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Foro/ Carreras de la Salud/ Nutrición/

El hierro como factor generador de enfermedades

El hierro como factor generador de enfermedades

  1. Avatar de krisnesh
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    #1
    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:
    • Serum ferritin (normal values are 12-200 mcg/l of serum)
    • Serum iron
    • Total iron binding capacity (TIBC)
    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.
    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]


    Poljak-Blazi M.
    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.
    Editado por Ragamuffin en 11-Oct-2008 a las 04:17 PM
  2. Avatar de krisnesh
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    Iron: the Redox-active center of oxidative stress in Alzheimer disease.

    Castellani RJ, Moreira PI, Liu G, Dobson J, Perry G, Smith MA, Zhu X.
    Department of Pathology, University of Maryland, Baltimore, MD, USA.
    Although iron is essential in maintaining the function of the central nervous system, it is a potent source of reactive oxygen species. Excessive iron accumulation occurs in many neurodegenerative diseases including Alzheimer disease (AD), Parkinson's disease, and Creutzfeldt-Jakob disease, raising the possibility that oxidative stress is intimately involved in the neurodegenerative process. AD in particular is associated with accumulation of numerous markers of oxidative stress; moreover, oxidative stress has been shown to precede hallmark neuropathological lesions early in the disease process, and such lesions, once present, further accumulate iron, among other markers of oxidative stress. In this review, we discuss the role of iron in the progression of AD.
    PMID: 17508283 [PubMed - indexed for MEDLINE]



    Traducción
    A pesar de que el hierro es esencial en mantener la función del sistema nervioso central, es una fuente potencial de formación de especies reactivas de oxígeno. La acumulación excesiva de hierro ocurre en muchas enfermedades neurodegenerativas incluyendo la Enfermedad de Alzheimer, la enfermedad de Parkinson, y la enfermedad de Creutzfedt Jacob, incrementando la posibilidad de que el estrés oxidativo sea participativo en el proceso de neurodegeneración. El Alzheimer en particular, está asociado con numerosos marcadores de estrés oxidativo. Aun mas, el estrés oxidativo se ha visto que ocurre antes de las lesiones neuropatologicas características, y esas lesiones , una vez presentes , comienzan a acumular hierro, entre otros marcadores de estrés oxidativo.





    Role of Iron in progressive renal disease

    SHAH Sudhir V. (1)

    (1) Department of Medicine, Division of Nephrology, University of Arkansas for Medical Sciences and Central Arkansas Veterans Healthcare System, Little Rock, AR, ETATS-UNIS

    Résumé / Abstract

    ○ The Importance of iron in renal injury is derived from the ease with which iron is reversibly oxidized or reduced, enabling it to participate in the production of free radicals. Experimental evidence for the role of oxidants and iron in progressive renal disease falls into two broad categories. First, considerable data implicate oxidants in the proteinuria of glomerular disease. To the extent that proteinuria is an Important determinant of progression, reduction of proteinuria would result in retardation of progression. Evidence also suggests a role of oxidants and iron in diabetic nephropathy, a major cause of end-stage kidney disease. Second, more direct studies have examined the role of oxidants and iron in models of progressive renal disease. These studies include the demonstration of increased iron in the kidney in models of progressive kidney disease; enhanced generation of oxidants, providing a mechanism by which iron can be mobilized; and more direct evidence of the beneficial effect of iron-deficient diets and Iron chelators. Although the collective Information on the role of oxidants and iron derived from in vitro studies and animal models of glomerular disease and progressive renal failure is impressive, control studies of patients are needed to show the efficacy of antioxidants and/or iron chelators in retarding the progression of renal failure and may offer an important therapeutic modality to patients with renal disease.





    Revue / Journal Title

    American journal of kidney diseases ISSN 0272-6386

    Oxidants and iron in chronic kidney disease

    Author: Shah, Sudhir V.
    Source: Kidney International, Volume 66, Supplement 91, October 2004 , pp. S50-S55(1)



    Abstract:
    Oxidants and iron in chronic kidney disease. 
    Oxidants derived either from leukocytes in proliferative glomerular nephritis or from resident glomerular cells in nonproliferative glomerulonephritis have been shown to have several biologic effects relevant to chronic kidney disease. These include: the ability of oxidants to damage glomerular basement membrane (GBM) and to directly induce proteinuria; effects that would lead to a fall in the glomerular filtration rate; and effects that would account for the morphologic changes observed in chronic kidney disease. In experimental models the role of oxidants has been demonstrated in both proliferative glomerulonephritis (e.g., anti-GBM antibody disease) as well as experimental models of minimal change disease and membranous nephropathy. Oxidants have also been shown to be an important mediator of the various pathways that have been implicated in diabetic nephropathy. Antioxidants and iron chelators have also been shown to retard functional and morphologic changes observed in progressive kidney disease. Taken together, these experimental studies suggest an important role of oxidants in chronic kidney disease.



