Acceptance is Always the Key!

acceptance 12311303_828542240604643_2357851135095776878_n

Glad to see other people have the same markings on their Big Book too! I have the same fluorescent yellow marker pen scrolls and deep pen lines across the page and under the words.

I was so desperate not to let a word go by, and to understand everything the Big Book of AA has to teach about alcoholism and the solution to it that I tied my developing understanding to the pages with yellow and black ink lines. Often returning to also add these #s and to note well, NB!

Every time I read it I got new understanding. The longer I have gone on in recovery the more I have seen and understood.

Reading the BB over the years help me see how my brain is recovering as I see things more clearly with every passing years. It reminds me of previous times when I have read it, gives me a memory snapshot of where I was at in previous periods of recovery. What I used to think and feel compared to what i think and feel now. What I agreed with then and what I disagree with now.

How I have healed.

It is strange how I see other things, not underlined, as gaining more in importance as recovery goes on.

This excerpt above is from a “share” or a personal story at the back of the Big Book. The story is known by two names, “Doctor, Alcoholic, Addict” or “Acceptance was the Answer” depending on which edition you bought.

It is referred to so often in meetings that it is almost a supplement to the first 164 pages.  It has common sense words of wisdom which can greatly help with your recovery – I keep returning to it over and over again.

Here is a link to it, have a read and hopefully it will help you in the same profound way it helped me and millions of others!

It is the last story in this section –

Here he is speaking at an AA convention. I have found these “shares” crucial to my own recovery in terms of  identifying with other other recovering alcoholics.

It is in listening to their shares that I could see that I am like these people and they act in a way I do, feel in a way I do, think and make decisions in a way I do and even have had experiences throughout their lives and drinking careers which are also so like mine so I guess I figured that  I must be a sort of alcoholic like all these people.

Maybe I was an alcoholic too!?


The journey in recovery often starts with identifying with others, their problems and how they have solved their problems.

I hope it does for you too!

My very first meeting I identified with the AAs talking about how difficult they found living life on life’s terms, their emotional disease etc. It was this that convinced me I was like them. Not the drinking or drugging, but the internal spiritual malady, the ISM that goes with the alcohol to create alcoholism.

Identifying with others like me, saved my life and is the reason I have been recovery ten years.

You are not alone.

So how is your decision making?


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Distressed Based Impulsivity?

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

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

These findings highlight a specific role for emotion.

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

The impact of emotional processing on cognitive performance.

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

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

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

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

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

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

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

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

The impact of emotion on impulsive action and decision making

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Looking Inside the Brain

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

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

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

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

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

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

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

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

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

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

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

The future is now in other words.

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

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


References (to  be included)


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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





How Research Helped Saved My Life!

One Christmas, I nearly relapsed.

I did not wish to relapse, in fact I would rather put a gun to my head and blow my brains out!

Nonetheless, I was indeed about to relapse. It seemed urgently inevitable. The emotional distress I had suffered all over Christmas, prompted by sad unresolved feelings about my deceased parents’s had built up, aided by a few bitter arguments with my frustrated wife, into into a sheer, blind terror.

My emotions overwhelmed me and had started to rush like a startled herd of fear through the remaining mental barricades,  exploding into a crashing cascade of stress chemicals rushing around my whole body, making my limbs weak, achy and feeble.

Somehow I had the sense to shakily climb the stairs to the top of the house to tell my wife that I was in trouble. Real nauseatingly frightening trouble. I needed help. “Let’s stop arguing, I am in danger!”

My wife’s facial expression quickly flickered from hurt to heightened concern. She could tell by my quivering voice and ashen complexion that I was in trouble.

I shakily walked over to sit near her. Out of the corner of my eye I could see a bottle of white spirits, which glowed invitingly with some spiritual lustre.

My attention seemed ‘locked into’ this bottle of spirits. Somewhere there was voice in my head saying “You could drink that, soon get rid of this terror” My wife had been trying to talk to me, get through to me. I looked at her. I recognised her face but couldn’t remember her name or the fact she was my wife. It was as if some habitual behaviour, some automatic pilot had activated my legs and brought me here for help.

My wife and I couldn’t remember her name!!? What the ….? I was consumed with a rampant rampaging terror that flipped by guts. Hallucinatory terror. I was going to drink the white spirits. I have never drunk white spirits during my active alcoholism but had heard of plenty of alcoholics who had, and their wife’s perfume and many other such unthinkable liquids. It had, via these accounts, become a viable option. Something I could drink if need be!

It seemed like this was one of those moments.

“What do you normally do?” was all I heard. What? “What do you mean, what do I normally do….?” I hesitantly replied in a hushed almost child-like voice.  “When you are like this, what do you normally do?” her voicing becoming more urgent . I could see the white spirits glisten and almost feel it evaporate, on my tongue, harshly as it  deeply burnt my chest with a warm reassuring heat,  move glowingly outwards from there in little dendritic branches of smoothing warmth and the whispering promised of blessed relief  and good cheer. When alcoholism whispers sweet nothings it is sweeter than your lover.

“You better drink it” sounded in my head.  I couldn’t remember what I normally do, or who was this asking this  I head was jumbled and terrified. “You’d better do it”, the internal voice insisted.  All I could feel was huge surges of stress chemicals surging through my veins like little scuttling manic spiders, speeding through my veins, up and down the insides of my legs, my limbs, scurrying frantically.

 For some inexplicable reason, I thought, or a thought occurred to me “once I would have thought this a massive craving!” but now I felt I knew better. This wasn’t an appetitive craving, I didn’t fancy a wee drinky winky, wouldn’t that be nice.  I knew this was a stress based urge and nothing to do with desire.

Nonetheless, I would kill for a drink, but paradoxically I didn’t even want one!? It wasn’t for pleasure but to escape this escalating aversion.

