lol. Trump and RFK says it harms people and these dopes believe it.
It does. The data shows it. Pregnant women who use tylenol on a regular basis thru their pregnancy increase the chances of developmental harm to their unborn kids. All the data supports this
"all?" the metastudy author you are referring to even admits there are counter studies, he just disputes their quality.
Of course Tylenol doesn’t. You know what does? Excessive masturbation. Before you proudly gotcha interrupt with “then how come three-year-olds are diagnosed with autism?”, it’s not the child stupid, it’s the parents. If you masturbate a lot before procreating, the physiological semen rejuvenation process causes advanced ejaculation and glycation end products that epigenetically makes new sperm cells increasingly likely to possess the autism mutation.
There. That’s my theory. Prove me wrong. Hah, hoo!
That would mean every letsrun poster would have Autistic kids.
actually, if you take their argument literally, if aspirin use among mothers is pervasive, but autism/ASD merely a percent risk, they are at best saying aspirin causes autism in 1-3% of cases -- the prevalence we are tossing around. trump would be fibbing even about that risk level.
in reality, the primary cause of autism is understood to be polygenic, followed by preemies. there are few environmental theories.
so it would really at best be a percent of the percent. some tiny chunk of 1-3% of births.
and that's a correlation and not proven.
at which point, using their best case scenario, we also need to do comparative risk. what is the percent risk a sick mother dies or cooks their baby without treating fever, vs. what is the risk aspirin causes autism.
the same sh*t argument was done on covid. if the risk of dying or being disabled from covid unvaxxed exceeds theoretical vax risk, only an idiot obsesses about the downside risk. and the deal is the unvax risk is calculable, while the downside risk is generally speculation and theoretical.
you can post all the studies you want. when the fact based world has dealt with this question (a) FDA still allows aspirin to be used by moms. (b) the court said the expert was unreliable.
(a) says the agency FDA empowered to police drugs is not convinced. if it was, it would be banned. or "black boxed."
(b) says the court viewed this autism theory as so unconvincing it did not even see a jury.
setting aside (c) what the psychologists and neurologists and whatnot think. which is not this theory. they think it's mostly genetics or preemie babies who are hypoxic or something like that. my brother is aspberger's. he was a briefly hypoxic preemie.
that is the reality based community talking.
trump can go say whatever he wants to cameras.
and to circle back to my brother. in terms of the numbers. he would not have counted as autistic under the original definition. he counts only when it broadens to ASD and includes aspberger's. that's your statistical uptick right there.
quit wasting people's time with conspiracy theories.
i mean, make your minds up whether it's caused by MMR or aspirin or being a browns fan. you can't even keep that story straight.
this is such a d@mned waste of time. autism is hereditary and polygenic, there are 100s of identified autism genes and the more you have the bigger your risk. there are studies showing twins and siblings having similar rates of autism.
if autism is sometimes environmental, that's rare. one rare explanation is being a premature birth. another is fetal exposure to mother taking VPA.
it's a fib to suggest aspirin "causes it" entirely. based on the limited environmental rate and inconsistent studies you are at best chasing another rare tertiary cause.
my brother fits ASD. i know he was preemie. that's not aspirin.
trump wants it to be aspirin instead of genetics because he can control the FDA by claiming it's caused by a drug. he can't control your genes or use genetics as a lever for political reasons.
From 1 in 10k to 1 in 30 in the past 35 years.
Amazing how much genetics have changed in such a short time.
It does. The data shows it. Pregnant women who use tylenol on a regular basis thru their pregnancy increase the chances of developmental harm to their unborn kids. All the data supports this
"all?" the metastudy author you are referring to even admits there are counter studies, he just disputes their quality.
Yes. No studies done. All we have is data. And the data proves this
"Physicians, researchers on the very studies cited in support of Trump’s position and even other members of the president’s administration are largely united on a few key facts: untreated fevers in pregnancy pose real risks to the fetus, acetaminophen (Tylenol’s active ingredient) remains the safest medication to treat them and any pregnant person seeking advice on the issue should consult their doctor."
“All that we should be asking of the medical profession [is] to actually weigh the risks and benefits for the women, with the women, and be cautious about chronic use of pain medications,” said Dr. Beate Ritz, a UCLA professor of epidemiology who co-authored a paper published last month that the White House cited as evidence for the link between Tylenol and autism."
