Saccharomyces boulardii

    Categorized as a probiotic under the World Health Organization’s definition of a “live microorganism that confers a health benefit on the host,” S. boulardii differs from bacterial probiotics as a eukaryotic probiotic yeast. Although similar to Saccharomyces cerevisiae or baker’s yeast, S. boulardii has “distinct taxonomic, physiological, metabolic and genetic properties.”

    S. boulardii has an optimum growth temperature of 37 degrees Celsius, consistent with human body temperature. The yeast can maintain 65% viability up to 52 degrees Celsius, allowing for a shelf-stable product.

    While other treatments may be challenged by the gastrointestinal environment, S. boulardii is resistant to low and high pH and bile acids, allowing it to survive in the gastrointestinal tract for up to 3 hours. To support supplementation, encapsulation in sodium alginate or gelatin allows S. boulardii to remain viable in the presence of bile salts for longer.

    With a half-life of six hours, consistent administration of S. boulardii results in a stable concentration after three days of administration, with a further 2-5 days of clearance from the point of discontinuation.

    Transient and unable to effectively colonize the gut over the long term due to its inability to adhere to the epithelium, S. boulardii can influence the microbial profile of the individual to some extent, based on the pre-existing gastrointestinal microbial composition. This selective action of S. boulardii on the microbiota differentiates it from the actions of other probiotics.

 

Recommended Doses of Saccharomyces boulardii

 

General digestive function and microbiota support 500-1000 mg (10-20 billion)

Clinical dysbiosis following antibiotic therapy 750 mg (15 billion)

Prevention of traveler's diarrhea 250-1000 mg (5-20 billion)

Acute diarrhea in adults 500-750 mg (10-15 billion)

Antibiotic-associated diarrhea 250-1000 mg (5-20 billion)

Prevention of recurrence of Clostridium difficile infection 500-1000 mg (10-20 billion)

Treatment of Clostridium difficile infection 1000 mg (20 billion)

Giardiasis 500 mg (10 billion)

Treatment of enteral nutrition-related diarrhea 2000 mg (40 billion)

Helicobacter pylori eradication and reduction of antibiotic side effects 250-1000 mg (5-20 billion)

Ulcerative colitis adjunctive therapy 750 mg (15 billion)

Crohn’s disease 500-1000 mg (10-20 billion)

Irritable bowel syndrome 750-1000+ mg (10-20 billion)

HIV-related diarrhea 3000 mg (60 billion)

HIV-related gut integrity and microbiota modulation 339 mg (approx. 7 billion)

SIBO in systemic sclerosis 400 mg (8 billion)

 

Mechanism of action of S. boulardii:

 

Antitoxin/antimicrobial effect

-S. boulardii acts as a decoy receptor, blocking the receptor sites of pathogenic toxins and directly destroying pathogens, including Clostridium difficile.

-Acetic acid production by S. boulardii inhibits Esherichia coli survival while operating to lower pH, allowing antimicrobial activity of SCFAs.

-Stimulates secretion of proteins to cleave microbial toxins and reduce cAMP levels.

 

Physiological protection

-Preservation of enterocyte tight junctions and intestinal permeability, subsequently preventing fluid loss and bacterial translocation.

 

Modulation of the microbiota

-S. boulardii has little impact on the healthy microbiome, however, in the presence of antibiotic use, S. boulardii can support colonization of Enterobacteriaceae and Bacteriodes populations while decreasing Clostridium coccoides and Eubacterium rectale populations in the days following antibiotic use, as observed in animal studies.

-Provision of replacement microflora following disruption of the microbiota due to antibiotics, illness or surgery.

-Inhibition of the proliferation of opportunistic bacteria within the gastrointestinal tract, known as 'colonisation resistance'.

 

Metabolic regulation

-Capable of regulating the production of SCFAs, particularly following illness, preventing adverse changes in colonic fermentation.

 

Nutritional and trophic effect (endocrine gland stimulation)

-Reduction of mucositis - the inflammatory state of the gastrointestinal tract, including the mouth, often associated with chemotherapy.

-Improved protein (lactase, maltase, sucrase) and energy production1 supporting a reduction in lactose intolerance.

-Support for enterocyte maturation through the release of polyamines, spermine and spermidine involved in cell proliferation.

-Beneficial for the expression of intestinal digestive enzymes and nutrient absorption transporters.

-Support for intestinal glucose absorption.

 

Immune Modulation

-Working to reduce pathogen penetration across the intestinal epithelium, S. boulardii promotes immune exclusion by modulating the immune response, supporting the structure of gastrointestinal epithelial tight junctions, and increasing the concentration of secretory IgA and mucus in both intestinal fluid and cryptic cells to quarantine microorganisms.

-Stimulates secretion of intestinal secretory IgA as a first-line defense, preventing adhesion of pathogens, including C. difficile toxins.

-Modulation of the immune response, including stimulation and suppression of the inflammatory response1 by influencing levels of pro-inflammatory cytokines, including interleukin-8 and mitogen-activated protein kinases.

-Increases anti-inflammatory cytokines, including interleukin-4 and interleukin-10.

-Beta-glucan contained in the cell wall of S. boulardii is known for its immune modulation capacity.

-Inhibition of the growth of pathogens, including Candida albicans, S. typhimurum, Yersenia enterocolitium and Aeromonas hemolysin.

-Increases the production of IgM and Kupffer cells (liver macrophages).

-Interception of signal transduction pathways mediated by Nuclear Factor-kB involved in cytokine production and inflammation.

-Reversal of the action of the pro-inflammatory cytokine lipopolysaccharide by bacteria, reducing IL-6 and TNF-alpha.

-Secretion of proteins to minimize the adhesion of Citrobacter rodentium to epithelial cells.