Drinking less still causes gut damage
Alcohol consumption, even at low levels, contributes to an increased risk of developing gastric precancerous lesions, such as atrophic gastritis (AG) and intestinal metaplasia (IM), a study has found.
The study followed 202,675 Korean adults who underwent repeated endoscopic examinations over a mean follow-up of 4.7 years. Lifetime alcohol abstainers tended to be older and female and have a medication history of dyslipidaemia and cardiovascular disease. Among current drinkers, on the other hand, increasing alcohol consumption positively correlated with blood pressure, glucose, liver enzymes, HOMA-IR, salt intake, total energy intake, and unfavorable lipid profiles.
During follow-up, 64,853 incident AG cases and 4,536 IM cases occurred. Alcohol consumption, including drinking frequency, quantity, and binge drinking, had a dose-response association with the risk of both AG and IM.
Multivariable Cox proportional hazard models revealed that compared with lifetime abstinence, alcohol consumption conferred a risk increase for IM. The adjusted hazard ratios (aHRs) associated with intakes of <10, 10 to <20, 20 to <40, and ≥40 g/day were 1.27 (95 percent confidence interval [CI], 1.02–1.56), 1.34 (95 percent CI, 1.07–1.66), 1.50 (95 percent CI, 1.20–1.86), and 1.54 (95 percent CI, 1.23–1.93), respectively.
The corresponding aHRs for AG were 1.08 (95 percent CI, 1.03–1.13), 1.15 (95 percent CI, 1.09–1.20), 1.20 (95 percent CI, 1.14–1.26), and 1.24 (95 percent CI, 1.18–1.31).
Former drinkers were also at a higher risk of both AG and IM compared with lifetime abstainers. The associations were consistent in never smokers and in time-dependent analyses.
The findings suggest that alcohol consumption even from low-level drinking may promote gastric carcinogenesis.