for iron overload syndromes, as it stimulates hepcidin activity.25


and renal support support formulations (depending on the condition priority) are recommended, provided they are derived from whole food and non-synthetic, quality- controlled sources, and that their constituents meet the condition criteria discussed.


glycoprotein extracted from bovine colostrum and whey protein isolates, has both iron-binding properties and immune modulating in conditions involving chronic inammation, infection, and trauma.24


Hepatic, digestive, Lactoferrin, an iron-binding


enhance absorption of non-heme iron by overcoming formation of insoluble iron compounds and for enhanced reduction of ferric iron to ferrous iron.1


Astragalus is useful


Dong Quai (Angelica sinensis) possesses properties that suppress activity of hepcidin that may be useful in IDA, in paradoxical conditions where iron is best not supplemented.26


Center - Iron. Oregon State University. Institute. http://lpi.oregonstate.edu


Linus Pauling


3. Iron deciency anaemia: assessment, prevention and control - A guide for programme managers. (2001). World Health Organization, United Nations Children’s Fund, United Nations University.


4. Conde Diez, S., de Las Cuevas Allende, R., Conde Garca, E. (2017). Current status of iron metabolism: Clinical and therapeutic implications. Med Clin (Barc). pii:S0025-7753(16)30664-9. 2016.10.047. doi: 10.1016/j. medcli.


5. Fukushima, T. (2016). The role of zinc in chronic kidney disease. Nihon Rinsho. Jul;74(7): 1138-43.


6. Nelson, R.L., Persky, V., Davis, F., Becker, E. (2001). Risk of disease in siblings of patients with hereditaryhemochromatosis. Digestion. 64(2):120-4.


7. Charles, G., heng, C., Lehmann-Horn, F., Jurkat-Rott, K., Levitt, J. (2013). Characterization of hyperkalemic periodic paralysis: a survey of genetically diagnosed individuals. J Neurol. Oct;260(10):2606-13.


Follow-up care involves re-testing relevant clinical laboratory markers in two to four month intervals to monitor evidence of change as well as soliciting changes in symptoms. Relevant routine in-ofce exam inventories are also re-checked for evidence of clinical change within a reasonable time in which to expect changes to occur, e.g., two to four months‘ time.


References 1. Gropper, S.S. & Smith, J.L. (2013). Advanced Nutrition and Human Metabolism (6th ed.). Belmont, CA: Wadsworth, Cengage Learning.


2. Delage, B., Higdon, J. (2016). Micronutrient Information


8. hou, H., Fischer, H.P. (2008). Hereditary hemochromatosis, alpha-1-antitrypsin deciency and Wilsons disease. Pathogenesis, clinical ndings and pathways to diagnosis. Pathologe. Feb;29(1):73-83. 9. Alpha-1-antitrypsin


deciency. (2017). Genetics Home


Reference. U.S. National Library of Medicine. Bethesda, MD. https://ghr.nlm.nih.gov/condition/alpha-1-antitrypsin- deciency.


10. Mocchegiani, E., Costarelli, L., Giacconi, R., Piacenza, F., Basso, A., Malavolta, M. (2012). Micronutrient (n, Cu, Fe)-gene interactions in ageing and inammatory age-related diseases: implications for treatments. Ageing Res Rev. Apr;11(2):297-319.


11. Lindner, S. (2016). Iron. Panopto Power Point Recording Figure 1. Pathophysiology of hemochromatosis and anemia of chronic disease. 13


THE ORIGINAL INTERNIST MARCH 2017


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