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Anti-oxidants help CFS, studies I ran across

Discussion in 'Antivirals, Antibiotics and Immune Modulators' started by triffid113, Oct 5, 2013.

  1. triffid113

    triffid113 Day of the Square Peg

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    Basic Clin Pharmacol Toxicol. 2010 Jun;106(6):490-6. doi: 10.1111/j.1742-7843.2009.00525.x. Epub 2010 Jan 18.

    Protective effect of epigallocatechin gallate in murine water-immersion stress model of chronic fatigue syndrome.

    Sachdeva AK, Kuhad A, Tiwari V, Arora V, Chopra K.

    Source

    Pharmacology Research Laboratory, University Institute of Pharmaceutical Sciences, UGC Centre of Advanced Study, Panjab University, Chandigarh, India.

    Abstract

    Chronic fatigue syndrome (CFS) is a specific clinical condition that characterizes unexplained disabling fatigue. In the present study, chronic fatigue was produced in mice by subjecting them to forced swim inside a rectangular jar of specific dimensions for 6 min. daily for 15 days. Epigallocatechin gallate (EGCG; 25, 50 and 100 mg/kg, p.o.) was administered daily 30 min. before forced swim session. Immobility period and post-swim fatigue was assessed on alternate days. On the 16th day, after assessment of various behavioural parameters, mice were killed to harvest the brain, spleen and thymus. There was significant increase in oxidative-nitrosative stress and tumour necrosis factor-alpha levels in the brain of mice subjected to water-immersion stress as compared with naive group. These behavioural and biochemical alterations were restored after chronic treatment with EGCG. The present study points out that EGCG could be of therapeutic potential in the treatment of chronic fatigue.

    Behav Brain Res. 2009 Dec 28;205(2):414-20. doi: 10.1016/j.bbr.2009.07.020. Epub 2009 Jul 28.

    Epigallocatechin gallate ameliorates chronic fatigue syndrome in mice: behavioral and biochemical evidence.

    Sachdeva AK, Kuhad A, Tiwari V, Chopra K.

    Source

    Pharmacology Research Laboratory, University Institute of Pharmaceutical Sciences, UGC Centre of Advanced Study, Punjab University, Chandigarh 160 014, India.

    Abstract

    Three decades after the coining of the term chronic fatigue syndrome, the diagnosis of this illness is still symptom based and the aetiology remains elusive. Chronic fatigue syndrome pathogenesis seems to be multifactorial and the possible involvement of immune system is supported. The present study was designed to evaluate the effects of the epigallocatechin gallate in a mouse model of immunologically induced chronic fatigue. On 19th day, after lipopolysaccharide/Brucella abortus administration, the mice showed significant increase in immobility period, post swim fatigue and thermal hyperalgesia. Behavioral deficits were coupled with enhanced oxidative-nitrosative stress as evident by increased lipid peroxidation, nitrite levels and decreased endogenous antioxidant enzymes (superoxide dismutase, reduced glutathione and catalase) and inflammation (increased levels of tumor necrosis factor-alpha and tissue growth factor-beta). Chronic treatment with epigallocatechin gallate restored these behavioral and biochemical alterations in mice. The present study points out towards the beneficial effect of epigallocatechin gallate in the amelioration of chronic fatigue syndrome and thus may provide a new, effective and powerful strategy to treat chronic fatigue syndrome.

    Brain Res Bull. 2011 Oct 10;86(3-4):165-72. doi: 10.1016/j.brainresbull.2011.06.007. Epub 2011 Jul 28.

    Epigallocatechin gallate ameliorates behavioral and biochemical deficits in rat model of load-induced chronic fatigue syndrome.

    Sachdeva AK, Kuhad A, Chopra K.

    Source

    University Institute of Pharmaceutical Sciences, UGC Centre of Advanced Study, Panjab University, Chandigarh, India.

