Environmental enteropathy is believed to result in chronic malnutrition and subsequent growth stunting (low height-for-age measurement) as well as other child development deficits.

EE is rarely symptomatic and is considered a subclinical condition. However, adults may have mild symptoms or malabsorption such as altered stool consistency, increased stool frequency and weight loss.

Fibrosing colonopathy is a disease that arises in patients with cystic fibrosis treated with enteric coated pancreatic enzyme supplements. The disease is associated with high dose of these supplements. The clinical presentation of fibrosing colonopathy is non-specific. Abdominal pain, distension, vomiting, and constipation are frequent

features and have led initially to confusion with distal intestinal obstruction syndrome. In some instances, the clinical and radiological features were suggestive of Crohn's disease or inflammatory colitis.

While the causes of IBS are still unknown, it is believed that the entire gut–brain axis is affected.

The risk of developing IBS increases six-fold after acute gastrointestinal infection. Postinfection, further risk factors are young age, prolonged fever, anxiety, and depression. Psychological factors, such as depression or anxiety, have not been shown to cause or influence the onset of IBS, but may play a role in the persistence and perceived severity of symptoms. Nevertheless, they may worsen IBS symptoms and the patient quality of life. Antibiotic use also appears to increase the risk of developing IBS. Research has found that genetic defects in innate immunity and epithelial homeostasis increase the risk of developing both post-infectious as well as other forms of IBS.

Approximately 10 percent of IBS cases are triggered by an acute gastroenteritis infection. Genetic defects relating to the innate immune system and epithelial barrier as well as high stress and anxiety levels appear to increase the risk of developing post-infectious IBS. Post-infectious IBS usually manifests itself as the diarrhea-predominant subtype. Evidence has demonstrated that the release of high levels of proinflammatory cytokines during acute enteric infection causes increased gut permeability leading to translocation of the commensal bacteria across the epithelial barrier resulting in significant damage to local tissues, which can result in chronic gut abnormalities in sensitive individuals. However, increased gut permeability is strongly associated with IBS regardless of whether IBS was initiated by an infection or not. A link between small intestinal bacterial overgrowth and tropical sprue has been proposed to be involved in the aetiology of post-infectious IBS.

While IBD can limit quality of life because of pain, vomiting, diarrhea, and other socially undesired symptoms, it is rarely fatal on its own. Fatalities due to complications such as toxic megacolon, bowel perforation and surgical complications are also rare..

Around one-third of individuals with IBD experience persistent gastrointestinal symptoms similar to irritable bowel syndrome (IBS) in the absence of objective evidence of disease activity. Despite enduring the side-effects of long-term therapies, this cohort has a quality of life that is not significantly different to that of individuals with uncontrolled, objectively active disease, and escalation of therapy to biological agents is typically ineffective in resolving their symptoms. The cause of these IBS-like symptoms is unclear, but it has been suggested that changes in the gut-brain axis, epithelial barrier dysfunction, and the gut flora may be partially responsible.

While patients of IBD do have an increased risk of colorectal cancer, this is usually caught much earlier than the general population in routine surveillance of the colon by colonoscopy, and therefore patients are much more likely to survive.

New evidence suggests that patients with IBD may have an elevated risk of endothelial dysfunction and coronary artery disease.

A recent literature review by Gandhi et al. described that IBD patients over the age of 65 and females are at increased risk of coronary artery disease despite the lack of traditional risk factors.

The goal of treatment is toward achieving remission, after which the patient is usually switched to a lighter drug with fewer potential side effects. Every so often, an acute resurgence of the original symptoms may appear; this is known as a "flare-up". Depending on the circumstances, it may go away on its own or require medication. The time between flare-ups may be anywhere from weeks to years, and varies wildly between patients – a few have never experienced a flare-up.

Life with IBD can be challenging, however, it should not impede your ability to live a normal life. Patients with IBD can go to college, hold a normal job, get married, have children etc. As is the nature of any chronic, unpredictable disease, there will be ups and downs. The progress made in IBD research and treatment is astounding and will only improve in the years to come.

Although living with IBD can be difficult, there are numerous resources available to help families navigate the ins and out of IBD. The Crohn's and Colitis Foundation of America (CCFA) is an excellent resource. CCFA is a vital resource to getting questions answered and finding support about life with IBD.

IBD resulted in a global total of 51,000 deaths in 2013 and 55,000 deaths in 1990. The increased incidence of IBD since World War 2 has been linked to the increase in meat consumption worldwide, supporting the claim that animal protein intake is associated with IBD. Inflammatory bowel diseases are increasing in Europe.

It is a serious medical disorder and the mortality rate can be as high as 30%. The high mortality rate is likely a measure that this syndrome is seen in critically ill patients, rather than this syndrome being in itself lethal, although it can also present in otherwise healthy individuals (especially if the disorder was induced by pharmacologic agents). Drug induced megacolon (i.e. from Clozapine) has been associated with mortality as high as 27.5%.

