I wonder how they did this study?!!! Did they do a challenge with a chelator prior to testing?!!! If not the levels in the blood stream would be irrelevant since neurotypical children have an intact liver or at least less affect one... that is able to produce GLUTATHIONE...... the ASD kids are unable therefore it will go from blood to cells (where they will harm them even further!!!)...

Had to post this, and hope it's not too late to get some notice....I found a small article that stated the augmenting labor with pitocin reduced glutathione

http://www.hindawi.com/journals/ogi/2009/807659.html

The implications of this is enormous, yet another glutathione bomb destroyer, routinely done, and correlates with incidence and rise in autism...along with HEP B vaccines...which contain mercury!

All should go through the PPT slides of Dr Walsh please look at page 35 of his slide, in which he found NO mercury in the brain of autistics, rather, found high levels of iron, calcium, etc...the sex differences in those metals was interesting...boys have high iron, girls have high calcium. Look on your biomed tests, you may find almost all girls with autism have high calcium, sometimes boys, but not as much. Boys have low ferritin with high iron (freed and toxic). This is also found in other neurological disorders. Note he found NO autism in tissues, by PCR DNA. Could the mercury in fact be a hit and run event? Damages just the same, just doesn't stick around, but maybe it is only in bones at this point when we chelate? And maybe the effects of chelation is adding more antioxidants in the body? These things I would like to know more about?

Steve, go away. You are out of your depth here.

Let's do some more math here. Let's say in 1998 a two month old baby recived 62.5 mcg of mercury via 3 vaccinations (Hepatitis B, DTaP, and HIB) in one "stay well" visit. This was a pretty common combination. Now a two month old has about 0.5 liters of total blood. So, 62.5 mcg divided by 0.5 liter = 125 mcg/l. Ouch! That's a little bit more than, "the geometric mean for typically developing children of 0.28 mcg/L.

For what it's worth, I have just read a few texts on mercury poisoning and if there is anything definitive in the literature it is that the symptoms and outcomes are extremly dependent on the method, amount, and type of mercury involved. What this data shows is that it is unlikely that autistic children process the type of mercury they studied differently from the way no autistic children do. I think this is a legitimate conclusion to make from this data and while not a major conclusion, every new bit of data helps narrow down the picture. Instead of tearing it down, we can use it a step forward.

The lead author said
"Just as autism is complex, with great variation in severity and presentation, it is highly likely that its causes will be found to be equally complex. It's time to abandon the idea that a single 'smoking gun' will emerge to explain why so many children are developing autism. The evidence to date suggests that, without taking account of both genetic susceptibility and environmental factors, the story will remain incomplete. Few studies, however, are taking this kind of multi-faceted approach," Hertz-Picciotto said."

I don't understand the point of this study unless it was a first step in a series that goes on to investigate excretion after challenge. Not everything coming out of MIND is gold. Case in point, David Amaral.

There was nothing in our kids' direct blood levels. No one ever expected there to be. On challenge, the levels of mercury were through the roof along with dangerous levels of cadmium and lead. Excreted mercury levels matched severity of diagnosis and levels also matched what the earlier porphyrins predicted.

Furthermore, our son talked in sentences for the first time, potty trained himself, taught himself to whistle and assembled a construction kit designed for kids four to five years older than himself, all on the tenth round. I know that not all kids respond so dramatically to chelation but we all know some do. That should have been the study.

All kinds of reactions were out in emails following the latest study showing mercury levels are the same for autistic/non-autistic kids.

TWO RESPONSES ARE BELOW:
I've long asked to hear from any toxicologist willing to lay his or her reputation on the line defending the practice of injecting mercury into humans---especially pregnant womem and children. I've never heard about any who would do so. Paul Offit, Thomas Frieden, and Thomas Insel vouch for the safety of vaccines BUT THERE'S NEVER A TOXICOLOGIST SITTING BESIDE THEM BACKING UP THEIR CLAIMS.
Maybe this is why.....
This comment on the UC Davis study came from an autism mom who is an incredible researcher in her own right:
As maddening as this study is, it is much more an embarrassment. It exemplifies precisely why and how the mercury issue is being misunderstood. Anyone who truly knows mercury toxicity knows that it's not the blood you look at for an accurate body burden of it.

