negative urgency

Inability to make fine-grained distinctions regarding negative emotions prompts impulsivity.

Posted on by alcoholicsguide

When I first came into recovery I was assigned a task which has gone on to shape much of my thinking about my alcoholism and addiction. I was prompted by my wife to sit with my emotions, that is, to sit in one place beside my wife and not suddenly get up and go elsewhere to avoid whatever emotional state consumed me, terrified me.

I have to say it was the bizarre experience. In my drinking any negative emotions would prime my thoughts towards alcohol and any increased intensity of such thoughts would practically have me skipping to the nearest drinking establishment.

Ever since I was a child, emotions were something to be avoided, tamed or feared. They were destructive, counterproductive things which somehow weakened you.

Now I was being asked to do something I had never accomplished in over thirty years. To sit with, not run from, whatever emotions starting to arise in my mind. As the first undifferentiated blobs of emotions arose I was struck my how I could not recognise them or say with any conviction what emotions they were exactly. In this undifferentiated state they felt like waves of feeling, like possessions, like being haunting by mute poltergeists!

The urge to flee these unpleasant feeling states was overwhelming. I asked my wife for help “what was happening to me!?” “What are these feeling things?”

My wife calmly said they are simply feelings, you are experiencing emotions in their entirety. It was horrible. How the hell had I not done this before, sat with my emotions instead to constantly escaping them somehow?

In fact, I am willing to say that I knew next to nothing about emotions when I arrive in recovery. These is why they have come to fascinate me and inspired my research into affective and clinical/psychiatric neuroscience.

How is it that a grown man got to this stage, to the stage where all his undifferentiated emotions propelled him into movement away from them?

The answer to this question may have been demonstrated in this study (1).

 

rumination2

“Affective functioning plays a prominent role in several etiological models of substance use (e.g., Kassel et al., 2010; McCarthy, Curtin, Piper, & Baker, 2010; Simons, Wills, & Neal, in press). These models suggest that individuals with poor affect regulation show a diminished capacity to handle intense emotion states and often rely upon maladaptive coping strategies, such as substance or alcohol use, to manage their emotions (Lavallo, 2007; Spence & Courbasson, 2012).

One factor related to emotion regulation is emotion differentiation. Emotion differentiation is the ability to make fine grained distinctions between similarly valenced emotion states (Feldman Barrett, 2004). Individuals differ greatly in their ability to differentiate their affective experiences. Some tend to describe their emotional experiences in more global terms, such as feeling “good” or feeling “bad” and find it difficult to make more subtle distinctions, while others make these nuanced differentiations easily. These differences have been shown to impact the ability to regulate emotions and consequential behaviors (Feldman Barrett, Gross, Conner Christensen, & Benvenuto, 2001; Tugade, Fredrickson, & Feldman Barrett, 2004). In support of this, emotional differentiation has been shown to moderate associations between negative emotion and alcohol consumption (Kashdan, Ferssizidis, Collins, & Muraven, 2010).

This research suggests that the inability to differentiate emotion may foster maladaptive behavior when emotionally aroused.

Hence, it is possible that the inability to differentiate emotions may
be related to urgency, defined as rash action in response to intense emotion. Along these lines, research on alexithymia, a construct related to deficits in identifying and describing emotions, shows that these deficits are positively associated with urgency, with urgency often fully mediating the relationship between alexithymia and problematic outcomes, including alcohol consequences (Gaher, Hofman, Simons, & Hunsaker, 2013; Shishido, Gaher, & Simons, 2013).

Moreover, alexithymia has been shown to mediate the relationship between childhood maltreatment (Gaher, Arens, & Shishido, 2013) as well as trauma history
(Gaher, Hofman, et al., 2013) and urgency, suggesting that deficits in
emotional understanding may underlie urgent responding.

The findings of this study (1) showed that negative emotion differentiation was associated with both negative urgency and alcohol which suggests that the inability to make fine-grained distinctions regarding the experience of negative emotions contributes to behavioral disinhibition when in a state of high emotional arousal.

References

1. Emery, N. N., Simons, J. S., Clarke, J. C., & Gaher, R. M. (2014). Emotion Differentiation and Alcohol-Related Problems: The Mediating Role of Urgency.Addictive Behaviors.

 

“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.

Feeding Distress-based action.

Posted on by alcoholicsguide

Even as I a child I had difficulties controlling my impulses and my behaviours, “I was into everything”. I did not use much forethought in decisions making and would generally react and always be after something that I wanted desperately that very moment. Now in fact!

I believe I had sugar addiction, and chocolate and playing, and girl chasing addictive behaviours way before I ever got near alcohol in my early teens, with a six month, and quite disastrous period of poker machine gambling in between. And of course you couldn’t get me off the “Space Invader” machine.  I just couldn’t get enough of anything, ever. Always wanted more, more and some more. My mother would call for me to come home in the darkening hours of evening. I had to be scraped off the playing fields in order to come home. Exhausted.

So why this constant overdoing of everything!!?

Why couldn’t I stop once in a while, ponder the consequences of my decisions, employ some, goal-directed, action-outcome type of thinking?

Following on for our very recent blog which described the neural mechanisms implicated in negative urgency we now look at at an article which attempts to  bring together some of our most consuming research interests by attempting to explain whether there is  a  link between emotional processing deficits (alexithymia)  negative urgency and dysregulated behaviours.

This study (1) looked at whether whether negative urgency (distress-based impulsivity)  would be the link in relationship between alexithymia and dysregulated behaviors.

Dysregulated behaviors have been defined as behaviors that are difficult to control, and often  result in functional impairment for the affected individual (Selby & Joiner, 2009).

