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AIMS: To investigate the association of accelerometer-measured intensity-specific physical activity (PA) with all-cause and cause-specific mortality among individuals with cardiovascular disease (CVD). METHODS: In this prospective cohort study, 8,024 individuals with pre-existing CVD (mean age: 66.6 years, female: 34.1%) from the UK Biobank had their PA measured using wrist-worn accelerometers over a 7-day period in 2013-2015. All-cause, cancer, and CVD mortality was ascertained from death registries. Cox regression modelling and restricted cubic splines were used to assess the associations. Population-attributable fractions (PAFs) were used to estimate the proportion of preventable deaths if more PA were undertaken. RESULTS: During an average of 6.8 years of follow-up, 691 deaths (273 from cancer and 219 from CVD) were recorded. An inverse non-linear association was found between PA duration and all-cause mortality risk, irrespective of PA intensity. The hazard ratio (HR) of all-cause mortality plateaued at 1800 minutes/week for light-intensity PA (LPA), 320 minutes/week for moderate-intensity PA (MPA) and 15 minutes/week for vigorous-intensity PA (VPA). The highest quartile of PA associated lower risks for all-cause mortality, with HRs of 0.63 (95% confidence interval [CI]: 0.51-0.79), 0.42 (0.33-0.54) and 0.47 (0.37-0.60) for LPA, MPA, and VPA, respectively. Similar associations were observed for cancer and CVD mortality. Additionally, the highest PAF were noted for VPA, followed by MPA. CONCLUSION: We found an inverse non-linear association between all intensities of PA (LPA, MPA, VPA, and MVPA) and mortality risk in CVD patients using accelerometer-derived data, but with larger magnitude of the associations than that in previous studies based on self-reported PA.
This study investigated the associations of accelerometer-derived intensity-specific physical activity (PA) with the risks of all-cause and cause-specific mortality among individuals with cardiovascular disease (CVD). L-shaped dose-response relationships between the duration of PA and all-cause mortality were observed across all levels of PA intensities. The risk reduction for mortality exhibited a sharp decline from 0 to 1800 minutes/week of light-intensity PA, followed by reaching a plateau. Notably, the inflection points for moderate-intensity PA and vigorous-intensity PA were found at 320 and 15 minutes per week, respectively. The population-attributable fraction analysis indicated that a significant number of deaths could potentially be prevented if individuals with CVD engaged in more vigorous physical activities.
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Physical activity (PA) has been shown to reduce diabetes mortality, but largely based on imprecise self-reported data, which may hinder the development of related recommendations. Here, we perform a prospective cohort study of 19,624 individuals with type 2 diabetes (T2D) from the UK Biobank with a median follow-up of 6.9 years. Duration and intensity of PA are measured by wrist-worn accelerometers over a 7-day period. We observe L-shaped associations of longer duration of PA, regardless of PA intensity, with risks of all-cause and cancer mortality, as well as a negatively linear association with cardiovascular disease mortality. 12.7%, 15.8%, and 22.3% of deaths are attributable to the lowest level of light-intensity, moderate-intensity PA, and vigorous-intensity PA, respectively. Collectively, our findings provide insights for clinical guidelines that should highlight the potential value of adherence to greater intensity and duration of PA for patients with T2D.
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Acelerometria , Diabetes Mellitus Tipo 2 , Exercício Físico , Humanos , Diabetes Mellitus Tipo 2/mortalidade , Acelerometria/instrumentação , Feminino , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Idoso , Doenças Cardiovasculares/mortalidade , Adulto , Neoplasias/mortalidade , Reino Unido/epidemiologiaRESUMO
OBJECTIVES: To investigate the associations of recreational screen time with risks of brain-related disorders (dementia, stroke, and Parkinson's disease) and neuroimaging features. DESIGN: Prospective cohort study. SETTING AND PARTICIPANTS: A total of 407,792 participants from the UK Biobank who were free of dementia, stroke, or Parkinson's disease at enrollment (2006-2010). METHODS: TV viewing and time spent using the computer were self-reported at baseline. Among a subsample of 40,692 participants, neuroimaging features were measured by magnetic resonance imaging in 2014. Data were analyzed using Cox proportional hazard models, restricted cubic spline models, and general linear regression models. RESULTS: During a median follow-up of 12.6 years, 5227 incident dementia, 6822 stroke, and 2308 Parkinson's disease cases were identified. Compared with TV viewing >0-1 h/day, watching TV ≥5 h/day was associated with higher risks of dementia [hazard ratio (HR), 1.44; 95% confidence interval (CI), 1.28-1.62], stroke (HR, 1.12; 95% CI, 1.01-1.25), and Parkinson's disease (HR, 1.28; 95% CI, 1.06-1.54). Moreover, we observed inverse associations between TV viewing time and both gray matter volume and hippocampus volume (Ptrend <.001). However, we did not observe the significant associations between discretional computer use and brain-related disorders or neuroimaging features. CONCLUSIONS AND IMPLICATIONS: Our findings suggest that high TV viewing time is associated with increased risk of various brain-related disorders, highlighting recreational TV viewing could have an important impact on brain-related health.