    Macrophage Iron, Hepcidin, and Atherosclerotic Plaque Stability

    Jerome l. Sullivan1,2

    Department of Pathology, Immunology, and Laboratory Medicine, University of Florida, College of Medicine, Gainesville, Florida 32610
    To whom requests for reprints should be addressed at 1 4475 Old Bear Run, Winter Park, FL 32792. E-mail: jlsullivan3@gmail.com

    Hepcidin has emerged as the key hormone in the regulation of iron balance and recycling. Elevated levels increase iron in macrophages and inhibit gastrointestinal iron uptake. The physiology of hepcidin suggests an additional mechanism by which iron depletion could protect against atherosclerotic lesion progression. Without hepcidin, macrophages retain less iron. Very low hepcidin levels occur in iron deficiency anemia and also in homozygous hemochromatosis. There is defective retention of iron in macrophages in hemochromatosis and also evidently no increase in atherosclerosis in this disorder. In normal subjects with intact hepcidin responses, atherosclerotic plaque has been reported to have roughly an order of magnitude higher iron concentration than that in healthy arterial wall. Hepcidin may promote plaque destabilization by preventing iron mobilization from macrophages within atherosclerotic lesions; the absence of this mobilization may result in increased cellular iron loads, lipid peroxidation, and progression to foam cells. Marked downregulation of hepcidin (e.g., by induction of iron deficiency anemia) could accelerate iron loss from intralesional macrophages. It is proposed that the minimally proatherogenic level of hepcidin is near the low levels associated with iron deficiency anemia or homozygous hemochromatosis. Induced iron deficiency anemia intensely mobilizes macrophage iron throughout the body to support erythropoiesis. Macrophage iron in the interior of atherosclerotic plaques is not exempt from this process. Decreases in both intralesional iron and lesion size by systemic iron reduction have been shown in animal studies. It remains to be confirmed in humans that a period of systemic iron depletion can decrease lesion size and increase lesion stability as demonstrated in animal studies. The proposed effects of hepcidin and iron in plaque progression offer an explanation of the paradox of no increase in atherosclerosis in patients with hemochromatosis despite a key role of iron in atherogenesis in normal subjects.

    Traducción

    La hepcidina emergió como una hormona clave en la regulación del balance de hierro y su reciclado. Elevados niveles de hepcidina incrementan los niveles de hierro en macrofagos e inhibe la absorción intestinal de hierro. La fisiología de la hepcidina sugiere un mecanismo adicional, por el cual , la depleción de hierro podría actuar como mecanismo protectivo contra la progresión de las lesiones arteriosecleroticas.
    Sin hepcidina , los macrofagos retienen menos hierro. Un muy bajo nivel de hepcidina ocurre en la anemia ferropenica (anemia por deficiencia de hierro) y también en hemocromatosis homocigota. Existe una defectiva retención de hierro por parte de los macrofagos y un freno en el desarrollo de arteriosclerosis en la hemocromatosis. En sujetos normales con respuestas intactas de la hepcidina, las placas arterioscleróticas se ha reportado que tienen aproximadamente de 10 veces mas de hierro que las paredes de arterias sanas. La hepcidina puede promover el deterioro de la placa al prevenir la movilización del hierro desde los macrofagos de las placas ateromatosas. La no movilización puede resultar en un incremento celular de hierro, peroxidación lipidica , y la progresión a celulas espumosas (aclaración: dentro de las placas ateromatosas los monocitos como los macrofagos incorporan grandes cantidades de lípidos, y estos últimos se los llama células espumosas)
    El descenso de hepcidina (por ej, inducido por una anemia por deficiencia de hierro – anemia ferropénica) puede acelerar la pérdida de hierro (movilización ) desde los macrofagos que estan dentro de la lesion ateromatosa. Se ha propuesto que la actividad mínima de pro aterogenicidad de la hepcidina corresponde a sus niveles bajos, asociados con la anemia ferropenica o la hemocromatosis homocigota.
    Anamia por deficiencia de hierro inducida, intensamente moviliza el hierro de los macrofagos en todo el cuerpo para mantener la eritropoyesis. El hierro de los macrofago que están dentro de las placas ateromatosas también es movilizado.
    En estudios en animales se ha observado la disminución del hierro dentro de la placa ateromatosa, como el tamaño de la placa, por disminución del hierro sistémico. Queda por confirmar en humanos el periodo de depleción sistemica de hierro que pueda disminuir el tamañó de la placa e incrementar la estabilidad de la lesión , como se demostró en estudios en animales.
    Los efectos que se sugieren de la hepcidina y del hierro en la progresión de la placa ateromatosa, ofrecen una explicación de la paradoja del no incremento de la arteriosclerosis en pacientes con hemocromatosis, a pesar del importante rol del hierro en la aterogenesis en pacientes normales.
    Editado por LuMi en 23-Nov-2008 a las 11:13 AM
  3. Avatar de krisnesh
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    Heme and non-heme iron consumption and risk of gallstone disease in men