I knew somewhere, and know more now, that the stress chemicals swirling around my nervous system were activating my reward (or survival) brain systems. I knew it because I had read about it. Many, many times. Enough times. Stress and emotional distress activated  the inner beast.


Massive amounts of stress and distress cuts off the action outcome memory, the explicit memory, the remembering of knowledge of what I would normally do in this type of situation, the “what do you normally doing this situation?” my wife had implored me to recall.  It was completely cut off, I couldn’t get to it, access it. It might as well have belonged to someone else.

In there, in that explicit memory, was my wife’s name and other life saving stuff like what I normally did when faced with inevitable relapse, apart from staring at a bottle of spirits and salivating! Stuff like the tips of recovery that I had learnt so proficiently that they were ingrained in my explicit memory, for occasions such as this one!?

Some of this recovery memory had become habitualized in my implicit memory too, thank God. It was this memory that had prompted me to climb the stairs to my wife’s help on my uncertain legs.  To automatically ask for help. This was implicit recovery. The very memory I could now not access now was explicit, because the excessive stress had cut if off. The what to do now I have asked for help memory. I knew this from my research as well.

The “flight or fight “mechanism, a cascade of noradrenaline, the actions of chronic stress on switching explicit to implicit memory from the action outcome to the stimulus response, to the compulsive automatised, you see it and then you do it, memory. The stimulus response memory.

The distress was the stimulus and drinking to alleviate it would be the response. Your life can depend on this memory, like when fleeing an approaching tiger, so it does not ease it’s grip on your mind too readily or easily. This is the memory with no insight of future negative consequence. It acts now and too hell with the later consequences. The “let’s deal with this now!” memory, not later.

The “what I usually did as a chronic drinking  alcoholic during extreme moments of distress”, a compulsive action hardwired into my brain. I drank alcohol previously at such prompting. It had become a unpremeditated, compulsive reaction to distress. It was how I survived back then.

But then was now.

Not only did it shut off my escape route via my explicit memory and knowledge of how to get out of this life threatening crisis but it locked me into “your life is in danger, act without thinking, just do the thing your have normally done over the past 25 odd years” routine. It showed me images of doing it before, drinking, in case I had forgotten, fleeting glimpses of the people I did it with and where, when, and whispered to me that this this person was actually the real me. Not this quivering sober fraud, in this torturous alien sober reality. That I was kidding myself.

The response was positively motoric. Get up and go over there and…drink! Lots! Drink, although you would rather kill yourself than drink.

Where was the choice there in this? Where had it gone, disappeared with my explicit memory no doubt? As my wife further implored me to do something,  the voice in my heading was now screeching orders at me “Drink now!” “Drink now or you..will, die!!!” Drink for God’s sake, drink!!”

So it wasn’t to be a case of I will relapse because “hey one will not hurt” sort of reasoning, rationalising and justification.  I was being implored to drink because my life was at risk if I did not!! I could die. I could die if I didn’t!

How badly is an alcoholics reward/survival system hijacked…usurped when this brain is imploring him to do the very thing that will kill him? And in order to help, save him from this nightmare, help him survive like some psychotic caregiver would suggest. How far down the road from full cognitive control over one’s behaviour had I gone. Answer: about as far as I could go! How much stress surges through the alcoholics brain to close down the mnemonic survival kit. When you can’t access your “recovery” survival kit, the old alcoholic one kicks in! The alcoholic self schema overrides the recovering alcoholic schema.

I slumped to my knees and implored through tear blurred eyes for help from somewhere. I gave in profoundly, I was beat. I surrendered. The stress retreated like waves scuttling away from a beach.  All action stations became deactivated and the red swirling light in my head and the honking siren turned off. I was emotionally traumatised but still sober.

I had given up on the idea that I, my self, could solve this terrifying dilemma. The answer was outside of my self, my survival network, it was in letting go. Letting go of the distress and all the brain regions it was activating; memory, attention. emotion, reward/survival. It is regions that make up the self that are taken over in the course of alcoholism. The self can no longer be fully trusted in matters  such as these.  It needs to escape to brain regions outside of self or to the helping arms and reassurance of someone who knows how to help, and external prefrontal cortex of reason.  One armed combat with the self will end up in crushing defeat. At certain times we are beyond our own mental control.

It was the most terrifying eureka moment imaginable. I have confirmed in experiential terms what I had spent the previous two years researching. Research had partly saved my life and I hope it also does yours or at the very least help you understand this disease more fully. It had proved my ‘theory’ as far as I was concerned, highlighted the mechanisms of my torture, the psycho-neural pullies and the strings.


It is this and other related theories that we hope to share while posting to this blog.  Emotional distress appears to lie at the very heart of my alcoholism, my “emotional disease”, as I have heard many alcoholics in recovery call it or this parasite that feeds on( my poorly regulated and processed) emotions, as described to me by a treatment centre counselor.  The same emotional difficulties that had made alcohol such a stupendous release and comfort, such a seemingly wonderful way to regulate my emotions, to approach and be with people who used to scare and confuse me, to belong among them, however fleetingly; now the thrill had long gone, my emotional difficulties were what remained, the daily managing of this emotional dysregulation is at the heart of my recovery. If we do not manage them then they manage us.

So there we have it: how research saved my life. Researchers need to consult and observe, listen and learn from those they study. As one researcher said about educational theories, the best way to disprove or ruin your beloved theory was to set it in a classroom environment. I suggest that researchers into alcoholisim and addiction ruin or disprove their own cherished theories by applying them to those they meet at a treatment centre. Who knows they may even improve on their theories, and in doing so treatment of the alcoholics and addicts they research.

The Distress at the Heart of Addiction and Alcoholism

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

“Fear based” is distress based.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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