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Does Candida Contribute to Crohns? Find out...
Candida is a popular yeast known to cause infections in the mucosal surfaces of the genitals and throat. However, it can also invade the gastrointestinal mucosa where it triggers Crohn’s disease. The link between Candida albicans and Crohn’s disease is well established and discussed in this article. But how does candida overcome the gut flora? What is the danger of candida invasion of the gut? And who is most at risk of candida overgrowth? Read on to find out.
Candida refers to a big family of yeasts. Most of the fungal species in the candida genus are harmless and even helpful. They can be found growing naturally on the skin, in the gastrointestinal tract and in the genital and urinary tracts.
However, changes in their growth environments can turn candida yeasts pathogenic. Such changes include reduced acidity of the stomach, antibiotic destruction of the intestinal bacterial flora and even transfer to a different location in the body.
The most popular member of the candida genus is Candida albicans. This species of candida normally grows in small numbers on the mucosal layers of the gastrointestinal, respiratory and genital tracts.
In the gut, Candida albicans turns sucrose into acid and glucose into acid and gas. It can be distinguished from other Candida species because it does not break down lactose.
Candida species can cause systemic infections when they and/or their toxins pass into the bloodstream. This form of candida infection known as invasive candidiasis is rare in the general population but common among patients with impaired immunity.
Clinical data show that the mortality rate from such infections is 40 – 50%.
Candida overgrowth in the gut can be treated with probiotics especially the bacterium, Saccharomyces boulardii.
Some of the drugs used in Crohn’s disease treatment can leave the gastrointestinal tract open to candida overgrowth.
When drugs such as oral antibiotics and steroids are taken by patients with this inflammatory disease over a long period of time, the right environment for candida invasion is created in the gut.
Broad-spectrum antibiotics wipe out both beneficial and pathogenic bacteria in the gut. This creates an imbalance in the normal gut microflora and leaves the intestinal mucosa open to opportunistic infections.
In addition, steroids such as prednisone are known to act by depressing immune reaction. Therefore, their actions may further weaken the already impaired immune system in Crohn’s disease.
The combination of immunosuppression and total bacterial wipeout in the gut not only increases the odds of unchecked growth of Candida albicans in the gut but also turns the otherwise beneficial yeast into a destructive pathogen.
When the population of candida fungi increases in the gut, they need more nutrients to sustain their growth. As they thrive and compete with other microbes in the gut, they turn pathogenic.
To ensure its survival, candida yeast releases mycotoxins in its immediate environment. These toxins irritate the gastrointestinal mucosa and also erode the lining of the stomach and intestines. These actions directly lead to the formation of lesions.
If the yeast growth is not stopped and reversed, the damage done by candida to the mucosa turn lesions to ulcers and then fissures.
The destruction caused by the invasive candida population as well as its metabolism can result in a number of symptoms including belching, gas, bloating, indigestion, acid reflux, constipation and diarrhea. These are the same symptoms commonly experienced by people with Crohn’s disease.
Therefore, candida overgrowth may be quite common in Crohn’s disease and some experts believe that this yeast is responsible for most of the gastrointestinal symptoms of inflammatory bowel diseases.
However, the harm done by candida invasion of the gut does not stop at the gut.
Both the yeast and its toxin can now penetrate the damaged lining of the intestine and get into the bloodstream.
Once in the blood, candida infections can cause fever as well as spread to other organs of the body.
A 2010 study published in the journal, Trends in Immunology, examined the genetic link between candida and Crohn’s disease.
The authors of the study identified a protein called NLRP3 (NOD-like receptor pyrin domain-containing protein 3) as one of the body’s defenses against candida overgrowth. They noted that activating the protein stops the growth and translocation of candida.
However, a defect in the activating mechanism of NLRP3 can open the gastrointestinal mucosa to microbes such as Candida albicans and quickly lead to the formation of inflammatory lesions as seen in Crohn’s disease.
A 2006 study published in the Journal of Clinical Microbiology investigated a different perspective of the genetic link between candida and Crohn’s disease.
In this study, the researchers linked the strains of C. albicans found in different members of 35 families with Crohn’s disease.
By isolating C. albicans from the digestive tracts of 234 participants from 25 families with Crohn’s disease and 10 control families, the researchers were able to determine the relationship between the strains of the yeast prevalent in each family.
First, the study showed that the prevalence of C. albicans in families with Crohn’s disease was 53.4% and in the control families, the yeast was found in 46.5% of the subject.
This result showed that C. albicans is a natural member of the gut flora even in healthy people.
