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%
Magnésio
Vitaminas 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 Fontes
Oxigénio Ar e água
Hidrogénio Ar e água
Carbono Base estrutural de todos os
alimentos
Nitrogénio Proteínas
Restantes elementos Distribuição heterogénea em
vários alimentos
Colgan, M. Sports nutrition guide – Minerals, vitamins & antioxidants for athletes. Apple Publications, 2002
4. VITAMINAS E OUTROS NUTRIENTES
Vitaminas Vitaminas Outros
hidrossolúveis 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 Níquel
Colgan, 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
see
tween
–1
as
A. central
94
tral
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
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 Control
re 2. Forest PlotsForest Plots ComparingHip and Nonvertebral Fractures Between Vitamin D (700-800 IU/d and 400IU/d and 400 IU/d) and Con
ps 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
19. 3, Vol 78 Musculoskeletal Pain and Severe Hypovitaminosis D 1463
vere Hypovitaminosis D in Patients
Nonspecific Musculoskeletal Pain Vol 78
Mayo Clin Proc, December 2003, Musculoskeletal Pain and
F, Original Article
MD, MTS, AND JOANNA M. QUIGLEY, BA
mine the prevalence of hypovita- whom were younger than 30 years. Five patients, 4 of whom
care outpatients with persistent, were aged 35 years or younger, had vitamin D serum levels
Prevalence of Severe Hypovitaminosis D in Patients
etal pain syndromes refractory to below the level of detection. The severity of deficiency was
disproportionate by age for young women (P<.001), by sex
ds: 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 ye
ng/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 to
of 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) 26:1895–1901
DOI 10.1007/s10067-007-0603-4
ORIGINAL ARTICLE
Hypovitaminosis D in female patients with chronic
low back pain
Ahmed Lotfi & Ahmed M. Abdel-Nasser &
Ahmed Hamdy & Ahmed A. Omran &
Mahmoud A. El-Rehany
Received: 7 October 2006 / Revised: 4 March 2007 / Accepted: 5 March 2007 / Published online: 22 March 2007
# Clinical Rheumatology 2007
Abstract 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 g
analyze 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 ARTICLE
Association between nonspecific skeletal pain and vitamin
D deficiency
Behzad HEIDARI,1 Javad Shokri SHIRVANI,1 Alireza FIROUZJAHI,2 Parnaz HEIDARI3 and
Karim O. HAJIAN-TILAKI4
1
Deparment of Medicine, Division of Rheumatology, 2Deparment of Pathology and Laboratory Medicine, Rouhani Hospital, Babol
University 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 CÉLULAS
Catelicidina
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
synthesis
Increased VDR
Increased 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 control
Figure 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
ap
Figure
season 2
Incidence of reported cold/influenza symptoms according to In
Incidence ofJJ, Zasloff M, Garland CF, Scragg R, Giovannucci E. Virol symptoms
Cannell reported cold/influenza J. 2008 Feb 25;5:29.
lu
according to season. The 104 subjects in the placebo m
25.
26. Diabetologia (2008) 51:1391–1398 1393
45
Sardinia, Italy
40
Finland
35
Aberdeen, UK
Diabetes 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,
29. NÍVEL IDEAL DE 25OHD PARA ÓPTIMA FUNÇÃO MUSCULAR
NOS MEMBROS INFERIORES
30. the growt
Prostate cell inhibit pr
1α,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
31. 453
death Table 3 The estimated relationship between serum calcidiol and death
arately from prostate cancer among patients receiving hormone therapy (n ¼ 97)
III RR Model I Model II Model III
CI) 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
32. 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 aggressive
e 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,
baseline
than 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 in
viduals 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
33. 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) as
by 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 baseline
with 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 was
viduals 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
34. 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/beem
13
Why the minimum desirable serum 25-hydroxyvitamin D
level 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, Canada
b
Department of Laboratory Medicine and Pathobiology, University of Toronto, Canada
c
Pathology and Laboratory Medicine, Mount Sinai Hospital, 600 University Ave, Toronto, Ontario, Canada M5G 1X5
Keywords:
The Institutes of Medicine (IOM) recently revised the recom-
mended dietary allowances (RDA) for vitamin D, to maintain
40. 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/ano
Figure 1. The potential for synthesis of previtamin D3 in lightly pigmented human skin computed from annual average UVMED. The highest annual
values 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 throughout
the 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 month
of 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
41. Sunlight, UV-Radiation, Vitamin D and Skin Cancer 5
Figure 3. Influence of season, time of day in July and latitude on the synthesis of previtamin
D3 in Boston (42°N)-o-, Edmonton (52°N)-n-, Bergen (60°) - ^ - . The hour is the end of the
one 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 and
bone 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 calcium
in the kidneys (Fig. 5).
42. 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, USA
gressively 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, USA
ng 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, USA
mmunity 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 triggers
e 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 human
influenza 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 triggers
stice. 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 the
a 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 in
pulation 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 Business
ning 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