THE ARISING · Longevity & Healthspan
Probiotic Strain BL-99 Speeds Sluggish Gut Transit in Older Adults, Trial Finds
A single probiotic strain shortened the time food takes to travel through the gut in older adults, according to a randomized, double-blind trial published in Nature Communications.
The strain is Bifidobacterium animalis subsp. lactis BL-99. The trial's main measure was whole-gut transit time, the total time food takes to pass through the digestive tract. BL-99 significantly reduced it. The randomized, double-blind trial enrolled 73 older adults with functional constipation and prolonged transit: 37 received BL-99 and 36 placebo for four weeks. It was registered as ChiCTR2300077583. At week four, the adjusted difference in transit time was 28.6 hours shorter with BL-99 (95% confidence interval 20.4 to 36.8 hours shorter). The researchers also ran experiments in naturally aged mice.
Slow gut movement is common with age. The authors describe the weakening of smooth muscle contraction as a major trigger of age-related intestinal hypomotility, meaning sluggish movement through the gut. They note that the condition places a substantial burden on healthcare and that no effective targeted therapy exists.
The trial also tracked bowel movement frequency, symptom severity and quality-of-life measures as secondary endpoints. The main result, though, was the shorter transit time. Quality-of-life scores did not show a significant treatment effect. No adverse events were reported, but this small, short trial cannot establish long-term safety.
The team also looked at how the strain might work. In both the trial and the aged mice, BL-99 reshaped the gut microbiota. It suppressed bacteria that produce an enzyme called bile salt hydrolase. That enzyme breaks down bile acids, the digestive compounds made by the liver. With fewer of these bacteria, the pool of conjugated bile acids was preserved. One of them is taurochenodeoxycholic acid, or TCDCA.
In mouse colon smooth muscle cells, BL-99 was associated with higher activity of a gene-control pathway known as the serum response factor–myocardin axis. This restored contractile proteins, including α-SMA and SM-MHC, which help muscle cells contract.
In the accompanying preclinical experiments, giving TCDCA on its own reproduced the effect of BL-99 on these muscle proteins. It did so by inhibiting a cell-signaling pathway called PI3K/AKT. The authors describe this as a microbiota–bile acid–smooth muscle signaling axis, and they name both BL-99 and TCDCA as candidate therapies aimed at gut muscle dysfunction.
For anyone weighing probiotics for slow digestion, the finding is specific to this one strain. The result applies to BL-99, not to probiotics as a group.
Next to watch: whether larger and longer trials confirm the transit-time result, and whether the bile acid pathway seen in mice and the gut microbiota is borne out as the mechanism in people.