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Background Understanding which factors influence participation in physical activity is important to improve the public health. The aim of the present review of reviews was to summarize and present updated evidence on personal and environmental factors associated with physical activity. Methods MEDLINE and EMBASE were searched for reviews published up to 31 Jan . 2017 reporting on potential factors of physical activity in adults aged over 18 years. The quality of each review was appraised with the Assessing the Methodological Quality of Systematic Reviews (AMSTAR) checklist. The corrected covered area (CCA) was calculated as a measure of overlap for the primary publications in each review. Results Twenty-five articles met the inclusion criteria which reviewed 90 personal and 27 environmental factors. The average quality of the studies was moderate, and the CCA ranged from 0 to 4.3%. For personal factors, self-efficacy was shown as the strongest factor for participation in physical activity (7 out of 9). Intention to exercise, outcome expectation, perceived behavioral control and perceived fitness were positively associated with physical activity in more than 3 reviews, while age and bad status of health or fitness were negatively associated with participation in physical activity in more than 3 reviews. For environmental factors, accessibility to facilities, presence of sidewalks, and aesthetics were positively associated with participation in physical activity. Conclusions The findings of this review of reviews suggest that some personal and environmental factors were related with participation in physical activity. However, an association of various factors with physical activity could not be established because of the lack of primary studies to build up the organized evidence. More studies with a prospective design should be conducted to understand the potential causes for physical activity.

A systematic review and meta-analysis of randomized controlled trials (RCTs) and observational studies was conducted to assess the association between menopausal hormone therapy and cardiovascular disease. The PubMed and EMBASE databases were searched for articles published from 2000 to 2019, using review methods based on a previous Cochrane review. Quality assessment of RCTs and observational studies was conducted using the Jadad scale and the Newcastle–Ottawa Scale, respectively. A total of 26 RCTs and 47 observational studies were identified. The study populations in the RCTs were older and had more underlying diseases than those in the observational studies. Increased risks of venous thromboembolism [summary estimate (SE), 95% confidence interval (CI): RCTs, 1.70, 1.33–2.16; observational studies, 1.32, 1.13–1.54] were consistently identified in both study types, whereas an increased risk of stroke in RCTs (SE: 1.14, 95% CI: 1.04–1.25) and a decreased risk of myocardial infarction in observational studies (SE: 0.79, 95% CI: 0.75–0.84) were observed. Differential clinical effects depending on timing of initiation, underlying disease, regimen type, and route of administration were identified through subgroup analyses. These findings suggest that underlying disease and timing of initiation should be carefully considered before starting therapy in postmenopausal women.

Despite the ongoing spread of MERS, there is limited knowledge of the factors affecting its severity and outcomes. We analyzed clinical data and specimens from fourteen MERS patients treated in a hospital who collectively represent a wide spectrum of disease severity, ranging from mild febrile illness to fatal pneumonia, and classified the patients into four groups based on severity and mortality. Comparative and kinetic analyses revealed that high viral loads, weak antibody responses, and lymphopenia accompanying thrombocytopenia were associated with disease mortality, whereas persistent and gradual increases in lymphocyte responses might be required for effective immunity against MERS-CoV infection. Leukocytosis, primarily due to increased neutrophils and monocytes, was generally observed in more severe and fatal cases. The blood levels of cytokines such as IL-10, IL-15, TGF-β, and EGF were either positively or negatively correlated with disease mortality. Robust induction of various chemokines with differential kinetics was more prominent in patients that recovered from pneumonia than in patients with mild febrile illness or deceased patients. The correlation of the virological and immunological responses with disease severity and mortality, as well as their responses to current antiviral therapy, may have prognostic significance during the early phase of MERS.

