Showing papers on "B vitamins published in 2002"

Prevalence of micronutrient malnutrition worldwide.

Abstract: Recent estimates indicate that globally over two billion people are at risk for vitamin A, iodine, and/or iron deficiency, in spite of recent efforts in the prevention and control of these deficiencies. The prevalence is especially high in Southeast Asia and sub-Saharan Africa, and pregnant women and young children are at greatest risk. Other micronutrient deficiencies of public health concern include zinc, folate, and the B vitamins. However, there is limited data on the actual prevalence of these deficiencies. Finally, in many settings, more than one micronutrient deficiency exists, suggesting the need for simple approaches that evaluate and address multiple micronutrient malnutrition.

The royal college of physicians report on alcohol: guidelines for managing wernicke’s encephalopathy in the accident and emergency department

Abstract: The Royal College of Physicians (London) recently published its latest report on alcohol misuse entitled ‘Alcohol — Can the NHS Afford It?’. Part of this document, encompassing our views, has made specific recommendations for the management of patients in the Accident and Emergency (A&E) Department who may possibly have, or are at risk of developing, Wernicke’s encephalopathy. Patients showing evidence of chronic alcohol misuse and suspected of having a poor diet should be treated at the outset with B vitamins intravenously or intramuscularly, especially when the clinical signs are initially masked by drunkenness at presentation to the A&E Department. This commentary offers a review of the scientific foundations on which these recommendations have been made.

Randomized trial of vitamin supplements in relation to transmission of HIV-1 through breastfeeding and early child mortality.

Abstract: Background: HIV-1 transmission through breastfeeding is a global problem and has been associated with poor maternal micronutrient status. Methods: A total of 1078 HIV-infected pregnant women from Tanzania were randomly assigned to vitamin A or multivitamins excluding A from approximately 20 weeks’ gestation and throughout lactation. Results: Multivitamins excluding A had no effect on the total risk of HIV-1 transmission (RR 1.04, 95% CI 0.82–1.32, P = 0.76). Vitamin A increased the risk of transmission (RR 1.38, 95% CI 1.09–1.76, P = 0.009). Multivitamins were associated with non-statistically significant reductions in transmission through breastfeeding, and mortality by 24 months among those alive and not infected at 6 weeks. Multivitamins significantly reduced breastfeeding transmission in infants of mothers with low baseline lymphocyte counts (RR 0.37; 95% CI 0.16–0.85, P = 0.02) compared with infants of mothers with higher counts (RR 0.99, 95% CI 0.68–1.45, P = 0.97; P-for-interaction 0.03). Multivitamins also protected against transmission among mothers with a high erythrocyte sedimentation rate (P-for-interaction 0.06), low hemoglobin (P-for-interaction 0.06), and low birthweight babies (P-for-interaction 0.04). Multivitamins reduced death and prolonged HIV-free survival significantly among children born to women with low maternal immunological or nutritional status. Vitamin A alone increased breastfeeding transmission but had no effect on mortality by 24 months. Conclusion: Vitamin A increased the risk of HIV-1 transmission. Multivitamin (B, C, and E) supplementation of breastfeeding mothers reduced child mortality and HIV-1 transmission through breastfeeding among immunologically and nutritionally compromised women. The provision of these supplements to HIV-infected lactating women should be considered.

Short-Term Folate, Vitamin B-12 or Vitamin B-6 Supplementation Slightly Affects Memory Performance But Not Mood in Women of Various Ages

Abstract: Based on research demonstrating associations between folate, B-12 and B-6 vitamins and cognition and mood, we investigated the effects of short-term supplementation in 211 healthy younger, middle-aged and older women who took either 750 microg of folate, 15 microg of vitamin B-12, 75 mg of vitamin B-6 or a placebo daily for 35 d. In addition, we examined associations between dietary intake of these vitamins and cognition and mood. Usual dietary intake status was estimated using a retrospective, self-report, quantified food frequency questionnaire. Participants completed alternate forms of standardized tests of cognitive processing resources, memory, executive function, verbal ability and self-report mood measures before and after supplementation. Supplementation had a significant positive effect on some measures of memory performance only, and no effect on mood. Dietary intake status was associated with speed of processing, recall and recognition and verbal ability.

