If there is one concept that I wish every person aged 40-70 understood about their health, it is this: insulin resistance is not a diabetes problem. It is a hormonal problem. It is a metabolic problem. It is a brain problem. It is an inflammation problem. And it is almost certainly already affecting you — even if your doctor has never mentioned it, even if your blood sugar is "normal," and even if you have never been told you are at risk for diabetes.
Ben Bikman, PhD — one of the world's leading researchers on insulin resistance — has argued compellingly that insulin resistance is the common root cause of nearly every chronic disease of modern civilisation. I have been making this argument in clinical practice for 30 years. The research has finally caught up with what functional medicine physicians have been observing in patients for decades.
What Insulin Resistance Actually Is
Insulin is a hormone produced by the pancreas in response to rising blood glucose. Its primary job is to facilitate the uptake of glucose into cells — particularly muscle cells, liver cells, and fat cells — for energy production or storage. When cells become resistant to insulin's signal, the pancreas compensates by producing more insulin. For a period of time, this compensation maintains normal blood glucose levels. But the elevated insulin itself — hyperinsulinemia — is causing damage throughout the body long before blood glucose becomes abnormal.
This is the critical point that conventional medicine misses: the damage from insulin resistance is caused by elevated insulin, not by elevated glucose. By the time blood glucose rises above the "normal" threshold, the patient has typically had elevated insulin for 10-15 years. The hormonal damage has been accumulating for a decade before the conventional diagnostic criteria are met.
The Conventional Range Is Clinically Indefensible
The conventional reference range for fasting insulin is below 25 µIU/mL. In some laboratories, it is below 20 µIU/mL. These ranges were established by measuring fasting insulin in a population that is, by current estimates, 88% metabolically unhealthy. The range reflects what is statistically average in a sick population — not what is physiologically optimal.
My functional optimal target for fasting insulin is below 5 µIU/mL. This is the level associated with optimal insulin sensitivity, optimal hormonal function, and the lowest risk of metabolic and cardiovascular disease. A fasting insulin of 10 µIU/mL — which is "normal" by conventional standards — is already associated with measurable insulin resistance and significant hormonal disruption. A fasting insulin of 15 µIU/mL is causing substantial damage to the hormonal system, even though it is well within the conventional "normal" range.
How Insulin Resistance Disrupts Every Hormone System
The hormonal consequences of insulin resistance are pervasive and interconnected. Understanding these connections is essential to understanding why treating insulin resistance is not just about preventing diabetes — it is about restoring the entire hormonal network.
Estrogen and SHBG. Elevated insulin suppresses the production of sex hormone binding globulin (SHBG) in the liver. SHBG is the protein that binds and transports sex hormones in the bloodstream, keeping them in an inactive, bound form until they are needed. When SHBG is suppressed, more estrogen circulates in its free, biologically active form — driving estrogen dominance. Simultaneously, elevated insulin drives the enzyme aromatase in adipose tissue, converting androgens into estrogen and further amplifying the estrogenic burden. This is why insulin resistance is the primary metabolic driver of estrogen dominance in women aged 35-55.
Testosterone in Men. In men, elevated insulin suppresses testosterone production through multiple mechanisms: it reduces LH (luteinising hormone) production from the pituitary, it drives aromatase activity (converting testosterone to estrogen), and it impairs the Leydig cells in the testes that produce testosterone. A man with a fasting insulin of 15 µIU/mL will have measurably lower testosterone than the same man with a fasting insulin of 4 µIU/mL — regardless of what his total testosterone number shows on a lab report.
Thyroid Conversion. Insulin resistance impairs the conversion of inactive T4 to active T3 in the liver and peripheral tissues. This is one of the most important and least discussed connections in hormonal medicine. A patient with insulin resistance will have suboptimal Free T3 levels even if their TSH and T4 are normal — because the metabolic machinery required for T4-to-T3 conversion is impaired by the insulin-resistant state. Treating insulin resistance consistently improves thyroid conversion and reduces hypothyroid symptoms in patients who have been told their thyroid is "fine."
