Why a spiritual solution?

The Alcoholics Guide to Alcoholism

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…

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Are Alcoholics Emotionally Immature?

Concerted attempts have been made to relate personality factors to alcohol dependence.

In fact, for many years, research attempted to define the so-called alcoholic personality. Attempts to do so have dwindled in recent years.

Potential alcoholics tend to be emotionally immature, expect a great deal of the world, require an inordinate amount of praise and appreciation, react to failure with marked feelings of hurt and inferiority, have a low frustration tolerance, and feel inadequate and unsure of their abilities to fulfil expected male or female roles.1

Although the obvious emotional immaturity often seen in alcoholics seems to cover a number of the more recent findings on bio-psychologcal aspects a alcoholism.

For example, if we partly defined emotional immaturity as containing some of the following, then we appear to be covering a number of much researched and demonstrated aspects of alcoholism. Do these then not come under an umbrella term of emotional immaturity? This list was complied by Psych Central

Dimensions of Emotional maturity

  1. The ability to modulate emotional responses.  Addicts tend to have an all or nothing emotional response.  When they respond they become overly emotional and take a longer time to return to baseline.  They are easily flooded with emotion to the point of impairing functioning.
  1. The ability to tolerate frustration.  Addicts tend to respond to frustrating situations as disasters rather than having any perspective.
  1. The ability to delay gratification.  Emotionally immature people have trouble planning and working toward goals.  The ability to give up immediate gratification is necessary for anyone to go about life in a successful way.
  1. The ability to control impulses.  The mature self has the ability to see that feeling the urge to do something is not the same as doing it.  The recovering addict has a level of control over his or her behavior and can put boundaries around what is inappropriate to say or do.
  1. The ability to be reliable and accountable.  Addicts are often self centered and not good at dealing with the everyday requirements of life like being on time, fulfilling obligations and telling the truth.  As they gain emotional maturity they gain the ability to get out of themselves and think about the impact of their actions on others and on their own lives as well.

 

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According to a list drawn up by alcoholrehab.com

If people are emotionally immature, they may exhibit some of the following symptoms:

* Such individuals will often find it hard to deal with the normal challenges of life. When they are faced with problems they feel unable to cope. They may have developed a psychological state known as learned helplessness.

They struggle to develop meaningful relationships with other people. They may appear too needy or a bit overbearing.
* Those people who are emotionally immature will tend to have a pessimistic outlook on life. They may see the future as a threatening and hostile place.
* This type of person will usually have low self-esteem. This means that they do not value themselves highly so will be willing to accept very little in life as being all they deserve.
* They find it almost impossible to live in the present moment. They are either reliving the past or worrying about the future.
* They can easily lose their temper at the slightest provocation. When they are dealing with uncomfortable emotions they will tend to take things out on other people.

* People who are emotionally immature can have unrealistically high expectations. This means that they are frequently disappointed. Such and individual can have impossibly high expectations for other people yet low expectations for themselves.
* Such individuals can suffer from severe mood swings. This instability of mood can make life a bit uncomfortable.
* If people are emotionally immature, they find it much harder to control their own behavior.

Recognize any of these symptoms?

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We were completely like this before doing the 12 steps.

We, however, do not think that anyone, alcoholics or otherwise choose to behave in this emotional immature way.

We have already looked at the emotional distress accompanies alcoholism and addiction, and will be examining more in the months ahead and it is difficult not to see the above emotional immaturity as all being products of a distress state.

In the course of addiction the alcoholic in particular grows in emotional distress as the stress and emotional dysregulation associated with addiction increases.

This means the brain “collapses” from more cortical, goal-directed (and emotionally regulated) areas of the brain to more sub-cortical areas which are more automatic, unthinking and compulsive.

Emotional distress activates these areas of habit-like compulsive behaviour, acting as a stimulus response, distress the stimulus and compulsive (unthinking)  responding as the response.

This is like a distress based or “fight or flight” reality or a heightened emotional state or “emergency” state. It seems to us that alcoholics live in this region more than cortical regions. They are primed to go off!

They then have a tendency to either run away from situations or to fight “everybody and everything”, to be intolerant of uncertainty, to catastrophize, to be fear-based people to be over reactive, hypervigilant, perfectionist etc These are all distress based states.

Are aspects of the  apparent emotional immaturity mentioned above not also not  a surface manifestation of these deep subcortical processes?

It is this state of heightened uncertainty and fear that whittles away at the alcoholic psyche. This amount of stress/distress promotes implicit, do, memory, over explicit, reflective, evaluative, memory. Distress makes one act without much thought of consequence, it makes one choose short term over greater long term gain, it makes one want to act impulsively or compulsively to alleviate distress. It is this distress that is in charge of action and emotional behaviour. It calls the shots.  A state of emergency has been called in the brain of the alcoholic.

I know it is widely shared at AA meetings that we got stuck in the emotional age of our first drink, in the early teens and never developed our emotional selves or capacity to regulate and process emotions. We are not sure this is completely true as the stress that accompanies alcoholism, as alcohol is literally classified as a pharmacological stressor,  not only causes chronic stress dysregulation but also the emotional dysregulation which accompanies this. It is emotional parts of the brain and the cortical areas that are supposed to keep them in check that are most impaired via chronic alcoholism.

