This paper proposes a single upstream mechanism linking artificial light at night (ALAN) to depression, allergic disease, breast cancer, and broad multimorbidity: collapse of circadian light-dark amplitude eliminates the melatonin-mediated nocturnal resetting cycle of mast cells. A self-sustaining feedback loop — in which mast cell-derived TNF-α suppresses both SCN clock gene expression and pineal AANAT, further reducing melatonin synthesis — explains chronification and treatment resistance. The paper further proposes that the cross-syndrome efficacy of SSRIs, tricyclics, mirtazapine, and SNRIs is explained by shared mast cell stabilization through off-target pathways, independent of serotonin reuptake inhibition. Eight falsifiable predictions are proposed.
Julian Vester (Fri,) studied this question.