Sunday, June 04, 2006

Effectiveness of Chelation Therapy

Nothing is known for certain about the effectiveness of Chelation Therapy as a treatment for autism. Jim Adams, a professor of chemistry at Arizona State University and parent of an autistic daughter, is conducting the first double blind, placebo controlled study on chelation. It's expected to be completed by the winter of 2006. The study was featured by Dateline on Sunday June 4, 2006.

Jim Adams is a DAN! doctor. But I trust that Dr. Adams will conduct this research in a proper manner, following all the rules required of a double-blind study. He's got a prior study on vitamin supplements, where he documents some significant improvement in gastrointestinal and sleep problems, but negligible improvement in autistic symptoms.

[Note: I just finished watching the Dateline segment. They used the "devastating" word and showed some kids who were said to be recovered from autism. It wasn't at all obvious that they were no longer autistic. And it wasn't at all obvious that they were severely affected before chelation. After watching Jim Adams, I'm sure many bloggers at Autism Hub would easily imagine why his daughter is autistic. I immediately thought of the fictional researcher from Apology from an autism researcher. His daughter is verbal and I wouldn't say she's "low functioning" from what little was shown. At this point it appears that Jim Adams is pretty close to the acceptance phase regarding his daughter. He's one of those parents who'd been told that he would have to institutionalize his daughter. Dateline did mention the CDC thimerosal studies, chelation deaths, and interviewed a researcher who said chelation is useless in autism.]

What should we expect of the chelation study? Probably nothing remarkable. In the past, Chelation Therapy has been touted as beneficial for a number of conditions, but placebo-controlled studies have failed to substantiate anecdotal accounts.

I will list some studies below. I'm only including studies that have a control group on placebo. Feel free to list any studies I've missed in the comments section.

Neurological & Behavioral Problems

Dietrich et al (2004) - Lead Exposure - Succimer
"Chelation therapy with succimer lowered average blood lead levels for 6 months but resulted in no benefit in cognitive, behavioral, and neuromotor endpoints... Chelation therapy with succimer cannot be recommended for children with blood lead levels between 20 and 44 µg/dL (0.96-2.12 µmol/L)."

Rogan et al (2001) - Lead Exposure - Succimer
"Treatment with succimer lowered blood lead levels but did not improve scores on tests of cognition, behavior, or neuropsychological function in children with blood lead levels below 45 microg per deciliter. Since succimer is as effective as any lead chelator currently available, chelation therapy is not indicated for children with these blood lead levels."

Liu et al (2002) - Lead Exposure - Succimer
"The improvement in scores in the placebo group only implies that factors other than declining blood lead levels per se are responsible for cognitive improvement; it is possible but less likely that succimer, the active drug, impairs cognition."

Arthur et al (1997) - Cerebral vasospasm in rabbits - Deferiprone
"The present study demonstrates that deferiprone is effective in attenuating experimental cerebral vasospasm. Because of its stability, lipophilicity, and ability to penetrate the blood-brain barrier, deferiprone represents an attractive candidate for the treatment of cerebral vasospasm."

Gordeuk et al (1992) - Coma due to cerebral malaria - Deferoxamine
"Iron chelation therapy may hasten the clearance of parasitemia and enhance recovery from deep coma in cerebral malaria."

McLachlan et al (1993) - Alzheimer's - Desferrioxamine
"The trivalent chelating agent desferrioxamine (DFO), 125 mg i.m. twice daily five days per week, was used in a randomized single-blind, oral lecithin, placebo-controlled clinical trial in 48 patients with AD... Analysis showed that the treatment and no-treatment groups were closely matched at entry into the trial but that the rate of decline, as measured by the VHB over 2 years of observation, was twice as rapid in the no-treatment group compared with the DFO-treated group."

Ziegler et al (2004) - Diabetic Polyneuropathy - ALA
"The results of this meta-analysis provide evidence that treatment with alpha-lipoic acid (600 mg/day i.v.) over 3 weeks is safe and significantly improves both positive neuropathic symptoms and neuropathic deficits to a clinically meaningful degree in diabetic patients with symptomatic polyneuropathy."


Peterson et al (2004) - Growth - Succimer
"Although succimer lowers blood lead in moderately lead-poisoned children, it does not have a beneficial effect on growth and may have an adverse effect."

