Vitamins are essential micronutrients obtained from the diet, required by the body in small amounts daily for proper metabolism. Monitoring their levels is necessary for detecting deficiencies and guiding supplementation in certain clinical conditions. This study aimed to update the reference values for vitamins A, B1, B6, and E, and some related ratios, adjusted to the adult population of our health reference area using liquid chromatography in a direct approach calculation (n = 146, age: 21-64 years, 64% females). No significant differences in vitamin levels or ratios were observed based on age and sex. We obtained reliable and updated reference values: 1.1-2.8 ‍μmol/L and 18.9-42.2 ‍μmol/L for vitamins A and E respectively, 85.9-181.6 nmol/L and 57.0-165.7 nmol/L for vitamins B1 and B6 respectively; and related ratios of 246.2-561.1 ‍ng/g for vitamin B1 corrected by hemoglobin; 5.2-8.9 ‍μmol/mmol and 4.5-7.4 ‍μmol/mmol for vitamin E corrected by cholesterol and total lipids, respectively. These reference values significantly differ from those provided by the reagent manufacturer currently in use. While correcting vitamin E for lipids and vitamin B1 for hemoglobin is not recommended for the general population, these adjustments may be useful in interpreting results in certain pathological conditions.

Recently, there has been an increasing interest in how diet and nutrition influence both physical and mental health. Numerous studies have highlighted the potential role of B vitamins in neuropsychiatric disorders (NPDs), yet the exact causal relationship between these nutrients and NPDs remains unclear. In our Mendelian randomization (MR) meta-analysis, we examined the links between B vitamins (VB6, VB12, and folate) and NPDs, utilizing data from previous MR studies, the UK Biobank, and FinnGen databases. Our MR analysis revealed a complex, multifaceted association: VB6 appears to protect against Alzheimer's disease (AD) but may increase the risk for conditions such as major depressive disorder and post-traumatic stress disorder. VB12 seems protective against autism spectrum disorder (ASD) but may heighten the risk for bipolar disorder (BD). Folate has shown protective effects against AD and intellectual disability (ID). The meta-analysis suggests that B vitamins may protect against certain disorders like AD and Parkinson's disease, but they might also be risk factors for anxiety and other psychiatric conditions. Further subgroup analysis indicates that VB6 protects against epilepsy and schizophrenia but increases the risk of mania; VB12 protects against ID and ASD but raises the risk of schizophrenia and BD; folate protects against schizophrenia, AD, and ID. These findings reveal the intricate influence of B vitamins on mental health, emphasizing that different B vitamins have distinct impacts on various NPDs. This complexity underscores the importance of personalized supplementation in developing future therapeutic approaches for NPDs.

Background Falls in older adults, specifically causing proximal femoral fractures, greatly affect daily functioning and life expectancy. Peripheral neuropathy is an established risk factor for falls. However, the relationship between nerve conduction velocity (CV), action potential (AP), and fall risk or functional recovery after rehabilitation is not well understood. This study aimed to clarify whether sural nerve function can predict fall risk and functional improvement in activities of daily living. Methods We assessed elderly patients hospitalized with proximal femoral fractures in a convalescent rehabilitation ward. Sural nerve function was evaluated using the DPNCheck (NeuroMetrix, Inc., Woburn, MA, USA), with additional data collected on demographics, blood tests, medication use at admission and discharge, incidence of falls during hospitalization, physical function (Short Physical Performance Battery, or SPPB), and activities of daily living (Functional Independence Measure, or FIM). Statistical analyses explored the associations between the sural nerve CV/AP and the collected measures. Results In 27 patients (7 men and 20 women), sural nerve CV and AP were significantly correlated with both SPPB and FIM scores. Logistic regression identified FIM toileting as a significant predictor of reduced sural nerve AP (<5 μV; odds ratio: 3.22, p = 0.025). Multiple regression analysis showed that age and AP were significant predictors of the total FIM cognitive scores at discharge, with an adjusted R² of 0.464. Conclusion This study suggests that sural nerve function may help predict functional abilities in patients with proximal femoral fractures, particularly in the FIM motor tasks. Assessing peripheral nerve function can enhance rehabilitation plans by targeting fall risk management and promoting improvements in daily activities.

