San Diego
Well-Known Member
Do you think it’s helped with EBV? Everything takes so long it’s really hard to know what’s working.
What Antioxidants Do You Use
- Thread starter Strike me lucky
- Start date
IrisRV
Well-Known Member
Ain't that the truth!
I don't take any supplements I actually expect to cure anything and then be done with them, so I don't have to try to sort out whether they worked or not. Most of the ones I do take, I challenge periodically. That is, I quit taking one and if I start feeling worse, I put in back in my regime. If I don't feel worse, I quit taking it on the assumption it's not helping. Not very solid, I realize, but it's the best I can do for determining what's working and what's not. Antioxidants are the hardest. I generally stick to the ones my specialist recommends on the theory that she has a lot more experience than I do with what tends to work for ME patients and what doesn't.
My prescription meds are a little easier because most don't take as long to see an improvement. I can also notice or measure fairly quickly if I deteriorate when I go off them.
But in all honesty, it's really hard to know for sure if many things are working the way i'm expecting or hoping. Mostly I have to go with the judgement of my ME specialist.
Last edited:
San Diego
Well-Known Member
Exactly. After using many supplements for a couple of years, with no noticeable improvement, I slowly went through this process myself. As a result, I’m down to just a few key things - mostly antioxidants recommended by my doc.
Strike me lucky
Well-Known Member
I think supplements can help general health but if expecting a treatment from them probably not so. I think for long term cfsers we need to worry about other risk factors from decreased activity and oxidative and inflammatory stress such as heart disease, osteoporosis, etc
After all that i added resveratrol 2 weeks ago. I cant say its a cure yet but its said to improve leptin resistance which they find common in cfsers. Hopefully it helps me lose weight, look younger and have a full head of hair lol
After all that i added resveratrol 2 weeks ago. I cant say its a cure yet but its said to improve leptin resistance which they find common in cfsers. Hopefully it helps me lose weight, look younger and have a full head of hair lol
San Diego
Well-Known Member
Will it also do my dishes and put money in my bank account?
Most definitely...........I am feeling better...........but it has been a long process. I can look back though and see how far I've come............but still have a ways to go.
IrisRV
Well-Known Member
I know what you mean! I just can't get into that "green" flavor. I took it in berrie smoothies to mask the flavor, which worked minimally. The best think I've found for me is vegetable juice -- V8 or the like. At least then the green feels like it belongs.OK, @IrisRV, I bought some of these ORAC greens and put it into my morning protein shake. All I have to say is that chocolate flavored greens...better make me feel fantastic fast!
My daughter decided to go with the capsules. They're more expensive, but you don't taste the stuff. You just have to be willing to choke down 8 capsules a day. At the moment, I'm taking a break from the powder and am doing a stretch of the pills. I'm trying only 4, so half strength. I'll see how that goes.
Veet
Well-Known Member
I've just returned to olive leaf extract. I'm using an extra strength liquid. Has allowed me to reduce some of my food antioxidants, which is a good thing.
None of those are supplements are antioxidants.
The only antioxidants and enzymes in our body. Here is a list of a few of them.
Superoxide Dimutase - Reduces superoxides to hydrogen peroxide
Dual Oxidase - Reduces superoxides to hydrogen peroxide
Glutathione Peroxidase - Reduces hydrogen peroxide to water. Depends on glutathione and selenium, as well as riboflavin.
Catalase - Reduces hydrogen peroxide to water and oxygen.
Thyroid peroxidase - reduces hydrogen peroxide in to water
Peroxiredoxin - Reduces hydrogen peroxide to water.
Lactoperoxidase -Reduces hydrogen peroxide to water.(Note that this is also anti-microbal)
Supplements can increase antioxidant enzyme activity, but they are not antioxidants. For example, Manganese will increase Superoxide Dimutase (SOD2 activity and calcium will increase thyroid peroxidase (TPO) activity.
It is important to understand as well that both TPO and SOD2 activity will be increased when there is more hydrogen peroxide and this will in turn deplete both Manganese and calcium. So when research jounals say that "x increases SOD2 activity" it might not be for a good reason.
As far as Vitamin C, E and Coq10, their role is more distant and more complicated:
[bimg=no-lightbox]http://www.intechopen.com/source/html/39159/media/image1.jpeg[/bimg]
I have a reason for being so nit picky about the wording, which you will understand as I post more.
