An Addicted Brain but a Recovering Mind

This blog used excerpts from

Do I still have an “Alcoholic Mind”!?


When I first came into recovery I used to get frightened by other abstinent  alcoholics proclaim that they were so glad they did not get the “wet tongue” when they saw alcohol or people drinking alcohol.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

I call this a physiological urge, distinct from craving.

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

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

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

Lives can depend on this.

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

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

Let me explain.

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

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

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

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

If I consciously engage, emotionally react, to these thoughts either because I want a drink (elaboration of these thoughts as in embellishing a desire state) or the thought scares the life out of me (averse reaction) I can end up in a mental obsession.

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

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

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



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

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

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

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

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

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

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


How Mindfulness could help Recovery?

Mindfulness training modifies cognitive, affective, and physiological mechanisms implicated in alcohol dependence.

Yesterday we looked a how low heart rate variability in alcoholics (active and in recovery) may influence self, emotion and stress regulation, and have a limited effect on impulsivity, and result in a “locked in” attention to alcohol-related cues, all of which have obvious consequences for relapse.

Here we cite and use excerpts from an article by Eric Garland et al (1) which addresses the effects of mindfulness  meditation on those with alcohol dependence.

Although Garland suggest mindfulness could be an alternative to other treatment and recovery programs, I suggest that it can be used most effectively with other treatment and recovery programs, e.g. with step 11 of 12 step programs.

I believe the consequence of emotion dysregulation  over many years of addiction leaves behind numerous unprocessed emotions which have not been consigned to long term memory and as a result float around the mind as resentments, shame and guilt based memories etc.

Emotion dysregulation has not allowed us to consigned them properly to the past (the so-called wreckage of the past) or long term memory and only an intensive process of emotional processing these e.g. via step 4 or 5 or via an alternative stock taking of our pasts seems to resolve this problem.

I know from my previous experience of intensive meditation involving various 10 day intensive courses and meditating on a very regular basis, before realising I am an alcoholic, would always result in relapse via the distress of the past being resurgent in my mind.

Some method of addressing all of these past behaviours, which invariably have hurt someone, need to be addressed and processed, even making amends to those hurt by our previous behaviours,  before we profoundly ease the distress of the past and help facilitate a greater recovery and more effective meditation practice.

Anyway, that’s my vies, on with the article…

“When attention is fixated on visual or olfactory alcohol cues, alcohol dependent individuals exhibit significant psychophysiological reactivity (Carter & Tiffany 1999). In turn, this alcohol cue-reactivity may lead to increased craving, which can trigger alcohol consumption as a means of reducing distress. Many persons recovering from alcohol use disorders attempt to suppress cravings, which, paradoxically, can serve to increase intrusive, automatic alcohol-related cognitions (Palfai, Monti, Colby, & Rohsenow 1997), dysphoria, and autonomic arousal (Wenzlaff & Wegner 2000). Indeed, among alcohol dependent persons, thought suppression is negatively correlated with vagally-mediated heart rate variability (Ingjaldsson, Laberg, & Thayer 2003), a putative index of emotion regulation and parasympathetic inhibition of stress reactions (Thayer & Lane 2000).

As thoughts of drinking intensify and are coupled with psychobiological distress, the impulse to consume alcohol as a form of palliative coping may overcome depleted self-regulation strength (Muraven, Collins, & Nienhaus 2002; Muraven & Shmueli 2006) leading to relapse. The attempt to avoid distress or allay its impact through compulsive alcohol consumption results in negative reinforcement conditioning that may perpetuate this cycle by further sensitizing the brain to future stressful encounters via allostatic dysregulation of neuroendocrine systems (Koob 2003). Components of this risk chain may be especially malleable to targeted behavioral therapies.

One such intervention, mindfulness training, which originates from Buddhist traditions but has been co-opted by Western clinicians, has recently gained prominence in the psychological and medical literatures for its salutary effects on stress-related biobehavioral conditions (Baer & Krietemeyer 2006; Ludwig & Kabat-Zinn 2008). Mindfulness involves self-regulation of a metacognitive form of attention: a nonreactive, non-evaluative monitoring of moment-by-moment cognition, emotion, perception, and physiological state without fixation on thoughts of past or future (Garland 2007). A growing body of research suggests that mindfulness affects implicit cognition and attentional processes (e.g., Jha, Krompinger, & Baime 2007; Lutz, Slagter, Dunne, & Davidson 2008; Wenk-Sormaz 2005) as well as heart rate variability indices of parasympathetic regulation (Tang et al. 2009).


Mindfulness treatments may enhance clinical outcomes in substance-abusing populations.

Bowen et al. (2007) found that mindfulness training of incarcerated inmates reduced post-release substance use, substance-related problems, and psychiatric symptoms to a greater extent than standard chemical dependency services offered at the prison. Other pilot studies of mindfulness-based interventions with substance abusers have found significant reductions in distress, negative affect, stress-related biomarkers, and substance use (Marcus, Fine, & Kouzekanani 2001; Marcus et al. 2003;Zgierska et al. 2008).

To that end, a randomized, controlled design was used to compare the therapeutic effects of a mindfulness-oriented recovery enhancement (MORE) intervention to those of an evidence-based alcohol dependence support group (ASG).

We hypothesized that, relative to ASG, MORE would result in significantly greaterdecreases in perceived stress, impaired alcohol response inhibition, craving for alcohol, psychiatric symptoms, and thought suppression and significantly greater increases in mindfulness and in heart rate variability (HRV) recovery from stress-primed alcohol cues.



Among recovering alcohol-dependent individuals, mindfulness training appears to be a potentially effective stress reduction technique. MORE reduced perceived stress to a greater extent than did ASG, which is noteworthy given that social support reduces stress reactivity and buffers deleterious effects of stressful life events (Christenfeld & Gerin 2000). The stress reduction effects of mindfulness training among nonclinical populations are well known in the literature (Grossman, Niemann, Schmidt, & Walach 2004), but it is notable that significant effects were obtained in a sample of clinically-disordered, alcohol-dependent adults with extensive trauma histories who may be more vulnerable to stress-precipitated relapse due to allostatic dysregulation of neural stress circuitry (Valdez & Koob 2004).

