Gut Microorganisms and Autism: the Latest Research

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Ammonia, Bacterias and LPS

Children with autism have a higher rate of ammonia levels than typical children. We also know that children with autism have the tendency to crave carbohydrates so we cannot blame this difference on a higher meat consumption.

Sophie Rousseneau had discovered that children with autism have a very high rate of gram negative bacteria in their bodies. Scientists have found connections between gram negative bacteria and high ammonia levels. O'Grady found that the bacterias that are producing the ammonia in the human gut are mostly the gram negative ones.[1] He also reported that foods that contain good probiotics decrease the amount of gram negative pathogens. O'Grady mentioned cheese and milk as examples of foods that contain beneficial probiotics.[1]

Furthermore, it was discovered that LPS, the poison found on gram negative bacteria, impairs hepatic ammonia detoxification. [2] This results in the following situation: the high number of gram negative bacteria inside ASD children produce an excessive amount of ammonia and their bacterial poison impairs the liver's ability to detoxify the ammonia.


[1] Click here to view this article on PubMed Central.

(The article begins on right side of the web page)

[2] Click here to view this article on PubMed.

1: Hepatology. 2005 May;41(5):1065-73.

Comment in: Hepatology. 2005 May;41(5):980-2.

Lipopolysaccharide-induced tyrosine nitration and inactivation of hepatic glutamine synthetase in the rat.
Görg B, Wettstein M, Metzger S, Schliess F, Häussinger D.

Clinic for Gastroenterology, Hepatology, and Infectiology, Heinrich-Heine-University, Düsseldorf, Germany.

Glutamine synthetase (GS) in the liver is restricted to a small perivenous hepatocyte population and plays an important role in the scavenging of ammonia that has escaped the periportal urea-synthesizing compartment. We examined the effect of a single intraperitoneal injection of lipopolysaccharide (LPS) in vivo on glutamine synthesis in rat liver. LPS injection induced expression of inducible nitric oxide synthase, which was maximal after 6 to 12 hours but returned toward control levels within 24 hours. Twenty-four hours after LPS injection, an approximately fivefold increase in tyrosine-nitrated proteins in liver was found, and GS protein expression was decreased by approximately 20%, whereas GS activity was lowered by 40% to 50%. GS was found to be tyrosine-nitrated in response to LPS, and immunodepletion of tyrosine-nitrated proteins decreased GS protein by approximately 50% but had no effect on GS activity. Together with the finding via mass spectrometry that peroxynitrite-induced inactivation of purified GS is associated with nitration of the active site tyrosine residue, our data suggest that tyrosine nitration critically contributes to inactivation of the enzyme. In line with GS inactivation, glutamine synthesis from ammonia (0.3 mmol/L) in perfused livers from 24-hour LPS-treated rats was decreased by approximately 50%, whereas urea synthesis was not significantly affected. In conclusion, LPS impairs hepatic ammonia detoxification by both downregulation of GS and its inactivation because of tyrosine nitration. The resulting defect of perivenous scavenger cell function with regard to ammonia elimination may contribute to sepsis-induced development of hyperammonemia in patients who have cirrhosis.

PMID: 15830392 [PubMed - indexed for MEDLINE]