Both vitamin B6 deficiency and vitamin B12 deficiency can present with symptoms that appear like polyneuropathy, organomegaly, endocrinopathy, M protein, and skin changes (POEMS) syndrome, with painful peripheral neuropathy and sensorimotor dysfunction. There are rare reports of an association between vitamin B12 deficiency and POEMS syndrome, and even rarer reports of an association between vitamin B6 deficiency and POEMS syndrome. To our knowledge, this is the first described case with deficiencies in both vitamin B6 and vitamin B12 in association with POEMS syndrome.

A man in his 40s presented with fatigue, imbalance, and painful numbness and tingling. Initial evaluation revealed low vitamin B12 level, and he received oral and IV supplementation for one month with an improvement in vitamin B12 levels, but without improvement in symptoms. Further evaluation revealed both a vitamin B6 deficiency and an IgA lambda monoclonal spike, prompting further investigation and an eventual diagnosis of POEMS syndrome. He underwent an autologous stem cell transplant and has had improvement in his symptoms.

Patients with POEMS syndrome may have symptoms that are difficult to distinguish from deficiencies in vitamin B6 or vitamin B12. Management of POEMS should include screening of vitamin B6 and B12 to ensure other possible associated causes of symptoms are appropriately treated.

Vitamin B6 deficiency is linked to neurological disorders. However, supplementation with high doses of vitamin B6 has also been linked to neuropathy as an adverse drug reaction. Review of cases from the Dutch Spontaneous Reporting System (SRS) and other data led to a regulatory action to lower the maximum daily dose (DD) of vitamin B6 in supplements to 21 mg/day from October 1, 2018.

The aim of this study was to investigate if there was an effect of the regulatory action in 2018 on maximum daily dosage for vitamin B6 on the reporting pattern of neuropathy to the SRS in the Netherlands.

We investigated trends in the number of reports received until December 31, 2023, DD mentioned in the reports, and the correlation between DD and plasma vitamin B6 levels. A change point analysis was used to get insight into the pattern of reports over time.

Two hundred and twenty-four reports were included. After the regulatory action for dose maximization from October 2018, only one report mentions a dosage which is much higher than the recommended 21 mg DD. Only 15% of the variability in plasma levels mentioned in reports can be explained by the DD. Twelve statistical change points were noted, especially around some peaks in the reporting pattern for instance in 2018. However, from the second half of 2019, the number of reports on vitamin B6 and neuropathy per time period is lower and no change points were detected.

Although our study has limitations, we clearly see an effect of regulatory action on the doses of vitamin B6 used in neuropathy reports. However, some cases describing neuropathy related to vitamin B6 supplementation with lower doses are still reported after the regulatory action in 2018. Therefore, the association between low-dose vitamin B6 products and neuropathy should be studied further.

Endogenous carbonyl stress leads to the formation of advanced glycation end products (AGEs). AGEs represent a potential target to prevent or treat diabetic sensorimotor polyneuropathy (DSPN). The current study aimed to characterize cutaneous carbonyl stress, oxidative stress, immune cells, and endothelial cell damage in early type 2 diabetes compared with normal glucose tolerance (NGT) using novel cutaneous biomarkers.

Included were 160 individuals recently (≤12 months) diagnosed with type 2 diabetes and 144 with NGT from the German Diabetes Study baseline cohort. Nerve function was assessed using electrophysiological, quantitative sensory, and clinical testing. Skin biopsies were obtained to analyze intraepidermal nerve fiber density, AGE autofluorescence, argpyrimidine area, and endothelial cell area. In addition, skin autofluorescence was measured noninvasively using the AGE reader. A subgroup with type 2 diabetes (n = 80) was reassessed 5 years later.

