As we enter the heart of flu season, industry pressure to rehabilitate thimerosal (the ethyl mercury-based vaccine preservative) has been escalating. Just last week, The Wall Street Journal ran an opinion piece blaming swine flu vaccine shortages on the demand for mercury-free formulations. According to the author, venture capitalist Scott Gottlieb, one of the main reasons you can’t get the swine flu vaccine is that the Obama administration has been “too cautious” in managing vaccine safety. He blamed three “fateful policy decisions” for restricting swine flu production, one of which was that “the government demanded single-dose syringes because they contain smaller amounts of thimerosal than multi-dose vials.” According to Gottlieb, “This mercury-containing vaccine preservative continues to stir concern it can trigger childhood autism, even though this has been firmly disproven.”
Coming from Gottlieb, this argument should be taken with a grain of salt (Gottlieb has acknowledged relevant conflicts. As a former FDA official in the Bush administration, see (HERE), he had to recuse himself from decisions involving Eli Lilly drug approvals; Eli Lilly sponsored research led to the invention of thimerosal). But Gottlieb was merely the point man for a commonly held view in the vaccine and medical industries. And over the last few months the vaccine industry has shifted their promotional activities into overdrive, eagerly exploiting the opportunity to market the novel threat of the swine flu. In the process they have bundled their full throttle marketing of flu vaccines with a renewed push to eliminate what they see as unnecessary obstacles to flu vaccine production (what others might call prudent product safety measures).
But this new propaganda blitz suggesting that thimerosal is safe—and that merely providing a thimerosal free option is excessively cautious—has scant scientific evidence to support it. Indeed, the overwhelming weight of evidence from animal studies suggests that exposing infants and fetuses to ethyl mercury always was, and continues to be, a bad idea.
In September, a new animal study from a group at the Institute of Psychiatry and Neurology in Warsaw provided the latest evidence of harm to infants from vaccine level doses of thimerosal. One of the methods they used, a heat sensitivity assessment called the “hot plate test”, had a special resonance for me. I saw my daughter flunk a real life version of this test just a few days before she got her formal diagnosis of autism.
[The] epidemic of autism spectrum disorders (ASD) is one of the most alarming public health problems, as the prevalence of autism has been dramatically increasing during the past 20 years world-wide with tragic personal and social consequences. Before 1970 the incidence of ASD was 1 in 2000 children, now in the USA and many other developed countries it is 1 in 150 children. The etiology of ASDs is multifactorial, having both genetic and environmental components, but the evidence strongly suggests that early-life – prenatal and postnatal – exposure to hazardous substances may be responsible for the observed rise in the incidence of autism.
The objective of this research project is to investigate, in a combination of multidisciplinary clinical and preclinical studies, the biological mechanisms of neurodevelopmental toxicity induced in children by certain environmental toxins, particularly mercury and lead.
Conference abstracts often provide the first signals of future publication results and the sponsor group’s abstract, entitled “Vaccine Preservative, Thimerosal, Causes Wide-Spread Neurodevelopmental Disturbances in Young Rats”, provided just such a clue. The abstract didn’t provide much detail, but it made clear that the research was showing evidence of harm to infant rats after receiving an exposure to thimerosal similar to that received under the American childhood immunization schedule during the 1990s.
And in a September article published on line in the journal Brain Research, the Warsaw team revealed their first peer-reviewed findings (HERE). The study design was simple and the results unambiguous. But the methods might strike close to home for some autism parents unfamiliar with the term “nociception.” They certainly struck home for me, and I’ll admit I had to look the word up.
The Warsaw group’s paper followed a protocol for thimerosal administration in rodents first designed by Mady Hornig at Columbia University. Hornig’s group used two different genetic mouse strains (one that was susceptible to autoimmunity and another that was not) and in each strain compared unexposed infant mice to those injected with thimerosal (injections were on days 7, 9, 11 and 15) on a schedule designed to mimic the typical vaccine schedule for human infants (with vaccinations at months 2, 4, 6 and 15) and at comparable weight adjusted doses. The Warsaw team followed the same plan of thimerosal injections with infant rats of two different strains and followed up the exposures with measures of mercury metabolism and infant development, comparing rats injected with thimerosal to those injected with a saline placebo.
