Gastro

#Anti-histamínicos podem ajudar pacientes com #diarreia crônica

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medica sorrindo para paciente

 

De acordo com uma recente série de casos publicada no Annals of Allergy, Asthma & Immunology, alguns pacientes com diarreia pós-prandial idiopática (DPP) podem responder ao tratamento com anti-histamínicos.

“O PPD anti-histamínico é visto em pacientes com urticária idiopática crônica e/ou dermatografia, e pode ser distinguido da síndrome de ativação de mastócitos (MCAS). Essa síndrome também deve ser considerada no diagnóstico diferencial de pacientes que apresentam intolerância alimentar após a exclusão de alergia alimentar e outros distúrbios gastrointestinais”, explica a médica Yasmin Hassoun, da Universidade de Cincinnati, em Ohio, nos Estados Unidos.

A diarreia crônica é um problema comum que afeta até 5% dos adultos, e o PPD compreende um subconjunto dessa condição.

Os autores do estudo relatam a ocorrência de DPP idiopática em cinco pacientes com idade entre 26 e 63 anos, com duração da diarreia de oito semanas a 13 anos. Todos os cinco pacientes tiveram dermatografias concomitantes. Três pacientes (duas mulheres e um homem) também tinham uma história atual ou anterior de urticária crônica, e três mulheres possuíam uma história atual ou anterior de angioedema.

Nenhum dos pacientes havia experimentado um evento desencadeante inicial, como doença viral. Em todos os cinco casos, a diarreia ocorreu apenas após as refeições ou lanches, e dentro de três horas após a ingestão da comida.

No entanto, nenhum dos pacientes mostrou qualquer evidência de alergia alimentar ou intolerância alimentar. O soro de quatro dos cinco pacientes foi rastreado para IgE específica para alimentos e testado como negativo. Três dos pacientes também realizaram uma dieta isenta de lactose e outras dietas de eliminação sem qualquer melhoria nos sintomas.

Testes adicionais foram realizados em alguns casos, incluindo anti-transglutaminase IgA tecidual (em quatro pacientes) para descartar doença celíaca , triptase sérica (em quatro pacientes), prostaglandina F urinária de 24 horas (em três pacientes) e 24 horas N-metil-histamina urinária (em dois pacientes) para investigar a possibilidade de MCAS. Todos esses testes foram normais.

Quatro dos pacientes também foram submetidos à endoscopia digestiva alta e colonoscopia. Lesões foram encontradas em apenas dois desses pacientes. Uma mulher de 55 anos apresentou colite linfocítica e outra mulher de 63 anos apresentou inflamação gástrica e úlcera. No entanto, esses achados não poderiam explicar um distúrbio gastrointestinal subjacente para explicar a diarreia.

Após eliminar a alergia ou intolerância alimentar subjacente, a doença gastrointestinal ou o MCAS como causa da DPP, todos os cinco pacientes receberam pré-tratamento diário com anti-histamínicos H 1 e H 2.

Este tratamento resolveu o PPD para dois pacientes e aliviou-o para os três restantes. “As respostas benéficas nesses pacientes aos bloqueadores de receptores H1 e H2 sugerem que a histamina liberada pelos mastócitos GI é um mediador chave da diarreia pós-prandial”, escreveu Yasmin Hassoun.

Embora o mecanismo exato pelo qual o alimento estimula os mastócitos GI seja desconhecido, os pesquisadores supõem que o peristaltismo possa ter um papel na ativação dos mastócitos.

 

O médico David I. Bernstein, também da Universidade de Cincinnati, disse ao Medscape Medical News que esperaria que a maioria dos pacientes com DPP idiopática e urticária idiopática crônica concomitante e/ou dermatografia respondesse a esse tipo de terapia anti-histamínica. “Mas há graus variáveis ​​de resposta, de 60% a 100% de controle dos sintomas gastrointestinais”, enfatizou.

Embora não se saiba com que frequência este subgrupo de pacientes visita clínicas de alergia ou gastroenterologia, a equipe de David Bernstein está planejando mais estudos para determinar isso.

Estas são “observações de caso único interessantes com benefício do tratamento combinado com bloqueadores H1 e H2 “, disse Michael Camilleri, professor de medicina, farmacologia e fisiologia na Mayo Clinic em Rochester, Minnesota, em uma entrevista Medscape Medical News.

A afirmação dos autores de que “o papel fisiológico dos mastócitos no trato gastrointestinal não foi claramente definido” é apropriada, pois segundo Michael Camilleri. esta associação pode ser mais relevante, como sugerido, em pacientes com urticária crônica ou angioedema.

