relapse

From a Drinking Problem to a Thinking Problem?

 

In early recovery I was amazed that some people in recovery said they never thought about alcohol after a few weeks into recovery. Or rather than thoughts related to alcohol rarely drifted across their minds.

I was alarmed by this as thoughts of alcohol rarely left my mind in early recovery.

They came to me rather than me actively going to retrieve thoughts about alcohol myself, consciously or deliberately.

I now realise that this was due to two main reasons.

First of all, fear of drinking is a distress which activates thoughts of alcohol as distress and negative emotions (and negative self perception/schema) seem to automatically retrieve thoughts of alcohol as there has been some habitual fusion of negative emotion with urge to drink in the alcoholic brain.

This is because my alcoholism resulted in compulsive drinking, i.e. my drinking was mainly to do with relieving distress, and that is what compulsion is, automatic behaviours that relieve distress.

Secondly and tied to this point, is that this compulsive drinking in itself is also linked to how chronic my drinking became.

I was completely addicted to alcohol at the end of my drinking so my alcoholism is very chronic.

In terms of neuroscience this means any distress activates a motoric part of my brain, the dorsal striatum,  a part of the brain that deals with stimulus response or automatic response the internal stimulus of distress, which activates an automatic approach or preparation of movement towards getting a drink.

This is expressed in terms of instruction in the brain as automatically occurring intrusive thoughts about drinking alcohol. This is also called an alcohol use schema because as a schema it is procedural way to deal with distress, i.e. have distress automatically deal with it by drinking.

I still find it fascinating that even automatic behaviours have thoughts that accompany them. Although nothing is completely automatic and we have a brief period of time in which to react or not.

By not reacting or acting on this thoughts they appear to lessen in intensity.  The more we do not react the less intense these thoughts become. Finding new ways to cope with distress lessens their grip on us too and eventually they practically disappear.

I have found I have to be very very distressed in recovery for thoughts of alcohol to come revisiting my mind.

This involuntary retrieval of drug related thoughts is thus a hallmark of addicted populations as it happens automatically, implicitly without you having to consciously and explicitly retrieve these thoughts and associated images from your memory banks. They just pop up without your permission.

The intensity of obsessive thoughts about alcohol is said to predict relapse rates (1), with addicts motivated to use drugs to “silence” obsessive thoughts (2).

The idea that abstinence automatically decreases alcohol-related thoughts is challenged by research (3) and supported by clinical observation that among abstinent alcohol abusers, alcohol-related thoughts and intrusions are the rule rather than exception (4).

Modell and colleagues (1992) highlighted symptomatic similarities between addiction and obsessive compulsive disorder with subjective craving for drugs or alcohol characterized as having obsessive elements. (eg, the compulsive drive to consume alcohol, recurrent and persistent thoughts about alcohol, and the struggle to control these drives and thoughts) similar to the thought patterns and behaviours of patients with obsessive-compulsive illness (5).

Modell et al. also point to the potential similarities in underlying neural pathways implicated in the two disorders, suggesting that they may share a similar aetiology.

The Obsessive Compulsive Drinking Scale (OCDS) implies 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 (6).

This may also be a reflection of addiction severity too! As addicts and alcoholics become more addictive brain imaging shows a shift in “reward processing” from the ventral striatum to the dorsal striatum.

The DS as stated above is in charge of more automatic, compulsive reaction.

This shift from VS to DS  may also be marked by an increased emergence of automatic thoughts, which the authors also suggested as the cognitive thoughts and images of automatized drug action schemata (2).

In fact, this is demonstrated by correlations indicating that dorsal striatum activation is lowest in participants with low OCDS scores. And vice versa, highers OCDS scores with increased DS activation.

 

This means, in simple terms, that more severe addiction may be associated with more intrusive/obsessive thoughts and less severe with less thoughts.  

So if you are in a meeting or in other treatment environments and someone in recovery says they never have any obsessive thoughts or intrusive thoughts consider the possibility that their addiction did not become as severe as your addiction?

Either way these thoughts are not your own but the automatic thoughts of addiction so be careful not to react to them.

They are frightening at first, but gradually becoming irritating and annoying before occurring less and less as recovery and your non reaction progress.

If you learn to habitually not to react emotionally to them they start to lose their grip and become less severely intrusive.

Most days I do not have any intrusive thoughts. This is because my recovery has progressed.

In many ways, recovery usually goes in the opposite direction to addiction.

