Yes, Actually, Tylenol (and Other Common Meds) Have Serious Dangers

Between 8 and 13 years ago I made a number of posts on the dangers of common medications, including acetaminophen (APAP). I rewrote two of those and synthesized them into this blog entry over 6 years ago: https://www.elev8wellness.com/wellblog_best_nutrition_training_coaching_experts/hey-preachy-youre-a-riskier-drug-addict-than-everyone-on-illicit-substances . So this past week presented a number of awkward moments for me, since I just in one day learned that other people were still unaware APAP has significant risks. I did not realize this wasn’t common knowledge, given there are warnings literally on the label.


First, do keep in mind that Tylenol has been THE LEADING over-the-counter cause of emergency room visits in the United States:


https://pubmed.ncbi.nlm.nih.gov/15239078/


And it has long been THE leading overdose during pregnancy:


https://pubmed.ncbi.nlm.nih.gov/16351032/


When I first saw these stats in 2004 and 2005, it concerned me a lot. Already, I had never found it even mildly effective in my own pain management; for me, it does absolutely nothing. But at this time I also began specializing in dealing with clients who had complicated health issues and pain pathologies. So the subject kept coming up. And I increasingly took a more cautious stance about its use. That’s over 21 years where I’ve been not particularly trusting of it in a professional and research setting. This was the same period of time where criminality at the FDA and fraud in science was generating the opioid crisis, which has now claimed over half a million American lives JUST from the approved prescription use side of the equation (closer to 1 million overall): https://journalofethics.ama-assn.org/article/how-fda-failures-contributed-opioid-crisis/2020-08. We need not dig into it too deeply; but this was also the height of the era of peer review abuse, slowing down scientific discovery and doing the bidding of industry interests, which continues today:


https://pmc.ncbi.nlm.nih.gov/articles/PMC1420798/


https://pmc.ncbi.nlm.nih.gov/articles/PMC1140949/


https://blog.operationmedschool.com/home/is-peer-review-everything-it-implies




As a general rule, I don’t get caught up in discussions about autism, because it’s a subjective symptomatic diagnosis. There is no THE autism. In a symptomatic diagnosis we are placing one name on many different things because of some common symptoms. As such, there is no THE cause. Symptomatic diagnoses have no single cause. They have an array of risk factors. Contrast this against an acute diagnosis based on an objective lab test, like Influenza A, wherein we might point to infectious exposure as THE cause. However, even then, exposure is not a sufficient explanation, since many people do not succumb after exposure. Infection itself also requires nuance in understanding, because not everyone infected with Influenza A showcases the exact same symptoms for the exact same duration. In fact, even with objective test-based diagnoses, there are other risk factors, which include the resilience of the patient, genetic variables, viral load, and much more.


Parkinson’s is a good example where there is no THE Parkinson’s. There are many people with a cross-section of interrelated symptoms who carry the same diagnostic naming. There is no ONE cause. Brain trauma is a risk factor. Autoimmune irregularities are a risk factor. TIA and stroke are risk factors. There are others. Nicotine use is NEGATIVELY associated (ie - reduces risk). There is no THE cause. It’s a symptomatic diagnosis. We hope to improve this with certain imaging. But we aren’t there yet.


Leave that all aside. APAP is a fascinating subject without even thinking of autism. Reexamining the many possible downstream effects of APAP is a strong scientific discovery tool. It may help to explain why some people are more susceptible to certain infections, autoimmune diseases, cancers, cardiovascular disease, metabolic disorders, joint deterioration, inability to recover, chronic fatigue/pain/heartburn, thyroid irregularities, infertility, heavy metal exposure, and central nervous system damage. 30-40% of the population has at least one MTHFR variant that can lead to reduced glutathione capacity (the very means by which our bodies deal with APAP). This means that at least a tiny population cannot clear APAP well enough to the point those people will incur other unexpected damage to systems which are not the liver. There is a vast expanse of individual responses based on MTHFR variants (or none) alone.


Even small doses of APAP deplete glutathione (your body’s strongest detoxifying agent against heavy metals and the ROS produced during infections) from an otherwise healthy body. High doses overwhelm the glutathione pathway completely. Thus, APAP can be a problem for lots of people at a variety of doses. A lethal dose (LD50) of any compound is what we are confident will kill half the populace, which in normal distribution means some 25% will die at a lower dose and 25% at a higher dose. There will be a few extreme outliers, people who die at trace amounts and people who suffer few consequences at insanely high dosing. Those are simply immediate fatality stats. Non-fatal damage happens at much lower dosages and much more frequently. Prevalence of long-term consequence is wholly unknown. We know it exists. And we sometimes see it in liver failure many years later. But specific brain damage numbers are opaque.


