Vitamin B6 Deficiency Research Articles

Long-Term Maintenance of Normal Serum Vitamin B1 Levels Is Associated with Better Outcomes in Patients with Heart Failure.

Deficiency of vitamin B1 (VB1), an essential micronutrient, causes heart failure (HF). A recent randomized controlled trial failed to show any improvement in HF prognosis after short-term VB1 supplementation. In the current study, we investigated the efficacy of long-term maintenance of normal blood VB1 levels in preventing adverse outcomes in patients with HF.This study included 88 consecutive patients with HF who received guideline-directed medical therapy at Arida Municipal Hospital. The patients were divided into 3 groups: a control group with normal VB1 levels and no VB1 supplementation (normal group, n = 25), and those presenting with VB1 deficiency, who either required short-term VB1 supplementation (short-term supplementation group, n = 25), or long-term maintenance of normal blood VB1 levels (long-term maintenance group, n = 38). The time to the first appearance of composite outcomes, including cardiovascular death and hospitalization for HF, was compared between the 3 groups.VB1 deficiency was observed in 63 (72%) patients. The Kaplan-Meier curve showed that the long-term maintenance group had better outcomes than the other 2 groups. In the multivariate analysis, long-term maintenance of normal blood VB1 levels and age were independent predictors of composite outcomes.VB1 deficiency is frequently observed, and the long-term maintenance of normal blood VB1 levels may result in better outcomes in patients with HF. Our results suggest that the detection of VB1 deficiency and long-term restoration of VB1 levels may be part of the overall therapeutic strategy for HF.

Deficiency of thiamine and Wernicke-Korsakoff syndrome – review of pathophysiology, clinical presentation , diagnostics and treatment

Introduction and aim of the study: Thiamine is a water-soluble vitamine, which bioactive form is necessary for energy metabolism in all cells. Deficiency of thiamine may be caused by malnutrition, alcoholism and certain diseases and it leads to an acute neuropsychiatric disorder called Wernicke encephalopathy. Untreated patients can develop a residual syndrome called Korsakoff syndrome. The aim of our study is to present current knowledge of history, pathophysiology, causes, symptoms and treatment of vitamine B1 depletion and Wernicke-Korsakoff’s syndrome. Material and methods: Our review is based on the analysis of materials collected in „Pubmed”, „Google Scholar” and other scientific articles using keywords: „thiamine”, „thiamine deficiency”, „Wernicke encephalopathy”, „Korsakoff syndrome”. Conclusions: Despite numerous studies, Wernicke encephalopathy is still difficult to diagnose. Attention should be paid to the possibility of vitamin B1 deficiency in people who are at risk of it like alcoholics, malnourished or psychiatric patients. Wernicke encephalopathy is an acute neuropsychiatric disorder so the treatment should be started as soon as possible to reduce the risk of developing Korsakoff syndrome.

Vitamin B1 Supplementation Ameliorates Obesogenic Effects of a High Fat Diet in Male Mice

