More questions about acetaminophen: Does it cause ADHD?



“Will Tylenol harm my baby?”


Pharmacists are among the most accessible of health professionals, and so we receive a lot of questions from the public. No appointment required, and the advice is free. Among the most frequent sources of questions are women seeking advice on drug use in pregnancy. This is an area where some health professionals are reluctant to tread. Some prefer to redirect all of these questions to physicians. But physicians are not always easily accessible, and few want to make an appointment just to ask what appears to be a simple question: Is it safe, or not? Admittedly, addressing questions about drug use in pregnancy can be challenging. There are no randomized controlled trials we can look to — there’s only messier, less definitive data. Our responses are filled with cautious hedging about risk and benefit, describing what we know (and don’t know) about fetal effects. In the pharmacy, one of the most common questions from pregnant women is about the use of acetaminophen (aka paracetamol aka APAP), more commonly known by the brand name Tylenol. Google “Tylenol and pregnancy” and you get 4.8 million results. Which source should you trust?

It should come as no surprise that acetaminophen has generated several posts over the years at SBM. It’s one of the most commonly-used medicines worldwide, starting in infancy for fever, right through towards end-of-life pain control in the elderly. As an ingredient, acetaminophen is packaged into hundreds of prescription and non-prescription drugs. Acetaminophen has a good safety profile when used appropriately. However it is among the most harmful of drugs in overdose, and the ease at which overdose can occur makes acetaminophen the cause of hundreds of cases of liver failure per year. Given this frequency of use, and a unique risk profile, there are continued questions about its safety and efficacy. Regulators (and manufacturers) continue to experiment with ways to make the drug available, while minimizing the risk of unintentional harm.

Pain in pregnancy, and the desire to treat it, is common. Beyond the non-pregnancy causes everyone can experience, like headaches and colds, the pregnant body is undergoing a rapid transformation that may not be painless. Weight gain of 25 or more pounds leads to posture changes and painful joints from head to toe. Low back pain is common, and it can be worse at night, leading to insomnia. Pelvis pain, knee pain, and hip pain are also common, and can be quite debilitating. While non-drug measures should always be attempted before considering drug treatment, severe or prolonged pregnancy pain may require the consideration of drug treatment.

Acetaminophen is the current go-to drug for pain control in pregnancy. There is good evidence to show that it does not increase the risk of major birth defects above the baseline risk (2-3%) that is inherent to any pregnancy. Acetaminophen can be used throughout pregnancy, and as long as the dosing is appropriate, side effects are remarkably rare. With a safe history of use and a low risk of side effects, acetaminophen is widely used when pain control with drugs is required.

The risks and benefits of drug use in pregnancy can’t be looked at in isolation. There is always an alternative, and the relative risks and benefits must be weighed. Doing nothing is always an alternative for pain, so the consequences of untreated pain need to be considered. But when pain is severe, other drugs might be considered. Stacked up against the alternatives, acetaminophen looks pretty good. Anti-inflammatory drugs like ibuprofen must be avoided in the later stages of pregnancy, due to the concerns about cardiovascular toxicity. Compared to the anti-inflammatory drugs, acetaminophen is unlikely to cause gastrointestinal ulcers, blood disorders, or kidney problems. Nor does acetaminophen appear to increase the risk of cardiovascular events such as heart attacks and strokes. Compared to the anti-inflammatory drugs, acetaminophen also has few interactions with other drugs, so it can safely be used for pain relief in pregnant women on other medications, or with other medical conditions where other pain relievers might have unwanted effects.

Beyond acetaminophen and the anti-inflammatories are the narcotics. The addictive properties of narcotics are well known, and they affect the fetus, too. Compared to a drug like codeine or morphine, acetaminophen provides a non-addictive alternative that may be more appropriate for short-term or long-term pain issues when drug treatment is being considered.

Now there’s a new study suggesting that the risk and benefit of acetaminophen in pregnancy may not be so clear. The paper is from JAMA Pediatrics, and it’s entitled “Acetaminophen Use During Pregnancy, Behavioral Problems, and Hyperkinetic Disorders”. Zeyan Liew and colleagues conducted a study of over 64,000 children and mothers who were enrolled in the Danish National Birth Cohort between 1996 and 2002. The Cohort was established to ask (and answer) questions about pregnancy and early childhood and the relationship to diseases that emerge later in life. Pregnant women were recruited with the intention to conduct long-term studies as these women (and their children) age.

The design of the study was straightforward. Acetaminophen use was assessed through telephone interviews before and after birth. Measurements of ADHD and hyperkinetic disorders after birth were measured by:

  • using a standardized questionnaire in parents once children reached age 7
  • looked for hyperkinetic disorder diagnoses in hospital and psychiatric registries
  • looked for prescriptions for ADHD medications through a national registry

Not surprisingly for a drug that is recommended for use in pregnancy, more than half of all of the study’s participants used acetaminophen at some point during pregnancy. There was a relationship found: Children whose mother used acetaminophen during pregnancy had a higher risk of a hospital diagnosis of HKD (hazard ratio 1.37, confidence intervals 1.19-1.59), receipt of ADHD medication (hazard ratio 1.29, confidence intervals 1.15-1.44) or having ADHD-like behaviors as defined by the standardized questionnaire (hazard ratio 1.01-1.27). There was also a positive relationship with the number of trimesters of use. Numerous confounders were studied and there was no relationship found.

There are a lot of strengths to this study that merit a close consideration of the findings. It’s a big data set that was powerful enough to detect a very subtle difference. The analysis was generally very well done. It was prospective, so the risk of bias due to time and memory (“recall bias”) was minimal. There were three independent data points collected, and two (hospital diagnoses and prescriptions) were objective measurements. There was a consistent trend observed: The risks appeared higher with use in more than one trimester, and when the duration of use (in weeks) increased. This was observed across the different endpoints. We can never say correlation equals causation with a non-randomized study, but does this study suggest it’s time to change the guidance on acetaminophen?

There were a few important limitations. Investigators failed to fully evaluate the family history of behavior disorders in parents. In diseases where there is good evidence for genetics having a substantial role, this is a significant limitation. The use of ADHD-prescriptions may not be a great measure either, given the lack of certainty about the diagnosis of ADHD (although this should have affected both groups equally). It could also be that acetaminophen use is just a signal or proxy for something else — and the acetaminophen is just what we’re noticing, and not the actual cause. It could be another condition or cause that the pregnant women are taking acetaminophen for. Finally there’s considerable uncertainty about the dosing and timing. The measurements of exposure was not ideal — in some cases it had to be estimated for women who could not recall when they took the drug. In addition, the overall dosing (e.g., average number of tablets) wasn’t available).

