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Candidiasis is a fungal infection caused by Candida, a genus of yeast that lives on the skin and inside of the mouth, throat, vagina, and GI tract. Intestinal candidiasis refers specifically to an abnormally high level of Candida detected in samples from feces, rectal swabs, or (rarely) the intestinal mucosa (the lining of the stomach or intestinal tract).
Fungi make up a very small portion of the gut microbiome, with a population estimated at around 1 billion out of the 10 trillion microbes residing there. Most fungi in the gut are forms of yeast, such as Candida, Saccharomyces, and Malassezia. The genus Candida includes many species, but the most common is C. albicans. Depending on the sampling site and preparation, yeasts are detected in the feces of 4—97% of healthy people.
The fungal microbiome, or mycobiome, of the human gut is poorly understood. It is much lower in abundance, diversity, and stability than the bacterial microbiome but more unique to each individual. Some evidence suggests that most fungi aren’t inhabitants of the gut at all, but rather ingested with food and saliva (from the oral mycobiome).
To further complicate matters, fungi are dimorphic, meaning they can exist in different forms, and can change to a hyphal form, which is less adapted to the human gastrointestinal (GI) tract and potentially more pathogenic (likely to cause disease). Because gene expression differs between the fungal and hyphal forms of the same species, accurate identification and quantification (measuring the number) is challenging.
The role of the mycobiome in human health and disease is largely unknown. Some yeast species, such as C. albicans, exist as pathobionts, which are potential pathogens that remain harmless or even beneficial under normal conditions. Others, such as Saccharomyces boulardii, have known probiotic effects.
Though intestinal colonization is normal and harmless in healthy individuals, certain species of yeast can cause disease in immunocompromised individuals, premature newborns, and cases of surgery or inflammatory bowel disease (IBD) that damage the physical barrier of the intestinal wall. In these cases, microbes that reside in the gut can easily overcome the cellular or physical defenses of the immune system, escaping the intestines and entering the circulatory system. Yeast may also play a role in the development of antibiotic-associated diarrhea and certain respiratory and skin allergies, but more research is needed to establish causality.
Some species of yeast can cause disease in certain individuals, but most are considered normal (harmless) inhabitants of the human body. Research on the mycobiome is still emerging, so its role in health and disease is poorly understood.
Controversial publications from the 1970s and ’80s claimed that intestinal Candida overgrowth lead to a long list of ailments, including chronic fatigue, GI discomfort, recurring vaginal yeast infections, arthritis, acne, migraines, menstrual symptoms, and heart issues. Most of these claims have been debunked, however, and IC does not appear to have perceptible symptoms.
Exploratory studies suggest that Candida overgrowth could play a role in diarrhea associated with antibiotics and a specific subgroup of irritable bowel syndrome with diarrhea (IBS-D), but more research is needed.
Intestinal yeast colonization is estimated from rectal swabs, fecal samples, mucosal samples, or duodenal samples (from the area connecting the stomach and small intestine). In the past, swabs from these samples were grown on a plate, or cultured, before being counted, but recent technology allows researchers to estimate the number and types of yeast based on their genetic material within the sample. Breath tests cannot diagnose IC.
An average fecal sample is expected to contain less than 104 colony-forming units (CFU) per milliliter (mL). Studies generally classify a concentration of 103 to 105 CFU/mL as IC, but there is no consensus on the correct threshold for IC diagnosis.
The presence of IC alone doesn’t strongly predict the development of a systemic fungal infection, however. Clinical scoring systems, such as the Candida score and Candida index, estimate the risk of developing systemic fungal infections in critically ill patients. They include the extent of Candida colonization at multiple body sites in conjunction with other factors, such as length of hospital stay, prior use of antibiotics, prior surgery, and severity of the patient’s illness. Components of fungal cell walls can also be detected in serum, so blood testing can be used to indicate an early fungal infection like invasive candidiasis, a complication of IC.
IC may lead to invasive candidiasis in susceptible individuals, such as critically ill or immunosuppressed patients and premature babies. This occurs when fungi — most commonly the Candida species — escape the intestinal tract and infect other areas, such as the blood, brain, or heart. This leads to a fever that doesn’t go away after treatment with antibiotics, and can eventually progress to sepsis (a life-threatening immune system response) and death if untreated.