Dietary deficiencies in vitamins such as thiamine (Vitamin B1) are common even in developed countries and can have a range of deleterious health effects. This trend in Vitamin B1 deficiency coincides with increased fat consumption in the American diet, particularly of soybean oil, the most widely consumed cooking oil in the U.S. which is also present in many processed foods. Here, we hypothesized that the concurrent malnutrition caused by a soybean oil-based high fat diet (SO-HFD) and a physiological deficiency in thiamine can exacerbate conditions such as obesity, diabetes, and fatty liver that are associated with consumption of HFDs. To test this, C57BL/6N male mice (N=8-10 per group) were fed either a low-fat chow or an SO-HFD, with or without supplementation with 640 mg/kg of the thiamine analog thiamine tetrahydrofurfuryl disulfide (TTFD), for 18 weeks. Our results showed that the SO-HFD supplemented with TTFD leads to significantly decreased weight gain and delayed the onset of glucose intolerance compared to SO-HFD without added TTFD (p<0.05). In contrast, TTFD supplementation did not have any effect on body weight or glucose intolerance in the context of a low-fat diet. Metabolomic analysis revealed that the SO-HFD decreased absolute thiamine levels both in the blood and liver tissue compared to the low fat control diet (p<0.05); this decrease was reversed by TTFD supplementation suggesting that some of the negative effects of the SO-HFD may be due to its impact on the Vitamin B1 pathway. Untargeted metabolomic analysis identified several other metabolites — such as amino acids, organic acids, methylamine osmolytes and those involved in nucleotide metabolism — that were also affected by TTFD supplementation, but in a beneficial fashion. Transcriptomic analysis of the liver and intestines revealed alterations in thiamine absorption and metabolic pathways by the SO-HFD; effects of TTFD on hepatic gene expression and fatty liver will be presented. TTFD supplementation given after the onset of SO-HFD-induced obesity was not able to reverse the phenotype, suggesting that the deleterious effects of the SO-HFD-induced Vitamin B1 deficiency may be permanent. In conclusion, our findings indicate that consumption of an SO-enriched diet, similar in fat content to what is consumed by most Americans, can result in a Vitamin B1 deficiency. Although TTFD supplementation may mitigate some of the adverse metabolic effects of this diet, this intervention must be done at an early stage. Funding: The Thiamine Advocacy Foundation Research Grant (FMS, PHD, PD); NIH R01DK127082 (FMS)Acknowledgements: UCR Genomics Core Facility, UCR Metabolomics Core Facility, UCR High Performance Computing Center (HPCC). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Vitamin B1 supplementation ameliorates high-fat diet induced exercise fatigue and improves grip strength in male mice

Dietary deficiencies in vitamins such as thiamine (Vitamin B1) are common even in developed countries and can have a range of deleterious health effects. This trend in Vitamin B1 deficiency coincides with increased fat consumption in the American diet, particularly of soybean oil, the most widely consumed cooking oil in the U.S. which is also present in many processed foods. Here, we hypothesize that the concurrent malnutrition caused by a soybean oil-based high fat diet (SO-HFD) and a physiological deficiency in thiamine can impact regional gene expression in the brain and behavior. To test this, C57BL/6N male mice (N=10-12 per group) were fed either a low-fat chow (OSD) or an SO-HFD, with or without supplementation with 640 mg/kg of the thiamine analog thiamine tetrahydrofurfuryl disulfide (TTFD), for 18 weeks. Mice were subjected to a series of behavioral tests designed to evaluate cognition (passive avoidance test, PAT), strength (modified grip strength test, MGS), exercise endurance (treadmill test, EE), and locomotor/habituation activity (open field test, OFT). Our results showed no difference across groups on the PAT. On the MGS test, the force generated when normalized to body weight was lesser on all test days for SO-HFD as compared to OSD (p<0.05-0.0001). The TTFD supplementation improved MGS only in the SO group (p<0.05). On EE, OSD ran significantly longer before exhaustion as compared to SO (p<0.05-0.001). For one subset of animals TTFD supplementation improved the EE score in SO but not OSD (p<0.05-0.001). During the one-hour OFT, distance traveled decreased over time for both TTFD-supplemented groups only (p<0.05-0.01), indicating improvement in habituation/learning. Transcriptomic analysis of the hypothalamus and hippocampus from these mice revealed differentially expressed genes (p<0.05) that may contribute to alterations observed in the behavioral tests. Our results indicate that TTFD supplementation ameliorates HFD-induced deficits in strength and exercise endurance. TTFD supplementation improved habituation/learning on OFT regardless of diet. The Thiamine Advocacy Foundation, NIH R01DK127082 (FMS), DOD GW180072 (MCC). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Wernicke encephalopathy in combination with acute polyneuropathy under the guise of a demyelinating disease in a teenager with an eating disorder

