UV-blocking sunglasses for outdoors, appropriate dietary intake of fresh fruit and leafy green vegetables, antioxidant vitamin supplements, and regular intake of dietary omega-3 very-long-chain fatty acids are all recommended. One study found that a dietary supplement of lutein increases macular pigment levels in patients with choroideremia. Over a long period of time, these elevated levels of pigmentation "could" slow retinal degeneration. Additional interventions that may be needed include surgical correction of retinal detachment and cataracts, low vision services, and  counseling to help cope with depression, loss of independence, and anxiety over job loss. Gene therapy
Gene therapy is currently not a treatment option, however human clinical trials for both choroideremia and Lebers congenital amaurosis (LCA) have produced somewhat promising results.Clinical trials of gene therapy for patients with LCA began in 2008 at three different sites. In general, these studies found the therapy to be safe, somewhat effective, and promising as a future treatment for similar retinal diseases. In 2011, the first gene therapy treatment for choroideremia was administered. The surgery was performed by Robert MacLaren, Professor of Ophthalmology at the University of Oxford and leader of the Clinical Ophthalmology Research Group at the Nuffield Laboratory of Ophthalmology (NLO). In the study, 2 doses of the AAV.REP1 vector were injected subretinally in 12 patients with choroideremia.
Megaloblastic Anemia
It reflects DNA disturbance which affects the blood cells (erythrocytes, leukocytes, platelets) and the bone marrow, and it is characterized by large and immature blood cells in the bone marrow (macrocytic anemia), mainly caused by both vitamins B9 (Folic Acid) and B12. Anemia of Protein-Energy Malnutrition
As explained before, hemoglobin is a protein which means that its production requires adequate and enough intake of protein from the diet, but in case of protein-energy malnutrition, hemoglobin will not be produced sufficiently leading to anemia. As a result there is a reduction in cell mass and thus fewer RBCs are required to oxygenate the tissue ( reduced number of RBCs with a low hemoglobin). Copper Deficiency Anemia
Copper and copper proteins are needed for adequate hemoglobin formation, use of iron by the developing erythrocyte (ceruloplasmin), optimal functions of the erythrocyte membrane. Ceruloplasmin (copper containing protein) is required for normal mobilization of iron from its storage sites. Thus, in a copper- deficient state; iron cannot be released à low serum iron and hemoglobin levels (even in the presence of normal iron stores). Sideroblastic Anemia
It is an inherited defect of heme synthesis enzyme which results in derangement in the final pathway of heme synthesis and buildup of immature Fe- containing RBCs. It is classified as microcytic and hypochromic type of anemia and it is nutritional because it is Vitamin B6-responsive. Hemolytic Anemia
A defect in RBC membranes causes oxidative damage and lysis the cells. Vitamin E has shown to be protective as it has an antioxidative function.