Elaine Gottschall's Comments on the Jyonouchi Paper
(Elaine Gottschall had read the comments by Mark Blaxhill concerning the Jyonouchi Paper and included them in her explanation.)

The abstract of Jyonouchi's paper says that children with autism spectrum disorder (ASD) frequently reveal various gastrointestinal (GI) symptoms that may resolve with an elimination diet along with apparent improvement of some of the behavorial symptoms. Evidence suggests that ASD may be accompanied by aberrant (inflammatory) innate immune responses. THIS MAY PREDISPOSE ASD CHILDREN TO SENSITIVIES TO COMMON DIETARY PROTEINS LEADING TO GI INFLAMMATION AND AGGRAVATION OF SOME BEHAVIORAL SYMPTOMS."

The authors demonstrate conclusively that there is an abnormal immune response to cow's milk protein and wheat protein (gliadin) and soy in ASD. What is interesting is that the diet model is NOT THE SAME AS THE OPIOID MODEL BUT IS BASED ON A VARIABLE IMMUNE RESPONSE IN WHICH NOT EVERY CHILD WILL SHOW SENSITIVITY TO EVERY FOOD. But the punch line is: The authors suggest that the root cause of the food protein sensitivity may be an underlying sensitivity to endotoxin or lipopolysaccharides (LPS) which comes from the surfaces of gram negative bacteria in the gut.

Summary: This response to the bacterial endotoxin (LPS) PREDISPOSES THESE CHILDREN TO SENSITIZATION TO DIETARY PROTEINS. This is consistent with a model of abnormal gut flora development that promotes immune response to gut bacteria. This means that ASD kids may develop a kind of autoimmunie response to their own gut flora.

The Jyonouchi Paper

*Neuropsychobiology. 2002;46(2):76-84)

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve&db=PubMed&list_uids=12378124&dopt=Abstract

Innate immunity associated with inflammatory responses and cytokine production against common dietary proteins in patients with autism spectrum disorder.

Jyonouchi H, Sun S, Itokazu N.
Department of Pediatrics, University of Minnesota, Minneapolis, Minn, USA.

OBJECTIVES: Children with autism spectrum disorder (ASD) frequently reveal various gastrointestinal (GI) symptoms that may resolve with an elimination diet along with apparent improvement of some of the behavioral symptoms. Evidence suggests that ASD may be accompanied by aberrant (inflammatory) innate immune responses. This may predispose ASD children to sensitization to common dietary proteins (DP), leading to GI inflammation and aggravation of some behavioral symptoms.

METHODS: We measured IFN-gamma, IL-5, and TNF-alpha production against representative DPs [gliadin, cow's milk protein (CMP), and soy] by peripheral blood mononuclear cells (PBMCs) from ASD and control children [those with DP intolerance (DPI), ASD siblings, and healthy unrelated children]. We evaluated the results in association with proinflammatory and counter-regulatory cytokine production with endotoxin (LPS), a microbial product of intestinal flora and a surrogate stimulant for innate immune responses. RESULTS: ASD PBMCs produced elevated IFN-gamma and TNF-alpha, but not IL-5 with common DPs at high frequency as observed in DPI PBMCs.

ASD PBMCs revealed increased proinflammatory cytokine responses with LPS at high frequency with positive correlation between proinflammatory cytokine production with LPS and IFN-gamma and TNF-alpha production against DPs. Such correlation was less evident in DPI PBMCs. CONCLUSION: Immune reactivity to DPs may be associated with apparent DPI and GI inflammation in ASD children that may be partly associated with aberrant innate immune response against endotoxin, a product of the gut bacteria. Copyright 2002 S. Karger AG, Basel

PMID: 12378124 [PubMed - indexed for MEDLINE]

Research Paper that Shows that Malabsorbed Starch Increases the Concentrations of Starch-Fermenting Bacteria

The research article below proves that Acarbose, a starch inhibitor changes the type content of bacteria in the gut. This experiments reveals that having unabsorbed carbs in our children's guts increases the concentrations of starch-fermenting bacteria. Starch fermenting bacteria are gram-negative bacteria and contain lipolysaccharide, a bacterial TOXIN.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=retrieve&db=pubmed&list_uids=9164992&dopt=Abstract

J Nutr. 1997 May;127(5):717-23.

Acarbose enhances human colonic butyrate production.
Weaver GA, Tangel CT, Krause JA, Parfitt MM, Jenkins PL, Rader JM, Lewis BA, Miller TL, Wolin MJ.
Department of Medicine, The Mary Imogene Bassett Hospital, Cooperstown, NY 13326, USA.

Earlier studies suggest that butyrate has colonic differentiating and nutritional effects and that acarbose increases butyrate production. To determine the effects of acarbose on colonic fermentation, subjects were given 50-200 mg acarbose or placebo (cornstarch), three times per day, with meals in a double-blind crossover study. Fecal concentrations of starch and starch-fermenting bacteria were measured and fecal fermentation products determined after incubation of fecal suspensions with and without added substrate for 6 and 24 h. Substrate additions were cornstarch, cornstarch plus acarbose and potato starch. Dietary starch consumption was similar during acarbose and placebo treatment periods, but fecal starch concentrations were found to be significantly greater with acarbose treatment.

Ratios of starch-fermenting to total anaerobic bacteria were also significantly greater with acarbose treatment. Butyrate in feces, measured either as concentration or as percentage of total short-chain fatty acids, was significantly greater with acarbose treatment than with placebo treatment. Butyrate ranged from 22.3 to 27.5 mol/100 mol for the 50-200 mg, three times per day doses of acarbose compared with 18.3-19.3 mol/100 mol for the comparable placebo periods. The propionate in fecal total short-chain fatty acids was significantly less with acarbose treatment (10.7-12.1 mol/100 mol) than with placebo treatment (13.7-14.2 mol/100 mol). Butyrate production was significantly greater in fermentations in samples collected during acarbose treatment, whereas production of acetate and propionate was significantly less. Fermentation decreased when acarbose was added directly to cornstarch fermentations. Acarbose effectively augmented colonic butyrate production by several mechanisms; it reduced starch absorption, expanded concentrations of starch-fermenting and butyrate-producing bacteria and inhibited starch use by acetate- and propionate-producing bacteria.

PMID: 9164992 [PubMed - indexed for MEDLINE]

Full article:

http://jn.nutrition.org/cgi/content/full/127/5/717? ijkey=58e2782750a9cf2edbfd225e0db1e2139da53ea9

Gram Negative Bacteria and Starch Fermenting Bacteria are the Same Type of Bacteria

Proof that Gram negative bacteria and starch fermenting bacteria are the same can be found in the second paragraph of the article below:

http://www.puyallup.wsu.edu/dairy/shortcourse/readArticle.asp? intArticleID=86&intSCID=11

"Gram negative bacteria (starch fermenting bacteria) are more resistant to the action of Rumensin than the gram positive bacteria (fiber fermenting bacteria)."

The use of parenthesis indicates that Gram negative bacteria and starch fermenting bacteria are the same.