A polêmica em torno do projeto 03/2013, que foi sancionado pela presidente Dilma Rousseff (PT) tornando lei o aborto ou o direito de matar.

 abortistas

A polêmica em torno do projeto 03/2013, que foi sancionado pela presidente Dilma Rousseff (PT) tornando lei o fornecimento de “pílulas do dia seguinte” para mulheres vítimas de estupro, continua.

Um grupo de entidades cristãs e outras instituições religiosas, formado pela Aliança de Batistas do Brasil, Centro de Estudos Bíblicos (CEBI), Católicas pelo Direito de Decidir, Conselho Latino-Americano de Igrejas – Região Brasil (CLAI) e a Rede Ecumênica da Juventude (REJU), publicou uma carta manifestando apoio à decisão da presidente de sancionar o projeto.

“Nós mulheres e homens de fé, biblistas, teólogas e teólogos de diferentes igrejas cristãs, integrantes dos diferentes organismos abaixo subscritos, apoiamos e solicitamos a sanção integral e imediata da PLC 3/2013, que dispõe sobre o atendimento obrigatório e integral de pessoas em situação de violência sexual. E assumimos o compromisso de participar do processo de informação e formação das mulheres sobre seus direitos reforçados no PL 3/2013 e de reforço de normas técnicas já existentes sobre o assunto nos aspectos de atendimento universal, integral e de qualidade à saúde ameaçada de mulheres e adolescentes vítimas de violência”, afirmaram os integrantes do grupo.

Segundo informações publicadas no site da Universidade Metodista, a justificativa para essa tomada de posição foi a necessidade de combater a violência sexual e suas consequências: “Ao nos dedicarmos ao estudo da Bíblia como expressão de nossa fidelidade ao evangelho de Jesus, afirmamos o amor e a justiça como dinâmicas vitais de nossa fé; afirmamos ainda que mulheres e homens partilham de modo integral de toda dignidade e beleza na vivência do mais sagrado e do mais humano. Na Bíblia encontramos relatos do passado em que comunidades são chamadas a afirmar o amor e a justiça em seus contextos. Muitas das questões ainda nos desafiam hoje, entretanto as respostas estão condicionadas aos equipamentos simbólicos e materiais disponíveis em cada tempo. O exercício da interpretação bíblica, quando não feito de maneira fundamentalista, nos ajuda a manter o exercício da crítica em relação às respostas sociais disponíveis”.

Críticas

De acordo com informações do jornal Folha de S. Paulo, o pastor e deputado federal Roberto de Lucena (PV-SP) seguiu o mesmo caminho do pastor Marco Feliciano (PSC-SP) e criticou a postura adotada por Dilma Rousseff.

Num discurso na tribuna da Câmara, Lucena afirmou que a bancada evangélica deveria retomar a discussão do tema, pois o uso do termo “profilaxia da gravidez”, ao invés de “pílula do dia seguinte”, ludibriou os parlamentares e os levou a aprovarem o projeto por unanimidade.

“Haverá de ser encaminhado ao Congresso projeto esclarecendo expressamente que o termo profilaxia da gravidez não significa aborto. Na verdade, absolutamente, nós não estamos aqui tratando de uma discussão religiosa. A discussão que envolveu este assunto é, sobretudo, ética”, completou, demonstrando preocupação por acreditar que, como está, o PLC 03/2013 pode “abrir uma brecha para a prática do aborto”.

Por Tiago Chagas

http://noticias.gospelmais.com.br/entidades-cristas-manifestam-apoio-projeto-autorizar-aborto-59072.html

 

O PROJETO DE LEI 03/2013 LEGALIZOU O ABORTO NO BRASIL, AGORA FALTA APENAS A SANÇÃO PRESIDENCIAL, QUE SERÁ DADA POR DILMA.

https://objetodignidade.wordpress.com/2013/07/12/o-projeto-de-lei-032013-legalizou-o-aborto-no-brasil-agora-falta-apenas-a-sancao-presidencial-que-sera-dada-por-dilma/

ABORTO – PLC 03/2013 – A AUTORIZAÇÃO LEGAL PARA QUE MENTIRA POSSA SEMPRE SER CONSIDERADA COMO VERDADE

https://objetodignidade.wordpress.com/2013/07/24/aborto-plc-032013-a-autorizacao-legal-para-que-mentira-possa-sempre-ser-considerada-como-verdade/

 

 

 

Pessoas que ocupam o Poder Executivo e mantêm sua administração na ilegalidade, na verdade, exercem a ditadura.

 

https://objetodignidade.wordpress.com/2013/07/28/pessoas-que-ocupam-o-poder-executivo-e-mantem-sua-administracao-na-ilegalidade-na-verdade-exercem-a-ditadura/

 

 

 

TOTALITARISMO, ILEGALIDADE, CRIME ORGANIZADO É DESGOVERNO PT LULA-DILMA e FORO de SP – agem para LEGALIZAR CRIMES POR MEIO DE ARTIFÍCIOS JURÍDICOS E ALTERAR A CONSTITUIÇÃO BRASILEIRA, ELIMIINAR DIREITOS FUNDAMENTAIS COMO O DIREITO À VIDA E SAÚDE

 

 

 

https://objetodignidade.wordpress.com/2013/07/27/totalitarismo-ilegalidade-crime-organizado-e-desgoverno-pt-lula-dilma-e-foro-de-sp-agem-para-legalizar-crimes-por-meio-de-artificios-juridicos-e-alterar-a-constituicao-brasileira-elimiinar-direi/

 

 

 

 

 

ABORTO – PLC 03/2013 – A AUTORIZAÇÃO LEGAL PARA QUE MENTIRA POSSA SEMPRE SER CONSIDERADA COMO VERDADE

 

https://objetodignidade.wordpress.com/2013/07/24/aborto-plc-032013-a-autorizacao-legal-para-que-mentira-possa-sempre-ser-considerada-como-verdade/

 

 

 

 

 

Aborto: debate na TV Justiça, no STF, em junho de 2007.

 

http://biodireitomedicina.wordpress.com/?s=Aborto%3A+debate+na+TV+Justi%C3%A7a%2C+no+STF%2C+em+junho+de+2007

 

 

 

https://objetodignidade.wordpress.com/2013/07/26/aborto-debate-na-tv-justica-no-stf-em-junho-de-2007/

 

 

 

 

 

– ADPF54 > Ação de Descumprimento de Preceito Fundamental para desconsiderar a vida das crianças com deficiência – a meroanencefalia, e liberar o aborto. Dias Tofoli na Advocacia Geral da União defendendo aborto de feto anencéfalo no STF. A Advocacia Geral da União pode defender aborto de feto anencéfalo no STF?

 

http://biodireitomedicina.wordpress.com/2009/04/09/agu-defende-aborto-de-feto-anencefalo-no-stf/    

 

 

 

 

 

Os “defensores da vida” – incluindo o petista Jaime Ferreira Lopes, que protegeu Lula em 2006, quando preparei questionamentos técnicos sobre sua posição como futuro presidente respeito do aborto – DEIXARAM Dilma dizer apenas “EU não sou a favor do aborto”. Não fizeram a ela se defrontar com a pergunta que REALMENTE decidia sua posição: “SE FOR ELEITA PRESIDENTE _VETARÁ OU NÃO VETARÁ_ EVENTUAL LEGISLAÇÃO ABORTISTA?”

 

https://objetodignidade.wordpress.com/2013/07/14/os-defensores-da-vida-incluindo-o-petista-jaime-ferreira-lopes-que-protegeu-lula-em-2006-quando-preparei-questionamentos-tecnicos-sobre-sua-posicao-como-futuro-presidente-respeito-do-aborto/

 

 

 

 

 

Aborto e Direitos Humanos. Inconstitucionalidade e impunidade hedionda da violabilidade da vida na “common law” do STF

 

19/07/2012 — celsogallicoimbra

 

http://biodireitomedicina.wordpress.com/2012/07/19/aborto-e-direitos-humanos-inconstitucionalidade-e-impunidade-hedionda-da-violabilidade-da-vida-na-common-law-do-stf/

 

 

 

 

 

 

 

Aborto: debate na TV Justiça, no STF, em junho de 2007.

 

http://biodireitomedicina.wordpress.com/?s=Aborto%3A+debate+na+TV+Justi%C3%A7a%2C+no+STF%2C+em+junho+de+2007

 

 

 

https://objetodignidade.wordpress.com/2013/07/26/aborto-debate-na-tv-justica-no-stf-em-junho-de-2007/

 

 

 

 

 

Os “defensores da vida” – incluindo o petista Jaime Ferreira Lopes, que protegeu Lula em 2006, quando preparei questionamentos técnicos sobre sua posição como futuro presidente respeito do aborto – DEIXARAM Dilma dizer apenas “EU não sou a favor do aborto”. Não fizeram a ela se defrontar com a pergunta que REALMENTE decidia sua posição: “SE FOR ELEITA PRESIDENTE _VETARÁ OU NÃO VETARÁ_ EVENTUAL LEGISLAÇÃO ABORTISTA?”

 

 

 

Aborto e Direitos Humanos. Inconstitucionalidade e impunidade hedionda da violabilidade da vida na “common law” do STF

 

19/07/2012 — celsogallicoimbra

 

 

 

http://biodireitomedicina.wordpress.com/2012/07/19/aborto-e-direitos-humanos-inconstitucionalidade-e-impunidade-hedionda-da-violabilidade-da-vida-na-common-law-do-stf/

 

 

 

Acrescento: o STF legislou – usurpou competência de outro Poder – e proferiu decisão na ADPF 54  com Relator IMPEDIDO de participar do julgamento com base no Artigo 36, inciso III, da Lei Orgânica da Magistratura Nacional [1], por ter antecipado seu voto de forma reiterada na mídia antes do julgamento. O Artigo 485 do CPC [2], no seu inciso II, considera esta situação uma das hipóteses objetivas de AÇÃO RESCISÓRIA. Portanto, esta é uma decisão que pode ser objeto de AÇÃO RESCISÓRIA.

 

 

 

 

 

  1. Art. 36 da LOMAN – É vedado ao magistrado:(…) III – manifestar, por qualquer meio de comunicação, opinião sobre processo pendente de julgamento, seu ou de outrem, ou juízo depreciativo sobre despachos, votos ou sentenças, de órgãos judiciais, ressalvada a crítica nos autos e em obras técnicas ou no exercício do magistério.

 

 

 

 

 

  1. Art. 485 do Código de Processo Civil:  A setença de mérito, transitada em julgado, pode ser rescindida quando: (…) II – proferida por juiz impedido ou absolutamente incompetente; (…)

 

 

 

Ler:

 

 

 

  1. 1.     http://biodireitomedicina.wordpress.com/2012/04/10/por-que-o-meio-pro-vida-nao-protocola-no-stf-e-no-congresso-nacional-requerimento-de-suspeicao-do-ministro-marco-aurelio-de-mello-antes-do-julgamento-da-adpf-54/

 

 

 

 

 

  1. http://biodireitomedicina.wordpress.com/2008/11/22/impossibilidade-de-legalizacao-do-aborto-no-brasil-desde-sua-proibicao-constitucional-de-ir-a-deliberacao-pelo-poder-legislativo/

 

 

 

 

 

Celso Galli Coimbra

 

 

 

OABRS 11352

 

 

 

cgcoimbra@gmail.com

 

 

 

EM 19 de julho de 2012.

 

 

 

 

 

 

 

 

O PROJETO DE LEI 03/2013 LEGALIZOU O ABORTO NO BRASIL, AGORA FALTA APENAS A SANÇÃO PRESIDENCIAL, QUE SERÁ DADA POR DILMA.

 

https://objetodignidade.wordpress.com/2013/07/12/o-projeto-de-lei-032013-legalizou-o-aborto-no-brasil-agora-falta-apenas-a-sancao-presidencial-que-sera-dada-por-dilma/

 

 

 

 

 

ABORTO – PLC 03/2013 – A AUTORIZAÇÃO LEGAL PARA QUE MENTIRA POSSA SEMPRE SER CONSIDERADA COMO VERDADE

 

https://objetodignidade.wordpress.com/2013/07/24/aborto-plc-032013-a-autorizacao-legal-para-que-mentira-possa-sempre-ser-considerada-como-verdade/

 

 

 

Aborto: debate na TV Justiça, no STF, em 18 de junho de 2007 por escrito. O que aconteceu até hoje, desde o encontro, e o que se pode esperar.

 

https://objetodignidade.wordpress.com/2013/07/13/aborto-debate-na-tv-justica-no-stf-em-18-de-junho-de-2007-por-escrito-o-que-aconteceu-ate-hoje-desde-o-encontro-e-o-que-se-pode-esperar/

 

 

 

A inconstitucionalidade da tramitação de legislação legalizadora do aborto no Brasil por Celso Galli Coimbra

 

https://objetodignidade.wordpress.com/2012/02/08/a-inconstitucionalidade-da-tramitacao-de-legislacao-legalizadora-do-aborto-no-brasil-por-celso-galli-coimbra/

 

 

 

Projeto do Novo Código Penal: aborto, desinformação e impedimentos legislativos « Celso Galli Coimbra – OABRS 11352

 

http://biodireitomedicina.wordpress.com/2012/05/09/projeto-do-novo-codigo-penal-aborto-desinformacao-e-impedimentos-legislativos/

 

 

 

O PROJETO DE LEI 03/2013 LEGALIZOU O ABORTO NO BRASIL, AGORA FALTA APENAS A SANÇÃO PRESIDENCIAL, QUE SERÁ DADA POR DILMA.

 

https://objetodignidade.wordpress.com/2013/07/12/o-projeto-de-lei-032013-legalizou-o-aborto-no-brasil-agora-falta-apenas-a-sancao-presidencial-que-sera-dada-por-dilma/

 

 

 

Livros do MEC promovem MST, racismo, prostituição, incesto, estupro, pedofilia e agressão a professores para alunos do ensino fundamental – aborto, saude e tráfico de pessoas

 

https://objetodignidade.wordpress.com/2012/09/30/livros-do-mec-promovem-mst-racismo-prostituicao-incesto-estupro-pedofilia-e-agressao-a-professores-para-alunos-do-ensino-fundamental-aborto-saude-e-trafico-de-pessoas/

 

 

 

Dilma Vana Roussef PT quer “liberar” a prática do aborto até os 9 meses de gestação para, além da implantação de clínicas estrangeiras no Brasil, tornar o pais um exportador de matéria-prima humana – fetos – usada em plásticas, cosméticos, transplantes, alimentação e indústria farmacêutica.

 

 

 

https://objetodignidade.wordpress.com/2012/09/05/dilma-vana-roussef-pt-quer-liberar-a-pratica-do-aborto-ate-os-9-meses-de-gestacao-para-alem-da-implantacao-de-clinicas-estrangeiras-no-brasil-tornar-o-pais-um-exportador-de-materia/

 

 

 

 

 

lula mandou encampar essa “‘reforma”‘ pra inglês ver E principalmente CALAR O POVO ou SILENCIAR PROTESTOS. Além de distrair as atenções internacionais e nós brasileiros, movimenta dinheiro público

 

https://objetodignidade.wordpress.com/2013/07/02/lula-mandou-encampar-essa-reforma-pra-ingles-ver-e-principalmente-calar-o-povo-ou-silenciar-protestos-alem-de-distrair-as-atencoes-internacionais-e-nos-brasileiros-movimenta-dinheiro-publico/

 

 

 

Plebiscito inviável em 2013, concluiu Ministra Cármem Lucia, presidente do TSE

 

https://objetodignidade.wordpress.com/2013/07/04/plebiscito-inviavel-em-2013-concluiu-ministra-carmem-lucia-presidente-do-tse/

 

 

 

Ativo nos bastidores, Lula comanda Dilma presidente “Encampar reforma política”

 

https://objetodignidade.wordpress.com/2013/06/30/ativo-nos-bastidores-lula-comanda-dilma-presidente-encampar-reforma-politica/

 

 

 

PNDH3   Aborto, saude publica e industria multimilionaria. As razoes petistas – PT, Dilma e Lula, para o fim do Estado de Direito: O PNDH-3 PREVE A LIBERAÇÃO DE CRIMES

 

https://objetodignidade.wordpress.com/2012/03/05/aborto-saude-publica-e-industria-multimilionaria-as-razoes-petistas-pt-dilma-e-lula-para-o-fim-do-estado-de-direito-o-pndh-3-preve-a-liberacao-de-crimes/

 

 

 

Constituição e o genocídio no Brasil.

