Vitafit

Prospective study of plasma vitamin B6 and risk of colorectal cancer in men

مطالعه ارتباط بین ویتامین ب6 و خطر سرطان کولورکتال در مردان

Lee JE , Li H , Giovannucci E , Lee IM , Selhub J , Stampfer M , Ma J .

Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA

Cancer Epidemiol Biomarkers Prev. 2009

Vitamin B(6) may lower risk of colorectal cancer by preventing aberrations in one-carbon metabolism or by anti-inflammatory effects. We prospectively evaluated the association between plasma levels of pyridoxal 5'-phosphate (PLP; the active form of vitamin B(6)) and risk of colorectal cancer in a nested case-control study within the Physicians' Health Study. Among 14,916 men who provided blood specimens in 1982 to 1984, we identified 197 incident colorectal cancer cases through 2000 and individually matched them to 371 controls by age and smoking status. Plasma PLP levels were positively correlated with cold cereal intake and plasma levels of folate and vitamin B(12) (age- and smoking-adjusted partial correction r = 0.28-0.48) and slightly inversely correlated with body mass index (r = -0.11) and plasma levels of homocysteine, C-reactive protein, tumor necrosis factor-alpha receptor 2, and interleukin-6 (r = -0.23 to -0.14). With control for these factors and known risk factors for colorectal cancer, plasma PLP levels were significantly inversely associated with risk of colorectal cancer; compared with men in the lowest quartile, those with PLP in quartiles 2 to 4 had relative risks (95% confidence interval) of 0.92 (0.55-1.56), 0.42 (0.23-0.75), and 0.49 (0.26-0.92; P(trend) = 0.01), respectively. In conclusion, vitamin B(6) may protect against colorectal cancer independent of other one-carbon metabolites and inflammatory biomarkers.

NAD+ and vitamin B3: from metabolism to therapies

نیکوتین آمید آدنین و ویتامین ب3: از متابولیسم تا درمان

Sauve AA .

Department of Pharmacology, Weill Medical College of Cornell University, 1300 York Avenue, New York, NY 10021, USA

J Pharmacol Exp Ther. 2008

The role of NAD(+) metabolism in health and disease is of increased interest as the use of niacin (nicotinic acid) has emerged as a major therapy for treatment of hyperlipidemias and with the recognition that nicotinamide can protect tissues and NAD(+) metabolism in a variety of disease states, including ischemia/reperfusion. In addition, a growing body of evidence supports the view that NAD(+) metabolism regulates important biological effects, including lifespan. NAD(+) exerts potent effects through the poly(ADP-ribose) polymerases, mono-ADP-ribosyltransferases, and the recently characterized sirtuin enzymes. These enzymes catalyze protein modifications, such as ADP-ribosylation and deacetylation, leading to changes in protein function. These enzymes regulate apoptosis, DNA repair, stress resistance, metabolism, and endocrine signaling, suggesting that these enzymes and/or NAD(+) metabolism could be targeted for therapeutic benefit. This review considers current knowledge of NAD(+) metabolism in humans and microbes, including new insights into mechanisms that regulate NAD(+) biosynthetic pathways, current use of nicotinamide and nicotinic acid as pharmacological agents, and opportunities for drug design that are directed at modulation of NAD(+) biosynthesis for treatment of human disorders and infections.

Dietary intake of folate, other B vitamins, and omega-3 polyunsaturated fatty acids in relation to depressive symptoms in Japanese adults.

تاثیر جذب غذائی فولات و سایر ویتامین های گروه ب واسید های چرب غیر اشباع امگا 3 در رابطه با علائم افسردگی در افراد ژاپنی

Murakami K , Mizoue T , Sasaki S , Ohta M , Sato M , Matsushita Y , Mishima N .

Department of Epidemiology and International Health, Research Institute, International Medical Center of Japan, Tokyo, Japan

