The Danger of B12 Deficiency in the Elderly

1998 ◽  
Vol 12 (4) ◽  
pp. 215-226 ◽  
Author(s):  
Margaret Wynn ◽  
Arthur Wynn

Vitamin B12 deficiency damages nerve cells and aggravates nervous system disorders even in the absence of evidence of anaemia. Prevalence of B12 deficiency increases with age especially over 65 and is frequently associated with Alzheimer's disease. Recent American surveys record a higher prevalence of B12 deficiency and of undiagnosed and untreated pernicious anaemia in the elderly than reported earlier. B12 deficiency is also reported to be a risk factor for heart disease, stroke and accelerated ageing.

2003 ◽  
Vol 3 (4) ◽  
pp. 335-339
Author(s):  
No Author

1. The Ocular Manifestations Of Nutritional Disease. Mc Laren, D.S & Halasa, A. Postgraduate Med. J. 1964, Dec., v.40, No. 470, 711-16, 2 figs, (15 refs).2. Lead Intoxication And The Nervous System. Fazlullah S. and Ramamurthi B. J. Ind, Med. Asso. 1965, 44, 644-3. Neonatal Candidiasis. Sharma N.L., Gupta S.P., Philip Elsie, Goel K.M. Indian J. Pediat. 1965, 32, 157.4. Stress, Tobacco and Heart Disease. Russek H.I. JAMA, 1965, 192, 189.5. Autoimmune Addition' Disease. Koang N.K. & Hsing-Chiung C. Chinese M.J. 1965, 84;343.6. Metformin-Chlorpropamide Therapy. Clarke B.F., Duncan L.J.P. Lancet, (1965), i, 12487. Nutritional Vitamin B12 Deficiency among Hindus. Habib, G.G. Trop. & Geograph. Med. Haarlem. 1964, sept., v.16 no.3 206-15. (73 refs)


2010 ◽  
Vol 80 (45) ◽  
pp. 330-335 ◽  
Author(s):  
Lindsay Helen Allen

Vitamin B12 deficiency is common in people of all ages who consume a low intake of animal-source foods, including populations in developing countries. It is also prevalent among the elderly, even in wealthier countries, due to their malabsorption of B12 from food. Several methods have been applied to diagnose vitamin B12 malabsorption, including Schilling’s test, which is now used rarely, but these do not quantify percent bioavailability. Most of the information on B12 bioavailability from foods was collected 40 to 50 years ago, using radioactive isotopes of cobalt to label the corrinoid ring. The data are sparse, and the level of radioactivity required for in vivo labeling of animal tissues can be prohibitive. A newer method under development uses a low dose of radioactivity as 14C-labeled B12, with measurement of the isotope excreted in urine and feces by accelerator mass spectrometry. This test has revealed that the unabsorbed vitamin is degraded in the intestine. The percent bioavailability is inversely proportional to the dose consumed due to saturation of the active absorption process, even within the range of usual intake from foods. This has important implications for the assessment and interpretation of bioavailability values, setting dietary requirements, and interpreting relationships between intake and status of the vitamin.


Author(s):  
Nishant Kumar Singh ◽  
Hirni J. Patel ◽  
Mohit Buddhadev ◽  
S P Srinivas Nayak ◽  
Gunosindhu Chakraborthy

Peripheral nerves are susceptible to damage by a wide array of toxins, medications, and vitamin deficiencies. Vitamin B12 (VB12) deficiency neuropathy is a rare debilitating disease that affects mostly the elderly. It is important to consider these etiologies when approaching patients with a variety of neuropathic presentations in this review were have included most relevant and latest information on mechanisms causing Peripheral neuropathy in VB12 deficiency. We also have included cardiovascular disorders and their management. Hyperhomocysteinemia has been implicated in endothelial dysfunction and cardiovascular disease. The association of homocysteine (Hcy) and VB12 with cardiovascular risk factors in patients with coronary artery disease (CAD) has also been studied Keywords: Peripheral Neuropathy, Vitamin B12 Deficiency, Cardiovascular Disease and Homocysteine.


1974 ◽  
Vol 47 (6) ◽  
pp. 617-630
Author(s):  
A. Lavoie ◽  
E. Tripp ◽  
A. V. Hoffbrand

1. The uptake of 14C from [methyl-14C]methyItetrahydrofolate was significantly reduced in the phytohaemagglutinin (PHA)-stimulated lymphocytes from nine patients with untreated pernicious anaemia compared with the uptake in seven normal subjects. 2. The uptake of 14C from [14C]methyltetrahydrofolate by the lymphocytes from seven of the patients with pernicious anaemia was consistently increased by addition of vitamin B12in vitro. 3. The proportion of 14C taken up from [14C]methyltetrahydrofolate transferred to non-folate compounds was found to be significantly reduced in the PHA-stimulated lymphocytes from nine patients with untreated pernicious anaemia compared with the proportion transferred in the PHA-stimulated lymphocytes from seven normal subjects. Addition of vitamin B12in vitro consistently increased the transfer in vitamin B12-deficient cells but had no consistent effect in normal cells. 4. Normal and vitamin B12-deficient PHA-stimulated lymphocytes took up [3H]folic acid and after 72 h incubation converted this largely into pteroylpolyglutamate forms. 5. The proportion of labelled lymphocyte folate as pteroylpolyglutamate after incubation with [3H]folic acid was the same in vitamin B12-deficient as in normal lymphocytes and the proportion of pteroylpolyglutamates formed in vitamin B12-deficient lymphocytes was unaffected by addition of vitamin B12in vitro. 6. No radioactivity could be decteted in pteroylpolyglutamates after incubating normal PHA-stimulated lymphocytes with [14C]methyltetrahydrofolate for 72 h, suggesting that pteroylpolyglutamate forms of folate cannot be made directly from methyltetrahydrofolate. 7. These results are consistent with the ‘methyltetrahydrofolate trap’ hypothesis in vitamin B12 deficiency. It is suggested that reduced synthesis of pteroylpolyglutamates reported by others in vitamin B12-deficient cells may be secondary to the failure of removal of the methyl group from methyltetrahydrofolate rather than to a direct effect of vitamin B12 deficiency on the enzyme responsible for pteroylpolyglutamate synthesis. 8. Reduced entry of methyltetrahydrofolate into vitamin B12-deficient cells may be secondary to failure of conversion of this compound into tetrahydrofolate.


