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The treatment of inflammatory bowel disease by complementary medicine
COMPLEMENTARY THERAPIES
Common diseases
The treatment of inflammatory bowel disease by complementary medicine D. DOWSON
Centre for the Study of Complementary Medicine, Southampton, UK In this paper the main conditionsconsideredunder the broad heading of inflammatorybowel disease (IBD), are ulcerativecolitis and Crohn’s disease. Considerationis given to the known pathologicaland histological changes in these conditions, and as to the possible aetiologicalcauses in orthodoxterms. The role of diet in ini’kmunatorybowel disease has, in the opinion of many practitionerswithin the complementaryfield, been largely overlooked,and this is discussedas one of the major possible causes of IBD, with evidence for dietary elimination being an effectiveform of management. In addition, the importanceof dysbiosis, or alteration of the normal ecologicalbacterialflora of the intestine is mentioned, togetherwith the treatment of this condition using herbal, homoeopathicand naturopathicmethods. Where appropriate,evidence for the effixtiveness of complementarytherapiesis given, and for practitioners who are unfamiliar with complementaryapproaches,dietaryrestriction,as discussed as an experimentalform of treatment,may well be worthwhile. SUMMARY.
INTRODUCTION
CAUSE OF IBD
Within the group of conditions encompassing inflammatory bowel disease (IBD), the main ones to be considered all: ulcerative colitis and Crohn’s disease. Diverticulitis should also be included in view of the associated inflammation. In terms of prognosis, however, it is of less importance and, although commoner, is of course a secondary condition developing from the underlying pathology of diverticulosis. Ulcerative colitis and Crohn’s disease were once thought to be related, but the former affects the large bowel only whereas Crohn’s diseaseis predominantly,but not exclusively, a condition of the small intestine. In addition, the histology is distinctively different in that Crohn’s disease affects alI layers of the intestine, whereas ulcerative colitis produces lesions only within the mucosa of tbe colon.
The fundamental cause for these conditions remains unknown. An infective cause has been suggested although none has been found. At one time a relationship between tuberculosis and Crohn’s disease was considered in view of the similarity in histology, but this has not been demonstrated. An ischaemic aetiology has been suggested’ although the cause of the ischaemia is not known. To the layman it would appear obvious that dietary factorsmay be important in bowel disorders in view of the logical association but, surprisingly, conventional medicine has largely tended to ignore this possibility. This is even more surprising as antigens to cows’ milk have been shown in patients with ulcerative colitis? In addition, other conditions which are known or suspected to have an allergenic basis, such as hay-fever, eczema, and polyarthritis, are more common in patients with ulcerative colitis and in their relatives. Recently, a high level of endothelin-1, a potent vasoconstrktor, has been demonstmted in patients with both ulcerative colitis
David Dowson MB, ChB, Co-Diitoc, Care for the Study of Corn-plementary Medicine. 51 Bedford Place. !Xouthampton SO1 2DG. UK.
139
140 ComplementaryTherapiesin Medicine : Common diseases
and Crohn’s di~ease,~and this may cause the underlying ischaemic lesions mentioned above. However, this does not explain why the endothelin-1 is produced initially. A psychological cause has been proposed, as patients often display similar personality traits in that they tend to be emotionally immature, fussy, and dependent individuals. But this might well be a result rather than the cause of the condition.
TREATMENT OF IBD Conventional treatment Drug treatment remains the mainstay of management when the conditions am relatively mild. Salicylate-telated medications, such as sulphasilizine, tend to be the first line treatment, which initially seems illogical, as many sufferers find that their condition is aggravated by aspirin. In addition, side effects from these medications are common, occurring in up to 55% of patienk4 Steroid treatment, either locally in the form of enemas in ulcerative colitis or systemically in Crohn’s disease, ate used when symptoms are more severe. Other patho-immune suppressive agents have been used to manage this condition, all presenting the consolation of fairly adverse rcactions. Surgerymay be essential if symptoms arc not adequately controlled. However, this is a risky procedure, especially in Crohn’s disease, as the development of fistulae creates a real chance of peritonitis and septicaemia. In addition, the severity of the diarrhoea as part of the condition has commonly resulted in nutritional deficiencies, which may result in poor healing and recovery. For these reasons the disease may become terminal within the postoperative period.
