negative affect

“I don’t know how I feel, therefore I act!”

Posted on by alcoholicsguide

One of my pet hates in experimental study is researchers suggesting that one can generalise findings from a non-clinical group of participants in a particular study to a clinical  group, not in the study. For example, most studies in Psychology and in Neuroscience are conducted on very well informed, healthy undergraduate Psychology students with the suggestion that the findings will also be seen in a clinical groups such as alcoholics or addicts. That the findings have ecological validity, they will also be observed in the reality of addicts in real everyday life.

Obviously this is very controversial. How can you one really say that brain processes in a perfectly healthy undergraduate psychology student are similar to those suffering from a mental disorder such as addiction?

It is clear that the behavioural responses of someone with an addictive disorder will be different to those with a perfectly healthy adaptive brain and adaptive behavioural choices. The point of addiction, is that individuals with an addictive disorder often make maladaptive choices and make poor decisions as many brain processes and mechanisms have become chronically impaired. They tend to choose now over then, be very emotional reactive, use “fight or flight” responding to situations rather than reflective, evaluative, goal-directed, action-outcome type of thinking…the list goes on and on, believe me!

In other words, they tend to act in a very different way to healthy undergraduate studies!

I do not have a problem with using undergraduate studies but please do not attempt to generalise findings to a clinical group, or in other words, a group suffering a psychiatric disorder. It is like saying that a study observed in healthy 19-20 year olds could also be said to exist or occur in middle aged schizophrenics? Most rational people would view this as quite peculiar, to say the least. So why do this very same thing with those suffering another mental disorder, called addiction?

 

lab-rat

So why do it at all, use students as participants? Well the study I refer to in this blog shows why using a student sample may have utility. If nothing else this sampling of students provides a control group – that is a group that can act as a “healthy” group compared to a later study  which has used a clinical group as participants. This way we can compare results to observe differences in both sample groups and this can highlight fundamental differences (and sometimes similarities) in healthy and clinical groups and may help highlight specific difficulties which may need to be considered in treating these clinical groups.

Also, and importantly for our overall discussion, through many of our blogs thus far,  regarding the role of emotional processing deficits in impulsivity and decision making deficits in addiction, this type of study can look at “proof of concept” which can then be studied in clinical groups such as those with addictive disorders.

But one must also have the proviso that generalising to this clinical group is not without it’s pitfalls. Just because a certain behavioral manifestation is seen in one healthy group, which has also been seen in a more severe from in a clinical  group , it does not follow that this severity is simple down to using a substance more chronically.

Severity may also be a function of genetic expression within a specific type of environment, e.g. a genetic vulnerability in an “at risk” son of an alcoholic reared in a emotionally abusive background may be a main reason for certain behavioural manifestation rather than simply chronic substance use. Altered stress systems may represent in a similar manner to the chronic toxic effects of chronic drug use but not actually be driven by the same mechanisms or underlying processes.

Regardless on these many sensible caveats, it is still possible to look at certain psychological  traits and relate them to certain behaviours before testing whether these are also observed in a clinical  group such as those with addictive disorders.

The study we refer to here (1) used a large sample of 429 undergraduate students and examined the nature of the relationship between alexithymia and impulsivity.  “Alexithymia is a multifaceted personality construct that is characterized by difficulty identifying and describing feelings  (Taylor, 2000). Alexithymia is associated with a range of disorders, many of which are associated with poor impulse control (Parker, Wood, Bond, & Shaughnessy, 2005; Thorberg, Young, Sullivan, & Lyvers, 2009).
The development of emotional awareness and skills to express feelings are strongly linked to cognitive development because humans use language to identify and express their feelings. According to Taylor, Bagby, and Parker (1997), all individuals have emotions (i.e., neurophysiological arousal), but how we feel the emotions differ
based on our subjective cognitive understanding and experiences.
Without adequate words to describe various neurophysiological stimuli, we cannot feel (identify and describe) them accurately and precisely, and thus we have difficulties regulating our behaviors that follow the emotions (Lane & Schwartz, 1987; Taylor et al., 1997).
The emotional awareness theory presented by Lane and Schwartz (1987) has provided some explanations for the development of alexithymia (Taylor, 2000; Taylor et al., 1997). According to this theory, individuals with alexithymia are considered to be on the first two levels of emotional awareness (i.e., sensorimotor reflexive and sensorimotor enactive) as their abilities to cognitively identify
various feelings precisely by recognizing specific physiological signs of emotions are not yet fully developed (Taylor et al., 1997).
Perhaps, lack of cognitive representations for neurophysiological stimuli may make individuals with alexithymia distressed…and thus they may use alcohol to alleviate their discomfort (Kauhanen et al., 1992; Thorberg et al., 2009; Uzun, 2003)… impulsive individuals tend to rely on reflexive affective (emotional) processes rather than on reflective cognitive processes, to lead their behaviors (Lieberman, 2007; Metcalfe & Mischel, 1999)… impulsivity and alexithymia research emphasize the necessity of using reflective and sophisticated cognitive processes in order to
better regulate emotions and behaviors (Carlson, 2007; Cyders & Smith, 2008)… it is plausible that alexithymia and impulsivity are related under a higher order structure, namely neuroticism, and thus they robustly predict behaviors associated with emotion dysregulation.

