At Risk Adolescents have Emotional Dysregulation?

Following up from our previous blog on the abnormalities in the ventromedial prefrontal cortex  (vmPFC) in alcoholics,  brain regions which govern emotional regulation, we came across another study which appears to show that adolescents at increased risk for later alcohol use disorders (AUDs) may also be showing an emotion regulation difficulty.

This emotional regulation difficulty may be a biomarker for later alcoholism, which is in keeping with our previous proposals that an emotional processing and regulation difficulty or disorder underpins the aetiolgy of of alcoholism. In order words it is part of the pathomechanism – or the mechanism by which a pathological condition occurs- of later alcoholism.




The area in this study, the vmPFC,   showed relatively increased cerebral blood flow (CBF) in bilateral amygdala and vmPFC and relatively decreased CBF in bilateral insula, right dorsal anterior cingulate cortex (ACC) and occipital lobe cuneus of high-risk adolescents. This suggests that adolescents at relatively high-risk for AUD exhibit altered patterns of resting CBF in distributed corticolimbic regions supporting emotional behaviors.

The authors’ hypothesized that the relatively increased amygdala and ventromedial prefrontal CBF may contribute to increased emotional reactivity and sensitivity to environmental stressors in these individuals while diminished insula/occipital cuneus and dorsal anterior cingulate cortex (ACC) CBF may lead to poor integration of visceral and sensory changes accompanying such emotional stress responses and top-down regulation of amygdala reactivity.

Thus we see our model in a snapshot even in adolescents potentially.  The emotional processing deficits we have discussed previously implicate the insula and ACC, as there appears to be a difficulty in alcoholics in reading emotional or somatic signals/states and integrating these signals into the identifying, labelling and processing of emotions. Equally there appears to be a hyperactivty in the vmPFC and amgydala as with alcoholics which implies emotional dysregulation, a hyper reactive emotional response and a tendency perhaps to a more “fight or flight” response, distress based impulsivity and short termist decision making, wanting it NOW rather than later.


References Lin, A. L., Glahn, D. C., Hariri, A. R., & Williamson, D. E. (2008). Basal Perfusion in Adolescents at Risk for Alcohol Use Disorders. In Proc. Intl. Soc. Mag. Reson. Med (Vol. 16, p. 60).

One Christmas I nearly relapsed!


One Christmas I nearly relapsed!