Wernicke encephalopathy is a neuropsychiatric syndrome characterized by three main symptoms: oculomotor disturbances, cerebellar ataxia, and psychiatric disturbances. The condition is associated with a high mortality and morbidity rate. Wernicke encephalopathy is most commonly seen in adolescent children presenting with a vitamin B1 deficiency. Thiamine deficiency may also cause polyneuritis syndrome, with or without the aforementioned symptoms. The condition is characterized by sensory-motor impairments in a symmetrical pattern, dysarthria, and paresis or even paralysis of the lower limbs. This report focuses on an adolescent case presenting acute oculomotor paresis, nystagmus, leg weakness, impaired gait, decreased deep tendon reflexes, cognitive impairment, and a history of recurrent vomiting, prolonged starvation, and eating behaviour disorders. The magnetic resonance imaging scan reveals symmetrical pathological foci of increased intensity in T2 in the periaqueductal region, at the Magendie’s central aperture. The patient displays a mixed motor-sensory polyneuropathic syndrome affecting both lower limbs, primarily of the axonopathy type, based on electroneuromyography data. Positive outcomes such as restored eyeball movement, enhanced gait, increased muscle strength in the lower legs and feet, and better management of sensory disorders have occurred due to thiamine treatment.

Subnormal Serum Liver Enzyme Levels: A Review of Pathophysiology and Clinical Significance.

Subnormal levels of liver enzymes, below the lower limit of normal on local laboratory reports, can be useful diagnostically. For instance, subnormal levels of aminotransferases can be observed in vitamin B6 deficiency and chronic kidney disease. Subnormal alkaline phosphatase levels may indicate the presence of hypophosphatasia, Wilson's disease, deficiencies of divalent ions, or malnutrition. Subnormal levels of gamma glutamyl transferase may be seen in cases of acute intrahepatic cholestasis, the use of certain medications, and in bone disease. Finally, subnormal levels of 5'-nucleotidase have been reported in lead poisoning and nonspherocytic hemolytic anemia. The aim of this review is to bring attention to the fact that subnormal levels of these enzymes should not be ignored as they may indicate pathological conditions and provide a means of early diagnosis.

Hyperhomocysteinemia is a risk factor for vascular complications in patients with chronic kidney disease

Hyperhomocysteinemia is considered a risk factor for many diseases, including thrombosis. Patients with chronic kidney disease often have vascular complications in the form of arterial or venous thrombosis, and it is important to consider the blood homocysteine level as a predictor of thrombophilia. The causes of hyperhomocysteinemia can be both genetic mutations and deficiency of homocysteine metabolism enzymes, as well as deficiency of folic acid, vitamin B12 and, to a lesser extent, deficiency of vitamin B6, which affects methionine metabolism. Given the role of hyperhomocysteinemia as a predictor of cardiovascular events in patients with kidney diseases, in our opinion, the multifactorial nature of increased homocysteine requires further research into some links of its pathogenesis in chronic kidney disease and the development of targeted therapeutic interventions.

Vitamin deficiencies in children: Lessons from clinical and neuroimaging findings

