Showing papers on "B vitamins published in 2006"

Homocysteine Lowering with Folic Acid and B Vitamins in Vascular Disease

Abstract: risk, 0.95; 95 percent confidence interval, 0.84 to 1.07; P = 0.41). As compared with placebo, active treatment did not significantly decrease the risk of death from cardiovascular causes (relative risk, 0.96; 95 percent confidence interval, 0.81 to 1.13), myocardial infarction (relative risk, 0.98; 95 percent confidence interval, 0.85 to 1.14), or any of the secondary outcomes. Fewer patients assigned to active treatment than to placebo had a stroke (relative risk, 0.75; 95 percent confidence interval, 0.59 to 0.97). More patients in the active-treatment group were hospitalized for unstable angina (relative risk, 1.24; 95 percent confidence interval, 1.04 to 1.49). Conclusions Supplements combining folic acid and vitamins B 6 and B 12 did not reduce the risk of major cardiovascular events in patients with vascular disease. (ClinicalTrials.gov number, NCT00106886; Current Controlled Trials number, ISRCTN14017017.)

Homocysteine lowering and cardiovascular events after acute myocardial infarction.

Abstract: BACKGROUND Homocysteine is a risk factor for cardiovascular disease. We evaluated the efficacy of homocysteine-lowering treatment with B vitamins for secondary prevention in patients who had had an acute myocardial infarction. METHODS The trial included 3749 men and women who had had an acute myocardial infarction within seven days before randomization. Patients were randomly assigned, in a twoby-two factorial design, to receive one of the following four daily treatments: 0.8 mg of folic acid, 0.4 mg of vitamin B 12 , and 40 mg of vitamin B 6 ; 0.8 mg of folic acid and 0.4 mg of vitamin B 12 ; 40 mg of vitamin B 6 ; or placebo. The primary end point during a median follow-up of 40 months was a composite of recurrent myocardial infarction, stroke, and sudden death attributed to coronary artery disease. RESULTS The mean total homocysteine level was lowered by 27 percent among patients given folic acid plus vitamin B 12 , but such treatment had no significant effect on the primary end point (risk ratio, 1.08; 95 percent confidence interval, 0.93 to 1.25; P = 0.31). Also, treatment with vitamin B 6 was not associated with any significant benefit with regard to the primary end point (relative risk of the primary end point, 1.14; 95 percent confidence interval, 0.98 to 1.32; P = 0.09). In the group given folic acid, vitamin B 12 , and vitamin B 6 , there was a trend toward an increased risk (relative risk, 1.22; 95 percent confidence interval, 1.00 to 1.50; P = 0.05). CONCLUSIONS Treatment with B vitamins did not lower the risk of recurrent cardiovascular disease after acute myocardial infarction. A harmful effect from combined B vitamin treatment was suggested. Such treatment should therefore not be recommended. (ClinicalTrials.gov number, NCT00266487.)

An assessment of incremental coronary risk prediction using C-reactive protein and other novel risk markers: the atherosclerosis risk in communities study.

Abstract: Background There has been interest in recent years in whether additional, and in particular novel, risk factors or blood markers, such as C-reactive protein, can enhance existing coronary heart disease (CHD) prediction models. Methods Using a series of case-cohort studies, the prospective Atherosclerosis Risk in Communities (ARIC) Study assessed the association of 19 novel risk markers with incident CHD in 15 792 adults followed up since 1987-1989. Novel markers included measures of inflammation, endothelial function, fibrin formation, fibrinolysis, B vitamins, and antibodies to infectious agents. Change in the area under the receiver operating characteristic curve (AUC) was used to assess the additional contribution of novel risk markers to CHD prediction beyond that of traditional risk factors. Results The basic risk factor model, which included traditional risk factors (age, race, sex, total and high-density lipoprotein cholesterol levels, systolic blood pressure, antihypertensive medication use, smoking status, and diabetes), predicted CHD well, as evidenced by an AUC of approximately 0.8. The C-reactive protein level did not add significantly to the AUC (increase in AUC of 0.003), and neither did most other novel risk factors. Of the 19 markers studied, lipoprotein-associated phospholipase A 2 , vitamin B 6 , interleukin 6, and soluble thrombomodulin added the most to the AUC (range, 0.006-0.011). Conclusions Our findings suggest that routine measurement of these novel markers is not warranted for risk assessment. On the other hand, our findings reinforce the utility of major, modifiable risk factor assessment to identify individuals at risk for CHD for preventive action.

