THE Fatigue   AIHA of CFIDS is proof EGBE is the root cause 

 CFIDS Fatigue

Hemolytic Anemias

Rarely (if AIHA of CFIDS ... more often than found by doctors), anemia is due to problems that cause the red blood cells to break down prematurely. Normally, red cells live in the blood for about 4 months. In hemolytic anemia, this time is shortened, sometimes to only a few days.

Sickle cell anemia is a hereditary problem that can cause minor difficulties as the “trait” (when you carry one mutated gene from one of your parents) but severe clinical problems as the “disease” (when you carry two mutated genes, one from each of your parents). The red blood cells are misshapen and clog the blood vessels, causing pain and anemia. Screening is usually done on newborns – particularly those of African descent. Treatment is usually based on the symptoms.

Thalassemia is a hereditary abnormality of hemoglobin production and causes small red blood cells that resemble those seen in iron deficiency. In its most severe form, the red cells have a shortened life span. In milder forms, anemia is usually mild or absent, and the disease may be detected by finding small blood cells on a routine CBC. This genetic disease is found frequently in people of Mediterranean, African, and Asian heritage. The defect in production may involve any of the two major components of hemoglobin, and the disease is defined as betal thalassemia or alpha thalassemia accordingly. The "beta minor" form (sometimes called beta thal trait, as with sickle cell) occurs when a person inherits half normal genes and half beta thalassemia genes. It causes a mild anemia and no symptoms. The "beta major" form (due to inheriting two beta thalassemia genes and also called Cooley’s anemia) is more severe and may result in growth problems, jaundice (yellowing of the skin and whites of the eyes), and severe anemia. The hemoglobin electrophoresis shows an increase in hemoglobin A2 and/or hemoglobin F in beta thalassemia form, but may be relatively normal in the other form.