Author(s):  
Saskia LM van Loon ◽  
Anna M Wilbik ◽  
Uzay Kaymak ◽  
Edwin R van den Heuvel ◽  
Volkher Scharnhorst ◽  
...  

Background Methylmalonic acid (MMA) can detect functional vitamin B12 deficiencies as it accumulates early when intracellular deficits arise. However, impaired clearance of MMA from blood due to decreased glomerular filtration rate (eGFR) also results in elevated plasma MMA concentrations. Alternative to clinical trials, a data mining approach was chosen to quantify and compensate for the effect of decreased eGFR on MMA concentration. Methods Comprehensive data on patient’s vitamin B12, eGFR and MMA concentrations were collected ( n = 2906). The relationship between vitamin B12, renal function (eGFR) and MMA was modelled using weighted multiple linear regression. The obtained model was used to estimate the influence of decreased eGFR on MMA. Clinical impact was examined by comparing the number of patients labelled vitamin B12 deficient with and without adjustment in MMA. Results Adjusting measured MMA concentrations for eGFR in the group of patients with low-normal vitamin B12 concentrations (90–300 pmol/L) showed that the use of unadjusted MMA concentrations overestimates vitamin B12 deficiency by 40%. Conclusions Through a data mining approach, the influence of eGFR on the relation between MMA and vitamin B12 can be quantified and used to correct the measured MMA concentration for decreased eGFR. Especially in the elderly, eGFR-based correction of MMA may prevent over-diagnosis of vitamin B12 deficiency and corresponding treatment.


2013 ◽  
Vol 2013 (sep29 1) ◽  
pp. bcr2013200380-bcr2013200380 ◽  
Author(s):  
H. B. Gowdappa ◽  
M. Mahesh ◽  
K. V. K. S. N. Murthy ◽  
M. G. Narahari

1993 ◽  
Vol 50 (8) ◽  
pp. 807-811 ◽  
Author(s):  
K. R. Robertson ◽  
R. A. Stern ◽  
C. D. Hall ◽  
D. O. Perkins ◽  
J. W. Wilkins ◽  
...  

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 932-932
Author(s):  
Gyllian Yahn ◽  
Brandi Wasek ◽  
Terry Bottiglieri ◽  
Nafisa Jadavji

Abstract Objectives The majority of the world's population is growing older, in 2000, 10% of the total population of the world was over 60 years old and is projected to increase to 21% by 2050. Brain vasculature is unique, and its aging has been scarcely investigated at the cellular, and molecular levels, as well as in the context of age-related comorbidities. Nutrition is a modifiable risk factor for stroke, as people age their ability to absorb some nutrients decreases. A primary example is vitamin B12, the majority of older adults are deficient in vitamin B12 because of changes in breakdown and absorption of the vitamin. Furthermore, a vitamin B12 deficiency results in elevated levels of homocysteine which is a risk factor for cardiovascular diseases, such as stroke. Using a mouse model system, the aim of this study was to understand the role of vitamin B12 deficiency in ischemic stroke outcome and investigate mechanistic changes in the brain. Methods At 10-weeks of age male and female C57Bl/6J mice were put on control (0.025 mg/kg of vitamin B12) or vitamin B12 deficient (0 mg/kg of vitamin B12) diets for 4-weeks prior to ischemic damage. At 14 weeks of age we induced ischemic stroke in the sensorimotor cortex using the photothrombosis model, all animals received damage. Animals continued on diets for 4 weeks after damage. At 18 weeks of age we assessed stroke outcome using the accelerating rotarod and forepaw placement task. After the collection of behavioral data, we euthanized animals and collected brain, blood, and liver tissue to assess histological and biochemical measurements. Plasma was used to measure total homocysteine and methylmalonic acid. Results All animals maintained on the vitamin B12 deficient diet had increased levels of total homocysteine in plasma and liver tissue. Male and female mice maintained on a vitamin B12 deficient diet had impairments in balance and coordination on the accelerating rotarod compared to animals maintained on a control diet. Conclusions Vitamin B12 deficiency impacts motor function in older adult male and female mice. We are investigating damage volume and potential mechanisms within the damage brain tissue. Funding Sources Midwestern University Start-Up Funds.


Author(s):  
Niloofar Khodabandehloo ◽  
Masoud Vakili ◽  
Zahra Hashemian ◽  
Hadi Zare Zardini

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