New Study Shows GliSODin Supplementation Increases SOD Leve

[Jacob]

New Study Shows GliSODin Supplementation Increases SOD Levels and Protects Against Oxidative Stress

MORRISTOWN, NJ (March 9, 2005) PL Thomas (PLT) today announced the results of a new study using its exclusive dietary supplement ingredient, GliSODin, published in Phytotherapy Research March 1, 2005. The study concluded that supplementation with Glisodin promoted cellular antioxidant status and protected against oxidative stress-induced cell death.

According to PL Thomas President Paul Flowerman, This is the third and most important study conducted on the mechanism of action of GliSODin. This study validates the concept of GliSODin as an antioxidant catalyst, showing significant promotion of internal antioxidant production, including superoxide dismutase (SOD), catalase and glutathione peroxidase.

This study supports previously published human research (Free Radical Research, September 2004) where GliSODin supplementation was shown to protect against induced oxidative damage in a double-blind, placebo-controlled clinical trial.1

GliSODin is a radical new approach to antioxidant supplementation, one that is entirely different from conventional dietary antioxidants, such as vitamins (vitamins A, C and E), minerals (selenium, zinc, copper and manganese) and other substances, including polyphenols found in grapes and green tea. While important, these dietary antioxidants play a secondary role to the primary antioxidants produced by the body at the cellular level.

According to the new study, Supplementation with GliSODin in normal mice for 28 days was found to promote the circulating antioxidant enzymes SOD, catalase and Gpx. This was specific to GliSODin, because non-protected SOD extract or gliadin alone were unable to promote these antioxidants.

This increase in blood antioxidant activities correlated with an increased resistance of red blood cells to oxidative stress-induced cell death. GliSODin was further shown to increase antioxidant levels in the liver, and demonstrated an enhanced resistance to oxidative stress-induced cell death.

http://www.npicenter.com/anm/templates/ ... &zoneid=28

[Jacob]

This is just one example..so no I'm not saying it's going to do this for you.
I can't copy/paste but here's a list of "observational studies". See "Hair color & growth".

http://www.superglisodin.com/observations.html

The stuff is available at numerous places online.

[HairLossFight.com]

Jacob,

I recall reading somewhere that increased SOD internally could be associated with Parkinson's. I don't want anyone to freak out because it could have been total hearsay that I read on some forum somewhere, but do you have any info on this?

My guess is that the chances of this are really slim. I guess it would be nice to know what the potential side-effects of Glisodin are.

Regards,
Sam

[Jacob]

Well it is true that anything taken..too much of anti-oxidants..can be bad. Maybe I can dig up a discussion on that sometime. I've read that lack of enough glutathione can cause "bad sod" to build up or whatever they meant with their mumble jumble. There's a liposomal glut product out there...the only glut product taken internally that makes sense. But it's very expensive.


Here's some stuff I came across on Parkinson's and SOD:

SOD tends to be low in the area of the brain involved in Parkinsons disease. In theory, therefore, low levels of zinc and copper could leave the brain susceptible to free radical damage. However, copper and zinc (as well as iron) taken in excess can also act as pro-oxidants, and all have been associated with an increased risk of developing Parkinsons disease in preliminary research.57 58 Insufficient evidence currently exists for either recommending or avoiding supplementation with zinc and copper.

During the last decade studies of the pathogenesis of PD have centred on the oxidative damage to the substantia nigra pars compacta. An increased free radical production and an inadequate antioxidant defence system have been reported, which could contribute to the biopathology of PD. The GSH levels in the brain are decreased,and iron levels in the substantia nigra are elevated. Moreover there are changes in SOD with an increased activity in the substantia nigra. The possible implication of oxidative stress in cell loss has encouraged research into the role of certain antioxidant agents, such as dietary compounds and drugs, as protective agents against PD"