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Riboflavin, in its cofactor forms flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN), plays fundamental roles in energy metabolism, cellular antioxidant potential, and metabolic interactions with other micronutrients, including iron, vitamin B6, and folate. Severe riboflavin deficiency, largely confined to low-income countries, clinically manifests as cheilosis, angular stomatitis, glossitis, seborrheic dermatitis, and severe anemia with erythroid hypoplasia. Subclinical deficiency may be much more widespread, including in high-income countries, but typically goes undetected because riboflavin biomarkers are rarely measured in human studies. There are adverse health consequences of low and deficient riboflavin status throughout the life cycle, including anemia and hypertension, that could contribute substantially to the global burden of disease. This review considers the available evidence on causes, detection, and consequences of riboflavin deficiency, ranging from clinical deficiency signs to manifestations associated with less severe deficiency, and the related research, public health, and policy priorities. [ABSTRACT FROM AUTHOR]

The relationship between endometriosis and subclinical atherosclerosis represents an emerging topic in women's health, as women with endometriosis are at higher risk of cardiovascular disease later in life. We investigated metabolic parameters and indirect endothelial markers related to atherosclerosis, in women suffering from stage III/IV of endometriosis compared with women without endometriosis. The study population comprised 643 women: 92 women (14.3%) with stage III/IV of endometriosis and 551 (85.7%) without endometriosis. By analyzing biohumoral parameters we observed a significant increased total cholesterol (p = 0.01), LDL-C (p = 0.01), triglycerides (p = 0.05) and homocysteinaemia (p = 0.04), lower vitamin B6 and folate (p = 0.07 and p = 0.03, respectively) values, and higher high-sensitive C reactive protein (p = 0.05) concentrations in stage III/IV in comparison to those observed in women without endometriosis. After adjustment for traditional cardiovascular risk factors, the poorer lipid profile (total cholesterol, LDL-C), as well as Lipoprotein (a), remained significantly associated with severity of endometriosis (p = 0.01 and p = 0.03, respectively). Our findings highlight the role of endometriosis as a gender-specific cardiovascular risk factor. The clinical relevance of our study lies in identifying women with stage III/IV of endometriosis at higher risk of atherosclerotic disease, who could benefit from an early cardiovascular screening to control future cardiovascular risk. [ABSTRACT FROM AUTHOR]

The occurrence of anorectal malformations (ARM) is thought to be reduced with sufficient folate intake. However, there is no apparent evidence. We focused on enzyme cofactors for one-carbon metabolism, including folate (vitamin B9), vitamin B6 and vitamin B12, and explored the association between maternal combined intake of these B vitamins and the risk of ARM. Using baseline data from a Japanese nationwide birth cohort study between 2011 and 2014, we analysed data of 89 235 women (mean age at delivery = 31·2 years) who delivered singleton live births without chromosomal anomalies. Information on dietary intake was obtained via a FFQ focused on early pregnancy and used to estimate B vitamin intake. We also collected information on the frequency of folic acid supplement use. ARM occurrence was ascertained from medical records. We identified forty-three cases of ARM diagnosed up to the first month after birth (4·8 per 10 000 live births). In terms of individual intake of the respective B vitamins, high vitamin B6 intake was non-significantly associated with reduced odds of ARM. Compared with women in the low combined B vitamin intake group, the OR of having an infant with ARM was 0·4 (95 % CI 0·2, 1·0) in the high intake group (folate ≥400 μg/d, and upper half of vitamin B6 and/or vitamin B12). In conclusion, our cohort analysis suggested an inverse association between the combined intake of one-carbon metabolism-related B vitamins in early pregnancy and ARM occurrence. [ABSTRACT FROM AUTHOR]

L'anémie sidéroblastique est une cause rare d'anémie microcytaire, caractérisée par la présence de sidéroblastes en couronne au myélogramme. Cette anémie peut être congénitale ou bien acquise, due à une myélodysplasie ou favorisée par des carences, des médicaments et des toxiques. Nous rapportons le cas d'un homme alcoolique de 49 ans présentant une anémie microcytaire sidéroblastique sévère reliée à une carence en pyridoxine (vitamine B6). Il a aussi été identifié une carence en folates. L'hémogramme s'est corrigé en un mois avec une supplémentation vitaminique. Chez les sujets à risque, une carence en pyridoxine doit être évoquée devant une anémie sidéroblastique. Sideroblastic anemia is a rare cause of microcytic anemia, which is characterized by ring sideroblasts on bone marrow aspirate. This anemia can be congenital or acquired. We report the case of an alcoholic 49-year-old man who presented with a severe microcytic sideroblastic anemia related to pyridoxine (B6 vitamin) deficiency. Acid folic deficiency was associated. The blood count normalized within one month after vitamin supplementation. Pyridoxine deficiency must be sought in sideroblastic anemia in patients at risk. [ABSTRACT FROM AUTHOR]