Background and aimsWater-soluble vitamins play an essential coenzyme role in the nervous system. Acquired vitamin deficiencies are easily treatable, however, without treatment, they can lead to irreversible complications. This study aimed to provide clinical, laboratory parameters and neuroimaging data on vitamin deficiencies in an attempt to facilitate early diagnosis and prompt supplementation. MethodsFrom July 1998 to July 2023, patients at Necker-Enfants-Malades Hospital presenting with acute neurological symptoms attributed to acquired vitamin deficiency were included. Clinical data were extracted from Dr Warehouse database. Neuroimaging, biochemical and electrophysiological data were reviewed. ResultsPatients with vitamin B1 deficiency exhibited abnormal eye movements (n = 4/4), fluctuations in consciousness (n = 3/4), and ataxia (n = 3/4). Brain MRI showed alterations of fourth ventricle region (n = 4/4), periaqueductal region (n = 4/4), tectum (n = 3/4), and median thalami (n = 3/4). Patients with vitamin B2 deficiency presented with early onset hypotonia (n = 3/4), hyperlactatemia (n = 4/4), and hyperammonemia (n = 4/4). Plasma acylcarnitines revealed a multiple acyl-coA dehydrogenase deficiency-like profile (n = 4/4). In vitamin B12 deficiency, young children presented with developmental delay (n = 7/7) and older children with proprioceptive ataxia (n = 3/3). Brain MRI revealed atrophy (n = 7/7) and spinal MRI hyperintensity in posterior cervical columns (n = 3/3). Metabolic findings showed elevated methylmalonic acid (n = 6/7) and hyperhomocysteinemia (n = 6/7). Patients with vitamin C deficiency exhibited gait disturbances and muscle weakness (n = 2/2). ConclusionsAcquired vitamin deficiencies may display reversible clinical symptoms mimicking inherited metabolic disorders. Some situations raise suspicion for diagnosis: concordant clinical presentation, suggestive neuroimaging findings, and/or biochemical evidence. Any acute neurological condition should be treated without waiting for definitive biochemical confirmation.

A Gadolinium(III) Complex Based on Pyridoxine Molecule with Single-Ion Magnet and Magnetic Resonance Imaging Properties.

Pyridoxine (pyr) is a versatile molecule that forms part of the family of B vitamins. It is used to treat and prevent vitamin B6 deficiency and certain types of metabolic disorders. Moreover, the pyridoxine molecule has been investigated as a suitable ligand toward metal ions. Nevertheless, the study of the magnetic properties of metal complexes containing lanthanide(III) ions and this biomolecule is unexplored. We have synthesized and characterized a novel pyridoxine-based GdIII complex of formula [GdIII(pyr)2(H2O)4]Cl3 · 2 H2O (1) [pyr = pyridoxine]. 1 crystallizes in the triclinic system and space group Pī. In its crystal packing, cationic [Gd(pyr)2(H2O)4]3+ entities are connected through H-bonding interactions involving non-coordinating water molecules and chloride anions. In addition, Hirshfeld surfaces of 1 were calculated to further investigate their intermolecular interactions in the crystal lattice. Our investigation of the magnetic properties of 1, through ac magnetic susceptibility measurements, reveals the occurrence of a slow relaxation in magnetization in this mononuclear GdIII complex, indicating an unusual single-ion magnet (SIM) behavior for this pseudo-isotropic metal ion at very low temperatures. We also studied the relaxometric properties of 1, as a potential contrast agent for high-field magnetic resonance imaging (MRI), from solutions of 1 prepared in physiological serum (0.0-3.2 mM range) and measured at 3 T on a clinical MRI scanner. The values of relaxivity obtained for 1 are larger than those of some commercial MRI contrast agents based on mononuclear GdIII systems.

Assessment of blood one-carbon metabolism indexes during mid-to-late pregnancy in 397 Chinese pregnant women.