Lasky et al (2001) - Growth in Reshus Monkeys - Succimer
"Growth in weight, length, and head circumference did not vary significantly as a function of blood lead levels. Succimer chelation therapy did not significantly affect weight, length, or head circumference through 2 years of age."


Lasky et al (2001) - Auditory Function in Reshus Monkeys - Succimer
"Finally, the auditory evoked response at levels from the auditory nerve to the cerebral cortex did not significantly differ as a function of succimer treatment."

Apparent Heavy Metal Toxicity

Grandjean et al (1997) - Symptoms Attributed to Amalgam Fillings - Succimer
"Immediately after the treatment and 5 to 6 weeks later, most distress dimensions had improved considerably, but there was no difference between the succimer and placebo groups. These findings suggest that some patients with environmental illness may substantially benefit from placebo."

Sandborgh Englund et al (1994) - Alleged Mercury Poisoning - Succimer
"No treatment effect of DMSA was apparent on subjective symptoms and mood state. One statistically significant treatment effect was noted - a decrease in fatigue-inertia in the DMSA-group - but there was no demonstrable correlation with increased urinary excretion or decreased blood concentration of mercury. Three subjects showed hypersensitive reactions, probably DMSA-specific, at the end of the treatment period. This placebo-controlled study provides no scientific support for diagnostic or therapeutic administration of DMSA for symptoms allegedly associated with chronic mercury exposition from dental amalgam fillings."

True Heavy Metal Toxicity

O'Connor & Rich (1999) - Lead Poisoning - Succimer
"All children with BPb, in the range studied here, should receive environmental evaluation and remediation; DMSA does not improve long-term blood lead levels."

Mazumder et al (2001) - Arsenic Poisoning - 2,3-Dimercapto-1-propanesulfonate
"3-Dimercapto-1-propanesulfonate treatment caused significant improvement in the clinical score of patients suffering from chronic arsenic toxicity. Increased urinary excretion of arsenic during the period of therapy is the possible cause of this improvement."

Cardiovascular Disease

van Rij et al (1994) - Intermittent claudication - EDTA
"Multiple reports of excellent results in large numbers of patients have encouraged the use of this regimen... CONCLUSIONS: Chelation therapy has no significant beneficial effects over placebo in patients with intermittent claudication."

Knudtson et al (2002) - Ischemic Heart Disease - EDTA
"There is no evidence to support a beneficial effect of chelation therapy in patients with ischemic heart disease, stable angina, and a positive treadmill test for ischemia."

Chen et al (2006) - Blood Pressure - Succimer
"Overall, there is no association between blood lead and blood pressure in these children with moderately high lead exposure, nor does chelation with succimer change blood pressure."


Chelation therapy is somewhat effective in the treatment of true heavy metal toxicity, but does not appear to have discernible effects in cases of minor exposure (as would be the case with Pica) or after significant time passes following exposure.

Iron chelation (with agents specific for this purpose) seems to be beneficial in Cerebral vasospasm and in Coma due to cerebral malaria. But these conditions result in severe neurological damage that can ultimately cause death, and they are not caused by iron poisoning.

Padhye (2003) hypothesizes that "excess dietary iron is the root cause for increase in childhood autism and allergies." But this hypothesis appears to be falsified by Latif et al (2002) which found a high prevalence of iron deficiency in autistic children. Chelating iron out of autistic children does not seem advisable.

There's a finding of interest about Alzheimer's and chelation of aluminum, but it was a single-blind study that apparently has not been replicated.

Alpha Lipoic Acid (ALA), an anti-oxidant which is also used as a mercury chelating agent, appears to be helpful in diabetic neuropathy. This leads me to wonder if ALA could be treating peripheral neuropathy induced by excessive vitamin B6 supplementation.

In general, prior chelation studies in combination with prior placebo-controlled autism studies suggest that anecdotal accounts of improvement need to be taken with a grain of salt. There is no good reason to suppose that Dr. Adams will find anything of significance regarding chelation therapy and autism, particularly given what is known about autism in regards to heritability, neurobiology and cognition. Even if Dr. Adams does find a positive correlation, this would not necessarily implicate mercury, thimerosal or poisoning for that matter.