A controlled trial of homocysteine lowering and cognitive performance.

Abstract: Background The results of observational studies suggest that plasma homocysteine concentrations are inversely related to cognitive function in older people. Our objective was to test the hypothesis that lowering the plasma homocysteine concentration improves cognitive function in healthy older people. Methods We conducted a two-year, double-blind, placebo-controlled, randomized clinical trial involving 276 healthy participants, 65 years of age or older, with plasma homocysteine concentrations of at least 13 μmol per liter. Homocysteine-lowering treatment was a daily supplement containing folate (1000 μg) and vitamins B12 (500 μg) and B6 (10 mg). Tests of cognition were conducted at baseline and after one and two years of treatment. Treatment effects were adjusted for baseline values, sex, and education. Results On average, during the course of the study, the plasma homocysteine concentration was 4.36 μmol per liter (95 percent confidence interval, 3.81 to 4.91 μmol per liter) lower in the vitamin group than in the placebo group (P<0.001). Overall, there were no significant differences between the vitamin and placebo groups in the scores on tests of cognition. Conclusions The results of this trial do not support the hypothesis that homocysteine lowering with B vitamins improves cognitive performance. (Australian Clinical Trials registry number, ACTR NO 12605000030673.)

The role of nutrients in bone health, from A to Z.

Abstract: Osteoporosis is a major public health problem, affecting millions of individuals. Dietary intake is an important modifiable factor for bone health. Inadequate intake of nutrients important to bone increases the risk for bone loss and subsequent osteoporosis. The process of bone formation requires an adequate and constant supply of nutrients, such as calcium, protein, magnesium, phosphorus, vitamin D, potassium, and fluoride. However, there are several other vitamins and minerals needed for metabolic processes related to bone, including manganese, copper, boron, iron, zinc, vitamin A, vitamin K, vitamin C, and the B vitamins. Although the recommended levels of nutrients traditionally related to bone were aimed to promote bone mass and strength, the recommended levels of the other nutrients that also influence bone were set on different parameters, and may not be optimal for bone health, in view of recent epidemiological studies and clinical trials.

Phosphoinositide 3-kinase/Akt signaling pathway and its therapeutical implications for human acute myeloid leukemia.

Abstract: The phosphoinositide 3-kinase (PI3K)/Akt signaling pathway is crucial to many aspects of cell growth, survival and apoptosis, and its constitutive activation has been implicated in the both the pathogenesis and the progression of a wide variety of neoplasias. Hence, this pathway is an attractive target for the development of novel anticancer strategies. Recent studies showed that PI3K/Akt signaling is frequently activated in acute myeloid leukemia (AML) patient blasts and strongly contributes to proliferation, survival and drug resistance of these cells. Upregulation of the PI3K/Akt network in AML may be due to several reasons, including FLT3, Ras or c-Kit mutations. Small molecules designed to selectively target key components of this signal transduction cascade induce apoptosis and/or markedly increase conventional drug sensitivity of AML blasts in vitro. Thus, inhibitory molecules are currently being developed for clinical use either as single agents or in combination with conventional therapies. However, the PI3K/Akt pathway is important for many physiological cellular functions and, in particular, for insulin signaling, so that its blockade in vivo might cause severe systemic side effects. In this review, we summarize the existing knowledge about PI3K/Akt signaling in AML cells and we examine the rationale for targeting this fundamental signal transduction network by means of selective pharmacological inhibitors.

Homocysteine metabolism, hyperhomocysteinaemia and vascular disease: an overview.

Abstract: Hyperhomocysteinaemia has been regarded as a new modifiable risk factor for atherosclerosis and vascular disease. Homocysteine is a branch-point intermediate of methionine metabolism, which can be further metabolised via two alternative pathways: degraded irreversibly through the transsulphuration pathway or remethylated to methionine by the remethylation pathway. Both pathways are B-vitamin-dependent. Plasma homocysteine concentrations are determined by nongenetic and genetic factors. The metabolism of homocysteine, the role of B vitamins and the contribution of nongenetic and genetic determinants of homocysteine concentrations are reviewed. The mechanisms whereby homocysteine causes endothelial damage and vascular disease are not fully understood. Recently, a link has been postulated between homocysteine, or its intermediates, and an alterated DNA methylation pattern. The involvement of epigenetic mechanisms in the context of homocysteine and atherosclerosis, due to inhibition of transmethylation reactions, is briefly overviewed.

