The Antioxidant System

The Antioxidant System
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The Antioxidant System

Antioxidants are profoundly important to our health, yet just as profoundly misunderstood.

First, free radicals and other oxidants are actually good for us in the right amount and context. They support our thyroid health and our immune system, they help us regulate our energy metabolism, and they help us get lean and fit in response to exercise. In the wrong context, however, they can make us sick, contributing to aging skin, diabetes, thyroid diseases, and many other aspects of ill health. The role of the antioxidant system isn't to stop these oxidants in their tracks; it's to direct them into their healthful roles and prevent them from causing harm.

Second, nourishing the antioxidant system is about a lot more than fruits, vegetables, and the latest trendy superfoods. It's also about protein, fat, carbohydrate, minerals, and B vitamins. It's about a well rounded, nutrient-dense diet.

If we want to be able to harness the antioxidant system to support our health, we need to understand how it works.

This is a free 14-lesson series on the nuts and bolts of the antioxidant system, complete with videos, slides, and transcripts so that you can pick whatever format works best for you and learn how the system works at your own pace.

Everything you need is right here on this page. However, you can also watch the videos on YouTube or Facebook. You can always come back to this page with the easy-to-remember shortcut, “chrismasterjohnphd.com/antioxidant” If you love the class, share it on Facebook, retweet it, or like it on Instagram!

Have fun, and let me know what you think in the comments!

1. Physiological Roles of Oxidants



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Masterpass holders can read the transcript here.

2. Pathological Roles of Oxidants



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3. Introduction to the Antioxidant System



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4. Vitamin E



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5. Vitamin C



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6. Introduction to Glutathione



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7. Nutrition, Metabolism, and GSH Status



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8. Beneficial Toxins: Phytochemicals, Hormesis, and Nrf2



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9. Oxidative Stress, Green Tea, and Fatty Liver Disease



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10. Glutathione Reductase, B Vitamins, and Glucose



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11. Pentose Phosphate Enzymes, ATP, and B Vitamins



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12. Oxidative Stress and Heart Disease



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13. Vegetable Oils and Heart Disease: Examining the Controversy



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14. Wrapping Up the Antioxidant System


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8 Comments

  1. wondering if you could explore in your lite series why people seem to do well with oxidants such as hyperbaric oxygen, h202, and mms (chlorine dioxide)

  2. Hey Chris,
    I was wondering what could be done for someone who has a SNP within the G6PD gene. Since the this prevents the pentose phosphate pathway, would it be advisable to supplement with ribose and NADPH?

    Thanks in advance!

    Lisa

  3. Super stuff – thank for this.

    One other cause of thiamine deficiency is elevated sulfite, and elevated sulfite can be caused by oxidative stress, so oxidative stress might lead to low levels of B1 even when there is dietary sufficiency of it.

    e.g.

    Aust Vet J. 2005 Jul;83(7):412-7.
    Thiamine deficiency in dogs due to the feeding of sulphite preserved meat.

    Singh M1, Thompson M, Sullivan N, Child G.
    Author information
    Abstract
    A 6-year-old dog, a 4-year-old dog and three 7-week-old puppies were diagnosed with thiamine deficiency caused by feeding sulphite treated meat. The 6-year-old dog presented with a history of inappetence, weight loss and vomiting that rapidly progressed to signs of multifocal intracranial disease including mental dullness, paresis, seizures, spontaneous nystagmus and strabismus. Thiamine pyrophosphate effect was elevated at 58% and magnetic resonance imaging revealed bilaterally symmetrical hyperintensity of the caudate nucleus and rostral colliculi. The dog recovered with thiamine supplementation. The 4-year-old dog and three 7-week-old puppies also presented with rapidly progressive multifocal central nervous system signs including ataxia, paresis, increased muscle tone, seizures, nystagmus and exophthalmos. The 4-year-old dog made a rapid recovery with thiamine supplementation. Euthanasia and necropsy of a puppy revealed malacia of multiple brainstem nuclei and oedema of the cerebral cortex. These findings were consistent with thiamine deficiency.
    Comment in
    Thiamine deficiency due to sulphur dioxide preservative in ‘pet meat’–a case of déjà vu. [Aust Vet J. 2005]
    PMID: 16035180

    ———-

    Shock. 2005 Dec;24(6):529-34.
    Oxidative stress-dependent conversion of hydrogen sulfide to sulfite by activated neutrophils.