An inability to understand affective and physiological experiences inherent in alexithymia might prompt individuals to engage in maladaptive behaviors in an effort to regulate emotions. One type of behavior linked to alexithymia is binge eating. Wheeler and colleagues (2005) found that alexithymia was positively correlated with binge eating in a sample of females.

Carano and colleagues (2006) found that alexithymia was positively correlated with the severity of binge eating behaviors. Additionally, Speranza and colleagues (2007) found that alexithymia predicted eating disorder treatment outcome in a three year prospective study meaning high levels of alexithymia can interfere with treatment response even more than the actual severity of the presenting problem.

 

eating-disorder

Taylor and colleagues (1990) found that 50% of substance dependent males admitted to a drug and alcohol rehabilitation program were characterized as alexithymic. Similarly, Haviland and colleagues (1988) found that approximately 50% of individuals diagnosed as alcohol dependent were characterized as alexithymic. These numbers are significantly greater than the reported prevalence of alexithymia in the general population, which has been estimated to fall between 10 and 15% (Rybakowski et al., 1988; Parker et al., 1989), and suggests that alcohol and drug abuse is another example of a maladaptive behavior that may be used to modulate negative affective states when one is incapable of doing so in an adaptive way.

Loas and colleagues (1997) conducted a one year follow-up on individuals admitted to a psychiatric facility for alcohol treatment. Results suggested that individuals who remained abstinent from alcohol use one year post-treatment had
significantly lower scores on alexithymia measures.

“Why does the lack of understanding and expression of emotions have such a powerful influence over dysregulated behaviors?” 

Why  do individuals with high levels of alexithymia who experience negative affect seem to engage in dysregulated behaviors so frequently, while other individuals may simply cry, ruminate, or develop vegetative symptoms of depression?

Is negative urgency (Whiteside & Lynam, 2001; Cyders, Smith, Spillane, Fischer, Annus, & Peterson, 2007) the mechanism through which these behaviors are developed  and sustained?     It may be that the relationship between alexithymia and behavior is explained by a tendency on the part of individuals with high levels of alexithymia to act rashly in an attempt to immediately reduce psychological and physiological sensations associated with negative affect (negative mood, negative emotions, anxiety etc).

Negative urgency could be thought the  mechanism that drives dysregulated behaviors in individuals who experience difficulty recognizing and expressing their emotions.  

eating-disorder-clinic-300x250

The authors (1) concluded that when faced with negative affect, many individuals are able to recognize and process their emotions adaptively. However, if people are not able to identify or describe their emotions (the very definition of alexithymia), our results suggest that this confusing affective experience may be quite upsetting (or unpleasant) and could lead to negative urgency, or a tendency to act rashly when they experience any type of negative affect.

High alexithymia individuals appear to be highly motivated to alleviate negative affect, regardless of the consequences. It may be that the emotional confusion inherent in alexithymia prompts individuals high on negative urgency to engage in dysregulated behaviors, by acting out either
against themselves or others.

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As we mentioned in our previous blog  emotional processing deficits are common in addiction and in other dysregualted behaviours and these deficits may not recruit the goal-directed parts of the brain. They do not guide 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 used to anticipate future, long term consequence.

We disagree that it is not simply negative affect that prompts negative urgency but rather the chronic stress dsyregulation underpinning the manifestation of negative affect.

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. 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 emotional and stress dysregulation.

References for this blog

Fink, E. L., Anestis, M. D., Selby, E. A., & Joiner, T. E. (2010). Negative urgency fully mediates the relationship between alexithymia and dysregulated behaviours. Personality and Mental Health, 4(4), 284-293.

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.

 

Are Alcoholics Emotionally Immature?

Posted on by alcoholicsguide

Concerted attempts have been made to relate personality factors to alcohol dependence.

In fact, for many years, research attempted to define the so-called alcoholic personality. Attempts to do so have dwindled in recent years.

Potential alcoholics tend to be emotionally immature, expect a great deal of the world, require an inordinate amount of praise and appreciation, react to failure with marked feelings of hurt and inferiority, have a low frustration tolerance, and feel inadequate and unsure of their abilities to fulfil expected male or female roles.1

Although the obvious emotional immaturity often seen in alcoholics seems to cover a number of the more recent findings on bio-psychologcal aspects a alcoholism.

For example, if we partly defined emotional immaturity as containing some of the following, then we appear to be covering a number of much researched and demonstrated aspects of alcoholism. Do these then not come under an umbrella term of emotional immaturity? This list was complied by Psych Central

Dimensions of Emotional maturity

  1. The ability to modulate emotional responses.  Addicts tend to have an all or nothing emotional response.  When they respond they become overly emotional and take a longer time to return to baseline.  They are easily flooded with emotion to the point of impairing functioning.
  1. The ability to tolerate frustration.  Addicts tend to respond to frustrating situations as disasters rather than having any perspective.
  1. The ability to delay gratification.  Emotionally immature people have trouble planning and working toward goals.  The ability to give up immediate gratification is necessary for anyone to go about life in a successful way.
  1. The ability to control impulses.  The mature self has the ability to see that feeling the urge to do something is not the same as doing it.  The recovering addict has a level of control over his or her behavior and can put boundaries around what is inappropriate to say or do.
  1. The ability to be reliable and accountable.  Addicts are often self centered and not good at dealing with the everyday requirements of life like being on time, fulfilling obligations and telling the truth.  As they gain emotional maturity they gain the ability to get out of themselves and think about the impact of their actions on others and on their own lives as well.

 

 photo-for-emotional-maturity

 

According to a list drawn up by alcoholrehab.com

If people are emotionally immature, they may exhibit some of the following symptoms:

* Such individuals will often find it hard to deal with the normal challenges of life. When they are faced with problems they feel unable to cope. They may have developed a psychological state known as learned helplessness.

