El Paso Functional Medicine
I hope you have enjoyed our blog posts on various health, nutritional and injury related topics. Please don't hesitate in calling us or myself if you have questions when the need to seek care arises. Call the office or myself. Office 915-850-0900 - Cell 915-540-8444 Great Regards. Dr. J

Glutamine, Fiber & Fatty Acid Intake for IBD

1,064

[et_pb_section bb_built=”1″][et_pb_row][et_pb_column type=”4_4″][et_pb_text]

Inflammatory bowel disease, or IBD, is a term used to describe inflammation of the gastrointestinal mucosa of unknown etiology. There are a selection of hypotheses associated to the development and perpetuation of IBD. Three main theories emerge from the literature. The first implicates a persistent intestinal infection; the second demonstrates that the upcoming signs of IBD are due to a defective mucosal barrier to luminal antigens; and the next suggests a dysregulated host immune response to ubiquitous antigens.

 

What are the nutritional components, if any, behind inflammatory bowel disease?

 

It is believed that IBD has both genetic and environmental components, therefore it’s immunologically mediated. Information gathered from IBD patients showing cytokine profiles, permeability defects, response to treatment and natural history of disease, may indicate a heterogeneous group of disorders that fall under the headings of ulcerative colitis, or UC, and Crohn’s disease, or CD. Previous epidemiological data on diet in UC and CD are conflicting, partly as a result of the heterogeneity of those diseases, making it difficult to get reliable statistics and publication bias, such as in the case of negative structures from breastfeeding.

 

Glutamine, Fiber and Fatty Acids

 

Diets high in glutamine, a significant source of energy for enterocytes, in addition to being the preferred fuel of the small intestine, are used with varying success. Glutamine is bekieved to exert its trophic effects on the small intestine by increasing protein synthesis and producing alanine for enteric gluconeogenesis. There is proof that glutamine protects the small intestinal mucosa during acute disease. However, oral glutamine supplements do not restore to normal the increased intestinal permeability discovered in patients with CD and these supplements do not beneficially affect the sufferers’ CDAI or C-reactive protein, also abbreviated as CRP, levels. Similarly, a randomized controlled trial demonstrated no benefit was connected to the usage of glutamine-enriched polymeric formulas in children with CD.

 

In animal research studies, dietary fiber has been implicated in keeping the integrity of the intestine, as well as in preventing bacterial translocation from the gut to the mesenteric lymph nodes. Short-chain fatty acids (SCFA, C1 to C6 natural fatty acids), are created by the fermentation of dietary polysaccharides in the common anaerobic bacteria in the colon. These SCFA are a source of energy for the colonocytes, which together improve sodium and water absorption, and promote blood circulation. Decreased quantities of SCFA, particularly butyrate, and a defect in the oxidation of butyrate from colonocytes, are indicated as a mechanism in the pathogenesis of inflammatory bowel disease. Evidence to support that concept requires the observation of the oxidation of C-labelled butyrate, demonstrated to decrease in patients with active UC in comparison with healthy controls. However, researchers have failed to reveal the differences between UC patients and controls in the oxidation of rectally administered C-labelled butyrate.

 

TPN supplemented with SCFA improved function adaptation to intestinal resection in rats. It remains to be discovered when patients with short bowel syndrome may make the most of SCFA.

 

Butyrate (C4 fatty acid) administered to UC patients contributed to remission levels like corticosteroids and mesalamine. In patients with CD, both intestinal biopsies and lamina propria cells packaged with butyrate had substantially decreased levels of inflammatory cytokines (TNF), possibly due to a reduction in NFκB stimulation and IκB degradation.

 

Eicosanoids are inflammatory mediators, which have also been implicated in the pathogenesis of chronic inflammatory damage in the intestine. Specimens from patients with IBD show enhanced eicosanoid formation. High dietary intake of omega-6 polyunsaturated fatty acids, abbreviated as PUFAs, which reduces omega-3 intake, and may contribute to IBD development. The benefits of fish oil, which contain n3 fatty acids, that were shown in certain inflammatory disorders, such as psoriasis and rheumatoid arthritis. Epidemiological observations of this very low prevalence of IBD in Japanese and Inuit populations consuming substantial n3 fatty acid fish provided a justification for utilizing n3 fatty acids in IBD. The n3 fatty acids are considered to compete with n6 fatty acids as precursors of eicosanoid synthesis. The n3 products reveal a series of 5 leukotrienes, which have considerably less physiological activity when compared with the arachidonate established series 4 counterparts. In addition, fish oil might have an anti inflammatory effect.

 

Rats fed with fish oil that had TNBS-induced inflammatory lesions in the intestine showed less prostaglandin- and leukotriene-mediated resistant response. Parenteral lipid emulsions enhanced with n3 fatty acids reduce diarrhea, weaken morphological changes and decreased colonic concentrations of inflammatory mediators in an animal model of acetic acid induced colitis.

