Autism Science Digest: Aluminum Toxicity in Mitochondrial Dysfunction and ASD
Thank you to our friends at Autism Science Digest magazine for allowing us to excerpt this article.
Aluminum Toxicity in Mitochondrial Dysfunction and ASD
By Nancy Mullan, MD, and Amy Yasko, PhD, AMD, FAAIM
Currently, there is intense interest and discussion surrounding the high incidence of mitochondrial disease and/or dysfunction in children with autism spectrum disorders (ASDs). This interest is fueled at least in part by the 2008 Hannah Poling decision.1,2 In this landmark case, the federal government’s Vaccine Injury Compensation Program (VICP) agreed to award damages to the Poling family when their daughter Hannah, who had an underlying mitochondrial disorder, developed autism-like symptoms after receiving a series of vaccines in a single day. Because Hannah Poling’s father is a medical doctor who was in the department of neurology at Johns Hopkins Hospital at the time that his daughter’s vaccine injury occurred, her case carried great weight. The Poling case, therefore, served to draw a great deal more attention to mitochondrial disorders within autism than these disorders had previously received.
A carefully executed review and meta-analysis of mitochondrial dysfunction in ASD by Rossignol and Frye discerned that the prevalence of full syndrome mitochondrial disease in children with ASD is significantly higher than it is in children in general.3 Their analysis also revealed that many children with ASD have findings on laboratory tests that indicate some degree of mitochondrial dysfunction, although not full syndrome mitochondrial disease. Together, these findings indicate a high degree of abnormal mitochondrial function in children with ASD, which other research has corroborated.2,4-9
The cause of the high comorbidity between ASD and mitochondrial dysfunction remains obscure. Most ASD patients do not have a genetic abnormality that would explain the association.4 Nonetheless, there is a great deal of overlap between the symptoms of ASD and the symptoms of genetic mitochondrial diseases, many of which progressively affect multiple body systems. Genetic mitochondrial diseases especially impact organs that have high energy demands, such as the brain and nerves. Because the brain has the highest energy demand of any tissue, mitochondrial disease causes a variety of neurological problems, including intellectual disability, seizures, developmental regression, gastrointestinal problems, and lack of coordination. In addition, because muscles have a high demand for mitochondrial energy, low muscle tone, weakness, and fatigue are features of many mitochondrial diseases. These neurological and muscle-related symptoms are very commonly found in children with ASD as well, though patients who have ASD and biochemical evidence of mitochondrial dysfunction have relatively milder, non-progressive forms of mitochondrial dysfunction when compared with cases of mitochondrial disease caused by genetic aberrations.10
Searching for explanations
The search continues to identify the reason(s) why so many children with ASD have associated abnormal mitochondrial functioning and biomarkers (as shown by results of laboratory testing). Attention is turning away from genetics toward the environment. As a first line of evidence that environmental factors are involved, there is no question that increased free radicals impair mitochondrial function.11 This fact may be particularly significant for children with ASD since . . . read more at Aluminum Toxicity in Mitochondrial Dysfunction and ASD.
L carnitine: aluminum interferes with mitochondria oxidation phosphorylation complex I at least if not more, by interfering with L carnitine. Two studies.
The first one is those vaccine papers which every one dismisses as Oh, those tin hatters:
http://vaccinepapers.org/wp-content/uploads/The-disruption-of-L-carnitine-metabolism-by-aluminum-toxicity-and-oxidative-stress-promotes-dyslipidemia-in-human-astrocytic-and-hepatic-cells.pdf
But then Everybody loves the NIH sites, so trusted and all.
So, here is this: "An acetyl-L-carnitine switch on mitochondrial dysfunction and rescue in the metabolomics study on aluminum oxide nanoparticles"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4715336/
And then there is aspirin that helps uncouple phosphorylation in the mitochondria and that is a good thing.
https://pubmed.ncbi.nlm.nih.gov/1019575/
" Salicylate- and aspirin-induced uncoupling of oxidative phosphorylation in mitochondria isolated from the mucosal membrane of the stomach"
Posted by: Benedetta | July 26, 2020 at 10:44 AM
HOW ABOUT THIS: B12 INJECTIONS (CYANOCOBALAMIN) CONTAINING ALUMINUM, I FOUND THE HARD WAY,
AFTER ABOUT 3 YEARS OF INJECTIONS, (I LATER PUT IT TOGETHER). NEUROLOGICAL SYMPTOMS BEGAN BILATERALLY IN THE TOES AND PROGRESSING UPWARD , DIAGNOSIS "PERIPHERAL NEUROPATHY OF UNKNOWN ORIGIN".
