Reasons for Relapse

One Christmas I nearly relapsed!

Posted on by alcoholicsguide

 

One Christmas I nearly relapsed!

by alcoholicsguide
“One Christmas, I nearly relapsed. I did not wish to relapse, in fact I would rather put a gun to my head and blow my brains out! Nonetheless, I was indeed about to relapse. It seemed urgently inevitable.
The emotional distress I had suffered all over Christmas, prompted by sad unresolved feelings about my deceased parents’s had built up, aided by a few bitter arguments with my frustrated wife, into into a sheer, blind terror.
Somehow I had the sense to shakily climb the stairs to the top of the house to tell my wife that I was in trouble.My wife’s facial expression quickly flickered from hurt to heightened concern. She could tell by my quivering voice and ashen complexion that I was in trouble. I shakily walked over to sit near her. Out of the corner of my eye I could see a bottle of white spirits, which glowed invitingly with some spiritual lustre.
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My attention seemed ‘locked into’ this bottle of spirits. Somewhere there was voice in my head saying “You could drink that, soon get rid of this terror”
My wife had been trying to talk to me, get through to me. I looked at her. I recognised her face but couldn’t remember her name or the fact she was my wife. My wife and I couldn’t remember her name!!? What the ….? I was consumed with a rampant rampaging terror that flipped by guts. Hallucinatory terror.
I was going to drink the white spirits. I have never drunk white spirits during my active alcoholism but had heard of plenty of alcoholics who had, and their wife’s perfume and many other such unthinkable liquids. It had, via these accounts, become a viable option. Something I could drink if need be!
It seemed like this was one of those moments.
“What do you normally do?” was all I heard. What? “What do you mean, what do I normally do….?” I hesitantly replied in a hushed almost child-like voice. “When you are like this, what do you normally do?” her voicing becoming more urgent . I could see the white spirits glisten and almost feel it evaporate, on my tongue, harshly as it deeply burnt my chest with a warm reassuring heat, move glowingly outwards from there in little dendritic branches of smoothing warmth and the whispering promised of blessed relief and good cheer. When alcoholism whispers sweet nothings it is sweeter than your lover.
“You better drink it” sounded in my head. I couldn’t remember what I normally do, or who was this asking this I head was jumbled and terrified. “You’d better do it”, the internal voice insisted. All I could feel was huge surges of stress chemicals pulsating through my veins like little scuttling manic spiders, speeding through my veins, up and down the insides of my legs, my limbs, scurrying frantically.
For some inexplicable reason, I thought, or a thought occurred to me “once I would have thought this a massive craving!” but now I felt I knew better. This wasn’t an appetitive craving, I didn’t fancy a wee drinky winky, wouldn’t that be nice.
I knew this was a stress based urge and nothing to do with desire. Nonetheless, I would kill for a drink, but paradoxically I didn’t even want one!? It wasn’t for pleasure but to escape this escalating aversion.
I knew somewhere, and know more now, that the stress chemicals swirling around my nervous system were activating my reward (or survival) brain systems. I knew it because I had read about it. Many, many times. Enough times. Stress and emotional distress activated the inner beast.
Massive amounts of stress and distress cuts off the action outcome memory, the explicit memory, the remembering of knowledge of what I would normally do in this type of situation, the “what do you normally do in this situation?” my wife had implored me to recall. It was completely cut off, I couldn’t get to it, access it. It might as well have belonged to someone else.
In there, in that explicit memory, was my wife’s name and other life saving stuff like what I normally did when faced with inevitable relapse, apart from staring at a bottle of spirits and salivating!
Stuff like the tips of recovery that I had learnt so proficiently that they were ingrained in my explicit memory, for occasions such as this one!?
Some of this recovery memory had become habitualized in my implicit memory too, thank God. It was this memory that had prompted me to climb the stairs to my wife’s help on my uncertain legs. To automatically ask for help. This was implicit recovery.
The very memory I could now not access now was explicit, because the excessive stress had cut if off. The what to do now I have asked for help memory. I knew this from my research as well. The “flight or fight “mechanism, a cascade of noradrenaline, the actions of chronic stress on switching explicit to implicit memory from the action outcome to the stimulus response, to the compulsive automatised, you see it and then you do it, memory. The stimulus response memory.
The distress was the stimulus and drinking to alleviate it would be the response. Your life can depend on this memory, like when fleeing an approaching tiger, so it does not ease it’s grip on your mind too readily or easily. This is the memory with no insight of future negative consequence. It acts now and too hell with the later consequences. The “let’s deal with this now!” memory, not later.
The “what I usually did as a chronic drinking alcoholic during extreme moments of distress”, a compulsive action hardwired into my brain. I drank alcohol previously at such prompting. It had become a unpremeditated, compulsive reaction to distress. It was how I survived back then. But then was now.
Not only did it shut off my escape route via my explicit memory and knowledge of how to get out of this life threatening crisis but it locked me into “your life is in danger, act without thinking, just do the thing your have normally done over the past 25 odd years” routine.
It showed me fleeting images of doing it before, drinking, in case I had forgotten, floating airy glimpses of the people I did it with and where, when, and whispered to me that this this person was actually the real me. Not this quivering sober fraud, in this torturous alien sober reality. That I was kidding myself.
The response was positively motoric. Get up and go over there and…drink! Lots! I could feel my legs stiffen and steal themselves.
Drink, although you would rather kill yourself than drink. Where was the choice there in this? Where had it gone, disappeared with my explicit memory no doubt? As my wife further implored me to do something, the voice in my heading was now screeching orders at me “Drink now!” “Drink now or you..will, die!!!” Drink for God’s sake, drink!!”
So it wasn’t to be a case of I will relapse because “hey one will not hurt” sort of reasoning, rationalising and justification. I was being implored to drink because my life was at risk if I did not!! I could die. I could die if I didn’t!
How badly is an alcoholics reward/survival system hijacked…usurped when this brain is imploring him to do the very thing that will kill him? And in order to help, save him from this nightmare, help him survive like some psychotic caregiver would suggest. How far down the road from full cognitive control over one’s behaviour had I gone.
Answer: about as far as I could go! How much stress surges through the alcoholics brain to close down the mnemonic survival kit. When you can’t access your “recovery” survival kit, the old alcoholic one kicks in! The alcoholic self schema overrides the recovering alcoholic schema.
I slumped to my knees and implored through tear blurred eyes for help from somewhere. I gave in profoundly, I was beat. I surrendered. The stress retreated like waves scuttling away from a beach. All action stations became deactivated and the red swirling light in my head and the honking siren turned off. I was emotionally traumatised but still sober.” An abbreviated excerpt from “How Research Helped Save My Life” 
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I had given up on the idea that I, my self, could solve this terrifying dilemma. The answer was outside of my self, my survival network, it was in letting go. Letting go of the distress and all the brain regions it was activating; memory, attention. emotion, reward/survival. It is regions that make up the self that are taken over in the course of alcoholism. The self can no longer be fully trusted in matters such as these. It needs to escape to brain regions outside of self or to the helping arms and reassurance of someone who knows how to help, and external prefrontal cortex of reason. One armed combat with the self will end up in crushing defeat. At certain times we are beyond our own mental control.
                                            ———————–
This ancedotal evidence highlights why research is essential to the effective treatment of alcoholism and addiction as it clearly shows the neural mechanisms implicated in relapse in chronic addiction. Altered stress systems (and their affective manifestation of emotional distress) hijack memory systems. In “offlining” the prefrontal cortex and the explicit memory of the hippocampal region it makes it very difficult to access “recovery tools” and prevent relapse.
It is only in clearly understanding these mechanisms can we seek to prevent the very high level of relapse in these clinical groups. We have to fully understand the problem before we can effectively deal with it.
We have shown via this “case study” how one can almost relapse when one has no desire ever to drink again, we have shown how it is emotional distress that precipitates and prompts this type of relapse.
We have seem how the “self will” is greatly limited and the regulation of self usurped by the impact of stress systems on reward/motivation, attention, affective and memory systems. Systems all essential to regulating one’s behaviour.
Thus treatment may find it more profitable in addressing measures to alleviate distress, increase stress and emotional coping strategies and improve the emotional regulation that is key to recovery.

