Many hypotheses have been raised for environmental factors contributing to the pathogenesis of ulcerative colitis. They include the following:

- Diet: as the colon is exposed to many dietary substances which may encourage inflammation, dietary factors have been hypothesized to play a role in the pathogenesis of both ulcerative colitis and Crohn's disease. Few studies have investigated such an association; one study showed no association of refined sugar on the prevalence of ulcerative colitis. High intake of unsaturated fat and vitamin B6 may enhance the risk of developing ulcerative colitis. Other identified dietary factors that may influence the development and/or relapse of the disease include meat protein and alcoholic beverages. Specifically, sulfur has been investigated as being involved in the etiology of ulcerative colitis, but this is controversial. Sulfur restricted diets have been investigated in patients with UC and animal models of the disease. The theory of sulfur as an etiological factor is related to the gut microbiota and mucosal sulfide detoxification in addition to the diet.

- Breastfeeding: Some reports of the protection of breastfeeding in the development of inflammatory bowel disease contradict each other. One Italian study showed a potential protective effect.

- One study of isotretinoin found a small increase in the rate of ulcerative colitis.

The risk of colorectal cancer is significantly increased in patients with ulcerative colitis after ten years if involvement is beyond the splenic flexure. Those patients with only proctitis or rectosigmoiditis usually have no increased risk. It is recommended that patients have screening colonoscopies with random biopsies to look for dysplasia after eight years of disease activity, at one to two year intervals.

As a result of microbial symbiosis and immunity, alterations in enteral bacteria may contribute to inflammatory gut diseases. IBD-affected individuals have been found to have 30–50 percent reduced biodiversity of commensal bacteria, such as decreases in Firmicutes (namely Lachnospiraceae) and Bacteroidetes. Further evidence of the role of gut flora in the cause of inflammatory bowel disease is that IBD-affected individuals are more likely to have been prescribed antibiotics in the 2–5 year period before their diagnosis than unaffected individuals. The enteral bacteria can be altered by environmental factors, such as concentrated milk fats (a common ingredient of processed foods and confectionery) or oral medications such as antibiotics and oral iron preparations.

Incidence and prevalence of microscopic colitis nears those of ulcerative colitis and Crohn’s disease. Recent studies in North America found incidence rates of 7.1 per 100,000 person-years and 12.6 per 100,000 person-years for collagenous colitis for lymphocytic colitis, respectively.

A higher incidence of autoimmune diseases, for example arthritis, Sjögren's syndrome, thyroid disorders, and coeliac disease, has been reported in patients with microscopic colitis. Associations with various drugs have been found, especially proton pump inhibitors, H blockers, selective serotonin reuptake inhibitors (SSRIs), and non-steroidal anti-inflammatory drugs (NSAIDs). Bile acid diarrhea is found in 41% of patients with collagenous colitis and 29% with lymphocytic colitis. Additionally, smoking has been identified as a significant risk factor of microscopic colitis.

IBD is a complex disease which arises as a result of the interaction of environmental and genetic factors leading to immunological responses and inflammation in the intestine.

A subtype of infectious colitis is "Clostridium difficile" colitis, which is informally abbreviated as "c diff colitis". It classically forms and is often referred to as pseudomembranous colitis, which is its (nonspecific) histomorphologic description.

Enterohemorrhagic colitis may be caused by Shiga toxin in "Shigella dysenteriae" or "Shigatoxigenic group" of "Escherichia coli" (STEC), which includes serotype and other enterohemorrhagic "E. coli".

Parasitic infections, like those caused by "Entamoeba histolytica", can also cause colitis.

The increased incidence of Crohn's in the industrialized world indicates an environmental component. Crohn's is associated with an increased intake of animal protein, milk protein and an increased ratio of omega-6 to omega-3 polyunsaturated fatty acids.

Those who consume vegetable proteins appear to have a lower incidence of Crohn's disease. Consumption of fish protein has no association.

Smoking increases the risk of the return of active disease (flares). The introduction of hormonal contraception in the United States in the 1960s is associated with a dramatic increase in incidence, and one hypothesis is that these drugs work on the digestive system in ways similar to smoking. Isotretinoin is associated with Crohn's. Although stress is sometimes claimed to exacerbate Crohn's disease, there is no concrete evidence to support such claim. Dietary microparticles, such as those found in toothpaste, have been studied as they produce effects on immunity, but they were not consumed in greater amounts in patients with Crohn's.

