Exercise, Reactive Oxygen Species, and Fatigue.

weyland

Well-Known Member
At the 12th week of the experiment, the levels of catalase, SOD and GSH-Px were significantly lower in the riboflavin-deficient, T. spiralis-infected, and combined riboflavin-deficient and T. spiralis-infected, rats, compared to the control group. This may have been due to an increase in free oxygen radicals caused by riboflavin deficiency and parasitic infection.
Again, in the context of infection, in rats. Not proof that in humans a vitamin deficiency alone causes oxidative stress which is what you seem to be saying. Let me know if I am misunderstanding your assertions.

I forgot the link for that one, but here you go. I fail to understand how you do not see the connection.
http://bmb.oxfordjournals.org/content/68/1/95.full
I don't doubt that environmental exposure + infection leads to a worse outcome. In that case the damage comes directly or as a result from the pollutant, not from our body's protective response to it. That paper is talking about exposure to outside oxidants, probably in concentrations far greater than what our body can produce.

As was pointed out in the paper I linked, diminishing the body's oxidative response in the context of diseases can lead to worse outcomes.
When antioxidants are put to the test in randomized clinical trials they generally fail or, worse, show evidence of unexpected harm. For example, in a meta-analysis of nine clinical trials that evaluated the benefit of treating type 2 diabetes with antioxidants such as α-tocopherol (vitamin E) there was no benefit (Suksomboon et al., 2011). Like many purified antioxidant vitamins, vitamin E is a two-edged sword. The reasons for this are not entirely clear, but may relate to the fact that therapeutic dosing of purified micronutrients and antioxidants intervenes in regulatory pathways that produce biochemical symptoms associated with cell defense, but are not the actual cause of disease. Vitamin E supplementation, alone or in combination with β-carotene, was shown to increase the risk of lung cancer in smokers (The Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group, 1994). Vitamin C supplementation was found to double the risk of cancer death in nonobese women [relative risk (RR) = 2.0; 95% CI = 1.12–3.58], while having no effect in obese women (Lin et al., 2009). The SELECT clinical trial of vitamin E and selenium was terminated early because of an apparent increase in the risk of new onset diabetes in the selenium group and a 1.6-fold increased risk in prostate cancer in the vitamin E group (Lippman et al., 2009; Klein et al., 2011). If ROS are at the heart of cancer, diabetes, and heart disease, why are antioxidants so ineffective at preventing or treating these diseases?
But mice studies are useful and you dismiss it not to further our understanding, but only to try to appear intelligent.
There's no need to be adversarial. I'm trying to discuss the science with you. It's not controversial to point out that animal studies have limitations and don't prove anything in humans.

Listen, if you think that people with ME do not have enough oxidative stress to kill a virus or bacteria in the body show me some links to back up your hypotheisis.
Galbraith DN, Nairn C, Clements GB. Evidence for enteroviral persistence in humans.
Chia J, Chia A, Voeller M, Lee T, Chang R. Acute enterovirus infection followed by myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and viral persistence.
Chia JK, Chia AY. Chronic fatigue syndrome is associated with chronic enterovirus infection of the stomach.
Chia JK, Chia AY. Ribavirin and Interferon-a for the Treatment of Patients with Chronic Fatigue Syndrome Associated with Persistent Coxsackievirus B Infection: A Preliminary Observation.
Douche-Aourik F, Berlier W, Féasson L, Bourlet T, Harrath R, Omar S, Grattard F, Denis C, Pozzetto B. Detection of enterovirus in human skeletal muscle from patients with chronic inflammatory muscle disease or fibromyalgia and healthy subjects.
Galbraith DN, Nairn C, Clements GB. Phylogenetic analysis of short enteroviral sequences from patients with chronic fatigue syndrome.
Cunningham L, Bowles NE, Lane RJ, Dubowitz V, Archard LC. Persistence of enteroviral RNA in chronic fatigue syndrome is associated with the abnormal production of equal amounts of positive and negative strands of enteroviral RNA.
Gow JW, Behan WM, Clements GB, Woodall C, Riding M, Behan PO. Enteroviral RNA sequences detected by polymerase chain reaction in muscle of patients with postviral fatigue syndrome.
Archard LC, Bowles NE, Behan PO, Bell EJ, Doyle D. Postviral fatigue syndrome: persistence of enterovirus RNA in muscle and elevated creatine kinase.
E. G. Dowsett, A. M. Ramsay, R. A. McCartney, E. J. Bell Myalgic encephalomyelitis--a persistent enteroviral infection?
McGarry F, Gow J, Behan PO. Enterovirus in the chronic fatigue syndrome.
J. Richardson Viral Isolation from Brain in Myalgic Encephalomyelitis
Fegan KG, Behan PO, Bell EJ. Myalgic encephalomyelitis--report of an epidemic.