They struggle to develop meaningful relationships with other people. They may appear too needy or a bit overbearing.
* Those people who are emotionally immature will tend to have a pessimistic outlook on life. They may see the future as a threatening and hostile place.
* This type of person will usually have low self-esteem. This means that they do not value themselves highly so will be willing to accept very little in life as being all they deserve.
* They find it almost impossible to live in the present moment. They are either reliving the past or worrying about the future.
* They can easily lose their temper at the slightest provocation. When they are dealing with uncomfortable emotions they will tend to take things out on other people.

* People who are emotionally immature can have unrealistically high expectations. This means that they are frequently disappointed. Such and individual can have impossibly high expectations for other people yet low expectations for themselves.
* Such individuals can suffer from severe mood swings. This instability of mood can make life a bit uncomfortable.
* If people are emotionally immature, they find it much harder to control their own behavior.

Recognize any of these symptoms?

images (26)

We were completely like this before doing the 12 steps.

We, however, do not think that anyone, alcoholics or otherwise choose to behave in this emotional immature way.

We have already looked at the emotional distress accompanies alcoholism and addiction, and will be examining more in the months ahead and it is difficult not to see the above emotional immaturity as all being products of a distress state.

In the course of addiction the alcoholic in particular grows in emotional distress as the stress and emotional dysregulation associated with addiction increases.

This means the brain “collapses” from more cortical, goal-directed (and emotionally regulated) areas of the brain to more sub-cortical areas which are more automatic, unthinking and compulsive.

Emotional distress activates these areas of habit-like compulsive behaviour, acting as a stimulus response, distress the stimulus and compulsive (unthinking)  responding as the response.

This is like a distress based or “fight or flight” reality or a heightened emotional state or “emergency” state. It seems to us that alcoholics live in this region more than cortical regions. They are primed to go off!

They then have a tendency to either run away from situations or to fight “everybody and everything”, to be intolerant of uncertainty, to catastrophize, to be fear-based people to be over reactive, hypervigilant, perfectionist etc These are all distress based states.

Are aspects of the  apparent emotional immaturity mentioned above not also not  a surface manifestation of these deep subcortical processes?

It is this state of heightened uncertainty and fear that whittles away at the alcoholic psyche. This amount of stress/distress promotes implicit, do, memory, over explicit, reflective, evaluative, memory. Distress makes one act without much thought of consequence, it makes one choose short term over greater long term gain, it makes one want to act impulsively or compulsively to alleviate distress. It is this distress that is in charge of action and emotional behaviour. It calls the shots.  A state of emergency has been called in the brain of the alcoholic.

I know it is widely shared at AA meetings that we got stuck in the emotional age of our first drink, in the early teens and never developed our emotional selves or capacity to regulate and process emotions. We are not sure this is completely true as the stress that accompanies alcoholism, as alcohol is literally classified as a pharmacological stressor,  not only causes chronic stress dysregulation but also the emotional dysregulation which accompanies this. It is emotional parts of the brain and the cortical areas that are supposed to keep them in check that are most impaired via chronic alcoholism.

Dr. Stephanie Brown (2) has explored these developmental changes in cognition, which lead to “alcoholic thinking.” She states that these changes refer “not only to rationalization, denial and frame of mind, but also to character traits that frequently accompany drinking. These include grandiosity, omnipotence and low frustration tolerance.” (3) These traits appear to be directly associated with the addictive process rather than with the individual’s personality prior to establishing this abusive cycle.

As alcohol becomes more dominant, the need to deny these changes becomes greater. It appears that there is an interaction between physiological changes and psychological defenses which creates emotional immaturity, self-centeredness and irresponsibility. Alcoholism becomes a thought disorder as well as an addiction to alcohol.

This is the consequence we believe of prefrontal atrophy and subcortical hypertrophy caused by chronic alcohol consumption, a constant injection a pharmacological stressor into the brain, wrecking the ability to maturely deliberate and instead rely on “I want it now!”  type of thinking.

We firmly believe this progression is to a state of constant distress signal in the brain and a cortical hyperarousal.

The alcoholic may not be emotionally distressed all the time but his brain is never satisfied, it constantly needs more, it finds only transient balance, via allostasis, it never finds true balance, i.e. homeostasis. it is always seeking, never reaching satiety, never completely at rest. This is emotionally exhausting.

It may represent, on superficial observation to some, the “emotional immaturity, self-centeredness and irresponsibility” (4) but is it really this simple, seeing these as the primary defenses and interpersonal style typical of normal development in the first three years of life or to characterize the addictive part of self as a “two-year-old child”?

Isn’t it more apt to say instead of  a “two-year-old wounded part of self begins to “drive the bus” and create havoc for all concerned” to say chronic stress manifest  as emotional distress “driving the bus”?

Thus a valid question remains for us and we ask it to our normies or earthling friends (i.e. non-alcoholics), wouldn’t you act in a childish if you were this distressed most of the time, having to rely on impaired emotional regulation and processing parts of the brain?

 

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In fact, to all those normies or earthlings who are reading this blog, how well do you think or consider others when in a state of persistent and daily distress? In this heightened anxiety how good is your action outcome memory, goal-directed planning and awareness of future consequence?

Are you ever moody, emotionally volatile and over reactive in this state of high anxiety? Hyper sensitive? Ever strike out unthinkingly at others although you had not intended to? Leading to guilt and shame, and remorse and self pity which can in the fullest of time lead to depression? This is called a transient emotional dysregulation, distress leading to an emotional cascade. This is the brain of an alcoholic all the time. It can lead to dejection and relapse.

In this sate of nauseating anxiety, how well do you consider the consequence, negative or otherwise, or your fear-based decision making?  Do you choose the short term answer in these anxiety-filled moments just to simply relieve this distress this unpleasant feeling of doom? So do alcoholics!

