This is a bit long but I think it demonstrates the problems with AI spreading misinformation. Here is an item I have seen on the internet:
OP: I had an AI entity generate this exceptionally obvious abstract.
Abstract
Background: Acetaminophen (Tylenol) is widely used for pain relief and fever reduction during pregnancy; however, it is also a leading cause of acute liver failure in children due to overdose. This raises significant concerns about its safety, particularly regarding prenatal exposure. Emerging evidence suggests potential links between acetaminophen use during pregnancy and neurodevelopmental disorders, including autism spectrum disorders (ASD). This abstract aims to summarize the current understanding of the mechanisms by which acetaminophen may influence fetal development and contribute to the risk of autism.
Methods: A review of recent epidemiological studies and biological mechanisms was conducted to assess the relationship between prenatal acetaminophen exposure and the development of ASD. Key factors considered include the pharmacokinetics of acetaminophen in relation to fetal body mass, the role of toxic metabolites, and the impact of maternal health.
Results: Studies indicate that acetaminophen can cross the placental barrier, exposing the developing fetus to its effects. The fetal liver, still maturing, may be less capable of metabolizing acetaminophen, leading to the accumulation of toxic metabolites such as N-acetyl-p-benzoquinone imine (NAPQI). This accumulation can induce oxidative stress and inflammation, potentially disrupting normal neurodevelopment. Epidemiological data have shown associations between maternal acetaminophen use during pregnancy and increased risk of ASD in offspring, although causation remains to be definitively established.
Conclusion: The potential link between prenatal acetaminophen exposure and autism is a growing area of concern. Given the vulnerability of the developing fetus, particularly in terms of body mass and organ maturity, further research is essential to elucidate the mechanisms involved and to establish clear guidelines for acetaminophen use during pregnancy. Awareness of these risks is crucial for healthcare providers and expectant mothers to make informed decisions regarding pain management and fever treatment during pregnancy.
My response:
There is nothing that supports that Acetaminophen causes autism in peer reviewed literature. Correlation is not causation. One may as well make the claim that drinking dihydrogen monoxide during pregnancy is linked to autism. The “methods” demonstrate that no actual research was done, and postulating damage based upon metabolic pathways is pure speculation and is not a legitimate result when the metabolites you mention are directly measurable. So, the conclusion is absolute nonsense. One would need to demonstrate glutathione depletion and escape from NADPH-cytochrome P-450 reductase allowing NAPQI to enter the bloodstream before its binding with mitochondrial proteins in the liver. Furthermore, while NAPQI can be generated by the mitochondria in the brain, NAPQI is not seen in the brain even at hepatotoxic concentrations of Acetaminophen. This study completely disputes the ignorant assertion of the AI you use; Toxicol Sci . 2025 Jun 1;205(2):274-278.
The driver of neurodevelopment timing and expression are clusters of genes (and probably some pleiotropic regulators). Nothing is as impactful in the development of autism as genetics.
You have demonstrated that AI is susceptible to promoting misinformation and it gives new emphasis that ignorant opinion is not the same as expertise. Cherry picked Google and AI misinformation does not count as expertise.
OP: I had an AI entity generate this exceptionally obvious abstract.
Abstract
Background: Acetaminophen (Tylenol) is widely used for pain relief and fever reduction during pregnancy; however, it is also a leading cause of acute liver failure in children due to overdose. This raises significant concerns about its safety, particularly regarding prenatal exposure. Emerging evidence suggests potential links between acetaminophen use during pregnancy and neurodevelopmental disorders, including autism spectrum disorders (ASD). This abstract aims to summarize the current understanding of the mechanisms by which acetaminophen may influence fetal development and contribute to the risk of autism.
Methods: A review of recent epidemiological studies and biological mechanisms was conducted to assess the relationship between prenatal acetaminophen exposure and the development of ASD. Key factors considered include the pharmacokinetics of acetaminophen in relation to fetal body mass, the role of toxic metabolites, and the impact of maternal health.
Results: Studies indicate that acetaminophen can cross the placental barrier, exposing the developing fetus to its effects. The fetal liver, still maturing, may be less capable of metabolizing acetaminophen, leading to the accumulation of toxic metabolites such as N-acetyl-p-benzoquinone imine (NAPQI). This accumulation can induce oxidative stress and inflammation, potentially disrupting normal neurodevelopment. Epidemiological data have shown associations between maternal acetaminophen use during pregnancy and increased risk of ASD in offspring, although causation remains to be definitively established.
Conclusion: The potential link between prenatal acetaminophen exposure and autism is a growing area of concern. Given the vulnerability of the developing fetus, particularly in terms of body mass and organ maturity, further research is essential to elucidate the mechanisms involved and to establish clear guidelines for acetaminophen use during pregnancy. Awareness of these risks is crucial for healthcare providers and expectant mothers to make informed decisions regarding pain management and fever treatment during pregnancy.
My response:
There is nothing that supports that Acetaminophen causes autism in peer reviewed literature. Correlation is not causation. One may as well make the claim that drinking dihydrogen monoxide during pregnancy is linked to autism. The “methods” demonstrate that no actual research was done, and postulating damage based upon metabolic pathways is pure speculation and is not a legitimate result when the metabolites you mention are directly measurable. So, the conclusion is absolute nonsense. One would need to demonstrate glutathione depletion and escape from NADPH-cytochrome P-450 reductase allowing NAPQI to enter the bloodstream before its binding with mitochondrial proteins in the liver. Furthermore, while NAPQI can be generated by the mitochondria in the brain, NAPQI is not seen in the brain even at hepatotoxic concentrations of Acetaminophen. This study completely disputes the ignorant assertion of the AI you use; Toxicol Sci . 2025 Jun 1;205(2):274-278.
The driver of neurodevelopment timing and expression are clusters of genes (and probably some pleiotropic regulators). Nothing is as impactful in the development of autism as genetics.
You have demonstrated that AI is susceptible to promoting misinformation and it gives new emphasis that ignorant opinion is not the same as expertise. Cherry picked Google and AI misinformation does not count as expertise.