"The conclusion of the paper, which reviewed existing studies on the topic, was that the association between acetaminophen use in pregnancy and later diagnoses of neurodevelopmental disorders in kids was strong enough to merit doctors’ consideration when determining how to treat fever or pain in pregnancy. The group did not determine a causal relationship between the drug and autism, or suggest barring the drug altogether, she said. “Looking at all of these studies, yes, there is a risk,” Ritz said. “It’s not very big, but it’s there, but the risk increases are more seen in regular users of Tylenol. This is not a woman who has a fever and takes three Tylenols.”
"Her co-author, University of Massachusetts epidemiologist Ann Bauer, has made similar statements. “What we recommend is judicious use — the lowest effective dose [for] the shortest duration of time under medical guidance and supervision, tailored to the individual,”
“The FDA’s letter, while significantly more nuanced than the president’s comments on the issue, still gives too much weight to findings from poorly designed studies,” she said.
“Acetaminophen is one of the few options available to pregnant patients to treat pain and fever, which can be harmful to pregnant people when left untreated,”
But it's all a great distraction from the fact that noone's ever been really allowed to look thoroughly and seriously at the effects of nicotine in the mother's bloodstream, thanks to the cigarette industry stranglehold on research unflattering to it. And, of course, from the old BFF's files, and increasing signs of economic and foreign policy failure.
"list all meta-analysis and systematic reviews on acetaminophen and neurodevelopmental disorders and their conclusion" Grok PubMed: 29688261 + association PubMed: 30654621 + association PubMed: 29341895 + association PubMed: 34046850 + association but weak PubMed: 35175416 + association PubMed: 35989852 + association PubMed: 35206317 + association PubMed: 36939050 + association PubMed: 37321575 + association strong PubMed: 38255358 + association PubMed: 38592388 Null PubMed: 40804730 + association DOI: 10.1097/AOG.0000000000005802 + association 13 meta-analysis or systematic review from 2018-present, only 1 with a null association. Selecting the 1 is the very epitome of "cherry picking" And Ahlqvist et al has flaws one could drive a semi-truck through.
With such a vast body of knowledge and research, this rabbit hole is more like a Grand Canyon. Stay tuned...
"list all meta-analysis and systematic reviews on acetaminophen and neurodevelopmental disorders and their conclusion" Grok PubMed: 29688261 + association PubMed: 30654621 + association PubMed: 29341895 + association PubMed: 34046850 + association but weak PubMed: 35175416 + association PubMed: 35989852 + association PubMed: 35206317 + association PubMed: 36939050 + association PubMed: 37321575 + association strong PubMed: 38255358 + association PubMed: 38592388 Null PubMed: 40804730 + association DOI: 10.1097/AOG.0000000000005802 + association 13 meta-analysis or systematic review from 2018-present, only 1 with a null association. Selecting the 1 is the very epitome of "cherry picking" And Ahlqvist et al has flaws one could drive a semi-truck through.
With such a vast body of knowledge and research, this rabbit hole is more like a Grand Canyon. Stay tuned...
Missing Gustavson 2021. AI tools aren’t amazing research assistance if the goal is an exhaustive review.
Again, this is literally what Baccarelli tried to scam. Compile a bunch of crap studies and write off the two best (Gustavson and Ahlqvist).
You don’t seriously think that a proper analysis is just counting the number of studies on each side? I know you know better than that, but the lazy use of AI slop makes me suspicious.
this is such a d@mned waste of time. autism is hereditary and polygenic, there are 100s of identified autism genes and the more you have the bigger your risk. there are studies showing twins and siblings having similar rates of autism.
if autism is sometimes environmental, that's rare. one rare explanation is being a premature birth. another is fetal exposure to mother taking VPA.
it's a fib to suggest aspirin "causes it" entirely. based on the limited environmental rate and inconsistent studies you are at best chasing another rare tertiary cause.
my brother fits ASD. i know he was preemie. that's not aspirin.
trump wants it to be aspirin instead of genetics because he can control the FDA by claiming it's caused by a drug. he can't control your genes or use genetics as a lever for political reasons.
From 1 in 10k to 1 in 30 in the past 35 years.
Amazing how much genetics have changed in such a short time.
It’s all diagnostic changes.
Are you curious about the apparent rise in autism rates?
Are you fearful of an autism "epidemic" that might affect your kids?