One-carbon metabolism (OCM) significantly influences fetal growth and neurodevelopment through transferring methyl group to biomolecules, during which folate, methionine, choline and betaine function as methyl donor nutrients, while vitamin B2, B6, B12 function as enzyme cofactors, and homocysteine (Hcy) and S-adenosyl methionine (SAM) are functional metabolites. This study aimed to assess blood OCM index levels and explore their relationships among Chinese pregnant women. Data were obtained from the baseline of the Mother-Child Nutrition and Health Cohort Study. Pregnant women, voluntarily recruited from September 2020 to June 2022 during antenatal examinations in five Chinese cities at 24-32 gestational weeks, provided fasting venous blood samples. Measurements included RBC and serum folate, serum vitamin B2, B6, B12, choline, betaine, methionine, total Hcy (tHcy), and plasma SAM. Sociodemographic characteristics and pregnancy-related conditions were collected via a self-designed questionnaire. Of 397 participants, 82.6% were in mid-pregnancy (24-27 gestational weeks) and 17.4% were in late-pregnancy (28-32 gestational weeks). Serum folate, vitamin B6, and B12 deficiencies were 2.5, 1.3, and 8.3%, respectively. Elevated tHcy (≥10 μmol/L) was observed in 1.8% of pregnant women. Elderly pregnant women (aged 35 and above) exhibited significantly lower serum methionine levels (p < 0.05), while multiparous women had lower RBC folate levels (p < 0.05), and lower serum methionine and vitamin B12 levels (p < 0.10, not statistically significant). Partial correlation analysis revealed positive associations between RBC folate and cofactor vitamin B12 (r = 0.244, p < 0.05) in the folate cycle, as well as significant correlations between two methyl donor paths [serum folate was significantly related to serum choline (r = 0.172) and betaine (r = 0.193)]. As functional biomarkers of OCM, serum tHcy exhibited negative associations with RBC folate (β = -0.330, p < 0.05) and vitamin B6 (β = -0.317, p < 0.05), and plasma SAM displayed a positive association with serum betaine (β = 0.610, p < 0.05), while negatively associated with serum vitamin B6 (β = -0.181, p < 0.05). The blood OCM exhibited imbalances during mid-to-late pregnancy, characterized by lower levels of folate, vitamin B6, and B12, alongside elevated tHcy levels. Adequate folate and vitamin B6 emerged as significant predictors of lower tHcy levels. Additionally, serum betaine showed a positive correlation with plasma SAM. This suggests the importance of not only ensuring sufficient folate but also optimizing other OCM-related nutrients throughout pregnancy.

Effect of Pb-exposure and B vitamin deficiencies on δ-aminolevulinic acid dehydratase activity among workers from Pb recycling plants.

Previous studies reported that Pb exposure causes a negative association with delta-aminolevulinic acid dehydratase activity (δ-ALAD), but the impact of Pb exposure (dose and time), B vitamin deficiencies, and lifestyle factors needs to be explored. In this study, the impact of Pb exposure, B vitamin deficiencies, and lifestyle factors on δ-ALAD activity among workers exposed to Pb from the Pb-recycling process was evaluated. Blood lead levels (BLLs), B vitamins (B6, B9, and B12), hematological factors (Hb% and HCT), lifestyle factors, and δ-ALAD activity was assessed in 170 male Pb-exposed workers engaged in the Pb recycling process. BLLs are estimated using the ICP-OES method. B vitamins in serum samples from workers were determined using the ELISA method. The δ-ALAD activity in whole blood samples was determined using the spectrophotometer method. The lifestyle factors were collected using a standard questionnaire. The δ-ALAD activity was significantly decreased in workers with the habits of alcohol use, tobacco consumption, hematocrit < 41%, mild and moderate categories of anemia, vitamin B6 and B12 deficiency, and BLL categories of 10-30, 30-50, and > 50µg/dL. Multiple regression analysis revealed that the independent variables of alcohol consumption (β = -0.170; P = 0.025), BLLs (β = -0.589; P = 0.001) and Hb% (β = 0.183; P = 0.001) significantly influenced the δ-ALAD activity with 44.2% (R2 = 0.442). Among the workers exposed to Pb from the Pb recycling plant, δ-ALAD activity was considerably reduced by Pb exposure, B vitamin deficiency, hematological parameters, and lifestyle factors.

Wernicke Syndrome: Case Report and Literature Review of Contributing Factors—Can Malpractice Dynamics Be Identified?