This study demonstrated that individuals with alexithymia are more likely to act impulsively when experiencing heightened negative affect…and thus engage in more drinking or experience more negative consequences after drinking.

2013-05-en-Rat-Park-09

 

These results support the use of treatment models that emphasize awareness of feelings and psychological mindfulness as these treatment approaches help clients learn to identify and acknowledge their feelings first, in order to learn how to better regulate them. The results indicate that deficits in the cognitive representation of emotional experience may contribute to impulsive action when emotionally aroused. The current findings may help explain why alexithymia has been identified
as a risk factor for many psychological problems that involve emotional and behavioral regulation deficits, including substance use related disorders (Kauhanen et al., 1992; Troisi et al., 1997).”

Essentially this study on undergraduates has observed similar findings as seen in addicted individuals but this does mean the findings generalise. It means that there is theoretical utility in further exploring this link between emotional processing deficit, alexithymia, the psychological trait of impulsivity and the behavioural manifestation of chronic addiction. Finally it may also be possible by scrutinizing results to identify key differences between these two samples which may aid treatment, intervention and even prevention. We have often mentioned that prevention may in the future involve the identification of emotional processing and regulation deficits in “at risk” children and helping them process emotions more adaptively and effectively.

Addiction seems even more tragic if one considers addiction as the consequence of processes that could possible be rectified or improved in early childhood. Emotional dysregulation heightens the effects of drugs and alcohol also and sets up a viscous cycle of use that often leads to chronic addiction.

It may be the source or rather the heart of the problem.  Prevention would then need to act at the heart of this disorder.

 

References

Shishido, H., Gaher, R. M., & Simons, J. S. (2013). I don’t know how I feel, therefore I act: alexithymia, urgency, and alcohol problems. Addictive behaviors, 38(4), 2014-2017.

Explaining the negative consequences of Negative Urgency.

Posted on by alcoholicsguide

Explaining how negative Negative Urgency can be.

from Inside the Alcoholic Brain by alcoholicsguide

In various blogs we have suggested that one of the main aspects of addictive behaviours is to act as the result of distress-based impulsivity or negative urgency. Here we explore in more details what we mean by that term negative urgency.

Here we borrow from one article (1) which has an excellent review of  negative urgency (1).

The experience of emotion facilitates action. It has long been recognized that emotional processing appears to prepare the body for action (Frijda, 1986; Lang, 1993; Saami, Mumme, & Campos, 1998). In fact, to emote means, literally, to prepare for action (Maxwell & Davidson, 2007). Researchers have theorized that the relationship between emotional experiences and actions involve activation of the motor cortex by limbic structures (Morgenson, Jones, & Yim, 1980).

Some investigations have used neuroimaging techniques to document increased activity in motor areas of the brain during emotional processing (Bremner et al., 1999; Rauch et al., 1996), and nonhuman studies suggest the emotion-action interface may involve connections between the amygdala and the anterior cingulate cortex (ACC: Devinsky, Morrel, & Vogt, 1995).

Hajcak et al. (2007) found that emotionally arousing stimuli increase motor cortex excitability. The authors theorized that there may be individual difference in emotional reactivity that may relate to differences in the amount of activation of the motor cortex areas.

One takes action to meet the need identified by the emotion.Pinker (1997) makes this point by noting that “Most artificial intelligence researchers believe that freely behaving robots . . . will have to be programmed with something like emotions merely for them to know at every moment what to do next” (p. 374).

Intense emotions can undermine rational, advantageous decision making (Bechara, 2004, 2005;Dolan, 2007; Driesbach, 2006; Shiv et al., 2005). It also appears to be true that attempts to regulate negative emotions can impair one’s ability to continue self-control behaviors (Muraven & Baumeister, 2000; Tice & Bratslavsky, 2000; Tice,Bratslavsky, & Baumeister, 2001).

