Is DMSA safe and effective?
November 26th, 2009
Yes!
For lead poisoning.
And probably as a treatment for mercury and cadmium poisoning (but not for assessing the body burden of mercury).
And possibly as a treatment for arsenic and antimony poisoning.
But as a treatment for autism, it hasn’t been shown to be either effective or safe, despite the titles of two articles (or one two-part article) in BMC Clinical Pharmacology.
These two articles, published by a diverse group of authors - including Professor of Materials Science and Engineering James B. Adams, PhD (lead author), DAN! practitioner Jeff Bradstreet, MD and Professor of Pediatrics and Section Chief of Pediatric Allergy, Immunology and Rheumatology, Jane El-Dahr, MD - are titled:
Strangely enough, given that the lead author is on the faculty of Arizona State University and the “anchor” author is on the faculty of Tulane University, the study was done under the auspices (and approved by the IRB of) Southwest College of Naturopathic Medicine - which Dr. Adams lists as his academic affiliation in these articles.
Curious.
It’s almost as though they couldn’t get a real university IRB to approve their study. After all, Tulane University has an IRB, and so does Arizona State University, but they decided to go with the IRB at a naturopathic college, instead.
Again, that’s curious.
But that’s not the last curious thing about these studies. In fact, the next curiousity about these studies is the very…..eccentric nature of the study design.
Let me start by outlining the odd and circuitous path of their enquiry into the safety and efficacy of DMSA as a treatment for autism.
Perhaps it is the writing style or maybe it is the chaotic nature of their research showing through in the articles, but it is very hard to track exactly how many subjects were in each of the several “phases” and sub-phases of this study. Here is what I could extract from their writing:
The study began with 82 autistic children, ages 3 - 8 years, who underwent a physical examination, blood tests for kidney and liver function, blood counts, and red blood cell (RBC) glutathione. If the examination and blood tests (with the exception of RBC glutathione) were within normal range (the article uses the phrase “not below the normal range” - curious), they were “eleigible to participate in Phase 1″.
Each parent filled out an initial Autism Treatment Evaluation Checklist (ATEC - a test devised by Drs. Rimland and Edelson and never properly validated) and a “Heavy Metal Exposure Questionnaire”. The parents also collected a “baseline first-morning urine sample” - for “heavy metal testing”. (three guesses which lab did the testing)
Here’s where it gets weird: the next step was to randomly divide the subjects into two groups. One group got a glutathione-containing skin lotion (to be applied once a day for a week) and the other group got a placebo lotion. At this point, I found myself asking, “What’s up with the lotion? Who’s selling the glutathione lotion?“, because this meant that - at best - their results would be much harder to interpret.
Further complicating the study, they had every subject receive a single “round” of oral DMSA (10 mg/kg/dose, three doses a day for three days - nine doses in total) to test their “heavy metal excretion” (and here I thought that autistic children were “poor excretors”). Only those subjects who had post-chelation urine “toxic metals” (as defined by “Doctor’s Data Laboratories” - aluminium, antimony, arsenic, beryllium, bismuth, cadmium, lead, mercury, nickel, platinum, thallium, thorium, tin and tungsten) greater than the 95th percentile (for people who had not received a chelating agent) continued on to “Phase 2″. (see: Mercurial Laboratories for a more in-depth discussion)
Amazingly, eight (8) children had all of their “toxic metals” below the 95th percentile even after chelation. This deserves to be a published result on its own! In all, 17 subjects failed to complete “Phase 1″ (testing, glutathione lotion and one “round” of DMSA), leaving only 65 (79%) to move on to “Phase 2″.
In “Phase 2″, the subjects who had recieved the glutathione lotion were scheduled to receive oral DMSA and those who had received the “placebo” lotion received a placebo capsule. This was to go on for an additional 6 “rounds”, each “round” consisting of three days of 30 mg/kg DMSA (divided into three doses) followed by eleven days of no treatment. The article is a bit confusing about this, saying that the subjects took the DMSA or placebo for “…up to 3 rounds” in one place and a few paragraphs later saying that “When the participants finished Phase 2 (after either 3 or 6 rounds)…” The reason for this is that urine testing was done after the second “round” of DMSA in Phase 2 (third “round” total) and those who were not continuing to excrete elevated levels of “toxic metals” after three “rounds” of DMSA were considered to have completed Phase 2. Why some had an additional “round” after this testing is unclear.
