Neuroendocrine dysregulation in primary insomnia.
Level 5 - mechanism / opinion, no new human data
Narrative review and mechanism-based model without detailed methodology or direct reporting of primary trial data.
What was done
The authors synthesized findings from their research and existing literature examining neuroendocrine alterations—specifically evening/nocturnal plasma cortisol and nocturnal melatonin levels—in patients with primary insomnia and healthy controls to propose a mechanistic model of hypothalamic-pituitary-adrenal (HPA) axis dysregulation.
What was found
Patients with primary insomnia showed increased evening and nocturnal plasma cortisol concentrations and, in long-lasting cases, decreased nocturnal plasma melatonin. Evening cortisol secretion positively correlated with nocturnal awakenings in both insomniacs and controls. The abstract reports directional findings and correlations but provides no numerical data, effect sizes, or p-values.
Why it matters
This paper frames primary insomnia as a state of neuroendocrine hyperarousal, linking elevated evening cortisol directly to sleep fragmentation and the maintenance of chronic sleep disturbance.
Limits
The abstract describes a narrative review and theoretical model without reporting sample sizes, participant demographics, control matching, assay timing protocols, or exact quantitative values.
Cited by
- partial Patients with sleep maintenance insomnia exhibit an abnormal spike in cortisol in the middle of the night that predicts awakenings.