Status deficiente da vitamina D no sangue e o risco de doenças cronicas – Dr. Holick’s Responses to Participant Questions During the December 5, 2008 Live Webinar Presentation “Vitamin D & Chronic Disease Risk”

Status deficiente da vitamina D no sangue e o risco de doenças cronicas –

Dr. Holick’s Responses to Participant Questions During the December 5, 2008 Live Webinar Presentation “Vitamin D & Chronic Disease Risk”

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 Dr. Michael F. Holick

VitaminDHealth.org

vitamin-d-solution

Dr. Michael F. Holick on Vitamin D

http://vitamindhealth.org/

Articles by Category

Michael F. Holick, PhD, MD

Professor of Medicine, Physiology and Biophysics

Director of the General Clinical Research Center

Director of the Vitamin D, Skin and Bone Research Laboratory

Director, Biologic Effects of Light Research Center

Boston University Medical Center

Dr. Holick’s new book The Vitamin D Solution is now available! Click on the book cover for more information on how to order.

 

Vitamin D is not a vitamin but a hormone. It is unique in that it is made in the skin as a result of exposure to sunlight. Photosynthesis of vitamin D has been occurring on earth for more than 750 million years. Some of the earliest life forms that were exposed to sunlight for their energy requirement were also photosynthesizing vitamin D. Both children and adults have in the past depended on adequate sun exposure to satisfy their vitamin D requirement. It is well documented that at the turn of the last century upwards of 80% of children in the industrialized, polluted cities of northern Europe and northeastern United States suffered from the devastating consequences of vitamin D deficiency rickets. The skin has a large capacity to make vitamin D. Exposure of a person in a bathing suit to a minimal erythemal dose of sunlight, which is typically no more than 15-20 minutes on Cape Cod in June or July at noon time, is the equivalent to taking 20,000 IU of vitamin D orally. It is now well documented that in the absence of any sun exposure 1,000 IU of vitamin D3 a day is necessary to maintain healthy levels of 25-hydroxyvitamin D in the circulation. An analysis of the NHANES III data has demonstrated that neither children nor adults are receiving an adequate amount of vitamin D from their diet or from supplements.

Read more of this article »

 

Dr. Holick’s Responses to Participant Questions During the December 5, 2008 Live Webinar Presentation “Vitamin D & Chronic Disease Risk”

Posted by mfholick on under Cancer, Multiple Sclerosis, Osteomalacia, Osteoporosis, Rickets, Vitamin D | 57 Comments to Read

 

VITAMIN D AND DISEASE STATES

EPILEPSY

 

I have heard that vitamin D may play a role in epilepsy, possibly due to interaction with anti-epileptic drugs. Is this becoming an acknowledged effect? And how much vitamin D is necessary to combat the interaction to reduce seizures?

Response: Epileptic drugs will enhance the destruction of vitamin D making patients who are on anti-seizure medications at higher risk for developing vitamin D deficiency and osteomalacia or rickets. Measurement of 25-hydroxyvitamin D [25(OH)D] is important in patients on antiepileptic medications. Often twice as much vitamin D is required to maintain a blood level of 25(OH)D of > 30 ng/ml. Thus, 2,000-4,000 IU of vitamin D/d is usually needed. An alternative is to take 50,000 IU of vitamin D2 either once every week or once every two weeks depending on the serum 25-hydroxyvitamin D level.

 

MENTAL HEALTH

What is your position on vitamin D and depression and schizophrenia?

Response: There is evidence that vitamin D deficiency during pregnancy increases the risk of the child developing schizophrenia during their adult life. There is also evidence that vitamin D receptors exist in the brain, and that the active form of vitamin D, 1,25-dihydroxyvitamin D, Read more of this article »

 

Multiple Sclerosis and Vitamin D

Posted by admin on under Multiple Sclerosis, Vitamin D | 5 Comments to Read

It is known that if you are born above 35° latitude at approximately Atlanta, Georgia, and live at this latitude for the first ten years of your life that you have a 100% increase risk of developing multiple sclerosis. Recent studies have suggested that women and men who increase their vitamin D intake above 400 IU of vitamin D a day reduces risk of developing multiple sclerosis by approximately 40%.

 

References:

Munger KL, Zhang SM, O’Reilly E, Hernan MA, Olek MJ, Willett WC, Ascherio A. Vitamin D intake and incidence of multiple sclerosis. Neurology 2004; 62(1):60-5.

Munger KL, Levin LI, Hollis, BW, Howard NS, Ascheino A. Serum 25-hydroxyvitamin D levels and risk of multiple sclerosis. JAMA 2006; 296:2832-2838.

Ponsonby A-L, McMichael A, and van der Mei I. Ultraviolet radiation and autoimmune disease: insights from epidemiological research. Toxocology 2002;181-182:71-78.

 

Infectious Diseases and Vitamin D

Posted by admin on under Infectious Disease, Vitamin D | 2 Comments to Read

It has long been recognized that patients with tuberculous do better when treated with vitamin D or exposed to sunlight. It was recently recognized that the immune cell known as the macrophage needs vitamin D in order to produce a peptide which is responsible for killing infectious agents such as tuberculous. It has been speculated that one of the reasons that influenza occurs in the winter time in tepid climates is because the sun is unable to produce vitamin D, and the resulting vitamin D insufficiency may promote and enhance the infectivity of the influenza virus.

References: Adams,J.S., Gacad,M.A., Anders,A., Endres,D.B., and Sharma,O.P. 1986. Biochemical indicators of disordered vitamin D and calcium homeostasis in sarcoidosis. Sarcoidosis 3:1-6.

Gallo, R.L., Eisenberg, D., Hewison, M., Hollis, B.W., Adams, J.S., Bloom, B.R., Modlin, R.L. 2006. Toll-like receptor Triggering of a vitamin D-mediated human antimicrobial response. Sciencexpress. 3:1770-1773. Liu, P.T., Stenger, S., Li, H., Wenzel, L., Tan, B.H., Krutzik, S., Ochoa, M.T., Schauber, J., Wu, K., Meinken, C., Kamen, D.L., Wagner, M., Bals, R., Steinmeyer, A., Zugel, U.

 

Arthritis and Vitamin D

Posted by admin on under Arthritis, Vitamin D | 9 Comments to Read

Rheumatoid Arthritis and Osteoarthritis

Recent studies have revealed that women who ingest more than 400 IU of vitamin D a day reduce their risk of developing rheumatoid arthritis by as much as 42%.

Vitamin D deficiency has been associated with an increased risk of developing osteoarthritis.

Merlino LA, Curtis J, Mikuls TR, Cerhan JR, Criswell LA, and Saag KG. Vitamin D intake is inversely associated with rheumatoid arthritis. Arthritis & Rheumatism 2004; 50(1):72-77.

 

Diabetes and Vitamin D

Posted by admin on under Diabetes, Vitamin D | 6 Comments to Read

Diabetes mellitus type I

Studies in mice have suggested that pretreating mice that are prone to developing type I diabetes with the active form of vitamin D (1,25-hydroxyvitamin D [1,25(OH)2D]) reduces the development of type I diabetes by 80%. This study is supported by the observation in Finland where children in the 1960’s routinely received 2,000 IU of vitamin D a day during their first year of life. When these children were followed for the next 31 years, it was observed that these children had a reduced risk of developing type I diabetes by 78%. Children who were vitamin D deficient at the same time and also followed for 31 years had an almost 300% increased risk of developing type I diabetes.

Reference:

Hypponen E, Laara E, Jarvelin M-R, Virtanen SM. Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study. Lancet 2001;358:1500-1503.

Diabetes mellitus type II

The beta islet cells that produce insulin in the pancreas have a vitamin D receptor. The active form of vitamin D stimulates the pancreas to produce insulin. It has been observed that the relative risk of developing type II diabetes is reduced by as much as 33% in men and women who increase their intake of vitamin D above 800 IU/day along with 1,000 milligrams of calcium.

Reference:

Pittas AG, Dawson-Hughes B, Li T, et al. Vitamin D and calcium intake in relation to type 2 diabetes in women. Diabetes Care 2006:29:650-56.

 

Rickets and Vitamin D

Posted by admin on under Rickets, Vitamin D | 2 Comments to Read

Rickets occurs at approximately six months of age in children who are vitamin D deficient. They can present with growth retardation, skeletal deformities including bowing of the legs or knocked knees, prominent knob like projections along the ribs next to the sternum known as the rachitic rosary and muscle weakness. Infants with vitamin D deficiency also suffer from craniotabes which is a softening of the skull causing it to become square shaped. They can have increase in the bone formation in the front of the head which is known as frontal bossing.

References:

Holick, M.F. Resurrection of vitamin D deficiency and rickets. J Clin Invest 2006, 116(8):2062-2072..

Kreiter SR, Schwartz RP, Kirkman HN, Charlton PA, Calikoglu AS, Davenport M. Nutritional rickets in African American breast-fed infants. J Pediatr 2000;137:2-6.

Marksted, T., Halvorsen, S., Halvorsen, K.S., Aksnes, L., and Aarskog, D. 1984. Plasma concentrations of vitamin D metabolites before and during treatment of vitamin D deficiency rickets in children. Acta Padiatr Scand. 73:225-231.

 

Osteomalacia and Vitamin D

Posted by admin on under Osteomalacia, Vitamin D | Read the First Comment

Vitamin D deficiency causes a defect in the ability of the body to deposit calcium into the collagen jello-like matrix in the bone. As a result, the covering on the bone which contains pain sensing nerves is easily deformed resulting in throbbing aching bone pain. Patients with osteomalacia often complain of achiness in their muscles and bones. These non-specific aches and pains in the bones and muscles are often misdiagnoses as fibromyalgia or chronic fatigue syndrome. There have been several studies demonstrating that patients with severe bone and muscle pain and muscle weakness associated with osteomalacia have dramatic improvement in their symptoms when vitamin D deficiency is corrected. It takes months to years to develop osteomalacia and associated symptoms and it takes three to six months before significant improvement in symptoms results from correcting vitamin D deficiency.

References:

Holick, M.F. Vitamin D deficiency: What a Pain it is. Mayo Clin. Proc. 2003; 78(12): 1457-1459.

Malabanan AO, Turner AK, Holick MF. Severe generalized bone pain and osteoporosis in a premenopausal black female: effect of vitamin D replacement. J Clin Densitometr . 1998;1:201-204.

 

Osteoporosis and Vitamin D

Posted by admin on under Osteoporosis, Vitamin D | 3 Comments to Read

Vitamin D deficiency will cause removal of both the calcium and matrix from the bone, and as a result, will cause osteopenia and can precipitate and exacerbate osteoporosis. Unlike osteomalacia which causes bone pain, osteoporosis, which is porotic bone, i.e., holes in the bones and loss of bone does not cause bone pain unless there is an acute fracture. Typically this pain resolves as the fracture heals and can be easily distinguished from osteomalacia.

References:

Bischoff-Ferrari, HA, Giovannucci, E., Willett, W.C., Dietrich, T., and Dawson-Hughes, B. Estimation of optimal serum concentrations of 25-hydroxyvitamin D for multiple health outcomes. Am J Clin Nutr 2006; 84:18-28.

Boonen S, Bischoff-Ferrari A, Cooper C, Lips P, Ljunggren O, Meunier PJ, Reginster JY. Addressing the musculoskeletal components of fracture risk with calcium and vitamin D: a review of the evidence. Calcif Tissue Int 2006; 78(5):257-70.

Chapuy MC, Arlot ME, Duboeuf F, Brun J, Crouzet B, Arnaud S, Delmas PD, Meunier PJ. Vitamin D3 and calcium to prevent hip fractures in elderly women. N Engl J Med 1992; 327(23):1637-1642.

 

Cancer and Vitamin D

Posted by admin on under Cancer, Vitamin D | 6 Comments to Read

Cancer

As early as 1941, it was observed that people living at higher latitude were at higher risk of dying of cancer. In the 1980’s and the 1990’s, several reports surfaced revealed that living at higher latitude and being at higher risk of vitamin D deficiency increased risk of developing and dying of cancers of the colon, rectum, prostate, breast, ovary. More recently, vitamin D deficiency has been associated with increased risk of developing many other cancers including cancer of the esophagus, pancreas and leukemia. Read more of this article »

 

Obesity

Posted by admin on under Obesity, Vitamin D | 14 Comments to Read

Obesity is associated with vitamin D deficiency. The reason is that the vitamin D is trapped within the fat and cannot easily exit. As a result, obese patients need at least twice as much vitamin D as a normal weighted individual in order to maintain a normal vitamin D status with a 25(OH)D between 30-60 ng/ml.Wortsman J, Matsuoka LY, Chen TC, Lu Z, Holick MF. Decreased bioavailability of vitamin D in obesity. Am J Clin Nutr 2000;72: 690-693.

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1.       Vitamina D e doenças causadas pela deficiência

https://objetodignidade.wordpress.com/2013/06/04/vitamina-d-e-doencas-causadas-pela-deficiencia/

  1. The Vitamin Which Can Cut Your Flu Risk Nearly in Half

https://objetodignidade.wordpress.com/2013/04/24/the-vitamin-which-can-cut-your-flu-risk-nearly-in-half/

 

3.       20 razões para tomar Vitamina D

https://objetodignidade.wordpress.com/2013/04/24/20-razoes-para-tomar-vitamina-d/

 

4.       Vitamin D and Health

https://objetodignidade.wordpress.com/2013/04/24/vitamin-d-and-health-2/

 

5.       Vitamina D – contra envelhecimento e contra a gripe suína

https://objetodignidade.wordpress.com/2013/04/23/vitamina-d-contra-envelhecimento-e-contra-a-gripe-suina/

 

6.       Vitamin D Deficiency – Michael F. Holick, M.D., Ph.D.

https://objetodignidade.wordpress.com/2013/04/22/vitamin-d-deficiency-michael-f-holick-m-d-ph-d/

 

7.       Como funciona e qual é a relação entre vitamina D e proteção ao câncer

https://objetodignidade.wordpress.com/2013/04/21/como-funciona-e-qual-e-a-relacao-entre-vitamina-d-e-protecao-ao-cancer/

 

8.       Fatigue and Muscle Weakness From a Vitamin D Deficiency

https://objetodignidade.wordpress.com/2013/04/16/fatigue-and-muscle-weakness-from-a-vitamin-d-deficiency/

 

9.       Serum 25-Hydroxyvitamin D Levels and Risk of Multiple Sclerosis

https://objetodignidade.wordpress.com/2013/04/15/serum-25-hydroxyvitamin-d-levels-and-risk-of-multiple-sclerosis/

 

10.   Dr. Cícero Galli Coimbra, fundador e Presidente do Instituto de Investigação e Tratamento de Autoimunidade, médico neurologista, Phd., M.D., professor na Universidade Federal de São Paulo

https://objetodignidade.wordpress.com/2013/04/21/dr-cicero-galli-coimbra-fundador-e-presidente-do-instituto-de-investigacao-e-tratamento-de-autoimunidade-medico-neurologista-phd-m-d-professor-na-universidade-federal-de-sao-paulo/

 

  1. Estudo randomizado de suplementação de vitamina D para prevenir a gripe sazonal A em crianças em idade escolar – Randomized trial of vitamin D supplementation to prevent seasonal influenza A in schoolchildren

https://objetodignidade.wordpress.com/2013/04/29/estudo-randomizado-de-suplementacao-de-vitamina-d-para-prevenir-a-gripe-sazonal-a-em-criancas-em-idade-escolar-randomized-trial-of-vitamin-d-supplementation-to-prevent-seasonal-influenza-a-in-school/

 

  1. É preciso reconhecer os sintomas da deficiência de vitamina D, o hormonio esteroide imunoregulador

https://objetodignidade.wordpress.com/2013/04/29/e-preciso-reconhecer-os-sintomas-da-deficiencia-de-vitamina-d-o-hormonio-esteroide-imunoregulador/

 

13.   A suplementação de vitamina D aumentou a resposta à terapêutica anti-tuberculose em um estudo randomizado de pacientes com tuberculose pulmonar com baciloscopia positiva.

https://objetodignidade.wordpress.com/2013/04/30/a-suplementacao-de-vitamina-d-aumentou-a-resposta-a-terapeutica-anti-tuberculose-em-um-estudo-randomizado-de-pacientes-com-tuberculose-pulmonar-com-baciloscopia-positiva/

 

14.   Estudo controlado randomizado mostra ligação entre a vitamina D e rinite alérgica

https://objetodignidade.wordpress.com/2013/05/01/estudo-controlado-randomizado-mostra-ligacao-entre-a-vitamina-d-e-rinite-alergica/

 

15.   A pilot study assessing the effect of prolonged administration of high daily doses of vitamin D on the clinical course of vitiligo and psoriasis

https://objetodignidade.wordpress.com/2013/06/01/a-pilot-study-assessing-the-effect-of-prolonged-administration-of-high-daily-doses-of-vitamin-d-on-the-clinical-course-of-vitiligo-and-psoriasis/

15 . Traumatic Brain Injury and Aging: Is a Combination of Progesterone and Vitamin D Hormone a Simple Solution to a Complex Problem?

https://objetodignidade.wordpress.com/2013/06/02/traumatic-brain-injury-and-aging-is-a-combination-of-progesterone-and-vitamin-d-hormone-a-simple-solution-to-a-complex-problem/

16. O que você não sabe ou reconhece pode prejudicar a sua saúde

https://objetodignidade.wordpress.com/2013/05/31/o-que-voce-nao-sabe-ou-reconhece-pode-prejudicar-a-sua-saude/

17.  Câncer de mama: a vitamina D ou mastectomia

https://objetodignidade.wordpress.com/2013/05/30/cancer-de-mama-a-vitamina-d-ou-mastectomia/

18.  A vitamina D supera a vacina contra a gripe

https://objetodignidade.wordpress.com/2013/05/30/a-vitamina-d-supera-a-vacina-contra-a-gripe/

19.  Não patenteiem meus genes! Liberem os genes do câncer da mama!

https://objetodignidade.wordpress.com/2013/05/30/nao-patenteiem-meus-genes-liberem-os-genes-do-cancer-da-mama/

20.  Existe terapêutica natural e de baixo custo para doenças autoimunitárias. Depoimentos de pacientes com esclerose múltipla. Vitamina D – Dr. Cícero Galli Coimbra, PhD, MD.

https://objetodignidade.wordpress.com/2013/05/26/existe-terapeutica-natural-e-de-baixo-custo-para-doencas-autoimunitarias-depoimentos-de-pacientes-com-esclerose-multipla-vitamina-d-dr-cicero-galli-coimbra-phd-md/

21.  Vitamina D – Por uma outra terapia (p/ a esclerose múltipla) e todas as doenças autoimunes

https://www.youtube.com/watch?feature=player_detailpage&v=erAgu1XcY-U

  1. Vitamina D pode revolucionar o tratamento da esclerose múltipla*

http://biodireitomedicina.wordpress.com/category/doencas-autoimunes/

  1. POR UM NOVO PARADIGMA DE CONDUTA E TRATAMENTO http://www.institutodeautoimunidade.org.br/novo-paradigma.html

Por Dr. Cícero Galli Coimbra Médico Internista e Neurologista, Professor Associado Livre-Docente da Universidade Federal de São Paulo, Fundador e Presidente do Instituto de Investigação e Tratamento de Autoimunidade  

24.  Dr. Cícero Galli Coimbra – Doenças Autoimunes e Vitamina D

http://www.youtube.com/watch?v=4uJt1361aGw

25.  Mais de 10 anos de tratamento com a Vitamina D – Exijam que seus médicos se atualizem!

http://biodireitomedicina.wordpress.com/2012/12/23/mais-de-10-anos-de-tratamento-com-a-vitamina-d-exija-que-seus-medicos-se-atualizem/  – https://www.youtube.com/watch?v=fQN32qR_M2Y

 

26.  POR 30 ANOS, EXTENSA REVISÃO DE TODA A PESQUISA ANTERIOR CONFIRMA QUE BAIXO NÍVEL DE VITAMINA D É UMA SENTENÇA DE MORTE

http://biodireitomedicina.wordpress.com/2013/02/14/vitamina-d-reportagem-com-dr-cicero-galli-coimbra-e-daniel-cunha-na-rede-record/

27.  “As doses diárias de 10.000 unidades de colecalciferol devem ser tomadas por todas pessoas. Essa quantidade previne todas as doenças inclusive à autoimunidade. Com 10.000 unidades a pessoa sai da deficiencia de vitamina D. A dose de 1.000 unidades não tira as pessoas da deficiencia de vitamina D.’’ – Dr. Cicero Galli Coimbra, medico neurologista, Phd., professor na Universidade Federal de São Paulo, Presidente do Instituto de Investigação e Tratamento de Autoimunidade

https://objetodignidade.wordpress.com/2013/01/21/as-doses-diarias-de-10-000-unidades-de-colecalciferol-devem-ser-tomadas-por-todas-pessoas-essa-quantidade-previne-todas-as-doencas-inclusive-a-autoimunidade-com-10-000-unidades-a-pessoa-sai/

28.  Entrevistas com Dr. Cícero Galli Coimbra sobre o hormônio-vitamina D

http://www.youtube.com/playlist?list=PLeqEGmvbpULN2NfNfnLU6bYse4fp9alQS

  1. Dr. Cícero Galli Coimbra – Esclerose múltipla e o tratamento com a vitamina D – 28.01.13 – TV Mundi

https://objetodignidade.wordpress.com/2013/02/03/dr-cicero-galli-coimbra-esclerose-multipla-e-o-tratamento-com-a-vitamina-d-28-01-13-tv-mundi/

  1. Dr. Cícero Galli Coimbra – Esclerose múltipla e o tratamento com a vitamina D – 28.01.13 – TV Mundi

http://www.youtube.com/watch?v=hv6tD3B0Nlo&list=PLeqEGmvbpULNrc8biL5LF9Mp3-WbJT2Ao

http://www.youtube.com/watch?list=PLeqEGmvbpULNrc8biL5LF9Mp3-WbJT2Ao&feature=player_detailpage&v=hv6tD3B0Nlo

  1. “As doses diárias de 10.000 unidades de colecalciferol devem ser tomadas por todas pessoas. Essa quantidade previne todas as doenças inclusive à autoimunidade. Com 10.000 unidades a pessoa sai da deficiencia de vitamina D. A dose de 1.000 unidades não tira as pessoas da deficiencia de vitamina D.’’ – Dr. Cicero Galli Coimbra, medico neurologista, Phd., professor na Universidade Federal de São Paulo, Presidente do Instituto de Investigação e Tratamento de Autoimunidade

https://objetodignidade.wordpress.com/2013/01/21/as-doses-diarias-de-10-000-unidades-de-colecalciferol-devem-ser-tomadas-por-todas-pessoas-essa-quantidade-previne-todas-as-doencas-inclusive-a-autoimunidade-com-10-000-unidades-a-pessoa-sai/

32.  A responsabilidade Civil e Criminal Médica na Desinformação às pessoas – Revista VEJA, 2.304: “O que você não sabe sobre a Vitamina do Sol. Ela continua a surpreender a medicina com novos efeitos benéficos.”

https://objetodignidade.wordpress.com/2013/05/25/a-responsabilidade-civil-e-criminal-medica-na-desinformacao-as-pessoas-revista-veja-2-304-o-que-voce-nao-sabe-sobre-a-vitamina-do-sol-ela-continua-a-surpreender-a-medicina-com-novos-efe/

33.  Vitamina D: A Desinformação Médica e o Direito à Informação do Cidadão

https://objetodignidade.wordpress.com/2013/05/25/vitamina-d-a-desinformacao-medica-e-o-direito-a-informacao-do-cidadao-2/

34.  A suplementação de vitamina D aumentou a resposta à terapêutica anti-tuberculose em um estudo randomizado de pacientes com tuberculose pulmonar com baciloscopia positiva.

https://objetodignidade.wordpress.com/2013/04/30/a-suplementacao-de-vitamina-d-aumentou-a-resposta-a-terapeutica-anti-tuberculose-em-um-estudo-randomizado-de-pacientes-com-tuberculose-pulmonar-com-baciloscopia-positiva/

35.  Estudo randomizado de suplementação de vitamina D para prevenir a gripe sazonal A em crianças em idade escolar – Randomized trial of vitamin D supplementation to prevent seasonal influenza A in schoolchildren

https://objetodignidade.wordpress.com/2013/04/29/estudo-randomizado-de-suplementacao-de-vitamina-d-para-prevenir-a-gripe-sazonal-a-em-criancas-em-idade-escolar-randomized-trial-of-vitamin-d-supplementation-to-prevent-seasonal-influenza-a-in-school/

  1. É preciso reconhecer os sintomas da deficiência de vitamina D, o hormonio esteroide imunoregulador

https://objetodignidade.wordpress.com/2013/04/29/e-preciso-reconhecer-os-sintomas-da-deficiencia-de-vitamina-d-o-hormonio-esteroide-imunoregula

  1. The Vitamin Which Can Cut Your Flu Risk Nearly in Half

https://objetodignidade.wordpress.com/2013/04/24/the-vitamin-which-can-cut-your-flu-risk-nearly-in-half/

 

  1. 20 razões para tomar Vitamina D

https://objetodignidade.wordpress.com/2013/04/24/20-razoes-para-tomar-vitamina-d/

  1. Vitamin D and Health

https://objetodignidade.wordpress.com/2013/04/24/vitamin-d-and-health-2/

  1. Vitamina D – contra envelhecimento e contra a gripe suína

https://objetodignidade.wordpress.com/2013/04/23/vitamina-d-contra-envelhecimento-e-contra-a-gripe-suina/

  1. Vitamin D Deficiency – Michael F. Holick, M.D., Ph.D.

https://objetodignidade.wordpress.com/2013/04/22/vitamin-d-deficiency-michael-f-holick-m-d-ph-d/

  1. Como funciona e qual é a relação entre vitamina D e proteção ao câncer

https://objetodignidade.wordpress.com/2013/04/21/como-funciona-e-qual-e-a-relacao-entre-vitamina-d-e-protecao-ao-cancer/

  1. Fatigue and Muscle Weakness From a Vitamin D Deficiency

https://objetodignidade.wordpress.com/2013/04/16/fatigue-and-muscle-weakness-from-a-vitamin-d-deficiency/

  1. Serum 25-Hydroxyvitamin D Levels and Risk of Multiple Sclerosis

https://objetodignidade.wordpress.com/2013/04/15/serum-25-hydroxyvitamin-d-levels-and-risk-of-multiple-sclerosis/

  1. Dr. Cícero Galli Coimbra, fundador e Presidente do Instituto de Investigação e Tratamento de Autoimunidade, médico neurologista, Phd., M.D., professor na Universidade Federal de São Paulo

https://objetodignidade.wordpress.com/2013/04/21/dr-cicero-galli-coimbra-fundador-e-presidente-do-instituto-de-investigacao-e-tratamento-de-autoimunidade-medico-neurologista-phd-m-d-professor-na-universidade-federal-de-sao-paulo/

 

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Esclerose múltipla – sobre a gravidade da deficiência desse hormônio

Esclerose múltipla – sobre a gravidade da deficiência desse hormônio

CALCIFEROL

Daniel Cunha

Cicero

Vitamina D – Por uma outra terapia (p/ a esclerose múltipla)

http://www.youtube.com/watch?feature=player_detailpage&v=erAgu1XcY-U

] dc2

Mais de 10 anos com o tratamento com vitamina D p/ esclerose múltipla

http://www.youtube.com/watch?feature=player_detailpage&v=fQN32qR_M2Y

Entrevistas com Junia, Márcia e Nayra sobre a experiência da família com o tratamento da vitamina D. Nayra descobriu a EM há mais de 10 anos e é provavelmente uma das pacientes mais antigas tratando a EM com o Dr. Cícero Coimbra.

Esclerose múltipla, distúrbio metabólico – atualizado em 7/janeiro/2013

https://objetodignidade.wordpress.com/2013/01/07/esclerose-multipla-disturbio-metabolico-atualizado-em-7fevereiro2013/

“Infelizmente este conhecimento não tem sido levado aos livros textos de medicina e isso gera esse desconhecimento, não só do público em geral mas até da classe médica em relação á gravidade dessa situação sobre a deficiência desse hormonio esteroide, conhecido como vitamina D. Esta deficiencia torna as 229 funções do sistema imunológico do próprio organismo das pessoas desregulado, permitindo desenvolver qualquer doença, o que levou á pandemia do mundo atual.” – Dr. Cicero Galli Coimbra, medico neurologista, Phd., MD, neurocirurgião, neurocientista, professor na UNIFESP

 https://objetodignidade.wordpress.com/2012/12/09/por-um-novo-paradigma-de-conduta-e-tratamento-estamos-vivendo-uma-defasagem-entre-o-conhecimento-cientifico-e-a-pratica-medica-dr-cicero-galli-coimbra/

Vitamina D em medicina preventiva: estamos ignorando as provas?

“Os dados epidemiológicos indicam também um baixo status da vitamina D na tuberculose, artrite reumatóide, esclerose múltipla, doenças inflamatórias intestinais, hipertensão e certos tipos de câncer.”

https://objetodignidade.wordpress.com/2009/08/28/vitamina-d-em-medicina-preventiva-estamos-ignorando-as-provas/

Zittermann A .A Zittermann.

Department of Nutrition Science, University of Bonn, Endenicher Allee 11-13, 53115 Bonn, Germany. Departamento de Ciência da Nutrição, da Universidade de Bonn, Endenicher Allee 11-13, 53115 Bonn, Alemanha. a.zittermann@uni-bonn.de a.zittermann @ uni-bonn.de

Vitamin D is metabolised by a hepatic 25-hydroxylase into 25-hydroxyvitamin D (25(OH)D) and by a renal 1alpha-hydroxylase into the vitamin D hormone calcitriol. A vitamina D é metabolizado por uma 25-hidroxilase hepática em 25-hidroxi-vitamina D (25 (OH) D) e por um 1alpha renal-hidroxilase no hormônio calcitriol vitamina D.

Dispoível em

http://64.233.163.132/translate_c?hl=pt-BR&langpair=en%7Cpt&u=http://www.ncbi.nlm.nih.gov/pubmed/12720576&prev=/translate_s%3Fhl%3Dpt-BR%26q%3DVitamina%2BD%2Be%2Bdepress%25C3%25A3o%26sl%3Dpt%26tl%3Den&rurl=translate.google.com.br&usg=ALkJrhjspQEBlxCMyClVGNWHjrZsYK2BOA

Vitamina D é importantíssima para a saúde
Disponível em http://biodireitomedicina.wordpress.com/category/a-prevencao-de-doencas-neurodegenerativas/

Vitamina D pode revolucionar o tratamento da esclerose múltipla*
http://biodireitomedicina.wordpress.com/2010/08/03/vitamina-d-pode-revolucionar-o-tratamento-da-esclerose-multipla/
*Dr. Cícero Galli Coimbra
PHD Médico Neurologista e Professor Livre-Docente

O que é possível dizer em breves palavras, já oferece um quadro preocupante. A insuficiência de vitamina D tem desenvolvido muitas outras doenças, alem do raquitismo e da osteoporose, que já são aceitas como “comuns” e típicas da medicina das doenças crônicas.

 

Associadas á deficiencia de vitamina D estão o câncer, as diabetes, problemas cardiovasculares, transtorno bipolar, autismo, mal de Alzheimer e esquizofrenia, psoríase, depressão. O comercio industrial multimilionário da farmácia, não traz a cura, apresenta medicação cara e talvez paliativa.

 

Diz assim a medicina das doenças crônicas: “a sua doença não tem cura”… E, no entanto, todas essas doenças graves sequer teriam desenvolvido nas pessoas, se existisse o cuidado com a medicina preventiva com a suplementação da vitamina D3, o hormônio esteroide imunoregulador.

 

Os médicos vêm apresentando pesquisa que aponta o aumento de epidemias em todo planeta, por causa da falta de investimento dos governos em saúde preventiva com suplementação da vitamina D.

Vitamin D deficiency: a global perspectivehttps://objetodignidade.wordpress.com/2011/08/15/vitamin-d-deficiency-a-global-perspective/

Deficiência de vitamina D: uma epidemia global
https://objetodignidade.wordpress.com/2011/08/15/deficiencia-de-vitamina-d-uma-epidemia-global/

Symposium: Vitamin D Insufficiency: A Significant Risk Factor in Chronic Diseases and Potential Disease-Specific Biomarkers of Vitamin D Sufficiency Vitamin D Intake: A Global Perspective of Current Status
https://objetodignidade.wordpress.com/2011/08/15/symposium-vitamin-d-insufficiency-a-significant-risk-factor-in-chronic-diseases-and-potential-disease-specific-biomarkers-of-vitamin-d-sufficiency-vitamin-d-intake-a-global-perspective-of-current-s/

 

Brasil ainda investe pouco em saúde País investe apenas 8,7% do valor arrecadado com impostos em saúde. Número é inferior ao de países como Argentina, Chile e Venezuela. Um estudo realizado pela Fundação Instituto de Administração da Universidade de São Paulo (USP)
https://objetodignidade.wordpress.com/2011/08/05/brasil-ainda-investe-pouco-em-saude/

 

O aumento da Deficiência de vitamina D3 geralmente se apresentava como deformidade óssea (raquitismo) ou hipocalcemia na infância e como dor músculoesquelética e fraqueza em adultos.

 

Hoje os estudos são avançados e os médicos constataram muitos outros problemas de saúde, incluindo doenças cardiovasculares, diabetes, vários tipos de câncer, e autoimunes como mal de Alzheimer e esclerose múltipla, hipo e hipertireoidismo, artrite, vitiligo, associadas á alta insuficiência de vitamina D no sangue.

 

O status da vitamina D é mais confiável determinado pelo ensaio de soro de 25-hidroxivitamina D3 (25-OHD3).


O consenso entre os médicos definiu a medida da nanoterapia como ideal acima de 40 ng/ml de sangue. Abaixo de 40 já existe deficiencia mesmo que a pessoa ainda não apresente qualquer sintoma de doença. Isto significa que há meio de baixo custo para a prevenção de epidemias. A suplementação e reposição da colecalciferol, a vitamina D3 a vitamina D3, deve ser feita em altas doses. Muito alem das convencionadas 600 UI da medicina do passado, para ter uma idéia uma gota [0,05 ml] da solução de colecalciferol tem 1.000 UI [unidades internacionais].

 

O espectro dessas doenças comuns e graves, é particularmente preocupante porque os estudos observacionais têm demonstrado que a insuficiência de vitamina D3, desenvolve Raquitismo em crianças e osteomalacia em adultos são apenas manifestações clássicas de deficiência de vitamina D3 profunda. Nos últimos anos, no entanto, aparecem doenças não músculoesqueléticas condições incluindo câncer, síndrome metabólica, infecciosas e doenças autoimunes, esclerose múltipla, doenças que também foram encontrados associados aos baixos níveis de vitamina D. O Aumento da prevalência de distúrbios ligados à deficiência de VITAMINA D, É REFLETIDA NO AUMENTO DO NUMERO DE CRIANÇAS DOENTES.


EPIDEMIAS CRESCEM SE NÃO FOR DADA NUTRIÇÃO ADEQUADA E SUPLEMENTOS Á TODA POPULAÇÃO. Este é o cuidado que o governo brasileiro deve ter com todas as pessoas, indistintamente, em todas as idades.]

 

Dilma e Lula não sabem disso, e desde 2008 favorecem pesquisas com células de embriões e abortos.


“É interessante notar que as geografias de raquitismo (Hess, 1929) e MS são muito semelhantes, a geografia do raquitismo levou Sniadecki (citado por Holick, 1995) para sugerir em 1822 que o sol pode curar o raquitismo. Lamentavelmente, diz Hayes, o raquitismo continuou a aleijar crianças por um século inteiro antes de investigadores demonstrarem os benefícios da luz solar ou óleo de fígado de bacalhau (Hess & Unger, 1921; Chick et al. 1922). Hoje o óleo de fígado de bacalhau tornou-se a proteção do “inverno” para as crianças que vivem em latitudes setentrionais.”