Background Effects of confounders on associations between diet and colorectal cancer (CRC) in observational studies can be minimized in Mendelian randomization (MR) approach. This study aimed to investigate observational and genetically predicted associations between dietary intake and CRC using one-sample MR. Methods Using genetic data of over 93 million variants, we performed a genome-wide association study to find genomic risk loci associated with dietary intake in participants from the UK Biobank. Then we calculated genetic risk scores of diet-related variants and used them as instrumental variables in the two-stage least square MR framework to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs) for associations. We also performed observational analyses using age as a time-scale in Cox proportional hazard models. Results Allele scores were calculated from 399 genetic variants associated with the consumption of of red meat, processed meat, poultry, fish, milk, cheese, fruits, vegetables, coffee, tea, and alcohol in participants from the UK Biobank. In MR analysis, genetically predicted fruit intake was significantly associated with a 21% decreased risk of CRC (HR = 0.79, 95% CI = 0.66–0.95), and there was a marginally inverse association between vegetable intake and CRC (HR = 0.85, 95% CI = 0.71–1.02). However, null findings were observed in multivariable analysis, with HRs (95% CIs) of 0.99 (0.98–1.01) and 0.99 (0.98–1.00) per increment of daily servings of fruits and vegetables, respectively. Conclusion Dietary habits were attributable to genetic variations, which can be used as instrumental variables in the MR framework. Our study supported a causal relationship between fruit intake and a decreased risk of CRC and suggested an effective strategy of consuming fruits in the primary prevention of CRC.

Background This study aimed to explore the potential interaction between dietary intake and genetics on incident colorectal cancer (CRC) and whether adherence to healthy dietary habits could attenuate CRC risk in individuals at high genetic risk. Methods We analyzed prospective cohort data of 374,004 participants who were free of any cancers at enrollment in UK Biobank. Dietary scores were created based on three dietary recommendations of the World Cancer Research Fund (WCRF) and the overall effects of 11 foods on CRC risks using the inverse-variance (IV) method. Genetic risk was assessed using a polygenic risk score (PRS) capturing overall CRC risk. Cox proportional hazard models were used to calculate hazard ratios (HRs) and 95% CIs (confidence intervals) of associations. Interactions between dietary factors and the PRS were examined using a likelihood ratio test to compare models with and without the interaction term. Results During a median follow-up of 12.4 years, 4,686 CRC cases were newly diagnosed. Both low adherence to the WCRF recommendations (HR = 1.12, 95% CI = 1.05–1.19) and high IV-weighted dietary scores (HR = 1.27, 95% CI = 1.18–1.37) were associated with CRC risks. The PRS of 98 genetic variants was associated with an increased CRC risk (HR T3vsT1  = 2.12, 95% CI = 1.97–2.29). Participants with both unfavorable dietary habits and a high PRS had a more than twofold increased risk of developing CRC; however, the interaction was not significant. Adherence to an overall healthy diet might attenuate CRC risks in those with high genetic risks (HR = 1.21, 95% CI = 1.08–1.35 for high vs. low IV-weighted dietary scores), while adherence to WCRF dietary recommendations showed marginal effects only (HR = 1.09, 95% CI = 1.00–1.19 for low vs. high WCRF dietary scores). Conclusion Dietary habits and the PRS were independently associated with CRC risks. Adherence to healthy dietary habits may exert beneficial effects on CRC risk reduction in individuals at high genetic risk.

There is growing interest in the real-time assessment of physical activity (PA) and physiological variables. Acceleration, particularly those collected through wearable sensors, has been increasingly adopted as an objective measure of physical activity. However, sensor-based measures often pose challenges for large-scale studies due to their associated costs, inability to capture contextual information, and restricted user populations. Smartphone-delivered ecological momentary assessment (EMA) offers an unobtrusive and undemanding means to measure PA to address these limitations. This study aimed to evaluate the usability of EMA by comparing its measurement outcomes with 2 self-report assessments of PA: Global Physical Activity Questionnaire (GPAQ) and a modified version of Bouchard Physical Activity Record (BAR). A total of 235 participants (137 female, 98 male, and 94 repeated) participated in one or more 7-day studies. Waist-worn sensors provided by ActiGraph captured accelerometer data while participants completed 3 self-report measures of PA. The multilevel modeling method was used with EMA, GPAQ, and BAR as separate measures, with 6 subdomains of physiological activity (overall PA, overall excluding occupational, transport, exercise, occupational, and sedentary) to model accelerometer data. In addition, EMA and GPAQ were further compared with 6 domains of PA from the BAR as outcome measures. Among the 3 self-reporting instruments, EMA and BAR exhibited better overall performance in modeling the accelerometer data compared to GPAQ (eg EMA daily: β=.387, P<.001; BAR daily: β=.394, P<.001; GPAQ: β=.281, P<.001, based on repeated-only participants with step counts from accelerometer as dependent variables). Multilevel modeling on 3 self-report assessments of PA indicates that smartphone-delivered EMA is a valid and efficient method for assessing PA.

