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  • 1. VITAMINAS E MINERAISNutrição no Exercício Físico e Desporto Pedro Carrera Bastos, 2013
  • 2. COMPOSIÇÃO DO CORPO HUMANO Elementos gasosos Proporção no corpo humano Oxigénio 65% Hidrogénio 10% Nitrogénio 3% Subtotal 78% Minerais Carbono 18.5% Cálcio 1.2% Fósforo 1.0%Potássio, Enxofre, Sódio, Cloro, 1.2% MagnésioVitaminas e outros nutrientes 0.1% Total 100% Colgan, M. Sports nutrition guide – Minerals, vitamins & antioxidants for athletes. Apple Publications, 2002
  • 3. FONTES DE NUTRIENTES Nutrientes FontesOxigénio Ar e águaHidrogénio Ar e águaCarbono Base estrutural de todos os alimentosNitrogénio ProteínasRestantes elementos Distribuição heterogénea em vários alimentosColgan, M. Sports nutrition guide – Minerals, vitamins & antioxidants for athletes. Apple Publications, 2002
  • 4. VITAMINAS E OUTROS NUTRIENTES Vitaminas Vitaminas Outroshidrossolúveis Lipossolúveis micronutrientes Vitamina B1 Vitamina A Colina Vitamina B2 Vitamina D Betaína Vitamina B3 Vitamina E PABA Vitamina B5 Vitamina K Fitonutrientes Vitamina B6 Vitamina B12 Ácido Fólico Biotina Vitamina C Colgan, M. Sports nutrition guide – Minerals, vitamins & antioxidants for athletes. Apple Publications, 2002
  • 5. MINERAIS Macrominerais Microminerais Cálcio Ferro Fósforo Zinco Potássio Cobre Enxofre Iodo Sódio Crómio Cloro Selénio Magnésio Manganês Molibdénio Sílicio Boro Vanádio Flúor Cobalto Arsénico, Estanho e NíquelColgan, M. Sports nutrition guide – Minerals, vitamins & antioxidants for athletes. Apple Publications, 2002 Stipanuk. MH. Biochenical, Physiological, Molecular aspects of Human Nutrition. Saunders, 2006
  • 6. –1 –1 as 96 . A central seetween –1 asA. central94tral 1,25(OH)2D3 Vitamina D3 86 25OHD3 86,97,98 . α,97,98 . 86,97,98 . 99 α α Hart PH, et al. Nature Rev Immun 2011;11:584–596
  • 7. Ca
  • 8. Ca Duodeno: 8-10% Ceco e Cólon: % pequena Íleo: Maior parte
  • 9. Ca Duodeno: 8-10% Ceco e Cólon: % pequena Íleo: Maior parte
  • 10. Christakos S. Arch Biochem Biophys. 2012 Jul 1;523(1):73-6 Ca Ca Ca Ca Ca
  • 11. Christakos S. Arch Biochem Biophys. 2012 Jul 1;523(1):73-6 Ca Ca Ca Ca Ca
  • 12. Christakos S. Arch Biochem Biophys. 2012 Jul 1;523(1):73-6 Ca Ca Ca Ca Ca
  • 13. Christakos S. Arch Biochem Biophys. 2012 Jul 1;523(1):73-6 Ca Ca Ca Ca Ca
  • 14. Christakos S. Arch Biochem Biophys. 2012 Jul 1;523(1):73-6 Ca Ca Ca Ca Ca
  • 15. Christakos S. Arch Biochem Biophys. 2012 Jul 1;523(1):73-6 Ca TRPV6 Ca Ca Ca TRPV6 Ca
  • 16. Christakos S. Arch Biochem Biophys. 2012 Jul 1;523(1):73-6 Ca TRPV6 Ca Ca Ca TRPV6 Ca
  • 17. Figure 2. Comparing the Risk of the Risk of Hip and Nonvertebral Fractures Between Vitamin D (700-800 IU/d) and Controlre 2. Forest PlotsForest Plots ComparingHip and Nonvertebral Fractures Between Vitamin D (700-800 IU/d and 400IU/d and 400 IU/d) and Conps Groups Hip Fracture Hip Fracture Nonvertebral Fracture Nonvertebral Fracture Source Fracture Prevention With Favors Vitamin D Favors Control Favors Vitamin D Favors Control Source Favors Vitamin D Favors Vitamin D Favors Control Favors Control Vitamin D Supplementation Source Source Vitamin D 700-800 IU/d 700-800 IU/d Vitamin D Vitamin D 700-800 IU/d D 700-800 IU/d Vitamin 17 Pfeifer et al,15 2000 Chapuy et al,17 Chapuy et al, 2002 Pfeifer et al,15 2000 A Meta-analysis of Randomized Controlled Trials 2002 Chapuy et al,17 2002 Chapuy et al,17 2002 12 Chapuy et al,12 Chapuy et al, 1994 1994 Chapuy et al,12 1994 Heike A. Bischoff-Ferrari, MD, MPH Chapuy et al,12 1994 Context The role and dose of oral vitamin D supplementation in nonvertebral f 18 Walter C. Willett, DrPH ture Dawson-HughesDawson-Hughes well 14 1997 prevention have not been et al, established. Trivedi et al,18 2003 et al, 2003 Trivedi et al,14 1997 John B. Wong, MD Objective To estimate the effectiveness of vitamin D supplementation in prev Trivedi et 18 Trivedi et nonvertebral al, 2003 in older persons. 18 Edward Giovannucci, ScD ing hip and al, 2003 fractures Pooled Pooled Thomas Dietrich, MPH Data Sources A systematic review of English and non-English articles using MEDL Pooled Pooled and the Cochrane Controlled Trials Register (1960-2005), and EMBASE (1991-20 Bess Dawson-Hughes, MD Additional studies were identified by contacting clinical experts and searching bibl F 0.2 0.2 0.5 1.0 0.5 1.0 5.0 5.0 0.2 0.5 0.2 1.0 0.5 1.0 5.0 5. raphies and abstracts presented at the American Society for Bone and Mineral Rese RACTURES CONTRIBUTE SIGNIFI- (1995-2004). Search terms included randomized controlled trial (RCT), controlled c cantly to morbidity and mortal- cal trial, random allocation, double-blind method, cholecalciferol, ergocalciferol, Vitamin D 400 Vitamin D 400 IU/d IU/d ity of older persons. Hip frac- Vitamin D 400 humans, elderly, falls, and bone density. hydroxyvitaminIU/d fractures, IU/d Vitamin D 400 D, tures increase exponentially Study Selection Only double-blind RCTs of oral vitamin D supplementation (c Meyer et al,16 2002 et al,16 2002 Meyer Meyer et al,16 2002Meyer et al,16 2002 with age so that by the ninth decade of lecalciferol, ergocalciferol) with or without calcium supplementation vs calcium sup life, an estimated 1 in every 3 women mentation or placebo in older persons (Ն60 years) that examined hip or nonverte and 1 in every 6 men will have sus- fractures were included. tained a hip fracture.1 With the aging Data ExtractionLips et al,13 1996 extraction of articles by 2 authors using predef Lips et al,13 1996 et al,13 1996 Lips Lips et al,13 1996 Independent of the population, the number of hip data fields, including study quality indicators. fractures is projected to increase world- Data Synthesis All pooled analyses were based on random-effects models. Five R wide.2 The consequences of hip frac- for hip fracture (n=9294) and 7 RCTs for nonvertebral fracture risk (n=9820) met Pooled Pooled Pooled tures are severe: 50% of older persons inclusion criteria. All trials used cholecalciferol. Heterogeneity among studies for both Pooled have permanent functional disabili- and nonvertebral fracture prevention was observed, which disappeared after pooling R 0.2 15% to 25% require long-term 5.0 low-dose (400 IU/d) and higher-dose0.2 1.0 D 0.5 ties,0.5 0.2 1.0 0.5 1.0 5.0 with 0.2 0.5 vitamin (700-800 IU/d), separately.5. 1.0 5.0 A nursing home care, CI) Risk (95%20% die 2tamin D dose of 700 to 800 IU/d reduced the relative riskCI) Risk (95% CI) by 26% Relative Risk (95% and 10% to CI) Relative JAMA.   005;293:2257-­‐2264   Relative Risk (95% (RR) of hip fracture Relative within 1 year.3-6 Besides the personal RCTs with 5572 persons; pooled RR, 0.74; 95% confidence interval [CI], 0.61-0.88)es represent relative risks (RRs) and size(RRs) and sizeproportionalis proportionalthe the size of the fracture by95%represent 95% confidenceTrials are sortedTrials are so Squares represent relative risks of squares is of squares to the size ofany trials. Error bars represent bars confidence with 6098 persons; pooled RR, 0.77; 9 to nonvertebral trials. Error 23% (5 RCTs intervals (CIs). intervals (CIs). by burden, hip fractures account for sub- 12,17,18 12,17,18
  • 18. Holick  MF.  J  Clin  Invest.  2006  Aug;116(8):2062-­‐72   ×
  • 19. 3, Vol 78 Musculoskeletal Pain and Severe Hypovitaminosis D 1463vere Hypovitaminosis D in PatientsNonspecific Musculoskeletal Pain Vol 78 Mayo Clin Proc, December 2003, Musculoskeletal Pain andF, Original Article MD, MTS, AND JOANNA M. QUIGLEY, BAmine the prevalence of hypovita- whom were younger than 30 years. Five patients, 4 of whomcare outpatients with persistent, were aged 35 years or younger, had vitamin D serum levels Prevalence of Severe Hypovitaminosis D in Patientsetal pain syndromes refractory to below the level of detection. The severity of deficiency was disproportionate by age for young women (P<.001), by sexds: In this cross-sectional study, for East African patients (P<.001), and by race for African With Persistent, Nonspecific Musculoskeletal Pain consecutively between February h persistent, nonspecific muscu- American patients (P=.006). Season was not a significant factor in determining vitamin D serum levels (P=.06).mmunity University Health Care • Conclusion: All patients with persistent, nonspecific iliated inner city primary care musculoskeletal pain are at high risk for the consequences nn (45 north). Immigrant (n=83) of unrecognized and untreated severe hypovitaminosis D. G REGORYto A. P ) persons of both sexes, aged 10 LOTNIKOFF , MD, MTS, J AND OANNA This risk extends to those considered at low risk for vita- M. QUIGLEY, BA ethnic groups were screened for min D deficiency: nonelderly, nonhousebound, or nonimmi- 25-hydroxyvitamin D levels were grant persons of either sex. Nonimmigrant women of unoassay. childbearing age with such pain appear to be at greatest • Objective: To misdiagnosis or delayed diagnosis. Because osteo-can American, East African, His-dian patients, 100% had deficient risk for determine the prevalence of hypovita- malacia is a known cause of persistent, nonspecific muscu- whom were younger than 30 yeng/mL). Of all patients, 93% (140/D in primary screening all outpatients with such pain for minosis loskeletal pain, care outpatients with persistent, were aged 35 years or younger, nonspecific musculoskeletal pain standard practicerefractory toof vitamin D (mean, 12.08 ng/mL; hypovitaminosis D should be syndromes in clinical below the level of detection. Th , 11.18-12.99 ng/mL). Nonimmi- care. standard therapies.evels as deficient as immigrants Mayo Clin Proc. 2003;78:1463-1470 disproportionate by age for yo • Patients and Methods:of In thisCI = confidence interval; study,n D in men were as deficient as in tients, 28% (42/150) had severely ANOVA = analysis variance; cross-sectional for East African patients (P<.0 150 patients presented consecutively between February ls (≤8 ng/mL), including 55% of PTH = parathyroid hormone American patients (P=.006). S
  • 20. Clin Rheumatol (2007) 26:1895–1901DOI 10.1007/s10067-007-0603-4 ORIGINAL ARTICLEHypovitaminosis D in female patients with chroniclow back painAhmed Lotfi & Ahmed M. Abdel-Nasser &Ahmed Hamdy & Ahmed A. Omran &Mahmoud A. El-RehanyReceived: 7 October 2006 / Revised: 4 March 2007 / Accepted: 5 March 2007 / Published online: 22 March 2007# Clinical Rheumatology 2007Abstract Chronic low back pain (LBP) is an extremely had significantly lower 25 OHD levels (p<0.05)common problem in practice, where it is often labeled significantly higher PTH (p<0.05) and ALP (p<0.idiopathic. No sufficient studies have been conducted to than controls, although there were no significant ganalyze the contribution of hypovitaminosis D to the eti- differences in calcium and phosphorus. Hypovitaminos
  • 21. International Journal of Rheumatic Diseases 2010; 13: 340–346 ORIGINAL ARTICLEAssociation between nonspecific skeletal pain and vitaminD deficiencyBehzad HEIDARI,1 Javad Shokri SHIRVANI,1 Alireza FIROUZJAHI,2 Parnaz HEIDARI3 andKarim O. HAJIAN-TILAKI41 Deparment of Medicine, Division of Rheumatology, 2Deparment of Pathology and Laboratory Medicine, Rouhani Hospital, BabolUniversity of Medical Sciences, Babol, 3Faculty of Medicine, Islamic Azad University, Tehran and 4Department of Social Medicine,Babol University of Medical Sciences, Babol, Iran Abstract Background: Deficiency of vitamin D has been reported in patients with many types of musculoskeletal pain.
  • 22. RECEPTORES EM VÁRIAS CÉLULASCatelicidina   Holick  MF.  J  Clin  Invest.  2006  Aug;116(8):2062-­‐72  
  • 23. Lipopolysaccharide or tuberculosis TLR-2/1 tubercle Cytokine regulation Activated T lymphocyte VDR-RXR Increased Tuberculosis tubercle Immunoglobulin cathelicidin synthesisIncreased VDRIncreased 1-OHase 1,25(OH)2D Activated B lymphocyte 25(OH)D 1-OHase 1,25(OH)2D VDR–RXR 24-OHase 25(OH)D >30 ng/ml Calcitroic Acid Enhances p21 and p27 Inhibits angiogenesis Induces apoptosis 1-OHase VDR–RXR 1-OHase 1,25(OH)2D Increased 1,25(OH)2D insulin Decreased Decreased parathyroid renin hormone Holick M. NEJM 2007;357:266-81. Parathyroid hormone regulation Blood pressure regulation Blood sugar controlFigure 2. Metabolism of 25-Hydroxyvitamin D to 1,25-Dihydroxyvitamin D for Nonskeletal Functions.
  • 24. Virology Journal 2008, 5:29 VITAMINA D E GRIPE 25 cr N = 104 Placebo vs 104 Vit D ex 20 m 15 th a 10 se 5 of 0 Winter Spring Summer Autumn In Placebo 800 IU/d 2000 IU/d apFigureseason 2Incidence of reported cold/influenza symptoms according to InIncidence ofJJ, Zasloff M, Garland CF, Scragg R, Giovannucci E. Virol symptoms Cannell reported cold/influenza J. 2008 Feb 25;5:29. luaccording to season. The 104 subjects in the placebo m
  • 25. Diabetologia (2008) 51:1391–1398 1393 45 Sardinia, Italy 40 Finland 35 Aberdeen, UKDiabetes incidence rate per 100,000 30 Prince Edward Island, Sweden Canada 25 Canterbury, New Zealand Alberta, Canada Norway Oxford, Tierra del Fuego, Argentina 72 20 77 UK Kuwait Puerto Rico Plymouth, 40 61 64 UK Alabama, 71 15 US Virgin Islands USA 48 New South Wales, Lux . 97 68 49 The Netherlands Australia 45 50 44 10 Montevideo, 3 38 Estonia Uruguay 2 62 43 52 Lithuania 67 Sao Paulo, Brazil 63 Latvia Bogota, Dominica Cordoba, Argentina 31 39 59 36 Columbia Sudan 8 4 5 80 5 Oran, 65 Wielkopolska, 82 Barbados Algeria Poland Cuba 9 32 33 Santiago, Chile 87 7 29 34 23 16 10 88 90 25 17 21 0 –60 –50 –40 –30 –20 –10 0 10 20 30 40 50 60 70 Latitude (º)Fig. 1 Age-standardised incidence rates of type 1 diabetes per Madeira Island, Portugal; 64. Portalegre, Portugal; 65. Bucharest,100,000 boys <14 years of age, by latitude, in 51 regions worldwide, Romania; 67. Slovakia; 68. Catalonia, Spain; 71. Leicestershire, UK;2002. Data points are shown by dots; names shown adjacent to the 72. Northern Ireland, UK; 77. Allegheny, PA, USA; 80. Avellaneda,
  • 26. MS) IS 25-hydroxyvitamin D levels either by 2mmon partment of Defense Serumsome as yet Multiple sclerosis cases were identified through Repository. unknown effect on vita- 3ses in Army and Navy physical disabilitymetabolismfor 1992 through 2004, and diagnoses collection min D databases or, more likely, by Age at first serum sample ecting Serum 25-Hydroxyvitamin D Levels were confirmed by medicalchanges in behavior—because heat matched to 2 con- (%) unless o record review. Each case (n=257) was *Data are expressed as No. trols by age, sex, race/ethnicity, and dates of blood collection. Vitamin“Methods”to 100% of text forof mis commonly exacerbates MS symp- ‡See D status was †Does not total because Statesvailing and Risk of Multiple Sclerosis estimated by averaging 25-hydroxyvitamin D levels of 2 or more serum samples col- lected before the date of initial multiple sclerosis symptoms. section definine dis- Kassandra L. Munger, MSc Main Outcome Measures Odds ratios of multiple sclerosis evidence suggests thatcon- D Among W Context Ratios of MS and experimental associated with high Figure. Odds Epidemiologicalby Quantile of Serum 25-Hydroxyvitaminlevels of vi-ent or Lynn I. Levin, PhD, MPH tinuous or categorical levels (quantilespotent immunomodulator, may decrease the risk of multiple25- tamin D, a or a priori–defined this hypothesis. of serum sclerosis. There categories) are no prospective studies addressingnflam- Bruce W. Hollis, PhD hydroxyvitamin D within each racial/ethnic group. 3.0 Whites Objective To examine whether levels of 25-hydroxyvitamin D are associated withtion of Noel S. Howard, MD Results AmongDrPH (148 cases, multiple sclerosis. the risk of multiple sclerosis signifi- Alberto Ascherio, MD, whites risk of 296 controls), M cantly decreased with increasing levelsSetting, and military personnelD (oddsnested case-control studythe De- Design, ofmillion US Participants Prospective, serum samples for a in among 25-hydroxyvitamin who have ratio [OR] stored 1.36 al dis- ULTIPLE SCLEROSIS (MS) IS more than 7 1.07 1.07 50-nmol/L increase in 25-hydroxyvitaminDefense Serum Repository. Multipleinterval, 0.36-0.97). through among the most common partment of 1.0 0.59; 95% confidence sclerosis cases were identified 1 D, crease In categorical analyses using the lowest quintile (Ͻ63.3 nmol/L) as the 1992 through the ORs diagnoses neurological diseases in Army and Navy physical disability databases0.74 reference, 2004, and for 0.75 Odds Ratiotitude, young adults, affecting were confirmed by medical record review.(P=.02 (n = 257) was across to 2 con- Each case for each subsequent quintile were 0.57, 0.57, 0.74, and0.57 dates of blood collection. Vitamin D status was 0.57 0.38 for trend matched trols by age, sex, race/ethnicity, anduator.3 350 000 individuals in the United States estimated by averaging 25-hydroxyvitamin D levels of 2 or more serum samples col- quintiles). Only the OR for the highest quintile, corresponding to 0.40 25-hydroxyvitamin D 0.38 and 2 million worldwide.1 Prevailing lected before the date of initial multiple sclerosis symptoms. 0.30 0.30utes to thought higher thanautoimmune dis- was significantly different from 1.00 (OR, 0.38; 95% con- levels is that MS is an 99.1 nmol/L, in MS fidence interval, 0.19-0.75; or Main Outcome Measures Odds ratios of multiple sclerosis risk was with con- tinuous or categorical relation with multiple sclerosis associated order whereby an unknown agent P=.006). The inverse levels (quantiles or a priori–defined categories) of serum 25- 0.19 agents triggers astrong for 25-hydroxyvitamin D levels measured before age 20 years. Among particularly T cell–mediated inflam- hydroxyvitamin=D within each racial/ethnic group. ple of matory attack, causing demyelination of P .02 for Trend blacks and Hispanics (109 cases, 218 0.1 Among whites (148 cases, 296 controls), the risk of multiplelev- signifi- Resultscontrols), who had lower 25-hydroxyvitamin D sclerosisports a central nervous system tissue.2 els than whites, nothe global dis- associations between vitamin D and84.9-99.1 99.2-152.9 ratio [OR] for a A striking feature of 15.2-63.2 63.3-75.3 75.4-84.8 significant cantly decreased with increasing levels of 25-hydroxyvitamin D (odds risk multiple sclerosis ne po- were found. Quintile of 25-Hydroxyvitamin D, nmol/L 50-nmol/L increase in 25-hydroxyvitamin D, 0.59; 95% confidence interval, 0.36-0.97). 9 tribution of MS is a multifold increase In categorical analyses using the lowest quintile (Ͻ63.3 nmol/L) as the reference, the ORs a po- in incidence with increasing latitude, forCases subsequent quintile were 0.57, 0.57, 0.74, and 0.3818 each 41 29 27 33 (P=.02 for trend across Cts hor- Conclusion The results of ourquintiles).suggest that60 highest63 both north and south of the equator. 3 study Only56 OR for the circulating 57 Controls the high quintile, corresponding60 25-hydroxyvitamin D levels of vitamin D to C Genetic predisposition contributes to levelsmultiple 99.1 nmol/L, was significantly different from 1.00 (OR, 0.38; 95% con- are associated with a lower risk of higher than sclerosis.mental this variation,4 but the change in MS bars indicate 95% confidence intervals. inverse relation with multiple sclerosis risk was Error fidence interval, 0.19-0.75; P=.006). The JAMA. 2006;296:2832-2838 www.jama.com(EAE), risk with migration among people of particularly strong for 25-hydroxyvitamin D levels measured before age 20 years. Among e food common ancestry5 strongly supports a blacks and Hispanics (109 Association. All rights reserved. ©2006 American Medical cases, 218 controls), who had lower 25-hydroxyvitamin D lev- els than whites, no significant associations between vitamin D and multiple sclerosis risk
  • 27. RISCO RELATIVO DE QUEDAS AJUSTADO PARA A IDADE EM 124 IDOSOS    
  • 28. NÍVEL IDEAL DE 25OHD PARA ÓPTIMA FUNÇÃO MUSCULAR NOS MEMBROS INFERIORES  
  • 29. the growt Prostate cell inhibit pr1α,25(OH)2D3 25(OH)D3 Review line that TRENDS in Endocrinology and Metabolism Vol.14 No.9 November 2003 to the SV Mitochondria DU145 ce 1α-OHase Vitamin D and prostate cancer 25(OH)D3 1α,25(OH)2D3 of 24-OHa of Liaroz prevention and treatment 24-hydrox half-life o Tai C. Chen and Michael F. Holick Nucleus 1a,25(OH 1α,25(OH)D3 University School of Medicine, Boston, MA 02118, USA and in cel Vitamin D, Skin and Bone Research Laboratory, Section of Endocrinology, Diabetes and Nutrition, Department of Med VDR RXR might be Human prostate cells contain receptors for 1a,25-dihy- and prodifferentiation activities of 1a,25(OH droxyvitamin D, the active form of vitamin D. Prostate Apoptotic analogs in prostate cells in vitro and in vivo [ Gene transcription we summarize recent findings of: (1 cancer cells respond to vitamin D3 with increases in Here Under so differentiation and apoptosis, and decreases in prolifer- ation between vitamin D deficiency, UVR expo ation, invasiveness and metastasis. These findings risk of prostate cancer; (2) the mechanism of a induces 1 strongly support the use of vitamin D-based therapies Cell-cycle arrest Apoptosis Differentiation action; (3) the identification of terminal 1a-OHase in for prostate cancer and/or as a second-line therapy CDK2, p21, p27, p53, the evaluation of anti Bcl-2, Bcl-XL, Mcl-1 PSA, AR if and its implications; (4) BAG1L, deprivation fails. The association between Ki67, E-Cadherin 2D3 and itsnick in pro androgen XIAP, cIAP1 activity of 1a,25(OH) analogs end either decreased sun exposure or vitamin D deficiency cIAP2 risk of prostate cancer at an earlier culture, in animal models and inassociation be and the increased controversy that surrounds the clinical trials cytometri age, and with a more aggressive progression, indicates Blutt et polymorphism and the risk of prostate cancer that adequate vitamin D nutrition should be a priority TRENDS in Vitamin D Metabolism LNCaP c for men of all ages. Here we summarize recent advancesEndocrinology &deficiency, UV exposure and the in epidemiological and biochemical studies of the endo- prostate cancer downregu crine and autocrine systems associated with vitamin D An association between vitamin D deficiency a
  • 30. 453 death Table 3 The estimated relationship between serum calcidiol and deatharately from prostate cancer among patients receiving hormone therapy (n ¼ 97)III RR Model I Model II Model IIICI) Variables RR (95%CI) RR (95%CI) RR (95%CI) Calcidiol (nmol lÀ1) Low (<  50)   1.00 (ref) 1.00 (ref) 1.00 (ref) Medium (50-­‐80)   0.39 (0.19 – 0.81) 0.35 (0.17 – 0.73) 0.18 (0.07 – 0.46)– 0.77) High (>  80)   0.29 (0.12 – 0.68) 0.20 (0.08 – 0.50) 0.09 (0.03 – 0.27)– 0.43) Group status 0.08 (0.04 – 0.16) 0.06 (0.02 – 0.13)– 0.10) Age (1 year) 1.00 (0.94 – 1.03) Clinical Studies– 1.03) Functional status Good 1.00 (ref) Less good 1.19 (1.04 – 1.61)– 5.06)– 25.7) Differentiation gradea High 1.00 (ref) Moderate 0.85 (0.23 – 3.18) Low 5.63 (1.42 – 22.3)– 1.50) a British Journal of Cancer (2009) 100, 450 – 454 Differentiation grade of tumour tissue; WHO three-grade system. & 2009 Cancer Research UK All rights reserved 0007 – 0920/09 $32.00 www.bjcancer.com
  • 31. VITAMIN D FOR CANCER PREVENTION 470 Garland et al.arland et al. AEP Vol. AEP No. 7 No. 7 19, Vol. 19, TAMIN D FOR VITAMIN D FOR CANCER PREVENTION CANCER PREVENTION July 2009: 468–483 468–483 July 2009: 1.0 1.0 1.0 1.0 0.93 0.95 0.93 1.0 0.95 0.93 0.9 p trend = 0.02 p trend = 0.02 0.9 0.9 0.8 0.8 0.8 0.8 0.7 0.68 0.8 0.68 Relative risk 0.7 Relative risk 0.6 0.6 0.7 Relative risk 0.6 0.5 Relative risk RR=0.44 Relative risk 0.4 0.6 RR = 0.28 0.5 0.4 RR=0.44 0.6 RR = 0.28 p < 0.05 RR=0.28 0.4 0.3 0.2 p < 0.05 0.3 0.2 RR=0.28 0.5 0.20 0.4 0.08 0.1 RR = 0.28 0.11 0.0 0.2 0.20 0.4 0.08 < 62.5 nmol/L > 62.5 nmol/L 0.1 p < 0.05 < 50 nmol/L 50 to <80 nmol/L0.11 > 80 nmol/L FIGURE 1. Relative risk of breast cancer mortality, by baseline FIGURE 3. Relative risk of colon cancer mortality, by baseline 0.3 < 62.5 nmol/L > 62.5 nmol/L serum 25(OH)D concentration, divided at the median, 0.2 1988–2000. (Source: Drawn from data in serum nmol/L 50 to <80 nmol/L > 80 nmol/L < 50 25(OH)D concentration, in tertiles, NHANES cohort, NHANES III cohort,E 1. Relative risk of breast cancer mortality, by baseline FIGURE 3. Relative (Source: Drawn from data in Freedman et al. [56].) 0.2 1988-2000. risk of colon cancer mortality, by baseline Freedman et al. [56].) divided at the median,25(OH)D concentration, serum 25(OH)D concentration, 0.08in tertiles, NHANES cohort,ES III cohort, 1988–2000. (Source: Drawn from data in 25(OH)D and0.1 1988-2000. (10) found that physicians whoseet al. [56].) by quantiles of serum 25(OH)D provided a clear linear dose- (Source: Drawn from data in Freedman n et al. [56].) 0.0 1,25(OH)2D levels were both below the median, response gradient (61) (Fig. 4). A serum 25(OH)D level tiles of serum than 38 ng/mL (95 a clear<(top quintile) 62.5 nmol/L asso- greater25(OH)D providednmol/L)linear dose- was (10) found that of 28 ng/mL (70 nmol/L) and 1,25(OH)2D of 25(OH)D physicians whose 25(OH)D and > 62.5 nmol/L ciated with an odds ratio of 0.45 (95% CI 0.28–0.69), cor- 32 pg/mL (77 pmol/L) had twice the incidence of aggressivee gradient (61) (Fig. 4). A serum 25(OH)D level 1,25(OH)2D levels were both below the median, risk Relative risk of 25(OH)D prostateng/mL (odds ratioby and 1,25(OH) p ! 0.05) as responding to 55% lower1. of colorectal cancer compared FIGURE quintile) was asso- breast cancercancer (70 nmol/L) the median. 2D of FIGURE of 28 mortality, 2.1, 95% CI 1.2–3.4, baselinethan 38to individuals with 25(OH)D of less than 16 ng/mL (40 ng/mL (95 nmol/L) (top men whose levels were above serum 25(OH)D concentration, divided case-control incidence ofKaiser Foundation 25(with an nmol/L) (bottom quintile) CI 0.28–0.69), cor- odds ratio of 0.45 (95% (61). 32 pg/mL (77In a nested at the study of 90 aggressive serum pmol/L) had twice the median, prostate cancer (odds controls 95% CI 1.2–3.4, p ! 0.05) of serum NHANES III cohort, 1988–2000. (Source: ratio 2.1,matched on age, race, and dayas 1988-2000 ing to 55% lower risk of colorectal cancer compared cases and 91Drawn from data inviduals with 25(OH)D of less et al. [56].) (40 men whose levels were above the median. of prostate cancer was storage, the estimated relative risk Prostate Freedman than 16 ng/mL Cancer In a nested (not significant) in men inKaiser Foundation serum 0.41 case-control study of 90 the top quartile of) (bottom quintile) (61). Observational studies of the inverse association of prediag- and 91 controls metabolites, specifically, 25(OH)Dserum than cases vitamin D matched on age, race, and day of greater
