Treating Gastrointestinal Candida Colonisation

Passé? Or Something to Consider?

Nowadays, with any mention of digestive symptoms of constipation, diarrhoea, gas, or bloating, and a history of antibiotic or proton-pump inhibitor use, one of the first things most integrative healthcare practitioners will consider in the differential diagnosis list is gastrointestinal dysbiosis with testing for small intestinal bacterial overgrowth (SIBO).[1] SIBO has a lot of hype—and how can it not, with so many conferences, practitioners, and clinics focused on its treatment? Given that the lactulose breath test (LBT), commonly used for the diagnosis of SIBO, has a low sensitivity and frequently gives false-positive results (although sensitivity can be improved via three-hour methane and hydrogen testing), it can be overused for the ease of diagnosing, well, something.[2]^,[3]

Fortunately, for many diagnosed with SIBO, symptoms do improve with a combination of dietary modification, digestive support (supplemental hydrochloric acid, enzymes, and/or ox bile), and antibiotics and/or herbal antimicrobials—and, in those with constipation, support for normal motility. However, in some patients, SIBO is seemingly resistant to treatment, even after many cycles of otherwise effective therapies. In this population, it is imperative that we consider other factors that may coexist leading to the symptomology that we often ascribe to SIBO.

Many of the factors that contribute to SIBO are also well-documented to contribute to candida colonization. Although we medically recognize an overgrowth of candida on the skin, vulvovaginal tissues, oral cavity, and numerous other locations as an indication for treatment, medical guidelines state that the presence of Candida spp. is normal in the gastrointestinal (GI) tract, and does not warrant treatment,[4] even though multiple studies have shown higher faecal levels of candida in conditions such as antibiotic-associated diarrhea.[5]^,[6] In the gut, candida colonisation also is associated with constipation,[10] Increased faecal candida counts have been shown in patients with inflammatory bowel disease,⁸ and, in individuals with ulcerative colitis, the lack of treating these patients with an antifungal has been shown to be associated with an increased level of disease activity.[11]

Given this knowledge, is it really appropriate for us to neglect considering GI candida colonisation (and its treatment) completely, particularly in the presence of these often-chronic conditions? Much like the LBT for SIBO, testing is plagued by the lack of an absolute threshold at which treatment is indicated; however, there are tests that indicate the magnitude of overgrowth and candida viability (as indicated by culture), as well as sensitivity to different antifungal agents (both natural and pharmaceutical). Such tests give us a starting point for addressing candida colonisation—though, much like SIBO, many factors are necessary to consider for its successful resolution.

Taming Candida Overgrowth

Because the presence of candida is normal, we must consider the factors that lead to its overgrowth when addressing treatment. If we only use hard-hitting antifungals to eradicate candida, it will likely return in full force because we haven’t addressed the terrain that leads to colonisation to begin with. Immune system function. Below is a list of considerations for candida overgrowth and data supporting its use as a therapy:

• Saccharomyces boulardii: A probiotic yeast, boulardii has been shown to decrease candida colonisation and related inflammation.[19] S. boulardii inhibits candida filamentation, adhesion, and biofilm formation,[20] and also supports mucosal production of secretory IgA,[21] a factor that helps protect against candida and other infections.[22]
• Certain Lactobacillus: L. acidophilus,[23] L. casei, and L. rhamnosus GG[24] have been shown to reduce the formation of candida-related biofilms and candida colonisation via mechanisms similar to S. boulardii,[25] also improving tissue healing and resolution of inflammation.¹¹

• Colostrum and lactoferrin: Colostrum provides immunoglobulins, proline-rich peptides, and a small amount of lactoferrin, each factors that support a normal immune response and help protect against infection.[26] Colostrum also provides growth factors that support mucosal healing and repair, while lactoferrin exerts broad antimicrobial effects, with numerous studies showing its effectivity against candida in vitro and in vivo.[27]^{,[28],[29],[30]} Colostrum can be a particularly effective treatment for GI pathogens and dysbiosis in settings of immunodeficiency.[31]^,[32]

