Alcohol-induced heart rate response dampening during aversive and rewarding stress paradigms in subjects at risk for alcoholism

Croissant, Bernhard; Rist, Fred; Demmel, Ralf; Olbrich, Robert

doi:10.1016/j.ijpsycho.2005.10.016

Cited by 12 publications

(9 citation statements)

References 14 publications

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“…This effect is thought to encourage chronic self-medication because of the temporary negative reinforcement alcohol can provide (Morris et al 2005). Inconsistent empirical support for these models has underlined the importance of individual differences in risk for alcoholism (Sher and Levenson 1982), including gender, family history of alcoholism, and personality characteristics such as high novelty seeking and low harm avoidance (Croissant et al 2008; Croissant et al 2006). …”

Section: Discussionmentioning

confidence: 99%

Effect of the TaqIA polymorphism on ethanol response in the brain

London

Berman

Mohammadian

et al. 2009

Psychiatry Research: Neuroimaging

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Acute ethanol administration increases striatal dopamine release and decreases cerebral glucose metabolism. The A1 allele of the ANKK1 TaqIa polymorphism is associated with lower dopaminergic tone and greater risk for alcoholism, but the mechanisms are unclear. We hypothesized that ethanol would be more reinforcing in men with the A1 allele (A1+) than in men without it (A1−), as indicated by decreased anxiety and fatigue and altered activity in associated brain regions. In a pilot study, A1+ and A1− men (6/group) drank ethanol (0.75 ml/kg) or placebo beverages on each of two days. Positron emission tomography with [F-18]fluorodeoxyglucose (FDG) was used to assess regional cerebral glucose metabolism as a measure of relative brain activity while participants performed a vigilance task. Ethanol decreased anxiety and fatigue in A1+ men but increased them in A1− men (p = 0.008). Ethanol increased activity in the striatum (p = 0.005) and insula (p = 0.001) of A1+ men, but reduced activity in the anterior cingulate of A1− men (p = 0.03). Reduced anxiety and fatigue in A1+ men were significantly associated with greater activity within a right orbitofrontal region previously implicated in cognitive control, and less activity in structures associated with anxiety (amygdala), fatigue (thalamus), and craving/reinforcement (striatum). In contrast, anxiety and fatigue changes were unrelated to brain activity in A1− men. Although these results require replication in a larger sample, alcohol-induced negative reinforcement may explain the greater risk for alcoholism associated with the A1 allele.

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Section: Discussionmentioning

confidence: 99%

Effect of the TaqIA polymorphism on ethanol response in the brain

London

Berman

Mohammadian

et al. 2009

Psychiatry Research: Neuroimaging

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“…Affective response magnitude has been identified as an important parameter of affective style that may be governed by distinct neurocircuitry and display important individual differences (Davidson et al 2000). Croissant et al (2006) have provided recent indirect evidence to implicate affective response magnitude in alcohol SRD effects as well. Finally, we test the possible moderating role of SRD relevant individual differences in trait affectivity (positive emotionality, negative emotionality and constraint/disinhibition), alcohol use, and alcohol problems.…”

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confidence: 99%

Alcohol dose effects on stress response to cued threat vary by threat intensity

2011

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Rationale Clarification of alcohol’s effect on stress response during threat is critical to understand motivation for alcohol use and related alcohol-use disorders. Evaluation of stress response dampening (SRD) effects of alcohol has been limited by nonsystematic use of varied experimental methods and measures. Objectives This experiment parametrically varied alcohol dose and shock threat intensity among social drinkers to examine their effects on startle potentiation, a physiological measure of the affective component of the stress response. Methods 96 participants were assigned to one of four beverage groups: placebo and target blood alcohol concentration (BAC) groups of 0.04, 0.075, and 0.11%. Participants viewed colored cues presented in shock and no-shock blocks. Distinct colored cues predicted imminent low, moderate, or high intensity electric shock administration. Startle potentiation during shock threat relative to no-shock cues indexed affective response. Results High threat increased startle potentiation relative to moderate/low intensity threat. Startle potentiation decreased as BAC increased. Threat intensity moderated this BAC effect with the strongest BAC effect observed during high threat. Analysis of individual difference moderators revealed reduced effect of BAC among heavier, more problematic drinkers. Conclusions Clear alcohol SRD effects were observed. These SRD effects were greatest at higher BACs and during more potent threat. Failure to account for these factors may partially explain inconsistent findings in past laboratory SRD research. Furthermore, they suggest greater reinforcement from alcohol at higher doses and among individuals with greater stress. Moderation of SRD effects by alcohol consumption and problems point to possible important risk factors.

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“…Multigenerational FHP > FHN @ 20 minutes Conrod et al (1997a) Heart rate at rest Multigenerational FHP > FHN @ 10 to 40 minutes Conrod et al (1997b) Heart rate at rest Heavy drinkers > Light drinkers @ 30 to 35 minutes Conrod et al (1998) Heart rate at rest Multigenerational FHP > FHN @ 30 to 35 minutes Croissant et al (2006) Heart rate at rest Female FHP > Female FHN @ 25 minutes Sinha et al (1998) Heart rate at rest FHP (alcoholism and anxiety) > FHN @ 30 minutes Heart rate at rest FHP men > FHN men @ 30 minutes Pulse transit time at rest FHP (alcoholism and anxiety) > FHN @ 30 minutes Peterson et al (1996) Heart rate at rest Multigenerational FHP > FHN @ 15 minutes Heart rate at rest Alcoholics > Controls @ 15 minutes Beta-endorphin Heart rate responders > nonresponders @ 45 and 120 minutes Newlin and Thomson (1999) Pulse transit time at rest FHP > FHN @ 30 minutes Body sway FHP > FHN @ 30 minutes Cohen et al (1998) C z P200 decrements FHP > FHN @ 0-20 minutes Cohen et al (1993) Slow alpha at F3, F4, P4 FHP > FHN @ 35 minutes Gianoulakis et al (1996) Beta-endorphin FHP > FHN Lex et al (1991) Cortisol Women FHP > Women FHN @ 130 and 150 minutes Blekher et al (2002) Antisaccade latencies FHP > FHN @ 60 minutes Ramchandani et al (1999) BAES stimulation FHP > FHN @ 10 minutes Short term memory FHP > FHN @ 10 minutes Random saccades FHP > FHN @ 10 minutes Volitional saccades FHP > FHN @ 10 minutes P300 latency FHP > FHN @ 10 minutes Cowley et al (1994) ARCI MBG to diazepam FHP > FHN -diazepam Streeter et al (1998) ''Feeling'' drug (alprazolam) FHP > FHN @ 1 and 2 hours -alprazolam ''Liking'' drug (alprazolam) FHP > FHN @ 2 hours -alprazolam ARCI -MBG (alprazolam) FHP > FHN @ 1-2 hours -alprazolam…”

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confidence: 99%