emotion regulation

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.

Christianity_Jesus_meditating_golden_light

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.

 

 

 

The Heart of Recovery

How is low HRV related to longer term recovering alcoholics?

We cited and use excerpts from a study (2) into short term and longer term (3) of up to six months which shows that alcoholics with years of recovery still have low HRV although it improves although this is dependent of severity of the alcoholism.

“It is known that chronic and heavy alcohol use has a toxic effect on the nervous system,[2] including effects on autonomic nervous system.[3] Specifically, heavy alcohol use can cause cardiac autonomic neuropathy,[4] which in turn, is associated with greater mortality.

Resting cardiac autonomic function reportedly favors energy conservation by way of parasympathetic dominance over sympathetic influence. Heart rate is characterized by beat-to-beat variability over a wide range, which has been reported to indicate vagal dominance and thereby parasympathetic dominance.[5]

In those with alcohol dependence, HRV is lower than in healthy individuals even after several days of abstinence.[13,14] This decrement may improve with abstinence for long periods of time.[15,16]

A study of 24-h ambulatory HRV found significantly reduced HRV in alcohol-dependent men with established vagal neuropathy and in some without.[17] Alcohol dependence has been shown to compromise vagal output measured before sleep onset, which correlates with loss of delta sleep and morning sleep impairments.[18]

Reduced HRV was found in alcohol-dependent patients with negative mood states and compulsive drinking.[19] Rechlin et al.,[20] reported reductions in HRV in patients with alcohol dependence, and this has been consistently reported in subsequent studies.[21,22]”

 

“Heart rate variability (HRV) was studied in 11 chronic alcoholic subjects, 1–30 days after the beginning of abstinence and again 5, 12 and 24 weeks later. Two patients could be re-examined after 19 and 22 months, respectively. In the follow-up study, the total patient group showed a statistically significant increase in HRV with prolonged abstinence of at least 6 months.

No recovery of efferent vagal function was found in 4 patients. It is suggested that the vagal neuropathy may improve in chronic alcoholics, but perhaps only in patients with a short to moderately long duration of drinking history (3)”.

Thus it seems thee is a partial recovery in HRV as recovery proceeds although there may be work required depending on severity of one’s alcoholism.

In our next blog on HRV we will cite and use excerpts from one of the best articles authored by Thayer which is the best explanation of how low HRV keeps an alcoholics attention “locked in” to stuff he/she would rather it didn’t get locked into such as alcohol-related cues.

References

1. THAYER, J. F., AHS, F., FREDRIKSON, M., SOLLERS, J. J., & WAGER, T. D. (2012). A meta-analysis of heart rate variability and neuroimaging studies: Implications for heart rate variability as a marker of stress and health.Neuroscience and biobehavioral reviews, 36(2), 747-756.

2. Ganesha, S., Thirthalli, J., Muralidharan, K., Benegal, V., & Gangadhar, B. N. (2013). Heart rate variability during sleep in detoxified alcohol-dependent males: A comparison with healthy controls. Indian journal of psychiatry, 55(2), 173.

3. Weise, F., Müller, D., Krell, D., Kielstein, V., & Koch, R. D. (1986). Heart rate variability in chronic alcoholics: a follow-up study. Drug and alcohol dependence, 17(4), 365-368.

Recovery is a Journey from the Head to the Heart (and back)!

PART 2 

So what does this low HRV mean for the recovering alcoholic?

I have explained this to show that HRV is directly connected to areas of the the brain implicated in stress and emotion regulation.

If, via recovery practices, we can still our beating heart, become serene as well as clean, it will have neuroplastic effects on our brain and the regulation of emotion and stress.

Equally if we meditate and alter the functioning of areas implicated in this study such as areas of the medial PFC and cingulate gyrus we improve our control over our heart. Ultimately if we can learn to relieve the inherent distress at the heart of addiction we can recovery function of not only the heart but also of areas in the brain which interact with the heart in producing heart rate variability.

So ultimately we need only to know how to quell a distressed heart via prayer, meditation, loving others.

