Participation in Treatment and Alcoholics Anonymous

So keep taking the medicine…

“A 16-Year Follow-Up of Initially Untreated Individuals


This study focused on the duration of participation in professional treatment and Alcoholics Anonymous (AA) for previously untreated individuals with alcohol use disorders. These individuals were surveyed at baseline and 1 year, 3 years, 8 years, and 16 years later. Compared with individuals who remained untreated, individuals who obtained 27 weeks or more of treatment in the first year after seeking help had better 16-year alcohol-related outcomes. Similarly, individuals who participated in AA for 27 weeks or more had better 16-year outcomes. Subsequent AA involvement was also associated with better 16-year outcome…some of the association between treatment and long-term alcohol-related outcomes appears to be due to participation in AA.

We focus here on participation in professional treatment and AA among previously untreated individuals after these individuals initially sought help for their alcohol use disorders and address three sets of questions:

  1. Is the duration of treatment obtained in the first year after seeking help, and the duration of subsequent treatment, associated with individuals’ long-term (16-year) alcohol-related and psychosocial outcomes? Is participation in treatment in the second and third years … after initiating help seeking associated with additional benefits beyond those obtained from participation in the first year?
  2. Is the duration of participation in AA in the first year, and the duration of subsequent participation, associated with individuals’ long-term (16-year) outcomes? Is participation in AA in the second and third years associated with additional benefits beyond those obtained from participation in the first year?
  3. Many of the individuals who participate in one modality of help (professional treatment or AA) also participate in the other modality. Accordingly, we focus on whether the associations between the duration of participation in treatment and AA and 16-year outcomes are independent of participation in the other modality of help. We also consider interactions between the duration of treatment and AA in that, for example, one modality could compensate for or amplify the influence of the other.


Independent Contribution of Treatment and Alcoholics Anonymous

Patients who participate in both self-help groups and treatment tend to have better outcomes than do patients who are involved only in treatment (Fiorentine, 1999;Fiorentine & Hillhouse, 2000). According to Moos et al. (2001), patients with substance use disorders who attended more self-help group meetings had better 1-year outcomes.

Similarly, among patients discharged from intensive substance use care, participation in self-help groups was associated with better 1-year (Ouimette et al., 1998), 2-year, and 5-year (Ritsher, Moos, & Finney, 2002; Ritsher, McKellar, et al., 2002) outcomes, after controlling for outpatient mental health care. We focus here on whether the duration of participation in one modality of help (treatment or AA) contributes to long-term outcomes beyond the contribution of participation in the other modality.

Prior Findings With This Sample

In prior work with the current sample, we found that individuals who entered treatment or AA in the first year after seeking help had better alcohol-related outcomes and were more likely to be remitted (in recovery) than were individuals who did not obtain any help. Individuals who participated in treatment and/or in AA for a longer interval in the first year were more likely to be abstinent and had fewer drinking problems at 1-year and 8-year follow-ups (Moos & Moos, 2003; 2004a; 2005b; Timko, Moos, Finney, & Lesar, 2000).

In this article, the distinctive focus is on associations between the duration of participation in treatment and AA and 16-year outcomes. We also consider the independent contribution of participation in treatment and AA to 16-year outcomes.


Compared to individuals who did not enter treatment in the first year after they sought help, individuals who obtained treatment for 27 weeks or more experienced better 16-year alcohol-related outcomes. Individuals who participated in AA for 27 weeks or more in the first year, and in years 2 and 3, had better 16-year outcomes than did individuals who did not participate in AA. Some of the contribution of treatment reflected participation in AA, whereas the contribution of AA was essentially independent of the contribution of treatment.

Participation in Treatment and 16-Year Outcomes

About 60% of individuals who sought help for their alcohol use problems entered professional treatment within one year. These individuals obtained an average of 20 weeks of treatment. Compared to untreated individuals, individuals who obtained 27 weeks or more of treatment in the first year were more likely to be abstinent and less likely to have drinking problems at 16 years than were individuals who remained untreated. These findings extend earlier results on this sample (Moos & Moos, 2003; 2005b; Timko et al., 1999) and are consistent with prior studies that have shown an association between more-extended treatment and better substance use outcomes (Moos et al., 2000, 2001;Ouimette et al., 1998).

Participation in Alcoholics Anonymous and 16-Year Outcomes

The findings extend earlier results on this sample (Moos & Moos, 2004a; 2005b) and those of prior studies (Connors et al., 2001; Fiorentine, 1999; Ouimette et al., 1998;Watson et al., 1997) by showing that more extended participation in AA is associated with better alcohol-related and self-efficacy outcomes. The results support the benefit of extended engagement in AA, in that a longer duration of participation in the first year, and in the second and third years, was independently associated with better 16-year outcomes. In addition, our findings indicate that attendance for more than 52 weeks in a 5-year interval may be associated with a higher likelihood of abstinence than attendance of up to 52 weeks.

 Part of the association between AA attendance and better social functioning, which reflects the composition of the social network, is likely a direct function of participation in AA. In fact, for some individuals, involvement with a circle of abstinent friends may reflect a turning point that enables them to address their problems, build their coping skills, and establish more supportive social resources (Humphreys, 2004; Humphreys, Mankowski, Moos, & Finney, 1999). Participation in a mutual support group may enhance and amplify these changes in life context and coping to promote better long-term outcomes.

Independent Contribution of Treatment and Alcoholics Anonymous

Consistent with prior studies (Fiorentine, 1999; Fiorentine & Hillhouse, 2000; Moos et al., 2001; Ritsher, McKellar, et al., 2002; Ritsher, Moos, & Finney, 2002), longer participation in AA made a positive contribution to alcohol-related, self-efficacy, and social functioning outcomes, over and above the contribution of treatment.

An initial episode of professional treatment may have a beneficial influence on alcohol-related functioning; however, continued participation in a community-based self-help program, such as AA, appears to be a more important determinant of long-term outcomes.

Moreover, compared with individuals who participated only in treatment in the first year, individuals who participated in both treatment and AA were more likely to achieve 16-year remission (i.e. still be in recovery) (Moos & Moos, 2005a).

In interpreting these findings, it is important to remember that participation in treatment likely motivated some individuals to enter AA; thus, some of the contribution of AA to 16-year outcomes should be credited to treatment. Another consideration involves the differential selection processes into treatment versus AA. Individuals with more severe alcohol-related problems tend to obtain longer episodes of treatment, but this selection and allocation process is much less evident for AA.

These divergent selection processes may help to explain the finding that AA is more strongly associated with positive long-term outcomes than is treatment.”

…keep making the meetings!


Moos, R. H., & Moos, B. S. (2006). Participation in Treatment and Alcoholics Anonymous: A 16-Year Follow-Up of Initially Untreated Individuals. Journal of Clinical Psychology, 62(6), 735–750. doi:10.1002/jclp.20259


The Irrationality of Controlled Drinking?

The Irrationality of Controlled Drinking?

by alcoholicsguide

“Most of us have been unwilling to admit we were real alcoholics…Therefore, it is not surprising that our drinking careers have been characterized by countless vain attempts to prove we could drink like other people. The idea that somehow, someday, he will control and enjoy his drinking is the great obsession of every abnormal drinker. The persistence of this illusion is astonishing. Many pursue it into the gates of insanity or death.” (Alcoholics Anonymous, 1976, p. 30)


A number of very concerned people, people in recovery and family members of people in recovery have sent me a link to a journalistic piece entitled,  “The Irrationality of Alcoholics Anonymous “, written by  Gabrielle Glaser, who has moved onto writing about the highly emotive issue of alcoholism and so-called “controlled drinking” after having previously written on such diverse subjects as health and beauty, and interfaith marriage and appeared in magazines like Mademoiselle, Glamour, The Washington Post, and Health, among other publications.

They worry about the effect of this article may have on vulnerable alcoholics and new comers to recovery in particular.

In order to help newcomers and those out there in active addiction make an informed decision about an abstinence based recovery path, which is what I would strongly suggest for alcoholics, I will pick certain studies Glaser cites as being good example of research that demonstrate a return to controlled drinking in alcoholics and  why they are not.

I will then address many of her arguments  over the next series of blogs.

I believe there is no such phenomenon as a return to controlled drinking in alcoholics. To suggest otherwise is highly dangerous.

The Natural History of Alcoholism Revisited (1995) is a book by psychiatrist George E. Vaillant that describes two multi-decade studies of the lives of 600 American males, non-alcoholics at the outset, focusing on their lifelong drinking behaviours. By following the men from youth to old age it was possible to chart their drinking patterns and what factors may have contributed to alcoholism.

In other words, this studies show the “progression” of the disease of alcoholism.

The National Review hailed the first edition (1983) as “a genuine revolution in the field of alcoholism research” and said that “Vaillant has combined clinical experience with an unprecedented amount of empirical data to produce what may ultimately come to be viewed as the single most important contribution to the literature of alcoholism since the first edition of AA’s Big Book.”[1] Some of the main conclusions of Vaillant’s book are:

“Alcoholism can simultaneously reflect both a conditioned habit and a disease.”