 

  Ver Vitamin D: a natural inhibitor of multiple sclerosis, de Collen Hayes:
Disponivel em http://journals.cambridge.org/action/displayFulltext?type=1&fid=796912&jid=PNS&volumeId=59&issueId=04&aid=796900

“A evidência de que a vitamina D pode ser um inibidor natural de MS ou E.M. é irresistível. Examinando o benefício da suplementação de vitamina D para a prevenção de MS, a recusa desta verdade vai exigir um grande esforço por parte da comunidade científica, mas é claramente justificada diante dos atuais investimentos político-economicos”, diz Collen Hayes.

Ver Vitamin D: a natural inhibitor of multiple sclerosis, de Collen Hayes:
Disponivel em http://journals.cambridge.org/action/displayFulltext?type=1&fid=796912&jid=PNS&volumeId=59&issueId=04&aid=796900—-

 

As pessoas que têm doenças como Alzheimer, esclerose múltipla, lúpus, hipo e hipertireoidismo, artrite, vitiligo, diabetes, câncer e outras doenças autoimunitárias, hoje são orientadas por médicos e pesquisadores a consumir a solução oleosa [óleo de girassol ou oliva] de colecalciferol, a vitamina D3. A 25hidroxivitamin D3 é de fácil absorção pelo organismo. Passando do fígado aos rins e, depois de transformada em ativa, é absorvida por todas as células de todos os tecidos do corpo humano, como cálcio, fósforo e outras substancias, fortalecendo e recuperando inclusive o tecido neural.

 

A DEFICIENCIA ou INSUFICIENCIA DA VITAMINA D é verificada em exame de sangue, o 25[OH]D3 que o sistema de saúde publica do Brasil não oferece.


O consenso entre os médicos definiu a medida da nanoterapia como ideal acima de 40. Abaixo de 40 já existe deficiencia mesmo que a pessoa ainda não apresente qualquer sintoma de doença. Isto significa que há meio de baixo custo para a prevenção de epidemias. A suplementação e reposição da colecalciferol, a vitamina D3 a vitamina D3, deve ser feita em altas doses. Muito alem das convencionadas 600 UI da medicina do passado, para ter uma idéia uma gota [0,05 ml] da solução de colecalciferol tem 1.000 UI [unidades internacionais].

 

E há SIM UM DISTURBIO METABOLICO, pois, se as pessoas com resultado do exame de sangue abaixo de 50, já estiverem recebendo alimentação apropriada, existe indicio de dificuldade digestiva na absorção dos alimentos, depressão, estresse e tristeza que impedem a neurogenesis.

 

“Revisando-se a literatura, verificamos que a carne vermelha libera, durante a digestão, a substância hemina, que possui propriedades tóxicas, porque penetra as membranas celulares carregando ferro para o interior das células, onde este eleva a produção de radicais livres. Para evitar tal efeito, a hemina é destruída, em sua maior parte, na própria célula intestinal (e o restante, no fígado), utilizando a vitamina B2. Tornou-se claro, então, que o indivíduo absorve a hemina, não tendo então a B2 para destruí-la. Assim, solicitamos a parada completa da ingestão de carne”. Coimbra acrescenta que o tratamento tradicional contra a doença, à base de medicamentos, deve ser concomitante à dieta proposta pelos pesquisadores.
[…]
SBPC/Labjor – Brasil
SBPC/Labjor – Brasil
Disponível em http://www.comciencia.br/noticias/2003/06jun03/parkinson.htm
——

 

Vitamina D pode revolucionar o tratamento da esclerose múltipla*
http://biodireitomedicina.wordpress.com/2010/08/03/vitamina-d-pode-revolucionar-o-tratamento-da-esclerose-multipla/
*Dr. Cícero Galli Coimbra
PHD Médico Neurologista e Professor Livre-Docente

Informações médicas sobre a prevenção e tratamento de doenças neurodegenerativas e autoimunes, como Parkinson, Alzheimer, Lupus, Psoríase, Vitiligo, depressão
Dr. Cícero Galli Coimbra
PHD Médico Neurologista e Professor Livre-Docente
http://biodireitomedicina.wordpress.com/category/doencas-autoimunes/

 

“a situação fundamental é a mesma: a existência de um DISTÚRBIO METABÓLICO evidente e corrigível, capaz de explicar os eventos fisiopatológicos conhecidos, e cuja correção pode deter a progressão da doença (interrompendo a continuidade da morte neuronal crônica, recuperando células neuronais já afetadas pelo processo neurodegenerativo – mas que não atingiram ainda o ponto de irreversibilidade), promover a recuperação total em casos de início recente, ou ao menos parcial das deficiências neurológicas nos casos mais avançados (minimizando seqüelas permanentes) e impedir a morte.” [1]

 

Disponivel em
http://www.unifesp.br/dneuro/nexp/riboflavina/
—-
Dr. Cícero Galli Coimbra
PHD Médico Neurologista e Professor Livre-Docente
http://biodireitomedicina.wordpress.com/category/doencas-autoimunes/
—-

 

Vitamin D: a natural inhibitor of multiple sclerosis From Colleen E. Hayes Department of Biochemistry, University of Wisconsin-Madison, 433 Babcock
Disponivel em 
http://journals.cambridge.org/action/displayFulltext?type=1&fid=796912&jid=PNS&volumeId=59&issueId=04&aid=796900——

 

 

Vitamin D: its role and uses in immunology
HECTOR F. DELUCA2 and MARGHERITA T. CANTORNA*
Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA; and
* Department of Nutrition, Pennsylvania State University, University Park, Pennsylvania 16802, USA
http://www.fasebj.org/cgi/content/full/15/14/2579http://www.drtheo.com/vitaminD/documents/VitaminD-itsroleandusesinimmunology.pdf
(The FASEB Journal. 2001;15:2579-2585.)
—-

 

  1. 1.      Disponivel em
    http://www.unifesp.br/dneuro/nexp/riboflavina/
    —-
    Dr. Cícero Galli Coimbra
    PHD Médico Neurologista e Professor Livre-Docente
    http://biodireitomedicina.wordpress.com/category/doencas-autoimunes/
    —-

Vitamin D: a natural inhibitor of multiple sclerosis From Colleen E. Hayes Department of Biochemistry, University of Wisconsin-Madison, 433 Babcock Disponivel em http://journals.cambridge.org/action/displayFulltext?type=1&fid=796912&jid=PNS&volumeId=59&issueId=04&aid=796900——

Vitamin D: its role and uses in immunology
HECTOR F. DELUCA2 and MARGHERITA T. CANTORNA*
Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA; and
* Department of Nutrition, Pennsylvania State University, University Park, Pennsylvania 16802, USA
http://www.fasebj.org/cgi/content/full/15/14/2579http://www.drtheo.com/vitaminD/documents/VitaminD-itsroleandusesinimmunology.pdf
(The FASEB Journal. 2001;15:2579-2585.)
—-

High prevalence of vitamin D deficiency and reduced bone mass in multiple sclerosis
http://www.huffingtonpost.com/dr-david-perlmutter-md/vitamin-d-benefits_b_818912.html
High prevalence of vitamin D deficiency and reduced bone mass in multiple sclerosis
J. Nieves, PhD,
F. Cosman, MD,
J. Herbert, MD,
V. Shen, PhD and
R. Lindsay, MD
—-

Vitamin D and the immune system: new perspectives on an old theme
Endocrinol Metab Clin North Am. 2010 June; 39(2):
365–379.
Endocrinol Metab Clin North Am. Author manuscript; available in PMC 2011 June 1.Published in final edited form as:Endocrinol Metab Clin North Am. 2010 June; 39(2): 365–379. doi: 10.1016/j.ecl.2010.02.010

Martin Hewison, PhD
Martin Hewison, Professor in Residence, Department of Orthopaedic Surgery and Molecular Biology Institute, David Geffen School of Medicine at UCLA, 615 Charles E. Young Drive South, Los Angeles, CA 90095, USA;
National Center for Biotechnology Information, U.S. National Library of Medicine 8600 Rockville Pike, Bethesda MD, 20894 USA
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2879394/?tool=pubmed
—-

Lack of Vitamin D Linked to Alzheimer’s and Vascular Dementia
Friday, June 05, 2009 by: Sherry Baker, Health Sciences Editor
Sherry Baker is a widely published writer whose work has appeared in Newsweek, Health, the Atlanta Journal and Constitution, Yoga Journal, Optometry, Atlanta, Arthritis Today, Natural Healing Newsletter, OMNI, UCLA’s “Healthy Years” newsletter, Mount Sinai School of Medicine’s “Focus on Health Aging” newsletter, the Cleveland Clinic’s “Men’s Health Advisor” newsletter and many others.
Learn more:
http://www.naturalnews.com/026392_Vitamin_D_Alzheimers_disease.html#ixzz3HnBD71Qg
http://www.naturalnews.com/026392_Vitamin_D_Alzheimers_disease.html
—-

Factors in human vitamin D nutrition and in the production and cure of classical rickets Sítio canadense sobre e.m. DIRECT-MS
Fatores nutricionais e suplementares relacionados à esclerose múltipla.
http://www.direct-ms.org/
—-

“It is plausible that some 200 cases a year of MS might be prevented in Scotland alone by giving vitamin D to mothers and children,” he wrote.

disponivel emhttp://www.timesonline.co.uk/tol/life_and_style/health/article5663483.ece-VitaminD is ray of sunshine for multiple sclerosis patient
—-

Vitamin D in preventive medicine: are we ignoring the evidence? Vitamin D in preventive medicine: are we ignoring the evidence? A vitamina D em medicina preventiva: estamos ignorando as provas? Vitamina D em medicina preventiva: estamos ignorando as provas?
Dispoível em
http://64.233.163.132/translate_c?hl=pt-BR&langpair=en%7Cpt&u=http://www.ncbi.nlm.nih.gov/pubmed/12720576&prev=/translate_s%3Fhl%3Dpt-BR%26q%3DVitamina%2BD%2Be%2Bdepress%25C3%25A3o%26sl%3Dpt%26tl%3Den&rurl=translate.google.com.br&usg=ALkJrhjspQEBlxCMyClVGNWHjrZsYK2BOA


Vitamin D supplementation: Recommendations for Canadian mothers and infants. A suplementação de vitamina D: Recomendações para as mães e bebês canadenses.. 
Paediatr Child Health. . Paediatr Child Health. 2007 Sep; 12(7):583-98. 2007 Sep; 12 (7) :583-98.[Paediatr Child Health. [Paediatr Child Health. 2007] 2007]

Review Vitamin D and disease prevention with special reference to cardiovascular disease. Review vitamina D e prevenção de doenças, com especial referência à doença cardiovascular.Prog Biophys Mol Biol. Prog Biophys Mol Biol. 2006 Sep; 92(1):39-48. 2006 Sep; 92 (1) :39-48. Epub 2006 Feb 28. Epub 2006 Feb 28.[Prog Biophys Mol Biol. [Prog Biophys Mol Biol. 2006] 2006]

Vitamin D in health and disease. Vitamina D na saúde e na doença.Clin J Am Soc Nephrol. Clin J Am Soc Nephrol. 2008 Sep; 3(5):1535-41. 2008 Sep; 3 (5) :1535-41. Epub 2008 Jun 4. Epub 2008 Jun 4.[Clin J Am Soc Nephrol. [Clin J Am Soc Nephrol. 2008] 2008]

Review Sunlight and vitamin D for bone health and prevention of autoimmune diseases, cancers, and cardiovascular disease. Review Luz solar e vitamina D para a saúde óssea e prevenção de doenças auto-imunes, câncer e doenças cardiovasculares.Am J Clin Nutr. Am J Clin Nutr. 2004 Dec; 80(6 Suppl):1678S-88S. 2004 Dec; 80 (6 Suppl): 1678S-88S.[Am J Clin Nutr. [Am J Clin Nutr. 2004] 2004]
—-

Cristiane Rozicki, em junho 25, 2012 às 5:20 pm disse:

Referencias Médico-Científicas Sobre Tratamento, Cura e Prevenção, doenças neurodegenerativas e autoimunes. Vitamina D.

Referencias Médico-Científicas Sobre Tratamento, Cura e Prevenção, doenças neurodegenerativas e autoimunes. Vitamina D.

Vitamina D pode revolucionar o tratamento da esclerose múltipla*
http://biodireitomedicina.wordpress.com/category/doencas-autoimunes/

POR UM NOVO PARADIGMA DE CONDUTA E TRATAMENTO
http://www.institutodeautoimunidade.org.br/novo-paradigma.html

Por Dr. Cícero Galli Coimbra
Médico Internista e Neurologista
Professor Associado Livre-Docente da Universidade Federal de São Paulo
Presidente do Instituto de Investigação e Tratamento de Autoimunidade


O vídeo referido na reportagem dominical de 27.05.12 da Folha está no endereço:
Vitamina D – Por uma outra terapia (Vitamin D – For an alternative therapy)

http://biodireitomedicina.wordpress.com/2012/05/28/folha-de-sao-paulo-terapia-polemica-usa-vitamina-d-em-doses-altas-contra-esclerose-multipla/


Vitamina D pode revolucionar o tratamento da esclerose múltipla
http://biodireitomedicina.wordpress.com/2010/08/03/vitamina-d-pode-revolucionar-o-tratamento-da-esclerose-multipla/

Taxas baixas de vitamina D na maioria da população preocupam especialistas
http://biodireitomedicina.wordpress.com/2012/06/18/taxas-baixas-de-vitamina-d-na-maioria-da-populacao-preocupam-especialistas/

Pediatras dobram recomendação de consumo diário de vitamina D
http://biodireitomedicina.wordpress.com/2012/06/17/pediatras-dobram-recomendacao-de-consumo-diario-de-vitamina-d/

Doses diárias de Sol – nos horários certos e com os devidos cuidados
http://biodireitomedicina.wordpress.com/2012/06/12/doses-diarias-de-sol-nos-horarios-certos-e-com-os-devidos-cuidados/

“(…) cerca de 70% da população mundial apresenta taxas inadequadas de vitamina D, substância que, dentro do corpo, trabalha como um hormônio. O fenômeno da insuficiência não poupa nem países tropicais, como o Brasil, e a defasagem tende a ser maior nas grandes cidades, já que, dentro de casa, no carro ou no escritório, as pessoas acabam fugindo do sol. De acordo com o endocrinologista Geraldo Santana, do Instituto Mineiro de Endocrinologia, “a deficiência de vitamina D é um achado frequente e também preocupante devido à importante ação da substância no organismo.”
Celso Galli Coimbra
OABRS 11352
cgcoimbra@gmail.com
Em 19.06.2012
__

Vitamina D: A Desinformação Médica e o Direito à Informação do Cidadão
http://biodireitomedicina.wordpress.com/2012/06/20/vitamina-d-a-desinformacao-medica-e-o-direito-a-informacao-do-cidadao/

Vitamina D pode combater males que mais matam pessoas no mundo
http://biodireitomedicina.wordpress.com/2010/03/20/vitamina-d-pode-combater-males-que-mais-matam-pessoas-no-mundo/

Informações médicas sobre a prevenção e tratamento de doenças neurodegenerativas e autoimunes, Parkinson, Alzheimer, Lupus, Psoríase, Vitiligo, como depressão
http://biodireitomedicina.wordpress.com/2011/03/23/informacoes-medicas-sobre-a-prevencao-e-tratamento-de-doencas-neurodegenerativas-e-auto-imunes-como-parkinson-alzheimer-lupus-psoriase-vitiligo-depressao/

Vitamina D é importantíssima para a saúde
”Estudos realizados no Brasil e no exterior apontam a importância da substância na prevenção e no tratamento do câncer, diabetes e de doenças neurológicas, cardiovasculares e até degenerativas, como a esclerose múltipla.”
http://biodireitomedicina.wordpress.com/2009/09/22/vitamina-d-e-importantissima-para-a-saude/

A importância da colina para a regeneração neuronal
http://biodireitomedicina.wordpress.com/2009/09/18/a-volta-triunfal-do-ovo/
“A colina é especialmente importante na gravidez. “Vários estudos já mostraram que ela é tão ou mais importante do que o ácido fólico durante a gestação”
Antes inimigo da saúde cardiovascular, o alimento agora está liberado pelos médicos

O tratamento com vitamina D deve ser feito com indicação por médico atualizado
http://biodireitomedicina.wordpress.com/2012/06/22/o-tratamento-com-vitamina-d/

Taxas baixas de vitamina D na maioria da população preocupam especialistas
http://biodireitomedicina.wordpress.com/2012/06/18/taxas-baixas-de-vitamina-d-na-maioria-da-populacao-preocupam-especialistas/

Solução que vem do sol – com os devidos cuidados
http://biodireitomedicina.wordpress.com/2012/06/12/solucao-que-vem-do-sol-com-os-devidos-cuidados/
11 de junho de 2012
“A vitamina D, que precisa dos raios solares para ser sintetizada no corpo, é a base de uma alternativa revolucionária para tratar doenças autoimunes”

Informações médicas sobre a prevenção e tratamento de doenças neurodegenerativas e autoimunes, como Parkinson, Alzheimer, Lupus, Psoríase, Vitiligo, depressão
Entrevista em TV com o Dr. Cícero Galli Coimbra, professor neurologista da Universidade Federal de São Paulo – Unifesp.
http://biodireitomedicina.wordpress.com/2011/03/23/informacoes-medicas-sobre-a-prevencao-e-tratamento-de-doencas-neurodegenerativas-e-auto-imunes-como-parkinson-alzheimer-lupus-psoriase-vitiligo-depressao/


Vitamina D pode revolucionar o tratamento da esclerose múltipla
http://biodireitomedicina.wordpress.com/2010/08/03/vitamina-d-pode-revolucionar-o-tratamento-da-esclerose-multipla/
Sobre este assunto, assista: Vitamina D – por uma outra terapia
http://biodireitomedicina.wordpress.com/2012/04/12/vitamina-d-por-uma-outra-terapia/
http://biodireitomedicina.wordpress.com/2011/03/23/informacoes-medicas-sobre-a-prevencao-e-tratamento-de-doencas-neurodegenerativas-e-auto-imunes-como-parkinson-alzheimer-lupus-psoriase-vitiligo-depressao/
—-

Vitamina D pode combater males que mais matam pessoas no mundo
http://biodireitomedicina.wordpress.com/2010/03/20/vitamina-d-pode-combater-males-que-mais-matam-pessoas-no-mundo/

—-

“POR UM NOVO PARADIGMA DE CONDUTA E TRATAMENTO” – “Estamos vivendo uma defasagem entre o conhecimento científico e a prática médica” – Dr. Cicero Galli Coimbra, medico neurologista, Phd., professor na Universidade Federal de São Paulo,, em dezembro 9, 2012 às 7:16 pm disse:

[…] Esclerose múltipla, distúrbio metabólico. […]

·         Vitamina do Sol é sem protetor – a pele produz a Vitamina D, hormonio esteroide, na cura e na medicina preventiva

Vitamina D

o   http://biodireitomedicina.wordpress.com/category/vitamina-d/

.

Deficiência de vitamina D em grávidas

03/01/2013 — Celso Galli Coimbrahttp://biodireitomedicina.wordpress.com/2013/01/03/deficiencia-de-vitamina-d-em-gravidas/

__ Related articles

http://biodireitomedicina.wordpress.com/2012/07/23/bibiliografia-cientifica-internacional-sobre-vitamina-d-60-724-titulos-nesta-data-na-scirus/

__

POR UM NOVO PARADIGMA DE CONDUTA E TRATAMENTO

Por Dr. Cícero Galli Coimbra

Médico Internista e Neurologista

Professor Associado Livre-Docente da Universidade Federal de São Paulo

Presidente do Instituto de Investigação e Tratamento de Autoimunidade

http://www.institutodeautoimunidade.org.br/novo-paradigma.html

—-

 

A vital importância do hormônio conhecido por Vitamina D3 para a preservação ou recuperação de sua saúde de doenças autoimunes: exijam que seus médicos se atualizem

Por Celso Galli Coimbra

Celso Galli Coimbra – OABRS 11352
cgcoimbra@gmail.com
http://biodireitomedicina.wordpress.com/
https://www.facebook.com/celso.gallicoimbra
http://www.youtube.com/biodireitobioetica

http://biodireitomedicina.wordpress.com/2012/12/23/vitamina-d3-e-sua-saude/#comment-3220

 

VITAMINA D e a RESPONSABILIDADE CIVIL DO MÉDICO

 

”ATENÇÃO: o uso preventivo do Vitamina D3 é DIFERENTE do uso terapêutico deste hormônio-vitamina, que exige sempre a orientação e acompanhamento de médico com treinamento adequado para ser responsável pela avaliação caso a caso e a específica determinação de dosagem, em contrário haverá sérios danos à saúde.”

http://biodireitomedicina.wordpress.com/2012/12/23/vitamina-d3-e-sua-saude/

—-

Para estas pessoas que desenvolveram doenças autoimunes, a solução simples é o consumo de altas DOSES DE VITAMINA D QUE O MEDICO PRESCREVE SEGUNDO O CASO DE CADA PACIENTE. – Dr. Cicero Galli Coimbra, medico neurologista, Phd., professor na Universid, em fevereiro 28, 2013 às 4:21 pm disse:

[…] Esclerose múltipla, distúrbio metabólico – atualizado em 7/janeiro/2013 […]

A responsabilidade Civil e Criminal Médica na Desinformação às pessoas – Revista VEJA, 2.304: “O que você não sabe sobre a Vitamina do Sol. Ela continua a surpreender a medicina com novos efeitos benéficos.”

20/01/2013 — Celso Galli Coimbra

http://biodireitomedicina.wordpress.com/2013/01/20/a-responsabilidade-civil-e-criminal-medica-na-desinformacao-as-pessoas-revista-veja-2-304-o-que-voce-nao-sabe-sobre-a-vitamina-do-sol-ela-continua-a-surpreender-a-medicina-com-novos-efe/

Vitamina D – Entrevista com Dr. Cícero Galli Coimbra sobre esclerose múltipla e demais doenças autoimunitárias
28/01/2013 — Celso Galli Coimbra

http://biodireitomedicina.wordpress.com/2013/01/28/vitamina-d-entrevista-com-dr-cicero-galli-coimbra-sobre-esclerose-multipla-e-demais-doencas-autoimunitarias/
__

http://www.institutodeautoimunidade.org.br/novo-paradigma.html
Cícero Galli Coimbra
Médico Internista e Neurologista
Professor Associado Livre-Docente da Universidade Federal de São Paulo
Presidente do Instituto de Investigação e Tratamento de Autoimunidade

Vitamina D3 – 10.000 UI diárias é vital para à saúde
por Celso Galli Coimbra
http://www.youtube.com/playlist?list=PL301EAE2D5602A758
http://www.youtube.com/watch?v=Pn-swcSA7As&list=PL301EAE2D5602A758&index=25

Vídeos com pessoas que estão curadas e fizeram o tratamento com a Vitamina D. Mais de 10 anos que este tratamento eficiente é usado e autoimunidade tem cura sim.

Vitamina D – Por uma outra terapia (Vitamin D – For an alternative therapy)
http://www.youtube.com/watch?feature=player_detailpage&v=erAgu1XcY-U

Mais de 10 anos de tratamento com a Vitamina D – Exijam que seus médicos se atualizem!
23/12/2012 — Celso Galli Coimbra
http://biodireitomedicina.wordpress.com/2012/12/23/mais-de-10-anos-de-tratamento-com-a-vitamina-d-exija-que-seus-medicos-se-atualizem/
—-

Traíção de uma Nação: autoridades de saúde dos EUA estão protegendo a deficiência de Vitamina D para beneficiar a Indústria Farmacêutica. Betrayal of a Nation: Why U.S. health authorities are keeping you vitamin D deficient and who stands to gain
15/01/2013 — Celso Galli Coimbra
http://biodireitomedicina.wordpress.com/2013/01/15/traicao-de-uma-nacao-autoridades-de-saude-dos-eua-estao-protegendo-a-deficiencia-de-vitamina-d-para-benficiar-a-industria-farmaceutica-betrayal-of-a-nation-why-u-s-health-authorities-are-keeping-y/

Vitamina D – Por uma outra terapia (Vitamin D – For an alternative therapy)
http://www.youtube.com/watch?feature=player_detailpage&v=erAgu1XcY-U

Dr. Cícero Galli Coimbra – Doenças Autoimunes e Vitamina D
http://www.youtube.com/watch?feature=player_embedded&v=4uJt1361aGw

Vitamina D – Sem Censura – Dr. Cicero Galli Coimbra e Daniel Cunha
http://www.youtube.com/watch?feature=player_embedded&v=cIwIWim4hNM

Vitamina D – Por uma outra terapia (Vitamin D – For an alternative therapy)
http://www.youtube.com/watch?feature=player_detailpage&v=erAgu1XcY-U

Para estas pessoas que desenvolveram doenças autoimunes, a solução simples é o consumo de altas DOSES DE VITAMINA D QUE O MEDICO PRESCREVE SEGUNDO O CASO DE CADA PACIENTE. – Dr. Cicero Galli Coimbra, medico neurologista, Phd., professor na Universidade Federal de São Paulo, Presidente do Instituto de Investigação e Tratamento de Autoimunidade

“POR UM NOVO PARADIGMA DE CONDUTA E TRATAMENTO” – “Estamos vivendo uma defasagem entre o conhecimento científico e a prática médica” – Dr. Cicero Galli Coimbra, medico neurologista, Phd., professor na Universidade Federal de São Paulo, Presidente do Instituto de Investigação e Tratamento de Autoimunidade

Dr. Cícero Galli Coimbra – Doenças Autoimunes e Vitamina D
http://www.youtube.com/watch?feature=player_embedded&v=4uJt1361aGw
Vitamina D – Sem Censura – Dr. Cicero Galli Coimbra e Daniel Cunha
http://www.youtube.com/watch?feature=player_embedded&v=cIwIWim4hNM
Vitamina D – Por uma outra terapia (Vitamin D – For an alternative therapy)
http://www.youtube.com/watch?feature=player_detailpage&v=erAgu1XcY-U
Para estas pessoas que desenvolveram doenças autoimunes, a solução simples é o consumo de altas DOSES DE VITAMINA D QUE O MEDICO PRESCREVE SEGUNDO O CASO DE CADA PACIENTE. – Dr. Cicero Galli Coimbra, medico neurologista, Phd., professor na Universidade Federal de São Paulo, Presidente do Instituto de Investigação e Tratamento de Autoimunidade
———-
“por causa da deficiência de vitamina D, o hormonio esteroide do qual estamos falando, torna o sistema imunológico completamente desregulado, de tal modo que ele tem dificuldade de reagir contra infecções e permite o organismo ser atacado por qualquer outra doença.’’

“Há evidencias de que a carencia de vitamina D provoca e agrava a esclerose múltipla (Surtos da doença abalam o sistema nervoso central). Assim, também a deficiencia de Colecalciferol pode levar a problemas Cardiovasculares, AVCs, nascimento de crianças autistas, problemas na gestação, Alzheimer.”

(2) Bibiliografia científica internacional sobre Vitamina D – 60.724 títulos nesta data na SCIRUS
Acesse: “multiple sclerosis” (“vitamin D”)
http://www.scirus.com/srsapp/search?q=%22multiple+sclerosis%22+%28%22vitamin+D%22%29&t=all&sort=0&g=s
23/07/2012 — Celso Galli Coimbra – OABRS 11352
http://biodireitomedicina.wordpress.com/2012/07/23/bibiliografia-cientifica-internacional-sobre-vitamina-d-60-724-titulos-nesta-data-na-scirus/
__
“Infelizmente este conhecimento não tem sido levado aos livros textos de medicina e isso gera esse desconhecimento, não só do público em geral mas até da classe médica em relação á gravidade dessa situação sobre a deficiência desse hormonio esteroide. Esta deficiencia torna as 229 funções do sistema imunológico do próprio organismo das pessoas desregulado, permitindo desenvolver qualquer doença, o que levou á pandemia do mundo atual.”

http://www.institutodeautoimunidade.org.br/novo-paradigma.html
Cícero Galli Coimbra
Médico Internista e Neurologista
Professor Associado Livre-Docente da Universidade Federal de São Paulo
Presidente do Instituto de Investigação e Tratamento de Autoimunidade

Vitamina D

– –

Para estas pessoas que desenvolveram doenças autoimunes, a solução simples é o consumo de altas DOSES DE VITAMINA D QUE O MEDICO PRESCREVE SEGUNDO O CASO DE CADA PACIENTE. – Dr. Cicero Galli Coimbra, medico neurologista, Phd., professor na Universid, em fevereiro 28, 2013 às 4:21 pm disse:

[…] Esclerose múltipla, distúrbio metabólico – atualizado em 7/janeiro/2013 […]

Por 30 anos, extensa revisão de toda a pesquisa anterior confirma que baixo nível de vitamina D é uma sentença de morte
http://biodireitomedicina.wordpress.com/2013/02/13/por-30-anos-extensa-revisao-de-toda-a-pesquisa-anterior-confirma-que-baixo-nivel-de-vitamina-d-e-uma-sentenca-de-morte/
__
Hormônio-Vitamina D: quando a Medicina tem dois pesos e duas medidas e a saúde do paciente vale menos do que a saúde do médico
25/02/2013 — Celso Galli Coimbra
__
Constituição Federal, Art. 196. “A saúde é direito de todos e dever do Estado, garantido mediante políticas sociais e econômicas que visem à redução do risco de doença e de outros agravos e ao acesso universal e igualitário às ações e serviços para sua promoção, proteção e recuperação.”
http://biodireitomedicina.wordpress.com/2013/02/25/hormonio-vitamina-d-quando-a-medicina-tem-dois-pesos-e-duas-medidas-e-a-saude-do-paciente-vale-menos-do-que-a-saude-do-medico/

Informe-se:
Vitamina D3 – 10.000 UI diárias é vital para à saúde
http://www.youtube.com/watch?feature=player_embedded&list=PL301EAE2D5602A758&v=LGqg2-PiO8M
Aqui está o editorial do Multiple Sclerosis Journal :
VIt D for relative with MS
Celso Galli Coimbra
OABRS 11352
cgcoimbra@gmail.com
__
http://www.youtube.com/watch?feature=player_embedded&v=J3UvUK3_u0o
Vitamina D3 – 10.000 UI diárias é vital para preservar à saúde
https://www.youtube.com/playlist?list=PL301EAE2D5602A758
No Facebook apenas “curta” esta página e estará automaticamente inscrito:
Vitamina D é um hormônio vital para preservação da saúde
https://www.facebook.com/VitaminaD.HormonioVital
Leia também:
Por 30 anos, extensa revisão de toda a pesquisa anterior confirma que baixo nível de vitamina D é uma sentença de morte
http://biodireitomedicina.wordpress.com/2013/02/13/por-30-anos-extensa-revisao-de-toda-a-pesquisa-anterior-confirma-que-baixo-nivel-de-vitamina-d-e-uma-sentenca-de-morte/
Cientistas convocam para uma Ação de Saúde Pública tendo como modelo o uso do Hormônio-Vitamina D
http://biodireitomedicina.wordpress.com/2013/01/29/cientistas-convocam-para-uma-acao-de-saude-publica-tendo-como-modelo-o-uso-do-hormonio-vitamina-d/

__
http://www.youtube.com/watch?feature=player_embedded&v=J3UvUK3_u0o
Vitamina D3 – 10.000 UI diárias é vital para preservar à saúde
https://www.youtube.com/playlist?list=PL301EAE2D5602A758
No Facebook apenas “curta” esta página e estará automaticamente inscrito:
Vitamina D é um hormônio vital para preservação da saúde
https://www.facebook.com/VitaminaD.HormonioVital
Leia também:
Por 30 anos, extensa revisão de toda a pesquisa anterior confirma que baixo nível de vitamina D é uma sentença de morte
http://biodireitomedicina.wordpress.com/2013/02/13/por-30-anos-extensa-revisao-de-toda-a-pesquisa-anterior-confirma-que-baixo-nivel-de-vitamina-d-e-uma-sentenca-de-morte/
Cientistas convocam para uma Ação de Saúde Pública tendo como modelo o uso do Hormônio-Vitamina D
http://biodireitomedicina.wordpress.com/2013/01/29/cientistas-convocam-para-uma-acao-de-saude-publica-tendo-como-modelo-o-uso-do-hormonio-vitamina-d/

A responsabilidade Civil e Criminal Médica na Desinformação às pessoas – Revista VEJA, 2.304: “O que você não sabe sobre a Vitamina do Sol. Ela continua a surpreender a medicina com novos efeitos benéficos.”

20/01/2013 — Celso Galli Coimbra

http://biodireitomedicina.wordpress.com/2013/01/20/a-responsabilidade-civil-e-criminal-medica-na-desinformacao-as-pessoas-revista-veja-2-304-o-que-voce-nao-sabe-sobre-a-vitamina-do-sol-ela-continua-a-surpreender-a-medicina-com-novos-efe/

Para estas pessoas que desenvolveram doenças autoimunes, a solução simples é o consumo de altas DOSES DE VITAMINA D QUE O MEDICO PRESCREVE SEGUNDO O CASO DE CADA PACIENTE. – Dr. Cicero Galli Coimbra, medico neurologista, Phd., professor na Universid, em fevereiro 28, 2013 às 4:29 pm disse:

[…] Esclerose múltipla, distúrbio metabólico – atualizado em 7/janeiro/2013 […]

 

 […] Esclerose múltiplA responsabilidade Civil e Criminal Médica na Desinformação às pessoas – Revista VEJA, 2.304: “O que você não sabe sobre a Vitamina do Sol. Ela continua a surpreender a medicina com novos efeitos benéficos.”

20/01/2013 — Celso Galli Coimbra

http://biodireitomedicina.wordpress.com/2013/01/20/a-responsabilidade-civil-e-criminal-medica-na-desinformacao-as-pessoas-revista-veja-2-304-o-que-voce-nao-sabe-sobre-a-vitamina-do-sol-ela-continua-a-surpreender-a-medicina-com-novos-efe/

 

Há interesses na gestão da Medicina associados com os da Indústria Farmacêutica e não com a preservação da saúde

É impossível dimensionar a extensão CRIMINOSA dos interesses envolvidos em forçar cada vez mais o que já é comprovado pela CIÊNCIA:

SEM o hormônio conhecido por Vitamina D, em doses não inferiores a 10.000 UI diárias para pessoas AINDA saudáveis, o que a correta exposição ao SOL diariamente desenvolve pela [redundância] própria natureza através da pele HUMANA, de acordo com tipo de pele e idade, a saúde e a vida de todas as pessoas estão definitivamente comprometidas.

Os grandes beneficiários desta CONDUTA CRIMINOSA – em desinformar o que é OBRIGAÇÃO PROFISSIONAL MÉDICA informar – são os investidores da Indústria Farmacêutica e seus interesses em aumentar o universo de pessoas doentes e dependentes de inócua “medicação” de ALTO CUSTO” .

