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.

 

 

 

Intolerance of Uncertainty and Distorted thinking About the Future

Another common area I feel addiction has with obsessive compulsive disorder (OCD) is intolerance of uncertainty (IU).

In fact it is also associated with post traumatic stress disorder (PTSD)- there is actually a high co-morbidity  (at least around 40% comorbidity) with addiction and PTSD and it is one so-called co-morbidity that does not naturally dissipate like some others months into recovery such as Generalized Anxiety Disorder or Depression (the 14% rates of depression and GAD in recovery people are the same as for a normal population) but remains and often makes the symptomatic manifestations of addiction more severe, especially the tendency to engage in “fight or flight” reactions” to uncertainty and ambiguity.

I will blog more on this co-morbidity in later blogs.

The study we cite today in fact looks at IU in addicts who have suffered trauma (1).

Intolerance of uncertainty is a term that refers to a certain way in which some people perceive and respond to situations that are uncertain, and it has been found to be associated with the experience of PTSD symptoms.

Individuals who respond to uncertain or unpredictable situations in this way are considered to have an intolerance of uncertainty. People who are intolerant of uncertainty may begin to experience constant worry about what could happen in the future.

One study (1) demonstrated that negative emotion regulation strategy and intolerance of uncertainty can significantly explain the craving beliefs in addicts (especially those who have suffered a traumatic experience).

This result is consistent with that of Asadi Majareh, Abedini, Porsharifi and Nilkokar (2013) and Nasiri Shushi (2011).

Nasiri Shushi (2011) revealed that there is a significant difference among substance abuse and intolerance of ambiguity and tolerance of uncertainty in two groups of drug abusers.

The other results of this study showed that addicts have less tolerance of ambiguity and tolerance of uncertainty. In the implications of these results it should be expressed that tolerance of uncertainty is associated with cognitive features and addicts when they are faced with difficult situations act in very low levels of performance in terms of decision-making.

Studies carried out to investigate the characteristics of drug abusers suggest that they use substances to regulate a wide range of cognitive events. Undoubtedly unpleasant emotional states, particularly anxiety, depression and stress in addicts are associated with the cognitive consequences.”

The authors suggest that “Drug abusers are not able to tolerate the unpleasant situations and uncertainty in the stressful conditions and their sensitivity leads to mental and emotional problems, therefore, they more turn to substances to regulate their own cognitive experiences (Spada, Nikčević, Moneta, Wells, 2007).

The results of a study showed that individuals with lower tolerance to ambiguity find the ambiguous situations threatening… Many of them may find the substance use in the face of difficulties the only solution and therefore are not able to think or consider other solutions.”

“….While, those with high tolerance to ambiguity in face of unpleasant situation and uncertainty try to find a good solution to get rid of this condition as soon as possible…those with a low tolerance to ambiguity and uncertainty cannot find an appropriate solution…and consequently turn to undetected compromise strategies such as the use of the substance (Ahmadi-Tahoorsoltani and Najafy, 2012).”

I can relate to this study. As I still suffer from intolerance of uncertainty (IU) in recovery, and some years into recovery, it is safe to assume that I suffered form IU in addictive addiction also, if not more so?

For me dealing with an uncertain future can still provoke anxiety. In recovery groups, like AA, we often hear sensible suggestions such as do not “project into the future”, which basically means do not attempt to control future events by thinking about them because this is not only impossible but also anxiety inducing.

The main reason why I think me and other alcoholics cannot project into the future and reasonably reflect and deliberate possible outcomes is because we may have an intrinsic impairment in this regard.

We, or some of us, especially those who have suffered trauma in earlier years, may have IU, like OCD sufferers.

The number of times I rang my sponsor in early recovery to help me with projecting into the future was legion.

Having some one else to talk and share with helps us recruit the pre frontal part of the brain so that we can either see the sense in not not projecting into an unknown future or get help in reasoning through what is likely to occur then.

The difficulty I had and can still have is that my projection into the future is still negatively biased, it is still prompted by distress based cognitive distortions.

As we will see in later blogs these types of cognitive distortions proliferate across a wide range of addictive disorders such as eating disorders which we consider in our next blog.

Among this cognitive distortions is catastrophic thinking which is also distressed based. I will also blog on this at a later date. My head can still run away with itself and convince itself about something which is patently not the case. It can persuade me that this is person or that is doing this or that for these reasons. All of which on reflection are usually nonsense. For me this is like a type of delusion. It is a part of my condition that my head can trick me into believing a whole range of ideas that are delusional. Sometimes I realise this only weeks and months later.

And some people wonder why we turn our lives over to a power greater than ourselves!!?

All this distorted thinking is distressed based.

Which means there is chronically excessive stress chemicals like glucocorticoids being synthesized and whirling around one’s brain. If you give some one enough glucocorticoid there is a good chance they will end up in psychosis. In the 1950s glucocorticoids were used as an anti depressant until people started ending up in psychosis.

Ultimately when we engage in this negatively biased and distorted thinking we have potentially taken the first steps in a walk to relapse because that will eventually seem a whole lot better idea than psychosis?

These cognitive distortions (and there are many)  may even be at the heart of this condition of addictive behaviour.

They are also the consequence of an impaired ability to process emotions (and to avoid) them and thus regulate them. This leads to a tendency to fight or flight which only leads to an heightening of this anxiety, and an increased proliferation of distressing thoughts about future possiblilities, all of which can seem to become more and more catastrophic. How much these thoughts are specifically linked to trauma has to be further explored by research.

For me IU and thought action fusion, especially in early recovery caused as many problems as so-called defects of character. The only difficulty is that they are not mentioned in AA literature, or the Big Book. That does not mean that they do not exist simply because they were not discussed as psychological manifestations commonly known to alcoholics in the 1930s.

They are however known now, which is why I write this blog. To add to our sum of knowledge about this strange illness…

That is not to say having a reassuring sponsor and taking inventory cannot deal with these issues. It is useful however to be aware of them and to realise that not every one in recovery has suffered traumatic incidents. Those who have can have additional requirements in terms of recovery.

I always found it comforting to have a sponsor in the early days who was there and who could also relate to the trauma side of my alcoholism and addiction. It helped soothe me when I could not self soothe. Helped me realise I was not alone in this, that I could recover like this other trauma sufferer could. We can do stuff we can’t do alone.

Ultimately with such an impaired ability to see things reasonably and to make decisions rationally it is imperative to evoke a cardinal recovery rule for me, Accept, Let Go and Let God.

The most profound way to regulated emotions. To Let it Be.

I also used a thing I borrowed and rephrased from Jeffey Schwartz, a leading expert on OCD, how suggested OCD sufferers when in the grip of some obsession to say to themselves “It’s not me it’s my OCD”.