Protein Composition and Electron Microscopy Structure of Affinity-Purified Human Spliceosomal B Complexes Isolated under Physiological Conditions

Abstract: The spliceosomal B complex is the substrate that undergoes catalytic activation leading to catalysis of pre-mRNA splicing. Previous characterization of this complex was performed in the presence of heparin, which dissociates less stably associated components. To obtain a more comprehensive inventory of the B complex proteome, we isolated this complex under low-stringency conditions using two independent methods. MS2 affinity-selected B complexes supported splicing when incubated in nuclear extract depleted of snRNPs. Mass spectrometry identified over 110 proteins in both independently purified B complex preparations, including 50 non-snRNP proteins not previously found in the spliceosomal A complex. Unexpectedly, the heteromeric hPrp19/CDC5 complex and 10 additional hPrp19/CDC5-related proteins were detected, indicating that they are recruited prior to spliceosome activation. Electron microscopy studies revealed that MS2 affinity-selected B complexes exhibit a rhombic shape with a maximum dimension of 420 A and are structurally more homogeneous than B complexes treated with heparin. These data provide novel insights into the composition and structure of the spliceosome just prior to its catalytic activation and suggest a potential role in activation for proteins recruited at this stage. Furthermore, the spliceosomal complexes isolated here are well suited for complementation studies with purified proteins to dissect factor requirements for spliceosome activation and splicing catalysis. Pre-mRNA splicing is catalyzed by a large RNP molecular machine, termed the spliceosome, which consists of the U1, U2, U4/U6, and U5 snRNPs and a multitude of non-snRNP proteins (reviewed in reference 48). The active site(s) responsible for the catalysis of pre-mRNA splicing is not preformed but, rather, is created anew during the highly dynamic process of spliceosome assembly. The latter is an ordered process during which several intermediates, termed E, A, B, and B*, can be detected in vitro (reviewed in reference 48). Assembly is initiated by the ATP-independent interaction of the U1 snRNP with the conserved 5 splice site of the pre-mRNA, forming the E complex. At this stage, the U2 snRNP is loosely associated with the pre-mRNA (11). In a subsequent step requiring ATP, the U2 snRNP stably interacts with the pre-mRNA’s branch site, leading to formation of the A complex (also called the prespliceosome). Spliceosome assembly culminates with the formation of the spliceosomal B complex, during which the preformed U4/U6.U5 tri-snRNP particle interacts with the A complex. The B complex thus contains a full set of U snRNAs in a precatalytic state. It subsequently undergoes major rearrangements, including destabilization or loss of the U1 and U4 snRNPs, leading to catalytic activation and the formation of the so-called activated spliceosome (B* complex).

Risk factors of vitamin B(12) deficiency in patients receiving metformin.

Abstract: Background Identification of risk factors for metformin-related vitamin B 12 deficiency has major potential implications regarding the management of diabetes mellitus. Methods We conducted a nested case-control study from a database in which the source population consisted of subjects who had levels of both serum vitamin B 12 and hemoglobin A 1c checked in a central laboratory. We identified 155 cases of diabetes mellitus and vitamin B 12 deficiency secondary to metformin treatment. Another 310 controls were selected from the cohort who did not have vitamin B 12 deficiency while taking metformin. Results A total of 155 patients with metformin-related vitamin B 12 deficiency (mean ± SD serum vitamin B 12 concentration, 148.6 ± 40.4 pg/mL [110 ± 30 pmol/L]) were compared with 310 matched controls (466.1 ± 330.4 pg/mL [344 ± 244 pmol/L]). After adjusting for confounders, we found clinically important and statistically significant association of vitamin B 12 deficiency with dose and duration of metformin use. Each 1-g/d metformin dose increment conferred an odds ratio of 2.88 (95% confidence interval, 2.15-3.87) for developing vitamin B 12 deficiency ( P P = .001) compared with those receiving metformin for less than 3 years. After exclusion of 113 subjects with borderline vitamin B 12 concentration, dose of metformin remained the strongest independent predictor of vitamin B 12 deficiency. Conclusions Our results indicate an increased risk of vitamin B 12 deficiency associated with current dose and duration of metformin use despite adjustment for many potential confounders. The risk factors identified have implications for planning screening or prevention strategies in metformin-treated patients.

