domingo, 3 de julho de 2016

ESTRATÉGIA FODMAPs - Você ainda ouvirá falar muito sobre ela


ESTRATÉGIA FODMAP (EF) E SENSIBILIDADE NÃO CELÍACA AO GLÚTEN 

FODMAPs, acrônimo de Fermentable Oligo-Di-Monosaccharides And Polyols, são carboidratos de:
  1. Cadeia curta,
  2. Difícil absorção,
  3. Pelo seu poder osmótico, aumentam o volume de líquido na luz intestinal,
  4. São fermentados pelas bactérias do intestino, produzindo gazes, dor abdominal, distensão abdominal, cólicas, diarréia. 
Pesquisas recentes apontam esses carboidratos como “vilões” para o desencadeamento dos sintomas da Síndrome do Intestino Irritável e outros distúrbios gastrintestinais funcionais. Os distúrbios do trato digestivo funcionais são transtornos que não podem ser atribuídos a anormalidades estruturais ou anatômicas e nem a alterações bioquímicas e metabólicas.

Os Oligossacarídeos (fructanos e os galactanos) são formados pela união de até 10 moléculas de monossacarídeos. 

Os fructanos, constituídos por uma cadeia curta de frutose ligada a uma molécula de glicose, não são absorvidos porque o intestino não tem a uma enzima hidrolase específica para quebrar as ligações frutose-frutose. 

O trigo é a maior fonte de frutanos da dieta, mas eles estão também presentes na cebola, alho, aspargos, brócolis, beterraba e melancia. Os galactanos, formados por uma cadeia de galactose unida a uma molécula de frutose, também não são absorvidos, sendo então fermentados no intestino. Dentre outros alimentos, estão presentes no feijão, ervilha e soja.

Os Dissacarídeos (sacarose e lactose) são hidrolisados por enzimas presentes na mucosa intestinal. 

A sacarose (açúcar comum) é quebrada nos monossacarídeos frutose e glicose, facilmente absorvidos. A lactose é quebrada pela lactase, localizada na superfície das células intestinais, originando glicose e galactose, que também são absorvidas. Porém, quando existe deficiência de lactase, o que é frequente na população, ocorre má absorção de lactose. 

A má absorção de lactose por deficiência de lactase apresenta a mesma proporção tanto em indivíduos saudáveis como em pacientes com Síndrome do Intestino Irritável, porém os sintomas são mais intensos nos pacientes com SII (Clinical Gastroenterology and Hepatology 2013;11:262). Com frequência, observamos isso na prática clínica: os indivíduos com deficiência de lactase, sem problemas digestivos, podem até tolerar a ingestão de um copo de leite por dia. Já, os pacientes com Síndrome do Intestino Irritável e com deficiência de lactase, ao ingerirem alimentos que contenham lactose, apresentam dor abdominal, gases e diarréia.

Os Monossacarídeos (glicose, galactose, frutose) são absorvidos rapidamente. A frutose, quando presente em excesso em relação à glicose, é absorvida com dificuldade. Isto pode ocorrer com ingestão de grande quantidade de mel e de alguns sucos de frutas, como maçã, manga, pera, melancia. Tem-se diagnosticado muitos casos de intolerância à frutose e na maioria das vezes esse distúrbio é transitório, podendo ser oriundo de alteração na microbiota intestinal, assim como por alteração no metabolismo dos monossacarídeos, fazendo com que eles permaneçam na luz intestinal, promovendo efeito osmótico, sendo fermentados por bactérias e com isso gerando gases abdominais, dores e até mesmo diarréia. 

Os Polióis (sorbitol, manitol, xilitol) adoçantes artificiais presentes em chicletes e balas sem açúcar e em algumas frutas (pera, maçã, abacate, manga) têm absorção lenta, por difusão passiva, através de poros no epitélio intestinal e são fermentados.

Em 2005, os pesquisadores Peter Gibson  e Susan Shepherd, da Monash University (Melbourne), começaram a perceber que uma série de alimentos eram mais ligados a piora dos sintomas da Síndrome do intestino irritável (SII), assim como dos distúrbios funcionais do trato gastrintestinal. Percebendo a composição desses alimentos, viram que esses carboidratos fermentáveis poderiam ser a causa dos sintomas em tais pacientes. Surgiu então a abordagem, ou Estratégia FODMAPs (EF) como alguns denominam. 

A EF sugere um novo enfoque de dieta como forma de reduzir os sintomas deste distúrbio. Suas crescentes evidências vêm ganhando destaque e atenção cada vez maiores no meio científico em todo o mundo. Mensalmente saem estudos mostrando que ela realmente pode reduzir até 70% dos sintomas nos portadores de SII.

A Síndrome do Intestino Irritável (SII) é caracterizada por sintomas de longa duração relacionados ao intestino, como dor e distensão abdominal por gazes, associados com alterações no hábito intestinal (diarreia ou constipação ou alternância de ambos). É de alta prevalência em todo o mundo, sendo que 20% dos adultos e adolescentes apresentam queixas compatíveis com o diagnóstico. Os medicamentos, mesmo os mais recentes, têm sido pouco eficientes e a maioria dos pacientes relata que os alimentos são os responsáveis pelo início e manutenção dos sintomas.

Os critérios para diagnóstico de SII são baseados nos critérios de ROMA III:

Os critérios* diagnósticos devem incluir todos os itens a seguir:
Dor ou desconforto abdominal recorrente** pelo menos 3 dias/mês, nos últimos 3 meses, associada com dois ou mais dos seguintes:
1. Melhora com a defecação;
2. Início associado com mudança na frequência das evacuações;
3. Início associado com mudança no formato (aparência) das fezes.
* Critérios preenchidos nos últimos 3 meses com início dos sintomas pelo menos 6 meses antes do diagnóstico. 
** “Desconforto” significa uma sensação desconfortável não descrita como dor.
Recomenda-se que, para uma pessoa possa participar e ser incluída nos protocolos de pesquisas de fisiopatologia e em estudos clínicos, tenha frequência de dor/desconforto de ao menos 2 dias por semana durante o período de avaliação.

Outros distúrbios funcionais intestinais são:

1) Estufamento/Empachamento funcional: Os critérios* diagnósticos devem incluir os dois itens a seguir:
1. Sensação recorrente de estufamento/empachamento ou distensão visível por pelo menos 3 dias/mês em 3 meses
2. Critérios insuficientes para diagnóstico de dispepsia funcional, síndrome do intestino irritável ou outro distúrbio
gastrointestinal funcional
* Critérios preenchidos nos últimos 3 meses com início dos sintomas pelo menos 6 meses antes do diagnóstico.

2) Constipação funcional: Os critérios* diagnósticos devem incluir:
1. Dois ou mais dos seguintes:
a. Esforço evacuatório durante pelo menos 25% das defecações;
b. Fezes grumosas ou duras em pelo menos 25% das defecações;
c. Sensação de evacuação incompleta em pelo menos 25% das defecações;
d. Sensação de obstrução/bloqueio anorretal das fezes em pelo menos 25% das defecações;
e. Manobras manuais para facilitar pelo menos 25% das defecações (por exemplo, evacuação com ajuda digital, apoio do assoalho pélvico);
f. Menos de três evacuações por semana.
2. Fezes moles estão raramente presentes sem o uso de laxantes;
3. Critérios insuficientes para SII.
* Critérios preenchidos nos últimos 3 meses com início dos sintomas pelo menos 6 meses antes do diagnóstico.

