⬡ Core speculation
Glycine deficiency → NMDA receptor hypofunction in the prefrontal cortex compromises executive braking over the amygdala. The window between emotional trigger and reactive impulse narrows, increasing vulnerability to self-harm, reckless behaviour, and sudden relationship ruptures.
🧠 Neuroanatomical refinement
The “pause” depends on the prefrontal–amygdala circuit. Glycine deficiency impairs NMDA receptors on inhibitory interneurons in the mPFC, reducing top‑down control. Concurrently, compensatory glutamate release creates metabolic noise, further narrowing the impulse window.
⚠️ Clinical caveat — this is not likely a simple dietary deficiency. In most cases, it may reflect NMDA receptor resistance, elevated kynurenic acid (glycine‑site blocker), or chronic cortisol‑induced mPFC changes. Even with normal glycine, the system may be dysfunctional.
⟡ In short — the proposed mechanism is biologically plausible: NMDA hypofunction in the PFC shortens the impulse‑pause and biases the brain toward reactive, all‑or‑none responses. However, the root cause is likely systemic (receptor dysfunction, metabolic stress, trauma) rather than isolated glycine lack.