Cholesterol Metabolism

This marker assesses your microbiome's ability to actively reduce cholesterol levels in your body. Certain gut bacteria possess unique enzymes that transform cholesterol into an unabsorbable substance called coprostanol, facilitating its direct elimination through feces and providing a natural cardiovascular protective mechanism.

The cholesterol circulating through your large intestine comes from two sources: the food you eat and the bile that your own liver secretes to aid in digestion. If this cholesterol remains intact in the digestive tract, a large portion of it is reabsorbed into the bloodstream, raising your systemic levels.

Fortunately, we host bacteria that act as lipid treatment agents. These microorganisms use cholesterol for their own metabolism or simply structurally modify it, converting it into coprostanol. The design of the human intestine does not allow coprostanol to be absorbed, so it is expelled through feces. In short: the more active cholesterol-consuming bacteria you have in your ecosystem, the more efficient your body will be at eliminating excess cholesterol.

The ability of your flora to metabolize cholesterol has a direct and measurable impact on your cardiovascular health:

• Reduction of Blood Cholesterol (LDL): Multiple studies have shown that individuals with a microbiome that has a high capacity to degrade intestinal cholesterol into coprostanol have significantly lower levels of total cholesterol and LDL (the "bad" cholesterol) in their routine blood tests.
• Cardiovascular Protection: By naturally decreasing the burden of circulating lipids, these bacteria provide a biological shield that helps prevent plaque buildup in the arteries (atherosclerosis), reducing long-term risk.
• Dietary Synergy: A low level of this bacterial function indicates that you depend almost exclusively on your diet and liver genetics to control cholesterol. In these cases, increasing the consumption of soluble fibers (mucilage, oats, chia) becomes even more crucial, as these fibers physically "trap" cholesterol to compensate for the lack of bacterial assistance.

The evaluation of the microbial degradation of cholesterol is performed by quantifying the presence of the genetic pathways responsible for the reduction of cholesterol's double bond.

Recently, the scientific literature identified the gene ismA (Intestinal SMetabolizing A) as the main marker gene responsible for this transformation to coprostanol in the human intestinal ecosystem. Using metagenomic Shotgun sequencing, our bioinformatics pipeline maps DNA reads against this gene and the genomes of the key species that carry it (historically associated with unculturable clades, as well as specific strains of Eubacterium coprostanoligenes, and some species of Bacteroides and Bifidobacterium).

The conversion potential is reported based on the normalized abundance of these genes. An absence or low detection of the ismA gene indicates a deficit in the main pathway of bacterial cholesterol excretion, suggesting a higher rate of intestinal reabsorption and the need for compensatory nutritional interventions (such as phytosterols or viscous fiber).