So if your head gets into a downward spiral over some event your head distorts into being and likely to happen in the dark, threatening, Gothic never never world of the future, say to your self “It’s not me it’s my illness.”

In the UK it is called the fanatic in the attic.

It does the thinking for you, if you allow it. Guaranteed.

 

References

Fizollahi, S., Abolghasemi, A., & Babazadeh, A. THE ROLE OF EMOTION REGULATION, DISSOCIATIVE EXPERIENCES AND INTOLERANCE OF UNCERTAINTY IN THE PREDICTION OF CRAVING BELIEFS IN DRUG ABUSERS WITH TRAUMATIC EXPERIENCE.

They can fuck you up, your mum and dad.

They fuck you up, your mum and dad.
    They may not mean to, but they do.
They fill you with the faults they had
    And add some extra, just for you.

Phillip Larkin – This Be The Verse

Looking back on my own childhood it is easier now to observe the fertile ground from which my genetic seeds of alcoholism started to flourish. I have long maintained that growing up in a dysfunctional family environment did not create my alcoholism but certainly did not help. A family environment were emotional expression was limited and veered between sentimentality and  outright anger.

It is difficult to see how I learnt the essential adaptive skills of emotional regulation then; how to identify, label and express emotions freely without sanction, verbally, and non-verbally. For me emotions where something you cut off, experientially avoided, resisted. The more you did not let them get to you the tougher you were mentally somehow. Emotions were strangely dangerous things almost.

Emotions, having them, made you weak! People who indulged in them were weak.

I also grew up with a father who was a boxer and alcoholic (abstinent, thank God, via the local Church) who insisted emotions had to tolerated like a man, like some tough  hombre in a 1950s Western. I had a host of uncles and a Grandad who agreed and they all set out to toughen me up. I even had boxing matches with cousins at various homes to show how I was progressing!

When I started drinking I found that this tough guy routine was greatly enhanced. Alcohol made me bullet proof. I drank and grew up to manhood in one go. Or so I thought – I didn’t realise that I stayed at that emotionally  impaired 14 years old for nearly three decades later.

The worst effect on my emotional regulation  skills was my relationship with my mother who struggled with valium abuse most of her adult life. This meant she was emotionally distant a lot of the time. Wose than that, she mixed mawkishness with being cold as a stone. It was an insecure attachment.  You were never sure, emotionally, where you were at with her. It made me insecure, anxious and eventually very very angry. Cold blue angry.

But did this also have an effect on my ability to processing emotions. How could maternal emotional deprivation have an effect on my emotional processing skills? Andd how could this emotional processing difficulty affect the amount I craved alcohol??

I recently came across this article (1) which looked at this very question.  I refer widely from it here.

Attachment theory is a widely used framework for understanding emotion regulation as well as alexithymia, and this perspective has also been applied to understand alcohol use disorders. One hypothesized function of attachment is the interpersonal regulation of affective experiences (Shaver & Mikulincer, 2007; Sroufe, 1977).

One hypothesized function of attachment is the interpersonal regulation of affective experiences (Shaver & Mikulincer, 2007; Sroufe, 1977). In the development of alexithymia, attachment theories stress the importance of significant others in childhood (Krystal & Krystal, 1988; Nemiah, 1977; Taylor et al., 1997). Evidence suggests that alexithymia is related to dysfunctional parenting (Thorberg, Young, Sullivan & Lyvers, in press).

Insecure attachment is associated with alexithymia and both harmful drinking and alcohol-dependence (Cooper, Shaver, & Collins, 1998; De Rick & Vanheule, 2006; Thorberg & Lyvers, 2006; Thorberg, Young, Sullivan, Lyvers, Connor & Feeney, 2009). In addition, alcohol abuse has been hypothesized to be a consequence of alexithymia (Taylor, Bagby, & Parker, 1997).

Research on alexithymia (1) has found significant positive associations between alexithymia, difficulties identifying feelings, difficulties describing feelings and alcohol problems (Thorberg, Young, Sullivan, & Lyvers, 2009; Thorberg, Young, Sullivan, Lyvers, Connor & Feeney, 2010). Individuals with alcohol-dependence and alexithymia report more severe alcohol problems compared to those with alcohol-dependence alone (Sakuraba, Kubo, Komoda, & Yamana, 2005; Uzun, Ates, Cansever, & Ozsahin, 2003). They also have poorer treatment outcomes (Loas, Fremaux, Otmani, Lecercle, & Delahousse, 1997; Ziolkowski, Gruss, & Rybakowski, 1995).

Individuals may use alcohol to escape feelings of rejection and establish a “secure attachment base” (Hofler & Kooyman, 1996), given alcohol’s stress and anxiety reducing effects.

In this study (1)  results highlight the importance of alexithymia and difficulties identifying and describing feelings as related to preoccupation, obsessions and compulsive behaviors regarding drinking in those with alcohol-dependence. Or in more simple terms between alexithymia and craving.  In this study 32.4% of this alcohol dependent groups were alexithymic. This is less than previously reported prevalence rates of 45-67% (Thorberg et al., 2009).

In this study (1)  alcohol-dependence severity, alexithymia and insecure attachment were associated with more intrusive and interfering cognitions, ideas and impulses about alcohol, including an impaired ability to control these thoughts and impulses. This cognitively based “craving” as measured by the Obsessive Compulsive Drinking Scale (OCDS; Anton, Moak, & Latham, 1995), which is designed to assess obsessive thoughts and compulsive behavior toward drinking.

Hence there was a demonstrated relationships between alexithymia, craving, anxious attachment and alcohol problems in an alcohol-dependent sample. Higher levels of alexithymia led to a stronger desire for alcohol that was partially explained by an underlying mechanism, anxious attachment. One possible reason for this  it may reflect an impairment in affect regulation.

Findings of the RAAS-Anxiety scale measured insecure attachment as related to a current or previous relationship, these findings may suggest that worries about being rejected, not cared for or unloved lead to an increased craving for alcohol.

One explanation for this mediational relationship may perhaps be that increased relationship stress is associated with a fear of intimacy and anxious attachment that leads to increased craving and perhaps a stronger attachment to alcohol. In other words, the alexithymia of insecure attachment may cause a stress dysregulation which prompts craving particularly as craving is a consequence of dysregulated stress systems. Stress dysregulations is also implicated in increased or more chronic alexithymia as suggested by George Koob in various articles. This has also been observed in other studies – this relationships of negative affect (anxiety, negative mood and emotion) with both alexithymia and craving (Sinha & Li, 2007).

To summarise, the results of this study support important relationships between alexithymia, difficulties identifying and describing feelings in relation to alcohol craving. These relationships extend to significantly higher levels of obsessive thoughts and compulsive behaviors in relation to alcohol use and alcoholism severity amongst individuals with combined alexithymia and alcohol-dependence, compared with alcohol-dependence alone. This study identified anxious attachment as a potentially important mechanism, in the relationship between alexithymia and alcohol craving.

