vitamin B deficiency

Choline and betaine are nutrients involved in one-carbon metabolism. Choline is essential for neurodevelopment and brain function. We studied the associations between cognitive function and plasma concentrations of free choline and betaine. In a cross-sectional study, 2195 subjects (55 % women), aged 70-74 years, underwent extensive cognitive testing including the Kendrick Object Learning Test (KOLT), Trail Making Test (part A, TMT-A), modified versions of the Digit Symbol Test (m-DST), Block Design (m-BD), Mini-Mental State Examination (m-MMSE) and Controlled Oral Word Association Test (COWAT). Compared with low concentrations, high choline (.8·4 mmol/l) was associated with better test scores in the TMT-A (56·0 v. 61·5, P¼ 0·004), m-DST (10·5 v. 9·8, P¼ 0·005) and m-MMSE (11·5 v. 11·4, P¼ 0·01). A generalised additive regression model showed a positive dose -response relationship between the m-MMSE and choline (P¼0·012 from a corresponding linear regression model). Betaine was associated with the KOLT, TMT-A and COWAT, but after adjustments for potential confounders, the associations lost significance. Risk ratios (RR) for poor test performance roughly tripled when low choline was combined with either low plasma vitamin B 12 (# 257 pmol/l) concentrations (RR KOLT ¼ 2·6, 95 % CI 1·1, 6·1; RR m-MMSE ¼ 2·7, 95 % CI 1·1, 6·6; RR COWAT ¼ 3·1, 95 % CI 1·4, 7·2) or high methylmalonic acid (MMA) ($3·95 mmol/l) concentrations (RR m-BD ¼ 2·8, 95 % CI 1·3, 6·1). Low betaine (# 31·1 mmol/l) combined with high MMA was associated with elevated RR on KOLT (RR KOLT ¼ 2·5, 95 % CI 1·0, 6·2). Low plasma free choline concentrations are associated with poor cognitive performance. There were significant interactions between low choline or betaine and low vitamin B 12 or high MMA on cognitive performance.

Vitamin B 12 deficiency is a common problem in elderly subjects. If a serum cobalamin level of about 150 pmol/L (200 pg/mL) is considered normal, 10 -15% of the elderly are deficient. Today, however, a threshold of 220 -258 pmol/L (300 -350 pg/mL) is recognized as desirable in the elderly, or else sensitive markers like the blood concentration of homocysteine or methylmalonic acid (MMA) are used. Then the prevalence of cobalamin deficiency rises to up to 43%. In the elderly, this high prevalence of poor cobalamin status is predominantly caused by atrophic gastritis type B. Atrophic gastritis results in declining gastric acid and pepsinogen secretion, and hence decreasing intestinal absorption of the cobalamin protein complexes from food. About 20 -50% of the elderly are affected. Furthermore, the reduced acid secretion leads to an alkalinization of the small intestine, which may result in bacterial overgrowth and thus to a further decrease of the bioavailability of the vitamin. In addition, some drugs such as proton pump inhibitors or H2 receptor antagonists inhibit the intestinal absorption of vitamin B 12 . An already moderately reduced vitamin B 12 level is associated with vascular disease and neurocognitive disorders such as depression and impaired cognitive performance. Furthermore, a poor vitamin B 12 status is assumed to be involved in the development and progression of dementia (e.g., Alzheimer's dementia). This is especially observable if the folic acid status is reduced as well. Due to the insecure supply, the cobalamin status of elderly persons (z60 years) should be regularly controlled and a general supplementation with vitamin B 12 (>50 Ag/day) should be considered.

Psychiatric disturbance was alluded to in Addison's original description of pernicious anaemia, and nowadays the disorder is recognised as being associated with depression, mania, psychosis and dementia. 1 It is also known that psychiatric symptoms can precede the onset of anaemia or neurological features and can sometimes be seen in the absence of macrocytosis. 2 A case report has recently added catatonia to the list of psychiatric syndromes associated with B 12 deficiency. Here we present a further case, where catatonia was the presenting -and only -psychiatric feature of what turned out to be autoimmune B 12 deficiency. Haematological abnormality was absent and neurological abnormality was subtle to the point of being easy to dismiss.

