Distorted Thinking!!

We have a new page!!.

This page will look at the myriad of cognitive distortions and preservative (and deluded) thinking that appears to be part of the condition of many different addictive behaviours.

 

 

So far in this blog we have looked at how altered stress systems effect emotion processing and regulation and how this results in the increasingly compulsive need to use substances and behaviours to regulate subsequent negative emotions and affect.

Now we will be looking at the third strata of this disorder of addictive behaviour, that of distorted preservative thinking. Perseverative thinking is when someone gets an idea or thoughts in their head and just can’t get them out.

It is commonly shared in 12 step meeting show we have a problem with our thinking and hence our decision making. We find this to be true for us also.

Some addictive behaviours have their own specific cognitive distortions such as with gambling and eating disorders in addition to a more generalized pattern of cognitive distortions associated with all additive behaviours and psychopathology more generally.

Unlike those who feel cognitive distortions cause psychopathology we believe cognitive distortions are the consequence of impaired stress systems and emotion dysregulation which implicate a hyperactive amgydaloid region of the brain.

We feel that persistent negative and distorted thinking is the direct consequence and manifestation of stress and emotion dysregulation. It is how stress and emotion dysregulation manifests  in thought processes; these thought processes obviously worsen this stress and emotion dysregulation and vice versa.

In recovery by addressing either stress, negative affect or our distorted thinking we automatically deal with the other factors.  Hence distress is at the heart of our addictive behaviour.

If we reduce our distress we reduce stress reactivity, the effect of negative emotions and their manifest distorted thoughts.

Hence addictive behaviour is a three level ( tri strata) disorder of stress hyper reactivity, emotion dysregulation and distorted thoughts, all interconnectedly reactive.

 

 

In other words, the thinking of addicted individuals seems to be “fear-based” or distress prompted which leaves perception and reaction to it rather it distorted.

Along with these thoughts there is a reciprocal increase in stress chemical reactivity and increasingly impaired e motion regulation and processing of emotions.

Hence these unregulated negative emotions act with heigthen stress reactivity and spiraling distorted thinking to increase relapse vulnerability.

As a result we believe that distorted preservative thinking, thinking that persists and gets increasingly distorted,  is a part of the aetiology of addictive behaviour.

Equally we believe it is the consequence of a distress state activated by a hyperactive amgydala which increases stress reactivity, emotion dysregulation and then distorted thinking in a viscous circle.

We believe, based on our own research and experience of recovery that this is viscous circle is a common feature of all addictive behaviours.

 

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!

 

References

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.

A Message of Hope at Christmas – We Do Recover!!

I have heard various statistics about rates of recovery of the years, especially in AA. Some of the figures were depressing low and often go unchallenged which can be demotivating for those seeking recovery.

Why AAs in particular spread distorted statistics which suggest hardly any one recovers is open to question?

Out of all the people I know who were in treatment before me and in the group after me, as well as with me and who completed the entire course of treatment most of them, i.e. a high majority of at least 3/4s, are still in recovery.

This suggests to me that those who seek treatment, whether 12 step based treatment or via taking the steps, with fearlessness and honesty, do actually recover long term. So why is this sort of statistic not well know?

There can be no greater motivation to recover than knowing that the vast majority of people who do engage in treatment do actually recover! 

I recently came across an excellent article on this by Dr. Omar Manejwala,  former Medical Director for Hazelden Foundation, one of the nations oldest and largest addiction centers in the US.

I will quote from his blog here.

“…the recent tragic overdose death of Phillip Seymour Hoffman, whom many have noted was reportedly abstinent from alcohol and drugs for over two decades, raises another set of important questions:

  • Do people who get sober actually stay sober?

  • Can’t you ever be free of addiction? Are you always at risk of relapse?

  • Is there some period when, like cancer, you are considered to be “cured”?

  • Isn’t staying sober for a long time at least somewhat protective?

In my experience treating thousands of addicts, I’ve learned that cases like these can often diminish hope and create a perception that these conditions aren’t treatable, or that addicts can never be trusted.

When is an addict or alcoholic sober long enough to be considered at least relatively safe? Do most people with addiction who have been sober a long time eventually relapse?  In scientific terms, what is the natural history of recovery from alcohol and drug addiction?