Wernicke Encephalopathy (WE) is a neurological acute syndrome related to vitamin B1 deficiency and is relatively common in patients with chronic alcoholism. In the case of Hyperemesis Gravidarum, thiamine body stores become unable to meet the increased demand, resulting in acute deficiency. WE is associated with typical clinical and radiological findings. Treatment pathways rely on thiamine replacement. The case herein reported is centered around a 33-year-old diabetic patient at 12 weeks of gestation, with WE due to hyperemesis gravidarum. The disease manifested itself with weakness, mental confusion, headache, and impaired vision. The diagnosis was established after the detection of typical findings by MRI. Thirty days after therapy was started, most of the patient’s neurological disorders were resolved. The patient was discharged 40 days later with instructions to continue daily thiamine supplementation. The pregnancy outcome was good. Unfortunately, mild ataxia persisted in 2-year follow-up as a long-term consequence. When diagnosed and treated, WE has a favorable prognosis. However, roughly 80% of patients experience memory loss, which may continue for a long time, while gait disorders reportedly affect about 35% of patients. Mild ataxia and dysmetria may persist, too. We reviewed the scientific literature on WE in women with HG until February 2023. Hardly any authors report data on long-term sequelae. Our report emphasizes how important it is to take into consideration this complication in clinical practice, referring to published guidelines and recommendations. Neurological maternal sequelae can demonstrably persist despite early diagnosis and appropriate management. For this reason, a long-term follow-up is recommended. Wernicke syndrome management cannot yet rely on well-established conclusive guidelines; hence, a cautionary approach ought to be prioritized in order to ensure medicolegal soundness.

Relationship of Low Vitamin B6 Status with Sarcopenia, Frailty, and Mortality: A Narrative Review.

Marginal vitamin B6 (B6) deficiency is a widespread global concern. Inadequate B6 levels have been linked to an increased risk of age-related chronic diseases such as cardiovascular diseases and cancers. In recent years, the growing concern over sarcopenia (the age-related loss of muscle mass and strength) and frailty (a decline in physiological resilience and increased vulnerability associated with aging) is particularly relevant due to the emergence of super-aged societies in developed countries. Notably, among the thirty-one studies included in this review, twenty-five showed a significant association of B6 status with sarcopenia, frailty, and all-cause mortality in adults (p < 0.05), while six showed no association. Emerging studies have suggested novel mechanisms underlying this association. These mechanisms involve P2X7 receptor-mediated NLRP3 inflammasome signaling, AMPK signaling, PD-L1 signaling, and satellite cell-mediated myogenesis. Furthermore, the modulation of PLP-dependent enzymes due to B6 deficiency is associated with impaired metabolic processes, affecting energy utilization, imidazole peptide production, and hydrogen sulfide production, as well as the kynurenine pathway, all of which play vital roles in skeletal muscle health and pathophysiology. This narrative review provides an up-to-date assessment of our current understanding of the potential role of nutritional B6 status in combating sarcopenia, frailty, and mortality.

Vitamin B6 and vitamin D deficiency co-occurrence in geriatric memory patients.

Vitamin B6 and D levels are not assessed routinely in geriatric memory patients. This study examined vitamin levels to determine the potential effects on cognition. A chart review was conducted of 203 consecutive patients over a 12-month period. Levels of vitamins B1, B6, B12, and D were obtained on the day of clinic to identify deficiencies. A mental status exam (Mini Mental State Examination [MMSE]) was also performed. One hundred sixty-seven patients had one or more vitamin levels obtained on the day of clinical evaluation. Vitamin B6 deficiency was the most common (37.5%), followed by vitamin D deficiency (36.8%). A chi-square test revealed significant co-occurrence of deficiency of vitamins B6 and D (p<0.001). Vitamin B6 and D deficiencies were associated with lower MMSE scores (p<0.05). Vitamin B6 and D deficiencies are common in geriatric patients. The coexistence of these vitamin deficiencies has a significant association with cognitive performance, indicating the clinical importance of monitoring and supplementation.

