Powerless over Thinking!

When I first came into recovery I would be plagued by intrusive thoughts about drinking, I would have thoughts about drinking, at certain times of the day in particular, on sunny days etc.

These thoughts used to greatly distress me and I would end fighting with these thoughts which only seemed to make things worse, the thoughts seem to increase rather than decrease and I got increasingly distressed.

I had no control over these thoughts and would get into a terrible emotional state over this. All before I decided it was now a good time to ring my sponsor. I always waited until I was in as much emotional pain as possible before ringing my sponsor!

I thought I could go it alone – that I did not need any help. I was in control of this.

Geez, surely I could control my own thoughts for flips sake!

Hmmm…afraid not!?

In early recovery I was as powerless over thinking as well as my drinking.

It was obvious I had lost control of my thinking like my drinking – it took a lot longer (and I still forget this even today!) to realise I have no  control over my thinking.

It chatters away regardless of my will, my wishes. It I have found is not usually a friend.

So like everything else in recovery I decided to research this! To find out why my thinking seemed out to get me, to negatively affect my recovery. To find out why my thinking did not seem to help me in recovery.

I found out that the idea that abstinence will automatically also decrease alcohol-related intrusive thoughts had been dismissed by research and vast anecdotal evidence.

Practically all therapies for alcoholism e.g  AA, SMART and so on suggest that urges create automatic thoughts about drinking.

This has been demonstrated in research that distress automatically gives rise to intrusive thoughts about alcohol. (1) This reflects emotional dysregulation as these intrusive thoughts are correlated to emotional dysregulation (2).

These thoughts to the recovering/abstinent individual can be seen as egodystonic which is a psychological term referring to behaviors, values, feelings that are not in harmony with or acceptable to the needs and goals of the ego, or consistent with one’s self image.

Other conditions, such as OCD, have these egodystonic thoughts creating the distress that drives a compulsive need to act on them, rather than letting them pass.

In other words, these thoughts are seen as distressing and threatening and compel one to act to reduce this escalating sense of distress. A similar process can happen to those in early recovery.

Thoughts about drinking or using when you now wish to remain in recovery are egodystonic, they are contrary to the view of oneself as a person in recovery.  The main problem occurs when we think we can control these thoughts are that these thoughts mean we want to drink or are going to relapse!

Early recovery is a period marked by heightened emotional dysregulation and the proliferation of intrusive thoughts about alcohol .

In fact,  research demonstrates that alcohol-related thoughts can resemble obsessive-compulsive thinking (3,4).

In fact, one way to measure “craving” in alcoholics is by scale called the Obsessive Compulsive Drinking Scale (5) , thus highlighting certain similarities between alcoholism and OCD.

This finding is also supported by clinical observation and leads to the expectation that among abstinent alcohol abusers, alcohol-related thoughts and intrusions are the rule rather than the exception (6)

Relatively little is known about how alcohol abusers appraise their alcohol-related thoughts. Are they aware that alcohol-related thoughts occur naturally and are highly likely during abstinence?

Or do they interpret these thoughts in a negative way, for example, as unexpected, shameful, and bothersome? Misinterpretations of naturally occurring thoughts or emotional reaction to them  may be detrimental for abstinence (7).

 

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A number of papers and  studies have shown that individuals’ appraisal of their intrusive thoughts as detrimental and potentially out of their control may lead them to dysfunctional and counterproductive efforts to control their thinking.

Alcohol-related thoughts cause an individual to experience strong emotional reactions; however, alcohol abusers will increase their efforts to control their thinking only when they have negative beliefs about these thoughts.

For instance, spontaneous positive memories about alcohol (‘‘It was so nice to hang out at parties and to drink with my buddies’’) may be appraised—and misinterpreted—as ‘‘the first steps toward a relapse’’.

Such an appraisal of one’s thoughts about alcohol as problematic may instigate thought suppression and other efforts to control the thoughts.

These efforts must be assumed to be counterproductive and  will increase rather than prevent negative feelings and thoughts, and they may even demoralize alcohol abusers who are trying to remain abstinent

On the other hand if positive alcohol-related thoughts are not appraised as problematic but as a normal part of abstinence, the awareness of these thoughts might even lead to the selection of more adaptive coping responses, which could help to reduce the risk of relapse, such as talking to someone about them or just simply letting these thoughts go.

 

In one study (8), participants who reported on their thoughts about alcohol in the previous 24 hours, 92% reported experiencing at least some thoughts about drinking that ‘‘just pop in and vanish’’ without an attempt to eliminate them. This suggests that if both suppression and elaboration can be avoided, many intrusive thoughts will be relatively transient.

An “accept and move on’’ strategy provides an opportunity for the intrusion to remain a fleeting thought.

In other words, just let go.

This means the thoughts go, and the distress which activates them, too.

This is recovery a lo of the time.  Getting embroiled in thinking and then letting go, repeat…

That is why helping others is important  -it takes us out of our crazy heads

References

1. Zack, M., Toneatto, T., & MacLeod, C. M. (1999). Implicit activation of alcohol concepts by negative affective cues distinguishes between problem drinkers with high and low psychiatric distress. Journal of Abnormal Psychology108(3), 518.

2. 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 Psychiatry54(12), 1427-1436.

3. Caetano, R. (1985). Alcohol dependence and the need to drink: A compulsion? Psychological Medicine, 15(3), 463–469

4. Modell, J. G., Glaser, F. B., Mountz, J. M., Schmaltz, S., & Cyr, L. (1992). Obsessive and compulsive characteristics of alcohol abuse and dependence: Quantification by a newly developed questionnaire. Alcoholism: Clinical and Experimental Research, 16(2), 266–271.

5. Anton, R. F., Moak, D. H., & Latham, P. (1995). The Obsessive Compulsive Drinking Scale: A self-rated
instrument for the quantification of thoughts about alcohol and drinking behavior. Alcoholism:
Clinical and Experimental Research, 19, 92–99.

6. Hoyer, J., Hacker, J., & Lindenmeyer, J. (2007). Metacognition in alcohol abusers: How are alcohol-related intrusions appraised?. Cognitive Therapy and Research31(6), 817-831.

7. Marlatt, G. A., & Gordon, J. R. (Eds.). (1985). Relapse prevention: Maintenance strategies in the
treatment of addictive behaviors. New York: Guilford Press

8. Kavanagh, D. J., Andrade, J., & May, J. (2005). Imaginary relish and exquisite torture: the elaborated intrusion theory of desire. Psychological review112(2), 446.