 

Loeschke et al conducted a placebo-controlled trial of n3 fatty acids in preventing relapse in UC. Patients in remission who got n3 fatty acids experienced fewer relapses than did those receiving placebo. Unfortunately, the favorable results of this research study did not last throughout the total amount of the two year research, possibly due to diminished compliance punctually. In a multicenter placebo controlled relapse prevention trial, Belluzzi et al found a significant drop in the relapse rate in CD patients given an exceptional formula designed to allow postponed ileal release of n3 fatty acids. A fish oil diet has been shown to increase eicosapentanoic and docosahexanoic acids in the intestinal mucosal lipids of IBD sufferers, also demonstrating a reduction in arachadonic acid. A gain in the synthesis of leukotriene B5 along with a 53 percent decrease of leukotriene B4 was shown in UC patients, whereas the fish oil treatment revealed a nonsignificant trend to faster remission. Fish oil supplementation results in clinical improvement of active mild to moderate disease, but was not associated with a significant reduction in leukotriene B4 production. Consequently, fish oil supplementation of the diet may provide some short-term benefit to people with CD or UC. Using probiotics and prebiotics has received much attention; the interested reader is referred to recent reviews in this area.

 

Clinical Implications

 

It is widely known that nutritional deficiencies are common in people with CD and UC, and people have to be expected, diagnosed and treated. There are no special diets which may be recommended for all patients with IBD; dietary therapy needs to be individualized. TPN or TEN may be necessary to restore nutrient equilibrium in selected IBD patients with malnutrition, but in adults these interventions do not provide an essential decision to modify disease activity. The omega-3 PUFAs in fish oil may reduce disease activity in UC and CD when used at the short term together with regular medical therapy. Their mechanism of action is to enhance the activity of the amino acids PPAR, or peroxisome proliferator-activated receptors, in the intestine, inhibiting the AP-1 signaling pathway and NF-κB, weakening pro-inflammatory cytokine receptor expression. Future research will focus on the identification and use of certain dietary lipids to reduce intestinal inflammatory activity and also to maintain long-term disease remission.

 

Information referenced from the National Center for Biotechnology Information (NCBI) and the National University of Health Sciences. The scope of our information is limited to chiropractic and spinal injuries and conditions. To discuss the subject matter, please feel free to ask Dr. Jimenez or contact us at 915-850-0900 .

 

By Dr. Alex Jimenez

 

Green-Call-Now-Button-24H-150x150-2-3.png

 

Additional Topics: Wellness

 

Overall health and wellness are essential towards maintaining the proper mental and physical balance in the body. From eating a balanced nutrition as well as exercising and participating in physical activities, to sleeping a healthy amount of time on a regular basis, following the best health and wellness tips can ultimately help maintain overall well-being. Eating plenty of fruits and vegetables can go a long way towards helping people become healthy.

 

blog picture of cartoon paperboy big news

 

WELLNESS TOPIC: EXTRA EXTRA: Managing Workplace Stress

 

 

[/et_pb_text][et_pb_accordion _builder_version=”3.0.95″][et_pb_accordion_item _builder_version=”3.0.95″ title=”Blank” use_background_color_gradient=”off” background_color_gradient_start=”#2b87da” background_color_gradient_end=”#29c4a9″ background_color_gradient_type=”linear” background_color_gradient_direction=”180deg” background_color_gradient_direction_radial=”center” background_color_gradient_start_position=”0%” background_color_gradient_end_position=”100%” background_color_gradient_overlays_image=”off” parallax=”off” parallax_method=”on” background_size=”cover” background_position=”center” background_repeat=”no-repeat” background_blend=”normal” allow_player_pause=”off” custom_css_main_element=”display:none;” /][et_pb_accordion_item _builder_version=”3.0.95″ title=”References” use_background_color_gradient=”off” background_color_gradient_start=”#2b87da” background_color_gradient_end=”#29c4a9″ background_color_gradient_type=”linear” background_color_gradient_direction=”180deg” background_color_gradient_direction_radial=”center” background_color_gradient_start_position=”0%” background_color_gradient_end_position=”100%” background_color_gradient_overlays_image=”off” parallax=”off” parallax_method=”on” background_size=”cover” background_position=”center” background_repeat=”no-repeat” background_blend=”normal” allow_player_pause=”off”]

1. Liu Y, van Kruiningen HJ, West AB, Cartun RW, Cortot A, Colombel JF. Immunocytochemical evidence of Listeria, Escherichia coli, and Streptococcus antigens in Crohn’s disease. Gastroenterology. 1995;108:1396–1404. [PubMed]
2. Sartor R. Microbial factors in the pathogenesis of Crohn’s disease, ulcerative colitis and experimental intestinal inflammation. Baltimore: Williams & Wilkins; 1995.
3. Wakefield AJ, Ekbom A, Dhillon AP, Pittilo RM, Pounder RE. Crohn’s disease: pathogenesis and persistent measles virus infection. Gastroenterology. 1995;108:911–916. [PubMed]
4. Sartor RB. Current concepts of the etiology and pathogenesis of ulcerative colitis and Crohn’s disease. Gastroenterol Clin North Am. 1995;24:475–507. [PubMed]
5. Sartor RB. Pathogenesis and immune mechanisms of chronic inflammatory bowel diseases. Am J Gastroenterol. 1997;92:5S–11S. [PubMed]
6. MacDermott RP. Alterations in the mucosal immune system in ulcerative colitis and Crohn’s disease. Med Clin North Am. 1994;78:1207–1231. [PubMed]
7. Podolsky DK. Inflammatory bowel disease (1) N Engl J Med. 1991;325:928–937. [PubMed]
8. Podolsky DK. Inflammatory bowel disease (2) N Engl J Med. 1991;325:1008–1016. [PubMed]
9. Yang H, Rotter J. The genetics of inflammatory disease. Baltimore: Williams & Wilkins; 1994.
10. Wurzelmann JI, Lyles CM, Sandler RS. Childhood infections and the risk of inflammatory bowel disease. Dig Dis Sci. 1994;39:555–560. [PubMed]
11. Knoflach P, Park BH, Cunningham R, Weiser MM, Albini B. Serum antibodies to cow’s milk proteins in ulcerative colitis and Crohn’s disease. Gastroenterology. 1987;92:479–485. [PubMed]
12. De Palma GD, Catanzano C. Removable self-expanding metal stents: a pilot study for treatment of achalasia of the esophagus. Endoscopy. 1998;30:S95–S96. [PubMed]
13. Bernstein CN, Ament M, Artinian L, Ridgeway J, Shanahan F. Milk tolerance in adults with ulcerative colitis. Am J Gastroenterol. 1994;89:872–877. [PubMed]
14. Matsui T, Iida M, Fujishima M, Imai K, Yao T. Increased sugar consumption in Japanese patients with Crohn’s disease. Gastroenterol Jpn. 1990;25:271. [PubMed]
15. Kelly DG, Fleming CR. Nutritional considerations in inflammatory bowel diseases. Gastroenterol Clin North Am. 1995;24:597–611. [PubMed]
16. Geerling BJ, Dagnelie PC, Badart-Smook A, Russel MG, Stockbrügger RW, Brummer RJ. Diet as a risk factor for the development of ulcerative colitis. Am J Gastroenterol. 2000;95:1008–1013. [PubMed]
17. Dudrick SJ, Latifi R, Schrager R. Nutritional management of inflammatory bowel disease. Surg Clin North Am. 1991;71:609–623. [PubMed]
18. D’Odorico A, Bortolan S, Cardin R, D’Inca’ R, Martines D, Ferronato A, Sturniolo GC. Reduced plasma antioxidant concentrations and increased oxidative DNA damage in inflammatory bowel disease. Scand J Gastroenterol. 2001;36:1289–1294. [PubMed]
19. Reimund JM, Hirth C, Koehl C, Baumann R, Duclos B. Antioxidant and immune status in active Crohn’s disease. A possible relationship. Clin Nutr. 2000;19:43–48. [PubMed]
20. Romagnuolo J, Fedorak RN, Dias VC, Bamforth F, Teltscher M. Hyperhomocysteinemia and inflammatory bowel disease: prevalence and predictors in a cross-sectional study. Am J Gastroenterol. 2001;96:2143–2149. [PubMed]
21. Lewis JD, Fisher RL. Nutrition support in inflammatory bowel disease. Med Clin North Am. 1994;78:1443–1456. [PubMed]
22. Azcue M, Rashid M, Griffiths A, Pencharz PB. Energy expenditure and body composition in children with Crohn’s disease: effect of enteral nutrition and treatment with prednisolone. Gut. 1997;41:203–208.[PMC free article] [PubMed]
23. Mingrone G, Capristo E, Greco AV, Benedetti G, De Gaetano A, Tataranni PA, Gasbarrini G. Elevated diet-induced thermogenesis and lipid oxidation rate in Crohn disease. Am J Clin Nutr. 1999;69:325–330.[PubMed]
24. Bjarnason I, Macpherson A, Mackintosh C, Buxton-Thomas M, Forgacs I, Moniz C. Reduced bone density in patients with inflammatory bowel disease. Gut. 1997;40:228–233. [PMC free article] [PubMed]
25. Griffiths AM, Nguyen P, Smith C, MacMillan JH, Sherman PM. Growth and clinical course of children with Crohn’s disease. Gut. 1993;34:939–943. [PMC free article] [PubMed]
26. Fischer JE, Foster GS, Abel RM, Abbott WM, Ryan JA. Hyperalimentation as primary therapy for inflammatory bowel disease. Am J Surg. 1973;125:165–175. [PubMed]
27. Reilly J, Ryan JA, Strole W, Fischer JE. Hyperalimentation in inflammatory bowel disease. Am J Surg. 1976;131:192–200. [PubMed]
