Re: Mitochondrial Dysfunction in Autism

[Guest guest]

All competent physicians know or can easily look up that heavy metal poisoning

has a lot of its effect through impairing mitochondrial function.

Thus of course when doctors study babies they poisoned it is easy to pretend to

find out they have mitochondrial dysfunction - they really do - but the root

cause is being poisoned by quacks. It isn't genetic. It's iatrogenic.

People who want their mitochondrially impaired autistic child to get better can

chelate them, people who want to keep them sick can give them 'mitochondrial

rescussitation cocktails.'

BTW, mercury and especially arsenic are known to elevate pyruvate levels through

blocking the transport protein that moves it into mitochondria, and the protein

that helps get it into the Krebs cycle. You'll find this in standard textbooks

like Devlin's Biochemistry with Clinical Applications, or Stryer's Biochemistry.

Andy

http://www.noamalgam.com/index.html

Amalgam Illness: Diagnosis and Treatment

http://www.noamalgam.com/hairtestbook.html

Hair Test Interpretation: Finding Hidden Toxicities

http://www.noamalgam.com/nourishinghope.html

Nourishing Hope for Autism: Nutrition Intervention for Healing Our Children

http://www.noamalgam.com/biologicaltreatments.html

Biological Treatments for Autism and PDD

>

>

> Mitochondrial Dysfunction in Autism

>

> Cecilia Giulivi, PhD; Yi-Fan Zhang, BS; Alicja Omanska-Klusek, MS;

> Ross-Inta, BS; Wong, BS; Irva Hertz-Picciotto, PhD; Flora Tassone,

> PhD; Isaac N. Pessah, PhD

>

> JAMA. 2010;304(21) :2389-2396. doi:10.1001/ jama.2010. 1706

>

> ABSTRACT

>

> Context Impaired mitochondrial function may influence processes highly

> dependent on energy, such as neurodevelopment, and contribute to autism. No

> studies have evaluated mitochondrial dysfunction and mitochondrial DNA

> (mtDNA) abnormalities in a well-defined population of children with autism.

>

> Objective To evaluate mitochondrial defects in children with autism.

>

> Design, Setting, and Patients Observational study using data collected from

> patients aged 2 to 5 years who were a subset of children participating in

> the Childhood Autism Risk From Genes and Environment study in California,

> which is a population-based, case-control investigation with confirmed

> autism cases and age-matched, genetically unrelated, typically developing

> controls, that was launched in 2003 and is still ongoing. Mitochondrial

> dysfunction and mtDNA abnormalities were evaluated in lymphocytes from 10

> children with autism and 10 controls.

>

> Main Outcome Measures Oxidative phosphorylation capacity, mtDNA copy number

> and deletions, mitochondrial rate of hydrogen peroxide production, and

> plasma lactate and pyruvate.

>

> Results The reduced nicotinamide adenine dinucleotide (NADH) oxidase

> activity (normalized to citrate synthase activity) in lymphocytic

> mitochondria from children with autism was significantly lower compared with

> controls (mean, 4.4 [95% confidence interval {CI}, 2.8-6.0] vs 12 [95% CI,

> 8-16], respectively; P = .001). The majority of children with autism (6 of

> 10) had complex I activity below control range values. Higher plasma

> pyruvate levels were found in children with autism compared with controls

> (0.23 mM [95% CI, 0.15-0.31 mM] vs 0.08 mM [95% CI, 0.04-0.12 mM],

> respectively; P = .02). Eight of 10 cases had higher pyruvate levels but

> only 2 cases had higher lactate levels compared with controls. These results

> were consistent with the lower pyruvate dehydrogenase activity observed in

> children with autism compared with controls (1.0 [95% CI, 0.6-1.4] nmol x

> [min x mg protein]-1 vs 2.3 [95% CI, 1.7-2.9] nmol x [min x mg protein]-1,

> respectively; P = .01). Children with autism had higher mitochondrial rates

> of hydrogen peroxide production compared with controls (0.34 [95% CI,

> 0.26-0.42] nmol x [min x mg of protein]-1 vs 0.16 [95% CI, 0.12-0.20] nmol x

> [min x mg protein]-1 by complex III; P = .02). Mitochondrial DNA

> overreplication was found in 5 cases (mean ratio of mtDNA to nuclear DNA:

> 239 [95% CI, 217-239] vs 179 [95% CI, 165-193] in controls; P = 10-4).