Crohn's disease can lead to several mechanical complications within the intestines, including obstruction, fistulae, and abscesses. Obstruction typically occurs from strictures or adhesions that narrow the lumen, blocking the passage of the intestinal contents. A fistula can develop between two loops of bowel, between the bowel and bladder, between the bowel and vagina, and between the bowel and skin. Abscesses are walled off concentrations of infection, which can occur in the abdomen or in the perianal area. Crohn's is responsible for 10% of vesicoenteric fistulae, and is the most common cause of ileovesical fistulae.

Crohn's disease also increases the risk of cancer in the area of inflammation. For example, individuals with Crohn's disease involving the small bowel are at higher risk for small intestinal cancer. Similarly, people with Crohn's colitis have a relative risk of 5.6 for developing colon cancer. Screening for colon cancer with colonoscopy is recommended for anyone who has had Crohn's colitis for at least eight years. Some studies suggest there is a role for chemoprotection in the prevention of colorectal cancer in Crohn's involving the colon; two agents have been suggested, folate and mesalamine preparations. Also, immunomodulators and biologic agents used to treat this disease may promote developing extra-intestinal cancers.

Individuals with Crohn's disease are at risk of malnutrition for many reasons, including decreased food intake and malabsorption. The risk increases following resection of the small bowel. Such individuals may require oral supplements to increase their caloric intake, or in severe cases, total parenteral nutrition (TPN). Most people with moderate or severe Crohn's disease are referred to a dietitian for assistance in nutrition.

The major significant complications of Crohn's disease include bowel obstruction, abscesses, free perforation and hemorrhage, which in rare cases may be fatal.

Crohn's disease can be problematic during pregnancy, and some medications can cause adverse outcomes for the fetus or mother. Consultation with an obstetrician and gastroenterologist about Crohn's disease and all medications facilitates preventative measures. In some cases, remission occurs during pregnancy. Certain medications can also lower sperm count or otherwise adversely affect a man's fertility.

There are many types of colitis. They are usually classified by the cause.

Types of colitis include:

Pancolitis or universal colitis is a very severe form of ulcerative colitis. This form of ulcerative colitis is spread throughout the entire large intestine including the right colon, the left colon, the transverse colon, descending colon, and the rectum. A diagnosis can be made using a number of techniques but the most accurate method is direct visualization via a colonoscopy. Symptoms are similar to those of ulcerative colitis but more severe and affect the entire large intestine. Patients with ulcerative colitis generally exhibit symptoms including rectal bleeding as a result of ulcers, pain in the abdominal region, inflammation in varying degrees, and diarrhea (often containing blood). Pancolitis patients exhibit these symptoms and may also experience fatigue, fever, and night sweats. Due to the loss of function in the large intestine patients may lose large amounts of weight from being unable to procure nutrients from food. In other cases the blood loss from ulcers can result in anemia which can be treated with iron supplements. Additionally, due to the chronic nature of most cases of pancolitis, patients have a higher chance of developing colon cancer.

Pancolitis is a kind of inflammatory bowel disease (IBD) that affects the entire internal lining of the colon. The precise causes of this inflammatory disorder are unclear, although physicians currently believe that autoimmune diseases and genetic predispositions might play a role in its progress. Genes that are known to put individuals at risk for Crohn’s disease have been shown to also increase risk of other IBD including pancolitis. Furthermore, an individual may also develop pancolitis if ulcerative colitis of only a small portion of the colon is left untreated or worsens. Current treatment of pancolitis is focused on forcing the disease into remission, a state where the majority of the symptoms subside. Ultimately, the goal is to reach an improved quality of life, reduction in need for medicine, and minimization of the risk of cancer. Medication utilized in treatment includes anti-inflammatory agents and corticosteroids to alleviate inflammation and immunomodulators which act to suppress the immune system. Immunomodulators are used in severe cases of ulcerative colitis and often utilized to treat patients with pancolitis who have shown little improvement with anti-inflammatories and corticosteroids. However, in this case it can further expose the patient to other diseases due to the compromised immune system. A final option of treatment is available in the form of surgery. Generally, this option is reserved for only the cases in which cancer development is highly suspected or major hemorrhaging from ulcers occurs. In this case the entire colon and rectum are removed which both cures the pancolitis and prevents any chance of colon cancer. Patients who undergo surgery either must have their stool collect in a reservoir made in place of the rectum or have the end of the small intestine attached to the anus. In the latter case the diseased portion of the anus must be removed, but the muscles are left intact, allowing bowel movement to still take place.

Chemical colitis is a type of colitis, an inflammation of the large intestine or colon, caused by the introduction of harsh chemicals to the colon by an enema or other procedure. Chemical colitis can resemble ulcerative colitis, infectious colitis and pseudomembranous colitis endoscopically.

