Hyperalgesia After a Drinking Episode in Young Adult Binge Drinkers

A Cross-Sectional Study

Dokyoung S. You; Hunter A. Hahn; Thomas H. Welsh Jr.; Mary W. Meagher

Disclosures

Alcohol Alcohol. 2020;55(6):608-615. 

In This Article

Results

Pain Sensitivity

To examine group differences in cutaneous mechanical, heat and muscle PPTs, a MANOVA was conducted. The results revealed a significant main effect of group, Wilk's Λ = 0.80, P < 0.001. Follow-up univariate analysis indicated that only muscle PPT was different between the groups, F(4, 165) = 7.10, P < 0.001, partial η 2 = 0.14. LSD post-hoc analysis indicated that the binge group without recent drinking, lnM = 1.02, lnSD = 0.50, showed lower muscle PPTs when compared to the moderate drinking group without recent drinking, lnM = 1.27, lnSD = 0.47, P = 0.013 (Figure 2). These results indicate the divergent effects of alcohol consumption on muscle PPT. Specifically, moderate drinking was associated with an increase in PPT, whereas binge drinking was associated with a decrease in PPT. Notably, the binge group with recent drinking, lnM = 0.67, lnSD = 0.51, showed reduced PPT compared to all the other groups, Ps < 0.005. Lastly, neither cutaneous MPT (P = 0.148) nor heat pain threshold (P = 0.393) differed significantly between groups, suggesting that binge drinking and alcohol withdrawal were unrelated to cutaneous mechanical and heat pain thresholds in young adult binge drinkers.

Figure 2.

Comparison of muscle pressure pain, cutaneous mechanical and heat pain thresholds between the groups with different drinking patterns (Error bars = SEM).

Stress Hormones in Relation to Drinking Patterns and Pain Sensitivity

A time × gender × group repeated measures ANOVA was conducted for epinephrine (Figure 3, Upper Left). The results showed no significant time (P = 0.296) nor interaction effects (Ps > 0.245, Figure 3, upper right). There were significant main effects of group, F(4, 167) = 2.66, P = 0.035, and gender, F(1, 167) = 10.62, P = 0.001, but no significant gender x group interaction (P = 0.834). The main effect of gender on basal epinephrine was driven by higher levels in men, = 14.91, = 6.15, compared to women, = 11.78, = 6.58.

Figure 3.

Comparison of epinephrine (upper left) and cortisol concentrations (lower left) between the groups with different drinking patterns (Error bar = SEM).

An LSD post-hoc analysis showed that binge drinkers without recent drinking, = 15.43, = 5.99, showed elevated epinephrine levels compared to abstainers, = 11.56, = 5.67, and moderate drinkers without recent drinking, = 12.34, = 5.95. Different from expectation, no significant difference was found between the binge group with and without recent drinking (P = 0.562). These results suggest that binge drinking, but not alcohol withdrawal, was associated with an increase in basal epinephrine levels. A subsequent ANCOVA controlling for basal epinephrine levels indicated that the group difference in muscle PPT remained significant, F(4, 171) = 6.21, P < 0.001, but the effect size was reduced by 7%, partial η 2 = 0.13, suggesting basal epinephrine levels explained a small portion of the variance in binge drinking-associated hyperalgesia.

Next, a time x gender x group repeated measures ANOVA was conducted on cortisol. The results showed a significant effect of time, F(4, 167) = 127.85, P < 0.001, but no other significant main or interaction effects (ps > 0.138). Cortisol levels decreased after the QSTs (M = −26.8, SD = 30.5, Figure 3, Lower right). The lack of a group difference in cortisol suggests cortisol was unrelated to the group difference in PPT.

Negative Effect in Relation to Drinking Patterns and Pain Sensitivity

Because baseline depressive symptoms were significantly higher in drinkers regardless of drinking patterns, no additional tests were conducted. No significant changes in STAI scores by the three QSTs were observed (M = 0.07, SD = 2.42), P = 0.732.

Physiological Responses to Pain Testing

Changes in HR, SCL and RR were compared between the groups with a 3 (time: baseline, pain testing and final) by 5 (group) repeated measures ANOVA. Results revealed significant effects only on time, Ps < 0.001. LSD post-hoc analyses indicated that HR was elevated during pain testing (M = 74.7, SD = 9.5) and after pain testing (M = 74.5, SD = 9.7) compared to baseline (M = 73.6, SD = 9.8). Secondly, compared to baseline (M = 2.3, SD = 0.7), SCL was elevated during (M = 2.8, SD = 0.6) and after pain testing (M = 2.7, SD = 0.6). Thirdly, RRs were elevated during (M = 14.9, SD = 2.3) and after pain testing (M = 14.6, SD = 2.8) compared to baseline (M = 13.8, SD = 3.3). A post-hoc test was conducted for SCL because a significant time by group interaction effect was observed, F(5, 214) = 3.17, P = 0.009. The results indicated that initially different SCLs were no longer different during, P = 0.382, and after pain testing, P = 0.414.

Taken together, psychophysiological responses to pain testing were similar across the groups and paralleled the lack of group differences observed in epinephrine and cortisol responses to pain testing.

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