References

1.. 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.

2. 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.

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

4. 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.

5. 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, 266-271.

6. 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.

7. Vollstädt‐Klein, S., Wichert, S., Rabinstein, J., Bühler, M., Klein, O., Ende, G., … & Mann, K. (2010). Initial, habitual and compulsive alcohol use is characterized by a shift of cue processing from ventral to dorsal striatum.Addiction, 105(10), 1741-1749.

 

 

 

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).

 

Image

 

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 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.

 

Gambling Disorder and Emotional Dysfunction

Following on from our recent blog on emotional dysfunction in sexual addiction we continue our series which explores the inherent role of  emotional dysfunction in all addictive disorders.

We will explore eating disorders later.

Here we use excerpts from a very interesting article (1)  on

Deficits in emotion regulation associated with pathological gambling.

 

“Pathological gambling is recognized as an impulse-control disorder characterized by a loss of control over gambling, deception about the extent of one’s involvement with gambling, and significant family or job disruption (American Psychiatric Association, 1994). Failures in self-control, therefore, represent a defining feature of pathological gambling. Self-control involves over-riding impulses by substituting another response in its place (Tice & Bratslavsky, 2000), and failures in self-control are primarily associated with the desire for short-term gains despite associated long-term negative consequences (Baumeister, 1997, Baumeister, Heatherton, & Tice, 1993).

Failures in control over gambling are likely to be influenced by individual coping styles. Problem-focused coping includes active and effortful problem solving, while emotion-focused coping includes escape and avoidance behaviours (Lazarus & Folkman, 1984). Scannell, Quirk, Smith, Maddern, and Dickerson (2000) suggested that loss of control over gambling is associated with emotion-focused coping such as avoidance or escape. This suggestionhas been supported by evidence that gamblers demonstrate deficits in coping repertoires (McCormick, 1994) and some rely on gambling to provide an escape from personal or familial problems (Corless & Dickerson, 1989; Lesieur & Rosenthal, 1991). Finally, in a sample of adolescent gamblers, those identified as at-risk for developing pathological gambling behaviours were those who exhibited more emotion-focused coping styles
(Gupta & Derevensky, 2001).

Gambling behaviours, therefore, seem to be associated with a deficit in self-control
processes that may be exacerbated by reliance on coping styles characterized by
avoidance and escape. At a more basic level, difficulties managing emotions effectively may contribute to the use of maladaptive coping strategies and result in failures in self regulation and impulse control. Optimal self-regulation relies on being able to focus on long-term goals in the presence of emotional distress that tends to shift attention to the immediate present (Tice & Bratslavsky, 2000). In addition, struggling with one’s feelings may deplete coping resources and leads to decreased self-control (Baumeister, Muraven, & Tice, 2000), leading to increased risk of disinhibited or impulsive behaviour.

Finally, individuals who are feeling acute emotional distress will likely wish to escape via activities that promise immediate pleasure (Tice, Bratslavsky, & Baumeister, 2001) and pathological gamblers often report using gambling to escape from negative mood states (Blaszczynski & McConaghy, 1989; Getty, Watson, & Frisch, 2000).

Emotion regulation refers to strategies to influence, experience, and modulate
emotions (Gross, 1999). Although there are several factors that influence whether a
certain emotion-regulation strategy is adaptive in a particular situation, certain strategies appear to be costly and maladaptive. For example, suppression or avoidance of emotions is associated with increased negative effect and anxiety, physiological activity, and physical pain (Campbell-Sills, Barlow, Brown, & Hoffman, 2006; Gross & Levenson, 1997; Levitt, Brown, Orsillo, & Barlow, 2004; Masedo & Esteve, 2007). Experimental investigations also support the notion that the effort of suppressing emotions drains mental resources (Richards & Gross, 2000), which could lead to decreased self-control.

Ricketts and Macaskill (2003) investigated several techniques that gamblers use to
modify their emotions, one of which was the technique of ‘shutting off’ or using gambling in order to stop an unpleasant emotional state. Participants receiving treatment for gambling were interviewed or watched during treatment sessions and administered questionnaires. Patients who used the technique of ‘shutting off’ were often the ones who also reported poorly tolerating emotional discomfort (Ricketts & Macaskill, 2003).

According to Baumeister, Zell, and Tice (2007), emotional distress leads to an increase in self-awareness, which consequently leads to a desire to decrease ones self-awareness, but at the cost of self-regulation. If one is unable to self-regulate, this could lead to an addiction or a relapse of an addictive behaviour (Sayette, 2004).