 

An Addicted Brain but a Recovering Mind

This blog used excerpts from

Do I still have an “Alcoholic Mind”!?

 

When I first came into recovery I used to get frightened by other abstinent  alcoholics proclaim that they were so glad they did not get the “wet tongue” when they saw alcohol or people drinking alcohol.

I used to feel ashamed as I did have an instantaneous “wet tongue” or mild salivation (Pavlovian response) and still do  years later when I see people drinking alcohol. Is this a “craving” for alcohol, do I still want to drink? Do I still have an “alcoholic mind?“. Did I do my steps properly?

It used to churn me up, these so-called alcoholics who had no physiological response to alcohol-related “cues”. By “cues” I mean the sight, sound and smell of alcohol and alcohol  related  stimuli, like wine gulping , glasses clinking, people having a good time, etc.

Part me also thought it was linked to addiction severity, how bad or chronic one’s alcoholism become, how far down the line or how low your rock bottom was? There may some validity in that observation.

It was partly because of mixed messages from alcoholics that I decided to take matters into my own hands and do some research into my alcoholic brain.

What I have discovered is that I have an “alcoholic brain” and not a “alcoholic mind” and there is a huge difference.

I found there is a difference between by addicted brain that has been altered by chronic abuse of alcohol and drugs and my recovering alcoholic mind, that  essence of me that is dedicated to recovery from alcoholism and addiction. These are very distinct – let me explain – on a daily basis I use my mind to help my brain recover.

For example, I meditate, I ignore the incessant chattering of my “illness”.

Both these are the function of my mind affecting the neuroplasticity of my brain.

In other words my mind is in control of my brain, the brain’s functions and structure can be shaped by my mind.    This is in effect, recovery.

For example, meditation can strengthen my control over emotional states, especially negative emotional states, by building yo the neural “muscles” of brain regions which regulate emotion.

Hence my mind and brain are distinct from each other, one effects the other.

So if there are people out there relatively new to recovery, listen up.

For chronic alcoholics there is an automatic physiological response when we see cues such as other people drinking. Mild salivation, quickening heart rate etc.

These are automatic, habitual, these responses happens to us rather than us wanting or willing it to happen. It happens unconsciously without our say so!

If you get a “wet tongue” i.e. you mildly salivate, then this is what happens when you have crossed the line into chronic alcoholism.

Loads of studies have shown there is this automatic response and have also shown there is also an attentional bias to alcohol cues. We notice alcohol cues in the environment before anything else. They have a heightened “noticeableness”.

Have you ever been in a new town and counted the number of drinking establishments automatically or had a heightened awareness of half drunken bottles of alcohol lying in the street? This is an attentional bias, we notice alcohol related stuff before anything else.

Some researchers in science call this a craving. I disagree.

I call this a physiological urge, distinct from craving.

I think a craving is more akin to a “mental obsession” about alcohol.

Alcohol has only had ‘luring’ effect on me while very emotional distressed or in the early days of recovery I was very scared that  I would drink but, looking back, I never had any desire to.

It is hugely important for recovering persons that we distinguish between urges and craving, in a clear manner that science seems to have been unable to do!

Lives can depend on this.

We are so vulnerable in early recover that we need sound direction on what is happening to us automatically and what we are encouraging to happen, consciously.

An urge for me is a physiological response to cues, external and internal (e.g. stress). A craving is different but interlinked.

Let me explain.

If I have an urge and it becomes accompanied by automatic intrusive thoughts such as a drink would be nice, and maybe a suggestion on where to get this drink, this does not mean I want a drink.

It is simply automatically prompted intrusive thoughts, the type of thought I used to get all the time and so became habitual, stored away in an automatized addiction schema or addiction action plan.

If I realize this and simply let these thoughts go, i.e. do not react to them, then they lessen and dissipate altogether.

This is not a craving. I have not consciously and emotionally engaged with these intrusive thoughts (although we often do in early recovery when they scare the life out of us!).

If I consciously engage, emotionally react, to these thoughts either because I want a drink (elaboration of these thoughts as in embellishing a desire state) or the thought scares the life out of me (averse reaction) I can end up in a mental obsession.

If in recovery, we try to suppress these thoughts then they will come back stronger than before which will raise  already high stress levels and recruit a whole host of memories of why I should drink, with who, where, and how much I will enjoy it.

They will also activate an Alcoholic Self Schema (different to the recovery self schema still being formed in early recovery).

Then I have a memory Hydra effect where attempting to suppress this terrible flowering of desire based memories or to cut off the heads of these thoughts and memories leads to them increasing and increasing.

 

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Then there are lots of these memories driving you crazy and scaring the life out of you.  And this is in someone who does not want to drink but wants to remain in recovery!!?

The other guy who is embellishing these thoughts is kinda thinking about drinking or toying with the possibility, so but again he is reacting cognitively and consciously to these intrusive thoughts. He is elaborating on them. He is using a different more cognitive part of the brain and a different memory system to those activated when he was simply having unconscious, habitual, automatic intrusive thoughts. He is now involved in this process rather than it simply happening to him.

So what I am saying is that there is no simple urge state that automatically leads to drink. We have to cognitively and emotionally react to it.

In my time in recovery, I have rarely heard of or witnessed  someone lured siren-like by a cue to a drink and when I have it is because he wanted to drink really, was testing their alcoholism, or he was in huge emotional distress and went “to hell with it!”

As we will see in later blogs,  there has to be a  cognitive-emotional reaction which mediates between an urge and a relapse!

If you have urges of a “wet tongue” accept this fact, that it is because you are an alcoholic. Non alcoholics are bedeviled with these things, only alcoholics are.

Thank the heavens you have had this reminder of your alcoholism. I used to replace this urge states with gratitude, and thank God for giving me another insight into my condition.

 

How Mindfulness could help Recovery?

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

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

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

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

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

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

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

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

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

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

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

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

 

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

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

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

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

 

MINDFULNESS TRAINING REDUCES STRESS AND THOUGHT SUPPRESSION

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

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

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

CONCLUSION

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

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

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

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

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

I personally meditate using both  Christian and Buddhist meditation techniques.

