Is there such a thing as intestinal candida overgrowth?

Not according to Tamara Duker Freuman, writing in the health section of US News & World Report. According to Freuman, candida overgrowth is “health misinformation couched in pseudoscience”, “One of the more common online health fictions”, “a mythical condition”.

If you’re not familiar with candida (Candida albicans), it is a species of yeast that lives in your gut, which is also home to bacteria, with which we have a symbiotic relationship. You probably already know that eating yogurt or fermented vegetables can help populate your gut with “good” bacteria, which play an important role in gut health and immune function.

Candida overgrowth is when the normal balance of intestinal flora becomes upset and the yeast takes over.

In my own research into this subject, I have noticed a tendency in the mainstream to dismiss candida overgrowth. One doctor I know described it as “fringe” medicine when I brought it up in conversation. My own primary care physician likewise dismissed it when I mentioned it to him. I’ve encountered abundant articles online doing likewise, including Freuman’s, which kept popping up in Google search results. According to her,

Candida does not infect the small intestine nor does it overgrow in the colon. In fact, searching the term “Candida overgrowth” in PubMed, the national database of over 22 million published biomedical research studies maintained by the National Institutes of Health, turns up nothing. Unless every medical researcher who studies Candida, digestive health, infectious disease or immunology is in on a conspiracy to hide the truth, it’s pretty safe to say that “Candida overgrowth” is not an actual phenomenon.”[1]

This is extraordinary ignorance.

Going back as far as 1985, a study of hamsters showed that antiobiotic treatment killed off beneficial bacteria in the animals’ guts, which “predisposed hamsters to gastrointestinal overgrowth and subsequent systemic dissemination by C. albicans in 86% of the animals.” They suggested that “the indigenous intestinal microflora suppress C. albicans colonization and dissemination from the gut by inhibiting Candida-mucosal association and reducing C. albicans population levels in the gut.”[2]

A follow-up study two years later showed that treating mice with antibiotics “allowed C. albicans to proliferate in the gut and, subsequently, disseminate from the GI tract to visceral organs.” They again suggested that the gut bacteria “are responsible for the inhibition of C. albicans adhesion, colonization and dissemination from the GI tract.”[3]

Another follow-up study in 1987 compared mice treated with antibiotics to untreated mice, showing that “Candida cells only penetrated into the mucosa of animals in which the ecology of the intestinal microflora had been disrupted.”[4]

A 1999 study noted that while candida is found in the GI tract of healthy people, in people with a compromised immune system, “local gastrointestinal candidiasis and disseminated invasive infection are through to arise from gastrointestinal colonization and overgrowth of C. albicans.” Candida overgrowth has been “associated with a variety of clinical symptoms,” including diarrhea, psoriasis, and dermatitis. The study stated that “Infections due to Candida albicans occur readily in situations in which ample glucose is available. In mice, dietary refined carbohydrate supplementation leads to higher rates of Candida growth in the gastrointestinal tract and favors mucosal invasion.” It concluded that a high-sugar diet did not result in candida overgrowth in healthy individuals and noted the role that bacteria play, stating that the gut bacteria “are known to modulate candida growth”.[5]

In sum, there is a balance of flora in the gut and if this balance is disrupted (dysbiosis), such as through the use of antibiotics, which kill off beneficial gut bacteria, an overgrowth of candida can occur.

Furthermore, a 2000 study published in the Journal of Clinical Microbiology noted that, “Despite the association between intestinal lesions and systemic disease, gastrointestinal candidiasis has not been well studied. The interactions of C. albicans with the gastrointestinal mucosa are not well defined, and the mechanisms of invasion and systemic dissemination have not been identified.” Newborn piglets were orally inoculated with candida, which “led to the development of extensive mucocutaneous candidiasis, intestinal lesions, and disseminated disease. The intestinal lesions likely represent a significant portal of entry for the organism into the bloodstream.” The paper notes that, “Although intestinal candidiasis is not commonly diagnosed, human cases of infection have been reported and studied…. Autopsy studies of infants and children infected with Candida demonstrate that the small intestine is one of the most common sites of infection….” The study’s results supported “the hypothesis that virulent organisms create lesions and significantly damage the GI tract, allowing them to escape the GI tract, overwhelm the host defense mechanisms, and become hematogenously disseminated.[6]

A 2001 paper in Clinical and Vaccine Immunology stated that “Increased intestinal colonization is generally accepted as a major risk factor that predisposes high-risk patients to systemic candidiasis.”[7]

A 2002 paper in the British Journal of Nutrition stated that “Overgrowth of candida in the gut is also a frequent consequence of antibiotic therapy.”[8]

A 2005 study in Gut (a journal of The BMJ, formerly the British Medical Journal) “hypothesized that Candida colonization promotes food allergy, which is known to contribute to a pathogenic response in atopic dermatitis.” The results of a study in mice suggested “that gastrointestinal Candida colonisation promotes sensitisation against food antigens, at least partly due to mast cell mediated hyperpermeability in the gastrointestinal mucosa of mice.”[9]

In other words, an overgrowth of candida can result in a damaged gut lining, leading to increased intestinal permeability—commonly known as “leaky gut” (a whole other area about which there is similar institutional ignorance)—which in turn can cause food allergies.

