SummaryBackground and objectives Chronic kidney disease (CKD) is known to be associated with increased allcause and cardiovascular mortality, but no large studies examined the cancer-specific mortality in non-dialysis-dependent CKD patients. Such outcome data are needed for proper allocation of resources and would help to develop better preventive services. Between 1998 and 1999, 123,717 adults were recruited from four health screening centers in Taiwan. The estimated glomerular filtration rate was calculated using the four-variable Modification of Diet in Renal Disease Study equation for the Chinese. Mortality was ascertained by computer linkage to the national death registry after a median follow-up of 7.06 years. Cox proportional hazards regression models were used to estimate the impact of CKD on cancer-specific mortality. Design, setting, participants, & measurementsResults A higher risk for overall cancer mortality was found in CKD patients compared with non-CKD patients (adjusted hazard ratio, 1.2). CKD was associated with increased mortality from liver cancer, kidney cancer, and urinary tract cancer, with an adjusted hazard ratio of 1.74, 3.3, and 7.3, respectively. A graded relationship between the severity of renal impairment and cancer mortality was also found. ConclusionsPatients with CKD had a higher mortality risk of liver cancer, kidney cancer, and urinary tract cancer. This is the first large study that showed an inverse association between renal function and liver cancer mortality. The increased mortality could be caused by higher cancer incidence or worse response to cancer treatment. Future research is warranted to clarify the mechanism.

PurposeDyslipidemia is considered as one mechanism causing cardiovascular sequelae in obstructive sleep apnea (OSA). Continuous positive airway pressure (CPAP) can reduce cardiovascular morbidities but its effect on lipid profiles is inconclusive. This study aimed to investigate the effects of CPAP on lipid profiles by a meta-analysis of the existing randomized controlled trials.MethodsStudies were retrieved from MEDLINE/PubMed, EMBASE, CENTRAL, commercial websites, and article references up to August 2013 following the protocols (PROSPERO CRD42012002636). Randomized controlled trials investigating the CPAP effects on changes in lipid profiles in adult patients with OSA were included. Two independent researchers extracted relevant data in duplicate. The pooled effect was analyzed by fixed-effect generic inverse variance, and the heterogeneity was assessed using the I2 statistic.ResultsSix trials with 348 patients and 351 controls were included. CPAP significantly lowered total cholesterol (mean, −6.23 mg/dl; 95% CI, −8.73 to –3.73; I2, 0 %; p < 0.001), triglyceride (mean, −12.60 mg/dl; 95% CI, −18.80 to −6.41; I2, 25 %; p < 0.001), and high-density lipoprotein (mean, −1.05 mg/dl; 95% CI, −1.69 to −0.40; I2, 0 %; p = 0.001), but not low-density lipoprotein (mean, −1.01 mg/dl; 95% CI, −5.04 to 3.02; I2, 0 %; p = 0.62). The lipid-lowering effects were homogeneous across the studies. By subgroup analysis, the reductions of lipid profiles were associated with the cross-over design, subtherapeutic CPAP as placebo, enrolled patients with moderate-to-severe OSA or daytime sleepiness, and CPAP treatment with short-term duration or good compliance.ConclusionsThis meta-analysis validates the observation that CPAP can reduce lipid profiles in patients with OSA.Electronic supplementary materialThe online version of this article (doi:10.1007/s11325-014-1082-x) contains supplementary material, which is available to authorized users.

This study aimed to identify lifestyle factors associated with cognitive change and to explore whether the effect of lifestyle varies by socioeconomic status (SES). Participants aged 65 years and older were recruited from elderly health checkup programs from 2011 to 2013 in Taiwan. Neuropsychological tests, including tests of global cognition, logical memory, executive function, verbal fluency and attention, were administered at baseline (N = 603) and 2 years later (N = 509). After literature review, 9 lifestyle factors and 3 SES indicators were chosen and their effects on cognitive change were evaluated using linear regression adjusting for age, sex, education, APOE ε4 status, and baseline cognitive score. Five lifestyle factors (high vegetable and fish intake, regular exercise, not smoking, and light to moderate alcohol consumption) and 3 SES indicators [annual household income (> 33,333 USD vs. less), occupational complexity (high vs. low mental demanding job), and years of education (> 12 years vs. less)] were found to be protective against cognitive decline (P < 0.1 in any cognitive domains, ß ranging from 0.06 to 0.38). After further adjusting for all the lifestyle and SES factors, fish intake, higher income and occupational complexity remained protective. Significant interactions were found between a healthful lifestyle (defined as having ≥ 3 healthful lifestyle factors) and income on changes of global cognition and verbal fluency (Pinteraction = 0.02 and 0.04). The protective effect of a healthful lifestyle was observed only among participants with lower income in global cognition and logical memory [ß = 0.17, 95% confidence interval (CI) = 0.07–0.26; ß = 0.30, 95% CI = 0.14–0.46]. To the best of our knowledge, this study for the first time explored how the interactions of lifestyle and SES affect cognitive change. Our findings will aid in developing dementia prevention programs and reduce health inequalities.