Emotional Dysregulation, recovery and relapse

Throughout our blogs thus far, we have attempted to highlight how emotional dysregulation appears to prevalent to all aspects of alcoholism and addiction from pre-morbid vulnerability to endpoint compulsive addictive behaviours.

Here we highlight a few articles which have considered how prevalent is emotional dysregulation in alcoholism and addiction in early abstinence/recovery. 

Early abstinence from chronic alcohol dependence is associated with increased emotional sensitivity to stress-related craving as well as changes in brain systems associated with stress and emotional processing.

Early abstinence from alcohol is associated with changes in neural stress and reward systems that can include atrophy in subcortical and frontomesal regions (1).

Moreover, recent imaging studies have shown that these brain regions are also associated with the experience and regulation of emotion (2).

While alcohol-related changes in emotion, stress and reward-related brain regions have been well documented difficulties in emotion regulation (ER) have not been studied much.

bar_of_destruction_1874__medium

One study (3) examined ER in early abstinent alcohol-dependent individuals compared with social drinkers using the Difficulties in Emotion Regulation Scale (DERS).

The DERS is an inclusive scale and defines ER in terms of four major factors: the understanding of emotion, the acceptance of emotion, the ability to control impulsive behavior and the ability to access ER strategies benefiting the individual and the specific goals of the situation. The scale has been validated in cocaine dependent patients (4) and on alcohol dependent individuals.

ER difficulties in treatment-engaged alcohol dependent (AD) patients during a period of early abstinence that is marked by an overall distress state. AD patients reported an overall problem with emotion regulation compared with SDs in the first few days of abstinence; in particular with emotional awareness and impulse control. Following protracted abstinence, AD patients significantly improved awareness and clarity of their emotional experience, and only significant problems with impulse control persisted.

This is consistent with neuro-imaging studies showing chronic alcohol abuse to be associated with stress and cue-related neuroadaptations in the medial prefrontal and anterior cingulate regions of the brain (6), which are strongly implicated in the self-regulation of emotion and behavioral self-control (7). As impulsivity in distress states may reflect a change in priority from self-control to affect regulation (8 ).

As we have seen in other blogs and articles (5) these areas are those which improve in short term abstinence/recovery.

Cocaine-dependent individuals also report emotion regulation difficulties, particularly during early abstinence (4). Additionally, protracted distress-related impulse control problems suggest potential relapse vulnerability Difficulties concerning emotional clarity and awareness compared with controls were observed which suggests that cocaine dependent individuals were less able to acknowledge and/or have a clear understanding of their emotions.

Clarity and awareness of emotions could represent early processing components of emotional competence (9) and may be integral to the maintenance of drug use.

The cocaine addicts appeared to have greater difficulty in developing effective emotional coping strategies  (i.e. they would be more likely to believe that little could be  done to change an emotionally stressful situations.) They were also found to report significantly higher scores on the Impulse subscale of the DERS compared with controls, indicating difficulties with regard to inhibiting inappropriate or impulse behaviors under stressful situations which can prompt relapse.

References

1. Bartsch, A. J., Homola, G., Biller, A., Smith, S. M., Weijers, H. G., Wiesbeck, G. A., et al. (2007). Manifestations of early brain recovery associated with abstinence from alcoholism. Brain, 130(Pt 1), 36−47

2. Fox, H. C., Hong, K. A., & Sinha, R. (2008). Difficulties in emotion regulation and impulse control in recently abstinent alcoholics compared with social drinkers. Addictive Behaviors33(2), 388-394.

3. Ochsner, K.N., Gross, J.J., 2005. The cognitive control of emotion. Trends Cogn. Sci. 9, 242–249

4. Fox, H. C., Hong, K. A., & Sinha, R. (2008). Difficulties in emotion regulation and impulse control in recently abstinent alcoholics compared with social drinkers. Addictive Behaviors33(2), 388-394.

5. Sinha, R., & Li, C. S. (2007). Imaging stress- and cue-induced drug and alcohol craving: Association with relapse and clinical implications. Drug and Alcohol Review, 26(1), 25−31.