Like stress, thought suppression significantly decreased over the course of ten weeks of mindfulness training. In turn, decreases in thought suppression among MORE participants were significantly correlated with decreases in impaired alcohol response inhibition, raising the possibility that participants who improved their ability to regulate drinking urges may have done so via reductions in thought suppression.

In the context of alcohol dependence, thought suppression seems to enhance the conscious awareness of alcohol-related cognitions and affective reactions. MORE, with its emphasis on nonjudgmental, metacognitive awareness of present-moment experience, appeared to counter this deleterious cognitive strategy and therefore may have prevented post-suppression rebound effects from exacerbating negative affect and intrusive alcohol-related cognitions that can promote relapse.


In sum, the unwitting attempts of recovering alcohol dependent persons to suppress appetitive cognitive-emotional reactions towards alcohol may obscure these responses from consciousness only to perpetuate and intensify them within the cognitive unconscious. In the domain of unconscious mental life, automatic processes run smoothly and efficiently uninhibited by volitional control (Kihlstrom 1987). Hence, by shunting appetitive reactions into the unconscious, the alcohol dependent individual may increase the very appetitive response towards alcohol he or she is trying to suppress and exacerbate psychophysiological reactivity to alcohol cues. Mindfulness training may serve to undo this process, making unconscious responses conscious. Thus, practice of mindfulness may promote the recovery of alcohol dependent persons through: a) deautomatization of alcohol use action schema, resulting in diminished attentional bias towards subliminal alcohol cues and increased craving as a result of disrupted automaticity; and b) decreased thought suppression resulting in increased awareness of alcohol urges over time, increased HRV recovery from alcohol cue-exposure, and improved ability to inhibit appetitive responses.

Accordingly, mindfulness training may be a tractable means of promoting enduring behavior change. Although brief motivational interventions may be highly effective at impelling the desire towards sobriety, participants of such motivational enhancement therapies remain prone to eventual relapse; indeed, relapse is often a part of the recovery process. As such, interventions that consolidate short-term treatment gains into broader lifestyle change are of major significance to the addictions treatment field. During the gradual practice of mindfulness, one learns to work with negative emotions in a metacognitive context, resulting in nonreactivity to difficult mental contents and improved self-regulation in the face of stressors. The developmental process of cultivating and embedding mindfulness principles into all aspects of one’s life may solidify gains made in prior treatment and provide an effective, long-term approach to coping with stress-precipitated relapse.

Despite evidence suggesting that stress appraisal and attentional biases are key components of alcohol dependence, the form of addictions treatment most available to poor and marginalized persons, social support groups, does not target these pathogenic mechanisms directly. In contrast, practice of mindfulness may attenuate stress reactivity and thought suppression while disrupting addictive automaticity, resulting in increased awareness of craving and greater ability to cope with and recover from alcohol urges in stressful contexts. Hence, mindfulness training may hold promise as an alternative, targeted treatment for stress-precipitated alcohol dependence among vulnerable members of society.”

Equally mindfulness meditation may be used alongside other treatment regimes. For example, it can be used in a daily manner as part of step 11 in the 12 step program. It is also used as part of DBT, for example.

I think that there are ideas out there, is so-called different treatment regimes, which can simply compliment each other. Whatever works, works.

I personally meditate using both  Christian and Buddhist meditation techniques.

Sometimes appreciating the therapeutic strengths of different treatment philosophies and practice can augment one’s own main treatment and recovery program.


1.  Garland, E. L., Gaylord, S. A., Boettiger, C. A., & Howard, M. O. (2010). Mindfulness training modifies cognitive, affective, and physiological mechanisms implicated in alcohol dependence: results of a randomized controlled pilot trial. Journal of psychoactive drugs, 42(2), 177-192.


The terror of “Locked In” Attention!

I remember when I was in the first days, weeks and months of early recovery I used to give myself such a hard time when my attention was drawn to some alcohol-related cue, like someone drinking ,or finding it difficult not dealing with some  reminder of people places and things from my alcohol abusing past; finding that I found it nigh on impossible dragging my attention away from these and related memories associated with my drinking past.

It was as if I was entranced by it, in some of tunnel vision. It used to scare the life out of me.

I rarely found these thoughts appetitive but if I dwelt on these thoughts or trained my attention on cues I would find that the adverse, fearful things would turn to more desire based physiological reactions like salivating and so on.

I took these to mean that I actually wanted to drink and not stay sober. My sponsor at the time said two things which helped – a. I have an alcoholic brain that wants to drink period, 2. cues from my past may always have this effect on me. Accept it, don’t fight it.

That was what I had been doing in fact. Fighting it, these cues reminders and their automatically occurring intrusive thoughts about the past. It is in fighting these thoughts that they proliferate and then become “craving”.

Years later after much research I found that all alcoholics seem to have an attentional bias towards alcohol-related cues which leads to a cue reactivity.

Originally I thought this meant that I simply wanted to drink but found out that in  any manifestation of urge to drink (which is slightly different from a craving which requires an affective response on the part of the alcoholic in order to become a craving similar to mental obsession of the Big Book ) there is a stress reponse like the hear beat quickening, differences in galvanic skin conductance, increased saliva production etc .

Thus this cue reactivty seems to involve not only appetitive or desire states, i.e. it activates the reward system in the brain to motivate one to drink but also contains a stress based reactivity.

Any so-called “craving” state also manifests as either an anxiety state in simple cue reactivity e.g. the sight of alcohol or in negative emotions such as fear, anger and sadness in terms of a stress based craving.

Together, i.e. a cue based reactivity in the face stress/distress leads to a greater urge to drink than by either alone. By reacting to these one is increasing the stress/distress.

