thought suppression

Powerless over Thinking!

When I first came into recovery I would be plagued by intrusive thoughts about drinking, I would have thoughts about drinking, at certain times of the day in particular, on sunny days etc.

These thoughts used to greatly distress me and I would end fighting with these thoughts which only seemed to make things worse, the thoughts seem to increase rather than decrease and I got increasingly distressed.

I had no control over these thoughts and would get into a terrible emotional state over this. All before I decided it was now a good time to ring my sponsor. I always waited until I was in as much emotional pain as possible before ringing my sponsor!

I thought I could go it alone – that I did not need any help. I was in control of this.

Geez, surely I could control my own thoughts for flips sake!

Hmmm…afraid not!?

In early recovery I was as powerless over thinking as well as my drinking.

It was obvious I had lost control of my thinking like my drinking – it took a lot longer (and I still forget this even today!) to realise I have no  control over my thinking.

It chatters away regardless of my will, my wishes. It I have found is not usually a friend.

So like everything else in recovery I decided to research this! To find out why my thinking seemed out to get me, to negatively affect my recovery. To find out why my thinking did not seem to help me in recovery.

I found out that the idea that abstinence will automatically also decrease alcohol-related intrusive thoughts had 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 not 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,  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 between alcoholism 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? Misinterpretations of naturally occurring thoughts or emotional reaction to them  may be detrimental for abstinence (7).

 

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A number of papers and  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.

These efforts must be assumed to be counterproductive and  will increase rather than prevent negative feelings and thoughts, and they may even demoralize alcohol abusers who are trying to remain abstinent

On the other hand 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, such as talking to someone about them or just simply letting these thoughts go.

 

In one 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.

In other words, just let go.

This means the thoughts go, and the distress which activates them, too.

This is recovery a lo of the time.  Getting embroiled in thinking and then letting go, repeat…

That is why helping others is important  -it takes us out of our crazy heads

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.

 

How Mindfulness could help Recovery?

Mindfulness training modifies cognitive, affective, and physiological mechanisms implicated in alcohol dependence.

Posted on May 7, 2015 | Leave a comment

Yesterday we looked a how low heart rate variability in alcoholics (active and in recovery) may influence self, emotion and stress regulation, and have a limited effect on impulsivity, and result in a “locked in” attention to alcohol-related cues, all of which have obvious consequences for relapse.

Here we cite and use excerpts from an article by Eric Garland et al (1) which addresses the effects of mindfulness  meditation on those with alcohol dependence.

Although Garland suggest mindfulness could be an alternative to other treatment and recovery programs, I suggest that it can be used most effectively with other treatment and recovery programs, e.g. with step 11 of 12 step programs.

I believe the consequence of emotion dysregulation  over many years of addiction leaves behind numerous unprocessed emotions which have not been consigned to long term memory and as a result float around the mind as resentments, shame and guilt based memories etc.

Emotion dysregulation has not allowed us to consigned them properly to the past (the so-called wreckage of the past) or long term memory and only an intensive process of emotional processing these e.g. via step 4 or 5 or via an alternative stock taking of our pasts seems to resolve this problem.

I know from my previous experience of intensive meditation involving various 10 day intensive courses and meditating on a very regular basis, before realising I am an alcoholic, would always result in relapse via the distress of the past being resurgent in my mind.

Some method of addressing all of these past behaviours, which invariably have hurt someone, need to be addressed and processed, even making amends to those hurt by our previous behaviours,  before we profoundly ease the distress of the past and help facilitate a greater recovery and more effective meditation practice.

Anyway, that’s my vies, on with the article…

“When attention is fixated on visual or olfactory alcohol cues, alcohol dependent individuals exhibit significant psychophysiological reactivity (Carter & Tiffany 1999). In turn, this alcohol cue-reactivity may lead to increased craving, which can trigger alcohol consumption as a means of reducing distress. Many persons recovering from alcohol use disorders attempt to suppress cravings, which, paradoxically, can serve to increase intrusive, automatic alcohol-related cognitions (Palfai, Monti, Colby, & Rohsenow 1997), dysphoria, and autonomic arousal (Wenzlaff & Wegner 2000). Indeed, among alcohol dependent persons, thought suppression is negatively correlated with vagally-mediated heart rate variability (Ingjaldsson, Laberg, & Thayer 2003), a putative index of emotion regulation and parasympathetic inhibition of stress reactions (Thayer & Lane 2000).

As thoughts of drinking intensify and are coupled with psychobiological distress, the impulse to consume alcohol as a form of palliative coping may overcome depleted self-regulation strength (Muraven, Collins, & Nienhaus 2002; Muraven & Shmueli 2006) leading to relapse. The attempt to avoid distress or allay its impact through compulsive alcohol consumption results in negative reinforcement conditioning that may perpetuate this cycle by further sensitizing the brain to future stressful encounters via allostatic dysregulation of neuroendocrine systems (Koob 2003). Components of this risk chain may be especially malleable to targeted behavioral therapies.

