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Information about Vitamin B12

Vitamin B12 has an essential role in the function of only two enzymes in the body, MethylmalonylCoA mutase, essential for obtaining energy from several amino acids and fatty acids, and methionine synthase, 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.

Potential Uses of vitamin B12

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, 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 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 and the Brain

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, and cannot be achieved by any oral dosing system.

Vitamin B12 and Treatment of Cognitive Decline

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).  

Vitamin B12 and CFS/ME Treatment

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.  

Vitamin B12 and Vitamin B2

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.

Vitamin B12 and Autism Treatment

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.

Vitamin B12, Sciatica and Neuropathic Pain

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.

Vitamin B12 and Food Intolerance

Many foods contain histamine and lack of vitamin B12 can result in a reduced ability to inactivate histamine.

Vitamin B12 and IBS

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.

Vitamin B12 and Sleep

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.

Vitamin B12 and Hypothyroidism

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.

Further Information on Vitamin B12 Deficiency

Information on vitamin B12 deficiency can be found at the following sites

https://vitaminb12deficiency.info

www.vitaminb12deficiency.net.au

http://b12awareness.org/

http://preventingdementia.org

Pacholok, S.M. and Stuart, J. J. Could it be B12? An epidemic of misdiagnosis.

 

 

 

 

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