Before entering Phase 2, the 65 remaining subjects underwent further blood tests and also had the ADOS administered. The ADOS testing found that 7% of those who completed Phase 2 did not meet the criteria for Autistic Spectrum Disorder - we are not told how many of those entering Phase 2 failed to meet criteria. The authors did not seem particularly bothered by the fact that 7% of their subjects were apparently not autistic or on the “autistic spectrum” - they explained this away by stating that “All children continued on in the study, since they all had a previous clinical diagnosis of ASD.” [emphasis added]
In addition to the ADOS, the parents filled out the Pervasive Developmental Disorders - Behavior Inventory (PDD-BI - a screening test evaluated only by its originators) and the Severity of Autism Scale (SAS - a test developed by the authors and not validated).
Following completion of Phase 2, the 41 remaining subjects (50% of starting subjects) underwent repeat blood testing and an ADOS evaluation. The parents filled out the ATEC, PDD-BI and SAS questionnaires again, as well as a Parental Global Impression (PGI - a new test not yet validated) questionnaire.
Let’s recap the study so far:
The study consisted of three arms:
[1] Subjects who received placebo lotion and one “round” of DMSA - 15 subjects.
[2] Subjects who received glutathione lotion and three or four “rounds” of DMSA. It appears that five subjects were in this group - it remains unclear why some had three and some had four.
[3] Subjects who recieved glutathione lotion and seven “rounds” of DMSA - 21 subjects.
The testing consisted of RBC glutathione, complete blood counts, liver function tests, renal function tests, and urinary “toxic” and “essential” metal excretion as well as the ATEC (an un-validated test), PDD-BI (a screening test), the SAS (an unvalidated test), the PGI (new and unvalidated) and the ADOS (validated for autism diagnosis, but not severity rating).
The problems with this study are legion, but their results were the most damning part of the whole mess, because the results don’t say what the authors think they do.
Behavioral Testing:
In the behavioral testing, only the ADOS (which - as I mentioned before - is not valid for comparing autism severity) showed any diffrerence between the “got one round of DMSA and placebo lotion” and “got three to seven rounds of DMSA and glutathione lotion” groups. The other tests showed no statistically significant difference. Of course, the authors try to spin that as best they can, but the results speak for themselves.
Safety Testing:
DMSA’s safety was studied long before than this study, and its side effects are well known: reduction of white cell count (generally reversible), reduction in platelet count (generally reversible), liver injury (generally reversible) and some subtle decrease in intellectual function when given to children (and rats) with low (or zero) lead levels (not reversible).
The “safety testing” in these articles, strangely enough, did not include measures of the most significant (and the only irreversible) side effect that has been noted with DMSA, namely cognitive/intellectual functions (see: Dietrich et al and Stangle et al). Thus, in a supreme moment of irony, the authors have done exactly what some of them have long claimed that “the government” has done - failed to research the correct mode of toxicity.
The authors (and many, many other practitioners) are giving DMSA to children with low levels of heavy metals - exactly the group found to be at risk for permanent intellectual impairment. Yet they do no intellectual testing. They could have gone to Dietrich et al and read it right out of their paper, yet they didn’t.
Curious.
Biochemical Effects:
This area, which the authors call “Medical Effects” has the most bizarre results ever. Rather than spend the next year discussing them all, I’ll give my “highlights”:
[1] “Toxic metal” excretion.
Not surprisingly, lead excretion was up significantly - this is what DMSA does. However, in a major upset for the autism-is-mercury-poisoning hard-core, mercury excretion was fifth, after tin (?), bismuth (??) and uranium (????). Who knew that autistic children were so heavily contaminated with uranium? There was even more thallium excreted than mercury, over the inital “round” of DMSA administration.
