BACKGROUND: Sleep disordered breathing (SDB) is broadly recognized to be associated with neurobehavioral deficits, which have significant impacts on developing-aged children and adolescents. Therefore, our study aimed to quantify the proportion of neurobehavioral impairments attributed to SDB in general children and adolescents by population attributable fraction (PAF).
METHODS: The study was registered at PROSPERO (ID: CRD42023388143). We collected two types of literature on the prevalence of SDB and the risk of SDB-related neurobehavioral deficits from ten electronic databases and registers, respectively. The pooled effect sizes (Pe, Pc, RR) by random-effects meta-analysis were separately substituted into Levin\'s formula and Miettinen\'s formula to calculate PAFs.
RESULTS: Three prevalence literature and 2 risk literature, all with moderate/high quality, were included in the quantitative analysis individually. The prevalence of SDB was 11% (95%CI 2%-20%) in children and adolescents (Pe), while the SDB prevalence was 25% (95%CI 7%-42%) in neurobehavioral patients (Pc). SDB diagnosis at baseline was probably associated with about threefold subsequent incidence of neurobehavioral deficits (pooled RR 3.24, 95%CI 1.25-8.41), after multi-adjustment for key confounders. Up to 19.8% or 17.3% of neurobehavioral consequences may be attributed to SDB from Levin\'s formula and Miettinen\'s formula, respectively.
CONCLUSIONS: A certain number of neurobehavioral consequences may be attributable to SDB. It is essential for clinicians to identify and treat SDB timely, as well as screen for SDB in patients with neurobehavioral impairments. More longitudinal studies of SDB and neurobehavioral deficits are needed in the future to further certify the association between them.

This study aimed to update the association between Helicobacter pylori (H. pylori) infection and gastric cancer (GC).
We searched PubMed, Embase, and Cochrane Library from 1990 to December 2021 to identify prospective studies. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were summarized to validate the relationship between H. pylori infection and GC.
Including 27 studies, findings indicated a strong link between H. pylori and non-cardia gastric cancer (NCGC) in both Europe/North America (OR=5.37, 95%CI:4.39-6.57) and Asia (OR = 2.50, 95%CI:1.89-3.32), and a positive association with cardia gastric cancer (CGC) in Asia (OR = 1.74, 95%CI:1.38-2.19), but an inverse association in European/American populations (OR = 0.64, 95%CI: 0.51 to 0.79). Furthermore, the strength of association was greater in studies that detected H. pylori by immunoblotting versus ELISA, and also in studies testing for H. pylori detection further back in time prior to cancer diagnosis (Ptrend<0.05). Approximately 79% of NCGC in Asia and 87% in Europe/North America, along with 62% of CGC in Asia, could be attributable to H. pylori infection.
The meta-analysis supports the significant attributable risk of H. pylori infection for GC and underscores the potential impact of targeting H. pylori in GC prevention programs.
CRD42021274120.

This meta-analysis aimed at estimating the prevalence of postpartum depression (PPD) at different postpartum timepoints in women with antenatal depression (AD) in the three trimesters. We also examined the association between AD and PPD, and estimated the population attributable fraction of PPD to AD.
This systematic review and meta-analysis identified cohort studies that determined the prevalence of PPD in women who had AD, and those that examined the association between AD and PPD from PubMed, Embase, MEDLINE, CINAHL and PsycINFO. Articles were appraised using the modified Newcastle Ottawa Scale and data were analyzed using Comprehensive Meta-Analysis.
Eighty-eight (88) cohort studies with a combined sample size of 1,042,448 perinatal women contributed to the meta-analysis. About 37% pregnant women who had AD, later had PPD. Those with AD had four times higher odds of developing PPD (OR: 4.58; 95% CI = 3.52-5.96). The odds of having PPD were higher when AD was observed in the first or third trimester compared to the second trimester. About 12.8% of PPD cases were attributable to AD.
The findings should inform future clinical guidelines on the screening, the frequency of screening, and follow-up care in maternal-mental health.

The number of cases of dementia attributable to physical inactivity remains unclear due to heterogeneity in physical inactivity definitions and statistical approaches used.
Studies that used population-based samples to estimate the population attributable fraction (PAF) of physical inactivity for dementia were included in this review. Weighted PAFs were adjusted for communality among the risk factors (i.e., inactive persons may also share other risk factors) analyzed. Values were reported as percentage (%) of cases of dementia attributable to physical inactivity.
We included 22 studies. The overall impact of physical inactivity, defined by any criteria, on dementia ranged from 6.6% (95% CI: 3.6%, 9.6%; weighted) to 16.6% (95% CI: 14.4%, 18.9%; unweighted). Studies using the WHO criterion for physical inactivity estimated a higher unweighted impact (β = 7.3%; 95% CI: 2.0%, 12.6%) than studies using other criteria.
Conservatively, one in 15 cases of dementia may be attributable to physical inactivity, defined by any criteria.

