"Hoping someone will chime in with more info on this and MMR..."
Please read carefully, because this is very long, but very important:
I'm going to start off by saying outright that I strongly believe that Tylenol is behind the rise of not only autism, but the other childhood "A" disorders, including asthma, allergies and ADHD.
It's only a very strong hunch, but after countless hours researching this issue, all signs point right back at Tylenol.
A few months ago, my 14 year old autistic son began exhibiting extremely aggressive behaviors. They coincided around the time we started working with a behavioral analyst who would give him skittles as a reinforcer. Over a period of about 5 days, he had ingested quite a few of these. (Ordinarily, I don't let him have very much of that sort of thing, but his behavioral analyst made it clear that we needed to have some sort of "reward" for him.) Over that 5 day period, he became very agitated, waking during the night, and just constantly wandering throught the house, acting very strangely. He attacked me, pulling my hair, and biting me. He also engaged in self-injurious behavior, hitting his head with whatever was close by, and lying down on the floor, violently banging his head into it. His behavioral analyst was at my house during one of these attacks, and we both agreed that this was very strange, and she thought maybe he was acting out because he was in pain. I gave him some Tylenol that evening, and took him to his pediatrician the next morning, to have her look him over. She couldn't find anything obviously wrong with him, other than his throat appearing a little red. I mentioned that his behavioral analyst had recently gotten over strep throat, and maybe he had been exposed. He wouldn't allow her to get a throat culture, so she gave me a prescription for an antibiotic and some Tylenol #3 and instructed me to give this to him for a couple of days to see if pain really was the problem. After a couple of days of round the clock dosing with the antibiotic and Tylenol #3, there was absolutely no improvement in behaviors, so I discontinued both and started researching online. I came across the Southampton study wrt food dyes/sodium benzoate.http://www.telegraph.co.uk/news/ukne...additives.html
This made perfect sense to me, since the behaviors had started within days of the skittles. So, I eliminated everything in my house that contained FD&C food colorings, and over a period of a few days, the behaviors went away, and didn't return for about 3 weeks.
The behaviors slowly started coming back though, which led me to trying the Feingold diet, (the ADHD diet) and we had a few weeks of good behavior, but there were still times that I felt he was reacting to certain foods, because I was noticing his ears turning red, and he seemed headachey, (rubbing his head a lot). Tylenol is the only OTC pain med approved on Feingold, so each time he had these red ear/headachey episodes, I would give him a dose.
We eventually got to a point where he seemed to be reacting to everything he ingested. His behaviors were becoming out of control again, and he even ended up in the state hospital on 3 separate occasions over a 2 month period, due to his self-injurious and aggressive outbursts. I wasn't getting anywhere with any of the doctors that saw him up to this point, so a googling I went again, and found this:http://www.newtreatments.org/Sulfur/...photransferase
Dr. Rosemary Waring's research shows that the lack of sulfate is the
primary problem in 73% of these children (another study found low
levels in 92%), but all of those Waring checked had a low PST level
too. Similar sulfate deficiencies have been reported in people with
migraine, rheumatoid arthritis, jaundice, and other allergic
conditions all of which are anecdotally reported as common in the
families of people with autism. Adequate sulfoxidation requires
adequate supplies of B-vitamins, especially vitamin B6. The PST
enzymes are inhibited or overloaded by chocolate, bananas, orange
juice, vanillin, and food colorants such as tartrazine. Removal of
these from the diet and supplementation of sulfates may well relieve
all these symptoms.
The lack of sulfation could well be due to the
largely carbohydrate diet of most of these children. It is likely a
combination of all these things. In any case, toxic compounds of
these aforementioned chemicals can build to dangerous levels. A high
value for the tIAG (?) as well as a high reading for DHPPA (rather
HPHPA-a phenolic metabolite of tyrosine) both indicate a PST problem.
I read with horror this paragraph:
"Since sulfur intake is low, and its oxidation is slow in many
autistic children, sulfate is low, and PST activity is slower than it
would be otherwise. It would seem that this sub optimality of
sulphotransferase activity is a function of low plasma sulfate levels
rather than of deficits in the actual enzyme. Cellular level
enzymatic effects of mercury's binding with proteins include blockage
of sulfur oxidation processes and of the neurotransmitter amino
acids. These have been found to be significant factors in many
autistics. Thus, mercury, and any foodstuff that requires or uses up
sulfate ions during its metabolism, will make the situation worse.