I’ve seen numerous experts speak up in the wake of Hoffman’s death, but few have offered hard science on what we really know about how a person’s duration of sobriety is related to their chances of being sober in the subsequent years. Fortunately, there are data to support the idea that recovery is durable, and that the vast majority of people who stay sober for a long time will continue to stay sober afterwards.

The most thorough attempt to understand what happens to addicts and alcoholics who stay sober is an eight-year study of nearly 1200 addicts. They were able to follow up on over 94% of the study participants, and they found that extended abstinence really does predict long term recovery. Some takeaways from this research are:

  • Only about a third of people who are abstinent less than a year will remain abstinent.

  • For those who achieve a year of sobriety, less than half will relapse.

  • If you can make it to 5 years of sobriety, your chance of relapse is less than 15 percent.

 

Of course, there are many people with 10, 20, 30 or even 40 years of abstinence…. My experience is that people with decades of abstinence clearly can and do relapse, but the incidence is very low. Like Hoffman and many others, it’s always heartbreaking when it happens. I’ve seen it triggered by opiate prescriptions, acute pain and other life stressors. Often the people who relapse have stopped engaging in the recovery-oriented practices that served them well during their earlier sobriety.

Every death from addiction is tragic. But cases like Hoffman’s are definitely the exception and not the rule.”

Copyright Omar Manejwala, M.D. 2013.

 

 

 

Link/reference

http://www.manejwala.com/#!single-post/cyqt/1

Dennis, M. L., Foss, M. A., & Scott, C. K. (2007). An eight-year perspective on the relationship between the duration of abstinence and other aspects of recovery. Evaluation Review, 31(6), 585-612.

When the Nuggets Lose their Lustre!

Good little animation, although the animation misses the bit about lying and cheating family and friends, the general degradation of the kiwi’s being etc and the frenzied attempts to do any thing to get the next glow, however increasingly dim that glow has become. In recovery we need to watch out for euphoric recall of that glow and also getting that glow in different ways, through different behaviours.

Why a “Spiritual Solution” to a Neurobiological Disease?

because it says it all! and for our newcomers…

Inside The Alcoholic Brain

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

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

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

View original post 2,028 more words

Feeding Distress-based action.

Even as I a child I had difficulties controlling my impulses and my behaviours, “I was into everything”. I did not use much forethought in decisions making and would generally react and always be after something that I wanted desperately that very moment. Now in fact!

I believe I had sugar addiction, and chocolate and playing, and girl chasing addictive behaviours way before I ever got near alcohol in my early teens, with a six month, and quite disastrous period of poker machine gambling in between. And of course you couldn’t get me off the “Space Invader” machine.  I just couldn’t get enough of anything, ever. Always wanted more, more and some more. My mother would call for me to come home in the darkening hours of evening. I had to be scraped off the playing fields in order to come home. Exhausted.

So why this constant overdoing of everything!!?

Why couldn’t I stop once in a while, ponder the consequences of my decisions, employ some, goal-directed, action-outcome type of thinking?

Following on for our very recent blog which described the neural mechanisms implicated in negative urgency we now look at at an article which attempts to  bring together some of our most consuming research interests by attempting to explain whether there is  a  link between emotional processing deficits (alexithymia)  negative urgency and dysregulated behaviours.

This study (1) looked at whether whether negative urgency (distress-based impulsivity)  would be the link in relationship between alexithymia and dysregulated behaviors.

Dysregulated behaviors have been defined as behaviors that are difficult to control, and often  result in functional impairment for the affected individual (Selby & Joiner, 2009).

An inability to understand affective and physiological experiences inherent in alexithymia might prompt individuals to engage in maladaptive behaviors in an effort to regulate emotions. One type of behavior linked to alexithymia is binge eating. Wheeler and colleagues (2005) found that alexithymia was positively correlated with binge eating in a sample of females.

Carano and colleagues (2006) found that alexithymia was positively correlated with the severity of binge eating behaviors. Additionally, Speranza and colleagues (2007) found that alexithymia predicted eating disorder treatment outcome in a three year prospective study meaning high levels of alexithymia can interfere with treatment response even more than the actual severity of the presenting problem.