That alcoholism was generally the cause of co-occurring depression, anxiety …not the result.

… it is therapeutically effective to explain it as a disease to patients. The disease concept encourages patients to take responsibility for their drinking, without debilitating guilt.

That there is as yet no cure for alcoholism…

That for most alcoholics, attempts at controlled drinking in the long term end in either abstinence or a return to alcoholism.

Successful return to controlled drinking is…just  a rare and unstable outcome that in the long term usually ends in relapse or abstinence, especially for the more severe cases.[48]

“by the time an alcoholic is ill enough to require clinic treatment, return to asymptomatic drinking is the exception not the rule.”[47]

Vaillant, when asked whether controlled drinkingis advisable as a therapeutic goal, he concluded that “training alcohol-dependent individuals to achieve stable return to controlled drinking is a mirage.”[47]

Glaser struggles with this concept of progression of alcoholism I feel in her article. She describes alcoholism as a spectrum when it is in fact more accurately a continuum – it not a static disorder but a disorder which has transitory phases, most commonly called use, abuse and addiction. If one does not understand this progression then they could be saying that abusers and not alcoholics can return to controlled drinking which is different. If that is even the case.

Some people can also  meet a diagnostic criteria for alcohol dependence for certain periods of time in their lives but are not alcoholic per se.  For example, they may be drinking heavily for a period of time due to a bereavement over the loss of a loved one.

As I will go into later in other blogs, neuroscience can certainly give us a good indication of the progression to chronic alcoholism in terms of brain imaging regions of the brain. A classic example is the switch in reward – motivation processing from the ventral to dorsal striatum in the brain of chronic alcoholics.

The dorsal striatum is more involved in compulsive behaviour common to endpoint addiction.

Other diagnostic help in assessing alcoholism in terms of chronicity is the severity of automatically occurring thoughts about alcohol related subject matter or obsessive thinking about drinking as measured by the Obsessive Compulsive Drinking Scale which also shows that more chronic alcoholics activate not only the dorsal striatum when viewing alcohol related cues but also obsessively think about these cues more also.

This the shift to dorsal regions of the striatum is reflected in cognitive terms and is also reflective of affective mechanisms such as a low heart rate variability which is a measure of emotion regulation in the face of these cues.

Alcoholics simply react differently to alcohol cues, salivate more etc than those who are not alcoholic. These measures are reflective to “that invisible line” alcoholics cross in switching for abusive to alcoholic drinking.

Unless scientific enquiry starts using these and other biomarkers of alcoholism it will be impossible for them to conclude that their studies are actually observing the behaviour of alcoholics. You can not predict behaviour accurately unless you have accurately defined what it is you are observing?

This is basic Science.

Glaser determines whether the people she is talking about are or were actual alcoholics by relying on self reports.

She also takes these people on face value although she may have heeded Vaillant when he suggests alcoholics present special challenges for researchers because they are good at concealing their drunkenness.[16] Vaillant asserts that “Alcoholics are expert forgetters,”[17] have inaccurate memories,[18] and give persuasive denials[16] that manifest “an extraordinary ability to deny the consequences of their drinking.”[19]

For the above reasons we have to be especially skeptical of studies supposedly about alcoholics. Most studies on alcoholics showing the markers I have mentioned above have no chance of returning to asymptomatic drinking whatsoever, to do so would lead to relapse and possible early death. This highlights the importance of detailed research, mainly because superficial research can have terrible if not life threatening effect on vulnerable alcoholics looking for help.

I will give an example of this by looking more closely at a study by certain researchers cited by Glaser in her article. To directly quote from Glaser’s article,

“ To many, though, the idea of non-abstinent recovery is anathema. No one knows that better than Mark and Linda Sobell, who are both psychologists. In the 1970s, the couple conducted a study with a group of 20 patients in Southern California who had been diagnosed with alcohol dependence.

Over the course of 17 sessions, they taught the patients how to identify their triggers, how to refuse drinks, and other strategies to help them drink safely. In a follow-up study two years later, the patients had fewer days of heavy drinking, and more days of no drinking, than did a group of 20 alcohol-dependent patients who were told to abstain from drinking entirely. (Both groups were given a standard hospital treatment, which included group therapy, AA meetings, and medications.) The Sobells published their findings in peer-reviewed journals.

In 1980, the University of Toronto recruited the couple to conduct research at its prestigious Addiction Research Foundation. “We didn’t set out to challenge tradition,” Mark Sobell told me. “We just set out to do good research.”

The Sobells returned to the United States in the mid-1990s to teach and conduct research at Nova Southeastern University, in Fort Lauderdale, Florida. They also run a clinic.”

What Glaser failed to mention was that in a subsequent study (4) 10-year follow-up of the original 20 experimental subjects showed that only one, who apparently had not experienced physical withdrawal symptoms (thus possibly not alcoholic), maintained a pattern of controlled drinking;

eight continued to drink excessively–regularly or intermittently–despite repeated damaging consequences;

six abandoned their efforts to engage in controlled drinking and became abstinent;

four died from alcohol-related causes;

and one, certified about a year after discharge from the research project as gravely disabled because of drinking, was missing.

Why did Glaser failed to mention this research, a follow up study to the one she mentions and cites?

Also why has Glaser not mentioned either that the the Sobells have stated since that it is those with less severe problems who often improve by moderating their drinking. Alcoholic abusers.

The Sobells’ implication – that the focus on non-dependent problem drinkers and on harm reduction could take the teeth out of the controlled drinking controversy – was again strangely also not mentioned by Glaser?

It is worth noting that some supporters of controlled or moderation drinking have also hidden their own difficulties with the drink. Audrey Kishline, the founder of Moderation Management (MM), a non-abstinence-oriented self-help group for individuals whose alcohol problems stop short of dependence, killed two people in a head-on vehicular collision with a not very moderate blood alcohol content measured at .26.

She started attending AA soon afterwards.

I will be dissecting the Glaser over the next few weeks – next up will be a blog on the infamous Rand Report of the 1970s and other studies which have purportedly demonstrated a return of controlled drinking in a small minority of so-called alcoholics?


Until then, all I can say is  a very heart felt but at the same time sad thank you to those friends in AA who were chronic alcoholics like me, who showed me what I need to know about this disease. They all relapsed and died,  to never become abstinent and in recovery again?

This was, is and will always be proof enough for me! Ultimately when it comes down to it, my experience and what my eyes see will always outrank academic theorising.

The BB states clearly ” If anyone who is showing inability to control his drinking can do the right-about- face and drink like a gentleman, our hats are off to him. Heaven knows, we have tried hard enough and long enough to drink like other people!”

What I am trying to do and will continue to do is demonstrate where research  is often inaccurate and sometimes downright dangerous.

Also, to end, these studies and diagnostic criteria all seem to focus on alcohol not the underlying condition of alcoholism. If alcohol was my only problem I would simply have stopped drinking as I stopped smoking, stopped taking drugs, stopped eating meat.

Going to an AA meeting and subsequently has shown me that I needed to accept first my alcoholism before accepting that alcoholism is more than alcohol, that I need a solution to my every day living problem.

I have a stress and emotional dysregulation problem, which precedes alcohol and which remains after alcohol.

Until we grasp, finally, what is wrong with alcoholics, we may be destined to go around in the same circuitous fashion.

AA has taught me how to live with others in this world, in a way I never previously could, and no amount of words can never convey how grateful I am for that blessing.



1. Alcoholics Anonymous. (2001). Alcoholics Anonymous, 4th Edition. New York: A.A. World Service

2.Vaillant, George E. (1995). The Natural History of Alcoholism Revisited. Cambridge, Massachusetts: Harvard University Press. ISBN 0-674-60378-8.

Vaillant, George E. (2003). “A 60-year follow-up of alcoholic men”. Addiction, 98, 1043–1051.

4. Pendery, M. L., Maltzman, I. M., & West, L. J. (1982). Controlled drinking by alcoholics? New findings and a reevaluation of a major affirmative study.Science, 217(4555), 169-175.



“Staying in Action” Part 3

In this third part of our blog on the gambling addicts version of “dry drunk” we look at further “symptoms” of this. We hasten to add that a good 12 step program would soon iron out  most of these emotional and behavourial manifestations and maintenance of our “emotional sobriety” via steps 10-12 keep them in manageable order.

Nonetheless, this article (1) gives us good insight into the emotional malady we suffer from without a therapeutic solution, and which can creep up on us in many ways even when trying to “work our program” .

Other manifestations of “Staying in Action” –


Gamblers who rely on avoidance as a defense mechanism are frequently flooded with feelings and memories when they become abstinent. This can occur in several ways. Most commonly the gambler becomes overwhelmed with guilt as he or she remembers things that were done, people that were hurt, episodes of lying and cheating. A common refrain is “I can’t believe I did that.”

