The terror of “Locked In” Attention!

I remember when I was in the first days, weeks and months of early recovery I used to give myself such a hard time when my attention was drawn to some alcohol-related cue, like someone drinking ,or finding it difficult not dealing with some  reminder of people places and things from my alcohol abusing past; finding that I found it nigh on impossible dragging my attention away from these and related memories associated with my drinking past.

It was as if I was entranced by it, in some of tunnel vision. It used to scare the life out of me.

I rarely found these thoughts appetitive but if I dwelt on these thoughts or trained my attention on cues I would find that the adverse, fearful things would turn to more desire based physiological reactions like salivating and so on.

I took these to mean that I actually wanted to drink and not stay sober. My sponsor at the time said two things which helped – a. I have an alcoholic brain that wants to drink period, 2. cues from my past may always have this effect on me. Accept it, don’t fight it.

That was what I had been doing in fact. Fighting it, these cues reminders and their automatically occurring intrusive thoughts about the past. It is in fighting these thoughts that they proliferate and then become “craving”.

Years later after much research I found that all alcoholics seem to have an attentional bias towards alcohol-related cues which leads to a cue reactivity.

Originally I thought this meant that I simply wanted to drink but found out that in  any manifestation of urge to drink (which is slightly different from a craving which requires an affective response on the part of the alcoholic in order to become a craving similar to mental obsession of the Big Book ) there is a stress reponse like the hear beat quickening, differences in galvanic skin conductance, increased saliva production etc .

Thus this cue reactivty seems to involve not only appetitive or desire states, i.e. it activates the reward system in the brain to motivate one to drink but also contains a stress based reactivity.

Any so-called “craving” state also manifests as either an anxiety state in simple cue reactivity e.g. the sight of alcohol or in negative emotions such as fear, anger and sadness in terms of a stress based craving.

Together, i.e. a cue based reactivity in the face stress/distress leads to a greater urge to drink than by either alone. By reacting to these one is increasing the stress/distress.

To the alcoholic brain having a drink or the desire to drink is the brain suggesting to us as alcoholics that this is the best way to attain transient homeostasis from an allostatic state of distress because this is how we used to balance the effects of emotional distress when we were drinking. We experience distress and automatically had thoughts about drinking. Thus alcoholism is a distress-based condition. We think it is us wanting the drink but it is the distress prompting the wanting of the drink!!

The distress does the drinking for us, itgets us out of our seats and down the street to the bar, it gets us on the bar stool….We may think it is our actions as we use rationalisng and justifying schemata afterwards to justify behaviour that had, in fact, been automatic or compulsive, compulsive meaning to relieve a distress state.

As a schema, which is implicit, i.e. it is automatically prompted and activated by distress also. We are not even in charge of this. We feel and think that we are in control over behaviour bit this is not the case as self control has become so impaired and limited it is distress doing the action and the subsequent rationalising.

The compusive part of the brain, the dorsal striatum, is the only part of the brain that requires us to make a post hoc rationalisation of why we did an action that was essentially automatic and compulsive.

We have become passengers in our own lives. Distress is now doing the driving.

So the brain thinks it is simply telling us the best way to survive this distress or in other words to regulate this distress. Thus it is an incredibly impaired way to regulate stress and emotional distress.

I want to further explain how some of this is linked to low heart rate variability. If we have low HRV we find it difficult inhibiting automatic responses and in changing behaviour. We become behaviourally rigid, and locked into attending to things like cues when we don’t really want to.

This is often the result of distress reducing the ability of the heart rate variability to inform and change our responses.

I cite and use excerpts form one of my favourite articles again by co-authored by Julian Thayer (1).

 

“The recovering alcoholic must face the difficulty of having his or her ambition to remain abstinent challenged in various situations in which memories about the pleasurable effects of alcohol are activated and the striving for abstinence no longer seems meaningful (Anton 1999; Marlatt and Gordon 1985). The odds for successful coping with such temptations are related to numerous factors, such as one’s subjective affective state and the ability to shift one’s focus from the automatic impulse to drink toward a cognitive reconstruction of the situation (Palfai et al 1997b; Tiffany 1990). Despite the importance of  attentional flexibility in effectively modulating such “highrisk” situations, research on the topic is scarce.

