Long term supplementation

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B12 info

In patients with liver disease, cholesterol and/or phospholipids become deposited on the membranes of circulating red blood cells, leading to larger than normal cells.[1]

Causes of non-megaloblastic macrocytosis
•There may also be folate deficiency due to a poor diet
•Liver disease.

•Serum folate levels are readily available but most laboratories offer red cell folate that is more specific.

It should be remembered that serum B12 is not always an accurate reflection of deficiency at a cellular level. It is perhaps for this reason that some patients become symptomatic if the frequency of their injections is reduced, despite having normal serum B12 levels.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1570488/

http://www.medscape.com/viewarticle/410469_4

A low serum folate level may indicate only a decrease in folate intake over the preceding few days. [26] A better indicator of tissue folate status is RBC folate concentration, [27] which remains relatively unchanged while a red cell is in the circulation and thus provides an assessment of folate turnover during the 2 or 3 months preceding measurement. Also, low RBC folate levels correlate better with the degree of megaloblastic changes in the bone marrow than do low serum folate levels. When there is coexistent Iron deficiency, liver disease, serum and RBC folate levels may be normal -- and serum B 12 levels may be normal or even elevated -- but tissue Vitamin deficiency can be present. This is only demonstrable via subtle hypersegmentation and/or deoxyuridine suppression test and is subsequently confirmed by response to vitamin therapy. Decreased serum total folate-binding capacity is another test that may indicate hidden folate deficiency.

An elevated MCV is also associated with alcoholism[3] (as are an elevated GGT and a ratio of AST:ALT of 2:1). Vitamin B12 and/or folic acid deficiency has also been associated with macrocytic anemia (high MCV numbers).