433 results on '"de Courten B."'
Search Results
2. Association of low carbohydrate diet score with the risk of type 2 diabetes in an Australian population: A longitudinal study.
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Kabthymer, RH, Karim, MN, Itsiopoulos, C, Hodge, AM, De Courten, B, Kabthymer, RH, Karim, MN, Itsiopoulos, C, Hodge, AM, and De Courten, B
- Abstract
AIMS: We aimed to assess the association of a low carbohydrate diet score (LCD) with the incidence of type 2 diabetes (T2D) using Melbourne Collaborative Cohort Study (MCCS) data. METHODS: Between 1990 and 1994, the MCCS recruited 41,513 people aged 40-69 years. The first and second follow-ups were conducted in 1995-1998 and 2003-2007, respectively. We analyzed data from 39,185 participants. LCD score was calculated at baseline as the percentage of energy from carbohydrate, fat, and protein. The higher the score the less percentage of carbohydrates contributed to energy intake. The association of LCD quintiles with the incidence of diabetes was assessed using modified Poisson regression, adjusted for lifestyle, obesity, socioeconomic and other confounders. Mediation of the association by adiposity (BMI) was assessed. RESULTS: LCD was positively associated with diabetes risk. Higher LCD score (p for trend = 0.001) was associated with increased risk of T2D. Quintile 5 (38 % energy from carbohydrates) versus quintile 1 (55 % energy from carbohydrates) showed a 20 % increased diabetes risk (incidence risk ratio (IRR) = 1.20 (95 % CI: 1.05-1.37)). A further adjustment for BMI (Body Mass Index) and WHR (Waist-to-Hip-Ratio) eliminated the association. Mediation analysis demonstrated that BMI mediated 76 % of the LCD & diabetes association. CONCLUSIONS: Consuming a low carbohydrate diet, reflected as a high LCD score, may increase the risk of T2D which is largely explained by obesity. Results highlight the need for further studies, including clinical trials investigating the effects of a low carbohydrate diet in T2D.
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- 2024
3. Sarcopenia and type 2 diabetes mellitus: a bidirectional relationship
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Mesinovic J, Zengin A, De Courten B, Ebeling PR, and Scott D
- Subjects
type 2 diabetes mellitus ,sarcopenia ,metabolic health ,muscle health ,obesity. ,Specialties of internal medicine ,RC581-951 - Abstract
Jakub Mesinovic,1 Ayse Zengin,1 Barbora De Courten,2 Peter R Ebeling,1,3 David Scott,1,31Department of Medicine, School of Clinical Sciences at Monash Health, Faculty of Medicine, Nursing and Health Sciences, Monash University, Clayton, Melbourne, VIC, Australia; 2Monash Centre for Health Research and Implementation, School of Public Health and Preventive Medicine, Monash University, Clayton, Melbourne, VIC, Australia; 3Australian Institute for Musculoskeletal Science (AIMSS), Department of Medicine - Western Health, Melbourne Medical School, The University of Melbourne, St Albans, Melbourne, VIC, AustraliaAbstract: The incidence and prevalence of metabolic and musculoskeletal diseases are increasing. Type 2 diabetes mellitus (T2DM) is characterized by insulin resistance, inflammation, advanced glycation end-product accumulation and increased oxidative stress. These characteristics can negatively affect various aspects of muscle health, including muscle mass, strength, quality and function through impairments in protein metabolism, vascular and mitochondrial dysfunction, and cell death. Sarcopenia is a term used to describe the age-related loss in skeletal muscle mass and function and has been implicated as both a cause and consequence of T2DM. Sarcopenia may contribute to the development and progression of T2DM through altered glucose disposal due to low muscle mass, and also increased localized inflammation, which can arise through inter- and intramuscular adipose tissue accumulation. Lifestyle modifications are important for improving and maintaining mobility and metabolic health in individuals with T2DM and sarcopenia. However, evidence for the most effective and feasible exercise and dietary interventions in this population is lacking. In this review, we discuss the current literature highlighting the bidirectional relationship between T2DM and sarcopenia, highlight current research gaps and treatments, and provide recommendations for future research.Keywords: type 2 diabetes mellitus, sarcopenia, metabolic health, muscle health, obesity
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- 2019
4. The burden and trend of diseases and their risk factors in Australia, 1990-2019: a systematic analysis for the Global Burden of Disease Study 2019
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Islam, SMS, Uddin, R, Maddison, R, Ball, K, Livingstone, KM, Khan, A, Salmon, J, Ackerman, IN, Adair, T, Adegboye, OA, Ademi, Z, Adhikary, RK, Ahinkorah, BO, Alam, K, Alene, KA, Alif, SM, Amare, AT, Ameyaw, EK, Aminde, LN, Anderlini, D, Angell, B, Ansar, A, Antony, B, Anyasodor, AE, Arnet, VK, Astell-Burt, T, Atorkey, P, Awoke, MA, Quintanilla, BPA, Ayano, G, Bagheri, N, Barnett, A, Baune, BT, Bhandari, D, Bhaskar, S, Biswas, RK, Borschmann, R, Boufous, S, Briggs, AM, Buchbinder, R, Bulamu, NB, Burns, RA, Carvalho, AF, Cerin, E, Cherbuin, N, Chowdhury, EK, Ciobanu, LG, Clark, SR, Cross, M, Dadi, AF, de Courten, B, De Leo, D, de Luca, K, Doyle, KE, Edvardsson, D, Edvardsson, K, Efendi, F, Endalamaw, A, Fauk, NK, Feng, X, Fitzgibbon, BM, Flavel, J, Gebreyohannes, EAA, Gesesew, HA, Gill, TK, Godinho, MA, Gupta, B, Gupta, VK, Hambisa, MT, Hamiduzzaman, M, Hankey, GJ, Hassanian-Moghaddam, H, Hay, SI, Hebert, JJ, Huda, MM, Huda, TM, Islam, MM, Islam, MS, Islam, RM, Kaambwa, B, Kandel, H, Kassie, GM, Kelly, JT, Kerr, JA, Kiross, GT, Knibbs, LD, Kulkarni, VV, Lalloo, R, Le, LKD, Leigh, J, Leung, J, Li, S, Mahumud, RA, Mamun, AA, Marzan, MB, McGrath, JJ, Mehlman, ML, Meretoja, A, Mersha, AG, Miller, TR, Mitchell, PB, Mokdad, AH, Morawska, L, Mpundu-Kaambwa, C, Mude, W, Murray, CJL, Kandel, SN, Nyanhanda, T, Obamiro, KO, Peden, AE, Pesudovs, K, Polkinghorne, KR, Rahman, A, Rahman, MA, Ratan, ZA, Rawal, L, Reifels, L, Renzaho, AMN, Robinson, SR, Roshandel, D, Rumisha, SF, Saunders, PA, Sawyer, SM, Schlaich, MP, Schutte, AE, Seidu, A-A, Sharma, S, Shorofi, SA, Siabani, S, Singh, A, Singh, BB, Slater, H, Stephens, JH, Stokes, MA, Subedi, NS, Sumi, CD, Sun, J, Sundstrom, J, Szoeke, CEI, Tadakamadla, SK, Takahashi, K, Taylor, J, Tessema, MBT, Thrift, AG, To, QG, Tollosa, DN, Tran, MTN, Vandelanotte, C, Varghese, BM, Veerman, LJ, Wang, N, Ward, P, Woodward, M, Wubishet, BL, Xu, X, Ye, P, Bin Zaman, S, Zarghami, A, Zhang, J, Crawford, DA, Islam, SMS, Uddin, R, Maddison, R, Ball, K, Livingstone, KM, Khan, A, Salmon, J, Ackerman, IN, Adair, T, Adegboye, OA, Ademi, Z, Adhikary, RK, Ahinkorah, BO, Alam, K, Alene, KA, Alif, SM, Amare, AT, Ameyaw, EK, Aminde, LN, Anderlini, D, Angell, B, Ansar, A, Antony, B, Anyasodor, AE, Arnet, VK, Astell-Burt, T, Atorkey, P, Awoke, MA, Quintanilla, BPA, Ayano, G, Bagheri, N, Barnett, A, Baune, BT, Bhandari, D, Bhaskar, S, Biswas, RK, Borschmann, R, Boufous, S, Briggs, AM, Buchbinder, R, Bulamu, NB, Burns, RA, Carvalho, AF, Cerin, E, Cherbuin, N, Chowdhury, EK, Ciobanu, LG, Clark, SR, Cross, M, Dadi, AF, de Courten, B, De Leo, D, de Luca, K, Doyle, KE, Edvardsson, D, Edvardsson, K, Efendi, F, Endalamaw, A, Fauk, NK, Feng, X, Fitzgibbon, BM, Flavel, J, Gebreyohannes, EAA, Gesesew, HA, Gill, TK, Godinho, MA, Gupta, B, Gupta, VK, Hambisa, MT, Hamiduzzaman, M, Hankey, GJ, Hassanian-Moghaddam, H, Hay, SI, Hebert, JJ, Huda, MM, Huda, TM, Islam, MM, Islam, MS, Islam, RM, Kaambwa, B, Kandel, H, Kassie, GM, Kelly, JT, Kerr, JA, Kiross, GT, Knibbs, LD, Kulkarni, VV, Lalloo, R, Le, LKD, Leigh, J, Leung, J, Li, S, Mahumud, RA, Mamun, AA, Marzan, MB, McGrath, JJ, Mehlman, ML, Meretoja, A, Mersha, AG, Miller, TR, Mitchell, PB, Mokdad, AH, Morawska, L, Mpundu-Kaambwa, C, Mude, W, Murray, CJL, Kandel, SN, Nyanhanda, T, Obamiro, KO, Peden, AE, Pesudovs, K, Polkinghorne, KR, Rahman, A, Rahman, MA, Ratan, ZA, Rawal, L, Reifels, L, Renzaho, AMN, Robinson, SR, Roshandel, D, Rumisha, SF, Saunders, PA, Sawyer, SM, Schlaich, MP, Schutte, AE, Seidu, A-A, Sharma, S, Shorofi, SA, Siabani, S, Singh, A, Singh, BB, Slater, H, Stephens, JH, Stokes, MA, Subedi, NS, Sumi, CD, Sun, J, Sundstrom, J, Szoeke, CEI, Tadakamadla, SK, Takahashi, K, Taylor, J, Tessema, MBT, Thrift, AG, To, QG, Tollosa, DN, Tran, MTN, Vandelanotte, C, Varghese, BM, Veerman, LJ, Wang, N, Ward, P, Woodward, M, Wubishet, BL, Xu, X, Ye, P, Bin Zaman, S, Zarghami, A, Zhang, J, and Crawford, DA
- Abstract
BACKGROUND: A comprehensive understanding of temporal trends in the disease burden in Australia is lacking, and these trends are required to inform health service planning and improve population health. We explored the burden and trends of diseases and their risk factors in Australia from 1990 to 2019 through a comprehensive analysis of the Global Burden of Disease Study (GBD) 2019. METHODS: In this systematic analysis for GBD 2019, we estimated all-cause mortality using the standardised GBD methodology. Data sources included primarily vital registration systems with additional data from sample registrations, censuses, surveys, surveillance, registries, and verbal autopsies. A composite measure of health loss caused by fatal and non-fatal disease burden (disability-adjusted life-years [DALYs]) was calculated as the sum of years of life lost (YLLs) and years of life lived with disability (YLDs). Comparisons between Australia and 14 other high-income countries were made. FINDINGS: Life expectancy at birth in Australia improved from 77·0 years (95% uncertainty interval [UI] 76·9-77·1) in 1990 to 82·9 years (82·7-83·1) in 2019. Between 1990 and 2019, the age-standardised death rate decreased from 637·7 deaths (95% UI 634·1-641·3) to 389·2 deaths (381·4-397·6) per 100 000 population. In 2019, non-communicable diseases remained the major cause of mortality in Australia, accounting for 90·9% (95% UI 90·4-91·9) of total deaths, followed by injuries (5·7%, 5·3-6·1) and communicable, maternal, neonatal, and nutritional diseases (3·3%, 2·9-3·7). Ischaemic heart disease, self-harm, tracheal, bronchus, and lung cancer, stroke, and colorectal cancer were the leading causes of YLLs. The leading causes of YLDs were low back pain, depressive disorders, other musculoskeletal diseases, falls, and anxiety disorders. The leading risk factors for DALYs were high BMI, smoking, high blood pressure, high fasting plasma glucose, and drug use. Between 1990 and 2019, all-cause DALYs decreased
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- 2023
5. High cereal fibre but not total fibre is associated with a lower risk of type 2 diabetes: Evidence from the Melbourne Collaborative Cohort Study
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Kabthymer, RH, Karim, MN, Hodge, AM, de Courten, B, Kabthymer, RH, Karim, MN, Hodge, AM, and de Courten, B