I read the first study. It's sad this this is considered one of the best studies we have on acetaminophen.
It collected prescription-issued data and on a small subset, self-reported data but only for the first 12 weeks of pregnancy and only a yes/no response! Major questions were left unanswered.
When did the acetaminophen group take it? Specifically, during what trimester? How many consecutive days did they take it? What dosages were they taking? How many times did they take it during pregnancy? Did the women reporting yes take one pill or one bottle a month? In the self-reported group, what did they take AFTER the first 12 weeks of pregnancy?
The study provides no answers to ANY of these questions! A far better approach would be to follow several thousand pregnancies over a few years and get answers to all of these questions.
Frustrated with this study, I did a few searches on my own and found this.
Prevalence of autism in US: ~3.0%
Prevalence of autism, Sweden: ~0.4%
Sweden consumes ~ 3x more acetaminophen than the US.
My takeaway (after wasting nearly a day on this) is that something is causing autism at higher rates in the US and it's *probably* not acetaminophen. I put the * * around probably because when acetaminophen metabolizes, a very small amount of NAPQI is created as a byproduct. The body uses glutathione to break down NAPQI, but that depletes the body's store of glutathione. Once glutathione is depleted, NAPQI can cause fatal liver damage. Also, low glutathione levels are present in Parkinson's, Alzheimers, and autism.
In short, chronic use of acetaminophen should be avoided by everyone. It has a very important use, and from what I've learned recently, it's the best drug we have to treat fever during pregnancy.
My point is that we shouldn't be taking it like candy.... AND we should keep looking for the cause of autism.
There must be something protective in the genetics or diet of Swedes... or something damaging in our diet and/or environment in the US to cause the US to have a 7x greater prevalence of autism than Sweden.
I don't really want to get yelled at or to yell at anyone else. That's just my opinion. I'm sharing what I found because I realize that most of you have jobs or are in school and don't have time to look all this up.
I'm open to any constructive feedback.
This makes sense. I agree.
I would look at diagnostic criteria differences between the two countries. The relatively high autism rate in the US may be explained by our aggressive diagnosing (and possibly by some warped incentives with aid to individuals and schools)
I definitely don’t agree with this author on everything but his writing on autism is good:
"list all meta-analysis and systematic reviews on acetaminophen and neurodevelopmental disorders and their conclusion" Grok PubMed: 29688261 + association PubMed: 30654621 + association PubMed: 29341895 + association PubMed: 34046850 + association but weak PubMed: 35175416 + association PubMed: 35989852 + association PubMed: 35206317 + association PubMed: 36939050 + association PubMed: 37321575 + association strong PubMed: 38255358 + association PubMed: 38592388 Null PubMed: 40804730 + association DOI: 10.1097/AOG.0000000000005802 + association 13 meta-analysis or systematic review from 2018-present, only 1 with a null association. Selecting the 1 is the very epitome of "cherry picking" And Ahlqvist et al has flaws one could drive a semi-truck through.
With such a vast body of knowledge and research, this rabbit hole is more like a Grand Canyon. Stay tuned...
I’ll add, I’m laughing that you disappeared for several days and came back to regurgitate the exact same old, weaker studies except this time you garbled it through an AI tool that did an even worse job than you had previously.
The newest, strongest studies refute this argument, as they have for the last week. You need new material or you need to explain why we should believe weaker, older studies with smaller samples sizes and less sophisticated designs.
This post was edited 21 seconds after it was posted.
I’ll add, I’m laughing that you disappeared for several days and came back to regurgitate the exact same old, weaker studies except this time you garbled it through an AI tool that did an even worse job than you had previously.
The newest, strongest studies refute this argument, as they have for the last week. You need new material or you need to explain why we should believe weaker, older studies with smaller samples sizes and less sophisticated designs.
I laugh because you have no life and I do. You're also mad because everything you say has been proven to be either a lie or utter garbage. First, as noted, what was returned via AI is from 2018 and newer so they're not "old". Second, the question presented to AI is very clear, specific and to the point - the exact opposite of everything you whine about without basis.