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

References

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

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The terror of “Locked In” Attention!

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 

References

1. Ingjaldsson, J. T., Laberg, J. C., & Thayer, J. F. (2003). Reduced heart rate variability in chronic alcohol abuse: relationship with negative mood, chronic thought suppression, and compulsive drinking. Biological Psychiatry54(12), 1427-1436.

 

 

 

Intolerance of Uncertainty and Distorted thinking About the Future

Another common area I feel addiction has with obsessive compulsive disorder (OCD) is intolerance of uncertainty (IU).

In fact it is also associated with post traumatic stress disorder (PTSD)- there is actually a high co-morbidity  (at least around 40% comorbidity) with addiction and PTSD and it is one so-called co-morbidity that does not naturally dissipate like some others months into recovery such as Generalized Anxiety Disorder or Depression (the 14% rates of depression and GAD in recovery people are the same as for a normal population) but remains and often makes the symptomatic manifestations of addiction more severe, especially the tendency to engage in “fight or flight” reactions” to uncertainty and ambiguity.

I will blog more on this co-morbidity in later blogs.

The study we cite today in fact looks at IU in addicts who have suffered trauma (1).

Intolerance of uncertainty is a term that refers to a certain way in which some people perceive and respond to situations that are uncertain, and it has been found to be associated with the experience of PTSD symptoms.

Individuals who respond to uncertain or unpredictable situations in this way are considered to have an intolerance of uncertainty. People who are intolerant of uncertainty may begin to experience constant worry about what could happen in the future.

One study (1) demonstrated that negative emotion regulation strategy and intolerance of uncertainty can significantly explain the craving beliefs in addicts (especially those who have suffered a traumatic experience).

This result is consistent with that of Asadi Majareh, Abedini, Porsharifi and Nilkokar (2013) and Nasiri Shushi (2011).

Nasiri Shushi (2011) revealed that there is a significant difference among substance abuse and intolerance of ambiguity and tolerance of uncertainty in two groups of drug abusers.

The other results of this study showed that addicts have less tolerance of ambiguity and tolerance of uncertainty. In the implications of these results it should be expressed that tolerance of uncertainty is associated with cognitive features and addicts when they are faced with difficult situations act in very low levels of performance in terms of decision-making.

Studies carried out to investigate the characteristics of drug abusers suggest that they use substances to regulate a wide range of cognitive events. Undoubtedly unpleasant emotional states, particularly anxiety, depression and stress in addicts are associated with the cognitive consequences.”

The authors suggest that “Drug abusers are not able to tolerate the unpleasant situations and uncertainty in the stressful conditions and their sensitivity leads to mental and emotional problems, therefore, they more turn to substances to regulate their own cognitive experiences (Spada, Nikčević, Moneta, Wells, 2007).

The results of a study showed that individuals with lower tolerance to ambiguity find the ambiguous situations threatening… Many of them may find the substance use in the face of difficulties the only solution and therefore are not able to think or consider other solutions.”

“….While, those with high tolerance to ambiguity in face of unpleasant situation and uncertainty try to find a good solution to get rid of this condition as soon as possible…those with a low tolerance to ambiguity and uncertainty cannot find an appropriate solution…and consequently turn to undetected compromise strategies such as the use of the substance (Ahmadi-Tahoorsoltani and Najafy, 2012).”

I can relate to this study. As I still suffer from intolerance of uncertainty (IU) in recovery, and some years into recovery, it is safe to assume that I suffered form IU in addictive addiction also, if not more so?

For me dealing with an uncertain future can still provoke anxiety. In recovery groups, like AA, we often hear sensible suggestions such as do not “project into the future”, which basically means do not attempt to control future events by thinking about them because this is not only impossible but also anxiety inducing.

The main reason why I think me and other alcoholics cannot project into the future and reasonably reflect and deliberate possible outcomes is because we may have an intrinsic impairment in this regard.

We, or some of us, especially those who have suffered trauma in earlier years, may have IU, like OCD sufferers.

The number of times I rang my sponsor in early recovery to help me with projecting into the future was legion.

Having some one else to talk and share with helps us recruit the pre frontal part of the brain so that we can either see the sense in not not projecting into an unknown future or get help in reasoning through what is likely to occur then.

The difficulty I had and can still have is that my projection into the future is still negatively biased, it is still prompted by distress based cognitive distortions.

As we will see in later blogs these types of cognitive distortions proliferate across a wide range of addictive disorders such as eating disorders which we consider in our next blog.

Among this cognitive distortions is catastrophic thinking which is also distressed based. I will also blog on this at a later date. My head can still run away with itself and convince itself about something which is patently not the case. It can persuade me that this is person or that is doing this or that for these reasons. All of which on reflection are usually nonsense. For me this is like a type of delusion. It is a part of my condition that my head can trick me into believing a whole range of ideas that are delusional. Sometimes I realise this only weeks and months later.

And some people wonder why we turn our lives over to a power greater than ourselves!!?

All this distorted thinking is distressed based.

Which means there is chronically excessive stress chemicals like glucocorticoids being synthesized and whirling around one’s brain. If you give some one enough glucocorticoid there is a good chance they will end up in psychosis. In the 1950s glucocorticoids were used as an anti depressant until people started ending up in psychosis.

Ultimately when we engage in this negatively biased and distorted thinking we have potentially taken the first steps in a walk to relapse because that will eventually seem a whole lot better idea than psychosis?

These cognitive distortions (and there are many)  may even be at the heart of this condition of addictive behaviour.

They are also the consequence of an impaired ability to process emotions (and to avoid) them and thus regulate them. This leads to a tendency to fight or flight which only leads to an heightening of this anxiety, and an increased proliferation of distressing thoughts about future possiblilities, all of which can seem to become more and more catastrophic. How much these thoughts are specifically linked to trauma has to be further explored by research.

For me IU and thought action fusion, especially in early recovery caused as many problems as so-called defects of character. The only difficulty is that they are not mentioned in AA literature, or the Big Book. That does not mean that they do not exist simply because they were not discussed as psychological manifestations commonly known to alcoholics in the 1930s.

They are however known now, which is why I write this blog. To add to our sum of knowledge about this strange illness…

That is not to say having a reassuring sponsor and taking inventory cannot deal with these issues. It is useful however to be aware of them and to realise that not every one in recovery has suffered traumatic incidents. Those who have can have additional requirements in terms of recovery.