Background: Vitamin B deficiency and elevated total plasma homocysteine have been associated with cognitive impairment and dementia in later life, although it is unknown if treatment with these vitamins improves cognitive outcomes. Objectives: The objectives of this study were to examine the efficacy of treatment with vitamin B12, vitamin B6, or folic acid in slowing cognitive decline amongst older adults with and without cognitive impairment. Methods: We summarized findings from previous systematic reviews of clinical trials and performed a new systematic review and meta-analysis of 31 English-language, randomized placebo-controlled trials of B-vitamin supplementation of individuals with and without existing cognitive impairment. Results: Previous reviews have generally reported no effect of B vitamins on cognitive function in older adults with or without cognitive impairment at study entry, although these vitamins effectively lowered total plasma homocysteine levels in participants. Ten randomized placebo-controlled trials of 1925 participants with pre-existing cognitive impairment and 21 trials of 15,104 participants without cognitive impairment have been completed to date but these generally confirmed findings from previous reviews with the exception of two trials that showed a modest but clinically uncertain benefit for vitamins in people with elevated plasma homocysteine. B-vitamin supplementation did not show an improvement in Mini-Mental State Examination scores for individuals with (mean difference 0.16, 95% confidence interval − 0.18 to 0.51) and without (mean difference 0.04, 95% confidence interval − 0.10 to 0.18) cognitive impairment compared to placebo. Conclusions: Raised total plasma homocysteine is associated with an increased risk of cognitive impairment and dementia, although available evidence from randomized controlled trials shows no obvious cognitive benefit of lowering homocysteine using B vitamins. Existing trials vary greatly in the type of supplementation, population sampled, study quality, and duration of treatment, thereby making it difficult to draw firm conclusions from existing data. Findings should therefore be viewed in the context of the limitations of the available data and the lack of evidence of effect should not necessarily be interpreted as evidence of no effect. [ABSTRACT FROM AUTHOR]

This review offers an update on a group of inborn errors of metabolism causing severe epilepsy with the onset in pediatric age (but also other neurological manifestations such as developmental delay or movement disorders) with available effective or potentially effective treatments. The main pathogenic and clinical features and general recommendations for the diagnostic and therapeutic workup of the following disorders are discussed: vitamin B6-dependent epilepsies, cerebral folate deficiency, congenital disorders of serine metabolism, biotinidase deficiency, inborn errors of creatine metabolism, molybdenum cofactor deficiency, and glucose transporter 1 deficiency. Available treatments are more effective on epileptic manifestations (with the possibility of complete seizure control) and motor symptoms, whereas the benefits on cognitive outcome are usually minor. [ABSTRACT FROM AUTHOR]

B vitamin deficiency is a leading cause of neurological impairment and disability throughout the world. Multiple B vitamin deficiencies often coexist, and thus an understanding of the complex relationships between the different biochemical pathways regulated in the brain by these vitamins may facilitate prompter diagnosis and improved treatment. Particular populations at risk for multiple B vitamin deficiencies include the elderly, people with alcoholism, patients with heart failure, patients with recent obesity surgery, and vegetarians/vegans. Recently, new clinical settings that predispose individuals to B vitamin deficiency have been highlighted. Moreover, other data indicate a possible pathogenetic role of subclinical chronic B vitamin deficiency in neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. In light of these findings, this review examines the clinical manifestations of B vitamin deficiency and the effect of B vitamin deficiency on the adult nervous system. The interrelationships of multiple B vitamin deficiencies are emphasized, along with the clinical phenotypes related to B vitamin deficiencies. Recent advances in the clinical determinants and diagnostic clues of B vitamin deficiency, as well as the suggested therapies for B vitamin disorders, are described. [ABSTRACT FROM AUTHOR]