 

eating-disorder

Taylor and colleagues (1990) found that 50% of substance dependent males admitted to a drug and alcohol rehabilitation program were characterized as alexithymic. Similarly, Haviland and colleagues (1988) found that approximately 50% of individuals diagnosed as alcohol dependent were characterized as alexithymic. These numbers are significantly greater than the reported prevalence of alexithymia in the general population, which has been estimated to fall between 10 and 15% (Rybakowski et al., 1988; Parker et al., 1989), and suggests that alcohol and drug abuse is another example of a maladaptive behavior that may be used to modulate negative affective states when one is incapable of doing so in an adaptive way.

Loas and colleagues (1997) conducted a one year follow-up on individuals admitted to a psychiatric facility for alcohol treatment. Results suggested that individuals who remained abstinent from alcohol use one year post-treatment had
significantly lower scores on alexithymia measures.

“Why does the lack of understanding and expression of emotions have such a powerful influence over dysregulated behaviors?” 

Why  do individuals with high levels of alexithymia who experience negative affect seem to engage in dysregulated behaviors so frequently, while other individuals may simply cry, ruminate, or develop vegetative symptoms of depression?

Is negative urgency (Whiteside & Lynam, 2001; Cyders, Smith, Spillane, Fischer, Annus, & Peterson, 2007) the mechanism through which these behaviors are developed  and sustained?     It may be that the relationship between alexithymia and behavior is explained by a tendency on the part of individuals with high levels of alexithymia to act rashly in an attempt to immediately reduce psychological and physiological sensations associated with negative affect (negative mood, negative emotions, anxiety etc).

Negative urgency could be thought the  mechanism that drives dysregulated behaviors in individuals who experience difficulty recognizing and expressing their emotions.  

eating-disorder-clinic-300x250

The authors (1) concluded that when faced with negative affect, many individuals are able to recognize and process their emotions adaptively. However, if people are not able to identify or describe their emotions (the very definition of alexithymia), our results suggest that this confusing affective experience may be quite upsetting (or unpleasant) and could lead to negative urgency, or a tendency to act rashly when they experience any type of negative affect.

High alexithymia individuals appear to be highly motivated to alleviate negative affect, regardless of the consequences. It may be that the emotional confusion inherent in alexithymia prompts individuals high on negative urgency to engage in dysregulated behaviors, by acting out either
against themselves or others.

—————————————————————————————————

As we mentioned in our previous blog  emotional processing deficits are common in addiction and in other dysregualted behaviours and these deficits may not recruit the goal-directed parts of the brain. They do not guide action or choices effectively. As a result they manifest in perhaps crude, undifferentiated or processed forms as distress signals instead and recruit more limbic, motoric regions of the brain.  Hence they are not used to anticipate future, long term consequence.

We disagree that it is not simply negative affect that prompts negative urgency but rather the chronic stress dsyregulation underpinning the manifestation of negative affect.

We are simply adding that as addiction becomes more chronic, so does stress and emotional distress and this appears to lead to a distress-based “fight or flight” responding to decision making. Addicts increasing appear to recruit sub-cortical or limbic areas in decision making and this is prevalent in abstinence as in active using. It is the consequence of chronic emotional and stress dysregulation.

References for this blog

Fink, E. L., Anestis, M. D., Selby, E. A., & Joiner, T. E. (2010). Negative urgency fully mediates the relationship between alexithymia and dysregulated behaviours. Personality and Mental Health, 4(4), 284-293.

Why a spiritual solution?

The Alcoholics Guide to Alcoholism

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

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

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

View original post 2,028 more words

Understanding Emotional Processing Deficits in Addiction – Guest Blog

Understanding Emotional Processing Deficits in Addiction

by alcoholicsguide

We recently blogged on how alcoholics, and children of alcoholics, have difficulty with recognizing and differentiating external signs of emotions such as facial emotional expressions, now we will consider increasing evidence that alcoholics have difficulties with identifying and differentiating internal emotional states also.

Both these areas of research point to real difficulties in alcoholics in relation to the processing of emotion.

As we shall explain below, this deficit in emotional processing has real consequence for decision making capabilities and this has an important role to play in the initiation and maintenance of substance abuse and eventual addiction.

