How do I calculate the AIP?

AIP = log10 (TG mmol/L / HDL-C mmol/L). First convert values to mmol/L: TG mmol/L = TG mg/dL ÷ 88.57; HDL mmol/L = HDL mg/dL ÷ 38.67. Then divide TG by HDL and take the base-10 logarithm (log10). Example: TG = 180 mg/dL = 2.03 mmol/L; HDL = 40 mg/dL = 1.03 mmol/L: AIP = log10(2.03/1.03) = log10(1.97) = 0.29 (high risk).

How can I improve my AIP?

AIP can be reduced through interventions targeting both TG (numerator) and HDL (denominator): (1) Reduce refined carbohydrates, sugar, and alcohol — primary drivers of TG elevation. (2) Increase omega-3 fatty acid intake (fatty fish, flaxseed) — reduces TG. (3) Aerobic exercise (150+ min/week) — raises HDL and lowers TG. (4) Weight loss: 5-10% body weight reduction improves AIP. (5) Fibrates or prescription omega-3 (icosapent ethyl) for TG >200-500 mg/dL. (6) SGLT2 inhibitors and GLP-1 agonists in T2DM improve TG and HDL simultaneously.

Does AIP predict cardiovascular risk better than LDL alone?

AIP captures cardiovascular risk from atherogenic dyslipidemia that is missed by LDL-C measurement alone. In populations with metabolic syndrome, T2DM, or obesity (where atherogenic dyslipidemia is prevalent), AIP adds significant risk discrimination beyond LDL-C. A meta-analysis (Zhong et al., Cardiovasc Diabetol 2021) confirmed AIP as an independent predictor of cardiovascular events. AIP is most informative when LDL appears normal but TG is high and HDL is low.

What is the difference between AIP and TG/HDL ratio?

AIP = log10(TG/HDL) using mmol/L; TG/HDL ratio = TG divided by HDL (commonly in mg/dL in the US). The US TG/HDL ratio in mg/dL >3.0 correlates with small dense LDL and insulin resistance. AIP uses log10 transformation and mmol/L units from European/international convention. Both indices capture the same atherogenic dyslipidemia concept. AIP and TG/HDL ratio are mathematically related — AIP is essentially the log-transformed TG/HDL ratio adjusted for unit scale.

What medications improve AIP?

Medications that lower AIP: (1) Fibrates (fenofibrate 145 mg/day, gemfibrozil) — reduce TG by 30-50%, raise HDL by 10-15%. (2) Prescription omega-3 fatty acids (icosapent ethyl 4g/day — REDUCE-IT) — reduce TG by 50%, proven CV event reduction. (3) SGLT2 inhibitors — reduce TG modestly, improve metabolic profile. (4) GLP-1 agonists — reduce TG and weight. (5) Niacin — raises HDL and reduces TG (limited use due to side effects). Statins reduce LDL primarily and have modest TG/HDL effects — may not sufficiently normalize AIP in atherogenic dyslipidemia.

Is AIP elevated in PCOS?

Yes. PCOS is commonly associated with atherogenic dyslipidemia — elevated TG and low HDL — even in normal-weight women, due to underlying insulin resistance and hyperandrogenism. Multiple studies confirm AIP is significantly higher in women with PCOS compared to healthy controls, and AIP correlates with androgen levels and insulin resistance severity in PCOS. Monitoring AIP in PCOS patients helps quantify lipid atherogenicity and track improvement with metformin, combined oral contraceptives, or lifestyle changes.

What is the relationship between AIP and statin therapy?

Statins primarily lower LDL-C and have modest effects on TG (10-30% reduction) and HDL (5-10% increase). Patients on statin therapy who achieve LDL goals but have persistently elevated AIP (high TG, low HDL) have residual lipid risk from atherogenic dyslipidemia. REDUCE-IT (icosapent ethyl) and ACCORD-Lipid (fenofibrate add-on to statin) addressed this residual TG/HDL risk. For patients with TG >200 mg/dL despite statin, consider add-on icosapent ethyl per REDUCE-IT evidence for cardiovascular event reduction.

