) and dorsal medial prefrontal cortex (MPFC).[2] This suggests that meditators have a stronger processing of conflict/distraction and are more engaged in emotional regulation. However as the meditators become more efficient at focused attention, regulation becomes unnecessary and consequentially decreases activation of ACC in the long term.[3]

  • The cortical thickness in the dorsal ACC was also found to be greater in the of gray matter of experienced meditators.[4]

Body awareness

Body awareness refers to focusing on an object/task within the body such as breathing

  • Meditators showed a greater cortical thicknesss [8] and greater gray matterconcentration in the right anterior insula.[9]

 

 

The insula is responsible for awareness to stimuli and the thickness of its gray matter correlates to the accuracy and detection of the stimuli by the nervous system.[11][12] Since there is no quantitative evidence suggesting that mindfulness meditation impacts body awareness, this component is not well understood.

Emotion regulation

Cognitive regulation (in terms of mindfulness meditation) means having control over giving attention to a particular stimuli or by changing the response to that stimuli.The cognitive change is achieved through reappraisal (interpreting the stimulus in a more positive manner) and extinction (reversing the response to the stimulus). Behavioral regulationrefers to inhibiting the expression of certain behaviors in response to a stimuli. Research suggests two main mechanisms for how mindfulness meditationinfluences the emotional response to a stimuli.

  • Mindfulness meditation regulates emotions via increased activation of the dorso-medial PFC and rostral ACC.[2]
  • Increased activation of the ventrolateral PFC can regulate emotion by decreasing the activity of the amygdala.[13][14][15] This was also predicted by a study in which they observed the effect of a person’s mood/attitude during mindfulness on brain activation.[16]

Lateral prefrontal cortex (lPFC) is important for selective attention while ventral prefrontal cortex (vPFC) is involved in inhibiting a response. As noted before, anterior cingulate cortex (ACC) has been noted for maintaining attention to a stimulus. The amygdala is responsible for generating emotions. Mindfulness meditation is believed to be able to regulate negative thoughts and decrease emotional reactivity through these regions of the brain.

 

Alcoholics Anonymous and Reduced Impulsivity: A Novel Mechanism of Change

Impulsivity or lack of behaviour inhibition, especially when distressed, is one psychological mechanisms which is implicated in all addictive behaviour from substance addiction to behaviour addiction.

It is, in my view, linked to the impaired emotion processing as I have elucidated upon in various blogs on this site.

This impulsivity is present for example in those vulnerable to later alcoholism, i.e. sons and daughters of alcoholic parents or children  from a family that has a relatively high or concentrated density of alcoholics in the family history, right through to old timers, people who have decades of recovery from alcoholism.

It is an ever present and as a result part of a pathomechanism of alcoholism, that is it is fundamental to driving alcoholism to it’s chronic endpoint.

It partly drives addiction via it’s impact on decision making – research shows people of varying addictive behaviours choose now over later, even if it is a smaller short term gain over a greater long term gain. We seem to react to relieve a distress signal in the brain rather than in response to considering and evaluating the long term consequences of a decision or act.

No doubt this improves in recovery as it has with me. Nonetheless, this tendency for rash action with limited consideration of long term consequence is clearly a part of the addictive profile. Not only do we choose now over then, we appear to have an intolerance of uncertainty, which means we have difficulties coping with uncertain outcomes. In other words we struggle with things in the future particularly if they are worrying or concerning things, like a day in court etc. The future can continually intrude into the present. A thought becomes a near certain action, again similar to the though-action fusion of obsessive compulsive disorder. It is as if the thought and possible future action are almost fused, as if they are happening in unison.

Although simple, less worrying events can also make me struggle with leaving the future to the future instead of endless and fruitlessly ruminating about it in the now. In early recovery  especially I found that I had real difficulty dealing with the uncertainty of future events and always thought they would turn out bad. It is akin to catastrophic thinking.

If a thought of a drink entered into my head it was so distressing, almost as if I was being dragged by some invisible magnet to the nearest bar. It was horrendous. Fortunately I created my own thought action fusion to oppose this.

Any time I felt this distressing lure of the bar like some unavoidable siren call of alcohol I would turn that thought into the action of ringing my sponsor. This is why sponsees should ring sponsors about whatever, whenever in order to habitualize these responses to counteract the automatic responses of the addicted brain.

I think it is again based on an inherent emotion dysregulation. Obsessive thoughts are linked to emotion dysregulation.

My emotions can still sometimes control me and not the other way around.

Apparently we need to recruit the frontal part of the brain to regulate these emotions and this is the area most damaged by chronic alcohol consumption.

As a result we find it difficult to recruit this brain area which not only helps regulate emotion but is instrumental in making reflective, evaluative decisions about future, more long term consequence. As a result addicts of all types appear to use a “bottom up” sub-cortical part of the brain centred on the amgydala region to make responses to decisions instead of a “top down” more cortical part of the brain to make evaluative decisions.

We thus react, and rashly act to relieve the distress of undifferentiated emotions, the result of unprocessed emotion rather than using processed emotions to recruit the more cortical parts of the brain.