    Abstract

    Chronic fatigue syndrome is a heterogeneous disorder with unknown pathogenesis and etiology, characterized by tiredness, difficulty in concentration and memory, and concomitant skeletal and muscular pain, thus affecting both mental and physical domains. The pathogenesis of chronic fatigue syndrome is multifactorial and involves increased oxido-nitrosative stress along with generation of pro-inflammatory cytokines such as TNF-α. In the present study chronic fatigue was produced in rats by plunging a load of 10 ± 2% body weight and subjecting them to forced swim inside a rectangular jar daily for 28 days. Endurance capacity and post-swim fatigue were assessed on 1st, 7th, 14th, 21st and 28th days. EGCG was administered daily by oral gavage 30 min before forced swim session. On the 29th day, after assessment of various behavioral parameters, blood was collected through tail vein, and animals were sacrificed to harvest the brains, spleens and thymus. Chronic fatigue group exhibited significant behavioral alterations along with enhanced oxido-nitrosative stress and serum TNF-α level as compared to naive group. Chronic treatment with EGCG restored all the behavioral and biochemical alterations associated with chronic fatigue syndrome. The present study signifies the therapeutic potential of EGCG for the treatment of chronic fatigue syndrome.

    J Med Food. 2005 Spring;8(1):47-52.

    Green tea extract and catechin ameliorate chronic fatigue-induced oxidative stress in mice.

    Singal A, Kaur S, Tirkey N, Chopra K.

    Source

    Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh, India.

    Abstract

    Chronic fatigue syndrome (CFS) is an illness characterized by persistent and relapsing fatigue, often accompanied by numerous symptoms involving various body systems. The etiology of CFS remains unclear, but a number of studies have shown that oxidative stress may be involved in its pathogenesis. The present study was designed to investigate the protective effect of green tea extract (GTE) and catechin in the mouse model of CFS. Animals were subjected to a forced swimming test session of 6 minutes every day for 7 days; a significant increase in immobility time on successive days represented the CFS in mice. Biochemical analysis revealed that the chronic swim test significantly increased lipid peroxidation levels and decreased glutathione levels in mouse whole-brain homogenate. Treatment with GTE (25 or 50 mg/kg, i.p.) and catechin (50 or 100 mg/kg, i.p.) for 7 days reversed the increase in immobility time. Protection was correlated with the lowered levels of lipid peroxidation and restoration of reduced glutathione levels in the brains of fatigued mice. These findings strongly suggest the pivotal role of oxidative stress in the pathophysiology of CFS and that GTE and catechin could be used as potential agents in the management of CFS and warrant the inclusion of GTE and catechin in the treatment regimen of CFS patients.

    Fundam Clin Pharmacol. 2009 Jun;23(3):331-7. doi: 10.1111/j.1472-8206.2009.00675.x. Epub 2009 Mar 11.

    Modulation of antigen-induced chronic fatigue in mouse model of water immersion stress by naringin, a polyphenolic antioxidant.


    Vij G, Gupta A, Chopra K.

    Source


    Pharmacology Division, University Institute of Pharmaceutical Sciences, Punjab University, Chandigarh-160014, India.

    Abstract


    It is believed that physical stress, infection and oxidative stress are involved in the development of chronic fatigue syndrome. There is little evidence stating the beneficial role of nutritional supplements in chronic fatigue syndrome. Based on this, this study was designed to evaluate the effect of naringin, a natural polyphenol, in a mouse model of immunologically-induced fatigue, wherein purified lipopolysaccharide (LPS) as well as Brucella abortus (BA) antigen was used as immunogens. The assessment of chronic fatigue syndrome was based on chronic water-immersion stress test for 10 mins as well as measurement of hyperalgesia for 19 days. Immobility time and tail withdrawal latency as well as oxidative stress were taken as the markers of fatigue. Mice challenged with LPS or BA for 19 days showed significant increase in the immobility time, hyperalgesia and oxidative stress on 19th day. Serum tumor necrosis factor-alpha (TNF-alpha) levels markedly increased with LPS or BA challenge. Concurrent treatment with naringin resulted in the significant decrease in the immobility time as well as hyperalgesia. There was significant attenuation of oxidative stress as well as in TNF-alpha levels. Present findings strongly suggest the role of oxidative stress and immunological activation in the pathophysiology of chronic fatigue syndrome, and treatment with naringin can be a valuable option in chronic fatigue syndrome.

    Fundam Clin Pharmacol. 2009 Feb;23(1):89-95. doi: 10.1111/j.1472-8206.2008.00638.x. Epub 2009 Jan 10.

    Protective effects of antidepressants against chronic fatigue syndrome-induced behavioral changes and biochemical alterations.

    Kumar A, Garg R.