Cortisol and the HPA Axis. Insulin resistance and cortisol dysregulation are mutually reinforcing. Elevated cortisol drives insulin resistance by stimulating gluconeogenesis (glucose production in the liver) and reducing insulin sensitivity in peripheral tissues. Insulin resistance, in turn, activates the HPA axis and elevates cortisol. This creates a vicious cycle that is one of the most common and most difficult hormonal patterns to break — and one of the most important to address.
Progesterone. Insulin resistance reduces progesterone synthesis through multiple pathways: it impairs the function of the corpus luteum (the ovarian structure that produces progesterone after ovulation), it drives the pregnenolone steal (diverting the progesterone precursor toward cortisol production), and it disrupts the LH surge that triggers ovulation. Without ovulation, there is no corpus luteum and no progesterone. This is why insulin resistance is the primary driver of PCOS — a condition characterised by anovulation, androgen excess, and progesterone deficiency.
The Markers That Actually Matter
A complete metabolic assessment for insulin resistance includes fasting insulin (the most important single marker — should be below 5 µIU/mL), fasting glucose (target 75-85 mg/dL, not just "below 100"), HbA1c (target below 5.3%, not just "below 5.7%"), HOMA-IR (calculated from fasting insulin and glucose — target below 1.0), triglycerides (target below 80 mg/dL — the most sensitive early marker of insulin resistance), HDL cholesterol (target above 60 mg/dL in women, above 50 mg/dL in men — low HDL is a reliable marker of insulin resistance), and the triglyceride-to-HDL ratio (target below 1.5 — one of the most powerful predictors of insulin resistance and cardiovascular risk).
The LCHPMF Protocol for Insulin Resistance
The most powerful intervention for insulin resistance is not a medication. It is the LCHPMF nutritional framework, combined with targeted exercise and evidence-based supplementation.
The dietary foundation reduces refined carbohydrates to 50-100g per day from whole-food sources, eliminates seed oils entirely (canola, soybean, corn, sunflower, safflower — the most inflammatory fats in the modern diet), and anchors every meal in protein (1g per pound of ideal body weight daily). This combination reduces insulin secretion, improves insulin sensitivity, and reduces the inflammatory load that drives insulin resistance.
Exercise is the most powerful insulin sensitiser available. Resistance training — lifting weights — is more effective than any other form of exercise for improving insulin sensitivity, because muscle tissue is the primary site of glucose disposal. Three sessions of resistance training per week, combined with 150 minutes of Zone 2 cardio (a pace at which you can hold a conversation), produces dramatic improvements in fasting insulin within 8-12 weeks. Post-meal walks of 10 minutes reduce the postprandial glucose spike by approximately 30% — a simple, powerful intervention that requires no equipment.
The targeted supplement protocol for insulin resistance includes berberine (500mg three times daily with meals — as effective as metformin in multiple clinical trials for reducing fasting glucose, HbA1c, and triglycerides), chromium picolinate (400mcg daily — enhances insulin receptor sensitivity), alpha-lipoic acid (600mg daily — improves insulin sensitivity and reduces oxidative stress), and inositol (2g myo-inositol plus 200mg d-chiro-inositol daily — particularly effective for PCOS-driven insulin resistance).
The Timeline
Patients who implement the LCHPMF framework with consistent resistance training and the targeted supplement protocol typically see fasting insulin drop from 15-20 µIU/mL to below 5 µIU/mL within 90-120 days. The hormonal consequences follow: estrogen dominance symptoms reduce, testosterone improves in men, thyroid conversion improves, progesterone production normalises, and the HPA axis begins to recover. These are not theoretical outcomes — they are what I observe in clinical practice, consistently, in patients who commit to the protocol.
Insulin resistance is not a life sentence. It is a metabolic pattern that responds predictably to targeted intervention. The question is not whether you can reverse it. The question is whether you are willing to implement the protocol that will.
— Dr. Jay Wrigley, NMD