carnitine deficiency - mitochondrial disorder- toxins

[Guest guest]

Listmates - We have discussed and debated this topic in the past. I

strongly urge you to do some further research on your own and then

take what you find to your practicioner.

I confirmed that my globally dyspraxic son has mitochondrial

dysfunction back in October. He was nearly 5 years old - he had very

scary/serious symtoms back when he was 2 that were blown off. We

have to push our trusted Dr.'s to go an extra yard beyond mainstream

media. A good Dr. is a detective.

Since this IS a common thread - please check it out, at least to rule

it out. THIS IS NOT UNIQUE (like you are reading in the newpaper and

hearing on the news) THIS IS VERY, VERY, VERY COMMON, and common to

apraxia as it is to Autism and all that there in between.

The ONLY reason we didn't loose my son to " the other world " called

Autism - is because we stopped vaccinating at 6 mos. PURE luck! His

mito problem was NOT genetic - it was AQUIRED from (vaccine) toxic

exposure.

http://www.emedicine.com/PED/topic321.htm

Mortality/Morbidity

Sudden death: Unfortunately, the first clinical manifestation in

asymptomatic individuals with primary carnitine deficiency may be

sudden death. This also may occur in patients with secondary

carnitine deficiency as a consequence of ventricular tachycardia or

fibrillation.

Heart failure: Patients with primary carnitine deficiency develop a

progressive cardiomyopathy that usually presents at a later age. The

cardiac function does not respond to inotropes or diuretics. If the

condition is not diagnosed correctly and no carnitine is

supplemented, progressive heart failure eventually leads to death.

Heart failure caused by dilated cardiomyopathy may be the presenting

syndrome in patients with secondary carnitine deficiency caused by

defects in beta-oxidation, such as long-chain 3-hydroxyacyl-CoA

dehydrogenase (LCHAD) and very long-chain acyl-CoA dehydrogenase

(VLCAD) deficiency.

Hypoglycemic hypoketotic encephalopathy: Acute encephalopathy

accompanied by hypoketotic hypoglycemic episodes usually presents in

younger infants with primary carnitine deficiency. Periods of fasting

in association with viral illness trigger these acute episodes. Some

patients have developmental delay and central nervous system

dysfunction associated with these episodes. If no carnitine

replacement is given, recurrent episodes of encephalopathy may ensue.

..

THIMEROSAL in published studies, PROVOKES mito failure.(study below)

Lyn Redwood from SAFEMINDS has provided the CDC ACIP (Vaccine

Advisory) panel with this information over and over again.

Mitochondrial Mediated Thimerosal-Induced Apoptosis in a Human

Neuroblastoma Cell Line (SK-N-SH)

L. Humphreya, Marsha P. Coleb, C. Pendergrassc and

Kinsley K. Kininghama, Corresponding Author Contact Information, E-

mail The Corresponding Author

aDepartment of Pharmacology, Joan C. School of Medicine,

Marshall University, 1542 Spring Valley Drive, Huntington, WV 25704-

9388, USA

bGraduate Center for Toxicology, University of Kentucky, Lexington,

KY 40536, USA

cAffinity Labeling Technologies, Inc., Lexington, KY 40508, USA

Received 6 December 2004; accepted 25 February 2005. Available online

24 May 2005.

Abstract

Environmental exposure to mercurials continues to be a public health

issue due to their deleterious effects on immune, renal and

neurological function. Recently the safety of thimerosal, an ethyl

mercury-containing preservative used in vaccines, has been questioned

due to exposure of infants during immunization. Mercurials have been

reported to cause apoptosis in cultured neurons; however, the

signaling pathways resulting in cell death have not been well

characterized. Therefore, the objective of this study was to identify

the mode of cell death in an in vitro model of thimerosal-induced

neurotoxicity, and more specifically, to elucidate signaling pathways

which might serve as pharmacological targets. Within 2 h of

thimerosal exposure (5 µM) to the human neuroblastoma cell line, SK-N-

SH, morphological changes, including membrane alterations and cell

shrinkage, were observed. Cell viability, assessed by measurement of

lactate dehydrogenase (LDH) activity in the medium, as well as the 3-

[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT)

