An Addicted Brain but a Recovering Mind

This blog used excerpts from

Do I still have an “Alcoholic Mind”!?

I used to feel ashamed as I did have an instantaneous “wet tongue” or mild salivation (Pavlovian response) and still do years later when I see people drinking alcohol. Is this a “craving” for alcohol, do I still want to drink? Do I still have an “alcoholic mind?“. Did I do my steps properly?

It used to churn me up, these so-called alcoholics who had no physiological response to alcohol-related “cues”. By “cues” I mean the sight, sound and smell of alcohol and alcohol related stimuli, like wine gulping , glasses clinking, people having a good time, etc.

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

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

What I have discovered is that I have an “alcoholic brain” and not a “alcoholic mind” and there is a huge difference.

I found there is a difference between by addicted brain that has been altered by chronic abuse of alcohol and drugs and my recovering alcoholic mind, that essence of me that is dedicated to recovery from alcoholism and addiction. These are very distinct – let me explain – on a daily basis I use my mind to help my brain recover.

For example, I meditate, I ignore the incessant chattering of my “illness”.

Both these are the function of my mind affecting the neuroplasticity of my brain.

In other words my mind is in control of my brain, the brain’s functions and structure can be shaped by my mind. This is in effect, recovery.

For example, meditation can strengthen my control over emotional states, especially negative emotional states, by building yo the neural “muscles” of brain regions which regulate emotion.

Hence my mind and brain are distinct from each other, one effects the other.

So if there are people out there relatively new to recovery, listen up.

For chronic alcoholics there is an automatic physiological response when we see cues such as other people drinking. Mild salivation, quickening heart rate etc.

These are automatic, habitual, these responses happens to us rather than us wanting or willing it to happen. It happens unconsciously without our say so!

If you get a “wet tongue” i.e. you mildly salivate, then this is what happens when you have crossed the line into chronic alcoholism.

Loads of studies have shown there is this automatic response and have also shown there is also an attentional bias to alcohol cues. We notice alcohol cues in the environment before anything else. They have a heightened “noticeableness”.

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

Some researchers in science call this a craving. I disagree.

I call this a physiological urge, distinct from craving.

I think a craving is more akin to a “mental obsession” about alcohol.

Alcohol has only had ‘luring’ effect on me while very emotional distressed or in the early days of recovery I was very scared that I would drink but, looking back, I never had any desire to.

It is hugely important for recovering persons that we distinguish between urges and craving, in a clear manner that science seems to have been unable to do!

Lives can depend on this.

We are so vulnerable in early recover that we need sound direction on what is happening to us automatically and what we are encouraging to happen, consciously.

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

Let me explain.

If I have an urge and it becomes accompanied by automatic intrusive thoughts such as a drink would be nice, and maybe a suggestion on where to get this drink, this does not mean I want a drink.

It is simply automatically prompted intrusive thoughts, the type of thought I used to get all the time and so became habitual, stored away in an automatized addiction schema or addiction action plan.

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

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

If in recovery, we try to suppress these thoughts then they will come back stronger than before which will raise already high stress levels and recruit a whole host of memories of why I should drink, with who, where, and how much I will enjoy it.

They will also activate an Alcoholic Self Schema (different to the recovery self schema still being formed in early recovery).

Then I have a memory Hydra effect where attempting to suppress this terrible flowering of desire based memories or to cut off the heads of these thoughts and memories leads to them increasing and increasing.

Then there are lots of these memories driving you crazy and scaring the life out of you. And this is in someone who does not want to drink but wants to remain in recovery!!?

The other guy who is embellishing these thoughts is kinda thinking about drinking or toying with the possibility, so but again he is reacting cognitively and consciously to these intrusive thoughts. He is elaborating on them. He is using a different more cognitive part of the brain and a different memory system to those activated when he was simply having unconscious, habitual, automatic intrusive thoughts. He is now involved in this process rather than it simply happening to him.

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

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

As we will see in later blogs, there has to be a cognitive-emotional reaction which mediates between an urge and a relapse!