Genetic effects of methylation diets

Abstract: ▪ Abstract DNA methylation at cytosines in CpG dinucleotides can lead to changes in gene expression and function without altering the primary sequence of the DNA. Methylation can be affected by dietary levels of methyl-donor components, such as folic acid. This may be an important mechanism for environmentally induced changes in gene expression. Recent literature supports a role for DNA-methylation changes in a number of adult-onset disorders and during development. These changes may be significant for better understanding certain birth defects (e.g., neural tube defects) and the long-term consequences of early environmental influences on gene expression (metabolic programming). Optimal “methylation diets” should be investigated as part of the prevention and treatment of all these conditions, as well as in disorders such as Rett syndrome, whose primary defects may lie in DNA methylation-dependent gene regulation.

Folic acid, ageing, depression, and dementia

Abstract: It is becoming clear that folic acid affects mood and cognitive function, especially in older people. Edward Reynolds draws together the evidence Folic acid is important for functioning of the nervous system at all ages.1–4 In the fetus the relation between maternal folate status and the risk of neural tube defects is well established: clinical trials have shown that periconceptual preventive treatment with 400 μg or higher of folic acid significantly reduces the risks of such defects.4 In neonates, infants, children, and adolescents, inborn errors of folate transport and metabolism are associated with a variety of overlapping syndromes which are influenced by age of clinical presentation. These include developmental delay, cognitive deterioration, motor and gait abnormalities, behavioural or psychiatric symptoms, seizures, signs of demyelination or failure of myelination, and vascular changes seen on magnetic resonance imaging or postmortem examination.4 Less commonly, subacute combined degeneration and peripheral neuropathy may also occur. In adult patients presenting with megaloblastic anaemia due to folate deficiency, approximately two thirds have neuropsychiatric disorders which overlap considerably with those associated with anaemia due to vitamin B-12 deficiency. 2 5 However, depression is commoner in patients with folate deficiency, and subacute combined degeneration with peripheral neuropathy is more frequent in those with vitamin B-12 deficiency. The degree of anaemia is poorly correlated with the presence of neuropsychiatric disorders, but if these anaemias were left untreated nearly all patients would eventually develop neuropsychiatric complications.2 Over the past 35 years numerous studies have shown a high incidence of folate deficiency correlated with mental symptoms, especially depression and cognitive decline in epileptic, neurological, psychiatric, geriatric, and psychogeriatric populations. 3 4 Furthermore, recent studies in elderly people suggest a link between folic acid, homocysteine, ageing, depression, and dementia, including Alzheimer's disease and vascular disease. 4 6 …

B-vitamin intake, metabolic genes, and colorectal cancer risk (United States).

Abstract: Objective: This population-based case–control study was designed to investigate the interrelationships between polymorphisms in the methylenetetrahydrofolate (MTHFR C677T and A1298C) gene and other genes (MTR A2756G; MTRR A66G and CBS 844ins68), intake of B-vitamins and colorectal cancer risk (CRC). Methods: We interviewed 727 CRC cases of Japanese, Caucasian, or Native Hawaiian origin and 727 controls matched on sex, age, and ethnicity. Results: Compared to the homozygous wild-type genotype, the odds ratios for subjects with one or two MTHFR 677T variant alleles were 0.8 (0.6–1.1) and 0.7 (0.5–1.1), respectively (p for gene–dosage effect: 0.04). The TT genotype was associated with a 50–60% decrease in CRC risk among subjects with high intake of folate or vitamin B6, compared to those with the CC genotype and low levels of intake. The MTHFR 1298C and CBS8 44ins68 variant alleles were also found to be weakly protective against CRC and to act jointly with the 677T allele. Conclusions: This study provides additional evidence for a decreased CRC risk for subjects with the MTHFR 677T allele, particularly at high levels of folate and vitamin B6 intake. Our data also suggest that the relationships between CRC and the MTHFR A1298C and CBS 844ins68 polymorphisms warrant further study.

