Geographic Disparities in Stroke Action Awareness in China: A National Survey.

While atopic dermatitis (AD) has been linked to individual psychiatric disorders, the cumulative contribution of psychiatric multimorbidity to incident AD has been insufficiently characterized. This study shows that psychiatric disorder-related traits, especially co-occurring conditions and higher weighted psychiatric burden, are associated with increased long-term AD risk. Serum vitamin D modified these associations, but the finding should not be interpreted as proof that supplementation prevents AD. Metabolomic mediation was statistically significant but modest, and the prioritized plasma proteins likely reflect shared inflammatory activity rather than AD-specific biomarkers. Psychiatric disorders occupy a prominent share of the global disease landscape, accounting for 17.2% of total years lived with disability worldwide in 2021. Among them, depression and anxiety disorder stand out – not only for their disabling nature but also for their tendency to co-occur with each other (, ). Beyond psychological suffering, individuals with psychiatric disorders often contend with physical comorbidities, particularly skin diseases such as atopic dermatitis (AD), which are far more common in this population than in the general public (). The brain and the skin are tightly linked by neuro-immunological pathways. Studies have shown that psychiatric disorders disrupt this balance, enhancing sympathetic nervous system activity while dampening parasympathetic tone – an imbalance that can ignite inflammatory cascades in the skin (–). The result is a chronic, proinflammatory cutaneous state, which may erode the skin’s barrier function and set the stage for AD (). Although the concept of the brain–skin axis is well established, most longitudinal studies and many Mendelian randomization (MR) analyses have emphasized the direction from AD to later depression, anxiety disorder or other psychiatric outcomes (, ). Recent genetic studies have begun to evaluate the reverse direction and suggest that liability to selected neuropsychiatric disorders may also contribute to AD or eczema risk, although the effect sizes are generally modest and phenotype-specific (). What remains insufficiently defined is the long-term dermatological consequence of cumulative psychiatric burden within the same individual. This gap is clinically important because psychiatric conditions rarely occur in isolation; they cluster through shared genetic, neurobiological, behavioural and inflammatory pathways (). Failing to account for psychiatric multimorbidity may therefore underestimate the combined burden relevant to AD risk stratification. A weighted composite score offers a more nuanced way to quantify the cumulative psychiatric load that may contribute to AD susceptibility. In addition, psychiatric conditions often have a biological footprint marked by proinflammatory cytokines, innate immune activation, metabolic disturbance and altered neuroendocrine signalling. These shared mechanisms raise the possibility that circulating biomarkers may help explain, but not fully determine, the association between psychiatric burden and AD (–).