If you have urges of a “wet tongue” accept this fact, that it is because you are an alcoholic. Non alcoholics are bedeviled with these things, only alcoholics are.

Thank the heavens you have had this reminder of your alcoholism. I used to replace this urge states with gratitude, and thank God for giving me another insight into my condition.

Filling that “Hole in the Soul”

When I first arrived in AA I was told by a big scary looking man that in AA you will get better.

That “we will help you by loving you back to health”.

I was quite alarmed by this situation to be honest “loved back to health”? Was this guy some relic from the hippy era?

What he said, was very threatening to me. It suggested unconditional love, a concept that I was only partially familiar with.

I had always knew my father loved my unconditionally but this was less the case with my mother. I knew she loved me in her vague, through a distant Valium haze but part of me was always reaching out, crying out for more. More love.

I found that love in liquid form in alcohol. Or so I felt. Alcohol was constant. It always delivered without fail, transported me to the person I would much rather be. Allowed me to escape the person I did not want to be.

I now accept my mother suffered from addiction just like me and I have immense compassion for her because of that, she did the best she could under the circumstances. I forgive her completely and love her completely.

She was not a bad person she as an ill person just like me.

Did this relationship with my primary care giver have any effect on my teenage drinking and later alcoholism?

Like many alcoholics I have spoken to over the years I too seemed to suffer from the “hole in the soul” they spoke of.

That not feeling whole, like something in you, some part of you was missing.

Having a curious mind, I always wondered what it could be? It must be something that can be discovered? I wasn’t happy to leave it was a vague spiritual condition.

It felt too emotional just to be a spiritual thing, although it is also that.

It felt like I was lacking in something, something in my make up was not there or in diluted measure?

Later I found out that this relationship with my mother was called an insecure attachment and that lots of people in recovery had this insecure attachment with their mothers or whoever reared them.

This insecure attachment they said often resulted in novelty seeking and hunting out some “secure attachment” elsewhere, in a bottle, syringe, sex, a poker machine, food or other addictive behaviours.

It is lonely recently that I found there is a brain chemical linked to this insecure attachment called oxytocin, the “love chemical” which effects all the neurochemical said to be involved in addiction.

Oxytocin is badly affected by the stress reaction to insecure attachment, abuse trauma and a tough upbringing. The oxytocin is then reduced which reduces the other chemicals too and we search for these at the bottom of a glass.

Unfortunately alcohol seems to give us cocktail of these chemicals in liquid form. But never enough.

For a while anyway, it gives us the illusion of attachment, of that fleeting feeling of being part, of being loved.

Through the years all these chemicals start running dry and the drink stops working.

We are then left with the problems we had before we put a glass to our mouths.

So when the drink stopped working and I had to go to AA – not one wants to go there, let’s face it, it’s because we have to!

So the big scary guy may have been right all along. I have found that he is right over the years of attending AA.

I have found a new, surrogate family in AA, a “learnt attachment” within the fellowship of others in the same boat as me, who have felt the same as me. I have found this attachment to others, by being looked after and trying to help others – my oxytocin, the “love chemical” the “cuddle chemical” has gone up dramatically while my stress has plummeted as I have bonded with others in recovery.

This connectedness is my spiritual solution to a neurobiological problem.

I now feel part of for the first time, I have filled the hole in the soul with love given and received.

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.

View original post 2,028 more words

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.

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.

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)

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.

Do I still have an “Alcoholic Mind”!?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Factors in relapse

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

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

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

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

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

How does conditioning methodology adequately explain this group?

Attentional Bias

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

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

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

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

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

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

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

References

1. El, S., Salah El, G., & Bashir, T. Z. (2004). High-risk relapse situations and self-efficacy: Comparison between alcoholics and heroin addicts. Addictive behaviors, 29(4), 753-758.

2. Hammerbacher, M., & Lyvers, M. (2006). Factors associated with relapse among clients in Australian substance disorder treatment facilities. Journal of substance use, 11(6), 387-394.

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

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

5. Townshend JM, Duka T . Attentional bias associated with alcohol cues: differences between heavy and occasional social drinkers. Psychopharmacology (Berl)2001;157:67–74.

