Hace varios años que se ha comenzado a ubicar al hierro como un factor independiente de muchas enfermedades.
Este tema , ya cada vez crece mas, por que el hierro, por que es considerado uno o el mas oxidante de los nutrientes.
Ya no quedan dudas en el rol de los oxidantes en la generación de daños bioquimicos, fisiologico e histologico en el cuerpo humano , asi como en modelos animales.
Que enfermedades aumentaría el riesgo de generarlas, o de potenciarlas el hierro?
Infarto de miocardio, varios cánceres, diabetes, enfermedades neurodegerativas, aumento del riesgo de ciertas infecciones (cuando hay carga alimanticia de hierro, durante un proceso infeccioso), entre otras. Y son esas, enfermedades de alto impacto en la salud mundial.
Building Your Strength Against Cancer - Iron: The Double-Edged Sword
Iron encourages the formation of cancer-causing free radicals. Of course, the body needs a certain amount of iron for healthy blood cells. But beyond this rather small amount, iron becomes a dangerous substance, acting as a catalyst for the formation of free radicals. Because of this, research studies have shown that higher amounts of iron in the blood mean higher cancer risk.23
Once iron is absorbed by the digestive tract, the body stores it. Most of us accumulate much more iron than we need. In spite of the advertising from iron supplement manufacturers, "iron overload" is much more common in America than iron deficiency. The reason is the daily diet of red meats, which contributes much more iron than most people can safely handle over the long run. A diet of grains, vegetables, fruits, and beans provides adequate iron, without the risk of overload.
It is easy to check whether your body has accumulated too much stored iron. The following set of tests will check for both iron deficiency and iron overload. The more general hemoglobin and hematocrit tests are not sufficient. Although general guidelines are given here, the tests should be interpreted by your doctor:
Doctors divide the serum-iron value by the TIBC. The result should be 16 to 50 percent for women and 16 to 62 percent for men. Results above these norms indicate excess iron. Results below these norms indicate iron deficiency. A further test sometimes used to check for iron deficiency is the red cell protoporphyrin test. A result greater than 70 units is considered abnormal. If two of these three values (serum ferritin, serum iron/TIBC, and red cell protoporphyrin) are normal, iron-deficiency anemia is not likely. Serum iron and TIBC should be measured after fasting overnight.
- Serum ferritin (normal values are 12-200 mcg/l of serum)
- Serum iron
- Total iron binding capacity (TIBC)
Unfortunately, the body has no way to rid itself of excess iron. Believe it or not, the only way to predictably reduce excessive iron stores is by donating blood. So this altruistic act can have health benefits for the donor as well.
Fuente: The Cancer Porject
Cancer Project / Iron: The Double-Edged Sword
Iron, zinc, and alcohol consumption and mortality from cardiovascular diseases: the Iowa Women's Health Study1,2,3
Duk-Hee Lee, Aaron R Folsom and David R Jacobs, Jr
Background: The relation between iron status and atherosclerosis has long been a topic of debate.
Objective: We examined associations of cardiovascular disease (CVD) mortality with dietary intakes of iron (a possible prooxidant), zinc (a possible antioxidant), and alcohol (a disruptor of iron homeostasis).
Design: Postmenopausal women (n = 34 492) aged 55–69 y at baseline, who completed a food-frequency questionnaire, were followed for CVD mortality over 15 y.
Results: Among women who consumed 10 g alcohol/d, after adjustment for CVD risk factors in a model that contained dietary heme iron, nonheme iron, and zinc intakes, dietary heme iron showed a positive association, dietary nonheme iron showed a U-shaped association, and dietary zinc showed an inverse association with CVD mortality. For example, the relative risks (RRs) for categories of dietary heme iron were 1.0, 1.46, 1.52, 1.73, and 2.47 (P for trend = 0.04); corresponding RRs for dietary nonheme iron were 1.0, 0.93, 0.63, 0.83, and 1.20 (P for quadratic term = 0.02). The corresponding RRs for dietary zinc were 1.0, 0.61, 0.59, 0.57, and 0.37 (P for trend = 0.07). In an analysis restricted to those who consumed 30 g alcohol/d, the risk gradients strengthened.
Conclusions: Our results suggest that a higher intake of heme iron might be harmful, whereas a higher intake of zinc might be beneficial in relation to CVD mortality in the presence of a trigger that can disturb iron homeostasis, such as alcohol consumption.