6. Connolly, C. G., Foxe, J. J., Nierenberg, J., Shpaner, M., & Garavan, H. (2012). The neurobiology of cognitive control in successful cocaine abstinence. Drug and alcohol dependence121(1), 45-53.

7. Baumeister, R.F., Heatherton, T.F., Tice, D.M., 1994. Loosing Control: How and Why People Fail at Self-regulation. Academic Press, San Diego, CA

8.  Tice, D.M., Bratslavsky, E., Baumeister, R.F., 2001. Emotional distress regulation takes precedence over impulse control: if you feel bad, do it! J. Pers Soc. Psychol. 80, 53–67.

9. Salovey, P., Stroud, L.R., Woolery, A., Epel, E.S., 2002. Perceived emotional intelligence, stress reactivity, and symptom reports: further explorations using the trait Meta-mood scale. Psychol. Health 17, 611–627

 

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 Psychology108(3), 518.

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

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

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

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

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

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

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

 

Do I still have an “Alcoholic Mind”!?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 

Image

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

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

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

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

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

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

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

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

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

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

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

 

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 behaviors29(4), 753-758.

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

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

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

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

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

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

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

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 Health23(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 Psychiatry54(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

How meditation helps with “emotional sobriety”!

In this blog we have considered two main and fundamental areas:-

1. that alcoholism appears to be an emotional regulation and processing disorder which implicates impaired functioning of brain regions and neural networks involved in regulation and processing emotion such as the insular cortex, anterior cingulate cortex and dorsolateral prefrontal cortex.

2. that in early and later recovery there appears to be increased functioning in these areas especially the dorsolateral prefrontal cortex (dlPFC) and anterior cingulate cortex (ACC) which is important not only in regulating emotions but also in abstinence success.

Our third point is that mediation, of various types, appears to strengthen the very areas implicated in emotional regulation and processing, which ultimately helps with “emotional sobriety” and long term recovery.

Various studies have shown that mindfulness mediation training in expert meditators, as well as novices,  influenced areas of the brain involved in attention, awareness and emotion (1,2).

 

Meditation-in-Brain-660

 

A key feature of mindfulness meditators may be the ability to recognise and accurately label emotions (3). Brain FMRI studies have shown more mindful people having increased ability to control emotional reactions in various areas associated with emotional regulation such as the amgydala, dlPFC, and ACC (4).

In a study (5) on the the effects of long term meditation on physical structure of the above brain regions, practitioners of mindful meditation who meditated 30-40 minutes a day, had increased thickness due to neuroplasticity of meditation in brain regions associated with attention and interoception (sensitivity to somatic or internal bodily stimuli) than the matched controls used in this study. Again the regions observed to have greater thickness via increased neural activity (neuroplasticity) were the PFC, right insula (interoception and this increased appreciation of bodily sensations and emotions) as well as the ACC in attention (and possible self awareness as ACC is also linked to consciousness) .

A structural MRI study (6) showed that experienced mindfulness meditators also had increased grey matter the right interior insula and PFC as well as, in unpublished data, in the hippocampus, which is implicated in memory but also in stress regulation. Thus mindfulness meditation and the fMRI and MRI studies show it is possible to train the mind to change brain morphology and functionality through the neuroplastic behaviour of meditating.

Brain regions consistently strengthen or which grow additonal “neural muscles” are those associated with emotional regulation and processing such as the dlPFC, ACC, insula and amgydala.   Thus if we want, as recovering individuals,  to shore up our early recovery, by strengthening the brain regions implicated in recovery success we meditate on a regular basis, daily, so that we can also improve those underlying difficulties in emotional regulation and processing.

By relieving emotional distress we greatly lessen the grip our condition has on us on a daily basis, We recover these functions.  We will discuss the role of meditation on reducing emotional distress in later blogs.

 

Image

 

References

1. Cahn, B. R., & Polich, J. (2006). Meditation states and traits: EEG, ERP, and neuroimaging studies. Psychological bulletin132(2), 180.

2,  Lutz, A., Slagter, H. A., Dunne, J. D., & Davidson, R. J. (2008). Attention regulation and monitoring in meditation. Trends in cognitive sciences12(4), 163-169.