A similar experience is the sudden realization of time wasted. During the years they had been gambling, their lives had gone on and they are now older. There is an acute sense of lost opportunities, and of lost youth and innocence. Disappointment becomes self-pity and there is an impulse to give up or to punish oneself by a return to gambling or some other self-destructive behavior.

A third kind of flooding involves the sudden remembrance of painful and traumatic memories of childhood—physical or sexual abuse, extreme neglect, disturbed parents. This may occur when the patient stops gambling or quits other addictive behaviors.

(( we dealt with these ourselves in steps 4 through to seven, followed up with amends 8-9)  As we have already blogged on previously the steps 4-7 in particular allow one to process memories from the past via the adaptive processing of emotions attached to these memories as well as the realisation they we were in the grip of a profound affective and addictive disorder.   Also as the Big Book states “No matter how far down the scale we have gone, we will see how our experience can benefit others. That feeling of uselessness and self pity will disappear. We will lose interest in selfish things and gain interest in our fellows. Self seeking will slip away. Our whole attitude and outlook upon life will change. Fear of people and of economic insecurity will leave us. We will intuitively know how to handle situations which used to baffle us. We will suddenly realize that God is doing for us what we could not do for ourselves.”

This transforms our self pity and sense of wasted years into a powerful transformative tool for helping others. It is no longer wasted but the most precious thing we possess in helping others, in sharing our experience, in being there for others because we know what it’s like to feel the way they do, to be where they are at. )


According to the description in DSM-IV, as well as the writings of most clinicians (for example, Custer & Milt, 1985, p. 52), the typical pathological gambler is “restless, and easily bored.”  This proneness to boredom has been the focus of two studies (Blaszczynski, McConaghy, & Frankova, 1990; Elia, 1995) that compared pathological gamblers to normal controls; boredom scores were significantly higher for the pathological gamblers.

(Again this ties in with alcoholics without a recovery as per the BB ” being restless, irritable, and discontented”, page xxvi).

For early onset male gamblers, particularly if there have been decades of gambling activity, the gambling was typically how they defined themselves. Without their identity as a gambler, they do not know who they are. Giving up gambling leaves a large vacuum or hole in their lives. They have no other interests, and there are few activities that can compete with the excitement of gambling.

As already noted, boredom can mean understimulated. when they stop gambling and “get off the roller coaster” of strong sensations and self-created crises, they may find the underlying restlessness unbearable.

Patients who are manic also need time to adjust to being normal. What others regard as normal feels like being in slow motion to them, or as if something is missing. They describe it as strange and uncomfortable.

Boredom can mean that individuals cannot be alone because of problems in self-soothing. Boredom can mean that they are left alone with intolerable feelings, such as depression, helplessness, shame, or guilt. There is a need to escape, to get away from themselves.

(as an alcoholic the main reason I gave for drinking was “to get away from myself!”) 

For some, being alone means an intolerable state of emptiness or deadness. Those individuals who did not bond in infancy may carry within themselves an image of parental rejection or disgust, or affects engendered by an overwhelmed mother. Being alone and quiet means experiencing these intolerable affects, which they instead try to externalize through addictive substances and behavior.

Problems with intimacy and commitment

By the time the gambler is in treatment and has stopped gambling, spouse and family members are aware of the debts and depleted finances, the pattern of lying, and other problems. The response is usually one of anger, helplessness, and betrayal. Not infrequently, it is only after the gambling has stopped that the brunt of the spouse’s anger is expressed. This is often difficult for the gambler to understand. The anger is often proportional to the fear of being hurt and betrayed again. Holding on to the anger is a way for family members to protect themselves.

Mistrust of the gambler continues longer than it does with other addictive disorders because a relapse can be so devastating in terms of a family’s financial situation, and also because it is so much more difficult to recognize. As frequently stated, gambling is not something that a wife can smell on her husband’s breath nor observe by his gait or coordination. Nor are there blood or urine tests so that one can detect it with certainty. What we need to emphasize with both patient and family is that reestablishing trust will take time, and that if treatment is successful there will be observable changes in personality as well as behavior.

There are usually problems with intimacy that precede the gambling, in which case they will be there after the individual has stopped. Pathological gamblers often have difficulty being open and vulnerable and depending upon others in a meaningful way.

(I can relate to all of the above too – waking up to an awkward and at times profoundly troubling and distressing emotional illiteracy  is perhaps the last thing one needs in the early days of prolonged withdrawal and feelings of almost overwhelming emotional distress that can sometimes accompany the early weeks and months of recovery)

They have learned to suppress their feelings and to detach from potentially painful situations. Much of the work in therapy has to do with identifying emotions and learning how to express them.

Family members have their own issues which if not dealt with may sabotage the gambler’s recovery (Heineman, 1987; Lorenz, 1989). For example, some of the wives of recovering gamblers will admit that they miss the gifts they received when their husband came home after winning. They confess to a wish that he could have just one more big win, which would allow them to pay off their debts. They may realize they had been living vicariously through him, particularly if he was an “action” or “high stakes” gambler. His optimism and grandiosity were contagious. Initially they may have been attracted to him because he was a man with big dreams, a risk-taker, and big spender. According to Heineman (1987) and others, many wives of compulsive gamblers are adult children of alcoholics or of compulsive gamblers. Living from crisis to crisis may be familiar and exciting for them. In some cases there is a need for the gambler to remain “sick” so that they can take care of him.

Many pathological gamblers were brought up in a home in which intimacy was lacking.  They tolerate financial indebtedness far better than they do emotional indebtedness. Many experience claustrophobia in their personal relationships (Rosenthal, 1986), in fact in any meaningful situation. Commitment is experienced as a trap. They have difficulty saying no, or setting limits. This is related to an excessive need for other people’s approval and validation. When they say they feel trapped by another person, what they mean is that they feel trapped by their own feelings about the other person. They may have projected various expectations or demands on to the other, so that they are overly concerned about disappointing them, or about not being adequate to the task.

Excessive reliance on these projective mechanisms leaves them uncertain as to their boundaries, between inner and outer, self and other. A question they frequently ask themselves: what am I entitled to?

Male gamblers, in particular, are preoccupied with power games (Rosenthal, 1986). Power, as opposed to strength,3 is defined in relation to others, and is invariably gained at someone’s expense.

Relationships take on a seesaw quality, with the gambler battling for power and control.

Due to unresolved guilt about his gambling, a patient felt “onedown” in relation to his wife. He felt unworthy of her and not entitled to be treated decently. He did not verbalize this, but instead provoked fights at home. Similarly, his self-esteem was based on material success. When they had to scale down their lifestyle, he felt diminished. Again feeling like a failure, he blamed others and took it out on those closest to him. Compulsive gamblers are often good at “turning the tables,” so that it is the spouse who feels helpless and inadequate or is apologizing to the gambler and seeking forgiveness. For male gamblers, particularly action seekers, relationships are typically adversarial.

In light of the above, it is not surprising that there are frequent sexual problems (Daghestani, 1987; Steinberg, 1990, 1993). Adkins, Rugle, and Taber (1985) found a 14 percent incidence of sexual addiction within a sample of 100 inpatient male compulsive gamblers. When “womanizing” patterns are investigated, the incidence is closer to 50 percent (Steinberg, 1990, also personal communication). The excitement associated with the pursuit and conquest of women resembles the excitement and “big win” mentality of gambling.

In treating early onset male gamblers, in particular, one typically encounters two patterns of aberrant sexual behavior: (1) celibacy or a kind of phobic avoidance of sexual relationships, and (2) compulsive sexual behavior consisting of promiscuous womanizing, or compulsive masturbation related to various forms of pornography. The two patterns may be mixed.


A closely related problem has to do with difficulties handling success. It may be blown out of proportion. For example, in some parts of the country a GA birthday is a cross between a bar mitzvah and a Friar’s Club roast. Gamblers compete with each other in seeing how many people will attend and who will receive the most glowing testimonials. It is a critical time, in that the achievement of a year’s abstinence, or some other landmark, poses an immediate risk for relapse.

There frequently are unrealistic expectations of what success will mean, so that its achievement leads to disappointment and depression. Sometimes the gambler abstained in order to prove something to someone, in effect to win a mind bet. Sometimes they were doing it for their family or for the therapist, so that after a period of abstinence they feel justified in saying “Okay, I was  good for a year. Now I feel something is owed me so I’m going out to have some fun.” Fun, in this case, of course, means gambling.




Sometimes their successes are attributed to omnipotent parts of the personality (Rosenthal, 1986). Success can trigger mania.

They get high on their success and grandiosity takes over. Some gamblers are fearful of success, and there is a subset of gamblers with masochistic character disorders. Some of them feel more alive when they are in debt and having to work hard to pay creditors. A critical time is when they are just beginning to get in the black, when they can start to have something for themselves.

The gambler’s relationship with reality may be adversarial, persecutory, or humiliating. The gambler may want to see himself as an exception—exceptional among people, and an exception to the rules. Not wanting to be pinned down, he is looking for “an edge,” or for loopholes. This search for “freedom” is often what gets him into trouble.