De acordo com Camilleri, os receptores de histamina H1 também mostraram estar envolvidos na modulação da sensação de dor em pacientes com síndrome do intestino irritável (SII). Em um estudo recente, a ebastina, um antagonista anti-H1 seletivo, reduziu hipersensibilidade visceral, sintomas, e dor abdominal em pacientes com IBS.

Estudos adicionais podem incluir a avaliação da prevalência e história natural deste PPD e dos esquemas terapêuticos ideais.

#Desenvolvido exame não invasivo para doenças intestinais

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Fonte de imagem: Valter Longo Foundation

Futuramente, o diagnóstico e monitorização de doenças dos intestinos poderão ser efetuados de forma não invasiva, com apenas uma amostra de sangue e fezes.

Uma equipa de investigadores do Laboratório do Centro para Investigação Pré-clínica, da Universidade de Medicina de Varsóvia, Polónia, está a desenvolver uma nova análise não invasiva que avalia a função dos intestinos.

A nova análise poderá ajudar a fazer o rastreio e a monitorizar o tratamento das doenças dos intestinos apenas com uma pequena amostra de 1ml de sangue e fezes. O funcionamento dos intestinos é avaliado pela barreira intestinal.

A barreira intestinal consiste num sistema complexo de múltiplas camadas, que é comparável a um filtro finamente sintonizado que controla rigorosamente a passagem de nutrientes e bloqueia a passagem de bactérias desde o interior dos intestinos para a corrente sanguínea.

Os pacientes com doença inflamatória do intestino (DII) e outras doenças intestinais têm a barreira intestinal danificada. A parede intestinal passa a atuar de forma semelhante a uma manga rasgada, permitindo a passagem de produtos bacterianos (produzidos pelas bactérias durante o metabolismo) dos intestinos para a corrente sanguínea.

Chama-se a este fenómeno síndrome do intestino permeável.

É precisamente a concentração de produtos bacterianos intestinais que a nova análise mede no sangue e fezes do paciente.

O método de diagnosticar e monitorizar a DII é atualmente baseado na colonoscopia. Além de ser invasiva, a colonoscopia requer frequentemente anestesia e apenas avalia lesões estruturais em vez de problemas no funcionamento dos intestinos.

Outro problema é que as doenças intestinais podem desenvolver-se antes de qualquer alteração estrutural ser visível.

A avaliação do funcionamento intestinal pode permitir aos médicos diagnosticar as doenças numa fase mais precoce, o que permitirá controlar os sintomas antes que se tornem severos, melhorando a qualidade de vida do paciente.

BancodaSaúde

#En busca de un #gen modulador que proteja frente al #Crohn

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Actúan como unos sensores de la expresión de los genes de susceptibilidad y se activan para impedir el desarrollo de la enfermedad de Crohn.

¿Por qué hay personas que tienen genes que les predisponen a sufrir la enfermedad de Crohn y no la padecen? ¿Por qué hay otras que no tienen ese perfil genético y, sin embargo, la desarrollan? Son preguntas que la investigación que dirige Urko Martínez Marigorta tratará de responder. El punto de partida es una hipótesis que deriva de las conclusiones de un estudio realizado en Estados Unidos y en el que participó: hay una interacción entre genes moduladores y genes de susceptibilidad, de manera que los primeros actúan como sensores de la expresión de los segundos y se activan para evitar el desarrollo de la enfermedad.

Urko Martinez Marigort.

La existencia de genes buenos no es una novedad para la ciencia. Se han asociado con la longevidad o con la resistencia al VIH, a la hepatitis C y al cáncer. Desde que se descifró el genoma humano, es factible averiguar el perfil genético de cualquier individuo, lo que puede ser muy útil en medicina siempre que se gestione bien esa información. Es necesario recordar que el que una persona tenga determinados genes asociados con alguna enfermedad no significa, la mayoría de las veces, que vaya a padecerla. “Esta realidad nos descubre una capa de individuos que evidentemente tienen algo que les protege”, añade Urko Martínez.

Su investigación, financiada por la Fundación La Caixa y que se lleva a cabo en el CIC BioGUNE del País Vasco, se centra en la enfermedad de Crohn y, en última instancia, busca adaptar la terapia a las características genéticas de los pacientes. En concreto, se fija en las personas que genéticamente están predispuestas y no la tienen, y al revés, en las que no lo están y la desarrollan”.

