India is coming to grips with a stage of nutrition transition. According to the Food Safety and Standards Authority of India (FSSAI), preventable micronutrient deficiency is arising public health precedence in India. However, the foremost public health concern is the lack of national prevalence data. The present study was carried out to estimate the pooled age-wise prevalence of six preventable micronutrient deficiencies (vitamin A, vitamin B12, vitamin D, iron, iodine and folic acid) in India. A systematic review was carried out on PubMed and Global Index Medicus databases using the Boolean search strategy. Statistical analyses were done using R software, version 3.6. 2. PRISMA guidelines were strictly adhered to during the review. A preliminary literature search yielded 4302 articles; however, 270 original research articles were found eligible to be included in quantitative synthesis. The estimated overall prevalence was 17 % [95 % confidence interval (CI) 0⋅07, 0⋅26] for iodine deficiency, 37 % (95 % CI 0⋅27, 0⋅46) for folic acid deficiency, 54 % (95 % CI 0⋅49, 0⋅59) for iron deficiency, 53 % (95 % CI 0⋅41, 0⋅64) for vitamin B12 deficiency, 19 % (95 % CI 0⋅09, 0⋅29) for vitamin A deficiency and 61 % (95 % CI 0⋅07, 0⋅26) for vitamin D with high heterogeneity. We classified the population into infants (0–5 years), adolescents (<18 years), adults (>18 years) and pregnant women. Iron deficiency was most prevalent (61 %) in pregnant women. The results of the present study reinforce the data on micronutrient deficiency in India and warrant the immediate need for further active public health interventions to address these deficiencies. The study is registered with PROSPERO (CRD42020205043).

Vitamin B12 deficiency can result in a variety of neurological and psychiatric disorders. We describe a young patient in whom vitamin B12 deficiency presented as dementia with only mild hematological disease and no spinal cord disease.

Objectives: 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.

Methods: 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.

Results: Ordering serum vitamin B12 to assess cobalamin deficiency among patients with unexplained fatigue was not cost-effective in any patient population, irrespective of pretest prevalence of this deficiency. For patients with a pretest prevalence above 1 percent, treating all with oral vitamin B12 supplements without testing was most cost-effective, whereas watchful waiting with symptoms monitoring was most cost-effective for patients with lower pretest prevalence probabilities.

Conclusions: Substantial evidence gaps exist for parameter estimation: questionable cobalamin deficiency levels in the fatigued; debatable treatment methods; unknown natural history of the condition. Despite this, we reveal a robust path for disinvestment decision making in the face of a paradox between the evidence required to inform disinvestment compared with its paucity in informing initial funding decisions.

The aim of the present study was to elucidate the mechanism of the vitamin B12 deficiency-induced changes of the serine dehydratase (SDH) and tyrosine aminotransferase (TAT) activities in the rat liver. When rats were maintained on a vitamin B12-deficient diet, the activities of these two enzymes in the liver were significantly reduced compared with those in the B12-sufficient control rats (SDH 2·8 (sd 0·56) v. 17·5 (sd 6·22) nmol/mg protein per min (n 5); P < 0·05) (TAT 25·2 (sd 5·22) v. 41·3 (sd 8·11) nmol/mg protein per min (n 5); P < 0·05). In the B12-deficient rats, the level of SDH induction in response to the administration of glucagon and dexamethasone was significantly lower than in the B12-sufficient controls. Dexamethasone induced a significant increase in TAT activity in the primary culture of the hepatocytes prepared from the deficient rats, as well as in the cells from the control rats. However, a further increase in TAT activity was not observed in the hepatocytes from the deficient rats, in contrast to the cells from the controls, when glucagon was added simultaneously with dexamethasone. The glucagon-stimulated production of cAMP was significantly reduced in the hepatocytes from the deficient rats relative to the cells from the control rats. Furthermore, the glucagon-stimulated adenylyl cyclase activity in the liver was significantly lower in the deficient rats than in the controls. These results suggest that vitamin B12 deficiency results in decreases in SDH and TAT activities correlated with the impairment of the glucagon signal transduction through the activation of the adenylyl cyclase system in the liver.

In the UK vitamin B12 deficiency occurs in approximately 20% of adults aged >65 years. This incidence is significantly higher than that among the general population. The reported incidence invariably depends on the criteria of deficiency used, and in fact estimates rise to 24% and 46% among free-living and institutionalised elderly respectively when methylmalonic acid is used as a marker of vitamin B12 status. The incidence of, and the criteria for diagnosis of, deficiency have drawn much attention recently in the wake of the implementation of folic acid fortification of flour in the USA. This fortification strategy has proved to be extremely successful in increasing folic acid intakes pre-conceptually and thereby reducing the incidence of neural-tube defects among babies born in the USA since 1998. However, in successfully delivering additional folic acid to pregnant women fortification also increases the consumption of folic acid of everyone who consumes products containing flour, including the elderly. It is argued that consuming additional folic acid (as ‘synthetic’ pteroylglutamic acid) from fortified foods increases the risk of ‘masking’ megaloblastic anaemia caused by vitamin B12 deficiency. Thus, a number of issues arise for discussion. Are clinicians forced to rely on megaloblastic anaemia as the only sign of possible vitamin B12 deficiency? Is serum vitamin B12 alone adequate to confirm vitamin B12 deficiency or should other diagnostic markers be used routinely in clinical practice? Is the level of intake of folic acid among the elderly (post-fortification) likely to be so high as to cure or ‘mask’ the anaemia associated with vitamin B12 deficiency?

To clarify the bioavailability of vitamin B12 in lyophylized purple laver (nori; Porphyra yezoensis), total vitamin B12 and vitamin B12 analogue contents in the laver were determined, and the effects of feeding the laver to vitamin B12-deficient rats were investigated. The amount of total vitamin B12 in the dried purple laver was estimated to be 54.5 and 58.6 (SE 5.3 and 7.5 respectively) ΜG/100 g dry weight by lactobacillus bioassay and chemiluminescent assay with hog intrinsic factor respectively. the purple laver contained five types of biologically active vitamin b12 compounds (cyano-, hydroxo-, sulfito-, adenosyl- and methylcobalamin), in which the vitamin b12 coezymes (adenosyl- and methylcobalamin) comprised about 60 % of the total vitamin b12. when 9-week-old vitamin b12-deficient rats, which excreted substantial amounts of methylmalonic acid (71.7(se 20.2) μmol/d) in urine, were fed the diet supplemented with dried purple laver (10 μg/kg diet) for 20 d, urinary methylmalonic acid excretion (as an index of vitamin B12 deficiency) became undetectable and hepatic vitamin B12 (especially adenosylcobalamin) levels were significantly increased. These results indicate that vitamin B12 in dried purple laver is bioavailable to rats.