These kinds of studies always demonstrate what my brother, a med student at the time, told me when I sought out his help to try and help my daughter.

"I wish I could, but unfortunately, we don't take toxicology in medical school."

AND FROM OUR OWN BOYD HALEY:

In 1977 a report from a Toronto Hospital stated that 10 of 13 treated children (infected umbilical cords) died of mercury toxicity with the source being identified as topically applied thimerosal (in Merthiolate, a trade name of the topical antiseptic). Many adolescents were treated with this same Merthiolate without any noticeable toxicity. WHY? Because adolescents have a fully developed bilary transport system and infants do not. Mercury and other toxicants are removed from humans primarily through the bilary transport system and this is why infants are much more susceptible to most toxicants. This aspect is different from the “retention toxicity” but do keep this in mind.

Children who are exposed to levels of mercury that could be described as average can become ill if they are unable to excrete mercury effectively due and retain it in their cells. They will have little mercury detected in their blood or urine and will still be toxic. Children who are reasonable excretors will also become ill if exposed to excess mercury or a combination of mercury plus other toxic heavy metals like lead----but they will have mercury in their blood and urine.

It is never just the amount of anything that identifies the toxicity, it is the amount delivered plus the toxicity induced by that amount. Vaccines have toxic levels of thimerosal and it just shows the total ignorance of the medical community when they ignore this---especially of a toxin known to have retention toxic effects.

The bottom line is that it would be important to classify the age the child was exposed for any study. It would also be important to know the level of other toxic metals that act synergistically with mercury to induce higher toxicity. Finally, why doesn’t this reporting group (who seem to be adequately funded) do a study on vaccinated vs unvaccinated children?

Boyd E. Haley, PhD

Professor Emeritus

University of Kentucky

Chemistry Department

All, please take the time to view this hour length talk on how PR firms shape our mindsets on the hazards of our world. Deflection, change the subject, attention wondering, etc...this is a massive problem in todays society. Turn your TV off, and listen to this....

http://www.youtube.com/watch?v=UUY9ahSCMG0&feature=related

A couple of years ago I questioned a MIND Institute scientist regarding the Holmes/Blaxill/Haley baby hair study. There seemed to be a knowledge gap regarding brain-bound mercury and lack of excretion. Why this perseveration on blood levels from people who should know better?

Indian J Med Res. 2008 Oct;128(4):501-23
Heavy metal induced oxidative stress & its possible reversal by chelation therapy.Flora SJ, Mittal M, Mehta A.
Division of Pharmacology & Toxicology, Defence Research & Development Establishment, Gwalior, India.

Exposure to heavy metals is a common phenomenon due to their environmental pervasiveness. Metal intoxication particularly neurotoxicity, genotoxicity, or carcinogenicity is widely known. This review summarizes our current understanding about the mechanism by which metalloids or heavy metals (particularly arsenic, lead, cadmium and mercury) induce their toxic effects. The unifying factor in determining toxicity and carcinogenicity for all these metals is the generation of reactive oxygen and nitrogen species. The toxic manifestations of these metals are caused primarily due to imbalance between pro-oxidant and antioxidant homeostasis which is termed as oxidative stress. Besides these metals have high affinity for thiol groups containing enzymes and proteins, which are responsible for normal cellular defense mechanism. Long term exposure to these metals could lead to apoptosis. Signaling components affected by metals include growth factor receptors, G-proteins, MAP kinases and transcription factors. Chelation therapy with chelating agents like calcium disodium ethylenediamine tetra acetic acid (CaNa(2)EDTA), British Anti Lewisite (BAL), sodium 2,3-dimercaptopropane 1-sulfonate (DMPS), meso 2,3-dimercaptosuccinic acid (DMSA) etc., is considered to be the best known treatment against metal poisoning. Despite many years of research we are still far away from effective treatment against toxicity caused due to exposure to heavy metals/metalloids. The treatment with these chelating agents is compromised with number of serious side-effects. Studies show that supplementation of antioxidants along-with a chelating agent prove to be a better treatment regimen than monotherapy with chelating agents. This review attempts a comprehensive account of recent developments in the research on heavy metal poisoning particularly the role of oxidative stress/free radicals in the toxic manifestation, an update about the recent strategies for the treatment with chelating agents and a possible beneficial role of antioxidants supplementation to achieve the optimum effects. We have selected only arsenic, lead, mercury and cadmium for this article keeping in view current concerns and literature available.