Who would have though emotions were so instrumental in us making decisions? Two parts of the brain that hold emotions in check so that they can be used to serve goal directed behaviour are the orbitofrontal cortex and the ventromedial prefrontal cortex.

120px-Orbital_gyrus_animation_small2

 

These areas also keep amgydaloid responding in check. Unfortunately these two areas are impaired in alcoholics and other addictive behaviours so their influence on and regulation of the amgydala is also impaired.

This means the sub cortical areas of the amgydala and related regions are over active and prompt not a goal directed response to decision making but a “fight or flight” response to alleviate distress and not facilitate goal directed behaviour.

128px-Amyg

 

Sorry for so much detail. I have read so much about medication recently which does this or that to reduce craving or to control  drinking but what about the underlying conditions of alcoholism and addictive behaviour? These are rarely mentioned or considered at all.

 

We always in recovery have to deal with alcoholism not just it’s symptomatic manifestation of that which is chronic alcohol consumption. This is a relatively simple point and observation that somehow alludes academics, researchers and so-called commentators on this fascinating subject.

Anyway that is some background to this study which demonstrates that long term AA membership can reduce this impulsivity and perhaps adds validity to the above arguments that improved behaviour inhibition and reducing impulsivity is a very possible mechanism of change brought about by AA membership and the 12 step recovery program.

It shows how we can learn about a pathology from the recovery from it!

Indeed when one looks back at one’s step 4 and 5 how many times was this distress based impulsivity the real reason for “stepping on the toes of others” and for their retaliation?

Were we not partly dominated by the world because we could not keep ourselves in check? Didn’t all our decisions get us to AA because they were inherently based on a decision making weakness? Isn’t this why it is always useful to have a sponsor, someone to discuss possible decisions with?

Weren’t we out of control, regardless of alcohol or substance or behaviour addiction? Isn’t this at the heart of our unmanageability?

I think we can all see how we still are effected by a tendency not to think things through and to act rashly.

The trouble it has caused is quite staggeringly really?

Again we cite a study (1) which has Rudolf H. Moos as a co-author. Moos has authored and co-authored a numbered of fine papers on the effectiveness of AA and is a rationale beacon in a sea of sometimes quite controversial and ignorant studies on AA, and alcoholism in general.

“Abstract

Reduced impulsivity is a novel, yet plausible, mechanism of change associated with the salutary effects of Alcoholics Anonymous (AA). Here, we review our work on links between AA attendance and reduced impulsivity using a 16-year prospective study of men and women with alcohol use disorders (AUD) who were initially untreated for their drinking problems. Across the study period, there were significant mean-level decreases in impulsivity, and longer AA duration was associated with reductions in impulsivity…

Among individuals with alcohol use disorders (AUD), Alcoholics Anonymous (AA) is linked to improved functioning across a number of domains [1, 2]. 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 [3]. To our knowledge, however, there have been no efforts to examine links between AA and reductions in impulsivity-a dimension of personality marked by deficits in self-control and self-regulation, and tendencies to take risks and respond to stimuli with minimal forethought.

In this article, we discuss the conceptual rationale for reduced impulsivity as a mechanism of change associated with AA, review our research on links between AA and reduced impulsivity, and discuss potential implications of the findings for future research on AA and, more broadly, interventions for individuals with AUD.

Impulsivity and related traits of disinhibition are core risk factors for AUD [5, 6]. In cross-sectional research, impulsivity is typically higher among individuals in AUD treatment than among those in the general population [7] and, in prospective studies, impulse control deficits tend to predate the onset of drinking problems [8–11]

Although traditionally viewed as static variables, contemporary research has revealed that traits such as impulsivity can change over time [17]. For example, traits related to impulsivity exhibit significant mean- and individual-level decreases over the lifespan [18], as do symptoms of personality disorders that include impulsivity as an essential feature [21, 22]. Moreover, entry into social roles that press for increased responsibility and self-control predict decreases in impulsivity [16, 23, 24]. Hence, individual levels of impulsivity can be modified by systematic changes in one’s life circumstances [25].

Substance use-focused mutual-help groups 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 [26]. 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.

…the idea of reduced impulsivity as a mechanism of change…it is consistent with contemporary definitions of recovery from substance use disorders that emphasize improved citizenship and global health [31], AA’s vision of recovery as a broad transformation of character [32], and efforts to explore individual differences in emotional and behavioral functioning as potential mechanisms of change (e.g., negative affect [33,34]).

Several findings are notable from our research on associations between AA attendance and reduced impulsivity. First, consistent with the idea of impulsivity as a dynamic construct [18, 19], mean-levels of impulsivity decreased significantly in our AUD sample. Second, consistent with the notion that impulsivity can be modified by contextual factors [25], individuals who participated in AA longer tended to show larger decreases in impulsivity across all assessment intervals.

References

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.

Forgiving Others is the Number One Healer!?

