The idea that mercury poisoning causes autism was first put forward in a paper by Sally Bernard and others entitled Autism: a novel form of mercury poisoning.
This was published in a journal called Medical Hypotheses. As you might tell from the title, Medical Hypotheses presents hypotheses-not proven ideas. The journal has no peer review process. Instead, they basically print “…will publish radical ideas, so long as they are coherent and clearly expressed”. If you write well and pay to publish, it will likely get in. Keep that in mind with any paper from “Medical Hypotheses”.
In this paper, the put forth the hypothesis that mercury causes autism. To support this idea, they compare the symptoms of autism and mercury intoxication.
In the Autism Omnibus Proceedings, Dr. Patricia Rodier spoke on specifically the Bernard paper. Dr. Rodier has a unique position in the United States, and likely the world: she is an expert on both mercury poisoning and autism. Below is a rough transcription based on the audio recording of that testimony.
She starts out by stating that she has many criticism of the Bernard paper. She also mentioned a response to that paper had already been published by Nelson and Bauman. That paper is worth reading, and it’s free on the Pediatrics website.
Dr. Rodier then discusses the comparisons made between mercury poisoning and autism, based on her experience with both. If you want the short version: there is no comparison.
First, many of the symptoms or characteristics that are discussed in the Bernard paper are not specific to either autism or mercury poisoning. These include, nausea, vomiting, irritability and temper tantrums. Basically, these are things that happen for all of us at times.
Other symptoms are common across many disabilities: mental retardation, depression and abnormal gait. Again, these are not specific to either autism or mercury poisoning.
Almost all the symptoms used for mercury poisoning are taken from “Mad Hatter’s” disease: the result of a very high exposure to inorganic mercury vapor. Only a few symptoms listed were from ethyl mercury exposure. Since the exposure from vaccines is due to ethyl mercury (thimerosal breaks down to ethyl mercury) that would be the valid comparison.
Dr. Rodier, in her testimony, then discussed how the Bernard paper doesn’t actually do what it purports to do. The comparison isn’t valid since the actual symptoms of autism and mercury poisoning do not match up in a comparison.
She then goes on to discuss many of the comparisons made by Bernard, et al., and show that the comparisons are not valid.
1. Under psychiatric disturbances, the paper discusses depression, flat affect, depressive traits, mood swings, impaired face recognition
1a. Depression is a symptom of acrodynia. This is an exposure to inorganic mercury, not ethyl mercury. While some, possibly many, autistics suffer from depression, it is not a characteristic of autism.
1b. Mood swings are a characteristic of Mad Hatters disease. Again, this is not an autism symptom or characteristic.
1c. Flat affect is a diagnostic trait for autism but not mercury poisoning . Also, this is the opposite of mood swings, a characteristic of mercury poisoning noted in ii, above.
1d. Impaired face recognition occurs in autism, but hasn’t even been tested in any kind of mercury poisoning.
So, in this first group of four: there is no overlap for the above 4 ‘symptoms’. If it happens in mercury poisoning, it doesn’t happen in autism and vice versa.
2. Under speech and language deficits, the paper describes:
2a. Verbalizing and word retrieval. This is a problem is observed in Mad Hatters disease but not autism. But, this is compared to ecololia and word use and pragmatic errors. These never happen in mercury poisoning. It is an autism trait.
3. Again under psychiatric disturbances, the paper lists “Lacks eye contact”, and “impaired vision” under mercury toxicity, compared to “problems with joint attention” as the ‘similar’ autism trait
3a. “lacks eye contact” is a symptom of autism, but not of mercury poisoning. Likewise, impaired visual fixation is a symptom of methyl mercury poisoning-the brain control of the eye muscles are impaired which doesn’t allow you to fixate on something-but is not a symptom of autism. Joint attention has nothing to do with vision. It is not a feature of any kind of mercury poisoning. It is a social impairment, not a vision issue.
4) Under CNS structure, they compare “progressive microcephaly” for mercury poisoning with “progressive microcephaly and macrocephaly” for autism.
4a. progressive microcephally is given as a symptom of mercury poisoning. The idea of ‘progressive’ is incorrect here. Also, microcephaly is a sign of methyl mercury toxicity prenatally, not postnatal exposure. Children are born with it.
4b. Progressive macrocephally is a sign of autism. However, it has never been reported in mercury poisoning.
5) Under Neurochemistry, they list “Causes demyelinating neuropathy” under mercury poisoning.
5a. Demyelinating nerorpathy results from a chronic exposure to inorganic mercury. It is not reported in autism.
5b) They list “demyelination in brain” as a characteristic of autism, but no one has ever listed this in autism and the reference doesn’t address it.
