The Alcohol Flushing Response: An Unrecognized Risk Factor for Esophageal Cancer from Alcohol Consumption

Philip J Brooks,Akira Yokoyama,David Goldman,Mary-Anne Enoch,Ting-Kai Li

doi:10.1371/journal.pmed.1000050

Abstract

Philip Brooks and colleagues discuss evidence linking the alcohol flushing response (predominantly due to ALDH2 deficiency) with a much higher risk of esophageal cancer from alcohol consumption.

Highlights

SÈ +NOWLEDGEÈOFÈTHEÈFLUSHINGÈRESPONSEÈISÈ useful clinically, as it allows doctors to identify their aldehyde dehydrogenase 2 (ALDH2)-deficient patients in a simple, cost-effective, and noninvasive manner
Reduce alcohol consumption, and high-risk patients can be assessed for endoscopic cancer screening
In a population of this size, even a small reduction in the incidence of esophageal cancer could result in a substantial reduction in esophageal cancer deaths worldwide

Summary

Introduction

SÈ +NOWLEDGEÈOFÈTHEÈFLUSHINGÈRESPONSEÈISÈ useful clinically, as it allows doctors to identify their ALDH2-deficient patients in a simple, cost-effective, and noninvasive manner. Alcohol consumed by ALDH2deficient individuals is metabolized to acetaldehyde, which accumulates in the body due to absent ALDH2 activity and results in facial flushing (Figure 1), nausea, and tachycardia [2]. This observation provided evidence for a causative role for ethanol in esophageal cancer, and a key role for acetaldehyde paradoxically, it is the more common low-activity ALDH2 heterozygous genotype that is associated with greatest risk of esophageal cancer from drinking alcohol.

Results

Conclusion