These foodstuffs include foods that supply neurotransmitters, like
bananas (serotonin), chocolate (phenylethylamine), and cheese
(tyramine), apple juice (and one mother reports her child drank a
quart a day!), citrus fruit juices, and paracetamol (Tylenol™). For
instance, one or two minutes after a dose of Tylenol™, the entire
supply of sulfate in the liver is gone!"
I couldn't believe it, because I had indeed given him Tylenol multiple times, and this explained why he was reacting to everything, in addition to craving foods like bananas and apples!
After the second admission, I contacted Thoughtful House in Austin for help. The psychiatrists that were seeing him were of absolutely no help. They insisted that this was a hormonal change, and that boys with autism act this way when they hit puberty, and my only options were to medicate him or institutionalize him. This was unacceptable. I knew there was more to it, and so did the staff at Thoughtful House. It's a long story, but he is doing better now as a result of the elemental diet they placed him on.
While at the local hospital, awaiting transfer to the state hospital, a news story came on about a link between Tylenol and asthma. I was intrigued, but didn't have time to study it too closely at that time. After my son was discharged from the hospital, and seemed to be doing better, I was able to devote more time to this Tylenol issue.
I found the story about the link between prenatal Tylenol use and asthma, and went to pubmed, to see if I could find the original study. To my surprise, I found SEVERAL studies, going back almost TEN years that show a link to Tylenol and asthma and allergies. I was stunned.http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum
A growing number of studies show that regular use of acetaminophen (paracetamol) carries a dose-dependent risk of developing allergies in general and asthma in particular and of worsening other respiratory diseases and lung function. The most disturbing finding has come from the population-based Avon Longitudinal Study of Parents and Children, in which use of paracetamol-but not aspirin-in late pregnancy was positively associated with asthma when comparing children whose mothers took paracetamol "sometimes" and "most days/daily" with those whose mothers never took it. Assuming a causal relationship, the percentage of asthma attributable to paracetamol use in late pregnancy was 7%. In this review, we present data from the most important studies published since 2000. Although the pathophysiology remains unclear, the available data justify a warning to the general public that the uncritical use of over-the-counter acetaminophen can lead to the development of allergies and asthma, even in utero.http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum
The prevalence of asthma has increased worldwide. The reasons for this rise remain unclear. Various studies have reported an association between acetaminophen, a widely used analgesic, and diagnosed asthma. In a prospective cohort study, the rate of newly diagnosed asthma was 63% higher among frequent acetaminophen users than nonusers in multivariate analyses. Studies of patients with asthma suggest that acetaminophen challenge can precipitate a decline in FEV(1) > 15% among sensitive individuals. This article reviews the existing literature and evaluates the epidemiologic and pathophysiologic evidence underlying a possible link between acetaminophen and asthma.http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum
INTRODUCTION: A link between regular paracetamol intake and asthma in adults has recently been postulated. Detoxification of paracetamol may deplete stores of glutathione, which is one of the major antioxidants present in the lung. A reduced source of glutathione in the lung may lead to increased oxidative damage to the epithelium and hence increased frequency and severity of asthma attacks in susceptible individuals. AIM OF STUDY: This study aimed to determine whether regular intake of maximum therapeutic doses of paracetamol reduced serum antioxidant capacity in healthy volunteers. METHODS: Fifteen young healthy volunteers (nine men, six women, mean age 21.3 years, range 19-32) took maximum therapeutic doses of paracetamol (1 g four times a day) for 14 days. On days 0 and 14 blood samples were taken at baseline and hourly for a period of 4 h following ingestion of 1 g paracetamol. Single venous blood samples were collected 1 h after ingestion of 1 g paracetamol on days 4, 7 and 10. Blood samples were analysed for serum paracetamol concentration and total antioxidant capacity. RESULTS: Mean total antioxidant capacity was significantly reduced over the 3-h post-dosing on both days 0 and 14 (P < 0.01). The results from days 4, 7 and 10 showed a trend towards reduced antioxidant activity over time. On day 14 values were consistently lower compared with the corresponding times on day 0 (P < 0.01 at 0, 1, 3 and 4 h, P < 0.05 at 2 h). CONCLUSIONS: Chronic ingestion of maximum therapeutic doses of paracetamol depletes serum antioxidant capacity in healthy volunteers in as few as 14 days, possibly by a reduction in glutathione. This may have implications for analgesic use in asthmatic individuals. Further studies are now required to assess the impact of paracetamol on antioxidant defences in the lung.
