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Targeted Nutritional Strategies

Several dietary constituents have been investigated for their ability to treat iron overload. They work by either reducing or inhibiting iron absorption from the gut, or binding excess iron in the blood and tissues to help draw it out of the body. Additionally, the significant contribution of free radical damage to the progression of iron-overload associated diseases suggests a role for increasing antioxidant consumption.

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).