6. Tiffany, S. T. (1990). A cognitive model of drug urges and drug-use behavior: role of automatic and nonautomatic processes. Psychological review, 97(2), 147.

7. Bar-Haim, Y., Lamy, D., Pergamin, L., Bakermans-Kranenburg, M. J., & van IJzendoorn, M. H. (2007). Threat-related attentional bias in anxious and nonanxious individuals: a meta-analytic study. Psychological bulletin, 133(1), 1.

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

What is craving?

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

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

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

Some researchers in science call this a craving. I disagree. I call this an physiological urge, distinct from craving. I think a craving is more akin to a “mental obsession” about alcohol.

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

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

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

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

This is not a craving. I have not consciously and emotionally engaged with these intrusive thoughts.

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

In my time in recovery, I have rarely heard of or witnessed someone lured siren-like by a cue to a drink and when I have it is because he wanted to drink really, were testing their alcoholism, or that he was in huge emotional distress and went to “hell with it!”. As we will see below, stress and cues certainly do not mix but again there is still a cognitive-emotional reaction which mediates between an urge and a relapse!

In the first of a four part series of blogs we discuss “what is craving?” and consider whether the emotional dysregulation we consider to be at the heart of alcoholism and addiction also plays a role in both craving and relapse.

We start this series by considering the neurobiological accounts of craving and will then consider how well these accounts explain craving and relapse in abstinent, treatment seeking, or recovering alcoholics and addicts.

Part 1

What is craving?

Craving persists years into abstinence (1).

Precise definitions of craving have remained elusive (2-5). Two general categories are based on conditioning and cognitive mechanisms (6) but are not mutually exclusive.

A Neuroadaptive Model of Craving – Scientists believe that a gradual and, perhaps, permanent adaptation of brain function (i.e., neuroadaptation) to the presence of alcohol is a central feature in the development of alcohol dependence (7,8).

Conditioning Models – The “conditioning” models posit that cues elicit the same physiological and psychological response as drug consumption itself with these ‘respondent’ conditioning theories predicting that responses to drug-related cues either reflect aversive abstinence symptoms or mimic drug effects have dominated explanatory models in cue reactivity studies (9).

The definition of addiction by the American Society of Addiction Medicine (ASAM) includes the terms craving and persistent risk, and emphasises risk of relapse after periods of abstinence triggered by exposure to substance-related cues and emotional stressors (10).

This conceptualisation points to the role of substance-related cues, e.g., environmental stimuli that are strongly associated with the effects of the administration of substances and acquire incentive salience through Pavlovian conditioning, as well as stress (an internal cue), as major determinants of relapse.

The Incentive Sensitisation (IS) Model (11), addiction is the result of neural sensitisation of reward circuits (centred in the ventral striatum (VS)) by the neurotransmitter dopamine. Positive reinforcement mechanisms lead to a non-associative learning process, referred to as sensitization, in which repeated confrontation with a substance-related cue (which acts as a reinforcer) results in the progressive amplification of a response (substance seeking).

This ‘sensitisation’ or hypersensitivity may be independent of negative withdrawal symptoms or an individual’s general negative emotional state and leads to compulsive substance-seeking and substance-taking. These mechanisms of positive reinforcement leave addicts vulnerable to relapse when confronted with substance-related cues that trigger a pathological “wanting”. In short, IS produces a bias of attentional processing towards substance-associated stimuli and a pathological wanting of alcohol or substances. Sensitisation and attentional bias have been demonstrated in various studies (12,13).

Negative reinforcement model of addiction Basic negative reinforcement models pose that addictive behaviour is the consequence of persistent negative affect (NA). This NA is associated with maladaptive changes in the brain’s stress and reward circuits, which leave addicts vulnerable to cue-associated stimuli prompting a desire to relieve their negative emotional states (14).

One prominent stress-based negative reinforcement model, the Hedonic Dysregulation (HD) Model, mainly associated with Koob and le Moal (14), In sum, the HD model posits that, in substance dependent individuals, an overactive stress axis creates a progressive allostasis in the brain reward systems which underlies transition from substance use to addiction and creates a persistent state of NA (altered and excessive stress) and emotional reaction to “cues”. These changes continue to persist even when an addicted individual experiences a state of protracted abstinence.