Probably the biggest fault to the study isn’t actually a flaw — it’s one of how meaningful these results really are. The absolute risks of ADHD remain tiny. Most of the headlines mention the relative risk: (“30% MORE LIKELY TO EXHIBIT ADHD”) when it’s the absolute risk that needs to be considered. The biggest difference as measured at age seven was the variation in the standardized questionnaire: 34 per 1 000 in the group “ever took acetaminophen”, versus 25 per 1 000 in the “never took acetaminophen” group. Recall, that’s a survey result — not a diagnosis. On balance, if the effect is real, it very minor, and the vast majority of the cases of ADHD are being detected in women who took no acetaminophen at all.


I have mixed feelings about these studies. On one hand, these databases give us the ability to evaluate very subtle effects that we could never otherwise identify. They also allow us to make inferences about relationships when randomization isn’t feasible or even ethically possible. And they may lead to further studies to help us better understand risk and benefit. When it comes to acetaminophen and ADHD, we can be reassured that if there is any causal effect from acetaminophen, then the effect is very slight. There’s no evidence to suggest that acetaminophen is driving the perception of growing incidence of ADHD. And studies like these are also a reminder to health professionals that we cannot take anything for granted — we need to look carefully yet critically at any new evidence. But there’s a downside to studies like these. Unwarranted panic is one, often driven by reporting that hypes the “statistically significant” without providing insight and context. Pushing women towards other, less safe alternatives could cause more harm.

Does the study change how we manage pain in pregnancy? It shouldn’t. No drug should be taken in pregnancy unless it’s necessary — acetaminophen is no exception. But there’s no reason for pregnant women to suffer from pain unnecessarily. Acetaminophen remains the drug of choice when pain control is necessary in pregnancy.


Liew Z., Ritz B., Rebordosa C., Lee P.C. & Olsen J. Acetaminophen Use During Pregnancy, Behavioral Problems, and Hyperkinetic Disorders, JAMA Pediatrics, DOI:

Photo from flickr user summerbl4ck used under a CC licence.

Posted in: Science and Medicine

Leave a Comment (59) ↓

59 thoughts on “More questions about acetaminophen: Does it cause ADHD?

  1. Jen in TX says:

    This is actually the second study showing adverse neurodevelopmental outcomes from prenatal acetaminophen use.

    1. Autismepi says:

      This first, well done study found much stronger effects. The prolonged use of acetaminophen in pregnancy increased the risk of behavioral problems and problems with motor skill development by almost 70% and doubled the risk of language problems in 3 year olds.

  2. Thurber says:

    “No drug should be taken in pregnancy unless it’s necessary – acetaminophen is no exception. ”

    I think that’s it in a nutshell. Pushing women towards other, less safe alternatives could cause more harm. When my wife was pregnant, she was prescribed a multi-vitamin, but I remember all the bad alternative-medicine advice we got from well-meaning friends we ignored.

    By the way, I recently read the following about wikipedia:

    “The Association for Comprehensive Energy Psychology (ACEP) set up a petition asking Wikipedia to make it easier to post crazy pseudo-science to Wikipedia, specifically information about “Energy Medicine, Energy Psychology, and specific approaches such as the Emotional Freedom Techniques, Thought Field Therapy, and the Tapas Acupressure Technique.”

    In response, Wikipedia co-founder Jimmy Wales said “no,” very emphatically. He told the petitioners that Wikipedia would continue to accept material published in peer-reviewed scientific journals, but would not “pretend that the work of lunatic charlatans is the equivalent of ‘true scientific discourse.’ It isn’t.”

  3. Liz says:

    What about aspirin for pain during pregnancy?

    1. WilliamLawrenceUtridge says:

      Not recommended:

      Though it’s complicated:

      But the latter applies when you’re trying to prevent preeclampsia.

      This is a little more comprehensive:

    2. Harriet Hall says:

      There are concerns about aspirin in pregnancy: bleeding complications and other potential problems. Tylenol is generally considered to be preferable.

  4. steney01 says:

    Some of the correlation could be attributed to a link between a mother’s willingness to use medication for herself and her willingness to medicate her children. If mothers who use acetaminophen during pregnancy are simply more open to pursuing medication or a medical diagnosis in response to their children’s behavior, or conversely, women who don’t need or don’t want to use acetaminophen are less likely to medicate their children then you have a built in bias for any study of this kind. The authors could potentially account for this if they had data on the use of other medications or disease diagnosis in children born to mothers in this study.
    I’m also concerned that they had to exclude almost 30,000 cases upfront where the mother didn’t complete the 3 scheduled interviews, another 6000 due to unsuccessful pregnancies, and then another 20,000 when they wanted to correlate with the children’s behavior at age 7 but the mother didn’t complete the questionnaire. There could be a lot of bias introduced by those exclusions. I can imagine a scenario where the mothers who are more vigilant about completing the interviews and questionnaires are also more vigilant about their recall of acetaminophen use and possibly more vigilant about diagnosing adhd in their children.
    Add that to the confounding factors mentioned above, specifically the spotty investigation of the family history of behavioral problems, and it seems we still we need more data on this question.

    1. Angora Rabbit says:

      “then another 20,000 when they wanted to correlate with the children’s behavior at age 7 but the mother didn’t complete the questionnaire.”

      That’s a good catch. And which families are more likely to participate, those having a child with behavioral issues or those whose kid is “just fine now go away”? That strikes me as huge selective bias. It’s about 1/3 to 1/4 of their cohort.

      1. Dr Robert Peers MBBS [UniMelb] says:

        Hi Dr Rabbit,

        Any thoughts on the [prospective] Norwegian study cited in comment #1, by Jen in TX?

        Might have been some selection bias there as well, judging by the abstract.

        Cheers, Rob

        1. Angora Rabbits says:

          Thanks for the question and glad I caught it. There’s multiple possible interpretations and doubtless you’ve already thought of them. Foremost is that the single greatest challenge of any epi study is that it is correlation, never causation. The way we would phrase this study is that, for those pregnancies with increased use, the offspring had an increased risk for y outcomes.

          Thus the question is, what was going on in those pregnancies. And immediately we ask, was there a reason why the acetamin. use was greater? And could that reason also by why those outcomes were greater? And thus, could the acetamin. use been causative or a instead a marker for the real causative agent.

          Here’s an example. Children born closer to major airports have higher risk for developmental delays and adverse outcomes. Wow – airplanes cause DDs! No, it is more likely that folks who live near major airports have lower incomes and can’t move away from the noise and congestion. In other words, it’s an SES marker. (Though there are some interesting studies about hearing.)

          Ultimately, since the rules for building brain are fairly similar across mammals, we’d like to see animal studies that show parallel outcomes.