Though IC doesn’t require treatment in otherwise healthy people, it may be treated in at-risk individuals to prevent invasive candidiasis. In premature babies and critically ill patients, reducing or limiting intestinal Candida colonization lowers the risk of developing a systemic fungal infection. This is commonly done with antifungal drugs, but certain probiotics are also effective.
Oral or intravenous antifungal drugs kill or destroy fungi similar to the way antibiotics treat bacterial infections, suppressing their ability to overcome the immune system and intestinal barrier. However, preventive use seems to be more effective in preterm newborns compared with critically ill or surgical patients.   (Inappropriate use of antifungal drugs leads to drug resistance, so it is important to use these as directed by a physician.)
A recent meta-analysis of seven studies on 1,371 preterm infants total found that probiotics are unlikely to prevent (and cannot treat) invasive fungal infections, but they may reduce the risk of Candida colonization by about 43% in preterm babies. Two studies have shown that Saccharomyces boulardii and Lactobacillus reuteri are as effective as the antifungal drug nystatin for reducing the occurrence of Candida colonization (but not for treating invasive candidiasis) in this population.
Probiotics have also been studied in a group of critically ill, hospitalized children taking antibiotics. After 2 weeks, 50% of the placebo group was colonized by Candida, compared with 31% of the group who took a multi-strain probiotic supplement. However, the prevalence of candidemia was similar between the groups.
Vitamin D–supplemented yogurt and medium-chain triglycerides (MCT) have also been studied in children and infants, respectively, and have shown promising results for reducing Candida colonization or rates of invasive infection, but more research is needed. Read more.
It is important to note that total elimination of Candida and other fungi is likely impossible. Though antifungal drugs may reduce colonization below the detection limits of diagnostic tests, yeasts reach detectable levels again once the medications are stopped. This wouldn’t occur without some organisms surviving to multiply after treatment.
Antifungal drugs and certain probiotics can prevent IC from progressing to a systemic infection, but this is only necessary in at-risk individuals. Total elimination of intestinal fungi is likely impossible.
Most cases of IC (and subsequent invasive infection) are seen in preterm infants and critically ill or immunocompromised individuals. Certain medications, such as antibiotics and steroids, can also increase the risk of developing IC.
Immature immune systems, permeable intestines, invasive surgical procedures, hospitalization, and the use of broad-spectrum antibiotics make premature infants more prone to IC and invasive infections. (A suppressed immune system also increases the risk of oral and esophageal candidiasis in people with HIV or cancer, but whether this translates to IC is unknown.)
Emerging research suggests that people with diabetes may also be more prone to IC, but these findings are complicated by the participants’ use of antifungals, antibiotics, and steroids to control inflammation. Intestinal Candida counts can also be elevated as a result of swallowing oral Candida, and oral candidiasis (overgrowth of yeast in the mouth and throat) can occur in people who wear dentures or take the aforementioned medications.
Healthy people may experience a relative increase in Candida compared to bacteria while taking antibiotics, but the actual numbers of Candida may not reach abnormally high levels consistent with IC. This has been connected to antibiotic-associated diarrhea, but a causal relationship hasn’t been established. Early studies detected Candida in the stools of people with antibiotic-associated diarrhea, but they lacked a control group, so no conclusions could be drawn. Evidence from a small, uncontrolled study showed that antibiotic-associated diarrhea occurred in patients regardless of Candida colonization. Though antifungal medications resolved diarrhea in five of the seven colonized patients, diarrhea also resolved without treatment in two patients and didn’t resolve until after antibiotics were ceased in the non-colonized patients.
Long-term hospitalization, low or suppressed immune function, and certain medications can increase the risk of developing IC.
Many microbes in the intestines are potentially pathogenic, which means they could cause disease in certain circumstances. Their potential for causing disease is controlled by immune cells, the physical barrier of the intestinal walls, and other resident microbes of the GI tract.
In healthy people, the innate immune system controls Candida colonization by initiating the production of antimicrobial peptides (amino acid chains), and neutrophils (cells of the innate immune system) prevent Candida from escaping the GI tract and causing infection. Other microbes may communicate with the innate immune system to induce an antimicrobial response or produce metabolites, which suppress Candida growth.