Tricho-hepato-enteric syndrome (THE), also known as syndromic or phenotypic diarrhea, is an extremely rare congenital bowel disorder which manifests itself as intractable diarrhea in infants with intrauterine growth retardation, hair and facial abnormalities. Many also have liver disease and abnormalities of the immune system. The associated malabsorption leads to malnutrition and failure to thrive.

It is thought to be a genetic disorder with an autosomal recessive inheritance pattern, although responsible genes have not been found and the exact cause remains unknown. Prognosis is poor; many patients die before the age of 5 (mainly from infections or cirrhosis), although most patients nowadays survive with intravenous feeding (parenteral nutrition).

Tricho-hepato-enteric syndrome is estimated to affect 1 in 300,000 to 400,000 live births in Western Europe. This syndrome was first reported in 1982 with a report on 2 siblings, and as of 2008 there were around 25 published cases in medical journals. There seem to be no racial differences in its occurrence. It might be more common, as many genetic diseases, in areas with high levels of consanguinity.

Inflammation can spread to other parts of the gut in patients with typhlitis. The condition can also cause the cecum to become distended and can cut off its blood supply. This and other factors can result in necrosis and perforation of the bowel, which can cause peritonitis and sepsis.

Historically, the mortality rate for typhlitis was as high as 50%, mostly because it is frequently associated with bowel perforation. More recent studies have demonstrated better outcomes with prompt medical management, generally with resolution of symptoms with neutrophil recovery without death

Some situations that increase the need for folate include the following:

- hemorrhage

- kidney dialysis

- liver disease

- malabsorption, including celiac disease and fructose malabsorption

- pregnancy and lactation (breastfeeding)

- tobacco smoking

- alcohol consumption

Folate is found in leafy green vegetables. Multi-vitamins also tend to include Folate as well as many other B vitamins. B vitamins, such as Folate, are water-soluble and excess is excreted in the urine.

When cooking, use of steaming, a food steamer, or a microwave oven can help keep more folate content in the cooked foods, thus helping to prevent folate deficiency.

Folate deficiency during human pregnancy has been associated with an increased risk of infant neural tube defects. Such deficiency during the first four weeks of gestation can result in structural and developmental problems. NIH guidelines recommend oral B vitamin supplements to decrease these risks near the time of conception and during the first month of pregnancy.

The condition is usually caused by Gram-positive enteric commensal bacteria of the gut (gut flora). "Clostridium difficile" is a species of Gram-positive bacteria that commonly causes severe diarrhea and other intestinal diseases when competing bacteria are wiped out by antibiotics, causing pseudomembranous colitis, whereas Clostridium septicum is responsible for most cases of neutropenic enterocolitis.

Typhlitis most commonly occurs in immunocompromised patients, such as those undergoing chemotherapy, patients with AIDS, kidney transplant patients, or the elderly.

Ogilvie syndrome is the acute dilation of the colon in the absence of any mechanical obstruction in severely ill patients.

Colonic pseudo-obstruction is characterized by massive dilatation of the cecum (diameter > 10 cm) and right colon on abdominal X-ray. It is a type of megacolon, sometimes referred to as "acute megacolon", to distinguish it from toxic megacolon.

The condition carries the name of the British surgeon Sir (1887–1971), who first reported it in 1948.

The diagnosis of enteric neuropathy is rather difficult, in that many symptoms present in ways that are common to many other bowel- and gut-related diseases. It is common that many people undergo many surgeries, sometimes over several years, to attempt to combat other possible diseases. The diagnosis itself is conducted by a physician based on multiple tests and is subjective rather than definitive, which for those who have enteric neuropathy will show signs of severe abnormalities in the movement of the gut. An operation to take a section of muscle for biopsy which, if it shows signs of nerve degradation, assists in the diagnosis.

Enteric neuropathy is a degenerative neuromuscular condition of the digestive system. In simple terms the gut stops functioning, due to degradation of the nerves and muscles. The condition affects all parts of the digestive tract. There is no known cure or treatment for enteric neuropathy at this time; it is only possible to work on symptom management.

The name enteric neuropathy only seems to be used for diagnosis within the UK. The most common name worldwide for this condition is Intestinal pseudoobstruction.

An enterocutaneous fistula (ECF) is an abnormal communication between the small or large bowel and the skin that allows the contents of the stomach or intestines to leak through an opening in the skin.

Little is currently known on brain dysfunction in feather-plucking. However, it may be hypothesized that abnormal brain function is involved, especially in those cases that appear sensitive to treatment with behavioural intervention and/or environmental changes. Psychotropic therapy for birds has been suggested as treatment for feather-plucking although responses seem variable.

