Acetaldehyde and gastric cancer

Abstract

Aldehyde dehydrogenase (ALDH2) and alcohol dehydrogenase (ADH) gene polymorphisms associating with enhanced acetaldehyde exposure and markedly increased cancer risk in alcohol drinkers provide undisputable evidence for acetaldehyde being a local carcinogen not only in esophageal but also in gastric cancer. Accordingly, acetaldehyde associated with alcoholic beverages has recently been classified as a Group 1 carcinogen to humans. Microbes are responsible for the bulk of acetaldehyde production from ethanol both in saliva and Helicobacter pylori-infected and achlorhydric stomach. Acetaldehyde is the most abundant carcinogen in tobacco smoke and it readily dissolves into saliva during smoking. Many foodstuffs and 'non-alcoholic' beverages are important but unrecognized sources of local acetaldehyde exposure. The cumulative cancer risk associated with increasing acetaldehyde exposure suggests the need for worldwide screening of the acetaldehyde levels of alcoholic beverages and as well of the ethanol and acetaldehyde of food produced by fermentation. The generally regarded as safe status of acetaldehyde should be re-evaluated. The as low as reasonably achievable principle should be applied to the acetaldehyde of alcoholic and non-alcoholic beverages and food. Risk groups with ADH-and ALDH2 gene polymorphisms, H. pylori infection or achlorhydric atrophic gastritis, or both, should be screened and educated in this health issue. L-cysteine formulations binding carcinogenic acetaldehyde locally in the stomach provide new means for intervention studies.

Combined Extracts of Artemisia and Green Tea, Mitigated Alcoholic Gastritis Via Enhanced Heat-shock Protein 27

“…[27][28][29] Although not studied in the current study, acetaldehyde associated with alcoholic beverages has been classified as a Group 1, definite, carcinogen in humans. 30 The cumulative cancer risk associated with increasing alcohol exposure has necessitated intervention studies, such as slow-release L-cysteine capsules 31 or agents to reduce the mutagenic actions of alcohol. 32 Although there is significant evidence, in the current study, ethanol exposure decreased the expression of 15-PGDH.…”

Upper Gastrointestinal Tract Cancers as Double-cancers in Elderly Patients with Oral Squamous Cell Carcinoma

“…The esophagus is directly exposed to carcinogens in tobacco smoke entering it from the larynx, and indirectly exposed to carcinogens mixed in saliva 14) . Histological differences are also known to exist between the oral and esophageal mucosas and the gastric mucosa: the former are lined with stratified squamous epithelium, whereas the latter comprises single-layer columnar epithelium.…”

“…However, others found that most double-cancer patients had smoking and drinking habits 22) . Moreover, smoking and drinking have been listed as risk factors for esophageal cancer 11,14) , and they are also thought to contribute to the development of OSCC 8) . In the present survey, OSCC patients with esophageal cancer as a double-cancer did not show a significant association with smoking or drinking history.…”

Geographic particularities in incidence and etiopathogenesis of sporadic gastric cancer

“…On the other hand, the International Agency for Research on Cancer (IARC) revealed that the concentration of acetaldehyde, a group 1 human carcinogen and a water-soluble compound, is over 1000-fold in cigarette smoke; during active smoking, it dissolves in saliva and reaches high concentrations by modifying the oral flora to produce more of the compound from ethanol. Together, smoking and alcohol intake seem to have a seven-fold effect in increasing exposure of the upper gastrointestinal tract to acetaldehyde [7,36], although there are authors who even deny the carcinogenic role of alcohol in gastric carcinogenesis [37] or consider that the risk of non-cardia intestinal-type GC is higher in patients whose intake is ≥ 60 g alcohol/day, 2-7 days/week, for a medium period of 9-10 years [38]. Regarding the type of the ingested alcohol, heavy wine drinkers are more predisposed than consumers of beer or vodka [39].…”