I was delighted to be asked and honored to take part in one of the excellent “The Hope Interviews” with Steve Jones for the recovery newspaper “Keys to Recovery” – our interview is on page 9 and it was a experience strength and hope type interview from both a 12 step recovery and a neuro-psychological perspective, showing how these perspectives are very compatible and how we need a spiritual solution to a neuro-psychological problem.
The main reason I am alive today, sober and have recovered from a seemingly hopeless condition of alcoholism is simple!
Or rather the first step can be simple.
The first step on my recovery journey was to identify with the life stories of other recovering alcoholics.
Not necessarily with where they grew up, or the damage alcoholism had inflicted on their lives. Although many alcoholics talk themselves, or their illness talks them, out of the possibility of recovery by saying I am not as bad as that guy, or that woman.
You may not be as bad “YET!” – the “yets” are often talked about in AA – you may not have done the damage others have, yet? Keep drinking and you are bound to. You, like them, will have no choice.
Alcoholism increasingly takes away choice.
It takes over your self will.
Your self will, your self regulation, is a combination of your emotional, attentional, memory and reward/survival/motivation networks.
Alcoholism takes over these networks, progressively, over time.
Neuroscience has shown this, over the last twenty odd years.
A superb longitudinal study, “The Natural History of Alcoholism” by George Vaillant clearly showed this progression in six hundred alcoholics over a 60 year period!
In my own research and in articles, with two highly respected Professors at a UK University, I have shown how the alcoholic brain progressively “collapses inwards” to subcortical responding.
In other words, we end up with a near constant “fight or flight” reaction to the world, with alcoholism causing distress based compulsion at the endpoint of this addiction.
All the above neural circuits become governed by a region of the brain which deals with automatic, compulsive behaviour. All the self regulation parts of the brain progress to an automatic compulsive behaviour called alcoholism and we are then often without mental defence against the next drink!
I identified with this one simple fact – the progression of this neurobiological, emotional, and spiritual disease state called alcoholism. I saw it in my own life, this progression over years of drinking.
The “invisible line” that is crossed, according to AA members, can be viewed on a brain image, I believe.
Can you see it in your life?
Like these recovering alcoholics I had not taken my first drink hoping to end up an alcoholic
It was something that had happened to me, happened despite my very strong will not because my will is weak. I am as wilful a person as you would hope to me. How come I became an alcoholic then?
I did also relate to other things these people shared.
I identified with the damage caused by alcoholism in their lives and the lives of their family. How this illness affects everyone in the immediate and even extended family.
I had never considered the effect on others, apart from me?
I listened and identified with how they talked about a “hole in the soul”, how they never felt part of, felt different from others, detached. I related to this. That was me too.
Alcohol made me feel more me! I became attached to it and grew to love it like someone would love another person, more so perhaps? Alcohol came first, loved ones second.
Alcoholism takes away all the good things in life and then your life too.
All of this was the case with me too.
I identified with all this.
I identified too with their solution.
I identified with and wanted what these now happy people in recovery had.
I decided to take the same steps as they had towards this happiness.
There is a solution.
We do recover!
I have blogged recently about how insecure attachment is linked to various addictive behaviours.
What is important is to establish a mechanism by which insecure attachment contributes to later addictive disorders. It may not be enough to say attachment and addiction are linked but that they are linked via a pathomechanism of some sort.
I have argued many times before that I believe this pathomechanism, the mechanism by which a pathological condition occurs, or the mechanism that drives a disease state (or disorder) is emotion processing and regulation deficits.
We look here (1) at a study that demonstrates how insecure attachment correlates in alcoholics with difficulties in emotion processing and regulation difficulties. I believe this is how addiction is driven to it’s endpoint of chronic, compulsive behaviour, although this study is only a correlational study and makes no such claims about causation.
“Attachment theory has been conceptualised as an affect regulation theory, proposing that attachment is associated with the expression and recognition of emotions as well as interpersonal functioning… the objective of the present study was to investigate potential associations between attachment, Negative Mood Regulation (NMR) expectancies, fear of intimacy and self-differentiation…(with) findings support broad attachment theory suggesting that attachment is associated with and predicts affect regulation abilities, difficulties with intimacy and intrapersonal as well as interpersonal functioning in a sample of substance use disorder inpatients.
Attachment is associated with the expression and regulation of emotion. Early attachment theory postulates that early bonding
with a significant caregiver is essential for the development of internal working models for communication, regulation of emotions and interpersonal behaviour.
These early attachment experiences are associated with adult attachment styles. Adult attachment styles are relatively stable and influence attitudes, emotions, affect regulation and behavioural strategies in relationships…Empirical evidence has indicated associations between insecure attachment, fear of intimacy and
emotion regulation difficulties and between secure attachment
and a higher capacity for intimacy, emotional awareness and empathy.
Substance abuse has been proposed to be a consequence of emotion regulation difficulties with individuals using alcohol/drugs to avoid
intimacy or rejection, to ease pain, anger and ambivalence and possibly establish a “secure base”.
Negative mood regulation (NMR) expectancies are beliefs regarding a person’s ability to terminate or alleviate a negative mood state.