    Chung-Jyi Tsai, Michael F Leitzmann, Walter C Willett and Edward L Giovannucci

    1 From the Division of Digestive Diseases and Nutrition, University of Kentucky Medical Center, Lexington, Kentucky (C-JT); the Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (C-JT, WCW, and ELG); the Departments of Nutrition and Epidemiology, Harvard School of Public Health, Boston, MA (WCW and ELG); and the Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD (MFL)
    2 Supported by research grants (CA55075 and DK46200) from the National Institutes of Health.
    3 Reprints not available. Address correspondence to C-J Tsai, Division of Digestive Diseases and Nutrition, University of Kentucky Medical Center, 800 Rose Street, Lexington, Kentucky 40536-0298. E-mail: hpcjt@channing.harvard.edu .



    Background:Excessive iron intake can promote biliary cholesterol crystal formation in experimental studies. The absorption of heme iron is more complete than that of non-heme iron in humans; however, the effect of long-term consumption of heme and non-heme iron on the risk of gallstones is unknown.
    Objective:The objective of the study was to examine long-term iron intake in relation to the occurrence of gallstone disease.
    Design:We prospectively studied intakes of heme and non-heme iron and the risk of gallstone disease in a cohort of 44 758 US men from 1986 to 2002. Iron consumption was assessed by using a validated semiquantitative food-frequency questionnaire. Newly diagnosed gallstone disease was ascertained biennially.
    Results:We documented 2468 incident cases of symptomatic gallstones during 597 699 person-years of follow-up. The age-adjusted relative risks (RRs) for men with intakes of heme iron and non-heme iron, when the highest and lowest quintiles were compared, were 1.21 (95% CI: 1.06, 1.37; P for trend = 0.0008) and 1.02 (95% CI: 0.90, 1.16; P for trend = 0.45), respectively. After adjustment for multiple potential confounding variables, when extreme quintiles were compared, the multivariate RR of heme iron intake was not significantly changed and remained significant with a dose-response relation (RR = 1.21; 95% CI: 1.03, 1.42; P for trend = 0.01), and that of non-heme iron intake was not significant (RR = 1.14; 95% CI: 0.99, 1.31; P for trend = 0.18). Conclusion:Our findings suggest that a higher consumption of heme iron is associated with a greater risk of gallstone disease among men.

    Conclusiones: Nuestros hallazgos sugieren que un elevado consumo de hierro está asociado con un muy elevado riesgo de cálculos biliares entre hombres.



    Gallstone disease is very common in Western countries and increasingly is a major cause of abdominal morbidity (1). Approximately 80% of gallstones in Western populations are cholesterol stones (2). Many factors have been associated with the risk of cholesterol gallstones, but cholesterol-saturated bile is an important determinant of gallstone formation (2). High plasma triacylglycerol concentrations are associated with a greater risk of cholesterol gallstones (2).

