alcohol related thoughts

The terror of “Locked In” Attention!

Posted on by alcoholicsguide

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 Psychiatry, 54(12), 1427-1436.

 

 

 

Alcoholics Anonymous and Reduced Impulsivity: A Novel Mechanism of Change

Posted on by alcoholicsguide

Impulsivity or lack of behaviour inhibition, especially when distressed, is one psychological mechanisms which is implicated in all addictive behaviour from substance addiction to behaviour addiction.

It is, in my view, linked to the impaired emotion processing as I have elucidated upon in various blogs on this site.

This impulsivity is present for example in those vulnerable to later alcoholism, i.e. sons and daughters of alcoholic parents or children  from a family that has a relatively high or concentrated density of alcoholics in the family history, right through to old timers, people who have decades of recovery from alcoholism.

It is an ever present and as a result part of a pathomechanism of alcoholism, that is it is fundamental to driving alcoholism to it’s chronic endpoint.

It partly drives addiction via it’s impact on decision making – research shows people of varying addictive behaviours choose now over later, even if it is a smaller short term gain over a greater long term gain. We seem to react to relieve a distress signal in the brain rather than in response to considering and evaluating the long term consequences of a decision or act.

No doubt this improves in recovery as it has with me. Nonetheless, this tendency for rash action with limited consideration of long term consequence is clearly a part of the addictive profile. Not only do we choose now over then, we appear to have an intolerance of uncertainty, which means we have difficulties coping with uncertain outcomes. In other words we struggle with things in the future particularly if they are worrying or concerning things, like a day in court etc. The future can continually intrude into the present. A thought becomes a near certain action, again similar to the though-action fusion of obsessive compulsive disorder. It is as if the thought and possible future action are almost fused, as if they are happening in unison.

Although simple, less worrying events can also make me struggle with leaving the future to the future instead of endless and fruitlessly ruminating about it in the now. In early recovery  especially I found that I had real difficulty dealing with the uncertainty of future events and always thought they would turn out bad. It is akin to catastrophic thinking.

If a thought of a drink entered into my head it was so distressing, almost as if I was being dragged by some invisible magnet to the nearest bar. It was horrendous. Fortunately I created my own thought action fusion to oppose this.

Any time I felt this distressing lure of the bar like some unavoidable siren call of alcohol I would turn that thought into the action of ringing my sponsor. This is why sponsees should ring sponsors about whatever, whenever in order to habitualize these responses to counteract the automatic responses of the addicted brain.

I think it is again based on an inherent emotion dysregulation. Obsessive thoughts are linked to emotion dysregulation.

My emotions can still sometimes control me and not the other way around.

Apparently we need to recruit the frontal part of the brain to regulate these emotions and this is the area most damaged by chronic alcohol consumption.

As a result we find it difficult to recruit this brain area which not only helps regulate emotion but is instrumental in making reflective, evaluative decisions about future, more long term consequence. As a result addicts of all types appear to use a “bottom up” sub-cortical part of the brain centred on the amgydala region to make responses to decisions instead of a “top down” more cortical part of the brain to make evaluative decisions.

We thus react, and rashly act to relieve the distress of undifferentiated emotions, the result of unprocessed emotion rather than using processed emotions to recruit the more cortical parts of the brain.

Who would have though emotions were so instrumental in us making decisions? Two parts of the brain that hold emotions in check so that they can be used to serve goal directed behaviour are the orbitofrontal cortex and the ventromedial prefrontal cortex.

120px-Orbital_gyrus_animation_small2

 

These areas also keep amgydaloid responding in check. Unfortunately these two areas are impaired in alcoholics and other addictive behaviours so their influence on and regulation of the amgydala is also impaired.

This means the sub cortical areas of the amgydala and related regions are over active and prompt not a goal directed response to decision making but a “fight or flight” response to alleviate distress and not facilitate goal directed behaviour.

128px-Amyg

 

Sorry for so much detail. I have read so much about medication recently which does this or that to reduce craving or to control  drinking but what about the underlying conditions of alcoholism and addictive behaviour? These are rarely mentioned or considered at all.

 

We always in recovery have to deal with alcoholism not just it’s symptomatic manifestation of that which is chronic alcohol consumption. This is a relatively simple point and observation that somehow alludes academics, researchers and so-called commentators on this fascinating subject.

Anyway that is some background to this study which demonstrates that long term AA membership can reduce this impulsivity and perhaps adds validity to the above arguments that improved behaviour inhibition and reducing impulsivity is a very possible mechanism of change brought about by AA membership and the 12 step recovery program.

It shows how we can learn about a pathology from the recovery from it!

Indeed when one looks back at one’s step 4 and 5 how many times was this distress based impulsivity the real reason for “stepping on the toes of others” and for their retaliation?