One such intervention, mindfulness training, which originates from Buddhist traditions but has been co-opted by Western clinicians, has recently gained prominence in the psychological and medical literatures for its salutary effects on stress-related biobehavioral conditions (Baer & Krietemeyer 2006; Ludwig & Kabat-Zinn 2008). Mindfulness involves self-regulation of a metacognitive form of attention: a nonreactive, non-evaluative monitoring of moment-by-moment cognition, emotion, perception, and physiological state without fixation on thoughts of past or future (Garland 2007). A growing body of research suggests that mindfulness affects implicit cognition and attentional processes (e.g., Jha, Krompinger, & Baime 2007; Lutz, Slagter, Dunne, & Davidson 2008; Wenk-Sormaz 2005) as well as heart rate variability indices of parasympathetic regulation (Tang et al. 2009).

 

Mindfulness treatments may enhance clinical outcomes in substance-abusing populations.

Bowen et al. (2007) found that mindfulness training of incarcerated inmates reduced post-release substance use, substance-related problems, and psychiatric symptoms to a greater extent than standard chemical dependency services offered at the prison. Other pilot studies of mindfulness-based interventions with substance abusers have found significant reductions in distress, negative affect, stress-related biomarkers, and substance use (Marcus, Fine, & Kouzekanani 2001; Marcus et al. 2003;Zgierska et al. 2008).

To that end, a randomized, controlled design was used to compare the therapeutic effects of a mindfulness-oriented recovery enhancement (MORE) intervention to those of an evidence-based alcohol dependence support group (ASG).

We hypothesized that, relative to ASG, MORE would result in significantly greaterdecreases in perceived stress, impaired alcohol response inhibition, craving for alcohol, psychiatric symptoms, and thought suppression and significantly greater increases in mindfulness and in heart rate variability (HRV) recovery from stress-primed alcohol cues.

 

MINDFULNESS TRAINING REDUCES STRESS AND THOUGHT SUPPRESSION

Among recovering alcohol-dependent individuals, mindfulness training appears to be a potentially effective stress reduction technique. MORE reduced perceived stress to a greater extent than did ASG, which is noteworthy given that social support reduces stress reactivity and buffers deleterious effects of stressful life events (Christenfeld & Gerin 2000). The stress reduction effects of mindfulness training among nonclinical populations are well known in the literature (Grossman, Niemann, Schmidt, & Walach 2004), but it is notable that significant effects were obtained in a sample of clinically-disordered, alcohol-dependent adults with extensive trauma histories who may be more vulnerable to stress-precipitated relapse due to allostatic dysregulation of neural stress circuitry (Valdez & Koob 2004).

Like stress, thought suppression significantly decreased over the course of ten weeks of mindfulness training. In turn, decreases in thought suppression among MORE participants were significantly correlated with decreases in impaired alcohol response inhibition, raising the possibility that participants who improved their ability to regulate drinking urges may have done so via reductions in thought suppression.

In the context of alcohol dependence, thought suppression seems to enhance the conscious awareness of alcohol-related cognitions and affective reactions. MORE, with its emphasis on nonjudgmental, metacognitive awareness of present-moment experience, appeared to counter this deleterious cognitive strategy and therefore may have prevented post-suppression rebound effects from exacerbating negative affect and intrusive alcohol-related cognitions that can promote relapse.

CONCLUSION

In sum, the unwitting attempts of recovering alcohol dependent persons to suppress appetitive cognitive-emotional reactions towards alcohol may obscure these responses from consciousness only to perpetuate and intensify them within the cognitive unconscious. In the domain of unconscious mental life, automatic processes run smoothly and efficiently uninhibited by volitional control (Kihlstrom 1987). Hence, by shunting appetitive reactions into the unconscious, the alcohol dependent individual may increase the very appetitive response towards alcohol he or she is trying to suppress and exacerbate psychophysiological reactivity to alcohol cues. Mindfulness training may serve to undo this process, making unconscious responses conscious. Thus, practice of mindfulness may promote the recovery of alcohol dependent persons through: a) deautomatization of alcohol use action schema, resulting in diminished attentional bias towards subliminal alcohol cues and increased craving as a result of disrupted automaticity; and b) decreased thought suppression resulting in increased awareness of alcohol urges over time, increased HRV recovery from alcohol cue-exposure, and improved ability to inhibit appetitive responses.