Conclusiones: Nuestros resultados sugieren que una gran consumo de hierro hemínico podría ser perdjudicial , mientras que alto consumo de zinc podría ser benefico en relación a la muerte por enfermedades cardiovasculares , en presencia de un detonador que altere la homeostasis del hierro, como es el consumo del alcohol.
[The role of iron in neoplasms]
[Article in Croatian]
Zavod za molekularnu medicinu, Institut Ruder Bosković, Bijenicka cesta 54, 10001 Zagreb.
The purpose of this review is to concisely summarize the current knowledge of iron participation in the carcinogenic process, especially from the standpoint of redox regulation, and to introduce a hypothesis for the mechanism. In both animals and humans, primary neoplasms develop more frequently at body sites of excessive iron deposits. Iron exerts its carcinogenic effects by catalysing formation of hydroxil radicals, suppressing activity of host defence cells and promoting cancer cell multiplication. Manipulations of cellular iron metabolism for modulating normal and malignant cell proliferation is described. Quantitative evaluation of body iron and iron-withholding proteins has prognostic value in cancer patients. Procedures associated with lowering host iron intake and inducing host cell iron efflux can assist in prevention and management of neoplastic disease.
Traducción: En ambos, animals y humanos, neoplasmas primarios se desarrollan mas frecuentemente en lugares del cuerpo donde existen depositos altos de hierro. El hierro ejerce los efectos cancerígenos al catalizar (acelerar) la formación de radicales hidroxilo , supresión de las células defensivas y promoviendo la multiplicación de células cancerígenas. La evaluación cuantitativa de la cantidad de hierro en el organismo, y de proteinas contenedoras de hierro, tiene valor pronóstico para el cáncer. Procedimientos asociados a la baja del consumo de hierro e induciendo a la eliminación del hierro corporal pueden asistir en la prevención y manejo del cáncer.
Decreased Cancer Risk After Iron Reduction in Patients With Peripheral Arterial Disease: Results From a Randomized Trial
Leo R. Zacharski, Bruce K. Chow, Paula S. Howes, Galina Shamayeva, John A. Baron, Ronald L. Dalman, David J. Malenka, C. Keith Ozaki, Philip W. Lavori
Background: Excess iron has been implicated in cancer risk through increased iron-catalyzed free radical–mediated oxidative stress.
Methods: A multicenter randomized, controlled, single-blinded clinical trial (VA Cooperative Study #410) tested the hypothesis that reducing iron stores by phlebotomy would influence vascular outcomes in patients with peripheral arterial disease. Patients without a visceral malignancy in the last 5 years (n = 1277) were randomly assigned to control (n = 641) or iron reduction (n = 636). Occurrence of new visceral malignancy and cause-specific mortality data were collected prospectively. Cancer and mortality outcomes in the two arms were compared using intent-to-treat analysis with a Cox proportional hazards regression model. Statistical tests were two-sided.
Results: Patients were followed up for an average of 4.5 years. Ferritin levels were similar in both groups at baseline but were lower in iron reduction patients than control patients across all 6-month visits (mean = 79.7 ng/mL, 95% confidence interval [CI] = 73.8 to 85.5 ng/mL vs 122.5 ng/mL, 95% CI = 115.5 to 129.5 ng/mL; P < .001). Risk of new visceral malignancy was lower in the iron reduction group than in the control group (38 vs 60, hazard ratio [HR] = 0.65, 95% CI = 0.43 to 0.97; P = .036), and, among patients with new cancers, those in the iron reduction group had lower cancer-specific and all-cause mortality (HR = 0.39, 95% CI = 0.21 to 0.72; P = .003; and HR = 0.49, 95% CI = 0.29 to 0.83; P = .009, respectively) than those in the control group. Mean ferritin levels across all 6-monthly visits were similar in patients in the iron reduction and control groups who developed cancer but were lower among all patients who did not develop cancer than among those who did (76.4 ng/mL, 95% CI = 71.4 to 81.4 ng/mL, vs 127.1 ng/mL, 95% CI = 71.2 to 183.0 ng/mL; P = .017).
Conclusions: Iron reduction was associated with lower cancer risk and mortality. Further studies are needed to define the role of body iron in cancer risk.
Conclusiones: la reducción coroporal del hierro, fue asociada con bajos riesgos de desarrollo de cáncer y muerte por cáncer. Mas estudios son necesarios para definir el rol del hiero en el riesgo del cáncer.