The mnemonic FRIENDS can be used to memorize characteristics which impede the closure of ECF.

F Foreign body

R Radiation

I Infection or Inflammatory bowel disease

E Epithelialization

N Neoplasm

D Distal obstruction

S Short tract (<2 cm)

In stage III disease, fistulae left undiscovered, undiagnosed, or untreated, can lead to the development of squamous cell carcinoma, a rare cancer, in the anus or other affected areas. Other stage III chronic sequelae may also include anemia, multilocalized infections, amyloidosis, and arthropathy. Stage III complications have been known to lead to sepsis, but clinical data is still uncertain.

In epidemiology, environmental diseases are diseases that can be directly attributed to environmental factors (as distinct from genetic factors or infection). Apart from the true monogenic genetic disorders, environmental diseases may determine the development of disease in those genetically predisposed to a particular condition. Stress, physical and mental abuse, diet, exposure to toxins, pathogens, radiation, and chemicals found in almost all personal care products and household cleaners are possible causes of a large segment of non-hereditary disease. If a disease process is concluded to be the result of a combination of genetic and "environmental factor" influences, its etiological origin can be referred to as having a multifactorial pattern.

There are many different types of environmental disease including:

- Lifestyle disease such as cardiovascular disease, diseases caused by substance abuse such as alcoholism, and smoking-related disease

- Disease caused by physical factors in the environment, such as skin cancer caused by excessive exposure to ultraviolet radiation in sunlight

- Disease caused by exposure to toxic or irritant chemicals in the environment such as toxic metals

==Environmental Diseases vs. Pollution-

Related Diseases==

Environmental diseases are a direct result from the environment. This includes diseases caused by substance abuse, exposure to toxic chemicals, and physical factors in the environment, like UV radiation from the sun, as well as genetic predisposition. Meanwhile, pollution-related diseases are attributed to exposure to toxins in the air, water, and soil. Therefore all pollution-related disease are environmental diseases, but not all environmental diseases are pollution-related diseases.

Toxic optic neuropathy refers to the ingestion of a toxin or an adverse drug reaction that results in vision loss from optic nerve damage. Patients may report either a sudden loss of vision in both eyes, in the setting of an acute intoxication, or an insidious asymmetric loss of vision from an adverse drug reaction. The most important aspect of treatment is recognition and drug withdrawal.

Among the many causes of TON, the top 10 toxins include:

- Medications

- Ethambutol, rifampin, isoniazid, streptomycin (tuberculosis treatment)

- Linezolid (taken for bacterial infections, including pneumonia)

- Chloramphenicol (taken for serious infections not helped by other antibiotics)

- Isoretinoin (taken for severe acne that fails to respond to other treatments)

- Ciclosporin (widely used immunosuppressant)

- Acute Toxins

- Methanol (component of some moonshine, and some cleaning products)

- Ethylene glycol (present in anti-freeze and hydraulic brake fluid)

Metabolic disorders may also cause this version of disease. Systemic problems such as diabetes mellitus, kidney failure, and thyroid disease can cause optic neuropathy, which is likely through buildup of toxic substances within the body. In most cases, the cause of the toxic neuropathy impairs the tissue’s vascular supply or metabolism. It remains unknown as to why certain agents are toxic to the optic nerve while others are not and why particularly the papillomacular bundle gets affected.

TAA is an old term for a constellation of elements that can lead to a mitochondrial optic neuropathy. The classic patient is a man with a history of heavy alcohol and tobacco consumption. Respectively, this combines nutritional mitochondrial impairment, from vitamin deficiencies (folate and B-12) classically seen in alcoholics, with tobacco-derived products, such as cyanide and ROS. It has been suggested that the additive effect of the cyanide toxicity, ROS, and deficiencies of thiamine, riboflavin, pyridoxine, and b12 result in TAA.

Additionally, there are environmental diseases caused by the aromatic carbon compounds including : benzene, hexachlorocyclohexane, toluene diisocyanate, phenol, pentachlorophenol, quinone and hydroquinone.

Also included are the aromatic nitro-, amino-, and pyridilium-deratives: nitrobenzene, dinitrobenzene, trinitrotoluene, paramethylaminophenol sulfate (Metol), dinitro-ortho-cresol, aniline, trinitrophenylmethylnitramine (tetryl), hexanitrodiphenylamine (aurantia), phenylenediamines, and paraquat.

The aliphatic carbon compounds can also cause environmental disease. Included in these are methanol, nitroglycerine, nitrocellulose, dimethylnitrosamine, and the halogenated hydrocarbons: methyl chloride, methyl bromide, trichloroethylene, carbon tetrachloride, and the chlorinated naphthalenes. Also included are glycols: ethylene chlorhydrin and diethylene dioxide as well as carbon disulfide, acrylonitrile, acrylamide, and vinyl chloride.