The only supplement I take that reduces all of my oxidative stress is a form of B2 (riboflavin) called Flavin Mononucleotide. For me, it helps not only reduce superoxides, but hydrogen peroxide as well (logical assumption). Note that I have cured myself with pharmacological doses of riboflavin, but this is only true for me because of my genetics, I am not saying it will work for all ME patients.
It is becoming increasingly clear, brought to us by the field of Nutiritional Genomics, that each of us have very specific supplement and dietary needs to reduce ROS. And that if one guesses they can actually increase ROS production by taking the wrong supplement. Our genetic differences are mostly what explains the variation in reaction to supplements. I have a feeling now that the two main vitamin cofactors deficiencies that can trigger ME are either Niacin, Riboflavin or a combination of the two. This has to do with an enzyme called NADPH Oxidase.
The following study looks at the ROS produced by phagocytes, not total body ROS production. Why is this important? Because most of out body systems have feedback mechanisms. So when phagocytes start producing ROS they will get a signal from the environment that they are producing too much and another chemical signal will make them stop. So ROS produced outside the phagocytes sends a signal that tells the phagocyctes to stop making ROS! THIS is why stress makes people more prone to colds and flu and other virii and bacterium, and it is why people with autoimmune diseases (CFS/ME) suffer infection more often. It is not that we have MORE EBV, it is that our phagocytes are turned off so we cannot fight them.
The redox-sensitive cation channel TRPM2 modulates phagocyte ROS production and inflammation
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3242890/
Phagocytes keep the ROS production local to the pathogen. This is why we get inflammation in the area of a cut or phlem when we have a cold. This is called respiratory burst.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2491708/
The cofactors for NADPH oxidase are riboflavin and niacin.
http://www.uniprot.org/uniprot/Q9Y5S8
And for the grand finale....
Immune and hemorheological changes in Chronic Fatigue Syndrome
http://nutritionj.biomedcentral.com/articles/10.1186/1475-2891-7-29
In fact, I beleive this to be the case with all autoimmune diseases.
It is becoming increasingly clear, brought to us by the field of Nutiritional Genomics, that each of us have very specific supplement and dietary needs to reduce ROS. And that if one guesses they can actually increase ROS production by taking the wrong supplement. Our genetic differences are mostly what explains the variation in reaction to supplements. I have a feeling now that the two main vitamin cofactors deficiencies that can trigger ME are either Niacin, Riboflavin or a combination of the two. This has to do with an enzyme called NADPH Oxidase.
The following study looks at the ROS produced by phagocytes, not total body ROS production. Why is this important? Because most of out body systems have feedback mechanisms. So when phagocytes start producing ROS they will get a signal from the environment that they are producing too much and another chemical signal will make them stop. So ROS produced outside the phagocytes sends a signal that tells the phagocyctes to stop making ROS! THIS is why stress makes people more prone to colds and flu and other virii and bacterium, and it is why people with autoimmune diseases (CFS/ME) suffer infection more often. It is not that we have MORE EBV, it is that our phagocytes are turned off so we cannot fight them.
The redox-sensitive cation channel TRPM2 modulates phagocyte ROS production and inflammation
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3242890/
The NADPH oxidase activity of phagocytes and its generation of reactive oxygen species (ROS) is critical for host-defense, but ROS overproduction can also lead to inflammation and tissue injury. Here we report that TRPM2, a non-selective and redox-sensitive cation channel, inhibits ROS production in phagocytic cells and prevents endotoxin-induced lung inflammation in mice. TRPM2-deficient mice challenged with endotoxin (lipopolysaccharide) showed an increased inflammatory signature and decreased survival compared to controls. TRPM2 functions by dampening NADPH oxidase-mediated ROS production through depolarization of the plasma membrane in phagocytes. Since ROS also activates TRPM2, our findings establish a negative feedback mechanism inactivating ROS production through inhibition of the membrane potential-sensitive NADPH oxidase.
Phagocytes keep the ROS production local to the pathogen. This is why we get inflammation in the area of a cut or phlem when we have a cold. This is called respiratory burst.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2491708/
To combat infections, immune cells use NADPH oxidase to reduce O2 to oxygen free radical and then H2O2. Neutrophils and monocytes utilize myeloperoxidase to further combine H2O2 with Cl− to produce hypochlorite, which plays a role in destroying bacteria.