While lead is still ubiquitous in urban areas - a legacy of decades of tetraethyl lead in gasoline, where are these children getting their exposure to tin, bismuth and uranium? Or is this yet another problem with the laboratory? The authors make a brave stab at explaining how their results differ from an earlier Bradstreet “study”, but it doesn’t really work too well.
[2] “Essential metal” excretion:
Several studies have looked at “essential mineral” excretion with DMSA administration - most have found that DMSA increases the excretion of zinc and copper to a minor degree. However, Adams et al found that potassium and chromium were the most significant losses during DMSA treatment.
Part of this comes from their…..eccentric way of looking at “essential mineral” losses as a percent of the RDA. This artificially elevates the “significance” of micronutrients like chromium (children in this age range should have about 15 micrograms a day).
The major problem with their analysis of this section is that they appear to have no idea how these elements get into the urine. Potassium, for example, is found in almost all foods and the urinary levels will fluctuate depending on how much there is in the diet and how much the body needs. DMSA has no effect on an alkali metal ion like potassium and the authors’ discussion makes it appear that their knowledge of basic physiology and biochemistry is inadequate.
[3] RBC glutathione:
This is a bit harder to interpret for a number of reasons. First off, the mean RBC glutathione doesn’t change significantly (it goes down in those treated with DMSA, but apparently not significantly). The baseline of all 72 subjects who had RBC glutathione done was a mean of 501 (+/- 246) - those 38 (this is confusing - which 38 are they referring to? Why not 41?) who went on to receive a second measurement in “Phase 2″ had a baseline mean of 523 (+/- 280). Two months after one “round” of DMSA, the ”38″ remaining had a mean of 478 (+/- 83). Another graph shows that those with higher RBC glutathione ended up with lower RBC glutathione after treatment and vice versa.
Secondly, their laboratory (Immunosciences) uses an odd “reference range for adults” - 427 - 714 micromolar (I assume it is micromolar - the article never gives the units - curious). There are a number of references (e.g. Richie et al 1996) that looked at large numbers of “normal” adults and found the range to be higher (670 - 1600 micromolar in whole blood; 1600 - 2800 micromolar in RBC’s).
There was also the problem of determining how the glutathione was measured. The authors state that Immunosciences Lab used an Oxis Research kit in which “…the absorbance measured at 405nm is directly proportional to the GSH concentration.” It may be nit-picking, but currently available Oxis Research glutathione measurement kits use absorbance at 400 nm, 420 nm and 412 nm - none use absorbance at 405 nm. Maybe it was an old kit.
Still, the change in the standard deviation of the RBC glutathione is curious (there’s that word again), but not terribly significant unless they can explain how reducing half of the subjects’ RBC glutathione is a “good thing”. Their presentation of the data raises more questions than it answers, such as “Why don’t you have RBC gluathione for all 41 subjects who completed Phase 2?” and many, many others.
Another point that the authors didn’t address about the RBC glutathione tests is that they don’t seem to show any positive effect of the glutathione lotion. Of course, they don’t break it out for us to show differences (if any) between the glutathione lotion and placebo lotion, but I suspect they would have if there had been any indication that the glutathione lotion had an effect.
[4] Platelets:
According to my university’s hospital lab, the “normal range” for platelets in children 3 - 6 years old is 204,000 - 402,000 per microliter of blood. This study showed that the baseline platelet count of their subjects who completed the study (n=41; I wish they would explain why the numbers keep bouncing around - I suspect it is because they didn’t get a full set of data on all of their subjects) had a mean (a rather useless value - median would be so much better) of 388,000 per microliter (+/- 274,000). Rather than give us a before and after number, they only give the percent above an below the “reference range” after one “round” of DMSA treatment. It’s almost as though they’re trying to hide something.
