The glucose problem
Standard NHS metabolic screening checks fasting glucose and, in some cases, HbA1c. If glucose is below 6.0 mmol/L and HbA1c is below 48 mmol/mol, you're told everything is fine. You're not diabetic. You're not even pre-diabetic. Come back in a few years.
The problem is that glucose is a late-stage marker. By the time fasting glucose rises consistently above 5.6 mmol/L — the conventional pre-diabetes threshold — the underlying metabolic dysfunction has typically been present for a decade or more.
What rises first — years before glucose — is insulin.
What insulin actually does
When you eat carbohydrates, your pancreas releases insulin to shuttle glucose into cells. In a healthy metabolic state, a small amount of insulin does this efficiently. Fasting insulin in a genuinely healthy person sits between 2 and 6 μIU/mL.
When cells start to become resistant to insulin's signal — when they stop responding as sensitively as they should — the pancreas compensates by releasing more insulin to achieve the same effect. Fasting insulin creeps up. 8. Then 12. Then 18. Then 25.
All while fasting glucose looks completely normal.
This compensation phase can last many years. The pancreas is working harder and harder to maintain glucose in the normal range, and succeeding. So the standard test shows nothing wrong. Meanwhile, elevated insulin is driving inflammation, fat storage (particularly visceral abdominal fat), hormonal disruption, and cardiovascular risk — silently, for years.
Fasting insulin at 15–18 μIU/mL with normal glucose is not a normal result. It is a compensation result. The system is working overtime to maintain appearances. The question is how much longer it can sustain that effort.
What HOMA-IR actually is
HOMA-IR stands for Homeostatic Model Assessment of Insulin Resistance. It's calculated from two numbers you probably already have on a blood test: fasting glucose and fasting insulin.
The formula is straightforward: fasting insulin (μIU/mL) × fasting glucose (mmol/L) ÷ 22.5.
The result gives you a single number that reflects how much insulin your body is requiring to maintain normal glucose levels — a direct proxy for insulin sensitivity.
Why isn't it on a standard blood panel?
Two reasons. First, fasting insulin isn't routinely measured by the NHS. It's not in the standard metabolic screening protocol. You can request it, but most GPs will only run it if there's a specific clinical indication — and "your glucose is normal but you have symptoms consistent with insulin resistance" generally doesn't qualify.
Second, even when both fasting glucose and fasting insulin are run, HOMA-IR is rarely calculated. The two numbers sit in different sections of the report. Nobody joins the dots.
This isn't a conspiracy. It's a system designed to diagnose disease, not optimise health. Insulin resistance that hasn't yet manifested as pre-diabetes isn't considered a disease state worth treating. By the time it does manifest, interventions are more expensive, less effective, and considerably more disruptive to the patient's life.
What symptoms suggest insulin resistance before glucose rises?
The classic presentation I see clinically is a cluster of symptoms that appears to have no obvious connection:
Energy crashes 90 to 120 minutes after meals — not hunger exactly, more a sudden drop in energy and concentration that feels disproportionate to what was eaten.
Waking at 2–4am — particularly common when the dysglycaemic pattern involves overnight glucose instability. Glucose drops, cortisol spikes to mobilise energy stores, the client wakes with racing thoughts and can't return to sleep.
Strong carbohydrate cravings — particularly in the afternoon, often for something sweet or starchy. The body is seeking a quick glucose fix to compensate for the crash.
Difficulty losing weight despite eating reasonably — chronically elevated insulin is a fat-storage signal. The body is receiving a constant instruction to store rather than burn.
Brain fog and poor concentration — the brain is highly glucose-dependent. When glucose delivery becomes erratic, cognitive function follows.
Fatigue that isn't explained by sleep quality — cellular energy production is compromised when insulin signalling is impaired.
None of these symptoms would trigger a metabolic screen in a standard consultation. They're more likely to result in a referral for depression, anxiety, or — if the patient is female and of a certain age — an assumption that it's perimenopause. The metabolic component goes undetected.
HOMA-IR in the context of the full picture
HOMA-IR is most useful not in isolation but in the context of other markers. In functional medicine practice, I look at the cluster:
Fasting insulin — the raw fuel gauge. Optimal is 2–6 μIU/mL. Above 10 starts to become clinically meaningful even with normal glucose.
Fasting glucose — the later-stage marker. Functional optimal is 4.0–5.0 mmol/L. Above 5.0 with elevated insulin is a significant finding.
HbA1c — the three-month average. Functional optimal is below 35 mmol/mol, not the NHS threshold of 48.
Triglycerides — often elevated with insulin resistance. Functional optimal is below 1.0 mmol/L. The triglyceride-to-HDL ratio is one of the most underused metabolic risk markers available.
HOMA-IR — the calculated bridge between the glucose and insulin story.
Together, these five numbers tell a metabolic story that no single marker can tell alone. A client with fasting insulin of 14, fasting glucose of 5.2, HbA1c of 36, triglycerides of 1.8, and HOMA-IR of 3.3 is not metabolically healthy regardless of what a standard blood panel reports.
What to do if your HOMA-IR is elevated
The intervention hierarchy matters here. Before reaching for supplements, the foundational variables need addressing:
Meal composition and sequencing — eating protein and fat before carbohydrate at each meal significantly blunts the insulin response. Not a diet, a sequencing strategy.
Movement timing — a 10 to 15 minute walk after meals is one of the most evidence-backed interventions for post-meal glucose management available. Simple, free, and immediately effective.
Sleep quality — a single night of poor sleep measurably impairs insulin sensitivity the following day. Chronically disrupted sleep drives insulin resistance independent of diet.
Stress management — cortisol raises blood glucose. Chronic stress chronically elevates cortisol. The metabolic and stress systems are not separate.
Reducing refined carbohydrate load — particularly liquid calories, refined sugars, and ultra-processed foods. The goal is not zero carbohydrate but appropriate carbohydrate relative to individual metabolic capacity, which varies significantly between people.
Only once these foundations are addressed does targeted supplementation become relevant. Berberine, magnesium, alpha lipoic acid, and inositol all have evidence in insulin resistance contexts — but they're Layer 7 on the intervention hierarchy, not Layer 1.
The bottom line
HOMA-IR is not a difficult test. It's not expensive. It requires two blood markers that are already available from any laboratory. The calculation takes thirty seconds.
The reason it isn't routinely run is not technical — it's systemic. Standard medical practice is designed to catch disease at the point it becomes diagnosable, not to identify the decade of dysfunction that precedes it.
By the time fasting glucose crosses the pre-diabetes threshold, the window for the simplest and most effective interventions has largely passed. Identifying insulin resistance through HOMA-IR when fasting insulin is 12 and glucose is still 4.8 gives a clinically actionable window that waiting for the glucose to rise does not.
This is why functional reference ranges exist. Not to pathologise normal variation, but to identify the trajectory before it becomes the destination.