by alcoholicsguide

“One Christmas, I nearly relapsed. I did not wish to relapse, in fact I would rather put a gun to my head and blow my brains out! Nonetheless, I was indeed about to relapse. It seemed urgently inevitable.
The emotional distress I had suffered all over Christmas, prompted by sad unresolved feelings about my deceased parents’s had built up, aided by a few bitter arguments with my frustrated wife, into into a sheer, blind terror.
Somehow I had the sense to shakily climb the stairs to the top of the house to tell my wife that I was in trouble.My wife’s facial expression quickly flickered from hurt to heightened concern. She could tell by my quivering voice and ashen complexion that I was in trouble. I shakily walked over to sit near her. Out of the corner of my eye I could see a bottle of white spirits, which glowed invitingly with some spiritual lustre.
My attention seemed ‘locked into’ this bottle of spirits. Somewhere there was voice in my head saying “You could drink that, soon get rid of this terror”
My wife had been trying to talk to me, get through to me. I looked at her. I recognised her face but couldn’t remember her name or the fact she was my wife. My wife and I couldn’t remember her name!!? What the ….? I was consumed with a rampant rampaging terror that flipped by guts. Hallucinatory terror.
I was going to drink the white spirits. I have never drunk white spirits during my active alcoholism but had heard of plenty of alcoholics who had, and their wife’s perfume and many other such unthinkable liquids. It had, via these accounts, become a viable option. Something I could drink if need be!
It seemed like this was one of those moments.
“What do you normally do?” was all I heard. What? “What do you mean, what do I normally do….?” I hesitantly replied in a hushed almost child-like voice. “When you are like this, what do you normally do?” her voicing becoming more urgent . I could see the white spirits glisten and almost feel it evaporate, on my tongue, harshly as it deeply burnt my chest with a warm reassuring heat, move glowingly outwards from there in little dendritic branches of smoothing warmth and the whispering promised of blessed relief and good cheer. When alcoholism whispers sweet nothings it is sweeter than your lover.
“You better drink it” sounded in my head. I couldn’t remember what I normally do, or who was this asking this I head was jumbled and terrified. “You’d better do it”, the internal voice insisted. All I could feel was huge surges of stress chemicals pulsating through my veins like little scuttling manic spiders, speeding through my veins, up and down the insides of my legs, my limbs, scurrying frantically.
For some inexplicable reason, I thought, or a thought occurred to me “once I would have thought this a massive craving!” but now I felt I knew better. This wasn’t an appetitive craving, I didn’t fancy a wee drinky winky, wouldn’t that be nice.
I knew this was a stress based urge and nothing to do with desire. Nonetheless, I would kill for a drink, but paradoxically I didn’t even want one!? It wasn’t for pleasure but to escape this escalating aversion.
I knew somewhere, and know more now, that the stress chemicals swirling around my nervous system were activating my reward (or survival) brain systems. I knew it because I had read about it. Many, many times. Enough times. Stress and emotional distress activated the inner beast.
Massive amounts of stress and distress cuts off the action outcome memory, the explicit memory, the remembering of knowledge of what I would normally do in this type of situation, the “what do you normally do in this situation?” my wife had implored me to recall. It was completely cut off, I couldn’t get to it, access it. It might as well have belonged to someone else.
In there, in that explicit memory, was my wife’s name and other life saving stuff like what I normally did when faced with inevitable relapse, apart from staring at a bottle of spirits and salivating!
Stuff like the tips of recovery that I had learnt so proficiently that they were ingrained in my explicit memory, for occasions such as this one!?
Some of this recovery memory had become habitualized in my implicit memory too, thank God. It was this memory that had prompted me to climb the stairs to my wife’s help on my uncertain legs. To automatically ask for help. This was implicit recovery.
The very memory I could now not access now was explicit, because the excessive stress had cut if off. The what to do now I have asked for help memory. I knew this from my research as well. The “flight or fight “mechanism, a cascade of noradrenaline, the actions of chronic stress on switching explicit to implicit memory from the action outcome to the stimulus response, to the compulsive automatised, you see it and then you do it, memory. The stimulus response memory.
The distress was the stimulus and drinking to alleviate it would be the response. Your life can depend on this memory, like when fleeing an approaching tiger, so it does not ease it’s grip on your mind too readily or easily. This is the memory with no insight of future negative consequence. It acts now and too hell with the later consequences. The “let’s deal with this now!” memory, not later.
The “what I usually did as a chronic drinking alcoholic during extreme moments of distress”, a compulsive action hardwired into my brain. I drank alcohol previously at such prompting. It had become a unpremeditated, compulsive reaction to distress. It was how I survived back then. But then was now.
Not only did it shut off my escape route via my explicit memory and knowledge of how to get out of this life threatening crisis but it locked me into “your life is in danger, act without thinking, just do the thing your have normally done over the past 25 odd years” routine.
It showed me fleeting images of doing it before, drinking, in case I had forgotten, floating airy glimpses of the people I did it with and where, when, and whispered to me that this this person was actually the real me. Not this quivering sober fraud, in this torturous alien sober reality. That I was kidding myself.
The response was positively motoric. Get up and go over there and…drink! Lots! I could feel my legs stiffen and steal themselves.
Drink, although you would rather kill yourself than drink. Where was the choice there in this? Where had it gone, disappeared with my explicit memory no doubt? As my wife further implored me to do something, the voice in my heading was now screeching orders at me “Drink now!” “Drink now or you..will, die!!!” Drink for God’s sake, drink!!”
So it wasn’t to be a case of I will relapse because “hey one will not hurt” sort of reasoning, rationalising and justification. I was being implored to drink because my life was at risk if I did not!! I could die. I could die if I didn’t!
How badly is an alcoholics reward/survival system hijacked…usurped when this brain is imploring him to do the very thing that will kill him? And in order to help, save him from this nightmare, help him survive like some psychotic caregiver would suggest. How far down the road from full cognitive control over one’s behaviour had I gone.
Answer: about as far as I could go! How much stress surges through the alcoholics brain to close down the mnemonic survival kit. When you can’t access your “recovery” survival kit, the old alcoholic one kicks in! The alcoholic self schema overrides the recovering alcoholic schema.
I slumped to my knees and implored through tear blurred eyes for help from somewhere. I gave in profoundly, I was beat. I surrendered. The stress retreated like waves scuttling away from a beach. All action stations became deactivated and the red swirling light in my head and the honking siren turned off. I was emotionally traumatised but still sober.” An abbreviated excerpt from “How Research Helped Save My Life” 
I had given up on the idea that I, my self, could solve this terrifying dilemma. The answer was outside of my self, my survival network, it was in letting go. Letting go of the distress and all the brain regions it was activating; memory, attention. emotion, reward/survival. It is regions that make up the self that are taken over in the course of alcoholism. The self can no longer be fully trusted in matters such as these. It needs to escape to brain regions outside of self or to the helping arms and reassurance of someone who knows how to help, and external prefrontal cortex of reason. One armed combat with the self will end up in crushing defeat. At certain times we are beyond our own mental control.
This ancedotal evidence highlights why research is essential to the effective treatment of alcoholism and addiction as it clearly shows the neural mechanisms implicated in relapse in chronic addiction. Altered stress systems (and their affective manifestation of emotional distress) hijack memory systems. In “offlining” the prefrontal cortex and the explicit memory of the hippocampal region it makes it very difficult to access “recovery tools” and prevent relapse.
It is only in clearly understanding these mechanisms can we seek to prevent the very high level of relapse in these clinical groups. We have to fully understand the problem before we can effectively deal with it.
We have shown via this “case study” how one can almost relapse when one has no desire ever to drink again, we have shown how it is emotional distress that precipitates and prompts this type of relapse.
We have seem how the “self will” is greatly limited and the regulation of self usurped by the impact of stress systems on reward/motivation, attention, affective and memory systems. Systems all essential to regulating one’s behaviour.
Thus treatment may find it more profitable in addressing measures to alleviate distress, increase stress and emotional coping strategies and improve the emotional regulation that is key to recovery.

