allostasis

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.

Addiction – A Parasite that feeds off your Emotions?

When I was in treatment at a local treatment centre, when we were in group therapy to be exact, one of our facilitators, after someone had given an example of their “powerlessness and damage” while drinking, suddenly described alcoholism and addiction as a being like a parasite that feeds on the addict’s emotions.

I was shocked initially by this remark, feeling that this would be an insidious illness indeed if that were the case. A disorder or disease that fed on one’s emotional state. Not only negative emotions I must add as so called happy emotions such as “elation” can also propel a vulnerable recovering person to relapse.

All emotions which are extreme seem to have the capacity to activate a pathological “wanting” in the brain and can prompt relapse. That is why we are often advised to keep a check on the emotions to make sure they are neither too high or too low. Too extreme. This is also called emotional regulation. When emotions are tempered and not so overwhelming or not too labile (changeable).

We know from previous blogs that emotional dysregulation, not controlling or tempering emotions but reacting to them can heighten a sense or a feeling of “wanting”, so intense it feels like a “needing”, in the brain. This is partly due to having excess stress chemicals in the brain.

In the course of addiction or during the so-called “addiction cycle” the brain’s stress systems become increasingly out of kilter, dysregulated, and this creates a brain allostasis rather than the normal homeostasis. With homeostasis the brain regulates itself within given parameters and within regionalised areas of the brain. An example of homeostatic imbalances, such as high core temperature, a high concentration of salt in the blood, or low concentration of oxygen, can generate homeostatic emotions (such as warmth, thirst, or breathlessness), which motivate behavior aimed at restoring homeostasis (such as removing a sweater, drinking or slowing down).

Allostasis is the process of achieving stability, or homeostasis, through physiological or behavioral change. This can be carried out by means of alteration in HPA axis hormones, the autonomic nervous system etc.

Wingfield states: The concept of allostasis, maintaining stability through change, is a fundamental process through which organisms actively adjust to both predictable and unpredictable events… Allostatic load refers to the cumulative cost to the body of allostasis, with allostatic overload… being a state in which serious pathophysiology can occur… (Wingfield 2003).

Allsotasis means adaption via change, it is fleeting homeostasis but “at a price”. One of the prices of excess or chronic levels of stress in addiction  is normally a reduction in dopamine, a brain chemical involved in wanting, motivation, reward, learning and memory and habits.

When there is a heighten stress or emotional distress there is often a rise in dopamine and an increased wanting in an attempt to create a homeostasis. In the case of addiction this dopaminergic wanting, augmented by stress chemicals, usually makes an addicted person want what has previously created a temporary “homeostasis” ie drinking alcohol or taking drugs etc to relieve a distress. Hence stress activates dopamine brain circuits involved in attention, memory, emotion, reward/motivation and habit behaviours. Hence heightened stress levels can pretty much activate one’s addiction and the physiological urge to use or drink. This is the reason stress factors are implicated in the majority of relapse situations.

So to summarise, instead of one or more specialist areas of the brain regulating within given parameters the whole brain can be engaged in attempting to create a fleeting homeostasis. The brain becomes global, i.e. different areas and functions of the brain are recruited. For example, previous experience, memories and so on are activated in governing action and behaviour.

In addiction these memories, for example, are activated by excess stress normally caused by negative emotions and failure to regulate them. The brain will suddenly suggests via these memories and previous experience that the previous way to create a fleeting homeostasis while in a negative emotions would be to drink or use drugs. It would suggest this present distress, this alien state,  is solvable and that drug use is the “normal” way to survive it.

In effect the brain is saying that previously we used drugs to regulate these emotions which at a bio-chemical level also created a fleeting homeostasis, or a fleeting resolution to emotional distress.

As we know this is a far from perfect way to regulate emotions. Hence we use more drink and drugs to regulate emotion which ultimately leads to increased emotional and stress dysregulation which leads to needing drink and drugs more and more. It creates a tolerance, whereby we need more of a certain substance (or behaviour) to reach a fleeting ” balance”. The more stress we have the more we need to restore “homeostais” by using more drugs. The more we reduce dopamine the more we need to use drugs to get more dopamine and other neurotransmitters. It is stress chemicals in the brain  that controls addiction in the end.

