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Background and Objectives: Telomere length (TL) has been acknowledged as biomarker of biological aging. Numerous investigations have examined associations between individual early life factors and leukocyte TL; however, the findings were far from consistent. Research Design and Methods: We evaluated the relationship between individual and combined early life factors and leukocytes TL in middle and late life using data from the UK Biobank. The early life factors (eg, maternal smoking, breastfeeding, birth weight, and comparative body size and height to peers at age 10) were measured. The regression coefficients (β) and 95% confidence interval (CI) were applied to assess the link of the early life factors and TL in adulthood. Flexible parametric survival models incorporated age to calculate the relationship between early life factors and life expectancy. Results: Exposure to maternal smoking, lack of breastfeeding, low birth weight, and shorter height compared to peers at age 10 were identified to be associated with shorter TL in middle and older age according to the large population-based study with 197 504 participants. Individuals who experienced more than 3 adverse early life factors had the shortest TL in middle and late life (β = −0.053; 95% CI = −0.069 to −0.038; p < .0001), as well as an average of 0.54 years of life loss at the age of 45 and 0.49 years of life loss at the age of 60, compared to those who were not exposed to any early life risk factors. Discussion and Implications: Early life factors including maternal smoking, non-breastfed, low birth weight, and shorter height compared to peers at age 10 were associated with shorter TL in later life. In addition, an increased number of the aforementioned factors was associated with a greater likelihood of shorter TL in adulthood, as well as a reduced life expectancy. [ABSTRACT FROM AUTHOR]

Background: Sedentary behavior (SB) has emerged as a significant health concern that deserves attention. This study aimed to examine the associations between prolonged sedentary behavior and the risk of all-cause and cause-specific mortality as well as to explore desirable alternatives to sitting in terms of physical activity (PA). Methods: Two prospective cohort investigations were conducted using the UK Biobank and NHANES datasets, with a total of 490,659 and 33,534 participants, respectively. Cox proportional hazards regression models were used to estimate the associations between SB and the risk of all-cause and cause-specific mortality due to cancer, cardiovascular disease (CVD), respiratory diseases, and digestive diseases. In addition, we employed isotemporal substitution models to examine the protective effect of replacing sitting with various forms of PA. Results: During the average follow-up times of 13.5 and 6.7 years, 36,109 and 3057 deaths were documented in the UK Biobank and NHANES, respectively. Both cohorts demonstrated that, compared with individuals sitting less than 5 h per day, individuals with longer periods of sitting had higher risks of all-cause and cause-specific mortality due to cancer, CVD, and respiratory diseases but not digestive diseases. Moreover, replacing SB per day with PA, even substituting 30 min of walking for pleasure, reduced the risk of all-cause mortality by 3.5% (hazard ratio [HR] 0.965, 95% confidence interval [CI] 0.954–0.977), whereas cause-specific mortality from cancer, CVD, and respiratory diseases was reduced by 1.6% (HR 0.984, 95% CI 0.968–1.000), 4.4% (HR 0.956, 95% CI 0.930–0.982), and 15.5% (HR 0.845, 95% CI 0.795–0.899), respectively. Furthermore, the protective effects of substitution became more pronounced as the intensity of exercise increased or the alternative duration was extended to 1 h. Conclusions: SB was significantly correlated with substantially increased risks of all-cause mortality and cause-specific mortality from cancer, CVD, and respiratory diseases. However, substituting sitting with various forms of PA, even for short periods involving relatively light and relaxing physical activity, effectively reduced the risk of both overall and cause-specific mortality. [ABSTRACT FROM AUTHOR]

A recent study published in the journal Clinical & Experimental Allergy examined the association between sleep patterns, lifestyle behaviors, genetic predisposition, and the risk of adult-onset asthma. The study found that poor sleep patterns increased the risk of developing asthma in adults. The association between sleep patterns and asthma risk was influenced by lifestyle behaviors and genetic vulnerability. Individuals with poor lifestyles and high genetic susceptibility had a higher risk of developing asthma. The study highlights the importance of integrated interventions targeting sleep and lifestyle factors in preventing adult-onset asthma. [Extracted from the article]

