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Place · Level 3
腺苷 + SCN + HPA 三轴失调 · CBT-I A 级证据 · melatonin 是时钟信号不是安眠药· Z 药慎用
synergy · 3
Bidirectional: training improves sleep (Kredlow 2015 latency ↓13 min); sleep improves training adaptation (Mah 2011 Stanford basketball). Without sleep, training effects run at 50-70%.
Mg²⁺ plugs NMDA receptors and boosts GABA-A — insomnia + anxiety + cramps form a classic Mg-deficient triad.
Yamadera 2007 RCT: 3 g glycine pre-bed improved PSG metrics and morning freshness via peripheral vasodilation + core-temp drop.
antagonism · 1
When insomnia comes with sleep apnoea, hypnotics work against you: they relax upper-airway muscle and blunt the arousal response, making breathing events longer and deeper. The route here is CPAP, not a sleeping pill.
regulates · 11
The strongest comorbidity in psychiatry: insomnia independently predicts depression relapse; depression is the single strongest chronifier of insomnia. CBT-I alone improves mild-moderate depression; SSRIs alone don't always fix insomnia. Treat both.
Kredlow 2015 meta: sleep latency ↓13 min, TST ↑19 min, PSQI ↓0.31 SD. Comparable to CBT-I, exceeds melatonin. Morning training best; post-9pm high-intensity disrupts sleep.
Caffeine's half-life is 5-7 hours — half of your 3pm cup is still in you when you lie down. It doesn't have to keep you awake to count: it cuts deep sleep even when you do fall asleep. So 'I sleep fine after coffee' and 'that cup had no effect on me' are two different statements.
CBT-I is the A-level first line for chronic insomnia, not a sleep tip: stimulus control rebuilds the bed as a sleep cue, sleep restriction compresses fragmented sleep back into a block. Reaching for drugs first inverts the order.
One of insomnia's three axes is the clock: darkness triggers melatonin, morning light resets the phase. Melatonin here is a timing signal, not a sedative — and the commoner mistake is the hour, not the dose.
Perimenopausal insomnia is not psychological: allopregnanolone, a progesterone metabolite, is a GABA modulator, so the high-progesterone luteal phase was helping sleep. In this window progesterone swings hard, and all three patterns — onset, maintenance, early waking — become common.
↔Sleep Architecture & Sleep Debt
Sleep is not switching off but active, staged, ordered neural engineering: 4-6 cycles a night, deep sleep loaded into the first half, REM into the second. Seeing how the building goes up is what lets you see which floor insomnia fails on.
Insomnia is a top-3 migraine trigger; reverse — migraine night waking + chronic pain → insomnia. Co-occurrence ~50%. CBT-I has indirect evidence for migraine frequency reduction. Treating one often treats both.
The first month of a chronic-fatigue work-up is crossing off reversible causes one at a time, and insomnia is one of them: found, it goes to CBT-I rather than the tiredness being filed as the diagnosis.
←GERD
Nocturnal reflux is an easily missed physical cause of insomnia: lying flat makes regurgitation easier and heartburn pulls the sleeper out of light sleep. Here, treating the reflux first works better than treating the sleep.
The third axis is the HPA: chronically high cortisol makes sleep onset hard and sleep light. Ashwagandha is sold against exactly that axis, as an adjunct — any of the three axes (sleep pressure, clock, stress) can cause insomnia, so first work out which one.
contrast · 2
Two different channels, not to be treated as one: an all-nighter is acute sleep pressure and pays back; repeated all-nighters on top of trouble sleeping anyway is chronic insomnia, which goes down the CBT-I road.
Screens do two separate things — to eyes and to sleep — and blue-light marketing fuses them: eye strain is dry eye from blink rate dropping to a third plus sustained focusing effort, while evening screens act on melatonin timing. The first needs 20-20-20, the second needs light scheduling.