Gut Microorganisms and Autism: the Latest Research

LPS and Autism

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Mitochondrial Disease and LPS

Mitochondrial disease or dysfunction is a very serious and possibly fatal condition. It is very rare among the general population but is surprisingly common among children with autism. It is estimated by different researchers that 7% or 20% of children with autism have mitochondrial disease. [4]

A very large amount of scientific studies demonstrate the fact that the bacterial toxin, LPS, damages the mitochondria. We know that children with ASD have an overload of the gram negative bacteria that contain LPS. It is therefore easy to understand why such a high percentage of children with autism have mitochondrial disease.

There are plenty of scientific articles showing that LPS, damages the mitochondria.
Click here to view these article on PubMed.

There is also evidence that LPS can cause the biochemical changes that are used as markers for mitochondrial dysfunction. One research articles suggest the following as being markers for mitochondria in children with autism: High lactate, ammonia and alanine levels with reduced values of carnitine and pyruvate. [1] Another article suggests hyperlactacidemia and increased ratios of lactate/pyruvate. We have found research articles that demonstrate that LPS can induce these conditions.[2]
Click here to view these article on PubMed.

At the American Academy of Neurology 60th Annual Meeting, investigator John Shoffner, MD, reported that many children with ASD had indicators of underlying mitochondrial disease. His findings were reported in Medscape [2] and reprinted on the Autism Speaks website. John Shoffner's analysis found defects in oxidative phosphorylation to be common among these children. He also found that a small number of them had defects in mtDNA. LPS affects both oxidative phosphorylation and mtDNA and all the other issues mentioned in the article.
Click here to view these article on PubMed.

It has been suggested that mitochondrial disease is a result of heavy metal contamination. This is not surprising since many heavy metals disable the enzymes needed for carbohydrate digestion[5] and thus bring about an overgrowth of bacteria. Unfortunately children who have both ASD and mitochondrial disease tend to have liver dysfunction. The Mitochondrial and Metabolic Disease Center at the University of California San Diego has an article on their website material about the role of nutrition in mitochondrial disease. That article states:

"Some children with lactic acidemia have demonstrated carbohydrate sensitivity. They may respond to a higher fat, lower carbohydrate and or fructose restricted diet".[3]

It is important to remember that the scientific research indicates that autistic children with mitochondria tend to have high levels of lactic acidemia.

A leading authority on mitochondrial disease has stated that there is no cure for this devastating disorder.[2] Therefore, there is an urgent need to advise parents that they should implement a diet that eliminates the bacterial toxins.

References

[1] Click here to view this article on PubMed

1: J Autism Dev Disord. 2004 Dec;34(6):615-23.
Relative carnitine deficiency in autism.
Filipek PA, Juranek J, Nguyen MT, Cummings C, Gargus JJ.

Department of Pediatrics, College of Medicine, University of California, Irvine, CA, USA. filipek@uci.edu

A random retrospective chart review was conducted to document serum carnitine levels on 100 children with autism. Concurrently drawn serum pyruvate, lactate, ammonia, and alanine levels were also available in many of these children. Values of free and total carnitine (p < 0.001), and pyruvate (p = 0.006) were significantly reduced while ammonia and alanine levels were considerably elevated (p < 0.001) in our autistic subjects. The relative carnitine deficiency in these patients, accompanied by slight elevations in lactate and significant elevations in alanine and ammonia levels, is suggestive of mild mitochondrial dysfunction. It is hypothesized that a mitochondrial defect may be the origin of the carnitine deficiency in these autistic children.

PMID: 15679182 [PubMed - indexed for MEDLINE]


[2] Click here to view this article on Medscape.com


[3]Mitochondrial and Metabolic Disorders: A Primary Care Physician's Guide. The Role of Nutrition in Mitochondrial and Metabolic Diseases, pages 15-16.
Click here to view this online.


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

1: Dev Med Child Neurol. 2005 Mar;47(3):185-9.
Mitochondrial dysfunction in autism spectrum disorders: a population-based study.
Oliveira G, Diogo L, Grazina M, Garcia P, Ataíde A, Marques C, Miguel T, Borges L, Vicente AM, Oliveira CR.

Outpatient Clinic of Autism, Centro de Desenvolvimento da Criança, Hospital Pediátrico de Coimbra, 3000-076 Coimbra, Portugal. guiomar@hpc.chc.min-saude.pt

A minority of cases of autism has been associated with several different organic conditions, including bioenergetic metabolism deficiency. In a population-based study, we screened associated medical conditions in a group of 120 children with autism (current age range 11y 5mo to 14y 4mo, mean age 12y 11mo [SD 9.6mo], male:female ratio 2.9:1). Children were diagnosed using Diagnostic and Statistical Manual of Mental Disorders criteria, the Autism Diagnostic Interview--Revised, and the Childhood Autism Rating Scale; 76% were diagnosed with typical autism and 24% with atypical autism. Cognitive functional level was assessed with the Griffiths scale and the Wechsler Intelligence Scale for Children and was in the normal range in 17%. Epilepsy was present in 19 patients. Plasma lactate levels were measured in 69 patients, and in 14 we found hyperlactacidemia. Five of 11 patients studied were classified with definite mitochondrial respiratory chain disorder, suggesting that this might be one of the most common disorders associated with autism (5 of 69; 7.2%) and warranting further investigation.

PMID: 15739723 [PubMed - indexed for MEDLINE]


[5] Click here to view this article on PubMed

1: J Appl Toxicol. 1982 Dec;2(6):275-7.

Co-enzyme effects of inorganic mercury in the liver of a freshwater fish Channa punctatus.

Rana SV, Sharma R.

Mercury is known to modify enzyme activity through oxidation of thiol groups and respective reverse reactions in vitro and in vivo. However, variations in the activity of carbohydrates, and the significance of this variation after mercury poisoning in different species, has not been established. In the present report, the effects of inorganic mercury on selected hepatic enzymes was studied in the freshwater fish Channa punctatus. Quantitative data clearly showed a dose-response relationship between the amount of mercury retained in the liver and inhibition of enzymes (i.e. alkaline phosphatase, glucose-6-phosphatase, amylase, maltase, lactase, lipase and dehydrogenases). Mechanisms and significance of their modification have also been discussed.

PMID: 7185906 [PubMed - indexed for MEDLINE]