Background: Previous observational studies investigated the relationship between coffee and tea intake and the risk of asthma, however, the conclusions were inconsistent. Further, the combined effect of coffee and tea consumption on asthma has rarely been studied. Methods: We examined associations between the self-reported intake of tea and coffee and the risk of incident asthma in a total of 424,725 participants aged from 39 to 73 years old from the UK Biobank. Cox proportional hazards models were used to estimate the associations between coffee/tea consumption and incident adult-onset asthma, adjusting for age, sex, race, smoking status, body mass index (BMI), education, and Townsend deprivation index. Results: Cox models with penalized splines showed J-shaped associations of coffee, tea, caffeinated coffee, and caffeine intake from coffee and tea with the risk of adult-onset asthma (p for nonlinear <0.01). Coffee intake of 2 to 3 cups/d (hazard ratio [HR] 0.877, 95% confidence interval [CI] 0.826–0.931) or tea intake of 0.5 to 1 cups/d (HR 0.889, 95% CI 0.816–0.968) or caffeinated coffee intake of 2 to 3 cups/d (HR 0.858, 95% CI 0.806–0.915) or combination caffeine intake from tea and coffee of 160.0 to 235.0 mg per day (HR 0.899, 95% CI 0.842–0.961) were linked with the lowest hazard ratio of incident asthma after adjustment for age, sex, race, smoking status, BMI, qualification, and Townsend deprivation index. Conclusions: Collectively, the study showed light-to-moderate coffee and tea consumption was associated with a reduced risk of adult-onset asthma and controlling total caffeine intake from coffee and tea for a moderate caffeine dose of 160.0 to 305.0 mg/day may be protective against adult-onset asthma. Further investigation on the possible preventive role of caffeine in asthma is warranted. [ABSTRACT FROM AUTHOR]

Numerous studies have explored the association of air pollution with asthma but have yielded conflicting results. The exact role of air pollution in the incidence of adult-onset asthma and whether this effect is modified by genetic risk, lifestyle, or their interaction remain uncertain. We conducted a prospective cohort study on 298,738 participants (aged 37–73 years) registered in the UK Biobank. Cox proportional hazard models were used to evaluate the association of air pollution, including particulate matter (PM 2.5 , PM coarse , and PM 10), nitrogen dioxide (NO 2), and nitrogen oxides (NO x), with asthma incidence. We constructed genetic risk and lifestyle scores, assessed whether the impact of air pollution on adult-onset asthma risk was modified by genetic susceptibility or lifestyle factors, and evaluated the identified interactions. We found that each interquartile range increase in annual concentrations of PM 2.5 , NO 2 , and NO x was related to 1.04 (95% confidence interval [CI]: 1.01, 1.08), 1.04 (95% CI: 1.00, 1.08), and 1.03 (95% CI: 1.00, 1.06) times the risk of adult-onset asthma, respectively. The size of the effect of air pollution was greater among subpopulations with low genetic risk or unfavorable lifestyles. We also identified an additive interaction effect of air pollution with lifestyle factors, but not with genetic risk, on the risk of adult-onset asthma. Our analyses show that air pollution increases the risk of adult-onset asthma, but that the size of the effect is modified by lifestyle and genetic risk. These findings emphasize the need for integrated interventions for environmental pollution by the government as well as adherence to healthy lifestyles to prevent adult-onset asthma. [Display omitted] • Air pollution significantly increased the incidence of adult-onset asthma. • The effect of air pollution on asthma was modified by lifestyle or genetic risk. • Air pollution and lifestyle factors demonstrate additive interactions. [ABSTRACT FROM AUTHOR]

The effect of air pollution exposure on incident lung cancer remains uncertain, and the modifying role of lifestyle and genetic susceptibility in association between air pollution and lung cancer is ambiguous. A total of 367,623 participants from UK biobank cohort were enrolled in the analysis. The concentrations of particle matter (PM 2.5 , PM 10), nitrogen dioxide (NO 2), and nitrogen oxides (NO x), were evaluated by land-use regression model. Cox proportional hazard model was applied to assess the associations between air pollution and incident lung cancer. A lifestyle risk score and a polygenic risk score were established to investigate whether lifestyle and heritable risk could modify the effect of air pollution on lung cancer risk. Per interquartile range (IQR) increment in annual concentrations of PM 2.5 (HR = 1.22, 95% CI, 1.15∼1.30), NO 2 (HR = 1.19, 95% CI, 1.10∼1.27), and NO x (HR = 1.14, 95% CI, 1.09∼1.20) were associated with increased risk of lung cancer. We observed an additive interaction between air pollution including PM 2.5 and NO x and lifestyle or genetic risk. Individuals with high air pollution exposure, poor lifestyle and high genetic risk had the highest risk of incident lung cancer. Long-term exposures to air pollution is associated with increased risk of lung cancer, and this effect was modified by lifestyle or genetic risk. Integrated interventions for environmental pollution by government and adherence to healthy lifestyle by individuals are advocated for lung cancer prevention. • Exposure to air pollution was associated with increased risk of lung cancer. • The effect of air pollution was modified by lifestyle and genetic risk. • Improving air pollution is important in lung cancer prevention. • Adherence to healthy lifestyle is necessary in lung cancer prevention. [ABSTRACT FROM AUTHOR]