References De Rick, A., Vanheule, S., & Verhaeghe, P. (2009). Alcohol addiction and the attachment system: an empirical study of attachment style, alexithymia, and psychiatric disorders in alcoholic inpatients. Substance use & misuse,44(1), 99-114.

Why erase addiction memories when they can help others?

According to one UK newspaper The Independent, dated the 9th July 2014 “Substance abusers could have their memories of drug addiction wiped in a bid to stop them using illegal narcotics, an award-winning neuroscientist has said.

According to new research by Cambridge University’s Professor Barry Everitt: disrupting the memory pathways of drug users could weaken powerful “compel” cravings, reduce “drug seeking behaviour” and open a new field of addiction therapy.

Professor Everitt  told this week’s Federation of European Neuroscience Societies (FENS) how his research in rodents had found that targeting “memory plasticity” in rats was able to reduce the impact of maladaptive drug memories.

He added that this knowledge could offer a radical new method of treatment of drug addiction in humans, where researchers have already established that the path to addiction operates by shifting behavioural control from one area of the brain to another. This process sees drug use go from a voluntary act to a goal directed one, before finally becoming an compulsive act.

It was this process that Professor Everitt’s research is trying to “prevent” by targeting “maladaptive drug-related memories” to “prevent them from triggering drug-taking and replaces”.

In humans this could potentially be done by blocking brain chemicals.

“It’s the emotional intrusiveness of drug and fear memoirs that can be diminished, rather than an individual’s episodic memory that they did in the past take drugs or had a traumatic experience,” he told The Independent. “Conscious remembering is intact after consolidation blockade, but the emotional arousal [that] leads to drug seeking or distressing feelings of fear that are diminished.”

His research group discovered that when drug memories are reactivated by retrieval in the brain, they enter a pliable and unstable state. By putting rats in this state Professor Everitt was able to prevent memory reconsolidation by blocking brain chemicals or inactivating key genes.

In one study, the team diminished drug seeking behaviours by obstructing a brain chemical receptor linked to learning and memory, thus erasing memories, while in another study it found they could weaken drug use memories by altering a particular gene in the amygdala, a brain area processing emotional memory.

“Of course, inactivating genes in the brain is not feasible in humans,” the professor told FENS. “So we’re directing our research to better identify the underlying brain mechanisms of memory reconsolidation.”

He added: “We specifically examined how we could target these maladaptive drug-related memories, and prevent them from triggering drug-taking and relapse.”

So to recap, this new treatment is based on altering genes in rats!

There is no need to actually wipe an alcoholics’ addiction memories.

In fact it may be very counter productive to recovery from alcoholism. One 80 year old and hyper ecologically valid experiment into the mnemonics of “treating addiction memories”  has shown that by honestly looking at the consequences of one’s actions as the result of one’s alcoholic drinking that the positive associations of previous drinking were reappraised in light of the damage done to oneself, one’s loved ones and family and society at large.

Addiction memories via this profound reappraisal were then more accurately processed in long term explicit memory. Implicit schematic memory was also altered fro a self schema in which one is a drinking alcoholic to one in which one is a recovering alcoholic.

So-called positive associations in long term episodic and explicit memory were,  when labile via recall, then challenged and replaced by more accurate negative associations in long term memory – no memories needed to be erased just reappraised more accurately.

 

mad scientist

 

This type of ongoing experiment is happening on a daily basis at an AA meeting near you.

AA groups have found that memories need not be erased, with possible deleterious knock on effects on fear processing and amgydaloid performance, but rather memories simply need to be faced up to, and via honesty appraisal reprocessed more adaptively in long term memory.

This also means alcoholics in recovery can use their addiction memories in not only clearing away the wreckage of the past, repairing broken relationships with loved ones and society as a whole by  making amends to those involved in this wreckage and also put the memories of the past to excellent therapeutic use by using it to help others with similar memory difficulties.

In fact even academic researchers have found and have demonstrated that abstinent, treatment seeking individuals also have a different cognitive or/and memory bias to active alcoholics. This has been illustrated in findings that the greater “accessibility” for positive vs. negative alcohol- associations in heavy vs. light drinkers was not found to be generalized to alcoholics in treatment vs. social drinkers (2). Rather, there was a trend for treated inpatients, motivated to attain abstinence, to show greater availability and accessibility for negative alcohol-related information.

This is how to use memories of addiction to the best possible use, instead of erasing them, wiping them our and hoping for the best, memories of our addiction can be used to great purpose in helping others. Also “addiction memory” is often activated by those who have not come to terms with their alcoholism and still want to drink. Unless some one has come to terms with their alcoholism little can be done, by erasing memories or otherwise. These are sticking plasters on a gaping wound. They will be replaced with other “addiction memory” as there an underlying condition to alcoholism ( we believe it to be emotional regulation and processing deficits) and it is this that drives this fear-based condition called alcoholism, memories are the result of this malady. Address the underlying conditions and the rest takes care of itself.

It is not brain regions which are the problem either such as activation of the amgydala, it is how this sometimes errant and overactive brain region in alcoholics is tamed via the serenity found in the AA program of recovery.

The compel parts of the brain, Everitt mentions,  are activated by emotional distress, so treat the distress not the symptom of it. He also confuses implicit, automatic memory, with explicit, conscious memory. Either way they are both activated by stress/distress, and are thus both emotional memories.  Again treat the emotional dysregulation, the primary problem not the secondary manifestation of the problem.

As I mentioned above, there has been an ongoing experiment into recovery from alcoholism going on for nearly 80 years now, there is a lab in most areas of town.

It would benefit the world and science, in particular, if neuroscientists would pop in for a coffee and check our our findings.

 

References

2. McCusker CG  Cognitive biases and addiction: an evolution in theory and methodAddiction 2001;96:4756.

 

One Christmas I nearly relapsed!

 

One Christmas I nearly relapsed!

by alcoholicsguide

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

When fighting your neural ghosts make sure to surrender!!

When I was in early recovery, in the first weeks and months my brain would continually trick me into thinking I was not an alcoholic and it did this via a combination of  stress and memory.

The process went like this – first I would have an intrusive thought about alcohol and drinking which I did not want and had not consciously put in my own head. Which used to annoy me! So what was it doing there then? I must have put it there right? why else would it be there?

So I must still have wanted to drink?

I would find this thought very threatening, frightening and upsetting. I would try to get rid of it by suppressing it, pushing it out of my consciousness. The problem was this didn’t work.