If we can do so, we improve our emotion and stress regulation.

But do we need to do this if we have been in recovery long term?

Let me give you an example of allostasis in action.

In an allostatic system like addiction there is stress dysregulation coupled with reward dysfunction (I believe there is a pre-morbid allostasis in those addicts who have experienced abuse, trauma and insecure attachment also which means there is a stress and emotion dysregulation from an early age which leads to a heightened reward sensitivity which means we start to regulate negative emotions from an early age via impulsively  using or consuming stuff we really really like, or seem to like more than healthy people, to make ourselves feel better).

These adolescents at risk also have low HRV and the effects of alcohol have a pronounced effect on HRV.

This sets the chain of addiction in action from the start for many addicts.

So when we decide we want something this leads to a feeling of pathological wanting and then needing simply because we have altered reward systems as they are linked to our “out of kilter” stress systems .

Buying something in the store, if thwarted, soon becomes a life and death like struggle. Ever had that feeling?

I remember a 75 year old recovering person with 30 odd years of recovery  sharing in a meeting how she went to a store to get something, to find that something wasn’t there, so she was instructed to drive somewhere else to get that something, and when she got there they didn’t have it, so she had an argument with them and then with her husband in the car, then off to another store which did not have the something either, then back home on the internet, found a online store that stocked the something and ordered it.

It arrived the next day because she paid a lot of money for it to arrive the very next day! When it arrived she found that she had not only completely forgot about ordering the something but did not really want the something even. So off she sloped to apologise to her husband for being so emotionally abusive and immature over the something on her way to the Post Office to post back the something that she never really wanted in the first place!!?

This is also my head still, even after a few years of recovery. It is not as bad it was, by a long shot! It does, however, get distressed, I become impulsive and  want, need, that thing now!!! On occasion.

So I think this is one area recovery people always need to be aware of. Wanting stuff.

As it can lead to pathological wanting fairly quickly – then people get in the way of those things and we get angry, frustrated, distressed, our emotions overwhelm us or we are mean to our fellow human beings all because they are getting in the way of the thing I really really want.. NEED God damn it!…

We lose our emotional sobriety.

When we have either got it, regardless of the the human or emotional cost, we often find we do not want it or never really wanted it…that much….

Not compared to the cost of getting it!?

How do we solve this problem? We let go, we calm down, talk to someone, express our feelings, try to establish a transient homeostasis, let our stress systems subside and start again, trying to managing these chaotic brain systems.

Amends time.

If you are like that you have a low HRV and a stress/emotion regulation problem and probably always will.

But if can be manged and it can vastly improve. Then one day we learn that it is in living with our hearts forefront to our decisions and not our heads that brings lasting everyday happiness.

That is why in recovery we travel from our at times over zealous heads to our hearts. The wisdom and direction and basis of our decision making lives their not in our heads. It is not to say we do not use these wondrous instruments but we incorporate the help of our hearts in activating the reasoning of the brain.

Solve the heart issue, and the rest comes.

 

Neural structures associated with HRV

Over the past several years however a number of human neuroimaging studies have appeared in which researchers have explicitly examined the brain structures associated with HRV. In the present paper we provide a meta-analysis of eight published studies in which HRV has been related to functional brain activity using either PET or fMRI

The goal of this meta-analysis was to identify areas that were consistently associated with HRV.

In the overall analyses three regions show significant activations One region in the medial PFC (MPFC) is the right pregenual cingulate (BA 24/32).

Brodmann Cytoarchitectonics 24.pngBrodmann Cytoarchitectonics 32.png

 

Another MPFC region is the right subgenual cingulate (BA 25).

Brodmann Cytoarchitectonics 25.png

The third region is the left sublenticular extended amygdala/ventral striatum (SLEA). This region extends into the basolateral amygdalar complex, and also covers the superior amygdala (central nucleus) and extends into the ventral striatum.

 

 

More generally, the pgACC/rmPFC correlation with HRV in our meta-analysis suggests thatthis region is part, and the most reliably activated part in studies to date, of a descending “visceromotor” system that controls the autonomic nervous system and possibly other responses (neuroendocrine) based on emotional context.