I have a strong feeling I know you from PR.
And?
 

RuthAnn

Well-Known Member
Croatoan said:
Listen, if you think that people with ME do not have enough oxidative stress to kill a virus or bacteria in the body show me some links to back up your hypotheisis.​
And @weyland added:

Galbraith DN, Nairn C, Clements GB. Evidence for enteroviral persistence in humans.
Chia J, Chia A, Voeller M, Lee T, Chang R. Acute enterovirus infection followed by myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and viral persistence.
Chia JK, Chia AY. Chronic fatigue syndrome is associated with chronic enterovirus infection of the stomach.
Chia JK, Chia AY. Ribavirin and Interferon-a for the Treatment of Patients with Chronic Fatigue Syndrome Associated with Persistent Coxsackievirus B Infection: A Preliminary Observation.
Douche-Aourik F, Berlier W, Féasson L, Bourlet T, Harrath R, Omar S, Grattard F, Denis C, Pozzetto B. Detection of enterovirus in human skeletal muscle from patients with chronic inflammatory muscle disease or fibromyalgia and healthy subjects.
Galbraith DN, Nairn C, Clements GB. Phylogenetic analysis of short enteroviral sequences from patients with chronic fatigue syndrome.
Cunningham L, Bowles NE, Lane RJ, Dubowitz V, Archard LC. Persistence of enteroviral RNA in chronic fatigue syndrome is associated with the abnormal production of equal amounts of positive and negative strands of enteroviral RNA.
Gow JW, Behan WM, Clements GB, Woodall C, Riding M, Behan PO.Enteroviral RNA sequences detected by polymerase chain reaction in muscle of patients with postviral fatigue syndrome.
Archard LC, Bowles NE, Behan PO, Bell EJ, Doyle D. Postviral fatigue syndrome: persistence of enterovirus RNA in muscle and elevated creatine kinase.
E. G. Dowsett, A. M. Ramsay, R. A. McCartney, E. J. Bell Myalgic encephalomyelitis--a persistent enteroviral infection?
McGarry F, Gow J, Behan PO. Enterovirus in the chronic fatigue syndrome.
J. Richardson Viral Isolation from Brain in Myalgic Encephalomyelitis
Fegan KG, Behan PO, Bell EJ. Myalgic encephalomyelitis--report of an epidemic.


I think the logic of Croatoan's statement meant that certainly those of us have a lot of oxidative stress already, and if oxidative stress were going to kill the viruses, we would be okay. In other words, it doesn't make sense to say that we should aim for more oxidative stress.
If anyone thinks they don't have a lot of oxidative stress going on, and they are wondering if it could be the cause of their symptoms, they might want to start googling to see what they can find.
 

RuthAnn

Well-Known Member
Again, in the context of infection, in rats. Not proof that in humans a vitamin deficiency alone causes oxidative stress which is what you seem to be saying. Let me know if I am misunderstanding your assertions.
Would information at Linus Pauling institute be considered good information about Vitamin B2 (riboflavin) deficiency causing oxidative stress?

http://lpi.oregonstate.edu/mic/vitamins/riboflavin
 

weyland

Well-Known Member
In other words, it doesn't make sense to say that we should aim for more oxidative stress.
I never said we should try to increase ROS production. I'm saying that ROS production is a natural part of the immune response and it may not be wise to block it when we don't know what is causing the immune response in the first place.

