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Flint Father: My Wife Has to Take Care of Me


Adam Murphy speaks about the effects of lead poisoning at the TYT’s town hall.

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Video Credit: TYT Politics


  1. This information is for the person in the video with the caveat that I am not a doctor in any way I am just a person who is interested in neuroprotection and environmental health. This links are abstracts and links to studies on pubmed that look like they might impart some useful info. I would definitely take NAC if I was in that situation, this is just one of dozens of similar papers. NAC is commonly taken orally. Its available as 600 mg capsules, they are fairly cheap- you can also buy it in bulk and encapsulate it yourself. Its a mild chelator of some metals- Its biggest benefit is as a precursor of glutathione.

    I take NAC several times a day with water. I would ask your doctor about this – get familiar with pubmed. There are a fair number of papers on pubmed suggesting that NAC is helpful in that situation but I would read up on it, and ask your doctor- NAC is just a good thing to take. It may prevent birth defects to boost glutathione levels.


    Biol Trace Elem Res. 2012 Jun;147(1-3):292-8. doi: 10.1007/s12011-012-9320-1. Epub 2012 Jan 13.
    N-acetylcysteine attenuates copper overload-induced oxidative injury in brain of rat.

    Ozcelik D1, Uzun H, Nazıroglu M.
    Author information
    Copper is an integral part of many important enzymes involved in a number of vital biological processes. Even though it is essential to life, at elevated tissue concentrations, copper can become toxic to cells. Recent studies have reported oxidative damage due to copper in various tissues. Considering the vulnerability of the brain to oxidative stress, this study was undertaken to explore possible beneficial antioxidant effects of N-acetylcysteine on oxidative stress induced by copper overload in brain tissue of rats. Thirty-two Wistar rats were equally divided into four groups. The first group was used as control. The second, third, and fourth groups were given 1 g/L copper in their drinking water for 1 month. At the end of this period, the group 2 rats were sacrificed. During the next 2 weeks, the rats in group 3 were injected intraperitoneally with physiological saline and those in group 4 with 20 mg/kg intraperitoneal injections of N-acetylcysteine. In group 2 the lipid peroxidation and nitric oxide levels were increased in the brain cortex while the activities of superoxide dismutase and catalase and the concentration of glutathione were decreased. In rats treated with N-acetylcysteine, lipid peroxidation decreased and the activities of antioxidant enzyme improved in the brain cortex. In conclusion, treatment with N-acetylcysteine modulated the antioxidant redox system and reduced brain oxidative stress induced by copper.
    PMID: 22246790 DOI: 10.1007/s12011-012-9320-1

    Next one-


    Toxicology. 2003 Jul 15;189(1-2):147-63.
    Copper toxicity, oxidative stress, and antioxidant nutrients.

    Gaetke LM1, Chow CK.
    Author information
    Copper (Cu) is an integral part of many important enzymes involved in a number of vital biological processes. Although normally bound to proteins, Cu may be released and become free to catalyze the formation of highly reactive hydroxyl radicals. Data obtained from in vitro and cell culture studies are largely supportive of Cu’s capacity to initiate oxidative damage and interfere with important cellular events. Oxidative damage has been linked to chronic Cu-overload and/or exposure to excess Cu caused by accidents, occupational hazards, and environmental contamination. Additionally, Cu-induced oxidative damage has been implicated in disorders associated with abnormal Cu metabolism and neurodegenerative changes. Interestingly, a deficiency in dietary Cu also increases cellular susceptibility to oxidative damage. A number of nutrients have been shown to interact with Cu and alter its cellular effects. Vitamin E is generally protective against Cu-induced oxidative damage. While most in vitro or cell culture studies show that ascorbic acid aggravates Cu-induced oxidative damage, results obtained from available animal studies suggest that the compound is protective. High intakes of ascorbic acid and zinc may provide protection against Cu toxicity by preventing excess Cu uptake. Zinc also removes Cu from its binding site, where it may cause free radical formation. Beta-carotene, alpha-lipoic acid and polyphenols (chris comment resveratrol, curcumin, quercetin are examples ask your doctor- they reduce inflammation ) have also been shown to attenuate Cu-induced oxidative damage. Further studies are needed to better understand the cellular effects of this essential, but potentially toxic, trace mineral and its functional interaction with other nutrients.

    PMID: 12821289

    Biol Trace Elem Res. 2009 Jan;127(1):45-52. doi: 10.1007/s12011-008-8219-3. Epub 2008 Sep 12.
    Copper intoxication; antioxidant defenses and oxidative damage in rat brain.

    (Taking NAC (N-acetyl cysteine) increases GSH – Glycine may help too. )

    Ozcelik D1, Uzun H.
    Author information
    Copper (Cu) is an integral part of many important enzymes involved in a number of vital biological processes. Even though Cu is essential to life, it can become toxic to cells, at elevated tissue concentrations. Oxidative damage due to Cu has been reported in recent studies in various tissues. In this study, we aimed to determine the effect of excess Cu on oxidative and anti-oxidative substances in brain tissue in a rat model. Sixteen male Wistar albino rats were divided into two groups: the control group, which was given normal tap water, and the experimental group, which received water containing Cu in a dose of 1 g/l. All rats were sacrificed at the end of 4 wk, under ether anesthesia. Cu concentration in the liver and in plasma alanine aminotransferase (ALT) and aspartate transaminase (AST) activities were determined. There were multiparameter changes with significant ALT and AST activity elevation and increased liver Cu concentration. In brain tissue, Cu concentration, superoxide dismutase (SOD) activities, malondialdehyde (MDA) levels and glutathione (GSH) concentrations were determined. Brain Cu concentration was significantly higher in rats receiving excess Cu, compared with control rats (p < 0.05). Our results showed that SOD activities and GSH levels in brain tissue of the Cu-intoxicated animals were significantly lower than in the control group (p < 0.01 and p < 0,001, respectively). The brain MDA levels were found to be significantly higher in the experimental group than in the control group (p < 0.001). The present results indicate that excessive Cu accumulation in the brain depressed SOD activities and GSH levels and resulted in high MDA levels in brain homogenate due to the lipid peroxidation induced by the Cu overload.
    PMID: 18784908 DOI: 10.1007/s12011-008-8219-3


    Check out these links and then follow the related links at the side.. learn how to use PubMed. You may want to also search on lead poisoning or the other toxicants found in test results.

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