Complementary treatment
Whenconsidering approacheswith complementarymethods to the management of bowel disease in general, some understanding of unconventional views of bowel physiology is essential. These are concepts, well-recognised within the complementary field, which are not, as yet, fully accepted by most orthodox practitioners, but which are particularlyrelevant in the treatment of gastro-intestinal disease. These are: 1. Dysbiosis 2. Food Sensitivity 1. Dysbiosis
The concept of dysbiosis is one which is readily accepted on the Continent but which is relatively ignored in the UK.
Fundamentally it refers to an abnormal balance of the usual commensal bacteria in the intestine or the presence of abnormal bacteria. Most bowel bacteria are anaerobic, and there is a symbiotic relationship which enhances health both by stimulating normal digestive processes and by immune system stimulation. It has been shown that the normal commensal organisms vary according to diet. Broadly speaking, two forms of bacteria ate present - coliform organisms and lactic acid fermenters. In most Westernerslactobacillipredominate and sudden dietary change may cause gastro-intestinal symptoms as the bacteriado not alter until after modification of the diet. The ingestion of excessive or unnecessary antibiotics may affect the commensal bacteriaby altering the balance between the two groups of bacteria and causing a dysbiosis. Symptomsof dysbiosis: The primary symptoms of dys-
biosis are alteration of bowel action, excessive flatulence, and abdominal distension. Secondary symptoms may be caused if factors caused by the dysbiosis develop. Indeed dysbiosis is probably present in the majority of patients with gastro-intestinaldisease. Causes of dysbiosis: As mentioned, antibiotics are common cause, particularlyif takenover a long period of time. An episode of infective diarrhoea,simply by emptying the bowel content, may also induce a temporary dysbiosis which, in turn, prolongs the symptoms. As diarrhoea is a universal symptom of inflammatory gastro-intestinaldiseases, these too will enhance a dysbiosis and thus add to the problems in treating the condition. Pancreatic dysfunction will alter the pH of the gastro-intestinaltract, and a carefully controlled pH is essential for maintenance of the normal floral balance. Consequently,inadequate pmduction of pancreatic enzymes or altered gastric secretion will predispose to dysbiosis. A number of hypotheses have emerged which have suggested a very close link between food sensitivities and bowel fermentation.5 Resultsof dysbiosis: The commensal bacteria provide a
degree of protection from a number of secondary conditions. If present in inadequate numbers, the ‘leaky’intcstine develops. In this, large molecules can pass through the gastro-intestinalmucosa into the portal circulation. If proteins arc not reduced to their constituent amino-acids they will be absorbed and can induce symptoms via a numkr of different immune reactions. Dysbiosis also predisposes to the development of yeast overgrowth in the bowel (popularly,but somewhat incorrectly, termed ‘candida’). The treatmentof dysbiosis: The treatment of dysbiosis is primarily the replacement of the normal commensal bacteria. However, this must be accompanied, if necessary, by correction of the normal pH of the bowel and treatment
Inflammatory bowel disfzase 141
of the liver and pancreas, to restore normal enzyme excretion. Probiotics, which are widely available in health stores and similar outlets, am concemrations of the normalbowel bacteria. They are normally given orally, and as the normal bowel contains several trillion bacteria, these have to be given in high concentrations. Even then, probably 70% are destroyed by the stomach acid, so only a small proportion reach the small intestine. Commercially available probiotics tend to contain either the colifomi bacteria or, more commonly, the lactic acid fermenting bacteria. A mixture of both is ideal as adjustment then naturally takes place according to need. 2. Food sensitivity Whilst immediate hypersensitivity reactions to food (commonly shellfish and strawberries) are well recognised as genuine IgE mediated allergies, there is only limited acceptance of the late onset reaction - or sensitivity - which is not mediated by usual allergic mechanisms. However, cows’ milk intolerance, due to lactase deficiency, is now acknowledged as a reality, and there is increasing evidence that other foodstuffs may produce a similar delayed reaction. The mechanisms for these effects are not necessarily through usual immunoglobulin allergy reactions. One study6 demonstrated improvement in patients with ulcerative colitis on removal of cows’ milk from the diet, but subsequent studies were at variance in the presence of cows’ milk antibodies in patients.7’8 It would seem that if diet is a significant factor in the aetiology of IBD, it is probably due to other non-IgE mediated mechanisms. Apparently, it is more likely that the reactions are due to one of three abnormal activities: +
Enzyme deficiencies
+
Direct pharmacological effects, or
+
Altered metabolic systems.