Thayer and Lane (2000) suggested that the interplay between positive (excitatory) and negative (inhibitory) feedback circuits in the nervous system (NS) allows for flexible and adaptive behavior across a wide range of situations. The uniqueness of this model lies with its emphasis on the importance of inhibitory processes in effective modulation of affective experience. In short, these researchers propose that the defects in neurovisceral regulation of affective experience seen in various psychiatric conditions (e.g., anxiety disorders) may be better explained by faulty inhibitory function in the NS than by unitary arousal models.

Tonic heart rate variability (HRV) may be a physiologic indicator of such inhibitory processes (Friedman and Thayer 1998a; Porges 1995). Heart rate variability refers to the complex beat-to-beat variation in heart rate produced by the interplay of sympathetic and parasympathetic (vagal) neural activity at the sinus node of the heart.

Importantly, heart rate (HR) is under tonic inhibitory control via the vagus nerve (Levy 1990). These neural connections to the heart are linked to brain structures involved in goal-directed behavior and adaptability (Thayer and Lane 2000). Compelling evidence now exists to show that high levels of HRV are related to cognitive flexibility (Johnsen et al 2003), modulation of affect and emotion (see Bazhenova 1995, cited in Porges 1995), and increased impulse control (Allen et al 2000; Porges et al 1996).

The hypothesis that reduced HRV is related to defective affective and emotional regulation has been supported in recent research in which reduced HRV was present in clinical disorders such as generalized anxiety disorder (Thayer et al 1996), panic disorder (Friedman and Thayer 1998b), posttraumatic stress disorder (Cohen et al 1997) several scientific arguments suggest that impaired inhibitory function may play a role in chronic alcohol abuse.

First, alcoholics have repeatedly been shown to have problems shifting attention and directing their attention away from task-irrelevant information (Johnsen et al 1994; Setter et al 1994; Stormark et al 2000). Second, frontal areas of the brain are most affected by the acute and chronic effects of alcohol, and these structures are of crucial importance in inhibitory functioning and self-control (Lyvers 2000). Third, acute effects of alcohol ingestion result in reductions in HRV, implying that chronic alcohol ingestion may result in a long-lasting impairment of the vagal modulation of HR (Reed et al 1999; Weise et al 1986)

Fourth, severely dependent alcoholics show a sustained phasic HR acceleration when processing alcohol information, indicating defective vagal modulation of cardiac function (Stormark et al 1998). Tonic HRV has similarly been found to be a useful measure of physiologic activity in challenging situations (Thayer and Lane 2000). Appropriate modulation of HRV (increases, decreases, or no change) depends on the type of challenge and the characteristics of individuals as they interact with specific contextual manipulation (Friedman and Thayer 1998a; Hughes and Stoney 2000; Porges et al 1996; Thayer et al 1996).

For example, during attention demanding tasks, healthy individuals show appropriate reductions in HRV (Porges 1995). In general, high tonic levels of HRV allow for the flexible deployment of organism resources to meet environmental challenges. With respect to attention, it is suggested that high levels of HRV reflect flexible attentional focus, whereas low HRV is related to “locked in attention” (Porges et al 1996). Moreover, increased tonic vagal activity is related to adaptive development and lack of behavioral and emotional problems (Hughes and Stoney 2000; Porges et al 1996).

Furthermore, it has been demonstrated that increases in vagal activity during challenging tasks discriminates between individuals who have experienced traumatic events and managed to recover from them and those who still suffer from chronic symptoms of posttraumatic stress (Sahr et al 2001). Such increases in vagal activity during challenging tasks are particularly interesting because studies on alcohol abusers have found increases in HRV after exposure to alcohol-related cues (Jansma et al 2000; Rajan et al 1998).

One could speculate that such enhanced vagal activity could be a sign of compensatory coping aimed at taming automatic drinking related processes (Larimer et al 1999). Such an interpretation is in agreement with cognitive theories predicting that alcoholics and other drug users do not simply respond passively to exposure to drug-related cues, but, on the contrary, in such situations conscious processes are invoked, inhibiting execution of drug-related cognition (Tiffany 1990, 1995). If this explanation is correct, alcoholics who have more effective coping resources should show stronger increases in vagal activity during such challenging exposure than alcoholics who express greater difficulty in resisting drinking-related impulses.

Also  general differences in HRV between alcoholics and nonalcoholics are interesting indicators of defective inhibitory functioning, a measure of rigid thought-control strategies and lack of cognitive control should be an important indicator of defective inhibitory function and “positive feedback loops” reflected as low HRV (Wegner and Zanakos 1994).

