Vitamin B12 has an essential role in the function of only two enzymes in the body, MethylmalonylCoA mutase,
which uses AdenosylB12 (Adenosylcolabamin), essential for obtaining energy from several amino acids and fatty acids, and methionine synthase,
which uses MethylB12 (Methylcobalamin), an essential enzyme in the methylation cycle
While the daily requirement for vitamin B12 is very small (less than 6 ug/day), a deficiency in the vitamin affects over 200 methylation reactions in the body, and can lead to debilitating fatigue, weight loss and
demyelination of the nervous system, with disastrous consequences, Lack of
methyl B12, through its role in the methylation cycle results in greatly reduced
production of CoQ10 and also of creatine. Functional vitamin B12 deficiency has
been strongly linked to developmental delay in children.
Traditionally vitamin B12 has been used to treat pernicious
anemia, however, more recently vitamin B12 supplementation has
has been used in the treatment of various conditions
related to sub-clinical deficiency of vitamin such as
treatment to prevent memory loss, dementia, Alzheimer's disease, autism, chronic
fatigue syndrome, depression,
poor concentration, reducing the signs of ageing, incontinence, asthma,
allergies (such as in atopic allergy and eczema), amyotrophic lateral sclerosis
(Lou Gehring's disease), vitiligo, ringing in the ears (tinitis), boosting
energy, incontinence, lack of libido, male and female infertility, poor balance,
hearing loss, and psoriasis.
High dose of
hydroxocobalamin injected intravenously has been used for treatment of heavy
metal poisoning and cyanide intoxication. High dose methyl cobalamin (injected)
has been used to successfully treat the sign and symptoms of Alzheimer's
disease. Similar success has not been achieved with oral preparations of vitamin
B12.
Vitamin B12, either
alone, or in combination with vitamin B2, folate and vitamin B6, has also been used to
reduce serum homocysteine levels, which have been associated with cardiovascular
disease, vascular dementia and mild cognitive decline.
Vitamin B12 "loading" of the brain occurs during
fetal life, with very little vitamin B12 entering the brain after birth. There
is a general decline in B12 levels over time, and it has not been possible to
restock the brain with any oral form of B12. Overcoming deficiency in the brain
requires prolonged high dose parenteral administration of vitamin B12, or
TransdermOil™ B12, and
cannot be achieved by any oral dosing system.
Deficiency of
folate and particularly vitamin B12 can lead to an inability to properly process
homocysteine, with the result that in many individuals who are deficient in
these vitamins can have elevated levels of Homocysteine (Hcy) in both the serum and the brain.
Elevated Hcy has been found to occur in 9-14% of people over 60 and has been
correlated with an increased incidence/severity of cardiovascular disease and
the development of mild cognitive impairment. High dose vitamin B12
supplementation in with folate and vitamin B6 has been shown to reduce the level
of brain shrinkage in subjects with elevated serum homocysteine levels (Douaud
etal, 2013, Smith etal, 2010). High dose intravenous methylcobalamin has been
shown to reverse the symptoms of Alzheimer's disease (Ikeda etal, 1992).
It has been found that CFS/ME may be related to defects in
either folate metabolism and/or the methylation cycle, as a high
incidence of sufferers have genetic mutations in the MTHFR, MTR, MTRR, MTS
and/or SHMT genes. In addition many CFS/ME individuals have genetically similar
vitamin D receptor genes. It is possible that CFS/ME sufferers have had these
"inborn errors of metabolism" for much of their life, without experiencing any
significant problem until some precipitating event such as stress or a chronic
infection has triggered chemical changes inside the body thereby resulting in
CFS/ME. Many, many different treatments have been tried in an
attempt to cure CFS/ME, with little success. Recently, however, it has been found
that many people have obtained significant benefit from repeated dose treatment
with high levels of vitamin D3, adenosylcobalamin and methylcobalamin. It is
believed that this repeated high dose supplementation is required to stock both
the body's methylcobalamin levels but also the adenosylcobalamin levels. Over time, and
with the addition of high dose vitamin D supplementation the subjects appear to
return to their pre-CFS status.