A Cognitive Model of Craving – Pt 3

Posted on by alcoholicsguide

In an earlier blog we asked the question whether  neurobiological or “conditioning” or reinforcement models of craving predict relapse in abstinent alcoholics and addicts?

For us this is the most essential question. How do we explain relapse in those individuals motivated to remain abstinent, especially when they have followed some form of treatment, including 12 step groups.

We have seen that most relapse seems to be prompted by psychological stressors such as interpersonal relationships and the failure to cope with these.

This is very different to conditioning or reinforcement models that simply posit that people relapse because of the lure of alcohol or drug related stimuli, “cues”, or cues in the presence of stress or negative emotions, which we believe does have some affect.

Equally we have shown that in treatment seeking individuals there seems to be an automatic avoidance of cues so attentional bias does not really apply to this group plus there is a negative memory association bias in this abstinent, treatment seeking group also. So why do these people relapse?

What is the craving process prior to relapse for this group? . This is hugely important as neurobiological accounts do not predict relapse, so what does?

Over the next two blogs we will forward a model of craving or “mental obsessing” which we believe more accurately models the mechanisms which lead these individuals committed to staying sober and in recovery to relapse.

Ultimately we believe it may the maladaptive cognitive-affective reaction to naturally occurring  intrusive thoughts about alcohol or drugs (which are also the function of emotional dysregulation) that creates a proliferation of such thoughts, until they become obsessive, and which escalates stress and emotional distress to such an extent that the individual relapses to silence these tortuous obsessive thoughts.

