<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>2183-5985</journal-id>
<journal-title><![CDATA[Acta Portuguesa de Nutrição]]></journal-title>
<abbrev-journal-title><![CDATA[Acta Port Nutr]]></abbrev-journal-title>
<issn>2183-5985</issn>
<publisher>
<publisher-name><![CDATA[Associação Portuguesa de Nutrição]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S2183-59852017000400005</article-id>
<title-group>
<article-title xml:lang="pt"><![CDATA[Nutrição e Alimentação na prevenção e terapêutica da Demência]]></article-title>
<article-title xml:lang="en"><![CDATA[Diet and Nutrition in the Prevention and Treatment of Dementia]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Cardoso]]></surname>
<given-names><![CDATA[Sofia Alves]]></given-names>
</name>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Paiva]]></surname>
<given-names><![CDATA[Isabel]]></given-names>
</name>
<xref ref-type="aff" rid="A01"/>
</contrib>
</contrib-group>
<aff id="A01">
<institution><![CDATA[,ACES Porto Oriental Unidade de Recursos Assistenciais Partilhados ]]></institution>
<addr-line><![CDATA[Porto ]]></addr-line>
<country>Portugal</country>
</aff>
<pub-date pub-type="pub">
<day>31</day>
<month>12</month>
<year>2017</year>
</pub-date>
<pub-date pub-type="epub">
<day>31</day>
<month>12</month>
<year>2017</year>
</pub-date>
<numero>11</numero>
<fpage>30</fpage>
<lpage>34</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://scielo.pt/scielo.php?script=sci_arttext&amp;pid=S2183-59852017000400005&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.pt/scielo.php?script=sci_abstract&amp;pid=S2183-59852017000400005&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.pt/scielo.php?script=sci_pdf&amp;pid=S2183-59852017000400005&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="pt"><p><![CDATA[Atualmente, a demência é uma epidemia global com grande impacto social, económico e na saúde, sendo urgente aumentar o conhecimento sobre a sua prevenção e tratamento. Diversos macro e micronutrientes, alimentos e padrões alimentares têm sido estudados como potenciais fatores de risco e de proteção, e agentes no tratamento. Para além da potencial modulação dos fatores de risco vascular, os fatores nutricionais poderão ter uma ação direta na patogénese. Embora ainda não haja evidência consistente e definitiva de ensaios controlados randomizados sobre o efeito dos fatores nutricionais na demência, vários trabalhos sugerem que estratégias nutricionais podem ser custo-efetivas, seguras e fáceis de implementar. Desta forma, é necessário realizar mais investigação para esclarecer o papel da nutrição e alimentação e estabelecer recomendações preventivas e terapêuticas na demência.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Currently, dementia is a global epidemic with great impact at social, economic and health levels. Thus, it is urgent to improve knowledge about prevention and treatment. Various macro- and micronutrients, specific foods and food patterns have been studied as potential risk and protection factors and treatment agents. Besides potential modulation of vascular risk factors, nutritional factors may have a direct action in pathogenesis. Albeit there is still no consistent and definitive evidence from randomized controlled studies about the role of nutritional factors in dementia, studies suggest nutritional strategies may be cost-effective, safe and easy to implement. Therefore, the role of nutrition and diet needs to be further investigated to clarify their role and to draw preventive and therapeutic recommendations.]]></p></abstract>
<kwd-group>
<kwd lng="pt"><![CDATA[Alimentação]]></kwd>
<kwd lng="pt"><![CDATA[Demência]]></kwd>
<kwd lng="pt"><![CDATA[Demência Vascular]]></kwd>
<kwd lng="pt"><![CDATA[Doença de Alzheimer]]></kwd>
<kwd lng="pt"><![CDATA[Nutrição]]></kwd>
<kwd lng="pt"><![CDATA[Prevenção]]></kwd>
<kwd lng="pt"><![CDATA[Tratamento]]></kwd>
<kwd lng="en"><![CDATA[Diet]]></kwd>
