The average age of onset is 40 to 60 years, and men are affected more often than women. Adults with Ménétrier disease have a higher risk of developing gastric adenocarcinoma.

The condition most commonly affects people between the ages of 30 and 60. The prevalence in unknown, but estimated to be about 1 per 100,000 people.

Gastrinoma causes the following symptoms:

- Hypergastrinemia

- Ulcers of the duodenum, stomach, and small intestine.

- Severe diarrhea.

- Generalized cancer symptoms.

A gastrinoma is a tumor in the pancreas or duodenum that secretes excess of gastrin leading to ulceration in the duodenum, stomach and the small intestine. There is hypersecretion of HCl acid into the duodenum, which causes the ulcers. Excessive HCl acid production also causes hyperperistalsis, and inhibits the activity of lipase, causing severe diarrhea.

It is frequently the source of the gastrin in Zollinger-Ellison syndrome.

It is usually found in the duodenum, although it may arise in the stomach or pancreas. Those occurring in the pancreas have a greater potential for malignancy. Most gastrinomas are found in the gastrinoma triangle; this is bound by the junction of cystic and common bile ducts, junction of the second and third parts of the duodenum, and the junction of the neck and body of the pancreas.

Zollinger–Ellison syndrome (ZES) is a disease in which tumors cause the stomach to produce too much acid, resulting in peptic ulcers. Symptoms include abdominal pain and diarrhea.

The syndrome is caused by a gastrinoma, a neuroendocrine tumor that secretes a hormone called gastrin. The tumor causes excessive production of gastric acid, which leads to the growth of gastric mucosa and proliferation of parietal and ECL cells.

ZES may occur on its own or as part of an autosomal dominant syndrome called multiple endocrine neoplasia type 1 (MEN 1). The primary tumor is usually located in the pancreas, duodenum or abdominal lymph nodes, but ectopic locations (e.g., heart, ovary, gallbladder, liver, and kidney) have also been described.

The cause of Ménétrier disease is unknown, but it has been associated with HCMV infection in children and "H. pylori "infections in adults. Additionally, increased TGF-α has been noted in the gastric mucosa of patients with the disease.

Little is known on the prognosis of achlorhydria, although there have been reports of an increased risk of gastric cancer.

A 2007 review article noted that non-"Helicobacter" bacterial species can be cultured from achlorhydric (pH > 4.0) stomachs, whereas normal stomach pH only permits the growth of "Helicobacter" species. Bacterial overgrowth may cause false positive H. Pylori test results due to the change in pH from urease activity.

Small bowel bacterial overgrowth is a chronic condition. Retreatment may be necessary once every 1–6 months. Prudent use of antibacterials now calls for an antibacterial stewardship policy to manage antibiotic resistance.

Recent research has shown that AMAG is a result of the immune system attacking the parietal cells.

"Environmental Metaplastic Atrophic Gastritis" (EMAG) is due to environmental factors, such as diet and "H. pylori" infection. EMAG is typically confined to the body of the stomach. Patients with EMAG are also at increased risk of gastric carcinoma.

Patients with atrophic gastritis are also at increased risk for the development of gastric adenocarcinoma. The optimal endoscopic surveillance strategy is not known but all nodules and polyps should be removed in these patients.

Hyperchlorhydria, sometimes called chlorhydria, refers to the state in the stomach where gastric acid levels are higher than the reference range. The combining forms of the name ("" + ""), referring to chlorine and hydrogen, are the same as those in the name of hydrochloric acid, which is the active constituent of gastric acid.

In humans, the normal pH is around 1 to 3, which varies throughout the day. The highest basal secretion levels are in the late evening (around 12 A.M. to 3 A.M.). Hyperchlorhydria is usually defined as having a pH less than 2. It has no negative consequences unless other conditions are also present such as gastroesophageal reflux disease (GERD).

Smoking has been linked to a variety of disorders of the stomach. Tobacco is known to stimulate acid production and impairs production of the protective mucus. This leads to development of ulcers in the majority of smokers.