Dr. Stephanie Brown (2) has explored these developmental changes in cognition, which lead to “alcoholic thinking.” She states that these changes refer “not only to rationalization, denial and frame of mind, but also to character traits that frequently accompany drinking. These include grandiosity, omnipotence and low frustration tolerance.” (3) These traits appear to be directly associated with the addictive process rather than with the individual’s personality prior to establishing this abusive cycle.

As alcohol becomes more dominant, the need to deny these changes becomes greater. It appears that there is an interaction between physiological changes and psychological defenses which creates emotional immaturity, self-centeredness and irresponsibility. Alcoholism becomes a thought disorder as well as an addiction to alcohol.

This is the consequence we believe of prefrontal atrophy and subcortical hypertrophy caused by chronic alcohol consumption, a constant injection a pharmacological stressor into the brain, wrecking the ability to maturely deliberate and instead rely on “I want it now!”  type of thinking.

We firmly believe this progression is to a state of constant distress signal in the brain and a cortical hyperarousal.

The alcoholic may not be emotionally distressed all the time but his brain is never satisfied, it constantly needs more, it finds only transient balance, via allostasis, it never finds true balance, i.e. homeostasis. it is always seeking, never reaching satiety, never completely at rest. This is emotionally exhausting.

It may represent, on superficial observation to some, the “emotional immaturity, self-centeredness and irresponsibility” (4) but is it really this simple, seeing these as the primary defenses and interpersonal style typical of normal development in the first three years of life or to characterize the addictive part of self as a “two-year-old child”?

Isn’t it more apt to say instead of  a “two-year-old wounded part of self begins to “drive the bus” and create havoc for all concerned” to say chronic stress manifest  as emotional distress “driving the bus”?

Thus a valid question remains for us and we ask it to our normies or earthling friends (i.e. non-alcoholics), wouldn’t you act in a childish if you were this distressed most of the time, having to rely on impaired emotional regulation and processing parts of the brain?

 

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In fact, to all those normies or earthlings who are reading this blog, how well do you think or consider others when in a state of persistent and daily distress? In this heightened anxiety how good is your action outcome memory, goal-directed planning and awareness of future consequence?

Are you ever moody, emotionally volatile and over reactive in this state of high anxiety? Hyper sensitive? Ever strike out unthinkingly at others although you had not intended to? Leading to guilt and shame, and remorse and self pity which can in the fullest of time lead to depression? This is called a transient emotional dysregulation, distress leading to an emotional cascade. This is the brain of an alcoholic all the time. It can lead to dejection and relapse.

In this sate of nauseating anxiety, how well do you consider the consequence, negative or otherwise, or your fear-based decision making?  Do you choose the short term answer in these anxiety-filled moments just to simply relieve this distress this unpleasant feeling of doom? So do alcoholics!

It is not enough to call the alcoholic emotional immature or stuck in the “terrible twos”, although let’s face it the evidence for it is compelling at times!! Let’s instead understand the reasons for it. Would you like to be in a state of distress most of the time? It’s not a whole lot of fun!

The 12 steps help solve these issues, there is a solution to emotional immaturity – it leads to emotional maturity or emotional sobriety which is blogged about here also.

The next time the alcoholic is your life acts in an immature way don’t ask them why they are acting that way, ask them how they feel. instead. Get them to identify, label and process their feelings  by verbalizing them.

When the anxious amgydala has quelled and  it’s feverish responding quietened,  get them to an AA meeting where many tens of thousands of alcoholics are doing the same, “sharing”, processing their emotions by talking about them and how they really feel.

 

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Not running away from them or intellectualizing about them, not fighting them. Simply saying in words how they feel.

It is a miracle awakening for us in recovery, the emotional regulation normies and earthlings take for granted.

The age of miracles is amongst us and it starts by opening your mouth, asking for help, getting help and getting real about what you are really feeling.

It is through sharing our deepest feelings that we start to mature and grow up.

 

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References

1. Chaudhury, S.K. Das, B. Ukil,  Psychological assessment of alcoholism in males Indian J Psychiatry. 2006 Apr-Jun; 48(2): 114–117. doi: 10.4103/0019-5545.31602

2. Brown S. (1985). Treating the Alcoholic: A Developmental Model of Recovery. New York: John Wiley & Sons, Spring.

3. Brown, S. (1988). Treating Adult Children of Alcoholics: A Developmental Perspective. New York: John Wiley and Sons.

4. http://www.cairforyou.com/alchoholdrugs/alcoholcharacter.htm

 

Processing Emotions by verbalising them!?

The Therapeutic Benefits of “Sharing”

In early recovery I did not have a clue what emotions I was experiencing. I was not able to identify, label or process them. As a result of his failure to process emotions I seemed to be constantly distressed and and, as we seen in previous blogs, this distress leads to a distress-based impulsivity and a negative urgency to either engage in “fight or flight” behaviour, i.e. running away from fearful situations or ignoring the Big Book of AA’s recommendation not to fight anybody or anything.

The only way I could handle these troublesome and frightening emotions was by talking about them to my sponsor or my wife or other people in recovery.

In recent years it has become evident to that what I have been doing all these years have been using a technique of verbalising my emotions to actually process them. I now believe this is a fundamental part of my recovery and that I sometimes need to verbalise my emotions in order to process them. How does this work?

I recently came across an article (1) which might shed some light on this process.

Putting feelings into words (affect labeling) has long been thought to help manage negative emotional experiences. Affect labeling or naming emotions diminishes the response of the amygdala and other limbic regions to negative emotional images.  A  brain imaging study by UCLA psychologists reveals why verbalizing our feelings makes our sadness, anger and pain less intense.

