“Staggeringly”! I hope you got that. By what mechanism I wondered? That was absolutely crucial. Huge toxic loads of mercury caused Pink disease (acrodynia). Thimerosal is ethylmercury rapidly removed from the body, monitored to the nth degree to ensure safe exposure. Teething powders contained 65,000 micrograms per dose of mercurous chloride which decomposed into elemental mercury and poisonous mercuric chloride on exposure to sunlight.

Thousands of children died – between 10 and 33% of cases. Yet not all exposed children suffered acrodynia – it was a minority of 0.2%. Are they thus suggesting a pre-existing inherited genetic susceptibility or susceptibility brought on by acrodynia, which was known to cause infertility? How did parents of children in the Swinburne study fare, in view of other studies linking high maternal exposure to mercury to autism in offspring? How robust was the data collation?

Kerrie Shandley and David W. Austin return to The Journal of Toxicology and Environmental Health to publish Ancestry of Pink Disease (Infantile Acrodynia) Identified as a Risk Factor for Autism Spectrum Disorders. Yes, that Journal of Toxicology…. The one that provides succour to Dr. Mark Geier of chemical castration and misdiagnosis fame in his “ASD Centers” across eight USA states. In 2007 the journal published A Case Series of Children with Apparent Mercury Toxic Encephalopathies Manifesting with Clinical Symptoms of Regressive Autistic Disorders by the infamous father and son team of, to say the least, dubious reputation. Geier senior is presently watching as his medical licence is suspended in consecutive US states.

We can learn quite a bit of these author’s intentions, hence the quality of research, simply by checking their track record. In 2008 Shandley and Austin published An Investigation of Porphyrinuria in Australian Children. They leap straight into citing from known offenders perpetuating the mercury-autism link – Geier and Geier, Nataf et al., Bernard et al., Mutter et al., – in the abstract claiming;

These (atypical urinary porphyrin profiles in children with an autism spectrum disorder) serve as an indirect measure of environmental toxicity generally, and mercury (Hg) toxicity specifically, with the latter being a variable proposed as a causal mechanism of ASD…. To examine whether this phenomenon occurred in a sample of Australian children with ASD, an analysis of urinary porphyrin profiles was conducted. [….] Three independent studies from three continents have now demonstrated that porphyrinuria is concomitant with ASD, and that Hg may be a likely xenobiotic to produce porphyrin profiles of this nature.

The discussion is far more circumspect about this correlation [italics mine], despite the authoritative recommendation [in my bold];

 Furthermore, this study provides further evidence suggestive of an environmental toxicant variable, consistent with Hg, contributing to the maintenance, and possibly development, of ASD.

Given the consistency of the emerging research, health authorities worldwide need to move without delay to further elucidate the specific nature of the toxic insult.

The bibliography is rather short but as well as the above includes Edward Yazbak, Mark Blaxill – editor from Age of Autism – and Sally Bernard et al.’s Autism: a novel form of poisoning from Medical Hypotheses 2001. It’s a Who’s Who of vaccines cause autism mythology whose work is featured by Generation Rescue, The Australian Vaccination Network, Age of Autism and their ilk. Shandley and Austin write erroneously, citing Yazbak, that autism [the disease – not the diagnosis frequency] is “increasing at epidemic rates” then cite Blaxill et al, arguing it;

…. cannot be accounted for by changing diagnostic criteria or improved diagnostic systems

In fact changing criteria has been proposed for years by many paediatricians including Gillian Baird and quantified recently by Brugha et al, who used current diagnostic criteria to uncover a population of autistic adults only 2% smaller than the child population. However, whilst porphyrinuria may indicate environmental exposure to heavy metals including lead and mercury other studies have shown correlation to autism and not Aspergers. Yet this heavy metal/autism mechanism, and what it exactly means is even less certain.

Porphyrins are oxidised byproducts that have “escaped” the heme biosynthetic pathway. We expect to see elevated levels in the urine of elderly, nutritionally deficient, regularly medicated and physiologically distressed individuals. The body can generally physiologically manage toxic build up. Hepatic and renal pathways of elimination serve as detoxification routes for the body. Porphyrinuria heralds a drop in efficacy of biosynthesis or environmental toxic exposure.

If the autistic sample is not recently exposed to environmental toxicity – or as the authors may argue, mercury – then we have to accept compromised biosynthesis. Whether this is due to autism, which does accompany a range of physiological challenges, or whether compromised biosynthesis indicated by porphyrinuria is contributing to autism, is unknown. It’s worth noting that enzymatic and physiological abnormality at the molecular level has been hypothesised as contributing to hypo’ and hypersensitivity in autism. The pathophysiology of autism sufferers is extensive and well documented. The angle Shandley and Austin take is the dramatic call to discover the nature of the “toxic insult” potentially causing ASD. Reading between the lines, and all academic company considered, that “toxic insult” is mercury in vaccines.

