
Anonymous wrote:Anonymous wrote:Anonymous wrote:So, in a few years, insurance companies will deny all autism coverage by saying they shouldn’t have to pay for treatments because mom intentionally gave her kid autism by taking Tylenol. Mothers of autistic kids will be pariahs.
What will they do with me? I have fraternal twins. One has autism and the other is neurotypical. Did all of the Tylenol only go to one baby?
I’m also an autism parent. I hope your family is doing well and that you all are hanging in there. I say this with respect and compassion, but it’s odd to me that your experience leads you to parody people positing an environmental component. Plenty of people will say that autism “is genetic,” insinuating (or even outright saying) that whether a child has autism follows ineluctably from that child’s genes, when, in fact, the experience of twins (including monozygotic twins) shows that it surely is much more complicated than that.
Anonymous wrote: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.
Anonymous wrote:Anonymous wrote:Anonymous wrote:So, in a few years, insurance companies will deny all autism coverage by saying they shouldn’t have to pay for treatments because mom intentionally gave her kid autism by taking Tylenol. Mothers of autistic kids will be pariahs.
What will they do with me? I have fraternal twins. One has autism and the other is neurotypical. Did all of the Tylenol only go to one baby?
I’m also an autism parent. I hope your family is doing well and that you all are hanging in there. I say this with respect and compassion, but it’s odd to me that your experience leads you to parody people positing an environmental component. Plenty of people will say that autism “is genetic,” insinuating (or even outright saying) that whether a child has autism follows ineluctably from that child’s genes, when, in fact, the experience of twins (including monozygotic twins) shows that it surely is much more complicated than that.
Anonymous wrote:Anonymous wrote:Anonymous wrote:Sone people believe that 1 in 12 are born with autism. How many of you know children who are disabled with autism?
Disabled with autism, or experience life differently than others in part because of autism?
Disabled. Because people experiencing life differently should not be included in the autism diagnosis. It takes services away from the children who will never have a conversation with anyone, will never live alone, will never get married, have children, who will be stunted at the age of a child. That’s what autism is.
Anonymous wrote:Anonymous wrote:Anonymous wrote:Anonymous wrote:Anonymous wrote: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.
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?
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.
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.
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 wrote:Anonymous wrote:Anonymous wrote:Anonymous wrote: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.
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?
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.
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 wrote:Anonymous wrote:Anonymous wrote:Anonymous wrote: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.
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?
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.
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.
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.
Anonymous wrote:Anonymous wrote:Anonymous wrote: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.
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?
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 wrote:Anonymous wrote: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.
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?
Anonymous wrote:I’m surprised they went with Tylenol vs SSRIs.