I always found it comforting to have a sponsor in the early days who was there and who could also relate to the trauma side of my alcoholism and addiction. It helped soothe me when I could not self soothe. Helped me realise I was not alone in this, that I could recover like this other trauma sufferer could. We can do stuff we can’t do alone.

Ultimately with such an impaired ability to see things reasonably and to make decisions rationally it is imperative to evoke a cardinal recovery rule for me, Accept, Let Go and Let God.

The most profound way to regulated emotions. To Let it Be.

I also used a thing I borrowed and rephrased from Jeffey Schwartz, a leading expert on OCD, how suggested OCD sufferers when in the grip of some obsession to say to themselves “It’s not me it’s my OCD”.

So if your head gets into a downward spiral over some event your head distorts into being and likely to happen in the dark, threatening, Gothic never never world of the future, say to your self “It’s not me it’s my illness.”

In the UK it is called the fanatic in the attic.

It does the thinking for you, if you allow it. Guaranteed.

 

References

Fizollahi, S., Abolghasemi, A., & Babazadeh, A. THE ROLE OF EMOTION REGULATION, DISSOCIATIVE EXPERIENCES AND INTOLERANCE OF UNCERTAINTY IN THE PREDICTION OF CRAVING BELIEFS IN DRUG ABUSERS WITH TRAUMATIC EXPERIENCE.

They can fuck you up, your mum and dad.

They fuck you up, your mum and dad.
    They may not mean to, but they do.
They fill you with the faults they had
    And add some extra, just for you.

Phillip Larkin – This Be The Verse

Looking back on my own childhood it is easier now to observe the fertile ground from which my genetic seeds of alcoholism started to flourish. I have long maintained that growing up in a dysfunctional family environment did not create my alcoholism but certainly did not help. A family environment were emotional expression was limited and veered between sentimentality and  outright anger.

It is difficult to see how I learnt the essential adaptive skills of emotional regulation then; how to identify, label and express emotions freely without sanction, verbally, and non-verbally. For me emotions where something you cut off, experientially avoided, resisted. The more you did not let them get to you the tougher you were mentally somehow. Emotions were strangely dangerous things almost.

Emotions, having them, made you weak! People who indulged in them were weak.

I also grew up with a father who was a boxer and alcoholic (abstinent, thank God, via the local Church) who insisted emotions had to tolerated like a man, like some tough  hombre in a 1950s Western. I had a host of uncles and a Grandad who agreed and they all set out to toughen me up. I even had boxing matches with cousins at various homes to show how I was progressing!

When I started drinking I found that this tough guy routine was greatly enhanced. Alcohol made me bullet proof. I drank and grew up to manhood in one go. Or so I thought – I didn’t realise that I stayed at that emotionally  impaired 14 years old for nearly three decades later.

The worst effect on my emotional regulation  skills was my relationship with my mother who struggled with valium abuse most of her adult life. This meant she was emotionally distant a lot of the time. Wose than that, she mixed mawkishness with being cold as a stone. It was an insecure attachment.  You were never sure, emotionally, where you were at with her. It made me insecure, anxious and eventually very very angry. Cold blue angry.

But did this also have an effect on my ability to processing emotions. How could maternal emotional deprivation have an effect on my emotional processing skills? Andd how could this emotional processing difficulty affect the amount I craved alcohol??

I recently came across this article (1) which looked at this very question.  I refer widely from it here.

Attachment theory is a widely used framework for understanding emotion regulation as well as alexithymia, and this perspective has also been applied to understand alcohol use disorders. One hypothesized function of attachment is the interpersonal regulation of affective experiences (Shaver & Mikulincer, 2007; Sroufe, 1977).

One hypothesized function of attachment is the interpersonal regulation of affective experiences (Shaver & Mikulincer, 2007; Sroufe, 1977). In the development of alexithymia, attachment theories stress the importance of significant others in childhood (Krystal & Krystal, 1988; Nemiah, 1977; Taylor et al., 1997). Evidence suggests that alexithymia is related to dysfunctional parenting (Thorberg, Young, Sullivan & Lyvers, in press).

Insecure attachment is associated with alexithymia and both harmful drinking and alcohol-dependence (Cooper, Shaver, & Collins, 1998; De Rick & Vanheule, 2006; Thorberg & Lyvers, 2006; Thorberg, Young, Sullivan, Lyvers, Connor & Feeney, 2009). In addition, alcohol abuse has been hypothesized to be a consequence of alexithymia (Taylor, Bagby, & Parker, 1997).

Research on alexithymia (1) has found significant positive associations between alexithymia, difficulties identifying feelings, difficulties describing feelings and alcohol problems (Thorberg, Young, Sullivan, & Lyvers, 2009; Thorberg, Young, Sullivan, Lyvers, Connor & Feeney, 2010). Individuals with alcohol-dependence and alexithymia report more severe alcohol problems compared to those with alcohol-dependence alone (Sakuraba, Kubo, Komoda, & Yamana, 2005; Uzun, Ates, Cansever, & Ozsahin, 2003). They also have poorer treatment outcomes (Loas, Fremaux, Otmani, Lecercle, & Delahousse, 1997; Ziolkowski, Gruss, & Rybakowski, 1995).

Individuals may use alcohol to escape feelings of rejection and establish a “secure attachment base” (Hofler & Kooyman, 1996), given alcohol’s stress and anxiety reducing effects.

In this study (1)  results highlight the importance of alexithymia and difficulties identifying and describing feelings as related to preoccupation, obsessions and compulsive behaviors regarding drinking in those with alcohol-dependence. Or in more simple terms between alexithymia and craving.  In this study 32.4% of this alcohol dependent groups were alexithymic. This is less than previously reported prevalence rates of 45-67% (Thorberg et al., 2009).

In this study (1)  alcohol-dependence severity, alexithymia and insecure attachment were associated with more intrusive and interfering cognitions, ideas and impulses about alcohol, including an impaired ability to control these thoughts and impulses. This cognitively based “craving” as measured by the Obsessive Compulsive Drinking Scale (OCDS; Anton, Moak, & Latham, 1995), which is designed to assess obsessive thoughts and compulsive behavior toward drinking.