This is brought home strongly by Austin’s lone foray the same year in The International Journal of Risk and Safety in Medicine. An epidemiological analysis of the ‘autism as mercury poisoning’ hypothesis, is a scruffy 11 point synopsis concluding that mercury does indeed cause autism. In point 9, he addresses “Mercury levels are higher in autistic than non-autistic children”. He argues that the “causal” hypothesis would suggest that mercury levels would be higher in autistic children. Of course, that’s just what we find chopping into this straw man. Nataf et al., Geier and Geier, Bradstreet and Geier et al., make up three references. The fourth is DeSoto and Hitlan who court ample controversy not least for citing Geier and Geier excessively.

He notes that either mercury causes autism or autism causes mercury. The second notion being “patently nonsensical” and unsupported by literature. Which is unusual because with the cause of autism unknown and the many times exposure to mercury has been ruled out the same could be said of the first notion. We do know that biologically, neurologically and physiologically autistic individuals face many hurdles, and as I suggest above biosynthetic dynamics can’t be ruled out or in.

I was treated once again to a fallacy I’ve had shoved at me in other areas in public health in which robust data indicate no causation between variables. A type of “better to be safe than sorry”, usually proffered by those bent on ideology. Austin here hijacks the “Precautionary Principle (‘First, do no harm’)” as point 10;

The science behind the autism as mercury poisoning hypothesis meets all epidemiological criteria across too many independent studies to be dismissed as coincidence. So, the hypothesis that mercury likely causes autism is confirmed epidemiologically.

He also rewrites history on Pink Disease in point 9, by suggesting that “despite limited evidence” mercury containing compounds were recalled. This is nonsense. Fierce resistance to accepting mercury poisoning was the norm with medical focus being on a physiological cause. It’s argued the mercury hypothesis gained stronger ground only when opponents “became old and disappeared from the scene”. Gaining credibility via attrition of opposition is not application of the precautionary principle. Austin here is exposed as deceptive, misleading readers for his own purposes.

He concludes his plunge from the windowsill of academic integrity with;

The existing literature provides grounds for suspicion that mercury plays a causal role in the development of autism. [….] …it would be negligent to continue to expose pregnant and nursing mothers and infant children to any amount of avoidable mercury. Health authorities worldwide should move without hesitation to ban and remove all mercury in all medical products at the earliest possible date.

Again with the dramatic calls. Where is this mercury really coming from? Ethylmercury or methylmercury in the diet, pre-term maternal diet, breast feeding or toxic exposure? We can infer with a good deal of accuracy he alludes to thimerosal in vaccines. It’s a shocking paper without even an acknowledgement of the impact of changing diagnostic criteria. The bibliography continues to fail with Boyd Haley, who pops up twice, Mark Blaxill again along with another showing from Sally Bernard. Indeed the “epidemiological analysis” of “existing literature” is a predetermined collation of biased and discredited publications.

Still, we can now return to the most recent paper with a clear understanding of these authors’ predetermined agenda.

To begin with they wheel out all the veteran offending authors, including their previous work to make the case there’s a relationship between mercury and autism. Well, third time lucky just doesn’t apply here. In the tradition of discerning character from the company one keeps, I think we can indeed confirm intention from citations. From the abstract they propose susceptibility and genetic predisposition to explain the small subset of Pink disease sufferers and of autism diagnoses today;

Pink disease (infantile acrodynia) was especially prevalent in the first half of the 20th century. Primarily attributed to exposure to mercury (Hg) commonly found in teething powders, the condition was developed by approximately 1 in 500 exposed children. The differential risk factor was identified as an idiosyncratic sensitivity to Hg. Autism spectrum disorders (ASD) have also been postulated to be produced by Hg. Analogous to the pink disease experience, Hg exposure is widespread yet only a fraction of exposed children develop an ASD, suggesting sensitivity to Hg may also be present in children with an ASD. The objective of this study was to test the hypothesis that individuals with a known hypersensitivity to Hg (pink disease survivors) may be more likely to have descendants with an ASD.

Fair enough. Yet as we’ll see both the genetic component and the exposure to mercury in subsequent generations is unconvincing. Besides, where might this mercury today be coming from?

Mercury contained in vaccines (as a preservative under the tradename Merthiolate, but more commonly known as thiomersal/thimerosal), dental amalgams (silver fillings), seafood, and the atmosphere is argued to be the primary set of sources of Hg exposure for infants both in utero and in their early years.

Well that’s pretty clear. Small children awaiting first or second teeth won’t be worrying about dental filings. Big Atmosphere is here to stay and dietary sources are by choice. In short the only tantrum one need throw is over vaccines. They continue firming the dual hypothesis of susceptibility and exposure to mercury;

… the Hg-autism hypothesis is, in reality, a two-part hypothesis that states that Hg exposure combined with a genetic/physiological sensitivity to Hg or a predisposition to impaired Hg excretion capacity leads to a chronic elevation of Hg in the brain and body.