The meta-analysis provides supportfor the idea that HRV may index the degree to which a mPFC-guided “core integration” system is integrated with the brainstem nuclei that directly regulate the heart. Thus these results support Claude Bernard’s idea that the vagus serves as a structural and functional link between the brain and the heart. We have proposed that this neural system essentially operates as a “super-system” that integrates the activity in perceptual, motor, interoceptive, and memory systems into gestalt representations of situations and likely adaptive responses. These findings suggest that HRV may index important organism functions associated with adaptability and health.”

References

1. THAYER, J. F., AHS, F., FREDRIKSON, M., SOLLERS, J. J., & WAGER, T. D. (2012). A meta-analysis of heart rate variability and neuroimaging studies: Implications for heart rate variability as a marker of stress and health.Neuroscience and biobehavioral reviews, 36(2), 747-756.

Journey from the Head to the Heart (and back)!

Part 1

Over this week leading up to my interview/podcast with sincerightnow http://www.sincerightnow.com/upcoming/ http://www.sincerightnow.com/pdcst/

I want to look at the “neuroscience of alcoholism and addiction from another angle. I want to look at the evident difficulties seen in alcoholics in terms of impaired self and emotion regulation by looking at the relationship of the heart to the brain.

Some may find this a more clear, easier way to understand what is impaired in terms of brain functioning in alcoholics. I know I do and looking at the role of the heart in alcoholism has helped me understand the issues more clearly. I hope it does for you too.

I will seek to explain how the emotional, stress and thus self dysregulation seen in alcoholics and addicts is indexed or can be seen clearly in terms of a reduced heart rate variability  compared to normal healthy individuals.

I will explain as we go, how low HRV is linked to this dysregulation gives rise to a stress and emotion reactivity and an impulsivity seen commonly in alcoholics in particular.

This low HRV has a interactive effect in the emotion regulation  parts of the brain also with one effecting the other. So in terms of say reducing distress, stress and thus craving, for example, we could suggest instead use measures to improve low HRV such as mediation and so on. If we get the heart under more control, the neurotransmission of the brain and stress chemicals too seem also to be affected.

It certainly ties in with treatment regimes which advocate strategies of letting go of distress and maintaining balance and serenity.

Personally I find it fascinating how the heart can affect the workings of the brain.

Before we look at the concept of heart rate variability in relation to alcoholism we need to first to look at the interaction between the head and the heart.

We cite and use excerpts from a review (1) by Julian Thayer, one of the leading experts on the subject of heart rate variability (HRV) and it’s relationship to impaired self and emotion regulation.

“The intimate connection between the brain and the heart was enunciated by Claude Bernard over 150 years ago.

Heart rate variability may provide an index of how strongly ‘top–down’ appraisals, mediated by cortical-subcortical pathways, shape brainstem activity and autonomic responses in the body.

Thus, HRV may serve as a proxy for ‘vertical integration’ of the brain mechanisms that guide flexible control over behavior.

We have proposed that a core set of neural structures provides an organism with the ability to integrate signals from inside and outside the body and adaptively regulate cognition,perception, action, and physiology.

This system essentially operates as a “super-system” that integrates the activity in perceptual, motor, interoceptive, and memory systems into gestalt representations of situations and likely adaptive responses. Thus, it is undoubtedly extremely complex. However, it is still possible that physiological measures exist that can serve as indices ofthe degree to which this system provides flexible, adaptive regulation of its component systems. In a number of papers (Thayer and Brosschot, 2005; Thayer and Lane, 2000, 2009), we have proposed that heart rate variability (HRV) may provide just such an index.