This review brings together human and animal studies and reviews that examine the possible role of maternal vitamin B12 (B12) on fetal growth and its programming for susceptibility to chronic disease. A selective literature review was undertaken to identify studies and reviews that investigate these issues, particularly in the context of a vegetarian diet that may be low in B12 and protein and high in carbohydrate. Evidence is accumulating that maternal B12 status influences fetal growth and development. Low maternal vitamin B12 status and protein intake are associated with increased risk of neural tube defect, low lean mass and excess adiposity, increased insulin resistance, impaired neurodevelopment and altered risk of cancer in the offspring. Vitamin B12 is a key nutrient associated with one carbon metabolic pathways related to substrate metabolism, synthesis and stability of nucleic acids and methylation of DNA which regulates gene expression. Understanding of factors regulating maternal-fetal one carbon metabolism and its role in fetal programming of non communicable diseases could help design effective interventions, starting with maternal nutrition before conception.

A 61-year-old eutrophic male was diagnosed with vitamin B12 deficiency and megaloblastic anemia. A modified Schilling test suggested intestinal malabsorption unrelated to intrinsic factor deficiency. Subsequent colonoscopy revealed the presence of a Taenia tapeworm. The anemia resolved within days under therapy with niclosamide and temporary vitamin B12 supplements. The present case suggests that, in addition to other wellknown parasitic agents, e.g., Diphyllobothrium latum and Giardia lamblia, Taenia infestation can also be a cause of intestinal vitamin B12 malabsorption.

Background Cobalamin deficiency is prevalent in vegetarians and has been associated with increased risk of osteoporosis. Aim of the study To examine the association between cobalamin status and bone mineral density in adolescents formerly fed a macrobiotic diet and in their counterparts. Methods In this cross–sectional study bone mineral density (BMD) and bone mineral content (BMC) were determined by DEXA in 73 adolescents (9–15 y) who were fed a macrobiotic diet up to the age of 6 years followed by a lacto–(–ovo–) vegetarian or omnivorous diet. Data from 94 adolescents having consumed an omnivorous diet throughout their lives were used as controls. Serum concentrations of cobalamin, methylmalonic acid (MMA) and homocysteine were measured and calcium intake was assessed by questionnaire. Analysis of covariance (MANCOVA) was performed to calculate adjusted means for vitamin B12 and MMA for low and normal BMC and BMD groups. Results Serum cobalamin concentrations were significantly lower (geometric mean (GM) 246 pmol/L vs. 469 pmol/L) and MMA concentrations were significantly higher (GM 0.27 µmol/L vs. 0.16 µmol/L) in the formerly macrobiotic–fed adolescents compared to their counterparts. In the total study population, after adjusting for height, weight, bone area, percent lean body mass, age, puberty and calcium intake, serum MMA was significantly higher in subjects with a low BMD (p = 0.0003) than in subjects with a normal BMD. Vitamin B12 was significantly lower in the group with low BMD (p = 0.0035) or BMC (p = 0.0038) than in the group with normal BMD or BMC. When analyses were restricted to the group of formerly macrobiotic–fed adolescents, MMA concentration remained higher in the low BMD group compared to the normal BMD group. Conclusion In adolescents, signs of an impaired cobalamin status, as judged by elevated concentrations of methylmalonic acid, were associated with low BMD. This was especially true in adolescents fed a macrobiotic diet during the first years of life, where cobalamin deficiency was more prominent.