Martínez Marigorta, en colaboración con Azucena Salas, gastroenteróloga del Hospital Clínico de Barcelona, ha reclutado a cien pacientes del Departamento de Gastroenterología que dirige Julián Panes en el centro hospitalario catalán. El primer objetivo es averiguar cuáles son los genes moduladores de la enfermedad y el mecanismo por el que compensan la acción negativa de los genes de susceptibilidad.

El precedente inmediato es el estudio de Estados Unidos, que duró diez años y en el que participaron 1.500 pacientes de Crohn: “La idea era ver qué niños iban a evitar la cirugía. Medimos la expresión de los genes y vimos que había genes relacionados con la enfermedad de Crohn que retornaban a niveles normales en los niños con mejor evolución”, explica.

Dos candidatos

Los investigadores detectaron, al menos, dos genes que posiblemente son activados para ejercer una actividad moduladora que podría evitar la aparición de esta patología o al menos su curso más agresivo. El primero es CD226, un receptor de inmunoglobulinas implicado en el control de las infecciones víricas: “Pese a que los enfermos de Crohn suelen tener una variante que disminuye la expresión de CD226, aquellos pacientes que consiguen revertir esta tendencia, aumentando los niveles de expresión de este gen más allá de los niveles medios vistos en personas sanas, acaban teniendo una prognosis más suave”.

El otro gen es TNFRSF18, implicado en mantener la inmunotolerancia y que también está particularmente elevado en pacientes con buen perfil patológico.

El objetivo es identificar los genes moduladores y el mecanismo por el que compensan a los de susceptibilidad en Crohn

El hecho de que en ambos casos la variante genética típica de los enfermos sea la que hace disminuir sus niveles de expresión, mientras que aquellos pacientes que muestran mejor curso de la enfermedad consiguen elevarlos al máximo, podría significar que estos dos genes actúan como sensores de riesgo y que se estimulan como mecanismo de protección ante la acción de otros genes de susceptibilidad o factores de riesgo ambientales (infecciones víricas, estrés o tabaquismo): “De este modo, quizás se activan para modular el riesgo una vez que el cuerpo ha entrado en una fase de peligro, como por ejemplo altos niveles de inflamación crónicos en el intestino”. La identificación de todos esos genes buenos y entender cómo se produce su efecto modulador para que los genes malos disminuyan su expresión, permitirá hacer una predicción más afinada y menos determinista. “Además, es necesario conocer el riesgo genético de manera dinámica, a lo largo de toda la vida”, puntualiza el director del estudio.

Las mediciones se realizarán durante los próximos seis meses. Los investigadores evaluarán los niveles de expresión genética en tres momentos: al inicio del tratamiento con tres biológicos (infliximab, ustekinumab y vedolizumab), transcurridas 14 semanas y, finalmente, a las 46 semanas: “Describiremos el perfil genético de cada paciente, los clasificaremos en alto y bajo riesgo, y observaremos qué genes cambian los niveles de expresión”.
Ese perfil genético de riesgo se calculará en función de las variantes genéticas presentes en más de 250 genes malos. Entre éstos, destacan el NOD2, un gen clásico para Crohn y el primero que se descubrió implicado en el riesgo de esta enfermedad; el ATG16L1, un gen que se asocia a la autofagia celular, que es un proceso que no se sospechaba que estaba relacionado con la enfermedad inflamatoria intestinal; o los genes de la familia TNF y otras citocinas, como TNF-alpha o IL23, que estimulan la acción inflamatoria de las células T y son las dianas terapéuticas que están más de moda en el diseño de fármacos para enfermedades autoinmunes.

Un mecanismo en otras enfermedades

El líder de la investigación, Urko M. Marigorta, pone el acento en las posibilidades para el tratamiento de la enfermedad de Crohn que se pueden plantear si se logra entender bien el mecanismo celular que se produce entre los genes moduladores y los de susceptibilidad, ya que las compañías farmacéuticas podrían explorar este camino para trabajar en nuevas terapias. Asimismo, ayudaría a comprender las razones por las que un grupo de pacientes no responden al tratamiento con biológicos, sobre el que hay evidencia científica acerca de su efectividad reduciendo la inflamación e impidiendo la progresión de la enfermedad en otras muchas personas.

Por otra parte, Marigorta está convencido de que esta hipótesis se puede aplicar a otras dolencias: “Me gustaría aplicar estos mismos modelos a cualquier enfermedad”. De hecho, en este estudio también trabajará con pacientes que sufren colitis ulcerosa, que, como el Crohn, es un subtipo de la enfermedad inflamatoria intestinal.