 

[…] Esclerose múltipla, distúrbio metabólico – atualizado em 7/janeiro/2013 […]

Dr. Cícero Galli Coimbra – Doenças Autoimunes e Vitamina D
http://www.youtube.com/watch?feature=player_embedded&v=4uJt1361aGw

Vitamina D – Sem Censura – Dr. Cicero Galli Coimbra e Daniel Cunha
http://www.youtube.com/watch?feature=player_embedded&v=cIwIWim4hNM

Vitamina D – Por uma outra terapia (Vitamin D – For an alternative therapy)
http://www.youtube.com/watch?feature=player_detailpage&v=erAgu1XcY-U

Para estas pessoas que desenvolveram doenças autoimunes, a solução simples é o consumo de altas DOSES DE VITAMINA D QUE O MEDICO PRESCREVE SEGUNDO O CASO DE CADA PACIENTE. – Dr. Cicero Galli Coimbra, medico neurologista, Phd., professor na Universidade Federal de São Paulo, Presidente do Instituto de Investigação e Tratamento de Autoimunidade

·       A Autoimunidade tem cura com a Vitamina D – Instituto de Investigação e Tratamento da Autoimunidade

——–

Influence of Vitamin D Status and Vitamin D3 Supplementation on Genome Wide Expression of White Blood Cells: A Randomized Double-Blind Clinical Trial

Lançamento nova publicação (26 de março de 2013)

por Michael F. Holick, Ph.D, MD

“Influência da vitamina D e suplementação de vitamina D3 sobre o genoma. Expressão clinica da variedade de células brancas do sangue: um estudo duplo-cego randomizado” foi recentemente publicado na PLoS e está disponível online.

dr_%20holick%20photoArticle

Influence of Vitamin D Status and Vitamin D3 Supplementation on Genome Wide Expression of White Blood Cells: A Randomized Double-Blind Clinical Trial

  • Arash Hossein-nezhad,

Affiliation: Department of Medicine, Section of Endocrinology, Nutrition, and Diabetes, Vitamin D, Skin and Bone Research Laboratory, Boston University Medical Center, Boston, Massachusetts, United States of America

X

  • Avrum Spira,

Affiliation: Department of Medicine, Section of Computational Biomedicine, Boston University Medical Center, Boston, Massachusetts, United States of America

X

  • Michael F. Holick mail

* E-mail: mfholick@bu.edu

Affiliation: Department of Medicine, Section of Endocrinology, Nutrition, and Diabetes, Vitamin D, Skin and Bone Research Laboratory, Boston University Medical Center, Boston, Massachusetts, United States of America

Abstract

Background

Although there have been numerous observations of vitamin D deficiency and its links to chronic diseases, no studies have reported on how vitamin D status and vitamin D3 supplementation affects broad gene expression in humans. The objective of this study was to determine the effect of vitamin D status and subsequent vitamin D supplementation on broad gene expression in healthy adults. (Trial registration: ClinicalTrials.gov NCT01696409).

Methods and Findings

A randomized, double-blind, single center pilot trial was conducted for comparing vitamin D supplementation with either 400 IUs (n = 3) or 2000 IUs (n = 5) vitamin D3 daily for 2 months on broad gene expression in the white blood cells collected from 8 healthy adults in the winter. Microarrays of the 16 buffy coats from eight subjects passed the quality control filters and normalized with the RMA method. Vitamin D3 supplementation that improved serum 25-hydroxyvitamin D concentrations was associated with at least a 1.5 fold alteration in the expression of 291 genes. There was a significant difference in the expression of 66 genes between subjects at baseline with vitamin D deficiency (25(OH)D<20 ng/ml) and subjects with a 25(OH)D>20 ng/ml. After vitamin D3 supplementation gene expression of these 66 genes was similar for both groups. Seventeen vitamin D-regulated genes with new candidate vitamin D response elements including TRIM27, CD83, COPB2, YRNA and CETN3 which have been shown to be important for transcriptional regulation, immune function, response to stress and DNA repair were identified.

Conclusion/Significance

Our data suggest that any improvement in vitamin D status will significantly affect expression of genes that have a wide variety of biologic functions of more than 160 pathways linked to cancer, autoimmune disorders and cardiovascular disease with have been associated with vitamin D deficiency. This study reveals for the first time molecular finger prints that help explain the nonskeletal health benefits of vitamin D.

Trial Registration

ClinicalTrials.gov NCT01696409

Citation: Hossein-nezhad A, Spira A, Holick MF (2013) Influence of Vitamin D Status and Vitamin D3 Supplementation on Genome Wide Expression of White Blood Cells: A Randomized Double-Blind Clinical Trial. PLoS ONE 8(3): e58725. doi:10.1371/journal.pone.0058725

Editor: Moray Campbell, Roswell Park Cancer Institute, United States of America

Received: October 3, 2012; Accepted: February 5, 2013; Published: March 20, 2013

Copyright: © 2013 Hossein-nezhad et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: This work was supported by a pilot grant from the National Institutes of Health Clinical Translational Science Institute Grant UL-1-RR-25711. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have declared that no competing interests exist.

Introduction

Vitamin D deficiency defined as a serum concentration of 25-hydroxyvitamin D [25(OH)D]<20 ng/ml is the largest pandemic in the world [1],[2]. The musculoskeletal consequences of inadequate vitamin D are well-established [2],[3]. In addition to its traditional role in calcium homeostasis, a growing number of other conditions have also been linked to vitamin D insufficiency including cancers, autoimmune diseases, infectious diseases, type 2 diabetes and cardiovascular disease [1],[2],[3],[4].

Epidemiological studies have suggested that adequate levels of 25(OH)D are critical for the prevention of various solid tumors, including breast, ovarian and colon cancers [4],[5]. The risk of developing and dying of these cancers appears to be inversely correlated with sun exposure, and/or vitamin D status, suggesting that vitamin D has chemopreventive properties [4],[5]. Studies based on immunomodulatory effects of vitamin D have recommended vitamin D supplementation for prevention of autoimmune diseases and several forms of cancer [4],[6],[7].

Vitamin D requires two metabolic conversions, 25-hydroxylation in the liver and 1α-hydroxylation in the kidney, before its hormonal form, 1,25-dihydroxyvitamin D[1,25(OH)2D], can bind to the vitamin D receptor (VDR) to modulate gene transcription. The VDR is present in a wide variety of cells and tissues and 1,25(OH)2D via its receptor directly or indirectly have been reported to have effects on cell cycling and proliferation, differentiation, apoptosis and the production of cathelicidin, renin and insulin [2],[3],[4].

The wide distribution of VDR and the plethora of biologic actions reported for 1,25(OH)2D may explain how vitamin D can prevent a variety of diseases. Recent genetic association studies reported the effects of 1,25(OH)2D on gene expression and its influence on some epigenetic modifications [8],[9],[10]. It is estimated that VDR activation may regulate directly and/or indirectly the expression of a very large number of genes (0.5–5% of the total human genome i.e., 100–1250 genes) [1],[9],[10].

Our knowledge of both the molecular events controlling regulation of gene transcription by the VDR and the target genes underlying its physiological functions has benefited tremendously in the last decade by the advent of techniques for genome-wide analysis of transcriptional regulation[11]. In vitro microarray studies in cultured human cells provided insights into some target genes underlying the broad physiological actions of 1,25(OH)2D3 [11],[12]. These in vitro findings have helped provide a molecular genetic basis for the wide variety of biological and physiological responses regulated by 1,25(OH)2D3 [9],[11],[12].

Early microarray studies performed in squamous carcinoma cells derived from a tumor of the oral cavity revealed that an analog of 1,25(OH)2D3 regulated the expression of numerous genes implicated in immune function[12]. Genome-wide microarray analysis of 1,25(OH)2D3-treated human osteoblasts revealed an interplay of critical regulatory and metabolic pathways and supported the hypothesis that 1,25(OH)2D3 can modulate the coagulation process through osteoblasts, activate osteoclastogenesis through inflammation signaling and modulate the effects of monoamines by affecting their reuptake[11].

Although there have been numerous observations of vitamin D deficiency and its links to chronic diseases, a study on how a person’s vitamin D status and improvement with vitamin D supplementation affects genomic expression in vivo in humans has not been reported. The objective of this study was to determine the effect of vitamin D status and subsequent vitamin D supplementation on broad gene expression in the white blood cells collected from healthy adults before and two months after daily supplementation with either 400 or 2000 IU vitamin D3. (Trial registration: ClinicalTrials.gov NCT01696409; http://clinicaltrials.gov/ct2/show/NCT01​696409?term=Holick&rank=4).

Methods

Trial design

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This research study was a randomized, controlled, double-blind, investigator-initiated, single center pilot trial. The study protocol approved by the Boston University Medical Campus Institutional Review Board and registered in ClinicalTrials.gov with Identifier: NCT01696409. The protocol for this trial and supporting CONSORT checklist are available as supporting information; see Checklist S1 and Protocol S1. A total of 11 adult subjects were recruited for this study. However, two subjects dropped out before using supplement and the nine subjects were randomly assigned to 1 of 2 groups (Group I and Group II) using a computer-generated simple randomization scheme. Four subjects were assigned to Group I to receive 400 IU/d of vitamin D3 for 8 weeks, and five subjects were assigned to Group II to receive 2,000 IU/d of vitamin D3 for 8 weeks. After signing a consent form and receiving the supplement, one subject from group I refused further participating in the study. The eight remaining subjects included 3 subjects in group I and 5 subjects in group II who received vitamin D3 for 8 weeks and were assigned to the final analysis for studying the effect of vitamin D supplementation on broad gene expression. Based on vitamin D status at baseline, 4 subjects were vitamin D deficient and the other four subjects were insufficient or sufficient. Comparing gene expression in these two groups (deficient vs. insufficient or sufficient) led us to study the effect of vitamin D status on broad gene expression. The consent form was signed before the subjects were given the supplement so that we could evaluate the influence of vitamin D status and vitamin D3 supplementation on genome wide expression in white blood cells. None of the recruited subjects refused to give consent. To minimize sun exposure as a confounding factor, the study was conducted in the winter months. Study visits were conducted at the General Clinical Research Unit (GCRU) at Boston Medical Center. Subject demographics and total 25(OH)D levels before and after vitamin D3 supplementation are shown in Table 1.

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Table 1. Subject demographics and total 25(OH)D levels before and after 400 IU/d or 2000 IU/d of vitamin D3 supplementation for 8 weeks.

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Study Subjects

Healthy, non-patient English speaking adult males and females of all ethnic groups age 18 and older were recruited for this study. Before any study procedures were initiated for any subject in this study, a written informed consent was properly executed and documented as approved by the Boston University Medical Campus Institutional Review Board. A Federal wide Assurance Number FWA00000301 has been approved for Boston University Medical Center. The informed consent form is available as supporting information; see Informed consent form. The exclusion criteria included: pregnant/lactating women; current or recent history of hepatic or renal disease; supplementation of greater than 400 IUs vitamin D2 or vitamin D3; current antiseizure medications or glucocorticoids; tanning for more than 8 hours within the past month; history of intestinal malabsorption; and unwillingness to consent to the study.

Visits

During the subjects’ first and second visits to the GCRU, demographic data, body weight, height, body mass index (BMI), past vitamin D use, urine pregnancy test (females only), diet, current medication usage and/or anticipated medication usage during the study period were collected on data collection forms. The subjects also received a bottle containing vitamin D3 capsules that contained either 400 IUs or 2000 IUs of vitamin D3 for the 8-week period. The vitamin D3 supplements were produced by Tishcon Laboratories (Westbury, NY 11590) and were found to have contained stated vitamin D content as previously described [13].

The second visit occurred 8 weeks after the first visit. Subjects returned with their vitamin D3 bottles and the investigators counted how many capsules remained and determined compliance.

Blood sample collection

Ten ml of blood was also collected at each visit and sera were collected for evaluation at Quest Diagnostics and the BUMC Corelab and utilized to determine serum levels of 25(OH)D by liquid chromatography tandem mass spectroscopy as previously described [14]. Another 10 ml of blood was collected to obtain a buffy coat including white blood cells and platelets.

The white blood cells were collected to purify total RNA, including small RNAs. Purified RNA was stored at -86 degrees Celsius and sent for analysis to the Boston University Pulmonary Center’s Microarray Resource Facility.

Microarray Data Acquisition and Preprocessing

All procedures were performed at the Boston University Microarray Resource Facility as described in the GeneChip® Whole Transcript (WT) Sense Target Labeling Assay Manual (Affymetrix, Santa Clara, CA). Total RNA was isolated using QIAGEN’s RNeasy kit as described in manual (Qiagen, Valencia, CA). For each sample, integrity was verified using RNA 6000 Nano Assay RNA chips run in Agilent 2100 Bioanalyzer (Agilent Technologies, Palo Alto, CA). RNA was reverse transcribed using Whole Transcript cDNA Synthesis kit (Affymetrix, Santa Clara, CA). The obtained antisense cRNA was purified using GeneChip Sample Cleanup Module (Affymetrix, Santa Clara, CA), and used as a template for reverse transcription (Whole Transcript cDNA Synthesis kit, Affymetrix, Santa Clara, CA) to produce single-stranded DNA in the sense orientation. During this step dUTP was incorporated. DNA was then fragmented using uracil DNA glycosylase (UDG) and apurinic/apyrimidinic endonuclease 1 (APE 1) and labeled with DNA Labeling Reagent that is covalently linked to biotin using terminal deoxynucleotidyl transferase (TdT, Whole Transcript Terminal Labeling kit, Affymetrix, Santa Clara, CA). IVT and cDNA fragmentation quality controls were carried out by running an mRNA Nano assay in the Agilent 2100 Bioanalyzer.

The labeled fragmented DNA was hybridized to the Gene Array 1.0ST for 16–18 hours in GeneChip Hybridization oven 640 at 45°C with 60 rpm rotation. The hybridized samples were washed and stained using Affymetrix fluidics station 450. The first stain used was streptavidin-R-phycoerythrin (SAPE) followed by signal amplification using a biotinilated goat anti-streptavidin antibody and another SAPE staining (Hybridization, Washing and Sataining Kit, Affymetrix, Santa Clara, CA). Microarrays were immediately scanned using Affymetrix GeneArray Scanner 3000 7G Plus (Affymetrix, Santa Clara, CA). The resulting CEL files were summarized using Affymetrix Expression Console (current version 1.1). Robust Multi-Array Average (RMA) algorithm was used to generate gene-level data.

Real time –PCR verification

The cDNA was then used to check for the gene expression of four specific genes, via qRT-PCR. This was done in duplicate, so that a total of 32 samples were tested for each gene (2×16 samples). This was accomplished by adding 2.5 uL of each of the 16 samples into a 96-well plate. 22.5 uL of the TaqMan Master Mix was then added to each sample in the plate. The TaqMan Master Mix (per sample) included 12.5 uL of 2× TaqMan, 1.25 uL of oligonucleotide ribosomal RNA (rRNA), and 8.75 uL H2O. The expression of an 18S rRNA was also tested. Since the 18S gene is expressed in all cells it was used as an endogenous control. Each 96-well plate was covered and centrifuged at 1,500 rpm and 4oC for 5 minutes. After spinning the plate was put into the Applied Biosystems StepOnePlus Real-Time PCR system to check for gene expression. The total run time for each plate in the StepOnePlus was about 40 min. The raw data was saved on a computer and later analyzed.

Searching for candidate vitamin D response elements

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To investigate the role of VDR binding in vitamin D mediated gene expression, we searched for VDR binding domain within 60 kb (especially in 5 kb) of the transcriptional start site (TSS) of vitamin D responsive genes. From the 291 genes influenced by vitamin D3 supplementation 17 genes that were most affected by vitamin D3 supplementation were selected for vitamin D response element (VDRE) analysis.

For our analysis we first evaluated known VDREs that are shown in Table S1. These motifs were entered in to the CLC workbench (version6.2) as new motifs to search for novel VDREs as shown in Table S2.

This structural study was also performed on 12 housekeeping genes. The housekeeping genes were used as negative controls for candidate VDREs. Expressions of these housekeeping genes after vitamin D3 supplementation were not changed. There were no sequences of candidate VDREs in 100 kb upstream of the TSS of these housekeeping genes. The list of these housekeeping genes and the region of the study is summarized in Table S3.

As positive controls the known target genes for 1,25(OH)2D3 and reported VDREs in them were used (Table S1). In some VDRE candidates the same sequence was found like the VDRE in the RANKL gene (Table 2). In some genes the first hexameric motif was similar to the first part in VDRE in the one target gene and the second part similar to the second part of the another genes’ VDRE. The similarity of the candidate VDREs with the known VDREs are demonstrated in Table 2. For example the candidate VDRE in coatomer protein complex, subunit beta 2 (COPB2), a gene that was stimulated at least 1.5 fold by vitamin D3 supplementation, had two hexameric binding motifs associated with the VDRE. The first binding motif (TGAACT) was similar to the VDRE in receptor activator of NFkB ligand (RANKL) and the second binding motif (AGGTGA) was similar to VDRE in cytochrome P450, family 24, subfamily A, polypeptide 1 (25-hydroxyvitamin D-24-hydroxylase, CYP24A1).

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Table 2. The motif sequences of 17 genes that were most response to vitamin D3 supplementation that is identical or similar to other known VDRE sequences.

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Sample size estimation

The sample size in this pilot study was estimated based on the pilot funding and on results from previous report of vitamin D impact on broad gene expression in vitro model [11],[12], it was estimated that vitamin D could reduce expression in some genes or increase expression in other genes between one to three fold. A two-sided risk of type 1 error, α, of 0.05; a type 2 error risk, β, of 20%; (power of 80%), changing relative expression from 1.5 to 3, standard deviation of 1(0.3 to 1) and equal group size, the sample size (N) for was calculated to N = 4 for each group.

The actual inclusion of 8 subjects in the two supplemented groups or based on their vitamin D status resulted in a power of 57%–92% for the effect of vitamin D status and vitamin D supplementation on expression of TRIM27, CD83, COPB2, YRNA and CETN3.

Data Analysis

The sample size for this study was 8 subjects. Since each subject had two samples (baseline and follow-up visits), a total of 16 samples were analyzed and linked to experimental factors of supplementation and time. All 16 arrays were normalized with the RMA method as described above. For data quality control regarding the similarity of the samples within and between the groups, the Principal Component Analysis (PCA) method was used. Microarray data normalization was conducted to correct for the mean intensity for each array. To identify the differentially expressed genes before versus after supplementation and between two kinds of supplementation (400 IUs or 2000 IUs), a 2-way ANOVA in the linear model was applied. To assess the results, the p<0.01 was used as a cutoff due a small sample size. Also all subjects were classified based on basal levels of 25(OH)D. Four subjects were vitamin D deficient with 25(OH)D of 16±3.8 ng/ml and the other four subjects were insufficient or sufficient [2] with a 25(OH)D of 27.6±5.4 ng/ml.

It is standard practice in biostatistics to use a p value threshold of 0.05 for the decision as to whether a difference is significant or not. This p value is the probability of getting a false positive result, so on average we would expect to get a false positive result about once every 20 times the test was used [15]. Thus in this study the level of statistical significance was defined as alpha <0.01 i,e. there was a 1% maximum chance of incorrectly rejecting the null hypothesis that there is no association between vitamin D supplementation and genetic expression. The FDR <0.1, (False Discovery Rate) was applied to a list of genes, not any particular gene. We conducted appropriate correction for multiple testing that included using a 1.5 fold change of gene expression combined with false discovery rate (Fdr) < 0.1 in our main analysis. Using a 1.5 fold change of gene expression combined with ANOVA in our subgroup analysis. Using P <0.01 for decreasing false positive and technique validation with the real replicate time PCR. Significant enrichment of GO biological process categories were tested for using EASE software (version 2.0) with P<0.05 [16].

Results

Demographic and other baseline characteristics

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Eight subjects who met the inclusion/exclusion criteria were enrolled. No recruited subjects refused to give consent. Sixteen microarrays (baseline and after 2 months of vitamin D3 supplementation) from eight subjects (3 women) passed the quality control filters and normalized with the RMA method. Mean of age, BMI and serum 25(OH)D levels were 26.5±4 years, 27±5.9 kg/m2 and 21.8±8.6 ng/ml respectively and all of them were white. Three participants received 400 IUs of vitamin D3 daily and five participants received 2000 IUs of vitamin D3 daily (Figure 1). After eight weeks of vitamin D3 supplementation serum 25(OH)D levels in the group that received daily 2000 IUs had a 2-fold increase (9.8±4.9 ng/ml) compared to subjects who received and had an increase of 5.6±4.9 ng/ml (Table 1).

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Figure 1. Flow Diagram of Study Subjects.

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Impact of vitamin D3 supplementation on expression of genes in human white blood cells

To explore gene-expression relationships between and within the 400 IU and 2000 IU groups principal component analysis (PCA) was performed. Total variability of individual chips after normalization is illustrated in Figure 2. There wasn’t a significant difference in order to explore gene-expression relationships between and within the 400 IU and 2000 IU groups. Regarding all participants, with false discovery rate (Fdr)<0.1, and a 1.5 fold change, 291 genes were found to have a statistically significant difference in expression from baseline to follow-up after vitamin D3 supplementation (Figure 3). The list of these 291 genes is shown in Table S4. There was at least a 1.5 fold inhibition of 82 genes (top ~30% of the heat map) whose expression was dramatically reduced and at least a 1.5 fold induction of 209 genes (bottom ~70% of the heat map) whose expression was significantly increased after supplementation with either 400 or 2000 IU of vitamin D3 for 2 months.

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Figure 2. Principal Component Analysis across 16 microarray samples.

There is no grouping of samples along the first or second principal components (representing 18.6% and 17.9% of the variance in gene expression, respectively) based on the expression of these genes. Sample types of each group before or after vitamin D3 supplementation are color-coded for the dose of vitamin D3 supplementation. Red = 2000 IUs and blue = 400 IUs (PoV = Possibility of Variance.)

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Figure 3. Heatmaps of vitamin D responsive genes whose expression levels change after 2 months vitamin D3 supplementation.

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Before supplementation (light green) four subjects were vitamin D deficient with 25(OH)D of 16.2±4.2 ng/ml (dark purple) and the other four subjects were insufficient or sufficient with a 25(OH)D of 27.5±8.4 ng/ml(light purple). After supplementation (dark green) serum levels of 25(OH)D in vitamin D insufficient/sufficient subjects increased to 35.2±8.2 ng/ml (light purple) and in the vitamin deficient subjects increased to 25.1± 4.7 ng/ml(dark purple). Two groups of gene-expression changes are seen based on stimulation (brown) or inhibition (blue) of gene expression post vitamin D3 supplementation. (Colors ranged from blue to brown; High expression = brown, average expression = white, low expression = blue). Clustering of the 291 genes affected by vitamin D3 supplementation was based on stimulation (brown) or inhibition (blue) of gene expression. The list of the 291 genes is shown in Table S1.

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For verification candidate of gene expression changes real-time PCR was performed for four genes including CD83, TNFAIP3, KLF10 and SBDS (Figure 4). The results showed gene expression changes concordant with those observed by microarray.

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Figure 4. Verification of microarray gene expression by Real-time PCR.

For verification of gene expression real-time PCR was performed for four genes including CD83, TNFAIP3, KLF10 and SBDS. Relationship between two sets of data from microarray and real-time PCR is shown by linear regression with 95% mean prediction interval. The results showed the relative expression of these genes was consistent with the expression observed from the broad gene expression by microarray.

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The effect of vitamin D status on gene expressio

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A subgroup analysis of participants was evaluated based on the baseline serum 25(OH)D levels (Figure 3 and 5) in order to determine what if any influence vitamin D status had on the basal expression of the 291 genes identified as being affected by 2 months of vitamin D3 supplementation. Four subjects were vitamin D deficient with 25(OH)D 16.2±4.2 ng/ml (range 10–19 ng/ml) and the other four subjects were insufficient or sufficient with a 25(OH)D of 27.5±8.4 ng/ml (range 22–40 ng/ml).

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Figure 5. Heatmaps of vitamin D responsive genes affected by vitamin D status.

Before supplementation (light green) four subjects were vitamin D deficient with 25(OH)D of 16.2±4.2 ng/ml (dark purple) and the other four subjects were insufficient or sufficient with a 25(OH)D of 27.5±8.4 ng/ml(light purple). After supplementation (dark green) serum levels of 25(OH)D in vitamin D insufficient/sufficient subjects increased to 35.2±8.2 ng/ml (light purple) and in the vitamin deficient subjects increased to 25(OH)D of 25.1±4.7 ng/ml(dark purple). Two groups of gene-expression changes are seen based on stimulation (brown) or inhibition (blue) of gene expression post vitamin D3 supplementation. (Colors ranged from blue to brown; High expression = brown, average expression = white, low expression = blue).Expression of 66 genes before supplementation was significantly different in the vitamin D deficient group (dark purple) compared to the vitamin D insufficient/sufficient group (light purple). Clustering of the 66 genes affected by vitamin D status and vitamin D3 supplementation was based on stimulation (brown) or inhibition (blue) of gene expression.

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This subgroup analysis of the baseline gene expression for the 291 genes (Figure 3) in the vitamin D deficient group compared to the vitamin D insufficient/sufficient group revealed that, expression of 66 genes were significantly different between the two groups (p<0.01 and fold change>1.5). (Figure 5) There was at least a 1.5 fold increase in gene expression (brown-orange) of 14 genes and at least a 1.5 fold decrease in the expression (yellow-white) of 52 genes in the vitamin D deficient adults compared to those who were vitamin D insufficient or sufficient at baseline (Figure 5). After vitamin D3 supplementation the serum 25(OH)D increased from 16.2±4.2 to 25.1±4.7 ng/ml and 27.5±8.4 to 35.2±8.2 ng/ml in the adults who were vitamin D deficient and vitamin D insufficient or sufficient respectively. After vitamin D3 supplementation gene expression in the vitamin D deficient group was similar to vitamin D insufficient/sufficient group and there was no longer a significant difference between two groups in the expression of these 66 genes.

Structural evidence for the effect of vitamin D3 supplementation on gene expression

To learn which of these genes affected by vitamin D3 supplementation contained VDR binding domains near the transcriptional start site (TSS), we performed a VDRE analysis as described in Materials and Methods.

Of the 66 genes that were influenced by at least 1.5 fold in their expression by the baseline serum 25(OH)D concentration, 17 of these genes that were significantly changed after vitamin D3 supplementation in both deficient and insufficient/sufficient groups (p<0.01) were selected for VDRE analysis.

The details of searching for candidate VDRE sequences is explained in Methods and shown in Table S1-3. We found at least one candidate VDRE in the upstream region within 30 kb of the TSS in these 17 genes (Table 1). For example, the candidate VDRE in coatomer protein complex, subunit beta 2 (COPB2), a gene that was stimulated at least 1.5 fold by vitamin D3 supplementation, had two hexameric binding motifs associated with the VDRE. The first binding motif (TGAACT) was similar to the VDRE in receptor activator of NFkB ligand (RANKL) and the second binding motif (AGGTGA) was similar to the VDRE in cytochrome P450, family 24, subfamily A, polypeptide 1 (25-hydroxyvitamin D-24-hydroxylase, CYP24A1).

The motif sequence for VDR/RXR hetrodimeric binding sites is shown in Figure 6.

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The motif sequence of candidate VDREs (6A) are compared with known VDREs (6B). All of these sequences are summarized in one motif sequence (6C). The location of other transcription factor binding sites are shown in Figure S1. These are associated with known steroidogenic factor 1 (SF-1), CTF1/nuclear factor 1 (NF1), CCAAT enhancer binding protein-β (C/EBPβ), NF-KB and RNA polymerase (TATA box) motifs. For example pseudouridylate synthase 3 (PUS3), a gene that was stimulated 1.6 fold by vitamin D3 supplementation has five VDREs (Table 2) that one of them is shown in Figure 6D located at position -1027, the TATA box located at -276 and location of other transcription factor sites near this VDRE was determined (6D).

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Figure 6. Sequence of candidate VDREs compared with known VDREs.

(A) The candidate sequences of VDREs (B), motifs created based on known VDRE sequences previously reported and (C) motifs based on the sum of these sequences and (D) the location of candidate VDREs of pseudouridylate synthase 3 (PUS3) and the location of other transcription regulation sites in this gene including TATA box, SF1and CCAAT. The major structure of candidate VDREs are based on the consensus sequence RGKTSA (R = A or G, K = G or T, and S = C or G).

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This study was also performed on 12 housekeeping genes to serve as negative controls. There were no sequences of candidate VDREs in 100 kb upstream of TSS of these housekeeping genes (Table S3). The expression of these housekeeping genes after vitamin D3 supplementation was not changed.

Biological functions for vitamin D responsive genes

An analysis of the 291 genes affected by the vitamin D3 supplementation was associated with at least a 1.5 fold induced expression of genes related to 81 pathways and at least a 1.5 fold inhibition of genes affecting 88 pathways (Table S5, S6)(p<0.05). The most relevant biological functions resulting from these changes in gene expression by vitamin D3 supplementation are listed in Table 3 and the complete list is in Tables S5 and S6. Gene ontology analysis showed that the differentially expressed genes were significantly enriched with those associated with immune functions, transcriptional regulation, cell cycle activity, DNA replication and response to stress (Figure 7).

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Figure 7. Biological functions for genes whose expression levels were altered after 2 months of vitamin D3 supplementation.

After receiving vitamin D3 supplementation we identified 291 genes whose expression was significantly decreased or increased. Some of these genes influence several pathways that are involved in response to stress and DNA repair, DNA replication, immune regulation, epigenetic modification, transcriptional regulation and other biological functions. In addition vitamin D3 supplementation influenced the expression of Y RNA and CETN3 that are involved in DNA repair in response to UVR exposure.

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Table 3. List of biological functions of the 291 genes whose expression was influenced by vitamin D3 supplementation.

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Discussion

This genome-wide expression analysis provides the first insight into the global transcriptional activity that underlies the effects of vitamin D status and vitamin D3 supplementation in cells on the human buffy coat that include immune cells. As shown in Figure 3, vitamin D supplementation caused at least a 1.5 fold change in the expression of 291 genes that are involved in apoptosis, immune function, transcriptional regulation, epigenetic modification, response to stress, cell cycle activity and differentiation (Table 3). This finding is consistent with previous in vitro studies that showed 1,25(OH)2D3 directly or indirectly controlled more than 200 genes, including genes responsible for the regulation of cellular proliferation, differentiation, angiogenesis and immunomodulatory activities on both innate and adaptive immune responses [3],[4],[6]. Our observations support previous reports that have estimated that VDR activation may regulate directly and/or indirectly the expression of a very large number of genes (0.5–5% of the total human genome i.e., 100–1250 genes) [3],[4],[8],[11],[17].

In a recent genome-wide microarray analysis of 1,25(OH)2D3-treated human osteoblasts revealed modulation of 158 genes involved in vitamin D metabolism (CYP24A1), immune function (CD14), neurotransmitter transporters (SLC1A1, SLC22A3), and coagulation [17]. A study of the human genome screened for VDREs reported 157 genes to be regulated in SCC- 25 cells, of which 126 were induced and 31 were repressed [17]. The researchers found 2,776 binding sites for the vitamin D receptor along the length of the genome. Among them included 229 genes associated with susceptibility to autoimmune disorders, and cancers including chronic lymphocytic leukemia and colorectal cancer [17]. All of these studies reporting the effect of 1,25(OH)2D3 on gene expression were in vitro studies in different cell types.

There have been two genome wide association studies that have related genomic variation on vitamin D status [18],[19]. However little is known about what effect vitamin D status has on gene expression or what happens to gene expression in response to vitamin D supplementation. We observed that 291 genes were at least a 1.5 fold stimulated or inhibited in response to vitamin D3 supplementation. We identified 66 genes, that were most significantly affected by the subjects’ vitamin D status i e those who were vitamin D deficient with 25(OH)D of 16.2±4.2 ng/ml compared to adults who had a 25(OH)D of 27.5±8.4 ng/ml at baseline. Nineteen of these 66 genes are the same reported by in vitro studies [12], [17]. Thus we have identified an additional 47 genes that were influenced by vitamin D3 status.

Of these 66 genes, 17 genes whose expression significantly changed after vitamin D3 supplementation in both deficient and insufficient/sufficient groups were found to have novel VDREs (Table 2).

After receiving 400 IUs or 2000 IUs for 8 weeks of vitamin D3 dramatic changes occurred in the expression of these 66 genes while no significant change was seen in 12 housekeeping genes. We did not see a significant dose dependent difference in the alteration in gene expression 8 weeks after the adults received daily either 400 IUs or 2000 IUs vitamin D3. This could be due to the small number of subjects studied or that any improvement in serum 25(OH)D levels can lead to significant changes in gene expression whether the person is vitamin D deficient, insufficient or sufficient. We observed the same trend in gene expression in the subjects who received 400 or 2000 IUs vitamin D3 whether the baseline 25(OH)D was 16.2±4.2 or 27.5±8.4 ng/ml. There was however a trend for a larger change in the expression of these genes for the group who received 2000 IUs vitamin D3/d compared to the group who received 400 IUs vitamin D3/d. Even the subject who had a 25(OH)D of 40 ng/ml after 2000 IUs vitamin D3 daily for two months had at least a 1-fold change in 10 genes and at least a 0.5 fold change in the expression of 33 genes from this pool of 66 genes.

Of the 66 genes, 52 increased their expression in response to vitamin D3 supplementation. The greatest increases were in genes that coded for apoptosis, T Cell intracellular antigen-1 (TIA1) (26-fold), immune function, zinc finger protein 287(ZNF287) (6.8-fold), response to cellular stress, Y-RNA(2-fold), centrin3(CETN3) (1.5-fold) and heat shock 105 kDa/110 kDa protein 1(HSPH1) (1.5-fold), tRNA processing, mitochondrial translation optimization 1 homolog (MTO1)(5-fold) and pseudouridylate synthase 3 (PUS3)(2-fold), transcriptional regulation such as ZNF 701 (2.3-fold), and genes involved in DNA repair, general transcription factor IIH, polypeptide 1 (GTF2H1) (7-fold) and chromatin modification small subunit processome component, homolog (UTP3) (4-fold).

The other 14 genes decreased their expression in response to vitamin D3 supplementation. The greatest decreases were in genes that coded for histone modification; H1 histone family, member X (H1FX) (12-fold), transcriptional regulation; early growth response 1 (EGR1)(2.8-fold). Two of the genes that had reduced expression; the cluster of differentiation 83(CD83) (2-fold) and tumor necrosis factor alpha-induced protein 3 (TNFAIP3)(1.5-fold) that are known to affect immune function also were found to have reduced expression by real-time PCR.

Our observation that vitamin D3 supplementation increased serum 25(OH)D levels resulting in the suppression of CD83 (2-fold) is consistent with the observation that 1,25(OH)2D3 inhibited CD83 expression in cultured dendritic cells[20]. This suggests that local synthesis of 1,25(OH)2D3 in immune cells including macrophages[21] regulates genes that affect immune function and improve immune health resulting in reducing risk for developing autoimmune diseases such as multiple sclerosis and type 1 diabetes[20].

The role of TNFAIP3 in antiapoptotic function [22] and the association of its’ mutations with Crohn’s disease, rheumatoid arthritis, systemic lupus erythematous, psoriasis, type 1 diabetes [23] could explain the association of vitamin D sufficiency in the prevention of chronic inflammation and autoimmune diseases. Also vitamin D’s influence on the expression of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (NFKBIA)(1.5-fold) may affect immune and proinflammatory responses [24],[25].

Vitamin D3 supplementation resulted in a 1.5 fold increase in the expression of tripartite motif containing protein 27 (TRIM27) a gene that negatively regulates CD4 T cells by ubiquitinating and inhibiting the class II phosphatidylinositol 3 kinase C2β (PI3KC2β)2β [26]. TRIM27 over expression conferred resistance to oxidative stress, by decreasing the expression of thioredoxin binding protein-2 [26]. Also TRIM27 was as recently identified an important negative regulator of mast cells in vivo, and suggests that PI3KC2β is a potential new pharmacologic target to treat IgE mediated disease [25][26]. Our finding has identified a potential new pathway for vitamin D affecting the immune system, allergy risk and oxidative stress via TRIM27. Coatomer protein complex, subunit beta 2 (COPB2) was another vitamin D responsive gene in our study whose expression significantly increased (1.5-fold) after vitamin D3 supplementation. COPB2’s role in apoptosis and tumor growth suppression [27], may help explain the association of improving vitamin D status in cancer prevention [7],[17].

