Nos EUA, Suprema Corte recusa patente de partes de DNA

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A Suprema Corte dos Estados Unidos decidiu ontem que as empresas não podem patentear partes específicas do DNA, em uma decisão ambígua que também reconheceu os direitos da indústria de biotecnologia, que movimenta US$ 83 bilhões por ano, sobre produtos genéticos sintéticos.

Animation of the structure of a section of DNA...

Animation of the structure of a section of DNA. The bases lie horizontally between the two spiraling strands. (Photo credit: Wikipedia)

Os juízes decidiram que o DNA sintético – filamentos de material genético modificados em laboratório – podem ser patenteados porque esse processo envolve alguma ingerência humana. A decisão da corte invalidou as patentes que a Myriad Genetics, uma companhia de biotecnologia sediada em Utah,  havia registrado sobre dois genes humanos: o BRCA1 e o BRCA2.

Mutações nesses genes estão ligadas ao câncer nos seios e ovários – as mesmas mutações que a atriz Angelina Jolie  confirmou em testes e que a levaram a optar por uma mastectomia dupla preventiva.

Mark Skolnick, um dos fundadores da Myriad, tornou-se o primeiro cientista a isolar e sequenciar os dois genes, garantindo patentes de 20 anos sobre eles na metade da década de 90. A Myriad realiza testes dos genes.

Cientistas e organizações de defesa dos direitos humanos, liderados neste caso pela Association for Molecular Pathology,  contestaram os direitos exclusivos da Myriad sobre os genes, alegando que “produtos da natureza” não podem ser patenteados.

Mas a Myriad respondeu que os genes se enquadram na categoria de “invenção humana” porque os fragmentos do DNA tiveram que ser isolados. A corte concordou com os cientistas. “Um segmento de DNA ocorre naturalmente, é um produto da natureza e não pode ser patenteado simplesmente por ter sido isolado”, escreveu o juiz Clarence Thomas na decisão unânime.

A Myriad “encontrou um gene importante e útil,  mas descobertas inovadoras ou mesmo brilhantes não justificam por si só a patente”, escreveu ele.

Mas a decisão da corte foi limitada e o preço da ação da Myriad subiu imediatamente.  Ao meio-dia de ontem, ela era negociada a US$ 36,55, uma alta de 10,6%.

De fato, a corte disse que o DNA sintético ou complementar, conhecido como cDNA, pode ser patenteado por não ocorrer naturalmente. “O cDNA não apresenta os mesmos obstáculos à capacidade de receber patente que os segmentos isolados de DNA, que ocorrem naturalmente”, escreveu em nome da corte o juiz Thomas.

“Os técnicos de um laboratório indiscutivelmente criam algo novo quando o cDNA é feito”, disse ele, acrescentando que o cDNA não é um “produto da natureza” e, desse mod, pode ser patenteado.

A Myriad, que afirma ter mais de 500 reivindicações válidas e exequíveis em 24 patentes diferentes relacionadas ao seu teste de genes, disse que a corte “manteve apropriadamente” suas reivindicações sobre o cDNA.

Companhias farmacêuticas que incluem a Amgen, GlaxoSmithKline e Monsanto têm sido citadas como detentoras de patentes que poderão ser afetadas pela decisão da Myriad.

Fonte: Valor Econômico Jornalista: Anna Fifield e Andrew Jack, Financial Times Data: 14/06/2013

 

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Suprema Corte dos Estados Unidos proíbe patentear DNA humano natural

 

Por Lawrence HurleyWASHINGTON, 13 Jun (Reuters) – Em sua primeira sentença desse tipo sobre a genética humana, a Suprema Corte dos Estados Unidos decidiu por unanimidade nesta quinta-feira que material genético produzido sinteticamente pode ser patenteado, mas que isso não se aplica ao DNA natural.Os nove juízes concederam vitória parcial à empresa de biotecnologia Myriad Genetics, de Salt Lake City (Utah), detentora das patentes em questão.O principal órgão judicial dos Estados Unidos preservou importantes proteções de patentes que beneficiam a indústria de biotecnologia, mas deixou claro que isso não abrange o DNA extraído do corpo humano.Pesquisadores e defensores dos pacientes dizem que isso pode baratear os exames genéticos que apontam riscos de doenças.O tribunal se pronunciou em uma ação movida por pesquisadores médicos e outros interessados, envolvendo sete patentes detidas ou licenciadas pela Myriad, relacionados a dois genes associados aos cânceres de mama e ovário.O trabalho da Myriad nos diagnósticos preventivos atraiu a atenção mundial neste ano, quando a atriz Angelina Jolie anunciou que havia extraído as duas mamas depois que um exame apontou que ela tinha um risco extremamente elevado de desenvolver câncer de mama.O setor de biotecnologia viu algo de bom na decisão, observando que os juízes mantiveram intactas as proteções de patente sobre as formas de DNA produzidas por cientistas em laboratórios, e os processos usados para realizar os exames que prognosticam o câncer e outras doenças. O setor vinha alertando que uma condenação mais rigorosa à Myriad ameaçaria um investimento de bilhões de dólares.Em voto redigido pelo juiz Clarence Thomas, a corte disse que o chamado cDNA (“c” de “complementar, por ser “editado” em laboratório) pode ser patenteado, pois não ocorre naturalmente, o que lhe garantiria proteção sob a lei federal.Um laboratorista, escreveu ele, “inquestionavelmente cria algo novo quando o cDNA é feito”. Thomas observou que a chamada patente metodológica, que abrange os procedimentos técnicos para a realização de determinado processo, não foi afetada pela sentença.O acordo intermediário, que havia sido recomendado aos juízes pelo governo Obama, terá menos impacto sobre a Myriad do que se o tribunal tivesse proibido as patentes de todo tipo de material genético. Todas as patentes contestadas da Myriad expiram em 2015, mas a empresa diz deter outras que protegerão seus exames até 2018 e potencialmente depois.As ações da Myriad tiveram alta superior a 10 por cento depois da sentença devido à expectativa de que ela continuará lucrando com seus exames de diagnóstico preventivo do câncer.Mas essa alta acabou sendo revertida mais tarde, à medida que analistas de Wall Street questionaram as implicações em mais longo prazo sobre as ferramentas genéticas de diagnóstico.(Com reportagem adicional de Diane Bartz, Sharon Begley e Bill Berkrot)

Anúncios

Suprema Corte dos Estados Unidos proíbe patentear DNA humano natural

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Em sua primeira sentença desse tipo sobre a genética humana, a Suprema Corte dos Estados Unidos decidiu por unanimidade nesta quinta-feira que material genético produzido sinteticamente pode ser patenteado, mas que isso não se aplica ao DNA natural.

Os nove juízes concederam vitória parcial à empresa de biotecnologia Myriad Genetics, de Salt Lake City (Utah), detentora das patentes em questão.

dna humano

O principal órgão judicial dos Estados Unidos preservou importantes proteções de patentes que beneficiam a indústria de biotecnologia, mas deixou claro que isso não abrange o DNA extraído do corpo humano.

Pesquisadores e defensores dos pacientes dizem que isso pode baratear os exames genéticos que apontam riscos de doenças.

O tribunal se pronunciou em uma ação movida por pesquisadores médicos e outros interessados, envolvendo sete patentes detidas ou licenciadas pela Myriad, relacionados a dois genes associados aos cânceres de mama e ovário.

O trabalho da Myriad nos diagnósticos preventivos atraiu a atenção mundial neste ano, quando a atriz Angelina Jolie anunciou que havia extraído as duas mamas depois que um exame apontou que ela tinha um risco extremamente elevado de desenvolver câncer de mama.

O setor de biotecnologia viu algo de bom na decisão, observando que os juízes mantiveram intactas as proteções de patente sobre as formas de DNA produzidas por cientistas em laboratórios, e os processos usados para realizar os exames que prognosticam o câncer e outras doenças. O setor vinha alertando que uma condenação mais rigorosa à Myriad ameaçaria um investimento de bilhões de dólares.