> Deletions at the segment of cytochrome b were observed in 2 cases (ratio of

> cytochrome b to ND1: 0.80 [95% CI, 0.68-0.92] vs 0.99 [95% CI, 0.93-1.05]

> for controls; P = .01).

>

> Conclusion In this exploratory study, children with autism were more likely

> to have mitochondrial dysfunction, mtDNA overreplication, and mtDNA

> deletions than typically developing children.

>

> A link to the whole article:

> <http://xa.yimg.com/kq/groups/1957724/635851927/name/Giulivi+

> et+al_JAMA_2010.pdf>

>

> ------------ --------- --------- --------- -------

>

> 1. Thimerosal induces neuronal cell apoptosis by causing cytochrome c

> and apoptosis-inducing factor release from mitochondria.

> < <http://www.ncbi.nlm.nih.gov/pubmed/16273274>

> <http://www.ncbi.nlm.nih.gov/pubmed/16273274>

> Yel L, Brown LE, Su K, Gollapudi S, Gupta S.

> Int J Mol Med. 2005 Dec;16(6):971- 7.PMID: 16273274

>

> 2. Mitochondrial mediated thimerosal-induced apoptosis in a human

> neuroblastoma cell line (SK-N-SH).

> < <http://www.ncbi.nlm.nih.gov/pubmed/15869795>

> <http://www.ncbi.nlm.nih.gov/pubmed/15869795>

> Humphrey ML, Cole MP, Pendergrass JC, Kiningham KK.

> Neurotoxicology. 2005 Jun;26(3):407- 16.PMID: 15869795

>

> 3. Biochemical and molecular basis of thimerosal-induced apoptosis in T

> cells: a major role of mitochondrial pathway.

> < <http://www.ncbi.nlm.nih.gov/pubmed/12140745>

> <http://www.ncbi.nlm.nih.gov/pubmed/12140745>

> Makani S, Gollapudi S, Yel L, Chiplunkar S, Gupta S.

> Genes Immun. 2002 Aug;3(5):270- 8.PMID: 12140745

>

> 4. Cellular and mitochondrial glutathione redox imbalance in

> lymphoblastoid cells derived from children with autism.

> < <http://www.ncbi.nlm.nih.gov/pubmed/19307255>

> <http://www.ncbi.nlm.nih.gov/pubmed/19307255>

> SJ, Rose S, Melnyk S, Jernigan S, Blossom S, Pavliv O, Gaylor DW.

> FASEB J. 2009 Aug;23(8):2374- 83.

>

> 5. Developmental regression and mitochondrial dysfunction in a child

> with autism. < <http://www.ncbi.nlm.nih.gov/pubmed/16566887>

> <http://www.ncbi.nlm.nih.gov/pubmed/16566887>

> Poling JS, Frye RE, Shoffner J, Zimmerman AW.

> J Child Neurol. 2006 Feb;21(2):170- 2.PMID: 16566887

>

> > UC study finds children with *autism* have mitochondrial

> > dysfunction

> > < <http://www.eurekale rt.org/pub_ releases/ 2010-11/uoc- -uds112410. php>

> http://www.eurekale rt.org/pub_ releases/ 2010-11/uoc- -uds112410. php>

> > EurekAlert (press release) -

> > <http://www.eurekale rt.org/pub_ releases/ 2010-11/uoc- -uds112410. php>

> http://www.eurekale rt.org/pub_ releases/ 2010-11/uoc- -uds112410. php

> >

> > Evidence of *mitochondrial dysfunction *in autism and ...

> > <

> <http://hstrial- astephens3. homestead. com/Evidence_ of_Mitochondrial

> _Dysfuncti

> on_in_Autism_ and_Implications _for_Treatment. pdf>

> http://hstrial- astephens3. homestead. com/Evidence_ of_Mitochondrial

> _Dysfunctio

> n_in_Autism_ and_Implications _for_Treatment. pdf>

> >

> > Biomarker-guided interventions of clinically relevant conditions

> > associated with autism spectrum disorders and attention deficit

> > hyperactivity disorder. < <http://www.ncbi. nlm.nih.gov/ pubmed/20359266>

> http://www.ncbi. nlm.nih.gov/ pubmed/20359266>

> > Bradstreet JJ, S, Baral M, Rossignol DA.

> > Altern Med Rev. 2010 Apr;15(1):15- 32. Review.

