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The road to diabetes takes 15 years. Here's what your labs look like along the way. Year 1: Everything looks normal. Fasting glucose 82. HbA1c 5.1%. Your doctor says you're healthy. But nobody checked fasting insulin. It's already 10. Year 5: Glucose still normal at 88. HbA1c 5.3%. But fasting insulin has crept to 14. Triglycerides are 130. HDL dropped to 42. Your doctor doesn't connect these dots because each value is "within range." Year 10: Glucose 97. "Still normal." HbA1c 5.6%. Doctor says "let's keep an eye on it." Fasting insulin is 22. Triglycerides 180. You've gained 30 pounds, mostly around your middle. Year 15: Glucose 128. HbA1c 6.7%. "You have type 2 diabetes." Prescription for metformin. The disease didn't arrive at year 15. It started at year 1. The labs to detect it existed the entire time. Nobody ordered them.
Fasting insulin is the earliest lab marker of metabolic dysfunction. It rises 5-10 years before glucose does.
As cells become resistant to insulin's signal, the pancreas compensates by producing more insulin. Blood sugar stays normal because insulin is working overtime to keep it there. The elevated insulin is invisible on standard lab work because fasting insulin isn't part of routine screening.
Dr. Joseph Kraft performed over 14,000 insulin response tests during his career at St. Joseph Hospital in Chicago. He found that abnormal insulin patterns preceded glucose abnormalities by years, and that 80% of people with "normal" glucose already showed pathological insulin responses. His work, published in Diabetes Research and Clinical Practice (2011), demonstrated that diabetes should be diagnosed by insulin, not glucose.
Optimal fasting insulin: below 6 uIU/mL. Early insulin resistance: 6-10. Moderate insulin resistance: 10-15. Severe insulin resistance: above 15.
Most labs don't flag insulin as abnormal until 25 or higher. By that point, you've been insulin resistant for a decade.
Fasting insulin costs about $20-30 at direct-to-consumer labs. It's the single most cost-effective preventive test available for metabolic disease.
HOMA-IR (Homeostatic Model Assessment of Insulin Resistance) is calculated from two values you already have if you order fasting glucose and fasting insulin.
Formula: (Fasting Glucose mg/dL x Fasting Insulin uIU/mL) / 405.
Originally published by Matthews and colleagues in Diabetologia (1985), HOMA-IR has become the standard research tool for quantifying insulin resistance without requiring the complex hyperinsulinemic-euglycemic clamp (the gold standard but impractical for clinical use).
Optimal: below 1.0. Early IR: 1.0-2.0. Established IR: 2.0-3.0. Severe IR: above 3.0.
Example calculation: Fasting glucose 90, fasting insulin 12. HOMA-IR = (90 x 12) / 405 = 2.67. This is established insulin resistance.
Another person: Fasting glucose 82, fasting insulin 4. HOMA-IR = (82 x 4) / 405 = 0.81. This is optimal.
Both people have "normal" fasting glucose. Their metabolic realities are completely different.
HOMA-IR makes the invisible visible. It turns two "normal" lab values into a meaningful assessment of metabolic health. No additional blood draw required. Just simple math.
Track HOMA-IR over time. It should decrease as you implement dietary changes, exercise, and improve sleep.
Don't have fasting insulin? Calculate your triglyceride/HDL ratio from a standard lipid panel. It's the best surrogate marker for insulin resistance from routine blood work.
Simply divide your triglycerides by your HDL cholesterol.
McLaughlin and colleagues published in the Annals of Internal Medicine (2003) that TG/HDL ratio above 3.0 identified insulin-resistant individuals with sensitivity and specificity comparable to formal insulin testing.
Optimal: below 1.0. Acceptable: 1.0-2.0. Insulin resistance likely: 2.0-3.0. Severe insulin resistance: above 3.0.
Example: Triglycerides 150, HDL 40. Ratio: 3.75. Severe insulin resistance. Another person: Triglycerides 60, HDL 70. Ratio: 0.86. Optimal.
This ratio correlates with small dense LDL particles, visceral fat, and cardiovascular risk better than LDL cholesterol alone.
Here's what makes this powerful: your doctor already orders a lipid panel. The data exists. Nobody is calculating this ratio. It's sitting right there on the lab report, hiding in plain sight.
Next time you get labs back, divide your triglycerides by your HDL. If the number is above 2, you have insulin resistance. Address it now.
Fasting glucose and HbA1c are the tests your doctor relies on for diabetes screening. They work, but they catch the disease far too late.
Fasting glucose: Conventional "normal" extends to 99 mg/dL. Prediabetes starts at 100. Diabetes at 126.
But functional medicine knows that fasting glucose in the high 80s and 90s already reflects insulin resistance. Your pancreas is working harder to keep glucose from rising. The system is stressed.