AFTER 10 YEARS AND PROGRESSION THAT PREVENTED ANY POSITION ENABLING SLEEP, I JUST THRASHED AROUND, AND HAD LASER SPINE SURGERY DUE TO THE SYMPTOMS , WHICH ONLY HELPED MINIMALLY IF AT ALL.
ONE DAY I WAS ACCIDENTALLY GIVEN THE PACKAGE INSERT FOR MY B12 INJECTION BOTTLE. (guess what ? aluminum in the B12 cyano I had been taking for 10 years ! Precautions listed aluminum 's known neurotoxicity, with numbness & tingling of the toes, and working its way up the legs...)
Also beginning in the 3rd year of the B12 cyano, my hearing, and my balance ever so slightly, began to suffer, and progress; I do not think it was any coincidence.
Finally I found that the methylcobalamin was form of B12 was no longer made, and did find Liquid B12 for under tongue absorption. It seems to have stopped the upward progression, but the hearing loss progressed.
In view of all the vaccines as well as the "geoengineering" (the "sky writing" {it's not !] that is being done, everywhere on earth to put aerial aluminum, barium and God knows what else, SPRAYED OVER US TO SUPPOSEDLY KEEP THE SUN FROM HEATING THE EARTH IS NOW MONUMENTALLY CONTAMINATING THE EARTH's SOIL AND THE PLANTS WE THAT AND ALL LIFE DEPEND UPON FOR SUSTENANCE MAKES ME WONDER IF THE INSTIGATORS ARE SO REMOVED FROM NATURE THAT THEY THINK THERE'S NOT A PROBLEM. (or maybe they are complying with the United Nations' plan for denying ownership of personal property and population control: Agenda 21, is killing us off to comply !)
I have found that the ONLY place to find deodorant that is lacking aluminum is the health food store, and it uses grapefruit skin extract, to work very well.
When researching this problem, it becomes clear that aluminum is most increasingly pervasive in our environment, and will be cumulative, though unrecognized by doctors as causing anything until it's done its damages.
Even our "non stick" aluminum pans are a source of very toxic fluorine (goitrogenic) compounds, which give off toxic fumes when heating. Aluminum is known to have detrimental effects in all biological systems, yet they put it in vaccines and are increasingly giving more & more shots straight into the bloodstream of babies. (INSANITY !)
I just read that Codex Alimenterius (the UN/WTO edict making controls of commerce that is supposed to protect the food supplys' ingredients) has refused to consider regulating the prevalence of aluminum in our foods (Baking powder for example, among many others) Just like GMO's, the commercial production by the
transnatinonal corporations financed by the Banksters must go on... they don 't feel a thing.
Aluminum is known to attack the thyroid gland, and thus is attacking both the origins of energy production and the regulation of calcium trough the calcitonin also produced in the thyroid.
There is a lot more, but the information is available on the net, if you just look.
Medscape is a good source, but you need to be a health professional to sign on.... ( I don't think they investigate the source.)
Posted by: Patty Reynolds | April 28, 2013 at 04:52 AM
http://www.umdf.org/site/c.jtJWJaMMIsE/b.4090097/
The above is a link to the United Mitochondrial Disease Foundation
Information you will find there are patients writing in asking questions and describing their symptoms
Reading the Docs answers - the dieting stuff and the ketogenic diet gets complicated.
KENT WHERE ARE YOU ON THIS DIETING BUSINESS????
ALso reading this - Thank God for this Web site.
The docs will never ever, ever, ever blame the vaccines.
If ask if a child that has reacted to each and every one of its vaccines -- and has gotten some better -- if they should vaccinate again -- the docs say talk to your doctor and hell yes.
