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Increasing evidence highlights the role of disrupted circadian rhythms in the neural dysfunctions and sleep disturbances observed in autism spectrum disorder and attention-deficit/hyperactivity disorder. However, the causality and directionality of these associations remain unclear. In this study, we employed a bidirectional two-sample Mendelian randomization framework, leveraging genome-wide association study data from the UK Biobank (n = 85,670) and FinnGen (n = 377,277). Genetic variants served as instrumental variables to infer causation, and objective accelerometer-derived metrics identified circadian rhythm and sleep genetic instruments. The results showed that the timing of the most active 10 h was significantly linked to higher odds of autism spectrum disorder and attention-deficit/hyperactivity disorder. Independently, higher sleep efficiency predicted a lower risk of autism spectrum disorder, while attention-deficit/hyperactivity disorder was linked to an increase in nocturnal sleep episodes. Heterogeneity and sensitivity analyses confirmed these findings. Our study establishes causal links between circadian alterations and autism spectrum disorder and attention-deficit/hyperactivity disorder, distinguishing the independent and protective role of sleep efficiency in autism spectrum disorder from circadian rhythms. In attention-deficit/hyperactivity disorder, however, disrupted sleep appears as a consequence, not a cause. These insights highlight divergent interactions with sleep factors in autism spectrum disorder and attention-deficit/hyperactivity disorder, laying the groundwork for tailored therapeutic strategies that recognize the distinct influences of sleep quality and circadian rhythms in each disorder.

Despite the importance of a thriving workforce in sustaining organizational success, prior research pays little attention to how individualized human resource (HR) practices can help individual employees to thrive at work. Drawing on the theoretical underpinnings of conservation of resources theory, we investigate whether, how, and when development idiosyncratic deals (i‐deals) can contribute to individual thriving. We contend that possessing development i‐deals will motivate individuals to engage in approach job crafting, which in turn promotes their experience of thriving at work. We further contend that high‐quality leader–member exchange will enhance the function of development i‐deals in triggering approach job crafting and subsequent thriving experiences. Results from a two‐wave survey involving 278 managers in a pharmaceutical firm in China and a three‐wave survey among 178 managers working in various organizations in the UK support our hypotheses. Our findings provide new insights for practitioners seeking to design customized HR practices to support a thriving workforce. [ABSTRACT FROM AUTHOR]

This paper explores Sustainable Development Goals (SDGs) knowledge and behavioural differences of university students in the United Kingdom and Malaysia. The researchers also explore gender as an indicator of students' SDG awareness and behaviours as few studies to date have explored this area. This study employed a sustainability consciousness questionnaire (SCQ) that was developed to measure SDG knowledge based on the UNESCO framework for sustainability behaviour. Questionnaires were distributed to 156 university students in the UK and Malaysia. Malaysian university students reported higher scores for understanding SDG content and scope and the specific SDGs of their country compared to British students, although British students have been receiving formal education on SDGs. University students in the UK were also unable to transform their SDG knowledge into sustainability behaviours, although they had a certain level of understanding of the topic covered by the SDGs. Malaysian university students exhibited a closer relationship between SDG knowledge and sustainable behaviours given the sufficient institutional and policy support and customised university programs. SDG knowledge and sustainability behaviours were the same for male and female students in both countries. In conclusion, integrating SDG knowledge into university education will inevitably lead students to work towards SDG goals in the future. This can be achieved with proper planning of the university curriculum and the enforcement of educational policies.

Digital technologies have been widely used in higher education (HE) for years, and the benefits have been recognised by both students and academics. Although many universities have developed their own digital technology strategies, many do not share either their vision or implementation strategies with staff. This research explores differences and similarities in the perception of digital technology by lecturers and academic managers. The purpose of this paper is to compare and contrast motivations, barriers and support systems required for the use and adoption of digital strategies. Interviews were conducted with a group of 20 lecturers and academic managers in the HE sector. The results reveal that both groups shared a common view that the introduction of digital technology can have a clear set of benefits to students; however, their motivations for introducing new approaches differed significantly. Whilst it is important not to generalise too much given the lack of homogeneity in the two groups and also the crossover between managers and lecturers, managers tended to take a performance goal-based approach to its introduction whilst lecturers were more learning goal orientated. This difference can cause significant difficulties in the implementation of new approaches to learning.

The extensive and intensive online teaching and learning during the pandemic has provided good opportunities for academic staff and students to experiment with learning and teaching using synchronous communication technology and learning platforms. This experience is highly valuable for helping higher education institutions move learning and teaching practices forward after the pandemic. Indeed, many universities are considering adopting blended learning in the new era. However, it is worth noting that a number of emerging issues related to student behaviour also appeared during online learning, such as teaching to blank screens, students' inappropriate use of social media icons, languages and their inappropriate outfits. It appears that these issues have not yet been investigated properly, and are not addressed by the existing codes of conduct, since these have been written mainly for face-to-face teaching. This study offers some important insights into students' unprofessional online behaviour from tutors' perspective, and also the experiences of academic tutors in managing such behaviour in formal online learning and teaching environments. It used semi-structured interviews to collect data, and analysed the narratives of 20 academic staff working in UK universities. The findings report and describe students' unprofessional online behaviours witnessed by academic tutors in different academic disciplines. The findings also suggest that special attention needs to be paid to policymaking regarding online learning, in particular, in the area of students' online professionalism.

This article examines the dynamics of heritage language (HL) identity development by analysing the life history accounts of three Chinese heritage language (CHL) learners growing up in the UK. Drawing on narrative data, the study contributes to the growing body of HL identity research by capturing the individual trajectories of CHL learners engaging with different interlocutors, at multiple sites, and across the lifespan. We report the various ways our participants are positioned by the essentialist discourses of Chineseness and how they learn to (re)position themselves as competent HL learners and legitimate members of the diasporic community. The findings highlight the need to understand HL learners' identity and agency as emergent from varied social interactions embedded within one's personal history. In light of the findings, we propose an original model to theorise the dynamics of HL identity development from a historical, spatial, and relational lens, and conclude with practical suggestions to encourage HL learning and maintenance.

The association between the American Heart Association (AHA) Life's Essential 8 (LE8) and the risk of pancreatic cancer (PC) remains unclear. Our goal was to assess the relationships between LE8, genetic susceptibility, and PC risk. This cohort consisted of 234,102 participants from the UK Biobank. The components of LE8 include diet, nicotine exposure, sleep, physical activity, blood glucose, body mass index, blood lipids, and blood pressure. LE8 is classified into three categories: low cardiovascular health (CVH), moderate CVH, and high CVH. Measurements were made using Cox proportional risk models to estimate impact of associations between LE8, genetic susceptibility, and incidence of PC in participants. Compared to participants with low LE8 scores, those with moderate and high LE8 scores had a 53% (HR, 0.47; 95% CI, 0.39–0.57) and 70% (HR, 0.30; 95% CI, 0.22–0.41) lower risk of developing PC, respectively. Interestingly, among individuals with high genetic risk, high LE8 scores were associated with greater benefits (HR, 0.24; 95% CI, 0.15–0.40), whereas the protective effect was weaker among those with low genetic risk (HR, 0.40; 95% CI, 0.21–0.75). Participants with a high LE8 score and a low polygenic risk score (PRS) had the lowest risk of PC (HR, 0.19; 95% CI: 0.11–0.33). Furthermore, we observed a significant additive interaction between LE8 and PRS. A higher LE8 score is associated with a lower risk of PC, especially for participants with a high PRS. These findings have important implications for participants most genetically predisposed to PC and for targeted strategies for PC prevention. [ABSTRACT FROM AUTHOR]

Increasing evidence highlights the role of disrupted circadian rhythms in the neural dysfunctions and sleep disturbances observed in autism spectrum disorder and attention-deficit/hyperactivity disorder. However, the causality and directionality of these associations remain unclear. In this study, we employed a bidirectional two-sample Mendelian randomization framework, leveraging genome-wide association study data from the UK Biobank (n = 85,670) and FinnGen (n = 377,277). Genetic variants served as instrumental variables to infer causation, and objective accelerometer-derived metrics identified circadian rhythm and sleep genetic instruments. The results showed that the timing of the most active 10 h was significantly linked to higher odds of autism spectrum disorder and attention-deficit/hyperactivity disorder. Independently, higher sleep efficiency predicted a lower risk of autism spectrum disorder, while attention-deficit/hyperactivity disorder was linked to an increase in nocturnal sleep episodes. Heterogeneity and sensitivity analyses confirmed these findings. Our study establishes causal links between circadian alterations and autism spectrum disorder and attention-deficit/hyperactivity disorder, distinguishing the independent and protective role of sleep efficiency in autism spectrum disorder from circadian rhythms. In attention-deficit/hyperactivity disorder, however, disrupted sleep appears as a consequence, not a cause. These insights highlight divergent interactions with sleep factors in autism spectrum disorder and attention-deficit/hyperactivity disorder, laying the groundwork for tailored therapeutic strategies that recognize the distinct influences of sleep quality and circadian rhythms in each disorder. Research shows that people with autism spectrum disorder and attention-deficit/hyperactivity disorder often have sleep issues and problems with the body's natural daily rhythms, known as circadian rhythms. By exploring the genetic variants associated with these rhythms and the conditions, this study reveals that these rhythm changes and sleep patterns are directly linked to autism spectrum disorder and attention-deficit/hyperactivity disorder. It found that the timing of one's most active hours can increase the likelihood of having both autism spectrum disorder and attention-deficit/hyperactivity disorder. Importantly, it also shows that good sleep quality might protect against autism spectrum disorder, while disturbed sleep in people with attention-deficit/hyperactivity disorder seems to be a result rather than the cause of the condition. This understanding can help doctors and researchers develop better treatment approaches that focus on the specific ways sleep and body rhythms affect those with autism spectrum disorder and attention-deficit/hyperactivity disorder, considering their unique associations with circadian rhythms and sleep patterns. Understanding these unique links can lead to more effective, personalized care for those affected by these conditions. [ABSTRACT FROM AUTHOR]

