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Special Issue "Vitamin B12 and Human Health"

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A special issue of Nutrients (ISSN 2072-6643).

Deadline for manuscript submissions: closed (30 June 2013)

Special Issue Editor

Guest Editor
Dr. Kristina Pentieva (Website)

School of Biomedical Sciences, University of Ulster at Coleraine, Northern Ireland, BT52 1SA, UK
Fax: +44 28 703 249 65
Interests: B-vitamin requirements and recommendations for intake in humans; B-vitamins in health and disease; B-vitamins and epigenetics; food folate bioavailability; food folate analysis; food fortification; functional foods

Special Issue Information

Submission

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Nutrients is an international peer-reviewed Open Access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1500 CHF (Swiss Francs).


Keywords

  • clinical and subclinical vitamin B12 deficiency
  • biochemical markers for vitamin B12 deficiency
  • total mortality
  • cognitive function
  • osteoporosis
  • cancer
  • cardiovascular diseases
  • neural tube defects

Published Papers (7 papers)

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Research

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Open AccessArticle Vitamin B12 and Folic Acid Imbalance Modifies NK Cytotoxicity, Lymphocytes B and Lymphoprolipheration in Aged Rats
Nutrients 2013, 5(12), 4836-4848; doi:10.3390/nu5124836
Received: 30 September 2013 / Revised: 6 November 2013 / Accepted: 14 November 2013 / Published: 26 November 2013
Cited by 5 | PDF Full-text (244 KB) | HTML Full-text | XML Full-text
Abstract
Different vitamin B12 and folic acid concentrations could exacerbate the immune response. The aim was to evaluate different dietary folic acid and vitamin B12 levels on the immune response in aged rats. Male Sprague Dawley aged rats were assigned to [...] Read more.
Different vitamin B12 and folic acid concentrations could exacerbate the immune response. The aim was to evaluate different dietary folic acid and vitamin B12 levels on the immune response in aged rats. Male Sprague Dawley aged rats were assigned to three folic acid groups (deficient, control, supplemented) each in absence of vitamin B12 for 30 days. Several parameters of innate and acquired immune responses were measured. Serum and hepatic folate levels increased according to folic acid dietary level, while vitamin B12 levels decreased. There was a significant decrease in natural killer cell-mediated cytotoxicity in the spleen for the vitamin B12 deficient diet and folic acid control diet groups. Significant changes in CD45 lymphocyte subsets were also observed according to dietary imbalance. Lymphoproliferative response to concanavalin A and phytohemagglutinin did not differ significantly between groups. The spleen response to lipopolysaccharide increased significantly, but was unmodified for the other organs. An imbalance between dietary vitamin B12 and folic acid concentrations alters some immunological parameters in aged rats. Therefore, the ratio between folate and vitamin B12 could be as important as their absolute dietary concentrations. Full article
(This article belongs to the Special Issue Vitamin B12 and Human Health)
Open AccessArticle Vitamin B12 Deficiency in Relation to Functional Disabilities
Nutrients 2013, 5(11), 4462-4475; doi:10.3390/nu5114462
Received: 8 August 2013 / Revised: 16 September 2013 / Accepted: 4 November 2013 / Published: 12 November 2013
Cited by 6 | PDF Full-text (401 KB) | HTML Full-text | XML Full-text
Abstract
This study was designed to assess whether symptoms, functional measures, and reported disabilities were associated with vitamin B12 (B12) deficiency when defined in three ways. Participants, aged 60 or more years of age, in 1999–2002 National Health and Nutrition Examination Surveys (NHANES) [...] Read more.
This study was designed to assess whether symptoms, functional measures, and reported disabilities were associated with vitamin B12 (B12) deficiency when defined in three ways. Participants, aged 60 or more years of age, in 1999–2002 National Health and Nutrition Examination Surveys (NHANES) were categorized in relation to three previously used definitions of B12 deficiency: (1) serum B12 < 148 pmol/L; (2) serum B12 < 200 pmol/L and serum homocysteine > 20 μmol/L; and (3) serum B12 < 258 pmol/L or serum methylmalonic acid > 0.21 μmol/L. Functional measures of peripheral neuropathy, balance, cognitive function, gait speed, along with self-reported disability (including activities of daily living) were examined with standardized instruments by trained NHANES interviewers and technicians. Individuals identified as B12 deficient by definition 2 were more likely to manifest peripheral neuropathy OR (odds) (95% confidence intervals), p value: 9.70 (2.24, 42.07), 0.004 and report greater total disability, 19.61 (6.22, 61.86) 0.0001 after adjustments for age, sex, race, serum creatinine, and ferritin concentrations, smoking, diabetes, and peripheral artery disease. Smaller, but significantly increased, odds of peripheral neuropathy and total disability were also observed when definition 3 was applied. Functional measures and reported disabilities were associated with B12 deficiency definitions that include B12 biomarkers (homocysteine or methylmalonic acid). Further study of these definitions is needed to alert clinicians of possible subclinical B12 deficiency because functional decline amongst older adults may be correctable if the individual is B12 replete. Full article