OBJECTIVE: To assess the region-specific relative risk of cardia/non-cardia gastric cancer (CGC/NCGC) associated with Helicobacter pylori (H. pylori) and quantify its contribution to gastric cancer burden using population attributable fraction (PAF).
METHODS: PubMed, EMBASE, Web of Science, and Cochrane Central databases were searched by two reviewers until April 20, 2022. The association between H. pylori infection and NCGC/CGC was assessed using pooled odds ratios (ORs) with 95% confidence intervals (CIs). PAF was calculated using the formula of H. pylori prevalence and the pooled OR.
RESULTS: One hundred and eight studies were included. A significant association was observed between H. pylori infection and NCGC in East Asia (OR, 4.36; 95% CI: 3.54-5.37) and the West (OR, 4.03; 95% CI: 2.59-6.27). Regarding CGC, a significant association was found only in East Asia (OR, 2.86; 95% CI: 2.26-3.63), not in the West (OR, 0.80; 95% CI: 0.61-1.05). For studies with a follow-up time of ≥10 years, pooled ORs for NCGC and CGC in East Asia were 5.58 (95% CI: 4.08-7.64) and 3.86 (95% CI: 2.69-5.55), respectively. Pooled OR for NCGC was 6.80 (95% CI: 3.78-12.25) in the West. PAFs showed that H. pylori infection accounted for 71.2% of NCGC, 60.7% of CGC in East Asia, and 73.2% of NCGC in the West.
CONCLUSIONS: Gastric cancer burden associated with H. pylori infection exhibits important geographical differences. Prolonged follow-up period could overcome the underestimation of the magnitude of the association between H. pylori infection and CGC/NCGC. Customized strategies for H. pylori screening and eradication should be implemented to prevent gastric cancer.

The long-term associations between the consumption of sugar-sweetened beverages (SSBs) and low-calorie sweetened beverages (LCSBs) with cardiovascular diseases (CVDs) remains inconsistent. To synthesize the evidence, we conducted a meta-analysis of prospective cohort studies published up to 1 December, 2019 on the associations between SSB and LCSB intake and the risk of CVD incidence and mortality. Out of 5301 articles retrieved from our literature search, 11 articles evaluating the consumption of SSBs (16,915 incident CVD cases, 18,042 CVD deaths) and 8 articles evaluating the consumption of LCSBs (18,077 incident CVD cases, 14,114 CVD deaths) were included in the meta-analysis. A 1 serving/d increment of SSBs was associated with an 8% (RR: 1.08; 95% CI: 1.02, 1.14, I2 = 43.0%) and 8% (RR: 1.08; 95% CI: 1.04, 1.13, I2 = 40.6%) higher risk of CVD incidence and CVD mortality, respectively. A 1 serving/d increment of LCSBs was associated with a 7% (RR: 1.07; 95% CI: 1.05, 1.10, I2 = 0.0%) higher risk of CVD incidence. The association between LCSBs and CVD mortality appeared to be nonlinear (P = 0.003 for nonlinearity) with significant associations observed at high intake levels (>2 servings/d). Under an assumption of causality, the consumption of SSBs may be linked to 9.3% (95% CI: 6.6%, 11.9%) of predicted CVD incidence in the USA from 2015 to 2025, among men and nonpregnant women, who were aged 40-79 y in 2015-2016. The habitual consumption of SSBs was associated with a higher risk of CVD morbidity and mortality in a dose-response manner. LCSBs were also associated with a higher risk of these outcomes, however, the interpretation of these findings may be complicated by reverse causation and residual confounding.

Our aim was to provide a systematic review of studies on the burden of disease due to second-hand smoke (SHS) exposure, reviewing methods, exposure assessment, diseases causally linked to SHS, health outcomes, and estimates available to date. A literature review of studies on the burden of disease from SHS exposure, available in PubMed and SCOPUS, published 2007-2018 in English language, was carried out following the PRISMA recommendations. Overall, 588 studies were first identified, and 94 were eligible. Seventy-two studies were included in the systematic review. Most of them were based on the comparative risk assessment approach, assessing SHS exposure using mainly surveys on exposure at home/workplaces. Diseases more frequently studied were: lung cancer, ischemic heart disease, stroke, chronic obstructive pulmonary disease, asthma and breast cancer in adults; lower respiratory tract infection, otitis media, asthma, sudden infant death syndrome and low birth weight in children. The SHS exposure assessment and the reported population attributable fractions (PAF) were largely heterogeneous. As an example, the PAF from lung cancer varied between 0.6% and 20.5%. Moreover, PAF were estimated applying relative risks and SHS exposures with no consistent definitions or with different age classes. The research gap on the SHS exposure burden is shrinking. However, estimates are not yet available for a number of countries, particularly the Middle Eastern and African countries, and not all diseases with the strongest evidence of causation, such as sudden infant death syndrome, have been explored. Moreover, in some cases the applied methodology revealed relatively low quality of data.