Background: Circulating metabolites, which playa crucial role in our health, have been reported to be disordered in basal cell carcinoma (BCC). Despite these findings, evidence is still lacking to determine whether these metabolites directly promote or prevent BCC's progression. Therefore, our study aims to examine the potential effects of circulating metabolites on BCC progression. Material and methods: We conducted a two-sample Mendelian randomization (MR) analysis using data from two separate genome-wide association studies (GWAS). The primary study included data for 123 blood metabolites from a GWAS with 25,000 Finnish individuals, while the secondary study had data for 249 blood metabolites from a GWAS with 114,000 UK Biobank participants.GWAS data for BCC were obtained from the UK Biobank for the primary analysis and the FinnGen consortium for the secondary analysis. Sensitivity analyses were performed to assess heterogeneity and pleiotropy. Results: In the primary analysis, significant causal relationships were found between six metabolic traits and BCC with the inverse variance weighted (IVW) method after multiple testing [P < 4 x 10-4 (0.05/123)]. Four metabolic traits were discovered to be significantly linked with BCC in the secondary analysis, with a significance level of P < 2 x 10-4 (0.05/249). We found that all the significant traits are linked to Polyunsaturated Fatty Acids (PUFAs) and their degree of unsaturation. Conclusion: Our research has revealed a direct link between the susceptibility of BCC and Polyunsaturated Fatty Acids and their degree of unsaturation. This discovery implies screening and prevention of BCC. [ABSTRACT FROM AUTHOR]

Several characteristics distinguish lung cancer in female patients from that in male patients, with adenocarcinoma being more prevalent in female patients and occurring more frequently in female patients who do not smoke. Uncertainty surrounds the relationship between female-specific reproductive factors and lung cancer risk. Are sex-specific reproductive factors associated with risk of lung cancer in different genetic risk groups and histologic types? A Cox proportional hazard model was used to evaluate the association between multiple reproductive factors and the risk of lung cancer developing in a prospective cohort study involving 273,190 female individuals from the UK Biobank. Subgroup analyses stratified by age, smoking status, BMI, genetic risk, and histologic subtype were conducted to emphasize the modification effects further. A total of 1,182 cases of lung cancer in female patients were recorded over a median follow-up period of 12.0 years in the cohort study. In multivariable-adjusted models, early menarche (age ≤ 11 years: hazard ratio [HR], 1.22; 95% CI, 1.03-1.46), early menopause (age ≤ 46 years: HR, 1.49; 95% CI, 1.19-1.86), a shorter reproductive span (≤ 32 years: HR, 1.42; 95% CI, 1.18-1.71; and 33-35 years: HR, 1.24; 95% CI, 1.00-1.53), and early age at first birth (age ≤ 20 years: HR, 1.63; 95% CI, 1.33-2.01) were associated with a higher risk of lung cancer. Stratified analysis revealed that several reproductive factors, including early age at menopause, shortened reproductive span, and early age at first birth, showed a substantially stronger relationship with an elevated risk of lung cancer, particularly of lung adenocarcinoma, in populations with high genetic risk and more detrimental behaviors. Early age at menopause, a shortened reproductive life span, and early age at first birth were associated with higher risks of lung cancer, particularly of lung adenocarcinoma, in a subpopulation with higher genetic susceptibility and detrimental behaviors. The evidence provided by this study emphasizes the significance of screening for multiple reproductive factors to prevent lung cancer among female individuals. [Display omitted] [ABSTRACT FROM AUTHOR]

Adverse childhood experiences (ACEs) are widely recognized as associated with stress-associated digestive disorders, yet their comprehensive relationship with gastro-esophageal diseases as well as the potential mechanisms of depression remains underexplored. The prospective study included 133,638 participants aged 40–69 from UK Biobank with full information on ACEs, depression, and gastro-esophageal diseases. ACEs were retrospectively measured both as individual types (physical, emotional, and sexual abuse, and physical and emotional neglect) and cumulative scores of experienced types. Cox proportional hazards model was utilized to assess the association of ACEs with the overall and type-specific risks of diseases. Two-sample Mendelian randomization (TSMR) was conducted utilizing data from a genome-wide association study of ACEs (N = 185,414) to further examine the causal relationship. Mediation analysis was performed to quantify the role of depression. During a median follow-up of 13.3 years, those who had a history of ACEs were observed with a 15 % higher overall risk of gastro-esophageal diseases (HR, 1.15; 95%CI, 1.12–1.19) and 10–25 % increased type-specific risks compared to unexposed participants. Among five individual types of ACEs, the association was more prominent for emotional abuse (1.22, 1.17–1.27) and sexual abuse (1.24, 1.18–1.30). TSMR analysis consistently reported positive associations between ACE and four subtypes of gastro-esophageal diseases. Depression was found to mediate 17.2 % (13.5 %, 24.0 %) of the aforementioned relationship. Our findings highlight the importance of early screening and intervention on ACEs to reduce the long-term risk of gastro-esophageal diseases, and stress the potential of depression as a ponderable indirect intervention target. • Adverse childhood experiences are associated with gastro-esophageal diseases risks. • Emotional and sexual abuse show more prominent association among all childhood adversity types. • Depression partly mediates the link between childhood adversities and gastro-esophageal diseases. [ABSTRACT FROM AUTHOR]

Higher Education Institutions (HEIs) have mission statements as a matter of course. This article analyses 127 mission statements from UK HEIs, comprising 76.048% of the mainstream UK higher education sector. The statements were divided into the categories of Russell Group; Other; and Specialist Institution. A mixed methods research approach was adopted. The article identifies the fifty-seven most frequently used terms in mission statements. It also identifies the average lengths for each of the three categories. The article also analyses claims made and language used in mission statements: selected statements were subjected to close analysis. The article shows mission statements from Russell Group universities tend to be shorter, whereas HEIs outside the Russell Group make more detailed statements of their provision and credentials. Structurally, mission statements are distinct between the three categories. Linguistically, there is less distinction, though there is some difference in the most frequently used terms in each category.

Context/Objectives: Hydroxychoroquine has hypoglycemic effects and may reduce the risk of diabetes mellitus (DM). We determined the association between hydroxychoroquine use and the incidence of DM in a population-based cohort of pations with Rheumatic disease Methods: A prospective cohort study among 502392 Potentially eligible participants in the context of UK Biobank, recruitment to the database began between 2006 and 2010. Patients diagnosed with diabetes and fasting glucose greater than or equal to 7 mmol/L at baseline (n=619) were excluded and patients diagnosed with either RA or SLE at baseline (n=6793) were followed up until 2022. Diagnosis was recorded using the International Classification of Diseases, tenth edition (ICD-10) code. The mean follow-up was 13.78 years and the primary outcome was newly recorded type 2 diabetes mellitus (T2DM), with the time of onset of diabetes as the follow-up endpoint date. Results: During a median follow-up period of 13.78 (12.93, 14.49) years, diabetes developed in 537 participants, with an incidence of 7.9%. New diabetes cases not taking hydroxychloroquine and taking hydroxychloroquine was 504 (8.03%) and 33 (6.36%), respectively. In univariate models, the hazard ratio for diabetes was 0.89 (95% confidence interval, 0.81-0.98, P =0.014) for hydroxychloroquine users compared with those not taking hydroxychloroquine. After adjusting for age, sex, race, education level, and BMI the hazard ratio for incident diabetes among hydroxychloroquine users was 0.88 (95% confidence interval, 0.80-0.97, P =0.008). In complete multivariate model hazard ratio for hydroxychloroquine was 0.87 (95% confidence interval, 0.79- 0.96, P =0.005). Conclusion: Hydroxychloroquine was associated with decreased risk of DM among rheumatoid arthritis patients, our data taken together with correlational studies, warrant further investigation of the potential preventive effect of hydroxychloroquine against T2DM. [ABSTRACT FROM AUTHOR]

This study examines potential negative human resource consequences of leadership development. Applying theoretical perspectives on job demands and resources, we argue that leadership development may result in potential negative outcomes by introducing new and different demands on workers, requiring adjustment and adaptation. We further argue that the pervasiveness of this risk increases as leadership training is distributed across an organisation. We examine the effects of the implementation of a leadership development programme across a whole organisation (N = 9471), analysing data on incidences of withdrawal (absenteeism) and conflict (formal grievances) over a four-year period. We analyse data using fixed-effects modelling, and our findings indicated that increases in the proportions of leaders undertaking development in nineteen service units of the organisation over this period predicted increases in absenteeism and grievances raised by staff. Implications for theory in leadership development, and the management of development initiatives are discussed. [ABSTRACT FROM AUTHOR]

