The observation, stated once
Hypermobility is found substantially more often in autistic and ADHD populations than in matched controls, across several independent samples.
Through the mechanism
Proprioception depends on receptors embedded in ligament and joint capsule. Where that tissue is more compliant, end-range feedback arrives later and weaker, so the brain's map of where the limbs are is genuinely blurrier.
Sensory filtering and interoception are the same integrative machinery. A body sending late, noisy positional data and unreliable internal signals gives that machinery a harder job from early development.
This is why the practical consequences look alike from both directions: clumsiness at end range, difficulty judging effort, delayed recognition of fatigue or a full bladder, and a strong preference for deep pressure and predictable input.
Autonomic involvement joins from the tissue side rather than the neurological one, which is why orthostatic symptoms belong in a neurodivergence workup at all.
What it changes in practice
- Motor-control and proprioceptive work matters more here than flexibility work, which is often the opposite of what has already been prescribed.
- Pacing taught from external data rather than from felt effort.
- Screen for orthostatic intolerance rather than attributing lightheadedness to anxiety.
Hold this loosely
The association is consistently observed; the causal mechanism is a well-argued hypothesis, not established fact.