Alcohol and Gastritis

Ethyl alcohol

Ethyl alcohol is a NON nutritional macro molecule that provides 7 kcal per gram; it is contained in alcoholic beverages obtained by fermentation (wine, beer, etc.) or distillation (grappa, whiskey, etc.) thanks to the degradation of carbohydrates (both simple than complexes) by some microorganisms or yeasts, called saccharomycetes.

Alcohol is a nerve and therefore acts in a toxic way in ALL the tissues of the body, however, some areas are more vulnerable than others. The cells of the digestive mucosa are the first to be affected by the introduction of alcohol; in fact, the absorption of ethanol occurs by simple diffusion in the epithelium of the mouth, in the gastric mucosa and in the small intestine.

Once absorbed, ethyl alcohol enters the circulation and reaches all the peripheries, where it manifests its toxic function in a more or less evident way; the most easily identifiable effect is that on the central nervous system (CNS): sensation of heat , disinhibition, alteration of coordination and lengthening of reaction times to stimuli. However, although asymptomatic, cytolysis occurs in parallel in all histological forms of the body: kidney cells, pancreatic cells, liver cells, etc. Ethyl alcohol also causes a hormonal reaction very similar to the intake of a strong glycemic load with a surge of insulin, causing an increase in the fortified fat deposit by its conversion into fatty acids since, NOT being a nutrient, its energetic oxidation It is NEVER of the direct type.

The disposal of ethanol takes place above all in the liver thanks to specific enzymatic processes; however, following ethyl poisoning also the hepatocytes undergo cytolytic lesions identifiable with the blood detection of trans-aminases.
The frequent use of ethyl alcohol represents a major risk factor for chronic abuse, which can determine the onset of psychiatric syndrome of alcoholism.

Alcohol and gastritis

At the gastric level, ethyl alcohol performs a markedly deleterious function; it can give rise to both acute and chronic complications, the manifestation of which depends above all on the level of individual predisposition and the presence of other inappropriate behaviors (poor diet, smoking, nervousness, etc. .). The most frequent clinical manifestations are:

• Acute gastritis
• Chronic superficial gastritis
• Chronic atrophic gastritis

The etiopathogenesis of gastritis - whether acute or chronic - depends on:

• Reduced mucus synthesis
• Alteration of submucosal blood flow
• Alteration of cell permeability
• Blocking the synthesis of cyclic Adenosine Monophosphate (cyclic AMP - messenger involved in signal transduction)
• Alteration of cell membrane potential

The most frequent complications of ethyl abuse gastritis are acute and chronic; among the acute ones it is possible to find gastric haemorrhages identifiable with the onset of haematic vomiting, while in the long term, the presence of mucosal pathologies can become chronic, facilitating the onset of gastric carcinoma.

Acute hemorrhagic gastritis

This kind of pathological manifestation is fundamentally attributable (20-40% of cases) to two etiological causes: the abuse of alcohol and the use of gastro-damaging drugs (anti-inflammatory NSAIDs); while it is more rare that it is caused by the ingestion of corrosive agents. The pathogenetic mechanisms linked to the onset of acute hemorrhagic gastritis are linked to the direct epithelial action of alcohol on the mucosa, to the gastric hyper-secretion and to the vascular congestion submucosa.
Acute hemorrhagic gastritis manifests itself with lesions of the gastric mucosa (which sometimes reach perforation of the digestive tract) associated with erosions, ulcers and hemorrhagic extravasations, therefore with both occult and abundant bleeding; these organic alterations are linked to symptoms such as epigastric pain, postprandial heartburn, nausea and blood vomiting. Sometimes systemic manifestations such as fever, tachycardia, paleness and sweating can be seen. The most severe forms of acute ulcerative gastritis evolve into electrolyte alterations (induced by vomiting) and into cardio-circulatory shock and / or collapse; in general the prognosis is benign and of short duration (about 2-7 days), but in the most serious forms, very serious complications are not excluded.

Bibliography:                                                                                                                                                                      

• The Italian book of alcology. Volume 1 - A. Allamani, D. Orlandini, G. Bardazzi, A. Quartini, A. Morettini - SEE Florence - page 215
• Alcohol. Alcoholism. What changes? - B. Sanfilippo, G. L. Galimberti, A. Lucchini - FrancoAngeli - page 96

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