It's interesting that you also experienced arthritis with iron...it took us like a month to put the two things together and realize that was likely the culprit. So frustrating that the things we need to take cause other problems!
When you do (if you do) resume iron supplementation at some point, you might want to consider trying it in the form of Bisglycinate (which is what I've been using for years - I buy Solgar, 25mg per capsule). There is some research that indicates this form is a bit more bioavailable and helpful for ferritin replenishment than fumarate and other iron salts. Plus, this form is gentle on the stomach (Solgar actually calls it "Gentle Iron".) Since I'm prone to constipation, this is pretty important for me, and in fact this form doesn't seem to make me constipated at all. You can do a general internet search to compare the various forms. One I found was from
http://www.biomath.info/Protocols/Duke/docs/HarperJason.pdf and even though it's specifically about Celiac patients, it does compare ferritin levels when given fumarate vs. bisglycinate:
"In the treatment of iron deficiency, multiple formulations of iron are available. In general, the iron salts (i.e. ferrous fumarate, ferrous sulfate and ferrous gluconate) are prescribed as iron supplements in cases of iron deficiency, and these are the most common formulations found in over-the-counter formulations as well. However, there are multiple other formulations of elemental iron available, including some that are complexed to amino acid chelators, such as FeNaEDTA or ferrous bisglycinate. Some studies have suggested that these forms of iron are more bioavailable in select populations. One such study looked at an in vitro model of iron absorption using human colonic adenocarcinoma cells, and found that a wheat-based cereal fortified with NaFeEDTA and ferrous bisglycinate led to increased cell ferritin formation in comparison to traditional iron salts.x In another study, 40 infants diagnosed with iron-deficiency anemia were treated with ferrous sulfate versus iron bisglycinate for 28 days.
While both groups showed an equivalent rise in hemoglobin, the group treated with iron bisglycinate had a significantly greater increase in serum ferritin as well, suggesting better restoration of tissue iron stores."
If only I could well explain the nitric oxide cycle...I would be really impressed with myself! I'll try to do my best, but just keep in mind that I don't have a biochemistry background at all, so hopefully I don't make a mistake with what I understand so far:
Nitric Oxide plays a really complex role. It is both pro-inflammatory and anti-inflammatory (and both an antioxidant and a free radical). Having too little is a big problem, but having too much is just as much of a problem. NO plays so many various roles in the body, I don't think I could list them all if I tried. What's important to know is that in the right amounts, NO is critical for good health.
NO is our body's first line defense against "simple" pathogens like many types of bacteria...Basically, NO is like a poison gas that the body produces to kill off these invaders (Th1). For the most part, it's a really efficient way to kill off many pathogens and this approach works well. However, not all pathogens are killed by NO gas...such as many viruses, some molds, some other bacteria, environmental toxins, etc... When the body produces a huge poison NO attack but it doesn't work, then the body shifts to using strategy #2: B cells (Th2). If there is a legitimate pathogen to attack, the B cells attack it and hopefully eliminate the infection. However, in some people, it seems that once the B cells are activated, they never seem to deactivate as they should. There are some suggestions for why this happens:
1) NO (Th1) is actually the correct strategy to use against a particular pathogen, but the body doesn't have enough of the co-factors to produce it, therefore it is 'forced' to rely on the (Th2) B cell strategy, which isn't effective, but since it has no other choice, it just keeps on using it -this creates a state of chronic B cell activation.
or:
2) For some unknown reason the 'kill switch' (which I believe is called TReg) isn't pulled on the Th2 system, so it is in a constant state of war with no invader...this is why it starts attacking the body and results in creating autoimmune problems.
Additionally, when NO combines with Superoxide (a free radical that on its own is not much of a big deal) it creates Peroxynitrite...a VERY big deal! It's a super oxidizing agent that is much more powerful than the components it's made from. Cheney, for example, believes that CFS is largely due to an excessive amount of Peroxynitrite (which then leads to massive inflammation in addition to other damage faster than it can be repaired.
Right now, there are several CFS doctors who are treating patients with antivirals. Since the amount of time it takes for patients to improve happens to be the same amount of time it takes for B cells (Th2) to be replaced, I actually think that it's likely that of the people who are improving with this treatment, they are improving because the antivirals are modulating the Th2 system that is overproducing B cells, rather than any actual viral infection. If you think about it, Artesunate is used to treat Malaria, which is a real son of a bitch viral infection, and the Artesunate eliminates it in days. Same thing with antibiotics - if an active infection isn't cured in a week or two, then doctors know they aren't using the right antibiotic and they switch to something else. Even with chronic Lyme, you have to treat it aggressively to get it into remission (you have more experience than I do with this, so correct me if I'm wrong), which generally means changing the medication on a regular basis so the Lyme doesn't become immune to it. It doesn't make any sense to me that other viral infections require months of the same anti-viral treatment before any improvement is seen. But I'm going on a tangent here, and probably some people will disagree with me, so I'll move on.
This system is highly complex, and I've skimmed over a huge amount of it, but this how I'm understanding it so far. Ultimately, Nitric Oxide is super important, but having not enough (because you don't have the cofactors to produce it) or having too much which then goes on to eventually produce peroxynitrite is a major problem.
At this point, it seems that one of the most important pieces of the Nitric Oxide puzzle is Glutathione, which is a powerful antioxidant produced by the body that controls peroxynitrite damage by neutralizing it. In fact, people with CFS (and other illnesses) have often show improvement when they are able to increase their glutathione levels and many of the CFS specialists have protocols that focus on trying to increase Glutathione while reducing peroxynitrite formation.
Here is one great link that has way more information than I summed up:
http://www.medicalinsider.com/cardiac3.html#pall that maybe can fill out the areas that I skipped over. There is also an article here on PR that is pretty good:
http://phoenixrising.me/archives/18836
And lastly, this thread has a lot of interesting and useful information:
http://forums.phoenixrising.me/inde...isease-martin-pall-website.34969/#post-550190
While I know the Nitric Oxide cycle is critical, I also know that it's not the whole thing. But much like methylation, I think it's a really important part of the puzzle.
