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The detection and correction of vitamin B12 (B12) deficiency prevents megaloblastic anaemia and potentially irreversible neuropathy and neuropsychiatric changes. B12 status is commonly estimated using the abundance of the vitamin in serum, with ∼148 pmol/L (200 ng/L) typically set as the threshold for diagnosing deficiency. Serum B12 assays measure the sum of haptocorrin-bound and transcobalamin-bound (known as holotranscobalamin) B12. It is only holotranscobalamin that is taken up by cells to meet metabolic demand. Although receiver operator characteristic curves show holotranscobalamin measurement to be a moderately more reliable marker of B12 status than serum B12, both assays have an indeterminate range. Biochemical evidence of metabolic abnormalities consistent with B12 insufficiency is frequently detected despite an apparently sufficient abundance of the vitamin. Laboratory B12 status markers that reflect cellular utilisation rather than abundance are available. Two forms of B12 act as coenzymes for two different reactions. Methionine synthase requires methylcobalamin for the remethylation of methionine from homocysteine. A homocysteine concentration >20 µmol/L may suggest B12 deficiency in folate-replete patients. In the second B12-dependent reaction, methylmalonyl-CoA mutase uses adenosylcobalamin to convert methylmalonyl-CoA to succinyl-CoA. In B12 deficiency excess methylmalonyl-CoA is hydrolysed to methylmalonic acid. A serum concentration >280 nmol/L may suggest suboptimal status in young patients with normal renal function. No single laboratory marker is suitable for the assessment of B12 status in all patients. Sequential assay selection algorithms or the combination of multiple markers into a single diagnostic indicator are both approaches that can be used to mitigate inherent limitations of each marker when used independently.

Disorders of cobalamin (vitamin B12) metabolism are increasingly recognized in small animal medicine and have a variety of causes ranging from chronic gastrointestinal disease to hereditary defects in cobalamin metabolism. Measurement of serum cobalamin concentration, often in combination with serum folate concentration, is routinely performed as a diagnostic test in clinical practice. While the detection of hypocobalaminemia has therapeutic implications, interpretation of cobalamin status in dogs can be challenging. The aim of this review is to define hypocobalaminemia and cobalamin deficiency, normocobalaminemia, and hypercobalaminemia in dogs, describe known cobalamin deficiency states, breed predispositions in dogs, discuss the different biomarkers of importance for evaluating cobalamin status in dogs, and discuss the management of dogs with hypocobalaminemia.

Background/Objectives: Severe mental illnesses such as schizophrenia, major depressive disorder, and bipolar disorder are often accompanied by metabolic comorbidities. While the role of vitamins in physical health is well-established, their involvement in psychiatric disorders has garnered increasing attention in recent years. Methods: We conducted a cross-sectional analysis of 1003 patients diagnosed with severe mental illnesses. Vitamin D, B9, and B12 serum levels were measured, and deficiencies were defined using established clinical cutoffs. Multivariate regression analyses were performed to identify associations between vitamin deficiencies and clinical outcomes. Results: Our findings revealed that vitamin deficiencies were prevalent across all diagnostic groups, with particularly high rates in patients with schizophrenia and major depressive disorder. Vitamin D deficiency was significantly associated with worse psychiatric outcomes, including increased depressive symptoms (adjusted OR = 1.89, p = 0.018), lower Global Assessment of Functioning scores (adjusted OR = −0.18, p < 0.001), and higher rates of metabolic syndrome (adjusted OR = 1.97, p = 0.007). Folate and B12 deficiencies were also linked to greater psychiatric symptom severity and metabolic disturbances, including increased risks of obesity and dyslipidemia. Conclusions: Our study highlights the critical role of vitamins deficiencies in both psychiatric and metabolic health of patients with severe mental illnesses. These findings underscore the importance of routine screening and correction of these deficiencies as part of comprehensive care in psychiatric populations. The integration of nutritional interventions may offer a novel and holistic approach to improving both mental and physical health outcomes.

Vitamin B12 (cobalamin) is a critical micronutrient involved in hematopoiesis and neurological function. Its deficiency, commonly presenting with anemia and neurological symptoms, is particularly relevant in oncology. While anemia affects up to 60% of cancer patients, the contribution of vitamin B12 deficiency to cancer-related anemia remains underexplored. Additionally, cobalamin-related neuropathy manifests or exacerbates existing chemotherapy-induced peripheral neuropathy (CIPN), a serious side effect of chemotherapy. Prevalence estimates in cancer populations range widely (6–48%), with higher rates in elderly and gastrointestinal cancer patients. This review summarizes current evidence on the prevalence and implications of both vitamin B12 deficiency and excess in patients with solid tumors. It discusses laboratory markers (such as serum vitamin B12, holotranscobalamin, methylmalonic acid, and homocysteine) that could improve diagnostic accuracy in oncology settings. Additionally, it evaluates supplementation strategies and discusses its role in mitigating CIPN. Additionally, it addresses B12′s emerging immunological role in cancer therapy.