  • 32. AEP Vol. 19, No. 7 July 2009: 468–483 470 Garland et al. arland et al. AEP Vol. AEP No. 7 No. 7 19, Vol. 19, TAMIN D FOR VITAMIN D FOR CANCER PREVENTION CANCER PREVENTION July 2009: 468–483 468–483 July 2009: 1.0 1.0 0.95 1.0 0.95 0.93 1.0 0.95 0.93 0.9 p = 0.02 0.9 0.9 p trend = 0.02= 0.02trend p trend 0.8 0.8 0.8 0.68 0.7 0.8 0.68 Relative risk 0.7 Relative risk 0.6 0.6 Relative risk 0.7 0.6 0.5 0.68 RR=0.44 0.4 RR = 0.28 Relative risk 0.5 0.4 RR=0.44 0.6 RR = 0.28 p < 0.05 0.4 0.3 RR=0.28 0.2 p < 0.05 0.2 RR=0.28 0.5 0.3 RR=0.44 0.20 0.08 0.1 0.11 0.2 0.20 0.0 < 62.5 nmol/L 0.4 0.08 > 62.5 nmol/L 0.1 < 50 nmol/L 50 to <80 nmol/L0.11 > 80 nmol/L 0.3 > 62.5 nmol/L FIGURE 1. Relative risk of breast cancer mortality, by baseline FIGURE 3. Relative risk ofRR=0.28 mortality, by baseline colon cancer < 62.5 nmol/L serum 25(OH)D concentration, divided at the median, serum nmol/L 50 to <80 nmol/L > 80 nmol/L < 50 25(OH)D concentration, in tertiles, NHANES cohort,E 1. Relative risk of breast cancer mortality, by baseline from data in NHANES III cohort, 1988–2000. (Source: Drawn 0.2 FIGURE 3. Relative (Source: Drawn from data in Freedman et al. [56].) 1988-2000. risk of colon cancer mortality, by baseline Freedman et al. [56].) divided at the median,25(OH)D concentration, 0.20 serum 25(OH)D concentration, in tertiles, NHANES cohort,ES III cohort, 1988–2000. (Source: Drawn from data in 0.1 1988-2000. (10) found that physicians whoseet al. [56].) (Source: Drawn from data in Freedman 25(OH)D and by quantiles of serum 25(OH)D provided a clear linear dose- n et al. [56].) 0.11 response gradient (61) (Fig. 4). A serum 25(OH)D level 1,25(OH)2D levels were both below the median, greater25(OH)D providednmol/L)linear dose- was (10) found that of 28 ng/mL (70 nmol/L) and 1,25(OH)2D of than 38 ng/mL (95 a clear (top quintile) asso- 25(OH)D physicians whose 25(OH)D and L of serum with an odds ratio of 0.45 (95% CI 0.28–0.69), cor- 50 to <80 nmol/L tiles ciated < 50 nmol/L 32 pg/mL (77 pmol/L) had 80 nmol/L > twice the incidence of aggressive e gradient (61) (Fig. 4). A serum 25(OH)D level 1,25(OH)2D levels were both below the median, responding to 55% lower risk of colorectal cancer compared prostate cancer (odds ratio 2.1, 95% CI 1.2–3.4, p ! 0.05) asby baseline (95 nmol/L) (top quintile) Relative risk(40 colon cancer(70 nmol/L) and 1,25(OH)2D of FIGURE 3. than 16 than 38to individuals with 25(OH)D of lesswas asso- ng/mL of ng/mL 25(OH)D men whose levels were above the median. of 28 ng/mL mortality, by baselinewith an nmol/L) (bottom serum CI 0.28–0.69), cor- 32 pg/mL (77 pmol/L) had twice the incidence of aggressive median, of 0.45 (95% (61). odds ratio quintile) 25(OH)D concentration, In a tertiles, NHANES 90 Kaiser Foundation in nested case-controlCI 1.2–3.4,cohort, of study of p ! 0.05) prostate cancer (odds ratio 2.1,matched on age, race, and dayas serum 95% ing to 55% lower risk of colorectal cancer compared cases and 91 controls m data in 1988-2000. (Source: Drawn whose levels wereestimated relativeet al. prostate cancer wasviduals with 25(OH)D of less than 16 ng/mL (40 men from data in above the median. of [56].) storage, the Freedman risk Prostate Cancer In a nested (not significant) in men inKaiser Foundation serum 0.41 case-control study of 90 the top quartile of) (bottom quintile) (61). Observational studies of the inverse association of prediag- and 91 controls metabolites, specifically, 25(OH)Dserum than cases vitamin D matched on age, race, and day of greater
  • 33. Best Practice & Research Clinical Endocrinology & Metabolism 25 (2011) 681–691 Contents lists available at ScienceDirect Best Practice & Research Clinical Endocrinology & Metabolism journal homepage: www.elsevier.com/locate/beem13Why the minimum desirable serum 25-hydroxyvitamin Dlevel should be 75 nmol/L (30 ng/ml)Reinhold Vieth, Ph.D., F.C.A.C.B., Professor a, b, c, *a Department of Nutritional Sciences, University of Toronto, Canadab Department of Laboratory Medicine and Pathobiology, University of Toronto, Canadac Pathology and Laboratory Medicine, Mount Sinai Hospital, 600 University Ave, Toronto, Ontario, Canada M5G 1X5Keywords: The Institutes of Medicine (IOM) recently revised the recom- mended dietary allowances (RDA) for vitamin D, to maintain
  • 34. RELAÇÃO ENTRE INGESTÃO CÁLCIO E NÍVEIS SÉRICOS DE 25OHD Ingestão  de  300  mg  Cálcio   Heaney R P Am J Clin Nutr 2008;88:541S-544S©2008 by American Society for Nutrition
  • 35. [Dermato-Endocrinology 1:4, 207-214; July/August 2009]; ©2009 Landes BioscienceReviewIn defense of the sunAn estimate of changes in mortality rates in the United States if mean serum 25-hydroxyvitamin Dlevels were raised to 45 ng/mL by solar ultraviolet-B irradianceWilliam B. GrantSunlight, Nutrition and Health Research Center (SUNARC); San Francisco, CA USAKey words: cancer, cardiovascular diseases, melanoma, respiratory infections, skin cancer, vitamin D, ultraviolet-B Emerging scientific evidence strongly supports the beneficial rates of other diseases such as type 2 diabetes mellitus,9,10 coronaryrole of vitamin D in reducing the risk of incidence and death heart disease (CHD)11 and congestive heart failure.12from many chronic and infectious diseases. This study esti- Let us put vitamin D production into the context of humanmates increases in melanoma and nonmelanoma skin cancer history on Earth. The human species originated in the easternmortality rates and decreases in chronic and infectious disease portion of tropical Africa. Skin pigmentation in that region wasmortality rates in the US from the standpoint of approximately very dark to protect against the adverse effects of solar UVR,doubling population doses of solar UVB to increase mean primarily free radical production and DNA damage leading toserum 25-hydroxyvitamin D levels from 16 ng/mL for black melanoma and other skin cancer.13 Because UVB doses wereAmericans and 25 ng/mL for white Americans to 45 ng/mL. high and clothes were not worn, sufficient UVB penetrated the
  • 36. The n e w e ng l a n d j o u r na l of m e dic i n e droxylase Circulation review article Medical Progress Vitamin D Deficiency Michael F. Holick, M.D., Ph.D. O rom the Department of Medicine, Sec- nce foods were fortified with vitamin d and rickets appeared ion of Endocrinology, Nutrition, and Di- to have been conquered, many health care professionals thought the major betes, the Vitamin D, Skin, and BoneResearch Laboratory, Boston University Reference range health problems resulting from vitamin D deficiency had been resolved. How-Medical Center, Boston. Address reprint ever, rickets can be considered the tip of the vitamin D–deficiency iceberg. In fact, <20 ng/ml equests to Dr. Holick at Boston UniversitySchool of Medicine, 715 Albany St., M-1013, 20–100 ng/ml vitamin D deficiency remains common in children and adults. In utero and during >150 ng/ml childhood, vitamin D deficiency can cause growth retardation and skeletal deformi-Boston, MA 02118, or at mfholick@bu.edu. ties and may increase the risk of hip fracture later in life. Vitamin D deficiency in adults etabolite)N Engl J Med 2007;357:266-81. opyright © 2007 Massachusetts Medical Society. can precipitate or exacerbate osteopenia and osteoporosis, cause osteomalacia and muscle weakness, and increase the risk of fracture. Deficiency Preferred range Intoxication The discovery that most tissues and cells in the body have a vitamin D receptor and that several possess the enzymatic machinery to convert the primary circulating form of vitamin D, 25-hydroxyvitamin D, to the active form, 1,25-dihydroxyvitamin D, has 30–60 ng/ml provided new insights into the function of this vitamin. Of great interest is the role it can play in decreasing the risk of many chronic illnesses, including common can- cers, autoimmune diseases, infectious diseases, and cardiovascular disease. In this review I consider the nature of vitamin D deficiency, discuss its role in skeletal and _ nonskeletal health, and suggest M. NEJM 2007;357:266-81. and treatment. Holick strategies for its prevention S ource s a nd Me ta bol ism of V i ta min D
  • 37. PORQUE EXISTE DEFICIÊNCIA
  • 38. Webb AR, Kline L, Holick MF. J Clin Endocrinol Metab. 1988 Aug;67(2):373-8.
  • 39. RADIAÇÃO UV E VITAMINA D 68 Défice de Vitamina D 6 ou + meses/ano Défice de Vitamina D 1 ou + meses/ano . .   .  Vitamina D todo o ano Défice de Vitamina D 1 ou + meses/ano Défice de Vitamina D 6 ou + meses/anoFigure 1. The potential for synthesis of previtamin D3 in lightly pigmented human skin computed from annual average UVMED. The highest annualvalues for UVMED are shown in light violet, with incrementally lower values in dark 2000 Jul;39(1):57-106 shades of blue, orange, green and gray Jablonski NG, Chaplin G. J Hum Evol. violet, then in light to dark(64 classes). White denotes areas for which no UVMED data exist. Mercator projection. In the tropics, the zone of adequate UV radiation throughoutthe year (Zone 1) is delimited by bold black lines. Light stippling indicates Zone 2, in which there is not sufficient UV radiation during at least one monthof the year to produce previtamin D3 in human skin. Zone 3, in which there is not sufficient UV radiation for previtamin D3 synthesis on average for
  • 40. Sunlight, UV-Radiation, Vitamin D and Skin Cancer 5Figure 3. Influence of season, time of day in July and latitude on the synthesis of previtaminD3 in Boston (42°N)-o-, Edmonton (52°N)-n-, Bergen (60°) - ^ - . The hour is the end of theone hour exposure time in July. Holick copyright 2007 with permission.cells in the kidneys. l,25(OH)2D is responsible for the maintenance of calcium homeostasis andbone health by increasing the efficiency ofExp Med Biol.calcium absorption, stimulating osteoblast Holick MF. Adv intestinal 2008;624:1-15.function and increase bone calcium resorption. It also enhances the tubular resorption of calciumin the kidneys (Fig. 5).
  • 41. Epidemiol. Infect. (2006), 134, 1129–1140. f 2006 Cambridge University Press doi:10.1017/S0950268806007175 Printed in the United Kingdom Epidemiol. Infect. (2006), 134, 1129–1140. f 2006 Cambridge University Press REVIEW ARTICLE doi:10.1017/S0950268806007175 Printed in the United Kingdom Epidemic influenza and vitamin D REVIEW ARTICLE Epidemic influenza and vitamin D Epidemic influenza and vitamin D J. J. C A N N E L L 1*, R. V IE T H 2, J. C. U M H A U 3, M. F. H O L IC K 4, W. B. G R A N T 5, 1131 S. M A D R O N I C H 6, C. F. G A R LA N D 7 A N D E. G I O V A N N U C C I 8 1 Atascadero State Hospital, 10333 El Camino Real, Atascadero, CA, USA 2 J. J. C A NNHospital, PathologyT H 2Laboratory Medicine,, Department of IC K 4, W. B. GR A NT 5, Mount Sinai E L L 1*, R. V IE and , J. C. UM H A U 3 M. F. H O L Medicine, Toronto, Ontario,ess despite being a 35 Canada S. M A D R O N I C H 6, C. F. G A R LA ND 7 A N D E. G I O V A N N U C C I 8 3 Laboratory of Clinical and Translational Studies, National Institute on Alcohol Abuse and Alcoholism,mmune population National Institutes of Health, 10333 El Camino Real, Atascadero, CA, USA 1 4 2 Atascadero State Hospital, Bethesda, MD Departments of Medicine and Physiology, Boston University School of Medicine, Boston, MA, USA Mount Sinai Hospital, Pathology and Laboratory Medicine, Department of Medicine, Toronto, Ontario, rates increased in 30 5 SUNARC, San Francisco, CA, USA Canada 25(OH)D (ng/ml) 6 3 Atmospheric Chemistry Division, National Center for Atmospheric Research, Boulder, CO, USA 7 Laboratory of Clinical and Translational Studies, National Institute on Alcohol Abuse and Alcoholism, Department of Family and Preventive Medicine, University of California San Diego, La Jolla, CA, USAgressively lower in National Institutes of Health, Bethesda, MD 8 4 Departments of Nutrition and Epidemiology, Harvard School of Public Health, Boston, MA, USA 25Departments of Medicine and Physiology, Boston University School of Medicine, Boston, MA, USA 5 SUNARC, San Francisco, CA, USAng until the winter (Accepted 5 August 2006, first published Center for Atmospheric Research, Boulder, CO, USA 6 7 Atmospheric Chemistry Division, National online 7 September 2006) Department of Family and Preventive Medicine, University of California San Diego, La Jolla, CA, USAmmunity outbreaks 20 8 Departments of Nutrition and Epidemiology, Harvard School of Public Health, Boston, MA, USA SUMMARY eaked for several (Accepted 5Edgar Hope-Simpson proposed that a ‘ seasonal stimulus ’ intimately associated with In 1981, R. August 2006, first published online 7 September 2006) 15 solar radiation explained the remarkable seasonality of epidemic influenza. Solar radiation triggerse higher in the sky S U M M A R Y vitamin D production in the skin ; vitamin D deficiency is common in the winter, robust seasonal and activated vitamin D, 1,25(OH)2D, a steroid hormone, has profound effects on humaninfluenza virtually 10 In 1981, R.1,25(OH)2D acts as an immune system a ‘seasonal stimulus ’ intimately associated with immunity. Edgar Hope-Simpson proposed that modulator, preventing excessive expression solar radiation explained the remarkable seasonality of burst ’ potential of macrophages. Perhaps of inflammatory cytokines and increasing the ‘ oxidative epidemic influenza. Solar radiation triggersstice. Clinical case robust seasonal vitamin D production Jan. skin ; vitamin of potentMayJune JulyAug. Aug. Sep. Oct.Nov.Dec. in the Feb. Mar.Apr. anti-microbial in the winter, most importantly, it dramatically stimulates the expression D deficiency is commonpeptides, Month and activated neutrophils,1,25(OH)2D,natural killer cells, and in epithelialeffects on human which exist in vitamin D, monocytes, a steroid hormone, has profound cells lining thea increased from immunity. 1,25(OH)2Dthey play a immune system modulator, preventinginfection. Volunteers respiratory tract where acts as an major role in protecting the lung from excessive expression of inflammatory cytokines and influenza virus ‘oxidative burst ’ potentialfever and serological inoculated with live attenuated increasing the are more likely to develop of macrophages. Perhaps again in the days Fig. 3. Seasonal variation of 25(OH)D levels in a popu- evidence of an immune response in the winter. Vitamin D deficiency predisposes children to most importantly, it dramatically stimulates the expression of potent anti-microbial peptides, which exist infections. Ultraviolet radiation (either from artificial sources or cells lining the reduces respiratory in neutrophils, monocytes, natural killer cells, and in epithelial from sunlight) n though a much lation-based sample of inhabitants of a small southern respiratory tractviral respiratory infections, as does cod liver the (which contains vitamin D). An the incidence of where they play a major role in protecting oil lung from infection. Volunteers German town, aged 50–80 years. (Reproduced/amended inoculated with live attenuated influenza D reducesmore likely to of respiratory and serological interventional study showed that vitamin virus are the incidence develop fever infections inpulation had virus- evidence of an immune response in D, or lack of it, may D deficiency predisposes children to ’. children. We conclude that vitamin the winter. Vitamin be Hope-Simpson’s ‘ seasonal stimulus with respiratory infections. Ultraviolet of Springer artificial sourcesand sunlight) reduces kind permission radiation (either from Science or from Businessning of the lethal the incidence of viral respiratory infections, as does cod liver oil (which contains vitamin D). An Media, R O D U CstudyNS.H., 1998.)D reduces the incidence of respiratory infections in might I N T Scharla, TIO … the characteristic microbe of a disease be a interventional showed that vitamin symptom instead of a cause. e beginning of its children. wishes to investigate medicine properly of it, may be Hope-Simpson’s ‘seasonal stimulus ’. Bernard Shaw Whoever We conclude that vitamin D, or lack should proceed thus : in the first place to consider the seasons of the George
  • 42. Table 4 shows 25(OH)D levels by study centre, for the study(38), where unexpectedly only 3·5 % of the analysedwhole group split by sex. The highest levels were obtained European elderly presented optimum 25(OH)D levels British Journal of Nutrition, page 1 of 10 doi:10.1017/S0007114511003527in Rome, Athens, Vienna q The Authors 2011 and Zaragoza, and the lowest (. 60 nmol/l), public health authorities have been concernedlevels were found in Dortmund, Heraklion and Ghent for about the widespread 25(OH)D deficiency in the Europeanthe whole group, where the sampling procedure adolescents in Europe: the Healthy Lifestyle our knowledge, the data obtained Vitamin D status among went on population. To the best offor most of the academic year. In none of the in Adolescence studythe framework of the HELENA study are the first to aim at in Europe by Nutrition cities were inmean levels above the proposed cut-off of 75 nmol/l. Girls establishing descriptive 25(OH)D status in adolescents at ahad higher mean levels in all Gonzalez-Gross *†, Jara Valtuena †, Christina Breidenassel2level.A.According to the Institute of Medicine report Marcela cities except for Athens, ´ 3 1,2 6 ˜ 1,3 European , Luis8 Moreno4,5,3 7 Marika Ferrari , Matilde Kersting , Stefaan De Henauw , Frederic Gottrand , Elena Azzini ,Pecs and Lille. Deficient levels (,50 nmol/l) were highest Manios11 and Peter vitamin behalf of the for bone health should correspond to Kurt Widhalm9, Anthony Kafatos10, Yannis in 2011, Stehle2 on D intake HELENA Study Group 1 Department of Health and Human Performance, Faculty of Physical Activity and Sport Sciences (INEF), Universidad ´ ´ Politecnica de Madrid, C/Martın Fierro, 7, 28040 Madrid, Spain 40 ¨ 2 ¨ ¨ ¨ Institut fur Ernahrungs- und Lebensmittelwissenschaften – Humanernahrung, Rheinische Friedrich-Wilhelms Universitat, Bonn, Germany 3 National Research Institute on Food and Nutrition, Rome, Italy 4 Growth, Exercise, Nutrition and Development (GENUD) Research Group, Universidad de Zaragoza, Zaragoza, Spain 5 British Journal of Nutrition Escuela Universitaria de Ciencias de la Salud, Universidad de Zaragoza, Zaragoza, Spain 6 ¨ Research Institute of Child Nutrition Dortmund, Rheinische Friedrich-Wilhelms Universitat, Bonn, Germany 7 Department of Public Health, Ghent University, Ghent, Belgium 30 8 Inserm U995, IFR114, University Lille 2, Lille, France 9 Department of Paediatrics, Medical University of Vienna, Vienna, Austria 10 Preventive Medicine and Nutrition Clinic, University of Crete School of Medicine, Iraclion, Crete, Greece 11 Department of Nutrition and Dietetics, Harokopio University, Athens, Greece Subjects (%) (Received 12 November 2010 – Revised 23 May 2011 – Accepted 31 May 2011) 20 Abstract 38·8 An adequate vitamin D status is essential during childhood and adolescence, for its important role in cell growth, skeletal structure and development. It also reduces the risk of conditions such as CVD, osteoporosis, diabetes mellitus, infections and autoimmune disease. As comparable data on the European level are lacking, assessment of vitamin D concentrations was included in the Healthy Lifestyle in 27·4 Europe by Nutrition in Adolescence (HELENA) study. Fasting blood samples were obtained from a subsample of 1006 adolescents (470 males; 46·8 %) with an age range of 12·5– 17·5 years, selected in the ten HELENA cities in the nine European countries participating in this cross-sectional study, and analysed for 25-hydroxycholecalciferol (25(OH)D) by ELISA using EDTA plasma. As specific reference 10 18·9 values for adolescents are missing, percentile distribution were computed by age and sex. Median 25(OH)D levels for the whole popu- lation were 57·1 nmol/l (5th percentile 24·3 nmol/l, 95th percentile 99·05 nmol/l). Vitamin D status was classified into four groups according 15·0 to international guidelines (sufficiency/optimal levels $75 nmol/l; insufficiency 50 –75 nmol/l; deficiency 27·5 – 49·99 nmol/l and severe deficiency ,27·5 nmol/l). About 80 % of the sample had suboptimal levels (39 % had insufficient, 27 % deficient and 15 % severely deficient levels). Vitamin D concentrations increased with age (P,0·01) and tended to decrease according to BMI. Geographical differences were also identified. Our study results indicate that vitamin D deficiency is a highly prevalent condition in European adolescents and should be a matter of concern for public health authorities. 0 Key words: Adolescents: Vitamin D: Prevention: Europe Severe deficiency Deficient Insufficient Sufficient (<27·5 nmol/l) group for malnutrition Adolescents are considered as a risk (27·5–50 nmol/l) (50–756)nmol/l)cognitive function and concen- osteomalacia (4 – , impaired (>75 nmol/l) because of their increasing needs of nutrients and energy tration problems(7), hyperactivity(8) and immune system deficiency(4). Inadequate vitamin D levels have also been for adequate growth and development that vary with 25(OH)D age(1 – 3). Specifically different levels of vitamin D deficiency status groups related to other diseases such as diabetes, multiple sclerosisFig. 1. 25-Hydroxycholecalciferol (25(OH)D) statuscould be considered a risk factor for at these early ages classification. and cancer(9 – 11). One of the most important applications
  • 43. DEFICIÊNCIA DE VITAMINA D EM ATLETASModalidades 25OHD3 Referências ng/mlMulheresFinlandesas Lehtonen-Veromaa M, et al. 67%: < 15 Eur J Clin Nutr. 1999;53(9):746–51.(corredoras eginastas)Ginástica 77%: < 35 Willis KS, Peterson NJ, Larson-Meyer DE. Int J Sport Nutr Exerc Metab.(Alemanha) 37%: < 10 2008;18:204–24.Ginástica 83%: < 30 Lovell G. Clin J Sport Med. 2008;18(2):(EUA - Mulheres) 33%: < 20 159–61.Ciclistas franceses Maïmoun L, et al.(treino de 16 h/dia) Média: 32 Int J Sports Med. 2006;27(2):105–11. PERFORMANCE AUMENTA NOS MESES DE VERÃO USO DE RADIAÇÃO UVB EM ATLETAS MELHORA PERFORMANCE Cannell JJ, et al. Med Sci Sports Exerc. 2009 May;41(5):1102-10
  • 44. ENVELHECIMENTO vitamin D and ellular growth. in the skin ab- (preD3). Once mation to vita- D3 and vitamin g from the diet5(OH)D3 in the eenters the cir- 25(OH)D3 1␣- m phosphorusD. 1,25(OH)2Dmajor target tis- destruction by (24-OHase). FIGURE 4. A: Circulating concentrations of vitamin D3 after a single llular growth. exposure to 1 MED of simulated sunlight, with a sunscreen (SPF 8) or a topical placebo Holick M. Am J Circulating concentrations of vitamin D in re- cream. B: Clin Nutr 2004;80(suppl):1678S– 88S. sponse to whole-body exposure to 1 MED among healthy young and elderly subjects. Reproduced with permission from reference 3.
  • 45. toon- Albedo from lighter-colored ground and, especially, from snow 7).ted UVBonsnin ur-hasernan- calerethe ich of msent ost ol-the Jablonski NG, Chaplin G. Proc Natl Acad Sci U S A. 2010 May 11;107 Suppl 2:8962-8and
  • 46. Pele pouco pigmentada54 mJ/cm2 Pele muito pigmentada Pele muito320 mJ/cm2 pigmentada Holick M. Am J Clin Nutr 2004;80(suppl):1678S– 88S.!
  • 47. Pele pouco pigmentada54 mJ/cm2 Pele muito pigmentada Pele muito320 mJ/cm2 pigmentada Holick M. Am J Clin Nutr 2004;80(suppl):1678S– 88S.!
  • 48. Pele pouco pigmentada54 mJ/cm2 Pele muito pigmentada Pele muito320 mJ/cm2 pigmentada Holick M. Am J Clin Nutr 2004;80(suppl):1678S– 88S.!
  • 49. MEDO DO SOL
  • 50. PROTECTOR SOLARü  SPF de 8 diminui a capacidade de produzir Vitamina D3 em 95%ü  SPF de 15 diminui a capacidade de produzir Vitamina D3 em 98% Holick M. Am J Clin Nutr 2004;80(suppl):1678S– 88S.!
