Alcohol consumption and cancer of the gastrointestinal tract

被引:55
作者
Salaspuro, MP [1 ]
机构
[1] Univ Helsinki, Biomed Helsinki, Res Unit Subst Abuse Med, Cent Hosp, Helsinki 00029, Finland
关键词
acetaldehyde; alcohol; alcohol dehydrogenase; aldehyde dehydrogenase; atrophic gastritis; bacteria; cancer; colon cancer; oesophageal cancer; digestive tract; ethanol; gastric cancer; gut flora; microbes; oral cancer;
D O I
10.1016/S1521-6918(03)00035-0
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Excessive alcohol consumption and heavy smoking are the main risk factors for upper digestive tract cancers. Cancer risk is dose-dependent and alcohol and smoking have synergistic effects. Alcohol is not carcinogenic. However, its first metabolite acetaldehyde-has recently been shown to be a local carcinogen in humans. Microbes representing normal human gut flora are able to produce acetaldehyde from ethanol. This results in high local acetaldehyde concentrations in the saliva and contents of the large intestine. Asian heavy drinkers with a genetic deficiency for detoxifying acetaldehyde form an exceptional human 'knockout' model for long-term acetaldehyde exposure. The risk of alcohol-related digestive tract cancers is particularly high among this population. All mechanisms that have an effect on salivary or intracolonic acetaldehyde concentration are of importance. The message for prevention is that one should take care to have good oral hygiene and to avoid smoking, heavy drinking and drinking to intoxication.
引用
收藏
页码:679 / 694
页数:16
相关论文
共 103 条
[11]  
657::AID-IJC7&gt
[12]  
3.0.CO
[13]  
2-C
[14]   Interaction between the functional polymorphisms of the alcohol-metabolism genes in protection against alcoholism [J].
Chen, CC ;
Lu, RB ;
Chen, YC ;
Wang, MF ;
Chang, YC ;
Li, TK ;
Yin, SJ .
AMERICAN JOURNAL OF HUMAN GENETICS, 1999, 65 (03) :795-807
[15]   CELL-PROLIFERATION IN CARCINOGENESIS [J].
COHEN, SM ;
ELLWEIN, LB .
SCIENCE, 1990, 249 (4972) :1007-1011
[16]  
Colman G, 1976, Aust Dent J, V21, P111
[17]   Laryngeal and oropharyngeal cancer, and alcohol dehydrogenase 3 and glutathione S-transferase M1 polymorphisms [J].
Coutelle, C ;
Ward, PJ ;
Fleury, B ;
Quattrocchi, P ;
Chambrin, H ;
Iron, A ;
Couzigou, P ;
Cassaigne, A .
HUMAN GENETICS, 1997, 99 (03) :319-325
[18]   GENOTYPES FOR ALDEHYDE DEHYDROGENASE-DEFICIENCY AND ALCOHOL SENSITIVITY - THE INACTIVE ALDH22 ALLELE IS DOMINANT [J].
CRABB, DW ;
EDENBERG, HJ ;
BOSRON, WF ;
LI, TK .
JOURNAL OF CLINICAL INVESTIGATION, 1989, 83 (01) :314-316
[19]  
DAY NE, 1975, CANCER RES, V35, P3304
[20]  
Doll R, 1999, HLTH ISSUES RELATED, P351