          Maybe the women taking the acetamin. had fevers, which we know is a risk factor. Maybe they had joint pain from being overweight, which is a risk factor. Maybe they were having hang-overs from drinking, which is definitely a risk factor. Even within families, there are can be influences that differ between pregnancies. And remember, siblings share only half their DNA and in utero environments can still differ.

          Hope this helps!

  5. goodnightirene says:

    “Investigators failed to fully evaluate the family history of behavior disorders in parents. In diseases where there is good evidence for genetics having a substantial role, this is a significant limitation.”

    I gained 75 lbs (I’m 5’2”) with the last two pregnancies (of four) and had no discomfort other than finding a way to flop onto the sofa. I never took any pain meds in pregnancy and have three children with ADHD–which is rampant on both sides of the family.

    Note. I quickly lost the weight after birth. I also had my children while relatively young by today’s standards.

    1. Dr Robert Peers MBBS [UniMelb] says:

      Good Morning Irene!

      Mr Gavura, and several commentators on this story, clearly believe ADHD to be highly heritable. This is not a proven scientific fact, as the genetic hypothesis is actually highly controversial, given that no single common gene has been found, that is directly causative of the disorder.

      From the handful of genes–of unexpectedly modest effect–found so far, occasional gene combinations might be found, that have a more direct effect. But such combinations may break up in a family tree, so may not explain familial aggregation, that you describe in your own family line.

      A few rare copy number variations have been found, that may have a stronger or more directly causative role–but [being rare] would not explain the majority of cases.

      ADHD genetics researchers, humbled and surprised by the few shrivelled fruits they have picked off what looked like a big juicy tree a few years ago, are now reduced to pleading for funding to look for: yep, rare-but-strong variations.

      Anything will do: copy number variations, rare-but-strong variations, epigenetic variants, epistatic combinations, exon sequencing, whole genome sequencing–so long as it keeps the research dollar rolling in, until the evil day arrives when the big funding agencies simultaneously wake up and lose interest.

      What, spend tens of millions more dollars, to fund even more gigantic international multi-site genome-wide studies, to find that the missing heritability stays missing?

      So it’s not the genes, so MUST be something else? But what?

      This is the Genome Era, as Francis Collins calls it. And something has gone wrong.
      If the NIH had a Thinker-in-Residence, here is what he would say:

      ADHD is only THOUGHT to be genetic, because those entrusted with the task of finding its cause ASSUME, at the very start, that it is indeed genetic–and then set out to confirm their hunch, at great public expense.

      Without the basic wits to ask if ADHD might have a dietary, or toxic, or obscure microbial cause, these scientific dwarfs leap straight into Quantitative Genetics: estimating heritability via twin, family and adoption studies.

      1. ADHD clusters in families. Dr Joe Biederman, a Harvard man not lacking in confidence, says somewhere that that alone indicates heredity. Funny thing, I once met venerable genetics man Dr Vincent McKusick, and asked him about genes for common diseases.

      His reply was very similar to the opinion of a wise old European geneticist I met in Melbourne, at a varsity dinner: the more common the disease, the less likely that genes play any part–no more than a predisposing role, at best, and then only in a fraction of cases. The European said “it must be clearly hereditary, judging by the pedigree, because in a disease of high prevalence, familial aggregation may be entirely fortuitous”.

      Id est, if ADHD was to be both familial and very uncommon, even a high school nitwit could have a stab at it being inherited. But it is common–AND seems to vary greatly, in both space and time. Twice as common in N Carolina as in Calif–how so? Rare or unknown among the Amish. Why?

      How to explain a single case in a family with no family history of it at all? Or several affected siblings, but nothing in either parent, or anywhere else in the family tree? Or kid[s] and one or both parents affected, but nothing seen in the four grandparents, or in aunties and uncles, and great-aunts and great-uncles??

      2. An adopted kid with ADHD is more likely to have an affected biological, than adoptive mother. What, in every case? Could the real mother have eaten the wrong thing, or consumed some unsuspected toxin, that the adopting family have been lucky to avoid?

      3. Family and adoption studies, therefore, tell us nothing, if confounding environmental factors are not looked for–actual alternative explanations of the disease. But now come the twin studies–surely those will wrap it up?

      More one-egg twin pairs are concordant for ADHD, than are two-egg twin pairs. And from the concordance data, one can work out the proportion of the variance of something or other, to finally arrive at an estimate of heritability. Which is, in ADHD, very high indeed–over 80%. Dr Stephen Faraone, a decade ago, called ADHD by far the most highly inherited of all psychiatric disorders. Hasn’t got much to say recently, though.

      So is it really, after all this exciting genetic research, due to some quite unexpected and completely unpredictable environmental cause or causes, and the genes do no more than predispose, and then only in a minority of cases?

      I believe so–and my own investigations into ADHD, ironically, began in 1990, with PARACETAMOL!!! That’s what we call acetaminophen, in proper English-speaking countries. I was looking for a simple cause of Alzheimer’s disease [AD] at the time, after attending a lecture at Melbourne Uni, by a post-doc in Prof Colin Masters’ Department, a leading AD research centre.

      I later asked Colin about the epidemiology–which is the fast road to solving common diseases–and he put me onto Prof A S Henderson, a mere social psychiatrist in Canberra [“who does no work of his own”]–but who wrote a paper in a Swedish journal in 1988, on AD risk factors.

      It turned out to be a goldmine–AD rare or unknown in West Africa; twin discordance can occur; may not co-exist with diabetes; safflower oil [refined] impairs memory in rats; PHENACETIN causes AD, in analgesic abusers; and even Masters’ German colleague, Dr Konrad Bayreuther, is cited, asking for more research into membrane damage, lipid peroxidation and vitamin E [which he still takes, himself].

      Phenacetin is a pro-drug for PARACETAMOL; abuse of the former causes renal failure, which then prolongs the half-life of phenacetin, exposing even the brain to the toxic effects of high local concentrations of derived paracetamol. My free radical book said paracetamol toxicity is mediated mostly by the benzoquinone-imine metabolite, which severely depletes protective glutathione levels, leaving it free to attack thiol [sulfhydryl] groups on proteins, which kills the cell.

      And that, alone, might cause AD, by imitating the neurotoxic synaptic effects of reactive certain electrophilic toxins that hit the same thiol groups, which include those on the key beta-amyloid degrading synaptic enzyme neprilysin. But the book also hints that the same toxic metabolite of paracetamol also attacks cell membranes directly–Bayreuther’s membrane damage!!

      And THAT would be enough to cause AD, all on its own, because lipid peroxidation breaks Arachidonic Acid, in the synaptic membrane, into fragments, one of which [4-hydroxynonenal] is a reactive aldehydic electrophile, that is now known to hit all the above protein thiol groups in the synapse, including those on neprilysin–meaning that beta-amyloid will accumulate, to cause AD.