Thin-layer chromatography and bioautography were used to study the cobalamin pattern of plasma, erythrocytes, and hepatic tissue from patients with cobalamin deficiency on maintenance therapy with hydroxocobalamin (Vibeden), a cyanocobalamin depot preparation (Betolvex), or cyanocobalamin tablets (Behepan). The cobalamin pattern in plasma is dominated by the form in which it is administered. The results of assaying the erythrocytes and liver biopsies show that the cobalamins administered are converted to the coenzyme forms in vivo, irrespective of the type of cobalamin preparation.

insulin-like activity or of transforming growth factor-a, which is thought to interact with the epidermal growth factor receptor. 3 Insulin level was normal in the present patient but we do not know if the present patient had a relative insuline resistance. We believe that other etiopathologic or stimulating factors, which are unknown, yet may play a role in the development of AN, as in the present case.

In summary, rosacea-like eruptions may be a dermatological side effect of nilotinib treatment. To date, there have been few clinical reports about the cutaneous adverse effects of nilotinib. Additional case reports and research are needed to determine the mechanism by which nilotinib induces rosacea-like eruptions.

The importance of folate in reproduction can be appreciated by considering that the existence of the vitamin was first suspected from efforts to explain a potentially fatal megaloblastic anemia in young pregnant women in India. Today, low maternal folate status during pregnancy and lactation remains a significant cause of maternal morbidity in some communities. The folate status of the neonate tends to be protected at the expense of maternal stores; nevertheless, there is mounting evidence that inadequate maternal folate status during pregnancy may lead to low infant birthweight, thereby conferring risk of developmental and long-term adverse health outcomes. Moreover, folate-related anemia during childhood and adolescence might predispose children to further infections and disease. The role of folic acid in prevention of neural tube defects (NTD) is now established, and several studies suggest that this protection may extend to some other birth defects. In terms of maternal health, clinical vitamin B12 deficiency may be a cause of infertility or recurrent spontaneous abortion. Starting pregnancy with an inadequate vitamin B12 status may increase risk of birth defects such as NTD, and may contribute to preterm delivery, although this needs further evaluation. Furthermore, inadequate vitamin B12 status in the mother may lead to frank deficiency in the infant if sufficient fetal stores of vitamin B12 are not laid down during pregnancy or are not available in breastmilk. However, the implications of starting pregnancy and lactation with low vitamin B12 status have not been sufficiently researched.

The concentration of total homocysteine (tHcy) in serum and plasma is elevated in both folate and cobalamin deficiencies, whereas methylmalonic acid (MMA) in serum, plasma, or urine is a specific marker of cobalamin function. The combined measurement of both metabolites is useful for the diagnosis and follow-up of these deficiency states. In addition, tHcy is elevated under various pathologic states (eg, renal failure), and hyperhomocysteinemia is associated with an increased risk of cardiovascular disease, cognitive dysfunction, and adverse pregnancy outcomes. The diagnostic utility of tHcy and MMA concentrations as markers of folate and cobalamin deficiencies in healthy and diseased children has been documented. This article briefly summarizes the biochemical background of tHcy and MMA and the associations of tHcy and MMA with various disease states and focuses on novel data obtained in infants, children, and adolescents, with emphasis on cobalamin status in infants. The utility o...

Fortification of food with folic acid to reduce the number of neural tube defects was introduced 10 y ago in North America. Many countries are considering whether to adopt this policy. When fortification is introduced, several hundred thousand people are exposed to an increased intake of folic acid for each neural tube defect pregnancy that is prevented. Are the benefits to the few outweighed by possible harm to some of the many exposed? In animals, a folic acid-rich diet can influence DNA and histone methylation, which leads to phenotypic changes in subsequent generations. In humans, increased folic acid intake leads to elevated blood concentrations of naturally occurring folates and of unmetabolized folic acid. High blood concentrations of folic acid may be related to decreased natural killer cell cytotoxicity, and high folate status may reduce the response to antifolate drugs used against malaria, rheumatoid arthritis, psoriasis, and cancer. In the elderly, a combination of high folate levels and low vitamin B-12 status may be associated with an increased risk of cognitive impairment and anemia and, in pregnant women, with an increased risk of insulin resistance and obesity in their children. Folate has a dual effect on cancer, protecting against cancer initiation but facilitating progression and growth of preneoplastic cells and subclinical cancers, which are common in the population. Thus, a high folic acid intake may be harmful for some people. Nations considering fortification should be cautious and stimulate further research to identify the effects, good and bad, caused by a high intake of folic acid from fortified food or dietary supplements. Only then can authorities develop the right strategies for the population as a whole.

