Delta-sleep-inducing peptide (DSIP): an update.
Graf. M V MV; Kastin. A J AJ
Key Findings
- DSIP reliably induces or supports sleep in animal studies.
- It has been investigated as a potential treatment for insomnia, pain relief, and withdrawal symptoms.
- Immunohistochemical work shows DSIP‑like material is naturally present in various tissues, hinting at broader physiological roles.
- A possible mechanism may involve modulation of adrenergic (adrenaline) transmission, but this is not yet proven.
Practical Outcomes
- For biohackers, DSIP is an interesting experimental sleep aid, but the literature offers no clear dosing guidelines or safety data. It may be worth monitoring future studies, but current evidence is insufficient to recommend a concrete protocol.
Summary
Delta‑sleep‑inducing peptide (DSIP) is a small protein that has been shown to help animals fall asleep and has been studied for possible use in treating insomnia, pain and drug‑withdrawal symptoms. Researchers have also found DSIP‑like material naturally in the body and think it might affect the adrenaline system, but the exact way it works is still unclear.
Abstract
The isolation and characterization of delta-sleep-inducing peptide (DSIP) achieved from 1963 to 1977 were reviewed in 1984. The first reports describing sleep as well as extra-sleep effects of DSIP also were included in that work. Only two years later, much additional literature concerning DSIP has accumulated. Besides further sleep-inducing and/or -supporting effects of DSIP in animals, considerable work has been carried out to evaluate the potential use of the peptide for therapeutic purposes such as treatment of insomnia, pain, and withdrawal. Immunohistochemical as well as radioimmunochemical studies provided further insights into the natural occurrence of the nonpeptide and the distribution of DSIP-like material in the body, suggesting possible relations of the peptide to certain diseases. Various physiological functions of DSIP and a possible mechanism of action involving the modulation of adrenergic transmission remain to be established.
Study Information
pubmed
1986
1986-11-01T00:00:00.000Z
10.1016/0196-9781(86)90148-8
100
162