- Abstract
AIM: To assess the associations of total dietary fibre and fibre from different food sources (ie, cereal, fruit and vegetables) with the risk of diabetes. MATERIALS AND METHODS: The Melbourne Collaborative Cohort Study enrolled 41 513 participants aged 40 to 69 years from 1990 to 1994. The first and second follow-ups were conducted in 1994 to 1998 and 2003 to 2007, respectively. Self-reported diabetes incidence was recorded at both follow-ups. We analysed data from 39 185 participants, with a mean follow-up of 13.8 years. The relationships between dietary fibre intake (total, fruit, vegetable and cereal fibre) and the incidence of diabetes were assessed using modified Poisson regression, adjusted for dietary, lifestyle, obesity, socioeconomic and other possible confounders. Fibre intake was categorized into quintiles. RESULTS: At total of 1989 incident cases were identified over both follow-up surveys. Total fibre intake was not associated with diabetes risk. Higher intake of cereal fibre (P for trend = 0.003), but not fruit (P for trend = 0.3) and vegetable fibre (P for trend = 0.5), was protective against diabetes. For cereal fibre, quintile 5 versus quintile 1 showed a 25% reduction in diabetes risk (incidence risk ratio [IRR] 0.75, 95% confidence interval [CI] 0.63-0.88). For fruit fibre, only quintile 2 versus quintile 1 showed a 16% risk reduction (IRR 0.84, 95% CI 0.73-0.96). Adjustment for body mass index (BMI) and waist-to-hip ratio eliminated the association and mediation analysis showed that BMI mediated 36% of the relationship between fibre and diabetes. CONCLUSION: Intake of cereal fibre and, to a lesser extent, fruit fibre, may reduce the risk of diabetes, while total fibre showed no association. Our data suggest that specific recommendations regarding dietary fibre intake may be needed to prevent diabetes.
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- 2023
6. Supplementation-Induced Change in Muscle Carnosine is Paralleled by Changes in Muscle Metabolism, Protein Glycation and Reactive Carbonyl Species Sequestering
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SCHÖN, M, primary, JUST, I, additional, KRUMPOLEC, P, additional, BLAŽÍČEK, P, additional, VALKOVIČ, L, additional, ALDINI, G, additional, TSAI, C-L, additional, DE COURTEN, B, additional, KRŠŠÁK, M, additional, UKROPCOVÁ, B, additional, and UKROPEC, J, additional
- Published
- 2023
- Full Text
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7. Emergency treatment of hypoglycaemia: a guideline and evidence review
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Villani, M., de Courten, B., and Zoungas, S.
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- 2017
- Full Text
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8. Nurses' harm prevention practices during admission of an older person to the hospital: A multi-method qualitative study.
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Redley B., Douglas T., Hoon L., de Courten B., Hutchinson A.M., Redley B., Douglas T., Hoon L., de Courten B., and Hutchinson A.M.
- Abstract
BACKGROUND: Nurses' harm prevention practices during the admission of older persons to hospital have important consequences for patient safety, preventable patient harm and length of hospital stay. Novel solutions are needed to assist nurses to balance complexity, high workload burden and patient safety during admission processes. AIM: Explore the nurses' experiences of harm prevention practices during the admission of an older person to the hospital. DESIGN: A multi-method qualitative study informed by frameworks of behaviour change and human-centred co-design. METHOD(S): The purposive sample included 44 nurses, 5 clinicians from other disciplines and 3 consumers recruited from five general medicine wards across three hospitals of a large public health service in metropolitan Melbourne, Australia. Data were collected over 12 h of naturalistic observations of nurses during eight patient admissions, and during four participatory human-centred co-design workshops between August 2019 and January 2020. Observation, field notes and workshop artefact data were integrated for qualitative content and thematic analysis. RESULT(S): Analysis revealed a 5-step journey map, with a temporal logic, that captured nurses' experiences, as well as the enablers and barriers to harm prevention practices when admitting an older person to the hospital. The consensus was reached on three priority features to assist nurses to implement harm prevention practices when they admit an older person to the hospital: (1) prioritize important care; (2) tailor care to the individual and (3) see the big picture for the patient. CONCLUSION(S): The novel research approach identified five steps in nurses' activities and harm prevention practices during admission of an older person to the hospital, and key features for a solution to assist nurses to keep patients safe. The findings provide the foundation for further research to develop interventions to assist nurses to manage high workloads during this co
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- 2022
9. The Cost-Effectiveness of Supplemental Carnosine in Type 2 Diabetes
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Menon, K, de Courten, B, Magliano, DJ, Ademi, Z, Liew, D, Zomer, E, Menon, K, de Courten, B, Magliano, DJ, Ademi, Z, Liew, D, and Zomer, E
- Abstract
In this paper, we assess the cost-effectiveness of 1 g daily of carnosine (an over the counter supplement) in addition to standard care for the management of type 2 diabetes and compare it to standard care alone. Dynamic multistate life table models were constructed in order to estimate both clinical outcomes and costs of Australians aged 18 years and above with and without type 2 diabetes over a ten-year period, 2020 to 2029. The dynamic nature of the model allowed for population change over time (migration and deaths) and accounted for the development of new cases of diabetes. The three health states were 'Alive without type 2 diabetes', 'Alive with type 2 diabetes' and 'Dead'. Transition probabilities, costs, and utilities were obtained from published sources. The main outcome of interest was the incremental cost-effectiveness ratio (ICER) in terms of cost per year of life saved (YoLS) and cost per quality-adjusted life year (QALY) gained. Over the ten-year period, the addition of carnosine to standard care treatment resulted in ICERs (discounted) of AUD 34,836 per YoLS and AUD 43,270 per QALY gained. Assuming the commonly accepted willingness to pay threshold of AUD 50,000 per QALY gained, supplemental dietary carnosine may be a cost-effective treatment option for people with type 2 diabetes in Australia.
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- 2022
10. Estimating the benefits of obesity prevention on productivity: an Australian perspective
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Menon, K, de Courten, B, Ademi, Z, Owen, AJ, Liew, D, Zomer, E, Menon, K, de Courten, B, Ademi, Z, Owen, AJ, Liew, D, and Zomer, E
- Abstract
BACKGROUND/OBJECTIVES: Obesity poses one of the biggest public health challenges globally. In addition to the high costs of obesity to the healthcare system, obesity also impacts work productivity. We aimed to estimate the benefits of preventing obesity in terms of years of life, productivity-adjusted life years (PALYs) and associated costs over 10 years. SUBJECTS/METHODS: Dynamic life table models were constructed to estimate years of life and PALYs saved if all new cases of obesity were prevented among Australians aged 20-69 years from 2021 to 2030. Life tables were sex specific and the population was classified into normal weight, overweight and obese. The model simulation was first undertaken assuming currently observed age-specific incidences of obesity, and then repeated assuming all new cases of obesity were reduced by 2 and 5%. The differences in outcomes (years of life, PALYs, and costs) between the two modelled outputs reflected the potential benefits that could be achieved through obesity prevention. All outcomes were discounted by 5% per annum. RESULTS: Over the next 10 years, 132 million years of life and 81 million PALYs would be lived by Australians aged 20-69 years, contributing AU$17.0 trillion to the Australian economy in terms of GDP. A 5% reduction in new cases of obesity led to a gain of 663 years of life and 1229 PALYs, equivalent to AU$262 million in GDP. CONCLUSIONS: Prevention of obesity is projected to result in substantial economic gains due to improved health and productivity. This further emphasises the need for public health prevention strategies to reduce this growing epidemic.
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- 2022
11. The dietary inflammatory index, obesity, type 2 diabetes, and cardiovascular risk factors and diseases
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Hariharan, R, Odjidja, EN, Scott, D, Shivappa, N, Hebert, JR, Hodge, A, de Courten, B, Hariharan, R, Odjidja, EN, Scott, D, Shivappa, N, Hebert, JR, Hodge, A, and de Courten, B
- Abstract
An unhealthy diet is a recognized risk factor in the pathophysiology of numerous chronic noncommunicable diseases (NCD), including obesity, type 2 diabetes (T2DM), and cardiovascular diseases (CVD). This is, at least in part, due to unhealthy diets causing chronic low-grade inflammation in the gut and systemically. To characterize the inflammatory potential of diet, we developed the Dietary Inflammatory Index (DII®). Following this development, around 500 papers have been published, which examined the association between the DII, energy-adjusted DII (E-DII™), and the children's DII (C-DII™) and many chronic NCDs including obesity and cardiometabolic diseases. Although a previous narrative review published in 2019 briefly summarized the evidence in this area, there was a significant increase in papers on this topic since 2020. Therefore, the purpose of this narrative review is to provide an in-depth updated review by including all papers until July 2021 on DII and its relationship with obesity, T2DM, and CVD. Furthermore, we aim to identify potential gaps in the literature and provide future directions for research. Most studies found that DII was associated with an increased risk of obesity, T2DM, and CVD with some relationships being sex-specific. However, we identified the paucity of papers describing associations between dietary inflammation and T2DM and its risk factors. Few studies used gold-standard measures of cardiometabolic risk factors. We also identified the lack of interventional studies designed to change the inflammatory potential of diets and study its effect on cardiometabolic risk factors and diseases. We recommend that such interventional studies are needed to assess if changes in DII, representing the inflammatory potential of diet, independently of changes in body composition can modulate cardiometabolic risk factors and diseases.