“Pienso que se puede estudiar en otras enfermedades porque se ha visto que existen los llamados genes malos en muchas y, sin embargo, la mayoría de las personas no desarrollan esas patologías, así que creo que la interacción entre los genes buenos y malos se puede dar en cualquier enfermedad”, señala el investigador.

La diabetes tipo 2 ilustra perfectamente esta situación. Recientemente se ha visto que el riesgo de desarrollar esta enfermedad se triplica para el 5% de la población con más carga genética asociada a diabetes. Considerando que la prevalencia de esta enfermedad en España es del 12%, alrededor de un tercio de los individuos de este subgrupo desarrollarán diabetes tipo 2 en algún momento de su vida. Pero al mismo tiempo, este pronóstico no se cumplirá con los otros dos tercios de las personas con más carga genética. Entender las razones puede significar una clave esencial para identificar dianas terapéuticas que han permanecido ocultas hasta ahora.

#El equilibrio de la #microbiota intestinal alarga la vida

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Un estudio liderado por científicos españoles analiza la relación entre un microbioma sano y mayor longevidad.

Imagen de la bacteria Akkermansia muciniphila.

Bacterias, virus, hongos y otros microorganismos que conviven en nuestro intestino tienen voz y voto no sólo en la aparición de enfermedades como la diabetes y la obesidad, también en la esperanza de vida. Un estudio pionero con apellido español demuestra que las alteraciones de la microbiota intestinal contribuyen al envejecimiento acelerado.

“Identificamos varias clases de proteobacterias asociadas”, explica Carlos López-Otín, uno de los líderes del trabajo que acaba de publicar la revista Nature Medicine. La bacteria más destacada: la Akkermansia muciniphila. Así como en recientes estudios ha demostrado un efecto positivo en la respuesta a inmunoterapia de pacientes con cáncer, ahora se postula como clave en el incremento de los años de vida.

Tras el análisis de la microbiota de centenarios españoles, “observamos un aumento de bacterias beneficiosas como Akkermansia muciniphila“. Precisamente este microorganismo aparecía en una proporción más reducida en las muestras examinadas de los ratones con progeria, una rara enfermedad que provoca un envejecimiento acelerado durante la infancia y conduce a la muerte prematura de los pacientes. Le ocurre a una de cada cuatro millones de personas.

El equipo de científicos de la Universidad de Oviedo estudió también la microbiota de cinco pacientes con progeria. Se ha demostrado que los ratones y los pacientes afectados presentan un desequilibrio de la microbiota intestinal (disbiosis intestinal) y el objetivo era identificar las alteraciones causantes y “analizar si las bacterias cuyos niveles estaban alterados ejercían un papel beneficioso o perjudicial”, argumenta López-Otín.

Clea Bárcena y Pedro M. Quirós, principales autores del trabajo.

Clea Bárcena y Pedro M. Quirós, principales autores del trabajo.

Reconocida la bacteria Akkermansia muciniphila, el grupo de investigadores puso en marcha dos vías de tratamiento en los ratones enfermos: el trasplante fecal de sus semejantes sanos y la terapia con la bacteria probiótica Akkermansia muciniphila. Así se consiguió extender sus vidas. Como explica la primera firmante del trabajo, Clea Bárcena, “el reemplazo de la microbiota endógena de los ratones con progeria por microbiota proveniente de ratones sanos mejoró diversos parámetros metabólicos, además de alargar la esperanza de vida; en cambio, los ratones sanos que recibieron un trasplante con microbiota de ratones con progeria mostraron alteraciones metabólicas como aumento de peso y de los niveles de glucosa en sangre”.

En definitiva, este trabajo demuestra que el desequilibrio intestinal podría solventarse con un trasplante de microbiota y establecerse como futura terapia de afecciones relacionadas con el envejecimiento. Esta técnica ha sido claramente exitosa para las infecciones recurrentes con Clostridium difficile (una bateria que causa diarrea) existen múltiples ensayos clínicos para otras enfermedades (colon irritable o la enfermedad de Crohn), pero todavía existen muchos aspectos que deben ser resueltos antes de extender este tipo de tratamientos a otras enfermedades. “Hay que ser muy prudentes para evitar banalizar los trasplantes fecales, lo cual puede llevar a situaciones fatales. Por ello, dadas las dificultades y riesgos derivados de administrar tratamientos basados en flora intestinal completa, será de gran interés definir qué organismos concretos es conveniente administrar en cada caso”, aclara uno de los principales autores de la investigación.