Diagnosis and treatment of vitamin B12 deficiency--an update.

Abstract: We represent an update on diagnosing and treatment of vitamin B12 deficiency. Vitamin B12 deficiency should be suspected in all patients with unexplained anaemia and/or neurological symptoms,as well as in patients at risk of developing vitamin B12 deficiency such as the elderly and patients with intestinal diseases. Measurement of plasma cobalamins is suggested as the primary analysis followed by measurement of plasma methylmalonic acid in unsettled cases. Accumulating evidence indicates that the biologically active cobalamin,plasma holotranscobalamin (holoTC),may be superior to plasma cobalamins, and measurement of holoTC is currently introduced in the clinical setting. No consensus exists concerning evaluation of the cause for vitamin B12 deficiency,and pros and cons on the different tests mainly aiming at evaluation of the function of the gastric mucosa are presented. Once the diagnosis of vitamin B12 deficiency has been confirmed efficient treatment can be ensured either by injections every 2-3 month or by a daily dose of 1 mg vitamin B12.

Low maternal vitamin B12 status is associated with intrauterine growth retardation in urban South Indians.

Abstract: To assess the maternal sociodemographic, anthropometric, dietary and micronutrient status in apparently healthy pregnant women in order to determine their associations with intrauterine growth retardation (IUGR). Prospective observational study. Bangalore City, India. A total of 478 women were recruited at 12.9±3.3 weeks of gestation and followed up at the first, second and third trimesters of pregnancy and at delivery. The dropout rate was 8.5%. None. Birth weight was measured at hospital delivery. The mean birth weight was 2.85±0.45 kg. In all, 28.6% of newborns were IUGR. There was a strong inverse relationship between maternal educational level and risk of IUGR. A low body weight at baseline was also associated with a high risk of IUGR. Compared with women in the highest quartile for second trimester weight gain, those in the lowest quartile had a significantly higher adjusted odds ratio (AOR: 3.98; 95% CI: 1.83, 8.65) for IUGR. Women in the lowest tertile for serum vitamin B12 concentration during each of the three trimesters of pregnancy had significantly higher risk of IUGR (AOR: 5.98, 9.28 and 2.81 for trimesters 1–3, respectively). The present study demonstrates associations between educational status, maternal weight and gestational weight gain with IUGR. Importantly, in a subsample, there were strong associations of vitamin B12 status with IUGR, suggesting that better socioeconomic conditions, improved nutritional status and early detection of vitamin B12 deficiency in pregnancy combined with appropriate interventions are likely to play an important role in reducing IUGR. This research was partly supported by the GlaxoSmithKline Consumer Healthcare Ltd, India.

Crystal structure of the SOCS2–elongin C–elongin B complex defines a prototypical SOCS box ubiquitin ligase

Abstract: Growth hormone (GH) signaling is tightly controlled by ubiquitination of GH receptors, phosphorylation levels, and accessibility of binding sites for downstream signaling partners. Members of the suppressors of cytokine signaling (SOCS) family function as key regulators at all levels of this pathway, and mouse knockout studies implicate SOCS2 as the primary suppressor. To elucidate the structural basis for SOCS2 function, we determined the 1.9-A crystal structure of the ternary complex of SOCS2 with elongin C and elongin B. The structure defines a prototypical SOCS box ubiquitin ligase with a Src homology 2 (SH2) domain as a substrate recognition motif. Overall, the SOCS box and SH2 domain show a conserved spatial domain arrangement with the BC box and substrate recognition domain of the von Hippel-Lindau (VHL) tumor suppressor protein, suggesting a common mechanism of ubiquitination in these cullin-dependent E3 ligases. The SOCS box binds elongin BC in a similar fashion to the VHL BC box and shows extended structural conservation with the F box of the Skp2 ubiquitin ligase. A previously unrecognized feature of the SOCS box is revealed with the burial of the C terminus, which packs together with the N-terminal extended SH2 subdomain to create a stable interface between the SOCS box and SH2 domain. This domain organization is conserved in SOCS1-3 and CIS1, which share a strictly conserved length of their C termini, but not in SOCS4, 5, and 7, which have extended C termini defining two distinct classes of inter- and intramolecular SOCS box interactions.