 

https://objetodignidade.wordpress.com/2011/08/18/constituicao-e-o-genocidio-no-brasil/

 

 

 

Brasil é lanterna em investimento na saúde

 

https://objetodignidade.wordpress.com/2011/08/05/brasil-e-lanterna-em-investimento-na-saude/

 

 

 

Impossibilidade de legalização do aborto no Brasil desde sua proibição constitucional de ir à deliberação pelo Poder Legislativo

 

http://biodireitomedicina.wordpress.com/2008/11/22/impossibilidade-de-legalizacao-do-aborto-no-brasil-desde-sua-proibicao-constitucional-de-ir-a-deliberacao-pelo-poder-legislativo/

 

 

 

As células-tronco de embriões nunca foram necessárias para “curar”. Esta foi a grande mentira milionária de uma Medicina meramente comercial, industria farmaceutica e laboratórios multinacionais e clínicas – inclusive abortistas.

 

https://objetodignidade.wordpress.com/2012/02/18/a-cura-e-prevencao-ocorrem-por-terapia-natural-suplementacao-de-vitaminas-dieta-alimentar/

 

 

 

 

 

Brasil, de 2002 a 2012 passa pela fase totalitária: ilegalidade e ilegitimidade são tipicas na ditadura civil.

 

https://objetodignidade.wordpress.com/2012/08/03/brasil-de-2002-a-2012-passa-pela-fase-totalitaria-ilegalidade-e-ilegitimidade-sao-tipicas-na-ditadura-civil/

 

 

 

O governador do Arizona Jan Brewer assinou uma lei que proíbe os provedores de aborto como a Planned Parenthood de receber dinheiro por meio do Estado, seu escritório disse em um comunicado.

 

 

 

https://objetodignidade.wordpress.com/2012/08/22/o-governador-do-arizona-jan-brewer-assinou-uma-lei-que-proibe-os-provedores-de-aborto-como-a-planned-parenthood-de-receber-dinheiro-por-meio-do-estado-seu-escritorio-disse-em-um-comunicado/

 

 

 

PORQUE O ABORTO

 

 

 

https://objetodignidade.wordpress.com/2012/08/20/porque-o-aborto/

 

 

 

LEGALIZAR O ABORTO? – A quem interessa?

 

 

 

https://objetodignidade.wordpress.com/2012/08/20/legalizar-o-aborto-a-quem-interessa/

 

 

 

A que interessa o aborto no Brasil e a deslavada má fé de quem acompanha os fins espúrios de um governo que usa da ilegalidade há 10 anos – parte 1

 

 

 

https://objetodignidade.wordpress.com/2012/08/17/a-que-interessa-o-aborto-no-brasil-e-a-deslavada-ma-fe-de-quem-acompanha-os-fins-espurios-de-um-governo-que-usa-da-ilegalidade-ha-10-anos-parte-1/

 

 

 

El aborto genera en España un negocio de 100 millones€ en diez años

 

 

 

https://objetodignidade.wordpress.com/2012/05/20/el-aborto-genera-en-espana-un-negocio-de-100-millonese-en-diez-anos/

 

 

 

Projeto do Novo Código Penal: aborto, desinformação e impedimentos legislativos

 

 

 

https://objetodignidade.wordpress.com/2012/05/10/projeto-do-novo-codigo-penal-aborto-desinformacao-e-impedimentos-legislativos/

 

 

 

Os países que têm o aborto liberado, a interrupção voluntaria da gravidez descriminalzada, são os que têm os mais altas taxas de MORBIDADE e de MORTALIDADE DAS MULHERES

 

 

 

https://objetodignidade.wordpress.com/2012/03/23/os-paises-que-tem-o-aborto-liberado-a-interrupcao-voluntaria-da-gravidez-descriminalzada-sao-os-que-tem-os-mais-altas-taxas-de-morbidade-e-de-mortalidade-das-mulheres/

 

 

 

Crimes sexuais que têm por objeto as crianças, correspondem ao terceiro mais rentável comércio mundial, que perde apenas para a indústria de armas e do narcotráfico.

 

https://objetodignidade.wordpress.com/2012/10/27/crimes-sexuais-que-tem-por-objeto-as-criancas-correspondem-ao-terceiro-mais-rentavel-comercio-mundial-que-perde-apenas-para-a-industria-de-armas-e-do-narcotrafico/

 

 

 

Gastos públicos crescem no governo Lula. Mas saúde e educação são os setores menos beneficiados

 

https://objetodignidade.wordpress.com/2012/09/30/gastos-publicos-crescem-no-governo-lula-mas-saude-e-educacao-sao-os-setores-menos-beneficiados/

 

 

 

Livros do MEC promovem MST, racismo, prostituição, incesto, estupro, pedofilia e agressão a professores para alunos do ensino fundamental – aborto, saude e tráfico de pessoas

 

https://objetodignidade.wordpress.com/2012/09/30/livros-do-mec-promovem-mst-racismo-prostituicao-incesto-estupro-pedofilia-e-agressao-a-professores-para-alunos-do-ensino-fundamental-aborto-saude-e-trafico-de-pessoas/

 

 

 

Senado e alteração ao Código Penal – Inconstitucionalidade – Ameaça ao Direito à Vida. Artifícios jurídicos

 

https://objetodignidade.wordpress.com/2012/09/27/senado-e-alteracao-ao-codigo-penal-inconstitucionalidade-ameaca-ao-direito-a-vida-artificios-juridicos/

 

 

 

Imprensa do Canadá sobre o purgatório do Brasil. A forma mais cruel de populismo. “This is a fascist economy, in its purest definition. The reason is that they retain the old veneer in fake cultural causes… they tell you how to live your private life. Censorship or “media control” is in Dilma’s agenda”.

 

 

 

Dilma Vana Roussef PT quer “liberar” a prática do aborto até os 9 meses de gestação para, além da implantação de clínicas estrangeiras no Brasil, tornar o pais um exportador de matéria-prima humana – fetos – usada em plásticas, cosméticos, transplantes, alimentação e indústria farmacêutica.

 

 

 

Tráfico de órgãos é terceiro mais lucrativo crime organizado no mundo, segundo Polícia Federal

 

https://objetodignidade.wordpress.com/2012/08/25/trafico-de-orgaos-e-terceiro-mais-lucrativo-crime-organizado-no-mundo-segundo-policia-federal-co-de-orgaos-e-terceiro-mais-lucra/

 

 

 

O governador do Arizona Jan Brewer assinou uma lei que proíbe os provedores de aborto como a Planned Parenthood de receber dinheiro por meio do Estado, seu escritório disse em um comunicado.

 

https://objetodignidade.wordpress.com/2012/08/22/o-governador-do-arizona-jan-brewer-assinou-uma-lei-que-proibe-os-provedores-de-aborto-como-a-planned-parenthood-de-receber-dinheiro-por-meio-do-estado-seu-escritorio-disse-em-um-comunicado/

 

 

 

LEGALIZAR O ABORTO? – A quem interessa

 

https://objetodignidade.wordpress.com/2012/08/20/legalizar-o-aborto-a-quem-interessa/

 

 

 

Brasil, de 2002 a 2012 passa pela fase totalitária: ilegalidade e ilegitimidade são tipicas na ditadura civil.

 

https://objetodignidade.wordpress.com/2012/08/03/brasil-de-2002-a-2012-passa-pela-fase-totalitaria-ilegalidade-e-ilegitimidade-sao-tipicas-na-ditadura-civil/

 

 

 

Tribunal de Apelações do Texas permite excluir Planned Parenthood

 

https://objetodignidade.wordpress.com/2012/06/30/tribunal-de-apelacoes-do-texas-permite-excluir-planned-parenthood/

 

 

 

O PNDH-3 PREVE A LIBERAÇÃO DE CRIMES, fim do Estado de Direito.

 

https://objetodignidade.wordpress.com/2011/08/23/o-pndh-3-preve-a-liberacao-de-crimes-fim-do-estado-de-direito/

 

 

 

Projeto do Novo Código Penal: aborto, desinformação e impedimentos legislativos

 

09/05/2012 — Celso Galli Coimbra

 

http://biodireitomedicina.wordpress.com/2012/05/09/projeto-do-novo-codigo-penal-aborto-desinformacao-e-impedimentos-legislativos/

 

 

 

The Wholesalers of aborted babies

 

https://objetodignidade.wordpress.com/2012/06/28/the-wholesalers-of-aborted-babies/

 

 

 

O generocídio acontece nos EUA. Video de Bound4Life apresenta centros da Planned Parenthood Federation of America (PPFA), a maior organização abortista do mundo.

 

https://objetodignidade.wordpress.com/2012/06/26/o-generocidio-acontece-nos-eua-video-de-bound4life-apresenta-centros-da-planned-parenthood-federation-of-america-ppfa-a-maior-organizacao-abortista-do-mundo/

 

 

 

IBGE: população brasileira envelhece em ritmo acelerado

 

https://objetodignidade.wordpress.com/2012/06/15/ibge-populacao-brasileira-envelhece-em-ritmo-acelerado/

 

 

 

China pede desculpas à mulher forçada a abortar feto de 7 meses

 

https://objetodignidade.wordpress.com/2012/06/15/china-pede-desculpas-a-mulher-forcada-a-abortar-feto-de-7-meses/

 

 

 

Imagem de feto resultado de aborto forçado choca chineses

 

 

 

Ministro de Justiça reconhece e defende o direito de viver dos embriões.

 

https://objetodignidade.wordpress.com/2012/05/20/ministro-de-justica-reconhece-e-defende-o-direito-de-viver-dos-embrioes/

 

 

 

‘No nos resignamos’: Los ciudadanos europeos, en pie por la cultura de la vida

 

https://objetodignidade.wordpress.com/2012/05/20/no-nos-resignamos-los-ciudadanos-europeos-en-pie-por-la-cultura-de-la-vida/

 

 

 

El aborto genera en España un negocio de 100 millones€ en diez años

 

https://objetodignidade.wordpress.com/2012/05/20/el-aborto-genera-en-espana-un-negocio-de-100-millonese-en-diez-anos/

 

 

 

Infanticídio feminino e mortalidade materna, assassinato em massa de mulheres e deficientes, um genocídio por responsabilidade do governo

 

https://objetodignidade.wordpress.com/2012/05/02/infanticidio-feminino-e-mortalidade-materna-assassinato-em-massa-de-mulheres-e-deficientes-um-genocidio-por-responsabilidade-do-governo/

 

 

 

All Girls Allowed – China Gendercide

 

https://objetodignidade.wordpress.com/2012/05/01/all-girls-allowed-china-gendercide/

 

 

 

Gendercide – The war on baby girls

 

https://objetodignidade.wordpress.com/2012/04/30/gendercide-the-war-on-baby-girls/

 

 

 

The world at seven billion

 

https://objetodignidade.wordpress.com/2012/04/29/the-world-at-seven-billion/

 

 

 

Experimentação médica em humanos nos Estados Unidos: A história chocante da verdade da medicina moderna e psiquiatria (1833-1965 a parte de 1965-2005). Os riscos e perigos ‘a saúde de quem utiliza drogas psiquiatricas. Vale lembrar que as mulheres que abortam comumente tém, entre as sequelas fisico-psiquicas e o cancer, doenças psiquiatricas alem da perda da fecundidade.

 

 

 

Sobre política usa como argumentos a ideia espuria de ajudar a saude das mulheres pobres mantendo a criminosa industria multimilionaria de abortamento – como fazem aqui no Brasil no plano político nacional do PT e presidente Dilma, e a Rede Feminista de Saúde e de Direitos Reprodutivos no Conselho Nacional dos Direitos das Mulheres-, quando todo o planeta ja sabe que as mulheres que abortam tém risco elevado de desenvolver cancer de mamas.

 

 

 

Os países que têm o aborto liberado, a interrupção voluntaria da gravidez descriminalzada, são os que têm os mais altas taxas de MORBIDADE e de MORTALIDADE DAS MULHERES

 

https://objetodignidade.wordpress.com/2012/03/23/os-paises-que-tem-o-aborto-liberado-a-interrupcao-voluntaria-da-gravidez-descriminalzada-sao-os-que-tem-os-mais-altas-taxas-de-morbidade-e-de-mortalidade-das-mulheres/

 

 

 

Aborto na Rússia: “triste recorde mundial”

 

https://objetodignidade.wordpress.com/2012/02/08/aborto-na-russia-triste-recorde-mundial/

 

 

 

Abortos Causam Transtornos Mentais na Mulher. Estudo na Nova Zelândia Requer Menos Abortos.

 

https://objetodignidade.wordpress.com/2011/09/29/abortos-causam-transtornos-mentais-na-mulher-estudo-na-nova-zelandia-requer-menos-abortos/

 

 

 

A criança como sujeito de experimentação científica: uma analise histórica dos aspectos éticos – limpeza social de incapazes e incompetendes

 

https://objetodignidade.wordpress.com/2011/09/23/a-crianca-como-sujeito-de-experimentacao-cientifica-uma-analise-historica-dos-aspectos-eticos-limpeza-social-de-incapazes-e-incompetendes/

 

 

 

Aborto: debate na TV Justiça, no STF, em junho de 2007 e HOJE

 

https://objetodignidade.wordpress.com/2011/09/12/aborto-debate-na-tv-justica-no-stf-em-junho-de-2007-e-hoje/

 

 

 

Estudo Requer aos Médicos que façam Menos Abortos. Abortos Causam Transtornos Mentais na Mulher

 

https://objetodignidade.wordpress.com/2011/09/10/estudo-requer-aos-medicos-que-facam-menos-abortos-abortos-causam-transtornos-mentais-na-mulher-2/

 

 

 

Roe versus Reality — Abortion and Women’s Health

 

https://objetodignidade.wordpress.com/2011/09/10/roe-versus-reality-abortion-and-womens-health/

 

 

 

OS RISCOS DE ABORTAR – perigos físicos e emocionais do aborto

 

https://objetodignidade.wordpress.com/2011/09/10/os-riscos-de-abortar-perigos-fisicos-e-emocionais-do-aborto/https://objetodignidade.wordpress.com/2011/09/10/os-riscos-de-abortar-perigos-fisicos-e-emocionais-do-aborto/

 

 

 

The Breast Cancer Epidemic: Modeling and Forecasts Based on Abortion and Other Risk Factors

 

https://objetodignidade.wordpress.com/2011/09/09/the-breast-cancer-epidemic-modeling-and-forecasts-based-on-abortion-and-other-risk-factors/

 

 

 

Relação entre aborto e cancro da mama

 

https://objetodignidade.wordpress.com/2011/09/06/relacao-entre-aborto-e-cancro-da-mama/

 

 

 

Constituição e o genocídio no Brasil.

 

https://objetodignidade.wordpress.com/2011/08/18/constituicao-e-o-genocidio-no-brasil/

 

 

 

Projeto genocida

 

https://objetodignidade.wordpress.com/2011/08/18/projeto-genocida-2/

 

 

 

Aborto: a quem interessa?

 

https://objetodignidade.wordpress.com/2011/08/18/aborto-a-quem-interessa-2/

 

 

 

A indústria da morte: cenário frankenstein

 

https://objetodignidade.wordpress.com/2011/07/28/a-industria-da-morte-cenario-frankenstein-2/

 

 

——-

 

 

 

 

Vitamin C use has been an alternative therapy for many years. Many doctors do not hesitate to recommend doses of 1 to 5gm or more per day. The Third National Health and Nutrition Survey, also called NHANES III, showed that 11% of nonsmoking women and 21% of nonsmoking men

Vitamin C (Ascorbic Acid): Overview

http://www.diagnose-me.com/treat/T50562.html

 

Alternative Names: Ascorbic Acid.

 

http://www.googleadservices.com/pagead/aclk?sa=L&ai=Be72Ma5ZwT5D7MfGO2gW0nez4C_WErKgD3YWj4zmluOrpReDFCBABGAEglfLnAzgAUJ2C6dn______wFgzdjqgKgDoAHju4vcA7IBE3d3dy5kaWFnbm9zZS1tZS5jb226AQozMDB4MjUwX2FzyAEC2gEsaHR0cDovL3d3dy5kaWFnbm9zZS1tZS5jb20vdHJlYXQvVDUwNTYyLmh0bWzgAQLAAgbIAtW86BWoAwHIAx3oA-0B6AOjA-gDyAPoA48B9QMAAADE9QMAAAAQiAYBoAYC&num=1&cid=5Gj1vgM4uDBXHr14WhdL0bv4&sig=AOD64_0ATSOOlQpi7OY5m_CCg1aVgY1sXg&client=ca-pub-9775460366133772&adurl=http://www.lumosity.com/landing%3Frefer%3D694%26a%3DBTG-PlayNow_300x250_Image%26Network%3DContent%26kw%3D%26ad%3D15438085533%26SiteTarget%3Dwww.diagnose-me.com%26ll_ad_id%3D699&nm=12&nx=148&ny=55

Vitamin C use has been an alternative therapy for many years. Many doctors do not hesitate to recommend doses of 1 to 5gm or more per day. The Third National Health and Nutrition Survey, also called NHANES III, showed that 11% of nonsmoking women and 21% of nonsmoking men in the United States do not get enough vitamin C.  (Article continues below…)

Concerned about your state of health?  Or just curious?  Click below…
 Questionnaire


The Analyst™ gathers all the information it needs when you complete the extensive drill-down multiple-choice questionnaire
Questionnaire

 Diagnosis


Using your questionnaire, The Analyst™ produces a prioritized personal diagnosis showing condition likelihood, seriousness, ‘rule out’s, risks and informational links
Diagnosis

 Suggestions


Your report includes prioritized personal recommendations such as lab testing, medicines, diet and lifestyle changes, supplement suggestions and prevention
Consult a doctor before taking action

Suggestions

 LifeMeter®


LifeMeter® shows overall state of health scored from 100 (perfect) to 0 (mortality)
Select this option at your own risk

LifeMeter®

 Doctor Review (optional)


Optionally and for a small fee, one of our doctors can review your case, respond to your notes and questions, review lab tests, and be available for follow-up questions
Review (optional)

 Full Explanations


Your report includes detailed explanations to support all reasoning, conclusions and recommendations
Explanation

Start The AnalystPlease note that it is extremely important to obtain an accurate diagnosis before trying to find a cure.  Many diseases and conditions share common symptoms: if you treat yourself for the wrong illness or a specific symptom of a complex disease, you may delay legitimate treatment of a serious underlying problem.  In other words, the greatest danger in self-treatment may be self-diagnosis. If you do not know what you really have, you can not treat it!

Knowing how difficult it is to weed out misinformation and piece together countless facts in order to see the “big picture”, we now provide simple online access to The Analyst™.  Used by doctors and patients alike, The Analyst™ is a computerized diagnostic tool that sits on a vast accumulation of knowledge and research.  By combining thousands of connections between signs, symptoms, risk factors, conditions and treatments, The Analyst™ will help to build an accurate picture of your current health status, the risks you are running and courses of action (including appropriate lab testing) that should be considered.

One of the most talked about vitamins in recent decades, vitamin C activity was first identified hundreds of years ago for it’s ability to prevent and treat scurvy. There are few conditions for which Vitamin C has not been promoted for, and in many cases had some effect. Essentially, ascorbic acid is the main water soluble anti-oxidant of the body. It is considered a vitamin in man because we cannot synthesize it. There are thousands of articles and hundreds of books describing the benefits of supplementation with ascorbic acid.

In contrast with the findings from epidemiologic studies based on foods, observational studies of nutrients consumed in supplements and recent experimental trials provide little support for a strong protective role for vitamins C or E against cancer. If vitamins C or E are indeed protective against cancer, that protection may derive from their consumption in complex mixtures with other nutrients and with other bioactive compounds as found in the matrix provided by whole foods.

One of the main objections to mega-dose vitamin C use has been the possibility of developing kidney stones from elevated oxalic acid levels in the urine. This myth has been slow to die. It turns out that elevated levels of oxalic acid seen in some urine samples of people taking vitamin C were misleading. The particular testing method used could not distinguish between oxalic acid and vitamin C, thus giving a false positive reading for oxalic acid. More accurate testing methods have shown there are no oxalic acid elevations in vitamin C users.

Urinary oxalate excretion generally does not increase significantly for both normal subjects and stone-formers with ascorbic acid supplementation unless doses exceed 6gm daily; however, oxalate excretion even at those high doses is still usually in the range achievable by dietary influences alone. The exceptions derive from anecdotal reports of a small number of cases and from one poorly controlled trial with unstated methodology and questionable assay techniques (Piesse JW. Nutritional factors in calcium-containing kidney stones with particular emphasis on vitamin C.) [Int Clin Nutr Rev 5(3): pp.110-29, 1985] A study did not find a correlation between a high daily intake of vitamin C or vitamin B6 and the risk of stone formation, even when consumed in large doses. [J Urol, 1996 Jun, 155:6, pp.1847-51]

Source


Most ascorbic acid is synthesized by the oxidation of l-sorbose (usually derived from corn). High quality ascorbic acid will be 99% pure and contain no residues of corn. To get the maximum effect of ascorbic acid supplements, one should combine them with plant flavonoids. Flavonoids, the so-called vitamin P, have been shown to increase the effectiveness of ascorbic acid as well as direct its usage to the areas most needed.

The best sources of vitamin C are fruits and vegetables. Citrus fruits such as oranges, grapefruit, and tangerines are excellent sources. Other good natural sources of vitamin C are: broccoli, cabbage, brussels sprouts, tomatoes, green peppers, melons, cantaloupe, kiwifruit, strawberries, sweet peppers, potatoes with skin, and alfalfa sprouts.

Here are some guidelines for eating fruits and vegetables with a high vitamin C content: Choose fresh or frozen fruits and vegetables over canned products; cook vegetables only for a short time in a small amount of water; eat raw vegetables; eat sliced fruits and vegetables shortly after they’re cut; keep fruits and vegetables refrigerated, and eat them while they’re fresh.

Acerola is a small cherry-like fruit of the small shrub Malpighia glabra. As one of the richest natural sources of vitamin C, fruits have between 1-4.5% vitamin C. The dried extraction (usually about 10:1) of the fruit juice may have between 10-18% Vitamin C content, although many of the products on the market above 10% are adulterated with commercial asorbic acid. Acerola also contains such other vitamins as vitamin A, thiamin, riboflavin and niacin in similar proportions as other fruits.

Reasons for Use


It is not known for sure if mega doses of antioxidants, such as vitamin C, can help decrease the risk for chronic diseases. Much of the current information is conflicting. More research is needed. In a review of recent studies, it was suggested that an intake of 90mg per day provides the optimal health benefits related to heart disease and cancer.

Directions


High oral doses of vitamin C have been used safely for decades. If the amount you are using causes diarrhea, the dosage needs to be reduced. However, in some conditions, in order for vitamin C to be effective it has to be used in doses that come very close to causing diarrhea. Unless this “bowel tolerance” dose is found and maintained, the condition for which the vitamin C was recommended may not resolve. If you are consuming doses of vitamin C greater than perhaps 500mg per day, do not stop its use abruptly. It is best to taper your dose down over several days. A sudden reduction may result in a temporary deficit (“rebound scurvy“) and a negative influence on your resistance to infection.

The RDA for vitamin C is 75mg for women and 90mg men. The RDA for pregnant women is 85mg; women who breastfeed should consume 120mg per day. Several groups are recommending that 120-200mg should be considered the recommended daily intake.

Side-Effects; Counter-Indicators and Warnings

 

Consuming more than 2,000mg per day of vitamin C can cause stomach upset and diarrhea and possibly other adverse effects.

Caution must be advised regarding any use of vitamin C in cases of renal failure or dialysis.

 

 

 

 

 

 

Dietary micronutrients/antioxidants and their relationship with bronchial asthma severity

Dietary micronutrients/antioxidants and their relationship with bronchial asthma severity

 

  1. 1.    C. Picado1,
  2. 2.    R. Deulofeu2,
  3. 3.    R. Lleonart3,
  4. 4.    M. Agustí3,
  5. 5.    J. Mullol3,
  6. 6.    M. Torra4,
  7. 7.    L. Quintó4

 

Article first published online: 23 SEP 2008

DOI: 10.1034/j.1398-9995.2001.00793.x

Issue

 

 

Allergy

Volume 56, Issue 1, pages 43–49, January 2001

http://onlinelibrary.wiley.com/doi/10.1034/j.1398-9995.2001.00793.x/full

 

Keywords:

  • ·         antioxidants;
  • ·         bronchial asthma;
  • ·         diet;
  • ·         micronutrients

 

Abstract

  1. 1.   Top of page
  2. 2.   Abstract
  3. 3.   Material and methods
  4. 4.   Results
  5. 5.   Discussion
  6. 6.   Acknowledgments
  7. 7.   References

Background: Because little is known about micronutrient/antioxidant intake and asthma severity, we investigated dietary intake and plasma/serum levels of micronutrients/antioxidants in a group of asthma patients with various degrees of severity, and compared the results with healthy subjects.

Methods: A case control study was carried out on 118 asthma patients and 121 healthy subjects. The severity of the disease was classified by division of patients into four groups. Normal dietary micronutrient/antioxidant intake was estimated from a food frequency questionnaire. Plasma/serum levels of vitamins C, E, and A, selenium, magnesium, zinc, and platelet glutathione peroxidase (GSH-Px) activity were also determined.

Results: No differences in daily micronutrient/antioxidant intake were seen between patients and healthy subjects. The severity of the disease showed no significant relationship with micronutrient/antioxidant intake. There were no differences in plasma/serum levels in any of the micronutrients/antioxidants between healthy subjects and asthmatics. Nor were any differences found between asthma groups in severity in the biochemical measures, except in platelet GSH-Px activity, which was significantly lower in the most severe groups.

Conclusions: In this study, we found no evidence of any association between micronutrient/antioxidant intake or plasma/serum levels of micronutrients/antioxidants and asthma. Reduction of platelet GSH-Px activity in the most severe patients suggests that these patients have a diminished capacity to restore part of the antioxidant defences.

Recent studies suggest that an association may exist between a low intake of certain micronutrients and asthma (1). It has also been hypothesized that a deficient antioxidant capacity may also play a role in the patho-genesis of asthma (2).

Human antioxidant defences include ascorbic acid (vitamin C), α-tocopherol (vitamin E), vitamin A, enzymes such as glutathione peroxidase, and trace elements including selenium and zinc.

Low intake of vitamin C has been associated with wheezing (3, 4), increased risk of bronchial hyperresponsiveness (5), and reduced levels of FEV1 (6, 7). Dietary intake of vitamin E has a positive influence on wheezing (8) and lung function (8). Low dietary intake of vitamin A has been shown to be associated with airflow limitation (9).

Selenium is an essential component of glutathione peroxidase (GSH-Px). It has been suggested that lowered GSH-Px activity due to a low intake of selenium may play a role in asthma (10–13).

Many studies have evaluated the effect of the dietary intake of micronutrients and antioxidants on wheeze (3, 4, 8), lung function (6–9), and bronchial hyperreactivity (5), as assessed by challenge tests. However, neither the presence of wheeze, the demonstration of bronchial hyperresponsiveness, nor low lung function can be used as a substitute for the diagnosis of asthma.

In epidemiologic studies the potential impact of both the severity of the disease and its treatment on the characteristics of asthma patients’ diet should also be considered. One example of the possible influence of asthma therapy on the diet is the severe corticosteroid-dependent patient who modifies his/her diet to reduce caloric intake in order to prevent weight gain resulting from the use of systemic corticosteroids. Reduction or modification of dietary intake in these patients can be accompanied by a low intake of micronutrients and antioxidants. Therefore, in order to elucidate the role of dietary factors in asthma, it is important to perform studies on patients with a clearly defined diagnosis of asthma. In addition, only patients with diets not influ-enced by food supplementation or avoidance should be included in the study. In a recent study, we reported that asthma is associated with a decrease in energy intake (14). We also found severe asthma with regular oral corticosteroid therapy to be associated with reduced plasma protein and albumin levels (14).

Although a number of studies have evaluated the possible role of dietary micronutrients/antioxidants in asthma, little is known about the influence of either the severity of the disease and/or its treatment on intake and on the plasma/serum levels of these micronutrients.

The objective of our study was to investigate whether a relationship exists between the dietary intake of micronutrients/antioxidants and asthma. We also studied the effects of asthma severity on plasma/serum levels of vitamins, selenium, magnesium, and zinc, and platelet GSH-Px activity.

Material and methods

  1. 1.   Top of page
  2. 2.   Abstract
  3. 3.   Material and methods
  4. 4.   Results
  5. 5.   Discussion
  6. 6.   Acknowledgments
  7. 7.   References

 

Study subjects

A total of 150 consecutive asthmatic patients attending the outpatient clinic were asked to take part in the study. They all presented a history of intermittent wheezing, shortness of breath, and chest tightness; they all had a diagnosis of asthma and were taking asthma medication. The severity of the disease was characterized in four groups of patients by a method similar to the one proposed in the Global Initiative for Asthma (GINA) (15). This method was modified in order to include the characteristics of therapy in the classification of the severity of disease. The four groups were as follows: intermittent (group 1), mild persistent (group 2), moderate persistent (group 3), and severe (group 4). Group 1 comprised patients who were on β2-adrenergic agents on demand. Group 2 comprised patients who regularly used β2-adrenergic agents, with or without low doses of inhaled corticosteroids. Group 3 comprised patients with a continuing history of episodic asthma, most of whom were on regular inhaled corticosteroid therapy, and group 4 comprised patients with a current history of chronic unremitting asthma requiring high doses of inhaled corticosteroids and regular oral corticosteroid therapy, or frequent short courses of oral corticosteroids.

Aspirin-intolerant asthma was deduced from the patient’s history. In patients with only one attack precipitated by aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs), aspirin intolerance was confirmed by an oral challenge test with aspirin. In patients with two or more asthma attacks precipitated by aspirin or NSAIDs, the oral test was not carried out.

A total of 150 healthy volunteers were selected as a control population from various sources, including neighbors of patients (n=112), relatives of the staff members (n=10), and the blood donor population (n=28). The control subjects had never had any episode of breathlessness and/or wheezing and had never used asthma medication.

All subjects lived in the area surrounding the hospital with a very homogeneous middle-class population.

Only subjects (patients and healthy volunteers) from the native population were included in the study. Smokers, subjects receiving vitamin supplements, or those who were on an exclusion diet were excluded.

A total of 118 patients and 121 subjects met all the inclusion criteria and agreed to participate in the study. The subjects gave informed consent to the study, which was approved by the ethics committee of the institution.

The skin prick test was performed with common allergens (Dermatophagoides pteronyssinus, D. farinae, cat, dog, grass-pollen mixture, tree-pollen mixture, Parietaria judaica, Aspergillus fumigatus, Alternaria tenuis, and cockroach) (Ifidesa-Arístegui, Bilbao, Spain). Histamine (10 mg/ml) and glycerol were used as positive and negative controls. A skin prick reaction was regarded as positive if the wheal size was over 3 mm. Subjects were considered to be atopic if they had a positive reaction to any of the allergens in the testing panel.