Hence there was a demonstrated relationships between alexithymia, craving, anxious attachment and alcohol problems in an alcohol-dependent sample. Higher levels of alexithymia led to a stronger desire for alcohol that was partially explained by an underlying mechanism, anxious attachment. One possible reason for this  it may reflect an impairment in affect regulation.

Findings of the RAAS-Anxiety scale measured insecure attachment as related to a current or previous relationship, these findings may suggest that worries about being rejected, not cared for or unloved lead to an increased craving for alcohol.

One explanation for this mediational relationship may perhaps be that increased relationship stress is associated with a fear of intimacy and anxious attachment that leads to increased craving and perhaps a stronger attachment to alcohol. In other words, the alexithymia of insecure attachment may cause a stress dysregulation which prompts craving particularly as craving is a consequence of dysregulated stress systems. Stress dysregulations is also implicated in increased or more chronic alexithymia as suggested by George Koob in various articles. This has also been observed in other studies – this relationships of negative affect (anxiety, negative mood and emotion) with both alexithymia and craving (Sinha & Li, 2007).

To summarise, the results of this study support important relationships between alexithymia, difficulties identifying and describing feelings in relation to alcohol craving. These relationships extend to significantly higher levels of obsessive thoughts and compulsive behaviors in relation to alcohol use and alcoholism severity amongst individuals with combined alexithymia and alcohol-dependence, compared with alcohol-dependence alone. This study identified anxious attachment as a potentially important mechanism, in the relationship between alexithymia and alcohol craving.

References De Rick, A., Vanheule, S., & Verhaeghe, P. (2009). Alcohol addiction and the attachment system: an empirical study of attachment style, alexithymia, and psychiatric disorders in alcoholic inpatients. Substance use & misuse,44(1), 99-114.

When fighting your neural ghosts make sure to surrender!!

When I was in early recovery, in the first weeks and months my brain would continually trick me into thinking I was not an alcoholic and it did this via a combination of  stress and memory.

The process went like this – first I would have an intrusive thought about alcohol and drinking which I did not want and had not consciously put in my own head. Which used to annoy me! So what was it doing there then? I must have put it there right? why else would it be there?

So I must still have wanted to drink?

I would find this thought very threatening, frightening and upsetting. I would try to get rid of it by suppressing it, pushing it out of my consciousness. The problem was this didn’t work.

Image

In fact, it made the situation a whole lot worse. The intial intrusive thoughts about drinking would then proliferate and there would be other thoughts about drinking; where, at what time, who would be there. I would then have a visual read out of all these scenarios. In the bar, the sunlight streaming through the window, the golden glistening pint of lager in the summer sun matched only by the pearly white smile of the beautiful buxom bar maid slowly pulling my pint, looking at me longingly etc. in a busy atmosphere, full of happy your attractive people laughing and enjoying themselves. people dancing and hugging. Sweet music drifting acorss the bar. You get the picture.

Delusion! This was nothing like the last bar I drank in a can assure you!! It was however the image my brain was evoking partly via memory association partly by motivational embellishment.

I have an alcoholic brain which wants me to drink. It uses, still, memories from the past, to whisper sweet nothings. It never casts images across my feverish mind of violently vomiting, bent over the downstairs toilet, or me staring through half blind eyes at my severely jaundiced face in the bathroom mirror. Or being thrown out of various bars onto the hard concrete pavement outside, on my head. Or the tears and violent rows. And the distress and confusion on loved ones’ faces.

No my alcoholism never accesses these images. Ignores them completely. Instead, as my alcoholic brain wants nothing more or else than to drink, it sends memories like neural ghosts into my head to cast a spell of delusional images and suggestive ideas, mainly promoting the idea of how good it was.

This is why in AA it is said we should wind the tape forward a bit to the disgustingly horrible reality of our final drinking. The constantly wretching and living in isolaton in our alcohol induced psychosis and the shivering terror of delirium tremens.

We have a inner voice of alcoholism that quite simply lies. Distorts our memories. The motivational voice of our alcoholism is a pathological liar. It only wants to drink because it is like a psychotic carer who thinks that drinking is the thing to do when we are in full of stress or in emotional distress. It automatically says hold one I have a solution to this distress, DRINK!

This is what the brain has become hardwired to do when distressed enough.  it is a habitual response of our implicit memory which then recruits our explicit memory which paints the picture of why drinking would be such a good idea.

I have a distress based illness, so I do get distressed from time to time. Sometimes over the most innocuous things sometimes.

Not as badly as in early recovery.  No, things have improved beyond belief since then.

The neural ghosts of my motivation were like intoxicating sirens in early recovery. My impaired reward systems implored me to have liquid release. Both combined to conjure an alternative view of myself from that of my recovering self, which was still in it”s infancy. They seemed to have control of my brain!  I suddenly had a problem beyond my own will power, I couldn’t resolve these things under my own steam.

The thoughts would come and I would suppress them and the thoughts would multiply and then the memories would all chain link  and pretty soon I would have an Amazon warehouse store of memories, all providing evidence against those guys in AA, who were not telling me truth about me being an alcoholic, They were wrong…sure I liked to drink, especially given by traumatic upbringing and all?

All these thoughts and memories floating across my mind like edits in a movie to show me as a drinking person who wasn’t an alcoholic. Not many disorders go to such profound trouble!!

I would fight these images, memories and thoughts to such an extent my brain would quite simply end up paralysed, my brain felt like it had become locked and there was nothing I could do about it. It had frozen into a terrifying inertia. Stalemate. No resolution apart from increased suffering.

Fortunately whatever I had learnt in AA even in the early days would rescue me. I had learnt to habitually grasp at something close to hand, my mobile phone. After a few puzzling moments of indecision I realised I could get help from somewhere. Ring my sponsor!!!!

I had to use someone else’s head to help me with my head, my newly recovering alcoholic head. I needed a recovered head who knew what I was going through and could help me through it! I felt all fragile like a jaundiced chick.

Recovery is tough in the early days, let’s never forget that! Life without a sponsor and right from the start is a key to surviving this alcoholic possession by these deluded memories and these neural ghosts.

This is the most vital period, to keeping those who need help in recovery. Saying someone doesn’t want it enough doesn’t cut it for me anymore. Better to show them what they are missing, namely a solution to their problems. Who ultimately doesn’t want that?

If you have never trusted anyone in your life, like me, this is the time to start if you want to recover. Trust at least one person on God’s earth. One, that’s all. This is the start to a new world in recovery. A world beyond your alcoholic brain’s comprehension.