Worldwide, the burden of cancer is rising, stimulating efforts to develop strategies to control these diseases. Primary prevention, a key control strategy, aims to reduce cancer incidence through programs directed towards reducing population exposure to known causal factors. Before enacting such strategies, it is necessary to estimate the likely effect on cancer incidence if exposures to known causal factors were reduced or eliminated. The population attributable fraction (PAF) is the epidemiological measure which quantifies this potential reduction in incidence. We surveyed the literature to document and summarise the proportions of cancers across the globe attributable to modifiable causes, specifically tobacco smoke, alcohol, overweight/obesity, insufficient physical activity, solar ultraviolet (UV) radiation and dietary factors (insufficient fruit, non-starchy vegetables and fibre; red/processed meat; salt). In total, we identified 55 articles that presented PAF estimates for one or more causes. Information coverage was not uniform, with many articles reporting cancer PAFs due to overweight/obesity, alcohol and tobacco, but fewer reporting PAFs for dietary factors or solar UV radiation. At all cancer sites attributable to tobacco and alcohol, median PAFs were markedly lower for women than men. Smoking contributed to very high median PAFs (>50%) for cancers of the lung and larynx. Median PAFs for men, attributable to alcohol, were high (25-50%) for cancers of the oesophagus, oral cavity/pharynx, larynx and liver. For cancers causally associated with overweight/obesity, high median PAFs were reported for oesophageal adenocarcinoma (men 29%, women 37%), gallbladder (men 11%, women 42%) and endometrium (36%). The cancer PAF literature is growing rapidly. Repeating this survey in the future should lead to more precise estimates of the potentially preventable fractions of cancer.

BACKGROUND: Literature supports a strong relationship between childhood maltreatment and mental illness but most studies reviewed are cross-sectional and/or use recall to assess maltreatment and are thus prone to temporality and recall bias. Research on the potential prospective impact of maltreatment reduction on the incidence of psychiatric disorders is scarce.
METHODS: Electronic databases and grey literature from 1990 to 2014 were searched for English-language cohort studies with criteria for depression and/or anxiety and non-recall measurement of childhood maltreatment. Systematic review with meta-analysis synthesized the results. Study quality, heterogeneity, and publication bias were examined. Initial screening of titles and abstracts resulted in 199 papers being reviewed. Eight high-quality articles met eligibility criteria. Population attributable fractions (PAFs) estimated potential preventive impact.
RESULTS: The pooled odds ratio (OR) between any type of maltreatment and depression was 2.03 [95% confidence interval (CI) 1.37-3.01] and 2.70 (95% CI 2.10-3.47) for anxiety. For specific types of maltreatment and depression or anxiety disorders, the ORs were: physical abuse (OR 2.00, 95% CI 1.25-3.19), sexual abuse (OR 2.66, 95% CI 1.88-3.75), and neglect (OR 1.74, 95% CI 1.35-2.23). PAFs suggest that over one-half of global depression and anxiety cases are potentially attributable to self-reported childhood maltreatment. A 10-25% reduction in maltreatment could potentially prevent 31.4-80.3 million depression and anxiety cases worldwide.
CONCLUSIONS: This review provides robust evidence of childhood maltreatment increasing the risk for depression and anxiety, and reinforces the need for effective programs and policies to reduce its occurrence.

BACKGROUND: The aetiology of pancreatic cancer (PC) has been extensively studied and is the subject of numerous meta-analyses and pooled analyses. We have summarized results from these pooled and meta-analytical studies to estimate the fraction of PCs attributable to each of the identified risk factors.
METHODS: Using a comprehensive strategy, we retrieved 117 meta-analytical or pooled reports dealing with the association between specific risk factors and PC risk. We combined estimates of relative risk and estimates of exposure to calculate the fraction of PCs caused or prevented by a particular exposure.
RESULTS: Tobacco smoking (\'strong\' evidence) and Helicobacter pylori infection (\'moderate\' evidence) are the major risk factors associated with PC, with respective estimated population attributable fractions of 11-32% and 4-25%. The major protective factors are history of allergy (\'strong\' evidence) and increasing fruit or folate intake (\'moderate\' evidence), with respective population preventable fractions of 3-7% and 0-12%.
CONCLUSIONS: We summarized results of 117 meta-analytical or pooled data reports dealing with 37 aetiological exposures, to obtain robust information about the suspected causes of PC. By combining these estimates with their prevalences in the population, we calculated population attributable or population preventable fractions. About two-thirds of the major risk factors associated with PC are potentially modifiable, affording a unique opportunity for preventing one of our deadliest cancers.