Impulse control represents one of the major behavioural aspects of emotion regulation (Gratz & Roemer, 2004) and has been identified as an important component of addictive processes (Evenden, 1999). More specifically, research has demonstrated that failures of emotion regulation are associated with addictive behaviours (Coffey & Hartman, 2008; Fox, Axelrod, Paliwal, Sleeper, & Sinha, 2007; Goudriaan, Oosterlaan, De Beurs, & Van Den Brink, 2008; Lakey, Campbell, Brown, & Goodie, 2007).

Several recent studies have employed the Difficulties in Emotion-Regulation Scale (DERS), a recently developed and validated measure of emotion regulation, in assessing behavioural addictions (Bonn-Miller, Vujanovic, & Zvolensky, 2008; Fox et al., 2007; Fox, Hong, & Sinha, 2008). The DERS assesses both general deficits in emotion regulation and deficits in specific domains of regulation. It is based on a model of emotion dysregulation that includes: (1) deficits in awareness and understanding of emotional experience (i.e., clarity), (2) minimal access to strategies to manage one’s emotions, (3) non-acceptance of emotions (i.e., reactivity to one’s emotional state), and (4) impaired ability to act in desired ways regardless of emotional state (i.e., impulsivity and an inability to engage in goal-directed behaviour).

The goal of the present study was therefore to examine emotion regulation difficulties among individuals being treated in a specialist gambling clinic and
to compare the use of strategies to a mixed clinical comparison group and a sample
of healthy community controls. Specifically, we investigated the association between
emotion-regulation deficits and gambling pathology using two measures of emotion
regulation, the DERS and the Emotional Regulation Questionnaire (ERQ; Gross & John, 2003). The ERQ examines the habitual use of two specific emotion-regulation strategies, namely expressive suppression and cognitive reappraisal. The use of suppression reduces the outward expression of emotions in the short term, but is less effective in reducing emotions in the long term and is, therefore, considered a maladaptive emotion-regulation strategy (Gross, 1998; John & Gross, 2004). Cognitive reappraisal involves changing the meaning associated with a particular situation so that the emotional impact is altered (Gross, 1999; Siemer, Mauss, & Gross, 2007). Reappraisal is considered an adaptive strategy to regulate one’s internal states and is associated with higher self-reported positive emotions and fewer depressive symptoms (Gross & John, 2003; Mauss, Cook, Cheng, & Gross, 2007).

gambling-slots-cover (1)

 

 

Discussion

As expected, we found a significant relationship between self-reported problem,
gambling behaviour, and negative effect as measured by the DASS, as well as deficits
in emotion regulation as measured by the DERS.

With respect to group differences, the gambling group reported a greater lack
of awareness of their emotions compared to both comparison groups.

With respect to the overall findings of emotional dysregulation, Blaszczynski and
Nower (2002) proposed a pathway model of the determinants of gambling and identified three separate trajectories into problem gambling. Of relevance to the current study, the authors identified an emotionally vulnerable group of problem gamblers who used gambling as a way to regulate affective states by providing either emotional escape or arousal.

According to the pathway model, once a habitual pattern of gambling behaviours has been established, the combination of emotional vulnerabilities, conditioned responses, distorted cognitions, and decision-making deficits maintain the cycle of pathological gambling. Blaszczynski and Nower (2002) suggest that such emotional vulnerabilities make treatment more difficult in this particular group of gamblers and emphasize the need to address these underlying vulnerabilities in addition to directly targeting gambling behaviours in therapy. It may, therefore, be of therapeutic benefit to specifically assess for and target emotion-regulation strategies in this population of gamblers.

Given the gamblers in the current study demonstrated limited access to effective strategies for managing difficult emotions, it may be important for clinicians to address coping strategies (including emotion-focussed strategies) as a part of any comprehensive treatment package. Gamblers need to be able to recognize and modify unhelpful thinking patterns (both in relation to problem gambling situations and, more generally, to other life stressors).

It is also important that the clinician is aware of any deficits in emotion-regulation strategies to ensure that the client is prepared to guard against relapse, given that the ability to tolerate distress is associated with increased length of abstinence from gambling (Daughters et al., 2005).