Persistent NA increases their incentive salience and desire to use substances in an attempt to relieve this NA.

Evidence for the involvement of both the reward and the stress system of the brain comes from imaging studies of addicted individuals during withdrawal or protracted abstinence, which have shown decreases in dopamine D2 receptor density (hypothesized to reflect hypodopaminergic function) (15) as well as alteration in brain stress systems, such as increase in CRF and glucocorticoids (16).

These models to me appear to be describing urges based on cues and the effect of cues with stress/emotional distress. This last one can impact on recovery and relapse mentioned in another blog.

The question remains however whether these neurobiological models predict relapse in abstinent alcoholics and addicts?

References

1. Anton, R. F. (1999). What is craving. Alcohol Research and Health, 23(3), 165-173.

2. LUDWIG, A.M., AND STARK, L.H. Alcohol craving: Subjective and situational aspects. Quarterly Journal of Studies on Alcohol 35:899–905, 1974.

3. KOZLOWSKI, L.T., AND WILKINSON, D.A. Use and misuse of the concept of craving by alcohol, tobacco, and drug researchers. British Journal of Medicine 82:31–45, 1987.

4. KOZLOWSKI, L.T.; MANN, R.E.; WILKINSON, D.A.; AND POULOS, C.X. “Cravings” are ambiguous: Ask about urges and desires. Addictive Behaviors 14:443–445, 1989

5. SITHARTHAN, T.; MCGRATH, D.; SITHARTHAN, G.; AND SAUNDERS, J.B. Meaning of craving in research on addiction. Psychological Reports 71:823–826, 1992.

6. SINGLETON, E.G., AND GORELICK, D.A. Mechanisms of alcohol craving and their clinical implications. In: Galanter, M., ed. Recent Developments in Alcoholism: Volume 14. The Consequences of Alcoholism. New
York: Plenum Press, 1998. pp. 177–195.

7. Robinson, T.E., & Berridge, K.C. (1993). The neural basis of drug craving: An incentive-sensitization theory of addiction. Brain Research, 18, 247-291

8. Koob GF, Le Moal M. Drug abuse: hedonic homeostatic dysregulation. Science. 1997;278:52–58

9. Ingjaldsson, J. T., Laberg, J. C., & Thayer, J. F. (2003). Reduced heart rate variability in chronic alcohol abuse: relationship with negative mood, chronic thought suppression, and compulsive drinking. Biological Psychiatry, 54(12), 1427-1436.

10. Morse RM, Flavin DK (1992). “The definition of alcoholism. The Joint Committee of the National Council on Alcoholism and Drug Dependence and the American Society of Addiction Medicine to Study the Definition and Criteria for the Diagnosis of Alcoholism“. JAMA 268 (8): 1012–4

11. Robinson, T. E., & Berridge, K. C. (2008). The incentive sensitization theory of addiction: some current issues. Philosophical Transactions of the Royal Society B: Biological Sciences, 363(1507), 3137-3146

12. Leyton M. Conditioned and sensitized responses to stimulant drugs in humans. Prog. Neuropsychopharmacol. Biol. Psychiatry. 2007;31:1601–1613.

13. Franken, I. H. (2003). Drug craving and addiction: integrating psychological and neuropsychopharmacological approaches. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 27(4), 563-579

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

15. Volkow ND, Wang GJ, Fowler JS, et al. Decreased striatal dopaminergic responsiveness in detoxified cocaine-dependent subjects. Nature. 1997;386:830–3.

16.. Koob GF, Le Moal M. Addiction and the brain antireward system. Annu Rev Psychol. 2008;59:29–53

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 therapy, 42(3), 378-386.

Euphoria Re-experienced not Recalled?

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

This does not mean I will not drink again however.

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

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

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

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

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

Now what is it to be?

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

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

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

I would drink.