Background: Deficiency of vitamin B-6, vitamin B-12, folate, folic acid, or methionine may lead to dysregulation of DNA methylation, which might lead to disturbed energy and lipid metabolism. Objective: We aimed to explore whether intakes of vitamin B-6, vitamin B-12, folate, folic acid, and methionine at 1 y are associated with measures of growth and body composition at the age of 6 y. Methods: This study was performed in 2922 children participating in The Generation R Study, a population-based prospective cohort study. Dietary intakes of vitamins B-6 and B-12, folate, folic acid, and methionine were assessed at a median age of 12.9 mo by using a validated food-frequency questionnaire. At the age of 6 y, height and weight were measured, and body mass index (BMI; in kg/m²) was calculated. Body fat was measured with dual-energy X-ray absorptiometry, and body fat percentage and the ratio of android fat mass to gynoid fat mass (android:gynoid) were calculated. Results: In models adjusted for maternal and child characteristics, children with folic acid intakes in the highest tertile had a 0.16 SD score (SDS) lower weight (95% CI: -0.31, -0.02 SDS) and a 0.14 SDS lower BMI (95% CI: -0.26, -0.01 SDS) than children in the lowest tertile. Children with vitamin B-12 intakes in the highest tertile had a 0.13 SDS higher android:gynoid (95% CI: 0.00, 0.25 SDS) than children in the lowest tertile. In addition, children with intakes in the highest tertile of methionine had a 0.09 SDS higher BMI (95% CI: 0.01, 0.17) and a 0.12 SDS higher android:gynoid (95% CI: 0.02, 0.22) than children in the lowest tertile. Vitamin B-6 and folate intakes were not associated with any of the body composition outcomes measured. Conclusions: In this population of children, early high folic acid intakes were associated with a lower body weight and BMI at the age of 6 y. In contrast, early higher methionine intakes were associated with unfavorable body composition at the age of 6 y. Future studies should investigate long-term consequences of these outcomes on health. [ABSTRACT FROM AUTHOR]

Précis Abnormal methionine challenge test results cannot be explained by a deficiency in pyridoxal phosphate, folic acid, or cobalamin. The methionine challenge test is reliable for demonstrating hyperhomocysteinemia. Objective. To research the status of pyridoxal phosphate, folic acid, and cobalamin as part of an examination for hyperhomocysteinemia and to establish their relationship to the results of methionine challenge tests in women, who were tested at least 3 months after they had ended a pregnancy which was complicated by preeclampsia or other vascular-related pregnancy complications. Methods. In the Isala clinics in Zwolle, women with vascular-related complications of pregnancy were tested at least 3 months postpartum for hyperhomocysteinemia, by performing a methionine challenge test, as well as tests to measure their vitamin status. The diagnosis of hyperhomocysteinemia was made after two abnormal test results. The χ2 test was used to compare the vitamin status of the group with normal results to those with an abnormal result of methionine challenge tests. Results. No statistically significant differences in the vitamin status were found between the group of women with an abnormal and the group with normal results of the methionine challenge tests. Conclusion. Abnormal methionine challenge test results cannot be explained by a deficiency in pyridoxal phosphate, folic acid, or cobalamin. We demonstrate that, when women are tested 3 months postpartum, the methionine challenge test is reliable for demonstrating hyperhomocysteinemia as a risk factor for vascular-related complications of pregnancy. [ABSTRACT FROM AUTHOR]

Deficiencies of the vitamins folate, B, and B 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. [ABSTRACT FROM AUTHOR]

Objective: To find out the prevalence of hyperhomocysteinemia, and deficiencies of folate, vitamin B6 and vitamin B12 in an urban population in Karachi, Pakistan. Methodology: In a pre and post experimental study, eight hundred and seventy-two apparently healthy adults (aged 18-60 years; 355 males and 517 females) were recruited from a low-income urban locality in East of Karachi from February 2006 to March 2007. Fasting venous blood was obtained. Serum was analyzed for folate and vitamin B12. Plasma was analyzed for pyridoxal phosphate (PLP, coenzymic form of B6) and total homocysteine. A group of vitamin-deficient individuals (n=194) was given 3-week supplementation with folic acid (5mg/ day), methycobalamin (0.5mg/day) and pyridoxine hydrochloride (vitamin B6, 50 mg/day). After supplementation, serum/plasma levels of folate, vitamin B12, PLP and homocysteine were again determined. Results: Prevalence of hyperhomocysteinemia (>15μmol/l) was 32%. Similarly percent values of folate deficiency (<3.5ng/ml), vitamin B6 deficiency (PLP<20 nmol/l) and vitamin B12 deficiency (<200pg/ml) in the study population were 27.5%, 33.7% and 9.74%, respectively. Hyperhomocysteinemia was associated with male sex, folate deficiency, vitamin B12 deficiency [OR (95%CI), 8.3(5.7-12.1); 2.5(1.76-3.58); 2.6(1.5-4.5), respectively]. A 3-week supplementation with folic acid, methycobalamin and pyridoxine hydrochloride in vitamindeficient subjects decreased plasma homocysteine levels by 37%. Conclusion: High prevalence estimates of folate, vitamin B12, and vitamin B6 deficiencies appear to be the major determinants of hyperhomocysteinemia in a low income general population in Karachi. [ABSTRACT FROM AUTHOR]