It does not appear advisable to try chelation at the moment "just in case" considering its potential adverse effects. And I do hope Dr. Adams documents negative placebo effects and adverse effects in his study.

Further Reading

- Green, Saul. Chelation Therapy: Unproven Claims and Unsound Theories. Quackwatch.

- Laidler, James. Can Chelation Help Autism?. Reproduced with permission at Neurodiversity weblog.

- AP. Boy With Autism Dies After Chelation Therapy. MSNBC.

- Leitch, Kevin. Chelation: Dangerous & Experimental. Left Brain/Right Brain Blog.

- DeNoon, Daniel. Experts: Chelation Therapy Not Worth the Risk. MedScape Today.


  1. Thanks for gathering all this together. Chelation seems to be a treatment used for so many different ailments that I wonder at its specific efficacy for certain "symptoms" of autism.

  2. Hi Joseph
    I think that the first step to clarify the issue is to find a trustable and complete way to detect/discard HM poisoning in autistic people.
    If you are interested I can post some studies about detection- by the combination of different tests- HM poisoning following available literature (excluding challenge tests). I think that in this field the research and the current knowledge is incomplete.Please let me know.
    María Luján

  3. Joe;
    You forgot to include "Amalgam Illness" by Andrew Hall Cutler in your suggested reading. If you want to seem credible, you should include protocols that actually work.

  4. Hi Kristina,

    Chelation seems to be a treatment used for so many different ailments that I wonder at its specific efficacy for certain "symptoms" of autism.

    I doubt even that will be the case. It's possible some things used as chelating agents, like ALA, might be helpful for reasons other than chelation of heavy metals. But this study is using DMSA (Succimer).

    I was thinking that because developmentally delayed kids tend to have Pica, a positive correlation might be found. But the Succimer studies on lead exposed children have not yielded results.

  5. Hi María,

    I think that the first step to clarify the issue is to find a trustable and complete way to detect/discard HM poisoning in autistic people.

    Is it different with autistic people?

    If you are interested I can post some studies about detection- by the combination of different tests- HM poisoning following available literature (excluding challenge tests).

    Go ahead. (I prefer if they are hyperlinks as opposed to URLs).

  6. Fore Sam:

    You forgot to include "Amalgam Illness" by Andrew Hall Cutler in your suggested reading.

    I only listed studies that have a placebo-controlled group. I did post a study on alleged mercury poisoning due to dental amalgams. You're welcome to post a link.

  7. I forgot to mention that Dateline goofed up their prevalence numbers. I heard 1 in 100,000 in the 1980s. I'm sure they wanted to say 1 in 10,000, which is what Generation Rescue claims. The earliest data I've found is Wing (1976) which documented a prevalence of 4-5 in 10,000. Once you note that this was a prevalence of Kanner autism, and the current prevalence of 60 in 10,000 refers to ASD (DSM-IV autistic disorder, PDD-NOS and Asperger's syndrome) the increase claim is not so impressive anymore.

  8. I missed Dateline, so I appreciate your comments. I missed it because we went to see the latest X-Men movie.

    All the time I was watching this movie about mutants with a possible cure... I could not help think about the "cure autism" discussions I have read on the Autism Hub.

  9. The transcript of the segment is here.

    At one point Jim Adams is quoted as saying:

    "There have been a number of epidemiology studies looking at [thimerosal], Some showing absolutely no link, some showing a very strong link."

    At first I thought, which studies show a very strong link? But then I remembered Geier & Geier. I'm sure that's what he's talking about. Are there any others? In other words, studies that claim VAERS can be used as an indication of the prevalence of autism; studies where it's claimed that incidence can be calculated by substracting administrative caseload one quarter minus that of the previous quarter; and studies that use prevalence by birth year cohort as fixed numbers.

    Jim Adams apparently likes to compare oranges with rotten apples.

  10. Regarding Prevalence the earliest study cited by Wing is Lotter, V. (1966). Epidemiology of autistic conditions in young children: I. Prevalence. Social Psychiatry, 1, 124-137 which gave a finding of 4.5:10000. This was for Kanner's autism using these two defining criteria
    1. a profound lack of affective contact
    2. repetitive, ritualistic behaviour, which must be of an elaborate kind.

  11. Thanks for that info, Mike.

    I think someone should do a prevalence study on autism using Kanner's criteria; you know, just to settle the issue.

