August 1, 2011

Ancestry of Pink Disease (Infantile Acrodynia) a Risk Factor for Autism

Ancestry of pink disease (infantile acrodynia) identified as a risk factor for autism spectrum disorders.

J Toxicol Environ Health A. 2011 Sep 15;74(18):1185-94. Shandley K, Austin DW.

Swinburne Autism Bio-Research Initiative (SABRI), Brain and Psychological Sciences Research Centre , Swinburne University of Technology , Hawthorn , Victoria , Australia.

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. Autismspectrum 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. 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 22) 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.


Jeff C said...

Thanks for posting on this Ginger, I sure would like to get a copy of this study. What a beautifully thought out hypothesis and test.

It is inarguable that mercury caused pink disease as it disappered almost overnight once the powder was banned. It is also uncontested that the great majority of those that used the teething powder containing mercury did not get pink disease. It has long been settled that those who got pink disease had a genetic predisposition (susceptibility to mercury) coupled with an environmental trigger (mercury from the teething powder). Lo an behold, their decendants have ASD at 8 times the rate of those without pink disease.

So what does it mean? Nothing good for the needle nuts as far as I can tell. The best outcome is that the same genetic predisposition has two different triggers, mercury in pink disease and something else (totally unrelated to vaccines of course) in the case of ASD. Sounds like a hard sell.

I hope the author's methodology was impeccable and he has no skeletons in his closet. I have a feeling he is about to get the equivalent of a full body cavity search.

You can tell this one has them scared as left brain right brain has already jumped all over it.

Jim Thompson said...


Here is an excerpt from “Thalidomide and the Power of the Drug Companies by Sjostrom and Nilsson (1972) that shows a common thread in the arguments about cause and effect from Calomel, Thalidomide, and Thimerosal:

“Finally there have been some objections which were supposed to cast doubt on the causal relationships between thalidomide and malformations, but which actually have no relevance to this question…Mothers who claim to have taken thalidomide during the critical phase, have given birth to absolutely normal children. It is not known in how many cases this has occurred and the power of thalidomide to produce malformations is still being discussed. However, all seem to agree that thalidomide is an extremely potent teratogen, producing malformations when taken during the sensitive period in 60 to 100 per cent of the cases. In monkeys, where malformations remarkably similar to those seen in man have been produced, and where a controlled test can he made, the malformation frequency is almost 100 per cent, which supports its high effectiveness found in man. It is, for obvious reasons, sometimes quite difficult to check in retrospect, for example, that thalidomide really was consumed during the sensitive period and not a short time before or after. In some of these cases although the children had no striking, easily visible malformations, they were later found on thorough examination to have minor defects of the thumbs or internal organs.

If thalidomide caused these special malformations it is in principle of no importance whether thalidomide resulted in malformed children in 70 per cent, 80 per cent or 95 per cent of the cases where the drug was taken during the sensitive phase. Every biologist knows that within a group of living organisms there is always an individual variation in the sensitivity towards, for example, a poison or a drug. Because of natural biological variation some individuals are affected more than others and some are perhaps not affected at all. If about 0.5 milligrams of strychnine is given by intraperitoneal injection to a certain strain of rats, approximately 50 per cent of the animals will die. The fact that the other 50 per cent survive cannot, of course, be taken as evidence against a causal relation between the intake of strychnine and death in rats.”