emotional dysregulation

Why erase addiction memories when they can help others?

Posted on by alcoholicsguide

According to one UK newspaper The Independent, dated the 9th July 2014 “Substance abusers could have their memories of drug addiction wiped in a bid to stop them using illegal narcotics, an award-winning neuroscientist has said.

According to new research by Cambridge University’s Professor Barry Everitt: disrupting the memory pathways of drug users could weaken powerful “compel” cravings, reduce “drug seeking behaviour” and open a new field of addiction therapy.

Professor Everitt  told this week’s Federation of European Neuroscience Societies (FENS) how his research in rodents had found that targeting “memory plasticity” in rats was able to reduce the impact of maladaptive drug memories.

He added that this knowledge could offer a radical new method of treatment of drug addiction in humans, where researchers have already established that the path to addiction operates by shifting behavioural control from one area of the brain to another. This process sees drug use go from a voluntary act to a goal directed one, before finally becoming an compulsive act.

It was this process that Professor Everitt’s research is trying to “prevent” by targeting “maladaptive drug-related memories” to “prevent them from triggering drug-taking and replaces”.

In humans this could potentially be done by blocking brain chemicals.

“It’s the emotional intrusiveness of drug and fear memoirs that can be diminished, rather than an individual’s episodic memory that they did in the past take drugs or had a traumatic experience,” he told The Independent. “Conscious remembering is intact after consolidation blockade, but the emotional arousal [that] leads to drug seeking or distressing feelings of fear that are diminished.”

His research group discovered that when drug memories are reactivated by retrieval in the brain, they enter a pliable and unstable state. By putting rats in this state Professor Everitt was able to prevent memory reconsolidation by blocking brain chemicals or inactivating key genes.

In one study, the team diminished drug seeking behaviours by obstructing a brain chemical receptor linked to learning and memory, thus erasing memories, while in another study it found they could weaken drug use memories by altering a particular gene in the amygdala, a brain area processing emotional memory.

“Of course, inactivating genes in the brain is not feasible in humans,” the professor told FENS. “So we’re directing our research to better identify the underlying brain mechanisms of memory reconsolidation.”

He added: “We specifically examined how we could target these maladaptive drug-related memories, and prevent them from triggering drug-taking and relapse.”

So to recap, this new treatment is based on altering genes in rats!

There is no need to actually wipe an alcoholics’ addiction memories.

In fact it may be very counter productive to recovery from alcoholism. One 80 year old and hyper ecologically valid experiment into the mnemonics of “treating addiction memories”  has shown that by honestly looking at the consequences of one’s actions as the result of one’s alcoholic drinking that the positive associations of previous drinking were reappraised in light of the damage done to oneself, one’s loved ones and family and society at large.

Addiction memories via this profound reappraisal were then more accurately processed in long term explicit memory. Implicit schematic memory was also altered fro a self schema in which one is a drinking alcoholic to one in which one is a recovering alcoholic.

So-called positive associations in long term episodic and explicit memory were,  when labile via recall, then challenged and replaced by more accurate negative associations in long term memory – no memories needed to be erased just reappraised more accurately.

 

mad scientist

 

This type of ongoing experiment is happening on a daily basis at an AA meeting near you.

AA groups have found that memories need not be erased, with possible deleterious knock on effects on fear processing and amgydaloid performance, but rather memories simply need to be faced up to, and via honesty appraisal reprocessed more adaptively in long term memory.

This also means alcoholics in recovery can use their addiction memories in not only clearing away the wreckage of the past, repairing broken relationships with loved ones and society as a whole by  making amends to those involved in this wreckage and also put the memories of the past to excellent therapeutic use by using it to help others with similar memory difficulties.

In fact even academic researchers have found and have demonstrated that abstinent, treatment seeking individuals also have a different cognitive or/and memory bias to active alcoholics. This has been illustrated in findings that the greater “accessibility” for positive vs. negative alcohol- associations in heavy vs. light drinkers was not found to be generalized to alcoholics in treatment vs. social drinkers (2). Rather, there was a trend for treated inpatients, motivated to attain abstinence, to show greater availability and accessibility for negative alcohol-related information.

This is how to use memories of addiction to the best possible use, instead of erasing them, wiping them our and hoping for the best, memories of our addiction can be used to great purpose in helping others. Also “addiction memory” is often activated by those who have not come to terms with their alcoholism and still want to drink. Unless some one has come to terms with their alcoholism little can be done, by erasing memories or otherwise. These are sticking plasters on a gaping wound. They will be replaced with other “addiction memory” as there an underlying condition to alcoholism ( we believe it to be emotional regulation and processing deficits) and it is this that drives this fear-based condition called alcoholism, memories are the result of this malady. Address the underlying conditions and the rest takes care of itself.

It is not brain regions which are the problem either such as activation of the amgydala, it is how this sometimes errant and overactive brain region in alcoholics is tamed via the serenity found in the AA program of recovery.

The compel parts of the brain, Everitt mentions,  are activated by emotional distress, so treat the distress not the symptom of it. He also confuses implicit, automatic memory, with explicit, conscious memory. Either way they are both activated by stress/distress, and are thus both emotional memories.  Again treat the emotional dysregulation, the primary problem not the secondary manifestation of the problem.

As I mentioned above, there has been an ongoing experiment into recovery from alcoholism going on for nearly 80 years now, there is a lab in most areas of town.

It would benefit the world and science, in particular, if neuroscientists would pop in for a coffee and check our our findings.

 

References

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

 

Why a spiritual solution?

Posted on by alcoholicsguide

In the first in a series of blogs we discuss the topic of why does the solution to one’s alcoholism and addiction require a spiritual recovery.

This is a much asked question within academic research, although the health benefits of meditation are well known and life styles incorporating religious affiliation are known to increase health and span of life.