  12. I have Wing's study as a word doc if you want it.

  13. Hi Joseph
    I tried to post with hyperlinks but the web says that tag is not allowed. Can I e-mail to you?
    Ma Luján

  14. Hi Joseph

    I think you pointed out to the discussion several key points, when you answer to me my prompt

    I think that the first step to clarify the issue is to find a trustable and complete way to detect/discard HM poisoning in autistic people.

    Is it different with autistic people?

    I think we must go back to this point, before to go to the discussion of the tests, and less to the discussion of the chelation treatment, that IMHO, must be based on appropiate tests.

    Therefore the questions are

    1-Are autistic people different as population in terms of HM susceptibility to poisoning, based on genetics-epigenetics-proteomics-metabolomics? Are there any evidence of bioaccumulation of HM in autistic people?

    2-What are the appropiate tests to detect HM poisoning in this subgroup of autistic people?

    I will begin with the first because I think that the second is related to the first. If the autistic people are different in the management of xenobiotics, tests must be different and “common tests” are not trustable or give no information. If bioaccumulation in tissues is possible-because of lack of excretion-, no common tests in blood, urine, fecal or hair would provide evidence at least at the best of the published literature in the topic, after the initial exposure.

    First, no complete study on the issue of HM genetic susceptibility/predisposition to bioaccumulation because of metabolic disruption in metal transport/excretion in autistics is available today (even when some metabolic studies on some biomarkers-such as glutathione and the pathway of gluthathione transferase and other enzymes are available-but are partial). Therefore I consider these studies on genetic susceptibility in the general population and autistic people almost not done yet. If we think in ASD as a genetic predisposition distributed in the general population and see the interaction with the environment as important, the importance of some key polymorphisms in the HM management can give clues to look at in ASD people.
    To give some insight to this question 1- that I consider is far from being solved from the published available science, I will present some studies about some polymorphisms in general population that have been detected that would be important to study in ASD vs controls to evaluate importance-beyond the ApoE that has been published with contradictory results.

    Transport of toxic metals by molecular mimicry
    points the importance of transport of toxic metals

    Transporters of divalent cations

    -DCT1 (divalent cation transporter-1; also known as NRAMP2 or DMT1) is considered to be a major cellular uptake mechanism for Fe(2+) and other essential divalent metals, but this protein also mediates uptake of Cd(2+), Pb(2+), and possibly of other toxic divalent metals (Hg+2 ??)

    -the apically located MRP2 (multidrug resistance-associated protein 2) transporter, a member of the adenosine triphosphate-binding cassette protein superfamily.

    Personally it intrigues to me the nature of the heavy metals considered as insults in autism:
    -Hg, Pb, Cd ( all of them with the possibility of +2 oxidation state in inorganic form)
    -Al , that presents the +3 oxidation state

    Adverse reactions after injection of adsorbed diphtheria-pertussis-tetanus (DPT) vaccine are not due only to pertussis organisms or pertussis components in the vaccine

    Nielsen AO, et al. [Aluminum allergy caused by DTP vaccine]. Ugeskr Laeger. 1992 Jun 29;154(27):1900-1. Danish.

    -As, that also has available the +3 oxidation state and others. Arsenite (As+3) compounds are lipid soluble. Within 24 hours of absorption, arsenic distributes over the body, where it bind to the SH groups of tissue proteins. As can replace phosphorus in bones (from Textbook of modernToxicology Hogdson)

    “We know that the toxicity of arsenic is dependent on its oxidation state, chemical form and solubility in the biological media and that the scale of toxicity decreases in the order: arsine > inorganic As(III) > organic As(III) > inorganic As(V) > organic As(V) > arsonium compounds and elemental arsenic. We also know that the toxicity of As(III) is about ten times that of AS(V) “

    -Ni, Cu (both of them have +2 as oxidation state available)

    Main elements in the body are present as +2 (Mg, Ca and Zn). Molecular mimicry is worrisome in these circunstances, as a possibility, with the potential of disruption of Ca channels and Zn ”fingers”,beyond a lot of enzymes and metabolic paths involving Mg.