Anyway, remember that in the feverish brain of a person in early recovery who ends up engaged in this neurobiological possession, thought straightjacket and fighting for his or her life against a mnemonic Hydra when it is the last thing they should be doing, the only way to win is to give in. Surrender!

Ultimately, how we appraise and react to naturally occurring alcohol or drug related thoughts and associated memories  will determine if this process of “craving” is activated. If we use strategies such as acceptance of these thoughts as transitory then the thoughts will not affect this process and if we “Let Go and Let God” then the distress which initially activates this process will not do so. How we react to our thoughts and accompanying distress (as they appear be be coupled) will determine whether the mental obsession mentioned above will be provoked.

Also see Cognitive Craving Part 3  and Part 4

Don’t fight your thoughts!

The idea that abstinence will automatically also decrease alcohol-related intrusive thoughts has been dismissed by research and vast anecdotal evidence.

Practically all therapies for alcoholism e.g  AA, SMART and so on suggest that urges create automatic thoughts about drinking. This has been demonstrated in research that distress automatically gives rise to intrusive thoughts about alcohol. (1) This reflects emotional dysregulation as these intrusive thoughts are correlated to emotional dysregulation (2).

These thoughts to the recovering/abstinent individual can be seen as egodystonic which is a psychological term referring to behaviors, values, feelings that are in harmony with or acceptable to the needs and goals of the ego, or consistent with one’s self image.  Other conditions, such as OCD, have these egodystonic thoughts creating the distress that drives a compulsive need to act on them, rather than letting them pass. In other words, these thoughts are seen as distressing and threatening and compel one to act to reduce this escalating sense of distress. A similar process can happen to those in early recovery. Thoughts about drinking or using when you now wish to remain in recovery are egodystonic, they are contrary to the view of oneself as a person in recovery.  The main problem occurs when we think we can control these thoughts are that these thoughts mean we want to drink or are going to relapse!

Early recovery is a period marked by heightened emotional dysregulation and the proliferation of intrusive thoughts about alcohol .

In fact, empirical research demonstrates that alcohol-related thoughts can resemble obsessive-compulsive thinking (3,4).

In fact, one way to measure “craving” in alcoholics is by scale called the Obsessive Compulsive Drinking Scale (5) , thus highlighting certain similarities in pathomechanisms between alcohol and OCD.

This finding is also supported by clinical observation and leads to the expectation that among abstinent alcohol abusers, alcohol-related thoughts and intrusions are the rule rather than the exception (6)

Relatively little is known about how alcohol abusers appraise their alcohol-related thoughts. Are they aware that alcohol-related thoughts occur naturally and are highly likely during abstinence? Or do they interpret these thoughts in a negative way, for example, as unexpected, shameful, and bothersome? Answers to these questions obviously inform with implications for relapse prevention, because misinterpretations of naturally occurring thoughts may be detrimental for abstinence (7).

 

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A number of conceptual papers and empirical studies have shown that individuals’ appraisal of their intrusive thoughts as detrimental and potentially out of their control may lead them to dysfunctional and counterproductive efforts to control their thinking. Alcohol-related thoughts cause an individual to experience strong emotional reactions; however, alcohol abusers will increase their efforts to control their thinking only when they have negative beliefs about these thoughts. For instance, spontaneous positive memories about alcohol (‘‘It was so nice to hang out at parties and to drink with my buddies’’) may be appraised—and misinterpreted—as ‘‘the first steps toward a relapse’’.

Such an appraisal of one’s thoughts about alcohol as problematic may instigate thought suppression and other efforts to control the thoughts. Because these efforts must be assumed to be counterproductive (Fehm & Hoyer, 2004), they will increase rather than prevent negative feelings and thoughts, and they may even demoralize alcohol abusers who are trying to remain abstinent

If positive alcohol-related thoughts are not appraised as problematic but as a normal part of abstinence, the awareness of these thoughts might even lead to the selection of more adaptive coping responses, which could help to reduce the risk of relapse.

In the context of mental health, metacognition can be loosely defined as the process that “reinforces one’s subjective sense of being a self and allows for becoming aware that some of one’s thoughts and feelings are symptoms of an illness.”

The assumption that metacognition mediates reactions to alcohol-related cues may help to explain why “craving” does not inevitably lead to relapse.

In one reported study (8), participants who reported on their thoughts about alcohol in the previous 24 hours, 92% reported experiencing at least some thoughts about drinking that ‘‘just pop in and vanish’’ without an attempt to eliminate them. This suggests that if both suppression and elaboration can be avoided, many intrusive thoughts will be relatively transient.

An “accept and move on’’ strategy provides an opportunity for the intrusion to remain a fleeting thought.

 

References

1. Zack, M., Toneatto, T., & MacLeod, C. M. (1999). Implicit activation of alcohol concepts by negative affective cues distinguishes between problem drinkers with high and low psychiatric distress. Journal of Abnormal Psychology108(3), 518.

2. 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 Psychiatry54(12), 1427-1436.

3. Caetano, R. (1985). Alcohol dependence and the need to drink: A compulsion? Psychological Medicine, 15(3), 463–469

4. Modell, J. G., Glaser, F. B., Mountz, J. M., Schmaltz, S., & Cyr, L. (1992). Obsessive and compulsive characteristics of alcohol abuse and dependence: Quantification by a newly developed questionnaire. Alcoholism: Clinical and Experimental Research, 16(2), 266–271.

5. Anton, R. F., Moak, D. H., & Latham, P. (1995). The Obsessive Compulsive Drinking Scale: A self-rated
instrument for the quantification of thoughts about alcohol and drinking behavior. Alcoholism:
Clinical and Experimental Research, 19, 92–99.

6. Hoyer, J., Hacker, J., & Lindenmeyer, J. (2007). Metacognition in alcohol abusers: How are alcohol-related intrusions appraised?. Cognitive Therapy and Research31(6), 817-831.

7. Marlatt, G. A., & Gordon, J. R. (Eds.). (1985). Relapse prevention: Maintenance strategies in the
treatment of addictive behaviors. New York: Guilford Press

8. Kavanagh, D. J., Andrade, J., & May, J. (2005). Imaginary relish and exquisite torture: the elaborated intrusion theory of desire. Psychological review112(2), 446.