Imagine you have an infection and fever. You take an aspirin and the fever goes away, you feel better. Did the aspirin cure the infection? No, and in fact it might actually help the infection because increasing body temperature is one way the body attempts to limit infection, at the expense of our temporary comfort. Same idea with ROS production. ROS is generated to help limit and cordon off infected or metastatic tissue. It will make us feel horrible, but it's in an attempt to save us. The problem in ME is that this response goes on and on for years, but we need to figure out what is provoking this response in the first place in order to solve it.
 

weyland

Well-Known Member
Would information at Linus Pauling institute be considered good information about Vitamin B2 (riboflavin) deficiency causing oxidative stress?
If you saw some human studies referenced in there that showed that vitamin deficiency alone causes ROS production and ME symptoms then flag them up, sure.

Vitamin deficiency states are pretty well documented in humans and as far as I'm aware none of them really match the clinical picture of ME. If vitamins cured ME I think we would see a lot more success stories. Most ME patients that I've talked to are on extensive supplement regimes with little or no improvement in overall function.
 

RuthAnn

Well-Known Member
If you saw some human studies referenced in there that showed that vitamin deficiency alone causes ROS production and ME symptoms then flag them up, sure.

Vitamin deficiency states are pretty well documented in humans and as far as I'm aware none of them really match the clinical picture of ME. If vitamins cured ME I think we would see a lot more success stories. Most ME patients that I've talked to are on extensive supplement regimes with little or no improvement in overall function.
We have a few people here already who are having improvement from some of these supplements, riboflavin in particular.
 

RuthAnn

Well-Known Member
Again, in the context of infection, in rats. Not proof that in humans a vitamin deficiency alone causes oxidative stress which is what you seem to be saying
The Linus Pauling link was in reference to this statement of yours.
Do you see the information about riboflavin deficiency causing oxidative stress? If not, I'll copy and paste it.
 
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Croatoan

Well-Known Member
@Croatoan, what happens to all those H+ 's coming off the electron transport chain?
They are used to produce ATP, the energy molecule.

http://chemwiki.ucdavis.edu/Core/Biological_Chemistry/Metabolism/Electron_Transport_Chain

"Metabolic processes use NADH and [FADH2] to transport electrons in the form of hydride ions (H-). These electrons are passed from NADH or [FADH2] to membrane bound electron carriers which are then passed on to other electron carriers until they are finally given to oxygen resulting in the production of water. As electrons are passed from one electron carrier to another hydrogen ions are transported into the intermembrane space at three specific points in the chain. The transportation of hydrogen ions creates a greater concentration of hydrogen ions in the intermembrane space than in the matrix which can then be used to drive ATP Synthase and produce ATP (a high energy molecule). "
 

weyland

Well-Known Member
We have a few people here already who are having improvement from some of these supplements, riboflavin in particular.
Again, I don't doubt that symptomatic improvements may be found (similar to taking aspirin for fever) but I don't think they are curative or address the underlying pathology. If they are still posting here then I'm guessing they are still not recovered so the disease process is still active.
 

Croatoan

Well-Known Member
If you saw some human studies referenced in there that showed that vitamin deficiency alone causes ROS production and ME symptoms then flag them up, sure.
How many would it take to prove it to you?
Cell death caused by selenium deficiency and protective effect of antioxidants.
Manganese superoxide dismutase deficiency triggers mitochondrial uncoupling and the Warburg effect.
Role of reactive oxygen species in zinc deficiency-induced hepatic stellate cell activation

Vitamin deficiency states are pretty well documented in humans and as far as I'm aware none of them really match the clinical picture of ME. If vitamins cured ME I think we would see a lot more success stories. Most ME patients that I've talked to are on extensive supplement regimes with little or no improvement in overall function.
Vitamin deficiencies are not well documented because it is so difficult to get a doctor to do these tests, specifically with riboflavin since serum ribofalvin does not tell the whole story. There is a test called EGRac (erythrocyte glutathione reductase activity coefficient ) that is a better measure but it is expensive. And whenever the do tests for deficiency, well...

I met with a woman who was on this study when I was in Vancouver:
High rates of riboflavin deficiency in women of childbearing age in Cambodia and Canada
http://www.fasebj.org/content/28/1_Supplement/1041.12
the biggest surprise was:
"67% of Canadians had a suboptimal riboflavin status (EGRac >1.3). The data suggests suboptimal riboflavin status and deficiency may be widespread in both developed and developing countries and merits further investigation."
she said that they thought it would be closer to 10%
Here is another interesting one that proves they are unclear what a deficiency is:
http://www.ncbi.nlm.nih.gov/pubmed/21525198
Correcting a marginal riboflavin deficiency improves hematologic status in young women in the United Kingdom
The results also suggest that consideration should be given to raising the currently accepted EGRAC threshold for deficiency.

