People who have Fatigue report that their energy has increased after taking an Nrf2 activator. Following the testimonials are current research articles that report new information about the cause of Fatigue and how Nrf2 activators can be effective in treating it at the cellular level where it starts.
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Jeremy Bensemon: "When you workout more you're creating a lot more oxidative stress, especially when you're lifting heavy. You're creating more oxidative stress which means your body is not recovering. Your body is taking it's toll as you go along. Whenever you're working out, if you're running, if you're weight lifting, you're metabolizing more. Your body is creating more cells, and those cells are creating more oxidative stress. When you heal you're getting stronger, not when you're lifting. Protandim is reducing that oxidative stress. It's making your body healthier, it's making your body better.
"Protandim cuts my time down in between sets. The older I've been getting, the longer I have to wait in between sets. Since I've been taking the stuff I can wait a minute or less and go back and do another one. It's a lot faster in between so I'm getting a lot better workout. My joints were going way down real fast. I don't have that problem any more. If you watched me about 6 months ago, I would have an arm band on here when I benched, and I don't have to do that no more. My knees have torn ligaments in both, and when I'd go to squat it would be just a nightmare. It's not like that no more. I love squatting. I was taking it about two and a half weeks when I noticed my joints were feeling better, and after about a month they were just one hundred percent better." (See him tell his story)
Vanessa Nishikubo: I'm a 45-year-old woman and sometimes I have to be careful staying up late. Like going to 2 back-to-back karate classes on just 4 hours of sleep is really asking for trouble. I did that a few times over the last few years with disastrous results. I would feel queasy, faint, and when I'd see myself in the mirror my face would LOOK EXHAUSTED. Which was downright embarrassing because the teacher would always get mad at me for looking like such a blob. Well, I started Vivix on August 14th with my husband. Friday, August 22nd I stayed up until 5:15 am watching old movies and catching up on office stuff etc. I got up today, Saturday, at 10:30 am and felt fine. I matter-of-factly got together my karate gear and the kid's gear and we scooted (literally) over to karate. When I walked into the dojo I noticed it right away. I felt really LIGHT. Not light-headed but I felt at ease, and GOOD! I changed and joined the class and I felt so full of energy, so ready to go! We were stretching on the floor and I saw myself in the mirror and I looked like a person who¹d gotten plenty of sleep. I'm not saying this is going to become my habit of getting very little sleep but I was amazed at how I felt.
As the class (which I've taken for 2 year and which is called ENDURANCE) progresses usually I get more and more tired. Usually I hit a plateau when I feel I can't go on. Instead, today I never really hit that plateau. At one point I looked around at the class (by the way we lined up by weight and I was the 4th lightest person in a class of 48 people...thank you Cinch!) and noticed people were covered in sweat and red faced and looking EXHAUSTED and I didn't even feel tired. I wasn't sweating and my heart wasn't pumping like crazy as usual. It didn't feel like a really intense workout. I felt as though this workout wasn't challenging me, and this was unusual. I began at one point doing knee kicks on my own just to up the cardio for me and students in the class looked at me like, 'there goes energizing bunny!' Interesting experience with Vivix thus far. Go to source.
Cody Waite: My body takes a beating as an Xterra off-road triathlete. Typical distances are about a one mile swim, 20 mile off-road mountain bike, and a typical race is usually about six miles. The off-road component makes it quite challenging. I believe ASEA has helped me to achieve a higher level ofathletic performance. If my body is working properly at the cellular level everything is coming together. http://discoverredoxsignalingmolecules.com/testimonials/
JOURNAL ARTICLE (from pubmed.gov)
Neuro Endocrinol Lett. 2014 Dec;35(7):577-85.Attenuation of autoimmune responses to oxidative specific epitopes, but not nitroso-adducts, is associated with a better clinical outcome in Myalgic Encephalomyelitis/chronic fatigue syndrome.