<kwd lng="en"><![CDATA[Dementia]]></kwd>
<kwd lng="en"><![CDATA[Vascular Dementia]]></kwd>
<kwd lng="en"><![CDATA[Alzheimer&#8217;s Disease]]></kwd>
<kwd lng="en"><![CDATA[Nutrition]]></kwd>
<kwd lng="en"><![CDATA[Prevention]]></kwd>
<kwd lng="en"><![CDATA[Treatment]]></kwd>
</kwd-group>
</article-meta>
</front><body><![CDATA[ <p align="right"><b>ARTIGO DE REVIS&#195;O</b></p>     <p>     <p><b>Nutri&ccedil;&atilde;o e Alimenta&ccedil;&atilde;o na preven&ccedil;&atilde;o e terap&ecirc;utica da Dem&ecirc;ncia</b></p>     <p><b>Diet and Nutrition in the Prevention and Treatment of Dementia</b></p>     <p><b>Sofia Alves Cardoso<sup>1</sup>; Isabel Paiva<sup>2*</sup></b></p>     <p><sup>1</sup>&nbsp;Nutricionista</p>     <p><sup>2</sup>Unidade de Recursos Assistenciais Partilhados do ACES Porto Oriental, Rua do Vale Formoso, n.&ordm; 466, 4200-510 Porto, Portugal</p>     <p></p> <a href="#c0">Endere&#231;o para correspond&#234;ncia</a><a name="topc0"></a></b></p>     <p>&nbsp;</p>     <p><b>RESUMO</b></p>     ]]></body>
<body><![CDATA[<p>Atualmente, a dem&ecirc;ncia &eacute; uma epidemia global com grande impacto social, econ&oacute;mico e na sa&uacute;de, sendo urgente aumentar o conhecimento sobre a sua preven&ccedil;&atilde;o e tratamento. Diversos macro e micronutrientes, alimentos e padr&otilde;es alimentares t&ecirc;m sido estudados como potenciais fatores de risco e de prote&ccedil;&atilde;o, e agentes no tratamento. Para al&eacute;m da potencial modula&ccedil;&atilde;o dos fatores de risco vascular, os fatores nutricionais poder&atilde;o ter uma a&ccedil;&atilde;o direta na patog&eacute;nese. Embora ainda n&atilde;o haja evid&ecirc;ncia consistente e definitiva de ensaios controlados randomizados sobre o efeito dos fatores nutricionais na dem&ecirc;ncia, v&aacute;rios trabalhos sugerem que estrat&eacute;gias nutricionais podem ser custo-efetivas, seguras e f&aacute;ceis de implementar. Desta forma, &eacute; necess&aacute;rio realizar mais investiga&ccedil;&atilde;o para esclarecer o papel da nutri&ccedil;&atilde;o e alimenta&ccedil;&atilde;o e estabelecer recomenda&ccedil;&otilde;es preventivas e terap&ecirc;uticas na dem&ecirc;ncia.</p>     <p><b>PALAVRAS-CHAVE</b></p>     <p>Alimenta&ccedil;&atilde;o, Dem&ecirc;ncia, Dem&ecirc;ncia Vascular, Doen&ccedil;a de Alzheimer, Nutri&ccedil;&atilde;o, Preven&ccedil;&atilde;o, Tratamento</p>     <p>&nbsp;</p>  <hr>     <p>&nbsp;</p>     <p><b>ABSTRACT</b></p>     <p>Currently, dementia is a global epidemic with great impact at social, economic and health levels. Thus, it is urgent to improve knowledge about prevention and treatment. Various macro- and micronutrients, specific foods and food patterns have been studied as potential risk and protection factors and treatment agents. Besides potential modulation of vascular risk factors, nutritional factors may have a direct action in pathogenesis. Albeit there is still no consistent and definitive evidence from randomized controlled studies about the role of nutritional factors in dementia, studies suggest nutritional strategies may be cost-effective, safe and easy to implement. Therefore, the role of nutrition and diet needs to be further investigated to clarify their role and to draw preventive and therapeutic recommendations.</p>     <p><b>KEYWORDS</b></p>     <p>Diet, Dementia, Vascular Dementia, Alzheimer&rsquo;s Disease, Nutrition, Prevention, Treatment</p>     <p>&nbsp;</p>  <hr>     ]]></body>