    Transport of toxic metals by molecular mimicry
    points the importance of transport of toxic metals

    Heavy metals can have impact in the regulation of genes

    Transcriptional regulation of the NAD(P)H:quinone oxidoreductase 1 and glutathione S-transferase ya genes by mercury, lead, and copper.

    Transporters can be cationic or anionic

    Research on Metal transport

    Identification of polymorphisms in the promoter region of the human NRF2 gene..

    Polymorphisms in xenobiotic metabolism genes and autism.

    “We performed family-based association studies of polymorphisms in metal-regulatory transcription factor 1(MTF1), a multispecific organic anion transporter (ABCC1), proton-coupled divalent metal ion transporters (SLC11A3 and SLC11A2), paraoxonase 1 (PON1), and glutathione S-transferase (GSTP1) genes in 196 autistic disorder families. There was deviation from the expected pattern of transmission for polymorphisms in MTF1 (Single nucleotide polymorphism database reference identification number, dbSNP rs3790625, P = .02) and divalent metal ion transporter SLC11A3 (dbSNP rs2304704, P = .07) genes. Although these results might represent chance finding, further investigations of genetic variations of metal metabolism in autism are warranted.”

    The possibility of chance finding must be analyzed with care

    Chronic low-level mercury exposure, BDNF polymorphism, and associations with cognitive and motor function..

    Chronic low-level mercury exposure, BDNF polymorphism, and associations self-reported symptoms and mood..

    Mutation screen of the brain derived neurotrophic factor gene (BDNF): identification of several genetic variants and association studies in patients with obesity, eating disorders, and attention-deficit/hyperactivity disorder..

    DMT1: which metals does it transport?

    Phenotypic variation in xenobiotic metabolism and adverse environmental response: focus on sulfur-dependent detoxification pathways.

    The association between a genetic polymorphism of coproporphyrinogen oxidase, dental mercury exposure and neurobehavioral response in humans.

    A cascade analysis of the interaction of mercury and coproporphyrinogen oxidase (CPOX) polymorphism on the heme biosynthetic pathway and porphyrin production.

    Therefore it seems that GMST1, BDNF, CPOX, SLC11A3 and SLC11A2, (ABCC1), (PON1), 1(MTF1) DCT1 would be important to study, considering the anecdotic evidence for science of HM poisoning in autism ( including Hg). Basically, focusing in the xenobiotics metabolism and divalent metal transport, including the aminoacid transport system, I think that some further clues would be provided if a coherent, highly scientific and prudent approach is done. Selective inhibition of BLM carriers implicated the involvement of organic anion transporter(s) (Oat1 and/or Oat3; Slc22a6 and Slc22a8), amino acid transporter system ASC (Slc7a10), the dibasic amino acid transporter (Slc3a1), and the sodium-dicarboxylate carrier (SDCT2 or NADC3; Slc13a3). After this knowledge about the how the bioaccumulation can / is taking place (if any) in a subgroup of ASD children, THEREFORE the best tests to detect can be planned and diagnostic/test research can be designed to confirm HM poisoning.
    For example

    Analysis of case-parent trios at a locus with a deletion allele: association of GSTM1 with autism

    High levels of homocysteine and low serum paraoxonase 1 arylesterase activity in children with autism

    Mercuric conjugates of cysteine are transported by the amino acid transporter system b(0,+): implications of molecular mimicry.

    Linkage and association of the mitochondrial aspartate/glutamate carrier SLC25A12 gene with autism.

    Plasma amino acids profiles in children with autism: potential risk of nutritional deficiencies. .

    Plasma amino acid levels in children with autism and their families. .

    Imbalance of plasma amino acids in patients with autism and subjects with attention deficit/hyperactivity disorder .

    Low serum tryptophan to large neutral amino acids ratio in idiopathic infantile autism. .

    Serotonin and amino acid content in platelets of autistic children.

    If we consider that in some group of autistic people it has been published that
    1- there are problems with proteins metabolism/aminoacids, with some published evidence of defficiency in essential and non-essential aminoacids
    2- there are problems with the enzymes ( concentration and activities), cofactors and regulations of the xenobiotics management from glutathione conjugates , cytochromes , phase I and Phase II of the liver and the excretion as mercapturic acid conjugates (as I posted before) – GSH, GSMT (recently published a positive correlation with ASD, etc)
    I think that we need lot more research than current on these issues in ASD.

