What Is Insulin Resistance — And Why Is It Hiding in Your Labs?
If you have been trying to lose weight, struggling with energy that won't come back, dealing with hormone imbalances that don't fully respond to treatment, or watching your body composition shift in the wrong direction despite genuine effort — there is one metabolic variable I want to make sure has been properly evaluated.
Fasting insulin.
Not fasting glucose. Fasting insulin.
These are different tests. Most standard panels run one and not the other. And the one that gets skipped is the one that reveals the problem years before anything shows up on the test that gets ordered.
What Insulin Actually Does
Insulin is a hormone produced by the pancreas in response to rising blood sugar. When you eat — particularly carbohydrates — glucose enters the bloodstream and insulin is released to help cells absorb and use that glucose for energy. In a healthy metabolic state, this process is efficient and responsive. Blood sugar rises after eating, insulin is released, cells absorb the glucose, blood sugar returns to baseline.
Insulin resistance is what happens when that process breaks down. The cells — particularly in muscle, liver, and fat tissue — begin to respond less efficiently to insulin's signal. The pancreas compensates by producing more insulin to achieve the same effect. Blood sugar stays controlled — for a while — but only because insulin levels are running higher than they should be to maintain it.
This is the critical piece: blood sugar can appear completely normal on a standard panel while insulin is already significantly elevated. The pancreas is compensating. The dysfunction exists. But the test that would reveal it — fasting insulin — wasn't ordered.
This state can persist for years, even decades, before fasting glucose finally moves out of range and someone gets a diagnosis of prediabetes or type 2 diabetes. By that point, the metabolic dysfunction has been building quietly in the background — driving weight gain, disrupting hormones, degrading energy, and compounding inflammation — the entire time.
Why It Matters Beyond Blood Sugar
Most people think of insulin resistance as a precursor to diabetes. That framing is accurate but incomplete. Insulin resistance is a systemic metabolic condition with effects that extend well beyond glucose regulation — and those effects are exactly what most of my patients are dealing with when they walk through the door.
Weight gain and fat storage. Chronically elevated insulin is one of the most potent fat storage signals in the body. Insulin actively suppresses fat burning and promotes fat accumulation — particularly in the abdomen. A person with significant insulin resistance who is eating a reasonable diet can still be in a constant state of fat storage mode because their insulin levels never fully drop between meals. This is a physiological barrier to weight loss, not a behavioral one. No amount of caloric restriction fully overcomes it without addressing the underlying insulin dynamics.
Disrupted hormone balance. Insulin resistance is directly connected to testosterone and estrogen dysregulation in both men and women. In women, elevated insulin stimulates the ovaries to produce excess androgens — a pattern central to polycystic ovary syndrome and a contributor to hormonal acne, cycle irregularity, and difficulty conceiving. In men, insulin resistance drives increased conversion of testosterone to estrogen through aromatization, simultaneously lowering testosterone and raising estradiol. Treating testosterone levels without addressing insulin resistance in this context produces limited and temporary results.
SHBG suppression. Insulin resistance lowers sex hormone-binding globulin — which sounds like it should help, since lower SHBG means more free sex hormones. But the hormones being freed into circulation include estrogen as well as testosterone, and the overall hormonal picture in insulin-resistant patients tends toward imbalance rather than optimization. This is one of the reasons why lab values can look confusing — total hormones appear adequate, free hormones are elevated, but the pattern still produces symptoms.
Thyroid interference. Insulin resistance impairs the conversion of T4 — the storage form of thyroid hormone — into active T3. This means that even in patients with normal TSH and adequate T4 production, insulin resistance can be quietly limiting how much active thyroid hormone reaches the cells. We covered this pattern in the thyroid post — Reverse T3 elevation driven by metabolic dysfunction — and insulin resistance is one of its primary drivers.
Chronic inflammation. Elevated insulin drives inflammatory signaling throughout the body. Chronically elevated insulin is associated with higher levels of hs-CRP, IL-6, and other inflammatory markers — contributing to the low-grade systemic inflammation that undermines recovery, accelerates aging processes, and compounds nearly every other health condition we try to address clinically.
Energy dysregulation. When cells are resistant to insulin, they are less efficient at using glucose for energy. The result is a cellular energy deficit despite adequate caloric intake — a persistent fatigue that is metabolic in origin and that doesn't respond to caffeine, sleep, or rest the way normal tiredness does. This is one of the most common presentations of insulin resistance that goes completely unidentified because nobody checked the fasting insulin.