<body><![CDATA[<p>&nbsp;</p>      <p><b>INTRODU&Ccedil;&Atilde;O</b></p>     <p>A dem&ecirc;ncia &eacute; uma s&iacute;ndrome que pode ser definida como uma deteriora&ccedil;&atilde;o adquirida das capacidades cognitivas, que compromete a performance das atividades de vida di&aacute;ria (1). A maioria dos casos &eacute; de natureza cr&oacute;nica e progressiva e surge ap&oacute;s os 65 anos de idade (2, 3).</p>     <p>Os tipos de dem&ecirc;ncia mais comuns s&atilde;o a Doen&ccedil;a de Alzheimer (DA) e a Dem&ecirc;ncia Vascular, podendo ser coexistentes (4). Os marcadores neuropatol&oacute;gicos da DA s&atilde;o os novelos neurofibrilares e as placas neur&iacute;ticas resultantes de agregados de prote&iacute;na beta-amiloide (A&beta;), que levam &agrave; morte neuronal (5). A Dem&ecirc;ncia Vascular deve-se &agrave; insufici&ecirc;ncia cerebrovascular (6).</p>     <p>Atualmente, a preval&ecirc;ncia mundial &eacute; de 47 milh&otilde;es de pessoas e dever&aacute; triplicar at&eacute; 2050, sendo considerada uma epidemia global (7). Em 2012 a dem&ecirc;ncia afetava 1,7% da popula&ccedil;&atilde;o portuguesa (8). O presente cen&aacute;rio tem impacto a n&iacute;vel social, econ&oacute;mico e da sa&uacute;de, acarretando custos que tender&atilde;o a agravar-se (9).</p>     <p>O atual tratamento farmacol&oacute;gico da dem&ecirc;ncia &eacute; sintom&aacute;tico (10) e apesar de as causas exatas n&atilde;o estarem esclarecidas, sabe-se que fatores gen&eacute;ticos e ambientais interv&ecirc;m na etiologia e evolu&ccedil;&atilde;o (5, 6).</p>     <p>Para fazer face a este desafio de sa&uacute;de p&uacute;blica, &eacute; urgente ampliar o conhecimento sobre os fatores ambientais influentes e estrat&eacute;gias preventivas (5, 6). Fatores de risco modific&aacute;veis que englobam os estilos de vida, como a alimenta&ccedil;&atilde;o e a atividade f&iacute;sica, e fatores de risco vascular t&ecirc;m sido alvo de investiga&ccedil;&atilde;o (6). A preven&ccedil;&atilde;o deve focar-se na modula&ccedil;&atilde;o destes fatores, nomeadamente nos de risco vascular (6, 11).</p>     <p>Diversos estudos sugerem que os fatores nutricionais, incluindo micro e macronutrientes, alimentos, bebidas e padr&otilde;es alimentares, podem modificar o risco e atrasar a ocorr&ecirc;ncia de dem&ecirc;ncia (12-14). Por outro lado, tamb&eacute;m t&ecirc;m sido estudados no &acirc;mbito do tratamento, quer no atraso da progress&atilde;o da dem&ecirc;ncia, de decl&iacute;nio e de comprometimento cognitivo, quer na melhoria da fun&ccedil;&atilde;o cognitiva e dos sintomas (15-17). O presente artigo pretende analisar o papel da nutri&ccedil;&atilde;o e alimenta&ccedil;&atilde;o na preven&ccedil;&atilde;o e na terap&ecirc;utica da dem&ecirc;ncia, atrav&eacute;s da revis&atilde;o da literatura existente, focando os principais fatores nutricionais investigados e os poss&iacute;veis mecanismos subjacentes.</p>     <p><b>Fatores de risco vascular</b></p>     <p>Os fatores de risco vascular incluem les&otilde;es cerebrovasculares, doen&ccedil;as cardiovasculares (CV), diabetes&nbsp;Mellitus&nbsp;tipo 2, hipercolesterolemia e hipertens&atilde;o arterial na meia-idade (16, 17). Em geral, a presen&ccedil;a destes fatores duplica o risco de desenvolver dem&ecirc;ncia (16). Alguns autores incluem ainda a hiperhomocistein&eacute;mia e a obesidade na meia-idade (16-18). A defini&ccedil;&atilde;o de &ldquo;meia-idade&rdquo; dos estudos &eacute; vari&aacute;vel, mas a maioria refere idades entre os 35 e os 65 anos. Os fatores poder&atilde;o interagir entre si e com aspetos gen&eacute;ticos (nomeadamente o alelo para a apolipoprote&iacute;na-E &epsilon;4), aumentando o risco de dem&ecirc;ncia (16). Os mecanismos subjacentes ainda s&atilde;o desconhecidos, mas poder&atilde;o iniciar-se d&eacute;cadas antes da manifesta&ccedil;&atilde;o cl&iacute;nica (16, 19). A obesidade poder&aacute; aumentar o risco devido ao perfil inflamat&oacute;rio da adiposidade e ao maior risco de comorbilidades como a hipertens&atilde;o arterial (16, 17). A sua poss&iacute;vel influ&ecirc;ncia &eacute; complexa e carece de mais estudos (17).</p>     ]]></body>