There is evidence that inflammatory, oxidative and nitrosative stress (IO&NS) pathways participate in the pathophysiology of a subgroup of patients with Myalgic Encephalomyelitis/chronic fatigue syndrome (ME/CFS). Increased IgM-related autoimmune responses to oxidative specific epitopes (OSEs), including malondialdehyde (MDA), oleic acid and phosphatidyl inositol (Pi), and nitroso-(NO)-adducts, including NO-tryptophan (NOW), NO-arginine and NO-cysteinyl, are frequently observed in ME/CFS. Autoimmune responses in ME/CFS may be driven by increased bacterial translocation as measured by IgM and IgA responses to LPS of gram negative bacteria.METHODS:
The aim of this study is to examine whether IgM responses to OSEs and NO-adducts are related to a better outcome as measured by the Fibromyalgia and Fatigue Rating Scale (FF). 76 ME/CFS patients with initially abnormal autoimmune responses were treated with care-as-usual, including nutraceuticals with anti-IO&NS effects (NAIOS), such as L-carnitine, coenzyme Q10, taurine + lipoic acid, with or without curcumine + quercitine or N-acetyl-cysteine, zinc + glutamine.RESULTS:
We found that use of these NAIOS was associated with highly significant reductions in initially increased IgM-mediated autoimmune responses to OSEs and NO-adducts. A greater reduction in autoimmune responses to OSEs during intake of these NAIOS was associated with a lower FF score. Reductions in IgM responses to oleic acid, MDA and Pi, but not in any of the NO-adducts, were associated with reductions in severity of illness. These associations remained significant after adjusting for possible effects of increased bacterial translocation (leaky gut).CONCLUSIONS:
Our results show that autoimmune responses to OSEs are involved in the pathophysiology of ME/CFS and that these pathways are a new drug target in a subgroup of ME/CFS patients. Although hypernitrosylation and nitrosative stress play a role in ME/CFS, reductions in these pathways are not associated with lowered severity of illness. Randomized controlled trials with NAIOS should be carried out in the subgroup of ME/CFS patients with initially increased autoimmune responses to OSEs.
PMID: 25617880 [PubMed - in process]
[INTERPRETATION: Chronic fatigue is caused by oxidative stress (cell damage by free radicals), nitrosative stress, and inflammation. Reduction of these problems reduced the severity of the illness. The new treatment is to reduce the pathways of oxidation and inflammation.]
ARTICLE (from pubmed.gov)
2015 Jan 20. [Epub ahead of print]
patients with systemic immune-inflammatory and neuro-inflammatory disorders,
including depression, rheumatoid arthritis, systemic lupus erythematosus,
Sjögren's disease, cancer, cardiovascular disorder, Parkinson's disease,
multiple sclerosis, stroke, and chronic fatigue syndrome/myalgic
encephalomyelitis, endure pathological levels of fatigue. The aim of this
narrative review is to delineate the wide array of pathways that may underpin
the incapacitating fatigue occurring in systemic and neuro-inflammatory
disorders. A wide array of immune, inflammatory, oxidative and nitrosative
stress (O&NS), bioenergetic, and neurophysiological abnormalities are
involved in the etiopathology of these disease states and may underpin the
incapacitating fatigue that accompanies these disorders. This range of
abnormalities comprises: increased levels of pro-inflammatory cytokines, e.g.,
interleukin-1 (IL-1), IL-6, tumor necrosis factor (TNF) α and interferon (IFN)
α; O&NS-induced muscle fatigue; activation of the Toll-Like Receptor Cycle
through pathogen-associated (PAMPs) and damage-associated (DAMPs) molecular
patterns, including heat shock proteins; altered glutaminergic and dopaminergic
neurotransmission; mitochondrial dysfunctions; and O&NS-induced
defects in the sodium-potassium pump. Fatigue is also associated with
altered activities in specific brain regions and muscle pathology, such as
reductions in maximum voluntary muscle force, downregulation of the
mitochondrial biogenesis master gene peroxisome proliferator-activated
receptor gamma coactivator 1-alpha, a shift to glycolysis and buildup of
toxic metabolites within myocytes. As such, both mental and physical
fatigue, which frequently accompany immune-inflammatory and neuro-inflammatory
disorders, are the consequence of interactions between multiple systemic and
PMID: 25598355 [PubMed - as
supplied by publisher]
[INTERPRETATION: Fatigue is caused by several factors at the cellular level including inflammation, oxidative stress (cell damage by oxidants), and mitochondria dysfunction. There are many diseases associated with fatigue.]