I guess people are curious as to how the spirit changes matter or material being when it should perhaps be rephrased to how does application of the ephemral mind affect neuroplasticity of the brain. Or in other words how does behaviour linked to a particular faith/belief system alter the functions and structure of the brain. We have discussed these points in two blogs previously and will do so again in later blogs. Here I just want to highlight in a short summary why spiritual practice helps alcoholics and addicts with with regulating themselves especially when the areas of their brains which govern self regulation have been taken over by the action of drugs and alcohol, so that they have very limited control over their own selves and their own behaviour.

This seems to be at the heart of addiction and alcoholism, this increasingly limited self control over addictive behaviors. In addressing this need for a spiritual solution we also hope to address choice versus limited control arguments. As we will see, the addicted or alcoholic brain is usurped to such a profound extent by effects of drugs and alcohol and this brain acts so frequently without conscious awareness of the negative consequences of these actions that it is appears undoubtedly the case that addicts and alcoholics have profoundly diminished control over their choices of behaviour.

This is especially pertinent in chronic addicts and alcoholics were the thrill is long gone so why would they continue doing something which has little reward other than because they are compelled to.

In addiction, vital regions of the brain and processes essential to adaptive survival of the species become hijacked or usurped or “taken over” by the combination of the effects of alcohol or drugs or addictive compulsive behaviours (acting as pharmacological stressors)  on pre-existing impairment in certain parts and functions of the brain. The actions of drugs and alcohol lead to a hyperactive stress system which enhances the rewarding aspects of drugs and alcohol in initial use, especially in those with maladaptive stress response such as individuals who have altered stress systems in the brain due to abusive childhood experiences (1-3).

In the second abusing phase, stress interacts with various neurotransmitters especially dopamine to drive this abusive cycle. In this phase of the addiction cycle  stress heightens attention towards cues and creates an  heightened attentional bias towards drugs and alcohol (4,5). Stress chemicals also increase activation of “addiction memory” (6,7). Thus there is multi-network usurping of function in the brain as the addiction cycle progresses (8). Recruited of attention, reward and memory networks are enhanced by the effects of stress chemicals.

Stress also enhances the rewarding effects of alcohol and drugs so makes us want them more (9). Enjoy them more. These are the so-called “good times” some of us look back on, in our euphoric recall.

In the final endpoint phase of addiction, stress incorporates more compulsive parts of the brain, partly by the stimulus response of emotional distress which automatically activates a compulsive response to approach drug and alcohol use while in distress, which is a common reality for chronic addicts and alcoholics.

 

10350601_792571304116059_8113905016770358871_n

 

Thus stress chemicals acting on mainly dopamine  circuits in the brain and other neurotransmitters eventually take over control of the brain in terms of the control of behaviour (8).

In usurping  “survival” or self regulation networks in the brain, control over behaviour “implodes” or collapses inwards, from control over behaviour moving inwards from the action outcome, or goal directed, conscious prefrontal cortex to the unconscious automatic, motoric, subcortical  parts of the brain (10).

This greatly limits one’s conscious self control over one’s own behaviour  if one is addicted or chronically alcoholic. Control of behaviour appears to have becomes a function of hyperactive stress systems in the brain and their manifestation as emotional distress (11,12).

This emotional distress constantly activates a “flight or flight” response in the brain and this means behaviour is carried out without reflection or without explicit knowledge of consequences, usually negative in the case of addiction (13,14).

The alcoholic or addicted brain becomes a reactionary brain not a forward thinking, considering of all possible options type of brain. The addict or alcoholic becomes driven by his brain and to a great extent a passenger in his own reality. Automatic survival networks act or react continually as if the addicted brain is on a constant state of emergency, constantly under threat.

There is a profoundly reduced conscious cognitive control over behaviour. This heighted, excessive and chronic stress and distress cuts off explicit memory of previous negative consequences of our past drinking and drug use and recruits implicit memory systems which are mainly habitual and procedural, they are “do” or “act” without conscious deliberation systems of the brain (14) .

It is as if our alcoholic or addicted brains are doing the thinking for us. Or not as the case may be. Alcoholics are on automatic pilot, fuelled by distress.  This neuroscientific explanation fits almost perfectly with the description of alcoholism in the Big Book of Alcoholics Anonymous, “The  fact is that most alcoholics…have lost choice in drink. Our so-called will power becomes practically nonexistent. We are unable , at certain times,  to bring into our consciousness with sufficient force the memory of the suffering and humiliation of even a week or month ago. We are without defense against the first drink”

The” suffering and humiliation” are now called “negative consequences” in current definitions of addiction…”continued use despite negative consequences”. (15)

images (15)

 

We “cannot bring into our consciousness with sufficient force the memory” because this is an explicit memory cut off by the effects of excessive stress which “offlines” the prefrontal cortex and hippocampal memory in favour of unconscious habitual, implicit or procedural memory (14,16). The memory of drinking not the memory of the “ situations surrounding this drinking”. How is this not a disorder  that has placed us “ beyond human aid” and beyond our own human aid” ? 

The “unable at certain times” are possibly times of great distress or emotional dysregulation and they leave the alcoholic and addict vulnerable to  relapse.

“Once more: The alcoholic, at certain times, has no effective mental defence against the first drink.”

“His defence must come from a Higher Power”

In later blogs we will discuss, in terms of the brain, why we need to recruit parts of the brain, via selfless behaviours, which activate areas outside those implicated in self regulation.

The cited  power greater than ourselves in AA meetings, for example, often follows an experiential trajectory – first it is the first person an alcoholic asks for help whether a family member, loved one or a G.P. – this often leads to an AA meeting or a treatment centre – then they are presented with other alcoholics who suffer from the same disorder – in AA parlance this is the first, and for many alcoholics in recovery, their only experience or attempt to find G.O.D. – this Group. of. Drunks. is like all that preceded it, a power greater than ourselves, regardless on whether we attain a spiritual connection with God after that.

