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Blood Disorders
(Anemia, Leukopenia, and Thrombocytopenia)

Targeted Natural Interventions

Anemia

Treatment of anemia typically involves supplemental iron and B-vitamins; both of these interventions are discussed in the section of this protocol pertaining to conventional anemia treatment. However, a variety of natural interventions may complement conventional anemia treatments and support healthy red blood cell development and function.

Multinutrient formulas (multivitamins). Multivitamin/multimineral supplements may be beneficial in anemia by simultaneously fulfilling multiple nutritional requirements. One study showed that in as little as 26 weeks, a multiple micronutrient supplement taken twice weekly significantly increased hemoglobin levels in anemic but otherwise healthy young girls (Ahmed 2010). Another study showed that a multiple micronutrient supplement improved hemoglobin synthesis as well as an iron supplement, despite containing less iron, in a population of pregnant women (Allen 2009). These supplements also improved pregnancy outcomes (in terms of small-for-gestational-age births) compared to iron-folate supplementation alone (Haider 2011).

Taurine. Taurine (a derivative of the amino acid cysteine) plays an important role in the body’s response to acute inflammation and has antioxidant properties (Marcinkiewicz 2012; Laidlaw 1988). It is found naturally in animal meat and seafood. One study demonstrated a significantly reduced taurine status in vegans (Laidlaw 1988), a population in which anemia appears frequently. Interestingly, taurine itself may have a role in treating anemia. In a study on iron deficiency anemics, the addition of 1000 mg taurine to 325 mg iron daily for 20 weeks resulted in significantly better improvements in hemoglobin, red blood cell count, and iron status compared to iron alone (Sirdah 2002).

Vitamin D. There are some interesting correlates between vitamin D and red blood cell function, which suggest this vitamin might play an important role in maintaining the health of red blood cells. For example, vitamin D can potentiate erythropoietin in stimulating red blood cell synthesis (Alon 2002). Another study showed a significant correlation between vitamin D status and the prevalence of anemia in heart disease patients (Zittermann 2011). This result has been independently confirmed in a larger cross-sectional study (Sim 2010). Furthermore, high dose vitamin D supplements were shown to completely abrogate pain symptoms in a patient with sickle cell anemia (Osunkwo 2011). Life Extension recommends an optimal 25-hydroxy vitamin D blood level of 50 – 80 ng/mL.

N-acetylcysteine. In addition to its well-established effects as a potent antioxidant (Sagias 2010; Czubkowski 2011; Radtke 2012), N-acetylcysteine (NAC) has demonstrated efficacy in anemia. One study showed that 200 mg NAC taken three times daily significantly increased red blood cells and reduced oxidative stress in a population of patients with anemia and end-stage kidney disease on hemodialysis (Hsu 2010). Taking 600 mg NAC twice daily for 10 days also significantly attenuated the increase in oxidative stress associated with intravenous iron administration in a similar population (Swarnalatha 2010). A study of NAC in treating sickle cell anemia showed that 1200–2400 mg daily for 6 weeks significantly improved red blood cell profile and reduced oxidative stress compared to placebo (Nur 2012).

Leukopenia and Thrombocytopenia

Shark Liver Oil. Shark liver oil is a potent source of alkylglycerols, which are bioactive lipid compounds with a wide range of health-promoting properties (Deniau 2010). They have been shown to prevent the decline in leukocytes and thrombocytes in patients undergoing radiation treatment, which resulted in reduced mortality (Magnusson 2011). In another study in humans, shark liver oil improved blood antioxidant status while enhancing neutrophil function (Lewkowicz 2005), suggesting that it may benefit patients with oxidative stress-induced hemolytic anemia and neutropenia. Furthermore, data from animal studies show that alkylglycerols stimulate the formation of red blood cells as well as platelet aggregation (Iannitti 2010).

Chlorophyllin. Chlorophyllin is a component of the plant pigment chlorophyll. Studies suggest that it may protect against toxin-induced DNA damage (Egner 2003; Shaughnessy 2011). In addition, one study on 105 leukopenic subjects found 60–120 mg of chlorophyllin daily to be about as effect as a medication containing filgrastim (a ganulocyte colony-stimulating factor that stimulates development of white blood cells) in the treatment of leukopenia (Gao 2005).

Astragalus. The adaptogenic herb Astragalus membranaceus has been used traditionally for centuries in the treatment of many common health complaints (AMR 2003). In a study on 115 subjects with leukopenia, an astragalus preparation, administered twice daily for 8 weeks, was shown to increase white blood cell counts in a dose-dependent manner (Weng 1995). In an animal experiment, another adaptogenic herbal preparation containing astragalus boosted the white blood cell count of mice with chemically-induced leukopenia (Huang 2007).

Active hexose correlated compound (AHCC). AHCC, a compound derived from the family of fungi to which the shiitake mushroom belongs, has immune-modulating properties and has been shown to be well-tolerated in human study subjects (Spierings 2007). In one animal experiment, AHCC prolonged survival of leukopenic mice subject to lethal infection and raised their white blood cell counts (Ikeda 2003). A similar experiment found that AHCC increased the ability of leukopenic mice to resist the lethal effects of methicillin-resistant Staphylococcus areus (MRSA) (Ishibashi 2000). These findings suggest that AHCC may help improve immune defenses during leukopenia, which is associated with increased susceptibility to opportunistic infections.

Nutrients Potentially Beneficial in Multiple Blood Disorders

The following natural interventions may generally support blood health and potentially provide benefit in more than one of the blood disorders described in this protocol.