Em voto redigido pelo juiz Clarence Thomas, a corte disse que o chamado cDNA (“c” de “complementar, por ser “editado” em laboratório) pode ser patenteado, pois não ocorre naturalmente, o que lhe garantiria proteção sob a lei federal.

Um laboratorista, escreveu ele, “inquestionavelmente cria algo novo quando o cDNA é feito”. Thomas observou que a chamada patente metodológica, que abrange os procedimentos técnicos para a realização de determinado processo, não foi afetada pela sentença.

O acordo intermediário, que havia sido recomendado aos juízes pelo governo Obama, terá menos impacto sobre a Myriad do que se o tribunal tivesse proibido as patentes de todo tipo de material genético. Todas as patentes contestadas da Myriad expiram em 2015, mas a empresa diz deter outras que protegerão seus exames até 2018 e potencialmente depois.

As ações da Myriad tiveram alta superior a 10 por cento depois da sentença devido à expectativa de que ela continuará lucrando com seus exames de diagnóstico preventivo do câncer.

Mas essa alta acabou sendo revertida mais tarde, à medida que analistas de Wall Street questionaram as implicações em mais longo prazo sobre as ferramentas genéticas de diagnóstico.

Com reportagem adicional de Diane Bartz, Sharon Begley e Bill Berkrot
Reuters

http://noticias.terra.com.br/mundo/estados-unidos/suprema-corte-dos-estados-unidos-proibe-patentear-dna-humano-natural,04c54b65d463f310VgnCLD2000000dc6eb0aRCRD.html

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Genética influi pouco em doenças autoimunes

English: Angelina Jolie at the Cannes film fes...

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Luis Ricardo Goulart Filho, o estudo ajuda a esclarecer suspeitas que sempre existiam na área médica. “Existem doenças, como o diabetes, que conseguimos identificar o gene responsável pelo desencadeamento dela, mas muitas outras enfermidades dessa magnitude são causadas por fatores externos. Como esse estudo mostra, seria bastante complicado definir os agentes só no DNA da pessoa”, destaca o pesquisador. O geneticista diz ainda que as pessoas com um gene relacionado a alguma doença podem não desenvolvê-la. “Podemos usar como exemplo o caso da Angelina Jolie, que tinha cerca de 80% de chances de ter câncer de mama. Isso significa que 20% (de pacientes como ela) não desenvolvem. Por isso, não podemos generalizar e dizer que a hereditariedade seria a principal causa. Temos fatores, como o estresse e a poluição, que podem fazer diferença”, destaca.

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Cientistas da Universidade Queen Mary, de Londres, realizaram o sequenciamento genético de mais de 40 milpessoas

Em um estudo publicado na revista Nature, pesquisadores ingleses fizeram um mapeamento genético de grandes proporções em busca de indícios que ligassem a origem das doenças autoimunes a fatores genéticos. O objetivo da equipe era encontrar uma maneira de combater essas enfermidades em sua formação inicial, mas o resultado mostrou que o enfoque nos genes pode não ser muito efetivo, pois outros importantes fatores parecem estar por trás do desencadeamento desses males.

Os cientistas da Universidade Queen Mary, de Londres, realizaram o sequenciamento genético de mais de 40 mil pessoas. A investigação usou como base seis quadros autoimunes: doenças da tireoide, doença celíaca, doença de Crohn (enfermidade crônica inflamatória intestinal), psoríase, esclerose múltipla e diabetes tipo 1. O mapeamento dos participantes foi dividido em dois grupos, sendo que 24.892 voluntários tinham algum desses males, e 17.019 eram saudáveis. Ao analisar os genes dos dois conjuntos de indivíduos e compará-los, os estudiosos perceberam que o fator genético das doenças é pequeno (na ordem de 3%). Logo, outros fatores seriam grandes responsáveis por esse tipo de condição.

De acordo com David Van Heel, professor de genética gastrointestinal de Queen Mary e líder do estudo, os genes que foram identificados não são suficientes para que um tratamento mais eficaz possa ser desenvolvido. “Para cada doença, deve haver centenas de fatores, e o risco genético é provavelmente herdado de um grande número de variantes de ambos os genitores. Se for esse o caso, talvez seja possível prever com exatidão as chances de um indivíduo desenvolver doenças autoimunes. Entretanto, os resultados não fornecem informações essenciais sobre a base biológica dessas condições e sobre as vias envolvidas”, destaca o pesquisador no trabalho.

Para o geneticista da Universidade Federal de Uberlândia (UFU) Luis Ricardo Goulart Filho, o estudo ajuda a esclarecer suspeitas que sempre existiam na área médica. “Existem doenças, como o diabetes, que conseguimos identificar o gene responsável pelo desencadeamento dela, mas muitas outras enfermidades dessa magnitude são causadas por fatores externos. Como esse estudo mostra, seria bastante complicado definir os agentes só no DNA da pessoa”, destaca o pesquisador. O geneticista diz ainda que as pessoas com um gene relacionado a alguma doença podem não desenvolvê-la. “Podemos usar como exemplo o caso da Angelina Jolie, que tinha cerca de 80% de chances de ter câncer de mama. Isso significa que 20% (de pacientes como ela) não desenvolvem. Por isso, não podemos generalizar e dizer que a hereditariedade seria a principal causa. Temos fatores, como o estresse e a poluição, que podem fazer diferença”, destaca. (VS)

 

Fogo amigo
Doenças autoimunes são quadros que ocorrem quando o sistema imunológico ataca e destrói os tecidos saudáveis do corpo, como se fosse incapaz de distinguir o que é prejudicial e o que faz parte do próprio organismo. Existem mais de 80 tipos dessas enfermidades.

http://sites.uai.com.br/app/noticia/saudeplena/noticias/2013/05/23/noticia_saudeplena,143471/genetica-influi-pouco-em-doencas-autoimunes.shtml

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Study Accidentally Finds Chemotherapy Makes Cancer Far Worse

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A team of researchers looking into why cancer cells are so resilient accidentally stumbled upon a far more important discovery. While conducting their research, the team discovered that chemotherapy actually heavily damages healthy cells and subsequently triggers them to release a protein that sustains and fuels tumor growth. Beyond that, it even makes the tumor highly resistant to future treatment.

Chemotherapy

 

Reporting their findings in the journal Nature Medicine, the scientists report that the findings were ‘completely unexpected’. Finding evidence of significant DNA damage when examining the effects of chemotherapy on tissue derived from men with prostate cancer, the writings are a big slap in the face to mainstream medical organizations who have been pushing chemotherapy as the only option to cancer patients for years.

The news comes after it was previously ousted by similarly-breaking research that expensive cancer drugs not only fail to treat tumors, but actually make them far worse. The cancer drugs were found to make tumors ‘metasize’ and grow massively in size after consumption. As a result, the drugs killed the patients more quickly.

Read more: http://naturalsociety.com/chemotherapy-makes-cancer-far-worse/#ixzz2JB7sUIYw

Known as WNT16B, scientists who performed the research say that this protein created from chemo treatment boosts cancer cell survival and is the reason that chemotherapy actually ends lives more quickly. Co-author Peter Nelson of the Fred Hutchinson Cancer Research Center in Seattle explains:

“WNT16B, when secreted, would interact with nearby tumour cells and cause them to grow, invade, and importantly, resist subsequent therapy.”

The team then complimented the statement with a word of their own:

“Our results indicate that damage responses in benign cells… may directly contribute to enhanced tumour growth kinetics.”

Meanwhile, dirt cheap substances like turmeric and ginger have consistently been found to effectively shrink tumors and combat the spread of cancer. In a review of 11 studies, it was found that turmeric use reduced brain tumor size by a shocking 81%. Further research has also shown that turmeric is capable of halting cancer cell growth altogether. One woman recently hit the mainstream headlines byrevealing her victory against cancer with the principal spice used being turmeric.