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- 2022
12. The global, regional, and national burden of cirrhosis by cause in 195 countries and territories, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017
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Sepanlou, S, Safiri, S, Bisignano, C, Ikuta, K, Merat, S, Saberifiroozi, M, Poustchi, H, Tsoi, D, Colombara, D, Abdoli, A, Adedoyin, R, Afarideh, M, Agrawal, S, Ahmad, S, Ahmadian, E, Ahmadpour, E, Akinyemiju, T, Akunna, C, Alipour, V, Almasi-Hashiani, A, Almulhim, A, Al-Raddadi, R, Alvis-Guzman, N, Anber, N, Angus, C, Anoushiravani, A, Arabloo, J, Araya, E, Asmelash, D, Ataeinia, B, Ataro, Z, Atout, M, Ausloos, F, Awasthi, A, Badawi, A, Banach, M, Bejarano Ramirez, D, Bhagavathula, A, Bhala, N, Bhattacharyya, K, Biondi, A, Bolla, S, Boloor, A, Borzì, A, Butt, Z, Cámera, L, Campos-Nonato, I, Carvalho, F, Chu, D, Chung, S, Cortesi, P, Costa, V, Cowie, B, Daryani, A, de Courten, B, Demoz, G, Desai, R, Dharmaratne, S, Djalalinia, S, Do, H, Dorostkar, F, Drake, T, Dubey, M, Duncan, B, Effiong, A, Eftekhari, A, Elsharkawy, A, Etemadi, A, Farahmand, M, Farzadfar, F, Fernandes, E, Filip, I, Fischer, F, Gebremedhin, K, Geta, B, Gilani, S, Gill, P, Gutirrez, R, Haile, M, Haj-Mirzaian, A, Hamid, S, Hasankhani, M, Hasanzadeh, A, Hashemian, M, Hassen, H, Hay, S, Hayat, K, Heidari, B, Henok, A, Hoang, C, Hostiuc, M, Hostiuc, S, Hsieh, V, Igumbor, E, Ilesanmi, O, Irvani, S, Jafari Balalami, N, James, S, Jeemon, P, Jha, R, Jonas, J, Jozwiak, J, Kabir, A, Kasaeian, A, Kassaye, H, Kefale, A, Khalilov, R, Khan, M, Khan, E, Khater, A, Kim, Y, Koyanagi, A, La Vecchia, C, Lim, L, Lopez, A, Lorkowski, S, Lotufo, P, Lozano, R, Magdy Abd El Razek, M, Mai, H, Manafi, N, Manafi, A, Mansournia, M, Mantovani, L, Mazzaglia, G, Mehta, D, Mendoza, W, Menezes, R, Mengesha, M, Meretoja, T, Mestrovic, T, Miazgowski, B, Miller, T, Mirrakhimov, E, Mithra, P, Moazen, B, Moghadaszadeh, M, Mohammadian-Hafshejani, A, Mohammed, S, Mokdad, A, Montero-Zamora, P, Moradi, G, Naimzada, M, Nayak, V, Negoi, I, Nguyen, T, Ofori-Asenso, R, Oh, I, Olagunju, T, Padubidri, J, Pakshir, K, Pana, A, Pathak, M, Pourshams, A, Rabiee, N, Radfar, A, Rafiei, A, Ramezanzadeh, K, Rana, S, Rawaf, S, Rawaf, D, Reiner RC, J, Roever, L, Room, R, Roshandel, G, Safari, S, Samy, A, Sanabria, J, Sartorius, B, Schmidt, M, Senthilkumaran, S, Shaikh, M, Sharif, M, Sharifi, A, Shigematsu, M, Singh, J, Soheili, A, Suleria, H, Teklehaimanot, B, Tesfay, B, Vacante, M, Vahedian-Azimi, A, Valdez, P, Vasankari, T, Vu, G, Waheed, Y, Weldegwergs, K, Werdecker, A, Westerman, R, Wondafrash, D, Wondmieneh, A, Yeshitila, Y, Yonemoto, N, Yu, C, Zaidi, Z, Zarghi, A, Zelber-Sagi, S, Zewdie, K, Zhang, Z, Zhao, X, Naghavi, M, Malekzadeh, R, Sepanlou SG, Safiri S, Bisignano C, Ikuta KS, Merat S, Saberifiroozi M, Poustchi H, Tsoi D, Colombara DV, Abdoli A, Adedoyin RA, Afarideh M, Agrawal S, Ahmad S, Ahmadian E, Ahmadpour E, Akinyemiju T, Akunna CJ, Alipour V, Almasi-Hashiani A, Almulhim AM, Al-Raddadi RM, Alvis-Guzman N, Anber NH, Angus C, Anoushiravani A, Arabloo J, Araya EM, Asmelash D, Ataeinia B, Ataro Z, Atout MMW, Ausloos F, Awasthi A, Badawi A, Banach M, Bejarano Ramirez DF, Bhagavathula AS, Bhala N, Bhattacharyya K, Biondi A, Bolla SR, Boloor A, Borzì AM, Butt ZA, Cámera LA, Campos-Nonato IR, Carvalho F, Chu DT, Chung SC, Cortesi PA, Costa VM, Cowie BC, Daryani A, de Courten B, Demoz GT, Desai R, Dharmaratne SD, Djalalinia S, Do HT, Dorostkar F, Drake TM, Dubey M, Duncan BB, Effiong A, Eftekhari A, Elsharkawy A, Etemadi A, Farahmand M, Farzadfar F, Fernandes E, Filip I, Fischer F, Gebremedhin KBB, Geta B, Gilani SA, Gill PS, Gutirrez RA, Haile MT, Haj-Mirzaian A, Hamid SS, Hasankhani M, Hasanzadeh A, Hashemian M, Hassen HY, Hay SI, Hayat K, Heidari B, Henok A, Hoang CL, Hostiuc M, Hostiuc S, Hsieh VC, Igumbor EU, Ilesanmi OS, Irvani SSN, Jafari Balalami N, James SL, Jeemon P, Jha RP, Jonas JB, Jozwiak JJ, Kabir A, Kasaeian A, Kassaye HG, Kefale AT, Khalilov R, Khan MA, Khan EA, Khater A, Kim YJ, Koyanagi A, La Vecchia C, Lim LL, Lopez AD, Lorkowski S, Lotufo PA, Lozano R, Magdy Abd El Razek M, Mai HT, Manafi N, Manafi A, Mansournia MA, Mantovani LG, Mazzaglia G, Mehta D, Mendoza W, Menezes RG, Mengesha MM, Meretoja TJ, Mestrovic T, Miazgowski B, Miller TR, Mirrakhimov EM, Mithra P, Moazen B, Moghadaszadeh M, Mohammadian-Hafshejani A, Mohammed S, Mokdad AH, Montero-Zamora PA, Moradi G, Naimzada MD, Nayak V, Negoi I, Nguyen TH, Ofori-Asenso R, Oh IH, Olagunju TO, Padubidri JR, Pakshir K, Pana A, Pathak M, Pourshams A, Rabiee N, Radfar A, Rafiei A, Ramezanzadeh K, Rana SMM, Rawaf S, Rawaf DL, Reiner RC Jr, Roever L, Room R, Roshandel G, Safari S, Samy AM, Sanabria J, Sartorius B, Schmidt MI, Senthilkumaran S, Shaikh MA, Sharif M, Sharifi A, Shigematsu M, Singh JA, Soheili A, Suleria HAR, Teklehaimanot BF, Tesfay BE, Vacante M, Vahedian-Azimi A, Valdez PR, Vasankari TJ, Vu GT, Waheed Y, Weldegwergs KG, Werdecker A, Westerman R, Wondafrash DZ, Wondmieneh AB, Yeshitila YG, Yonemoto N, Yu C, Zaidi Z, Zarghi A, Zelber-Sagi S, Zewdie KA, Zhang ZJ, Zhao XJ, Naghavi M, Malekzadeh R., Sepanlou, S, Safiri, S, Bisignano, C, Ikuta, K, Merat, S, Saberifiroozi, M, Poustchi, H, Tsoi, D, Colombara, D, 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Hostiuc, M, Hostiuc, S, Hsieh, V, Igumbor, E, Ilesanmi, O, Irvani, S, Jafari Balalami, N, James, S, Jeemon, P, Jha, R, Jonas, J, Jozwiak, J, Kabir, A, Kasaeian, A, Kassaye, H, Kefale, A, Khalilov, R, Khan, M, Khan, E, Khater, A, Kim, Y, Koyanagi, A, La Vecchia, C, Lim, L, Lopez, A, Lorkowski, S, Lotufo, P, Lozano, R, Magdy Abd El Razek, M, Mai, H, Manafi, N, Manafi, A, Mansournia, M, Mantovani, L, Mazzaglia, G, Mehta, D, Mendoza, W, Menezes, R, Mengesha, M, Meretoja, T, Mestrovic, T, Miazgowski, B, Miller, T, Mirrakhimov, E, Mithra, P, Moazen, B, Moghadaszadeh, M, Mohammadian-Hafshejani, A, Mohammed, S, Mokdad, A, Montero-Zamora, P, Moradi, G, Naimzada, M, Nayak, V, Negoi, I, Nguyen, T, Ofori-Asenso, R, Oh, I, Olagunju, T, Padubidri, J, Pakshir, K, Pana, A, Pathak, M, Pourshams, A, Rabiee, N, Radfar, A, Rafiei, A, Ramezanzadeh, K, Rana, S, Rawaf, S, Rawaf, D, Reiner RC, J, Roever, L, Room, R, Roshandel, G, Safari, S, Samy, A, Sanabria, J, Sartorius, B, Schmidt, M, Senthilkumaran, S, 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- Abstract
Background: Cirrhosis and other chronic liver diseases (collectively referred to as cirrhosis in this paper) are a major cause of morbidity and mortality globally, although the burden and underlying causes differ across locations and demographic groups. We report on results from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017 on the burden of cirrhosis and its trends since 1990, by cause, sex, and age, for 195 countries and territories. Methods: We used data from vital registrations, vital registration samples, and verbal autopsies to estimate mortality. We modelled prevalence of total, compensated, and decompensated cirrhosis on the basis of hospital and claims data. Disability-adjusted life-years (DALYs) were calculated as the sum of years of life lost due to premature death and years lived with disability. Estimates are presented as numbers and age-standardised or age-specific rates per 100 000 population, with 95% uncertainty intervals (UIs). All estimates are presented for five causes of cirrhosis: hepatitis B, hepatitis C, alcohol-related liver disease, non-alcoholic steatohepatitis (NASH), and other causes. We compared mortality, prevalence, and DALY estimates with those expected according to the Socio-demographic Index (SDI) as a proxy for the development status of regions and countries. Findings: In 2017, cirrhosis caused more than 1·32 million (95% UI 1·27–1·45) deaths (440 000 [416 000–518 000; 33·3%] in females and 883 000 [838 000–967 000; 66·7%] in males) globally, compared with less than 899 000 (829 000–948 000) deaths in 1990. Deaths due to cirrhosis constituted 2·4% (2·3–2·6) of total deaths globally in 2017 compared with 1·9% (1·8–2·0) in 1990. Despite an increase in the number of deaths, the age-standardised death rate decreased from 21·0 (19·2–22·3) per 100 000 population in 1990 to 16·5 (15·8–18·1) per 100 000 population in 2017. Sub-Saharan Africa had the highest age-standardised death rate among GBD super-regions fo
- Published
- 2020
13. Prevalence and attributable health burden of chronic respiratory diseases, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017