3) Diarreia funcionalCritérios diagnósticos*
Fezes moles ou aquosas sem dor, ocorrendo em pelo menos 75% das evacuações.
* Critérios preenchidos nos últimos 3 meses com início dos sintomas pelo menos 6 meses antes do diagnóstico

4) Distúrbio intestinal funcional inespecífico: Critérios diagnósticos*
Sintomas intestinais não atribuíveis a uma etiologia orgânica e que não preenchem critérios para as categorias definidas previamente.
* Critérios preenchidos nos últimos 3 meses com início dos sintomas pelo menos 6 meses antes do diagnóstico.

A EF está conquistando atenção e interesse crescentes, devido a sua eficácia no gerenciamento dos sintomas descritos acima, o que evidencia a importância de estudarmos mais e acrescentarmos mais esta ferramenta em nossa prática clínica, tendo sempre em conta que os pacientes com distúrbios digestivos funcionais devem ser orientados caso a caso, respeitando intolerâncias individuais e influências emocionais. 

Descobri a estratégia em 2013 quando um amigo nutrólogo me disse que a "epidemia de sensibilidade ao glúten" era provavelmente ocasionada não pelo glúten, mas sim pelos fructanos presentes no trigo, centeio e cevada. Na época haviam poucas pesquisas e ano após ano, os estudos vem mostrando os diversos benefícios da EF. Em 2016 surgiram metanálises mostrando que realmente é uma estratégia eficaz no controle dos sintomas.

Tive que treinar algumas nutricionistas em Goiânia, já que por se tratar de um tema novo e restrito ao meio da gastroenterologia, poucas tinham conhecimento. Em pleno 2016 a maioria ainda desconhece a EF. Conclusão: muitas vezes sobra pra mim, a tarefa de preparar cardápio para os pacientes. Sendo esta uma atividade privativa de nutricionistas e não devendo ser delegada a médicos.

VANTAGENS DA EF

Ela consegue detectar de forma precisa (desde que seguida a metodologia corretamente), os alimentos que mais geram sintomas nos pacientes. Portanto deve ser feita em acompanhamento com médico e nutricionista. É composta por duas fases. Uma de restrição e outra de introdução. Ou seja, a dieta restritiva não é para toda a vida. 

Na fase 1: O paciente deve colaborar, permanecendo no mínimo 6 semanas sem ingerir nenhum alimento rico em FODMAP (e isso não é fácil). 
Na fase 2: Inicia-se a reintrodução gradativa (de acordo com grupos: fructanos, galactanos, lactose, frutose, polióis), associada a observação. Uma vez detectada a intolerância deve-se testar quantidades menores de respectivo alimento e verificar em qual dose ele começa a gerar sintomas. Exemplo, alguns pacientes podem tolerar pequenas ingestões dos alimentos aqui relacionados, outros não. Ou podem tolerar um copo de leite, desde que naquela refeição não consumam trigo.  

Resumindo, é um duplo trabalho de detetive: do paciente que deve observar o que ingere versus sintomas provocados e do médico que deve orientar e acompanhar sua dieta, de forma personalizada, rastreando os alimentos e/ou as combinações de alimentos que maximizam ou minimizam os efeitos indesejáveis.

TABELA DE FODMAPS


Acima uma exemplificação de alimentos pobres e ricos em FODMAPs. No consultório entrego uma lista bem mais ampla, com inúmeras sugestões (modo de manipular alguns alimentos ricos em fodmaps) e dicas para amenizar as dificuldades da dieta. Também entrego uma sugestão de cardápio (caso o paciente queira), mas o mais indicado é que ele procure uma nutricionista que tenha experiência e treinamento em EF. 

EF NÃO DEU CERTO, E AGORA?

Essa é uma das perguntas comuns dos pacientes que sofrem com SII , distúrbios funcionais e múltiplas intolerâncias alimentares.  30% dos pacientes pertencem a esse grupo e nesse caso o paciente deverá fazer acompanhamento conjunto do nutrólogo com o gastroenterologista. Aprofunda-se então no trabalho duplo de detetive. 

Inicia-se a suspensão de alimentos ricos em determinadas substâncias (salicilatos, aminas, cafeína, glutamato etç) que podem induzir a sintomatologia gastrintestinal.

EF É SÓ DIETA?

 Na EF a dieta é a parte mais importante, porém a tentativa de alteração da microbiota intestinal, mudando o perfil de cepas, tem se mostrado promissor na SII. A questão é, quais cepas de probióticos são recomendadas? Qual a dose indicada? Por quanto tempo? São perguntas que gastroenterologistas, nutrólogos e alergistas se fazem e ainda não temos certezas. 


Bibliografia: 




http://www.medcenter.com/contentnews.aspx?pageid=128787&tax_id=279&id=232032&EMKT=1&langtype=1046&utm_source=Icommarketing&utm_medium=Email&utm_content=NL_GASTRO_BR_07_2016&utm_campaign=Icommarketing%20-%20_NEWSLETTER%20ESPEC%20BR%20-%20NL_GASTRO_BR_07_2016&esp_id=202

Uma mudança na dieta pode melhorar a vida das pessoas diagnosticadas com uma afecção intestinal frequente, mas difícil de tratar.

Esse é o resultado de um estudo do Sistema de Saúde da Universidade de Michigan apresentado na Semana da Enfermidade Digestiva, que estudou pela primeira vez nos Estados Unidos o resultado de cumprir uma dieta cuidadosamente controlada para melhorar os sintomas e a qualidade de vida saqueles com síndrome do intestino irritável (SII).

O estudo, o maior de seu tipo, mediu o grau de alívio com uma dieta com baixo conteúdo em FODMAP que se recomenda habitualmente e que significa comumente recomendado e isso significa oligo, di-, monossacarídeos e polióis fermentáveis (por sua sigla em inglês).

Esta dieta exclui muitos compostos encontrados no trigo, certas frutas e vegetais, alho, cebola e substitutos do açúcar.

"Este é o único estudo clínico com rigorosa metodologia que demonstra que um tratamento baseado na dieta pode não só pode melhorar os sintomas, mas também a qualidade de vida em pacientes com SII", disse a professora assistente de clínica na U-M e gastroenterologista Shanti Eswaran, MD, que investigou o papel da dieta e de alimentação em doenças funcionais do intestino, tais como SII.

A síndrome do intestino irritável pode ser muito debilitante, se não virtualmente paralisante, afetando o trabalho, o sono e as relações pessoais e familiares.

A maioria dos tratamentos baseia-se em medicamentos que com frequência são caros, habitualmente ineficazes e frequentemente provocam efeitos colaterais indesejáveis. E, infelizmente, não há cura. Muitos médicos e pacientes consideram a dieta como possível tratamento, mas muitas das recomendações dietéticas não têm o apoio de estudos clínicos.