Sigh.
It is murder, don't you think.
Posted by: Benedetta | January 06, 2013 at 08:44 PM
I found this while reading about metoformins
http://cmajopen.com/content/173/5/505.full
"Recent discoveries indicate that the enzyme AMP (adenosine monophosphate)-kinase is activated.14 AMP-kinase is activated under physiologic conditions by elevation in cellular AMP concentration, which occurs during exercise or fasting. "
Could this be the reason that ketogenic diets and the 15 carb Atkins diet that mimics starvation works -- it activates adenosine monophopsate?
Oh meteformin may inhibit or deplete or something B 12 -- I am not sure on that one. If any one is out there bothering to read this---- they might check on that one.
Meteformin works through the kidneys so anyone with renal failure may be in more danger of what the most dangerous thing about this drug is and it is Lactic acidosis. The same reason all the doctors got all big eyed when I mentioned ketogenic diet or the Atkins diet.
Posted by: Benedetta | January 04, 2013 at 05:33 PM
The below link was from researchers in India
this link is from researchers in Italy
http://www.ncbi.nlm.nih.gov/pubmed/12797472
"The effect of Al3+ on lipid peroxidation of HDL was observed at aluminium concentrations similar to those observed in the brain of patients affected by neurological diseases. Aluminium-induced oxidative damage of HDL could be involved in the development of neurological diseases."
Remember way back in my first post that I found that the lipids in the matrix (inter wall of the mitochondria) was leaking out electron nad these caused peroxids that further damaged lipid production.
By the way the link from India below mentions the Alzeheimers.
When my husband developed high cholesterol at a young age - then of course we started on a low fat diet - and I poured tons of oat bran into everything. My son grew up with oat bran and salmon patties-- and mostly stuff from the garden which was tomatoes, corn, and greens.
My son is not what he was borned into this world to be - but he is not bad.
THe only time thought that we were able to get the cholesterol down was the Atkins diet!!!
OH feat the Atkins diet for all those fats?
And it brings the cholesterol they are measuring down?
Posted by: Benedetta | January 04, 2013 at 11:12 AM
http://www.lipidworld.com/content/3/1/13
in this study in the abstract it says:
"Effect of long-term (90–100 days) exposure of rats to soluble salt of aluminum (AlCl3) on myelin lipid profile was examined. The long-term exposure to AlCl3 resulted in a 60 % decrease in the total phospholipid (TPL) content while the cholesterol (CHL) content increased by 55 % "
It sounds like to me that phospholiipids are not being made but cholesterol (a certian type is)
cholesterol is only the prescurser of all the hormones - including the sex hormones.
The middle age men - in this epidemic that started falling over dead with heart attacks back in the 60s and 70s may have been the first victims of vaccines.
Posted by: Benedetta | January 04, 2013 at 10:56 AM
No Hera;
It may just be your computer.
Here is another symptom that I think is very related that my husband had after his first reaction - he developed high cholesterol - although he was perfect weight, at age 28.
They do know something because a couple years later after his second reacton and the doctor sent him down to Emory Clinic and he was dignoised with oxidation phosphoralation on he complex I and complex III (eyes cross as usual here) -- his doctor that sent him told him he could never take statin drugs to lower his cholesterol - it would kill him
Years later a different doctor - had this genius idea that she could give him a drug that absorbed fat out of the intestine before it reache the blood and he would be okay.
She congradulated him on being able to lower his cholesterol levels 230 to 200-- as he was beginning to be unable to concentrate at work, turning a very pale gray skin color -- a week after that she was putting him in the hospital all while his boss was threatening to fire him.
MY husband a senior researcher.
Posted by: Benedetta | January 04, 2013 at 10:49 AM
Hi Taximom;
I think its basically that aluminium depletes glutathione levels. Low glutathione effects lipid metabolism.
( And of course low glutathione is common in kids with autism)
By the way, I'm having a lot of trouble logging on to this site over the last couple of weeks. Is there a problem for others too?
