Filling the Empty Self

In the first part of this two part blog – we looked at how addicts in recovery move from a more negative (perhaps chronically negative) self schema to a more positive recovering self schema and how this now sense of self and the new interrelatedness with others which develops in recovery drives recovery and an increased self empowerment.

The self, via schema, is increasingly positive in outlook, attitude and action. In other words recovery does for the self schema, sense of self, what we could not do for our own selves, our own self schemas. The self and the self schema becomes a vehicle for increasing well being and not further disease and disorder.

It is a vehicle by which we recover.  For me it helped recover the person who I was meant to be, the person who had become so lost to alcoholism for so long. It in some ways introduced me to a person I did not really know and in many ways am still getting to know.

The fascinating thing also is that negative self perception, as we know from previous blogs, generates a brain frequency very similar to thinking about drinking and not similar to drinking itself. We presume a positive self perception does not and this not only does not lead one back to drinking but very much in the opposite direction.

We again cite from the same article as before (1) to demonstrate perhaps how self schema, especially, the recovering self schema, is so vital to recovery for alcoholism.

“….From this perspective, specific disturbances in the underlying structure of the self-concept are considered intermediary factors that serve as important mechanisms that link more distal factors (e.g., genetic factors, family history of alcohol problems) to alcohol
use. A person with a self-concept composed of few positive and many negative and highly interrelated self-schemas would not have the internal motivation necessary to facilitate adaptive behavior. The negative affect stemming from such a self-concept configuration
would be likely to motivate maladaptive
behavior in an attempt to escape the negative self views
(Baumeister, 1990) and “fill up” the empty self (Cushman, 1990).

Persons with a family history of alcohol problems or other risk factors for alcohol problems would be likely to turn to alcohol (versus other types of maladaptive behavior) as a means to escape the negative emotions. A core belief about the self in relation
to alcohol (drinker self-schema) would be likely to form as drinking experience accumulates and similarities across drinking-related incidents are abstracted. Such a drinking-related self-schema
would serve to motivate schema-consistent (drinking)
behavior.
According to the hypothesized model, a person in sustained recovery (long-term abstinence) would have a more well-developed self-concept—one that consists of newly developed positive self-schemas and a recoveryrelated
self-schema. The recovery self-schema is conceptualized
as central to the recovery process as it would serve to motivate schema-consistent (recovery) behaviors.

During the process of recovery, new positive self-schemas are likely to form as a result of new relationships, activities, and involvements. The development of new positive self-schemas would diminish the proportion of negative self-schemas and the overall level of interrelatedness among the self-schemas.

 

How-To-Fill-The-Inner-Emptiness-Of-Addiction-PhysicianHealthProgram

 

TESTING THE THEORETICAL MODEL

… findings provide empirical evidence that (a) young adults with early-onset alcohol dependence have impaired self-concepts that are characterized by many negative self-schemas, a tendency toward few positive self-schemas, and an elaborated self-schema related to alcohol; and (b) young adults in recovery have healthier self-concepts characterized by few negative self-schemas, a tendency toward many positive self-schemas, and an elaborated recovery related self-schema.

If further longitudinal research studies demonstrate that the self-concept configuration that we found in persons with early-onset alcohol dependence contributes to the development of the disorder,
then prevention strategies aimed at children and adolescents
could be beneficial, particularly for those children who are at risk for alcohol problems based on the presence of other risk factors (e.g., familial alcohol problems, conduct problems). More specifically, interventions designed to build a healthy self-concept (by
fostering the development of a diverse collection of positive self-schemas, thereby decreasing the relative proportion of negative self-schemas) may serve as a protective factor that buffers the effects of the more distal risk factors.

 

At the other end of the spectrum, the data from our study suggest that interventions may also profitably focus on fostering the development of a recovery self schema in persons with alcohol dependence. 

…the nature of any recovery related intervention would depend on how ready the person is to change. For a person who does not yet recognize that alcohol is a problem, the goal would not be
to foster the development of a recovery schema but to help him or her identify that drinking is a problem.

One possible way to do this is to assist the person to make associative links across the multitude of negative alcohol-related outcomes so that rather than a series of unrelated incidents, the individual begins to see a pattern of repeated, enduring, and pervasive alcohol-related problems.

when the individual is able to pull unpleasant alcohol related episodic memories together to identify that he or she indeed has a problem with alcohol. So whereas
assisting the person to increase his or her awareness
of problems with alcohol is consistent with the basic
tenets of motivational interviewing (Miller & Rollnick,
2002), fostering the development of a recovery self schema
is not.

For people who recognize that they have a problem with alcohol or people who are seeking treatment for alcohol problems, one strategy may be to foster the idea that they can be recovering persons— that is, that recovery is possible for them. Fostering communication with other recovering persons and encouraging involvement in recovery-related activities may help to form a recovery-related “possible self”—a future-oriented conception of the self one “hopes to be,” that is, a recovering person.

Imagining the self in the future by developing detailed images of what one would be like in recovery is an important part of this process. Participation in 12-step recovery programs such as Alcoholics Anonymous that explicitly foster the development of a recovery related identity may also be helpful…

In fact, one plausible explanation…for an emerging recovery related self-schema is that the alcohol dependent participants were in a treatment  facility based on such a 12-step recovery program.

 

 

Reference

1. Corte, C. (2007). Schema model of the self-concept to examine the role of the self-concept in alcohol dependence and recovery.Journal of the American Psychiatric Nurses Association, 13(1), 31-41.

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.

Reference

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