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New member
Sep 27, 2004

I'm new to this forum. I'm curious to know if anyone has tried using R(+)Alpha lipoic acid to slow the progression of their disease. I am a 47 year old male and have been taking it now for about six weeks along with Acetyl-l-carnitine (ALCAR), and biotin, and I believe it may be helping my symptoms. I appear to be stronger and more coordinated, and my feet are not dropping as much as they were. I've been doing research, and I've developed some of my own ideas:

I think there is some evidence that oxidation (particularly within mitochondria) may play a central role in the pathogenesis of this disease.

Researchers have developed a transgenic ALS mouse model. These mice, showing classical symptoms of ALS, have a mutation of a certain gene: G93A. This gene is responsible for producing a mammal's most important anti-oxidant enzyme: Cu,Zn superoxide dismutase, aka SOD. The mutation interferes with the ability to correctly produce this primary antioxidant enzyme. Since the bulk of most ROS (reactive oxygen species) are produced within the mitochondria, this makes the mitochondria especially susceptible to damage from oxidation. Mitochondria are the "powerhouses" of cells, producing all the energy the cell needs. When they become damaged, the whole cell eventually suffers, especially since they (unlike all other organelles) contain their own DNA separate from nuclear DNA. I believe that this may occur in particular types of cells in ALS, namely muscle, motorneuron, etc at a greater rate.

The R(+) form of Alpha lipoic acid (a popular supplement and research chemical), is one of the most effective exogenous mitochondrial antioxidants known at this point. It has been estimated to be 1000 times more powerful than vitamin C and E combined, and has the ability to cross the mitochondrial membrane and neutralize free radicals much more effectively than most other antioxidants. Recent research has shown that the R(+) form is superior to the ordinary racemic form which most know simply as alpha lipoic acid. -- (There are multiple websites discussing the differences).

As a mitochondrial antioxidant (the body produces tiny amounts of it), R(+)alpha-lipoic acid can cross the mitochondrial membrane and neutralize many of the ROS which SOD would ordinarily take care of.

In healthy cells producing normal SOD, SOD will react with ROS producing hydrogen peroxide and water. Other antioxidant enzymes, like protein catalase, will then neutralize the resulting hydrogen peroxide. This is one of the primary mechanisms the body has for dealing with oxidative stress.

Anti-oxidants work a little bit differently. ROS are lacking an electron, which it steals from other molecules of the cell in a chain reaction, thus damaging (oxidizing) the cell and its DNA and repair mechanisms. Anti-oxidants help to break this chain by donating an electron. This takes away much of the "punch". The oxidized anti-oxidant only has a relatively weak need to obtain another electron, thereby helping to reduce oxidative stress. It does not work as perfectly as the body's own mechanisms for this reason, but R(+)ALA is, nonetheless, very effective at neutralizing free radicals.

Actual SOD mimetics have been developed, such as EUK-189. EUK-189 performs the function of both SOD and catalase. Many people interested in "anti-aging" take antioxidants like R(+)ALA and EUK-189 in an effort to slow aging. (The two most popular theories of aging involve oxidation and mitochondrial damage).

In addition, spin traps are being developed. Spin traps, unlike anti-oxidants, cannot become pro-oxidants after neutralizing ROS. Examples are NtBHA, and the amazingly powerful "STAZN" which is under development at this time. I'm thinking about adding NtBHA, which can be purchased at the current time. Studies have shown that it is very effective in dealing with inter-mitochondrial oxidative stress.
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R(+)ALA should be taken as part of a trio along with Acetyl-l-carnitine and biotin. I am taking 750 mg of the potassium salt of R(+)ALA daily in divided dosages, along with 8mg biotin, and 4 grams of ALCAR.

The typical racemic form of ALA has been shown to "significantly" increase the lifespan of the transgenic mice. (See study below). You might notice that a copper chelator has also been shown to extend lifespan in these animals. This may be because copper is actually responsible for forming much of the ROS in the first place, through a process known as the "fenton reaction".

I don't want to give false hope. This is just an idea of mine, based on the fact that it has been shown effective in the mutant rodents. The study is below. These three supplements are available from many sources on the internet. Many already healthy people take them daily for anti-aging purposes.

Exp Neurol. 2001 Apr;168(2):419-24. Related Articles, Links

Effects of an inhibitor of poly(ADP-ribose) polymerase, desmethylselegiline, trientine, and lipoic acid in transgenic ALS mice.

Andreassen OA, Dedeoglu A, Friedlich A, Ferrante KL, Hughes D, Szabo C, Beal MF.

Neurochemistry Laboratory, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.

The development of transgenic mouse models of amyotrophic lateral sclerosis (ALS) allows the testing of neuroprotective agents. We evaluated the effects of five agents in transgenic mice with the G93A Cu,Zn superoxide dismutase mutation. A novel inhibitor of poly(ADP-ribose) polymerase showed no effects on survival. Desmethylselegiline and CGP3466 are agents that exert antiapoptotic effects in vitro by preventing nuclear translocation of glyceraldehyde-3-phosphate dehydrogenase. They had no significant effects on survival in the G93A mice. Trientine, a copper chelator, produced a modest significant increase in survival. Similarly administration of lipoic acid in the diet produced a significant improvement in survival. These results therefore provide evidence for potential therapeutic effects of copper chelators and lipoic acid in the treatment of ALS.
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