Were we not partly dominated by the world because we could not keep ourselves in check? Didn’t all our decisions get us to AA because they were inherently based on a decision making weakness? Isn’t this why it is always useful to have a sponsor, someone to discuss possible decisions with?

Weren’t we out of control, regardless of alcohol or substance or behaviour addiction? Isn’t this at the heart of our unmanageability?

I think we can all see how we still are effected by a tendency not to think things through and to act rashly.

The trouble it has caused is quite staggeringly really?

Again we cite a study (1) which has Rudolf H. Moos as a co-author. Moos has authored and co-authored a numbered of fine papers on the effectiveness of AA and is a rationale beacon in a sea of sometimes quite controversial and ignorant studies on AA, and alcoholism in general.

“Abstract

Reduced impulsivity is a novel, yet plausible, mechanism of change associated with the salutary effects of Alcoholics Anonymous (AA). Here, we review our work on links between AA attendance and reduced impulsivity using a 16-year prospective study of men and women with alcohol use disorders (AUD) who were initially untreated for their drinking problems. Across the study period, there were significant mean-level decreases in impulsivity, and longer AA duration was associated with reductions in impulsivity…

Among individuals with alcohol use disorders (AUD), Alcoholics Anonymous (AA) is linked to improved functioning across a number of domains [1, 2]. As the evidence for the effectiveness of AA has accumulated, so too have efforts to identify the mechanisms of change associated with participation in this mutual-help group [3]. To our knowledge, however, there have been no efforts to examine links between AA and reductions in impulsivity-a dimension of personality marked by deficits in self-control and self-regulation, and tendencies to take risks and respond to stimuli with minimal forethought.

In this article, we discuss the conceptual rationale for reduced impulsivity as a mechanism of change associated with AA, review our research on links between AA and reduced impulsivity, and discuss potential implications of the findings for future research on AA and, more broadly, interventions for individuals with AUD.

Impulsivity and related traits of disinhibition are core risk factors for AUD [5, 6]. In cross-sectional research, impulsivity is typically higher among individuals in AUD treatment than among those in the general population [7] and, in prospective studies, impulse control deficits tend to predate the onset of drinking problems [8–11]

Although traditionally viewed as static variables, contemporary research has revealed that traits such as impulsivity can change over time [17]. For example, traits related to impulsivity exhibit significant mean- and individual-level decreases over the lifespan [18], as do symptoms of personality disorders that include impulsivity as an essential feature [21, 22]. Moreover, entry into social roles that press for increased responsibility and self-control predict decreases in impulsivity [16, 23, 24]. Hence, individual levels of impulsivity can be modified by systematic changes in one’s life circumstances [25].

Substance use-focused mutual-help groups may promote such changes, given that they seek to bolster self-efficacy and coping skills aimed at controlling substance use, encourage members to be more structured in their daily lives, and target deficits in self-regulation [26]. Such “active ingredients” may curb the immediate self-gratification characteristic of disinhibition and provide the conceptual grounds to expect that AA participation can press for a reduction in impulsive inclinations.

…the idea of reduced impulsivity as a mechanism of change…it is consistent with contemporary definitions of recovery from substance use disorders that emphasize improved citizenship and global health [31], AA’s vision of recovery as a broad transformation of character [32], and efforts to explore individual differences in emotional and behavioral functioning as potential mechanisms of change (e.g., negative affect [33,34]).

Several findings are notable from our research on associations between AA attendance and reduced impulsivity. First, consistent with the idea of impulsivity as a dynamic construct [18, 19], mean-levels of impulsivity decreased significantly in our AUD sample. Second, consistent with the notion that impulsivity can be modified by contextual factors [25], individuals who participated in AA longer tended to show larger decreases in impulsivity across all assessment intervals.

References

Blonigen, D. M., Timko, C., & Moos, R. H. (2013). Alcoholics anonymous and reduced impulsivity: a novel mechanism of change. Substance abuse, 34(1), 4-12.

When fighting your neural ghosts make sure to surrender!!

Posted on by alcoholicsguide

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.

Image

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

Posted on by alcoholicsguide

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 review, 30(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 psychology, 52(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. Addiction, 91(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 review, 97(2), 147.

5. Bottlender, M., & Soyka, M. (2004). Impact of craving on alcohol relapse during, and 12 months following, outpatient treatment. Alcohol and Alcoholism, 39(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 23, 108–114.

(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?

Posted on by alcoholicsguide

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 Alcoholism, 39(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 review, 97(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 Research, 31(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.Addiction, 105(10), 1741-1749.

 

 

Don’t fight your thoughts!

Posted on by alcoholicsguide

The idea that abstinence will automatically also decrease alcohol-related intrusive thoughts has been dismissed by research and vast anecdotal evidence.

Practically all therapies for alcoholism e.g  AA, SMART and so on suggest that urges create automatic thoughts about drinking. This has been demonstrated in research that distress automatically gives rise to intrusive thoughts about alcohol. (1) This reflects emotional dysregulation as these intrusive thoughts are correlated to emotional dysregulation (2).