Durante um processo de 6 semanas, nutricionistas licenciados capacitaram e monitoraram o progresso de mais de 90 pacientes com SII. Aproximadamente a metade seguiu uma dieta com baixo conteúdo de FODMAP e a outra metade foi um grupo controle que usou um regime criterioso, suspendendo grandes refeições, comer fora de hora e irritantes conhecidos como cafeína e álcool.

Os resultados foram impressionantes: mais de 50% dos pacientes com dieta de baixo conteúdo  de FODMAP apresentaram uma melhora importante da dor abdominal, em comparação com 20% no grupo de controle.

Também foi observado melhoria de outros sintomas desagradáveis em comparação com o grupo controle: inchaço, diarreia e urgência para defecar.

Eswaran colaborou com William Chey, MD, professor de medicina interna, Kenya Jackson, Sivaram G. Pillai, Samuel W. Chey e Theresa Han-Markey, M.S., R.D., da Universidade de Michigan, no resumo do estudo publicado na revista Gastroenterology.

As 4 semanas, a proporção de pacientes com uma melhora significativa na qualidade de vida relacionada com o SII foi significativamente maior no grupo com baixo conteúdo de FODMAP, em comparação com o grupo de controle: 61% contra 27%.

Embora os resultados sejam muito encorajadores para aqueles que sofrem de SII, existem algumas ressalvas importantes, disse Eswaran.

Porque pouco se sabe sobre as causas químicas e desencadeantes do SII, a lista de alimentos "maus" é abrangente e vaga, por isso recomenda-se veementemente a ajuda de um nutricionista.

"A dieta com baixo conteúdo de FODMAP não é um tratamento novo, mas agora estamos convencidos de que realmente funciona", disse. "Nosso próximo passo será determinar com mais precisão a bioquímica subjacente à forma e o motivo pelo qual alimentos específicos podem provocar resultados dramaticamente diferentes em pessoas diferentes. Enquanto isso, recomendamos de forma veemente que os pacientes com SII trabalhem com seu médico e com um nutricionista para conhecer a dieta com baixo conteúdo FODMAP e controlar seus sintomas de SII”.  

Referências:

Shanti L. Eswaran et al, 821 A Low FODMAP Diet Improves Quality of Life, Reduces Activity Impairment, and Improves Sleep Quality in Patients With Irritable Bowel Syndrome and Diarrhea: Results From a U.S. Randomized, Controlled Trial. Gastroenterology, 2016; 150 (4): S172 DOI: 10.1016/S0016-5085(16)30665-5




Irritable Bowel Syndrome: Little Evidence for FODMAP Diet

Yael Waknine
August 14, 2015
There is "very limited evidence" to support a diet low in short-chain carbohydrates, also known as FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols), for patients with irritable bowel syndrome (IBS), according to a review published online August 6 in the Drug and Therapeutics Bulletin.
"Evidence for the efficacy of the low FODMAP diet to improve symptoms of [IBS] is based on a few relatively small, short-term unblinded or single-blinded controlled trials of varying duration," write James Cave, OBE, FRCGP, editor-in-chief of theDrug and Therapeutics Bulletin, and colleagues, noting that improper use could lead to dietary insufficiencies.
Developed in Australia, the FODMAP diet is based on the premise that patients with IBS have a limited ability to process the small-chain carbohydrates found in wheat, onions, legumes, milk, high-fructose corn syrup, and artificial sweeteners. FODMAP fermentation in the large intestine results in luminal distension, causing pain, bloating, and changes in motility.
Two recent review articles had conflicting conclusions: one concluded there is high-quality evidence supporting the efficacy of low FODMAP diet for IBS, whereas the other "was more cautious in its conclusion," report Dr Cave and colleagues.
In an effort to achieve consensus, researchers evaluated some of the same data but also included a 6-week study of 123 patients randomly assigned to a low FODMAP diet, Lactobacillussupplementation, or a regular Danish diet. Results revealed that both interventions yielded clinically significant symptom improvement, as evaluated using the 101-point IBS severity scoring system. Notably, 15 participants dropped out of the study, citing difficulties in dietary adherence.
The other studies also reported some level of symptom improvement, albeit with considerable variations in what was tested and how. One found that the median time to symptom resolution was 3.5 weeks; another concluded that breath-test evidence of fructose malabsorption "had no bearing on the benefit."
Because none of the randomized controlled studies exceeded 6 weeks' duration, the long-term effect of the FODMAP diet remains unknown. Restrictive or exclusion diets do carry a risk for nutritional inadequacy or harmful changes to the gut microbiota, the authors write. One study found a reduction in beneficial bifidobacteria, but further evaluation is needed to determine whether the effect is temporary or permanent.
"Some guidelines suggest that a low FODMAP diet may be appropriate for motivated patients for whom other therapies have not offered sufficient symptomatic relief; and that advice on a low FODMAP diet should be provided by a dietician with specialist knowledge of this type of intervention," the researchers state. "However, we believe that patients should be advised that there is very limited evidence for its use, the ideal duration of treatment has not been assessed in a clinical trial and its place in the management of IBS has not been fully established."
A Treatment Option
In an interview with Medscape Medical News, David Johnson, MD, MACG, FASGE, professor of medicine and chief of gastroenterology at Eastern Virginia Medical School in Norfolk, expressed his support of the FODMAP diet as an option in IBS.
"[The FODMAP diet] is worth a shot. It may help patients feel better, and they don't have to take an expensive medication or get approval from insurance. I tell patients to try it for 2 to 4 weeks; they can tell pretty quickly if something is affecting them," Dr Johnson said.
"There are a number of reports where the FODMAP diet has been used successfully in patients with IBS. Most gastroenterologists would accept that it has good scientific rationale with a relatively weak base of evidence," he added, noting the difficulties of controlling for other variables in this type of study.
"It's important not to throw the concept out just because of a lack of strong evidence. In some of my patients, [the FODMAP diet] has been very beneficial," he concluded.
The authors and Dr Johnson have disclosed no relevant financial relationships. Dr Johnson is an advisory board member for Medscape.
Drug Therapeutics Bull. Published online August 6, 2015. Abstract







Sensitivity to Wheat, Gluten and FODMAPs in IBS

FACTS OR FICTION?

Roberto De Giorgio; Umberto Volta; Peter R Gibson
 |Disclosures
Gut. 2016;65(1):169-178. 

ABSTRACT AND INTRODUCTION

Abstract

IBS is one of the most common types of functional bowel disorder. Increasing attention has been paid to the causative role of food in IBS. Food ingestion precipitates or exacerbates symptoms, such as abdominal pain and bloating in patients with IBS through different hypothesised mechanisms including immune and mast cell activation, mechanoreceptor stimulation and chemosensory activation. Wheat is regarded as one of the most relevant IBS triggers, although which component(s) of this cereal is/are involved remain(s) unknown. Gluten, other wheat proteins, for example, amylase-trypsin inhibitors, and fructans (the latter belonging to fermentable oligo-di-mono-saccharides and polyols (FODMAPs)), have been identified as possible factors for symptom generation/exacerbation. This uncertainty on the true culprit(s) opened a scenario of semantic definitions favoured by the discordant results of double-blind placebo-controlled trials, which have generated various terms ranging from non-coeliac gluten sensitivity to the broader one of non-coeliac wheat or wheat protein sensitivity or, even, FODMAP sensitivity. The role of FODMAPs in eliciting the clinical picture of IBS goes further since these short-chain carbohydrates are found in many other dietary components, including vegetables and fruits. In this review, we assessed current literature in order to unravel whether gluten/wheat/FODMAP sensitivity represent 'facts' and not 'fiction' in IBS symptoms. This knowledge is expected to promote standardisation in dietary strategies (gluten/wheat-free and low FODMAP) as effective measures for the management of IBS symptoms.