“Resentment is the “number one” offender. It destroys more alcoholics than anything else… In dealing with resentments, we set them on paper. We listed people, institutions or principles with whom we were angry… The first thing apparent was that this world and its people were often quite wrong. To conclude that others were wrong was as far as most of us ever got. The usual outcome was that people continued to wrong us and we stayed sore. Sometimes it was remorse and then we were sore at ourselves. But the more we fought and tried to have our own way, the worse matters got…It is plain that a life which includes deep resentment leads only to futility and unhappiness…If we were to live, we had to be free of anger. The grouch and the brainstorm were not for us. They may be the dubious luxury of normal men, but for alcoholics these things are poison…We saw that these resentments must be mastered, but how?… (1)”

Later, p.77, it suggests  “a helpful and forgiving spirit.”

In the 12 Steps and 12  Traditions, p.78, in reference to step 8 it suggests “why shouldn’t we start out by forgiving them, one and all?

These truncated passages from the Big Book (1)  and the 12 and 12 (3) illustrates how resentments cause relapse and that they need to by treated with the antidote of forgiveness.

We suggest also that the myriad of resentments which swirl around our minds in early recovery are also negative emotions unprocessed and thus unregulated from the past. They continually haunt us because we have not put them “to bed” in long term memory.

We have not dealt with them, by clearly identifying, labelling, sharing via verbalising them with others and then by letting go of them via forgiveness. “Letting go” is another emotional regulatory strategy that healthy people use.

res images (42)

Instead of constantly holding on to memories and incidents from the past, endlessly ruminating on them we maturely face up to them and consign them to the past.

We were thus interested in a study which was not using 12 step recovery but which came to the same conclusion but via another route (2).

“Anger and related emotions have been identified as triggers in substance use. Forgiveness therapy (FT) targets anger, anxiety, and depression as foci of treatment. Fourteen patients with substance dependence from a local residential treatment facility were randomly assigned to and completed either 12 approximately twice-weekly sessions of individual FT or 12 approximately twice-weekly sessions of an alternative individual treatment based. Participants who completed FT had significantly more improvement in total and trait anger, depression, total and trait anxiety, self-esteem, forgiveness, and vulnerability to drug use than did the alternative treatment group. Most benefits of FT remained significant at 4-month follow-up.

The levels of anger and violence observed among alcohol and other substance abusers are far higher than the levels found in the general population.

Alcohol and other substance abusers administered the State-Trait Anger Expression Inventory typically have been shown to have higher state and trait anger, to be more likely to express anger to others, and to have less control of their anger.

Reducing levels of anger and its related emotions is now seen as an important feature of recovery programs. For example, according to the Project Match 12-step facilitation therapy manual, “Anger and resentment are pivotal emotions for most recovering alcoholics. Anger that evokes anxiety drives the alcoholic to drink in order to anesthetize it. Resentment, which comes from unexpressed (denied) anger, represents a constant threat to sobriety for the same reason” (Nowinski, Baker, & Carroll, 1999, p. 83).

Marlatt (1985) emphasized the importance of anger and frustration as triggers for relapse in both the intrapersonal and interpersonal domains. He noted that 29% of relapses are related to intrapersonal frustration and anger and that 16% are related to interpersonal conflict and associated anger and frustration.

Litt, Cooney, and Morse (2000) reported that those alcoholics who had urges to use after treatment had higher degrees of alcohol dependence, anxiety, and trait anger than those without such urges.

Forgiveness is an important way to resolve anger and restore hope (Enright & Fitzgibbons, 2000). In helping clients move toward forgiveness, it is essential to differentiate forgiving from condoning, pardoning, reconciling, or forgetting.

Forgiveness is a personal decision to give up resentment and to respond with beneficence toward the person responsible for a severe injustice that caused deep, lasting hurt. FT helps the wronged person examine the injustice, consider forgiveness as an option, make a decision to forgive or not, and learn the skills to forgive.

Findings – Our clients came to the program with trait anxiety and trait anger scores substantially above the published norms for adults; after treatment, however, FT participants exhibited scores comparable to the average.  In other words, the treatment did not lead simply to a change in anxiety and anger (particularly the reportedly more stable trait anxiety) but to a change toward normal profiles. In contrast, patients in the alternative treatment condition had anxiety scores well above average, especially in terms of trait anxiety, which showed little change at post test and only minimal improvement at follow-up.

FT did not focus on drug vulnerabilities, whereas the alternative treatment did. Urges to use substances are not necessary for relapse, they are important indicators.

FT  treatment is centered more on clients’ thoughts, feelings, and behaviors about someone other than themselves: an offender who hurt them deeply and unfairly. In FT, a potential reason for substance use is examined, that of avoiding painful memories of betrayal, violence, or abuse. When patients are allowed to heal, their motivation to abuse substances may be substantially reduced…(it) is worth considering as a way to address core issues of emotional pain.

resentment

 

This can lead to a reduction in negative emotions and increases in self-esteem and forgiveness… it moves to the heart of the matter for some clients. Deep hurts borne out of unfair treatment seem to play a part in substance use and abuse. Even when clients have many people to forgive…we find that they seem to know which person is most crucial to forgive first before moving to other offenders. Substance use, from this perspective, is a symptom of underlying resentments and related emotional disruptions.

If we fail to realize this, we may end up treating only symptoms rather than underlying causes. ”

 

This process seems practically the same as the inventory of Step 4 and the forgiveness implicit to steps 8 and 9. This study also highlights that we through forgiveness we actually tackle the underlying condition of emotional dysregulation. It is this emotion dysregulation (or spiritual disease) which appears to drive addiction so needs to be fundamentally addressed. By addressing these issues via the steps especially step 4 we begin to see how it works!