Plasma Total Homocysteine Level and Bone Mineral Density: The Hordaland Homocysteine Study

Abstract: Background Plasma total homocysteine (tHcy) has been associated with hip fracture but not directly with bone mineral density (BMD). We examined the association of hip BMD with levels of plasma tHcy, folate, and vitamin B 12 and the methylenetetrahydrofolate reductase ( MTHFR ) 677C→T and 1298A→C polymorphisms. Methods Bone mineral density was measured between 1997 and 2000 in 2268 men and 3070 women, aged 47 to 50 and 71 to 75 years, from the Hordaland Homocysteine Study cohort. Low BMD was defined as BMD in the lowest quintile for each sex and age group. Linear, logistic, and generalized additive regression models were used. Results Plasma levels of tHcy were inversely related to BMD among middle-aged and elderly women ( P 12 level or the MTHFR polymorphisms. Conclusions Elevated tHcy and low folate levels were associated with reduced BMD in women but not in men. These findings suggest that tHcy may be a potential modifiable risk factor for osteoporosis in women.

Altered D-chiro-inositol urinary clearance in women with polycystic ovary syndrome.

Abstract: OBJECTIVE —Evidence suggests that some actions of insulin are effected by inositolphosphoglycan (IPG) mediators. We hypothesize that a deficiency in D- chiro -inositol (DCI) and/or a DCI-containing IPG (DCI-IPG) may contribute to insulin resistance in humans. RESEARCH DESIGN AND METHODS —To assess this possibility in polycystic ovary syndrome (PCOS), we determined insulin sensitivity ( S i by frequently sampled intravenous glucose tolerance test), plasma and urinary DCI and myo -inositol (MYO) levels (by gas chromatography/mass spectrometry), and the release of insulin and DCI-IPG during the oral glucose tolerance test (area under the curve [AUC]) in 23 women with PCOS and 26 normal women. RESULTS —Women with PCOS were heavier than control subjects ( P = 0.002 for BMI), but also had decreased S i ( P insulin ( P DCI ) was increased almost sixfold in PCOS compared with normal women ( P = 0.001), but not MYO clearance ( P = 0.10). uCl DCI correlated inversely with S i when all women were analyzed together ( n = 49, r = −0.50, P S i . Finally, the ratio of AUC DCI-IPG to AUC insulin was decreased threefold in women with PCOS ( P CONCLUSIONS —uCl DCI is inversely correlated with insulin sensitivity in women and is a strong independent predictor of insulin resistance in multivariate models. PCOS, which is characterized by insulin resistance, is associated with a selective increase in uCl DCI and impaired DCI-IPG release in response to insulin. These findings are consistent with a defect in tissue availability or utilization of DCI in PCOS that may contribute to the insulin resistance of the syndrome.

Greater Fish, Fruit, and Vegetable Intakes Are Related to Lower Incidence of Venous Thromboembolism The Longitudinal Investigation of Thromboembolism Etiology

Abstract: Background— Little is known about the role of dietary intake in the development of deep vein thrombosis or pulmonary embolus (venous thromboembolism [VTE]). Homocysteine, factor VIII, and von Willebrand factor levels, risk factors for VTE, are influenced by dietary intake. We tested the hypothesis that foods rich in B vitamins and ω-3 fatty acids are negatively associated and meat intake is positively associated with incidence of VTE. Methods and Results— In a prospective study over 12 years, 14 962 middle-aged adults participating in the Atherosclerosis Risk in Communities study were followed up for incident VTE. All hospitalizations were identified, and 196 VTEs were validated by chart review. A food frequency questionnaire assessed dietary intake at baseline and year 6. In separate proportional hazards regression analyses, risk of developing VTE was computed across quintiles of selected nutrients, major food groups, and the Western diet pattern, with adjustment for demographic and lifestyle factors, bo...

Mediterranean diet and depression

Abstract: Objective: The adherence to a Mediterranean Dietary Pattern ensures an adequate intake of B vitamins and w-3 fatty acids. A protective role on depression has been suggested for both nutrients. Design: Cross-sectional analysis from the SUN (Seguimiento Universidad de Navarra) prospective cohort study. Data from 9670 participants (4211 men and 5459 women) were analised. Logistic regression analyses were fitted to assess the association between B-vitamins and w-3 fatty acids intake (quintiles) and the prevalence of depression. Results: Folate intake was inversely associated with depression prevalence among men, especially smokers. Among women, B12 vitamin intake was inversely associated with depression, especially among smokers and physically active women. No significant associations were observed for w-3 fatty acids intake. Conclusions: The adherence to a Mediterranean Dietary Pattern ensures an adequate intake of fruits, nuts, vegetables, cereals, legumes or fish, important sources of nutrients linked to depression prevention.