Deficiencies of the vitamins folate, B 12 , and B 6 are associated with neurological and psychological dysfunction and with congenital defects. In the elderly, cognitive impairment and incident dementia may be related to the high prevalence of inadequate B vitamin status and to elevations of plasma homocysteine. Plausible mechanisms include homocysteine neurotoxicity, vasotoxicity, and impaired S-adenosylmethionine-dependent methylation reactions vital to central nervous system function. In light of this, it is imperative to find safe ways of improving vitamin B status in the elderly without exposing some individuals to undue risk.

for hemoglobin, B12, methylmalonic acid (MMA), total homocysteine (tHcy), ferritin and serum transferrin receptor, C-reactive protein (CRP) and alpha-1-acid glycoprotein (AGP). Vitamin B12 was also assessed in breast milk. H1N1-specific antibodies were determined in plasma and colostrum/breast milk. Results At baseline, 26 % women were B12 deficient (<150 pmol/L), 40 % had marginal status (150-220 pmol/L), 43 % had elevated MMA (>271 nmol/L), and 31 % had elevated tHcy (>10 μmol/L). Supplementation increased B12 in plasma, colostrums and breast milk (p < 0.05) and lowered MMA in neonates, mothers and infants at 3 months (p < 0.05). B12 supplementation significantly increased H1N1-specific IgA responses in plasma and colostrums in mothers and reduced proportion of infants with elevated AGP and CRP compared with placebo. Conclusion Supplementation with 250 μg/day B12 during pregnancy and lactation substantially improved maternal, infant and breast milk B12 status. Maternal supplementation improved H1N1 vaccine-specific responses in mothers only and may alleviate inflammatory responses in infants.

Objective: To investigate the association of serum vitamin B 12 , folic acid, iron, calcium, magnesium, and phosphorus levels as well as family history and cigarette smoking with recurrent aphthous stomatitis (RAS). Methods: Thirty-four patients with RAS and 32 control subjects were included in this controlled prospective screening study. Both groups received a questionnaire, and serum screening tests were performed. The collected data were analyzed using v 2 test and binary logistic regression analysis. Results: Family history was found to be the most significant predisposing factor for RAS among the investigated ones. Regarding the serum tests, only vitamin B 12 was found to have significant correlation with RAS. Patients with vitamin B 12 deficiency, positive family history, and nonsmoking status have been found to have the highest risk for having RAS. Conclusions: RAS is a multifactorial disease. Positive family history, vitamin B 12 deficiency, and nonsmoking status are among the important predisposing factors. D

The aim of this international guideline on dementia was to present a peer-reviewed evidence-based statement for the guidance of practice for clinical neurologists, geriatricians, psychiatrists, and other specialist physicians responsible for the care of patients with dementia. It covers major aspects of diagnostic evaluation and treatment, with particular emphasis on the type of patient often referred to the specialist physician. The main focus is Alzheimer's disease, but many of the recommendations apply to dementia disorders in general. The task force working group considered and classified evidence from original research reports, meta-analysis, and systematic reviews, published before January 2006. The evidence was classified and consensus recommendations graded according to the EFNS guidance. Where there was a lack of evidence, but clear consensus, good practice points were provided. The recommendations for clinical diagnosis, blood tests, neuroimaging, electroencephalography (EEG), cerebrospinal fluid (CSF) analysis, genetic testing, tissue biopsy, disclosure of diagnosis, treatment of Alzheimer's disease, and counselling and support for caregivers were all revised when compared with the previous EFNS guideline. New recommendations were added for the treatment of vascular dementia, Parkinson's disease dementia, and dementia with Lewy bodies, for monitoring treatment, for treatment of behavioural and psychological symptoms in dementia, and for legal issues. The specialist physician plays an important role together with primary care physicians in the multidisciplinary dementia teams, which have been established throughout Europe. This guideline may contribute to the definition of the role of the specialist physician in providing dementia health care.