At endpoint addiction and in early recovery we seem to be left with a whole lot of stress in the brain, emotional and stress dysregulation; so severe we may not even be able to guess what emotion we are actually having and a desire to leave this alien state of sobriety and return to the previously “normal” state of intoxication that is so profound only an addict can really understand it’s overwhelming intensity.

Thus craving is also stress based. If we regulate our stress we regulate our emotions and our illness is quietened and tempered. Hence we suffer from a distress based illness.

Sorry for so much detail but this is important to know.

The article (1) here set us on a research voyage to a large extent as it confirmed to us that one of the reason people relapse is because sobriety is initially so foreign, so alien, so troubling. We do not really have the tools to cope with it. Hence we need a whole lot of help to recovery. Our illness has effectively taken over our survival mechanisms and appears to speak to us with our own voice although it is essentially the motivational voice of addiction imploring us to survive by re-using.

It is like a psychotic care-giver who is convinced the best way to survive is to employ a way of living that is destined to take your life away and then kill you.

This article showed that  the “euphoric recall” often mentioned in recovery circles is not only instantly retrieved from memory but is immediate. The euphoria is actually re-experienced rather than re-called as such. it is re-felt in terms of brain frequency. Thinking about drinking activates a similar brain frequency to actually drinking itself.

Also it may be also that experience of a negative self perception may activate this brain frequency also and instantly remind one of alcohol or drugs as a way to deal with this negative self perceptions, these distressing negative emotions. This brain frequency suggests we consume substances in order to do the most basic of survival strategies, to regulate our emotional states. Our emotions have become the slaves of substance abuse and behavioural addictions. Addiction does, after all, mean to be bound. We are bound to our addictions for the basic of human needs.

This article (1) – which we comment on as we proceed, italics as we feel it is describing allostasis although it does explicitly say so – appears to be saying in scientific terms what our facilitator at the treatment centre was saying from a therapeutic and observational point of view, from great and profound ancedotal evidence. That substances appear to take over our emotional states and regulation. In this case, alcohol seems to have become intrinsic to our emotional regulation.

How can we say this? In this experiment the researchers found that not only does simply thinking about alcohol create a very similar brain frequency in the brain as actually drinking but that this brain frequency is also seen when we are having negative emotions about ourselves (as alcoholics).

To us this means our negative self perception and emotional regulation itself has become absolutely connected to drinking and taking drugs, in other words, negative emotional states automatically give rise to a desire state a need to drink or use drugs. It has become a automatic habitualised and compulsive reaction and response to negative emotions and adverse self perception.

How we feel about ourselves has ultimately driven our addiction. Hence we need to start think differently about ourselves real soon in recovery because for many years our alcohol, drugs or addictive behaviours may have been doing the thinking and feeling for us!

One thing that kept me sober in early recovery was not listening to my self-centred thoughts (as much as I could because these thoughts have your voice attached so are kinda hard to completely ignore!)  as my thoughts were the product of negative emotions which then caused more negative emotions and then brought memories of past drinking etc and the people, places and things attached with this drinking. My sponsor said it is the voice of your illness and this helped immeasurably.

I tell sponsees this now.

Here we go…” Evidence demonstrates that attachment and interactions between parents and child play a significant role in normal development; alternatively,
impaired parental bonding appears to be a major risk factor for development of mental illness, substance abuse and possible substance dependence later in life (Canetti et al. 1997; Newcomb and Felix-Ortiz 1992; Petraitis et al. 1995; Brook et al. 1989) – It is within this context that this study and the Self-Perception and Experiential Schemata Assessment (SPESA) were formulated. The SPESA is designed for sensitivity to negative, average or positive perceptions of self, experiences and self in-experience in three life domains; childhood, adolescence and adulthood.

