Association between Helicobacter pylori antibodies determined by multiplex serology and gastric cancer risk: A meta-analysis.

BACKGROUND AND AIMS: Previous studies have reported the association between limited number of Helicobacter pylori (H. pylori) antigens and gastric cancer (GC) risk. The present study evaluated the association between serum antibodies against 15 different H. pylori proteins measured by using multiplex serology assay and GC risk. METHODS: We searched PubMed databases, Embase, Web of Science, and Cochrane Library for relevant articles. A meta-analysis was used to pool studies and to estimate odds ratios (ORs) with 95% confidence intervals (95%CIs) of different H. pylori antigens associated with GC risk. Heterogeneity was investigated using Cochran's Q test and I-squared statistic. RESULTS: Nine studies were identified, with a total of 3209 GC cases and 6964 controls. Five H. pylori virulence factors were significantly associated with non-cardia GC risk at p-value <0.0033 including: CagA (OR = 3.22, 95%CI: 2.10-4.94), HP0305 (OR = 1.72, 95%CI: 1.32-2.25), HyuA (OR = 1.42, 95%CI: 1.13-1.79), Omp (OR = 1.83, 95%CI: 1.30-2.58), and VacA (OR = 2.05, 95%CI: 1.67-2.52). However, none of the 15 antigens was associated with cardia GC risk. In subgroup analysis by ethnicity, we identified 7 antigens associated with the risk of non-cardia GC among East Asian while only two antigens were identified in European population. Nevertheless, CagA and GroEL showed a stronger association in Caucasian (CagA OR = 5.83, 95%CI: 3.31-10.26; GroEL OR = 3.66, 95%CI: 1.58-8.50) compared with East Asian (CagA OR = 2.20, 95% CI: 1.85-2.61; GroEL OR = 1.47, 95%CI: 1.29-1.68). CONCLUSIONS: This study determined that H. pylori infection increases the risk of non-cardia GC with differential effects by its virulence factors and with different patterns among East Asian and European populations. These results advance the understanding of the effect of H. pylori on GC.

Investigation of the relationships between sleep behaviors and risk of healthspan termination: a prospective cohort study based on 323,373 UK-Biobank participants.

OBJECTIVES: To examine the associations between four sleep behaviors and the risk of healthspan termination. METHODS: This study included 323,373 participants, free of terminated healthspan at baseline, from the UK-Biobank (UKB). We applied multivariable-adjusted Cox regression models to estimate the risk of terminated healthspan based on four sleep behaviors (insomnia/sleeplessness, napping, daytime sleepiness, and difficulty getting up from bed), which were self-reported and measured on Likert scales from "usually" to "never/rarely" experiences. In this study, healthspan was defined based on eight events that are strongly associated with longevity (congestive heart failure, myocardial infarction, chronic obstructive pulmonary disease, stroke, dementia, diabetes, cancer, and death). RESULTS: Participants who reported the following unhealthy sleep behaviors had a significantly higher risk of terminated healthspan: "usually experience sleeplessness/insomnia" (HR = 1.05, 95% CI: 1.03-1.07; P < 0.001); "usually nap" (HR = 1.22, 95% CI: 1.18-1.26; P < 0.01); "excessive daytime sleepiness" (HR = 1.25, 95% CI: 1.19-1.32; P < 0.001); and "difficult getting up from bed" (HR = 1.08, 95% CI: 1.05-1.10; P < 0.001). The corresponding population attributable risk percentage (PAR%) indicated that about 7% of healthspan termination in this cohort would have been eliminated if all participants had healthy sleep behaviors. CONCLUSION: Participants who reported "usually experience sleeplessness/insomnia," "usually nap," "excessive daytime sleepiness," and "difficult getting up from bed" had increased risk of shortened healthspan. Therefore, adherence to healthy sleep behavior is significant for the extension of healthspan.

Type 2 diabetes, glycaemic traits and upper gastrointestinal cancer risk: a prospective cohort study.

BACKGROUND: Type 2 diabetes (T2D) has been linked with site-specific upper gastrointestinal (UGI) cancers during the past decades, but associations are still inconclusive. This study aimed to determine the association between T2D, glycaemic traits (random blood glucose and HbA1c) and UGI cancer (oesophageal and gastric cancer). METHODS: In the present study, based on the large-scale prospective cohort of UK Biobank, we included 452 631 eligible participants. T2D was defined according to baseline self-report data, clinical data and biochemistry data. Random blood glucose and HbA1c were measured at baseline. Polygenic risk score was used to classify individuals into different UGI cancer genetic risks. Multivariable Cox regression models were used to estimate HRs and 95% CIs. RESULTS: During a median follow-up of 10.26 years (IQR: 9.47-10.97), 1392 incident UGI cancer cases were identified. T2D was significantly associated with a 44% increment in UGI cancer risk (95% CI 1.22 to 1.70, p<0.001). Moreover, per SD increase in random blood glucose and HbA1c was associated with 7% (95% CI 1.03 to 1.12, p<0.001) and 6% (95% CI 1.04 to 1.09, p<0.001) increased hazards of developing UGI cancer, respectively. Patients with T2D at high genetic risk had a 2.33-fold hazard of UGI cancer (95% CI 1.66 to 3.28, p<0.001), compared with non-T2D individuals at low genetic risk. CONCLUSION: Our results indicate that T2D and elevated levels of glycaemic traits may be risk factors for incident UGI cancer. Individuals with a high genetic risk and T2D have a significantly increased risk of developing UGI cancer.