•Vitamin B12 (B12) is a nutrient of particular concern in plant-based diets, and should be readily supplemented on a continuous basis to ensure adequate B12 levels and to prevent deficiencies.•A short-term B12 supplement intake cessation might be well tolerated by vegans with an adequate B12 status, an interruption of more than 8 wk could signify B12 loss approaching suboptimal status.•The present case study reiterates the need for continuous B12 supplementation in persons following an unfortified plant-based diet. Healthy plant-based diets, such as the lacto-ovo-vegetarian and the vegan diet, offer numerous benefits to human health. Poorly designed plant-based diets, however, bear the risk for vitamin- and micronutrient deficiencies. Vitamin B12 (B12, cobalamin) is a nutrient of particular concern in both diets, and should be readily supplemented on a continuous basis to ensure adequate B12 levels and to prevent deficiencies. This case reports describes the history of a healthy man in his mid-30s who adopted a vegan diet approximately 10 y ago. Well informed about the risks of vitamin B12 deficiency on a plant-based diet, he regularly supplemented methylcobalamin for years (single oral dose: 500 µg, 3–4 times a week) in order to maintain an adequate vitamin B12 status. In late 2023, however, he decided to cease B12 supplementation for undisclosed reasons. Subsequent to this decision, we closely monitored his B12 status and longitudinally measured serum B12, homocysteine, and holotranscobalamin (holo-TC). Total serum folate was also determined as it is a modifier of homocysteine concentration. A gradual decrease in holo-TC and vitamin B12 levels was observed after 4 weeks and supplements had to be re-introduced after 16 weeks. Homocysteine increased concomitantly up to 18.2 μmol/L after 20 weeks. While a short-term B12 supplement intake cessation might be well tolerated by vegans with an adequate B12 status, an interruption of more than 8 weeks could signify B12 loss approaching suboptimal status. This case report reiterates the need for continuous B12 supplementation in persons following an unfortified plant-based diet.

This study aimed to evaluate whether being metabolically healthy (MHO) provides protection against micronutrient deficiencies, particularly vitamin B12 deficiency, in obese children and to investigate the relationship between vitamin B12 levels and metabolic health parameters. 296 obese children (mean age: 11.3 years) and 138 age- and sex-matched healthy controls were included. Cases are classified as Metabolically Unhealthy Obese (MUO): One or more of the following criteria: glucose ≥ 100 mg/dL, triglycerides ≥ 150 mg/dL, HDL ≤ 40 mg/dL, or systolic/diastolic blood pressure ≥ 95th percentile, and MHO: absence of all these criteria.Vitamin B12 was categorized as deficient (< 148 pmol/L (200 pg/mL)), borderline (148–221 pmol/L(200–300 pg/mL)), or sufficient (> 221 pmol/L(> 300 pg/mL)). Using multivariate regression, vitamin B12 levels and metabolic indicators were examined. Of obese children,54.3% were in MUO.MHO and MUO groups had similar vitamin B12 levels( p  = 0.051) but considerably lower than the healthy controls. Vitamin B12 insufficiency was detected in 34.3% of obese children compared with 16.1% of controls ( p  = 0.015). MHO group had a mean B12 level of 281.6 pg/mL, considerably lower than the controls(388.5 pg/mL; p  = 0.001).Higher BMI SDS raised B12 insufficiency risk by 4.3-fold (OR = 4.307). Multivariate logistic regression analysis identified statistically significant associations between vitamin B12 deficiency and free T4 ( p  < 0.001, OR:0.001), AST ( p  = 0.011,OR:0.897), triglycerides ( p  = 0.032,OR:1.054), HDL ( p  = 0.029, OR:0.847), TG/HDL( p  = 0.017,OR:0.092), and uric acid ( p  = 0.047,OR:1.491). Vitamin B12 deficiency is more common in obese children than in healthy controls, regardless of metabolic phenotype. Being metabolically healthy does not appear to offer protection against low vitamin B12 levels. Increased adiposity and associated metabolic alterations may also contribute to vitamin B12 deficiency. These findings underscore the importance of routinely monitoring micronutrient deficiencies in childhood obesity.

Deficiency of vitamin B 12 (B 12 or cobalamin), an essential water-soluble vitamin, leads to neurological damage, which can be irreversible and anaemia, and is sometimes associated with chronic disorders such as osteoporosis and cardiovascular diseases. Clinical tests to detect B 12 deficiency lack specificity and sensitivity. Delays in detecting B 12 deficiency pose a major threat because the progressive decline in organ functions may go unnoticed until the damage is advanced or irreversible. Here, using targeted unbiased metabolomic profiling in the sera of subjects with low B 12 levels v control individuals, we set out to identify biomarker(s) of B 12 insufficiency. Metabolomic profiling identified seventy-seven metabolites, and partial least squares discriminant analysis and hierarchical clustering analysis showed a differential abundance of taurine, xanthine, hypoxanthine, chenodeoxycholic acid, neopterin and glycocholic acid in subjects with low B 12 levels. Random forest multivariate analysis identified a taurine/chenodeoxycholic acid ratio, with an AUC score of 1, to be the best biomarker to predict low B 12 levels. Mechanistic studies using a mouse model of B 12 deficiency showed that B 12 deficiency reshaped the transcriptomic and metabolomic landscape of the cell, identifying a downregulation of methionine, taurine, urea cycle and nucleotide metabolism and an upregulation of Krebs cycle. Thus, we propose taurine/chenodeoxycholic acid ratio in serum as a potential biomarker of low B 12 levels in humans and elucidate using a mouse model of cellular metabolic pathways regulated by B 12 deficiency.