There is also some evidence that the GI tract in mammals induces specific characteristics in Candida that make it less likely to cause disease. In other words, it trades its virulence (or ability to cause disease) for better chances of survival in the human gut.
Candidiasis can occur in the mouth and throat (often referred to as thrush), esophagus, or vagina (commonly called a yeast infection). Invasive candidiasis is an infection of other parts of the body, including the brain, blood, and heart. Candidemia, or a blood infection, is the most common form of invasive candidiasis. Candiduria, or Candida in the urine, is also a sign of invasive infection.
Small Intestinal Fungal Overgrowth (SIFO) is characterized by high numbers of fungi in the small intestine, while Small Intestinal Bacterial Overgrowth (SIBO) is caused by elevated numbers of bacteria. Much more is known about bacterial overgrowth, but it’s still poorly understood. It is thought that microbial overgrowth could play a role in unexplained GI symptoms such as gas, bloating, and abdominal pain.
Recent studies have used more accurate sampling and quantification methods to detect Candida_ and other forms of fungi in the small intestine. Though sampling this way can accurately detect intestinal overgrowth of bacteria and fungi, these studies found that the rates of unexplained GI symptoms were similar in participants regardless of their fungal colonization.
In a study that sampled the gastric (stomach) mucosa of people with dyspepsia (indigestion) or ulcer complaints, Candida was present in approximately 27% of the participants (with no control samples for comparison). A follow-up study compared participants with and without SIFO, and found no differences in the severity of the participants’ GI symptoms. In that study, 25% of the participants with unexplained digestive complaints also had SIFO.
Though prescription antacid medications and altered gut motility (organized muscular contractions) may increase the risk of developing SIBO, they aren’t associated with SIFO.
Controversial publications from the 1970s and ’80s claimed that intestinal C. albicans overgrowth impaired immune, thyroid, digestive, and adrenal function. This “Candidiasis Hypersensitivity Syndrome” allegedly led to a long list of ailments, including chronic fatigue, GI discomfort, recurrent vaginal yeast infections, arthritis, acne, migraines, menstrual symptoms, and heart issues.
An observational study of 26 participants with chronic fatigue syndrome and 50 healthy controls revealed no differences in the concentration of Candida antibodies in their blood samples, which indicates that Candida infections don’t play a role in chronic fatigue.
A more informative study compared antifungal treatment to a placebo in 42 women with alleged Candidiasis Hypersensitivity Syndrome and recurring vaginal yeast infections. Though the antifungal treatment resolved the vaginal yeast infections much more effectively than the placebo did, both were equally effective in reducing the systemic symptoms, such as fatigue, and psychological effects. This evidence strongly suggests that Candida colonization played no role in their physical symptoms.
The Executive Committee of the American Academy of Allergy, Asthma & Immunology released a position statement about this syndrome, critiquing the lack of evidence for any of its claims and the potential dangers of long-term antifungal drugs recommended by the program.
Though it’s unclear whether Candida plays a causal role, researchers have found low or altered fungal diversity in patients with IBD, and emerging evidence indicates that Candida species tend to predominate in the mycobiomes of patients with IBD.
Some species of Candida can colonize and delay the healing of gastric and intestinal ulcers. One small observational study found that certain species were detectable in inflamed regions of the intestines in Crohn’s disease but absent from the non-inflamed areas. One nonrandomized, uncontrolled study reported that two weeks of antifungal treatment in patients with ulcerative colitis and significant fungal colonization reduced disease activity and mucosal inflammation.
Without diagnostic criteria or the quantification of Candida colonization in these studies, however, it’s impossible to determine whether these cases would be characterized as IC or some form of fungal imbalance. Patients with IBD often use certain medications that increase the risk for fungal disease, which could also explain these findings.
Candida abundance is also associated with visceral hypersensitivity (a heightened sense of pain in response to normal gut functions) in a subgroup of IBS that responds well to antifungal treatment. Exploratory studies have noted that higher Candida abundance is associated with more severe bloating. Though Candida species are present in people with and without IBS, other emerging evidence suggests that C. albicans in people with IBS is genetically distinct from the same species in healthy people. The correlations between Candida and certain bacteria also differ between people with IBS-D and healthy controls. There is still no conclusive link between IBS and Candida, though. Despite some unique variations in IBS versus healthy controls, the mycobiome isn’t a useful biomarker for IBS due to high levels of individual variability and lack of any causal relationships.
