Epidemiological studies have reported inconsistent association between obesity and risk of bladder cancer, and the dose-response relationship between them has not been clearly defined. We carried out a meta-analysis to summarize available evidence from epidemiological studies on this point. Relevant articles were identified by searching the PubMed and Web of Science databases through September 30, 2014. We pooled the relative risks from individual studies using random-effect model, and the dose—response relationship was estimated by using restricted cubic spline model. Fifteen cohort studies with 38,072 bladder cancer cases among 14,201,500 participants were included. Compared to normal weight, the pooled relative risks and corresponding 95% confidence intervals of bladder cancer were 1.07(1.01-1.14) and 1.10(1.06-1.14) for preobese and obesity, with moderate (I² = 37.6%, P = 0.029) and low (I² = 15.5%, P = 0.241) heterogeneities between studies, respectively. In a dose-response meta-analysis, body mass index (BMI) was associated with bladder cancer risk in a linear fashion (P_{non-linearity} = 0.467) and the risk increased by 4.2% for each 5 kg/m² increase. No significant publication bias was found (P = 0.912 for Begg’s test, P = 0.712 for Egger’s test). Findings from this dose-response meta-analysis suggest obesity is associated with linear-increased risk of bladder cancer.

Background and purpose: The objective was to assess the ability of eight commonly measured blood markers to serve as prognostic biomarkers in amyotrophic lateral sclerosis (ALS).Methods: A cohort study was conducted of 399 individuals with newly diagnosed ALS between 2006 and 2011 in Stockholm, Sweden. Information on eight blood markers, including creatinine, albumin, haemoglobin, C‐reactive protein (CRP), glucose, potassium, sodium and calcium, measured at or after the date of ALS diagnosis, was collected. The Cox regression model and joint model were used to explore the associations between biomarkers and risk of mortality.Results: The mean age at ALS diagnosis was 66.25 years and 58% of the patients were male. A lower than median level of serum creatinine [hazard ratio (HR) 1.67; 95% confidence interval (CI) 1.31–2.12] or albumin (HR 1.49, 95% CI 1.13–1.96) whereas a higher than median level of log‐transformed CRP (HR 1.33, 95% CI 1.04–1.71) or glucose (HR 1.34, 95% CI 1.01–1.78) at baseline was associated with a higher mortality risk. Taking all available measurements after ALS diagnosis into account, an association was found between per standard deviation (SD) decrease in serum creatinine (HR 2.23, 95% CI 1.81–2.75) or albumin (HR 1.83, 95% CI 1.43–2.36) as well as per SD increase of log(CRP) (HR 1.96, 95% CI 1.58–2.43) or glucose (HR 1.61, 95% CI 1.21–2.12) and a higher mortality risk. No clear association was found for haemoglobin, potassium, sodium or calcium.Conclusions: This study suggests that serum creatinine, albumin, CRP and glucose measured at the time of ALS diagnosis as well as their temporal changes after ALS diagnosis could serve as additional prognostic biomarkers for ALS. Their values in routine clinical practice and clinical trials of ALS need to be investigated further.

Metabolic dysfunction-associated steatotic liver disease (MASLD; formerly NAFLD) is the fastest growing cause of hepatocellular carcinoma (HCC) worldwide. However, whether family members of individuals with MASLD also share an increased risk of developing HCC is unknown. This nationwide multigenerational cohort study involved family members of all Swedish adults diagnosed with biopsy-proven MASLD (1969-2017), and matched general population comparators. Using the Swedish Multi-generation Register, we identified 38,018 first-degree relatives (FDRs: parents, siblings, offspring) and 9,381 spouses of patients with MASLD, as well as 197,303 comparator FDRs and 47,572 comparator spouses. We used Cox proportional hazards models to calculate adjusted hazard ratios (aHRs) for HCC, major adverse liver outcomes (cirrhosis, decompensated liver disease or liver transplantation), liver-related mortality, extrahepatic cancer, and non-liver-related mortality. Over a median of 17.6 years, the rate of the primary outcome HCC was higher in MASLD FDRs vs. comparator FDRs (13 vs. 8/100,000 person-years [PY]; aHR 1.80, 95% CI 1.36-2.37). The HCC risk was further increased in FDRs of individuals with liver fibrosis/cirrhosis (aHR 2.14, 95% CI 1.07-4.27; P_{Heterogeneity} = 0.03). MASLD FDRs also had higher rates of major adverse liver outcomes (73 vs. 51/100,000 PY; aHR 1.52, 95% CI 1.36-1.69) and liver-related mortality (20 vs. 11/100,000 PY; aHR 2.14, 95% CI 1.67-2.74). MASLD FDRs with any concomitant chronic liver condition experienced accelerated progression of liver disease (aHR 1.47, 95% CI 1.29-1.67). MASLD spouses were at higher risks of major adverse liver outcomes (86 vs. 74/100,000 PY; aHR 1.23, 95% CI 1.01-1.51) and liver-related mortality (25 vs. 19/100,000 PY; aHR 1.93, 95% CI 1.15-3.23), but not of HCC (aHR 1.43, 95% CI 0.87-2.35). There is distinct familial clustering of adverse liver-related outcomes in families of individuals with biopsy-proven MASLD, with higher relative risks of HCC, progressive liver disease, and liver-related mortality, but absolute risks are low. Metabolic dysfunction-associated steatotic liver disease (MASLD; formerly termed NAFLD) clusters in families with high genetic susceptibility and shared environmental risk factors, but the risks of developing hepatocellular carcinoma and other major liver-related outcomes in family members of individuals with MASLD are largely unknown. This large nationwide multigenerational cohort study involving family members (first-degree relatives and spouses) of individuals with biopsy-proven MASLD and of matched general population comparators found slightly increased risks of hepatocellular carcinoma in first-degree relatives, and of developing cirrhosis and liver-related mortality in all family members of individuals with biopsy-proven MASLD. The findings of this study provide large-scale evidence to inform clinical practice guidelines for recommendations on the early identification of individuals at higher risk of liver-related morbidity and mortality.

Findings on the association between television (TV) viewing and all-cause mortality in epidemiologic studies have been inconsistent. Therefore, we conducted a meta-analysis of data from prospective cohort studies to quantify this association. Relevant articles were identified by searching MEDLINE (PubMed; National Library of Medicine, Bethesda, Maryland) and EMBASE (Elsevier B.V., Amsterdam, the Netherlands) from inception to March 1, 2015, and reviewing the reference lists of retrieved articles. Study-specific results were pooled using a random-effects model. Of 2,578 citations identified by the search strategy, 10 cohort studies (61,494 deaths among 647,475 individuals) met the inclusion criteria. The summary relative risk of all-cause mortality for the highest category of TV viewing time versus the lowest was 1.33 (95% confidence interval: 1.20, 1.47), with heterogeneity among studies (I² = 66.7%, P_{heterogeneity} = 0.001). In dose-response meta-analysis, TV viewing time was statistically significantly associated with all-cause mortality risk in a J-shaped fashion (P_nonlinearity = 0.001). These results indicate that prolonged TV viewing time might increase the risk of all-cause mortality. Given the high prevalence of excessive TV viewing, public health recommendations or interventions aimed at decreasing the amount of TV viewing time in modern societies are warranted.