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In fact, it made the situation a whole lot worse. The intial intrusive thoughts about drinking would then proliferate and there would be other thoughts about drinking; where, at what time, who would be there. I would then have a visual read out of all these scenarios. In the bar, the sunlight streaming through the window, the golden glistening pint of lager in the summer sun matched only by the pearly white smile of the beautiful buxom bar maid slowly pulling my pint, looking at me longingly etc. in a busy atmosphere, full of happy your attractive people laughing and enjoying themselves. people dancing and hugging. Sweet music drifting acorss the bar. You get the picture.

Delusion! This was nothing like the last bar I drank in a can assure you!! It was however the image my brain was evoking partly via memory association partly by motivational embellishment.

I have an alcoholic brain which wants me to drink. It uses, still, memories from the past, to whisper sweet nothings. It never casts images across my feverish mind of violently vomiting, bent over the downstairs toilet, or me staring through half blind eyes at my severely jaundiced face in the bathroom mirror. Or being thrown out of various bars onto the hard concrete pavement outside, on my head. Or the tears and violent rows. And the distress and confusion on loved ones’ faces.

No my alcoholism never accesses these images. Ignores them completely. Instead, as my alcoholic brain wants nothing more or else than to drink, it sends memories like neural ghosts into my head to cast a spell of delusional images and suggestive ideas, mainly promoting the idea of how good it was.

This is why in AA it is said we should wind the tape forward a bit to the disgustingly horrible reality of our final drinking. The constantly wretching and living in isolaton in our alcohol induced psychosis and the shivering terror of delirium tremens.

We have a inner voice of alcoholism that quite simply lies. Distorts our memories. The motivational voice of our alcoholism is a pathological liar. It only wants to drink because it is like a psychotic carer who thinks that drinking is the thing to do when we are in full of stress or in emotional distress. It automatically says hold one I have a solution to this distress, DRINK!

This is what the brain has become hardwired to do when distressed enough.  it is a habitual response of our implicit memory which then recruits our explicit memory which paints the picture of why drinking would be such a good idea.

I have a distress based illness, so I do get distressed from time to time. Sometimes over the most innocuous things sometimes.

Not as badly as in early recovery.  No, things have improved beyond belief since then.

The neural ghosts of my motivation were like intoxicating sirens in early recovery. My impaired reward systems implored me to have liquid release. Both combined to conjure an alternative view of myself from that of my recovering self, which was still in it”s infancy. They seemed to have control of my brain!  I suddenly had a problem beyond my own will power, I couldn’t resolve these things under my own steam.

The thoughts would come and I would suppress them and the thoughts would multiply and then the memories would all chain link  and pretty soon I would have an Amazon warehouse store of memories, all providing evidence against those guys in AA, who were not telling me truth about me being an alcoholic, They were wrong…sure I liked to drink, especially given by traumatic upbringing and all?

All these thoughts and memories floating across my mind like edits in a movie to show me as a drinking person who wasn’t an alcoholic. Not many disorders go to such profound trouble!!

I would fight these images, memories and thoughts to such an extent my brain would quite simply end up paralysed, my brain felt like it had become locked and there was nothing I could do about it. It had frozen into a terrifying inertia. Stalemate. No resolution apart from increased suffering.

Fortunately whatever I had learnt in AA even in the early days would rescue me. I had learnt to habitually grasp at something close to hand, my mobile phone. After a few puzzling moments of indecision I realised I could get help from somewhere. Ring my sponsor!!!!

I had to use someone else’s head to help me with my head, my newly recovering alcoholic head. I needed a recovered head who knew what I was going through and could help me through it! I felt all fragile like a jaundiced chick.

Recovery is tough in the early days, let’s never forget that! Life without a sponsor and right from the start is a key to surviving this alcoholic possession by these deluded memories and these neural ghosts.

This is the most vital period, to keeping those who need help in recovery. Saying someone doesn’t want it enough doesn’t cut it for me anymore. Better to show them what they are missing, namely a solution to their problems. Who ultimately doesn’t want that?

If you have never trusted anyone in your life, like me, this is the time to start if you want to recover. Trust at least one person on God’s earth. One, that’s all. This is the start to a new world in recovery. A world beyond your alcoholic brain’s comprehension.

Anyway, remember that in the feverish brain of a person in early recovery who ends up engaged in this neurobiological possession, thought straightjacket and fighting for his or her life against a mnemonic Hydra when it is the last thing they should be doing, the only way to win is to give in. Surrender!

Ultimately, how we appraise and react to naturally occurring alcohol or drug related thoughts and associated memories  will determine if this process of “craving” is activated. If we use strategies such as acceptance of these thoughts as transitory then the thoughts will not affect this process and if we “Let Go and Let God” then the distress which initially activates this process will not do so. How we react to our thoughts and accompanying distress (as they appear be be coupled) will determine whether the mental obsession mentioned above will be provoked.

Also see Cognitive Craving Part 3  and Part 4

A Cognitive Model of Craving – Pt 3

In an earlier blog we asked the question whether  neurobiological or “conditioning” or reinforcement models of craving predict relapse in abstinent alcoholics and addicts?

For us this is the most essential question. How do we explain relapse in those individuals motivated to remain abstinent, especially when they have followed some form of treatment, including 12 step groups.

We have seen that most relapse seems to be prompted by psychological stressors such as interpersonal relationships and the failure to cope with these.

This is very different to conditioning or reinforcement models that simply posit that people relapse because of the lure of alcohol or drug related stimuli, “cues”, or cues in the presence of stress or negative emotions, which we believe does have some affect.

Equally we have shown that in treatment seeking individuals there seems to be an automatic avoidance of cues so attentional bias does not really apply to this group plus there is a negative memory association bias in this abstinent, treatment seeking group also. So why do these people relapse?

What is the craving process prior to relapse for this group? . This is hugely important as neurobiological accounts do not predict relapse, so what does?

Over the next two blogs we will forward a model of craving or “mental obsessing” which we believe more accurately models the mechanisms which lead these individuals committed to staying sober and in recovery to relapse.

Ultimately we believe it may the maladaptive cognitive-affective reaction to naturally occurring  intrusive thoughts about alcohol or drugs (which are also the function of emotional dysregulation) that creates a proliferation of such thoughts, until they become obsessive, and which escalates stress and emotional distress to such an extent that the individual relapses to silence these tortuous obsessive thoughts.

These thoughts may not always be about alcohol or drugs. They may also contain negative perceptions of self, such as low self esteem and negative self schemas as the consequence of abusive early childhoods. These may result in “I am not good enough” thinking or “to hell with it!” relapse which have little to do with an appetitive urge to drink as in some reinforcement models. They are more akin to escape from self.

So models of addiction tend to focus on neurobiological substrates underlying addiction rather than on how affective (and cognitive) processing mediate addictive behaviours (1) although 80% of problem drinkers after outpatient treatment reported drinking episodes aimed at manipulating thoughts or emotions (2), with the majority of treatment clients attributing their relapse to interpersonal stress or negative emotions (3).