High NMR presumably reflects the ability to cope successfully with bad moods, whereas having low NMR may lead to less efficacious or maladaptive ways of coping… high NMR may be associated with secure attachment, as securely attached individuals tend to seek comfort from others when emotionally upset, and utilise constructive coping mechanisms to decrease the intensity of distress.
By contrast, low NMR may potentially be associated with anxious attachment as well as substance abuse...insecure attachment is a fearful attachment style characterised by a fear of intimacy and rejection, high emotional reactivity and a self-belief associated with being deserving of rejection. Some have argued that fear of intimacy (FIS) is associated with mental health issues and substance use problems…FIS research to date has largely reported significant associations with loneliness, lack of self-disclosure, low social interaction and low relationship quality.
Differentiation of self is defined as the degree to which an individual is able to balance emotional and intellectual functioning, intimacy and autonomy in relationships…Individuals with lower
self-differentiation experience higher levels of chronic anxiety, emotion regulation difficulties, mood disturbances and substance abuse.
In addition, previous studies have reported higher levels of mood regulation and interpersonal difficulties in substance abusers compared to controls…(As) attachment has been hypothesised to be associated with relationship functioning and mood regulation (and) addiction has been proposed to be an attachment disorder, potential relationships of attachment with mood regulation and interpersonal functioning in substance abusers may
potentially inform the development of future treatment approaches.
The results (of this study) indicated a significant negative association between anxious attachment and NMR…suggesting that anxious attachment may be associated with lower abilities to regulate one’s negative moods. This is in accordance with other research evidence suggesting that insecurely attached individuals tend to show poor affect regulation.
The present investigation also found that attachment was a strong predictor of FIS (and) the present results suggest that adult
attachment is related to difficulties in intimacy and interpersonal functioning, in accordance with previous evidence that reported a significant association between insecure attachment and relationship problems as well as lower levels of trust, interdependence and commitment.
The present investigation also found that anxious attachment significantly predicted emotional reactivity (ER).
These data support the predictive power of anxious attachment in relation to being more emotionally reactive, having difficulties with emotion regulation and maladjustment in those with substance dependence…The predictive utility of attachment was also related to Emotional cut-off (EC)…This is in line with previous research suggesting a link between attachment and EC in those with substance abuse and implies that attachment style is related to traits of emotional aloofness, anxiety, isolation from others and exaggerated independence…EC may be associated with, or a consequence of alexithymia, a personality trait associated with difficulties in identifying and describing feelings.”
The above sounds so familiar, doesn’t it? Sounds like most newcomers to recovery that I have ever come cross, including me.
1. Thorberg, F. A., & Lyvers, M. (2009). Attachment in relation to affect regulation and interpersonal functioning among substance use disorder in patients.Addiction Research & Theory, 18(4), 464-478.
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 .
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  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 . 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 .
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 , 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 , drug abuse , reckless driving and sexual practices , lower quality of interpersonal relationships , and poor health  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.
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I come from a family of four siblings, two of whom are alcoholic and two who are not. I have often wondered why this is the case? Why is it the case that certain children of alcoholic parents will grow up to become alcoholics and why some will not? What is it that makes certain children vulnerable to alcoholism and other children, from the very same family, protected. What do these children have that protects them from later alcoholism?
This is especially important to know in terms of prevention strategies to help children at risk.
Obviously environment has an impact on vulnerability but does an inherited protectiveness help prevent this sometimes dysfunctional and abusive childhood environment of alcoholic parenting from having the same impact as those children who have inherited a genetic vulnerability?
Throughout our blogs has been a thread suggesting alcoholics, and children of alcoholics, may have difficulties in processing and regulating emotions. Is this the vulnerability, is there a difference in affective/emotional circuitry in the brain?
We cite a very interesting article here Affective circuitry and risk for alcoholism in late adolescence: Differences in frontostriatal responses between vulnerable and resilient children of alcoholic parents
in setting out an argument that children of alcoholics who are at greater risk of later alcoholism may have inherited impairments in brain neural circuitry which is responsible for affective/emotional processing.
Children of alcoholics (COAs) are at elevated risk for alcohol use disorders (AUD), yet not all COAs will develop AUD. One aim of this study was to identify neural activation mechanisms that may mark protection or vulnerability to AUD in COAs.
Some differences between alcohol abusers and control samples may precede alcoholism onset and thus constitute markers of precursive risk. After all, behavioral and affective markers early in life can predict later alcoholism (Caspi et al., 1996; Mayzer et al., 2001). Thus, it is reasonable to hypothesize that pre-alcoholic differences in the functioning of relevant neural systems will be related to risk for alcoholism.
In hoping to identify neural activation mechanisms that may mark protection or vulnerability to AUD in children of alcoholic fathers, the guiding conceptual framework was that the functioning of affective and behavioral regulation networks in the brain may serve as such mechanisms.
Consistent with that framework, the resilient and vulnerable groups were distinguished from one another by remarkably consistent inverse or opposite patterns of activation in the brain in response to the processing of emotional stimuli and which were most apparent with regard to negative affective stimuli and the vulnerable group.
