Insulin resistance calculator
Two honest routes to the same question. Give it your fasting glucose and insulin and it runs HOMA-IR. Give it nothing but a tape measure and it runs the proxy score instead.
6
Questions
0
Labs required
405
The HOMA divisor
It asks one thing at a time
Insulin Resistance
Question 1 of 6
Helpful, not required
- Fasting glucose (mg/dL)
- Fasting insulin (µU/mL or mIU/L)
- Triglycerides ÷ HDL from any lipid panel
- A typical systolic blood pressure
Skip any of them. A tape measure and your height are enough to get a usable answer.
Measure it properly
Waist at the navel, first thing in the morning, after a normal exhale — not sucked in, not over clothing. A 4 cm error in the tape changes your waist-to-height ratio by roughly 0.02, which is enough to move you a band.
The thresholds, without the hand-waving
These are the conventional clinical bands. Drag the slider to see what each one actually implies — and where the model stops being trustworthy.
Drag to explore the cut-points
Wallace 2004 · Diabetes Care
2.4HOMA-IR
Borderline
The pancreas is starting to push harder for the same result. Trajectory matters more than the single reading here.
HOMA-IR is a screening model, not a diagnosis. It performs poorly at the extremes of insulin secretion and in very lean, highly trained adults.
Insulin resistance is a storage problem before it is a sugar problem
Petersen and Shulman’s mechanism reviews trace the lesion to ectopic lipid — fat deposited inside liver and muscle cells, where it interferes with insulin-receptor signalling. That sequence explains why fasting insulin rises years before fasting glucose does.
Fat lands where it shouldn’t
Lipid accumulates inside liver and skeletal-muscle cells rather than in fat tissue built to hold it.
The receptor signal degrades
Diacylglycerol activates PKCε, which blunts insulin-receptor signalling inside the cell.
The pancreas compensates
Beta cells raise insulin output to force the same glucose disposal. Fasting insulin climbs first.
Glucose moves last
Fasting glucose only drifts up once compensation starts failing — which is why a normal glucose can be falsely reassuring.
Four levers with real evidence behind them
None of these are novel and none of them are exciting. That is rather the point — they are the ones that keep showing up in controlled trials rather than in marketing.
A sustained, unheroic deficit
The Newcastle and DiRECT work points at hepatic and intramyocellular lipid as the thing that has to fall. Weight loss is the vehicle, not the point.
Resistance training
Muscle is the largest glucose sink you own. Strasser’s 2013 review found resistance training improved insulin sensitivity independently of fat loss.
Fewer ultra-processed calories
Not a moral position — a mechanical one. UPF-heavy patterns drive surplus intake, and surplus lands preferentially in the wrong depots.
Sleep that isn’t an afterthought
Buxton 2012 produced prediabetic-grade insulin resistance in healthy adults with three weeks of restricted, misaligned sleep. Diet was not the variable.
A note on honesty: we will not tell you how much weight you will lose or how fast your markers will move. Nobody can know that about you. What the research supports is that these levers may help support better insulin sensitivity in many people, and that adherence predicts the outcome more reliably than which protocol you pick.
Straight answers
What people ask about this number
If you give it fasting glucose and fasting insulin, it runs HOMA-IR — the Homeostatic Model Assessment, which is glucose in mg/dL multiplied by insulin in µU/mL, divided by 405. That single number estimates how hard your pancreas is working to keep your fasting glucose where it is.
If you don’t have labs, it switches to a 0–10 proxy score built from waist-to-height ratio, plus any of fasting glucose, the triglyceride-to-HDL ratio and systolic blood pressure that you happen to know. The proxy is a screen for whether testing is worth asking for — it is not a substitute for the test.
Screening estimates only. None of the above is a diagnosis or a treatment plan.
Free · 2 minutes · No card
One marker is a clue. Your profile is the answer.
The assessment reads insulin resistance against your sleep, training, dietary pattern and weight history — then points you at the protocol the evidence supports for that combination.
References
- 01Wallace TM, Levy JC, Matthews DR (2004). Use and abuse of HOMA modeling. Diabetes Care. PubMed 15161807
- 02Petersen MC, Shulman GI (2018). Mechanisms of Insulin Action and Insulin Resistance. Physiological Reviews. PubMed 30067154
- 03Samuel VT, Shulman GI (2016). The pathogenesis of insulin resistance: integrating signaling pathways and substrate flux. Journal of Clinical Investigation. PubMed 26727229
- 04Lim EL, Hollingsworth KG, Aribisala BS, Chen MJ, Mathers JC, Taylor R (2011). Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol. Diabetologia. PubMed 21656330
- 05Lean MEJ et al. (2018). Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial. The Lancet. PubMed 29221645
- 06Taylor R et al. (2024). Beta-cell function and remission of type 2 diabetes (5-year DiRECT extension). The Lancet Diabetes & Endocrinology. PubMed 38301678
- 07Buxton OM et al. (2012). Adverse metabolic consequences in humans of prolonged sleep restriction combined with circadian disruption. Science Translational Medicine. PubMed 22496545
- 08Strasser B, Pesta D (2013). Resistance training for diabetes prevention and therapy: experimental findings and molecular mechanisms. BioMed Research International. PubMed 24455726
Educational only, not medical advice. This calculator produces a screening estimate, not a diagnosis. Consult your physician before major dietary changes or altering prescribed medication, including metformin, insulin or GLP-1 drugs. These statements have not been evaluated by the Food and Drug Administration. Individual results vary; no outcome is guaranteed.