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Demência , Imageamento por Ressonância Magnética , Tempo de Tela , Humanos , Estudos Prospectivos , Masculino , Feminino , Idoso , Pessoa de Meia-Idade , Demência/epidemiologia , Doença de Parkinson/diagnóstico por imagem , Acidente Vascular Cerebral/epidemiologia , Reino Unido/epidemiologia , Neuroimagem , Encéfalo/diagnóstico por imagem , Modelos de Riscos Proporcionais , Recreação , Televisão/estatística & dados numéricosRESUMO
BACKGROUND: Cumulative evidence suggests a correlation between physical or mental activity and the risk of stroke. However, the combined impact of these activities on stroke onset remains unexplored. This study identified physical and mental activity patterns using principal component analysis and investigated their associations with risk of incident stroke in the general population. METHODS: Our study was sourced from the UK Biobank cohort between 2006 and 2010. Information on physical and mental-related activities were obtained through a touch-screen questionnaire. The incident stroke was diagnosed by physicians and subsequently verified through linkage to Hospital Episode Statistics. Principal component analysis was used to identify potential physical and mental activity patterns. Cox proportional hazard regression models were performed to calculate hazard ratios (HRs) and 95% CIs of incident stroke, adjusting for potential confounders. RESULTS: The initial UK Biobank cohort originally consisted of 502â 411 individuals, of whom a total of 386â 902 participants (aged 38-79 years) without any history of stroke at baseline were included in our study. During a median follow-up of 7.7 years, 6983 (1.8%) cases of stroke were documented. The mean age of the included participants was 55.9 years, and the proportion of women was 55.1%. We found that multiple individual items related to physical and mental activity showed significant associations with risk of stroke. We identified 4 patterns of physical activity and 3 patterns of mental activity using principal component analysis. The adherence to activity patterns of vigorous exercise, housework, and walking predominant patterns were associated with a lower risk of stroke by 17% (HR, 0.83 [95% CI, 0.78-0.89]; 20% (HR, 0.80 [95% CI, 0.75-0.85]; and 20% (HR, 0.80 [95% CI, 0.75-0.86), respectively. Additionally, the transportation predominant pattern (HR, 1.36 [95% CI, 1.28-1.45) and watching TV pattern (HR, 1.43 [95% CI, 1.33-1.53) were found to be significantly associated with a higher risk of stroke. These associations remained consistent across all subtypes of stroke. CONCLUSIONS: Activity patterns mainly related to frequent vigorous exercise, housework, and walking were associated with lower risks of stroke and all its subtypes. Our findings provide new insights for promoting suitable patterns of physical and mental activity for primary prevention of stroke.
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BACKGROUND: Atrial fibrillation (AF) is the most common sustained arrhythmia and is associated with significant morbidity and mortality. Hearing impairment has been linked to several cardiovascular diseases. However, the association between hearing disorders, genetic predisposition, and new-onset AF remains largely unknown. METHODS: A total of 476,773 participants (mean age 56.5 years) free of AF at baseline (from 2006 to 2010) were included from the UK Biobank study. The presence of hearing disorders including hearing difficulty and tinnitus was self-reported through the touchscreen questionnaire. AF was defined using ICD-10 code: I48 and was followed till February 1st. 2022. The Cox model was used to calculate hazard ratios (HRs) and 95% confidence intervals (95% CI). RESULTS: During a median follow-up of 13.0 years, the AF incidence rate was 2.9 per 1000 person-years. After adjustments for potential confounders, the presence of hearing difficulty (HR, 1.35; 95% CI: 1.32-1.39) and the use of hearing aid (1.45; 1.37-1.53) were significantly associated with risk of new-onset AF. Compared to individuals without tinnitus, the AF risk increased by 17% among those who experienced tinnitus occasionally (1.17; 1.09-1.25), 23% among those who experienced tinnitus frequently (1.23; 1.10-1.39), and 32% among those who experienced tinnitus consistently (1.32; 1.22-1.42). No significant difference was observed across different groups of genetic risk score for AF onset. CONCLUSIONS: Our study provides evidence regarding significant associations of hearing difficulty, use of hearing aid, and tinnitus with risk of incident AF. Findings highlight the potential that screening hearing disorders can benefit AF prevention.