Calcium/Calmodulin‐Dependent Protein Kinase II Is Associated with NR2A/B Subunits of NMDA Receptor in Postsynaptic Densities

Abstract: NMDA receptors and Ca2+/calmodulin-dependent kinase II (CaMKII) have been reported to be highly concentrated in the postsynaptic density (PSD). Although the possibility that CaMKII in PSD might be associated with specific proteins has been put forward, the protein or proteins determining the targeting of the kinase in PSD have not yet been identified. Here we report that CaMKII binds to NR2A and NR2B subunits of NMDA receptors in PSD isolated from cortex and hippocampus. The association of NMDA receptor subunits and CaMKII was assessed by immunoprecipitating PSD proteins with antibodies specific for NR2A/B and CaMKII: CaMKII coprecipitated with NR2A/B and NR1 but not with other glutamate ionotropic receptor subunits, such as GluR1 and GluR2-3. A direct association between CaMKII and NR2A/B subunits was further confirmed by overlay experiments using either 32P-autophosphorylated CaMKII or 32P-NR2A/B and by evaluating the formation of a CaMKII-NR2A/B complex by means of the cross-linker disuccimidyl suberate. These data demonstrate an association between the NMDA receptor complex and CaMKII in the postsynaptic compartment, suggesting that this colocalization may be relevant for synaptic plasticity.

Homocysteine, vitamin B6, and vascular disease in AD patients

Abstract: Background: Cerebrovascular disease is a cause of dementia and is associated with elevated plasma levels of homocysteine Patients with AD tend to have unexplained elevations of homocysteine concentrations vs healthy control subjects Vitamin B 6 status, a potential determinant of plasma homocysteine, has not been characterized in patients with AD Objective: To investigate plasma homocysteine, vitamin B 6 status, and the occurrence of vascular disease in patients with AD Methods: Forty-three patients with AD and 37 control subjects without AD were studied for homocysteine, B vitamin status (folate, vitamin B 12 , pyridoxal-5′-phosphate [PLP]), kidney function (creatinine), and thyroid function (thyroid-stimulating hormone, thyroxin) In addition, the presence of vascular disease was assessed by reviewing both medical histories and brain imaging data provided by CT and MRI Results: The OR for elevated plasma homocysteine (>12 μmol/L) was only 22 (not significant) for subjects with AD In contrast, the OR was 100 ( p = 003) for subjects with vascular disease (n = 26) The OR for low plasma PLP ( p = 001) for patients with AD No significant relationship was observed between vascular disease and PLP level or between plasma homocysteine and PLP concentrations Conclusions: Elevated plasma homocysteine in patients with AD appears related to vascular disease and not AD pathology In addition, low vitamin B 6 status is prevalent in patients with AD It remains to be determined if elevated plasma homocysteine or low vitamin B 6 status directly influences AD pathogenesis or progression

Endothelial dysfunction and atherothrombosis in mild hyperhomocysteinemia

Abstract: Mildly elevated plasma homocysteine levels are an independent risk factor for atherothrombotic vascular disease in the coronary, cerebrovascular, and peripheral arterial circulation. Endothelial dysfunction as manifested by impaired endothelium-dependent regulation of vascular tone and blood flow, by increased recruitment and adhesion of circulating inflammatory cells to the endothelium, and by a loss of endothelial cell antithrombotic function contributes to the vascular disorders linked to hyperhomocysteinemia. Increased vascular oxidant stress through imbalanced thiol redox status and inhibition of important antioxidant enzymes by homocysteine results in decreased bioavailability of the endothelium-derived signaling molecule nitric oxide via oxidative inactivation. This plays a central role in the molecular mechanisms underlying the effects of homocysteine on endothelial function. Supplementation of folic acid and vitamin B12 has been demonstrated to be efficient in lowering mildly elevated plasma homocysteine levels and in reversing homocysteine-induced impairment of endothelium-dependent vasoreactivity. Results from ongoing intervention trials will determine whether homocysteine-lowering therapies contribute to the prevention and reduction of atherothrombotic vascular disease and may thereby provide support for the causal relationship between hyperhomocysteinemia and atherothrombosis.

Dietary Recommendations and Athletic Menstrual Dysfunction

Abstract: Exercise-induced or athletic menstrual dysfunction (amenorrhoea, oligomenorrhoea, anovulation, luteal phase deficiency, delayed menarche) is more common in active women and can significantly affect health and sport performance. Although athletic amenorrhoea represents the most extreme form of menstrual dysfunction, other forms can also result in suppressed estrogen levels and affect bone health and fertility. A number of factors, such as energy balance, exercise intensity and training practices, bodyweight and composition, disordered eating behaviours, and physical and emotional stress levels, may contribute to the development of athletic menstrual dysfunction. There also appears to be a high degree of individual variation with respect to the susceptibility of the reproductive axis to exercise and diet-related stresses. The dietary issues of the female athlete with athletic menstrual dysfunction are similar to those of her eumenorrhoeic counterpart. The most common nutrition issues in active women are poor energy intake and/or poor food selection, which can lead to poor intakes of protein, carbohydrate and essential fatty acids. The most common micronutrients to be low are the bone-building nutrients, especially calcium, the B vitamins, iron and zinc. If energy drain is the primary contributing factor to athletic menstrual dysfunction, improved energy balance will improve overall nutritional status and may reverse the menstrual dysfunction, thus returning the athlete to normal reproductive function. Because bone health can be compromised in female athletes with menstrual dysfunction, intakes of bone-building nutrients are especially important. Iron and zinc are typically low in the diets of female athletes if meat products are avoided. Adequate intake of the B vitamins is also important to ensure adequate energy production and the building and repair of muscle tissue. This review briefly discusses the various factors that may affect athletic menstrual dysfunction and two of the proposed mechanisms: the energy-drain and exercise-intensity hypotheses. Because energy drain can be a primary contributor to athletic menstrual dysfunction, recommendations for energy and the macro- and micronutrients are reviewed. Methods for helping the female athlete to reverse athletic menstrual dysfunction are discussed. The health consequences of trying to restrict energy intake too dramatically while training are also reviewed, as is the importance of screening athletes for disordered eating. Vitamins and minerals of greatest concern for the female athlete are addressed and recommendations for intake are given.

Diffusion-weighted imaging abnormalities in Wernicke encephalopathy: Reversible cytotoxic edema?

Abstract: Background Wernicke encephalopathy (WE) is a metabolic disorder of the central nervous system resulting from vitamin B 1 deficiency. The exact mechanisms underlying the pathogenesis of the lesions in WE are not completely understood. Vitamin B 1 deficiency is associated with intracellular and extracellular edema by glutamate N-methyl-D-aspartate receptor–mediated excitotoxicity. Conventional magnetic resonance imaging (MRI) cannot differentiate the types of edema. Diffusion-weighted imaging (DWI) has been reported to detect early ischemic damage (cytotoxic edema) as bright areas of high signal intensity (SI) and vasogenic edema as areas of heterogeneous SI. Objectives To describe the DWI findings and to characterize the types of edema in WE using DWI. Setting Tertiary referral center. Design and Methods Two patients with WE underwent DWI and conventional MRI with gadolinium enhancement. Wernicke encephalopathy was diagnosed with salient conventional MRI findings (high SIs in the paramedian thalamus, periaqueductal gray matter, and mamillary bodies) and typical clinical history and symptoms. Apparent diffusion coefficient (ADC) values were measured in abnormal lesions by visual inspection of DWIs and T2-weighted echo planar images. Results T2-weighted and fluid-attenuated inversion recovery MRIs showed high SIs in the bilateral paramedian thalamus, mamillary bodies, and periaqueductal gray matter. The DWIs showed bright high SI in the corresponding lesions, and ADC values were decreased (patient 1: 512-545 × 10 −6 mm 2 /s; patient 2: 576-612 × 10 −6 mm 2 /s). The ADC decrease and the DWI high SI were normalized in 2 weeks with administration of thiamine hydrochloride. Conclusions Abnormalities on DWI and ADC decrease became normalized with adequate therapy. The MRI abnormalities in WE might be owing to the "reversible cytotoxic edema" caused by vitamin B 1 deficiency.

A randomized, double-blind, placebo-controlled study of oral vitamin B12 supplementation in older patients with subnormal or borderline serum vitamin B12 concentrations.

