A milk-adapted gut bacterium that thrives on sugars found almost only in human milk. Newborn evidence is strong for bowel injury and eczema; adult evidence is thin and partly from a strain later moved to another organism. Nothing persists after dosing stops. Confirmed serious harm is limited to extremely premature or severely immune-suppressed patients. Much research is company-funded. (Full Review)
| Marker | Target | Why |
|---|---|---|
| hs-CRP | Below 1.0 mg/L | Tracks the body-wide inflammation this organism is claimed to lower |
| Faecal calprotectin | Below 50 µg/g | Direct read-out of gut-lining inflammation, the proposed local effect |
| Stool pH | 5.5–6.5 | Falls when the organism ferments carbohydrate to acetate and lactate |
| Faecal B. longum subsp. infantis abundance | No established target; track change from the individual's own baseline | Confirms the organism is actually present rather than passing through |
| Complete blood count with differential | Absolute neutrophil count above 1,500 per µL | Screens for the immune suppression that turns a harmless resident organism into a pathogen |
| Serum immunoglobulin A | 70–400 mg/dL | Selective deficiency alters mucosal handling of live organisms |
| Glucose breath test | Hydrogen rise below 12 ppm over baseline | Small intestinal bacterial overgrowth is the setting linked to lactic acidosis |
Cadence: Baseline for inflammation, stool and immune-screening markers; stool measurement repeated at 4 weeks, inflammation markers at 8 to 12 weeks, and both every 6 to 12 months if use continues; a further stool measurement 4 weeks after any planned stop. Immune-screening tests are baseline-only for healthy adults; the glucose breath test is ordered only where bloating with mental cloudiness appears.