I feel I can resolve a few possible anomalies suggested by Dr Bradley and others:
Firstly, when it comes to treating B12 deficiency, it should be noted that back in the 1950’s, E. Lester Smith and his team were assigned to establishing dosage for treating the anaemia aspect of the illness. The effective dosage for treating neurological injury was assigned to another team at a hospital in England. Because at the time it was believed that the anaemia caused the neuro damage, then once Smith’s team had established dosages effective for reversing the anaemia it was this information which was released by Glaxo - the effective treatment for neurological injury was archived - and there it remains.
Secondly, as Dr Bradley quite rightly observes, there is an inconsistency between the common causes of B12 deficiency listed in the review and the number of people said to suffer from it. One aspect rarely focused upon today is that previous to 1926 it was well known that all patients suffering from pernicious anaemia (all B12 deficiencies then went under this classification) also had acholorhydria or hypochlorhydria. At the time it was reported, by such authorities as Hurst and James Samuel Risien Russell, that 100% of these patients had this condition. Later research, by I believe, Kinnier-Wilson, claimed it to be 75%. Either way the statistics are staggering. Yet, despite these figures and the fact that stomach acid needs to be acidic rather than alkaline to cleave B12 from food, few patients are tested for this condition. In fact there is no test available to primary care physicians throughout Europe. The new Best Practice Guidelines from the BMJ do suggest checking for increased gastrin levels which would suggest alkaline stomach acid, however it remains to be seen whether this suggestion is taken on board or whether a direct pH test will be introduced.
Another issue remaining is the contradiction relating to the progression of the illness: is anaemia ‘end stage’ as we often hear, or does it precede the neurological damage? Certainly it can’t always be both and certainly patients do present with the anaemia and few signs of neurological injury, whereas others present with severe neuro injury and few signs of anaemia. Worth noting may be the fact that in the late 1800s and early 1900s, only about 20% of patients were recorded as dying from anaemia. The remainder died from neuro degeneration or associated heart attacks/strokes etc. The patients identified by Addison (1847) did die of anaemia, but they were later (from the 1880s onwards) considered to be the 20% arm.
In short, it would seem that a primary causation of this illness, alkaline stomach acid, requires more investigation, and also consideration should be given to the possibility that anaemia is only one possible symptom which may appear at any stage of the disease progression as well as appearing in isolation.
Competing interests:
In December 2016 Mike Newman and Karen Thompson wrote Vitamin B12 Deficiency and Chronic Illness, published by CreateSpace Independent Publishing Platform. [Response modified on 4 July 2017 by Sharon Davies, The BMJ]
Rapid Response:
Re: Vitamin B12 deficiency
I feel I can resolve a few possible anomalies suggested by Dr Bradley and others:
Firstly, when it comes to treating B12 deficiency, it should be noted that back in the 1950’s, E. Lester Smith and his team were assigned to establishing dosage for treating the anaemia aspect of the illness. The effective dosage for treating neurological injury was assigned to another team at a hospital in England. Because at the time it was believed that the anaemia caused the neuro damage, then once Smith’s team had established dosages effective for reversing the anaemia it was this information which was released by Glaxo - the effective treatment for neurological injury was archived - and there it remains.
Secondly, as Dr Bradley quite rightly observes, there is an inconsistency between the common causes of B12 deficiency listed in the review and the number of people said to suffer from it. One aspect rarely focused upon today is that previous to 1926 it was well known that all patients suffering from pernicious anaemia (all B12 deficiencies then went under this classification) also had acholorhydria or hypochlorhydria. At the time it was reported, by such authorities as Hurst and James Samuel Risien Russell, that 100% of these patients had this condition. Later research, by I believe, Kinnier-Wilson, claimed it to be 75%. Either way the statistics are staggering. Yet, despite these figures and the fact that stomach acid needs to be acidic rather than alkaline to cleave B12 from food, few patients are tested for this condition. In fact there is no test available to primary care physicians throughout Europe. The new Best Practice Guidelines from the BMJ do suggest checking for increased gastrin levels which would suggest alkaline stomach acid, however it remains to be seen whether this suggestion is taken on board or whether a direct pH test will be introduced.
Another issue remaining is the contradiction relating to the progression of the illness: is anaemia ‘end stage’ as we often hear, or does it precede the neurological damage? Certainly it can’t always be both and certainly patients do present with the anaemia and few signs of neurological injury, whereas others present with severe neuro injury and few signs of anaemia. Worth noting may be the fact that in the late 1800s and early 1900s, only about 20% of patients were recorded as dying from anaemia. The remainder died from neuro degeneration or associated heart attacks/strokes etc. The patients identified by Addison (1847) did die of anaemia, but they were later (from the 1880s onwards) considered to be the 20% arm.
In short, it would seem that a primary causation of this illness, alkaline stomach acid, requires more investigation, and also consideration should be given to the possibility that anaemia is only one possible symptom which may appear at any stage of the disease progression as well as appearing in isolation.
Competing interests: In December 2016 Mike Newman and Karen Thompson wrote Vitamin B12 Deficiency and Chronic Illness, published by CreateSpace Independent Publishing Platform. [Response modified on 4 July 2017 by Sharon Davies, The BMJ]