Thus, it is not surprising that individuals engage in other strategies to manage intense emotions that are ill-considered and maladaptive, in that they work against one’s long-term interests. For example, heavy alcohol use may be used to manage emotion. Daily diary studies of alcohol use indicate that individuals drink more on days when they experience anxiety and stress (Swendson et al., 2000).

Indeed, negative affect states have been shown to correlate with a greater frequency of many maladaptive, addictive behaviors, including alcohol and drug abuse (Colder & Chassin, 1997;Cooper, 1994; Cooper et al., 2000; Martin & Sher, 1994;Peveler & Fairburn, 1990). This pattern also is true of bulimic behaviors; individuals tend to participate in more binge eating and purging behaviors on days during which they experienced negative emotions (Agras & Telch, 1998; Smyth et al., 2007). Emotions such as shame, guilt, anger, depression, loneliness, stress, anxiety, boredom, and rejection are often cited as triggers for binge and purge episodes (Jeppson, Richards, Hardman, & Granley, 2003). For bulimic women, engaging in binge eating produces a decline in the earlier negative emotion (Smyth et al., 2007). Because actions like these do appear to reduce negative affect, they are reinforced.

Brain Pathways Related to Emotion-Based Action

Brain system involved in emotion and action -the amygdala, the orbitofrontal cortex (OFC) and its medial sector (the ventromedial prefrontal cortex, or VM PFC:Bechara, 2005), and other areas of the prefrontal cortex (PFC:Barbas, 2007). The amygdala appears to be heavily involved in the experience of negative affect; more broadly, it is thought to play a role in directing attention to emotionally salient stimuli, particularly stressful or disturbing stimuli (Davidson, 2003).

orbitofrontaler_cortex

The OFC appears to be involved in the modulation of emotion-based reactivity (Davidson, 2003).

OFC activity overrides emotional responses, apparently by providing information and a bias toward long-term, goal-directed behavior (Lewis & Todd, 2007).

Davidson and his colleagues (Davidson, 1998, 2000,2003;Davidson & Irwin, 1999; Davidson, Putnam, & Larson, 2000) suggest the experience of intense emotion, and its accompanying potential actions, is inconsistent with one’s long-term goals. The OFC, perhaps particularly the left VM PFC, provides a biasing signal to avoid immediate reward, and thus maintain one’s pursuit of one’s longer-term goals. Davidson (2003) refers to this process as affect-guided planning and anticipation: with healthy left VMPFC functioning, one gains access to the emotion associated with anticipated outcomes consistent with one’s long-term goals. The ability to do so is, Davidson argues, the hallmark of adaptive, emotion-based decision making. At times, long-term affect-guided planning is difficult: the experience of intense emotions unrelated to one’s long-term interests may disrupt processing with regard to those interests (Gray, 1999; Preston, Buchanan, Stansfield, & Bechara, 2007). But healthy functioning of the left VM PFC helps one maintain an affective connection to one’s longer-term goals, and thus plan accordingly.

Damage to the OFC, and perhaps damage specifically to the VM PFC, results in affective lability and rash action particularly in inhibiting the action of amygdaloid reactivity.

Parasagittal_MRI_of_human_head_in_patient_with_benign_familial_macrocephaly_prior_to_brain_injury_(ANIMATED)

 

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The authors of this study put forward various reasons why OFC and VM PFC damage can cause rash action – we consider these before forwarding our own ideas of why OFC/ VM PFC damage may prompt distress based impulsivity.

The OFC, perhaps particularly the left VM PFC, provides a biasing signal to avoid immediate reward, and thus maintain one’s pursuit of one’s longer-term goals. Davidson (2003) refers to this process as affect-guided planning and anticipation: with healthy left VM PFC functioning, one gains access to the emotion associated with anticipated outcomes consistent with one’s long-term goals. Activation of the left VM PFC also appears to inhibit amygdalar activity (Davidson, 1998), thus shortening the time course of the experience of negative affect and attention to stressful stimuli. Because negative affect stimulates autonomic nervous system (ANS) activity, which provides support for action in response to distress, prolonged negative affect leads to prolonged ANS arousal (Davidson, 2000). Perhaps a greater duration of ANS arousal increases the likelihood of affect-triggered action. Activity in the amygdala appears to facilitate this process.

Damage to the OFC, and perhaps damage specifically to the VM PFC, results in affective lability and rash action. Individuals with PFC damage, and with OFC damage in particular, do not; they do not appear to have the normal anticipatory affective response to potential punishment (Bechara, 2004; Bechara, Tranel, Damasio, & Damasio, 1996; Cardinal et al., 2002).