Figure 5 gives away part of the secret: like the RBC glutathione levels, the platelet counts show a reduction in standard deviation without a significant change in mean (or median - from my reading of the chart). While this may be an “interesting” (or “curious”) finding, it will take a lot more work to show that it means anything.
Bottom line:
These studies show neither efficacy nor safety of DMSA in the treatment of autism. This is not surprising, given the poor design of the study.
In fact, if I were to try to design a study that couldn’t show any results, I would be hard-pressed to do better than this one. The fact that the authors are so convinced that the DMSA did work is a testament to their pre-conceived notions.
In the end, this study gathered a bunch of data and then threw it against the wall to see what stuck.
And not much - if any - did stick.
Considering how long we’ve been hearing that DMSA treatment is dramatically ”curing” or “recovering” autistic children, the results from this study are distinctly underwhelming. It shows that there is no clinically significant difference between a single “round” of DMSA and multiple “rounds”, which suggests that DMSA doesn’t work at all. The authors’ assessment that a single dose of DMSA “did the trick” is a pathetic post hoc attempt at spinning the results in favor of their preferred outcome.
About the only thing it shows for certain is that glutatione lotion doesn’t increase RBC glutathione. But they didn’t address the efficacy of the glutathione lotion at all.
Curious.
Prometheus
Filed under: Autism Practitioners, Autism Science, Autism Treatments
November 27th, 2009 at 1:28 pm
1) One would expect (assuming independence of exposure) that roughly 51% of unchelated subjects would be “high” on at least one of those metals.
2) My first thought was “why not uranium?” though it later turns out that they did look for that. Possible source of uranium exposure is pica, since uranium is a common constituent of soil.
3) I get this persistent mental picture of Doctors’ Data staff throwing darts at a copy of the Periodic Table to determine what tests they’re going to offer. The thought of their using the same procedure to determine the results they supply is tempting, though for legal reasons I must emphasize that I have no valid reason to assume that that is in fact their procedure.
November 27th, 2009 at 6:20 pm
“some subtle decrease in intellectual function when given to children (and rats) with low (or zero) lead levels (not reversible).”
Maybe I am missing something, but it does not appear that either Dietrich or Stangle say that chelation causes a decrease in intellectual function.
Dietrich seems to say that there was no benefit to treating low levels of lead with a chelating agent but they say in their result section -
“In our study, succimer seemed to be a safe drug in the sense that no important or irreversible side effects could be attributed directly to its administration”
This statement seems to be at odds with with your assertion. I assume that the study authors would consider a decrease in intellectual function an important side effect.
Stangle et al is more on point but is the result of a few month experiment on rats and as such the results might not be a reliable measure of the long term effect on people. The main outcome is that treatment with a chelating agent does alleviate cognitive defects due to lead exposure but there is a warning about chelating when there is no elevated level of lead or other heavy metal.
This warning is based on the results of using chelating agent in a group of rats that had no exposure to lead. If I am not mistaken, most children today do have some detectable exposure to lead. And if you look at the (rather confusing) results from the current study (Table 2), you will see that the children did excrete lead both before and after the chelating agent was administered. So I would have to question whether the decrease in function from a no-exposure groups of rats would be directly applicable to the normal low-exposure that children have.
Also, if you notice the warning is written to include “other heavy metals”. This is the theory that the study authors are working on - specifically they children with autism have a hard time getting rid of heavy metals. So if this theory is true, the warning would not apply.
I would tend to agree that, based on the available evidence, chelation is a rather pointless thing to do for autism but I don’t think either of the studies you quoted demonstrate that irreversible cognitive impairments is a known side effect of chelation.
November 27th, 2009 at 8:23 pm
MJ,
The bit on cognitive impairment is on page 25, left-hand column, first paragraph. It is a minor finding, which the authors mention without much comment, largely because it was small.
This finding was replicated by Stangle et al in rats.
The reason this is of concern is that while the benefits of treating children with high lead levels with DMSA is clear, children who have more modestly elevated lead levels haven’t shown the same benefits.
Dietrich et al were studying children who had lead levels that were above the “reference range” (without “provocation”) but lower than the threshold for treating with DMSA.
