Where does B12 come from?

No animals can digest the cellulose that makes up plants.  Some animals such as cattle and sheep (ruminants) get around this by filling their stomach with bacteria, fungi and yeasts.  These microbes can digest cellulose and manufacture a whole range of nutrients (including B12) which the cattle and sheep can then absorb.  The microbes get a safe place to live and the cattle and sheep can use the grass and leaves they eat. The microbes produce a lot of B12  and all of that extra vitamin B12 gets stored in the muscle and meat for us to eat. 
However we know that modern farming methods require farmers to inject B12  (90% of the world’s production of Vitamin B12  is for farm animals).  It could be because of the speed animals are grown, or pesticides/ fertilisers on the grass, or antibiotics fed to keep the animals free from disease.

Natural cattle and sheep probably have very high levels of B12 in their meat.  If a farmer injects B12, he or she will only do so if it’s really needed, and will only inject enough to grow the animal fast.  Therefore we’re probably getting less than we used to from our food.

Microwave ovens

B12 is a robust molecule and survives cooking.  One of the few things that can break it is a microwave oven.  Even if you don’t use a microwave yourself, it’s possible that foods containing B12 have been irradiated to stop microbes growing, which might break down B12.

[i] Eating large quantities of liver or drinking liver juice reversed the impact of anaemia in dogs and pernicious anaemia in humans.  During 1920s it was found that the effects were totally different (anaemia was cured by iron from the liver, whereas pernicious anaemia was cured by something else in liver juice).  In 1928 the chemist Edwin Cohn prepared a liver extract that was the first workable treatment for the disease, and for their initial work in pointing a way to a working treatment, George Whipple, George Minot and William Murphy shared the 1934 Nobel Prize in Medicine.  The active ingredient was not isolated until 1948 and its structure eventually in 1956. .  (4)

[ii]the pressures accompanying the management of patients with leukaemia has led to decreasing interest in other blood disorders.  The simple elucidation of the cause of megaloblastic anaemia is poorly done, criteria on which diagnosis is made are often inadequate and conclusions reached are often incorrect.  An evaluation of the response of physicians to a report of low serum cobalamin following a request which they had initiated was adequate in only one-third of patients, and in more than 40% of 250 patients the report was ignored” Chanarin I “The Megaloblastic Anaemias” 3rd edition, Chapter 1 pg 1(Chanarin, The Megaloblastic Anaemias, 1986)

A pragmatic approach

Selenium deficiency in a lambNorman writes:

Dear All , 

This  confirms  Dr  Chandy's  approach  to  the  treatment  of  VB12  deficiency [that the best way to tell if there is a deficiency is to use a therapeutic trial - if the symptoms go away with B12 replacement therapy, then keep treating],  albeit  in  farm  animals .
Interestingly,  it  confirms  that  some  malfunctions  require  more  intake  than  others. Also,  if  there  is  a  shortage,  the  body  distributes  it to  the  vital  functions  first.
If  there  are  cobalt  deficiencies  ,  this  would  apply.

Selenium deficiency is widespread and often severe in UK soils, as demonstrated by analysis of soils on livestock farms, by the frequency of symptoms of subclinical deficiency in cattle and sheep, and by the low intake of UK citizens from home-grown food and their falling blood levels. There is overwhelming evidence that MAFF's reference values for an adequate selenium intake are too low for cattle and sheep.The only valid test for an adequate intake is the response ie the correction of a malfunction be it infertility, depressed immune system etc. Certain malfunctions may require higher intakes. There is evidence that when selenium supplies are limited, it is distributed to those tissues most vital to the organism, leaving others to go short.

Discovering Vitamin B12

The active ingredient in liver was not isolated until 1948 by the chemists Karl A. Folkers of the United States and Alexander R. Todd of Great Britain. The substance was a cobalamin called vitamin B12. It could also be injected directly into muscle, making it possible to treat pernicious anemia more easily.

The chemical structure of the molecule was determined by Dorothy Crowfoot Hodgkin and her team in 1956, based on crystallographic data. Eventually, methods of producing the vitamin in large quantities from bacteria cultures were developed in the 1950s, and these led to the modern form of treatment for the disease (the above from [6]). It is a large protein of molecular weight 1355.5 (ie 1 Molecular Weight (mol) =6.022*1023 (Avogadro’s constant) molecules of vitamin B12 would weigh 1,355.5g if it could be isolated in pure form – see the table on comparing weight concentration with mol concentration in Diagnosis)

More on vitamin B12 can be found on this page.




1.            Chanarin, I., The Megaloblastic Anaemias. 3rd ed. 1986, Oxford: Blackwell Scientific Publications.

2.            Addison, T., Anaemia: disease of the supra-renal capsules. London Medical Gazette 1849. 43: p. 517-518.

3.            Biermer, A., Über eine Form von progressiver perniciöser Anämie. Correspondenz-Blatt Schw. Ärzte., 1872. 2: p. 15-17.

4.            Russell, J.S.R., F.E. Batten, and J. Collier, Subacute Combined Degeneration of the Spinal Cord. Brain, 1900. 23: p. 39-110.

5.            Minot, G.R. and W.P. Murphy, Treatment of pernicious anemia by a special diet. 1926. Yale J Biol Med, 2001. 74(5): p. 341-53.

6.            Wikipedia. Vitamin B12. [web page] 2009  [cited 2009 2 Oct]; Description of Vitamin B12 (cobalamin) including description of discovery of cure for Pernicious anaemia and structure of B12]. Available from: http://en.wikipedia.org/wiki/Vitamin_B12.