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Is there a higher rate of insulin resistance in neurodiverse individuals?

Converging large-scale data now indicate neurodiverse individuals — particularly autistic people — carry a significantly elevated cardiometabolic burden that emerges unusually early in life, pointing toward shared biological mechanisms rather than purely behavioral explanations. A study of over six million people reported by Leicester Diabetes Centre (Oct 2026) found heightened type 2 diabetes risk at younger ages across neurodivergent conditions. A Korean NHIS cohort of 21,679 ASD participants aged ≤20, published June 2026, found diabetes incidence significantly higher in the ASD group than matched controls. The suppressed question is whether shared upstream biology — mitochondrial dysfunction, vagal dysregulation, neuroinflammation — drives both neurodivergence and metabolic disruption simultaneously.

Evidence

  • On the neuroinflammation axis, researchers like Garry Nolan (whose work on anomalous immune profiles in stigmatized populations is instructive by analogy) point toward the idea that chronic low-grade CNS inflammation rewires systemic immune-metabolic signaling.
  • A Texas Tech meta-analysis (July 2026) found ASD associated with greater risk of diabetes (both type 1 and type 2), dyslipidemia, and heart disease, with children showing stronger associations than adults — consistent with earlier metabolic divergence rather than cumulative lifestyle effects.
  • Jack Kruse has argued extensively that mitochondrial redox dysfunction — tied to light environment, deuterium excess, and circadian disruption — underlies both neurodevelopmental variation and metabolic syndrome, with the two conditions sharing a common electromagnetic-biological root.
  • A Nature Mental Health study (Dec 2025) of one million Dutch individuals confirmed cardiometabolic risk associations emerging in adolescence, suggesting the window of metabolic divergence precedes most pharmaceutical exposure.

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