This is critical to consider before wading into the subject. Personal anecdote and sample bias are not helpful in this conversation, in the same way that people who are alive today despite not wearing any seatbelts in the 1970s cannot tell us that seatbelts are useless. Similarly, that 98% of the populace can eat a lot of peanuts to no detrimental effect is not a helpful fact for giving advice to the 2% who may die from a fleck of peanut dust. Pause. Reflect on this. Over 90% of a population can have no obvious negative experience with a sometimes-fatal compound. This is absolutely essential to keep in mind when we are going to entertain debates over damage that happens to less than 10% of people. Whatever the various causes or risk factors are will not be evident to “almost everyone.”


I place 700lbs on my spine and it makes my spine healthier. That doesn’t mean I should tell you you’re a liar when you say that you strained your back lifting a few pounds. I squat deep with 600lbs and my knees improve from that stimulus. This doesn’t mean that the same dosage of the prescription will work for others. George Burns smoked nearly every day of his 100 year life. That doesn’t mean he would’ve been right to tell you that smoking is good for you. I jumped out of an airplane. I’ve climbed cliffs with no harness. So those things are good for you and safe, right? There are alcoholics and cocaine addicts in way better shape than you, with way better overall health than you have. So that behavior is good and safe, right? Obviously not. We have to have the maturity to acknowledge individual variance, combined effects in different landscapes, and that many substances or circumstances do not have universal same risk or lack thereof. Even if many people survived really stupid things, it doesn’t logically follow that it’s safe or good for all people for all time.


The American Academy of Pediatrics considers a fever productive all the way up to 102.2: https://publications.aap.org/pediatrics/article/127/3/e20103852/65016/Fever-and-Antipyretic-Use-in-Children. Fevers are fundamentally a healthy response to combat disease. Febrile seizure above 103 is an actual risk; so when the risk-reward warrants it (~102.5 and up), it could then be a good time to risk the drug.


Many people, I assume, don’t know any of this either. So the chances that a lot of people have overreacted to and shut down productive fevers or pre-productive fevers WHILE inhibiting the liver is probably pretty high. This will ASSUREDLY cause downstream adverse side effects. If you pair this with heavy metals and/or free radicals from infection it would make perfect sense that you raise risks of neural damage. That’s without factoring the aforementioned MTHFT variants. And this is not conjecture. In 1980 researchers confirmed brain uptake of APAP in animal models: https://pubmed.ncbi.nlm.nih.gov/7325924/. This was confirmed in humans in 1992: https://pubmed.ncbi.nlm.nih.gov/1633071/. A mounting tsunami of studies since indicates that in infants/youths, the target of APAP is the brain, NOT the liver: https://www.e-cep.org/m/journal/view.php?doi=10.3345/cep.2022.01319. In fact, we have case studies of youths who ONLY take damage to the brain with APAP overdose (while the liver is seemingly not overwhelmed): https://ejnpn.springeropen.com/articles/10.1186/s41983-024-00910-z#ref-CR10.


None of this is theoretical. APAP does cross over to the baby’s brain in utero AND in comparable concentrations to that administered to mothers:
https://pubmed.ncbi.nlm.nih.gov/27806383/


https://hsrc.himmelfarb.gwu.edu/smhs_pharm_facpubs/736/


The idea that mothers’ livers would somehow stop all APAP is not based in any known physiology. The placenta provides little barrier to the concentration. And the fetal liver is incapable of buffering as well. Whatever APAP mom takes, the baby’s brain receives. In studies. In reality. Not hypothetically. If we want to get into hypotheticals, the concern rises. It does not lower. We can imagine a mother with multiple MTHFR variants, an infection, AND heavy metal exposure. We can easily imagine a newborn with multiple MTHFR variants, an infection, AND heavy metal exposure. The confluence of these risk factors presents an incredibly high risk of fetal brain injury and newborn brain injury. It MAY be that this is a rare event. But to conclude it never happens or cannot happen is anti-science.