Estrategias anti-envejecimiento

Con las conclusiones de este estudio español sobre la mesa, ahora toca definir con mayor precisión las alteraciones de la microbiota más relevantes en el proceso de envejecimiento con técnicas de mayor resolución y, como explica López-Otín, “también será importante explorar los mecanismos moleculares responsables de los efectos beneficiosos o perjudiciales causados por los microorganismos identificados”.

El objetivo: tratar de diseñar estrategias anti-envejecimiento y anti-progeria basadas en combinaciones de probióticos o de determinados componentes moleculares derivados de estos microorganismos.

El científico español reconocido en todo el mundo lleva los últimos 20 años de su carrera profesional trabajando sobre el envejecimiento, el normal y el patológico. Precisamente en el año 2013, cuando estaba preparando un trabajo acerca de las claves de la longevidad (The Hallmarks of Aging), empezó a plantearse el estudio del microbioma. A medida que cumplimos años, argumenta López-Otín, “se produce una pérdida de la homeostasis celular y una degeneración de los tejidos, lo que genera una alteración del ambiente que lleva a una disbiosis que va a favorecer el envejecimiento”.

Dados los sólidos resultados encontrados en ratones, “posiblemente en el futuro podamos mejorar e incluso curar las alteraciones en la microbiota con trasplantes personalizados de ciertas bacterias”, puntualiza el investigador español. Sin embargo, hacen falta más estudios para confirmar los efectos en humanos. De momento, “la mejor forma de mantener una microbiota sana es con una vida y alimentación sana, con un consumo adecuado de verduras, legumbres y frutas; evitar el consumo de tóxicos como el alcohol, el tabaco y las drogas; tomar fármacos y antibióticos únicamente cuando es necesario y ha sido prescrito por un médico, permanecer lo más posible en armonía y equilibrio emocional…

En cuanto a la ingesta de probióticos, puntualiza López-Otín, “no siempre son beneficiosos. Puede ocurrir que la población de bacterias probióticas crezca demasiado, provocando un segundo desequilibrio en la simbiosis de la microbiota. Como con todo, el uso de los probióticos debe ser racional y personalizado para cada caso”.

#Signs and symptoms of colon cancer in men

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Resultado de imagem para colon cancer

The digestive system is complex, which makes the symptoms of colon cancer difficult to catch. As a result, it is vital to attend regular colon cancer screenings.

Colon cancer, which is also called colorectal cancer, is the third leading cause of cancer-related deaths in both men and women in the United States. For men, the overall risk of developing colon cancer is about one in 22, which equates to 4.49 percent.

Many symptoms can indicate colon cancer, but if someone has these symptoms, it does not necessarily mean that they have this disease. There are many other explanations for the symptoms, such as infections or inflammatory bowel disease (IBD).

However, anyone experiencing new symptoms may wish to visit a doctor for a diagnosis.

The symptoms of colon cancer are the same in men and women and include the following:

1. Changes in bowel habits

Man speaking to doctor in waiting room about symptoms of colon cancer in men.

A person who suspects that they may have colon cancer should speak to a doctor.

An upset stomach or a minor infection can often cause changes in the bowels, such as constipationdiarrhea, or very narrow, thin stools. However, these issues usually resolve within a few days as the illness subsides.

Changes in the bowels that last more than a few days may be a sign of an underlying health issue.

If a person has these symptoms regularly or for longer than a few days, they should see a doctor.

2. Cramps and bloating

Occasional cramps or bloating are common digestive issues that can occur due to an upset stomach, gas, or eating certain foods.

Experiencing frequent, unexplained cramps and bloating can be a sign of colon cancer, though these symptoms are more often the result of other health issues.

3. Feeling as though the bowels are not empty

If a growth turns into a blockage in the colon, it may cause the person to feel as though they can never empty their bowels.

Even if their bowels are empty, they will still feel the need to use the restroom again.

4. Blood in the stool

Seeing blood in the stool can be frightening. The stool may have streaks of fresh red blood, or the whole stool may have a darker, tarry appearance.

There are many other possible causes of bloody stools, such as hemorrhoids. However, anyone experiencing blood in their stool should still see a doctor for a diagnosis.

5. Unexplained weight loss

Suddenly and unexpectedly losing weight is a sign of several types of cancer. Unintentionally losing 10 pounds or more within 6 months may be a sign to report to a doctor.

In people with cancer, the weight loss may be due to cancer cells consuming more of the body’s energy. The immune system is also working hard to fight the cancer cells.