These thoughts may not always be about alcohol or drugs. They may also contain negative perceptions of self, such as low self esteem and negative self schemas as the consequence of abusive early childhoods. These may result in “I am not good enough” thinking or “to hell with it!” relapse which have little to do with an appetitive urge to drink as in some reinforcement models. They are more akin to escape from self.

So models of addiction tend to focus on neurobiological substrates underlying addiction rather than on how affective (and cognitive) processing mediate addictive behaviours (1) although 80% of problem drinkers after outpatient treatment reported drinking episodes aimed at manipulating thoughts or emotions (2), with the majority of treatment clients attributing their relapse to interpersonal stress or negative emotions (3).

Also the involuntary retrieval of drug related thoughts is a hallmark of addicted populations. Over 70% of smokers stated that urges disrupted their thinking or functioning (4). Intensity of obsessive thoughts about alcohol predict relapse rate (5), with addicts motivated to use drugs to “silence” obsessive thoughts (6).  The idea that abstinence automatically decreases alcohol-related thoughts is challenged by research and supported by clinical observation that among abstinent alcohol abusers, alcohol-related thoughts and intrusions are the rule rather than exception (7).

So if emotion regulation difficulties and related intrusive thoughts are so prevalent in recovering abstinent addicts and alcoholics how do we account for this in a satisfactory and comprehensive theory of craving?

One study important to the conceptual framework set out here (6) used heart rate variability (HRV) measures, as a putative index of emotional regulation, to illustrate how craving involves cognitive-emotional processing and how conditioning models may not fully explain  ‘craving’.  This is consistent with the increasing concern in the literature about the applicably of such “one-dimensional” conditioning models explaining the results of cue reactivity studies (6). This study, among various findings, showed a link between HRV and obsessive thoughts,  in simple terms, the greater the emotional dysregulation, the greater the obsessive thoughts about alcohol.

It may even be that these “conditioning” reinforcement models or dopaminergic or stress-based models are describing “urges” rather than craving.  For us “craving” is distinct but interdependent on this “urge” state, it is partly triggered by it, if you like.

As an alternative to such passive “respondent” or “conditioning” models, some researchers have advocated the use of information-processing theory to understand how dependent individuals react in their encounter with “drug-related” cues (external and internal, e.g. stress or negative emotions) (6). Craving may thus be a different phenomenological experience to that of the physiological urges, although one may prompt the other.

According to one ‘info-processing’ view of craving, forwarded by Stephen Tiffany (4), ‘craving’,  occurs only when the automatic approach behaviour commonly seen in addicts in thwarted. This is particularly pertinent to those abstinent, treatment seeking individuals. In addiction, drug use behaviour develops various rituals around the seeking, preparation and consumption of drugs. These habitual procedures become stored in memory, in automatized action schemata  or action plans.

Encoded within these unitized memory systems are prompts such as external events (e.g. sight of a hypodermic syringe,) or internal events such as physical states (e.g. NA). Although activation of these memory structures may not be a sufficient for addicts to respond to ‘urges’, via actual drug seeking, they may stimulate approach behaviours.

Tiffany (1990) proposed “urges”, or what we call craving, are said to be associated with conscious efforts to inhibit the operation of drug use action plans (e.g. prevention of relapse or suppressive reaction to intrusive using-related thoughts). In abstinence, these “urges” involve non-automatic (i.e. conscious, effortful) cognitions that compete with automatic (unconscious effortless) drug use related plans. Thus, relapse may occur under two circumstances: when the action plan operates autonomously and when conscious processes to inhibit the action plan (thought suppression) backfire and are unsuccessful.

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We agree with Tiffany’s (1990) assertion that, like other stereotypic motor acts, some aspects of the drug-use ritual are susceptible to automatization. In fact in relation to automatic using schemas it is only the “nonautomatic” processing where cognitive resources are consciously devoted to disrupting the course of a perceive threat of relapse and prior experience of these self same affective states in the context of use that activate drug- and alcohol related memories (Bradizza, Stasiewcz, & Maisto, 1994.) and cause “craving”.

The “exhaustive and effortful” effects of “urges” (craving)  in abstinent addicts (Tiffany, 1990 p.158) may reflect consciously trying to inhibit these by thought suppression. Whereas, drug using schemas are firmly established and neurally embedded and require few resources to operate, the “abstinence plan” is poorly established and demands vigilance (i.e. attention) and effort to maintain. It is also a relatively new internal voice and not as familiar to the addict. Therefore, it not surprising that many addicts take the path of least resistance and relapse.

Addictive behaviours thus become increasingly automatic or compulsive in the addiction cycle, which supports Tiffany’s ‘cognitive’ model of automatic action plans. ‘Cravings’ are generated, in our model, by non-automatic, cognitive processes which are invoked to thwart (or interfere) with these drug use action plans.

For example, in abstinent addicts, internal stress/emotional distress provokes automatic action plans (and accompanying intrusive thoughts). These individuals then use non-automatic processing i.e. cognitive control/thought suppression) to ‘fight’ these threatening (naturally occurring) automatic thoughts.