Abstract: Epidemiological and clinical studies indicate that elevated circulating level of homocysteine (Hcy) is a risk factor for developing Alzheimer’s disease (AD). Dietary deficiency of folate, vitamin B6 and B12 results in a significant increase of Hcy levels, a condition also known as hyperhomocysteinemia (HHcy). In the present study we tested the hypothesis that a diet deficient for these three important factors when administered to a mouse model of AD, i.e. Tg2576, will result in HHcy and in an acceleration of their amylodotic phenotype. Compared with Tg2576 mice on regular chow, the ones receiving the diet deficient for folate, B6 and B12 developed HHcy. This condition was associated with a significant increase in Aβ levels in the cortex and hippocampus, and an elevation of Aβ deposits in the same regions. No significant changes were observed for steady-state levels of total APP, BACE-1, ADAM-10, PS1 and nicastrin in the brains of mice with HHcy. No differences were observed for the main Aβ catabolic pathways, i.e. IDE and neprilysin proteins, or the Aβ chaperone apolipoprotein E. Our findings demonstrate that a dietary condition which leads to HHcy may also result in increased Aβ levels and deposition in a transgenic mouse model of AD-like amylodosis. They further support the concept that dietary factors can contribute to the development of AD neuropathology. [Copyright &y& Elsevier]

Little is known about the micronutrient status of Chinese women of childbearing age. We assessed nonfasting plasma concentrations of folic acid, vitamin B-12, vitamin B-6 (as pyridoxal-5'-phosphate), hemoglobin (Hb), ferritin and transferrin receptor (TfR) in 563 nonpregnant textile workers aged 21-34 y from Anqing, China. All women had obtained permission to become pregnant and were participating in a prospective study of pregnancy outcomes. Mean (SD) plasma concentrations were 9.7 (4.1) nmol/L folic acid, 367 (128) pmol/L vitamin B-12, 40.2 (15.8) nmol/L vitamin B-6, 108 (12. 9) g/L Hb, 42.6 (34.2) microgram/L ferritin and 5.2 (2.7) mg/L TfR. Twenty-three percent of women had biochemical evidence of folic acid deficiency, 26% were deficient in vitamin B-6 and 10% had low vitamin B-12. Overall, 44% of women were deficient in at least one B vitamin. Although anemia (Hb < 120 g/L) was detected in 80% of women, only 17% had depleted iron stores (ferritin < 12 microgram/L); 11% had elevated TfR concentrations. Distinct seasonal trends were observed in the prevalence of moderate anemia (Hb < 100 g/L) and deficiencies of folic acid and vitamin B-6, with significantly lower concentrations of folate and Hb occurring in summer and lower concentrations of vitamin B-6 occurring in winter and spring than in other seasons. We conclude that deficiencies of folic acid, vitamin B-6 and iron were relatively common in this sample of Chinese women of childbearing age and were contributing to the high prevalence of anemia. Without appropriate supplementation, these deficiencies could jeopardize the women's health and increase their risk of adverse pregnancy outcomes. [ABSTRACT FROM AUTHOR]

The article presents evidence that deficiencies of folic acid, vitamin B12, thiamine, riboflavin, pyridoxine and ascorbic acid have certain associations with psychiatric disorders. According to the author, such deficiencies are frequently found in depression and alcoholism. The author reveals that vitamin B12 deficiencies are usually associated with organic psychosis and affective symptoms. The author adds that thiamine deficiency is linked with a wide variety of mental symptoms and is probably secondary to anorexia and malnutrition.

The plasma homocysteine response to methionine loading was assessed in vitamin B-6- and folate-deficient rats. Rats fed vitamin B-6-or folate-deficient diets for 4 wk were administered a gastric gavage of methioninc (100 mg/kg body wt). Subsequent plasma analyses revealed a peak post-methionine load increase in plasma homocysteine concentration of > 300 µmol/L in the vitamin B-6-deficient rats. Folate-dcficient rats exhibited no significant changes in plasma homocysteinc after the load. These disparate responses can be explained by the observed increase in hepatic S-adenosylmethionine (SAM) concentration because of the load. In vitamin B-6 deficiency, increased SAM inhibits homocysteine remethylation, which, in conjunction with the impaired homocysteine catabolism due to the deficiency and the increased synthesis of homocysteine due to the methionine load, leads to a large elevation of homocysteine in the blood. In folate deficiency, increased SAM activates homocysteine catabolism, which compensates for the increased synthesis of homocysteine due to the load and thus no change in blood homocysteine is observed. These results have significant bearing on the interpretation of both positive and negative responses to methionine loading in humans. [ABSTRACT FROM AUTHOR]