  • 51. T-score Documento descargado de http://www.elsevier.es el 19/08/2011. Copia para uso personal, se prohíbe la transmisión de este documento por ± 0,8 0,2 cualquier medio o formato. 0,4 ± 1,2 0,223 Trocánter (g/cm2 ) 0,743 ± 0,104 0,789 ± 0,960 0,722 ± 0,101 0,003 T-score Endocrinol Nutr. 2011;58(6):267—273 0,1 ± 0,8 0,4 ± 1,2 0,189 2 Intertrocánter (g/cm ) 1,138 ± 0,151 1,213 ± 0,134 1,104 ± 0,147 0,001 T-score 0,1 ± 0,8 0,4 ± 1,3 0,218 ENDOCRINOLOGÍA Y NUTRICIÓN www.elsevier.es/endo Tabla 6 Valores de ultrasonidos medidos en el calcáneo QUS ORIGINAL los alumnos Todos Varones Mujeres Valor de p BUA (dB/MHz) 76,8 (13,7) 80,3 (12,8) 75,1 (14) Elevada prevalencia de hipovitaminosis D en los estudiantes de 0,084 T-score —0,2 ± 0,7 —0,2 ± 0,9 0,733 medicina de Gran Canaria, Islas Canarias (Espa˜a) n SOS (m/s) 1.561,8 (24,5) 1.560,4 (25,7) 1.562,5 (24,1) 0,692 T-score —0,2b±Elisa González-Rodríguez a , ± 0,8 a Esther González-Padilla , Adela Soria López , 0,8 —0,1 0,529 a a QUI 102,7 (18) 102,8 (15,7) Marco a , Sabrina García-Santana , Ana Mirallave-Pescador , María del Val Groba102,6 (19,1) 0,960 c T-score Gómez y Manuel Sosa Henríquez a,e,∗ 1 d Pedro Saavedra , José Manuel Quesada —0,1 ± 0,8 —0,1 ± 0,514 a Grupo de Investigación en Osteoporosis y Metabolismo Mineral, Universidad de Las Palmas de Gran Canaria, Gran Canaria, Espa˜a n b Servicio de Bioquímica Clínica, Hospital Universitario Insular, Las Palmas de Gran Canaria, Gran Canaria, Espa˜a n c Departamento de Matemáticas, Universidad de Las Palmas de Gran Canaria, Gran Canaria, Espa˜a n Tabla 7 Prevalencia deUnidad de Investigación,deficiencia de vitamina D (%)Metabolismo Mineral, Servicio de Endocrinología, Hospital d insuficiencia y Iniciativas y Desarrollo, Sanyres y Unidad de Universitario Reina Sofía, RETICEF, Córdoba. Espa˜an e Todos los estudiantes Unidad Metabólica Ósea, Hospital Universitario Insular, Gran Canaria, Espa˜an Varones Mujeres Valor de p Deficiencia (25-HCC < 30 Recibido el 3 de agosto de 2010; aceptado el 9 de marzo de 2011 ng/dl) 32,6 48,3 26,1 0,048 Disponible en Internet el 8 de mayo de 2011 Insuficiencia (25-HCC < 20 ng/dl) 28,6 27,6 29 0,927 Deficiencia e insuficiencia conjuntas 61,2 75,9 55,1 0,081 Valores óptimos (> 30 ng/ml) PALABRAS CLAVE 38,8 Resumen 24,1 44,9 0,081 Vitamina D; Fundamento: Se ha descrito la existencia de deficiencia de vitamina D tanto en la población Deficiencia; general como en un gran número de enfermedades. Sin embargo, se han publicado pocos estu- Insuficiencia; dios realizados en población joven y sana en Espa˜a. Teóricamente no debería encontrarse n Estudiantes; deficiencia de vitamina D entre los estudiantes de Medicina de la Universidad de Las Palmas de Exposición solar; Gran Canaria, porque disponen de todos los medios para evitarla.que fueron estadísticamente Canarias Islas superiores en todos los lugares 25-HCC que es el metabolito utilizado para valorar el estado Objetivo: Estimar la prevalencia de deficiencia de vitamina D en una población de estudiantes de Medicina de ambos sexos de la Universidad de Las Palmas de Gran Canaria. 18,19anatómicos de la extremidad proximal del fémur. de vitamina D en el organismo . Método: Se estudiaron 103 alumnos de Medicina de ambos sexos de la Universidad de Las Palmas Gran  Canária:  Aunque no existe un consenso sobre cuáles son los niveles La tabla 6 muestra los parámetros ultrasonográficos 28º  N   de Gran Canaria. A todos se les realizó un cuestionario y una exploración física. Se determinó la vitamina D 25-hidroxicolecalciferol (25-HCC), la hormona paratiroidea, varios marcadoresmedidos en el calcáneo. No se observaron diferencias esta- óptimos de 25-HCC, hoy en día se acepta la clasificación de bioquímicos de remodelado óseo y un estudio bioquímico general. Se estimó la densidad mineraldísticamente significativas entre ambos sexos en ninguno de deficiencia de vitamina D cuando los valores de 25-HCC son ósea por absorciometría radiológica dual en la columna lumbar y en la extremidad proximal del fémur. Asimismo, se midieron los parámetros ultrasonográficos en el calcáneo. 20los parámetros estudiados: BUA, SOS y QUI. inferiores a 20 ng/ml e insuficiencia cuando las cifras de Resultados: Sólo el 38,8% de los estudiantes de Medicina (el 42,1% de los varones y el 44,9% de las mujeres) presentaron niveles de 25-HCC superiores a 30 ng/dl tal y como se recomienda 3,21 Finalmente, en la tabla 7 se muestra la prevalencia 25-HCC están por debajo de 30 ng/ml .de insuficiencia y deficiencia de vitamina D en la pobla- Las personas que viven cerca del Ecuador, expuestas ación estudiada. El 48,3% de los varones y el 26,1% de las la luz solar sin protección, habitualmente tienen unos nive- 3
  • 52. mined by RIA being approximately 6.8 ng/ml higher than by doi: 10.1210/jc.2006-2250 HPLC. Thus, if the Diasorin RIA had been used to determine the prevalence of low vitamin D status (using a cutpoint ofLow 30 ng/ml), fewer individuals would have been classified as Vitamin D Status despite Abundant Sun ExposureN. Binkley, R. Novotny, D. Krueger, T. using the RIA, 25% of this population and “low.” However, even Kawahara, Y. G. Daida, G. Lensmeyer, B. W. Hollis, would be classified as having low vitamin D status. Finally,M. K. DreznerUniversity of Wisconsin Osteoporosis Clinical Research Program (N.B., D.K., T.K., M.K.D.), Madison, Wisconsin 53705;Human Nutrition, Food and Animal Sciences (R.N., Y.G.D.), University of Hawaii at Manoa, Honolulu, Hawaii 96822; Hawai:  21º  N  Laboratory Medicine (G.L.), University of Wisconsin, Madison, Wisconsin 53792; and Medical University of South Carolina(B.W.H.), Charleston, South Carolina 29425Context: Lack of sun exposure is widely accepted as the primary cause Main Outcome Measures: Serum 25(OH)D concentration was mea-of epidemic low vitamin D status worldwide. However, some individuals sured using a precise HPLC assay. Low vitamin D status was definedwith seemingly adequate UV exposure have been reported to have low as a circulating 25(OH)D concentration less than 30 ng/ml.serum 25-hydroxyvitamin D [25(OH)D] concentration, results thatmight have been confounded by imprecision of the assays used. Results: Mean serum 25(OH)D concentration was 31.6 ng/ml. Using a cutpoint of 30 ng/ml, 51% of this population had low vitamin DObjective: The aim was to document the 25(OH)D status of healthy status. The highest 25(OH)D concentration was 62 ng/ml.individuals with habitually high sun exposure. Conclusions: These data suggest that variable responsiveness toSetting: This study was conducted in a convenience sample of adults UVB radiation is evident among individuals, causing some to havein Honolulu, Hawaii (latitude 21°). low vitamin D status despite abundant sun exposure. In addition, because the maximal 25(OH)D concentration produced by natural UVParticipants: The study population consisted of 93 adults (30 women exposure appears to be approximately 60 ng/ml, it seems prudent toand 63 men) with a mean (SEM) age and body mass index of 24.0 yr (0.7) use this value as an upper limit when prescribing vitamin Dand 23.6 kg/m2 (0.4), respectively. Their self-reported sun exposure was supplementation. (J Clin Endocrinol Metab 92: 2130 –2135, 2007)28.9 (1.5) h/wk, yielding a calculated sun exposure index of 11.1 (0.7).L OW VITAMIN D status1 is extremely common (1– 4), and may contribute to the development of osteopo-rosis and osteomalacia/rickets, as well as increase the risk The high prevalence of low vitamin D status is assumed to result from inadequate sun exposure. Because highly sun- exposed individuals likely possess normal vitamin D statusfor falls (5, 6). Moreover, low vitamin D status may play from an evolutionary standpoint, the use of such individualsa role in nonmusculoskeletal diseases, including a variety to define normal 25(OH)D status has been proposed (19).of cancers, multiple sclerosis, infection, hypertension, and This argument is based on the view that contemporary hu-diabetes mellitus (7, 8). Although it is widely accepted that mans are genetically adapted to the environment of ourvitamin D status is determined by the measurement of the ancestors and that the profound lifestyle changes that havecirculating concentration of 25-hydroxyvitamin D occurred over the past approximately 10,000 yr (importantly[25(OH)D] (9), the cutoff value to define low vitamin D including reduced sun exposure) have been much too rapidstatus and a definition for success of vitamin D repletion for the human genome to adjust (20, 21). The current studytherapy remain controversial (10, 11). This is partially due was designed to assess whether, in fact, people living IGa low Comparison of 25(OH) F at . 4.to the variability2. vitamin D concentration by geograph- FIG. of Low vitamin D status in highly sun-exposed subjects. When haveAlthough the correlation betwee latitude with high amounts of sun exposure adequateical location and differences in assay methodology (12–16). vitamin D status, as expected, D status, a target6.8 ng/ml is present using th and to identifyDespite this controversy, cutpoint of 30 ng/ml is usedof 25(OH)D for use in vitamin D therapy. an accepted clinicians often endeavor to cor- to define low vitamin of value 51% of these subjects (open bars) are low.rect vitamin D deficiency by prescribing high-dose vita- HPLC assay used in this studymin D (17). However, the goal for such therapy is unclearand could include achieving a serum 25(OH)D level Subjects and Methodsgreater than an accepted cutpoint (e.g. 30 ng/ml) or, al- Subjects and study designternatively, the upper Journal  of  Clinical  Endocrinology  &  Metabolism  92(6):2130–2135   The   limit of normal, a value that varies Subjects older than 18 yr were recruited approximately equally frombetween laboratories (18). the University of Hawaii at Manoa (UH) and from patrons of the A’ala Park Board Shop, Honolulu, Hawaii (latitude 21° north), in late March 2005. The A’ala Park Board Shop is a skateboard shop frequented by First Published Online April 3, 2007 young adults. Recruitment was performed by posted notice at the Board
  • 53. Table 1. Predictors of risk of death from melanoma in a population-based tion. Compared withstudy of residents from Connecticut awareness, individual No. of Hazard ratio lower risk of death fro Total melanoma (95% condence reported skin self-exaVariable no.* deaths interval) P value were not statistically Demographic variables from melanoma (P =Sex When melanoma- Male 272 33 1.0 (referent) .33 multivariable setting Female 256 25 0.8 (0.5 to 1.3) univariate analysis aAge at diagnosis 528 58 1.2 (1.0 to 1.4) .08 death from other cau 10-year increase remained statisticallyEducation anatomic site, Breslo Up to high school 202 28 1.0 (referent) .11 In addition, the point Greater than 326 30 0.7 (0.4 to 1.1) high school tivariable model for i CI = 0.3 to 1.1) and Sun exposure variables CI = 0.4 to 1.1) chaEver severely sunburned (Table 1), but the co No 173 27 1.0 (referent) .02 rose, both to 0.12. In Yes 353 31 0.5 (0.3 to 0.9) the 80% of subjects fIntermittent sun containing nevus cou exposure index count in association w Low 189 27 1.0 (referent) .04 val for melanoma inc High 328 28 0.6 (0.3 to 1.0) value. The point estiSolar elastosis Absent 254 Cancer  Inst  2005;97:195–9   (referent) 36 1.0 .02 variables in this mode J  Natl   Present 268 21 0.5 (0.3 to 0.9) Table 2. Screening variables
  • 54. FONTES DE VITAMINA D Alimentos Vit. D (UI)Óleo de Fígado de Peixe (10 g) 1360Sardinha (105 g) 500Atum (105 g) 402Salmão Cozinhado (105 g) 360Ovo (Unidade) 20Fígado de Vitela cozinhado (105 g) 15 Ozkan  B.  J  Clin  Res  Pediatr  Endocrinol.  2010  Dec;2(4):137-­‐43  
  • 55. The Journal of Nutrition Symposium: Food-Based Approaches to Combating Micronutrient Deficiencies in Children of Developing Countries Local Cultural Animal Food Contributes High Levels of Nutrients for Arctic Canadian Indigenous Adults and Children1,2 Harriet V. Kuhnlein3,4* and Olivier Receveur5 3 Centre for Indigenous Peoples’ Nutrition and Environment (CINE) and 4School of Dietetics and Human Nutrition, McGill University, Ste. Anne de Bellevue H9X3V9, Canada and 5Department of Nutrition, University of Montreal, Montreal J3C3KS, Canada ´ ´ TF  –  Alimentos  Tradicionais   1  mcg  V 4  40  UI   ´ Óleo de Fígado de Peixe: 8400 IUTABLE it  D  =Micronutrient intake on days with and without TF for Yukon, Dene/Metis, and Inuit adults and Yukon and Dene children " Abstract Adults1 Children1 Downloaded from jn.nutrition.org at Lund University Libraries on September 20, 2011 Food systems of Canadian Arctic Indigenous Peoples contain many species of traditional animal and plant food, but the Yukon ´ Dene/Metis Inuit extent of use today is limited because purchased food displaces much of the traditional species from the diet. Frequency Yukon and Dene Days with Days without Days with Days without Days with Days without and 24-h dietary interviews of Arctic adults and children were used to investigate these trends. The most frequently Days with Days withoutNutrient consumed Arctic foods were derived from (n ¼ 661) fish. TF adults 346) foods contributed 6–40%TF daily energy of TF (n ¼ 410) TF (n ¼ 387) TF animals and In (n ¼ these TF (n ¼ 968) of (n ¼ 632) TF (n ¼ 58) TF (n ¼ 40) adults. Children ate much less, 0.4–15% of energy, and .40% of their total energy was contributed by ‘‘sweet’’ and ‘‘fat’’Iron, mg 23.3 6 0.6a 14.1 6 0.7b 26.5 6 0.9a 15.6 6 1.3b 37.4 6 1.1a 15.0 6 1.4b food sources. Nevertheless, for adults and children, even a single portion of local animal or fish food resulted in increased 16 6 0.6a 14 6 0.7bZinc, mg (P , 6 0.9alevels of energy, protein, vitamin D, vitamin E, riboflavin, b vitamin B-6, iron, zinc, copper, magnesium, 27.7 0.05) 13.1 6 1.1b 23.8 6 1.0a 15.4 6 1.3 21.5 6 0.5a 9.5 6 0.6b 11 6 0.5a 8.6 6 0.6bCopper, mg 1655 6 46a phosphorus, 6 53b manganese, 2025 6 89a had 6 122b 2076 6 44a 1041 not b 1163 and potassium; although children 1439similar results for these nutrients, they did6 58reach 1293 6 41a 1066 6 48b significance for energy, vitaminbD, or manganese. Because market foods are the major source of energy in the Arctic,Phosphorus, mg 1602 6 35a 1155 6 40 1759 6 31a 1224 6 43b 1663 6 27a 947 6 36b 1044 6 32a 924 6 37b traditional animal-source foods are extremely important to ensure high dietary quality of both adults and children. J. Nutr. a b a b a b aPotassium, mg 3520 6 76 2608 6 87 3516 6 63 2561 6 86 2997 6 53 1999 6 0 2291 6 86 2043 6 99b 137: 1110–1114, 2007.Magnesium, mg 297 6 6a 240 6 7b 305 6 5a 237 6 7b 597 6 31a 280 6 40b 203 6 5.7a 182 6 6.6bManganese, mg 3.7 6 0.1a 3.3 6 0.1b 3.6 6 0.1a 3.3 6 0.1b 3.3 6 0.1a 2.7 6 0.1b 2.4 6 0.1 2.1 6 0.2 a b a b a b aRiboflavin, mg 2.2 6 0.1 1.5 6 0.1 2.5 6 0.1 1.6 6 0.1 2.9 6 0.1 1.3 6 0.1 1.6 6 0.07 1.2 6 0.08b 6bVitamin B-6, mg Animal-source foods (ASF) are viewed 6 0.1a 3.3 6 0.1a 1.7 6 0.1 3.7 as essential in1.9 6 0.1btheir derivatives0.1a their possible 0.1b most 4.0 6 and 1.4 6 contribution 1.9 the 0.08a to 6 nutrition 1.6 6 0.09b human societies because of their high nutrient content. In food- btransition in developing societies (2,3). In Canadian Arctic food a b a a bVitamin D, mg 7.3 6 0.6 2.1 6 0.7 7.9 6 0.9 based approaches to ameliorating multiple micronutrient defi- 3.5 6 1.3 systems 25.1 6are abundant animals and fish 3.2 6 0.4 there 1.3 8.6 6 1.7 in addition to 2.5 6 0.5Vitamin E, mg 4.8 6 0.1a 3.5 6 0.2b 6.5 6 0.4a use of ASF6 0.5bpurchased foods. Studies of 3.1 6 0.3b Nations, Dene/Metis, ciencies, particularly in developing countries, the 3.9 in 5.4 6 0.2a Yukon First 3.5 6 0.2a ´ 3.1 6 0.2b combination with plant foods is seen as effective and efficacious and Inuit cultural groups demonstrate extensive knowledge of1 Significant differences in nutrient intakes cultural and without TF are represented by are presence offood sources, unique (a, b). Absence of superscripts means results are not (1) provided that with TF and household-level constraints the diverse different superscripts foods with exceptional nutrient Downloaded from jsignificantly different. Adults, P , 0.01;(2). Successful0.05. accommodated children P , efforts to increase intake of ASF quality, and unique patterns of food use incorporating varying have been documented, yet concerns have been expressed about levels of local cultural food with purchased market food (MF)result of fortification of frequently consumed commercial bev- or the amount of saturated fat and additional energy from ASF significantlyarticle, we present data on dietary food sources for phosphorus, (4–9). In this more iron, zinc, copper, magnesium, Kuhnlein HV, Receveur O. J Nutr. 2007 Apr;137(4):1110-4!selected samples of Dene (10,11) adults of these 3 groups anderages (not shown) (8). potassium, vitamin E, riboflavin, and vitamin B-6 than did recall and Inuit children. Presented as part of amounts ‘‘Food-Based Approaches to Combating days with no TF. It is very clear that traditional ASF are For children, even with smallthe symposium of TF being consumed, 1 Micronutrient Deficiencies in Children of Developing Countries’’ given at the Methods of data collection
  • 56. INGESTÃO PROLONGADA DE 100 IU/DIA DE VITAMINA D3RESULTA NUM AUMENTO DE 25(OH)D DE 2,5 NMOL/L (1 NG/ML) Heaney  RP.  Journal  of  Steroid  Biochemistry  &  Molecular  Biology  103  (2007)  635–641  
  • 57. 1550 Clinical Journal of the American Society of Nephrology calcium metabolism lating cellular prolif wide variety of other immune function, m renin and insulin sy although increasing lead to an increase i believed that raising vides an adequate a version of 25(OH)D t cells. Once 1,25(OH) the cell, it then indu creasing the expressi ylase (CYP24R; 24-OFigure 2. Comparison of the percentage increase in serum25(OH)D levels of healthy adults who were in a bathing suit Clinical Uses oand exposed to suberythemal doses (0.5 MED) of ultraviolet B Activity of 1,25radiation once a week for 3 mo with healthy adults who re- Epidermal cells haceived either 1000 IU of vitamin D2 or 1000 IU of vitamin D3 ited by 1,25(OH)2D3daily during the winter and early spring for a period of 11 wk. that 1,25(OH)2D3 coFifty percent increase represented approximately 10 ng/ml skin disorder psoriasfrom baseline 18 Ϯ 3 to 28 Ϯ 4 ng/ml. Skin type is based on the found to be very effFitzpatrickHolick  MF.  Clin  J  Am  Salways burns, sometimes tans; type III scale: Type II oc  Nephrol.  2008  Sep;3(5):1548-­‐54   ward toxicity (42). 1always burns, always tans; type IV sometimes burns, always now one of the first-
  • 58. EXPOSIÇÃO SOLAR!Todo o corpo (1 MED): 10 000 – 25 000 UI !             (20 000-50 000 UI em suplemento)"Braços e pernas (0,25 – 0,5 MED): 2 000 – 4 000 UI!!  Mãos e cara: 200 UI! Holick M. The Vitamin D Solution. 2010. Hudson Street Press!
  • 59. EDITORIAL 1109 FIGURE 1. Photochemical pathway occurring in the skin that describes the production of vitamin D3 (cholecalciferol) from 7-dehydrocholesterol. Norman AW. Am J Clin Nutr 1998;67:1108–10A brief description of the cellular anatomy of skin is provided in the text. The starting point is the irradiation of a provitamin D, which contains themandatory ⌬5,7-conjugated double bonds; in the skin the highest concentrations of 7-dehydrocholesterol are present in the stratum spinosum and stra-
  • 60. TIPOS DE PEL TIPO! DESCRIÇÃO!Tipo I ! Queima-se sempre, nunca se bronzeia, pele muito clara com cabelo louro ou ruivo"Tipo II ! Queima-se rápido, bronzeia-se com dificultade, pele clara"Tipo III ! Queima-se ocasionalmente, bronzeia-se gradualmente (origen mediterrânica e do médio oriente)"Tipo IV! Muito raro queimar-se, bronzeia-se sempre (Médio Oriente, Índia, Paquistão)"Tipo V! África, Sudeste asiático, alguns nativos de India e Paquistão"Tipo VI ! África, Tamils de Ásia (Índia, Sri Lanka), Nativos de Papua-Nova Guiné, Aborígenes Australianos" Holick M. The Vitamin D Solution. 2010. Hudson Street Press!
  • 61. PENÍNSULA IBÉRICA 8-11 H / 15 – 18 HTipo de Nov-Fev Mar-Maio Jun-Ag Sep-OctPeleTipo 1 15-20 min 10-15 min 15-20 minTipo II 20-30 min 15-20 min 20-30 minTipo III 30-40 min 20-30 min 30-40 minTipo IV 40-60 min 30-40 min 40-60 minTipo V e VI 60-75 min 40-60 min 60-75 min Holick M. The Vitamin D Solution. 2010. Hudson Street Press
  • 62. PENÍNSULA IBÉRICA 11 - 15 HTipo de Nov-Fev Mar-Maio Jun-Ag Sep-OctPeleTipo 1 10-15 min 2-8 min 10-15 minTipo II 15-20 min 5-10 min 15-20 minTipo III 20-30 min 15-20 min 20-30 minTipo IV 30-40 min 20-25 min 30-40 minTipo V e VI 40-60 min 25-35 min 40-60 min Holick M. The Vitamin D Solution. 2010. Hudson Street Press
  • 63. DEFICIÊNCIA EM VITAMINA D65 Holick MF, Chen TC. Am J Clin Nutr. 2008 Apr;87(4):1080S-6S
  • 64. DISTRIBUIÇÃO NO CORPO HUMANOSangue e tecidos moles: 1% Ossos e dentes: 99% Mataix J. Nutrición y Alimentación Humana – Tomo I: Nutrientes y Alimentos. Ergon, 2002.
  • 65. FUNÇÕESo  Mineralização óssea e dentária;o  Vasoconstrição e vasodilatação;o  Transmissão de impulsos nervosos;o  Contracção muscular;o  Secreção e sensbilidade à Insulina;o  Lipólise;o  Ritmo cardíaco, Pressão Arterial e coagulação Mataix J. Nutrición y Alimentación Humana – Tomo I: Nutrientes y Alimentos. Ergon, 2002. Stipanuk. MH. Biochemical, Physiological, Molecular aspects of Human Nutrition. Saunders, 2006
  • 66. ABSORÇÃOü  Infância: 60%ü  Antes da puberdade: 28%ü  Puberdade: 34%ü  Adolescência e idade adulta: 25 a 30%ü  Gravidez: Aumentaü  Envelhecimento: Diminui 0.21% por anoü  Menopausa: Diminui 2% Mataix J. Nutrición y Alimentación Humana – Tomo I: Nutrientes y Alimentos. Ergon, 2002.Shils M.E., Shike M., Ross A.C. et al. Modern Nutrition in Health and Disease. Lippincott Williams & Wilkins, US; 10Rev Ed edition, 2005 Stipanuk. MH. Biochemical, Physiological, Molecular aspects of Human Nutrition. Saunders, 2006
  • 67. ABSORÇÃO DE CÁLCIOü  Ácido Hidroclorídrico ü  Gorduraü  Ácido Ascórbico ü  Fósforoü  Ácido Cítrico ü  Sódio, potássio, estrôncio y Magnésioü  Glicina e Lisina ü  Ácido Fíticoü  Fibra solúvel ü  Mais potente: Ácidoü  Lactose (crianças) Oxálico Mataix J. Nutrición y Alimentación Humana – Tomo I: Nutrientes y Alimentos. Ergon, 2002. Institute for Functional Medicine. Clinical Nutrition – A functional approach. IFM, 2004Shils M.E., Shike M., Ross A.C. et al. Modern Nutrition in Health and Disease. Lippincott Williams & Wilkins, US; 10Rev Ed edition, 2005
  • 68. ABSORÇÃO ACTIVA DE CÁLCIO Sem  Transporte  Accvo:     ü  Absorção  =  0  à  Ingestão  =  1100  mg   ü  Absorção  =  200  mg  à  Ingestão  =  3000  mg   Heaney R P Am J Clin Nutr 2008;88:541S-544S©2008 by American Society for Nutrition
  • 69. % ABSORÇÃO DE CaN= 13 (Cross-over)200 mg Ca (marcado com 45Ca) por alimento 30% 25% 20% 15% 10% 5% 0% Espinafre Leite Heaney RP, Weaver CM, Recker RR. Am J Clin Nutr. 1988 Apr;47(4):707-9.
  • 70. % ABSORÇÃO DE CaN= 16 (Cross-over)100 mg Ca (marcado com 45Ca) por alimento 45% 40% 35% 30% 25% 20% 15% 10% 5% 0% Soja alta Fitato Leite Soja baixa Fitato Heaney RP, Weaver CM, Fitzsimmons ML. Am J Clin Nutr. 1991 Mar;53(3):745-7.
  • 71. EXCREÇÃO DE CÁLCIOü  Cafeína??ü  Álcoolü  Excesso de Sódioü  Excesso de Proteínaü  Aspartameü  Glucoseü  Hiperinsulinemiaü  Carga Ácida >0 Mataix J. Nutrición y Alimentación Humana – Tomo I: Nutrientes y Alimentos. Ergon, 2002. Institute for Functional Medicine. Clinical Nutrition – A functional approach. IFM, 2004 Shils M.E., Shike M., Ross A.C. et al. Modern Nutrition in Health and Disease. Lippincott Williams & Wilkins, US; 10Rev Ed edition, 2005
  • 72. EQUILÍBRIO ÁCIDO-BASE
  • 73. PH ARTERIAL pH = 7,62 + log HCO3- /PCO2 (Henderson-­‐Hasselbach)   H+ PCO2 HCO3- pH (nanoeq/L) mmHg (mEq/L)Sangue Arterial 7,37-7,43 37-43 36-44 22-26 Rose BD, Post TW. Clinical Physiology of Acid-base and Electrolyte Disorders. McGraw-Hill, 2001.  
  • 74. PRODUÇÃO ÁCIDA ENDÓGENA LÍQUIDA
  • 75. PAELProdução de Ácido Sulfúrico + Produção de Ácidos orgânicos - Produção de Bicarbonato Sebastian A, et al. Am J Clin Nutr. 2002 Dec;76(6):1308-16
  • 76. PAELü  Produção de Ácido sulfúrico resulta do metabolismo dos aminoácidos sulfurados metionina e cisteína.ü  Produção de Ácidos orgânicos resulta da combustão incompleta dos hidratos de carbono e dos ácidos gordos.ü  Produção de Bicarbonato (PB) = ∑ catiões inorganicos - ∑ aniões inorganicos Corrigido para a taxa de absorção intestinalPB = 0.95 Na+ + 0.8 K+ + 0.25 Ca2+ + 0.32 Mg2+ - 0.95 Cl - 0.63 Pi Sebastian A, et al. Am J Clin Nutr. 2002 Dec;76(6):1308-16
  • 77. PRAL DE ALGUNS GRUPOS DE ALIMENTOS ACIDIFICANTES   ALCALINIZANTES   PRAL(mEq/100  kcal)   PRAL  (mEq/100  kcal)   Peixe 14,6 Oleaginosas -1,1 Carne 12,4 Fruta -5,2 Aves 7,8 Tubérculos -5,4 Ovo 7,3 Cogumelos -11,2Marisco 7,3 RaízesQueijo 3,3 (cenoura, nabo) -17,1 Leite 1,3 Tomate -17,5Cereais 1,1 Hortaliças -23,4 NEUTROS   PAEL  (mEq/100  kcal)   Para  cálculo  da  PAEL  da  dieta,  há  que  somar   32.9  mEq/d  que  é  a  produção  ácida  orgânica  Leguminosas -0,4 basal  independente  da  dieta.     Frassetto L.A. et al. J Nephrol. 2006 Mar-Apr;19 Suppl 9:S33-40.
  • 78. CLORO NaCl determina ~ 50% da PAELFrassetto LA, Morris RC Jr, Sebastian A. Am J Physiol Renal Physiol. 2007 Aug;293(2):F521-5
  • 79. Jajoo R, et al. J Am Coll Nutr. 2006 Jun;25(3):224-30.
  • 80. ü  40 H e M > 50 anosü  Duração 60 diasü  2 Grupos: GRUPO 1: Elevada ingestão de Fruta e Vegetais GRUPO 2: Fruta e Vegetais substituídas por Cereaisü  RESULTADOS: Jajoo R, et al. J Am Coll Nutr. 2006 Jun;25(3):224-30.
  • 81. GRUPO 2:•  PTH•  Excreção UCa•  Excreção urinária de N-Telopéptido Jajoo R, et al. J Am Coll Nutr. 2006 Jun;25(3):224-30.