      Driven by the powerful clue of twin discordance, I soon identified a biologically plausible dietary factor, already suspected to cause lipid peroxidation in various lab experiments: a toxic factor I call TDL, found in refined seed oils.

      A small pilot case/control study in my own patients confirmed my suspicion that lifelong exposure to refined seed oils [or even from about age 40-50], was strongly associated with AD outcome. But what about ADHD??!!

      This one was pure serendipity: knowing that lipid peroxidation would strike mostly the highly polyunsaturated brain and retina, I was looking for mild memory faults, plus some sort of visual effect, in my adult patients consuming refined seed oils. I soon identified a whole Seed Oil Syndrome: subjective memory impairment, glare sensitivity [photophobia] and night blindness.

      I soon became aware that affected parents frequently had hyperactive kids–so frequently that I wondered if these same oils might cause ADHD during gestation. The free radical literature said, hey, natural low-level [physiological] lipid peroxidation promotes cell differentiation and even apoptosis [cell death], of tumour cells or self-reactive auto-immune clones.

      And even a slight increase into the pathological range will inhibit the growth of virtually any rapidly growing tissue or organ–including cancer and foetal brain.

      So I collected 160 kids, over 2 years–80 ADHD, and 80 controls–and found, via retrospective maternal diet history [concealing my interest in ADHD, to minimise recall bias], a very strong association between “oily” maternal diet in pregnancy and ADHD outcome.

      Clearly, this pilot study needed replication, so I asked a Royal Children’s Hospital paediatrician for help. He was interested, but his post-doc got sick and couldn’t proceed. I called the hospital’s Psychiatry Prof, Dr Robert Adler, with unexpected results [see below].

      Only once has a {probably refined] seed oil been given to pregnant test animals [rat moms]–and the pups showed a hyperactive phenotype, including lack of stimulation by amphetamine. The nearest thing to the real thing is to deprive Mother Rat of omega-3, which imitates the peroxidative loss of omega-3 induced by peroxiding omega-6 oils, but without the additional synaptic toxicity of HNE.

      Sheila Innis, Ephraim Yavin, and Beth Levant have all done this, and report growth cone damage [impaired neurite extension], reduced axonal branching in cortex, delayed neuronal migration, and even a specific ADHD effect [potential dopamine terminal damage or death]. Wow.

      And that’s without the destructive, anti-growth effect of HNE. HNE is now known to inhibit a key synaptic protein, SNAP25, mutations in which are a risk factor for ADHD!! SNAP25 is involved not only in dopamine release, but ALSO in foetal brain development, including neuronal migration and neurite extension. Wow.

      So are the twin studies wrong? I have emailed a little essay, called The ADHD Paradox, to various ADHD gene folks: only one replied, agreeing it was probably a multifactorial thing. But which is the bigger factor–genes or maternal diet?

      Obviously, these weak genes, when present, must have some effect. But do they account for the lower concordance rate in two-egg twins? A serious weakness in twin studies is the Equal Environment Assumption–a real stinker of a thing used in all twin studies I have ever seen.

      Not being nutritional geniuses, twin researchers simply assume that unlike twins eat exactly the same diet, and so do like twins. That may not be the case, for various reasons. Furthermore, exactly the same refined seed oils that may be the true prenatal cause of the disorder appear to AGGRAVATE the condition during childhood, if currently consumed [worse symptoms correlate with low blood omega-3 levels, that may indicate current peroxidative DHA losses in brain].

      So the answer to the Paradox may be: when identical twins are discordant, on categorical or continuous measures, the unaffected one might not be eating these oils, currently—as a simple diet history might reveal, if gene dudes had the curiosity to follow up, which they never do. Ditto for the greater discordance seen in fraternal twins–who may well differ more in their dietary habits and preferences. Assumptions combined with incuriosity does not add up to Science.

      This aggravating effect of post natal refined oil exposure may be the key to solving the ADHD Paradox. Future twin studies should analyse diet very carefully, to avoid fatal confounding. I predict that diet will prove to be the main, and directly causative factor, while the interesting [but weak] genes will turn out to play no more than a mild predisposing role–when present: not necessary, not sufficient, and simply too weak to be directly causative, on their own.

      As for the Psychiatry Professor mentioned above: after I asked for his help, to confirm a link between maternal refined oil exposure and ADHD in offspring, he wrote a secret letter to the Medical Board, questioning my fitness to practise. The Board did not process this as a complaint, that I could defend at an informal hearing–and clear the air. It went in my file as evidence for a much later Formal Hearing, in 1996, at which my research on AD and ADHD was vilified by a number of psychiatrists, and was dismissed as a psychotic delusion. I was later arrested, certified insane, locked up, confined in isolation, and injected with potent antipsychotic drugs that induced prolonged vegetative neuroleptic dysphoria. Upon recovering a year later, I was forced to abandon my solo practice, to work under supervision indefinitely.

      Dr Adler, meanwhile, got himself onto the Board, and rose to President eventually. At a meeting in 2001, he barely managed to restrain himself from suspending me from practice, after seeing a vicious report from Victoria’s Chief Psychiatrist, Dr Norman James. Luckily, Adler had seen in my Board file an informal paper on my ADHD research, and had studied it. He let me go, saying “Dr Peers, there does seem to be some substance in what you’ve been saying.”

      After much consideration, I have decided not to publish my completed hypotheses on AD and ADHD, until I get an official Inquiry, and substantial damages, from the Medical Board of Australia. So far, they refuse to negotiate.

      If anybody wants to know what TDL is, just google Dr Robert Adler, Millswyn Clinic, South Yarra, Melbourne, and write to him, asking what the hell is going on in Darkest Victoria.

      1. Harriet Hall says:

        Dr. Peers’ posts invariably consist of grandiose untested claims for inositol (up to and including “cures Alzheimer’s”), based only on speculations about basic science and on his personal experiences treating patients. His admission that he was certified insane, was diagnosed with psychotic delusions, was locked up, and is only allowed to practice under supervision does nothing to bolster his credibility. I wouldn’t venture to diagnose him, and his claims for inositol may prove to be true; but his writings certainly make him look like a crank. We haven’t heard the psychiatrists’ version of events. I can’t help but wonder if he should go back on his meds. If he is sane, he is clearly not ethical, since he refuses to publish and allow patients other than his own to benefit from his discoveries.

        1. Calli Arcale says:

          I must say, though, I am impressed at his ability to castigate people for thinking there may be a genetic link when no gene has been found yet, while simultaneously being quite happy to seize on acetominophen/paracetamol as a definitive causative agent, based on a fishing expedition looking for a cause of Alzheimer’s Disease, which is related to ADHD only insofar as it also involves the brain, with absolutely no defined mechanism whatsoever.