If the tumor is large, it may lead to blockages in the colon, which can cause bowel changes and further weight loss.

6. Fatigue

People with colon cancer may feel constant fatigue or weakness, possibly due to the cancer cells using extra energy and the stress of bowel symptoms. Although feeling tired now and then is normal, chronic fatigue does not go away with rest.

Chronic fatigue is generally a symptom of an underlying condition. Anyone experiencing fatigue should see a doctor to help determine the cause.

7. Shortness of breath

Once cancer begins to drain energy from the body and fatigue sets in, it is common for people to experience related symptoms, such as shortness of breath.

They may find it difficult to catch their breath or might become winded very quickly from something as simple as walking a short distance or laughing.

Risk factors

Senior african american black father with son in army uniform at home.

African-Americans have a higher risk of developing colon cancer than people from other ethnic backgrounds.

Some factors may increase a person’s risk of developing colon cancer, including:

  • a personal history of digestive issues, such as colorectal polyps or IBD
  • a family history of polyps or colorectal cancer
  • some inherited gene mutations, such as hereditary nonpolyposis colorectal cancer (HNPCC)
  • getting older
  • having type 2 diabetes
  • some ethnic backgrounds, including being African American or Ashkenazi Jewish

It is not possible to prevent cancer in all cases, but making lifestyle changes to eliminate some risk factors may help a person reduce their likelihood of developing colon cancer.

Diet

As the American Cancer Society (ACS) note, a diet that is high in red meat or processed meat products increases the risk of colorectal cancer.

These foods include:

  • beef
  • pork
  • lamb
  • venison
  • liver
  • hot dogs
  • deli cuts
  • luncheon meat

Cooking meats at very high temperatures, such as on the grill or in a broiler or deep fryer, releases carcinogenic chemicals. These chemicals may also increase the risk of a person getting colon cancer, though the relationship between meat cooking methods and cancer is still unclear.

Weight

Being overweight or having obesity increases a person’s risk of developing or dying from colon cancer.

According to the ACS, the link between obesity and colorectal cancer also seems to be stronger in men. Losing weight can help reduce the risk.

Inactivity

Being physically inactive increases the risk of developing colon cancer. Staying active by doing even light workouts each day may help reduce this risk.

Alcohol use

People who drink heavily or regularly may also be putting themselves at greater risk of colon cancer. Men should limit their drinking to no more than two drinks per day.

Smoking

People who smoke are more likely to develop or die from colon cancer than those who do not. Smoking cigarettes also increases the risk of many other types of cancer.

Treatment

Surgery is a common treatment for colon cancer.

Surgery is a common treatment for colon cancer.

Colon cancer is highly treatable and often curable if the diagnosis takes place at an early stage when the cancer is only in the bowel and has not spread to other areas of the body.

Surgery is the most common first-line treatment for colon cancer, and it has a cure rate of about50 percent.

A surgeon will remove the cancerous growth and any nearby lymph nodes as well as a section of healthy tissue surrounding the growth. They will then reconnect the healthy parts of the bowel.

Many early forms of colon cancer do not require further treatment.

If the cancer is advanced, surgeons may need to remove more of the colon, and if the disease reaches too low into the rectum, the surgeon may remove this part of the large intestine.

Sometimes, doctors recommend chemotherapy to people who may have a higher risk of recurring tumors.

When to see a doctor

In most cases, digestive symptoms do not indicate cancer. However, if the symptoms are unusual, appear more regularly, or steadily get worse, it is best to see a doctor as there is no other way to diagnose these issues.

Even if the underlying cause is not colon cancer, the doctor may be able to identify and diagnose a separate disorder for which they can recommend treatment.

Many people with colon cancer do not show any early symptoms so experiencing symptoms can be a sign that the cancer is growing or spreading. The ACS recommend that men and women with an average risk of colon, or colorectal, cancer begin screening at the age of 45 years. Doctors can diagnose and treat colon cancer in the early stages if a person regularly attends screenings.

Outlook

Anyone who notices new, unexplained digestive symptoms or is uncertain about their symptoms should see a doctor.

Early screening and diagnosis are crucial in people with colon cancer. When doctors diagnose colon cancer before it spreads, the 5-year relative survival rate is 92 percent. However, survival rates are lower among people who do not get a diagnosis until a later stage.

MedicalNewsToday

#Pro-inflammatory diet linked to #colorectal cancer risk

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    •  Univadis Medical News

A new study published in the journal Nutrients suggests a link between a pro-inflammatory diet (e.g. refined carbohydrates, mono-sodium glutamate, gluten, aspartame, alcohol and trans fats) and risk for colon cancer.

