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.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.
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.I forgot the link for that one, but here you go. I fail to understand how you do not see the connection.
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?
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.But mice studies are useful and you dismiss it not to further our understanding, but only to try to appear intelligent.
Galbraith DN, Nairn C, Clements GB. Evidence for enteroviral persistence 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.
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?I have a strong feeling I know you from PR.