In IBD there is evidence that food sensitivity may play an important role. Total pamnteral nutrition is of proven valueinactiveCrohn’sdiseaseg-l’andthereareanumber of reports suggesting that elemental dieting - removing the yzsrtscommon food allergens from the diet - is beneficial. ’ As previously mentioned, immunoglobulins to cows’ milk have been identified in some sufferers2 In addition, desenitisation by the technique known as enzyme potentiated desensitisation (see below) has also been shown to lessen the severity of ulcerative colitis.r4 Chemical sensitivity: Specific, naturally occurring, chemicals have been identified in foods which may cause sensitivity problems. Some, such as nicotine andcaffeine, are known to have pharmacological effects, and others in pure form are directly toxic. Capsaicin, for example, which is present in peppers, is neurotoxic when applied dermally. It appears that idiosyncratic sensitivity to these
chemicals may be the underlying problem in many cases of food intolerance. One report, based on the case histories of just four patients, lends support to the suggestion that one chemical may be particularly implicated in IBD.” Phenylisothiocyanate is a potent inflammatory substance in pure form, but is present in a wide variety of foods. Further, more controlled research is needed in order to elucidate the role of this and other natural chemicals in these conditions. Enzyme potentiateddesensitisation: In this method of treatment extremely small doses of potentially allergenic foods are mixed with beta-glucuronidase and 1,3, cyciohexanediol. This is then administered to the patient by injection at monthly, then 3 and 6 monthly intervals. One study has shown that this approach significantly reduces the exacerbations of ulcerative colitis, indicatin~4again that food sensitivity may be the underlying cause. Vitaminand mineral supplementation: Because of the malabsorption associated with the conditions of IBD, deficiencies of essential minerals and vitamins are common. Zinc has been shown to be deficient in patients and replacement therapy, either through injection or intravenous infusion, may be needed.
CONCLUSION The major complementary therapies that can be used to approach IBD primarily involve the use of dietary manipulation. There is some clear evidence to suggest that food exclusion diets and enzyme potentiated desensitisation may have a significant effect in these conditions. It is possible that gut fermentation and the subsequent dysbiosis caused by an abnormal gut fermentation is an important patho-physiological process in the development both of irritable bowel and of inflammatory bowel disease. However, dysbiosis and its direct therapeutic implications have not been adequately tested in the context of properly controlled clinical trials. It is certainly worthwhile considering food exclusion in inflammatory bowel disease, and a trial of 2 to 3 months on an appropriate food exclusion diet may avoid the necessity for powerful and potentially dangerous conventional medication. A wide range of other complementary approaches have been suggested for IBD. These include acupuncture, homoeopathy, and hypnosis. While there is clear evidence that food exclusions can provide significant help in a proportion of those suffering from Crohn’s disease and colitis, there is little evidence to substantiate some of the claims made by other complementary therapists. These other therapies may well prove to be effective, but clinical trials are not yet available.
142 Complementary Therapies in Medicine : Common diseases
Suggestions for further reading Davies S, Stewart A. Nutritional medicine: the drug-free guide to better family healtk London: Pan Boo4 1987. Lewith G, Kenyon J, Dowson D. Allergy & intohxance: a complete guide to envimnmental medicine. London: Green Print, 1992.
10. 11.
12.
References 1. Waketield AJ, Dhillon AP, Pittico RM, et al. Pathogenesis of
2. 3. 4.
5. 6. 7. 8. 9.
C&n’s disease: multifocal gasttointestinal infarction. Lancet 1989; ii@671 4Nov): 1057-1062. Tmelove SC, Wright R. A controlled therapeutic trial of various diets in Ctohn’s disease. BMJ 1%5; 2: 138-141. Murch SH. et al. High endothelin-1 immunomactivity in Cmhn’s disease and ulcerative colitis. Lancet 1992; 339: 381-384. Das KM, Eastwood MA, McManus JPA, Sircus W. Adverse teattions during salicylazosulphapyridine therapy and the relation with dtug metabolism and acetylator phenotype. N Engl J Med 1973; 289 (6 Sept): 491-495. Hunter JO. Food allergy or entem metabolic disorder. Lancet 1991; 338 (8765): 495-496. Wright R, Ttuelove SC. A controlled therapeutic trial of various diets in ulcerative colitis. Am J Dig Dis 1966.11: 831-846. Taylor KB, Truelove SC. Circulating antibodies to milk proteins in ulcerative colitis. BMJ l%l; 2: 924-929. Jewel1DP, Truelove SC. Reaginic hypersensitivity in ulcerative colitis. Gut 1972, 13: 903-906. Dickinson RJ, Ashton MG. Axon AT, et al. Controlled trial of in-
13.
14.
15.
travenous hyperahmentation and total bowel rest as an adjunct to routine therapy of acute colitis. Gasttoenterology 1980; 79: 11991204. Driscoll Jr RH, Rosenberg JH. Total patenteral nutrition in inflammatory bowel disease. Med Clin N Am 1978; 62: 185-201. FischerJE, Foster JS, Abel RM, et al. Hyperahmemation as primary therapy for inflammatory bowel disease. Am J Surg 1973; 125: 165-173. Morin CL, RoutJet M, Roy CC, et al. Continuous elemental entend alimentation in the treatment of children and adolescents with Cmhn’s disease. J Patent Nutr 1982.6: 194-199. Sanderson JR, Udeen S, Davies PSW, et al. Remission induced by an elemental diet in small bowel Crohn’s disease. Arch Dis Childh 1987; 62 (2): 123-127. McEwen LM. A double blind controlled trial of enzyme potentiated hyposensitisation for the treatment of ulcerative colitis. Clin Ecol1987; 5 (2): 47-5 1. Dowson D. C&n’s disease: a dietary approach. Compl Med Res 1991; 5 (1): 44-45.
Useful addresses British Society of Allergy and Environmental Medicine Cadley Mews, Cadley, Marlborough, Wilts, UK. British Society for Nutritional Medicine 4 Museum Street, York YO12Es. UK.
Common diseases
The treatment of inflammatory bowel disease by complementary medicine D. DOWSON
Centre for the Study of Complementary Medicine, Southampton, UK In this paper the main conditionsconsideredunder the broad heading of inflammatorybowel disease (IBD), are ulcerativecolitis and Crohn’s disease. Considerationis given to the known pathologicaland histological changes in these conditions, and as to the possible aetiologicalcauses in orthodoxterms. The role of diet in ini’kmunatorybowel disease has, in the opinion of many practitionerswithin the complementaryfield, been largely overlooked,and this is discussedas one of the major possible causes of IBD, with evidence for dietary elimination being an effectiveform of management. In addition, the importanceof dysbiosis, or alteration of the normal ecologicalbacterialflora of the intestine is mentioned, togetherwith the treatment of this condition using herbal, homoeopathicand naturopathicmethods. Where appropriate,evidence for the effixtiveness of complementarytherapiesis given, and for practitioners who are unfamiliar with complementaryapproaches,dietaryrestriction,as discussed as an experimentalform of treatment,may well be worthwhile. SUMMARY.
INTRODUCTION
CAUSE OF IBD
Within the group of conditions encompassing inflammatory bowel disease (IBD), the main ones to be considered all: ulcerative colitis and Crohn’s disease. Diverticulitis should also be included in view of the associated inflammation. In terms of prognosis, however, it is of less importance and, although commoner, is of course a secondary condition developing from the underlying pathology of diverticulosis. Ulcerative colitis and Crohn’s disease were once thought to be related, but the former affects the large bowel only whereas Crohn’s diseaseis predominantly,but not exclusively, a condition of the small intestine. In addition, the histology is distinctively different in that Crohn’s disease affects alI layers of the intestine, whereas ulcerative colitis produces lesions only within the mucosa of tbe colon.