The purpose of the present study was to test the Hg-autism hypothesis. If the hypothesis is indeed correct, and a sensitivity to Hg is heritable (genetic), the prevalence of ASD among the descendants of a cohort confirmed as having a hypersensitivity to Hg (pink disease survivors) should be higher than a comparable general population prevalence.

Results were reported in the media release and in Fairfax: Mercury poison linked to autism. We can also check back to the abstract for a more telling summary;

Five hundred and twenty-two participants who had previously been diagnosed with pink disease completed a survey on the health outcomes of their descendants. The prevalence rates of ASD and a variety of other clinical conditions diagnosed in childhood (attention deficit hyperactivity disorder, epilepsy, Fragile X syndrome, and Down syndrome) were compared to well-established general population prevalence rates. The results showed the prevalence rate of ASD among the grandchildren of pink disease survivors (1 in 25) to be significantly higher than the comparable general population prevalence rate (1 in 160). The results support the hypothesis that Hg sensitivity may be a heritable/genetic risk factor for ASD.

The most telling flaw is the efforts gone to in constructing the apparent genetic susceptibility to mercury leading to autism in grandchildren of acrodynia sufferers.

As identified earlier, numerous studies demonstrated a relationship between ASD and Hg. Our results suggest that this variable may have a heritable component and therefore, of course, a genetic basis. What our results do not do, however, is enable an understanding of the degree to which the susceptibility is inheritable and the mechanism by which this may occur.

Firstly if there’s a genetic component, why did the grandparents – and indeed the entire cohort of acrodynia children – not show prominent autism diagnoses. Secondly, how did the parents of the children escape autism? They lived in an era of mercury in house paint, mercury compounds in worming treatments, mercurochrome was a standard in First Aid kits – then suddenly vanished, industrial waste spilled into local rivers where kids regularly swam as standards of control were far more lax and mercury was used in the manufacturing of more products.

In short the parents with the same, “…heritable component and therefore, of course, a genetic basis”, were exposed to much more environmental mercury. Yet they emerge unscathed. Surely we should be seeing a reduction in ASD. Each subsequent generation is exposed to less mercury and the genetic component is halved. Unless there’s some incredible generational leap. Yet the authors themselves answer my initial question on mechanism – it’s unknown – and can offer no insight into the degree of genetic susceptibility.

So we must examine data collation. A survey completed by 522 infantile acrondyia sufferers. Self reporting data is perhaps the least reliable source of data in the absence of correction or follow up. In this case to correct for response bias it was crucial to chase up each and every one of the 522 respondents grandchildren to confirm that yes, they meet Australia’s criteria for autistic diagnosis. After all the authors are using the 1 in 160 frequency figure gained this way to claim “a six times higher” prevalence. The problem of perceived but undiagnosed autistic disorders may be impacting on results.

But they didn’t do this. The Age reports;

The authors said although they did not validate the autism diagnoses provided by the survivors in the surveys their study added to mounting evidence of a link between genetics, mercury sensitivity and autism spectrum disorders.

“The authors said”, eh? Right. It’s not as if they’re biased or anything – just look at their body of work. This emerging train wreck gets worse in that they likely promoted response bias. The study was advertised on the Pink Disease Support Group site. Yet the author’s write;

In order to minimize response bias, the true purpose of the study was not included on recruitment materials sent out to potential participants; instead, recruitment materials indicated that the purpose of the study was to investigate the general health outcomes of the descendants of pink disease survivors.

All up 23% of surveys were returned. What of the other 77%? Perhaps they had no descendants with health problems and thus were not motivated. Members of this support group with ill descendants are far more likely to respond, if not initially being prompted to join for the very reason the authors favour. Surely this “mounting evidence” would reach the ears of many Pink disease survivors. It’s even more likely those with autistic descendants would know of the hysteria over mercury in vaccines and thus reply, skewing results.

It is in fact arguable that some members of PDSG with autistic descendants – or who perceive they have autistic descendants, or have been told – gravitated toward membership because of the wide coverage of mercury being linked to autism. This point is just as likely as the supposed “six times higher” frequency rate. In truth we just don’t know. This is bad science that merely postulates a hand-me-down trick to breathe more life into the “mercury causes autism” corpse.

So in conclusion, we have two highly biased authors with a well documented track record of being unable to source reputable and bipartisan material on the issue of mercury and autism. They have a demonstrated propensity to argue against thimerosal in vaccines and immerse themselves in research and writing that we can only describe as being fringe or by known crackpots. David Austin in particular has previously written deceptive rubbish and aligned himself with known culprits in perpetuating known myths.

Shandley and Austin have a demonstrable predetermined agenda. Together they’ve come up with an appalling hypothesis because of this yet continue to cite these same biased sources. Their methodology is fatally flawed. Their conclusions are bordering on the absurd as they fail to justify the degree or mechanism of their observation which is based on unreliable data. To battle through this mess they cite over and again the same disreputable sources, which does not strengthen their argument. No dissenting citations are presented and challenged. They have published in a journal of dubious integrity and made public claims that remain scientifically unsubstantiated.

What.A.Mess. There’s nothing to see here – move along, move along.