Recent studies suggest an association between greater dietary inflammatory index (DII) and higher biological ageing. As α -Klotho has been considered as a longevity protein, we examined whether α -Klotho plays a role in the association between DII and ageing. We included 3054 participants from the National Health and Nutrition Examination Survey. The associations of DII with biological and phenotypic age were assessed by multivariable linear regression, and the mediating role of α -Klotho was evaluated by mediation analyses. Participants' mean age was 58·0 years (sd 11·0), with a median DII score of 1·85 and interquartile range from 0·44 to 2·79. After adjusting for age, sex, race/ethnicity, BMI, education, marital status, poverty income ratio, serum cotinine, alcohol, physical activity, a higher DII was associated with both older biological age and phenotypic age, with per DII score increment being associated with a 1·01-year increase in biological age (1·01 (95 % CI: 1·005, 1·02)) and 1·01-year increase in phenotypic age (1·01 (1·001, 1·02)). Negative associations of DII with α -Klotho (β = –1·01 pg/ml, 95 % CI: –1·02, –1·006) and α -Klotho with biological age (β = –1·07 years, 95 % CI: –1·13, –1·02) and phenotypic age (β = –1·03 years, 95 % CI: –1·05, –1·01) were found. Furthermore, α -Klotho mediated 10·13 % (P < 0·001) and 9·61 % (P < 0·001) of the association of DII with biological and phenotypic age, respectively. Higher DII was associated with older biological and phenotypic age, and the potential detrimental effects could be partly mediated through α -Klotho. [ABSTRACT FROM AUTHOR]

We aimed to investigate the associations of individual and area-level socioeconomic status (SES) with incident cardiovascular diseases (CVD) alone, cancer alone, and comorbid CVD and cancer, and the mediation role of cardiovascular health score in these associations. This was a population-based prospective cohort study. We used data from the UK Biobank, a population-based prospective cohort study. Latent class analysis was used to create an individual-level SES index based on three indicators (household income, education level, and employment status), and the Townsend Index was defined as the area-level socioeconomic status. We used the American Heart Association's (AHA) Life's Simple 7 (smoking, body weight, physical activity, diet, blood pressure, blood glucose, and total cholesterol) to calculate the cardiovascular health score. We used Cox proportional hazard regression models to estimate the hazard ratio (HR) and 95% confidence interval (CI) adjusted for demographic, environmental, and genetic factors. Compared with high SES, the HRs in participants with low individual and area-level SES were 1.33 (95% confidence interval [CI] 1.29 to 1.38) and 1.24 (95% CI 1.20 to 1.29) for incident CVD, 0.96 (95% CI 0.93 to 0.99) and 0.95 (95%CI 0.92 to 0.98) for incident cancer, 1.32 (95%CI 1.24 to 1.40) and 1.15 (95%CI 1.08 to 1.22) for incident comorbid CVD and cancer, respectively. Additionally, the mediation proportion of CVD score for individual and area-level SES was 47.93% and 48.87% for incident CVD, 44.83% and 59.93% for incident comorbid CVD and cancer. The interactions between individual-level SES and CVD scores were significant on incident CVD, and comorbid CVD and cancer, and the protective associations were stronger in participants with high individual-level SES. Life's Simple 7 significantly mediated the associations between SES and comorbid CVD and cancer, while almost half of the associations remained unclear. [ABSTRACT FROM AUTHOR]

This study aimed to investigate the independent and joint associations of accelerometer-derived sleep duration and physical activity (PA) in different intensities with the risk of incident heart failure (HF). The study included 89,572 participants (mean age 62.2 ± 7.8 years, 42.8% male) from the UK Biobank. Sleep duration (short: <6 h/day; normal: 6–8 h/day; long: >8 h/day) and PA [total PA, light PA (LPA), moderate-to-vigorous PA (MVPA), vigorous PA (VPA)] were measured using accelerometers over 7 days. MVPA and VPA were categorized according to the World Health Organization's recommended levels, while LPA and total PA were categorized based on the median. HF cases were identified through hospital records or death registries. Over a 7-year follow-up period, 1324 participants (2.1%; incidence rate, 2.1 per 1000 person-years) developed HF. Short, but not long, sleep duration was linked to a 33% increased risk of HF [hazard ratio (HR) 1.33, 95% confidence interval (CI): 1.11–1.59]. This increased risk associated with short sleep could be mitigated by increasing PA, especially to the levels of recommended MVPA or VPA. In joint analyses, compared to participants meeting the recommended MVPA and with normal sleep duration, those not meeting the MVPA recommendation and with short sleep had the highest HF risk (HR 1.78, 95% CI: 1.42–2.25). Accelerometer-derived short, but not long, sleep duration was associated with a higher risk of incident HF. Engaging in sufficient PA, especially recommended MVPA or VPA, can partially mitigate this risk. [Display omitted] • Accelerometer-measured short sleep duration is independently associated with a higher risk of heart failure. • Higher physical activity levels, regardless of intensity, reduce the heart failure risk linked to short sleep duration. • Our study suggests for promoting recommended levels of PA, especially in situations where sleep duration may be compromised. [ABSTRACT FROM AUTHOR]

Background: It remains unknown how the patterns of change of social isolation and loneliness are associated with the onset of cardiovascular disease (CVD) and mortality. We aimed to investigate the longitudinal association of changes in social isolation and loneliness with incident CVD, all-cause mortality, CVD mortality and subsequent cardiac function. Methods: This prospective cohort study included 18,258 participants aged 38–73 years who participated in visit 0 (2006–2010) and visit 1 (2012–2013) using UK Biobank (mean age 57.1, standard deviation [SD] 7.4; 48.7% males). Social isolation or loneliness was categorized into four patterns: never, transient, incident, and persistent. Incident CVD, all-cause and CVD mortality were ascertained through linkage data. Cardiac function was assessed by cardiovascular magnetic resonance imaging in a subsample (N = 5188; visit 2, since 2014). Results: Over a median follow-up of 8.3 (interquartile range [IQR] 8.1–8.6) years, compared with never social isolation, persistent social isolation was associated with the higher risk of incident CVD (hazard ratio [HR] 1.17, 95% confidence interval [CI] 1.03–1.33), all-cause (1.42, 1.12–1.81) and CVD (1.53, 1.05–2.23) mortality. Likewise, persistent loneliness was strongly associated with the greater risk of incident CVD (1.13, 1.00–1.27), all-cause (1.28, 1.02–1.61) and CVD mortality (1.52, 1.06–2.18). Conclusions: Persistent social isolation and loneliness posed a substantially higher risk for incident CVD, all-cause and CVD mortality, and cardiac dysfunction than other patterns. Persistent social isolation and loneliness, along with an increasing cumulative score, are associated with lower cardiac function. [ABSTRACT FROM AUTHOR]

Background: Sex disparity between metabolic-obesity (defined by body mass index, BMI) phenotypes and obesity-related cancer (ORC) remains unknown. Considering BMI reflecting overall obesity but not fat distribution, we aimed to systematically assess the association of our newly proposed metabolic-anthropometric phenotypes with risk of overall and site-specific ORC by sex. Methods: A total of 141,579 men (mean age: 56.37 years, mean follow-up time: 12.04 years) and 131,047 women (mean age: 56.22 years, mean follow up time: 11.82 years) from the UK Biobank was included, and designated as metabolic-anthropometric phenotypes based on metabolic status (metabolically healthy/unhealthy), BMI (non-obesity/obesity) and body shape (pear/slim/apple/wide). The sex-specific association of different phenotypes with overall and site-specific ORC was assessed by hazard ratios (HRs) and 95% confidence intervals (CIs) using Cox proportional hazards regression models. Results: We found metabolically unhealthy and/or obesity phenotypes conveyed a higher risk in men than in women for overall ORC and colorectal cancer compared with metabolically healthy non-obesity phenotype (Pinteraction < 0.05). Of note, metabolically healthy obesity phenotype contributed to increased risks of most ORC in men (HRs: 1.58 ~ 2.91), but only correlated with higher risks of endometrial (HR = 1.89, 95% CI: 1.54–2.32) and postmenopausal breast cancers (HR = 1.17, 95% CI: 1.05–1.31) in women. Similarly, even under metabolically healthy, men carrying apple and wide shapes phenotypes (metabolically healthy apple/wide and metabolically healthy non-obesity apple/wide) suffered an increased risk of ORC (mainly colorectal, liver, gastric cardia, and renal cancers, HRs: 1.20 ~ 3.81) in comparison with pear shape or non-obesity pear shape. Conclusions: There was a significant sex disparity between metabolic-anthropometric phenotypes and ORC risk. We advised future ORC prevention and control worth taking body shape and sex disparity into account. [ABSTRACT FROM AUTHOR]

Background: Lipid pathways play a crucial role in psoriatic arthritis development, and some lipid-lowering drugs are believed to have therapeutic benefits due to their anti-inflammatory properties. Traditional observational studies face issues with confounding factors, complicating the interpretation of causality. This study seeks to determine the genetic link between these medications and the risk of psoriatic arthritis. Methods: This drug target study utilized the Mendelian randomization strategy. We harnessed high-quality data from population-level genome-wide association studies sourced from the UK Biobank and FinnGen databases. The inverse variance-weighted method, complemented by robust pleiotropy methods, was employed. We examined the causal relationships between three lipid-lowering agents and psoriatic arthritis to unveil the underlying mechanisms. Results: A significant association was observed between genetically represented proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibition and a decreased risk of psoriatic arthritis (odds ratio [OR]: 0.51; 95% CI 0.14–0.88; P < 0.01). This association was further corroborated in an independent dataset (OR 0.60; 95% CI 0.25–0.94; P = 0.03). Sensitivity analyses affirmed the absence of statistical evidence for pleiotropic or genetic confounding biases. However, no substantial associations were identified for either 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors or Niemann–Pick C1-like 1 inhibitors. Conclusions: This Mendelian randomization analysis underscores the pivotal role of PCSK9 in the etiology of psoriatic arthritis. Inhibition of PCSK9 is associated with reduced psoriatic arthritis risk, highlighting the potential therapeutic benefits of existing PCSK9 inhibitors. [ABSTRACT FROM AUTHOR]