How do resentments become the Number one Offender!?

Research suggests (1) suggest individuals with poorly regulated emotions often turn to alcohol to escape from or down-regulate their emotions, creating a risk for diagnosable problems in relation to alcohol  difficulties as this impairment in emotion regulation is associated with alcohol-related disorders  and substance-related disorders (2).

Experiential avoidance of thoughts, emotions, sensations,memories, and urges can lead to a variety of negative outcomes such as problems with substance use, because it paradoxically increases negative thoughts (3)

Thus risk factors include suppression (including both expressive suppression and thought suppression), avoidance (including both experiential avoidance and behavioral avoidance), and rumination.

Emotional distress, which is chronically higher in people with emotion dysregulation, appears to potentiate (heighten) reward systems in the brain (1), and this potentiation may be even greater in individuals high in reward sensitivity, increasing the chances they will turn to alcohol. Intake of alcohol will be reinforced both by the satisfaction of high appetitive drives and by the reduction of negative emotions these individuals otherwise cannot regulate. Thus, the combination of emotional dysregulation and high reward sensitivity should be a potent risk factor for the development and/or maintenance of substance abuse and eating disorder.

Emotion dysregulation may occur if emotions are experienced as intense and overwhelming, when individuals have not learned how or when to apply effective strategies, when strategies are not applied flexibly, when the strategies fail, or when strategies are overused, emotion regulation patterns may interfere with the ability to successfully achieve goals. Emotion dysregulation still involves attempts at regulation, but the process leads to maladjustment rather than adjustment. For example, emotion dysregulation may result in poor interpersonal relationships, difficulty concentrating, feeling overwhelmed by emotions, or inability to inhibit destructive behaviors.

Components of emotional dysregulation include a tendency for emotions to spiral out of control, change rapidly, get expressed in intense and unmodified forms, and/or overwhelm both coping capacity and reasoning. (4)

Self regulatory deficits like these may emerge from an interaction of intrinsic biological factors as well as from chaotic or stressful early life experiences, particularly child abuse and problematic attachments with caregivers.

Emotional Dysregualtion may be present in  overly restricted emotional expression and avoidance or excessive emotionality and excitement seeking. This research (4) highlighted that the idea that emotional dysregualtion is a distinct construct, related to but not reducible to negative effect (anxiety, mood, negative emotions) and may be seen as the result of the developmental capacity to adaptively regulate emotions being disturbed by early disruptive experiences. In other words, abuse in early childhood can help determine how we cope with our emotions.

Maladaptive cognitive emotion regulation strategies such as rumination    (5 ) and thought suppression (6) have been linked to a number of negative psychological outcomes. Binge-eating (7), and other impulsive behaviors (8) may all be a result of emotion dysregulation.