In the population-based multi-case-controlled study, researchers in Spain calculated the energy-adjusted dietary inflammatory index (E-DII) and total dietary non-enzymatic antioxidant capacity (NEAC) in 1,852 colorectal cancer and 1,486 breast cancer cases, along with 3,447 and 1,652 population controls, respectively.

Analysis of the data revealed that E-DII was associated with increased risk for colorectal cancer (highest versus lowest quartile odds ratio [OR] 1.93; 95% CI 1.60-2.32; Ptrend<.001). The association was observed for both colon and rectal cancer. The association was less pronounced for breast cancer (highest versus lowest quartile OR 1.22; 95% CI 0.99-1.52; Ptrend>.10).

The combination of high E-DII scores and low antioxidant values was associated with colorectal cancer risk (highest versus lowest quartile OR 1.48; 95% CI 1.26-1.74; Ptrend<.001), but not breast cancer.

The authors concluded that the findings provide evidence that a pro-inflammatory diet is associated with increased colorectal cancer risk, while findings for breast cancer are less consistent.

#High blood pressure: Could gut bacteria play a role?

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We investigate whether the bacteria that live in our guts could influence our blood pressure. If so, could they guide future treatment?
Blood pressure home monitor

Hypertension is growing in prevalence, but can we blame gut bacteria?

Scientists are growing increasingly interested in the role of gut bacteria.

Each week, journals publish many study papers that examine how these microscopic visitors might play a role in health and disease.

As it stands, because the microbiome is a relatively new field of study, the full scope of gut bacteria’s role in health is still up for debate.

However, it is becoming increasingly clear that the bacteria in our gut can open new avenues in our understanding of a wide range of conditions.

Scientists have studied the role of gut bacteria in conditions as varied as obesityParkinson’s diseasedepression, and blood pressure.

This Spotlight focuses on their role in hypertension. Elevated blood pressure is a risk factor for cardiovascular disease and affects almost 1 in 3 adults in the United States.

Because of this, it is vital that medical scientists unearth the various mechanisms that underpin blood pressure regulation.

One study paper puts hypertension’s impact into sobering context: “Over 400 ,000 deaths in the United States are related to [hypertension] every year, more than all the Americans who died through all of World War II.”

Beyond standard risk factors

Although researchers have established certain risk factors for hypertension — such as smoking, obesity, and drinking excessive amounts of alcohol — there appears to be more to the condition.

More than 19% of the U.S. adults with hypertension have a treatment-resistant form of the condition, wherein medications do not bring blood pressure down to a healthful level. Also, lifestyle interventions do not work for everyone.

Some scientists are considering dysfunction of the immune system and autonomic nervous system. This is the branch of the nervous system that controls “automatic” functions, such as breathing, digestion, and blood pressure.

A relatively new addition to this list of potential risk factors is gut dysbiosis, which refers to an imbalanced microbial community.

A study in the journal Microbiome analyzed the gut bacteria of 41 people with ideal blood pressure levels, 99 individuals with hypertension, and 56 people with prehypertension.

Prehypertension refers to high blood pressure that is not yet high enough for a person to receive a diagnosis of hypertension. People in this range have an increased risk of developing hypertension in the future.

They found that in the participants with prehypertension or hypertension, there was a reduction in the diversity of gut bacteria. In particular, species such as Prevotella and Klebsiella tended to be overgrown.

Next, the scientists transplanted fecal matter from the participants into germ-free mice, which are animals that lack gut bacteria. The mice that received fecal matter from people with hypertension also developed hypertension.

Conversely, the authors of a 2019 study in the journal Frontiers in Physiology transplanted feces from mice without hypertension into mice with hypertension. This resulted in a reduction in blood pressure in the mice with hypertension.

Another study investigated the bacterial residents of pregnant women with obesity and overweight pregnant women, both of whom are at increased risk of hypertension. They found that in both sets of participants, bacteria of the genus Odoribacter were significantly rarer.

Those with the lowest levels of Odoribacter had the highest blood pressure readings.

How do gut bacteria affect blood pressure?

Although evidence is mounting that gut bacteria can influence hypertension, most of the studies to date have been observational.

Anatomy model

From the gut, chemicals can quickly enter the rest of the body.

This means that it has not been possible to determine whether changes in gut bacteria influence blood pressure, or whether hypertension (or the factors that produce it) alter gut bacteria.