To evaluate the associations of periodontal disease (PD) with systemic diseases, including diabetes mellitus (DM) and cardiovascular disease (CVD), as well as the reciprocal association. The CVD included the cases of coronary heart disease and heart failure. A prospective study was conducted from 2007 to 2019 using linked data from three databases in Korea. Three separate study groups were formed to individually determine the risks of PD (n = 10,533), DM (n = 14,523) and CVD (n = 14,315). All diseases were confirmed based on physicians’ diagnoses using medical records and self-reports. Cox proportional hazard regression was applied with 95% confidence intervals (CIs) to obtain hazard ratios (HRs). PD was significantly associated with an elevated risk of DM (HR [95% CI]: 1.22 [1.07–1.39]) after full adjustment for age, sex, lifestyle factors, body mass index, dental behaviour and CVD. PD was also found to increase the risk of CVD (1.27 [1.03–1.57]), whereas CVD increased the risk of PD (1.20 [1.09–1.32]) after full adjustment for other covariates including DM. This study found a bidirectional association between PD and CVD, as well as a positive association of PD with DM.

Various risk factors have been associated with epithelial ovarian cancer risk in observational epidemiological studies. However, the causal nature of the risk factors reported, and thus their suitability as effective intervention targets, is unclear given the susceptibility of conventional observational designs to residual confounding and reverse causation. Mendelian randomization (MR) uses genetic variants as proxies for risk factors to strengthen causal inference in observational studies. We used MR to evaluate the association of 12 previously reported risk factors (reproductive, anthropometric, clinical, lifestyle, and molecular factors) with risk of invasive epithelial ovarian cancer, invasive epithelial ovarian cancer histotypes, and low malignant potential tumours. Genetic instruments to proxy 12 risk factors were constructed by identifying single nucleotide polymorphisms (SNPs) that were robustly (P < 5 × 10-8) and independently associated with each respective risk factor in previously reported genome-wide association studies. These risk factors included genetic liability to 3 factors (endometriosis, polycystic ovary syndrome, type 2 diabetes) scaled to reflect a 50% higher odds liability to disease. We obtained summary statistics for the association of these SNPs with risk of overall and histotype-specific invasive epithelial ovarian cancer (22,406 cases; 40,941 controls) and low malignant potential tumours (3,103 cases; 40,941 controls) from the Ovarian Cancer Association Consortium (OCAC). The OCAC dataset comprises 63 genotyping project/case-control sets with participants of European ancestry recruited from 14 countries (US, Australia, Belarus, Germany, Belgium, Denmark, Finland, Norway, Canada, Poland, UK, Spain, Netherlands, and Sweden). SNPs were combined into multi-allelic inverse-variance-weighted fixed or random effects models to generate effect estimates and 95% confidence intervals (CIs). Three complementary sensitivity analyses were performed to examine violations of MR assumptions: MR-Egger regression and weighted median and mode estimators. A Bonferroni-corrected P value threshold was used to establish strong evidence (P < 0.0042) and suggestive evidence (0.0042 < P < 0.05) for associations. In MR analyses, there was strong or suggestive evidence that 2 of the 12 risk factors were associated with invasive epithelial ovarian cancer and 8 of the 12 were associated with 1 or more invasive epithelial ovarian cancer histotypes. There was strong evidence that genetic liability to endometriosis was associated with an increased risk of invasive epithelial ovarian cancer (odds ratio [OR] per 50% higher odds liability: 1.10, 95% CI 1.06-1.15; P = 6.94 × 10-7) and suggestive evidence that lifetime smoking exposure was associated with an increased risk of invasive epithelial ovarian cancer (OR per unit increase in smoking score: 1.36, 95% CI 1.04-1.78; P = 0.02). In analyses examining histotypes and low malignant potential tumours, the strongest associations found were between height and clear cell carcinoma (OR per SD increase: 1.36, 95% CI 1.15-1.61; P = 0.0003); age at natural menopause and endometrioid carcinoma (OR per year later onset: 1.09, 95% CI 1.02-1.16; P = 0.007); and genetic liability to polycystic ovary syndrome and endometrioid carcinoma (OR per 50% higher odds liability: 0.89, 95% CI 0.82-0.96; P = 0.002). There was little evidence for an association of genetic liability to type 2 diabetes, parity, or circulating levels of 25-hydroxyvitamin D and sex hormone binding globulin with ovarian cancer or its subtypes. The primary limitations of this analysis include the modest statistical power for analyses of risk factors in relation to some less common ovarian cancer histotypes (low grade serous, mucinous, and clear cell carcinomas), the inability to directly examine the association of some ovarian cancer risk factors that did not have robust genetic variants available to serve as proxies (e.g., oral contraceptive use, hormone replacement therapy), and the assumption of linear relationships between risk factors and ovarian cancer risk. Our comprehensive examination of possible aetiological drivers of ovarian carcinogenesis using germline genetic variants to proxy risk factors supports a role for few of these factors in invasive epithelial ovarian cancer overall and suggests distinct aetiologies across histotypes. The identification of novel risk factors remains an important priority for the prevention of epithelial ovarian cancer.

