The metabolic root that connects almost everything.

There’s a thread that runs through almost every chronic condition I see in clinical practice, and it took me longer than I’d like to admit to fully appreciate how central it is.

Insulin resistance.

It shows up in the woman with Hashimoto’s whose thyroid medication isn’t making her feel better. It shows up in the man with declining testosterone who’s been told his levels are “normal for his age.” It shows up in the person with stubborn weight gain, the person with worsening anxiety, the person whose inflammatory markers are quietly elevated while everyone tells them they look fine. It shows up in the people I wrote about in “But They Were So Healthy”—the ones who look great from the outside while their labs tell a completely different story.

Insulin resistance isn’t a diagnosis most people receive. It’s not on the standard lab panel. It’s not something most providers check for unless the situation has already progressed to prediabetes or type 2 diabetes—by which point the dysfunction has been running for years, sometimes decades, doing damage the entire time.

That’s the gap I want to address in this post: what insulin resistance actually is, why the system misses it, what it connects to, and what you can do about it. In plain English; no biochemistry degree required.

What Insulin Resistance Actually Is

The simplest way I can explain it: insulin resistance is what happens when the cells in your body stop responding efficiently to insulin.

Insulin is a hormone produced by the pancreas. Its primary job is to shuttle glucose—blood sugar—out of the bloodstream and into cells, where it’s used for energy. Under normal conditions, you eat something, your blood sugar rises, the pancreas releases insulin, insulin tells the cells to open up and accept the glucose, and blood sugar comes back down. It’s an elegant system.

When insulin resistance develops, the cells become less responsive to that signal. Insulin shows up at the door, knocks, and the cells take longer to answer—or don’t answer at all. The pancreas responds the only way it knows how: by producing more insulin. Louder knocking. More force. For a while, this compensatory mechanism works—blood sugar stays in the normal range because the pancreas is overproducing insulin to compensate for the cells’ reduced sensitivity.

This is the critical window that conventional screening almost always misses. Because blood sugar looks “normal” on a standard lab panel, everything appears fine. Nobody checks the insulin level—the signal that’s being overproduced behind the scenes to maintain that normal blood sugar. It’s like checking whether the car is moving and concluding the engine is fine, without noticing that the engine is redlining to maintain a speed it used to handle effortlessly.

By the time fasting glucose starts to creep up—the marker that actually gets flagged on standard labs—the insulin resistance has typically been present for years—sometimes a decade or more. That’s years of elevated insulin quietly driving inflammation, hormonal disruption, fat storage, and metabolic dysfunction without anyone knowing.

Why the Standard Panel Misses It

This is the part that frustrates me, because the test exists. Fasting insulin is a simple, inexpensive blood test. It tells you how hard the pancreas is working to maintain blood sugar control—and when that number is elevated, it’s one of the earliest signals that metabolic dysfunction is developing.

The standard metabolic panel measures fasting glucose. Glucose is the last thing to go. Insulin rises years before glucose does. By the time your fasting glucose is flagged as “high,” you’ve been insulin resistant for a long time.

It’s not that providers don’t care. The system wasn’t built for this kind of early detection. The standard panel was designed around a model of care that catches disease after it’s developed, not metabolic dysfunction before it has a name. Fasting insulin isn’t part of the standard order because the standard of care doesn’t require it. The infrastructure wasn’t built to ask the question, so the question doesn’t get asked.

If you take nothing else from this post, take this: ask for a fasting insulin level the next time you get bloodwork done. It’s inexpensive, it’s widely available, and it gives you information about your metabolic trajectory that fasting glucose alone simply cannot provide. Pair it with the other markers I’ve written about before—hsCRP, a full thyroid panel, lipid panel with context—and you have a picture that’s dramatically more complete than what the standard panel offers.

What Insulin Resistance Connects To

This is where the scope of the problem comes into focus, and honestly, it’s staggering once you start mapping the connections.

Weight gain and inability to lose weight. Insulin is a storage hormone. When insulin levels are chronically elevated, the body is getting a persistent signal to store energy as fat and to resist releasing stored fat for fuel. This is why so many people hit a wall with weight loss despite doing “everything right”—they’re exercising, they’re watching what they eat, and the scale won’t budge. The hormonal environment created by insulin resistance makes fat loss physiologically difficult, regardless of effort or willpower.