Selby (9 ) addresses the issues of why does emotion dysregulation appear to result in behavioral dysregulation?  The connection may lay in the use of certain cognitive emotion regulation strategies (cognitive emotion dysregulation) that actually increase the intensity of negative emotions and cause an individual to engage in maladaptive behavioral emotion regulation strategies (behavioral dysregulation) in order to down-regulate these intense emotions.

In essence, the way we regulate our emotions may actually cause us to lose control of them. These are often  considered “impulsive” behaviors, without premeditation. While not a behavioral emotion regulation strategy per se, urgency may be part of what causes certain individuals to engage in behavioral dysregulation. Individuals who exhibit high levels of urgency, feeling the need to act when faced with emotional distress, may be more likely to engage in maladaptive behaviors such as substance abuse as a result of emotion dysregulation.

The best characterized cognitive emotion regulation strategy is rumination. Rumination (5) is the tendency to repetitively think about the causes, situational factors, and consequences of one’s emotional experience.  Rumination is an important risk factor for substance abuse (10)

Thought suppression is another emotion regulation strategy as is catastrophizing (11) the tendency to continuously think about how bad a situation is and the negative effects that the current situation has on the future. Using catastrophizing as an emotion regulation strategy has been found to increase emotional distress (12)

All of the cognitive emotion strategies discussed (rumination, thought suppression, and catastrophizing) appear to have a common theme: they all focus attention on emotionally relevant stimuli, usually negative.

Furthermore, evidence has shown that ruminative processes tend to amplify the effect of negative affect.

Yet the tendency to ruminate on negative emotional thoughts increases levels of negative affect, and in turn the increase in negative affect increases levels of rumination followed by a flood of racing negative emotional thoughts, which in turn increase levels of negative affect in a vicious, repetitive cycle – an emotional cascade.

As a recovering alcoholic, this rumination and catastrophizing is very similar to what we call resentments the constant resending of negative emotions and accompany thoughts, each cycle making the emotions and thoughts more distressing.

Mixed with the self elaboration we discussed in another blog, then more has a heady cocktail of distressing resentments.

As the Big Book of Alcoholics Anonymous says “resentments kill more alcoholics than anything else”

It is thus difficult to see alcoholism as anything other than a disorder of emotional regulation.


1. Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010). Emotion-regulation strategies across psychopathology: A meta-analytic review. Clinical psychology review30(2), 217-237.

2. Berking, M., Margraf, M., Ebert, D., Wupperman, P., Hofmann, S. G., & Junghanns, K. (2011). Deficits in emotion-regulation skills predict alcohol use during and after cognitive–behavioral therapy for alcohol dependence. Journal of consulting and clinical psychology79(3), 307.

3.  Hayes, S. C., Strosahl, K. D., & Wilson, K. G. (1999). Acceptance and commitment therapy: An experiential approach to behavior change. New York: Guilford Press.

4.  Bradley, B., DeFife, J. A., Guarnaccia, C., Phifer, J., Fani, N., Ressler, K. J., & Westen, D. (2011). Emotion dysregulation and negative affect: Association with psychiatric symptoms. Journal of Clinical Psychiatry72(5), 685-691.

5. Nolen-Hoeksema, S. (1991). Responses to depression and their effects on the duration of depressive episodes. Journal of Abnormal
Psychology, 100(4), 555–561.

6. Wegner, D. M., Schneider, D. J., Carter, S. R., & White, T. L. (1987). Paradoxical effects of thought suppression. Journal of Personality
and Social Psychology, 53, 5–13.

7.  Anestis, M. D., Selby, E. A., Fink, E., & Joiner, T. E. (2007). The multifaceted role of distress tolerance in dysregulated eating behaviors.
International Journal of Eating Disorders, 40, 718–726.

8. Whiteside, S. P., & Lynam, D. R. (2001). The five-factor model and impulsivity: Using a structural model of personality to understand
impulsivity. Personality and Individual Differences, 30, 669–689.

9. Selby, E. A., Anestis, M. D., & Joiner, T. E. (2008). Understanding the relationship between emotional and behavioral dysregulation: Emotional cascades. Behaviour Research and Therapy46(5), 593-611.

10. Nolen-Hoeksema, S., Stice, E., Wade, E., & Bohon, C. (2007). Reciprocal relations between rumination and bulimic, substance abuse, and depressive symptoms in female adolescents. Journal of abnormal psychology116(1), 198.