    Source

    Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh 160014, India. kumaruips@yahoo.com

    Abstract

    Chronic fatigue syndrome (CFS) is characterized by profound fatigue, which substantially interferes with daily activities. The aim of this study was to explore the protective effects of antidepressants in an animal model of CFS in mice. Male albino mice were forced to swim individually for a period of 6-min session each for 7 days. Imipramine (10 and 20 mg/kg), desipramine (10 and 20 mg/kg) and citalopram (5 and 10 mg/kg) were administered 30 min before forced swimming test on each day. Various behavior tests (immobility time, locomotor activity, anxiety-like behavior by plus maze and mirror chamber) followed by biochemical parameters (lipid peroxidation, reduced glutathione, catalase and nitrite level) were assessed in chronic stressed mice. Chronic forced swimming for 7 days significantly caused increase in immobility period, impairment in locomotor activity, anxiety-like behavior, and oxidative stress (raised lipid peroxidation, nitrite activity and reduced glutathione and catalase activity) as compared with naïve mice (P < 0.05). Seven days of pretreatment with imipramine (10 and 20 mg/kg), desipramine (10 and 20 mg/kg), and citalopram (5 and 10 mg/kg) significantly reduced immobility time, improved locomotor activity and anti-anxiety effect (in both plus maze and mirror chamber test), and attenuated oxidative stress in chronic stressed mice as compared with control (chronic fatigues) (P < 0.05). These results suggested that these drugs have protective effect and could be used in the management of chronic fatigue like conditions.

    J Neuroimmunol. 2010 Sep 14;226(1-2):3-7. doi: 10.1016/j.jneuroim.2010.05.021. Epub 2010 May 26.

    Possible role of oxidative stress and immunological activation in mouse model of chronic fatigue syndrome and its attenuation by olive extract.

    Gupta A, Vij G, Chopra K.

    Source

    Pharmacology Division, University Institute of Pharmaceutical Sciences, UGC Center of Advanced Study, Panjab University, Chandigarh 160014, India.

    Abstract

    Various putative theories involved in the development of chronic fatigue syndrome revolve around the role of stress, infection and oxidative stress. Scientific evidence highlighting the protective role of nutritional supplements in chronic fatigue syndrome is lacking. Based on these assumptions, the present study was designed to evaluate the effect of olive extract in a mouse model of immunologically-induced fatigue, wherein purified lipopolysaccharide (LPS) and Brucella abortus (BA) antigen were used as immunogens. The assessment of chronic fatigue syndrome was based on immobility period during chronic water-immersion stress test for 10 min daily. The stress-induced hyperalgesia was measured by tail withdrawal latency. Mice challenged with LPS or BA for 19 days showed significant increase in the immobility time, hyperalgesia and oxidative stress on the 19th day. Serum tumor necrosis factor-alpha (TNF-α) levels were also markedly increased with LPS or BA challenge. Concurrent treatment with olive extract resulted in a significant decrease in the immobility time as well as hyperalgesia. There was significant attenuation of oxidative stress as well as serum TNF-α levels. The results of the present study strongly indicate the role of oxidative stress and immunological activation in the pathophysiology of chronic fatigue syndrome and highlight the valuable role of olive extract in combating chronic fatigue syndrome.

    Immunobiology. 2009;214(1):33-9. doi: 10.1016/j.imbio.2008.04.003. Epub 2008 Jun 17.

    Curcumin, a polyphenolic antioxidant, attenuates chronic fatigue syndrome in murine water immersion stress model.

    Gupta A, Vij G, Sharma S, Tirkey N, Rishi P, Chopra K.

    Source

    Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh 160014, India.

    Abstract

    Chronic fatigue syndrome, infection and oxidative stress are interrelated in epidemiological case studies. However, data demonstrating scientific validation of epidemiological claims regarding effectiveness of nutritional supplements for chronic fatigue syndrome are lacking. This study is designed to evaluate the effect of natural polyphenol, curcumin, in a mouse model of immunologically induced fatigue, where purified lipopolysaccharide (LPS) and Brucella abortus (BA) antigens were used as immunogens. The assessment of chronic fatigue syndrome was based on chronic water-immersion stress test for 10 min daily for 19 days and the immobility time was taken as the marker of fatigue. Mice challenged with LPS or BA for 19 days showed significant increase in the immobility time and hyperalgesia on day 19, as well as marked increase in serum tumor necrosis factor-alpha (TNF-alpha) levels. Concurrent treatment with curcumin resulted in significantly decreased immobility time as well as hyperalgesia. There was significant attenuation of oxidative stress as well as TNF-alpha levels. These findings strongly suggest that during immunological activation, there is significant increase in oxidative stress and curcumin can be a valuable option in the treatment of chronic fatigue syndrome.

