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ARPatACHRI
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08 Jul 2013, 9:39 am

Mitochondrial dysfunction is becoming recognized as one of the most common metabolic abnormalities associated with autism spectrum disorder (ASD). Recent studies have also implicated oxidative stress and redox abnormalities as associated with ASD. Despite the fact that the mitochondria is both the source and target of reactive oxygen species resulting from abnormal redox metabolism, the connection between mitochondrial dysfunction and abnormal redox metabolism has not been investigated until now. A group of researchers led by Dr. Richard Frye, Director of the Autism Research Program at Arkansas Children’s Hospital Research Institute, examined redox abnormalities in two sub groups of children with ASD, those with mitochondrial disease (MD) and those without any biological markers or symptoms of MD. Results showed that both ASD groups manifested abnormal redox and immune metabolism, but in different ways. The research also demonstrated differences between the two groups in clinical and developmental characteristics -- those with MD had reduced scores in communication and daily living skills. Interestingly, redox metabolism was relative to developmental characteristics of the ASD group with MD but not the ASD group without MD. These findings suggest that different subgroups of children with ASD have different redox abnormalities, which may arise from different sources. The findings also suggest it is important to identify children with ASD and MD as they may respond differently to specific treatments because of their specific metabolic profile.

The article can be found by searching for the author (Frye) and the article title (Redox metabolism abnormalities in autistic children associated with mitochondrial disease). Please let me know if you cannot find it and I will message you the link to public article (I am not able to post the link here.)



Fnord
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08 Jul 2013, 9:46 am

I have an Autism Spectrum Disorder, and no mitochondrial dysfunction.

You can type out the link.



ARPatACHRI
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08 Jul 2013, 10:11 am

Unfortunately I have not yet posted 5 items yet and so am not able to include links in my posts (This is a measure the site uses to prevent spam). I have tried posting the link again and am still not allowed to do so.



Anomiel
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08 Jul 2013, 10:17 am

Very fascinating. Here's the link http://www.ncbi.nlm.nih.gov/pubmed/23778583

Here's a little information on mitochondria, to put this into perspective.

http://encyclopedia2.thefreedictionary.com/Mitochondria wrote:
Mammalian mtDNAs accumulate mutations at high rates and evolve correspondingly fast (up to 12–15 times faster than single-copy genes in nuclear DNA and up to 100 times faster for rRNA and tRNA genes). This behavior reflects both a high incidence of mutations and a high probability of their fixation. The first is probably related to oxidative damage to mtDNA by oxygen free radicals produced as by-products of electron transfer through the respiratory chain. The second has been attributed to the lack of efficient DNA repair (mitochondria lack nucleotide-excision repair) and to a relatively high tolerance of many mitochondrial gene products to mutational change.

The rapid rate of sequence evolution of mammalian mtDNAs makes these genomes highly sensitive indicators of recent evolutionary relationships. Unlike their nuclear counterparts, mtDNAs do not undergo recombination during sexual transmission and are strictly maternally inherited. Sequence changes in mtDNA therefore provide a clear record of the history of the female lineages through which this DNA has been transmitted.



Anomiel
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08 Jul 2013, 10:33 am

Fnord wrote:
I have an Autism Spectrum Disorder, and no mitochondrial dysfunction.

You can type out the link.


They tested 2 groups, autistics with mitochondrial disease and those without. This study found that if you have autism, you probably have redox abnormalities. http://www.hindawi.com/journals/bcri/2012/896751/

http://www.ncbi.nlm.nih.gov/pubmed/23778583 wrote:
Plasma markers of oxidative stress and measures of cognitive and language development and ASD behavior were obtained from 18 children diagnosed with ASD who met criteria for probable or definite MD per the Morava et al. criteria (ASD/MD) and 18 age and gender-matched ASD children without any biological markers or symptoms of MD (ASD/NoMD).'
[...]
Children with ASD/MD demonstrated significantly higher levels of fGSH/GSSG and lower levels of GSSG as compared with children with ASD/NoMD, suggesting an overall more favourable glutathione redox status in the ASD/MD group. However, compare with controls, both ASD groups demonstrated lower fGSH and fGSH/GSSG, demonstrating that both groups suffer from redox abnormalities.
[...]
Overall, our findings suggest that ASD/MD children with a more chronic oxidized microenvironment have better development. We interpret this finding in light of the fact that more active mitochondrial can create a greater oxidized microenvironment especially when dysfunctional. Thus, compensatory upregulation of mitochondria which are dysfunctional may both increase activity and function at the expense of a more oxidized microenvironment.



OddDuckNash99
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08 Jul 2013, 2:53 pm

I think with ASDs in particular it's going to be hard to fully believe in a mitochondrial factor. ASDs are more prevalent in males, meaning that there should be more fathers than mothers affected, and the mitochondrial genome is only passed on by the mother. This caveat makes mitochondrial involvement in neuropsychiatric disorders rather puzzling genetically.


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Anomiel
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08 Jul 2013, 3:19 pm

"Belief" is not a factor in research. Unless the mothers have the mutations too they are de novo mutations, meaning they arose in the affected person. Autistics have genomic instability, meaning we are very prone to mutations. There is absolutely nothing to "believe".



Mara_Jade
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13 Jul 2013, 6:28 pm

Anomiel wrote:
"Belief" is not a factor in research. Unless the mothers have the mutations too they are de novo mutations, meaning they arose in the affected person. Autistics have genomic instability, meaning we are very prone to mutations. There is absolutely nothing to "believe".


I agree. Our daughter with Autism also has a dx of clinical mitochondrial disease. She does not have the inherited mtDNA form but rather hers happened spontaneously or due to disease processes.



Maxwel
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13 Dec 2013, 11:03 pm

Dr. Richard Kellys research along with a Dr. Suzanne Goh are saying

L Carnatine, Vitamin E, Vitamin C, Vitamin CoQ10, in the right balance can within 3 to 6 months can rebalance the biochemistry for proper mitochondrial function in people within the Autism umbrella.

I'm using mitospectra for my 18 year old son and I'm seeing excellent early indications that this making a difference. As a parent this is one of my favorite protocols because its so easy to implement.

I used a limited time holiday discount code SPECTRUM20 when ordering.

I don't understand all the science but I do know I am using some of these ingredients in my work out powders that I take before during and after the gym.

Not that I am having my son take this integrated vitamin for building muscle but he is gaining muscle mass density and he is of a slight build so its not terrible side effect.

I see early signs of improved capabilities and eye contact too.

I know I need to do at least 3 to 6 months to see the best results.

.I'm so excited about results I'm seeing so far I'm doing that I'm googling mitochondrial discussion forums to learn more.

Thanks guys!