So we can see how a pollution, psychological stress, combined with a vitamin deficiency and/or genetics can trigger production of ROS outside of the phagocyte and tell that phagocyte to stop doing its job. This is the definition of an autoimmune disease.The cofactors for NADPH oxidase are riboflavin and niacin.
http://www.uniprot.org/uniprot/Q9Y5S8
And for the grand finale....
Immune and hemorheological changes in Chronic Fatigue Syndrome
These results indicate immune dysfunction as potential contributors to the mechanism of CFS, as indicated by decreases in neutrophil respiratory burst, NK cell activity and NK phenotypes. Thus, immune cell function and phenotypes may be important diagnostic markers for CFS. The absence of rheological changes may indicate no abnormalities in erythrocytes of CFS patients.
And I quote this as well:http://nutritionj.biomedcentral.com/articles/10.1186/1475-2891-7-29
Moreover, it has been demonstrated that a micronutrient deficiency can be the cause of suppression of immune function affecting both innate T-cell-mediated immune response and adaptive antibody response, thus altering the balanced host response. Therefore, an adequate intake of vitamins and antioxidant elements seems to be essential for an efficient function of the immune system.
I think that rests my case that ME is not caused by an infection, but rather, caused by the bodies inability to fight infection because of excessive non-phagocitic ROS production and a genetic susceptibility to certain vitamin deficiencies.In fact, I beleive this to be the case with all autoimmune diseases.
Selenium can help with formation of antioxidant enzymes.
http://lpi.oregonstate.edu/mic/minerals/selenium
http://lpi.oregonstate.edu/mic/minerals/selenium
- Five glutathione peroxidases, three thioredoxin reductases, three iodothyronine deiodinases, and one methionine sulfoxide reductase B1 are among the best characterized selenoproteins with known functions. (More information)
- Preliminary evidence from randomized controlled trials suggests that seleniumsupplementation may prevent viral load progression and increase immune cell count in HIV-positive patients. (More information)
Remy
Administrator
If you look at the thread I posted on selenium, it looks like it helps with the formation of antioxidant enzymes to help fix the damage it causes. Selenium is now thought to be toxic in levels commonly used in supplementation.
I would not take selenium unless you have tested low on something like a SpectraCell analysis.
From the above article from Linus Pauling Institute:
Five selenium-containing glutathione peroxidases (GPx1-4 and GPx6) have been identified: GPx1 (cytosolic GPx), GPx2 (epithelial cell-specific GPx expressed in intestinal lining and lungs), GPx3 (highly expressed in thyroid gland and kidneys), GPx4 (phospholipid-hydroperoxide GPx; PHGPx), and GPx6 (expressed in the olfactory epithelium) (4). GPx isoenzymes are all antioxidant enzymes that reduce potentially damaging reactive oxygen species (ROS), such as hydrogen peroxide and lipid hydroperoxides, to harmless products like water and alcohols by coupling their reduction with the oxidation of glutathione
Five selenium-containing glutathione peroxidases (GPx1-4 and GPx6) have been identified: GPx1 (cytosolic GPx), GPx2 (epithelial cell-specific GPx expressed in intestinal lining and lungs), GPx3 (highly expressed in thyroid gland and kidneys), GPx4 (phospholipid-hydroperoxide GPx; PHGPx), and GPx6 (expressed in the olfactory epithelium) (4). GPx isoenzymes are all antioxidant enzymes that reduce potentially damaging reactive oxygen species (ROS), such as hydrogen peroxide and lipid hydroperoxides, to harmless products like water and alcohols by coupling their reduction with the oxidation of glutathione
Sorry! I missed this!
Thioredoxin is like glutathinone. Thioredoxin reductase uses FAD as a cofactor and helps "reduce" Thioredoxin, meaning it adds a hydrogen atom. It serves the same purpose as Glutathione Reductase, reducing H2O2 into water and oxygen.
Here is a good image. Note the electron transport chain at the top.
http://jgp.rupress.org/content/early/2012/05/08/jgp.201210772/F1.expansion.html
If someone takes high doses of selenium but do not take Riboflavin with it, I think it will lead to a deficiency of Riboflavin which increases oxidative stress and causes disease. I say this because many of the symptoms of Selenosis are the same as riboflavin deficiency, like Alopecia
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3681114/
Oh, that makes sense! Thanks for the heads up!
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