However if component systems are become unbalanced, and a particular process can come to dominate the system’s behavior, rendering it unresponsive to the normal range of inputs. In the context of physiological regulation, and regulation of the heart specifically, a balanced system is healthy, because the system can respond to physical and environmental demands (Thayer and Sternberg, 2006). A system that is “locked in” to a particular pattern is dysregulated. This is why the heart rate of a healthy heart oscillates spontaneously (i.e., shows high HRV), whereas a diseased heart shows almost no variability under certain conditions. A critical idea is that HRV may be more than just an index of healthy heart function, and may in fact provide an index of the degree to which the brain’s “integrative” system for adaptive regulation provides flexible control over the periphery. Thus, HRV may serve as an easily measured output of this neural network that may provide valuable information about the capacity of the organism to effectively function in a complex environment.

 

Hear Rate Variability

Like many organs in the body, the heart is dually innervated. Although a wide range of physiologic factors determine cardiac functions such as heart rate (HR), the autonomic nervous system (ANS) is the most prominent with Although a wide range of physiologic factors determine cardiac functions such as heart rate (HR), the autonomic nervous system (ANS) is the most prominentwith  both cardiac vagal (the primary parasympathetic nerve) and sympathetic inputs.

 

 

The heart is under tonic inhibitory control by parasympathetic influences. Thus, resting cardiac autonomic balance favors energy conservation by way of parasympathetic dominance over sympathetic influences. In addition, the HR time series is characterized by beat-to-beat variability over a wide range, which also implicates vagal dominance as the sympathetic influence on the heart is too slow to produce beat to beat changes.

Low heart rate variability (HRV) is associated with increased risk of all-cause mortality, and low HRV has been proposed as a marker for disease (Thayer and Lane, 2007; Thayer et al., 2010b). The basic data for the calculation of all the measures of HRV is the sequence of time intervals between heart beats. This interbeat interval time series is used to calculate the variability in the timing of the heart beat. As mentioned earlier the heart is dually innervated by the autonomic nervous system such that relative increases in sympathetic activity are associated with heart rate increases and relative increases in parasympathetic activity are associated with heart rate decreases.

Thus relative sympathetic increases cause the time between heart beats (the interbeat interval) to become shorter and relative parasympathetic increases cause the interbeat interval to become longer.

The differential effects of the ANS on…s the timing of the heart beats, are due to the differential effects of the neurotransmitters for the sympathetic (norepinephrine) and parasympathetic (acetylcholine) nervous systems. The sympathetic effects are slow, on the time scale of seconds, whereas the parasympathetic effects are fast, on the time scale of milliseconds. Therefore the parasympathetic influences are the only ones capable of producing rapid changes in the beat to beat timing of the heart.

In summary, the heart and the brain are connected bidirectionally. Efferent outflow from the brain affects the heart and afferent outflow from the heart affects the brain. Importantly, the vagus is an integral part of this heart–brain system and vagally mediated HRV appears to be capable of providing valuable information about the functioning of this system.

 

HRV and emotional regulation In addition to being linked to vmPFC and amygdala modulation, emotion regulation is linked to HRV (Appelhans and Luecken, 2006; Thayer and Brosschot, 2005). Individuals with greater emotion regulation ability have been shown to have greater levels of restingHRV(Appelhans andLuecken,2006; Thayer andLane,2009). In addition, during successful performance on emotion regulation tasks HRV appears to be increased (Butler et al., 2006; Ingjaldsson et al., 2003; Smith et al., 2011).

We have investigated the role of HRV in emotional regulation attwo differentlevels of analysis. One level is at the trait or tonic level where individual differences in resting HRV have been associated with differences in emotional regulation. We have shown that individuals with higher levels of resting HRV, compared to those with lower resting levels, produce context appropriate emotional responses as indexed by emotion-modulated startle responses, fear-potentiated startle responses, and phasic heart rate responses in addition to behavioral and self-reported emotional responses (Melzig et al., 2009; Ruiz-Padial et al., 2003; Thayer and Brosschot, 2005). In addition, we have recently shown that individuals with low resting HRV show delayed recovery from psychological stressors of cardiovascular, endocrine, and immune responses compared to those with higher levels of resting HRV (Weber et al., 2010). Thus, individuals with higher resting levels of HRV appear more able to produce context appropriate responses including appropriate recovery after the stressor has ended.