The SPESA takes less than 10 min to administer and 10 min to score. It provides important insight into the perceptual, visceral, affective and cognitive processes that may preclude the actual physical or psychological substance abuse or dependence. This instrument divulges perceptual information regarding the endogenous and exogenous experiences of the individual; including, physical, sexual or emotional abuse, self-efficacy, self image, view of self in relation to family and peers, in addition to perceptions of alienation and inadequacy .

Individuals with a family history of alcoholism show increased alpha activity (brain frequency) in posterior regions after alcohol consumption and rate it more difficult to resist further drinking than controls (Kaplan et al. 1988). Males at risk for alcoholism show increased low-alpha EEG activity (7.5–10 Hz) after ingesting alcohol as compared to males at low risk (Cohen et al. 1993).
Michael et al. (1993) found higher central alpha and slow-beta coherence in frontal and parietal electrodes in relatives of alcoholics and lower parietal alpha and slow beta coherence in males with alcohol dependence.

Notably, other findings indicate that morphine, alcohol and marjuana increase alpha 2 power in the spectral EEG and relate this to the euphoric state produced by the drugs (Lukas 1991, 1993; Lukas et al. 1995).

Elevated alpha power amplitude is suggested to be a potential threat indicator for the development of alcoholism and men with fathers having alcohol use disorders are more likely to have high-voltage alpha than men with unaffected fathers at baseline or after receiving placebo (Ehlers and Schuckit 1988, 1990, 1991; Ehlers et al. 1989).

We define experiential schemata (ES) as a neurologic progression in human development involving a fundamental self-organization process. This process is based in the formulation of concepts of self originating in perceptions  of self (endogenous) formed through interactions with others and the environment (exogenous). These encoded schemata become the foundation for prevailing emotions, motivations, attitudes, and attributions relating to self and self-in-the-world that are maintained, reinforced and entrenched in neural coding mechanisms formed through dendritic arborization (spreading of neural networks) over the lifespan.

In normal development ES involving experiences, behaviors, learning and organization of self are engrained or reinforced in neural circuits with much of the
acquired information being necessary for social functioning, and overall survival in most circumstances. The drawback to this process is that it can be extremely difficult
to introduce new concepts relating to self—identity to an individual as well as novel learning material.

Based upon critical concepts from a variety disciplines contributing to addiction research, we propose that a common neurophysiological pattern exists in recovering alcoholics (RSA)  when evaluating self and self-in-experience that is significantly different from non-clinical controls.

This is the first study of its kind to evaluate EEG patterns of self-perception and experiential schemata in a group of RSA as well as controls. The significant differences between groups in the SPESA condition may provide insight into a very probable neural pathway which stands to be an idiosyncratic neurologic anomaly for the RSA population  in this study, in addition to a possible antecedent to Substance Use Disorders (SUDs).

The excess alpha activity in SUD when processing perception of self and self-in experience may reflect a state of desynchronization (or an idling fear and evaluator
response guided by maladaptive ES) within the individual, given that alpha is generated in the thalamus (Lorincz et al. 2008) and is known to be involved in both attention and memory processes (Cannon et al. in press-a).

(Obviously this desynchronisation may reflect the allostasis mentioned above also)

This alpha excess possibly places demands on resources otherwise employed for the homeostatic functioning of the individual; including, autonomic, perceptual, attentional, social, cognitive and sensory processes.

(Equally it may in fact relate to allostasis and the recruiting of these various brain function in anticipating homeostatic/physiological need)

Notably, research demonstrates the use of certain chemicals produces widespread
alpha power increases in the cortex thereby, at least for this study group and their reports of ‘using’and ‘drinking’ thought patterns, bringing the brain into synchrony, if only for a very short period of time.

(Again we would add that these thoughts are acting allostatically as a homoestatic facsimile if you like)

We believe this to be the euphoria addicted individuals speak of so fondly and is one possible reason for the difficulty in treating these disorders in addition to the high relapse rates.
The excess alpha activity during the task is possibly attributable to ES and the associated emotions relating to internal and external conflict and confusion distinguishing past from present and the brain’s reaction to re-experiencing the past.