<body><![CDATA[<p><b>Papel da Nutri&ccedil;&atilde;o e Alimenta&ccedil;&atilde;o</b></p>     <p>Os fatores protetores de doen&ccedil;as CV, como h&aacute;bitos alimentares adequados, poder&atilde;o estar associados a um menor risco de desenvolver DA e outras dem&ecirc;ncias (20, 21). Por outro lado, sugere-se que v&aacute;rios nutrientes e alimentos possam agir de uma forma mais direta, interferindo na capacidade de regenera&ccedil;&atilde;o celular e nas vias patog&eacute;nicas da dem&ecirc;ncia (16, 22). A sinergia entre v&aacute;rios nutrientes presentes nos alimentos poder&aacute; ser importante para se verificar um efeito protetor (17). Para al&eacute;m de nutrientes, o efeito do consumo de alguns alimentos, bebidas e outros compostos tamb&eacute;m tem sido estudado (16).</p>     <p>Desta forma, discutir-se-&atilde;o primeiro os nutrientes mais investigados, em segundo, alimentos, bebidas e outros compostos e, em terceiro, a sua combina&ccedil;&atilde;o atrav&eacute;s de padr&otilde;es alimentares. Por &uacute;ltimo, abordam-se formula&ccedil;&otilde;es nutricionais que est&atilde;o a ser alvo de pesquisa no tratamento da dem&ecirc;ncia. A <a href ="/img/revistas/apn/n11/n11a05f1.jpg">Figura 1</a> sumaria os potenciais fatores nutricionais protetores e de risco de dem&ecirc;ncia e/ou DA, abordados com maior &ecirc;nfase no presente artigo.</p>     
<p><u>Antioxidantes</u></p>     <p>As vitaminas E e C, o sel&eacute;nio e os flavonoides protegem de danos oxidativos que podem surgir como causa e/ou consequ&ecirc;ncia da dem&ecirc;ncia (17, 23). V&aacute;rios estudos mostram que estes fatores s&atilde;o potencialmente protetores na incid&ecirc;ncia de dem&ecirc;ncia e que a sua obten&ccedil;&atilde;o na alimenta&ccedil;&atilde;o poder&aacute; ser prefer&iacute;vel &agrave; suplementa&ccedil;&atilde;o (21, 24). Apesar de n&atilde;o haver evid&ecirc;ncia de que a toma de vitamina E (alfa-tocoferol) melhore fun&ccedil;&atilde;o cognitiva na DA, um estudo apresentou um atraso do decl&iacute;nio funcional (25).</p>     <p><u>Vitaminas do complexo B e Folato</u></p>     <p>A maioria das vitaminas do complexo B e o folato t&ecirc;m demonstrado associa&ccedil;&atilde;o com a sa&uacute;de neuronal, intervindo nas suas vias metab&oacute;licas (17). Adicionalmente, o d&eacute;fice destas vitaminas pode levar ao aumento da homociste&iacute;na plasm&aacute;tica. Diversos trabalhos mostram uma associa&ccedil;&atilde;o entre a ingest&atilde;o de vitaminas do complexo B e um menor risco de dem&ecirc;ncia; e que altos n&iacute;veis de homociste&iacute;na e baixos n&iacute;veis de vitamina B12 se associam a um maior risco de DA (17, 26). Tal como para os antioxidantes, o seu papel no tratamento tem sido pouco estudado e com resultados conflituosos (15, 27). Uma meta-an&aacute;lise verificou efeitos moderados da suplementa&ccedil;&atilde;o de vitaminas do complexo B na melhoria da mem&oacute;ria em casos de comprometimento cognitivo, mas n&atilde;o de DA (28). A sua toma foi ainda associada a uma redu&ccedil;&atilde;o da homociste&iacute;na (29). A suplementa&ccedil;&atilde;o em &aacute;cido f&oacute;lico (com ou sem vitamina B12) n&atilde;o estabilizou nem atrasou o decl&iacute;nio em doentes com DA (28). N&atilde;o obstante, mais estudos s&atilde;o necess&aacute;rios nesta &aacute;rea (28).</p>     <p><u>Vitamina D</u></p>     <p>A vitamina D pode ser importante na prote&ccedil;&atilde;o de doen&ccedil;as CV e na neuroprote&ccedil;&atilde;o (30). Baixos n&iacute;veis ou d&eacute;fice de vitamina D t&ecirc;m sido associados a doen&ccedil;as cerebrovasculares e a um maior risco de dem&ecirc;ncia (31). Os mecanismos subjacentes podem envolver as vias da prote&iacute;na A&beta;, vasculares, metab&oacute;licas, anti-inflamat&oacute;rias e antioxidantes (32). O d&eacute;fice desta vitamina &eacute; comum e pode agravar a DA, sendo importante garantir n&iacute;veis adequados (6).</p>     <p><u>&Aacute;cidos Gordos</u></p>     ]]></body>