Another level of analysis is at the state or phasic level where HRV values increase during the successful regulation of emotion during emotion regulation tasks. Thus, it has been shown that phasic increases in HRV in response to situations that require emotional regulation facilitate effective emotional regulation. In an early study, we showed that HRV increased in recovering alcoholics in response to alcohol cues but only if they later reported an increased ability to resist a drink. Those recovering alcoholics that later reported an urge to drink did not exhibit increased HRV during the alcohol cues (Ingjaldsson et al., 2003). A recent replication and extension of this work reported increased HRV during the successful regulation of emotion by either reappraisal or suppression (Butler et al., 2006). We have recently shown that the increase in HRV associated with emotional regulation is accompanied by concomitant cerebral blood flow changes in areas identified as being important in emotional regulation and inhibitory processes (Lane et al., 2009).

, the amygdala, which has outputs to autonomic, endocrine, and other physiological regulation systems, and becomes active during threat and uncertainty, is under tonic inhibitory control via GABAergic mediated projections from the prefrontal cortex (Davidson, 2000; Thayer, 2006).

. Thayer and Lane (2000) suggested that a common reciprocal inhibitory cortico-subcortical neural circuit serves as the structural link between psychological processes like emotion and cognition, and health-related physiological processes, and that this circuit can be indexed with HRV. Thus, because of these reciprocally interconnected neural structures that allow prefrontal cortex to exert an inhibitory influence on sub-cortical structures, the organism is able to respond to demands from the environment, and organize their behavior effectively. In the next section we briefly review the evidence for the relationship of HRV to this network of neural structures and further specify the prefrontal regions involved in the inhibitory control of the heart.

 

TBC

References

1. Thayer, J. F., Åhs, F., Fredrikson, M., Sollers, J. J., & Wager, T. D. (2012). A meta-analysis of heart rate variability and neuroimaging studies: implications for heart rate variability as a marker of stress and health. Neuroscience & Biobehavioral Reviews, 36(2), 747-756.

 

 

 

 

 

 

 

 

 

 

 

 

Are There Two Types of Alcoholic

In this three part blog we sill start to look more closely at the genetics of alcoholism, a subject area slightly neglected so far on this blog site.

I have often sat in the rooms of AA and wondered if there are different types of alcoholics. One old timer once said to me there were as many types of alcoholism as there are alcoholics but I disagree with this observation.

I do think there are certain types. In fact the “Doctor’s Opinion” in the Big Book of Alcoholics Anonymous mentions various types, however accurate or inaccurate these categories of alcoholics may be.

Generally I agree with Cloninger who states after much factoral analysis that there are essentially two types of alcoholics.

I think his observations of an alcoholic who is a more anxious type and an alcoholic who is more impulsive, conduct problem-based has been observed very roughly in the many meetings I have sat in over the years.

 Cloninger states there are  two “types” of alcoholics and two  pathways into alcoholism; the “externalising”, Type II alcoholics, usually the offpspring of alcoholics  which implicates lack of inhibition over impulsive behaviours, sensation seeking, risky behaviours and conduct problems and Type I  “internalizing” which is posited as involving affective dysregulation with drinking to medicate anxiety like symptoms – both also posited to be linked to the “warrior” and the “worrier” of the dopamine COMT  gene variants, Val158 and Met158 respectively.

I am the Type II alcoholic according to this typology.

As we shall observe in the next two blogs these gene varients of COMT are linked to emotion regulation – Met carriers are more anxious and do not process emotion as efficiently as Val carriers who are more efficient but more impulsive. Thus their type of emotion processing difficulty appears to result more in impulsive responding, which is as we have seen may be linked to lack of emotion differentiation when labeling emotions, resulting in impulsive decision making.

In simple terms Met leads to a slower more rigid responding and Val a quicker responding marked by lack of inhibition over action and behaviour.

Two different pathways to the same problem of alcohol dependence but useful to observe in terms of treatment specificity.

