By David Kirby
When the US Government conceded that vaccines had contributed to the development of autism in nine-year-old Hannah Poling, there was much speculation about what could trigger autistic regression in children with low cellular energy from mitochondrial dysfunction.
Many experts who oppose the idea that vaccines could be linked to autism – including those at the CDC - first suggested that a single-point mutation in Hannah’s mitochondrial DNA, inherited from her mother, was the actual underlying cause of her neurological problems.
The vaccines, they said, only made a bad situation worse. Many went so far as to insist that Hannah’s precarious genetic situation would have deteriorated into “features of autism” anyway - with or without the vaccines.
But that explanation fell apart: Hannah’s mother has the exact same mitochondrial mutation, and yet she never developed any neuro-psychological disorders. Moreover, Hannah does not have “classic” mitochondrial disease – a rare, inherited, and usually very serious disorder.
Instead, Hannah had a moderate dysfunction of her mitochondria, one that was so mild and asymptomatic that it went undetected – and apparently undisturbed – until July 19, 2000, when she received nine vaccinations at once.
The rest is medical history.
The government stated in its second concession statement in February, (in which her epilepsy was also determined to be vaccine-related), that the “cause” of Hannah’s “autistic encephalopathy” was:
“Underlying mitochondrial dysfunction, exacerbated by vaccine-induced
fever and immune stimulation that exceeded metabolic reserves.”
Many people jumped on the “vaccine induced fever” part of that sentence, and they are still running with it. Some have inferred that it is a well known fact that children with disorders of their mitochondria can readily regress into autistic encephalopathy – if they encounter any number of infant febrile infections.
This idea was supported by one of the experts on mitochondrial dysfunction and autism that I interviewed, who has studied 30 children with regressive ASD at the same clinic. He discovered that all 30 patients have the same markers for mild mitochondrial dysfunction: in this case, slightly abnormal levels or ratios of the same amino acids and liver enzymes.
One of the 30 children was Hannah Poling.
This doctor told me that, of the 30 regressive autism cases, only two -- Hannah and one other child – or 6 percent of the total, had received any vaccines within 7 days of the first sign of encephalopathy. The rest, he said, regressed because of fevers unrelated to immunization – a contention that is sure to be challenged when these data are made public..
The researcher said that children with mitochondrial dysfunction have a particularly pronounced window of vulnerability during the time when language skills are usually developing – between one and two years of age. They are, in essence, little walking, ticking time bombs: Anything that stressed their relatively fragile systems, including fever or vaccines, could push them over the edge and into ASD.
For this reason, doctors such as Paul Offit of Philadelphia say that children with mitochondrial problems should be quickly vaccinated against any disease that could cause a fever and overtax their systems.
Some estimates of the percentage of ASD children who also have mitochondrial dysfunction put the number at about 20% - though this very preliminary figure needs to be thoroughly studied.
But if 20% of ASD kids have a mito disorder, and six percent of those kids regressed due to vaccines, then just 1% of all autism could be attributed to vaccine induced “mitochondrial regression.”
If 1% of all autism cases were actually vaccine-induced mitochondrial regression, this would suggest that another 19% of ASD cases may be mitochondrial regression induced by fever alone.
Estimates of US autism cases vary wildly, but, for argument’s sake let’s say it’s a million people (many will argue that it’s far lower than that). That would mean some 190,000 Americans with mito issues who, after normal births and development, suddenly stopped talking and regressed into autism following some kind of childhood fever.
That may be the case, but then a number of questions are left wanting for an answer.
To begin with, I have confirmed that Hannah – who was sick several times in her first year or so of life, to the extent that her parents delayed some of her vaccines – suffered a number of high fevers several times before July 19, 2000 (a day when her doctor pronounced her a picture of neurological health, by the way).
Hannah was precocious, and began forming words at nine months of age, and quickly developed a vocabulary after that, despite the fact that she had a number of subsequent fevers, including one at 13 months of age.
So my first question is: If non-vaccine related fevers could have triggered her regression, why didn’t they? Why did Hannah continue to develop language following several fevers, right up until her vaccination date in July, 2000?
The idea that millions of children each year suddenly develop autism following some routine fever, and that this has been going on for hundreds or thousands of years, also raises many interesting questions.
