Omega 3 Testing
Measures percentages of omega-3 fatty acids EPA, DPA and DHA as a potential indicator of various health risks.
DHA Testing
Indicates whether mothers are providing adequate DHA levels to their infants through breastfeeding.
Hair Cortisol Analysis
Provides a complementary method of monitoring stress and cortisol exposure in the body over longer periods of time.
IgG Food Sensitivity
A valuable tool often used to help design elimination diets for patients with several chronic conditions.
Hair Mineral Analysis
Provides the basis for a nutritional balancing program to establish and maintain optimal levels of wellness.

Role of Copper in Iron Localization in Developing Erythrocytes

Copper deficiency in the experimental animal results in a hypochromic microcytic anemia,”2 similar to that observed in certain conditions characterized by defective hemoglobin synthesis. Thus, a role for copper in the production of hemoglobin was proposed and actively investigated by Cartwright, Wintrobe, Lee and coworkers37 in copper-deficient swine. Their studies indicated that copper deficiency produces a defect in the release of iron to the circulation from the intestinal mucosa, reticuloendothelial system and the hepatocyte3-5; the pathways of porphyrin and heme synthesis in the developing erythrocyte are not affected.6 However, swine receiving iron supplementation accumulated large amounts of stainable iron in erythroid precursor cells, even though they remained somewhat anemic.5 This suggested an additional defect of intracellular iron metabolism in the copper-deficient animal. When we examined the localization of ferritin or electron-dense iron accumulations in developing erythrocytes of copper-deficient rats, ferritin was present in the vesicles of erythroid precursors but not in the mitochondria, where iron combines with protoporphyrin to form heme. Some conditions that interfere with heme or globin synthesis, e.g., lead poisoning,8 thalassemia,#{176} porphyria cutanea tarda,1#{176}result in an accumulation of iron in the mitochondna. In our study, normal animals treated with lead accumulated iron within storage vesicles and in mitochondria, as reported previously.8 In contrast, copper-deficient rats treated with lead accumulated iron in the vesicles but not in the mitochondria of erythroid precursors.

Joseph R. Goodman and Peter R. Dallman (www.bloodjournal.org, October 1, 2009)