Abstract: Objectives To determine the effect of small doses of oral cyanocobalamin supplements in older patients with low or borderline serum vitamin B12 concentrations but no other evidence of pernicious anemia (PA). Design Randomized, double-blind, placebo-controlled study assessing the efficacy of oral cyanocobalamin 10 microg and 50 microg daily for 1 month. Setting Two geriatric hospitals in the North Western Health Care Network, Melbourne, Australia. Participants Thirty-one inpatients with serum vitamin B12 levels between 100 and 150 pmol/L, without PA, other malabsorption disorders, or progressive neurological or terminal illness. The mean age was 81.4 years. Intervention After informed consent, a medical and drug history was taken and the Mini-Mental State Examination (MMSE) completed. A dietitian made assessment of oral cobalamin intake. Blood was taken for serum vitamin B12, serum and red cell folate assay, full blood examination, fasting serum gastrin, parietal and intrinsic factor antibodies, fasting serum homocysteine, and creatinine. Patients were then randomized to receive 10 microg oral cyanocobalamin, 50 microg oral cyanocobalamin, or placebo treatment for 1 month, after which the investigations and clinical examinations were repeated. Measurements Percentage change in the level of vitamin B12, homocysteine, folate, and red cell parameters and absolute changes in MMSE were calculated and compared between groups. The groups were compared on the number of responders who improved their level of B12 by 20%. Chi-square calculations on changes in serum vitamin B12 concentration were also performed. Results Mean serum vitamin B12 +/- standard deviation improved by 51.7 +/- 47.1% in the 50-microg group, 40.2 +/- 34.4% in the 10-microg group, and 11.7 +/- 24.5% in the placebo group. The change in the 50-microg cyanocobalamin group was significantly greater than that in the placebo group (P=.044). The change in the 10-microg cyanocobalamin group was not significantly different from that in the placebo group (P=.186). Eight of 10 subjects in each treatment group were classified as responders, compared with two of 11 in the placebo group (P=.004). Homocysteine levels fell in patients receiving cyanocobalamin, but this fall failed to reach statistical significance. There were no significant changes in the other parameters measured. Conclusion Cyanocobalamin supplementation of 50 microg but not 10 microg daily produced a significant increase in serum vitamin B12. This result has implications for the management of patients with subnormal or borderline serum vitamin B12 concentrations and for food fortification with vitamin B12.

Smoking and plasma homocysteine

Abstract: Background Smoking is known to be associated with an increased plasma homocysteine level. Both are associated with an increased risk of cardiovascular disease. B-vitamins modulate plasma homocysteine levels. Aims To investigate the relationships between smoking, plasma homocysteine, nutrient levels and risk of cardiovascular disease. Methods The European Concerted Action Project case control study of 750 cases and 800 age- and sex-matched controls aged less than 60 years from 19 centres in 10 European countries. Results Smokers were at increased risk of vascular disease. This risk was greatly increased in the presence of a raised plasma homocysteine; cigarette smokers with a plasma homocysteine above 12μmol.l−1 had a 12-fold increased risk of cardiovascular disease (OR 12·4 95% CI 7·3 to 21·2) compared with non-smokers with a normal plasma homocysteine. In both cases and controls the current smokers had a higher plasma homocysteine level than the never smokers (11·7μmol.l−1 vs 10·07μmol.l−1, P 20.day−1 8·19, after adjustment for B6, B12, folate OR 7·09). Conclusions This case control study suggests that smokers with high plasma homocysteine are at greatly increased risk of cardiovascular disease and should therefore be offered intensive advice to help them cease smoking. They also have reduced levels of those B-vitamins (folate, vitamin B6 and vitamin B12) that modulate homocysteine metabolism. While this finding may reflect a direct effect of smoking or reduced B-vitamin intake, supplementation of these nutrients may be appropriate in smokers with high homocysteine levels.

Hyperhomocysteinemia, and low intakes of folic acid and vitamin B12 in urban North India

Abstract: Background and Aim An adverse coronary risk profile has been reported amongst rural-to-urban migrant population living in urban slums undergoing stressful socio-economic transition. These individuals are likely to have low intakes of folic acid and vitamin B12, which may have an adverse impact on serum levels of homocysteine (Hcy). To test this hypothesis, we studied serum levels of Hcy in subjects living in an urban slum of North India and healthy subjects from urban non-slum area. Methods Group I consisted of 46 subjects (22 males and 24 females) living in an urban slum, while group II consisted of healthy subjects (n = 26, 13 males and 13 females) living in the adjacent non-slum area. Anthropometric measurements, biochemical profile (fasting blood glucose, total cholesterol, serum triglycerides, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol) and fasting serum levels of Hcy were measured. Dietary intakes of folic acid, vitamin B12, vitamin B1, and iron were calculated by the 24-hour dietary recall method. Serum levels of Hcy were correlated with dietary intakes of nutrients, anthropometry, and metabolic variables. Results Sex-adjusted serum levels of Hcy in mmol/L (Mean ± SD) were high, though statistically comparable, in both the groups (group I: 20.8 ± 5.9 and group II: 23.2 ± 5.9). Overall, higher than normal serum levels of Hcy (> 15 μmol/L) were recorded in 84 % of the subjects. A substantial proportion of subjects in both groups had daily nutrient intakes below that recommended for the Asian Indian population (folic acid: 93.4 % in group I and 96.7 % in group II, vitamin B12: 76.1 % in group I and 88.4 % in group II). However, between the two groups, average daily dietary intakes of both the nutrients were statistically comparable. As compared to non-vegetarians, vegetarians showed lower intakes of folic acid (p < 0.01) and vitamin B12 (p < 0.01) in both groups. On multivariate linear regression analysis with serum Hcy as the response variable and vegetarian/non-vegetarian status and sex (male/female) as predictor variables, higher serum levels of Hcy were observed in vegetarians vs non-vegetarians (β = 4.6, p < 0.05) and males vs females (β = 5.3, p < 0.01). Conclusions Low intakes of folic acid and vitamin B12, and hyperhomocysteinemia, in both the healthy population living in urban slums and adjacent urban non-slum areas, are important observations for the prevention of nutritional and cardiovascular diseases in the Indian subcontinent.