Folate, vitamin B 12 and human health During the past decade the role of folate and vitamin B 12 in human nutrition have been under constant re-examination. Basic knowledge on the metabolism and interactions between these essential nutrients has expanded and multiple complexities have been unraveled. ese micronutrients have shared functions and intertwined metabolic pathways that dene the size of the &quot;methyl donor&quot; pool utilized in multiple metabolic pathways; these include DNA methylation and synthesis of nucleic acids. In Chile, folate deciency is virtually nonexis-tent, while vitamin B 12 deciency aects approximately 8.5-51% depending on the cut-o value used to dene deciency. Folate is found naturally mainly in vegetables or added as folic acid to staple foods. Vitamin B 12 in its natural form is present only in foods of animal origin, which is why decit is more common among strict vegetarians and populations with a low intake of animal foods. Poor folate status in vuln...

BACKGROUND: Conventional tests for vitamin B 12 deficiency measure total serum vitamin B 12 , whereas only that portion of vitamin B 12 carried by transcobalamin (holotranscobalamin) is metabolically active. Measurement of holotranscobalamin (holoTC) may be more diagnostically accurate for detecting B 12 deficiency that requires therapy. We developed an automated assay for holoTC that can be used on the Abbott AxSYM immunoassay analyzer.

The prevalence of vitamin B 12 deficiency increases in the elderly, mainly because atrophic gastritis decreases the production of the acid and digestive enzymes needed to cleave protein-bound vitamin B 12 from the natural chemical form of vitamin B 12 found in meat, poultry, fish, and dairy foods. Depending on the biochemical criterion that is used, 5% to more than 20% of older adults have marginal or frank vitamin B 12 deficiency. Adults over 50 years of age should meet the Recommended Dietary Allowance by consuming vitamin B 12 in the crystalline form, which does not require gastric acid or enzymes for initial digestion. A recent clinical trial suggests that an oral dose of 500 g/d of crystalline vitamin B 12 is needed to reverse biochemical signs of vitamin B 12 deficiency in older adults.

During the past decade the role of folate and vitamin B 12 in human nutrition have been under constant re-examination. Basic knowledge on the metabolism and interactions between these essential nutrients has expanded and multiple complexities have been unraveled. These micronutrients have shared functions and intertwined metabolic pathways that define the size of the "methyl donor" pool utilized in multiple metabolic pathways; these include DNA methylation and synthesis of nucleic acids. In Chile, folate deficiency is virtually nonexistent, while vitamin B 12 deficiency affects approximately 8.5-51% depending on the cut-off value used to define deficiency. Folate is found naturally mainly in vegetables or added as folic acid to staple foods. Vitamin B 12 in its natural form is present only in foods of animal origin, which is why deficit is more common among strict vegetarians and populations with a low intake of animal foods. Poor folate status in vulnerable women of childbearing age increases the risk of neural tube birth defects, so the critical time for the contribution of folic acid is several months before conception since neural tube closure occurs during the first weeks of life. The absorption of vitamin B 12 from food is lower in older adults, who are considered to have higher risk of gastric mucosa atrophy, altered production of intrinsic factor and acid secretion. Deficiency of these vitamins is associated with hematological disorders. Vitamin B 12 deficiency can also induce clinical and sub-clinical neurological and of other disorders. The purpose of this review is to provide an update on recent advances in the basic and applied knowledge of these vitamins relative to human health. (Rev Med Chile 2012; 140: 1464-1475.

