Thinking You Are Bullet Proof might just Kill You.

Alcohol seemed to fortify me, make me stronger limbed, heroic, thrusting and invincible. With alcohol in me I communed with the Gods.

The blood seemed to flow around my body better, muscles seemed to get enhanced. I was less inhibited, funnier, nicer, more humane, better company. I looked on the world and it’s troubles with a kinder, gladder heart. People sought me out for advice. I was often sage-like. Especially compared to the insecure, disconnected from people, sober me.

People would comment on how transformed I became with the drink, nicer, more trusting, more human, more warmed up and less distant.

Alcohol was my first profound spiritual awakening –  alcohol brought about a profound alteration in how I felt and thought about the world and it’s people. How I acted towards them.  It made me connect with humanity, become a part of, not separate.  It made me exhale and go “phew”.  My wife said the main reason I gave for drinking when I was in the midst of chronic alcoholism was to escape from myself – not to get drunk but to escape the unbearable lightness of being ME.

The second, and most vital and absolutely necessary profound spiritual awakening I had was when I came into recovery via the 12 steps. Then I found a program that also enabled let me go “phew” and also connected me to my fellow human beings. With much less damage and tragedy wrought!

Don’t get me wrong I wasn’t some shy kid, fidgeting in the corner.  I was not. I was not all there, a character, wired to the moon some would say. I was extrovert, but I was also insecure, uncertain, distrusting of people. Sure I was someone who appeared to get  on with people but in a manipulative way. People worried me so I have a whole bundle of strategies to keep them happy, at arms reach. This included my family.

I was also less than whole when sober. Not properly filled in, felt like I was missing something or was protecting some indescribable weakness or deficit in me, although I was never sure want this was, this undefined sense of lacking. Always attending to, protecting some invisible psychic wound.

When drinking I underwent some transformation of spirit. I connected better with my fellow human beings. I became someone I liked more than the sober me. Other people seemed to like the sober me less also and much preferred the company of the wisecracking, fun seeking drinking me.

The drinking me was a shinier, more colourful me, expansive, inclusive, connecting, less manipulative. The sober me was greyer, more insular, cut off and suspicious of people.

When I drank I could drink a lot and rarely had the negative impairments to speech, gait and behaviour that I saw frequently in friends and others.

Alcohol did not make me drowsy or make me want to hug my friends and family. It made me slap people on the back, high five. It was not a sedative it was a major stimulant and much more. A wonderful cocktail of effects. For me it is the most brilliantly designed concoction of effect, and I have tried quite a few other drugs in my time.

In fact it wasn’t a drug to me so much as a homecoming to myself.

If you could mix cocaine with opium in liquid form then that was what  alcohol was me. Not only did it give me a warm glow of absolute well being, in a way no other drug has – although opium was pretty good at that! – it also made me feel that I could conquer the world, that everything was possible. It made me dream big dreams, plan my next imaginary offensive.

 

drinking-makes-you-happy

 

Alcohol made me more me! Seemed to make me work better. I became more the  me I wanted to be, that is before  the magic began to dissipate in later years until the point in the end of drinking the alcohol had not affect but to calm the delirium tremens or stave off that imminent alcoholic fit, or momentarily quietened the auditory and visual hallucinations, before reigniting and refuelling them again. Alcoholism gives you many heavenly feelings as it drags you to hell!

The thrill was long gone by this stage. So why did alcohol have this effect. Is it only alcoholics that get this euphoric alive and kicking reaction to alcohol? And for years I got away with the physiological withdrawals and hangovers too. Alcohol made me feel bullet proof, it made me stronger. Invincible, like my internal organs were steam powered and made of metal. That I was beyond human.

In this response to alcohol, in this lack of impairing effects of alcohol, in this thinking I was invincible, that the drink was my greatest ally may well have lain the seeds of my eventually destruction. In this combination of impulsive seeking and stimulative effects of alcohol was an alcohol fuelled propulsion into eventual chronic alcoholism and compulsive addictive behaviours. Alcoholism would never be something I ever had to consider because I was good, very good, at drinking!!

Right?

We cite and quote directly from a very interesting article on how a family history of alcoholism contributes to impulsivity, the one psychological domain that turns up repeatedly and is supported in studies of alcoholics, addicts and those at risk genetically from these addictive disorders. Impulsivity from an early age is one variable that appears central to later addictive disorders.

“A family history of alcoholism (FHA) doubles the risk of alcohol dependence (Nurnberger et al., 2004). Beyond the risk for alcohol use disorders, familial alcoholism is also significantly associated with impulsive and externalizing behaviors (Marmorstein et al., 2009)–behaviors thought to be relevant to drinking initiation, escalation, and treatment relapse (Perry & Carroll, 2008).