This accidental finding reached by scientists further shows the lack of real science behind many ‘old paradigm’ treatments, despite what many health officials would like you to believe. The truth of the matter is that natural alternatives do not even receive nearly as much funding as pharmaceutical drugs and medical interventions because there’s simply no room for profit. If everyone was using turmeric and vitamin D for cancer (better yet cancer prevention), major drug companies would lose out.

Additional sources:

Pubmed/21775121

Pubmed/19138983

Read more: http://naturalsociety.com/chemotherapy-makes-cancer-far-worse/#ixzz2JB81UnNu

Fonte: http://naturalsociety.com/chemotherapy-makes-cancer-far-worse/

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Vitamina D influencia mais de 200 genes – Vitamin D, Genome Research, Inglaterra 2010

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Em 2010, um novo estudo acaba de ampliar - de maneira contundente - as evidências de que a deficiência de vitamina D pode aumentar os riscos de desenvolvimento de muitas doenças. [Imagem: FRL/UCR]

Em 2010, um novo estudo ampliou – de maneira contundente – as evidências de que a deficiência de vitamina D pode aumentar os riscos de desenvolvimento de muitas doenças. [Imagem: FRL/UCR]

Com este trabalho realizado em 2010 na Inglaterra,  publicado na revista Genome Research, que relacionou pontos nos quais a vitamina D interage com o DNA e identificou mais de 200 genes que são influenciados diretamente por esta vitamina, e com seu enorme desenvolvimento até o momento presente, que já se tornou público e notório até mesmo para leigos em medicina – junto com os resultados além de qualquer expectativa obtidos na clínica médica, médico algum que se pretenda um profissional sério e atualizado,  pode dizer que a terapia com o hormônio vitamina D é  “experimental”,  “não tem base científica” e, MUITO MENOS, recusar esta terapia para seus pacientes.

Caso estes “médicos” não saibam, é dever legal deles esgotar os recursos terapêuticos em FAVOR de seus pacientes, e não a favor do lucro fácil e mortal da indústria farmacêutica que privilegia atendimentos de alta complexidade e alto custo EM DETRIMENTO dos atendimentos de baixa complexidade, alta eficácia, baixo custo.   O mesmo diz respeito aos governos que apoiam os primeiros interesses com suas “políticas de saúde pública” incompetentes ou mais frequentemente corruptas mesmo.

Já passou o  momento de os pacientes cidadãos assumirem que têm direitos no atendimento qualificado à saúde, como tal previstos na legislação brasileira, a começar pela de maior hierarquia, a Constituição Federal – que garante o direito à saúde e com isto o direito ao melhor atendimento e à mais eficiente terapia, sobretudo sempre com orientação preventiva.

Contudo, a maioria dos cidadãos esquece ou não sabe que, direitos não exigidos e substituídos por direitos implorados,  faz com que eles sejam gradualmente perdidos com o passar do tempo.   A questão resume-se a simples atitude: é direito seu? SIM.  Então, EXIJA respeito desde o início, a começar pelo médico acomodado ou incompetente que diz ser esta terapia “experimental”, “sem base científica”.  Ele está mentindo, porque não pode alegar à seu favor ignorância profissional.

 Celso Galli Coimbra
OABRS 11352
cgcoimbra@gmail.com
https://biodireitomedicina.wordpress.com/
https://www.youtube.com/user/biodireitobioetica
https://www.facebook.com/VitaminaD.HormonioVital

Genome Research

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Vitamina genética

Um novo estudo acaba de ampliar – de maneira contundente – as evidências de que a deficiência de vitamina D pode aumentar os riscos de desenvolvimento de muitas doenças.

A pesquisa, cujos resultados foram publicados nesta segunda-feira na revista Genome Research, relacionou pontos nos quais a vitamina D interage com o DNA e identificou mais de 200 genes que são influenciados diretamente pela vitamina.

De acordo com o estudo, estima-se que 1 bilhão de pessoas no mundo tenham carência de vitamina D, devido a fatores como insuficiência de exposição ao sol ou uma dieta pobre em nutrientes – veja, por exemplo, Jovens brasileiros têm insuficiência de vitamina D.

Ativadora de genes

Além de ser conhecida como fator de risco para o desenvolvimento de raquitismo, há evidências de que a falta de vitamina D também estaria relacionada ao aumento da suscetibilidade a condições como esclerose múltipla, artrite reumatoide e diabetes, bem como demência e alguns tipos de câncer.

No novo estudo, feito no Reino Unido, os cientistas utilizaram tecnologia de sequenciamento genético para criar um mapa das ligações dos receptores de vitamina D pelo genoma.

Esse receptor é uma proteína ativada pela própria vitamina, que, por sua vez, liga-se ao DNA e influencia quais proteínas são feitas a partir do código genético.

Os pesquisadores identificaram 2.776 pontos de ligação para o receptor por toda a extensão do genoma humano e verificaram que esses locais estão concentrados anormalmente próximos a genes associados a suscetibilidade a problemas no sistema imunológico.

Influência da vitamina D

O trabalho também mostrou que a vitamina D tem um efeito importante na atividade de 229 genes, entre os quais o IRF8, que já foi associado com esclerose múltipla, e o PTPN2, ligado a diabetes do tipo 1 e com a doença de Crohn, que atinge o intestino.

“O estudo mostra dramaticamente a ampla influência que a vitamina D tem sobre nossa saúde”, disse Andreas Heger, da Universidade de Oxford, um dos autores da pesquisa.

Fonte: http://www.diariodasaude.com.br/news.php?article=vitamina-d-influencia-genes&id=5652

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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

English: Autism awareness ribbon Português: Fi...

English: Autism awareness ribbon Português: Fita símbolo da conscientização a respeito do autismo (Photo credit: Wikipedia)

 

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Segundo este artigo publicado em revista de pediatria americana, o autismo estaria relacionado com falta de vitamina D.

E parte do tratamento seriam suplementos de vitamina D.

 

 

 

Source: Dermato-Endocrinologia

 

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Autism prevalence in the United States with respect to solar UV-B doses: An ecological study

 

 

 

Volume 4, Issue 4   October/November/December 2012
Keywords: 25(OH)D, African American, Asian American, autism, ecological, pregnancy, serum 25-hydroxyvitamin D, ultraviolet-B, vitamin D

 

Authors: William B. Grant and John J. Cannell

 
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Abstract: 
Evidence is mounting that vitamin D deficiency is intimately involved in autism. We report on autism prevalence by US state for those aged 6–17 y in 2010 with respect to indices of solar UV-B (UVB) doses. We calculated autism prevalence rates for white, black and Asian Americans by using total prevalence and relative populations of minors for each ethnic group by state. Analyses omit AK and HI (considered extreme cases), WY (no data), along with AZ and ND for black Americans (low numbers) and DC, ME, MT, ND and SD for Asian Americans (low numbers). For white Americans, the regression coefficient for solar UVB doses and autism prevalence ranged from -0.52 in January to -0.57 in October. For black Americans, the regression coefficient for latitude was 0.61, whereas those for solar UVB ranged from -0.55 to -0.61. For Asian Americans, the values for solar UVB ranged from -0.28 to -0.38. The inverse correlation between solar UVB and autism prevalence is similar to that for many types of cancer in the US. The journal literature indicates that adverse effects on fetal brain development during pregnancy due to vitamin D deficiency can explain these findings. However, we cannot rule out a role of vitamin D deficiency in early life. These results add to the evidence that vitamin D deficiency may be an important risk factor for autism and suggest that pregnant women and autistic individuals raise their serum 25-hydroxyvitamin D concentrations above 30 ng/ml.

