Hemochromatosis

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See also: iron overload

HFE C282Y

This gene mutation arose about 6,000 years ago in northern latitutes and wet environments [1]. Part of this reason could be drinking water from shallow wells that was infected with iron bacteria including potentially Pseudomonas and/or siderophilic bacteria that live on the released iron.

Can be caused by immune reactivity to hepcidin or at least low pro-hepcidin (precursor)[2]

HFE, the gene that is knocked out in hemochromatosis, stimulates hepcidin production. [3] So using an herb that stimulates hepcidin might be a great treatment.

When hepcidin is down in this disease, ferroportin is unchanged in hepatocytes in the liver leading to iron accumulation there but ferroportin is increased in macrophages leading to a iron deficiency in them. [4] what this means is when macrophages are low on iron they produce less il-6 and tnf-a and more pge2 and in some cases or perhaps parts of the body like the scalp in baldness? pgd2.

Doxycycline seems to induce ferroportin expression which might be linked to fatal familial insomnia which is thought to be due to prions. [5] but it seemsthat it is just doxycycline inducible ferroportin overexpressers [6] but who knows if any humans contain doxycycline inducible transgenes.

Benefits for the mutation

Intracellular bacteria like salmonella, chlamydia, ajd mycobacterium are inhibited since elevated ferroportin makes macrophages have less iron [7]. Also Listeria and Brucella the latter strongly promotes hepcidin [8] which could be a huge reason for the body to delete the gene.

Bacterial causes

Chlamydia due to mismaking of heme for porphyrins [9] [10].

Links

Overview of hemochromatosis including chronic fatigue and arthritis as most common symptoms [11]

Retinoids low in hemochromatosis [12].

Tests you can get [13].

Other pages that link to Hemochromatosis:

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