>

>

>

>

>

>

[Guest guest]

Thanks for being so blunt about this Dr. A. Cutler. I hear so much about

mitochondrial cocktails, and such, sophisticated sounding stuff, perhaps (How

some people seem to love sophisticated sounding stuff, (BWBS?) especially where

they can carry it to the point of baffling the other, it seems

Perhaps your message should be repeated over and over in that respect, of what

seems to be prevailing? Stupidity seems to be repeated over and over (that seems

to take hold? where it does?) so why not what is truer, to reason, and

understanding more, of the facts? (if not The feeling/s) of what works, seems to

work? I wouldn't think it would take nearly as many repetitions to make sense to

those trying to make sense of things

Best wishes in that respect

Glavic

P. S.-

Also repeating what is said below, of such treatment, and appreciation.

Where simplicity is the essence of genius, I'd be thinkin', for understanding

more by as much, (but what else?) that anything else should matter... Of all

there is, well, you seem to Know how It goes by now.. . And thanks for all

you're doing in that respect.

BWT

> >

> >

> > Mitochondrial Dysfunction in Autism

> >

> > Cecilia Giulivi, PhD; Yi-Fan Zhang, BS; Alicja Omanska-Klusek, MS;

> > Ross-Inta, BS; Wong, BS; Irva Hertz-Picciotto, PhD; Flora Tassone,

> > PhD; Isaac N. Pessah, PhD

> >

> > JAMA. 2010;304(21) :2389-2396. doi:10.1001/ jama.2010. 1706

> >

> > ABSTRACT

> >

> > Context Impaired mitochondrial function may influence processes highly

> > dependent on energy, such as neurodevelopment, and contribute to autism. No

> > studies have evaluated mitochondrial dysfunction and mitochondrial DNA

> > (mtDNA) abnormalities in a well-defined population of children with autism.

> >

> > Objective To evaluate mitochondrial defects in children with autism.

> >

> > Design, Setting, and Patients Observational study using data collected from

> > patients aged 2 to 5 years who were a subset of children participating in

> > the Childhood Autism Risk From Genes and Environment study in California,

> > which is a population-based, case-control investigation with confirmed

> > autism cases and age-matched, genetically unrelated, typically developing

> > controls, that was launched in 2003 and is still ongoing. Mitochondrial

> > dysfunction and mtDNA abnormalities were evaluated in lymphocytes from 10

> > children with autism and 10 controls.

> >

> > Main Outcome Measures Oxidative phosphorylation capacity, mtDNA copy number

> > and deletions, mitochondrial rate of hydrogen peroxide production, and

> > plasma lactate and pyruvate.

> >

> > Results The reduced nicotinamide adenine dinucleotide (NADH) oxidase

> > activity (normalized to citrate synthase activity) in lymphocytic

> > mitochondria from children with autism was significantly lower compared with

> > controls (mean, 4.4 [95% confidence interval {CI}, 2.8-6.0] vs 12 [95% CI,

> > 8-16], respectively; P = .001). The majority of children with autism (6 of

> > 10) had complex I activity below control range values. Higher plasma

> > pyruvate levels were found in children with autism compared with controls

> > (0.23 mM [95% CI, 0.15-0.31 mM] vs 0.08 mM [95% CI, 0.04-0.12 mM],

> > respectively; P = .02). Eight of 10 cases had higher pyruvate levels but

> > only 2 cases had higher lactate levels compared with controls. These results

> > were consistent with the lower pyruvate dehydrogenase activity observed in

> > children with autism compared with controls (1.0 [95% CI, 0.6-1.4] nmol x

> > [min x mg protein]-1 vs 2.3 [95% CI, 1.7-2.9] nmol x [min x mg protein]-1,

> > respectively; P = .01). Children with autism had higher mitochondrial rates

> > of hydrogen peroxide production compared with controls (0.34 [95% CI,

> > 0.26-0.42] nmol x [min x mg of protein]-1 vs 0.16 [95% CI, 0.12-0.20] nmol x

> > [min x mg protein]-1 by complex III; P = .02). Mitochondrial DNA

> > overreplication was found in 5 cases (mean ratio of mtDNA to nuclear DNA:

> > 239 [95% CI, 217-239] vs 179 [95% CI, 165-193] in controls; P = 10-4).

> > Deletions at the segment of cytochrome b were observed in 2 cases (ratio of

> > cytochrome b to ND1: 0.80 [95% CI, 0.68-0.92] vs 0.99 [95% CI, 0.93-1.05]

> > for controls; P = .01).