Also the involuntary retrieval of drug related thoughts is a hallmark of addicted populations. Over 70% of smokers stated that urges disrupted their thinking or functioning (4). Intensity of obsessive thoughts about alcohol predict relapse rate (5), with addicts motivated to use drugs to “silence” obsessive thoughts (6).  The idea that abstinence automatically decreases alcohol-related thoughts is challenged by research and supported by clinical observation that among abstinent alcohol abusers, alcohol-related thoughts and intrusions are the rule rather than exception (7).

So if emotion regulation difficulties and related intrusive thoughts are so prevalent in recovering abstinent addicts and alcoholics how do we account for this in a satisfactory and comprehensive theory of craving?

One study important to the conceptual framework set out here (6) used heart rate variability (HRV) measures, as a putative index of emotional regulation, to illustrate how craving involves cognitive-emotional processing and how conditioning models may not fully explain  ‘craving’.  This is consistent with the increasing concern in the literature about the applicably of such “one-dimensional” conditioning models explaining the results of cue reactivity studies (6). This study, among various findings, showed a link between HRV and obsessive thoughts,  in simple terms, the greater the emotional dysregulation, the greater the obsessive thoughts about alcohol.

It may even be that these “conditioning” reinforcement models or dopaminergic or stress-based models are describing “urges” rather than craving.  For us “craving” is distinct but interdependent on this “urge” state, it is partly triggered by it, if you like.

As an alternative to such passive “respondent” or “conditioning” models, some researchers have advocated the use of information-processing theory to understand how dependent individuals react in their encounter with “drug-related” cues (external and internal, e.g. stress or negative emotions) (6). Craving may thus be a different phenomenological experience to that of the physiological urges, although one may prompt the other.

According to one ‘info-processing’ view of craving, forwarded by Stephen Tiffany (4), ‘craving’,  occurs only when the automatic approach behaviour commonly seen in addicts in thwarted. This is particularly pertinent to those abstinent, treatment seeking individuals. In addiction, drug use behaviour develops various rituals around the seeking, preparation and consumption of drugs. These habitual procedures become stored in memory, in automatized action schemata  or action plans.

Encoded within these unitized memory systems are prompts such as external events (e.g. sight of a hypodermic syringe,) or internal events such as physical states (e.g. NA). Although activation of these memory structures may not be a sufficient for addicts to respond to ‘urges’, via actual drug seeking, they may stimulate approach behaviours.

Tiffany (1990) proposed “urges”, or what we call craving, are said to be associated with conscious efforts to inhibit the operation of drug use action plans (e.g. prevention of relapse or suppressive reaction to intrusive using-related thoughts). In abstinence, these “urges” involve non-automatic (i.e. conscious, effortful) cognitions that compete with automatic (unconscious effortless) drug use related plans. Thus, relapse may occur under two circumstances: when the action plan operates autonomously and when conscious processes to inhibit the action plan (thought suppression) backfire and are unsuccessful.

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We agree with Tiffany’s (1990) assertion that, like other stereotypic motor acts, some aspects of the drug-use ritual are susceptible to automatization. In fact in relation to automatic using schemas it is only the “nonautomatic” processing where cognitive resources are consciously devoted to disrupting the course of a perceive threat of relapse and prior experience of these self same affective states in the context of use that activate drug- and alcohol related memories (Bradizza, Stasiewcz, & Maisto, 1994.) and cause “craving”.

The “exhaustive and effortful” effects of “urges” (craving)  in abstinent addicts (Tiffany, 1990 p.158) may reflect consciously trying to inhibit these by thought suppression. Whereas, drug using schemas are firmly established and neurally embedded and require few resources to operate, the “abstinence plan” is poorly established and demands vigilance (i.e. attention) and effort to maintain. It is also a relatively new internal voice and not as familiar to the addict. Therefore, it not surprising that many addicts take the path of least resistance and relapse.

Addictive behaviours thus become increasingly automatic or compulsive in the addiction cycle, which supports Tiffany’s ‘cognitive’ model of automatic action plans. ‘Cravings’ are generated, in our model, by non-automatic, cognitive processes which are invoked to thwart (or interfere) with these drug use action plans.

For example, in abstinent addicts, internal stress/emotional distress provokes automatic action plans (and accompanying intrusive thoughts). These individuals then use non-automatic processing i.e. cognitive control/thought suppression) to ‘fight’ these threatening (naturally occurring) automatic thoughts.

The anterior cingualte cortex (ACC) acts a gateway between what is known as explicit (hippocampal) memory (remembered knowledge about things – e.g. where we drank, with whom, how it felt, noises, smells, atmosphere and ourselves in those situations etc) and implicit (dorsal striatal)  memory (the procedural, how to do memory-  the habitualised procedure of Tiffany’s automatic addiction action plans). The dorsal medial striatum (DMS) plays an important part orchestrating the switching between these memories through a “hippocampal-to-striatal pathway” passing through the ACC (41). It may be ACC hypofunctioning, under extreme stress, which aids transition between explicit and implicit memory networks (42).

Addiction severity is suggested as being represented by a shift in reward processing from ventral stiatum (VS) to DS (28) with this marked by an emergence of automatic thoughts, which the authors suggested as the cognitive thoughts and images of automatized drug action schemata (Tiffany 1990). As addiction escalates there appears to be a greater reliance on implicit rather than explicit (hippocampal) memory too. Also emotional distress is known to recruit the DS region also. So in effect the DS becomes involved in memory, reward and affect in later addiction.  So emotional dysregulation will not only provoke intrusive thoughts, but activate automatic approach behaviour, i.e. will prompt a movement towards getting and consuming drugs and alcohol.

Modell et al, 1992, distinguished between  intrusive thoughts – and memories – in a cognitive component to craving and in compulsions, which is more motoric and action component –  the cognitive component may be governed by the dorsal medial which has connections with the ‘associative’ PFC and lateral DS which is more involved in habitual motor activity As we have already discussed, addiction severity corresponds with the extent of obsessive thoughts as measured by the Obsessive Compulsive Drinking Scale (OCDS) which suggest that as the severity of this illness progresses, so does the intensity of the obsessive thoughts about alcohol and the compulsive behaviours to use alcohol. Kranzler et al. (1999) showed relapsers who scored higher in ‘obsessions’ craving measured by the OCDS predicted relapse in the 12 months after treatment completion. It is tempting to ad that emotional dysregulation also worsens as addiction becomes more severe(  ).

‘Cravings’ are thus generated by non-automatic, cognitive processes which are invoked to thwart (or interfere) with these drug use action plans.  The DMS may be very important in the relapse mechanism we are about to explore.