<body><![CDATA[<p>Os &aacute;cidos gordos &oacute;mega 3 (AGn-3) diminuem os n&iacute;veis de colesterol s&eacute;rico e inflama&ccedil;&atilde;o sist&eacute;mica e inibem a agrega&ccedil;&atilde;o plaquet&aacute;ria (26), e podem estar envolvidos nas vias vasculares, inflamat&oacute;rias e amiloides da DA e da Dem&ecirc;ncia Vascular (17). Diversos estudos observacionais sugerem um papel protetor dos AGn-3 na preven&ccedil;&atilde;o da dem&ecirc;ncia. Suplementos de &oacute;leo de peixe, &aacute;cido docosahexaen&oacute;ico (DHA) e &aacute;cido eicosapentaen&oacute;ico (EPA) t&ecirc;m sido investigados, mas ainda n&atilde;o &eacute; claro qual a melhor fonte ou combina&ccedil;&atilde;o (16, 17, 26). Relativamente ao tratamento, apesar de algumas interven&ccedil;&otilde;es com suplementos terem verificado melhorias cognitivas em doentes com DA ou decl&iacute;nio cognitivo, comparando com o placebo (26), uma revis&atilde;o n&atilde;o encontrou efeito ben&eacute;fico em indiv&iacute;duos com DA ligeira ou moderada (33). Quanto aos AG saturados, existe uma associa&ccedil;&atilde;o positiva entre a sua ingest&atilde;o e o risco de dem&ecirc;ncia e de DA (34, 35). Num estudo, indiv&iacute;duos com um r&aacute;cio superior entre a ingest&atilde;o de AG polinsaturados e AG saturados, apresentaram uma redu&ccedil;&atilde;o de 70% no risco de desenvolver DA (34). No entanto, um r&aacute;cio superior de AGn-6:AGn-3 associa-se a um maior risco de dem&ecirc;ncia (36).</p>     <p><u>Peixe</u></p>     <p>Alguns estudos revelam uma associa&ccedil;&atilde;o entre o consumo de peixes gordos e de &oacute;leo de peixe e um menor risco de dem&ecirc;ncia e/ou DA (26). Huang et al (2005) verificaram que uma ingest&atilde;o de peixe gordo superior a 2 vezes/semana estava associada a uma redu&ccedil;&atilde;o de risco de dem&ecirc;ncia e de DA em 28% e em 41%, respetivamente, comparando com ingest&atilde;o inferior a 1 vez/m&ecirc;s (37). Enquanto os estilos de vida saud&aacute;veis e a escolaridade s&atilde;o poss&iacute;veis confundidores desta associa&ccedil;&atilde;o, a presen&ccedil;a do alelo da apolipoprote&iacute;na-E &epsilon;4 e uma ingest&atilde;o elevada de AGn-6 podem contribuir para a aus&ecirc;ncia da associa&ccedil;&atilde;o (17, 26).</p>     <p><u>Hortofrut&iacute;colas</u></p>     <p>O consumo de hortofrut&iacute;colas tem sido associado a um menor risco de dem&ecirc;ncia e DA, e o consumo de hort&iacute;colas tem sido associado a um abrandamento do decl&iacute;nio cognitivo (32, 38).</p>     <p><u>Bebidas com cafe&iacute;na (caf&eacute; e ch&aacute;)</u></p>     <p>Os potenciais efeitos protetores de bebidas com cafe&iacute;na, especialmente caf&eacute;, tamb&eacute;m t&ecirc;m sido investigados (16, 32, 39). Uma meta-an&aacute;lise indicou um poss&iacute;vel efeito protetor da ingest&atilde;o de cafe&iacute;na, atrav&eacute;s de caf&eacute; e/ou ch&aacute;, na dem&ecirc;ncia, DA ou no decl&iacute;nio cognitivo (39). A cafe&iacute;na poder&aacute; intervir na neurodegenera&ccedil;&atilde;o atrav&eacute;s da diminui&ccedil;&atilde;o da produ&ccedil;&atilde;o de prote&iacute;na A&beta;, do poder anti-inflamat&oacute;rio e antioxidante e da antagoniza&ccedil;&atilde;o do recetor A2 da adenosina (40).</p>     <p><u>Bebidas alco&oacute;licas</u></p>     <p>A ingest&atilde;o baixa a moderada de bebidas alco&oacute;licas, sobretudo de vinho, tem sido indicada como protetora do decl&iacute;nio cognitivo e de dem&ecirc;ncia, em alguns trabalhos, mas a sua interpreta&ccedil;&atilde;o deve ser cautelosa (16, 41, 42). Embora seja dif&iacute;cil estabelecer uma dose que conduza a estes benef&iacute;cios (43), sugere-se uma curva em U ou em J para representar a rela&ccedil;&atilde;o entre a quantidade ingerida e o risco de dem&ecirc;ncia (5, 6). O mecanismo ainda &eacute; desconhecido, mas verifica-se que a ingest&atilde;o moderada auxilia a reduzir o risco de eventos CV e poder&aacute; estimular a acetilcolina no hipocampus (6, 44). Os efeitos do vinho tinto na redu&ccedil;&atilde;o do risco de DA poder&atilde;o dever-se ao etanol e/ou aos polifen&oacute;is, que diminuem a forma&ccedil;&atilde;o de placa neur&iacute;tica e protegem contra a neurotoxicidade da prote&iacute;na A&beta; (32, 43). Inversamente, a ingest&atilde;o excessiva de bebidas alco&oacute;licas &eacute; prejudicial &agrave; sa&uacute;de, aumentando o risco de dem&ecirc;ncia (16, 45). A sua recomenda&ccedil;&atilde;o a abst&eacute;mios n&atilde;o tem justifica&ccedil;&atilde;o cient&iacute;fica e indiv&iacute;duos que possuem o h&aacute;bito de consumir estas bebidas, n&atilde;o devem ultrapassar os limites da ingest&atilde;o moderada (mulheres: 1 por&ccedil;&atilde;o/dia e homens: 2 por&ccedil;&otilde;es/dia) (46). Devido aos seus riscos devem realizar-se mais estudos (41).