Once initial problems have been dealt with and abstinence established, gamblers are often at greatest risk when life starts becoming predictable. Meeting responsibilities and living a “normal” life leads to a feeling of being trapped for those gamblers who have not yet internalized a value system based on facing responsibility. Rather than viewing their new life as a self determined one, gamblers are more likely to see such behavior as externally imposed. Feeling controlled by their own schedule, they experience a need to rebel.


Staying in action is, for the pathological gambler, equivalent to the alcoholic’s dry drunk. It is a way to maintain attitudes and behaviors associated with gambling while superficially complying with treatment and Gamblers Anonymous. After the patient has initially achieved abstinence, it is important to look for more covert forms of gambling and other ways in which the patient may still be in action.

Lasting abstinence requires personality change. At a minimum, there is a need to identify and confront whatever it is from which the gambler is escaping. This would include the intolerable situation and feelings as well as the mechanism of their avoidance. Honesty means more than not lying to others about one’s gambling; it means being honest with oneself about one’s feelings. One learns to take honest emotional risks, rather than those based on the need to manipulate or control external events.

As is true for all addicts, gamblers at the beginning of treatment cannot trust themselves. Self-trust requires self-knowledge, which in turn requires curiosity about oneself. Stated differently, “The key to building self-trust” (Kramer & Alstad, 1993, p. 252) “is the ability to utilize one’s own experience, including (one’s) mistakes, to change.”

(This article (1)  is worthy in addressing the oft unspoken realities of abstinence/sobriety when the emotional dysfunction and emotional immaturity once solely regulated via addictive behaviours seeps into sober life also and the formerly habitualised compulsive approaches to life re-surface in abstinence. There can be quick and profound self transformation in recovery but many of the habitualised behavioural patterns continue to stalk our every day lives, as we ” trudge the road of Happy Destiny”. They are there waitng to resurface. They are normally the consequence of reacting to the world as opposed to acting responsibly in it.

I have an addicted brain and a recovering mind, they do not always mix very well. They pull me in opposite directions and have sometimes heated arguments in my head.

I have to manage my illness. It hasn’t gone away. The drink did not make me ill. It didn’t help but it did not solely make me an alcoholic, some emotional dysfunction worsened by alcohol, drugs and other addictive behaviours did. I had a vulnerability and a propensity to later addictive behaviours. I was primed to go off. If alcohol or drugs were the sole problem I quite simply would have given them up. As I did with cigarettes etc

If I do not try to remain manageable or emotionally sober I can still react and “still go off on one”, on temporary, fleeting dry drunks.

Hey I appear even to have many  “stay in action” similarities and I haven’t gambled since I was 14 years old. Perhaps these emotional and behavioural manifestations have certain commonalities among addictive disorders?  A spiritual malady or emotional dysfunction which activates “old patterns of behaving” ?  

Then again I only gave up gambling on poker machines because I was losing all my drinking money on gambling machines!!))  



1. Rosenthal, R. J. (2005). Staying in action: The pathological gambler’s equivalent of the dry drunk. Journal of Gambling Issues.





It Works if you Work It!

Alcoholism takes away your life and then kills you.

We look at a study from 8 years ago to show the extent of premature deaths caused by alcoholism and how membership of Alcoholics Anonymous helps in reducing the risk of premature death from alcoholism.

This study (1) of women and men, over 16 years,  observed that those initiating help-seeking careers have better chances of long-term survival. Of the individuals for whom cause of death was known, of the 121 participants known to have died, 76 did so between the 8- and 16-year follow-ups.and 68% died of alcohol-related causes.

Men were more likely to die than were women. When gender was controlled, individuals who were older and unmarried and had more alcohol dependence
symptoms at baseline were more likely to die over the 16-year period.

“It is well documented that the course of alcohol use disorders (AUDs) may end in premature death (Rivara et al., 2004; Room et al., 2005) and …that remission may reduce the risk of premature mortality (Fillmore et al., 2003; Miller, 1999), there is little information about whether an initial course of
professional treatment, or participation in Alcoholics Anonymous (AA), can counteract the connection between AUDs and heightened mortality risk.

To address these issues, we examined mortality in a sample of individuals who had just initiated help-seeking for their AUDs at the start of the study and were followed for 16 years. Specifically, we ascertained the proportions of women and men who died and how these rates compared with matched general population rates…

It Works If You Work It


Data on mortality are much more extensive for treated than for untreated individuals with AUDs. Finney and Moos (1991) reviewed long-term studies of mortality among treated individuals. Overall mortality rates ranged from 15% to 42% and were higher when the duration of follow-up was longer (see also Nielsen et al., 2005).

…Among individuals treated for AUDs, mortality rates were higher for men than for women (Feurerlein et al., 1994; Hurt et al., 1996). In addition, in community samples, rates of mortality due to alcohol use were higher in
men than in women (John and Hanke, 2002; Zureik and Ducimetiere, 1996). Premature death due to alcohol abuse or dependence is particularly more likely among men than among women in young and middle-aged groups (Moller-Leimkuhler, 2003)…

…A more severe and longer duration of alcohol abuse predicts premature death (Liskow et al., 2000; Ojesjo, 1981)…. In an 11-year follow-up, Smith et al. (1983) found that women who developed their AUD early and engaged in binge drinking were more likely to die. Consistently, more alcohol consumption and having recognized at a younger age that drinking was a problem were related to more years of life lost to an AUD (Marshall et al., 1994).

…Mackenzie et al. (1986) found that men who were hospitalized for AUDs more frequently were more likely to die over an 8-year follow-up. Inpatient treatment occurring throughout the course of alcoholism may be a marker for a more severe and chronic disorder because such treatment is sought in response to a relapse (Timko et al., 2000). In a study of inpatients with AUDs, de Lint and Levinson (1975) found that death rates were lower in the first 2 years postdischarge than thereafter. They speculated  that intensive outpatient aftercare may delay or prevent the high rate of mortality that often occurs shortly after discharge.

Among individuals treated for AUDs, those who subsequently attended AA were less likely to have died by a 2-year follow-up than those who did not attend (Masudomi et al., 2004)…

… For inpatient care, longer duration appears to be an indicator of greater disorder severity and thus should be associated with higher mortality…However, for outpatient care and help from AA, a longer duration predicts better substance use disorder outcomes and so may  indicate continuing motivation to stop drinking (Moos and Moos, 2003a, 2004a). From this perspective, a longer duration of outpatient treatment or AA affiliation should be associated with lower mortality.

…Furthermore, those who relapsed after treatment were 3 to 5 times more likely to die as those who remained abstinent (Bullock et al., 1992; Feurerlein et al., 1994)…

(This study found)…individuals who are just beginning their help-seeking…have a better chance of long-term survival than do women and men with more chronic disorders.
That is, individuals entering an initial episode of help-seeking may be successful at preventing or reducing the harm associated with excessive drinking that is also potentially causal in death. In contrast, repeated episodes of AUD treatment are often a reflection of the chronic and severe alcoholism known to cause premature death. As other studies have found, men were more likely to die than were women (Feurerlein et al., 1994; Hurt et al., 1996; John and Hanke, 2002; Zureik and Ducimetiere, 1996). Of the individuals who died, over two-thirds died of causes related to alcohol use.

…individuals who were olderand had more alcohol dependence symptoms (Finney and Moos, 1992; Liskow et al., 2000) and were unmarried were
more likely to die over the 16-year observation period.
Alcohol-related mortality tends to be lower among married persons (Agren and Romelsjo, 1992; Lewis et al., 1995)…



…continuous abstinence, had a positive effect on the survival of individuals with AUDs. Studies comparing stable abstinence with reduced frequency and
quantity of abusive drinking found that only stable abstinence prevented a higher mortality risk (Bullock et al., 1992; Gerdner and Berglund, 1997). Our results are consistent with those findings…


…Longer duration of AA attendance during the first follow-up year (specifically, attendance for more than 4 months) combined with better 1-year drinking outcomes was associated with a lower likelihood of death in the subsequent 15 years.

Alcoholics Anonymous participation may delay mortality not only by
reducing drinking and drinking-related, including medical,
problems, as outpatient treatment does, but also by increasing social resources and reducing…friendship stressors (Humphreys and Noke, 1997; Kaskutas et al., 2002; Masudomi et al., 2004).



Timko, C., DeBenedetti, A., Moos, B. S., & Moos, R. H. (2006). Predictors of 16‐year mortality among individuals initiating help‐seeking for an alcoholic use disorder. Alcoholism: Clinical and Experimental Research, 30(10), 1711-1720.

Why a spiritual solution?

The Alcoholics Guide to Alcoholism

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

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

I guess people are curious as to how the spirit changes matter or material being when it should perhaps be rephrased to how does application of the ephemral mind affect neuroplasticity of the brain. Or in other words how does behaviour linked to a particular faith/belief system alter the functions and structure of the brain. We have discussed these points in two blogs previously and will do so again in later blogs. Here I just want to highlight in a short summary why spiritual practice helps alcoholics and addicts with with…

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AA helps to reduce Impulsivity


One constant in studies on addiction and in alcoholism, in particular is the  fundamental role played by impulsivity in these disorders. It is seen to be present in early use but appears to be more distress based (i.e. more negative urgency based) as the addiction cycle becomes more chronic. This impulsivity has obvious consequences for propelling these disorders via impulsive behaviours and decision making difficulties.