After adjustment for sex, age, HbA1c, LDL cholesterol, and BMI, argpyrimidine area (17.5 ± 18.8 vs. 11.7 ± 12.7%) was higher in recent-onset type 2 diabetes than in NGT (P < 0.05). AGE autofluorescence was inversely correlated with nerve conduction (e.g., peroneal motor nerve conduction velocity: r = -0.346) and positively with AGE reader measurements in type 2 diabetes (r = 0.358, all P < 0.05), but not in NGT. Higher baseline AGE autofluorescence and lower endothelial cell area predicted the deterioration of clinical and neurophysiological measures after 5 years.

Cutaneous AGE markers were associated with neurophysiological deficits in recent-onset type 2 diabetes and predicted their progression after 5 years, substantiating the role of carbonyl stress in the development of early DSPN.

Background/Objectives: Radiculopathy leads to pain, consequently reducing patient's quality of life (QoL). Research indicates that certain nucleotides, such as cytidine and uridine, along with vitamins B1 and B12, may help alleviate pain and enhance QoL. This study assessed the impact of adding a supplement containing cytidine and uridine nucleotides and vitamins B1 and B12, alongside standard treatment, on radiculopathy-associated pain. Methods: A multicenter, prospective, two-cohort, randomized, open-label study was conducted. The control group received standard treatment, while the experimental group received standard treatment plus the supplement. The primary endpoint was pain reduction measured by a Visual Analog Scale (VAS). Secondary endpoints included functional improvement (Roland Morris questionnaire), clinical improvement (Clinical Global Impression [CGI] scale), and QoL improvement (EQ-5D-5L questionnaire). Results: A total of 122 patients were included from 17 centers across Spain. Both groups showed pain improvement, but the VAS reduction (control: 24.58 vs. experimental: 31.35) was not statistically significant. The Roland Morris score decreased significantly in the experimental group (estimate: -1.70, 95% CI -3.29 to -0.10; p = 0.038), and these patients were 5 times more likely to progress to a better CGI category (OR = 0.20, 95% CI 0.07 to 0.57; p = 0.003). No significant differences were observed in EQ-5D-5L scores or analgesic consumption. Conclusions: The addition of supplemental pyrimidine nucleotides and vitamins B1 and B12 to standard of care treatment improved radiculopathy functional and clinical outcomes. Regarding pain, however, although there was a numerical improvement, it did not reach statistical significance.

Numerous studies have suggested a link between dietary micronutrient intake and the onset of constipation. Nevertheless, there has not been much research done on the potential relationship between vitamin B6 and constipation. The purpose of this study was to determine whether dietary vitamin B6 consumption and chronic constipation are related among adult participants in the National Health and Nutrition Examination Survey (NHANES).

The study made use of information from the 2009-2010 NHANES health and nutrition survey. Respondents' dietary information was gathered using 24-h dietary recalls. A range of statistical techniques, including as interaction tests, subgroup analyses, and curve fitting analyses, were used to examine the connection between dietary vitamin B6 intake and chronic constipation.

This study included 3,643 patients, with 270 (7.41%) diagnosed with persistent constipation. A fully adjusted multiple logistic regression analysis found that increasing dietary vitamin B6 consumption (OR = 0.78, 95% CI: 0.68-0.89) was linked to a lower incidence of constipation, with significance at p < 0.05. After accounting for numerous factors, the odds ratio and 95% confidence interval for the third tertile compared to the reference group (first tertile) were 0.85 (0.74, 0.98), with statistical significance at p < 0.05. Furthermore, subgroup analysis and interaction assessments revealed a substantial negative link between vitamin B6 intake and the occurrence of constipation, particularly in males and alcohol drinkers (all p-values were less than 0.05).

This study found an inverse connection between vitamin B6 consumption and the prevalence of persistent constipation. More extensive prospective trials are needed to fully examine the long-term influence of vitamin B6 on persistent constipation.

Evidence regarding the associations of pyridoxal 5'-phosphate level in plasma and dietary intake of vitamin B6 with depression risk is scarce. Accordingly, we investigated the aforementioned associations in US adults.