If that is the case, then why is there little mention in the literature – medical or otherwise – of normally developing children who developed a fever and, soon after that, stopped talking and developed features of autism?
Doesn’t it seem likely that such a disorder would have been given a name during all those years, perhaps even a folksy one, such as, say, “Mute Fever” (much like some Africans used to call AIDS “Slims Disease”)?
And speaking of Africa and other developing nations, wouldn’t this tragic phenomenon be a common, everyday part of life throughout the world? And wouldn’t the documented rate of regressive autism be far higher in countries where childhood illnesses are much more endemic than in places like the United States? (Perhaps they are, but there is no evidence of this).
Moreover, shouldn’t we have seen a steady decline in reported ASD cases over the years in America, as increased vaccination, improved sanitation and wider access to medical care reduced the occurrence of at least some fever inducing infections?
I have also learned that Hannah has suffered from extensive bouts of fever ever since her autism diagnosis. Like with many ASD kids, her symptoms actually improve remarkably during these episodes, and when they happen, she seems to temporarily “come of her cloud.”
This temporary improvement was documented in the December, 2007 issue of Pediatrics in a study titled, “Fever May Briefly Alleviate Autism Symptoms.” The authors reported that, out of 30 ASD children observed before and after a 100.4 degree fever, more than 80% showed some improvement in behavior and other signs, and 30% showed “significant improvement.” Changes included longer concentration span, increased amount of talking and improved eye contact.
So my next question is: Hannah did not regress from fevers prior to 19 months of age and, after that point, fevers made her ASD symptoms actually improve – But wouldn’t her ASD symptoms be expected to deteriorate further, rather than improve temporarily?
Still other questions arise from the government’s move, which conceded that Hannah’s autism was, "caused by vaccine induced fever and immune stimulation that exceeded metabolic reserves."
There are at least two ways of interpreting this statement:
1) Hannah’s vaccines induced a fever, which IN TURN caused immune stimulation that exceeded metabolic reserves.
2) Hannah’s vaccines induced a fever, AND ALSO caused immune stimulation that exceeded metabolic reserves.
It's an important distinction.
In Hannah’s case, it is not at all clear that vaccine-induced fever, alone, would have caused an immune stimulation that “exceeded metabolic reserves.”
Isn’t it reasonable to ask if the immune stimulation that exceeded reserves was induced directly by the nine vaccine antigens, three live viruses, 50 micrograms of ethylmercury and many times more of aluminum (which is added to vaccines precisely in order to stimulate the immune system) given to her simultaneously?
In other words, were two separate biological events happening at the same time: Vaccine-induced fever AND vaccine-induced immune stimulation?
I know of several regressive ASD cases with documented diagnoses of mito dysfunction, but no fevers present during the period around the onset of encephalopathy. What happened in these cases? Is it possible that “vaccine-induced immune stimulation” alone could have triggered their regression, even without fever?
That will be the theory that is tested in the Krakow case, which was initially chosen to replace Hannah Poling as the first test case of the thimerosal causation theory. It turns out the Krakow boy tested positive for many of the same mitochondrial markers as Hannah, and he was promptly withdrawn as a thimerosal test case.
In this boy, the signs of autistic regression began after receiving a thimerosal containing vaccine, though no sign of fever was noted at the time. A month later, the child received a second mercury-containing shot and, once again, showed further (and more serious) signs of regressive encephalopathy – again without the involvement of any fever.
But do these mito children who regressed after vaccines, but not fever, really comprise just 1% of all autism cases in the country? The answer is we don’t know.
But even CDC Director Dr. Julie Gerberding has hinted that fever alone may not always be enough to trigger “ mitochondrial regression. On March 29, she told CNN’s Dr. Sanjay Gupta that, “If a child was immunized, got a fever, had other complications from the vaccines, and was pre-disposed with the mitochondrial disorder, it can certainly set off some damage (including) symptoms that have characteristics of autism.”
Dr. Gerberding needs to tell us exactly what kind of “other complications from the vaccines” befell Hannah just before she regressed..
Meanwhile, we need to find out how many more Hannah Polings are still out there, waiting to be counted.