Measuring the “Psychic” Change

a change in consciousness brought about the 12 step program of recovery can be demonstrated.

The Alcoholics Guide to Alcoholism

Prolonged Abstinence and Changes in Alcoholic Personality?

When I came into AA I remember hearing the words “the need for a psychic change” which was the product of a spiritual awakening (as the result of doing the 12 steps).

The big Book of Alcoholics Anonymous clearly states this need “The great fact is just this, and nothing less: That we have had deep and effective spiritual experiences* which have revolutionised our whole attitude toward life, towards our fellows and toward God’s universe.”

This is the cornerstone of AA recovery; thinking, feeling and acting differently about the world to when we were active drinkers. Otherwise one does the same things and ends up in the same places, doing the same things, namely drinking. It is a behavioural revolution; a sea change in how we perceive and act.

In line with this thinking, we came across this French study which measured via…

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Getting out of “self” via Prayer and meditation

when we meditate and pray we can get “out of self” – here’s proof.

The Alcoholics Guide to Alcoholism

When I first came into recovery I constantly heard the refrain about “getting out of self” – in fact steps 10-12 help one do so. Step 12, by helping others in recovery and step 11 which encourages prayer and mediation.

Can we get out of “self” by prayer and mediation? I will be dedicating a number of blogs to mediation so will just briefly consider prayer here.

In one study Franciscan nuns had their brains imaged via SPECT which looked at blood-flow in their brains while they were engaged in a type of mystic union called  ‘centring prayer’ which involves opening themselves to being in  the presence of God (and not in “self”).

In centring prayer the nuns had a “loss of usual forms of space  During prayer there was demonstrated increase in blood flow in the PFC inferior parietal and inferior frontal lobes  and a decreased flow in the…

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Maintaining emotional sobriety (and sanity) via Steps 10-12

Thoughts on how to remain relatively sane via steps 10-12! Hope it helps someone.

The Alcoholics Guide to Alcoholism

When I have did my steps 4-7, noting the situations, the people, the institutions  that have caused persistent resentments in me, then examining what parts of my self have been affected,  I also, thanks to one sponsor was asked me to,  put down exactly what “sins” or defects of character I also experienced during these resentments. This jotting down of the exact sins I was in during these resentments  has proved to be very useful in my recovery ever since.  What I noticed was that I had the same array of sins or negatively (immaturely) expressed emotions in relation to all resentments regardless of the situation or the person I had the resentment, the same web of sins was weaved in every situation.  For me this shows clearly how I do not process and regulate my emotions properly, how it has a canalized form of reaction.

I have found increasingly…

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

This is How It Works for me and my emotional disease! Hope it helps you and yours.

The Alcoholics Guide to Alcoholism



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

by alcoholicsguide

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

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

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

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

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Living with an alcoholic is like living in a war zone!

Strength and hope for friends and families of problem drinkers

Al-Anon Family Groups

About one in ten children in the United States lives with a parent with an alcohol misuse problem.

In a word, “devastating.” That’s how Dr. George Koob describes the impact of a loved one’s alcoholism on family members and friends. Dr. Koob is the Director of the National Institute on Alcohol Abuse and Alcoholism (NIAAA), which is the leading funder of alcohol research in the world.

In this exclusive interview—released today—with Pamela Walters, Marketing Information Analyst for Al-Anon Family Group Headquarters, Inc., Dr. Koob is candid about concerns, not only for the person who drinks, but for those affected by the drinker.

“Children, particularly adolescents, but even younger children, friends and family members, all can be affected by an individual with an alcohol use disorder,” said Dr. Koob. He continued, “They often are experiencing negative emotions. They feel stressed. They feel alienated. They can become aggressive. These symptoms can lead to low self-esteem.”

In focusing on how children are affected by a parent’s drinking, Dr. Koob said, “About one in ten children in the United States lives with a parent with an alcohol misuse problem.” Dr. Koob commented on the subsequent, negative effects on a child’s development. Parents struggling with alcohol use disorders are sometimes “barely able to maintain themselves, much less take care of a child,” he said.