Linking these measures to the physiologic index of HRV makes a stronger case for attributing reduced vagal tone (HRV) to a defective regulatory mechanism resulting in unpleasant affective states and maladaptive coping with psychologic stressors

The main results of our study may be summed as follows. First, as expected, alcoholic participants had lower HRV compared with the nonalcoholic control group. Second, the imaginary alcohol exposure increased HRV in the alcoholic participants. Third, across the groups, an inverse association was found between HRV and negative mood and a positive association between positive mood and HRV. Fourth, HRV was negatively correlated with compulsive drinking during the imaginary alcohol exposure in the alcoholic participants. Fifth, within the alcoholic group, HRV was negatively associated with chronic thought suppression (WBSI).

Generally, these findings are in agreement with the neurovisceral integration model and the polyvagal theory that suggests HRV is a marker of the level of cognitive, behavioral, and emotional regulatory abilities (Thayer and Lane 2000).

The fact that the alcoholic group had generally lower tonic HRV compared with the nonalcoholic control group indicates that such reduced HRV may also be a factor in alcohol abuse; however, such group differences in HRV provide only indirect support for the theory that low HRV in alcoholics may be related to impaired inhibitory mechanisms

Because HRV is related to activity in frontal brain areas involved in cognition and impulse control (Thayer and Lane 2000), we speculated that tonic HRV would be an index of nonautomatic inhibitory processes aimed at suppressing and controlling automatic drug-related cognitions. To test this hypothesis more directly, the association between HRV and problems with controlling drinking-related impulses were studied.

Consistent with this hypothesis, the compulsive subscale of the OCDS was found to be inversely associated with HRV in the alcohol-exposure condition, thus suggesting that HRV may be an indirect indicator of the level of impulse control associated with drinking. These findings are therefore consistent with Stormark et al (1998), who found that sustained HR acceleration (lack of vagal inhibition) when processing alcohol-related information was related to compulsive drinking and “locked-in attention.”

Post hoc analysis further suggested that alcoholics who expressed a relatively high ability to resist impulses to drink (OCDS) had the clearest increase in HRV under the alcohol exposure this study suggests that alcoholics may actively inhibit or compensate for their involuntary attraction to alcohol-related information by activation of higher nonautomatic cognitive processes (Tiffany 1995). Such conscious avoidance has previously been demonstrated in studies on attentional processes in alcoholics (Stormark et al 1997) and by the fact that frontal brain structures involved in inhibition and control of affective information are often highly activated in the processing of alcohol related cues (Anton 1999). Furthermore, this interpretation is in agreement with other studies suggesting that high HRV during challenging tasks is associated with recovery from acute stress disorders (Sahr et al 2001).

Several studies have indicated that low HRV is associated with impaired cognitive control and perseverative thinking (Thayer and Lane 2002). Consistent with these reports a negative association was found between HRV and chronic thought suppression. The WBSI assesses efforts to eliminate thoughts from awareness while experiencing frequent intrusions of such “forbidden” thoughts and thus represents an interesting and well-validated measure of ineffective thought control (Wegner and Zanakos 1994). Thought suppression has been found to be an especially counterproductive strategy for coping with urges and craving (Palfai et al 1997a, 1997b) and may even play a causal role in maintaining various clinical disorders (Wenzlaff and Wegner 2000).

To our knowledge, this is the first time a link between physiologic indicators of a lack of cognitive flexibility (low HRV) and chronic thought suppression has been demonstrated.

Thayer and Friedman (2002) have reviewed evidence indicating that there is an association between vagally mediated HRV and the inhibitory role of the prefrontal cortex. Consistent with Thayer and Lane (2000), this study suggests that impaired inhibitory processes are significantly related to ineffective thought control.

The fact that this association between HRV and WBSI was only found in the alcoholics may be related to the fact that only this clinical group shows signs of such faulty thought control.

Wegner and Zanakos (1994) suggested that thought suppression is particularly ineffective when the strategic resources involved in intentional suppression are inhibited or blocked (Wegner 1994). Consistent with this hypothesis, our findings show that those reporting high scores on WBSI show signs of impaired inhibitory functioning as indexed by low vagally mediated HRV.”