- Author
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Soriano, J, Kendrick, P, Paulson, K, Gupta, V, Abrams, E, Adedoyin, R, Adhikari, T, Advani, S, Agrawal, A, Ahmadian, E, Alahdab, F, Aljunid, S, Altirkawi, K, Alvis-Guzman, N, Anber, N, Andrei, C, Anjomshoa, M, Ansari, F, Anto, J, Arabloo, J, Athari, S, Awoke, N, Badawi, A, Banoub, J, Bennett, D, Bensenor, I, Berfield, K, Bernstein, R, Bhattacharyya, K, Bijani, A, Brauer, M, Bukhman, G, Butt, Z, Camera, L, Car, J, Carrero, J, Carvalho, F, Castaneda-Orjuela, C, Choi, J, Christopher, D, Cohen, A, Dandona, L, Dandona, R, Dang, A, Daryani, A, de Courten, B, Demeke, F, Demoz, G, De Neve, J, Desai, R, Dharmaratne, S, Diaz, D, Douiri, A, Driscoll, T, Duken, E, Eftekhari, A, Elkout, H, Endries, A, Fadhil, I, Faro, A, Farzadfar, F, Fernandes, E, Filip, I, Fischer, F, Foroutan, M, Garcia-Gordillo, M, Gebre, A, Gebremedhin, K, Gebremeskel, G, Gezae, K, Ghoshal, A, Gill, P, Gillum, R, Goudarzi, H, Guo, Y, Gupta, R, Hailu, G, Hasanzadeh, A, Hassen, H, Hay, S, Hoang, C, Hole, M, Horita, N, Hosgood, H, Hostiuc, M, Househ, M, Ilesanmi, O, Ilic, M, Irvani, S, Islam, S, Jakovljevic, M, Jamal, A, Jha, R, Jonas, J, Kabir, Z, Kasaeian, A, Kasahun, G, Kassa, G, Kefale, A, Kengne, A, Khader, Y, Khafaie, M, Khan, E, Khan, J, Khubchandani, J, Kim, Y, Kisa, S, Kisa, A, Knibbs, L, Komaki, H, Koul, P, Koyanagi, A, Kumar, G, Lan, Q, Lasrado, S, Lauriola, P, La Vecchia, C, Le, T, Leigh, J, Levi, M, Li, S, Lopez, A, Lotufo, P, Madotto, F, Mahotra, N, Majdan, M, Majeed, A, Malekzadeh, R, Mamun, A, Manafi, N, Manafi, F, Mantovani, L, Meharie, B, Meles, H, Meles, G, Menezes, R, Mestrovic, T, Miller, T, Mini, G, Mirrakhimov, E, Moazen, B, Mohammad, K, Mohammed, S, Mohebi, F, Mokdad, A, Molokhia, M, Monasta, L, Moradi, M, Moradi, G, Morawska, L, Mousavi, S, Musa, K, Mustafa, G, Naderi, M, Naghavi, M, Naik, G, Nair, S, Nangia, V, Nansseu, J, Nazari, J, Ndwandwe, D, Negoi, R, Nguyen, T, Nguyen, C, Nguyen, H, Nixon, M, Ofori-Asenso, R, Ogbo, F, Olagunju, A, Olagunju, T, Oren, E, Ortiz, J, Owolabi, M, P A, M, Pakhale, S, Pana, A, Panda-Jonas, S, Park, E, Pham, H, Postma, M, Pourjafar, H, Poustchi, H, Radfar, A, Rafiei, A, Rahim, F, Rahman, M, Rawaf, S, Rawaf, D, Rawal, L, Reiner, R, Reitsma, M, Roever, L, Ronfani, L, Roro, E, Roshandel, G, Rudd, K, Sabde, Y, Sabour, S, Saddik, B, Safari, S, Saleem, K, Samy, A, Santric-Milicevic, M, Sao Jose, B, Sartorius, B, Satpathy, M, Savic, M, Sawhney, M, Sepanlou, S, Shaikh, M, Sheikh, A, Shigematsu, M, Shirkoohi, R, Si, S, Siabani, S, Singh, V, Singh, J, Soljak, M, Somayaji, R, Soofi, M, Soyiri, I, Tefera, Y, Temsah, M, Tesfay, B, Thakur, J, Toma, A, Tortajada-Girbes, M, Tran, K, Tran, B, Tudor Car, L, Ullah, I, Vacante, M, Valdez, P, van Boven, J, Vasankari, T, Veisani, Y, Violante, F, Wagner, G, Westerman, R, Wolfe, C, Wondafrash, D, Wondmieneh, A, Yonemoto, N, Yoon, S, Zaidi, Z, Zamani, M, Zar, H, Zhang, Y, Vos, T, Soriano J. 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G., Gill P. S., Gillum R. F., Goudarzi H., Guo Y., Gupta R., Hailu G. B., Hasanzadeh A., Hassen H. Y., Hay S. I., Hoang C. L., Hole M. K., Horita N., Hosgood H. D., Hostiuc M., Househ M., Ilesanmi O. S., Ilic M. D., Irvani S. S. N., Islam S. M. S., Jakovljevic M., Jamal A. A., Jha R. P., Jonas J. B., Kabir Z., Kasaeian A., Kasahun G. G., Kassa G. M., Kefale A. T., Kengne A. P., Khader Y. S., Khafaie M. A., Khan E. A., Khan J., Khubchandani J., Kim Y. -E., Kim Y. J., Kisa S., Kisa A., Knibbs L. D., Komaki H., Koul P. A., Koyanagi A., Kumar G. A., Lan Q., Lasrado S., Lauriola P., La Vecchia C., Le T. T., Leigh J., Levi M., Li S., Lopez A. D., Lotufo P. A., Madotto F., Mahotra N. B., Majdan M., Majeed A., Malekzadeh R., Mamun A. A., Manafi N., Manafi F., Mantovani L. G., Meharie B. G., Meles H. G., Meles G. G., Menezes R. G., Mestrovic T., Miller T. R., Mini G. K., Mirrakhimov E. M., Moazen B., Mohammad K. A., Mohammed S., Mohebi F., Mokdad A. H., Molokhia M., Monasta L., Moradi M., Moradi G., Morawska L., Mousavi S. M., Musa K. I., Mustafa G., Naderi M., Naghavi M., Naik G., Nair S., Nangia V., Nansseu J. R., Nazari J., Ndwandwe D. E., Negoi R. I., Nguyen T. H., Nguyen C. T., Nguyen H. L. T., Nixon M. R., Ofori-Asenso R., Ogbo F. A., Olagunju A. T., Olagunju T. O., Oren E., Ortiz J. R., Owolabi M. O., P A M., Pakhale S., Pana A., Panda-Jonas S., Park E. -K., Pham H. Q., Postma M. J., Pourjafar H., Poustchi H., Radfar A., Rafiei A., Rahim F., Rahman M. H. U., Rahman M. A., Rawaf S., Rawaf D. L., Rawal L., Reiner R. C., Reitsma M. B., Roever L., Ronfani L., Roro E. M., Roshandel G., Rudd K. E., Sabde Y. D., Sabour S., Saddik B., Safari S., Saleem K., Samy A. M., Santric-Milicevic M. M., Sao Jose B. P., Sartorius B., Satpathy M., Savic M., Sawhney M., Sepanlou S. G., Shaikh M. A., Sheikh A., Shigematsu M., Shirkoohi R., Si S., Siabani S., Singh V., Singh J. A., Soljak M., Somayaji R., Soofi M., Soyiri I. N., Tefera Y. M., Temsah M. -H., Tesfay B. E., Thakur J. S., Toma A. T., Tortajada-Girbes M., Tran K. B., Tran B. X., Tudor Car L., Ullah I., Vacante M., Valdez P. R., van Boven J. F. M., Vasankari T. J., Veisani Y., Violante F. S., Wagner G. R., Westerman R., Wolfe C. D. A., Wondafrash D. Z., Wondmieneh A. B., Yonemoto N., Yoon S. -J., Zaidi Z., Zamani M., Zar H. J., Zhang Y., Vos T., Soriano, J, Kendrick, P, Paulson, K, Gupta, V, Abrams, E, Adedoyin, R, Adhikari, T, Advani, S, Agrawal, A, Ahmadian, E, Alahdab, F, Aljunid, S, Altirkawi, K, Alvis-Guzman, N, Anber, N, Andrei, C, Anjomshoa, M, Ansari, F, Anto, J, Arabloo, J, Athari, S, Awoke, N, Badawi, A, Banoub, J, Bennett, D, Bensenor, I, Berfield, K, Bernstein, R, Bhattacharyya, K, Bijani, A, Brauer, M, Bukhman, G, Butt, Z, Camera, L, Car, J, Carrero, J, Carvalho, F, Castaneda-Orjuela, C, Choi, J, Christopher, D, Cohen, A, Dandona, L, Dandona, R, Dang, A, Daryani, A, de Courten, B, Demeke, F, Demoz, G, De Neve, J, Desai, R, Dharmaratne, S, Diaz, D, Douiri, A, Driscoll, T, Duken, E, Eftekhari, A, Elkout, H, Endries, A, Fadhil, I, Faro, A, Farzadfar, F, Fernandes, E, Filip, I, Fischer, F, Foroutan, M, Garcia-Gordillo, M, Gebre, A, Gebremedhin, K, Gebremeskel, G, Gezae, K, Ghoshal, A, Gill, P, Gillum, R, Goudarzi, H, Guo, Y, Gupta, R, Hailu, G, Hasanzadeh, A, Hassen, H, Hay, S, Hoang, C, Hole, M, Horita, N, Hosgood, H, Hostiuc, M, Househ, M, Ilesanmi, O, Ilic, M, Irvani, S, Islam, S, Jakovljevic, M, Jamal, A, Jha, R, Jonas, J, Kabir, Z, Kasaeian, A, Kasahun, G, Kassa, G, Kefale, A, Kengne, A, Khader, Y, Khafaie, M, Khan, E, Khan, J, Khubchandani, J, Kim, Y, Kisa, S, Kisa, A, Knibbs, L, Komaki, H, Koul, P, Koyanagi, A, Kumar, G, Lan, Q, Lasrado, S, Lauriola, P, La Vecchia, C, Le, T, Leigh, J, Levi, M, Li, S, Lopez, A, Lotufo, P, Madotto, F, Mahotra, N, Majdan, M, Majeed, A, Malekzadeh, R, Mamun, A, Manafi, N, Manafi, F, Mantovani, L, Meharie, B, Meles, H, Meles, G, Menezes, R, Mestrovic, T, Miller, T, Mini, G, Mirrakhimov, E, Moazen, B, Mohammad, K, Mohammed, S, Mohebi, F, Mokdad, A, Molokhia, M, Monasta, L, Moradi, M, Moradi, G, Morawska, L, Mousavi, S, Musa, K, Mustafa, G, Naderi, M, Naghavi, M, Naik, G, Nair, S, Nangia, V, Nansseu, J, Nazari, J, Ndwandwe, D, Negoi, R, Nguyen, T, Nguyen, C, Nguyen, H, Nixon, M, Ofori-Asenso, R, Ogbo, F, Olagunju, A, Olagunju, T, Oren, E, Ortiz, J, Owolabi, M, P A, M, Pakhale, S, Pana, A, Panda-Jonas, S, Park, E, Pham, H, Postma, M, Pourjafar, H, Poustchi, H, Radfar, A, Rafiei, A, Rahim, F, Rahman, M, Rawaf, S, Rawaf, D, Rawal, L, Reiner, R, Reitsma, M, Roever, L, Ronfani, L, Roro, E, Roshandel, G, Rudd, K, Sabde, Y, Sabour, S, Saddik, B, Safari, S, Saleem, K, Samy, A, Santric-Milicevic, M, Sao Jose, B, Sartorius, B, Satpathy, M, Savic, M, Sawhney, M, Sepanlou, S, Shaikh, M, Sheikh, A, Shigematsu, M, Shirkoohi, R, Si, S, Siabani, S, Singh, V, Singh, J, Soljak, M, Somayaji, R, Soofi, M, Soyiri, I, Tefera, Y, Temsah, M, Tesfay, B, Thakur, J, Toma, A, Tortajada-Girbes, M, Tran, K, Tran, B, Tudor Car, L, Ullah, I, Vacante, M, Valdez, P, van Boven, J, Vasankari, T, Veisani, Y, Violante, F, Wagner, G, Westerman, R, Wolfe, C, Wondafrash, D, Wondmieneh, A, Yonemoto, N, Yoon, S, Zaidi, Z, Zamani, M, Zar, H, Zhang, Y, Vos, T, Soriano J. B., Kendrick P. J., Paulson K. R., Gupta V., Abrams E. M., Adedoyin R. A., Adhikari T. B., Advani S. M., Agrawal A., Ahmadian E., Alahdab F., Aljunid S. M., Altirkawi K. A., Alvis-Guzman