These thoughts to the recovering/abstinent individual can be seen as egodystonic which is a psychological term referring to behaviors, values, feelings that are in harmony with or acceptable to the needs and goals of the ego, or consistent with one’s self image.  Other conditions, such as OCD, have these egodystonic thoughts creating the distress that drives a compulsive need to act on them, rather than letting them pass. In other words, these thoughts are seen as distressing and threatening and compel one to act to reduce this escalating sense of distress. A similar process can happen to those in early recovery. Thoughts about drinking or using when you now wish to remain in recovery are egodystonic, they are contrary to the view of oneself as a person in recovery.  The main problem occurs when we think we can control these thoughts are that these thoughts mean we want to drink or are going to relapse!

Early recovery is a period marked by heightened emotional dysregulation and the proliferation of intrusive thoughts about alcohol .

In fact, empirical research demonstrates that alcohol-related thoughts can resemble obsessive-compulsive thinking (3,4).

In fact, one way to measure “craving” in alcoholics is by scale called the Obsessive Compulsive Drinking Scale (5) , thus highlighting certain similarities in pathomechanisms between alcohol and OCD.

This finding is also supported by clinical observation and leads to the expectation that among abstinent alcohol abusers, alcohol-related thoughts and intrusions are the rule rather than the exception (6)

Relatively little is known about how alcohol abusers appraise their alcohol-related thoughts. Are they aware that alcohol-related thoughts occur naturally and are highly likely during abstinence? Or do they interpret these thoughts in a negative way, for example, as unexpected, shameful, and bothersome? Answers to these questions obviously inform with implications for relapse prevention, because misinterpretations of naturally occurring thoughts may be detrimental for abstinence (7).

 

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A number of conceptual papers and empirical studies have shown that individuals’ appraisal of their intrusive thoughts as detrimental and potentially out of their control may lead them to dysfunctional and counterproductive efforts to control their thinking. Alcohol-related thoughts cause an individual to experience strong emotional reactions; however, alcohol abusers will increase their efforts to control their thinking only when they have negative beliefs about these thoughts. For instance, spontaneous positive memories about alcohol (‘‘It was so nice to hang out at parties and to drink with my buddies’’) may be appraised—and misinterpreted—as ‘‘the first steps toward a relapse’’.

Such an appraisal of one’s thoughts about alcohol as problematic may instigate thought suppression and other efforts to control the thoughts. Because these efforts must be assumed to be counterproductive (Fehm & Hoyer, 2004), they will increase rather than prevent negative feelings and thoughts, and they may even demoralize alcohol abusers who are trying to remain abstinent

If positive alcohol-related thoughts are not appraised as problematic but as a normal part of abstinence, the awareness of these thoughts might even lead to the selection of more adaptive coping responses, which could help to reduce the risk of relapse.

In the context of mental health, metacognition can be loosely defined as the process that “reinforces one’s subjective sense of being a self and allows for becoming aware that some of one’s thoughts and feelings are symptoms of an illness.”

The assumption that metacognition mediates reactions to alcohol-related cues may help to explain why “craving” does not inevitably lead to relapse.

In one reported study (8), participants who reported on their thoughts about alcohol in the previous 24 hours, 92% reported experiencing at least some thoughts about drinking that ‘‘just pop in and vanish’’ without an attempt to eliminate them. This suggests that if both suppression and elaboration can be avoided, many intrusive thoughts will be relatively transient.

An “accept and move on’’ strategy provides an opportunity for the intrusion to remain a fleeting thought.

 

References

1. Zack, M., Toneatto, T., & MacLeod, C. M. (1999). Implicit activation of alcohol concepts by negative affective cues distinguishes between problem drinkers with high and low psychiatric distress. Journal of Abnormal Psychology, 108(3), 518.

2. 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 Psychiatry, 54(12), 1427-1436.

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

4. 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(2), 266–271.

5. Anton, R. F., Moak, D. H., & Latham, P. (1995). The Obsessive Compulsive Drinking Scale: A self-rated
instrument for the quantification of thoughts about alcohol and drinking behavior. Alcoholism:
Clinical and Experimental Research, 19, 92–99.

6. Hoyer, J., Hacker, J., & Lindenmeyer, J. (2007). Metacognition in alcohol abusers: How are alcohol-related intrusions appraised?. Cognitive Therapy and Research, 31(6), 817-831.

7. Marlatt, G. A., & Gordon, J. R. (Eds.). (1985). Relapse prevention: Maintenance strategies in the
treatment of addictive behaviors. New York: Guilford Press

8. Kavanagh, D. J., Andrade, J., & May, J. (2005). Imaginary relish and exquisite torture: the elaborated intrusion theory of desire. Psychological review, 112(2), 446.