Chronic stomach problems have also been linked to excess intake of alcohol. It has been shown that alcohol intake can cause stomach ulcer, gastritis and even stomach cancer. Thus, avoidance of smoking and excess alcohol consumption can help prevent the majority of chronic stomach disorders.

One of the most causes of chronic stomach problems is use of medications. Use of aspirin and other non-steroidal anti-inflammatory drugs to treat various pain disorders can damage lining of the stomach and cause ulcers. Other medications like narcotics can interfere with stomach emptying and cause bloating, nausea, or vomiting.

The majority of chronic stomach problems are treated medically. However, there is evidence that a change in life style may help. Even though there is no specific food responsible for causing chronic stomach problems, experts recommend eating a healthy diet which consists of fruits and vegetables. Lean meat should be limited. Moreover, people should keep a diary of foods that cause problems and avoid them.

The mechanism of development of Cushing ulcers is thought to be due to direct stimulation of vagal nuclei as a result of increased intracranial pressure. Alternatively, it may also be a direct result of Cushing reaction. Efferent fibers of the vagus nerve then release acetylcholine onto gastric parietal cell M receptors, causing insertion of hydrogen potassium ATPase vesicles into the apical plasma membrane. The end result is increased secretion of gastric acid with eventual ulceration of the gastric mucosa.

Cancers of the stomach are rare and the incidence has been declining worldwide. Stomach cancers usually occur due to fluctuations in acidity level and may present with vague symptoms of abdominal fullness, weight loss and pain. The actual cause of stomach cancer is not known but has been linked to infection with "Helicobacter pylori", pernicious anemia, Menetriere's disease, and nitrogenous preservatives in food.

Evidence does not support a role for specific foods including spicy foods and coffee in the development of peptic ulcers. People are usually advised to avoid foods that bother them.

Achlorhydria or hypochlorhydria refers to states where the production of hydrochloric acid in gastric secretions of the stomach and other digestive organs is absent or low, respectively. It is associated with various other medical problems.

A Cushing ulcer, named after Harvey Cushing, is a gastric ulcer associated with elevated intracranial pressure. It is also called von Rokitansky-Cushing syndrome. Apart from in the stomach, ulcers may also develop in the proximal duodenum and distal esophagus.

The literature, from 1953 through 2010, often cited that the cause of gastric antral vascular ectasia is unknown. The causal connection between cirrhosis and GAVE has not been proven. A connective tissue disease has been suspected in some cases.

Autoimmunity may have something to do with it, as 25% of all sclerosis patients who had a certain anti-RNA marker have GAVE. RNA autoimmunity has been suspected as a cause or marker since at least 1996. Gastrin levels may indicate a hormonal connection.

Gastritis may also develop after major surgery or traumatic injury ("Cushing ulcer"), burns ("Curling ulcer"), or severe infections. Gastritis may also occur in those who have had weight loss surgery resulting in the banding or reconstruction of the digestive tract.

Dietary factors such as spice consumption, were hypothesized to cause ulcers until late in the 20th century, but have been shown to be of relatively minor importance. Caffeine and coffee, also commonly thought to cause or exacerbate ulcers, appear to have little effect. Similarly, while studies have found that alcohol consumption increases risk when associated with "H. pylori" infection, it does not seem to independently increase risk. Even when coupled with "H. pylori" infection, the increase is modest in comparison to the primary risk factor.

Transient gastroparesis may arise in acute illness of any kind, as a consequence of certain cancer treatments or other drugs which affect digestive action, or due to abnormal eating patterns.

It is frequently caused by autonomic neuropathy. This may occur in people with type 1 or type 2 diabetes. In fact, diabetes mellitus has been named as the most common cause of gastroparesis, as high levels of blood glucose may effect chemical changes in the nerves. The vagus nerve becomes damaged by years of high blood glucose or insufficient transport of glucose into cells resulting in gastroparesis. Gastroparesis has also been associated with connective tissue diseases such as scleroderma and Ehlers–Danlos syndrome, and neurological conditions such as Parkinson's disease. It may also occur as part of a mitochondrial disease. Opioids and anticholinergic medications can cause medication-induced gastroparesis.