Tylenol is known to deplete glutathione, (this is why an overdose will kill you-it exhausts the body's supply of glutathione, and the liver can no longer excrete it) which my son's metabolic profile did show that he was deficient in. Glutathione is the body's "master antioxidant" and is essential for eliminating toxins, including mercury, from the body. Studies are showing that many autistic kids are deficient in glutathione, and also have abnormalities with sulfation.
Lots of good information here, too...http://findarticles.com/p/articles/m...1155402/pg_10/
I believe that this may possibly explain why babies so often get ear infections that first year of life. I believe that the Tylenol that is taken by the pregnant mother, as well as the tylenol given along with vaccines is depleting glutathione to a small degree in the ear canal, making it harder to the body to fight off the infection on its own.http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum
BACKGROUND: The inflammatory cells documented in chronic otitis media with effusion (OME) spontaneously release oxidants which can induce middle ear (ME) epithelial cell damage. Glutathione (GSH), a major extracellular antioxidant in humans, plays a central role in antioxidant defense. PURPOSE: To evaluate the effects of GSH treatment on chronic otitis media with effusion (OME). SUBJECTS AND INTERVENTION: Sixty children with chronic OME were enrolled, 30 of whom were randomly assigned to the treatment group and 30 to the placebo group. Patients in the treatment group received 600 mg glutathione in 4 mL saline per day subdivided into five 2-minute administrations given by nasal aerosol every 3 or 4 waking hours for 2 weeks. Patients in the control group received 4 mL saline per day following the same procedure as for GSH treatment. RESULTS: Three months after therapy improvement had occurred in 66.6% of patients in the GSH-treated group and in 8% of the control subjects (P <.01). CONCLUSION: On the basis of these results, GSH treatment could be considered for the nonsurgical management of chronic OME.
I believe these frequent ear infections in the first year of life, and the medications used to treat them are setting these kids up for a perfect storm by depleting their sulfates, stripping their gut flora, and depleting their glutathione. The MMR is one in which very high fevers are often reported, and if the gut integrity is already under stress, and more Tylenol is administered, you're only asking for trouble.
For years, I had thought that only vaccines were the cause of my older son's autism. So much so, that I refused to vaccinate my younger son. However, that child also started showing signs of autism, (mostly in the way of speech delay-he is nowhere near as severly autistic as my older son, and will likely lose his diagnosis of PDD-NOS as he gets older.) I took Tylenol very frequently during the end of my pregnancy, due to severe back pain, as well as taking Tylox (which contains acetaminophen) for pain after my cesarean. My younger child also has mild asthma.
Many of the medications that are given to women after birth contain acetaminophen (Tylox, Darvocet, Lorcet, Lortab, etc).
Another thing that I discovered is that the practice of administering Tylenol before vaccinations is not supported by scientific evidence.
I've also found evidence that Tylenol causes mitochondrial damage:http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum
Since the first mitochondrial dysfunction was described in the 1960s, the medicine has advanced in its understanding the role mitochondria play in health and disease. Damage to mitochondria is now understood to play a role in the pathogenesis of a wide range of seemingly unrelated disorders such as schizophrenia, bipolar disease, dementia, Alzheimer's disease, epilepsy, migraine headaches, strokes, neuropathic pain, Parkinson's disease, ataxia, transient ischemic attack, cardiomyopathy, coronary artery disease, chronic fatigue syndrome, fibromyalgia, retinitis pigmentosa, diabetes, hepatitis C, and primary biliary cirrhosis. Medications have now emerged as a major cause of mitochondrial damage, which may explain many adverse effects. All classes of psychotropic drugs have been documented to damage mitochondria, as have stain medications, analgesics such as acetaminophen, and many others.
While targeted nutrient therapies using antioxidants or their precursors (e. g., N-acetylcysteine) hold promise for improving mitochondrial function, there are large gaps in our knowledge. The most rational approach is to understand the mechanisms underlying mitochondrial damage for specific medications and attempt to counteract their deleterious effects with nutritional therapies. This article reviews our basic understanding of how mitochondria function and how medications damage mitochondria to create their occasionally fatal adverse effects.
The 4 "A" disorders are all becoming more frequent in children over the past 20 years, coinciding with the timing of aspirin's link to Reye's Syndrome. I do not believe this to be just a coincidence.
I know this has been long, and I've only scratched the surface of what I've learned, but I thank you if you've read this entire post.
Please use Tylenol with extreme caution.