    Some thoughts and questions

    1-If aminoacids transporter system is involved, diet/nutrition/biochemistry can be important in the management of HM-and Al- (in terms of digestion/proteins/peptides/aminoacids), especially if GI issues are involved
    2-Adequate test of metabolites or biomarkers of disrupted detox system of xenobiotics would allow a better understanding of the issue.
    3-Adequate levels of aminoacids could be important in this role (methionine levels).
    How would exclusion diet affect the protein/polypeptides/aminaocids balances. IF digestive enzymes are disrupted, what about gluten and casein exclusion and effect in aminoacids balance in the body-without the supposed disruption of peptides as interfirients, if adequate testing for leaky gut is present?
    And how these diets (such as GFCF diet) would affect the HM transport in the body (levels of HM in blood, urine, fecal stool) in ASD during diet related to food allergies- celiac disease and milk allergy for example- that are related to protein/polypeptides management and immune answers to them if ALSO leaky gut is present?

    Again, with this picture I can not say that the management of xenobiotics is similar in autistics than in non autistics because there are no complete published studies about, but there are a lot of clues that are pointing that the answer is no. How, when and why is another history. The lack of published research in these fields is almost total today.

    Finally, in this point, I have more questions than answers (and a lot of anecdotic information for science that has not been adequately analyzed and systematically organized and considered). I think that asking for further research in the issue is the right thing to do, considering the medical research for population of ASD. Meanwhile, many of us must deal with the lack of consideration –only anecdotes- and knowledge about our personal and individual experiences and do the best we can.

    BTW, thank you for the link to the hyper link. It was a problem of reordering of the URLs to make them fit correctly in the sentence.

    María Luján

  15. Sure María. You have my address. (Blogger should allow b, i and a tags).

  16. Hi Joseph
    Although the links were shown when I included them, in the page the links do not work. Sorry
    María Luján

  17. María,

    I think some line breaks got in your URLs. Sorry for not answering right now. It's a lot of information.

  18. I happened to come across an article by Wing where she discusses the early prevalence study Mike commented on:

    "One of us (LW) was involved in the planning of the study by Vic Lotter of 78,000 children aged 8, 9, and 10 years living in the former English county of Middlesex. This was the study in which the 4-5 in 10,000 prevalence rate was first found. I (LW) know what sorts of children were included as classically autistic because I was one of the small group (Neil O'Connor, John Wing, Vic Lotter and myself) who decided on the criteria. In those days we were interested only in really classic Kanner's syndrome and Vic was determined to keep the criteria as narrow as possible. Later, in the Camberwell study described above, Vic was shown case histories of the children Judy Gould and I thought fitted Kanner's descriptions - to our surprise, Vic said we ought to exclude some because they were not classic enough! I think it is fair to say that, when Vic specified narrow criteria, they were NARROW.

    When Judy Gould and I started the Camberwell study, we still thought that Kanner's autism could easily be differentiated from other developmental disorders.. By the end of the study our ideas had been turned upside down. We had learnt from direct experience that the psychological dysfunctions underlying autism were manifested in many different ways, far beyond the boundaries of Kanner's syndrome. We developed the hypothesis of an autistic spectrum based on the triad of impairments of social interaction, communication and imagination. Because we concentrated on the children with learning disabilities (IQ under 70) we saw very few with the pattern described by Asperger. We had to wait for the study by Christopher Gillberg in Gothenberg to find out how many children with IQ of 70 and above were also in the autistic spectrum. As described above, combining the results of these two studies gave an overall prevalence rate for the whole autistic spectrum, including those with the most subtle manifestations, of 91 per 10,000 - nearly 1% of the general population."

    There you have it: 91 in 10,000 for the whole autism spectrum. As I've said before, I think it's about 150 in 10,000 if you count those who might escape a diagnosis for various reasons, such as being too high functioning.

  19. Re Dateline and hype, I came across a precedent:

    "In 1998, a case series (1) and television program (NBC Dateline) described children whose symptoms of autism improved remarkably after secretin infusion for a gastrointestinal procedure. These and other testimonials sparked a huge demand for off-label secretin use."

  20. for regular (and supportive) reports on chelation check the issues from the nineties (a voice for eco-agriculture).