Dr. Koob continued, “We know that a child with a parent who binge drinks is much more likely to binge drink than a child whose parents do not binge drink. We know that it can lead to dynamics in the family that contribute to the development of alcohol use disorders in the children themselves, when they grow up.” He went on to reference research the Institute is conducting to get the word out about the family cycle of alcoholism, and to encourage those who are affected by a parent’s, or anyone’s, problem drinking to seek help from Al-Anon.

“I’ve had many of my colleagues over the years who joined Al-Anon because their parents had alcohol problems, and they found it very, very helpful for protecting them against their own vulnerabilities,” Dr. Koob said. He encourages friends and family members to get help for themselves in dealing with a problem drinker. “And that then can lead to a strengthening of yourself, but also of your ability to get help for intervention,” he said.

Find all of Dr. Koob’s comments in “NIAAA Director talks about the impacts of alcoholism on family members and friends,” as part of the “First Steps to Al-Anon Recovery” podcast series at

The National Institute on Alcohol Abuse and Alcoholism is one of the 27 institutes and centers that comprise the National Institutes of Health (NIH). NIAAA supports and conducts research on the impact of alcohol use on human health and well-being. It is the leading funder of alcohol research in the world.

Al-Anon Family Groups are for families and friends who have been affected by a loved one’s drinking. Nearly 16,000 local groups meet throughout the U.S., Canada, Bermuda, and Puerto Rico every week. Al-Anon Family Groups meet in more than 130 countries, and Al-Anon literature is available in more than 40 languages. Al-Anon Family Groups have been offering strength and support to families and friends of problem drinkers since 1951. Al-Anon Family Group Headquarters, Inc. acts as the clearinghouse worldwide for inquiries from those who need help or want information about Al-Anon Family Groups and Alateen, its program for teenage members.

For more information about Al-Anon Family Groups, go to and read a copy of Al-Anon’s annual public outreach magazine “Al-Anon Faces Alcoholism 2015.”

Is the Impulsive Behaviour that Precedes Addiction Hardwired into the Brain?

In various blogs we have forwarded the idea that emotional and stress dysregulation are that the heart of addiction and alcoholism and are also possible present in those at risk to these disorders.

Essentially we suggest that the behavioural endpoint of addictive behaviours, the distress based impulsivity (negative urgency) seen in alcoholics and addicts which shapes decision making may be the consequence of chronic neurotoxic activity (as the consequence of chronic alcohol and drug use)  on brain areas which have a pre-existing impairments or vulnerability such as brain regions involved in emotional regulation, processing, inhibition and stress and reward response.

Here we cite an article (1) which looks at some of these brain regions, specifically those involved in emotional regulation and impulsivity and considers whether these deficits may be “hardwired” into the brain in terms of white and grey matter impairments.


Brain areas actively developing during adolescence include the prefrontal cortex, limbic system areas, and white matter myelin ( electrically insulating material that forms a layer, the myelin sheath – the yellow insulation below), usually around only the axon of a neuron. It is essential for the proper functioning of the nervous system.)


These areas serving cognitive, behavioral, and emotional regulation may be particularly vulnerable to adverse alcohol effects.

Alternatively, deficits or developmental delays in these structures and their functions may underlie liability to accelerated alcohol use trajectories in adolescence.

The prefrontal cortex, limbic brain regions, white matter ( composed of bundles of myelinated nerve cell axons which connect various grey matter areas (the locations of nerve cell bodies) of the brain to each other (see below – grey on outside, white inside) and carry nerve impulses between neurons. Myelin acts as an insulator, increasing the speed of transmission of all nerve signals, and reward circuits undergo active development during adolescence (Chambers et al., 2003; Spear, 2000).




These structures and their functions, involving behavioral, emotional and cognitive regulation, may be particularly vulnerable to the adverse effects of alcohol exposure during adolescence.

Delays or deficits in the development of neural substrates necessary for these psychological regulation abilities to fully develop may be termed neurodevelopmental dysmaturation.

download (6)


Psychological Dysregulation

The development of accelerated alcohol involvement in adolescence is not an isolated phenomenon, but is typically presaged by persistent behavioral characteristics including attentional deficits, conduct problems, and irritability (Chassin et al., 1999; Clark et al., 1997a, 2005; Tapert et al., 2002).