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Fibrilação Atrial , Zumbido , Humanos , Pessoa de Meia-Idade , Fibrilação Atrial/diagnóstico , Fibrilação Atrial/epidemiologia , Fibrilação Atrial/genética , Estudos Prospectivos , Zumbido/diagnóstico , Zumbido/epidemiologia , Zumbido/genética , Bancos de Espécimes Biológicos , Biobanco do Reino Unido , Incidência , Predisposição Genética para Doença , Fatores de RiscoRESUMO
Background: The evidence regarding the association between leucocyte telomere length (LTL) and brain health is sparse and inconclusive. Aims: To investigate the associations of LTL with brain structure and the risk of dementia based on a large-scale prospective study. Methods: LTL in the peripheral blood was measured by the quantitative polymerase chain reaction (qPCR) assay from 439 961 individuals in the UK Biobank recruited between 2006 and 2010 and followed up until 2020. Electronic health records were used to record the incidence of dementia, including Alzheimer's disease (AD) and vascular dementia (VD). The brain structure, including total and regional brain volume, of 38 740 participants was then assessed by magnetic resonance imaging (MRI). Results: During a median follow-up of 11.6 years, a total of 5 820 (1.3%) dementia cases were documented. The restricted cubic spline model showed significant overall associations between LTL and the risk of dementia and AD (p for overall <0.05). The multivariable adjusted hazard ratios (HRs) for the lowest LTL tertile compared with the highest LTL tertile were 1.14 (95% confidence interval (CI): 1.06 to 1.21) for dementia, 1.28 (95% CI: 1.12 to 1.46) for AD and 1.18 (95% CI: 0.98 to 1.42) for VD. Furthermore, we found that shorter LTL was associated with smaller total brain volume (ß=-0.012 8, p=0.003), white matter volume (ß=-0.022 4, p<0.001), hippocampus volume (ß=-0.017 2, p<0.001), thalamus volume (ß=-0.023 9, p<0.001) and accumbens (ß=-0.015 5, p=0.001). Conclusions: Shorter LTL is associated with total and regional brain structure and a higher risk of incident dementia and AD, implying the potential of telomere length as a predictive biomarker of brain health.
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BACKGROUND: Diet is increasingly recognized as an important risk factor for mental health. However, evidence regarding the association between diet pattern and depressive and anxiety symptoms is limited. We aimed to investigate the associations of dietary patterns characterized by a set of nutrients of interest with depressive and anxiety symptoms. METHODS: The analyses included a total of 126,819 participants in the UK Biobank who had completed at least two dietary questionnaires. Dietary data were obtained through 24-h dietary assessment at baseline between 2006 and 2010 and four rounds of online follow-ups between 2011 and 2012. Reduced rank regression was applied to derive dietary patterns (DPs) explaining variability in energy density, free sugars, saturated fat, and fiber intakes. Depressive and anxiety symptoms were measured by the Patient Health Questionnaire-9 and General Anxiety Disorder-7 between 2016 and 2017, respectively. Logistic regression models were performed to investigate the associations between dietary patterns and depressive and anxiety symptoms. RESULTS: During a mean follow-up of 7.6 years, 2746 cases of depressive symptoms and 2202 cases of anxiety symptoms were recorded. Three major DPs were derived, explaining 74% of the variation in nutrients hypothesized to be related to depressive and anxiety symptoms. DP1 was characterized by high intakes of chocolate, confectionery, butter, and low vegetable/fruit intakes. Compared to the lowest quintile of DP1, the odds ratio (95% confidence interval) of depressive symptoms for Q2-Q5 was 0.82 (0.72-0.93), 0.86 (0.76-0.98), 1.02 (0.90-1.15), and 1.17 (1.03-1.32), respectively. Compared to the lowest quintile of DP1, the odds ratio (95% CI) of anxiety symptoms for Q2-Q5 was 0.84 (0.73-0.97), 0.91 (0.79-1.05), 1.01 (0.88-1.15), and 1.18 (1.03-1.35), respectively. DP2 featured high intakes of sugar-sweetened beverages, added sugars, and low intakes of butter/cheese but showed no significant links to depressive or anxiety symptoms. DP3 was characterized by high butter and milk desserts and low alcohol/bread intakes. Compared to the lowest quintile of DP3, the odds ratio (95% CI) of depressive symptoms for Q2-Q5 was 0.90 (0.79-1.01), 1.00 (0.88-1.13), 1.06 (0.94-1.20), and 1.17 (1.03-1.32), respectively. Compared to the lowest quintile of DP3, the odds ratio (95% CI) of anxiety symptoms for Q2-Q5 was 0.90 (0.78-1.04), 1.05 (0.91-1.20), 1.02 (0.89-1.17), and 1.21 (1.05-1.38), respectively. CONCLUSIONS: A DP characterized by high intakes of chocolate and confectionery, butter, high-fat cheese, added sugars, along with low intakes of fresh fruit and vegetables, is associated with a higher risk of depressive and anxiety symptoms.