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Impulsive behavior is associated with both alcohol use disorders and a family history of alcoholism (FHA). One operational definition of impulsive behavior is the stop signal task (SST), which measures the time needed to stop a ballistic hand movement.

Stop signal reaction time (SSRT) is distinct from delay discounting, which measures impulsive devaluing of reward as a function of time, the motor impulsiveness assessed by SSRT represents the speed  (or slowness) with which an individual can accommodate an environmental demand to halt a behavior. Using the stop signal task (SST) to quantify SSRT, Nigg et al. (2004) found that alcohol-naïve adolescent offspring of alcoholic fathers had slower SSRTs than children from control families, and that SSRT predicted aggregate future alcohol and drug problems (Nigg et al., 2006).

Twenty two family history positive (FHP; age = 22.7 years, SD= 1.9) and 18 family history negative (FHN; age = 23.7, SD= 1.8) subjects performed the SST in fMRI in two randomized visits: once during intravenous infusion of alcohol. The results showed FHP being less sensitive to alcohol’s effects.

Beyond its potential as a reflection of baseline behavioral impulsiveness, SSRT and inhibition success (but not choice reaction time) are worsened by alcohol intoxication (e.g., De Wit et al., 2000; Fillmore & Vogel-Sprott, 1999).

Thus, as inhibitory control worsens during intoxication, so does ad lib alcohol consumption (Weafer & Fillmore, 2008), speaking to a potential mechanism in the loss of control of drinking.

The principal finding from this experiment (1) was a significant interaction between alcohol exposure and those with family history of alcoholism (FHA) in right prefrontal BOLD activation during motor inhibition. During clamped alcohol infusion, however, this right frontal activation in FHN was significantly reduced, while in FHP activation remained essentially unchanged. Those subjects with a smaller right prefrontal BOLD response during behavioral inhibition (FHN) also tended to need more time (had a longer SSRT) to successfully inhibit their behavioral responses so SSRT may have been lengthened by alcohol infusion.

While we found only an insignificantly smaller difference in frontal responses to correct stop signal responses in FHP subjects, which is consistent with data on another task measuring impulsivity, the Go/No-Go, of Schweinsburg, et al. (2004), which showed only FHN subjects’ activation frontal activation was significantly reduced by alcohol.

Schuckit et al. (1980) first proposed that individuals with FHA are less sensitive to alcohol’s effects. A recent meta-analysis (Quinn & Fromme, 2011) found that, when compared to lower drinkers, heavier drinkers are more sensitive to alcohol’s stimulant effects, and less sensitive to alcohol’s sedative effects.

The data form this study (1)  the data are generally consistent with the concept that FHP subjects are less susceptible to (in this case, the adverse cognitive) effects of alcohol exposure in a brain region that plays an important role in behavioral inhibition.

…a resistance to the cognitively impairing effects of intoxication may carry its own risks, as subjects may perceive a reduced vulnerability to alcohol’s punishing consequences— or in this case the adverse effects in brain systems regulating behavioral control. Thus, the combination of an increased sensitivity to reward and a tolerance to alcohol’s cognitively impairing effects could represent a mechanism of increased risk of progression to heavier drinking, in particular by creating expectancies in drinkers that they can increase their consumption without adverse consequences to their behavior (Vogel-Sprott & Sdao-Jarvie, 1989).”

So to summarise, solely from our own perspective, it may not be the effect of alcohol that prompts  impulsive, loss of control drinking observed in alcohol dependent individuals but impulsivity that prompts drinking behaviour initially and with an apparent lack of cognitive impairment as the result of drinking then leading some individuals to thinking they can “handle the drink” and it negative psychological effects and consequences when, over time and chronic use, it may be progressively contributing to an increased impulsive behaviour to the point where this impulsivity becomes  compulsivity.

It may be that in thinking they are “in control” of drinking and it’s consequences that this paradoxically gives rise to loss of control in drinking via an increased compulsivity but much more on this another time!

References

1. Kareken, D. A., Dzemidzic, M., Wetherill, L., Eiler II, W., Oberlin, B. G., Harezlak, J., … & O’Connor, S. J. (2013). Family history of alcoholism interacts with alcohol to affect brain regions involved in behavioral inhibition.Psychopharmacology, 228(2), 335-345.

 

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

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!”

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.

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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.

That “Warm Glow” of the First Drink Might Take You To Hell!

In a recent blog we looked at the possibility that those  with a positive family history of alcoholism, experience a heightened stimulant response to alcohol in addition to a blunted response to more negative impairing effects. 

In other words sons and daughters of alcoholics at risk for later alcoholism appear to have a greater kick from alcohol and can also hold their liquor without the negatives that go with it such as falling around the place, etc. I think we all know, alcoholic and non-alcoholic, what these negative   impairing effects may be.  In fact I suspect we all have rather vivid memories of experiencing such negative impairing effects.