The anterior cingualte cortex (ACC) acts a gateway between what is known as explicit (hippocampal) memory (remembered knowledge about things – e.g. where we drank, with whom, how it felt, noises, smells, atmosphere and ourselves in those situations etc) and implicit (dorsal striatal)  memory (the procedural, how to do memory-  the habitualised procedure of Tiffany’s automatic addiction action plans). The dorsal medial striatum (DMS) plays an important part orchestrating the switching between these memories through a “hippocampal-to-striatal pathway” passing through the ACC (41). It may be ACC hypofunctioning, under extreme stress, which aids transition between explicit and implicit memory networks (42).

Addiction severity is suggested as being represented by a shift in reward processing from ventral stiatum (VS) to DS (28) with this marked by an emergence of automatic thoughts, which the authors suggested as the cognitive thoughts and images of automatized drug action schemata (Tiffany 1990). As addiction escalates there appears to be a greater reliance on implicit rather than explicit (hippocampal) memory too. Also emotional distress is known to recruit the DS region also. So in effect the DS becomes involved in memory, reward and affect in later addiction.  So emotional dysregulation will not only provoke intrusive thoughts, but activate automatic approach behaviour, i.e. will prompt a movement towards getting and consuming drugs and alcohol.

Modell et al, 1992, distinguished between  intrusive thoughts – and memories – in a cognitive component to craving and in compulsions, which is more motoric and action component –  the cognitive component may be governed by the dorsal medial which has connections with the ‘associative’ PFC and lateral DS which is more involved in habitual motor activity As we have already discussed, addiction severity corresponds with the extent of obsessive thoughts as measured by the Obsessive Compulsive Drinking Scale (OCDS) which suggest that as the severity of this illness progresses, so does the intensity of the obsessive thoughts about alcohol and the compulsive behaviours to use alcohol. Kranzler et al. (1999) showed relapsers who scored higher in ‘obsessions’ craving measured by the OCDS predicted relapse in the 12 months after treatment completion. It is tempting to ad that emotional dysregulation also worsens as addiction becomes more severe(  ).

‘Cravings’ are thus generated by non-automatic, cognitive processes which are invoked to thwart (or interfere) with these drug use action plans.  The DMS may be very important in the relapse mechanism we are about to explore.

The DMS may have a potential role in cognitive control of behaviour flexibility and mediating behaviours by hippocampal guidance. As such the DMS and DLS may either compete (Misumori, Yeshenko, Gill and Davis, 2004) or cooperate (Devan, MacDonald, White 1999) under different conditions.  For example, DMS may be activated when a reversal of a previously reinforced response, i.e. habitual response, is required (Eichenbaum et al, 1989). Thus in attempting to inhibit stimulus response, i.e. the automatic alcohol approach behaviour of the DLS,    the DMS activates action-outcome pathways

Thus the ‘cognition and imagery of automatized schema’ becomes increasingly obsessive as the consequence of the anterior cingulate cortex (ACC) detecting conflict between memory intrusions and alerting the prefrontal cortex (PFC) to actively suppress unwanted thoughts (169). This only serves to intensify these thoughts as thought suppression ‘rebounds’ unwanted thoughts more intensely and prolifically into consciousness (170).

This, in abstinent addicts, appears to make the situation worse leading to greater stress reactivity and  need to further inhibit habitual response which activates even more action-outcome memory, e.g. the automatic activation of mental representations in associated memory networks of what course of action has normally been followed to affect the outcome of reducing this distress, i.e. which normally has been to drink.

Whereas the DMS normally in adaptive processes competes with the DLS to resolve a situation, for the abstinent addict, it only increases the problem by suggesting solutions which in fact make the situation more acutely adverse.

For the addict attempting to maintain abstinence, declarative memory and controlled processes may often be “corrupted” in service of promoting or rationalizing drug use. This will occur because negative affect is aversive and intrinsically primes escape and avoidance strategies.

Thus the ACC in recruiting explicit memory to counteract the automatic alcohol related thoughts of the DS may unwittingly be increasing memories of drinking and explicit prompts to drink as this is what has normally been the course of action in such situations of negative emotions.

The best and most well-intentioned efforts to remain sober/clean threaten sobriety most; producing a mnemonic ‘Hydra Effect’ whereby attempts to cut off this terrible flowering of intrusive thoughts leads to increased proliferation of these thoughts and accompanying emotional distress.

 

This, we posit, is what occurs in the mind of a recovering/abstinent alcoholic and is more akin to the “mental obsession” of the Big Book that purely neurobiological/physiological urge states.

Equally it should be noted that craving or mental obsession does not suggest that the alcoholic or addict in recovery/abstinence is actually motivated or even wants to relapse to former use. One can engage in this “mental obsession” or cognitive craving simply via a maladaptive emotional dysregulation whereby a defective emotional strategy such as thought suppression of threatening intrusive thoughts can set up a chain of reactions which lead to an unfortunate proliferation of thoughts and memories which promote alcohol and drug use to relieve escalating emotional distress which leads to relapse even if the alcoholic or addict in recovery did not even wish it! What else is this other than a craving beyond one’s mental (cognitive) control!