11. Garfnefski, N., Kraaij, V., & Spinhoven, P. (2001). Negative life events, cognitive emotion regulation, and emotional problems.
Personality and Individual Differences, 30, 1311–1327.

12.  Sullivan, M. J. L., Bishop, S. R., & Pivik, J. (1995). The pain catastrophizing scale: Development and validation. Psychological
Assessment, 7, 524–532.


An Emotional Disease?

Is Addiction an Emotional Disease!?

“Addiction”, is widely viewed as a chronic, relapsing, neurobiological disorder, characterized by compulsive use of alcohol or substances, despite serious negative consequences. It involves both physiological and psychological dependence and leads to the emergence of a negative emotional state.  The Diagnostic and Statistical Manual of Mental Disorders, DSM-5, combines DSM-IV categories of substance abuse and dependence into a single disorder, on a continuum from mild to severe.  The previous definition of addiction by the American Society of Addiction Medicine (ASAM) includes the terms, craving, persistent risk, and emphasizes risk of relapse after periods of abstinence triggered by exposure to substance-related cues and emotional stressors . This conceptualisation points to the role of substance-related cues, e.g., environmental stimuli that are strongly associated with the effects of the administration of substances and acquire incentive salience through Pavlovian conditioning, as well as stress (an internal cue), as major determinants of relapse.

For example in terms of the reasons for relapse implicated in much research, alcoholics relapse due to ‘cue-reactivity’ i.e. they see ‘people, places, or things’ associated with their drinking past and they are drawn to it and simply relapse.

 In some years of recovery, we have rarely heard of a committed abstinent alcoholic addict in recovery who relapsed simply because he/she was lured siren like to some cue associated stimuli. That is not to say cue reactivity is not a valid construct, it is obviously. Recovering alcoholics  exhibit an automatic, that is involuntary,  attentional bias towards drug and alcohol-related “cues”. This is a torturous aspect of early recovery thus most therapeutic regimes advise those in early abstinence and recovery to avoid “people, places and things” that act as  cue-associated stimuli. In fact, some in early recovery do challenge this only to learn painfully as the result by thinking they can spend time, like before, in drinking establishments,  only to find that it is “like sitting in a hairdressors  all day and not expecting to eventually get a haircut!”

A more recent  ASAM definition includes “Addiction is a primary, chronic disease of brain reward, motivation, memory and related circuitry. Dysfunction in these circuits leads to characteristic biological, psychological, social and spiritual manifestations. Addiction is characterized by inability to consistently abstain, impairment in behavioral control, craving, diminished recognition of significant problems with one’s behaviors and interpersonal relationships, and a dysfunctional emotional response.”

We appreciate the role now afforded to “dysfunctional emotional response” in this new definition as we believe it is dysfunctional emotional response which is at the heart of alcoholism and addiction.

Our own experience of recovery, coupled with our neuroscientific research over several years, has  made us curious as why the ways addicts and alcoholics talk about their condition or the explanations they forward all generally point to what they would call an “emotional disease” or “a parasite the feeds on their emotions”, an “emotional cancer” or a “fear based disease” yet these are rarely countenanced in any theory of addiction, whether neurobiological, psychological, psycho-analytical (although there have been very interesting ideas based on attachment within this methodology).

How could addicts and alcoholics be so wrong about themselves and what ails them? Especially when they see it also in hundreds of others with the same condition? We doubt that they are wrong, in fact, we have in recent years taken the opposite approach and started to explore, in terms of research, if addiction and alcoholism, especially, have their roots in emotional dysregulation and emotional processing deficits

In even more recent times, we have been encouraged that these difficulties also shape decision making difficulties, distress based impulsivity (leading to compulsivity) lack of inhibition across various psychological domains, as well as more revealingly the cognitive and executive dysfunctions and ‘flight or flight’ reactions which seem common to this group, over reacting in other words.

There appears to be a short term decision making profile which we suggest is distress based, which implicates more emotive-motoric “automatic,compulsive”regions of the brain rather than goal-directed. A more “let’s do it NOW!”way of making decisions.  This is also seen in children of alcoholics.

