A $50 million program is going beyond genes to find answers about what's causing rising prevalence of autism, emphasizing a need to look at "under-studied" factors
The intervention aspect is very important and innovative. Intervention studies have already been done regarding early life screen exposure and the manifestation of autistic-like symptoms in toddlers. Parent training, stopping the affected child's screen time, and greatly increasing social interactions and play with non-electronic playthings has been shown to greatly lessen autistic-resembling symptoms in affected children. Some background: https://durablehuman.com/VirtualAutism
Very interesting. I don't think the effort will result in anything but some researchers getting paid, but maybe that's some benefit. Bobby Kennedy is an expert at doing this kind of flashy, political posturing that looks like something is getting accomplished even when it isn't.
As to your hypothesis that toxins cause epigenetic problems in parents' sperm and ova that results in autism, how would you ever be able to test that hypothesis? Since you can't do experiments on humans, the only option is causal inference, and it would be very hard to get the data to support that tool's use.
It does remind me, though, of when Richard Doll and AB Hill went out and interviewed so many lung cancer patients to see what caused their cancer. There were lots of possible suspects -- Richard Doll thought tar used to pave roads the most likely culprit. But as he said, as they talked to more and more people, 2/3 of the way into the study he gave up smoking.
Richard Doll and AB Hill had a debate with Ronald Fisher about just what was a valid test of the smoking causes lung cancer hypothesis. Even today it's unclear how to infer causes, but thanks to people like Judea Pearl, the causation toolkit has expanded.
As a side note, I was interested to see that sevoflurane may be causing epigenetic harm. Back in 1992 when I was working as a lawyer in Japan I did the legal work on the deal between Maruishi, Abbott, Baxter and Central Glass that gave worldwide rights to use the drug. It's a shame that it might have these terrible consequences.
I didn’t go into detail here, but using two-generation datasets (available to varying degrees in Israel, Sweden, Denmark, some US cohorts, and more) this “F1 exposure, F2 outcome” hypothesis could indeed be explored. Yes, as with all epidemiology the results would show associations only unless the cohort also had data on transcriptional irregularities in F2. Actually I think the RFA would allow for creation of brain cortical organoids of F2. Maybe.
In any event your analogy to cigarettes and lung cancer is apt. I’ve surveyed about 350 autism parents about these sorts of associations, eg F1 history of surgeries and F2 neurodevelopmental outcomes, which gave rise to this hypothesis.
Re sevoflurane— how interesting re your personal connection to its history. I definitely encourage you to watch my Harvard presentation….
And please explain the Judea Pearl work. I’m a fan of his. His daughter incidentally has done research on maternal smoking and autism risk (not finding much)
The intervention aspect is very important and innovative. Intervention studies have already been done regarding early life screen exposure and the manifestation of autistic-like symptoms in toddlers. Parent training, stopping the affected child's screen time, and greatly increasing social interactions and play with non-electronic playthings has been shown to greatly lessen autistic-resembling symptoms in affected children. Some background: https://durablehuman.com/VirtualAutism
Very interesting. I don't think the effort will result in anything but some researchers getting paid, but maybe that's some benefit. Bobby Kennedy is an expert at doing this kind of flashy, political posturing that looks like something is getting accomplished even when it isn't.
As to your hypothesis that toxins cause epigenetic problems in parents' sperm and ova that results in autism, how would you ever be able to test that hypothesis? Since you can't do experiments on humans, the only option is causal inference, and it would be very hard to get the data to support that tool's use.
It does remind me, though, of when Richard Doll and AB Hill went out and interviewed so many lung cancer patients to see what caused their cancer. There were lots of possible suspects -- Richard Doll thought tar used to pave roads the most likely culprit. But as he said, as they talked to more and more people, 2/3 of the way into the study he gave up smoking.
Richard Doll and AB Hill had a debate with Ronald Fisher about just what was a valid test of the smoking causes lung cancer hypothesis. Even today it's unclear how to infer causes, but thanks to people like Judea Pearl, the causation toolkit has expanded.
As a side note, I was interested to see that sevoflurane may be causing epigenetic harm. Back in 1992 when I was working as a lawyer in Japan I did the legal work on the deal between Maruishi, Abbott, Baxter and Central Glass that gave worldwide rights to use the drug. It's a shame that it might have these terrible consequences.
I didn’t go into detail here, but using two-generation datasets (available to varying degrees in Israel, Sweden, Denmark, some US cohorts, and more) this “F1 exposure, F2 outcome” hypothesis could indeed be explored. Yes, as with all epidemiology the results would show associations only unless the cohort also had data on transcriptional irregularities in F2. Actually I think the RFA would allow for creation of brain cortical organoids of F2. Maybe.
In any event your analogy to cigarettes and lung cancer is apt. I’ve surveyed about 350 autism parents about these sorts of associations, eg F1 history of surgeries and F2 neurodevelopmental outcomes, which gave rise to this hypothesis.
Re sevoflurane— how interesting re your personal connection to its history. I definitely encourage you to watch my Harvard presentation….
And please explain the Judea Pearl work. I’m a fan of his. His daughter incidentally has done research on maternal smoking and autism risk (not finding much)