. More specifically, given the finding that gamblers were less aware of their feelings, mindfulness strategies may be useful to increase awareness of one’s
emotions. This could potentially be helpful in reducing automatic and habitual responses, particularly in high-risk situations. Decreasing emotional avoidance through mindfulness may also assist pathological gamblers in better understanding the impact of various mood states on their behaviour. Individuals who experience heightened awareness of emotions, and who learn to observe and act in a more aware manner, are less likely to engage in maladaptive behaviours such as gambling (Lakey et al., 2007).”

 

References

1. Williams, A. D., Grisham, J. R., Erskine, A., & Cassedy, E. (2012). Deficits in emotion regulation associated with pathological gambling. British Journal of Clinical Psychology, 51(2), 223-238.

Predicting relapse via extent of emotional dysregulation?

Predicting relapse via extent of emotional dysregulation?

by alcoholicsguide

Even the most experienced counselors have difficultly spotting a recovering alcoholic in danger of relapse. Brain imaging scans might do a better job according to a study last year by researchers at  Yale University.

They suggested that alcoholics with abnormal activity in areas of the brain that control emotions and desires (reward) are eight times more likely to relapse and drink heavily than alcoholics with more normal patterns of activity or healthy individuals (1)

“These areas in the prefrontal cortex are involved in regulating emotion and in controlling responses to reward,” said Rajita Sinha, the Foundations Fund Professor of Psychiatry and professor in the Child Study Center and of Department of Neurobiology. “They are damaged by high levels of alcohol and stress and just do not function well.”

Or both perhaps, i.e. chronic alcohol use impacting on already impaired emotional regulation networks in the brain.

 

Figure6_ADHC_revised_2_7_12

 

This graphic highlights areas of the brain where Yale researchers found significant differences in responses to stress and relaxation-inducing stimuli between alcoholics and healthy controls. Alcoholics who exhibited such patterns of activity during fMRI scans were much more likely to relapse than alcoholics that more closely resembled control subjects.

Areas of the brain governing emotional regulation such as the ventromedial prefrontal cortex which suggests chronic difficulties in emotional dysregulation, which  potentiates the reward network, lying adjacent, and promotes higher relapse – click image for study. 

 

Ironically, the damage shows up on fMRI scans when alcoholics imagine being in their own most relaxing scenarios, like sitting at the beach listening to the waves, or taking a bubble bath. In non-alcoholics, these brain regions regulating emotion show markedly reduced activity during relaxing imagery, as anticipated. However, in alcoholics most likely to relapse, those brain regions remain hyperactive. On the other hand, when recovering alcoholics imagine their own recent stressful events, these control regions of the brain show little change, while in non-alcoholics, they show marked activation in response to stress. Such disrupted responses in areas of the brain governing emotions and reward lead to high cravings in the recovering alcoholic and an increased likelihood of subsequent relapse.

These brain scans in the future might serve as a diagnostic test to help professionals identify those most at risk of relapsing and suggest specific interventions to normalize brain function and prevent high rates of alcohol relapse, Sinha said.

“The findings show the prefrontal region is important for maintaining recovery for alcoholism,” Sinha said.

This is in accord with much of our writing in this blog – alcoholics, in recovery or otherwise, appear to have profound difficulties in regulating stress and emotion, as if the hyperactivity in the ventromedial pefrontal cortex, seen here, is indicative of a brain that never emotionally shuts off, is always on the go (whether this is the consequence of allostasis, the continual readjustment of the brain to stress needs to be further explored) and is primed to relapse effectively via a “fight of flight mechanism, or a distress based impulsivity.

 

References

Dongju Seo; R Todd Constable; Kwang-Ik Hong; Cheryl Lacadie; Keri Tuit; Rajita Sinha
Disrupted ventromedial prefrontal function, alcohol craving, and subsequent relapse risk.
JAMA psychiatry (Chicago, Ill.) 2013;70(7):727-39.

 

Is the “mental obsession” of the Big Book relative to how severe your addiction is?

Involuntary retrieval of drug related thoughts is a hallmark of addicted populations.

Intensity of obsessive thoughts about alcohol predict relapse rate (1), with addicts motivated to use drugs to “silence” obsessive thoughts (2).  The idea that abstinence automatically decreases alcohol-related thoughts is challenged by research (3) and supported by clinical observation that among abstinent alcohol abusers, alcohol-related thoughts and intrusions are the rule rather than exception (4).

