Vitamin B12 Deficiency



Vitamin B12


Vitamin B12 (also known as cobalamin), has a deep red colour and is a highly water soluble member of the B group vitamins. The daily requirement for vitamin B12 is very small (~ 6 ug). Despite this the vitamin plays an essential role in the synthesis of fatty acids for the myelin sheath on nerves, and in the processing of some fatty acids and amino acids for energy, with folate is essential for DNA synthesis. There are two main cobalamins in the body which are used by only two enzymes in the body, methionine synthase and L-methylmalonyl-CoA, but lack of vitamin B12 affects the activity of over two hundred enzymes involved in methylation. Deficiency of vitamin B12 can therefore have disastrous ramifications and can produce haematological, neurological and gut symptoms, and can cause sensory disturbances in the extremities, energy loss with exercise intolerance and fatigue, as well as cognitive changes such as memory loss, brain fog and dementia.


Vitamin B12 deficiency


Vitamin B12 deficiency can affect individuals of all ages and evidence of deficiency can be "seen" to affect even the foetus. Whilst it was originally thought that deficiency was a result of inadequate intake, or inadequate bioavailability or absorption, it is now known that there are many other causes of vitamin B12 deficiency.


Clinical deficiency was formerly defined by classic haematological and neurological symptoms, however more recently many other symptoms of vitamin B12 deficiency have been described. Such "sublinical" deficiency symptoms affect between 5-25% of the population and often vitamin B12 deficiency is disregarded as a possible cause.


Severe lack of vitamin B12 can result in anaemia, whilst even a moderate continued lack has been associated with several conditions including fatigue, incontinence, brain fog, adrenal fatigue, IBS, histamine intolerance, neuritis, multiple sclerosis, cognitive impairment, psychoses and dementia.

Vitamin B12 deficiency is frequently under-diagnosed and misdiagnosed in the community. This site aims to describe some of the many conditions associated with vitamin B12 deficiency in an attempt to better educate those who may suffer from the condition, who may not, nor be able to get treatment for the condition, or may be unresponsive to vitamin B12 therapy.


In order to cover this broad subject with even some degree of thoroughness we have deemed it necessary to provide suitable reference material and so have included references to scientific publications where possible. Many aspects of vitamin B12 deficiency are not understood by the majority of clinicians nor apparently by the majority of researchers who have performed supplementations studies in a diverse range of areas such as dementia, schizophrenia, depression, chronic fatigue syndrome, multiple sclerosis, and autism to name but a few. Such studies would be typified by the many, many studies on oral administration of cyanocobalamin without due reference to the small amount of vitamin B12 that reaches not only the circulation following oral administration, let alone the pitifully small amount that traverses into the brain. Further, over and over studies have been performed with cyanocobalamin without the inclusion of the necessary support by vitamin B2 (riboflavin) or it co-commitments, Iodine, Selenium and Molybdenum. This is despite it being known for over 40 years that vitamin B2 plays an essential role in remethylation of methyl B12 through it being a co-factor for MTHFR, and the additional role of vitamin B2 in regeneration of oxidized Co(II)B12, which has been known for over 20 years.


Vitamin B12 deficiency is typified by the many conditions associated with mitochondrial disease, including autism, chronic fatigue syndrome, dementia, multiple sclerosis, depression, Parkinson's disease, ALS, etc. Total disregard seems to have been taken of vitamin B12's important contribution to energy production through the formation of CoQ10, creatine and carnitine, and the generation of iron-sulphur proteins, and the neurotransmitter hydrogen sulphide.


There has been an over-reliance on postulates of damage to the body due to elevated homocysteine levels with scant regard to the accompanying deficiency of methylation and the 200 or so enzymes that rely on methylation for function, and also the accompanying reduction in hydrogen sulphide production, reduction in glutathione levels, and more importantly the reduced production of iron-sulphur proteins, each of which must accompany elevations in homocysteine.


In general the measurement of serum levels of vitamin B12 rather the metabolic markers of vitamin B12 deficiency, including Methylmalonic acid, and homocysteine, but also potentially including VMA, HVA and QA, has misled many researchers in their data interpretation.


It is the purpose of this site is to describe more recent advances in the diagnosis and treatment of vitamin B12 deficiency, as well as describing some of the less well known conditions associated with the condition.  




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The statements on this site compose a compendium of generally recognized signs of vitamin B12 deficiency, and problems that can then ensue They also are formulated from a summary of relevant scientific publications. In addition they may contain some forward looking statements of a general nature.
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