 

Food frequency questionnaire

All subjects completed a food frequency questionnaire (FFQ). We used a 150-item semiquantitative FFQ to assess usual dietary intake over the previous 6 months. A trained dietitian who was unaware of the subjects’ characteristics administered the FFQ to all the subjects. Micronutrient/antioxidant intake was computed from the reported frequency of consumption of each specified unit of food or beverage, and from published data on the micronutrient/antioxidant content of the specified portions. To help the subjects to quantify food consumption, the dietitian used photographs of servings with six progressive portions of the reported consumed foods.

Biochemical measurements

A fasting 100-ml sample of venous blood was taken between 8 and 9 a.m. Serum α-tocopherol (vitamin E) was measured by high-performance liquid chromatography (HPLC), by the method of Shearer (16). Serum retinol (vitamin A) was measured by HPLC by the method of Catigiani & Bieri (17). Whole-blood total ascorbic acid (vitamin C), which includes ascorbic and dehydroascorbic acid, was measured by HPLC by the method of Speek et al. (18). Methods for vitamin measurements were initially calibrated with the standard reference material 968b for fat-soluble vitamins, from the National Institute for Standards and Technology (NIST) (Gaithersburg, MD, USA), and were periodically controlled by participation in the Micronutrients Measurement Quality Assurance Program, also from the NIST.

Serum selenium concentration was determined by the direct electrothermal atomic absorption spectrophotometric method with palladium as matrix modifier. We used a Perkin-Elmer 3030 spectrometer, HGA-600 fur-nace and AS-60 automatic sampler. The L’vov platform, Zeemand background correction, and other specifications of the STPF (stabilised temperature platform furnace) concept were followed (19). Within-day precision, between-day precision, and the accuracy of the method were confirmed by the analysis of Standard Reference Material SERONORMTR (selenium certified value=86 µg/l).

Zinc was measured by atomic absorption spectrophotometry.

Platelet GSH-Px activity was determined by a spectrophotometric assay based on the oxidation of NADPH, by a method previously described in detail elsewhere (20).

Statistics

Dietary intake of selenium, vitamin A, vitamin C, and magnesium was skewed; therefore, a logarithmic trans-formation was applied to the data before formal analy-sis. However, summary statistics are reported in the original scale in the text and the tables. Serum vitamin E values were adjusted for total cholesterol (μM vitamin E: mM total cholesterol). Dietary information was analyzed by the method of Willett (21). Correlation between dietary and serum vitamin levels was tested by simple Pearson correlation analyses with crude values. Means of dietary intake and biochemical measurements (adjusted to total energy intake) were compared between patients and controls, and between the four groups of patients, by an ANOVA model adjusting for age and sex. Results were considered statistically significant if the observed two-sided significance level (P value) was not greater than 0.05. Values in the test and tables are means±SEM. Statistical analysis was carried out using SPSSWIN 6.1.3 statistical software (SPSS, Inc., 1989–95).

We calculated the empirical power of the study, defined as the percentage of significant tests over 1000 samples, by bootstrapping (22).

Jump to…

Results

  1. 1.   Top of page
  2. 2.   Abstract
  3. 3.   Material and methods
  4. 4.   Results
  5. 5.   Discussion
  6. 6.   Acknowledgments
  7. 7.   References

 

Demographic and clinical characteristics

Demographic characteristics were similar in patients with asthma and control subjects (Table 1). The distrib-ution of patients as regards severity is shown in Table 2. Patients from group 1 were significantly (ANOVA, P<0.01) younger than those with moderate (groups 2 and 3) and severe asthma (group 4).

Table 1.  Demographic data from patients and controls expressed as mean±SEM (range), P value

 

Asthma

Controls

P

n 118 121  
Sex (M/F) 48/70 45/76 NS
Age (years) 41.6±1.4 (16–72) 38.8±1.3 (17–74) NS
Weight (kg) 65.8±1.2 (40–101) 66.2±1.3 (45–98) NS
Height (cm) 164.0±0.8 (146–186) 164.8±1.0 (150–188) NS
Table 2.  Demographic data from asthmatic patients according to severity expressed as mean±SEM (range), P value, ANOVA

Severity

1

2

3

4

P

  1. * Groups 1, 2 vs 4.
n 30 40 24 24  
Age (years) 29.5±2.2 (16–63) 40.8±2.2 (19–72) 47.2±2.9 (19–67) 50.4±2.3 (44–99) <0.05*
Weight (kg) 63.0±2.6 (44–99) 64.8±2 (47–101) 65.9±1.7 (48–79) 70.2±3 (40–96) NS
Height (cm) 165.8±1.6 (150–182) 163.7±1.6 (148–186) 161.7±1.7 (146–180) 165.0±1.9 (148–186) NS
FEV1 (%) 86.0±1.1 (80–93) 83.0±1.01 (77–91) 74.0±1.2 (62–86) 62.0±2.1 (46–75) <0.05*
FVC (%) 91.0±1.3 (82–101) 87.0±0.9 (81–95) 84.0±1.2 (75–94) 78.0±1.9 (68–88) <0.05*
Atopy (%) 67 61 59 39 <0.05*
                 

In group 1, there were no patients on inhaled corticosteroids. In group 2, 22 out of 40 patients were on inhaled corticosteroids (180±100 mg/day, range 0–400 for 11±19 months). Seventeen out of 24 patients in group 3 were on inhaled corticosteroid therapy (380± 260 mg/day, range 0–800 for 10±15 months), and 19 out of 24 patients in group 4 were on this therapy (1060± 380 mg/day, range 800–2000, for 9±16 months). The mean dose of inhaled corticosteroids was significantly higher (P<0.05) in groups 3 and 4 than in group 2. The difference was also significantly different (P<0.05) between groups 3 and 4. Patients from group 4 had a significantly lower FEV1 (ANOVA, P<0.001) and FVC (ANOVA, P<0.01) than those from groups 1 and 2 (Table 2).

The prevalence of atopy defined according to the results of the prick test was significantly higher in groups 1 (67%) and 2 (61%) with respect to group 4 (39%) (Table 2).

Eighteen patients were aspirin-intolerant. They all belonged to groups 3 (14 patients) and 4 (four patients).

Only patients from group 4 were on regular oral cor-ticosteroid therapy (mean 11.5 mg/day, range 5–20 mg/day) or were receiving frequent short courses of oral steroids.

Food frequency questionnaire

The daily micronutrient/antioxidant intakes are given by asthma and control groups in Table 3. No differences in daily micronutrient/antioxidant intake were seen between patients and healthy subjects.

Table 3.  Daily micronutrient/antioxidant intake (crude values) for patients and controls, mean±SEM. ANOVA adjusted for total energy intake, sex, and age

 

Patients

Controls

P

Magnesium (mg/day) 330.0±120   363.0±168  NS
Zinc (mg/day)    10.0±3    11.0±3.3  NS
Selenium (μg/day)   73.0±20     78.0±35  NS
Vitamin A (μg/day) 882.0±685   827.0±704  NS
Vitamin C (mg/day)   159.0±75    165.0±98 NS
Vitamin E (mg/day)   6.7±2   6.7±2.4   NS

No differences in micronutrient/antioxidant intake were found between the four groups of asthma patients (Table 4).

Table 4.  Daily micronutrient/antioxidant intake (crude values) for patients according to severity. Mean±SEM. ANOVA adjusted for total energy intake, sex, and age

 

Severity

 

1

2

3

4

P

Patients (n) 30   40 24 24  
Magnesium (mg/dl) 358.0±155  321.0±78 336.0±153 328.0±69 NS
Selenium (mg/day) 79.0±17   68.0±16 67.0±16 75.5±27 NS
Zinc (mg/day) 11.3±3.6   9.9±2.4 9.6±2.2 10.3±3.4 NS
Retinol (vitamin A) (μg/day) 1005.0±981 673.2±419 990.0±581 968.0±658 NS
Vitamin C (mg/day) 177.0±76   147.0±69.9 162.0±82  152.0±74 NS
Vitamin E (mg/day)  7.6±1.8       6.4±1.8   6.5±2.0 6.4±2.1 NS

No differences in the characteristics of micronutrient/antioxidant intake were found between atopic and nonatopic subjects after adjusting by age and sex (data not shown).

The empirical power of the study calculated by bootstrapping ranged from low levels for vitamin E (12%, 95% confidence interval 9–16) to moderate levels for vitamin C (42%, 95% confidence interval 36–46).

 

Biochemical measurements

There were no differences in plasma/serum levels in any of the micronutrients/antioxidants between healthy subjects and asthmatics (Tables 5 and 6). Nor were any differences found between asthma groups as regards severity in the biochemical measurements, except in platelet GSH-Px activity (ANOVA, P<0.05), which was significantly lower in the most severe groups (groups 3 and 4).

Table 5.  Plasma/serum values in patients and controls. Results are presented as mean±SEM. ANOVA adjusted for sex and age

 

Patients

Controls

P

Magnesium (mg/dl) 2.0±1.2   2.0±1.1   NS
Zinc (mg/dl)  78±16     80±13    NS
Selenium (μg/dl) 79.0±1.1  77.5±2.7  NS
Vitamin A (μg/dl)  73±25     72±24    NS
Vitamin C (μmol/l)  54±17     58±19    NS
Vitamin E (μmol/l)    28±7      29±7   NS
Vitamin E/Chol (mmol/mg) 0.13±0.01 0.14±0.01 NS
GSH-Px (mU/109 platelets) 156.9±5.2 145.4±6.2 NS
Table 6.  Plasma/serum values in patients according to disease severity. Mean±SEM

 

Severity

 

1

2

3

4

P

  1. * Groups 1 and 2 vs 3 and 4. ANOVA adjusted for sex and age.
n 30 40 24 24  
Magnesium (mg/dl) 2.0±0.2 2.0±0.2 2.0±0.1 2.0±0.2 NS
Zinc (mg/dl) 84.0±14 77.0±18 77.0±16 75.0±11 NS
Selenium (μg/dl) 77.5±2.7 76.5±2.2 77.1±3.1 79.9±3.1 NS
Retinol (vitamin A) (μg/dl) 82.0±23 76.0±19 77.0±27 75.0±33 NS
Vitamin C (mmol/l) 53.0±16 53.0±6 55.0±17 50.0±25 NS
Vitamin E (mmol/l) 26.0±7 28.0±6 29.0±9 30.0±8 NS
GSH-Px (mU/109 platelets) 162.5±9.3 152.7±11.1 125.0±13.4 122.5±16 0.03*
                 

Aspirin-intolerant patients did not show any signifi-cant difference in micronutrients/antioxidants, either in dietary intake or biochemical measurements, in comparison with aspirin-tolerant patients.

Correlations between food frequency questionnaire and biochemical measures

Correlation between vitamin C intake and blood levels was statistically significant between crude values (r=0.47, P<0.001). After adjustment by total energy intake, the correlation coefficient between vitamin C intake and blood levels was 0.099 (95% confidence intervals, 0.067–0.131). This means that the relationship between vitamin C intake and blood levels was 1/100 (for each 100 units of ingested vitamin C, the blood level increased by 1 unit). No correlation was found between dietary values (crude and total energy adjusted) and biochemical measures of α-tocopherol, retinol, selenium, magnesium, and zinc.

Jump to…

Discussion

  1. 1.     We investigated differences in dietary micronutrient/antioxidant intake between asthmatics and nonasthmatics. Only patients with clearly defined asthma and with diets not compromised by food supplementation or avoidance were included. The usual dietary intake was measured by an FFQ. FFQs have been found to relate well to more detailed methods of dietary evaluation (21).

The FFQ-estimated intake of vitamin C was correlated with blood concentration (r=0.47). However, we did not find any correlation between dietary nutrient intake and biochemical measurements with the other tested micronutrients/antioxidants. This is in keeping with previous studies, which have generally shown little or no correlation between dietary intake evaluation and biochemical quantification of these micronutrients/antioxidants (21, 23). Significant correlations are more often found in studies in which at least some of the recruited subjects are on supplemented diets (23). However, in our study, these subjects were excluded. Moreover, there are two reasons to explain why plasma/serum levels of micronutrients/antioxidants may not be correlated with dietary intake:

  • ·       a single plasma/serum measurement of a micronutrient may be a poor marker of long-term intake detected by FFQ
  • ·       plasma/serum levels of some micronutrients/antioxidants do not always reflect the level of their stores (liver, skeleton, and kidney).

We found no evidence of any association between either dietary intake or plasma/serum levels of micronutrients/antioxidants and asthma. Nor did we find evidence that the severity of the disease has any influence on the plasma/serum levels of these substances.

According to our results, no relationship exists between asthma and retinol intake. Troisi et al. (24) found that vitamin E may have a modest effect on the incidence of asthma. We did not find any difference in either vitamin E intake or serum levels between asthma patients and nonasthmatic controls.

Some studies have reported short-term effects of vitamin C in the bronchoprovocation test and improvements in the lung-function test (25), but a beneficial effect of vitamin C was not detected in other studies (26). Olusi et al. (27) and Aderele et al. (28) found significantly higher plasma concentrations of vitamin C in controls than in asthma patients. However, no relationship was detected between vitamin C levels and asthma severity. In contrast, Troisi et al. (24) found no relationship between vitamin C intake and the subsequent development of asthma in women. Nor could Cook et al. (29) find any relationship between plasma vitamin C levels and wheezing.

Selenium is an essential component of glutathione peroxidase

Selenium is an essential component of glutathione peroxidase (GSH-Px), which reduces hydrogen peroxidase and other organic peroxides to nontoxic substances. Studies performed to determine a possible relationship between selenium levels and asthma have yielded contradictory results. Stone et al. (13) found that patients with asthma have lower concentrations of selenium in plasma and whole blood, but not in platelets, than controls. However, there was no concomitant reduction in GSH-Px activity in whole blood or platelets. In contrast, Flatt et al. (10) found that in whole blood, but not in plasma, selenium concentration and GSH-Px activity were lower in asthmatics than in healthy subjects. Similarly, reduced platelet GSH-Px activity was found by Misso et al. (11) in patients with asthma. Pearson et al. (12) found that aspirin-tolerant asthmatics had higher serum selenium concentrations than either aspirin-intolerant patients or control subjects. However, only aspirin-intolerant patients with asthma were found to have reduced platelet GSH-Px activity. In contrast, Plaza et al. (20) could not find any significant difference between platelet GSH-Px activity in aspirin-intolerant asthmatics and that in either aspirin-tolerant patients or healthy subjects. It has been suggested that GSH-Px levels may reflect the intensity of the inflammatory activity in asthma. Bibi et al. (30) demonstrated a close correlation between asthma severity and erythrocyte GSH-Px activity. Similarly, Pearson & Suarez-Mendez (31) also observed that platelet GSH-Px activity was lower in patients with severe asthma than in those with mild asthma. In keeping with this study, we found that platelet GSH-Px activity was significantly lower in patients with the most severe asthma. Since all these studies were cross-sectional, they could not determine whether the low platelet GSH-Px activity is responsible for asthma severity or is merely the consequence of an increased consumption of antioxidants in patients with a more active inflammatory process. In any case, the restoration of normal GSH-Px activity by increasing selenium intake might be a therapeutic alternative in asthma. Hasselmark et al. (32) found that selenium supplementation improved clinical symptoms in asthma patients, suggesting that the restoration of GSH-Px may improve control of bronchial inflammation.

Although Britton et al. (33) found that dietary intake of magnesium was related to lung function, airway hyperreactivity, and self-reported wheezing in the gen-eral population, we could not find any difference, either in dietary intake or magnesium serum levels, between patients and healthy subjects. Like us, de Valk et al. (34), and Falker et al. (35) did not find any magnesium deficiency in asthmatics with respect to nonasthmatics, nor did the severity of the disease correlate with serum magnesium levels (35).

The statistical power of our study was low to moder-ate (20–40%). Therefore, the lack of statistically signifi-cant differences in micronutrient/antioxidant intake between asthma and controls may have resulted from the study’s being underpowered, resulting in a type 1 error.