Contrary to popular belief about 'Candida cleanse diets', refined carbohydrate intake doesn’t increase the risk of developing IC, and most yeast found in stool is likely derived from food and saliva.
Unlike the microbiome, the mycobiome is more closely associated with recent dietary patterns than with long-term habits. Some of the diet-Candida interactions could actually be artifacts of relationships between fungi and bacteria, the latter of which is more sensitive to dietary habits. For example, Candida are positively associated with short-term high-carbohydrate diets, but they’re also associated with Prevotella (a bacterial genus) and Methanobrevibacter (a major methane-consuming domain of single-celled organisms), both of which are also linked to high carbohydrate intake. These microbes could exist in symbiosis, supported by any form of carbohydrate ingested, since Candida can break down complex carbohydrates that could then be fermented by Prevotella, resulting in end products consumed by Methanobrevibacter.
The effects of refined carbohydrate intake were explored in a study of 28 healthy men and women. After a six-week baseline period, during which saliva and stool were collected weekly, participants’ total energy intake was increased by adding 110 grams of sugar to their diet for one week. Stool and saliva samples were collected on the third and seventh days of that week. Participants then followed their regular diet for another four weeks, and stool and saliva samples were collected weekly. Participants with higher levels of oral Candida also had higher levels of Candida in their stool, and only the 12 with the highest oral counts had an elevation in stool concentrations after the intervention. The sugar had no effect on the rest of the participants’ Candida counts. The authors concluded that the observed changes were minimal and healthy people aren’t at risk of developing candidiasis from high-sugar diets.
A low-yeast diet and frequent toothbrushing may reduce the amount of Candida and other yeast in stool samples. In a small study that controlled both diet and oral hygiene habits, four participants were placed on diets known to be low in fungi, while a fifth continued their regular diet. Their fecal samples contained fungi that were present in their saliva or recently consumed foods. In a case study, a participant followed a diet free of a specific form of yeast for two weeks, resulting in undetectable levels of that yeast in their stool until the foods were reintroduced.
In a similar pilot study, two participants were asked to alternate between brushing their teeth after every meal and brushing once per day, for two days at a time. The amount of Candida in their stool samples was significantly lower after more frequent brushing, which supports the idea that some portion of Candida in stool samples is actually derived from the mouth, not the intestines.)
A low-yeast, low-sugar diet has been suggested to treat the supposed C. albicans overgrowth alleged by some to cause chronic fatigue syndrome. In a 24-week randomized, controlled trial, 52 participants with chronic fatigue syndrome were assigned to a low-sugar, low-yeast diet or a healthy eating intervention based on guidelines from the United Kingdom’s department of health. The diets led to similar improvements in ratings of fatigue and general health, but more participants dropped out of the low-sugar, low-yeast group. Other evidence for this intervention is limited to anecdotes and a couple of small, flawed studies that lacked standardization or validated health questionnaires.
Though dietary interventions might change the yeast content of fecal samples, this is most likely due to changes in the amount of yeast ingested with food. The sugar content of the diet has little impact on intestinal Candida colonization.
Vitamin D–supplemented yogurt drinks have been studied in children, with promising results. In a randomized, controlled trial of 416 pediatric patients, the prevalence of candidemia and candiduria in the group receiving vitamin D supplementation (300 international units per day) was roughly half that of the placebo group, and the vitamin D group’s hospital stays were about four days shorter. (Intestinal colonization wasn’t reported at any point, so the effects on IC are unknown, but these results are more relevant to clinical outcomes.)
MCT supplementation was explored in a small randomized controlled trial of 12 preterm infants with Candida colonization. MCT oil is high in caprylic acid. During the three-week treatment period, infants receiving MCT experienced an average 84% reduction in fecal Candida colonization, while the control group exhibited a threefold increase. However, the infants’ diets weren’t standardized, so dose-dependent effects couldn’t be determined. Larger studies with dietary controls are needed to confirm these results.
Certain compounds extracted from oregano, pine, cinnamon, and coffee suppress Candida growth in cell culture models and denture stomatitis (mild oral inflammation due to thrush in denture-wearers), but these haven't been studied in the human GI tract.