Introduction

IBS can be considered the prototype of all functional bowel disorders for its high prevalence worldwide and impact on patients' quality of life.[1,2] Patients with IBS suffer from abdominal pain or discomfort associated with bowel habit changes. In the absence of established biomarkers, for which research is actively ongoing, the diagnosis relies upon symptom evaluation according to the well-known Rome III criteria, which are currently the benchmark for IBS identification.[1,2] Current estimates indicate that IBS prevalence ranges from 10% to 25% in the general population with a typical predominance of young adult women (3:1 F:M ratio).[3–6] Usually regarded as a harmless disorder, IBS is known to severely hamper the patient's quality of life at least as much as organic disorders and is responsible for repeated absence from work as well as suboptimal performance on the workplace with relevant social costs.
The mechanisms leading to symptom generation in IBS remain highly debated, although growing knowledge indicates that multiple factors are involved. Altered brain–gut axis with gut dysmotility and hypersensitivity, immune activation, leaky gut barrier function, changes in gut microbiome, genetic factors, infections, as well as psychological/psychiatric factors, can all contribute to symptom generation.[5,7,8] The interest of the scientific community for these mechanisms has somehow obscured one of the most logical pathogenic factors—the role of food in triggering and perpetuating IBS symptoms. Recently, however, a number of studies linking type of food consumption to functional symptoms refuelled the interest in dietary factors in IBS, thus opening new avenues to treatment strategies.[9]This review aims first to briefly address some key mechanisms involved in food-related symptom genesis; and second, to address the ongoing controversy about wheat, gluten and fermentable oligo-di-mono-saccharides and polyols (FODMAPs) in IBS, a controversy that is generating much debate and a growing body of research that is slowly sorting fact from fiction

MECHANISMS BY WHICH FOOD MIGHT INDUCE SYMPTOMS

Common clinical experience indicates that food ingestion precipitates or exacerbates symptoms, such as abdominal pain and bloating, in about 60% of patients with IBS. The onset or worsening of symptoms can occur rapidly after meal ingestion, namely, within 15 min in 28%, up to 3 h in 93% of patients with IBS.[10] Foods can trigger symptoms in IBS via several possible mechanisms, which include immune and mast cell activation, mechanoreceptor activation via luminal distension associated with visceral hypersensitivity and altered motility, and chemosensory activation by bioactive molecule activity ('food chemicals') (figure 1).[11]

Figure 1.

Synopsis illustrating the interplay among several dietary factors, such as gluten, wheat and fermentable oligo-di-mono-saccharides and polyols (FODMAPs), that contribute to generate a wide array of symptoms in patients with IBS. For example, in the gut lumen, the interaction between dietary factors (carbohydrates, lipids and proteins) and the microbiota results in gas production and/or passage of noxious macromolecules triggering the release of mast cell mediators and the activation of the immune system. These mechanisms are at the base of mechanoreceptor and sensory nerve pathway activation ultimately responsible for commonly reported symptoms, such as abdominal pain, bloating and distension, especially in genetically predisposed patients. Moreover, stress or gliadomorphin evoked anxiety/depression, can directly impair intestinal barrier function, thus favouring passage of previously mentioned noxious macromolecules. ENS, enteric nervous system; IgE, immunoglobulin E; IgG, immunoglobulin G; IL4, interleukin-4; INF-γ, interferon-γ; TNFα, tumour necrosis factor α.

Immune and Mast Cell Activation

Low-grade inflammation (mainly characterised by a dense mast cell infiltrate) is present in colonic mucosal biopsies of about two-thirds of patients with IBS.[12] Mast cells are known to release a variety of mediators, including serine proteases, which evoke neuronal hyperexcitability, a major factor for functional symptom generation (eg, pain).[13,14] Food components, particularly proteins, may be pathogenically involved with this process, either primarily or secondarily. One possible interpretation of such mucosal changes is that food components/antigens pass through a leaky (ie, more permeable) epithelial barrier, leading to mast cell infiltration and activation, thereby leading to IBS symptoms.[5,8] Mast cells can be activated by allergy-like mechanisms, such as those involving food-specific immunoglobulin E (IgE). However, tests for food allergy detection that use the systemic immune compartment, such as skin-prick tests, have a poor sensitivity and specificity.[15] Thus, immune response to food in IBS may require more sophisticated approaches to be demonstrated.
One method is to present the offending protein to the gut immune compartment. A sort of 'mucosal prick test' renamed as colonoscopic allergen provocation (COLAP) test involves colonoscopy-guided submucosal injection to unravel food hypersensitivity.[16] Seventy-seven per cent of a population with gut symptoms thought possibly related to food hypersensitivity had a positive COLAP test, which was consistently negative in the few control subjects. A more refined technique (confocal laser endomicroscopy) demonstrated that submucosal injection of food antigens caused increased infiltration with intraepithelial lymphocytes (IEL), formation of epithelial leaks/gaps and widening of intervillous spaces in more than half of IBS, and not in a small group of controls.[17] These changes occurred within a few minutes of food antigen injection and predicted the clinical response to specific food withdrawal. Alternatively, circulating basophils have been used to determine allergens in vitro without the need to risk an allergic reaction when the patient is challenged. Indeed, basophil activation when exposed in vitro to dietary proteins, especially of wheat and milk origin, correlated with clinical responsiveness to dietary restriction of the relevant protein by one group,[18] but another could find no specificity for basophil activation.[19]Overall, these studies do suggest that reaction to food, whether it be via allergic, other immune or epithelial-damaging mechanisms, may play a role in the genesis of symptoms in some patients presenting with IBS. Confirmatory studies are needed before reaching diagnostic relevance.

Mechanoreceptor Activation

Many different foods can evoke intestinal (luminal) distension, which, in the presence of visceral hypersensitivity and abnormal gut motility, may trigger bloating, abdominal pain and changes in bowel habit. Dietary FODMAPs are believed to act via luminal distension as discussed later.[20–22]

Chemosensory Activation by Bioactive Molecules

A wide array of foods contains potentially bioactive chemicals, such as salicylates, amines, benzoates and glutamate, which can elicit neurally and/or mast cell-mediated mechanisms contributing to IBS symptoms.[11,23,24] However, a specific cause–effect mechanism between bioactive chemicals and symptoms is still far from being established. Empirical clinical experience indicates an improvement of IBS symptoms as a result of reduction of the dietary intake of bioactive chemicals. Nonetheless, clinicians should have a cautionary approach before advising dietary restrictions as nutritional defects may became a serious issue for the patient.