Two main psychological factors have been identified: (1) Behavioral Undercontrol, comprised of conduct disorder symptoms and personality characteristics including aggression and diminished constraint, and (2) Negative Emotionality, comprised of depression, anxiety and stress reactivity variables (Martin et al., 2000).

These two factors were significantly correlated. These correlated characteristics have been hypothesized to comprise the early phenotypic manifestations of a core liability for SUDs (Tarter et al., 1999).

The proposed construct manifested by these psychopathologic features has been termed psychological dysregulation (Clark and Winters, 2002). Psychological dysregulation is a deficiency in the ability to regulate attention, emotions and behavior in response to environmental challenges. Psychological regulation is thus the ability to modulate prepotent responses in order to optimize reward opportunities. The skills involved in psychological regulation include executive cognitive functioning (ECF), behavioral inhibition and emotional management.

Deficiencies in psychological regulation may be the result of delays or persistent deficits in the acquisition of behavioral, emotional, and cognitive regulation skills.

Adolescents at risk for developing SUDs exhibit deficits in psychological regulation. Childhood psychological dysregulation, or neurobehaviour disinhibition, correlates with parental substance use disorders (SUDs) and prospectively predicts adolescent alcohol and other substance use as well as related disorders (Clark et al., 2005; Tarter et al., 2003).

The psychological dysregulation dimension integrates several psycho patholological dimensions heretofore considered distinct, including affective disorders and SUDS themselves (Krueger et al., 2002).

Neurobiological Basis of Psychological Dysregulation

The functions subsumed under the construct of psychological dysregulation are thought to be served by the prefrontal cortex (Koechlin and Summerfield, 2007). The capabilities that comprise psychological regulation improve during adolescence (Levin et al., 1991; Welsh et al., 1991). The ongoing development of the prefrontal cortex has been hypothesized to be the primary neurobiological foundation for the advancement of these abilities (Happaney et al., 2004; Spear, 2000). Developmental abnormalities in the frontal cortex have been found in children and adolescents with behavioral problems reflecting psychological dysregulation (Rubia et al., 2000; Spear, 2000).

Diffusion tensor imaging (DTI) studies  indicated that white matter organization increases from early childhood to young adulthood (Klingberg et al., 1999; Nagy et al., 2004; Schmithorst et al., 2002; Zhang et al., 2005).White matter development may underlie advancing executive functioning. The prefrontal cortex is a brain region undergoing relatively late gray matter pruning, and volumes of gray matter appear to decrease over adolescence (Gogtay et al., 2004; Lenroot and Giedd, 2006; Sowell et al., 2001, 2004). Unlike grey matter volume, white matter volume appears to increase during adolescence, particularly in the prefrontal area (Ashtari et al., 2007;Barnea-Goraly et al., 2005; Lenroot and Giedd, 2006).





White Matter Development and Alcohol Exposure

Selective white matter loss has been reported among adults with Alcohol Use Disorders (AUDs) (Carlen et al., 1978, 1986) and with fMRI (Agartz et al., 2003), and postmortem specimens (Krill et al., 1997).  Compared with controls, adolescents with AUDs have been found to have smaller prefrontal white matter volumes (DeBellis et al., 2005). Prefrontal grey and white matter volumes were compared in adolescents with AUDs. Compared with control subjects, subjects with AUDs had significantly smaller prefrontal white matter volumes.Marijuana use has also been found to be associated with smaller white matter volumes in adolescents (Medina et al., 2007b). While these volumetric findings suggest problematic frontal development among adolescents with AUD, the emergence of neuroimaging techniques developed to examine white matter organization may prove to be more specifically relevant to understanding the effects of alcohol on neurodevelopmental maturation.

Changes in gene expression may be involved in alteration of white matter structure in AUDs.  In a postmortem study, myelin-related genes were found to be down-regulated in the AUD group (Lewohl et al., 2000).