The DMS may have a potential role in cognitive control of behaviour flexibility and mediating behaviours by hippocampal guidance. As such the DMS and DLS may either compete (Misumori, Yeshenko, Gill and Davis, 2004) or cooperate (Devan, MacDonald, White 1999) under different conditions.  For example, DMS may be activated when a reversal of a previously reinforced response, i.e. habitual response, is required (Eichenbaum et al, 1989). Thus in attempting to inhibit stimulus response, i.e. the automatic alcohol approach behaviour of the DLS,    the DMS activates action-outcome pathways

Thus the ‘cognition and imagery of automatized schema’ becomes increasingly obsessive as the consequence of the anterior cingulate cortex (ACC) detecting conflict between memory intrusions and alerting the prefrontal cortex (PFC) to actively suppress unwanted thoughts (169). This only serves to intensify these thoughts as thought suppression ‘rebounds’ unwanted thoughts more intensely and prolifically into consciousness (170).

This, in abstinent addicts, appears to make the situation worse leading to greater stress reactivity and  need to further inhibit habitual response which activates even more action-outcome memory, e.g. the automatic activation of mental representations in associated memory networks of what course of action has normally been followed to affect the outcome of reducing this distress, i.e. which normally has been to drink.

Whereas the DMS normally in adaptive processes competes with the DLS to resolve a situation, for the abstinent addict, it only increases the problem by suggesting solutions which in fact make the situation more acutely adverse.

For the addict attempting to maintain abstinence, declarative memory and controlled processes may often be “corrupted” in service of promoting or rationalizing drug use. This will occur because negative affect is aversive and intrinsically primes escape and avoidance strategies.

Thus the ACC in recruiting explicit memory to counteract the automatic alcohol related thoughts of the DS may unwittingly be increasing memories of drinking and explicit prompts to drink as this is what has normally been the course of action in such situations of negative emotions.

The best and most well-intentioned efforts to remain sober/clean threaten sobriety most; producing a mnemonic ‘Hydra Effect’ whereby attempts to cut off this terrible flowering of intrusive thoughts leads to increased proliferation of these thoughts and accompanying emotional distress.

 

This, we posit, is what occurs in the mind of a recovering/abstinent alcoholic and is more akin to the “mental obsession” of the Big Book that purely neurobiological/physiological urge states.

Equally it should be noted that craving or mental obsession does not suggest that the alcoholic or addict in recovery/abstinence is actually motivated or even wants to relapse to former use. One can engage in this “mental obsession” or cognitive craving simply via a maladaptive emotional dysregulation whereby a defective emotional strategy such as thought suppression of threatening intrusive thoughts can set up a chain of reactions which lead to an unfortunate proliferation of thoughts and memories which promote alcohol and drug use to relieve escalating emotional distress which leads to relapse even if the alcoholic or addict in recovery did not even wish it! What else is this other than a craving beyond one’s mental (cognitive) control!

Relapse can happen to an alcoholic or addict if he does not manage his underlying condition of emotional dysregulation, in other words.

 

 

References (to follow)

1. Cheetham, A., Allen, N. B., Yücel, M., & Lubman, D. I. (2010). The role of affective dysregulation in drug addiction. Clinical psychology review30(6), 621-634.

2. Sanchez-Craig, M., Annis, H. M., Bronet, A. R., & MacDonald, K. R. (1984). Random assignment to abstinence and controlled drinking: evaluation of a cognitive-behavioral program for problem drinkers. Journal of consulting and clinical psychology52(3), 390.

3. Lowman, C., Allen, J., Stout, R. L., & Group, T. R. R. (1996). Replication and extension of Marlatt’s taxonomy of relapse precipitants: overview of procedures and results. Addiction91(12s1), 51-72.

4. Tiffany, S. T. (1990). A cognitive model of drug urges and drug-use behavior: role of automatic and nonautomatic processes. Psychological review97(2), 147.

5. Bottlender, M., & Soyka, M. (2004). Impact of craving on alcohol relapse during, and 12 months following, outpatient treatment. Alcohol and Alcoholism39(4), 357-361.

6. Ingjaldsson JT, Laberg JC, Thayer JF. Reduced heart rate variability in chronic alcohol abuse: relationship with negative mood, chronic thought suppression, and compulsive drinking. Biological Psychiatry. 2003;54(12):1427–1436.

7.  Hoyer, J., Hacker, J., & Lindenmeyer, J. (2007). Metacognition in alcohol abusers: How are alcohol-related intrusions appraised?

 

. Bradizza, C. M., Stasiewicz, P. R., & Maisto, S. A. (1994). A conditioning reinterpretation of cognitive events in alcohol and drug cue exposure. Journal of Behavior Therapy and Experimental Psychiatry, 25, 15 – 22

Modell, J. G., Glaser, F. B., Cyr, L. & Mountz, J. M. (1992) Obsessive and compulsive characteristics of craving for alcohol in alcohol abuse and dependence. Alcoholism: Clinical and Experimental Research, 16, 272–274.

. Kranzler, H. R., Mulgrew, C. L., Modesto-Lowe, V. and Burleson, J. A. (1999) Validity of the obsessive compulsive drinking scale (OCDS): Does craving predict drinking behavior? Alcoholism: Clinical and Experimental Research 23108–114.

(Misumori, Yeshenko, Gill and Davis, 2004)

(Devan, MacDonald, White 1999)

(Eichenbaum et al, 1989).

Is the “mental obsession” of the Big Book relative to how severe your addiction is?

Involuntary retrieval of drug related thoughts is a hallmark of addicted populations.

Intensity of obsessive thoughts about alcohol predict relapse rate (1), with addicts motivated to use drugs to “silence” obsessive thoughts (2).  The idea that abstinence automatically decreases alcohol-related thoughts is challenged by research (3) and supported by clinical observation that among abstinent alcohol abusers, alcohol-related thoughts and intrusions are the rule rather than exception (4).

Modell and colleagues (1992) highlighted symptomatic similarities between addiction and obsessive compulsive disorder with subjective craving for drugs or alcohol characterized as having obsessive elements. (eg, the compulsive drive to consume alcohol, recurrent and persistent thoughts about alcohol, and the struggle to control these drives and thoughts) similar to the thought patterns and behaviours of patients with obsessive-compulsive illness (5).

Modell et al. also point to the potential similarities in underlying neural pathways implicated in the two disorders, suggesting that they may share a similar aetiology. The Obsessive Compulsive Drinking Scale (OCDS) implies that as the severity of this illness progresses, so does the intensity of the obsessive thoughts about alcohol and the compulsive behaviours to use alcohol.

Kranzler et al. (1999) showed relapsers who scored higher in ‘obsessions’ craving measured by the OCDS predicted relapse in the 12 months after treatment completion (6).

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This may also be a reflection of addiction severity too! As addicts and alcoholics become more addictive brain imaging shows a shift in “reward processing” from the ventral striatum to the dorsal striatum. The DS is in charge of more automatic, compulsive reaction.  This shift from VS to DS  may also be marked by an increased emergence of automatic thoughts, which the authors suggested as the cognitive thoughts and images of automatized drug action schemata (2).