Introduction: A strong association was previously established between body mass index (BMI) and female reproductive system tumors; however, the causal relationship is unclear. We conducted a Mendelian randomization (MR) study to further explore this association. Methods: Genetic information for BMI was retrieved from a published genome-wide association study involving 339,224 participants. Genetic associations with five common female reproductive system tumors were obtained from the FinnGen, UK Biobank studies, and other large consortia. Results: Genetic predisposition towards BMI exhibits a significant association with multiple tumors of the female reproductive system. Specifically, for every 1-unit increase in BMI log-transformed odds ratio (OR). The OR fluctuations overall for patients with breast cancer ranged from 0.661 to 0.996 (95% confidence interval [CI],0.544-1.000, P < 0.05). When stratified by estrogen receptor (ER) status, the OR for patients with ER (+) breast cancer ranged from 0.782 to 0.844 (95% CI, 0.616-0.994, P < 0.05) and that for those with ER (-) breast cancer ranged from 0.663 to 0.789 (95% CI, 0.498-0.991, P < 0.05). Additionally, ORs were as follows for cancer types: 1.577–1.908 (95% CI, 1.049-2.371, P < 0.05) for endometrial carcinoma; 1.216–1.303 (95% CI, 1.021-1.591, P < 0.05) for high-grade serous ovarian cancer; 1.217 (95% CI, 1.034-1.432, P < 0.05) for low-grade malignant serous ovarian cancer; and 1.502 (95% CI, 1.112-2.029, P < 0.05) for endometrioid ovarian carcinoma. Furthermore, our findings indicated that genetic predisposition towards BMI did not exhibit a causal association with uterine fibroids, cervical precancerous lesions, or cervical cancer itself. Conclusion: A genetic association was established between a high BMI and high risk of developing multiple tumors of the female reproductive system and their associated subtypes. This underscores the significance of taking measures to prevent reproductive system tumors in women who have a high BMI. [ABSTRACT FROM AUTHOR]

Aims: To estimate the association between long‐term changes in frailty and the risk of incident type 2 diabetes (T2DM) and to evaluate the effect of preventing the worsening of frailty on the risk of T2DM. Methods: We included 348 205 participants free of baseline T2DM and with frailty phenotype (FP) data from the UK Biobank; among them, 36 175 had at least one follow‐up assessment. According to their FP score, participants were grouped into nonfrailty, prefrailty and frailty groups. Frailty assessed at baseline and at follow‐up was used to derive the trajectory of frailty (ΔFP). Cox regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Results: Compared with those in the nonfrailty group at baseline, the HRs of T2DM for the prefrailty and frailty groups were 1.38 (95% CI 1.33–1.43) and 1.69 (95% CI 1.59–1.79), respectively (both p < 0.001), in the multivariable‐adjusted model. During a median follow‐up of 5.4 years after the final assessment, data for 472 T2DM patients were recorded. A 1‐point increase in the final FP was associated with a 25% (95% CI 1.14–1.38; p < 0.001) increased risk of T2DM. For the trajectory of frailty, each 0.5‐point/year increase in ΔFP was associated with a 52% (95% CI 1.18–1.97; p < 0.001) greater risk of T2DM, independent of the FP score at baseline. Compared with those that remained in the nonfrailty group, the greatest risk of T2DM over time was prefrailty aggravation (HR 3.03, 95% CI 2.00–4.58; p < 0.001). Using the frailty index did not materially change the results. Conclusions: Long‐term changes in frailty were associated with the risk of incident T2DM, irrespective of baseline frailty status. Preventing the worsening of frailty may reduce T2DM risk. [ABSTRACT FROM AUTHOR]

Background: Exposure to famine in the prenatal period is associated with an increased risk of metabolic disease, including obesity and type 2 diabetes. We employed nuclear magnetic resonance (NMR) metabolomic profiling to identify the metabolic changes that are associated with survival of prenatal famine exposure during the Dutch Famine at the end of World War II and subsequently assess their link to disease. Methods: NMR metabolomics data were generated from serum in 480 individuals prenatally exposed to famine (mean 58.8 years, 0.5 SD) and 464 controls (mean 57.9 years, 5.4 SD). We tested associations of prenatal famine exposure with levels of 168 individual metabolic biomarkers and compared the metabolic biomarker signature of famine exposure with those of 154 common diseases. Results: Prenatal famine exposure was associated with higher concentrations of branched-chain amino acids ((iso)-leucine), aromatic amino acid (tyrosine), and glucose in later life (0.2–0.3 SD, p < 3 × 10−3). The metabolic biomarker signature of prenatal famine exposure was positively correlated to that of incident type 2 diabetes from the UK Biobank (r = 0.77, p = 3 × 10−27), also when re-estimating the signature of prenatal famine exposure among individuals without diabetes (r = 0.67, p = 1 × 10−18). Remarkably, this association extended to 115 common diseases for which signatures were available (0.3 ≤ r ≤ 0.9, p < 3.2 × 10−4). Correlations among metabolic signatures of famine exposure and disease outcomes were attenuated when the famine signature was adjusted for body mass index. Conclusions: Prenatal famine exposure is associated with a metabolic biomarker signature that strongly resembles signatures of a diverse set of diseases, an observation that can in part be attributed to a shared involvement of obesity. [ABSTRACT FROM AUTHOR]

The UK Biobank (UKB) has the largest adult brain imaging dataset, which encompasses over 40,000 participants. A significant number of Mendelian randomization (MR) studies based on UKB neuroimaging data have been published to validate potential causal relationships identified in observational studies. Relevant articles published before December 2023 were identified following the PRISMA protocol. Included studies (n = 34) revealed that there were causal relationships between various lifestyles, diseases, biomarkers, and brain image-derived phenotypes (BIDPs). In terms of lifestyle habits and environmental factors, there were causal relationships between alcohol consumption, tea intake, coffee consumption, smoking, educational attainment, and certain BIDPs. Additionally, some BIDPs could serve as mediators between leisure/physical inactivity and major depressive disorder. Regarding diseases, BIDPs have been found to have causal relationships not only with Alzheimer's disease, stroke, psychiatric disorders, and migraine, but also with cardiovascular diseases, diabetes, poor oral health, osteoporosis, and ankle sprain. In addition, there were causal relationships between certain biological markers and BIDPs, such as blood pressure, LDL-C, IL-6, telomere length, and more. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the genetic correlation and causal links between sleep traits (including sleep duration, chronotype, and insomnia) and myopia. Methods: Summary data on three sleep traits (sleep duration, chronotype and insomnia) and myopia from FinnGen (n = 214,211) and UK Biobank (n = 460,536) were analyzed using linkage disequilibrium score regression (LD Score), univariable and multivariable mendelian randomization (MR) experiments and Causal Analysis Using Summary Effect (CAUSE) estimation. Results: LD Score regression detected candidate genetic correlation between sleep traits and myopia, such as sleep duration, chronotype (Genetic Correlation Z-score >10.00, h2_observed_p < 0.005, Lambda GC > 1.05, p > 0.05). Univariable MR analyses indicated that increased sleep duration has a promotional effect on the occurrence of myopia (p = 0.046 < 0.05, P_FDR = 0.138 < 0.2, OR = 2.872, 95% CI: 1.018-8.101). However, after accounting for potential confounding factors, multivariable MR and CAUSE analysis did not provide evidence for a causal effect of the three sleep traits on myopia. Conclusion: There may be a potential genetic correlation between sleep duration, chronotype and myopia. However, neither of sleep duration, chronotype or insomnia had causal effect on myopia. [ABSTRACT FROM AUTHOR]

Background: To investigate the association between cigarette smoking, smoking cessation and the trajectory of cardiometabolic multimorbidity (CMM), and further to examine the association of age at smoking initiation and smoking cessation with CMM. Methods: This study included 298,984 UK Biobank participants without cardiometabolic diseases (CMDs) (including type 2 diabetes, coronary heart diseases, stroke, and hypertension) at baseline. Smoking status was categorized into former, current, and never smokers, with age at smoking initiation and smoking cessation as a proxy for current and former smokers. The multi-state model was performed to evaluate the association between cigarette smoking, smoking cessation and CMM. Results: During a median follow-up of 13.2 years, 59,193 participants developed first cardiometabolic disease (FCMD), 14,090 further developed CMM, and 16,487 died. Compared to former smokers, current smokers had higher risk at all transitions, with hazard ratio (95% confidence interval) = 1.59 (1.55 ∼ 1.63) vs. 1.18 (1.16 ∼ 1.21) (P = 1.48 × 10− 118) from health to FCMD, 1.40 (1.33 ∼ 1.47) vs. 1.09 (1.05 ∼ 1.14) (P = 1.50 × 10− 18) from FCMD to CMM, and 2.87 (2.72 ∼ 3.03) vs. 1.38 (1.32 ∼ 1.45) (P < 0.001) from health, 2.16 (1.98 ∼ 2.35) vs. 1.25 (1.16 ∼ 1.34) (P = 1.18 × 10− 46) from FCMD, 2.02 (1.79 ∼ 2.28) vs. 1.22 (1.09 ∼ 1.35) (P = 3.93 × 10− 17) from CMM to death; whereas quitting smoking reduced the risk attributed to cigarette smoking by approximately 76.5% across all transitions. Reduced risks of smoking cessation were also identified when age at quitting smoking was used as a proxy for former smokers. Conclusions: Cigarette smoking was associated with a higher risk of CMM across all transitions; however, smoking cessation, especially before the age of 35, was associated with a significant decrease in CMM risk attributed to cigarette smoking. [ABSTRACT FROM AUTHOR]

