People who have Joint Problems report that their symptoms have decreased after taking an Nrf2 activator. Following the testimonials are current research articles that report new information about the cause of Joint Problems and how Nrf2 activators can be effective in treating them at the cellular level where they start.
Dale Ross: I have Rheumatoid Arthritis this is my Protandim testimonial. I ran into a distributor for LifeVantage and he offered me Protandim I thought right, and I expected it not to work. I have been given many other supplements that I feel are ineffective, to say the least, and why should this be any different. I have had Rheumatoid Arthritis for 40 years now, and it has gotten so severe that many of my joints are now fused. I was scheduled to have Ankle Fusion surgery by a leading ankle surgeon. I can not believe only after taking Protandim for just under 2 weeks I then canceled my surgery, and I no longer use crutches anymore. Though I am not cured, but way better off than before, and I have now been on Protandim for 2 1/2 weeks. (from jsuddsblog.blogspot.com)
"My chiropractor asked me to try Protandim. He didn't tell me a whole lot about it except the science behind it at first, and he didn't tell me what to expect. He just said he wanted to see what would happen. I started taking it. Five days later I woke up to find I had slept nine and a half hours. It was the first time I had done that in a long time. I woke up feeling pretty refreshed. Normally I wake up spending hours in a fog. That was just amazing to me. On day eleven I noticed my knuckles weren't swollen and red any more, and my hands didn't hurt, and I noticed that my knees hadn't been hurting like they used to, and my elbows didn't hurt.
"On day 31 I found that I was sleeping seven and a half hours a night. When I wake up I don't feel like I'm in a fog. I feel great. All during the day things seem to be clearer. A wrist that I broke when I was 14 years old used to pop and crack and snap. Well, it doesn't make a sound anymore, and it doesn't hurt to move it. On day 36 I noticed that I had dropped a few pounds. When I started off I was 195 pounds. On day 36 I was at 182. I am 6 foot tall. The 182 put me right in the center of the BMI for normal weight, where before I was overweight. I think I had been in a bit of depression also. On day 36 I noticed also things were brighter, I feel better, and I'm positive I was in a depression before. My joints no longer hurt and ache. I can walk up the stairs just fine. My pain level was a 3 to a 6 every day. Now it's a 0 or a one. I feel fantastic. I haven't felt this good for years.
"On day 42 I noticed that my skin is softer. The backs of my hands don't have the old age wrinkles like I used to. On day 56 I was driving home late at night and noticed that headlights weren't bothering me. I have pretty bad astigmatism, and that is what my doctor said gave me the problem of seeing stars and halos around headlights at night. Then looking back at the road it was hard to refocus on what was ahead of me. So I didn't drive at night usually. That night the headlights looked clear so it was much easier to drive at night. My vision is clearer, especially at night." youtube.com
RESEARCH ARTICLE (from pubmed.gov):
Ann Rheum Dis. 2014 Dec 4. pii: annrheumdis-2014-206295. doi: 10.1136/annrheumdis-2014-206295. [Epub ahead of print]Oxidative changes and signalling pathways are pivotal in initiating age-related changes in articular cartilage. Author information Abstract OBJECTIVE:
To use a computational approach to investigate the cellular and extracellular matrix changes that occur with age in the knee joints of mice.METHODS:
Knee joints from an inbred C57/BL1/6 (ICRFa) mouse colony were harvested at 3-30 months of age. Sections were stained with H&E, Safranin-O, Picro-sirius red and antibodies to matrix metalloproteinase-13 (MMP-13), nitrotyrosine, LC-3B, Bcl-2, and cleaved type II collagen used for immunohistochemistry. Based on this and other data from the literature, a computer simulation model was built using the Systems Biology Markup Language using an iterative approach of data analysis and modelling. Individual parameters were subsequently altered to assess their effect on the model.RESULTS:
A progressive loss of cartilage matrix occurred with age. Nitrotyrosine, MMP-13 and activin receptor-like kinase-1 (ALK1) staining in cartilage increased with age with a concomitant decrease in LC-3B and Bcl-2. Stochastic simulations from the computational model showed a good agreement with these data, once transforming growth factor-β signalling via ALK1/ALK5 receptors was included. Oxidative stress and the interleukin 1 pathway were identified as key factors in driving the cartilage breakdown associated with ageing.CONCLUSIONS:
A progressive loss of cartilage matrix and cellularity occurs with age. This is accompanied with increased levels of oxidative stress, apoptosis and MMP-13 and a decrease in chondrocyte autophagy. These changes explain the marked predisposition of joints to develop osteoarthritis with age. Computational modelling provides useful insights into the underlying mechanisms involved in age-related changes in musculoskeletal tissues.
Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
PMID: 25475114 [PubMed - as supplied by publisher]
[INTERPRETATION: Knee and other joints lose cartilage over time because of increased levels of oxidative stress (cell damage by oxidants) and apoptosis (cell destruction by oxidants). So the oxidants ultimately cause arthritis in the joints.]
ARTICLE (from pubmed.gov):
Rheumatol. 2014 Dec;66(12):3300-10. doi: 10.1002/art.38822.
arthritis is associated with joint inflammation, synovial tissue proliferation,
and degradation of articular cartilage and bone. Angiogenesis is an early
and fundamental component of synovial inflammation. Oxygen metabolism is
recognized as an important mediator of joint vascular remodeling. The aim
of this study was to determine whether in vivo synovial hypoxia (tissue PO2
[tPO2 ]) and tumor necrosis factor (TNF) blocking therapy alter synovial
vascular expression of NADPH oxidase (NOX) and how this action regulates
protein and messenger RNA expression was examined in patients with inflammatory
arthritis before and after receiving TNF inhibitor (TNFi) therapy and in mice
with collagen-induced arthritis (CIA). Proangiogenic processes were assessed in
human microvascular endothelial cells (HMVECs) following culture with NOX-2
activators (TNFα and 4-hydroxynonenal), small interfering RNA (siRNA) for NOX,
and the inhibitor diphenyleneiodonium (DPI) under conditions of normoxia or 3%
demonstrated significantly increased NOX-2 expression in the joints of patients
with inflammatory arthritis and the joints of mice with CIA as compared to
expression was higher in patients with synovial tPO2 levels <3% than in
those with tPO2 levels >3% (P < 0.05), and correlated with in vivo
macroscopic/microscopic measures of angiogenesis, such as vascularity and
levels of vascular endothelial growth factor, angiopoietin 2, factor VIII,
neural cell adhesion molecule, and α-smooth muscle actin (P < 0.05 for all).
A decrease in NOX-2 expression was paralleled by an increase in in vivo tPO2
levels only in those patients who were defined as TNFi responders. In vitro NOX-2
activators and 3% hypoxia significantly promoted HMVEC migration, angiogenic
tube formation, and secretion of proangiogenic mediators, effects that were
blocked by siRNA for NOX-2 or the NOX-2 inhibitor DPI.
demonstrated that hypoxia activates NOX-2 protein expression, and NOX-2-induced
oxidative stress may be an initiating factor in driving angiogenesis.
© 2014 by the American College of Rheumatology.
[PubMed - in process]
[INTERPRETATION: Oxidants (NOX) are abnormally high in the joints of patients who have arthritis. Oxidative stress (cell damage by oxidants) causes arthritis, movement of cells, and the tubes associated with arthritis.]