This study aimed to understand the biological process related to the prevention of cardiovascular & metabolic diseases (CMD), including diabetes, hypertension, and dyslipidemia via regular exercise. This study included 17,053 subjects aged 40–69 years in the Health Examinees Study from 2004 to 2012. Participation in regular exercise was investigated by questionnaires. Data on 42 biomarkers were collected from anthropometric measures and laboratory tests. We examined the associations between regular exercise and biomarkers using general linear models, between biomarkers and the risk of CMD using cox proportional hazard models, and the mediation effect of biomarkers using mediation analyses. Biomarker networks were constructed based on the significant differential correlations ( p  < 0.05) between the exercise and non-exercise groups in men and women, respectively. We observed significant mediators in 14 and 16 of the biomarkers in men and women, respectively. Triglyceride level was a noteworthy mediator in decreasing the risk of CMD with exercise, explaining 23.79% in men and 58.20% in women. The biomarker network showed comprehensive relationships and associations among exercise, biomarkers, and CMD. Body composition-related biomarkers were likely to play major roles in men, while obesity-related biomarkers seemed to be key factors in women.

This study aimed to investigate the association of sleep duration and quality with high-sensitivity C-reactive protein (hs-CRP) among middle-aged and elderly Koreans. Among a total of 74,867 participants (25,069 men and 49,798 women) recruited for the Health Examinees (HEXA) study, adjusted geometric means of hs-CRP level were compared across categories of sleep duration (3 mg/L) associated with sleep characteristics were estimated using multivariable-adjusted logistic regression models. Men who slept [greater than or equal to]10 hours per day were significantly associated with elevated hs-CRP (OR = 1.47, 95% CI 1.11-1.95). Whereas in women, difficulty in initiating sleep (OR = 1.28, 95% CI 1.04-1.57 for \"Always\"), and maintaining sleep was significantly associated with elevated hs-CRP levels (OR = 1.13, 95% CI 1.02-1.26 for \"Often\"; OR = 1.11, 95% CI 0.97-1.28 for \"Always\"). Additionally, women who experienced poor sleep quality presented an elevated level of hs-CRP (OR = 1.13, 95% CI 1.03-1.23). Our findings suggest that excessive sleep duration and poor sleep quality are significantly associated with the elevated inflammatory marker, specifically hs-CRP. Further research is needed to examine the effect of sleep interventions focused on these factors.