Key Benefits

• See your balance of harmful versus protective cholesterol in one number.
• Spot atherogenic imbalance that raises long-term heart and stroke risk.
• Clarify risk when LDL seems fine but HDL is low.
• Guide lifestyle to lower bad cholesterol particles and raise protective HDL.
• Explain treatment need when this ratio stays high despite good LDL.
• Track lipid quality improvements beyond single LDL or HDL targets.
• Flag cardiometabolic patterns often linked to insulin resistance and fatty liver.
• Interpret best with full lipid panel, triglycerides, ApoB, and overall risk.

What is an Atherogenic Coefficient blood test?

The Atherogenic Coefficient (AC) is a calculated marker from a standard cholesterol blood test, not a substance in the blood. It describes how cholesterol is distributed among lipoproteins. Specifically, it compares the cholesterol carried by potentially plaque-forming particles (non-HDL lipoproteins: LDL, VLDL, IDL, and remnants) to the cholesterol carried by the protective scavenger particle (HDL). The AC is computed using routine values for total cholesterol and HDL cholesterol, drawn from the same sample used for a basic lipid panel.

Biologically, it reflects the balance between cholesterol delivery to tissues and artery walls by apoB-containing particles (atherogenic lipoproteins) and cholesterol removal back to the liver by HDL (reverse cholesterol transport). By condensing this balance into a single ratio, the AC provides a compact view of the atherogenicity of a person’s lipid profile. It helps characterize the overall lipoprotein mix and its tendency toward cholesterol deposition versus removal in artery walls.

Why is an Atherogenic Coefficient blood test important?

The atherogenic coefficient (AC) captures the balance between cholesterol particles that promote plaque and those that help clear it. Calculated as (total cholesterol − HDL cholesterol) divided by HDL cholesterol, it reflects the push–pull between apoB-containing “atherogenic” lipoproteins and HDL-mediated reverse cholesterol transport. It integrates liver metabolism, vascular inflammation, insulin signaling, and hormonal status into one cardiovascular risk signal. Many labs report AC values around 1–3 as typical, with lower values generally indicating lower risk and persistent values above 3 suggesting higher atherogenic burden.

When the value sits toward the lower end, HDL is relatively plentiful or efficient, non-HDL particles are fewer, and cholesterol trafficking favors removal from artery walls. Endothelial tone and nitric oxide signaling are better preserved, so blood pressure regulation and microvascular function tend to be healthier. This state is usually asymptomatic. Premenopausal women commonly have lower AC than men due to higher HDL; children also tend to have lower values unless a familial disorder is present.

Values drifting higher indicate more atherogenic particles relative to HDL, greater endothelial activation, and accelerated plaque formation. People may feel nothing for years, yet subtle signs—reduced exercise tolerance, erectile dysfunction in men, or rising blood pressure—can reflect early vascular stiffness. After menopause, AC often rises in women; during pregnancy, lipids increase physiologically and AC can climb, though marked elevations may signal heightened cardiometabolic strain.

Big picture: AC links lipid transport, liver and adipose biology, and vascular health. It complements LDL-C, non-HDL-C, triglycerides, and markers of insulin resistance, refining long-term risk for atherosclerotic cardiovascular disease and its downstream effects on heart, brain, kidneys, and metabolic resilience.

What insights will I get?

The atherogenic coefficient (AC) is a ratio derived from a standard lipid panel: non-HDL cholesterol divided by HDL cholesterol, often expressed as (total cholesterol − HDL)/HDL. It estimates the balance between cholesterol carried in artery-depositing particles (LDL, VLDL, remnants) and cholesterol carried for clearance (HDL). This balance influences vascular inflammation, energy handling, and tissue perfusion, linking to cardiovascular risk, metabolic resilience, and brain and reproductive health.

Low values usually reflect low atherogenic particles and/or relatively higher HDL. Physiology points to efficient reverse cholesterol transport and less endothelial stress. Children and premenopausal women commonly sit lower. Very low results can also appear with malnutrition, overactive thyroid (thyrotoxicosis), chronic liver disease, or rare genetic hypolipidemias, and occasionally with unusually high but sometimes dysfunctional HDL.

Being in range suggests a stable lipoprotein mix that supports healthy arterial function, adequate tissue oxygen delivery, and balanced hormone and membrane lipid supply. Epidemiologically, risk tends to fall as AC moves toward the lower end of its reference interval, aligned with favorable non-HDL and apolipoprotein B profiles.

High values usually reflect excess LDL/VLDL or low HDL, signaling greater cholesterol deposition, foam-cell formation, and endothelial dysfunction. It commonly tracks with insulin resistance, visceral adiposity, hypothyroidism, kidney or liver disorders, and chronic inflammation. Values tend to be higher in men, rise with age and after menopause, and can increase in late pregnancy due to physiologic hyperlipidemia.

Notes: Fasting status, acute illness, and laboratory methods can shift components and the ratio. Many drugs and hormones (statins, fibrates, steroids, androgens/estrogens, beta-blockers, retinoids) alter lipids. Because AC is a ratio, changes may arise from the numerator, denominator, or both; pairing with non-HDL cholesterol or apoB helps context.