When the rats reached 6 weeks of age (an human equivalent age just under 3 years), the Warsaw experimenters tested them for impaired “nociception”, or the “neural processes of encoding and processing noxious stimuli.” In this case, they tested the rats to see how sensitive they were to heat by placing the infant rats on a hot plate (a little over 130 degrees Fahrenheit) and seeing how long it took them to show their discomfort, either by licking their paws or jumping from the plate. This “hot plate test” is a highly standardized animal protocol for pain sensitivity testing, finely tuned to provide just enough heat to generate discomfort but not enough to actually burn the baby rodents (after 30 seconds on the hot plate, the infants were removed “to prevent tissue damage” if they didn’t show any reaction). The amount of time before paw-licking or jumping is measured using a stop watch.
In the susceptible strain, the Warsaw team found that the difference between the infant rats exposed to thimerosal and those with no exposure was highly significant. Unexposed rats took about 10 seconds before they demonstrated discomfort on the hot plate (8 seconds for males and 11 seconds for females); rats exposed to vaccine level doses of thimerosal took about twice as long before they reacted to the heat (over 15 seconds for the males and close to 25 seconds for the females). The researchers concluded that this was the result of “long term neurodevelopmental alterations in brain organization and function.”
This finding of harm due to thimerosal exposure is by no means the first in such animal models. In a 2004 paper, Hornig’s susceptible strain of mice showed clear evidence of developmental delay and altered brain development when compared with unexposed mice. In 2007, Peruvian researchers published similar experimental evidence using hamsters; they followed Hornig’s protocol and found clear evidence of developmental delay and brain injury (HERE).
Interestingly, neither of these two studies exposed the study animals to thimerosal at birth. When a recent study group from the University of Pittsburgh and Thoughtful House examined infant primates to see whether a birth dose of thimerosal-containing hepatitis B vaccine influenced development (HERE), they found significant delays in a group of survival reflexes in the exposed infant monkeys.
In the only other study performed on mice, a group from the University of California that was funded by NIH attempted to replicate Hornig’s mouse model, but found little effect from thimerosal. This apparent contradiction left open the question, which group was correct, California or Columbia? Based on several recent studies, the weight of the evidence seems clear: only the NIH group has been unable to replicate Hornig’s work (suggesting the California team’s methods may have been flawed), while researchers from Peru to Poland have supported the Columbia findings.
In short, Hornig was right. Thimerosal in vaccines is dangerous to infants.
When science imitates life
In late August 1998, our family took a vacation at a friend’s house on the Gulf Coast of Florida. One sunny day, I was sitting in a chair reading a book when I noticed my daughter Michaela, who was then just shy of three years old, toddle up to a reading lamp that was standing right next to my chair. It was early in the afternoon, the room was full of light and I thought the lamp was turned off. She put her fingers up to the light bulb and just after touching it pulled her hand back sharply. Then she just wandered on about the room, with no further reaction or indication of discomfort. I was concerned, however, so I reached up to check the lamp and was surprised to find that the bulb was scalding hot. It was one of those adjustable brightness lamps, and someone had turned the brightness all the way down without switching the light all the way off. I watched Michaela a bit more, waiting for the inevitable wail of pain that never came. Figuring there was nothing to worry about, I switched off the light and continued reading.
The next day, we were all walking towards the beach when I reached down to hold Michaela’s hand as we were about to cross the street. I noticed that her fingers had an angry burn on them where she had touched the light bulb the day before. Her skin had started blistering and it was clear that her brief encounter with the standing lamp had given her what must have been a painful burn. I told my wife about what had happened and we went back to the house to tend to her wound.
But what amazed me most was that my little girl never showed a hint of distress. If I hadn’t seen her pull her hand back from the bulb I would never have known what had happened. She never cried; she never displayed any sign of pain or “nociception”; she barely even noticed.
And, of course, she never spoke a word because she wasn’t speaking at all back then. Just a week later, on the Friday before Labor Day, we had a meeting with a developmental pediatrician at Boston Children’s Hospital and received official notification that Michaela was autistic. The Labor Day weekend that followed was a time of profound shock, and that Friday was the day our lives changed forever.
But in my mind’s eye, I often return to that image, just a few short days before, of Michaela touching the light bulb. It was for me, the single most vivid demonstration that something wasn’t quite right with my little girl. Looking back, it’s clear that she had stumbled into a domestic version of the hot plate test, one operating at temperatures that would provoke charges of cruelty in an animal experiment, but one with starkly similar results. Born in November 1995, Michaela received almost the identical weight-adjusted thimerosal doses as the Columbia University mice, the Peruvian hamsters and the Warsaw rats (more, in fact, since she had also received the birth dose that the Pittsburgh primates had received). So reading this new study from Warsaw meant more to me than most other scientific papers; it was one of the handful of papers I’ve ever read where the experiment literally jumped off the page.
After all, I’d already seen it with my own eyes.
Mark Blaxill is Editor At Large for Age of Autism.
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