This is probably lower than the lead (and other heavy metal) levels seen in the subjects in the Adams et al study (we’ll never know, because Adams et al didn’t do “unprovoked” tests), so an obvious test - if they were serious about addressing safety - would have been to do cognitive tests like those done by Dietrich et al. They didn’t.
Remember that an NIH study into chelation for autism was cancelled because the results of Stangle et al suggested that the findings in Dietrich et al might not have been an anomaly.
While this isn’t “hard and fast” proof that DMSA can cause irreversible cognitive impairment in children with low (or zero) lead/mercury/etc. levels, it is a good reason to think twice (or even more often) about using DMSA in the absence of true lead or mercury toxicity (i.e. without elevated blood or unprovoked urine metal levels). It is also a good reason to include cognitive testing in any “safety study” of DMSA in children with lead/mercury/etc. levels below the usual threshold of treatment with DMSA. Given all of the testing that the authors of Adams et al did, it is a significant oversight that they omitted the one test that could have answered the safety concerns that Dietrich et al and Stangle et al have raised.
I am also aware that the authors of Adams et al are still labouring under the mistaken belief that autistic children are “poor excretors” of heavy metals - a hypothesis that is without any supporting data. The lamentable Holmes et al “study” which was first used to advance this hypothesis has been repeatedly shot down by me and many others.
Prometheus
November 27th, 2009 at 9:17 pm
Prometheus,
“The bit on cognitive impairment is on page 25, left-hand column, first paragraph.”
That explains why I didn’t notice it when I skimmed the paper. This is a minor finding and I have to wonder at the validity of it even with Stangle showing a related effect. But you right that chelation is not something that you would want to undertake lightly.
“Given all of the testing that the authors of Adams et al did”
I think they were picking random tests at random and the overall impression is that they were rather disorganized. But I am not sure how they would have been able to detect a slight difference in cognitive ability in such a small group - children with autism tend to perform inconsistently on IQ tests even under normal circumstances.
“I am also aware that the authors of Adams et al are still labouring under the mistaken belief that autistic children are “poor excretors” of heavy metals - a hypothesis that is without any supporting data.”
Did you happen to see these two studies that were published recently?
http://www.ncbi.nlm.nih.gov/pubmed/19921347?dopt=Abstract
http://www.ncbi.nlm.nih.gov/pubmed/19937285?dopt=Abstract
I haven’t finished reading them completely but they seen to hint that children with autism react differently to lead and mercury.
November 28th, 2009 at 3:04 pm
It’s also interesting to read comments of Drs. Richard Deth and Ray Palmer, the “peer reviewers.” They basically amount to “this paper was great.”
November 29th, 2009 at 10:25 am
Curious, indeed.
“In fact, if I were to try to design a study that couldn’t show any results, I would be hard-pressed to do better than this one.”
Thank you for the laugh! In my H1N1-addled state, this brightened my day!
November 29th, 2009 at 1:40 pm
If one works for a university and conducts a study with human subjects overseen by an IRB outside the university isn’t one required to at least have the university agree to an “IRB of record?” This would include a review of the IRB by the university’s IRB.
November 29th, 2009 at 2:51 pm
MJ,
Thanks for bringing those two studies to my attention. I’ve given them a quick look and - as I suspected - they are very similar to the sort of gene-expression studies that were done ten years ago in bacteria and smaller eukarya.
By this, I mean that the development of gene microarrays and “gene chips” allowed researchers to look at the changes in gene expression with changes in a dizzying variety of cellular conditions, generating tons of data. At first, this looked like it would revolutionise the world of molecular biology, but in the end it turned out that there was often more noise than signal.
There are two major problems with these studies:
[1] They are using “blood cells” (white blood cells, since red blood cells don’t have ANY gene expression). White blood cells are terminally differentiated and do not necessarily represent the gene expression of any other tissue.