    The human body has a considerable capacity to store iron, but there is no regulated iron excretion in dietary iron overload (3). Homeostatic mechanisms increase iron absorption from the intestine in iron deficiency, but its down-regulation in high intakes of iron, particularly intakes of heme iron, is insufficient to prevent the accumulation of high iron stores (3, 4). Iron is the most abundant transition metal in the body because of its roles in oxygen binding and electron transport (5, 6). During adulthood, iron stores gradually increase almost linearly with age in men (3, 7). Dietary iron overload in adults may be of concern in the United States (8). Elevated iron stores, aside from primary and secondary pathologic forms of iron overload, may be harmful because of their associations with several chronic diseases, including the metabolic syndrome (9-13).
    In experimental studies, a high iron diet can elevate plasma triacylglycerol concentrations (14). Iron is a prooxidant prone to produce reactive oxygen metabolites that may promote cholesterol crystal formation in the bile (15). The relation between iron intake and the molar percent cholesterol concentration in the bile in human and animal studies, however, is mixed (16, 17). The effect of long-term iron consumption on the incidence of gallstones in humans is unknown. In a large cohort of US men, we examined long-term iron intake in relation to the occurrence of gallstone disease.





    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
    J Natl Cancer Inst. 2008;100(14):996-1002. ©2008 Oxford University Press
    Posted 09/15/2008

    Abstract and Introduction

    Abstract

    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.
    Introduction

    Body iron stores accumulate imperceptibly with aging because intake exceeds loss and no biologic mechanism exists for excretion of iron in excess of physiological requirements.[1] Iron accumulation has been implicated in the risk of several chronic diseases, including cardiovascular disease and cancer, through increased iron-catalyzed free radical-mediated oxidative stress.[1-9] Clinical cohort studies have found that measures of body iron stores or dietary iron intake may be associated with increased risk of cancer and cancer mortality.[9-14] Colorectal cancer has received particular attention in this regard.[6,11] Cancer risk rises after menopause in women[5,12] in association with rising iron stores.[1] A cause-and-effect relationship between levels of iron stores and cancer risk is suggested by studies showing that blood donation (which reduces body iron) is associated with lower cancer risk[13,14] and that blood transfusion (delivery of an iron load) adversely affects cancer outcome.[15,16] Kato et al. [17] reported a cohort of patients with hepatitis C who were treated with iron reduction and followed for 12 years. These patients had a statistically significantly lower risk of developing hepatocellular carcinoma compared with a demographically similar cohort not treated with iron reduction. Although studies in animal models suggest that limitation or removal of iron may prevent cancer occurrence and growth,[18-20] no such data exist for malignancy in humans.
    A randomized trial of calibrated phlebotomy was conducted in patients with advanced peripheral arterial disease.[21-24] Although this clinical trial was designed as a cardiovascular disease study, it provided a setting for controlled, prospective collection of data on risk of new malignancy. The occurrence of new visceral malignancy according to histological type and organ of origin and death according to cause was determined in this cohort of patients, who had no clinical evidence of visceral malignancy within the preceding 5 years.
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    Dietary and stored iron as predictors of breast cancer risk: A nested case-control study in Shanghai.

    Moore AB, Shannon J, Chen C, Lampe JW, Ray RM, Lewis SK, Lin M, Stalsberg H, Thomas DB.
    Department of Public Health and Preventive Medicine, Oregon Health and Sciences University, Portland, OR.
    Increases in risk of breast cancer in successive generations of migrants to the United States from China and rapid temporal changes in incidence rates in China following social and economic changes clearly implicate environmental factors in the etiology of this disease. Case-control and cohort studies have provided evidence that at least some of these factors may be dietary. Iron, an essential element necessary for cell function, has also been demonstrated to have potential carcinogenic and co-carcinogenic activities. Iron overload, which was previously uncommon, has become more common in the United States than iron deficiency and may be increasing in China concurrently with dramatic increases in meat consumption. A case-control study nested in a cohort of women in Shanghai, China, was conducted to evaluate possible associations between risk of proliferative and nonproliferative fibrocystic changes as well as breast cancer and dietary iron intake and plasma ferritin levels. Plasma ferritin levels and reported dietary iron intake were compared in 346 women with fibrocystic changes, 248 breast cancer cases and 1,040 controls. Increasing ferritin levels were significantly associated with increasing risk of nonproliferative fibrocystic changes (OR: 2.51, 95% CI: 1.16-5.45, p trend = 0.04). Similar, but weaker, trends were observed for proliferative changes and for breast cancer. Risk of breast cancer relative to the risk of fibrocystic changes was associated with dietary iron intake in women with nonproliferative fibrocystic changes (OR: 2.63, 95% CI: 1.04-6.68, p = 0.02). In conclusion, this study finds significant associations between iron (stored and dietary) and fibrocystic disease and breast cancer.