To the alcoholic brain having a drink or the desire to drink is the brain suggesting to us as alcoholics that this is the best way to attain transient homeostasis from an allostatic state of distress because this is how we used to balance the effects of emotional distress when we were drinking. We experience distress and automatically had thoughts about drinking. Thus alcoholism is a distress-based condition. We think it is us wanting the drink but it is the distress prompting the wanting of the drink!!

The distress does the drinking for us, itgets us out of our seats and down the street to the bar, it gets us on the bar stool….We may think it is our actions as we use rationalisng and justifying schemata afterwards to justify behaviour that had, in fact, been automatic or compulsive, compulsive meaning to relieve a distress state.

As a schema, which is implicit, i.e. it is automatically prompted and activated by distress also. We are not even in charge of this. We feel and think that we are in control over behaviour bit this is not the case as self control has become so impaired and limited it is distress doing the action and the subsequent rationalising.

The compusive part of the brain, the dorsal striatum, is the only part of the brain that requires us to make a post hoc rationalisation of why we did an action that was essentially automatic and compulsive.

We have become passengers in our own lives. Distress is now doing the driving.

So the brain thinks it is simply telling us the best way to survive this distress or in other words to regulate this distress. Thus it is an incredibly impaired way to regulate stress and emotional distress.

I want to further explain how some of this is linked to low heart rate variability. If we have low HRV we find it difficult inhibiting automatic responses and in changing behaviour. We become behaviourally rigid, and locked into attending to things like cues when we don’t really want to.

This is often the result of distress reducing the ability of the heart rate variability to inform and change our responses.

I cite and use excerpts form one of my favourite articles again by co-authored by Julian Thayer (1).


“The recovering alcoholic must face the difficulty of having his or her ambition to remain abstinent challenged in various situations in which memories about the pleasurable effects of alcohol are activated and the striving for abstinence no longer seems meaningful (Anton 1999; Marlatt and Gordon 1985). The odds for successful coping with such temptations are related to numerous factors, such as one’s subjective affective state and the ability to shift one’s focus from the automatic impulse to drink toward a cognitive reconstruction of the situation (Palfai et al 1997b; Tiffany 1990). Despite the importance of  attentional flexibility in effectively modulating such “highrisk” situations, research on the topic is scarce.

Thayer and Lane (2000) suggested that the interplay between positive (excitatory) and negative (inhibitory) feedback circuits in the nervous system (NS) allows for flexible and adaptive behavior across a wide range of situations. The uniqueness of this model lies with its emphasis on the importance of inhibitory processes in effective modulation of affective experience. In short, these researchers propose that the defects in neurovisceral regulation of affective experience seen in various psychiatric conditions (e.g., anxiety disorders) may be better explained by faulty inhibitory function in the NS than by unitary arousal models.

Tonic heart rate variability (HRV) may be a physiologic indicator of such inhibitory processes (Friedman and Thayer 1998a; Porges 1995). Heart rate variability refers to the complex beat-to-beat variation in heart rate produced by the interplay of sympathetic and parasympathetic (vagal) neural activity at the sinus node of the heart.

Importantly, heart rate (HR) is under tonic inhibitory control via the vagus nerve (Levy 1990). These neural connections to the heart are linked to brain structures involved in goal-directed behavior and adaptability (Thayer and Lane 2000). Compelling evidence now exists to show that high levels of HRV are related to cognitive flexibility (Johnsen et al 2003), modulation of affect and emotion (see Bazhenova 1995, cited in Porges 1995), and increased impulse control (Allen et al 2000; Porges et al 1996).

The hypothesis that reduced HRV is related to defective affective and emotional regulation has been supported in recent research in which reduced HRV was present in clinical disorders such as generalized anxiety disorder (Thayer et al 1996), panic disorder (Friedman and Thayer 1998b), posttraumatic stress disorder (Cohen et al 1997) several scientific arguments suggest that impaired inhibitory function may play a role in chronic alcohol abuse.

First, alcoholics have repeatedly been shown to have problems shifting attention and directing their attention away from task-irrelevant information (Johnsen et al 1994; Setter et al 1994; Stormark et al 2000). Second, frontal areas of the brain are most affected by the acute and chronic effects of alcohol, and these structures are of crucial importance in inhibitory functioning and self-control (Lyvers 2000). Third, acute effects of alcohol ingestion result in reductions in HRV, implying that chronic alcohol ingestion may result in a long-lasting impairment of the vagal modulation of HR (Reed et al 1999; Weise et al 1986)

Fourth, severely dependent alcoholics show a sustained phasic HR acceleration when processing alcohol information, indicating defective vagal modulation of cardiac function (Stormark et al 1998). Tonic HRV has similarly been found to be a useful measure of physiologic activity in challenging situations (Thayer and Lane 2000). Appropriate modulation of HRV (increases, decreases, or no change) depends on the type of challenge and the characteristics of individuals as they interact with specific contextual manipulation (Friedman and Thayer 1998a; Hughes and Stoney 2000; Porges et al 1996; Thayer et al 1996).

For example, during attention demanding tasks, healthy individuals show appropriate reductions in HRV (Porges 1995). In general, high tonic levels of HRV allow for the flexible deployment of organism resources to meet environmental challenges. With respect to attention, it is suggested that high levels of HRV reflect flexible attentional focus, whereas low HRV is related to “locked in attention” (Porges et al 1996). Moreover, increased tonic vagal activity is related to adaptive development and lack of behavioral and emotional problems (Hughes and Stoney 2000; Porges et al 1996).

Furthermore, it has been demonstrated that increases in vagal activity during challenging tasks discriminates between individuals who have experienced traumatic events and managed to recover from them and those who still suffer from chronic symptoms of posttraumatic stress (Sahr et al 2001). Such increases in vagal activity during challenging tasks are particularly interesting because studies on alcohol abusers have found increases in HRV after exposure to alcohol-related cues (Jansma et al 2000; Rajan et al 1998).