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Dieta , Verduras , Humanos , Estudos Prospectivos , Dieta/efeitos adversos , Ansiedade/epidemiologia , Manteiga , AçúcaresRESUMO
Accumulating evidence has reported the associations of coffee consumption with physical conditions and mortality, but the associations with mental disorders were limited. The objective of this study was to examine the associations of coffee consumption with incident depression and anxiety, and to assess whether the associations differed by coffee subtypes (instant, ground, and decaffeinated coffee) or additives (milk, sugar-sweetened, and artificial-sweetened). In this prospective cohort study, we utilized data from the UK Biobank and included a total of 146,566 participants who completed the touchscreen questionnaire at baseline between 2006 and 2010. During the follow-up, incident depression and anxiety were measured in 2016 using the Patient Health Questionnaire (PHQ)-9 and the Generalised Anxiety Disorder Assessment (GAD)-7, respectively. Multivariable-adjusted logistic regression models and restricted cubic splines were used to assess the associations. Approximately 80.7% of participants reported consuming coffee, and most drank 2 to 3 cups per day (41.2%). We found J-shaped associations between coffee consumption and both incident depression and anxiety, with the lowest risk of the mental disorders occurring at around 2-3 cups per day. Results were similar for participants who drank 2-3 cups of ground coffee, milk-coffee, or unsweetened coffee. Our findings highlight that 2-3 cups of coffee consumption could be recommended as part of a healthy lifestyle to improve mental health.
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BACKGROUND: Sleep behaviors are potentially modifiable risk factors for common mental disorders and cardiovascular disease (CVD). However, the associations between combined sleep behaviors and common mental disorders among individuals with CVD remain unclear. METHODS: A total of 18,776 participants with a history of CVD from UK Biobank, who were free of depression or anxiety from 2006 to 2010 were included. A composite healthy sleep score was constructed based on five sleep behaviors (chronotype, sleep duration, insomnia, snoring, and excessive daytime sleepiness). Cox proportional hazard regression models were performed to calculate hazard ratios (HRs) and 95 % confidence intervals (CIs) for incident depression and anxiety. RESULTS: During a median follow-up of 11.8 years, 965 depression and 812 anxiety cases were recorded. The adjusted HRs for participants with a healthy sleep pattern compared with a poor sleep pattern were 0.45 (95 % CI: 0.35-0.57) for depression and 0.77 (95 % CI: 0.58-1.03) for anxiety. There was a linear dose-response association of healthy sleep score with incident depression and anxiety (HR = 0.82, 95 % CI: 0.77-0.87; HR = 0.92, 95 % CI: 0.86-0.99 per 1-score increase, respectively). Likewise, these associations were observed among individuals with coronary heart disease, stroke, heart failure and atrial fibrillation. CONCLUSIONS: A healthy sleep pattern is significantly associated with a lower risk of depression among individuals with CVD, highlighting the importance of monitoring and improving sleep health in the prevention of common mental disorders among individuals with CVD.
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Doenças Cardiovasculares , Insuficiência Cardíaca , Distúrbios do Início e da Manutenção do Sono , Humanos , Doenças Cardiovasculares/epidemiologia , Estudos Prospectivos , Sono/fisiologia , Distúrbios do Início e da Manutenção do Sono/epidemiologia , Fatores de RiscoRESUMO
SCOPE: Evidence suggests a positive association between ultra-processed food (UPF) consumption and the incidence of cardiovascular disease (CVD). The study aims to investigate associations between UPF intake and respiratory disease, CVD, and their multimorbidity in a large prospective cohort. METHODS AND RESULTS: Within the UK Biobank, participants who are free from respiratory disease or CVD at baseline and completed at least two times 24-h dietary records are included in this study. After adjusting for socioeconomic status and lifestyle factors, the hazard ratios (95% confidence interval) for each 10% increase in UPF are 1.06 (1.04, 1.09) for CVD, 1.04 (1.02, 1.06) for respiratory disease, 1.15 (1.08, 1.22) for CVD mortality, and 1.06 (1.01, 1.12) for their multimorbidity, respectively. In addition, replacing 20% of UPF weight in diet with an equivalent proportion of unprocessed or minimally processed foods is estimated to be associated with 11% lower risk of CVD, 7% lower risk of respiratory disease, 25% lower risk of CVD mortality, and 11% lower risk of CVD and respiratory disease multimorbidity. CONCLUSION: In this prospective cohort study, higher consumption of UPF is associated with higher risks of CVD and respiratory disease multimorbidity. Further longitudinal studies are needed to confirm these findings.
