Absolutely. S. Boulardii is the real deal. When I was really sick, I always knew S. Boulardii was working because whenever I would take it, I would get WICKED GAS. I mean like the type of hot flatulence that could choke a horse. As I got better, S. Boulardii didn't give me nearly as much gas, until eventually, there was no change when taking it whatsoever.

Yes I think SB is the best probiotic for Candida. The only concern is that a lot of people with Candida are allergic to yeast. I know I am.

Summary
Saccharomyces boulardii is a non-pathogenic yeast with biotherapeutic properties that has been used successfully to prevent and to treat various infectious and antibiotic-associated diarrheas. The intestinal microbiota is responsible for colonization resistance and immune response to pathogens but can be disrupted by Antibiotics and lose its barrier effect. Dendritic cells (DCs) are professional antigen-presenting cells of the immune system with the ability to initiate a primary immune response or immune tolerance. In a human microbiota-associated mouse model, we evaluated the influence of S. boulardii on the composition of the microbiota and on the properties of dendritic cells in normal homeostatic conditions and after antibiotic-induced stress. The DCs were derived from splenic precursors. Membrane antigen expression and phagocytosis of FITC-latex beads by DCs were evaluated by flow cytometry. The molecular analysis of the microbiota was performed with fluorescence in situ hybridization (FISH) combined with flow cytometry or confocal microscopy using group specific 16S rRNA targeted probes. This evaluation was conducted during and after a 7-day oral treatment with amoxicillin-clavulanic acid alone and in combination with the administration of the yeast. The Antibiotic treatment increased the phagocytic activity of DCs. Their antigen presenting function (MHC class II antigen and CD 86 costimulatory molecule membrane expression) was up-regulated. This reflects a functional activation of DCs. In the presence of S. boulardii, the modification of membrane antigen expression was down regulated. To correlate these modifications to the microbiota disruption, we analyzed in parallel the composition of the intestinal microbiota. As previously shown, the amoxicillin-clavulanic acid treatment, both alone and with S. boulardii, did not quantitatively alter the total microbiota. In contrast, after one day of the Antibiotic treatment the Clostridium coccoides group decreased dramatically in the two groups of mice treated with the antibiotic. The level then increased regularly, and at days 17, 22 and 24 it increased faster (P < 0.05) in the AB+ Sb group than in the AB group, reaching the initial level at day 29. The Bacteroides group in the two groups of mice increased during the Antibiotic treatment and decreased after the antibiotic was stopped, reaching the initial level. The rate of decrease was faster for the AB+ Sb group than for the AB group, with a significant difference (P < 0.05) at days 17 and 22. During antibiotic treatment, the Enterobacteriaceae group became detectable and its level increased in both groups of mice. After discontinuation of the antibiotic, its level decreased to become undetectable at day 29, without significant difference between the two groups. These results showed that S. boulardii treatment tends to restore the balance of the dominant anaerobic microbiota more rapidly in human microbiota associated-mice treated with amoxicillin-clavulanic acid; the results also suggest that the yeast has a role in modulating the specific immune response to microbial associated-molecular patterns. This may explain, at least in part, the beneficial effects of S. boulardii in preventing antibiotic-associated diarrhea. This also suggests that the yeast plays a role in maintaining intestinal homeostasis.
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Summary
This review summarizes the probiotic mechanisms of action of Saccharomyces boulardii (S. boulardii) against inflammatory and non-inflammatory diarrheal conditions. S. boulardii is distributed in lyophilized form in many countries and used for the prevention of diarrhea in children and adults, including Clostridium difficile (C. difficile) associated infection. The main mechanisms of action of S. boulardii include inhibition of activities of bacterial pathogenic products, trophic effects on the intestinal mucosa, as well as modification of host signaling pathways involved in inflammatory and non-inflammatory intestinal diseases. S. boulardii inhibits production of pro-inflammatory cytokines by inhibiting main regulators of inflammation, including nuclear factor κB (NF-κB), and mitogen-activated protein kinases (MAP kinases), ERK1/2 and p38, but stimulates production of anti-inflammatory molecules such a speroxisome proliferator-activated receptor-gamma (PPAR-γ). Moreover, S. boulardii suppresses bacterial infection by inhibiting adhesion and/or overgrowth of bacteria, produces a serine protease that cleaves C. difficile toxin A, and stimulates antibody production against this toxin. Furthermore, S. boulardii may interfere with pathogenesis of Inflammatory Bowel Disease (IBD) by acting on T cells and acts in diarrheal conditions by improving the fecal biostructure in patients with diarrhea. These diverse mechanisms exerted by S. boulardii provide molecular clues for its effectiveness in diarrheal diseases and intestinal inflammatory conditions with an inflammatory component.

f you are taking s boulardii for candida, consider adding SAMe to increase treatment efficacy -- see research below.

S-Adenosyl-L-Methionine protects the probiotic yeast, Saccharomyces boulardii, from acid-induced cell death (Vincent Cascio, Daniel Gittings, Kristen Merloni, Matthew Hurton, David Laprade, Nicanor Austriaco OP)

"Abstract
Background
Saccharomyces boulardii is a probiotic yeast routinely used to prevent and to treat gastrointestinal disorders, including the antibiotic-associated diarrhea caused by Clostridium difficile infections. However, only 1-3% of the yeast administered orally is recovered alive in the feces suggesting that this yeast is unable to survive the acidic environment of the gastrointestinal tract.
Results
We provide evidence that suggests that S. boulardii undergoes programmed cell death (PCD) in acidic environments, which is accompanied by the generation of reactive oxygen species and the appearance of caspase-like activity. To better understand the mechanism of cell death at the molecular level, we generated microarray gene expression profiles of S. boulardii cells cultured in an acidic environment. Significantly, functional annotation revealed that the up-regulated genes were significantly over-represented in cell death pathways Finally, we show that S-adenosyl-L-methionine (AdoMet), a commercially available, FDA-approved dietary supplement, enhances the viability of S. boulardii in acidic environments, most likely by preventing programmed cell death.
Conclusions
In toto, given the observation that many of the proven health benefits of S. boulardii are dependent on cell viability, our data suggests that taking S. boulardii and AdoMet together may be a more effective treatment for gastrointestinal disorders than taking the probiotic yeast alone."