Thus, OFC damage appears to impair affective anticipation of potential risk to one’s actions.

Bechara, Damasio, Damasio, and Anderson (1994) described OFC-damaged individuals as oblivious to the future consequences of their actions, but sensitive to immediate reinforcement and punishment. Thus, their actions tend to be guided by immediate consequences only. These patients had otherwise retained their intellectual capacities, including abstract reasoning skills. They could even describe possible future consequences in realistic language. They appeared simply to lack the anticipatory affect that others have; thus perhaps lacking the affect-guided anticipation described byDavidson (2003).

The authors then  suggest that  associations between the OFC/VM PFC-amygdala system and psychopathy are  consistent with their claim of an association between this system and the urgency traits. In other words, individuals high in psychopathy have reduced VM PFC functioning, and hence lack an affective connection to the consequences of their actions. Other studies have also documented similar OFC functioning deficits among psychopaths (Blair et al., 2006; Mitchell, Colledge, Leonard, & Blair, 2002).

This model is interesting but there is not mention of stress systems in this model although the authors mention distress and negative affect but not the stress chemicals underpinning these affective manifestations.

The authors also do no mention two hugely important points we believe;

a. that this amgydaloid (hyper) activity, caused by PFC dysfunction can also “offline” PFC activity (fig.1)

b. in favour of the compulsive, emotive-motoric behaviour of the dorsal striatum which drives rash action, distress-based impulsivity or compulsivity rendering the individual remote to negative consequence of actions, although he/she may be able to explain clearly these consequences. prior to or after seeming to not consider them. It is chronic stress dysregulation in addiction that “cuts off” access to action-outcome or goal-directed parts of the brain and recruits stimulus response, implicit, “must do” action instead.

fig 1.

nihms197465f5 (1)

This we believe is the mechanism of negative urgency rather than as the authors suggest in this article, but not included, that VMPFC damage renders individuals unknowing of consequence, when rather, consequence, negative or otherwise, has been cut off by this amygdaolid activity rendering action  outcome associations remote to consciousness.  The brain acts implicitly, procedurally or in a stimulus response way to distress we believe in addictive disorders when heightened amgydaloid reactivity  is in charge of behaviour with VMPFC deficit contributing to this amgydaloid dysfunction.

An argument against simply seeing rash behaviour as the result of OFC or VMPFC damage which leads to lack of knowledge of consequence is that it does not really consider the chronic stress that accompanies addictive behaviours and which creates a near constant distress which acts in the way we describe above.

This does not mean that there is a lack of emotionally guided behaviour or action on the part of addicts. It would appear, as discussed in previous blogs, that emotional processing deficits are common in addiction and may not recruit the goal-directed parts of the brain as the authors suggest. They do not guided action or choices effectively. As a result they manifest in perhaps crude, undifferentiated or processed forms as distress signals instead and recruit more limbic, motoric regions of the brain.  Hence they are not use to anticipate future, long term consequence.

We are simply adding that as addiction becomes more chronic, so does stress and emotional distress and this appears to lead to a distress-based “fight or flight” responding to decision making that the authors have mentioned in this article but not elucidated as above. Addicts increasing appear to recruit sub-cortical or limbic areas in decision making and this is prevalent in abstinence as in active using. it is the consequence of chronic and stress dysregulation.

We suggest that this chronic stress prompts negative urgency via an hypofunctioning ACC (2) and by a “emotional arousal habit bias” as seen in post traumatic stress disorder (3) whereby chronic emotional distress increasingly during the addiction cycle comes to implicitly activate dorsal striatal responding “offlining” the PFC in a similar manner to fig. 1.

References

1. Cyders, M. A., & Smith, G. T. (2008). Emotion-based dispositions to rash action: positive and negative urgency. Psychological bulletin, 134(6), 807.

2. Li, C. S. R., & Sinha, R. (2008). Inhibitory control and emotional stress regulation: neuroimaging evidence for frontal–limbic dysfunction in psycho-stimulant addiction. Neuroscience & Biobehavioral Reviews,32(3), 581-597.

3. Goodman, J., Leong, K. C., & Packard, M. G. (2012). Emotional modulation of multiple memory systems: implications for the neurobiology of post-traumatic stress disorder.

 

Understanding Emotional Processing Deficits in Addiction – Guest Blog

Posted on by alcoholicsguide

Understanding Emotional Processing Deficits in Addiction

by alcoholicsguide

We recently blogged on how alcoholics, and children of alcoholics, have difficulty with recognizing and differentiating external signs of emotions such as facial emotional expressions, now we will consider increasing evidence that alcoholics have difficulties with identifying and differentiating internal emotional states also.