Curr Top Med Chem. 2001 Dec;1(6):529-39. Links
Toxic metals and oxidative stress part I: mechanisms involved in metal-induced oxidative damage.Ercal N, Gurer-Orhan H, Aykin-Burns N.
University of Missouri-Rolla, Department of Chemistry, 65409-0010, USA. [email protected]

Toxic metals (lead, cadmium, mercury and arsenic) are widely found in our environment. Humans are exposed to these metals from numerous sources, including contaminated air, water, soil and food. Recent studies indicate that transition metals act as catalysts in the oxidative reactions of biological macromolecules therefore the toxicities associated with these metals might be due to oxidative tissue damage. Redox-active metals, such as iron, copper and chromium, undergo redox cycling whereas redox-inactive metals, such as lead, cadmium, mercury and others deplete cells' major antioxidants, particularly thiol-containing antioxidants and enzymes. Either redox-active or redox-inactive metals may cause an increase in production of reactive oxygen species (ROS) such as hydroxyl radical (HO.), superoxide radical (O2.-) or hydrogen peroxide (H2O2). Enhanced generation of ROS can overwhelm cells' intrinsic antioxidant defenses, and result in a condition known as "oxidative stress". Cells under oxidative stress display various dysfunctions due to lesions caused by ROS to lipids, proteins and DNA. Consequently, it is suggested that metal-induced oxidative stress in cells can be partially responsible for the toxic effects of heavy metals. Several studies are underway to determine the effect of antioxidant supplementation following heavy metal exposure. Data suggest that antioxidants may play an important role in abating some hazards of heavy metals. In order to prove the importance of using antioxidants in heavy metal poisoning, pertinent biochemical mechanisms for metal-induced oxidative stress should be reviewed.

For example in the case of mercury there are reports of this kind
Clin Pediatr (Phila). 2007 Nov;46(9):844-6. Epub 2007 Jul 19. Links
Mercury intoxication: lack of correlation between symptoms and levels.Gattineni J, Weiser S, Becker AM, Baum M.
Department of Pediatrics, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75235-9063, USA.

The incidence of mercury intoxication has decreased considerably because of stricter public health regulations. However, it has not been completely eliminated and should be considered in a child with unexplained tachycardia, hypertension, mood changes, weight loss, and acrodynia. Mercury intoxication can be difficult to differentiate from pheochromocytoma and Kawasaki's disease. Here, the authors report the case of an 8-year-old boy with history of mercury exposure, signs and symptoms suggestive of mercury intoxication, and good response to chelation therapy, but with only mild increase in urinary mercury levels. This case highlights the fact that urinary mercury levels do not necessarily correlate with the severity of clinical signs and symptoms of mercury intoxication.

Toxicology. 2007 May 20;234(3):145-56. Epub 2007 Mar 1.
The role of thiols, dithiols, nutritional factors and interacting ligands in the toxicology of mercury.Rooney JP.
Centre for Synthesis and Chemical Biology, Department of Pharmaceutical and Medicinal Chemistry, Royal College of Surgeons in Ireland, Dublin 2, Ireland.

Mercury has been a known as a toxic substance for centuries. Whilst the clinical features of acute mercury poisoning have been well described, chronic low dose exposure to mercury remains poorly characterised and its potential role in various chronic disease states remains controversial. Low molecular weight thiols, i.e. sulfhydryl containing molecules such as cysteine, are emerging as important factors in the transport and distribution of mercury throughout the body due to the phenomenon of "Molecular Mimicry" and its role in the molecular transport of mercury. Chelation agents such as the dithiols sodium 2,3-dimercaptopropanesulfate (DMPS) and meso-2,3-dimercaptosuccinic acid (DMSA) are the treatments of choice for mercury toxicity. Alpha-lipoic acid (ALA), a disulfide, and its metabolite dihydrolipoic acid (DHLA), a dithiol, have also been shown to have chelation properties when used in an appropriate manner. Whilst N-acetyl-cysteine (NAC) and glutathione (GSH) have been recommended in the treatment of mercury toxicity in the past, an examination of available evidence suggests these agents may in fact be counterproductive. Zinc and selenium have also been shown to exert protective effects against mercury toxicity, most likely mediated by induction of the metal binding proteins metallothionein and selenoprotein-P. Evidence suggests however that the co-administration of selenium and dithiol chelation agents during treatment may also be counter-productive. Finally, the issue of diagnostic testing for chronic, historical or low dose mercury poisoning is considered including an analysis of the influence of ligand interactions and nutritional factors upon the accuracy of "chelation challenge" tests.