I am not saying B2 is the cause of everyone's ME, but unless they start doing EGRac tests on people with ME we do not know. As I said in other posts, there are multiple causes to ME but the root is the same; too much ROS.

The reason you do not see success in treating ME (yet you fail to see me as a success) with diet changes AND cofactor supplements is because people are not looking at their genetics. It is called Nutritional Genomics.

Watch this, this is what I am doing:

watch this by Dr. Steven Ziesel of the UNC Nutrition Research institute. He also talks about why nutrition studies have been useless because they do not take into account genetics:

Another good one:
 

Croatoan

Well-Known Member
Again, I don't doubt that symptomatic improvements may be found (similar to taking aspirin for fever) but I don't think they are curative or address the underlying pathology. If they are still posting here then I'm guessing they are still not recovered so the disease process is still active.
Aspirin does is not a cofcator for enzymes in the body so it is not similar. It is not that the underlying pathology is any different from anyone else, it is that our ROS genetics do not give us the ability to handle the pathology like everyone else. Give two people the same flu, why does one get sicker than the other?

I am recovered 100%. I am posting here to see if I can help other people. Are you not curious about what I did and how I did it? The fact that you do not care tells me that you are stuck in the "it is caused by a virii or bactirium" paradigim. I am saying that that idea is only half right.
 

Croatoan

Well-Known Member
I never said we should try to increase ROS production. I'm saying that ROS production is a natural part of the immune response and it may not be wise to block it when we don't know what is causing the immune response in the first place.
You have a great logical fallacy there; Begs the question.

They do not say HOW MUCH ROS is needed to kill the bacteria. Maybe they needs to be so little that we would not even sense the increase in ROS. Maybe the fact that ROS gets takes care of so quickly after it is used leaves up with no cold symptoms?

So we all need to be deathly ill when we get the flu?

Imagine you have an infection and fever. You take an aspirin and the fever goes away, you feel better. Did the aspirin cure the infection? No, and in fact it might actually help the infection because increasing body temperature is one way the body attempts to limit infection, at the expense of our temporary comfort. Same idea with ROS production. ROS is generated to help limit and cordon off infected or metastatic tissue. It will make us feel horrible, but it's in an attempt to save us. The problem in ME is that this response goes on and on for years, but we need to figure out what is provoking this response in the first place in order to solve it.
So why do people have high ROS with no infection, like vitamin deficiency? Why do ME people have symptoms with no fever if they have an infection? The difference is that the infection is an acute disease, but ME is a chronic disease. I am saying that the acute disease triggers the chronic disease because of vitamin deficiencies in the antioxidant pathways.

But you have no proof, PROOF, that infection is the cause for all ME cases. That is just a theory, which I consider AND fits well with my hypothesis.
 

Croatoan

Well-Known Member
Again, in the context of infection, in rats. Not proof that in humans a vitamin deficiency alone causes oxidative stress which is what you seem to be saying. Let me know if I am misunderstanding your assertions.


I don't doubt that environmental exposure + infection leads to a worse outcome. In that case the damage comes directly or as a result from the pollutant, not from our body's protective response to it. That paper is talking about exposure to outside oxidants, probably in concentrations far greater than what our body can produce.

As was pointed out in the paper I linked, diminishing the body's oxidative response in the context of diseases can lead to worse outcomes.



There's no need to be adversarial. I'm trying to discuss the science with you. It's not controversial to point out that animal studies have limitations and don't prove anything in humans.