Alexythymia and Addiction

Effective emotion regulation skills include the ability to be aware of emotions, identify and label emotions, correctly interpret emotion-related bodily sensations, and accept and tolerate negative emotions (2,3).

Alexithymia is characterized by difficulties identifying, differentiating and expressing feelings. The prevalence rate of alexithymia in alcohol use disorders is between 45 to 67% (4,5)

Finn, Martin and Pihl (1987) investigated the presence of alexithymia among males at varying levels of genetic risk for alcoholism. They found that the high risk for alcoholism group was more likely to be alexithymic than the moderate and low genetic risk groups (6).

Higher scores on alexithymia were associated poorer emotion regulation skills, fewer percent days abstinent, greater alcohol dependence severity (7). Some studies have emphasized a right hemisphere deficit in alexithymia [8,9] based on the hypothesis that right hemisphere plays a more important role in emotion processing than the left [10, 11].

Dysfunction of the anterior cingulate cortex has been frequently argued, e.g., [12], and others have focused on neural substrates, such as the amygdala, insula, and orbitofrontal cortex (see the review in [13]). All different components of the the emotional regulation  network.

These models may interact with each other and also map onto the brain region morphological vulnerability mentioned as being prevalent in alcoholics.

Magnetic resonance imaging and post-mortem neuropathological studies of alcoholics indicate that the greatest cortical loss occurs in the frontal lobes, with concurrent thinning of the corpus callosum. Additional damage has been documented for the amygdala and hippocampus, as well as in the white matter of the cerebellum. All of the critical areas of alcoholism-related brain damage are important for normal emotional functioning (14) .

One might speculate that thinning of the corpus collosum may render alcoholics less able to inhibit negative affect in right hemisphere circuits.

Alcoholics are thus vulnerable to thinning of the corpus collosum and perhaps even to emotional processing difficulties (15 ). The inability to identify and describe affective and physiological experiences is itself associated with the elevated negative affect (16) commonly seen in alcoholics, even in recovery (17.

Thus, this unpleasant experience might prompt individuals to engage in maladaptive behaviors, such as excessive alcohol consumption, in an effort to regulate emotions, or, more specifically, cope with negative emotional states (18 )

One neuroimaging study (19) looked at and compared  various models of alexithymia showing people with alexithymia showed reduced activation in the dorsal ACC and right anterior insula (AI), and suggested individuals who exhibit impaired recognition of their own emotional states may be due to a dysfunction of the ACC-AI network, given these regions’ important role in self-awareness. These studies suggest alexithymics may not be able to use feelings to guide their behaviour appropriately.

The Iowa gambling task (IGT) was developed to assess decision-making processes based on emotion-guided evaluation. When alexithymics perform the IGT, they fail to learn an advantageous decision-making strategy and show reduced activity in the medial prefrontal cortex, a key area for successful performance of the IGT, and increased activity in the caudate, a region associated with impulsive choice (20).

ep neg

The neural machinery in alexithymia is therefore activated more on the physiologic, motor-expressive level, similar to the study on children of alcoholics and thus may represent a vulnerability.

The function of the caudate is to regulate or control impulsivity and disinhibition. Individuals with alexithymia may work on the IGT impulsively rather than by using emotion-based signals. This IGT study suggests that individuals with alexithymia may be unable to use feelings to guide their behavior appropriately.

Alexithymic individuals thus may be unable to use emotion for flexible cognitive regulation. Thus, there may be dysfunction in the interaction of the aspects of the emotional response system in alexithymia with greater activation in the caudate (basal ganglia) and less activation in the mPFC in alexithymics during the IGT.

Thus alexithymics show weak responses in structures necessary for the representation of emotion used in conscious cognition and stronger responses at levels focused on action. This ties in with the blog on an emotional disease? and also  so how is your decision making? which suggested that alcoholics do not use emotion to guide decision making and rely on more motor, or automatic/compulsive parts of the brain to make decisions.

Consequently, alexithymics experience inflexible cognitive regulation, owing to impairment of the emotion guiding system. These dysregulated physiological responses over many years may result in untoward health effects such as drug addiction.

To illustrate this, one study demonstrated that patients with cocaine dependence had higher alexithymia scores compared with healthy control subjects (21).