Thus it then follows that any treatment of these addictive disorders must have treatment of impulsivity at the core as it appears to a fundamental pathomechanism.


Here, we review a study that on links  AA attendance and reduced impulsivity using a 16-year prospective study of men and women, who were initially untreated for their drinking problems. Across the study period, there were significant l decreases in impulsivity, and longer AA duration was associated with reductions in impulsivity.

Alcoholics Anonymous (AA) is linked to improved functioning across a number of domains [2,3]. As the evidence for the effectiveness of AA has accumulated, so too have efforts to identify the mechanisms of change associated with participation in this mutual-help group [4].

This study concluded that help-seeking and exposure to the “active ingredients” of various types of help (i.e., AA principles/practices, sponsors), which, in turn, leads to improvements in reduced impulsivity.

Impulsivity is typically higher among individuals in AUD treatment than among those in the general population [5] and, impulse control deficits tend to predate the onset of drinking problems [6-9].

Contemporary research has revealed that traits such as impulsivity can change over time [10]. Mutual-help groups like AA may promote such changes, given that they seek to bolster self-efficacy and coping skills aimed at controlling substance use, encourage members to be more structured in their daily lives, and target deficits in self-regulation [11].


impulse control.preview


Such “active ingredients” may curb the immediate self-gratification characteristic of disinhibition and provide the conceptual grounds to expect that AA participation can press for a reduction in impulsive inclinations. In turn, given the range of outcomes related to impulsivity (e.g., legal, alcohol-related, and psychosocial problems), decreases in impulsivity may account for part of the association between AA participation and improvements in these outcomes.

AA’s vision of recovery as a broad transformation of character [12], and  explores individual differences in emotional and behavioural functioning as potential mechanisms of change (13,14).

Such groups encourage members to be more structured and goal-directed, which may translate into greater efforts to delay gratification of one’s impulses and  to improve clients’ general coping skills (e.g., reduce avoidance coping).

Given that impulsivity is a risk factor for a host of problematic behaviors and outcomes beyond drinking-e.g., criminality [15], drug abuse [16], reckless driving and sexual practices [17],  lower quality of interpersonal relationships [18], and poor health [19] this reduced impulsivty is beneficial in other aspects too.

Notably, this effect was buffered by a higher quality of social support-a probable active ingredient of AA. Thus, the impact of reducing impulsivity may be widespread across a range of outcomes that are critical for long-term sobriety.


Our main caveat on this study is that it does not distinguish between different types of impulsivity and does not mention negative urgency (or distress-based impulsivity) which is more commonly seen is this sample group.

AA’s “active ingredients” may reduce distress, via a new found emotional regulation gained via the steps and use of a sponsor (acting as an external prefrontal cortex to help us inhibit our impulsive and distress based responses)  which in turns reduces our tendency to impulsive decision making and behaviour.


It would have been interesting in this study to have also measure how emotional dysregulation changed in the time span of 16 years (using the DERS scale) and to have used a different impulsivity scale i.e. used the UPPS-P scale which would both have helped more specificallylook  at the interaction of how emotional regulation and impulse control changed over the 16 year period.




1.  Blonigen, D. M., Timko, C., & Moos, R. H. (2013). Alcoholics anonymous and reduced impulsivity: a novel mechanism of change. Substance abuse, 34(1), 4-12.

2. Humphreys, K. Circles of recovery: Self-help organizations for addictions. Cambridge Univ Pr; 2004.

3.. Tonigan JS, Toscova R, Miller WR. Meta-analysis of the literature on Alcoholics Anonymous: Sample and study characteristics moderate findings. Journal of Studies on Alcohol. 1995

4. Kelly JF, Magill M, Stout RL. How do people recover from alcohol dependence? A systematic review of the research on mechanisms of behavior change in Alcoholics Anonymous. Addiction Research & Theory. 2009; 17(3):236–259.

5. Conway KP, et al. Personality, drug of choice, and comorbid psychopathology among substance abusers. Drug and alcohol dependence. 2002; 65(3):225–234. [PubMed: 11841894]

6. Caspi A, et al. Behavioral observations at age 3 years predict adult psychiatric disorders: Longitudinal evidence from a birth cohort. Archives of General Psychiatry. 1996; 53(11):1033. [PubMed: 8911226]

7. Cloninger CR, Sigvardsson S, Bohman M. Childhood personality predicts alcohol abuse in young adults. Alcoholism: Clinical and Experimental Research. 1988; 12(4):494–505.

8. Elkins IJ, et al. Personality traits and the development of nicotine, alcohol, and illicit drug disorders: Prospective links from adolescence to young adulthood. Journal of abnormal psychology. 2006; 115(1):26. [PubMed: 16492093]

9. Sher KJ, Bartholow BD, Wood MD. Personality and substance use disorders: A prospective study. Journal of Consulting and Clinical Psychology. 2000; 68(5):818. [PubMed: 11068968]

10. Caspi A, Roberts BW, Shiner RL. Personality development: Stability and change. Annual Review of Psychology. 2005; 56:453–484

11. Moos RH. Active ingredients of substance use focused self help groups. Addiction. 2008; 103(3):387–396. [PubMed: 18269361]

12. White WL. Commentary on Kelly et al. (2010): Alcoholics Anonymous, alcoholism recovery, global health and quality of life. Addiction. 2010; 205:637–638. [PubMed: 20403015]

13. Kelly JF, et al. Mechanisms of behavior change in alcoholics anonymous: does Alcoholics Anonymous lead to better alcohol use outcomes by reducing depression symptoms? Addiction. 105(4):626–636. [PubMed: 20102345]

14. KELLY JF, et al. Negative Affect, Relapse, and Alcoholics Anonymous (AA): Does AA Work by Reducing Anger? Journal of studies on alcohol and drugs.

15. Krueger RF, et al. Personality traits are linked to crime among men and women: Evidence from a birth cohort. Journal of abnormal psychology. 1994; 103(2):328. [PubMed: 8040502]

16. McGue M, Slutske W, Iacono WG. Personality and substance use disorders: II. Alcoholism versus drug use disorders. Journal of Consulting and Clinical Psychology. 1999; 67(3):394. [PubMed: 10369060]

17. Caspi A, et al. Personality differences predict health-risk behaviors in young adulthood: Evidence from a longitudinal study. Journal of Personality and Social Psychology. 1997; 73(5):1052. [PubMed: 9364760]

18. Ozer DJ, Benet-Martinez V. Personality and the prediction of consequential outcomes. Annu. Rev. Psychol. 2006; 57:401–421. [PubMed: 16318601]

19. Bogg T, Roberts BW. Conscientiousness and Health-Related Behaviors: A Meta-Analysis of the Leading Behavioral Contributors to Mortality. Psychological Bulletin. 2004; 130(6):887. [PubMed: 15535742]









Predicting relapse via extent of emotional dysregulation?

Predicting relapse via extent of emotional dysregulation?

by alcoholicsguide

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

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

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

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




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

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


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

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

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

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



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


When fighting your neural ghosts make sure to surrender!!

When I was in early recovery, in the first weeks and months my brain would continually trick me into thinking I was not an alcoholic and it did this via a combination of  stress and memory.

The process went like this – first I would have an intrusive thought about alcohol and drinking which I did not want and had not consciously put in my own head. Which used to annoy me! So what was it doing there then? I must have put it there right? why else would it be there?

So I must still have wanted to drink?

I would find this thought very threatening, frightening and upsetting. I would try to get rid of it by suppressing it, pushing it out of my consciousness. The problem was this didn’t work.


In fact, it made the situation a whole lot worse. The intial intrusive thoughts about drinking would then proliferate and there would be other thoughts about drinking; where, at what time, who would be there. I would then have a visual read out of all these scenarios. In the bar, the sunlight streaming through the window, the golden glistening pint of lager in the summer sun matched only by the pearly white smile of the beautiful buxom bar maid slowly pulling my pint, looking at me longingly etc. in a busy atmosphere, full of happy your attractive people laughing and enjoying themselves. people dancing and hugging. Sweet music drifting acorss the bar. You get the picture.

Delusion! This was nothing like the last bar I drank in a can assure you!! It was however the image my brain was evoking partly via memory association partly by motivational embellishment.

I have an alcoholic brain which wants me to drink. It uses, still, memories from the past, to whisper sweet nothings. It never casts images across my feverish mind of violently vomiting, bent over the downstairs toilet, or me staring through half blind eyes at my severely jaundiced face in the bathroom mirror. Or being thrown out of various bars onto the hard concrete pavement outside, on my head. Or the tears and violent rows. And the distress and confusion on loved ones’ faces.