Relapse can happen to an alcoholic or addict if he does not manage his underlying condition of emotional dysregulation, in other words.

 

 

References (to follow)

1. Cheetham, A., Allen, N. B., Yücel, M., & Lubman, D. I. (2010). The role of affective dysregulation in drug addiction. Clinical psychology review, 30(6), 621-634.

2. Sanchez-Craig, M., Annis, H. M., Bronet, A. R., & MacDonald, K. R. (1984). Random assignment to abstinence and controlled drinking: evaluation of a cognitive-behavioral program for problem drinkers. Journal of consulting and clinical psychology, 52(3), 390.

3. Lowman, C., Allen, J., Stout, R. L., & Group, T. R. R. (1996). Replication and extension of Marlatt’s taxonomy of relapse precipitants: overview of procedures and results. Addiction, 91(12s1), 51-72.

4. Tiffany, S. T. (1990). A cognitive model of drug urges and drug-use behavior: role of automatic and nonautomatic processes. Psychological review, 97(2), 147.

5. Bottlender, M., & Soyka, M. (2004). Impact of craving on alcohol relapse during, and 12 months following, outpatient treatment. Alcohol and Alcoholism, 39(4), 357-361.

6. Ingjaldsson JT, Laberg JC, Thayer JF. Reduced heart rate variability in chronic alcohol abuse: relationship with negative mood, chronic thought suppression, and compulsive drinking. Biological Psychiatry. 2003;54(12):1427–1436.

7.  Hoyer, J., Hacker, J., & Lindenmeyer, J. (2007). Metacognition in alcohol abusers: How are alcohol-related intrusions appraised?

 

. Bradizza, C. M., Stasiewicz, P. R., & Maisto, S. A. (1994). A conditioning reinterpretation of cognitive events in alcohol and drug cue exposure. Journal of Behavior Therapy and Experimental Psychiatry, 25, 15 – 22

Modell, J. G., Glaser, F. B., Cyr, L. & Mountz, J. M. (1992) Obsessive and compulsive characteristics of craving for alcohol in alcohol abuse and dependence. Alcoholism: Clinical and Experimental Research, 16, 272–274.

. Kranzler, H. R., Mulgrew, C. L., Modesto-Lowe, V. and Burleson, J. A. (1999) Validity of the obsessive compulsive drinking scale (OCDS): Does craving predict drinking behavior? Alcoholism: Clinical and Experimental Research 23, 108–114.

(Misumori, Yeshenko, Gill and Davis, 2004)

(Devan, MacDonald, White 1999)

(Eichenbaum et al, 1989).

Don’t fight your thoughts!

Posted on by alcoholicsguide

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 Psychology, 108(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 Psychiatry, 54(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 Research, 31(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 review, 112(2), 446.

 

Do I still have an “Alcoholic Mind”!?

Posted on by alcoholicsguide

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

Posted on by alcoholicsguide

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.

 

PowerPoint Presentation

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 behaviors, 29(4), 753-758.

2.  Hammerbacher, M., & Lyvers, M. (2006). Factors associated with relapse among clients in Australian substance disorder treatment facilities. Journal of substance use, 11(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 JM, Duka T . Attentional bias associated with alcohol cues: differences between heavy and occasional social drinkers. Psychopharmacology (Berl)2001;157:67–74.

6. Tiffany, S. T. (1990). A cognitive model of drug urges and drug-use behavior: role of automatic and nonautomatic processes. Psychological review, 97(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 bulletin, 133(1), 1.

8.  McCusker CG  Cognitive biases and addiction: an evolution in theory and method. Addiction 2001;96:47–56.

What is craving?

Posted on by alcoholicsguide

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” 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?“.

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

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. Automatic, habitual, it happens to us rather than us wanting or willing it to happen. It happens unconsciously without our say so!

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.

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 so 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.

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, became stored away in an automatized addiction schema or addiction action plan.

If I realize this and simply  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.

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, were testing their alcoholism, or that he was in huge emotional distress and went to “hell with it!”. As we will see below, stress and cues certainly do not mix but again there is still a cognitive-emotional reaction which mediates between an urge and a relapse!

In the first of a four part series of blogs we discuss “what is craving?” and consider whether the emotional dysregulation we consider to be at the heart of alcoholism and addiction also plays a role in both craving and relapse.

We start this series by considering the neurobiological accounts of craving and will then consider how well these accounts explain craving and relapse in abstinent, treatment seeking, or recovering alcoholics and addicts.

Part 1

What is craving?

Craving persists years into abstinence (1).

Precise definitions of craving have remained elusive (2-5). Two general categories are based on conditioning and cognitive mechanisms (6) but are not mutually exclusive.