Особенности диагностики энцефалопатии Вернике: клинический случай

Wernicke's encephalopathy (WE) is a rare neurological disorder caused by vitamin B1 (thiamine) deficiency and is associated with a significant risk of developing persistent neurological deficiency, chronification, disability and ultimately death if the aetiopathogenetic therapy with high doses of vitamin B1 is initiated late. Objective: to raise awareness among physicians about the characteristics of clinics, diagnostics and treatment of Wernicke's encephalopathy. Materials and methods. Retrospective analysis of the medical records of a patient with alcoholic Wernicke's encephalopathy. Results. This paper presents the own clinical observation of a patient with newly diagnosed alcoholic Wernicke's encephalopathy, clinical manifestations and MRI picture, describes the main features of aetiology and pathogenesis of this pathological process. Conclusion. An important role in the diagnosis of WE is played by the correct collection of anamnestic data and magnetic resonance imaging (MRI) of the brain, which has a sufficiently high specificity and is the only diagnostic method that allows this disease to be identified with high reliability. Thus, it is the thorough collection of anamnesis and the timely MRI examination that allow the doctor to point in the right direction of the diagnostic search in a timely manner.

ЭНЦЕФАЛОПАТИЯ ВЕРНИКЕ ПОСЛЕ БАРИАТРИЧЕСКОЙ ОПЕРАЦИИ: СЛУЧАЙ ИЗ ПРАКТИКИ

Objective: To review the signs and symptoms of Wernicke encephalopathy (WE) after bariatric surgery based on 2 case reports and a literature data analysis. Methods: We present two case reports of WE. In these patients, thiamine deficiency developed due to bariatric gastric surgery, which was performed to treat class III obesity, formerly known as morbid obesity. The patients underwent comprehensive physical and neurological examinations; clinical, laboratory, and instrumental data were collected from medical records and analyzed. The researchers also performed a computerized search using the keywords "Wernicke encephalopathy after bariatric surgery" to find relevant publications in the PubMed/Medline, Scopus, and Web of Science databases. Results: The presented acute neurological condition related to vitamin B1 deficiency in two patients after undergoing a weight loss surgery, specifically a mini-gastric bypass. The clinical picture in one patient was dominated by memory impairment, ataxic, and polyneuritic syndrome, while in the other, it was only polyneuritic syndrome. Conclusion: The initial symptoms of WE are often overlooked, leading to the progression of the disease with the development of severe neurological deficits. To prevent the progression of encephalopathy, it is necessary to begin treatment with high doses of parenteral thiamine replacement therapy as early as possible. Keywords: Obesity, bariatric surgery, Wernicke encephalopathy, thiamine, case report

Использование витаминов группы В в профилактических и лечебных дозах при сахарном диабете 2-го типа

Polyhypovitaminosis is a risk factor for many diseases. Adequate dietary intake of vitamins may help prevent/reduce the risk of progression of several diseases, including type 2 diabetes (T2D). Objective. To analyze the sufficiency of B vitamins and efficacy of their administration in patients with T2D depending on the dose. Vitamin deficiencies typical for patients with T2D worsen the course of the disease and increase the risk of complications. Higher intake of vitamins B1, B2 and folate is associated with a lower risk of T2D, and higher intake of folate and vitamin B6 is associated with a lower risk of cardiovascular diseases in patients with T2D. Higher intake of vitamin B6 by individuals with T2D is associated with a lower incidence of diabetic retinopathy. In T2D patients, low levels of the coenzyme form of vitamin B6 and high serum levels of 4-pyridoxic acid increase the risk of all-cause mortality. Patients with diabetic retinopathy have significantly reduced levels of vitamin B12. The incidence of vitamin B2 deficiency based on serum levels is found in approximately 30–40% of patients with T2D and diabetic nephropathy. Metformin administration worsens vitamin B12 supply and increases the risk of T2D complications. The need to eliminate vitamin deficiencies and improve the sufficiency of B vitamins is undeniable. There are prophylactic and therapeutic doses of vitamins. Continuous intake of multivitamin supplements with a complete set of all B vitamins in prophylactic doses consistent with the recommended daily intake (RDI) will reduce the risk of T2D progression. Administration of B vitamins during 1 month to 5 years in therapeutic doses well above the RDI results in improvement of carbohydrate metabolism, antioxidant and clinical status in patients with T2D, but may lead to undesirable effects. Conclusion. When prescribing B vitamins to T2D patients, it is recommended to distinguish between prophylactic doses of vitamins that meet the body’s needs and can and should be taken continuously, and therapeutic doses, that are close to the upper safe intake level and may cause adverse reactions. Key words: type 2 diabetes, B vitamins, sufficiency, prophylactic and therapeutic doses of vitamins

