I"ve been researching Hepcidin, the link between the immune system, inflammation and how your body treats iron.
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http://rheumatology.oxfordjournals.org/ ... /1323.fullThe 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.
Hepcidin: inflammation's iron curtain
Rheumatology Vol. 43 No. 11 © British Society for Rheumatology 2004; all rights reserved
I need to further note that, since this article this year De Sousa published that lymphocytes also produce Hepcidin. The missing link between immune response and iron storage.
I find this so interesting, as it explains why someone who is aneamic can have iron overloaded macrophages, and the iron is not available for them, but it is non the less in their body with more likelyhood of free radicals and inflammation. Prescribing iron supplements in this situation seems ludicrous.