 

Full Text

Introduction

Evidence is mounting that vitamin D deficiency is a risk factor for autism. Cannell1 [2008] first proposed and later extended2 [2010] the UV-B (UVB)-vitamin D-autism hypothesis. Kinney and colleagues3 reviewed the autism and vitamin D connection and suggested that “Vitamin D plays important roles in repairing DNA damage and protecting against oxidative stress—a key cause of DNA damage.” Mostafa and Al-Ayadhi recently studied autistic children and found a strong correlation between better autism rating scales and higher 25(OH)D levels and between higher anti-neural antibodies and lower 25(OH)D levels.4 Kočovská and colleagues5 reviewed the evidence supporting this hypothesis and called for “urgent research” into vitamin D and autism. Despite the mounting evidence, the working hypothesis has not been accepted among autism researchers. .

A map of autism rates by state for children aged 6–17 y in the Los Angeles Times in December 20116 prompted this ecological study. The map showed highest rates in the Northeast and on the West Coast and lowest among the Southern and Plains states. The trend of high rates in the Northeast and lowest rates in the Southern states is similar to that of many types of cancer,7 which were linked to solar UVB doses for July.8,9Thus, we thought that the data, when analyzed in greater detail, might show an inverse correlation between solar UVB doses and prevalence of autism.

 

Results

Table 1 gives the regression results for solar UVB doses for several different months as well as latitude. For white and Asian Americans, the regression fits for UVB in March, July and October were similar and stronger than those for UVB in January or latitude. However, for black Americans, the results for latitude were similar to those for UVB. The regression fits for black Americans were slightly stronger than for white Americans.
Table 1. Regression results, autism aged 6–17 y in the US in 2010 by state

Race, states Factor Linear fit (r, adjusted R2p) Power law fit (r)
White Americans (AK,
HI, WY omitted)
UVB-vit D, Oct -0.57, 0.31, * 0.60
UVB-vit D Mar -0.55, 0.29, * 0.58
UVB Jul -0.55, 0.28, * 0.57
UVB-vit D, Jul -0.54, 0.28, * 0.60
UVB-vit D, Jan -0.52, 0.25, * 0.52
Latitude 0.48, 0.22, * 0.48
Black Americans (AK, AZ, HI, ND, WY omitted) Latitude × latitude 0.63, 0.38, * 0.63
Latitude 0.61, 0.36, * 0.63
UVB-vit D, Oct -0.61, 0.36, * 0.69
UVB-vit D Mar -0.59, 0.33, * 0.62
UVB Jul -0.57, 0.31, * 0.60
UVB-vit D, Jan -0.56, 0.31, * 0.65
UVB-vit D, Jul -0.55, 0.29, * 0.63
Asian Americans (AK, DC, HI, ME, MT, ND, SD, WY omitted) UVB-vit D, Jul -0.38, 0.13, 0.01 0.38
UVB Jul -0.36, 0.11, 0.02 0.35
UVB-vit D, Oct -0.32, 0.08, 0.04 0.33
UVB-vit D Mar -0.30, 0.07, 0.06 0.30
Latitude × latitude 0.29, 0.06, 0.06 0.27
Latitude 0.28, 0.05, 0.08 0.27
UVB-vit D, Jan -0.28, 0.05, 0.08 0.34

*

, p < 0.001; UVB-vit D, data for vitamin D production from UVB;12 UVB Jul, data from reference 54.
No significant correlations emerged for other possible risk-modifying factors such as air pollution, alcohol consumption, obesity, poverty, or smoking.

Figures 1–3 are scatter plots of the autism prevalence data with respect to solar UVB doses. Figure 1 shows the results for white Americans with respect to October UVB vitamin D production with both linear and power-law fits to the data. Figure 2 does the same for black Americans. Figure 3shows the results for Asian Americans with respect to July UVB vitamin D production. The linear regression fits to the data show ratios for low to high UVB of 2.4 for white Americans, 3.6 for black Americans and 1.7 for Asian Americans. In all three cases, prevalence of autism with respect to changes in solar UVB decreases faster at lower UVB doses than at higher doses.

Figure 1. Scatter plot of autism prevalence for white Americans vs. solar UVB doses for October13 with linear and power-law fits to the data. Prevalence data are in arbitrary units. Omitted states: AK, HI and WY.

Figure 3. Same as Figure 1 but for Asian Americans. Omitted states: AK, DC, HI, ME, MT, ND, SD and WY.

Figure 2. Same as Figure 1 but for black Americans. Omitted states: AK, AZ, HI, ND and WY.

 

Discussion

The finding that, for both white and Asian Americans, solar UVB doses for March, July and October are much stronger than UVB doses in January or latitude suggests that vitamin D’s effect is associated with vitamin D production from solar UVB when doses are relatively high. This finding is similar to those for many types of cancer.8,9 Other ecological studies directly correlated multiple sclerosis prevalence rates with latitude.10,11 The latitudinal dependence in the United States is considered an index of wintertime solar UVB doses12 because summertime solar UVB doses are highly asymmetrical, being highest in the Southwest and lowest in the Northeast.13 Low serum 25(OH)D concentrations in winter are associated with infectious diseases such as influenza,14 which peaks in winter. However, for black Americans, the results for latitude are comparable to those for UVB.

If we assume that solar UVB production of vitamin D is an important factor in reducing risk of autism, an important question is how vitamin D deficiency before and during pregnancy and in early life affects risk. Reasonable evidence exists that autism is due in part to genetic factors. For example, evidence indicates that vitamin D status affects both male and female fertility,15 which could be due to potential genetic effects on the fetus. In addition, monozygotic twins are more likely to be concordant for autism than dizygotic twins.16 Good evidence also exists that vitamin D deficiency during pregnancy leads to adverse birth outcomes. Maternal metabolic conditions during pregnancy (diabetes, hypertension and obesity) are associated with increased risk of offspring diagnosed with autism by age 5 y.17 Vitamin D deficiency is a risk factor for diabetes,18and obesity is associated with lower serum 25(OH)D concentrations.19 Animal model studies have documented adverse effects on fetal brain development for vitamin D-deficient mothers.20 Although prompted by an interest in schizophrenia, Sullivan and colleagues21 associated family history of schizophrenia with increased risk of autism.

A study in Australia “found that the risk of women with vitamin D insufficiency (≤46 nmol/L) during pregnancy having a child with clinically significant language difficulties was increased close to twofold compared with women with vitamin D levels >70 nmol/L.”22 A study in the UK found that there were excess birth rates in April for several immune-mediated diseases found to be related to vitamin D deficiency in other studies, thereby providing evidence that vitamin D deficiency during fetal development is a risk factor for these diseases.23

Season of birth (or conception) affects risk of autism. In the 1980s and 1990s, excess birth rates for autism occurred around March.24,25However, Zerbo and colleagues26 associated wintertime conception with increased risk of autism. Maternal infection during pregnancy is associated with increased risk of autism,3,27 as is elevated maternal temperature. See Edwards29 for an explanation of how infection through increasing body temperature, is a risk factor for adverse birth outcomes.

Vitamin D reduces risk of both bacterial and viral infection.30 Lower respiratory infections are relatively common during pregnancy.31 Influenza infection during pregnancy is associated with increased risk of schizophrenia in offspring.32 Vitamin D may reduce the risk of influenza32,33 as well as that of other acute respiratory infections.34

A study in Denmark found significantly increased risk of epilepsy for those born to mothers who experienced elevated temperature during pregnancy associated with infections.35 Both epilepsy and autism have elevated birth rates in winter and lower birth rates in summer or fall.24,36

Although the journal literature supports the evidence for vitamin D deficiency before or during pregnancy as an important risk factor for autism, this ecological study cannot determine whether vitamin D status after birth plays a role although Mostafa and Al-Ayadhi’s recent study indicates such a connection.4 Both genetics and environment affect risk of autism.16 However, separating genetic from environmental factors is difficult.37

Since differences were found for those with different skin pigmentation, there might be some effects of solar irradiance other than vitamin D production involved in the link between solar UVB doses and prevalence of autism. A number of papers have reviewed the neuroendocrinology of the skin.3841 For example, keratinocytes stimulated by UVR can produce and secrete a number of cytokines.38 A recent study found that children with autism were “more likely to have decreased levels of both T helper-1(Th-1)-like cytokines (i.e. IFN-γ) and Th-2like cytokines (i.e. IL-4, IL-10).”42 Since darker pigmentation reduces the effect of UVR on keratinocytes, those with darker skin should produce fewer cytokines. Certainly more research is needed in this area.

UVA can increase serotonin production and reduce melatonin concentrations.43 “Low maternal plasma serotonin may be a risk factor for autism through effects on fetal brain development..”44 Those with autism may have a deficit of melatonin since supplementing them with melatonin improves sleep patterns.45 Since dark skin reduces the production of serotonin and degradation of melatonin, those with lighter skin have an decreased risk of autism and a recent review showed the opposite.46 Obviously, more work needs to be done in this area.

There is some evidence that UVR contributed to regulation of the hypothalamic-pituitary-adrenal (HPA) axis and the inflammatory response system and that they may have systemic effects.41 Prenatal stressors should increase the risk of autism and maternal stress during pregnancy is weakly associated with raised maternal cortisol.47 Thus, more research is needed in this area.

 

Vitamin D recommendations

,

The Institute of Medicine determined that pregnant women require only 600 IU/d (15 µg/day) of vitamin D3 (recommending the same for a 300-pound professional football lineman) and opine that a serum 25(OH)D concentration of 20 ng/ml is adequate.48 In the US, serum 25(OH)D concentrations during pregnancy are already low,49,50 and black Americans have much lower serum 25(OH)D concentrations than white Americans in general.51 The optimal serum 25(OH)D concentration during pregnancy is above 30 ng/ml based on a number of observational studies. Representative studies reporting that levels above 30 ng/ml are optimal include those related to pregnancy outcomes such as bacterial vaginosis,52 birth weight,53 primary Cesarean section delivery,54 and pre-eclampsia.55 In addition, gestational 25(OH)D concentrations are associated with normal fetal brain development20,56 and levels above 30 ng/ml are associated with reduced risk of childhood neuropsychological impairments,57 and development language difficulties.58

There is also evidence that serum 25(OH)D concentrations above 40 ng/ml might be considered optimal during pregnancy since optimal production of 1,25-dihydroxyvitamin D was achieved above this value in a randomized controlled trial with pregnant women.59,60 No adverse effects on calcium metabolism or other parameters were apparent in pregnant women taking 4000 IU/d of vitamin D3.60 A recent study of 25(OH)D levels in women living a traditional life style near the equator found mean serum 25(OH)D levels of nearly 60 ng/ml in pregnancy, approximately triple that of pregnant women in more developed poleward countries who putatively live and work indoors.61

The optimum 25(OH)D levels for children with autism are unknown although Mostafa and Al-Ayadhi found a strong negative correlation between autism rating scales and 25(OH)D levels in children with autism.4 They did not report a flattening of the association with higher vitamin D levels and improved autism scores although their study was limited by both the sample size and the low number of children with higher vitamin D levels. They also found autistic children have lower 25(OH)D levels than do control children although both groups reported similar time outdoors.

Mean “natural” 25(OH)D levels (as opposed to “normal” 25(OH)D levels) are around 46 ng/ml, as recently discovered by Luxwolda et al. who studied 25(OH)D levels of hunter-gatherers in equatorial Tanzania.62 Such “natural” 25(OH)D levels were common among tanned lifeguards in Missouri.63

 

Conclusion

This ecological study finds that autism prevalence among those aged 6–17 y in 2010 was significantly inversely correlated with solar UVB doses. Taken together, these results and other findings strongly implicate vitamin D deficiency as an important risk factor for developing autism. Maternal vitamin D deficiency appears to play an important role although we cannot discount a role of vitamin D deficiency in early life. Further studies should evaluate the UVB-vitamin D-autism hypothesis in both pregnant women and children with autism.

 

Methods

WBG obtained prevalence data from the Data Accountability Center associated with the Individuals with Disabilities Education Act data. The numbers of children by state with autism in 2010 are from Part B, Child Count (https://www.ideadata.org/PartBChildCount.asp (accessed Dec 16, 2011). Data used included the number of children with autism aged 6–17 y; those aged 6–21 y; and number of Asian, black and white children aged 6–21 y with autism. The data for those aged 6–17 y were not separated by race. WBG used the data by race for those aged 6–21 y with autism to estimate the number by race of those aged 6–17 y.

The data for total population aged 6–17 y by state are from Part C, Population and Enrollment Data, Table C-4, Number of and percentage change in estimated resident population ages 6–17, by state: 2001, 2009 and 2010 (https://www.ideadata.org/PopulationData.asp#2010[accessed Dec 16, 2011]).

WBG calculated the estimated population by race and state for children aged 6–17 y, he calculated numbers of autism children for each race and state. WBG obtained racial populations by state for children aged 5–17 y in 2009 from the US. Census Bureau (http://www.census.gov/compendia/statab/cats/population/estimates_and_projections_by_age_sex_raceethnicity.html [accessed Dec 18, 2011]). The fractions for single races were as follows: white (including Hispanics), 0.760; black, 0.151; and Asian, 0.043. WBG used these values to apportion the population by state into the three racial categories to calculate autism rates by race and state.

The independent variables used in this ecological study were solar UVB doses and latitude. WBG used two sets of data for UVB doses. One was DNA-weighted surface UVB doses from the Total Ozone Mapping Spectrometer (TOMS) for noon for July 1992.64 Grant and Garland9 used these data in an ecological study of cancer mortality rates. The other data set was monthly solar UVB doses weighted for vitamin D production from TOMS, validated using ground-based measurements and averaged over the period 1980–1990 for 12:00–12:59 p.m. local time.13 Solar UVB doses in the US in summer are highly asymmetric, with levels highest in the Southwest, lowest in the Northeast. The reasons for this asymmetry include that surface elevations are higher in the West, whereas stratospheric ozone column contents are lower. In addition, the Northeast has greater aerosol loading and cloud cover. For both sets of data, WBG estimated the UVB dose for each state from the maps in an effort to weight it by each state’s population distribution. A problem with the data maps from Fioletov and colleagues is that the contours are closely spaced in the Southwest, making this graphical approach less reliable for those states.

Latitude is an index for wintertime solar UVB dose and vitamin D production because solar zenith angle is much more important in winter than is surface elevation and stratospheric ozone column content. WBG chose latitude data to be near the center of population for each state. The second-order regression with latitude yielded the best model for multiple sclerosis prevalence among veterans of World War II and the Korean War in the US10 Scientists have linked multiple sclerosis to the Epstein-Barr virus, and other diseases linked to this virus have peak rates in March.65

This report omits data for AK and HI because those states are at the extreme latitudes and were not used in other ecological studies such as those regarding solar UVB and cancer.8 No data were available for Wyoming. In addition, some states have few Asians and/or blacks with autism, yielding poor estimates of autism rates. For black Americans, analyses omitted AZ and ND. For Asian Americans, DC, ME, MT, ND and SD were also omitted.

The analyses also used data for several possible risk-modifying factors, as has been done for cancer.9 These factors included alcohol consumption, lung cancer mortality rates for females, obesity, fraction of population living below poverty level and particulate air pollution concentrations.

WBG conducted linear regression analyses with the SPSS 20.0 statistical package (IBM/SPSS, Chicago, IL) and power law regression analyses with KaleidaGraph version 4.02 (Synergy Software, Reading, PA). Graphs were prepared using KaleidaGraph.

 

Disclosure of Potential Conflicts of Interest

W.B.G. receives funding from the UV Foundation (McLean, VA), Bio-Tech Pharmacal (Fayetteville, AR), the Vitamin D Council (San Luis Obispo, CA), the Vitamin D Society (Canada) and the Sunlight Research Forum (Veldhoven). J.J.C. is president of the Vitamin D Council and receives remuneration from Purity Products, Inc.