Nutrition. 2008

OBJECTIVE: Although a favorable effect of dietary folate and omega-3 polyunsaturated fatty acids (PUFAs) on depression is suggested from epidemiologic studies in Western countries, evidence from non-Western populations is lacking. We examined cross-sectional associations between the intake of folate, other B vitamins, and omega-3 PUFAs and depressive symptoms in Japanese adults. METHODS: Subjects were 309 Japanese men and 208 Japanese women 21-67 y of age. Dietary intake was assessed with a validated, brief, self-administered diet history questionnaire. Depressive symptoms were defined as present when subjects had a Center for Epidemiologic Studies Depression scale score > or =16. Adjustment was made for age, body mass index, work place, marital status, occupational physical activity, leisure-time physical activity, current smoking, current alcohol drinking, and job stress score. RESULTS: The prevalences of depressive symptoms were 36% for men and 37% for women. Folate intake showed a statistically significant, inverse, and linear association with depressive symptoms in men but not in women. The multivariate odds ratios (95% confidence intervals) for depressive symptoms for men in the first, second, third, and fourth quartiles of folate intake were 1.00 (reference), 0.78 (0.38-1.63), 0.57 (0.27-1.18), and 0.50 (0.23-1.06), respectively (P for trend = 0.045). No statistically significant linear association was observed for the intake of riboflavin, pyridoxine, cobalamin, total omega-3 PUFAs, alpha-linolenic acid, eicosapentaenoic acid, or docosahexaenoic acid in either sex. CONCLUSION: Higher dietary intake of folate was associated with a lower prevalence of depressive symptoms in Japanese men but not women.

 Folate-responsive neurologic diseases

بیماری های عصبی پاسخ دهنده به مصرف فولات

Djukic A .

Department of Neurology, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY 10467, USA.

Pediatr Neurol. 2007

Folate is a water-soluble vitamin of the B complex group, and is required for optimal health, growth, and development. In humans, it cannot be synthesized de novo. As a cofactor or coenzyme, folate plays key biological roles in a variety of physiologic processes: maintenance and repair of the genome, regulation of gene expression, amino-acid metabolism, neurotransmitter synthesis, and the formation of myelin. Dietary folates must undergo multiple, tightly regulated absorption and metabolic processes before their cellular utilization occurs. Clinical conditions associated with abnormal body folate status are very diverse. They range from genetic syndromes defined prior to conception, to malformations that develop during embryogenesis (neural tube defects), to disorders that are postnatally acquired and progressive (e.g., cerebral folate deficiency, or folinic acid-responsive seizures). Central nervous system folate deficiency or impaired availability can occur in the settings of normal or decreased systemic folate levels. Because the majority of patients respond to treatment with folinic acid, pediatric neurologists should remain vigilant to the possibility of deficiencies of folate in patients with unexplained neurologic disorders. The deleterious outcomes of untreated patients underscore the importance of making an early diagnosis.

Biotin

بیوتین

Zempleni J , Wijeratne SS , Hassan YI .

Department of Nutrition and Health Sciences, University of Nebraska-Lincoln, 316 Ruth Leverton Hall, Lincoln, NE 68583-0806, USA.

Biofactors. 2009

Biotin is a water-soluble vitamin and serves as a coenzyme for five carboxylases in humans. Biotin is also covalently attached to distinct lysine residues in histones, affecting chromatin structure and mediating gene regulation. This review describes mammalian biotin metabolism, biotin analysis, markers of biotin status, and biological functions of biotin. Proteins such as holocarboxylase synthetase, biotinidase, and the biotin transporters SMVT and MCT1 play crucial roles in biotin homeostasis, and these roles are reviewed here. Possible effects of inadequate biotin intake, drug interactions, and inborn errors of metabolism are discussed, including putative effects on birth defects

Update on the role of vitamin K in skeletal health

نقش ویتامین K در سلامت سیستم اسکلتی

Shea MK , Booth SL .

Vitamin K Laboratory, USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA

Nutr Rev. 2008

A protective role for vitamin K in bone health has been suggested based on its role as an enzymatic cofactor. In observational studies, vitamin K insufficiency is generally associated with lower bone mass and increased hip fracture risk. However, these findings are not supported in randomized controlled trials (RCT) of phylloquinone (vitamin K(1)) supplementation and bone loss at the hip in the elderly. This suggests that increased vegetable and legume intakes may simultaneously improve measures of vitamin K status and skeletal health, even though the mechanisms underlying these improvements may be independent of each other. Menaquinone-4 (vitamin K(2)), when given at pharmacological doses, appears to protect against fracture risk and bone loss at the spine. However, there are emerging data that suggest the efficacy of vitamin K supplementation on bone loss is inconclusive.

 Effect of vitamin K supplementation on bone loss in elderly men and women

تاثیر مکمل ویتامین کا درکاهش میزان از دست دادن حجم استخوان در مردان و زنان سالخورده

Booth SL , Dallal G , Shea MK , Gundberg C , Peterson JW , Dawson-Hughes B .

U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, 711 Washington Street, Boston, Massachusetts 02111, USA

J Clin Endocrinol Metab. 2008

CONTEXT: Vitamin K has been implicated in bone health, primarily in observational studies. However, little is known about the role of phylloquinone supplementation on prevention of bone loss in men and women. OBJECTIVE: The objective of this study was to determine the effect of 3-yr phylloquinone supplementation on change in bone mineral density (BMD) of the femoral neck bone in older men and women who were calcium and vitamin D replete. DESIGN, PARTICIPANTS, AND INTERVENTION: In this 3-yr, double-blind, controlled trial, 452 men and women (60-80 yr) were randomized equally to receive a multivitamin that contained either 500 mug/d or no phylloquinone plus a daily calcium (600 mg elemental calcium) and vitamin D (400 IU) supplement. MAIN OUTCOME MEASURES: Measurements of the femoral neck, spine (L2-L4), and total-body BMD, bone turnover, and vitamins K and D status were measured every 6-12 months. Intent-to-treat analysis was used to compare change in measures in 401 participants who completed the trial. RESULTS: There were no differences in changes in BMD measurements at any of the anatomical sites measured between the two groups. The group that received the phylloquinone supplement had significantly higher phylloquinone and significantly lower percent undercarboxylated osteocalcin concentrations compared with the group that did not receive phylloquinone. No other biochemical measures differed between the two groups. CONCLUSIONS: Phylloquinone supplementation in a dose attainable in the diet does not confer any additional benefit for bone health at the spine or hip when taken with recommended amounts of calcium and vitamin D.

Micronutrient status, cognition and behavioral problems in childhood

میزان ریزمغذی ها در بدن به هنگام کودکی و ارتباط آن با اختلالات شناختی و رفتاری

Benton D ; ILSI Europe a.i.s.b.l .

Department of Psychology, University of Swansea, Swansea, Wales, SA2 8PP, UK

Eur J Nutr. 2008

It is widely accepted that the rapid rate of growth of the brain during the last third of gestation and the early postnatal stage makes it vulnerable to an inadequate diet, although brain development continues into adulthood and micronutrient status can influence functioning beyond infancy. A deficiency of various micro-nutrients in developing countries has been found to have long-term implication for cognitive development. Vitamin A plays a critical role in visual perception and a deficiency is the leading cause of childhood blindness. A lack of iodine during a critical period in brain development is associated with reduced intellectual ability. Iron shortage is a widespread problem in the developing world but also in industrialized countries. There is evidence that iron deficiency in early life adversely effects brain development. In addition in industrialized countries a role for folate in the prevention of neural tube defects is well established and in a few individuals impaired cognitive functioning is associated with the inadequate provision of vitamin B(12. )The controversial suggestions that sub-clinical deficiencies of micronutrients may in industrialized societies influence anti-social behavior and intelligence are also discussed.

Zinc: mechanisms of host defense

روی : مکانیسم های دفاعی میزبان

Prasad AS .

Department of Internal Medicine, Division of Hematology, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, Michigan

J Nutr. 2007 May

Zinc deficiency in humans decreases the activity of serum thymulin (a thymic hormone), which is required for maturation of T-helper cells. T-helper 1 (Th(1)) cytokines are decreased but T-helper 2 (Th(2)) cytokines are not affected by zinc deficiency in humans. This shift of Th (1) to Th (2) function results in cell-mediated immune dysfunction. Because IL-2 production (Th (1) cytokine) is decreased, this leads to decreased activities of natural-killer cell and T cytolytic cells, which are involved in killing viruses, bacteria, and tumor cells. In humans, zinc deficiency may decrease the generation of new CD4+ T cells from the thymus. In cell culture studies (HUT-78, a Th(0) human malignant lymphoblastoid cell line), as a result of zinc deficiency, nuclear factor-kappaB (NF-kappaB) activation, phosphorylation of IkappaB, and binding of NF-kappaB to DNA are decreased and this results in decreased Th(1) cytokine production. In another study, zinc supplementation to humans decreased the gene expression and production of pro-inflammatory cytokines and decreased oxidative stress markers. In HL-60 cells (a human pro-myelocytic leukemia cell line), zinc deficiency increased the levels of TNF-alpha , IL -1beta, and IL-8 cytokines and mRNA. In these cells, zinc induced A20, a zinc finger protein that inhibited NF-kappaB activation via tumor necrosis factor receptor associated factor pathway, and this decreased gene expression of pro-inflammatory cytokines and oxidative stress markers. We conclude that zinc has an important role in cell-mediated immune functions and also functions as antiinflammatory and antioxidant agent.