is RKFJr's "Tylenol(TM) causes autism" just a shakedown for extortion money from the company?
![[Post New]](/jforum/templates/default/images/icon_minipost_new.gif){kind=icon}
Anonymous
|
Yes. And so many women will take home from this that Tylenol use in pregnancy is dangerous (which it is not), and so they will reach for NSAIDs, which have a high risk of closing the fetal PDA and resulting in miscarriage or stillbirth. |
Anonymous
| I’m surprised they went with Tylenol vs SSRIs. |
Anonymous
Tylenol is easier to say. |
Anonymous
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. |
Anonymous
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. |
Anonymous
It's almost like there is an entire infrastructure to repetitively test children and keep them in a setting where they are forced to interact with each other, and where if the child falling behind -- unlike for adults, when you are on your own -- there is another entire infrastructure with legal requirements for supports to be given and then reassessed. Oh yeah. It's called school. |
Anonymous
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. |
Anonymous
DSM IV to V made diagnosis a wider net. We also standardized screening children earlier to be able to provide interventions earlier. We cast a wide net to help those who need it and yes, that increased diagnosis rates. |
Anonymous
+1 and I used to do research with animals |
Anonymous
|
The irony is that while there is no solid evidence linking Tylenol use in pregnancy to autism, there IS solid evidence linking second trimester fevers to autism. Just one example: https://pubmed.ncbi.nlm.nih.gov/28607458/.
I did not hesitate to take Tylenol when I had a fever during one of my pregnancies because I was familiar with the research on maternal immune activation and potentially mega rive effects on the developing brain. The evidence to date suggests it’s better for the baby to get a fever under control than to let it rage. |
Anonymous
You are DEAD WRONG. Have you parented one of these children? If not then STFU. |
Anonymous
There genetic components already located. It’s also closely related to Schizophrenia. Regarding twins - Studies have found that autism spectrum disorder (ASD) aggregates in families, and twin studies estimate the proportion of the phenotype variance due to genetic factors (heritability) to be about 90%. https://pmc.ncbi.nlm.nih.gov/articles/PMC5818813/#:~:text=Studies%20have%20found%20that%20autism,)%20to%20be%20about%2090%25. I don’t know why people can’t understand how genetic mutations happen and how far science has come with identifying where disorders come from. Identifying the genes that can mutate is the one of the steps needed to intervene and one day completely eliminate. |
Anonymous
I’m too tired to read the full text versions of these articles, which are probably behind a paywall anyway. Do any of them mention the possibility that the condition/reasons that prompted the frequent Tylenol use could underlie the link to autism? For example, a parent might give a really fussy infant Tylenol thinking they are in chronic pain. But the fussiness is actually due to their brain wiring being different, leading to sensory overload/irritability that they cannot communicate so they just cry. The gold standard is RCTs which we can’t do for ethical reasons. Data based on retrospective self reports can be quite flawed. Just because something for published in a journal doesn’t make it a great study. |
Anonymous
It is more complicated. There is something called epigenetic changes which don’t always affect monozygotic twins equally. There’s also a really interesting thing called endophenotypes. These are behavioral or cognitive traits relevant to a psych disorder, that people can show without fully meeting the diagnostic criteria. If a family has enough of these endophenotyes, they can “pile up” in an offspring and tip them over into meeting the full diagnostic criteria. So a child with autism might have a parent who is very rigid, an uncle who always had social difficulties, a grandparent who showed restricted interests, etc. |
Anonymous
In addition to all the other debunkings of 1-7 PP, autism diagnoses doubled from 2008 to 2018 (sample of 8 yr olds), before DSM-V was published.
|