The findings of 2011 study of mice similarly suggested “that C. albicans gut colonization in mice aggravates inflammation in allergic and autoimmune diseases, not only in the gut but also in the extra-gut tissues and underscores the necessity of investigating the pathogenic role of C. albicans gut colonization in immune diseases in humans.”[10]

A 2012 study noted that “The bacterial microbiota of the stomach is vital in promoting gastric colonization resistance against the opportunistic pathogen C. albicans.” It stated that the use of an antibiotic “can promote C. albicans overgrowth in mice and humans, suggesting that its spectrum of activity encompasses bacteria that are critical for colonization resistance against C. albicans outgrowth or invasion.” It concluded that “The role of the microbiome in regulating inflammatory responses to members of the indigenous microbiome is an area of current interest for a number of diseases. The potential ramification of understanding the process of C. albicans colonization is illustrated by research from our lab and others that has demonstrated that gastrointestinal colonization by C. albicans in mice can promote sensitization against intranasally and orally delivered antigens, such as food.”[11]

This is by no means an exhaustive list, just a number of the studies I have come across in my own quest for better health. Anyone who knows how to use Google can do a search of the scientific literature on the subject[12]—a body of literature Tamara Duker Freuman claims doesn’t even exist.

So, no, it isn’t a myth. And, no, believing that it is real doesn’t mean you must also think that there is some kind of conspiracy theory to cover up its existence. There is no conspiracy. There are just a lot of ignorant professionals out there—including many and probably most doctors—who just don’t know what they are talking about because they haven’t done any kind of proper research.

Freuman provides an instructive example of this by actually telling us all the research she did before writing her article: “searching the term ‘Candida overgrowth’ in PubMed”—which would exclude results I found, for example, containing the following: “…overgrowth and subsequent systemic dissemination by C. albicans…” and “…gastrointestinal colonization and overgrowth of C. albicans…”, “Overgrowth of candida in the gut…”, and so on.

So, yes, candida overgrowth is very real and well-established in the scientific literature, including its potential role in causing leaky gut and the development of food allergies. There are people out there suffering from it. For them to be told that the cause of their symptoms doesn’t exist and for their intelligence to be insulted if they beg to differ is the height of unprofessionalism.

References

[1] Tamara Duker Freuman, “We All Have Candida (And it’s OK!)US News & World Report, December 10, 2013.

[2] M J Kennedy and P A Volz, “Ecology of Candida albicans gut colonization: inhibition of Candida adhesion, colonization, and dissemination from the gastrointestinal tract by bacterial antagonism,” Infection and Immunity, September 1985, 654-663.

[3] Michael J. Kennedy and Paul A. Volz, “Effect of various antibiotics on gastrointestinal colonization and dissemination by Candida albicans,Medical Mycology, 1985, Vol. 23, No. 4, 265-273.

[4] M. J. Kennedy, P. A. Volz, C. A. Edwards, and R. J. Yancey, “Mechanisms of association of Candida albicans with intestinal mucosa,Journal of Medical Microbiology, December 1987, Vol. 24, No. 4, 333-341.

[5] Michael Weig, Edgar Werner, Matthias Frosch, and Heinrich Kasper, “Limited effect of refined carbohycrate dietary supplementation on colonization of the gastrointestinal tract of healthy subjects by Candida albicans,” American Journal of Clinical Nutrition, June 1999, Vol. 69, No. 6, 170-1173.

[6] Karl A. Andrutis, Perry J. Riggle, Carol A. Kumamoto, and Saul Tzipori, “Intestinal Lesions Associated with Disseminated Candidiasis in an Experimental Animal Model,” Journal of Clinical Microbiology, June 2000, Vol. 38, No. 6, 2317-2323.

[7] Stephen M. Wiesner, et al, “Gastrointestinal Colonization by Candida albicans Mutant Strains in Antibiotic-Treated Mice,” Clinical and Vaccine Immunology, January 2001, Vol. 8, No. 1, 192-195.

[8] L. J. Fooks and G. R. Gibson, “Probiotics as modulators of the gut flora,” British Journal of Nutrition, September 2002, Vol. 88, Suplement S1, 39-49.

[9] N Yamaguchi, et al, “Gastrointestinal Candida colonization promotes sensitization against food antigens by affecting the mucosal barrier in mice,” Gut, January 2006, Vol. 55, Issue 7.

[10] Kei Sonoyama, et al, “Gut colonization by Candida albicans aggravates inflammation in the gut and extra-gut tissues in mice,” Medical Mycology, 2011, Vol. 39, Issue 3, 237-247.

[11] Katie L. Mason, et al, “Interplay between the Gastric Bacterial Microbiota and Candida albicans during Postantibiotic Recolonization and Gastritis,” Infection and Immunity, January 2012, Vol. 80, No. 1, 150-158.

[12] http://scholar.google.com/.

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