Personally speaking I used to love having a good laugh at my friends, enemies and acquaintances having these negative impairing effects and would often remind them of these the following hungover-cursed morning.

I rarely got plastered, swayed madly across the street, puked up or made a complete fool of myself. Not in the early days of drinking anyway!!

In this study from a few months ago, it is clearly suggested that  heavy social drinkers who report greater stimulation and reward from alcohol are more likely to develop alcohol use disorder over time.

A team led by Andrea King, PhD, professor of psychiatry and behavioral neuroscience at the University of Chicago, analyzed the subjective response of 104 young adult heavy social drinkers to alcohol and tracked their long-term drinking habits.

“Heavy drinkers who felt alcohol’s stimulant and pleasurable effects at the highest levels in their 20s were the ones with the riskiest drinking profiles in the future and most likely to go on and have alcohol problems in their 30s,” King said, “In comparison, participants reporting fewer positive effects of alcohol were more likely to mature out of binge drinking as they aged.”

“We knew that at age 25, there were binge drinkers who were sensitive to alcohol’s more positive effects,” King said. “We just didn’t know what was going to happen to them. Now we show that they’re the ones more likely to go on to experience more alcohol problems.”

Journal Reference

  1. Andrea C. King, Patrick J. McNamara, Deborah S. Hasin, Dingcai Cao. Alcohol Challenge Responses Predict Future Alcohol Use Disorder Symptoms: A 6-Year Prospective Study. Biological Psychiatry, 2014; 75 (10): 798 DOI:10.1016/j.biopsych.2013.08.001

Journalist Article Reference

  1. University of Chicago Medical Center. “Effects of alcohol in young binge drinkers predicts future alcoholism.” ScienceDaily. ScienceDaily, 15 May 2014. <www.sciencedaily.com/releases/2014/05/140515103702.htm>.

The ability to ‘hold one’s liquor’ indicates risk of developing alcohol problems

When I was starting out on my drinking career around 14/15 years old, I prided myself on my ability to hold my drink or as they say in the US to hold my liquor. It made me feel like a man for some reason especially as I could easily drink grown men under the table. Was this due to my budding alcoholism? Did this innate ability to drink large amounts of alcohol mark me out as at risk for future alcoholism?

 

A study from last year  showed that an ability to “hold one’s liquor” is likely to become a risk factor for longer-term problems as tolerance to alcohol develops.

“People who feel less impaired after drinking are at increased risk for developing AUDs,” said William R. Corbin, associate professor and director of clinical training in the department of psychology at Arizona State University. “A low subjective response (SR)  to alcohol may result from differences in drinking history.”

It should be noted that this low SR precedes the development of alcohol problems, as distinct from acquired tolerance – whereby individuals feel less intoxicated than they used to at the same level of consumption –  is a symptom in itself.

This study examined the unique role of initial SR and tolerance in a sample of heavy drinking young adults.

Corbin and his colleagues examined associations between early subjective response and acquired tolerance, and both drinking behavior and alcohol-related problems, within a sample of 113 heavy drinking young adults (75 men, 38 women) who had volunteered for a clinical trial of naltrexone in combination with brief motivational counseling.

“Consistent with the one prior study on this topic, we found that both initial SR and tolerance were related to drinking behavior, with heavier drinking among those with a low initial SR and greater acquired tolerance,” said Corbin.

“The participants in our sample were young heavy drinkers who had not yet passed through the peak period of risk for alcohol use disorders (AUDs),” said Corbin. “We speculate that protection against alcohol-related problems among young heavy drinkers with a low SR may allow them to continue to drink more heavily as they miss the ‘stop’ signal to cease drinking. A continued escalation in heavy drinking may ultimately contribute to an increased risk for AUDs.”

Corbin said this study provides further evidence for differential roles of initial SR and acquired tolerance. “Whereas both were associated with drinking behavior, only initial SR was related to AUDs among heavy drinkers with considerable acquired tolerance,” he said.

“In this study, the responses measured are primarily sedative and unpleasant, hence playing a stronger protective role in individuals who have negative responses to alcohol. However, and as noted by the authors, this sample is characterized by heavy drinkers who may differ in terms of their genetic make up and predisposition to problem drinking”.sujective rep

“In addition,” said Corbin, “there is evidence that individuals at increased risk for alcohol problems, such as heavy drinkers and those with a positive family history of alcoholism, experience a heightened stimulant response to alcohol in addition to a blunted response to more negative impairing effects.”

 

References

Alcoholism: Clinical & Experimental Research. “The ability to ‘hold one’s liquor’ indicates risk of developing alcohol problems.” ScienceDaily. ScienceDaily, 22 January 2013. <www.sciencedaily.com/releases/2013/01/130122162238.htm>.