A lab-made fatty acid the body cannot burn, so it acts as a lasting signal that switches on fat-burning genes and calms inflammation. Small, short human studies modestly lowered bad cholesterol and triglycerides but did not improve blood sugar or weight. Safety data are brief, supply is unregulated, and long-term value remains unproven. (Full Review)
| Marker | Target | Why |
|---|---|---|
| LDL cholesterol | <100 mg/dL | Primary efficacy target; TTA's clearest human effect |
| Triglycerides | <100 mg/dL | Storage-fat marker responsive to TTA |
| HDL and LDL/HDL ratio | HDL >50 mg/dL; LDL/HDL <2.0 | Captures the ratio improvement seen in trials |
| ALT and AST (liver enzymes) | ALT <25 U/L (men) / <20 U/L (women); AST <25 U/L | Detects class-based liver stress |
| Creatine kinase (CK) | 30–150 U/L | Detects muscle toxicity, especially with statins |
| Creatinine and eGFR | eGFR >90 mL/min/1.73 m² | Class agents can raise creatinine |
| Fasting glucose and HbA1c | Glucose 70–90 mg/dL; HbA1c <5.4% | Confirms no adverse glucose effect |
| hs-CRP (inflammation) | <1.0 mg/L | Tracks the anti-inflammatory signal |
| Omega-3 index (EPA + DHA) | >8% of red-cell fatty acids | TTA depletes omega-3s; guides fish-oil pairing |
Cadence: Baseline, then ~4 weeks, ~12 weeks, then every 3–6 months