WHEAT SENSITIVITY

Wheat is considered one of the foods known to evoke IBS symptoms.[25] However, which component(s) of wheat is/are actually responsible for these clinical effects still remain(s) an unsettled issue.[26] The two parts of wheat that are thought to have a mechanistic effect comprise proteins (primarily, but not exclusively, gluten) and carbohydrates (primarily indigestible short-chain components, FODMAPs). Two distinct views characterise the clinical debate: one line identifies wheat proteins as a precipitating/perpetuating factor leading to symptoms, while the other believes that FODMAPs are the major trigger for IBS.

The Controversy Over Nomenclature

If gluten is a major trigger for IBS, it expands the gluten-related disorders by adding a new entity now referred to as non-coeliac gluten sensitivity (NCGS).[27] Indeed, coeliac disease-like abnormalities were reported in a subgroup of patients with IBS many years ago.[28] A recent expert group of researchers reached unanimous consensus attesting the existence of a syndrome triggered by gluten ingestion.[29] This syndrome recognises a wide spectrum of symptoms and manifestations including an IBS-like phenotype, along with an extra-intestinal phenotype, that is, malaise, fatigue, headache, numbness, mental confusion ('brain fog'), anxiety, sleep abnormalities, fibromyalgia-like symptoms and skin rash. In addition, other possible clinical features include gastro-oesophageal reflux disease, aphthous stomatitis, anaemia, depression, asthma and rhinitis. Symptoms or other manifestations occur shortly after gluten consumption and disappear or recur in a few hours (or days) after gluten withdrawal or challenge. A fundamental prerequisite for suspecting NCGS is to rule out all the established gluten/wheat disorders, comprising coeliac disease (CD), gluten ataxia, dermatitis herpetiformis and wheat allergy. The major issue not addressed by the consensus opinion was that gluten is only one protein contained within wheat. Other proteins, such as amylase-trypsin inhibitors (ATIs),[30] are strong activators of innate immune responses in monocytes, macrophages and dendritic cells. Furthermore, wheat germ agglutinin, which has epithelial-damaging and immune effects at very low doses at least in vitro, might also contribute to both intestinal and extraintestinal manifestations of NCGS.[31]
Consequently, a further development of this research field led to suggestions of a broader term, non-coeliac wheat sensitivity (NCWS). The problems with this term are twofold. First, rye and barley may be inappropriately excluded. Second, the term will refer to any wheat component that might be causally related to induction of symptoms and, therefore, will also include fructans (FODMAPs). It will then have a very non-specific connotation in IBS. A more correct term would then be non-coeliac wheat protein sensitivity (NCWPS) since this does not attribute effects to gluten without evidence of such specificity, eliminates the issue of fructan-induced symptoms and avoids the unknown contribution of rye and barley proteins to the symptoms. Both NCGS, the currently accepted term, and NCWPS will be used subsequently in this paper.

Evidence for Involvement of Sensitivity to Wheat Proteins in IBS

Due to the lack of biomarkers, the diagnosis of NCGS still challenges clinicians as it remains based only on clinical criteria.[32,33] In addition, one of the major diagnostic criteria for NCGS, which is the improvement of symptoms after wheat protein/gluten exclusion, might be influenced by a placebo effect experienced by patients after food elimination from their usual diet.[34] This is compounded by a huge media drive, via publications, printed media, television and the internet supported strongly by celebrity endorsement where a gluten-free diet (GFD) has been embraced not only as a solution to many symptoms but also with the erroneous belief that it is healthy not to eat gluten and, even more, that GFD helps to lose weight. As a result, a high proportion of US population, for example, switched to GFD with a marked increase of the global sale of gluten-free foods.[35] Because of these facts, it has been hypothesised that NCGS might be a false problem created by media rather than an emerging clinical entity.[36] However, recent studies have provided strong signals that wheat protein/gluten may specifically induce GI and extraintestinal, including psychological, symptoms in at least some patients with NCGS.[37–39]
Although epidemiological data are still scanty and approximate, NCGS may be at least as common as CD (ie, occurring in ≥1% of the general population).[40] Similarly to IBS, NCGS affects more young (third decade of life) women (F:M ratio >3:1), while, in contrast to IBS, NCGS is diagnosed more commonly in tertiary than primary care centres. According to the National Health and Nutrition Examination Survey, a primary care programme, NCGS was found in 0.6% over 7762 subjects,[41]whereas at the Celiac Disease Center (University of Maryland) 6% over 5896 subjects were identified as NCGS.[42] In an Italian multicentre prospective survey carried out on 38 referral paediatric and adult centres for the diagnosis of gluten-related disorders, NCGS and CD were respectively diagnosed in 391 (3.2%) and 340 (2.8%) over 12 255 patients consecutively studied in a 1-year period.[40] Such data have to be viewed, however, in the light of the failure to actually prove specific sensitivity to gluten/wheat proteins in double-blind placebo-controlled (DBPC) cross-over studies in most patients fulfilling the criteria for NCGS.[39,43]
Although still a matter of debate, several factors have been postulated to play a role in NCGS pathogenesis. First, NCGS may be an immune-mediated disorder evoked by innate immunity, as highlighted by the increased expression of toll-like-receptors (TLRs), mainly TLR2, in the intestinal mucosa.[44] More recently, however, the evidence of an increased level of interferon-γ in small intestinal biopsies of patients with NCGS after a short (3-day) gluten challenge lends support to a possible role exerted by adaptive immunity in this syndrome.[45] In line with the latter findings, the detection of antigliadin antibodies in >50% of patients with NCGS provides further support to adaptive immunity in NCGS pathogenesis.[46]Second, discordant data exist on epithelial barrier dysfunction. Initial studies showed a reduced intestinal permeability in NCGS, thus suggesting an increased intestinal barrier function. This finding has been also supported by a significantly higher expression of claudin-4 mRNA, a marker of reduced permeability, in duodenal biopsies of patients with NCGS.[44] However, more recently, some evidence for increased intestinal permeability in a subgroup of patients with IBS-D carrying the human leucocyte antigen (HLA)-DQ2+/DQ8+ was reported when consuming a gluten-containing diet compared with a GFD.[47]Further studies are needed. Third, changes of gut microbiota, as detected in CD,[48] might also occur in patients with NCGS. Finally, a further aspect potentially linking NCGS with IBS is that HLA-DQ8 transgenic mice sensitised by gliadin displayed an increased secretion of acetylcholine from the myenteric plexus, enhancing muscle contractility and epithelial hypersecretion. Gluten withdrawal reversed both abnormalities.[49]

