Smoking increases the risk of developing gastric cancer significantly, from 40% increased risk for current smokers to 82% increase for heavy smokers. Gastric cancers due to smoking mostly occur in the upper part of the stomach near the esophagus. Some studies show increased risk with alcohol consumption as well.

Dietary factors are not proven causes, but some foods including smoked foods, salt and salt-rich foods, red meat, processed meat, pickled vegetables, and bracken are associated with a higher risk of stomach cancer. Nitrates and nitrites in cured meats can be converted by certain bacteria, including "H. pylori", into compounds that have been found to cause stomach cancer in animals.

Fresh fruit and vegetable intake, citrus fruit intake, and antioxidant intake are associated with a lower risk of stomach cancer. A Mediterranean diet is associated with lower rates of stomach cancer, as is regular aspirin use.

Obesity is a physical risk factor that has been found to increase the risk of gastric adenocarcinoma by contributing to the development of gastroesophageal reflux disease (GERD). The exact mechanism by which obesity causes GERD is not completely known. Studies hypothesize that increased dietary fat leading to increased pressure on the stomach and the lower esophageal sphincter, due to excess adipose tissue, could play a role, yet no statistically significant data has been collected. However, the risk of gastric cardia adenocarcinoma, with GERD present, has been found to increase more than 2 times for an obese person. There is a correlation between iodine deficiency and gastric cancer.

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.

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.

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.

Linitis plastica, also known as Brinton's disease or leather bottle stomach, is a morphological variant of diffuse (or infiltrating) stomach cancer.

Causes of linitis plastica could be lye ingestion or metastatic infiltration of the stomach, particularly breast and lung carcinoma. It is not associated with H. pylori infection or chronic gastritis. The risk factors are undefined, except for rare inherited mutations in E-cadherin, which are found in about 50% of diffuse-type gastric carcinomas.

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.

Fundic gland polyps are found in 0.8 to 1.9% of patients who undergo esophagogastroduodenoscopy, and are more common in middle aged women.

The most important consideration in evaluating patients with FGPs is distinguishing between sporadic form (patients without any other gastrointestinal condition, usually in middle age with female prevalence) and syndromic form. This is to ascertain the risk of development of gastric cancer, and to ascertain the risk of concomitant colon cancer.

FGPs can be found in association with the following genetic conditions:

- familial adenomatous polyposis

- attenuated familial adenomatous polyposis syndromes

- Zollinger-Ellison syndrome

- gastric adenocarcinoma associated with proxymal polyposis of the stomach (GAPPS): this condition, described in three families is characterized by development of antral adenomas and FGPs, with early development of severe dysplasia and gastric cancer, in absence of overt intestinal polyposis. This condition has been recently characterized by a point mutation in exon 1B of APC gene.

Sporadic FGPs have been associated with:

- chronic use of proton pump inhibitors (proposed by some authors, denied by others)

- "Helicobacter pylori" infection: there is a reverse relationship between infection and fundic gland polyps, and infection by "H pylori" causes polyps regression.

Napoleon Bonaparte and many members of his family are thought to have died from this type of cancer, although it is believed by others that he may have died from arsenic poisoning.

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.

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.

As a general rule, GDV is of greatest risk to deep-chested dogs. The five breeds at greatest risk are Great Danes, Weimaraners, St. Bernards, Gordon Setters, and Irish Setters. In fact, the lifetime risk for a Great Dane to develop GDV has been estimated to be close to 37 percent. Standard Poodles are also at risk for this health problem, as are Irish Wolfhound, Doberman Pinschers, Rottweilers, German Shorthaired Pointer, German Shepherds, Rhodesian Ridgebacks. Basset Hounds and Dachshunds have the greatest risk for dogs less than .

Immediate treatment is the most important factor in a favorable prognosis. A delay in treatment greater than six hours or the presence of peritonitis, sepsis, hypotension, or disseminated intravascular coagulation are negative prognostic indicators.

Historically, GDV has held a guarded prognosis. Although "early studies showed mortality rates between 33% and 68% for dogs with GDV," studies from 2007 to 2012 "reported mortality rates between 10% and 26.8%". Mortality rates approach 10% to 40% even with treatment. A study determined that with prompt treatment and good preoperative stabilization of the patient, mortality is significantly lessened to 10% overall (in a referral setting). Negative prognostic indicators following surgical intervention include postoperative cardiac arrhythmia, splenectomy, or splenectomy with partial gastric resection. Interestingly, a longer time from presentation to surgery was associated with a lower mortality, presumably because these dogs had received more complete preoperative fluid resuscitation and were thus better cardiovascularly stabilized prior to the procedure.

The causes are divided into benign or malignant.

