hemochromatosis
Definicion:
Hereditary hemochromatosis (he-moe-kroe-muh-TOE-sis) causes your body to absorb too much iron from the food you eat. The excess iron is stored in your organs, especially your liver, heart and pancreas. The excess iron can poison these organs, leading to life-threatening conditions such as cancer, heart arrhythmias and cirrhosis.
Many people inherit the faulty genes that cause hemochromatosis — it is the most common genetic disease in Caucasians. But only a minority of those with the genes develop serious problems. Hemochromatosis is more likely to be serious in men.
Signs and symptoms of hereditary hemochromatosis usually appear in midlife. Iron can be dropped to safe levels by regularly removing blood from your body.
Vamos que cuando me miro al espejo me veo de acero puro.. y motivos no me faltan!
Tengo una rarisima combinacion genetica que me llevara a tener hemochromatosis al menos leve… un familiar directo murio de cirrosis que es una de las consecuencias y toda su vida estuvo amarillo, y yo llevo anios con lecturas altas y no han conseguido encontrar el motivo.
En este hilo comentare la dieta baja en hierro y los alimentos que evitan la absorcion del hierro.. aun asi es probable que en algun momento tenga que tener tratamientos de limpieza del hierro sobrante en mi sangre.
Es bueno saberlo… gracias a los analisis geneticos!
Otro motivo mas para seguir con el te verde y el turmeric (suplementos-vitaminas-f114/turmeric-curcumin-t1489-20.html):
Certain phenolic-rich herbs and spices, such as green tea and rosemary, can reduce iron absorption4
The primary polyphenol in turmeric known as curcumin actually acts as an iron chelator, and in mice studies, diets supplemented with this spice extract exhibited a decline in levels of ferritin in the liver
Astaxanthin, which has been researched to have over 100 potential health benefits, has been shown to reduce iron-induced oxidative damage (http://www.huffingtonpost.com/suzy-cohe … 50910.html), lo que nos lleva a las maravillas de comer salmon! (suplementos-vitaminas-f114/pescado-azul-mercurio-t1499-20.html)
Segun Mayo Clinic:
You may reduce your risk of complications from hemochromatosis if you:
Avoid iron supplements and multivitamins containing iron. These can increase your iron levels even more.
Avoid vitamin C supplements, especially with food. Vitamin C increases absorption of iron. Try to drink vitamin C-rich juices, such as orange juice, between meals.
Avoid alcohol. Alcohol increases the risk of liver damage. If you have liver disease and hereditary hemochromatosis, avoid alcohol completely.
Avoid eating raw shellfish. People with hereditary hemochromatosis are susceptible to infections, especially those caused by certain bacteria in raw shellfish.
Drink tea. Some evidence suggests that drinking tannin-rich tea may slow the storage of iron.
Al parecer Curcumin, Te verde, Quercetina, Granada, ALA, ALCAR y Cardo (Milk Thistle) son utilies para eliminar hierro.
http://www.lef.org/magazine/mag2012/mar … ion_01.htm
Too much iron accelerates mitochondrial decay and inflicts system-wide free radical damage to healthy tissues. Age-related iron overload is a known contributor to multiple degenerative diseases, including liver fibrosis, heart attack, and cancer.
Iron accumulation is often a consequence of aging. In the laboratory, total iron content has been shown to increase exponentially as cells age, resulting in 10-fold higher levels of iron compared to young cells.
Results of a groundbreaking UCLA study published late last year conclusively linking excess iron accumulation in brain tissue to neurodegenerative brain disorders like Alzheimer’s and Parkinson’s.
Experts now typically recommend that older adults limit their intake of red meat, which is our major natural dietary source of iron.
A number of nutrients can help reduce your body’s total exposure to iron through chelation (binding to free iron atoms) and antioxidant activity, including quercetin, curcumin, R-lipoic acid, and silymarin.
Curcuma para quitarle hierro al asunto! Ojo que para otros puede suponer una deficiencia de hierro. http://www.sciencedirect.com/science/ar … 1714000330
Curcumin supplementation reduces iron stores in the liver and spleen but does not affect zinc and copper content in either tissue.
A 6 month dietary supplementation with 0.2% curcumin in C57BL/6J mice led to a significant reduction in iron, but not zinc and copper stores, in the liver and the spleen, and suppressed liver hepcidin and ferritin expression. Furthermore, the expression of the iron-importing transport proteins divalent metal transporter (DMT) 1 and transferrin receptor (TfR) 1 was induced in the curcumin-fed mice. These data suggest that long-term curcumin supplementation and a Western-type diet may aggravate iron deficiency.
One small study found that drinking a cup of coffee while eating lowered the amount of nonheme iron absorbed from the meal by 39 percent; a cup of tea reduced absorption by 64 percent. Red wine also appears to have a potent iron-blocking effect, based on other research. But the beverages don’t appear to block absorption of the other main type of iron, heme iron, which is found in meat.
Pollo y cerdo como carnes… otras carnes de firma excepcional y con un un cafecito y/o te!