One could speculate that such enhanced vagal activity could be a sign of compensatory coping aimed at taming automatic drinking related processes (Larimer et al 1999). Such an interpretation is in agreement with cognitive theories predicting that alcoholics and other drug users do not simply respond passively to exposure to drug-related cues, but, on the contrary, in such situations conscious processes are invoked, inhibiting execution of drug-related cognition (Tiffany 1990, 1995). If this explanation is correct, alcoholics who have more effective coping resources should show stronger increases in vagal activity during such challenging exposure than alcoholics who express greater difficulty in resisting drinking-related impulses.

Also  general differences in HRV between alcoholics and nonalcoholics are interesting indicators of defective inhibitory functioning, a measure of rigid thought-control strategies and lack of cognitive control should be an important indicator of defective inhibitory function and “positive feedback loops” reflected as low HRV (Wegner and Zanakos 1994).

Linking these measures to the physiologic index of HRV makes a stronger case for attributing reduced vagal tone (HRV) to a defective regulatory mechanism resulting in unpleasant affective states and maladaptive coping with psychologic stressors

The main results of our study may be summed as follows. First, as expected, alcoholic participants had lower HRV compared with the nonalcoholic control group. Second, the imaginary alcohol exposure increased HRV in the alcoholic participants. Third, across the groups, an inverse association was found between HRV and negative mood and a positive association between positive mood and HRV. Fourth, HRV was negatively correlated with compulsive drinking during the imaginary alcohol exposure in the alcoholic participants. Fifth, within the alcoholic group, HRV was negatively associated with chronic thought suppression (WBSI).

Generally, these findings are in agreement with the neurovisceral integration model and the polyvagal theory that suggests HRV is a marker of the level of cognitive, behavioral, and emotional regulatory abilities (Thayer and Lane 2000).

The fact that the alcoholic group had generally lower tonic HRV compared with the nonalcoholic control group indicates that such reduced HRV may also be a factor in alcohol abuse; however, such group differences in HRV provide only indirect support for the theory that low HRV in alcoholics may be related to impaired inhibitory mechanisms

Because HRV is related to activity in frontal brain areas involved in cognition and impulse control (Thayer and Lane 2000), we speculated that tonic HRV would be an index of nonautomatic inhibitory processes aimed at suppressing and controlling automatic drug-related cognitions. To test this hypothesis more directly, the association between HRV and problems with controlling drinking-related impulses were studied.

Consistent with this hypothesis, the compulsive subscale of the OCDS was found to be inversely associated with HRV in the alcohol-exposure condition, thus suggesting that HRV may be an indirect indicator of the level of impulse control associated with drinking. These findings are therefore consistent with Stormark et al (1998), who found that sustained HR acceleration (lack of vagal inhibition) when processing alcohol-related information was related to compulsive drinking and “locked-in attention.”

Post hoc analysis further suggested that alcoholics who expressed a relatively high ability to resist impulses to drink (OCDS) had the clearest increase in HRV under the alcohol exposure this study suggests that alcoholics may actively inhibit or compensate for their involuntary attraction to alcohol-related information by activation of higher nonautomatic cognitive processes (Tiffany 1995). Such conscious avoidance has previously been demonstrated in studies on attentional processes in alcoholics (Stormark et al 1997) and by the fact that frontal brain structures involved in inhibition and control of affective information are often highly activated in the processing of alcohol related cues (Anton 1999). Furthermore, this interpretation is in agreement with other studies suggesting that high HRV during challenging tasks is associated with recovery from acute stress disorders (Sahr et al 2001).

Several studies have indicated that low HRV is associated with impaired cognitive control and perseverative thinking (Thayer and Lane 2002). Consistent with these reports a negative association was found between HRV and chronic thought suppression. The WBSI assesses efforts to eliminate thoughts from awareness while experiencing frequent intrusions of such “forbidden” thoughts and thus represents an interesting and well-validated measure of ineffective thought control (Wegner and Zanakos 1994). Thought suppression has been found to be an especially counterproductive strategy for coping with urges and craving (Palfai et al 1997a, 1997b) and may even play a causal role in maintaining various clinical disorders (Wenzlaff and Wegner 2000).

To our knowledge, this is the first time a link between physiologic indicators of a lack of cognitive flexibility (low HRV) and chronic thought suppression has been demonstrated.

Thayer and Friedman (2002) have reviewed evidence indicating that there is an association between vagally mediated HRV and the inhibitory role of the prefrontal cortex. Consistent with Thayer and Lane (2000), this study suggests that impaired inhibitory processes are significantly related to ineffective thought control.

The fact that this association between HRV and WBSI was only found in the alcoholics may be related to the fact that only this clinical group shows signs of such faulty thought control.

Wegner and Zanakos (1994) suggested that thought suppression is particularly ineffective when the strategic resources involved in intentional suppression are inhibited or blocked (Wegner 1994). Consistent with this hypothesis, our findings show that those reporting high scores on WBSI show signs of impaired inhibitory functioning as indexed by low vagally mediated HRV.”

This excellent article fro me is also alluding to the fact that those with increased HRV was related to successfully related to regulating negative emotion,  stress/distress and affect, not just the thoughts that these affective states gave rise to .

Thus any strategies that help with improving  the ability to increase HRV will likely have positive results in coping with cue associated materials.

We look at one of these therapeutic strategies next…that of mindfulness meditation.



1. Ingjaldsson, J. T., Laberg, J. C., & Thayer, J. F. (2003). Reduced heart rate variability in chronic alcohol abuse: relationship with negative mood, chronic thought suppression, and compulsive drinking. Biological Psychiatry54(12), 1427-1436.




Childhood Maltreatment and later Alcoholism/Addiction

One old timer I know often says two things that I often take issue with – 1. there are as many alcoholisms as alcoholics and that 2. we all come to AA in different boats but end up in the same dock.