Introduction: Vitamin D has been known to be associated with asthma, particularly in children, while the evidence among adults is limited and inconclusive. This study aimed to investigate the association between serum, vitamin D concentrations, and the incidence of adult-onset asthma and also the modified effect caused by sleep patterns and genetic risks., Methods: A prospective cohort study with 307,872 participants aged between 37 and 73 years was conducted based on the UK Biobank, with a median follow-up of 12 years. The Cox proportional hazard model was applied to evaluate the association between vitamin D status and incident adult-onset asthma, and the modified effect was investigated by conducting stratified analysis according to sleep pattern score and genetic risk score, and subgroup analyses were performed by sex, age, BMI, and smoking status as well., Results: Individuals with optimal vitamin D concentration were associated with 11.1% reduced risk of incident asthma compared to those participants with deficient vitamin D (HR = 0.889; 95% CI: 0.820-0.964; p = 0.005). Moreover, stratification analysis demonstrated that the protective effect of vitamin D on asthma risk was modified by sleep patterns or genetic susceptibility, with the strongest protective effect being observed in the subpopulation with a moderate sleep pattern (HR = 0.883; 95% CI: 0.797-0.977; p = 0.016) and a moderate genetic risk (HR = 0.817; 95% CI: 0.711-0.938; p = 0.004). In subgroup analyses, the protective effect of optimal vitamin D levels was only significant among men, individuals younger than 60 years of age, overweight individuals, and current or previous smokers., Conclusion: Increased serum vitamin D levels were associated with a lower risk of incident adult-onset asthma, and this association was modified by sleep patterns and genetic predisposition to some extent., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Chang, Zhu, Zhou, Liang, Li, Cheng, Pan and Zhang.)

Background: Both genetic and lifestyle factors contribute to the development of asthma, but whether unfavourable lifestyle is associated with similar increases in risk of developing asthma among individuals with varying genetic risk levels remains unknown., Methods: A healthy lifestyle score was constructed using body mass index, smoking status, physical activities and dietary pattern to further categorise into ideal, intermediate and poor groups. Genetic risk of asthma was also categorised as three groups based on the tertiles of polygenic risk score established using 212 reported and verified single-nucleotide polymorphisms of European ancestry in the UK Biobank study. We examined the risk of incident asthma related with each lifestyle level in each genetic risk group by Cox regression models., Results: Finally, 327 124 participants without baseline asthma were included, and 157 320 (48.1%) were male. During follow-up, 6238 participants (1.9%) developed asthma. Compared to ideal lifestyle in a low genetic risk group, poor lifestyle was associated with a hazard ratio of up to 3.87 (95% CI, 2.98-5.02) for developing asthma in a high genetic risk group. There was interaction between genetic risk and lifestyle, and the population-attributable fraction of lifestyle and genetic risk were 30.2% and 30.0% respectively., Conclusion: In this large contemporary population, lifestyle and genetic factors jointly play critical roles in the development of asthma, and the effect values of lifestyle on incident adult-onset asthma were greater than that of genetic risk. Our findings highlighted the necessity of a comprehensive intervention for the prevention of asthma despite the genetic risk., Competing Interests: Conflict of interest: The authors declare no conflict of interests., (Copyright ©The authors 2023.)

Purpose: Leptospirosis is a zoonotic disease caused by pathogenic spirochetes of the genus Leptospira. However, there is currently no consensual definition or diagnostic criteria for severe and different forms of leptospirosis. Therefore, more insight on clinical manifestations, risk factors, and outcomes of leptospirosis is warranted. The identification of leptospirosis with distinct clinical manifestations and prognosis in our population., Methods: Multiple correspondence analysis and hierarchical classification on principal components were presented to identify different clinical types of leptospirosis. The outcomes were clinical phenotypes, laboratory and imaging findings, and prognosis., Results: The 95 enrolled patients had median values of 54.0 years (39.0-65.0) for age, 9.0 (7.0-14.0) for total hospital stay lengths, of whom 86.3% was male and 40.0% was transferred to ICU. Three clinical types were distinguished: mild leptospirosis (n=43, 45.3%) with less organ dysfunction and shorter hospital stays; respiratory leptospirosis (n=28, 29.5%) with hemoptysis, and respiratory and circulatory failure; and hepato-renal leptospirosis (n=24, 25.3%) with worst liver and kidney dysfunction. Total hospital mortality was 15.8% and was associated with dyspnea and high levels of neutrophil counts., Conclusions: The identification of leptospirosis with distinct clinical manifestations and prognosis in our population may assist clinicians to distinguish leptospirosis-like disease. Moreover, dyspnea and neutrophil count were found to be independent risk factors for severe leptospirosis progression., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Li, Liang, Yi, Xiao, Zhu, Chang, Zhou, Liu, He, Liu, Fan, Cheng, Wang, Zhang and Pan.)

Background: Vitamin D has been known to be associated with asthma. However, the association between vitamin D status and asthma, lung function as well as hospitalization among adults remains unclear., Objective: To investigate the role of serum vitamin D in asthma prevalence, lung function, and asthma control in adults., Methods: Multivariable logistic regression was applied to assess the relationship between serum vitamin D and asthma prevalence, lung function (FEV1, FVC, and FEV1/FVC), current wheeze, and asthma-linked hospitalizations in a cross-sectional study of 435,040 adults aged 37-73 years old from the UK Biobank., Results: Compared to vitamin D deficiency, the odds of asthma were decreased by 6.4% [adjusted odds ratio ( aOR ) = 0.936; 95% CI : 0.911-0.962; p < 0.001] and 9.8% ( aOR = 0. 0.902; 95% CI : 0.877-0. 0.927; p < 0.001) in individuals with insufficient and optimal vitamin D concentration, respectively, in the fully adjusted model. In total asthmatic patients, serum vitamin D was obviously and positively related with FEV1 (β = 1.328 ml, 95% CI = 0.575-2.080), FVC (β = 2.018 ml, 95% CI = 1.127-2.908), and FEV1/FVC (β = 0.006%, 95% CI = 0.002-0.010). Asthmatic patients whose vitamin D level was in the deficient category had 9.3-19.9% higher odds of current wheeze than insufficient categories ( aOR = 0.907; 95% CI : 0.861-0.957; p < 0.001) and optimal categories ( aOR = 0.801; 95% CI : 0.759-0.845; p < 0.001), but the relationship between vitamin D and asthma hospitalization was not significant., Conclusion: Vitamin D deficiency was related to higher odds of asthma and current wheeze, and lower lung function in a large sample size study of British adults. Our results indicate a potential positive impact of serum vitamin D on asthma occurrence and disease control in adults., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Zhu, Jing, Liang, Li, Chang, Shen, Pan, Liu and Zhang.)

Objective: Talaromyces marneffei (TM) is an opportunistic fungus that is predominantly prevalent among patients who are HIV-positive in South-East Asia. However, few studies focused on the clinical features, laboratory findings, and prognosis across varying immune states., Methods: A total of 54 patients with TM infection in Xiangya Hospital of Central South University from January 1, 2006 to October 31, 2021 were retrospectively analyzed. Clinical profiles were compared across the different immune statuses by HIV-positive (HIV group, n = 18), HIV negative but with immunocompromised conditions (Non-HIV with IC Group, n = 11), and immunocompetent patients ( n = 25)., Results: All the patients were diagnosed by pathogen culture or by metagenomic next-generation sequencing (mNGS). The median age was 50, and patients with HIV were much younger compared to the other two groups. The most common symptom at presentation was fever (79.6%), followed by cough (70.4%), weight loss (61.1%), and expectoration (53.7%). The patients with HIV were more likely to develop into a subtype of disseminated TM affecting multiple organs including lymph node, liver, skin, and spleen, thus, resulting in higher hospital mortality compared to the other two groups. Patients without HIV but with immunocompromised conditions presented similar hospital mortality rates compared to immunocompetent patients, while experiencing longer days of hospitalization to recover from the diseases. Additionally, in this study, the pathogen culture easily confirmed the patients with HIV. However, mNGS presented as a promising tool to confirm TM infection in those suspicious patients without HIV., Conclusions: In summary, patients with HIV were more likely to develop into disseminated TM, resulting in higher mortality compared to those patients without HIV. Additionally, mNGS presented as an important supplementary tool to confirm TM infection in patients without HIV, particularly in those with immunocompromised diseases., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Li, Liang, Zhu, Chang, Pan and Zhang.)