Introduction: Walking stands as the most prevalent physical activity in the daily lives of individuals and is closely associated with physical functioning and the aging process. Nonetheless, the precise cause-and-effect connection between walking and aging remains unexplored. The epigenetic clock emerges as the most promising biological indicator of aging, capable of mirroring the biological age of the human body and facilitating an investigation into the association between walking and aging. Our primary objective is to investigate the causal impact of walking with epigenetic age acceleration (EAA). Methods: We conducted a two-sample two-way Mendelian randomization (MR) study to investigate the causal relationship between walking and EAA. Walking and Leisure sedentary behavior data were sourced from UK Biobank, while EAA data were gathered from a total of 28 cohorts. The MR analysis was carried out using several methods, including the inverse variance weighted (IVW), weighted median, MR-Egger, and robust adjusted profile score (RAPS). To ensure the robustness of our findings, we conducted sensitivity analyses, which involved the MR-Egger intercept test, Cochran's Q test, and MR-PRESSO, to account for and mitigate potential pleiotropy. Results: The IVW MR results indicate a significant impact of usual walking pace on GrimAge (BETA = − 1.84, 95% CI (− 2.94, − 0.75)), PhenoAge (BETA = − 1.57, 95% CI (− 3.05, − 0.08)), Horvath (BETA = − 1.09 (− 2.14, − 0.04)), and Hannum (BETA = − 1.63, 95% CI (− 2.70, − 0.56)). Usual walking pace is significantly associated with a delay in epigenetic aging acceleration (EAA) (P < 0.05). Moreover, the direction of effect predicted by the gene remained consistent across RAPS outcomes and sensitivity MR analyses. There is a lack of robust causal relationships between other walking conditions, such as walking duration and walking frequency, on EAA (P > 0.05). Conclusion: Our evidence demonstrates that a higher usual walking pace is associated with a deceleration of the acceleration of all four classical epigenetic clocks acceleration. Key messages: In recent years, observational studies have found that there is a correlation between walking and aging, but the specific relationship is not clear We used a Mendelian randomization approach to test the causal effect of walking and sedentarism on epigenetic clock acceleration Mendelian randomization studies have found that faster walking speed may delay physiological aging through causal analysis at the genetic level [ABSTRACT FROM AUTHOR]

Background: Potentially modifiable risk factors for hepatocellular carcinoma (HCC) have been investigated in observational epidemiology studies in East Asian and European populations, whereas the causal associations of most of these risk factors remain unclear. Methods: We collected genome-wide association summary statistics of 22 modifiable risk factors in East Asians and 33 risk factors in Europeans. Genetic summary statistics of HCC were sourced from the Biobank Japan study (1,866 cases and 195,745 controls) for East Asians, and the deCODE genetics study (406 cases and 49,302 controls) and the UK Biobank (168 cases and 372 016 controls) for Europeans. Two-sample Mendelian randomization (MR) analyses were performed independently for East Asian and European populations. Results: In East Asians, genetically predicted alcohol frequency, ever drinkers, aspartate aminotransferase (AST), hypothyroidism, chronic hepatitis B, and chronic hepatitis C, metabolic dysfunction-associated steatotic liver disease (MASLD), and autoimmune hepatitis were significantly associated with an increased HCC risk (P < 0.05/22). Among European population, alanine transaminase, AST, MASLD, percent liver fat, and liver iron content were significantly associated with a higher risk of HCC (P < 0.05/33). The replication dataset and meta-analysis further confirmed these results. Conclusions: Although East Asian and European populations have different factors for HCC, their common modifiable risk factors AST and MASLD for HCC, offer valuable insights for targeted intervention strategies to mitigate society burden of HCC. [ABSTRACT FROM AUTHOR]

Objective: Numerous studies have reported that metformin can reduce the risk of tumor development. However, some of the results of these studies are conflicting, necessitating a more reliable evaluation. Methods: We conducted a Mendelian randomization phenome-wide association study (MR-PheWAS) of tumors to explore the causal relationship between metformin and tumors. Two cohorts of patients taking metformin were obtained from the UK Biobank. Complete phenotype data of the tumors were obtained from FinnGen_R10. We elucidated the causal relationship using a two-sample Mendelian randomization (MR) analysis. More importantly, we conducted a meta-analysis to ensure relatively unbiased results. In the MR analysis, we used the inverse-variance weighted (IVW) method as the main outcome indicator. Subsequently, two cohorts were integrated for the meta-analysis. Finally, we investigated the mechanisms through mediational MR analysis. Results: MR analysis revealed that metformin might have a causal relationship with 13 tumor-associated phenotypes in the training cohort. Four phenotypes were validated in the testing cohort. In the training and testing cohorts, metformin exhibited a protective effect against brain meningiomas and malignant neoplasms of the breast (HER-positive), oral cavity, tonsils, and the base of the tongue. Intriguingly, after integrating the results of the two cohorts for the meta-analysis, 12 results were statistically significant. Mediational MR analysis suggested that the effects of metformin on brain meningiomas may be weakened by the presence of the family Oxalobacteraceae. Conclusion: Metformin exhibits potential preventive and therapeutic effects on four types of tumors: brain meningioma, malignant neoplasms of the breast (HER-positive), oral cavity and tonsils, and the base of the tongue. Large randomized controlled trials are required to confirm these findings. [ABSTRACT FROM AUTHOR]

Aim: To prospectively assess the association of smoking timing with the risk of type 2 diabetes (T2D) and examine whether smoking amount or genetic susceptibility might modify the relationship. Materials and Methods: A total of 294 815 participants without diabetes from the UK Biobank, including non‐smokers and smokers with data on the time from waking to first cigarette, were included. Cox proportional hazards models were used to evaluate the association between smoking timing and the risk of incident T2D. Results: During a median follow‐up time of 12 years, a total of 9937 incident cases of T2D were documented. Compared with non‐smokers, a shorter time from waking to first cigarette was significantly associated with a higher risk of incident T2D (P for trend <.001). In the fully adjusted model, the hazard ratios (HRs) (95% confidence interval) associated with smoking timing were 1.46 (1.17–1.81) for more than 2 hours, 1.51 (1.21–1.87) for 1–2 hours, 1.58 (1.34–1.85) for 30–60 minutes, 1.86 (1.57–2.21) for 5–15 minutes and 2.01 (1.60–2.54) for less than 5 minutes. We found that even among those who reported being light smokers, those with the shortest time from waking to first cigarette had a 105% higher risk of T2D with an HR of 2.05 (1.52–2.76), which was comparable with heavy smokers. The genetic risk score for T2D did not modify this association (P‐interaction =.51). Conclusions: Our findings indicate that shorter time from waking to first cigarette is significantly associated with a higher risk of incident T2D. [ABSTRACT FROM AUTHOR]

Background: It's unclear if excess visceral adipose tissue (VAT) mass in individuals with prediabetes can be countered by adherence to a Mediterranean lifestyle (MEDLIFE). We aimed to examine VAT mass, MEDLIFE adherence, and their impact on type 2 diabetes (T2D) and diabetic microvascular complications (DMC) in individuals with prediabetes. Methods: 11,267 individuals with prediabetes from the UK Biobank cohort were included. VAT mass was predicted using a non-linear model, and adherence to the MEDLIFE was evaluated using the 25-item MEDLIFE index, encompassing categories such as "Mediterranean food consumption," "Mediterranean dietary habits," and "Physical activity, rest, social habits, and conviviality." Both VAT and MEDLIFE were categorized into quartiles, resulting in 16 combinations. Incident cases of T2D and related DMC were identified through clinical records. Cox proportional-hazards regression models were employed to examine associations, adjusting for potential confounding factors. Results: Over a median follow-up of 13.77 years, we observed 1408 incident cases of T2D and 714 cases of any DMC. High adherence to the MEDLIFE, compared to the lowest quartile, reduced a 16% risk of incident T2D (HR: 0.84, 95% CI: 0.71–0.98) and 31% for incident DMC (0.69, 0.56–0.86). Conversely, compared to the lowest quartile of VAT, the highest quartile increased the risk of T2D (5.95, 4.72–7.49) and incident any DMC (1.79, 1.36–2.35). We observed an inverse dose-response relationship between MEDLIFE and T2D/DMC, and a dose-response relationship between VAT and all outcomes (P for trend < 0.05). Restricted cubic spline analysis confirmed a nearly linear dose-response pattern across all associations. Compared to individuals with the lowest MEDLIFE quartile and highest VAT quartile, those with the lowest T2D risk had the lowest VAT and highest MEDLIFE (0.12, 0.08–0.19). High MEDLIFE was linked to reduced T2D risk across all VAT categories, except in those with the highest VAT quartile. Similar trends were seen for DMC. Conclusion: High adherence to MEDLIFE reduced T2D and MDC risk in individuals with prediabetes, while high VAT mass increases it, but MEDLIFE adherence may offset VAT's risk partly. The Mediterranean lifestyle's adaptability to diverse populations suggests promise for preventing T2D. [ABSTRACT FROM AUTHOR]

Complicated associations between multiplexed environmental factors and aging are poorly understood. We manipulated aging using multidimensional metrics such as phenotypic age, brain age, and brain volumes in the UK Biobank. Weighted quantile sum regression was used to examine the relative individual contributions of multiplexed environmental factors to aging, and self-organizing maps (SOMs) were used to examine joint effects. Air pollution presented a relatively large contribution in most cases. We also found fair heterogeneities in which the same environmental factor contributed inconsistently to different aging metrics. Particulate matter contributed the most to variance in aging, while noise and green space showed considerable contribution to brain volumes. SOM identified five subpopulations with distinct environmental exposure patterns and the air pollution subpopulation had the worst aging status. This study reveals the heterogeneous associations of multiplexed environmental factors with multidimensional aging metrics and serves as a proof of concept when analyzing multifactors and multiple outcomes. Complicated associations between multiplexed environmental factors and aging are poorly understood. Here, authors show heterogeneous associations of multiplexed environmental factors with multidimensional aging metrics. [ABSTRACT FROM AUTHOR]

