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Foods that cause Gastritis


Types of Gastritis

Notes on the classification of gastritis

Gastritis is classified in two ways: the first is called system Sydney-Huston and is based on the histological and endoscopic entity, etiological mechanisms and type of lesion. The discriminatory variables in the classification of gastritis according to Sydney-Huston are:

  1. Presence of Helicobacter Pylori
  2. Extent of infiltration of immune cells (white blood cells)
  3. Importance of glandular atrophy and presence of intestinal metaplasia

Severity scale of variables in gastritis

The second method, however, focuses above all on the etiological agents that determine it:

The most serious complications of gastritis are linked to possible bleeding and compromised digestive capacity. Gastritis can induce one or more erosions of the gastric mucosa which, if left untreated, risk evolving into actual gastric ulcers; the differentiation between one or the other condition is based on the depth of the lesion.
Gastritis bleeding can be treated directly and/or indirectly with:


Bleeding gastritis causes constant blood loss in the stomach; this complication, especially in fertile women who already suffer monthly losses with menstruation, can lead to a significant reduction in hematocrit, inducing or worsening the anemic condition.

At the gastric level, the mucous membranes secrete the so-called intrinsic factor, a molecule indispensable for the intestinal absorption (in the terminal ileum) of vitamin B12 (cobalamin). The possible atrophy of the mucous membranes induced by gastritis, or worse the evolution into intestinal metaplasia, determine the reduction of the ability to secrete intrinsic factor and absorb cobalamin. The consequence of chronic vitamin B12 deficiency – in addition to being particularly serious for the pregnant woman, as it increases the risk of complications in the neural development of the fetus – could give rise to or significantly aggravate the defined anemic form pernicious.

UNTREATED gastritis can develop into an ulcer; this can be defined as such if the erosion, in addition to compromising the mucosa (gastritis), also reaches the basement membrane and/or goes beyond it, to the point of becoming a perforating ulcer. The perforating ulcer can be very serious and sometimes fatal; however, the correlation between gastritis and the onset of perforating ulcers is rather modest.

Foods and Gastritis

Among the foods that trigger gastritis or worsen its course we remember:

It is appropriate to specify that foods potentially responsible for gastritis are among those to be abolished in nutritional therapy for the treatment of the disease itself; however, many foods to be avoided during treatment (for example milk, stewed meat, raw meat, large portions of cheese, etc.) DO NOT have any pathogenic effect in healthy subjects, in whom, provided they are taken in portions and with adequate frequency, they do not cause any type of gastritis.
Caffeine and other sympathomimetic amines: in particularly sensitive subjects, even the mere consumption of one or two cups of coffee per day (80-160mg of caffeine) can cause significant irritation of the gastric mucosa, especially if the drink is taken at fast. In fact, caffeine, just like theine, represents a stimulant of acid secretion; these drinks, which in themselves constitute a potentially (even if subjectively) harmful food for the stomach, must be COMPLETELY abolished both in cases of hypersensitivity and in the treatment of gastritis.
The same goes for alcoholic beverages; ethyl alcohol is a powerful acid stimulator which, if taken on an empty stomach, stimulates the secretion of hydrochloric acid, irritating or eroding the mucosa; if taken on a full stomach, however, alcohol causes a slowdown in gastric digestion due to an excessive lowering of the pH of the chyme (food mush being digested between the stomach and the intestine). Susceptibility to alcohol is also absolutely subjective and in most cases a single unit of alcohol during the main meals does NOT cause strong irritative symptoms of the gastric mucosa.
Not least nicotine; this is ingested in very high quantities by tobacco chewers (who fortunately have almost disappeared today) and by the most avid smokers. Smoking causes continuous ingestion of nicotine, which, like alcohol and caffeine, causes a lowering of gastric pH due to hyper acid secretion.
A group of foods which, contrary to what is mentioned above, represents a DIRECTLY irritating element for the stomach, is that of acidic and carbonated drinks; the most striking example is that of cola-type drinks. These, in addition to containing caffeine, are also characterized by a pH low enough to create instant irritation of the mucosa and, in the long term, cause gastritis. As if that weren't enough, these drinks provide an excessive intake of carbon dioxide, which greatly affects gastric hyper-distension, worsening the painful symptoms of gastritis.
Salty foods contain excessive amounts of sodium chloride (NaCl); this salt has a powerful osmotic effect towards the mucous membranes of the stomach, dehydrating it; at the same time, table salt represents a further stimulator of gastric secretion; furthermore, considering that generally the saltiest foods (except for some baked products such as crackers and breadsticks or similar) contain good quantities of proteins (salted meats, sausages, mature cheeses, etc.) which in turn determine an increase in hydrochloric acid and of pepsin, it is possible to state that (if consumed frequently) salty foods can determine a further factor in the onset of gastritis.
The foods that cause gastritis are few but they must be eaten frequently and in very limited portions; their etiological importance depends greatly on individual susceptibility, however, even in a normal subject, the association of several potentially harmful eating habits could determine the pathological onset of this disorder.


  • Inflammation in gastroenterology – A. Martin – Piccin – p. 71:1
  • Internal and systemic medicine. Sixth edition – C. Rugarli – Elsevier Masson – page 648:656
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