Evidence the U.S. autism epidemic initiated by acetaminophen (Tylenol)

is aggravated by oral antibiotic amoxicillin/clavulanate (Augmentin)

and now exponentially by herbicide glyphosate (Roundup)


Clinical Nutrition ESPEN 2017;17:1–13


SUMMARY


Because certain hereditary diseases show autistic behavior, and autism often runs in families, researchers seek genes underlying the pathophysiology of autism, thus core behaviors. Other researchers argue environmental factors are decisive, citing compelling evidence of an autism epidemic in the United States beginning about 1980. Recognition that environmental factors influence gene expression led to synthesis of these views – an ‘epigenetic epidemic’ provoked by pervasive environmental agents altering expression of vulnerable genes, inducing characteristic autistic biochemistries in many mothers and infants. Two toxins most implicated in the U.S. autism epidemic are analgesic/antipyretic acetaminophen (Tylenol) and oral antibiotic amoxicillin/clavulanate (Augmentin). Recently herbicide glyphosate (Roundup) was exponentially implicated. What do these toxins have in common? Acetaminophen depletes sulfate and glutathione required to detoxify it. Oral antibiotics kill and glyphosate inhibits intestinal bacteria that synthesize methionine (precursor of sulfate and glutathione, and required to methylate DNA), bacteria that synthesize tryptophan (sole precursor of neuroinhibitor serotonin), and bacteria that restrain ammonia-generating anaerobes. Sulfate plus glutathione normally sulfate fetal adrenal androgen dehydroepiandrosterone to DHEAS – major precursor of placental/postnatal estrogens. Glyphosate (and heavy metals) also inhibit aromatase that turns androgens to estrogens. Placental/postnatal estrogens dehydrate/mature brain myelin sheaths, mature corpus callosum and left hemisphere preferentially, dilate brain blood vessels, and elevate brain serotonin and oxytocin. Stress-induced weak androgens and estrogen depletion coherently explain white matter asymmetry and dysconnection in autism, extreme male brain, low brain blood flow, hyperexcitability, social anxiety, and insufficient maternal oxytocin at birth to limit fetal brain chloride/water and mature GABA.


INTRODUCTION


[F]or every disease there is a single key mechanism that dominates all others. If one can find it, and then think one's way around it, one can control the disorder…. In short, I believe that the major diseases of human beings have become approachable biological puzzles, ultimately solvable. 

Lewis Thomas The Medusa and the Snail


Certain aspects of autistic disorders (ASD) are obvious though little understood. As different as autistic behavior looks from child to child, it is recognizably autistic. Martha Herbert noted many behavioral, neurological, and metabolic autisms – and that transient autistic behavior has been seen in many different disorders, including metabolic, allergic and epileptic conditions. “What is it about brain biology that may allow many different underlying biological mechanisms to produce a set of behaviors that look so similar?” she asked. [3]


Clearly these diverse mechanisms have some pathophysiology in common. Lewis Thomas noted several diseases with multiple environ-mental causes and multiple pathologies linked to a “single key mechanism”: “This generalization is harder to prove, and arguable – it is more like a strong hunch than a scientific assertion – but I believe that the record thus far tends to support it. The most complicated, multicell, multitissue, and multiorgan diseases I know of are tertiary syphilis, chronic tuberculosis, and pernicious anemia …. Before they came under scientific appraisal each was thought to be what we now call a ‘multifactorial’ disease, far too complex to allow for any single causative mechanism. And yet, when all the necessary facts were in, it was clear that by simply switching off one thing – the spirochete, the tubercle bacillus, or a single vitamin deficiency – the whole array of disordered and seemingly unrelated pathologic mechanisms could be switched off, at once.” [2]


Thomas's view of pathological mechanisms switched on or off is apt as researchers investigate genetic vulnerabilities in autism. Although gene structure (DNA) remains stable over a lifetime (except for muta-tions) gene expression is very labile. Genes are readily turned on or off by epigenetic mechanisms – environmental factors like toxins and even stress [4,5]. Three environmental toxins most implicated in the U.S. autism epidemic are (1) analgesic/antipyretic acetaminophen (Tylenol), (2) oral antibiotic amoxicillin/clavulanate (Augmentin), and most recently (3) herbicide glyphosate (Roundup). Do these toxins have a common “key mechanism”?


(pdf)