  • 82. RECOMENDAÇÕES DE CÁLCIO Etapas da vida Dose adequada Limite mg mg 0-6 meses 210 N.D. 7-12 meses 270 N.D. 1-3 anos 500 2500 4-8 anos 800 2500 9-18 anos 1300 2500 19-50 anos 1000 2500 > 50 anos 1200 2500Gravidez e Amamentação Até 18 anos 1300 2500 > 18 anos 1000 2500 National Academy of Sciences. Dietary Reference Intakes: National Academy Press; 1 edition (Dec 2006)
  • 83. FONTES DE CALCIO NÃO LÁCTEAS Nº de doses necessárias Alimento Dose Cálcio para = Cálcio absorvido a (mg) partir de 225 ml de leite Leite 225 ml 300 1 Couve chinesa * ½ chávena 239 1,3 Repolho chinês * 55 g 79 2,3 Feijão branco ½ chávena 113 3,9 Brócolo * ½ chávena 35 4,5 Ruibarbo ½ chávena 174 9,5 Feijão vermelho ½ chávena 41 9,7 Espinafre ½ chávena 115 16,3* Não acumulam oxalatos como mecanismo para desentoxicar excesso de cálcio, de modo a prevenir a morte celular Institute for Functional Medicine. Clinical Nutrition – A functional approach. IFM, 2004 Shils M.E., Shike M., Ross A.C. et al. Modern Nutrition in Health and Disease. Lippincott Williams & Wilkins, US; 10Rev Ed edition, 2005
  • 84. % ABSORÇÃO DE CaN= 11 (Cross-over)300 mg Ca (marcado com 47Ca) por alimento 45% 40% 35% 30% 25% 20% 15% 10% 5% 0% Leite Couve Heaney RP, Weaver CM. Am J Clin Nutr. 1990 Apr;51(4):656-7
  • 85. HORTÍCOLAS PORTUGUESES COMO FONTES DE CÁLCIO Alimento Ca (mg) Crú Cozido Couve-Galega 286 264 Grelo de Couve 147 131 Grelo de Nabo 131 106 Couve-Portuguesa 76 71 Brócolo 67 56 Couve-Lombarda 51 46 Couve-Branca 50 45 Couve-De-Bruxelas 26 20 Couve-Flor 21 19 Instituto Ricardo Jorge, 2006
  • 86. DEFICIÊNCIA E TOXICIDADE
  • 87. SESSÃO DE BASQUETEBOL (2 H) à PERDA DE Ca (SUOR) DE 400 MG. .Kiesges RC, et al. JAMA. 1996 Jul 17;276(3):226-30
  • 88. DEFICIÊNCIA o  Cãibras, o  Espasmos musculares, o  Hipertensão, o  Osteopenia, o  Osteomalacia. Mataix J. Nutrición y Alimentación Humana – Tomo I: Nutrientes y Alimentos. Ergon, 2002.Shils M.E., Shike M., Ross A.C. et al. Modern Nutrition in Health and Disease. Lippincott Williams & Wilkins, US; 10Rev Ed edition, 2005 Stipanuk. MH. Biochemical, Physiological, Molecular aspects of Human Nutrition. Saunders, 2006
  • 89. TOXICIDADE> 2500 mg/dia: ü Cálculos renais ü Perturba o equilíbrio de Fe, Mg e Zn A partir de 5 gramas/dia pode afectar a função renal. Mataix J. Nutrición y Alimentación Humana – Tomo I: Nutrientes y Alimentos. Ergon, 2002.Shils M.E., Shike M., Ross A.C. et al. Modern Nutrition in Health and Disease. Lippincott Williams & Wilkins, US; 10Rev Ed edition, 2005 Stipanuk. MH. Biochemical, Physiological, Molecular aspects of Human Nutrition. Saunders, 2006
  • 90. RESEARCH Effect of calcium supplements on risk of myocardial infarction and cardiovascular events: meta-analysis Mark J Bolland, senior research fellow,1 Alison Avenell, clinical senior lecturer,2 John A Baron, professor,3 1651 Andrew Grey, associate professor,1 Graeme S MacLennan, senior research fellow,2 Greg D Gamble, research fellow,1 Ian R Reid, professor1nfarction 1 ABSTRACT INTRODUCTION67, P=0.035 Department of Medicine, Faculty of Medical and Health Sciences, Relative Risk of Myocardial Infarction cause Weightand mor- Objective To investigate whether calcium supplements Osteoporosis is a major of morbidity Study University of Auckland, Private Bag [95% Confidence Interval] risk of fracture, and most guidelines increase the risk of cardiovascular events. (%) 1 92 019, Auckland 1142, New tality in older people. Calcium supplements margin- Zealand Design Patient level and trial level meta-analyses. ally reduce the 23 2 Health Services Research Unit, Data sources Medline, Embase, and Cochrane Central recommend adequate calcium intake as an integral University of Aberdeen 3 Baron 1999 Register of Controlled Trials (1966-March 2010), part of the prevention or treatment13 of osteoporosis.4 5 Department of Medicine, and Department of Community and reference lists of meta-analyses of calcium supplements, Consequently, calcium supplements are commonly Grant 2005 Family Medicine, Dartmouth and two clinical trial registries. Initial searches were 29 used by people over the age of 50. Observational stu- Medical School, NH, USA carried out in November 2007, with electronic database dies suggest that high calcium intake might protect Grant 2005 Vit D Correspondence to: I R Reid i.reid@auckland.ac.nz searches repeated in March 2010. Study selection Eligible studies were randomised, 26 against vascular disease,6-8 and the findings are consis- tent with those of interventional studies of calcium sup- Cite this as: BMJ 2010;341:c3691 placebo controlled trials of calcium supplements doi:10.1136/bmj.c3691 Prince 2006 (≥500 mg/day), with 100 or more participants of mean 13 plements that show improvement in some vascular risk factors.9-11 In contrast, calcium supplements accelerate age more than 40 years and study duration more than one vascular calcification and increase mortality in patients Reid 2006 year. The lead authors of eligible trials supplied data. 17 with renal failure, in both dialysis and predialysis Cardiovascular outcomes were obtained from self reports, populations. 12-14 Furthermore, a five year randomised Calcium Lappe 2007 hospital admissions, and death certificates. 1 controlled trial of calcium supplements in healthy Results 15 trials were eligible for inclusion, five with older women, in which cardiovascular events were Placebo Reid 2008 patient level data (8151 participants, median follow-up 3.6 years, interquartile range 2.7-4.3 years) and 11 with prespecified as secondary end 1 points, recently reported possible increases in rates of myocardial trial level data (11 921 participants, mean duration Total infarction and cardiovascular events in women allo- 4 5 4.0 years). In the five studies contributing patient level data, 143 people allocated to calcium had a myocardial cated to calcium.15 16 We carried out a meta-analysis Test for heterogeneity: I² = 0%, 111= 0.96 to placebo infarction compared with P allocated 1.27 [1.01-1.59]events P=0.038 trials of cal- of cardiovascular in randomiseds (hazard ratio 1.31, 95% confidence interval 1.02 to 1.67, cium supplements. P=0.035). Non-significant increases occurred in the 0.5 0.8 1 1.2 METHODS 2 incidence of stroke (1.20, 0.96 to 1.50, P=0.11), the 1.5 370 1294 373 In November 2007 we searched Medline, Embase, and Favours calcium composite end point of myocardial infarction, stroke, or Favours placebo of Controlled Trials for the Cochrane Central Register28 1320 388 sudden death (1.18, 1.00 to 1.39, P=0.057), and death (1.09, 0.96 to 1.23, P=0.18). The meta-analysis of trial randomised placebo controlled trials of calcium sup- level data showed similar results: 296 people had a plements, using the terms “calcium”, “randomised myocardial infarction (166 allocated to calcium, 130 to controlled trial”, and “placebo” as text words, and cor-
  • 91. .       .     ü  7 estudos prospectivos, 170         991 mulheres, 2954     fracturas da anca. ü  5 estudos prospectivos, 68 606 Homens, 214 fracturas da anca. ü  5 intervenções (5666 Mulheres + 1074 Homens), 814 fracturas não-vertebrais. ü  4 intervenções c/ resultados separados para fracturas da anca (6504 pessoas, 139 fracturas da anca).Bischoff-Ferrari HA, Dawson-Hughes B, Baron JA, et al. Am J Clin Nutr. 2007 Dec;86(6):1780-90
  • 92. Total n: 252,841 NÃO MOSTRAM ü Estudos Prospectivos ASSOCIAÇÃO ENTRE INGESTÃO DE CA E FRACTURAS DA ANCA em Homens e Mulheres LIGEIRO AUMENTO DO ü RCTs observam um RISCO DE FRACTURAS DA ANCA com a SUPLEMENTAÇÃO DE CA . .100 Bischoff-Ferrari HA, Dawson-Hughes B, Baron JA, et al. Am J Clin Nutr. 2007 Dec;86(6):1780-900
  • 93. Total n: 252,841 NÃO MOSTRAM ü Estudos Prospectivos ASSOCIAÇÃO ENTRE INGESTÃO DE CA E FRACTURAS DA ANCA em Homens e Mulheres LIGEIRO AUMENTO DO ü RCTs observam um RISCO DE FRACTURAS DA ANCA com a SUPLEMENTAÇÃO DE CA . .101 Bischoff-Ferrari HA, Dawson-Hughes B, Baron JA, et al. Am J Clin Nutr. 2007 Dec;86(6):1780-900
  • 94. Reid IR, Bolland MJ, Grey A. Osteoporos Int. 2008 Aug;19(8):1119-23.
  • 95. LEITE E FRACTURAS" SEM ASSOCIAÇÃO EM ADULTOS RR/+1glass"Pooled analysis for categories of milk intake and hip fracture risk in womenfrom prospective cohort studies (6 studies, 195 102 women, 3574 fractures). ! Bischoff-Ferrari HA et al. J Bone Mineral Res 2011; online Oct 2010, DOI 10.1002/jbmr.279!
  • 96. MAGNÉSIO ü Distribuição: o  Ossos e dentes: 60 a 65% o  Músculo: 27% o  Outras células: 6 a 7% o  Líquido extracelular: menos de 1% Mataix J. Nutrición y Alimentación Humana – Tomo I: Nutrientes y Alimentos. Ergon, 2002.Shils M.E., Shike M., Ross A.C. et al. Modern Nutrition in Health and Disease. Lippincott Williams & Wilkins, US; 10Rev Ed edition, 2005 Stipanuk. MH. Biochemical, Physiological, Molecular aspects of Human Nutrition. Saunders, 2006
  • 97. Mg-ATP and Mg-DNA complexes: Mg está envolvido em todos os enzimas que usam ATP eMg2+todos os all enzymes envolvidos naenzymes inde ADN RNA synthesis involved in enzimas using ATP and all síntese DNA and e RNA Mg-ATP complexes: triphosphates are normally found with Mg2+. If the Mg2+content of a system is Mg-DNA complexes: Mg2+>Co2+> Ni2+> low the enzymes using triphosphates as Mn 2+> Zn2+>Cd2+>Cu2+ substrates cease function
  • 98. Mg(1)  gamma-Glutamylcysteine synthetase; (2) glutathione synthetase; (3) phytochelatine synthase; (4) glutathione S-transferase (GST).
  • 99. W-6 W-3 Ácido Linoleico Ácido Alfa Linolénico 18:2 w6 18:3 w3 Enzima Delta-6- Ácido -desaturase Mg Ácido Gama Linoleico Estearidónico 18:3 w6 18:4 w3 Enzima Elongase Ácido Ácido Dihomogama Eicosatetraenoico Linoleico 20:4 w3 20:3 w6 Enzima Delta-5- -desaturase EPA 20:5 w3 Ácido Delta-6- Araquidónico -desaturase 20:4 w611 DHA3Bastos P. An Nutr Esp Func 2007; 7(36): 17-24 22:6 w3
  • 100. Santos DA, Matias CN, Monteiro CP, Silva AM, Rocha PM, Minderico CS, Bettencourt Sardinha L, Laires MJ. Magnes Res. 2011 Dec;24(4):215-9
  • 101. DOSES DE MAGNÉSIO FOOD AND NUTRITION BOARD Homens RDA/AI* Limite (mg) Mulheres RDA/AI* (mg) Limite (mg) (mg) suplemento suplemento 0-6 meses 30* N.D. 0-6 meses 30* N.D. 7-12 meses 75* N.D. 7-12 meses 75* N.D. 1-3 anos 80 65 1-3 anos 80 65 4-8 anos 130 110 4-8 anos 130 110 9-13 anos 240 350 9-13 anos 240 350 14-18 anos 410 350 14-18 anos 360 350 19-30 anos 400 350 19-30 anos 310 350 > 30 anos 420 350 > 30 anos 320 350 Gravidez Até 18 anos 400 350 Sugestão de 19-30 anos 350 350 Seelig 6 mg/kg peso(Am J Clin Nutr 31-50 anos 360 3501964, 14:342-90) Lactação Até 18 anos 360 350 19-30 anos 310 350 31-50 anos 320 350
  • 102. FONTES DE MAGNÉSIOAlimentos   Dose  (g)  Magnésio  (mg)   Alimentos   Dose  (g)   Magnésio  (mg)  Semente  de  sésamo   30   102   Feijão  Preto  cozido   150   70  Semente  de  abóbora   30   159   LenYlha  cozida   100   36  Amêndoa   30   91   Ervilha  cozida   100   29  Avelã   30   85   Pão  Integral   60   51  Caju   30   72   Arroz  Integral  cozido   100   43  Castanha  do  Pará   30   71   Arroz  Branco  cozido   100   12  Noz   30   50   Aveia  cozida   100   24  Pistachio   30   47   Farelo  de  Aveia   10   22  Semente  de  girassol   30   36   Beterraba  fresca  cozida   100   68  Macadâmia   30   34   Alcachofra  cozida   100   60  Banana   120   35   Couve  Cozida   100   23  Melancia   250   26   Brócolo  cozido   100   22  Kiwi   75   23   Pescada   100   29  Abacate   50   20   Atum   100   28  Manga   200   17   Sardinha   100   25  Morango   150   16   Linguado   100   25  Papaia   140   14   Gambas   100   42  Sumo  de  Laranja  natural   250   27   Leite     250   29  Sumo  de  Uva   250   25   Iogurte   125   22   Hands ES. Nutrients in Food. Lippincott Williams & Wilkins; 2003.
  • 103. ABSORÇÃOü Gorduraü Fitatos e Oxalatosü Cálcio e Fósforoü Ácidos biliaresü Ingestão proteica < 30 grs/díaü Ingestão de Cálcio >2 grs juntamente con Mgü Ingestão elevada de Zn (> 100 mg)ü Hipocloridria PDR, 2001 Mataix, 2002 Linus Pauling Institute, 2003 IFM, 2004
  • 104. ABSORÇÃO o Lactose o FOS o Boro PDR, 2001 Mataix, 2002 Linus Pauling Institute, 2003 IFM, 2004
  • 105. EXCREÇÃO DE MAGNÉSIO o  Excesso de Na, Ca, açúcar, cafeína e álcool o  Diuréticos o  Diabetes o  Dieta com PAEL > 0 PDR,  2001      Mataix,  2002        Linus  Pauling  Ins;tute,  2003      IFM,  2004   J.  Nutr.  2006;  136:2374-­‐2377  
  • 106. SINAIS DE DEFICIÊNCIACãibras Diminuição dos níveis de Ca e KEspasmos musculares Alteração do perfil lipídicoFadiga RIInsónia Arritmia cardíacaIrritabilidade e Sintomas Depressão Aumento PA com Stress Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ. Modern Nutrition in Health and Disease. Lippincott Williams & Wilkins; 2005. Gibney MJ, et al. Introduction to Human Nutrition (Nutrition Society Textbook). 2nd ed. Wiley-Blackwell; 2009.
  • 107. DEFICIÊNCIAS DE MICRONUTRIENTES (POPULAÇÃO GERAL - EUA)Nutriente %H %H %H %M %M %M 14-18 a 19-30 a 31-50 a 14-18 a 19-30 a 31-50 aVit E 97 89 90 97 97 97Magnésio 78 55 61 91 64 65Vit C 26 37 40 42 40 41Zinco 4 6 4 26 13 11Folato 4 6 <3 19 14 16Ferro <3 <3 <3 16 15 17 USDA  What  we  Eat  in  America  (NHANES  2001-­‐2002)  Sept.  2005     Disponível  em:   hmp://www.ars.usda.gov/SP2UserFiles/Place/12355000/pdf/usualintaketables2001-­‐02.pdf    
  • 108. DEFICIÊNCIAS DE MAGNÉSIO EM ATLETASModalidades % DDR ReferênciasBasquetebol 66 Hickson JF Jr, Schrader J, Trischler LC.(Mulheres) J Am Diet Assoc 1986;86: 251–3Ginástica 66 Hickson JF Jr, Schrader J, Trischler LC. J Am Diet Assoc 1986;86: 251–3(Mulheres)Futebol Americano 69 Hickson JF, et al. Nutr Res 1987;7:27–34.Futebol 90 Hickson JF, et al. Nutr Rep Int 1986;34:85–91Atletismo 53 Zierath J, Kaiserauer S, Snyder AC.(Mulheres com Med Sci Sports Exerc 1986; 18(suppl):S55–6amenorreia)Atletismo 89 Zierath J, Kaiserauer S, Snyder AC.(Mulheres sem Med Sci Sports Exerc 1986; 18(suppl):S55–6amenorreia)Triatlo (Homens) 91 Worme JD, et al. Am J Clin Nutr 1990;51:690–7 Adaptado  de  Lukaski  HC.  Am  J  Clin  Nutr.  2000  Aug;72(2  Suppl):585S-­‐93S  
  • 109. TOXICIDADEo  Diarreia (pode surgir a partir de 600 mg/dia);o  Hipotensão que pode levar a tonturas, letargia, confusão e alteração do ritmo cardíacoo  Grave: debilidade, dificultade em respirar e paragem cardíaca. ü Atenção a quem tem Insuficiência Renal ü Doses de Suplementos: Comum entre 100 e 1000 mg/dia             PDR, 2001, Colgan, 2002, IFM, 2004, Linus Pauling Institute, 2003 Seelig e Rosanoff 2003
  • 110. VITAMINA K
  • 111. Best practice Vit K Vit K Vit K Vit K Figure 1 Pathways of the human coagulation system.Morley SL. Management of up these pathways are foundacute paediatrics. Arch Dis Child Educ Pract Ed. 2011 Apr;96(2):49-60. acquired coagulopathy in in plasma, almost all The clotting cascade contains a number of the reactions in the cascade occur on the surface anticoagulants that help to prevent excessive of platelets, endothelial cells or other blood cells. clot formation. Protein C is activated by throm- Normal endothelium cannot support coagulation bin into activated protein C (aPC) and forms a
  • 112. of around 3 days. The kinetic of the half-life of MK-7 -glutamyl carboxylation of coagulation factors.is biphasic; within the first 1.5h it lasts 6-8h, where- However, vitamin K2 has a more wide-spread tissueas in a second phase the half-life is around 50h, sug- distribution and is thus also involved in the car-gesting initial redistribution and tissue uptake followed boxylation of osteocalcin and MGP. Osteocalcin (OC),by the incorporation of vitamin K2 in lipoproteins and also called bone Gla-protein (BGP), is exclusivelyFigure 1The Vitamin-K-Cycle (from Stafford, 2005) Krueger T. Port J Nephrol Hypert 2008; 22(2): 143-148
  • 113. DOSES DE VITAMINA K FOOD AND NUTRITION BOARD Homens AI (mcg) Limite (mcg) Mulheres AI Limite (mcg) (mcg)0-12 meses 2.0-2.5 Nd 0-12 meses 2.0-2.5 Nd 1-3 anos 30 Nd 1-3 anos 30 Nd 4-8 anos 55 Nd 4-8 anos 55 Nd9-13 anos 60 Nd 9-13 anos 60 Nd14-18 anos 75 Nd 14-18 anos 75 Nd >18 anos 120 Nd >18 anos 90 Nd Gravidez (<18 anos) 75 Nd Gravidez (>18 anos) 90 Nd Lactação (<18 anos) 75 Nd Lactação (>18 anos) 90 Nd
  • 114. Alimentos Vitamina K1 (mcg)Couve Galega cozida (130 g) 1146Espinafre cozido (180 g) 888Couve-de-Bruxelas cozida (155 g) 300Brócolo cozido (156) 220Cebola crua (100 g) 207 USDA  Naconal  Nutrient  Database  for  Standard  Reference,  Release  20  
  • 115. CALCIFICAÇÃO DA AORTA
  • 116. MORTALIDADE CARDIOVASCULAR
  • 117. 2/121 (hip); 0/120 (hip); 5/121 (nonspine) 1/120 (nonspine) 52 (0) 52 (0) NA NA 1.1 (spine) neral density; CI, confidence interval; NA, not applicable.s who underwent follow-up for outcome. rate. ns low to de- OR % t asymmetry Study Favors Vitamin K Favors Control (95% Cl) WeightPvertebral = .61; Hipl inspection Sato et al,33 1998 0.36 (0.02 to 5.90) 6.3 Shiraki et al,36 2000 0.26 (0.03 to 2.55) 9.4 no evidence Sato et al,34 2002 0.19 (0.05 to 0.75) 26.4 ).24 In terms Ishida and Kawai,26 2004 0.37 (0.02 to 5.90) 6.3 Sato et al,35 2005 0.22 (0.08 to 0.59) 51.6only 2 stud- Subtotal 0.23 (0.12 to 0.47) 100.0 ey had used Vertebralg the alloca- Sasaki et al,32 2005 0.35 (0.02 to 6.00) 2.9 Shiraki et al,36 2000 0.39 (0.20 to 0.75) 54.4ion, another Iwamoto et al,29 2001 0.32 (0.07 to 1.46) 10.4 ranged from Ishida and Kawai,26 2004 0.47 (0.20 to 1.10) 32.3 Subtotal 0.40 (0.25 to 0.65) 100.0 All Nonvertebral Sato et al,33 1998 0.36 (0.02 to 5.90) 4.5 NTS Shiraki et al,36 2000 0.26 (0.05 to 1.30) 13.4 Sato et al,34 2002 0.17 (0.05 to 0.58) 23.0 serious ad- Ishida and Kawai,26 2004 0.22 (0.03 to 1.56) 8.9 Sato et al,35 2005 0.18 (0.08 to 0.41) 50.2d with vita- Subtotal 0.19 (0.11 to 0.35) 100.0 gastrointes-reported by 0.05 0.1 0.2 0.5 1 2 5 10 20 OR Figure 2. Meta-analysis of treatmentArch  Intern  Med.  2006;166:1256-­‐1261   (ORs) with 95% confidence effects on fractures. Peto odds ratios intervals (CIs).
  • 118. Alimentos (100 g) Vitamina K2 (mcg)Natto 1103Paté de fígado de Ganso 369Queijos envelhecidos 76,3Queijos gordos 56Gema de ovo 15-32Coxa de Ganso 21Manteiga 15Fígado de Galinha 14Coxa de Galinha 8,5Bife de vaca 8,1 Elder  SJ,  et  al.  J  Agric  Food  Chem.  2006;  54:  463-­‐467     Schurgers  LJ,  Vermeer  C.  Haemostasis.  2000;  30:  298-­‐307.        
  • 119. VITAMINA K1 E OSTEOCALCINA Binkley  NC.  Am  J  Clin  Nutr.  2002  Nov;76(5):1055-­‐60.    
  • 120. 0.07 Mean transvalvular gradient 24 Ϯ 12 21 Ϯ 14 0.37 0.0001 (mm Hg) 0.23 Peak aortic velocity (m/s) 3.14 Ϯ 0.72 2.93 Ϯ 0.85 0.31 0.61 0.14 Data are presented as numbers (percentages) or means Ϯ SDs. 1.00 * Peak aortic velocity between 2 and 3 m/s. † 0.47 Peak aortic velocity between 3.1 and 3.9 m/s. ‡ 0.63 Peak aortic velocity Ն4 m/s. 0.79 es). Table 3 Valvular and coronary calcium scores assessed by multislice spiral computed tomography stratified by anticoagulation statusts using a Variable Oral Anticoagulants pVingmed, Valuecardiogra- Yes (n ϭ 23) No (n ϭ 63)al area ofrtic valve Valvular Agatston 2,409.9 Ϯ 1,758.5 1,070.1 Ϯ 1,084.6 0.002 score0 m/s on Coronary Agatston 1,561.3 Ϯ 1,140.5 738.2 Ϯ 977.5 0.024 of Otto et scorebetween 2h a peak Koos  R,  et  al.  Am  J  Cardiol.  2005  Sep  15;96(6):747-­‐9.  aortic ste- tion for OAC therapy was chronic atrial fibrillation in 16 ad severe patients (70%), cardiomyopathy with a low ejection fraction
  • 121. ORIGINAL ARTICLE E n d o c r i n e C a r e — B r i e f R e p o r t Reduced Bone Mineral Density Is Associated with Breast Arterial Calcification Jhansi Reddy, John P. Bilezikian, Suzanne J. Smith, and Lori Mosca Department of Obstetrics, Gynecology, and Reproductive Biology (J.R.), Brigham and Women’s Hospital, Boston, Massachusetts 02115; 210 Reddy et al. of Medicine (J.P.B., L.M.), Pharmacology (J.P.B.), and Radiology (S.J.S.), Columbia University College of Physicians and Departments Bone Density and Arterial Calcification J Clin Surgeons, New York, New York 10032 Background: Arterial calcification, a marker of atherosclerosis, results from a complex process of biomineralization resembling bone formation. Breast arterial calcification (BAC) has been associ- TABLE 2. Multivariate adjusted odds ratios (OR) and 95% cohort than the general p ated with angiographic and clinical cardiovascular disease. The purpose of this study was to de- confidence intervals (CI) for predictors of BAC termine the association between reduced bone mineral density (BMD) and BAC, which may share generalized to the popula a common pathophysiology. data were ascertained fro Methods: We conducted a retrospective study ofOR women (55% 95% CI Variable 228 Hispanic, mean age 64 a physician’s diagnosis o Ϯ10 yr) who had both mammography and BMD evaluation at Columbia University Medical Center from Age (10 2001–2003. Each mammogram was reviewed for the presence of BAC using standardized methods. the systematic d yr) 1.5 1.0 –2.2 cluded HispanicBMD was measured using dual-energy x-ray absorptiometry and categorized as normal, low bone 3.1 1.5– 6.3 particular the diagnosis o density (osteopenia), or osteoporosis as defined by the World Health Organization. Univariate and Menopause 4.1 0.8 –21association between multivariate logistic regression analyses were performed to evaluate the 23 study participants. O mellitusa Diabetesreduced BMD and BAC. 1.6 0.7–3.7 Hypertensiona The prevalence of BAC, low bone density (osteopenia), and osteoporosis was 39, and BAC, however, were Results: 0.9 0.5–1.7 42, and Bone densityrespectively. Women with BAC were significantly more likely to be older, Hispanic, and 29%, was limited to white and Low bone density and have osteoporosis as compared with women1.1– 6.8 In age-adjusted not be generalized postmenopausal (osteopenia) 2.7 without BAC. may analyses, women with BAC were more likely to have reduced BMD (odds ratio 3.0, P Ͻ 0.01) as Osteoporosis with women without BAC. Furthermore, osteoporosis was strongly associated with the compared 4.4 1.6 –12 significance of the correl presence of BAC (odds ratio 3.5, P Ͻ 0.01). a Total n ϭ 205 due to missing data on 23 patients. who may need further ev Conclusion: These data suggest that osteoporosis and arterial calcification are strongly and inde- pendently correlated. Reduced BMD may identify women at risk of vascular disease. (J Clin Endo- The paradigm of CV sclerosis measured 93: 208carotid artery ultrasound and reduced crinol Metab on –211, 2008) replaced by the growing r bone density. J,  et  al.  J  Clin  Endocrinol  Metab  93:  208–211,  2008   Reddy   risk. It is important to iC ardiovascular disease (CVD) and osteoporosis are signifi- Several studies have suggested that BAC is an at risk of future clinical cardiovas- cant causes of morbidity and mortality among older testing may identify women cular events (6 –9). independent vascular disease so optim
  • 122. Bolland  MJ,  et  al.  BMJ.  2008  Feb  2;336(7638):262-­‐6   PORQUÊ?? Talvez Déficit Vit. K
  • 123. DOSES DE POTÁSSIO FOOD AND NUTRITION BOARDFases da vida AI Limite grs 0-6 meses 0.4 N.D. 7-12 meses 0.7 N.D. 1-3 anos 3.0 N.D 4-8 anos 3.8 N.D 9-13 anos 4.5 N.D > 13 anos 4.7 N.D Gravidez 4.7 N.D Lactação 5.1 N.D
  • 124. FONTES DE POTÁSSIO LPI, 2004 Alimentos Dose Qtd de Potássio mgBanana 1 média 467Batata cozida com casca 1 média 721Sumo de ameixa 180 ml 530Sumo de laranja 180 ml 354Laranja 1 média 237Sumo de tomate 180 ml 400Tomate 1 médio 273Passas ½ chávena 598Alcachofra cozida 1 média 425Espinafres cozidos ½ chávena 419Amêndoas 30 g 211
  • 125. CONCENTRAÇÕES DE ELECTRÓLITOS NO SORO E SUOR, E CONCENTRAÇÕES DE HC E ELECTRÓLITOS EM ALGUMAS BEBIDAS COMUNS. Na+                        K+                          Ca2+                    Mg2+                  Cl-­‐                            Osmolalidade            CHO   (mEq.L-­‐1)    (mEq.L-­‐1)    (mEq.L-­‐1)      (mEq.L-­‐1)      (mEq.L-­‐1)      (mOsm.L-­‐1  )                    (g.L-­‐1  )  Plasma                140                                        4,5                        2,5                            1,5-­‐2,1                      110                                          300                                          -­‐              Suor                    60-­‐80                                  4,5                        1,5                                  3,3                          40-­‐90                                170-­‐220                                  -­‐    Coca-­‐Cola      3,0                                        -­‐                                -­‐                                        -­‐                                  1,0                                          650                                      107  Gatorade          23,0                                3,0                            -­‐                                        -­‐                                14,0                                        280                                          62  Sumo  Fruta    0,5                                  58,0                        -­‐                                        -­‐                                      -­‐                                              690                                      118  Pepsi  Cola      1,7                          VesYgios                  -­‐                                      -­‐                          Vesbgios                                568                                          81  Àgua                Vesbgios                Vesbgios                  -­‐                                        -­‐                        Vesbgios                              10-­‐20                                        -­‐       McArdle  W,  Katch  F,  Katch  V.  Sports  &  Exercise  Nutricon,    2nd  Edicon.  Lippincom  Williams  &  Wilkins,  2005  
  • 126. PERDA DE FERRO:ü  SUOR: 0.4 A 0.6 MG/HORAü  HEMÓLISE: 0.25 a 0.75 mgü  HEMORRAGIA GASTROINTESTINAL, ACIDOSE E PEROXIDAÇÃO DAS MEMBRANAS CELULARES POR RL: 0.5-1 MG/DIA Colgan, M. Sports nutrition guide – Minerals, vitamins & antioxidants for athletes. Apple Publications, 2002 SHILS, M.E. et al. Modern Nutrition in Health and Disease. 10 ed. Lippincott Williams & Wilkins, 2005.
  • 127. NECESSIDADES DE ATLETAS EM TREINO INTENSO:ü  HOMENS = 3,25 MG (PERDAS) + 1 MG (FUNÇÕES BÁSICAS) = 4,25MG/DIAü  MULHERES = 3,25 MG (PERDAS) + 1 MG (FUNÇÕES BÁSICAS) + 0.5MG (MENSTRUAÇÃO) = 4,75MG/DIA ABSORÇÃO: ENTRE 1 A 25% Colgan, M. Sports nutrition guide – Minerals, vitamins & antioxidants for athletes. Apple Publications, 2002 SHILS, M.E. et al. Modern Nutrition in Health and Disease. 10 ed. Lippincott Williams & Wilkins, 2005.
  • 128. FONTES DE FERRO144  
  • 129. PERDA DE Zn:ü SUOR: 3 A 12 MG/DIAü UTILIZAÇÃO PELA SOD Colgan, M. Sports nutrition guide – Minerals, vitamins & antioxidants for athletes. Apple Publications, 2002
  • 130. DEFICIÊNCIAS DE ZINCO EM ATLETASModalidades % DDR ReferênciasAtletismo 86 Deuster PA, et al. Am J Clin Nutr 1989;49:1295–301(Mulheres)Maratonistas 73 Lukaski HC. Am J Clin Nutr. 2000 Aug;72(2 Suppl): 585S-93S(Mulheres)Velocistas 81 Lukaski HC. Am J Clin Nutr. 2000 Aug;72(2 Suppl): 585S-93S(Mulheres)Triatlo 88 Worme JD, et al. Am J Clin Nutr 1990;51:690–7(Mulheres)Triatlo (Homens) 91 Worme JD, et al. Am J Clin Nutr 1990;51:690–7 Adaptado  de  Lukaski  HC.  Am  J  Clin  Nutr.  2000  Aug;72(2  Suppl):585S-­‐93S  
  • 131. DOSES DE ZINCO FOOD AND NUTRITION BOARD Homens RDA/AI*  (mg) Limite  (mg) Mulheres RDA/AI*  (mg) Limite   (mg)0-­‐6  meses 2* 4 0-­‐6  meses 2* 47-­‐12  meses 3 5 7-­‐12  meses 3 5 1-­‐3  anos 3 7 1-­‐3  anos 3 7 4-­‐8  anos 5 12 4-­‐8  anos 5 12 9-­‐13  anos 8 23 9-­‐13  anos 8 2314-­‐18  anos 11 34 14-­‐18  anos 9 34 >  18  anos 11 40 >  18  anos 8 40 Gravidez Até  18  anos 12 34 19-­‐50  anos 11 40 Lactação Até  18  anos 13 34 19-­‐50 12 40
  • 132. FONTES DE ZINCO Alimentos   Dose Qtd  de  Zinco  (mg) Ostras 6  médias  (cozidas) 43,4 Caranguejo 90  g  (cozido) 4,6 Bife  de  vaca 90  g  (cozido) 5,8 Carne  de  porco 90  g  (cozido) 2,2Galinha  (coxa  e  asa) 90  g  (cozido) 2,4 Perú  (coxa  e  asa)   90  g  (cozido) 3,5 Queijo 30  g 0,9 Leite 240  ml 1,0 Amêndoas 30  g 1,0 Amendoins 30  g 0,9 Feijão  cozido ½  chávena 1,8 Grão  de  bico ½  chávena 1,3
  • 133. FITATOSDIMINUI A ABSORÇÃO DE: ü  Ferro ü  Zinco ü  Cálcio ü  Magnésio     Cordain  L.  World  Rev  Nutr  Diet  1999;  84:19-­‐73.       Bohn  T,  et  al.  Am  J  Clin  Nutr.  2004  Mar;79(3):418-­‐23.  