    Now that I am passing out tips, may as mention a maverick sociologist of autism: Andrew Lehman, reviewed here: review of

  21. My son was diagnosed in september of '05 with low functioning autism, we were reluctant to try chelation because of fear. We had several blood tests for heavy metals all came back as within normal range, now he's 5 yrs old and we got him a urine test which came back with aluminum exceeding 5x the upper expected limit, lead and tin 3x and cadmium twice the upper expected limit. He was diagnosed in june of '09 with severe mental retardation. Now after 6 months of chelation he is gaining skills rapidly after years of regression. We did not start chelation because he has autism, but because he is heavy metal poisoned. He used to have a lot of pica as a baby which I am assuming caused the toxicity. We don't expect him to be "cured" but he is definitely recovering. There will be lasting brain damage but my point is that the symptoms of heavy metal poisoning are often mistaken for autism and I am sure there are many more children like my son out there. We noticed positive results from the very first round of chelation that's why we are continuing until he no longer has elevated metals in his urine, then he will be a candidate for hyperbaric oxygen therapy to try to repair some of the pathways destroyed by these metals. Some children need chelation autism diagnosis or not!

  22. @Anon: You should note that aluminum is not a heavy metal. Aluminum is the most abundant metal on the surface of Earth and it's commonly found in food. Now, you didn't say which lab you used. I'm assuming that was provoked testing.

    I'm glad to hear your child is gaining skills.

  23. "then he will be a candidate for hyperbaric oxygen therapy to try to repair some of the pathways destroyed by these metals."

    I don't know who told you that pathways in the brain can be 'repaired' when the nerve tracts have been destroyed... they can't. When brain tissue is destroyed, it stays destroyed. Any learning that has been done by the making of neural connections between those tracts of nerve tissue and others in the brain is lost or corrupted and has to be re-learned.

    "There will be lasting brain damage but my point is that the symptoms of heavy metal poisoning are often mistaken for autism and I am sure there are many more children like my son out there."

    I wish you could see how incorrect what you've been told about this actually is: there may be some lunatic practitioners who will tell you that they are often confused one for the other, but the signs of autistic development are radically different from the signs and symptoms of heavy metal poisoning. Any competent diagnostician would have no problem making the distinction between them. The ones who most often mistake these issues for each other are the DAN! practitioners, in whose best interests it is to do so - they get to profit from it.

    As Joseph is, so I am also glad that you child is gaining skills. It should be noted, however, that even children diagnosed as low-functioning can begin to quite quickly acquire skills... so skill acquisition is not a reliable indicator of chelation "working".

    Also, if - as Joseph suspects - the blood-work was based on a provocation test, it should be pointed out here that such testing is not (based on the available scientific evidence) reliable as a means of confirming a diagnosis of heavy metal toxiaemia.

    Regarding "LFA" and severe mental retardation as diagnoses... no clinician can actually diagnose "LFA" (as opposed to any other functioning-level of autism) since these labels are not specified in the diagnostic manuals. A diagnosis of severe mental retardation requires an intellectual assessment result of 20-34 as well as evidence of severe problems in two or more areas of adaptive behaviour (such as self-help/daily-living skills, communication skills or social skills). There is, on this basis alone, a chance that misdiagnosis could be made, particularly by an inexperienced diagnostician... which is why a good one will use structured interviews for this purpose. If, however, there was any sort of regression involved, and you state that there was such, then a diagnosis of mental retardation would be incorrect in any case, since it does not explain the situation better than other diagnoses might (such as, for example) Heller's syndrome, which definitely does involve a loss of skills. And if the Heller diagnosis were to explain best the situation, then the autism diagnosis would also be incorrect. And in regressive cases, Heller's syndrome is really the more appropriate diagnosis to be made.

  24. Also, if - as Joseph suspects - the blood-work was based on a provocation test, it should be pointed out here that such testing is not (based on the available scientific evidence) reliable as a means of confirming a diagnosis of heavy metal toxiaemia.

    You're being generous, David. Those sorts of tests are better described as a scam.

  25. Of course, Joseph... you are absolutely correct: they are a scam. I merely state why ;)

    And now ... to bed. Up early in the morning - travelling halfway across southern Finland to lecture for half an hour to a bunch of interested people at the Newlands Disability Services Foundation, one of the more progressive organisations in Finland.