 

Do I still have an “Alcoholic Mind”!?

When I first came into recovery I used to get frightened by other abstinent  alcoholics proclaim that they were so glad they did not get the “wet tongue” when they saw alcohol or people drinking alcohol.  I used to feel ashamed as I did have an instantaneous “wet tongue” or mild salivation (Pavlovian response) and still do  years later when I see people drinking alcohol. Is this a “craving” for alcohol, do I still want to drink? Do I still have an “alcoholic mind?“. Did I do my steps properly?

It used to churn me up, these so-called alcoholics who had no physiological response to alcohol-related “cues”.

Part me also thought it was linked to addiction severity, how bad or chronic one’s alcoholism become, how far down the line or how low your rock bottom was? There may some validity in that observation.

It was partly because of mixed messages from alcoholics and from various medical doctors that I decided to take matters into my own hands and do some research into my alcoholic brain.

What I have discovered is that I have an “alcoholic brain” and not a “alcoholic mind” and there is a huge difference. So if there are people out there relatively new to recovery, listen up. For chronic alcoholics there is an automatic physiological response when we see cues such as other people drinking. Mild salivation, quickening heart rate etc. These are automatic, habitual, it happens to us rather than us wanting or willing it to happen. It happens unconsciously without our say so!

If you get a “wet tongue” i.e. you mildly salivate, then this is what happens when you have crossed the line into chronic alcoholism. Loads of studies have shown there is this automatic response and have also shown there is also an attentional bias to alcohol cues. We notice alcohol cues in the environment before anything else. They have a heightened “noticeableness”.

Have ever been in a new town and counted the number of drinking establishments automatically or had a heightened awareness of half drunken bottles of alcohol lying in the street? This is an attentional bias, we notice alcohol related stuff before anything else.

Some researchers in science call this a craving. I disagree. I call this an physiological urge, distinct from craving. I think a craving is more akin to a “mental obsession” about alcohol. Alcohol has only had ‘luring’ effect on me while very emotional distressed or in the early days of recovery I was very scared that  I would drink but, looking back, I never had any desire to.

It is hugely important for recovering persons that we distinguish between urges and craving, in a clear manner that science seems to have been unable to do! Lives can depend on this. We are so vulnerable in early recover that we need sound direction on what is happening to us automatically and what we are encouraging to happen, consciously.

An urge for me is a physiological response to cues, external and internal (e.g. stress). A craving is different but interlinked.

Let me explain. If I have an urge and it becomes accompanied by automatic intrusive thoughts such as a drink would be nice, and maybe a suggestion on where to get this drink, this does not mean I want a drink. It is simply automatically prompted intrusive thoughts, the type of thought I used to get all the time and so became habitual, stored away in an automatized addiction schema or addiction action plan.

If I realize this and simply let these thoughts go, i.e. do not react to them, then they lessen and dissipate altogether.

This is not a craving. I have not consciously and emotionally engaged with these intrusive thoughts (although we often do in early recovery when they scare the life out of us!).

If I consciously engage, emotionally react, to these thoughts either because I want a drink (elaboration of these thoughts as in embellishing a desire state) or the thought scares the life out of me (averse reaction) I can end up in a mental obsession. If in recovery, we try to suppress these thoughts then they will come back stronger than before which will raise  already high stress levels and recruit a whole host of memories of why I should drink, with who, where, and how much I will enjoy it. They will also activate an Alcoholic Self Schema (different to the recovery self schema still being formed in early recovery).  Then I have a memory Hydra effect where attempting to suppress this terrible flowering of desire based memories or to cut off the heads of these thoughts and memories leads to them increasing and increasing.

 

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Then there are lots of these memories driving you crazy and scaring the life out of you.  And this is in someone who does not want to drink but wants to remain in recovery!!? The other guy who is embellishing these thoughts is kinda thinking about drinking or toying with the possibility, so but again he is reacting cognitively and consciously to these intrusive thoughts. He is elaborating on them. He is using a different more cognitive part of the brain and a different memory system to those activated when he was simply having unconscious, habitual, automatic intrusive thoughts. He is now involved in this process rather than it simply happening to him.

So what I am saying is that there is no simple urge state that automatically leads to drink. We have to cognitively and emotionally react to it.

In my time in recovery, I have rarely heard of or witnessed  someone lured siren-like by a cue to a drink and when I have it is because he wanted to drink really, was testing their alcoholism, or e was in huge emotional distress and went “to hell with it!”

As we will see in later blogs, stress and cues certainly do not mix but again there is still a cognitive-emotional reaction which mediates between an urge and a relapse!

What is craving – do neurobiological accounts explain relapse in recovering alcoholics? Pt 2

If you want to drink, you will. It you do not, and depending on your regulation of emotions and stress, you may still relapse, even if one never intended to drink again.

In our previous blog we looked at automatic physiological response to cues that alcoholics appear to experience. These habitual responses are well explained by reinforcement, conditioning or neurobiological models of addiction.

However, do these neurobiological models predict relapse in abstinent alcoholics and addicts? In other words, do recovering alcoholics act and react to cues and have the same attentional bias, i.e. are they lured siren-like to alcohol or drug cues like lemmings to a drink or a drug or are there more  cognitive-affective processes at work in the craving than these models suggest!?

Does the mind play a role in transmuting these physiological urges into “craving”.

When I have seen a new comer to recovery craving they do not seem to walk around like a robot, salivating and rubbing their sweaty hands together. I have seen that when I was in active drinking and was like that innumerable times myself while under the spell of this “fleshy hunger” called having a pathological urge for a drink.

I am not downplaying this urge state, it is quite horrendous, it is like craving a glass of water after days in the desert. It feels like your very life depends on it, in other words. It can be a life or death feeling.

 

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In recovery, this urge state becomes more complicated and various other brain regions may become involved in this “craving” and there may be a interplay between regions rather than regions simply acting in concert – we will explore this more in series 3 of this theme of “craving”.

For now we examine how well do neurobiological accounts (i.e. accounts which focus primarily on impairments in neurotransmitter and stress systems and brain function in areas which create a cascade of ‘knock on’ impairment and dysfunction in areas of the prefrontal cortex which deals with cognitive control of behaviour with resultant dysfunction in areas which deal with reward, motivation stress and emotional response and more motoric, habitualized action) predict behaviour in abstinent, treatment seeking individuals?