  • 134. A biodisponibilidade de minerais emamostras chinesas de vários tipos de arroz é <4%.
  • 135. DOSES DE COBRE FOOD AND NUTRITION BOARDFases  da  vida RDA/AI*  (mcg) Limite  (mcg) 0-­‐6  meses 200* N.D. 7-­‐12  meses 220* N.D. 1-­‐3  anos 340 1,000 4-­‐8  anos 440 3,000 9-­‐13  anos 700 5,000 14-­‐18  anos 890 8,000 >  18  anos 900 10,000 Gravidez Até  18  anos 1000 8,000 >  18  anos 1000 10,000 Lactação Até  18  anos 1300 8,000 >  18  anos 1300 10,000
  • 136. FONTES DE COBRE Alimentos  100  grs Qtd  de  Cobre  Alimentos  100  grs Qtd  de  Cobre   mg mg Cereais 0,02-­‐0,4 Carne 0,2-­‐1,1 Pão  branco 0,02 Lombo  de  porco 0,4 Pão  de  centeio 0,1 Frango 0,2 Trigo  inteiro 0,2 Mariscos 0,3-­‐13,7 Verduras  e  hortaliças 0,04-­‐0,3 Amêijoa 0,3 Cenouras 0,3 Lacccínios 0,02-­‐0,4 Espargos 0,04 Leite  inteiro 0,02 Couve  galega 0,1 Leite  desnatado 0,2 Frutas 0,07-­‐0,14 Leguminosas 0,14-­‐1,2 Banana 0,1 Ervilhas 1,2 Maçã 0,1 LenYlhas 0,1 Gorduras 0,1-­‐0,3 Frutos  secos 0,8-­‐2,4 Azeite 0,3 Amêndoas 1,4 Manteiga 0,4 Amendoins 0,8 Condimentos 0,3-­‐2,4 Nozes 1,3 Alho 0,3 Pimentão 0,6
  • 137. DOSES DE SELÉNIO FOOD AND NUTRITION BOARDFases  da  vida RDA/AI*   Limite   (mcg) (mcg) 0-­‐6  meses 15* 45 7-­‐12  meses 20* 60 1-­‐3  anos 20 90 4-­‐8  anos 30 150 9-­‐13  anos 40 280 >  14 55 400 Gravidez 60 400 Lactação 70 400
  • 138. FONTES DE SELÉNIO Alimentos   Dose Qtd  de  Selenio  (mcg)Castanha  do  Pará 30  g  (6  a  8  unidades) 839 Camarão   90  g  (10  a  12   34 pequeno unidades) Caranguejo 90  g 40 Salmão 90  g 40 Arroz  integral   1  chávena 19 cozidoPeito  de  galinha 90  g 20 Bife  de  porco 90  g 33 Bife  de  vaca 90  g 17 Pão  de  trigo   2  faYas 15 integral Leite 240  ml 5 Nozes 30  g 5
  • 139. VITAMINA B1
  • 140. DOSE DIÁRIA RECOMENDADA DE TIAMINA FOOD AND NUTRITION BOARD Homens RDA/AI* Limite (mg) Mulheres RDA/AI* Limite (mg) (mg) (mg)0-12 meses 0.2-0.3* Nd 0-12 meses 0.2-0.3* Nd 1-8 anos 0.5-0.6 Nd 1-8 anos 0.5-0.6 Nd9-13 anos 0.9 Nd 9-13 anos 0.9 Nd> 14 anos 1.2 nd 14-18 anos 1.0 Nd < 18 anos 1.1 Nd Gravidez 1.4 Nd Lactação 1.4 Nd
  • 141. FONTES DE TIAMINA Cereais Tiamina Carne, Leite e Tiamina Oleaginosas Tiamina (mg/100g) Levedura (mg/100g) (mg/100g)Gérmen de Trigo 2 Levedura de Cerveja 15,61 Sem. Girassol 1,96Farelo de Trigo 0,72 Bife de Porco 0,93 Pinhão 1,28Trigo Integral 0,4-0,5 Coração de Borrego 0,45 Amendoim 1,14Centeio Integral 0,43 Fígado de Borrego 0,4 Castanha do Pará 0,96Millet 0,73 Fígado de Vaca 0,25 Pistácio 0,67Trigo Sarraceno 0,6 Bife de Vaca 0,3 Avelã 0,46Aveia 0,6 Bife de Borrego 0,2 Caju 0,43Farelo de Arroz 2,3 Leite de Vaca 0,04 Noz 0,33Arroz Integral 0,5 Frango 0,1 Amêndoa 0,24Arroz polido 0,03 Sem. de abóbora 0,24Arroz Selvagem 0,45 Leguminosas Tiamina Sem. Sésamo 0,18 (mg/100g) Farinha de soja 0,85 Feijão Vermelho 0,84 Ervilha 0,74 Lentilhas 0,37 Grão 0,31 Rebentos de soja 0,23 Liska D, Quinn S, Lukaczer D, et al. Clinical Nutrition: A Functional Approach. Second Edition. IFM; 2004. Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ. Modern Nutrition in Health and Disease. Lippincott Williams & Wilkins; 2005.
  • 142. FACTORES QUE AFECTAM ESTADO DE TIAMINA Tiaminases Como (Degradam a Alimentos Acção eliminar Tiamina) Algumas plantas, Peixe Actuam durante oTiaminase 1 Crú, marisco Crú, armazenamento Clostridium thiaminolyticus dos alimentos ou TemperaturaTiaminase 2 Candida aneurinolytica durante a passagem pelo tracto gastrointestinalShils ME, Shike M, Ross AC, Caballero B, Cousins RJ. Modern Nutrition in Health and Disease. Lippincott Williams & Wilkins; 2005. Gibney MJ, et al. Introduction to Human Nutrition (Nutrition Society Textbook). 2nd ed. Wiley-Blackwell; 2009.
  • 143. FACTORES QUE AFECTAM ESTADO DE TIAMINA1.  Compostos anti-tiamina, que são termoestáveis: Tanino (chá)2.  Sulfitos destroem a Tiamina3.  Perda significativa na água da cozedura4.  Temperatura destrói Tiamina (incluindo pasteurização do Leite)5.  Exposição às luz solar (p.e. alimentos numa montra expostos à luz solar)6.  Ingestão crónica e excessiva de Álcool (reduz absorção intestinal e transporte celular de Tiamina e a sua conversão em co-factor)7.  Envenenamento por Arsénico (Bloqueia uso celular da Tiamina)Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ. Modern Nutrition in Health and Disease. Lippincott Williams & Wilkins; 2005. Gibney MJ, et al. Introduction to Human Nutrition (Nutrition Society Textbook). 2nd ed. Wiley-Blackwell; 2009.
  • 144. Tiamina éco-factor
  • 145. Tiamina é co-factorTiamina éco-factor
  • 146. Tiamina éco-factor
  • 147. Tiamina é co-factorTiamina éco-factor
  • 148. DEFICIÊNCIABeriberi “Seco” (Neuropatia periférica)Beriberi “Molhado” (Neuropatia Periférica, Edema, Taquicardia, Cardiomegalia, Insuficiência Cardíaca)Beriberi Infantil (Vómitios, Taquicardia, Convulsões e Morte)Estomatite Angular (Irritação e fissuras nos cantos dos lábios)Encefalopatia AlcoólicaLesões neurológicas Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ. Modern Nutrition in Health and Disease. Lippincott Williams & Wilkins; 2005. Gibney MJ, et al. Introduction to Human Nutrition (Nutrition Society Textbook). 2nd ed. Wiley-Blackwell; 2009.
  • 149. VITAMINA B6
  • 150. DOSE DIÁRIA RECOMENDADA DE VITAMINA B6 FOOD AND NUTRITION BOARDHomens RDA/AI* Limite (mg) Mulheres RDA/AI* Limite (mg) (mg) (mg) 0-12 0.1-0.3* Nd 0-12 meses 0.1-0.3* Nd meses1-8 anos 0.5-0.6 30-40 1-8 anos 0.5-0.6 30-409-13 anos 1.0 60 9-13 anos 1.0 60 14-50 1.3 80-100 14-18 anos 1.2 80 anos> 50 anos 1.7 100 19-50 anos 1.3 100 > 50 anos 1.5 100 Gravidez 1.9 80-100 Lactação 2.0 80-100
  • 151. FONTES DE VITAMINA B6
  • 152. BIODISPONIBILIDADE DA B6 EM CEREAIS É BAIXAü  Pode chegar a ser de 25-20%ü  Nos alimentos de origem animal: biodisponibilidade de quase 100%ü  Baixo status de vitamina B6 em vegetarianos Cordain  L.  World  Rev  Nutr  Diet  1999;  84:19-­‐73.    
  • 153. SÍNTESE DE HEMEPLP
  • 154. SÍNTESE DE CARNITINAPLP
  • 155. PLP GLICOGENÓLISE
  • 156. DOPAMINA, SEROTONINA, GABA E HISTAMINA Giardina G et al. PNAS 2011;108:20514-20519©2011 by National Academy of Sciences
  • 157. SINTOMAS DE DEFICIÊNCIA Dermatite Irritabilidade Convulsões Anemia microcitica (Diminuição da Hemoglobina) Diminuição da Proliferação Linfocitária Hiperhomocisteinemia Neuropatia PeriféricaShils ME, Shike M, Ross AC, Caballero B, Cousins RJ. Modern Nutrition in Health and Disease. Lippincott Williams & Wilkins; 2005. Gibney MJ, et al. Introduction to Human Nutrition (Nutrition Society Textbook). 2nd ed. Wiley-Blackwell; 2009.
  • 158. EXCESSO Neuropatias (> 500 mg, mas casos isolados com dosagens > 100 mg) Inibição da Lactação na Mulher (> 150 mg)Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ. Modern Nutrition in Health and Disease. Lippincott Williams & Wilkins; 2005. Gibney MJ, et al. Introduction to Human Nutrition (Nutrition Society Textbook). 2nd ed. Wiley-Blackwell; 2009.
  • 159. HOMOCISTEÍNA
  • 160. FOLATO
  • 161. DOSE DIÁRIA RECOMENDADA DE FOLATO FOOD AND NUTRITION BOARDHomens RDA/AI* Limite (mcg) Mulheres RDA/AI* Limite (mcg) (mcg) (mcg) 0-12 65-80* Nd 0-12 meses 65-80* Nd meses1-8 anos 150-200 300 1-8 anos 150-200 3009-18 anos 300-400 600-800 9-13 anos 300-400 600-800 Adultos 400 1000 Adultos 400 1000 Gravidez (<18 anos) 600 800 Gravidez ( >18 anos) 600 1000 Lactação (> 18 anos) 500 800 Lactação (> 18 anos) 500 1000
  • 162. FONTES DIETÉTICAS DE FOLATO184  
  • 163. FOLATOMiller  AL,  Kelley  GS.    Altern  Med  Rev.  1996;1(4):220-­‐235      
  • 164. L-5-methyl-THF was not feasible until its stable calcium salt they are metabolized to L-5-methyl-THF during theirwas developed (Metafolin®; Merck Eprova AG, Schaffhausen, across the intestinal mucosa (figure 1). Folie acid is ÁCIDO F by theSwitzerland), Since then, folie acid has been replaced ÓLICO ≠toFOLATO (DHF) and then to tetrahydrofolate dihydrofolate alcium salt of L-5-methyl-THF in several vitamin supplements by DHF reductase (DHFR) in the mucosal cell, a Folie acid Folie acid Folk: acid >200 ng Polyglutamates DHF Food folates Monoglutamates THF * 5,10-methyiene-THF 5-­‐MTHFR   L-5-methyl-THF * L-5-methyl-THF L-5-methyl-THFig. 1. Intestinal folate absorption (from ttie brush border membrane ttirough the mucosal cell via the portal vein into the peripheral cHF = dihydrofolate; THF=tetrahydrofolate. , _ 2010 Adis Data information BV. All rights reserved. Pietrzik  K,  Bailey  L,  Shane  B.  Clin  Pharmacokinet.  2010  Aug;49(8):535-­‐48.   Clin Piiarmacoidne
  • 165. G Model CANEP-315; No. of Pages 4G ModelCANEP-315; No. of Pages 4 Cancer Epidemiology xxx (2011) xxx–xxx Cancer Epidemiology xxx (2011) available Contents lists xxx–xxx at ScienceDirect Cancer Epidemiology Contents lists available at ScienceDirect The International Journal of Cancer Epidemiology, Detection, and Prevention Cancer Epidemiology journal homepage: www.cancerepidemiology.net The International Journal of Cancer Epidemiology, Detection, and Prevention journal homepage: www.cancerepidemiology.net Meta-analysis of cancer risk in folic acid supplementation trials G Model CANEP-315; No. of Pages 4Meta-analysis of Baggott a,risk inA. Oster b, Tsunenobu Tamura a,* trials Joseph E. cancer Robert folic acid supplementation a Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, AL 35294, USAJoseph E. Baggott a, Robert A. Oster b, Tsunenobu Tamura a,AL 35294, USAJ.E. Baggott et al. / Cancer Epidemiology xxx (2011) xxx–xxx b Department of Medicine, University of Alabama at Birmingham, Birmingham, * 2a Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, AL 35294, USAb Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA A R T I C L E I N F O A B S T R A C T group, a description of the dailyA R T I C L E I N F O Article history: A B S T R A C T Several reports suggest that folate has a procarcinogenic effect. Folate hasfolic acidbecauseplacebo), the numb a unique role or a its Received 5 November 2010 coenzymes are needed for de novo purine and thymine nucleotide biosynthesis. Antifolates, such as Received in revised form 29 April 2011 group, and the duration of the st methotrexate, are used in cancer treatment. Using a meta-analysis weighted for the duration of folic acidArticle history: Accepted 6 May 2011 Several reports suggest that folate has a procarcinogenic effect. Folate has a unique role because its coenzymes are needed for de novo purine and thymine nucleotide biosynthesis. Antifolates,served as the weighting factor. ThReceived 5 November 2010 online xxx (pteroylglutamic acid) supplementation, we analyzed the cancer incidence of six previously published Available such asReceived in revised form 29 April 2011 large prospective folic acid-supplementation trials in men and women. These articles were carefully methotrexate, are used in cancer treatment. Using a meta-analysis weighted for the duration of folic acidAccepted 6 May 2011 (pteroylglutamic acid) supplementation, we analyzed the cancer incidence excluded, where possible, fro selected from over 1100 identified using PubMed search.of sixanalyses suggest that cancer incidences Our previously publishedAvailable online xxx Keywords: large prospective were acid-supplementation trials in men and women. than the non-folic acid-supplemented groups folic higher in the folic acid-supplemented groups These articles were carefully Folic acid Cancer risk investigators [2,4,6] or by us [1 selected from over 1100 identified using PubMed search. Our analyses suggest that cancer incidences trials should be (relative risk = 1.21 [95% confidence interval: 1.05–1.39]). Folic acid-supplementationKeywords:Folic acid Supplementation trials performed with careful monitoring than the non-folic acid-supplemented groups types of skin cancer were unkno were higher in the folic acid-supplemented groupsof cancer incidence. Solid monitoring systems to detect side effects, Meta-analysis (relative risk = 1.21 [95% confidence in cancer risk, should be established before the initiation of folic acid supplementation including increase interval: 1.05–1.39]). Folic acid-supplementation trials should beCancer riskSupplementation trials percentage increase in risk of c trials.monitoring of cancer incidence. Solid monitoring systems to detect side effects, performed with careful including increase in cancer risk, should be established before the initiation of folicß 2011 Elsevier Ltd. All rights reserved. acid supplementationMeta-analysis trials. (95% CIs) associated with the ca 1), and the weights as a percenta ß 2011 Elsevier Ltd. All rights reserved. 1. Introduction 2. Methods risk ratio was compared to a null1. Introduction Several research groups have conducted large 2. Methods prospective Haenszel test. Statistical analy A weighted meta-analysis of six trials that involved folic acid clinical trials to evaluate the effect of the supplementation of B- supplementation in men and women(version 11.1; StataCorp LP, Coll was performed. We vitamins including conducted large prospective Several research groups have folic acid (pteroylglutamic acid) to evaluate its identified a total of 1124 articles by a folic acid A weighted meta-analysis of six trials that involvedPubMed search using keyclinical trials to effect on the effect of the supplementation of B- evaluate the risk of occlusive vascular disease and neoplasm in not adjusted for dropouts or de words, ‘‘folic acid,’’ limiting only performed. We supplementation in men and women was in ‘‘randomized-controlled trial,’’vitamins including folic acidand women [1–6]. Someevaluate its performed be the same both men (pteroylglutamic acid) to of these were identified a total of 1124 articles by a PubMed search using key 2009). Of thesein folic acid su ‘‘humans,’’ and ‘‘English’’ (access date: June 11, because a higher occlusive and neoplasm ineffect on the risk of occlusive vascular disease vascular disease incidence ‘‘folic acid,’’ limiting only in ‘‘randomized-controlled trial,’’ words, was articles, 370 involved the use of folate supplements withboth men and associated with higher these were performed ‘‘humans,’’ anticancer drugs and June 11, 2009). supplemented women [1–6]. Some of homocysteine concentration in theand ‘‘English’’ (access date:were eliminated,Of these 754. Of these,groups. leavingbecause a higher occlusive vascular be lowered by supplementation of folic circulation, which can disease incidence was articles, 370 involved the use of folate supplements with case-controlled 343 were cross-sectional or metabolic studies,associated with higher vitamins B-12 and B-6. Based on cancer incidences in drugs and were eliminated, leaving 754. Of these, acid and homocysteine concentration in the anticancer investigations, methodological articles, reviews and letters to thecirculation, which cantrials, researcherssupplementation the folic 3. Results 343 were cross-sectional or metabolic these, 303 studies lasted for less than these be lowered by commented on of possibility that folic editor, leaving 411. Of studies, case-controlledacid and vitamins B-12 and B-6. Based on cancer incidences of various cancers acid supplementation increases the incidence in investigations, methodological articles, reviews trials lastedto the 2–3; 3–6; and one year (63; 68; 70; 73; and 29 and letters for <1;these trials, researchers commented on the possibility thatintake would reduce [7–9]. It is possible that increased folate folic editor, leaving 411. Of these, respectively).lasteddurations than 12 months or 6–12 months, 303 studies The for less were Fig. 1. Weighted meta-analysis of cancerone year (63; folic for the remaining108 prospective trialsacid supplementation increases the incidence of various cancers risk during more acid supplementation Investigators cancer incidence, because of the role of folate coenzymes in purine 68; 70; 73; and 29 trials lasted for <1; 2–3; 3–6; andinvolving folate used daily supp trials. increased diamonds are risk ratios with 95% confidence intervals (95% CI) 12 use of anticancer drugs. Of[7–9]. It is possible thatThe de novo and thymidylate reduce biosynthesis solid folate intake would synthesis. 6–12 months, respectively). without the concomitantmonths or Therefore, supplements The durations were
  • 166. GENOTIPO MTHFR TT ingestão ≅ 254mcg/día ≅ 254mcg/día ≅ 254mcg/díaAshfield-­‐Wam  PAL  et  al.  Am  J  Clin  Nutr  2002;76:180-­‐6.  
  • 167. Photodegradation of 5-methyltetrahydrofolate: Biophysical Aspects Arnfinn Hykkerud Steindal* , ? Asta Juzeniene, Anders Johnsson and Johan Moan13 Department of Radiation Biology, Institute for Cancer Research, The Norwegian Radium Hospital, Montebello, N-0310Oslo, Norway 2Department of Physics, Norwegian University of Science and Technology - NTNU, N-7491 Trondheim, Norway 3Department of Physics, University of Oslo, N-0316 Oslo, Norway Received 09 June 2006; accepted 24 July 2006; published online 31 July 2006 DOI: 10.1562/2006-06-09-RA-915 Photochemistry and Photobiology, 2006, 82: 1651-1 655 ABSTRACT MATERIALS AND METHODS Chemicals. (6R,S)-5-methyl-5,6,7,8-tetrahydrofolate calcium salt and (6R,S)- 5-methyltetrahydrofolate(SMTHF) absorbs UV radiation and Photodegradation of 5-methyltetrahydrofolat 5-methyl-5,6-dihydrofolateammonium salt was purchased from Schircks has an absorption coefficient of 24250 f 1170 M- cm- at Laboratories (JoM, Switzerland), while p-aminobenzoyl-L-glutamicacid 290 nm.It has a weak fluorescence emission in the wavelength was purchased from Sigma Chemical Co. (St. Louis, MO). Dulbeccos Arnfinn Hykkerud Steindal*, ? Asta Juzeniene, Anders Johnss region around 360 nm. Our data demonstrated induction of 5methyldihydrofolate by exposure to UVB and, after con- ü  5MTHF absorve UVB, sendo phosphate buffered saline (PBS) was purchased from PAA Laboratories GmbH (Paschmg, Austria).Departmentwere Radiation Biology, Institute for Cancer Research, The Norw The solutions of freshly made in PBS before the instability N-0310Oslo, Norway tinues irradiation,p-aminobenzoyl-L-glutamic acid was found. oxidado a 5MDHF each experiment. Because ofMontebello, of the compounds, the solutions were always kept on ice before use. 2Department of Physics, Norwegian University of Science and Technology The photodegradation of SMTHF follows a first order kinetic UVIVis absorption and fluorescence measurements. Absorption spectmOslo, N-0316 Oslo, Norway I 3Department of Physics, University of with a degradation rate constant of 9.2 X min- under were registered with a Perkin-Elmer Lambda 40 UVPis spectrometer 1 poaH our conditions (fluence rate of 2.15 mW crn-, exposure wave- (Shelton, CT). Fluorescence emission and June 2006; accepted 24 July 2006; published online 31 July 2006 Received 09 excitation spectra were recorded lJV lengths from 280 to 350 nm). Our results indicate that a direct ü  5MDHF não volta a entrar no by means of a Perkin-Elmer LS5OB luminescence spectrometer equipped with a Hamamatsu R-928 photomultiplier (Iwata, Japan). All measurements degradation of SMTHF by UV exposure in humans in vivo is were performed in standard 10 mm quartz cuvettes. rather unlikely. 5MTHF mainly absorbs, and is degraded by, ciclo de folato ABSTRACT Photoolysis. Solutions of 5MTHF were exposed to UV radiation in closed quartz cuvettes (1 mL). The radiation source was a broad-band UVB lamp MATER UVB and UVC, radiation that does not penetrate the earths Chemicals. ( with five Philips TL 2OW/12 RS UVB tubes (Amsterdam).(SMTHF) absorbs UV radiation and 5-methyltetrahydrofolate The fluence rate atmosphere and the human skin well. after each experiment with an UVB 24250 of the lamp was measuredhas an absorption coefficient of detector f 1170 M- cm- at 5-methyl-5,6 Laboratories 500 INTRODUCTION ü  UVA, através de ROS (PMA2106) connected to a photometer (PMA2200), both from Solar Light 290 nm.It at the sample position was 2.15 Co. (Philadelphia, PA). The intensity has a weak fluorescence emission in the wavelength region around 360innm. wavelength region Our data demonstrated induction of was purchas phosphate b mW an-*, the radiation was emitted mainly the and Folate is an important vitamin for human health (1). Folate defi- produzidos por 280-350 nm with a maximum at 3 12 nm. The temperaturesexposure to UVB and, after con- 5methyldihydrofolate by of the samples were approximately 25 to tinues irradiation,p-aminobenzoyl-L-glutamic 30°C. All experiments were performed in con- acid was found. GmbH (Pasc each experimon spectra of 5 ciency, or impairment of the folate metabolism in an organism, were always20 and 150 min. leads to several diseases, including megaloblastic anemia (1) and fotosensibilizadores (ex: stant dim light in order to avoid photodegradation of SMTHF follows a first order kinetic The external, uncontrolled light exposure. One point that must be stressed is the fact that our UV source contains with a degradation rate constant of 9.2 X min- under UVIVis ab were registe complications arising in pregnancy, such as neural tube defects (2). radiationthat is not present in the solar radiation (9). In the starting phase of or the emission Folate deficiency may also increase the risk of developing cardio- flavinas, porfirinas, our project we used a narrow-band UVB lamp (Phillips TL 20W/01mW crn-, exposure wave- our conditions (fluence rate of 2.15 RS, lengths from 280 to broad-band UVB lamp, 312 nm peak). The results were the same as for the 350 nm). Our results indicate that a direct (Shelton, CT by means o vascular diseases (3) and cancer (4). with a Hama It has been suggested that exposure to large doses of solar bilirrubina, etc), oxida 5MTHF because 5MTHF SMTHF at UV exposure but the process was slower degradation ofabsorbs lessby 312 nm than at in humans in vivo is shorter wavelengths. SMTHF is rather unstable in vibo, mainly absorbs, and is degraded by, rather unlikely. 5MTHF so we decided to were perform Photoolysiexcitation and Unknown molecule + radiation may lead to folate deficiency, and that sun-induced folate degradation may play a key role in evolution of human skin color. use the broad-band UVB lamp. UVB and UVC, radiation that does not penetrate the earths quartz cuvet with five Ph atmosphere and the human skin well. of the lampVB exposure. This hypothesis was first proposed by Branda and Eaton (5) and Ha further developed by Jablonski and Chaplin (6). No definite con- RESULTS AND DISCUSSION (PMA2106)radiation, the Absorption measurements INTRODUCTION Co. (Philad Figure 8. A possibleclusion about theAs a first step folate photodegradation inproblem, scheme of thepossibility of in the elucidation of this vivo has photodegradation of SMTHF. mW an-*, aat at least one been drawn yet. Folate is an concentrations of 5MTHF are health (1). Folate defi- The absorption spectra of different important vitamin for human 280-350 nm investigations of the photophysics and photochemistry of folate in were approx than SMTHF simple model systems would be of great value. shown in Fig. 2. SMTHF absorbs radiation in the the folate metabolism in an organism, ciency, or impairment of UV region and stant dim lig has an absorption peak at 290 to several diseases, including megaloblastic anemia (1) and leads nm. At wavelengths longer than 340 One poin constant is five times larger than that ofofan unirradiated solution of the The photodegradation folic acid (FA), a synthetic form nm, the absorption is weak. The insert shows apregnancy, such as neural tube defects (2). complications arising in linear plot of the radiationthaes higher than (1.8 x folate, has been thoroughly studied (7,s). 5-methyltetrahydrofolate min-I). (SMTHF) belongs to the naturally occurring folates. In the present absorbance at 290 nm as a function of concentration. The the risk of developing cardio- Folate deficiency may also increase linear our project 312 nm pea y explain the In Fig. 8 a scheme workSMTHF photodegradation is proposed. of we have investigated the photodegradation kinetic of SMTHF relationship between absorbancediseases (3) and cancer (4). that vascular and concentration indicates but the proc the absorbance of SMTHF follows the Beer-Lambert exposure to large doses of solar It has been suggested that law, thus shorter wav F and then the The unknown molecule is probably a reduced form of a chemical by absorption and fluoresence measurements. The pterin. struc- radiation may lead to folate deficiency, and that sun-induced folate aggregation plays no major role. use the broa ture of SMTHF is shown in Fig. 1. It consists of three groups:
