The terror of “Locked In” Attention!

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 

References

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

 

 

 

The Heart of Recovery

How is low HRV related to longer term recovering alcoholics?

We cited and use excerpts from a study (2) into short term and longer term (3) of up to six months which shows that alcoholics with years of recovery still have low HRV although it improves although this is dependent of severity of the alcoholism.

“It is known that chronic and heavy alcohol use has a toxic effect on the nervous system,[2] including effects on autonomic nervous system.[3] Specifically, heavy alcohol use can cause cardiac autonomic neuropathy,[4] which in turn, is associated with greater mortality.

Resting cardiac autonomic function reportedly favors energy conservation by way of parasympathetic dominance over sympathetic influence. Heart rate is characterized by beat-to-beat variability over a wide range, which has been reported to indicate vagal dominance and thereby parasympathetic dominance.[5]

In those with alcohol dependence, HRV is lower than in healthy individuals even after several days of abstinence.[13,14] This decrement may improve with abstinence for long periods of time.[15,16]

A study of 24-h ambulatory HRV found significantly reduced HRV in alcohol-dependent men with established vagal neuropathy and in some without.[17] Alcohol dependence has been shown to compromise vagal output measured before sleep onset, which correlates with loss of delta sleep and morning sleep impairments.[18]

Reduced HRV was found in alcohol-dependent patients with negative mood states and compulsive drinking.[19] Rechlin et al.,[20] reported reductions in HRV in patients with alcohol dependence, and this has been consistently reported in subsequent studies.[21,22]”

 

“Heart rate variability (HRV) was studied in 11 chronic alcoholic subjects, 1–30 days after the beginning of abstinence and again 5, 12 and 24 weeks later. Two patients could be re-examined after 19 and 22 months, respectively. In the follow-up study, the total patient group showed a statistically significant increase in HRV with prolonged abstinence of at least 6 months.

No recovery of efferent vagal function was found in 4 patients. It is suggested that the vagal neuropathy may improve in chronic alcoholics, but perhaps only in patients with a short to moderately long duration of drinking history (3)”.

Thus it seems thee is a partial recovery in HRV as recovery proceeds although there may be work required depending on severity of one’s alcoholism.

In our next blog on HRV we will cite and use excerpts from one of the best articles authored by Thayer which is the best explanation of how low HRV keeps an alcoholics attention “locked in” to stuff he/she would rather it didn’t get locked into such as alcohol-related cues.

References

1. THAYER, J. F., AHS, F., FREDRIKSON, M., SOLLERS, J. J., & WAGER, T. D. (2012). A meta-analysis of heart rate variability and neuroimaging studies: Implications for heart rate variability as a marker of stress and health.Neuroscience and biobehavioral reviews, 36(2), 747-756.

2. Ganesha, S., Thirthalli, J., Muralidharan, K., Benegal, V., & Gangadhar, B. N. (2013). Heart rate variability during sleep in detoxified alcohol-dependent males: A comparison with healthy controls. Indian journal of psychiatry, 55(2), 173.

3. Weise, F., Müller, D., Krell, D., Kielstein, V., & Koch, R. D. (1986). Heart rate variability in chronic alcoholics: a follow-up study. Drug and alcohol dependence, 17(4), 365-368.

Recovery is a Journey from the Head to the Heart (and back)!

PART 2 

So what does this low HRV mean for the recovering alcoholic?

I have explained this to show that HRV is directly connected to areas of the the brain implicated in stress and emotion regulation.

If, via recovery practices, we can still our beating heart, become serene as well as clean, it will have neuroplastic effects on our brain and the regulation of emotion and stress.

Equally if we meditate and alter the functioning of areas implicated in this study such as areas of the medial PFC and cingulate gyrus we improve our control over our heart. Ultimately if we can learn to relieve the inherent distress at the heart of addiction we can recovery function of not only the heart but also of areas in the brain which interact with the heart in producing heart rate variability.

So ultimately we need only to know how to quell a distressed heart via prayer, meditation, loving others.

If we can do so, we improve our emotion and stress regulation.

But do we need to do this if we have been in recovery long term?

Let me give you an example of allostasis in action.

In an allostatic system like addiction there is stress dysregulation coupled with reward dysfunction (I believe there is a pre-morbid allostasis in those addicts who have experienced abuse, trauma and insecure attachment also which means there is a stress and emotion dysregulation from an early age which leads to a heightened reward sensitivity which means we start to regulate negative emotions from an early age via impulsively  using or consuming stuff we really really like, or seem to like more than healthy people, to make ourselves feel better).