Higher serum concentrations of 25(OH)D at baseline and improvement in serum concentrations of 25(OH)D with either 400 IUs or 2000 IUs of vitamin D3 resulted in a 2.5 fold decrease in the expression of EGR-1, a gene that is a transcriptional regulator of not only differentiation and mitogenesis but also plays an important function in vascular health [28],[29]. An analogue of 1,25(OH)2D3, calcipotriol which a potent inhibitor of keratinocyte proliferation and used for treating the hyperproliferative skin disorder psoriasis was found to inhibit EGR-1 expression in cultured human keratinocyte[30]. It has been estimated that as a transcription factor EGR-1 affects the expression of more than 300 genes [31]. Thus by altering the expression of EGR1 with vitamin D supplementation has the potential cascading effect of altering an additional 300 genes. This could help explain the observation that vitamin D can directly or indirectly influence up to 5% of the human genome [4],[17].

These data suggest that there is a continuum in gene expression in response to increasing serum 25(OH)D levels. The definitions of vitamin D deficiency and insufficiency and sufficiency are somewhat arbitrary. As shown in Figure 3, our data suggest that any improvement in vitamin D status will improve expression of genes that have a wide variety of biologic functions that are associated with cellular proliferation, differentiation, immune function, DNA repair etc whether the 25(OH)D concentration is as low as 10 ng/ml or as high as 40 ng/ml. These genes are linked to cancer, autoimmune disorders and cardiovascular disease and have been associated with vitamin D deficiency [1],[5],[6].

These results suggest that to maximize vitamin D’s effect on gene expression may require even higher doses than 2000 IUs of vitamin D3 daily. The current observation showed the specific pattern for broad gene expression of vitamin D deficiency and significant changes with increases in serum levels of 25(OH)D. Although larger studies are required to explain the clinically relevant gene expression patterns, the present genome-wide microarray study in human buffy coat for the first time identified a wide range of critical regulatory and metabolic pathways influenced by vitamin D3 supplementation that supports the vitamin D immunomodulatory effects and potential role in response to stress and DNA repair.

The major limitation of the study is the small number of subjects studied and thus the results are reported as an exploratory study. Although gene expression was determined with a suitable false discovery rate only a few of the 291 vitamin D responsive genes were verified by real time PCR. Furthermore although our study did not identify actual VDR binding sites with a biologic function it does support vitamin D-responsive genes from in vitro studies [11],[12],[17] and suggests 17 potential novel candidate VDREs in vitamin D-regulated genes. This will need to confirm with experimental studies.

There are several strengths of the study that include accurately measuring serum 25(OH)D concentrations by the gold standard liquid chromatography tandem mass spectroscopy assay, comparing gene expression in the same individual at baseline and 2 months after vitamin D supplementation and performing this study in the winter when sunlight does not influence vitamin D status. An additional strength was provided by the real-time PCR analysis of two genes CD83 and TNFAIP3 from the 66 gene pool that were affected by vitamin D status and two genes KLF10 and SBDS from the 291 gene pool that were affected by vitamin D3 supplementation (Figure 4) that corroborated the microarray expression of these four genes (Figure 5).

In summary, this is the first report to reveal how vitamin D status and vitamin D3 supplementation affects gene expression in healthy adults. Nineteen of these vitamin D-induced genes have been previously reported to be regulated by 1,25(OH)2D3 in vitro and function on the immune system, apoptosis, transcription regulation and response to stress.

Vitamin D supplementation has proven skeletal health benefits [3],[4], particularly in individuals at risk for vitamin D deficiency. This study reveals for the first time molecular finger prints that help to explain some of the nonskeletal health benefits of vitamin D [2],[6].

Supporting Information

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The six gene upstream regions containing candidate VDRE sequences, and other transcription factors sites for steroidogenic factor 1 (SF-1), CTF1/nuclear factor 1 (NF1), CCAAT enhancer binding protein-β (C/EBPβ), NF-KB and RNA polymerase (TATA box). Arrows indicate direction of forward or revere strand. The VDREs are located at upstream region and disfigured by mines numbers relative to the ATG translation start site. The locations of other transcription factors binding sites are also shown.

Figure S1.

The six gene upstream regions containing candidate VDRE sequences, and other transcription factors sites for steroidogenic factor 1 (SF-1), CTF1/nuclear factor 1 (NF1), CCAAT enhancer binding protein-β (C/EBPβ), NF-KB and RNA polymerase (TATA box). Arrows indicate direction of forward or revere strand. The VDREs are located at upstream region and disfigured by mines numbers relative to the ATG translation start site. The locations of other transcription factors binding sites are also shown.

doi:10.1371/journal.pone.0058725.s001

(TIF)

Table S1.

The reported vitamin D response elements in known vitamin D target genes. The positions and sequences of nucleotide motifs from 5′ upstream to the transcriptional start site were identified.

doi:10.1371/journal.pone.0058725.s002

(DOCX)

Table S2.

Definition of new vitamin D response element motifs. The reported vitamin D response elements and related element collected and these definitions entered in CLC workbench (version6.2) as new motifs to search VDRE.

doi:10.1371/journal.pone.0058725.s003

(DOCX)

Table S3.

The housekeeping genes that used as negative control for VDREs searching. Expression of these housekeeping genes after vitamin D supplementation was not changed. There were no sequences of candidate VDREs in 100 kb upstream of TSS of these housekeeping genes. The list of these housekeeping genes and the region of the study is summarized in the table.

doi:10.1371/journal.pone.0058725.s004

(DOCX)

Table S4.

The complete list of 291 genes that affected by vitamin D3 supplementation.

doi:10.1371/journal.pone.0058725.s005

(DOCX)

Table S5.

The pathways enriched with down regulated genes after treatment (p<0.05).

doi:10.1371/journal.pone.0058725.s006

(DOCX)

Table S6.

Pathways enriched with up regulated genes after treatment (p<0.05).

doi:10.1371/journal.pone.0058725.s007

(DOCX)

Checklist S1.

CONSORT Checklist.

doi:10.1371/journal.pone.0058725.s008

(DOCX)

Protocol S1.

Trial Protocol.

doi:10.1371/journal.pone.0058725.s009

(PDF)

Acknowledgments

We appreciate the help from Cassandre Voltaire, Timothy K.M. Calvert, Leonierose N.Dacuycuy and Chlirim Zaku master’s degree students for subject recruitment and sample preparation and Dr. Stefan Shen for his helpful advice.

Author Contributions

Conceived and designed the experiments: AH MFH AS. Performed the experiments: AH MFH AS. Analyzed the data: AH MFH AS. Contributed reagents/materials/analysis tools: AH MFH AS. Wrote the paper: AH MFH AS.

References

1. Holick MF (2008) The vitamin D deficiency pandemic and consequences for nonskeletal health: mechanisms of action. Mol Aspects Med 29(6): 361–8. doi: 10.1016/j.mam.2008.08.008. Find this article online

2. Holick MF, Binkley NC, Bischoff-Ferrari HA, Gordon CM, Hanley DA, et al. (2011) Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 96(7): 1911–30. doi: 10.1210/jc.2011-0385. Find this article online

3. Adams JS, Hewison M (2010) Update in Vitamin D. J Clin Endocrinol Metab. 95(2): 471–478. Find this article online

4. Holick MF (2007) Vitamin D Deficiency. N Engl J Med 357: 266–281. Find this article online

5. Rosen CJ, Adams JS, Bikle DD, Black DM, Demay MB, et al. (2012) The nonskeletal effects of vitamin D: an Endocrine Society Scientific statement. Endocr Rev 33(3): 456–92. doi: 10.1210/er.2012-1000. Find this article online

6. Giovannucci E (2009) Expanding roles of vitamin D. J Clin Endocrinol Metab. 94: 418–420. Find this article online

7. Garland CF, Gorham ED, Mohr SB, Garland FC (2009) Vitamin D for cancer prevention: global perspective. Ann Epidemiol 19: 468–483. doi: 10.1016/j.annepidem.2009.03.021. Find this article online

8. Montecino M, Stein GS, Stein JL, Lian JB, Wijnen AJ, et al. (2008) Vitamin D control of gene expression: temporal and spatial parameters for organization of the regulatory machinery. Crit Rev Eukaryot Gene Expr 18(2): 163–72. doi: 10.1615/CritRevEukarGeneExpr.v18.i2.50. Find this article online

9. Zhang X, Ho SM (2011) Epigenetics meets endocrinology. J Mol Endocrinol 46(1): R11–32. doi: 10.1677/JME-10-0053. Find this article online

10. Yu S, Cantorna MT (2011) Epigenetic reduction in invariant NKT cells following in utero vitamin D deficiency in mice. J Immunol 186(3): 1384–90. doi: 10.4049/jimmunol.1002545. Find this article online

11. Tarroni P, Villa I, Mrak E, Zolezzi F, Mattioli M, et al. (2012) Microarray analysis of 1,25(OH)2D3 regulated gene expression in human primary osteoblasts. J Cell Biochem 113(2): 640–9. Find this article online

12. Wang TT, Tavera-Mendoza LE, Laperriere D, Libby E, MacLeod NB, et al. (2005) Large-scale in silico and microarray-based identification of direct 1,25-dihydroxyvitamin D3 target genes. Mol Endocrinol 19(11): 2685–95. doi: 10.1210/me.2005-0106. Find this article online

13. Holick MF, Biancuzzo RM, Chen TC, Klein EK, Young A, et al. (2007) Vitamin D2 is as effective as vitamin D3 in maintaining circulating concentrations of 25-hydroxyvitamin D. J Clin Endocrinol Metab. 93(3): 677–81. Find this article online

14. Holick MF, Siris ES, Binkley N, Beard MK, Khan A, et al. (2005) Prevalence of Vitamin D inadequacy among postmenopausal North American women receiving osteoporosis therapy. J Clin Endocrinol Metab 90(6): 3215–24. Find this article online

15. Pavlidis P (2003) Using ANOVA for gene selection from microarray studies of the nervous system. Methods 31: 282–289. doi: 10.1016/S1046-2023(03)00157-9. Find this article online

16. Ferraresso S, Milan M, Pellizzari C, Vitulo N, Reinhardt R, et al. (2010) Development of an oligo DNA microarray for the European sea bass and its application to expression profiling of jaw deformity. BMC Genomics 11: 354. doi: 10.1186/1471-2164-11-354. Find this article online

17. Ramagopalan SV, Heger A, Berlanga AJ, Maugeri NJ, Lincoln MR, et al. (2010) A ChIP-seq defined genome-wide map of vitamin D receptor binding: associations with disease and evolution. Genome Res 20(10): 1352–60. doi: 10.1101/gr.107920.110. Find this article online

18. Wang TJ, Zhang F, Richards JB, Kestenbaum B, van Meurs JB, et al. (2010) Common genetic determinants of vitamin D insufficiency: a genome-wide association study. Lancet 376(9736): 180–8. doi: 10.1016/S0140-6736(10)60588-0. Find this article online

19. Ahn J, Yu K, Stolzenberg-Solomon R, Simon KC, McCullough ML, et al. (2010) Genome-wide association study of circulating vitamin D levels. Hum Mol Genet 19(13): 2739–45. doi: 10.1093/hmg/ddq155. Find this article online

20. Bartosik-Psujek H, Tabarkiewicz J, Pocinska K, Stelmasiak Z (2010) Rolinski (2010) Immunomodulatory effects of vitamin D on monocyte-derived dendritic cells in multiple sclerosis. Mult Scler (12): 1513–6. doi: 10.1177/1352458510379611. Find this article online

21. Rosenblatt J, Bissonnette A, Ahmad R, Wu Z, Vasir B, et al. (2010) Immunomodulatory effects of vitamin D: implications for GVHD. Bone Marrow Transplant 45(9): 1463–8. doi: 10.1038/bmt.2009.366. Find this article online

22. Vereecke L, Beyaert R, van Loo G (2009) The ubiquitin-editing enzyme A20 (TNFAIP3) is a central regulator of immunopathology. Trends Immunol 30(8): 383–91. doi: 10.1016/j.it.2009.05.007. Find this article online

23. Maxwell JR, Gowers IR, Kuet KP, Barton A, Worthington J, et al. (2012) Expression of the autoimmunity associated TNFAIP3 is increased in rheumatoid arthritis but does not differ according to genotype at 6q23. Rheumatology (Oxford) 51(8): 1514–5. doi: 10.1093/rheumatology/kes134. Find this article online

24. Berry DM, Clark CS, Meckling-Gill KA (2002) 1alpha,25-dihydroxyvitamin D3 stimulates phosphorylation of IkappaBalpha and synergizes with TPA to induce nuclear translocation of NFkappaB during monocytic differentiation of NB4 leukemia cells. Exp Cell Res 272(2): 176–84. Find this article online

25. Kamen DL, Tangpricha V (2010) Vitamin D and molecular actions on the immune system: modulation of innate and autoimmunity. J Mol Med (Berl) 88(5): 441–50. doi: 10.1007/s00109-010-0590-9. Find this article online

26. Srivastava S, Cai X, Li Z, Sun Y, Skolnik EY (2012) Phosphatidylinositol-3-Kinase C2β and TRIM27 function to Positively and Negatively Regulate IgE Receptor Activation of Mast Cells. Mol Cell Biol 32(15): 3132–9. Find this article online

27. Sudo H, Tsuji AB, Sugyo A, Kohda M, Sogawa C, et al. (2010) Knockdown of COPA, identified by loss-of-function screen, induces apoptosis and suppresses tumor growth in mesothelioma mouse model. Genomics 95(4): 210–6. doi: 10.1016/j.ygeno.2010.02.002. Find this article online

28. Fu M, Zhu X, Zhang J, Liang J, Lin Y, et al. (2003) Egr-1 target genes in human endothelial cells identified by microarray analysis. Gene 2 315: 33–41. doi: 10.1016/S0378-1119(03)00730-3. Find this article online

29. Wada Y, Fujimori M, Suzuki J, Tsukioka K, Ito K, et al. (2003) Egr-1 in vascular smooth muscle cell proliferation in response to allo-antigen. J Surg Res 115(2): 294–302. doi: 10.1016/S0022-4804(03)00213-0. Find this article online

30. Kristl J, Slanc P, Krasna M, Berlec A, Jeras M, et al. (2008) Calcipotriol affects keratinocyte proliferation by decreasing expression of early growth response-1 and polo-like kinase-2. Pharm Res 25(3): 521–9. doi: 10.1007/s11095-007-9388-z. Find this article online

31. Arora S, Wang Y, Jia Z, Vardar-Sengul S, Munawar A, et al. (2008) Egr1 regulates the coordinated expression of numerous EGF receptor target genes as identified by ChIP-on-chip. Genome Biol 9(11): R166. doi: 10.1186/gb-2008-9-11-r166. Find this article online

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0058725

——

Vitamin D linked with lower risk of deadly prostate cancer

Vitamin D linked with lower risk of deadly prostate cancer

By Karen Rowan

Published April 18, 2012

MyHealthNewsDaily

Vitamin D does not protect men from getting prostate cancer, but it may lessen their chances of dying of it.

In a new study, men with the highest levels of vitamin D in their blood were 57 percent less likely than men with the lowest levels to succumb to prostate cancer.

However, no link was found between vitamin D levels and having prostate cancer, the researchers said.

“Prostate cancer is a very heterogeneous disease,” said study researcher Irene Shui, an epidemiologist at the Harvard School of Public Health. Some tumors progress quickly, spreading to other sites in the body and causing death, while others stay within the prostate for years and never affect a man’s health or life.

It remains unclear exactly why vitamin D would lower men’s risk of dying from prostate cancer if it has no influence at all on the risk of developing the cancer, Shui said. It may be that vitamin D specifically influences the cancer cells’ abilities to progress to later stages of the disease and spread through the body, but not the actual initiation of the cancer, she said.

Still, the study was observational, and it does not show a cause-and-effect link between vitamin D and prevention of deadly prostate cancer.

The new findings were published in online April 12 in the Journal of the National Cancer Institute.

Vitamin D and prostate cancer

“There is abundant laboratory evidence that vitamin D may have anticancer properties,” Shui said. But while studies conducted on prostate cancer cells growing in lab dishes have shown that vitamin D may thwart cancer’s progression, studies in people have shown that high levels of the vitamin don’t lower a man’s risk of getting cancer of the prostate, the gland surrounding a man’s urethra.

For their study, the researchers gathered data from men who had provided blood samples between 1993 and 1995 as part an ongoing study at Harvard University. The researchers looked at 1,260 men who had developed prostate cancer by 2004, and 1,331 men who were the same age but didn’t develop the disease.

By March 2011, when the study ended, 114 of the men with prostate cancer had died. When the researchers looked at these men’s levels of vitamin D, they found that 31 of them were among the men with the lowest levels of vitamin D in the study, whereas only 19 of them were among the men with the highest levels of vitamin D in the study.

However, vitamin D levels made no difference in terms of developing any prostate cancer — 310 of the men with the cancer were in the group with the lowest vitamin D levels, and 333 of the men with cancer were among those with the highest levels.

So should men try to get more vitamin D?

While the results of this study need to be replicated in future research, Shui said, vitamin D has been shown to have numerous effects on health. “Men who are concerned that they may be deficient in vitamin D should speak with their physicians about taking supplements or eating more foods rich in vitamin D,” she said.

The vitamin is also produced naturally by the skin when exposed to the sun. Getting about 30 minutes of sun exposure between 10 a.m. and 3 p.m. twice a week usually leads to sufficient vitamin D synthesis, according to the National Institutes of Health.

The study was limited in that most of the participants were white. “As vitamin D deficiency is even more prevalent in men of African descent, and this population also has a higher prostate cancer risk, studies conducted in men of other ethnicities would be helpful to see of our results are generalizable to those populations,” Shui said.

Read more: http://www.foxnews.com/health/2012/04/18/vitamin-d-linked-with-lower-risk-deadly-prostate-cancer/#ixzz2OktTqu4s

COMUNICADO DO CONSULTÓRIO DO DR. CÍCERO GALLI COIMBRA

COMUNICADO DO CONSULTÓRIO DO DR. CÍCERO.

http://www.institutodeautoimunidade.org.br/index.html
IITA

Os problemas com o telefone devem-se em grande parte à ineficiência da operadora contratada pelo prédio onde está instalado o consultório. Conseguiram agora mudar a operadora, mas, para fazer a portabilidade e manter o número, já tão conhecido, o telefone ficará mudo no próximo dia 26/03, pelo menos no período da manhã.

Informam também que:
– o número adequado para ligar é o (11) 5908 5969, pois o outro número é utilizado o tempo todo para fazer ligações.
– os horários menos congestionados no tel 5908-5969 são os seguintes: entre 8 às 9:30; entre 11 e 12:00; e entre 17 e 18:30h.

– quem já é paciente da clínica deve preferencialmente entrar em contato pelo e-mail da secretaria.

Não divulgam esse e-mail para todos porque não há como atender a demanda (pelo menos no momento). São inúmeros os e-mails e ligações.

– está sendo organizado um curso para médicos pelo Instituto de Autoimunidade e estão sendo treinados novos assistentes para ocupar completamente o tempo das 2 outras salas.

– ficam extremamente sensibilizados com os pacientes e estão trabalhando muito para oferecer alternativas.

CONSULTORIO DR. CÍCERO GALLI COIMBRA

CONSULTORIO DR. CÍCERO GALLI COIMBRA.

CONSULTORIO DR. CÍCERO GALLI COIMBRA

Rua Doutor Diogo de Faria 775  – Sala 94  Vila Mariana – em frente ao Hospital Paulista

COMUNICADO DO CONSULTÓRIO DO DR. CÍCERO.

– o número adequado para ligar é o (11) 5908 5969, pois o outro número é utilizado o tempo todo para fazer ligações.
– os horários menos congestionados no tel 5908-5969 são os seguintes: entre 8 às 9:30; entre 11 e 12:00; e entre 17 e 18:30h.

Consultorio Faz chamadas com 11 50844642

The Effects Of Low Vitamin D On The Body

0The Effects of Low Vitamin D on the Body

 oste1

Mar 28, 2011 | By Joseph Pritchard

Joseph Pritchard graduated from Our Lady of Fatima Medical School with a medical degree. He has spent almost a decade studying humanity. Dr. Pritchard writes as a San Francisco biology expert for a prominent website and thoroughly enjoys sharing the knowledge he has accumulated.

Photo Credit x-ray of bones image by Tammy Mobley from Fotolia.com

Your body needs 13 essential vitamins. Without these vitamins, which include vitamin A, B complex, C, D, E and K, your may suffer from complications ranging from heart disease to bone deformities. Vitamin D specifically has been linked to bone disease. In children vitamin D deficiency is called rickets and in adults it is called osteomalacia. In either case, low vitamin D has numerous detrimental effects on the body.

Vitamin D

Vitamin D is a fat soluble vitamin that the body is able to store in large amounts. Most often vitamin D is stored in the liver and in the fatty tissue. The body needs vitamin D to maintain normal blood levels of phosphorus and calcium, MayoClinic.com reports. These are the two main minerals involved in the formation of bone. Vitamin D also facilitates the absorption of calcium from the diet. Vitamin D may also be useful in preventing osteoporosis, high blood pressure, autoimmune disease and cancer.

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Rickets

Infants who suffer from severe vitamin D deficiency develop a condition called rickets. Often infants who only take in breast milk, darker-skinned babies and children with parents with vitamin D deficiency are at a greater risk for rickets. Symptoms include bone pain or tenderness, teeth deformities and cavities, growth retardation, frequent bone fractures, short stature, bowlegs, spine deformities and bumps in the chest and breastbone, according to Medline Plus, a service of the National Institutes of Health. Treatment for rickets focuses on administering vitamin D in order to normalize the child’s vitamin D levels. Braces and support can help prevent skeletal deformities, but some permanent defects may require corrective surgery.

Osteomalacia

In adults, vitamin D deficiency, or osteomalacia, often causes muscle and bone weakness. Adults are done growing by the time osteomalacia begins so they rarely develop skeletal deformities or growth problems. However, osteomalacia is correlated with a decrease in skeletal structural integrity, an article in “The American Journal of Clinical Nutrition” warns. These bones are weaker than normal bones and therefore the patient may experience aches and pains especially in the joints. Osteomalacia can also cause muscles pain and weakness. The diagnosis of vitamin D deficiency is sometimes difficult, but once the diagnosis is made treatment with vitamin D supplementation usually reverses the symptoms.

Sources of Vitamin D

The main source of vitamin D for humans comes from exposure to sunlight, “The American Journal of Clinical Nutrition” explains. Your skin is able to synthesize vitamin D when exposed to adequate amounts of sunlight. Furthermore, vitamin D found in foods such as salmon, mackerel and herring. Fish oil, like cod liver oil, also contains vitamin D. In the United States, some forms of milk, juice, breads, yogurts and cheesed are fortified with vitamin D. There are also dietary supplements and pharmaceutical preparations that contain vitamin D. These man-made forms of vitamin D are usually given to patients suffering from or at risk or developing vitamin D deficiency.

 

References

  • MedlinePlus; Rickets; Neil K. Kaneshiro, MD, MHA; August 3, 2010
  • Mayo Clinic; Vitamin D; December 1, 2010
  • “The American Journal of Clinical Nutrition”; Vitamin D deficiency: a worldwide problem with health consequences; Michael F Holick and Tai C Chen; May 1, 2007

Article reviewed by Jenna Marie Last updated on: Mar 28, 2011

Read more: http://www.livestrong.com/article/408333-the-effects-of-low-vitamin-d-on-the-body/#ixzz2HmHb3700

—-

 

Alta prevalência de quantidade inadequada/baixa de vitamina D e Implicações para a Saúde – High Prevalence of Vitamin D Inadequacy and Implications for Health

High Prevalence of Vitamin D Inadequacy and Implications for Health

 

Abstract

During the past decade, major advances have been made in vitamin D research that transcend the simple concept that vitamin D is important for the prevention of rickets in children and has little physiologic relevance for adults. Inadequate vitamin D, in addition to causing rickets, prevents children from attaining their genetically programmed peak bone mass, contributes to and exacerbates osteoporosis in adults, and causes the often painful bone disease osteomalacia. Adequate vitamin D is also important for proper muscle functioning, and controversial evidence suggests it may help prevent type 1 diabetes mellitus, hypertension, and many common cancers. Vitamin D inadequacy has been reported in approximately 36% of otherwise healthy young adults and up to 57% of general medicine inpatients in the United States and in even higher percentages in Europe. Recent epidemiological data document the high prevalence of vitamin D inadequacy among elderly patients and especially among patients with osteoporosis. Factors such as low sunlight exposure, age-related decreases in cutaneous synthesis, and diets low in vitamin D contribute to the high prevalence of vitamin D inadequacy. Vitamin D production from cutaneous synthesis or intake from the few vitamin D-rich or enriched foods typically occurs only intermittently. Supplemental doses of vitamin D and sensible sun exposure could prevent deficiency in most of the general population. The purposes of this article are to examine the prevalence of vitamin D inadequacy and to review the potential implications for skeletal and extraskeletal health.

Article

High Prevalence of Vitamin D Inadequacy and Implications for Health

 

 High Prevalence of Vitamin D Inadequacy and Implications for Health Mayo Clinic Proceedings, Volume 81, Issue 3, Pages 353-373 Michael F. Holick

 

 

  • ·       Vitamin D, Skin and Bone Research Laboratory, Section of Endocrinology, Diabetes, and Nutrition, Department of Medicine, Boston University School of Medicine, Boston, Mass

http://www.sciencedirect.com/science/article/pii/S0025619611614651

 

ScienceDirect

 

SOURCES OF VITAMIN D

VITAMIN D PHOTOBIOCHEMISTRY, METABOLISM, AND FUNCTIONS

1MHOLICK

ASSESSMENT OF VITAMIN D STATUS

2MHOLICK

EPIDEMIOLOGY OF VITAMIN D INADEQUACY

TABLE 1

FACTORS THAT CONTRIBUTE TO VITAMIN D INADEQUACY

SKELETAL CONSEQUENCES OF VITAMIN D INADEQUACY

3MHOLIC

TABLE 2

NEUROMUSCULAR FUNCTION

4MHOLICK

VITAMIN D AND EXTRASKELETAL HEALTH

VITAMIN D AND CANCER

VITAMIN D AND CARDIOVASCULAR DISEASE

VITAMIN D AND PSORIASIS

VITAMIN D AND MULTIPLE SCLEROSIS

VITAMIN D AND TYPE I DIABETES MELLITUS

VITAMIN D IN OTHER DISEASES

VITAMIN D DOSING, SUPPLEMENTATION, AND UV IRRADIATION AND/OR SENSIBLE SUN EXPOSURE

TREATMENT OF SEVERE VITAMIN D DEFICIENCY

CONCLUSION

Acknowledgments

REFERENCES

 

mholick

Mayo Clinic Proceedings

Volume 81, Issue 3, March 2006, Pages 353–373

REVIEW

High Prevalence of Vitamin D Inadequacy and Implications for Health

Michael F. Holick, PhD, MD,

Vitamin D, Skin and Bone Research Laboratory, Section of Endocrinology, Diabetes, and Nutrition, Department of Medicine, Boston University School of Medicine, Boston, Mass

 

Individual reprints of this article are not available. Address correspondence to Michael F. Holick, PhD, MD, Vitamin D, Skin and Bone Research Laboratory, Section of Endocrinology, Diabetes, and Nutrition, Department of Medicine, Boston University School of Medicine, 715 Albany St, Room M-1013, Boston, MA 02118

Available online 28 September 2011

http://dx.doi.org/10.4065/81.3.353, How to Cite or Link Using DOI

View full text

 

SOURCES OF VITAMIN D

VITAMIN D PHOTOBIOCHEMISTRY, METABOLISM, AND FUNCTIONS

ASSESSMENT OF VITAMIN D STATUS

EPIDEMIOLOGY OF VITAMIN D INADEQUACY

FACTORS THAT CONTRIBUTE TO VITAMIN D INADEQUACY

SKELETAL CONSEQUENCES OF VITAMIN D INADEQUACY

NEUROMUSCULAR FUNCTION

VITAMIN D AND EXTRASKELETAL HEALTH

VITAMIN D AND CANCER

VITAMIN D AND CARDIOVASCULAR DISEASE

VITAMIN D AND PSORIASIS

VITAMIN D AND MULTIPLE SCLEROSIS

VITAMIN D AND TYPE I DIABETES MELLITUS

VITAMIN D IN OTHER DISEASES

VITAMIN D DOSING, SUPPLEMENTATION, AND UV IRRADIATION AND/OR SENSIBLE SUN EXPOSURE

TREATMENT OF SEVERE VITAMIN D DEFICIENCY

CONCLUSION

Acknowledgments

REFERENCES

Refers to

Robert P. Heaney

Nutrition and Chronic Disease

Mayo Clinic Proceedings, Volume 81, Issue 3, March 2006, Pages 297-299

PDF (32 K)

Referred to by

Robert P. Heaney

Nutrition and Chronic Disease

Mayo Clinic Proceedings, Volume 81, Issue 3, March 2006, Pages 297-299

PDF (32 K)


 

During the past decade, major advances have been made in vitamin D research that transcend the simple concept that vitamin D is important for the prevention of rickets in children and has little physiologic relevance for adults. Inadequate vitamin D, in addition to causing rickets, prevents children from attaining their genetically programmed peak bone mass, contributes to and exacerbates osteoporosis in adults, and causes the often painful bone disease osteomalacia. Adequate vitamin D is also important for proper muscle functioning, and controversial evidence suggests it may help prevent type 1 diabetes mellitus, hypertension, and many common cancers. Vitamin D inadequacy has been reported in approximately 36% of otherwise healthy young adults and up to 57% of general medicine inpatients in the United States and in even higher percentages in Europe. Recent epidemiological data document the high prevalence of vitamin D inadequacy among elderly patients and especially among patients with osteoporosis. Factors such as low sunlight exposure, age-related decreases in cutaneous synthesis, and diets low in vitamin D contribute to the high prevalence of vitamin D inadequacy. Vitamin D production from cutaneous synthesis or intake from the few vitamin D-rich or enriched foods typically occurs only intermittently. Supplemental doses of vitamin D and sensible sun exposure could prevent deficiency in most of the general population. The purposes of this article are to examine the prevalence of vitamin D inadequacy and to review the potential implications for skeletal and extraskeletal health.

 

Keywords

1α(OH)D3, 1α-hydroxyvitamin D3;

1,25(OH)2D, 1,25-dihydroxyvitamin D;

25(OH)D, 25-hydroxyvitamin D;

BMD, bone mineral density;

PTH, parathyroid hormone;

RCT, randomized controlled trial;

RECORD, Record Evaluation of Calcium or Vitamin D;

VDR, vitamin D receptor


Figures and tables from this article:

 

FIGURE 1. Cutaneous production of vitamin D and its metabolism and regulation for calcium homeostasis and cellular growth. 7-Dehydrocholesterol or provitamin D3 (proD3) in the skin absorbs solar UV-B radiation and is converted to previtamin D3 (preD3). D3 undergoes thermally induced (δH) transformation to vitamin D3. Vitamin D from the diet or from the skin is metabolized in the liver by the vitamin D-25-hydroxylase to 25-hydroxyvitamin D3 (25[OH]D3). 25(OH)D3 is converted in the kidney by the 25(OH)D3-1α-hydroxylase to 1,25-dihydroxyvitamin D3 [1,25(OH)2D3]. A variety of factors, including serum phosphorus (PO2−4) and parathyroid hormone (PTH), regulate the renal production of 1,25(OH)2D3. 1,25(OH)2D regulates calcium metabolism through its interaction with its major target tissues, the bone and the intestine. From Osteoporos Int,21 with permission from Springer Science and Business Media.

 

FIGURE 2. Left, Relationship between serum 25-hydroxyvitamin D (25[OH]D) concentrations and mean ± SE (error bars) serum concentrations of parathyroid hormone in patients with osteoporosis receiving treatment. Right, Percentage of subjects with secondary hyperparathyroidism by 25(OH)D level. The percentage of subjects with secondary hyperparathyroidism (parathyroid hormone level >40 pg/mL) sorted by subgroups with serum 25(OH)D concentrations delineated by predefined cutoffs for analyses of 25(OH)D inadequacy. Left and right, From J Endocrinol Metab,30 with permission from The Endocrine Society, Copyright 2005.

 

 

FIGURE 3. Mean ± SD (error bars) serum 25-hydroxyvitamin D (25[OH]D) concentrations (shown as nmol/L and ng/mL) in women older than 70 years, stratified by supplement use and residential status. Adapted from J Clin Endocrinol Metab,97 with permission from The Endocrine Society, Copyright 1988.

 

 

FIGURE 4. Relative to therapy with 1200 mg/d of calcium for 12 weeks, daily therapy with 800 IU of vitamin D and 1200 mg of calcium accounted for a 49% reduction in the relative risk of falls among older women (mean age, 85.3 years) in long-term geriatric care. Ca = calcium; Ca + D = Ca plus vitamin D. Adapted from J Bone Miner Res,174 with permission from The American Society for Bone and Mineral Research.

 

 

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FIGURE 5. Endocrine and autocrine or paracrine functions of 1,25-dihydroxyvitamin D (1,25[OH]2D). The kidneys serve as the endocrine organ to convert 25-hydroxyvitamin D (25[OH]D) to 1,25(OH)2D. 1,25(OH)2D carries out its calcium-regulating functions for bone health by stimulating intestinal calcium and phosphorus absorption. The circulating levels of 1,25(OH)2D can also potentially influence the activity of other tissues and cells that have a vitamin D receptor (VDR) and have no function in regulating calcium homeostasis and bone health. These include, among others, the heart skeletal muscle, active T and B lymphocytes, breast, colon, and prostate. In addition, a multitude of in vitro studies with human and animal cells have shown that most tissues and cells not only express the VDR but also express the same 1α-hydroxylase as the kidney. Thus, it has been suggested that most cells, including lung, colon, prostate, and breast, locally produce 1,25(OH)2D3 to help regulate a variety of cellular functions including growth and differentiation. This may help explain the epidemiological evidence that sun exposure at lower altitudes and higher serum levels of 25(OH)D are related to a decreased risk of a wide variety of chronic illnesses. It has been speculated that when 25(OH)D levels are above 30 ng/mL this serves as the substrate for the external 25(OH)D3-1α-hydroxylase to produce 1,25(OH)2D in the colon, prostate, breast, and lung to modulate cell growth and reduce risk of the cells becoming malignant.

 

 

TABLE 1. Vitamin D Inadequacy in Osteoporosis: Summary of Reports Published in 2003 and 2004*

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TABLE 2. Hierarchy of Evidence for Studies Relating Vitamin D to Pathologic Conditions*

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This work was supported in part by National Institutes of Health grants MOIRR00533 and AR369637 and the UV Foundation.

Individual reprints of this article are not available. Address correspondence to Michael F. Holick, PhD, MD, Vitamin D, Skin and Bone Research Laboratory, Section of Endocrinology, Diabetes, and Nutrition, Department of Medicine, Boston University School of Medicine, 715 Albany St, Room M-1013, Boston, MA 02118

*

Dr Holick is an Academic Associate for Nichols Institute Diagnostics.

Copyright © 2006 Mayo Foundation for Medical Education and Research. Published by Elsevier Inc. All rights reserved.