It is not enough to call the alcoholic emotional immature or stuck in the “terrible twos”, although let’s face it the evidence for it is compelling at times!! Let’s instead understand the reasons for it. Would you like to be in a state of distress most of the time? It’s not a whole lot of fun!

The 12 steps help solve these issues, there is a solution to emotional immaturity – it leads to emotional maturity or emotional sobriety which is blogged about here also.

The next time the alcoholic is your life acts in an immature way don’t ask them why they are acting that way, ask them how they feel. instead. Get them to identify, label and process their feelings  by verbalizing them.

When the anxious amgydala has quelled and  it’s feverish responding quietened,  get them to an AA meeting where many tens of thousands of alcoholics are doing the same, “sharing”, processing their emotions by talking about them and how they really feel.

 

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Not running away from them or intellectualizing about them, not fighting them. Simply saying in words how they feel.

It is a miracle awakening for us in recovery, the emotional regulation normies and earthlings take for granted.

The age of miracles is amongst us and it starts by opening your mouth, asking for help, getting help and getting real about what you are really feeling.

It is through sharing our deepest feelings that we start to mature and grow up.

 

maturity-grown-up-300x225

 

References

1. Chaudhury, S.K. Das, B. Ukil,  Psychological assessment of alcoholism in males Indian J Psychiatry. 2006 Apr-Jun; 48(2): 114–117. doi: 10.4103/0019-5545.31602

2. Brown S. (1985). Treating the Alcoholic: A Developmental Model of Recovery. New York: John Wiley & Sons, Spring.

3. Brown, S. (1988). Treating Adult Children of Alcoholics: A Developmental Perspective. New York: John Wiley and Sons.

4. http://www.cairforyou.com/alchoholdrugs/alcoholcharacter.htm

 

Processing Emotions by verbalising them!?

Posted on by alcoholicsguide

The Therapeutic Benefits of “Sharing”

In early recovery I did not have a clue what emotions I was experiencing. I was not able to identify, label or process them. As a result of his failure to process emotions I seemed to be constantly distressed and and, as we seen in previous blogs, this distress leads to a distress-based impulsivity and a negative urgency to either engage in “fight or flight” behaviour, i.e. running away from fearful situations or ignoring the Big Book of AA’s recommendation not to fight anybody or anything.

The only way I could handle these troublesome and frightening emotions was by talking about them to my sponsor or my wife or other people in recovery.

In recent years it has become evident to that what I have been doing all these years have been using a technique of verbalising my emotions to actually process them. I now believe this is a fundamental part of my recovery and that I sometimes need to verbalise my emotions in order to process them. How does this work?

I recently came across an article (1) which might shed some light on this process.

Putting feelings into words (affect labeling) has long been thought to help manage negative emotional experiences. Affect labeling or naming emotions diminishes the response of the amygdala and other limbic regions to negative emotional images.  A  brain imaging study by UCLA psychologists reveals why verbalizing our feelings makes our sadness, anger and pain less intense.

When people see a photograph of an angry or fearful face,they have increased activity in a region of the brain called the amygdala, which serves as an alarm to activate a cascade of biological systems (including stress chemicals) to protect the body in times of danger. Scientists see a robust amygdala response even when they show such emotional photographs subliminally, so fast a person can’t even see them.

But does seeing an angry face and simply calling it an angry face change our brain response? The answer is yes, according to Matthew D.Lieberman, UCLA associate professor of psychology.

“When you attach the word ‘angry,’ you see a decreased response in the amygdala,” said Lieberman, lead author of the study. The study showed that while the amygdala was less active when an individual labeled the feeling, another region of the brain was more active: the right ventrolateral prefrontal cortex.

This region is located behind the forehead and eyes and has been associated with thinking in words about emotional experiences. It has also been implicated in inhibiting behavior and processing emotions.

“What we’re suggesting is when you start thinking in words about your emotions —labeling emotions — that might be part of what the right ventrolateral region is responsible for,” Lieberman said.

If a newcomer to recovery one is sad or angry or resentful , getting them person to talk or write may many have benefits.

In Lieberman’s study  participant’s viewed images of individuals making different emotional expressions. Below the picture of the face they either saw two words, such as “angry” and “fearful” and chose which emotion described the face, or they saw two names,such as “Harry” and “Sally,” and chose the gender-appropriate name that matched the face.

“When you attach the word ‘angry,’ you see a decreased response in the amygdala,” Lieberman said. “When you attach the name ‘Harry,’you don’t see the reduction in the amygdala response.

“When you put feelings into words, you’re activating this prefrontal region and seeing a reduced response in the amygdala,” he said. “In the same way you hit the brake when you’re driving when you see a yellow light,when you put feelings into words, you seem to be hitting the brakes on your emotional responses.”

As a result, an individual may feel less angry or less sad.

“This is ancient wisdom,” Lieberman said.

Putting our feelings into words helps us heal better and if we can get newcomers to talk about them, that  will make them feel better. They will experience part of the “solution” right way and be encouraged to come back for more.

So putting feelings into words helps with not only regulating and modulating the intensity of emotions, but helps with processing them, reduces distress and distress based impulsivity and shows there is a solution to unruly negative  emotions.

In my experience this process has been a fundamental part of how it works!

 

 References

Lieberman, M. D., Eisenberger, N. I., Crockett, M. J., Tom, S. M., Pfeifer, J. H., & Way, B. M. (2007). Putting feelings into words affect labeling disrupts amygdala activity in response to affective stimuli. Psychological Science, 18(5), 421-428.

 

lieberman_affect_labelling_scan_small

AA helps to reduce Impulsivity

Posted on by alcoholicsguide

 

One constant in studies on addiction and in alcoholism, in particular is the  fundamental role played by impulsivity in these disorders. It is seen to be present in early use but appears to be more distress based (i.e. more negative urgency based) as the addiction cycle becomes more chronic. This impulsivity has obvious consequences for propelling these disorders via impulsive behaviours and decision making difficulties.