N., Anber N. H., Andrei C. L., Anjomshoa M., Ansari F., Anto J. M., Arabloo J., Athari S. M., Athari S. S., Awoke N., Badawi A., Banoub J. A. M., Bennett D. A., Bensenor I. M., Berfield K. S. S., Bernstein R. S., Bhattacharyya K., Bijani A., Brauer M., Bukhman G., Butt Z. A., Camera L. A., Car J., Carrero J. J., Carvalho F., Castaneda-Orjuela C. A., Choi J. -Y. J., Christopher D. J., Cohen A. J., Dandona L., Dandona R., Dang A. K., Daryani A., de Courten B., Demeke F. M., Demoz G. T., De Neve J. -W., Desai R., Dharmaratne S. D., Diaz D., Douiri A., Driscoll T. R., Duken E. E., Eftekhari A., Elkout H., Endries A. Y., Fadhil I., Faro A., Farzadfar F., Fernandes E., Filip I., Fischer F., Foroutan M., Garcia-Gordillo M. A., Gebre A. K., Gebremedhin K. B., Gebremeskel G. G., Gezae K. E., Ghoshal A. G., Gill P. S., Gillum R. F., Goudarzi H., Guo Y., Gupta R., Hailu G. B., Hasanzadeh A., Hassen H. Y., Hay S. I., Hoang C. L., Hole M. K., Horita N., Hosgood H. D., Hostiuc M., Househ M., Ilesanmi O. S., Ilic M. D., Irvani S. S. N., Islam S. M. S., Jakovljevic M., Jamal A. A., Jha R. P., Jonas J. B., Kabir Z., Kasaeian A., Kasahun G. G., Kassa G. M., Kefale A. T., Kengne A. P., Khader Y. S., Khafaie M. A., Khan E. A., Khan J., Khubchandani J., Kim Y. -E., Kim Y. J., Kisa S., Kisa A., Knibbs L. D., Komaki H., Koul P. A., Koyanagi A., Kumar G. A., Lan Q., Lasrado S., Lauriola P., La Vecchia C., Le T. T., Leigh J., Levi M., Li S., Lopez A. D., Lotufo P. A., Madotto F., Mahotra N. B., Majdan M., Majeed A., Malekzadeh R., Mamun A. A., Manafi N., Manafi F., Mantovani L. G., Meharie B. G., Meles H. G., Meles G. G., Menezes R. G., Mestrovic T., Miller T. R., Mini G. K., Mirrakhimov E. M., Moazen B., Mohammad K. A., Mohammed S., Mohebi F., Mokdad A. H., Molokhia M., Monasta L., Moradi M., Moradi G., Morawska L., Mousavi S. M., Musa K. I., Mustafa G., Naderi M., Naghavi M., Naik G., Nair S., Nangia V., Nansseu J. R., Nazari J., Ndwandwe D. E., Negoi R. I., Nguyen T. H., Nguyen C. T., Nguyen H. L. T., Nixon M. R., Ofori-Asenso R., Ogbo F. A., Olagunju A. T., Olagunju T. O., Oren E., Ortiz J. R., Owolabi M. O., P A M., Pakhale S., Pana A., Panda-Jonas S., Park E. -K., Pham H. Q., Postma M. J., Pourjafar H., Poustchi H., Radfar A., Rafiei A., Rahim F., Rahman M. H. U., Rahman M. A., Rawaf S., Rawaf D. L., Rawal L., Reiner R. C., Reitsma M. B., Roever L., Ronfani L., Roro E. M., Roshandel G., Rudd K. E., Sabde Y. D., Sabour S., Saddik B., Safari S., Saleem K., Samy A. M., Santric-Milicevic M. M., Sao Jose B. P., Sartorius B., Satpathy M., Savic M., Sawhney M., Sepanlou S. G., Shaikh M. A., Sheikh A., Shigematsu M., Shirkoohi R., Si S., Siabani S., Singh V., Singh J. A., Soljak M., Somayaji R., Soofi M., Soyiri I. N., Tefera Y. M., Temsah M. -H., Tesfay B. E., Thakur J. S., Toma A. T., Tortajada-Girbes M., Tran K. B., Tran B. X., Tudor Car L., Ullah I., Vacante M., Valdez P. R., van Boven J. F. M., Vasankari T. J., Veisani Y., Violante F. S., Wagner G. R., Westerman R., Wolfe C. D. A., Wondafrash D. Z., Wondmieneh A. B., Yonemoto N., Yoon S. -J., Zaidi Z., Zamani M., Zar H. J., Zhang Y., and Vos T.
- Abstract
Background: Previous attempts to characterise the burden of chronic respiratory diseases have focused only on specific disease conditions, such as chronic obstructive pulmonary disease (COPD) or asthma. In this study, we aimed to characterise the burden of chronic respiratory diseases globally, providing a comprehensive and up-to-date analysis on geographical and time trends from 1990 to 2017. Methods: Using data from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017, we estimated the prevalence, morbidity, and mortality attributable to chronic respiratory diseases through an analysis of deaths, disability-adjusted life-years (DALYs), and years of life lost (YLL) by GBD super-region, from 1990 to 2017, stratified by age and sex. Specific diseases analysed included asthma, COPD, interstitial lung disease and pulmonary sarcoidosis, pneumoconiosis, and other chronic respiratory diseases. We also assessed the contribution of risk factors (smoking, second-hand smoke, ambient particulate matter and ozone pollution, household air pollution from solid fuels, and occupational risks) to chronic respiratory disease-attributable DALYs. Findings: In 2017, 544·9 million people (95% uncertainty interval [UI] 506·9–584·8) worldwide had a chronic respiratory disease, representing an increase of 39·8% compared with 1990. Chronic respiratory disease prevalence showed wide variability across GBD super-regions, with the highest prevalence among both males and females in high-income regions, and the lowest prevalence in sub-Saharan Africa and south Asia. The age-sex-specific prevalence of each chronic respiratory disease in 2017 was also highly variable geographically. Chronic respiratory diseases were the third leading cause of death in 2017 (7·0% [95% UI 6·8–7·2] of all deaths), behind cardiovascular diseases and neoplasms. Deaths due to chronic respiratory diseases numbered 3 914 196 (95% UI 3 790 578–4 044 819) in 2017, an increase of 18·0% since 1990, while
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- 2020
14. The effect of salsalate on insulin action and glucose tolerance in obese non-diabetic patients: results of a randomised double-blind placebo-controlled study
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Koska, J., Ortega, E., Bunt, J. C., Gasser, A., Impson, J., Hanson, R. L., Forbes, J., de Courten, B., and Krakoff, J.
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- 2009
- Full Text
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15. The dietary inflammatory index, obesity, type 2 diabetes, and cardiovascular risk factors and diseases.
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Hariharan R., Odjidja E.N., Scott D., Shivappa N., Hebert J.R., Hodge A., de Courten B., Hariharan R., Odjidja E.N., Scott D., Shivappa N., Hebert J.R., Hodge A., and de Courten B.
- Abstract
An unhealthy diet is a recognized risk factor in the pathophysiology of numerous chronic noncommunicable diseases (NCD), including obesity, type 2 diabetes (T2DM), and cardiovascular diseases (CVD). This is, at least in part, due to unhealthy diets causing chronic low-grade inflammation in the gut and systemically. To characterize the inflammatory potential of diet, we developed the Dietary Inflammatory Index (DII). Following this development, around 500 papers have been published, which examined the association between the DII, energy-adjusted DII (E-DIITM), and the children's DII (C-DIITM) and many chronic NCDs including obesity and cardiometabolic diseases. Although a previous narrative review published in 2019 briefly summarized the evidence in this area, there was a significant increase in papers on this topic since 2020. Therefore, the purpose of this narrative review is to provide an in-depth updated review by including all papers until July 2021 on DII and its relationship with obesity, T2DM, and CVD. Furthermore, we aim to identify potential gaps in the literature and provide future directions for research. Most studies found that DII was associated with an increased risk of obesity, T2DM, and CVD with some relationships being sex-specific. However, we identified the paucity of papers describing associations between dietary inflammation and T2DM and its risk factors. Few studies used gold-standard measures of cardiometabolic risk factors. We also identified the lack of interventional studies designed to change the inflammatory potential of diets and study its effect on cardiometabolic risk factors and diseases. We recommend that such interventional studies are needed to assess if changes in DII, representing the inflammatory potential of diet, independently of changes in body composition can modulate cardiometabolic risk factors and diseases.Copyright © 2021 World Obesity Federation
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- 2021
16. Effectiveness of community-based health education and home support program to reduce blood pressure among patients with uncontrolled hypertension in Nepal: A cluster-randomized trial.
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Khanal M.K., Dhungana R.R., Bhandari P., Rawal L.B., Gurung Y., Paudel K.N., Singh A., Devkota S., de Courten B., Khanal M.K., Dhungana R.R., Bhandari P., Rawal L.B., Gurung Y., Paudel K.N., Singh A., Devkota S., and de Courten B.