[2] Many of the genes the researchers find “correlated” to mercury and lead levels do not seem to be related to heavy metal toxicity. This is similar to what was found when microarrays were first available for bacteria. In bacteria - which are VASTLY simpler than a multicellular eukaryote like humans - most of the “correlating” genes had NOTHING to do with the exposure. The differences in expression turned out to be either generalised “stress responses” or were due to changes in the breakdown of the encoded protiens.
I will give these studies a closer examination and will probably feature them in a future posting.
Prometheus
November 29th, 2009 at 2:55 pm
Joseph,
Yes, the fact that the authors chose Richard Deth, a co-traveler in the DAN! circuit, speaks volumes about their confidence in their own work.
I am not familiar with Ray Palmer - what is his background?
Dick,
I’m not sure if that is a universal requirement. At my university, I am required to involve the IRB if I am doing human research under their auspices (i.e. on their facilities). Of course, if I were doing human research using the IRB from a naturopathic college, the university might wonder what I was up to.
Prometheus
November 30th, 2009 at 11:49 am
Prometheus,
Ray Palmer, I believe, is the lead author on the Texans near coal plants are more autistic studies. On top of the serious flaws in those studies, if I recall correctly, he is involved in vaccine litigation.
That aside, thanks for taking on these DMSA papers. I am amazed the editors let this through.
November 30th, 2009 at 11:57 am
Is there some form of qualification for IRBs? The Geigers were notorious for setting up their own, and this one doesn’t look any better. And are members of an IRB responsible for their approval decisions? If something goes severely wrong with a study like this and people get injured, is the IRB subject to “standard of care” review itself?
November 30th, 2009 at 3:25 pm
I am not familiar with Ray Palmer - what is his background?
Remember the Texas coal-fired power plants papers?
November 30th, 2009 at 5:35 pm
Ah! That Ray Palmer!
So, the two “peer reveiwers” the authors chose were BOTH co-religionists at the Church of Mercury Causes Autism.
Curious.
Prometheus
November 30th, 2009 at 7:18 pm
Jeff Bradstreet routinely diagnoses ‘metals poisoning’ in autistic children and uses chelation yet none of the authors declared any conflicts of interest on either of the studies. It seems to me that Dr. Bradstreet has an extraordinary interest in positive results of these studies, at the very least.
December 1st, 2009 at 1:00 am
[...] is the question posed by Prometheus over at A Photon in the Darkness blog. He blogged this in response to two papers recently [...]
December 1st, 2009 at 1:13 pm
Excellent and clear analysis of a rather ‘unclear’ paper.
One other point to make about the use of an ADOS - as well as not being appropriate as a measure of clinical change, it is generally advised that one doesn’t repeat an ADOS assessment within 1 year of the first one. The danger otherwise is the subject will be familiar with the materials and that you will get practice effects, which could, who knows, even make it look like there was some improvement in ASD symptoms when there is none…
Was there any comment about the time interval between assessments?
December 1st, 2009 at 6:38 pm
none of the authors declared any conflicts of interest on either of the studies
BTW, neither did the “peer reviewers.” The journal does define ‘competing interest’ as any possible interest in the results, be they political or monetary. I checked.
December 7th, 2009 at 1:30 pm
[...] there are, but they suck. The author has a great quote on this study: n fact, if I were to try to design a study that [...]
January 20th, 2010 at 7:36 am
[...] body burden of toxic metals.” (for more on that study, see Prometheus’ analysys, Is DMSA safe and effective?). One of the toxic metals reported in that [...]
January 21st, 2010 at 5:20 pm
I looked at the first array paper noted above (PMID: 19921347). They don’t seem to realize that for the 3 lists of “significant” genes (they use a very weak p<.05 criteria), where they get 2172, 1712 and 1829 qualifying, that for an array with 54675 probe-sets, we would expect to get 2734 with p<.05 (54675x.05) by chance alone.
For other people, when that happens, you call the experiment dead. An autopsy is all you can do.
For array wonks, there is much additional humor to be found in that paper. Where deceiving themselves ends and deceiving reader begins is hard to tell though, so compassion may be more appropriate than anger.