In a study of 46 inpatients with alcohol abuse or dependence, the total TAS (Toronto Alexithymia Scale) score was significantly higher among those who relapsed after discharge than among those who did not, even when depressive symptoms were taken into account(4)

Cocaine-dependent patients also failed to activate the anterior cingulate and other paralimbic regions during stress imagery, suggesting dysregulation of control under emotional distress in these patients (22).

Instead, cocaine-dependent patients demonstrated greater craving-related activation in the dorsal striatum, a region that has been implicated in reward processing and obsessive–compulsive behaviours. The greater activation associated with alexithymia in men in the right putamen during stress is broadly consistent with earlier studies implicating the striatum in emotional motor responses.

This also corresponds to  the study of  children of alcoholics show significantly more activation in the left dorsal anterior cingulate cortex and left caudate nucleus a region associated with impulsive choice, illustrating perhaps in children of alcoholics a bias in brain decision-making systems as an underlying  elevated risk for alcoholism.

We have also suggested previously a ‘compulsive’ emotional  habit bias in endpoint addiction which reflects a stiumulus response or automatic behaviour in the face of emotional distress, which then influences an automatic decision making profile. This may be the effect of chronic drug use impacting on an inherited emotional expressive-motor decision making vulnerability seen in children of alcoholics.

In simple terms, these vulnerable individuals may recruit more automatic rather than goal-directed areas of the brain when making decisions. This would result in impulsive/compulsive decisions which do not fully consider consequences, negative or otherwise, of their decisions and resultant actions. This decision making profile would then have obvious consequences in terms of a propensity to addiction.

 

References (to be finished)

1. Naqvi, N. H., & Bechara, A. (2009). The hidden island of addiction: the insula.Trends in neurosciences32(1), 56-67.

2. Berking M, Margraf M, Ebert D, Wupperman P, Hogmann SG, Junghanns K. Deficits in emotion-regulation skills predict alcohol use during and after cognitive-behavioral therapy for alcohol dependence. Journal of Consulting and Clinical Psychology. 2011;79:307–318

3. Gratz KL, Roemer L. Multidimensional assessment of emotion regulation and dysregulation: Development, factor structure, and initial validation of the Difficulties in Emotion Regulation Scale. Journal of Psychopathology and Behavioral Assessment.2004;26:41–54

4. Loas G, Fremaux D, Otmani O, Lecercle C, Delahousse J. Is alexithymia a negative factor for maintaining abstinence? A follow-up study. Comprehensive Psychiatry. 1997;38:296–299.

5. Ziolkowski M, Gruss T, Rybakowski JK. Does alexithymia in male alcoholics constitute a negative factor for maintaining abstinence. Psychotherapy and psychosomatics. 1995;63:169–173.

6.  Finn PR, Martin J, Pihl RO. Alexithymia in males at high genetic risk for alcoholism.Psychotherapy and Psychosomatics.1987;47:18–21

7.  Moriguchi, Y., & Komaki, G. (2013). Neuroimaging studies of alexithymia: physical, affective, and social perspectives. BioPsychoSocial medicine7(1), 8.

8. Miller L. Is alexithymia a disconnection syndrome? A neuropsychological perspective. Int J Psychiatry Med. 1986;7:199–209. doi: 10.2190/DAE0-EWPX-R7D6-LFNY.

9. Sifneos PE. Alexithymia and its relationship to hemispheric specialization, affect, and creativity.Psychiatr Clin North Am. 1988;7:287–292.

10. Buchanan DC, Waterhouse GJ, West SC Jr. A proposed neurophysiological basis of alexithymia. Psychother Psychosom. 1980;7:248–255. doi: 10.1159/000287465.

11. Shipko S. Further reflections on psychosomatic theory. Alexithymia and interhemispheric specialization. Psychotherapy and psychosomatics.

12. Lane RD, Reiman EM, Axelrod B, Yun LS, Holmes A, Schwartz GE. Neural correlates of levels of emotional awareness Evidence of an interaction between emotion and attention in the anterior cingulate cortex. J cognitive neuroscience. 1998;7:525–535. doi: 10.1162/089892998562924.