Both these areas of research point to real difficulties in alcoholics in relation to the processing of emotion.

As we shall explain below, this deficit in emotional processing has real consequence for decision making capabilities and this has an important role to play in the initiation and maintenance of substance abuse and eventual addiction.

Alexythymia and Addiction

Effective emotion regulation skills include the ability to be aware of emotions, identify and label emotions, correctly interpret emotion-related bodily sensations, and accept and tolerate negative emotions (2,3).

Alexithymia is characterized by difficulties identifying, differentiating and expressing feelings. The prevalence rate of alexithymia in alcohol use disorders is between 45 to 67% (4,5)

Finn, Martin and Pihl (1987) investigated the presence of alexithymia among males at varying levels of genetic risk for alcoholism. They found that the high risk for alcoholism group was more likely to be alexithymic than the moderate and low genetic risk groups (6).

Higher scores on alexithymia were associated poorer emotion regulation skills, fewer percent days abstinent, greater alcohol dependence severity (7). Some studies have emphasized a right hemisphere deficit in alexithymia [8,9] based on the hypothesis that right hemisphere plays a more important role in emotion processing than the left [10, 11].

Dysfunction of the anterior cingulate cortex has been frequently argued, e.g., [12], and others have focused on neural substrates, such as the amygdala, insula, and orbitofrontal cortex (see the review in [13]). All different components of the the emotional regulation  network.

These models may interact with each other and also map onto the brain region morphological vulnerability mentioned as being prevalent in alcoholics.

Magnetic resonance imaging and post-mortem neuropathological studies of alcoholics indicate that the greatest cortical loss occurs in the frontal lobes, with concurrent thinning of the corpus callosum. Additional damage has been documented for the amygdala and hippocampus, as well as in the white matter of the cerebellum. All of the critical areas of alcoholism-related brain damage are important for normal emotional functioning (14) .

One might speculate that thinning of the corpus collosum may render alcoholics less able to inhibit negative affect in right hemisphere circuits.

Alcoholics are thus vulnerable to thinning of the corpus collosum and perhaps even to emotional processing difficulties (15 ). The inability to identify and describe affective and physiological experiences is itself associated with the elevated negative affect (16) commonly seen in alcoholics, even in recovery (17.

Thus, this unpleasant experience might prompt individuals to engage in maladaptive behaviors, such as excessive alcohol consumption, in an effort to regulate emotions, or, more specifically, cope with negative emotional states (18 )

One neuroimaging study (19) looked at and compared  various models of alexithymia showing people with alexithymia showed reduced activation in the dorsal ACC and right anterior insula (AI), and suggested individuals who exhibit impaired recognition of their own emotional states may be due to a dysfunction of the ACC-AI network, given these regions’ important role in self-awareness. These studies suggest alexithymics may not be able to use feelings to guide their behaviour appropriately.

The Iowa gambling task (IGT) was developed to assess decision-making processes based on emotion-guided evaluation. When alexithymics perform the IGT, they fail to learn an advantageous decision-making strategy and show reduced activity in the medial prefrontal cortex, a key area for successful performance of the IGT, and increased activity in the caudate, a region associated with impulsive choice (20).

ep neg

The neural machinery in alexithymia is therefore activated more on the physiologic, motor-expressive level, similar to the study on children of alcoholics and thus may represent a vulnerability.

The function of the caudate is to regulate or control impulsivity and disinhibition. Individuals with alexithymia may work on the IGT impulsively rather than by using emotion-based signals. This IGT study suggests that individuals with alexithymia may be unable to use feelings to guide their behavior appropriately.

Alexithymic individuals thus may be unable to use emotion for flexible cognitive regulation. Thus, there may be dysfunction in the interaction of the aspects of the emotional response system in alexithymia with greater activation in the caudate (basal ganglia) and less activation in the mPFC in alexithymics during the IGT.

Thus alexithymics show weak responses in structures necessary for the representation of emotion used in conscious cognition and stronger responses at levels focused on action. This ties in with the blog on an emotional disease? and also  so how is your decision making? which suggested that alcoholics do not use emotion to guide decision making and rely on more motor, or automatic/compulsive parts of the brain to make decisions.

Consequently, alexithymics experience inflexible cognitive regulation, owing to impairment of the emotion guiding system. These dysregulated physiological responses over many years may result in untoward health effects such as drug addiction.

To illustrate this, one study demonstrated that patients with cocaine dependence had higher alexithymia scores compared with healthy control subjects (21).