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Doenças Cardiovasculares , Alimento Processado , Humanos , Estudos Prospectivos , Multimorbidade , Fast Foods/efeitos adversos , Dieta/efeitos adversos , Doenças Cardiovasculares/epidemiologia , Doenças Cardiovasculares/etiologia , Manipulação de AlimentosRESUMO
BACKGROUND: Accumulated evidence confirmed depression was positively associated with coronary heart disease (CHD). But evidence of the association between depression and premature CHD is still unknown. OBJECTIVES: To explore the association between depression and premature CHD, and to investigate whether and to what extent the association is mediated by metabolic factors and systemic immune-inflammation index (SII). METHODS: In this large population-based cohort study based on the UK Biobank, 176,428 CHD-free (mean age: 52.70) adults were followed up for 15 years to detect incident premature CHD. Depression and premature CHD (mean age: female, 54.53; male, 48.13) were ascertained from self-report data and linked hospital-based clinical diagnosis. Metabolic factors included central obesity, hypertension, dyslipidemia, hypertriglyceridemia, hyperglycemia, and hyperuricemia. Systemic inflammation was evaluated by calculating SII, which equals platelet count (/L) × neutrophil count (/L) / lymphocyte count (/L). Data were analyzed using Cox proportional hazards models and generalized structural equation model (GSEM). RESULTS: During follow-up (median: 8.0 years, interquartile range: 4.0 to 14.0 years), 2990 participants developed premature CHD (1.7 %). The adjusted hazard ratio (HR) and 95 % confidence interval (CI) of premature CHD related to depression were 1.72 (1.44-2.05). The association between depression and premature CHD was 32.9 % mediated by comprehensive metabolic factors (ß = 0.24, 95 % CI: 0.17-0.32) and 2.7 % by SII (ß = 0.02, 95 % CI = 0.01-0.04), respectively. Concerning metabolic factors, the strongest indirect association was for central obesity, accounting for 11.0 % of the association between depression and premature CHD (ß = 0.08, 95 % CI: 0.05-0.11). CONCLUSIONS: Depression was associated with an increased risk of premature CHD. Our study provided evidence that metabolic and inflammatory factors might play a mediating role in the association between depression and premature CHD, especially central obesity.
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Doença da Artéria Coronariana , Obesidade Abdominal , Adulto , Humanos , Masculino , Feminino , Pessoa de Meia-Idade , Estudos de Coortes , Depressão/epidemiologia , Fatores de Risco , Inflamação/epidemiologia , Obesidade , Modelos de Riscos Proporcionais , IncidênciaRESUMO
Older adults have been markedly impacted by the coronavirus disease 19 (COVID-19) pandemic, and many reports have cited concerns regarding potential psychiatric sequelae of coronavirus disease (COVID-19), but the actual effects of psychotropics on the COVID-19 are unclear. In this study, multivariate logistic regression was used to evaluate associations between the prescription of psychotropics and the risk of SARS-CoV-2 infection, and COVID-19-related death among the participants who were tested for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) before October 18, 2021, in UK Biobank. The psychotropics included 18 types of medications. Among 168,173 participants who underwent testing for SARS-CoV-2 RNA, 30,577 (18.2%) were positive, and 14,284 (8.5%) participants used psychotropics. Among 30,577 participants who were infected with SARS-CoV-2, 1,181 (3.9%) were COVID-19-related deaths, and 2,542 (8.3%) participants used psychotropics. In multivariate logistic regression, psychotropics use was significantly associated with the risk of SARS-CoV-2 infection (odds ratio [OR], 0.95; 95% confidence interval [CI], 0.88-0.98), and COVID-19-related death (OR, 0.78; 95% CI, 0.64-0.98). Interestingly, the use of diazepam was significantly associated with a 31% lower risk of SARS-CoV-2 infection (OR, 0.69; 95% CI, 0.53-0.88). The use of sertraline was significantly associated with a 89% lower risk of COVID-19-related death (OR, 0.11; 95% CI, 0.02-0.39). In conclusion, our findings suggested that the use of psychotropics was associated with a lower risk of SARS-CoV-2 infection and COVID-19-related deaths.