A sizable minority in AA remain agnostic or atheist. This does not mean they have not performed essentially “spiritual” acts such as asking for help, accepting powerless over their life at that present moment. These are all acts of humility of accepting one needs help from beyond oneself. They also attend meetings where no one is in charge apart from God as He may express Himself in our group conscience.

Our first sponsors (mentors) in AA are also a power beyond ourselves as are their sponsors and their sponsors and the people in all their lives who advise and support. From the moment one has wholeheartedly accepted the need for help, one has accepted that help will come from a power greater than themselves.  It is a humbling and I believe spiritual act. A new breath filling one’s life.

All these people are already doing something for us which we could not do ourselves, they are helping us recruit the prefrontal cortex and explicit memories of the disasters alcohol or drug addiction has wrought on our lives – they move, eventually, activity in the brain from the unthinking dorsal striatal to the reasoning prefrontal cortex, helped also by sharing our stories in meetings. They give us a new recovery alcoholic self schema to replace the former drinking alcoholic self schema and stores it in implicit memory.

These people helps us change positive memory association of alcohol with negative associations. They overturn old ideas about the good times with a deep awareness of how bad these so-called good times were. The attentional bias is avoided or is rarely activated as the distress and stress are greatly reduced so as not to activate it.

We find recovery rewarding in the way we formerly (but not latterly) found drinking. In fact we find recovery better than drinking even at it’s best. The worst day in recovery seems much better than the worst day in drinking. We learn how to regulate our emotions so as to avoid prolonged bouts of distress, we ring our sponsors when such moments arise, talk to a loved one.

Again an external prefrontal cortex helps us climb out of the sub-cortical “fear” areas of the dorsal striatum and the anxious amgydala. The solution  is in the prefrontal cortex, in it’s control over emotions, in it’s clear appraisal of our past, in it’s activation of negative, realistic  memories of the past and  in avoiding the people, places and things which remind us of drinking.

The prefrontal cortex becomes more in charge rather than our illness doing the thinking. The prefrontal also gets strengthened by us sharing our experience strength and hope at meetings, it uses a recovery narrative to reconcile the drinking self with the recovering self, making us whole,  it embeds in our mind the truth of the progressive nature of this illness. It helps us see what it was like, what happened and what it is today. It gives us the tools to help others.

In the follow up blog to this we will further explore how this works – this spiritual solution.

 

References

1. Cleck, J. N., & Blendy, J. A. (2008). Making a bad thing worse: adverse effects of stress on drug addiction. The Journal of clinical investigation, 118(2), 454.

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

3. Sinha, R. (2008). Chronic stress, drug abuse, and vulnerability to addiction. Annals of the New York Academy of Sciences, 1141, 105–130

4. Peciña, S., Schulkin, J., & Berridge, K. C. (2006). Nucleus accumbens corticotropin-releasing factor increases cue-triggered motivation for sucrose reward: paradoxical positive incentive effects in stress?  BMC biology, 4(1), 8.

5. Ventura, R., Latagliata, E. C., Morrone, C., La Mela, I., & Puglisi-Allegra, S. (2008). Prefrontal norepinephrine determines attribution of “high” motivational salience. PLoS One, 3(8), e3044

6. Hyman, S. E. (2007). Addiction: a disease of learning and memory. Focus, 5 (2), 220.

7.  Adinoff , B. (2004) Neurobiologic processes in drug reward and addiction, Harvard Review of Psychiatry

8. Duncan E, Boshoven W, Harenski K, Fiallos A, Tracy H, Jovanovic T, et al  (2007) An fMRI study of the interaction of stress and cocaine cues on cocaine craving in cocaine-dependent men. The American Journal on Addictions, 16: 174–182

9. Berridge, K. C., Ho, C. Y., Richard, J. M., & DiFeliceantonio, A. G. (2010). The tempted brain eats: pleasure and desire circuits in obesity and eating disorders.Brain research, 1350, 43-64.

10. Everitt, B. J., & Robbins, T. W. (2005). Neural systems of reinforcement for drug addiction: From actions to habits to compulsion. Nature Neuroscience, 8, 1481–1489

11. Sinha, R., Lacadie, C., Sludlarski, P., Fulbright, R. K., Rounsaville, B. J., Kosten, T. R., & Wexler, B. E. (2005). Neural activity associated with stress-induced cocaine craving: A functional magnetic resonance imaging study. Psychopharmacology, 183, 171–180.

12. Goodman, J., Leong, K. C., & Packard, M. G. (2012). Emotional modulation of multiple memory systems: implications for the neurobiology of post-traumatic stress disorder.

13. Schwabe, L., Tegenthoff, M., Höffken, O., & Wolf, O. T. (2010). Concurrent glucocorticoid and noradrenergic activity shifts instrumental behavior from goal-directed to habitual control. Journal of Neuroscience, 20, 8190–8196.

14. Schwabe, L., Dickinson, A., & Wolf, O. T. (2011). Stress, habits, and drug addiction: a psychoneuroendocrinological perspective. Experimental and clinical psychopharmacology, 19(1), 53.

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

16. Arnsten, A. F. (2009). Stress signalling pathways that impair prefrontal cortex structure and function. Nature Reviews Neuroscience, 10(6), 410-422.

 

At Risk Adolescents have Emotional Dysregulation?

Posted on by alcoholicsguide

Following up from our previous blog on the abnormalities in the ventromedial prefrontal cortex  (vmPFC) in alcoholics,  brain regions which govern emotional regulation, we came across another study which appears to show that adolescents at increased risk for later alcohol use disorders (AUDs) may also be showing an emotion regulation difficulty.

