Counterargument
What if the dominant driver is structural, endocrine, or autoimmune?
Strictures, adhesions, untreated thyroid disease, adrenal insufficiency, and autoimmune enteropathies can produce HCM-pattern symptoms while being a different problem entirely.
Where it is valid
Any case with imaging findings, abnormal endocrine workup, or seropositive autoimmune disease that has not been adequately treated.
What it challenges
Applying HCM before standard structural / endocrine / autoimmune workup is complete.
Host Capacity Model response
HCM is explicitly out of scope for these primary drivers. Gate 1 is designed to surface them and decline engagement when they appear to dominate the picture. The framework can sometimes provide adjunctive systems-biology context after the primary driver is being managed clinically.
Unresolved questions
- Where does host-capacity context add value alongside well-managed primary disease?
Evidence that would resolve this
- Studies of adjunctive substrate-supportive context in patients with treated primary endocrine or autoimmune disease.