28. Ganem D, Schneider RJ. Hepadnaviridae: The viruses and their replication. In: Knipe DM, Howley PM, editors. Fields Virology. Volume 2. Philadelphia: Lippincott, Williams & Wilkins; 2001. pp. 2923–2969.
29. Jones VA, Dickinson RJ, Workman E, Wilson AJ, Freeman AH, Hunter JO. Crohn’s disease: maintenance of remission by diet. Lancet. 1985;2:177–180. [PubMed]
30. Suzuki I, Kiyono H, Kitamura K, Green DR, McGhee JR. Abrogation of oral tolerance by contrasuppressor T cells suggests the presence of regulatory T-cell networks in the mucosal immune system. Nature. 1986;320:451–454. [PubMed]
31. Ostro MJ, Greenberg GR, Jeejeebhoy KN. Total parenteral nutrition and complete bowel rest in the management of Crohn’s disease. JPEN J Parenter Enteral Nutr. 1985;9:280–287. [PubMed]
32. Matuchansky C. Parenteral nutrition in inflammatory bowel disease. Gut. 1986;27 Suppl 1:81–84.[PMC free article] [PubMed]
33. Payne-James JJ, Silk DB. Total parenteral nutrition as primary treatment in Crohn’s disease–RIP? Gut. 1988;29:1304–1308. [PMC free article] [PubMed]
34. Shiloni E, Coronado E, Freund HR. Role of total parenteral nutrition in the treatment of Crohn’s disease. Am J Surg. 1989;157:180–185. [PubMed]
35. Dickinson RJ, Ashton MG, Axon AT, Smith RC, Yeung CK, Hill GL. Controlled trial of intravenous hyperalimentation and total bowel rest as an adjunct to the routine therapy of acute colitis. Gastroenterology. 1980;79:1199–1204. [PubMed]
36. McIntyre PB, Powell-Tuck J, Wood SR, Lennard-Jones JE, Lerebours E, Hecketsweiler P, Galmiche JP, Colin R. Controlled trial of bowel rest in the treatment of severe acute colitis. Gut. 1986;27:481–485.[PMC free article] [PubMed]
37. Greenberg GR, Fleming CR, Jeejeebhoy KN, Rosenberg IH, Sales D, Tremaine WJ. Controlled trial of bowel rest and nutritional support in the management of Crohn’s disease. Gut. 1988;29:1309–1315.[PMC free article] [PubMed]
38. Hughes CA, Bates T, Dowling RH. Cholecystokinin and secretin prevent the intestinal mucosal hypoplasia of total parenteral nutrition in the dog. Gastroenterology. 1978;75:34–41. [PubMed]
39. Stratton RJ, Smith TR. Role of enteral and parenteral nutrition in the patient with gastrointestinal and liver disease. Best Pract Res Clin Gastroenterol. 2006;20:441–466. [PubMed]
40. O’Sullivan M, O’Morain C. Nutrition in inflammatory bowel disease. Best Pract Res Clin Gastroenterol. 2006;20:561–573. [PubMed]
41. González-Huix F, Fernández-Bañares F, Esteve-Comas M, Abad-Lacruz A, Cabré E, Acero D, Figa M, Guilera M, Humbert P, de León R. Enteral versus parenteral nutrition as adjunct therapy in acute ulcerative colitis. Am J Gastroenterol. 1993;88:227–232. [PubMed]
42. Voitk AJ, Echave V, Feller JH, Brown RA, Gurd FN. Experience with elemental diet in the treatment of inflammatory bowel disease. Is this primary therapy? Arch Surg. 1973;107:329–333. [PubMed]
43. Axelsson C, Jarnum S. Assessment of the therapeutic value of an elemental diet in chronic inflammatory bowel disease. Scand J Gastroenterol. 1977;12:89–95. [PubMed]
44. Lochs H, Steinhardt HJ, Klaus-Wentz B, Zeitz M, Vogelsang H, Sommer H, Fleig WE, Bauer P, Schirrmeister J, Malchow H. Comparison of enteral nutrition and drug treatment in active Crohn’s disease. Results of the European Cooperative Crohn’s Disease Study. IV. Gastroenterology. 1991;101:881–888.[PubMed]
45. Malchow H, Steinhardt HJ, Lorenz-Meyer H, Strohm WD, Rasmussen S, Sommer H, Jarnum S, Brandes JW, Leonhardt H, Ewe K. Feasibility and effectiveness of a defined-formula diet regimen in treating active Crohn’s disease. European Cooperative Crohn’s Disease Study III. Scand J Gastroenterol. 1990;25:235–244. [PubMed]
46. O’Brien CJ, Giaffer MH, Cann PA, Holdsworth CD. Elemental diet in steroid-dependent and steroid-refractory Crohn’s disease. Am J Gastroenterol. 1991;86:1614–1618. [PubMed]
47. Okada M, Yao T, Yamamoto T, Takenaka K, Imamura K, Maeda K, Fujita K. Controlled trial comparing an elemental diet with prednisolone in the treatment of active Crohn’s disease. Hepatogastroenterology. 1990;37:72–80. [PubMed]
48. O’Moráin C, Segal AW, Levi AJ. Elemental diet as primary treatment of acute Crohn’s disease: a controlled trial. Br Med J (Clin Res Ed) 1984;288:1859–1862. [PMC free article] [PubMed]
49. Raouf AH, Hildrey V, Daniel J, Walker RJ, Krasner N, Elias E, Rhodes JM. Enteral feeding as sole treatment for Crohn’s disease: controlled trial of whole protein v amino acid based feed and a case study of dietary challenge. Gut. 1991;32:702–707. [PMC free article] [PubMed]
50. Rocchio MA, Cha CJ, Haas KF, Randall HT. Use of chemically defined diets in the management of patients with acute inflammatory bowel disease. Am J Surg. 1974;127:469–475. [PubMed]
51. Saverymuttu S, Hodgson HJ, Chadwick VS. Controlled trial comparing prednisolone with an elemental diet plus non-absorbable antibiotics in active Crohn’s disease. Gut. 1985;26:994–998. [PMC free article][PubMed]
52. Teahon K, Bjarnason I, Pearson M, Levi AJ. Ten years’ experience with an elemental diet in the management of Crohn’s disease. Gut. 1990;31:1133–1137. [PMC free article] [PubMed]
53. Teahon K, Smethurst P, Pearson M, Levi AJ, Bjarnason I. The effect of elemental diet on intestinal permeability and inflammation in Crohn’s disease. Gastroenterology. 1991;101:84–89. [PubMed]
54. Heuschkel RB, Menache CC, Megerian JT, Baird AE. Enteral nutrition and corticosteroids in the treatment of acute Crohn’s disease in children. J Pediatr Gastroenterol Nutr. 2000;31:8–15. [PubMed]
55. Sanderson IR, Boulton P, Menzies I, Walker-Smith JA. Improvement of abnormal lactulose/rhamnose permeability in active Crohn’s disease of the small bowel by an elemental diet. Gut. 1987;28:1073–1076.[PMC free article] [PubMed]
56. Sanderson IR, Udeen S, Davies PS, Savage MO, Walker-Smith JA. Remission induced by an elemental diet in small bowel Crohn’s disease. Arch Dis Child. 1987;62:123–127. [PMC free article] [PubMed]
57. Ruemmele FM, Roy CC, Levy E, Seidman EG. Nutrition as primary therapy in pediatric Crohn’s disease: fact or fantasy? J Pediatr. 2000;136:285–291. [PubMed]
58. O’Morain C, O’Sullivan M. Nutritional support in Crohn’s disease: current status and future directions. J Gastroenterol. 1995;30 Suppl 8:102–107. [PubMed]
59. Rigaud D, Cosnes J, Le Quintrec Y, René E, Gendre JP, Mignon M. Controlled trial comparing two types of enteral nutrition in treatment of active Crohn’s disease: elemental versus polymeric diet. Gut. 1991;32:1492–1497. [PMC free article] [PubMed]
60. Royall D, Wolever TM, Jeejeebhoy KN. Evidence for colonic conservation of malabsorbed carbohydrate in short bowel syndrome. Am J Gastroenterol. 1992;87:751–756. [PubMed]
61. Giaffer MH, North G, Holdsworth CD. Controlled trial of polymeric versus elemental diet in treatment of active Crohn’s disease. Lancet. 1990;335:816–819. [PubMed]
62. Verma S, Kirkwood B, Brown S, Giaffer MH. Oral nutritional supplementation is effective in the maintenance of remission in Crohn’s disease. Dig Liver Dis. 2000;32:769–774. [PubMed]
63. Levine GM, Deren JJ, Steiger E, Zinno R. Role of oral intake in maintenance of gut mass and disaccharide activity. Gastroenterology. 1974;67:975–982. [PubMed]
64. Weser E, Heller R, Tawil T. Stimulation of mucosal growth in the rat ileum by bile and pancreatic secretions after jejunal resection. Gastroenterology. 1977;73:524–529. [PubMed]
65. Fell JM, Paintin M, Arnaud-Battandier F, Beattie RM, Hollis A, Kitching P, Donnet-Hughes A, MacDonald TT, Walker-Smith JA. Mucosal healing and a fall in mucosal pro-inflammatory cytokine mRNA induced by a specific oral polymeric diet in paediatric Crohn’s disease. Aliment Pharmacol Ther. 2000;14:281–289. [PubMed]
66. Souba WW, Smith RJ, Wilmore DW. Glutamine metabolism by the intestinal tract. JPEN J Parenter Enteral Nutr. 1985;9:608–617. [PubMed]
67. Windmueller HG, Spaeth AE. Uptake and metabolism of plasma glutamine by the small intestine. J Biol Chem. 1974;249:5070–5079. [PubMed]
68. Higashiguchi T, Hasselgren PO, Wagner K, Fischer JE. Effect of glutamine on protein synthesis in isolated intestinal epithelial cells. JPEN J Parenter Enteral Nutr. 1993;17:307–314. [PubMed]
69. Burke DJ, Alverdy JC, Aoys E, Moss GS. Glutamine-supplemented total parenteral nutrition improves gut immune function. Arch Surg. 1989;124:1396–1399. [PubMed]
70. Souba WW, Herskowitz K, Klimberg VS, Salloum RM, Plumley DA, Flynn TC, Copeland EM. The effects of sepsis and endotoxemia on gut glutamine metabolism. Ann Surg. 1990;211:543–549; discussion 543-551;. [PMC free article] [PubMed]
71. Den Hond E, Hiele M, Peeters M, Ghoos Y, Rutgeerts P. Effect of long-term oral glutamine supplements on small intestinal permeability in patients with Crohn’s disease. JPEN J Parenter Enteral Nutr. 1999;23:7–11. [PubMed]
72. Akobeng AK, Miller V, Stanton J, Elbadri AM, Thomas AG. Double-blind randomized controlled trial of glutamine-enriched polymeric diet in the treatment of active Crohn’s disease. J Pediatr Gastroenterol Nutr. 2000;30:78–84. [PubMed]
73. Jacobs LR, Lupton JR. Effect of dietary fibers on rat large bowel mucosal growth and cell proliferation. Am J Physiol. 1984;246:G378–G385. [PubMed]
74. Spaeth G, Berg RD, Specian RD, Deitch EA. Food without fiber promotes bacterial translocation from the gut. Surgery. 1990;108:240–246; discussion 246-247;. [PubMed]
75. Roediger WE, Moore A. Effect of short-chaim fatty acid on sodium absorption in isolated human colon perfused through the vascular bed. Dig Dis Sci. 1981;26:100–106. [PubMed]
76. Sakata T. Stimulatory effect of short-chain fatty acids on epithelial cell proliferation in the rat intestine: a possible explanation for trophic effects of fermentable fibre, gut microbes and luminal trophic factors. Br J Nutr. 1987;58:95–103. [PubMed]
77. Roediger WE. The colonic epithelium in ulcerative colitis: an energy-deficiency disease? Lancet. 1980;2:712–715. [PubMed]
78. Chapman MA, Grahn MF, Boyle MA, Hutton M, Rogers J, Williams NS. Butyrate oxidation is impaired in the colonic mucosa of sufferers of quiescent ulcerative colitis. Gut. 1994;35:73–76.[PMC free article] [PubMed]
79. Den Hond E, Hiele M, Evenepoel P, Peeters M, Ghoos Y, Rutgeerts P. In vivo butyrate metabolism and colonic permeability in extensive ulcerative colitis. Gastroenterology. 1998;115:584–590. [PubMed]
80. Simpson EJ, Chapman MA, Dawson J, Berry D, Macdonald IA, Cole A. In vivo measurement of colonic butyrate metabolism in patients with quiescent ulcerative colitis. Gut. 2000;46:73–77.[PMC free article] [PubMed]
81. Tappenden KA, Thomson AB, Wild GE, McBurney MI. Short-chain fatty acid-supplemented total parenteral nutrition enhances functional adaptation to intestinal resection in rats. Gastroenterology. 1997;112:792–802. [PubMed]
82. Senagore AJ, MacKeigan JM, Scheider M, Ebrom JS. Short-chain fatty acid enemas: a cost-effective alternative in the treatment of nonspecific proctosigmoiditis. Dis Colon Rectum. 1992;35:923–927.[PubMed]
83. Segain JP, Raingeard de la Blétière D, Bourreille A, Leray V, Gervois N, Rosales C, Ferrier L, Bonnet C, Blottière HM, Galmiche JP. Butyrate inhibits inflammatory responses through NFkappaB inhibition: implications for Crohn’s disease. Gut. 2000;47:397–403. [PMC free article] [PubMed]
84. Aslan A, Triadafilopoulos G. Fish oil fatty acid supplementation in active ulcerative colitis: a double-blind, placebo-controlled, crossover study. Am J Gastroenterol. 1992;87:432–437. [PubMed]
85. Shoda R, Matsueda K, Yamato S, Umeda N. Epidemiologic analysis of Crohn disease in Japan: increased dietary intake of n-6 polyunsaturated fatty acids and animal protein relates to the increased incidence of Crohn disease in Japan. Am J Clin Nutr. 1996;63:741–745. [PubMed]
86. Vilaseca J, Salas A, Guarner F, Rodríguez R, Martínez M, Malagelada JR. Dietary fish oil reduces progression of chronic inflammatory lesions in a rat model of granulomatous colitis. Gut. 1990;31:539–544. [PMC free article] [PubMed]
87. Campos FG, Waitzberg DL, Habr-Gama A, Logullo AF, Noronha IL, Jancar S, Torrinhas RS, Fürst P. Impact of parenteral n-3 fatty acids on experimental acute colitis. Br J Nutr. 2002;87 Suppl 1:S83–S88.[PubMed]
88. Loeschke K, Ueberschaer B, Pietsch A, Gruber E, Ewe K, Wiebecke B, Heldwein W, Lorenz R. n-3 fatty acids only delay early relapse of ulcerative colitis in remission. Dig Dis Sci. 1996;41:2087–2094.[PubMed]
89. Belluzzi A, Brignola C, Campieri M, Pera A, Boschi S, Miglioli M. Effect of an enteric-coated fish-oil preparation on relapses in Crohn’s disease. N Engl J Med. 1996;334:1557–1560. [PubMed]
90. Hawthorne AB, Daneshmend TK, Hawkey CJ, Belluzzi A, Everitt SJ, Holmes GK, Malkinson C, Shaheen MZ, Willars JE. Treatment of ulcerative colitis with fish oil supplementation: a prospective 12 month randomised controlled trial. Gut. 1992;33:922–928. [PMC free article] [PubMed]
91. Hillier K, Jewell R, Dorrell L, Smith CL. Incorporation of fatty acids from fish oil and olive oil into colonic mucosal lipids and effects upon eicosanoid synthesis in inflammatory bowel disease. Gut. 1991;32:1151–1155. [PMC free article] [PubMed]
92. Lehmann JM, Moore LB, Smith-Oliver TA, Wilkison WO, Willson TM, Kliewer SA. An antidiabetic thiazolidinedione is a high affinity ligand for peroxisome proliferator-activated receptor gamma (PPAR gamma) J Biol Chem. 1995;270:12953–12956. [PubMed]
93. Lehmann JM, Lenhard JM, Oliver BB, Ringold GM, Kliewer SA. Peroxisome proliferator-activated receptors alpha and gamma are activated by indomethacin and other non-steroidal anti-inflammatory drugs. J Biol Chem. 1997;272:3406–3410. [PubMed]
94. Delerive P, Furman C, Teissier E, Fruchart J, Duriez P, Staels B. Oxidized phospholipids activate PPARalpha in a phospholipase A2-dependent manner. FEBS Lett. 2000;471:34–38. [PubMed]
95. Kliewer SA, Sundseth SS, Jones SA, Brown PJ, Wisely GB, Koble CS, Devchand P, Wahli W, Willson TM, Lenhard JM, et al. Fatty acids and eicosanoids regulate gene expression through direct interactions with peroxisome proliferator-activated receptors alpha and gamma. Proc Natl Acad Sci USA. 1997;94:4318–4323. [PMC free article] [PubMed]
96. Forman BM, Chen J, Evans RM. Hypolipidemic drugs, polyunsaturated fatty acids, and eicosanoids are ligands for peroxisome proliferator-activated receptors alpha and delta. Proc Natl Acad Sci USA. 1997;94:4312–4317. [PMC free article] [PubMed]
97. Mansén A, Guardiola-Diaz H, Rafter J, Branting C, Gustafsson JA. Expression of the peroxisome proliferator-activated receptor (PPAR) in the mouse colonic mucosa. Biochem Biophys Res Commun. 1996;222:844–851. [PubMed]
98. Desreumaux P, Ernst O, Geboes K, Gambiez L, Berrebi D, Müller-Alouf H, Hafraoui S, Emilie D, Ectors N, Peuchmaur M, et al. Inflammatory alterations in mesenteric adipose tissue in Crohn’s disease. Gastroenterology. 1999;117:73–81. [PubMed]
99. Su CG, Wen X, Bailey ST, Jiang W, Rangwala SM, Keilbaugh SA, Flanigan A, Murthy S, Lazar MA, Wu GD. A novel therapy for colitis utilizing PPAR-gamma ligands to inhibit the epithelial inflammatory response. J Clin Invest. 1999;104:383–389. [PMC free article] [PubMed]
100. Ricote M, Huang J, Fajas L, Li A, Welch J, Najib J, Witztum JL, Auwerx J, Palinski W, Glass CK. Expression of the peroxisome proliferator-activated receptor gamma (PPARgamma) in human atherosclerosis and regulation in macrophages by colony stimulating factors and oxidized low density lipoprotein. Proc Natl Acad Sci USA. 1998;95:7614–7619. [PMC free article] [PubMed]
101. Staels B, Koenig W, Habib A, Merval R, Lebret M, Torra IP, Delerive P, Fadel A, Chinetti G, Fruchart JC, et al. Activation of human aortic smooth-muscle cells is inhibited by PPARalpha but not by PPARgamma activators. Nature. 1998;393:790–793. [PubMed]
102. Marx N, Bourcier T, Sukhova GK, Libby P, Plutzky J. PPARgamma activation in human endothelial cells increases plasminogen activator inhibitor type-1 expression: PPARgamma as a potential mediator in vascular disease. Arterioscler Thromb Vasc Biol. 1999;19:546–551. [PubMed]
103. Delerive P, Martin-Nizard F, Chinetti G, Trottein F, Fruchart JC, Najib J, Duriez P, Staels B. Peroxisome proliferator-activated receptor activators inhibit thrombin-induced endothelin-1 production in human vascular endothelial cells by inhibiting the activator protein-1 signaling pathway. Circ Res. 1999;85:394–402. [PubMed]
104. Sakai M, Matsushima-Hibiya Y, Nishizawa M, Nishi S. Suppression of rat glutathione transferase P expression by peroxisome proliferators: interaction between Jun and peroxisome proliferator-activated receptor alpha. Cancer Res. 1995;55:5370–5376. [PubMed]
105. Zhou YC, Waxman DJ. STAT5b down-regulates peroxisome proliferator-activated receptor alpha transcription by inhibition of ligand-independent activation function region-1 trans-activation domain. J Biol Chem. 1999;274:29874–29882. [PubMed]
106. Desreumaux P, Dubuquoy L, Nutten S, Peuchmaur M, Englaro W, Schoonjans K, Derijard B, Desvergne B, Wahli W, Chambon P, et al. Attenuation of colon inflammation through activators of the retinoid X receptor (RXR)/peroxisome proliferator-activated receptor gamma (PPARgamma) heterodimer. A basis for new therapeutic strategies. J Exp Med. 2001;193:827–838. [PMC free article] [PubMed]
107. Lewis JD, Lichtenstein GR, Stein RB, Deren JJ, Judge TA, Fogt F, Furth EE, Demissie EJ, Hurd LB, Su CG, et al. An open-label trial of the PPAR-gamma ligand rosiglitazone for active ulcerative colitis. Am J Gastroenterol. 2001;96:3323–3328. [PubMed]
108. Göttlicher M, Widmark E, Li Q, Gustafsson JA. Fatty acids activate a chimera of the clofibric acid-activated receptor and the glucocorticoid receptor. Proc Natl Acad Sci USA. 1992;89:4653–4657.[PMC free article] [PubMed]

