Very Low-Density Lipoprotein Cholesterol
Lipids marker
VLDL Cholesterol
Very Low-Density Lipoprotein Cholesterol
Cholesterol carried by VLDL particles, which transport triglycerides from the liver. Usually estimated from triglycerides via the Friedewald equation (Triglycerides / 5 in mg/dL). Elevated levels indicate excess triglyceride-rich lipoprotein production and increased atherogenic risk.
PED Notes
Oral/17-alpha-alkylated AAS (oxandrolone, stanozolol, methandrostenolone) increase hepatic VLDL production while suppressing HDL, creating a broadly atherogenic profile. GH stimulates hepatic VLDL secretion by enhancing lipolysis and promoting insulin resistance. The combination of oral AAS + GH + high-calorie bulking diets creates maximal VLDL elevation through multiple converging pathways. Lipid effects from AAS are generally reversible, normalising 2.5 to 4 months after discontinuation.
When high
When elevated (>30 mg/dL):
Supplements:
- Omega-3 (EPA/DHA) -- 2-4g/day (most effective intervention; reduces hepatic VLDL synthesis and enhances triglyceride clearance)
- Berberine -- 500mg 2-3x/day before meals (improves insulin sensitivity, reduces hepatic lipogenesis)
- Niacin (extended-release) -- 500-1000mg/day (reduces hepatic VLDL production; discuss with physician)
Lifestyle:
- Reduce refined carbohydrates and sugar (primary dietary driver of hepatic VLDL production)
- Regular cardio 3-5x/week (improves insulin sensitivity, enhances lipoprotein lipase activity)
- Moderate alcohol intake or abstain entirely (alcohol increases hepatic triglyceride synthesis)
- Ensure 12h fasted blood draw for accurate VLDL estimation
PED-specific:
- If on oral AAS and VLDL is persistently elevated, consider switching to injectable compounds only
- If on GH, consider dose reduction; monitor alongside fasting glucose and insulin as an insulin resistance marker
- Avoid stacking oral AAS + GH + insulin simultaneously if lipids are severely impaired
- Between cycles, allow full lipid recovery (minimum 8-12 weeks off oral AAS) before starting another cycle
- Request ApoB alongside VLDL for a more complete picture of atherogenic particle burden
Pharmacological options (when supplements insufficient):
- Fenofibrate -- 145-200mg/day; PPAR-alpha agonist; reduces VLDL and triglycerides 30-50%; first-line prescription when triglycerides >5 mmol/L
- Icosapent ethyl (Vascepa) -- 2g 2x/day; purified EPA; reduces triglyceride-rich lipoproteins
- Semaglutide / Tirzepatide -- 0.25-2.4mg or 2.5-15mg subQ weekly; GLP-1 agonists reduce VLDL via insulin sensitisation; ideal for GH/MK-677 users
- Pemafibrate -- 0.2mg 2x/day where available; selective PPAR-alpha modulator with cleaner safety profile than fenofibrate
- Rosuvastatin 5-20mg/day reduces VLDL and LDL together; see LDL/ApoB markers for full statin protocol
- All require physician oversight and baseline liver/CK panel
When low
When low (<2 mg/dL):
- Generally favourable; indicates efficient triglyceride metabolism
- During contest prep, very low VLDL may reflect extreme caloric restriction; ensure adequate essential fatty acid intake
- No specific intervention typically required
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Frequently Asked Questions
Reference Ranges
Standard Range
VitalMetrics Range