(This article belongs to the Special Issue Vitamin B12 and Human Health)
Open AccessArticle Biological Variability and Impact of Oral Contraceptives on Vitamins B6, B12 and Folate Status in Women of Reproductive Age
Nutrients 2013, 5(9), 3634-3645; doi:10.3390/nu5093634
Received: 25 June 2013 / Revised: 9 August 2013 / Accepted: 12 August 2013 / Published: 16 September 2013
Cited by 3 | PDF Full-text (191 KB) | HTML Full-text | XML Full-text
Abstract
Vitamins B6, B12 and folate play crucial metabolic roles especially during the reproductive years for women. There is limited reporting of within-subject variability of these vitamins. This study aimed to determine the within and between subject variability in serum [...] Read more.
Vitamins B6, B12 and folate play crucial metabolic roles especially during the reproductive years for women. There is limited reporting of within-subject variability of these vitamins. This study aimed to determine the within and between subject variability in serum vitamins B6, B12, folate and erythrocyte folate concentrations in young women; identify factors that contribute to variability; and determine dietary intakes and sources of these vitamins. Data were obtained from the control group of a trial aimed at investigating the effect of iron on the nutritional status of young women (age 25.2 ± 4.2 year; BMI 21.9 ± 2.2 kg/m2). The coefficients of variability within-subject (CVI) and between-subject (CVG) for serum vitamins B6, B12 and folate, and erythrocyte folate were calculated. Food frequency questionnaires provided dietary data. CVI and CVG were in the range 16.1%–25.7% and 31.7%–62.2%, respectively. Oral contraceptive pill (OCP) use was associated (P = 0.042) with lower serum vitamin B12 concentrations. Initial values were 172 ± 16 pmol/L and 318 ± 51 pmol/L for OCP and non-OCP users, respectively; with differences maintained at four time points over 12 weeks. BMI, age, physical activity, alcohol intake and haematological variables did not affect serum or erythrocyte vitamin concentrations. Vitamin B12 intakes were derived from traditional and unexpected sources including commercial energy drinks. Young women using OCP had significantly lower serum vitamin B12 concentrations. This should be considered in clinical decision making and requires further investigation. Full article
(This article belongs to the Special Issue Vitamin B12 and Human Health)
Open AccessArticle Metformin Lowers Serum Cobalamin without Changing Other Markers of Cobalamin Status: A Study on Women with Polycystic Ovary Syndrome
Nutrients 2013, 5(7), 2475-2482; doi:10.3390/nu5072475
Received: 26 April 2013 / Revised: 5 June 2013 / Accepted: 7 June 2013 / Published: 5 July 2013
Cited by 3 | PDF Full-text (449 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Treatment with the anti-diabetic drug metformin is followed by a decline in plasma cobalamin, but it is unsettled whether this denotes an impaired cobalamin status. This study has explored changes in the markers of cobalamin status in women with Polycystic Ovary Syndrome [...] Read more.
Treatment with the anti-diabetic drug metformin is followed by a decline in plasma cobalamin, but it is unsettled whether this denotes an impaired cobalamin status. This study has explored changes in the markers of cobalamin status in women with Polycystic Ovary Syndrome treated with metformin (1.5–2.5 g per day) (n = 29) or placebo (n = 23) for six months. Serum samples were collected before and after two, four, and six months of treatment. We found serum cobalamin to decline and reach significant lower levels after six months of treatment (p = 0.003). Despite the decline in serum cobalamin, we observed no reductions in the physiological active part of cobalamin bound to transcobalamin (holotranscobalamin), or increase in the metabolic marker of cobalamin status, methylmalonic acid. Instead, the non-functional part of circulating cobalamin bound to haptocorrin declined (p = 0.0009). Our results have two implications: The data questions whether metformin treatment induces an impaired cobalamin status in PCOS patients, and further suggests that serum cobalamin is a futile marker for judging cobalamin status in metformin-treated patients. Full article
(This article belongs to the Special Issue Vitamin B12 and Human Health)

