What is insulin resistance, and why is it so often missed?

What's actually happening in the body with insulin resistance?

Insulin is the hormone made by the pancreas (the organ behind your stomach) that helps move sugar from your bloodstream into cells where it can be used for energy. In insulin resistance, cells stop responding well to that signal. To compensate, the pancreas produces more insulin to push sugar into cells anyway.

Elevated insulin has its own consequences. It promotes fat storage. It inhibits fat release. It contributes to inflammation. And eventually, the pancreas can't keep up with demand, blood sugar rises, and the diagnosis becomes prediabetes or type 2 diabetes.

How common is insulin resistance, and who has it?

Insulin resistance is far more common than most people realize. The age-standardized prevalence in nondiabetic US adults rose from 24.8% in 1999-2000 to 38.4% in 2017-2018, with hyperinsulinemia (elevated fasting insulin) now affecting roughly 41% of nondiabetic adults [PMID: 40364246]. The trajectory has been upward across all sociodemographic groups for decades.

It's more common with age, with abdominal weight, with family history of diabetes, and in certain ethnic groups (particularly Black, Hispanic, South Asian, and Native American populations). But it's also present in many people who don't fit any of those profiles.

What does the progression look like?

Insulin resistance progresses through recognizable stages, but slowly. Insulin starts rising while glucose stays normal. That phase can last 10 years or more. Then post-meal glucose starts spiking. Then fasting glucose creeps up, and the diagnosis becomes prediabetes (HbA1c 5.7 to 6.4% or fasting glucose 100 to 125 mg/dL) [Source: ADA 2024 Standards of Care, Classification and Diagnosis of Diabetes]. Eventually, if untreated, type 2 diabetes.

The earlier in this progression you catch it, the more reversible it is.

What labs actually pick it up early?

Several labs catch insulin resistance years before standard glucose testing would:

• Fasting insulin. This is the marker that changes first, often years before anything else. Most labs report a wide reference range (something like 2 to 25 µU/mL), but values around 10 or above are considered elevated in the research [PMID: 40364246]. Many precision physicians want this number on the lower end, not just inside the range
• HOMA-IR. A simple calculation that combines fasting insulin and fasting glucose into a single insulin sensitivity score. The lower, the better. Most insurance-based panels don't include this; you usually have to ask
• Triglyceride-to-HDL ratio. A useful clue from any standard lipid panel. Triglycerides are a type of blood fat; HDL is the so-called "good" cholesterol. When the ratio is elevated, insulin resistance is often the reason
• Continuous glucose monitor (CGM). A small wearable that shows exactly how blood sugar responds to food, sleep, exercise, and stress. Now available without a prescription [Source: FDA 510(k) clearance K234070, Dexcom Stelo 2024]. The patterns it reveals are often more informative than any single fasting blood draw
• Fasting glucose and HbA1c. These show up on most physicals. Fasting glucose is your blood sugar after an overnight fast; HbA1c is a 3-month average of your blood sugar. Both shift late in the progression. By the time they're abnormal, insulin resistance has been going on for years

What does insulin resistance actually look like?

Things that often accompany insulin resistance:

• Weight that creeps onto the midsection and won't come off
• Energy crashes after meals
• Sugar cravings
• Dark velvety patches of skin around the neck or armpits (a finding called acanthosis nigricans, often a visible sign of insulin resistance)
• Skin tags
• Irregular cycles or fertility issues in women
• Elevated liver enzymes on routine bloodwork that go unexplained
• Difficulty losing weight even with significant effort

Why does insulin resistance matter beyond weight?

Insulin resistance is the upstream driver of much of what shortens healthspan, the years of healthy, functional life. Type 2 diabetes is the obvious endpoint, but it's also a major contributor to cardiovascular disease, fatty liver, PCOS (polycystic ovary syndrome, a hormonal and metabolic condition affecting many women), certain cancers, and Alzheimer's disease. Researchers now sometimes refer to Alzheimer's as "type 3 diabetes" because brain insulin signaling looks similar to what happens in the body [PMID: 35269827].

Catching insulin resistance early changes a lot of long-term trajectories at once.

What actually reverses insulin resistance?

It's one of the most reversible chronic conditions in medicine when caught early. The interventions that consistently work:

• Strength training. Muscle is where most of the body's glucose ends up after a meal. Building muscle increases your capacity to handle carbohydrates and improves insulin sensitivity directly [PMID: 16394814], even when the muscle gain is modest. This is one of the highest-leverage things you can do
• Reducing refined carbohydrates and ultra-processed foods. Less work for the insulin system, more stable energy
• Sleep. Even a few nights of poor sleep can measurably worsen insulin sensitivity in healthy people. Chronic poor sleep is a slow drag on metabolism
• Time-restricted eating. Eating in a consistent window, often somewhere between 8 and 12 hours, gives the insulin system a daily rest
• Specific nutrients with research support. Magnesium, berberine (a plant compound used in traditional medicine), inositol (a vitamin-like compound, especially helpful for PCOS-related insulin resistance), and a few others
• Medications when appropriate. Metformin is the long-standing first-line option [Source: ADA 2024 Standards of Care]. GLP-1 medications work on a different mechanism and have changed what's possible for many patients with significant insulin resistance

What's the connection to PCOS?

Insulin resistance is the underlying driver of most cases of PCOS. The visible PCOS symptoms (acne, hirsutism meaning unwanted facial or body hair, weight resistance, irregular cycles) are largely downstream of insulin resistance. PCOS affects somewhere between 6 and 22% of women of reproductive age depending on which diagnostic criteria are used.

Treating the insulin resistance often resolves the visible PCOS features by addressing the upstream metabolic driver. This is why PCOS isn't just a reproductive condition; it's a metabolic condition with reproductive manifestations.

The deeper picture

Insulin resistance is rarely the only thing happening when it's present. It interacts with thyroid function, with cortisol (the body's main stress hormone), with sex hormones, with sleep, with inflammation. The lab numbers tell part of the story; how to act on them depends on the whole picture, and on the specific person.

The challenge with insulin resistance is that the standard screening focuses on glucose, which changes years after insulin resistance has started. The labs that catch it early are inexpensive, but most patients have to ask for them specifically. Extend's standard workup includes them as part of comprehensive metabolic assessment.