Methylenetetrahydrofolate reductase (MTHFR) is a critical folate-metabolising enzyme which requires riboflavin as its co-factor. A common polymorphism (677C→T) in the MTHFR gene results in reduced MTHFR activity in vivo which in turn leads to impaired folate metabolism and elevated homocysteine concentrations. Homozygosity for this polymorphism (TT genotype) is associated with an increased risk of a number of conditions including heart disease and stroke, but there is considerable variability in the extent of excess risk in various reports. The present review will explore the evidence which supports a role for this polymorphism as a risk factor for a number of adverse health outcomes, and the potential modulating roles for B-vitamins in alleviating disease risk. The evidence is convincing in the case which links this polymorphism with hypertension and hypertensive disorders of pregnancy, particularly preeclampsia. Furthermore, elevated blood pressure was found to be highly responsiv...

Background: Cobalamin deficiency has been described in children consuming macrobiotic diets. Objective: We investigated whether moderate consumption of animal products is sufficient for achieving normal cobalamin function in 73 adolescents who had received a macrobiotic diet until 6 y of age and had then switched to a lactovegetarian, lactoovovegetarian, or omnivorous diet (macrobiotic adolescents). Design: Hematologic indexes and serum concentrations of methylmalonic acid (MMA), total homocysteine (tHcy), and folate were measured. Current consumption frequency of animal products and cobalamin intake from dairy products were assessed by questionnaire. Data from 94 age-matched adolescents who received an omnivorous diet from birth were used as a reference. Results: Serum cobalamin concentrations were significantly lower and concentrations of MMA and folate and mean corpuscular volume (MCV) were significantly higher in macrobiotic adolescents than in control adolescents: of macrobiotic adolescents, 21% had abnormal MMA concentrations (> 0.41 mol/L), 37% had abnormal cobalamin concentrations (< 218 pmol/L), 10% had abnormal tHcy concentrations (> 12.8 mol/L), and 15% had abnormal MCV (> 89 fL). In macrobiotic adolescents, dairy products (200 g milk or yogurt and 22 g cheese/d) supplied on average 0.95 g cobalamin/d; additionally, these adolescents consumed fish, meat, or chicken 2-3 times/wk. In girls, meat consumption contributed more to cobalamin status than the consumption of dairy products, whereas in boys these food groups were equally important. Conclusions: A substantial number of the formerly strict macrobiotic adolescents still had impaired cobalamin function. Thus, moderate consumption of animal products is not sufficient for restoring normal cobalamin status in subjects with inadequate cobalamin intake during the early years of life.

Vitamin B6 is thought to be a most versatile coenzyme that participates in more than 100 biochemical reactions. It is involved in amino acid and homocysteine metabolism, glucose and lipid metabolism, neurotransmitter production and DNA/RNA synthesis. Vitamin B6 can also be a modulator of gene expression. Nowadays, clinically evident vitamin B6 deficiency is not a common disorder, at least in the general population. Nevertheless, a subclinical, undiagnosed deficiency may be present in some subjects, particularly in the elderly. This review gives a complete overview over the metabolism and interactions of vitamin B6. Further, we show which complications and deficiency symptoms can occur due to a lack of vitamin B6 and possibilities for public health and supplemental interventions. The database Medline (www.ncvi.nlm.nih.gov) was searched for terms like &quot;vitamin B6&quot;, &quot;pyridoxal&quot;, &quot;cancer&quot;, &quot;homocysteine&quot;, etc. For a complete understanding, we incl...

Neural tube defects (NTDs) are one of the commonest birth defects with a high incidence in India. However, few studies have systematically looked into the etio-pathogeneis of NTDs, which mainly includes nutritional deficiencies and genetic predisposition. Efforts are afoot for universal food fortification with folic acid in the hope of preventing NTDs, without factual evidence of folate deficiency in the target population. We conducted a review of Indian literature on NTDs focusing on the role of folate and vitamin B12 nutrition and common genetic polymorphisms in 1-carbon metabolism. We performed a literature search of Medline and Indian Medlars (www. indmed.nic.in) for articles using following search terms: Neural tube defect and India, published up to November 2008, on human subjects. We did not include individual case reports and case series describing surgical and medical management, genetic syndromes where NTD was only one of the features or unusual associations of NTDs with o...

