HDL vs LDL: Understanding Good and Bad Cholesterol for Athletes

HDL (high-density lipoprotein) and LDL (low-density lipoprotein) are the two most clinically discussed lipoproteins. Both transport cholesterol through the bloodstream, but in opposite directions and with opposite consequences for arterial health.

HDL is often called "good cholesterol" because it performs reverse cholesterol transport: it collects cholesterol from peripheral tissues and arterial walls and carries it back to the liver for excretion or recycling. HDL is the body's primary mechanism for removing cholesterol that has deposited in artery walls.

LDL is often called "bad cholesterol" because it delivers cholesterol from the liver to peripheral tissues. When LDL is elevated, excess cholesterol can deposit in arterial walls, forming atherosclerotic plaques that narrow and stiffen arteries over time.

Why both matter for athletes on AAS: Anabolic steroids produce a simultaneous double hit on the lipid profile. Oral 17-alpha-alkylated compounds and non-aromatising injectables suppress HDL (removing the protective reverse transport mechanism) while LDL rises (increasing delivery of cholesterol to arterial walls). This combination is more atherogenic than either change in isolation.

Direction of cholesterol transport:

• HDL: Outbound transport. Collects cholesterol from tissues and artery walls, returns it to the liver. Acts as a cardiovascular protective mechanism.
• LDL: Inbound delivery. Carries cholesterol from the liver to peripheral tissues. Excess LDL deposits cholesterol in artery walls.

Effect on cardiovascular risk:

• HDL: Inversely associated with cardiovascular disease risk. Higher HDL is protective. Every 1 mg/dL increase in HDL reduces cardiovascular risk by approximately 2-3%.
• LDL: Positively associated with cardiovascular disease risk. Higher LDL drives atherosclerosis. Every 1 mmol/L increase in LDL increases cardiovascular risk by approximately 20-25%.

Response to anabolic steroids:

• HDL: Uniformly suppressed by all anabolic steroids. Oral 17-AA compounds suppress it 30-70%. Trenbolone suppresses it 50-70%. Even testosterone at TRT doses reduces it 10-20%.
• LDL: Generally rises during AAS use, though the effect is more variable and sometimes modest with testosterone alone.

What raises each marker:

• Raises HDL: Aerobic exercise, omega-3 fatty acids, niacin, weight loss, alcohol in moderation, oestrogen, quitting smoking.
• Raises LDL: Saturated fat, trans fats, hypothyroidism, obesity, familial hypercholesterolaemia, certain medications, some anabolic steroids.

What lowers each marker:

• Lowers HDL: Anabolic steroids (all), physical inactivity, smoking, obesity, trans fats, high carbohydrate diet, diabetes.
• Lowers LDL: Statins, PCSK9 inhibitors, plant sterols, soluble fibre, dietary fat modification, exercise.

Key subfractions:

• HDL: HDL2 is the most protective subfraction (performs most reverse cholesterol transport); HDL3 is less protective. Stanozolol preferentially destroys HDL2 (-71% vs -33% for total HDL).
• LDL: LDL-P (particle number) and ApoB are more informative than LDL-C (cholesterol content). Small dense LDL particles are more atherogenic than large buoyant LDL particles.

Test both together as part of a standard lipid panel: HDL and LDL should never be assessed in isolation. Their relationship to each other is more clinically informative than either alone.

The total cholesterol:HDL ratio (also called the Castelli ratio) is often more useful than either marker individually:

• Below 4.0: low cardiovascular risk
• 4.0-5.0: moderate risk
• Above 5.0: elevated risk, warrants intervention

When HDL is the more urgent focus:

• During and after AAS cycles, especially with oral 17-AA compounds or trenbolone
• When monitoring for the acute lipid-suppressive effects of a new compound
• When HDL is below 35 mg/dL (below 25 mg/dL is considered critically low)

When LDL is the more urgent focus:

• Long-term cardiovascular risk assessment in users over 35-40
• When evaluating statin therapy need
• In users with family history of premature cardiovascular disease or familial hypercholesterolaemia

ApoB as a superior alternative: Both HDL and LDL can be estimated from standard lipid panels, but ApoB (apolipoprotein B) is a direct measure of all atherogenic particles and is increasingly preferred for cardiovascular risk stratification, particularly when triglycerides are elevated (common in bodybuilders on bulking diets or using GH).