  • 168. Mean values were significantly different from those of the raw food (paired t test: ***P, 0·005, ****P, 0·0001.† ‘Typical’ cooking procedures were established from the results of a consumer questionnaire (for details see p. 682).‡ Times shown reflect the duration required to cook the food item (determined from preliminary experiments, i.e. not ‘undercooked’ or ‘overcooked’; for details,Journal of Nutrition (2002), 88, 681–688 British see p. 683). q The Authors 2002 DOI: 10.1079/BJN2002733§ To avoid differences in moisture content as a result of different cooking procedures, spinach, broccoli and beef were weighed raw before cooking and values therefore given per 100 g raw weight. Values for potatoes relate to whole potatoes (skin and flesh) and are given per 100 g raw or cooked weight as appropriate (for details of procedures see p. 682). The effect of different cooking methods on folate retention in various foods that are amongst the major contributors to folate intake in the UK diet Derek J. McKillop, Kristina Pentieva*, Donna Daly, Joseph M. McPartlin, Joan Hughes, J. J. Strain, John M. Scott and Helene McNulty Northern Ireland Centre for Food and Health (NICHE), University of Ulster, Coleraine BT52 1SA, Northern Ireland, UK (Received 14 January 2002 – Revised 04 July 2002 – Accepted 15 August 2002) COZIDO  AO  VAPOR   Folate intake is strongly influenced by various methods of cooking that can degrade the natural forms of the vitamin in foods. The aim of the present study was to determine the effect of different cooking methods on folate retention in various foods that contribute to folate intake in the UK diet. Typical purchasing and cooking practices of representative food folate sources were determined from a questionnaire survey of local shoppers (n 100). Total folate was deter- mined by microbiological assay (Lactobacillus casei NCIMB 10463) following thermal extrac- tion and tri-enzyme (a-amylase, protease and conjugase) treatment in raw foods and after typical methods of cooking. Boiling for typical time periods resulted in only 49 % retention of folate in spinach (191·8 and 94·4 mg/100 g for raw and boiled spinach respectively; P, 0·005), and only 44 % in broccoli (177·1 and 77·0 mg/100 g for raw and boiled broccoli respectively, P, 0·0001). Steaming of spinach or broccoli, in contrast, resulted in no significant decrease in folate content, even for the maximum steaming periods of 4·5 min (spinach) and COZIDO  EM  ÁGUA   15·0 min (broccoli). Prolonged grilling of beef for the maximum period of 16·0 min did not result in a significant decrease in folate content (54·3 and 51·5 mg/100 g for raw and grilled beef respectively). Compared with raw values, boiling of whole potatoes (skin and flesh) for 60·0 min did not result in a significant change in folate content (125·1 and 102·8 mg/100 g for raw and boiled potato respectively), nor was there any effect on folate retention whether or not skin was retained during boiling. These current results show that the retention of folate in various foods is highly dependent both on the food in question and the method of cook- ing. Thus, public health efforts to increase folate intake in order to improve folate status should incorporate practical advice on cooking. Food folate retention: Cooking methods: Food folates: Dietary folate intake ESPINAFRE   Optimal folate status may have a role in the prevention of 400 mg folic acid/d in addition to normal dietary folate cardiovascular disease via plasma homocysteine-lowering intake to prevent the occurrence of neural tube defects. (Boushey et al. 1995), and possibly in the prevention of However, more recent studies suggest that an additional certain cancers (Branda & Blickenderfer, 1993; Kim et al. intake of 200 mg folic acid/d may be optimal both for the 1997; Jacob et al. 1998; Choi & Mason, 2000). However, prevention of neural tube defect occurrence (Daly et al. the most compelling evidence for the benefit of optimal 1997) and for the lowering of plasma homocysteine
  • 169. British Journal of Nutrition (2002), 88, 681–688 DOI: 10.1079/BJN2002733 q The Authors 2002 The effect of different cooking methods on folate retention in various foods that are amongst the major contributors to folate intake in the UK diet Derek J. McKillop, Kristina Pentieva*, Donna Daly, Joseph M. McPartlin, Joan Hughes, J. J. Strain, John M. Scott and Helene McNulty Northern Ireland Centre for Food and Health (NICHE), University of Ulster, Coleraine BT52 1SA, Northern Ireland, UK (Received 14 January 2002 – Revised 04 July 2002 – Accepted 15 August 2002) COZIDO  AO  VAPOR   Folate intake is strongly influenced by various methods of cooking that can degrade the natural forms of the vitamin in foods. The aim of the present study was to determine the effect of different cooking methods on folate retention in various foods that contribute to folate intake in the UK diet. Typical purchasing and cooking practices of representative food folate sources were determined from a questionnaire survey of local shoppers (n 100). Total folate was deter- mined by microbiological assay (Lactobacillus casei NCIMB 10463) following thermal extrac- tion and tri-enzyme (a-amylase, protease and conjugase) treatment in raw foods and after typical methods of cooking. Boiling for typical time periods resulted in only 49 % retention of folate in spinach (191·8 and 94·4 mg/100 g for raw and boiled spinach respectively; P, 0·005), and only 44 % in broccoli (177·1 and 77·0 mg/100 g for raw and boiled broccoli respectively, P, 0·0001). Steaming of spinach or broccoli, in contrast, resulted in no significant decrease in folate content, even for the maximum steaming periods of 4·5 min (spinach) and COZIDO  EM  ÁGUA   15·0 min (broccoli). Prolonged grilling of beef for the maximum period of 16·0 min did not result in a significant decrease in folate content (54·3 and 51·5 mg/100 g for raw and grilled beef respectively). Compared with raw values, boiling of whole potatoes (skin and flesh) for 60·0 min did not result in a significant change in folate content (125·1 and 102·8 mg/100 g for raw and boiled potato respectively), nor was there any effect on folate retention whether or not skin was retained during boiling. These current results show that the retention of folate in various foods is highly dependent both on the food in question and the method of cook- ing. Thus, public health efforts to increase folate intake in order to improve folate status should incorporate practical advice on cooking. Food folate retention: Cooking methods: Food folates: Dietary folate intakeBRÓCOLO   Optimal folate status may have a role in the prevention of 400 mg folic acid/d in addition to normal dietary folate cardiovascular disease via plasma homocysteine-lowering intake to prevent the occurrence of neural tube defects. (Boushey et al. 1995), and possibly in the prevention of However, more recent studies suggest that an additional certain cancers (Branda & Blickenderfer, 1993; Kim et al. intake of 200 mg folic acid/d may be optimal both for the 1997; Jacob et al. 1998; Choi & Mason, 2000). However, prevention of neural tube defect occurrence (Daly et al. Fig. 2. The effect of duration and method of cooking on folate retention in: (a), spinach; the most compelling evidence for the benefit of optimal 1997) and for the lowering of plasma homocysteine
  • 170. VITAMINA B12
  • 171. DOSE DIÁRIA RECOMENDADA DE VITAMINA B12 FOOD AND NUTRITION BOARDHomens RDA/AI* Limite (mcg) Mulheres RDA/ Limite (mcg) AI* (mcg) (mcg) 0-12 0.4-0.5* Nd 0-12 meses 0.4-0.5* Nd meses1-8 anos 0.9-1.2 Nd 1-8 anos 0.9-1.2 Nd9-13 anos 1.8 Nd 9-13 anos 1.8 Nd> 14 anos 2.4 Nd > 14 anos 2.4 Nd Gravidez 2.6 Nd Lactação 2.8 Nd
  • 172. FONTES DE VITAMINA B12195  
  • 173. TABLE 2 Vitamin B-12 and homocysteine status among vegetarians, vegans, and omnivores: summary of studies from different countries Study (reference) Plasma vitamin B-12 Plasma homocysteine pmol/L lmol/L Majchrzak et al, 2006, Austria (10) Vegetarians (n ¼ 36)1 238.5 6 99.1 14.0 6 5.4 Vegans (n ¼ 42)1 203.2 6 101.5 16.5 6 8.2 Omnivores (n ¼ 40)1 251.5 6 83.0 12.2 6 5.6 Koebnick et al, 2005, Germany (11) Vegetarians (n ¼ 38)2 143.2 (121.2–175.9) 17.1 (13.1–20.2) Vegans (n ¼ 39)2 126.2 (87.8–182.3) 18.5 (13.5–28.9) Omnivores (n ¼ 109) 2 174.5 (142.2–249.8) 14.7 (11.9–18.3) Herrmann et al, 2005, Germany (13) Vegetarians (n ¼ 66)3 192 (127–450) 10.6 (6.4–27.7) Vegans (n ¼ 29)3 148 (99–314) 12.8 (5.9–57.1) Omnivores (n ¼ 79)3 287 (190–471) 8.8 (5.5–16.1) Waldmann et al, 2004, Germany (12) Moderate vegans (n ¼ 45)3 185 (97.6–689) 12.3 (4.6–23.6) Downloaded from www.ajcn.org at Lund University Libraries on October 3, 2011 Strict vegans (n ¼ 86)3 122 (71.2–276) 13.4 (6.0–82.5) Huang et al, 2003, Taiwan (14) Vegetarians (n ¼ 37)4 191.8 (164.0, 220.0) 13.2 (10.6, 15.7) Omnivores (n ¼ 32)4 310.9 (278.2, 343.6) 9.8 (9.1, 10.6) Su et al, 2005, Taiwan (15)DEFICIÊNCIA DE Vegetarians (n ¼ 57)1 265.2 6 179.3 11.0 6 3.3 Omnivores (n ¼ 61)1 380.3 6 199.4 9.0 6 2.1 Hung et al, 2002, Taiwan (16)VITAMINA B12 Vegetarians (n ¼ 45)1 Omnivores (n ¼ 45)1 Bissoli et al, 2002, Italy (17) 207.7 6 127.1 403.5 6 138.9 11.20 6 4.27 8.64 6 2.06 Vegetarians (n ¼ 14)1 EM 163.8 6 57.1 17.4 6 11.1 Vegans (n ¼ 31)1 155 6 73.6 26.9 6 24.1 ˇ ´ ´ Kazimırova et al, 2006, Slovak Republic (18)VEGETARIANOS Vegetarians (n ¼ 24)5 Omnivores (n ¼ 24)5 Koebnick et al, 2004, Germany (19) 209.79 6 27.52 229.33 6 15.01 Not reported Not reported Vegetarian (n ¼ 60)6,7 159.6 (127–176) 6.7 (5.7–7.5) Omnivores (n ¼ 108)6,7 218.6 (169–249) 6.2 (5.7–6.7) Ambroszkiewicz et al, 2006, Poland (20) Vegetarians (n ¼ 32)1,8 404.9 6 106.6 6.1 6 1.2 Karabudak et al, 2008, Turkey (21) Vegetarian (n ¼ 26)1 200.5 6 137.3 12.6 6 5.97 Omnivores (n ¼ 26)1 269.1 6 234.2 10.8 6 3.72 Haddad et al, 1999, United States (22) Vegans (n ¼ 25)1 312 6 125 7.9 6 1.5 Omnivores (n ¼ 20)1 313 6 99 8.0 6 1.9 Hokin et al, 1999, Australia (23) Vegetarians (n ¼ 245)7 199 (58–538) Not reported Omnivores (n ¼ 53)7 292 (134–721) Not reported Leung et al, 2001, China (24) Vegetarians (n ¼ 51)7,9 389 (313–437) Not reported Refsum et al, 2001, India (26) Vegetarian (n ¼ 78)3 124 (66–625) 22 (9.6–48) Omnivores (n ¼ 126)3 161 (62–492) 19.4 (9.7–45.7) 1 All are means 6 SDs. values Elmadfa  I,  Singer  I.  Am  J  Clin  Nutr.  2009  May;89(5):1693S-­‐1698S   2 All values are medians; 25th to 75th percentiles in parentheses. 3 All values are medians, 5th to 95th percentiles in parentheses. 4 All values are means; 95% CIs in parentheses. 5
  • 174. adjusting for non-vegetarian food intake. Higher least alternate days (data not shown). Ninety-three meneducation andOriginal Article income were associated with lower had non-vegetarian food frequently (Table 1).plasma vitamin B12 and higher tHcy concentrations Approximately half of the men who ate non-veg food(p<0.05). These relations were not independent of intake frequently had low vitamin B12 concentration and VitaminSmoking and alcohol habits Hyperhomocysteinemia inof non-vegetarian foods. B12 Deficiency and hyperhomocysteinemia. Nine men had hyper-were not related to plasma vitamin B12 orIndiansred Rural and Urban tHcy or to homocysteinemia despite frequent non-vegetarian foodcell folate concentrations. intake, normal circulating vitamin B12, normal folate CS Yajnik*, Swapna S Deshpande*, Himangi G Lubree*, plasma creatinine concentrations. Intake ofAssociations with diet and gastrointestinal factors and SS Naik*, DS Bhat* Bhagyashree S Uradey*, Jyoti A Deshpande*, Sonali S Rege*, Helga Refsum**, was not related to plasma vegetables, milk and coffee Only 3 men Yudkin*** JS took vitamin supplements, none vitamin B12 and tHcy or red cell folate concentrations.containing vitamin B12. Daily energy intakes of thesemen were lower than those recommended by the Indian Plasma vitamin B12 and tHcy and red cell folate Abstract concentrations were not related to gastrointestinal Background : Low vitamin B12 concentration in South Asian Indians is common, but the exact prevalence is Table 2 : Circulating vitamin B12, total homocysteine and folate concentrations and haematological parameters and in not known. rural and urban men. The CRISIS study Aim : To investigate prevalence and associations of low vitamin B12 concentration and hyperhomocysteinemia in rural and urban Indian men living in and around Pune, Maharashtra. Rural(n=149) Slums(n=142) Urban middle-class(n=150) Method : We studied 441 middle-aged men (149 rural, 142 slum and 150 urban middle-class residents, meanPlasma vitamin B12age 39 y). Data on lifestyle, socio-economic status, nutrition and 145 (90, 241) were obtained. Circulating (pmol/L) 119 (73, 171) medical history ** 89 (58, 133) ++ concentrations of vitamin B12, folate, ferritin, total homocysteine (tHcy), and haematological indices, and <150 pmol/L (%) 68 51 * 81 *, +++ cardiovascular risk variables were measured.Total Hcy (µmol/L) 14.6 (12.0, 22.6) 14.2 (11.4, 19.7) 23.7 (15.3, 40.7) ***, +++ Results : Median plasma B12 concentration was low (110 pmol/L): Overall, 67% of men had low vitamin B12 >15 µmol/L (%) 48 47 79 **, ++ concentration (<150 pmol/L) and 58% had hyperhomocysteinemia (>15 µmol/L). Of the urban middle class,Red cell folate (nmol/L)had low vitamin B12 concentration and 79% had hyperhomocysteinemia.585) vitamin B12 concentration 707) ++ 81% 522 (424, 647) 461 (360, Low * 525 (406, <283 nmol/L (%)contributed 28% to the risk of hyperhomocysteinemia (population2 7 1 attributable risk) while low red cell folate 5 ++Haematological parameters 2%. Vegetarians had 4.4 times (95%CI 2.1, 9.4) higher risk of low vitamin B12 concentrations and contributedHaemoglobin (g/L) 3.0 times (95%CI 1.4, 6.5) higher risk of hyperhomocysteinemia compared to those who ate non-vegetarian 146) 140 (134,147) 143 (137,149) 141 (132, foods frequently. Urban middle-class residence was an additional independent risk factor ofAnemia (< 135 g/L)hyperhomocysteinemia (odds ratio 7.6 (95%CI 2.5, 22.6), compared to rural men). Low vitamin B12 (%) 25 19 31Mean corpuscular volume (fL) was related to lower blood haemoglobin concentration and higher mean corpuscular volume, concentration 85.7 (82.3, 89.0) 85.1 (81.8, 89.7) 85.3 (82.2,89.3)Macrocytosis (>100 fL) (%) but macrocytic anemia was rare. 1 2 1Microcytosis (<80 fL) (%) Conclusion : Low vitamin B12 1 5 14 15 concentration and hyperhomocysteinemia are common in Indian men, particularly in vegetarians and urban middle class residents. Further studies are needed to confirm theseThrombocytopenia (<140 * 10 9/L) (%) 4 4 2Leucopenia (<4.5*109/L) (%) other parts of India. © 8 findings in 1 5* 5*Plasma ferritin(<45.0 pmol/L) (%) 18 17 21Median (interquartile range) or INTRODUCTION percentages. *p<0.05, **p<0.01, ***p<0.001, different from to other ethnic groups. Inage concentration compared rural and adjusted for+ p<0.05, ++p<0.01, +++p<0.001, different from urban slums andCaucasian populations not eating folic acid fortified adjusted for age.778 E levated circulating total homocysteine (tHcy) concentration is a risk factor for cardiovascular food, hyperhomocysteinemia is usually explained by low blood folate concentrations. 10 In contrast, hyper- folate J  Assoc  Physicians  Ihomocysteinemia in Indians living in India is more • OCTOBER 2006 www.japi.org disease1,2 and elevated tHcy or lowS,  et  al.  and vitamin © JAPI • VOL. 54 Yajnik  C ndia.  2006  Oct;54:775-­‐82   B12 concentrations are a risk factor for birth defects, attributable to low concentrations of vitamin B12.4 poor pregnancy outcomes and neurocognitive performance.3-5 Indians in India 6,7 as well as those Eventhough low circulating vitamin B12 8, 9 concentration have been recognised in Indians for a long
  • 175. level of vitamin B12 of the study group (174 pmol/L) was of could well reach statistical journal homepage: www.nutritionjrnl.com borderline significance (P ¼ 0.067) compared with the control subjects were studied. AnaApplied nutritional investigation In the study group, only 4 of 24 participants group (269 pmol/L). difference in concentration of had plasma vitamin B12 levels below the lower limit of normalVegetarianism produces subclinical malnutrition, hyperhomocysteinemia groups (Table 2). In contrast,and atherogenesis cantly higher (18.6 mmol/L, P the control group (mean avYves Ingenbleek M.D. a, Kilmer S. McCully M.D. b, c, * !11.7 mmol/L). Plasma levelsa Table 2 Laboratory of Nutrition, Faculty of Pharmacy, University Louis Pasteur, Strasbourg, Francebc Pathology and Laboratory Medicine Service, VA Boston Healthcare System, West Roxbury, Massachusetts, USA Health and plasma indices Department of Pathology, Harvard Medical School, Boston, Massachusetts, USA 0.01) were significantly lower the control group. Indices Study group Control group P The Spearman correlationa r t i c l e i n f o a b s t r a c tArticle history: (n ¼ 24) (n ¼ 15) nutritional indicators, and di Objective: To explain why vegetarian subjects develop morbidity and mortality from cardiovascularReceived 30 December 2010 diseases unrelated to vitamin B status and Framingham criteria. Overall health status Methods: A study of 24 rural male subjects 18 to 30 y old and 15 urban male controls was con-Accepted 27 April 2011 Height (m) 1.68 Æ 0.3 1.73 Æ 0.3 NS ducted in the Sahel region of Chad. Food consumption was determined from a dietary question-Keywords: naire, and overall health status was assessed by body weight, body mass index, serum albumin, Weight (kg)Protein malnutrition 61.7 Æ 3.6 69.3 Æ 1.9 <0.05 plasma transthyretin, urinary nitrogen, and creatinine. Plasma lipids, vitamins B6, B9 and B12, Table 3Lean body mass 2Transthyretin Body mass index (kg/m ) 19.3 Æ 0.8 22.1 Æ 0.6 homocysteine, and related sulfur amino acids were measured as selected cardiovascular disease <0.05 Spearman correlation coefficients b risk factors.HomocysteineSulfur deficiency Serum albumin (g/L) Results: Body weight, body mass index, blood, and Æ 0.4 markers of protein status were signif- 3.8 Æ 0.6 4.3 urinary <0.05 indicators and significance Plasma transthyretin (mg/L)Cardiovascular disease 178.1 Æ 27.5 292.9 Æ 10.8 icantly lower, with an estimated 10% decrease of lean body mass in the study group compared <0.001 with urban controls. Neither lipid fractions nor plasma levels of vitamins B6, B9, and B12 were Nutritional indicator Study Urinary nitrogen (g/d) 9.6 Æ 0.9 11.2 Æ 0.9 <0.05 significantly different between the two groups. Although the mean consumption of sulfur amino À1 À1 Urinary creatinine (g/d) (10.4 mg$kg $dÀ1$dby0.37 subjects was significantly below the in the two groups. In acids allowances (13 mg$kg 1.18 )ÆÀ1),rural 1.43 Æ 0.26 <0.05 plasma methionine values were similar recommended dietary (n ¼ 2 Serum lipids contrast, homocysteine concentration was significantly increased (18.6 mmol/L, P < 0.001), and the levels of cysteine and glutathione were significantly decreased in the study group, demonstrating Triacylglycerols (mmol/L) of the trans-sulfuration pathway.1.08 Æ 0.41 correlation (r ¼ À0.71) between 0.85 Æ 0.55 NS r inhibition The strong negative Total cholesterol (mmol/L) transthyretin and homocysteine implicated lean body mass asNS critical determinant Body mass index 3.98 Æ 0.59 4.31 Æ 0.92 a of À0.139 hyperhomocysteinemia. HDL cholesterol (mmol/L) 1.21 Æ intake of protein and sulfur amino acids NS plant-eating population Conclusion: The low dietary 0.41 1.49 Æ 0.30 by a Serum albumin À0.273 LDL cholesterol (mmol/L) 2.27 Æ 0.32 2.12 Æ 0.25 NS leads to subclinical protein malnutrition, explaining the origin of hyperhomocysteinemia and the Plasma transthyretin À0.709 increased vulnerability of these vegetarian subjects to cardiovascular diseases. Plasma vitamins Urinary nitrogen Ó 2011 Elsevier Inc. All rights reserved. À0.357 Pyridoxine (B6, nmol/L) 41.9 Æ 7.4 52.4 Æ 13.8 NS Urinary creatinine À0.285 Folate (B9, nmol/L) 16.9 Æ 2.7 14.4 Æ 2.6 NS Triacylglycerols 0.215Introduction Cobalamin (B12, pmol/L) 174 Ædiabetes, and cancerÆ 36been documented by many investi- 28 269 have <0.06 Total cholesterol 0.188 Plasma SAAs gators [3,4], explaining their growing popularity in Westernized HDL cholesterol À0.315 According to World Health Organization estimates [1], 16.7 Methionine (mmol/L) 29.3 Æcountries during theÆ 4 several decades. It is estimated that cholesterol 3 28.0 past NS LDL 0.209million deaths are attributable to cardiovascular disease (CVD) about 2% to 5% of individuals living in developed countries have Homocysteine ( all deathseach year, accounting for 30% of mmol/L) worldwide 18.6 Æadopted vegetarianism as a lifestyle choice [5,6]. and 2.9 10.8 Æ 0.7 <0.001 Pyridoxine (B6) 0.189constituting an internationalmol/L) [2]. More than half of Æ 8.3 Cysteine (m pandemic 14.5 Plant-based regimens, however, do not optimally fulfill the 43.4 Æ 4.5 <0.001 Folate (B9) 0.237these deaths occur in developing countries where vegetarian nutritional requirements of population groups living in devel- Glutathione (mmol/L) and starchy foods Æoping countries, as illustrated by the increasing incidenceCobalamin (B12)diets consisting of several varieties of legumes 2.7 0.7 4.3 Æ 0.7 <0.01 of À0.175 Taurine (mmol/L)have prevailed for millennia. The beneficial health effects of such Æhyperhomocysteinemia 9 32 6 58 Æ (HHcy) states [7,8], now recognizedMethionine <0.01 as 0.260regimens in the prevention of chronic disorders such as CVD, a critical factor in occurrence of CVD and stroke [9]. HHcy was Cysteine À0.668 HDL, high-density lipoprotein; LDL, Nutricon.  2012  Feb;28(2):148-­‐53.   pathogenesis of atherosclerosis by originally associated with the Ingenbleek  Y,  McCully  KS.   low-density lipoprotein; SAA sulfur amino the study of the vascular pathology of children with inherited Glutathione À0.319 acid This work was funded by University Louis Pasteur, Strasbourg, France. disorders of methionine (Met) metabolism [10]. Dietary insuffi- * Corresponding author. Tel.: þ857-203-5990; fax: þ857-203-5623. Taurine À0.182 E-mailParameters of general health status and serum lipids, plasma vitamins, and address: kilmer.mccully@va.gov (K. S. McCully). ciency or malabsorption of any of three water-soluble B vitamins
  • 176. FONTES DE B12 BIODISPONÍVEL PARA VEGANSAlimento mcg/100  g !Brócolos, Espargos, Rebentos de feijão Mung >0,1  Folhas de Chá verde 0,1-­‐0,5  Folhas de Chá Vermelho 0,7  Folhas de chá preto 0,3-­‐1,2  Tempeh 0,7-­‐8  Natto 0,1-­‐1,5  Nori 32-­‐78  Alga Nostoc (Ishikurage) 99     (apenas  12%  é  accva)   Watanabe  F.  Exp  Biol  Med  (Maywood).  2007  Nov;232(10):1266-­‐74!
  • 177. VITAMINA B2
  • 178. DOSE DIÁRIA RECOMENDADA DE RIBOFLAVNA FOOD AND NUTRITION BOARDHomens RDA/AI* Limite (mg) Mulheres RDA/ Limi (mg) AI* te (mg) (mg) 0-12 0.3-0.4* Nd 0-12 meses 0.3-0.4 Nd meses *1-8 anos 0.5-0.6 Nd 1-8 anos 0.5-0.6 Nd 9-13 0.9 Nd 9-13 anos 0.9 Nd anos> 14 anos 1.3 Nd 14-18 anos 1.0 Nd < 18 anos 1.1 Nd Gravidez 1.4 Nd Lactação 1.6 Nd
  • 179. FONTES DE RIBOFLAVINA Cereais e Tiamina Carne, Leite e Tiamina Oleaginosas e Tiamina Leguminosas (mg/100g) Levedura (mg/100g) Hortaliças (mg/100g)Gérmen de Trigo 0,68 Levedura de Cerveja 4,28 Amêndoa 0,92Farelo de Trigo 0,35 Fígado de Borrego 3,28 Caju 0,25Centeio Integral 0,22 Fígado de Porco 3,03 Pinhão 0,23Millet 0,38 Fígado de Vitela 2,72 Sem. Girassol 0,23Arroz Selvagem 0,73 Fígado de Galinha 2,49 Cogumelos 0,46Farelo de Arroz 0,25 Gema de Ovo 0,44 Pimento vermelho 0,36Farinha de soja 0,35 Ovo 0,3 Couve 0,26Ervilha 0,29 Salmão 0,23 Salsa 0,26Lentilha 0,22 Bife de Porco 0,22 Brócolo 0,23Feijão Vermelho 0,21 Leite 0,18 Rábano 0,22Feijão Preto 0,21 Ameixa 0,22 Reservas duram 2-6 Semanas Liska D, Quinn S, Lukaczer D, et al. Clinical Nutrition: A Functional Approach. Second Edition. IFM; 2004.
  • 180. CONVERSÃO DA RIBOFLAVINA EM COENZIMAS OCORRE NO CITOPLASMA DE VÁRIAS CÉLULASShils ME, Shike M, Ross AC, Caballero B, Cousins RJ. Modern Nutrition in Health and Disease. Lippincott Williams & Wilkins; 2005.
  • 181. Marriage B, Clandinin MT, Glerum DM. Nutritional cofactor treatment in mitochondrial disorders. J Am Diet Assoc. 2003 Aug;103(8):1029-38
  • 182. VIT  B2  
  • 183. VITAMINA B3
  • 184. DOSE DIÁRIA RECOMENDADA DE NIACINA FOOD AND NUTRITION BOARDHomens RDA/AI* Limite (mg) Mulheres RDA/ Limit (mg) AI* e (mg) (mg) 0-12 2-4* Nd 0-12 meses 2-4* Nd meses1-8 anos 6-8 10-15 1-8 anos 6-8 10-159-18 anos 12-16 20-30 9-18 anos 12-16 20-30 Adultos 16 35 Adultos 14 35 Gravidez 18 30-35 Lactação 17 30-35
  • 185. FONTES DE VITAMINA B3210  
  • 186. 60 g B6, B2 Ferro, Cobre1g
  • 187. Marriage B, Clandinin MT, Glerum DM. Nutritional cofactor treatment in mitochondrial disorders. J Am Diet Assoc. 2003 Aug;103(8):1029-38
  • 188. EXCESSO Calor e rubor causado pela liberação de prostaglandinas durante a formação do ácido nicotinúrico (deriva da conjugada da niacina com a glicina) à Mais comum com Niacina de Libertação rápida Hepatotoxicidade à Mais comum com Niacina de Libertação lenta (a partir de 2 gramas) Diarreia, Náusea, Dispepsia, Dor Abdominal Resistência à Insulina Atraso no Crescimento em crianças à Mais comum com NicotinamidaShils ME, Shike M, Ross AC, Caballero B, Cousins RJ. Modern Nutrition in Health and Disease. Lippincott Williams & Wilkins; 2005. Gibney MJ, et al. Introduction to Human Nutrition (Nutrition Society Textbook). 2nd ed. Wiley-Blackwell; 2009.
