Hello tout le monde
Les récentes interventions échangées ici sont très intéréssantes et mériteraient bien volontier d'apparaitre dans un topic a part, afin de permettre a un plus grand nombre de les voir...je vais donc créér un nouveau sujet (je ne sais pas encore ou...

)et recopier ces messages la bas.
Bon compléter un peu a mon tour ce qui est dit ici, je voudrais rapeller que plusieures co-infections (et surtout babesia) sont très largement impactées dans les troubles de la nuque et de la tete. Le pb étant qu'il n'existe pas réellement a notre disposition de test (en tout cas pas en france, a ma connaissance, mais ailleurs oui) permettant de savoir si cette co-infection est présente chez les personnes ayant deja lyme. Klinghardt dit qu'environ 80% des personnes ayant lyme l'ont également, donc ça donne deja un ordre de grandeur. Le fait est que le traitement de cette co-infection (principalement par voie médicamenteuse (mepron) ou via l'artemesisin / cryptolepsis) a permis a bcp de personnes de grandement diminuer leur pbs de brainfob / nuque raide / maux de tete chroniques. Il s'agit dans ces cas la de véritable encéphalite, dont babesia a un grand role a jouer dedans (bien que ce n'est surement pas le seul co-facteur, comme nous le savons bien ici).
Ensuite et dans un deuxième temps, je rebondis sur ce qui a été dis sur les enzymes, l"homocystéine et le gluthation.
Le Dr Paul Cheney (pas français donc on peut le dire

) a écrit plusieurs articles très intéréssants sur la relation entre:
--> le phénomène de génération d'ATP dans les cellules - les différentes formes d'oxide nitrique - les antioxidants (SOD et glutathion peroxydase) - et l'apparation de l'élément meutrier "peroxynitrite" qui pose tant de soucis dans nos corps.
Il est possible qu'un grand nombre de personnes n'ai encore jamais entendu parlé de ce fameux peroxynitrite, alors je vous fais un copier/coller d'une partie d'un de ses articles (en anglais, sorry...