This emotional regulation difficulty may be a biomarker for later alcoholism, which is in keeping with our previous proposals that an emotional processing and regulation difficulty or disorder underpins the aetiolgy of of alcoholism. In order words it is part of the pathomechanism – or the mechanism by which a pathological condition occurs- of later alcoholism.

 

 ventromedial-prefrontal-cortex

 

The area in this study, the vmPFC,   showed relatively increased cerebral blood flow (CBF) in bilateral amygdala and vmPFC and relatively decreased CBF in bilateral insula, right dorsal anterior cingulate cortex (ACC) and occipital lobe cuneus of high-risk adolescents. This suggests that adolescents at relatively high-risk for AUD exhibit altered patterns of resting CBF in distributed corticolimbic regions supporting emotional behaviors.

The authors’ hypothesized that the relatively increased amygdala and ventromedial prefrontal CBF may contribute to increased emotional reactivity and sensitivity to environmental stressors in these individuals while diminished insula/occipital cuneus and dorsal anterior cingulate cortex (ACC) CBF may lead to poor integration of visceral and sensory changes accompanying such emotional stress responses and top-down regulation of amygdala reactivity.

Thus we see our model in a snapshot even in adolescents potentially.  The emotional processing deficits we have discussed previously implicate the insula and ACC, as there appears to be a difficulty in alcoholics in reading emotional or somatic signals/states and integrating these signals into the identifying, labelling and processing of emotions. Equally there appears to be a hyperactivty in the vmPFC and amgydala as with alcoholics which implies emotional dysregulation, a hyper reactive emotional response and a tendency perhaps to a more “fight or flight” response, distress based impulsivity and short termist decision making, wanting it NOW rather than later.

 

References Lin, A. L., Glahn, D. C., Hariri, A. R., & Williamson, D. E. (2008). Basal Perfusion in Adolescents at Risk for Alcohol Use Disorders. In Proc. Intl. Soc. Mag. Reson. Med (Vol. 16, p. 60).

Predicting relapse via extent of emotional dysregulation?

Posted on by alcoholicsguide

Predicting relapse via extent of emotional dysregulation?

by alcoholicsguide

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

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

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

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

 

Figure6_ADHC_revised_2_7_12

 

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

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

 

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

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

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

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

 

References

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

 

Processing the Past via the action steps, 4-12!

Posted on by alcoholicsguide

 

 

Processing the Past via the actions steps, 4-12!

by alcoholicsguide

How The Alcoholics Anonymous’ program of action helps with emotional dysregulation.

When I first came into recovery I was surprised how much more time I spent embroiled in thinking about past incidents and how I had numerous murderous resentments  about people who had supposedly done me wrong, than I did thinking about drinking.

The thought of drinking terrified me rather than enticed me. Fortunately it also made be nauseous and fortunately still does. A full year of vomiting on an empty stomach, throughout each and every interminable day and night, has had some aversion like effect.

I had literally hundreds of thoughts and negative emotions about the past streaming through and around my aching head and piercing my heart. They were like toxic mind darts that flipped my guts and almost made me physically ill. Even thinking back now makes me feel queasy.

It was a constant state of emotional distress, those early days of recovery.

I was shocked as the weeks trudged on painfully that I seemed to have problems other than the drink. I was reassured by many other AAs in meetings when they shared about how difficult life was on life’s terms – how they struggled with resentments and fears and their “emotional disease”. I was was glad it wasn’t just me.

I had finally found a club where I fitted in! After all these years. In fact most people I drank with were also alcoholic! So I have always sought the company of my own. I thought we could only be found in pubs! And here we had rooms of them talking about trying to stay “emotionally sober”. It wasn’t just sobriety it had to be emotional sobriety. I was, through my fading eyesight and mercifully abating alcoholic psychosis, greatly intrigued by this. My life, and their lives, had become unmanageable, they said,  not just because of the drink, but because of some underlying condition.

I was especially interested in why I was so cursed by memories of my past. Why hadn’t they gone away? Why had they come back so prolifically in early recovery. The alcohol must have keep some of them suppressed, at bay. Now they were teeming through, poisoning my mind just as effectively as any alcoholic withdrawal or rattling hangover ever did. It was difficult not to somehow see these rampant, rampaging negative thoughts and emotions as akin to a disease. When they spoke of spiritual disease, it seemed to describe what was happening in my head.

I have “done” the steps three times and each time has offered more insight into this spiritual malady which I call an emotional disease. Why? Well because the sure sign of a spiritual malady, I believe,  is the expression and lack of control over negative emotions. The emotional lability and volatility. The bad temperedness, the indignition at life’s flaws, the perfectionism, the need to control, the righteous anger. We sin via these negative emotions. Have you ever heard of someone sinning via positive emotions? “Yes he wronged me by being so kind and generous, thoughtful and loving, to hell with that man!” So why are we so scared of the e word, emotion.

We sin via, or have defects of character which are, negative expressions of emotion. Intolerance, or impatience, selfishness, fear based dishonesty and so on. All expressions of distress. A fear based illness?  I like the term defect of character because it suggests sometime intrinsic to alcoholics. I call this inherent aspect of this condition called alcoholism, emotional regulation and processing difficulties.

In this blog I will attempt to explain how the 12 steps of AA, principally the action steps 4 through to 12, have not only connected me with a power greater than myself  but they continue to treat, on a daily basis, my unmanageability.  An  unmanageability caused inherently by my difficulties processing and regulating emotions.

 

12 steps pic

 

I have looked hard for supporting evidence to substantiate what I am about to write and found this link to an interesting piece on the use of EMDR and other therapies in treating the unprocessed emotions caused by emotional dysregulation in those who suffer from trauma. I have used aspects of this to make it applicable to alcoholics. I believe profoundly that steps 4-12 facilitate a profound alteration in our ability to regulate and process emotions.