Evidence From Double-blind Placebo-controlled Trials

Consistent evidence indicates the existence of an overlap between IBS and gluten-related disorders. In fact, about 5% of patients with IBS tests positive for CD and, conversely, CD may present with typical IBS-like symptoms.[50,51] Moreover, IBS-like symptoms occur in the majority of patients with NCGS,[40] while about one-third of patients with IBS may have NCWPS.[37] Although wheat is now established to be linked to IBS, the component(s) that actually trigger(s) symptoms remain unknown. In this line, the only way to confirm the possible role of gluten or wheat as causative factors of NCGS/NCWPS is a DBPC strategy.[27] This is an expensive and time-consuming procedure and, therefore, it is not yet of routine use being confined to research setting.[37–39,43,52,53] So far, few DBPC trials have been performed. Their design and results are shown in Table 1. The findings are discordant with a variation from approximately 30% of 920 patients with IBS in a routine clinical setting being sensitive to wheat protein, of whom the majority has NCWPS associated with multiple food hypersensitivity,[37] to greater symptoms induction overall with gluten or wheat protein,[38,39,53] to gluten-specific responses for current feelings of depression but not for abdominal symptoms.[38,53]
Reasons for apparent heterogeneity of results require dissection. First, subject selection might be a factor. For example, contamination of the cohort with CD can unduly skew results. This is why the exclusion of CD by combined histological and serological assessment while consuming adequate gluten is so important. In this respect, a critical point is to decide whether patients carrying HLA-DQ2/DQ8 and showing increased IEL density should be excluded from DBPC. Since about 40% of patients with NCGS is HLA-DQ2/DQ8+ and shows an increased IEL density, their exclusion would represent a pre-selection bias. In addition, 30–90% with positive responses to wheat protein/gluten has elevated IEL density in several studies.[54] In the study in which 30% of patients with IBS showed sensitivity to wheat, there was a high incidence of eosinophilic infiltration of the mucosa and epithelium, features not described in the other reports, suggesting a different cohort being investigated.[37] Second, nocebo responses can be a problem in re-challenge arms as evident in most, but not all, cross-over studies reported above. In the Australian study, 3 of 37 patients had gluten-specific induction of symptoms, but none of those three had such specificity of responses when a further DBPC challenge was instituted.[43]The Italian study had 3 of 61 patients who demonstrated unequivocal specificity of gluten-induction of symptoms.[39] It would be interesting to see if this is reproducible on a further DBPC challenge. Third, the active product that was used for the challenge differed from carbohydrate-depleted wheat protein[43,53] to purified gluten[39]to whole wheat flour,[37,52] in its dose from low[39,43] to high,[37–39,52] and in its form of presentation from capsule[37,39] to food.[38,43,52]Finally, other design features including method of assessing the end-points and sample size differed.
Based on these findings, it is reasonable to speculate that gluten and/or other wheat proteins (such as ATIs)[30] can generate intestinal and extraintestinal manifestations in a subgroup of patients with IBS. This contention is supported by mechanistic studies demonstrating epithelial injury and innate and possibly adaptive immune activation in response to wheat proteins. However, gluten and wheat are not the only dietary proteins involved in IBS. Proteins derived from milk, yeast and soy maybe involved in some,[17,37] and IgE-mediated food allergy and nickel allergy have been reported in a significant proportion of patients with IBS and NCGS/NCWPS.[37,40] 

THE ROLE OF FODMAPS IN IBS

The Development of the FODMAP Story

Over many years, there have been multiple observations that ingestion of certain short-chain carbohydrates—lactose, fructose and sorbitol, and fructo-oligosaccharides and galacto-oligosaccharides—was able to induce IBS-like symptoms, and that their restriction in the diet was associated with apparent improvement in symptoms in some patients with IBS (as reviewed in detail[22]). These carbohydrates have several key features in common. They are small molecules, containing only 1–10 sugars, and hence are possible osmotically active substances in the lumen of the intestine. They are slowly absorbed in the small intestine if monosaccharides are not absorbed at all if they contain more than one sugar due to lack of suitable hydrolases. Hence, they are present in the small intestinal lumen for a prolonged time and do increase the intestinal luminal water content. Their malabsorption leads to their exposure to intestinal bacteria, which rapidly ferment them to release short-chain fatty acids and gases (hydrogen, carbon dioxide and, in some people, methane). Their effects on symptoms and gas production are also additive.
Two hypotheses were proposed: (1) the luminal distension evoked by FODMAPs was related to symptom generation; (2) in patients with IBS and its associated visceral hypersensitivity, reducing the intake of all those short-chain carbohydrates would optimally improve the symptom burden. This was different to previous dietary strategies in that only one or two species of those carbohydrates—for example, lactose in lactose malabsorbers, fructose alone or in combination with sorbitol or fructans in fructose malabsorbers—were restricted.

Structure and Implementation of the Low FODMAP Diet

A dietary approach was designed to reduce the intake of all FODMAP groups, by finding in each food group low-FODMAP alternatives. Other adjuncts to reducing FODMAP intake, such as the use of lactase in food or orally to reduce lactose content of relevant foods, and the use of co-ingestion of glucose with food containing an excess of free fructose, were also proposed in patients with IBS.[22] Knowledge of the FODMAP content of foods was patchy and limited, and an ongoing programme of detailed food analyses has corrected aberrant assumptions and filled in many gaps.[55–57] Such information has been made readily available by an application (the Monash University Low FODMAP Diet App) that is updated regularly.
The diet has been implemented by education via a dietitian trained in the principles of the diet. The dietitian would tailor the dietary advice to the eating patterns of the individual, ensure nutritional adequacy and provide written information and where to find accurate digital information. After 4–6 weeks, no or minimal response in an adherent patient should then lead to the abandonment of FODMAP restriction. If there has been a good response, consideration is then given to reducing the level of restriction by graded reintroduction of previously restricted foods with a focus on specific FODMAP groups. The patient is encouraged in the long term to restrict only to the level that is needed for symptomatic comfort.

