As we age and get less active, generally our dietary requirements also decrease, with the result that our intake of essential nutrients such as vitamins also is reduced. Whilst for many vitamins, this may not be a problem, as they are normally consumed in excess it is a significant problem with vitamin B12, as reducing the intake of red meat is also associated with reduced intake of vitamin B12. This reduced intake of vitamin B12 eventually leads to deficiency of the vitamin. Complicating the dietary reduction in vitamin B12, is the presence of atrophic gastritis (up to 30% of the elderly population), which can greatly reduce the ability to absorb vitamin B12, and the use of various medications such as MetforminÔ, ant-acids, cholestyramine, cymetidine, clofibrate, colchicine, methotrexate, methyldopa, neomycin, omeprazole, phenobarbital, ranitidine, tetracyclines, valproic acid,
Many of the conditions that we associate with ageing may actually be due to vitamin B12 deficiency, including forgetfulness, dementia, depression, an unstable gait, numbness and tingling in the hands and feet, bowel and bladder (urinary) incontinence, hearing loss, decreased energy and a feeling of tiredness, and an increased incidence of bone facture
Vitamin B12 is an essential vitamin for correct functioning of neurones and for the maintenance of the myelin sheath. As would be expected vitamin B12 deficiency may be associated with various neuronal conditions such as forgetfulness, dementia, depression, an unstable gait, numbness and tingling in the hands and feet, bowel and urinary incontinence and hearing loss. Preliminary evidence suggests that vitamin B12 deficiency may also be correlated with the macular degeneration and neuritis of the optic nerve.
Although incontinence can be thought of as a normal part of ageing, a number of studies have shown that high dose supplementation with vitamin B12 can reverse the inability to control the movements of bowel and bladder12.
Recently it has been discovered that elevated homocysteine, such as is found with vitamin B12 deficiency is a newly recognized risk factor for osteoporosis. Supplementation with high levels of vitamin B12 in combination with folate has been found to reduce the levels of serum homocysteine, and has potential in reducing the incidence of osteoporosis, as well as bone factures in the elderly, particularly hip fractures. The risk of fracture increases by 4% for every 50 pmol/L drop in vitamin B12. Other studies have shown a correlation with increased levels of MMA in serum, reduced vitamin B12 in serum, a decreased bone density, and an increased risk of fracture. .
As we age, many individuals experience a decrease in energy levels and a general feeling of tiredness. Energy generation is one of the prime functions of the mitochondria and vitamin B12 (adenosylcobalamin) is an essential part of energy generation. Further, methyl B12, through its role in the methylation cycle is also essential for the formation of creatine and CoQ10. Reduced levels of vitamin B12 are reflected upon reduced energy levels and in many individuals high doses of adenosylcobalamin have been shown to give the recipients a distinct energy boost.
There is an increasing incidence of hypothyroidism as we age, which is associated with many similar symptoms to vitamin B12 deficiency. In addition, it has been found that vitamin B12 deficiency is often associated with hypothyroidism, and as such both conditions can be confused with each other. Thus, if the condition is diagnosed as vitamin B12 deficiency, supplementation with vitamin B12 may be of little use, if the precipitating cause is hypothyroidism. Similarly if hypothyroidism is diagnosed and underlying vitamin B12 deficiency is missed, treatment may also be ineffective in reversing symptomatology. Symptoms share in common between hypothyroidism and vitamin B12 deficiency include Fatigue, Weakness, Muscle cramps and frequent muscle aches, Depression, Irritability, Memory loss, Abnormal menstrual cycles, Decreased libido
In elderly the brain shows a progressive atrophy. The rate of atrophy has been shown to be higher in those with mild cognitive impairment and early dementia and highest in Alzheimer’s disease. Various studies have shown that the degree of atrophy is correlated with the levels of serum homocysteine, a by-product of vitamin B12 (methylcobalamin) deficiency. High dose supplementation with vitamin B12, folate and vitamin D2 has been shown to reduce the levels of homocysteine in the circulation and to greatly reduce the rate of brain atrophy (shrinkage).
Deficiency of vitamin B12 correlates with the development of progressive dementia and may present without any signs of megaloblastic anaemia and can be accompanied by subacute combined degeneration of the spinal cord.
Repeated high dose injection of methylcobalamin over a period of 12 months has been shown to reduce brain atrophy in the elderly and to reverse signs of dementia. Supplementation studies addressing all of Adenosyl and Methyl B12 deficiency, plus the support required of vitamin B2, Iodine, Selenium, Molybdenum and folate have for some reason not yet been performed.
Clarke R, Smith AD, Jobst KA, Refsum H, Sutton L, et al. (1998) Folate, vitamin B12, and serum total homocysteine levels in confirmed Alzheimer disease. Arch Neurol 55: 1449–1455.
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Smith AD (2008) The worldwide challenge of the dementias: A role for B vitamins and homocysteine? Food Nutr Bull 29: S143–172.
Zylberstein DE, Lissner L, Bjorkelund C, Mehlig K, Thelle DS, et al. (2009) Midlife homocysteine and late-life dementia in women. A prospective population study. Neurobiol Aging Epub ahead of print.
Williams JH, Pereira EA, Budge MM, Bradley KM (2002) Minimal hippocampal width relates to plasma homocysteine in community-dwelling older people. Age Ageing 31: 440–444.
Sachdev PS, Valenzuela M, Wang XL, Looi JC, Brodaty H (2002) Relationship between plasma homocysteine levels and brain atrophy in healthy elderly individuals. Neurology 58: 1539–1541.
den Heijer T, Vermeer SE, Clarke R, Oudkerk M, Koudstaal PJ, et al. (2003) Homocysteine and brain atrophy on MRI of non-demented elderly. Brain 126: 170–175.
Yang LK, Wong KC, Wu MY, Liao SL, Kuo CS, et al. (2007) Correlations between folate, B12, homocysteine levels, and radiological markers of neuropathology in elderly post-stroke patients. J Am Coll Nutr 26: 272–278.
Seshadri S, Wolf PA, Beiser AS, Selhub J, Au R, et al. (2008) Association of plasma total homocysteine levels with subclinical brain injury: cerebral volumes, white matter hyperintensity, and silent brain infarcts at volumetric magnetic resonance imaging in the Framingham Offspring Study. Arch Neurol 65: 642–649.
Keser I, Ilich JZ, Vrkić N, Giljević Z, Colić Barić I. Folic acid and vitamin B12 supplementation lowers plasma homocysteine but has no effect on serum bone turnover markers in elderly women: a randomized, double-blind, placebo-controlled trial. Nutr Res. 2013 Mar;33(3):211-9. doi: 10.1016/j.nutres.2013.01.002. Epub 2013 Feb 1
Kurabayashi H, Kubota K, Kawada E, Tamura K, Tamura J, Shirakura T. Complete cure of urinary and faecal incontinence after intravenous vitamin B12 therapy in a patient with post-gastrectomy megaloblastic anaemia. J Intern Med. 1992 Mar;231(3):313-5.
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