Posted by: Hera | January 04, 2013 at 05:42 AM
Taximom,
This abstract seems to explain a mechanism, but I'm not qualified to interpret:
http://www.ncbi.nlm.nih.gov/pubmed/17762189
Aluminum-induced mitochondrial dysfunction leads to lipid accumulation in human hepatocytes: a link to obesity.
Mailloux R, Lemire J, Appanna V.
Source
Department of Chemistry and Biochemistry, Laurentian University, Ontario, Canada.
Abstract
Mitochondrial dysfunction is the cause of a variety of pathologies associated with high energy-requiring tissues like the brain and muscles. Here we show that aluminum (Al) perturbs oxidative-ATP production in human hepatocytes (HepG2 cells). This Al-induced mitochondrial dysfunction promotes enhanced lipogenesis and the accumulation of the very low density lipoprotein (VLDL). Al-stressed HepG2 cells secreted more cholesterol, lipids and proteins than control cells. The level of apolipoprotein B-100 (ApoB-100) was markedly increased in the culture medium of the cells exposed to Al. (13)C-NMR and HPLC studies revealed a metabolic profile favouring lipid production and lowered ATP synthesis in Al-treated cells. Electrophoretic and immunoblot analyses pointed to increased activities and expression of lipogenic enzymes such as glycerol 3-phosphate dehydrogenase (G3PDH), acetyl CoA carboxylase (ACC) and ATP-citrate lyase (CL) in the hepatocytes exposed to Al, and a sharp diminution of enzymes mediating oxidative phosphorylation. D-Fructose elicited the maximal secretion of VLDL in the Al-challenged cells. These results suggest that the Al-evoked metabolic shift favours the accumulation of lipids at the expense of oxidative energy production in hepatocytes.
Posted by: Jeannette Bishop | January 03, 2013 at 10:52 PM
Can someone explain exactly what the relationship is between aluminum/mercury and lipid metabolism problems?
Thanks.
Posted by: Taximom | January 03, 2013 at 08:02 PM
I am considering writing a letter to the neurologist on heads up on what would be the problem of prescribing metformin. Other than a chance of causing acidoisis.
This is just me talking - I have no medical degree or can even spell for that matter, so plenty I don't know about this.
Does anyone know anything about it?
I found this:
"FDA pregnancy category B. Metformin is not expected to be harmful to an unborn baby. Tell your doctor if you are pregnant or plan to become pregnant during treatment. It is not known whether metformin passes into breast milk or if it could harm a nursing baby. Do not take metformin without first talking to your doctor if you are breast-feeding a baby. Metformin should not be given to a child younger than 10 years old. Extended-release metformin (Glucophage XR) should not be given to a child younger than 17 years old."
So they know something that I don't.
Posted by: Benedetta | January 03, 2013 at 07:04 PM
Sarah pretty much sums it up for my family.
One of the lasting effects of Kawasakis is Lipid metabolism problems.
If you read the systems of Lipid metabolism symptoms they are identical to mitochondria myopathy of the complex I and complex III on the electron transfer system.
It may well be that the lipds that make up the wall of the matrix that keeps the electrons from leaking out.
A diet with lots of fats as in the ketogenic diet -that includes a lot of cream and fat from Medium chain triglycerides - made from coconut oil is able to repair this? Or perhaps the Atkin's diet - but more consideration of the kinds of fats used. I don't think that man made shortening is the thing to use.
With out proper lipid metabolism then carbohydrates can not be broken down and used for energy, nor can the manufacturing and use of the B vitamins either.
There is a diabetic drug that is known to tighten the lipids of the mitochondria at the complex I
Meteformin stops or slows down the permeability of the inter membrane of the mitochondria. It stops the flow of electrons flowing out --
The escaped electrons from the complex one means no energy is being
made or very little energy is being made. But that is not the only or perhaps even the biggest problem. It is the escape of the electrons that is the big problem. If they don't make energy they go on to peroxide in the
body> (free radicals) and interfere with lipid metabolism
Again: biggest problem that kids with Kawasakis developed later on was lipd metabolism)unless carried away by glutiothiione --the body uses N
-acetly cysteine to make glutithione.
meteformin. This is a vicious cycle.