assay, showed a time- and concentration-dependent decrease in cell

survival upon thimerosal exposure. In cells treated for 24 h with

thimerosal, fluorescence microscopy indicated cells undergoing both

apoptosis and oncosis/necrosis. To identify the apoptotic pathway

associated with thimerosal-mediated cell death, we first evaluated

the mitochondrial cascade, as both inorganic and organic mercurials

have been reported to accumulate in the organelle. Cytochrome c was

shown to leak from the mitochondria, followed by caspase 9 cleavage

within 8 h of treatment. In addition, poly(ADP-ribose) polymerase

(PARP) was cleaved to form a 85 kDa fragment following maximal

caspase 3 activation at 24 h. Taken together these findings suggest

deleterious effects on the cytoarchitecture by thimerosal and

initiation of mitochondrial-mediated apoptosis.

Keywords: Mercury; Thimerosal; Mitochondria; Neurotoxicity

[Guest guest]

This answers my question about carnitine for my friend with the

autistic kid who is not currently on dairy. Let's hear it for beef

and dairy if you can tolerate it:)

>

> Listmates - We have discussed and debated this topic in the past.

I

> strongly urge you to do some further research on your own and then

> take what you find to your practicioner.

>

> I confirmed that my globally dyspraxic son has mitochondrial

> dysfunction back in October. He was nearly 5 years old - he had

very

> scary/serious symtoms back when he was 2 that were blown off. We

> have to push our trusted Dr.'s to go an extra yard beyond

mainstream

> media. A good Dr. is a detective.

>

> Since this IS a common thread - please check it out, at least to

rule

> it out. THIS IS NOT UNIQUE (like you are reading in the newpaper

and

> hearing on the news) THIS IS VERY, VERY, VERY COMMON, and common

to

> apraxia as it is to Autism and all that there in between.

>

> The ONLY reason we didn't loose my son to " the other world " called

> Autism - is because we stopped vaccinating at 6 mos. PURE luck!

His

> mito problem was NOT genetic - it was AQUIRED from (vaccine) toxic

> exposure.

>

>

> http://www.emedicine.com/PED/topic321.htm

>

>

> Mortality/Morbidity

>

> Sudden death: Unfortunately, the first clinical manifestation in

> asymptomatic individuals with primary carnitine deficiency may be

> sudden death. This also may occur in patients with secondary

> carnitine deficiency as a consequence of ventricular tachycardia or

> fibrillation.

> Heart failure: Patients with primary carnitine deficiency develop a

> progressive cardiomyopathy that usually presents at a later age.

The

> cardiac function does not respond to inotropes or diuretics. If the

> condition is not diagnosed correctly and no carnitine is

> supplemented, progressive heart failure eventually leads to death.

> Heart failure caused by dilated cardiomyopathy may be the

presenting

> syndrome in patients with secondary carnitine deficiency caused by

> defects in beta-oxidation, such as long-chain 3-hydroxyacyl-CoA

> dehydrogenase (LCHAD) and very long-chain acyl-CoA dehydrogenase

> (VLCAD) deficiency.

> Hypoglycemic hypoketotic encephalopathy: Acute encephalopathy

> accompanied by hypoketotic hypoglycemic episodes usually presents

in

> younger infants with primary carnitine deficiency. Periods of

fasting

> in association with viral illness trigger these acute episodes.

Some

> patients have developmental delay and central nervous system

> dysfunction associated with these episodes. If no carnitine

> replacement is given, recurrent episodes of encephalopathy may

ensue.

> .

>

>

>

> THIMEROSAL in published studies, PROVOKES mito failure.(study below)

> Lyn Redwood from SAFEMINDS has provided the CDC ACIP (Vaccine

> Advisory) panel with this information over and over again.