Reduced folate carrier transports thiamine monophosphate: an alternative route for thiamine delivery into mammalian cells.

Abstract: Although the reduced folate carrier RFC1 and the thiamine transporters THTR-1 and THTR-2 share ∼40% of their identity in protein sequence, RFC1 does not transport thiamine and THTR-1 and THTR-2 do not transport folates. In the present study, we demonstrate that transport of thiamine monophosphate (TMP), an important thiamine metabolite present in plasma and cerebrospinal fluid, is mediated by RFC1 in L1210 murine leukemia cells. Transport of TMP was augmented by a factor of five in cells (R16) that overexpress RFC1 and was markedly inhibited by methotrexate, an RFC1 substrate, but not by thiamine. At a near-physiological concentration (50 nM), TMP influx mediated by RFC1 in wild-type L1210 cells was ∼50% of thiamine influx mediated by thiamine transporter(s). Within 1 min, the majority of TMP transported into R16 cells was hydrolyzed to thiamine with a component metabolized to thiamine pyrophosphate, the active enzyme cofactor. These data suggest that RFC1 may be one of the alternative transport routes available for TMP in some tissues when THTR-1 is mutated in the autosomal recessive disorder thiamine-responsive megaloblastic anemia.

Benefits and risks of folic acid to the nervous system.

Abstract: During three decades of neurological practice I have witnessed a remarkable change in attitudes to the benefits and risks of folic acid therapy in nervous system disorders. In the 1960s all that was known and taught was that folic acid was harmful to the nervous system, especially in precipitating or exacerbating the neurological complications of vitamin B12 deficiency. So deeply held was this view that the possibility of neuropsychological benefits from this vitamin was initially viewed with considerable scepticism.

Low plasma antioxidants and normal plasma B vitamins and homocysteine in patients with severe obesity

Abstract: BACKGROUND Obesity is among the well-established risk factors for cardiovascular morbidity and mortality. However, the exact mechanisms are not well understood. Low concentrations of vitamins (fat soluble antioxidants and B vitamins) are linked to accelerated atherosclerosis through increased oxidative stress and homocysteine. OBJECTIVE To compare plasma antioxidant vitamins (carotenoids and vitamin E), B vitamins (folic acid and B12) and homocysteine--all linked to increased cardiovascular morbidity--between patients with severe obesity and lean control subjects. METHODS We investigated plasma carotenoids, vitamin E, folic acid, B12, and homocysteine in 25 obese patients and their age-matched controls (body mass index 38 +/- 3 vs. 21 +/- 2 kg/m2), respectively), related to BMI and plasma insulin. RESULTS Patients with obesity had normal B vitamins and a non-significant decrease in plasma homocysteine as compared to controls (9.4 +/- 2.6 vs. 11.4 +/- 4.8 mumol/L, P = 0.07). There was a significant decrease in both plasma carotenoids and vitamin E (0.69 +/- 0.32 vs. 1.25 +/- 0.72 and 24 +/- 10 vs. 33 +/- 14 micrograms/ml, respectively; P < 0.01). Both vitamins were inversely related to BMI and plasma insulin, which was significantly increased in patients with obesity (22 +/- 21 vs. 6 +/- 2 microU/ml, P < 0.01). CONCLUSIONS Obese patients with BMI above 35 kg/m2 show low plasma antioxidants (carotenoids and vitamin E). This may result in increased oxidative stress and consequently enhanced atherosclerosis in these patients.

Hyperhomocysteinemia, vascular function and atherosclerosis: effects of vitamins.