Plant-based diets may increase the risk of vitamin B 12 deficiency due to limited intake of animal-source foods, while dietary folate increases when adhering to plant-based diets. In this cross-sectional study, we evaluated the B 12 and folate status of Norwegian vegans and vegetarians using dietary B 12 intake, B 12 and folic acid supplement use, and biomarkers (serum B 12 (B 12 ), plasma total homocysteine (tHcy), plasma methylmalonic acid (MMA) and serum folate). Vegans ( n 115) and vegetarians ( n 90) completed a 24-h dietary recall and a FFQ and provided a non-fasting blood sample. cB 12 , a combined indicator for evaluation of B 12 status, was calculated. B 12 status was adequate in both vegans and vegetarians according to the cB 12 indicator; however 4 % had elevated B 12 . Serum B 12 , tHcy, MMA concentrations and the cB 12 indicator (overall median: 357 pmol/l, 9·0 µmol/l, 0·18 µmol/l, 1·30 (cB 12 )) did not differ between vegans and vegetarians, unlike for folate (vegans: 25·8 nmol/l, vegetarians: 21·6 nmol/l, P = 0·027). Serum B 12 concentration < 221 pmol/l was found in 14 % of all participants. Vegetarians revealed the highest proportion of participants below the recommended daily intake of 2 µg/d including supplements (40 v . 18 %, P < 0·001). Predictors of higher serum B 12 concentrations were average daily supplement use and older age. Folate deficiency (< 10 nmol/l) was uncommon overall (< 2·5 %). The combined indicator cB 12 suggested that none of the participants was B 12 -depleted; however, low serum B 12 concentration was found in 14 % of the participants. Folate concentrations were adequate, indicating adequate folate intake in Norwegian vegans and vegetarians.

Hereditary hemorrhagic telangiectasia (HHT) leads to fragile blood vessels, causing frequent bleeding and anemia. Treatment mainly addresses iron levels and substitution. Although cobalamin (vitamin B12) is routinely tested in chronic anemia, its role in HHT has not been studied until now. This study examined its prevalence and related symptoms in HHT patients. Data from HHT patients treated between July 2019 and November 2022 were analyzed. Patients with cobalamin levels under 400 pg/ml underwent further testing and questioning. Among 155 patients, 42% were anemic, and 45% had cobalamin levels below 400 pg/ml. However, only 7 patients had a confirmed deficiency. Still, many reported symptoms commonly but not specifically linked to cobalamin deficiency, even with low-normal levels. Gastrointestinal lesions were significantly associated with these low-normal values ( p  = 0.027). Furthermore, 59% of patients had iron deficiency, and 67% were not receiving iron therapy at the time of their visit. This study is the first to show that true cobalamin deficiency is not more common in HHT than in the general population, though low-normal levels are frequent. In case of unexplained symptoms, evaluating cobalamin levels should be taken into consideration.

To compare the prevalence of vitamin B12 deficiency and peripheral neuropathy between two groups of type 2 diabetes mellitus (T2DM) patients treated with or without metformin, and to determine factors associated with vitamin B12 deficiency therapy and dietary intake of vitamin B12. In this retrospective study, we recruited 412 individuals with T2DM: 319 taking metformin, and 93 non-metformin users. Demographics, dietary assessment for vitamin B12 intakes, and medical history were collected. Participants were assessed for peripheral neuropathy. Blood specimens were collected and checked for serum vitamin B12 levels. The differences between the two groups were analyzed using an independent t-test for continuous data, and the Chi-squared or Fisher's exact test was used for categorical data. The relationship of vitamin B12 deficiency with demographics and clinical characteristics was modeled using logistic regression. The prevalence of B12 deficiency was 7.8% overall, but 9.4% and 2.2% in metformin users and non-metformin users, respectively. The odds ratio for serum vitamin B12 deficiency in metformin users was 4.72 (95% CI, 1.11-20.15, P = 0.036). There were no significant differences in a test of peripheral neuropathy between the metformin users and non-metformin users (P > 0.05). Low levels of vitamin B12 occurred when metformin was taken at a dose of more than 2,000 mg/day (AOR, 21.67; 95% CI, 2.87-163.47) or for more than 4 years (AOR, 6.35; 95% CI, 1.47-24.47). Individuals with T2DM treated with metformin, particularly those who use metformin at large dosages (> 2,000 mg/day) and for a longer duration (> 4 years), should be regularly screened for vitamin B12 deficiency and metformin is associated with B12 deficiency, but this is not associated with peripheral neuropathy.