Could this be an important vulnerabilty to alcoholism? In order to get this debate going we will now consider whether there are possibilities for re-defining the DSM criterion in relation to the manifest difficulties observed in these clinical groups in relation to emotional dysregulation. The “official” nosology (e.g. DSM IV) is largely limited to physical manifestations of addiction although addicted individuals display additional psychiatric symptoms that affect their well-being and social functioning but which have been relegated to the domain of psychiatric “comorbidity.” 

Although the relationship of these psychiatric symptoms with addiction is very close, substance abuse may modify pre-existing psychic structures and lead to addiction as a specific mental disorder, inclusive of symptoms pertaining to mood/anxiety, or impulse control dimensions, decision making difficulties or, as we suggest, the various characteristics of emotional dysregulation. All of which suggests the current DSM based nosology of addiction-related mental comorbidity does not consider the overlap of the biological substrates and neurophysiology of addictive processes and psychiatric symptoms associated with addiction, so fails to include specific mood, anxiety, and impulse control dimensions and decision making difficulties in the psychopathology of addictive processes.

Addiction reaches beyond the mere result of drug-elicited effects on the brain and cannot be peremptorily equated only with the use of drugs despite the adverse consequences produced. Addiction is a relapsing chronic condition in which these psychiatric manifestations play a crucial role. Thus it may be that the aetiology of addiction cannot be severed from its psychopathological underpinning, it’s roots.  In may have been initiated by these mechanisms and also the addiction cycle may be continually perpetuated by them. Particularly in view of the undeniable presence of symptoms, of their manifest contribution to the way addicted patients feel and behave, and to the role they play in maintaining the continued use of substances.

In other words, the latter symptoms frequently precede the addictive process constituting a predisposing psychological background on which substance effects and addictive processes interact, leading to a full-fledged psychiatric disorder. Within the frame of the current DSM, numerous relevant psychiatric issues in substance abuse disorders may have been overlooked.   Even in the absence of psychiatric diagnosis, specific psychological vulnerabilities may constitute a background for the development of  disorders. The neural circuitry implicated in affective reactivity and regulation is closely related to the circuitry proposed to underlie addictive behaviours.  Affect is related to dysfunctional decision-making processes and risky behaviours,  In fact, we suggest these affective processing difficulties cause inherent decision making difficulties and constitute a premorbid vulnerability.

Substance dependence is associated with significant emotional dysregulation that influences cognition via numerous mechanismsThis dysregulation comes in the form of heightened reward sensitivity to drug-related stimuli, reduced sensitivity to natural reward stimuli, and heightened sensitivity of the brain’s stress systems that respond to threats. Such disturbances have the effect of biasing attentional processing toward drugs with powerful rewarding and/or anxiolytic effects. 

Emotional dysregulation can also result in impulsive actions and influence decision-making. It appears clear in addiction and alcoholism (substance dependence)  and that emotional processing significantly impairs cognition in substance dependence. Emotionally influenced cognitive impairments have serious negative effects with both the resultant attentional bias and decision-making deficits being predictive of drug relapse. 

The influence of emotion is clearly detrimental in substance dependence, and many of the detrimental effects observed are due to the ability of drugs of abuse to mimic the effects of stimuli or events that have survival significance. Drugs of abuse effectively trick the brain’s emotional systems into thinking that they have survival significance!

They trick the alcoholic into thinking he needs to drink to survive! 

It is important to note that the neural mechanisms implicated in neurobiological accounts of the transition to endpoint addiction from initial use are also experienced emotionally in human beings, in addicted individuals. That human beings, addicted individuals have to live with these profound alterations and impairments of various regions and neural networks in the brain. And that it is in treating these human manifestation of this neurobiological disease, i.e. one’s “dysfunctional emotional responses” in every day life that is required for long term recovery. We have to manage the emotional difficulties which perpetuate this disease, this “parasite on our emotions”, otherwise these dysfunctional overwhelming emotions manage us.   

It is through this emotional dysregulation that the addiction cycle is experienced and via emotional means perpetuated! It is through living “emotionally light” and spiritually aware lives which help manage our emotions that perpetuate our long term recovery.

Emotional distress is at the heart of addiction and alcoholism, and relief from it on a continually, daily basis is at the heart of recovery.    


American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders (Fifth ed.). Arlington, VA: American Psychiatric Publishing. pp. 5–25.

Pani, Pier Paolo, et al. “Delineating the psychic structure of substance abuse and addictions: Should anxiety, mood and impulse-control dysregulation be included?.” Journal of affective disorders 122.3 (2010): 185-197.

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

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.