The Real Reason Acetaminophen Doubles ADHD and Autism Rates
Newsweek magazine recently published an article exposing new research that shows acetaminophen (Tylenol) doubles ADHD and Autism rates in children whose mothers took it during pregnancy.
In this article, Newsweek omits the science showing the connection leaving the reader with the dead-end phrase so often used in mainstream media: "There's a lot more work to be done here."
The connection between acetaminophen and ADHD and Autism is glutatione, the powerful substance your body makes the removes toxins from your body, including mercury.
Mercury, which has been associated with ADD, ADHD, OCD, and over 200 common diseases, is known to be intimately related to - and likely causal of - autism. Glutathione is a primary detoxifier of mercury in the body. When glutathione production is depleted, mercury is allowed to distribute in the body causing extensive damage. Much of this damage is neurological and hormonal resulting in change to personality, IQ, memory, and emotional stability.
Mainstream media has a long history of omission and disinformation related to autism. This is likely because all mainstream media is owned by 6 corporations that are intimately connected with the pharmaceutical industry. There is much information freely available online exposing this connection.
Acetaminophen decreases intracellular glutathione levels and modulates cytokine production in human alveolar macrophages and type II pneumocytes in vitro
Abstract
Recent epidemiological observations suggest that acetaminophen (paracetamol) may contribute to asthma morbidity. Impaired endogenous antioxidant defences may have a role in the pathogenesis of a number of inflammatory pulmonary diseases, including asthma. We studied the effect of acetaminophen on the intracellular level of reduced glutathione (GSH) with and without inhibitors of cytochrome P450 or prostaglandin H synthetase, and TNF-alpha, IL-6 and IL-8 protein production in human alveolar macrophages and type II pneumocytes in vitro. Following a 20 h incubation with acetaminophen, cytotoxicity was apparent from > or = 5 and > or = 10 mM in macrophages and type II pneumocytes, respectively. A time- and concentration-dependent decrease of intracellular GSH occurred after acetaminophen (0.05-1 mM) exposure (1-4 h) in pulmonary macrophages (up to 53%) and type II pneumocytes (up to 34%). Diethyldithiocarbamic acid, potassium ethyl xanthate, and indomethacin decreased significantly acetaminophen-induced GSH depletion in the two cell types tested, suggesting the involvement of cytochrome P450 (mainly CYP2E1) and/or prostaglandin H synthetase. In macrophages, acetaminophen decreased the secretion of TNF-alpha (at 4 and 24 h, concentration-related) and IL-6 (at 24 h, at 0.1 mM), and did not affect significantly IL-8 production. These in vitro observations demonstrate that clinically relevant concentrations of acetaminophen decreased: (i) intracellular GSH in human pulmonary macrophages and type II pneumocytes and (ii) the secretion of TNF-alpha and possibly IL-6 by human pulmonary macrophages. These findings provide experimental plausibility to the challenging observations that frequent use of APAP may be a risk factor for asthma morbidity.
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