In fact, this is demonstrated by correlations indicating that dorsal striatum activation is lowest in participants with low OCDS scores. This means, in simple terms, that more severe addiction may be associated with more intrusive/obsessive thoughts and less severe with less thoughts.  

 

References 

 

1.. Bottlender, M., & Soyka, M. (2004). Impact of craving on alcohol relapse during, and 12 months following, outpatient treatment. Alcohol and Alcoholism39(4), 357-361.

2. 6. Tiffany, S. T. (1990). A cognitive model of drug urges and drug-use behavior: role of automatic and nonautomatic processes. Psychological review97(2), 147.

3. Caetano, R. (1985). Alcohol dependence and the need to drink: A compulsion? Psychological Medicine,
15(3), 463–469.

4. Hoyer, J., Hacker, J., & Lindenmeyer, J. (2007). Metacognition in alcohol abusers: How are alcohol-related intrusions appraised?. Cognitive Therapy and Research31(6), 817-831.

5. Modell, J. G., Glaser, F. B., Mountz, J. M., Schmaltz, S., & Cyr, L. (1992). Obsessive and compulsive characteristics of alcohol abuse and dependence: Quantification by a newly developed questionnaire.
Alcoholism: Clinical and Experimental Research, 16, 266-271.

6. Kranzler, H. R., Mulgrew, C. L., Modesto-Lowe, V. and Burleson, J. A.
(1999) Validity of the obsessive compulsive drinking scale (OCDS): Does craving predict drinking behavior? Alcoholism: Clinical and Experimental Research 23, 108–114.

7. Vollstädt‐Klein, S., Wichert, S., Rabinstein, J., Bühler, M., Klein, O., Ende, G., … & Mann, K. (2010). Initial, habitual and compulsive alcohol use is characterized by a shift of cue processing from ventral to dorsal striatum.Addiction105(10), 1741-1749.

 

 

Do I still have an “Alcoholic Mind”!?

When I first came into recovery I used to get frightened by other abstinent  alcoholics proclaim that they were so glad they did not get the “wet tongue” when they saw alcohol or people drinking alcohol.  I used to feel ashamed as I did have an instantaneous “wet tongue” or mild salivation (Pavlovian response) and still do  years later when I see people drinking alcohol. Is this a “craving” for alcohol, do I still want to drink? Do I still have an “alcoholic mind?“. Did I do my steps properly?

It used to churn me up, these so-called alcoholics who had no physiological response to alcohol-related “cues”.

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

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

What I have discovered is that I have an “alcoholic brain” and not a “alcoholic mind” and there is a huge difference. So if there are people out there relatively new to recovery, listen up. For chronic alcoholics there is an automatic physiological response when we see cues such as other people drinking. Mild salivation, quickening heart rate etc. These are automatic, habitual, it happens to us rather than us wanting or willing it to happen. It happens unconsciously without our say so!

If you get a “wet tongue” i.e. you mildly salivate, then this is what happens when you have crossed the line into chronic alcoholism. Loads of studies have shown there is this automatic response and have also shown there is also an attentional bias to alcohol cues. We notice alcohol cues in the environment before anything else. They have a heightened “noticeableness”.

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

Some researchers in science call this a craving. I disagree. I call this an physiological urge, distinct from craving. I think a craving is more akin to a “mental obsession” about alcohol. Alcohol has only had ‘luring’ effect on me while very emotional distressed or in the early days of recovery I was very scared that  I would drink but, looking back, I never had any desire to.

It is hugely important for recovering persons that we distinguish between urges and craving, in a clear manner that science seems to have been unable to do! Lives can depend on this. We are so vulnerable in early recover that we need sound direction on what is happening to us automatically and what we are encouraging to happen, consciously.

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

Let me explain. If I have an urge and it becomes accompanied by automatic intrusive thoughts such as a drink would be nice, and maybe a suggestion on where to get this drink, this does not mean I want a drink. It is simply automatically prompted intrusive thoughts, the type of thought I used to get all the time and so became habitual, stored away in an automatized addiction schema or addiction action plan.

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

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

If I consciously engage, emotionally react, to these thoughts either because I want a drink (elaboration of these thoughts as in embellishing a desire state) or the thought scares the life out of me (averse reaction) I can end up in a mental obsession. If in recovery, we try to suppress these thoughts then they will come back stronger than before which will raise  already high stress levels and recruit a whole host of memories of why I should drink, with who, where, and how much I will enjoy it. They will also activate an Alcoholic Self Schema (different to the recovery self schema still being formed in early recovery).  Then I have a memory Hydra effect where attempting to suppress this terrible flowering of desire based memories or to cut off the heads of these thoughts and memories leads to them increasing and increasing.

 

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Then there are lots of these memories driving you crazy and scaring the life out of you.  And this is in someone who does not want to drink but wants to remain in recovery!!? The other guy who is embellishing these thoughts is kinda thinking about drinking or toying with the possibility, so but again he is reacting cognitively and consciously to these intrusive thoughts. He is elaborating on them. He is using a different more cognitive part of the brain and a different memory system to those activated when he was simply having unconscious, habitual, automatic intrusive thoughts. He is now involved in this process rather than it simply happening to him.

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

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

As we will see in later blogs, stress and cues certainly do not mix but again there is still a cognitive-emotional reaction which mediates between an urge and a relapse!

What is craving – do neurobiological accounts explain relapse in recovering alcoholics? Pt 2

If you want to drink, you will. It you do not, and depending on your regulation of emotions and stress, you may still relapse, even if one never intended to drink again.

In our previous blog we looked at automatic physiological response to cues that alcoholics appear to experience. These habitual responses are well explained by reinforcement, conditioning or neurobiological models of addiction.

However, do these neurobiological models predict relapse in abstinent alcoholics and addicts? In other words, do recovering alcoholics act and react to cues and have the same attentional bias, i.e. are they lured siren-like to alcohol or drug cues like lemmings to a drink or a drug or are there more  cognitive-affective processes at work in the craving than these models suggest!?

Does the mind play a role in transmuting these physiological urges into “craving”.

When I have seen a new comer to recovery craving they do not seem to walk around like a robot, salivating and rubbing their sweaty hands together. I have seen that when I was in active drinking and was like that innumerable times myself while under the spell of this “fleshy hunger” called having a pathological urge for a drink.

I am not downplaying this urge state, it is quite horrendous, it is like craving a glass of water after days in the desert. It feels like your very life depends on it, in other words. It can be a life or death feeling.

 

PowerPoint Presentation

In recovery, this urge state becomes more complicated and various other brain regions may become involved in this “craving” and there may be a interplay between regions rather than regions simply acting in concert – we will explore this more in series 3 of this theme of “craving”.