Prior to 1950, hydrogen peroxide enemas were commonly used for certain conditions. This practice will often result in chemical colitis.

Soap enemas may also cause chemical colitis.

Harsh chemicals, such as compounds used to clean colonoscopes, are sometimes accidentally introduced into the colon during colonoscopy or other procedures. This can also lead to chemical colitis.

Chemical colitis may trigger a flare of ulcerative colitis or Crohn's colitis. Symptoms of colitis are assessed using the Simple Clinical Colitis Activity Index.

Diseases of the hepatobiliary system affect the biliary tract (also known as the "biliary tree"), which secretes bile in order to aid digestion of fats. Diseases of the gallbladder and bile ducts are commonly diet-related, and may include the formation of gallstones that impact in the gallbladder (cholecystolithiasis) or in the common bile duct (choledocholithiasis).

Gallstones are a common cause of inflammation of the gallbladder, called cholecystitis. Inflammation of the biliary duct is called cholangitis, which may be associated with autoimmune disease, such as primary sclerosing cholangitis, or a result of bacterial infection, such as ascending cholangitis.

Disease of the biliary tree may cause pain in the upper right abdomen, particularly when pressed. Disease might be investigated using ultrasound or ERCP, and might be treated with drugs such as antibiotics or UDCA, or by the surgical removal of the gallbladder.

Epidemiology may differ between studies, as number of cases are small, with approximately 300 EG cases reported in published literature.

EG can present at any age and across all races, with a slightly higher incidence in males. Earlier studies showed higher incidence in the third to fifth decades of life.

Oesophageal diseases include a spectrum of disorders affecting the oesophagus. The most common condition of the oesophagus in Western countries is gastroesophageal reflux disease, which in chronic forms is thought to result in changes to the epithelium of the oesophagus, known as Barrett's oesophagus.

Acute disease might include infections such as oesophagitis, trauma caused ingestion of corrosive substances, or rupture of veins such as oesophageal varices, Boerhaave syndrome or Mallory-Weiss tears. Chronic diseases might include congenital diseases such as Zenker's diverticulum and esophageal webbing, and oesophageal motility disorders including the nutcracker oesophagus, achalasia, diffuse oesophageal spasm, and oesophageal stricture.

Oesophageal disease may result in a sore throat, throwing up blood, difficulty swallowing or vomiting. Chronic or congenital diseases might be investigated using barium swallows, endoscopy and biopsy, whereas acute diseases such as reflux may be investigated and diagnosed based on symptoms and a medical history alone.

Risperidone, an anti-psychotic medication, can result in megacolon.

Toxic megacolon is mainly seen in ulcerative colitis and pseudomembranous colitis, two chronic inflammations of the colon (and occasionally, in the other type of inflammatory bowel disease, Crohn's disease). Its mechanism is incompletely understood. It is probably due to an excessive production of nitric oxide, at least in ulcerative colitis. The prevalence is about the same for both sexes.

In patients with HIV/AIDS, cytomegalovirus (CMV) colitis is the leading cause of toxic megacolon and emergency laparotomy. CMV may also increase the risk of toxic megacolon in non-HIV/AIDS patients with IBD.

Once a diagnosis of pouchitis is made, the condition is further classified. The activity of pouchitis is stratified as:

- remission (no active pouchitis).

- mild to moderately active (increased stool frequency, urgency, infrequent incontinence).

- severely active (hospitalised for dehydration, frequent incontinence).

The duration of pouchitis is defined as acute (less than or equal to four weeks) or chronic (four weeks or more) and the pattern classified as infrequent (1-2 acute episodes), relapsing (three or fewer episodes) or continuous. Finally, the response to medical treatment as labelled as treatment responsive or treatment refractory, with the medication for either case being specified.

The development of any of the cancers associated with PSC predicts a poor prognosis. Complications from PSC-associated cancers account for 40% of deaths from PSC. Primary sclerosing cholangitis is one of the major known risk factors for cholangiocarcinoma, a cancer of the biliary tree, for which the lifetime risk among patients with PSC is 10-15%. This represents a 400-fold greater risk of developing cholangiocarcinoma compared to the general population. Surveillance for cholangiocarcinoma in patients with PSC is encouraged, with some experts recommending annual surveillance with a specialized imaging study and serum markers, although consensus regarding the modality and interval has yet to be established. Similarly, a screening colonoscopy is recommended in people who receive a new diagnosis of primary sclerosing cholangitis since their risk of colorectal cancer is 10 times higher than that of the general population.