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Vitamin D: importância na prevenção de cancros, diabetes, doenças do coração, e osteoporose – Vitamin D: importance in the prevention of cancers, type 1 diabetes, heart disease, and osteoporosis

Vitamin D: importance in the prevention of cancers, type 1 diabetes, heart disease, and osteoporosis1,2,3,4,5

  1. 1.    Michael F Holick

+ Author Affiliations

  1. 1.     1From the Vitamin D, Skin, and Bone Research Laboratory, Section of Endocrinology, Diabetes, and Nutrition, Department of Medicine, Boston University School of Medicine, Boston

Next Section Abstract The purpose of this review is to put into perspective the many health benefits of vitamin D and the role of vitamin D deficiency in increasing the risk of many common and serious diseases, including some common cancers, type 1 diabetes, cardiovascular disease, and osteoporosis. Numerous epidemiologic studies suggest that exposure to sunlight, which enhances the production of vitamin D3 in the skin, is important in preventing many chronic diseases. Because very few foods naturally contain vitamin D, sunlight supplies most of our vitamin D requirement. 25-Hydroxyvitamin D [25(OH)D] is the metabolite that should be measured in the blood to determine vitamin D status. Vitamin D deficiency is prevalent in infants who are solely breastfed and who do not receive vitamin D supplementation and in adults of all ages who have increased skin pigmentation or who always wear sun protection or limit their outdoor activities. Vitamin D deficiency is often misdiagnosed as fibromyalgia. A new dietary source of vitamin D is orange juice fortified with vitamin D. Studies in both human and animal models add strength to the hypothesis that the unrecognized epidemic of vitamin D deficiency worldwide is a contributing factor of many chronic debilitating diseases. Greater awareness of the insidious consequences of vitamin D deficiency is needed. Annual measurement of serum 25(OH)D is a reasonable approach to monitoring for vitamin D deficiency. The recommended adequate intakes for vitamin D are inadequate, and, in the absence of exposure to sunlight, a minimum of 1000 IU vitamin D/d is required to maintain a healthy concentration of 25(OH)D in the blood.

     Vitamin D

     sunlight

     25-hydroxyvitamin D

     cancer

     bone health

     diabetes

Previous SectionNext Section INTRODUCTION Once our sun ignited, it began to emit enormous amounts of energy. This energy bombarded all of its satellite planets. The third planet from the Sun (ie, Earth) had a huge ocean and a small land mass. In the bubbling, organically rich tide pools, life began to evolve and became dependent on solar energy for its very existence. Early in evolution, organisms captured the sun’s energy in the form of carbohydrates through the process of photosynthesis. As organisms evolved, they continued to make a wide variety of complex macromolecules, not only for the purpose of replication but also to sustain life’s functions. The life forms took advantage of their ocean environment and became dependent on calcium for signal transduction and metabolic functions. In addition, calcium became an important component for organisms that developed exoskeletons. The use of calcium for structural scaffolding became critically important in the evolution of ocean-dwelling vertebrates. The plentiful calcium in the oceans provided the ideal element to incorporate into a collagen-based matrix that gave rise to the structurally rigid vertebrate skeleton. The development of the vertebrate endoskeleton not only provided an opportunity for organisms to grow in size but also gave organisms the opportunity to venture onto land. As vertebrate organisms left their ocean environment for a land-based existence, they needed to develop an efficient method of utilizing the calcium that was absorbed into plants from the calcium-rich soil environment. Remarkably, it was the sun’s energy that was called on to promote the photosynthesis of vitamin D3 in the skin of vertebrates that was responsible for enhancing the efficiency of intestinal calcium absorption (1). Little is known about when vitamin D made its appearance on Earth and what its function was. However, it is known that some of the earliest phytoplankton and diatom life forms, including Emiliania huxlei, which has existed in the oceans for > 750 million years and which has used calcium for its structural support (it is a coccolithophore), produced ergosterol (provitamin D2). When exposed to simulated sunlight, the ergosterol in E huxlei was converted to previtamin D2 (which rapidly isomerized to vitamin D2; 2). Skeletonema menzelii, a diatom that also contained ergosterol, converted it to previtamin D2. Little is known about the biologic function of ergosterol, previtamin D2, and vitamin D2 in nonvertebrate species. It has been suggested that ergosterol and its photoproducts are an ideal sunscreening system because of their high absorption of ultraviolet radiation (1). Ergosterol, previtamin D2, vitamin D2, and their photoproducts efficiently absorb the ultraviolet radiation that is damaging to DNA, RNA, and protein—ie, 230-330 nm. Thus, before the ozone layer (which now efficiently absorbs all ultraviolet radiation < 290 nm) evolved, the ergosterol-vitamin D2 system may have played a critical role in protecting organisms from the high-energy ultraviolet radiation that could have damaged their ultraviolet-sensitive proteins, RNA, and DNA. It is also possible that, if ergosterol existed in the plasma membrane of early life forms, it altered the membrane’s permeability for calcium when it was converted to the structurally less rigid vitamin D2 (1, 2). Previous SectionNext Section PHOTOSYNTHESIS OF PREVITAMIN D Ergosterol is a plant and fungal sterol. Animals synthesize cholesterol. The immediate precursor in the cholesterol biosynthetic pathway is 7-dehydrocholesterol (provitamin D3). 7-Dehydrocholesterol is produced in relatively large quantities in the skin of many vertebrate animals, including humans. The few exceptions are some bat species, mole rats, cats, and dogs (35). During exposure to sunlight, the 7-dehydrocholesterol in the epidermal and dermal cells absorbs ultraviolet B (UVB) radiation with wavelengths of 290-315 nm. The absorption of this radiation results in a rearrangement of the 5,7-diene in the B-ring that causes a break in the B-ring to form the 9,10-secosterol, previtamin D3. Previtamin D3 is thermodynamically unstable, and it rearranges its double bonds to form the more thermodynamically stable vitamin D3 structure (Figure 1).

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FIGURE 1. F1MH Schematic representation of cutaneous production of vita-min D and its metabolism and regulation of calcium homeostasis and cellular growth. During exposure to sunlight, 7-dehydrocholesterol (7-DHC) in the skin absorbs solar ultraviolet B (UVB) radiation and is converted to previtamin D3 (preD3). Once formed, preD3 undergoes thermally induced transformation to vitamin D3. Further exposure to sunlight converts preD3 and vitamin D3 to biologically inert photoproducts. Vitamin D coming from the diet or from the skin enters the circulation and is metabolized in the liver by vitamin D-25-hydroxylase (25-OHase) to 25-hydroxyvitamin D3 [25(OH)D3]. 25(OH)D3 reenters the circulation and is converted in the kidney by 25-hydroxyvitamin D3-1α-hydroxylase (1-OHase) to 1,25-dihydroxyvitamin D3 [1,25(OH)2D3]. A variety of factors, including serum phosphorus (Pi) and parathyroid hormone (PTH), regulate the renal production of 1,25(OH)2D. 1,25(OH)2D regulates calcium metabolism through its interaction with its major target tissues, the bone, and the intestine. 1,25(OH)2D3 also induces its own destruction by enhancing the expression of 25-hydroxyvitamin D-24-hydroxylase (24-OHase). 25(OH)D is metabolized in other tissues for the purpose of regulation of cellular growth. VDR, vitamin D receptor. Velluz et al (6) were the first to identify previtamin D3 and to show the transformation of previtamin D3 to vitamin D3. At room temperature, this process took ≈12 d to complete (7). Although this transformation was remarkable, it would have been impractical for cold-blooded vertebrates to produce an amount of vitamin D3 in their skin that was adequate to sustain their calcium-needy skeletons. Previtamin D3 exists in 2 conformeric forms. Once 7-dehydrocholesterol undergoes its exocyclic ring opening, it converts to the 5, 6-cis, cis (cZc) conformer. However, this conformer is extremely unstable because of the steric interference of the C-19 methyl group, and it immediately rotates into the more stable 5, 6-trans,cis (tZc) previtamin D3. However, only the cZc conformer can convert to vitamin D3. To overcome this impediment, the 7-dehydrocholesterol was incorporated into the lipid bilayer of the plasma membrane. This resulted in the sandwiching of 7-dehydrocholesterol between the polar head group and the long-chain fatty acids. Thus, during exposure to sunlight, the 7-dehydrocholesterol immediately converted to cZc previtamin D3, which could not rotate into the favored tZc conformer, and that resulted in the rapid conversion of previtamin D3 to vitamin D3. This probably explains why the conversion of previtamin D3 to vitamin D3 in the skin is 10 times faster than that in an organic solvent (7). Previous SectionNext Section FACTORS THAT ALTER PHOTOSYNTHESIS OF PREVITAMIN D3 During exposure to sunlight, 7-dehydrocholesterol is converted to previtamin D3, which in turn is isomerized by a thermally induced process to vitamin D3. Once formed, vitamin D3, which is structurally incompatible with being sandwiched between the hydrophobic fatty acid chains of the plasma membrane, is ejected into the extracellular space. It is then drawn into the dermal capillary bed by the vitamin D-binding protein, which has a small but effective affinity for it (8). It is remarkable that lifeguards and sun worshippers have never suffered from vitamin D intoxication due to excessive exposure to the sun (9). The reason for this is that previtamin D3 and vitamin D3 efficiently absorb sunlight and are converted to a multitude of other photoproducts, including lumisterol, tachysterol, suprasterols, and toxisterols (1, 2, 9; Figure 1). Thus, because of this unique solar regulation, the skin can never generate quantities of vitamin D3 excessive enough to cause vitamin D3 intoxication (9). Because the production of previtamin D3 in the skin is directly related to the number of UVB photons that are absorbed by 7-dehydrocholesterol, any process that either decreases the number of UVB photons entering the epidermis or decreases the amount of 7-dehydrocholesterol in the skin will result in a significant reduction in or the complete elimination of vitamin D3 production in the skin. A heightened awareness of the role that excessive exposure to sunlight plays in increasing the risk of nonmelanoma skin cancer and wrinkles led to the widespread use of topical sunscreens. Sunscreens efficiently absorb UVB radiation and thus markedly diminish the total number of UVB photons that reach the 7-dehydrocholesterol in the skin’s cells. When used properly (ie, 2 mg/cm2 or 35 mL—ie, 1 oz—on the whole body one time), a sunscreen with an sun protection factor of 8 reduces cutaneous production of previtamin D3 by > 95% (10, 11). The proper use of a sunscreen with a sun protection factor of 15 reduces the capacity > 99%. The facts that most sunscreen users apply as little as 18% and no more than 35-50% of the recommended amount of sunscreen, and they do tan indicate that they are making sufficient amounts of vitamin D3 in their skin. The fact that they tan is a reflection of the fact that UVB penetrates the epidermis to stimulate the melanocytes and make vitamin D3. Melanin is a natural sunscreen that evolved to protect humans from blistering solar radiation as they evolved in equatorial regions of the world. This skin pigment is an extremely effective sunscreen with absorption properties from the ultraviolet C (200-280 nm) into the visible range (> 700 nm), and it competes quite well with 7-dehydrocholesterol for UVB photons. Thus, people of color who have greater amounts of melanin in their epidermis than do whites are less efficient in producing vitamin D3 than are whites (11, 12). A person with skin type 5/6 (dark skin, never develops a sunburn) requires 10-50 times the exposure to sunlight to produce the same amount of vitamin D3 in their skin as does a white person with skin type 2 or 3 (12). The stratospheric ozone layer is efficient in absorbing all solar radiation below 290 nm. However, the ozone layer also can absorb UVB radiation above 290 nm that is responsible for producing previtamin D3 in the skin. The ultraviolet radiation that can be absorbed by 7-dehydrocholesterol has energies down to 315 nm. Thus, when the angle of the sunlight (zenith angle) reaching the Earth’s surface is very oblique (ie, early morning, late afternoon, and winter), sunlight must pass through more ozone, which efficiently absorbs the previtamin D3-producing UVB photons, and thus very few, if any, reach the earth’s surface. Because the zenith angle is dependent on time of day, season of the year, and latitude, those factors have a dramatic effect on the cutaneous production of vitamin D3 (13, 14). Below ≈35°, the zenith angle is more direct, and therefore previtamin D3 synthesis can occur in the skin year-round. However, above 35° latitude, the angle of the sun is so oblique during the winter months that most, if not all, of the UVB photons below 315 nm are absorbed by the ozone layer, thereby either reducing or completely preventing the production of previtamin D3 in the skin. For example, residents of Boston (42 °N), Edmonton, Canada (52 °N), and Bergen, Norway (61 °N) cannot produce sufficient quantities of vitamin D3 in their skin for 4, 5, and 6 mo, respectively. We have conducted studies around the globe that provide guidelines for when, where, and at what time of day vitamin D3 can be produced in the skin (14; Figure 2).

F2MH

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FIGURE 2. Influence of season, time of day, and latitude on the synthesis of previtamin D3 in the northern (A and C: Boston, ○; Edmonton, □; Bergen, ▴) and southern (B: Buenos Aires, ○; Johannesburg, □; Cape Town, ▴; Ushuala, ▿; D: Buenos Aires, •; Johannesburg, □; Cape Town, ▵; Ushuala, ▾) hemispheres. The hour indicated in C and D is the end of the 1-h exposure time in July and January, respectively. Adapted with permission (14). Previous SectionNext Section SOURCES OF VITAMIN D Very few foods naturally contain vitamin D. Cod liver oil and oily fish such as salmon, mackerel, and sardines are good sources. Eating oily fish at least 3-4 times/wk will help satisfy the requirement for adequate intake. Some foods such as milk (100 IU/8 oz), orange juice (100 IU/8 oz), and some cereals and breads are fortified with vitamin D (11, 12, 15). The vitamin D content in milk is often less than the label proclaims it to be, and thus the contribution of vitamin D from the diet is highly variable. To satisfy the body’s requirement for vitamin D, most humans obtain it from casual exposure to sunlight. During the spring, summer, and fall, enough vitamin D3 is produced in the skin to be stored in the body fat, and it can be mobilized during winter months when little, if any, vitamin D3 is produced in the skin. The skin has a large capacity to produce vitamin D3. Blood concentrations of vitamin D3 were compared in healthy young and middle-aged adults who were exposed to simulated sunlight that was equivalent to being on a sunny beach and obtaining enough sun to cause a slight pinkness to the skin (1 minimal erythemal dose) and who took an oral dose of vitamin D2. The exposure was equivalent to an oral dose of ≈20 000 IU vitamin D2 (9; Figure 3). Although aging decreases the amount of 7-dehydrocholesterol produced in the skin by as much as 75% by the age of 70 y (16, 17), the skin has such a large capacity to make vitamin D3 that even elderly exposed to sunlight can achieve increased blood concentrations of vitamin D3 and 25(OH)D (1719).

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FIGURE 3. F3MH Serum vitamin D concentrations after a whole-body exposure to 1 minimal erythemal dose (MED) of simulated sunlight in a tanning bed and after a single oral dose of either 10 000 or 25 000 IU vitamin D2. UV, ultraviolet. Reproduced with permission (9). Previous SectionNext Section CAUSES AND CONSEQUENCES OF VITAMIN D DEFICIENCY It is estimated that 10 million households in the United States have a reptile as a pet. In their natural environment, reptiles are often exposed to sunlight. They are vertebrates, and, like humans, they require a source of calcium and vitamin D. Iguanas are at particular risk of severe vitamin D deficiency because they are herbivores that, as pets, often are fed a steady diet of lettuce and because they are housed in glass enclosures with a light source that is devoid of UVB transmission. Lettuce contains very little calcium and no vitamin D, and thus iguanas and other vertebrates who do not receive an adequate amount of calcium and vitamin D develop the metabolic bone diseases osteoporosis and osteomalacia that result in fractures and ultimately death. Most reptile owners are aware of the need not only to provide their precious pets with a commercial source of calcium supplementation, but also to provide them with a light that emits UVB radiation similar to sunlight so that the animals can produce vitamin D3 in their skin. Humans are no different. They need an adequate source of calcium and vitamin D. Without vitamin D, the small intestine absorbs no more than 10-15% of dietary calcium. In a person with vitamin D sufficiency, the small intestine absorbs, on average, 30% of dietary calcium; during growth, lactation, and pregnancy, the efficiency increases to 80%. Vitamin D deficiency during bone development and growth causes the bone-deforming disease rickets. In adults bone growth stops and bone remodeling continues. Vitamin D deficiency in adults causes secondary hyperparathyroidism that can precipitate and exacerbate osteoporosis (2, 9, 11). The secondary hyperparathyroidism associated with vitamin D deficiency often maintains the serum calcium concentration within the normal range, but it causes a loss of phosphorus in the urine. This loss results in inadequate serum calcium × phosphorus to promote mineralization of the osteoid in the bone, which in turn results in osteomalacia, ie, nonmineralization of the collagen matrix. Because the nonmineralized matrix cannot provide structural support, the risk of fracture is greater. How common is vitamin D deficiency? Surprisingly, it has made a resurgence in neonates and young children, in part because of the campaign to encourage all women to provide all of their infants’ nutrition through breastfeeding. Because there is very little, if any, vitamin D in human milk, infants, especially infants of women of color, are at high risk of developing vitaminD deficiency and rickets if they are not given a vitamin D supplement (20, 21). The elderly are at risk for vitamin D deficiency because of poor dietary vitamin D intake and decreased exposure to sunlight. We observed that 30%, 42%, and 84% of free-living white, Hispanic, and black elderly were vitamin D deficient [25(OH)D < 50 nmol/L] at the end of August in Boston (9). It has always been assumed that young and middle-aged adults are not at risk of vitamin D deficiency because of their outdoor activities and dietary intake. However, it was recently recognized that 42% of African American women aged 15-49 y throughout the United States were vitamin D deficient [25(OH)D < 40 nmol/L] at the end of the winter (22). Hard-working young and middle-aged adults who very seldom spend any time outdoors or always wear sun protection outdoors are also at high risk of vitamin D deficiency. We observed that 32% of healthy adults 18-29 y of age were vitamin D deficient [25(OH)D < 50 nmol/L] at the end of the winter in Boston (23). Obesity is often associated with vitamin D deficiency (24). It is now recognized that, whether vitamin D is ingested in the diet or obtained from exposure to sunlight, it is efficiently deposited in the large body fat stores and is not bioavailable (25; Figure 4). This is probably the reason that obese persons are chronically vitamin D deficient.

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FIGURE 4. F4MH A: Mean (± SEM) serum vitamin D3 concentrations before (▪) and 24 h after (□) whole-body irradiation (27 mJ/cm2) with ultraviolet B radiation. The response of the obese subjects was attenuated when compared with that of the control group. There was a significant time-by-group interaction, P = 0.003. *Significantly different from preradiation values (P < 0.05). B: Mean (± SEM) serum vitamin D2 concentrations in the control (•) and obese (○) groups before and 25 h after oral intake of vitamin D2 (50 000 IU, or 1.25 mg). *Significant time and group effects by ANOVA (P < 0.05) but no significant time-by-group interaction. The difference in peak concentrations between obese and nonobese control subjects was not significant. Reproduced with permission (25). Vitamin D deficiency often goes undiagnosed or, worse, is misdiagnosed (9, 2629). There are 3 reasons for this. First, it is believed that either exposure to sunlight or dietary intake of vitamin D is adequate, and, therefore, that Americans and Europeans are not at risk of vitamin D deficiency. Second, physicians who perform routine blood work-ups often obtain a blood calcium value. If they find it to be normal, they assume that the patient is vitamin D sufficient, which is not correct. Third, many physicians erroneously order an analysis for the active form of vitamin D, 1,25-dihydroxyvitamin D [1,25(OH)2D], to determine the vitamin D status of a patient. Unfortunately, 1,25(OH)2D not only is not a measure of vitamin D status, but its measurement also can mislead the physician into thinking that the patient is vitamin D sufficient. The reason for this is that, as a person becomes vitamin D-deficient, there is an increase in the concentration of parathyroid hormone (PTH), which increases the renal production of 1,25(OH)2D, the circulating concentrations of which often become normal or even elevated (9). The vitamin D metabolite that should be measured to determine vitamin D status is 25(OH)D, which is the major circulating form of vitamin D, circulating at 1000 times the concentration of 1,25(OH)2D and having a half-life of ≈2 wk (2, 9, 11). As a person becomes vitamin D-deficient, there is a decrease in the efficiency of intestinal calcium absorption. The ionized calcium concentrations begin to drop; this decrease is immediately recognized by the calcium sensor in the parathyroid glands, which increases the production of PTH (30). PTH compensates for the decrease in intestinal calcium absorption by increasing the mobilization of calcium stores from the skeleton and by increasing tubular reabsorption of calcium in the kidney (31, 32). Previous SectionNext Section NONSKELETAL CONSEQUENCES OF VITAMIN D DEFICIENCY It has long been recognized that people who live at higher latitudes face an increased risk of many chronic diseases, including common cancers (3339), multiple sclerosis (39, 40), and hypertension (41). As early as 1941, Apperly (37) observed that people living at higher latitudes, eg, Massachusetts and New Hampshire, had a higher risk of dying of the most common cancers than did people living in the South, eg, Georgia and South Carolina. In 1979, Rostand (41) reported that people living at higher latitudes in both the United States and Europe were at higher risk of hypertension. In the late 1980s and early 1990s, several investigators reported increased risks of dying of colon, prostate, and breast cancer in people living at higher latitudes in both the United States and Europe (3335). Grant (42) reported that ≥25% of the deaths due to breast cancer in women in Europe could be attributed to the women’s lack of UVB from exposure to sunlight. Both men and women are at higher risk of dying of cancer if they have minimum exposure to sunlight (38; Figure 5 A and B). In a retrospective study, Ahonen et al (44) reported that men on average begin to develop prostate cancer by the age of 52 y, whereas men exposed to more sunlight throughout their lives did not begin developing prostate cancer until 3-5 y later.

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FIGURE 5. F5MH A: Premature mortality due to cancer in white females, as determined on the basis of the July 1992 DNA-weighted ultraviolet B (UV-B) radiation by use of a total ozone mapping spectrometer. B: Premature mortality due to cancer in white males in the United States from 1970 through 1994, as determined on the basis of the July 1992 DNA-weighted UV-B radiation. Reproduced by permission of Wiley-Liss, Inc, a subsidiary of John Wiley & Sons, Inc (43). Copyright (2002) American Cancer Society. Previous SectionNext Section VITAMIN D METABOLISM AND NONCALCEMIC FUNCTIONS It has been known for > 30 y that vitamin D3 made in the skin or coming from the diet requires 2 obligate hydroxylations, first in the liver and then in the kidney, to create the active form of vitamin D, 1,25(OH)2D (Figure 1). 1,25(OH)2D interacts with its nuclear receptor in the intestine, bone, and kidney to regulate calcium and bone metabolism (9, 31, 45). Most tissues and cells in the body, including heart, stomach, pancreas, brain, skin, gonads, and activated T and B lymphocytes, have nuclear receptors for 1,25(OH)2D, called vitamin D receptors (4648). Thus, it is not at all surprising that 1,25(OH)2D has a multitude of biologic effects that are noncalcemic in nature (9, 31, 45). One of the most intriguing important and unappreciated biologic functions of 1,25(OH)2D is its ability to down-regulate hyperproliferative cell growth (9, 31, 49). Normal and cancer cells that have a vitamin D receptor often respond to 1,25(OH)2D by decreasing their proliferation and enhancing their maturation. This was the rationale for using 1,25(OH)2D3 and its analogs to treat the common hyperproliferative skin disorder psoriasis (50, 51). Vitamin D receptors are present in activated T and B lymphocytes and in activated macrophages. The most common autoimmune diseases, including type 1 diabetes, rheumatoid arthritis, and multiple sclerosis, have all been successfully prevented in models using mice that were prone to these diseases if they received 1,25(OH)2D3 early in life (45, 5255). When nonobese diabetic mice, who typically develop type 1 diabetes, received 1,25(OH)2D3 throughout their life, their risk of developing type 1 diabetes was reduced by 80% (52, 55). This is in good agreement with the recent observation by Hypponen et al (56) that children receiving 2000 IU vitamin D from age 1 y on decreased their risk of getting type 1 diabetes by 80%. Krause et al (57) reported that hypertensive patients exposed to UVB radiation for 3 mo had a > 180% increase in circulating concentrations of 25(OH)D and a 6 mm Hg decrease in their diastolic and systolic blood pressures, results similar to those expected if the patients had received a blood pressure medication (Figure 6). A similar group of patients who were exposed to ultraviolet A radiation and whose circulating concentrations of 25(OH)D did not increase continued to be hypertensive throughout the 3-mo study. The exact mechanism by which UVB radiation returned the blood pressure to normal [presumably due to increased blood concentrations of 25(OH)D] in these hypertensive adults is not well understood, but the observation by Li et al (58) sheds some light on the question. They observed in a mouse model that 1,25(OH)2D is effective in down-regulating renin and angiotensin and thereby decreasing blood pressure.

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FIGURE 6. F6MH Effect of ultraviolet B (UVB) and ultraviolet A (UVA) radiation from a tanning bed on ambulatory daytime and nighttime blood pressure in hypertensive adults before and after exposure to tanning bed radiation 3 times/wk for 3 mo. The daytime and nighttime blood pressures after UVB tanning bed radiation were significantly (P < 0.01) different from those before irradiation. The mean is indicated by the thick line. Reproduced with permission from Elsevier (57). Previous SectionNext Section THE CANCER-VITAMIN D CONNECTION Because an increased risk of vitamin D deficiency is one of the well-documented effects of living at higher latitudes on human health, it was reasonable to suggest that both living at higher latitudes and an increased risk of common diseases were associated with a decrease in the synthesis of vitamin D3 in the skin. It was intuitively obvious to many, on the basis of new information about vitamin D metabolism and action, that increased exposure to sunlight at lower latitudes would increase blood concentrations of 25(OH)D3, which could be activated in the kidney to 1,25(OH)2D3. Because 1,25(OH)2D3 is extremely potent in inhibiting cancer cell growth, this all seemed to make sense. Unfortunately, it was also well known that the renal production of 1,25(OH)2D was tightly regulated by PTH, calcium, and phosphorus (31). Indeed, neither increased exposure to sunlight nor increased oral intake of vitamin D raised blood concentrations of 1,25(OH)2D (5961). Thus, the question remained: how was it that increased exposure to sunlight was related, presumably by increasing the production of vitamin D3 in the skin, to a decreased risk of many common cancers and other chronic diseases? It had always been assumed that the kidney was the sole source for the body’s production of 1,25(OH)2D. This was based on many observations in animals and in humans whereby, in the absence of any renal function, there were little if any circulating concentrations of 1,25(OH)2D. It had been reported that the placenta, epidermal cells, and bone cells could produce 1,25(OH)2D, but the physiologic relevance of these observations was not well understood (62, 63). In 1985, Schwartz et al (64) reported that cultured prostate cancer cells expressed the enzymatic machinery to convert 25(OH)D to 1,25(OH)2D (Figure 7). Since that observation, it has been shown that a wide variety of normal tissues as well as various cancer cells, including colon cancer, breast cancer, and lung cancer, all have the ability to make 1,25(OH)2D (6567).

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FIGURE 7. F7MH Measurement of 25-hydroxyvitamin D-1α-hydroxylase (1α-OHase) activity in prostate cells that were either normal (▪), benign but hypertrophied (□), or cancerous (▧). The activity was measured by incubating the cells with [3H]25-hydroxyvitamin D3 and measuring the percentage of conversion to [3H]1,25-dihydroxyvitamin D3 after 24 h. Thus, it is reasonable to conclude that increased exposure to sunlight or increased intake of vitamin D leads to higher circulating concentrations (> 80 nmol/L) of 25(OH)D. 25(OH)D acts as a substrate for the 25-hydroxyvitamin D-1-hydroxylase in various tissues, including colon, breast, and lung. These tissues can produce 1,25(OH)2D, which acts in an autocrine fashion to regulate cell growth and decrease proliferative activity (Figure 8). It can also induce apoptosis when called on. Thus, 1,25(OH)2D3 can effectively manipulate cell growth and maintain it in a normal proliferative state under most circumstances. Once it accomplishes this, it induces the 25-hydroxyvitamin D-24-hydroyxlase, which hydroxylates the 1,25(OH)2D in the side chain on carbons 23 and 24, and this results in cleavage between carbons 23 and 24 that forms the water-soluble, biologically inert calcitroic acid (31, 68; Figure 1). This is the likely explanation for why patients with renal failure develop a 1,25(OH)2D deficiency that results in secondary hyperparathyroidism and renal osteodystrophy.

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FIGURE 8. F8MH Schematic representation of the multitude of other potential physiologic actions of vitamin D with respect to cardiovascular health, cancer prevention, regulation of immune function, and decreased risk of autoimmune diseases. 25(OH)D, 25-hydroxyvitamin D; 1,25(OH)2D, 1,25-dihydroxyvitamin D. Previous SectionNext Section CONCLUSIONS The Institute of Medicine reported in 1997 that the recommended vitamin D intake was inadequate for adults over the age of 50 y (69). They recommended that the adequate intake for children and adults up to the age of 50 be 200 IU vitamin D/d. However, adults aged 50-70 y and ≥ 70 y required 400 and 600 IU vitamin D/d, respectively. As noted in Heaney’s McCollum Award presentation (70) and as indicated in a considerable number of published reports, including that of Heaney et al (71), the new recommendations are totally inadequate, especially if a person has no exposure to sunlight. Without exposure to sunlight, a minimum of 1000 IU vitamin D/d is required. We gave healthy young and middle-aged adults 1000 IU vitamin D/d in orange juice from March through May. Their 25(OH)D concentrations increased by 150%, and what is considered to be a healthy 25(OH)D concentration, ie, 78-100 nmol/L (30-40 ng/mL), was maintained. Those adults receiving orange juice not fortified with vitamin D increased their blood concentration of 25(OH)D by 45%. This was due to their casual exposure to sunlight in the spring (15; Figure 9).

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FIGURE 9. F9M H Mean (± SEM) weekly 25-hydroxyvitamin D [25(OH)D] concentrations in healthy adults ingesting orange juice fortified with vitamin D (1000 IU · 8 oz−1 · d−1, •) or unfortified orange juice (▪). *P ≤ 0.01. Reproduced with permission (15). The easiest method of correcting vitamin D deficiency is to give the patient one pill that contains 50 000 IU vitamin D once a week for 8 wk (71). This will usually increase the 25(OH)D concentration to > 50 nmol/L (20 ng/mL; Figure 10). If not, the vitamin D “tank” may still not be full, and another 8-wk course of therapy usually corrects the vitamin D deficiency (67; Figure 10). One should suspect a fat-malabsorption problem or poor compliance if the 25(OH)D concentration does not increase by > 25% after these treatments. Exposure to sunlight or a tanning bed will correct vitamin D deficiency in patients with severe intestinal fat- malabsorption syndrome (72).

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FIGURE 10. F10MH A: Serum concentrations of 25-hydroxyvitamin D [25(OH)D; ▵] and parathyroid hormone (PTH; •) before and after therapy with 50 000 IU vitamin D2 and calcium supplementation once a week for 8 wk. *P < 0.05. B: Serum concentrations of PTH in patients who had 25(OH)D concentrations between 10 and 25 ng/mL and who were stratified in increments of 5 ng/mL before (•) and after (▵) receiving 50 000 IU vitamin D2 and calcium supplementation for 8 wk. *P < 0.05, **P < 0.01. Reproduced with permission (71). Why should we care about vitamin D deficiency? It is insidious and has both short- and long-term consequences. Infants and young children who are vitamin D deficient may be imprinted for the rest of their lives with increased risks of type 1 diabetes, multiple sclerosis, rheumatoid arthritis, and many common cancers (Figure 8). Adults are at increased risk of common cancers and cardiovascular disease. Recently, it has been reported that young adults with vitamin D deficiency were at greater risk of congestive heart failure than were their vitamin D-sufficient counterparts (73, 74). Therefore, to maximize health and reduce the risk of common diseases, it is reasonable to pay attention to the 25(OH)D concentration. Just as the blood concentration of cholesterol is often measured on an annual basis, so too should the blood concentration of 25(OH)D be measured. Indeed, vigilance in maintaining a healthy 25(OH)D concentration may have more important health ramifications than a simple lowering of a blood cholesterol concentration to prevent coronary artery disease. A minimum concentration of 25(OH)D should be 50 nmol/L, and, for maximum bone health and prevention of many chronic diseases, the 25(OH)D concentration should be 78-100 nmol/L. The simplest way to obtain vitamin D is from moderate exposure to sunlight. I recommend that exposure of hands, face and arms, or arms and legs to sunlight for a period equal to 25% of the time that it would take to cause a light pinkness to the skin (1 minimum erythemal dose) is sufficient not only to satisfy the body’s requirement, but also to make sufficient amounts of vitamin D to store in the body for use on rainy days and during times when sun exposure is inadequate to produce enough vitamin D in the skin. I have provided guidelines for the amount of sun exposure needed by people of all skin types to achieve their vitamin D requirement without significantly increasing the risk of skin damage and skin cancer (9, 39). Increasing the intakes of foods fortified with vitamin D, including milk, orange juice, cereals, and oily fish, is a reasonable approach to satisfying the body’s requirement. Taking > 1 multivitamin is counterproductive, because too much vitamin A would be ingested, and that increases the risk of birth defects and osteoporosis. Alternatively, one multivitamin containing 400 IU vitamin D and a vitamin D supplement containing either 400 or 1000 IU vitamin D is appropriate. Previous SectionNext Section Footnotes 2 Presented at the American Society for Clinical Nutrition 43rd Annual Meeting, April 12, 2003, San Diego. 3 Presentation of the Robert H Herman Memorial Award in Clinical Nutrition supported by Mrs Yaye Herman. 4 Supported by NIH grants M01RR0053 and AR36963. 5 Address reprint requests to MF Holick, Boston University School of Medicine, 715 Albany Street, M-1013, Boston, MA 02118-2394. E-mail: mfholick@bu.edu. Robert H Herman Memorial Award in Clinical Nutrition Lecture, 2003 Received June 23, 2003. Accepted September 12, 2003. Previous Section F11 REFERENCES