Dr. Rodier posed the question: since the authors are trying to show a connection between thimerosal containing vaccines and autism, why don’t they compare autism and ethyl mercury poisoning? Keep in mind, there are various forms of mercury (ethyl and methyl being two types of organic mercury). In their comparison, Bernard et al. have picked from ethyl, methyl and inorganic mercury symptoms. Dr. Rodier suggest the reason they didn’t stick to purely ethyl mercury symptoms because “It doesn’t make a good story”.
1) For example, in a paper by Zhang , 41 people were exposed to ethyl mercury from tainted rice. They knew dose from how much rice they ingested. The authors documented the symptoms. Doses varied from mild to death.
1a) The three most comment symptoms documented by Zhang were:
1a.i) Muscle Weakness
1a.ii) Loss of appetite
Dr. Rodier notes that “those don’t sound much like autism”.
1b) The next 10 symptoms listed by Zhang are
1b.ii) abdominal pain and diarrhea
1b.iv) numbness of the extreminties
1b.v) peresthesia and ataxia
1b.viii) unsteady gait
1b.ix) ringing in the ears
Dr. Rodier: again, none of these sound like any of the symptoms of autism that are used in diagnosis.
Dr. Rodier stresses at this point: there is really no correspondence between the symptoms of ethyl mercury poisoning and autism
The government’s attorney asked: the current hypothesis is that low levels of inorganic mercury cause oxidative stress or an inflammatory process which cause autism. Does that make sense? Dr. Rodier answered quite directly, “no”. In the opinion of that autism and mercury poisoning expert, the logic does not work.
She went on to point out that scientists try to disprove hypotheses, not just find support for their given hypothesis. (author’s note here: this is quite true. You need to test a hypothesis and make sure it doesn’t fail, not just collect the evidence that implies it is correct).
She points out that there is one piece of evidence that completely refutes the Bernard et al. hypothesis. There have been autopsy studies performed on people with acute ethyl mercury poisoning. While they indeed had high levels of organic mercury after the ethyl mercury was gone, these people recovered from the mercury toxicity symptoms after the ethyl mercury was gone and the had inorganic mercury was left.
This was the end of the discussion on the Bernard paper and mercury. It is pretty clear when an expert in both fields-mercury toxicity and autism-speaks on the comparison. Compare this to the authors who wrote the paper. Of the three, only one had a background in medicine. That is Lyndelle Redwood, a nurse. None of them are researchers, none experts in either autism or mercury poisoning.
From the above it is pretty clear: the hypothesis put forth by Bernard et al. was a poorly formed and is definitely incorrect.
In the Omnibus Proceeding, the discussion then moved away from mercury directly and into the question of environmental causes of autism. The question was posed: when does autism begin? The answer was that it almost always is determined pre birth.
This led to a discussion of known environmental factors that lead to autism. Dr. Rodier listed them and listed when the exposure has to occur to result in autism.
The known environmental causes are: Rubella, thalidomide, valproic acid, ethanol, misoprostol. All are involved during gestation. The timing of exposure to increase autism risk is:
1) Rubella (German measles): before the 9th week
2) Thalidamide: week 3 and 4
3) Valproic acid: week 3 and 4
4) Ethanol: week 3-5
5) Misoprostol: week 6
She noted that tuberous sclerosis is an example of autistic symptoms developing after birth as the tumors progress.
Terbutaline has been brought up a number of times by the plaintiffs (petitioners) in the Omnibus as an example of an environmental cause of autism. The question was raised as to why Dr. Rodier didn’t discuss this. She described that it is not an environmental cause study, but a genetic study.
Twin pairs were studied. Some were exposed to terbutaline and some were not. They compared the concordance: the rate of one twin having autism if the other did not. No significant increase was found in general in this study. So, the authors looked at a smaller subset, and still found no increase. Then, they looked only at male twins, where no autistic siblings were present in the family. In that case only, they found a significant effect.
Dr. Rodier goes on to discuss that even interpreting this part is difficult because we don’t know if the increased risk was due to the terbutaline, or the fact that the children were at risk of being born early (terbutaline is given to prevent premature delivery).
The judge (Special Master in this court) asked if this was because without the terbutaline the children would not have survived to be born. Dr. Rodier agreed and pointed out that the interpretation the plaintiffs are supplying is further confused because low birth weight is also an increased risk factor. This is from a very recent paper in Pediatrics. Since the turbutaline twins were low birth weight, that could be a factor in the increased autism risk found.
The plaintiffs lawyers have been using a study on rats as an example of a post-natal environmental exposure. The government lawyer asked if this was a valid interpretation. Could this be used to suggest a post-natal exposure could cause autism in humans? Dr. Rodier answered that this is not valid. Newborn rats are more developmentally immature than newborn humans. Newborn rats have closed eyes, no hair, and in other ways are very much more developmentally like prenatal humans. The study would compare better to late-gestation humans.
There was much more in her testimony, but that gets even farther away from the Bernard paper, so we can end this discussion here and let others pick up the rest of her testimony.