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VSL#3 is a probiotic supplement that contains as much as 900 billion live bacteria in each serving. VSL#3 probiotic is a probiotic nutritional supplement that contains 8 different strains of live lactic acid bacteria.
The supplement is officially classified as medical food due to its high potencies: this isn’t your average probiotic supplement you would pick up from Walmart.
The reason you need a prescription to buy VSL#3 DS is because it’s not classified as a nutritional supplement: it’s a medical food for the dietary management of an ileal pouch or ulcerative colitis. If you need to ask more questions or request a refund on your VSL#3 order, you can call customer service at 1-866-438-8753. VSL#3A® is a probiotic blend that is intended to be used under the supervision of a doctor. Many a€?healthya€? yoghurts are likely to be useless, as the a€?good bacteriaa€? they contain are destroyed in the stomach, according to a study. In some cases drinking probiotic yoghurts and drinks on an empty stomach was the only way to reap their benefits. Scientists from University College London tested eight probiotic brands, such as yoghurts and drinks, to see whether they delivered as much good bacteria as they claimed.
The brands were Actimel, Align, Symprove, Bio Balance, Probio 7, Yakult, VSL#3 and Bio-Kult.
Salcombea€™s first development of new properties right on the watera€™s edge for almost twenty years. Pouchitis affects those, typically with ulcerative colitis, who have undergone ileal pouch-anal anastomosis (also known as j-pouch surgery), to create a surgical alternative to the colon. Evidence from clinical experience also supports this theory, concluding that the disorder "appears to be associated with high concentrations of bacteria"1. Although it must be said that research is in its early days, initial evidence for the use of probiotics in the treatment of ileal-anal pouch inflammation is promising. Each serving contains 112.5 billion live bacteria, although there are different versions of the supplement that contain 225 billion, 450 billion, and 900 billion live bacteria as well. It’s a pharmaceutical-grade medical food designed to treat the symptoms of ulcerative colitis, irritable bowel syndrome, and other harmful diseases. These bacteria line the walls of your GI tract, protecting your gut from pathogens and harmful bacteria.
Pouchitis occurs when this surgically created pouch, known as an ileal-anal pouch or J-pouch, becomes inflamed.
There is, however, to date not enough evidence to suggest that probiotics are of use in treating acute, severe pouchitis a€“ more research is needed into this aspect and indeed into the clinical use of probiotics for pouchitis in general. However, you’ll need a prescription to buy VSL#3-DS (it has 900 billion live bacteria in each serving). This condition affects approximately thirty-two percent of patients with an ileo-anal pouch.
Illumina 16S sequencing demonstrated that VSL#3 significantly decreased (16-fold) the abundance of a bacterial taxon assigned to genus Clostridium in the mucosally-adherent microbiota.
Mediation analysis by linear models suggested that this taxon was a contributing factor to increased tumorigenesis in VSL#3-fed mice. Animal models and human clinical trials indicate that probiotics may reduce inflammation and alleviate symptoms of IBD4, and it is tantalizing to consider that beneficial effects may also extend to CRC.

The majority of probiotic research has centered around effects on the mammalian host with less emphasis on exploring the impact of probiotics on commensal microbes inhabiting the GI tract, commonly referred to as the gut microbiota.The gut microbiota is a population of an estimated 100 trillions of microbes that reside within the GI tract and participate in a symbiotic relationship with their mammalian host. This population of microbes harbors 100-fold more genes than are found in the human genome, and its enzymatic capacity rivals that of the human liver5. Alteration in the composition of the gut microbiota, termed intestinal dysbiosis, is now regarded as a driving force behind the pathogenic features of IBD and appears to similarly impact the development of CRC6,7,8.
Culture-independent rRNA sequence analyses have revealed differences in community composition of the luminal and mucosally-adherent microbiota between human IBD patients and healthy controls9,10. Similar analyses on human CRC patients have revealed significant differences in the luminal microbiota of cases vs.
Although it remains unclear which specific microbial taxa promote development of inflammation and CRC, several bacterial groups have been consistently identified as altered in these disease states. Bacteroidetes, a dominant phylum of the gut microbiota, were found to be less abundant in the tissue of adenoma-bearing patients and human colorectal tumors relative to that of healthy controls4,13,15. Bulgaricus, Lactobacillus paracasei, Lactobacillus acidophilus, Bifidobacterium breve, Bifidobacterium longum, Bifidobacterium infantis, and Streptococcus salivarius subsp. Orally administered VSL#3 has shown success in ameliorating symptoms and reducing inflammation in human pouchitis20,21 and ulcerative colitis22,23.
The mechanisms underlying the beneficial functions of VSL#3 are not well understood, but likely involve direct effects of probiotic activity on the mammalian host as well as indirect effects by altering the population dynamics of the gut microbiota as a whole. In the rat TNBS model of inflammation-associated CRC, early administration of VSL#3 altered microbial diversity and delayed the transition from inflammation to dysplasia31,32.
Thus it is clear that VSL#3 probiotic has the capability to prevent inflammation and carcinogenesis when used as a preventative strategy. However, the therapeutic potential of VSL#3 probiotic administered after the onset of inflammation remains unknown.The goal of the present study was to assess the ability of probiotic cocktail VSL#3 to alter the colonic microbiota and decrease inflammation-associated cancer when administered as interventional therapy. In fact, we observed increased tumorigenesis in one of two cohorts of VSL#3-fed mice, relative to VSL#3-untreated mice. Illumina sequencing of this microbiota revealed that microbial community composition of the stool and mucosally-adherent compartments were significantly altered by VSL#3 administration.
Depletion of a bacterial taxon assigned to genus Clostridium from the mucosally-adherent microbiota was identified as a mediator of VSL#3-enhanced tumorigenesis in this cohort. Conventionalizing mice born and raised in GF conditions negates the confounding factor of familial transmission of the microbiota. However, macroscopic assessment of tumor penetrance revealed no significant effect of VSL#3 on tumorigenesis, assessed seventeen weeks after the initial AOM injection (Fig. There was a potential trend towards greater depth of tumor invasion in VSL#3-treated animals that did not reach significance (Fig. Seventeen weeks after the initiation of tumorigenesis with AOM, miniature endoscopy of live anesthetized mice revealed large macroscopic lesions in VSL#3-treated animals that were rarely seen in VSL#3-untreated animals (Fig. Macroscopic examination of harvested colon tissue revealed that VSL#3-treatment induced visible tumors in 91% of mice, a significantly greater amount than the 38% observed in VSL#3-untreated mice that developed macroscopic lesions (Fig. Tumor multiplicity was also significantly enhanced by VSL#3, with an average of 1.64 macroscopic tumors per mouse vs. Histologic analysis of colonic sections revealed a significantly enhanced dysplasia score in VSL#3-treated animals (Fig.
As observed in the first cohort, the cancer in VSL#3-fed animals was highly penetrant, with nearly all animals exhibiting advanced neoplasia (Fig.

The majority of the VSL#3-fed mice harbored invasive adenocarcinomas (79% of mice), in contrast to only 13% of VSL#3-untreated mice (Fig. To gain greater insight into the inflammatory environment of the colon, we measured inflammatory cytokine mRNA in colon tissue biopsies using an Inflammation PCR Array.
There were no significant differences in the expression of common IBD- and CRC-associated cytokines including Ifng, Il18, Tnf, Il1b, Il23a, and Il6 (Fig.
To determine the extent to which VSL#3 alters the microbiota, we utilized Illumina HiSeq2000 high-throughput sequencing. We extracted DNA from stool samples to assess the luminal microbiota and from colon tissue biopsies to assess the mucosally-adherent microbiota and sequenced the hypervariable V6 region of the 16S rRNA gene8.
We sequenced the luminal microbiota of all animals, and one representative animal per cage for the mucosally-adherent microbiota. Analysis of similarity (ANOSIM) was used to test for dissimilarity between groups, where R = 1 is maximum dissimilarity.
VSL#3-treated animals exhibited a significant contraction of Verrucomicrobia and expansion of Proteobacteria in the mucosally-adherent microbiota.
SPF = 10 mice in 4 cages, SPF + VSL#3 = 14 mice in 5 cages.Full size imageDepletion of a Clostridium bacterial group is associated with VSL#3 administration and tumorigenesisTo determine if microbial alterations in the mucosally-adherent microbiota mediate the effects of VSL#3 on tumorigenesis, we performed mediation by linear models analysis40 (Figure 8a and Methods section). We next applied model 2 to test the association of the relative abundance of all OTUs of the mucosally-adherent microbiota with dysplasia. We found that only a single taxon of the mucosal niche, OTU#199, had a significant association with dysplasia score (Benjamini and Hotchberg FDR corrected p = 0.0518).
The Benjamini and Hotchberg FDR adjustment was applied for multiple testing correction (model 2). We tested the effect of VSL#3 on dysplasia score without the influence of OTU#199, and found a high P-value (0.9399), which indicates that VSL#3 treatment is not directly associated with dysplasia. In contrast, when we tested the effect of OTU#199 on dysplasia score without the influence of VSL#3, we found a low P-value (FDR corrected P = 0.0692), supporting that the abundance of OTU#199 is associated with dysplasia. Although some of the beneficial impacts of probiotics have been scientifically documented, mechanisms of action and impact on established disease remained unclear. Introduction of billions of bacteria in a confined ecosystem such as the intestine is likely to impact the microbial community. Earlier work employing molecular fingerprinting analyses, including terminal restriction fragment length polymorphism (TRFLP) and denaturing gradient gel electrophoresis (DGGE), have revealed that administration of VSL#3 probiotic can alter microbial community composition of mice and rats23,29,43,44. Interventional administration of VSL#3 altered the composition of the luminal and mucosally-adherent microbiota with phylum level changes in the luminal microbiota (decrease in Bacteroidetes) and mucosally-adherent microbiota (decrease in Verrucomicrobia and increase in Proteobacteria).
Depletion of specific bacterial groups at the family level, with Verrucomicrobiaceae in the adherent compartment and Porphyromonadaceae in the luminal and adherent compartments, was observed in VSL#3-exposed mice. Although we detected a non-significant increase in the abundance of VSL#3 bacterial groups Firmicutes and Lactobacillaceae, the major differences were detected in non-VSL#3 bacterial groups, indicating that administration of VSL#3 can exert pressure to induce broad changes in the microbial population of the intestine.
In the current study, VSL#3 was therapeutically administered after the onset of inflammation and in the context of a dysbiotic microbiota.

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