The possible relationship between asthma and dietary intake of micronutients has been deduced from studies which investigated the prevalence of wheezing (3, 4, 8, 33) or the presence of bronchial hyperresponsiveness (5). However, up to 10% of normal subjects are hyper-responsive to bronchoconstrictor stimuli, and wheezing is more prevalent than asthma in the general population (36).

A reduced intake of vitamins A, E, or C is associated with an increased level of airflow obstruction (6–9). Since subjects with nonasthmatic airflow limitation demonstrate histamine or methacholine airway hyperresponsiveness (37), it may well be that a reduced vita-mins A, E, or C intake may predispose to bronchial hyperresponsiveness, simply by reducing airway diameter rather than by inducing asthma.

If the important question is to know whether or not changes in the diet are associated with asthma, it seems more logical to investigate the relationship of diet and asthma than the association of dietary intake and indicators of asthma such as wheezing and hyperresponsiveness.

In summary, we could not find any association bet-ween micronutrient/antioxidant intake or plasma/serum levels of micronutrients/antioxidants and asthma. Re-duction of platelet GSH-Px activity in the most severe patients suggests that their capacity to restore part of the antioxidant defences is diminished.

Acknowledgments

 

This study was supported by grants from Fondo de Investigaciones Sanitarias (FIS-92/698 and 94/337), Sociedad Española de Neumo-logía y Cirugía Torácica (SEPAR), and CIRIT (1998GR-00112). J.M. was supported in part by a grant from Ministerio de Educación y Ciencia (Spain).

References

  1. 1.    
  • ·       1

Monteleone CA, Sherman AR. Nutrition and asthma. Arch Intern Med 1997;157:23–34.

Hatch GE. Asthma, inhaled oxidants, and dietary antioxidants. Am J Clin Nutr 1995;61 Suppl 3:625S–630S.

  • ·       3

Schwartz J, Weiss ST. Dietary factors and their relationship to respiratory symptoms: the second National Health and Nutrition Examination Survey. Am J Epidemiol 1990;132:67–76.

Bodner G, Godden D, Brown K, Little J, Ross S, Seaton A. Antioxidant intake and adult-onset wheeze: a case-control study. Eur Respir J 1999;13:22–30.

Soutar A, Seaton A, Brown K. Bronchial reactivity and dietary antioxidants. Thorax 1997;52:166–170.

Britton JR, Pavord ID, Richards HA, et al. Dietary antioxidant vitamin intake and lung function in the general population. Am J Respir Crit Care Med 1995;151:1383–1387.

Schwartz J, Weiss ST. The relationship of dietary vitamin C intake to level of pulmonary function in the First National Health and Nutrition Survey (NHANES I). Am J Clin Nutr 1994;59: :110–114.

Dow L, Tracey M, Villar A, et al. Does dietary intake of vitamins C and E influence lung function in older people? Am J Respir Crit Care Med 1996;154:1401–1404.

Morabia A, Serenson A, Kumanyiki S, et al. Vitamin A, cigarette smoking and airway obstruction. Am J Respir Crit Care Med 1989;140:1312–1316.

Flatt A, Pearce N, Thomson CD, Sears MR, Robinson MF, Beasley R. Reduced selenium in asthmatic subjects in New Zealand. Thorax 1990;45:95–99.

Misso NL, Powers KA, Gillon RL, Stwart GA, Thompson PJ. Reduced platelet glutathione peroxidase activity and serum selenium concentration in atopic asthmatic patients. Clin Exp Allergy 1996;26:838–847.

Direct Link:

Pearson DJ, Suarez-Mendez VJ, Day JP, Miller PF. Selenium status in relation to reduced glutathione peroxidase activity in aspirin-sensitive asthma. Clin Exp Allergy 1991;21:203–208.

Direct Link:

Stone J, Hinks LJ, Beasley R, Holgate ST, Clayton BA. Reduced selenium status of patients with asthma. Clin Sci 1989;77:495–500.

Picado C, Deulofeu R, Lleonart R, et al. Lipid and protein metabolism in asthma. Effects of diet and cortico-steroid therapy. Allergy 1999;55:569–575.

Direct Link:

Global Initiative for Asthma. Global strategy for asthma management and prevention. NHLBI/WHO workshop. National Institutes of Health, National Heart, Lung and Blood Institute 1995, Publication no. 95;3659:1–176.

  • ·       16

Shearer MJ. Vitamin E. In: CK LIM, editor. HPLC of small molecules. London: Oxford University Press, 1986: 177–182.

  • ·       17

Catigiani GL, Bieri JG. Measurement of serum retinol by high performance liquid chromatography. Clin Chem 1983;29:708–712.

Speek AJ, Schrijver J, Schreurs WHP. Measurement of total ascorbic acid in biological fluids. J Chromatogr 1984;305:53–59.

Van Cauwenberg R, Robberecht H, Van Dael P, Deelstra H. Direct selenium determination in human whole blood by graphite furnace atomic absorption spectrometry with deuterium correction using a L’vov platform, a Pd/Mg matrix modification and appropriate dilution. J Trace Elem Electrolytes Health Dis 1990;4:127–131.

Plaza V, Prat J, Rossello J, et al. In vitro release of arachidonic acid metabolites, glutathione peroxidase, and oxygen-free radicals from platelets of asthmatic patients with and without aspirin intolerance. Thorax 1995;50:490–496.

Willett WC. Nutritional epidemiology. New York: Oxford University Press, 1990.

  • ·       22

Bradly E, Tibshirani RJ. An introduction to Bootstrap. New York: Chapman & Hall, 1993.

  • ·       23

Jacques PF, Sulsky SI, Sadowski JA, Phillips JCC, Rush D, Willett WC. Comparison of micronutrient intake measured by a dietary questionnaire and biochemical indicators of micro-nutrient status. Am J Clin Nutr 1993;57:182–189.

Troisi RJ, Willett WC, Weiss ST, Trichopoulos D, Rosner B, Speizer FE. A prospective study of diet and adult-onset asthma. Am J Respir Crit Care Med 1995;151:1401–1408.

Cohen HA, Neuman I, Nahum H. Blocking effect of vitamin C in exercise-induced asthma. Arch Pediatr Adolesc Med 1997;151:367–370.

Malo JL, Cartier A. Lack of acute effects of ascorbic acid on spirometry and airway responsiveness to histamine in subjects with asthma. J Allergy Clin Immunol 1986;78:1153–1158.

Olusi SO, Ojutiku OO, Jessop WJE, Iboko MI. Plasma and white blood cell ascorbic acid concentrations in patients with bronchial asthma. Clin Chim Acta 1979;92:161–166.

Aderele WR, Ette SI, Oduwoule O, Ikpeme SJ. Plasma vitamin C (ascorbic acid) levels in asthmatic children. Afr J Med Sci 1985;14:115–120.

  • o            CAS
  • ·       29

Cook DG, Carey IM, Whincup PH, et al. Effect of fresh fruit consumption on lung function and wheeze in children. Thorax 1997;52:628–633.

Bibi H, Schlesinger M, Tabachnik E, Schwartz Y, Iscovitz H, Iaina A. Erythrocyte glutathione peroxidase activity in asthmatic children. Ann Allergy 1988;61:339–340.

Pearson J, Suarez-Mendez J. Abnormal platelet hydrogen peroxide metabolism in aspirin hypersensitivity. Clin Exp Allergy 1990;20:157–163.

Direct Link:

Hasselmark L, Malmgren R, Zetterström O, Unge G. Selenium supplementation in intrinsic asthma. Allergy 1993;48:30–36.

Britton J, Pavord I, Wisniewski A, et al. Dietary magnesium, lung function, wheezing, and airway hyperreactivity in a random adult population. Lancet 1994;344:357–362.

De Valk HW, Kok PT, Struyvenberg A, et al. Extracellular and intracellular magnesium concentrations in asthmatic patients. Eur Respir J 1993;6:1122–1125.

Falker D, Glauser J, Allen M. Serum magnesium levels in asthmatic patients during acute exacerbations of asthma. Am J Emerg Med 1992;10:1–3.

Cockcroft DW. Airway hyper-responsiveness. Relevance of random population data to clinical usefulness. Am Rev Respir Dis 1990;142:497–500.

Ramsdale EH, Morris MM, Roberts RS, Hargrave FE. Bronchial responsiveness to methacholine in chronic bronchitis: relationship to airflow obstruction and cold air responsiveness. Thorax 1984;39:912–918.

Get PDF (82K)

—-

Vitamina D em medicina preventiva: estamos ignorando as provas?

A vitamina D em medicina preventiva: estamos ignorando as provas?

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.
Calcitriol receptors are present in more than thirty different tissues. Receptores de calcitriol estão presentes em mais de trinta diferentes tecidos. Apart from the kidney, several tissues also possess the enzyme 1alpha-hydroxylase, which is able to use circulating 25(OH)D as a substrate. Para além do rim, vários tecidos também possuem a enzima 1alpha-hidroxilase, que é capaz de usar circulam 25 (OH) D como substrato. Serum levels of 25(OH)D are the best indicator to assess vitamin D deficiency, insufficiency, hypovitaminosis, adequacy, and toxicity. Os níveis séricos de 25 (OH) D é o melhor indicador para avaliar a deficiência de vitamina D, insuficiência, hipovitaminose, adequação e toxicidade.
European children and young adults often have circulating 25(OH)D levels in the insufficiency range during wintertime. Crianças europeias e adultos jovens têm frequentemente circulam 25 (OH) níveis de D na faixa de insuficiência durante o inverno.Elderly subjects have mean 25(OH)D levels in the insufficiency range throughout the year. Idosos têm média de 25 (OH) níveis de D na faixa de insuficiência longo do ano. In institutionalized subjects 25(OH)D levels are often in the deficiency range. Em indivíduos institucionalizados 25 (OH) níveis de D são freqüentemente na faixa de deficiência. There is now general agreement that a low vitamin D status is involved in the pathogenesis of osteoporosis. Há agora um acordo geral de que o baixo status da vitamina D está envolvida na patogênese da osteoporose. Moreover, vitamin D insufficiency can lead to a disturbed muscle function. Além disso, a insuficiência de vitamina D pode levar a uma função muscular perturbado. Epidemiological data also indicate a low vitamin D status in tuberculosis, rheumatoid arthritis, multiple sclerosis, inflammatory bowel diseases, hypertension, and specific types of cancer. 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.Some intervention trials have demonstrated that supplementation with vitamin D or its metabolites is able: (i) to reduce blood pressure in hypertensive patients; (ii) to improve blood glucose levels in diabetics; (iii) to improve symptoms of rheumatoid arthritis and multiple sclerosis. Alguns estudos de intervenção têm demonstrado que a suplementação com vitamina D ou seus metabólitos é capaz: (i) reduzir a pressão arterial em pacientes hipertensos, (ii) para melhorar os níveis de glicose no sangue em diabéticos, (iii) para melhorar os sintomas da artrite reumatóide e esclerose múltipla .The oral dose necessary to achieve adequate serum 25(OH)D levels is probably much higher than the current recommendations of 5-15 microg/d. A dose oral necessária para atingir adequado soro 25 (OH) níveis de D é provavelmente muito maior do que as atuais recomendações de 5-15 microg / d.PMID: 12720576 [PubMed – indexed for MEDLINE]
Related articles Artigos relacionados
Dispoível em

Vitamina B2 ajuda a combater Parkinson, mostra pesquisa

Vitamina B2 ajuda a combater Parkinson, mostra pesquisa

26/05/2003 – 10h36

da France Presse, em Brasília

Reverter o mal de Parkinson, revela um estudo conduzido na Universidade Federal de São Paulo (Unifesp).

Doses elevadas de vitamina B2, ou riboflavina, aliadas à retirada de carne vermelha do cardápio, ajudam a reverter o mal de Parkinson, revela um estudo conduzido na Universidade Federal de São Paulo (Unifesp).

De acordo com a pesquisa, os pacientes que seguiram esse molde de dieta recuperaram em média 18% de suas funções motoras no primeiro mês, 39% no segundo e 62% no terceiro mês de tratamento.

O estudo começou em setembro, com um número reduzido de pacientes do Hospital Municipal dos Funcionários Públicos. Segundo o professor do Departamento de Neurologia da Unifesp e responsável pelo estudo, Cícero Galli Coimbra, a pesquisa começou depois de ficar comprovado que 100% dos portadores de Parkinson apresentavam no organismo um nível baixo de vitamina B2 –necessária para o processo de respiração celular e responsável por mais de cem reações químicas.

A carne vermelha dificulta a absorção da vitamina B2. Aqueles que estavam na fase avançada da doença recuperaram boa parte de suas funções motoras, e alguns já conseguem dirigir, disse o professor. Os dados preliminares da pesquisa foram apresentados no 6º Congresso Internacional sobre doença de Alzheimer e Parkinson, realizado em Sevilha, Espanha, no começo do mês.

O mal de Parkinson surge quando 60% das células nervosas da região do cérebro responsável pelas funções motoras estão prejudicadas. O leite é um dos alimentos com maior concentração de vitamina B2.

disponivel em

http://www.doencadeparkinson.com.br/b2.htm

Dieta especial pode regredir Parkinson

Dieta especial pode regredir Parkinson
17 de Junho de 2003 (Bibliomed)

Dieta especial pode regredir Parkinson

Uma simples alteração na dieta de portadores da doença de Parkinson – tirar a carne vermelha e incluir vitamina B2, encontrada principalmente no leite – é capaz não apenas de estagnar a doença como também de regredi-la. Um estudo realizado na Universidade Federal de São Paulo constatou que a recuperação da função motora de 31 pacientes em tratamento no Hospital do Servidor Público Municipal saltou, em média, de 44% para 70% em apenas três meses de tratamento e dieta.

“Os melhores resultados são encontrados nos pacientes que estão nas fases iniciais da doença. Entretanto, existem casos de pessoas que se tratam há muito tempo e que tiveram uma melhora na função motora de 15% para 90% após a intervenção”, disse o pesquisador Cícero Galli Coimbra, que é neurologista e professor livre-docente de Neurologia Experimental da Unifesp. Os dados preliminares da pesquisa foram apresentados no 6º Congresso Internacional sobre doença de Alzheimer e Parkinson, realizado em Sevilha, Espanha, no começo de maio.

O pesquisador explica que é do conhecimento médico que a carne vermelha produz uma substância chamada hemina, extremamente tóxica para as células do organismo, originando a produção de radicais livres. “Para serem eliminados, esses radicais livres precisam de uma substância chamada glutationa que, depois de utilizada, só pode ser recuperada com vitamina B2. A falta da glutationa é a primeira alteração neuroquímica presente nas células cerebrais que estão degenerando com a doença de Parkinson”, explicou.

Com a reposição da vitamina, Coimbra esperava que a doença parasse de progredir, mas ela começou a regredir. O neurologista ainda não sabe explicar se esse fenômeno se deve à neurogênese (processo que leva à formação do sistema nervoso) ou à recuperação de células que não funcionavam, mas encontravam-se ainda vivas na substância negra do encéfalo, principal região afetada pelo processo neurodegenerativo. “De qualquer forma, o nível de recuperação alcançado em tão pouco tempo é surpreendente, pois estima-se que cerca de 60% das células dessa região já foram perdidas quando surgem os primeiros sintomas”, comemorou.

A doença de Parkinson é uma alteração do sistema nervoso central que afeta principalmente o sistema motor, provocando tremores, rigidez muscular e alterações posturais, além de comprometimento de memória, depressão e alterações do sono. Segundo o neurologista João Carlos Papaterra Limongi, do Departamento de Neurologia do Hospital das Clínicas da Universidade de São Paulo, apenas 5% dos portadores da doença apresentam forte componente hereditário. Em 20% dos casos é possível identificar uma causa medicamentosa, tóxica, infecciosa ou traumática para o desenvolvimento da doença. Os 75% restantes ainda desafiam a ciência a descobrir a causa.