Here we simply consider how well aspects of these theories, such as the ideas relating to craving (urge) via cue reactivity (an attentional bias towards alcohol and drug associated cues in the environment)  and positive memory associations for previous alcohol or drug use, relate to, or are relevent to the experiential reality of everyday recovering alcoholics and addicts.

In simple terms, it is the duty of science to attempt to predict behaviour, so how well do these models, especially the positive reinforcement model, predict the behaviour of treatment seeking abstinent alcoholics and addicts. 

Factors in relapse

Cues, external especially, which is a central part of positive reinforcement models, seem to be only one of various factors in relapse. They are present in a relatively small minority of studies or interact with other variables such as stress and negative affect (NA). So how well does this then validate this theory of addiction, when it is only present in a minor way in relapse and usually alongside stress and NA. Does this mean it plays a role when interacting with these variables of stress/NA. Does it play a role on it’s own?

I forward this question because the looking at an alcohol cue by an alcoholic even in recovery/abstinence invokes stress reactions such as anxiety or negative emotions such as anger, sadness ( ). Can we say there is a non-stress influenced cue-reactivity? Is there a purely dopaminergic cue reactivity? It doesn’t appear so.

In fact moving on from noting this intrinsic stress response in cue reactivity, various studies show that the highest high-risk relapse situations are negative emotions, testing personal control, social pressure, and urge and temptations  (1), that 62 –73% of relapse episodes were due to negative emotion and social pressure. Heroin addicts relapse primarily because of NE and lack of social supports. Mood state, along with social isolation and family factors, was more likely to be related to relapse incidences with a positive correlation between NE and alcohol-seeking behaviour. Thus the most commonly cited reason for relapse was negative mood states, consistent with previous studies of relapse factors (2).  Also reasons for relapse did not differ in relation to the primary drug of dependence (alcohol, methamphetamine, heroin), reflecting the commonality of relapse processes across diverse types of substances.

Marlatt (3,4) , views relapse as an unfolding process in which resumption of substance use is the last event in a long sequence of maladaptive responses to internal or extemal stressors such as negative emotional states, interpersonal conflicts, and social pressures. In fact negative emotional states ….coping, self-efficacy and stressful life events appeared to be of greater import in determining relapse than ‘cues’.

It would appear that cue associated stimuli plays a minor role in relapse, with stress and NA appearing to be a more important determinant of relapse. So conditioning models do not appear to give a comprehensive account of relapse and this may be particularly the case in abstinent, treatment seeking alcoholics.

How does conditioning methodology adequately explain this group?

Attentional Bias

Do treatment seeking alcoholic have the same attentional bias as non treatment seeking active alcoholics?

In fact, studies seem to show a negative attentional bias in alcohol-dependent patients that may be interpreted as an avoidance of alcohol-related stimuli.

Townshend and Duka (2007) propose that treatment seeking individuals have established active avoiding strategies and  are able to disengage their attention from alcohol cues (5). In fact is suggested that a positive attentional bias towards alcohol cues occurs when stimuli were presented shortly (50 ms), followed by a disengagement from alcohol cues in the 500 ms interval of cue presentation. This corresponds with a cognitive model of craving of Tiffany (6) where the 50ms may represent automatic approach before this automatic bias is interfered with by cognitive control, perhaps resulting in ‘craving’.

Does this visual approach–disengagement pattern reflect an  attentional bias which is appetitive or threat based? If there is avoidance are cues similar as  seen as in those with trait anxiety who have attentional bias for threat-related cues (7). A large body of evidence indicates that aversive emotional states are associated with biases in cognitive processing and, specifically, with increased attentional processing of threat-related cues.Is this also how treatment seeking addicted individuals are responding to substance-related cues? It may that stress heightens the salience of attractiveness of the cues so that abstinent individual relapse because of stress based response which makes relapse via internal and external cues a solution to their chronic stress/emotional distress?

Or it may be that relapse is based on difficulties coping with the manifestation of chronic stress, emotional distress and that  relapse  is a more complicated process than simply being lured, siren-like, to relapse via cues.

In most of the relapses we have encountered it has been a ongoing build up to relapse. There has been a period of emotional dyregulation whereby individuals get more and more distressed, often in inter-personal relationships, and have a “to hell with it!” relapse to relieve escalating emotional distress and the distorted thinking that goes with it. It is not due to automatic or motoric proceses, it is mediated via affective-cognitive mechanisms and this is why the information processing model, with some modifications, appears to explain craving and relapse more satisfactorily.

If you want to drink, you will, it you do not, and depending on your regulation of emotions and stress, you may still relapse, even if one never intended to drink again, due to the torturous intrusive thoughts which accompany this cognitive and emotionally based “craving”, more akin to the “mental obsession ” of AA’s Big Book than purely physiological urges.

References

1. El, S., Salah El, G., & Bashir, T. Z. (2004). High-risk relapse situations and self-efficacy: Comparison between alcoholics and heroin addicts. Addictive behaviors29(4), 753-758.

2.  Hammerbacher, M., & Lyvers, M. (2006). Factors associated with relapse among clients in Australian substance disorder treatment facilities. Journal of substance use11(6), 387-394.

3. Marlatt, G.A. (1978) Craving for alcohol, loss of control and relapse: Cognitive behavioural analysis. In: Nathan, P.E., Marlatt, G.A., and Loberg, T. eds. Alcoholism: new directions in behavioural research and treatment. Plenum Press, New York, 271-314.

4. Marlatt, G.A., and Gordon, J.R. (1985). Relapse prevention: maintenance strategies in the treatment of addictive behaviors. Guilford  Press, New York.

5. Townshend JMDuka Attentional bias associated with alcohol cues: differences between heavy and occasional social drinkersPsychopharmacology (Berl)2001;157:6774.

6. Tiffany, S. T. (1990). A cognitive model of drug urges and drug-use behavior: role of automatic and nonautomatic processes. Psychological review97(2), 147.

7.  Bar-Haim, Y., Lamy, D., Pergamin, L., Bakermans-Kranenburg, M. J., & van IJzendoorn, M. H. (2007). Threat-related attentional bias in anxious and nonanxious individuals: a meta-analytic study. Psychological bulletin133(1), 1.

8.  McCusker CG  Cognitive biases and addiction: an evolution in theory and methodAddiction 2001;96:4756.