Thanks to having a wife in Al Anon I have had the benefit of her insight and from other al-anons who state how remarkably similar we alcoholics are in our behaviour, particularly in dealing/coping with distress and stress, our emotional reactivity and at times immaturity (or so-called defects of character), I disagree that we are so different in our addictive behaviours.

All addictive behaviours from alcoholism, substance addiction, eating disorders to hypersexual disorder seem to be based on an inherent problem with emotion and stress dysregulation.

I believe I have a distress based condition. It results in what appear to be distress based reactions such as perfectionism, distress intolerance and frustration intolerance, normally exemplified in my shouting at my PC when it doesn’t work quickly enough or crashes!

I also believe I have distress based impulsivity, I want that thing, whatever it is, NOW. That anything!

In fact I have noticed when I want something, anything, I end up pathological wanting it in no time at all! It seems then like I NEED it. I too think this is based on distress and heighten stress reactivity.

In fact it is through this pathological wanting that my so-called defects of character that my examples  of emotional dysregulation appear.

If I can’t get what I want, all range of negative emotions spill forth such as intolerance, impatience, arrogance, pride, shame, selfishness etc .  They only appear when I want something and you are getting in the way of me having it!!

So there is a link between my motivation (which is dysregulated due to the effects of chronic stress which turns simple wanting into something more akin to “needing”) and my subsequent emotional dysregulation.

So where does this distress come from? Is it purely the effects of chronic stress dysregulation caused by years of neuro toxic brain damage or does it go back further, into childhood?

I do not think we all have separate alcoholisms, I feel we have remarkably similar reactions to life and these centre on an inherent difficulty regulating stress and emotion.

I also believe we have come to recovery in similar boats. In fact the majority of us have come to recovery in a remarkable similar boat so much so that it would resemble a gigantic ship rather than a boat. That boat is the ship of childhood maltreatment.

Child maltreatment has been frequently identified in the life histories of adolescents and adults in treatment for substance use disorders, as well as in epidemiological studies of risk factors for substance use and abuse.

 Child Maltreatment

One study (1) suggests there is ample evidence exists for higher rates of substance abuse and dependence among maltreated individuals.

In clinical samples undergoing treatment for substance use disorders, between one third and two thirds evince child abuse and neglect histories (Dembo, Dertke, Borders, Washburn, & Schmeidler, 1988Edwall, Hoffman, & Harrison, 1989Pribor & DiWiddie, 1992Schaefer, Sobieragi, & Hollyfield, 1988).

In the US a survey of over 100,000 youth in 6th though 12th grade, Harrison, Fulkerson, and Beebe (1997) Harrison, Fulkerson, and Beebe (1997) found that those reporting either physical or sexual abuse in childhood were from 2 to 4 times more likely to be using drugs than those not reporting abuse; the rates were even higher for youth reporting multiple forms of child maltreatment. Similar findings have been reported by Rodgers et al. (2004) and Moran, Vuchinich, and Hall (2004).

Among youth with Child Protective Services documented maltreatment, Kelly, Thornberry, and Smith (1999) reported one-third higher risk for drug use among those with an abuse history. In a large epidemiological study, Fergusson, Boden, and Horwood (2008) have shown physical abuse and particularly sexual abuse to be related to illicit drug use, as well as abuse and dependence.

Another Study (2) study would suggest the figures are much higher –   data were collected on 178 patients–101 in the United States and 77 in Australia–in treatment for drug/alcohol addiction. The purpose of the study was to determine the degree to which a correlation exists between child abuse/neglect and the later onset of drug/alcohol addiction patterns in the abuse victims. The questionnaire explored such issues as family intactness, parental violence/abuse/neglect, parental drug abuse, sibling relationships and personal physical/sexual abuse histories, including incest and rape. The study determined that 84% of the sample reported a history of child abuse/neglect.

A third study (1) stated that, using the Childhood Trauma Questionnaire-Short Form (CTQ-SF; Bernstein & Fink, 1998; Bernstein et al., 2003) to assess childhood maltreatment in a community sample of active drug users, Medrano, Hatch, Zule, and Desmond (2002) found that 53% of women and 23% of men were sexually abused, 53% of women and 43% of men were physically abused, 58% of women and 39% of men were emotionally abused, 52% of women and 50% of men were physically neglected, and 65% of women and 52% of men were emotionally neglected.

Substance abusers, in addition to having higher rates of childhood maltreatment than members of the general population, have been found to have levels of psychological distress that increase with increasing severity of all types of childhood maltreatment (Medrano et al., 2002). This association is important considering that stress increases an individual’s vulnerability to addiction and addiction relapse (Goeders, 2003; Sinha, 2001;Wills & Hirky, 1996).

There is also evidence that the way in which people cope with stress is related to substance use. For example, researchers have found that greater use of avoidance stress-coping strategies (i.e., disengaging from investing effort to cope with a problem) is related to a greater likelihood of drug use initiation, higher levels of ongoing drug use, and a greater probability of relapse, whereas greater use of active stress-coping strategies (i.e., taking steps to deal with a problem) most consistently functions to protect individuals from substance use initiation and relapse (Wagner, Myers, & McIninch, 1999; Wills & Hirky, 1996).

Childhood maltreatment may influence substance use behavior through its effect on stress and coping. There is emerging evidence that childhood maltreatment may negatively affect the maturation of self-regulatory systems that enable an individual to modulate and tolerate aversive emotional states (Cicchetti & Toth, 2005; Hein, Cohen, & Campbell, 2005). Childhood maltreatment may disrupt neurobiological development and elevate subjective stress by biologically altering the brain’s response to stress (Bugental, 2004;DeBellis, 2002; Heim & Nemeroff, 2001; Heim et al., 2000; Sinha, 2005; Wills & Hirky, 1996). Childhood maltreatment may also affect an individual’s characteristic style of coping with stress so that he or she may be more likely to rely upon maladaptive strategies, such as avoidance of problems, wishful thinking, and social withdrawal, rather than active strategies, such as seeking information and advice from others (Bal, Crombez, Van Oost, & Debourdeaudhuij, 2003; Futa, Nash, Hansen, & Garbin, 2003; Krause, Mendelson, & Lynch, 2003; Leitenberg, Gibson, & Novy, 2004; Thabet, Tischler, & Vostanis, 2004).