Objective: We describe a case of irreversible subacute sclerotic combined degeneration of the spinal cord in a Western vegan subject. Methods: A 57-y-old man, member of a vegan cult for 13 y, developed weakness, paraplegia, hyper-reflexia, distal symmetric muscular hypotrophy, impairment of superficial sensation in the hands and feet, loss of deep sensation in the lower limbs, and neurogenic bladder and bowel. Magnetic resonance imaging of the cervical and dorsal spine disclosed abnormally increased signal intensity on T 2 -weighted sections in the posterior and lateral columns. Subacute sclerotic combined degeneration of the spinal cord was diagnosed and treatment with cobalamin was started. Results: Despite rehabilitative treatment, the patient developed spastic hypertonia with mild improvement of paresthesias. Six months later, vitamin B12 plasma levels and hematological analysis were normal. One year later, spastic paraplegia was still present and the patient was unable to walk despite improvement on magnetic resonance imaging. Conclusion: Irreversible subacute sclerotic combined degeneration of the spinal cord is a rare but possible effect of a strict vegetarian diet.

A compromised vitamin B 12 status is common in older people despite dietary intakes that typically far exceed current recommendations. The maintenance of an optimal status of vitamin B 12 is not only dependent on adequate dietary intake but more critically on effective absorption which diminishes with age. The measurement of vitamin B 12 is complicated by the lack of a gold standard assay. There are a number of direct and functional indicators of vitamin B 12 status; however, none of these are without limitations and should be used in combination. Vitamin B 12 is of public health importance, not only because deficiency leads to megaloblastic anaemia and irreversible nerve damage, but also because emerging evidence links low B 12 to an increased risk of a number of age-related diseases, including cardiovascular disease, cognitive dysfunction, dementia and osteoporosis. Furthermore, there are concerns relating to potential adverse effects for older adults with low vitamin B 12 status of over-exposure to folic acid in countries where there is mandatory fortification of food with folic acid. The aim of this review is to examine the known and emerging issues related to vitamin B 12 in ageing, its assessment and inter-relationship with folate.

Poor vitamin B 12 status may lead to the development of cognitive decline and dementia but there is a large variation in the quality, design of and results reported from these investigations. We have undertaken a systematic review of the evidence for the association between vitamin B 12 status and cognitive decline in older adults. A database search of the literature to 2011 was undertaken, using keywords related to vitamin B 12 and cognition. All prospective cohort studies assessing the association of serum vitamin B 12 or biomarkers were included. Quality assessment and extraction of the data were undertaken by two researchers. The quality assessment tool assigns a positive, neutral or negative rating. Of 3772 published articles, thirty-five cohort studies (n 14 325 subjects) were identified and evaluated. No association between serum vitamin B 12 concentrations and cognitive decline or dementia was found. However, four studies that used newer biomarkers of vitamin B 12 status (methylmalonic acid and holotranscobalamin (holoTC)) showed associations between poor vitamin B 12 status and the increased risk of cognitive decline or dementia diagnosis. In general, the studies were of reasonable quality (twenty-one positive, ten neutral and four negative quality) but of short duration and inadequate subject numbers to determine whether an effect exists. Future studies should be of adequate duration (at least 6 years), recruit subjects from the seventh decade, choose markers of vitamin B 12 status with adequate specificity such as holoTC and/or methylmalonic acid and employ standardised neurocognitive assessment tools and not screening tests in order to ascertain any relationship between vitamin B 12 status and cognitive decline.

Vitamin B 12 deficiency anemia may have psychiatric manifestations preceding the hematological symptoms. Although a variety of symptoms are described, there are only sparse data on the role of vitamin B 12 in depression. We report a case of vitamin B 12 deficiency presenting with recurrent episodes of depression.