    (c) 2009 UICC.



    La conclusión de este estudio es que existe asociación significativa entre el hierro en depósitos y el dietario y el desarrollo de enfermedades fibrocísictica y cáncer de mama.
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    Iron toxicity in diseases of aging: Alzheimer's disease, Parkinson's disease and atherosclerosis.

    Altamura S, Muckenthaler MU.
    Department of Pediatric Oncology, Haematology and Immunology, University Hospital of Heidelberg, Molecular Medicine Partnership Unit, Heidelberg, Germany.
    Excess free iron generates oxidative stress that hallmarks diseases of aging. The observation that patients with Alzheimer's disease or Parkinson's disease show a dramatic increase in their brain iron content has opened the possibility that disturbances in brain iron homeostasis may contribute to the pathogenesis of these disorders. While the reason for iron accumulation is unknown, iron localization correlates with the production of reactive oxygen species in those areas of the brain that are prone to neurodegeneration. A role for iron is also proposed in atherosclerosis, a further frequent disorder of aging. We will review experimental evidences for an involvement of iron in these diseases and discuss some mouse models with impairment in iron-related genes that may be useful to study the role of iron in these disorders.
  6. Avatar de krisnesh
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    Una nueva investigación asocia más directamente al hierro acumulado en el cerebro y el desarrollo del Alzhemier...


    Increased Iron and Free Radical Generation in Preclinical Alzheimer Disease and Mild Cognitive Impairment
    Mark A. Smith,a Xiongwei Zhu,a Massimo Tabaton,b Gang Liu,c Daniel W. McKeel, Jr.,d Mark L. Cohen,a Xinglong Wang,a Sandra L. Siedlak,a Takaaki Hayashi,e Masao Nakamura,f Akihiko Nunomura,g and George Perryah
    aDepartment of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
    bDepartment of Neuroscience, Ophthalmology, and Genetics, University of Genoa, Genoa, Italy
    cDepartment of Radiology, University of Utah, Salt Lake City, Utah, USA
    dDepartments of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri, USA
    eHokkaido Institute of Public Health, Kita 19, Nishi 12, Kita-ku, Sapporo, Japan
    fDepartment of Chemistry, Asahikawa Medical College, Asahikawa, Japan
    gDepartment of Neuropsychiatry, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo, Yamanashi, Japan
    hUTSA Neurosciences Institute and Department of Biology, College of Sciences, University of Texas at San Antonio, San Antonio, Texas, USA
    Correspondence to: Mark A. Smith, Ph.D., Department of Pathology, Case Western Reserve University, 2103 Cornell Road, Cleveland, Ohio 44106 USA; Tel: 216-368-3670, Fax: 216-368-8964, Email: mark.smith@case.edu


    Abstract

    It is now established that oxidative stress is one of the earliest, if not the earliest, change that occurs in the pathogenesis of Alzheimer's disease (AD). Consistent with this, mild cognitive impairment (MCI), the clinical precursor of AD, is also characterized by elevations in oxidative stress. Since such stress does not operate in vacuo, in this study we sought to determine whether redox-active iron, a potent source of free radicals, was elevated in MCI and preclinical AD as compared to cognitively-intact age-matched control patients. Increased iron was found at the highest levels both in the cortex and cerebellum from the pre-clinical AD/MCI cases. Interestingly, glial accumulations of redox-active iron in the cerebellum were also evident in preclinical AD patients and tend to increase as patients became progressively cognitively impaired. Our findings suggests that an imbalance in iron homeostasis is a precursor to the neurodegenerative processes leading to AD and that iron imbalance is not necessarily unique to affected regions. In fact, an understanding of iron deposition in other regions of the brain may provide insights into neuroprotective strategies. Iron deposition at the preclinical stage of AD may be useful as a diagnostic tool, using iron imaging methods, as well as a potential therapeutic target, through metal ion chelators.


    los que quiern leer el paper entero, este es link


    Increased Iron and Free Radical Generation in Preclinical Alzheimer Disease and Mild Cognitive Impairment
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