Chronic gastroparesis can be caused by other types of damage to the vagus nerve, such as abdominal surgery. Heavy cigarette smoking is also a plausible cause since smoking causes damage to the stomach lining.

Idiopathic gastroparesis (gastroparesis with no known cause) accounts for a third of all chronic cases; it is thought that many of these cases are due to an autoimmune response triggered by an acute viral infection. Gastroenteritis, mononucleosis, and other ailments have been anecdotally linked to the onset of the condition, but no systematic study has proven a link.

Gastroparesis sufferers are disproportionately female. One possible explanation for this finding is that women have an inherently slower stomach emptying time than men. A hormonal link has been suggested, as gastroparesis symptoms tend to worsen the week before menstruation when progesterone levels are highest. Neither theory has been proven definitively.

Gastroparesis can also be connected to hypochlorhydria and be caused by chloride, sodium and/or zinc deficiency, as these minerals are needed for the stomach to produce adequate levels of gastric acid (HCl) in order to properly empty itself of a meal.

GAVE is associated with a number of conditions, including portal hypertension, chronic kidney failure, and collagen vascular diseases.

Watermelon stomach also occurs particularly with scleroderma, and especially the subtype known as systemic sclerosis. A full 5.7% of persons with sclerosis have GAVE, and 25% of all sclerosis patients who had a certain anti-RNA marker have GAVE. In fact:

The endoscopic appearance of GAVE is similar to portal hypertensive gastropathy, but is not the same condition, and may be concurrent with cirrhosis of the liver. 30% of all patients have cirrhosis associated with GAVE.

Sjögren's syndrome has been associated with at least one patient.

The first case of ectopic pancreas associated with watermelon stomach was reported in 2010.

Patients with GAVE may have elevated gastrin levels.

The Genetic and Rare Diseases Information Center (GARD) states that pernicious anemia is one of the conditions associated with GAVE's, and one separate study showed that over three-fourths of the patients in the study with GAVE's had some kind of Vitamin B12 deficiency including the associated condition pernicious anemia.

Intestinal permeability and diverticulitis may occur in some patients with GAVE.

Stress due to serious health problems such as those requiring treatment in an intensive care unit is well described as a cause of peptic ulcers, which are termed stress ulcers.

While chronic life stress was once believed to be the main cause of ulcers, this is no longer the case. It is, however, still occasionally believed to play a role. This may be by increasing the risk in those with other causes such as "H. pylori" or NSAID use.

Among those in the intensive care unit, ulceration resulting in bleeding is very rare.

While emergency surgery was once the only treatment, combination therapies including enteral feeding with powerful antacids such as H-receptor antagonists or, more recently, proton pump inhibitors such as omeprazole have made Curling's ulcer a rare complication.

There is a risk of development of cancer with fundic gland polyposis, but it varies based on the underlying cause of the polyposis. The risk is highest with congenital polyposis syndromes, and is lowest in acquired causes. As a result, it is recommended that patients with multiple fundic polyps have a colonoscopy to evaluate the colon. If there are polyps seen on colonoscopy, genetic testing and testing of family members is recommended.

In the gastric adenocarcinoma associated with proximal polyposis of the stomach (GAPPS), there is a high risk of early development of proximal gastric adenocarcinoma.

It is still unclear which patients would benefit with surveillance gastroscopy, but most physicians recommend endoscopy every one to three years to survey polyps for dysplasia or cancer. In the event of high grade dysplasia, polypectomy, which is done through the endoscopy, or partial gastrectomy may be recommended. One study showed the benefit of NSAID therapy in regression of gastric polyps, but the efficacy of this strategy (given the side effects of NSAIDs) is still dubious.