Colorectal cancer protective effects and the dietary micronutrients folate, methionine, vitamins B6, B12, C, E, selenium, and lycopene.

Abstract: The data reported here were obtained from the case-control arm of a large, comprehensive, population-based investigation of colorectal cancer incidence, etiology, and survival, the Melbourne Colorectal Cancer Study, conducted in Melbourne, Australia. This part of the case-control study was designed to identify dietary factors associated with colorectal cancer risk in 715 incident cases compared with 727 age/sex frequency-matched randomly chosen community controls, in which a quantitative assessment of all foods eaten was made. New data are presented on the potential of two groups of micronutrients as protective agents, namely, those involved in DNA methylation, synthesis, and repair (folate, methionine, and vitamins B6 and B12) and those with antioxidant properties (selenium, vitamins E and C, and lycopene). The adjusted odds ratios showed that for folate there was significant protection for rectal cancer in second and third quintiles of consumption but not for colon cancer, and this was similar for methionine consumption. Vitamin B6 consumption was significantly protective for both colon and rectal cancer at the higher quintiles, and this was similar for vitamin B12. Dietary selenium was significantly protective at middle quintiles of consumption at both cancer sites. Dietary vitamins E and C were statistically significantly protective for both colon and rectal cancer at all levels of consumption, and for both vitamins there was a dose-response effect of increasing protection, particularly so for colon cancer. Lycopene was not associated with colorectal cancer risk. A combined model included vitamins E, C, and B12 and selenium as micronutrients protective for colorectal cancer and folate, which, however, showed an increased risk at the highest level of consumption. These data support the proposition that a diet containing the dietary micronutrients involved in DNA methylation (folate, methionine, and vitamins B6 and B12) and some of those with antioxidant properties (selenium and vitamins E and C) may have a role to play in lowering colorectal cancer risk and also that such protection can be achieved by dietary means alone.

Niacinamide: A B Vitamin that Improves Aging Facial Skin Appearance

Abstract: Background. In multiple chronic clinical studies, topical niacinamide (vitamin B3) has been observed to be well tolerated by skin and to provide a broad array of improvements in the appearance of aging facial skin (eg, reduction in the appearance of hyperpigmentated spots and red blotchiness). Objective. To clinically determine the effect of topical niacinamide on additional skin appearance and property end points (wrinkles, yellowing, and elasticity). Methods. Female white subjects (N = 50) with clinical signs of facial photoaging (fine lines and wrinkles, poor texture, and hyperpigmented spots) applied 5% niacinamide to half of the face and its vehicle control to the other half twice daily for 12 weeks (double blind, left-right randomized). Facial images and instrumental measures were obtained at baseline and at 4-week intervals. Results. Analyses of the data revealed a variety of significant skin appearance improvement effects for topical niacinamide: reductions in fine lines and wrinkles, hyperpigmented spots, red blotchiness, and skin sallowness (yellowing). In addition, elasticity (as measured via cutometry) was improved. Corresponding mechanistic information is presented. Conclusion. In addition to previously observed benefits for topical niacinamide, additional effects were identified (improved appearance of skin wrinkles and yellowing and improved elasticity). ALL OF THE AUTHORS ARE EMPLOYED BY THE PROCTER & GAMBLE COMPANY, WHICH FUNDED THIS STUDY.

B-Vitamins and Exercise: Does Exercise Alter Requirements?

Abstract: The B-vitamins (thiamin, riboflavin, vitamin B-6) are necessary in the energy-producing pathways of the body, while folate and vitamin B-12 are required for the synthesis of new cells, such as the red blood cells, and for the repair of damaged cells. Active individuals with poor or marginal nutritional status for a B-vitamin may have decreased ability to perform exercise at high intensities. This review focuses on the B-vitamins and their role in energy metabolism and cell regeneration. For each vitamin, function related to physical activity, requirement, and status measures are given. Research examining dietary intakes and nutritional status in active individuals is also presented. Current research suggests that exercise may increase the requirements for riboflavin and vitamin B-6, while data for folate and vitamin B-12 are limited. Athletes who have poor diets, especially those restricting energy intakes or eliminating food groups from the diet, should consider supplementing with a multivitamin/mineral supplement.