The relationship between ω-3 and ω-6 fatty acids consumption and sleep disorders or duration are controversial. Therefore, we used the data of the National Health and Nutrition Examination Survey 2007–2016 in this cross-sectional study to explore their relationships. ω-3 and ω-6 fatty acids consumption was assessed using two 24 h dietary recall interviews. Sleep disorders and sleep duration were based on self-reported data. Logistic regression models and restricted cubic spline analyses were used. Compared with tertile one, the odds ratios (ORs) and 95% confidence intervals (CIs) of sleep disorders for the second tertile of ω-6 fatty acid intake and the highest tertile of ω-6:ω-3 ratio were 1.30 (1.04–1.62) and 1.36 (1.08–1.70), respectively. Inverse U-shaped and linear dose–response relationships were observed between dietary ω-6 fatty acid intake and ω-6:ω-3 ratio and sleep disorders, respectively. In addition, ω-3 fatty acid consumption was adversely related to sleep disorders in men and the OR (95% CI) was 0.68 (0.49–0.95). Compared with normal sleep duration, ω-3 fatty acid consumption was negatively related to very short, short, and long sleep duration risk. The relative risk ratios (RRRs) were 0.53 (0.35–0.81), 0.79 (0.67–0.93), and 0.81 (068–0.98), respectively. The RRR of very short sleep for ω-6 fatty acid consumption was 0.57 (0.45–0.73). Our study indicates that ω-6 fatty acid consumption and the ω-6:ω-3 ratio are positively associated with the risk of sleep disorders, while the negative association between ω-3 fatty acids and sleep disorders may exist only in men. Furthermore, ω-3 and ω-6 fatty acid consumption are negatively related to the risk of non-normal sleep duration.

Objective: This cross-sectional study aimed to explore the association between smoking cessation and depressive symptoms and investigate the mediating role of dietary quality. Methods: We used data from the 2007–2014 National Health and Nutrition Examination Survey. Logistic regression models were applied to evaluate the associations between smoking cessation and depressive symptoms. Stratified analysis was performed according to different HEI levels. We examined the mediating role of HEI in the relationship between depressive symptoms and cessation duration using the Karlson–Holm–Breen (KHB) method. Results: A total of 20,004 participants aged 20 years or older were included in the analyses. There were significant correlations between years for smoking cessation and depressive symptoms (OR: 0.985, 95% CI: 0.971~0.999) after adjusting for correlation covariables. A likelihood ratio test showed that there was an interaction between smoking cessation and diet quality (p = 0.047). In the mediation analysis, we estimated that the increase in HEI scores after quitting smoking could explain the 6.91% decline in depressive symptoms. Conclusion: In this cross-sectional study, smoking cessation showed a protective effect on depressive symptoms and that diet quality can influence and mediate this association.

The evidence on the relationship of pyridoxal 5′-phosphate (PLP) with sleep-related problems is limited and controversial. Notably, there is a lack of studies on the general population and studies of the dose–response relationship. Therefore, we conducted a cross-sectional study to examine the associations between serum PLP concentration and sleep-related problems (sleep quality and sleep duration) in adults, using the data of the National Health and Nutrition Examination Survey 2005–2010. High-performance liquid chromatography (HPLC) was used to test PLP in blood samples. Sleep quality and sleep duration were based on self-reported data, with sleep quality categorized as sleep disorder, trouble falling asleep, waking up during the night, and daytime sleepiness. The primary analyses utilized logistic regression models and restricted cubic spline. Compared with the first quartile (Q1), the odds ratios (ORs) and 95% confidence intervals (CIs) of daytime sleepiness for the Q2 and Q3 of serum PLP concentrations were 0.76 (0.59–0.99) and 0.78 (0.62–0.98), respectively. The relationship was only significant for males. Furthermore, a non-linear dose–response relationship was observed between serum PLP concentration and the risk of daytime sleepiness. Compared with the normal sleep duration group, serum PLP concentrations were negatively associated with the risks of very short, short, and long sleep duration, with relative risk ratios (RRRs) of 0.58 (0.43–0.81) (Q4), 0.71 (0.61–0.83) (Q4) and 0.62 (0.34–0.94) (Q3), respectively. The average serum PLP concentrations were higher in people with normal sleep duration, suggesting a non-linear dose–response relationship. Our study indicated that serum PLP concentrations were negatively associated with daytime sleepiness, and this association may only exist in males. Moreover, it was also inversely related to abnormal sleep duration (very short, short, long) compared to normal sleep duration.