Accordingly, mindfulness training may be a tractable means of promoting enduring behavior change. Although brief motivational interventions may be highly effective at impelling the desire towards sobriety, participants of such motivational enhancement therapies remain prone to eventual relapse; indeed, relapse is often a part of the recovery process. As such, interventions that consolidate short-term treatment gains into broader lifestyle change are of major significance to the addictions treatment field. During the gradual practice of mindfulness, one learns to work with negative emotions in a metacognitive context, resulting in nonreactivity to difficult mental contents and improved self-regulation in the face of stressors. The developmental process of cultivating and embedding mindfulness principles into all aspects of one’s life may solidify gains made in prior treatment and provide an effective, long-term approach to coping with stress-precipitated relapse.

Despite evidence suggesting that stress appraisal and attentional biases are key components of alcohol dependence, the form of addictions treatment most available to poor and marginalized persons, social support groups, does not target these pathogenic mechanisms directly. In contrast, practice of mindfulness may attenuate stress reactivity and thought suppression while disrupting addictive automaticity, resulting in increased awareness of craving and greater ability to cope with and recover from alcohol urges in stressful contexts. Hence, mindfulness training may hold promise as an alternative, targeted treatment for stress-precipitated alcohol dependence among vulnerable members of society.”

Equally mindfulness meditation may be used alongside other treatment regimes. For example, it can be used in a daily manner as part of step 11 in the 12 step program. It is also used as part of DBT, for example.

I think that there are ideas out there, is so-called different treatment regimes, which can simply compliment each other. Whatever works, works.

I personally meditate using both  Christian and Buddhist meditation techniques.

Sometimes appreciating the therapeutic strengths of different treatment philosophies and practice can augment one’s own main treatment and recovery program.

References

1.  Garland, E. L., Gaylord, S. A., Boettiger, C. A., & Howard, M. O. (2010). Mindfulness training modifies cognitive, affective, and physiological mechanisms implicated in alcohol dependence: results of a randomized controlled pilot trial. Journal of psychoactive drugs, 42(2), 177-192.

Christianity_Jesus_meditating_golden_light

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 Psychiatry, 54(12), 1427-1436.

 

 

 

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.

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

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 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!

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.

 

How do resentments become the Number one Offender!?

Research suggests (1) suggest individuals with poorly regulated emotions often turn to alcohol to escape from or down-regulate their emotions, creating a risk for diagnosable problems in relation to alcohol  difficulties as this impairment in emotion regulation is associated with alcohol-related disorders  and substance-related disorders (2).

Experiential avoidance of thoughts, emotions, sensations,memories, and urges can lead to a variety of negative outcomes such as problems with substance use, because it paradoxically increases negative thoughts (3)

Thus risk factors include suppression (including both expressive suppression and thought suppression), avoidance (including both experiential avoidance and behavioral avoidance), and rumination.

Emotional distress, which is chronically higher in people with emotion dysregulation, appears to potentiate (heighten) reward systems in the brain (1), and this potentiation may be even greater in individuals high in reward sensitivity, increasing the chances they will turn to alcohol. Intake of alcohol will be reinforced both by the satisfaction of high appetitive drives and by the reduction of negative emotions these individuals otherwise cannot regulate. Thus, the combination of emotional dysregulation and high reward sensitivity should be a potent risk factor for the development and/or maintenance of substance abuse and eating disorder.

Emotion dysregulation may occur if emotions are experienced as intense and overwhelming, when individuals have not learned how or when to apply effective strategies, when strategies are not applied flexibly, when the strategies fail, or when strategies are overused, emotion regulation patterns may interfere with the ability to successfully achieve goals. Emotion dysregulation still involves attempts at regulation, but the process leads to maladjustment rather than adjustment. For example, emotion dysregulation may result in poor interpersonal relationships, difficulty concentrating, feeling overwhelmed by emotions, or inability to inhibit destructive behaviors.

Components of emotional dysregulation include a tendency for emotions to spiral out of control, change rapidly, get expressed in intense and unmodified forms, and/or overwhelm both coping capacity and reasoning. (4)

Self regulatory deficits like these may emerge from an interaction of intrinsic biological factors as well as from chaotic or stressful early life experiences, particularly child abuse and problematic attachments with caregivers.

Emotional Dysregualtion may be present in  overly restricted emotional expression and avoidance or excessive emotionality and excitement seeking. This research (4) highlighted that the idea that emotional dysregualtion is a distinct construct, related to but not reducible to negative effect (anxiety, mood, negative emotions) and may be seen as the result of the developmental capacity to adaptively regulate emotions being disturbed by early disruptive experiences. In other words, abuse in early childhood can help determine how we cope with our emotions.

Maladaptive cognitive emotion regulation strategies such as rumination    (5 ) and thought suppression (6) have been linked to a number of negative psychological outcomes. Binge-eating (7), and other impulsive behaviors (8) may all be a result of emotion dysregulation.