          It is quite impressive to be so grand, so eloquent, and so verbose on the subject without noticing this hypocrisy in the least. Truly, he has a dizzying intellect.

  6. LadyAtheist says:

    “Children whose mother used acetaminophen during pregnancy had a higher risk of a hospital diagnosis of HKD (hazard ratio 1.37, confidence intervals 1.19-1.59), receipt of ADHD medication”

    Could this mean that women who were likely to take a pill for one condition were more inclined to take a pill for other conditions?

    1. Andrey Pavlov says:

      Could this mean that women who were likely to take a pill for one condition were more inclined to take a pill for other conditions?

      Yes. This study can’t identify causation. So it is conceivable that there is some condition, unidentified, which leads to increased pain during pregnancy and ADHD and that the tylenol is incidental.

      That is not as likely as the tylenol itself having some (very small) effect, at least in terms of the Bayesian you would assign each, but not impossible.

  7. Angora Rabbit says:

    As a professional teratologist, it blows my mind that people obsess over gestational exposure to, say, acetaminophen or caffeine, compounds that have a very low threshold of risk, and then don’t think twice about having that glass of wine or a beer during pregnancy. Or refuse to take iron supplements because of the gastric side effects. Worse, their ob/gyns are telling these women that it’s okay to to drink during pregnancy because “they’ve never seen one of those FAS kids.” Not that they would recognize one.

    This highlights how irrational people can be. They like wine and so dismiss the huge and powerful database of 40yrs that show alcohol is the most common teratogen in use and has far worse and lasting effects than, say, the caffeine or acetaminophen. It’s a perfect example of how people misunderstand risk and rationalize away concerns that are inconvenient to their immediate needs or lifestyle.

    As I said. Blows my mind.

    1. nancy brownlee says:

      “This highlights how irrational people can be. They like wine and so dismiss the huge and powerful database of 40yrs that show alcohol is the most common teratogen in use and has far worse and lasting effects than, say, the caffeine or acetaminophen”

      That’s certainly true, and probably true of all of us- in varying degrees. Awareness of teratogenic effects of ordinary meds and OTC drugs has increased hugely in my adult life, I think because the thalidomide horror opened up a world of possibility and evaluation that had never been thoroughly explored. Even now, pregnant women are encouraged to continue using psychoactive drugs, antidepressants et al, and I don’t believe that anyone has a clue about the extended use of these drugs by pregnant women. The drugs haven’t been around long enough.

      But- all of us who are boomers and older are intensely aware that we ourselves and virtually every child we knew who was born before 1980 had a mother who probably smoked (and if not who nevertheless lived in a cloud of second-hand smoke), who occasionally had a beer or a highball before dinner, and who swallowed a couple of aspirin (later Tylenol) when she had a headache. The kids were, mostly, just fine. Ordinary observation – correlation of cause and effect, our usual method of evaluating risk- isn’t good enough. But that’s counterintuitive, and it must be learned. We’re not very good at it.

    2. Angora Rabbit says:

      Weeeellll….there’s fine and there’s fine. I think a good case can be made that my generation (same as yours, methinks) and generations before did have effects from the booze and ciggies. But it isn’t a comfortable message to hear. There are also SES influences and in general other behaviors such as increased health awareness, better access to perinatal care, low stress, etc, can offer a mitigating influence.

      I disagree, however, that pregnant women are encouraged to use drugs. Physicians are supposed to be aware of risks. There is good testing that goes on for the physical defects, but a good case can also be made that the neurobehavioral testing needs significant expansion. It can be a challenge when a woman becomes pregnant who needs Drug X (say an anti-depressive) and removing Drug X creates a new set of problems. What do we do? Do we tell her she has to suffer manic episodes or depression and too bad?

      Completely agree with your statement about cause-and-effect and our inability to rationally estimate risk. Cheers!

      1. mouse says:

        AngoraRabbit “What do we do? Do we tell her she has to suffer manic episodes or depression and too bad? ”

        Excellent point. It’s also to good understand the consequences of not taking medication. People who are in manic episode may have little impulse control and have serious problems with binge drinking and drug use as a result. Suicide or suicidal behavior is a risk in a depressive episode.

      2. nancy brownlee says:

        You know infinitely more than I about drugs, physician, and the latter’s awareness of the former. My (Pretty useless) experience comes second hand, via a daughter-in-law and her contemporaries. They report that their OBs, essentially, leave the decision up to them, having told them that their babies will “probably” be alright. None are manic or bipolar; all are diagnosed ‘mildly to moderately’ depressive.

        Second guessing the OBs with only third-hand information to go on is undoubtedly unfair, but it’s hard not to wonder about it.

      3. Jessica S says:

        “It can be a challenge when a woman becomes pregnant who needs Drug X (say an anti-depressive) and removing Drug X creates a new set of problems. What do we do? Do we tell her she has to suffer manic episodes or depression and too bad?”

        I’m one of those women. :) I have a three and a half year old boy and I’m 24wks along with “the baby sister”, as he calls her”. I talked extensively with my psychiatrist and reg doc about the risks of the meds I take; luckily there was good background on both meds I take and everything was fine (meaning no obvious birth defects). With this pregnancy, I had a consult with a high risk OB at the Univ of WA Medical Center – she’s professor of some sort, too – and she really helped put my mind at ease, giving me all the pros and cons. She said “in order to have a healthy baby, we need a healthy mom. With some women, that means managing mental health, which is just as important to deal with.”

        All that said, it still weighs on me, which is one reason having two is plenty for me. :) I wonder about the subtle effects the meds could have that will be a real problem later on. But I know that without the meds, I wouldn’t have been able to function. I’m grateful for people such as yourself and the OB at UWMC that spend their time studying the risks. :)

        1. WilliamLawrenceUtridge says:

          In addition to “healthy baby needs a healthy mom”, there’s the idea that there is merit to mom simply being healthy in her own right. She doesn’t cease to be a person as soon as she has a baby, and the idea that all of her needs must come behind even the smallest need or possible risk to maximizing every potential opportunity in a child’s life, both strike me as distasteful.

          I suppose my comments mostly come from my opinions on the over-emphasis on the importance of breastfeeding, but in general the idea irks me. “No, you have to stay home, not shower, not exercise and not socialize, because your baby might need you”. But now I’m shading into my prejudices against attachment parenting.

          1. Jessica S says:

            I love everything about this response, particularly b/c I didn’t breastfeed for the sake of my sanity. I didn’t even need to try it to know I would be completely overwhelmed with it, on top of the overwhelm of being a new mother. People have asked me why I’m not going to try with the second, since I’m more familiar with babies. Um, because I will be figuring out how to handle life as a mom of two without kidnapping my husband and running away (kids safely at nana and papa’s of course!).