    J Med Food. 2002 Winter;5(4):211-20.

    Effect of natural and synthetic antioxidants in a mouse model of chronic fatigue syndrome.

    Singh A, Naidu PS, Gupta S, Kulkarni SK.

    Source

    Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh 160014, India.

    Abstract

    Chronic fatigue syndrome (CFS) is an illness characterized by persistent and relapsing fatigue, often accompanied by numerous symptoms involving various body systems. The etiology of CFS remains unclear; however, a number of studies have shown that oxidative stress may be involved in its pathogenesis. In the present study, a mouse model of CFS was used in which mice were forced to swim for one 6-minute session on each day for 15 days and the immobility period was recorded. There was a significant increase in immobility period in saline-treated mice on successive days. Intraperitoneal treatment with the potent antioxidants carvedilol (5 mg/kg) and melatonin (5 mg/kg) produced a significant reduction in immobility period. Similar results were observed with herbal preparations administered orally: Withania somnifera (100 mg/kg), quercetin (50 mg/kg), and St. John's wort (Hypericum perforatum L., 10 mg/kg). Biochemical analysis revealed that chronic swimming significantly induced lipid peroxidation and decreased glutathione (GSH) levels in the brains of mice. The rats also showed decreased levels of antioxidant defense enzymes, superoxide dismutase (SOD), and catalase. Co-administration of antioxidants carvedilol, melatonin, W. somnifera, quercetin or St. John's wort significantly reduced lipid peroxidation and restored the GSH levels decreased by chronic swimming in mice. Further, the treatment increased levels of SOD in the forebrain and of catalase. The findings strongly suggest that oxidative stress plays a significant role in the pathophysiology of CFS and that antioxidants could be useful in the treatment of CFS.



    Indian J Exp Biol. 2002 Nov;40(11):1240-4.

    Role of antioxidants in chronic fatigue syndrome in mice.


    Singh A, Garg V, Gupta S, Kulkarni SK.

    Source


    Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh 160 014, India.

    Abstract


    The present study was carried out using mice model of chronic fatigue syndrome (CFS) in which mice were forced to swim everyday for 7 days for a 6 min session. There was a significant increase in despair behavior (immobility period) in saline treated mice on successive days. Treatment with potent antioxidants carvedilol (5 mg/kg, i.p.) and melatonin (10 mg/kg, i.p.) produced a significant reduction in immobility period. Similar results were observed with herbal products St. John's Wort (Hypericum perforatum L) (10 mg/kg, p.o.) and GS-02 (20 mg/kg, p.o.). Fluoxetine, a selective serotonin reuptake inhibitor produced a significant effect only on first and second day of its treatment. Biochemical analysis revealed that chronic swim test significantly increased lipid peroxidation and catalase levels in whole brains of mice. There was a decrease in the levels of super oxide dismutase (SOD) and glutathione reductase (GSH) in the brain. Administration of carvedilol, melatonin, GS-02 and St. John's Wort restored the levels of lipid peroxidation and glutathione. The enzymes SOD and catalase were also restored. Fluoxetine affected the biochemical variables not to the same extent as other treatments. The findings of the present study suggest that oxidative stress might play a significant role in the pathophysiology of CFS. Thus antioxidants and herbal products like St. Johns wort and GS-02 could be useful in the treatment of CFS.

    Curr Top Med Chem. 2011;11(14):1767-79.

    Effects of antioxidant polyphenols on TNF-alpha-related diseases.

    Kawaguchi K, Matsumoto T, Kumazawa Y.

    Source

    Laboratory of Pharmacognosy, Faculty of Pharmacy, Iwaki Meisei University, 5-5-1 Chuodai-Iino, Iwaki, Fukushima 970-8551, Japan. kiichi-k@iwakimu.ac.jp

    Abstract

    Oxidative stress and inflammatory responses sustained for a long period of time cause many diseases. A proinflammatory cytokine, tumor necrosis factor α (TNF-α), plays a pivotal role in the pathogenesis of chronic and auto-immune diseases. The present review, supplemented by hitherto unpublished data of the authors and their coworkers, shows that the intake of polyphenols contained in natural sources, such as hydroxytyrosol, tyrosol, oleuropein (olives), naringin and hesperidin (Citrus fruits), resveratrol, procyanidins or oligomeric procyanidin (grapes or grape seed extracts), (-)-epigallocatechin gallate (green tea) and quercetin (grapes, green tea) etc., are able to modulate chronic inflammatory diseases, such as type 2 diabetes, rheumatoid arthritis, inflammatory bowel disease, and affect the formation and interaction of advanced glycation end products with their respective receptors. Furthermore, potent activities of fermented grape marc, prepared as a fine lyophilized powder from fresh skin and seeds of a Japanese grape strain (Koshu) and then fermented with Lactobacillus plantarum, are described. Finally, the bioavailability of representative polyphenols will be discussed.



