What you should know about vitamin B12 deficiency: problems with detecting and treating a vitamin B12 deficiency.
The difficulty of detecting a vitamin B12 deficiency starts at the standard vitamin B12 serum test that is used:
The B12 serum test is the standard test performed by general practitioners to detect a vitamin B12 deficiency. This test has the following issues:
B12 serum level | Interpretation |
---|---|
< 200 ng/L | Vitamin B12 deficiency (in the Netherlands) |
< 340 ng/L | Grey zone according to NHG 5 |
< 400 to < 600 ng/L | Grey zone B12 (according to authorities worldwide) 6 |
< 745 ng/L | Scientifically proven grey zone s3 4 |
Key message NHG: Key message NHG Methylmalonic acid test and, to a lesser extent, the Homocysteïnetest. 5
There is a difference between symptoms that have been scientifically proven to be caused by a vitamin B12-deficiency and symptoms that are related to a vitamin B12 deficiency according to the NHG.
According to the NHG, only the following symptoms are related to a B12-deficiency:5
The following scientific claims have been sufficiently proved according to the European Commission:7
Sciences have proven over 150 symptoms more that can be related to a vitamin B12 deficiency, for these symptoms check out the list of symptoms.
It makes sense that a vitamin B12 deficiency can cause so many symptoms, since vitamin B12 contributes to, among others, a healthy cell division and the production of red blood cells.
Because there is no test which can diagnose a vitamin B12 deficiency with absolute certainty, a test treatment is often initiated. This test treatment can be done with injections or lozenges.
Treatment of a vitamin B12 deficiency may be done with injections or lozenges (oral supplementation).
The NHG states: In patients presenting with symptoms and a vitamin B12 level below 200 ng/L, treatment with 1000microgram a day should be initiated. This can be taken orally, even if pernicious anaemia is present, because with this high dose the absence of intrinsic factor is sufficiently countered by passive diffusion. 5 9 10 11
There are 4 forms of vitamin B12:
Cyanocobalamin and Hydroxocobalamin are both forms of vitamin B12 that have to be converted by the body (into Methylcobalamin and Adenosylcobalamin). A vitamin B12 deficiency mostly arises because of a conversion problem in the gastrointestinal tract. The body cannot converse vitamin B12 into the active form and therefore cannot transport it properly into the bloodstream.
A conversion disorder mostly causes a vitamin B12 deficiency in the gastrointestinal tract, which may have been going on for years. Therefore, symptoms will not resolve overnight. Most people experience positive effects after 6 to 12 weeks of taking vitamin B12 supplements. Depending on your physical and mental condition, you may notice a change earlier or later.
During the first 6 to 8 weeks of taking vitamin B12 supplements, it is important to drink 6 to 8 glasses of water a day. The body will start to detoxify and by drinking 6 to 8 glasses of water a day, your body can appropriately get rid of the toxics.
A vitamin B12 deficiency can be treated with vitamin B12 injections. The procedure of vitamin B12 injections is as follows in the Netherlands:
The first 5 weeks you receive 2 injections a week.
After that, you continue with 1 injection a week and this interval will slowly be expanded.
The B12 deficiency foundation states a minimum frequency of an injection once every 2 months is required. 12
In the Netherlands, injections contain 1000mcg of Hydroxocobalamin. In Belgium, two types of injections are used: one containing 1000mcg Hydroxocobalamin and another one containing 1000mcg Cyanocobalamin. Hydroxocobalamin has a preference. In Germany and Italy, injections contain the active form of vitamin B12: Methylcobalamin and Adenosylcobalamin. The address of the pharmacy where you can get these injections can be found here.
Important when being treated with injections:
A vitamin B12 deficiency can be treated with vitamin B12 lozenges. When taking vitamin B12 sublingually, it will be directly absorbed into the bloodstream through the oral mucosa, with this bypassing the conversion problem in the gastrointestinal tract.
It is important to take an active form of vitamin B12, such as Methylcobalamin or Adenosylcobalamin. The body will have to convert other forms of vitamin B12 (Cyanocobalamin and Hydroxocobalamin) into the active form.
Important when taking lozenges:
You can combine injections with lozenges. You should always discuss this with your general practitioner.
A lot of people combine injections with lozenges because they notice a higher dose of vitamin B12 is needed to resolve their symptoms. Or because the interval between injections is too long and their vitamin B12 deficiency symptoms are reoccurring.
