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The identification of hepcidin opens the door to therapeutic approaches for several disorders and to proscriptions regarding the use of iron. Recombinant hepcidin may be the ideal therapeutic agent for those with some forms of juvenile haemochromatosis and with the less severe but more common form of haemochromatosis caused by mutations in the HFE gene [26]. Hepcidin-induced iron deprivation may prove helpful in preventing the development of resistant bacterial biofilms [10]. For the anaemia of inflammation, often resistant to erythropoietin therapy [27], inhibitors of hepcidin, by releasing sequestered iron, could restore haemoglobin levels and conceivably correct an iron lack in myoglobin and cytochromes as well. Finally, of related interest is a recent report that moderate alcohol intake reduces levels of C-reactive protein and IL-6 [28], the principle chemokine for the generation of hepcidin mRNA, extrapolating to a possible ameliorative role of alcohol in both inflammation and the anaemia of inflammation.
As to proscriptions, iron supplements should be monitored, not only because the resulting increase in hepcidin can fuel antimicrobial engines unnecessarily, but because hepcidin increases macrophage iron sequestration in the synovium as elsewhere. Synovial iron has the propensity to generate oxygen free radicals that have been linked to the chronicity and erosiveness of joint disease in RA [29]. In fact, intramuscular injections of iron have long ago been reported to cause acute flares of joint inflammation in RA [30]. A broader phlogistic potential of iron towards the joint comes from a recent report that iron depletion by serial phlebotomies diminishes recurrences of gouty arthritis [31]. If one adds all of the above to the reported links of iron sufficiency to colon cancer [32], diabetes mellitus [33], chronic hepatitis [34] and atherosclerosis [35], it would seem best to phase out gratuitous iron supplementation altogether.
The discovery of hepcidin provides a thread that ties together the perplexing triad of decreased serum iron, increased macrophage iron and chronic inflammation. In addition, it offers a unique opportunity for determining the effects of iron on disease, the usefulness of hepcidin inhibitors or promoters to control iron kinetics, and the proper means of iron administration. In the aggregate, these will represent a step forward in the treatment of a variety of diseases.
The authors have declared no conflicts of interest.

Merlyn wrote: Being vegetarian, it is doubtful that you have iron overload, and further I assume that molecular mimicry is not heavily involved, simply due to the lack of animal-based protein. I am just trying to figure out why in the world this bloodletting is so useful/helpful.

There has to be some inflammatory component in our blood that is causing venous damage, damage to the endothelial cells.

And you are right about vegetarianism, over the years I have noticed a number of people with MS that are vegetarian.
B12? Do you take supplements of methylcobalamin? One lady I knew totally reversed her MS symptoms when I suggested that she take various forms of B12 (she was a lifelong vegetarian), but she was an exception, her reversal of symptoms was very rapid. She took all four kinds in high doses. I have injected methylcobalamin, hydroxyl cobalamin, cyanocobalamin and I never received any benefit. But for some it might make all the difference in the world.

(8) As of 2004 no plant sources of vitamin B12 had been found, though many had been tested including various seaweeds, algae and fermented foods. Where claims have been made as to B12 being present in a plant source, it has not been based on the test for MMA levels, and any subsequent tests have found no reduction in MMA, proving the presence only of inactive analogues.