A Neuroadaptive Model of Craving – Scientists believe that a gradual and, perhaps, permanent adaptation of brain function (i.e., neuroadaptation) to the presence of alcohol is a central feature in the development of alcohol dependence (7,8).

Conditioning Models – The “conditioning” models posit that cues elicit the same physiological and psychological response as drug consumption itself  with these ‘respondent’ conditioning theories predicting that responses to drug-related cues either reflect aversive abstinence symptoms or mimic drug effects  have dominated explanatory models in cue reactivity studies (9).

The definition of addiction by the American Society of Addiction Medicine (ASAM) includes the terms craving and persistent risk, and emphasises risk of relapse after periods of abstinence triggered by exposure to substance-related cues and emotional stressors (10).

This conceptualisation points to the role of substance-related cues, e.g., environmental stimuli that are strongly associated with the effects of the administration of substances and acquire incentive salience through Pavlovian conditioning, as well as stress (an internal cue), as major determinants of relapse.

The Incentive Sensitisation (IS) Model (11), addiction is the result of neural sensitisation of reward circuits (centred in the ventral striatum (VS)) by the neurotransmitter dopamine. Positive reinforcement mechanisms lead to a non-associative learning process, referred to as sensitization, in which repeated confrontation with a substance-related cue (which acts as a reinforcer) results in the progressive amplification of a response (substance seeking).

This ‘sensitisation’ or hypersensitivity may be independent of negative withdrawal symptoms or an individual’s general negative emotional state and leads to compulsive substance-seeking and substance-taking. These mechanisms of positive reinforcement leave addicts vulnerable to relapse when confronted with substance-related cues that trigger a pathological “wanting”. In short, IS produces a bias of attentional processing towards substance-associated stimuli and a pathological wanting of alcohol or substances. Sensitisation and attentional bias have been demonstrated in various studies (12,13).

Negative reinforcement model of addiction Basic negative reinforcement models pose that addictive behaviour is the consequence of persistent negative affect (NA). This NA is associated with maladaptive changes in the brain’s stress and reward circuits, which leave addicts vulnerable to cue-associated stimuli prompting a desire to relieve their negative emotional states (14).

One prominent stress-based negative reinforcement model, the Hedonic Dysregulation (HD) Model, mainly associated with Koob and le Moal (14), In sum, the HD model posits that, in substance dependent individuals,  an overactive stress  axis creates a progressive allostasis in the brain reward systems which underlies transition from substance use to addiction and creates a persistent state of NA (altered and excessive stress) and emotional reaction to “cues”. These changes continue to persist even when an addicted individual experiences a state of protracted abstinence.

Persistent NA increases their incentive salience and desire to use substances in an attempt to relieve this NA.

Evidence for the involvement of both the reward and the stress system of the brain  comes from imaging studies of addicted individuals during withdrawal or protracted abstinence, which have shown decreases in dopamine D2 receptor density (hypothesized to reflect hypodopaminergic function) (15) as well as alteration in brain stress systems, such as increase in CRF and glucocorticoids (16).

These models to me appear to be describing urges based on cues and the effect of cues with stress/emotional distress. This last one can impact on recovery and relapse mentioned in another blog.

The question remains however whether these neurobiological models predict relapse in abstinent alcoholics and addicts?

 

References 

1.  Anton, R. F. (1999). What is craving. Alcohol Research and Health, 23(3), 165-173.

2. LUDWIG, A.M., AND STARK, L.H. Alcohol craving: Subjective and situational aspects. Quarterly Journal of Studies on Alcohol 35:899–905, 1974.

3. KOZLOWSKI, L.T., AND WILKINSON, D.A. Use and misuse of the concept of craving by alcohol, tobacco, and drug researchers. British Journal of Medicine 82:31–45, 1987.

4.  KOZLOWSKI, L.T.; MANN, R.E.; WILKINSON, D.A.; AND POULOS, C.X. “Cravings” are ambiguous: Ask about urges and desires. Addictive Behaviors 14:443–445, 1989

5.  SITHARTHAN, T.; MCGRATH, D.; SITHARTHAN, G.; AND SAUNDERS, J.B. Meaning of craving in research on addiction. Psychological Reports 71:823–826, 1992.

6. SINGLETON, E.G., AND GORELICK, D.A. Mechanisms of alcohol craving and their clinical implications. In: Galanter, M., ed. Recent Developments in Alcoholism: Volume 14. The Consequences of Alcoholism. New
York: Plenum Press, 1998. pp. 177–195.

7. Robinson, T.E., & Berridge, K.C. (1993). The neural basis of drug craving: An incentive-sensitization theory of addiction. Brain Research, 18, 247-291

8. Koob GF, Le Moal M. Drug abuse: hedonic homeostatic dysregulation. Science. 1997;278:52–58

9.  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.