  • 189. Antioxidants prevent health-promoting effects of physical exercise in humans ¨ Michael Ristowa,b,1,2, Kim Zarsea,2, Andreas Oberbachc,2, Nora Klotingc, Marc Birringera, Michael Kiehntopfd, ¨ Michael Stumvollc, C. Ronald Kahne, and Matthias Bluherc,2 aDepartment of Human Nutrition, Institute of Nutrition, University of Jena, Jena D-07743, Germany; bGerman Institute of Human Nutrition, Potsdam-Rehbrucke D-14558, Germany; cDepartment of Medicine, University of Leipzig, Leipzig D-04103, Germany; dInstitute of Clinical Chemistry and ¨ Laboratory Medicine, University of Jena, Jena D-07743, Germany; and eResearch Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215 Contributed by C. Ronald Kahn, March 31, 2009 (sent for review March 14, 2009) Exercise promotes longevity and ameliorates type 2 diabetes olism has been functionally connected with type 2 diabetes (11). mellitus and insulin resistance. However, exercise also increases Mitochondria, however, are also the main source of reactive mitochondrial formation of presumably harmful reactive oxygen oxygen species (ROS), which are inevitable by-products of species (ROS). Antioxidants are widely used as supplements but oxidative glucose metabolism. Muscle is also known to generate whether they affect the health-promoting effects of exercise is free radicals, especially during contraction and physical exercise unknown. We evaluated the effects of a combination of vitamin C (12). It has been suggested that ROS may mediate some health-ion on expression of (1000 mg/day) and vitamin E (400 IU/day) on insulin sensitivity as promoting effects, at least in nonprimate model systems (13–17). measured by glucose infusion rates (GIR) during a hyperinsuline- We here evaluated the possibility that ROS are required for tion of vitamins by mic, euglycemic clamp in previously untrained (n ‫ )91 ؍‬and pre- the insulin-sensitizing capabilities of physical exercise in healthy trained (n ‫ )02 ؍‬healthy young men. Before and after a 4 week humans and that commonly used antioxidants, such as vitamin intervention of physical exercise, GIR was determined, and muscle C and vitamin E, may abrogate the health-promoting effects ofhat physical exercise biopsies for gene expression analyses as well as plasma samples were obtained to compare changes over baseline and potential both physical exercise and oxidative stress in humans. Resultssulin sensitivity irre- influences of vitamins on exercise effects. Exercise increased pa- rameters of insulin sensitivity (GIR and plasma adiponectin) only in Baseline Characteristics. Of the 40 individuals included in thehat this induction is the absence of antioxidants in both previously untrained (P < 0.001) and pretrained (P < 0.001) individuals. This was paralleled present study, 20 were known to be previously trained, and 20 were previously untrained. Study subject characteristics in thetation. by increased expression of ROS-sensitive transcriptional regulators of insulin sensitivity and ROS defense capacity, peroxisome- preinterventional state are given in Table 1. No significant differences in age, height, body mass index, fat free mass, or VO2 proliferator-activated receptor gamma (PPAR␥), and PPAR␥ coac- maximum were observed within the groups (Table 1) and no tivators PGC1␣ and PGC1␤ only in the absence of antioxidants (P < significant differences in age, height and body mass index were fense Following Phys- 0.001 for all). Molecular mediators of endogenous ROS defense observed between untrained and pretrained groups. Not sur- (superoxide dismutases 1 and 2; glutathione peroxidase) were also prisingly, pretrained individuals had a significantly higher fat The transcriptional induced by exercise, and this effect too was blocked by antioxidant free mass (P ϭ 0.03) and VO2 maximum (P Ͻ 0.001). supplementation. Consistent with the concept of mitohormesis, Half of the previously untrained and previously trained groups only been linked to were randomly assigned to either antioxidant supplementation MEDICAL SCIENCES exercise-induced oxidative stress ameliorates insulin resistance as described in Methods or to no supplementation (creating 4een shown to induce and causes an adaptive response promoting endogenous antiox- idant defense capacity. Supplementation with antioxidants may groups of 10 each) (supporting information (SI) Fig. S1). All involved into detox- preclude these health-promoting effects of exercise in humans. subjects underwent a 4 week exercise training program irrespec- tive of antioxidant supplementation and previous training status. ncluding superoxide aging ͉ hormesis ͉ insulin resistance ͉ oxidative stress ͉ reactive oxygen species One untrained individual withdrew during the study for personal reasons unrelated to the experimental protocol.dase 1 (GPx1) and T ype 2 diabetes mellitus is increasing worldwide at epidemic Induction of Oxidative Stress by Short-Term Exercise. It is well-mical function (20). established that physical exercise increases ROS formation in Fig. rates complications (1). with both microvascular is caused by skeletal muscle (12); however, it is not knownof the health- 3. and is associated Type 2 diabetes mellitus and macro- Mitohormesis links physical exercise and subsequent formation if vascularexercise resulted in a a combination of insulin resistance involving sensitivity promoting effects of exercise are partly due to this effect. To reactive oxygen species to insulin a number of and antioxidant defense. Physical our specific replicate the ROS-inducing capacity of exercise in peripheral tissues, including skeletal muscle (2, 3), and an 2 G and H, Left pair exercise exerts ameliorating effectsincreased experimental set-up, bysubjected previously untrained individ- inadequate ␤-cell response despite normal or even on insulin resistance we increasing mito- uals to 3 days of exercise with muscle biopsy before (Fig. S1,g. 2 I and J, Left pair chondrialcirculating insulin. of reactive oxygen species in skeletal muscle to induceS1, ‘‘early’’). amounts of formation Physical exercise exerts numerous favorable effects on general ‘‘pre’’) and after this short-term intervention (Fig.
  • 190. Antioxidants prevent health-promoting effects of physical exercise in humans ¨ Michael Ristowa,b,1,2, Kim Zarsea,2, Andreas Oberbachc,2, Nora Klotingc, Marc Birringera, Michael Kiehntopfd, ¨ Michael Stumvollc, C. Ronald Kahne, and Matthias Bluherc,2 aDepartment of Human Nutrition, Institute of Nutrition, University of Jena, Jena D-07743, Germany; bGerman Institute of Human Nutrition, Potsdam-Rehbrucke D-14558, Germany; cDepartment of Medicine, University of Leipzig, Leipzig D-04103, Germany; dInstitute of Clinical Chemistry and ¨ Laboratory Medicine, University of Jena, Jena D-07743, Germany; and eResearch Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215 Contributed by C. Ronald Kahn, March 31, 2009 (sent for review March 14, 2009) Exercise promotes longevity and ameliorates type 2 diabetes olism has been functionally connected with type 2 diabetes (11). mellitus and insulin resistance. However, exercise also increases Mitochondria, however, are also the main source of reactive mitochondrial formation of presumably harmful reactive oxygen oxygen species (ROS), which are inevitable by-products of species (ROS). Antioxidants are widely used as supplements but oxidative glucose metabolism. Muscle is also known to generate whether they affect the health-promoting effects of exercise is free radicals, especially during contraction and physical exercise unknown. We evaluated the effects of a combination of vitamin C (12). It has been suggested that ROS may mediate some health-ion on expression of (1000 mg/day) and vitamin E (400 IU/day) on insulin sensitivity as promoting effects, at least in nonprimate model systems (13–17). measured by glucose infusion rates (GIR) during a hyperinsuline- We here evaluated the possibility that ROS are required for tion of vitamins by mic, euglycemic clamp in previously untrained (n ‫ )91 ؍‬and pre- the insulin-sensitizing capabilities of physical exercise in healthy trained (n ‫ )02 ؍‬healthy young men. Before and after a 4 week humans and that commonly used antioxidants, such as vitamin intervention of physical exercise, GIR was determined, and muscle C and vitamin E, may abrogate the health-promoting effects ofhat physical exercise biopsies for gene expression analyses as well as plasma samples were obtained to compare changes over baseline and potential both physical exercise and oxidative stress in humans. Resultssulin sensitivity irre- influences of vitamins on exercise effects. Exercise increased pa- rameters of insulin sensitivity (GIR and plasma adiponectin) only in Baseline Characteristics. Of the 40 individuals included in thehat this induction is the absence of antioxidants in both previously untrained (P < 0.001) and pretrained (P < 0.001) individuals. This was paralleled present study, 20 were known to be previously trained, and 20 were previously untrained. Study subject characteristics in thetation. by increased expression of ROS-sensitive transcriptional regulators of insulin sensitivity and ROS defense capacity, peroxisome- preinterventional state are given in Table 1. No significant differences in age, height, body mass index, fat free mass, or VO2 proliferator-activated receptor gamma (PPAR␥), and PPAR␥ coac- maximum were observed within the groups (Table 1) and no tivators PGC1␣ and PGC1␤ only in the absence of antioxidants (P < significant differences in age, height and body mass index were fense Following Phys- 0.001 for all). Molecular mediators of endogenous ROS defense observed between untrained and pretrained groups. Not sur- (superoxide dismutases 1 and 2; glutathione peroxidase) were also prisingly, pretrained individuals had a significantly higher fat The transcriptional induced by exercise, and this effect too was blocked by antioxidant free mass (P ϭ 0.03) and VO2 maximum (P Ͻ 0.001). supplementation. Consistent with the concept of mitohormesis, Half of the previously untrained and previously trained groups only been linked to were randomly assigned to either antioxidant supplementation MEDICAL SCIENCES exercise-induced oxidative stress ameliorates insulin resistance as described in Methods or to no supplementation (creating 4een shown to induce and causes an adaptive response promoting endogenous antiox- idant defense capacity. Supplementation with antioxidants may groups of 10 each) (supporting information (SI) Fig. S1). All involved into detox- preclude these health-promoting effects of exercise in humans. subjects underwent a 4 week exercise training program irrespec- tive of antioxidant supplementation and previous training status. ncluding superoxide aging ͉ hormesis ͉ insulin resistance ͉ oxidative stress ͉ reactive oxygen species One untrained individual withdrew during the study for personal reasons unrelated to the experimental protocol.dase 1 (GPx1) and T ype 2 diabetes mellitus is increasing worldwide at epidemic Induction of Oxidative Stress by Short-Term Exercise. It is well-mical function (20). established that physical exercise increases ROS formation in Fig. rates complications (1). with both microvascular is caused by skeletal muscle (12); however, it is not knownof the health- 3. and is associated Type 2 diabetes mellitus and macro- Mitohormesis links physical exercise and subsequent formation if vascularexercise resulted in a a combination of insulin resistance involving sensitivity promoting effects of exercise are partly due to this effect. To reactive oxygen species to insulin a number of and antioxidant defense. Physical our specific replicate the ROS-inducing capacity of exercise in peripheral tissues, including skeletal muscle (2, 3), and an 2 G and H, Left pair exercise exerts ameliorating effectsincreased experimental set-up, bysubjected previously untrained individ- inadequate ␤-cell response despite normal or even on insulin resistance we increasing mito- uals to 3 days of exercise with muscle biopsy before (Fig. S1,g. 2 I and J, Left pair chondrialcirculating insulin. of reactive oxygen species in skeletal muscle to induceS1, ‘‘early’’). amounts of formation Physical exercise exerts numerous favorable effects on general ‘‘pre’’) and after this short-term intervention (Fig.
  • 191. 2, shaded of the adipocyte-derived secretory protein adiponectin havengs (12), been shown to be positively correlated with insulin sensitivity in exercise humans and inversely correlated with type 2 diabetes risk (19).tioxidant Antioxidants prevent health-promoting effects We observe an increase in circulating adiponectin levels follow- st 3 days. of physical exercise inpreviously untrained humans ing physicalRistow , Kim Zarse , Andreas Oberbach , Nora Klo¨ting , Marc Birringer , Michaelindividuals exercise in both Michael a,b,1,2 a,2 c,2 c Kiehntopf , a d (Fig. 1C, Left pairC. of bars,and Matthias Blu¨her and pretrained individuals Michael Stumvoll , Ronald Kahn , P Ͻ 0.001) c e c,2g Physical (Fig. 1D, Left pair of bars, P Ͻ 0.001). In contrast, previously aDepartment of Human Nutrition, Institute of Nutrition, University of Jena, Jena D-07743, Germany; bGerman Institute of Human Nutrition, Potsdam-Rehbrucke D-14558, Germany; cDepartment of Medicine, University of Leipzig, Leipzig D-04103, Germany; dInstitute of Clinical Chemistry and ¨ Laboratory Medicine, University of Jena, Jena D-07743, Germany; and eResearch Division, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215 shown to Contributed by C. Ronald Kahn, March 31, 2009 (sent for review March 14, 2009) tabolism Exercise promotes longevity and ameliorates type 2 diabetes mellitus and insulin resistance. However, exercise also increases olism has been functionally connected with type 2 diabetes (11). Mitochondria, however, are also the main source of reactivey trained mitochondrial formation of presumably harmful reactive oxygen oxygen species (ROS), which are inevitable by-products of species (ROS). Antioxidants are widely used as supplements but oxidative glucose metabolism. Muscle is also known to generate whether they affect the health-promoting effects of exercise is free radicals, especially during contraction and physical exercise 85 min unknown. We evaluated the effects of a combination of vitamin C (1000 mg/day) and vitamin E (400 IU/day) on insulin sensitivity as (12). It has been suggested that ROS may mediate some health- promoting effects, at least in nonprimate model systems (13–17). (with or measured by glucose infusion rates (GIR) during a hyperinsuline- mic, euglycemic clamp in previously untrained (n ‫ )91 ؍‬and pre- We here evaluated the possibility that ROS are required for the insulin-sensitizing capabilities of physical exercise in healthymeasure- trained (n ‫ )02 ؍‬healthy young men. Before and after a 4 week humans and that commonly used antioxidants, such as vitamin intervention of physical exercise, GIR was determined, and muscle C and vitamin E, may abrogate the health-promoting effects of biopsies for gene expression analyses as well as plasma samples both physical exercise and oxidative stress in humans.R) during were obtained to compare changes over baseline and potential influences of vitamins on exercise effects. Exercise increased pa- Resultscted (5), rameters of insulin sensitivity (GIR and plasma adiponectin) only in the absence of antioxidants in both previously untrained (P < Baseline Characteristics. Of the 40 individuals included in the present study, 20 were known to be previously trained, and 20crease in 0.001) and pretrained (P < 0.001) individuals. This was paralleled were previously untrained. Study subject characteristics in the by increased expression of ROS-sensitive transcriptional regulators preinterventional state are given in Table 1. No significant of insulin sensitivity and ROS defense capacity, peroxisome- differences in age, height, body mass index, fat free mass, or VO2 exercise proliferator-activated receptor gamma (PPAR␥), and PPAR␥ coac- tivators PGC1␣ and PGC1␤ only in the absence of antioxidants (P < maximum were observed within the groups (Table 1) and no significant differences in age, height and body mass index werentrained: 0.001 for all). Molecular mediators of endogenous ROS defense (superoxide dismutases 1 and 2; glutathione peroxidase) were also observed between untrained and pretrained groups. Not sur- prisingly, pretrained individuals had a significantly higher fat ned: Fig. induced by exercise, and this effect too was blocked by antioxidant supplementation. Consistent with the concept of mitohormesis, free mass (P ϭ 0.03) and VO2 maximum (P Ͻ 0.001). Half of the previously untrained and previously trained groups were randomly assigned to either antioxidant supplementation MEDICAL SCIENCES exercise-induced oxidative stress ameliorates insulin resistance findings and causes an adaptive response promoting endogenous antiox- idant defense capacity. Supplementation with antioxidants may as described in Methods or to no supplementation (creating 4 groups of 10 each) (supporting information (SI) Fig. S1). All tivity. By preclude these health-promoting effects of exercise in humans. subjects underwent a 4 week exercise training program irrespec- tive of antioxidant supplementation and previous training status.retrained aging ͉ hormesis ͉ insulin resistance ͉ oxidative stress ͉ reactive oxygen species One untrained individual withdrew during the study for personal reasons unrelated to the experimental protocol. gnificant T ype 2 diabetes mellitus is increasing worldwide at epidemic Induction of Oxidative Stress by Short-Term Exercise. It is well- established that physical exercise increases ROS formation in rates and is associated with both microvascular and macro- r of bars, vascular complications (1). Type 2 diabetes mellitus is caused by a combination of insulin resistance involving a number of skeletal muscle (12); however, it is not known if the health- promoting effects of exercise are partly due to this effect. To physical peripheral tissues, including skeletal muscle (2, 3), and an inadequate ␤-cell response despite normal or even increased replicate the ROS-inducing capacity of exercise in our specific experimental set-up, we subjected previously untrained individ- uals to 3 days of exercise with muscle biopsy before (Fig. S1, ly in the Fig. 1. amounts of circulating insulin. Antioxidants prevent exercise-dependent induction of insulin sensi- Physical exercise exerts numerous favorable effects on general ‘‘pre’’) and after this short-term intervention (Fig. S1, ‘‘early’’).
  • 192. Mari-Carmen Gomez-Cabrera, Elena Domenech, Marco Romagnoli, Alessandro Arduini, Consuelo Borras,one concentrations and increases ˜ a muscle and blood glutathi-oxidative stress, as indicated by alteredFederico V Pallardo, Juan Sastre, and Jose Vinin protein, DNA, and lipid peroxi- beneficial eff exerts processesdation. There is, and increases inC decreases muscle regarding the bene- one concentrations however, considerable debate lipid peroxi-ABSTRACT Oral administration of vitamin protein, DNA, and processes (10) and ha mitochondrial can exert favorable effects and c and mice dation. There is, and hampers training-induced adaptationstheendurance and mice (12). however, considerable debate regarding 9). Thus, ROS genes (8, bene-Background: Exercise practitioners vitamin C supplementation. in process of training adaptation. Up-regulatificial biogenesis 1–3 of often take vitamin C supple- involved in the health effects The m ficial health effects of vitamin C supplementation.endogenous antioxidant systemsThe maximal capa performancements because intense muscular contractile activity can result inObjective: This study was designedglutathi- effect of vitamin C in the preventionduringVtra Objective: This study altered muscle Marcoto study the Arduini, Consuelo Borras,oxidative stress, as indicated by was designed blood and to studyexerts effect of vitamin in responseof chronic˙ di the beneficial effects during exercise is ex C to regular O Mari-Carmen Gomez-Cabrera, Elena Domenech, Romagnoli, Alessandroone concentrations efficiencyprotein, Vina and lipidhumans.on training Vefficiency in ratsrats in humans. on trainingPallardo, Juan Sastre, in and Federico and increases in and Jose DNA, and in peroxi-dation. There is, however, considerable debate regarding the bene- ˜ processes (10) and has also been related to longevity of a and mice (12). limit in flies limit of a person’s or aDesign:The Exercise practitionerssupplementation. double-blindROSofcan exert adaptation.effects and canFour-transport and runnin Design: effectshuman study waswassupple- genes (8, in the process The maximal capacity to take up, during a utilize ox ABSTRACTficial health The human study double-blind and randomized. Four- belevel Background: of vitamin C often take vitamin C involved 9). Thus, and randomized. of training favorable Up-regulation level duri ments because intense muscular contractilestudy the effect of vitamin C activity can result in endogenous antioxidant systems in response to˙regular trainingObjective: Thisstress, as indicated by altered muscle and blood glutathi- 8 wk. Fiveduring exercise is VO2max (13). Endurance is defined as the teen men (27–36designed to were trained for 8 wk. inthepreventionthe diseasestudies of humans wi oxidative study was old) were trained forteenmen (27–36 increases in protein, DNA, and lipid peroxi- exerts beneficial effects Five of longevitymen were to maintain a specific p y y old) of the men were of chronic studies ofon training efficiency and rats and in humans. one concentrations in processes (10) and has also beena person’s or animal’s ability limit of related to in flies (11)Design: The health effects of daily withoral oral dose mice (12).g vitamin C. In the animallow aerobic exesupplemented vitaminwith an anandthe bene- 1 gof 1 capacity to take up, transport and utilize oxygenthat Large-scale epidemio supplemented however,was double-blind dose of and Four- levelIn theaanimal protocol (14). dation. There is, study considerable debate regarding randomized. vitamin C. ficial human daily C supplementation. during running that low The maximal Downloaded from www.ajcn.org by on June 29, 2009teen menObjective: This studywere trained forthe effect of vitamin C men were 2isdifferent protocolsasand without cardiovascular diseasestudy,24 male Wistar ratsrats vitamin exercised or that 2ability to maintain a specific power study,on 24 male Wistar were exercised under (27–36 y old) was designed to study 8 wk. Five of the during exercise VO max (13).of humans with the timemortality than are oth ˙ studies Endurance is definedsupplemented daily withinanwas double-blind and gwereFour-In the animal under low aerobic exercise capacity is an stronger predict limit of a person’s animal’s different protocols mortality 2 training efficiency rats and in humans. 1 oral dose of randomized. C. for 3 and Wistar ratswere trained for 8 wk. Five of the2men were level during running and withoutthan are other established risk factors, such as diab Design:6 wk. study The human Twelve of the rats were treateda withprotocol (14). Large-scale epidemiologicstudy,3 teen men (27–36 y old) were exercised under different studies of humans with a daily dose of showsmoking, hypertensifor andsupplemented daily with anthe rats2wereof C. In the animaldaily doseaerobic exercise capacitycardiovascular diseasedose of 24 and 6 wk. Twelve male 6 C (0.24 of Twelve mg/cm undertreated protocols the rats were treated with an stronger predictor of oral dose of 1 g vitamin surface area). of protocols mortality a daily vitaminwk.male Wistar rats were exercisedbody with a mortality than are other established risk factors, such as diabetes,ease obstructive pulmonary smoking,for 3 2 2 different that low smoking, hypertension, or chronic (15–18). These isvitaminand wk. Twelve body surface area). vitamin C significantlychronic҃ 0.014) dis-impaired regulation for 3 C (0.24 mg/cm study, 24 2 body surface area).ease (P obstructive pulmonaryvitamin C (0.246 mg/cm of the rats were treated with a daily dose of smoking, hypertension, or (15–18). These observations are consistent with the ro Results: The administration of 2 ease (15–Results: Results: The administration of vitamin C significantly (P ҃ 0.014) ҃ vitamin C (0.24 mg/cm body surface area). C significantly (P ease0.014) These observations are consistent with the role ofResults:administration ofcapacity.ofThe C may impaired regulationofmitochondrial(19). The(Paerobic capacity (19). Thefor an impo The vitamin (15–18).hampered endurance capacity. hampered endurance administration of vitamin effects impaired regulation of mitochondrial function as low a hampered enduranceThe adverse effects effects adverseC may significantlylow an҃amongmechanism relations am Thecapacity. The adverse vitamin ofvitamin C low aerobic capacity for may important mechanism for mechanism C relations of vitamin function as 0.014) impairedresult from its capacity to reduce the mitochondrial biogenesis.expression muscle effects ofendurance of C capacity, endurance capacityhamperedits capacity to reduce the to exercise-inducedof adverse oxidativemax, muscle oxidativeforVO2max, muscle ox result resulttranscriptioncapacity exercise-induced expressionexercise-induced2 expression discussed andmay from its factors involved incapacity. The maximal aerobic workload capacity, have been capacity, ˙ endurance reduce the VO capacity vitamin ˙ mechanis from 2 ˙ VO max, of keykey transcription factors involved in mitochondrial biogenesis. maximal aerobic workload capacity have been discusse These factors are peroxisome proliferator–activated receptor co-resultactivator 1, nuclear respiratory prevented mitochondrial transcrip- receptor co-the mitochondrialbiogenesis. al major concluded aerobic oxid key transcription factors to reduce in capacity (ie, from its capacity involved mitochondrial (20). Davies etThese factors are Vitamin C alsofactor 1, andthe exercise-induced ex-the exercise-induced muscle) was a (21)maximalthat O2max, tion factor A. peroxisome proliferator–activated years content of expression of years (20). Davies et al (21) concluded that muscle oxidative ˙ ˙ Vmuscle wo determinant of endurance capacity, whereas VO max was onlyactivator pression of cytochrome C (aperoxisome content) and of transcrip- to endurance capacity thewas directly relatedyears (20). Daviesa e These 1,factors are marker of mitochondrial proliferator–activated receptor co-key transcription factor 1, andtheinvolved exerciserelated capacity (ie, but mitochondrial content of muscle) was m nuclear respiratory factors mitochondrial indirectlyex-mitochondrial biogenesis. in 2 the antioxidant enzymes superoxide dismutase and glutathione per-tion factor A. Vitamin C also prevented exercise-induced intensity.determinant of endurance capacity, whereas VO2max was to In eukaryotic cells, mitochondrial biogen- maximal ˙ activator 1, oxidase. nuclear respiratory factor 1, and requires gene products from 2 physically separated ge-capacity (ie, the mitopression of cytochrome Care peroxisome proliferator–activated receptor co- esis mitochondrial transcrip-These factors it (a marker ofcellular adaptations content) andone contained within the organelle and the other con- capacity but years (20 mitochondrial Conclusion: Vitamin C supplementation decreases training nomes— of indirectly related to endurance was directly re tion factorenzymes superoxide dismutase and glutathione within the nucleus. Peroxisome proliferator–activateddeterminant of endur efficiency A. Vitamin C also prevented the exercise-induced ex- because prevents somethe antioxidant Am J Clin Nutr 2008;87:142–9. to tained per-activator 1, nuclear respiratory factor 1, nuclear receptors. Itrequires induces mRNA eukaryotic cells, mitochondrial biooxidase. exercise. of to exercise intensity. In receptor and mitochondrial transcrip- co-activator 1 (PGC-1) is a recently identified coacti- pression of cytochromeVCmax, antioxidant enzymes,mitochondrial content)factors such as expres-indirectly related to e (a marker of vatorfor important nuclear transcription and of nuclear from 2 physically separated esis powerfully gene products capacityConclusion: Vitamin Vitamin C also prevented the exercise-induced ex-tion factorsupplements, exercise, exhaustion, vitamins,decreases sion factor 1nomes— one contained within the organelle and the other antioxidant A. KEY WORDS Free radicals, ˙ O C supplementation gene ex- training determin 2 the antioxidant it preventsspecies cellular adaptations toandtained and mitochondrial transcriptionPeroxisome proliferator–acti enzymes someefficiency because reactive oxygen pression, hormesis, superoxide dismutase respiratory glutathione per- (NRF-1) within the nucleus. to exercise intensity.pression Am cytochrome C (a marker of mitochondrial content) and ofarequires gene co oxidase. of J Clin Nutr 2008;87:142–9.exercise. 1 receptor co-activator 1 (PGC-1) is recently identified p From the Department of Physiology, Faculty of Medicine, University of Valencia, Valencia, Spain (M-CG-C, ED, AA, FVP, JS, and JV); the Catholic esis indirectly INTRODUCTIONthe WORDSphysicalFreeenzymesmax, antioxidant enzymes, decreasesnuclear receptors. It powerfully inducesexercis antioxidant radicals, VO supplementation Conclusion: Vitamin augmented generation of re- Acute exercise induces C 2 ˙ superoxide dismutase and glutathione nomes— one such as exKEY active oxygen species (ROS) in muscle and in other organs (1–3). vator of training University of Valencia, Valencia, Spain (CB); and the Polytechnic Univer- sity of Valencia, Valencia, Spain (MR). 2 sion for important nuclear transcription per- factors mRNA nu to contain Supported by grants no. SAF 2004-03755 (to JV) and GV06/289 (toantioxidant supplements, exercise, accepted over the pastsome gene ex-oxidase. of that,thehas been generally antioxidants withinvitamins, cellular respiratory factor 1to efficiency because it prevents 20 y adaptations (NRF-1) and mitochondrial the ntained within transcri Because that increasing it concentrations of exhaustion,pression,cle cell should provide greaterClin speciesthese oxidizing hormesis, reactive oxygen Nutr 2008;87:142–9. M-CG-C) and by la Red Tematica de investigacion cooperativa en enveje- ´ ´ cimiento y fragilidad (RETICEF) from the Instituto de Salud Carlos III a mus- esis requ exercise.Conclusion:Am fatigue (4 –7). However, thesupplementation From the Department oftraining of Medicine, Univer J protection C Vitaminagainst functional (ISCIII2006-RED13-027). 3 decreases Physiology, Faculty co-activator receptor nomes— Reprints not available. Address correspondence to J Vina, Department of 1 agents and should reduce Physiology, Faculty of Medicine, Blasco Ibanez, 15, Valencia, Spain 46010. ˜ significance of exercise-induced oxidative stress is open to dis-