- Abstract
Background Hypertension is a major global public health problem. Elevated blood pressure can cause cardiovascular and kidney diseases. We assessed the effectiveness of health education sessions and home support programs in reducing blood pressure among patients with uncontrolled hypertension in a suburban community of Nepal. Methods We conducted a community-based, open-level, parallel-group, cluster randomized controlled trial in Birendranagar municipality of Surkhet, Nepal. We randomly assigned four clusters (wards) into intervention and control arms. We provided four health education sessions, frequent home and usual care for intervention groups over six months. The participants of the control arm received only usual care from health facilities. The primary outcome of this study was the proportion of controlled systolic blood pressure (SBP). The analysis included all participants who completed follow-up at six months. Results 125 participants were assigned to either the intervention (n = 63) or the control (n = 62) group. Of them, 60 participants in each group completed six months follow-up. The proportion of controlled SBP was significantly higher among the intervention participants compared to the control (58.3% vs. 40%). Odds ratio of this was 2.1 with 95% CI: 1.01-4.35 (p = 0.046) and that of controlled diastolic blood pressure (DBP) was 1.31 (0.63-2.72) (p = 0.600). The mean change (follow-up minus baseline) in SBP was significantly higher in the intervention than in the usual care (-18.7 mmHg vs. -11.2 mmHg, p = 0.041). Such mean change of DBP was also higher in the intervention (-10.95 mmHg vs. -5.53 mmHg, p = 0.065). The knowledge score on hypertension improved by 2.38 (SD 2.4) in the intervention arm, which was significantly different from that of the control group, 0.13 (1.8) (p<0.001). Conclusions Multiple health education sessions complemented by frequent household visits by health volunteers can effectively improve knowledge on hypertension and reduce
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- 2021
17. Diet scores and prediction of general and abdominal obesity in the Melbourne Collaborative Cohort Study.
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Hodge A.M., Karim M.N., Hebert J.R., Shivappa N., Milne R.L., de Courten B., Hodge A.M., Karim M.N., Hebert J.R., Shivappa N., Milne R.L., and de Courten B.
- Abstract
OBJECTIVE: To ascertain which of the Alternative Healthy Eating Index 2010 (AHEI), Dietary Inflammatory Index (DII) and Mediterranean Diet Score (MDS) best predicted body mass index (BMI) and waist-to-hip circumference ratio (WHR). DESIGN: Body size was measured at baseline (1990-94) and in 2003-7. Diet was assessed at baseline using a food frequency questionnaire, along with age, sex, socioeconomic status, smoking, alcohol drinking, physical activity, and country of birth. Regression coefficients and 95% confidence intervals for the association of baseline dietary scores with follow-up BMI and WHR were generated using multivariable linear regression, adjusting for baseline body-size, confounders and energy intake. SETTING: Population-based cohort in Melbourne, Australia. PARTICIPANTS: Included were data from 11,030 men and 16,774 women aged 40 to 69 years at baseline. RESULT(S): Median (IQR) follow up was 11.6 (10.7 - 12.8) years. BMI and WHR at follow-up were associated with baseline DII (Q5 vs Q1 (BMI 0.41 95%CI (0.21, 0.61) and WHR 0.009 95%CI (0.006, 0.013)), and AHEI (Q5 vs Q1 (BMI -0.51 95%CI (-0.68, -0.35) and WHR -0.011 95%CI (-0.013, -0.008)). WHR, but not BMI, at follow-up was associated with baseline MDS (Group 3 most Mediterranean vs G1 (BMI -0.05 95%CI (-0.23, 0.13) and WHR -0.004 95%CI (-0.007, -0.001)). Based on Akaike's Information Criterion and Bayesian Information Criterion statistics, AHEI was a stronger predictor of body size than the other diet scores. CONCLUSION(S): Poor quality or pro-inflammatory diets predicted overall and central obesity. The AHEI may provide the best way to assess the obesogenic potential of diet.
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- 2021
18. Exercise attenuates bone mineral density loss during diet-induced weight loss in adults with overweight and obesity: A systematic review and meta-analysis.
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Mesinovic J., Jansons P., Zengin A., de Courten B., Rodriguez A.J., Daly R.M., Ebeling P.R., Scott D., Mesinovic J., Jansons P., Zengin A., de Courten B., Rodriguez A.J., Daly R.M., Ebeling P.R., and Scott D.
- Abstract
Background: Weight-loss-induced fat loss improves cardiometabolic health in individuals with overweight and obesity; however, weight loss can also result in bone loss and increased fracture risk. Weight-loss-induced bone loss may be attenuated with exercise. Our aim was to compare changes in bone mineral density (BMD) in adults with overweight and obesity who undertook diet-induced weight loss alone or in combination with exercise. Method(s): We included randomized controlled trials (RCTs) in adults with overweight or obesity (aged >=18 years; body mass index >=25 kg/m2) that prescribed diet-induced weight loss alone or in combination with supervised exercise, and measured any bone structural parameters. Risk of bias was assessed using the Cochrane Risk of Bias tool. Random-effects meta-analyses determined mean changes and net mean differences (95% confidence intervals (95%CIs)) in the percentage of areal BMD (aBMD) change between groups. Result(s): We included 9 RCTs. Diet-induced weight loss led to significant losses in femoral neck aBMD (mean change: -1.73% (95%CI: -2.39 to -1.07), p < 0.001) and total hip aBMD (-2.19% (95%CI: -3.84 to -0.54), p = 0.009). Femoral neck aBMD losses were significantly greater in the diet-induced weight loss group compared to the exercise plus diet-induced weight loss group (net difference: -0.88% (95%CI: -1.73 to -0.03)); however, there were no differences in aBMD changes at any other skeletal site: total hip (-1.96% (95%CI: -4.59 to 0.68)) and lumbar spine (-0.48% (95%CI: -1.81 to 0.86)). aBMD changes did not differ significantly according to exercise modality (resistance exercise, aerobic exercise, or a combination of the two) during diet-induced weight loss. Conclusion(s): Diet-induced weight loss led to greater femoral neck bone loss compared to diet-induced weight loss plus exercise. Bone loss at the total hip and lumbar spine was not attenuated by exercise during diet-induced weight loss. The lack of consistent skeletal benefi
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- 2021
19. Sexual dysfunction in men with multiple sclerosis.
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Grech L.B., Allan M., de Courten B., Grech L.B., Allan M., and de Courten B.
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- 2021
20. Potentially inappropriate prescribing and its associations with health-related and system-related outcomes in hospitalised older adults: A systematic review and meta-analysis.
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Mekonnen A.B., Redley B., de Courten B., Manias E., Mekonnen A.B., Redley B., de Courten B., and Manias E.
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Aims: To synthesise associations of potentially inappropriate prescribing (PIP) with health-related and system-related outcomes in inpatient hospital settings. Method(s): Six electronic databases were searched: Medline Complete, EMBASE, CINAHL, PyscInfo, IPA and Cochrane library. Studies published between 1 January 1991 and 31 January 2021 investigating associations between PIP and health-related and system-related outcomes of older adults in hospital settings, were included. A random effects model was employed using the generic inverse variance method to pool risk estimates. Result(s): Overall, 63 studies were included. Pooled risk estimates did not show a significant association with all-cause mortality (adjusted odds ratio [AOR] 1.10, 95% confidence interval [CI] 0.90-1.36; adjusted hazard ratio 1.02, 83% CI 0.90-1.16), and hospital readmission (AOR 1.11, 95% CI 0.76-1.63; adjusted hazard ratio 1.02, 95% CI 0.89-1.18). PIP was associated with 91%, 60% and 26% increased odds of adverse drug event-related hospital admissions (AOR 1.91, 95% CI 1.21-3.01), functional decline (AOR 1.60, 95% CI 1.28-2.01), and adverse drug reactions and adverse drug events (AOR 1.26, 95% CI 1.11-1.43), respectively. PIP was associated with falls (2/2 studies). The impact of PIP on emergency department visits, length of stay, and health-related quality of life was inconclusive. Economic cost of PIP reported in 3 studies, comprised various cost estimation methods. Conclusion(s): PIP was significantly associated with a range of health-related and system-related outcomes. It is important to optimise older adults' prescriptions to facilitate improved outcomes of care.Copyright © 2021 The Authors. British Journal of Clinical Pharmacology published by John Wiley & Sons Ltd on behalf of British Pharmacological Society.
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- 2021
21. Exercise attenuates bone mineral density loss during diet-induced weight loss in adults with overweight and obesity: A systematic review and meta-analysis
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Mesinovic, Jakub, Jansons, Paul, Zengin, A, de Courten, B, Rodriguez, AJ, Daly, Robin, Ebeling, PR, Scott, David, Mesinovic, Jakub, Jansons, Paul, Zengin, A, de Courten, B, Rodriguez, AJ, Daly, Robin, Ebeling, PR, and Scott, David
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- 2021
22. Potentially inappropriate prescribing and its associations with health-related and system-related outcomes in hospitalised older adults: A systematic review and meta-analysis
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Mekonnen, Alemayehu, Redley, Bernice, de Courten, B, Manias, Elizabeth, Mekonnen, Alemayehu, Redley, Bernice, de Courten, B, and Manias, Elizabeth
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- 2021
23. Novel Relationship Between Plasmalogen Lipid Signatures and Carnosine in Humans
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Mayneris-Perxachs, J, Meikle, P, Mousa, A, Naderpoor, N, Fernandez-Real, JM, de Courten, B, Mayneris-Perxachs, J, Meikle, P, Mousa, A, Naderpoor, N, Fernandez-Real, JM, and de Courten, B
- Abstract
INTRODUCTION: Carnosine is a naturally occurring dipeptide abundant in the skeletal and cardiac muscle and brain, which has been shown to improve glucose metabolism and cardiovascular risk. This study showed that carnosine supplementation had positive changes on plasma lipidome. Here, this study aimed to establish the relationship of muscle carnosine and serum carnosinase-1 with cardiometabolic risk factors and the lipidome. METHODS AND RESULTS: This study profiles >450 lipid species in 65 overweight/obese nondiabetic individuals. Intensive metabolic testing is conducted using direct gold-standard measures of adiposity, insulin sensitivity and secretion, as well as measurement of serum inflammatory cytokines and adipokines. Muscle carnosine is negatively associated with 2-h glucose concentrations, whereas serum carnosinase-1 levels are negatively associated with insulin sensitivity and positively with IL-18. O-PLS and machine learning analyses reveal a strong association of muscle carnosine with ether lipids, particularly arachidonic acid-containing plasmalogens. Carnosinase-1 levels are positively associated with total phosphatidylethanolamines, but negatively with lysoalkylphosphatidylcholines, trihexosylceramides, and gangliosides. In particular, alkylphosphatidylethanolamine species containing arachidonic acid are positively associated with carnosinase-1. CONCLUSION: These associations reinforce the role of muscle carnosine and serum carnosinase-1 in the interplay among low-grade chronic inflammation, glucose homeostasis, and insulin sensitivity.
