Skip to content
All life stages
Life stage

Chronic insomnia

Difficulty falling or staying asleep most nights for ≥3 months — distinct from occasional sleep disruption. Affects 10–15% of adults.

What changes during this transition

Chronic insomnia is a diagnosis, not just "sleeping badly" — the first-line care path is cognitive behavioral therapy for insomnia (CBT-I), which outperforms every pharmacological option for long-term outcomes. Peptides relevant here cluster around two distinct mechanisms: direct sleep-architecture work (DSIP from the Italian 1980s clinical tradition — registered abroad for sleep disorders; epithalon via the pineal/melatonin axis) and slow-wave-sleep enhancement via GH-axis amplification (CJC-1295, MK-677 — well-documented EEG-level effect on SWS but SWS-enhancement is NOT the same as treating insomnia; sleep onset and maintenance metrics aren't reliably moved). Selank addresses the anxiety component when insomnia is anxiety-driven — distinct mechanism from the GH-axis or pineal entries. None of these substitute for CBT-I or for proper workup of sleep apnea, restless legs, depression, or thyroid dysfunction.

Important caveat

Rule out medical causes first: sleep apnea (consider an at-home sleep study if you snore, wake gasping, or have AM headaches), depression, thyroid dysfunction (TSH + free T4), restless legs, caffeine/alcohol patterns, and prescription medications (stimulants, steroids, SSRIs). GH-axis peptides are CONTRAINDICATED in insulin resistance — chronic GH stimulation worsens fasting glucose. Sex-differential matters: SWS-enhancement is more reliable in elderly men than in women.

Peptides editorially relevant to chronic insomnia

5 peptides from the library — each evidence-tiered honestly.

Want this list to grow? The library is editorial — if there’s a peptide you think belongs on this page with documented or mechanistically-clear evidence, send us a note with the citation and we’ll review it under the same evidence-tier discipline as every other entry.