Also, it is still unclear exactly how gut bacteria drive these changes.

Although the gut and blood pressure might not seem like obvious companions, the connection is not, perhaps, so surprising.

Many of the factors that increase the risk of hypertension — such as the consumption of alcohol and salty food — enter the body through the digestive system.

Nutrients, along with certain chemicals that bacteria produce, have the opportunity to enter the blood supply; once in circulation, the body is their oyster.

Also, the gastrointestinal tract hosts a number of processes that have the potential to play a role in hypertension, including metabolism, the production of hormones, and a direct connection with the nervous system.

Short chain fatty acids

Some researchers believe that one of the links between the gut and hypertension could be short chain fatty acids (SCFAs). Some gut bacteria produce these molecules as they digest dietary fiber.

After bacteria have produced SCFAs, the host’s blood suppy absorbs them. SCFAs affect a range of physiological processes, one of which appears to be blood pressure.

Backing this theory up, one study found differences in gut bacterial populations between participants with and without hypertension. Individuals with higher blood pressure had lower levels of certain species that produce SCFAs, including Roseburia spp. and Faecalibacterium prausnitzii.

One paper in the journal Hypertension investigated the role of gut bacteria in sleep apnea-induced hypertension. Sleep apnea is a condition wherein an individual’s breathing is disrupted during sleep.

The scientists simulated sleep apnea in rats. To so do, they fed half of the rats a standard diet and the other half a high fat diet. Hypertension only appeared in the rats that ate the fatty diet.

Next, they assessed the mice’s microbiome and found that the high fat group had a significant reduction in numbers of bacteria responsible for producing SCFAs.

Finally, the scientists transplanted bacteria from the hypertensive rats into the rats who ate a normal diet and demonstrated normal blood pressure.

This fecal transplant produced hypertension in the previously healthy animals.

Nervous control

Most likely, if gut bacteria truly do have the power to produce hypertension, it is likely to be via a number of interlinked routes. Scientists have several theories. For instance, some experts see a role for the autonomic nervous system.

Nervous system anatomy

How does gut bacteria influence the nervous system?

Studies have shown that hypertension is associated with increased sympathetic nerve activity (a branch of the autonomic nervous system). This increases gut permeability.

If the gut walls become more permeable, it is easier for the gut’s contents to leak through into the rest of the body.

This change in permeability impacts the gut environment and alters the microbiome. At the same time, bacterial products can pass more easily into the blood.

Interestingly, other factors — including smoking tobacco and being stressed — also alter the sympathetic system. This could help provide further reasons why these factors can also lead to cardiovascular changes.

A probiotic for hypertension?

Designing a probiotic that reliably reduces high blood pressure will take some time, but some researchers are looking at this option.

2013 meta-analysis examined the effect of probiotic fermented milk on blood pressure. In all, they took data from 14 studies, which included 702 participants. Although the authors write that “[s]ome evidence of publication bias was present,” they concluded that:

[P]robiotic fermented milk has blood pressure-lowering effects in prehypertensive and hypertensive [people].”

2014 systematic review and meta-analysis investigated probiotics more generally. Its authors only included randomized controlled trials, and their search only turned up nine papers that fit their criteria.

Overall, they concluded, “The present meta-analysis suggests that consuming probiotics may improve [blood pressure] by a modest degree.”

They also noted that the effect appeared to be more pronounced for people whose initial blood pressure readings were high, when the study used multiple bacterial species, and when the researchers tested the intervention for more than 8 weeks.

In the current scientific climate, the public has a substantial appetite for probiotics; however, outside of a small number of specific conditions, there is little evidence that they can benefit human health substantially or reliably.

With that in mind, it is likely to be a long time before a probiotic will bring blood pressure down.

For the future

Science is relatively new to the question of gut bacteria’s impact on blood pressure, so plenty more work will be needed. Although some evidence now supports the interaction between gut bacteria and hypertension, it is a complex beast to dissect.

Our diet, the drugs we take (particularly antibiotics), other health conditions we might have, and many more variables can all influence our gut bacteria.

Bacteriophages (viruses that attack bacteria), fungi, and parasites also find a home in the gut and influence both bacterial populations and our physiology.

This mystery will only unravel slowly, but at least the wheels of research are now in motion. As one reviewer writes:

Evidence is rapidly accumulating implicating gut dysbiosis in hypertension. However, we are far from understanding whether this is a cause or consequence of [hypertension], and how to best translate this fundamental knowledge to advance the management of [hypertension].”

MedicalNewsToday