10.  Morse RM, Flavin DK (1992). “The definition of alcoholism. The Joint Committee of the National Council on Alcoholism and Drug Dependence and the American Society of Addiction Medicine to Study the Definition and Criteria for the Diagnosis of Alcoholism“. JAMA 268 (8): 1012–4

11. Robinson, T. E., & Berridge, K. C. (2008). The incentive sensitization theory of addiction: some current issues. Philosophical Transactions of the Royal Society B: Biological Sciences, 363(1507), 3137-3146

12. Leyton M. Conditioned and sensitized responses to stimulant drugs in humans. Prog. Neuropsychopharmacol. Biol. Psychiatry. 2007;31:1601–1613.

13. Franken, I. H. (2003). Drug craving and addiction: integrating psychological and neuropsychopharmacological approaches. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 27(4), 563-579

14. Koob, G. F., & LeMoal, M. (2001). Drug addiction, dysregulation of reward, and allostasis. Neuropsychopharmacology, 24, 97–129.

15. Volkow ND, Wang GJ, Fowler JS, et al. Decreased striatal dopaminergic responsiveness in detoxified cocaine-dependent subjects. Nature. 1997;386:830–3.

16.. Koob GF, Le Moal M. Addiction and the brain antireward system. Annu Rev Psychol. 2008;59:29–53

An Emotional Disease?

Posted on by alcoholicsguide

Is Addiction an Emotional Disease!?

“Addiction”, is widely viewed as a chronic, relapsing, neurobiological disorder, characterized by compulsive use of alcohol or substances, despite serious negative consequences. It involves both physiological and psychological dependence and leads to the emergence of a negative emotional state.  The Diagnostic and Statistical Manual of Mental Disorders, DSM-5, combines DSM-IV categories of substance abuse and dependence into a single disorder, on a continuum from mild to severe.  The previous definition of addiction by the American Society of Addiction Medicine (ASAM) includes the terms, craving, persistent risk, and emphasizes risk of relapse after periods of abstinence triggered by exposure to substance-related cues and emotional stressors . This conceptualisation points to the role of substance-related cues, e.g., environmental stimuli that are strongly associated with the effects of the administration of substances and acquire incentive salience through Pavlovian conditioning, as well as stress (an internal cue), as major determinants of relapse.

For example in terms of the reasons for relapse implicated in much research, alcoholics relapse due to ‘cue-reactivity’ i.e. they see ‘people, places, or things’ associated with their drinking past and they are drawn to it and simply relapse.

 In some years of recovery, we have rarely heard of a committed abstinent alcoholic addict in recovery who relapsed simply because he/she was lured siren like to some cue associated stimuli. That is not to say cue reactivity is not a valid construct, it is obviously. Recovering alcoholics  exhibit an automatic, that is involuntary,  attentional bias towards drug and alcohol-related “cues”. This is a torturous aspect of early recovery thus most therapeutic regimes advise those in early abstinence and recovery to avoid “people, places and things” that act as  cue-associated stimuli. In fact, some in early recovery do challenge this only to learn painfully as the result by thinking they can spend time, like before, in drinking establishments,  only to find that it is “like sitting in a hairdressors  all day and not expecting to eventually get a haircut!”

A more recent  ASAM definition includes “Addiction is a primary, chronic disease of brain reward, motivation, memory and related circuitry. Dysfunction in these circuits leads to characteristic biological, psychological, social and spiritual manifestations. Addiction is characterized by inability to consistently abstain, impairment in behavioral control, craving, diminished recognition of significant problems with one’s behaviors and interpersonal relationships, and a dysfunctional emotional response.”

We appreciate the role now afforded to “dysfunctional emotional response” in this new definition as we believe it is dysfunctional emotional response which is at the heart of alcoholism and addiction.

Our own experience of recovery, coupled with our neuroscientific research over several years, has  made us curious as why the ways addicts and alcoholics talk about their condition or the explanations they forward all generally point to what they would call an “emotional disease” or “a parasite the feeds on their emotions”, an “emotional cancer” or a “fear based disease” yet these are rarely countenanced in any theory of addiction, whether neurobiological, psychological, psycho-analytical (although there have been very interesting ideas based on attachment within this methodology).

How could addicts and alcoholics be so wrong about themselves and what ails them? Especially when they see it also in hundreds of others with the same condition? We doubt that they are wrong, in fact, we have in recent years taken the opposite approach and started to explore, in terms of research, if addiction and alcoholism, especially, have their roots in emotional dysregulation and emotional processing deficits

In even more recent times, we have been encouraged that these difficulties also shape decision making difficulties, distress based impulsivity (leading to compulsivity) lack of inhibition across various psychological domains, as well as more revealingly the cognitive and executive dysfunctions and ‘flight or flight’ reactions which seem common to this group, over reacting in other words.

There appears to be a short term decision making profile which we suggest is distress based, which implicates more emotive-motoric “automatic,compulsive”regions of the brain rather than goal-directed. A more “let’s do it NOW!”way of making decisions.  This is also seen in children of alcoholics.