The fundamental cause for these conditions remains unknown. An infective cause has been suggested although none has been found. At one time a relationship between tuberculosis and Crohn’s disease was considered in view of the similarity in histology, but this has not been demonstrated. An ischaemic aetiology has been suggested’ although the cause of the ischaemia is not known. To the layman it would appear obvious that dietary factorsmay be important in bowel disorders in view of the logical association but, surprisingly, conventional medicine has largely tended to ignore this possibility. This is even more surprising as antigens to cows’ milk have been shown in patients with ulcerative colitis? In addition, other conditions which are known or suspected to have an allergenic basis, such as hay-fever, eczema, and polyarthritis, are more common in patients with ulcerative colitis and in their relatives. Recently, a high level of endothelin-1, a potent vasoconstrktor, has been demonstmted in patients with both ulcerative colitis
David Dowson MB, ChB, Co-Diitoc, Care for the Study of Corn-plementary Medicine. 51 Bedford Place. !Xouthampton SO1 2DG. UK.
139
140 ComplementaryTherapiesin Medicine : Common diseases
and Crohn’s di~ease,~and this may cause the underlying ischaemic lesions mentioned above. However, this does not explain why the endothelin-1 is produced initially. A psychological cause has been proposed, as patients often display similar personality traits in that they tend to be emotionally immature, fussy, and dependent individuals. But this might well be a result rather than the cause of the condition.
TREATMENT OF IBD Conventional treatment Drug treatment remains the mainstay of management when the conditions am relatively mild. Salicylate-telated medications, such as sulphasilizine, tend to be the first line treatment, which initially seems illogical, as many sufferers find that their condition is aggravated by aspirin. In addition, side effects from these medications are common, occurring in up to 55% of patienk4 Steroid treatment, either locally in the form of enemas in ulcerative colitis or systemically in Crohn’s disease, ate used when symptoms are more severe. Other patho-immune suppressive agents have been used to manage this condition, all presenting the consolation of fairly adverse rcactions. Surgerymay be essential if symptoms arc not adequately controlled. However, this is a risky procedure, especially in Crohn’s disease, as the development of fistulae creates a real chance of peritonitis and septicaemia. In addition, the severity of the diarrhoea as part of the condition has commonly resulted in nutritional deficiencies, which may result in poor healing and recovery. For these reasons the disease may become terminal within the postoperative period.
Complementary treatment
Whenconsidering approacheswith complementarymethods to the management of bowel disease in general, some understanding of unconventional views of bowel physiology is essential. These are concepts, well-recognised within the complementary field, which are not, as yet, fully accepted by most orthodox practitioners, but which are particularlyrelevant in the treatment of gastro-intestinal disease. These are: 1. Dysbiosis 2. Food Sensitivity 1. Dysbiosis
The concept of dysbiosis is one which is readily accepted on the Continent but which is relatively ignored in the UK.
Fundamentally it refers to an abnormal balance of the usual commensal bacteria in the intestine or the presence of abnormal bacteria. Most bowel bacteria are anaerobic, and there is a symbiotic relationship which enhances health both by stimulating normal digestive processes and by immune system stimulation. It has been shown that the normal commensal organisms vary according to diet. Broadly speaking, two forms of bacteria ate present - coliform organisms and lactic acid fermenters. In most Westernerslactobacillipredominate and sudden dietary change may cause gastro-intestinal symptoms as the bacteriado not alter until after modification of the diet. The ingestion of excessive or unnecessary antibiotics may affect the commensal bacteriaby altering the balance between the two groups of bacteria and causing a dysbiosis. Symptomsof dysbiosis: The primary symptoms of dys-
biosis are alteration of bowel action, excessive flatulence, and abdominal distension. Secondary symptoms may be caused if factors caused by the dysbiosis develop. Indeed dysbiosis is probably present in the majority of patients with gastro-intestinaldisease. Causes of dysbiosis: As mentioned, antibiotics are common cause, particularlyif takenover a long period of time. An episode of infective diarrhoea,simply by emptying the bowel content, may also induce a temporary dysbiosis which, in turn, prolongs the symptoms. As diarrhoea is a universal symptom of inflammatory gastro-intestinaldiseases, these too will enhance a dysbiosis and thus add to the problems in treating the condition. Pancreatic dysfunction will alter the pH of the gastro-intestinaltract, and a carefully controlled pH is essential for maintenance of the normal floral balance. Consequently,inadequate pmduction of pancreatic enzymes or altered gastric secretion will predispose to dysbiosis. A number of hypotheses have emerged which have suggested a very close link between food sensitivities and bowel fermentation.5 Resultsof dysbiosis: The commensal bacteria provide a
