Ingesting a small amount of beer reduces arterial stiffness in healthy humans

Abstract

Epidemiological studies reveal a J-shaped association between alcohol consumption and arterial stiffness, with arterial stiffening lower among mild-to-moderate drinkers than heavy drinkers or nondrinkers. This study aimed to examine the effects of ingesting a small amount of beer, corresponding to the amount consumed per day by a mild drinker, on arterial stiffness. Eleven men (20-22 years) participated, in random order and on different days, in four separate trials. The participants each drank 200 or 350 mL of alcohol-free beer (AFB200 and AFB350) or beer (B200 and B350), and were monitored for 90 min postingestion. There were no significant changes in arterial stiffness among trials that ingested AF200 or AF350. However, among trials ingesting B200 and B350, breath alcohol concentrations increased significantly, while indexes of arterial stiffness decreased significantly for approximately 60 min: carotid-femoral pulse wave velocity (B200: -0.6 ± 0.2 m/sec; B350: -0.6 ± 0.2 m/sec); brachial-ankle pulse wave velocity (B200: -53 ± 18 cm/sec; B350: -57 ± 19 cm/sec); and cardio-ankle vascular index (B200: -0.4 ± 0.1 unit; B350: -0.3 ± 0.1 unit). Furthermore, AFB showed no effect on arterial stiffness, regardless of whether or not it contained sugar, and no significant difference in antioxidant capacity was found between AFB and B. This is the first study to demonstrate that acute ingestion of relatively small amounts of beer reduces arterial stiffness (for approximately 60 min). Our data also suggest that the reduction in arterial stiffness induced by ingestion of beer is largely attributable to the effects of alcohol.

Keywords: Alcohol; arterial stiffening; arteriosclerosis; cardio‐ankle vascular index; pulse wave velocity.

Figure 1

Time course of the experiment. Solid arrows, time points of measurements of breath alcohol level, brachial‐ankle pulse wave velocity, cardio‐ankle vascular index, and hemodynamics; broken arrows, time points of measurements of carotid‐femoral pulse wave velocity; AF, alcohol‐free.

Figure 2

Effects of ingesting a small amount of beer on breath alcohol level (A), cfPWV (B), baPWV (C), and CAVI (D). Broken lines, time point of each beverage ingestion; Pre, baseline; cfPWV, carotid‐femoral pulse wave velocity, which is the gold‐standard indicator of central arterial stiffness; baPWV, brachial‐ankle pulse wave velocity, which reflects systemic arterial stiffness; CAVI, cardio‐ankle vascular index of arterial stiffness (adjusted for blood pressure); AF200 and AF350, alcohol‐free beer ingestion at 200 and 350 mL, respectively; B200 and B350, beer ingestion at 200 and 350 mL, respectively; *P < 0.05 versus each pre; **P < 0.01 versus each pre; †P < 0.05 versus each AF trial; ††P < 0.01 versus each AF trial. Data are expressed as mean ± SE.

Figure 3

Supplementary experimental data for baPWV (A), CAVI (B), and antioxidant capacity (C). Broken lines, time points of each beverage ingestion; Pre, baseline; AF, alcohol‐free beer without sugar; AFS, alcohol‐free beer with sugar; PW, pure water; B, beer; baPWV, brachial‐ankle pulse wave velocity; CAVI, cardio‐ankle vascular index; **P < 0.01 versus PW; ††P < 0.01 versus AFS. Data are expressed as mean ± SE.