Evidence to Support the Low FODMAP Approach

It is timely to critically review whether the FODMAP concept and the use of a low FODMAP diet in patients with IBS are supported by evidence.
Mechanisms of Action. Water output from the small bowel varied by a mean of 20% between diets of moderate and low intake in ileostomates,[58] and the volume of water in the small intestinal lumen as shown by MRI was markedly increased following the ingestion of mannitol, fructose or fructans compared with that following glucose.[59,60] Furthermore, the luminal distension induced by fructose was independent of whether any fructose reached the large bowel (as shown by breath hydrogen production).[60,61] Diets differing in FODMAP content also lead to marked differences in breath hydrogen production.[62] In addition in methane producers, high FODMAP intake favoured hydrogen production while low FODMAP intake preferentially led to the production of methane, which takes up one-fifth of the volume per hydrogen atom generated than does hydrogen gas.[62] Thus, there is close correlation between mechanoreceptor stimulation via small and large intestinal luminal distension and symptom genesis. Importantly, the degree of luminal distension is unlikely to differ overall between patients with IBS and healthy controls since small intestinal distension occurs similarly in both[59]and breath hydrogen production does not differ when fed diets high or low in FODMAPs.[61,62] The difference in symptom generation relates more to the presence of visceral hypersensitivity as shown with regard to symptom generation with lactose malabsorption.[63]
Unanswered questions include the mechanism by which FODMAP intake increases gastro-oesophageal reflux[64] or induces tiredness.[62] The role of chemoreceptor stimulation via taste receptors or short-chain fatty acid receptors with subsequent hormonal changes warrants further exploration. Likewise, the relationship of the efficacy of the diet with specific alterations in the microbiome, immune activation, specific patterns of dysmotility and the role of changes of gut microbiota when FODMAP intake is reduced[65] in ongoing efficacy have yet to be explored.
Heterogeneity of Physiological Effects Across FODMAPs. The principle that all FODMAPs have similar physiological effects and therefore should be considered together is true only to a limited extent. While all are capable of exerting an osmotic effect, this will vary according to the molecular weight and the rapidity of absorption. Thus, fructose and polyols have a greater osmotic effect per molecule than fructans and galacto-oligosaccharides, but the number of molecules in the lumen will fall more distally with fructose and polyols associated with their slow absorption as opposed to no absorption for oligosaccharides. Nevertheless, imaging does show greater small intestinal distension with fructose and mannitol or sorbitol.[59,60] Conversely, oligosaccharides will have greater fermentative effects as they are not absorbed as opposed to absorption of fructose and polyols across the small intestinal wall, which is likely to vary according to the dose and speed of intestinal transit, and, for fructose, the luminal glucose content (glucose facilitates fructose absorption[22]) and individual absorptive capacity via fructose-specific transporters. While all FODMAPs are readily fermented, the relative speeds of fermentation of individual FODMAP groups have not been specifically studied. Each FODMAP group may have different effects on the structure and function of microbiota, but this has not been systematically assessed. In clinical practice, patients report different sensitivities to FODMAP groups, but such observations have not been formally studied.
Efficacy of the Low FODMAP Diet. Seven studies with a variety of designs examining the efficacy of the low FODMAP diet have been published, and these are outlined in Table 2.[62,66–72] The studies uniformly show efficacy in around 70% of patients with IBS of any bowel habit type. The limitations of the evidence presented above include the choice of placebo (such as habitual diet), the short-term nature of the studies (3 days to 6 weeks), the lack of blinding in many and questions about the success of blinding in others.[73,74] Such issues are endemic in dietary intervention studies often without ready solutions as reviewed by Yao et al.[75] However, the consistency of findings is somewhat reassuring, and durability of the benefits has been supported by an observational study with a median duration over 12 months.[72]
Implementation of the Low FODMAP Diet. The low FODMAP diet restricts all FODMAP groups in its induction phase, followed by a step-down in restriction after 4–6 weeks if efficacious, but each aspect of this plan has not been subject to specific study. First, the need to restrict across all FODMAP groups should theoretically be associated with the highest chance of response, but this has not been tested. In observational studies, poorly defined diets that restricted fructose±sorbitol claimed benefits in 40–81% of patients with IBS or functional bloating.[76–78] Similarly, a diet that restricted fructose and fructans in 62 patients with IBS and fructose malabsorption reported benefit in 74%; step-up to other FODMAPs was only used if response was poor.[79] Second, while controlled trials have shown that maximal response in symptom reduction occurs within 7 days when all food is provided and a high degree of adherence is achieved, there is no evidence-base behind a 4–6 week induction. This duration was proposed give the patient time to learn the diet and to ensure persistence of the symptomatic improvement. It also offers a practical timeframe for review.
Adherence and Degree of Difficulty in Following the Diet. Adherence was high where all food was provided on the basis of dietary diaries and breath hydrogen testing.[67] However, where the diet is taught in a clinical setting, the ease to which patients can apply the diet and the consequent adherence are important issues. In a prospective evaluation of 90 patients with IBS in New Zealand, in which the diet was taught by a dietitian via one or two consultations, 61% of participants stated that the diet was easy to follow and 44% were able to incorporate the diet easily into their life.[72]Adherence rates were also high, possibly because non-adherence was associated with symptom induction.
Risks of a Diet low in FODMAPs. Broad dietary change is associated with several risks that might include the following. First, nutritional adequacy of the low FODMAP diet has been evaluated in one study, where dietary calcium intake was compromised in some patients, presumably those who restricted lactose. The low FODMAP diet can be associated with reduction of fibre intake unless action is taken to seek non-wheat sources of fibre, as is instructed by dietitians delivering the diet. The nutritional adequacy of the low FODMAP diet needs to be assessed in a larger population, particularly in those who are self-taught. Second, the psychosocial risks of imposing dietary change cannot be underplayed. These range from difficulties in socialisation and eating away from home through to the precipitation of eating disorders such as orthorexia nervosa.[80] Third, the physiological effects of reducing FODMAP intake beyond those targeted to improve symptoms may have other implications. The major effect documented to date is alteration by varying FODMAP intake of gut microbiota, such as changing total bacteria abundance and altering the relative abundance of Bifidobacteria.[69] Diets differing in their FODMAP content were also associated with changes in the relative abundance of strongly butyrate-producing Clostridal groups or the mucus-associated bacterium Akkermansia muciniphila, both of which are positively associated with health.[65] Interestingly, the changes in these bacteria comprised increased relative abundance in association with greater FODMAP intake than with the low FODMAP diet arm per se in comparison to the habitual diet. The health implications of such changes are not known but raise concerns about strict restriction of FODMAPs in the long term.

DIETARY THERAPY IN IBS AND PERCEIVED WHEAT SENSITIVITY

Patients appear to be increasingly recognising an association of induction of gut symptoms and/or fatigue with the ingestion of wheat products such as bread and pasta. An Australian survey of 1184 adults identified that 8% avoid wheat or are gluten-free to relieve such symptoms.[25] Because of the coexistence of fructans and gluten in wheat,[57] the dilemma from a clinical point of view is which of the two evidence-based dietary approaches—GFD or low FODMAP diet—does one advise after excluding coeliac disease. A low FODMAP diet may offer a higher chance of symptomatic response, but GFD involves attacking a specific pathogenic factor if the injurious nature of wheat protein is integral to the genesis of visceral hypersensitivity or other gut-related physiological changes. In the absence of a biomarker of NCWPS, the only available means of identifying specific sensitivity to wheat protein is a trial of exclusion diet (strict GFD) and then DBPC re-challenge using purified wheat protein or gluten with symptoms as the read-out, as discussed earlier.
There is no consensus regarding the choice of approach. Comparisons between the two dietary approaches are shown in Table 3. The GFD approach might be preferable if the clinic is geared towards exclusion diet followed by DBPC re-challenge. Those having a negative response could have a trial with low FODMAP diet. Alternatively, the re-challenge methodology might be better applied in those with biomarkers suggesting relevant pathogenic events occurring in the intestine. Increased duodenal IEL density (>25/100 enterocytes), raised faecal eosinophilic cationic protein and tryptase,[81] basophil activation in vitro[18] or circulating antibodies to whole gliadin might enable better targeting of wheat protein challenges.[37] A third alternative is that the low FODMAP diet is applied initially and, in those with insufficient response, gluten is also removed from the diet. If an adequate response occurs, then non-wheat-based FODMAP intake can be cautiously increased in a step-wise fashion to determine whether that is necessary. 