 

References

1. Cannell JJ. Autism and vitamin D. Med Hypotheses 2008; 70:750-9; PMID: 17920208; DOI: 10.1016/j.mehy.2007.08.016.
2. Cannell JJ. On the aetiology of autism. Acta Paediatr 2010; 99:1128-30; PMID: 20491697; DOI: 10.1111/j.1651-2227.2010.01883.x.
3. Kinney DK, Barch DH, Chayka B, Napoleon S, Munir KM. Environmental risk factors for autism: do they help cause de novo genetic mutations that contribute to the disorder?. Med Hypotheses 2010; 74:102-6; PMID: 19699591; DOI: 10.1016/j.mehy.2009.07.052.
4. Mostafa GA, Al-Ayadhi LY. Reduced serum concentrations of 25-hydroxy vitamin D in children with autism: relation to autoimmunity. J Neuroinflammation 2012; 9:201; PMID: 22898564; DOI: 10.1186/1742-2094-9-201.
5. Kočovská E, Fernell E, Billstedt E, Minnis H, Gillberg C. Vitamin D and autism: clinical review. Res Dev Disabil 2012; 33:1541-50; PMID: 22522213; DOI: 10.1016/j.ridd.2012.02.015.
6. Los Angeles Times. Autism rates by state, December 9, 2011; Credits: Interactivity: Pesce A. | Research: Poindexter S, Smith D, Zarembo A. [http://graphics.latimes.com/usmap-autism-rates-state/, accessed July 3, 2012]
7. Devesa SS, Grauman DJ, Blot WJ, Pennello GA, Hoover RN, Fraumeni JF Jr. Atlas of Cancer Mortality in the United States, 1950-1994. NIH Publication No. 99-4564, 1999.
8. Grant WB. An estimate of premature cancer mortality in the U.S. due to inadequate doses of solar ultraviolet-B radiation. Cancer 2002; 94:1867-75; PMID: 11920550; DOI: 10.1002/cncr.10427.
9. Grant WB, Garland CF. The association of solar ultraviolet B (UVB) with reducing risk of cancer: multifactorial ecologic analysis of geographic variation in age-adjusted cancer mortality rates. Anticancer Res 2006; 26:2687-99; PMID: 16886679.
10. Kurtzke JF. Epidemiologic evidence for multiple sclerosis as an infection. Clin Microbiol Rev 1993; 6:382-427; PMID: 8269393.
11. Grant WB, Holick MF. Benefits and requirements of vitamin D for optimal health: a review. Altern Med Rev 2005; 10:94-111; PMID: 15989379.
12. Grant WB. Hypothesis–ultraviolet-B irradiance and vitamin D reduce the risk of viral infections and thus their sequelae, including autoimmune diseases and some cancers. Photochem Photobiol 2008; 84:356-65; PMID: 18179620; DOI: 10.1111/j.1751-1097.2007.00266.x.
13. Fioletov VE, McArthur LJ, Mathews TW, Marrett L. Estimated ultraviolet exposure levels for a sufficient vitamin D status in North America. J Photochem Photobiol B 2010; 100:57-66; PMID: 20554218; DOI: 10.1016/j.jphotobiol.2010.05.002.
14. Cannell JJ, Vieth R, Umhau JC, Holick MF, Grant WB, Madronich S, et al. Epidemic influenza and vitamin D. Epidemiol Infect 2006; 134:1129-40; PMID: 16959053; DOI: 10.1017/S0950268806007175.
15. Lerchbaum E, Obermayer-Pietsch B. Vitamin D and fertility: a systematic review. Eur J Endocrinol 2012; 166:765-78; PMID: 22275473; DOI: 10.1530/EJE-11-0984.
16. Hallmayer J, Cleveland S, Torres A, Phillips J, Cohen B, Torigoe T, et al. Genetic heritability and shared environmental factors among twin pairs with autism. Arch Gen Psychiatry 2011; 68:1095-102; PMID: 21727249; DOI: 10.1001/archgenpsychiatry.2011.76.
17. Krakowiak P, Walker CK, Bremer AA, Baker AS, Ozonoff S, Hansen RL, et al. Maternal metabolic conditions and risk for autism and other neurodevelopmental disorders. Pediatrics 2012; 129:e1121-8; PMID: 22492772; DOI: 10.1542/peds.2011-2583.
18. Pittas AG, Nelson J, Mitri J, Hillmann W, Garganta C, Nathan DM, et al. Plasma 25-hydroxyvitamin D and progression to diabetes in patients at risk for diabetes: an ancillary analysis in the Diabetes Prevention Program. Diabetes Care 2012; 35:565-73; PMID: 22323410; DOI: 10.2337/dc11-1795.
19. Drincic AT, Armas LA, Van Diest EE, Heaney RP. Volumetric dilution, rather than sequestration best explains the low vitamin D status of obesity. Obesity (Silver Spring) 2012; 20:1444-8; PMID: 22262154; DOI: 10.1038/oby.2011.404.
20. Eyles D, Burne T, McGrath J. Vitamin D in fetal brain development. Semin Cell Dev Biol 2011; 22:629-36; PMID: 21664981; DOI: 10.1016/j.semcdb.2011.05.004.
21. Sullivan PF, Magnusson C, Reichenberg A, Boman M, Dalman C, Davidson M, et al. Family history of schizophrenia and bipolar disorder as risk factors for autism. Arch Gen Psychiatry 2012; :1-5; PMID: 22752149.
22. Whitehouse AJ, Holt BJ, Serralha M, Holt PG, Kusel MM, Hart PH. Maternal serum vitamin D levels during pregnancy and offspring neurocognitive development. Pediatrics 2012; 129:485-93; PMID: 22331333; DOI: 10.1542/peds.2011-2644.
23. Disanto G, Chaplin G, Morahan JM, Giovannoni G, Hypponen E, Ebers GC, et al. Month of birth, vitamin D and risk of immune mediated disease: a case control study. BMC Med 2012; 10:69; PMID: 22764877; DOI: 10.1186/1741-7015-10-69.
24. Gillberg C. Do children with autism have March birthdays?. Acta Psychiatr Scand 1990; 82:152-6; PMID: 2239360; DOI: 10.1111/j.1600-0447.1990.tb01373.x.
25. Grant WB, Soles CM. Epidemiologic evidence supporting the role of maternal vitamin D deficiency as a risk factor for the development of infantile autism. Dermatoendocrinol 2009; 1:223-8; PMID: 20592795.
26. Zerbo O, Iosif AM, Delwiche L, Walker C, Hertz-Picciotto I. Month of conception and risk of autism. Epidemiology 2011; 22:469-75; PMID: 21543984; DOI: 10.1097/EDE.0b013e31821d0b53.
27. Brown AS. Epidemiologic studies of exposure to prenatal infection and risk of schizophrenia and autism. Dev Neurobiol 2012; 72:1272-6; PMID: 22488761; DOI: 10.1002/dneu.22024.
28. Zerbo O, Iosif AM, Walker C, Ozonoff S, Hansen RL, Hertz-Picciotto I. Is maternal influenza or fever during pregnancy associated with autism or developmental delays? Results from the CHARGE (CHildhood Autism Risks from Genetics and Environment) Study. J Autism Dev Disord 2012; ; PMID: 22562209; DOI: 10.1007/s10803-012-1540-x.
29. Edwards MJ. Review: Hyperthermia and fever during pregnancy. Birth Defects Res A Clin Mol Teratol 2006; 76:507-16; PMID: 16933304; DOI: 10.1002/bdra.20277.
30. Gombart AF. The vitamin D-antimicrobial peptide pathway and its role in protection against infection. Future Microbiol 2009; 4:1151-65; PMID: 19895218; DOI: 10.2217/fmb.09.87.
31. Lim U, Freedman DM, Hollis BW, Horst RL, Purdue MP, Chatterjee N, et al. A prospective investigation of serum 25-hydroxyvitamin D and risk of lymphoid cancers. Int J Cancer 2009; 124:979-86; PMID: 19035445; DOI: 10.1002/ijc.23984.
32. McGrath JJ, Welham JL. Season of birth and schizophrenia: a systematic review and meta-analysis of data from the Southern Hemisphere. Schizophr Res 1999; 35:237-42; PMID: 10093868; DOI: 10.1016/S0920-9964(98)00139-X.
33. Urashima M, Segawa T, Okazaki M, Kurihara M, Wada Y, Ida H. Randomized trial of vitamin D supplementation to prevent seasonal influenza A in schoolchildren. Am J Clin Nutr 2010; 91:1255-60; PMID: 20219962; DOI: 10.3945/ajcn.2009.29094.