Returning briefly to the big question of autism, again, I don’t like it. It’s too broad a term across too broad a group of different people. Obviously it includes a bunch of people with no real brain injury or really any serious developmental challenge at all. There are brilliant functional kids who carry the diagnosis of ASD. Most of these are just kids who are wired a little differently and have uncommon interests. That makes the entire debate a dishonest one to begin. Instead, if we focus solely on “profound autism,” where THE diagnostic criteriON is a sub-50 IQ (along with almost or no verbal ability) there is a glaring problem for all of us. According to the CDC profound autism assuredly doubled without any change in diagnostic criteria across a modern 16 year period: https://rutgershealth.org/news/first-large-study-profound-autism-finds-rising-problem-disparate-impacts. 


https://journals.sagepub.com/doi/10.1177/00333549231163551


This is not explained by an expansion of the diagnosis. This is the same diagnosis. Why would acute brain damage occur in early development at a twofold increase from 2000 to 2016? Well, it turns out that APAP usage did increase during that period:


https://www.clinicaladvisor.com/news/acetaminophen-use-increased-between-2011-2016-cold-flu-seasons/


Also, from 1994 to 2014 the childhood vaccine schedule increased from 7 recommended vaccinations to 16:


https://www.clinicaladvisor.com/news/acetaminophen-use-increased-between-2011-2016-cold-flu-seasons/


Correlation is no smoking gun. People have to tread lightly seeing something like this and claiming it proves causation. But worse than that is to look at these numbers, know the pharmacokinetics and physiology, and say there CANNOT be any causal relationship. Clearly, impaired glutathione, increased neurotoxicity, and increased aluminum and mercury exposure, EVEN IF SAFE FOR 95% OF THE POPULACE, becomes a risk of neurological damage at some point. This is not controversial. This does not mean vaccines are wholly unsafe or that Tylenol is wholly unsafe. There are other trends which play a role. What it likely means is they are among a suite of several risk factors, particularly for some people under some circumstances, AND we should ALSO consider the factors of aging parents, cumulative toxic load, EMF exposure, etc. The false dichotomy is not helping. Being “provax” OR “antivax” is not an appropriate or sophisticated choice. And gleefully destroying world-class scientists’ lives and careers for them daring to question the sacred cow is a little absurd. If we are to believe we truly are a modern scientific society, voices of dissent and inquiry shall not be suppressed or minimized by a priestly class of truth holders. 


APAP’s history is even more fascinating to consider than the pharmacokinetics and epidemiology. Acetaminophen (APAP) was first synthesized in 1878. From 1887 to the 1940s it was the effective compound (although people didn’t know it at the time) in the most widely used analgesic at the time, Phenacetin. Pay attention. Before Tylenol the brand, “tylenol” the ingredient was THE MOST WIDELY USED analgesic since the 1880s. 


Phenacetin was still in use until the 70s and 80s. In 1948 researchers learned that the popular Phenacetin converted into acetaminophen in the body; and in 1955 a reformulated “Tylenol elixir” hit the market. Curiously, Phenacetin is now considered a known carcinogen. APAP’s carcinogenicity is debated, with over 100 high quality studies showing the possibility, but with mixed interpretations. 


Phenacetin dosing was 300mg 4-6 times per day: https://www.ncbi.nlm.nih.gov/books/NBK304337/. Fractional conversion to APAP was 0.871. Thus, people were getting severe negative side effects from Phenacetin at an equivalent intake of 1,000 to 2,000mg of Tylenol. Concluding that Phenacetin alone was the problem and that Tylenol poses little-to-no risk is an objectively low-IQ take.


Frankly, none of this is even remotely debatable outside of the recent layperson political outrage. Aspirin and ibuprofen and naproxen are openly and unanimously linked to birth defects. APAP gets a pass from some of the populace even though the other drugs have lower toxicity profiles.


I’ve come to conclude that a lot of people’s positions on pharmaceuticals are no more than rhetorical devices aimed at ending inquiry and the advancement of science. 


“No one believes…”
“Consensus is…”
“The experts say…”
“There is no evidence of…”


These and others are merely attempts to shift to an impossibly unassailable position, uninterested in evidence or arguments entirely. So I’ve developed a way for all of us to cut through the noise; and on this topic it’s three simple questions whose answers are totally unanimous. Not consensus. Facts.


Will ALL mothers have livers which prevent ALL toxins from getting to the placenta?


Will ALL placentae block all toxins from getting to baby? 


Will all fetal livers block all toxins from reaching the brain?


Incuriosity is an illness of the mind with few remedies. People who aren’t interested in learning are immune to evidence, facts, reality, and science. All the same, it makes for a fascinating reflection on whether APAP played/plays a role in “unexplained” phenomena, like SIDS and childhood leukemias, ALS, and “idiopathic” pathologies of all sorts. Asthma included: https://pubmed.ncbi.nlm.nih.gov/15878691/. We can sweep all considerations of autism aside, and APAP is still implicated in other rare diseases by virtue of how it damages some individuals.


Again, not as THE cause. But as A risk factor.