Hormonal disruption. Insulin resistance drives aromatase activity, converting testosterone to estrogen in men. In women, it disrupts the balance between estrogen and progesterone, worsens menopausal symptoms, and can contribute to PCOS. Thyroid function is affected indirectly—elevated insulin promotes inflammation and shifts the hormonal milieu in ways that compromise thyroid signaling.

Inflammation. Insulin resistance and chronic inflammation have a bidirectional relationship—each drives the other. Elevated insulin promotes the production of pro-inflammatory cytokines. Chronic inflammation, in turn, worsens insulin sensitivity at the cellular level. This loop is one of the reasons why metabolic dysfunction, once established, tends to deepen rather than self-correct without intervention.

Mental health. The brain is profoundly affected by insulin resistance. When brain cells can’t efficiently utilize glucose—their primary fuel source—cognitive function, mood, and emotional regulation all suffer. The research linking insulin resistance to depression, anxiety, and even more severe psychiatric conditions is growing rapidly. In my clinical experience, improving insulin sensitivity is one of the most reliable paths to improved mood and cognitive clarity.

Cardiovascular risk. Elevated insulin promotes endothelial dysfunction, increases triglycerides, shifts LDL particle size toward the small-dense pattern that’s actually dangerous, and drives hypertension through sodium retention and vascular smooth muscle growth. The cardiovascular risk attributed to cholesterol is, in many cases, more accurately attributed to the metabolic dysfunction underneath it.

Immune function. Insulin resistance impairs the immune system’s ability to respond to threats effectively—contributing to the terrain problem that makes some people more susceptible to infections and slower to recover.

Gut health. The insulin-inflammation loop affects the gut microbiome, promotes bacterial overgrowth, and contributes to intestinal permeability—which in turn drives further immune activation and autoimmune reactivity.

The point isn’t to be overwhelming—it’s to illustrate that insulin resistance isn’t a standalone metabolic issue. It’s a root-level dysfunction that expresses itself differently in different people depending on their genetics, their sex, their stress load, and their individual vulnerabilities. The women warriors in my practice tend to express it through thyroid and autoimmune pathways. The men tend to express it through cardiovascular and hormonal pathways. The downstream expression varies; the upstream driver is often the same.

What Drives Insulin Resistance

The factors that drive insulin resistance won’t surprise you if you’ve been following this blog; they’re the same factors that drive almost everything else we talk about here.

The standard American diet is the primary driver. Chronically elevated blood sugar from refined carbohydrates, added sugars, and ultra-processed foods forces the pancreas to produce more and more insulin over time. The cells adapt to the constant signal by becoming less responsive to it—the same way you stop noticing a sound that plays continuously in the background. Seed oils add to the problem by promoting cellular inflammation that further impairs insulin signaling.

Physical inactivity reduces the number of insulin receptors on muscle cells and decreases the body’s ability to utilize glucose without insulin assistance. Muscle is the largest glucose sink in the body; when it’s not being used, that sink shrinks.

Chronic stress elevates cortisol, which directly raises blood sugar and opposes insulin’s effects. The stress loop that I see in so many of my clients drives insulin resistance even when the diet is reasonable.

Poor sleep disrupts glucose regulation and insulin sensitivity measurably, even in a single night. Chronic sleep deprivation compounds the effect, creating a sustained state of metabolic compromise.

Environmental factors include endocrine disruptors—phthalates, BPA, pesticide residues—that interfere with insulin signaling at the cellular level. The modern environment delivers these exposures constantly, and their cumulative effect on metabolic function is real.

What I See When People Reverse It

This is the part that gets me out of bed in the morning—because functional insulin resistance is exactly that: functional. It’s a response to an environment. Change the environment, and the cells start responding again.

When someone moves from a processed, high-carbohydrate diet to a well-formulated ketogenic or carnivore approach, insulin levels start dropping. Sometimes quickly, sometimes gradually, but the direction is consistent. As insulin comes down, the downstream effects begin to unwind—fat loss becomes possible again, hormones start to recalibrate, inflammation decreases, mental clarity returns, energy stabilizes.