Gestational Malnutrition is Still the Skeleton in the Closet: Where Are the Malnutrition Risk Screening Criteria?

In 2020 there were 3,613,647 live births in the US. Fifty to 90% of those pregnancies were affected by nausea and vomiting of pregnancy (NVP) while the most severe NVP, known as hyperemesis gravidarum (HG) affected 1.5- 3.0% of those gravidas. In 2014 58,436 gravidas were hospitalized with HG. While hospital admissions for HG were down 42%, the number seen in Emergency departments rose by 27.7%. Although HG has been viewed as a positive predictor of a favorable pregnancy outcome, patients who also demonstrate weight loss and electrolyte disturbance may be a distinct entity and at greater risk for growth retardation and fetal anomalies. Poorly managed HG can result in compounded maternal injuries, increased rates of therapeutic abortions and suicide ideation, as well as a high rate of fetal loss. This study focuses on one of the most severe catastrophes originating from HG: Wernicke’s encephalopathy (WE) continues to be an under-recognized and often misunderstood disease in all populations. The acknowledged cause of WE is vitamin B1 or thiamin deficiency, a specific form of malnutrition. Unfortunately, this syndrome is most often recognized at autopsy, especially among non-alcoholics. One manifestation of WE is cognitive dysfunction which may explain the increase in suicidal ideation and/or elected terminations. The current mounting legislation of pregnancy termination limits will complicate the decision to abort for critically ill gravidas and their medical providers. However, antecedent events to WE are extremely poor nutritional intake leading to excessive weight loss and delayed nutritional interventions which can mitigate these situations.

Refractory seizures and polyneuropathy associated with vitamin B6 deficiency in a patient treated with oral levodopa/carbidopa: A case report

Refractory seizures and polyneuropathy associated with vitamin B6 deficiency in a patient treated with oral levodopa/carbidopa: A case report

Micronutrient gaps during the complementary feeding period in seven countries in Southeast Asia: A Comprehensive Nutrient Gap Assessment

AbstractThe complementary feeding period is a critical stage of child development when micronutrient needs are high and challenging to meet. Understanding if specific micronutrient gaps exist during this period is critical for effective programming. A Comprehensive Nutrient Gap Assessment (CONGA) was conducted in seven countries in Southeast Asia to estimate gaps in micronutrients commonly lacking in the diets of children aged 6–23 months and to establish the certainty of available evidence for each identified gap. Sixty‐eight evidence sources were identified during this analysis, and 310 micronutrient‐specific data points were identified across all seven countries. Data points varied in recency, representativeness and evidence type. The CONGA methodology enabled the estimation of a gap burden rating for each micronutrient in each country, as well as a rating of their evidence certainty. Micronutrient gaps were identified in vitamin D, zinc and iron and a potential gap was identified in calcium during the complementary feeding period in the region. Evidence relevant to intake and deficiency of folate, vitamin B12, thiamine, niacin, vitamin C and vitamin B6 was limited across the region. Proven strategies to address these gaps include increasing the availability and consumption of nutrient‐dense foods, micronutrient supplementation, large‐scale fortification of staple foods and condiments and point‐of‐use fortification through multiple micronutrient powders and fortified speciality foods. More recent data on micronutrient availability, intake and deficiency is urgently needed in Southeast Asia.