Thus it then follows that any treatment of these addictive disorders must have treatment of impulsivity at the core as it appears to a fundamental pathomechanism.

 

Here, we review a study that on links  AA attendance and reduced impulsivity using a 16-year prospective study of men and women, who were initially untreated for their drinking problems. Across the study period, there were significant l decreases in impulsivity, and longer AA duration was associated with reductions in impulsivity.

Alcoholics Anonymous (AA) is linked to improved functioning across a number of domains [2,3]. As the evidence for the effectiveness of AA has accumulated, so too have efforts to identify the mechanisms of change associated with participation in this mutual-help group [4].

This study concluded that help-seeking and exposure to the “active ingredients” of various types of help (i.e., AA principles/practices, sponsors), which, in turn, leads to improvements in reduced impulsivity.

Impulsivity is typically higher among individuals in AUD treatment than among those in the general population [5] and, impulse control deficits tend to predate the onset of drinking problems [6-9].

Contemporary research has revealed that traits such as impulsivity can change over time [10]. Mutual-help groups like AA may promote such changes, given that they seek to bolster self-efficacy and coping skills aimed at controlling substance use, encourage members to be more structured in their daily lives, and target deficits in self-regulation [11].

 

impulse control.preview

 

Such “active ingredients” may curb the immediate self-gratification characteristic of disinhibition and provide the conceptual grounds to expect that AA participation can press for a reduction in impulsive inclinations. In turn, given the range of outcomes related to impulsivity (e.g., legal, alcohol-related, and psychosocial problems), decreases in impulsivity may account for part of the association between AA participation and improvements in these outcomes.

AA’s vision of recovery as a broad transformation of character [12], and  explores individual differences in emotional and behavioural functioning as potential mechanisms of change (13,14).

Such groups encourage members to be more structured and goal-directed, which may translate into greater efforts to delay gratification of one’s impulses and  to improve clients’ general coping skills (e.g., reduce avoidance coping).

Given that impulsivity is a risk factor for a host of problematic behaviors and outcomes beyond drinking-e.g., criminality [15], drug abuse [16], reckless driving and sexual practices [17],  lower quality of interpersonal relationships [18], and poor health [19] this reduced impulsivty is beneficial in other aspects too.

Notably, this effect was buffered by a higher quality of social support-a probable active ingredient of AA. Thus, the impact of reducing impulsivity may be widespread across a range of outcomes that are critical for long-term sobriety.

 

Our main caveat on this study is that it does not distinguish between different types of impulsivity and does not mention negative urgency (or distress-based impulsivity) which is more commonly seen is this sample group.

AA’s “active ingredients” may reduce distress, via a new found emotional regulation gained via the steps and use of a sponsor (acting as an external prefrontal cortex to help us inhibit our impulsive and distress based responses)  which in turns reduces our tendency to impulsive decision making and behaviour.

 

It would have been interesting in this study to have also measure how emotional dysregulation changed in the time span of 16 years (using the DERS scale) and to have used a different impulsivity scale i.e. used the UPPS-P scale which would both have helped more specificallylook  at the interaction of how emotional regulation and impulse control changed over the 16 year period.

 

References

 

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

2. Humphreys, K. Circles of recovery: Self-help organizations for addictions. Cambridge Univ Pr; 2004.

3.. Tonigan JS, Toscova R, Miller WR. Meta-analysis of the literature on Alcoholics Anonymous: Sample and study characteristics moderate findings. Journal of Studies on Alcohol. 1995

4. Kelly JF, Magill M, Stout RL. How do people recover from alcohol dependence? A systematic review of the research on mechanisms of behavior change in Alcoholics Anonymous. Addiction Research & Theory. 2009; 17(3):236–259.

5. Conway KP, et al. Personality, drug of choice, and comorbid psychopathology among substance abusers. Drug and alcohol dependence. 2002; 65(3):225–234. [PubMed: 11841894]

6. Caspi A, et al. Behavioral observations at age 3 years predict adult psychiatric disorders: Longitudinal evidence from a birth cohort. Archives of General Psychiatry. 1996; 53(11):1033. [PubMed: 8911226]

7. Cloninger CR, Sigvardsson S, Bohman M. Childhood personality predicts alcohol abuse in young adults. Alcoholism: Clinical and Experimental Research. 1988; 12(4):494–505.

8. Elkins IJ, et al. Personality traits and the development of nicotine, alcohol, and illicit drug disorders: Prospective links from adolescence to young adulthood. Journal of abnormal psychology. 2006; 115(1):26. [PubMed: 16492093]

9. Sher KJ, Bartholow BD, Wood MD. Personality and substance use disorders: A prospective study. Journal of Consulting and Clinical Psychology. 2000; 68(5):818. [PubMed: 11068968]

10. Caspi A, Roberts BW, Shiner RL. Personality development: Stability and change. Annual Review of Psychology. 2005; 56:453–484

11. Moos RH. Active ingredients of substance use focused self help groups. Addiction. 2008; 103(3):387–396. [PubMed: 18269361]

12. White WL. Commentary on Kelly et al. (2010): Alcoholics Anonymous, alcoholism recovery, global health and quality of life. Addiction. 2010; 205:637–638. [PubMed: 20403015]

13. Kelly JF, et al. Mechanisms of behavior change in alcoholics anonymous: does Alcoholics Anonymous lead to better alcohol use outcomes by reducing depression symptoms? Addiction. 105(4):626–636. [PubMed: 20102345]

14. KELLY JF, et al. Negative Affect, Relapse, and Alcoholics Anonymous (AA): Does AA Work by Reducing Anger? Journal of studies on alcohol and drugs.