3.  Analayo. (2003). Satipatthana: The Direct Path to Awakening. Birmingham, UK: Windhorse Publications.

4.  Creswell, J. D., Way, B. M., Eisenberger, N. I., & Lieberman, M. D. (2007). Neural correlates of dispositional mindfulness during affect labeling.Psychosomatic Medicine69(6), 560-565.

5.  Lazar, S. W., Kerr, C. E., Wasserman, R. H., Gray, J. R., Greve, D. N., Treadway, M. T., … & Fischl, B. (2005). Meditation experience is associated with increased cortical thickness. Neuroreport16(17), 1893.

6. Hölzel, B. K., Ott, U., Hempel, H., Hackl, A., Wolf, K., Stark, R., & Vaitl, D. (2007). Differential engagement of anterior cingulate and adjacent medial frontal cortex in adept meditators and non-meditators. Neuroscience letters421(1), 16-21.

 

see also  Hijacking the Brain

What recovers in Recovery? – Cognitive Control over emotions?

A core aspect of alcohol dependence is poor regulation of behavior and emotion.

Alcohol dependent individuals show an inability to manage the appropriate experience and expression of emotion (e.g., extremes in emotional responsiveness to social situations, negative affect, mood swings) (1,2). Dysfunctional emotion regulation has been considered a primary trigger for relapse (1,3) and has been associated with prefrontal dysfunction.

While current alcohol dependence is associated with exaggerated bottom-up (sub-cortical) and compromised top-down (prefrontal cortex) neural network functioning, there is evidence suggesting that abstinent individuals may have overcome these dysfunctional patterns of network functioning (4) .

Neuro-imaging studies showing chronic alcohol abuse to be associated with stress neuroadaptations in the medial prefrontal and anterior cingulate regions of the brain (5 ), which are strongly implicated in the self-regulation of emotion and behavioral self-control (6).

One study (2) looking at how emotional dysregulation related to relapse, showed compared with social drinkers, alcohol-dependent patients reported significant differences in emotional awareness and impulse control during week 1 of treatment. Significant improvements in awareness and clarity of emotion were observed following 5 weeks of protracted abstinence.

Another study (7) which did not look specifically at emotional regulation but rather on the recovering of prefrontal areas of the brain known to be involved also in the inhibition of  impulsive behaviour and emotional regulation showed that differences between the short- and long-abstinence groups in the patterns of functional recruitment suggest different cognitive control demands at different stages in abstinence.

The long-term abstinent group (n=9) had not consumed cocaine for on average 69 weeks, the short-term abstinent (SA) group (n=9) had an average 0f 2.4 weeks.

Relative to controls, abstinent cocaine abusers have been shown to have reduced metabolism in left anterior cingulate cortex (ACC) and right dorsolateral prefrontal cortex (DLPFC), and greater activation in right ACC.

In this study  the abstinent groups of cocaine addicts showed more elevated activity in the DLPFC ; a finding that has also been observed in abstinent marijuana users (8).

The elevation of frontal activity also appears to undergo a shift from the left to right hemisphere over the course of abstinence.  Furthermore, the left inferior frontal gyrus (IFG) has recently been shown to be important for response inhibition (9) and in a task similar to that described here, older adults have been shown to rely more on left PFC (10). Activity observed in these regions is therefore likely to be response inhibition related.

The reliance of the SA group on this region suggests that early in abstinence users may adopt an alternative cognitive strategy in that they may recruit the LIFG in a manner akin to children and older adults to achieve behavioral results similar to the other groups.

In longer,  prolonged abstinence a pattern topographically typical of normal, healthy controls may emerge.
In short-term abstinence there was an increased inhibition-related dorsolateral and inferior frontal activity indicative of the need for increased inhibitory control over behaviour,  while long-term abstinence showed increased error-related ACC activity indicative of heightened behavioral monitoring.
The results suggest that the improvements in prefrontal systems that underlie cognitive control functions may be an important characteristic of successful long-term abstinence.

Another study (11) noted the loss of grey matter in alcoholism that last from 6–9 months to more than a year or, in some reports, up to at least 6 years following abstinence (12 -14).