34. Sabetta JR, DePetrillo P, Cipriani RJ, Smardin J, Burns LA, Landry ML. Serum 25-hydroxyvitamin d and the incidence of acute viral respiratory tract infections in healthy adults. PLoS ONE 2010; 5:e11088; PMID: 20559424; DOI: 10.1371/journal.pone.0011088.
35. Sun Y, Vestergaard M, Christensen J, Olsen J. Prenatal exposure to elevated maternal body temperature and risk of epilepsy in childhood: a population-based pregnancy cohort study. Paediatr Perinat Epidemiol 2011; 25:53-9; PMID: 21133969; DOI: 10.1111/j.1365-3016.2010.01143.x.
36. Torrey EF, Miller J, Rawlings R, Yolken RH. Seasonal birth patterns of neurological disorders. Neuroepidemiology 2000; 19:177-85; PMID: 10859496; DOI: 10.1159/000026253.
37. Anderson GM. Twin studies in autism: what might they say about genetic and environmental influences. J Autism Dev Disord 2012; 42:1526-7; PMID: 22610470; DOI: 10.1007/s10803-012-1552-6.
38. Slominski A, Wortsman J. Neuroendocrinology of the skin. Endocr Rev 2000; 21:457-87; PMID: 11041445; DOI: 10.1210/er.21.5.457.
39. Slominski A, Tobin DJ, Shibahara S, Wortsman J. Melanin pigmentation in mammalian skin and its hormonal regulation. Physiol Rev 2004; 84:1155-228; PMID: 15383650; DOI: 10.1152/physrev.00044.2003.
40. Slominski A. Neuroendocrine activity of the melanocyte. Exp Dermatol 2009; 18:760-3; PMID: 19558501; DOI: 10.1111/j.1600-0625.2009.00892.x.
41. Slominski AT, Zmijewski MA, Skobowiat C, Zbytek B, Slominski RM, Steketee JD. Sensing the environment: regulation of local and global homeostasis by the skin’s neuroendocrine system. Adv Anat Embryol Cell Biol 2012; 212:v-, vii, 1-115; PMID: 22894052.
42. Abdallah MW, Larsen N, Mortensen EL, Atladóttir HÓ, Nørgaard-Pedersen B, Bonefeld-Jørgensen EC, et al. Neonatal levels of cytokines and risk of autism spectrum disorders: an exploratory register-based historic birth cohort study utilizing the Danish Newborn Screening Biobank. J Neuroimmunol 2012; 252:75-82; PMID: 22917523; DOI: 10.1016/j.jneuroim.2012.07.013.
43. Gambichler T, Bader A, Vojvodic M, Bechara FG, Sauermann K, Altmeyer P, et al. Impact of UVA exposure on psychological parameters and circulating serotonin and melatonin. BMC Dermatol 2002; 2:6; PMID: 11952999; DOI: 10.1186/1471-5945-2-6.
44. Connors SL, Matteson KJ, Sega GA, Lozzio CB, Carroll RC, Zimmerman AW. Plasma serotonin in autism. Pediatr Neurol 2006; 35:182-6; PMID: 16939857; DOI: 10.1016/j.pediatrneurol.2006.02.010.
45. Doyen C, Mighiu D, Kaye K, Colineaux C, Beaumanoir C, Mouraeff Y, et al. Melatonin in children with autistic spectrum disorders: recent and practical data. Eur Child Adolesc Psychiatry 2011; 20:231-9; PMID: 21359552; DOI: 10.1007/s00787-011-0162-8.
46. Dealberto MJ. Prevalence of autism according to maternal immigrant status and ethnic origin. Acta Psychiatr Scand 2011; 123:339-48; PMID: 21219265; DOI: 10.1111/j.1600-0447.2010.01662.x.
47. O’Donnell K, O’Connor TG, Glover V. Prenatal stress and neurodevelopment of the child: focus on the HPA axis and role of the placenta. Dev Neurosci 2009; 31:285-92; PMID: 19546565; DOI: 10.1159/000216539.
48. Ross AC, Manson JE, Abrams SA, Aloia JF, Brannon PM, Clinton SK, et al. The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: what clinicians need to know. J Clin Endocrinol Metab 2011; 96:53-8; PMID: 21118827; DOI: 10.1210/jc.2010-2704.
49. Bodnar LM, Simhan HN, Powers RW, Frank MP, Cooperstein E, Roberts JM. High prevalence of vitamin D insufficiency in black and white pregnant women residing in the northern United States and their neonates. J Nutr 2007; 137:447-52; PMID: 17237325.
50. Ginde AA, Sullivan AF, Mansbach JM, Camargo CA. Vitamin D insufficiency in pregnant and nonpregnant women of childbearing age in the United States. Am J Obstet Gynecol 2010; 202:436-, e1-8; PMID: 20060512; DOI: 10.1016/j.ajog.2009.11.036.
51. Ginde AA, Liu MC, Camargo CA. Demographic differences and trends of vitamin D insufficiency in the US population, 1988-2004. Arch Intern Med 2009; 169:626-32; PMID: 19307527; DOI: 10.1001/archinternmed.2008.604.
52. Bodnar LM, Krohn MA, Simhan HN. Maternal vitamin D deficiency is associated with bacterial vaginosis in the first trimester of pregnancy. J Nutr 2009; 139:1157-61; PMID: 19357214; DOI: 10.3945/jn.108.103168.
53. Bodnar LM, Catov JM, Zmuda JM, Cooper ME, Parrott MS, Roberts JM, et al. Maternal serum 25-hydroxyvitamin D concentrations are associated with small-for-gestational age births in white women. J Nutr 2010; 140:999-1006; PMID: 20200114; DOI: 10.3945/jn.109.119636.
54. Merewood A, Mehta SD, Chen TC, Bauchner H, Holick MF. Association between vitamin D deficiency and primary cesarean section. J Clin Endocrinol Metab 2009; 94:940-5; PMID: 19106272; DOI: 10.1210/jc.2008-1217.
55. Bodnar LM, Catov JM, Simhan HN, Holick MF, Powers RW, Roberts JM. Maternal vitamin D deficiency increases the risk of preeclampsia. J Clin Endocrinol Metab 2007; 92:3517-22; PMID: 17535985; DOI: 10.1210/jc.2007-0718.
56. Harms LR, Burne TH, Eyles DW, McGrath JJ. Vitamin D and the brain. Best Pract Res Clin Endocrinol Metab 2011; 25:657-69; PMID: 21872806; DOI: 10.1016/j.beem.2011.05.009.
57. Morales E, Guxens M, Llop S, Rodríguez-Bernal CL, Tardón A, Riaño I, et al. Circulating 25-hydroxyvitamin D3 in pregnancy and infant neuropsychological development. Pediatrics 2012; 130:e913-20; PMID: 22987876; DOI: 10.1542/peds.2011-3289.
58. Whitehouse AJ, Holt BJ, Serralha M, Holt PG, Kusel MM, Hart PH. Maternal serum vitamin D levels during pregnancy and offspring neurocognitive development. Pediatrics 2012; 129:485-93; PMID: 22331333; DOI: 10.1542/peds.2011-2644.
59. Hollis BW, Wagner CL. Vitamin D requirements and supplementation during pregnancy. Curr Opin Endocrinol Diabetes Obes 2011; 18:371-5; PMID: 21857221.
60. Hollis BW, Johnson D, Hulsey TC, Ebeling M, Wagner CL. Vitamin D supplementation during pregnancy: double-blind, randomized clinical trial of safety and effectiveness. J Bone Miner Res 2011; 26:2341-57; PMID: 21706518; DOI: 10.1002/jbmr.463.
61. Luxwolda MF, Kuipers RS, Kema IP, van der Veer E, Dijck-Brouwer DA, Muskiet FA. Vitamin D status indicators in indigenous populations in East Africa. Eur J Nutr 2012; ; PMID: 22878781; DOI: 10.1007/s00394-012-0421-6.
62. Luxwolda MF, Kuipers RS, Kema IP, Janneke Dijck-Brouwer DA, Muskiet FA. Traditionally living populations in East Africa have a mean serum 25-hydroxyvitamin D concentration of 115 nmol/l. Br J Nutr 2012; 108:1557-61; PMID: 22264449; DOI: 10.1017/S0007114511007161.
63. Haddad JG, Chyu KJ. Competitive protein-binding radioassay for 25-hydroxycholecalciferol. J Clin Endocrinol Metab 1971; 33:992-5; PMID: 4332615; DOI: 10.1210/jcem-33-6-992.
64. Leffell DJ, Brash DE. Sunlight and skin cancer. Sci Am 1996; 275:52-3, 56-9; PMID: 8658110; DOI: 10.1038/scientificamerican0796-52.
65. Douglas AS, Brown T, Reid D. Infectious mononucleosis and Hodgkin’s disease–a similar seasonality. Leuk Lymphoma 1996; 23:323-31; PMID: 9031113; DOI: 10.3109/10428199609054835.