15. Krueger RF, et al. Personality traits are linked to crime among men and women: Evidence from a birth cohort. Journal of abnormal psychology. 1994; 103(2):328. [PubMed: 8040502]

16. McGue M, Slutske W, Iacono WG. Personality and substance use disorders: II. Alcoholism versus drug use disorders. Journal of Consulting and Clinical Psychology. 1999; 67(3):394. [PubMed: 10369060]

17. Caspi A, et al. Personality differences predict health-risk behaviors in young adulthood: Evidence from a longitudinal study. Journal of Personality and Social Psychology. 1997; 73(5):1052. [PubMed: 9364760]

18. Ozer DJ, Benet-Martinez V. Personality and the prediction of consequential outcomes. Annu. Rev. Psychol. 2006; 57:401–421. [PubMed: 16318601]

19. Bogg T, Roberts BW. Conscientiousness and Health-Related Behaviors: A Meta-Analysis of the Leading Behavioral Contributors to Mortality. Psychological Bulletin. 2004; 130(6):887. [PubMed: 15535742]

 

 

 

 

 

 

 

 

Do alcoholics drive through life with Faulty Brakes!

Posted on by alcoholicsguide

There has been a lot of debate in the last thirty – forty years about genetic inheritance – with at least half of children of alcoholic families at risk for later alcoholism. What is less known is what exactly is inherited in our genes? What marks us out for later alcoholism? Prior to drinking are there aspects of our behaviour, personality or emotional responding that marks us out compared to so-called normal healthy types.

Recently research has looked at brain systems which overlap in decision making such as cognitive control over impulsive behaviour and also emotional processing. Children from alcoholics seem to have difficulties with both these overlapping circuits in the brain – they are not only impulsive but also do not seem to process emotions in the same way their “health” peers do. Research has also begun  to show that emotional processing is indeed important to making decisions, as is the ability to inhibit impulsive responses.

It seems  young alcoholics in the making, are not using our emotions  to make decisions and  are also prone to being impulsive. This difficulty with making decisions must shape all other future decisions ?

Youth for families with a history of alcoholism (FH+) are more likely to engage in early adolescent alcohol use (1), they may be more prone to experience the neurotoxic effects of alcohol use during adolescence.

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Heavy alcohol use during adolescence is related to poorer neuropsychological functioning, including response inhibition (2), working memory (3-5), and decision-making (6).

Neuroimaging studies have shown that alcohol abusing teens have atypical grey matter volume in the PFC (7,8), and subcortical structures, such as the hippocampus (9,10) OFC and the amgydala.

Further, they have reduced integrity of white matter pathways, in both long-range connections between frontal and parietal brain regions as well as in pathways connecting subcortical and higher-order brain areas (11,12).

FMRI studies have found reduced BOLD response in adolescent alcohol abusers
in brain regions important affective decision-making (13).

The raging debate in research has been to whether these deficits are a consequence of heavy alcohol use or if genetic and environmental factors, such as family history of alcoholism, may contribute.

Risk Factor for Alcohol Use Disorders (AUDs): Family History of Alcoholism

The observation that alcoholism runs in families has long been documented
(14-16). Over the past few decades, adoption (17,18) and twin (19)
studies have suggested that there is an increased likelihood of individuals with a family history of alcoholism to develop the disorder themselves (20, 21).

These studies indicate that familial alcoholism is one of the most robust predictors of the development of an AUD during one’s lifetime. Furthermore, this risk factor appears to be stable over time, since it also predicts the chronicity of alcohol dependence at multiple time points (22).
This indicates that higher familial density is often associated with greater
risk (23), with genetic vulnerability accounting for about 30-50% of
individual risk (24-26).

 

One of the best characterized findings in individuals with familial alcoholism are greater impulsivity and difficulties in response inhibition which are commonly seen in this population (27,28), and FH+ individuals are less able to delay reward gratification compared with their peers (29).

Emotional processing and its relationship with executive control has received much less
attention in FH+ individuals.

Alcohol Use Disorders and Emotional Processing

Emotion Recognition and Affective Processing – Research suggests that alcohol use disorder (AUDs)  are associated with deficits in emotion recognition
(30-33), which may be related to atypical brain structure and functioning observed in the
limbic system among alcoholics (34-37).

Alcoholics not only tend to overestimate the intensity of emotions seen in faces  but they also make more negative emotional attributions and often confuse one emotion for another, such as mislabeling disgust as anger or contempt (32). Additionally, these deficits seem to be specific to alcoholism, since alcoholics, both recently abstinent and long-term abstinent, perform poorer on emotion recognition tasks than individuals with other drug abuse history (38). Alcoholics have also been shown to have slower reaction time when recognizing emotions (39).
Furthermore, poorer accuracy on emotion recognition tasks in alcoholics does not improve across the duration of the task, even though better performance is seen over time with other drug abusers (38).

Polysubstance abusing adults, the majority of whom were alcohol abusers, showed emotion recognition deficits on angry, disgusted, fearful, and sad faces (40). Based on the evidence of emotion recognition deficits in alcoholics, it is necessary to determine whether similar difficulties are present in FH+ youth that could be disruptive to emotional functioning and may contribute to the ultimately higher prevalence of alcohol abuse in this population.

Ultimately we may be observing here external emotional processing difficulties in the same manner we observed “internal” emotional processing difficulties in those with alexithymia, the reduced ability to “read” internal emotions of which a majority of alcoholics appear to suffer.

In summary, alcoholics and children of alcoholic families appear to have both external, i.e. recognition of other people’s emotions as well as their own and these may relate to immature development of brain regions which govern emotional, processing, recognition and regulation, which appears to contribute greatly to the initiation and progression of alcohol abuse.

