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.

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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).

 

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

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

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

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

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

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

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

 

References

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

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

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

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

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

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

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

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

 

Do I still have an “Alcoholic Mind”!?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 

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

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

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

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

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

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

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

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

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

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

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

 

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

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

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

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

Factors in relapse

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

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

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

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

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

How does conditioning methodology adequately explain this group?

Attentional Bias

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

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

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

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

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

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

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

References

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

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

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

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

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

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

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

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

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.

 

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.

The Distress at the Heart of Addiction and Alcoholism

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

“Fear based” is distress based.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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