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COVID-19 , Pessoa de Meia-Idade , Humanos , Idoso , SARS-CoV-2 , RNA Viral , Psicotrópicos/uso terapêutico , Progressão da DoençaRESUMO
BACKGROUND: Growing evidence has showed an association between habitual glucosamine use and type 2 diabetes (T2D). However, the effect of habitual glucosamine use on risk of dementia remains poorly understood. Our study aimed to examine the association between glucosamine use and risk of dementia and further to identify the mediating role of T2D in the association. METHODS: A total of 495,942 participants from UK Biobank who completed a questionnaire on habitual glucosamine use were included at baseline (2006-2010) and then followed up for incidence of dementia until 2020. Cox proportional hazard regressions were performed to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for incident dementia. Markov multi-state models were used to explore the role of incidence of T2D during the follow-up in the association. RESULTS: Overall, 18.80% of the participants reported habitual use of glucosamine at baseline. A total of 6831 dementia events were recorded during a median follow-up of 11 years. In fully adjusted models, habitual glucosamine use was associated with a significantly lower risk of dementia (HR = 0.87, 95% CI: 0.82-0.93). Multi-state models showed that the association between glucosamine use and dementia was mediated by the incidence of T2D during the follow-up (HR of dementia without T2D: 0.92, 95% CI: 0.86-0.99; HR of post-T2D dementia: 0.79, 95% CI: 0.67-0.93). CONCLUSIONS: Our findings reveal that habitual use of glucosamine supplement is associated with a lower risk of dementia, which might be explained by incidence of T2D.
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Demência , Diabetes Mellitus Tipo 2 , Humanos , Diabetes Mellitus Tipo 2/epidemiologia , Glucosamina/uso terapêutico , Fatores de Risco , Estudos Prospectivos , Incidência , Demência/epidemiologia , Demência/complicaçõesRESUMO
OBJECTIVE: to examine the association between different patterns of impaired lung function with the incident risk of dementia and magnetic resonance imaging (MRI)-based brain structural features. METHODS: in UK Biobank, a total of 308,534 dementia-free participants with valid lung function measures (forced expiratory volume in 1 s [FEV1] and forced vital capacity [FVC]) were included. Association was assessed using Cox proportional hazards regression model. Furthermore, the association between impaired lung function and brain MRI biomarkers related to cognitive function was analysed among 30,159 participants. RESULTS: during a median follow-up of 12.6 years, 3,607 incident all-cause dementia cases were recorded. Restrictive impairment (hazard ratio [HR], 1.42; 95% confidence interval [CI], 1.27-1.60) and obstructive impairment (HR, 1.28; 95% CI, 1.15-1.42) were associated with higher risk of all-cause dementia. The restricted cubic splines indicated FEV1% predicted and FVC % predicted had reversed J-shaped associations with dementia. Participants with impaired lung function have higher risks of all-cause dementia across all apolipoprotein E (APOE) risk categories, whereas associations were stronger among those of low APOE risk (P for interaction = 0.034). In addition, restrictive and obstructive impairment were linked to lower total (ß: -0.075, SE: 0.021, Pfdr = 0.002; ß: -0.033, SE: 0.017, Pfdr = 0.069) and frontoparietal grey matter volumes, higher white matter hyperintensity, poorer white matter integrity, lower hippocampus (ß: -0.066, SE: 0.024, Pfdr = 0.017; ß: -0.051, SE: 0.019, Pfdr = 0.019) and other subcortical volumes. CONCLUSIONS: participants with restrictive and obstructive impairments had a higher risk of dementia. Brain MRI indices further supported adverse effects and provided insight into potential pathophysiology biomarkers.