>

> Mitochondrial Mediated Thimerosal-Induced Apoptosis in a Human

> Neuroblastoma Cell Line (SK-N-SH)

>

> L. Humphreya, Marsha P. Coleb, C. Pendergrassc and

> Kinsley K. Kininghama, Corresponding Author Contact Information, E-

> mail The Corresponding Author

> aDepartment of Pharmacology, Joan C. School of Medicine,

> Marshall University, 1542 Spring Valley Drive, Huntington, WV 25704-

> 9388, USA

> bGraduate Center for Toxicology, University of Kentucky, Lexington,

> KY 40536, USA

> cAffinity Labeling Technologies, Inc., Lexington, KY 40508, USA

> Received 6 December 2004; accepted 25 February 2005. Available

online

> 24 May 2005.

>

> Abstract

>

> Environmental exposure to mercurials continues to be a public

health

> issue due to their deleterious effects on immune, renal and

> neurological function. Recently the safety of thimerosal, an ethyl

> mercury-containing preservative used in vaccines, has been

questioned

> due to exposure of infants during immunization. Mercurials have

been

> reported to cause apoptosis in cultured neurons; however, the

> signaling pathways resulting in cell death have not been well

> characterized. Therefore, the objective of this study was to

identify

> the mode of cell death in an in vitro model of thimerosal-induced

> neurotoxicity, and more specifically, to elucidate signaling

pathways

> which might serve as pharmacological targets. Within 2 h of

> thimerosal exposure (5 µM) to the human neuroblastoma cell line, SK-

N-

> SH, morphological changes, including membrane alterations and cell

> shrinkage, were observed. Cell viability, assessed by measurement

of

> lactate dehydrogenase (LDH) activity in the medium, as well as the

3-

> [4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT)

> assay, showed a time- and concentration-dependent decrease in cell

> survival upon thimerosal exposure. In cells treated for 24 h with

> thimerosal, fluorescence microscopy indicated cells undergoing both

> apoptosis and oncosis/necrosis. To identify the apoptotic pathway

> associated with thimerosal-mediated cell death, we first evaluated

> the mitochondrial cascade, as both inorganic and organic mercurials

> have been reported to accumulate in the organelle. Cytochrome c was

> shown to leak from the mitochondria, followed by caspase 9 cleavage

> within 8 h of treatment. In addition, poly(ADP-ribose) polymerase

> (PARP) was cleaved to form a 85 kDa fragment following maximal

> caspase 3 activation at 24 h. Taken together these findings suggest

> deleterious effects on the cytoarchitecture by thimerosal and

> initiation of mitochondrial-mediated apoptosis.

>

> Keywords: Mercury; Thimerosal; Mitochondria; Neurotoxicity

>

[Guest guest]

,

I believe that Mark has some type of acquired mitochondrea dysfunction and that

it too was acquired.

Janice

[sPAM][ ] carnitine deficiency - mitochondrial

disorder- toxins

Listmates - We have discussed and debated this topic in the past. I

strongly urge you to do some further research on your own and then

take what you find to your practicioner.

I confirmed that my globally dyspraxic son has mitochondrial

dysfunction back in October. He was nearly 5 years old - he had very

scary/serious symtoms back when he was 2 that were blown off. We

have to push our trusted Dr.'s to go an extra yard beyond mainstream

media. A good Dr. is a detective.

Since this IS a common thread - please check it out, at least to rule

it out. THIS IS NOT UNIQUE (like you are reading in the newpaper and

hearing on the news) THIS IS VERY, VERY, VERY COMMON, and common to

apraxia as it is to Autism and all that there in between.

The ONLY reason we didn't loose my son to " the other world " called

Autism - is because we stopped vaccinating at 6 mos. PURE luck! His

mito problem was NOT genetic - it was AQUIRED from (vaccine) toxic

exposure.

http://www.emedicine.com/PED/topic321.htm

Mortality/Morbidity

Sudden death: Unfortunately, the first clinical manifestation in

asymptomatic individuals with primary carnitine deficiency may be

sudden death. This also may occur in patients with secondary

carnitine deficiency as a consequence of ventricular tachycardia or

fibrillation.