13. Wingbermühle E, Theunissen H, Verhoeven WMA, Kessels RPC, Egger JIM. The neurocognition of alexithymia: evidence from neuropsychological and neuroimaging studies.Acta Neuropsychiatrica. 2012;7:67–80. doi: 10.1111/j.1601-5215.2011.00613.x.

14. Oscar-Berman, M., & Bowirrat, A. (2005). Genetic influences in emotional dysfunction and alcoholism-related brain damage.

15. Sperling W, Frank H, Martus P, et al. The concept of abnormal hemispheric organization in addiction research. Alcohol Alcohol.2000;35:394–9.

16.  Connelly M, Denney DR. Regulation of emotions during experimental stress in alexithymia. Journal of Psychosomatic Research. 2007;62:649–656

17. Stasiewicz, P. R., Bradizza, C. M., Gudleski, G. D., Coffey, S. F., Schlauch, R. C., Bailey, S. T., … & Gulliver, S. B. (2012). The relationship of alexithymia to emotional dysregulation within an alcohol dependent treatment sample.Addictive Behaviors37(4), 469-476.

18.  Thorberg FA, Young RM, Sullivan KA, Lyvers M, Hurst CP, Connor JP, Feeney GFX. Alexithymia in alcohol dependent patients is partially mediated by alcohol expectancy. Drug and Alcohol Dependence. 2011;116:238–241

19. Moriguchi, Y., & Komaki, G. (2013). Neuroimaging studies of alexithymia: physical, affective, and social perspectives. BioPsychoSocial medicine7(1), 8.

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22.  Sinha, R., Lacadie, C., Skudlarski, P., Fulbright, R. K., Rounsaville, B. J., Kosten, T. R., & Wexler, B. E. (2005). Neural activity associated with stress-induced cocaine craving: a functional magnetic resonance imaging study.Psychopharmacology183(2), 171-180.

Why a spiritual solution?

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

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

I guess people are curious as to how the spirit changes matter or material being when it should perhaps be rephrased to how does application of the ephemral mind affect neuroplasticity of the brain. Or in other words how does behaviour linked to a particular faith/belief system alter the functions and structure of the brain. We have discussed these points in two blogs previously and will do so again in later blogs. Here I just want to highlight in a short summary why spiritual practice helps alcoholics and addicts with with regulating themselves especially when the areas of their brains which govern self regulation have been taken over by the action of drugs and alcohol, so that they have very limited control over their own selves and their own behaviour.

This seems to be at the heart of addiction and alcoholism, this increasingly limited self control over addictive behaviors. In addressing this need for a spiritual solution we also hope to address choice versus limited control arguments. As we will see, the addicted or alcoholic brain is usurped to such a profound extent by effects of drugs and alcohol and this brain acts so frequently without conscious awareness of the negative consequences of these actions that it is appears undoubtedly the case that addicts and alcoholics have profoundly diminished control over their choices of behaviour.

This is especially pertinent in chronic addicts and alcoholics were the thrill is long gone so why would they continue doing something which has little reward other than because they are compelled to.

In addiction, vital regions of the brain and processes essential to adaptive survival of the species become hijacked or usurped or “taken over” by the combination of the effects of alcohol or drugs or addictive compulsive behaviours (acting as pharmacological stressors)  on pre-existing impairment in certain parts and functions of the brain. The actions of drugs and alcohol lead to a hyperactive stress system which enhances the rewarding aspects of drugs and alcohol in initial use, especially in those with maladaptive stress response such as individuals who have altered stress systems in the brain due to abusive childhood experiences (1-3).

In the second abusing phase, stress interacts with various neurotransmitters especially dopamine to drive this abusive cycle. In this phase of the addiction cycle  stress heightens attention towards cues and creates an  heightened attentional bias towards drugs and alcohol (4,5). Stress chemicals also increase activation of “addiction memory” (6,7). Thus there is multi-network usurping of function in the brain as the addiction cycle progresses (8). Recruited of attention, reward and memory networks are enhanced by the effects of stress chemicals.

Stress also enhances the rewarding effects of alcohol and drugs so makes us want them more (9). Enjoy them more. These are the so-called “good times” some of us look back on, in our euphoric recall.