When people see a photograph of an angry or fearful face,they have increased activity in a region of the brain called the amygdala, which serves as an alarm to activate a cascade of biological systems (including stress chemicals) to protect the body in times of danger. Scientists see a robust amygdala response even when they show such emotional photographs subliminally, so fast a person can’t even see them.

But does seeing an angry face and simply calling it an angry face change our brain response? The answer is yes, according to Matthew D.Lieberman, UCLA associate professor of psychology.

“When you attach the word ‘angry,’ you see a decreased response in the amygdala,” said Lieberman, lead author of the study. The study showed that while the amygdala was less active when an individual labeled the feeling, another region of the brain was more active: the right ventrolateral prefrontal cortex.

This region is located behind the forehead and eyes and has been associated with thinking in words about emotional experiences. It has also been implicated in inhibiting behavior and processing emotions.

“What we’re suggesting is when you start thinking in words about your emotions —labeling emotions — that might be part of what the right ventrolateral region is responsible for,” Lieberman said.

If a newcomer to recovery one is sad or angry or resentful , getting them person to talk or write may many have benefits.

In Lieberman’s study  participant’s viewed images of individuals making different emotional expressions. Below the picture of the face they either saw two words, such as “angry” and “fearful” and chose which emotion described the face, or they saw two names,such as “Harry” and “Sally,” and chose the gender-appropriate name that matched the face.

“When you attach the word ‘angry,’ you see a decreased response in the amygdala,” Lieberman said. “When you attach the name ‘Harry,’you don’t see the reduction in the amygdala response.

“When you put feelings into words, you’re activating this prefrontal region and seeing a reduced response in the amygdala,” he said. “In the same way you hit the brake when you’re driving when you see a yellow light,when you put feelings into words, you seem to be hitting the brakes on your emotional responses.”

As a result, an individual may feel less angry or less sad.

“This is ancient wisdom,” Lieberman said.

Putting our feelings into words helps us heal better and if we can get newcomers to talk about them, that  will make them feel better. They will experience part of the “solution” right way and be encouraged to come back for more.

So putting feelings into words helps with not only regulating and modulating the intensity of emotions, but helps with processing them, reduces distress and distress based impulsivity and shows there is a solution to unruly negative  emotions.

In my experience this process has been a fundamental part of how it works!

 

 References

Lieberman, M. D., Eisenberger, N. I., Crockett, M. J., Tom, S. M., Pfeifer, J. H., & Way, B. M. (2007). Putting feelings into words affect labeling disrupts amygdala activity in response to affective stimuli. Psychological Science, 18(5), 421-428.

 

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Why a spiritual solution?

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.

 

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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)

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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 research1350, 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 psychopharmacology19(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.

 

One Christmas I nearly relapsed!

 

One Christmas I nearly relapsed!

by alcoholicsguide

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

Intolerance of Uncertainty

Like many recovering alcoholics I know I have a real problem with “Not projecting into the future” but staying in the moment or even the day. Why is this? When I “project” or even consider a near future event I can feel distressed by it. I want to do something about it now! Not later.

The future seems to be urgently now.

I have long researched why this is? I seem to become overwhelmed at times by future tense and it is not even due to future events being that distressing in themselves. I just have this constant need to act now rather than later. I have an urgency or a negative urgency or in other words a  distress based impulsivity which prompts a desire to act now, make a decision now rather than later. I call this a compulsion to act  because a distress state compels me to make a decision to act now.

As I have mentioned in previous blogs, alcoholics appear to have a bias in decision making towards choose the short term solution over a long term one, even though the long term solution will yield greater gains. There are various  theories on why this is so. Sometimes it appears like a “fight or flight” response!

My theory is that I am very poor at tolerating uncertainty and what is the future but uncertain. I have  an “unconscious” negative bias about the future, linked at times to a tendency to then catastrophize.

This intolerance of uncertainty is seen in other disorders, such as anxiety, obsessive-compulsive and post traumatic stress disorders as well as in eating disorders but it is rarely researched in alcoholism.

I believe when confronted with a decision about the future I often make a decision to relieve a distress which manifests as an unpleasant feeling state which compels me, via a stimulus response to act now. Distress is the stimulus, acting now is the response.

I am not saying that I have to be in a negative frame of mind for this to occur. It is simply a decision making bias I have when left to my own devices.   It is the reason I speak to others when making important decisions in life because the need to relief distress can show in the mind as a good idea when it is often on reflection not such a great idea.

This is due to distress being a stress-fuelled experience and excessive stress reduces the awareness of future consequence of a decision. It seems like a good idea at the time because it relieves distress. To the brain this is a good idea.  It is a automatic response of the dorsal striatum, an implicit memory (procedural) system, that requires one to retrospectively rationalise and justify the automatic responding of this area of the brain, it justifies a previous action in other words, thus a decision is represented in the mind as a good idea, what was most urgently required!

These rationalisations and justifications through time can become automatic schemas and are automatically activated following a compulsive response. Some of us are probably familiar with these schemas being a big part of our alcohol and drug use. As we needed to use, we had automatic addiction schemas following shortly after our decisions to head to the pub or to score some drugs or even to propel some decisions, as the consequence of distress states. It is these habitual response, based on distress states which bias decisions making to acting now, even in recovery.