This excellent article fro me is also alluding to the fact that those with increased HRV was related to successfully related to regulating negative emotion,  stress/distress and affect, not just the thoughts that these affective states gave rise to .

Thus any strategies that help with improving  the ability to increase HRV will likely have positive results in coping with cue associated materials.

We look at one of these therapeutic strategies next…that of mindfulness meditation.

 

References

1. Ingjaldsson, J. T., Laberg, J. C., & Thayer, J. F. (2003). Reduced heart rate variability in chronic alcohol abuse: relationship with negative mood, chronic thought suppression, and compulsive drinking. Biological Psychiatry54(12), 1427-1436.

 

 

 

How it (Mindfulness) Works? (Part 2)

“Mindfulness Training Ameliorates Addiction by Targeting Neurocognitive Mechanisms

ATTENTIONAL BIAS

Given that drug-use action schemas may be evoked by cues associated with past substance use episodes, activation of addictive habits may be interrupted by re-orienting attention from substance-related stimuli to neutral or salutary objects and events. MBIs may be especially efficacious in that regard. Focused attention and open monitoring mindfulness practices capitalize on attentional orienting, alerting, and conflict monitoring – the fundamental components of attentional control (89, 90). Consequently, studies indicate that mindfulness is linked with enhanced attention regulation (61, 91). For instance, mindfulness training is associated with strengthening of functional connectivity within a dorsal attentional network (92) and MBIs can increase attentional re-orienting capacity, i.e., the ability to engage, disengage, and shift attention efficiently from one object to another subserved by dorsal attentional systems (93, 94). Other studies demonstrate that long-term mindfulness training strengthens alerting (93,95), i.e., a vigilant preparedness to detect and attend to incoming stimuli, subserved by the ventral attentional stream. In addition, dispositional mindfulness is positively associated with self-reported attentional control (68) and behavioral indices of sustained attention capacity (70). Recently, data from a randomized controlled trial indicated that 8 weeks of Mindfulness-Oriented Recovery Enhancement led to significant reductions in attentional bias to pain-related cues in a sample of opioid-misusing chronic pain patients (96).

MBIs may target addiction attentional bias by facilitating attentional disengagement from substance-related stimuli. In support of this hypothesis, a study of alcohol dependent adults in residential treatment identified a significant negative correlation between dispositional mindfulness and alcohol attentional bias for stimuli presented for 2000 ms that remained robust even after controlling for alcohol dependence severity, craving, and perceived stress (1). Hypothetically, alcohol dependent persons higher in dispositional mindfulness might exhibit increased capacity for attentional disengagement from alcohol cues by virtue of enhanced PFC and anterior cingulate cortex functionality, as these brain structures have been implicated in addiction attentional bias (9799). Concomitantly, the degree to which alcohol dependent individuals higher in dispositional mindfulness were better able to disengage their attention from alcohol cues than their less mindful counterparts predicted the extent of heart-rate variability (HRV) recovery (an index of prefrontal-autonomic regulation) from stress-primed alcohol cue-exposure (67). Mindfulness training may also affect attentional orienting to substance-related cues. Among a sample of alcohol dependent adults in inpatient treatment, Mindfulness-Oriented Recovery Enhancement was found to result in significant effects on alcohol attentional bias for cues presented for 200 ms (7), indicating modulation of automatic initial orienting to alcohol cues [c.f. (23)]. In individual difference analyses, reductions in attentional bias following Mindfulness-Oriented Recovery Enhancement were significantly associated with decreases in thought suppression, which were, in turn, correlated with increases in HRV recovery from alcohol cue-exposure and improvements in self-reported ability to regulate alcohol urges.

Hence, mindfulness training may strengthen the capacity to regulate attention in the face of conditioned stimuli associated with past substance use, countering attentional biases by refocusing attention on neutral or health-promoting stimuli (e.g., the sensation of one’s own breath or a beautiful sunset). Repeatedly redirecting attention from substance-related cues toward innocuous stimuli may foster extinction of associations between substance-related cues and drug-use action schema. This potential mechanism may explain how attentional bias modification among addicts leads to decreased substance use and improved treatment outcomes (100,101). Future research could evaluate the effects of mindfulness training and MBIs on addiction attentional bias with the use of a dot probe task alone or coupled with eye tracking and analysis of event-related potentials (ERPs) to determine at what stage of attentional selection (initial orienting vs. later attentional disengagement) training has significant effects.

