Your A1c Is Fine. That Doesn't Mean You're Fine.

Your A1c Is Fine. That Doesn't Mean You're Fine.

Dr. Jeff Kindred, DO

A patient comes in — mid-40s, no major complaints. Maybe a little more fatigue than a few years ago, but nothing alarming. Blood pressure is reasonable. Weight is up slightly but not dramatically. They eat reasonably well, exercise occasionally, and their last doctor told them their labs looked great.

We run a full panel. And there it is.

Fasting insulin: elevated. Fasting glucose: creeping up, still technically normal. Triglycerides: high. A1c: completely unremarkable.

By the standard checklist — the one most primary care visits run through — this patient is fine. No diabetes. No metabolic syndrome, technically. Nothing that would trigger a conversation beyond "watch your diet and come back in a year."

But something is clearly wrong. And the window to fix it without medication, without a diagnosis, without the downstream consequences of a decade of ignored insulin resistance — that window is open right now.

What A1c Misses

A1c tells you your average blood sugar over the past three months. It's a useful number. But it's a lagging indicator — it rises after insulin resistance has been building for years, sometimes decades.

Here's what happens before A1c moves: your pancreas starts working harder to keep blood sugar in check. Insulin goes up. Blood sugar stays normal — for a while — because your beta cells are compensating. You look fine on paper. But the underlying driver, insulin resistance at the tissue level, is already there and already doing damage.

By the time A1c crosses the prediabetes threshold, you're not catching this early. You're catching it late.

The test that catches it early is fasting insulin. It's cheap, it's widely available, and most people have never had it ordered.

The HOMA-IR Formula

Fasting insulin alone is useful, but even more useful in combination with fasting glucose. The HOMA-IR score — Homeostatic Model Assessment of Insulin Resistance — combines both into a single number that reflects how hard your body is working to maintain metabolic control.

The math is straightforward: multiply your fasting glucose (in mg/dL) by your fasting insulin (in µIU/mL), then divide by 405. A score below 1.0 is excellent. Above 1.9 is a signal worth taking seriously. Above 2.9 is frankly elevated.

For the patient I described, the HOMA-IR wasn't through the roof. It was 2.4. Not a crisis — but not fine either. Paired with the triglyceride picture, it told a coherent story: someone whose metabolism is starting to struggle, years before any standard marker would trigger an alarm.

Why This Matters More Than the Number

Think of insulin resistance as the trunk of the tree. What grows off it — the branches — are conditions we tend to treat as separate problems: cardiovascular disease, type 2 diabetes, fatty liver, low testosterone, cognitive decline, and a meaningful share of certain cancers. They look different in the clinic. They often land in different specialists' offices. But they share a common root, and if you're not looking at the root, you're managing symptoms while the underlying biology keeps running.

Atherosclerosis accelerates in the setting of insulin resistance — not just because of the glucose, but because of the dyslipidemia that comes with it (high triglycerides, low HDL, small dense LDL particles). Fatty liver develops silently — and here's the part most patients don't know: liver enzymes can be completely normal while this process is already underway. An AST and ALT in the normal range does not mean the liver is fine. It means the damage hasn't yet crossed the threshold where enzymes leak. By the time those numbers move, you're further down the road than you needed to be.

Testosterone suppression follows a similar pattern — insulin resistance disrupts the hormonal signaling that supports normal testosterone production, and men who come in with low energy and low libido often assume the problem is their testosterone, when the actual driver is metabolic. Treating the branch without addressing the trunk is why some of those conversations don't go the way patients hope.

The cognitive piece is less intuitive but increasingly hard to ignore. There's a reason some researchers refer to Alzheimer's as "type 3 diabetes" — the brain's sensitivity to insulin plays a direct role in neuronal health and synaptic function. This is an area where the science is still developing, but the signal is consistent enough that it belongs in any serious conversation about long-term risk. [1]

All of this — before a single diagnosis. Before A1c moves. Before liver enzymes flag. Before testosterone falls far enough to show up on a standard panel.

That's what makes the fasting insulin and HOMA-IR conversation so important. It's not about catching a disease. It's about seeing the direction before the destination is fixed.

The Test You Probably Haven't Had

If you've had a standard metabolic panel and been told your blood sugar is normal, that's genuinely good news. But it's not the complete picture.

Fasting insulin isn't on the standard panel. It's not part of the routine A1c conversation. In most primary care settings, it simply doesn't get ordered unless something has already gone wrong — which, by definition, means you're not catching it early.

Asking for it isn't paranoid. It's the kind of question that gets asked when you're trying to know where you actually stand, not just whether you've crossed a threshold that was set decades ago.

For most people with early insulin resistance, there's a meaningful window — sometimes a decade or more — where the trajectory is genuinely changeable. Reduced refined carbohydrate, increased dietary protein, consistent Zone 2 exercise, and improved sleep quality can move these numbers meaningfully when insulin resistance is early and compensated. The pancreas is still doing its job. The goal is to stop making it work so hard.

We retested that same patient at 90 days. Fasting insulin was down. Triglycerides improved. HOMA-IR dropped to 1.4. No medication. No diagnosis. Just early signal, early action.

If you're noticing the kind of subtle metabolic drift that often gets chalked up to stress or aging — fatigue, weight creeping up despite consistency, recovery that takes longer than it used to — this is worth knowing about. You just have to be in an environment where someone thinks to look.

Working With Us

If you've never had fasting insulin or HOMA-IR checked, or you've been told your metabolic labs look fine but something still doesn't feel right, that's exactly the kind of conversation we have at Hi, Finch Health. Our concierge medicine model is built around having enough time to look at the full picture — not just the numbers that fit on a standard panel.

Set up a consultation with Dr. Kindred.

Related Reading from the Hi, Finch Playbook

References

  1. De Felice FG, Lourenco MV, Ferreira ST. How does brain insulin resistance develop in Alzheimer's disease? Alzheimers Dement. 2014;10(1 Suppl):S26–32. PMID 24529521
  2. Matthews DR, et al. Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28(7):412–419. PMID 3899825
  3. Reaven GM. Banting Lecture 1988. Role of insulin resistance in human disease. Diabetes. 1988;37(12):1595–1607. PMID 3056758
  4. Lonardo A, et al. Insulin resistance in nonalcoholic fatty liver disease. Metab Syndr Relat Disord. 2011;9(4):251–262. PMID 20370677
  5. Facchini FS, et al. Insulin resistance as a predictor of age-related diseases. J Clin Endocrinol Metab.2001;86(8):3574–3578. PMID 11502781
  6. Ding EL, et al. Sex differences of endogenous sex hormones and risk of type 2 diabetes. JAMA.2006;295(11):1288–1299. PMID 16537739 — on the bidirectional relationship between insulin resistance and testosterone.

Hi, Finch Health is a concierge medicine practice in Nashville, Tennessee. We practice evidence-based preventive medicine — which means we look beyond the standard panel to find what actually matters for your long-term health.

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