Steps 4 -7,  in particular help us to embed the numerous unprocessed memories from childhood onwards, that all seem to have been tied together in a terrible mnemonic mesh by aspects of emotional dysregulation such as resentments.  It is in addressing all these that we finally process these associated negative emotions in our memory banks and finally embed all these memories in long term memory.

In short, the Steps allow us to adaptively and healthily process our disturbed pasts. They also allow us to maintain a health and adaptive emotional regulation  on a daily basis and via steps 10-12 in particular allow us to greatly improve our emotional regulation.

I am not rewriting the Big Book of AA here, only to add another angle to understanding it and how it works, so that others in related therapeutic fields can have some insight into how it may work and those who need help feel more inclined to come to AA for help.

http://www.thebody.com/content/art48754.html   – Refer also to the work of Francine Shapiro (1) and her work which shaped development of the EMDR therapy which treats trauma (PTSD) and other disorders. I know it works for PTSD as my wife suffered PTSD after a car accident, and was greatly helped by this type of treatment. It is Shapiro’s insight into the role of unprocessed emotions in causing emotional volatility and a “volcano of unresolved distressing effects” (2) and that  chronic dysfunctional perceptions, responses, attitudes, self-concept, and personality traits are all symptoms of unprocessed memories (3) that shapes my thinking, partly, on how the steps allow us to put the past to bed.

I have to add also that I believe myself to be a sufferer of PTSD also. I have stressed that alcoholism is a psychiatric disorder in it’s own right but would never be silly enough to suggest it does not have co-occurring disorders such as PTSD, as the result of abuse and trauma in earlier life experience. Especially as there as up to 2/3s of dependent people may have had abuse in their early lives and that PTSD sufferers have up to a 50 % co-morbidity with alcoholism and addiction. Perhaps this is why this work by Shapiro strikes a cord with me. I think it is naive to say that abusive early life does not play a role in alcoholism and addition and that this environmental influence on genetic inheritance (alcoholism has a a generic heritability of some 50 – 70% making one of the most inheritable disorders). In other words, some 50 – 70% of alcoholics have alcoholism in their genes.

Throughout our lives, we all experience significant events that impact our perceptions of the world and determine how we interpret and respond to future experiences. These moments represent painful experiences so severe that they overwhelm our ability to cope with the rush of thoughts and feelings they elicit and If left unresolved, these feelings can persist for years in unprocessed emotions.

As a general rule, anything destructive that is left untreated — disease, trauma, stress, psychological disorders, addiction — can become progressively worse over time. Coming to terms with the past is often referred to as “integration,”  of these errant unprocessed emotions and achieving resolution. One way this resolution can be accomplished is by verbally and somatically (by being aware of how they affect one bodily) reprocessing these, like in step 5 when discussing one’s inventory, and the rewards can be transformative.

Mental networks contain visual images of the previous experiences  as well as related thoughts, emotions, and sensations. Previous experiences — including every physical sensation, every emotion, and every perception or interpretation — are encoded and stored in the brain and throughout the body. The processing of information about previous events may be incomplete, perhaps because the person has not developed the emotional or mental faculties to effectively manage or correctly interpret the situation (often the case with children who have faced abuse, trauma, insecure attachment to caregivers) or because processing is hindered by strong negative feelings (such as shame, helplessness, and denial) which I believe may be the consequence of emotional dysregulation.

images (3)

 

The memory of the previous experiences can  therefore be improperly stored without appropriate associative connections and with many elements still unprocessed. This incomplete processing prevents the forging of connections with more adaptive information or new learning which might help the person release the abusive, traumatising, misrepresented, resented, emotionally dysregualted and unprocessed experiences from the past. Finally when we do process these experiences then we can consign them to, embed them, happily in long term memory.

In a previous blog we say how one maladaptive emotional regulations strategies that of self elaboration, where one regulates a negative emotional experience by filtering in through the self and then elaborating on this in a ruminating manner, i.e. only seeing an event in relation to themselves, in self- reference (similar to a resentment)  and that our minds in early recovery are thus filled with these unprocessed memories as the consequence of this type if emotional dysregulation which filtered everything through a self centredness. In many cases we began to see in our step 4 inventory that it was often our emotional dysregultation that caused others to act in certain ways which we interpret, whether for valid reasons or not, in a self centred and distorted way which was base on emotional reasoning. These unprocessed emotions and memories thus lingered on in our minds for decades, festering as resentments and fuelling our drinking and drug use.

Doesn’t Step 4 allow us to record these unprocessed memories, get them down in black and white, with the unprocessed emotions, the resentments and other negative unprocessed emotions, such as anger, fear, selfishness, self-centredness, dishonesty and son on.  Doesn’t it let us use our proper reasoning to see through our purely emotional reasoning?

Don’t we start to process these emotions and thus the attached memories by verbalizing them in a therapeutic sense to our sponsors, mentors, respected religious or spiritual guides, counsellors etc? Don’t we learn to see what has kept us enslaved in feelings of injustice, resentment, of being wronged? Doesn’t it help us see how our emotional dysregulation distorts our perception of reality, and leads to a negative bias in our thinking about life and the people in it? Doesn’t it show us our underlying problem, our underlying psychiatric condition, which the steps helps us then to manage, to help us become manageable. We are not powerless over alcohol when we manage our negative emotions.

The Steps 6 and 7 allow us to have these removed. I believe God remove my many previous unprocessed emotions and memories, helped me consign then to the past and my long term memory. They did not go into ether as i fist thought, but into were processed in long term memory. This is no way lessens the Grace of God or his mercy.  He helps me do what i cannot, He goes deep! Steps 8 and 9 process these emotions even more via making amends for our wrongdoings and getting rid of the potential distress associated with unresolved situations from our past.  The final recognition of the effects our emotional dysregulation has had on our wider community.