    Mitsuhashi H1, Yamashita S, Ikeuchi H, Kuroiwa T, Kaneko Y, Hiromura K, Ueki K, Nojima Y.
    Author information
    Abstract
    Sulfite, which is known as a major constituent of volcanic gas, is endogenously produced in mammals, and its concentration in serum is increased in patients with pneumonia. It has been reported that sulfite is produced by oxidation from hydrogen sulfide (H2S) as an intermediate in the mammalian body. The objective of this study was to investigate the ability of reactive oxygen species from neutrophils to produce sulfite from H2S. Sulfite production from activated neutrophils stimulated with N-formyl-methionyl-leucyl-phenylalanine gradually increased with an increased concentration of sodium hydrosulfide (NaHS) in the medium. The production of sulfite was markedly suppressed with an NADPH oxidase inhibitor, diphenyleneiodonium. When NaHS was added to the supernatant of activated neutrophils, a significant amount of sulfite was synthesized in the test tubes. Furthermore, when a medium containing NaHS was incubated with a water-soluble radical initiator, 2,2′-azobis-(amidinopropane) dihydrochloride, sulfite was formed in the solution and this increase was markedly suppressed by ascorbic acid. Finally, we determined serum concentrations of sulfite and H2S in an in vivo model of neutrophil activation induced by systemic injection of lipopolysaccharide (LPS) into rats. We found a significant increase in serum sulfite and H2S after LPS injection. Importantly, coadministration of ascorbic acid with LPS further increased serum H2S but suppressed sulfite levels. This finding implies that oxidative stress-dependent conversion of H2S to sulfite might occur in vivo. Thus, the oxidation of H2S is a novel sulfite production pathway in the inflammatory condition, and this chemical synthesis might be responsible for the upregulation of sulfite production in inflammatory conditions such as pneumonia.
    PMID: 16317383

    1. Interesting. Can you shed more light on the mechanism? Doesn’t sound so much like producing thiamin deficiency as raising the need for thiamin.

      Chris

  4. Hi Chris,

    First of all, thanks for putting this material together. However, my general biology and chemistry knowledge is quite rusty, so I was wondering if you can recommend a resource (perhaps one of the courses on Kahn Academy?) to use in relearning the fundamentals to get the most out of this course as well as future courses?

    Thanks!

    1. Hi Jeff, Khan Academy is pretty good. Right now I’m releasing a class in energy metabolism where I review basic chemistry concepts as I go along. Perhaps if enough people want it, I could even do basic courses.

  5. Hi Chris, Excellent series. I have one area I would ask you to clear up if you can. You seem to be inferring that omega-3 is as bad as omega-6 with regard to oxidation potential in human tissues. You may not be inferring this. I have a copy of your How Essential Are the Essential
    Fatty Acids? paper. I have also read a lot of Bill Lands work including:
    Consequences of Essential Fatty Acids https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3475243/
    Historical perspectives on the impact of n-3 and n-6 nutrients on health https://www.sciencedirect.com/science/article/pii/S0163782714000253
    Healthy intakes of n−3 and n−6 fatty acids: estimations considering worldwide diversity https://ajcn.nutrition.org/content/83/6/S1483.full
    and lots of others.
    All of these articles indicate are large benefit in reducing the omega-6 intake and maintaining a healthy ratio between omega-3 and omega-6.
    In Consequences of Essential Fatty Acids Bill Lands states “Tissue phospholipids undergo a continual remodeling process that allows cellular membranes to fairly rapidly accumulate HUFA at the 2-position.” He mentions this 2-position a couple of times. I get the impression that its going to have either omega-9, 6, or 3 on it and it should be a majority of omega-3. Am I reading it correctly and if so does that mean we are best to ensure we get enough (not much) omega-3 and 6 to create the correct HUFA balance.
    Although Bill Lands also says we don’t need much of either 3 or 6 he doesn’t talk about excess omega 3 as a problem. If the eaten in the correct ratio within reasonable amounts wouldn’t any excess of just be used as energy?

    1. Hi Adrian, you’re creating a conflict between different things that have no conflict between them. Omega-3 fatty acids are more vulnerable to peroxidation than omega-six because they have more double bonds. You don’t cite any arguments otherwise. You simply state that Bill Lands has pointed out problems with not getting enough omega-3 and has not pointed out problems of getting too much. First of all, one is a question of chemistry and the other of nutrition. Second, I don’t know why Bill Lands didn’t point out that they are vulnerable to peroxidation, but this isn’t even slightly controversial. The net effect of consuming them in the diet can be very controversial, because the number of peroxidizable carbons is not the only thing that relates to human health, and isn’t even the only thing that relates to the question of whether they will become peroxidized. But they are still very peroxidizable.

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