CUE-ELICITED CRAVING

The urge to seek intoxication from addictive substances is driven, in part, by reactivity to substance-related stimuli which have been conferred incentive salience, and is magnified by negative affective states. Several studies demonstrate that MBIs can produce significant reductions in craving (4,8,102105). However, other studies have failed to identify significant reductions in craving among participants of MBIs (7, 106108).

Mindfulness-based interventions may positively influence craving-related processes in several ways. First, mindfulness training may decrease bottom-up reactivity to drug-related stimuli, as mediated by reduced activation in the subgenual anterior cingulate cortex and striatum during exposure to substance cues (105). Second, mindfulness training may decouple negative emotion from craving. Although negative emotion is a common precipitant of craving and subsequent relapse (109), mindfulness training may extinguish this association, such that an addict experiencing sadness, fear, or anger could allow these emotions to arise and pass without triggering an appetitive reaction. Indeed, substance dependent individuals participating in Mindfulness-Based Relapse Prevention were less likely to experience craving in response to depressed mood, and this reduced craving and reactivity to negative emotion predicted fewer days of substance use (110).

MBIs may also produce therapeutic effects by increasing awareness of implicit craving responses. Tiffany (20) proposed that conscious craving occurs when an activated drug-use action schema is blocked from obtaining the goal of drug consumption. As such, persons in acute withdrawal, persons unable to obtain drugs (e.g., due to lack of funds or availability), or persons attempting to maintain abstinence in the face of triggers may experience an upwelling of craving for substances. In contrast, according to this theory, addicts who are able to obtain and use drugs in an unimpeded fashion would not experience craving. Similarly, persons in long-term residential treatment who are isolated from drug-related cues are unlikely to be conscious of craving. Without awareness of craving, the addict may unwittingly remain in high-risk situations and thus be especially subject to relapse. Indeed, lack of awareness of substance craving has been shown to be predictive of future relapse (111). MBIs may increase conscious access to the appetitive drive to use substances by virtue of their effects on increasing interoceptive awareness (78, 112). In that regard, mindfulness training has been shown to increase activity in the anterior insula during provocations by emotionally salient stimuli (113, 114). The anterior insula subserves interoception and awareness of the physical condition of the body, among other related processes (115). Increased neural activity in the insula during mindfulness meditation may index heightened access to interoceptive information.

In synthesizing the findings regarding attentional bias and cue-induced craving, we suggest that MBIs may restructure attentional bias away from drug-related reinforcing stimuli (e.g., drug-cues, negative affective stimuli) and facilitate the addict’s attempts to deal with associated cravings. We posit that mindfulness-centered regulation of cue-elicited appetitive responses occurs as a result of strengthening frontal-executive circuit-function and enhancing neural communication to the hippocampus and thalamus through formal and informal mindfulness meditation practices. The hippocampus is critical for context-dependent learning and memory – with reciprocal connectivity to brain regions that code for reward (ventral striatum), interoception (insula), affect (amygdala), and thalamus. In turn, the thalamus, a complex structure that is generally considered to serve as a relay station between limbic, striatal, and cortical circuits, contains efferent and afferent projections with striatal, limbic, somatosensory, ACC, lateral and medial PFC, and OFC. Thus, the recovering addict may utilize mindfulness training to become aware of which cues are under the spotlight of attention, and become more sensitive to how those cues may trigger changes in body state and motivation drive.

Hence, mindfulness may increase awareness of craving and thereby facilitate cognitive control of otherwise automatic appetitive impulses. In that regard, a recent study found that participation in Mindfulness-Oriented Recovery Enhancement was associated with decreased correlation strength between opioid craving and opioid misuse, suggesting that mindfulness training may have decoupled appetitive responses from addictive behaviors (8). This mechanism may explain the disparate findings vis-a-vis the effects of mindfulness on craving: because of potential underreporting of baseline levels of craving among individuals with impaired insight into their addiction (34), this increased awareness may confound researchers’ attempts to measure the impact of mindfulness training on craving, resulting in an apparent lack of change in craving over time.

