The present review summarizes the clinically relevant effects of acute and chronic alcohol consumption on motility, mucosal inflammation and cancer of the esophagus and the stomach. Alcohol consumption results in a significant increase in the morbidity of these two organs, the most important probably being the significant increase in the development of esophageal cancer. This review refers to epidemiologic and systematic experimental data to elucidate the clinical impact of alcohol consumption as well as the underlying alcohol-induced pathophysiologic mechanisms for these esophageal and gastric diseases. Much research is still needed to clarify the effects of alcohol itself and the byproducts that result during the production of the different types of alcoholic beverages on dismotility and mucosal injury to the esophagus and stomach.

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The secretory response of gastric acid to pure ethanol and alcoholic beverages may be different because the action of the nonethanolic contents of the beverage may overwhelm that of ethanol. Pure ethanol in low concentrations (<5% vol/vol) is a mild stimulant of acid secretion whereas at higher concentrations it has either no effect or a mildly inhibitory one. Pure ethanol given by any route does not cause release of gastrin in humans. Alcoholic beverages with low ethanol content (beer and wine) are strong stimulants of gastric acid secretion and gastrin release, the effect of beer being equal to the maximal acid output. Beverages with a higher ethanol content (whisky, gin, cognac) do not stimulate gastric acid secretion or release ofgastrin. The powerfdul stimulants of gastric acid secretion present in beer, which are yet to be identified, are thermostable and anionic polar substances. The effect of chronic alcohol abuse on gastric acid secretion is not as predictable. Chronic alcoholic patients may have normal, enhanced, or diminished acid secretory capacity; hypochlorhydria being associated histologically with atrophic gastritis. There are no studies on the acute effect of alcohol intake on gastric acid secretion in chronic alcoholic patients. The acid stimulatory component of beer and wine needs to be characterised and its possible role in the causation of alcohol induced gastrointestinal diseases needs to be investigated. (Gut 1993; 34: 843-847) Effects of acute exposure of non-alcoholic subjects to alcohol on gastric acid secretion The effect of pure ethanol on gastric acid secretion has been investigated by several workers.Early uncontrolled experiments3'4 suggested that alcohol had a stimulatory effect on gastric acid secretion; thus an 'ethanol test meal' was introduced to clinically evaluate acid secretory state in humans. Recent controlled studies have served to clarify the different aspects of the interaction between alcohol and gastric acid secretion. Gastric acid secretion is influenced by a number of factors such as pH, volume, osmotic activity, and caloric value of the infusate. The ideal osmotic control for ethanol is distilled water5 and not hypertonic glucose or saline as has been used in some studies.' This is because ethanol is a non-electrolyte of small molecular weight that diffuses rapidly in and through biological membranes. Consequently the effective osmotic pressure that it exerts on biological membranes is far less than its osmotic pressure measured by an osmometer. Distilled water has an identical effect and is pharmacologically inactive. It is, therefore, considered the ideal osmotic control for ethanol (for detailed discussion see5). Because alcohol is also a source of energy (1 g of ethanol provides 7 1 kcal), it is necessary to have an additional caloric control. An equicaloric glucose solution is used for this purpose. To compare the effect of different substances on gastric acid secretion proper control solutions comparable with the test solution should be used. Unfo...