Damasio (1994) discusses  the continuous monitoring of the body by the brain
as specific content and images are processed, exacting not only changes in brain electrical activity but also chemical reactions. Thus, as the brain communicates and orchestrates  the affective state of the individual in response to these contents and images relating to self and self-in-experience; it is plausible that a large scale feedback loop is formed involving not only perceptual processes but relative autonomic functioning. This process possibly reinforces the addicted person to become habituated to an aroused cortical state (i.e. increased alpha/beta activity) and when there is a shift to ‘normalcy’ it is errantly perceived as abnormal thereby increasing the desire or need for a substance to return to the aroused (or perceived normal) state.  

(This for us explains why initial sobriety and recovery feels so alien, the brain is not used to the cortical state of not using or drinking and tries to get the now recovering person to return to this cortical aroused state of using and drinking)

Also this study offers support to the idea of increased the dopamine roduction within limbic regions in addicted populations (Blum et al. 2007; Kohnke et al. 2003) as increased dopamine producion may be reflected in excitatory frequency domains observed.

(although obviously this heightened dopamine production may also be reflective of stress augmented dopamine activity consistent with allostasis) 

The possibility that substance abuse interacts with specific brain regions in
specific frequencies for specific time intervals appears to be a valid concept, noting the paradox that the resulting self destruction and self-deprecation to achieve a desired state or to change or alter an undesired state transcends immediate comprehension.

(again this can be understood in terms of allostasis as survival has been usurped, taken over, by stress systems acting on, among other systems, dopamine systems of the brain)

Many of the individuals in the RSA group with 3 or more years of continuous abstinence report a consistent effort to intervene on their initial reactions to
external cues and seek additional outside interpretations from counselors, peers or family members for suggestions in how to deal with life events, rather than go on their first instinct.”

(again we believe this can also be explained in terms of allostatically driven distressed-based impulsivity)

To conclude this article set us on a train of research which we believe has led to answers to some of the questions implicit in this research. We believe the increased alpha activity of brain frequency and other points mentioned can all be explained in terms of the brain constantly seeking a new homeostatic setpoint. A return to “normalcy” however maladaptive and self destructive that so-called normality is.

Stress systems usurp survival systems in the brain and the alpha activity reflects a drive for homeostasis whereby allostasis via memory and other mechanisms augment dopamine to facilitate the brain to want or need the substance least required in terms of survival, the alcohol or drugs that have usurped via stress means, the survival network in the first place.

The euphoric recall is allostasis sounding it’s bugle, activating the brain to return to former ways of regulating emotion and behaviour.

The increased brain frequency is a siren to a fleeting brain balance, which will give way via drug and alcohol use to even greater stress based wanting and a brain even more out of homeostatic sync.

An endless, fruitless cycle to find an elusive, fleeting balance that comes and goes.

Amazingly recovery offers alternatives to achieving this fleeting homeostasis and even prolonging it. Prayer, meditation and helping others can keep one in balance for as long as you do it.

Now that is food for thought. In helping others we help ourselves more and in a more profound way than we can ever do by ourselves. Being in self activates our illness and being out of self treats it.

Reference

Cannon, R., Lubar, J., & Baldwin, D. (2008). Self-perception and experiential schemata in the addicted brain. Applied psychophysiology and biofeedback,33(4), 223-238.

The Distress at the Heart of Addiction and Alcoholism

This blog is written for alcoholics and those who love and live with them, by alcoholics in recovery. For those who know what it is like to live with alcoholism but would also like to know why alcoholism affects the alcoholic and those around him in the way it does.

We write this blog to help us and you understand how the alcoholic brain works; why they do the things the do, why they act the way they do. Why is it everything is going great and suddenly the alcoholic in your life “flies off the handle’ and acts in an emotionally immature way, which can often cause hurt to others around them? What is the reason behind this “Jekyll and Hide” emotional responding?