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Encéfalo , Pneumopatias , Humanos , Estudos Longitudinais , Encéfalo/diagnóstico por imagem , Imageamento por Ressonância Magnética/métodos , Pulmão/diagnóstico por imagem , Apolipoproteínas E , BiomarcadoresRESUMO
BACKGROUND: We aimed to assess the impact of healthy cardiovascular health (CVH) on diabetic complications, mortality, and life expectancy among people with type 2 diabetes and to explore whether inflammation marker mediate these associations. METHODS: This prospective cohort study included 33,236 participants (aged 40-72) with type 2 diabetes from the UK Biobank with annual follow-up from 2006 to 2010 to 2020. Type 2 diabetes was ascertained from self-report, glycated hemoglobin ≥ 6.5%, hospital inpatient registry, or glucose-lowering medication use. Information on mortality was derived from the national death registry. Favorable CVH metrics consisted of non-smoker, regular physical activity, a healthy diet, non-overweight, untreated resting blood pressure < 120/<80 mm Hg, and untreated total cholesterol < 200 mg/dL. Participants were categorized into three groups according to the number of favorable CVH metrics: unfavorable (0 or 1); intermediate (any 2 or 3); and favorable (4 or more). Inflammation marker, as measured by C-reactive protein (CRP), was assessed at baseline and categorized as low (≤ 3 mg/L) and high (> 3 mg/L). Data were analyzed using Cox regression models, flexible parametric survival models, and mediation models. RESULTS: During the follow-up (median: 11.7 years), 3133 (9.4%) cases of diabetes complications and 4701 (14.1%) deaths occurred. Compared to unfavorable CVH, favorable CVH was associated with a reduced risk of diabetes complications (HR, 0.35; 95% CI, 0.26-0.47) and all-cause mortality (HR, 0.53; 95% CI, 0.43-0.65). In participants with unfavorable CVH, life expectancy at age 45 had a significantly reduction of 7.20 (95% CI, 5.48-8.92) years compared to those with a favorable CVH. Among people with type 2 diabetes, the proportions of diabetes complications and all-cause mortality that would be reduced by promoting the favorable CVH was 61.5% and 39.1%, respectively. CRP level mediated 14.3% and 29.7% of the associations between CVH and diabetic complication and all-cause mortality, respectively. CONCLUSION: A favorable CVH was associated with lower risk of diabetes complications and mortality risk, and was associated with a longer life expectancy among people with type 2 diabetes. This association may be in part accounted for by inflammatory processes. Our findings highlight the importance of favorable CVH for the prevention of diabetic complications and all-cause mortality among people with type 2 diabetes, and underscores the need to monitor inflammation among people with unfavorable CVH.
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SCOPE: Since associations between coffee and tea consumption with cardiovascular disease (CVD) and chronic respiratory disease (CRD) remain controversial. This study aims to investigate the separate and combined associations of coffee and tea consumption with CVD, CRD, and their comorbidity. METHODS AND RESULTS: Within the UK Biobank, 390 039 participants (56.2 ± 8.1 years) free of CVD and CRD are included. Coffee and tea consumption are self-reported at baseline. During a median follow-up of 12.1 years, 31126 CVD, 34132 CRD, and 6071 CVD-CRD comorbidity cases are identified. J-shaped associations between coffee and tea consumption with CVD, CRD, and CVD-CRD comorbidity are observed (p for nonlinearity <0.001). Compared with neither coffee nor tea consumption, hazard ratios (HRs) and 95% confidence intervals (CIs) of combined consumption of moderate coffee and tea (each 2-3 cups per day) are 0.88 (0.81-0.96) for CVD, 0.78 (0.72-0.84) for CRD, and 0.74 (0.61-0.91) for CVD-CRD comorbidity. CONCLUSION: Moderate consumption of coffee and tea separately or in combination are associated with lower risks of CVD, CRD, and their comorbidity.
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Doenças Cardiovasculares , Café , Humanos , Doenças Cardiovasculares/epidemiologia , Chá , Fatores de Risco , ComorbidadeRESUMO
BACKGROUND AND OBJECTIVES: There has been a growing body of evidence associating consumption of ultraprocessed foods (UPF) with adverse health outcomes including depression, cardiovascular disease, and all-cause mortality. However, whether UPF are associated with dementia is unknown. The authors investigated the associations between UPF and dementia incidence in the UK Biobank. METHODS: We included 72,083 participants (55 years or older) who were free from dementia at baseline and provided at least 2 times 24-hour dietary assessments from the UK Biobank study. Follow-up occurred through March 2021. UPF were defined according to the NOVA classification. Incident all-cause dementia comprising Alzheimer disease (AD) and vascular dementia was ascertained through electronic linkages to hospital and mortality records. Cox proportional hazards were used to estimate the association between the proportion (%) of UPF in the diet and the subsequent risk of dementia. In addition, substitution analysis was used to estimate the risk of dementia when substituting UPF with an equivalent proportion of unprocessed or minimally processed foods. RESULTS: During a total of 717,333 person-years of follow-up (median 10.0 years), 518 participants developed dementia, of whom 287 developed AD and 119 developed vascular dementia. In the fully adjusted model, consumption of UPF was associated with higher risk of dementia (hazard ratio [HR] for 10% increase in UPF 1.25; 95% CI 1.14-1.37), AD (HR 1.14; 95% CI 1.00-1.30), and vascular dementia (HR 1.28; 95% CI 1.06-1.55), respectively. In addition, replacing 10% of UPF weight in diet with an equivalent proportion of unprocessed or minimally processed foods was estimated to be associated with a 19% lower risk of dementia (HR 0.81; 95% CI 0.74-0.89). DISCUSSION: In this prospective cohort study, higher consumption of UPF was associated with higher risk of dementia, whereas substituting unprocessed or minimally processed foods for UPF was associated with lower risk of dementia.