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- 2021
24. Exercise attenuates bone mineral density loss during diet-induced weight loss in adults with overweight and obesity: A systematic review and meta-analysis
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Mesinovic, J, Jansons, P, Zengin, A, de Courten, B, Rodriguez, AJ, Daly, RM, Ebeling, PR, Scott, D, Mesinovic, J, Jansons, P, Zengin, A, de Courten, B, Rodriguez, AJ, Daly, RM, Ebeling, PR, and Scott, D
- Abstract
BACKGROUND: Weight-loss-induced fat loss improves cardiometabolic health in individuals with overweight and obesity; however, weight loss can also result in bone loss and increased fracture risk. Weight-loss-induced bone loss may be attenuated with exercise. Our aim was to compare changes in bone mineral density (BMD) in adults with overweight and obesity who undertook diet-induced weight loss alone or in combination with exercise. METHODS: We included randomized controlled trials (RCTs) in adults with overweight or obesity (aged ≥18 years; body mass index ≥25 kg/m2) that prescribed diet-induced weight loss alone or in combination with supervised exercise, and measured any bone structural parameters. Risk of bias was assessed using the Cochrane Risk of Bias tool. Random-effects meta-analyses determined mean changes and net mean differences (95% confidence intervals (95%CIs)) in the percentage of areal BMD (aBMD) change between groups. RESULTS: We included 9 RCTs. Diet-induced weight loss led to significant losses in femoral neck aBMD (mean change: -1.73% (95%CI: -2.39% to -1.07%), p < 0.001) and total hip aBMD (-2.19% (95%CI: -3.84% to -0.54%), p = 0.009). Femoral neck aBMD losses were significantly greater in the diet-induced weight loss group compared to the exercise plus diet-induced weight loss group (net difference: -0.88% (95%CI: -1.73% to -0.03%)); however, there were no differences in aBMD changes at any other skeletal site: total hip (-1.96% (95%CI: -4.59% to 0.68%)) and lumbar spine (-0.48% (95%CI: -1.81% to 0.86%)). aBMD changes did not differ significantly according to exercise modality (resistance exercise, aerobic exercise, or a combination of the two) during diet-induced weight loss. CONCLUSION: Diet-induced weight loss led to greater femoral neck bone loss compared to diet-induced weight loss plus exercise. Bone loss at the total hip and lumbar spine was not attenuated by exercise during diet-induced weight loss. The lack of consistent skeletal benef
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- 2021
25. Sexual dysfunction in men with multiple sclerosis
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Grech, LB, Allan, M, de Courten, B, Grech, LB, Allan, M, and de Courten, B
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- 2021
26. Potentially inappropriate prescribing and its associations with health-related and system-related outcomes in hospitalised older adults: A systematic review and meta-analysis.
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Mekonnen, AB, Redley, B, de Courten, B, Manias, E, Mekonnen, AB, Redley, B, de Courten, B, and Manias, E
- Abstract
AIMS: To synthesise associations of potentially inappropriate prescribing (PIP) with health-related and system-related outcomes in inpatient hospital settings. METHODS: Six electronic databases were searched: Medline Complete, EMBASE, CINAHL, PyscInfo, IPA and Cochrane library. Studies published between 1 January 1991 and 31 January 2021 investigating associations between PIP and health-related and system-related outcomes of older adults in hospital settings, were included. A random effects model was employed using the generic inverse variance method to pool risk estimates. RESULTS: Overall, 63 studies were included. Pooled risk estimates did not show a significant association with all-cause mortality (adjusted odds ratio [AOR] 1.10, 95% confidence interval [CI] 0.90-1.36; adjusted hazard ratio 1.02, 83% CI 0.90-1.16), and hospital readmission (AOR 1.11, 95% CI 0.76-1.63; adjusted hazard ratio 1.02, 95% CI 0.89-1.18). PIP was associated with 91%, 60% and 26% increased odds of adverse drug event-related hospital admissions (AOR 1.91, 95% CI 1.21-3.01), functional decline (AOR 1.60, 95% CI 1.28-2.01), and adverse drug reactions and adverse drug events (AOR 1.26, 95% CI 1.11-1.43), respectively. PIP was associated with falls (2/2 studies). The impact of PIP on emergency department visits, length of stay, and health-related quality of life was inconclusive. Economic cost of PIP reported in 3 studies, comprised various cost estimation methods. CONCLUSIONS: PIP was significantly associated with a range of health-related and system-related outcomes. It is important to optimise older adults' prescriptions to facilitate improved outcomes of care.
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- 2021
27. Nutritional Interventions for COVID-19: A Role for Carnosine?
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Feehan, J, de Courten, M, Apostolopoulos, V, de Courten, B, Feehan, J, de Courten, M, Apostolopoulos, V, and de Courten, B
- Abstract
As COVID-19 continues to take an enormous toll on global health, the effort to find effective preventive and treatment strategies has been unparalleled in recent history [...].
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- 2021
28. Effectiveness of community-based health education and home support program to reduce blood pressure among patients with uncontrolled hypertension in Nepal: A cluster-randomized trial
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Fukumoto, Y, Khanal, MK, Bhandari, P, Dhungana, RR, Rawal, LB, Gurung, Y, Paudel, KN, Singh, A, Devkota, S, de Courten, B, Fukumoto, Y, Khanal, MK, Bhandari, P, Dhungana, RR, Rawal, LB, Gurung, Y, Paudel, KN, Singh, A, Devkota, S, and de Courten, B
- Abstract
BACKGROUND: Hypertension is a major global public health problem. Elevated blood pressure can cause cardiovascular and kidney diseases. We assessed the effectiveness of health education sessions and home support programs in reducing blood pressure among patients with uncontrolled hypertension in a suburban community of Nepal. METHODS: We conducted a community-based, open-level, parallel-group, cluster randomized controlled trial in Birendranagar municipality of Surkhet, Nepal. We randomly assigned four clusters (wards) into intervention and control arms. We provided four health education sessions, frequent home and usual care for intervention groups over six months. The participants of the control arm received only usual care from health facilities. The primary outcome of this study was the proportion of controlled systolic blood pressure (SBP). The analysis included all participants who completed follow-up at six months. RESULTS: 125 participants were assigned to either the intervention (n = 63) or the control (n = 62) group. Of them, 60 participants in each group completed six months follow-up. The proportion of controlled SBP was significantly higher among the intervention participants compared to the control (58.3% vs. 40%). Odds ratio of this was 2.1 with 95% CI: 1.01-4.35 (p = 0.046) and that of controlled diastolic blood pressure (DBP) was 1.31 (0.63-2.72) (p = 0.600). The mean change (follow-up minus baseline) in SBP was significantly higher in the intervention than in the usual care (-18.7 mmHg vs. -11.2 mmHg, p = 0.041). Such mean change of DBP was also higher in the intervention (-10.95 mmHg vs. -5.53 mmHg, p = 0.065). The knowledge score on hypertension improved by 2.38 (SD 2.4) in the intervention arm, which was significantly different from that of the control group, 0.13 (1.8) (p<0.001). CONCLUSIONS: Multiple health education sessions complemented by frequent household visits by health volunteers can effectively improve knowledge on hypertension and re
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- 2021
29. Association between Diet Quality Indices and Incidence of Type 2 Diabetes in the Melbourne Collaborative Cohort Study
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Hodge, AM, Karim, MN, Hebert, JR, Shivappa, N, de Courten, B, Hodge, AM, Karim, MN, Hebert, JR, Shivappa, N, and de Courten, B
- Abstract
Type 2 diabetes mellitus is a common condition whose incidence is increasing worldwide, and for which obesity and diet are important risk factors. The aim of this study was to assess the association of three diet quality scores with diabetes risk and how much of the association was mediated through body size. The Melbourne Collaborative Cohort Study recruited 41,513 men and women aged 40-69 years during 1990-1994. At baseline, data were collected on lifestyle and diet, anthropometric measures were performed. Incident diabetes was assessed by self-report at follow-up surveys in 1994-1998 and 2003-2007. The associations between the dietary inflammatory index (DII®), Mediterranean Diet Score (MDS) and the Alternative Healthy Eating Index-2010 and incident diabetes were assessed using Poisson regression, adjusting for age, sex, physical activity, smoking, alcohol consumption, socio-economic status (area based) and family history of diabetes. Data from 39,185 participants were included in the analysis and 1989 cases of diabetes were identified. Both DII and AHEI-2010 were associated with diabetes incidence, but MDS was not. In the top quintile of DII (most pro-inflammatory) vs. the least inflammatory quintile IRR was 1.49 95% CI (1.30, 1.72), p trend across quintiles <0.001. For AHEI-2010 the IRR was 0.67 (0.58, 0.78), p trend <0.001 for the healthiest vs. the least healthy quintile. Mediation analysis indicated that body size (body mass index/waist to hip ratio) mediated 35-48% of the association with incident diabetes for the AHEI and DII. Healthier diets may reduce risk of diabetes both by reducing weight gain and other mechanisms such as reducing inflammation.
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- 2021
30. The activity of nuclear factor-κB (NF-κB) circulating mononuclear cells but not in subcutaneous adipose tissue or in muscle is associated with insulin sensitivity in healthy non-diabetic adults
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de Courten, B, Lyons, J, Sourris, K, Dougherty, S, Penfold, S, Gasser, A, Henstrige, D, de Courten, M, Duffy, S, Cooper, M, Kingwell, B, and Forbes, J
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- 2008
31. Sex-specific associations between insulin resistance and bone parameters in overweight and obese older adults.
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Mesinovic J., Ebeling P.R., De Courten B., Zengin A., Shore-Lorenti C., McMillan L.B., Scott D., Mesinovic J., Ebeling P.R., De Courten B., Zengin A., Shore-Lorenti C., McMillan L.B., and Scott D.
- Abstract
Objectives: To determine sex-specific associations between insulin resistance and bone parameters measured by peripheral quantitative computed tomography in overweight and obese community-dwelling older adults. Study design: Cross-sectional study of 79 community-dwelling overweight and obese adults (mean +/- SD age 62.8 +/- 7.9 years; body mass index 32.3 +/- 6.1 kg/m2; 58% women). Main Outcome Measure(s): Peripheral quantitative computed tomography assessed distal radius and tibia trabecular volumetric bone mineral density (vBMD) and proximal radius and tibia cortical vBMD, periosteal circumference, endosteal circumference and stress-strain index. The Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) score was calculated from fasting glucose and insulin values. Lean mass was assessed using dual-energy X-ray absorptiometry. Total minutes of moderate and vigorous physical activity (MVPA) were calculated using the Active Australia Survey. Result(s): Men and women in this cohort had no significant differences in fasting glucose and insulin concentrations, HOMA-IR values and diabetes prevalence (all P > 0.05). In women, HOMA-IR was positively correlated with proximal radius periosteal and endosteal circumference (r = 0.331; P = 0.034 and r = 0.325; P = 0.038, respectively). These associations became nonsignificant in multivariable regression analyses; however, HOMA-IR was negatively associated with proximal radius cortical vBMD (B = -4.79; 95% CI -8.66, -0.92) after adjusting for age, lean mass and MVPA. All associations between HOMA-IR and bone parameters became nonsignificant in a sensitivity analysis excluding individuals with diabetes, or self-reported use of glucose-lowering medications. There were no associations between HOMA-IR and bone parameters in men. Conclusion(s): Homeostatic Model Assessment of Insulin Resistance was negatively associated with radial cortical vBMD in overweight and obese older women, but not in men. Further studies are needed to
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- 2020
32. The relationship between vitamin d metabolites and androgens in women with polycystic ovary syndrome.
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Lambert E.A., Naderpoor N., de Courten B., Mesinovic J., Teede H.J., Shorakae S., Lambert G.W., Lambert E.A., Naderpoor N., de Courten B., Mesinovic J., Teede H.J., Shorakae S., and Lambert G.W.
