Insulin Resistance

Insulin resistance is the physiological state in which insulin-responsive tissues — muscle, liver, and adipose — respond less to a given concentration of insulin than they did before. The pancreas compensates by producing more insulin to achieve the same glucose-lowering effect. Over time, this compensation can fail, and the blood-glucose control the body previously maintained breaks down.

The progression

1. Early resistance: normal fasting glucose, elevated fasting insulin. Subclinical; often undetected unless an insulin level is specifically measured.
2. Pre-diabetes: fasting glucose 100–125 mg/dL, HbA1c 5.7–6.4%. Post-meal glucose excursions elevated.
3. Type 2 diabetes: fasting glucose ≥ 126 mg/dL, HbA1c ≥ 6.5%, or 2-hour OGTT glucose ≥ 200. Pancreatic compensation failing.

Mechanisms

• Muscle — GLUT4 translocation to the cell membrane is impaired; less glucose enters muscle per unit of insulin signalling.
• Liver — hepatic insulin resistance means the liver continues gluconeogenesis even in the presence of insulin, contributing to elevated fasting glucose.
• Adipose tissue — reduced suppression of lipolysis, elevated circulating free fatty acids, which themselves worsen insulin resistance (a vicious cycle).
• Inflammation — chronic low-grade inflammation in adipose tissue produces cytokines (TNF-α, IL-6) that interfere with insulin-receptor signalling.

Drivers

• Visceral fat accumulation. The strongest modifiable driver. Subcutaneous fat is far less metabolically damaging at the same mass.
• Chronic caloric surplus, especially with persistent carbohydrate loading and low training volume.
• Sedentary behaviour. Independent of total exercise, sitting time associates with worse sensitivity.
• Sleep deprivation. A single night of short sleep reduces sensitivity; chronic deprivation compounds.
• Genetics. Strong familial and ethnic component; South Asian, East Asian, and certain Indigenous populations develop resistance at lower body-mass thresholds.
• Certain medications. Long-term corticosteroids, some antipsychotics, some antiretrovirals.

Reversibility

In the early-to-moderate stages, insulin resistance is substantially reversible with:

• Weight loss — 5–10% of body weight often substantially normalises fasting glucose and insulin.
• Resistance training — improves muscle insulin sensitivity within weeks.
• Diet quality shift — Mediterranean, DASH, or whole-food plant-based patterns improve markers.
• Sleep optimisation — often underestimated; can produce measurable short-term improvement.

In established type 2 diabetes, reversibility is harder but still possible — the DiRECT trial (Lean et al. 2018) demonstrated meaningful T2D remission in roughly half of subjects via a structured, intensive dietary intervention.

Tracking implications

For consumer trackers without diagnosed dysglycemia, insulin resistance is typically a background concern rather than a tracked variable. CGM adoption has given some users an accessible window into their glucose-response patterns, which is a useful proxy. For anyone with actual metabolic-syndrome markers, tracking should happen in concert with a physician and a registered dietitian — calorie-tracking alone does not treat insulin resistance without the broader lifestyle intervention.