The Test That Reveals It
Fasting insulin is a simple blood test drawn after an overnight fast — the same conditions as a standard fasting glucose. It costs roughly the same as most basic labs. It is available on virtually every lab panel. And it is almost never included in a standard annual panel.
Optimal fasting insulin is generally considered to be below 5 to 7 mIU/L. The conventional "normal" range extends to 25 mIU/L or higher — meaning a patient with a fasting insulin of 18 can be told their insulin is normal while running at more than double what is considered metabolically optimal. That patient will struggle to lose weight, struggle to balance their hormones, and struggle to maintain energy — and be told by conventional medicine that nothing is wrong.
I pair fasting insulin with HbA1c — which reflects average blood sugar over approximately three months — and sometimes with a fasting glucose and a post-meal glucose reading when the clinical picture warrants it. Together, these markers tell the story of how well glucose metabolism is actually functioning — not just what's happening in a single fasting snapshot.
The HOMA-IR calculation — Homeostatic Model Assessment of Insulin Resistance — uses fasting insulin and fasting glucose together to produce a single number that quantifies insulin resistance. A HOMA-IR above 1.9 is generally considered to indicate early insulin resistance. Above 2.9, significant insulin resistance. This is a simple calculation from two standard lab values that most patients have never had performed or discussed with a provider.
What Drives It — And What Reverses It
Insulin resistance develops through the intersection of several factors that are increasingly common in modern life: excess body fat — particularly visceral fat — a diet high in processed carbohydrates and refined sugars, physical inactivity, chronic sleep deprivation, sustained psychological stress, and the cumulative effects of chronic low-grade inflammation.
The same factors appear in reverse when it comes to addressing it.
Resistance training is the most powerful insulin-sensitizing intervention available. Skeletal muscle is the primary site of glucose disposal in the body — meaning the more muscle you have and the more actively you use it, the more efficiently your body clears glucose from the bloodstream. A single resistance training session improves insulin sensitivity for 24 to 48 hours. Regular resistance training produces sustained improvements that compound over time. This is one of the reasons resistance training belongs at the center of every metabolic health plan, regardless of what medications or therapies are also being used.
Dietary modification — specifically reducing processed carbohydrates and refined sugars while increasing protein and fiber — reduces the glucose load that requires insulin management and allows insulin levels to fall between meals. This is not about eliminating carbohydrates entirely. It is about choosing carbohydrates that digest more slowly, paired with protein that buffers the glucose response. The practical version of this is what we've discussed in earlier posts: protein first at every meal, complex carbohydrates over simple ones, and consistent meal timing that allows meaningful insulin recovery windows between eating.
Sleep — inadequate sleep directly worsens insulin sensitivity, as we covered in the sleep post. One week of poor sleep produces measurable reductions in insulin sensitivity in otherwise healthy adults. Addressing insulin resistance while continuing to sleep poorly is fighting uphill in a meaningful way.
Stress management and cortisol reduction matter because chronically elevated cortisol directly raises blood glucose and suppresses insulin sensitivity. The cortisol-insulin connection is bidirectional — each drives the other in a cycle that's difficult to break from either end alone.
GLP-1 medications — semaglutide, tirzepatide, and retatrutide — improve insulin sensitivity as part of their mechanism of action, alongside the appetite suppression they're primarily known for. For patients with significant insulin resistance who haven't responded adequately to lifestyle modifications alone, these medications can meaningfully shift the metabolic picture while other interventions are built up. They work best as part of a comprehensive approach rather than as a standalone solution.
What We Look For at NOVA
Fasting insulin and HbA1c are on every initial comprehensive panel we run. They are not optional additions or advanced testing. They are foundational markers that belong in every evaluation of metabolic health — full stop.
When fasting insulin is elevated, we don't just note it and move on. We look at how it connects to the rest of the picture: the patient's body composition, their sleep, their stress burden, their hormone levels, their inflammatory markers. Insulin resistance is almost never an isolated finding. It is part of a pattern — and addressing it requires looking at the full pattern, not just the number.
If you've been working hard on your health and not getting the results your effort deserves — this is one of the first places I look. It is often the answer that was missing.
Book a free 30-minute consultation at novawellnessut.com or call and text us at (801) 449-1402. We draw labs right here in the office — no separate lab visit required.
Matt Nelson, NP
NOVA Wellness — Orem, Utah
(801) 449-1402 · novawellnessut.com