[/et_pb_accordion_item][et_pb_accordion_item _builder_version=”3.0.95″ title=”Close Accordion” use_background_color_gradient=”off” background_color_gradient_start=”#2b87da” background_color_gradient_end=”#29c4a9″ background_color_gradient_type=”linear” background_color_gradient_direction=”180deg” background_color_gradient_direction_radial=”center” background_color_gradient_start_position=”0%” background_color_gradient_end_position=”100%” background_color_gradient_overlays_image=”off” parallax=”off” parallax_method=”on” background_size=”cover” background_position=”center” background_repeat=”no-repeat” background_blend=”normal” allow_player_pause=”off” open_toggle_background_color=”#ffffff” closed_toggle_background_color=”#ffffff” custom_css_main_element=”border:none;” custom_css_toggle_title=”font-size:0.8em;” custom_css_toggle_icon=”display:none;” /][/et_pb_accordion][/et_pb_column][/et_pb_row][/et_pb_section]

Post Disclaimer

Professional Scope of Practice *

The information herein on "Glutamine, Fiber & Fatty Acid Intake for IBD" is not intended to replace a one-on-one relationship with a qualified health care professional or licensed physician and is not medical advice. We encourage you to make healthcare decisions based on your research and partnership with a qualified healthcare professional.

Blog Information & Scope Discussions

Our information scope is limited to Chiropractic, musculoskeletal, physical medicines, wellness, contributing etiological viscerosomatic disturbances within clinical presentations, associated somatovisceral reflex clinical dynamics, subluxation complexes, sensitive health issues, and/or functional medicine articles, topics, and discussions.

We provide and present clinical collaboration with specialists from various disciplines. Each specialist is governed by their professional scope of practice and their jurisdiction of licensure. We use functional health & wellness protocols to treat and support care for the injuries or disorders of the musculoskeletal system.

Our videos, posts, topics, subjects, and insights cover clinical matters, issues, and topics that relate to and directly or indirectly support our clinical scope of practice.*

Our office has reasonably attempted to provide supportive citations and has identified the relevant research study or studies supporting our posts. We provide copies of supporting research studies available to regulatory boards and the public upon request.

We understand that we cover matters that require an additional explanation of how it may assist in a particular care plan or treatment protocol; therefore, to further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez, DC, or contact us at 915-850-0900.

We are here to help you and your family.

Blessings

Dr. Alex Jimenez DC, MSACP, RN*, CCST, IFMCP*, CIFM*, ATN*

email: coach@elpasofunctionalmedicine.com

Licensed as a Doctor of Chiropractic (DC) in Texas & New Mexico*
Texas DC License # TX5807, New Mexico DC License # NM-DC2182

Licensed as a Registered Nurse (RN*) in Florida
Florida License RN License # RN9617241 (Control No. 3558029)
License Compact Status: Multi-State License: Authorized to Practice in 40 States*
Presently Matriculated: ICHS: MSN* FNP (Family Nurse Practitioner Program)

Dr. Alex Jimenez DC, MSACP, RN* CIFM*, IFMCP*, ATN*, CCST
My Digital Business Card