degree of protection from a number of secondary conditions. If present in inadequate numbers, the ‘leaky’intcstine develops. In this, large molecules can pass through the gastro-intestinalmucosa into the portal circulation. If proteins arc not reduced to their constituent amino-acids they will be absorbed and can induce symptoms via a numkr of different immune reactions. Dysbiosis also predisposes to the development of yeast overgrowth in the bowel (popularly,but somewhat incorrectly, termed ‘candida’). The treatmentof dysbiosis: The treatment of dysbiosis is primarily the replacement of the normal commensal bacteria. However, this must be accompanied, if necessary, by correction of the normal pH of the bowel and treatment
Inflammatory bowel disfzase 141
of the liver and pancreas, to restore normal enzyme excretion. Probiotics, which are widely available in health stores and similar outlets, am concemrations of the normalbowel bacteria. They are normally given orally, and as the normal bowel contains several trillion bacteria, these have to be given in high concentrations. Even then, probably 70% are destroyed by the stomach acid, so only a small proportion reach the small intestine. Commercially available probiotics tend to contain either the colifomi bacteria or, more commonly, the lactic acid fermenting bacteria. A mixture of both is ideal as adjustment then naturally takes place according to need. 2. Food sensitivity Whilst immediate hypersensitivity reactions to food (commonly shellfish and strawberries) are well recognised as genuine IgE mediated allergies, there is only limited acceptance of the late onset reaction - or sensitivity - which is not mediated by usual allergic mechanisms. However, cows’ milk intolerance, due to lactase deficiency, is now acknowledged as a reality, and there is increasing evidence that other foodstuffs may produce a similar delayed reaction. The mechanisms for these effects are not necessarily through usual immunoglobulin allergy reactions. One study6 demonstrated improvement in patients with ulcerative colitis on removal of cows’ milk from the diet, but subsequent studies were at variance in the presence of cows’ milk antibodies in patients.7’8 It would seem that if diet is a significant factor in the aetiology of IBD, it is probably due to other non-IgE mediated mechanisms. Apparently, it is more likely that the reactions are due to one of three abnormal activities: +
Enzyme deficiencies
+
Direct pharmacological effects, or
+
Altered metabolic systems.
In IBD there is evidence that food sensitivity may play an important role. Total pamnteral nutrition is of proven valueinactiveCrohn’sdiseaseg-l’andthereareanumber of reports suggesting that elemental dieting - removing the yzsrtscommon food allergens from the diet - is beneficial. ’ As previously mentioned, immunoglobulins to cows’ milk have been identified in some sufferers2 In addition, desenitisation by the technique known as enzyme potentiated desensitisation (see below) has also been shown to lessen the severity of ulcerative colitis.r4 Chemical sensitivity: Specific, naturally occurring, chemicals have been identified in foods which may cause sensitivity problems. Some, such as nicotine andcaffeine, are known to have pharmacological effects, and others in pure form are directly toxic. Capsaicin, for example, which is present in peppers, is neurotoxic when applied dermally. It appears that idiosyncratic sensitivity to these
chemicals may be the underlying problem in many cases of food intolerance. One report, based on the case histories of just four patients, lends support to the suggestion that one chemical may be particularly implicated in IBD.” Phenylisothiocyanate is a potent inflammatory substance in pure form, but is present in a wide variety of foods. Further, more controlled research is needed in order to elucidate the role of this and other natural chemicals in these conditions. Enzyme potentiateddesensitisation: In this method of treatment extremely small doses of potentially allergenic foods are mixed with beta-glucuronidase and 1,3, cyciohexanediol. This is then administered to the patient by injection at monthly, then 3 and 6 monthly intervals. One study has shown that this approach significantly reduces the exacerbations of ulcerative colitis, indicatin~4again that food sensitivity may be the underlying cause. Vitaminand mineral supplementation: Because of the malabsorption associated with the conditions of IBD, deficiencies of essential minerals and vitamins are common. Zinc has been shown to be deficient in patients and replacement therapy, either through injection or intravenous infusion, may be needed.