Competent review, where have you gone?
January 21st, 2010 at 5:45 pm
Dear Late,
I’ve looked through the array papers and have them “on my list” to address. I do a lot of microarray work and I think that the authors simply aren’t familiar with the shortcomings of microarrays.
Even if they had acheived statistically significant results, the genes they find “correlated” with autism and mercury exposure are either part of very general systems OR are “so what” results.
If the authors are not familiar with the rather steep learning curve that microbial physiologists went through in their use of microarrays, they should spend a few days going through some of the review papers in the field. From what I can see, they not only made all of the mistakes the bacterial physiologists made, they appear to have invented some new ones.
Thanks for your analysis!
Prometheus
January 22nd, 2010 at 11:36 am
The second paper is in the same issue of Neurotox Res. It is PMID 19927285. It is similar to the first paper but looks at mRNAs correlated to mercury rather than lead. They are again looking for mRNAs (‘transcripts’) whose correlation in autistic kids (AU) differs from the correlation in typically developing (TD) kids, that is, a mercury by group (AU vs. TD) interaction. They again use Affymetrix U133 plus_2 array data, which have 54675 probe-sets. Their signal processing and statistical analysis sounds more sophisticated this time, using GC-RMA algorithms for processing and log-transformation (pretty good method), and modeling array batch effects in addition to age, mercury and group effects. It appears there are thinking people doing this work so far.
However, for the test of mercury by group interactions they get 1113 probe-sets with p<.05, whereas again, 2734 (54675 * 0.05) are expected to be that good by chance alone, a deadly result. To restate, if I just randomly label the samples AU and TD, I expect to get more significant mRNAs than that. A eulogy is in order.
This time, they admit it. “No genes passed a False-Discovery Rate filter in any of these models”. In discussion too, “No gene reported here passed a multiple comparison correction for statistical significance”. That’s honest. They have some broken logical to talk their way out of that, and apparently the authors, reviewers, and editors bought it. That is astonishing. It reflects very poorly on science, and the journal.
To be slightly fair, I see another paper by about this same group in Genomics (PMID: 18006270) where they appear to obtained some real signal just comparing AU with general population (it has nothing to do with lead or mercury). There they report lists of genes where the false discovery rate for the list is 0.05. That is, they found more differences than expected from just random data for this question. That data-set is public (GEO series GSE6575) - good journals demand that. This data and paper might be useful to students of autism, presuming the identified differences are not merely due to some confounding with technical sources of variation (cell types obtained, sample handling, or quality of RNA for example). It might be a good example data-set for bioinformatics students to work on too. Again though, it’s not about heavy metals.
March 23rd, 2010 at 12:07 pm
Is alpha lipoic acid safe to use following the AC protocol of every 3-4 hrs for 3 days?
March 27th, 2010 at 10:35 pm
Cisco,
Is alpha-lipoic acid so rapidly excreted that you need to dose it every 3-4 hours???
Is the “AC protocol” safe? Who knows? Probably, but it has never been tested. Is it effective, though? Maybe yes, maybe no - it has never been tested.
So here is the quick and dirty risk:benefits analysis on the “AC protocol” for alpha-lipoic acid:
Risk: probably very low.
Benefit: unknown, probably nil.
risk:benefit ratio - highly skewed in favor of “risk”.
It’s not enough that a treatment be “safe” - it also needs to be effective for the risk:benefit ratio to favor its use.
Prometheus
June 7th, 2010 at 2:40 pm
Off thread, but, thought you’d be interested since you blogged about “stem cell treatments” offered in Costa Rica in the past. See, FEATURE - Costa Rica puts brakes on popular stem cell tourism (Reuters Mon Jun 7, 2010)
http://in.reuters.com/article/idINIndia-49088520100607
June 10th, 2010 at 3:25 pm
WFAJ,
I’m going to put a copy of your comment on the stem cell post.
Prometheus
June 10th, 2010 at 5:49 pm
Thanks. I was in a rush and didn’t have time to look for the right post.