The healing phase is real. The timeline varies. What I’ve seen across hundreds of people is that the body is remarkably responsive once the input changes—once the chronic demand for insulin production stops, the cells begin to resensitize. It’s not a linear process, and there are bumps along the way, but the trajectory is consistent enough that I’m comfortable saying this: for the vast majority of people with functional insulin resistance, dietary and lifestyle change is the most powerful intervention available.

That’s not a dismissal of medication for people who need it. Metformin has a place. GLP-1 agonists have a place. But they work best when they’re supporting a foundation of dietary and lifestyle change, not substituting for it. The medication manages the number; the lifestyle change addresses the driver. Both can coexist; only one addresses the root.

Starting the Investigation

If anything in this post resonated—if you’ve been struggling with symptoms that don’t seem to have a clear explanation, or if you’ve been told you’re “fine” based on a standard lab panel that never checked the most informative marker—here’s where I’d start:

Ask for a fasting insulin test. It’s inexpensive, widely available, and it gives you a window into your metabolic health that fasting glucose alone cannot provide. A fasting insulin above 5–7 µIU/mL in someone who’s metabolically optimized is worth investigating further. The conventional “normal” range goes much higher than that—because the reference range is based on a population that is increasingly insulin resistant.

Track the proxy markers I outlined in “But They Were So Healthy”—energy patterns, sleep quality, digestion, skin health, recovery, mood and cognitive clarity, body composition in context. These daily signals give you continuous information about your metabolic state without waiting for a lab order.

Consider your dietary foundation. The single most impactful intervention for insulin resistance is reducing the demand for insulin production—and the most effective way to do that is to reduce the dietary inputs that drive insulin secretion. Carbohydrate restriction, in its various forms, is the most direct path.

Move your body. Muscle contraction activates glucose uptake pathways that work independently of insulin. Regular movement—particularly resistance training—increases insulin sensitivity directly, at the cellular level.

Prioritize sleep and stress management. Both affect insulin sensitivity measurably and are often the first places to look when the dietary foundation is solid but the numbers aren’t moving as expected.

All That to Say—

Insulin resistance is the metabolic root that connects more dots than almost any other single factor in chronic disease. It’s also one of the most reversible—when it’s caught early enough and addressed with the right interventions.

The problem isn’t that it’s hard to fix. The problem is that it’s hard to find—because the system that screens for it was designed to catch the house fire, not the electrical short that’s been sparking in the walls for a decade. By the time the fire is visible, the damage is extensive. The short was detectable the whole time; nobody had the right instrument pointed at the right wall.

You deserve to know what’s happening in your body before it becomes a diagnosis. The tools to investigate are simple, accessible, and informative. The foundational changes that address insulin resistance are the same ones that improve virtually every other marker in metabolic health. The body wants to be insulin sensitive; it just needs the environment to make that possible.

I hope this gives someone the language and the framework to start asking better questions—of their providers, of the research, and of themselves.

Rance Edwards is a National Board Certified Health and Wellness Coach (NBC-HWC) with over 2,000 clinical hours of experience, specializing in chronic disease management and lifestyle medicine.

If you’ve been told you’re “fine” but something feels off—or if insulin resistance is already on your radar and you want a partner who understands the metabolic picture—I’d love to talk. Book a free discovery call—no pressure, just a conversation about where you are and what the next step might look like.

Sources

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  • Schulte, D.M., et al. (2013). Caloric restriction increases serum testosterone concentrations in obese male subjects by two distinct mechanisms. Hormone and Metabolic Research, 46(4), 283–286. DOI: 10.1055/s-0033-1358678
  • Shin, J., & Choi, J.Y. (2021). The risk of incident type 2 diabetes in statin users: a meta-analysis. Cardiovascular Drugs and Therapy, 36, 969–978. DOI: 10.1007/s40256-021-00516-3
  • Aquilani, R., et al. (2023). Several dementia subtypes and mild cognitive impairment share brain reduction of neurotransmitter precursor amino acids. Frontiers in Aging Neuroscience, 15, 1237469. DOI: 10.3389/fnagi.2023.1237469