While evidence has been presented that alcohol consumption may disrupt white matter organization, the possibility remains that delayed or diminished white matter organization may presage alcohol involvement and constitute a risk factor for AUDs. Immaturity of white matter development and the related deficits in the functional integration of brain areas may in part explain individual differences in psychological regulation during adolescence. For example, disruptive behavior disorders in childhood, particularly conduct disorder, have been found to predict accelerated trajectories of alcohol use, cannabis use, and substance-related problems in adolescence (Clark et al., 1999).

Limbic System Development and Alcohol Exposure

The limbic system is central to the processing of affective stimuli, the successful formation of new memories, and the implementation of related responses. Limbic system structures, including the hippocampus and amygdala, may be susceptible to alcohol-induced dysmaturation.

Smaller hippocampal volumes have been reported in adults with AUDs compared with control adults (Sullivan et al., 1995). As hippocampal development progresses in adolescence (Gogtay et al., 2006), this brain area may be particularly susceptible to the adverse effects of alcohol involvement during this developmental period.

DeBellis et al. (2000) compared the hippocampal volumes of 12 adolescents and young adults with adolescent-onset AUD to those of 24 control subjects. Both left and right hippocampi were significantly smaller in AUD subjects compared to the volumes in controls. Specifically, left hippocampal volumes were smaller in teens with AUD than demographically similar controls, and youth with greater severity of AUD had the smallest left hippocampal volumes (Medina et al., 2007a; Nagel et al., 2005).

The amygdala may also be important for understanding the neurodevelopmental effects of alcohol exposure. The amygdala, along with ventral striatum, has been hypothesized to be involved in reward mechanisms and thereby critical for understanding alcohol use trajectories (Koob, 1999). Amygdala volumes have been found to be relatively smaller in high-risk older adolescents and adults with SUDs compared to that in control subjects (Hill et al., 2001; Makris et al., 2004). Lack of correlation with use levels has led to the suggestion that this may be a predisposing characteristics rather than a substance effect.

Interacting brain areas are involved in reward processing (McClure et al., 2004), motivation (Chambers et al., 2003), and decision-making (Verdejo-Garcia et al., 2006).  The interactions between the prefrontal cortex and subcortical areas, including the amygdala and nucleus accumbens, constitute the neurocircuitry involved in reward responding. In the affective component of reward responding, the amygdala appears to be a network node involved in reactivity to emotional stimuli (Hariri et al., 2006; Schwartz et al., 2003). An understanding of the adolescent development of neural circuits underlying reward processing and decision making is central to considering the role of these systems in the development of alcohol involvement.

Impulsivity, defined as acting without forethought, progressively decreases from childhood into adulthood. This change has been thought to occur as a result of neuromaturation in the prefrontal cortex (Casey et al., 2005).

The generation of behaviors optimizing long-term reward opportunities often involves behavioral inhibition. The activation of prefrontal cortical areas during response inhibition tasks has been found to increase from childhood through adolescence, a change corresponding to the development of abilities to suppress prepotent behaviors (Luna and Sweeney, 2004; Luna et al., 2004). The ability to select an optimally adaptive behavioral response while suppressing a predominant or prepotent response with problematic consequences defines impulse control and is fundamental to psychological regulation skills. Improved abilities in response inhibition and related prefrontal activation during adolescence are thought to involve maturation of functional connectivity subserved by ongoing myelination.

Adolescents with psychopathology predictive of SUDs, similar to adults with alcohol dependence, have difficulty with behavioral inhibition during laboratory tasks (Bjork et al., 2004a; Dougherty et al., 2003; Schweinsburg et al., 2004). Furthermore, adolescents with histories of substantial marijuana use, compared with control adolescents, showed more activation in frontal cortical areas during behavioral inhibition tasks (Tapert et al., 2007). More activitation suggests greater effort was required by the marijuana using group.



1.  Clark, D. B., Thatcher, D. L., & Tapert, S. F. (2008). Alcohol, psychological dysregulation, and adolescent brain development. Alcoholism: Clinical and Experimental Research, 32(3), 375-385.