Elevated stress and maladaptive coping related to childhood maltreatment may translate to greater substance use behavior by making the coping motives of substance use appear more attractive (Wills & Hirky, 1996). Indeed, substance users commonly report using psychoactive substances such as alcohol, cannabis, and cocaine to cope with stress and regulate affect (Boys, Marsden, & Strang, 2001)

Most cocaine dependent inpatients reported multiple types of childhood maltreatment, and only 15% reported no maltreatment at all, (similar figures to study 2).

“Our findings suggest that the severity of overall childhood maltreatment experienced by recently abstinent cocaine dependent adults has a significant relationship with perceived stress and avoidance coping in adulthood.

Our findings suggest that having a more severe childhood maltreatment history may result in a greater sensitivity to stress…basic coping skills training may not be adequate in decreasing distress and avoidant coping in order to decrease substance use and relapse. Additional interventions that focus on stress tolerance, altering appraisals of stress, stress desensitization, and affect and emotion regulation skills may be of particular benefit to patients with childhood maltreatment histories.

The fact that childhood maltreatment is a preventable phenomenon that occurs early in life and affects psychological functioning well into adulthood makes our findings relevant to clinical practice with children as well. Early identification and treatment of maltreated children may help prevent stress sensitivity or the development of a less adaptive style of coping. Assessment of coping ability and the implementation of coping skills and stress tolerance training may also be indicated for maltreated children in an effort to increase their coping efficacy and decrease their vulnerability to stress later in life.”

I may have been in recovery for a number of years now but coping with stress/distress is still central to my recovery. Dealing with the effects of childhood maltreatment not only via negative self esteem and self schema but in the real sense of coping with every day stress/distress, mainly prompted in my interpersonal relationships (other people!) and with my PC!



1. Rogosch, F. A., Oshri, A., & Cicchetti, D. (2010). From child maltreatment to adolescent cannabis abuse and dependence: A developmental cascade model.Development and psychopathology, 22(04), 883-897.

2. Cohen, F. S., & Densen-Gerber, J. (1982). A study of the relationship between child abuse and drug addiction in 178 patients: Preliminary results. Child Abuse & Neglect, 6(4), 383-387.

3.  Hyman, S. M., Paliwal, P., & Sinha, R. (2007). Childhood maltreatment, perceived stress, and stress-related coping in recently abstinent cocaine dependent adults. Psychology of Addictive Behaviors, 21(2), 233.

Addiction – A Parasite that feeds off your Emotions?

When I was in treatment at a local treatment centre, when we were in group therapy to be exact, one of our facilitators, after someone had given an example of their “powerlessness and damage” while drinking, suddenly described alcoholism and addiction as a being like a parasite that feeds on the addict’s emotions.

I was shocked initially by this remark, feeling that this would be an insidious illness indeed if that were the case. A disorder or disease that fed on one’s emotional state. Not only negative emotions I must add as so called happy emotions such as “elation” can also propel a vulnerable recovering person to relapse.

All emotions which are extreme seem to have the capacity to activate a pathological “wanting” in the brain and can prompt relapse. That is why we are often advised to keep a check on the emotions to make sure they are neither too high or too low. Too extreme. This is also called emotional regulation. When emotions are tempered and not so overwhelming or not too labile (changeable).

We know from previous blogs that emotional dysregulation, not controlling or tempering emotions but reacting to them can heighten a sense or a feeling of “wanting”, so intense it feels like a “needing”, in the brain. This is partly due to having excess stress chemicals in the brain.

In the course of addiction or during the so-called “addiction cycle” the brain’s stress systems become increasingly out of kilter, dysregulated, and this creates a brain allostasis rather than the normal homeostasis. With homeostasis the brain regulates itself within given parameters and within regionalised areas of the brain. An example of homeostatic imbalances, such as high core temperature, a high concentration of salt in the blood, or low concentration of oxygen, can generate homeostatic emotions (such as warmth, thirst, or breathlessness), which motivate behavior aimed at restoring homeostasis (such as removing a sweater, drinking or slowing down).

Allostasis is the process of achieving stability, or homeostasis, through physiological or behavioral change. This can be carried out by means of alteration in HPA axis hormones, the autonomic nervous system etc.

Wingfield states: The concept of allostasis, maintaining stability through change, is a fundamental process through which organisms actively adjust to both predictable and unpredictable events… Allostatic load refers to the cumulative cost to the body of allostasis, with allostatic overload… being a state in which serious pathophysiology can occur… (Wingfield 2003).

Allsotasis means adaption via change, it is fleeting homeostasis but “at a price”. One of the prices of excess or chronic levels of stress in addiction  is normally a reduction in dopamine, a brain chemical involved in wanting, motivation, reward, learning and memory and habits.

When there is a heighten stress or emotional distress there is often a rise in dopamine and an increased wanting in an attempt to create a homeostasis. In the case of addiction this dopaminergic wanting, augmented by stress chemicals, usually makes an addicted person want what has previously created a temporary “homeostasis” ie drinking alcohol or taking drugs etc to relieve a distress. Hence stress activates dopamine brain circuits involved in attention, memory, emotion, reward/motivation and habit behaviours. Hence heightened stress levels can pretty much activate one’s addiction and the physiological urge to use or drink. This is the reason stress factors are implicated in the majority of relapse situations.

So to summarise, instead of one or more specialist areas of the brain regulating within given parameters the whole brain can be engaged in attempting to create a fleeting homeostasis. The brain becomes global, i.e. different areas and functions of the brain are recruited. For example, previous experience, memories and so on are activated in governing action and behaviour.