Modell and colleagues (1992) highlighted symptomatic similarities between addiction and obsessive compulsive disorder with subjective craving for drugs or alcohol characterized as having obsessive elements. (eg, the compulsive drive to consume alcohol, recurrent and persistent thoughts about alcohol, and the struggle to control these drives and thoughts) similar to the thought patterns and behaviours of patients with obsessive-compulsive illness (5).

Modell et al. also point to the potential similarities in underlying neural pathways implicated in the two disorders, suggesting that they may share a similar aetiology. The Obsessive Compulsive Drinking Scale (OCDS) implies 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 (6).

Image

 

 

This may also be a reflection of addiction severity too! As addicts and alcoholics become more addictive brain imaging shows a shift in “reward processing” from the ventral striatum to the dorsal striatum. The DS is in charge of more automatic, compulsive reaction.  This shift from VS to DS  may also be marked by an increased emergence of automatic thoughts, which the authors suggested as the cognitive thoughts and images of automatized drug action schemata (2).

In fact, this is demonstrated by correlations indicating that dorsal striatum activation is lowest in participants with low OCDS scores. This means, in simple terms, that more severe addiction may be associated with more intrusive/obsessive thoughts and less severe with less thoughts.  

 

References 

 

1.. 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.

2. 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.

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

4. 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.

5. 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, 266-271.

6. 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.

7. Vollstädt‐Klein, S., Wichert, S., Rabinstein, J., Bühler, M., Klein, O., Ende, G., … & Mann, K. (2010). Initial, habitual and compulsive alcohol use is characterized by a shift of cue processing from ventral to dorsal striatum.Addiction, 105(10), 1741-1749.

 

 

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).

 

Image

 

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.

 

What is craving?

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

Euphoria Re-experienced not Recalled?

I never, never want to drink again, I would rather kill myself.

This does not mean I will not drink again however.

A possible relapse is thus not down to desire for a drink, it is because something in my brain and in my heart goes awry.

I remember being in early recovery and thinking the following line from the Big Book of Alcoholics Anonymous was very strange  “Remember that we deal with  alcohol—cunning, baffling, powerful! Without help it is too much for us”

What did they mean, alcohol was cunning, baffling, powerful? Surely they meant, alcoholism was cunning, baffling, powerful? Right?

Alcohol itself has not got magical powers? It isn’t a ghost or a spirit that can come and get you lured you back into drinking? Why be wary of a substance?

I suffer from alcoholism not alcohol, don’t I? ISM – I, self, me, the internal spiritual malady treated formerly by alcohol. Right? Alcohol was symptomatic?  “Bottles were only a symbol”

Now what is it to be?

In AA, I used to think alcohol got off light, considering the damage it causes to the brain. I always felt alcohol and it’s comprehensive deleterious neuro-toxic effects on my brain have greatly contributed to my difficulties with emotions and thinking and memory and perception etc. The list does go on and on.

One only has to look at a brain image from a fMRI scan to realise  that the damage to the brain wrought by alcohol is extensive and some of it irreversible although there is extensive repair in certain regions of the brain in recovery. I have felt for some time that alcohol gradually help change, over years,  how I felt and thought and perceived this world.

Alcohol literally moulded my brain. If I emotionally reacted or  thought in the same distorted way as I did while drinking or perceived this world in the same jaundiced way I did while drinking ,but while in recovery, then the same behaviours would soon follow.

I would drink.

Like a lot of alcoholics, I had a terrible sense of self, a very negative self perception in other words. I thought I was the lowest of the low, that I had screwed up my life and squandered my talents, that I didn’t even deserve recovery or to recover. I was not even worth that. It was this shame and guilt-fuelled lack of self esteem, this devalued sense of self that helped drive my drinking and which threatened to ruin any chances of recovery.

But what does this have to do with alcohol being cunning, baffling, powerful I hear you ask? Lots, is the answer. This negative self perception, I have had since early childhood,  well since I could reflect on my self and the product of emotional and mental abuse and traumatic parenting is ingrained in my brain.

Even now when I reflect on myself I have a tendency to think negatively or poorly about myself and my achievements, I have a negative bias in my thinking about me. It could depress me even, if I indulged in thinking about me for too long.

Again what does this have to do with alcohol? Well these negative perceptions, ingrained in neural structures in my brain have had more than a helping hand by alcohol. Alcohol has helped reinforced this faulty image of my self.