  • 193. soreness following muscle-damaging exercise but may delay the recoveryprocess British Journal of Nutrition (2006), 95, 976–981 DOI: 10.1079/BJN20061732 q The Authors 2006Graeme L. Close1*, Tony Ashton2, Tim Cable1, Dominic Doran1, Chris Holloway1, Frank McArdle2 Ascorbic acid supplementation does not attenuate post-exercise muscleand Don P. M. MacLaren1 soreness following muscle-damaging exercise but may delay the recovery1 process Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Henry Cotton Campus, 15– 21Webster Street, Liverpool L3 2ET, UK2 School of Clinical Sciences,L. Close1*, Tony Ashton2, Tim Cable1, Dominic Doran1, Chris Hollowayof Frank McArdle2 Graeme Division of Metabolic and Cellular Medicine, University 1, Liverpool, Liverpool L69 3GA, UK and Don P. M. MacLaren1(Received 7 October 2005 –Research Institute for Sport 2005 – Accepted 19 Liverpool John Moores University, Henry Cotton Campus, 15– 21 1 Revised 15 December and Exercise Sciences, December 2005) Webster Street, Liverpool L3 2ET, UK 2 School of Clinical Sciences, Division of Metabolic and Cellular Medicine, University of Liverpool, Liverpool L69 3GA, UK (Received 7 October 2005 – Revised 15 December 2005 – Accepted 19 December 2005)Exercise involving lengthening muscle actions, such as downhill running, results in delayed onset muscle soreness (DOMS), which may be attribu-table to reactive oxygen species (ROS). Although exercise causes oxidative stress, any link between ROS and DOMS remains speculative. There isemerging evidence to suggest reactiveROS play an important physiological role, inany link between the and DOMS remains speculative. There is Exercise involving lengthening muscle actions, such as downhill running, results delayed onset muscle soreness (DOMS), which may be attribu- table to that oxygen species (ROS). Although exercise causes oxidative stress,assisting in ROS recovery process and protecting the cell from futuredamage; however, this has not been fully established. Despite this uncertainty as tointhe recovery process and protecting the cell from future emerging evidence to suggest that ROS play an important physiological role, assisting the precise role of ROS, attempts to prevent post-exercise ROSproduction through antioxidant intervention been fully established. common. The study investigated precise role of effectsacid supplementation on ROS ROS damage; however, this has not Despite this uncertainty as to the of ROS, attempts to prevent post-exercise production through antioxidantare still common. The study investigated the ascorbic of ascorbic acid supplementation on ROS pro- intervention are still the effects pro-duction and DOMS following and DOMS following downhill running. Subjects were assigned to two groups. The ascorbic acid group (group AA)group (group AA) received 1 g ascorbic duction downhill running. Subjects were assigned to two groups. The ascorbic acid received 1 g ascorbic acid 2 h pre-, and for 14 d post-downhill running, whilst the placebo group (Pl group) received a placebo. Blood samples were drawn pre-sup-acid 2 h pre-, and for 14plement, pre- and post-exercise, and then 1, 2, 3,the7 placebo group (Pl analysis of ascorbate, malonaldehyde and Blood samples were drawn pre-sup- d post-downhill running, whilst 4, and 14 d post-exercise for group) received a placebo. total glutathione.plement, pre- and post-exercise, and then a 2, analogue and 14 d post-exercise for analysis of ascorbate, malonaldehyde and total glutathione. DOMS was assessed using 1, visual3, 4, 7 scale and pressure algometry. Muscle function was assessed using isokinetic dynamometry. Plasma ascorbate was elevated throughout in group AA compared with the Pl group. Downhill running resulted in DOMS in both groups.DOMS was assessed using a visual analogue scale inand groups, although a delayed recovery was noted in group AA. Malonaldehyde increased 4 d isokinetic dynamometry. Muscle function was impaired post-exercise both pressure algometry. Muscle function was assessed usingPlasma ascorbate was elevated throughout in group AA supplementation with the Plproduction following downhill running, without affecting DOMS in both groups. post-exercise in the Pl group only. Ascorbic acid compared attenuates ROS group. Downhill running resulted in DOMS. Furthermore, ascorbic acid supplementation may inhibit the recovery of muscle function.Muscle function was impaired post-exercise in both groups, although a delayed recovery was noted in group AA. Malonaldehyde increased 4 dpost-exercise in the Pl group oxygen species: Exercise: Eccentric muscle torque: Antioxidants: Muscle damage Reactive only. Ascorbic acid supplementation attenuates ROS production following downhill running, without affectingDOMS. Furthermore, ascorbic acid supplementation may inhibit the recovery of muscle function. Unaccustomed or excessive exercise often results in the sen- or is an essential physiological process assisting in the recov-Reactive oxygen species: Exercise: Eccentric and pain that is characterised sation of muscular discomfort muscle torque: Antioxidants: Muscle damage reason for this is that merely ery from the initial trauma. The by its delay in onset and has been termed ‘delayed onset the presence of ROS cannot determine if their production is muscle soreness’ (DOMS) (Newham et al. 1983). DOMS is involved in the observed pathology. The only way that ROS often first noticed 24 h post-exercise and presents as a dull can be confirmed to be involved in the pathology is through ache similar to that of a bruise. Despite extensive research specific intervention (Jackson, 1999). Despite this uncertaintyUnaccustomed or excessive exercise often results in the sen- into DOMS, the underlying causes and methods of prevention asor is an essential physiological process assisting in the recov- to the exact role of ROS following contraction-induced remain unresolved (Close et al. 2005). damage, it is common practice for athletes to use antioxidantsation of muscular discomfort and pain that is characterised We have previously demonstrated that 30 min of downhill therapy from the initial trauma. The reason for this is that merely ery to prevent post-exercise ROS production and, further-by its delay in onsetand a significantbeen intensity ‘delayed damage running at a sub-maximaltermed results in muscleonset and has increase in reactive oxygen species (ROS) more, there is still extensive research investigating ways to if their production is the presence of ROS cannot determine prevent DOMS and muscle damage using antioxidant sup-muscle soreness’ (DOMS) (Newham etlipid peroxidation DOMS is production and subsequent al. 1983). in the days fol- plementation (Jakeman & observed pathology. The only way that ROS involved in the Maxwell, 1993; Goldfarb, 1999;often first noticed 24lipidpost-exercise speculated to be due as increase in lowing the exercise (Close et presentsThis a dull h peroxidation was and al. 2004). to phagocyte- Thompson et confirmed to be involved in the pathology is through al. 2001a). can beacid is a water-soluble, dietary antioxidant present Ascorbicache similar to that of a bruise. Despite extensive research derived superoxide (O2z2) production resulting in the sub- in specific intervention the cell and the 1999). Despite this uncertainty the cytosolic compartment of (Jackson, extracellularinto DOMS, the underlying formation is still methods of hydroxyl of ROS sequent causes and unclear ifpotentproduction radical (zOH). However, it of the more this prevention fluid, and is known to be a powerful inhibitor of lipid peroxi- as to the exact role of ROS following contraction-induced dation (Powers et al. 2004), in conjunction with a-tocopherol
  • 194. soreness following muscle-damaging exercise but may delay the recoveryprocess British Journal of Nutrition (2006), 95, 976–981 DOI: 10.1079/BJN20061732 q The Authors 2006Graeme L. Close1*, Tony Ashton2, Tim Cable1, Dominic Doran1, Chris Holloway1, Frank McArdle2 Ascorbic acid supplementation does not attenuate post-exercise muscleand Don P. M. MacLaren1 soreness following muscle-damaging exercise but may delay the recovery1 process Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Henry Cotton Campus, 15– 21Webster Street, Liverpool L3 2ET, UK2 School of Clinical Sciences,L. Close1*, Tony Ashton2, Tim Cable1, Dominic Doran1, Chris Hollowayof Frank McArdle2 Graeme Division of Metabolic and Cellular Medicine, University 1, Liverpool, Liverpool L69 3GA, UK and Don P. M. MacLaren1(Received 7 October 2005 –Research Institute for Sport 2005 – Accepted 19 Liverpool John Moores University, Henry Cotton Campus, 15– 21 1 Revised 15 December and Exercise Sciences, December 2005) Webster Street, Liverpool L3 2ET, UK 2 School of Clinical Sciences, Division of Metabolic and Cellular Medicine, University of Liverpool, Liverpool L69 3GA, UK (Received 7 October 2005 – Revised 15 December 2005 – Accepted 19 December 2005)Exercise involving lengthening muscle actions, such as downhill running, results in delayed onset muscle soreness (DOMS), which may be attribu-table to reactive oxygen species (ROS). Although exercise causes oxidative stress, any link between ROS and DOMS remains speculative. There isemerging evidence to suggest reactiveROS play an important physiological role, inany link between the and DOMS remains speculative. There is Exercise involving lengthening muscle actions, such as downhill running, results delayed onset muscle soreness (DOMS), which may be attribu- table to that oxygen species (ROS). Although exercise causes oxidative stress,assisting in ROS recovery process and protecting the cell from futuredamage; however, this has not been fully established. Despite this uncertainty as tointhe recovery process and protecting the cell from future emerging evidence to suggest that ROS play an important physiological role, assisting the precise role of ROS, attempts to prevent post-exercise ROSproduction through antioxidant intervention been fully established. common. The study investigated precise role of effectsacid supplementation on ROS ROS damage; however, this has not Despite this uncertainty as to the of ROS, attempts to prevent post-exercise production through antioxidantare still common. The study investigated the ascorbic of ascorbic acid supplementation on ROS pro- intervention are still the effects pro-duction and DOMS following and DOMS following downhill running. Subjects were assigned to two groups. The ascorbic acid group (group AA)group (group AA) received 1 g ascorbic duction downhill running. Subjects were assigned to two groups. The ascorbic acid received 1 g ascorbic acid 2 h pre-, and for 14 d post-downhill running, whilst the placebo group (Pl group) received a placebo. Blood samples were drawn pre-sup-acid 2 h pre-, and for 14plement, pre- and post-exercise, and then 1, 2, 3,the7 placebo group (Pl analysis of ascorbate, malonaldehyde and Blood samples were drawn pre-sup- d post-downhill running, whilst 4, and 14 d post-exercise for group) received a placebo. total glutathione.ASCORBIC ACID SUPPLEMENTATION ATTENUATES ROS PRODUCTIONplement, pre- and post-exercise, and then a 2, analogue and 14 d post-exercise for analysis of ascorbate, malonaldehyde and total glutathione. DOMS was assessed using 1, visual3, 4, 7 scale and pressure algometry. Muscle function was assessed using isokinetic dynamometry. Plasma ascorbate was elevated throughout in group AA compared with the Pl group. Downhill running resulted in DOMS in both groups.DOMS was assessed using a visual analogue scale inand groups, although a delayed recovery was noted in group AA. Malonaldehyde increased 4 d isokinetic dynamometry. Muscle function was impaired post-exercise both pressure algometry. Muscle function was assessed using FOLLOWING DOWNHILL RUNNING, WITHOUT AFFECTING DOMS.Plasma ascorbate was elevated throughout in group AA supplementation with the Plproduction following downhill running, without affecting DOMS in both groups. post-exercise in the Pl group only. Ascorbic acid compared attenuates ROS group. Downhill running resulted in DOMS. Furthermore, ascorbic acid supplementation may inhibit the recovery of muscle function.Muscle function was impaired post-exercise in both groups, although a delayed recovery was noted in group AA. Malonaldehyde increased 4 dFURTHERMORE, ASCORBIC ACID SUPPLEMENTATION MAY INHIBIT THEpost-exercise in the Pl group oxygen species: Exercise: Eccentric muscle torque: Antioxidants: Muscle damage Reactive only. Ascorbic acid supplementation attenuates ROS production following downhill running, without affectingDOMS. Furthermore, ascorbic acid supplementation may inhibit the recovery of muscle function. RECOVERY OF MUSCLE FUNCTION. Unaccustomed or excessive exercise often results in the sen- or is an essential physiological process assisting in the recov-Reactive oxygen species: Exercise: Eccentric muscle torque: Antioxidants: Muscle damage sation of muscular discomfort and pain that is characterised ery from the initial trauma. The reason for this is that merely by its delay in onset and has been termed ‘delayed onset the presence of ROS cannot determine if their production is muscle soreness’ (DOMS) (Newham et al. 1983). DOMS is involved in the observed pathology. The only way that ROS often first noticed 24 h post-exercise and presents as a dull can be confirmed to be involved in the pathology is through ache similar to that of a bruise. Despite extensive research specific intervention (Jackson, 1999). Despite this uncertaintyUnaccustomed or excessive exercise often results in the sen- into DOMS, the underlying causes and methods of prevention asor is an essential physiological process assisting in the recov- to the exact role of ROS following contraction-induced remain unresolved (Close et al. 2005). damage, it is common practice for athletes to use antioxidantsation of muscular discomfort and pain that is characterised We have previously demonstrated that 30 min of downhill therapy from the initial trauma. The reason for this is that merely ery to prevent post-exercise ROS production and, further-by its delay in onsetand a significantbeen intensity ‘delayed damage running at a sub-maximaltermed results in muscleonset and has increase in reactive oxygen species (ROS) more, there is still extensive research investigating ways to if their production is the presence of ROS cannot determine prevent DOMS and muscle damage using antioxidant sup-muscle soreness’ (DOMS) (Newham etlipid peroxidation DOMS is production and subsequent al. 1983). in the days fol- plementation (Jakeman & observed pathology. The only way that ROS involved in the Maxwell, 1993; Goldfarb, 1999;often first noticed 24lipidpost-exercise speculated to be due as increase in lowing the exercise (Close et presentsThis a dull h peroxidation was and al. 2004). to phagocyte- Thompson et confirmed to be involved in the pathology is through al. 2001a). can beacid is a water-soluble, dietary antioxidant present Ascorbicache similar to that of a bruise. Despite extensive research derived superoxide (O2z2) production resulting in the sub- in specific intervention the cell and the 1999). Despite this uncertainty the cytosolic compartment of (Jackson, extracellularinto DOMS, the underlying formation is still methods of hydroxyl of ROS sequent causes and unclear ifpotentproduction radical (zOH). However, it of the more this prevention fluid, and is known to be a powerful inhibitor of lipid peroxi- as to the exact role of ROS following contraction-induced dation (Powers et al. 2004), in conjunction with a-tocopherol
  • 195. ys a ory,nses rainwth, andatedROS rain ugh 83]; cor- tiontion, the the s of Fig. 1. The redoxRadak  Z,  Chung  HY,  Goto  S.  Free  Radic  Biol  changes as a result of single bout of homeostasis-associated Med.  2008  Jan  15;44(2):153-­‐9.   exercise and regular exercise compared to physical inactivity. Sedentary
  • 196. Z. Radak et al. / Ageing Research Reviews 7 (2008) 34–42mesis curve and the effects of exercise. Moderate exercise increases the physiological function of different orgainst diseases and improves quality of life. Physical inactivity and strenuous exercise and overtraining in
  • 197. Pflügers Arch - Eur J Physiol (2002) 443:791–797 DOI 10.1007/s00424-001-0770-0 O R I G I N A L A RT I C L E P. Tauler · A. Aguiló · E. Fuentespina · J. A. Tur A. Pons Diet supplementation with vitamin E, vitamin C and β-carotene cocktail enhances basal neutrophil antioxidant enzymes in athletes 795Table 2 Basal neutrophil glutathione of/ Accepted: 10 October 2001 / Published online: 31 January 2002 Received: 14 June 2001 sportsmen before and after supplementation with antioxidants. The results are the mean ±s.e.m.of ten subjects in the placebo group 2002 ten subjects in the antioxidant-supplemented group © Springer-Verlag and Initial Final ANOVA Abstract Exercise increases oxygen consumption and Introduction causesPlacebo a disturbance of intracellular pro-oxidant-antioxi- Supplemented Placebo Supplemented G×T G T dant homeostasis. Few data are available as to the cumu- Exercise increases oxygen consumption and causes a lative effects of exercise on the antioxidant defenses of disturbance of intracellular pro-oxidant-antioxidant ho-Total glutathione the neutrophil. We studied the effects of 90 days’ supple- meostasis [21]. The mitochondrial electron transportnmol/ml of blood mentation with placebo or2.41±0.09a cocktail of vi- chain [26], 2.36±0.16a 2.34±0.08a an antioxidant 2.06±0.20b polymorphonuclear neutrophils [27],* and * *nmol/109neutrophils tamin E (500 mg/day) and991±37a (30 mg/day) 793±33b 961±33a β-carotene and xanthine oxidase [29] have been identified as major 989±41a * * * the last 15 days also with vitamin C (1 g/day) on sports- sources of intracellular reactive oxygen species (ROS) men’s basal neutrophil antioxidant defenses. We ana- and free radical generation during exercise. The cellularGSH lyzed the activities of catalase, glutathione peroxidase, antioxidant defense systems have demonstrated great ad-nmol/ml of blood 2.18±0.12 the activities 1.99±0.12 2.22±0.10# glutathione reductase and 2.20±0.14 and levels of su- aptation to acute and chronic exercise [32]. However, ex- *nmol/10 9 neutrophils peroxide dismutase, glutathione and glutathione disul- treme physical exercise causes oxidative damage to * 887±33 900±37 700±39 901±48# well- fide in neutrophils purified from antecubital vein blood trained athletes, as indicated by an increase in plasma of sportsmen before and after diet supplementation. Plas- levels of malondialdehyde [22, 28] and conjugated di-GSSG ma vitamin E, β-carotene and vitamin C concentrations enes [28] or by an increase in urine 8-hydroxydeoxygua-nmol/ml of blood in the0.10±0.01 0.10±0.01 0.13±0.01& 0.11±0.01a antioxidant-supplemented group were approxi- nosine (8-OhdG) after an ultra-marathon [41] and as also *nmol/10 9 neutrophils mately 1.6, 10, and 1.2 times higher respectively 52.7±1.3& 44.1±3.3 45.0±2.7 than indicated by46.9±1.6a in erythrocyte catalase activity an increase * those of the placebo group. The antioxidant-supplement- after a duathlon competition [45]: in these situations ofGSH/GSSG ed group presented a significantly higher glutathione strenuous exercise the# antioxidant defenses are over- 20.2±1.9 20.5±2.3 13.8±1.8 19.4±2.0 * versus glutathione disulfide ratio in neutrophils (about whelmed [28]. Recent studies point to negative effects of* Significant effects of20%) than the or the interaction G×Tsupplementation Significant differences between placebo of and supplemented factor G, T placebo one. Antioxidant (two-way # oxidative stress in sportsmen on the functionality dif- enhances the antioxidant enzyme activity of superoxide ferent cells of the immune system [38]. EpidemiologicalANOVA). Factor G representsand catalase antioxidant supplementa- groups (Student’shigher risk of upper respiratory tract in- dismutase the diet in neutrophils. reports suggest a t-test for unpaired data, P<0.05)tion; factor T represents the training and competition period; G×T & Significant differences betweenprolonged and final values (Stu- fection in endurance athletes due to initial exercise,represents the interaction between the two factors. Different letters dent’s t-test for unpaired data, P<0.05)perturbation of Keywords Antioxidants · Exercise · Glutathione · which leads to a transient yet significantindicate significant Neutrophil · values (ANOVA one-way test, different Oxidative stress immune and host defenses [39]. Some studies haveP<0.05) when a significant G×T interaction is observed shown that diet supplementation with vitamin C reduces the risk of upper respiratory tract infection [39]. The phagocytic cell of the immune system, which is
  • 198. Alimento Ascorbato (mg)Acerola 1300Pimientos Vermelhos 369Goiaba 242Couve 186Pimentos verdes 128Brócolos 113Couve de Bruxelas 102Couve-Flor 78Morango 59Papaia 56Espinafre 51Laranja 50Toranja 38Manga 35Tangerina 31
  • 199. COUVES DE BRUXELAS CONGELADAS DURANTE 6 MESES APRESENTAMMENOS 14 A 32% DE VITAMINA C EM RELAÇÃO AO MOMENTO DA COLHEITA. Kmiecik  W,  Lisiewska  Z.  Rocz  Panstw  Zakl  Hig.  1989;40(3):215-­‐22.  
  • 200. bic acid content when it is affected by different pressure levels. They determinedthat after low pressures the Ascorbic acid content was greater than after highpressures. J. Nutr. Sci. Vitaminol., 36, S7-S15, 1990 Of course, cooking duration and the type of foodstuff play an important role asshown by some of our unpublished tests. Products, which need a long cookingperiod, like cabbage and Vitamin soup, showed a higher Ascorbic acid content after Comparison of bean Losses in Vegetables Due to Variouspressure cooking than after steaming. On the other hand, products, which require Cooking Methodsonly a short cooking period, like spinach and kohlrabi in slices, contained a higherconcentration of Ascorbic acid after steaming rather than after pressure cooking D. RUMM-KREUTER and I. DEMMEL(Rumm-Kreuter, 1986). Alfa Institut Eltville (FDG) Further interesting cooking methods are stirfrying and microwave cooking. Summary Preparing vegetables with heat the contents of their con Table 1.stituents will acid contents (mg/100g) in fresh spinach and in spinach after Ascorbic change to a various extend. Particularly the water-soluble different and the heat-sensitive vitamins are affected. At an early stage the vitamin cooking methods. C losses were investigated, because of vitamin Cs indicating function for oxidations and leaching-out processes (1, 2, 7, 11-13, 15, 17). The degree of vitamin losses is influenced by various factors, for example the type of food, variety of vegetables, the way of cutting, preparation, duration and method of cooking. The influence of the various cooking methods with regard to the losses of certain water-soluble vitamins will be discussed. Key Words cooking methods, ascorbic acid, folic acid, thiamine, ribo flavin, niacin, pyridoxine Blumenthal (1980). J. Nutr. Sci. Vitaminol. Foods are prepared in order to become edible and enjoyable. The choice of the cooking method depends on the individual or cultural dietary habits. By preparing food with heat, not only alterations in carbohydrates, fats and
  • 201. Each value is mean±SD of three replicate samples. Values 580 Yuan et al. / J Zhejiang Univ Sci B 2009 10(8):580-588not sharing a common letter are significantly different at Journal of Zhejiang University SCIENCE B ISSN 1673-1581 (Print); ISSN 1862-1783 (Online) www.zju.edu.cn/jzus; www.springerlink.com E-mail: jzus@zju.edu.cnP<0.05. Cooking methods: 1. Raw; 2. Boiled; 3. Streamed; Effects of different cooking methods on health-promoting4. Microwaved; 5. Stir-fried;of6. Stir-fried/boiled compounds broccoli * Gao-feng YUAN1, Bo SUN1, Jing YUAN1, Qiao-mei WANG†‡1,2 120 (1Department of Horticulture, Zhejiang University, Hangzhou 310029, China) a 2 ( Key Laboratory of Horticultural Plant Growth, Development and Quality Improvement, Ministry of Agriculture, Hangzhou 310029, China) Crudo   † a E-mail: qmwang@zju.edu.cn Vapor   Received Feb. 24, 2009; Revision accepted Apr. 20, 2009; Crosschecked July 14, 2009 Micro-­‐   100 b Ondas   Abstract: The effects of five domestic cooking methods, including steaming, microwaving, boiling, stir-frying, and stir-frying followed by boiling (stir-frying/boiling), on the nutrients and health-promoting compounds of broccoli were investigated. The c results show that all cooking treatments, except steaming, caused significant losses of chlorophyll and vitamin C and significant Frito   decreases of total soluble proteins and soluble sugars. Total aliphatic and indole glucosinolates were significantly modified by allVitamin C content 80 d cooking treatments but not by steaming. In general, the steaming led to the lowest loss of total glucosinolates, while stir-frying and Cozido   Cozido   (mg/100 g FW) stir-frying/boiling presented the highest loss. Stir-frying and stir-frying/boiling, the two most popular methods for most homemade dishes in China, cause great losses of chlorophyll, soluble protein, soluble sugar, vitamin C, and glucosinolates, but the steaming method appears the best in retention of the nutrients in cooking broccoli. e y  frito   Key words: Broccoli, Cooking, Glucosinolates, Vitamin C, Chlorophyll, Soluble sugar 60 doi:10.1631/jzus.B0920051 Document code: A CLC number: S635 INTRODUCTION ferent compartments of the plant cells to separate 40 Broccoli (Brassica oleracea var. italica) con- from glucosinolates. When plant tissues are damaged, myrosinase rapidly hydrolyzes the glucosinolates to tains high levels of vitamins, antioxidants, and anti- glucose and other unstable intermediates, which carcinogenic compounds and has been described as a spontaneously rearrange to a variety of biologically vegetable with high nutritional value. Glucosinolates, active products, including isothiocyanates, thiocy- 20 a diverse class of sulfur- and nitrogen-containing anates, epithionitriles, or nitriles depending on secondary metabolites, are found in Brassica vegeta- chemical conditions (Jia et al., 2009). The hydrolysis bles including broccoli. These compounds have products vary depending largely upon the level and gained renewed interest in recent years due to the activity of myrosinase, presence of specifier protein, 0 chemoprotective properties of their major hydrolysis e.g., epithiospecifier protein, and hydrolysis condi- products, isothiocyanates. Glucosinolates are chemi- tions, e.g., pH, metal ions and temperature, and these 14 cally stable until they come inYuan  et  awithhejiang  Univ  canBbe009  10(8):580-­‐588   contact l.  J  Z the deg- Sci    2 influenced by species, cultivar, and cooking cohydrolase, EC 3.2.1.147), which is stored in dif- a radation enzyme myrosinase ( -thioglucoside glu- time and conditions (Verkerk et al., 2008). Epidemi- ological studies and experimental researches with cell
  • 202. Research Article Received: 21 September 2009 Revised: 8 January 2010 Accepted: 20 February 2010 Published online in Wiley Interscience: (www.interscience.wiley.com) DOI 10.1002/jsfa.3967 Vitamin C, total phenolics and antioxidative activity in tip-cut green beans (Phaseolus vulgaris) and swede rods (Brassica napus var. napobrassica) processed by methods used in catering Pernille Baardseth,a∗ Frøydis Bjerke,b Berit K Martinsena and Grete Skredea Abstract BACKGROUND: Retention of nutrients in vegetables during blanching/freezing, cooking and warm-holding is crucial in the preparation of both standard and therapeutic diets. In the present study, conventional cooking in water, and cooking by pouch technology (boil-in-bag, sous vide) were compared in their ability to retain vitamin C, total phenolics and antioxidative activityPERDE-­‐SE  13  –  42  %  DA  VITAMINA  C  E  COMPOSTOS  FENÓLICOS   (DPPH and FRAP) in industrially blanched/frozen tip-cut green beans and swede rods. RESULTS: After conventional cooking, 50.4% total ascorbic acid, 76.7% total phenolics, 55.7% DPPH and 59.0% FRAP were NA  ÁGUA  DA  COZEDURA   recovered in the drained beans. After boil-in-bag cooking, significantly (P < 0.05) higher recoveries were obtained, i.e. 80.5% total ascorbic acid, 89.2% total phenolics, 94.8% DPPH and 92.9% FRAP. Recoveries after sous vide cooking were comparable to those of boil-in-bag cooking. By conventional cooking, 13.5–42.8% of the nutrients leaked into the cooking water; by sous vide about 10% leaked to the exuded liquid, while no leakage occurred by boil-in-bag cooking. Warm-holding beans after cooking reduced recoveries in all components. Recoveries in swede rods were comparable but overall slightly lower. CONCLUSION: Industrially blanched/frozen vegetables should preferably be cooked by pouch technology, rather than conventional cooking in water. Including cooking water or exuded liquid into the final dish will increase the level of nutrients in a meal. Warm-holding of vegetables after cooking should be avoided. c 2010 Society of Chemical Industry Keywords: green beans; swede; cooking; boil-in-bag; sous vide; warm-holding; vitamin C; total phenolics; DPPH; FRAP INTRODUCTION conventional cooking in water,6,10 – 17 baking in oven,10 heating by Consumption of vegetables rich in nutrients and phytochemicals microwave,6,10,11,13 – 15,17,18 steam,7,11,13,15 stir-frying,6,10,12,14,16,17 is today recommended as a means to ensure a health-beneficial cook–chill,8,19 or the more recent technologies of sous vide20 diet.1 – 3 Many vegetables are consumed fresh, but others are and boil-in-bag21 cooking. Both intentional19,22 and unintentional processed to various extents in the catering and foodservice warm-holding after cooking are also practised in many cases. The industries or in the private home prior to consumption. Processing pouch technologies, boil-in-bag and sous vide, will most likely
  • 203. smokers had significantly lower plasma ␤-carotene concentra-smokers and nonsmokers, but in neither case were the concentra- tions than did the nonsmokers. The smokers and passive smok-tions in the passive smoking group significantly different from ers had higher plasma ␥-tocopherol concentrations than did the Smoking and exposure to environmental tobacco smoke decreasethose in either of the other groups. In summary, after adjustment for race, age, sex, BMI, alco- nonsmokers. All of these comparisons were significant with the use of Tukey-Kramer’s correction with a 5% procedure-wise some plasma antioxidants and increase ␥-tocopherol in vivo afterhol intake, fruit and vegetable intakes, the respective dietary error rate.antioxidant, and triacylgycerol (for lipid-soluble antioxidants 1–3 The importance of other covariates on plasma antioxidant con- adjustment for dietary antioxidant intakesonly), the smokers had significantly lower plasma concentra- centrations is also notable. BMI was highly significant for severaltions of ␤-carotene, total ascorbic acid, ␤-cryptoxanthin, and carotenoids (data not shown), consistent with earlier findings on Marion Dietrich, Gladys Block, Edward P Norkus, Mark Hudes, Maret G Traber, Carroll E Cross, and Lester Packerlutein and zeaxanthin than did the nonsmokers. The passive the importance of body weight to plasma ascorbic acid status (40). ABSTRACT radicals cause oxidative damage to macromolecules such as lipids, Background: Free radicals in cigarette smoke may cause oxida-TABLE 3 proteins, and DNA, they are believed to be involved in the patho-Plasma antioxidant concentrations in the 159 subjects byto cardiovascular tive damage to macromolecules, contributing study group after adjustment for race, age, sex, body mass index, alcohol intake, fruit and genesis of cardiovascular diseases and cancer (2–5). Free radicals 1vegetable intake, the respective dietaryplasma antioxidant concentrations diseases and cancer. Decreased antioxidant, and triacylglycerol concentrationCS deplete some plasma antioxidants in vitro (4, 6), and several in may indicate cigarette smoke–related oxidative stress. Nonsmokers Passive smokers lower plasma antioxidant concentrations in smok- studies found Smokers Objective: We compared the effects on plasma antioxidant con- (n = 36) ers (n = 40) (7–13). Less information is available on the effect 2of in vivo (n = 83) P centrations in cotinine-confirmed active and passive smokers with CS exposure on plasma antioxidant concentrations in passive␣-Tocopherol (␮mol/L) 30.0 30.4 29.7 0.933 those in nonsmokers, independent of differences in dietary intakes␥-Tocopherol (␮mol/L) 6.5a smokers b(14–18). 7.8 7.8b 0.032 and other covariates.Total ascorbic acid (␮mol/L) 54.5 b It 54.6b been difficult to determine whether differences in has 43.6 a 0.014 Design:(␮mol/L) samples from 83 smokers, 40 passive smokers,␣-Carotene Plasma 0.05 plasma antioxidants between smokers and nonsmokers are 0.210 0.04 0.04 actu-␤-Carotene nonsmokers were analyzed for total ascorbic and 36 (␮mol/L) 0.24 bacid, ␣- and ally due to 0.15 a the effect of CS exposure or are due instead to dif- 0.17 a 0.026 ␥-tocopherols, 5 carotenoids, retinol, and cotinine. Groups wereTotal carotenoids (␮mol/L) 1.80 ferences in dietary antioxidant intakes or in other covariates [eg, 1.60 1.53 0.141 compared by using analysis of variance with adjustment for sex,␤-Cryptoxanthin (␮mol/L) 0.16b body 0.16b index (BMI; in kg/m 2a Epidemiologic studies mass 0.12)]. 0.034 b a,b aLutein and zeaxanthin (␮mol/L) 0.41 age, race, body mass index, alcohol intake, triacylglycerol con- 0.36 0.33 0.047 showed that cigarette smokers consume fewer fruits and vegeta-Lycopene (␮mol/L) and vegetable intakes, and dietary antioxidants. centration, fruit 0.71 0.70 0.71 bles than do nonsmokers (19–23). In addition, cigarette smok-0.977Retinol (␮mol/L) adjustment for dietary antioxidant intakes and other Results: After 2.15 2.15 2.26 ers consume fewer vitamin supplements than do nonsmokers 0.549 covariates, smokers and passive smokerswas performed for lipid-soluble antioxidants only. Valueshabitssame row with different superscript letters 1 Adjustment for triacylglycerol concentration had significantly lower (24–26). The dietary in the of passive smokers were found to beare plasma ␤-carotene at a 5% procedure-wise did nonsmokers (0.15, significantly different concentrations than error rate. intermediate between those of smokers and nonsmokers (27). 2 Overall general linear model. 0.17, and 0.24 ␮mol/L, respectively) and significantly higher Few of the existing studies of the effect of smoking on plasma ␥-tocopherol concentrations (7.8, 7.8, and 6.5 ␮mol/L, respec- antioxidant status adjusted for dietary or supplement intake (8, tively). Smokers had significantly lower plasma ascorbic acid and 9), and only one study on passive smokers did so (17). As a ␤-cryptoxanthin concentrations than did nonsmokers and passive result, the in vivo effect of smoking or passive smoking on smokers (ascorbic acid: 43.6, 54.5, and 54.6 ␮mol/L, respectively; plasma antioxidant status remains unclear. ␤-cryptoxanthin: 0.12, 0.16, and 0.16 ␮mol/L, respectively) and In this study, we confirmed active smoking, passive smoking, or significantly lower concentrations of lutein and zeaxanthin than nonsmoking status with plasma cotinine measures, excluded cur- did nonsmokers (0.33 compared with 0.41 ␮mol/L). et  al.  Avalues Nutr.  2003  recent vitamin supplement users, and adjusted for dietary Dietrich  M,   The P m  J  Clin   rent or Jan;77(1):160-­‐6.   for all the differences described above were < 0.05. No significant antioxidant intakes and other covariates. This permitted us to differences in plasma concentrations of ␣-tocopherol, ␣-carotene,
  • 204. OBRIGADO 
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