- Benign

- Peptic ulcer disease

- Infections, such as tuberculosis; and infiltrative diseases, such as amyloidosis.

- A rare cause of gastric outlet obstruction is blockage with a gallstone, also termed "Bouveret's syndrome".

- In children congenital pyloric stenosis / congenital hypertrophic pyloric stenosis may be a cause.

- A pancreatic pseudocyst can cause gastric compression.

- Pyloric mucosal diaphragm could be a rare cause.

- Malignant

- Tumours of the stomach, including adenocarcinoma (and its linitis plastica variant), lymphoma, and gastrointestinal stromal tumours

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.

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.

In a peptic ulcer it is believed to be a result of edema and scarring of the ulcer, followed by healing and fibrosis, which leads to obstruction of the gastroduodenal junction (usually an ulcer in the first part of the duodenum).

Industrialized nations, with the exception of Japan, have high rates of epithelial ovarian cancer, which may be due to diet in those countries. Caucasian are at a 30–40% higher risk for ovarian cancer when compared to Black and Hispanic people, likely due to socioeconomic factors; white women tend to have fewer children and different rates of gynecologic surgeries that affect risk for ovarian cancer.

Cohort studies have found a correlation between dairy consumption and ovarian cancer, but case-control studies do not show this correlation. There is mixed evidence regarding the effect of red meat and processed meat in ovarian cancer.

Tentative evidence suggests that talc, pesticides, and herbicides increase the risk of ovarian cancer. The American Cancer Society notes that as of now, no study has been able to accurately link any single chemical in the environment, or in the human diet, directly to mutations that cause ovarian cancer.

Alcohol consumption does not appear to be related to ovarian cancer. Other factors that have been investigated, such as smoking, low levels of vitamin D in the blood, presence of inclusion ovarian cysts, and infection with human papilloma virus (the cause of some cases of cervical cancer), have been disproven as risk factors for ovarian cancer. The carcinogenicity of perineal talc is controversial, because it can act as an irritant if it travels through the reproductive tract to the ovaries. Case-control studies have shown that use of perineal talc does increase the risk of ovarian cancer, but using talc more often does not create a greater risk. Use of talc elsewhere on the body is unrelated to ovarian cancer. Sitting regularly for prolonged periods is associated with higher mortality from epithelial ovarian cancer. The risk is not negated by regular exercise, though it is lowered.

Increased age (up to the 70s) is a risk factor for epithelial ovarian cancer because more mutations in cells can accumulate and eventually cause cancer. Those over 80 are at slightly lower risk.

Smoking tobacco is associated with a higher risk of mucinous ovarian cancer; after smoking cessation, the risk eventually returns to normal.A diet high in animal fats may be associated with ovarian cancer, but the connection is unclear. Diet seems to play a very small role, if any, in ovarian cancer risk.

Higher levels of C-reactive protein are associated with a higher risk of developing ovarian cancer.

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.

Most damage to the pyloric valve occurs as a complication of gastric surgery. Other causes of biliary reflux may be:

- Peptic ulcer

- Gallbladder surgery (cholecystectomy)

A significant fraction of cases are idiopathic, with no identified specific etiology.

A gastrojejunocolic fistula is a disorder of the human gastrointestinal tract. It may form between the transverse colon and the upper jejunum after a Billroth II surgical procedure. (The Billroth procedure attaches the jejunum to the remainder of the stomach). Fecal matter thereby passes improperly from the colon to the stomach, and causes halitosis.

Patients may present with diarrhea, weight loss and halitosis as a result of fecal matter passing through the fistula from the colon into the stomach.

Biliary reflux, bile reflux or duodenogastric reflux is a condition that occurs when bile flows upward (refluxes) from the duodenum into the stomach and esophagus.

Biliary reflux can be confused with acid reflux, also known as gastroesophageal reflux disease (GERD). While bile reflux involves fluid from the small intestine flowing into the stomach and esophagus, acid reflux is backflow of stomach acid into the esophagus. These conditions are often related, and differentiating between the two can be difficult.

Bile is a digestive fluid made by the liver, stored in the gallbladder, and discharged into duodenum after food is ingested to aid in the digestion of fat. Normally, the pyloric sphincter prevents bile from entering the stomach. When the pyloric sphincter is damaged or fails to work correctly, bile can enter the stomach and then be transported into the esophagus as in gastric reflux. The presence of small amounts of bile in the stomach is relatively common and usually asymptomatic, but excessive refluxed bile causes irritation and inflammation.

Gastric volvulus of unknown cause comprises two thirds of cases and is presumably due to abnormal laxity of the gastrosplenic, gastroduodenal, gastrophrenic, and gastrohepatic ligaments. Type 1 gastric volvulus is more common in adults but has been reported in children.

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.