Selby (9 ) addresses the issues of why does emotion dysregulation appear to result in behavioral dysregulation?  The connection may lay in the use of certain cognitive emotion regulation strategies (cognitive emotion dysregulation) that actually increase the intensity of negative emotions and cause an individual to engage in maladaptive behavioral emotion regulation strategies (behavioral dysregulation) in order to down-regulate these intense emotions.

In essence, the way we regulate our emotions may actually cause us to lose control of them. These are often  considered “impulsive” behaviors, without premeditation. While not a behavioral emotion regulation strategy per se, urgency may be part of what causes certain individuals to engage in behavioral dysregulation. Individuals who exhibit high levels of urgency, feeling the need to act when faced with emotional distress, may be more likely to engage in maladaptive behaviors such as substance abuse as a result of emotion dysregulation.

The best characterized cognitive emotion regulation strategy is rumination. Rumination (5) is the tendency to repetitively think about the causes, situational factors, and consequences of one’s emotional experience.  Rumination is an important risk factor for substance abuse (10)

Thought suppression is another emotion regulation strategy as is catastrophizing (11) the tendency to continuously think about how bad a situation is and the negative effects that the current situation has on the future. Using catastrophizing as an emotion regulation strategy has been found to increase emotional distress (12)

All of the cognitive emotion strategies discussed (rumination, thought suppression, and catastrophizing) appear to have a common theme: they all focus attention on emotionally relevant stimuli, usually negative.

Furthermore, evidence has shown that ruminative processes tend to amplify the effect of negative affect.

Yet the tendency to ruminate on negative emotional thoughts increases levels of negative affect, and in turn the increase in negative affect increases levels of rumination followed by a flood of racing negative emotional thoughts, which in turn increase levels of negative affect in a vicious, repetitive cycle – an emotional cascade.

As a recovering alcoholic, this rumination and catastrophizing is very similar to what we call resentments the constant resending of negative emotions and accompany thoughts, each cycle making the emotions and thoughts more distressing.

Mixed with the self elaboration we discussed in another blog, then more has a heady cocktail of distressing resentments.

As the Big Book of Alcoholics Anonymous says “resentments kill more alcoholics than anything else”

It is thus difficult to see alcoholism as anything other than a disorder of emotional regulation.

References

1. Aldao, A., Nolen-Hoeksema, S., & Schweizer, S. (2010). Emotion-regulation strategies across psychopathology: A meta-analytic review. Clinical psychology review, 30(2), 217-237.

2. Berking, M., Margraf, M., Ebert, D., Wupperman, P., Hofmann, S. G., & Junghanns, K. (2011). Deficits in emotion-regulation skills predict alcohol use during and after cognitive–behavioral therapy for alcohol dependence. Journal of consulting and clinical psychology, 79(3), 307.

3.  Hayes, S. C., Strosahl, K. D., & Wilson, K. G. (1999). Acceptance and commitment therapy: An experiential approach to behavior change. New York: Guilford Press.

4.  Bradley, B., DeFife, J. A., Guarnaccia, C., Phifer, J., Fani, N., Ressler, K. J., & Westen, D. (2011). Emotion dysregulation and negative affect: Association with psychiatric symptoms. Journal of Clinical Psychiatry, 72(5), 685-691.

5. Nolen-Hoeksema, S. (1991). Responses to depression and their effects on the duration of depressive episodes. Journal of Abnormal
Psychology, 100(4), 555–561.

6. Wegner, D. M., Schneider, D. J., Carter, S. R., & White, T. L. (1987). Paradoxical effects of thought suppression. Journal of Personality
and Social Psychology, 53, 5–13.

7.  Anestis, M. D., Selby, E. A., Fink, E., & Joiner, T. E. (2007). The multifaceted role of distress tolerance in dysregulated eating behaviors.
International Journal of Eating Disorders, 40, 718–726.

8. Whiteside, S. P., & Lynam, D. R. (2001). The five-factor model and impulsivity: Using a structural model of personality to understand
impulsivity. Personality and Individual Differences, 30, 669–689.

9. Selby, E. A., Anestis, M. D., & Joiner, T. E. (2008). Understanding the relationship between emotional and behavioral dysregulation: Emotional cascades. Behaviour Research and Therapy, 46(5), 593-611.

10. Nolen-Hoeksema, S., Stice, E., Wade, E., & Bohon, C. (2007). Reciprocal relations between rumination and bulimic, substance abuse, and depressive symptoms in female adolescents. Journal of abnormal psychology, 116(1), 198.

11. Garfnefski, N., Kraaij, V., & Spinhoven, P. (2001). Negative life events, cognitive emotion regulation, and emotional problems.
Personality and Individual Differences, 30, 1311–1327.

12.  Sullivan, M. J. L., Bishop, S. R., & Pivik, J. (1995). The pain catastrophizing scale: Development and validation. Psychological
Assessment, 7, 524–532.