A 1982 human study was conducted to assess the effect of various drinks on iron absorption. A subject ate a standard meal of a hamburger, string beans, mashed potatoes and water. When green tea was drunk instead of water, iron absorption was reduced by 62 percent. Coffee reduced iron absorption by 35 percent, whereas orange juice (as a source of vitamin C) increased absorption by 85 percent. Contrary to other studies, milk and beer had no significant effect.
Seguiremos con el te verde! (alimentos-saludables-f112/verde-t1215.html)
Bioflavonoids (found in berries, coffee, green tea, pine bark, quercetin and the rind of citrus fruits, particularly blueberry, cranberry, elderberry and grape seed) and phytic acid (a component of whole grains and seeds such as sesame) bind to iron and other minerals in the gastric tract and help to limit iron availability
Lactoferrin. Lactoferrin is an iron-binding protein analogous to the iron transporter transferrin; it binds and sequesters iron in areas outside of the bloodstream such as the mucous membranes, gastrointestinal tract, and reproductive tissues (Jiang 2011). It is present at high concentrations in milk, and is secreted by immune cells (neutrophils) as an antibacterial compound at sites of infection or inflammation (Paesano 2009; Brock 2012).
The antimicrobial effects of lactoferrin are attributed to its ability to deprive pathogenic microorganisms of the iron needed for growth (Brock 2012). Experiments also suggest lactoferrin may have antioxidant and anti-inflammatory properties, and may influence the expression of inflammatory genes (Scarino 2007; Paesano 2009; Mulder 2008). Evidence suggests low-iron apolactoferrin may be protective against iron-mediated free radical damage; it reduced iron-catalyzed formation of hydroxyl radicals in vitro (Baldwin 1984).
Polyphenols. Polyphenols such as chlorogenic acid (Kono 1998), quercetin, rutin, chrysin (Guo 2007), punicalagins (from pomegranate) (Kulkarni 2007), and proanthocyanidins (from cranberry) have been shown to bind iron in vitro (Lin 2011). In an in vitro binding study of 26 flavonoids (a type of polyphenol) isolated from a variety of sources (including tea catechins, hesperidin, naringenin, and diosmin), several were nearly as effective as desferoxamine at chelating ferrous iron when supplied at a 10:1 flavonoid/iron ratio. When supplied at a 1:1 ratio, quercetin, myrcetin, and baicalein (a flavonoid from skullcap) continued to chelate iron with the same efficiency as desferoxamine (Mladěnka 2011). As antioxidants, polyphenols may also reduce iron-catalyzed free-radical generation (Minakata 2011).
In a mouse model of iron overload (over 2,000 mg iron/g of liver weight), both quercetin and baicalin (fed as 1% of water, which is roughly equivalent to 15 grams for a 70 kg human) reduced iron-induced lipid peroxidation and protein oxidation in the liver, decreased liver iron stores as well as serum ferritin, and increased fecal excretion of iron (Zhang 2006). Clinical studies are necessary to confirm polyphenol’s effect(s) in humans.
Pectin. Pectin is an indigestible fiber that binds tightly to non-heme iron, thus interfering with its absorption. In a small study of 13 patients with idiopathic hemochromatosis (conducted before the genetics of hemochromatosis had been discovered), iron absorption decreased by nearly half following a loading dose of 9 grams/m2 of pectin (about 15 grams for the average adult). Cellulose fiber had no effect on iron binding (Monnier 1980).
Milk Thistle. Milk thistle and its flavonoid constituent (i.e., silymarin) have iron chelation and hydroxyl radial quenching properties (Borsari 2001; Abenavoli 2010). In HFE hemochromatosis patients, 140 mg of silybin (the main component of silymarin) taken with a test meal containing about 14 mg of non-heme iron reduced iron absorption by over 40% (Hutchinson 2010). When combined with soy phosphatidylcholine, silybin treatment for 12 weeks demonstrated a modest (13%) reduction in serum ferritin (indicative of reduced total body iron stores) in patients with chronic hepatitis C (Bares 2008). When combined with the injectable iron chelator desferoxamine, silymarin resulted in more effective reductions in serum ferritin than desferoxamine alone in patients with β-thalassemia (Gharagozloo 2009).
Curcumin. Curcuminoids, which are derived from the spice turmeric, are antioxidants and iron chelators. In experimental models, they have been shown to reduce iron-catalyzed oxidative damage of DNA (García 2012), liver damage associated with iron-associated lipid peroxidation (Reddy 1996), and free-radical damage due to iron in amyloid plaques characteristic of Alzheimer’s disease (Atamna 2006). In β-thalassemic mice, curcumin bound iron in the blood reduced cardiac iron deposits in mice fed a high-iron diet (Thephinlap 2011), and reduced iron-associated lipid peroxidation when combined with the IV chelator deferiprone (Thephinlap 2009). The iron chelation effects of curcumin in the liver depend upon total iron intake. At low dietary iron concentrations, curcumin demonstrated a significant reduction in transferrin saturation and plasma iron in mice given curcumin as 2% of their diet (Jiao 2009). Mice on high iron diets, however, saw significant decreases in liver ferritin (indicative of a decrease in iron storage capacity), but no changes in total plasma iron or transferrin saturation when given curcumin as 2% of their diet (Jiao 2006; Jiao 2009).