No my alcoholism never accesses these images. Ignores them completely. Instead, as my alcoholic brain wants nothing more or else than to drink, it sends memories like neural ghosts into my head to cast a spell of delusional images and suggestive ideas, mainly promoting the idea of how good it was.

This is why in AA it is said we should wind the tape forward a bit to the disgustingly horrible reality of our final drinking. The constantly wretching and living in isolaton in our alcohol induced psychosis and the shivering terror of delirium tremens.

We have a inner voice of alcoholism that quite simply lies. Distorts our memories. The motivational voice of our alcoholism is a pathological liar. It only wants to drink because it is like a psychotic carer who thinks that drinking is the thing to do when we are in full of stress or in emotional distress. It automatically says hold one I have a solution to this distress, DRINK!

This is what the brain has become hardwired to do when distressed enough.  it is a habitual response of our implicit memory which then recruits our explicit memory which paints the picture of why drinking would be such a good idea.

I have a distress based illness, so I do get distressed from time to time. Sometimes over the most innocuous things sometimes.

Not as badly as in early recovery.  No, things have improved beyond belief since then.

The neural ghosts of my motivation were like intoxicating sirens in early recovery. My impaired reward systems implored me to have liquid release. Both combined to conjure an alternative view of myself from that of my recovering self, which was still in it”s infancy. They seemed to have control of my brain!  I suddenly had a problem beyond my own will power, I couldn’t resolve these things under my own steam.

The thoughts would come and I would suppress them and the thoughts would multiply and then the memories would all chain link  and pretty soon I would have an Amazon warehouse store of memories, all providing evidence against those guys in AA, who were not telling me truth about me being an alcoholic, They were wrong…sure I liked to drink, especially given by traumatic upbringing and all?

All these thoughts and memories floating across my mind like edits in a movie to show me as a drinking person who wasn’t an alcoholic. Not many disorders go to such profound trouble!!

I would fight these images, memories and thoughts to such an extent my brain would quite simply end up paralysed, my brain felt like it had become locked and there was nothing I could do about it. It had frozen into a terrifying inertia. Stalemate. No resolution apart from increased suffering.

Fortunately whatever I had learnt in AA even in the early days would rescue me. I had learnt to habitually grasp at something close to hand, my mobile phone. After a few puzzling moments of indecision I realised I could get help from somewhere. Ring my sponsor!!!!

I had to use someone else’s head to help me with my head, my newly recovering alcoholic head. I needed a recovered head who knew what I was going through and could help me through it! I felt all fragile like a jaundiced chick.

Recovery is tough in the early days, let’s never forget that! Life without a sponsor and right from the start is a key to surviving this alcoholic possession by these deluded memories and these neural ghosts.

This is the most vital period, to keeping those who need help in recovery. Saying someone doesn’t want it enough doesn’t cut it for me anymore. Better to show them what they are missing, namely a solution to their problems. Who ultimately doesn’t want that?

If you have never trusted anyone in your life, like me, this is the time to start if you want to recover. Trust at least one person on God’s earth. One, that’s all. This is the start to a new world in recovery. A world beyond your alcoholic brain’s comprehension.

Anyway, remember that in the feverish brain of a person in early recovery who ends up engaged in this neurobiological possession, thought straightjacket and fighting for his or her life against a mnemonic Hydra when it is the last thing they should be doing, the only way to win is to give in. Surrender!

Ultimately, how we appraise and react to naturally occurring alcohol or drug related thoughts and associated memories  will determine if this process of “craving” is activated. If we use strategies such as acceptance of these thoughts as transitory then the thoughts will not affect this process and if we “Let Go and Let God” then the distress which initially activates this process will not do so. How we react to our thoughts and accompanying distress (as they appear be be coupled) will determine whether the mental obsession mentioned above will be provoked.

Also see Cognitive Craving Part 3  and Part 4

A Cognitive Model of Craving – Pt 3

In an earlier blog we asked the question whether  neurobiological or “conditioning” or reinforcement models of craving predict relapse in abstinent alcoholics and addicts?

For us this is the most essential question. How do we explain relapse in those individuals motivated to remain abstinent, especially when they have followed some form of treatment, including 12 step groups.

We have seen that most relapse seems to be prompted by psychological stressors such as interpersonal relationships and the failure to cope with these.

This is very different to conditioning or reinforcement models that simply posit that people relapse because of the lure of alcohol or drug related stimuli, “cues”, or cues in the presence of stress or negative emotions, which we believe does have some affect.

Equally we have shown that in treatment seeking individuals there seems to be an automatic avoidance of cues so attentional bias does not really apply to this group plus there is a negative memory association bias in this abstinent, treatment seeking group also. So why do these people relapse?

What is the craving process prior to relapse for this group? . This is hugely important as neurobiological accounts do not predict relapse, so what does?

Over the next two blogs we will forward a model of craving or “mental obsessing” which we believe more accurately models the mechanisms which lead these individuals committed to staying sober and in recovery to relapse.

Ultimately we believe it may the maladaptive cognitive-affective reaction to naturally occurring  intrusive thoughts about alcohol or drugs (which are also the function of emotional dysregulation) that creates a proliferation of such thoughts, until they become obsessive, and which escalates stress and emotional distress to such an extent that the individual relapses to silence these tortuous obsessive thoughts.

These thoughts may not always be about alcohol or drugs. They may also contain negative perceptions of self, such as low self esteem and negative self schemas as the consequence of abusive early childhoods. These may result in “I am not good enough” thinking or “to hell with it!” relapse which have little to do with an appetitive urge to drink as in some reinforcement models. They are more akin to escape from self.

So models of addiction tend to focus on neurobiological substrates underlying addiction rather than on how affective (and cognitive) processing mediate addictive behaviours (1) although 80% of problem drinkers after outpatient treatment reported drinking episodes aimed at manipulating thoughts or emotions (2), with the majority of treatment clients attributing their relapse to interpersonal stress or negative emotions (3).

Also the involuntary retrieval of drug related thoughts is a hallmark of addicted populations. Over 70% of smokers stated that urges disrupted their thinking or functioning (4). Intensity of obsessive thoughts about alcohol predict relapse rate (5), with addicts motivated to use drugs to “silence” obsessive thoughts (6).  The idea that abstinence automatically decreases alcohol-related thoughts is challenged by research and supported by clinical observation that among abstinent alcohol abusers, alcohol-related thoughts and intrusions are the rule rather than exception (7).

So if emotion regulation difficulties and related intrusive thoughts are so prevalent in recovering abstinent addicts and alcoholics how do we account for this in a satisfactory and comprehensive theory of craving?

One study important to the conceptual framework set out here (6) used heart rate variability (HRV) measures, as a putative index of emotional regulation, to illustrate how craving involves cognitive-emotional processing and how conditioning models may not fully explain  ‘craving’.  This is consistent with the increasing concern in the literature about the applicably of such “one-dimensional” conditioning models explaining the results of cue reactivity studies (6). This study, among various findings, showed a link between HRV and obsessive thoughts,  in simple terms, the greater the emotional dysregulation, the greater the obsessive thoughts about alcohol.

It may even be that these “conditioning” reinforcement models or dopaminergic or stress-based models are describing “urges” rather than craving.  For us “craving” is distinct but interdependent on this “urge” state, it is partly triggered by it, if you like.

As an alternative to such passive “respondent” or “conditioning” models, some researchers have advocated the use of information-processing theory to understand how dependent individuals react in their encounter with “drug-related” cues (external and internal, e.g. stress or negative emotions) (6). Craving may thus be a different phenomenological experience to that of the physiological urges, although one may prompt the other.

According to one ‘info-processing’ view of craving, forwarded by Stephen Tiffany (4), ‘craving’,  occurs only when the automatic approach behaviour commonly seen in addicts in thwarted. This is particularly pertinent to those abstinent, treatment seeking individuals. In addiction, drug use behaviour develops various rituals around the seeking, preparation and consumption of drugs. These habitual procedures become stored in memory, in automatized action schemata  or action plans.

Encoded within these unitized memory systems are prompts such as external events (e.g. sight of a hypodermic syringe,) or internal events such as physical states (e.g. NA). Although activation of these memory structures may not be a sufficient for addicts to respond to ‘urges’, via actual drug seeking, they may stimulate approach behaviours.

Tiffany (1990) proposed “urges”, or what we call craving, are said to be associated with conscious efforts to inhibit the operation of drug use action plans (e.g. prevention of relapse or suppressive reaction to intrusive using-related thoughts). In abstinence, these “urges” involve non-automatic (i.e. conscious, effortful) cognitions that compete with automatic (unconscious effortless) drug use related plans. Thus, relapse may occur under two circumstances: when the action plan operates autonomously and when conscious processes to inhibit the action plan (thought suppression) backfire and are unsuccessful.



We agree with Tiffany’s (1990) assertion that, like other stereotypic motor acts, some aspects of the drug-use ritual are susceptible to automatization. In fact in relation to automatic using schemas it is only the “nonautomatic” processing where cognitive resources are consciously devoted to disrupting the course of a perceive threat of relapse and prior experience of these self same affective states in the context of use that activate drug- and alcohol related memories (Bradizza, Stasiewcz, & Maisto, 1994.) and cause “craving”.

