People with CFS typically are severely exhausted, even bedridden like Elaine above, but they CANNOT get sufficient or quality sleep.

And if you’re able to go to college and write a paper about anything…then it’s unlikely you have true CFS.

I do not come from a medical background but I am desperately trying to find answers—

Is it possible to overdose on l- arginine?

What would the effects be?

a) effects if one had Adrenal Fatigue
b) kidney malfunction
c) underactive thyroid?

Interesting thoughts, in particular why dont people who use Nitro’s get CFS side-effects when elevated NO. I myself have CFS, have fully recovered for 8 yrs then are 2 yrs into relapse. I think the disease is more than NO depletion or elevation, but it does play a role. Im sure the underlying physiology of the disease sits on the axis between normal and coma, the brain gets an insult – Infection etc and goes into an autoprotection mode , which is where infected tissue is reprogrammed to function in a lower O2 environment which upgraded genetically the NO gene. However when the brain is confronted with having to produce extra energy , the NO gene is stimulated, producing excess NO. With more o2 being consumed during activity – this stimulate the L-Arginine NO pathway, producing those nasty by products. This is vicious cycle b/c the by procducts cause NS damage. Recently it have been mentioned 02 toxicity and ME. I only have theories like yourself, but this disease resembles Hashimoto Encephalopathy, Lymphatic Hypophositis, Atypical Addison,s, however it is a seperate entity b/c no disease has delayed 24-72 post-exertional fatigue, although one phenonemon that is strikingly similar is drug withdrawal – whereby pts get rebound excitatory neurotoxicity once the inhibitory substance is removed. I think when the brain goes into lock down mode – evidence SPECT Scans perfusion anolomies, slowed signalling on QEEG, HPA deficiencies – low temperature, slowed cortisol response, ( all markers of the shut down – inhibitory effect ), then once the NO pathway is induced the brain swings to NMDA neurotoxicity as seen in o2 toxicity. Depending on the level of activity ( o2 consumption ) and the shut down will determine how much post – exertional NS poisoning will occur. Finally yes, I have a medical background – Reg Nurse and was the Southern Regional Manager for a large drug company for 8 yrs.If thsi disease is a virus it is unique, i think that this disease is like cancer is that cells are reprogrammed, not producing tumours but major malfunction.
Good luck – Ash G.

I disagree with the Pall hypothesis that too much NO causes the production of peroxynitrite. That is incorrect. Peroxynitrite is only caused by near stoichiometric fluxes of NO and superoxide. The presence of peroxynitrite damage is a sign of not enough NO, not of too much.

NO/NOx physiology is under intense regulation. It is extremely difficult to perturb artificially. Essentially every non-physiological mechanism causes rebound. That is what supplemental L-arginine does.

Viagra does that too. I am pretty sure that Viagra will make CFS worse. It inhibits the phosphodiesterase that reduces cGMP, causing high cGMP levels, that turns off nitric oxide synthase earlier, and reduces the effects of NO that are not mediated through cGMP. There are a lot of NO effects not mediated through cGMP, breathing for example. Viagra makes obstructive sleep apnea worse via that mechanism (my hypothesis).

My blog is about NO physiology and at some point I will post about CFS. Right now I am working on a post about peripheral vascular damage.

Some of the symptoms of CFS and what is called Morgellons are the same. I think that Morgellons is low NO in the skin, CFS is low NO in the skeletal muscle. There are systemic effect too, and they are mostly the same. I have a blog about Morgellons.