In a study of 46 inpatients with alcohol abuse or dependence, the total TAS (Toronto Alexithymia Scale) score was significantly higher among those who relapsed after discharge than among those who did not, even when depressive symptoms were taken into account(4)

Cocaine-dependent patients also failed to activate the anterior cingulate and other paralimbic regions during stress imagery, suggesting dysregulation of control under emotional distress in these patients (22).

Instead, cocaine-dependent patients demonstrated greater craving-related activation in the dorsal striatum, a region that has been implicated in reward processing and obsessive–compulsive behaviours. The greater activation associated with alexithymia in men in the right putamen during stress is broadly consistent with earlier studies implicating the striatum in emotional motor responses.

This also corresponds to  the study of  children of alcoholics show significantly more activation in the left dorsal anterior cingulate cortex and left caudate nucleus a region associated with impulsive choice, illustrating perhaps in children of alcoholics a bias in brain decision-making systems as an underlying  elevated risk for alcoholism.

We have also suggested previously a ‘compulsive’ emotional  habit bias in endpoint addiction which reflects a stiumulus response or automatic behaviour in the face of emotional distress, which then influences an automatic decision making profile. This may be the effect of chronic drug use impacting on an inherited emotional expressive-motor decision making vulnerability seen in children of alcoholics.

In simple terms, these vulnerable individuals may recruit more automatic rather than goal-directed areas of the brain when making decisions. This would result in impulsive/compulsive decisions which do not fully consider consequences, negative or otherwise, of their decisions and resultant actions. This decision making profile would then have obvious consequences in terms of a propensity to addiction.

 

References (to be finished)

1. Naqvi, N. H., & Bechara, A. (2009). The hidden island of addiction: the insula.Trends in neurosciences, 32(1), 56-67.

2. Berking M, Margraf M, Ebert D, Wupperman P, Hogmann SG, Junghanns K. Deficits in emotion-regulation skills predict alcohol use during and after cognitive-behavioral therapy for alcohol dependence. Journal of Consulting and Clinical Psychology. 2011;79:307–318

3. Gratz KL, Roemer L. Multidimensional assessment of emotion regulation and dysregulation: Development, factor structure, and initial validation of the Difficulties in Emotion Regulation Scale. Journal of Psychopathology and Behavioral Assessment.2004;26:41–54

4. Loas G, Fremaux D, Otmani O, Lecercle C, Delahousse J. Is alexithymia a negative factor for maintaining abstinence? A follow-up study. Comprehensive Psychiatry. 1997;38:296–299.

5. Ziolkowski M, Gruss T, Rybakowski JK. Does alexithymia in male alcoholics constitute a negative factor for maintaining abstinence. Psychotherapy and psychosomatics. 1995;63:169–173.

6.  Finn PR, Martin J, Pihl RO. Alexithymia in males at high genetic risk for alcoholism.Psychotherapy and Psychosomatics.1987;47:18–21

7.  Moriguchi, Y., & Komaki, G. (2013). Neuroimaging studies of alexithymia: physical, affective, and social perspectives. BioPsychoSocial medicine, 7(1), 8.

8. Miller L. Is alexithymia a disconnection syndrome? A neuropsychological perspective. Int J Psychiatry Med. 1986;7:199–209. doi: 10.2190/DAE0-EWPX-R7D6-LFNY.

9. Sifneos PE. Alexithymia and its relationship to hemispheric specialization, affect, and creativity.Psychiatr Clin North Am. 1988;7:287–292.

10. Buchanan DC, Waterhouse GJ, West SC Jr. A proposed neurophysiological basis of alexithymia. Psychother Psychosom. 1980;7:248–255. doi: 10.1159/000287465.

11. Shipko S. Further reflections on psychosomatic theory. Alexithymia and interhemispheric specialization. Psychotherapy and psychosomatics.

12. Lane RD, Reiman EM, Axelrod B, Yun LS, Holmes A, Schwartz GE. Neural correlates of levels of emotional awareness Evidence of an interaction between emotion and attention in the anterior cingulate cortex. J cognitive neuroscience. 1998;7:525–535. doi: 10.1162/089892998562924.

13. Wingbermühle E, Theunissen H, Verhoeven WMA, Kessels RPC, Egger JIM. The neurocognition of alexithymia: evidence from neuropsychological and neuroimaging studies.Acta Neuropsychiatrica. 2012;7:67–80. doi: 10.1111/j.1601-5215.2011.00613.x.

14. Oscar-Berman, M., & Bowirrat, A. (2005). Genetic influences in emotional dysfunction and alcoholism-related brain damage.