However, a more important discovery was that the strains of C. albicans carried by members of each family were genetically identical. This result indicates that the yeast is easily transmitted between members of the same household.
In a rather curious twist, a group of researchers found that C. albicans infection can actually affect the bone even before Crohn’s disease is diagnosed. This means that is possible for the fungus to have reached the bloodstream even before patients see the classic symptoms of Crohn’s disease in the gastrointestinal tract.
In a paper published in the journal, Diseases of the Colon and Rectum, in 1998, four researchers detailed the case of a woman who was previously undiagnosed with Crohn’s disease but suffered from osteomyelitis caused by C. albicans.
The patient, a 48-year old woman, suffered from fever, chills, abdominal pain and knee pain.
Only after she was closely examined did her doctors discover that her small intestine had suffered from damage consistent with Crohn’s disease. Bone cultures also showed considerable colonization by C. albicans.
The doctors placed her on an aggressive treatment to get rid of the yeast in her bones and this prevented a full diagnosis of Crohn’s disease.
This unique case shows that even when there are no gastrointestinal symptoms and overt damage to the intestines, C. albicans colonization can proceed quietly and completely enough to reach and damage other organs of the body.
A 1991 study published in the journal, Gut, determined the difference between neutrophil activity in Crohn’s disease and in health subjects.
In this in vitro study, the researchers isolated neutrophils from normal subjects and patients with Crohn’s disease. Then they introduced C. albicans to these neutrophil samples before incubating them for 30 and 60 minutes.
The results showed that the neutrophils extracted from subjects with Crohn’s disease were less effective than those extracted from normal subjects.
In fact, the effectiveness of Crohn’s disease neutrophils decreased further at 60 minutes compared to 30 minutes.
Because neutrophils are the major immune cells responsible for phagocytosis (engulfment and destruction) of invading microbes, the impaired activity of these immune cells in Crohn’s disease can significantly affect the body’s ability to mount an effective immune response against the colonization of the gut by C. albicans.
This study shows that C. albicans disables the immune system’s offensive response to ensure its own survival.
Because foods are known triggers of Crohn’s disease, they can also influence the response of the immune system to the inflammatory bowel disease.
A study published in the journal, Inflammatory Bowel Diseases, in 2006 investigated such link between yeast and Crohn’s disease.
Yeast antigens are commonly found in foods and, over time, the body develops antibodies against these antigens. The most important antibodies developed against yeast antigen are known as ASCA (anti-Saccharomyces cerevisiae antibodies).
For this study, the researchers extracted lymphocytes from healthy subjects as well as patients suffering from ulcerative colitis and Crohn’s disease. These lymphocytes were challenged with yeast antigens such as mannan and ovalbumin.
The results of the study showed that
This study showed that yeast can trigger inflammatory response in Crohn’s disease.
Another study published in the journal, Clinical and Experimental Immunology, in 2004 examined another aspect of the genetic link between yeast and Crohn’s disease.
First, the researchers identified that ASCA differentiates Crohn’s disease from ulcerative colitis. Then they investigated possible links between ASCA and genes such as NOD2/CARD15 that are already known to contribute to Crohn’s disease.
By taking serums from 228 patients including 143 with Crohn’s disease, the researchers found out that ASCA was present in 57% of Crohn’s disease patients, 19% of patients with ulcerative colitis and 8% of healthy subjects.
Other conclusions from the study are:
Although ASCA have been identified as immune response to certain yeasts, the exact microbes (immunogen) that trigger the release of ASCA were once unknown.
A 2006 study published in the journal, Gastroenterology, identified C. albicans as an immunogen for ASCA.
To reach this conclusion, a group of researchers collected sera from patients with Crohn’s disease and systemic candidiasis as well as rabbits infected with C. albicans. The sera obtained were then purified and tested for ASCA.
The result of the study showed that in both humans and rabbits, ASCA were generated following the production of antibodies against C. albicans triggered by candida infections.
This result showed that C. albicans produced mannans that were functionally similar to the mannans in S. cerevisiae. Therefore, the immune system responded with ASCA thus making candida an immunogen for ASCA and the cause of impaired and misdirected immune response in Crohn’s disease.
A 2009 study published in the American Journal of Gastroenterology investigated the link between ASCA and C. albicans in families with genetic predisposition to Crohn’s disease.
The researchers noted that 50 – 60% of Crohn’s disease patients expressed ASCA and that these antibodies were also found in 20 – 25% healthy members of families with high risk of Crohn’s disease.
By taking samples from mouth swabs, stool specimens and sera of over 230 subjects from 41 Crohn’s disease families and 14 control families, the researchers were able to determine that
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