Aren’t the steps, primarily to help us manage our emotional dysregulation?

Isn’t this what was unmanageable? Wasn’t it this which gave King Alcohol power over us? Doesn’t the AA program of action help us in a similar way EMDR does with trauma victims?

Step 10 helps us on a daily basis look out for manifestations and examples on how we hurt others with our lack of control over our negative emotional response, our dysfunctional emotional response. It gives us a way to examine and process these emotions and to take action to apologise to those who experienced this emotional volatility. It helps encourage positive, healthy, adaptive emotional expression.

Step 11 helps us self soothe and this helps our emotional regulation, meditation improves  and strengthens the very brain areas which regulate emotion, the dlPFC and ACC, which help control our anxious amygdala, the very the heart of all distress.  And via Step 12 we regulate our emotions in one of the most profound ways possible by helping others. By showing love. There is little dyregulation in love, the most healthy of human  emotional expression. ..and in all our affairs! We do not become intolerance of other is upholding “Principles not personalities”

Love contains the positive assets hopefully also listed in your inventories; selfishness, consideration, patience, tolerance etc  – the aspects of healthy emotional being. Perhaps this is another reason why Step 12 is so profound in helping us manage the unmanageability of our emotional dysregulation.

And fellowship itself, gives us an “earned attachment” especially when many of us had insecure attachments with our parents, grew up in dysfunction, disrupted families, in abuse or trauma. It helps us finally “belong”.  Fellowship  allows us perhaps to express our emotions fully for the first time, allows us to verbalize our concerns and feelings, label them for the first time, regulate and process them. Provides a safe environment in which to emotionally mature. The list goes on and on. AA gives us loving feedback, nurtures us, nourishes us.  Home groups with regular members over many years obviously aid this process of caring and mutual self growth.

It has become more clear while writing this how AA manages this emotional disease we call alcoholism.

The AA program of action helps us change how we feel and think about the world.

References

1. Shapiro, F. EMDR Therapy: Adaptive Information Processing, Clinical Applications and Research Recommendations.

2. Courtois, C. A., & Ford, J. D. (Eds.). (2009). Treating complex traumatic stress disorders: An evidence-based guide. New York, NY: Guilford Press.

3  Alcoholics Anonymous. (2001). Alcoholics Anonymous, 4th Edition. New York: A.A. World Services.

Some references to follow.

How far have we come in understanding this emotional disorder?

Posted on by alcoholicsguide

A constant thread throughout our blogs so far has been an assertion that alcoholism and addiction are primarily emotional regulation and processing disorders.

So we were thus  very interested to find this article (1) which describes how we are not the first to view alcoholism and addiction this way.

Here we use this article to present a  brief history of research, dating back to the 1930s, that has viewed alcoholism and addiction in a similar way to we do now in 2014.

 

“Life, as we find it, is too hard for us; it brings us too many pains, disappointments and impossible tasks. In order to bear it we cannot dispense with palliative measures. (…), intoxicating substances, which make us insensitive to it” (Freud, 1930, p. 75).

 

Rado (1933) was the first to describe substance use as a way of coping with excessively difficult states of emotions (3).

Others subsequently interpret the phenomena as a maladaptive way of fighting against stress, anxiety, and depression (4-6). Krystal and Raskin(1970) emphasize the undifferentiated and archaic, somatically manifested, emotions of persons suffering from addictive disorders (7).

These emotions are fixed at this level owing to their early traumatic nature.

Later, McDougall (1984) also highlighted the importance of overflowing emotions in the case of people with addictive disorders (8). He identified substanceuse as a compulsive way of canalizing these overflowing emotions. Conclusively, we can see that in all of these mainly psychoanalytically oriented theories, substance use is present as an instrument to regulate emotions.

This approach is elaborated unequivocally in the theories of Leon Wurmser and Edward J. Khantzian. According to Wurmser (1974), people with addictive disorders are unable to regulate their undifferentiated feelings, impulses, and pervasive internal stress, and so they turn to psychoactive substances (9). Their substance use can thus be recognized as an attemptat “self-treatment.” The self-medication hypothesis of Khantzian (1985) also highlights emotion regulation in the background of addictions (10).

He asserts that drug use in fact emerges as the common result of psychopharmacological functioning and overwhelmingly painful emotions. Like Wurmser, Khantzian also points out that the choice of substance is specific to the person’s self-regulation and affect-regulation problems, as well as his/her personality dysfunctions (11).

More recently we have had Cheetham’s affect- centred theories of addiction (12).

Apparently, clinical observations highlight mainly those dimensions in the background of psychoactive substance use—primarily the presence of undifferentiated, overflowing, dominantly negative and painful feelings, and difficulties in emotional expression and emotional regulation—which appear to be basic components of the later Emotional Intelligence (EI)  construct (13). For instance, according to Mayer and Salovey (1997), the main components of EI are: (1) the perception, appraisal, and expression of emotions; (2) the emotional facilitation of thinking; (3) understanding and analyzing emotions, and employing emotional knowledge; and (4) the regulation of emotions.

The most important empirical findings regarding our topic may be those studies, which attempted to explore the relationship between addictions and alexithymia.

The concept of alexithymia (14) was created by Ruesch (1948) but the definition of Nemiah and Sifneos is more widely known (15,16).

The four main characteristics of alexithymia are: (1) difficulty identifying feelings and distinguishing between emotions and corresponding bodily sensations; (2) difficulty describing feelings to others; (3) constricted imaginal life and fantasies; and (4) externally oriented cognitive style (17).

The relationship between alexithymia and emotional consciousness or emotional intelligence was confirmed by several studies (18-20). These studies pointed out that a low level of EI correlates with a high level of alexithymia.

