Naringenin is the bitter grapefruit compound, concentrated into capsules. It shifts liver fat handling toward burning and slows export of cholesterol-carrying particles. The human record is thin: one small, short trial in overweight adults with fatty liver. Everything beyond rests on animals, cells or worms. The main concern is quiet interference with uptake of several prescription drugs. (Full Review)
| Marker | Target | Why |
|---|---|---|
| Triglycerides | 50–80 mg/dL | Primary lipid endpoint that moved in the trial |
| Low-density lipoprotein cholesterol | 70–100 mg/dL | Secondary lipid endpoint that fell on treatment |
| Apolipoprotein B | Under 80 mg/dL | Directly reflects the particle-export step naringenin suppresses |
| High-density lipoprotein cholesterol | Above 55 mg/dL (men), above 65 mg/dL (women) | Rose on treatment in the trial |
| Alanine aminotransferase | 10–26 U/L | Liver safety and liver-fat marker; the liver is the target organ |
| Aspartate aminotransferase | 10–26 U/L | Paired liver safety marker |
| Fasting insulin | 2–5 µIU/mL | Detects the conflicted insulin-sensitivity signal in either direction |
| High-sensitivity C-reactive protein | Under 0.5 mg/L | Tracks the inflammatory pathway naringenin targets |
| Liver fat fraction (imaging) | Under 5% | The primary endpoint that improved in the trial |
| Blood pressure (systolic) | 105–120 mmHg | Moved toward improvement without reaching significance in the trial |
| Concurrent drug level (where measurable) | No established target; track against the individual's own pre-supplement level | Detects silent absorption interference |
Cadence: Baseline before starting; lipid and liver panels repeated at 8 weeks, again at 6 months, then every 6 to 12 months while use continues. Concurrent drug levels are checked at 4 weeks and after any dose change.