These results suggest separate pathways of risk and resilience in the COA’s. First, the COA group that was not prone to early problem drinking (the resilient group) had more activation of the orbital frontal gyrus (OFG) than controls in response particularly to negative affect stimuli, but also to some extent in response to positive affect stimuli. The OFG is involved in the monitoring and evaluation of the affective value of stimuli, allowing for appropriate behavioral responses (Kringelbach and Rolls, 2004; Rolls, 2004).
The resilient group also had increased left insula activation to negative words. The insula is involved in evaluating internally generated emotions and the monitoring of ongoing internal emotional state (Phan et al., 2002).
The present findings, then, are consistent with the hypothesis that resilient youth have enhanced monitoring of emotionally arousing stimuli, even compared to typically developing youth. Yet, in an important nuance, they did not suppress the emotional experience.
They were prepared to modify behavioral response while maintaining affective response to these stimuli. This pattern of response in resilient youth may represent increased flexibility in emotional and social behavior. These youth may be exhibiting precisely an ability to delay external response to arousing stimuli, while internally processing those stimuli. In short, this may be a “reflective” pattern of approach to the world.
It is not difficult to speculate how this pattern might protect these at risk youth from substance misuse: they are able to respond to the emotional stimuli, but demonstrate enhanced monitoring that may allow for the inhibition of inappropriate responding, buying time for flexible response options based on well-processed information.
Interestingly, the vulnerable group displayed no differences from the control group in emotional monitoring and behavioral regulation systems (OFG and insula), suggesting that weakness in that system is not a risk factor. Rather, they demonstrated over-activation of DMPFC and an atypical under-activation of key emotion processing regions (particularly extended amygdala and ventral striatum). This pattern was more notable in regard to negative affect, it was also observed to a lesser extent with positive affect.
All of this may be consistent with a reactive approach to the world, in which affect is not fully processed.
Supporting this interpretation, neuroimaging studies have consistently shown the involvement of the DMPFC with conscious self-monitoring of emotional responses (Beauregard et al., 2001; Kuchinke et al., 2006; Levesque et al., 2003; Levesque et al., 2004; Phan et al., 2005). For example, during the voluntary suppression of negative affect in healthy adults, activation in the dorsal medial and lateral prefrontal cortex increased and that in the nucleus accumbens and extended amygdala decreased (Phan et al., 2005). It has been suggested that emotional information is conveyed from limbic regions to the prefrontal cortex allowing conscious, voluntary emotional self-regulation (Levesque et al., 2003; Levesque et al., 2004).
Therefore, one interpretation of the present findings is that the vulnerable youth were recruiting an emotional control system that was suppressing emotional response.
Heitzeg, M. M., Nigg, J. T., Yau, W. Y. W., Zubieta, J. K., & Zucker, R. A. (2008). Affective circuitry and risk for alcoholism in late adolescence: differences in frontostriatal responses between vulnerable and resilient children of alcoholic parents. Alcoholism: Clinical and Experimental Research, 32(3), 414-426.
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.
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.
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.
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.
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Following up from our previous blog on the abnormalities in the ventromedial prefrontal cortex (vmPFC) in alcoholics, brain regions which govern emotional regulation, we came across another study which appears to show that adolescents at increased risk for later alcohol use disorders (AUDs) may also be showing an emotion regulation difficulty.
This emotional regulation difficulty may be a biomarker for later alcoholism, which is in keeping with our previous proposals that an emotional processing and regulation difficulty or disorder underpins the aetiolgy of of alcoholism. In order words it is part of the pathomechanism – or the mechanism by which a pathological condition occurs- of later alcoholism.
The area in this study, the vmPFC, showed relatively increased cerebral blood flow (CBF) in bilateral amygdala and vmPFC and relatively decreased CBF in bilateral insula, right dorsal anterior cingulate cortex (ACC) and occipital lobe cuneus of high-risk adolescents. This suggests that adolescents at relatively high-risk for AUD exhibit altered patterns of resting CBF in distributed corticolimbic regions supporting emotional behaviors.
The authors’ hypothesized that the relatively increased amygdala and ventromedial prefrontal CBF may contribute to increased emotional reactivity and sensitivity to environmental stressors in these individuals while diminished insula/occipital cuneus and dorsal anterior cingulate cortex (ACC) CBF may lead to poor integration of visceral and sensory changes accompanying such emotional stress responses and top-down regulation of amygdala reactivity.
Thus we see our model in a snapshot even in adolescents potentially. The emotional processing deficits we have discussed previously implicate the insula and ACC, as there appears to be a difficulty in alcoholics in reading emotional or somatic signals/states and integrating these signals into the identifying, labelling and processing of emotions. Equally there appears to be a hyperactivty in the vmPFC and amgydala as with alcoholics which implies emotional dysregulation, a hyper reactive emotional response and a tendency perhaps to a more “fight or flight” response, distress based impulsivity and short termist decision making, wanting it NOW rather than later.
References Lin, A. L., Glahn, D. C., Hariri, A. R., & Williamson, D. E. (2008). Basal Perfusion in Adolescents at Risk for Alcohol Use Disorders. In Proc. Intl. Soc. Mag. Reson. Med (Vol. 16, p. 60).