These results are hardly surprising, given that the ability to identify and express emotions is an important component of EI.

Besides clinical observations (21), empirical studies have also shown that people with addictive disorders—mainly alcoholic patients or those diagnosed with eating disorders—have difficulties with the verbalization and expression of their feelings, so in their case the problem of alexithymia is more frequent than in the normal population (22-24)

One study looking at a meta analysis of research into emotional aspects of addiction (1) found – 12 of these studies solely measured the ability to identify emotions – Oscar-Berman and colleagues (1990) were the first to draw attention to the fact that alcohol addicts, especially those suffering from Korsakoff‘s syndrome, have difficulties in identifying and decoding emotions mediated by facial expressions (25).

Underlying the inaccuracy of decoding is the overestimation of intensity of emotions, especially negative ones, characteristic of alcohol patients (26-29). They also tend to associate negative emotions more often with each of the presented facial expressions (30). Furthermore, Kornreich and colleagues have pointed out that the ability to identify emotions is tightly and negatively associated with interpersonal problems, and these problems seem to be a mediating factor between emotional identification deficits and alcoholism (31). All of these findings may relate to results stating that people with alcohol addiction tend to interpret facial expressions, like sadness or disgust, falsely as emotions describing interpersonal conflicts, like anger or contempt (32).

This latter result is also supported by an Italian study (33). A further important outcome of these investigations showed that alcohol-addicted patients, in spite of their weaker capacity, rate these emotion-decoding tasks at the same difficulty level as do people from the control groups. It therefore seems as though they are not aware of their difficulties in identifying emotions.

At the same time, however, this distortion in the subjective ratings is not only characteristic of alcohol addiction, but is present in the case of opiate-addicted people as well (34,35). These studies also highlighted that alcoholism is associated with poorer emotion-decoding  abilities than compulsive use of opiates.

causes-of-addiction_mini

 

We have discussed emotional processing deficits in alcoholics and addicts in another blog.

The prevalence rate of alexithymia in alcohol use disorders is between 45 to 67% (36,37). Finn, Martin and Phil (1987) investigated the presence of alexithymia among males at varying levels of genetic risk for alcoholism. They found that the high risk for alcoholism group was more likely to be alexithymic than the moderate and low genetic risk groups (38).

The inability to identify and describe affective and physiological experiences is itself associated with the elevated negative affect (39) commonly seen in alcoholics, even in recovery (40). This latter study also highlighted the link between alexithymia and the emotional dysregulation inherent in addictive disorders.

Thus, the unpleasant “undifferentiated emotional” experience of early theories might prompt individuals to engage in maladaptive behaviors, such as excessive alcohol consumption, in an effort to regulate emotions, or, more specifically, cope with negative emotional states (41).

We now see how neurobiological models can marry statisfactorially wih psycho-analytic theories. This will be especially the case when we blog about alexithymia, addictive and theories of attachment.

We have thus moved from a mainly clinical perspective on the role of emotional difficulties in addiction to providing some neuroscientific evidence that these theories were actually on to something, namely these theories were pointing the way to further conceptualisations of addiction as a disorder of emotional regulation and processing. 

 

References

1. Kun, B., & Demetrovics, Z. (2010). Emotional intelligence and addictions: a systematic review. Substance use & misuse, 45(7-8), 1131-1160.

2. Freud, S. (1930). Civilization and its discontents. In J. Strachey (Ed.), The standard edition of the complete psychological works of Sigmund freud (Vol. 21, pp. 59–145). London: The Hogarth Press

3. Rado, S. (1933). The psychoanalysis of pharmacothymia (Drug Addiction). Psychoanalytic Quarterly, 2:1–23

4. Chein, I., Gerard, D. L., Lee, R. S., Rosenfeld, E. (1964). The road to H. New York: Basic Books

5. Fenichel, O. (1945). The psychoanalytic theory of neurosis. New York: Norton

6. Hartmann, D. (1969). A study of drug-taking adolescents. Psychoanalytic Study of the Child, 24:384–398.

7. Krystal, H., Raskin, H. A. (1970). Drug dependence. aspects of ego functions. Detroit: Wayne State University Press.

8.  McDougall, J. (1984). The “dis-affected” patient: reflections on affect pathology. Psychoanalytic Quarterly, 53:386–409.

9. Wurmser, L. (1974). Psychoanalytic considerations of the etiology of compulsive drug use. Journal of the American Psychoanalytic Association, 22:820–843.

10. Khantzian, E. J. (1985). The self-medication hypothesis of addictive disorders: focus on heroin and cocaine dependence. American Journal of Psychiatry, 142:1259–1264.

11. Khantzian, E. J. (1991). Self-regulation factors in cocaine dependence – a clinical perspective. NIDA Research Monograph, 110:211–226.

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

13.  Mayer, J. D., Salovey, P. (1997). What is emotional intelligence? In P. Salovey & D. Sluyter (Eds.), Emotional development and emotional intelligence: implications for educators(pp. 3–31). New York: Basic Books.

14. Ruesch, J. (1948). The infantile personality. Psychosomatic Medicine, 10:134–144

15. Nemiah, J. C., Sifneos, P. E. (1970). Affect and fantasy in patients with psychosomatic disorders. In O. W. Hill (Ed.), Modern trends in psychosomatic medicine (Vol. 2, pp. 26–35). London: Butterworths.

16. Sifneos, P. E. (1967). Clinical observations on some patients suffering from a variety of psychosomatic diseases. Acta Medica Psychosomatica, 7:1–10

17.  Nemiah, J. C., Freyberger, H., Sifneos, P. E. (1976). Alexithymia: a view of the psychosomatic process. In O. W. Hill (Ed.), Modern trends in psychosomatic medicine (Vol. 3, pp. 430–439). London: Butterworths

18. Austin, E. J., Saklofske, D. H., Egan, V. (2005). Personality, well-being and health correlates of trait emotional intelligence. Personality and Individual Differences, 38:547–558.

