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Originally Posted by Astral Mama 
I'm sorry, I've tried to explain it twice. I don't see how I can be clearer. But I'll try once more:
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Thank you for taking the time to reply, again.
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| It's not directly relevant to this question whether some people excrete mercury more or less quickly than others (or anything else specific about how the body handles mercury.) |
Why not? Surely exposure is only part of the picture? Why would you expect a uniform response across the population when exposed to anything?
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| The question is whether mercury exposure leads to ASDs. |
That is the question this study addresses, yes.
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| An interesting sub-question is whether mercury exposure leads to ASDs in some people but not others. (Whether that's because they excrete it more slowly, or, say, have some slightly altered protein or neurotransmitter that is somehow inactivated by mercury, or whatever else -- differing sensitivity to mercury could be caused by any number of different specific mechanisms.) |
I agree. It is an interesting question/subquestion. And one that I think is relevant.
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| The real question is not about whether some people excrete mercury more slowly, it's about whether or not some people develop ASDs because of exposure to mercury. |
I am not sure why you mean by 'the real question'? Is it an irrelevant question to ask if some people who were exposed to mercury were at more risk of damage due to a 'glitch' in their biology? If so,why?
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| But the thing is, even if it's only a subgroup, unless it was a very, very minuscule group, or the effect was very, very tiny, it would have shown up in this or some of the many other studies that have been done on thimerosal and ASDs, because at least some of those people would have been included in the study groups and they would have been disproportionately diagnosed with ASDs, thus resulting in a correlation between thimerosal exposure and ASD diagnosis. There isn't a correlation, in this study or in the other studies that have been done. |
I guess the part I am not understanding is how a correlation can be found between two phenomena without knowing if one of the phenomena exists or not. How could this study (or previous ones) have found this correlation if they were not measuring for it/did not even know if it is a real phenomena or not?
Also considering that 4 million new babies are born every year in the US, how many children would need to be in a study to get accurate data? Can 256 children represent the Autistic population in the US (approximately 750 000 from what I understand)?
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| There's no value in studying excretion of mercury -- at least not for this purpose -- because it doesn't actually get at the question (to whit: does mercury cause autism.) |
This is the part I am not understanding. It is subtle, but I think the question is probably CAN mercury cause Autism, and if so, under what conditions? Ruling out exposure alone within a relatively small sample does not rule it out altogether, or does it?
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| If there's some significant subpopulation that is liable to get autism from mercury exposure, a study like this wouldn't necessarily show that -- instead, it would show that the general population was liable to get autism from mercury exposure, because a random group of participants would include some mercury sensitives. |
I have read this a couple of times and I am still not sure I understand what you are saying. I will try and paraphrase.
Should a study be done that compares how well individuals in a sample excrete mercury, this would be not be valuable as it might suggest that mercury sensitivities are not associated with Autism, but something that exists in the population with no correlation to Autism?
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| I'm not trying to have it both ways. I don't understand why you find those two simple facts contradictory. I never said whether or not the actual rate of autism in the population was increasing. |
Repeating your statement without explaining it does not help me understand. However, I accept that I do no need to understand everyones point of view.
Perhaps there are others on this thread who understand more clearly what you are saying and can explain it to me more successfully.
Something that is on my mind with regards to the 'only the exposure is the relevant question.'
Prior to the vaccine being introduced, Hib was something pretty much every child was exposed to. Was exposure alone responsible for developing Hib Meningitis? No, only a very small percentage of children (20 - 60 cases per 100 000) were developing Hib meningitis, pointing to something specific to the child/Hib interaction, and not exposure alone. Taking a sample of 1000 children would not have helped identify who was at risk for Hib meningitis.
Anyway, I realise I am not about to crack the answer to these questions, but I am concerned that the action points given in the
first article posted in this thread:
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# Discuss with parents that data from a recent case control study indicates no increased risk of autism from prenatal and infant vaccination with thimerosal-containing vaccines.
# Further discuss with parents that this latest study adds to data collected from four previous studies, all of which fail to demonstrate any connection between the development of autism and prior exposure to thimerosal-containing vaccines. |
could be misleading. I do not know how many parents would know to ask whether exposure alone is what predicts whether a child develops Autism or not.
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