The ability to decode nonverbal cues is essential for effective cross-cultural communication. Despite the significance of nonverbal communication, research in this area has primarily focused on spoken language. This is particularly problematic during indirect communication, where there is a discrepancy between the surface meaning and the true intention (e.g., "Well, there is still room for improvement in your writing skills"). Misinterpretation of nonverbal cues during indirect communication can impede the decoding of true intention and potentially create hostile situations. The present study investigated cross-cultural differences in the use of nonverbal cues in decoding indirect messages. British and Chinese raters watched silent video clips and identified the types of replies from models of their own and the other culture. Results revealed that British raters were able to recognize indirect replies from British models but not from Chinese models above chance level, whereas Chinese raters were able to recognize indirect replies from models of both cultures above chance level. Furthermore, British raters showed higher accuracy and confidence in identifying indirect replies from British models than Chinese models. In contrast, Chinese raters were equally skilled and confident in identifying indirect replies from both British and Chinese models. Additionally, British and Chinese raters employed different nonverbal cues to recognize indirect replies from models of their respective cultures. These findings underscore the importance of cross-cultural differences in identifying indirect replies through nonverbal communication and provide insights to enhance intercultural communication between British and Chinese individuals. [ABSTRACT FROM AUTHOR]

Type 2 diabetes (T2D) is a global health concern with increasing prevalence. Comorbid hypothyroidism (HT) exacerbates kidney, cardiac, neurological and other complications of T2D; these risks can be mitigated pharmacologically upon detecting HT. The current HT standard of care (SOC) screening in T2D is infrequent, delaying HT diagnosis and treatment. We present a first-to-date machine learning algorithm (MLA) clinical decision tool to classify patients as low vs. high risk for developing HT comorbid with T2D; the MLA was developed using readily available patient data from harmonized multinational datasets. The MLA was trained on data from NIH All of US (AoU) and UK Biobank (UKBB) (Combined dataset) and achieved a high negative predictive value (NPV) of 0.989 and an AUROC of 0.762 in the Combined dataset, exceeding AUROCs for the models trained on AoU or UKBB alone (0.666 and 0.622, respectively), indicating that increasing dataset diversity for MLA training improves performance. This high-NPV automated tool can supplement SOC screening and rule out T2D patients with low HT risk, allowing for the prioritization of lab-based testing for at-risk patients. Conversely, an MLA output that designates a patient to be at risk of developing HT allows for tailored clinical management and thereby promotes improved patient outcomes. [ABSTRACT FROM AUTHOR]

Objective Whether metformin and its adenosine 5'monophosphate-activated protein kinase (AMPK) activation protect from psoriasis risk is unconcluded. We investigated the effect of AMPK, a pharmacological target of metformin, on the risk of psoriasis and its comorbidities and mortality among participants in the UK Biobank (UKB). Methods To avoid immortal time biases in pharmacoepidemiologic studies, Mendelian randomization was used to infer the AMPK pathway-dependent effects. The cut-off age for distinguishing early-onset/late-onset psoriasis (EOP/LOP) was set at 60 years, based on the incident psoriasis peak in UKB. A genetic instrument comprising 44 single-nucleotide polymorphisms associated with glycated haemoglobin (HbA1c), serving as a proxy for AMPK genetic risk score (negatively associated with AMPK activation), was employed as previously reported in the literature. Log-binomial models were used to estimate the effect size of AMPK regarding relative risk (RR) and 95% CI. Results A total of 407 159 participants were analysed, including 9126 EOP and 3324 LOP. The AMPK genetic risk score was associated with a 12.4% increase in the risk of LOP in men (RR = 1.124, 95% CI: 1.022–1.236). This association was not significant for EOP or women. AMPK genetic risk score exhibited an elevated risk of ischemic heart disease (RR = 1.217, 95% CI 1.062–1.395) in male psoriasis patients. Conclusions AMPK activation may protect against LOPs and associated ischemic heart disease in men. A sex-specific, comorbidity-targeted intervention for psoriasis is needed. [ABSTRACT FROM AUTHOR]

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Background: Both genetic factors and air pollution are risk factors for coronary artery disease (CAD), but their combined effects on CAD are uncertain. The study aimed to comprehensively investigate their separate, combined and interaction effects on the onset of CAD. Methods: We utilized data from the UK Biobank with a recruitment of 487,507 participants who were free of CAD at baseline from 2006 to 2010. We explored the separate, combined effect or interaction association among genetic factors, air pollution and CAD with the polygenic risk score (PRS) and Cox proportional hazard models. Results: The hazard ratios (HRs) [95% confidence interval (CI)] of CAD for 10-µg/m3 increases in PM2.5, NO2 and NOx concentrations were 1.25 (1.09, 1.44), 1.03 (1.01, 1.05) and 1.01 (1.00, 1.02), respectively. Participants with high PRS and air pollution exposure had a higher risk of CAD than those with the low genetic risk and low air pollution exposure, and the HRs (95% CI) of CAD in the PM2.5, PM10, NO2 and NOx high joint exposure groups were 1.56 (1.48, 1.64), 1.55(1.48, 1.63), 1.57 (1.49, 1.65), and 1.57 (1.49, 1.65), respectively. Air pollution and genetic factors exerted significant additive effects on the development of CAD (relative excess risk due to the interaction [RERI]: 0.12 (0.05, 0.19) for PM2.5, 0.17 (0.10, 0.24) for PM10, 0.14 (0.07, 0.21) for NO2, and 0.17 (0.10, 0.24) for NOx; attributable proportion due to the interaction [AP]: 0.09 (0.04, 0.14) for PM2.5, 0.12 (0.07, 0.18) for PM10, 0.11 (0.06, 0.16) for NO2, and 0.13 (0.08, 0.18) for NOx). Conclusion: Exposure to air pollution was significantly related to an increased CAD risk, which could be further strengthened by CAD gene susceptibility. Additionally, there were positive additive interactions between genetic factors and air pollution on the onset of CAD. This can provide a more comprehensive, precise and individualized scientific basis for the risk assessment, prevention and control of CAD. [ABSTRACT FROM AUTHOR]

Recognition of the huge variation between professional graduate degree programmes and employer requirements, especially in the construction industry, necessitated a need for assessing and developing competencies that aligned with professionally oriented programmes. The purpose of this research is to develop a competency mapping framework (CMF) in this case for quantity surveying honours degree programmes. The graduate competency threshold benchmark (GCTB) is a key component of the CMF. Therefore, the CMF contains the mapping process, the template documents and the benchmark. The research adopted literature review, pilot study, case studies (including semi-structured interviews) and expert forum in developing the framework. The framework developed in this research provides new insight into how degree programmes map against competencies. Thus, the framework can be applied more widely, to other professional degree programmes, for monitoring and improving the quality and professional standards of construction degree programmes by accrediting bodies. This should connect construction graduates more effectively to the industry.

Background: Previous retrospective studies have shown a correlation between depression and increased risk of infections, including a moderate rise in sepsis likelihood associated with severe depression and anxiety. To investigate the potential causal links between depression, sepsis, and mortality risks, while considering confounding factors, we employed a Mendelian randomization (MR) approach. Methods: In this two-sample Mendelian randomization study, we analyzed data from a large-scale genome-wide association study on depression, involving 807,553 European individuals (246,363 cases, 561,190 controls). We extracted SNP associations with sepsis and 28-day mortality from UK Biobank GWAS outcomes. The correlation analysis primarily employed the inverse-variance weighted method, supplemented by sensitivity analyses for heterogeneity and pleiotropy assessment. Results: Our analysis revealed a potential causal link between depression and an increased risk of sepsis (OR = 1.246, 95% CI: 1.076–1.442, P = 0.003), but no causal association was found with sepsis-induced mortality risk (OR = 1.274, 95% CI: 0.891–1.823, P = 0.184). Sensitivity analyses confirmed the robustness of these findings. Conclusions: We identified a potential causal association between depression and heightened sepsis risk, while no link was found with sepsis-induced mortality. These findings suggest that effective management of depression could be important in preventing sepsis. [ABSTRACT FROM AUTHOR]

Observational studies indicate that serum sex hormone-binding globulin (SHBG) levels are inversely correlated with blood lipid levels and coronary heart disease (CHD) risk. Given that dyslipidemia is an established risk factor for CHD, we aim to employ Mendelian randomization (MR) in conjunction with mediation analysis to confirm the mediating role of blood lipid levels in the association between SHBG and CHD. First, we assessed the causality between serum SHBG levels and five cardiovascular diseases using univariable MR. The results revealed causality between SHBG levels and reduced risk of CHD, myocardial infarction, as well as hypertension. Specifically, the most significant reduction was observed in CHD risk, with an odds ratio of 0.73 (95% CI 0.63–0.86) for each one-standard-deviation increase in SHBG. The summary-level data of serum SHBG levels and CHD are derived from a sex-specific genome-wide association study (GWAS) conducted by UK Biobank (sample size = 368,929) and a large-scale GWAS meta-analysis (60,801 cases and 123,504 controls), respectively. Subsequently, we further investigated the mediating role of blood lipid level in the association between SHBG and CHD. Mediation analysis clarified the mediation proportions for four mediators: high cholesterol (48%), very low-density lipoprotein cholesterol (25.1%), low-density lipoprotein cholesterol (18.5%), and triglycerides (44.3%). Summary-level data for each mediator were sourced from the UK Biobank and publicly available GWAS. The above results confirm negative causality between serum SHBG levels and the risk of CHD, myocardial infarction, and hypertension, with the causal effect on reducing CHD risk largely mediated by the improvement of blood lipid profiles. [ABSTRACT FROM AUTHOR]