It has been suggested cocaine abuse blunts responses in regions important to emotional regulation (15)

Given that emotional reactivity has been implicated as a factor in vulnerability to drug abuse (16)  this may be a preexisting factor that  increased the likelihood of the development and prolonging of drug abuse

If addiction can be characterized as a loss of self-directed volitional control (17),  then abstinence (recovery) and its maintenance may be characterized by a reassertion of these aspects of executive function (18)  as cocaine use has been shown to reduce grey matter in brain regions critical to executive function, such as the anterior cingulate, lateral prefrontal, orbitofrontal and insular cortices (19-24) .

The group of abstinent cocaine addicts (11) reported here show elevations in  (increased) grey matter in abstinence exceeded those of the healthy control in this study after 36 weeks, on average, of abstinence .

One possible explanation for this is that abstinence may require reassertion of cognitive control and behavior monitoring that is diminished during current cocaine dependence.

Reassertion of behavioral control may produce a expansion (25)  in grey matter  in regions such as the anterior insula, anterior cingulate, cerebellum, and dorsolateral prefrontal cortex .

All brain regions implicated in the processing and regulating of emotion. 

 

References

 

 

1. Berking M, Margraf M, Ebert D, Wupperman P, Hofmann SG, Junghanns K. Deficits in emotion-regulation skills predict alcohol use during and after cognitive-behavioral therapy for alcohol dependence. J Consult Clin Psychol. 2011;79:307–318.

2.  Fox HC, Hong KA, Sinha R. Difficulties in emotion regulation and impulse control in recently abstinent alcoholics compared with social drinkers. Alcohol Clin Exp Res. 2008;33:388–394.

3..Cooper ML, Frone MR, Russell M, Mudar P. Drinking to regulate positive and negative emotions: A motivational model of alcohol use. J Pers Soc Psychol. 1995;69:990

4. Camchong, J., Stenger, A., & Fein, G. (2013). Resting‐State Synchrony in Long‐Term Abstinent Alcoholics. Alcoholism: Clinical and Experimental Research37(1), 75-85.

5. Sinha, R., & Li, C. S. (2007). Imaging stress- and cue-induced drug and alcohol craving: Association with relapse and clinical
implications. Drug and Alcohol Review, 26(1), 25−31.

6. Beauregard, M., Lévesque, J., & Bourgouin, P. (2001). Neural correlates of conscious self-regulation of emotion. Journal of
Neuroscience, 21(18), RC165

7. Connolly, C. G., Foxe, J. J., Nierenberg, J., Shpaner, M., & Garavan, H. (2012). The neurobiology of cognitive control in successful cocaine abstinence. Drug and alcohol dependence121(1), 45-53.

8.  Tapert SF, Schweinsburg AD, Drummond SP, Paulus MP, Brown SA, Yang TT, Frank LR. Functional MRI of inhibitory processing in abstinent adolescent marijuana users.Psychopharmacology (Berl.) 2007;194:173–183.[PMC free article]

9. Swick D, Ashley V, Turken AU. Left inferior frontal gyrus is critical for response inhibition. BMC Neurosci. 2008;9:102.[PMC free article]

10. Garavan H, Hester R, Murphy K, Fassbender C, Kelly C. Individual differences in the functional neuroanatomy of inhibitory control. Brain Res. 2006;1105:130–142

11. Connolly, C. G., Bell, R. P., Foxe, J. J., & Garavan, H. (2013). Dissociated grey matter changes with prolonged addiction and extended abstinence in cocaine users. PloS one8(3), e59645.

12. Chanraud S, Pitel A-L, Rohlfing T, Pfefferbaum A, Sullivan EV (2010) Dual Tasking and Working Memory in Alcoholism: Relation to Frontocerebellar Circuitry. Neuropsychopharmacol 35: 1868–1878 doi:10.1038/npp.2010.56.

13.  Wobrock T, Falkai P, Schneider-Axmann T, Frommann N, Woelwer W, et al. (2009) Effects of abstinence on brain morphology in alcoholism. Eur Arch Psy Clin N 259: 143–150 doi:10.1007/s00406-008-0846-3.