What are the limitations of AIP for clinical use?

AIP limitations: (1) Units must be mmol/L — mg/dL values produce incorrect results; (2) Not a primary treatment target in any major lipid guideline (ACC/AHA, ESC); (3) Requires fasting sample; (4) Threshold heterogeneity across studies — no single validated clinical cutoff; (5) AIP alone cannot quantify LDL particle size — apoB or direct LDL particle measurement provides more precise atherogenic particle information; (6) AIP is an observational association marker — no RCT has specifically targeted AIP as a treatment goal with demonstrated outcome reduction. Use as supplementary risk information, not as a primary clinical decision driver.

Online Medical Tools — AIP Index

Printed on 9/2/2026

For informational purposes only. This is not medical advice.

Cardiology

AIP Index

AIP is calculated as log10(triglycerides/HDL-C) using molar concentrations. It reflects the balance between atherogenic and protective lipoprotein patterns and is associated with cardiovascular risk in multiple observational studies.

Formula: AIP = log10((TG [mmol/L]) / (HDL-C [mmol/L]))

Fasting Triglycerides

mg/dL

HDL Cholesterol

mg/dL

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How It Works

Obtain fasting lipid panel values

Collect fasting blood samples (8-12 hours fasting) and measure fasting triglycerides and HDL cholesterol. If values are reported in mg/dL (US convention), they must be converted to mmol/L for AIP calculation: divide triglycerides mg/dL by 88.57 to get mmol/L; divide HDL mg/dL by 38.67 to get mmol/L. Most published AIP cutoffs are based on mmol/L values.

Calculate AIP using log10

Apply the formula: AIP = log10 (base-10 logarithm) of (TG mmol/L divided by HDL-C mmol/L). Example: TG = 150 mg/dL = 1.69 mmol/L; HDL = 45 mg/dL = 1.16 mmol/L: AIP = log10(1.69/1.16) = log10(1.46) = 0.16. Note: log10 (base-10 logarithm) is used in AIP, not the natural log (ln) used in TyG index.

Interpret AIP atherogenicity risk

AIP <0 = low atherogenic risk (favorable lipid profile). AIP 0 to 0.1 = borderline atherogenic risk. AIP >0.1 = elevated atherogenic risk. AIP >0.21 = threshold most associated with significantly increased cardiovascular events in published studies. These thresholds are derived from observational data and vary across studies — AIP is a supplementary marker, not a primary treatment decision threshold in current guidelines.

Who Uses the AIP Index

Cardiovascular Risk Assessment Beyond LDL

Cardiologists, preventive medicine physicians, primary care physicians

AIP captures the atherogenic dyslipidemia pattern (high TG + low HDL) that is missed by standard LDL-C measurement. It provides supplementary cardiovascular risk information particularly valuable in patients with metabolic syndrome, T2DM, or obesity where LDL may be normal despite high residual cardiovascular risk.

Metabolic Syndrome Atherogenicity Evaluation

Endocrinologists, primary care physicians

Atherogenic dyslipidemia — high triglycerides combined with low HDL — is a defining feature of metabolic syndrome and insulin resistance. AIP directly quantifies this pattern on a single logarithmic scale, enabling easy tracking of atherogenic dyslipidemia improvement with lifestyle changes or pharmacotherapy.

PCOS Dyslipidemia Assessment

Gynecologists, endocrinologists

PCOS is associated with atherogenic dyslipidemia even in normal-weight women. AIP can quantify the lipid atherogenicity in PCOS patients and track improvement with weight loss, combined oral contraceptives, or metformin therapy.

Residual Cardiovascular Risk After Statin Therapy

Cardiologists, preventive medicine specialists

Patients on statin therapy who achieve LDL goals but have persistently high TG and low HDL may have elevated AIP despite normal or near-normal LDL-C. AIP identifies this residual lipid risk pattern, which may benefit from additional interventions such as fibrates, high-dose omega-3 fatty acids, or SGLT2 inhibitors.

Research in Non-Traditional Lipid Biomarkers

Cardiovascular researchers, lipidologists

AIP is widely used in observational research examining the association between lipid phenotypes and cardiovascular outcomes in populations with metabolic syndrome, diabetes, and insulin resistance. It complements apoB and LDL particle size measurements as a non-traditional lipid risk marker.

Pro Tips

AIP captures atherogenic dyslipidemia that LDL-C misses

The classic atherogenic dyslipidemia pattern — elevated triglycerides (>150 mg/dL) combined with low HDL-C (<40 mg/dL in men, <50 mg/dL in women) — is common in insulin resistance, T2DM, obesity, and metabolic syndrome. This pattern produces high AIP and is associated with small dense LDL particles, which are more atherogenic than large buoyant LDL. Standard LDL-C can appear normal even when AIP is elevated, underestimating true cardiovascular risk.

Fasting sample is essential — TG rises dramatically after meals

Triglycerides typically increase by 50-300 mg/dL above fasting baseline after meals, particularly after carbohydrate-rich or fatty meals. A non-fasting TG will significantly inflate AIP, producing a falsely elevated atherogenic index. Always confirm at least 8-12 hours of fasting before accepting the lipid panel for AIP calculation.

Convert mg/dL to mmol/L before calculating AIP

All published AIP cutoffs (low risk <0, borderline 0-0.1, high risk >0.1-0.21) are based on mmol/L values. Using mg/dL values in the AIP formula without converting produces a completely different numerical result that cannot be interpreted against published thresholds. Convert: TG mmol/L = TG mg/dL ÷ 88.57; HDL mmol/L = HDL mg/dL ÷ 38.67.

Lifestyle changes effectively lower AIP

AIP responds well to metabolic lifestyle interventions: carbohydrate restriction and Mediterranean diet reduce TG and raise HDL, improving AIP. Regular aerobic exercise raises HDL and reduces TG. Weight loss of 5-10% body weight substantially lowers TG and improves AIP. These lifestyle changes target the insulin resistance underlying atherogenic dyslipidemia.

Fibrates and omega-3 fatty acids dramatically lower TG and improve AIP

Fibrates (fenofibrate, gemfibrozil) reduce TG by 30-50% and raise HDL by 10-15%, substantially lowering AIP. High-dose prescription omega-3 fatty acids (icosapent ethyl at 4g/day — REDUCE-IT trial) reduce TG by ~50% and have proven cardiovascular event reduction in patients with high TG. Both agents are specifically indicated for atherogenic dyslipidemia AIP phenotype.

Statins have modest effects on TG and HDL — may not normalize AIP

Statins are the cornerstone of LDL-C reduction but have modest effects on TG (10-30% reduction) and HDL (5-10% increase). A patient may achieve LDL goal on statin therapy while AIP remains elevated due to persistent high TG and low HDL. This residual risk pattern may benefit from add-on fibrates or omega-3 fatty acids, particularly when TG >200 mg/dL despite statin therapy.

SGLT2 inhibitors and GLP-1 agonists improve AIP in T2DM

SGLT2 inhibitors (empagliflozin, dapagliflozin) and GLP-1 receptor agonists (semaglutide, liraglutide) both reduce TG and improve the lipid profile beyond glucose lowering. These agents are particularly beneficial in T2DM patients with elevated AIP (high TG, low HDL pattern), and their cardiovascular benefits in T2DM may partly operate through lipid and metabolic improvements.

AIP correlates with coronary artery calcium score progression

Several studies have shown that elevated AIP correlates with subclinical atherosclerosis as measured by coronary artery calcium (CAC) score progression over time. AIP may identify patients at risk of CAC progression who appear low-risk by standard lipid assessment, supporting its role as an adjunctive marker in intermediate-risk cardiovascular prevention decisions.

AIP is a supplementary marker — not a primary treatment target

AIP is not a recommended primary treatment target in ACC/AHA or ESC lipid management guidelines. LDL-C, non-HDL-C, and apoB are the established primary targets. AIP provides supplementary risk information and helps identify atherogenic dyslipidemia phenotype for additional intervention. Do not use AIP alone to initiate or escalate lipid-lowering therapy — it should complement, not replace, standard lipid management.

Common Questions About Your Results

AIP must be calculated using TG and HDL-C values in mmol/L (the SI unit system used in most of the world outside the United States). All published AIP cutoffs and clinical interpretations are based on mmol/L. If your lab reports values in mg/dL (standard in the US), convert: TG mmol/L = TG mg/dL ÷ 88.57; HDL mmol/L = HDL mg/dL ÷ 38.67. Using mg/dL values in the formula without conversion produces an incorrect result that cannot be compared to published thresholds.

AIP = log10(TG/HDL) in mmol/L, whereas TG/HDL ratio is the simple division of TG by HDL (often in mg/dL in US practice). The TG/HDL ratio in mg/dL >3.0 correlates with small dense LDL and insulin resistance (Siri-Tarino et al.). AIP and TG/HDL ratio are closely related mathematically (AIP is the log10-transformed TG/HDL ratio in mmol/L). AIP uses log transformation to normalize the distribution, which may improve its statistical properties in research analysis. Both capture similar atherogenic dyslipidemia information.

No. AIP is a supplementary atherogenic lipid marker, not a standalone cardiovascular risk tool. It should be interpreted alongside: the 10-year ASCVD risk score (PCE), LDL-C, non-HDL-C, blood pressure, HbA1c/diabetes status, and other risk-enhancing factors. AIP identifies atherogenic dyslipidemia that adds to ASCVD risk estimate, but it does not replace comprehensive cardiovascular risk assessment. Clinical management decisions should be based on integrated risk assessment, not AIP alone.

Yes. HDL-C is physiologically higher in women than men (mean ~10 mg/dL higher), which typically results in lower AIP in premenopausal women compared to men with similar TG levels. After menopause, the HDL advantage attenuates, and AIP may increase. Sex-specific AIP reference ranges have been proposed in some studies. When interpreting AIP, consider sex as a modifier of the normal range and be cautious applying male-derived cutoffs to premenopausal women.

AIP >0.21 was the threshold most consistently associated with significantly increased CAD risk in the AMORIS study (Walldius et al., JAMA 2001) and was validated in several subsequent studies. However, this threshold has heterogeneous support across different populations. Some studies use AIP >0.1 or >0.24 as the high-risk cutoff. Rather than treating any single threshold as definitive, interpret AIP as a continuous gradient — higher AIP consistently indicates greater atherogenic dyslipidemia burden regardless of which specific threshold is used.

Evidence-Based Methodology

AIP proposed by Dobiasova and Frohlich (Clin Biochem 2001). AMORIS study validation (Walldius et al., JAMA 2001, n=175,553): AIP >0.21 associated with significantly increased MI risk. Meta-analysis confirming AIP as independent CVD predictor: Zhong et al. (Cardiovasc Diabetol 2021, 14 studies). AIP in metabolic syndrome: Niroumand et al. (J Res Med Sci 2015). AIP in PCOS: Berneis et al. (Eur J Endocrinol 2009). AIP and CAC: Quispe et al. (J Clin Lipidol 2020). Units must be mmol/L for all published cutoffs.

Clinical Content Trust

Last reviewed:: April 21, 2026
Guideline version:: General evidence framework v2026.04
Source set version:: Primary-source set v1

How to Interpret Your Result

AIP summarizes the triglyceride-to-HDL relationship on a logarithmic scale. Higher values suggest a more atherogenic lipid phenotype and may indicate increased residual cardiovascular risk.

When to Use This Tool

Use AIP as an adjunctive lipid-risk marker in patients with mixed dyslipidemia, metabolic syndrome traits, or discordant traditional lipid markers.

Limitations

AIP is not currently the primary treatment target in major lipid guidelines. It should be interpreted as a supplementary marker alongside standard lipid and clinical risk metrics.

Disclaimer: This tool is for educational and informational purposes only. It is not a substitute for professional medical advice, diagnosis, or treatment. Always consult a qualified healthcare provider with questions about your health.

Changelog

April 21, 2026 · trust-baseline
Clinical trust metadata enabled for this tool page with structured review/version fields.

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Frequently Asked Questions

The Atherogenic Index of Plasma (AIP) is a lipid risk marker calculated as log10(TG/HDL-C), where both TG and HDL are in mmol/L. It quantifies the atherogenicity of the lipid profile by capturing the ratio of pro-atherogenic triglycerides to anti-atherogenic HDL cholesterol. AIP was proposed by Dobiasova and Frohlich (Clin Biochem 2001) and correlates with cardiovascular risk beyond standard LDL-C measurement.

Published AIP interpretation: AIP <0 = low atherogenic risk (TG/HDL ratio <1 in mmol/L, favorable lipid profile); AIP 0 to 0.1 = borderline risk; AIP >0.1 = elevated atherogenic risk; AIP >0.21 = significantly elevated risk associated with increased CAD events in AMORIS study. These thresholds vary somewhat across studies. AIP is best interpreted as a continuous spectrum — the higher the value, the greater the atherogenic lipid burden.

Elevated AIP indicates an atherogenic lipid phenotype characterized by high TG and low HDL — the pattern of atherogenic dyslipidemia associated with insulin resistance, metabolic syndrome, and small dense LDL particles. This phenotype predicts cardiovascular events independent of LDL-C. The AMORIS study (Walldius et al., JAMA 2001, n=175,553) showed AIP >0.21 associated with significantly increased MI risk, independent of total cholesterol and LDL.

AIP is elevated in metabolic syndrome because two of the five metabolic syndrome criteria are high TG (>150 mg/dL) and low HDL (<40 mg/dL in men, <50 mg/dL in women) — the same components that drive AIP. AIP correlates with insulin resistance, hyperglycemia, central obesity, and hypertension. AIP can serve as an integrated marker of the dyslipidemia component of metabolic syndrome and tracks improvement with lifestyle and pharmacological treatment.

Atherogenic dyslipidemia is a lipid pattern characterized by: elevated triglycerides (>150 mg/dL), reduced HDL cholesterol (<40 mg/dL men, <50 mg/dL women), and small dense LDL particles (which appear as near-normal LDL-C on standard testing). AIP captures the TG/HDL relationship on a log scale, providing an integrated measurement of this atherogenic pattern. High AIP reflects high TG combined with low HDL — the core of atherogenic dyslipidemia — without requiring advanced lipoprotein analysis.

Online Medical Tools — AIP Index

AIP Index

How It Works

Obtain fasting lipid panel values

Calculate AIP using log10

Interpret AIP atherogenicity risk

Who Uses the AIP Index

Cardiovascular Risk Assessment Beyond LDL

Metabolic Syndrome Atherogenicity Evaluation

PCOS Dyslipidemia Assessment

Residual Cardiovascular Risk After Statin Therapy

Research in Non-Traditional Lipid Biomarkers

Pro Tips

AIP captures atherogenic dyslipidemia that LDL-C misses

Fasting sample is essential — TG rises dramatically after meals

Convert mg/dL to mmol/L before calculating AIP

Lifestyle changes effectively lower AIP

Fibrates and omega-3 fatty acids dramatically lower TG and improve AIP

Statins have modest effects on TG and HDL — may not normalize AIP

SGLT2 inhibitors and GLP-1 agonists improve AIP in T2DM

AIP correlates with coronary artery calcium score progression

AIP is a supplementary marker — not a primary treatment target

Common Questions About Your Results

Evidence-Based Methodology

Clinical Content Trust

How to Interpret Your Result

When to Use This Tool

Limitations

Changelog

Related Tools

Cholesterol Ratio

LDL Calculator

ASCVD Risk Calculator

Further Reading

A Complete Guide to Cardiology: Risk Scores, Heart Failure, and Cardiovascular Disease Management

Frequently Asked Questions