Overt B12 Deficiency - Nerve Damage and Anemia
- Ways to Get B12 Deficiency
- Early, Noticeable Symptoms of Overt B12 Deficiency
- Other Symptoms of Overt B12 Deficiency
- Neurological Symptoms
- Theories of How B12 Deficiency Causes Nerve Damage
- When Is It Time to Call a Doctor?
The two main ways people get vitamin B12 deficiency are inadequate dietary intake and inadequate absorption from loss of intrinsic factor or lack of stomach acid. Other, much less common ways are listed in Ways to Get B12 Deficiency.
Please note that the symptoms listed below are found in overt vitamin B12 deficiency. You can be B12 deficient, increasing your risk of disease because of elevated homocysteine without suffering any noticeable symptoms.
Early, Noticeable Symptoms of Overt B12 Deficiency (1):
- Unusual fatigue
- Faulty digestion
- No appetite
- Loss of menstruation
- Numbness and tingling of the hands and feet (1)
- Nervousness (1)
- Diarrhea (2)
- Mild depression (1)
- Striking behavioral changes (1)
- Paranoia (1)
- Hyperactive reflexes (1)
- Fever (3)
- Frequent upper respiratory infections (4)
- Impotence (5)
- Impaired memory (5)
- Infertility (6)
- Sore tongue (2)
- Macrocytic anemia
- Low platelet count (3, 7) and increased bleeding (3)
- Neutropenia (3)
- Skin hyperpigmentation (dark skin with even darker spots) (13)
Neurological symptoms, often referred to as subacute combined degeneration (SCD), are the biggest concern regarding B12 deficiency. The damage can be irreversible if not caught early enough. SCD affects peripheral nerves and the spinal cord, and is normally different in children than adults (8).
There are 3 main theories as to how B12 deficiency causes nerve damage:
1. B12 deficiency produces a lack of methionine for conversion into S-adenosylmethionine (SAM) (9). SAM is required for the production of phosphatidylcholine (10) which is part of the myelin (the fatty material that insulates many nerves) (10). (See Figure: Methionine-Homocysteine-Folate-B12 Cycle.)
2. The inability to convert methylmalonyl-CoA (a 3-carbon molecule) to succinyl-CoA (a 4-carbon molecule) results in an accumulation of propionyl-CoA (a 3-carbon molecule). Fatty acids are normally made by adding 2 carbons at a time to an even numbered carbon molecule. In an overabundance of 3 carbon molecules, large amounts of unusual 15-carbon and 17-carbon fatty acids may be produced and incorporated into nerve sheets, causing altered nerve function (11).
3. Nerves are damaged by different hormone-like molecules (cytokines, tumor necrosis factor, and epidermal growth factor) which become unbalanced in the nerve tissue in B12 deficiency (8).
There are some serious diseases that have similarities to B12 deficiency, including Guillian-Barre syndrome, Lyme neuropathy, heavy metal intoxication, and lupus myelopathy (12). Anyone who develops symptoms of nerve damage should see a doctor immediately for treatment.
2. Lindenbaum J, Healton EB, Savage DG, Brust JC, Garrett TJ, Podell ER, Marcell PD, Stabler SP, Allen RH. Neuropsychiatric disorders caused by cobalamin deficiency in the absence of anemia or macrocytosis. N Engl J Med. 1988 Jun 30;318(26):1720-8.
3. Sarode R, Garewal G, Marwaha N, Marwaha RK, Varma S, Ghosh K, Mohanty D, Das KC. Pancytopenia in nutritional megaloblastic anaemia. A study from north-west India. Trop Geogr Med. 1989 Oct;41(4):331-6.
7. Refsum H, Yajnik CS, Gadkari M, Schneede J, Vollset SE, Orning L, Guttormsen AB, Joglekar A, Sayyad MG, Ulvik A, Ueland PM. Hyperhomocysteinemia and elevated methylmalonic acid indicate a high prevalence of cobalamin deficiency in Asian Indians. Am J Clin Nutr. 2001 Aug;74(2):233-41.
10. Grattan-Smith PJ, Wilcken B, Procopis PG, Wise GA. The neurological syndrome of infantile cobalamin deficiency: developmental regression and involuntary movements. Mov Disord. 1997 Jan;12(1):39-46.
13. Cherqaoui R, Husain M, Madduri S, Okolie P, Nunlee-Bland G, Williams J. A reversible cause of skin hyperpigmentation and postural hypotension. Case Rep Hematol. 2013;2013:680459. doi: 10.1155/2013/680459. Epub 2013 Jun 11. | link