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     Serum 25-Hydroxyvitamin D and Risks of Colon and Rectal Cancer in Finnish Men Am J Epidemiol 2011 173: 5 499-508
     Vitamin D and gastrointestinal diseases: inflammatory bowel disease and colorectal cancer Therapeutic Advances in Gastroenterology 2011 4: 1 49-62
     Daily Supplementation with 25 {micro}g Cholecalciferol Does Not Increase Calcium Absorption or Skeletal Retention in Adolescent Girls with Low Serum 25-Hydroxyvitamin D J. Nutr. 2010 140: 12 2139-2144
     Serum Vitamin D and Risk of Bladder Cancer Cancer Res. 2010 70: 22 9218-9223
     Nutritional Metabolic Bone Disease in Juvenile Veiled Chameleons (Chamaeleo calyptratus) and Its Prevention J. Nutr. 2010 140: 11 1923-1931
     Relationship Between Vitamin D Levels and Depressive Symptoms in Older Residents From a National Survey Population Psychosom. Med. 2010 72: 7 608-612
     Update in Pediatrics: Focus on Fat-Soluble Vitamins Nutr Clin Pract 2010 25: 4 340-346
     Circulating 25-Hydroxyvitamin D and Risk of Pancreatic Cancer: Cohort Consortium Vitamin D Pooling Project of Rarer Cancers Am J Epidemiol 2010 172: 1 81-93
     Fortification of orange juice with vitamin D2 or vitamin D3 is as effective as an oral supplement in maintaining vitamin D status in adults Am J Clin Nutr 2010 91: 6 1621-1626
     Colloquium Paper: Human skin pigmentation as an adaptation to UV radiation Proc. Natl. Acad. Sci. USA 2010 107: Supplement_2 8962-8968
     Cholecalciferol Supplementation in Hemodialysis Patients: Effects on Mineral Metabolism, Inflammation, and Cardiac Dimension Parameters CJASN 2010 5: 5 905-911
     Vitamin D Supplement Consumption Is Required to Achieve a Minimal Target 25-Hydroxyvitamin D Concentration of >=75 nmol/L in Older People J. Nutr. 2010 140: 3 551-556
     Vitamin D and the Immune System The Journal of Rheumatology 2010 37: 3 491-495
     A rare haplotype of the vitamin D receptor gene is protective against diabetic nephropathy Nephrol Dial Transplant 2010 25: 2 497-503
     Association of low serum 25-hydroxyvitamin D levels and high arterial blood pressure in the elderly Nephrol Dial Transplant 2010 25: 2 503-509
     Serum Vitamin D and Breast Density in Breast Cancer Survivors Cancer Epidemiol. Biomarkers Prev. 2010 19: 2 412-417
     Urgent action needed to improve vitamin D status among older people in England! Age Ageing 2010 39: 1 62-68
     Vitamin D Needs of Preterm Infants Neoreviews 2009 10: 12 e590-e599
     Predicting ambient ultraviolet from routine meteorological data; its potential use as an instrumental variable for vitamin D status in pregnancy in a longitudinal birth cohort in the UK Int J Epidemiol 2009 38: 6 1681-1688
     Serum 25-Hydroxyvitamin D Levels Among US Children Aged 1 to 11 Years: Do Children Need More Vitamin D? Pediatrics 2009 124: 5 1404-1410
     Effect of Vitamin D Deficiency and Replacement on Endothelial Function in Asymptomatic Subjects J. Clin. Endocrinol. Metab. 2009 94: 10 4023-4030
     Vitamin D: Bone Health and Beyond AMERICAN JOURNAL OF LIFESTYLE MEDICINE 2009 3: 5 386-393
     Heritability and Environmental Factors Affecting Vitamin D Status in Rural Chinese Adolescent Twins J. Clin. Endocrinol. Metab. 2009 94: 9 3273-3281
     The Dependency of Vitamin D Status on Body Mass Index, Gender, Age and Season Anticancer Res 2009 29: 9 3713-3720
     Up-Regulation of Transporters and Enzymes by the Vitamin D Receptor Ligands, 1{alpha},25-Dihydroxyvitamin D3 and Vitamin D Analogs, in the Caco-2 Cell Monolayer J. Pharmacol. Exp. Ther. 2009 330: 2 389-402
     Association between 25-hydroxyvitamin D levels and cognitive performance in middle-aged and older European men J. Neurol. Neurosurg. Psychiatry 2009 80: 7 722-729
     Metabolism of Vitamin D2 to 17,20,24-Trihydroxyvitamin
     Metabolism of Vitamin D2 to 17,20,24-Trihydroxyvitamin D2 by Cytochrome P450scc (CYP11A1) Drug Metab. Dispos. 2009 37: 4 761-767
     Vitamin D supplementation during Antarctic winter Am J Clin Nutr 2009 89: 4 1092-1098
     Vitamin D Deficiency in Older Men J. Clin. Endocrinol. Metab. 2009 94: 4 1214-1222
     Supplements of 20 {micro}g/d Cholecalciferol Optimized Serum 25-Hydroxyvitamin D Concentrations in 80% of Premenopausal Women in Winter J. Nutr. 2009 139: 3 540-546
     25-Hydroxyvitamin D3, arterial calcifications and cardiovascular risk markers in haemodialysis patients Nephrol Dial Transplant 2009 24: 2 611-618
     Association of oral calcitriol with improved survival in non-dialysed and dialysed patients with CKD Nephrol Dial Transplant 2009 24: 2 341-344
     A Comparison of Vitamin D Levels in Nondiabetic and Diabetic Patient Populations J. Am. Podiatr. Med. Assoc. 2009 99: 1 35-41
     Vitamin D Status and Its Relationship to Body Fat, Final Height, and Peak Bone Mass in Young Women J. Clin. Endocrinol. Metab. 2009 94: 1 67-73
     Efficacy of food fortification on serum 25-hydroxyvitamin D concentrations: systematic review Am J Clin Nutr 2008 88: 6 1528-1534
     Vitamin D Supplementation during Lactation to Support Infant and Mother J. Am. Coll. Nutr. 2008 27: 6 690-701
     Prevention of Rickets and Vitamin D Deficiency in Infants, Children, and Adolescents Pediatrics 2008 122: 5 1142-1152
     Vitamin D and Prevention of Colorectal Adenoma: A Meta-analysis Cancer Epidemiol. Biomarkers Prev. 2008 17: 11 2958-2969
     Vitamin D Deficiency in Children and Its Management: Review of Current Knowledge and Recommendations Pediatrics 2008 122: 2 398-417
     Higher Prevalence of Vitamin D Deficiency Is Associated with Immigrant Background among Children and Adolescents in Germany J. Nutr. 2008 138: 8 1482-1490
     Vitamin D insufficiency in a multiethnic cohort of breast cancer survivors Am J Clin Nutr 2008 88: 1 133-139
     Sun safety: what are the health messages? Perspectives in Public Health 2008 128: 4 164-169
     Serum Metabolite Profiles and Target Tissue Gene Expression Define the Effect of Cholecalciferol Intake on Calcium Metabolism in Rats and Mice J. Nutr. 2008 138: 6 1114-1120
     Use (or misuse) of vitamin D treatment in CKD and dialysis patients: A recent meta-analysis on vitamin D compounds in chronic kidney disease [1] and an editorial comment [2] accompanying this meta-analysis have already been published. We believe that these papers deserve some comments in the interest of the NDT readership Nephrol Dial Transplant 2008 23: 6 1786-1789
     From the Cover: Addressing the health benefits and risks, involving vitamin D or skin cancer, of increased sun exposure Proc. Natl. Acad. Sci. USA 2008 105: 2 668-673
     Association between 25-hydroxyvitamin D deficiency and cardiovascular disease in type 2 diabetic patients with mild kidney dysfunction Nephrol Dial Transplant 2008 23: 1 269-274
     A New Paradigm for the Treatment of Secondary Hyperparathyroidism Clin Kidney J 2008 1: suppl_1 i24-i28
     Dose response to vitamin D supplementation among postmenopausal African American women Am J Clin Nutr 2007 86: 6 1657-1662
     Vitamin D Levels in Men in a Single Primary Care Practice Near Boston Am J Mens Health 2007 1: 4 262-268
     Response to Teriparatide in Patients with Baseline 25-Hydroxyvitamin D Insufficiency or Sufficiency J. Clin. Endocrinol. Metab. 2007 92: 12 4630-4636
     Associations of diet, supplement use, and ultraviolet B radiation exposure with vitamin D status in Swedish women during winter Am J Clin Nutr 2007 86: 5 1399-1404
     Prepregnancy Obesity Predicts Poor Vitamin D Status in Mothers and Their Neonates J. Nutr. 2007 137: 11 2437-2442
     The Effects of Vitamin D Deficiency and Insufficiency on the Endocrine and Paracrine Systems Biol Res Nurs 2007 9: 2 117-129
     Mother-child vitamin D deficiency: an international perspective Arch. Dis. Child. 2007 92: 9 737-740
     Vitamin D status and parathyroid hormone in obese children before and after weight loss Eur J Endocrinol 2007 157: 2 225-232
     A Nested Case Control Study of Plasma 25-Hydroxyvitamin D Concentrations and Risk of Colorectal Cancer JNCI J Natl Cancer Inst 2007 99: 14 1120-1129
     Risk factors for low serum 25-hydroxyvitamin D concentrations in otherwise healthy children and adolescents Am J Clin Nutr 2007 86: 1 150-158
     Efficacy of daily and monthly high-dose calciferol in vitamin D-deficient nulliparous and lactating women Am J Clin Nutr 2007 85: 6 1565-1571
     Vitamin D and Its Role in Cancer and Immunity: A Prescription for Sunlight Nutr Clin Pract 2007 22: 3 305-322
     Vitamin D and Rehabilitation: Improving Functional Outcomes Nutr Clin Pract 2007 22: 3 297-304
     Synchronized Seasonal Variations of Mammographic Breast Density and Plasma 25-Hydroxyvitamin D Cancer Epidemiol. Biomarkers Prev. 2007 16: 5 929-933
     Plasma 25-Hydroxyvitamin D and 1,25-Dihydroxyvitamin D and Risk of Incident Ovarian Cancer Cancer Epidemiol. Biomarkers Prev. 2007 16: 4 783-788
     Lactating Women Restricting Milk Are Low on Select Nutrients J. Am. Coll. Nutr. 2007 26: 2 149-155
     Association Between Vitamin D Status and Physical Performance: The InCHIANTI Study J Gerontol A Biol Sci Med Sci 2007 62: 4 440-446
     Maternal intake of vitamin D during pregnancy and risk of recurrent wheeze in children at 3 y of age Am J Clin Nutr 2007 85: 3 788-795
     Sun Exposure and Non-Hodgkin Lymphoma Cancer Epidemiol. Biomarkers Prev. 2007 16: 3 396-400

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  1. Top
  2. Abstract
  3. INTRODUCTION
  4. PHOTOSYNTHESIS OF PREVITAMIN D
  5. FACTORS THAT ALTER PHOTOSYNTHESIS OF PREVITAMIN D3
  6. SOURCES OF VITAMIN D
  7. CAUSES AND CONSEQUENCES OF VITAMIN D DEFICIENCY
  8. NONSKELETAL CONSEQUENCES OF VITAMIN D DEFICIENCY
  9. VITAMIN D METABOLISM AND NONCALCEMIC FUNCTIONS
  10. THE CANCER-VITAMIN D CONNECTION
  11. CONCLUSIONS
  12. Footnotes
  13. REFERENCES

This Article

  1. 1.     Am J Clin Nutr March 2004 vol. 79 no. 3 362-371
  2. Abstract
  3. 2.    » Full Text
  4. 3.    Full Text (PDF)
  5. 4.    A correction has been published

Navigate This Article

  1. Top
  2. Abstract
  3. INTRODUCTION
  4. PHOTOSYNTHESIS OF PREVITAMIN D
  5. FACTORS THAT ALTER PHOTOSYNTHESIS OF PREVITAMIN D3
  6. SOURCES OF VITAMIN D
  7. CAUSES AND CONSEQUENCES OF VITAMIN D DEFICIENCY
  8. NONSKELETAL CONSEQUENCES OF VITAMIN D DEFICIENCY
  9. VITAMIN D METABOLISM AND NONCALCEMIC FUNCTIONS
  10. THE CANCER-VITAMIN D CONNECTION
  11. CONCLUSIONS
  12. Footnotes
  13. REFERENCES

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Dr. Cícero Galli Coimbra explica o Mal de Alzheimer: causas multifatoriais com destaque à depressão e a deficiência do hormonio imunoregulador vitamina D – um distúrbio metabólico.

Vitamina D é um hormônio vital para preservação e recuperação da saúde

http://www.facebook.com/VitaminaD.HormonioVital

CGC2013

Dr. Cícero Galli Coimbra explica o Mal de Alzheimer: causas multifatoriais com destaque à depressão e a deficiência do hormonio imunoregulador vitamina D – um distúrbio metabólico.

Dr. Cícero Galli Coimbra explica Mal de Alzheimer e sua relação com o Hormônio-Vitamina D

http://www.youtube.com/watch?feature=player_detailpage&v=v9fREuMywNo

 155336_345790338850350_1260490623_n

“POR UM NOVO PARADIGMA DE CONDUTA E TRATAMENTO” –  “Estamos vivendo uma defasagem entre o conhecimento científico e a prática médica” – Dr. Cicero Galli Coimbra, medico neurologista, Phd., professor na Universidade Federal de São Paulo, Presidente do Instituto de Investigação e Tratamento de Autoimunidade

 https://objetodignidade.wordpress.com/2012/12/09/por-um-novo-paradigma-de-conduta-e-tratamento-estamos-vivendo-uma-defasagem-entre-o-conhecimento-cientifico-e-a-pratica-medica-dr-cicero-galli-coimbra/ 

POR UM NOVO PARADIGMA DE CONDUTA E TRATAMENTO

Por Dr. Cícero Galli Coimbra
Médico Internista e Neurologista
Professor Associado Livre-Docente da Universidade Federal de São Paulo
Presidente do Instituto de Investigação e Tratamento de Autoimunidade

http://www.institutodeautoimunidade.org.br/novo-paradigma.html

 

Vitamina D é um hormônio vital para preservação e recuperação da saúde

http://www.facebook.com/VitaminaD.HormonioVital

Dr. Cícero Galli Coimbra explica Mal de Alzheimer e sua relação com o Hormônio-Vitamina D

Dr. Cícero Galli Coimbra explica Mal de Alzheimer e sua relação com o Hormônio-Vitamina D

http://www.youtube.com/watch?feature=player_detailpage&v=v9fREuMywNo

__________

Dr. Cícero Galli Coimbra explica o Mal de Alzheimer: causas multifatoriais com destaque à depressão e a deficiência do hormonio imunoregulador vitamina D – um distúrbio metabólico.               

Por Cristiane Rozicki

Hoje, está definitivamente reconhecida na medicina, há material científico para leitura, a importancia da terapia natural com hormonio vital à saúde, a vitamina D, na prevenção e na recuperação de doenças. Inclusive para o Alzheimer, a vitamina D, a hormona que no sangue é o metabólito ativo da vitamina D, o intermediário necessario e fundamental na produçao de novos neuronios, verificada a concentração da “25-hydroxyvitamin D” deficiente é feita a suplementação.

 

A vitamina D é um hormônio mestre que ajuda a regular a pressão arterial, densidade óssea, humor e comportamento, a força muscular, o crescimento do cabelo, função imune e a vida celular. Há receptores de vitamina D em todas as células do corpo humano, inclusive a parte nobre do cérebro, explica Dr. Cícero Galli Coimbra, sobre os neurônios e a capacidade cognitiva.

 

Obtêm-se a vitamina D através da conversão de compostos da pele após a exposição à luz UVB, a partir do sol.  A pessoa adulta jovem pode fazer até 50.000 UI de vitamina D na pele em um dia.  Já na meia e terceira idades, a quantidade da produção na nossa pele diminui muito, mesmo que deixemos a pele sob o sol diariamente. E com a quantidade insignificante que há nos alimentos (óleo de fígado de bacalhau contém 400 UI, e leite fortificado contém apenas 100 UI – apenas o suficiente para evitar o raquitismo), não é possível manter a quantidade normal deste hormônio fundamental à vida e saúde no sangue.

 

“A medida adequada/ideal, no sangue, determinada pela SOCIEDADE INTERNACIONAL DE ENDOCRINOLOGIA, é de 40 nanogramas por mililitro de sangue (40 ng/ml). Esta é a medida para uma pessoa com saude normal” sem doenças,  já explicou Dr. Cícero Galli Coimbra.

 

Pesquisas do Mount Sinai Hospital, do Canadá, indicam que doenças como transtorno bipolar, autismo, mal de Alzheimer e esquizofrenia são mais comuns em pessoas que têm uma quantidade menor da fonte natural de vitamina D no sangue.

Vitamina D é importantíssima para a saude”

Disponível em:

http://biodireitomedicina.wordpress.com/2009/09/22/vitamina-d-e-importantissima-para-a-saude/

Dr. Cícero Galli Coimbra sempre explica sobre o envelhecimento dos neurônios.

Estresse emocional, ansiedade, depressão, doenças cardiovasculares, neurodegenerativas e autoimunes. Prevenção e cura por terapia natural: Importância da Vitamina D

  

Um dos fatores desencadeantes de doenças é o estresse emocional, seja a extrema preocupação sejam excessivos temores, tristeza e depressão, ansiedade e mágoas, ressentimentos guardados.

 

Informações médicas sobre a prevenção e tratamento de doenças neurodegenerativas

 

http://www.youtube.com/watch?feature=player_detailpage&v=yRQkITHjZ5k

  

Os médicos descobriram que as fortes emoções alteram o corpo humano não apenas em seu aspecto funcional, hoje é conhecido que o estresse emocional produz também alterações estruturais. Estas alterações estruturais são verificadas com a perda de neuronios no encéfalo, exatamente, fortes emoções ou as células do cérebro. Estas emoções impedem a neogênese, que é a produção de novos neurônios.

 

Outros dois fatores desencadeantes de doenças que mais matam pessoas no mundo são a dieta inadequada e a deficiencia de vitaminas. Fatos já demonstrados pela ciência medica, no Brasil, desde 2002, têm evidenciado isso.

  

Quem não lembra da noticia: A interrupção da ingestão de carne e administração de B2 recupera o paciente acometido por Parkinson.

Em outubro de 2003 foi pública, no Brasil e no exterior, a informação medica-cientifica do artigo “High doses of riboflavin and the elimination of dietary red meat promote the recovery of some motor functions in Parkinson’s disease patients”, assinado por Cícero Galli Coimbra, professor do Departamento de Neurologia e Neurocirurgia da Universidade Federal de São Paulo, e por Virgínia Junqueira, do Centro de Estudos do Envelhecimento, da mesma universidade. A publicação deste artigo em Revista Medica Internacional foi decisiva para a erradicação do mal de Parkinson por terapia natural.

  

A interrupção da ingestão de carne vermelha e administração de altas doses de vitamina B2 somados ao fim da depressão, recupera portadores da doença de Parkinson. Pacientes conseguiram aumentar de 44% para 71% a reativação de funções motoras.

 

A noticia foi divulgada em vários jornais e revistas desde maio de 2003, com a Comunicação do Jornal da Paulista: Ano 16 – N° 179, Maio de 2003: “Dieta livre de carne e rica em vitamina B2 pode regredir Parkinson”

Disponível em

https://objetodignidade.wordpress.com/2009/08/02/dieta-livre-de-carne-e-rica-em-vitamina-b2-pode-regredir-parkinson/

  

E com a edição de outubro de 2003 no Brazilian Journal of Medical and Biological Research : Braz J Med Biol Res, October 2003, Volume 36(10) 1409-1417, disponivel em: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2003001000019&lng=pt&nrm=iso&tlng=en

  

Já era, nesta época, conhecimento medico de nova terapia para o mal de Alzheimer e prevenção da moléstia. Publicação na Edição brasileira da mais tradicional Revista mundial de divulgação científica SCIENTIFIC AMERICAN BRASIL, Ano 1 – Número 01, 16 de Junho de 2002, Páginas 18 e 19. www.sciam.com. “NOVO MODELO PARA ALZHEIMER. PESQUISA BRASILEIRA PODE ABRIR CAMINHO A TRATAMENTO PREVENTIVO”.

Disponível em

http://www2.uol.com.br/sciam/destq_junho.html

 

“Um modelo experimental do mal de Alzheimer, produzido pelo neurologista brasileiro Cícero Galli Coimbra, da Universidade Federal de São Paulo – Escola Paulista de Medicina, foi destacado como o mais importante estudo apresentado no Sgundo Congresso Internacional sobre Demência Vascular, realizado em Saelzburg, Áustria. Superando outros 82 trabalhos, apresentados por pesquisadores de 41 países, o modelo de Coimbra e colaboradores revoluciona nosso conhecimento acerca de uma das doenças mais preocupantes da atualidade.

 

Descoberto “[…] caminho para a prevenção efetiva do mal, por meio do monitoramento e manutenção dos níveis normais de homocisteína em todas pessoas idosas, a partir de uma certa idade. Pacientes portadores de outras doenças neurológicas, como o mal de Parkinson, igualmente caracterizado pela morte crônica de neurônios associada à elevada concentração de homocisteína no sangue, também podem vir a ser beneficiados por abordagens terapêuticas e preventivas semelhantes”.

  

Deve ser dito, a vitamina D, a hormona que no sangue é o metabólito ativo da vitamina D, a concentração da 25-hydroxyvitamin D, “é o principal determinante do estado de saúde do mundo moderno, hoje vivendo uma pandemia de doenças autoimunitárias, neurodegenerativas e todos os tipos de infecções.” –

 https://objetodignidade.wordpress.com/2012/12/09/por-um-novo-paradigma-de-conduta-e-tratamento-estamos-vivendo-uma-defasagem-entre-o-conhecimento-cientifico-e-a-pratica-medica-dr-cicero-galli-coimbra/

 

Cura e prevenção de doenças neurodegenerativas e autoimunes: Parkinson, Alzheimer, Lupus, Psoríase, Vitiligo, depressão, esclerose múltipla, câncer, artrite-reumatoide, diabetes, doenças cardiovasculares, diabetes, asma, infecções e todos os tipos de doenças. É a deficiencia da vitamina D no organismo que leva a essas doenças. Esta é a realidade do mundo moderno, o atual estilo de vida, a falta de tempo, pouca ou nenhuma exposição da pele ao sol, e a pandemia de doenças crônicas.

Vitamina D – Sem Censura – Dr. Cicero Galli Coimbra e Daniel Cunha – 18.junho.2012

http://www.youtube.com/watch?v=cIwIWim4hNM&feature=plcp

 

Sobre a vitamina D, Dr. Cícero Galli Coimbra explica que “essa substancia é na realidade um hormônio esteroide e que, por infelicidade, entre 1918 e 1922, foi chamada de vitamina D antes que se conhecesse qual era a verdadeira estrutura química dessa substancia. É importante que se saiba que este hormonio é o principal determinante do estado de saúde do mundo moderno, hoje vivendo uma pandemia de doenças autoimunitárias, neurodegenerativas e todos os tipos de infecções.”

 

Vitamina D é importantíssima para a saude”

Disponível em Biodireito Medicina:

http://biodireitomedicina.wordpress.com/2009/09/22/vitamina-d-e-importantissima-para-a-saude/


“Estudos realizados no Brasil e no exterior apontam a importância da substância na prevenção e no tratamento do câncer, diabetes e de doenças neurológicas, cardiovasculares e até degenerativas, como a esclerose múltipla.”

 

“Antigamente indicada para evitar o raquitismo na infância (quem não ouviu falar do famoso óleo de fígado de bacalhau?), a ciência ‘redescobre’ a vitamina D como poderoso preventivo da osteoporose e outras doenças do envelhecimento. “Pesquisas recentes também revelaram a ação positiva da substância nos sistemas nervoso e imununológico”, diz o neurologista Cícero Galli Coimbra, coordenador do Laboratório de Fisiopatologia Clínica e Experimental da Universidade Federal de São Paulo (Unifesp). Coimbra destaca que apenas sobre a esclerose múltipla, por exemplo, existem cerca de 700 artigos médicos internacionais, que atribuem a essa vitamina o papel de estimular as conexões dos neurônios. “Isso sem falar de estudos que mostram também a sua contribuição para a melhoria da qualidade de vida dos portadores de câncer, artrite reumatóide, vitiligo, psoríase, hiper e hipotireoidismo, entre outras patologias”, acrescenta”.

 

É preciso assinalar a fundamental importância da vitamina D. Baixos índices de vitamina D no sangue estão diretamente associados ao estresse emocional ou sofrimento. Em casos de doenças autoimunitárias, tais como a esclerose múltipla, artrite reumatoide, psoriase, hipertireoidismo, hipotireoidismo, lupus, vitiligo, por exemplo, existe deficiência de vitamina D confirmada em exames de sangue. Esta deficiência de vitamina D torna as pessoas mais sucetiveis à depressão e aos estados de sofrimento emocional, que são as condições adequadas à perda de massa neural, o envelhecimento do sistema nervoso. Por outro lado, a solução simples, para estas pessoas, é o consumo de altas doses de vitamina D. A vitamina D é capaz de produzir um estado de bem-estar indescritível. Unida ao estado de tranquilidade e suplementação adequada, a vitamina D permite a obtenção de uma condição de estabilização e recuperação do sistema nervoso. É importante que se saiba, em condições de equilíbrio — vitaminas deficientes complementadas e o aspecto emocional tranquilo –, voltam a nascer células-tronco, e novos neuronios, todos os dias. Dr. Cícero Galli Coimbra, entrevista em 2009, disponível em:

http://www.youtube.com/user/biodireitobioetica#p/u/5/yRQkITHjZ5k

 

 

[1] Dr. Cícero Galli Coimbra
PHD Médico Neurologista e Professor Livre-Docente
Departamento de Neurologia e Neurocirurgia – Universidade Federal de São Paulo – Unifesp/EPM –

 

“Os familiares de pacientes em coma – encarados como “potenciais doadores de órgãos” e submetidos ao teste da apnéia deveriam, em decorrência dos riscos do teste, ser apropriadamente informados, permitindo a realização do teste somente através de consentimento livre e esclarecido. No entanto, tornando-se obrigatória a obtenção de tal consentimento, o documento a ser assinado teria de expor, em linguagem compreensível ao leigo, todos os potenciais riscos, incluindo até mesmo a parada cardíaca irreversível (morte), que se contrapõem à ausência de benefícios ao paciente. Na prática, os familiares sequer ficam sabendo que o paciente em coma já foi submetido por uma ou duas vezes ao teste da apnéia, ao receberem a notícia de que a “morte encefálica” encontra-se declarada. Na realidade, a quase totalidade dos familiares que concordam com a doação de órgãos jamais ouviu falar ou vêm a tomar conhecimento da existência desse teste.”

 

Dr. Cícero Galli Coimbra

Este artigo: “Morte encefálica: implicações éticas e legais do reconhecimento de uma prática oportunista desenvolvida sobre conjecturas cuja validade científica encontra-se invalidada“ foi publicado na Revista DOSSIÊ AJURIS – Revista da Associação dos Juízes do Rio Grande do Sul – apresentado como matéria de capa da edição número 02, de 2007.

Disponível em

http://biodireitomedicina.wordpress.com/2009/03/14/revista-dossie-ajuris-ano-i-no-02-2007-a-morte-encefalica-em-xeque-pags-16-27/

 

Morte encefálica? Anestesia geral para os doadores de órgãos, recomendação da Revista dos Anestesistas

06/03/2013 — Celso Galli Coimbra

http://biodireitomedicina.wordpress.com/2013/03/06/morte-encefalica-anestesia-geral-para-os-doadores-de-orgaos-recomendacao-da-revista-dos-anestesistas/

 

Morte Encefálica: a verdade sobre o teste da apnéia na declaração de morte no Brasil

 

http://www.youtube.com/watch?feature=player_embedded&v=egD3g9K1qY8

Suplementos de vitamina D podem reduzir risco de Alzheimer – 10.000 UI, não menos

04/12/2012 — Celso Galli Coimbra

http://biodireitomedicina.wordpress.com/2012/12/04/suplementos-de-vitamina-d-podem-reduzir-risco-de-alzheimer-10-000-ui-nao-menos/

Alzheimer: Vitamina D diminui riscos das mulheres padecerem da doença

04/12/2012 — Celso Galli Coimbra

http://biodireitomedicina.wordpress.com/2012/12/04/alzheimer-vitamina-d-diminui-riscos-das-mulheres-padecerem-da-doenca/

Vitamina D e Alzheimer – Vitamin D may reduce the risk of dominantly inherited Alzheimer’s disease

26/07/2012 — Celso Galli Coimbra

http://biodireitomedicina.wordpress.com/2012/07/26/vitamina-d-e-alzheimer-vitamin-d-may-reduce-the-risk-of-dominantly-inherited-alzheimers-disease/


Nutrientes contra Parkinson e Alzheimer

17/09/2009 — Celso Galli Coimbra

http://biodireitomedicina.wordpress.com/2009/09/17/nutrientes-contra-parkinson-e-alzheimer/

 

a situação fundamental é a mesma: a existência de um DISTÚRBIO METABÓLICO evidente e corrigível, capaz de explicar os eventos fisiopatológicos conhecidos, e cuja correção pode deter a progressão da doença (interrompendo a continuidade da morte neuronal crônica) e impedir a morte.” [1]

Disponivel em
http://www.unifesp.br/dneuro/nexp/riboflavina/

Dr. Cícero Galli Coimbra
PHD Médico Neurologista e Professor Livre-Docente         

—-

“As doses diárias de 10.000 unidades de colecalciferol devem ser tomadas por todas pessoas. Essa quantidade previne todas as doenças inclusive à autoimunidade. Com 10.000 unidades a pessoa sai da deficiencia de vitamina D. A dose de 1.000 unidades não tira as pessoas da deficiencia de vitamina D.’’ – Dr. Cicero Galli Coimbra, medico neurologista, Phd., professor na Universidade Federal de São Paulo, Presidente do Instituto de Investigação e Tratamento de Autoimunidade

https://objetodignidade.wordpress.com/2013/01/21/as-doses-diarias-de-10-000-unidades-de-colecalciferol-devem-ser-tomadas-por-todas-pessoas-essa-quantidade-previne-todas-as-doencas-inclusive-a-autoimunidade-com-10-000-unidades-a-pessoa-sai/

A prescrição diária de 10.000 UIs de Vitamina D representaria para a indústria farmacêutica uma perda de 40% de uma receita de trilhões de dólares

A prescrição diária de 10.000 UIs de Vitamina D representaria para a indústria farmacêutica uma perda de 40% de uma receita de trilhões de dólares

15/01/2013 — Celso Galli Coimbra

__

Assista

Dr. Cícero Galli Coimbra – Doenças Autoimunes e Vitamina D

Vitamina D – Sem Censura – Dr. Cícero Galli Coimbra e Daniel Cunha

Vitamina D3 – 10.000 UI diárias é vital para à saúde

O Dr. John Cannell acusa pesquisadores da indústria farmacêutica norte-americana de estarem tentando alterar a molécula da vitamina D, para transformá-la em uma substância patenteável, ou seja, em remédio. A influência deles é tamanha, a ponto de se manterem unidos em comitês que “aconselham” o governo dos Estados Unidos a estabelecer a dose recomendável, entre 200 e no máximo 400 unidades por dia, bem aquém do necessário [SER, HOJE, EM DOSE PREVENTIVA 10.000 UI – NÃO MENOS].

“POR UM NOVO PARADIGMA DE CONDUTA E TRATAMENTO” – “Estamos vivendo uma defasagem entre o conhecimento científico e a prática médica” – Dr. Cicero Galli Coimbra, medico neurologista, Phd., professor na Universidade Federal de São Paulo, Presidente do Instituto de Investigação e Tratamento de Autoimunidade

https://objetodignidade.wordpress.com/2012/12/09/por-um-novo-paradigma-de-conduta-e-tratamento-estamos-vivendo-uma-defasagem-entre-o-conhecimento-cientifico-e-a-pratica-medica-dr-cicero-galli-coimbra/

Dr. Cícero Galli Coimbra – Doenças Autoimunes e Vitamina D – “Se a natureza não precisasse de 10.000 unidades todo o dia, não formava uma quantidade tão grande em tão poucos minutos.”

https://objetodignidade.wordpress.com/2012/11/04/dr-cicero-galli-coimbra-doencas-autoimunes-e-vitamina-d-se-a-natureza-nao-precisasse-de-10-000-unidades-todo-o-dia-nao-formava-uma-quantidade-tao-grande-em-tao-poucos-minutos/

Vitamin D status in a sunny country: Where has the sun gone?

https://objetodignidade.wordpress.com/2012/08/13/vitamin-d-status-in-a-sunny-country-where-has-the-sun-gone/

Instituto de Investigação e Tratamento da Autoimunidade

http://www.institutodeautoimunidade.org.br/

Vitamina D pode revolucionar o tratamento da esclerose múltipla*

http://biodireitomedicina.wordpress.com/2010/08/03/vitamina-d-pode-revolucionar-o-tratamento-da-esclerose-multipla/

*Dr. Cícero Galli Coimbra
PHD Médico Neurologista e Professor Livre-Docente

 

 Informações médicas sobre a prevenção e tratamento de doenças neurodegenerativas e autoimunes, como Parkinson, Alzheimer, Lupus, Psoríase, Vitiligo, depressão

Dr. Cícero Galli Coimbra
PHD Médico Neurologista e Professor Livre-Docente         

http://biodireitomedicina.wordpress.com/category/doencas-autoimunes/

 

Sistema nervoso – 06/02/2009. Entrevista com Dr. Cícero Galli Coimbra. Evitar o envelhecimento e a perda de neuronios.

http://www.youtube.com/watch?v=yRQkITHjZ5k&feature=player_embedded# —-

                                        

Disponivel em
http://www.unifesp.br/dneuro/nexp/riboflavina/

———————

“Os familiares de pacientes em coma – encarados como “potenciais doadores de órgãos” e submetidos ao teste da apnéia deveriam, em decorrência dos riscos do teste, ser apropriadamente informados, permitindo a realização do teste somente através de consentimento livre e esclarecido. No entanto, tornando-se obrigatória a obtenção de tal consentimento, o documento a ser assinado teria de expor, em linguagem compreensível ao leigo, todos os potenciais riscos, incluindo até mesmo a parada cardíaca irreversível (morte), que se contrapõem à ausência de benefícios ao paciente. Na prática, os familiares sequer ficam sabendo que o paciente em coma já foi submetido por uma ou duas vezes ao teste da apnéia, ao receberem a notícia de que a “morte encefálica” encontra-se declarada. Na realidade, a quase totalidade dos familiares que concordam com a doação de órgãos jamais ouviu falar ou vêm a tomar conhecimento da existência desse teste.”

 

Dr. Cícero Galli Coimbra

Este artigo: “Morte encefálica: implicações éticas e legais do reconhecimento de uma prática oportunista desenvolvida sobre conjecturas cuja validade científica encontra-se invalidada“ foi publicado na Revista DOSSIÊ AJURIS – Revista da Associação dos Juízes do Rio Grande do Sul – apresentado como matéria de capa da edição número 02, de 2007.

Disponível em

http://biodireitomedicina.wordpress.com/2009/03/14/revista-dossie-ajuris-ano-i-no-02-2007-a-morte-encefalica-em-xeque-pags-16-27/

 

 

Morte encefálica? Anestesia geral para os doadores de órgãos, recomendação da Revista dos Anestesistas

06/03/2013 — Celso Galli Coimbra

http://biodireitomedicina.wordpress.com/2013/03/06/morte-encefalica-anestesia-geral-para-os-doadores-de-orgaos-recomendacao-da-revista-dos-anestesistas/

 

Morte Encefálica: a verdade sobre o teste da apnéia na declaração de morte no Brasil

 

http://www.youtube.com/watch?feature=player_embedded&v=egD3g9K1qY8

 

·       2012/jun – A VITAMINA D, hormonio esteroide – Sol em contato com a pele – Dr. Cicero Galli Coimbra e Daniel Cunha – Sem Censura

·       Doenças autoimunes

·       Dr. Cícero Galli Coimbra – Informações médicas sobre a prevenção e tratamento de doenças neurodegenerativas

·       Dr. Cícero Galli Coimbra – Doenças Autoimunes e Vitamina D

·       Ingestão diária de vitamina D pode evitar doenças graves

·       Instituto de Investigação e Tratamento da Autoimunidade

·       Neurodegeneração, Parkinson, Vitamina D

·       Vitamina D

·       Vitamina D – Por uma outra terapia (Vitamin D – For an alternative therapy) –

·       Vitamina D – Por uma outra terapia (Vitamin D – For an alternative therapy) –

·       Vitamina D é um hormônio vital para preservação e recuperação da saúde

·       Vitamina D diminui o risco de autismo nas crianças – Autism prevalence in the United States with respect to solar UV-B doses: An ecological study

·       Vitamina D3 – 10.000 UI diárias é vital para à saúde por Celso Galli Coimbra

·       Vitamina D3 – 10.000 UI diárias é vital para à saúde por Celso Galli Coimbra

 

————-

Alzheimer: causas multifatoriais com destaque à depressão e a deficiência do hormonio imunoregulador vitamina D – um distúrbio metabólico.

CGC2013

Alzheimer: causas multifatoriais com destaque à depressão e a deficiência do hormonio imunoregulador vitamina D – um distúrbio metabólico.               

