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Reply to "is RKFJr's "Tylenol(TM) causes autism" just a shakedown for extortion money from the company? "
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[quote=Anonymous][quote=Anonymous][quote=Anonymous][quote=Anonymous][quote=Anonymous][quote=Anonymous]The JAMA study only looked at risk during pregnancy. There is more than one study that found an increased risk with Tylenol given after delivery to infants and children. https://pmc.ncbi.nlm.nih.gov/articles/PMC5536672/ https://pmc.ncbi.nlm.nih.gov/articles/PMC5044872/ https://pmc.ncbi.nlm.nih.gov/articles/PMC10915458/ https://pmc.ncbi.nlm.nih.gov/articles/PMC7017213/ Anecdotally, sample size of 1- I know someone who gave their baby Tylenol probably twice a day for nearly a year for "teething"... the child turned out severely autistic. Who knows if that was the cause, but I can't help but wonder whenever I see the child. [/quote] The first one you list isn't even a study, as it was called by you. It's a review article of theories. Did you read these studies, or are you just googling things and listing them without bothering to analyze them?[/quote] Autism has a very strong genetic (60-80%) component. It’s become more common largely because the diagnostic criteria are more expansive than before. The diagnostic criteria for autism previously only included around the top 1% of the human with the most severe behavioral symptoms, but now the current diagnostic threshold covers around the top 3% with the most severe behavioral symptoms. This is basically how almost all diseases work, there is a liability threshold where it becomes a condition, whether it is heart disease, osteoporosis or autism, things are not black and white. There is no discrete point where people have (most) diseases. There is just a liability threshold where the medical community has come to a scientific consensus that that treatment/diagnosis is clinically beneficial for people. [/quote] 1. To say that it has a genetic component is not to say that its presence or absence turns solely or even primarily on genes. The discipline of “epigenetics” tells us that genes can sometimes be altered by their environment. 2. The switch from the DSM-IV to DSM-V made it harder to get an autism diagnosis, not easier. 3. If liberalization of diagnostic criteria accounted for the increase in autism rates, we’d expect the fastest growing group to be the middle aged or seniors. In reality, it’s children whose ASD rate is rising fastest. 4. There is emerging research to suggest that non-genetic biomarkers may be found in, e.g., the hair and the gastrointestinal system. 5. If it were all genes, you’d expect identical twins to be either both NT or both autistic. That’s not what we see. One study of autistic monozygotic twins found a concordance rate of ~40%. 6. There are animal models of autism. To conduct those experiments, they need a way to get mice that show stereotypic behavior and restricted social abilities. Take a look at how they make them. (Hint: it’s not just “get the ones with the autism genes.”) 7. You can have a misleading correlation between genes and outcome. If you have two X chromosomes, it reduces your odds of being the president. That’s not because there’s a presidency gene; it’s because of sexism. [/quote] DP. You’re kind of contradicting yourself with 1 and 5. Epigenetic changes could affect monozygotic twins differently. With regard to 6, animal models of autism have serious limitations. We can only really model specific symptom domains and cannot recapitulate the whole disorder in an animal. We also can’t ask the mice whether their lack of social interaction is due to lack of interest or lack of understanding how to interact. It’s a huge leap to go from showing that a particular environmental factor increases repetitive behavior and decreases social and interaction to “this environmental factor causes autism”. Never mind that a lot of researchers doing the mouse model studies don’t do social behavior assays properly and overinterpret their results. [/quote] +1 and I used to do research with animals[/quote]
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