Why do they suddenly cut off their emotions so profoundly it leaves your emotions in limbo, confused and upset?

In this blog we seek to explain, as researchers,  in terms of the processes of the brain, why alcoholics, particularly  those in recovery, do the things the way they do, act the way they do.

We hope to explain this disease state, which alcoholics themselves call a “emotional disease’, a “cancer of the emotions’, a “parasite that feeds on the emotions” or quite simply  “a fear based illness”. It appears that alcoholics in recovery are aware to a large extent of what they suffer from. But why do they do what they do sometimes if they know what is going on? Why do they not seem to be able to help themselves from engaging in certain responses and behaviours?

Why do they endless engage in self defeating resentments,  taking “other peoples’ inventory” or criticizing, why do they project into future scenarios and then get emotionally paralyzed by doing so, why do they run through the list of cognitive distortions on a daily basis, why do they get self absorbed and engage in “me, me, me” behaviour!? Why do they indulge in self pity to the extent they end up in full blown depression?

More importantly, perhaps, how do various therapeutic strategies deal with these behaviours and seek to challenge and address them? And do these therapies, in time through practice and the neuroplasticity (neural reshaping of the brain via behaviour) change how they act, feel and live in this life. In short, how does recovery change the brains of alcoholics for the better?

As we are personally well aware, self knowledge does not bring recovery – only action does. But this action can be based solidly on a better understanding of what goes on in the brain of an alcoholic for example, why should I mediate? What beneficial, adaptive change will that bring, how will that “help me recover”? What is the point of doing the steps, how exactly do they effect change in one’s alcoholic brain? Is there a good healthy neurobiological reason for going to mutual aid group meetings like AA or  SMART?

We also believe that academic research definitions of alcoholism are inadequate – the latest DSM V  equates the emotional difficulties we highlight here as ‘co-morbidities’,  conditions that occur alongside the condition of alcoholism. We disagree, we suggest these ‘co-morbidities’ (co-occurring psychiatric disorders) are a main reason why we become alcoholics, they are what make us vulnerable, along with genes and environment to becoming alcoholic.

Most alcoholics feel they never fitted in, were emotionally hyper “sensitive”,  engaged in risky behaviours, got into trouble without intending to, and other impulsive behaviours which we believe are illustrative of an emotional dysregulation which makes certain individuals vulnerable to becoming alcoholic.

Science tells us there are many such vulnerabilities in children of alcoholics. The alcohol regulated, medicated these errant emotions which caused such distress, even at an early age. It is these emotional processing deficits and emotional dysregualtion (i.e. poor control of emotions, especially when distressed!) which lie at the heart of the this psychopathology or if you like  this psychiatric disorder called alcoholism.

It is a distress-based condition, day in day out, and we formally believe that various therapeutic regimes like the 12 steps, DBT, ACT or CBT, etc all treat this inherent distress state in some way. It is this distress state that activates this “fear-based illness”, that makes one hyper aware of cues, alcohol, it is this distress that provokes memories of drinking, alcohol use schemata, that trains one attention on people places and things from the past. Without this distress our illness barely gets activated! 

For example, does your loved alcoholic, “over do things”on a regular basis, do they engage in short term thinking, or “quick fix ” thinking. Do they resist your attempts at sensible long term , goal directed, “thought through thinking”?

Does your alcoholic work himself to a frazzle, do they easily become exhausted by overdoing it, whatever it is? Do they have a series of new addictions? Are they perfectionist doing too much, or nothing anything at all? Perfectionism is distress based.

Does your alcoholic fear the future, but continually project their thinking into the future? Do they have an intolerance of uncertainty, do they endless ruminate about things, do they react rather than act? Do the most simple decisions provoke a “fight or flight” response? Do they frequently come up with “I know how to do this, I have a great idea!” Only for it to be the opposite of a great idea! Do they give people “rent free room in their heads” because of resentments – replying the same old tape in their minds, over and over and over again? All distress based?