 155336_345790338850350_1260490623_n

“POR UM NOVO PARADIGMA DE CONDUTA E TRATAMENTO” –  “Estamos vivendo uma defasagem entre o conhecimento científico e a prática médica” – Dr. Cicero Galli Coimbra, medico neurologista, Phd., professor na Universidade Federal de São Paulo, Presidente do Instituto de Investigação e Tratamento de Autoimunidade

 https://objetodignidade.wordpress.com/2012/12/09/por-um-novo-paradigma-de-conduta-e-tratamento-estamos-vivendo-uma-defasagem-entre-o-conhecimento-cientifico-e-a-pratica-medica-dr-cicero-galli-coimbra/ 

POR UM NOVO PARADIGMA DE CONDUTA E TRATAMENTO

Por Dr. Cícero Galli Coimbra
Médico Internista e Neurologista
Professor Associado Livre-Docente da Universidade Federal de São Paulo
Presidente do Instituto de Investigação e Tratamento de Autoimunidade

http://www.institutodeautoimunidade.org.br/novo-paradigma.html

 

Vitamina D é um hormônio vital para preservação e recuperação da saúde

http://www.facebook.com/VitaminaD.HormonioVital

Dr. Cícero Galli Coimbra explica Mal de Alzheimer e sua relação com o Hormônio-Vitamina D

 

Dr. Cícero Galli Coimbra explica Mal de Alzheimer e sua relação com o Hormônio-Vitamina D

http://www.youtube.com/watch?feature=player_detailpage&v=v9fREuMywNo

Suplementos de vitamina D podem reduzir risco de Alzheimer – 10.000 UI, não menos

04/12/2012 — Celso Galli Coimbra

http://biodireitomedicina.wordpress.com/2012/12/04/suplementos-de-vitamina-d-podem-reduzir-risco-de-alzheimer-10-000-ui-nao-menos/

Alzheimer: Vitamina D diminui riscos das mulheres padecerem da doença

04/12/2012 — Celso Galli Coimbra

http://biodireitomedicina.wordpress.com/2012/12/04/alzheimer-vitamina-d-diminui-riscos-das-mulheres-padecerem-da-doenca/

Vitamina D e Alzheimer – Vitamin D may reduce the risk of dominantly inherited Alzheimer’s disease

26/07/2012 — Celso Galli Coimbra

http://biodireitomedicina.wordpress.com/2012/07/26/vitamina-d-e-alzheimer-vitamin-d-may-reduce-the-risk-of-dominantly-inherited-alzheimers-disease/


Nutrientes contra Parkinson e Alzheimer

17/09/2009 — Celso Galli Coimbra

http://biodireitomedicina.wordpress.com/2009/09/17/nutrientes-contra-parkinson-e-alzheimer/

 

a situação fundamental é a mesma: a existência de um DISTÚRBIO METABÓLICO evidente e corrigível, capaz de explicar os eventos fisiopatológicos conhecidos, e cuja correção pode deter a progressão da doença (interrompendo a continuidade da morte neuronal crônica) e impedir a morte.” [1]

Disponivel em
http://www.unifesp.br/dneuro/nexp/riboflavina/

Dr. Cícero Galli Coimbra
PHD Médico Neurologista e Professor Livre-Docente         

—-

“As doses diárias de 10.000 unidades de colecalciferol devem ser tomadas por todas pessoas. Essa quantidade previne todas as doenças inclusive à autoimunidade. Com 10.000 unidades a pessoa sai da deficiencia de vitamina D. A dose de 1.000 unidades não tira as pessoas da deficiencia de vitamina D.’’ – Dr. Cicero Galli Coimbra, medico neurologista, Phd., professor na Universidade Federal de São Paulo, Presidente do Instituto de Investigação e Tratamento de Autoimunidade

https://objetodignidade.wordpress.com/2013/01/21/as-doses-diarias-de-10-000-unidades-de-colecalciferol-devem-ser-tomadas-por-todas-pessoas-essa-quantidade-previne-todas-as-doencas-inclusive-a-autoimunidade-com-10-000-unidades-a-pessoa-sai/

A prescrição diária de 10.000 UIs de Vitamina D representaria para a indústria farmacêutica uma perda de 40% de uma receita de trilhões de dólares

A prescrição diária de 10.000 UIs de Vitamina D representaria para a indústria farmacêutica uma perda de 40% de uma receita de trilhões de dólares

15/01/2013 — Celso Galli Coimbra

__

Assista

Dr. Cícero Galli Coimbra – Doenças Autoimunes e Vitamina D

Vitamina D – Sem Censura – Dr. Cícero Galli Coimbra e Daniel Cunha

Vitamina D3 – 10.000 UI diárias é vital para à saúde

O Dr. John Cannell acusa pesquisadores da indústria farmacêutica norte-americana de estarem tentando alterar a molécula da vitamina D, para transformá-la em uma substância patenteável, ou seja, em remédio. A influência deles é tamanha, a ponto de se manterem unidos em comitês que “aconselham” o governo dos Estados Unidos a estabelecer a dose recomendável, entre 200 e no máximo 400 unidades por dia, bem aquém do necessário [SER, HOJE, EM DOSE PREVENTIVA 10.000 UI – NÃO MENOS].

“POR UM NOVO PARADIGMA DE CONDUTA E TRATAMENTO” – “Estamos vivendo uma defasagem entre o conhecimento científico e a prática médica” – Dr. Cicero Galli Coimbra, medico neurologista, Phd., professor na Universidade Federal de São Paulo, Presidente do Instituto de Investigação e Tratamento de Autoimunidade

https://objetodignidade.wordpress.com/2012/12/09/por-um-novo-paradigma-de-conduta-e-tratamento-estamos-vivendo-uma-defasagem-entre-o-conhecimento-cientifico-e-a-pratica-medica-dr-cicero-galli-coimbra/

Dr. Cícero Galli Coimbra – Doenças Autoimunes e Vitamina D – “Se a natureza não precisasse de 10.000 unidades todo o dia, não formava uma quantidade tão grande em tão poucos minutos.”

https://objetodignidade.wordpress.com/2012/11/04/dr-cicero-galli-coimbra-doencas-autoimunes-e-vitamina-d-se-a-natureza-nao-precisasse-de-10-000-unidades-todo-o-dia-nao-formava-uma-quantidade-tao-grande-em-tao-poucos-minutos/

Vitamin D status in a sunny country: Where has the sun gone?

https://objetodignidade.wordpress.com/2012/08/13/vitamin-d-status-in-a-sunny-country-where-has-the-sun-gone/

Instituto de Investigação e Tratamento da Autoimunidade

http://www.institutodeautoimunidade.org.br/

Vitamina D pode revolucionar o tratamento da esclerose múltipla*

http://biodireitomedicina.wordpress.com/2010/08/03/vitamina-d-pode-revolucionar-o-tratamento-da-esclerose-multipla/

*Dr. Cícero Galli Coimbra
PHD Médico Neurologista e Professor Livre-Docente

 

 Informações médicas sobre a prevenção e tratamento de doenças neurodegenerativas e autoimunes, como Parkinson, Alzheimer, Lupus, Psoríase, Vitiligo, depressão

Dr. Cícero Galli Coimbra
PHD Médico Neurologista e Professor Livre-Docente         

http://biodireitomedicina.wordpress.com/category/doencas-autoimunes/

 

Sistema nervoso – 06/02/2009. Entrevista com Dr. Cícero Galli Coimbra. Evitar o envelhecimento e a perda de neuronios.

http://www.youtube.com/watch?v=yRQkITHjZ5k&feature=player_embedded# —-

                                        

Disponivel em
http://www.unifesp.br/dneuro/nexp/riboflavina/

—-

 

Hoje, está definitivamente reconhecida na medicina, há material científico para leitura, a importancia da terapia natural com hormonio vital à saúde, a vitamina D, na prevenção e na recuperação de doenças. Inclusive para o Alzheimer, a vitamina D, a hormona que no sangue é o metabólito ativo da vitamina D, o intermediário necessario e fundamental na produçao de novos neuronios, verificada a concentração da “25-hydroxyvitamin D” deficiente é feita a suplementação.

 

A vitamina D é um hormônio mestre que ajuda a regular a pressão arterial, densidade óssea, humor e comportamento, a força muscular, o crescimento do cabelo, função imune e a vida celular. Há receptores de vitamina D em todas as células do corpo humano, inclusive a parte nobre do cérebro, explica Dr. Cícero Galli Coimbra, sobre os neurônios e a capacidade cognitiva.

 

Obtêm-se a vitamina D através da conversão de compostos da pele após a exposição à luz UVB, a partir do sol.  A pessoa adulta jovem pode fazer até 50.000 UI de vitamina D na pele em um dia.  Já na meia e terceira idades, a quantidade da produção na nossa pele diminui muito, mesmo que deixemos a pele sob o sol diariamente. E com a quantidade insignificante que há nos alimentos (óleo de fígado de bacalhau contém 400 UI, e leite fortificado contém apenas 100 UI – apenas o suficiente para evitar o raquitismo), não é possível manter a quantidade normal deste hormônio fundamental à vida e saúde no sangue.

 

“A medida adequada/ideal, no sangue, determinada pela SOCIEDADE INTERNACIONAL DE ENDOCRINOLOGIA, é de 40 nanogramas por mililitro de sangue (40 ng/ml). Esta é a medida para uma pessoa com saude normal” sem doenças,  já explicou Dr. Cícero Galli Coimbra.

 

Pesquisas do Mount Sinai Hospital, do Canadá, indicam que doenças como transtorno bipolar, autismo, mal de Alzheimer e esquizofrenia são mais comuns em pessoas que têm uma quantidade menor da fonte natural de vitamina D no sangue.

Vitamina D é importantíssima para a saude”

Disponível em:

http://biodireitomedicina.wordpress.com/2009/09/22/vitamina-d-e-importantissima-para-a-saude/

Dr. Cícero Galli Coimbra sempre explica sobre o envelhecimento dos neurônios.

Estresse emocional, ansiedade, depressão, doenças cardiovasculares, neurodegenerativas e autoimunes. Prevenção e cura por terapia natural: Importância da Vitamina D

 

 

Um dos fatores desencadeantes de doenças é o estresse emocional, seja a extrema preocupação sejam excessivos temores, tristeza e depressão, ansiedade e mágoas, ressentimentos guardados.

 

Informações médicas sobre a prevenção e tratamento de doenças neurodegenerativas

 

http://www.youtube.com/watch?feature=player_detailpage&v=yRQkITHjZ5k

 

 

Os médicos descobriram que as fortes emoções alteram o corpo humano não apenas em seu aspecto funcional, hoje é conhecido que o estresse emocional produz também alterações estruturais. Estas alterações estruturais são verificadas com a perda de neuronios no encéfalo, exatamente, fortes emoções ou as células do cérebro. Estas emoções impedem a neogênese, que é a produção de novos neurônios.

 

 

Outros dois fatores desencadeantes de doenças que mais matam pessoas no mundo são a dieta inadequada e a deficiencia de vitaminas. Fatos já demonstrados pela ciência medica, no Brasil, desde 2002, têm evidenciado isso.

 

 

Quem não lembra da noticia: A interrupção da ingestão de carne e administração de B2 recupera o paciente acometido por Parkinson.

Em outubro de 2003 foi pública, no Brasil e no exterior, a informação medica-cientifica do artigo “High doses of riboflavin and the elimination of dietary red meat promote the recovery of some motor functions in Parkinson’s disease patients”, assinado por Cícero Galli Coimbra, professor do Departamento de Neurologia e Neurocirurgia da Universidade Federal de São Paulo, e por Virgínia Junqueira, do Centro de Estudos do Envelhecimento, da mesma universidade. A publicação deste artigo em Revista Medica Internacional foi decisiva para a erradicação do mal de Parkinson por terapia natural.

 

 

A interrupção da ingestão de carne vermelha e administração de altas doses de vitamina B2 somados ao fim da depressão, recupera portadores da doença de Parkinson. Pacientes conseguiram aumentar de 44% para 71% a reativação de funções motoras.

 

 

A noticia foi divulgada em vários jornais e revistas desde maio de 2003, com a Comunicação do Jornal da Paulista: Ano 16 – N° 179, Maio de 2003: “Dieta livre de carne e rica em vitamina B2 pode regredir Parkinson”

Disponível em

https://objetodignidade.wordpress.com/2009/08/02/dieta-livre-de-carne-e-rica-em-vitamina-b2-pode-regredir-parkinson/

 

 

E com a edição de outubro de 2003 no Brazilian Journal of Medical and Biological Research : Braz J Med Biol Res, October 2003, Volume 36(10) 1409-1417, disponivel em: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2003001000019&lng=pt&nrm=iso&tlng=en

 

 

 

Já era, nesta época, conhecimento medico de nova terapia para o mal de Alzheimer e prevenção da moléstia. Publicação na Edição brasileira da mais tradicional Revista mundial de divulgação científica SCIENTIFIC AMERICAN BRASIL, Ano 1 – Número 01, 16 de Junho de 2002, Páginas 18 e 19. www.sciam.com. “NOVO MODELO PARA ALZHEIMER. PESQUISA BRASILEIRA PODE ABRIR CAMINHO A TRATAMENTO PREVENTIVO”.

Disponível em

http://www2.uol.com.br/sciam/destq_junho.html

 

 

“Um modelo experimental do mal de Alzheimer, produzido pelo neurologista brasileiro Cícero Galli Coimbra, da Universidade Federal de São Paulo – Escola Paulista de Medicina, foi destacado como o mais importante estudo apresentado no Sgundo Congresso Internacional sobre Demência Vascular, realizado em Saelzburg, Áustria. Superando outros 82 trabalhos, apresentados por pesquisadores de 41 países, o modelo de Coimbra e colaboradores revoluciona nosso conhecimento acerca de uma das doenças mais preocupantes da atualidade.

 

 

Descoberto “[…] caminho para a prevenção efetiva do mal, por meio do monitoramento e manutenção dos níveis normais de homocisteína em todas pessoas idosas, a partir de uma certa idade. Pacientes portadores de outras doenças neurológicas, como o mal de Parkinson, igualmente caracterizado pela morte crônica de neurônios associada à elevada concentração de homocisteína no sangue, também podem vir a ser beneficiados por abordagens terapêuticas e preventivas semelhantes”.

 

 

Deve ser dito, a vitamina D, a hormona que no sangue é o metabólito ativo da vitamina D, a concentração da 25-hydroxyvitamin D, “é o principal determinante do estado de saúde do mundo moderno, hoje vivendo uma pandemia de doenças autoimunitárias, neurodegenerativas e todos os tipos de infecções.” –

 https://objetodignidade.wordpress.com/2012/12/09/por-um-novo-paradigma-de-conduta-e-tratamento-estamos-vivendo-uma-defasagem-entre-o-conhecimento-cientifico-e-a-pratica-medica-dr-cicero-galli-coimbra/

 

 

Cura e prevenção de doenças neurodegenerativas e autoimunes: Parkinson, Alzheimer, Lupus, Psoríase, Vitiligo, depressão, esclerose múltipla, câncer, artrite-reumatoide, diabetes, doenças cardiovasculares, diabetes, asma, infecções e todos os tipos de doenças. É a deficiencia da vitamina D no organismo que leva a essas doenças. Esta é a realidade do mundo moderno, o atual estilo de vida, a falta de tempo, pouca ou nenhuma exposição da pele ao sol, e a pandemia de doenças crônicas.

Vitamina D – Sem Censura – Dr. Cicero Galli Coimbra e Daniel Cunha – 18.junho.2012

http://www.youtube.com/watch?v=cIwIWim4hNM&feature=plcp

 

Sobre a vitamina D, Dr. Cícero Galli Coimbra explica que “essa substancia é na realidade um hormônio esteroide e que, por infelicidade, entre 1918 e 1922, foi chamada de vitamina D antes que se conhecesse qual era a verdadeira estrutura química dessa substancia. É importante que se saiba que este hormonio é o principal determinante do estado de saúde do mundo moderno, hoje vivendo uma pandemia de doenças autoimunitárias, neurodegenerativas e todos os tipos de infecções.”

 

 

 

 

Vitamina D é importantíssima para a saude”

Disponível em Biodireito Medicina:

http://biodireitomedicina.wordpress.com/2009/09/22/vitamina-d-e-importantissima-para-a-saude/


“Estudos realizados no Brasil e no exterior apontam a importância da substância na prevenção e no tratamento do câncer, diabetes e de doenças neurológicas, cardiovasculares e até degenerativas, como a esclerose múltipla.”

 

“Antigamente indicada para evitar o raquitismo na infância (quem não ouviu falar do famoso óleo de fígado de bacalhau?), a ciência ‘redescobre’ a vitamina D como poderoso preventivo da osteoporose e outras doenças do envelhecimento. “Pesquisas recentes também revelaram a ação positiva da substância nos sistemas nervoso e imununológico”, diz o neurologista Cícero Galli Coimbra, coordenador do Laboratório de Fisiopatologia Clínica e Experimental da Universidade Federal de São Paulo (Unifesp). Coimbra destaca que apenas sobre a esclerose múltipla, por exemplo, existem cerca de 700 artigos médicos internacionais, que atribuem a essa vitamina o papel de estimular as conexões dos neurônios. “Isso sem falar de estudos que mostram também a sua contribuição para a melhoria da qualidade de vida dos portadores de câncer, artrite reumatóide, vitiligo, psoríase, hiper e hipotireoidismo, entre outras patologias”, acrescenta”.

 

 

É preciso assinalar a fundamental importância da vitamina D. Baixos índices de vitamina D no sangue estão diretamente associados ao estresse emocional ou sofrimento. Em casos de doenças autoimunitárias, tais como a esclerose múltipla, artrite reumatoide, psoriase, hipertireoidismo, hipotireoidismo, lupus, vitiligo, por exemplo, existe deficiência de vitamina D confirmada em exames de sangue. Esta deficiência de vitamina D torna as pessoas mais sucetiveis à depressão e aos estados de sofrimento emocional, que são as condições adequadas à perda de massa neural, o envelhecimento do sistema nervoso. Por outro lado, a solução simples, para estas pessoas, é o consumo de altas doses de vitamina D. A vitamina D é capaz de produzir um estado de bem-estar indescritível. Unida ao estado de tranquilidade e suplementação adequada, a vitamina D permite a obtenção de uma condição de estabilização e recuperação do sistema nervoso. É importante que se saiba, em condições de equilíbrio — vitaminas deficientes complementadas e o aspecto emocional tranquilo –, voltam a nascer células-tronco, e novos neuronios, todos os dias. Dr. Cícero Galli Coimbra, entrevista em 2009, disponível em:

http://www.youtube.com/user/biodireitobioetica#p/u/5/yRQkITHjZ5k

 

 

[1] Dr. Cícero Galli Coimbra
PHD Médico Neurologista e Professor Livre-Docente
Departamento de Neurologia e Neurocirurgia – Universidade Federal de São Paulo – Unifesp/EPM –

———————

 

 

“Os familiares de pacientes em coma – encarados como “potenciais doadores de órgãos” e submetidos ao teste da apnéia deveriam, em decorrência dos riscos do teste, ser apropriadamente informados, permitindo a realização do teste somente através de consentimento livre e esclarecido. No entanto, tornando-se obrigatória a obtenção de tal consentimento, o documento a ser assinado teria de expor, em linguagem compreensível ao leigo, todos os potenciais riscos, incluindo até mesmo a parada cardíaca irreversível (morte), que se contrapõem à ausência de benefícios ao paciente. Na prática, os familiares sequer ficam sabendo que o paciente em coma já foi submetido por uma ou duas vezes ao teste da apnéia, ao receberem a notícia de que a “morte encefálica” encontra-se declarada. Na realidade, a quase totalidade dos familiares que concordam com a doação de órgãos jamais ouviu falar ou vêm a tomar conhecimento da existência desse teste.”

 

Dr. Cícero Galli Coimbra

Este artigo: “Morte encefálica: implicações éticas e legais do reconhecimento de uma prática oportunista desenvolvida sobre conjecturas cuja validade científica encontra-se invalidada“ foi publicado na Revista DOSSIÊ AJURIS – Revista da Associação dos Juízes do Rio Grande do Sul – apresentado como matéria de capa da edição número 02, de 2007.

Disponível em

http://biodireitomedicina.wordpress.com/2009/03/14/revista-dossie-ajuris-ano-i-no-02-2007-a-morte-encefalica-em-xeque-pags-16-27/

 

 

Morte encefálica? Anestesia geral para os doadores de órgãos, recomendação da Revista dos Anestesistas

06/03/2013 — Celso Galli Coimbra

http://biodireitomedicina.wordpress.com/2013/03/06/morte-encefalica-anestesia-geral-para-os-doadores-de-orgaos-recomendacao-da-revista-dos-anestesistas/

 

Morte Encefálica: a verdade sobre o teste da apnéia na declaração de morte no Brasil

 

http://www.youtube.com/watch?feature=player_embedded&v=egD3g9K1qY8

 

 

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Como a vitamina D trabalha no seu corpo?

 Vitamina do Sol, conhecida como vitamina D,  é UM HORMONIO esteroide produzido pela pele exposta ao UVB que é benefico. Hormonio esteroide, na cura e na medicina preventiva, é FUNDAMENTAL à vida e está presente em todos os seres vivos há mais de 500 milhões de anos.

Como a vitamina D trabalha no seu corpo?

nrc2196-f1

 

Baixos níveis de vitamina D

 As duas formas mais confiáveis ​​para aumentar o seu nível de vitamina D: obter exposição à luz solar mais direta e tomar suplementos de vitamina D3. Também é impossível uma overdose de vitamina D por exposiçao ao sol. A exposição solar oferece benefícios da vitamina D.

 

As pessoas estão envelhecendo muito rápido – então leia. Saiba e entenda o que acontece com as células de seu corpo.

 

” A vitamina D3 é realmente um hormônio, que atua como um hormônio mestre, que regula e orquestra o que o resto de hormônios do corpo estão fazendo.  Além disso, é responsável para a saúde do osso, a saúde cardiovascular, saúde emocional, a força, o crescimento do cabelo, a função imunitária, e duração de vida normal das células.  Pesquisas recentes sobre esta substância revelam o quão poderosa pode ser!” 

“As 10.000 unidades de 25hidroxivitaminaD têm função preventiva, sim. Para as pessoas que não estão doentes, esta abordagem é correta.”

“POR UM NOVO PARADIGMA DE CONDUTA E TRATAMENTO” – “Estamos vivendo uma defasagem entre o conhecimento científico e a prática médica” – Dr. Cicero Galli Coimbra, medico neurologista, Phd., professor na Universidade Federal de São Paulo, Presidente do Instituto de Investigação e Tratamento de Autoimunidade

Publicado em dezembro 9, 2012 por Cristiane Rozicki

https://objetodignidade.wordpress.com/2012/12/09/por-um-novo-paradigma-de-conduta-e-tratamento-estamos-vivendo-uma-defasagem-entre-o-conhecimento-cientifico-e-a-pratica-medica-dr-cicero-galli-coimbra/ ]

Vitamina D Reportagem com Dr Cícero Galli Coimbra e Daniel Cunha

http://www.youtube.com/watch?v=c52mdUEHFaQ

 

Dr. Cícero Coimbra sobre Vitamina D, esclerose múltipla e todas autoimunes 2 de 2 TV Mundi .wmv

Dr. Cícero Galli Coimbra – Esclerose múltipla e o tratamento  com a  vitamina D – 28.01.13 – TV Mundi

 

 

http://www.youtube.com/watch?v=hv6tD3B0Nlo&list=PLeqEGmvbpULNrc8biL5LF9Mp3-WbJT2Ao

 

http://www.youtube.com/watch?list=PLeqEGmvbpULNrc8biL5LF9Mp3-WbJT2Ao&feature=player_detailpage&v=hv6tD3B0Nlo

 

Celso Galli Coimbra·231 vídeos

Publicado em 28/01/2013

Entrevista com Dr. Cícero Galli Coimbra e Marcelo Palma sobre o hormônio-vitamina D e esclerose múltipla no Programa Superação da TV Mundi com a apresentação de Luise Wischermann.

 

Cristiane Rozicki

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Como a vitamina D trabalha no seu corpo?

 Um hormônio fantástico está trabalhando em seu corpo agora.  Tem sido chamado de um hormônio mestre, e que ajuda a regular a pressão arterial, densidade óssea, humor e comportamento, a força muscular, o crescimento do cabelo, função imune e morte celular programada.  Este processo de morte celular programada é chamado apoptose, e a vitamina D é importante para impedir a reprodução das células danificadas ou cancerosas.

 O que poderia ser a vitamina D?  O hormônio do crescimento?  Testosterona?  Insulina?

 Nenhuma das alternativas acima!  Na verdade, a medicina era ignorante de suas múltiplas funções, por tanto tempo, que foi nomeada uma vitamina, porque ao prevenir o raquitismo. Hoje se sabe das centenas de funções deste hormônio, a vitamina D!

 Considerando que até poucos anos atrás, os cientistas acreditavam que esta vitamina incrível controlava apenas a saúde dos ossos, e sabemos agora que há receptores de vitamina D em todas as células do corpo humano.

 Obtêm-se a vitamina D através da conversão de compostos da pele após a exposição à luz UVB, a partir do sol.  Nós podemos fazer até 50.000 UI de vitamina D na pele em um dia, apesar de 20.000 UI ser muito mais comum.  Como a quantidade da produção na nossa pele diminui, mantem-se o suprimento constante, desde que deixemos a pele sob o sol diariamente.

 Em comparação com a quantidade insignificante que há nos alimentos (óleo de fígado de bacalhau contém 400 UI, e leite fortificado contém apenas 100 UI-apenas o suficiente para evitar o raquitismo), a nossa pele foi claramente destinada a ser a nossa principal fonte de vitamina D. Mas existem vários problemas com obtenção de sua vitamina D apenas a partir do sol, especialmente no mundo moderno.

 O mais ao norte que se vai, menos vitamina D podemos fazer com nossa pele.  Os peritos dizem-nos que, no inverno, é impossível para aqueles que vivem acima do paralelo 37 obter quantidade suficiente de vitamina D da luz solar.  Isso representa uma linha de partida: em Santa Cruz, ao sul de San Francisco, Califórnia, continuando para o leste, na fronteira norte do Arizona, Novo México, Oklahoma, Arkansas, Tennessee e Carolina do Norte, e termina na costa.  A maioria dos americanos têm deficiência de vitamina D no inverno, mesmo que não use roupas e fique sob o sol o dia todo!

 Mesmo no verão, há muitos fatores que lutam contra nossa produção de vitamina D.  Dadas as preocupações sobre o câncer de pele e envelhecimento, muitas pessoas usam protetor solar diariamente.  Protetor solar aparece mesmo na maquiagem e loções.  Passamos a maior parte de nosso tempo dentro de 4 paredes e automóveis onde os blocos de vidro de janelas têm filtro, e nossa pele perde a luz UVB necessária para a produção da vitamina D.  Funções da pele mais pigmentada – vale como bloqueador solar natural -, de modo que se estima que a pele escura requer 5 a 6 vezes mais tempo para fazer a mesma quantidade de vitamina D que uma pele clara produz sob a luz solar.  A pele do idoso é menos eficiente na conversão, e as pessoas obesas também estão em alto risco de deficiência de vitamina D.

 Assim, vivendo no Sul, no verão, todos nós devemos ter a abundância de vitamina D, certo?  Errado de novo.  Os profissionais de saúde no sul ensolarado foram verificar os níveis de vitamina D nas pessoas, e, apesar da pele bem bronzeada, níveis normais de vitamina D são raros, mesmo no final do verão, quando os níveis deveriam ser mais altos.

 Então, como devemos buscar a nossa vitamina D?  E que tipo é melhor?  Completando a vitamina D, especificamente a D3, é necessário para a maioria das pessoas nos países industrializados.  A vitamina D3 é também chamada colecalciferol, e enquanto a dose diária recomendada de até 600 UI é apenas o suficiente para evitar o raquitismo, os especialistas estão chamando agora para valores muito mais elevados (até 10.000 UI) para colher todos os benefícios deste hormônio notável.

A vitamina D3 pode ser extraída a partir de lã de animais de uma forma amiga, assim como as ovelhas são tosquiadas, sem danos, de modo que a lã pode ser usada para vestuário. Aquisição de vitamina D a partir de lã realmente imita o que os animais fazem quando lambem sua pele para obter vitamina D.

 A vitamina D2, também chamada ergocalciferol, é feita a partir de cogumelos irradiados.  Esta substância tem um efeito muito fraco e um perfil muito elevado de efeitos colaterais.  Embora seja provavelmente este o tipo de vitamina D que o seu médico iria prescrever, saiba que a decisão dele é baseada em marketing da indústria farmacêutica e não preocupação com o que é mais saudável ou mais natural.  Eu nunca recomendaria a vitamina D2.

 Vitamina D3 ajuda a promover a saúde dos ossos, a saúde cardiovascular, saúde emocional, a força, o crescimento do cabelo, função imunológica, e vida normal das células.  Então, tome pelo menos 10.000 UI de colecalciferol, a vitamina D3, por dia para garantir a melhor saúde que você pode ter! 

 A vitamina D3, o hormônio

 A vitamina D3 é realmente um hormônio, que atua como um hormônio mestre, que regula e orquestra o que o resto de hormônios do corpo estão fazendo.  Além disso, é responsável para a saúde do osso, a saúde cardiovascular, saúde emocional, a força, o crescimento do cabelo, a função imunitária, e duração de vida normal das células.  Pesquisas recentes sobre esta substância revelam o quão poderosa pode ser! 

 Baixos níveis de vitamina D estão associados com a pressão arterial elevada, e uma série de estudos sugere melhora com a suplementação da vitamina D3.  Modelos animais sugerem que a associação de baixa vitamina D com a pressão arterial elevada é devido à sobre-activação do sistema renina-angiotensina, devido à deficiência de vitamina D3.  As pessoas com maiores níveis de vitamina D têm um risco diminuído de ataque cardíaco.

 Duplo papel no sistema imunológico: A DEFICIENCIENCIA da vitamina D3 tanto pode fazer doenças autoimunes, como artrite reumatóide, lúpus, ou diabetes, menos provável ou menos grave, e também significa maior capacidade de evitar infecções quando a pessoa não tem deficiência de vitamina D3 (“A medida adequada/ideal, no sangue, determinada pela SOCIEDADE INTERNACIONAL DE ENDOCRINOLOGIA, é de 40 nanogramas por mililitro de sangue. Esta é a medida para uma pessoa com saúde normal.”).  

Por exemplo, a vitamina D diz às células brancas do sangue para produzir o seu próprio antibiótico, chamado calthelicidin.  Antes, tínhamos os antibióticos, os médicos usaram vitamina D para o tratamento da tuberculose.  Pesquisadores modernos descobriram que uma dose única de vitamina D faz as pessoas que foram expostas à tuberculose menos suscetíveis do que aqueles que não receberam vitamina D.

 Um estudo realizado na Finlândia surpreendente mostrou que dando aos bebês 2.000 UI de vitamina D por dia durante um ano reduz o risco de diabetes tipo 1 em quase 80%!  O mais interessante, o efeito durou por 30 anos.  Embora a vitamina D3 não seja uma vacina, estes resultados comprovam a ter um histórico melhor do que qualquer vacina que já tivemos.

 Baixos níveis de vitamina D têm sido associados com 18 tipos diferentes de cancro, incluindo da mama, rectal, do cólon, da próstata, do pulmão, da boca, do estômago, do esófago, bexiga, ovário, renais, uterino, cervical, vesícula biliar, pâncreas, laringe, linfoma não-Hodgkin e linfoma de Hodgkin. 

 Os pesquisadores estavam interessados ​​em melhorar a saúde óssea em mulheres na menopausa norte do ‘sol’ (onde a exposição ao sol era inadequada para manter saudáveis ​​os níveis de vitamina D).  Deram um grupo um placebo, um outro grupo de 1000 mg de cálcio por dia, e o terceiro grupo de 1.000 mg de cálcio PLUS 1000 UI de vitamina D por dia.  A notícia flash foi a diminuição da incidência de câncer no grupo de vitamina D, o risco foi reduzido em 60% para todos os tipos de câncer.  Quando excluídos os casos de câncer diagnosticados no primeiro ano, que eram mais prováveis já estarem presentes quando a suplementação começou, o risco foi reduzido em 75%.

 A associação da suplementação com vitamina D e risco de fratura foi reduzida nos idosos e pode estar associado com os ossos mais fortes e os músculos mais fortes.  Mesmo pacientes cuja densidade mineral óssea não mudou foram menos propensos a experimentar ossos quebrados.  Isto pode ser devido a que os músculos mais fortes e quedas foram menos prováveis.

 Baixos níveis de vitamina D estão associados com a depressão e transtorno afetivo sazonal.  No entanto, mesmo as pessoas sem um transtorno de humor relataram melhora do humor em estudos controlados com placebo.  A vitamina D3 é necessária para o cérebro para fazer norepinefrina e epinefrina, e sem a presença destas substâncias, é difícil para o cérebro se sentir “feliz”.

 Vitamina D ajuda a promover a saúde dos ossos, a saúde cardiovascular, saúde emocional, a força, o crescimento do cabelo, função imunológica, e vida normal das células.  Então, tome pelo menos 10.000 UI por dia para obter a melhor saúde que você puder!

 Para saber mais sobre a vitamina D, confira

Sobre Vitamina D, assista ao vídeo do Programa Sem Censura:

Vitamina D – Sem Censura – Dr. Cicero Galli Coimbra e Daniel Cunha

__

http://www.scirus.com/srsapp/search?q=%22multiple+sclerosis%22+%28%22vitamin+D%22%29&t=all&sort=0&g=s

A entrevista de Dr. Cícero Galli Coimbra e Daniel Cunha – Vitamina D – Programa Sem Censura 06.2012

1. Entrevista no Programa Sem Censura – Vitamina D – Dr. Cícero Galli Coimbra e Daniel Cunha

2. Lista de médicos que proporcionam terapia com Vitamina D

3. Vitamin D – For an alternative therapy

4. Vitamina D – Por uma outra terapia

Informações Por Celso Galli Coimbra, disponível em:

29/junho/2012

“Dia 18 de junho, o Programa Sem Censura recebeu o jornalista Daniel Cunha e o neurologista Cícero Galli Coimbra para uma conversa sobre a nova terapia para tratamento de esclerose múltipla com vitamina D.”

http://www.youtube.com/watch?feature=player_embedded&v=cIwIWim4hNM

Veja links sobre o mesmo assunto:

1. http://biodireitomedicina.wordpress.com/2010/08/03/vitamina-d-pode-revolucionar-o-tratamento-da-esclerose-multipla/

2. http://biodireitomedicina.wordpress.com/2012/04/12/vitamina-d-por-uma-outra-terapia/

3. http://biodireitomedicina.wordpress.com/2011/03/23/informacoes-medicas-sobre-a-prevencao-e-tratamento-de-doencas-neurodegenerativas-e-auto-imunes-como-parkinson-alzheimer-lupus-psoriase-vitiligo-depressao/

4. http://biodireitomedicina.wordpress.com/2010/03/20/vitamina-d-pode-combater-males-que-mais-matam-pessoas-no-mundo/

5. http://biodireitomedicina.wordpress.com/2012/05/28/folha-de-sao-paulo-terapia-polemica-usa-vitamina-d-em-doses-altas-contra-esclerose-multipla/

6. http://biodireitomedicina.wordpress.com/2012/06/18/taxas-baixas-de-vitamina-d-na-maioria-da-populacao-preocupam-especialistas/

“(…) cerca de 70% da população mundial apresenta taxas inadequadas de vitamina D, substância que, dentro do corpo, trabalha como um hormônio. O fenômeno da insuficiência não poupa nem países tropicais, como o Brasil, e a defasagem tende a ser maior nas grandes cidades, já que, dentro de casa, no carro ou no escritório, as pessoas acabam fugindo do sol. De acordo com o endocrinologista Geraldo Santana, do Instituto Mineiro de Endocrinologia, “a deficiência de vitamina D é um achado frequente e também preocupante devido à importante ação da substância no organismo.”

http://biodireitomedicina.wordpress.com/2012/06/29/vitamina-d-sem-censura-dr-cicero-galli-coimbra-e-daniel-cunha/

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VitaminDCouncil

Vitamin D and Risk of Ischemic Heart Disease

http://www.youtube.com/watch?feature=player_detailpage&v=jTLwD7hpjCs

Apelo do Dr. Rath às pessoas da Alemanha, da Europa e de todo mundo, Berlim 13.03.2012

https://www.youtube.com/watch?feature=player_detailpage&list=HL1352566764&v=VFJsicKGho0

Vitamina D

visualizar lista de reprodução completa ( 5 vídeos)

http://www.youtube.com/watch?v=erAgu1XcY-U&list=PL301EAE2D5602A758&feature=g-all-a

Vitamina D – Por uma outra terapia (Vitamin D – For an alternative therapy)

http://www.youtube.com/watch?feature=player_detailpage&v=erAgu1XcY-U

◊ Dr. Cícero Galli Coimbra é médico graduado pela Universidade Federal do Rio Grande do Sul (1979), possui título de especialista em medicina interna (1981) e neurologia (1983) pela mesma instituição, e em neurologia pediátrica (1985) pelo Jackson Memorial Hospital da Universidade de Miami, EUA. Obteve o título de mestre (1988) e doutor (1991) em Neurologia pela Universidade Federal de São Paulo e pós-doutorado (1993) pela Universidade de Lund, Suécia. Atualmente é Professor Livre Docente do Departamento de Neurologia e Neurocirurgia da Universidade Federal de São Paulo, onde dirige o Laboratório de Fisiopatologia Clínica e Experimental. Atua na área de Medicina (Neurologia e Clínica Médica), com ênfase em doenças neurodegenerativas e autoimunitárias.