I came across an article (1) which looked at this intolerance of uncertainty in relation to decision making and came up with similar conclusions to the above. “high IU (intolerance of uncertainty) predicted shorter wait times and more frequent selection of the immediate, less valuable (and riskier) reward. We take this tendency as evidence that IU was associated with an aversion to waiting in a state of uncertainty. One might argue that choices for the more immediate, less valuable reward might reflect an aversion to waiting per se…, the delay associated with the more valuable reward in the
current study appears to have magnified the unpleasant affective responses to uncertainty… delay is provoking unpleasant affective responses, choices for the smaller, immediate reward can be seen as avoidance of distress.” Decisions are thus like an “escape route” and more based on emotional avoidance.  “That is, the affective consequences of uncertainty may play a more central role in determining behavior than uncertainty itself…decision  making tendencies among those high in IU may be maintained through negative reinforcement…to  reduce or eliminate affectively unpleasant circumstances that accompany waiting in uncertainty.”

These “unpleasant affective responses” are distress based and lead to a negative urgency to act now.

References

1. Luhmann, C. C., Ishida, K., & Hajcak, G. (2011). Intolerance of uncertainty and decisions about delayed, probabilistic rewards. Behavior therapy42(3), 378-386.

 

 

 

 

So how is your decision making?

 

In this blog we will look at something  which we believe is apparent in alcoholics,  the decision making difficulties very present  in active alcoholism and to a lesser extent in recovery.

By this we mean there is a tendency to use the short term fix over more long term considerations, a more “want it now” than delayed gratification. This may be down to internal body (somatic signals) which can give rise to an unpleasant feeling at times prior making a decision, as if we sometimes make decisions based on a distress feeling rather than forward thinking, that we choose a decision to alleviate this feeling. It has been suggested by some authors that emotions do not guide the decision making of alcoholics and addicts properly and this is the reason why they are maladpative.

Equally it may be that certain somatic states such as the so-called ‘primary inducers’ of feeling, mainly centring on  the “anxious” amgydala which helps in our responding to body states associated with chronic drug and alcohol abuse, such as alleviated, chronic stress (and it’s manifestation as emotional distress) have the potential to dominate decisions, to treat decisions in a habitual, automatic manner and not in via  a thoughtful consideration of the possible outcome of our decisions.  

Once science thought we make sensible reasonable decision based on pure reason but it has become clear in recent decades that we use emotional signals ,”gut feelings” to make decisions too.

It appears that if we don’t access these emotional signals we are destined to make the move decisions over and over again, regardless of their outcome and consequence.

The extreme example of emotions guiding decisions, would be running from a rampaging lion, this decision is make emotionally, via the quick and dirty route, the “low road” according to Le Doux. The amygdala, which directs signal traffic in the brain when danger lurks, receives quick and dirty information directly from the thalamus in a route that neuroscientist Joseph LeDoux dubs the low road.

This shortcut allows the brain to start responding to a threat within a few thousandths of a second. The amygdala also receives information via a high road from the cortex. Although the high road encodes much more detailed and specific information, the extra step takes at least twice as long— and could mean the difference between life and death. 

Emotional dysregulation and altered reward sensitivity may underpin impulsive behavior and poor decision-making.

Both of these tendencies can be seen in the “real-world” behavior of addicted individuals, but can also be studied using laboratory-based paradigms.

Addiction is associated with a loss of control over drug use which continues in spite of individuals’ awareness of serious negative consequences.

Increased reward  alone, as seen in alcoholics and resulting in attentional bias and automatic responding to cues (internal and external)  do not seem a sufficient explanation for this persistent maladaptive behavior of addiction.

Instead there must be additional deficits in decision-making and/or inhibiting these maladaptive behaviours and which critically involve  emotional factors exerting a detrimental effect on cognitive function.

The term “impulsivity” is often used to describe behavior characterized by excessive approach with an additional failure of effective inhibition (1) and has consistently been found to be associated with substance dependence (2,3).

Impulsivity is a complex multifaceted construct which has resulted in numerous additional definitions such as, “the tendency to react rapidly or in unplanned ways to internal or external stimuli without proper regard for negative consequences or inherent risks” (4), or “the tendency to engage in inappropriate or maladaptive behaviors” (2).

This we suggest could be the consequence of either the push or pull of dsyregulated emotions.

By this we mean we either do not use emotions properly to feel the right  decision as we cannot process them properly to use them as “guides” in decision making or these dsyregulated emotions become distressing and prompt more compulsive decision making, effectively to relieve the distress of these negative emotional states.

Either way it appears that not only do alcoholics, but also children of alcoholics, use a more motor-expressive style of decision making, i.e. they recruit more compulsive regions of the brain rather than prefrontal cortex areas normally used used to make planned, evaluative decisions.

It appears that emotional dsyregulation is at the heart of maladaptive decison making in alcoholics and addicts.

Distressed Based Impulsivity?

Emotional impulsivity more closely reflects the interaction between emotional and cognitive processes. Negative urgency,   the disposition to engage in rash action when experiencing extreme negative affect (mood, emotion or anxiety), or in simple terms, distress-based impulsivity, was found to be the best predictor of alcohol, drug, social, legal, medical, and employment problems (5).

Substance users frequently make decisions with a view to immediate gratification (6-10), and may be less sensitive to negative future outcome (‘myopia for the future’) (11,12). It has been hypothesized that substance users are less able to use negative feedback to guide and adjust ongoing behavior (12).