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In addition to emotional processing deficits, alcoholics have various structural
and functional abnormalities in affective processing brain regions. Studies of the limbic system have found reduced volume in subcortical structures, including the amygdala, thalamus, ventral striatum, and hippocampus among adult alcoholics (41,42). Alcoholics with smaller amygdalar volumes, are more likely to continue drinking after six months of abstinence (37).

Marinkovic et al. (2009) alcoholics exhibited both amygdalar and hippocampal hypoactivity during face encoding, and when recognizing deeply encoded faces, alcoholics had significantly reduced amygdalar activity to positive and negative emotional expressions compared with controls (35). These results help explain findings in behavioral studies of alcoholics that have found considerable evidence for emotion recognition deficits in this population.

Furthermore, during emotion identification, alcoholics showed comparable
performance to controls, but had reduced brain response in the affective division of the
anterior cingulate cortex (ACC) to disgust and sadness, with this lack of affective response to aversive stimuli believed to underlie disinhibitory traits in AUDs (36).

There is also evidence to suggest that non-alcohol abusing FHP individuals
share similar deficits in affective systems to alcohol abusers, including reduced
amygdalar volume, less amygdalar activity in response to emotional stimuli, and high
rates of internalizing symptoms such as anxiety and depression (37; 45-47).

Furthermore, research examining the relationship between emotional
processing and cognition has found that poor inhibition in individuals with co-morbid
substance and alcohol abuse is associated with atypical arousal in response to affective images (48), and affective measures in FH+ alcoholics also relate to deficits in executive functioning, e.g impulsivity (47).

This suggests that familial history of AUDs may put individuals at greater risk for problems with emotional processing and associated disruptions in executive functioning (47), which could, in turn, increase risk for alcohol abuse (49).

As we suggested previously, in relation to decision making profiles, in those at risk, those with alexithymia and also with cocaine addicts, decision making often involves more emotion expressive-motor areas of the brain like the caudate nucleus which is more of a “feel it-do it” type of reaction to decision making or a emotionally impaired or distress-based impulsivity. If there is a difficulty  processing emotions, these emotions can not be used as a signal to guide adaptive, optimal decisions. Decisions appear more compulsive and short term.

It may be this tendency to act now, rather than later,  that defines the vulnerability in FH+ children. It is like driving through life with faulty brakes on decision making, which sets up a chain of maladaptive choices such as alcohol abuse which then damages these affective based decision making regions of the brain even more, with increasing  deleterious consequences as the addiction cycle progresses until the endpoint of addiction of very limited choice of behaviour as emotional distress acts eventually as a stimulus response to alcohol use.  Emotional processing usurped by compulsive responding.

 

References

Main reference – Cservenka, A., Fair, D. A., & Nagel, B. J. (2014). Emotional Processing and Brain Activity in Youth at High Risk for Alcoholism. Alcoholism: Clinical and Experimental Research.

1.  Dawson, D.A., 2000. The link between family history and early onset alcoholism: earlier initiation of drinking or more rapid development of dependence? J Stud Alcohol 61, 637-646.

2. Ferrett, H.L., Cuzen, N.L., Thomas, K.G., Carey, P.D., Stein, D.J., Finn, P.R., Tapert, S.F., Fein, G., 2011. Characterization of South African adolescents with alcohol use disorders but without psychiatric or polysubstance comorbidity. Alcohol Clin Exp Res 35, 1705-1715.

3. Brown, S.A., Tapert, S.F., 2004. Adolescence and the trajectory of alcohol use: basic to clinical studies. Ann N Y Acad Sci 1021, 234-244.

4.   Brown, S.A., Tapert, S.F., Granholm, E., Delis, D.C., 2000. Neurocognitive functioning of adolescents: effects of protracted alcohol use. Alcohol Clin Exp Res 24, 164-171.

5.   Squeglia, L.M., Schweinsburg, A.D., Pulido, C., Tapert, S.F., 2011. Adolescent binge drinking linked to abnormal spatial working memory brain activation: differential gender effects. Alcohol Clin Exp Res 35, 1831-1841.

6. Johnson, C.A., Xiao, L., Palmer, P., Sun, P., Wang, Q., Wei, Y., Jia, Y., Grenard, J.L.,  Stacy, A.W., Bechara, A., 2008. Affective decision-making deficits, linked to a dysfunctional ventromedial prefrontal cortex, revealed in 10th grade Chinese adolescent binge drinkers. Neuropsychologia 46, 714-726.

7. De Bellis, M.D., Narasimhan, A., Thatcher, D.L., Keshavan, M.S., Soloff, P., Clark, D.B.,  2005. Prefrontal cortex, thalamus, and cerebellar volumes in adolescents and young adults with adolescent-onset alcohol use disorders and comorbid mental disorders. Alcohol Clin Exp Res 29, 1590-1600.

8.  Medina, K.L., McQueeny, T., Nagel, B.J., Hanson, K.L., Schweinsburg, A.D., Tapert, S.F., 2008. Prefrontal cortex volumes in adolescents with alcohol use disorders: unique gender effects. Alcohol Clin Exp Res 32, 386-394.

9.  De Bellis, M.D., Clark, D.B., Beers, S.R., Soloff, P.H., Boring, A.M., Hall, J., Kersh, A., Keshavan, M.S., 2000. Hippocampal volume in adolescent-onset alcohol use disorders. Am J Psychiatry 157, 737-744.

10.  Nagel, B.J., Schweinsburg, A.D., Phan, V., Tapert, S.F., 2005. Reduced hippocampal volume among adolescents with alcohol use disorders without psychiatric comorbidity. Psychiatry Res 139, 181-190.

11.  Bava, S., Jacobus, J., Thayer, R.E., Tapert, S.F., 2013. Longitudinal changes in white matter integrity among adolescent substance users. Alcohol Clin Exp Res 37 Suppl 1, E181-189.

