A study published in Nature a few days ago (Yin et al., 2026) showed that a gut bacterium produces pentadecanoic acid (C15:0), an odd-chain saturated fatty acid. In an experimental model of mice prone to atherosclerosis, this molecule reduces atherosclerotic plaques by about 50% and improves the lipid profile. The mechanism is direct: pentadecanoic acid inhibits the same enzyme targeted by statins, reduces hepatic cholesterol synthesis, and increases the expression of receptors that promote the removal of LDL cholesterol, the “bad” cholesterol.
In Bravo, pentadecanoic acid is present through several mechanisms. On the one hand, it derives from the dairy matrix itself: bovine milk and colostrum naturally contain this fatty acid, originating from the microbial metabolism of the rumen. On the other hand, some lactic acid bacteria typical of the Bravo formula (including strains of Lactococcus lactis and Lactobacillus paracasei) contain pentadecanoic acid in their membrane lipids.
Furthermore, Bravo exerts favorable effects on lipid metabolism through other well-established mechanisms of lactic acid bacteria and bifidobacteria: it increases the enzymatic activity that deconjugates bile acids and promotes their excretion; it reduces cholesterol assimilation; and it promotes the production of short-chain fatty acids (in particular butyrate), which modulate the activity of the enzyme targeted by statins and support a more balanced lipid profile.
Overall, these converging effects contribute to a protective action against the accumulation of atherosclerotic plaques, a protective action consistent with the role of the microbiota in regulating the gut-liver axis.