Background: Numerous observational studies have investigated the potential link between hypertensive disorders of pregnancy (HDPs) and the subsequent risks of gynecologic tumors, yet the findings have been inconsistent. In this study, we utilized Mendelian randomization (MR) approach to assess the influence of HDPs on the future risks of ovarian, cervical, endometrial, and breast cancer and uterine fibroids, controlling for confounding factors. Methods: The genome‐wide association studies (GWAS) summary data relevant to HDPs was obtained from the FinnGen databases (10,736 cases and 136,325 controls). Gynecologic tumor outcomes were extracted from the IEU Open GWAS project and UK Biobank (47,690 cases and 1, 092,073 controls). The inverse variance weighted (IVW) approach was selected as the principal method for MR analysis, supplemented by MR‐Egger, weighted median, weighted model, simple model methods, MR pleiotropy residual sum and outlier (MR‐PRESSO) test, and leave‐one‐out method. Multivariate MR (MVMR) analysis was conducted after adjusting systolic blood pressure (SBP), body mass index (BMI) and type 2 diabetes mellitus (T2DM). Results: Our univariate MR analysis (UVMR) results revealed no significant relationship between HDPs and the risks of ovarian cancer (odds ratio [OR] = 0.924, p = 0.360), cervical cancer (OR = 1.230, p = 0.738), endometrial cancer (OR = 1.006, p = 0.949), uterine fibroids (OR = 1.155, p = 0.158), and breast cancer (OR = 0.792, p = 0.241) by IVW test. Similar results were observed in gestational hypertension and preeclampsia/eclampsia. Additionally, our study detected neither heterogeneity nor pleiotropy. MVMR analysis also provided no evidence of a causal association between HDPs and common gynecologic tumors after adjusting SBP, BMI, and T2DM. Conclusion: We discovered no causal relationship between HDPs and ovarian, cervical, endometrial, breast cancer, and uterine fibroids in European populations. However, present analysis did not explore the effect of HDPs on the subtypes of gynecologic tumors across varied ethnic populations, which may require additional research. [ABSTRACT FROM AUTHOR]

Background: Peripheral glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) are sensitive markers of neuroinflammation and neuronal damage. Previous studies with highly selected participants have shown that peripheral GFAP and NfL levels are elevated in the pre-clinical phase of Alzheimer's disease (AD) and dementia. However, the predictive value of GFAP and NfL for dementia requires more evidence from population-based cohorts. Methods: This was a prospective cohort study to evaluate UK Biobank participants enrolled from 2006 to 2010 using plasma GFAP and NfL measurements measured by Olink Target Platform and prospectively followed up for dementia diagnosis. Primary outcome was the risk of clinical diagnosed dementia. Secondary outcomes were cognition. Linear regression was used to assess the associations between peripheral GFAP and NfL with cognition. Cox proportional hazard models with cross-validations were used to estimate associations between elevated GFAP and NfL with risk of dementia. All models were adjusted for covariates. Results: A subsample of 48,542 participants in the UK Biobank with peripheral GFAP and NfL measurements were evaluated. With an average follow-up of 13.18 ± 2.42 years, 1312 new all-cause dementia cases were identified. Peripheral GFAP and NfL increased up to 15 years before dementia diagnosis was made. After strictly adjusting for confounders, increment in NfL was found to be associated with decreased numeric memory and prolonged reaction time. A greater annualized rate of change in GFAP was significantly associated with faster global cognitive decline. Elevation of GFAP (hazard ratio (HR) ranges from 2.25 to 3.15) and NfL (HR ranges from 1.98 to 4.23) increased the risk for several types of dementia. GFAP and NfL significantly improved the predictive values for dementia using previous models (area under the curve (AUC) ranges from 0.80 to 0.89, C-index ranges from 0.86 to 0.91). The AD genetic risk score and number of APOE*E4 alleles strongly correlated with GFAP and NfL levels. Conclusions: These results suggest that peripheral GFAP and NfL are potential biomarkers for the early diagnosis of dementia. In addition, anti-inflammatory therapies in the initial stages of dementia may have potential benefits. [ABSTRACT FROM AUTHOR]

Objective: The non-motor symptoms of Parkinson's disease (PD) are an important part of PD. In recent years, more and more non-drug interventions have been applied to alleviate the non-motor symptoms of PD, but the relevant evidence is limited. This systematic review and meta-analysis was designed to evaluate the efficacy of non-drug interventions in patients with non-motor symptoms in patients with PD. Methods: Seven databases, including Pubmed, Embease, Cochrane Library, China National Knowledge Infrastructure (CNKI), Wanfang database (WANFANG), VIP database (VIP), and China Biomedical Literature Service System (CBM) were searched from the establishment of the database to December 2023. Non-drug interventions such as acupuncture, cognitive behavioral therapy (CBT), exercise, repetitive transcranial magnetic stimulation (rTMS), and non-motor symptoms of Parkinson's disease were selected as search words, and two independent evaluators evaluated the included literature's bias risk and data extraction. The therapeutic efficacy was evaluated by the Parkinson's Disease Sleep Scale (PDSS), Hamilton Depression Scale (HAMD), Beck Depression Inventory (BDI), Hamilton Anxiety Scale (HAMA), Montreal Cognitive Assessment (MoCA), Minimum Mental State Examination (MMSE), and Parkinson's Disease Questionnaire-39 (PDQ-39). RevMan 5.4.1 (Reviewer Manager Software 5.4.1). Cochrane Collaboration, Oxford, United Kingdom analyzed the data and estimated the average effect and the 95% confidence interval (CI). A heterogeneity test is used to assess differences in the efficacy of different non-drug treatments. Results: We selected 36 from 4,027 articles to participate in this meta-analysis, involving 2,158 participants. Our combined results show that: PDSS: [mean difference (MD) =-19.35, 95% CI (-30.4 to -8.28), p<0.0006]; HAMD: [MD = -2.98, 95% CI (-4.29 to -1.67), p<0.00001]; BDI: [MD = -2.69, 95% CI (-4.24 to 4.80), p = 0.006]; HAMA: [MD=-2.00, 95% CI (-2.83 to -1.17), p<0.00001]; MMSE: [MD = 1.20, 95% CI (0.71 to 1.68), p< 0.00001]; CoMA: [MD = 2.10, 95% CI (-0.97 to 3.23), p = 0.0003]; PDQ-39: [MD = -4.03, 95% CI (-5.96 to -1.57), p < 0.00001]. Conclusion: The four non-drug measures used in our review showed significant improvements in sleep, depression, anxiety, cognition, constipation, and quality of life compared with the control group, and no serious adverse events were reported in the included research evidence, and we found that there were some differences among the subgroups of different intervention methods, but due to the less literature included in the subgroup, and the comparison was more indirect. So, we should interpret these results carefully. [ABSTRACT FROM AUTHOR]

Drawing on oral histories of first-generation migrant women, this paper explores Chinese women's role in financing migrant households, mothering children and promoting the well-being of the British Chinese community after 1945. It argues that, with better educational attainment and wider participation in professional occupations Chinese migrant women played an increasingly essential yet unrecognised role in private and public lives. This paper expands knowledge of Chinese women's experiences in contemporary international migration and confirms the necessity of understanding migration through the lens of gender to reveal evolving gendered family roles within migrant households and migrant women's manifold but unrecognised merits. [ABSTRACT FROM AUTHOR]

Aims: The causal relationship between sarcopenia‐related traits and ischemic stroke (IS) remains poorly understood. This study aimed to explore the causal impact of sarcopenia‐related traits on IS and to identify key mediators of this association. Methods: We conducted univariable, multivariable two‐sample, and two‐step Mendelian randomization (MR) analyses using genome‐wide association study (GWAS) data. This included data for appendicular lean mass (ALM), hand grip strength (HGS), and usual walking pace (UWP) from the UK Biobank, and IS data from the MEGASTROKE consortium. Additionally, 21 candidate mediators were analyzed based on their respective GWAS data sets. Results: Each 1‐SD increase in genetically proxied ALM was associated with a 7.5% reduction in the risk of IS (95% CI: 0.879–0.974), and this correlation remained after controlling for levels of physical activity and adiposity‐related indices. Two‐step MR identified that six mediators partially mediated the protective effect of higher ALM on IS, with the most significant being coronary heart disease (CHD, mediating proportion: 39.94%), followed by systolic blood pressure (36.51%), hypertension (23.87%), diastolic blood pressure (15.39%), type‐2 diabetes mellitus (T2DM, 12.71%), and low‐density lipoprotein cholesterol (7.97%). Conclusion: Our study revealed a causal protective effect of higher ALM on IS, independent of physical activity and adiposity‐related indices. Moreover, we found that higher ALM could reduce susceptibility to IS partially by lowering the risk of vascular risk factors, including CHD, hypertension, T2DM, and hyperlipidemia. In brief, we elucidated another modifiable factor for IS and implied that maintaining sufficient muscle mass may reduce the risk of such disease. [ABSTRACT FROM AUTHOR]

