Background Given the projected trends in population ageing and population growth, the number of people with dementia is expected to increase. In addition, strong evidence has emerged supporting the importance of potentially modifiable risk factors for dementia. Characterising the distribution and magnitude of anticipated growth is crucial for public health planning and resource prioritisation. This study aimed to improve on previous forecasts of dementia prevalence by producing country-level estimates and incorporating information on selected risk factors. MethodsWe forecasted the prevalence of dementia attributable to the three dementia risk factors included in the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019 (high body-mass index, high fasting plasma glucose, and smoking) from 2019 to 2050, using relative risks and forecasted risk factor prevalence to predict GBD risk-attributable prevalence in 2050 globally and by world region and country. Using linear regression models with education included as an additional predictor, we then forecasted the prevalence of dementia not attributable to GBD risks. To assess the relative contribution of future trends in GBD risk factors, education, population growth, and population ageing, we did a decomposition analysis. FindingsWe estimated that the number of people with dementia would increase from 57•4 (95% uncertainty interval 50•4-65•1) million cases globally in 2019 to 152•8 (130•8-175•9) million cases in 2050. Despite large increases in the projected number of people living with dementia, age-standardised both-sex prevalence remained stable between 2019 and 2050 (global percentage change of 0•1% [-7•5 to 10•8]). We estimated that there were more women with dementia than men with dementia globally in 2019 (female-to-male ratio of 1•69 [1•64-1•73]), and we expect this pattern to continue to 2050 (female-to-male ratio of 1•67 [1•52-1•85]). There was geographical heterogeneity in the projected increases across countries and regions, with the smallest percentage changes in the number of projected dementia cases in high-income Asia Pacific (53% [41-67]) and western Europe (74% [58-90]), and the largest in north Africa and the Middle East (367% [329-403]) and eastern sub-Saharan Africa (357% [323-395]). Projected increases in cases could largely be attributed to population growth and population ageing, although their relative importance varied by world region, with population growth contributing most to the increases in sub-Saharan Africa and population ageing contributing most to the increases in east Asia. Interpretation Growth in the number of individuals living with dementia underscores the need for public health planning efforts and policy to address the needs of this group. Country-level estimates can be used to inform national planning efforts and decisions. Multifaceted approaches, including scaling up interventions to address modifiable risk factors and investing in research on biological mechanisms, will be key in addressing the expected incr...

Background Hearing loss affects access to spoken language, which can affect cognition and development, and can negatively affect social wellbeing. We present updated estimates from the Global Burden of Disease (GBD) study on the prevalence of hearing loss in 2019, as well as the condition's associated disability. Methods We did systematic reviews of population-representative surveys on hearing loss prevalence from 1990 to 2019. We fitted nested meta-regression models for severity-specific prevalence, accounting for hearing aid coverage, cause, and the presence of tinnitus. We also forecasted the prevalence of hearing loss until 2050. Findings An estimated 1•57 billion (95% uncertainty interval 1•51-1•64) people globally had hearing loss in 2019, accounting for one in five people (20•3% [19•5-21•1]). Of these, 403•3 million (357•3-449•5) people had hearing loss that was moderate or higher in severity after adjusting for hearing aid use, and 430•4 million (381•7-479•6) without adjustment. The largest number of people with moderate-to-complete hearing loss resided in the Western Pacific region (127•1 million people [112•3-142•6]). Of all people with a hearing impairment, 62•1% (60•2-63•9) were older than 50 years. The Healthcare Access and Quality (HAQ) Index explained 65•8% of the variation in national agestandardised rates of years lived with disability, because countries with a low HAQ Index had higher rates of years lived with disability. By 2050, a projected 2•45 billion (2•35-2•56) people will have hearing loss, a 56•1% (47•3-65•2) increase from 2019, despite stable age-standardised prevalence. Interpretation As populations age, the number of people with hearing loss will increase. Interventions such as childhood screening, hearing aids, effective management of otitis media and meningitis, and cochlear implants have the potential to ameliorate this burden. Because the burden of moderate-to-complete hearing loss is concentrated in countries with low health-care quality and access, stronger health-care provision mechanisms are needed to reduce the burden of unaddressed hearing loss in these settings. Funding Bill & Melinda Gates Foundation and WHO.

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Incense smoke is increasingly being recognized as a potential environmental contaminant and is linked to malignant and non-malignant respiratory diseases. The detoxification of environmental contaminants including polycyclic aromatic hydrocarbons (PAHs) involves the induction of cytochrome P-450 family enzymes (CYPs) by PAHs. However, the detoxification of PAHs also results in the generation of reactive and unstable intermediary metabolites which are implicated in the oxidative stress, DNA damage, and inflammation. It is unclear whether CYPs are similarly induced by incense smoke, which incidentally contains substantial amounts of PAHs. Here, we examined the impact of long-term incense smoke exposure on the induction of CYPs in male Wister Albino rats. Incense smoke exposure significantly induced the expression of CYP1A1, CYP1A2, and CYP1B1 mRNAs in both lung and liver tissues. The extent of CYP1A1 and CYP1B1 induction was significantly higher in the liver compared to that in the lung, while that of CYP1A2 was greater in the lung than in liver. Incense smoke exposure also increased malondialdehyde and reduced glutathione levels in lung and liver tissues, and the catalase activity in the liver tissues to significant levels. Furthermore incense smoke exposure led to a marked increase in TNF-α and IL-4 levels. The data demonstrate for the first time the capacity of incense smoke to induce CYP1 family enzymes in the target and non-target tissues. Induction of CYPs increased oxidative stress and inflammation appear to be intimately linked to promote the carcinogenesis and health complications in people chronically exposed to incense smoke.

~ ~~~~~~~~~~~~~Male broiler chicks (I-d-old; Ross one) were given either a control diet containing recommended levels of phosphorus, calcium and cholecalciferol or experimental diets low in P and with variable levels of Ca (normal and low) and cholecalciferol (normal or high). The low-P diet with normal levels of Ca and cholecalciferol induced a hypophosphataemia and a hypercalcaemia which was reflected in reduced tibia length and weight and in reduced Ca, P and magnesium contents of tibia. The phytate digestibility remained normal while the retention of P and Ca fell significantly. The lowering of Ca alone elevated phytate digestibility and restored P and Ca retention. The hypercalcaemia and hypophosphataemia remained and tibia mineralization remained impaired. The raising of cholecalciferol alone dramatically increased phytate digestibility and the retention of Ca and P. While this remedied the hypercalcaemia, the hypophosphataemia persisted as did the diminution of tibia weight. The simultaneous lowering of dietary Ca and elevation of cholecalciferol on low-P diets restored all variables to the levels for the control diet. Circulating levels of 1,25-dihydroxycholecalciferol were significantly elevated by low-P diets, more so with high cholecalciferol intakes. However, Ca did not influence 1,29dihydroxy-cholecalciferol levels in plasma.