This is a cross-sectional study that included data from two independent samples of 12,716 and 11,967 individuals (aged ≥ 20 years) participating in the National Health and Nutrition Examination Survey (NHANES) from 2005 to 2010. The associations of the pyridoxal 5'-phosphate level in plasma and dietary intake of vitamin B6 with depression risk were examined through multivariable logistic regression. In addition, we determined dose-response associations by fitting restricted cubic splines to the data.

In the multivariable model, the highest quarter of dietary intake of vitamin B6 was associated with a significantly lower risk of depression compared to the lowest quarter (OR = 0.63, 95% CI: 0.50, 0.79, p < 0.001). Similarly, the highest quartile of plasma PLP levels was linked to a reduced risk of depression compared to the lowest quartile (OR = 0.76, 95% CI: 0.62, 0.93, p < 0.01). With increasing quartiles of dietary intake of vitamin B6 and plasma PLP levels, the risk of depression also decreased accordingly (all p for trend < 0.01). Furthermore, the correlation analysis revealed that for every 1-SD increase in the level of plasma lutein + zeaxanthin and dietary intake of vitamin B6, the risk of depression showed a decreasing trend (all p < 0.01). The interaction test results indicated that the dietary consumption of vitamin B6 did not significantly interact with any of the stratification factors (all p for interaction > 0.05). Moreover, no significant interaction was found between the amount of plasma PLP and any hierarchical factors (all p for interaction > 0.05), except for gender-based subgroup analysis (p for interaction > 0.05). The dose-response relationship results showed a linear decrease trend in the relationship between dietary vitamin B6 intake and plasma pyridoxal 5'-phosphate with the risk of depression.

Plasma PLP levels and dietary vitamin B6 intake in the highest quartiles are associated with a lower risk of depression. These findings support the promotion of a balanced diet rich in vitamin B6. However, future randomized controlled trials are necessary to confirm the effects of vitamin B6 supplementation on depression risk. We should aim for a healthy and balanced diet in terms of nutritional supplementation.

Tuberculosis (TB) is the leading cause of infectious mortality and morbidity in the world, second only to coronavirus disease 2019. Patients with chronic kidney disease and kidney transplant recipients are at a higher risk of developing TB than the general population. Active TB is difficult to diagnose in this population due to close mimics. All transplant candidates should be screened for latent TB infection and given TB prophylaxis. Patients who develop active TB pre- or post-transplantation should receive multidrug combination therapy of antitubercular therapy for the recommended duration with optimal dose modification as per glomerular filtration rate.

Multiple clinical studies have observed a close relationship between serum trace elements and nutrients and diabetes and its complications, but it remains unclear whether there is a genetic causal effect between serum trace elements and nutrients and diabetes and its complications.

This study aims to investigate the causal effects of serum trace elements and nutrients on diabetes and its complications using Mendelian randomization methods.

The single nucleotide polymorphisms of serum trace elements and vitamins, as exposure factors, were sourced from the published UK Biobank database and public databases of genome-wide association studies. The genome-wide association study data of diabetes and its complications, as outcome events, were sourced from the FinnGen Biobank database. Mendelian randomization methods were employed to explore the causal relationships between 9 trace elements and 6 nutrients and diabetes and its complications. The causal relationships were inferred using inverse variance weighting, MR Egger, weighted median, simple model, and weighted model methods. Sensitivity analyses, including heterogeneity tests, horizontal pleiotropy tests, MR-PRESSO tests, and leave-one-out analysis, were conducted to evaluate the robustness of the study results. Finally, trace elements and nutrients with statistical significance in the IVW method and consistent Beta and OR directions in the five methods were selected as exposure factors with causal relationships with diabetes and its complications. This study also used multivariable Mendelian randomization methods to assess the combined effects of multiple exposure factors on the risk of diabetes and its complications.