It was interesting that forgiveness led to higher self esteem, as if being tied to the past was akin to being tied to a former negative self schema, that people from our pained past did actually have the power to control us! Especially how we feel about ourselves. We change how we feel about ourselves and our past by simply forgiving, it is such a powerful tool in recovery.

Importantly by viewing studies like this (2)  we get beyond negative views of 12 step recovery to show that the recovery program’s effectiveness is clearly highlighted by the success of other psychological treatments getting the same positive results by using exactly the same strategies.

12 step groups provide a battery of the most profoundly effective psychological therapies for addiction ever contained within one treatment philosophy.

Don’t we all need to re-appraise how we see 12 step recovery?

Can’t we all benefit from stepping to one side and looking via a different angle to see why 12 step recovery is effective?

 

Reference

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

2. Lin, W. F., Mack, D., Enright, R. D., Krahn, D., & Baskin, T. W. (2004). Effects of forgiveness therapy on anger, mood, and vulnerability to substance use among inpatient substance-dependent clients. Journal of consulting and clinical psychology, 72(6), 1114.

3.   Twelve steps and twelve traditions. (1989). New York, NY: Alcoholics Anonymous World Services

How the Brain Recovers in Abstinence and Recovery

If addiction is characterized by loss of control over the use of substances and behaviour and a severely diminished self control or volitional control over behaviour is recovery the regaining over control over behaviours?

 

This study (1)  looked at the recovery of grey matter (and brain function in cocaine addicts (CD).  This study used a brain imaging technique called voxel based morphometry (VBM) to assess how local grey matter (GM) volume varies with years of drug use and length of abstinence in a cross-sectional study of cocaine users (presently or formerly inpatients or outpatients at treatment centres) with various durations of abstinence (1–102 weeks) and years of use (0.3–24 years).

“Extensive evidence indicates that current and recently abstinent cocaine abusers compared to drug-naïve controls have decreased grey matter in regions such as the anterior cingulate, lateral prefrontal and insular cortex. Relatively little is known, however, about the persistence of these deficits in long-term abstinence despite the implications this has for recovery and relapse.

Lower grey matter volume associated with years of use was observed for several regions including anterior cingulate, inferior frontal gyrus and insular cortex. Conversely, higher grey matter volumes associated with abstinence duration were seen in regions that included the anterior and posterior cingulate, insular, right ventral and left dorsal prefrontal cortex. Grey matter volumes in cocaine dependent individuals crossed those of drug-naïve controls after 35 weeks of abstinence, with greater than normal volumes in users with longer abstinence.

The asymmetry between the regions showing alterations with extended years of use and prolonged abstinence suggest that recovery involves distinct neurobiological processes rather than being a reversal of disease-related changes. Specifically, the results suggest that regions critical to behavioral control may be important to prolonged, successful, abstinence.

Findings suggest a cumulative effect of cocaine use wherein the longer the period of substance use the lower the grey matter volume [22]. That these effects were observed in abstinent users is consistent with prior reports of GM deficits in alcoholism that last from 6–9 months to more than a year or, in some reports, up to at least 6 years following abstinence [42]–[44].

Similarly, decreased GM as a function of years of use of heroin [6], [45], [46] and cocaine [15] have previously been reported. in regions important to emotional regulation…given that emotional reactivity has been implicated as a factor modulating vulnerability to drug abuse [49], this may have been a preexisting factor that served to increase the likelihood of the development and prolongation of drug abuse.

If addiction can be characterized as a loss of self-directed volitional control [22], abstinence and its maintenance may be characterized by a reassertion of these aspects of executive function [24]

Current cocaine users demonstrate reduced GM in brain regions critical to executive function, such as the anterior cingulate, lateral prefrontal, orbitofrontal and insular cortices [6]–[11]. In contrast, the group of abstinent CD users reported here show elevations in GM as a function of abstinence duration that exceeds control levels after 36 weeks, on average, of abstinence. One possible explanation for this is that abstinence may require reassertion of cognitive control and behavior monitoring that is diminished during current cocaine dependence [11], [50], [51].

 

We, and others, have previously hypothesized that drug abusers may develop increased cerebellar activity to compensate for reduced prefrontal activity in tasks demanding elevated levels of cognitive control [52], [53] and that this may play a role in maintaining abstinence [24]. Reassertion of behavioral control may produce a practice-related expansion [54] in GM regions such as the anterior insula, anterior cingulate, cerebellum, and dorsolateral prefrontal cortex and is consistent with our previous reports of elevated activity levels, compared to controls, in long-term abstinent substance users [24], [55].

 

It should be noted that we also observed regions displaying increased GM with abstinence in bilateral cingulate gyri that did not overlap with those showing decreased GM with years of use. This suggests that the brain is capable of compensating in response to changes in demands, such as the maintenance of abstinence [54], [76].”