</p>     <p><u>Compostos naturais e outros alimentos</u></p>     ]]></body>
<body><![CDATA[<p>A huperzina A e a Ginkgo biloba t&ecirc;m demonstrado resultados positivos em alguns estudos em animais e/ou humanos na preven&ccedil;&atilde;o ou progress&atilde;o da dem&ecirc;ncia e melhorias cognitivas (16, 47). Uma meta-an&aacute;lise concluiu que a toma de 240 mg/dia de extrato de Ginkgo biloba estabilizou ou abrandou o decl&iacute;nio na cogni&ccedil;&atilde;o e no comportamento, em casos de comprometimento cognitivo e de dem&ecirc;ncia (48). Para desenvolver recomenda&ccedil;&otilde;es, &eacute; necess&aacute;rio obter evid&ecirc;ncia consistente de benef&iacute;cios e seguran&ccedil;a assim como acautelar intera&ccedil;&otilde;es com f&aacute;rmacos (16, 26, 49).</p>     <p><b>Padr&otilde;es alimentares</b></p>     <p>Diversos trabalhos t&ecirc;m investigado o efeito de padr&otilde;es alimentares no decl&iacute;nio cognitivo e dem&ecirc;ncia (17, 22). Como poss&iacute;veis protetores, destacam-se a Dieta Mediterr&acirc;nica (DiMe) (22) e a dieta MIND (<em>Mediterranean-DASH Intervention for Neurodegenerative Delay</em>), uma combina&ccedil;&atilde;o da DiMe e da DASH (<em>Dietary Approaches to Stop Hypertension</em>) (50). Estudos epidemiol&oacute;gicos mostram evid&ecirc;ncia moderada relativa a uma associa&ccedil;&atilde;o entre a ades&atilde;o &agrave; DiMe e um menor risco de dem&ecirc;ncia, assim como a uma potencial diminui&ccedil;&atilde;o do risco de progress&atilde;o de s&iacute;ndromes pr&eacute;-demenciais (17, 51). Uma revis&atilde;o sistem&aacute;tica de 2013 verificou que em nove dos doze estudos, uma maior ades&atilde;o &agrave; DiMe se associou a uma melhor fun&ccedil;&atilde;o cognitiva, menor taxa de decl&iacute;nio cognitivo e um risco reduzido de DA (52). Um estudo experimental testou esta associa&ccedil;&atilde;o, comparando o efeito da interven&ccedil;&atilde;o da DiMe suplementada com azeite virgem extra ou oleaginosas, com uma dieta controlo baixa em gordura. Ap&oacute;s 6,5 anos, os grupos de interven&ccedil;&atilde;o possu&iacute;am melhor fun&ccedil;&atilde;o cognitiva que o grupo de controlo (53), resultados semelhantes a outra investiga&ccedil;&atilde;o similar (54).</p>     <p>Os benef&iacute;cios da DiMe t&ecirc;m sido atribu&iacute;dos aos alimentos e aos micro e macronutrientes caracter&iacute;sticos, em particular aos AG poli- e monoinsaturados (predominantes no azeite) (51, 55). A redu&ccedil;&atilde;o do risco de doen&ccedil;as CV, o aumento de neurotrofinas e/ou a&ccedil;&otilde;es anti-inflamat&oacute;rias, poder&atilde;o explicar os seus efeitos ben&eacute;ficos (17).</p>     <p>A dieta ocidental, caracterizada por uma elevada ingest&atilde;o de AG saturados, colesterol e a&ccedil;&uacute;cares refinados e uma reduzida ingest&atilde;o de AG polinsaturados, foi associada a um maior risco de dem&ecirc;ncia e de decl&iacute;nio cognitivo (16, 26).