Galbraith DN, Nairn C, Clements GB. Evidence for enteroviral persistence in humans.
Chia J, Chia A, Voeller M, Lee T, Chang R. Acute enterovirus infection followed by myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and viral persistence.
Chia JK, Chia AY. Chronic fatigue syndrome is associated with chronic enterovirus infection of the stomach.
Chia JK, Chia AY. Ribavirin and Interferon-a for the Treatment of Patients with Chronic Fatigue Syndrome Associated with Persistent Coxsackievirus B Infection: A Preliminary Observation.
Douche-Aourik F, Berlier W, Féasson L, Bourlet T, Harrath R, Omar S, Grattard F, Denis C, Pozzetto B. Detection of enterovirus in human skeletal muscle from patients with chronic inflammatory muscle disease or fibromyalgia and healthy subjects.
Galbraith DN, Nairn C, Clements GB. Phylogenetic analysis of short enteroviral sequences from patients with chronic fatigue syndrome.
Cunningham L, Bowles NE, Lane RJ, Dubowitz V, Archard LC. Persistence of enteroviral RNA in chronic fatigue syndrome is associated with the abnormal production of equal amounts of positive and negative strands of enteroviral RNA.
Gow JW, Behan WM, Clements GB, Woodall C, Riding M, Behan PO. Enteroviral RNA sequences detected by polymerase chain reaction in muscle of patients with postviral fatigue syndrome.
Archard LC, Bowles NE, Behan PO, Bell EJ, Doyle D. Postviral fatigue syndrome: persistence of enterovirus RNA in muscle and elevated creatine kinase.
E. G. Dowsett, A. M. Ramsay, R. A. McCartney, E. J. Bell Myalgic encephalomyelitis--a persistent enteroviral infection?
McGarry F, Gow J, Behan PO. Enterovirus in the chronic fatigue syndrome.
J. Richardson Viral Isolation from Brain in Myalgic Encephalomyelitis
Fegan KG, Behan PO, Bell EJ. Myalgic encephalomyelitis--report of an epidemic.


And?
Note this:
http://www.merckmanuals.com/professional/infectious-diseases/enteroviruses/overview-of-enterovirus-infections
Healthy adults can be infected, but they tend to have few or no symptoms. Immunocompromised adults may have severe respiratory disease.​
Immunocomprimised meaning autoimmune disease meaning automatically producing too much ROS.

And here: genetics.
http://www.nature.com/tp/journal/v6/n2/abs/tp2015208a.html
Further examination of these polymorphisms may help identify contributing factors to the pathophysiology of ME/CFS, as well as categorize potential targets for medical intervention strategies.​

I am not responding to you anymore because you fail to see my point. If you want me to look at you genetics I will be glad to do so.
 

Croatoan

Well-Known Member
Note that they are classifying SEID and autoimmune disorder. If a virus can trigger the immune system to make ROS. An AUTOimmune disorder would mean the body is making ROS without a virus. So any autoimmune disease is just too much ROS.

‘Robust’ Evidence Found That Chronic Fatigue Syndrome Is a Physical Illness
http://www.healthline.com/health-news/evidence-found-that-chronic-fatigue-is-a-physical-illness-022715

A Common Culprit in Autoimmune Disorders
Interleukin-17A doesn’t only affect people with CFS.
High levels of this specific cytokine are associated with many chronic inflammatory conditions, such as multiple sclerosis, psoriasis, and rheumatoid arthritis.
Interleukin-17A is a potential target for biologic treatments designed to dampen the body’s immune system to relieve symptoms of these conditions.
In January, the U.S. Food and Drug Administration approved Cosentyx (secukinumab), a psoriasis drug that targets interleukin-17A to quiet the body’s immune response.
Psoriasis, an autoimmune disorder, can also be triggered by an infection. CFS is a common complaint of people with psoriatic arthritis, an inflammatory joint condition that can develop in people in late-stage psoriasis.
 

weyland

Well-Known Member
All in vitro work. I'm not dismissing it outright, but this type of work may not be as clear as it seems:
Cells in culture are typically grown under ambient oxygen tensions of approximately 100 Torr that result from diffusion from a 21% oxygen atmosphere at sea level. They are not usually grown at the 2 to 4% oxygen (15–30 Torr) that is normal in tissues. Because all of the proteins involved in antioxidant defense evolved under physiologic conditions of 15 to 30 Torr oxygen, they typically haveKm values for oxygen in the 15- to 30-Torr range. Cell culture hyperoxia in the 30- to 100-Torr range will naturally activate antioxidant and pro-oxidant proteins that would otherwise be quiescent and substrate-limited. This makes the interpretation of oxidative changes in cell culture seductively clear. The measurement of a myriad of reactive oxygen species such as superoxide and hydrogen peroxide and biomarkers of oxidation such as lipid peroxidation is technically simple in cultured cells. However, the judgment that these changes are deleterious in the context of the whole organism is biologically unsound.
Vitamin deficiencies are not well documented because it is so difficult to get a doctor to do these tests, specifically with riboflavin since serum ribofalvin does not tell the whole story. There is a test called EGRac (erythrocyte glutathione reductase activity coefficient ) that is a better measure but it is expensive. And whenever the do tests for deficiency, well...
Understood. In this case it's just easier (and far cheaper) to try taking the vitamins and see what happens. I've noticed no effects from R5P. In that case you would say I need a different form then?

