Micronutrientes

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Micronutrientes

  1. 1. VITAMINAS E MINERAISNutrição no Exercício Físico e Desporto Pedro Carrera Bastos, 2013
  2. 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. 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. 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. 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. 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. 7. Ca
  8. 8. Ca Duodeno: 8-10% Ceco e Cólon: % pequena Íleo: Maior parte
  9. 9. Ca Duodeno: 8-10% Ceco e Cólon: % pequena Íleo: Maior parte
  10. 10. Christakos S. Arch Biochem Biophys. 2012 Jul 1;523(1):73-6 Ca Ca Ca Ca Ca
  11. 11. Christakos S. Arch Biochem Biophys. 2012 Jul 1;523(1):73-6 Ca Ca Ca Ca Ca
  12. 12. Christakos S. Arch Biochem Biophys. 2012 Jul 1;523(1):73-6 Ca Ca Ca Ca Ca
  13. 13. Christakos S. Arch Biochem Biophys. 2012 Jul 1;523(1):73-6 Ca Ca Ca Ca Ca
  14. 14. Christakos S. Arch Biochem Biophys. 2012 Jul 1;523(1):73-6 Ca Ca Ca Ca Ca
  15. 15. Christakos S. Arch Biochem Biophys. 2012 Jul 1;523(1):73-6 Ca TRPV6 Ca Ca Ca TRPV6 Ca
  16. 16. Christakos S. Arch Biochem Biophys. 2012 Jul 1;523(1):73-6 Ca TRPV6 Ca Ca Ca TRPV6 Ca
  17. 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. 18. Holick  MF.  J  Clin  Invest.  2006  Aug;116(8):2062-­‐72   ×
  19. 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. 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. 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. 22. RECEPTORES EM VÁRIAS CÉLULASCatelicidina   Holick  MF.  J  Clin  Invest.  2006  Aug;116(8):2062-­‐72  
  23. 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. 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. 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. 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. 27. RISCO RELATIVO DE QUEDAS AJUSTADO PARA A IDADE EM 124 IDOSOS    
  28. 28. NÍVEL IDEAL DE 25OHD PARA ÓPTIMA FUNÇÃO MUSCULAR NOS MEMBROS INFERIORES  
  29. 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. 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. 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. 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. 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. 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. 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. 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. 37. PORQUE EXISTE DEFICIÊNCIA
  38. 38. Webb AR, Kline L, Holick MF. J Clin Endocrinol Metab. 1988 Aug;67(2):373-8.
  39. 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. 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. 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

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