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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vitaminb12deficiency.info. All Rights Reserved.
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.
Reproduction in whole or in part in any form or medium without express written
permission is prohibited