The reason you do not see success in treating ME (yet you fail to see me as a success) with diet changes AND cofactor supplements is because people are not looking at their genetics.
I said we'd see a lot more success stories, I didn't say there weren't any. I don't doubt that this approach helps some people because that is what they report. I think you are the first person I've seen to be 100% cured by this approach, perhaps you know of others.

The fact that you do not care tells me that you are stuck in the "it is caused by a virii or bactirium" paradigim.
At the end of the day I can only go by my n=1, as we all can. In my own case a persistent virus is what my serology, histopathology, and symptoms point to. This is one of the more well covered causes in the literature. I'm not saying there may not be other causes of similar symptom complexes.

So why do people have high ROS with no infection, like vitamin deficiency?
Again, I haven't seen anything pointing to that in human studies.

And how do we know there is no infection? Does every person with ME get tested for every known bacteria or virus? Is the testing that they do receive 100% accurate? I would say no, and there is evidence in the literature pointing to persistent viruses and anecdotal evidence from certain clinicians finding high incidence of chronic vector borne bacterial infections. Both great reasons to be seeing increased ROS production, in my opinion.

It's very easy to twist around cause and effect here and have it make sense both ways. You're saying deficiency causes excess ROS. I'd say that excess ROS might cause deficiency. Both seem plausible.

But you have no proof, PROOF, that infection is the cause for all ME cases.
Agreed, just as you don't have proof vitamin deficiency is the cause.
 

RuthAnn

Well-Known Member
Again, I haven't seen anything pointing to that in human studies.
@weyland
This site lists causes of oxidative stress not related to pathology.

https://doctordoni.com/2014/10/5-signs-of-oxidative-stress.html
What is Oxidative Stress?

The process of oxidation happens as our bodies metabolize (or process) the oxygen that we breathe and our cells produce energy from it. This process also produces free radicals –molecules that interact with the molecules within our cells resulting in damage (or stress) to nearby cells, mitochondria (which I will explain further in a coming article), and DNA.
Free radicals are normal and necessary to some degree. In addition to causing some damage, they also stimulate repair. It is only when so many free radicals are produced, and they overwhelm the repair processes, that it becomes an issue. That is what we call oxidative stress.
Oxidation happens under a number of circumstances including:
  • when our cells use glucose to make energy
  • when the immune system is fighting off bacteria and creating inflammation
  • when our bodies detoxify pollutants, pesticides, and cigarette smoke
In fact, there are millions of processes taking place in our bodies at any one moment that can result in oxidation.
It also increases when we are physically and/or emotionally stressed.
 

weyland

Well-Known Member
Immunocomprimised meaning autoimmune disease meaning automatically producing too much ROS.
What they're talking about specifically is hypogammaglobulinemic patients. Such patients develop chronic, disseminated, highly active enterovirus infections because neutralizing antibodies are required to clear enterovirus infections.
http://www.ncbi.nlm.nih.gov/pubmed/8268346

So any autoimmune disease is just too much ROS.
Well, it's not just that. It's mistaken recognition of a self protein as a foreign antigen and a corresponding chronic immune activation because of it, which of course includes ROS production. The treatment isn't antioxidants though, it's getting rid of the autoantibodies through plasmaspherisis, B cell depletion therapy, or other immune suppression therapy.
 

weyland

Well-Known Member
In fact, there are millions of processes taking place in our bodies at any one moment that can result in oxidation.
Of course, that's why our bodies produce glutathione, SOD, etc. Oxidation is damaging to life, that's why our bodies produce it as a defense mechanism against pathogens.
 

RuthAnn

Well-Known Member
Of course, that's why our bodies produce glutathione, SOD, etc. Oxidation is damaging to life, that's why our bodies produce it as a defense mechanism against pathogens.
Then why did you say you haven't seen anything pointing to that in human studies?
 

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