• Oregano (Origanum vulgare): The essential oil of oregano has broad-spectrum antimicrobial properties,[33] inhibiting candida growth and diminishing its virulence.[34]^,[35] Carvacrol, one of the primary antimicrobial constituents found in oregano, has been demonstrated to dramatically reduce candida colonisation in animal models of an immunocompromised host.[36]^,[37] Oregano also may help reduce colonisation of methanogenic bacteria,[38] commonly associated with constipation-type SIBO, and Blastocystis hominis,[39] a parasite that can lead to GI symptoms.[40]
• Black walnut (Juglans nigra): Tannins and juglone are among the antimicrobial constituents of black walnut hulls,[41]^,[42] which have a history of traditional use for the treatment of fungal and parasitic infections.[43] Clinical research has shown us that juglone and extracts from the walnut plant have antifungal properties,[44] including activity against numerous strains of albicans.[45]^,[46] In animals, treatment of C. albicans with a product containing a black walnut husk extract was shown to be similarly effective to the standard antifungal treatment.[47] The extract of black walnut husk was also shown to be effective against C. tropicalis and C. krusei,[48] which have both been implicated in recurrent or chronic vulvovaginal candidiasis (VVC).[49]
• Pau d’arco (common name referring to various Tabebuia): Pau d’arco is a tree that is native to tropical regions of South and Central America, used traditionally for a variety of bacterial and fungal infections as well as malaria and trypanosomiasis.[50] Although limited data exists with human trials, the two main bioactive components of pau d’arco (lapachol and beta-lapachone, extracted from the inner bark) have demonstrated considerable anti-inflammatory and antifungal effects in vitro. Extracts of pau d’arco or these isolates have been shown to effectively inhibit multiple species of candida including C. albicans, C. parapsilosis, and C. tropicalis.[51]^,[52]

• Caprylic acid: Caprylic acid is a medium-chain fatty acid, also known as octanoic acid, found at high levels in virgin coconut oil. Both coconut oil and caprylic acid have been shown to strongly inhibit candida in vitro.[53]^,[54] Caprylic acid and other similar fatty acids exert antifungal effects by disrupting cellular membranes and impeding critical metabolic processes,[55] as well as reducing albicans biofilm formation and inhibiting the yeast-to-hyphae transition.[56]^,[57] The observed anti-Candida action of S. boulardii may be largely due to its secretion of caprylic, capric, and other fatty acids with antifungal effects.[58]

• Biotin: Biotin, a B vitamin often recognised for its importance for skin, hair, and nail health,[59] also may be important in difficult-to-resolve Candida infections. In individuals with biotin deficiency, a chronic scaly, erythematous dermatitis around orifices may exist, from which C. albicans has often been cultured.[60] Biotin deficiency, in the absence of gross malnutrition or gastrointestinal disorders, is often attributable to biotinidase deficiency, an inborn error of metabolism present in approximately 1 of 123 individuals. Although the number of individuals experiencing a profound deficiency of this enzyme is low (and often is evident in infancy), a larger proportion of the population may have a partial deficiency, which leads to 10 to 30% of normal biotinidase function.[61] A case report discusses the resolution of a chronic, 14-month case of VVC (and prevention of its recurrence) in a woman with biotinidase deficiency after being treated with 20 mg of biotin daily.[62] Studies have shown that up to half of pregnant women in the U.S. are marginally biotin deficient (particularly by later stages of pregnancy), despite normal intake,[63]^,[64] which may contribute to the increased rate of VVC during pregnancy.

 

Clearly, a wide array of nutritional tools exist that may help to reduce candida colonisation and improve the body’s resistance to recurrent infection. Although not clinically “diagnosable,” gastrointestinal candida overgrowth, much like other states of dysbiosis, can be a factor in many chronic conditions and may be improved with natural treatments.

 References

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