“Fear based” is distress based.

A recent study showed that alcoholics have a part of the brain that helps process emotions but it doesn’t work properly so is overactive all the time; it is exhausting being on red alert, all the time , living on a state of emergency. Hence step 11 in the the 12 steps.

The problem with this hyperactive brain region, called the ventromedial prefrontal cortex, is that it  also cuts out , hypo-activates, when more or excessive stress is applied and another compulsive area of the brain, the basal ganglia, takes over. This part is automatic, habitualized, automatic, compulsive! It results in more more more, and is driven by distress not goal directed consideration. It simple does, does, does, without consideration of future consequence.    Sound familiar??

How did your loved alcoholic get to be this way? What happened to your own alcoholic brain? We believe there is a vulnerability to these aforementioned  emotional difficulties as certain brain areas which regulate emotion not working properly. This means they are smaller, impaired and do not function optimally or are not  connected properly.

Do you know an alcoholic who does not accurately know how he is feeling properly, does not know what emotion he is experiencing? Cannot label to emotion properly which makes processing of it difficult? Can’t rely on a neural feedback to tell himself when  he is tired, angry, hungry  and that he should HALT? This is the insular cortex not working properly.

Does your alcoholic see error everywhere (and worse still give a running commentary on it!?), always whinging about that not being right, or that being wrong. Why can’t they do things properly, be more perfect!! That is partly to do with impairment of the anterior cingulate cortex which monitors error in the environment.

This fear based stuff? That is a hyperactive amgydala, the “anxious amgydala”, and it also acts as a switch between memory systems, from explicit to implicit memory, and recruits the compulsive “go,go, go” area of the dorsal striatum from the always “on the go”, hyperactive, ventromedial cortex.

The amgydala is at the heart of alcoholism and addiction. It not only switches memory but also reward/motivation/ and emotional response so that distress provokes a habitualised “fight or flight response” in the dorsal striatum.

It is said that alcoholics are emotional thinkers, but this region is also an emotional “do” area which means emotional distress acts as a stimulus response. The brain responds to the stimulus of distress in other words. As addiction and alcoholism progress the ways addicts and alcoholics react  become limited in line with addiction severity. The further the alcoholic gets in alcoholism the more he will react out of distress, the more automatic his behaviours become, the more short term his decision making will be, the more he has to fight automatic urges and automatic drink-related thoughts, the more he has to contend with “fight or flight” thinking and feeling.

Add to this a brain that is out of balance, does not have homeostasis, natural neurochemical balance, but has a state called  allostasis, where the brain constantly attempts to finding stability via constant change, and the fact that the alcoholic brain has too much Glutamate,  an excitatory neurotransmitter, the “go neurochemical”, and not enough GABA,  an inhibitory  neurotransmitter, the brains’ natural brakes”, (and which is increased by drinking alcohol) the stop or slow down chemical and  that this also helps slow down an abnormal heart rate variability (HRV) found in alcoholics.

Alcoholics have a different heart rate variability meaning we have a heart rate more suited to being ready for the next (imagined) emergency.  The effects of alcohol are thus more profound on this group, and this HRV is also seen in children of alcoholics so represents a profound vulnerability to later alcoholism.

Add to that depleted levels of of  dopamine, which is very important in the addiction cycle. The problem with dopamine supplies is that our excessive levels of stress reduce our amount of dopamine,  that we are always on the look out for more dopamine. Add to this that stressful states increase our brain in “dopamine seeking” in an attempt at transient allostasis and you have a brain that is always trying to get a buzz out of something, especially when in distress states.

Then there is other deficits to the serotonin system, to the natural opioids  system, to oxytocin, all of which take a beating and are reduced by excessive stress systems. But all are increased via love and looking out for our fellow man, our families, loved ones and other’s in recovery. We can manipulate our brain chemistries, this is what happens in recovery in fact!