            I should mention, I had ADHD so everything is overwhelming to me. :) My life is never boring, but always drama-filled, of my own doing. :)

            1. WilliamLawrenceUtridge says:

              If you are ever interested in a critical look at the breastfeeding debate,, Bottled Up by Suzanne Barston has a quick overview. If you’re really interested in the research on breastfeeding, and criticisms thereof, Is Breast Best by Joan Wolf would be a great book to read.

              Treating breastmilk like Kostas Portokalos treats Windex is stupid.

              1. Anne G says:

                I read “Bottled Up” because it was recommended for the reasons you have stated. Although the prose was pleasant and readable, Barston seems to have an axe to grind because she assumed that the cultural hurdles did not apply to her, presumably because she is not part of the “lower SES”. She attempts in the book to create the impression that some people think breastfeeding is a moral imperative rather than a pragmatic health decsion. The content was mostly unsubstantiated opinion, coming from a place of disappointment and grief. I would not recommend it as a means of understanding the limitations of breastfeeding advocacy.

              2. WilliamLawrenceUtridge says:

                If you found Bottled Up too hysterical, then may I suggest the cool, dispassionate prose and analysis of Joan Wolf’s Is Breast Best? instead? Barston definitely writes from a place of pain, to convince laypeople, and delegates much of the research elsewhere and substitutes instead a lot of interviews. But she does make the quite solid point that breastfeeding is oversold, that not breastfeeding is portrayed as a risk rather than an alternative, and that the punitive way bottle feeding is handled harms disproportionately those who need it most. I found it unsatisfying, but by then I’d read a good half-dozen books on the matter.

                A lot of people do feel that breastfeeding is a moral imperative. Any of the Sears attachment nutters for instance, the Alpha Parent, the La Leche League, and oh, say, the City of Ottawa treat bottle feeding as a near-poison, and many of the books I read on the topic contain numerous other examples.

                Barston’s core point is that bottle or breast, both are healthy ways to feed you baby, and the slim advantages of breastfeeding is not worth the hysterics that seem to surround it. No parent should feel guilty for using formula, no matter the reason. The shame and discouragement that breastfeeding faced in the past is over, and it seems that the advocacy has swung to the other direction.

                But perhaps I’m only reading one side of things.

    3. irenegoodnight says:

      OMG–I didn’t think anyone ingested any alcohol while pregnant anymore–anyone even marginally informed and not already in the depths of addiction.

      I agonized over a beer or two I had before knowing I was pregnant, and you’re telling me women are doing this knowingly–ack!

      1. Angora Rabbit says:

        Oh, my goodness, they certainly are still drinking when pregnant. Search on “moderate drinking and pregnancy” and you will be horrified by the mommy pages that say it’s okay. Even US ABC and CBS news had reports saying it was okay w/in the past 4 yrs. Worse, we had reports that “moderate drinking makes your baby smarter.”

        It is horrifying. It is astonishing that, despite all the research and public education efforts, FASD rates haven’t dropped in western nations.

        1. mouse says:

          @Angora Rabbit – Wow! I’m kinda startled by that. I have never known a pregnant woman who drank more than a very occasional half glass of wine – that is one woman. The rest didn’t drink at all.

          Of course I’m far from expert, I probably haven’t even know the average number of pregnant women, since many of my friends don’t have children.

          So is there a particular demographic, age group, etc that is drinking an unsafe amount while pregnant or is the drinking pretty dispersed through the population?

          1. Andrey Pavlov says:

            The official recommendation is zero alcohol intake. I think that considering first-pass metabolism and the size of the human body (plus the extra plasma that women take on as they are further along in the pregnancy) means that a half or full glass of wine on occasion is highly unlikely to have any sort of effect. That said, it is impossible to predict if, by chance, that one glass managed to let enough ethanol slip by at just the wrong time in development to cause some sort of subtle difference. It is certainly the safer play to avoid it all together and unquestionably the advice that I would give to my patients (if it ever comes up – pregnant women and babies is precisely why I am picking a specialty geared to avoid them as best as possible).

            If my fiance ever actually becomes my wife and we do decide to procreate, she will be my designated driver for 9 months, but I would not take issue with her enjoying a single glass of wine or a beer on occasion (particularly after the first trimester). I just can’t fathom that it could have anything more beyond a change so subtle as to be undetectable. But perhaps I am wrong on that and AG can set me straight.

            (Obviously doing that every night or having more than a single drink or drinking that single drink in one gulp would increase risk accordingly. I am talking about nursing a single drink to minimize ethanol ingestion and maximize first pass metabolism)

            1. mouse says:

              AP “The official recommendation is zero alcohol intake.”.

              It appears that Angora Rabbit is saying that the official line is not being towed by some (a lot?) OBGYNs and the media?

              Personally, I’m kinda I said. Maybe things have just changed? Most the people I know having babies now are parents of my kids friends and are older (late 30’s) maybe it’s a demographic thing.

            2. Angora Rabbit says:

              Andrey, please don’t let her drink alcohol during pregnancy. The brain develops during every trimester – that some trimesters are more sensitive than others is a myth. Would you let a 2yr drink beer or wine? Then why is it okay to expose a fetus? Especially when (a) the placenta is no barrier to alcohol, (b) fetal liver is insufficiently mature and can’t metabolize alcohol appreciably, and (c) alcohol enters the amniotic fluid and the infant then swims in it until birth, since clearance from the amniotic fluid is very slow. Fetal brain is more sensitive to alcohol than is adult brain (true also for adolescent). Think about how you feel with a BAC of 0.02% – fetal brain will be more sensitive.

              There might be threshold, but we can’t tell you what it is. We can’t tell you what the variables are. Do you really want to play roulette?

              1. Andrey Pavlov says:

                I suppose it is a cultural difference. I had my first alcoholic beverage before I could really remember. Perhaps 4 or 5? My parents would give me something like a half ounce or ounce of wine mixed with water in a wine glass. By around 11 or so I was given a half glass wine or beer and had tasted a few sips of the Scotch my father liked to drink. Mind you this is not every night, but certainly not just a few special occasions a year. More on the order of twice a week or so.

                Of course that doesn’t necessarily make it safe to do so, but it obviously lended to forming my attitudes regarding imbibing ethanol.

                I do know that the idea that there are trimesters that are insensitive to any teratogen is bunk, but it seems to me that there should be at least a decrease in sensitivity over time, no? My quick review of some literature seems to support this (how low it goes ultimately I cannot say, and it indeed may not go low enough).