It would have been interesting to correlate the findings of this type of research with more information on the treatment undertaken, e.g. was it a 12 step facilitation treatment, to assess the nature of this behaviour-based neuro-plasticity. We need more research into translating the elements of “how it works” into the areas of the brain to observe where it works. In other words how do new attitudes and behaviours shape the brain literally. How does the brain recover volume, connectivity, functionality via behavioural change?

The brain areas which regain volume are implicated also in emotion regulation. It is interesting that the authors point to a possibility that the decreased brain volume in certain areas regulating emotion may also be a pre-existing condition, or in other words, a vulnerability to later addiction risk.

It may be that in recovery some of us learn to master or at least attempt to manage and control emotions in a way we could not previously.

For us this is an essential part of the pathomechanism of addictive  behaviours,  this emotion processing and regulation deficit; a deficit we learn to overcome in recovery. An unmanageability that we learn to manage in recovery.

In our next blog we will look at how these emotional factors drive the addiction cycle to it’s chronic endpoint.

We will look at how emotional dysregulation around forgiveness has contributed to a need to continually distance ourselves chemically from the incidents that needed our forgiveness. It will also look at how forgiveness itself is a emotional regulation strategy in itself, just like “letting go” is. We learn so many emotion regulation strategies in recovery and these appear essential to long term recovery.

References

1. Connolly, C. G., Bell, R. P., Foxe, J. J., & Garavan, H. (2013). Dissociated Grey Matter Changes with Prolonged Addiction and Extended Abstinence in Cocaine Users. PLoS ONE, 8(3), e59645. doi:10.1371/journal.pone.0059645

 

 

What recovers in Recovery? – Cognitive Control over emotions?

 In recent blogs we have called for an increase in research into the neurobiology of recovery to add to the extensive research already published on the neurobiology of the addiction cycle.
There has been extensive research into the neurobiology of addiction, most of this has focused on reward and motivation networks of the brain.  In effect this suggests there is a pathological wanting in addicts, an excessive motivation towards drug taking over all other rewarding activities.
This view does not fully consider that this pathological wanting is in itself a product of dysregulated stress systems in the brain, many the product of neglect, abuse and maltreatment in childhood. These stress factors are also reflective of the role of emotional distress in the addiction cycle . This distress is we feel a product of the emotion processing and regulation deficits commonly seen in all addictive behaviours such as alcohol and substance addiction, eating and gambling disorders and sex addiction etc (and often reflective of childhood maltreatment).
In fact , this emotion processing and  regulation deficit is also apparent in certain children of alcoholics and may be a vulnerability to later alcoholism as these children demonstrate a deficit in impulsivity (common to alcoholics and addicts) and a decision making profile based on choosing now over later (short term gains based) and which recruits more subcortical and motor expressive (compulsive) parts of the brain rather than cortical and reflective/evaluative parts of the brain.
This means they make decisions to alleviate the distress of decisions (as undifferentiated emotions appear to be distressing) not via evaluative processes). This has obvious consequence for decision making over a life span.
This emotion dysregulation is also seen in active addicts and alcoholics and at the endpoint of addiction there is a fairly complete reliance of this compulsive decision making profile, which begs the question, does the decision making deficits seen in at risk children simply get worse in the addiction cycle via the neuro toxic effects of substance abuse?
This emotion (and stress) dysregulation also potentiates reward (makes things more rewarding) so alcohol is seen as more stimulating than for non risk children. This vulnerability may lead to the need  to regulate, especially negative, emotions ( and low self esteem ) via the stimulating and highly rewarding effects of alcohol make perpetuate the addiction cycle to it’s chronic endpoint where chronic emotional distress acts as a compulsive stimulus to the responding of chronic alcohol and drug use.
This emotion dysregulation also seems to play a huge part in relapse – so it begs the question does this emotion regulation improve in time via recovery, particularly long term recovery?
In the next two blogs we look at how the emotion regulation areas of the brain become reinforced, strengthened by the process of recovery or in other words we appear to develop the brain capacity for controlling and regulating our emotions more adaptively and this reduces the stress/distress which often prompts relapse.
Personally, I can wholeheartedly say, that the one main aspect I have developed in my recovery has been the awareness and skills in regulating/controlling emotions. Via recovery I have learnt to identify, label, describe by verbalising and sharing with others how I feel. This processes and regulates the emotions that used to cause me so much distress.
I have also developed a more acute awareness of the the emotional expression and needs of yours. These were previously aspects of my life which were completely lacking and frustrating/confusing as a result.
By emotionally engaging in with the world, by becoming more emotionally literate, I can converse with the world in a way that was previously beyond my capabilities.
The research we look at in the next two blogs asks the question – is cognitive control over emotions, lacking in active addiction, one of the main brain functions that improve in recovery?
A core aspect of alcohol dependence is poor regulation of behavior and emotion.
Alcohol dependent individuals show an inability to manage the appropriate experience and expression of emotion (e.g., extremes in emotional responsiveness to social situations, negative affect, mood swings) (1,2). Dysfunctional emotion regulation has been considered a primary trigger for relapse (1,3) and has been associated with prefrontal dysfunction.
While current alcohol dependence is associated with exaggerated bottom-up (sub-cortical) and compromised top-down (prefrontal cortex) neural network functioning, there is evidence suggesting that abstinent individuals may have overcome these dysfunctional patterns of network functioning (4) .
Neuro-imaging studies showing chronic alcohol abuse to be associated with stress neuroadaptations in the medial prefrontal and anterior cingulate regions of the brain (5 ), which are strongly implicated in the self-regulation of emotion and behavioral self-control (6).
One study (2) looking at how emotional dysregulation related to relapse, showed compared with social drinkers, alcohol-dependent patients reported significant differences in emotional awareness and impulse control during week 1 of treatment. Significant improvements in awareness and clarity of emotion were observed following 5 weeks of protracted abstinence.
Another study (7) which did not look specifically at emotional regulation but rather on the recovering of prefrontal areas of the brain known to be involved also in the inhibition of  impulsive behaviour and emotional regulation showed that differences between the short- and long-abstinence groups in the patterns of functional recruitment suggest different cognitive control demands at different stages in abstinence.