  2. triffid113

    triffid113 Day of the Square Peg

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    I actually was looking into curcumin which is how I ran across the above. Notice the one about olive also. Some of the stronger antioxidants that also kill pathogens I know of are olive leaf extract and oil of oregano. These might be worth a try. I take 1g/day Olive Leaf Extract and it keeps me free of gut problems despite that I cannot intake enough zinc during allergy season to make HCL. I take oreganol when I have an infection...it's expensive. I never tried taking it every day. I just also read it helps with depression as it raises both dopamine eand serotonin ver time (or dopamine immediately).
  3. alex3619

    alex3619 Senior Member

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    I first became very interested in antioxidants for all this when I was a patient in some experimental treatments that used antioxidants. This was 1993. Most of that was never published. Antioxidants that were found to have a clinical impact were quercetin and fruit, particularly whole fruit (skin and all, though I don't fancy eating banana or orange skin). Of course fruit has issues that the skin is where pesticides might be (unless organic) and are high in fructose or sugar. This year I was going to blog on gut issues and a finding that the polyphenols in apple skin can help with one part of the biochemistry, at least in rat models iirc. That blog is on hold for now.
    SickOfSickness, justy and snowathlete like this.
  4. barbc56

    barbc56 Senior Member

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    Just pondering here. Will exposing mice to fatigue producing situations that mimic ME symptoms be comparable to actually having ME? We aren't sick because we are subjected to daily swimming exercises and stress that produces fatigue. Possibly these results might be more appropriatly extrapolated to people with "normal" fatigue? I have no idea what the answer is but this crossed my mind while reading these studies.

    Poor mice.
  5. alex3619

    alex3619 Senior Member

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    Here is the problem with these rodent models, quite aside from them being rodents and not humans. These are fatigue models. ME is not fatigue. ME is about things we do not yet understand, including a crash in metabolic capacity after activity, probably including mitochondrial dysfunction. This is not what these chronic fatigue models mimic.
    MeSci, SOC, Little Bluestem and 5 others like this.
  6. peggy-sue

    peggy-sue

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    These poor mice are simply being "burnt out".
    I do not, for one split second, believe these studies are of any use to anybody - an example of completely unneccessary cruelty.

    Driven by the political mess of the invention CFS.
    Had the scientists had a reasonable definition, if they were aware of what is going on, I would doubt they would have carried it out.
    (I'm an optimist!:redface: )
  7. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    Wessley could fix those mice with more exercise. They aren't fatigued they just think they are lol
  8. justy

    justy Senior Member

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    peggy-sue my thought exactly. Making mice exhausted by enforced swimming cannot in anyones mind be extrapolated to presume they now 'have' M.E/CFS etc and i'm not sure how the researchers would believe this was the same thing.

    BUT i am interested in the effects on these poor mice that were seen later on with

    The mitochondrial studies done at Acumen labs (Myhill et al) on my blood show very similar changes and issues with antioxidants. I have shown Oxidative stress, increased lipid peroxidation, decreased endogenous antioxidant enzymes, very low Co Enzyme Q10, a gene blockage on the Mn SODase gene and low glutathione to name but a few of my issues. This is one fo the reasons that Dr Myhill suggests daily B12 injections, which are to act as immediate antioxidant cover - i ahd some benefit from them for a year or more but then no furhter help. Taking Co Q 10 daily for many months has no noticeable affect on me, but i'm sure it could be helping with stopping even further damage. Dr Myhill also advocates total rest so as to stop any further tissue damage arising from this kind of scenario. This also helped and allowed me through a type or Aggresive Rest Therapy to gain a lot of functioning over the course of 3 years - however the ART made me worse at first and now, after a much better year i have gone backwards a couple of years again.

