Abstract Introduction Asthma and allergies impair the quality of life of a substantial proportion of patients worldwide. Previous findings in clinical samples suggest that individuals with asthma and allergies have high frequency of insomnia symptoms. Many studies have shown that insomnia with short sleep duration phenotype (ISSD) is associated with cardiovascular and metabolic disorders The aim of this study is to investigate whether ISSD is associated with asthma or allergies in a large random general population sample. Methods A total of 1741 participants from a general random sample of the Penn State Adult Cohort (52.3% women, aged 48.79± 13.56) underwent 8- hour polysomnographic evaluation. Asthma and allergic status were defined by the participant’s response to “Have you ever had asthma or allergies?” or the use of medication. Insomnia was defined by the presence of complaint of insomnia lasting ≥ 1 year or by the presence of complaint of difficulty falling asleep, staying asleep, nonrestorative sleep, or early morning awakening. Normal sleepers were defined by the absence of insomnia. Objective short sleep duration (SSD) was defined as 6 hours’ sleep based on polysomnography. Binary logistic regression was performed while controlling for age, sex, race, BMI, mental health problems, education, smoking, alcohol consumption, caffeine use, apnea-hypopnea index and sampling weight. Results The prevalence of asthma/allergies was 27.7%. Compared to normal sleepers with normal sleep duration, only ISSD phenotype was associated with significant risk for asthma or allergies (OR=1.80, 95%CI=1.25-2.55, p=0.001). In contrast, neither the insomnia normal sleep duration (INSD) phenotype nor the normal sleepers SSD group were associated with increased risk for asthma/allergies. Conclusion These findings suggest that ISSD but not INSD phenotype is associated with asthma/ allergies further supporting that ISSD is the more severe biologic type of insomnia. Previous studies indicate that patients with asthma/allergy not treated with inhaled corticosteroids show attenuated hypothalamic–pituitary–adrenal (HPA) axis responsiveness and increased levels of pro-inflammatory cytokines. Similar HPA axis and inflammation alterations have been demonstrated in men with ISSD, suggesting a shared pathophysiological pathway underlying these two conditions. Support (if any)
Athanasiou et al. (Fri,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: