The issue of sudden, rapid acceleration in Toyota vehicles presents an interesting case study of how our society approaches rare hazardous events, and a consideration of this history can shed light on how other such instances are handled that are of more direct interest to us here. It turns out that this issue has been with us for some time. About 1000 suspicious acceleration events have been recorded over eight years, with some 19 deaths registered in Toyotas since 2002.

Complaints of sudden, unintended acceleration rose rapidly after Toyota replaced mechanical throttles with electronic controls in 2002. By the time that this problem received significant attention, however, the hypothesis of causation by floor mats interfering with the gas pedal was well entrenched. So that hypothesis continued to be advanced even after it ceased to be very credible. After all, the problem occurred even in vehicles where the floor mats had been removed, and where nothing was engaging the gas pedal (as at a stoplight). As recently as a few months ago, our National Highway Safety Administration saw no reason to inquire beyond the mundane hypothesis involving floor mats. And the recall of 4.2 million cars is majorly targeted to the replacement of gas pedals so that they will be less confused by the floor mats.

The really unsettling problem with the electronics is still being kept in the background. The whole unfolding episode has aspects of pageantry, of skillful stage management of disagreeable facts to make them appear more benign. The floor mat problem could have multiple causation, thus diffusing responsibility; the electronic malfunction, on the other hand, is entirely the responsibility of the manufacturer. The society has much less tolerance for such failures, particularly when they have existed for so many years.

The Taser presents us with a similar issue. Literally hundreds of deaths have occurred in people immediately subsequent to having been tased, but the connection continues to be denied. The principal rationale for the Taser is that it offers a non-lethal alternative for subduing a person resisting arrest, so the tactic can’t also come with its own risk of mortality. It is amazing to see how disagreeable facts can be rendered innocuous when significant interests are at stake. In this case, the exculpating hypothesis is that the Taser is harmless in “normal” individuals, and if death occurred, then it must be attributed to whatever condition the “abnormal” person may have had.

Now consider the question of vaccine injury leading to autism in children. We are again confronted with a rare event, and matters are once again obscured by a non-operative hypothesis. When the instances of sudden onset of autism after the administration of vaccines first came to light, the field of medicine was still in thrall to two pillars of belief with respect to autism. The condition was deemed to be genetically mediated, and it was thought to be an untreatable psychiatric disorder. Vaccine-induced injury did not fit either of these models.

There was the additional concern that the whole vaccination regime was at risk on account of this issue. It helps to take the historical view here, because we have been here before. When the issue of vaccine-induced injury was first raised in connection with the DPT vaccine, the medical community also stood as one in opposition to the claims. And when doctors such as John Menkes spoke in support of the vaccine-induced injury hypothesis at trial, he was ostracized by his colleagues for breaking rank. Vaccine-induced injury was always rare, but it was often severe, and it typically involved neurological injury, on which Menkes was expert. (See http://www.eeginfo.com/newsletter/?p=341)

We had another instance of this when Dr. Wakefield and his colleagues surfaced evidence of intestinal inflammation subsequent to the MMR vaccine jab. This research showed that there may be real medical issues involved in the causal chain of autism. The work was met with solid opposition among his colleagues, and his medical career in Britain was effectively destroyed. Once again, the vaccination regime had been put at risk, and that was intolerable.

By now the whole public relations apparatus of American medicine has been put in the service of delousing and refurbishing the vaccination regime. The disagreeable facts, however, continue to accrue. In our office, we continue to see autistic children whose descent into autistic behavior was clearly correlated with an immediately prior vaccination. The picture is very much the same as it was with DPT: an occasional drastic descent into neurological dysfunction. The rare event cannot be dismissed here any more than it can be dismissed in the case of Toyota or the Taser.

In each of these cases, a statistical or “epidemiological” approach would have missed the story entirely. One could have queried 10,000 Toyota drivers randomly and very well not found a single case of rapid acceleration. It would still have been wrong to conclude that the problem does not exist. When it comes to the rare event, a statistical or epidemiological approach is categorically inappropriate. We have to study the events themselves.

Of course the very existence of vaccine-induced injury leading to autistic behavior does have broader implications for how we understand autism. So how do we sort that out? To date, the “genetic hypothesis” of autism has presented a huge barrier to broader thinking on this topic. And in fact, it is supported by the best of evidence—high concordance for autism among monozygotic twins. It is 70% for classic Kanner autism, but as high as 90% for the more inclusive category of autism spectrum disorders. On the other hand, recent genetic studies have surfaced a substantial genetic heterogeneity in the autistic spectrum. Consequently, one cannot coalesce on a few targets for focused research.

But we must inquire further. Some years ago a correlation was observed between the age of the father and the likelihood that his next child would be autistic. The father’s initial contribution to the child is largely genetic, so here we have a possible nexus of the genetics of autism and of environmental factors. Environmental influences on germline cells would have to be postulated, and this could be done without doing injury to the genetic model.

More recently we have had the finding of differences in the DNA between children and their parents. At issue here are “copy number variations” (CNVs), either dropped or duplicated segments of DNA. Substantially greater numbers of CNVs were found in a subset of autistic children. This subset (~10%) is small, but this initial search was deliberately at a gross level, and the vast majority of CNVs may simply have been missed. The CNVs were preferentially observed in families with an isolated autistic child, as opposed to where autism was more familial. Hence in addition to the transmittal by Mendelian inheritance we now have to add substantial risk of “spontaneous” mutation.

High concordance would still be observed under both of the above scenarios, irrespective of whether the mutation(s) occurred in the father or in the fertilized egg. While this may be a scientifically pleasing resolution of a conundrum, it represents a frightening prospect otherwise. We must now take a serious look at how our toxic environment is degrading our own gene pool even across a small number of generations. The rapid growth rate in autism incidence in the developed world could never be understood in terms of classical Mendelian inheritance. Now that we know the underlying genetics of autism to be exceedingly complex, this is even more apparent. If a genetic model is to be sustained, it has to be on the basis of de novo mutations, and now we have indisputable evidence that these in fact exist.

There has to be a mechanism (or mechanisms) for the burgeoning of genetic defects over the last sixty years, and we must look to environmental factors for an explanation. The CNV study suggests that the integrity of the cell division process may not be maintainable under existing environmental threats. Given the obvious heterogeneity in the etiology of autism, we have to look at the rare event as assiduously as we search for larger patterns. One of the key observations of the CNV study was that each of the individual findings was rare in the population. None of the variants was observed more than twice. Given this intrinsic heterogeneity, it is simply preposterous to preclude a role for mercury exposure and for vaccinations as a final insult to send a particularly vulnerable nervous system on its path to autistic expression. The biochemical environment we have created could even be a genetic hazard for us all at some level, and in this respect the autistic child may just be our canary in the coal mine.

Sources:
The Los Angeles Times

Jonathan Sebat et al, Strong Association of De Novo Copy Number Mutations with Autism, Science, published online 15 March 2007: 10.1126/science.1138659

Siegfried Othmer, PhD
drothmer.com

This entry was posted on Saturday, December 12th, 2009 at 12:55 am and is filed under Application of Neurofeedback, Autism, Commentary, Neurofeedback. You can follow any responses to this entry through the RSS 2.0 feed. You can leave a response, or trackback from your own site.