Deixar de comer carne vermelha ajuda a tratar Parkinson, diz estudo

Deixar de comer carne vermelha ajuda a tratar Parkinson, diz estudo

25/09/2003 – 13h50
Deixar de comer carne vermelha ajuda a tratar Parkinson, diz estudo
da Folha Online

Cortar todos os tipo de carne vermelha na alimentação faz com que pessoas afetadas pelo mal de Parkinson aumentem a recuperação de suas funções motoras de 44% para 71%, segundo uma pesquisa desenvolvida pela Unifesp (Universidade Federal de São Paulo).

O estudo, realizado por Cícero Galli Coimbra, professor do Departamento de Neurologia e Neurocirurgia da universidade, e por Virgínia Junqueira, do Centro de Estudos do Envelhecimento da mesma instituição, foi publicado na edição de outubro do “Brazilian Journal of Medical and Biological Research” e incluiu ainda a utilização de doses de 30 miligramas de riboflavina, ou vitamina B2, a cada oito horas.

O consumo de carne vermelha gera toxinas no corpo humano, que produzem alguns tipos de radicais livres. A eliminação desses elementos, que atacam as células, ocorre por meio de uma substância chamada glutationa, cuja recuperação natural depende da vitamina B2. Em pacientes com mal de Parkinson, os níveis de riboflavina são baixos.

Resultados

O estudo foi feito com um grupo de 19 pessoas (8 homens e 11 mulheres), que cortaram a carne vermelha de suas dietas e tomaram a vitamina por seis meses, ao mesmo tempo em que continuavam a utilizar seus remédios para controlar o mal de Parkinson.

Um mês depois de iniciado o estudo, o grupo já tinha níveis normais de riboflavina no sangue. Seis meses depois do início, os paciente tiveram uma estagnação dos sintomas da doença e apresentaram melhora motora expressiva.

Com os resultados, os pesquisadores pretendem entender melhor como funcionam os mecanismos sensíveis à vitamina B2 dentro do corpo e aplicar esse conhecimento no tratamento da doença.

As informações são da Agência Fapesp

http://www.doutorbusca.com/artigos/showquestion.asp?faq=6&fldAuto=152

Parkinson: Um passo a favor da saude

Parkinson: Um passo a favor da saude

sexta-feira, 19 de Setembro de 2003.


Um passo em favor da saúde

20030919_160138


Os médicos brasileiros descobriram que uma dieta sem carne vermelha atenua e pode até reverter os sintomas do mal de Parkinson. A pesquisa, coordenada pela Universidade Federal de São Paulo e pelo Hospital do Servidor Público Municipal, foi divulgada hoje.

A professora aposentada cuida de suas orquídeas, caminha e sobe escadas sem perder o equilíbrio, mas até o ano passado o mal de Parkinson impedia dona Cilei Joana Favaro de levar a vida como ela gosta.

“Eu não estava conseguindo andar. Eu já não tinha mais equilíbrio. Eu consegui lavar as costas sem pedir auxílio” – contou Cilei.

Aos 73 anos dona Cecília Simões tem disposição para fazer todos os serviços da casa, mas ela também já viveu o drama da doença que degenera o cérebro e afeta os movimentos.

“Eu anda devagar. Era um desânimo enorme. Eu pensei que não iria longe” – disse. Cecília.

O que está melhorando a vida de pessoas que sofrem do mal de Parkinson é uma descoberta de médicos brasileiros que usam dieta e vitamina para atacar uma das causas da doença.

Um pesquisa com pacientes revelou que eles comiam carne vermelha em excesso e tinham deficiência de vitamina B2.

“A carne vermelha na dieta libera uma toxina que necessita da vitamina B2 para ser destruída. Não havendo vitamina B2 em quantidade adequada, essa toxina não é destruída e atinge as células cerebrais, promovendo a destruição das células que regeneram na doença de Parkinson” – explicou o coordenador da pesquisa, Cícero Gale Coimbra.

Por isso, o tratamento elimina o consumo de carne vermelha e introduz o suplemento de vitamina B2. Os pacientes que seguiram a dieta começaram a sentir os resultado em alguns meses e puderam diminuir as doses dos remédios específicos para o mal de Parkinson.

É importante observar que a dieta com vitamina B2 e sem carnes vermelhas faz efeito em pacientes com um tipo específico de mal de Parkinson. Vale sempre lembrar que antes de iniciar qualquer tratamento é preciso consultar um médico.

= abaixo está o endereço com o vídeo desse programa:

http://wm.globo.com/webmedia/windows.asx?usuario=tvgjornalismo&tipo=ondemand&path=/video/jh/20030919/CRG_mat06jh_low.wmv&ext.asx

o endereço da publicação em revista médica internacional é o que segue:
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2003001000019&lng=pt&nrm=iso

Publicada cura do Parkinson em Revista Medica Internacional

Publicada cura do Parkinson em Revista Medica Internacional


Brazilian Journal of Medical and Biological Research – <B>High doses of riboflavin and the elimination of dietary red meat promote the recovery of some motor functions in Parkinson’s disease patients</B>

Brazilian Journal of Medical and Biological Research
ISSN 0100-879X versão impressa

®carregue o artigo em formato PDF

Braz J Med Biol Res, October 2003, Volume 36(10) 1409-1417


High doses of riboflavin and the elimination of dietary red meat promote the recovery of some motor functions in Parkinson’s disease patients

C.G. Coimbra1,2 and V.B.C. Junqueira3,4

1Setor de Neurologia, Hospital do Servidor Público Municipal de São Paulo, São Paulo, SP, Brasil
2Departamento de Neurologia e Neurocirurgia, Universidade Federal de São Paulo, São Paulo, SP, Brasil
3Disciplina de Geriatria, Departamento de Medicina, Centro de Estudos do Envelhecimento, Universidade Federal de São Paulo, São Paulo, SP, Brasil
4VITÆ – Cromatografia Líquida em Análises Clínicas S/C Ltda., São Paulo, SP, Brasil

Abstract
Introduction
Patients and Methods
Results
Discussion
References
Acknowledgments
Correspondence and Footnotes


Abstract

Abnormal riboflavin status in the absence of a dietary deficiency was detected in 31 consecutive outpatients with Parkinson’s disease (PD), while the classical determinants of homocysteine levels (B6, folic acid, and B12) were usually within normal limits. In contrast, only 3 of 10 consecutive outpatients with dementia without previous stroke had abnormal riboflavin status. The data for 12 patients who did not complete 6 months of therapy or did not comply with the proposed treatment paradigm were excluded from analysis. Nineteen PD patients (8 males and 11 females, mean age ± SD = 66.2 ± 8.6 years; 3, 3, 2, 5, and 6 patients in Hoehn and Yahr stages I to V) received riboflavin orally (30 mg every 8 h) plus their usual symptomatic medications and all red meat was eliminated from their diet. After 1 month the riboflavin status of the patients was normalized from 106.4 ± 34.9 to 179.2 ± 23 ng/ml (N = 9). Motor capacity was measured by a modification of the scoring system of Hoehn and Yahr, which reports motor capacity as percent. All 19 patients who completed 6 months of treatment showed improved motor capacity during the first three months and most reached a plateau while 5/19 continued to improve in the 3- to 6-month interval. Their average motor capacity increased from 44 to 71% after 6 months, increasing significantly every month compared with their own pretreatment status (P < 0.001, Wilcoxon signed rank test). Discontinuation of riboflavin for several days did not impair motor capacity and yellowish urine was the only side effect observed. The data show that the proposed treatment improves the clinical condition of PD patients. Riboflavin-sensitive mechanisms involved in PD may include glutathione depletion, cumulative mitochondrial DNA mutations, disturbed mitochondrial protein complexes, and abnormal iron metabolism. More studies are required to identify the mechanisms involved.

Key words: Parkinson’s disease, Riboflavin, Flavin-adenine dinucleotide, Glutathione, Iron, Hemin


Introduction

During absorption of riboflavin, flavokinase phosphorylates the vitamin to yield flavin mononucleotide (FMN) that, according to the cellular requirements, is transformed into flavin-adenine dinucleotide (FAD) by FAD synthase (1,2). Progressive deficiency of riboflavin is associated with co-factor loss in a controlled manner, apparently ensuring that essential catalytic activity such as that related to aerobic metabolism is preserved (3,4).

Low riboflavin status may also result from defective absorption. In spite of an adequate dietary intake of riboflavin (FAD, vitamin B2), 10-15% of the inhabitants of London and of Florence present low activities of two riboflavin-dependent enzymes – erythrocyte glutathione reductase (EGR) and pyridoxin(pyridoxamine)-phosphate oxidase (5). The activity of both enzymes was corrected by adding their respective co-factors (FAD or FMN) to a test tube assay or by administering high doses of riboflavin (24-30 mg per day for 5-8 weeks) to the affected individuals (6). The dependency of both FMN and FAD levels on riboflavin absorption (i.e., on flavokinase activity), and the normalization of the activities of both FMN- and FAD-dependent enzymes only at a high riboflavin intake, taken together, are consistent with the expression of flavokinase isoforms with low affinity for the substrate – riboflavin (5). Anderson et al. (5) suggested that the relatively large percent of persons with altered riboflavin absorption (10-15%) may reflect the situation in the world population rather than being a feature of a particular ethnic group.

Low EGR activity may explain glutathione depletion with impaired antioxidant defense, the earliest neurochemical abnormality in Parkinson’s disease (PD), already observed in the substantia nigra before the disorder becomes clinically evident (7). Moreover, the reduced bioavailability of FMN and/or FAD may also explain the impaired oxidative metabolism of PD patients (8-10).

The first objective of the present study was to determine the status of riboflavin in PD patients. The second was to evaluate the specificity of the alterations of riboflavin status for PD by measuring the levels of vitamin B2 and of other determinants of homocystinemia (vitamins B6, B12, and folic acid) in PD patients and comparing them with those of individuals with dementia (11-13). Third, we also determined the effect of normalization of riboflavin status on the motor capacity of PD patients. Part of the data reported here, obtained during the first 3 months of treatment, were reported at the 6th International Conference on Parkinson’s and Alzheimer’s Diseases (14).


Patients and Methods

This study was approved by the Ethics Committee for Clinical Research of the Hospital do Servidor Público Municipal de São Paulo (HSPM) and informed consent was obtained from all participants or persons responsible for them.

The diagnosis of sporadic PD was made according to current criteria (15) with special care taken to exclude confounding disorders, particularly in the early stages of the disease.

Vitamin and homocysteine determinations were performed on 31 sporadic PD patients (67.5 ± 9.3 years old, 13 males and 18 females): 3, 3, 3, 8, and 14 patients were assigned, early in the morning, to stages I to V of Hoehn and Yahr (16), respectively.

Ten individuals (77.5 ± 8.8 years old, 5 males and 5 females) with dementia without stroke (DwoSt) and a low Mini-Mental score (13) were used as the control group for blood chemistry. They had no history of stroke or evidence for ischemic lesions of the brain by CT or NMRI and had been consecutively attended in the Neurology Clinic of HSPM.

Blood samples were obtained after a 10- to 12-h fast for serum assays of vitamin B12 by electrochemiluminescence immunoassay (11820753 Roche Diagnostics GmbH, Mannheim, Germany) and of homocysteine by HPLC (17). Heparinized plasma was assayed for FAD (18), vitamin B6 (19), and folic acid (20) by HPLC, as well as for the determination of the EGR-activation coefficient (EGR-AC) (21) in red blood cell lysates (22).

A food questionnaire covered the weekly dietary habits of all PD and DwoSt patients from 5 years prior to the onset of PD until the appearance of spontaneous changes associated with the onset of chewing and/or swallowing impairment or until the medical interview in the absence of these impairments. The questionnaire also evaluated the adequacy of daily vitamin intake.

All PD patients received 30 mg riboflavin orally at about 8-h intervals (90 mg/day) and their usual symptomatic medications. This dosage was used to avoid decreased absorption associated with higher doses or shorter intervals between administrations. Due to the renal excretion of riboflavin (3), the treatment was only initiated after confirmation of normal blood levels of creatinine (0.5-1.4 mg/dl). Because the PD patients had a higher consumption of red meat (beef and pork) than sex-matched controls (19 healthy non-consanguineous relatives or neighbors of similar age recruited for controlling the dietary habits), all PD patients were required to eliminate all red meat from their diets. The symptomatic drugs for PD in use included L-DOPA with carbidopa (200/50 mg tablets), L-DOPA with benserazide hydrochloride (200/50 mg tablets), biperiden (2 or 4 mg tablets), amantadine hydrochloride (100 mg tablets), selegiline (5 mg tablets), and pramipexole (0.25 or 1.0 mg tablets) taken alone or in diverse combinations. The treatment paradigm with symptomatic drugs for PD for each patient when the study began was maintained.

The motor capacities of the 19 PD patients who complied with the proposed treatment for 6 months by early August 2003 were rated monthly according to a motor function scale (Table 1), and compared with their own pretreatment values. The scale was based on that of Hoehn and Yahr (16) and new categories were added in order to detect subtle changes in the patients’ motor capacity. In addition, the presence or absence of responses to symptomatic drugs for PD is also used for more accurate characterization of the residual motor capacity of PD patients (for instance, compare the descriptions corresponding to 0 and 15% of motor capacity, Table 1). Although there are no direct validation studies of this rating system, the different levels of motor capacity in Table 1 represent a simple increase in the number of components within stages I to V of the widely employed Hoehn and Yahr system (16).

After the first month of treatment, compliance with the dietary directions and vitamin intake was determined in all patients, and the fasting plasma levels of FAD and EGR-AC values were re-evaluated in 9 of them approximately 9-12 h after the latest riboflavin dose.

The blood chemistry data obtained from both groups were compared statistically by the Student t-test and the motor function data were analyzed statistically by the Wilcoxon signed rank test, with the level of significance set at P < 0.05.


Results

Diversified food intake, including daily ingestion of milk, which is particularly rich in vitamin B2, was confirmed in all patients, with PD patients frequently declaring a strong preference for red meat. The content of the daily family meals was usually adapted to meet the high demand for red meat of most PD patients. In contrast, all 10 DwoSt patients passively accepted the family diet. The estimated red meat consumption prior to the onset of impaired chewing/swallowing by 19 PD patients (8 males and 11 females, mean age ± SD = 66.2 ± 8.6 years) at lunch and dinner within a 7-day period was significantly higher (mean consumption = 2,044 ± 1,439 g/week, range = 0-5,100 g/week) than that of their 19 diet controls (8 males and 11 females, all healthy individuals of similar social and cultural background, recruited among non-consanguineous relatives and neighbors of PD patients of similar age; mean age = 64.6 ± 11.3 years, mean consumption = 789 ± 509 g/week, range = 150-1800 g/week; P < 0.01, Mann-Whitney U-test). The calorie intake did not differ significantly between the two groups.

The basal plasma concentrations of FAD of the PD patients (100.9 ± 22 ng/ml) were significantly lower than those observed in the patients with DwoSt (128.8 ± 25.6 ng/ml, P < 0.01, Student t-test) while other determinants of homocysteine levels (pyridoxine, folic acid, and methylcobalamin) were usually within normal limits, and did not differ significantly between the two groups (Table 2). The PD group also had significantly higher EGR-AC levels than DwoSt patients (1.43 ± 0.26 vs 1.20 ± 0.11, respectively, P < 0.01, Student t-test).

It is important to point out that all 31 PD patients (including 3 newly diagnosed individuals not on symptomatic drugs for PD) but only 3 of 10 DwoSt patients had low plasma riboflavin levels. Normalization of the plasma concentrations of riboflavin and EGR-AC values was confirmed after 1 month of treatment (from 106.4 ± 34.9 to 179.2 ± 23.0 ng/ml, and from 1.40 ± 0.25 to 1.11 ± 0.08, N = 9, respectively).

About 10 to 15 days after the beginning of high-dose riboflavin treatment, PD patients often reported better (progressively less interrupted) sleep at night, improved reasoning, higher motivation, and reduced depression. Their family members usually started noticing motor improvements after 20 days of treatment, but in some cases of advanced disability the patient was able to change body position in bed at night as early as on the third day of treatment.