In one study, the long-term abstinent group (n=9) had not consumed cocaine for on average 69 weeks, the short-term abstinent (SA) group (n=9) had an average 0f 2.4 weeks.

Relative to controls, abstinent cocaine abusers have been shown to have reduced metabolism in left anterior cingulate cortex (ACC) and right dorsolateral prefrontal cortex (DLPFC), and greater activation in right ACC.
In this study  the abstinent groups of cocaine addicts showed more elevated activity in the DLPFC ; a finding that has also been observed in abstinent marijuana users (8).
The elevation of frontal activity also appears to undergo a shift from the left to right hemisphere over the course of abstinence.  The right is used more in processing (labelling/identifying) of emotion.
Furthermore, the left inferior frontal gyrus (IFG) has recently been shown to be important for response inhibition (9) and in a task similar to that described here, older adults have been shown to rely more on left PFC (10). Activity observed in these regions is therefore likely to be response inhibition related.
The reliance of the SA group on this region suggests that early in abstinence users may adopt an alternative cognitive strategy in that they may recruit the LIFG in a manner akin to children and older adults to achieve behavioral results similar to the other groups.
In longer,  prolonged abstinence a pattern topographically typical of normal, healthy controls may emerge.
In short-term abstinence there was an increased inhibition-related dorsolateral and inferior frontal activity indicative of the need for increased inhibitory control over behaviour,  while long-term abstinence showed increased error-related ACC activity indicative of heightened behavioral monitoring.
The results suggest that the improvements in prefrontal systems that underlie cognitive control functions may be an important characteristic of successful long-term abstinence.
Another study (11) noted the loss of grey matter in alcoholism that last from 6–9 months to more than a year or, in some reports, up to at least 6 years following abstinence (12 -14).
It has been suggested cocaine abuse blunts responses in regions important to emotional regulation (15)
Given that emotional reactivity has been implicated as a factor in vulnerability to drug abuse (16)  this may be a preexisting factor that  increased the likelihood of the development and prolonging of drug abuse
If addiction can be characterized as a loss of self-directed volitional control (17),  then abstinence (recovery) and its maintenance may be characterized by a reassertion of these aspects of executive function (18)  as cocaine use has been shown to reduce grey matter in brain regions critical to executive function, such as the anterior cingulate, lateral prefrontal, orbitofrontal and insular cortices (19-24) .
The group of abstinent cocaine addicts (11) reported here show elevations in  (increased) grey matter in abstinence exceeded those of the healthy control in this study after 36 weeks, on average, of abstinence .
One possible explanation for this is that abstinence may require reassertion of cognitive control and behavior monitoring that is diminished during current cocaine dependence.
Reassertion of behavioral control may produce a expansion (25)  in grey matter  in regions such as the anterior insula, anterior cingulate, cerebellum, and dorsolateral prefrontal cortex .
All brain regions implicated in the processing and regulating of emotion. 
References
1. Berking M, Margraf M, Ebert D, Wupperman P, Hofmann SG, Junghanns K. Deficits in emotion-regulation skills predict alcohol use during and after cognitive-behavioral therapy for alcohol dependence. J Consult Clin Psychol. 2011;79:307–318.
2.  Fox HC, Hong KA, Sinha R. Difficulties in emotion regulation and impulse control in recently abstinent alcoholics compared with social drinkers. Alcohol Clin Exp Res. 2008;33:388–394.
3..Cooper ML, Frone MR, Russell M, Mudar P. Drinking to regulate positive and negative emotions: A motivational model of alcohol use. J Pers Soc Psychol. 1995;69:990
4. Camchong, J., Stenger, A., & Fein, G. (2013). Resting‐State Synchrony in Long‐Term Abstinent Alcoholics. Alcoholism: Clinical and Experimental Research, 37(1), 75-85.
5. Sinha, R., & Li, C. S. (2007). Imaging stress- and cue-induced drug and alcohol craving: Association with relapse and clinical