In the final endpoint phase of addiction, stress incorporates more compulsive parts of the brain, partly by the stimulus response of emotional distress which automatically activates a compulsive response to approach drug and alcohol use while in distress, which is a common reality for chronic addicts and alcoholics.

 

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Thus stress chemicals acting on mainly dopamine  circuits in the brain and other neurotransmitters eventually take over control of the brain in terms of the control of behaviour (8).

In usurping  “survival” or self regulation networks in the brain, control over behaviour “implodes” or collapses inwards, from control over behaviour moving inwards from the action outcome, or goal directed, conscious prefrontal cortex to the unconscious automatic, motoric, subcortical  parts of the brain (10).

This greatly limits one’s conscious self control over one’s own behaviour  if one is addicted or chronically alcoholic. Control of behaviour appears to have becomes a function of hyperactive stress systems in the brain and their manifestation as emotional distress (11,12).

This emotional distress constantly activates a “flight or flight” response in the brain and this means behaviour is carried out without reflection or without explicit knowledge of consequences, usually negative in the case of addiction (13,14).

The alcoholic or addicted brain becomes a reactionary brain not a forward thinking, considering of all possible options type of brain. The addict or alcoholic becomes driven by his brain and to a great extent a passenger in his own reality. Automatic survival networks act or react continually as if the addicted brain is on a constant state of emergency, constantly under threat.

There is a profoundly reduced conscious cognitive control over behaviour. This heighted, excessive and chronic stress and distress cuts off explicit memory of previous negative consequences of our past drinking and drug use and recruits implicit memory systems which are mainly habitual and procedural, they are “do” or “act” without conscious deliberation systems of the brain (14) .

It is as if our alcoholic or addicted brains are doing the thinking for us. Or not as the case may be. Alcoholics are on automatic pilot, fuelled by distress.  This neuroscientific explanation fits almost perfectly with the description of alcoholism in the Big Book of Alcoholics Anonymous, “The  fact is that most alcoholics…have lost choice in drink. Our so-called will power becomes practically nonexistent. We are unable , at certain times,  to bring into our consciousness with sufficient force the memory of the suffering and humiliation of even a week or month ago. We are without defense against the first drink”

The” suffering and humiliation” are now called “negative consequences” in current definitions of addiction…”continued use despite negative consequences”. (15)

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We “cannot bring into our consciousness with sufficient force the memory” because this is an explicit memory cut off by the effects of excessive stress which “offlines” the prefrontal cortex and hippocampal memory in favour of unconscious habitual, implicit or procedural memory (14,16). The memory of drinking not the memory of the “ situations surrounding this drinking”. How is this not a disorder  that has placed us “ beyond human aid” and beyond our own human aid” ? 

The “unable at certain times” are possibly times of great distress or emotional dysregulation and they leave the alcoholic and addict vulnerable to  relapse.

“Once more: The alcoholic, at certain times, has no effective mental defence against the first drink.”

“His defence must come from a Higher Power”

In later blogs we will discuss, in terms of the brain, why we need to recruit parts of the brain, via selfless behaviours, which activate areas outside those implicated in self regulation.

The cited  power greater than ourselves in AA meetings, for example, often follows an experiential trajectory – first it is the first person an alcoholic asks for help whether a family member, loved one or a G.P. – this often leads to an AA meeting or a treatment centre – then they are presented with other alcoholics who suffer from the same disorder – in AA parlance this is the first, and for many alcoholics in recovery, their only experience or attempt to find G.O.D. – this Group. of. Drunks. is like all that preceded it, a power greater than ourselves, regardless on whether we attain a spiritual connection with God after that.

A sizable minority in AA remain agnostic or atheist. This does not mean they have not performed essentially “spiritual” acts such as asking for help, accepting powerless over their life at that present moment. These are all acts of humility of accepting one needs help from beyond oneself. They also attend meetings where no one is in charge apart from God as He may express Himself in our group conscience.

Our first sponsors (mentors) in AA are also a power beyond ourselves as are their sponsors and their sponsors and the people in all their lives who advise and support. From the moment one has wholeheartedly accepted the need for help, one has accepted that help will come from a power greater than themselves.  It is a humbling and I believe spiritual act. A new breath filling one’s life.