14.  Makris N, Oscar-Berman M, Jaffin SK, Hodge SM, Kennedy DN, et al. (2008) Decreased volume of the brain reward system in alcoholism. Biol Psychiatry 64: 192–202 doi:10.1016/j.biopsych.2008.01.018.

15, Bolla K, Ernst M, Kiehl K, Mouratidis M, Eldreth D, et al. (2004) Prefrontal cortical dysfunction in abstinent cocaine abusers. J Neuropsychiatry Clin Neurosci 16: 456–464 doi:10.1176/appi.neuropsych.16.4.456.

16.  Piazza PV, Maccari S, Deminière JM, Le Moal M, Mormède P, et al. (1991) Corticosterone levels determine individual vulnerability to amphetamine self-administration. Proc Natl Acad Sci USA 88: 2088–2092. doi: 10.1073/pnas.88.6.2088

17.  Goldstein RZ, Volkow ND (2002) Drug addiction and its underlying neurobiological basis: neuroimaging evidence for the involvement of the frontal cortex. Am J Psychiatry 159: 1642–1652. doi: 10.1176/appi.ajp.159.10.1642

18. Connolly CG, Foxe JJ, Nierenberg J, Shpaner M, Garavan H (2012) The neurobiology of cognitive control in successful cocaine abstinence. Drug Alcohol Depend 121: 45–53 doi:10.1016/j.drugalcdep.2011.08.007.

19.  Liu X, Matochik JA, Cadet JL, London ED (1998) Smaller volume of prefrontal lobe in polysubstance abusers: a magnetic resonance imaging study. Neuropsychopharmacol 18: 243–252 doi:10.1016/S0893-133X(97)00143-7.

20.  Bartzokis G, Beckson M, Lu P, Nuechterlein K, Edwards N, et al. (2001) Age-related changes in frontal and temporal lobe volumes in men – A magnetic resonance imaging study. Arch Gen Psychiatry 58: 461–465. doi: 10.1001/archpsyc.58.5.461

21. Franklin TR, Acton PD, Maldjian JA, Gray JD, Croft JR, et al. (2002) Decreased gray matter concentration in the insular, orbitofrontal, cingulate, and temporal cortices of cocaine patients. Biol Psychiatry 51: 134–142. doi: 10.1016/s0006-3223(01)01269-0

22.  Matochik JA, London ED, Eldreth DA, Cadet J-L, Bolla KI (2003) Frontal cortical tissue composition in abstinent cocaine abusers: a magnetic resonance imaging study. NeuroImage 19: 1095–1102. doi: 10.1016/s1053-8119(03)00244-1

23.  Lim KO, Wozniak JR, Mueller BA, Franc DT, Specker SM, et al. (2008) Brain macrostructural and microstructural abnormalities in cocaine dependence. Drug Alcohol Depend 92: 164–172 doi:10.1016/j.drugalcdep.2007.07.019.

24.  Ersche KD, Barnes A, Jones PS, Morein-Zamir S, Robbins TW, et al. (2011) Abnormal structure of frontostriatal brain systems is associated with aspects of impulsivity and compulsivity in cocaine dependence. Brain 134: 2013–2024 doi:10.1093/brain/awr138.

25.  Ilg R, Wohlschlaeger AM, Gaser C, Liebau Y, Dauner R, et al. (2008) Gray matter increase induced by practice correlates with task-specific activation: A combined functional and morphometric magnetic resonance Imaging study. J Neurosci 28: 4210–4215 doi:10.1523/JNEUROSCI.5722-07.2008.

 

Do you have Emotional Regulation Difficulties!?

Emotions have always troubled me! I have always found them frightening, always had difficulties labeling and controlling them. I have always seemed to put in an extra effort to keep them in check.

I have recently read a very good chapter from a book (1) which looks at emotional regulation and the role it seems to play in psychopathology. In fact, it is my view that emotional dysregulation  lies at the heart of alcoholism, initiates, sustains and perpetuates this chronic disease state.

It was thus illuminating to see that emotional dysregulation is cited as being present in some 75% of disorders listed in The Diagnostic and Statistical Manual of Mental Disorders, DSM-5.