Alcohol had helped colour this jaundiced view of my self and this can has serious repercussions in recovery. This distorted view was partly the result of staring at my refection on the warped  glass of a wine bottle or on a glass of beer.  It cemented this view or “concretized” it in my self perception neural networks. Every drink helped dig the grave of my self worth.

I have seen many people in recovery relapse after a period of negative self reflection, after not thinking they are good enough to recover. It is immensely sad, tragic but nonetheless true. That is why they need love more than anything when they come into recovery. Not orders or dictats but love, plain and simple, make them feel part of, that they belong, that they have found their place, their surrogate home.

I have seen countless people who were so severely abused that they could not face the self disclosure at the heart of the 12 step program of recovery. I have seem than unconsciously “choose” to drink rather than take the steps. Part of this is something deep inside whispers a barely audible solution. To drink again.

Why is it barely audible? Because it is. It doesn’t actually have a voice. It is the whisper of a neural ghost (1). It is ghost that lives in the machinery of the brain. As alive as you are. It will probably remain to haunt you as an alcoholic  in some form  and at some time of weakness. Never think otherwise!

It is like a euphoria recalled but also it isn’t!? It may be worse than that; it is actually to a very great extent re-experienced.

Euphoria re-experienced not simply recalled.

Euphoria wasn’t just the pleasure you received but also relief from…negative emotions surrounding the self. Negative self perception, emotional distress and so on. It appears that negative affect (emotions, mood, anxiety) can automatically prompt thoughts of alcohol or drugs (2) and that the neural circuitries of affect, reward, memory and attention are taken over or ‘hijacked’ in the addiction cycle and often prompted into activation by emotional distress so that attention is directed to alcohol to relieve distress, with the resultant ‘craving’ coloured by numerous memory associations ingrained in the brain linked to habitually drinking to relieve negative emotional states.

Also, pertinent to this blog, negative self perception may also prompt relapse. I partly reconcile alcohol being cunning, baffling, powerful and alcoholism by reference to an article I read a while back by Rex Cannon(3).

His observations about a possible role for negative self perception in relapse was based on a study conducted  on recovering alcoholics. It found that by measuring their brain frequencies, when thinking about drinking and when thinking about self perception that there was a change in the frequency of their brain waves. In both cases, thinking about drinking and negative self perception, Cannon et al observed that widespread alpha power increases in the cortex, commonly seen by use of certain chemicals, were also present and in the same areas of a common neural circuitry for his study group during their reports of ‘using’ and ‘drinking’ thought patterns as well as in negative self perception.

These reports of ‘using’ and ‘drinking’ thought patterns as well as in negative self perception which appeared to bring the brain into synchrony, if only for a brief period of time, suggesting this to be the euphoria addicted individuals speak so fondly of and one possible reason for difficulty in treating these disorders.

In relation to using thoughts they suggested that “if the brain communicates and orchestrates the affective state of the individual in response to contents and images relating to self and self-in-experience – it is plausible that a large scale feedback loop is formed involving not only perceptual processes but relative automatic functioning.

This process reinforces the addicted person to become habituated to an aroused cortical state (i.e. increased alpha/beta activity) and when there is a shift to ‘normalcy’ (or recovery/sobriety) it is errantly perceived as abnormal thereby increasing the desire or need for a substance to return to the aroused (perceived as normal (or desired)) state”.

This would surely have a profound impact on addicts attempting to contain normal negative emotions when there is an automatic desire state suggesting, unconsciously, an alternative to wrestling with these torturous sober realities.

I have seen a similar process but over a much longer time frame in some alcoholics in recovery who relapse. They seem to disappear into themselves, right in front of you, like they were being lured by some internal, inaudible siren, into a self drowning.

Letting go of the life boat trying to keep them afloat. I have seen it many times, the dimming of the eye’s light, the turning inwards to the alcoholic darkness. A submerging into this illness.

It may be that indulging in one’s negative self perception recreates a neural based virtual reality. One is almost bodily transported back in time. Back to a drinking period. In a neural sense, back in the drink and not fully in sobriety, however fleetingly.

It does leave a neural taste for it, a torturous transient desire.

I remember it, particularly in early recovery, when the ‘recovery’ script was not written yet and I did not have a habitual recovery self schema to automatically activate, to pull me out of this neural reverie, this most bio-chemical vicarious pleasure.

The problem is that it happens to you without you asking it! You can be invoking a negative self schema automatically without wanting to reawaken this  ghost.