> >

> > Conclusion In this exploratory study, children with autism were more likely

> > to have mitochondrial dysfunction, mtDNA overreplication, and mtDNA

> > deletions than typically developing children.

> >

> > A link to the whole article:

> > <http://xa.yimg.com/kq/groups/1957724/635851927/name/Giulivi+

> > et+al_JAMA_2010.pdf>

> >

> > ------------ --------- --------- --------- -------

> >

> > 1. Thimerosal induces neuronal cell apoptosis by causing cytochrome c

> > and apoptosis-inducing factor release from mitochondria.

> > < <http://www.ncbi.nlm.nih.gov/pubmed/16273274>

> > <http://www.ncbi.nlm.nih.gov/pubmed/16273274>

> > Yel L, Brown LE, Su K, Gollapudi S, Gupta S.

> > Int J Mol Med. 2005 Dec;16(6):971- 7.PMID: 16273274

> >

> > 2. Mitochondrial mediated thimerosal-induced apoptosis in a human

> > neuroblastoma cell line (SK-N-SH).

> > < <http://www.ncbi.nlm.nih.gov/pubmed/15869795>

> > <http://www.ncbi.nlm.nih.gov/pubmed/15869795>

> > Humphrey ML, Cole MP, Pendergrass JC, Kiningham KK.

> > Neurotoxicology. 2005 Jun;26(3):407- 16.PMID: 15869795

> >

> > 3. Biochemical and molecular basis of thimerosal-induced apoptosis in T

> > cells: a major role of mitochondrial pathway.

> > < <http://www.ncbi.nlm.nih.gov/pubmed/12140745>

> > <http://www.ncbi.nlm.nih.gov/pubmed/12140745>

> > Makani S, Gollapudi S, Yel L, Chiplunkar S, Gupta S.

> > Genes Immun. 2002 Aug;3(5):270- 8.PMID: 12140745

> >

> > 4. Cellular and mitochondrial glutathione redox imbalance in

> > lymphoblastoid cells derived from children with autism.

> > < <http://www.ncbi.nlm.nih.gov/pubmed/19307255>

> > <http://www.ncbi.nlm.nih.gov/pubmed/19307255>

> > SJ, Rose S, Melnyk S, Jernigan S, Blossom S, Pavliv O, Gaylor DW.

> > FASEB J. 2009 Aug;23(8):2374- 83.

> >

> > 5. Developmental regression and mitochondrial dysfunction in a child

> > with autism. < <http://www.ncbi.nlm.nih.gov/pubmed/16566887>

> > <http://www.ncbi.nlm.nih.gov/pubmed/16566887>

> > Poling JS, Frye RE, Shoffner J, Zimmerman AW.

> > J Child Neurol. 2006 Feb;21(2):170- 2.PMID: 16566887

> >

> > > UC study finds children with *autism* have mitochondrial

> > > dysfunction

> > > < <http://www.eurekale rt.org/pub_ releases/ 2010-11/uoc- -uds112410. php>

> > http://www.eurekale rt.org/pub_ releases/ 2010-11/uoc- -uds112410. php>

> > > EurekAlert (press release) -

> > > <http://www.eurekale rt.org/pub_ releases/ 2010-11/uoc- -uds112410. php>

> > http://www.eurekale rt.org/pub_ releases/ 2010-11/uoc- -uds112410. php

> > >

> > > Evidence of *mitochondrial dysfunction *in autism and ...

> > > <

> > <http://hstrial- astephens3. homestead. com/Evidence_ of_Mitochondrial

> > _Dysfuncti

> > on_in_Autism_ and_Implications _for_Treatment. pdf>

> > http://hstrial- astephens3. homestead. com/Evidence_ of_Mitochondrial

> > _Dysfunctio

> > n_in_Autism_ and_Implications _for_Treatment. pdf>

> > >

> > > Biomarker-guided interventions of clinically relevant conditions

> > > associated with autism spectrum disorders and attention deficit

> > > hyperactivity disorder. < <http://www.ncbi. nlm.nih.gov/ pubmed/20359266>

> > http://www.ncbi. nlm.nih.gov/ pubmed/20359266>

> > > Bradstreet JJ, S, Baral M, Rossignol DA.

> > > Altern Med Rev. 2010 Apr;15(1):15- 32. Review.

> >

> >

> >

> >

> >

> >