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

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

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

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

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

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

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

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

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

Euphoria re-experienced not simply recalled.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

References

1. Zack, M., Toneatto, T., & MacLeod, C. M. (1999). Implicit activation of alcohol concepts by negative affective cues distinguishes between problem drinkers with high and low psychiatric distress. Journal of Abnormal Psychology, 108(3), 518.

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

3. Tiffany, S. T. (1990). A cognitive model of drug urges and drug-use behavior: role of automatic and nonautomatic processes. Psychological review, 97(2), 147.

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

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)

1 Hommer D. W., Bjork J. M., Gilman J. M. (2011). Imaging brain response to reward in addictive disorders. Ann. N.Y. Acad. Sci. 1216, 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 processes. Addict. Biol. 14, 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 control. Neuron 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 impulsivity. Addict. Behav. 37, 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 problems. Drug Alcohol Depend. 91, 213–219 10.1016/j.drugalcdep.2007.05.025

6. Aron A. R. (2007). The neural basis of inhibition in cognitive control. Neuroscientist 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 processes. Drug Alcohol Depend. 90Suppl. 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 controls. J. Exp. Psychol. Gen. 128, 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 controls. Psychopharmacology (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 cortex. Cognition 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 consequences. Neuropsychologia 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 controls. Addiction 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 individuals. Exp. Clin. Psychopharmacol. 11, 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 controls. Psychopharmacology (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 traits. Alcohol 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 addiction. Nat. Neurosci. 8, 1442–1444 10.1038/nn1105-1442

19. Stewart J. (2008). Review. Psychological and neural mechanisms of relapse. Philos. Trans. R. Soc. Lond. B Biol. Sci. 363, 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 parameters. J. Addict. Med. 5, 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 abstinence. Am. 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 cortex. Neurosci. Biobehav. Rev. 26, 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 amygdala. Neuron 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 action. Behav. Brain Res. 219, 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 control. J. Neurosci. 30, 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 psychiatry, 70(7), 727-739.

29. Daw N. D., Niv Y., Dayan P. (2005). Uncertainty-based competition between prefrontal and dorsolateral striatal systems for behavioral control. Nat. Neurosci. 8, 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 Sci. 31, 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 decision. Games Econ. Behav. 52, 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 perception. Biol. 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. Neurosci. 8, 365–371 10.1038/nn1399

34. Robbins T. W. (2005). Controlling stress: how the brain protects itself from depression. Nat. Neurosci. 8, 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 task. Neuroimage 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-making. Hum. Brain Mapp. 28, 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 patients. Drug Alcohol Depend. 95, 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 men. Drug Alcohol Depend. 68, 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 sample. Alcohol. Clin. Exp. Res. 34, 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 implications. Nat. Rev. Neurosci. 12, 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 traits. Biol. 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 use. Neurology 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 use. Neurology 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 individuals. Biol. 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 neuroscience, 6.

LeDoux J. (2007). The amygdala. Curr. Biol. 17, R868–R874 10.1016/j.cub.2007.08.005

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

LeDoux J. E. (2000). Emotion circuits in the brain. Annu. Rev. Neurosci. 23, 155–184 10.1146/annurev.neuro.23.1.155

	Brittany Palmer on An Addicted Brain but a Recove…
	Richard L Walz-Smith on Acceptance is the Key
	Chapter 10 – R… on “The Bottled Scream” A Disease…
	Chapter 1 “Rock Bott… on Do we have to Hit Rock Bottom…
	Chapter 4 – Wh… on Acceptance is Always the …
	Chapter 5 – My… on Simplifying the Complex?
	Chapter 4 – Wh… on The psychic change as continua…
	Chapter 3 – Th… on 12 Steps
	Chapter 1 “Rock Bott… on Do we have to Hit Rock Bottom…
	“The Bottled Scream”… on Chapter 5 – My Sobering…
	“The Bottled Scream”… on Chapter 3 – The First…
	“The Bottled Scream”… on Chapter 1 “Rock Bottom”
	The First Step Is Th… on “The Bottled Scream” A Disease…
	Don’t They Kno… on “The Bottled Scream” A Disease…
	A Chemical Colonisat… on “The Bottled Scream” A Disease…