A higher dietary diversity score (DDS) and a lower energy-adjusted dietary inflammatory index (E-DII) may be associated with lower risks of type 2 diabetes (T2D) and mortality. This cohort study aimed to investigate the associations of DDS and E-DII with all-cause mortality, incidence of T2D, and mortality of T2D, as well as the joint effects of these two dietary factors. A total of 181,360 participants without all types of diabetes at baseline from the UK Biobank and 42,139 participants from the US NHANES were included. Cox proportional hazards models were used to assess the associations of DDS and E-DII with outcomes. In the UK Biobank data, 8338 deaths, 3416 incident T2D cases, and 353 T2D deaths occurred during a median follow-up of 12.5 years. In the US NHANES data, 6803 all-cause deaths and 248 T2D-specific deaths were recorded during a median follow-up of 9.6 years. We observed that higher DDS and lower E-DII were significantly associated with lower risks of total mortality and incident T2D. Compared with low DDS, the hazard ratios (HRs) and 95% confidence intervals (CIs) of high DDS were 0.69 (0.64, 0.74) for all-cause mortality, 0.79 (0.70, 0.88) for incident T2D in the UK Biobank, and 0.69 (0.61, 0.78) for all-cause mortality in the US NHANES. Compared with participants in tertile 3 of E-DII, those in tertile 1 had a lower risk of overall death [HR 0.86 (95% CI: 0.81, 0.91) in UK Biobank; 0.83 (0.77, 0.88) in US NHANES] and incident T2D [0.86 (0.79, 0.94)] in UK Biobank. No evidence was observed of the interactive effects of DDS and E-DII on either all-cause mortality or the incidence and mortality of T2D. There was no significant association found between any exposure and T2D mortality in this study. In conclusion, our results revealed that higher DDS and lower E-DII were associated with both total mortality and incident T2D in UK and US adults.

Little is known about the independent and joint effects of the energy-adjusted dietary inflammatory index (E-DII) and dietary diversity score (DDS) on sarcopenia and its components (low muscle mass, low muscle strength, and low physical performance). A total of 155,669 UK Biobank participants with ≥1 (maximum 5) 24 h dietary assessments were included in this cross-sectional analysis. We used logistic regression models to investigate the associations of E-DII and DDS with sarcopenia and its three components. We further examined the joint effects of E-DII and DDS on sarcopenia and its components using additive and multiplicative interaction analyses. We observed that lower E-DII and higher DDS were associated with lower odds of sarcopenia and its components. There were significant joint associations of E-DII and DDS with sarcopenia and low physical performance (p-interaction < 0.05) on the multiplicative interactive scale. Our study suggests that lower dietary inflammatory potential and higher dietary diversity might be important protective factors against sarcopenia and its components. More cases of sarcopenia and low physical performance might be preventable by adherence to a more anti-inflammatory diet combined with a higher dietary diversity.

Some studies suggest an association between iron overload and cardiovascular diseases (CVDs). However, the relationship between dietary iron intake and atrial fibrillation (AF) remains uncertain, as does the role of genetic loci on this association. The study involved 179,565 participants from UK Biobank, tracking incident atrial fibrillation (AF) cases. Iron intake was categorized into low, moderate, and high groups based on dietary surveys conducted from 2009 to 2012. The Cox regression model was used to estimate the risk of AF in relation to iron intake, assessing the hazard ratio (HR) and 95% confidence interval (95% CI). It also examined the impact of 165 AF-related and 20 iron-related genetic variants on this association. Pathway enrichment analyses were performed using Metascape and FUMA. During a median follow-up period of 11.6 years, 6693 (3.97%) incident AF cases were recorded. A total of 35,874 (20.0%) participants had high iron intake. High iron intake was associated with increased risk of AF [HR: 1.13 (95% CI: 1.05, 1.22)] in a fully adjusted model. Importantly, there were 83 SNPs (11 iron-related SNPs) that could enhance the observed associations. These genes are mainly involved in cardiac development and cell signal transduction pathways. High dietary iron intake increases the risk of atrial fibrillation, especially when iron intake exceeds 16.95 mg. The association was particularly significant among the 83 SNPs associated with AF and iron, the individuals with these risk genes. Gene enrichment analysis revealed that these genes are significantly involved in cardiac development and cell signal transduction processes.

Sexual adaptation plays an important role in psychosexual health. Our study aimed to investigate the relationship between the family environment and sexual adaptability among adolescents with different personality traits. A cross-sectional study was conducted in Shanghai and Shanxi province. A total of 1106 participants aged 14–19 was surveyed in 2019, including 519 boys and 587 girls. Univariate analyses and mixed regression models were performed to assess the association. Girls had a significantly lower average score of sexual self-adaptation compared to boys (4.01 ± 0.77 vs. 4.32 ± 0.64, p < 0.001). We found that the family environment did not impact boys’ sexual adaptation in different personality groups. For girls in a balanced group, expressiveness factors improved their sexual adaptability (p < 0.05), intellectual–cultural orientation and organization promoted social adaptability (p < 0.05) and active–recreational orientation and control decreased their social adaptability (p < 0.05). In the high-neuroticism group, cohesion facilitated sexual control (p < 0.05), while conflict and organization reduced sexual control ability, and active–recreational orientation decreased sexual adaptation (p < 0.05). No factors associated with the family environment were found to influence sexual adaptability in groups with low neuroticism and high ratings in other personality factors. Compared with boys, girls demonstrated lower sexual self-adaptability, and their overall sexual adaptability was more susceptible to the family environment.

Background: The risk of atrial fibrillation (AF) is accentuated by age and comorbidities. Healthy lifestyle behaviors, based on Life’s Essential 8 (LE8), may modify the risk of new-onset AF mitigating the impact of multimorbidity. The aim of this study was to investigate the associations of LE8 with multimorbidity status, linked to AF incidence. Methods: A total of 255 280 participants free of AF were included. LE8 was assessed using eight metrics and categorized into low, moderate, and high cardiovascular health (CVH). Multimorbidity clusters were determined using latent class analysis using 36 long-term conditions (LTCs), categorized into five groups as follows: three multimorbidity clusters (noncardiovascular disease; mental health; and cardio-metabolic multimorbidity); no LTCs; and singular LTCs. The relationships between LE8 and multimorbidity status with AF incidence were evaluated using Cox models and counterfactual analyses. Results: During an average follow-up of 11.7 years (SD 2.2), 15 069 participants without AF at baseline (mean age 56.2; SD 8.1; 51.9% female and 48.1% male) developed AF. Individuals with high CVH had a 27% lower risk of AF than those with low CVH. Compared to individuals without multimorbidity, participants with singular LTC or multimorbidity clusters had higher AF risk. Up to 54.7% of the associations between multimorbidity status and AF were mediated by LE8. Counterfactual analysis showed increasing the LE8 score to 80 could reduce AF occurrence in multimorbidity individuals by 22.12% to 24.56%. Conclusion: Lower LE8 scores and multimorbidity were associated with higher AF incidence. Adherence to a healthy lifestyle, based on LE8 may prevent AF, especially in those with multimorbidity.