Where does B12 come from?

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HugoMinney's picture
Submitted by HugoMinney on Sat, 01/09/2010 - 11:39

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)

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