By the time of writing this report in August 2003, 19 PD patients (respectively, 3, 3, 2, 5, and 6 patients initially rated as stages I to V of Hoehn and Yahr (16)) had completed 6 months of treatment with riboflavin administration and dietary red meat elimination. The data in Figure 1A show that all of them improved their motor capacity during the first 3 months and most reached a plateau, while 5/19 continued to improve in the 3- to 6-month interval. Figure 1B shows that the average motor capacity for these 19 patients increased from 44 to 71%. Their motor capacity increased significantly during the first month and every month for the next 5 months of treatment compared with their own pretreatment status, demonstrating a progressive and marked improvement (P < 0.001, Wilcoxon signed rank test). The rate of motor recovery was higher in the first 3 months than in the last 3 months of treatment. No patient on high doses of riboflavin reported adverse effects.

Because they could stand and walk with improved (although still altered) balance by 2 months of treatment, two male patients (initially in stage V (16) with associated dementia and hallucinations) started striking imaginary persons and/or often attempted to leave home unaccompanied, reacting aggressively against the relative who tried to stop them. These episodes of agitation and aggressiveness were observed less often by the end of the third month of riboflavin treatment and disappeared thereafter, but caused transient concern and distress among their family members who initially regarded them as signs of neurological worsening.

Three patients (2 individuals initially in stage II and 1 in stage I of Hoehn and Yahr (16)) reached 100% motor capacity within the first 3 months of treatment (Figure 1A). Four patients had run out of riboflavin tablets for up to 7 days between two consecutive clinical appointments, but sustained the benefit already achieved by then.

Twelve of 31 patients initially assessed for riboflavin status who either did not complete 6 months of therapy or did not comply with the proposed treatment paradigm were excluded from statistical analysis.


Figure 1. Motor capacity of patients with Parkinson’s disease who received 30 mg riboflavin/8 h, orally (240 mg/day) and abstained from dietary red meat for 6 months. Motor capacity was evaluated monthly for each patient by a modification of the method of Hoehn and Yahr (16) to provide a score in percent (Table 1). A, Individual data for the evolution of motor capacity of 19 patients for 0 to 3 and 3 to 6 months of treatment. *P < 0.001 for values at 3 months (month 0) compared with those before treatment; **P < 0.05 for values at 6 months compared with those obtained at 3 months (Wilcoxon signed rank test). B, The height of the columns indicates the mean motor capacity values (see Table 1) after the indicated periods of treatment. When compared with their own basal levels (month 0), highly significant and progressively higher differences were observed for each consecutive month of treatment. *P < 0.001 (Wilcoxon signed rank test).

[View larger version of this image (29 K GIF file)]


Discussion

This study demonstrated a progressive and marked improvement of motor capacity in consecutively evaluated patients with sporadic PD who started with below normal laboratory indexes of riboflavin and who eliminated red meat from their diets while receiving high multiple daily doses of riboflavin over a period of 6 months while taking their usual symptomatic medications. The mean motor capacity of a group of 19 PD patients showed a progressive 50% recovery over a period of only 3 months – a most surprisingly high and fast improvement, considering that about 60% of nigral neurons have already been lost at the onset of manifestations of PD (15).

The initial riboflavin status was low in all 31 consecutively evaluated PD individuals, and significantly lower in PD patients compared with those with another neurodegenerative disease also associated with hyperhomocystinemia (DwoSt), suggesting that abnormal riboflavin status may be a specific feature of PD rather than a minor metabolic contributor to the degeneration of nigral neurons. Taken together with the rapid and profound neurological improvement associated with normalization of riboflavin status, this observation suggests that altered riboflavin status may be a cause of neurodegeneration in PD.

Although urinary excretion of riboflavin peaks within 1-2 h and returns to baseline within 5-6 h after a large oral dose (3), the benefit achieved did not vanish in four PD patients over a therapeutic interval of up to 7 days. This observation suggests the occurrence of steady plastic changes rather than a pharmacological effect of high-dose riboflavin treatment to account for the improved motor capacity shown in Figure 1. The steady build-up of the motor recovery observed during the first 3 months of treatment suggests that this treatment paradigm may inactivate fundamental neurodegenerative mechanisms (e.g., glutathione depletion, considered to be an early key event in the pathogenesis of PD (23,24)), possibly allowing regenerative plastic phenomena to occur.

The importance of the elimination of dietary red meat for the results reported here is not known. The content of vitamin B2 in meat in general is considerable (about 0.2 mg/100 g), and diverse cooking procedures cause only minor (7-18%) loss of this micronutrient (25). The daily requirement for individuals above the age of 14 years is £1.3 mg/day. Therefore, if the PD patients had a normal absorptive capacity for vitamin B2, their large ingestion of red meat (up to 700 g/day), associated with milk, rice and beans, fruits and vegetables, should have provided a normal riboflavin status. In contrast, 31 consecutive PD patients had laboratory evidence for riboflavin deficiency (Table 2) suggesting that patients with sporadic PD belong to the subset of the general population (10-15%) (3) that may express a flavokinase with low affinity for vitamin B2, leading to a decreased absorption.

However, the digestion of red meat releases hemin, a highly diffusible toxin that, when not properly inactivated, increases intracellular iron concentrations and enhances hydroxyl radical production (Fenton reaction). Most of the absorbed hemin is destroyed by the enzyme heme oxygenase (HO) in the digestive tract and liver (26). Because HO is oxidized during the catabolization of hemin to biliverdin, the HO molecules must be reduced through the coordinated activity of the flavoenzyme cytochrome P450 reductase for continued hemin inactivation (Figure 2) (27). Cytochrome P450 reductase is particularly sensitive to riboflavin deficiency because it requires both FMN and FAD as prosthetic groups (28). It is possible that individuals with decreased absorption of vitamin B2 may not completely inactivate high dietary levels of hemin, allowing this neurotoxic compound to reach the brain cells. Consistently, the staining for HO-1 isozyme is increased in astrocytes and reacts with neuronal Lewy bodies in the nigra of PD patients, suggesting that its overexpression may contribute to the pathological iron deposition and mitochondrial damage in PD (29). By binding glutathione (30) hemin may further decrease glutathione levels in the brains of PD patients through a direct mechanism.

Because humans lack efficient iron excretory mechanisms, iron excess is dealt with by increasing the synthesis of the iron-storage protein ferritin (31). Disturbed systemic (32) and brain (33) iron metabolism has been reported in PD, suggesting that a selective decrease in the levels of ferritin may result in an increase in intracellular free iron, thereby enhancing free radical production (34). Indeed, vitamin B2 deficiency in rodents is associated with low circulating iron concentrations, increased iron turnover and excretion into the intestinal lumen, which may occur in response to impaired ferritin synthesis (35,36). Therefore, the consistent finding of an abnormal riboflavin status in PD, as reported here, may help to explain the disturbed iron metabolism found in PD patients, with the underlying mechanisms possibly involving impaired hemin catabolism and reduced ferritin synthesis. Interestingly, the highest world prevalence of PD is found among the inhabitants of Buenos Aires (37), where the consumption of red meat is traditionally high. Similarly, the identification of high dietary animal fat as a risk factor for PD (37) may actually reflect a role of high dietary hemin in PD pathology.

Moreover, because FAD is required in the two alternative pathways of deoxynucleotide synthesis (2), DNA repair and replication are expected to be disturbed upon decreased bioavailability of riboflavin, and abnormal riboflavin status may also explain the cumulative mitochondrial DNA mutations reported in PD (38).

The present results with 19 PD patients who showed a significant improvement in motor function after treatment with riboflavin and the elimination of red meat from the diet suggest that an abnormal riboflavin status, possibly due to flavokinase deficiency, may be an essential requirement for triggering and sustaining the degeneration of dopaminergic neurons in PD. As a result of the reduced B2 bioavailability, ATP production is selectively preserved, while the less critical FAD- or FMN-dependent metabolic pathways are impaired (4). Consequently, free iron concentrations in the cytosol increase as a result of impaired ferritin synthesis and/or reduced hemin catabolism associated with hydrogen peroxide accumulation due to glutathione depletion, thereby triggering the Fenton reaction and ultimately leading to the selective formation of the potent neurotoxin 6(OH)DA in dopaminergic neurons.

Current concepts about the cause of sporadic PD suggest an inherited predisposition to environmental or endogenous toxic agents (39), and the data presented and reviewed here suggest that flavokinase deficiency should be considered in future research as a promising candidate to account for this inherited predisposition, while dietary factors such as red meat consumption may largely account for the environmental/endogenous toxicity. The administration of high doses of riboflavin combined or not with red meat elimination may be an effective therapeutic paradigm addressing the determinants of PD, capable of providing regression to earlier clinical stages, or even to the nonsymptomatic state without symptomatic drugs for PD (at least in some cases), rather than only disease stabilization or partial symptomatic relief.

Although the relentless progression of PD clearly contrasts with the results of the treatment paradigm reported here, a larger and more prolonged study is certainly required to document the steadiness and the full extent of the ongoing recovery. A scientifically desirable blinded clinical trial with a placebo would necessarily leave known riboflavin-deficient patients untreated for a long period of time, when their neurological disability may progress as a consequence of sustained loss of nigral neurons, possibly rendering the ultimate response to delayed normalization of their riboflavin levels less complete. Therefore, the need for controlled trials should be weighed ethically considering the contrast of the natural history of PD (progress of motor disability to death despite an increase in the efficacy of symptomatic drugs for PD treatment) with the outcome of the vitamin B2 treatment observed in larger and more prolonged studies without controls.


Figure 2. Dependency of hemin catabolism on riboflavin bioavailability. The elimination of hemin requires cyclic reduction of heme oxygenase by flavoprotein cytochrome P450 reductase that, in turn, utilizes both flavin mononucleotide (FMN) and flavin-adenine dinucleotide (FAD) as prosthetic groups. Average or increased red meat consumption may overload the capacity of this chain of reactions already compromised by impaired intestinal absorption of riboflavin (with decreased FMN and FAD synthesis), leading to increased hemin (iron) delivery to the CNS and increased utilization of riboflavin for hemin inactivation. Modified from Figure 1, box 21-1, page 783 of Ref. 2.

[View larger version of this image (17 K GIF file)]


References

1. Brody T (1999). Nutritional Biochemistry. Academic Press, San Diego, CA, USA.

2. Nelson DL & Cox MM (2000). Lehninger Principles of Biochemistry. Worth Publishers, New York.

3. Bates CJ (1997). Bioavailability of riboflavin. European Journal of Clinical Nutrition, 51: S38-S42.

4. Ross NS & Hansen TP (1992). Riboflavin deficiency is associated with selective preservation of critical flavoenzyme-dependent metabolic pathways. Biofactors, 3: 185-190.
[ Medline ]

5. Anderson BB, Scattoni M, Perry GM, Galvan P, Giuberti M, Buonocore G & Vullo C (1994). Is the flavin-deficient red blood cell common in Maremma, Italy, an important defense against malaria in this area? American Journal of Human Genetics, 55: 975-980.
[ Medline ]

6. Anderson BB, Perry GM, Modell CB, Child JA & Mollin DL (1979). Abnormal red-cell metabolism of pyridoxine associated with beta-thalassaemia. British Journal of Haematology, 41: 497-507.
[ Medline ]

7. Dexter DT, Sian J, Rose S, Hindmarsh JG, Mann VM, Cooper JM, Wells FR, Daniel SE, Lees AJ & Schapira AH (1994). Indices of oxidative stress and mitochondrial function in individuals with incidental Lewy body disease. Annals of Neurology, 35: 38-44.
[ Medline ]

8. Schapira AH, Cooper JM, Dexter D, Clark JB, Jenner P & Marsden CD (1990). Mitochondrial complex I deficiency in Parkinson’s disease. Journal of Neurochemistry, 54: 823-827.
[ Medline ]

9. Mytilineou C, Werner P, Molinari S, Di Rocco A, Cohen G & Yahr MD (1994). Impaired oxidative decarboxylation of pyruvate in fibroblasts from patients with Parkinson’s disease. Journal of Neural Transmission. Parkinson’s Disease and Dementia Section, 8: 223-228.

10. Mizuno Y, Matuda S, Yoshino H, Mori H, Hattori N & Ikebe S (1994). An immunohistochemical study on alpha-ketoglutarate dehydrogenase complex in Parkinson’s disease. Annals of Neurology, 35: 204-210.
[ Medline ]

11. Hustad S, Ueland PM, Vollset SE, Zhang Y, Bjørke-Monsen AL & Schneede J (2000). Riboflavin as a determinant of plasma total homocysteine: effect modification by the methylenetetrahydrofolate reductase C677T polymorphism. Clinical Chemistry, 46: 1065-1071.
[ Medline ]

12. Diaz-Arrastia R (2000). Homocysteine and neurologic disease. Archives of Neurology, 57: 1422-1427.
[ Medline ]

13. Crum RM, Anthony JC, Bassett SS & Folstein MF (1993). Population-based norms for the Mini-Mental State Examination by age and educational level. Journal of the American Medical Association, 269: 2386-2391.
[ Medline ]

14. Coimbra CG & Junqueira VBC (2003). Altered riboflavin metabolism in Parkinson’s disease: Pathophysiologic and therapeutic implications. 6th International Conference AD/PD. Alzheimer’s and Parkinson’s disease: new perspectives, Seville, Spain, May 8-12. Book of Abstracts, 96.

15. Fahn S & Przedborski S (2000). Parkinsonism. In: Rowland LP (Editor), Merrit’s Neurology. Lippincott Williams & Wilkins, Philadelphia, PA, USA.

16. Hoehn MM & Yahr MD (1967). Parkinsonism: onset, progression and mortality. Neurology, 17: 427-442.
[ Medline ]

17. Pfeiffer CM, Huff DL & Gunter EW (1999). Rapid and accurate HPLC assay for plasma total homocysteine and cysteine in a clinical laboratory setting. Clinical Chemistry, 45: 290-292.
[ Medline ]

18. Speek AJ, van Schaik F, Schrijver J & Schreurs WH (1982). Determination of the B2 vitamer flavin-adenine dinucleotide in whole blood by high-performance liquid chromatography with fluorometric detection. Journal of Chromatography, 228: 311-316.
[ Medline ]

19. Sharma SK & Dakshinamurti K (1992). Determination of vitamin B6 vitamers and pyridoxic acid in biological samples. Journal of Chromatography, 578: 45-51.
[ Medline ]

20. Kelly P, McPartlin J & Scott J (1996). A combined high-performance liquid chromatographic-microbiological assay for serum folic acid. Analytical Biochemistry, 238: 179-183.
[ Medline ]

21. Sauberlich HE, Judd JH, Nichoalds GE, Broquist HP & Darby WJ (1972). Application of the erythrocyte glutathione reductase assay in evaluating riboflavin nutritional status in a high school student population. American Journal of Clinical Nutrition, 25: 756-762.
[ Medline ]

22. Beutler E (1975). The preparation of red cells for assay. In: Beutler E (Editor), Red Cell Metabolism. A Manual of Biochemical Methods. 2nd edn. Grune and Straton, New York.

23. Jenner P, Dexter DT, Sian J, Shapira AHV & Marsden CD (1992). Oxidative stress as a cause of nigral cell death in Parkinson’s disease and incidental Lewy body disease. Annals of Neurology, 32: S82-S87.

24. Schulz JB, Lindenau J, Seyfried J & Dichgans J (2000). Glutathione, oxidative stress and neurodegeneration. European Journal of Biochemistry, 267: 4904-4911.
[ Medline ]

25. Pinheiro-Sant’ana HM, Stringueta PC & Penteado MDVC (1999). Stability of B-vitamins in meats prepared by foodservice. 2. Riboflavin. Foodservice Research International, 11: 53-67.

