Abstract
BACKGROUND: The insular cortex (IC), which includes anterior (AIC) and posterior (PIC) subdivisions, plays a role in numerous functions and behaviors, including chronic alcohol consumption. This study investigated acute alcohol effects on functional connectivity (FC) of the IC in healthy social drinkers. We hypothesized that acute alcohol consumption would significantly disrupt IC resting-state FC (rsFC) with the whole brain and would differentially modulate the rsFC of the AIC and PIC. This study also examined the association of alcohol-induced changes in IC rsFC with subjective intoxication and whether sex and family history of alcohol problems moderate the effect of acute alcohol intake on IC rsFC. METHODS: One hundred and seven healthy social drinkers (25-45 years) completed two counterbalanced laboratory sessions where they consumed either a placebo or alcohol-containing beverage (target breath alcohol concentration 0.08 g/dL), followed by a 9-min resting-state functional magnetic resonance imaging scan. Subjective intoxication was assessed using a visual analog scale from "not at all intoxicated" to "most intoxicated imaginable." Effects of alcohol on IC connectivity were assessed using the CONN toolbox with IC regions of interest (ROIs) defined using the atlas of intrinsic connectivity of homotopic areas (AICHA). RESULTS: Alcohol intake resulted in widespread changes in rsFC of the IC with other brain regions, including increased rsFC with nodes of the salience network. Alcohol also attenuated differences in rsFC between the AIC and PIC compared with placebo. Sex and family history of alcohol problems did not significantly moderate these effects. CONCLUSIONS: Acute alcohol intake altered the rsFC of the IC and its connections to numerous structures. Consistent with prior evidence that alcohol disrupts the brain's functional organization, alcohol intake tended to attenuate differences in the connectivity profiles of AIC and PIC. Additional research is needed to determine how these effects may underlie alcohol's broader neurobehavioral consequences.