But that is alcoholsim in a nutshell. It happens to you without your express permission. It takes over the brain step by step, while impairing ones’ ability to observe this progression.

That is why we are are the last to know. It is not just denial, it is brain impairment and limited ability to reflect on what has happened to one’s self.

The self has been ‘hijacked’ so it is nigh impossible to figure this out without the help of others.

It is others that lead you out of the fog, as one has become lost to oneself. If nothing else, in early recovery especially, before the steps are done, it is a dangerous place to visit, the self and it is safer to spend as much time as possible outside of it and working with others!

It is a horrible, frightening experience, the limbo between addicted self and recovery self schemas. It is fraught with danger! I remember bumping into people places and things from the past and experiencing the most excruciating cognitive dissonance of literally being caught in between two worlds and not knowing if I was a drinking or a recovering alcoholic; the sense of self as a drinking alcoholic was much stronger than the recovering self. I would hurry to my sponsor or wife to help pull my sense of self as a recovering alcoholic to the surface, out of the neural swamp of my drinking alcoholism.

But it felt alien as Cannon observes, this sober self.  All new, awkward, pained, exposed and frightened.  A constant vacillation between two worlds, that of active use and that of recovery. Recovery had not become “concretized” in my neural networks!

This left an oscillating experiential schism, with one caught in two realities almost simultaneously.

I see people relapse because they have no emotional sobriety and they seem to be emotionally drunk before they are actually drunk. Emotionally drunk seems to be like a virtual drunk, brings up the similar feelings or neurochemical reactions as actual drinking.

The best way to stay sober is to act sober and develop this habitual schema so that it can be retrieved instantaneously, automatically, without thinking. We achieve this schema through our actions, so in a sense is also an action schema. Tiffany (4) states that alcoholics and addicts are prompted to relapse by automatized schemata surrounding drug and alcohol use rituals, so we must have automatized schemata surrounding recovery rituals. Such as ringing a sponsor, mentor, friend, doing a  step ten, praying, meditating, working with others, letting go and letting God, re-appraising distress, regulating emotions, putting thoughts of others before thoughts of ourselves, living outside self.  There are so many automatic schemas in AA and other therapeutic regimes.

Either way, whatever path you choose, make your recovery  tools automatic, so that they come to hand without yourself having to think about them.

 

 

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

3.  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.

4.  Adinoff, B. (2004). Neurobiologic processes in drug reward and addiction.Harvard review of psychiatry, 12(6), 305-320. 

An Emotional Disease?

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.

How Research Helped Saved My Life!

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.

My emotions overwhelmed me and had started to rush like a startled herd of fear through the remaining mental barricades,  exploding into a crashing cascade of stress chemicals rushing around my whole body, making my limbs weak, achy and feeble.

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. Real nauseatingly frightening trouble. I needed help. “Let’s stop arguing, I am in danger!”

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.

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. It was as if some habitual behaviour, some automatic pilot had activated my legs and brought me here for help.

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 surging 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.

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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 doing 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 images of doing it before, drinking, in case I had forgotten, fleeting 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! 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.

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.

It was the most terrifying eureka moment imaginable. I have confirmed in experiential terms what I had spent the previous two years researching. Research had partly saved my life and I hope it also does yours or at the very least help you understand this disease more fully. It had proved my ‘theory’ as far as I was concerned, highlighted the mechanisms of my torture, the psycho-neural pullies and the strings.

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It is this and other related theories that we hope to share while posting to this blog.  Emotional distress appears to lie at the very heart of my alcoholism, my “emotional disease”, as I have heard many alcoholics in recovery call it or this parasite that feeds on( my poorly regulated and processed) emotions, as described to me by a treatment centre counselor.  The same emotional difficulties that had made alcohol such a stupendous release and comfort, such a seemingly wonderful way to regulate my emotions, to approach and be with people who used to scare and confuse me, to belong among them, however fleetingly; now the thrill had long gone, my emotional difficulties were what remained, the daily managing of this emotional dysregulation is at the heart of my recovery. If we do not manage them then they manage us.

So there we have it: how research saved my life. Researchers need to consult and observe, listen and learn from those they study. As one researcher said about educational theories, the best way to disprove or ruin your beloved theory was to set it in a classroom environment. I suggest that researchers into alcoholisim and addiction ruin or disprove their own cherished theories by applying them to those they meet at a treatment centre. Who knows they may even improve on their theories, and in doing so treatment of the alcoholics and addicts they research.