The role of the COMT gene, implicated in 60% of dopamine metabolism in the PFC, which plays a role in executive function as well as being associated with substance abuse, would be an interesting area to research in terms of genetic vulnerability, particularly as COMT also codes for noradrenaline (NE), another catecholamine involved in PFC and affective regulation. This may be particularly pertinent as COMT has been posited as having alleles responsible for separate functions, cognitive and affective regulation with the COMT Met allele linked to affective dysregulation while the Val allele has been associated with less efficient PFC activation during cognitive control.

A recent meta-analysis on fMRI data concluded that Val allele carriers show advantages in emotional but disadvantages in cognitive paradigms while the opposite pattern applies to Met allele carriers (Mier et al. 2010). This trade-off had been earlier termed the warrior/worrier model (Goldman et al. 2005; Stein et al. 2006).

Those with valine (Val158) alleles have increased greater COMT activity and lower prefrontal extracellular dopamine compared with those with the methionine (Met158) substitution. Val158 alleles may be associated with an advantage in the processing of aversive stimuli (warrior strategy), while Met158 alleles may be associated with an advantage in memory and attention tasks (worrier strategy).

How this latter proposed inhibitory control problems result in impulsivity, sensation-seeking and conduct difficulties that are mediated by family-related factors, including parental substance abuse and chronic early life stress, moderate the relationship between genotype and these observed phenotypes is worthy of investigation and has important consequences for prevention strategies.

COMT Val158Met may confer their risk of alcohol dependence through reduced dopamine receptor sensitivity in the prefrontal cortex (PFC) .

COMT Val158Met also modulates the effect of childhood adverse experiences on the risk of alcohol dependence, which have been shown to reduce dopamine activity in the PFC and other areas.

Citing this study (1) we first we look at how the Met variant (the worrier) is associated with higher rates of alcohol dependence (Tiihonen et al. 1999; Wang et al. 2001) . Notably, Val158Met was recently linked to post-treatment relapse in alcohol-dependent individuals, such that Met carriers were about twice as likely to relapse in the year following treatment as those without the variant (Wojnar et al. 2009).

It is proposed that the Met variant could confer increased risk by way of differential dopamine-modulated reinforcement from acute intoxication, diminished ability to cope with negative emotional states and/or deficits in cognitive flexibility and task switching (Bilder et al. 2004; Oroszi & Goldman 2004; Enoch 2006).

This study (2) suggests that Met carriers display reduced processing efficiency and/or heightened neurobehavioral responses when presented with emotionally evocative stimuli (Enoch 2006; Heinz & Smolka 2006).

Accordingly, associations of the Met variant with alcohol use have been speculated to involve motivational pathways specific to the regulation of negative affect (Bilder et al. 2004; Enoch 2006).

If Met carriers show heightened neurobiological responses to cues signalling negative affect and/or diminished capacity to disengage from negative emotional states, these scenarios could potentially increase the likelihood of alcohol use in the context of negative affect, consistent with the current finding that Met carriers showed stronger associations between implicit coping motives and alcohol consumption.

This all ties in with our idea that emotion not processed effectively leads to distressing states which prompts more “implicit” coping or coping activated by implicit parts of the brain which are those of the dorsal striatum which appears to link distress to more automatic (or compulsive) responding to this distress, more so as the addiction cycle progresses.

More on the Val warrier next time round.

TBC

 

Some References

1.  Schellekens, A. F., Franke, B., Ellenbroek, B., Cools, A., de Jong, C. A., Buitelaar, J. K., & Verkes, R. J. (2012). Reduced Dopamine Receptor Sensitivity as an Intermediate Phenotype in Alcohol Dependence and the Role of the COMT Val158Met and DRD2 Taq1A Genotypes. Archives of general psychiatry, 69(4), 339.

2. Hendershot, C. S., Lindgren, K. P., Liang, T., & Hutchison, K. E. (2012). COMT and ALDH2 polymorphisms moderate associations of implicit drinking motives with alcohol use. Addiction biology, 17(1), 192-201.

 

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.

 

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.