FUTURE PERSPECTIVES

Much of the controversy has been generated by the poor awareness of the potential components of wheat that can induce symptoms. Gluten has been assumed to be the culprit because of its unequivocal key role in the pathogenesis of coeliac disease. In this way, the use of 'gluten' should be restricted to situations where gluten is the documented inducer of symptoms, 'wheat protein' where that has been the challenged factor, and 'wheat' where wheat products, such as bread, are used as the challenging agent. Likewise, further consideration will be needed in the terminology of clinical syndromes so that the current confusion of NCGS, NCWS and NCWPS can be put to rest. The lack of biomarkers for food protein sensitivity per se or individual protein sources is a significant impediment to progress. There has been considerable advancement in the application of techniques, such as confocal endomicrosocopy,[17]which holds promise as gold standards upon which practical biomarkers might be compared.
For interventional studies, exclusion of CD is critical and non-gluten-dependent diagnostic tests such as detection of gluten-reactive T-cells ex vivo[82] are needed. Likewise, the design of such studies may benefit from expert consensus about several of the details to reduce heterogeneity and to improve the interpretation of outcomes. Long-term outcomes are also needed to reassure the durability of efficacy with various dietary strategies.
One missing aspect is whether the intestinal responses to the dietary proteins are actually translated into altered gut physiology such as visceral hypersensitivity or abnormal motility responses. If that can be proven, then it places even greater importance of defining methods of detecting such sensitivities accurately so that the underlying condition can potentially be cured rather than just symptomatically treated.

CONCLUSIONS

There has been considerable progress in the understanding of how dietary change might influence patient outcomes in IBS. The often heated arguments and controversies over the involvement of wheat and its components in inducing symptoms have led to a now productive and healthy state of enquiry, with several research groups pursuing an understanding of how proteins and carbohydrates can contribute to IBS symptoms. Considerable more research is needed, but the learnings are informing future research into other, non-wheat dietary proteins and into bioactive chemicals, for which there is growing interest. The place of diet, whether it be low FODMAP diet, GFD or other fancy diets, is now established in the therapeutic strategies that clinicians can offer their patients. While the truth remains clouded, facts are emerging from the fiction.




Uma fórmula com baixo conteúdo de FODMAP melhora a diarreia em pacientes hospitalizados que recebem alimentação por sonda
16/12/2015
De acordo com um estudo difundido na Revista Gastroenterología de México em setembro deste ano, a dieta baixa em FODMAP exclui fructanos, oligossacarídeos, dissacarídeos, monossacarídeos e polióis fermentáveis. Os autores deste estudo expõem que as evidências atuais indicam que estes hidratos de carbono são absorbidos insuficientemente no intestino delgado e alcançam o cólon, onde são fermentados produzindo gases e gerando distensão.
Explicam que os pacientes que padecem transtornos funcionais digestivos, habitualmente manifestam desconfortos que são associados a presença de excesso de gás intestinal, que se expressa sob a forma de distensão abdominal e flatulência.
Muitos estudos demonstraram a eficácia de uma dieta baixa em FODMAP para o manejo de certos transtornos digestivos, como por exemplo a síndrome de intestino irritável. 
Em outro estudo que foi divulgado no Nutrition Journal  no mês passado, explica-se que os oligossacarídeos, dissacarídeos, monossacáridos e polióis fermentáveis (FODMAP) são hidratos de carbono de cadeia curta que não se absorvem bem e que desempenham um papel importante em provocar sintomas funcionais intestinais.
Em sintonia com as evidências existentes até o momento, os autores do estudo afirmam que uma alimentação com baixo conteúdo de FODMAP melhora os sintomas abdominais em pacientes com enteropatia inflamatória e síndrome de intestino irritável. Mas também adverte que ainda não se dispõe de algum estudo sobre o efeito do conteúdo de FODMAP na intolerância digestiva e estado nutricional em pacientes que recebem alimentação por sonda. E esse foi o objetivo que se propuseram estudar.
Tratou-se de um estudo clínico randomizado, multicêntrico, duplo-cego, de 14 dias, os pacientes hospitalizados elegíveis que receberam alimentação por sonda (n = 100) foram atribuídos de maneira randomizada a três grupos; 84 pacientes concluíram o estudo (alimentação por sonda com baixo conteúdo de FODMAP, n = 30; alimentação por sonda com moderado conteúdo de FODMAP, n = 28; EN com alto conteúdo de FODMAP, n = 26).
Mediram-se as variáveis antropométricas e bioquímicas; foi realizada a avaliação das fezes utilizando o Esquema das Fezes de King e a definição clínica.
Quanto aos resultados, os investigadores comunicaram que os valores iniciais não foram significativamente diferentes entre os três grupos. Depois da intervenção de 14 dias, a diarreia melhorou em grau significativo mais no grupo com baixo conteúdo de FODMAP que nos grupos com conteúdos moderado e alto de FODMAP (p < 0,05).
Os escores fecais de King em sujeitos com diarreia diminuíram em grau significativo e constante no grupo que recebeu baixo conteúdo de FODMAP em comparação com os outros dois grupos (p < 0,05 para interação de tempo e tipo de alimentação por sonda).
O índice de massa corporal (IMC) aumentou significativamente nos grupos com baixo e alto conteúdo de FODMAP durante a intervenção (p < 0,05 para ambos) e demonstrou uma tendência para o incremento no grupo com conteúdo moderado de FODMAP (p < 0,10).
A pré-albúmina em soro aumentou significativamente em todos os grupos em 14 dias; até o dia três tinha aumentado às concentrações presentes no dia 14 no grupo que recebeu alimentação com baixo conteúdo de FODMAP.
No dia 14, a transferrina sérica tinha aumentado significativamente no grupo com FODMAP moderado. Além disso, foram classificados os sujeitos por seu estado final (não melhorado, manutenção normal, só melhorou a diarreia, só melhorou a constipação e melhorou a diarreia e a constipação recorrentes). Setenta e cinco por cento do grupo com melhoria da diarreia consumiram uma fórmula de alimentação por sonda com baixo conteúdo de FODMAP.
Do grupo com diarreia e constipação recorrentes que melhoraram, 38,5% e 46,2% consumiram a alimentação por sonda com baixo e moderado conteúdo de FODMAP, respectivamente. O IMC aumentou significativamente em todos os grupos exceto naquele que não melhorou.
As concentrações de pré-albúmina aumentaram significativamente nos grupos com melhoria da diarreia e com diarreia e constipação recorrentes no dia três e continuaram no dia 14, e no grupo com melhoria da constipação no dia 14. As concentrações de transferrina melhoraram significativamente nos grupos com melhoria da diarreia e com diarreia e constipação recorrentes no dia 14.
Os investigadores chegaram à conclusão de que a alimentação com sonda com baixo conteúdo de FODMAP pode melhorar a diarreia e dar por resultado um melhor estado nutricional e facilitar o restabelecimento rápido da doença.
Referências:
So Ra Yoon et al, Low-FODMAP formula improves diarrhea and nutritional status in hospitalized patients receiving enteral nutrition: a randomized, multicenter, double-blind clinical trial.Nutrition Journal 2015, 14:116  doi:10.1186/s12937-015-0106-0
Pérez y López N, Torres-López E, Zamarripa-Dorsey F. Respuesta clínica en pacientes mexicanos con síndrome de intestino irritable tratados con dieta baja en carbohidratos fermentables (FODMAP). Revista de Gastroenterología de México, Volume 80, Issue 3, July–September 2015, Pages 180–185


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