) qui est a mon sens important a comprendre, car c'est une partie du puzzle en plus!
Pti gars
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Pall: Nitric Oxide + Superoxide = Peroxynitrite
The pathophysiology [functional changes that accompany a disease] at the cellular level that underpins this pathophysiologic state is well elucidated by Martin Pall. [A search for "Martin Pall" on immunesupport.com will produce several articles.]
One nitric oxide molecule plus one superoxide molecule equals one peroxynitrite molecule. Peroxynitrite is a reactive oxygen species, is deadly, and highly damaging. At the cellular level, it is the proximate cause of human mortality. Even if you are healthy and your body handles peroxynitrite as well as possible, you will still die of old age.
"These molecules [nitric oxide and superoxide] have to be generated because they are essential for life. They are the end products of a complex scheme of oxidation reactions in the human body; necessary for, among other things, energy generation, and their production is inevitable. Indeed, if they weren't produced you would not be alive. But because they are produced, you will die of oxidation. If you live by the sword, you die by the sword. If you live by oxidation then, like any piece of iron set in an oxygen environment, you will eventually rust away, and we call that death by old age. This is called 'The Free Radical Theory of Aging.' "
What do humans die of, usually? The top killer is Coronary Artery Disease [CAD], and the next is cancer. It turns out that CAD and cancer are also driven in part by peroxynitrite formation. Neurodegenerative diseases like Parkinson's and Alzheimer's are also suspected of being driven by free radical formation. Even suicide is increasingly thought to be generated by oxidative stress in the central nervous system. And, of course, MS and autoimmune diseases. And finally ICM, the path down which you seem to be going, though halted by CFS itself.
But your path deviated right here, just above the Event Horizon to CFS, and you went down the CFS path for a very interesting reason. Why didn't you go down the cancer or MS or Parkinson's pathway? For some reason you started down the CFS pathway over those, and I think that's a result of preordained genetics and environmental influences that combined in a unique fashion to produce that particular road I went down—the ICM pathway. But I could not deviate [from the ICM path] because I never developed CFIDS and I went straight to a near-death experience and came back.
I want to talk a little bit about these two guys [nitric oxide and superoxide], show you why they're necessary and that you have to make them, and how they can modulate your disease process. Especially how they're related to etiology. [They cause many, if not most, of our symptoms—directly or indirectly.]
Nitric Oxide is made by iNOS, eNOS, and nNOS, so far identified. [The small letter in front indicates the source.] The iNOS is of particular interest because it comes from the immune system. When any kind of virus, bacteria, mold, toxin, microbe, or allergy activates your immune system, it induces iNOS, which makes copious amounts of Nitric Oxide. iNOS can make far more Nitric Oxide than eNOS and nNOS can ever make.
eNOS is made by the endothelial cells in the blood vessels and is responsible for regulating microcirculation, basically.
nNOS is made in neurons and is responsible for memory and learning. It is also, when highly activated, very much responsible for MCS, EMR sensitivity [electromagnetic radiation], light and noise sensitivity, and can make sleep difficult. Over-activation also amplifies pain.
Your body has to make nitric oxide. If you don't make it, you have no immune system, no circulation, no brain. The question isn't do you make it; the question is do you make a lot of it. If you make a lot of it there can be repercussions downstream. What those repercussions are depends on what you're [your body iu] doing with superoxide.
Now superoxide is produced by the act of making energy [ATP]. It's made in the mitochondria, and for every molecule of ATP generated, you generate one molecule of superoxide—one for one. The more energy you make, the more superoxide you make. However, superoxide is generally found inside the mitochondria. Generally. Nitric oxide is found outside the mitochondria. As long as superoxide stays in the mitochondria and never leaks out, there's no way you will make peroxynitrite, because it takes one nitric oxide plus one superoxide to make one molecule of peroxynitrite.
A Little Math
Now, let's stop here for a moment to talk about the coupling effect. If I have 50 molecules of nitric oxide, and five molecules of superoxide have leaked out of the mitochondria, how many peroxynitrite molecules do I generate? Five. If I make 10,000 nitric oxide molecules, and only 5 superoxide, how many peroxynitrite molecules do I generate? Again, five! Do you see what is happening? What dictates peroxynitrite is not the one with the highest amount, but rather the one with the lowest.
Super Oxide—Out of Control
Therefore, the primary driving force behind peroxynitrite is in fact the production of superoxide. However, if superoxide is well controlled, peroxynitrite formation is limited. However, if superoxide is out of control, there are few limits to the formation of peroxynitrite. It's purely a function of energy production. The more energy you produce, the higher the peroxynitrite may go, especially if nitric oxide is also out of control.
If everything worked as intended, the mitochondria would take in oxygen and nutrition, and output carbon dioxide, water, and ATP (energy). You have enzyme systems embedded in the mitochondria that can break superoxide down to water to prevent superoxide from leaking out of the mitochondria. One enzyme system is called Superoxide Dismutase (SOD). Actually, the enzyme breaks it down to hydrogen peroxide and then down to water, via Glutathione Peroxidase, which depends on selenium and glutathione. [Without proper amounts of selenium and glutathione, the enzyme cannot do its job.]
For the enzyme [SOD] to break superoxide down properly, selenium is supposed to bind to Glutathione Peroxidase. However, if mercury is present in any amount and you have no defense against it [and there are defenseu], it competes for that binding site and blocks the selenium. When mercury displaces selenium at the binding site, the function of that enzyme is knocked out. At that point, you have no way to oxidize superoxide down to water, and superoxide starts to leak out contributing to the formation of deadly peroxynitrite. How much superoxide leaks out depends on how much energy you're generating [and thus how much superoxide], as well as the presence of other defense mechanisms. CoEnzyme Q10 is one and Lipoic Acid is another.
CoQ10 within the mitochondria and Lipoic Acid in the cytoplasm bind excess superoxide so it's unavailable to couple with nitric oxide to produce peroxynitrite. Taking sufficient CoQ10 under certain redox state conditions, would allow you to make more energy and not get creamed with peroxynitrite. [Redox will be discussed in another article.] But, if you keep raising CoQ10 in an inappropriate redox state you may actually generate more superoxide, and that's when the CoQ10 bites you. [Some patients who cannot tolerate CoQ10 find that its analogue, Idebenone, works better.]
Glutathione production is linked to ATP production, because the more ATP (energy) you make, the more Glutathione you need to keep the enzyme breaking the resulting superoxide down to water. If you don't, then the lack of Glutathione will actually result in injury to the mitochondrial membrane and a drop in ATP. That's the Gibbs Free Energy Equation, which says that Glutathione concentration and ATP generation are intimately linked.
Which brings me to the most important statement I'll make about this peroxynitrite diagram. If you are immune-activated from virus, bacteria, mold, and/or toxin exposures, then you're generating an excess amount of nitric oxide. And if you also make a significant amount of ATP, it can result in superoxide, which then binds with the nitric oxide to produce large amounts of peroxynitrite. Then you're set up for major problems. [Oxygen transport, microcirculatory impairment, lack of tissue perfusion, etc.]