Melatonin. Melatonin is a multifunctional hormone with a variety of health-promoting properties independent of its more widely known effects on sleep quality. For example, as an antioxidant, 18 mg melatonin significantly blunted the oxidative stress induced by iron or erythropoietin infusions when administered 1 hour prior to treatment (Herrera 2001). This result was associated with increased activity of two native erythrocyte antioxidant enzymes, catalase and glutathione. The effects of melatonin on glutathione have been confirmed in human erythrocytes in vitro (Erat 2006). In another study, treatment with 6 mg melatonin nightly for 30 days in patients with anemia of chronic disease (ACD) resulted in significantly improved iron status and hemoglobin values. These results were almost completely reversed within 2 weeks of discontinuing melatonin treatment, suggesting a robust and specific effect of melatonin (Labonia 2005). Melatonin may also be beneficial in thrombocytopenia. Evidence suggests that the hormone plays a role in platelet generation. In a study on 200 thrombocytic patients, 20 mg of melatonin taken orally in the evenings for at least a month resulted in a rapid and significant increase in mean platelet number (Lissoni 1997,1999). Additionally, evidence suggests melatonin may modulate white blood cell turnover and benefit leukopenia. In an animal model of leukopenia, melatonin helped maintain hematopoietic function, leading the researchers to conclude “our results indicate that overall [melatonin] exerts a remarkable countering activity towards leukopenia and anemia…” (Pacini 2009). In a study on 6 human subjects whose blood cell production was impaired due to chemotherapy, 20 mg of melatonin administered orally each day improved red and white blood cell counts (Viviani 1990).

Antioxidants. Given their overall biological function, red blood cells are exposed to a high amount of oxygen and are thus likely to experience oxidative stress and benefit from antioxidant supplementation (Kosenko 2012). The fat-soluble antioxidant vitamin E has been shown to improve red blood cell profile in premature infants, hemolytic anemics, sickle cell anemics, and apparently healthy people with only modestly reduced hemoglobin levels (Jilani 2011). Vitamin C is helpful in iron deficiency anemia due to its ability to enhance non-heme-iron absorption; however, vitamin C also prevents oxidative damage within red blood cells, which is completely independent from its role in iron absorption (Berns 2005).

Polyphenols, found in blueberries and green tea, have demonstrated protection against oxidative damage in red blood cells (Youdim 2000). Carnosine, another potent antioxidant, has been shown in animal models to decrease age-related oxidative stress in red blood cells (Aydin 2010). Carnosine also protects erythrocytes from homocysteine-induced oxidative stress; high homocysteine levels can be caused by deficiency in folate and/or vitamin B12 (Arzumanyan 2008). Moreover, some antioxidants may also be of benefit in leukopenia and/or thrombocytopenia. For example, one study found that platelets from individuals with autoimmune thrombocytopenia expressed evidence of elevated oxidative stress, which is countered by antioxidants (Kamhieh-Milz 2012). In an intriguing laboratory experiment, scientists showed that a combination of the antioxidant nutrients blueberry, green tea catechins, carnosine, and vitamin D3 acted synergistically and dose-dependently to promote the proliferation of bone marrow stem cells. This groundbreaking study suggests that supplementation with multiple antioxidants might be an effective means of bolstering populations of red blood cells, white blood cells, and platelets (Bickford 2006).

  • Vitamins C and E. Iron-deficiency anemia occurs more frequently in vegetarians because iron from non-meat sources has poor bioavailability. However, vitamin C has been shown to improve nonheme-iron absorption (Atanasova 2005; Fishman 2000). One study showed that an intervention consisting of 500 mg vitamin C twice daily for 2 months improved iron status and corrected anemia in a population of vegetarians (Sharma 1995). Additionally, a comprehensive review of studies on anemics with end-stage kidney disease showed that vitamin C supplementation improved hemoglobin concentrations and reduced their average dose of erythropoietin (Deved 2009). In the context of thalassemia, at least one study suggests vitamin E supplementation may help support the integrity of red blood cell membranes (Sutipornpalangkul 2012). Supplementation with vitamin E may also be of benefit in children with sickle cell anemia, as one study showed that six weeks of alpha-tocopherol supplementation improved several metrics of diseases severity in this population (Jaja 2005). Vitamins C and E may also have some value in the management of leukopenia. One animal study showed that vitamin C, in combination with vitamin E, mitigated drug-induced leukopenia (Garcia-de-la-Asuncion 2007). In another animal study, vitamin E helped ease chemotherapy-induced leukopenia (Branda 2006).
  • Coenzyme Q10. Coenzyme Q10 is an endogenous antioxidant that assists in intracellular energy production. One study showed that patients with high blood pressure had reduced erythrocyte superoxide dismutase and increased oxidative stress relative to healthy people; this was completely corrected by supplementing with 120 mg of coenzyme Q10 daily for 12 weeks (Kedziora-Kornatowska 2010).

Copper and Zinc. Copper and zinc are cofactors for the endogenous antioxidant enzyme called superoxide dismutase. Copper is also required for iron absorption (Olivares 2006; Nazifi 2011). As such, deficiency in both or either of these minerals predisposes people to anemia (Bushra 2010; Hegazy 2010; De la Cruz-Gongora 2012; Maret 2006; Mocchegiani 2012; Salzman 2002). Moreover, copper deficiency is associated with leukopenia (Lazarchick 2012). It is important to note that copper and zinc should be taken together, since, for example, excess zinc consumption may lead to copper deficiency and subsequent leukopenia (Hoffman 1988; Salzman 2002; Porea 2000).