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Caliburn

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I hope someone reads this and takes notice. Im currently a student of pathobiology and developed diffuse fasciculations and muscle issues hyperreflexia, pain, spasticity after drinking alcohol and taking huge quantities of the vasodilator NOxplode. I know this is probably a shot in the dark, but ive read dozens of medical journal articles on the role of NO on excitotoxicity of motor neurons and the combined effects of alcohol on production of NO (nitric oxide) and while part of me hopes i dont have als, part of me does so that what caused it (if it is in fact huge amounts of l-arginine and alcohol) can be identified and thus help to produce a model for sporadic als. I hope i dont create any conflict with this post, just trying to contribute something; my muscle issues are getting so bad. Awaiting my second EMG and a new panel of blood tests. I found someone else who took this supplement who is having the same issues as me.
 
Interesting finding.
Should that be true, then it should be good to alert people who do not have ALS
to avoid these things. Now that I have this dreadful disease, I wouldn't want it upon anybody, not even my worst enemy. So whenever I find something that might trigger it, I would alert people to steer clear from those things.

Although, L-Arginine and some of its derivatives are being used and recommended by some PALS at ALS--TDI Forums as a treatment for the disease. I just wonder why.

NH
 
I agree with NH! In regards to arginine and NO...it is notable that NO is deficient in PALS (according to clinical studies) so while it might be bad for pre-ALS it may not be post?

That said..those of us taking 1:1 AAKG also take large quantifies of glutathione to scavenge free radicals such as NO.

Keep us posted but I sure hope your tests are negative...
 
Thanks. Ive just read so so so many papers on excess nitric oxide and mitochondrial damage in relation to increased Ca+ influx leading to motor neuron death it really makes me think. And yet, these have all been single journal articles, no follow up, its like nobody cares... People just keep looking at the familial mouse model for als and saying hmm... Thats strange.... Yeah its strange its a genetic mutation you idiots. Figure out how to cure genetic diseases and youll be all set! Now find a damn sporadic model! Im a Phd student and i can see that much.

And thanks dbltree, i hope theyre negative too.... But my positive attitude meter is just about on empty. Now im just angry.
 
In response to nighthawk, i personally believe that an initial traumatic occurrence (hypoxia/excess NO) leads to a breakdown of the NO synthesis pathway and causes some change that results in the breakdown of this pathway. All issues with mitochondria and neuronal death follow suit. In my opinion, worth a look.
 
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