In addiction these memories, for example, are activated by excess stress normally caused by negative emotions and failure to regulate them. The brain will suddenly suggests via these memories and previous experience that the previous way to create a fleeting homeostasis while in a negative emotions would be to drink or use drugs. It would suggest this present distress, this alien state,  is solvable and that drug use is the “normal” way to survive it.

In effect the brain is saying that previously we used drugs to regulate these emotions which at a bio-chemical level also created a fleeting homeostasis, or a fleeting resolution to emotional distress.

As we know this is a far from perfect way to regulate emotions. Hence we use more drink and drugs to regulate emotion which ultimately leads to increased emotional and stress dysregulation which leads to needing drink and drugs more and more. It creates a tolerance, whereby we need more of a certain substance (or behaviour) to reach a fleeting ” balance”. The more stress we have the more we need to restore “homeostais” by using more drugs. The more we reduce dopamine the more we need to use drugs to get more dopamine and other neurotransmitters. It is stress chemicals in the brain  that controls addiction in the end.

At endpoint addiction and in early recovery we seem to be left with a whole lot of stress in the brain, emotional and stress dysregulation; so severe we may not even be able to guess what emotion we are actually having and a desire to leave this alien state of sobriety and return to the previously “normal” state of intoxication that is so profound only an addict can really understand it’s overwhelming intensity.

Thus craving is also stress based. If we regulate our stress we regulate our emotions and our illness is quietened and tempered. Hence we suffer from a distress based illness.

Sorry for so much detail but this is important to know.

The article (1) here set us on a research voyage to a large extent as it confirmed to us that one of the reason people relapse is because sobriety is initially so foreign, so alien, so troubling. We do not really have the tools to cope with it. Hence we need a whole lot of help to recovery. Our illness has effectively taken over our survival mechanisms and appears to speak to us with our own voice although it is essentially the motivational voice of addiction imploring us to survive by re-using.

It is like a psychotic care-giver who is convinced the best way to survive is to employ a way of living that is destined to take your life away and then kill you.

This article showed that  the “euphoric recall” often mentioned in recovery circles is not only instantly retrieved from memory but is immediate. The euphoria is actually re-experienced rather than re-called as such. it is re-felt in terms of brain frequency. Thinking about drinking activates a similar brain frequency to actually drinking itself.

Also it may be also that experience of a negative self perception may activate this brain frequency also and instantly remind one of alcohol or drugs as a way to deal with this negative self perceptions, these distressing negative emotions. This brain frequency suggests we consume substances in order to do the most basic of survival strategies, to regulate our emotional states. Our emotions have become the slaves of substance abuse and behavioural addictions. Addiction does, after all, mean to be bound. We are bound to our addictions for the basic of human needs.

This article (1) – which we comment on as we proceed, italics as we feel it is describing allostasis although it does explicitly say so – appears to be saying in scientific terms what our facilitator at the treatment centre was saying from a therapeutic and observational point of view, from great and profound ancedotal evidence. That substances appear to take over our emotional states and regulation. In this case, alcohol seems to have become intrinsic to our emotional regulation.

How can we say this? In this experiment the researchers found that not only does simply thinking about alcohol create a very similar brain frequency in the brain as actually drinking but that this brain frequency is also seen when we are having negative emotions about ourselves (as alcoholics).

To us this means our negative self perception and emotional regulation itself has become absolutely connected to drinking and taking drugs, in other words, negative emotional states automatically give rise to a desire state a need to drink or use drugs. It has become a automatic habitualised and compulsive reaction and response to negative emotions and adverse self perception.

How we feel about ourselves has ultimately driven our addiction. Hence we need to start think differently about ourselves real soon in recovery because for many years our alcohol, drugs or addictive behaviours may have been doing the thinking and feeling for us!

One thing that kept me sober in early recovery was not listening to my self-centred thoughts (as much as I could because these thoughts have your voice attached so are kinda hard to completely ignore!)  as my thoughts were the product of negative emotions which then caused more negative emotions and then brought memories of past drinking etc and the people, places and things attached with this drinking. My sponsor said it is the voice of your illness and this helped immeasurably.

I tell sponsees this now.

Here we go…” Evidence demonstrates that attachment and interactions between parents and child play a significant role in normal development; alternatively,
impaired parental bonding appears to be a major risk factor for development of mental illness, substance abuse and possible substance dependence later in life (Canetti et al. 1997; Newcomb and Felix-Ortiz 1992; Petraitis et al. 1995; Brook et al. 1989) – It is within this context that this study and the Self-Perception and Experiential Schemata Assessment (SPESA) were formulated. The SPESA is designed for sensitivity to negative, average or positive perceptions of self, experiences and self in-experience in three life domains; childhood, adolescence and adulthood.

The SPESA takes less than 10 min to administer and 10 min to score. It provides important insight into the perceptual, visceral, affective and cognitive processes that may preclude the actual physical or psychological substance abuse or dependence. This instrument divulges perceptual information regarding the endogenous and exogenous experiences of the individual; including, physical, sexual or emotional abuse, self-efficacy, self image, view of self in relation to family and peers, in addition to perceptions of alienation and inadequacy .

Individuals with a family history of alcoholism show increased alpha activity (brain frequency) in posterior regions after alcohol consumption and rate it more difficult to resist further drinking than controls (Kaplan et al. 1988). Males at risk for alcoholism show increased low-alpha EEG activity (7.5–10 Hz) after ingesting alcohol as compared to males at low risk (Cohen et al. 1993).
Michael et al. (1993) found higher central alpha and slow-beta coherence in frontal and parietal electrodes in relatives of alcoholics and lower parietal alpha and slow beta coherence in males with alcohol dependence.

Notably, other findings indicate that morphine, alcohol and marjuana increase alpha 2 power in the spectral EEG and relate this to the euphoric state produced by the drugs (Lukas 1991, 1993; Lukas et al. 1995).

