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Association versus causation in patient tissue
The finding that human PEO muscle has low NAD+ establishes an association. It does not, by itself, prove that NAD+ depletion causes the myopathy rather than being a consequence of it — degenerating, energy-starved muscle might lose NAD+ secondarily. The mouse
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- The finding that human PEO muscle has low NAD+ establishes an association. It does not, by itself, prove that NAD+ depletion causes the myopathy rather than being a consequence of it — degenerating, energy-starved muscle might lose NAD+ secondarily. The mouse intervention studies argue for a causal contribution because raising NAD+ improved function, but that causal chain has not been demonstrated with the same rigor in humans. In people, the usual tools for disentangling cause from consequence are limited here: a low patient count precludes the kind of statistical adjustment that might separate NAD+ depletion from the broader metabolic wreckage of failing muscle, and the redox coupling described earlier means an OXPHOS defect can lower the effective NAD+ pool directly, so a measured deficit is at least partly expected as a downstream signature of the disease rather than its origin. The honest reading is therefore that low NAD+ is a robust, reproducible correlate of mitochondrial myopa