Vitamin B-12 is essential to growth, cell reproduction, hematopoiesis (the process of formation and development of the various types of blood cells and other formed elements), and nucleoprotein and myelin synthesis. The plasma level of the B-12 compound reaches its peak within 1 hour after an intramuscular injection. The liver is the main organ for vitamin B-12 storage.

Within 48 hours after injection of vitamin B-12, 50 to 98% of the injected dose may appear in the urine. The major portion is excreted within the first eight hours.

Gastrointestinal absorption of vitamin B-12 depends upon the presence of sufficient intrinsic factor and calcium ions. The average diet supplies about 5 to 15 mcg/day of vitamin B-12 in a protein-bound form that is available for absorption after "normal digestion." Vitamin B-12 is not present in foods of plant origin, but is abundant in foods of animal origin.

Vitamin B-12 is bound to intrinsic factor during transit through the stomach, separation occurs in the terminal ileum (last part of the small intestines) in the presence of calcium.

Vitamin B-12 deficiencies due to malabsorption may be associated with the following conditions:

-Addisonian (pernicious) anemia.
-Gastrointestinal pathology, dysfunction or surgery, including gluten enteropahty or sprue, small intestine bacterial overgrowth, total or partial gastrectomy.
-Fish tapeworm infestation.
-Malignancy of pancreas or bowel.
-Folic acid deficiency.

Warning – Vitamin B-12 deficiency that is allowed to progress for longer than 3 months may produce permanent degenerative lesions on the spinal cord.

Maximum dosage should not exceed 10 mcg daily. So, if you have the standard 1mg/mL vitamin B-12 this would be 1cc intramuscular injection per week.

Important Note:
Never Self Administer Intramuscular Vitamin B-12 Without Your Doctor’s Approval !!!

Serious complications can result from improper usage of this Vitamin. Anaphylactic shock and death have been reported with administration of Vitamin B-12.

This information was gathered from Steris Laboratories in Phoenix Arizona.

(Thank you Steris Labs for your help in gathering this info.)

Causes of hypoferremia (iron deficiency)
-Random transient variation in normal subject
-Deficient iron stores (relatively late occurrence in the development of iron deficiency)
-Chronic inflammatory or neoplastic disorders (see "anemia of chronic disease")

-Miscellaneous:
-----1) Iron levels can decrease quickly even in relatively mild/acute injuries and trivial infections (e.g., colds in humans).
-----2) Corticosteroid excess: causes decreased iron (as much as half).

Iron circulates in the blood bound to transferrin. Transferrin is responsible for shuttling iron between sites of absorption, storage and utilization for the biosynthesis of iron-containing macromolecules. Receptors have been identified on the surface of reticulocytes (young red blood cells), hepatocytes (a type of liver cell), lymphocytes (white blood cells) and fibroblasts (a type of cell in connective tissue).

The best way to confirm iron deficiency is to demonstrate lack of iron stores in bone marrow.