These adolescents at risk also have low HRV and the effects of alcohol have a pronounced effect on HRV.

This sets the chain of addiction in action from the start for many addicts.

So when we decide we want something this leads to a feeling of pathological wanting and then needing simply because we have altered reward systems as they are linked to our “out of kilter” stress systems .

Buying something in the store, if thwarted, soon becomes a life and death like struggle. Ever had that feeling?

I remember a 75 year old recovering person with 30 odd years of recovery  sharing in a meeting how she went to a store to get something, to find that something wasn’t there, so she was instructed to drive somewhere else to get that something, and when she got there they didn’t have it, so she had an argument with them and then with her husband in the car, then off to another store which did not have the something either, then back home on the internet, found a online store that stocked the something and ordered it.

It arrived the next day because she paid a lot of money for it to arrive the very next day! When it arrived she found that she had not only completely forgot about ordering the something but did not really want the something even. So off she sloped to apologise to her husband for being so emotionally abusive and immature over the something on her way to the Post Office to post back the something that she never really wanted in the first place!!?

This is also my head still, even after a few years of recovery. It is not as bad it was, by a long shot! It does, however, get distressed, I become impulsive and  want, need, that thing now!!! On occasion.

So I think this is one area recovery people always need to be aware of. Wanting stuff.

As it can lead to pathological wanting fairly quickly – then people get in the way of those things and we get angry, frustrated, distressed, our emotions overwhelm us or we are mean to our fellow human beings all because they are getting in the way of the thing I really really want.. NEED God damn it!…

We lose our emotional sobriety.

When we have either got it, regardless of the the human or emotional cost, we often find we do not want it or never really wanted it…that much….

Not compared to the cost of getting it!?

How do we solve this problem? We let go, we calm down, talk to someone, express our feelings, try to establish a transient homeostasis, let our stress systems subside and start again, trying to managing these chaotic brain systems.

Amends time.

If you are like that you have a low HRV and a stress/emotion regulation problem and probably always will.

But if can be manged and it can vastly improve. Then one day we learn that it is in living with our hearts forefront to our decisions and not our heads that brings lasting everyday happiness.

That is why in recovery we travel from our at times over zealous heads to our hearts. The wisdom and direction and basis of our decision making lives their not in our heads. It is not to say we do not use these wondrous instruments but we incorporate the help of our hearts in activating the reasoning of the brain.

Solve the heart issue, and the rest comes.

 

Neural structures associated with HRV

Over the past several years however a number of human neuroimaging studies have appeared in which researchers have explicitly examined the brain structures associated with HRV. In the present paper we provide a meta-analysis of eight published studies in which HRV has been related to functional brain activity using either PET or fMRI

The goal of this meta-analysis was to identify areas that were consistently associated with HRV.

In the overall analyses three regions show significant activations One region in the medial PFC (MPFC) is the right pregenual cingulate (BA 24/32).

Brodmann Cytoarchitectonics 24.pngBrodmann Cytoarchitectonics 32.png

 

Another MPFC region is the right subgenual cingulate (BA 25).

Brodmann Cytoarchitectonics 25.png

The third region is the left sublenticular extended amygdala/ventral striatum (SLEA). This region extends into the basolateral amygdalar complex, and also covers the superior amygdala (central nucleus) and extends into the ventral striatum.

 

 

More generally, the pgACC/rmPFC correlation with HRV in our meta-analysis suggests thatthis region is part, and the most reliably activated part in studies to date, of a descending “visceromotor” system that controls the autonomic nervous system and possibly other responses (neuroendocrine) based on emotional context.

The meta-analysis provides supportfor the idea that HRV may index the degree to which a mPFC-guided “core integration” system is integrated with the brainstem nuclei that directly regulate the heart. Thus these results support Claude Bernard’s idea that the vagus serves as a structural and functional link between the brain and the heart. We have proposed that this neural system essentially operates as a “super-system” that integrates the activity in perceptual, motor, interoceptive, and memory systems into gestalt representations of situations and likely adaptive responses. These findings suggest that HRV may index important organism functions associated with adaptability and health.”

References

1. THAYER, J. F., AHS, F., FREDRIKSON, M., SOLLERS, J. J., & WAGER, T. D. (2012). A meta-analysis of heart rate variability and neuroimaging studies: Implications for heart rate variability as a marker of stress and health.Neuroscience and biobehavioral reviews, 36(2), 747-756.

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.