For most of human evolutionary history, calories were scarce and unpredictable. The ability to store fat efficiently during times of plenty was a survival advantage — the “thrifty genotype.” In 2026, those same genes are contributing to a global epidemic of obesity and type 2 diabetes.
The mismatch
Geneticist James Neel proposed in 1962 that genes promoting rapid fat storage and efficient glucose utilisation were selected for in environments of alternating feast and famine. These same genes, in an environment of constant caloric availability, cheap processed carbohydrates, and minimal physical activity, promote obesity and insulin resistance.
The human pancreas and insulin response evolved for a diet of tubers, lean meat, seasonal fruit, and occasional honey — not for continuous access to refined sugar and seed oils. Insulin resistance is not a failure of the metabolic system. It is a metabolic system doing exactly what it was designed to do, in conditions it was never designed for.
Why this matters beyond glucose
Chronic insulin resistance drives systemic inflammation, disrupts hormonal signalling (PCOS, endometriosis, and uterine fibroids all have insulin-related components), and contributes to autonomic nervous system dysregulation. The metabolic and musculoskeletal systems are not separate — chronic inflammation from metabolic dysfunction affects how connective tissue heals, how pain is processed, and how the nervous system functions.
What this means at OQ
OQ does not treat diabetes directly. But we regularly treat patients whose chronic pain, fatigue, and joint problems exist in the context of metabolic dysfunction. Understanding the inflammatory and neurological dimension of insulin resistance changes how we think about the whole person in front of us.
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