Gastrointestinal function and disease

5.1. Gastrointestinal infections (Gracey, 1993; Savarino & Bourgeois, 1993)

Acute infections of the gut are usually self-limiting, characterized by diarrhoea and often vomiting. The principal pathogens are viruses and bacteria such as Escherichia coli, Campylobacter spp, Vibrio cholerae, Staphylococcus aureus, Bacillus cereus, Clostridium perfringens, Salmonella spp, Shigella spp, Yersinia spp and a number of protozoa, especially Giardia lamblia, Entamoeba histolytica and Cryptosporidium parvum.

Bacteria causing infection are usually classified according to whether they secrete an enterotoxin (toxigenic) or invade the bowel wall (invasive). Toxigenic diarrhoeas include cholera, and both enteropathogenic and enterotoxigenic E. coli, whilst the classic invasive organisms are Shigella (dysentery), Salmonella (typhoid) and entero-invasive E. coli. Rotaviruses are most commonly found in diarrhoea of children and invade the small-intestinal epithelium. Acute diarrhoea is responsible for 3-4 million deaths annually worldwide, many of which are children, in which it accounts for 20-30 % of all mortality.

Rotavirus is the most common cause of acute childhood diarrhoea. It is primarily seen in infants and young children, with a peak incidence between 6 months and 2 years of age. Rotaviruses invade the highly differentiated absorptive columnar cells of the small-intestinal epithelium, where they replicate. This results in partial disruption of the intestinal mucosa with loss of microvilli and decreased villus: crypt ratio. Rotavirus infection is associated with increased intestinal permeability. Jalonen et al. (1991) found increased lactulose: mannitol urinary recovery ratios in patients with acute diarrhoea compared with non-diarrhoeal patients. Concomitantly, the levels of immune complexes containing dietary j3-lactoglobulin in sera were significantly higher in patients with rotavirus diarrhoea than in non-diarrhoeal patients. Enhanced macromo-lecular absorption in rotavirus gastroenteritis has been shown in several studies (Heyman et al. 1987; Isolauri et al. 1993a, b). A local immunoinflammatory reaction impairs the intestine's barrier function. Impaired barrier function and defective handling of intraluminal antigens in the epithelial cells may be an important pathogenic mechanism in acute and chronic gastrointestinal disorders. It may abrogate tolerance to ubiquitous antigens, including bacteria residing in the intestine (Duchmann et al. 1995).

Chronic infection of the gut is much rarer and seen only in persons who have anatomical abnormalities of the gut such as blind loops, strictures or fistulas. Chronic infection with Tropheryma whippelli causes Whipple's disease and intestinal bacteria are responsible for tropical sprue. Tuberculosis affects the gut, especially the ileo-caecal region, and chronic carrier states occur with amoebas.

The main indigenous bacteria of the large intestine resist invasion by pathogenic species and this is part of the human host defence against diarrhoeal illness. This barrier function provided by the gut flora may be impaired during antibiotic use, where diarrhoea is common. Antibiotic-associated diarrhoea is usually due to invasion with toxin-producing species such as Clostridium difficile or Clostridium septicum.

5.2. Normal bowel habit (Cummings, 1993, 1994)

Bowel habit is defined by the amount of stool passed, frequency of defecation and consistency of stool. It varies very widely throughout the world with daily stool weights in the range 100-400 g/d and stool frequency of three times per day to three times per week. In European countries and North America, daily stool weight is of the order of 100-150 g/d (Cummings et al. 1992). Bowel habit is controlled principally by two factors, first diet, and second gut motor activity (transit time). The foods that affect bowel habit are those which reach the large intestine, i.e. are non-digestible. The dietary components falling into this category are lactose (in lactase-deficient individuals), sugar alcohols, non-digestible oligosaccharides, resistant starch and NSP. Dietary fat and protein have little effect on bowel habit unless they are rendered non-absorbable by some technique (e.g. sucrose polyester).

The mechanism by which non-digestible foods affect bowel habit depends on their fermentability. Foods that are not fermented appear in faeces and cause bulking depending on their inherent mass or water-holding capacity (i.e. bran and other intact cell-wall material). Most foods that reach the large intestine are fermented, yielding SCFA, which are absorbed and do not contribute to faecal bulk, and H2 and CH4, which can expand faecal bulk but not mass. Fermentation also stimulates bacterial growth to produce biomass, which is the principal mechanism of increasing stool mass. A final mechanism that needs to be borne in mind is the interrelationship between intestinal bulk and motor activity. As bulk in the large intestine increases, so motor activity is stimulated and, in general, the greater the bulk the more rapid the transit. Motor activity expressed as transit time may also modulate stool output independently of dietary bulk (Cummings, 1993, 1994).

5.3. Constipation

Constipation is a disorder of motor activity of the large bowel traditionally defined in terms of bowel frequency. The main symptom in constipation is straining at defecation, and discomfort, distension and incomplete rectal emptying are all considered part of the condition. Total gut transit time is generally prolonged in constipated subjects. There are many causes of constipation, with diet one of the common reasons, particularly low-NSP diets, gluten-free diets, 'low-residue' diets and enteral feeds. Treatment of simple constipation is usually in the first instance by dietary means. The principle is to increase fermentable carbohydrates in the diet, especially NSP from whole-grain cereals. Thus, diet has a major role to play in controlling bowel habit.

5.4. Irritable bowel syndrome (IBS) (Thompson & Heaton,

1980; Thompson & Gomborone, 1993)

IBS is one of the commonest disorders seen in the hospital gastroenterology clinic, but it is poorly understood. IBS (or irritable colon, mucus colitis, spastic colon) is a disorder of motor activity of the whole bowel, although colonic symptoms usually predominate. It occurs very widely throughout the world and is commoner in women. IBS has two main presenting features, abdominal pain and altered bowel habit (Thompson & Heaton, 1980).

The cause of IBS is unknown but it occurs in many patients following dysentery or antibiotic use. In addition, patients often volunteer that specific foods upset them (food intolerance) and stress is clearly contributory. Wheat bran and other bulk laxatives are frequently given, but results have been very variable. They may aggravate symptoms through gas production, although in patients who are predominantly constipated they are of benefit. Because of a postulated disturbance in the colonic microflora in IBS a number of groups are currently trying the use of probiotics to 'normalize' the flora.

5.5. Inflammatory bowel disease (Podolsky, 1991;

MacDonald, 1993; Tytgat et al. 1995)

Two major disorders, Crohn's disease and ulcerative colitis, are conventionally grouped together under the heading inflammatory bowel disease because both are characterized by chronic inflammation in the gut. However, it is best to consider them as separate conditions because they have characteristically different pathology, clinical courses, complications and management. The aetiology of neither is known.

5.5.1. Crohn's disease. Crohn's disease may affect any part of the gut from mouth to anus. Characteristically it occurs in the ileocaecal region and colon, and the inflammation is patchy or discontinuous. It frequently recurs after surgical resection of the affected areas of gut at or near the point of anastomosis of the bowel. The involved intestine is thickened, with ulceration of the mucosa, stricturing and fistula formation. Mouth ulcers and perianal abscesses are characteristic. Histologically there is transmural inflammation, with mononuclear cells, lymphoid aggregates and granulomata.

Crohn's disease occurs worldwide although it is uncommon in Central and South America, Africa and Asia. It is seen less frequently than ulcerative colitis, although rates have increased fivefold since 1950. It is predominantly a disease of the young with peak occurrence between the ages of 20 and 30 years with a second peak between 70 and 80 years. The cause is unknown but genetic factors are important with 10% of patients having a close relative with the disease. Diet has been implicated, especially sugar, but a multicentre trial in which a diet excluding sugars and rich in NSP was given did not result in any conclusive benefit in patient management (Ritchie et al. 1987). More likely aetiological factors include bacteria and other micro-organisms.

Diet has an important role to play in the management of Crohn's disease. For patients who do not respond to conventional treatment in Crohn's disease, various enteral and parenteral regimens providing bowel rest have been used. The rationale for such treatments is that the absence of food antigens in the bowel lumen reduces inflammatory immune reactions, motor and digestive activity, and gives the mucosa a chance to heal itself.

Most patients relapse soon after introduction of normal food following bowel rest regimens. It has been suggested that dietary modification to exclude foods likely to cause symptoms (predominantly cereals, dairy products and meat) can lead to extended periods of remission.

5.5.2. Ulcerative colitis. Ulcerative colitis is a chronic inflammatory condition of the mucosa of the large bowel that causes bloody diarrhoea. It is one of the diseases of modern civilization, being first described with certainty in 1909 and predominantly affecting industrialized populations. It has an overall prevalence of 40-120 cases per 100000 of the population in Western countries and is uncommon, although beginning to emerge, in Africa and India. It affects the sexes equally and usually presents between the ages of 20 and 40 years.

Its cause is unknown but there is probably a genetic component, with a 15-fold increased risk amongst close relatives of patients. Animal models point to an involvement of the immune system, but also to the necessary presence of bacteria in the colon to produce colitis. The observation that healthy colonocytes use butyrate for their metabolism and that this is defective in ulcerative colitis has raised the possibility of dietary factors in its aetiology. However, no convincing evidence for a dietary factor has emerged, although the inhibition of butyrate oxidation by S-compounds leaves the possibility of diet combining with the colonic microflora as a possible initiating factor of the inflammation (Pitcher & Cummings, 1996).

5.6. Food allergy (Isolauri, 1995)

Food allergy is defined as an immunologically mediated adverse reaction against dietary antigens. Food allergy can affect several organ systems, the symptoms commonly arising from the gut, skin and respiratory tract. Despite the wide spectrum of clinical manifestations, there are at least two prerequisites for the development of food allergy: dietary antigens must penetrate the intestine's mucosal barrier, and the absorbed antigens must cause harmful immune responses. The immaturity of the immune system and the gastrointestinal barrier may explain the peak prevalence of food allergies in infancy. In food allergy, intestinal inflammation and disturbances in intestinal permeability and antigen transfer occur when an allergen comes into contact with the intestinal mucosa. During dietary elimination of the antigen, the barrier and transfer functions of the mucosa are normal. It has, therefore, been concluded that impairment of the intestine's function is secondary to an abnormal intestinal immune response to the offending antigens.

5.7. Colorectal cancer (Faivre et al. 1985)

Colorectal cancer is unequally spread throughout the world (Burkitt, 1971). It is amongst the three most common malignancies in most industrialized countries including Western Europe, and its survival rate has improved little during the past decades, being of the order of 40% at 5 years. The most common locations in high-risk countries are the left colon and the rectum, whereas right-colon cancers are proportionally more common in low-risk areas such as Japan. About 5 % of colorectal cancers are truly genetic diseases (hereditary nonpolyposis colorectal cancer and familial polyposis coli), transmitted as autosomal dominant, but the majority of colorectal cancers are sporadic, and are mostly influenced by environmental factors, in particular diet, with a potential interaction between a genetic background and diet (Boutron et al. 1996). From 70 to 80% of left colon and rectal cancers in Western countries follow the so-called adenoma-carcinoma pathway, with possibly less in the case of right-colon cancers (Bedenne et al. 1992). This is of major importance as it provides the opportunity of studying precancerous lesions both in aetiological studies such as case-control and cohort studies, and for intervention studies, where studying adenoma recurrence or growth is easier and brings results more rapidly (Boutron & Faivre, 1993).

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