Green tea. Green tea catechins are potent antioxidants that demonstrate an iron chelating activity similar to the injectable chelator desferoxamine in test tube studies (Mandel 2006). The addition of green tea extract with a high epigallocatechin gallate (EGCG) content to blood samples from β-thalassemia patients rapidly chelated non-transferrin bound iron, and modestly reduced markers of lipid peroxidation (Srichairatanakool 2006). The ability of green tea catechins to cross the blood-brain barrier implicates them as possible agents for the chelation of abnormal iron deposits characteristic of several neurodegenerative disorders (Mandel 2006). Studies examining the effect(s) of green tea consumption on iron status in humans are conflicting. Several studies have shown no association between tea consumption and iron absorption, serum ferritin, or hemoglobin levels in individuals with adequate iron intake (Mennen 2007; Temme 2002; Cheng 2009). However, two studies did show reductions in serum ferritin and iron absorption with high consumption levels of green tea (Imai 1995) and green tea extract (Samman 2001) respectively.
Alpha lipoic acid. Alpha lipoic acid is an important antioxidant and enzyme co-factor. In cell culture, alpha-lipoic acid (in its reduced form, dihydrolipoic acid) protects neurons against oxidative damage catalyzed by iron or Alzheimer’s beta amyloid (Lovell 2003). In a preclinical trial, R-alpha-lipoic acid (R-LA) was fed to older rats with age-related accumulation of iron in the cerebral cortex. Following 2 weeks of R-LA supplementation, iron levels dropped to those indicative of younger rats (Suh 2005).
Carnitine. Carnitine is an internal shuttle that helps move fatty acids into the mitochondria for conversion into energy. Carnitine esters (acetyl-L-carnitine and propionyl-L-carnitine) are derivatives, which may have additional antioxidant activities that confer advantages over carnitine alone (Mingorance 2011). When combined with alpha lipoic acid, acetyl-L-carnitine attenuated the production of free radicals in cultures of iron-overloaded human fibroblasts (Lal 2008). In test tube studies, propionyl-L-carnitine inhibits superoxide radicals, and reduces lipid peroxidation catalyzed by hydrogen peroxide (Vanella 2000). It is also proposed that propionyl-L-carnitine can reduce the production of hydroxyl radicals generated by iron, because of its iron-chelating activity (Reznick 1992).
Despues de investigarlo bastante y hablarlo con mi medico, la probablidad que tengo de tener hemochormatosis es del 1%, no del 70% como habia leido, y el caso es que yo tengo dobles H63D y aunque en muchos sitios dicen que es el riesgo, en realidad no lo es, tal y como dicen aqui: http://www.hemochromatosisdna.com/dna-t … B1zqfmSwwo
Significance of Alleles
C282Y/C282Y Homozygote
Individuals who are homozygous for C282Y are at increased risk for developing hereditary hemochromatosis. C282Y is found in the homozygous state in approximately 85% of all individuals who are clinically affected with hereditary hemochromatosis. Iron overload is detected in 90% of males and 50% of females, and 2% will develop characteristic clinical end points (diabetes mellitus, hepatic cirrhosis, cardiomyopathy, etc.). Approximately 30% are asymptomatic. The C282Y mutation is associated with a more penetrant and severe phenotype than H63D and S65C.
H63D/H63D Homozygote
Individuals who are homozygous for H63D are only at a slightly increased risk of developing hereditary hemochromatosis. Iron overload is detected in 1% of males and 0.5% of females.
C282Y/H63D Compound Heterozygote
Individuals who are compound hereterozygous for C282Y/H63D are at an increased risk for developing a clinically milder form of hereditary hemochromatosis. This form is found in approximately 3 to 8% of individuals who are clinically affected with hereditary hemochromatosis. Approximately 1% to 2% of individuals with this genotype will develop clinical evidence of iron overload. While individuals with this genotype may have increased iron indices, many do not develop clinical disease without other precipitating factors (hepatitis, alcohol abuse).
C282Y/S65C Compound Heterozygote
Individuals who are compound heterozygous for C282Y and S65C may have a small risk for mild hemochromatosis. This rare variant displays a very low penetrance.
C282Y Heterozygote
Individuals who are heterozygous for C282Y may have mild symptoms of hemochromatosis such as lethargy, joint pain, and weakness but are unlikely to develop the disease.
H63D Heterozygote
Individuals who are heterozygous for H63D are unlikely to have symptoms of iron overload and are not at significantly increased risk of developing the disease.
Note: Individuals who are heterozygous for S65C or compound heterozygous H63D/S65C do not seem to be at a measurably increased risk for hereditary hemochromatosis. Accordingly, the S65C mutation is only reported when it is part of the C282Y/S65C compound heterozygous genotype.
El gran riesgo esta en tener dobles C282Y.
Y aqui vemos lo importante de investigar bien, y mirar muchos estudios para comprender el significado.