Heart failure: Patients with primary carnitine deficiency develop a

progressive cardiomyopathy that usually presents at a later age. The

cardiac function does not respond to inotropes or diuretics. If the

condition is not diagnosed correctly and no carnitine is

supplemented, progressive heart failure eventually leads to death.

Heart failure caused by dilated cardiomyopathy may be the presenting

syndrome in patients with secondary carnitine deficiency caused by

defects in beta-oxidation, such as long-chain 3-hydroxyacyl-CoA

dehydrogenase (LCHAD) and very long-chain acyl-CoA dehydrogenase

(VLCAD) deficiency.

Hypoglycemic hypoketotic encephalopathy: Acute encephalopathy

accompanied by hypoketotic hypoglycemic episodes usually presents in

younger infants with primary carnitine deficiency. Periods of fasting

in association with viral illness trigger these acute episodes. Some

patients have developmental delay and central nervous system

dysfunction associated with these episodes. If no carnitine

replacement is given, recurrent episodes of encephalopathy may ensue.

.

THIMEROSAL in published studies, PROVOKES mito failure.(study below)

Lyn Redwood from SAFEMINDS has provided the CDC ACIP (Vaccine

Advisory) panel with this information over and over again.

Mitochondrial Mediated Thimerosal-Induced Apoptosis in a Human

Neuroblastoma Cell Line (SK-N-SH)

L. Humphreya, Marsha P. Coleb, C. Pendergrassc and

Kinsley K. Kininghama, Corresponding Author Contact Information, E-

mail The Corresponding Author

aDepartment of Pharmacology, Joan C. School of Medicine,

Marshall University, 1542 Spring Valley Drive, Huntington, WV 25704-

9388, USA

bGraduate Center for Toxicology, University of Kentucky, Lexington,

KY 40536, USA

cAffinity Labeling Technologies, Inc., Lexington, KY 40508, USA

Received 6 December 2004; accepted 25 February 2005. Available online

24 May 2005.

Abstract

Environmental exposure to mercurials continues to be a public health

issue due to their deleterious effects on immune, renal and

neurological function. Recently the safety of thimerosal, an ethyl

mercury-containing preservative used in vaccines, has been questioned

due to exposure of infants during immunization. Mercurials have been

reported to cause apoptosis in cultured neurons; however, the

signaling pathways resulting in cell death have not been well

characterized. Therefore, the objective of this study was to identify

the mode of cell death in an in vitro model of thimerosal-induced

neurotoxicity, and more specifically, to elucidate signaling pathways

which might serve as pharmacological targets. Within 2 h of

thimerosal exposure (5 µM) to the human neuroblastoma cell line, SK-N-

SH, morphological changes, including membrane alterations and cell

shrinkage, were observed. Cell viability, assessed by measurement of

lactate dehydrogenase (LDH) activity in the medium, as well as the 3-

[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT)

assay, showed a time- and concentration-dependent decrease in cell

survival upon thimerosal exposure. In cells treated for 24 h with

thimerosal, fluorescence microscopy indicated cells undergoing both

apoptosis and oncosis/necrosis. To identify the apoptotic pathway

associated with thimerosal-mediated cell death, we first evaluated

the mitochondrial cascade, as both inorganic and organic mercurials

have been reported to accumulate in the organelle. Cytochrome c was

shown to leak from the mitochondria, followed by caspase 9 cleavage

within 8 h of treatment. In addition, poly(ADP-ribose) polymerase

(PARP) was cleaved to form a 85 kDa fragment following maximal

caspase 3 activation at 24 h. Taken together these findings suggest

deleterious effects on the cytoarchitecture by thimerosal and

initiation of mitochondrial-mediated apoptosis.

Keywords: Mercury; Thimerosal; Mitochondria; Neurotoxicity