These findings highlight a specific role for emotion.

Emotional impulsivity traits appear distinct from other impulsivity traits and particularly pertinent for dependence, reliably differentiating substance users from controls, and also predicting poorer outcomes in dependent individuals.

The impact of emotional processing on cognitive performance.

A common behavioral measure of impulsivity is the delay discounting task which measures the degree of temporal discounting. Participants are faced with the choice of a small immediate reward, or a larger delayed reward; choosing the smaller immediate reward indicates a higher degree of impulsivity.

Increased discounting of larger delayed rewards has been found in heroin- (13), cocaine- (14), and alcohol (15 -17) -dependent individuals.

Enhanced discounting is also seen during opiate withdrawal, possibly reflecting the emergence of negative affect states during withdrawal (18).

Withdrawal is a period of heightened noradrenaline ( a “stress” chemical”) and this excessive stress has a bearing on decision making, and in relapse.

High levels of negative affect, anxiety/stress sensitivity a in substance dependent individuals may therefore contribute to observed deficits on decision-making tasks. Stress mechanisms are considered to be important mechanisms underlying relapse (19), suggesting these emotional traits impair real life decision-making.

Studies directly assessing the role of emotional states on decision-making in opiate addiction have shown that trait and state anxiety are negatively correlated with performance on the the Iowa Gambling Task – IGT (20). Furthermore, stress induction using the Trier Social Stress Test, was shown to produce a significant deterioration in IGT performance in long term abstinence and newly abstinent heroin users, but not in comparison subjects.

Treatment with the B adrenocepter antagonist propranolol blocked the deleterious effect of stress on IGT performance, supporting the role of the noradrenergic system in the generation of negative emotional states in substance dependence (21).

These findings indicate that conditioned emotional responses, i.e. stress based emotional response, impair decision-making.

The impact of emotion on impulsive action and decision making

Planning systems (also referred to as deliberative, cognitive, reflective or executive systems) are “goal-directed” systems that allow an agent to consider the possible consequences or outcomes of its actions to guide behavior. Habit systems mediate behaviors that are triggered in response to certain stimuli or situations but without consideration of the consequences.

“Habit” systems do not mean we are calling addiction is a habit, it simply means behaviour is automatic, ingrained, individuals respond immediately, without future consequence  to certain stimulus, such as stress or emotional distress. It is a conditioned response!

Brain areas underlying these conditioned or Pavlovian responses include the amygdala, which identifies the emotional significance or value of external stimuli, and the ventral  striatum, which mediates motivational influences on instrumental responding (22), and their connections to motor circuits (23).

Thus, it has been argued that emotions constitute a decision-making system in their own right, exerting a dominant effect on choice in situations of opportunity or threat (24).

It should be noted here, that in the addiction cycle, as it progresses towards endpoint addiction and compulsive use of substances, there is a stress based reduction  in prefrontal cognitive control over behaviour, and a responding more based on automatic emotive-motoric regions of the brain such s the dorsal striatal (DS) (and basal ganglia). Reward processing moves to the DS also from the ventral striatum (VS).

Thus stress modulates instrumental action in favour of the DS-based habit system at the expense of the PFC-based goal-directed system, also seen in hypertrophy of the DS and hypotrophy of the PFC.

This shift from cognitive to automatic is also the result of  excessive engagement of habitual processes, by partly by affecting the contribution of multiple memory systems on behaviour. We suggest that emotional stress via amgydaloid activity knocks out the hippocampal (explicit) memory in favour of the DS which is also a memory system, that of implicit memory, the procedural memory.

In lien with addiction severity, the brain appears to implode inwards towards compulsive behaviours of sub-cortical areas such as the DS modulated by the amgydala from more conscious cognitive control areas of the cortex. In fact, it is possible to say that this conscious cognitive control diminishes.

Recent evidence suggests this role of stress in shifting goal-directed control to habitual control of behavior (25). This effect appears to be mediated by the action of both cortisol and noradrenaline (26).

More importantly, perhaps for our argument is that , this shift from hippcampal to DS memory is also a function of a “emotional arousal habit bias”, as seen in post traumatic stress disorder,  via amgydaloid hyperactivity, or distress based hyperactivity,  which results in emotional distress acting as a stimulus to the automatic responding of the DS. Affect related behaviour, in essence, becomes more compulsively controlled also.

In simple terms, negative urgency, may bias an automatic responding towards amgydaloid activation of the dorsal striatum and away from cortical areas such as the ventromedial cortex  – vmPFC (27 ) which is involved in emotionally guided decision making and this may have consequence for decision making as decision making involves  responding to stimulus such as emotionally provoking stimuli.

One study (28) showed this vmpfc to be hyperactive in recently abstinent alcoholics, perhaps as the result of altered stress systems which create a state called allostasis, and when further stressed responding moved to the more compulsive regions of the brain listed above. This suggest to us, that there are inherent difficulties with emotional dysregulation, particularly in early abstinence/recovery and that these resources when taxed further by seemingly stressful decision making may be dealt with via a need to make a decision to relieve this “distress” feeling rather than achieve a long term outcome. Relieving this distress is thus the outcome most urgent.

Thus for some alcoholics there is an overtaxing of the areas implicated in emotional regulation and thus emotionally guided decision making and under extreme stress we suggest this switches to more a more compulsive decision making profile.