Health technology reassessment and disinvestment can be difficult due to uncertainties regarding available evidence. Pathology testing to investigate cobalamin (vitamin B12) deficiency is a strong case in point. We conducted a 3-month economic evaluation of five strategies for diagnosing and treating cobalamin deficiency in adult patients hypothetically presenting with new unexplained fatigue in the primary care setting. The first consultation per patient was considered. Screening tests other than serum cobalamin were not included. A cost-effectiveness analysis was undertaken using a decision tree to represent the diagnostic / treatment pathways, with relevant cost and utility scores assigned to different stages in the evaluation process. Input parameter values were estimated from published evidence, supplemented by expert opinion, with sensitivity analysis undertaken to represent parameter uncertainty. Ordering serum vitamin B12 to assess cobalamin deficiency among patients with un...

The aim of the study was to induce B deficiency symptoms and to relate the generation of reactive oxygen species (ROS) and altered cellular redox environment with the effects of B deficiency in mulberry (Morus alba L.) cv. Kanva-2 plants. Study was undertaken on antioxidant responses, malondialdehyde (MDA) content as an indicator of oxidative damage and ratio of dehydroascorbate (DHA) to ascorbic acid (AsA) as an index of cellular redox environment in B-deficient (0.0 μM) and B-supraoptimal (33 μM) mulberry plants. B deficiency symptoms appeared as upward cupping of the young emerging leaves. Later on, B-deficient plants developed lenticels like cracks on major vein, petiole and stem. B-deficient leaves had higher water potential (Ψ) and relative water content (RWC), contained a lower concentration of B, less chloroplastic pigments and high tissue Fe, Mn and Zn concentrations compared to the controls. Hydrogen peroxide was accumulated in leaves of B-deficient and B-supraoptimal plants. B-supraoptimal plants also showed an increased DHA/AsA ratio. The activities of superoxide dismutase (SOD, EC 1.15.1.1), catalase (CAT, EC 1.11.1.6), peroxidase (POD, EC 1.11.1.7) and ascorbate peroxidase (APX, EC 1.11.1.11) were increased in B-deficient leaves. The activities of SOD and POD were decreased in B-supraoptimal plants. The results suggest that B deficiency aggravates oxidative stress through enhanced generation of ROS in mulberry plants.

T he consultation psychiatrist is frequently called upon to assess patients in medical settings with primary or secondary hematologic disorders. This article addresses psychiatric issues that are specific to patients who have selected hematologic disorders, including B 12 and folate deficiency, sickle cell disease, and hemophilia, discussing the diseases, their unique psychiatric manifestations, and approaches to management. A review of hematologic side effects of psychotropic medications is also included.

A roundtable to discuss the measurement of vitamin B-12 (cobalamin) status biomarkers in NHANES took place in July 2010. NHANES stopped measuring vitamin B-12-related biomarkers after 2006. The roundtable reviewed 3 biomarkers of vitamin B-12 status used in past NHANES-serum vitamin B-12, methylmalonic acid (MMA), and total homocysteine (tHcy)-and discussed the potential utility of measuring holotranscobalamin (holoTC) for future NHANES. The roundtable focused on public health considerations and the quality of the measurement procedures and reference methods and materials that past NHANES used or that are available for future NHANES. Roundtable members supported reinstating vitamin B-12 status measures in NHANES. They noted evolving concerns and uncertainties regarding whether subclinical (mild, asymptomatic) vitamin B-12 deficiency is a public health concern. They identified the need for evidence from clinical trials to address causal relations between subclinical vitamin B-12 deficiency and adverse health outcomes as well as appropriate cutoffs for interpreting vitamin B-12-related biomarkers. They agreed that problems with sensitivity and specificity of individual biomarkers underscore the need for including at least one biomarker of circulating vitamin B-12 (serum vitamin B-12 or holoTC) and one functional biomarker (MMA or tHcy) in NHANES. The inclusion of both serum vitamin B-12 and plasma MMA, which have been associated with cognitive dysfunction and anemia in NHANES and in other population-based studies, was preferable to provide continuity with past NHANES. Reliable measurement procedures are available, and National Institute of Standards and Technology reference materials are available or in development for serum vitamin B-12 and MMA.