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Demência Vascular , Dieta , Fast Foods/efeitos adversos , Manipulação de Alimentos , Humanos , Estudos ProspectivosRESUMO
BACKGROUND AND AIMS: Concerns regarding adverse events associated with the use of acid suppressants have increased. However, the impact of proton pump inhibitors (PPIs) and histamine-2 receptor antagonists (H2RAs) on the risk of atherosclerotic cardiovascular disease (ASCVD) remains unknown. This study aimed to estimate the risk of ASCVD in association with the use of PPIs and H2RAs. METHODS: This prospective cohort study included participants without cardiovascular diseases or anti-hypertensive treatment at baseline (2006-2010) in the UK Biobank. The outcomes were ASCVD and each subtype (coronary artery disease, myocardial infarction, peripheral artery disease, and ischemic stroke). The association was estimated by Cox proportional-hazards models. RESULTS: Among 316,730 individuals (aged 50-88 years), during a median of 12.5 years of follow-up, we documented 13,503 (4.3%) incident ASCVD. Regular PPIs use was associated with a higher risk of ASCVD (HR: 1.16, 95% CI: 1.09-1.23) and every subtype of ASCVD. Among each type of PPIs, omeprazole (HR: 1.19, 95% CI: 1.11-1.28), lansoprazole (HR: 1.11, 95% CI: 1.02-1.22), and pantoprazole (HR: 1.40, 95% CI: 1.00-1.97) were associated with a higher risk of ASCVD. Stratification analysis showed that PPIs use was associated with a higher risk of ASCVD among individuals without indications of medications for PPIs. In addition, use of H2RAs was not related to the risk of ASCVD (HR: 0.97, 95% CI: 0.85-1.11). CONCLUSIONS: PPIs were associated with increased risk of ASCVD, particularly amongst participants without indications for medication. Our findings are of important practical significance and suggest that clinicians should be cautious in prophylactic use of PPIs.
Assuntos
Aterosclerose , Doenças Cardiovasculares , Idoso , Anti-Hipertensivos/uso terapêutico , Aterosclerose/induzido quimicamente , Aterosclerose/tratamento farmacológico , Aterosclerose/epidemiologia , Doenças Cardiovasculares/tratamento farmacológico , Histamina , Humanos , Lansoprazol/efeitos adversos , Pessoa de Meia-Idade , Omeprazol , Pantoprazol , Estudos Prospectivos , Inibidores da Bomba de Prótons/efeitos adversos , Medição de Risco , Fatores de RiscoRESUMO
OBJECTIVE: To examine whether the association between cardiorespiratory fitness (CRF) and type 2 diabetes (T2D) is modified by genetic susceptibility and inflammation. PARTICIPANTS: The prospective study included 57,185 participants (40-70 years) who were free from T2D and received the CRF assessment at enrollment (2006-2010) in the UK biobank. CRF was examined through a submaximal cycle ergometer test and expressed in metabolic equivalent of tasks (METs), genetic susceptibility was quantified using a genetic risk score, and inflammation was assessed according to the concentration of C-reactive protein. All these three factors were categorized into tertiles. RESULTS: During a median follow-up of 10.4 years, 5477 (7.0%) cases of T2D were ascertained. CRF was inversely associated with the risk of T2D in a dose-response manner. The hazard ratio (HR) was 0.85 (95% confidence interval [CI]: 0.79-0.92) per 1 MET increment of CRF. There was a significant interaction between CRF and genetic susceptibility to T2D in relation to the risk of T2D (P for interaction = 0.03). Compared with participants with high CRF and low genetic susceptibility, the HR was 4.98 (95% CI: 3.17-7.82) for those with low CRF and high genetic susceptibility. A similar pattern was observed in participants with low CRF and high inflammation compared with those who had high CRF and low inflammation (HR = 2.53; 95% CI: 1.83-3.48), though the interaction between CRF and inflammation did not reach statistical significance. T2D risk declined progressively with increased CRF among different inflammation categories. CONCLUSION: Our study reveals that genetic susceptibility may modify the association between CRF and T2D, highlighting that risk of T2D associated with genetics could benefit most from interventions on improving CRF.