The habit system chooses actions based upon stored associations of their values from past experience; through training, an organism learns the best action to take in a certain situation. Upon recognition of the situation again this “best action” will automatically be initiated, without consideration of consequences of such an action. This process is very fast but inflexible, unable to adapt quickly to changes in the value of outcomes (29,30).

Thus although emotion can guide decision-making when it is integral to the task at hand, emotional responses that are excessive can be detrimental (31).

Dorsal prefrontal regions are also involved in the regulation of affective states (32). Excessive emotion is likely to require increased regulation by these areas (33,34).

Dorsal prefrontal regions are additionally important in decision-making and inhibitory control, thus high levels of emotion that require regulation may limit resources available for these functions, which may contribute to deficits in decision-making.

As we mentioned this PFC control becomes impaired in the addiction cycle with automatic responding becomes more prevalent. This is especially the result of the emotional manifestation of chronic stress which is distress. We suggest this distress can act as a switch between conscious and automatic (unconscious) responding and this has consequences for decision making.

Given the crucial role of emotions in the processes of decision-making as described above, it follows that dysregulation of emotional processing may contribute to the observed decision-making deficits observed in substance dependent individuals. Decisions are driven by distress or negative affect and appear to favour now over then/later.

Looking Inside the Brain

A consistent finding of neuroimaging studies of decision-making in substance dependence is hypoactivation of the prefrontal cortex (35-37), 

Chronic drug use is consistently associated with VPFC, DLPFC and antior cingulate or ACC  gray matter loss in cocaine and alcohol dependence (38-42) and reduced prefrontal neuronal viability in opiate dependence (43,44). VPFC and DLPFC loss have been shown to predict both impaired performance on the IGT (45) and preference for immediate gratification in delay discounting tasks (37)

These areas and others involved in emotional regulation such as the hippocampus, orbitofrontal cortex  and insula show morphological abnormalities and the  emotional regulation neural network as a whole appears to have functionality and connectivity impairments.

These all suggest emotions are not being utilized properly to guide decisions. This may even appear as unregulated and distressing with the brain experiencing this distress rather than processed emotions.

A similar decision making profile is seen in alexithymia, where there is a difficulty labelling and processing emotions and thus using them to guide decision making which appears to result in recruitment of more compulsive or motor expressive areas of the brain outlined here. There are also similar morphological, neurobiological and connectivity impairments as seen in addiction. Cocaine addicts also  have a similar decision making profile as do children of alcoholics, before they start to use substances.

Whether these separate groups all have distress prompting this decision making profile  or whether it is unpleasant feeling state based on not fully processing emotion is open to debate.

As the prefrontal regions of the planning system are impaired in substance dependence, this compromises both the ability to generate affective states relating to long term goals and the ability to exert executive inhibitory control over drug-seeking thoughts and actions .

Dorsal prefrontal regions are involved in the regulation of affective states . Therefore excessive anxiety  would require increased regulation by these areas. Studies have shown dorsal prefrontal regions to be important in regulating reducing amygdala activity . Considering these prefrontal regions are important for  decision-making and anxiety regulation would limit the resources available for effective decision-making within the planning system and would not be able to inhibit more amgydaloid, or compulsive responding.

Bechara  concluded that  an impaired ability to use affective signals to guide behavior underlie impaired decision-making in these individuals. We forward the idea that distress signals guide this decision making and behaviour via a compulsive desire to automatically act to relieve a distress state. Whether via an unprocessed emotional state or as the consequence of the addiction cycle and excessive chronic distress recruiting compulsive parts of the brain.

Either way emotional processing and regulation deficits lie at the heart of these decision making difficulties! 

Now is chosen instead of later, short term gains rather than long term higher gains, because of the negative urgency to act now, to relieve a distress, which automatically, not consciously, devalues future outcome.

The future is now in other words.

There is a distress based urgency to act this moment, not later.  It is this desire to compulsively act which may give rise to obsessive compulsive behaviours, based on the desire to relieve distress not on the relative merits of a future consequence.

It can appear as a “little emergency” not a choice, the “flight or fight” response that delay discounting could possible be measuring and that excessive noradrenaline and glucocorticoids (stress chemicals) prompt – it has to be done, needs to be done now!

 

References (to  be included)

 

Hommer D. W., Bjork J. M., Gilman J. M. (2011). Imaging brain response to reward in addictive disordersAnn. N.Y. Acad. Sci1216, 50–61 10.1111/j.1749-6632.2010.05898.x

2. de Wit H. (2009). Impulsivity as a determinant and consequence of drug use: a review of underlying processesAddict. Biol14, 22–31 10.1111/j.1369-1600.2008.00129.x [PMC free article]

3. Dalley J. W., Everitt B. J., Robbins T. W. (2011). Impulsivity, compulsivity, and top-down cognitive controlNeuron 69, 680–694 10.1016/j.neuron.2011.01.020 

4. Shin S. H., Hong H. G., Jeon S. M. (2012). Personality and alcohol use: the role of impulsivityAddict. Behav37, 102–107 10.1016/j.addbeh.2011.09.006 [PMC free article]

5.  Verdejo-Garcia A., Bechara A., Recknor E. C., Perez-Garcia M. (2007a). Negative emotion-driven impulsivity predicts substance dependence problemsDrug Alcohol Depend91, 213–219 10.1016/j.drugalcdep.2007.05.025