Posted by: Benedetta | January 03, 2013 at 06:09 PM
Mitochondrial Disease in Autism Spectrum Disorder Patients: A Cohort Analysis
Jacqueline R. Weissman, Affiliation: Cleveland Clinic Lerner College of Medicine, Cleveland Clinic, Cleveland, Ohio, United States of America
X Richard I. Kelley, Affiliation: Department of Pediatrics, Johns Hopkins University Medical Center and Division of Metabolism, Kennedy Krieger Institute, Baltimore, Maryland, United States of America
X Margaret L. Bauman, Affiliation: Department of Pediatrics and Learning and Developmental Disabilities Evaluation and Rehabilitation Services (LADDERS), Massachusetts General Hospital, Boston, Massachusetts, United States of America
X Bruce H. Cohen, Affiliation: Neurological Institute and Pediatrics Institute, Cleveland Clinic, Cleveland, Ohio, United States of America
X Katherine F. Murray, Affiliation: Department of Pediatrics and Learning and Developmental Disabilities Evaluation and Rehabilitation Services (LADDERS), Massachusetts General Hospital, Boston, Massachusetts, United States of America
X Rebecca L. Mitchell, Affiliation: Genomic Medicine Institute, Cleveland Clinic, Cleveland, Ohio, United States of America
X Rebecca L. Kern, Affiliation: Department of Pediatrics, Johns Hopkins University Medical Center and Division of Metabolism, Kennedy Krieger Institute, Baltimore, Maryland, United States of America
X Marvin R. Natowicz mail * E-mail: [email protected]
Affiliations: Cleveland Clinic Lerner College of Medicine, Cleveland Clinic, Cleveland, Ohio, United States of America, Neurological Institute and Pediatrics Institute, Cleveland Clinic, Cleveland, Ohio, United States of America, Genomic Medicine Institute, Cleveland Clinic, Cleveland, Ohio, United States of America, Pathology and Laboratory Medicine Institute, Cleveland Clinic, Cleveland, Ohio, United States of America
Previous reports indicate an association between autism spectrum disorders (ASD) and disorders of mitochondrial oxidative phosphorylation. One study suggested that children with both diagnoses are clinically indistinguishable from children with idiopathic autism.
There are, however, no detailed analyses of the clinical and laboratory findings in a large cohort of these children. Therefore, we undertook a comprehensive review of patients with ASD and a mitochondrial disorder.
Methodology/Principal Findings
We reviewed medical records of 25 patients with a primary diagnosis of ASD by DSM-IV-TR criteria, later determined to have enzyme- or mutation-defined mitochondrial electron transport chain (ETC) dysfunction. Twenty-four of 25 patients had one or more major clinical abnormalities uncommon in idiopathic autism. Twenty-one patients had histories of significant non-neurological medical problems. Nineteen patients exhibited constitutional symptoms, especially excessive fatigability. Fifteen patients had abnormal neurological findings. Unusual developmental phenotypes included marked delay in early gross motor milestones (32%) and unusual patterns of regression (40%). Levels of blood lactate, plasma alanine, and serum ALT and/or AST were increased at least once in 76%, 36%, and 52% of patients, respectively. The most common ETC disorders were deficiencies of complex I (64%) and complex III (20%). Two patients had rare mtDNA mutations of likely pathogenicity.
Conclusions/Significance
Although all patients' initial diagnosis was idiopathic autism, careful clinical and biochemical assessment identified clinical findings that differentiated them from children with idiopathic autism. These and prior data suggest a disturbance of mitochondrial energy production as an underlying pathophysiological mechanism in a subset of individuals with autism.
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0003815
Posted by: Sarah | January 03, 2013 at 01:19 PM
We might be able to figure out what aluminum does compared to what mercury does now that the flu shots contain no aluminum just mercury
and
the rest of the vaccines have much more aluminum and less mercury.
Mercury I think is more immediate and faster
the aluminium is much more slower.
Just what I observed in my own family. Other than that -- just like arsenic - heavy metal poisoing acts about the same.
Posted by: Benedetta | January 03, 2013 at 11:49 AM