implications. Drug and Alcohol Review, 26(1), 25−31.
6. Beauregard, M., Lévesque, J., & Bourgouin, P. (2001). Neural correlates of conscious self-regulation of emotion. Journal of
Neuroscience, 21(18), RC165
7. Connolly, C. G., Foxe, J. J., Nierenberg, J., Shpaner, M., & Garavan, H. (2012). The neurobiology of cognitive control in successful cocaine abstinence. Drug and alcohol dependence, 121(1), 45-53.
8.  Tapert SF, Schweinsburg AD, Drummond SP, Paulus MP, Brown SA, Yang TT, Frank LR. Functional MRI of inhibitory processing in abstinent adolescent marijuana users.Psychopharmacology (Berl.) 2007;194:173–183.[PMC free article]
9. Swick D, Ashley V, Turken AU. Left inferior frontal gyrus is critical for response inhibition. BMC Neurosci. 2008;9:102.[PMC free article]
10. Garavan H, Hester R, Murphy K, Fassbender C, Kelly C. Individual differences in the functional neuroanatomy of inhibitory control. Brain Res. 2006;1105:130–142
11. Connolly, C. G., Bell, R. P., Foxe, J. J., & Garavan, H. (2013). Dissociated grey matter changes with prolonged addiction and extended abstinence in cocaine users. PloS one, 8(3), e59645.
12. Chanraud S, Pitel A-L, Rohlfing T, Pfefferbaum A, Sullivan EV (2010) Dual Tasking and Working Memory in Alcoholism: Relation to Frontocerebellar Circuitry. Neuropsychopharmacol 35: 1868–1878 doi:10.1038/npp.2010.56.
13.  Wobrock T, Falkai P, Schneider-Axmann T, Frommann N, Woelwer W, et al. (2009) Effects of abstinence on brain morphology in alcoholism. Eur Arch Psy Clin N 259: 143–150 doi:10.1007/s00406-008-0846-3.
14.  Makris N, Oscar-Berman M, Jaffin SK, Hodge SM, Kennedy DN, et al. (2008) Decreased volume of the brain reward system in alcoholism. Biol Psychiatry 64: 192–202 doi:10.1016/j.biopsych.2008.01.018.
15, Bolla K, Ernst M, Kiehl K, Mouratidis M, Eldreth D, et al. (2004) Prefrontal cortical dysfunction in abstinent cocaine abusers. J Neuropsychiatry Clin Neurosci 16: 456–464 doi:10.1176/appi.neuropsych.16.4.456.
16.  Piazza PV, Maccari S, Deminière JM, Le Moal M, Mormède P, et al. (1991) Corticosterone levels determine individual vulnerability to amphetamine self-administration. Proc Natl Acad Sci USA 88: 2088–2092. doi: 10.1073/pnas.88.6.2088
17.  Goldstein RZ, Volkow ND (2002) Drug addiction and its underlying neurobiological basis: neuroimaging evidence for the involvement of the frontal cortex. Am J Psychiatry 159: 1642–1652. doi: 10.1176/appi.ajp.159.10.1642
18. Connolly CG, Foxe JJ, Nierenberg J, Shpaner M, Garavan H (2012) The neurobiology of cognitive control in successful cocaine abstinence. Drug Alcohol Depend 121: 45–53 doi:10.1016/j.drugalcdep.2011.08.007.
19.  Liu X, Matochik JA, Cadet JL, London ED (1998) Smaller volume of prefrontal lobe in polysubstance abusers: a magnetic resonance imaging study. Neuropsychopharmacol 18: 243–252 doi:10.1016/S0893-133X(97)00143-7.
20.  Bartzokis G, Beckson M, Lu P, Nuechterlein K, Edwards N, et al. (2001) Age-related changes in frontal and temporal lobe volumes in men – A magnetic resonance imaging study. Arch Gen Psychiatry 58: 461–465. doi: 10.1001/archpsyc.58.5.461
21. Franklin TR, Acton PD, Maldjian JA, Gray JD, Croft JR, et al. (2002) Decreased gray matter concentration in the insular, orbitofrontal, cingulate, and temporal cortices of cocaine patients. Biol Psychiatry 51: 134–142. doi: 10.1016/s0006-3223(01)01269-0
22.  Matochik JA, London ED, Eldreth DA, Cadet J-L, Bolla KI (2003) Frontal cortical tissue composition in abstinent cocaine abusers: a magnetic resonance imaging study. NeuroImage 19: 1095–1102. doi: 10.1016/s1053-8119(03)00244-1
23.  Lim KO, Wozniak JR, Mueller BA, Franc DT, Specker SM, et al. (2008) Brain macrostructural and microstructural abnormalities in cocaine dependence. Drug Alcohol Depend 92: 164–172 doi:10.1016/j.drugalcdep.2007.07.019.
24.  Ersche KD, Barnes A, Jones PS, Morein-Zamir S, Robbins TW, et al. (2011) Abnormal structure of frontostriatal brain systems is associated with aspects of impulsivity and compulsivity in cocaine dependence. Brain 134: 2013–2024 doi:10.1093/brain/awr138.
25.  Ilg R, Wohlschlaeger AM, Gaser C, Liebau Y, Dauner R, et al. (2008) Gray matter increase induced by practice correlates with task-specific activation: A combined functional and morphometric magnetic resonance Imaging study. J Neurosci 28: 4210–4215 doi:10.1523/JNEUROSCI.5722-07.2008.

Insecure attachment affects emotion regulation in alcoholics?