Third, you don't have the faintest clue WTF you're talking about as it regards this topic so, as usual, you fabricate an imaginary world to compensate. I'm actually reading the research, you're not. For one, I've already exposed some of the weaknesses to Ahlqvist et al which a TDS science denialist like you obviously must reject but regardless I'm happy to go into further detail. Not for you, because we all already know you wouldn't accept proof of the nose on your face let alone rational/logical discourse explaining Ahlqvist's massive failings - which you almost exclusively rely upon. But rather for those on the fence with regard to this science. We already know you're going to find a weak, pathetic excuse to reject what you ask for so your approval is irrelevant and not required.
Missing Gustavson 2021. AI tools aren’t amazing research assistance if the goal is an exhaustive review.
Again, this is literally what Baccarelli tried to scam. Compile a bunch of crap studies and write off the two best (Gustavson and Ahlqvist).
You don’t seriously think that a proper analysis is just counting the number of studies on each side? I know you know better than that, but the lazy use of AI slop makes me suspicious.
Gustavson and Ahlqvist ARE the crap studies. I will demonstrate...
First, and less importantly, why Gustovson et al is weak.
The need for genetically-informative designs in developmental science: Commentary on Gustavson et al. (2021) and Myers et al. (2021) wrote:
Gustavson et al.'s results do, however, highlight an important cautionary note when it comes to conducting sibling comparisons. Their initial sample size was very large. However, in a sibling comparison design, only the sibling pairs who are discordant for exposure and outcome contribute to the analyses. As a consequence, and as seen in Gustavson's paper, the sample size soon declines. Accordingly, confidence intervals are very wide for the sibling analyses, and so conclusions around familial confounding should be drawn with this in mind. Studies that pool data from multiple cohorts and perform meta-analyses of the results across cohorts have the potential to provide solutions to any issues with statistical power that may arise
Only sibling pairs where both exposure and outcome are different contribute to the analysis. Both Gustovson and Ahlquist et al begin with huge numbers but when we strip them down to siblings, and further down to discordant exposure/outcome, their numbers are tiny. Do that and their confidence intervals widen and any results obtained are weak. But that flaw is only the tip of the iceberg.
Also, notice the final note: meta-analyses and other systematic evaluations which test across multiple cohorts have greater statistical power. That's Baccarelli et al.
Two major reasons why Ahlqvist et al is weak, unreliable garbage:
They underestimated usage/exposure and
They eliminated the two dozen other lines of evidence (metabolic/pharmacologic etc) to NDDs/ASD.
As noted in the prior post, despite Ahlqvist et al starting with a large cohort, this number is substantially reduced when controlling for discordant siblings - siblings with both different exposures AND differing outcomes. The reduction is so substantial as to render its results very weak/unreliable. But that's only the beginning of the sibling failure.
Parker et al wrote:
The principal point highlighted in the study was that correction for effects of sibling pairs eliminated any risk attributed to acetaminophen. However, the vast majority of the raw (unadjusted for any potential confounding factor) risk was eliminated by adjustment for more than 20 inflammation-related or associated factors. That is to say, the vast majority of the risk was eliminated by adjusting for inflammation-associated factors in the analysis, not by adjustment for the sibling pairs[79].
Ahlqvist et al's Cox regression analysis eliminated dozens of potential cofactors in an attempt to identify/eliminate one cause when the cause may be a multivariate scenario. They eliminated medical/environmental conditions associated with inflammation and/or oxidative stress such as: BMI, migraine headaches, other types of headaches, chronic pain, infections, fevers, any neuropsychiatric condition, rheumatoid arthritis, analgesics, anti-seizure medications, antidepressants, smoking status, household education, income, utilization of medical resources, and cohabitation.
Ahlqvist et all eliminated the above cofactors that create aberrant metabolism of acetaminophen and that pharmacological/metabolic mechanism is causally related to NDDs/autism. This is proven in animal studies. It should be noted that even Ahlqvist's raw, unmodified results from the larger cohort showed a positive correlation.
The most important point to take away is that Ahlqvist's Cox regression only works to identify/eliminate a single cause (acetaminophen) so if ASD/NDDs are multi/cofactorial (acetaminophen + factor -> ASD/NDD) then the study will return a null result for acetaminophen and that result will be wrong.
The Parker et al study presents this in a very easy to understand video on its publication page here:
From this one paper you can delve into why ASD is 4-5 time more prevalent in boys than girls, the origins of it and also slows in exposure/usage (poisoning scares) coinciding with a slowing in prevalence. They all act as supporting evidence. It is, in fact, a mountain of evidence from dozens of completely different angles while they cling to a single research paper which is critically flawed.