    We Know PWME have problems with Oxidative stress and antioxidant status, but we also know that just giving them antioxidants doesnt cure them. Equally i have recently discovered that many PWME havE Thyroid dysfunction, but just giving them more thyroid hormones doesn't cure them. All of this has been known a long time by many.
    When are we going to start getting to the heart of the issue?


    All the best,
    Justy.
  9. peggy-sue

    peggy-sue

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    I've copied and pasted all the papers in the first posting and sent them to my wee brother for his opinion.
    (He's got a PhD in Biochemical Pharmacology and Toxicology.)
  10. peggy-sue

    peggy-sue

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    I told him they made mice overswim. He said exactly what I did. (we chat every sunday)
    He is going to give them a good going over.:thumbsup:

    The problem is, the scientists who were doing this obviously have no idea what ME is - because they have obtained their information from the psychobabblers.
    Just what a waste of time and effort and expense, torturing animals unneccessarily.

    :aghhh:perhaps a Eureka moment...

    Could anybody make a serious complaint about this study on the grounds of the completely unethical use of the animals - particularly as considerable suffering is entailed?
    justy likes this.
  11. PDXhausted

    PDXhausted Senior Member

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    I came across nobiletin recently, which sounded interesting:
    http://www.ncbi.nlm.nih.gov/m/pubmed/23714077/

    Not a CFS study, but I thought it sounded promising for increasing glutathione and MnSOD activity, as well as improving memory deficits and oxidative stress. I'm not sure if they sell this yet as a supplement, but it might be contained in a citrus peel extract.
    justy likes this.
  12. triffid113

    triffid113 Day of the Square Peg

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    YES. ALL of the above crossed my mind too. Still in some sense isn't fatigue fatigue? I mean anything that helps fatigue is bound to help. If the real cause is a virus then the fatigue-helping substance would have to be done over and over of course, but it should still help to some degree?
  13. triffid113

    triffid113 Day of the Square Peg

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    I just saw in the September LEF magazine that WHEY raises glutathione. I did not explore this on the internet yet, I am only reporting for anyone who wants to look into it.
  14. Valentijn

    Valentijn Activity Level: 3

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    Not really. Because "fatigue" is a pretty broad concept, which doesn't really accurately describe the symptoms which we ME/CFS patients experience. PEM is not simply "fatigue", and I don't think anyone who has experienced it would describe it as such. Sometimes orthostatic intolerance is described as "fatigue", until the patient realizes what is causing the symptoms - and then it's clear that they're feeling light-headedness or oxygen deprivation.

    Fatigue is a very sloppy term which has nothing to do with ME/CFS.
    peggy-sue and SOC like this.
  15. triffid113

    triffid113 Day of the Square Peg

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    Ok, but I think may Dad and relatives and even I experience PEM (my Dad/relatives were serious cases of it though). And I have speculated that it may be caused by the free radicals generated by exercise (in other words I tend to think the cause is insufficient anti-oxidants for the body to support more exertion at the time). I am not saying I think that is the prime cause as a lot of things will use up antioxidants (and any of those things would be the prime cause).

    If you cut yourself or if you have periodontal issues or any other type of wound and it hurts, I observe that antioxidants fix the hurt. In fact if you have a tooth infection and you choose an antioxidant that can actually get to the site of the infection (oil of oregano) and kill a gram negative infection, then you will note the hurt goes away (ok maybe that's not a good example because oil of oregano is not just an antioxidant, but it also kills pathogens). Anyway, I constantly get little cuts from cats or bug bites or even just pulling a bit of dry skin off a finger (bad habit) and I know right away if I have not got enough antioxidants - when I take more, the sting goes away. If I am out and cannot, it does not. So...idk what it feels like when muscles inside you make oxidants but since I read that they do I reason that antioxidants are going to help and that perhaps that is the basis of PEM. It's what I use as a model for me anyway.