</p>     <p><u>Formula&ccedil;&otilde;es nutricionais na progress&atilde;o da dem&ecirc;ncia</u></p>     <p>Sob investiga&ccedil;&atilde;o existem algumas formula&ccedil;&otilde;es de nutrientes com objetivo de melhorar sintomas da DA e cuja toma deve supervisionada medicamente (<em>medical foods</em>) (16, 26, 56). Um dos suplementos &eacute; Fortasyn Connect,&reg;&nbsp;composto por substratos e nutrientes antioxidantes com a&ccedil;&atilde;o na integridade neuronal, incluindo uridina monofosfato, colina, EPA, DHA, fosfol&iacute;pidos, vitaminas C, E, B6 e B12, sel&eacute;nio e &aacute;cido f&oacute;lico (57). Em alguns estudos, indiv&iacute;duos em fases precoces de DA, apresentaram melhorias no metabolismo fosfolip&iacute;dico (58) e nos testes de mem&oacute;ria ap&oacute;s a sua toma (59, 60), o que n&atilde;o se verificou em fases mais avan&ccedil;adas (61). Por&eacute;m, o estabelecimento da sua efic&aacute;cia e de recomenda&ccedil;&otilde;es s&oacute; ser&aacute; poss&iacute;vel com a realiza&ccedil;&atilde;o de mais estudos, particularmente estudos independentes (58, 62).</p>     <p><b>AN&Aacute;LISE CR&Iacute;TICA E CONCLUS&Otilde;ES</b></p>     <p>V&aacute;rios estudos, sobretudo epidemiol&oacute;gicos, mostram um papel promissor da nutri&ccedil;&atilde;o e alimenta&ccedil;&atilde;o na dem&ecirc;ncia, apesar de haver resultados discrepantes (26). &Agrave; exce&ccedil;&atilde;o da DiMe, ainda n&atilde;o h&aacute; evid&ecirc;ncia consistente e clara de um papel protetor dos fatores nutricionais aqui abordados, sendo necess&aacute;rio mais investiga&ccedil;&atilde;o (17, 63). Embora ainda n&atilde;o existam ensaios controlados randomizados que confirmem definitivamente o papel dos nutrientes e dos alimentos, &eacute; necess&aacute;rio atender &agrave; dificuldade da sua execu&ccedil;&atilde;o e adequa&ccedil;&atilde;o neste &acirc;mbito (63). As limita&ccedil;&otilde;es metodol&oacute;gicas e o reduzido n&uacute;mero de investiga&ccedil;&otilde;es contribuem para o desafio de estabelecer recomenda&ccedil;&otilde;es e estrat&eacute;gias preventivas (63). N&atilde;o obstante, determinados autores advogam que podem ser feitas recomenda&ccedil;&otilde;es nutricionais e alimentares cautelosas, nomeadamente as que diminuem o risco CV, como a ades&atilde;o &agrave; DiMe, pois parecem n&atilde;o acarretar efeitos adversos (26, 64, 65).</p>     <p>Como forma de reduzir o risco de dem&ecirc;ncia, pode recomendar-se o tratamento/controlo dos fatores de risco vascular (17).</p>     ]]></body>
<body><![CDATA[<p>Os d&eacute;fices nutricionais devem ser tratados, sugerindo-se que interven&ccedil;&atilde;o nutricional na dem&ecirc;ncia seja particularmente ben&eacute;fica nestes casos (17, 64).</p>     <p>Atualmente, em idosos, existe uma elevada preval&ecirc;ncia de patologias que s&atilde;o fatores de risco vascular, como a hipertens&atilde;o arterial (17, 66, 67). Neste grupo et&aacute;rio tamb&eacute;m &eacute; alta a preval&ecirc;ncia dos d&eacute;fices de vitaminas do complexo B, vitamina D e antioxidantes (17, 66, 67). Dado o seu poss&iacute;vel papel na dem&ecirc;ncia, torna-se ainda mais pertinente assegurar um bom estado nutricional da popula&ccedil;&atilde;o, prevenindo estados de d&eacute;fice e excesso (17, 26, 68).</p>     <p>Para a preven&ccedil;&atilde;o da dem&ecirc;ncia, ser&aacute; igualmente importante sensibilizar a popula&ccedil;&atilde;o e profissionais de sa&uacute;de acerca da s&iacute;ndrome, fatores de risco e poss&iacute;veis estrat&eacute;gias preventivas (68).</p>     <p>Desta forma, &eacute; plaus&iacute;vel que o nutricionista possa desempenhar um papel na preven&ccedil;&atilde;o da dem&ecirc;ncia atrav&eacute;s da interven&ccedil;&atilde;o no controlo, tratamento e preven&ccedil;&atilde;o dos fatores de risco vascular, ao longo da vida, nomeadamente a n&iacute;vel dos Cuidados de Sa&uacute;de Prim&aacute;rios.</p>     <p>As modifica&ccedil;&otilde;es nutricionais podem ser medidas-custo efetivas, f&aacute;ceis de implementar e geralmente seguras, na preven&ccedil;&atilde;o e terap&ecirc;utica da dem&ecirc;ncia, e &eacute; pertinente que continuem a ser alvo de investiga&ccedil;&atilde;o, nomeadamente em ensaios de controlo randomizados.</p>     <p>&nbsp;</p>     <p><b>REFER&Ecirc;NCIAS BIBLIOGR&Aacute;FICAS</b></p> <ol>     <li>Seeley WQ, Miler LB. Alzheimer&rsquo;s Disease and other Dementias. In: L. Hauser S, editor. Harrison&rsquo;s Neurology in Clinical Medicine. 3rd ed. New York: McGraw-Hill Education; 2013. p. 310-33.</li>     <li>American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders IV. 4th ed. Washington D.C.: American Psychiatric Association; 1994. p. 886.</li>     <li>Prince M, Albanese E, Guerchet M, Prina M. World Alzheimer Report 2014. Dementia and Risk Reduction. An analysis of protective and modifiable factors. Executive summary. London: Alzheimer&rsquo;s Disease International, 2014.</li>     ]]></body>
