Couple things in the works regarding proper research, but majorly - Upcoming Big One(statistically powerful, controlled.)on SCD: https://www.pcori.org/research-results/2016/comparative-effectiveness-specific-carbohydrate-and-mediterranean-diets-induce - This will be an effective statistical proof of the degree of effect of diet.
here is a synthesis of my current understanding:
Due to the insignificance of macronutrient ratio changes or the polymerization of proteins on the effectiveness of elemental/semi-elemental enteric nutrition(all of which require that carbohydrates be supplied as monosaccharides, in the form of glucose, while allowing the total macro percentages of fats/proteins/chain proteins/ carbs to vary), the overlap in effects on markers for crohn’s patients on either EEN or SCD, and the SCD diet's take on carbohydrates(most of which are required to be supplied as monosaccharides, in the form of glucose or fructose) it appears that the usage of monosaccharides becomes a unifying cause of the marker changes across studies. Interpreted in light of the microbiome and NOD2 functionality, it seems that the simplest explanation is that fermentative bacteria are quantitatively linked to inflammation.
Crohn’s SCD studies: 1. Clinical, Specific Carbohydrate Diet: Nutritional Therapy in Pediatric Crohn Disease: The Specific Carbohydrate Diet Suskind, David L https://www.ncbi.nlm.nih.gov/pubmed/24048168
Specific carbohydrate diet for pediatric inflammatory bowel disease in clinical practice within an academic IBD center, Obih C. https://www.ncbi.nlm.nih.gov/pubmed/26655069
Response to strict and liberalized specific carbohydrate diet in pediatric Crohn’s disease Burgis JC. https://www.ncbi.nlm.nih.gov/pubmed/26877615
The Specific Carbohydrate Diet for Inflammatory Bowel Disease: A Case Series
Kadokhar, Samir public: https://www.ncbi.nlm.nih.gov/pubmed/26210084
Supportive of SCD/ EEN overlap :
Exclusive enteral feeding as primary therapy for Crohn's disease in Australian children and adolescents: a feasible and effective approach. Day AS1 https://www.ncbi.nlm.nih.gov/pubmed/16928225
Sustained modulation of intestinal bacteria by exclusive enteral nutrition used to treat children with Crohn's disease. Leach ST1
5b. Exclusive enteral nutrition in children with Crohn’s disease
Microbiome Associations of Therapeutic Enteral Nutrition Rajesh Shah1
Dysfunction of the intestinal microbiome in inflammatory bowel disease and treatment Xochitl C Morgan
Diet to the Rescue: Cessation of Pharmacotherapy After Initiation of Exclusive Enteral Nutrition (EEN) Followed by Strict and Liberalized Specific Carbohydrate Diet (SCD) in Crohn's Disease. Nakayuenyongsuk W1
Enteral nutritional therapy for induction of remission in Crohn's disease Mary Zakos
Genetics: 11. The contribution of NOD2 gene mutations to the risk and site of disease in inflammatory bowel disease Cuthbert AP http://www.gastrojournal.org/article/S0016-5085(02)05677-9/fulltext
Mechanism of crohn's: recognition of cell wall markers in bacteria by our cell's receptors-> t-cells and nf-kb activation. Leaky gut allows these bacterial cells into the body, thereby inducing this response not locally but systemically and chaotically. This is a gross simplification. The upshot of NOD2 studies are that if you've got crohn's, there is a broken recognition protein in the intestinal immune system. This most likely acts by conferring inability of the immune system to recognize either harmful microbiota, or cytokines(inflammatory agents).
From https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4447044/: (note: MDP = muramyl dipeptide; present in bacterial cell walls, bound by NOD2 protein. PRR = pattern recognition protein (as immune system detector))
One major theory of how defective NOD2 leads to CD: normally, NOD2 senses MDP activating a number of innate immune responses and bacterial killing; defective NOD2 leads to defects in these pathways, resulting in persistence of intracellular bacteria and effects on antimicrobial functions in the lumen. Another major theory on NOD2: activation via MDP leads to modulating effects on the innate immune system, including suppression of cytokine effects (for example, IL-23-driven Th17 responses), suppression of other PRRs (for example, TLR-2 and TLR-4 responses), and induction of tolerance.
Current Situation: I have been getting less and less response from remicade over the past 6 months (been on it for nearly 6 years). I experienced a return of bouts of severe constipation about
a year or two ago, and wrist/hip/lower back pain a few months ago. I started getting the rib, upper back and groin pain I associate with crohn's bleeding - intense, like fishhooks in the lower bounds of my rib cage - around three months ago.
So, remicade was shot for me - due to time, as far as I know and can share. It was the only variable. I had a bad flare, and couldn't wake up fully or be comfortably pain-free. I was prescribed a big dose of prednisone; I took it. My flare went away the next day. When I hit about
half-dose in the taper, my flare came back. I got prescribed more steroids. I'm at a point in my life where I can experiment a bit, so I tried the SCD after reading about
the mechanism of action of crohn's.(investigate the role of NOD2, the gene, in maintaining the intestines against bacteria.)
A study showed that over 6 weeks, the SCD diet resolved crohn's flare into remission as effectively as prednisone treatment. So, I did the diet. Google enough, read the 3-4 clinical studies on the diet in crohn's. Worth it, to know the theory and evidence.
I'm a month into the diet, and two weeks overdue for my remicade (that I was mostly immune to.). I've had total resolution of symptoms. I have reacted to a few things the diet lists as ok, (peanut butter, coconut flour), but mostly I believe it is a good starting point.
I recommend taking Stage I and Stage II, and ignoring the baked meat and oils thing and feeling free to fry meats up at the start (because these factors didn't break it for me; success!).
Additional notes: I'm highly stressed right now (job search post-ungergraduation). I have managed both heavy drinking and smoking cigarettes while on the SCD, neither followed by a bad flare (both of these in the past 6 years in any amount have always caused intense, two-four day constipation to me. Have caused ER trips.). The implication is that instead of this formula: (red meat, cigs, drinking, stress -> crohns flares ) the real formula is this: (colon transit time of disacharrides and complex carbs goes up -> crohns flares). Working out(and carboloading afterwards) has in the past triggered flares for me - I can successfully do this on SCD, no problem.
Post Edited (wibblypig) : 7/28/2017 6:30:38 AM (GMT-6)