For now we examine how well do neurobiological accounts (i.e. accounts which focus primarily on impairments in neurotransmitter and stress systems and brain function in areas which create a cascade of ‘knock on’ impairment and dysfunction in areas of the prefrontal cortex which deals with cognitive control of behaviour with resultant dysfunction in areas which deal with reward, motivation stress and emotional response and more motoric, habitualized action) predict behaviour in abstinent, treatment seeking individuals?

Here we simply consider how well aspects of these theories, such as the ideas relating to craving (urge) via cue reactivity (an attentional bias towards alcohol and drug associated cues in the environment)  and positive memory associations for previous alcohol or drug use, relate to, or are relevent to the experiential reality of everyday recovering alcoholics and addicts.

In simple terms, it is the duty of science to attempt to predict behaviour, so how well do these models, especially the positive reinforcement model, predict the behaviour of treatment seeking abstinent alcoholics and addicts. 

Factors in relapse

Cues, external especially, which is a central part of positive reinforcement models, seem to be only one of various factors in relapse. They are present in a relatively small minority of studies or interact with other variables such as stress and negative affect (NA). So how well does this then validate this theory of addiction, when it is only present in a minor way in relapse and usually alongside stress and NA. Does this mean it plays a role when interacting with these variables of stress/NA. Does it play a role on it’s own?

I forward this question because the looking at an alcohol cue by an alcoholic even in recovery/abstinence invokes stress reactions such as anxiety or negative emotions such as anger, sadness ( ). Can we say there is a non-stress influenced cue-reactivity? Is there a purely dopaminergic cue reactivity? It doesn’t appear so.

In fact moving on from noting this intrinsic stress response in cue reactivity, various studies show that the highest high-risk relapse situations are negative emotions, testing personal control, social pressure, and urge and temptations  (1), that 62 –73% of relapse episodes were due to negative emotion and social pressure. Heroin addicts relapse primarily because of NE and lack of social supports. Mood state, along with social isolation and family factors, was more likely to be related to relapse incidences with a positive correlation between NE and alcohol-seeking behaviour. Thus the most commonly cited reason for relapse was negative mood states, consistent with previous studies of relapse factors (2).  Also reasons for relapse did not differ in relation to the primary drug of dependence (alcohol, methamphetamine, heroin), reflecting the commonality of relapse processes across diverse types of substances.

Marlatt (3,4) , views relapse as an unfolding process in which resumption of substance use is the last event in a long sequence of maladaptive responses to internal or extemal stressors such as negative emotional states, interpersonal conflicts, and social pressures. In fact negative emotional states ….coping, self-efficacy and stressful life events appeared to be of greater import in determining relapse than ‘cues’.

It would appear that cue associated stimuli plays a minor role in relapse, with stress and NA appearing to be a more important determinant of relapse. So conditioning models do not appear to give a comprehensive account of relapse and this may be particularly the case in abstinent, treatment seeking alcoholics.

How does conditioning methodology adequately explain this group?

Attentional Bias

Do treatment seeking alcoholic have the same attentional bias as non treatment seeking active alcoholics?

In fact, studies seem to show a negative attentional bias in alcohol-dependent patients that may be interpreted as an avoidance of alcohol-related stimuli.

Townshend and Duka (2007) propose that treatment seeking individuals have established active avoiding strategies and  are able to disengage their attention from alcohol cues (5). In fact is suggested that a positive attentional bias towards alcohol cues occurs when stimuli were presented shortly (50 ms), followed by a disengagement from alcohol cues in the 500 ms interval of cue presentation. This corresponds with a cognitive model of craving of Tiffany (6) where the 50ms may represent automatic approach before this automatic bias is interfered with by cognitive control, perhaps resulting in ‘craving’.

Does this visual approach–disengagement pattern reflect an  attentional bias which is appetitive or threat based? If there is avoidance are cues similar as  seen as in those with trait anxiety who have attentional bias for threat-related cues (7). A large body of evidence indicates that aversive emotional states are associated with biases in cognitive processing and, specifically, with increased attentional processing of threat-related cues.Is this also how treatment seeking addicted individuals are responding to substance-related cues? It may that stress heightens the salience of attractiveness of the cues so that abstinent individual relapse because of stress based response which makes relapse via internal and external cues a solution to their chronic stress/emotional distress?

Or it may be that relapse is based on difficulties coping with the manifestation of chronic stress, emotional distress and that  relapse  is a more complicated process than simply being lured, siren-like, to relapse via cues.

In most of the relapses we have encountered it has been a ongoing build up to relapse. There has been a period of emotional dyregulation whereby individuals get more and more distressed, often in inter-personal relationships, and have a “to hell with it!” relapse to relieve escalating emotional distress and the distorted thinking that goes with it. It is not due to automatic or motoric proceses, it is mediated via affective-cognitive mechanisms and this is why the information processing model, with some modifications, appears to explain craving and relapse more satisfactorily.

If you want to drink, you will, it you do not, and depending on your regulation of emotions and stress, you may still relapse, even if one never intended to drink again, due to the torturous intrusive thoughts which accompany this cognitive and emotionally based “craving”, more akin to the “mental obsession ” of AA’s Big Book than purely physiological urges.

References

1. El, S., Salah El, G., & Bashir, T. Z. (2004). High-risk relapse situations and self-efficacy: Comparison between alcoholics and heroin addicts. Addictive behaviors29(4), 753-758.

2.  Hammerbacher, M., & Lyvers, M. (2006). Factors associated with relapse among clients in Australian substance disorder treatment facilities. Journal of substance use11(6), 387-394.

3. Marlatt, G.A. (1978) Craving for alcohol, loss of control and relapse: Cognitive behavioural analysis. In: Nathan, P.E., Marlatt, G.A., and Loberg, T. eds. Alcoholism: new directions in behavioural research and treatment. Plenum Press, New York, 271-314.

4. Marlatt, G.A., and Gordon, J.R. (1985). Relapse prevention: maintenance strategies in the treatment of addictive behaviors. Guilford  Press, New York.

5. Townshend JMDuka Attentional bias associated with alcohol cues: differences between heavy and occasional social drinkersPsychopharmacology (Berl)2001;157:6774.

6. Tiffany, S. T. (1990). A cognitive model of drug urges and drug-use behavior: role of automatic and nonautomatic processes. Psychological review97(2), 147.

7.  Bar-Haim, Y., Lamy, D., Pergamin, L., Bakermans-Kranenburg, M. J., & van IJzendoorn, M. H. (2007). Threat-related attentional bias in anxious and nonanxious individuals: a meta-analytic study. Psychological bulletin133(1), 1.

8.  McCusker CG  Cognitive biases and addiction: an evolution in theory and methodAddiction 2001;96:4756.