Alcohol Dependence in the DSM has a narrow definition, I believe, of alcoholism as mentioned in previous blogs. It relegates all manifestation of emotional, mood, impulse difficulties to that of “co-morbidities” which means it thinks there is a difficulty with unregulated drinking but the unregulated thinking, emotions and impulsive behaviour it relegates to being the consequence of a co-occurring condition such as anxiety disorder, depression, post traumatic stress disorder and so on. This is not to say that some of these conditions do not co-occur with alcoholism. PTSD and alcoholism co-occur quite frequently.

What I am saying is that a number of conditions/disorders attributed to alcoholism as a co-morbidity may not be co-morbidities at all, for some. They may be aspects of this psychiatric disorder I call alcoholism.

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.

See blogs for more An Emotional Disease? and Current Definitions of Addiction – how accurate are they?

I do not want to rehash arguments mentioned elsewhere on this blog (especially as I want to discuss some emotional regulation difficulties I find are very pertinent to my alcoholism and maybe to yours?) Particularly “self elaboration” which seems to be at the heart of my alcoholism and appears very similar to the alcoholic mentioned in the Big Book of Alcoholics Anonymous.

Emotions are important in readying behavioral, motor,

and physiological responses, in facilitating decision making, in enhancing memory for important events, and for negotiating interpersonal relationships.

But emotions can also hurt as well as help! Emotions are  not always helpful!

Psychopathology is largely characterised by excessive negative emotion.  In those with emotional dysregulation,  emotional regulation strategies helpful in childhood are now unhelpful in adulthood,  such as use of an avoidant coping style where they down play threat and suppress feelings. This may have helped in surviving an abusive childhood but is not conducive to intimate adult relationships.

Another difficulty is not allowing a primary emotional response to proceed but instead suppressing it or resisting it e.g it is not okay for me to feel angry at my dying mother. Thereby, creating a maladaptive secondary emotional response e.g. guilt.

Secondary responses for resisted emotions coming from emotions
are experienced as anxiety producing, as reflected in rigid attentional
processes, lack of acceptance, and the activation of negative beliefs about emotions.

In order to ascertain if your emotional regulation is adaptive answer the questions below (and refer perhaps to your early recovery too!)

Do you not immediately react to the external situation or to one’s internal primary emotional response, but pause for a moment and give oneself some breathing room? Thus allowing  space for the emotion to begin to arise free of immediate avoidance (e.g., cognitive, behavioral, or emotional avoidance), immediate resistance (e.g., “I shouldn’t want to feel this way”), or impulsive behavioural reaction (e.g reacting angrily or fearfully)?

Are you aware of your primary emotional response and be able to identify what emotion one is having in order to effectively control it?

Can you determine how controllable the situation that
caused the emotion is and how controllable one’s internal reaction to the situation?

For situations or internal thoughts or emotions that are out of one’s control, adaptive regulation is to accept the situation and experience . This is common to most therapeutic regimes.

Finally,  how well do you  inhibit/control inappropriate or impulsive behaviors when experiencing negative emotions?

All of the above, from a personal perspective, have improved the longer I have been in recovery. Although tiredness, or distress can prompt a quick return to emotional dysregulation.

Emotion regulatory strategies

The two regualtory strategies are two that most apply to me as an alcoholic. Attentional Deployment and Cognitive Change

See if they relate to you too, or to a loved one.

Attentional Deployment

Specific forms of maladaptive attentional deployment include rumination, distraction and worry.

Rumination typically involves repetitive attentional focus on feelings associated with negative events, along with a negative evaluation of their consequences. It has been associated with increased levels of negative emotion. Rumination is constantly implicated in alcoholism.

We discuss this and catastrophizing in later blogs.

Cognitive Change

Before a situation that is attended to gives rise to emotion, the situation needs to be judged as important to one’s goals (i.e., appraisal).This stage of imbuing a situation with meaning can be influenced if one wishes to change the trajectory of the emotional response.

Cognitive change refers to changing how we appraise a situation to alter its emotional significance.