Too much stress on the brain spreads like a forest fire throughout the brain, lowering levels of  essential neurotransmitters,  impairing memory and turning one from a goal directed action to a compulsive reaction type of guy. The alcoholic brain is always primed to go off!!

Chronic stress also impairs the prefrontal cortex, the cognitive, conscious “top down” controller of the brain’s emotions and urges, instincts and so on. It doesn’t help that it doesn’t work too well in alcoholics. The brain of an alcoholic is a “spillover” brain, it is a brain that spills over into various types of disinhibition,  impulsivity and compulsivity . It often acts before considering, speaks before thinking. decides this is a great idea with out consulting, reacts without sufficient reason or cause.

It needs help, this alcoholic brain. From another brain, from someone other than himself.

Recovering alcoholics need an external prefrontal cortex to help with the top down cognitive control of the subcortical emotional and motivational states. The problem with emotions are they, in the alcoholic brain, have become entwined with reward. We feel a certain way, negative for example, and fix this negative feeling, with something rewarding, makes us feel better, more positive, less self reflective,  and it seems this has been the case with certain alcoholics since childhood. Dealing with emotions by the granting of treats.

Feeling better by consuming. Fixing feelings via external substances. Sub contracting our emotional regulation.  Finding different feelings in a bottle, or a pill, or a syringe or snorting them up one’s nose. Alcoholics need a spiritual awakening,  a psychic change, a change in consciousness, in self schema;  this sudden change in how we feel about the world (including memories of our past life) because the old feeling about the world will lead to the sane old behaviours. Plus alcohol and drugs were  crude approximates of this change in consciousness, this  spirit awakenings, they dramatically and very instantaneously helped change our feelings, thoughts, perceptions about the world around us. They helped us fit in.

This is the purpose of a spiritual awakening too, a sudden change of consciousness. We believe the best and most sudden way to achieve this is to let go of the thing that causes all the suffering in the first place, the self. It appears we can live without the “self” . It also appears helping others brings a bigger buzz than even helping ourselves.

Helping others reduces our distress. and many many other therapeutic benefits to brain chemistry. This brain also needs some one outside of self, outside the self regulation network in the brain which is so impaired and cannot be relied on because at times it is maladaptive. Can’t be counted on the make the right decision because it favours  short term over the long term, is based on “fight or flight “thinking and rational, hence is distorted by fear.

If we have been thinking in this maladaptive way all our lives it  is no wonder we ended up where we have. We used alcohol to deal with our errant and quite frightening emotions. I positively ran away from my own emotions.

I used to say to my wife, the main reason for my drinking is “to get away from my self”. Now we have to find a solution to living with oneself, these sometimes torturous alien state of emotional sobriety.

I remember being asked by a counsellor to sit with my emotions for half on a hour. I felt I was being possessed by some poltergeist,  the feelings associated with emotional regulation were so alien to me, so frightening. I didn’t know what they were even. I had to have by wife label them for me and help me process them.

I believe steps 4 and  of 12 step programs help one emotional regulation hundreds  and hundreds of unresolved, unprocessed emotions from the past otherwise they will continue to be in there, haunting us like “neural ghosts” from the past, adding emotional distress to our conscious daily experience and encouraging relapse.  This is the case for many newly recovering alcoholics.  Being haunted by a million thoughts produced by  rampant emotional dysregulation.

Resentments swirling around the mind and driving the newcomer back to relapse. What the newcomer finds is that the drink stops working, and the emotional difficulties remain, in fact much worsened by years and years of sticking a neurotoxin down our throats and in into our brains. Havoc is then further reaped on an already not fully functioning  brain.

In AA they often they say that they are stuck at the emotional age of when they started drinking which is usually around the early teens when the cognitive part of the brain that controls emotions is still developing.  But we act much more immaturely than that, we act like the terrible twos or children. Our emotional brains never really grew up. This emotional dysregulation apparent as teens then shaped all our future decisions and eventually our alcoholism. That is what they mean in AA, when they say all your best thinking got you here. So there you have it . Sound familiar? Recognize anyone here?