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 adaptado de

http://www.ehealthdiscoveries.com/vitamind.html

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A Vitamina D Tem Sido Utilizada Para Bloquear O Crescimento Do Cancro Da Mama.- Vitamin D has been shown to block breast cancer growth.

Baixos níveis de vitamina D

As duas formas mais confiáveis ​​para aumentar o seu nível de vitamina D: obter exposição à luz solar mais direta e tomar suplementos de vitamina D3. Também é impossível uma overdose de vitamina D por exposiçao ao sol. A exposição solar oferece benefícios da vitamina D.

 Cristiane Rozicki

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http://www.breastcancer.org/risk/factors/low_vit_d

PACIENTE COM CÂNCER MAMA

A VITAMINA D TEM SIDO UTILIZADA PARA BLOQUEAR O CRESCIMENTO DO CANCRO DA MAMA.

O câncer de mama é comum entre as mulheres. Nos Estados Unidos, a doença afeta cerca de 230 mil mulheres por ano em comparação com 2000 homens. Aproximadamente 20% das pessoas diagnosticadas com câncer de mama morrem da doença. As taxas de câncer de mama são muito maiores em países ocidentais do que nos países em desenvolvimento.

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OS FATORES DE RISCO

Dos fatores de risco associados com muitos câncer de mama, o mais importantes são:

• exposição estrogénio Lifetime – Isto inclui estrogénio produzido no corpo e tomado oralmente.

• A alta ingestão de carne e laticínios – Comer uma dieta rica em produtos de origem animal no início da vida faz com que o organismo a produzir mais estrogênio durante o curso de uma vida.

• O consumo de álcool – Estudos têm mostrado uma ligação entre álcool e câncer de mama.

• fatores reprodutivos – Geralmente, as mulheres que têm menos filhos ou não tem filhos, têm um maior risco de tumor.

• trabalho noturno – a exposição à luz elétrica Mais à noite reduz a produção de melatonina. Este hormônio pode diminuir o risco de câncer de mama.

Exposição à luz solar e risco de câncer de mama

O câncer de mama é diagnosticado com menos frequência no verão, quando há mais luz solar. Também é diagnosticado com menos frequência durante o Inverno, quando há menos luz solar, mas o corpo produz mais melatonina.

A luz do sol parece ter efeitos diretos e indiretos sobre o câncer de mama. A parte ultravioleta da luz solar estimula o organismo a produzir a vitamina D, que protege contra o câncer de mama. Mulheres que gastam uma quantidade moderada de tempo ao sol, especialmente durante o meio-dia, pode se beneficiar.

A melatonina tem sido encontrado para ser associado com um risco reduzido de cancro da mama. A melatonina é produzida pela glândula pineal, o qual está ligado aos olhos e é sensível à luz azul brilhante. À noite, quando não há luz azul brilhante, a melatonina é produzida. A melatonina é uma hormona que induz o sono e pode também reduzir o risco de cancro da mama. No entanto, durante os dias mais longos do verão, o corpo produz menos melatonina. Deste modo, a melatonina parece ajudar a reduzir o risco de cancro da mama no inverno.

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O número de casos de cancro da mama e da taxa de diagnósticos variam com a quantidade de luz solar e as estações do ano. De acordo com os estudos do cancro da mama e outros, são:

• Menores taxas no ensolarado sudoeste dos Estados Unidos e as taxas mais elevadas no Nordeste mais escura

• As taxas mais elevadas em países que estão mais afastados do equador e recebem menos luz solar

Para câncer de mama, estão:

• diagnósticos a menos no verão e no inverno

• diagnósticos mais na primavera e no outono

A VITAMINA D E CÂNCER DE MAMA

m3e

CÂNCER DE MAMA FOI UM DOS PRIMEIRO CÂNCERES IDENTIFICADAS COMO DE PROTECÇÃO DA VITAMINA D. AGORA HÁ AMPLA EVIDÊNCIA DE QUE A VITAMINA D REDUZ O RISCO DE CÂNCER DE MAMA.

OS NÍVEIS DE VITAMINA D

OS NÍVEIS SANGUÍNEOS DE VITAMINA D SUPERIOR A 40 NG / ML (100 NMOL / L) REDUZ O RISCO DE CANCRO DA MAMA

Com base em estudos de observação de níveis de vitamina D no momento do diagnóstico do cancro da mama ou de um a três anos mais tarde, o risco de cancro da mama diminui rapidamente à medida que os níveis de vitamina D aumentam a partir de níveis muito baixos [menos de 10 ng / ml  até níveis de cerca de 50 ng / ml (150 nmol / l).

A taxa de cancro da mama parece diminuir em cerca de 30%, quando os níveis de vitamina D no sangue são superiores a 40 ng / mL (100 nmol / L) em comparação com os níveis mais baixos de 20 ng / mL (50 nmol / L).

COMO A VITAMINA D FUNCIONA

A vitamina D tem sido mostrado para bloquear o crescimento de tumores de cancro da mama. Forma ativa da vitamina D, calcitriol, proporciona inúmeros benefícios contra o câncer. Esta forma de vitamina D estimula as células a adapta ao seu órgão ou cometer apoptose. Calcitriol também limita fornecimento de sangue para o tumor e reduz a propagação do cancro.

PREVENÇÃO

A MAIORIA, MAS NÃO TODOS, OS ESTUDOS INDICAM NÍVEIS ELEVADOS DE VITAMINA D ESTÃO ASSOCIADOS COM UM MENOR RISCO DE CANCRO DA MAMA.

OS ESTUDOS QUE AS TAXAS DE INCIDÊNCIA DE CÂNCER DE MAMA EM COMPARAÇÃO COM OS NÍVEIS DE VITAMINA D NO SANGUE OU INGESTÃO ORAL DE VITAMINA D DETERMINADOS DENTRO DE TRÊS ANOS APÓS O DIAGNÓSTICO QUASE SEMPRE ENCONTRARAM MENOR RISCO

Tratamento

Um estudo realizado em Toronto descobriram que as mulheres com mais de 30 ng / ml (75 nmol / l) no momento do diagnóstico do cancro da mama tinham metade da taxa de mortalidade por todas as causas das pessoas com menos de 10 ng / ml (25 nmol / l). Desde que a vitamina D protege contra diversos tipos de doença, este achado provavelmente se relaciona com as mortes por câncer de mama e outras causas.

Um estudo realizado na Noruega descobriu que mulheres diagnosticadas no verão tinha uma melhor taxa de sobrevivência de dois anos do que aqueles diagnosticados no inverno. Os níveis de vitamina D são maiores no verão do que no inverno, o que pode explicar os resultados.

Página Última edição: 17 jul 2012

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Breast cancer Patient friendly summary

Vitamin D has been shown to block breast cancer growth.

Breast cancer is common among women. In the United States, the disease affects about 230,000 females each year compared to 2,000 men. Approximately 20% of those diagnosed with breast cancer die from the disease. Breast cancer rates are much higher in Western countries than in developing countries.

Risk factors

Of the many risk factors associated with breast cancer, the most important include:

  • Lifetime estrogen exposure — This includes estrogen produced in the body and taken orally.

  • High intake of meat and dairy — Eating a diet high in animal products early in life causes the body to produce more estrogen during the course of a lifetime.

  • Alcohol consumption — Studies have shown a link between alcohol and breast cancer.

  • Reproductive factors — Generally, women who have fewer or no children have a higher tumor risk.

  • Night shift work — More electrical light exposure at night reduces melatonin production. This hormone may lower the risk of breast cancer.

Sunlight exposure and breast cancer risk

Breast cancer is diagnosed less often in summer, when there is more sunlight. It is also diagnosed less often in winter, when there is less sunlight, but the body produces more melatonin.

Sunlight appears to have both direct and indirect effects on breast cancer. The ultraviolet portion of sunlight stimulates the body to produce vitamin D, which protects against breast cancer. Women who spend a moderate amount of time in the sun, especially during midday, may benefit.

Melatonin has been found to be associated with reduced risk of breast cancer. Melatonin is made by the pineal gland, which is connected to the eyes and is sensitive to bright blue light. At night, when there is no bright blue light, melatonin is produced. Melatonin is a hormone that induces sleep and may also reduce the risk of breast cancer. However, during the longer days of summer, the body produces less melatonin. Thus, melatonin seems to help reduce the risk of breast cancer in winter.

The number of breast cancer cases and rate of diagnoses vary with the amount of sunlight and the seasons. According to breast and other cancer studies, there are:

  • Lower rates in the sunny Southwest United States and higher rates in the darker Northeast

  • Higher rates in countries that are further from the equator and receive less sunlight

For breast cancer, there are:

  • Fewer diagnoses in the summer and winter

  • More diagnoses in the spring and fall

Vitamin D and breast cancer

Breast cancer was one of the first cancers identified as having protection from vitamin D. Now there is ample evidence that vitamin D lowers breast cancer risk.

Vitamin D levels

Vitamin D blood levels greater than 40 ng/mL (100 nmol/L) reduce the risk of breast cancer by approximately 30%.

Based on observational studies of vitamin D levels at the time of breast cancer diagnosis or up to three years later, risk of breast cancer decreases rapidly as vitamin D levels increase from very low levels [less than 10 ng/ml (25 nmol/] out to 20-30 ng/ml, then decreases at a slower rate until levels about 50 ng/ml (150 nmol/l).

The rate of breast cancer appears to decrease by approximately 30% when vitamin D levels in the blood are greater than 40 ng/mL (100 nmol/L) compared to lower levels of 20 ng/mL (50 nmol/L).

How vitamin D works

Vitamin D has been shown to block the growth of breast cancer tumors. Vitamin D’s active form, calcitriol, provides numerous benefits against cancer. This form of vitamin D encourages cells to either adapt to their organ or commit apoptosis. Calcitriol also limits blood supply to the tumor and reduces the spread of cancer.

Prevention

Most, but not all, studies indicate high levels of vitamin D are associated with a lower risk of breast cancer. The studies that compared incidence rates of breast cancer with vitamin D blood levels or oral intake of vitamin D determined within three years of diagnosis nearly always found lower risk with higher level or intake. Those with longer times between measurement and diagnosis did not. The reason they did not is probably that since breast cancer can grow rapidly, even a drop of vitamin D for a short period can permit breast cancer to grow to where it can be detected.

Vitamin D and calcium

Studies have shown that the combination of vitamin D and calcium provides moderate breast cancer protection for premenopausal women. Calcium intake from diet or supplements of more than 1000 mg/day might be helpful.

Treatment

A study in Toronto found that women with more than 30 ng/ml (75 nmol/l) at time of breast cancer diagnosis had half the 12-year all-cause mortality rate of those with less than 10 ng/ml (25 nmol/l). Since vitamin D protects against many types of disease, this finding likely relates to deaths from breast cancer and other causes.

A study in Norway found that women diagnosed in summer had a better two-year survival rate than those diagnosed in winter. Vitamin D levels are higher in summer than winter, which may explain the findings.

There have not been any reported studies of treating women with breast cancer with vitamin D. However, some cancer treatment centers are now giving at least 5000 IU (125 mcg)/day vitamin D to patients with many types of cancer.

Need to know more? Read on with our detailed evidence summary for Breast Cancer.

Page last edited: 17 July 2012

*These statements have not been evaluated by the Food and Drug Administration

O papel da vitamina D na prevenção do cancer – The Role of Vitamin D in Cancer Prevention

O papel da vitamina D na prevenção do cancer – The Role of Vitamin D in Cancer Prevention

 vitamin

Vários tipos de cancer têm prevenção com a suplementação de colecalciferol, a Vitamina D3.

Por que, no Brasil, o governo não suplementa ao povo com este hormonio fundamental á saúde – natural e barato.

Cristiane Rozicki

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Am J Public Health. 2006 February; 96(2): 252–261. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1470481/

doi:  10.2105/AJPH.2004.045260

PMCID: PMC1470481

The Role of Vitamin D in Cancer Prevention

Cedric F. Garland, DrPH, Frank C. Garland, PhD, Edward D. Gorham, PhD, MPH, Martin Lipkin, MD, Harold Newmark, ScD, Sharif B. Mohr, MPH, and Michael F. Holick, MD, PhD

Author information ► Article notes ► Copyright and License information ►

This article has been cited by other articles in PMC.

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Abstract

Vitamin D status differs by latitude and race, with residents of the northeastern United States and individuals with more skin pigmentation being at increased risk of deficiency. A PubMed database search yielded 63 observational studies of vitamin D status in relation to cancer risk, including 30 of colon, 13 of breast, 26 of prostate, and 7 of ovarian cancer, and several that assessed the association of vitamin D receptor genotype with cancer risk.

The majority of studies found a protective relationship between sufficient vitamin D status and lower risk of cancer. The evidence suggests that efforts to improve vitamin D status, for example by vitamin D supplementation, could reduce cancer incidence and mortality at low cost, with few or no adverse effects.

ALTHOUGH VITAMIN D deficiency is known mainly for its association with fractures and bone disease,17 its newly recognized association with risk of several types of cancer is receiving considerable attention.811 The high prevalence of vitamin D deficiency, combined with the discovery of increased risks of certain types of cancer in those who are deficient, suggest that vitamin D deficiency may account for several thousand premature deaths from colon,12breast,13,14 ovarian,15 and prostate16 cancer annually.17 This discovery creates a new impetus for ensuring adequate vitamin D intake in order to reduce the risk of cancer.

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PREVALENCE OF VITAMIN D DEFICIENCY

A low serum level of 25(OH)D, the principal form of circulating vitamin D, is the main marker of vitamin D deficiency.1820 High prevalence of vitamin D deficiency is present in all races, even in temperate areas,1936 and is particularly high among Black Americans.19,2124 A recent survey found, for example, that 42% of Black women had seriously deficient 25(OH)D levels (< 15 ng/mL).19

Residents of the northern tier of the United States receive considerably less solar ultraviolet B (UVB) radiation than those in the South, owing to the longer length and severity of northern winters.3739 UVB is needed to make vitamin D, which cannot be photosynthesized by the skin in the Northeast from November through March.40 Although some sunscreens, such as zinc or titanium oxides, may reduce risk of some skin cancers,4143 everyday use of sunscreens that offer a high level of protection against the sun, which currently are used periodically by about half the US population,44 completely blocks photosynthesis of vitamin D45,46 and reduces circulating vitamin D metabolites.46 This results in 25(OH)D deficiency unless there is adequate oral intake.47

A clinical laboratory test is available to identify 25(OH)D deficiency; it is most useful during the fall and winter, when deficiency is prevalent29,30 owing to the 3-week half-life of 25(OH)D.18,48 With respect to osteoporosis, the range of 25(OH)D considered deficient is less than 15 to 20 ng/mL,49 whereas serum levels below 30 ng/mL are associated with increased risk of colon cancer.5052Levels above 150 ng/mL suggest potential toxicity.5355

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EPIDEMIOLOGICAL EVIDENCE

Most observational studies have reported that vitamin D has a beneficial effect on risk of colon, breast, prostate, and ovarian cancer. A PubMed search (in December 2004) for epidemiological studies of vitamin D, sunlight, ultraviolet radiation, and latitude in association with these cancers yielded 63 studies, including 30 of colon cancer, 13 of breast cancer, 26 of prostate cancer, and 7 of ovarian cancer (some studies included more than one site).

Of the 30 studies of colon cancer or adenomatous polyps, 20 found a statistically significant benefit of vitamin D, its serum metabolites, sunlight exposure, or another marker of vitamin D status on cancer risk or mortality12,13,5052,5666and incidence of adenomatous polyps,6770 including 1 study in which the association was limited to men65; 5 studies reported a beneficial effect (of borderline statistical significance) of vitamin D or its markers on risk of colon or rectal cancer,7175 and 5 reported no association.7680

Of the 13 studies of breast cancer, 9 reported a favorable association of vitamin D markers or sunlight with cancer risk,13,14,57,64,75,8184 including 1 where the association was limited to premenopausal women84; 1 study reported a favorable trend of borderline statistical significance85 and 3 found no association.66,80,86None reported adverse effects.

Thirteen of the 26 studies of prostate cancer found a statistically significant favorable association,16,17,64,75,8795 1 reported a favorable trend for serum 25(OH)D of borderline significance,96 and 11 reported no statistically significant association.66,80,97105 One reported a U-shaped association106 and 1 reported a significant inverse correlation with latitude, with a weaker correlation with UVB.94 Five of the 7 studies of ovarian cancer found higher mortality associated with lower regional sunlight15,17,64,75 or lower vitamin D intake,107 although 2 reported no association with sunlight.66,80

The consistency of the findings of dietary and serum studies with those of geographic studies allowed triangulation on vitamin D as a common factor in risk of colon cancer,12,13,17,5052,5659,6164 colonic adenomas,6770 breast cancer,14,17,57,64,75,81,82,84 prostate cancer,16,17,64,75,8795,108,109 and ovarian cancer.15,17,64,94,107

Dietary studies56,58,6063,7174,7679,84,100102,105,107 had certain limitations that contrasted with studies of serum.5052,59,67,68,82,86,88,90,97,98,110 Dietary studies in the United States were somewhat limited because it was difficult to fully separate associations of vitamin D from those of calcium, because both are in milk. There are many foods, however, that contain substantial amounts of vitamin D but little calcium, including fatty ocean fish.111,112 Higher intake of fatty fish was associated with lower mortality rates of colon113,114 and breast114,115 cancer in international comparisons, and of prostate cancer in cohort studies.116,117

Although serum studies have the advantage of measuring vitamin D status regardless of source, they can be confounded by associations with physical activity, particularly in studies of colon cancer. An association between greater physical activity and lower risk of colon cancer has been reported,118120although this was not always found.121 A common link could be that physical activity raises serum levels of 1,25(OH)2D, the most biologically active metabolite of vitamin D.122

Six of 7 prediagnostic serum studies of colon cancer or adenomas reported significantly higher risk of colon cancer5052 and adenomas6769 in those with low 25(OH)D levels, whereas 1 reported a trend suggestive of higher risk in those with low serum 25(OH)D.59 Both studies of the role of vitamin D in breast cancer analyzed 1,25(OH)2D, rather than 25(OH)D.82,86 One reported that the risk of breast cancer was markedly higher in women with low prediagnostic 1,25(OH)2D,82 but the other found no association.86 Lower levels of 25(OH)D90or 1,25(OH)2D88 were associated with higher risk of prostate cancer in 2 studies, but not in others.97,98,103,110 Some of the latter may not have detected an association with 1,25(OH)2D because its serum concentration is homeostatically regulated.123,124 On the other hand, some individuals with prolonged poor vitamin D status have below-average levels of 1,25(OH)2D,125,126 possibly accounting for the studies that found that individuals with low serum 1,25(OH)2D had high risk of breast82 and prostate88 cancer.

Vitamin D synthesis127 and serum 25(OH)D levels128130 are inversely correlated with latitude and positively correlated with sunlight, consistent with higher incidence or mortality rates for colon12,13,17,57,75 and breast cancer,13,14,17,57,75,81 especially in areas 37° or more from the equator. There are also north–south gradients for ovarian15,17,64,75 and prostate16,17,64,75,87,92,94 cancer. Some of the gradient for breast cancer may be associated with reproductive factors.131,132

UVB exposure and vitamin D intake increase serum 25(OH)D levels in a dose-dependent manner133135 by providing a higher concentration of 25(OH)D as substrate for synthesis of 1,25(OH)2D. Normal colon,136138 breast,139,140 and prostate141 epithelial cells have a vitamin D receptor (VDR) that is highly sensitive to 1,25(OH)2D. This could provide a mechanism of anticarcinogenic action for either circulating or locally synthesized 1,25(OH)2D.

Because synthesis of circulating 1,25(OH)2D is regulated in the kidney by parathyroid hormone,133 increased UVB exposure usually does not elevate circulating 1,25(OH)2D. 1,25(OH)2D is the most active vitamin D metabolite, although its concentration in serum is one thousandth that of 25(OH)D.142 It is synthesized from 25(OH)D by 1-α-hydroxylase enzymes in the colon,143prostate,144 breast,145 and other tissues146 through an autonomous mechanism not homeostatically regulated by parathyroid hormone.

The fact that 1,25(OH)2D is synthesized in colon epithelium provides a possible explanation for lower incidence rates of colon cancer5052 and adenomatous polyps6769 in individuals with higher levels of serum 25(OH)D. It also helps explain the association of residence at sunnier latitudes with lower mortality rates from colon,12,17,56,64 breast,13,14,17,64,85 ovary,15,17,64 and prostate16,17,64,87,90,91 cancer, because sunlight increases 25(OH)D levels, thereby providing more substrate for these tissues to make 1,25(OH)2D.

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RACIAL FACTORS

Blacks have levels of 25(OH)D approximately half those of Whites.19,20,23,147150 Blacks in northern cities with large Black populations (Chicago, Minneapolis, Detroit, Buffalo, Cleveland, and Toledo) have colon cancer mortality rates substantially higher than those of Whites.151 Case-fatality rates are higher among Blacks for colon,152154 breast,154 prostate,154 and ovarian155 cancer. Colon cancer mortality rates are 33% higher among Blacks, and incidence rates are 19% higher.156 Breast cancer mortality rates are 28% higher among Blacks, although incidence rates are slightly lower.156

There is a possibility of confounding by stage at diagnosis, since breast cancer tends to be diagnosed in more advanced stages in Blacks than in Whites.157However, differences in stage at diagnosis persisted after adjustment for socioeconomic status.158 Blacks have substantially poorer survival rates,159 even when mammographic screening rates are similar to those of Whites.160 Prostate cancer mortality rates are more than twice as high among Blacks as among Whites, and incidence is 1.6 times higher.156,159 Ovarian cancer mortality and incidence rates are higher among Whites, although they are rising among Blacks.156

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GENETIC FACTORS

There are several VDR genotypes.161 The most important of these regarding cancer is Bsm I,162,163 which has 3 variants: BB, Bb, and bb. The bb genotype occurs in 35% of the US population164 and is associated with lower circulating concentrations of 1,25(OH)2D.162 Men with the bb genotype were found to have twice the incidence of colon cancer162 as those with the BB genotype. In men below the median serum 25(OH)D level, those with the bb genotype had more than twice the incidence of prostate cancer as other men.162,165 Risk of breast cancer in women with the bb genotype was twice that of women with the BB genotype,166,167 although breast cancer findings have been mixed.168 Women with the bb genotype were 4 times more likely to develop metastases than those with the BB genotype.169 Approximately 40% of colon and prostate cancer may be related to the bb genotype, interacting adversely with low 25(OH)D.162

VDR polymorphisms also are associated with a more severe form of malignancy. Men with the VDR Taq I TT genotype, for example, were found to be 5 times more likely to develop a severe (Gleason grade≥ 5) prostate malignancy than those with other genotypes.170 This differs from previous inconclusive studies of associations of VDR genotypes with prostate cancer.171,172 Breast cancer cases with the TT genotype were twice as likely to have lymphatic metastases.173 The population prevalence of the TT genotype is 35%.174

These studies have helped define the role of vitamin D in cancer,162,163,165,167although most were exploratory, and only a few of the known VDR genotypes have been shown to be associated with risk of cancer.

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VITAMIN D AND COLON CANCER

Age-adjusted death rates for colon cancer tend to be high in areas with low levels of winter sunlight and low in sunny areas (Figure 1; the contour lines show the annual mean daily solar irradiance, measured in Langleys [calories/cm2]).

 fig 1

FIGURE 1—

Age-adjusted colon cancer mortality rates, by county area, and contours of annual mean daily solar irradiance in Langleys (calories/cm2), United States, 1970–1994.

Individuals with circulating 25(OH)D levels below 30 ng/mL had approximately twice the risk of colon cancer as those with higher levels in 2 studies,50,52 with doubling of incidence for those with less than 20 ng/mL in another.51 There was a consistent favorable, although non-significant, trend in a fourth.59 Individuals with 25(OH)D levels below 30 ng/mL also had higher incidence of colonic adenomas.68,69 The association of 25(OH)D with risk of colon cancer was present both early and late in follow-up,50,59 suggesting that vitamin D metabolites may have effects at all stages of carcinogenesis.175177

Seven epidemiological studies reported higher risk of colon cancer in individuals who consumed lower amounts of vitamin D, including the Western Electric Cohort Study,56 the Nurses’ Health Study,60 the Male Health Professionals’ Follow-Up Study,62 the Iowa Women’s Health Study,71 and the American Cancer Society Cancer Prevention Study II (CPS II) Cohort Study,65 and 2 case–control studies.63,73 The association in the CPS-II Cohort was limited to men.

One study reported a trend toward higher risk of colon cancer with lower vitamin D intake,71 and another reported an inverse association of vitamin D and calcium intake with risk of rectal cancer.72 Another found that lower vitamin D intake was associated with higher risk of adenomas.70 The findings of one study of colon cancer were no longer statistically significant after multivariate analysis.71 Five studies found no association.7679,178 Two of these were performed in sunny climates,76,178 where they could have been influenced by solar vitamin D synthesis. Although the latitude gradient helps to isolate the role of vitamin D, confounding is still possible.

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VITAMIN D AND BREAST CANCER

Breast cancer death rates tended to be higher in areas with low winter sunlight levels and lower in sunny areas (Figure 2).13,14 Women regularly exposed to sunlight, and consumers of above-average amounts of vitamin D, had significantly lower incidence rates of breast cancer.85 Women in the lowest quartile of serum 1,25(OH)2D had a risk of breast cancer 5 times higher than those in the highest quartile.82 Low 1,25(OH)2D levels were also associated with faster progression of metastatic breast cancer.179 Mortality rates of perimenopausal ovarian cancer also were lower in sunny regions,15,17,64,75although one study found no geographic association within a single country.80High intake of vitamin D and calcium markedly reduced incidence of mammary cancer in mice and rats consuming high-fat diets.9,180 Incidence of mammary cancer was only one quarter as high in rats that received high levels of vitamin D and calcium.181

 fig 2

FIGURE 2—

Age-adjusted breast cancer mortality rates, by county area, and contours of annual mean daily solar irradiance in Langleys (calories/cm2), United States, 1970–1994.

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VITAMIN D AND PROSTATE CANCER

Residents of sunny areas,16,87 and those with a history of exposure to high levels of sunlight,92,95,108 had lower risk of prostate cancer. In a study of 19000 men, those with 25(OH)D levels below 16 ng/mL had a 70% higher incidence rate of prostate cancer than those with levels above 16 ng/mL.90 For younger men with 25(OH)D levels below 16 ng/mL, incidence of prostate cancer was 3.5 times higher than for those with levels of 16 ng/mL or above and incidence of invasive cancer was 6.3 times higher.90 However, other studies have not found associations.80,97102,104106

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MECHANISM OF VITAMIN D EFFECTS

Vitamin D and its metabolites reduce the incidence of many types of cancer by inhibiting tumor angiogenesis,182185 stimulating mutual adherence of cells,186and enhancing intercellular communication through gap junctions,187 thereby strengthening the inhibition of proliferation that results from tight physical contact with adjacent cells within a tissue (contact inhibition). Vitamin D metabolites help maintain a normal calcium gradient in the colon epithelial crypts,188 and high serum levels of 25(OH)D are associated with markedly decreased proliferation of noncancerous but high-risk epithelial calls in the colon.189 1,25(OH)2D inhibits mitosis of breast epithelial cells.190 Pulsatile release of ion-ized calcium from intracellular stores, including the endoplasmic reticulum, induces terminal differentiation and apoptosis,176 and 1,25(OH)2D enhances this release.191

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RECOMMENDATIONS FOR VITAMIN D INTAKE

The National Academy of Sciences recommends the following daily intakes of vitamin D: 1 to 50 years of age, 200 international units (IU); 51 to 70 years, 400 IU; older than 71 years, 600 IU.192 In one study, 500 IU per day was associated with a 25(OH)D level of 30 ng/mL, although this included photosynthesized vitamin D.193 Sufficient vitamin D intake to achieve 30 to 35 ng/mL of 25(OH)D in serum was associated with reduced incidence of colonic adenomas,67,69 the latter in combination with adequate calcium intake. On the basis of the studies of serum 25(OH)D and risk of colorectal cancer cited in this article, the target range for serum 25(OH)D should be at least 30 ng/mL, but no more than 150 ng/mL.149,194 The National Academy of Sciences does not recommend a different intake of vitamin D by Blacks, although it suggests a need for further research on racial differences.192 On the basis of the markedly higher prevalence of 25(OH)D deficiency in Blacks,19,147 a higher level of supplementation is probably needed. Althought adverse VDR genotypes162,165167,169 are present in a large proportion of the population,164,174 different intakes according to genotype would not be practical.

Older adults need higher amounts of vitamin D owing to decreased absorption,195 and at any age, serum 25(OH)D rises as an inverse power function of vitamin D intake.196 Intake of 800 (IU) of vitamin D3 per day, for example, would increase serum 25(OH)D by only 6 ng/mL,193 so there is no reasonable concern about inducing toxicity with daily intake of 800 to 1000 IU per day.197The latter intake would be consistent with maintaining the serum 25(OH)D level at or above 30 ng/mL in most individuals.69,198 New vitamin D analogs have promising cellular effects, but are not currently used for prevention.199

Throughout the United States, the estimated daily solar exposure to maintain a serum 25(OH)D level of 30 ng/mL is 15 minutes in summer and 20 minutes in early fall or late spring, from 11:00 am to 2:00 pm under clear skies,18,40,200assuming exposure of arms, shoulders, and back. Blacks require twice as long.147During November to March, north of 37° latitude in the Northeastern and mid-Atlantic regions, no amount of solar exposure is sufficient,40 partly owing to a slightly thicker regional stratospheric ozone layer201 and denser tropospheric sulfate aerosol.202,203 In the Northwest and most other regions, some UVB is available during winter, although low ambient temperatures limit duration and area of exposure.37,38,40,127,147,200

Moderation is needed concerning sunlight exposure. Actinic changes are associated with exposure to ultraviolet radiation, and there is considerable evidence for its role in skin cancer.42,43 If sunlight is used as a source of vitamin D, exposure should be scrupulously monitored so that no reddening of the skin occurs,200,204 and intentional exposure of the face should be minimized. Individuals with skin type I or II, who tend to burn easily and tan poorly,205should not exceed 20 minutes per day in the sun. Exposure times much longer than 20 minutes would not appreciably increase vitamin D synthesis and could increase risk of skin cancer.206 Oral vitamin D3 supplementation, rather than solar exposure, should be used by fair-skinned or sun-sensitive persons, or by individuals taking medicines causing photosensitivity.

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POTENTIAL TOXICITY

Vitamin D dosages of up to 1000 IU per day have no reasonable likelihood of producing toxicity. Serum 25(OH)D levels of at least 30 ng/mL207 to 45 ng/mL143,208 are the minimum necessary to maintain normal parathyroid hormone levels, and at least 400 IU of supplemental vitamin D3 per day is needed to maintain serum 25(OH)D at a range consistent with normal parathyroid hormone levels in young and middle-aged adults; intake of at least 600 IU per day is required to maintain normal levels in adults aged older than 70 years.192The National Academy of Sciences–Institute of Medicine has indicated that 2000 IU per day is the safe upper limit of vitamin D intake.192 Typical recommended intakes are far below this.192,209

Potential toxic effects of vitamin D overdosage, such as bone demineralization, hypercalcemia, hypercalciuria, or nephrocalcinosis with renal failure, are encountered rarely, generally only when the daily dose exceeds 10 000 IU of vitamin D on a chronic basis.55 Concerns about vitamin D toxicity in the past have been because of massive overdoses in the range of 50 000 to 150 000 IU per day on a long-term basis.54,133 According to the National Academy of Sciences, no known health risks are associated with dosages of vitamin D in the normally encountered range of intake (up to 2000 IU/day).55,192,197,198,210,211

Relatively high oral intakes of vitamin D or serum levels of 25(OH)D are not a concern from a cardiovascular viewpoint, because most studies suggest that higher levels of 25(OH)D are associated with reduced cardiovascular risk. For example, higher serum 25(OH)D,212 1,25(OH)2D,213,214 and oral vitamin D215were associated with moderately but significantly lower blood pressure.

There also was a beneficial association between serum 25(OH)D and risk of myocardial infarction,216 ischemic heart disease mortality,217 and congestive heart failure,218 although other cardiovascular results have been mixed.219,220

Vitamin D supplementation was also associated with reduced incidence of type I diabetes221,222 and with improvement in type II diabetes.223,224 In Finland, vitamin D supplementation of infants was associated with reduction by four fifths in incidence of type I diabetes.221 Higher regional UVB levels have also been linked with lower age-adjusted death rates from endometrial and kidney cancers, Hodgkin’s lymphoma, non-Hodgkin’s lymphoma, multiple myeloma, and other malignancies.75

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ADOPTION OF VITAMIN D FOR CANCER PREVENTION

Supplemental vitamin D intake could address the high prevalence of vitamin D deficiency in the United States.1,55,198,225 Strong evidence indicates that intake or synthesis of vitamin D is associated with reduced incidence and death rates of colon, breast, prostate, and ovarian cancers. More than 1000 laboratory and epidemiological studies have been published concerning the association between vitamin D and its metabolites and cancer. Long-term studies have demonstrated the efficacy of moderate intake of vitamin D in reducing cancer risk and, when administered with calcium, in reducing the incidence of fractures.226 Despite these reassuring studies, the public health and medical communities have not adopted use of vitamin D for cancer prevention.

The cost of a daily dose of vitamin D3 (1000 IU) is less than 5 cents, which could be balanced against the high human and economic costs of treating cancer attributable to insufficiency of vitamin D. Leadership from the public health community will provide the best hope for action.

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Acknowledgments

This research was supported by a congressional allocation to the Hollings Cancer Center of the Medical University of South Carolina, Charleston, through the Department of the Navy, Bureau of Medicine and Surgery (Work Unit No. 60126 TR 03–1)7.

The authors thank William B. Grant of SUNARC, San Francisco, Calif, for reviewing the article and providing comments.

Note. The views expressed in this report are those of the authors and do not represent an official position of the Department of the Navy, Department of Defense, or the US Government.

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Notes

Peer Reviewed

Contributors
C. F. Garland, F. C. Garland, and E. D. Gorham jointly developed the plan and outline of the article, prepared the first draft, and reviewed and edited subsequent drafts. S.B. Mohr and C.F. Garland jointly performed the literature review, and S. B. Mohr edited drafts of the article. M. Lipkin, H. Newmark, and M. F. Holick reviewed and edited drafts.

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