Could this be an important vulnerabilty to alcoholism? In order to get this debate going we will now consider whether there are possibilities for re-defining the DSM criterion in relation to the manifest difficulties observed in these clinical groups in relation to emotional dysregulation. The “official” nosology (e.g. DSM IV) is largely limited to physical manifestations of addiction although addicted individuals display additional psychiatric symptoms that affect their well-being and social functioning but which have been relegated to the domain of psychiatric “comorbidity.” 

Although the relationship of these psychiatric symptoms with addiction is very close, substance abuse may modify pre-existing psychic structures and lead to addiction as a specific mental disorder, inclusive of symptoms pertaining to mood/anxiety, or impulse control dimensions, decision making difficulties or, as we suggest, the various characteristics of emotional dysregulation. All of which suggests the current DSM based nosology of addiction-related mental comorbidity does not consider the overlap of the biological substrates and neurophysiology of addictive processes and psychiatric symptoms associated with addiction, so fails to include specific mood, anxiety, and impulse control dimensions and decision making difficulties in the psychopathology of addictive processes.

Addiction reaches beyond the mere result of drug-elicited effects on the brain and cannot be peremptorily equated only with the use of drugs despite the adverse consequences produced. Addiction is a relapsing chronic condition in which these psychiatric manifestations play a crucial role. Thus it may be that the aetiology of addiction cannot be severed from its psychopathological underpinning, it’s roots.  In may have been initiated by these mechanisms and also the addiction cycle may be continually perpetuated by them. Particularly in view of the undeniable presence of symptoms, of their manifest contribution to the way addicted patients feel and behave, and to the role they play in maintaining the continued use of substances.

In other words, the latter symptoms frequently precede the addictive process constituting a predisposing psychological background on which substance effects and addictive processes interact, leading to a full-fledged psychiatric disorder. Within the frame of the current DSM, numerous relevant psychiatric issues in substance abuse disorders may have been overlooked.   Even in the absence of psychiatric diagnosis, specific psychological vulnerabilities may constitute a background for the development of  disorders. The neural circuitry implicated in affective reactivity and regulation is closely related to the circuitry proposed to underlie addictive behaviours.  Affect is related to dysfunctional decision-making processes and risky behaviours,  In fact, we suggest these affective processing difficulties cause inherent decision making difficulties and constitute a premorbid vulnerability.

Substance dependence is associated with significant emotional dysregulation that influences cognition via numerous mechanisms. This dysregulation comes in the form of heightened reward sensitivity to drug-related stimuli, reduced sensitivity to natural reward stimuli, and heightened sensitivity of the brain’s stress systems that respond to threats. Such disturbances have the effect of biasing attentional processing toward drugs with powerful rewarding and/or anxiolytic effects. 

Emotional dysregulation can also result in impulsive actions and influence decision-making. It appears clear in addiction and alcoholism (substance dependence)  and that emotional processing significantly impairs cognition in substance dependence. Emotionally influenced cognitive impairments have serious negative effects with both the resultant attentional bias and decision-making deficits being predictive of drug relapse. 

The influence of emotion is clearly detrimental in substance dependence, and many of the detrimental effects observed are due to the ability of drugs of abuse to mimic the effects of stimuli or events that have survival significance. Drugs of abuse effectively trick the brain’s emotional systems into thinking that they have survival significance!

They trick the alcoholic into thinking he needs to drink to survive! 

It is important to note that the neural mechanisms implicated in neurobiological accounts of the transition to endpoint addiction from initial use are also experienced emotionally in human beings, in addicted individuals. That human beings, addicted individuals have to live with these profound alterations and impairments of various regions and neural networks in the brain. And that it is in treating these human manifestation of this neurobiological disease, i.e. one’s “dysfunctional emotional responses” in every day life that is required for long term recovery. We have to manage the emotional difficulties which perpetuate this disease, this “parasite on our emotions”, otherwise these dysfunctional overwhelming emotions manage us.   

It is through this emotional dysregulation that the addiction cycle is experienced and via emotional means perpetuated! It is through living “emotionally light” and spiritually aware lives which help manage our emotions that perpetuate our long term recovery.

Emotional distress is at the heart of addiction and alcoholism, and relief from it on a continually, daily basis is at the heart of recovery.    

References

American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders (Fifth ed.). Arlington, VA: American Psychiatric Publishing. pp. 5–25.

Pani, Pier Paolo, et al. “Delineating the psychic structure of substance abuse and addictions: Should anxiety, mood and impulse-control dysregulation be included?.” Journal of affective disorders 122.3 (2010): 185-197.

Murphy, A., Taylor, E., & Elliott, R. (2012). The detrimental effects of emotional process dysregulation on decision-making in substance dependence. Frontiers in integrative neuroscience, 6.

Cheetham, A., Allen, N. B., Yücel, M., & Lubman, D. I. (2010). The role of affective dysregulation. in drug addiction. Clinical Psychology Review, 30(6), 621-634.