CONCLUSION The major complementary therapies that can be used to approach IBD primarily involve the use of dietary manipulation. There is some clear evidence to suggest that food exclusion diets and enzyme potentiated desensitisation may have a significant effect in these conditions. It is possible that gut fermentation and the subsequent dysbiosis caused by an abnormal gut fermentation is an important patho-physiological process in the development both of irritable bowel and of inflammatory bowel disease. However, dysbiosis and its direct therapeutic implications have not been adequately tested in the context of properly controlled clinical trials. It is certainly worthwhile considering food exclusion in inflammatory bowel disease, and a trial of 2 to 3 months on an appropriate food exclusion diet may avoid the necessity for powerful and potentially dangerous conventional medication. A wide range of other complementary approaches have been suggested for IBD. These include acupuncture, homoeopathy, and hypnosis. While there is clear evidence that food exclusions can provide significant help in a proportion of those suffering from Crohn’s disease and colitis, there is little evidence to substantiate some of the claims made by other complementary therapists. These other therapies may well prove to be effective, but clinical trials are not yet available.
142 Complementary Therapies in Medicine : Common diseases
Suggestions for further reading Davies S, Stewart A. Nutritional medicine: the drug-free guide to better family healtk London: Pan Boo4 1987. Lewith G, Kenyon J, Dowson D. Allergy & intohxance: a complete guide to envimnmental medicine. London: Green Print, 1992.
10. 11.
12.
References 1. Waketield AJ, Dhillon AP, Pittico RM, et al. Pathogenesis of
2. 3. 4.
5. 6. 7. 8. 9.
C&n’s disease: multifocal gasttointestinal infarction. Lancet 1989; ii@671 4Nov): 1057-1062. Tmelove SC, Wright R. A controlled therapeutic trial of various diets in Ctohn’s disease. BMJ 1%5; 2: 138-141. Murch SH. et al. High endothelin-1 immunomactivity in Cmhn’s disease and ulcerative colitis. Lancet 1992; 339: 381-384. Das KM, Eastwood MA, McManus JPA, Sircus W. Adverse teattions during salicylazosulphapyridine therapy and the relation with dtug metabolism and acetylator phenotype. N Engl J Med 1973; 289 (6 Sept): 491-495. Hunter JO. Food allergy or entem metabolic disorder. Lancet 1991; 338 (8765): 495-496. Wright R, Ttuelove SC. A controlled therapeutic trial of various diets in ulcerative colitis. Am J Dig Dis 1966.11: 831-846. Taylor KB, Truelove SC. Circulating antibodies to milk proteins in ulcerative colitis. BMJ l%l; 2: 924-929. Jewel1DP, Truelove SC. Reaginic hypersensitivity in ulcerative colitis. Gut 1972, 13: 903-906. Dickinson RJ, Ashton MG. Axon AT, et al. Controlled trial of in-
13.
14.
15.
travenous hyperahmentation and total bowel rest as an adjunct to routine therapy of acute colitis. Gasttoenterology 1980; 79: 11991204. Driscoll Jr RH, Rosenberg JH. Total patenteral nutrition in inflammatory bowel disease. Med Clin N Am 1978; 62: 185-201. FischerJE, Foster JS, Abel RM, et al. Hyperahmemation as primary therapy for inflammatory bowel disease. Am J Surg 1973; 125: 165-173. Morin CL, RoutJet M, Roy CC, et al. Continuous elemental entend alimentation in the treatment of children and adolescents with Cmhn’s disease. J Patent Nutr 1982.6: 194-199. Sanderson JR, Udeen S, Davies PSW, et al. Remission induced by an elemental diet in small bowel Crohn’s disease. Arch Dis Childh 1987; 62 (2): 123-127. McEwen LM. A double blind controlled trial of enzyme potentiated hyposensitisation for the treatment of ulcerative colitis. Clin Ecol1987; 5 (2): 47-5 1. Dowson D. C&n’s disease: a dietary approach. Compl Med Res 1991; 5 (1): 44-45.
Useful addresses British Society of Allergy and Environmental Medicine Cadley Mews, Cadley, Marlborough, Wilts, UK. British Society for Nutritional Medicine 4 Museum Street, York YO12Es. UK.