12.   McQueeny, T., Schweinsburg, B.C., Schweinsburg, A.D., Jacobus, J., Bava, S., Frank, L.R., Tapert, S.F., 2009. Altered white matter integrity in adolescent binge drinkers. Alcohol Clin Exp Res 33, 1278-1285.

13. Xiao, L., Bechara, A., Gong, Q., Huang, X., Li, X., Xue, G., Wong, S., Lu, Z.L., Palmer, P., Wei, Y., Jia, Y., Johnson, C.A., 2012. Abnormal Affective Decision Making Revealed in Adolescent Binge Drinkers Using a Functional Magnetic Resonance Imaging Study. Psychol Addict Behav.

14. Cotton, N.S., 1979. The familial incidence of alcoholism: a review. J Stud Alcohol 40, 89-116.

15. Goodwin, D.W., 1979. Alcoholism and heredity. A review and hypothesis. Arch Gen Psychiatry 36, 57-61.

16.  Schuckit, M.A., 1985. Genetics and the risk for alcoholism. Jama 254, 2614-2617

17. Bohman, M., 1978. Some genetic aspects of alcoholism and criminality. A population of adoptees. Arch Gen Psychiatry 35, 269-276.

18. Cloninger, C.R., Bohman, M., Sigvardsson, S., 1981. Inheritance of alcohol abuse. Cross-fostering analysis of adopted men. Arch Gen Psychiatry 38, 861-868.

19. Merikangas, K.R., Stolar, M., Stevens, D.E., Goulet, J., Preisig, M.A., Fenton, B., Zhang, H., O’Malley, S.S., Rounsaville, B.J., 1998. Familial transmission of substance use disorders. Arch Gen Psychiatry 55, 973-979

20. Finn, P.R., Kleinman, I., Pihl, R.O., 1990. The lifetime prevalence of psychopathology in men with multigenerational family histories of alcoholism. J Nerv Ment Dis 178, 500-504.

21. Goodwin, D.W., 1985. Alcoholism and genetics. The sins of the fathers. Arch Gen Psychiatry 42, 171-174.

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Intolerance of Uncertainty

Posted on by alcoholicsguide

Like many recovering alcoholics I know I have a real problem with “Not projecting into the future” but staying in the moment or even the day. Why is this? When I “project” or even consider a near future event I can feel distressed by it. I want to do something about it now! Not later.

The future seems to be urgently now.

I have long researched why this is? I seem to become overwhelmed at times by future tense and it is not even due to future events being that distressing in themselves. I just have this constant need to act now rather than later. I have an urgency or a negative urgency or in other words a  distress based impulsivity which prompts a desire to act now, make a decision now rather than later. I call this a compulsion to act  because a distress state compels me to make a decision to act now.

As I have mentioned in previous blogs, alcoholics appear to have a bias in decision making towards choose the short term solution over a long term one, even though the long term solution will yield greater gains. There are various  theories on why this is so. Sometimes it appears like a “fight or flight” response!

My theory is that I am very poor at tolerating uncertainty and what is the future but uncertain. I have  an “unconscious” negative bias about the future, linked at times to a tendency to then catastrophize.

This intolerance of uncertainty is seen in other disorders, such as anxiety, obsessive-compulsive and post traumatic stress disorders as well as in eating disorders but it is rarely researched in alcoholism.

I believe when confronted with a decision about the future I often make a decision to relieve a distress which manifests as an unpleasant feeling state which compels me, via a stimulus response to act now. Distress is the stimulus, acting now is the response.

I am not saying that I have to be in a negative frame of mind for this to occur. It is simply a decision making bias I have when left to my own devices.   It is the reason I speak to others when making important decisions in life because the need to relief distress can show in the mind as a good idea when it is often on reflection not such a great idea.

This is due to distress being a stress-fuelled experience and excessive stress reduces the awareness of future consequence of a decision. It seems like a good idea at the time because it relieves distress. To the brain this is a good idea.  It is a automatic response of the dorsal striatum, an implicit memory (procedural) system, that requires one to retrospectively rationalise and justify the automatic responding of this area of the brain, it justifies a previous action in other words, thus a decision is represented in the mind as a good idea, what was most urgently required!

These rationalisations and justifications through time can become automatic schemas and are automatically activated following a compulsive response. Some of us are probably familiar with these schemas being a big part of our alcohol and drug use. As we needed to use, we had automatic addiction schemas following shortly after our decisions to head to the pub or to score some drugs or even to propel some decisions, as the consequence of distress states. It is these habitual response, based on distress states which bias decisions making to acting now, even in recovery.

I came across an article (1) which looked at this intolerance of uncertainty in relation to decision making and came up with similar conclusions to the above. “high IU (intolerance of uncertainty) predicted shorter wait times and more frequent selection of the immediate, less valuable (and riskier) reward. We take this tendency as evidence that IU was associated with an aversion to waiting in a state of uncertainty. One might argue that choices for the more immediate, less valuable reward might reflect an aversion to waiting per se…, the delay associated with the more valuable reward in the
current study appears to have magnified the unpleasant affective responses to uncertainty… delay is provoking unpleasant affective responses, choices for the smaller, immediate reward can be seen as avoidance of distress.” Decisions are thus like an “escape route” and more based on emotional avoidance.  “That is, the affective consequences of uncertainty may play a more central role in determining behavior than uncertainty itself…decision  making tendencies among those high in IU may be maintained through negative reinforcement…to  reduce or eliminate affectively unpleasant circumstances that accompany waiting in uncertainty.”

These “unpleasant affective responses” are distress based and lead to a negative urgency to act now.

References

1. Luhmann, C. C., Ishida, K., & Hajcak, G. (2011). Intolerance of uncertainty and decisions about delayed, probabilistic rewards. Behavior therapy, 42(3), 378-386.