 

 

 

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“The Drugs that completely cure are not profitable” – Dr. Richard J. Roberts, Prêmio Nobel da Medicina 1993

Assista aos vídeos:

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

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The Real Story on Vitamin D

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“The Drugs that completely cure are not profitable”

Interview with Dr. Richard J. Roberts, Nobel Prize in Medicine 1993

(Original en español: http://www.lavanguardia.es/free/edicionimpresa/20070727/53380162760.html)

I’m 63 years old: the worst about getting older is that you consider many “truths” as holy: that’s when you need new questions. I was born in Derby, my mechanic father gave me a chemistry set … and I still enjoy playing. Married, four children, one quadriplegic by an accident, which keep me encouraged to continue investigating. I participate in the Campus for Excellence.

– Can research be planned?

If I were Minister of Science, I would seek enthusiastic people with interesting projects, just give them money so they wouldn’t need to do anything else than investigate and let them work ten years to surprise us.

– It seems like a good policy.

It is generally believed that to go very far, you have to support basic research, but if you want more immediate and profitable results, you must bet on the applied research …

– And is it not like this?

Often the most profitable discoveries have been made ​​from very basic questions. So was created the giant U.S. biotech billion-dollar industry where I work.

– How was it created?

Biotechnology appeared when passionate people started to wonder if they could clone genes and began to study and try to purify them.

– An adventure by itself!

Yes, but nobody expected to get rich with these questions. It was difficult to get funding to research the answers until Nixon launched the war against cancer in 1971.

– Was it scientifically productive?

It allowed much research (like mine), with an enormous amount of public funds, that didn’t work directly against cancer, but was useful for understanding the mechanisms that allow life.

– What did you discover?

Phillip Allen Sharp and I were rewarded by the discovery of introns in eukaryotic DNA and gene splicing mechanism.

– For what was it useful?

That discovery led to understand how DNA works, however, has only an indirect link with cancer.

– Which model seems more effective research for you, the American or the European?
It’s obvious that the U.S., where private capital has an active role, is much more efficient. Take for example the spectacular progress of the computer industry, where private money financed basic and applied research, but for the health industry … I have my reservations.

– I listen

Research on human health cannot depend only on its profitability. What’s good for the corporate dividends is not always good for people.

– Could you explain?

Pharmaceutical industry wants to serve the capital markets …

– As any other industry

It’s just not any other industry, we are talking about our health and our lives and our children and millions of human beings.

– But if they are profitable, they will research better.

If you only think about benefits, you stop worrying about serving people.

– For instance?

I’ve seen that in some cases researchers dependent on private funds would have discovered a very effective medicine that would have completely eliminated a disease …

– And why do they stop investigating?

Because drug companies often are not as interested in healing you as in getting your money, so that investigation, suddenly, is diverted to the discovery of drugs that do not heal completely, but chronify the disease and make you experience an improvement that disappears when you stop taking the drug.

– It’s a serious accusation.

It is usual that pharmaceutical companies are interested in research that doesn’t cure but only make illnesses chronic with more profitable drugs that the ones that would completely cure once and forever. You just need to follow the financial analysis of the pharmaceutical industry and verify what I say.

– There are killing dividends.

That’s why we say that health cannot be a market and cannot be understood merely as a means of earning money. And I think that the European model of mixed private and public capital is less likely to encourage such abuses.

– An example of such abuse?

Investigations with antibiotics have been stopped because they were too effective and completely cured. As no new antibiotics have been developed, infectious organisms have become resistant and today tuberculosis, which in my childhood had been defeated, reappears and has killed this past year a million people.
– Are you talking about the Third World?

That is another sad chapter: Third World diseases are hardly investigated, because the drugs that would fight them are unprofitable. But I’m talking about our First World: the medicine that completely heals is not profitable and therefore is not researched.

– Don’t get politicians involved?

Don’t get too excited: in our system, politicians are mere employees of big companies, who invest what is necessary so that “their kids” get elected, and if they are not elected, they buy those who were elected.
Money and big companies are only interested in multiply. Almost all politicians – and I know what I mean, depend shamelessly on these multinational pharmaceutical companies that fund their campaigns. The rest are words …

Note of Ariel: Revista ARIEL recommends its readers read the following links taken from Periodismo Humano, relating to this same topic:

Periodismo Humano: http://periodismohumano.com con la serie ‘Farmacéuticas: razones para el escepticismo’

La industria farmacéutica hoy. Cualquier producto que demuestre ser mejor que un placebo puede ser comercializado. La industria gasta el doble en promocionar los medicamentos que en su investigación y desarrollo.

http://periodismohumano.com/sociedad/salud/la-industria-farmaceutica-hoy.html

¿Y quién vigila a las farmacéuticas? La relación entre los organismos reguladores y las empresas a las que tienen que regular.

http://periodismohumano.com/sociedad/salud/¿y-quien-vigila-a-las-farmaceuticas.html

Promocionando enfermedades: medicinas para los sanos.Las farmacéuticas exageran sobre afecciones comunes para captar a más clientes. Dos ejemplos: el debilitamiento de los huesos y la disfunción sexual femenina.

http://periodismohumano.com/sociedad/salud/promocionando-enfermedades-medicinas-para-los-sanos.html

Farmacéuticas y médicos: cómo bailar con puercoespines.Congresos, regalos, viajes, relaciones personales, ¿cómo influye la industria en el trabajo de los profesionales de la salud?. En Toledo, un 77% de los médicos recibe a diario la visita de representantes de las farmacéuticas.

http://periodismohumano.com/sociedad/salud/farmaceuticas-y-medicos-como-bailar-con-puercoespines.html

Fonte: http://www.revista-ariel.org/index.php?option=com_content&view=article&id=992:interview-with-dr-richard-j-roberts-nobel-prize-in-medicine&catid=54:healthy-mind-healthy-body&Itemid=83

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