26. Brown EB, Hwang Y-F, Nichol S & Ternberg J (1968). Absorption of radioiron-labeled hemoglobin by dogs. Journal of Laboratory and Clinical Medicine, 72: 58-64.

27. Ryter SW & Tyrrel RM (2000). The heme synthesis and degradation pathways: role in oxidant sensitivity. Heme oxygenase has both pro- and antioxidant properties. Free Radical Biology and Medicine, 28: 289-309.
[ Medline ]

28. Wang M, Roberts DL, Paschke R, Shea TM, Masters BSS & Kim J-JP (1997). Three-dimensional structure of NADPH-cytochrome P450 reductase: Prototype for FMN- and FAD-containing enzymes. Proceedings of National Academy of Sciences, USA, 94: 8411-8416.

29. Shipper HM (2000). Heme oxygenase-1: role in brain aging and neurodegeneration. Experimental Gerontology, 35: 821-830.

30. Sahini VE, Dumitrescu M, Volanschi E, Birla L & Diaconu C (1966). Spectral interferometrical study of the interaction of hemin with glutathione. Biophysical Chemistry, 58: 245-253.

31. Casey JL, Hentze MW, Koeller DM, Caughman SW, Rouault TA & Klausner RD (1988). Iron-responsive elements: regulatory RNA sequences that control mRNA levels and translation. Science, 240: 924-928.
[ Medline ]

32. Logroscino G, Marder K, Graziano J, Freyer G, Slavkovich V, LoIacono N, Cote L & Mayeux R (1997). Altered systemic iron metabolism in Parkinson’s disease. Neurology, 49: 714-717.
[ Medline ]

33. Dexter DT, Carayon A, Vidailhet M, Ruberg M, Agid F, Agid Y, Lees AJ, Wells FR, Jenner P & Marsden CD (1990). Decreased ferritin levels in brain in Parkinson’s disease. Journal of Neurochemistry, 55: 16-20.
[ Medline ]

34. Mann VM, Cooper JM, Daniel SE, Srai K, Jenner P, Marsden CD & Schapira AH (1994). Complex I, iron, and ferritin in Parkinson’s disease substantia nigra. Annals of Neurology, 36: 876-881.
[ Medline ]

35. Adelekan DA & Thurnham DI (1986). A longitudinal study of the effect of riboflavin status on aspects of iron storage in the liver of growing rats. British Journal of Nutrition, 56: 171-179.

36. Powers HJ, Weaver LT, Austin S, Wright AJ & Fairweather-Tait SJ (1991). Riboflavin deficiency in the rat: effects on iron utilization and loss. British Journal of Nutrition, 65: 487-496.
[ Medline ]

37. Tanner CM, Goldman SM & Ross GW (2002). Etiology of Parkinson’s disease. In: Jankovik JJ & Tolosa E (Editors), Parkinson’s Disease and Movement Disorders. Lippincott Williams & Wilkins, Philadelphia, PA, USA.

38. Di Monte DA (1991). Mitochondrial DNA and Parkinson’s disease. Neurology, 41: 38-42.
[ Medline ]

39. Jenner P, Shapira AH & Marsden CD (1992). New insights into the cause of Parkinson’s disease. Neurology, 42: 2241-2250.
[ Medline ]


Acknowledgments

The authors are grateful to Mr. Terence O’Reilly (Novartis, Basel, Switzerland) for his suggestions about statistical analysis.


Correspondence and Footnotes

Address for correspondence: C.G. Coimbra, UNIFESP, Rua Pedro de Toledo, 781, 7º andar, 04039-032 São Paulo, SP, Brasil. Fax: +55-11-5539-3123. E-mail: coimbracg.nexp@epm.br

Publication supported by FAPESP. Received August 13, 2003. Accepted August 27, 2003.


© 2003  Brazilian Journal of Medical and Biological Research

Av. Bandeirantes, 3900
14049-900 Ribeirão Preto SP Brazil
Tel. / Fax: +55 16 633-3825

O estresse e o mal de Parkinson

O estresse e o mal de ParkinsonUm novíssimo estudo aponta que a tensão emocional influencia no desenvolvimento dessa doença neurológica, que afeta os movimentos e causa tremores no corpo

POR CACILDA GUERRA
FOTO MÁRIO LEITE
INTERFERÊNCIA GRÁFICA MARCELO GARCIA

Um indivíduo extremamente preocupado, exigente demais consigo mesmo, que vive para o trabalho, passou por períodos de tensão prolongados ou sofreu fortes abalos emocionais: esse é o perfil mais comum do portador do mal de Parkinson, distúrbio neurológico crônico e progressivo, que prejudica os movimentos e causa tremores por todo o corpo. A descrição é feita pelo médico Cícero Galli Coimbra, professor de Neurologia Experimental da Universidade Federal de São Paulo (Unifesp), que desde 2003 coordena um estudo sobre a doença.

Em um primeiro momento, a pesquisa esteve focada em um pequeno grupo de pessoas que se tratava no Hospital do Servidor Público Municipal, na capital paulista, revelando que os pao estresse e o mal de Parkinson Um novíssimo estudo aponta que a tensão emocional influencia no desenvolvimento dessa doença neurológica, que afeta os movimentos e causa tremores no corpo cientes tinham uma deficiência de vitamina B2 no sangue e ingeriam carne vermelha em excesso. A associação desses dois fatores foi a base do tratamento, que consistiu na reposição da vitamina e na eliminação da carne e seus derivados da dieta. Após três meses, a recuperação média da função motora passou de 44% para 70%.

O estudo prosseguiu e conta hoje com cerca de 600 indivíduos. “A novidade em relação àqueles dados preliminares, a ser apresentada em junho em um congresso sobre o mal de Parkinson em Berlim, na Alemanha, é a descoberta de que o estresse emocional também é fator de risco para a doença, até mais importante que o consumo excessivo de carne vermelha”, conta o neurologista da Unifesp.

O tratamento, que agora inclui medidas de redução do estresse, como psicoterapia e incentivo para que os pacientes encarem a vida de maneira mais leve, tem dado bons resultados. Entre eles, o desaparecimento dos problemas urinários, dos pesadelos e das dificuldades de raciocínio que alguns indivíduos apresentam nos estágios finais da enfermidade. “De modo geral, os sintomas regridem até o que eram um ano antes de a pessoa começar a se tratar. Alguém que esteja doente há oito meses, por exemplo, passa a não apresentar mais nenhum sinal. Daí a importância do diagnóstico precoce”, alerta Cícero Galli Coimbra.

COMO RECONHECER
Segundo o neurologista João Carlos Papaterra Limongi, professor da Faculdade de Medicina da Universidade de São Paulo e organizador do livro Conhecendo Melhor a Doença de Parkinson(ed. Summus), é difícil para o doente e a família identificarem a época exata em que surgiu o problema, já que este começa de maneira quase imperceptível. O primeiro sintoma pode ser um dos descritos a seguir:
 Cansaço ou mal-estar no fim do dia.
 Letra menor ou menos legível.
 Fala menos articulada.
 Depressão ou vontade de se isolar, sem motivo.
 Lapsos de memória.
 Dificuldade de concentração.
 Irritabilidade.
 Dores musculares, principalmente na região lombar.
 Menos movimento em uma dos braços ou em uma das pernas.
 Piscadas pouco freqüentes.
 Expressão facial rígida, ‘congelada’.
 Lentidão nos movimentos.
 Permanência na mesma posição por muito tempo.

Tremores, movimentos lentos e fala monótona
Quando se fala em Parkinson, muita gente associa a doença apenas a tremores nas mãos. Mas ela abrange um conjunto de alterações bem mais amplo, a começar pelos tremores propriamente ditos, que podem aparecer também nas pernas, pés, cabeça, queixo e lábios. Os movimentos, por sua vez, ficam mais lentos, o que leva a pessoa a realizar as atividades comuns do dia-a-dia com menos rapidez e destreza do que quando era saudável. Como os gestos perdem a amplitude, a caligrafia diminui de tamanho. A rigidez muscular é outra manifestação do distúrbio, afetando braços, pernas e pescoço. A marcha se caracteriza por passos mais curtos que o normal e pelo arrastar dos calcanhares no chão, enquanto o corpo se inclina para a frente – e esse desequilíbrio na postura provoca quedas freqüentes. Sinais que não estão relacionados com o sistema motor também costumam surgir, como depressão, insônia, pesadelos, tonturas, cãibras nos pés, problemas urinários e dificuldades respiratórias. Além disso, a voz tende a se tornar mais fraca, e a fala, monótona.

A evolução da doença é lenta e os especialistas a dividem em cinco fases. Na primeira, aparecem tremores, rigidez muscular ou ambos em apenas um lado do corpo. Na segunda, os dois lados passam a apresentar os mesmos sintomas. Quando surge a terceira, o doente adota uma postura permanentemente curvada, perde o equilíbrio ao dar passos para trás e, quando está caminhando, não consegue mudar de direção com rapidez. A rigidez muscular na quarta fase chega a tal ponto que o indivíduo precisa de ajuda para comer e cuidar da higiene pessoal. Por fim, na última etapa, ele não é mais capaz de levantar sozinho da cama ou da cadeira, a não ser que use uma bengala ou um outro apoio.

PÁGINAS :: 1 |

O estresse e o mal de Parkinson
Um novíssimo estudo aponta que a tensão emocional influencia no desenvolvimento dessa doença neurológica, que afeta os movimentos e causa tremores no corpo

A doença surge como conseqüência de uma degeneração neurológica na área do cérebro conhecida como ‘substância negra’. Nessa região se concentram neurônios (células nervosas) que produzem dopamina, matéria química que, entre outras funções, tem papel fundamental na manutenção das atividades motoras. No mal de Parkinson, por razões ainda desconhecidas, essas células param de funcionar ou são destruídas e morrem, levando a uma deficiência de dopamina no organismo. Homens e mulheres são afetados em igual proporção pelo distúrbio, que, segundo as estimativas, aflige cerca de 200 indivíduos em cada grupo de 100 mil. Ele aparece em geral a partir dos 60 anos e tem uma incidência maior na faixa entre 70 e 75. Porém também pode atacar, embora mais raramente, pessoas com menos de 45 anos.

ÁREA DO CONFLITO

Em um corte da parte média do cérebro é possível visualizar a substância negra, região em que se concentram os neurônios produtores de dopamina, fundamental para as atividades motoras.

Medicamentos e atividade física ajudam
Apesar de todo o progresso científico ocorrido desde que a enfermidade começou a ser estudada, a medicina ainda não conseguiu descobrir a cura. Felizmente, a qualidade de vida dos parkinsonianos hoje é bem melhor do que três décadas e meia atrás, quando não se conhecia nenhum tratamento e, nos estágios mais avançados, a doença se tornava totalmente incapacitante, confinando a pessoa a uma cama.

Em 1970, os neurologistas passaram a cuidar de seus pacientes com a levodopa, medicação que, ao se transformar em dopamina no organismo, repõe a quantidade que o cérebro não é mais capaz de produzir, suavizando drasticamente os sintomas. De lá para cá, outros remédios antiparkinsonianos vêm sendo desenvolvidos, para uso conjunto com a levodopa ou isoladamente.

Além dos medicamentos, os especialistas recomendam que se pratique atividades físicas diariamente, como caminhadas ou natação, e se faça sessões de fisioterapia, para fortalecer a musculatura e manter a flexibilidade das articulações. A terapia ocupacional também se mostra benéfica nos casos em que a depressão faz parte do quadro.

A alimentação deve ser rica em fibras, para evitar a prisão de ventre, causada tanto pelas drogas administradas como pelo enfraquecimento dos movimentos do intestino, que acompanha o processo degenerativo da enfermidade. Devido à possibilidade de quedas e conseqüentes fraturas, é fundamental ainda prevenir a osteoporose – com o consumo de produtos ricos em cálcio – e a obesidade.

Cientistas buscam deter o avanço
Como os remédios atualmente disponíveis combatem apenas os sintomas do mal, sem impedir que os neurônios produtores de dopamina continuem se deteriorando, inúmeras pesquisas vêm sendo feitas, em busca das possíveis causas da doença e de formas de tratamento mais eficazes. Recentemente, cientistas americanos divulgaram resultados de testes indicando que um antibiótico usado em casos de lepra e tuberculose pode bloquear reações químicas associadas à morte de neurônios – descoberta que, se confirmada em animais e, posteriormente, em seres humanos, abrirá caminhos para deter o avanço do distúrbio.

PÁGINAS ::| 2 |

O estresse e o mal de Parkinson
Um novíssimo estudo aponta que a tensão emocional influencia no desenvolvimento dessa doença neurológica, que afeta os movimentos e causa tremores no corpo

Em outro experimento, realizado no Japão, os pesquisadores transplantaram células-tronco de embriões de macacos para o cérebro de macacos que tinham uma doença semelhante ao Parkinson, revertendo os sintomas – um resultado animador para o tratamento de pessoas no futuro, mas também polêmico, uma vez que enfrenta a oposição daqueles que consideram antiético o uso de embriões humanos. Já estudos recentes nos Estados Unidos, envolvendo a comparação do DNA de famílias e indivíduos, mostraram que um gene defeituoso era a causa de 5% dos casos de mal de Parkinson hereditários e de 1,6% dos casos chamados ‘esporádicos’ (que não têm causa hereditária). Tal alteração, identificada futuramente em testes genéticos, poderá favorecer o diagnóstico precoce, isto é, antes que a doença se manifeste. E o tratamento será, então, iniciado rapidamente, permitindo melhor qualidade de vida ao portador.

PARKINSONIANOS FAMOSOS
Michael J. Fox
Lembrado sobretudo por sua participação na trilogia De Volta para o Futuro, o ator abandonou a carreira aos 39 anos, depois de revelar que estava com Parkinson. Criou a Michael J. Fox Foundation, organização que, desde 2000, já arrecadou mais de 40 milhões de dólares para pesquisas sobre a cura da doença. No ano passado, apoiou publicamente o candidato democrata à presidência dos Estados Unidos, John Kerry, por sua postura progressista em relação às pesquisas com células-tronco.

Papa João Paulo II
Apresentou em 1994 os primeiros sinais da doença, amenizados durante anos graças ao uso de remédios. De lá para cá, sua fragilidade física se acentuou de maneira drástica, em parte devido aos problemas decorrentes da velhice – o Papa tem hoje 84 anos. Nas últimas semanas seu estado de saúde se agravou e ele foi submetido a uma traqueostomia (intervenção cirúrgica para facilitar a respiração). Segundo especialistas, essa dificuldade para respirar também pode ser conseqüência do mal de Parkinson.

Fotos: DivulgaçãoMuhammad Ali
Um dos maiores boxeadores de todos os tempos, Ali iniciou a carreira aos 22 anos, época em que se converteu ao islamismo e abandonou o nome de batismo, Cassius Clay. Quando parou de lutar, em 1981, tinha acumulado 56 vitórias, contra apenas 5 derrotas. Descobriu que sofria do mal de Parkinson em 1984, e a notícia deu origem a rumores de que a doença fora causada pelos inúmeros e perigosos golpes recebidos na cabeça em treinos e lutas, o que nunca ficou comprovado.

Quem foi Parkinson?
Londres, 1817. O médico James Parkinson publica um livreto em que descreve os casos de seis pacientes homens, com idades entre 50 e 72 anos, todos com tremor involuntário, alterações no caminhar e tronco curvado para a frente – sinais da enfermidade à qual ele dá o nome de ‘paralisia agitante’. Só em 1875, porém, ela se tornaria mais conhecida no meio científico, graças aos estudos do famoso neurologista francês Jean Martin Charcot, que, em uma homenagem àquele que pela primeira vez a relatou, batizou-a como ‘mal de Parkinson’.

Produção: Patida Mauad. Assistente de produção: Odete Marietto. Maquiagem: Kaio Martinelli

PÁGINAS :: 3

Disponivel em

http://revistavivasaude.uol.com.br/Edicoes/11/artigo5894-1.asp

– – –

%d blogueiros gostam disto: