HOMA-IR: What It Is, Formula, Normal Range, and Meaning

HOMA-IR (Homeostatic Model Assessment of Insulin Resistance) is a calculated index that estimates insulin resistance using fasting glucose and fasting insulin levels. It helps detect early metabolic dysfunction before blood sugar levels rise into the prediabetes or diabetes range.

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What Is HOMA-IR?

HOMA-IR is a mathematical model developed in 1985 to estimate insulin resistance and beta-cell function using routine fasting lab values instead of complex metabolic testing such as the euglycemic clamp.

It is not a direct laboratory measurement. It is a derived calculation based on fasting glucose and fasting insulin.

Fast Facts about HOMA-IR:

  • HOMA-IR estimates insulin resistance

  • Calculated from fasting insulin and fasting glucose

  • Detects early metabolic dysfunction

  • Values above 2.0 often suggest developing insulin resistance

  • Should be interpreted in clinical context

HOMA-IR Formula (How to Calculate It)

Formula Using mg/dL (U.S. Standard)

HOMA-IR = (Fasting Insulin µIU/mL × Fasting Glucose mg/dL) ÷ 405

Formula Using mmol/L (SI Units)

HOMA-IR = (Fasting Insulin mIU/L × Fasting Glucose mmol/L) ÷ 22.5

What Is a Normal HOMA-IR?

There is no universal diagnostic cutoff, but common interpretation ranges are:

HOMA-IR Interpretation: Typical Adult Ranges
HOMA-IR is a calculated index using fasting insulin and fasting glucose. Exact thresholds vary by population and clinical context.
HOMA-IR Value Typical Interpretation
< 1.0 High insulin sensitivity; often seen in metabolically healthy individuals.
1.0–1.9 Generally favorable range in many adult populations.
2.0–2.9 Early insulin resistance; may indicate developing metabolic dysfunction.
3.0–4.9 Elevated insulin resistance; associated with higher cardiometabolic risk.
≥ 5.0 Marked insulin resistance; often seen in metabolic syndrome or type 2 diabetes.

These ranges are for educational purposes and may not reflect the specific reference intervals used by your laboratory. HOMA-IR exists on a continuum of metabolic risk and should be interpreted alongside A1c, fasting glucose, lipid markers, body composition, ethnicity, and overall cardiometabolic risk assessment in consultation with a qualified clinician.

HOMA-IR exists on a continuum of metabolic risk rather than a binary disease threshold. “The lower, the longer, the better.”

What Does an Elevated HOMA-IR Mean?

An elevated HOMA-IR suggests that the body requires higher insulin levels to maintain normal blood glucose. This condition is known as insulin resistance.

Over time, insulin resistance may contribute to:

  • Metabolic syndrome

  • Prediabetes and type 2 diabetes

  • Atherosclerotic cardiovascular disease

  • Fatty liver disease

  • Polycystic ovarian syndrome

In many individuals, HOMA-IR rises before A1c or fasting glucose becomes abnormal.

HOMA-IR vs A1c: What Is the Difference?

HOMA-IR measures current insulin resistance physiology.

A1c measures average blood glucose over approximately three months.

It is possible to have:

  • Normal A1c

  • Normal fasting glucose

  • Elevated HOMA-IR

That pattern often reflects early compensatory hyperinsulinemia.

HOMA-IR vs Fasting Insulin

Fasting insulin alone does not account for glucose levels. HOMA-IR integrates both values, improving context.

For example:

  • Insulin 15 µIU/mL + Glucose 85 mg/dL → HOMA-IR ≈ 3.15

  • Insulin 15 µIU/mL + Glucose 100 mg/dL → HOMA-IR ≈ 3.7

The second scenario reflects greater metabolic strain than fasting insulin alone, because it accounts for the added context of the individual’s current glycemic state.

HOMA-IR vs LP-IR

LP-IR is an insulin resistance score derived from lipoprotein particle characteristics measured by NMR.

Key differences:

  • HOMA-IR requires fasting

  • LP-IR does not

  • HOMA-IR uses insulin directly

  • LP-IR reflects metabolic patterns through lipoprotein particles

Both can provide insight into metabolic risk and may move in similar directions clinically.

When Is HOMA-IR Most Useful?

HOMA-IR adds value in:

  • Early metabolic risk screening

  • Lean individuals with family history of diabetes

  • Evaluation of metabolic syndrome features

  • NAFLD workup

  • PCOS evaluation

  • Cardiometabolic prevention programs

Limitations of HOMA-IR

HOMA-IR does have some limitations for practical use and should only be looked at in the context of the individual’s overall cardiometabolic health:

  • Requires accurate fasting insulin measurement

  • Assumes stable beta-cell function

  • Less reliable in advanced diabetes

  • No universally accepted clinical cutoff

  • Can vary by assay methodology

It is best used as a risk stratification tool rather than a standalone diagnostic test.

How to Improve HOMA-IR

HOMA-IR often improves with:

  • Weight reduction

  • Resistance training

  • Aerobic exercise

  • Sleep optimization

  • Reduced refined carbohydrate intake

  • GLP-1 receptor agonists

  • Metformin

  • SGLT2 inhibitors

Improvements frequently parallel reductions in visceral adiposity.

Remember, as insulin sensitivity improves, future risk for developing type 2 diabetes and metabolic syndrome also improve.

FAQs about ApoB

  • Almost always, the answer is, yes. ApoB is a direct measure of particle number and predicts cardiovascular risk more accurately, especially in metabolic syndrome or diabetes. LDL-C can miss risk in people who are discordant.

  • Typically at baseline and then periodically to monitor risk or treatment response. Your clinician can guide timing. Depending on individual risk and current interventions, this could be as frequently as about every 3 months or as long as a year.

  • Yes. This is called discordance, and it can identify hidden cardiovascular risk.

  • Both. Family history can influence particle production, but lifestyle and treatment can significantly modify ApoB levels.

Additional References: ApoB

American College of Cardiology / American Heart Association (ACC/AHA)

Grundy SM, et al. 2018 ACC/AHA Guideline on the Management of Blood Cholesterol. Journal of the American College of Cardiology. 2019;73(24):e285–e350.

https://www.acc.org/latest-in-cardiology/ten-points-to-remember/2018/11/08/14/24/2018-guideline-on-the-management-of-blood-cholesterol

Arnett DK, et al. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease. Circulation. 2019;140(11):e596–e646.

https://www.acc.org/latest-in-cardiology/ten-points-to-remember/2019/03/07/16/00/2019-acc-aha-guideline-on-primary-prevention-gl-prevention

National Lipid Association (NLA)

Lloyd-Jones DM, et al. Role of Apolipoprotein B in Clinical Management of Cardiovascular Risk in Adults: NLA Scientific Statement. Journal of Clinical Lipidology. 2022;16(4):e85–e120.

https://www.lipid.org/nla/role-apolipoprotein-b-clinical-management-cardiovascular-risk-adults-expert-clinical-consensus

European Society of Cardiology / European Atherosclerosis Society (ESC/EAS)

Mach F, et al. 2019 ESC/EAS Guidelines for the Management of Dyslipidaemias. European Heart Journal. 2020;41(1):111–188.

https://www.escardio.org/Guidelines/Clinical-Practice-Guidelines/Dyslipidaemias-Management-of

Canadian Cardiovascular Society (CCS)

Anderson TJ, et al. 2016 Canadian Cardiovascular Society Guidelines for the Diagnosis and Management of Dyslipidemia. Canadian Journal of Cardiology. 2016;32(11):1263–1282.

https://www.onlinecjc.ca/article/S0828-282X(16)30732-2/fulltext

(2021 Practice Update summary available here:)

https://www.onlinecjc.ca/article/S0828-282X(20)31052-3/fulltext

International Atherosclerosis Society (IAS)

Sniderman AD, et al. Apolipoprotein B Particles and Cardiovascular Disease Risk: IAS Position Statement. Journal of Clinical Lipidology. 2019;13(5):669–683.

https://www.lipidjournal.com/article/S1933-2874(19)30265-X/fulltext

American Diabetes Association (ADA)

American Diabetes Association. Standards of Medical Care in Diabetes – 2024: Cardiovascular Disease and Risk Management. Diabetes Care. 2024;47(Suppl 1):S190–S206.

https://diabetesjournals.org/care/issue/47/Supplement_1

Key Peer-Reviewed Research Supporting ApoB

Sniderman AD, et al. Apolipoprotein B Versus Non–HDL Cholesterol and LDL Cholesterol as a Cardiovascular Risk Marker. Lancet. 2003;361:777–780.

https://www.sciencedirect.com/science/article/pii/S0140673603127221

  1. Pencina MJ, et al. Discordance Between LDL-C and ApoB and Cardiovascular Risk. Circulation. 2015;132(13):1204–1211.

    https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.114.015669

  2. Ference BA, et al. Low-Density Lipoproteins Cause Atherosclerotic Cardiovascular Disease: 1st of 2 Part Series.European Heart Journal. 2017;38(32):2459–2472.

    https://academic.oup.com/eurheartj/article/38/32/2459/3745109

  3. Johannesen CDL, et al. ApoB and Risk of Myocardial Infarction in the General Population. Clinical Chemistry. 2020;66(5):706–716.

    https://academic.oup.com/clinchem/article/66/5/706/5680971

ASCVD Risk & ApoB Utility

Lloyd-Jones DM, et al. Use of ApoB as a Marker of Atherogenic Lipoprotein Burden in Guidelines and Prevention.Journal of the American College of Cardiology. 2020;75(6):550–562.

https://www.jacc.org/doi/10.1016/j.jacc.2019.12.030

  1. Toth PP, et al. Practical Application of ApoB in Clinical Decision-Making. Atherosclerosis. 2019;282:85–93.

    https://www.atherosclerosis-journal.com/article/S0021-9150(19)30157-0/fulltext