The effects of mindfulness on cognitive regulation of craving might be measured by utilizing neuroimaging methodology (e.g., fMRI) to investigate neural circuitry function while participants attempt to regulate their craving response to salient drug-cues. For example, cognitive regulation appears to decrease cigarette craving concomitant with increased activity in dACC (116) and prefrontal regions coupled with attenuated activity in striatal regions (117). A complementary approach to probing the effects of mindfulness on regulating craving may be to utilize real-time fMRI (rt-fMRI). rt-FMRI involves providing subjects with real-time feedback of the BOLD signal within a brain region of interest (ROI) while they attempt to regulate the response within that ROI. This approach has been used to manage pain (118) and reduce cigarette cue craving in nicotine dependent smokers during smoking cessation (119). Evaluating the effects of mindfulness-centered regulation of craving-related neural circuitry in real-time may include a number of benefits including: (a) directly measuring which circuits are being effectively modulated and which are not; (b) feedback to the subject that will help guide mindfulness efforts; and (c) identifying individual differences associated with differential effects of MBIs on specific neural mechanisms.

COGNITIVE APPRAISAL

Insofar as stress evokes automatic responses and impairs prefrontally mediated cognitive control functions (120), exposure to socioenvironmental stressors may render addicts in recovery vulnerable to relapse (1, 22, 121). Mindfulness training may allay stress-induced relapse by virtue of its stress-reductive effects (122). Although early theorists believed that mindfulness meditation reduced stress primarily by evoking a generalized relaxation response (123), modern research indicates that mindfulness practice may also attenuate stress by targeting cognitive mechanisms (1, 124). One potential target of mindfulness is cognitive appraisal, the process whereby stimuli and their environmental context are evaluated for their significance to the self (125). Appraisals of threat or harm elicit negative emotional reactions coupled with activation of stress physiology. When recurrent, such emotional reactivity biases perception, leading to exaggerated, overestimated appraisals of threat and underestimations of self-efficacy (126), and ultimately, sensitization to future stressors (127).

In contrast, mindfulness, which has been conceptualized as a non-reactive form of awareness (128) may enable the individual to cognitively appraise his or her present circumstances with less emotional bias, and to more accurately assess his or her ability to cope with present challenges (60). Thus, MBIs may impact both primary (rapid and implicit) and secondary (slow and explicit) appraisal processes (125). In partial support of this hypothesis, a recent neuroimaging study revealed that, in contrast to a meditation-naive control group, mindfulness meditation practitioners exhibited decreased reactivity to briefly presented negative emotional cues in frontal-executive brain regions (i.e., dorsolateral PFC) and less deterioration of positive affect in response to cue-elicited amygdala activation (31). These data suggest that mindfulness training may alter the allocation of cognitive resources during appraisal of negative emotional stimuli and attenuate the influence of limbic reactivity on mood state. Other research demonstrates that mindfulness training minimizes emotional interference from unpleasant stimuli [e.g., Ref. (129)]. In so doing, mindfulness training may reduce biases toward negative emotional information processing. Among persons with a history of depression, Mindfulness-Based Cognitive Therapy reduces overgeneral memories (130) and cognitive bias toward negative information (131). Among individuals suffering from chronic pain, Mindfulness-Oriented Recovery Enhancement decreases cognitive bias toward pain-related cues (96). Together, these findings suggest that MBIs may decrease negative emotional bias in initial cognitive appraisal processes, thereby reducing the downstream effects of stress on addictive behavior. As mindfulness-centered regulation enhances cortico-thalamic-limbic functional connectivity, the recovering addict becomes more aware of relations between attention, emotional state, and motivation. This awareness provides an opportunity to deploy cognitive strategies to respond to the environment in a more adaptable context-dependent manner, rather than responding from a pattern of overlearned reactive behaviors.

References

1. Garland, E. L., Froeliger, B., & Howard, M. O. (2013). Mindfulness  training targets neurocognitive mechanisms of addiction at the attention-appraisal-emotion interface. Frontiers in psychiatry, 4.

How does the First Drink really get you Drunk?

In treatment circles, I have constantly heard the refrain “one is not enough and two is too many!” and “the first drink gets you drunk” which points to a difficulty certain people have with stopping once they start drinking; a “loss of control” over drinking.

It is as if drinking gives you a thirst rather than taking it away. Many thousands of recovering alcoholics will tell you about this phenomenon – how they had only intended to have a couple but then lost a weekend to drinking instead.

It is an essential question to get to the bottom of, why do certain people not have the ability  or have a reduced ability to stop once they start.

I came across an article from a few years back which addressed this issue (1) .