The active forms of vitamin B2, FMN and FAD have a
critical role in the maintenance of functional methylcobalamin and
adenosylcobalamin, through the actions of the two enzymes Methylene-Tetrahydrofolate
Reductase (MTHFR) and Methionine Synthase Reductase (MTRR). Persons who are functionally deficient in vitamin B2 rapidly
become deficient in active vitamin B12. In this case no amount of added methyl
or adenosylB12 can overcome deficiency. It is therefore essential that
functional vitamin B2 deficiency be addressed before vitamin B12 deficiency.
Vitamin B2 deficiency can be due to lack of dietary intake of vitamin B2
(riboflavin) or Iodine, Selenium and/or Molybdenum, as each metal is essential
for enzymes involved in converting riboflavin to FMN and FAD. The potential role
of vitamin B2 in the development of functional vitamin B12 deficiency is not
well appreciated, yet the majority of persons who contact us are functionally
deficient in vitamin B2. Such persons often have higher than normal serum B12
levels, however the vitamin B12 is inactive as these individuals show elevated
MMA, homocysteine, and other markers of vitamin B12 deficiency. This
"Paradoxical vitamin B12 deficiency" is generally not known by many
practitioners dealing with individuals who are being treated for conditions
associated with vitamin B12 deficiency, yet it would arguably be the most common
form of undiagnosed vitamin B12 deficiency. Further, if such persons are treated
with cyanocobalamin or hydroxycobalamin they cannot convert these forms to the
active Methyl B12 and Adenosyl B12, and as such appear refractory to vitamin B12
treatment. More information can be found on Paradoxical B12 deficiency on the
Paradoxical site.
Examination of the metabolism of autistic
individuals has shown that they are highly deficient in vitamin B2 and both
adenosyl and methyl B12. Evidence is accumulating that similar deficiencies may
be present in children with Down Syndrome. The brains of autistic individuals
have been shown to have less than one third the levels of normal children, presumably
due to lack of loading of the brains of the children during fetal life.
Treatment involves correcting functional B2 deficiency first, and then fixing
the functional B12 deficiency (see
https://b12oils.com/research.htm )
Absolute or functional deficiency in vitamin B12
eventually leads to over-production of serotonin in the brain, which in turn
leads to the development of depression. This can be corrected by identifying the
cause of the functional B12 deficiency and then correcting that with subsequent
application of vitamin B12 (see
https://b12oils.com/depression.htm )
High dose treatment with methyl and
adenosylcobalamin has been found to help reduce the pain in many people
suffering sciatica and other types of neuropathic pain.
Many foods contain
histamine and lack of vitamin B12 can result in a reduced ability to inactivate
histamine.
Proper maturation and
functioning of the gut is dependent upon the production of melatonin.
Production of melatonin is reduced in vitamin B12 deficiency. Melatonin has
regulatory effects on gastrointestinal mobility and helps to alleviate abdominal
pain and abdominal distention common in IBS.
Subacute combined degeneration of the spinal cord is a neurological complication
of vitamin B12 (cobalamin) deficiency.
Poor sleep in a common
side-effect of vitamin B12 deficiency. Production of melatonin in the brain is
required for regular sleep, and since production of melatonin is reduced in
vitamin B12 deficiency, poor sleep (insomnia) is common in people with vitamin B12
deficiency.
Hypothyroidism can lead to vitamin B12 deficiency.
Persons with hypothyroidism should check their serum vitamin B12 levels, as well
as other B12 deficiency markers such as MMA and homocysteine, as
Paradoxical B12 deficiency is common in persons with Hypothyroidism.
Information on vitamin B12 deficiency can be found at the
following sites
https://vitaminb12deficiency.info
www.vitaminb12deficiency.net.au
https://www.understandingautism.com.au
Pacholok, S.M. and Stuart, J. J. Could it be B12? An
epidemic of misdiagnosis.
Copyright © 2014 B12 Oils. All Rights Reserved. Information
about Vitamin B12
Potential
Uses of vitamin B12
Vitamin B12
and the Brain
Vitamin B12
and Treatment of Cognitive Decline
Vitamin B12
and CFS/ME Treatment
Vitamin B12
and Vitamin B2
Vitamin B12
and Autism Treatment
Vitamin B12
Deficiency and Prolonged Depression
Vitamin B12, Sciatica
and Neuropathic Pain
Vitamin B12
and Food Intolerance
Vitamin B12
and IBS
Vitamin B12
and Subacute Combined Degeneration of the Spine
Vitamin B12
and Sleep
Vitamin B12 and
Hypothyroidism
Further Information
on Vitamin B12 Deficiency
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