6. Aron A. R. (2007). The neural basis of inhibition in cognitive controlNeuroscientist 13, 214–228 

7. Bickel W. K., Miller M. L., Yi R., Kowal B. P., Lindquist D. M., Pitcock J. A. (2007). Behavioral and neuroeconomics of drug addiction: competing neural systems and temporal discounting processesDrug Alcohol Depend90Suppl. 1, S85–S91 10.1016/j.drugalcdep.2006.09.016

8. Madden G. J., Bickel W. K., Jacobs E. A. (1999). Discounting of delayed rewards in opioid-dependent outpatients: exponential or hyperbolic discounting functions? Exp. Clin. Psychopharmacol.7, 284–293 10.1037/1064-1297.7.3.284

9. Kirby K. N., Petry N. M., Bickel W. K. (1999). Heroin addicts have higher discount rates for delayed rewards than non-drug-using controlsJ. Exp. Psychol. Gen128, 78–87 10.1037/0096-3445.128.1.78

10. Petry N. M. (2001). Delay discounting of money and alcohol in actively using alcoholics, currently abstinent alcoholics, and controlsPsychopharmacology (Berl.) 154, 243–250 

11.  Bechara A., Damasio A. R., Damasio H., Anderson S. W. (1994). Insensitivity to future consequences following damage to human prefrontal cortexCognition 50, 7–15

12. Bechara A., Damasio H. (2002). Decision-making and addiction (part I): impaired activation of somatic states in substance dependent individuals when pondering decisions with negative future consequencesNeuropsychologia 40, 1675–1689 10.1016/S0028-3932(02)00015-5

13.  Kirby K. N., Petry N. M. (2004). Heroin and cocaine abusers have higher discount rates for delayed rewards than alcoholics or non-drug-using controlsAddiction 99, 461–471 10.1111/j.1360-0443.2003.00669.x

14. Coffey S. F., Gudleski G. D., Saladin M. E., Brady K. T. (2003). Impulsivity and rapid discounting of delayed hypothetical rewards in cocaine-dependent individualsExp. Clin. Psychopharmacol11, 18–25 10.1037/1064-1297.11.1.18

15. Petry N. M. (2001). Delay discounting of money and alcohol in actively using alcoholics, currently abstinent alcoholics, and controlsPsychopharmacology (Berl.) 154, 243–250

16. Bjork J. M., Hommer D. W., Grant S. J., Danube C. (2004a).Impulsivity in abstinent alcohol-dependent patients: relation to control subjects and type 1-/type 2-like traitsAlcohol 34, 133–150

17. Mitchell J. M., Tavares V. C., Fields H. L., D’Esposito M., Boettiger C. A. (2007). Endogenous opioid blockade and impulsive responding in alcoholics and healthy controls.Neuropsychopharmacology 32, 439–449 10.1038/sj.npp.1301226 

18. Koob G. F., Le Moal M. (2005). Plasticity of reward neurocircuitry and the ‘dark side’ of drug addictionNat. Neurosci8, 1442–1444 10.1038/nn1105-1442

19. Stewart J. (2008). Review. Psychological and neural mechanisms of relapsePhilos. Trans. R. Soc. Lond. B Biol. Sci363, 3147–3158 10.1098/rstb.2008.0084 [PMC free article]

20. Lemenager T., Richter A., Reinhard I., Gelbke J., Beckmann B., Heinrich M., et al. (2011). Impaired decision making in opiate addiction correlates with anxiety and self-directedness but not substance use parametersJ. Addict. Med5, 203–213 10.1097/ADM.0b013e31820b3e3d

21. Zhang X. L., Shi J., Zhao L. Y., Sun L. L., Wang J., Wang G. B., et al. (2011). Effects of stress on decision-making deficits in formerly heroin-dependent patients after different durations of abstinenceAm. J. Psychiatry 168, 610–616 10.1176/appi.ajp.2010.10040499 

22. Cardinal R. N., Parkinson J. A., Hall J., Everitt B. J. (2002).Emotion and motivation: the role of the amygdala, ventral striatum, and prefrontal cortexNeurosci. Biobehav. Rev26, 321–352 10.1016/S0149-7634(02)00007-6

23. van der Meer M., Kurth-Nelson Z., Redish A. D. (2012).Information processing in decision-making systems.Neuroscientist 18, 342–359 10.1177/1073858411435128

24. Seymour B., Dolan R. (2008). Emotion, decision making, and the amygdalaNeuron 58, 662–671 10.1016/j.neuron.2008.05.020

25. Schwabe L., Wolf O. T. (2011). Stress-induced modulation of instrumental behavior: from goal-directed to habitual control of actionBehav. Brain Res219, 321–328 10.1016/j.bbr.2010.12.038

26. Schwabe L., Tegenthoff M., Hoffken O., Wolf O. T. (2010).Concurrent glucocorticoid and noradrenergic activity shifts instrumental behavior from goal-directed to habitual controlJ. Neurosci30, 8190–8196 10.1523/JNEUROSCI.0734-10.2010

27. Cyders, M. A., Dzemidzic, M., Eiler, W. J., Coskunpinar, A., Karyadi, K., & Kareken, D. A. (2013). Negative Urgency and Ventromedial Prefrontal Cortex Responses to Alcohol Cues: fMRI Evidence of Emotion‐Based Impulsivity.Alcoholism: Clinical and Experimental Research.

