January 25, 2013 at 10:47 pm #51Dan SKeymaster
Malaria and babesia parasites need iron to grow, and the more they get, the better for them. Both malaria and babesia have life cycles that include immature growth stage inside red blood cells, where they consume large amounts of iron. Protomyxzoa also have immature stages inside red blood cells, so its reasonable to assume that protomyxzoa also has a high need for iron.
I believe the first paper (“Iron deficiency protects…”) here might be very important for treating protomyxzoa. The paper shows that children with iron deficiency have much better outcomes when infected with malaria. In this case, its GOOD to have a nutrient deficiency!
Severe malaria was lower by an amazing 4-fold in children with iron deficiency.
I say its a good idea for people with protomyxzoa to induce iron deficiency. A good way to do that is by taking IP6 (inositol hexaphosphate).
Clin Infect Dis. 2012 Apr;54(8):1137-44. Epub 2012 Feb 21.
Iron deficiency protects against severe Plasmodium falciparum malaria and death in young children.
Gwamaka M, Kurtis JD, Sorensen BE, Holte S, Morrison R, Mutabingwa TK, Fried M, Duffy PE.
Mother-Offspring Malaria Studies Project, Seattle Biomedical Research Institute, Washington, USA.
Iron supplementation may increased malaria morbidity and mortality, but the effect of naturally occurring variation in iron status on malaria risk is not well studied.
A total of 785 Tanzanian children living in an area of intense malaria transmission were enrolled at birth, and intensively monitored for parasitemia and illness including malaria for up to 3 years, with an average of 47 blood smears. We assayed plasma samples collected at routine healthy-child visits, and evaluated the impact of iron deficiency (ID) on future malaria outcomes and mortality.
ID at routine, well-child visits significantly decreased the odds of subsequent parasitemia (23% decrease, P < .001) and subsequent severe malaria (38% decrease, P = .04). ID was also associated with 60% lower all-cause mortality (P = .04) and 66% lower malaria-associated mortality (P = .11). When sick visits as well as routine healthy-child visits are included in analyses (average of 3 iron status assays/child), ID reduced the prevalence of parasitemia (6.6-fold), hyperparasitemia (24.0-fold), and severe malaria (4.0-fold) at the time of sample collection (all P < .001).
Malaria risk is influenced by physiologic iron status, and therefore iron supplementation may have adverse effects even among children with ID. Future interventional studies should assess whether treatment for ID coupled with effective malaria control can mitigate the risks of iron supplementation for children in areas of malaria transmission.
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