Two categories of reappraisals associated with psychopathology are (1) self-elaboration (e.g. “Others must think poorly of me”) and (2) emotional resistance/non acceptance of one’s current emotional experience (e.g., “I shouldn’t feel bad” ).

I personally find this “self elaboration” very applicable to myself as an alcoholic,  this ” the self in reference to a situation can substantially increase the duration and complexity of emotional responses.” 

For example, instead of my negative thoughts and feelings being processed and put to bed, they can be reignited throughout the day and can leave me feeling negative for hours afterward rather than just for the period following whatever incident provoked this emotional response initially.

This and other maladaptive emotional regulation strategies like rumination are shared with other disorders such as depression but this doesn’t mean they are the same disorders or that they co-occur. They are disorders which share common emotional dysregulation but ultimately have different behavioural manifestation.

They are not co-morbid but similar in certain ways but not all.

Back to self elaboration  –  Following my lack of appropriate emotional response above, I may feel negative the rest of the day, I may decide to ruminate, or complain  or bitterly gossip with others,  I may exhibit all the “defects of character” that came out in my step four inventory, such as pride, arrogance, intolerance, self-centredness, selfishness, anger, resentment, fear, dishonesty and so, all of which I feel are secondary emotional responding or emotional cascades. In fact, I believe step four through to seven helped me process the various episodes of emotional dysregulation I had running around my head and tearing at my heart for the thirty odd years prior to doing the steps.

The more I gossip and backbite, the more I think the person who “wronged me” is incompetent, it’s all his fault, my feelings are down to him! He caused this distress didn’t he?  The injustice of it all!! These thoughts will reignite other emotions and thoughts – I should have stuck up for my self – guilt and this situation could be serious – fear.  And so the cascade continues.

“I wonder if others think the same way about me, perhaps they don’t like me, perhaps I am not very popular!? – shame, self pity and  maybe I am just not very lovable – despair ” and then it can delve into my distant past to my childhood, “well this is how my mother acted sometimes, maybe it is just me ! I’m the problem!”

It is difficult not to see this self-assassination as anything other than emotional dysregulation. My thinking, based on negative emotions, running away with themselves and increasing these negative emotions which then increased by distorted thinking, until “to hell with it, I’m not worth it, let’s get drunk!”

My emotional dysregulation is linked to a heightened reward sensitivity, I really like things that soothe my emotions like drink and  drugs and I used them to regulate my emotions. I did not ruminate forever as in depression, I fixed it my external means, I consumed things and they change how I felt.

This makes my condition different to depression although plenty of depressives drink and abuse drugs. For me this heightened reward sensitivity meant I enjoyed them a whole lot more, got a whole lot out of them and decided that they would be part of how I dealt with things, emotions, life.

Our abnormal rejection to drink and drugs is a big part of our condition, our psychopathology, our psychiatric disorder. It has similarities with other conditions based on emotional dysregulation but it is also very different, That is why it demands a different treatment.

The wrong treatment will not Work!

The self elaboration means that I would consider many  imagined scenarios all in relation or in reference to my self.  The self has to be involved. Unfortunately this elaborates the meaning of my emotional responses and the emotional responses. All of a sudden  there is a soap opera running in my head, a committee of wrongdoings, soon becoming a psycho drama. A friend of mine in AA calls it travelling via his intergalactic armchair!

Ruminating on things that did not occur as we think, will not occur as we think and have only caused a temporary insanity.

How is this not a psychiatric disorder!?

The emotions get increasing intense and proliferate. A many headed monster.

All usually because of my initial misperception of something that probably did not occur!

 

References

Werner, K., & Gross, J. J. (2010). Emotion regulation and psychopathology: A conceptual framework.

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  alcoholcunningbafflingpowerful! 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 Psychology108(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 review97(2), 147.

4.  Adinoff, B. (2004). Neurobiologic processes in drug reward and addiction.Harvard review of psychiatry12(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 mechanismsThis 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 neuroscience6.

Cheetham, A., Allen, N. B., Yücel, M., & Lubman, D. I. (2010). The role of affective dysregulation. in drug addiction. Clinical Psychology Review30(6), 621-634.