Optimal fasting glucose: 70-85 mg/dL. 86-94: early metabolic dysfunction. 95-99: significant insulin resistance (your doctor still says "normal"). 100-125: prediabetes. 126+: diabetes.
HbA1c measures average blood sugar over 2-3 months by looking at glycated hemoglobin (sugar stuck to red blood cells).
Conventional cutoff: prediabetes at 5.7%, diabetes at 6.5%. Functional optimal: below 5.3%.
Between 5.3% and 5.6%, metabolic damage is accumulating. Selvin and colleagues published in NEJM (2010) that cardiovascular risk increases linearly with HbA1c starting at 5.0%. There's no safe threshold below which risk disappears.
Every 0.1% increase above 5.0% correlates with measurably higher cardiovascular disease risk.
The problem with both tests: they respond slowly. Insulin resistance can exist for a decade before glucose or HbA1c becomes abnormal. By the time these markers move, significant metabolic damage has occurred.
They're useful for tracking progress once you know you have insulin resistance. They're terrible for early detection.
Two additional markers round out the insulin resistance assessment.
Uric acid is produced when the body metabolizes purines and fructose. Elevated uric acid (above 6.0 mg/dL in men, above 5.0 in women) signals fructose metabolism dysfunction and early insulin resistance.
Dr. Richard Johnson at the University of Colorado has published extensively on the uric acid-metabolic syndrome connection. His research, including a 2009 paper in BMC Nephrology, shows that uric acid isn't just a marker of disease. It's a mechanistic driver. High uric acid promotes insulin resistance, hypertension, and fatty liver through mitochondrial oxidative stress.
Functional optimal: below 5.5 mg/dL (men), below 4.5 (women).
Reducing fructose intake (especially high-fructose corn syrup) and alcohol lowers uric acid. Cherry extract and vitamin C also help.
C-peptide is a byproduct of insulin production. When proinsulin is cleaved to form insulin, C-peptide is released in a 1:1 ratio. Measuring C-peptide tells you how much insulin your pancreas is actually producing.
High C-peptide (above 3.0 ng/mL): Your pancreas is working overtime. Hyperinsulinemia. Insulin resistance is established and the pancreas is compensating.
Normal C-peptide with high glucose: The pancreas is starting to fail. Beta cells are burning out. This is the transition from insulin resistance to diabetes.
Low C-peptide (below 0.8 ng/mL) with high glucose: Beta-cell failure. The pancreas can no longer produce adequate insulin. This typically means long-standing diabetes or type 1 diabetes.
C-peptide helps you understand where you are on the insulin resistance timeline. Are you early (high insulin, normal glucose, high C-peptide)? Or late (high glucose, failing C-peptide)? The answer determines your treatment strategy.
Here's the good news about catching insulin resistance early: it's completely reversible.
At fasting insulin of 10 and HOMA-IR of 1.5, you're in the early stage. Dietary changes alone (reducing refined carbohydrates, eliminating sugar, eating more protein and healthy fat) can normalize insulin within 3-6 months.
At fasting insulin of 15 and HOMA-IR of 2.5, you have established insulin resistance. More aggressive intervention is needed: strict carbohydrate reduction (under 50g daily), time-restricted eating, resistance training, and possibly berberine or metformin. Reversal takes 6-12 months.
At fasting insulin above 20 with rising glucose and HbA1c above 5.7%, you're approaching the tipping point. Ketogenic diet, intermittent fasting, resistance training, targeted supplementation, and medical supervision. Reversal is still possible but requires commitment.
Once HbA1c exceeds 6.5% and you're diagnosed with diabetes, reversal is harder but not impossible. The DiRECT trial (published in Lancet, 2018) achieved 46% remission at one year with intensive dietary intervention. Virta Health's ketogenic protocol achieved 60% remission at two years.
The earlier you catch it, the easier it is to fix.
If your fasting insulin is 12 right now, you're at approximately year 5-7 on the diabetes timeline. You have time. But not forever.
Test your fasting insulin. Calculate HOMA-IR. Check your TG/HDL ratio. Know your number. Act on it.
Type 2 diabetes is the most predictable chronic disease in medicine. The labs that detect it early exist. They're cheap. They're widely available. Fasting insulin. HOMA-IR. TG/HDL ratio. Uric acid. These markers light up years before glucose and HbA1c sound the alarm. But nobody orders fasting insulin as part of routine screening. Nobody calculates TG/HDL ratio. Nobody teaches patients what HOMA-IR means. So 88 million Americans have prediabetes, and 84% of them don't know it. They don't know it because the tests that would catch it early aren't being run. You now know which tests to order and how to interpret them. Get them done. Calculate the ratios. If the numbers are off, you have a window, years wide, to reverse the trajectory. Don't wait for a diagnosis. Diagnose the trend. Fix it now.
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