The “exhaustive and effortful” effects of “urges” (craving)  in abstinent addicts (Tiffany, 1990 p.158) may reflect consciously trying to inhibit these by thought suppression. Whereas, drug using schemas are firmly established and neurally embedded and require few resources to operate, the “abstinence plan” is poorly established and demands vigilance (i.e. attention) and effort to maintain. It is also a relatively new internal voice and not as familiar to the addict. Therefore, it not surprising that many addicts take the path of least resistance and relapse.

Addictive behaviours thus become increasingly automatic or compulsive in the addiction cycle, which supports Tiffany’s ‘cognitive’ model of automatic action plans. ‘Cravings’ are generated, in our model, by non-automatic, cognitive processes which are invoked to thwart (or interfere) with these drug use action plans.

For example, in abstinent addicts, internal stress/emotional distress provokes automatic action plans (and accompanying intrusive thoughts). These individuals then use non-automatic processing i.e. cognitive control/thought suppression) to ‘fight’ these threatening (naturally occurring) automatic thoughts.

The anterior cingualte cortex (ACC) acts a gateway between what is known as explicit (hippocampal) memory (remembered knowledge about things – e.g. where we drank, with whom, how it felt, noises, smells, atmosphere and ourselves in those situations etc) and implicit (dorsal striatal)  memory (the procedural, how to do memory-  the habitualised procedure of Tiffany’s automatic addiction action plans). The dorsal medial striatum (DMS) plays an important part orchestrating the switching between these memories through a “hippocampal-to-striatal pathway” passing through the ACC (41). It may be ACC hypofunctioning, under extreme stress, which aids transition between explicit and implicit memory networks (42).

Addiction severity is suggested as being represented by a shift in reward processing from ventral stiatum (VS) to DS (28) with this marked by an emergence of automatic thoughts, which the authors suggested as the cognitive thoughts and images of automatized drug action schemata (Tiffany 1990). As addiction escalates there appears to be a greater reliance on implicit rather than explicit (hippocampal) memory too. Also emotional distress is known to recruit the DS region also. So in effect the DS becomes involved in memory, reward and affect in later addiction.  So emotional dysregulation will not only provoke intrusive thoughts, but activate automatic approach behaviour, i.e. will prompt a movement towards getting and consuming drugs and alcohol.

Modell et al, 1992, distinguished between  intrusive thoughts – and memories – in a cognitive component to craving and in compulsions, which is more motoric and action component –  the cognitive component may be governed by the dorsal medial which has connections with the ‘associative’ PFC and lateral DS which is more involved in habitual motor activity As we have already discussed, addiction severity corresponds with the extent of obsessive thoughts as measured by the Obsessive Compulsive Drinking Scale (OCDS) which suggest that as the severity of this illness progresses, so does the intensity of the obsessive thoughts about alcohol and the compulsive behaviours to use alcohol. Kranzler et al. (1999) showed relapsers who scored higher in ‘obsessions’ craving measured by the OCDS predicted relapse in the 12 months after treatment completion. It is tempting to ad that emotional dysregulation also worsens as addiction becomes more severe(  ).

‘Cravings’ are thus generated by non-automatic, cognitive processes which are invoked to thwart (or interfere) with these drug use action plans.  The DMS may be very important in the relapse mechanism we are about to explore.

The DMS may have a potential role in cognitive control of behaviour flexibility and mediating behaviours by hippocampal guidance. As such the DMS and DLS may either compete (Misumori, Yeshenko, Gill and Davis, 2004) or cooperate (Devan, MacDonald, White 1999) under different conditions.  For example, DMS may be activated when a reversal of a previously reinforced response, i.e. habitual response, is required (Eichenbaum et al, 1989). Thus in attempting to inhibit stimulus response, i.e. the automatic alcohol approach behaviour of the DLS,    the DMS activates action-outcome pathways

Thus the ‘cognition and imagery of automatized schema’ becomes increasingly obsessive as the consequence of the anterior cingulate cortex (ACC) detecting conflict between memory intrusions and alerting the prefrontal cortex (PFC) to actively suppress unwanted thoughts (169). This only serves to intensify these thoughts as thought suppression ‘rebounds’ unwanted thoughts more intensely and prolifically into consciousness (170).

This, in abstinent addicts, appears to make the situation worse leading to greater stress reactivity and  need to further inhibit habitual response which activates even more action-outcome memory, e.g. the automatic activation of mental representations in associated memory networks of what course of action has normally been followed to affect the outcome of reducing this distress, i.e. which normally has been to drink.

Whereas the DMS normally in adaptive processes competes with the DLS to resolve a situation, for the abstinent addict, it only increases the problem by suggesting solutions which in fact make the situation more acutely adverse.

For the addict attempting to maintain abstinence, declarative memory and controlled processes may often be “corrupted” in service of promoting or rationalizing drug use. This will occur because negative affect is aversive and intrinsically primes escape and avoidance strategies.

Thus the ACC in recruiting explicit memory to counteract the automatic alcohol related thoughts of the DS may unwittingly be increasing memories of drinking and explicit prompts to drink as this is what has normally been the course of action in such situations of negative emotions.

The best and most well-intentioned efforts to remain sober/clean threaten sobriety most; producing a mnemonic ‘Hydra Effect’ whereby attempts to cut off this terrible flowering of intrusive thoughts leads to increased proliferation of these thoughts and accompanying emotional distress.


This, we posit, is what occurs in the mind of a recovering/abstinent alcoholic and is more akin to the “mental obsession” of the Big Book that purely neurobiological/physiological urge states.

Equally it should be noted that craving or mental obsession does not suggest that the alcoholic or addict in recovery/abstinence is actually motivated or even wants to relapse to former use. One can engage in this “mental obsession” or cognitive craving simply via a maladaptive emotional dysregulation whereby a defective emotional strategy such as thought suppression of threatening intrusive thoughts can set up a chain of reactions which lead to an unfortunate proliferation of thoughts and memories which promote alcohol and drug use to relieve escalating emotional distress which leads to relapse even if the alcoholic or addict in recovery did not even wish it! What else is this other than a craving beyond one’s mental (cognitive) control!

Relapse can happen to an alcoholic or addict if he does not manage his underlying condition of emotional dysregulation, in other words.



References (to follow)

1. Cheetham, A., Allen, N. B., Yücel, M., & Lubman, D. I. (2010). The role of affective dysregulation in drug addiction. Clinical psychology review30(6), 621-634.

2. Sanchez-Craig, M., Annis, H. M., Bronet, A. R., & MacDonald, K. R. (1984). Random assignment to abstinence and controlled drinking: evaluation of a cognitive-behavioral program for problem drinkers. Journal of consulting and clinical psychology52(3), 390.

3. Lowman, C., Allen, J., Stout, R. L., & Group, T. R. R. (1996). Replication and extension of Marlatt’s taxonomy of relapse precipitants: overview of procedures and results. Addiction91(12s1), 51-72.

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

5. Bottlender, M., & Soyka, M. (2004). Impact of craving on alcohol relapse during, and 12 months following, outpatient treatment. Alcohol and Alcoholism39(4), 357-361.

6. Ingjaldsson JT, Laberg JC, Thayer JF. Reduced heart rate variability in chronic alcohol abuse: relationship with negative mood, chronic thought suppression, and compulsive drinking. Biological Psychiatry. 2003;54(12):1427–1436.

7.  Hoyer, J., Hacker, J., & Lindenmeyer, J. (2007). Metacognition in alcohol abusers: How are alcohol-related intrusions appraised?


. Bradizza, C. M., Stasiewicz, P. R., & Maisto, S. A. (1994). A conditioning reinterpretation of cognitive events in alcohol and drug cue exposure. Journal of Behavior Therapy and Experimental Psychiatry, 25, 15 – 22

Modell, J. G., Glaser, F. B., Cyr, L. & Mountz, J. M. (1992) Obsessive and compulsive characteristics of craving for alcohol in alcohol abuse and dependence. Alcoholism: Clinical and Experimental Research, 16, 272–274.

. Kranzler, H. R., Mulgrew, C. L., Modesto-Lowe, V. and Burleson, J. A. (1999) Validity of the obsessive compulsive drinking scale (OCDS): Does craving predict drinking behavior? Alcoholism: Clinical and Experimental Research 23108–114.

(Misumori, Yeshenko, Gill and Davis, 2004)

(Devan, MacDonald, White 1999)

(Eichenbaum et al, 1989).

Acceptance is the Key – Using Acceptance-Based Mindfulness to Promote Emotional Regulation

One of the leading researchers in the area of emotional regulation difficulties and the advocacy of acceptance-based Mindfulness in treatment of these emotional regulation problems is  Kim Gratz.