    I used to get that lactic acid burn during PMS as if I had done exercise and yet had done none. People at work would not believe me and said I must have doe some exercise, but o, when you get home late from work, somehow exercise is not high on your priority list. Well, maybe for someone else... Anyway, long ago I rationalized it was from not have the Kreb (aerobic) cycle work correctly because the anaerobic way of producing ATP not only produces only about a tenth of the number of ATP but also gives off lactic acid. So I have taken supplements to benefit the Kreb cycle for years. And yet, I never had this sort of trouble EXCEPT during PMS so I STRONGLY believe that hormones have so much more impact on gene expression that trying to fix things without considering hormones is like trying to climb Everest with your bare hands (Can be done but I'm no super star). I don't get those burning muscles with bioidentical hormone replacement (and I don't think nay of it helps but the DHEA...I mean estrogen, progesterone did nothing for me until I switched to DHEA). So while I believe it is a Kreb cycle issue, solving that issue is not as simple as tking B2, B3, Mg, malic acid, aB12, or even a "Krebs metabolites" pill I tried one time...
  16. triffid113

    triffid113 Day of the Square Peg

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    I agree. And idk, idk. However I want to help so let me ask a couple of things that may help a teensy bit: are you supplementing with ubiquinol or ubiquinone? Because if you are hypothyroid (even a little) you will have trouble making the active form of CoQ10 from the precursor (so u need ubiquinol). Next I question how it is 'known' that just giving antioxidants doesn't cure them (ok forget the word 'cure' because obviously if the reason for high free radicals is not fixed antioxidants could only hope to TREAT the problem)...so I am asking how it is 'known' that antioxidants won't TREAT the problem? The reason is because I would always suspect the doses were too low or the wrong antioxidanst were used (some are water-soluble, some are lipid soluble, some have affinity for different parts of the body, etc...so if you need the antioxidant selenium but only take E and C, it's not going to be enough for instance). (I am only saying I am not convinced antioxidants are of little help).

    Lastly I know I sound like a stuck record but I needed DHEA for my adrenal gland or nothing worked for me. I still have to fight judiciously for thyroid function (during allergen challenge and I am allergic to a lot of things) but not otherwise (so could not take a set amount of thyroid hormone). I am sure you must've tried DHEA. How did it work for you?

    I lastly want to say that I think your hormones (and idk which ones) govern how much metallothionein you make and w/o sufficient metallothionein you cannot absorb sufficient copper and zinc (and copper and zinc are required for proper thyroid, adrenal, and HCL function/production, to name a few). So if you are lucky and have nothing using up your zinc at a ferocious rate so that you need to absorb it in large quantity then maybe you age gracefully w/o supplements and hormone replacement. If you are not lucky, trying to do it w/o hormone replacement can be like climbing Everest on your hands and knees. (IMHO)
    justy likes this.
  17. triffid113

    triffid113 Day of the Square Peg

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    I believe the Animal Welfare Act allows this...in fact I think it is useless. I do not believe there is legal recourse. That is not to say that there are not other ways to bring about change. The group I know of working on this is Physicians Committee for Responsible Medicine (pcrm,.org).

    They have been doing EXACTLY this experiment (with different substances) since the 1960's (when I first read about this test in regards to Vitamin E at that time). I was shocked then. I...feel sad now, but lost the sense of shock. Thanks for reminding me. if there was a search engine whicj only searched for kinder gentler labs I would use it. If there was a way to outlaw such labs I would do it. Only way I know is to support pcrm or organizations like navs (national anti-vivisection society).
    MeSci likes this.
  18. alex3619

    alex3619 Senior Member

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    Logan, Queensland, Australia
    This was the new hot therapy for us in the late 90s through early 00s. I was on it for years. Cold-pressed whey protein is the key thing. Heat processed whey protein loses its bioactive properties. This research goes back to about 88 I think, when some researcher studying glutathione in rats found their levels suddenly dropped. They had been fed whey protein as a big part of their protein intake. Suddenly it was no longer working. the researcher tracked the manufacturers down, and found the pasteurization temperature had been increased. High temperatures denatures the protein, and it no longer triggers glutathione synthesis, even if it still provides some of the amino acids.
    justy, triffid113 and merylg like this.
  19. alex3619

    alex3619 Senior Member

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    Logan, Queensland, Australia
    [Satire] SW and PW might be able to go one step further. They can interpret the footprints on their questionnaires, and may conclude that the mice are happy with their progress, and recovered.
  20. peggy-sue

    peggy-sue

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    Scotland
    Triffid 13
    I was not referring to the experiment itself, (I know swimming is a legal method used in many experiments).

    - but to the blindingly obvious fact that it is not a valid model for CFS or ME.

    Not scientifically theoretically.
    Not even biopsychosocially theoretically!

    They have not been subjected to any "biopsychosocial" stressors, any maintaining factors, nothing.

    It is a model for sporty burn-out. Nothing more.

    On these grounds, the experiments were illegal.
    justy and Valentijn like this.

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