Abstract: Homocysteine is a metabolic product of methyl group donation by the amino acid methionine. Moderate elevation of plasma homocysteine (>15 μM) is most commonly caused by B-vitamin deficiencies, especially folic acid, B6 and B12. Genetic factors, certain drugs and renal impairment may also contribute. Homocysteine has several potentially deleterious vascular actions. These include increased oxidant stress, impaired endothelial function, stimulation of mitogenesis, and induction of thrombosis. Homocysteine also appears to increase arterial pressure. In humans, experimental induction of hyperhomocysteinemia by methionine loading rapidly causes profound impairment of endothelium-dependent dilatation in both resistance and conduit arteries. This endothelial dysfunction can be reversed by administration of antioxidants. Epidemiological evidence suggests that homocysteine acts as an independent risk factor for atherosclerosis, thrombosis and hypertension. Prospective studies have shown that elevated plasma homocysteine concentrations in the top quintile of the population (>12 μM) increase risk of cardiovascular disease by about 2-fold. There are currently no data available from randomized, controlled trials of the effects of lowering plasma homocysteine on atherothrombotic events. Nonetheless, it would seem appropriate to screen for and treat hyperhomocysteinemia in individuals with progressive or unexplained atherosclerosis. Folic acid and vitamins B6 and B12 are the mainstay of therapy. Treatment of moderately elevated plasma homocysteine in patients without atherosclerosis should be deferred until the completion of randomized outcome trials.

Megalin is essential for renal proximal tubule reabsorption and accumulation of transcobalamin-B(12).

Abstract: Megalin has previously been shown to bind and mediate endocytosis of transcobalamin (TC)-B12. However, the physiological significance of this has not been established, and other TC-B12 binding prot...

The role of diet and specific micronutrients in the etiology of oral carcinoma

Abstract: BACKGROUND Carcinoma of the oral cavity is one of the most common cancers worldwide. Tobacco smoking and the consumption of alcoholic beverages are significant risk factors but to the authors' knowledge the role of nutrition is not adequately understood. The authors undertook an epidemiologic study of oral carcinoma occurring in Greece, where tobacco smoking and alcohol consumption are common but the incidence of the disease is among the lowest reported in Europe. METHODS One hundred six patients with histologically confirmed incident oral carcinoma and an equal number of control subjects matched for age and gender were studied. Dietary information was assessed through a validated extensive food frequency questionnaire and the data were analyzed using conditional logistic regression. RESULTS After adjustment for energy intake, tobacco smoking, and alcohol consumption, there was evidence that the consumption of cereals, fruits, dairy products, and added lipids (which in Greece are represented mostly by olive oil) was found to be associated inversely with the risk of oral carcinoma. Only with respect to meat and meat products was there adequate evidence of a positive association with the risk of oral carcinoma. Among the micronutrients studied, riboflavin, magnesium, and iron appeared to be correlated inversely with the disease. CONCLUSIONS Fruits, cereals, dairy products, and olive oil appear to convey protection against oral carcinoma and their effects may be mediated through higher intakes of riboflavin, iron, and magnesium. The low incidence of oral carcinoma reported in Greece may be explained in part by the higher consumption of the food groups and micronutrients that appear to protect against the disease. Cancer 2002;94:2981–8. © 2002 American Cancer Society. DOI 10.1002/cncr.10560

Dissimilation of the C2 sulfonates.

Abstract: Organosulfonates are widespread in the environment, both as natural products and as xenobiotics; and they generally share the property of chemical stability. A wide range of phenomena has evolved in microorganisms able to utilize the sulfur or the carbon moiety of these compounds; and recent work has centered on bacteria. This Mini-Review centers on bacterial catabolism of the carbon moiety in the C2-sulfonates and the fate of the sulfonate group. Five of the six compounds examined are subject to catabolism, but information on the molecular nature of transport and regulation is based solely on sequencing data. Two mechanisms of desulfonation have been established. First, there is the specific monooxy-genation of ethanesulfonate or ethane-1,2-disulfonate. Second, the oxidative, reductive and fermentative modes of catabolism tend to yield the intermediate sulfoacetaldehyde, which is now known to be desulfonated to acetyl phosphate by a thiamin-diphosphate-dependent acetyltransferase. This enzyme is widespread and at least three subgroups can be recognized, some of them in genomic sequencing projects. These data emphasize the importance of acetyl phosphate in bacterial metabolism. A third mechanism of desulfonation is suggested: the hydrolysis of sulfoacetate.