To the best of my knowledge chelation therapy doesn't have the ability to bind to mercury that isn't in the blood. If you think otherwise, can you give me a link?

Hi Kathy
There are recent other studies on toxic elements in ASD
Biol Trace Elem Res. 2009 Aug 18. [Epub ahead of print] Links
Chromium, Cadmium, and Lead Levels in Urine of Children with Autism and Typically Developing Controls.Yorbik O, Kurt I, Haşimi A, Oztürk O.
Gülhane Military Medical Faculty Child Psychiatry Department, Etlik 06018, Ankara, Turkey,

Although potentially harmful effects of heavy metals are well known, limited numbers of studies exist regarding their relationship with autism. The aim of this study was to investigate urine levels of some heavy metals such as of chromium (Cr), cadmium (Cd), and lead (Pb) in children with autism and healthy subjects. Urine levels of Cr, Cd, and Pb were measured by atomic absorption spectrometry in 30 children with autism and compared with 20 healthy controls. Urine Cd and Pb levels were found as significantly decreased in children with autism compared to healthy subjects (p < 0.05). On the other hand, urine Cr levels were significantly higher in children with autism than healthy subjects (p < 0.05).

This study suggested that autism may be associated with significant decrease in excretion rate of Cd and Pb and a significant increase excretion rate in the levels of Cr in the urine. These results have indicated that further studies are warranted for investigation of possible roles of heavy metals in autism.

The abnormal metal (toxic and essential or oligoelements) metabolism should be the topic of research. As you say , not only one toxic element but several ( Al, Cd, Pb, As, Hg, etc) and not only toxic elements but essential ( Fe, Ca, Mg, Zn , Cu, etc) and oligoelements ( Se, V, Mo, etc).

Clin Biochem. 2009 Sep 23. Measurement of selected ions related to oxidative stress and energy metabolism in Saudi autistic children.El-Ansary A, Al-Daihan S, Al-Dbass A, Al-Ayadhi L.
Biochemistry Department, Science College, King Saud University, P.O Box 22452, Zip code 11495, Riyadh, Saudi Arabia.

OBJECTIVES:: Autism is a developmental disorder characterized by social and emotional deficits, language impairments and stereotyped behaviors that manifest in early postnatal life. This study aims to clarify the role of selected ions related to energy metabolism as a consequence of oxidative stress in the deterioration accompanied autism. MATERIALS AND METHODS:: Malonaldehyde as measure of lipid peroxidation, Na(+)/K(+) ion pump (ATPase), together with the concentrations of Na(+), K(+), Mg(2+), Ca(2+) and Pb(2+) were determined in plasma of 30 Saudi autistic patients and compared to 30 age-matching control samples. RESULTS:: The obtained data recorded that Saudi autistic patients have a remarkable higher activities of Na(+)/K(+) ATPase and high levels of lipid peroxidation compared to control. In addition, they have significantly elevated levels of K(+) and Pb(2+) while Ca(2+) recorded a significantly lower level compared to age-matching control subjects. On the other hand both Mg(2+) and Na(+) were non-significantly changed in autistic patients. CONCLUSION:: Alteration of the selected measured ions confirms that oxidative stress and defective mitochondrial energy production could represent the primary causative factor in the pathogenesis of autism.

The problems in the management of Ca+2 are known and published from time ago, such as those on Mg/Fe/Zn in selected sub-populations of ASD.

I thought blood levels of metals were not important. When we started chelation my child's blood test showed minimal lead and no other metals. Post chelation his urine showed extremely high lead, moderately high mercury aluminum and other metals. The point is the metals are sequestered in cells and not circulating in blood where they can be excreted.