Effects of stress and alcohol cues in men with and without problem gambling and alcohol use disorder.

BACKGROUND: Relapse is a serious challenge in problem gambling (PG), as it is in substance addiction. Stress and cues are implicated in relapse in both conditions. However, experimental research on motivational effects of stress in PG subjects is scant. This study examined subjective-motivational, cognitive and physiological effects of stress and alcohol cues in subjects with PG, alcohol use disorder (AD), co-occurring PG and AD (CO), and healthy controls (HC). METHODS: Fifty-two (12/clinical group; 16 HC) physically healthy men received stress in the form of 10-min uncontrollable noise (U-Noise vs. controllable noise; C-Noise) and cues (355 ml non-alcoholic 'placebo' beer; P-Beer vs. soft drink) under Separate or Combined conditions on two test sessions. Visual analogue scales assessed subjective effects. Emotional Stroop and Go/No-Go 'Shift' tasks assessed inhibitory control. Systolic blood pressure (SBP) indexed physiological reactivity. RESULTS: U-Noise and C-Noise increased desire for alcohol in all groups. U-Noise selectively inhibited desire to gamble in PG subjects. Both U-Noise and C-Noise inhibited desire to gamble in CO subjects. Neither manipulation reliably altered cognitive performance. Compared to Neutral words, Alcohol words impaired Stroop color-naming in all groups except PG, which displayed relatively faster color-naming of Alcohol words (facilitation). U-Noise increased SBP relative to C-Noise in AD and HC groups. U-Noise plus P-Beer and U-Noise per se decreased SBP in PG and CO groups, respectively. CONCLUSIONS: Noise stress has opposite motivational and physiological effects in men with problem gambling vs. alcohol use disorder. A homeostatic process may explain the impact of stress in problem gamblers.

Stress and alcohol cues exert conjoint effects on go and stop signal responding in male problem drinkers.

Stress, cues, and pharmacological priming are linked with relapse to addictive behavior. Increased salience and decreased inhibitory control are thought to mediate the effects of relapse-related stimuli. However, the functional relationship between these two processes is unclear. To address this issue, a modified Stop Signal Task was employed, which used Alcohol, Neutral, and Non-Words as Go stimuli, and lexical decision as the Go response. Subjects were 38 male problem drinkers (mean Alcohol Dependence Scale (ADS) score: 18.0). Uncontrollable noise (∼ 10 min at 110 dB) was the stressor; nonalcoholic placebo beer (P-Beer) was the cue manipulation, and alcohol (0.7 g/kg), the pharmacological prime. Half the sample received alcohol, and half P-Beer. Stress and beverage (test drink vs soft drink) were manipulated within subjects on two sessions, with half the sample receiving active manipulations together and half receiving them separately. Go response time (RT) and Stop Signal RT (SSRT) were slower to Alcohol than Neutral words. Stress augmented this bias. Alcohol and P-Beer impaired overall SSRT. Stress impaired neither overall SSRT nor Go RT. SSRT to Neutral words and Non-Words correlated inversely with Go RT to Alcohol and Neutral words, and Non-Words. ADS correlated directly with SSRT to Alcohol words. A resource allocation account was proposed, whereby diversion of limited resources to salient cues effectively yoked otherwise independent Go and Stop processes. Disturbances of prefrontal norepinephrine and dopamine were cited as possibly accounting for these effects. Treatments that optimize prefrontal catecholamine transmission may deter relapse by reducing disinhibitory effects of salient eliciting stimuli.