In the first in a series of blogs about how different treatments address the intrinsic emotional dysregulation at the heart of addiction we consider Gratz’s view on emotional regulations and the role of mindfulness in alleviating some of this dysregulation (1).

The idea of acceptance of things as they are is central to acceptance based treatments such as Mindfulness, DBT and 12 step programs (“acceptance is the key”).

Difficulties in emotion regulation underlie many of the clinically relevant behaviors and psychological difficulties for which clients seek treatment, including substance use (2,3), binge eating (4,5).

In response, treatments for a variety of difficulties are increasingly incorporating a focus on emotion regulation and seeking to promote adaptive emotion regulation skills (6- 8 ).

There has been a great deal of research in the past decade indicating that efforts to control, suppress, or avoid unwanted internal experiences (including emotions) may actually have paradoxical effects, increasing the frequency, severity, and accessibility of these experiences (9-10 ).

Studies in this area have focused on thought suppression (i.e., deliberately trying not to think about something). Consistent with the findings of this research, another approach to emotion regulation emphasizes the functionality of all emotions (11,12) and suggests that adaptive emotion regulation involves the ability to control one’s behaviors (e.g., by inhibiting impulsive behaviors)



These studies show that attempts to avoid or suppress internal experiences may actually have paradoxical effects (referred to as ironic processes (13)) were attempts to suppress thoughts leads to them increasingly rebounding in one’s mind so this has the opposite effect, ironic, to what one hopes to achieve, to lessen these thoughts.  More recently, researchers have  found similar results when attempting to suppress emotions (14). All in all, these findings suggest that conceptualizations of emotion regulation that equate regulation with  the control or avoidance of certain emotions may be counter productive to emotion regulation.

Some researchers have suggested suggests that adaptive emotion regulation involves the ability to control one’s behaviors when experiencing negative emotions, rather than the ability to directly control one’s emotions themselves (7,15). This approach distinguishes emotion regulation from emotional control and, instead, defines regulation as the control of behavior in the face of emotional distress

According to this approach, although adaptive regulation may involve efforts to modulate the intensity or duration of an emotion (16) these efforts are in the service of reducing the urgency associated with the emotion in order to control one’s behavior (rather than the emotion itself).

In other words, this approach suggests the potential utility of efforts to “take the edge off” an emotion or self-soothe when distressed, rather than to get rid of the emotion or escape it altogether.

Moreover, when it comes to efforts to modulate the intensity or duration of an emotion, attachment to the outcome of these efforts is thought to have paradoxical effects (as directly trying to reduce emotional arousal to a particular level or make an emotion end after a certain amount of time is considered to reflect an “emotional control” agenda indicative of emotional avoidance).

Some researchers conceptualize emotion regulation as any adaptive way of responding to one’s emotions, regardless of their intensity or reactivity.

Given evidence that many individuals who engage in maladaptive behaviors struggle with their emotions (17,18), treatments that focus on teaching individuals ways to avoid or control their emotions may not be useful, and may inadvertently reinforce a non-accepting, judgmental, and unhealthy stance toward emotions. Instead, the fact  that such individuals may be caught in a struggle with their emotions suggests that they may benefit from learning another (more adaptive) way of approaching and responding to their emotions

Acceptance- and mindfulness-based treatments may be particularly useful for promoting emotion regulation and facilitating the development of more adaptive ways of responding to emotions. For example, the process of observing and describing one’s emotions (an element common across many mindfulness- and acceptance-based treatments,) to promote emotional awareness and clarity, as clients are encouraged to observe their emotions as  they occur in the moment and to label them objectively.

Through this process, clients are increasing contact with these emotions and focusing attention on the different components of their emotional responses (expected to increase emotional awareness). Further, the process of describing emotions is expected to facilitate the ability to identify, label, and differentiate between emotional states.

Moreover, the emphasis on letting go of evaluations such as “good” or “bad”) and taking a nonjudgmental and non evaluative stance toward these emotions


images (9)


Given that the evaluation of emotions as bad or wrong likely both motivates attempts to avoid emotions and leads to the  development of secondary emotional responses (e.g., fear or shame), learning to approach emotions in a nonjudgmental fashion is expected to increase the willingness to  experience emotions and decrease secondary emotional reactions.

Indeed, it is likely this nonevaluative stance (i.e., the description of stimuli as “just is,” rather than as “bad” or “good”) that underlies many of the potential benefits of observing and describing one’s emotions

Mindfulness training may also promote the decoupling of emotions and behaviors, teaching clients that emotions can be experienced and tolerated without necessarily acting on them. As such, these skills may facilitate the ability to control one’s behaviors in the context of emotional distress.

One factor thought to interfere with the ability to control impulsive behaviors when emotionally distressed  is the experience of emotions as inseparable from behaviors, such that the emotion and the behavior that occurs in response to that emotion are experienced as one (e.g.,anxiety and taking an anxiolytic). Thus, the process of observing one’s emotions and their associated action urges is thought to facilitate awareness of the separateness of emotions and the behaviors that often accompany them, facilitating the ability to control one’s behaviors when distressed.


1. Gratz, K. L., & Tull, M. T. (in press). Emotion regulation as a mechanism of change in acceptance-and mindfulness-based treatments. In R. A. Baer (Ed.), Assessing mindfulness and acceptance: Illuminating the processes of change. Oakland, CA: New Harbinger Publications.

2. Fox, H. C., Axelrod, S. R., Paliwal, P., Sleeper, J., & Sinha, R. (2007). Difficulties in emotion regulation and impulse control during cocaine abstinence. Drug and Alcohol Dependence, 89, 298-301.
3.  Fox, H. C., Hong, K. A., & Sinha, R. (2008). Difficulties in emotion regulation and impulse control in recently abstinent alcoholics compared with social drinkers. Addictive Behaviors, 33, 388-394.

4. Leahey, T. M., Crowther, J. H., & Irwin, S. R. (2008). A cognitive-behavioral mindfulness group therapy intervention for the treatment of binge eating in bariatric surgery patients.  Cognitive and Behavioral Practice, 15, 364-375.

5.  Whiteside, U., Chen, E., Neighbors, C., Hunter, D., Lo, T., & Larimer, M. (2007). Difficulties regulating emotions: Do binge eaters have fewer strategies to modulate and tolerate negative affect? Eating Behaviors, 8, 162-169.

6. Gratz, K. L., & Gunderson, J. G. (2006). Preliminary data on an acceptance-based emotion regulation group intervention for deliberate self-harm among women with borderline personality disorder. Behavior Therapy, 37, 25-35.

7. Linehan, M. M. (1993). Cognitive-behavioral treatment of borderline personality disorder. New York, NY: Guilford Press.

8. Mennin, D. S. (2006). Emotion regulation therapy: An integrative approach to treatment-resistant anxiety disorders. Journal of Contemporary Psychotherapy, 36, 95-105

9. Hayes, S. C., Luoma, J. B., Bond, F. W., Masuda, A., & Lillis, J. (2006). Acceptance and Commitment Therapy: Model, processes, and outcomes. Behaviour Research and Therapy, 44, 1-25

10. Salters-Pedneault, K., Tull, M. T, & Roemer, L. (2004). The role of avoidance of emotional material in the anxiety disorders. Applied and Preventive Psychology, 11, 95-114

11. Cole, P. M., Michel, M. K., & Teti, L. O. (1994). The development of emotion regulation and  dysregulation: A clinical perspective. In N. A. Fox (Ed.), The development of emotion regulation: Biological and behavioral considerations. Monographs of the Society for Research in Child Development, 59, (pp. 73-100, Serial No. 240)

12. Thompson, R. A., & Calkins, S. D. (1996). The double-edged sword: Emotional regulation for children at risk. Development and Psychopathology, 8, 163-182.

13. Wegner, D. M. (1994). Ironic processes of mental control. Psychological Review, 101, 34-52.

14. Salters-Pedneault, K., Roemer, L., Tull, M. T., Rucker, L., & Mennin, D. S. (2006). Evidence of  broad deficits in emotion regulation associated with chronic worry and generalized anxiety disorder. Cognitive Therapy and Research, 30, 469-480.

15. Melnick, S. M., & Hinshaw, S. P. (2000). Emotion regulation and parenting in AD/HD and comparison boys: Linkages with social behaviors and peer preference. Journal of Abnormal Child Psychology, 28, 73-86.

16. Thompson, R. A. (1994). Emotion regulation: A theme in search of definition. In N. A. Fox  (Ed.), The development of emotion regulation: Biological and behavioral considerations. Monographs of the Society for Research in Child Development, 59, (pp. 25-52, Serial No.

17.   Chapman, A. L., Gratz, K. L., & Brown, M. Z. (2006). Solving the puzzle of deliberate self harm: The experiential avoidance model. Behaviour Research and Therapy, 44, 371-394.

18. Whiteside, U., Chen, E., Neighbors, C., Hunter, D., Lo, T., & Larimer, M. (2007). Difficulties regulating emotions: Do binge eaters have fewer strategies to modulate and tolerate  negative affect? Eating Behaviors, 8, 162-169