New Findings on Impacts of Anxiety and Insomnia on Immune Function
A recent cohort study found lower circulating natural killer (NK) cell counts and altered NK subtypes in young female students reporting anxiety, suggesting short-term impairment of frontline innate immunity.
In 60 female students aged 17–23, investigators measured absolute NK concentrations and subtype proportions. Participants with anxiety symptoms—particularly those with moderate to severe symptoms—had reduced total NK counts and declines in key circulating NK subgroups.
Lower NK numbers can blunt rapid cytotoxic responses that contain infected or transformed cells, increasing short-term vulnerability to viral spread and weakening tumor surveillance. Acute sympathetic activation and elevated catecholamines suppress NK cytotoxicity and trafficking, while shifts in cytokines (for example, IL-6, IL-10, and interferon pathways) can reprogram innate responses away from effective NK-mediated clearance. Disrupted sleep and altered nocturnal melatonin and cortisol rhythms further reduce NK counts and blunt functional responsiveness.
Within the cohort, participants reporting insomnia showed significantly lower NK measures across total circulating counts and the proportions of CD16+CD56dim and CD16+CD56high subgroups. Blood assays quantified both absolute NK cells per microliter and percentage distribution of primary NK subpopulations, enabling detection of numeric deficits and subgroup-balance changes that can modify overall cytotoxic potential.
These measurable changes are therefore plausibly linked to greater susceptibility to common viral—and in some contexts, bacterial— infections, given NK cells’ role in early containment and in shaping downstream adaptive responses.
Key Takeaways:
- Anxiety and insomnia correlated with lower circulating NK cells and altered NK subtypes in young female students.
- Mechanisms likely include sympathetic activation, cytokine shifts, and sleep-linked hormonal disruption that together impair NK-mediated early defenses.