PSC is strongly associated with inflammatory bowel disease (IBD), in particular ulcerative colitis (UC) and to a lesser extent Crohn's disease. As many as 5% of patients with IBD are co-diagnosed with PSC and approximately 70% of people with PSC have IBD. Of note, the presence of colitis appears to be associated with a greater risk of liver disease progression and bile duct cancer (cholangiocarcinoma) development, although this relationship remains poorly understood. Close monitoring of PSC patients is vital.

Various forms of gallbladder disease such as gallstones and gallbladder polyps are also common in those with PSC. Approximately 25% of people with PSC have gallstones. Ultrasound surveillance of the gallbladder every year is recommended for people with PSC. Any person with PSC who is found to have a mass in the gallbladder should undergo surgical removal of the gallbladder due to the high risk of cholangiocarcinoma. Osteoporosis (hepatic osteodystrophy) and hypothyroidism are also associated with PSC.

There is a 2-3:1 male-to-female predilection in primary sclerosing cholangitis. PSC can affect men and women at any age, although it is commonly diagnosed in the fourth decade of life, most often in the presence of inflammatory bowel disease (IBD). PSC progresses slowly and is often asymptomatic, so it can be present for years before it is diagnosed and before it causes clinically significant consequences. There is relatively little data on the prevalence and incidence of primary sclerosing cholangitis, with studies in different countries showing annual incidence of 0.068–1.3 per 100,000 people and prevalence 0.22–8.5 per 100,000; given that PSC is closely linked with ulcerative colitis, it is likely that the risk is higher in populations where UC is more common. In the United States, an estimated 29,000 individuals have PSC.

Pouchitis is inflammation of the ileal pouch (an artificial rectum surgically created out of ileal gut tissue in patients who have undergone a colectomy), which is created in the management of patients with ulcerative colitis, indeterminate colitis, FAP, or, rarely, other colitides.

A variety of pathophysiological mechanisms have been proposed for pouchitis, but the precise pathogenesis (biological cause) remains unknown. A pilot study on the effect of reducing dietary FODMAP intake on bowel function in patients without a colon ran by Croagh C, Shepherd SJ, Berryman M, Muir JG, Gibson PR indicates there might be a relation between Pouchitis and FODMAP content of diets.

The incidence of a first episode of pouchitis at 1, 5 and 10 years post-operatively is 15%, 33% and 45% respectively.

Patients with pouchitis typically present with bloody diarrhea, urgency in passing stools, or discomfort while passing stools. The loss of blood and/or dehydration resulting from the frequent stools will frequently result in nausea. Extreme cramping and pain can occur with pouchitis.

Endoscopy in patients with pouchitis usually reveals erythematous pouch mucosa, loss of pseudocolonic vasculature or other architecture, and friability of the mucosa. Biopsies show evidence of inflammatory cells or red blood cells in the lamina propria.

An increasing number of people are now surviving cancer, with improved treatments producing cure of the malignancy (cancer survivors). There are now over 14 million such people in the US, and this figure is expected to increase to 18 million by 2022. More than half are survivors of abdominal or pelvic cancers, with about 300,000 people receiving abdominal and pelvic radiation each year. It has been estimated there are 1.6 million people in the US with post-radiation intestinal dysfunction, a greater number than those with inflammatory bowel disease such as Crohn's disease or ulcerative colitis.

Pyostomatitis vegetans is an inflammatory stomatitis and most often seen in association with inflammatory bowel disease, namely ulcerative colitis and Crohn's disease. Uncommonly, it may be one of the features of orofacial granulomatosis.

Proctitis has many possible causes. It may occur idiopathically (idiopathic proctitis). Other causes include damage by irradiation (for example in radiation therapy for cervical cancer and prostate cancer) or as a sexually transmitted infection, as in lymphogranuloma venereum and herpes proctitis. Studies suggest a celiac disease-associated "proctitis" can result from an intolerance to gluten.

A common cause is engaging in anal sex with partner(s) infected with sexual transmitted diseases in men who have sex with men. Shared enema usage has been shown to facilitate the spread of Lymphogranuloma venereum proctitis.

Surgery-associated ischemia may contribute inflammation at the anal transitional zone.

Patients whose cuffitis is refractory to mesalamine and/or corticosteroids should be evaluated for other disease in the cuff area, such as fistula or anastomotic leaks. Cuffitis that is refractory to medication can also be a sign of Crohn's disease of the pouch.

Chronic cuffitis can also contribute to the development of anastomotic stricture.

Cuffitis that is refractory, Crohn's-related, or is associated with surgical complications can contribute to pouch failure.