                I am well aware that the placenta is no barrier and that the fetal liver is not going to process ethanol (it’s busy making blood cells). But the mother’s liver is functioning just fine. And first pass metabolism is in effect. Some back of the envelope math (if I am doing it right) tells me that a standard drink imbibed over 30 minutes will yield no more than 7g of ethanol in the bloodstream of an average female. This comes out to a BAC of 0.014% assuming the female to be 140lbs. Using an online BAC calculator the numbers I get seem to jibe.

                I’m not sure if it is reasonable to assume the fetal levels will be at equilibrium at 0.014% or lower (I think lower, but by how much I don’t know). And that is assuming a standard 140lb woman, rather than a pregnant one who will have more plasma volume thus making the concentration even lower. The question is what effect would this actually have?

                I don’t know the literature particularly well and my rapid review certainly does it no justice, but what I could find demonstrates that there are critical periods for various aspects of FAS to manifest, that there is a dose-response curve in animal models exposed to ethanol, and that the low end of the dose is only speculated to have “more subtle effects.” To me that indicates that there probably are effects (barring some sort of minimal threshold which I would agree is rather unlikely or hormesis which is also unlikely but probably more likely than a threshold), but they are too subtle to notice.

                I agree that the science says we should simply advocate no ethanol intake. It is unequivocally the safer option. I also did not realize or consider that the ethanol will build up in the amnion. That may actually be the game changer for me. But barring that, I just don’t know that I would find myself that concerned over effects so subtle they can’t be noticed. I wouldn’t advocate for any pregnant women to drink, but if my wife feels like she wants to sip on a glass of wine with dinner on occasion I don’t know that I would be concerned enough to dissuade her, particularly later in the pregnancy as all the effects will be more and more mitigated as the pregnancy progresses.

                It is undoubtedly my own cultural bias speaking though and the accumulation in the amnion is the only thing really sticking in my head at the moment. I don’t question that it would be playing roulette… but the risk just seems minimal to me. Not rigorously scientific of me, I know.

              2. brewandferment says:

                this is something I’ve wondered about for quite awhile: when traveling in Tuscany in late 2000, during weeks 28 – 30 of my 2nd pregnancy, I had discussions about alcohol consumption during pregnancy with various European guests at the farmstay and hotel.

                The general consensus amongst them all was that pregnant women would greatly decrease their consumption but that there was not anywhere the same “drink absolutely no alcohol, ever, during pregnancy or even when preparing to conceive” sense that there is in the US. A certain amount of chuckling about American attitudes toward sensual pleasures of all sorts then generally followed.

                Anyone with a better handle on this phenomenon care to shed more light on it? Is FAS as big or worse in Europe as in the US given their more relaxed attitudes about pregnant women drinking alcohol would seem to imply? or is there something about wine being consumed with a meal that is different from many American alcohol habits (ie not wine/beer and often seperate from a meal?)

    4. mouse says:

      AG “As a professional teratologist, it blows my mind that people obsess over gestational exposure to, say, acetaminophen or caffeine, compounds that have a very low threshold of risk, and then don’t think twice about having that glass of wine or a beer during pregnancy. Or refuse to take iron supplements because of the gastric side effects. Worse, their ob/gyns are telling these women that it’s okay to to drink during pregnancy because “they’ve never seen one of those FAS kids.” Not that they would recognize one.

      This highlights how irrational people can be. They like wine and so dismiss the huge and powerful database of 40yrs that show alcohol is the most common teratogen”

      It sounds like people are obsessing over the things that their doctors and the media are telling them are more a concern. If you are not a nutrition expert how are you supposed to understand, much less dismiss the database of 40yrs studies? Perhaps you are saying the irrational bias is on the part of the doctors or the media’s – which is fine if that’s the case.

      But you can’t expect the women to not trust their doctor on drinking alcohol during pregnancy, but trust their doctor on vaccines. And you can’t expect the majority of the population to have the time and aptitude to tell when the doctors are correct or incorrect.

    5. Sean Duggan says:

      I’ll freely admit that I had been swayed by the doctors and studies saying that light drinking was either not harmful or of such minimal harm that you’re risking more by the additional stress. Is it actually that severe of a problem or is it more a matter of that people are really bad at judging what “light drinking” is, so it’s easier to prohibit drinking entirely than to deal with people downing half a bottle as “light drinking”?

      1. Andrey Pavlov says:

        I would have thought the same, but AR’s comment has left me questioning that. Brewandferment’s comment regarding comparison between FAS rates in the US and Europe could shed light on it, but I doubt that it would be that easy to get a clear answer from the literature available (but if we could, that’d be handy).

  8. James Garry says:

    This is a burning question that what drugs can be takes as a pain killer during pregnancy but here as stated that Acetaminophen is the current go-to drug for pain control in pregnancy. And big thing is that there is good evidence to show that it does not increase the risk of major birth defects above the baseline risk (2-3%) that is inherent to any pregnancy. Acetaminophen can be used throughout pregnancy, and as long as the dosing is appropriate, side effects are remarkably rare.
    I really like that “With a safe history of use and a low risk of side effects, acetaminophen is widely used when pain control with drugs is required”.

    1. WilliamLawrenceUtridge says:

      Well, I’m calling it. Subtle spam, that might even pass a Turing test if you assume a non-native speaker, but still spam. Looks like “This is a burning question that what drugs can be takes as a pain killer during pregnancy but here as stated that” and “I really like that” are some sort of template text, and the robot behind the message just clips a couple sentences from other parts of the page. The actual weblink leads to a DSHEA-enabled nutraceuticals page.

      Still, better than that guy thanking God that his witchdoctor can cure AIDS.

      1. windriven says:

        Paul is very good about removing this sh!t, but only if there are no responses to it. I would like to respectfully request that when you see these in the future, copy and paste it into an email to Paul.

        1. WilliamLawrenceUtridge says:

          Even the funny ones? Did you see my reply to the vagina-tightening gel spam?

          But good suggestion, thanks.

          1. Sheesh, those are tricky to spot. I would definitely have missed these without a heads up — thanks. I nuked the other one.

  9. Hyperion says:

    There’s another fairly simple potential explanation as well: might a hyperactive child, during the third trimester, be more likely to be moving around and potentially causing discomfort? ADHD is a neurodevelopmental disorder, so it’s entirely possible for there to be some effects at that point.

    An even more obvious possibility, given the known hereditary nature of ADHD, is that a pregnant woman with ADHD might simply have more difficulty sitting still (which is a symptom of the disorder) and/or more accident prone (common in people with ADHD) and thus more likely to wind up with minor aches and sprains that result in using acetominophen.

    To be honest, it’s difficult to conclude that there is a causal effect, given the massive difference in risk between acetominophen use during pregnancy vs having a parent with ADHD.