15. Sperling W, Frank H, Martus P, et al. The concept of abnormal hemispheric organization in addiction research. Alcohol Alcohol.2000;35:394–9.

16.  Connelly M, Denney DR. Regulation of emotions during experimental stress in alexithymia. Journal of Psychosomatic Research. 2007;62:649–656

17. Stasiewicz, P. R., Bradizza, C. M., Gudleski, G. D., Coffey, S. F., Schlauch, R. C., Bailey, S. T., … & Gulliver, S. B. (2012). The relationship of alexithymia to emotional dysregulation within an alcohol dependent treatment sample.Addictive Behaviors, 37(4), 469-476.

18.  Thorberg FA, Young RM, Sullivan KA, Lyvers M, Hurst CP, Connor JP, Feeney GFX. Alexithymia in alcohol dependent patients is partially mediated by alcohol expectancy. Drug and Alcohol Dependence. 2011;116:238–241

19. Moriguchi, Y., & Komaki, G. (2013). Neuroimaging studies of alexithymia: physical, affective, and social perspectives. BioPsychoSocial medicine, 7(1), 8.

20.  Kano M, Fukudo S. The alexithymic brain: the neural pathways linking alexithymia to physical disorders. BioPsychoSocial medicine. 2013;7:1. doi: 10.1186/1751-0759-7-1.

21.  Li, C. S. R., & Sinha, R. (2006). Alexithymia and stress-induced brain activation in cocaine-dependent men and women. Journal of psychiatry & neuroscience,31(2).

22.  Sinha, R., Lacadie, C., Skudlarski, P., Fulbright, R. K., Rounsaville, B. J., Kosten, T. R., & Wexler, B. E. (2005). Neural activity associated with stress-induced cocaine craving: a functional magnetic resonance imaging study.Psychopharmacology, 183(2), 171-180.

What is craving?

Posted on by alcoholicsguide

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

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

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

Some researchers in science call this a craving. I disagree. I call this an physiological urge, distinct from craving. I think a craving is more akin to a “mental obsession” about alcohol.

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

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

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

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

This is not a craving. I have not consciously and emotionally engaged with these intrusive thoughts.

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

In my time in recovery, I have rarely heard of or witnessed  someone lured siren-like by a cue to a drink and when I have it is because he wanted to drink really, were testing their alcoholism, or that he was in huge emotional distress and went to “hell with it!”. As we will see below, stress and cues certainly do not mix but again there is still a cognitive-emotional reaction which mediates between an urge and a relapse!

In the first of a four part series of blogs we discuss “what is craving?” and consider whether the emotional dysregulation we consider to be at the heart of alcoholism and addiction also plays a role in both craving and relapse.

We start this series by considering the neurobiological accounts of craving and will then consider how well these accounts explain craving and relapse in abstinent, treatment seeking, or recovering alcoholics and addicts.

Part 1

What is craving?

Craving persists years into abstinence (1).

Precise definitions of craving have remained elusive (2-5). Two general categories are based on conditioning and cognitive mechanisms (6) but are not mutually exclusive.

A Neuroadaptive Model of Craving – Scientists believe that a gradual and, perhaps, permanent adaptation of brain function (i.e., neuroadaptation) to the presence of alcohol is a central feature in the development of alcohol dependence (7,8).

Conditioning Models – The “conditioning” models posit that cues elicit the same physiological and psychological response as drug consumption itself  with these ‘respondent’ conditioning theories predicting that responses to drug-related cues either reflect aversive abstinence symptoms or mimic drug effects  have dominated explanatory models in cue reactivity studies (9).

The definition of addiction by the American Society of Addiction Medicine (ASAM) includes the terms craving and persistent risk, and emphasises risk of relapse after periods of abstinence triggered by exposure to substance-related cues and emotional stressors (10).

This conceptualisation points to the role of substance-related cues, e.g., environmental stimuli that are strongly associated with the effects of the administration of substances and acquire incentive salience through Pavlovian conditioning, as well as stress (an internal cue), as major determinants of relapse.

The Incentive Sensitisation (IS) Model (11), addiction is the result of neural sensitisation of reward circuits (centred in the ventral striatum (VS)) by the neurotransmitter dopamine. Positive reinforcement mechanisms lead to a non-associative learning process, referred to as sensitization, in which repeated confrontation with a substance-related cue (which acts as a reinforcer) results in the progressive amplification of a response (substance seeking).