Mendelian randomization analysis revealed that selenium was linked to an elevated risk of T2D.Vitamin B6 was correlated with an increased risk of neurological complications in type 2 diabetes. Magnesium exhibited a negative causal relationship with the risk of T1D.Carotene was linked to a higher risk of renal complications in T1D.Vitamin B12 showed a negative causal relationship with renal complications in T1D.Carotene was connected to a higher risk of neurological complications in T1D.Potassium and vitamin B6 exhibited negative causal relationships with neurological complications in T1D.Vitamin E showed a negative causal relationship with peripheral circulation complications in T2D.Multivariable Mendelian randomization analysis suggested that vitamin B6 could independently influence neurological complications in both T1D and T2D, apart from other exposure factors. Vitamin B6 could also independently influence renal complications in T1D.Vitamin E could independently influence peripheral circulation complications in T1D, apart from other exposure factors.

The findings from univariable and multivariable Mendelian randomization studies substantiate the causal relationships between trace elements and nutrients and different subtypes of diabetes and their complications. These findings hold significant clinical implications for developing targeted prevention and treatment strategies for diabetes and its complications.

An increasing number of adult individuals are at risk of vitamin B12 deficiency, either from reduced nutritional intake or impaired gastrointestinal B12 absorption.

This study aims to review the current best practices for the diagnosis and treatment of individuals with vitamin B12 deficiency.

A narrative literature review of the diagnosis and treatment of vitamin B12 deficiency.

Prevention and early treatment of B12 deficiency is essential to avoid irreversible neurological consequences. Diagnosis is often difficult due to diverse symptoms, marked differences in diagnostic assays' performance and the unreliability of second-line biomarkers, including holo-transcobalamin, methylmalonic acid and total homocysteine. Reduced dietary intake of B12 requires oral supplementation. In B12 malabsorption, oral supplementation is likely insufficient, and parenteral (i.e. intramuscular) supplementation is preferred. There is no consensus on the optimal long-term management of B12 deficiency with intramuscular therapy. According to the British National Formulary guidelines, many individuals with B12 deficiency due to malabsorption can be managed with 1000 µg intramuscular hydroxocobalamin once every two months after the initial loading. Long-term B12 supplementation is effective and safe, but responses to treatment may vary considerably. Clinical and patient experience strongly suggests that up to 50% of individuals require individualized injection regimens with more frequent administration, ranging from daily or twice weekly to every 2-4 weeks, to remain symptom-free and maintain a normal quality of life. 'Titration' of injection frequency based on measuring biomarkers such as serum B12 or MMA should not be practiced. There is currently no evidence to support that oral/sublingual supplementation can safely and effectively replace injections.

This study highlights the interindividual differences in symptomatology and treatment of people with B12 deficiency. Treatment follows an individualized approach, based on the cause of the deficiency, and tailored to help someone to become and remain symptom-free.

Many inherited metabolic disorders (IMDs), including disorders of amino acid, fatty acid, and carbohydrate metabolism, are treated with a dietary reduction or exclusion of certain macronutrients, putting one at risk of a reduced intake of micronutrients. In this review, we aim to provide available evidence on the most common micronutrient deficits related to specific dietary approaches and on the management of their deficiency, in the meanwhile discussing the main critical points of each nutritional supplementation. The emerging concepts are that a great heterogeneity in clinical practice exists, as well as no univocal evidence on the most common micronutrient abnormalities. In phenylketonuria, for example, micronutrients are recommended to be supplemented through protein substitutes; however, not all formulas are equally supplemented and some of them are not added with micronutrients. Data on pyridoxine and riboflavin status in these patients are particularly scarce. In long-chain fatty acid oxidation disorders, no specific recommendations on micronutrient supplementation are available. Regarding carbohydrate metabolism disorders, the difficult-to-ascertain sugar content in supplementation formulas is still a matter of concern. A ketogenic diet may predispose one to both oligoelement deficits and their overload, and therefore deserves specific formulations. In conclusion, our overview points out the lack of unanimous approaches to micronutrient deficiencies, the need for specific formulations for IMDs, and the necessity of high-quality studies, particularly for some under-investigated deficits.

The interplay between nutrition and neurology has gained increasing recognition and various studies have emerged showing malnutrition and nutritional imbalances as a cause and result of certain neurological pathologies [...].