Elevated alpha power amplitude is suggested to be a potential threat indicator for the development of alcoholism and men with fathers having alcohol use disorders are more likely to have high-voltage alpha than men with unaffected fathers at baseline or after receiving placebo (Ehlers and Schuckit 1988, 1990, 1991; Ehlers et al. 1989).

We define experiential schemata (ES) as a neurologic progression in human development involving a fundamental self-organization process. This process is based in the formulation of concepts of self originating in perceptions  of self (endogenous) formed through interactions with others and the environment (exogenous). These encoded schemata become the foundation for prevailing emotions, motivations, attitudes, and attributions relating to self and self-in-the-world that are maintained, reinforced and entrenched in neural coding mechanisms formed through dendritic arborization (spreading of neural networks) over the lifespan.

In normal development ES involving experiences, behaviors, learning and organization of self are engrained or reinforced in neural circuits with much of the
acquired information being necessary for social functioning, and overall survival in most circumstances. The drawback to this process is that it can be extremely difficult
to introduce new concepts relating to self—identity to an individual as well as novel learning material.

Based upon critical concepts from a variety disciplines contributing to addiction research, we propose that a common neurophysiological pattern exists in recovering alcoholics (RSA)  when evaluating self and self-in-experience that is significantly different from non-clinical controls.

This is the first study of its kind to evaluate EEG patterns of self-perception and experiential schemata in a group of RSA as well as controls. The significant differences between groups in the SPESA condition may provide insight into a very probable neural pathway which stands to be an idiosyncratic neurologic anomaly for the RSA population  in this study, in addition to a possible antecedent to Substance Use Disorders (SUDs).

The excess alpha activity in SUD when processing perception of self and self-in experience may reflect a state of desynchronization (or an idling fear and evaluator
response guided by maladaptive ES) within the individual, given that alpha is generated in the thalamus (Lorincz et al. 2008) and is known to be involved in both attention and memory processes (Cannon et al. in press-a).

(Obviously this desynchronisation may reflect the allostasis mentioned above also)

This alpha excess possibly places demands on resources otherwise employed for the homeostatic functioning of the individual; including, autonomic, perceptual, attentional, social, cognitive and sensory processes.

(Equally it may in fact relate to allostasis and the recruiting of these various brain function in anticipating homeostatic/physiological need)

Notably, research demonstrates the use of certain chemicals produces widespread
alpha power increases in the cortex thereby, at least for this study group and their reports of ‘using’and ‘drinking’ thought patterns, bringing the brain into synchrony, if only for a very short period of time.

(Again we would add that these thoughts are acting allostatically as a homoestatic facsimile if you like)

We believe this to be the euphoria addicted individuals speak of so fondly and is one possible reason for the difficulty in treating these disorders in addition to the high relapse rates.
The excess alpha activity during the task is possibly attributable to ES and the associated emotions relating to internal and external conflict and confusion distinguishing past from present and the brain’s reaction to re-experiencing the past.

Damasio (1994) discusses  the continuous monitoring of the body by the brain
as specific content and images are processed, exacting not only changes in brain electrical activity but also chemical reactions. Thus, as the brain communicates and orchestrates  the affective state of the individual in response to these contents and images relating to self and self-in-experience; it is plausible that a large scale feedback loop is formed involving not only perceptual processes but relative autonomic functioning. This process possibly reinforces the addicted person to become habituated to an aroused cortical state (i.e. increased alpha/beta activity) and when there is a shift to ‘normalcy’ it is errantly perceived as abnormal thereby increasing the desire or need for a substance to return to the aroused (or perceived normal) state.  

(This for us explains why initial sobriety and recovery feels so alien, the brain is not used to the cortical state of not using or drinking and tries to get the now recovering person to return to this cortical aroused state of using and drinking)

Also this study offers support to the idea of increased the dopamine roduction within limbic regions in addicted populations (Blum et al. 2007; Kohnke et al. 2003) as increased dopamine producion may be reflected in excitatory frequency domains observed.

(although obviously this heightened dopamine production may also be reflective of stress augmented dopamine activity consistent with allostasis) 

The possibility that substance abuse interacts with specific brain regions in
specific frequencies for specific time intervals appears to be a valid concept, noting the paradox that the resulting self destruction and self-deprecation to achieve a desired state or to change or alter an undesired state transcends immediate comprehension.

(again this can be understood in terms of allostasis as survival has been usurped, taken over, by stress systems acting on, among other systems, dopamine systems of the brain)

Many of the individuals in the RSA group with 3 or more years of continuous abstinence report a consistent effort to intervene on their initial reactions to
external cues and seek additional outside interpretations from counselors, peers or family members for suggestions in how to deal with life events, rather than go on their first instinct.”

(again we believe this can also be explained in terms of allostatically driven distressed-based impulsivity)

To conclude this article set us on a train of research which we believe has led to answers to some of the questions implicit in this research. We believe the increased alpha activity of brain frequency and other points mentioned can all be explained in terms of the brain constantly seeking a new homeostatic setpoint. A return to “normalcy” however maladaptive and self destructive that so-called normality is.

Stress systems usurp survival systems in the brain and the alpha activity reflects a drive for homeostasis whereby allostasis via memory and other mechanisms augment dopamine to facilitate the brain to want or need the substance least required in terms of survival, the alcohol or drugs that have usurped via stress means, the survival network in the first place.

The euphoric recall is allostasis sounding it’s bugle, activating the brain to return to former ways of regulating emotion and behaviour.

The increased brain frequency is a siren to a fleeting brain balance, which will give way via drug and alcohol use to even greater stress based wanting and a brain even more out of homeostatic sync.

An endless, fruitless cycle to find an elusive, fleeting balance that comes and goes.

Amazingly recovery offers alternatives to achieving this fleeting homeostasis and even prolonging it. Prayer, meditation and helping others can keep one in balance for as long as you do it.

Now that is food for thought. In helping others we help ourselves more and in a more profound way than we can ever do by ourselves. Being in self activates our illness and being out of self treats it.


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