McFarlin · World journal of gastrointestinal pathophysiology 2017 · randomized controlled trial · n=75 screened (? randomized)

Oral spore-based probiotic supplementation was associated with reduced incidence of post-prandial dietary endotoxin, triglycerides, and disease risk biomarkers.

Cited 51 times in the scientific literature.

Level 2 - randomized trial

Randomized controlled trial

PubMed 28868181 · doi:10.4291/wjgp.v8.i3.117 · record verified 2026-08-27

What was done

Seventy-five apparently healthy adults were screened for post-prandial dietary endotoxemia, defined as a 5-fold or greater increase in serum endotoxin 5 hours after a meal challenge. Individuals meeting this responder criterion were randomized to 30 days of either a multi-species spore-based probiotic supplement (Bacillus indicus, Bacillus subtilis, Bacillus coagulans, Bacillus licheniformis, and Bacillus clausii) or a rice flour placebo. Serum endotoxin, triglycerides, and secondary inflammatory biomarkers (IL-12p70, IL-1β, ghrelin) were measured before and after the 30-day intervention.

What was found

Probiotic supplementation resulted in a 42% post-prandial endotoxin reduction (12.9 ± 3.5 vs 6.1 ± 2.6, P = 0.011) and a 24% triglyceride reduction (212 ± 28 vs 138 ± 12, P = 0.004). Placebo participants had a 36% increase in endotoxin (10.3 ± 3.4 vs 15.4 ± 4.1, P = 0.011) and a 5% drop in triglycerides (191 ± 24 vs 186 ± 28, P = 0.004). Probiotics also significantly decreased post-prandial IL-12p70 (24.3 ± 2.2 vs 21.5 ± 1.7, P = 0.017) and IL-1β (1.9 ± 0.2 vs 1.6 ± 0.1, P = 0.020), and resulted in lower post-supplementation ghrelin compared to placebo (6.8 ± 0.4 vs 8.3 ± 1.1, P = 0.017).

Why it matters

This study provides evidence that oral spore-forming Bacillus strains can reduce meal-triggered endotoxin translocation and related post-prandial lipid and cytokine elevations in susceptible individuals.

Limits

The total randomized sample size is not stated (75 were screened, but only an unspecified subset met the responder threshold). The study intentionally selected only high-responder individuals, limiting applicability to the general population. The 30-day intervention was short, and direct clinical disease endpoints were not evaluated.

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