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<body><![CDATA[<li>Li FJ, Shen L, Ji HF. Dietary intakes of vitamin E, vitamin C, and beta-carotene and risk of Alzheimer&rsquo;s disease: a meta-analysis. J Alzheimers Dis. 2012;31(2):253-8.</li>     <li>Farina N, Llewellyn D, Isaac M, Tabet N. Vitamin E for Alzheimer&rsquo;s dementia and mild cognitive impairment. Cochrane Database Syst Rev. 2017;4:CD002854.</li>     <li>Swaminathan A, Jicha GA. Nutrition and prevention of Alzheimer&rsquo;s dementia. Front Aging Neurosci. 2014;6:282.</li>     <li>Mecocci P, Polidori MC. Antioxidant clinical trials in mild cognitive impairment and Alzheimer&rsquo;s disease. Biochim Biophys Acta. 2012;1822(5):631-8.</li>     <li>Li MM, Yu JT, Wang HF, Jiang T, Wang J, Meng XF, et al. Efficacy of vitamins B supplementation on mild cognitive impairment and Alzheimer&rsquo;s disease: a systematic review and meta-analysis. Curr Alzheimer Res. 2014;11(9):844-52.</li>     <li>Agnew-Blais JC, Wassertheil-Smoller S, Kang JH, Hogan PE, Coker LH, Snetselaar LG, et al. Folate, vitamin B-6, and vitamin B-12 intake and mild cognitive impairment and probable dementia in the Women&rsquo;s Health Initiative Memory Study. J Acad Nutr Diet. 2015;115(2):231-41.</li>     <li>Grant WB. Does vitamin D reduce the risk of dementia? J Alzheimers Dis. 2009;17(1):151-9.</li>     <li>Annweiler C. Vitamin D in dementia prevention. Ann N Y Acad Sci. 2016;1367(1):57-63.</li>     <li>Hu N, Yu JT, Tan L, Wang YL, Sun L, Tan L. Nutrition and the risk of Alzheimer&rsquo;s disease. Biomed Res Int. 2013;2013:12.</li>     <li>Burckhardt M, Herke M, Wustmann T, Watzke S, Langer G, Fink A. Omega-3 fatty acids for the treatment of dementia. Cochrane Database Syst Rev. 2016;4:CD009002.</li>     ]]></body>
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<body><![CDATA[<li>Alzheimer&rsquo;s Australia, Dementia Collaborative Research Center. Dementia Risk Reduction: A Practical Guide for General Practitioners. An Australian Government Initiative. 2nd ed: Alzheimer&rsquo;s Australia; 2010. p. 48.</li>     <li>Baumgart M, Snyder HM, Carrillo MC, Fazio S, Kim H, Johns H. Summary of the evidence on modifiable risk factors for cognitive decline and dementia: A population-based perspective. Alzheimers Dement. 2015;11(6):718-26.</li>     <li>Gillette Guyonnet S, Abellan Van Kan G, Andrieu S, Barberger Gateau P, Berr C, Bonnefoy M, et al. IANA task force on nutrition and cognitive decline with aging. J Nutr Health Aging. 2007;11(2):132-52.</li>     <li>Alves M, Bastos M, Leit&atilde;o F, Marques G, Ribeiro G, Carrilho F. Vitamina D&ndash;import&acirc;ncia da avalia&ccedil;&atilde;o laboratorial. Rev Port Endocrinol Diabetes Metab. 2013;8(1):32-9.</li>     <li>National Institute for Health and Care Excellence (NICE). Dementia, disability and frailty in later life &ndash; mid-life approaches to delay or prevent onset (NG16). NICE guideline. 2015:62.</li>     </ol>     <p></p>     <p>&nbsp;</p>     <p>  <b><a href="#topc0">Endere&#231;o para correspond&#234;ncia</a><a name="c0"></a></b>     <p>Isabel Paiva</p>     ]]></body>
<body><![CDATA[<p>Rua Bar&atilde;o Nova Sintra, n.&ordm; 244, 4300-365 Porto, Portugal</p> <a href="mailto:ialexspaiva@gmail.com">ialexspaiva@gmail.com</a></p>     <p>&nbsp;</p>     <p>Recebido a 21 de mar&ccedil;o de 2017</p>     <p>Aceite a 30 de novembro de 2017</p>     <p>&nbsp;</p>      ]]></body><back>
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