Key Benefits

• Gauge your heart risk from the balance of triglycerides and HDL cholesterol.
• Flag insulin resistance and metabolic syndrome risk when triglycerides run high, HDL low.
• Explain residual risk when LDL cholesterol looks normal but risk remains elevated.
• Guide personalized risk reduction beyond LDL by highlighting triglyceride–HDL balance.
• Protect heart health with lifestyle and medications that lower triglycerides and raise HDL.
• Track changes over time to confirm your plan is improving arterial risk.
• Clarify when to add apolipoprotein B, non-HDL cholesterol, or glucose testing.
• Best interpreted alongside your full lipid panel and overall cardiometabolic profile.

What is Atherogenic Index of Plasma (AIP)?

The Atherogenic Index of Plasma (AIP) is a calculated marker derived from two routine blood measurements: triglycerides and HDL cholesterol. It condenses their relationship into a single number to reflect the balance of fat‑carrying particles in plasma. Technically, AIP is a log‑transformed ratio of triglycerides to HDL cholesterol (log‑transformed TG/HDL‑C). It is not a substance measured directly; it is computed from the lipid profile and represents the overall pattern of circulating lipoproteins.

What it reflects: AIP gauges how your lipid transport system is configured at a given time. It mirrors the interplay between triglyceride‑rich lipoproteins (VLDL and remnants) and protective HDL. When triglycerides dominate relative to HDL, lipid exchanges favor smaller, denser LDL and cholesterol‑rich remnant particles (sdLDL, remnant lipoproteins), which more readily enter artery walls. By summarizing these remodeling processes (lipolysis and CETP‑mediated exchange), AIP offers a compact readout of plasma atherogenicity—the tendency of circulating lipoproteins to promote cholesterol deposition in arterial tissue.

Why is Atherogenic Index of Plasma (AIP) important?

Atherogenic Index of Plasma (AIP) captures how your body is packaging and clearing fats, reflecting the balance between triglycerides and HDL cholesterol. It is calculated as the log of triglycerides divided by HDL and serves as a proxy for the presence of small, dense LDL particles—lipoproteins that more readily penetrate arteries and drive plaque formation. Lower values are generally better; values below about 0.1 are typically considered low risk, around 0.1–0.2 borderline, and above 0.2 higher risk.

When AIP is low, triglycerides are modest and HDL is relatively robust. The liver is producing fewer triglyceride‑rich particles, LDL particles are larger and more buoyant, and reverse cholesterol transport works efficiently. Blood vessels tend to be more resilient and less inflamed. This state is usually symptom‑free. Premenopausal women often sit lower due to estrogen‑related HDL advantages; lean, active children and teens commonly do as well.

When AIP is high, triglyceride‑rich remnant particles accumulate and HDL is comparatively low. This shifts LDL toward small, dense forms, promoting endothelial inflammation, oxidative stress, and plaque growth. It often tracks with insulin resistance, central adiposity, fatty liver, and rising blood pressure or glucose—typically silent until advanced. Men and postmenopausal women commonly run higher; during pregnancy, physiological triglyceride rises can elevate AIP, and very high triglycerides raise pancreatitis risk.

Big picture: AIP integrates liver lipid output, HDL function, and LDL particle quality, tying together metabolism, vascular biology, and inflammation. It complements LDL cholesterol by signaling cardiometabolic risk and long‑term hazards like heart attack and stroke.

What Insights Will I Get?

The Atherogenic Index of Plasma (AIP) is the logarithm of the triglyceride-to–HDL cholesterol ratio. It summarizes the balance between triglyceride-rich particles and HDL and correlates with small, dense LDL and remnant lipoproteins. Because these particles drive endothelial stress and plaque formation, AIP links lipid handling to cardiometabolic health, liver fat metabolism, vascular brain health, and kidney and reproductive function.

Low values usually reflect low triglycerides and/or higher HDL. This pattern indicates efficient fat clearance and insulin sensitivity, with larger, buoyant LDL and active reverse cholesterol transport. Systems-level effects include steadier energy use, lower vascular inflammation, and resilient microcirculation. Premenopausal women and children often have lower AIP.

Being in range suggests balanced lipoprotein transport, predominance of larger LDL, and coordinated hepatic and peripheral fat handling (good VLDL turnover and lipolysis). This typically aligns with metabolic flexibility and stable endothelial function. Consensus places “optimal” toward the low end of the usual reference range.

High values usually reflect high triglycerides and/or low HDL. This points to hepatic overproduction of VLDL and delayed clearance with insulin resistance, promoting cholesterol exchange (via CETP), small dense LDL, and endothelial activation. System effects include higher cardiometabolic risk, fatty liver susceptibility, and vascular cognitive strain. Higher AIP is more common in men, increases with age, rises after menopause, and physiologically increases in late pregnancy; it may track with PCOS patterns.

Notes: Interpretation is influenced by fasting status (triglycerides rise post-meal), acute illness, thyroid and kidney disorders, and alcohol. Medications such as oral estrogens, glucocorticoids, some beta-blockers, thiazides, and HIV protease inhibitors can raise AIP; lipid-lowering drugs often lower it. Use consistent timing and the same lab when comparing results.