Very Low-Density Lipoprotein Cholesterol

Lipids marker

VLDL Cholesterol

Very Low-Density Lipoprotein Cholesterol

Category: Lipids
Unit: mg/dL

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 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

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

References:

  • Nordestgaard, B. G. (2016). Triglyceride-rich lipoproteins and atherosclerotic cardiovascular disease: New insights from epidemiology, genetics, and biology. Circulation Research, 118(4), 547-563. DOI: 10.1161/CIRCRESAHA.115.306249
  • Baggish, A. L., Weiner, R. B., Kanayama, G., Hudson, J. I., Lu, M. T., Hoffmann, U., & Pope, H. G. (2017). Cardiovascular toxicity of illicit anabolic-androgenic steroid use. Circulation, 135(21), 1991-2002. DOI: 10.1161/CIRCULATIONAHA.116.026945
  • Calder, P. C. (2017). Omega-3 fatty acids and inflammatory processes: From molecules to man. Biochemical Society Transactions, 45(5), 1105-1115. DOI: 10.1042/BST20160474

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Frequently Asked Questions

Reference Ranges

Standard Range

2 - 30 mg/dL

VitalMetrics Range

2 - 40 mg/dL

Statistics