Insulin Resistance With Normal Blood Sugar

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Article: Insulin Resistance With Normal Blood Sugar  |  Category: Metabolic  |  Authored by: Brian Lamkin, DO

Normal Glucose Does Not Mean Normal Metabolism

One of the most common scenarios in my practice: a patient brings in a stack of lab results from their primary care physician and says "my doctor told me my blood sugar is fine." Fasting glucose is 92. HbA1c is 5.4. Everything checks out. Except the patient has gained 30 pounds in the last five years despite a reasonable diet, cannot lose weight on any intervention, has visible abdominal weight gain, feels tired after meals, and has a family history of type 2 diabetes. The labs told one story. The clinical picture told another. The discrepancy resolved the moment we ran fasting insulin. It was 22. The glucose was fine because the pancreas was working overtime to keep it that way.

The 10 to 20 Year Silent Period

Insulin resistance does not appear suddenly with the first abnormal HbA1c. It develops over a decade or two before glucose ever rises^[1]. During this silent period, the cells become progressively less responsive to insulin. The pancreas compensates by producing more insulin to force glucose into cells. This compensation is successful. Fasting glucose stays in the normal range. HbA1c stays below 5.7. Conventional diabetes screening flags nothing. But during this entire period, the patient has hyperinsulinemia, and hyperinsulinemia is itself a disease state. It drives weight gain, visceral adiposity, hypertension, dyslipidemia, fatty liver, inflammation, and accelerated aging years before glucose ever rises.

Why Fasting Insulin Is the Early Marker

Fasting insulin^[2] measures what the pancreas is doing to keep glucose normal. In a metabolically healthy person, the pancreas produces small amounts of insulin and tissues respond efficiently. Fasting insulin is low (ideally 2 to 5 mIU/L). In early insulin resistance, tissues require more insulin to move the same amount of glucose. The pancreas produces more. Fasting insulin rises (8, 12, 15, 20 mIU/L) while glucose stays normal. This is the compensation phase. It can last 10 to 20 years. Glucose does not rise until the pancreas can no longer produce enough insulin to maintain normal levels. By that point, significant damage has accumulated.

The Problem With Standard Lab Reference Ranges

Most laboratory reference ranges for fasting insulin extend up to 25 mIU/L, with some labs going as high as 29. A patient with fasting insulin of 22 is technically "in range" and typically told their labs are normal. But fasting insulin of 22 represents significant insulin resistance. The reference range reflects what is statistically common in the general population, not what is physiologically optimal. In functional medicine, the relevant ranges are:

Below 5 mIU/L: Optimal insulin sensitivity. This is what we see in metabolically healthy individuals. 5 to 8 mIU/L: Acceptable range. Still insulin sensitive but worth monitoring. 8 to 12 mIU/L: Early insulin resistance. Lifestyle intervention usually sufficient. 12 to 20 mIU/L: Moderate insulin resistance. Aggressive dietary and exercise intervention warranted, often with insulin sensitizers. Above 20 mIU/L: Significant insulin resistance. Requires structured intervention and comprehensive metabolic workup.

HOMA-IR: The Calculated Score

HOMA-IR (Homeostatic Model Assessment of Insulin Resistance)^[3] incorporates both fasting insulin and fasting glucose to produce a single score: (fasting insulin x fasting glucose) / 405. A HOMA-IR below 1.5 indicates insulin sensitivity. Between 1.5 and 2.5 is borderline. Above 2.5 confirms insulin resistance. HOMA-IR is more accurate than fasting insulin alone because it captures the relationship between insulin output and glucose control. A patient with fasting insulin of 10 and glucose of 95 has a HOMA-IR of 2.3 (borderline). A patient with fasting insulin of 15 and glucose of 98 has a HOMA-IR of 3.6 (significant insulin resistance). The calculation surfaces the pattern that the individual numbers obscure.

C-Peptide: When Insulin Alone Is Not Enough

C-peptide is released in equimolar amounts with insulin and has a longer half-life, making it a more stable marker of pancreatic insulin output. It is particularly useful in patients already on exogenous insulin (where measured insulin reflects injected insulin rather than pancreatic output) and in distinguishing type 1 from type 2 diabetes. In functional medicine practice, C-peptide complements fasting insulin when results are ambiguous or when evaluating pancreatic beta-cell function in advanced insulin resistance.

Clinical Signs That Insulin Should Be Tested Even With Normal Glucose

If any of the following are present, fasting insulin and HOMA-IR should be tested regardless of glucose or HbA1c: central abdominal weight gain, particularly visceral adiposity; skin tags or acanthosis nigricans (dark velvety skin in folds); reactive hypoglycemia (shakiness, fatigue, brain fog 2 to 4 hours after carbohydrate-containing meals); elevated triglycerides with low HDL; fatty liver on imaging; PCOS or hormonal imbalances; family history of type 2 diabetes; weight loss resistance despite diet and exercise; hypertension; elevated ALT on liver panel.

Cardiovascular and Inflammatory Consequences Before Glucose Rises

Hyperinsulinemia independently drives cardiovascular risk^[4] through mechanisms that do not require glucose elevation: sodium retention producing hypertension, hepatic triglyceride synthesis producing dyslipidemia, inflammatory cytokine elevation driving endothelial dysfunction, and direct atherogenic effects on the arterial wall. Waiting for glucose to rise before intervening means waiting through a decade or more of active cardiovascular damage. Early identification through fasting insulin allows intervention when the damage is preventable.

The Lamkin Clinic Approach

Every metabolic evaluation at The Lamkin Clinic includes fasting insulin and HOMA-IR alongside standard glucose and HbA1c. When insulin resistance is identified, treatment is matched to severity: early cases respond to low-glycemic dietary modification, resistance training, and sleep optimization. Moderate cases add magnesium repletion, berberine or inositol, and structured intermittent fasting. Advanced cases with significant hyperinsulinemia may benefit from pharmaceutical insulin sensitizers alongside the foundational interventions. The goal in every case is to identify the problem early, reverse it completely, and prevent the 10 to 20 year progression to frank diabetes.

The Lamkin Clinic, Edmond Oklahoma | lamkinclinic.com

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References and Further Reading

1. [1]Tabak AG, et al. The natural history of progression from normal glucose tolerance to type 2 diabetes. Lancet. 2009;373(9682):2215-2221.
2. [2]Blaak EE, et al. Fasting insulin as a clinical marker of insulin resistance. Diabetes Obes Metab. 2020;22(Suppl 3):35-45.
3. [3]Matthews DR, et al. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28(7):412-419.
4. [4]Reaven GM. Insulin resistance and hyperinsulinemia as cardiovascular risk factors. Am J Hypertens. 2016;29(1):20-26.