I have blogged recently about how insecure attachment is linked to various addictive behaviours.

What is important is to establish a mechanism by which insecure attachment contributes to later addictive disorders. It may not be enough to say attachment and addiction are linked but that they are linked via a pathomechanism of some sort.

I have argued many times before that I believe this pathomechanism, the mechanism by which a pathological condition occurs, or the mechanism that  drives a disease state (or disorder) is emotion processing and regulation deficits.

We look here (1) at a study that demonstrates how insecure attachment correlates in alcoholics with difficulties in emotion processing and regulation difficulties. I believe this is how addiction is driven to it’s endpoint of chronic, compulsive behaviour, although this study is only a correlational study and makes no such claims about causation.

“Attachment theory has been conceptualised as an affect regulation theory, proposing that attachment is associated with the expression and recognition of emotions as well as interpersonal functioning… the objective of the present study was to investigate potential associations between attachment, Negative Mood Regulation (NMR) expectancies, fear of intimacy and self-differentiation…(with)  findings support broad attachment theory suggesting that attachment is associated with and predicts affect regulation abilities, difficulties with intimacy and intrapersonal as well as interpersonal functioning in a sample of substance use disorder inpatients.

Attachment is associated with the expression and regulation of emotion. Early attachment theory postulates that early bonding
with a significant caregiver is essential for the development of internal working models for communication, regulation of emotions and interpersonal behaviour.

These early attachment experiences are associated with adult attachment styles. Adult attachment styles are relatively stable and influence attitudes, emotions, affect regulation and behavioural strategies in relationships…Empirical evidence has indicated associations between insecure attachment, fear of intimacy and
emotion regulation difficulties  and between secure attachment
and a higher capacity for intimacy, emotional awareness and empathy.

Substance abuse has been proposed to be a consequence of emotion regulation difficulties with individuals using alcohol/drugs to avoid
intimacy or rejection, to ease pain, anger and ambivalence and possibly establish a “secure base”.

Negative mood regulation (NMR) expectancies are beliefs regarding a person’s ability to terminate or alleviate a negative mood state.

High NMR presumably reflects the ability to cope successfully with bad moods, whereas having low NMR may lead to less efficacious or maladaptive ways of coping… high NMR may be associated with secure attachment, as securely attached individuals tend to seek comfort from others when emotionally upset, and utilise constructive coping mechanisms to decrease the intensity of distress.

By contrast, low NMR may potentially be associated with anxious attachment as well as substance abuse...insecure attachment is a fearful attachment style characterised by a fear of intimacy and rejection, high emotional reactivity and a self-belief associated with being deserving of rejection. Some have argued that fear of intimacy (FIS) is associated with mental health issues and substance use problems…FIS research to date has largely reported significant associations with loneliness, lack of self-disclosure, low social interaction and low relationship quality.

Differentiation of self is defined as the degree to which an individual is able to balance emotional and intellectual functioning, intimacy and autonomy in relationships…Individuals with lower
self-differentiation experience higher levels of chronic anxiety, emotion regulation difficulties, mood disturbances and substance abuse.

In addition, previous studies have reported higher levels of mood regulation and interpersonal difficulties in substance abusers compared to controls…(As) attachment has been hypothesised to be associated with relationship functioning and mood regulation (and)  addiction has been proposed to be an attachment disorder,  potential relationships of attachment with mood regulation and interpersonal functioning in substance abusers may
potentially inform the development of future treatment approaches.

The results (of this study) indicated a significant negative association between anxious attachment and NMR…suggesting that anxious attachment may be associated with lower abilities to regulate one’s negative moods. This is in accordance with other research evidence suggesting that insecurely attached individuals tend to show poor affect regulation.

The present investigation also found that attachment was a strong predictor of FIS (and)  the present results suggest that adult
attachment is related to difficulties in intimacy and interpersonal functioning, in accordance with previous evidence that reported a significant association between insecure attachment and relationship problems as well as lower levels of trust, interdependence and commitment.

The present investigation also found that anxious attachment significantly predicted emotional reactivity (ER).

These data support the predictive power of anxious attachment in relation to being more emotionally reactive, having difficulties with emotion regulation and maladjustment in those with substance dependence…The predictive utility of attachment was also related to Emotional cut-off (EC)…This is in line with previous research suggesting a link between attachment and EC  in those with substance abuse and implies that attachment style is related to traits of emotional aloofness, anxiety, isolation from others and exaggerated independence…EC may be associated with, or a consequence of alexithymia, a personality trait associated with difficulties in identifying and describing feelings.”

The above sounds so familiar, doesn’t it? Sounds like most newcomers to recovery that I have ever come cross, including me.

Reference

1.  Thorberg, F. A., & Lyvers, M. (2009). Attachment in relation to affect regulation and interpersonal functioning among substance use disorder in patients.Addiction Research & Theory, 18(4), 464-478.

 

 

 

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!

 

 References

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.

 

lieberman_affect_labelling_scan_small

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.

 

images (23)

 

 

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

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

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

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

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

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

 

References

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

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

 

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

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

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

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

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

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

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

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

 

Thoughtful little girl

 

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

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

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

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

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

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

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

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

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

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

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

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

 

References

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