Review

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Open AccessReview Neuroenhancement with Vitamin B12—Underestimated Neurological Significance
Nutrients 2013, 5(12), 5031-5045; doi:10.3390/nu5125031
Received: 6 June 2013 / Revised: 20 November 2013 / Accepted: 29 November 2013 / Published: 12 December 2013
Cited by 15 | PDF Full-text (278 KB) | HTML Full-text | XML Full-text
Abstract
Vitamin B12 is a cofactor of methionine synthase in the synthesis of methionine, the precursor of the universal methyl donor S-Adenosylmethionine (SAMe), which is involved in different epigenomic regulatory mechanisms and especially in brain development. A Vitamin B12 deficiency expresses itself by [...] Read more.
Vitamin B12 is a cofactor of methionine synthase in the synthesis of methionine, the precursor of the universal methyl donor S-Adenosylmethionine (SAMe), which is involved in different epigenomic regulatory mechanisms and especially in brain development. A Vitamin B12 deficiency expresses itself by a wide variety of neurological manifestations such as paraesthesias, skin numbness, coordination disorders and reduced nerve conduction velocity. In elderly people, a latent Vitamin B12 deficiency can be associated with a progressive brain atrophy. Moderately elevated concentrations of homocysteine (>10 µmol/L) have been associated with an increased risk of dementia, notably Alzheimer’s disease, in many cross-sectional and prospective studies. Raised plasma concentrations of homocysteine is also associated with both regional and whole brain atrophy, not only in Alzheimer’s disease but also in healthy elderly people. Clinician awareness should be raised to accurately diagnose and treat early Vitamin B12 deficiency to prevent irreversible structural brain damage. Full article
(This article belongs to the Special Issue Vitamin B12 and Human Health)
Open AccessReview Cobalamin Deficiency: Clinical Picture and Radiological Findings
Nutrients 2013, 5(11), 4521-4539; doi:10.3390/nu5114521
Received: 22 September 2013 / Revised: 18 October 2013 / Accepted: 28 October 2013 / Published: 15 November 2013
Cited by 13 | PDF Full-text (3128 KB) | HTML Full-text | XML Full-text
Abstract
Vitamin B12 deficiency causes a wide range of hematological, gastrointestinal, psychiatric and neurological disorders. Hematological presentation of cobalamin deficiency ranges from the incidental increase of mean corpuscular volume and neutrophil hypersegmentation to symptoms due to severe anemia, such as angor, dyspnea on [...] Read more.
Vitamin B12 deficiency causes a wide range of hematological, gastrointestinal, psychiatric and neurological disorders. Hematological presentation of cobalamin deficiency ranges from the incidental increase of mean corpuscular volume and neutrophil hypersegmentation to symptoms due to severe anemia, such as angor, dyspnea on exertion, fatigue or symptoms related to congestive heart failure, such as ankle edema, orthopnea and nocturia. Neuropsychiatric symptoms may precede hematologic signs and are represented by myelopathy, neuropathy, dementia and, less often, optic nerve atrophy. The spinal cord manifestation, subacute combined degeneration (SCD), is characterized by symmetric dysesthesia, disturbance of position sense and spastic paraparesis or tetraparesis. The most consistent MRI finding is a symmetrical abnormally increased T2 signal intensity confined to posterior or posterior and lateral columns in the cervical and thoracic spinal cord. Isolated peripheral neuropathy is less frequent, but likely overlooked. Vitamin B12 deficiency has been correlated negatively with cognitive functioning in healthy elderly subjects. Symptoms include slow mentation, memory impairment, attention deficits and dementia. Optic neuropathy occurs occasionally in adult patient. It is characterized by symmetric, painless and progressive visual loss. Parenteral replacement therapy should be started soon after the vitamin deficiency has been established. Full article
(This article belongs to the Special Issue Vitamin B12 and Human Health)
Figures

Open AccessReview Vitamin B12 Metabolism during Pregnancy and in Embryonic Mouse Models
Nutrients 2013, 5(9), 3531-3550; doi:10.3390/nu5093531
Received: 5 July 2013 / Revised: 10 August 2013 / Accepted: 23 August 2013 / Published: 10 September 2013
Cited by 4 | PDF Full-text (269 KB) | HTML Full-text | XML Full-text
Abstract
Vitamin B12 (cobalamin, Cbl) is required for cellular metabolism. It is an essential coenzyme in mammals for two reactions: the conversion of homocysteine to methionine by the enzyme methionine synthase and the conversion of methylmalonyl-CoA to succinyl-CoA by the enzyme methylmalonyl-CoA [...] Read more.
Vitamin B12 (cobalamin, Cbl) is required for cellular metabolism. It is an essential coenzyme in mammals for two reactions: the conversion of homocysteine to methionine by the enzyme methionine synthase and the conversion of methylmalonyl-CoA to succinyl-CoA by the enzyme methylmalonyl-CoA mutase. Symptoms of Cbl deficiency are hematological, neurological and cognitive, including megaloblastic anaemia, tingling and numbness of the extremities, gait abnormalities, visual disturbances, memory loss and dementia. During pregnancy Cbl is essential, presumably because of its role in DNA synthesis and methionine synthesis; however, there are conflicting studies regarding an association between early pregnancy loss and Cbl deficiency. We here review the literature about the requirement for Cbl during pregnancy, and summarized what is known of the expression pattern and function of genes required for Cbl metabolism in embryonic mouse models. Full article
(This article belongs to the Special Issue Vitamin B12 and Human Health)

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