28.  Seo, D., Lacadie, C. M., Tuit, K., Hong, K. I., Constable, R. T., & Sinha, R. (2013). Disrupted ventromedial prefrontal function, alcohol craving, and subsequent relapse risk. JAMA psychiatry70(7), 727-739.

29. Daw N. D., Niv Y., Dayan P. (2005). Uncertainty-based competition between prefrontal and dorsolateral striatal systems for behavioral controlNat. Neurosci8, 1704–1711 10.1038/nn1560

30. Redish A. D., Jensen S., Johnson A. (2008). A unified framework for addiction: vulnerabilities in the decision process.Behav. Brain Sci31, 415–437 discussion: 437–487. 10.1017/S0140525X0800472X [PMC free article]

31. Bechara A., Damasio A. R. (2005). The somatic marker hypothesis: a neural theory of economic decisionGames Econ. Behav52, 336–372

32. Phillips M. L., Drevets W. C., Rauch S. L., Lane R. (2003a).Neurobiology of emotion perception I: the neural basis of normal emotion perceptionBiol. Psychiatry 54, 504–514 10.1016/S0006-3223(03)00168-9

33. Amat J., Baratta M. V., Paul E., Bland S. T., Watkins L. R., Maier S. F. (2005). Medial prefrontal cortex determines how stressor controllability affects behavior and dorsal raphe nucleus.Nat. Neurosci8, 365–371 10.1038/nn1399

34. Robbins T. W. (2005). Controlling stress: how the brain protects itself from depressionNat. Neurosci8, 261–262 10.1038/nn0305-261 

35.  Bolla K. I., Eldreth D. A., London E. D., Kiehl K. A., Mouratidis M., Contoreggi C., et al. (2003). Orbitofrontal cortex dysfunction in abstinent cocaine abusers performing a decision-making taskNeuroimage 19, 1085–1094 10.1016/S1053-8119(03)00113-7 [PMC free article]

36. Tanabe J., Thompson L., Claus E., Dalwani M., Hutchison K., Banich M. T. (2007). Prefrontal cortex activity is reduced in gambling and nongambling substance users during decision-makingHum. Brain Mapp28, 1276–1286 10.1002/hbm.20344

37. Bjork J. M., Momenan R., Smith A. R., Hommer D. W. (2008b). Reduced posterior mesofrontal cortex activation by risky rewards in substance-dependent patientsDrug Alcohol Depend95, 115–128 10.1016/j.drugalcdep.2007.12.014[PMC free article]

38. Fein G., Di Sclafani V., Meyerhoff D. J. (2002b). Prefrontal cortical volume reduction associated with frontal cortex function deficit in 6-week abstinent crack-cocaine dependent menDrug Alcohol Depend68, 87–93 10.1016/S0376-8716(02)00110-2[PMC free article]

39. Makris N., Gasic G. P., Kennedy D. N., Hodge S. M., Kaiser J. R., Lee M. J., et al. (2008). Cortical thickness abnormalities in cocaine addiction-a reflection of both drug use and a pre-existing disposition to drug abuse? Neuron 60, 174–188 10.1016/j.neuron.2008.08.011 [PMC free article]

40. Fein G., Shimotsu R., Barakos J. (2010). Age-related gray matter shrinkage in a treatment naive actively drinking alcohol-dependent sampleAlcohol. Clin. Exp. Res34, 175–182 10.1111/j.1530-0277.2009.01079.x [PMC free article]

41. Goldstein R. Z., Volkow N. D. (2011). Dysfunction of the prefrontal cortex in addiction: neuroimaging findings and clinical implicationsNat. Rev. Neurosci12, 652–669 10.1038/nrn3119 [PMC free article]

42. Ersche K. D., Turton A. J., Pradhan S., Bullmore E. T., Robbins T. W. (2010b). Drug addiction endophenotypes: impulsive versus sensation-seeking personality traitsBiol. Psychiatry 68, 770–773 10.1016/j.biopsych.2010.06.015 [PMC free article]

43. Haselhorst R., Dursteler-MacFarland K. M., Scheffler K., Ladewig D., Muller-Spahn F., Stohler R., et al. (2002).Frontocortical N-acetylaspartate reduction associated with long-term i.v. heroin useNeurology 58, 305–307

44. Yucel et al.,2007Haselhorst R., Dursteler-MacFarland K. M., Scheffler K., Ladewig D., Muller-Spahn F., Stohler R., et al. (2002).Frontocortical N-acetylaspartate reduction associated with long-term i.v. heroin useNeurology 58, 305–307

45. Tanabe J., Tregellas J. R., Dalwani M., Thompson L., Owens E., Crowley T., et al. (2009). Medial orbitofrontal cortex gray matter is reduced in abstinent substance-dependent individualsBiol. Psychiatry 65, 160–164 10.1016/j.biopsych.2008.07.030[PMC free article]

46. Murphy, A., Taylor, E., & Elliott, R. (2012). The detrimental effects of emotional process dysregulation on decision-making in substance dependence. Frontiers in integrative neuroscience6.

LeDoux J. (2007). The amygdalaCurr. Biol17, R868–R874 10.1016/j.cub.2007.08.005

LeDoux J. (2012). Rethinking the emotional brainNeuron 73, 653–676 10.1016/j.neuron.2012.02.004 [PMC free article]

LeDoux J. E. (2000). Emotion circuits in the brainAnnu. Rev. Neurosci23, 155–184 10.1146/annurev.neuro.23.1.155

 

 

 

 

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.