In those with a family history of alcoholism,  drinking alcohol affects how the brain responds to an alcohol cue – in other words these individuals appear to want more compared to controls when they see alcohol cues. So drinking alcohol heightens a wanting for alcohol  rather than causing a  feeling of having had enough (not wanting). 

Although a family history of alcoholism is the strongest risk factor for developing alcohol dependence, there are few studies of the association between familial alcoholism and the human brain’s reward system activity. This study used a functional magnetic resonance imaging (fMRI) to determine how family history affects the brain’s response to subjects’ preferred alcoholic drink odors (AO).

A family history of alcoholism doubles the odds of developing alcoholism (Hasin et al., 1997; Nurnberger et al., 2004). While environmental influences exert considerable influence in early adolescence, twin studies show an increasingly larger genetic influence by age 18 (Dick, Rose, & Kaprio, 2006), with a family history of alcoholism being a significant factor in the transition from abusive to dependent drinking (Hasin, Paykin, & Endicott, 2001).

While a number of studies have examined the human cerebral response to alcohol-related cues, particularly in alcoholics (e.g., Bragulat et al., 2008; Filbey et al., 2008b;Kareken et al., 2004; Myrick et al., 2008; Tapert et al., 2004;Wrase et al., 2007), very little research shows how familial alcoholism affects the brain response to alcohol-related cues— particularly in at-risk individuals who have yet to become dependent.

 

041123_drunk_rats_hmed4p.grid-6x2

Animal research suggests that selective breeding for alcohol preference might affect the heavily dopaminergic mesocorticolimbic reward system. For example, rodents selectively bred to prefer alcohol have reduced dopamine in the striatum (see Murphy et al., 2002; Strother et al., 2005) and medial prefrontal cortex (Engleman et al., 2006), but greater striatal dopaminergic responses to alcohol itself (Bustamante et al., 2008; also see Smith & Weiss, 1999;Weiss et al., 1993). In at least one case, alcohol-preferring rats (compared to Wistar rats) showed a greater dopaminergic response in the ventral striatum during alcohol anticipation (Katner, Kerr, & Weiss, 1996). In non-abusive drinkers without a family history of alcoholism there is greater striatal dopamine receptor availability (Volkow et al., 2006), suggesting a potential protective factor.

Family history affects the brain’s response to alcohol’s olfactory (smell) cues in non-dependent, at-risk heavy drinkers and this study  sought to determine how acute alcohol exposure affects the reward system’s response to alcohol’s conditioned cues by using intravenous (IV) alcohol infusion— a method that prescribes a constant level of brain alcohol throughout functional imaging and avoids the highly variable time courses of breath alcohol concentrations that accompany oral consumption (O’Connor et al., 1998; Plawecki et al., 2007;Ramachandi et al., 2004; Ramchandani et al., 1999).

So in effect alcohol was infused rather than simply drunk.

The researchers hypothesized that a family history of alcoholism would be associated with stronger responses to alcoholic drink aromas in the mesocorticolimbic reward system, and that a low-level of steady-state brain exposure to alcohol would potentiate these stimulus-induced responses (Bragulat et al., 2008). Such a potentiation could reflect a possible substrate for priming, when alcohol exposure increases desire to drink (De WitDe Wit, 2000).

In this study (1) fourteen non-dependent heavy drinkers (HD) who were family history positive (FHP) participated, as did 12 HD who were family history negative (FHN). Subjects were imaged under both alcohol intoxication and placebo.

In this study alcohol intoxication dampened this “cued” response in the HD-FHP but potentiated (heightened)  it in the HD-FHN.

This suggests that a family history of alcoholism and brain exposure to alcohol interact in heavy drinkers to differentially affect how the brain responds to alcohol cues.

In conclusion, frontal regions thought to process reward value may respond differently to alcohol’s classically conditioned cues in subjects with a family history of alcoholism. While alcohol appears to dampen medial frontal responses to alcohol cues in HD-FHP, it may enhance it in HD-FHN. Genetic background may therefore determine when, and under what circumstances, cues activate the reward network

References

Kareken, D. A., Bragulat, V., Dzemidzic, M., Cox, C., Talavage, T., Davidson, D., & O’Connor, S. J. (2010). Family history of alcoholism mediates the frontal response to alcoholic drink odors and alcohol in at-risk drinkers. Neuroimage,50(1), 267-276.