Humans and other mammals are all born with a serum B12 level of about 2710 ng/L, which decline gradually throughout life.13
Doctor John Dommisse states: ‘‘The one major step that would bring B12 deficiency back into the mainstream of medicine and psychiatry would be the general recognition that the normal range should be regarded as 813 to 2710 ng/L. Below 745 to 813 ng/L, deficiencies start to appear in the cerebrospinal fluid, as shown by several papers over the past 20 to 30 years.’ 13
Dommisse states that older adults ought to have a vitamin B12 level of at least 813 to 2710 ng/L. For children, he recommends a level of 1355 to 2710 ng/L. 13
Vitamin B12 is a water-soluble vitamin. Any vitamin B12 consumed in excess will be excreted in the urine.
Overview of medication known to interfere with the absorption of vitamin B12.
The most comprehensive list of symptoms caused by a vitamin B12 deficiency!
Tests that can be performed to detect a vitamin B12 deficiency.
Research Hans Reijnen: active Vitamin B12 (Methylcobalamin en Adenosylcobalamin)
1 Nexo E, Christensen AL, Hvas AM, Petersen TE, Fedosov SN. Quantification of holo-transcobalamin, a marker of vitamin B12 deficiency. Clin Chem 2002;48:561–2 http://www.ncbi.nlm.nih.gov/pubmed/11861448 [Free Full Text]
2 van Tiggelen, C.J.M., et al., Assessment of vitamin-B12 status in CSF. American Journal of Psychiatry 141, 1:136-7
3 Mitsuyama, Y., Kogoh, H., Serum and cerebrospinal fluid vitamin B12 levels in demented patients with CH3 - B12 treatment - preliminary study. Japanese Journal of Psychiatry and Neurology 42,1: 65-71
4 van Tiggelen, C.J.M., Peperkamp, J.P.C., Tertoolen J.F.W., Vitamin-B12 levels of cerebrospinal fluid in patients with organic mental disorder. Journal of Orthomolecular Psychiatry 12, 305-311
5 NHG-Standpunt Diagnostiek van vitamine-B12-deficiëntie 2014 (PDF)
6 http://b12d.org
7 EU Register on nutrition and health claims http://ec.europa.eu/nuhclaims/?event=search&CFID=115735
8 “Is het Misschien B12-tekort?” Sally M. Pacholok en Jeffrey M. Stuart. ISBN 978-90-202-0490-2 - Blz. 119
9 Troilo A, Mecili M, Ciobanu E, Boddi V, D’Elios MM, Andres E. Efficacite et toler ance de la vitamine B12 par voie orale chez 31 patients avec une maladie de Biermer ou une maldigestion des cobalamines alimentaires. Presse Med 2010;39;e273-e279
10 Vidal-Alaball J, Butler CC, Cannings-John R, Goringe A, Hood K, McCaddon A, et al. Oral vitamin B12 versus intramuscular vitamin B12 for vitamin B12 deficiency. Cochrane Database Syst Rev 2005;CD004655
11 Andres E, Fothergill H, Mecili M. Efficacy of oral cobalamin (vitamin B12) therapy. Expert Opin Pharmacother 2010;11;249-56.
12 http://stichtingb12tekort.nl/vitamine-b12/ik-heb-een-b12-tekort-wat-nu/behandeling/
13 “Is het Misschien B12-tekort?” Sally M. Pacholok en Jeffrey M. Stuart. ISBN 978-90-202-0490-2 - Blz. 240
14 Gezondheidsraad. Voedingsnormen: vitamine B6, foliumzuur en vitamine B12. Publicatienr. 2003/04, Gezondheidsraad, Den Haag 2003 (PDF)
15 Matrana M.R., Gauthier C., Lafaye K.M. Paralysis and pernicious anemia in a young woman. J La State Med Soc. 2009 Jul-Aug;161(4):228-32.
16 Szupień E., Ositek B., Pniewski J. Difficulties in the diagnosis in the case of subacute paraplegia in a woman with Addison-Biermer disease. Neurol Neurochir Pol. 2004 Sep-Oct; 38(5): 431-6.
17 Mohammed al Essa et al. Inborn error of vitamin B12 metabolism: A treatable cause of childhood dementia/paralysis. Journal of child neurology 1998. Volume 13 (5) p. 239-243.
18 Shyambabu C., Sinha S., Taly A.B., Vijayan J., Kovoor J.M.E.. Serum vitamin B12 deficiency and hyperhomocystinemia: A reversible cause of acute chorea, cerebellar ataxia in an adult with cerebral ischemia. Journal of the Neurological Sciences; 273 (2008): 152–154.
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