Background: Mendelian randomization analysis was applied to elucidate the causal relationship between the basal metabolic rate (BMR) and common cardiovascular diseases. Method: We choose BMR as exposure. BMR is the metabolic rate of the body when the basic physiological activities (blood circulation, breathing and constant body temperature) are maintained. The normal BMR is 1507 kcal/day for men and 1276 kcal/day for women. The dataset was drawn from the public GWAS dataset (GWAS ID: ukb‐a‐268), collected and analysed by UK biobank, containing 331,307 European males and females. SNPs independently and strongly associated with BMR were used as instrumental variables in the inverse variance weighted analysis. MR‐Egger, weighted median, MR pleiotropy residual sum, and outlier methods were also performed, and the sensitivity was evaluated using horizontal pleiotropy and heterogeneity analyses to ensure the stability of the results. Results: An increased BMR is associated with a higher risk of cardiomyopathy (odds ratio [OR] = 2.00, 95% confidence interval [CI], 1.57–2.54, p = 1.87 × 10−8), heart failure (OR = 1.39, 95% CI, 1.27–2.51, p = 8.1 × 10−13), and valvular heart disease (OR = 1.18, 95% CI, 1.10–1.27, p =.00001). However, there was no clear association between BMR and the subtypes of other cardiovascular diseases, such as coronary disease (OR =.96, 95% CI,.85–1.08, p =.48651) and atrial fibrillation (AF) (OR = 1.85, 95% CI, 1.70–2.02, p = 6.28 × 10−44). Conclusion: Our study reveals a possible causal effect of BMR on the risk of cardiomyopathy, heart failure and valvular disease, but not for coronary disease and AF. [ABSTRACT FROM AUTHOR]

Background: Cutaneous melanoma (CM) of the skin stands as the leading cause of mortality among skin cancer-related deaths. Despite the successes achieved with novel therapies such as immunotherapy and targeted therapy, their efficacy remains limited, necessitating further exploration of new treatment modalities. The gut microbiota and CM may be linked, as indicated by a growing body of preclinical and observational research. Nevertheless, the exact correlation between the intestinal microbiota and CM remains to be determined. Therefore, this study aims to assess the potential causal relationship between the gut microbiota and CM. Methods: The study utilized exposure data obtained from the MiBioGen consortium's microbiome GWAS, which included a total of 18,340 samples gathered from 24 population-based cohorts. Data at the summary level for CM were acquired from the UK Biobank investigation. The main analytical strategy utilized in this research was the inverse variance weighted (IVW) technique, supported by quality assurance measures like the weighted median model, MR-Egger, simple model, and weighted model approaches. The Cochran's Q test was used to evaluate heterogeneity. To ascertain potential pleiotropy, we employed both the MR-Egger regression and the MR-PRESSO test. Sensitivity analysis was conducted using the leave-one-out method. Results: The study found that the class Bacteroidia (OR = 0.997, 95% CI: 0.995-0.999, p = 0.027), genus Parabacteroides (OR = 0.997, 95% CI: 0.994-0.999, p = 0.037), order Bacteroidales (OR = 0.997, 95% CI: 0.995-0.999, p = 0.027), and genus Veillonella (OR = 0.998, 95% CI: 0.996-0.999, p = 0.046) have protective effects on CM. On the order hand, the genus Blautia (OR = 1.003, 95% CI: 1-1.006, p = 0.001) and phylum Cyanobacteria (OR = 1.002, 95% CI: 1-1.004, p = 0.04) are identified as risk factors for CM. Conclusion: We comprehensively assessed the potential causal relationship between the gut microbiota and CM and identified associations between six gut microbiota and CM. Among these, four gut microbiota were identified as protective factors for CM, while two gut microbiota were identified as risk factors for CM. This study effectively established a causal relationship between the gut microbiota and CM, thereby providing valuable insights into the mechanistic pathways through which the microbiota impacts the progression of CM. [ABSTRACT FROM AUTHOR]

Background: The prevalence of depression among people with chronic pain remains unclear due to the heterogeneity of study samples and definitions of depression. We aimed to identify sources of variation in the prevalence of depression among people with chronic pain and generate clinical prediction models to estimate the probability of depression among individuals with chronic pain. Methods: Participants were from the UK Biobank. The primary outcome was a "lifetime" history of depression. The model's performance was evaluated using discrimination (optimism-corrected C statistic) and calibration (calibration plot). Results: Analyses included 24,405 patients with chronic pain (mean age 64.1 years). Among participants with chronic widespread pain, the prevalence of having a "lifetime" history of depression was 45.7% and varied (25.0–66.7%) depending on patient characteristics. The final clinical prediction model (optimism-corrected C statistic: 0.66; good calibration on the calibration plot) included age, BMI, smoking status, physical activity, socioeconomic status, gender, history of asthma, history of heart failure, and history of peripheral artery disease. Among participants with chronic regional pain, the prevalence of having a "lifetime" history of depression was 30.2% and varied (21.4–70.6%) depending on patient characteristics. The final clinical prediction model (optimism-corrected C statistic: 0.65; good calibration on the calibration plot) included age, gender, nature of pain, smoking status, regular opioid use, history of asthma, pain location that bothers you most, and BMI. Conclusions: There was substantial variability in the prevalence of depression among patients with chronic pain. Clinically relevant factors were selected to develop prediction models. Clinicians can use these models to assess patients' treatment needs. These predictors are convenient to collect during daily practice, making it easy for busy clinicians to use them. [ABSTRACT FROM AUTHOR]

The causal relationship between different hypothyroidism subtypes and the risk of major depression (MD) is yet to be fully elucidated. This study aimed to determine if there's a causal relationship between various hypothyroidism subtypes (and related factors) and the risk of MD. This genetic association study utilized a two-sample Mendelian Randomization (MR) approach to explore the causal relationships between various hypothyroidism subtypes and MD risk. Genome-Wide Association Study (GWAS) summary statistics were obtained from the FinnGen and the UK Biobank. Instrumental variables (IVs) were chosen based on single nucleotide polymorphisms (SNPs). Among the analyzed hypothyroidism subtypes and related factors, "Hypothyroidism, strict autoimmune" (HTCBSA) and "Hypothyroidism, levothyroxin purchases" (HT/LP) demonstrated a statistically significant positive causal relationship with MD, with odds ratios of 1.020 (95 % CI: 1.004–1.037) and 1.022 (95 % CI: 1.005–1.040), respectively. The sensitivity analysis supported the robustness of these findings, showing no significant horizontal pleiotropy and confirming the stability of results when individual SNPs were removed. "Congenital iodine-deficiency syndrome/hypothyroidism" (CIDS/HT), "Postinfectious hypothyroidism" (PHT), "Hypothyroidism due to medicaments and other exogenous substances" (HDTDM and OES), "Thyroid Stimulating Hormone" (TSH), "Thyrotropin-releasing hormone" (THRH), and "Hypothyroidism, strict autoimmune, 3 medication purchases required" (HTCBSA/3MPR) showed no significant causal relationship with MD. The study population was limited to individuals of European ancestry, and there may be certain genetic differences between different ethnic groups. This MR study suggests a potential causal relationship between certain hypothyroidism subtypes (specifically HTCBSA and HT/LP) and an increased risk of MD. • MR was applied to analyze the causal relationship between the hypothyroidism subtypes and MD. • HTCBSA and HT/LP hypothyroidism subtypes were related to the increased risk of MD. • The causal relationship between the therapy of hypothyroidism and MD was analyzed. [ABSTRACT FROM AUTHOR]

Background: Impaired glucose utilization influences myocardial contractile function. However, the prognostic importance of left ventricular global radial strain (LV-GRS), left ventricular global circumferential strain (LV-GCS), and left ventricular global longitudinal strain (LV-GLS) in predicting new-onset heart failure (HF) in a population with diabetes is unclear. Methods: The study design is prospective cohort from the UK Biobank. Totally 37,899 participants had a complete data of cardiac magnetic resonance (CMR), of which 940 patients with diabetes were included, and all the participants completed follow-up. LV-GRS, LV-GCS, and LV-GLS were measured by completely automated CMR with tissue tagging. Cox proportional hazards regression analysis and C-index was performed to evaluate the association between the strain parameters and the new-onset HF in patients suffering from diabetes. Results: The average age of the 940 participants was 57.67 ± 6.97 years, with males comprising 66.4% of the overall population. With an average follow-up period of 166.82 ± 15.26 months, 35 (3.72%) patients reached the endpoint (emergence of new-onset HF). Significant associations were found for the three strain parameters and the new-onset HF (LV-GRS--hazard ratio [HR]: 0.946, 95% CI: 0.916-0.976; LV-GCS--HR: 1.162, 95% CI: 1.086-1.244; LV-GCS--HR: 1.181, 95% CI: 1.082-1.289). LV-GRS, LV-GCS, and LV-GLS were closely related to the related indicators to HF, and showed a high relationship to new-onset HF in individuals with diabetes at 5 and 10 years: LV-GRS: 0.75 (95% CI, 0.41-0.94) and 0.76 (95% CI, 0.44-0.98), respectively; LV-GCS: 0.80 (95% CI, 0.50-0.96) and 0.75 (95% CI, 0.41-0.98), respectively; LV-GLS: 0.72 (95% CI, 0.40-0.93) and 0.76 (95% CI, 0.48-0.97), respectively. In addition, age, sex, body mass index (BMI), and presence of hypertension or coronary artery disease (CAD) made no impacts on the association between the global strain parameters and the incidence of HF. Conclusion: LV-GRS, LV-GCS, and LV-GLS is significantly related to new-onset HF in patients with diabetes at 5 and 10 years. [ABSTRACT FROM AUTHOR]