19. Lane, R. D., Sechrest, L., Reidel, R., Weldon, V., Kaszniak, A., Schwartz, G. E. (1996). Impaired verbal and nonverbal emotion recognition in alexithymia.Psychosomatic Medicine, 58:203–210

20. Parker, J. D. A., Taylor, G. J., Bagby, R. M. (2001). The relationship between emotional intelligence and alexithymia. Personality and Individual Differences, 30:107–115.

21. Krystal, H. (1995). Disorders of emotional development in addictive behavior. In S. Dowling (Ed.), The psychology and treatment of addictive behavior(pp. 65–100). Madison, CT: International Universities Press.

22. Handelsman, L., Stein, J. A., Bernstein, D. P., Oppenheim, S. E., Rosenblum, A., Magura, S. (2000). A latent variable analysis of coexisting emotional deficits in substance abusers: alexithymia,
hostility, and PTSD. Addictive Behaviors, 25:423–428

23. Speranza, M., Corcos, M., Loas, G., Stephan, P., Guilbaud, O., Perez-Diaz, F., et al. (2005). Depressive personality dimensions and alexithymia in eating disorders.Psychiatry Research, 135:153–163.

24.Troisi, A., Pasini, A., Saracco, M., Spalletta, G. (1998). Psychiatric symptoms in male cannabis users not using other illicit drugs. Addiction, 93:487–492

25. Oscar-Berman, M., Hancock, M., Mildworf, B., Hutner, N., Weber, D. A. (1990). Emotional perception and memory in alcoholism and aging. Alcoholism: Clinical and Experimental Research, 14:383–393.

26. Foisy, M. L., Kornreich, C., Fobe, A., D’Hondt, L., Pelc, I., Hanak, C., et al. (2007a). Impaired emotional facial expression recognition in alcohol dependence: do these deficits persist with midterm abstinence? Alcoholism: Clinical and Experimental Research, 31:404–410

27. Kornreich, C., Blairy, S., Philippot, P., Hess, U., Noel, X., Streel, E., et al. (2001b). Deficits in recognition of emotional facial expression are still present in alcoholics after mid- to long-term abstinence. Journal of Studies on Alcohol, 62:533–542

28. Philippot, P., Kornreich, C., Blairy, S., Baert, I., Den Dulk, A., Le Bon, O., et al. (1999). Alcoholics’ deficits in the decoding of emotional facial expression. Alcoholism: Clinical and Experimental Research, 23:1031–1038

29. Townshend, J. M., Duka, T. (2003). Mixed emotions: alcoholics’ impairments in the recognition of specific emotional facial expressions.Neuropsychologia, 41:773–782.

30. Foisy, M. L., Kornreich, C., Petiau, C., Parez, A., Hanak, C., Verbanck, P., et al. (2007b). Impaired emotional facial expression recognition in alcoholics: are these deficits specific to emotional cues? Psychiatry Research, 150:33–41.

31. Kornreich, C., Philippot, P., Foisy, M. L., Blairy, S., Raynaud, E., Dan, B., et al. (2002). Impaired emotional facial expression recognition is associated with interpersonal problems in alcoholism. Alcohol and Alcoholism, 37:394–400

33. Frigerio, E., Burt, D. M., Montagne, B., Murray, L. K., Perrett, D. I. (2002). Facial affect perception in alcoholics. Psychiatry Research, 113:161–171

34. Foisy, M. L., Philippot, P., Verbanck, P., Pelc, I., Van Der Straten, G., Kornreich, C. (2005). Emotional facial expression decoding impairment in persons dependent on multiple substances: impact of a history of alcohol dependence. Journal of Studies on Alcohol, 66:673–681

35. Kornreich, C., Foisy, M. L., Philippot, P., Dan, B., Tecco, J., Noel, X., et al. (2003). Impaired emotional facial expression recognition in alcoholics, opiate dependence subjects, methadone maintained subjects and mixed alcohol-opiate antecedents subjects compared with normal controls. Psychiatry Research, 119:251–260.

36. Loas G, Fremaux D, Otmani O, Lecercle C, Delahousse J. Is alexithymia a negative factor for maintaining abstinence? A follow-up study. Comprehensive Psychiatry. 1997;38:296–299.

37. . Ziolkowski M, Gruss T, Rybakowski JK. Does alexithymia in male alcoholics constitute a negative factor for maintaining abstinence. Psychotherapy and psychosomatics. 1995;63:169–173.

38. Finn PR, Martin J, Pihl RO. Alexithymia in males at high genetic risk for alcoholism.Psychotherapy and Psychosomatics.1987;47:18–21

39. 16.  Connelly M, Denney DR. Regulation of emotions during experimental stress in alexithymia. Journal of Psychosomatic Research. 2007;62:649–656

40. Stasiewicz, P. R., Bradizza, C. M., Gudleski, G. D., Coffey, S. F., Schlauch, R. C., Bailey, S. T., … & Gulliver, S. B. (2012). The relationship of alexithymia to emotional dysregulation within an alcohol dependent treatment sample.Addictive Behaviors, 37(4), 469-476.

 

41. Thorberg FA, Young RM, Sullivan KA, Lyvers M, Hurst CP, Connor JP, Feeney GFX. Alexithymia in alcohol dependent patients is partially mediated by alcohol expectancy. Drug and Alcohol Dependence. 2011;116:238–241

 

Emotional Dysregulation, recovery and relapse

Posted on by alcoholicsguide

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 Behaviors, 33(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 Behaviors, 33(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 dependence, 121(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

 

The Distress at the Heart of Addiction and Alcoholism

Posted on by alcoholicsguide

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?