All these people are already doing something for us which we could not do ourselves, they are helping us recruit the prefrontal cortex and explicit memories of the disasters alcohol or drug addiction has wrought on our lives – they move, eventually, activity in the brain from the unthinking dorsal striatal to the reasoning prefrontal cortex, helped also by sharing our stories in meetings. They give us a new recovery alcoholic self schema to replace the former drinking alcoholic self schema and stores it in implicit memory.

These people helps us change positive memory association of alcohol with negative associations. They overturn old ideas about the good times with a deep awareness of how bad these so-called good times were. The attentional bias is avoided or is rarely activated as the distress and stress are greatly reduced so as not to activate it.

We find recovery rewarding in the way we formerly (but not latterly) found drinking. In fact we find recovery better than drinking even at it’s best. The worst day in recovery seems much better than the worst day in drinking. We learn how to regulate our emotions so as to avoid prolonged bouts of distress, we ring our sponsors when such moments arise, talk to a loved one.

Again an external prefrontal cortex helps us climb out of the sub-cortical “fear” areas of the dorsal striatum and the anxious amgydala. The solution  is in the prefrontal cortex, in it’s control over emotions, in it’s clear appraisal of our past, in it’s activation of negative, realistic  memories of the past and  in avoiding the people, places and things which remind us of drinking.

The prefrontal cortex becomes more in charge rather than our illness doing the thinking. The prefrontal also gets strengthened by us sharing our experience strength and hope at meetings, it uses a recovery narrative to reconcile the drinking self with the recovering self, making us whole,  it embeds in our mind the truth of the progressive nature of this illness. It helps us see what it was like, what happened and what it is today. It gives us the tools to help others.

In the follow up blog to this we will further explore how this works – this spiritual solution.

 

References

1. Cleck, J. N., & Blendy, J. A. (2008). Making a bad thing worse: adverse effects of stress on drug addiction. The Journal of clinical investigation, 118(2), 454.

2. Koob, G. F., & LeMoal, M. (2001). Drug addiction, dysregulation of reward, and allostasis. Neuropsychopharmacology, 24, 97–129.

3. Sinha, R. (2008). Chronic stress, drug abuse, and vulnerability to addiction. Annals of the New York Academy of Sciences, 1141, 105–130

4. Peciña, S., Schulkin, J., & Berridge, K. C. (2006). Nucleus accumbens corticotropin-releasing factor increases cue-triggered motivation for sucrose reward: paradoxical positive incentive effects in stress?  BMC biology, 4(1), 8.

5. Ventura, R., Latagliata, E. C., Morrone, C., La Mela, I., & Puglisi-Allegra, S. (2008). Prefrontal norepinephrine determines attribution of “high” motivational salience. PLoS One, 3(8), e3044

6. Hyman, S. E. (2007). Addiction: a disease of learning and memory. Focus, 5 (2), 220.

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10. Everitt, B. J., & Robbins, T. W. (2005). Neural systems of reinforcement for drug addiction: From actions to habits to compulsion. Nature Neuroscience, 8, 1481–1489

11. Sinha, R., Lacadie, C., Sludlarski, P., Fulbright, R. K., Rounsaville, B. J., Kosten, T. R., & Wexler, B. E. (2005). Neural activity associated with stress-induced cocaine craving: A functional magnetic resonance imaging study. Psychopharmacology, 183, 171–180.

12. Goodman, J., Leong, K. C., & Packard, M. G. (2012). Emotional modulation of multiple memory systems: implications for the neurobiology of post-traumatic stress disorder.

13. Schwabe, L., Tegenthoff, M., Höffken, O., & Wolf, O. T. (2010). Concurrent glucocorticoid and noradrenergic activity shifts instrumental behavior from goal-directed to habitual control. Journal of Neuroscience, 20, 8190–8196.

14. Schwabe, L., Dickinson, A., & Wolf, O. T. (2011). Stress, habits, and drug addiction: a psychoneuroendocrinological perspective. Experimental and clinical psychopharmacology19(1), 53.

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

16. Arnsten, A. F. (2009). Stress signalling pathways that impair prefrontal cortex structure and function. Nature Reviews Neuroscience, 10(6), 410-422.