Risk of incident type 2 diabetes in male NAFLD and NAFLD-free smokers: a 7-year post-cessation study.

BACKGROUND: We aimed to investigate the post-cessation T2DM risk in male NAFLD and NAFLD-free smokers in a 7-year cohort study. METHODS: The study population was male adults who underwent annual health checkups in a 7-year cohort study. Recent quitters were categorized into four groups based on their weight gain during follow-up: < 0 kg, 0-1.9 kg, 2.0-3.9 kg, and ≥ 4.0 kg. Cox proportional hazard models, adjusted for various variables, were used to estimate hazard ratios (HRs) for the association between post-cessation weight gain and incident T2DM in NAFLD and NAFLD-free individuals. RESULTS: At baseline, we included 1,409 NAFLD and 5150 NAFLD-free individuals. During a total of 39,259 person-years of follow-up, 222 (15.8%) NAFLD patients and 621 (12.1%) NAFLD-free participants quit smoking, with the corresponding means (standard deviations) of post-cessation weight gain being 2.24 (3.26) kg and 1.15 (3.51) kg, respectively. Among NAFLD individuals, compared to current smokers, the fully adjusted HRs (95% CI) for incident T2DM were 0.41 (0.06-3.01), 2.39 (1.21-4.70), 4.48 (2.63-7.63), and 6.42 (3.68-11.23) for quitters with weight gains < 0 kg, 0.0-1.9 kg, 2.0-3.9 kg, and ≥ 4.0 kg, respectively. For NAFLD-free individuals, we only observed a significant association between post-cessation weight gain ≥ 4.0 kg and the risk of incident T2DM (P < 0.001). Further analysis revealed that the impact of post-cessation weight gain on T2DM risk was not affected by alcohol consumption or obesity status at baseline. CONCLUSIONS: Mild post-cessation weight gain significantly increased the risk of T2DM in male NAFLD patients but not in male NAFLD-free individuals. Therefore, it is recommended that individuals with NAFLD manage their weight after quitting smoking.

Circulating fatty acids and risk of hepatocellular carcinoma and chronic liver disease mortality in the UK Biobank.

Nuclear magnetic resonance (NMR)-based plasma fatty acids are objective biomarkers of many diseases. Herein, we aim to explore the associations of NMR-based plasma fatty acids with the risk of hepatocellular carcinoma (HCC) and chronic liver disease (CLD) mortality in 252,398 UK Biobank participants. Here we show plasma levels of n-3 poly-unsaturated fatty acids (PUFA) and n-6 PUFA are negatively associated with the risk of incident HCC [HRQ4vsQ1: 0.48 (95% CI: 0.33-0.69) and 0.48 (95% CI: 0.28-0.81), respectively] and CLD mortality [HRQ4vsQ1: 0.21 (95% CI: 0.13-0.33) and 0.15 (95% CI: 0.08-0.30), respectively], whereas plasma levels of saturated fatty acids are positively associated with these outcomes [HRQ4vsQ1: 3.55 (95% CI: 2.25-5.61) for HCC and 6.34 (95% CI: 3.68-10.92) for CLD mortality]. Furthermore, fibrosis stage significantly modifies the associations between PUFA and CLD mortality. This study contributes to the limited prospective evidence on the associations between plasma-specific fatty acids and end-stage liver outcomes.

Reconstructing the evolution history of networked complex systems.

The evolution processes of complex systems carry key information in the systems' functional properties. Applying machine learning algorithms, we demonstrate that the historical formation process of various networked complex systems can be extracted, including protein-protein interaction, ecology, and social network systems. The recovered evolution process has demonstrations of immense scientific values, such as interpreting the evolution of protein-protein interaction network, facilitating structure prediction, and particularly revealing the key co-evolution features of network structures such as preferential attachment, community structure, local clustering, degree-degree correlation that could not be explained collectively by previous theories. Intriguingly, we discover that for large networks, if the performance of the machine learning model is slightly better than a random guess on the pairwise order of links, reliable restoration of the overall network formation process can be achieved. This suggests that evolution history restoration is generally highly feasible on empirical networks.

Estimated small dense low-density lipoprotein cholesterol and nonalcoholic fatty liver disease in nonobese populations.

AIMS/INTRODUCTION: To explore the association between estimated small dense low-density lipoprotein cholesterol (sdLDL-C) and the risk of incident nonalcoholic fatty liver disease (NAFLD) in nonobese populations. MATERIALS AND METHODS: This study included participants who underwent health checkups in 2014 and were followed up until 2019. We carried out Cox proportional hazards regression analyses to evaluate the association of estimated sdLDL-C with NAFLD. Discordance analyses were carried out to estimate the relative NAFLD risk in estimated sdLDL-C versus low-density lipoprotein cholesterol (LDL-C) discordant/concordant groups. Estimated sdLDL-C was calculated by equations based on LDL-C and triglycerides. The diagnosis of NAFLD was based on the presence of abdominal ultrasonography after excluding other causes of chronic liver disease. RESULTS: Over a mean follow-up period of 26,694 person-years, 844 incident NAFLD cases were recorded. Compared with the first quartile of estimated sdLDL-C, the fourth quartile was associated with a 2.933-fold increased risk of NAFLD (95% confidence interval 2.095-4.107). With the increase in estimated sdLDL-C, the risk of NAFLD gradually increased both in participants within the normal range of LDL-C (hazard ratio 2.854, 95% confidence interval 1.650-5.617) and beyond the normal range of LDL-C (hazard ratio 2.636, 95% confidence interval 1.263-5.502). In addition, the inconsistent high estimated sdLDL-C/low LDL-C group was associated with an increased risk of NAFLD, but not the low estimated sdLDL-C/high LDL-C group. CONCLUSIONS: Estimated sdLDL-C was positively associated with the risk of incident NAFLD in a nonobese population, independent of LDL-C.

Association between gastroesophageal reflux disease and atrial fibrillation: a systematic review and meta-analysis

Background and objective: associations between gastroesophageal reflux disease (GERD) and atrial fibrillation (AF) are inconclusive. Some studies found that AF was a risk factor for GERD whereas other studies showed opposite results. The primary objective of this study was to systematically evaluate whether GERD and AF have a bidirectional association using a meta-analysis. Methods: a systematic review was conducted of studies on the association between GERD and AF, written in the English language and included in Cochrane CENTRAL, PubMed and EMBASE until February 2017. The search was limited to longitudinal, case-control, and cross-sectional studies. Results: among 548 studies found in the above-mentioned databases, seven fulfilled the inclusion criteria. Among these seven studies, two were longitudinal studies, two were case-control studies, and three were cross-sectional studies. The summary adjusted relative risks (RRs) for AF-induced GERD and GERD-induced AF were 1.54 (95% CI, 1.08-2.17) and 1.06 (95% CI, 0.86-1.31), respectively. The subgroup analysis showed that the associations were not significantly modified by sample size, study design, age, or geographic area. Conclusions: this meta-analysis supported the association of AF with increased risk of GERD

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