Source: ‘MedZ, Vakblad voor Huisartsen met eigen Praktijk’, 27 oktober 2017.
My first experiences with vitamin B12 as a GP was within my own family. As time went by I saw more and more patients with B12 deficiency, i.e. a pattern of symptoms I got to know increasingly better.
The reference values provided more confusion than clarity, for patients with a (low)-standard laboratory values frequently proved to benefit from a test treatment. I was also surprised at the growing number of people that seemed to have a B12 deficiency, and that B12 appeared to be a cure for anything and everything. My curiosity led me to start looking for scientific literature on the subject.
Although the entire pattern of pernicious anaemia symptoms combined with weakness, shortness of breath and palpitations was described by William Hunter (1) as early as 1901, only anaemia has been taken into the future as an acknowledged result.The serious neurological symptoms have remained only rarely mentioned. More than a hundred years later cell biological research into vitamin B12 and the cause and results of deficiency has taken an important lead in medical research practice.
Cell biologists have long been aware that mice and rats with vitamin B12 deficiency will have offspring with growth disorders and osteoporosis (2). They also know that rats with vitamin B12 deficiency cannot find their way in mazes and become anxious (3). The respect and interest for vitamin B12 paid by cell biology is in stark contract to the way medicine approaches it, considering it a hype.
It is therefore high time to translate the functions of vitamin B12 at a cellular level towards the symptoms experienced by vitamin B12 deficiency patients.
During our study of medicine we all learn that the liver contains a large supply of vitamin B12. I have even found some articles on this subject from the fifties. The authors ventured a small calculation, concluding that the liver has a B12 supply that could last for three years, if all of that vitamin would be functional and if every individual would use a fixed quantity (1 mcg a day) (4). Medicine and nutrition science has transposed this theory into the conviction that supplementing the liver supply is adequate treatment of B12 deficiency.
In practice, however, it is not that simple: patients complain that the effect of vitamin B12 treatment is not yet ideal, and disappeared quickly.
What if treatment would be more complicated than just simply filling the empty bucket? Without going into details, I found a satisfactory explanation of the whole range of symptoms in the normal functioning of vitamin B12, and, moreover, that long and frequent treatment seemed necessary to reach and hold on to the desired effect.
Oxidative stress, e.g., which may be caused by illness and mental stress, leads to excessive oxygen waste material, oxiding vitamin B12, and stop it functioning. More vitamin B12 will be needed to attain the necessary effect (5).
Vitamin B12 has the task to convert the metabolic situation within the body to the need for and the synthesis of new cells, enzymes and neurotransmitters. The need for B12 therefore will be larger when there is disease and stress. So far, I have been able to conclude from research literature together with the study of patient experiences that apart from nutritional deficiency and malabsorption, B12 deficiency can also be caused by an increased intake of B12. I also concluded that the results of treatment doesn’t always mean that other diseases can be excluded!
Research in order to define B12 deficiency clearly and correctly is really necessary, but since B12 deficiency can bring forth seriously invalidating symptoms I hope that most of my colleagues will not await this research quietly.
Drs. Annette Offringa, GP