This post is really a reference guide that includes an outline and framework for thinking about Crohn’s strategies in a differnent way, along with links to a series of studies that go into depth about each area. This is a good place to start research, and a good resource to share with your doctor.
“Nothing in biology (nutrition or medicine) makes sense except in the light of evolution”. Dr. Loren Cordain
Intestinal Barrier Function & Leaky Gut:
These studies provide the framework for all the rest. Essentially all modern diseases of inflammation can be linked to a series of mismatches between our genes and environmental factors. The origin of this inflammation starts in the gut with a breakdown in intestinal barrier function.
- The Western diet and lifestyle and diseases of civilization: Cordain, Research Reports in Clinical Cardiology: 2011 March
- Mechanisms of disease: the role of intestinal barrier function in the pathogenesis of gastrointestinal autoimmune diseases. Fasano Nat Clin Pract Gastroenterol Hepatol. 2005 Sep
Zonulin and Its Regulation of Intestinal Barrier Function: The Biological Door to Inflammation, Autoimmunity, and Cancer Alessio Fasano Physiol Rev 2011 Jan
- Leaky Gut and Autoimmune Diseases Fasano Clinic Rev Allerg Immunol 2011 Nov.
Below is a simple chart that list the stressors/environmental factors that either increase intestinal permeability directly or damage the balance of the gut flora, all leading to inflammation.
Increasing Intestestinal Permeability
Low Vitamin D
Omega 6 Fats
Below is a simple chart that list the environmental factors that either decrease intestinal permeability directly or improve the balance of the gut flora, all leading to reduced inflammation and healing.
Improving Intestestinal Permeability
Probiotics & Fermented Food
Mutaflor, VSL#3, Lactobacillus paracasei
Boswellia — 5Loxin
S. Boulardii, B. Coagulans
D3 & K2
Sleep, Meditation/Yoga, Acupuncture
IF & HIIT = Growth Hormone
- SCD — Pilot Testing a Novel Treatment for Inflammatory Bowel Disease Clinical and Translational Science Research Retreat. 2011 May.
- Does gluten cause gastrointestinal symptoms in subjects without coeliac disease? J Gastroenterol Hepatol. 2011 Apr
- Dietary Lectins as Disease Causing Toxicants Pakistan Journal of Nutrition 2009
- Evidence-based dietary management of functional gastrointestinal symptoms: The FODMAP approach. J Gastroenterol Hepatol. 2010 Feb
- Dietary fructooligosaccharides increase intestinal permeability in rats. J Nutr. 2005
- Indigestible disaccharides open tight junctions. Dig Dis Sci. 2004 Jan
- GAPS – www.gaps.me, SCD – www.scdlifestyle.com Paleo – www.robbwolf.com
- Linoleic Acid, a Dietary N-6 Polyunsaturated Fatty Acid, and the Aetiology of Ulcerative Colitis – A European Prospective Cohort Study. Gut 2009 July
- The Type of Dietary Fat Modulates Intestinal Tight Junction Integrity, Gut Permeability, and Hepatic Toll-Like Receptor Expression. Alcohol Clin Exp Res. 2011
- Conjugated linoleic acid modulates immune responses in patients with Mild to Moderately active Crohn’s disease. Clinical Nutrition 2012 March.
- Lipid based therapy for ulcerative colitis-modulation of intestinal mucus membrane phospholipids as a tool to influence inflammation. Int J Mol Sci. 2010 Oct
- Butyrate enhances the intestinal barrier by facilitating tight junction assembly via activation of AMP-activated protein kinase in Caco-2 cell monolayers. J Nutr. 2009
Microbiota & Probiotics:
- Gut Microbiota and Pediatric Disease Dig Dis 2011
- Association between the use of antibiotics and new diagnoses of Crohn’s disease and ulcerative colitis. Am J Gastroenterol. 2011 Dec
- Association of Repeated Exposure to Antibiotics With the Development of Pediatric Crohn’s Disease–A Nationwide, Register-based Finnish Case-Control Study. Am J Epidemiol. 2012 Apr
- Influence of Saccharomyces boulardii (Florastor) on the intestinal permeability of patients with Crohn’s disease in remission. Scand J Gastroenterol. 2008
- Anti-inflammatory effects of Saccharomyces boulardii mediated by myeloid dendritic cells from patients with Crohn’s disease and ulcerative colitis. Am J Physiol Gastrointest Liver Physiol. 2011 Dec
- The probiotic Escherichia coli Nissle 1917 (Mutaflor) reduces pathogen invasion and modulates cytokine expression in Caco-2 cells infected with Crohn’s disease-associated E. coli LF82. Trop Med Int Health. 2011 May
- Probiotic Bacteria Produce Conjugated Linoleic Acid Locally in the Gut That Targets Macrophage PPAR γ to Suppress Colitis. PLoS One. 2012
- Lactocepin Secreted By Lactobacillus Exerts Anti-Inflammatory Effects By Selectively Degrading Proinflammatory Chemokines Cell Host & Microbe 2012 April
- Helminthic therapy: improving mucosal barrier function. Trends Parasitol. 2012 Mar
- Vitamin D and gastrointestinal diseases: inflammatory bowel disease and colorectal cancer.Therap Adv Gastroenterol. 2011 Jan
|Target Vitamin D Levels 25(OH)D – 10,000 iu/day|
|Dr. Jaquelyn McCandless||65 – 90|
|Robb Wolf||60 – 80|
|www.VitaminDCouncil.org||50 – 80|
|www.GrassRootsHealth.net||40 – 60|
|Vitamin D IBD Study||30 – 60|
- Curcumin Ameliorates Hydrogen Peroxide-Induced Epithelial Barrier Disruption. Dig Dis Sci. 2012 March.
- Therapy of active Crohn disease with Boswellia. Z Gastroenterol. 2001 Jan
- Dietary supplementation of krill oil attenuates inflammation and oxidative stress in experimental ulcerative colitis. Scand J Gastroenterol. 2012 Jan
- Glutamine and Whey Protein Improve Intestinal Permeability and Morphology in Patients with Crohn’s Disease: A Randomized Controlled Trial. Dig Dis Sci. 2011 Oct
- Combined Glutamine and Arginine Decrease Proinflammatory Cytokine Production by Biopsies from Crohn’s Patients J Nutrition 2008
- Zinc supplementation tightens “leaky gut” in Crohn’s. Inflamm Bowel Dis. 2001 May
- Intestinal immune system influenced by cocoa-enriched diet. J Nutr Biochem. 2008 Aug
- Therapy with the opioid antagonist naltrexone promotes mucosal healing in active Crohn’s disease: a randomized placebo-controlled trial. Dig Dis Sci. Smith & Zagon 2011 Jul
- Rifaximin-extended intestinal release induces remission in patients with moderately active Crohn’s disease. Gastroenterology. 2012 May
- Cannabinoid-induced apoptosis in immune cells as a pathway to immunosuppression. Immunobiology. 2010 Aug
- Cannabinoids mediate opposing effects on inflammation-induced intestinal permeability British Journal of Pharmacology 2011
- Linaclotide in the management of gastrointestinal tract disorders. Drugs Today (Barc). 2012 Mar
- 5-aminosalicylate is not chemoprophylactic for colorectal cancer in IBD: a population based study. Am J Gastroenterol. 2011 Apr
- Efficacy of 5-aminosalicylates in Crohn’s disease: systematic review and meta-analysis. Am J Gastroenterol. 2011 Apr
In an article on their website entitled Opioid boost may ease Crohn’s symptoms, the CCFC gives Low Dose Naltrexone (LDN) a positive review. Of course they are cautious and don’t really endorse LDN, but this is at least a step in the right direction.
Dr. Keith Sharkey – the Crohn’s and Colitis Foundation of Canada Chair in IBD Research – believes it is worthwhile for patients interested in LDN to consider and discuss this treatment option with their doctors. “Talk to your doctor and ask whether it’s safe and appropriate for you,” he said. And he goes on to suggest that “further clinical trials are absolutely warranted and low-dose naltrexone has to be tested in a multi-centre study.”
LDN acts as a powerful anti-inflammatory and we’ve seen direct results of improved ESR and CRP with LDN. The clinical trial showed that it improved symptoms for 88% of those in the study, but 33% saw complete remission with endoscopic confirmation of mucosal healing within 12 weeks. All with no dietary changes.
It is important to note that the CCFC may never have paid any attention to LDN if it were not for the tireless efforts of Sara Craig who manages a support page on Facebook. Sara made the effort to collect LDN success stories from people like me and she presented them to the CCFC at a conference in October of 2011. It appears that her efforts were fruitful as she got Dr. Sharkey to do some research.
Since Naltrexone is an FDA approved drug, LDN can be prescribed “off-label” by your doctor right now, there is no reason to wait to begin using LDN. You can learn more about LDN, and find doctors that will prescribe it at http://www.ldnscience.org and http://www.lowdosenaltrexone.org If you are set on working with your current doctor, you could bring them the published results from the small clinical trial that was done at Penn State by Dr. Jill Smith. In fact, Dr. Smith will consult with your doctor if they call her office – 800-243-1455.
If your doctor still won’t cooperate, you can email Crystal Nason – email@example.com with where you live, and she will give you a list of LDN prescribing doctors. Of course, you can always get Naltrexone yourself without a prescription via a number of online pharmacies – http://www.alldaychemist.com & http://www.unitedpharmacies.com have the cheapest prices. You can get a years supply of LDN for about $100.
LDN is not a magic cure for Crohn’s but combined with other safe strategies it can make a huge difference. LDN, along with the SCD, GAPS or Paleo diet should be the first line of treatment. Maybe with exposure like this we’ll see some progress.
Alessio Fasano continues to lead the charge with the latest research on the connection between “leaky-gut” and all autoimmune diseases. It won’t be easy to create what really is a “Paradigm Shift” in the medical world but this is the kind of serious science we need to get there. What Fasano does here is take the next step in not only showing how leaky gut is behind these diseases, but that it is possible to heal from these diseases by repairing leaky gut.
Chris Kresser in his latest article & podcast – Can Autoimmune Disease Be Prevented And Reversed? http://chriskresser.com/rhr-can-autoimmune-disease-be-prevented-and-reversed discusses Fasano’s article. Worth listening to!
Mucosal Biology Research Center, University of Maryland School of Medicine, 20 Penn Street HSF II Building, Room S345, Baltimore, MD, 21201, USA, firstname.lastname@example.org.
Autoimmune diseases are characterized by tissue damage and loss of function due to an immune response that is directed against specific organs. This review is focused on the role of impaired intestinal barrier function on autoimmune pathogenesis. Together with the gut-associated lymphoid tissue and the neuroendocrine network, the intestinal epithelial barrier, with its intercellular tight junctions, controls the equilibrium between tolerance and immunity to non-self antigens. Zonulin is the only physiologic modulator of intercellular tight junctions described so far that is involved in trafficking of macromolecules and, therefore, in tolerance/immune response balance. When the zonulin pathway is deregulated in genetically susceptible individuals, autoimmune disorders can occur. This new paradigm subverts traditional theories underlying the development of these diseases and suggests that these processes can be arrested if the interplay between genes and environmental triggers is prevented by re-establishing the zonulin-dependent intestinal barrier function. Both animal models and recent clinical evidence support this new paradigm and provide the rationale for innovative approaches to prevent and treat autoimmune diseases.