This ‘sensitisation’ or hypersensitivity may be independent of negative withdrawal symptoms or an individual’s general negative emotional state and leads to compulsive substance-seeking and substance-taking. These mechanisms of positive reinforcement leave addicts vulnerable to relapse when confronted with substance-related cues that trigger a pathological “wanting”. In short, IS produces a bias of attentional processing towards substance-associated stimuli and a pathological wanting of alcohol or substances. Sensitisation and attentional bias have been demonstrated in various studies (12,13).

Negative reinforcement model of addiction Basic negative reinforcement models pose that addictive behaviour is the consequence of persistent negative affect (NA). This NA is associated with maladaptive changes in the brain’s stress and reward circuits, which leave addicts vulnerable to cue-associated stimuli prompting a desire to relieve their negative emotional states (14).

One prominent stress-based negative reinforcement model, the Hedonic Dysregulation (HD) Model, mainly associated with Koob and le Moal (14), In sum, the HD model posits that, in substance dependent individuals,  an overactive stress  axis creates a progressive allostasis in the brain reward systems which underlies transition from substance use to addiction and creates a persistent state of NA (altered and excessive stress) and emotional reaction to “cues”. These changes continue to persist even when an addicted individual experiences a state of protracted abstinence.

Persistent NA increases their incentive salience and desire to use substances in an attempt to relieve this NA.

Evidence for the involvement of both the reward and the stress system of the brain  comes from imaging studies of addicted individuals during withdrawal or protracted abstinence, which have shown decreases in dopamine D2 receptor density (hypothesized to reflect hypodopaminergic function) (15) as well as alteration in brain stress systems, such as increase in CRF and glucocorticoids (16).

These models to me appear to be describing urges based on cues and the effect of cues with stress/emotional distress. This last one can impact on recovery and relapse mentioned in another blog.

The question remains however whether these neurobiological models predict relapse in abstinent alcoholics and addicts?

 

References 

1.  Anton, R. F. (1999). What is craving. Alcohol Research and Health, 23(3), 165-173.

2. LUDWIG, A.M., AND STARK, L.H. Alcohol craving: Subjective and situational aspects. Quarterly Journal of Studies on Alcohol 35:899–905, 1974.

3. KOZLOWSKI, L.T., AND WILKINSON, D.A. Use and misuse of the concept of craving by alcohol, tobacco, and drug researchers. British Journal of Medicine 82:31–45, 1987.

4.  KOZLOWSKI, L.T.; MANN, R.E.; WILKINSON, D.A.; AND POULOS, C.X. “Cravings” are ambiguous: Ask about urges and desires. Addictive Behaviors 14:443–445, 1989

5.  SITHARTHAN, T.; MCGRATH, D.; SITHARTHAN, G.; AND SAUNDERS, J.B. Meaning of craving in research on addiction. Psychological Reports 71:823–826, 1992.

6. SINGLETON, E.G., AND GORELICK, D.A. Mechanisms of alcohol craving and their clinical implications. In: Galanter, M., ed. Recent Developments in Alcoholism: Volume 14. The Consequences of Alcoholism. New
York: Plenum Press, 1998. pp. 177–195.

7. Robinson, T.E., & Berridge, K.C. (1993). The neural basis of drug craving: An incentive-sensitization theory of addiction. Brain Research, 18, 247-291

8. Koob GF, Le Moal M. Drug abuse: hedonic homeostatic dysregulation. Science. 1997;278:52–58

9.  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.

10.  Morse RM, Flavin DK (1992). “The definition of alcoholism. The Joint Committee of the National Council on Alcoholism and Drug Dependence and the American Society of Addiction Medicine to Study the Definition and Criteria for the Diagnosis of Alcoholism“. JAMA 268 (8): 1012–4

11. Robinson, T. E., & Berridge, K. C. (2008). The incentive sensitization theory of addiction: some current issues. Philosophical Transactions of the Royal Society B: Biological Sciences, 363(1507), 3137-3146

12. Leyton M. Conditioned and sensitized responses to stimulant drugs in humans. Prog. Neuropsychopharmacol. Biol. Psychiatry. 2007;31:1601–1613.

13. Franken, I. H. (2003). Drug craving and addiction: integrating psychological and neuropsychopharmacological approaches. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 27(4), 563-579

14. Koob, G. F., & LeMoal, M. (2001). Drug addiction, dysregulation of reward, and allostasis. Neuropsychopharmacology, 24, 97–129.

15. Volkow ND, Wang GJ, Fowler JS, et al. Decreased striatal dopaminergic responsiveness in detoxified cocaine-dependent subjects. Nature. 1997;386:830–3.

16.. Koob GF, Le Moal M. Addiction and the brain antireward system. Annu Rev Psychol. 2008;59:29–53