    1. Calli Arcale says:

      Well, my second, who has ADHD, was very very VERY active in utero. As in, at 14 weeks, my husband could *see* her moving from the outside. And normally, that’s about when the mother might begin to feel the movements. She was . . . uncomfortable to carry. And of course she’s just as squirmy now, seven years later. ;-)

      But in my experience, acetominophen does absolutely bupkis for that. Take a Tylenol and ask somebody to poke you in the ribs every thirty seconds for five minutes a while later. It doesn’t help. Narcotics might help, but only by putting the baby to sleep, and that’s not really want you want. It’s definitely uncomfortable, but it’s not the kind of discomfort that you can take a pill for.

  10. Iqbal says:

    For starters, acetaminophen is not a medicine. It is a drug and therefore limiting its effects to ADHD is rather narrow vision.

    Then the article follows the same trajectory : benefits and risks. Good to check this out –


    Why should the thought be limited to ADHD? Are the other problems smaller?

    1. Sawyer says:

      “Why should the thought be limited to ADHD? Are the other problems smaller?”

      Um, didn’t the word “more” tip you off? This topic has been written about several times on this site. Here’s the most recent one:

      Both the sources you provided are not exactly the paragon of medical reporting. I like the Atlantic overall but their sloppy science is a constant problem.

      1. Iqbal says:

        The article referred many studies, including one from WHO. That is not important? The paper that publishes the article is more important? This is surprising.

        If the issue on paracetamol has included many such messages, what was the conclusion? At all times the final message is : continue as earlier.

        “Does the study change how we manage pain in pregnancy? It shouldn’t. No drug should be taken in pregnancy unless it’s necessary — acetaminophen is no exception. But there’s no reason for pregnant women to suffer from pain unnecessarily. Acetaminophen remains the drug of choice when pain control is necessary in pregnancy.”

        Why is not the pregnant women told of the possible consequences on the child and allowed to make her decision?

        I wrote the following message to doctors over the sites “ask the doctor” : If fever is an immune response of the body to act as defense mechanism against infection, why is Paracetamol prescribed by most doctors to reduce temperature? What would be the outcome at 104 F, if paracetamol is not administered?

        No doctor seems to be ready to take a stand.

        1. WilliamLawrenceUtridge says:

          You do realize that fevers can drive the temperature of the body high enough to denature brain proteins, right? Fever is not a panacea, it’s not always a good thing, and if you’re pregnant, it’s teratogenic.

          The doctors were probably unwilling to “take a stand” because you come across as a crank who has already made up their mind and is not asking a question to seek an answer, but is asking a question to make a point.

          1. Iqbal says:

            Actually I did get 2 responses:

            “Yes as you said Fever is an immune response of the body to act as defense mechanism against infection . Most of the time paracetamol is not needed if body temperature is not crossing >102F .

            But any temp >102F causes many biochemical and physiological damages . The enzymes in the body will not work properly . Heart rate increases a lot causing a strain on heart . Body oxygen consumption increase causing a strain on heart ..

            Body glucose utilisation increase and this coupled with loss of appetite and less food intake will cause profound weakness .

            Because of all this Paracetamol is used . ” and

            “Paracetamol in general is prescribed to relieve the discomfort till the disease is controlled. That has been a normal practice from years, all over the world. ”

            If paracetamol is not a medicine why should it be used? Does it nor alter symptoms for the doctor to make a proper diagnosis and actually end in doctor prescribing incorrect medication?

            1. WilliamLawrenceUtridge says:

              I’m not sure what you’re asking here. So, you asked the question of at least two doctors. They replied, with information that’s basically uncontroversial. Paracetamol rather obviously is used, is a medicine, is generally seen as safe, and has two specific indications here – high fever and to relieve pain. Taken appropriately, even assuming the results discussed in this post are real and not merely artifacts, it is safe and may contribute in a small way to children having ADHD. What is your objection? That all risks to the fetus be zero, for all possible conditions? Great, don’t take tylenol.

              But for everyone else’s sanity, don’t pretend that taking a tylenol will turn your baby into a serial killer or cause decerebrate birth. Over-react much?

        2. Harriet Hall says:

          “Why is not the pregnant women told of the possible consequences on the child and allowed to make her decision?”

          Women do make their own decisions. Most of my pregnant patients vigorously resisted taking any kind of medication, even antibiotics to treat serious infections. I spent a lot of time explaining that the known benefits of treatment strongly outweighed the small possibility of risk. And for purely symptomatic treatments like acetaminophen, I would tell them the safest course was not to take anything, but I would ask them to weigh their own comfort against a very small hypothetical possibility of risk and make their own informed decision. Even when a pregnant woman is prescribed medication, she may not take it. Example: a Canadian doctor had given a pregnant woman thalidomide samples for morning sickness; when he subsequently learned it was teratogenic, he agonized over whether to tell her. He didn’t, the baby was normal, and then he told her how worried he had been. She laughed and said he needn’t have worried – the tablets were still in her medicine cabinet; she had never taken a single one.

  11. weing says:

    “If fever is an immune response of the body to act as defense mechanism against infection, why is Paracetamol prescribed by most doctors to reduce temperature? What would be the outcome at 104 F, if paracetamol is not administered?

    No doctor seems to be ready to take a stand.”

    Are you sure about that?
    Here’s only one post dealing with this topic.

    1. Iqbal says:

      It would be have been good if doctors were reading such messages. They don’t seem to. They continue to prescribe paracetamol almost without thinking.

      Most families with small children learn from doctors and keep stock of this drug at home and use it at the least provocation!!!

      1. WilliamLawrenceUtridge says:

        Paracetamol isn’t generally prescribed, and if it is prescribed, it’s because it’s in the same pill as another drug (which, chances are, is considerably more dangerous). Tylenol is generally over the counter. Doctors may recommend it to patients as a safe drug for discomfort during pregnancy or to avert high fevers (which are in fact dangerous).

        Don’t you think you are over-reacting more than a bit? At worst, given the information discussed in this post, paracetamol is far less dangerous than alcohol, raises the risk of ADHD by an amount considerably less than the baseline rate anyway, and ADHD is hardly a condition to be viewed with horror. Unless, perhaps, you’re of the thought that parents can only love a perfect child? Or that all children who cause you inconvenience shouldn’t exist? It seems rather reasonable to conclude that these findings could be mentioned to pregnant women as part of their decision-making process regarding how to manage their symptoms. Tylenol is not thalidomide, please stop treating it like this paper makes it seem like it is.

        1. Iqbal says:


          ….. or to avert high fevers (which are in fact dangerous). ..

          What is high fever in degrees?

          1. WilliamLawrenceUtridge says:

            No idea, I’m not a doctor and I wouldn’t pretend to be one. But that being said, body temperature can reach a point that it is dangerous. What’s your point anyway?

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