- Abstract
Polycystic ovary syndrome (PCOS) is the most common endocrine disorder among women of reproductive age, with hyperandrogenism present in up to 90% of affected women. Some evidence suggests a link between vitamin D deficiency and PCOS features via insulin resistance and inflammation. Our aim was to explore the relationship between biochemical markers of vitamin D status and androgens in women with PCOS. This cross-sectional study used bio-banked samples from 46 pre-menopausal women with PCOS (mean +/- SD: age 30 +/- 6 years; BMI 29 +/- 6 kg/m2). We measured 25-hydroxyvitamin D (25[OH]D), vitamin D-binding protein (DBP), total testosterone, sex hormone-binding globulin (SHBG), and calculated the free androgen index (FAI) and bioavailable and free 25(OH)D. Fasting glucose and insulin were used to calculate the homeostatic model assessment of insulin resistance (HOMA-IR) and body fat percentage was determined via dual energy x-ray absorptiometry. High-sensitivity C-reactive protein (hs-CRP) was measured as a marker of inflammation. DBP was positively associated with total 25(OH)D and expectedly, negatively associated with free 25(OH)D. There were no associations between vitamin D metabolites and total testosterone, SHBG or FAI, even after adjusting for age, body fat percentage, HOMA-IR and hs-CRP. We found no associations between vitamin D metabolites and androgens in women with PCOS. Studies that have identified a vitamin D-androgen link have largely relied on methodology with numerous pitfalls; future studies should exclusively use gold-standard measures to confirm these findings in this population.Copyright © 2020 by the authors. Licensee MDPI, Basel, Switzerland.
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- 2020
33. Prevalence and attributable health burden of chronic respiratory diseases, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017
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Soriano, JB, Kendrick, PJ, Paulson, KR, Gupta, V, Vos, T, Abrams, EM, Adedoyin, RA, Adhikari, TB, Advani, SM, Agrawal, A, Ahmadian, E, Alahdab, F, Aljunid, SM, Altirkawi, KA, Alvis-Guzman, N, Anber, NH, Andrei, CL, Anjomshoa, M, Ansari, F, Anto, JM, Arabloo, J, Athari, SM, Athari, SS, Awoke, N, Badawi, A, Banoub, JAM, Bennett, DA, Bensenor, IM, Berfield, KS, Bernstein, RS, Bhattacharyya, K, Bijani, A, Brauer, M, Bukhman, G, Butt, ZA, Camera, LA, Car, J, Carrero, JJ, Carvalho, F, Castaneda-Orjuela, CA, Choi, J-YJ, Christopher, DJ, Cohen, AJ, Dandona, L, Dandona, R, Dang, AK, Daryani, A, de Courten, B, Demeke, FM, Demoz, GT, De Neve, J-W, Desai, R, Dharmaratne, SD, Diaz, D, Douiri, A, Driscoll, TR, Duken, EE, Eftekhari, A, Elkout, H, Endries, AY, Fadhil, I, Faro, A, Farzadfar, F, Fernandes, E, Filip, I, Fischer, F, Foroutan, M, Garcia-Gordillo, MA, Gebre, AK, Gebremedhin, KB, Gebremeskel, GG, Gezae, KE, Ghoshal, AG, Gill, PS, Gillum, RF, Goudarzi, H, Guo, Y, Gupta, R, Hailu, GB, Hasanzadeh, A, Hassen, HY, Hay, SI, Hoang, CL, Hole, MK, Horita, N, Hosgood, HD, Hostiuc, M, Househ, M, Ilesanmi, OS, Ilic, MD, Irvani, SSN, Islam, SMS, Jakovljevic, M, Jamal, AA, Jha, RP, Jonas, JB, Kabir, Z, Kasaeian, A, Kasahun, GG, Kassa, GM, Kefale, AT, Kengne, AP, Khader, YS, Khafaie, MA, Khan, EA, Khan, J, Khubchandani, J, Kim, Y-E, Kim, YJ, Kisa, S, Kisa, A, Knibbs, LD, Komaki, H, Koul, PA, Koyanagi, A, Kumar, GA, Lan, Q, Lasrado, S, Lauriola, P, La Vecchia, C, Tham, TL, Leigh, J, Levi, M, Li, S, Lopez, AD, Lotufo, PA, Madotto, F, Mahotra, NB, Majdan, M, Majeed, A, Malekzadeh, R, Mamun, AA, Manafi, N, Manafi, F, Mantovani, LG, Meharie, BG, Meles, HG, Meles, GG, Menezes, RG, Mestrovic, T, Miller, TR, Mini, GK, Mirrakhimov, EM, Moazen, B, Mohammad, KA, Mohammed, S, Mohebi, F, Mokdad, AH, Molokhia, M, Monasta, L, Moradi, M, Moradi, G, Morawska, L, Mousavi, SM, Musa, KI, Mustafa, G, Naderi, M, Naghavi, M, Naik, G, Nair, S, Nangia, V, Nansseu, JR, Nazari, J, Ndwandwe, DE, Negoi, RI, Trang, HN, Cuong, TN, Huong, LTN, Nixon, MR, Ofori-Asenso, R, Ogbo, FA, Olagunju, AT, Olagunju, TO, Oren, E, Ortiz, JR, Owolabi, MO, Mahesh, PA, Pakhale, S, Pana, A, Panda-Jonas, S, Park, E-K, Hai, QP, Postma, MJ, Pourjafar, H, Poustchi, H, Radfar, A, Rafiei, A, Rahim, F, Rahman, MHU, Rahman, MA, Rawaf, S, Rawaf, DL, Rawal, L, Reiner, RC, Reitsma, MB, Roever, L, Ronfani, L, Roro, EM, Roshandel, G, Rudd, KE, Sabde, YD, Sabour, S, Saddik, B, Safari, S, Saleem, K, Samy, AM, Santric-Milicevic, MM, Jose, BPS, Sartorius, B, Satpathy, M, Savic, M, Sawhney, M, Sepanlou, SG, Shaikh, MA, Sheikh, A, Shigematsu, M, Shirkoohi, R, Si, S, Siabani, S, Singh, V, Singh, JA, Soljak, M, Somayaji, R, Soofi, M, Soyiri, IN, Tefera, YM, Temsah, M-H, Tesfay, BE, Thakur, JS, Toma, AT, Tortajada-Girbes, M, Khanh, BT, Bach, XT, Car, LT, Ullah, I, Vacante, M, Valdez, PR, van Boven, JFM, Vasankari, TJ, Veisani, Y, Violante, FS, Wagner, GR, Westerman, R, Wolfe, CDA, Wondafrash, DZ, Wondmieneh, AB, Yonemoto, N, Yoon, S-J, Zaidi, Z, Zamani, M, Zar, HJ, Zhang, Y, Soriano, JB, Kendrick, PJ, Paulson, KR, Gupta, V, Vos, T, Abrams, EM, Adedoyin, RA, Adhikari, TB, Advani, SM, Agrawal, A, Ahmadian, E, Alahdab, F, Aljunid, SM, Altirkawi, KA, Alvis-Guzman, N, Anber, NH, Andrei, CL, Anjomshoa, M, Ansari, F, Anto, JM, Arabloo, J, Athari, SM, Athari, SS, Awoke, N, Badawi, A, Banoub, JAM, Bennett, DA, Bensenor, IM, Berfield, KS, Bernstein, RS, Bhattacharyya, K, Bijani, A, Brauer, M, Bukhman, G, Butt, ZA, Camera, LA, Car, J, Carrero, JJ, Carvalho, F, Castaneda-Orjuela, CA, Choi, J-YJ, Christopher, DJ, Cohen, AJ, Dandona, L, Dandona, R, Dang, AK, Daryani, A, de Courten, B, Demeke, FM, Demoz, GT, De Neve, J-W, Desai, R, Dharmaratne, SD, Diaz, D, Douiri, A, Driscoll, TR, Duken, EE, Eftekhari, A, Elkout, H, Endries, AY, Fadhil, I, Faro, A, Farzadfar, F, Fernandes, E, Filip, I, Fischer, F, Foroutan, M, Garcia-Gordillo, MA, Gebre, AK, Gebremedhin, KB, Gebremeskel, GG, Gezae, KE, Ghoshal, AG, Gill, PS, Gillum, RF, Goudarzi, H, Guo, Y, Gupta, R, Hailu, GB, Hasanzadeh, A, Hassen, HY, Hay, SI, Hoang, CL, Hole, MK, Horita, N, Hosgood, HD, Hostiuc, M, Househ, M, Ilesanmi, OS, Ilic, MD, Irvani, SSN, Islam, SMS, Jakovljevic, M, Jamal, AA, Jha, RP, Jonas, JB, Kabir, Z, Kasaeian, A, Kasahun, GG, Kassa, GM, Kefale, AT, Kengne, AP, Khader, YS, Khafaie, MA, Khan, EA, Khan, J, Khubchandani, J, Kim, Y-E, Kim, YJ, Kisa, S, Kisa, A, Knibbs, LD, Komaki, H, Koul, PA, Koyanagi, A, Kumar, GA, Lan, Q, Lasrado, S, Lauriola, P, La Vecchia, C, Tham, TL, Leigh, J, Levi, M, Li, S, Lopez, AD, Lotufo, PA, Madotto, F, Mahotra, NB, Majdan, M, Majeed, A, Malekzadeh, R, Mamun, AA, Manafi, N, Manafi, F, Mantovani, LG, Meharie, BG, Meles, HG, Meles, GG, Menezes, RG, Mestrovic, T, Miller, TR, Mini, GK, Mirrakhimov, EM, Moazen, B, Mohammad, KA, Mohammed, S, Mohebi, F, Mokdad, AH, Molokhia, M, Monasta, L, Moradi, M, Moradi, G, Morawska, L, Mousavi, SM, Musa, KI, Mustafa, G, Naderi, M, Naghavi, M, Naik, G, Nair, S, Nangia, V, Nansseu, JR, Nazari, J, Ndwandwe, DE, Negoi, RI, Trang, HN, Cuong, TN, Huong, LTN, Nixon, MR, Ofori-Asenso, R, Ogbo, FA, Olagunju, AT, Olagunju, TO, Oren, E, Ortiz, JR, Owolabi, MO, Mahesh, PA, Pakhale, S, Pana, A, Panda-Jonas, S, Park, E-K, Hai, QP, Postma, MJ, Pourjafar, H, Poustchi, H, Radfar, A, Rafiei, A, Rahim, F, Rahman, MHU, Rahman, MA, Rawaf, S, Rawaf, DL, Rawal, L, Reiner, RC, Reitsma, MB, Roever, L, Ronfani, L, Roro, EM, Roshandel, G, Rudd, KE, Sabde, YD, Sabour, S, Saddik, B, Safari, S, Saleem, K, Samy, AM, Santric-Milicevic, MM, Jose, BPS, Sartorius, B, Satpathy, M, Savic, M, Sawhney, M, Sepanlou, SG, Shaikh, MA, Sheikh, A, Shigematsu, M, Shirkoohi, R, Si, S, Siabani, S, Singh, V, Singh, JA, Soljak, M, Somayaji, R, Soofi, M, Soyiri, IN, Tefera, YM, Temsah, M-H, Tesfay, BE, Thakur, JS, Toma, AT, Tortajada-Girbes, M, Khanh, BT, Bach, XT, Car, LT, Ullah, I, Vacante, M, Valdez, PR, van Boven, JFM, Vasankari, TJ, Veisani, Y, Violante, FS, Wagner, GR, Westerman, R, Wolfe, CDA, Wondafrash, DZ, Wondmieneh, AB, Yonemoto, N, Yoon, S-J, Zaidi, Z, Zamani, M, Zar, HJ, and Zhang, Y
- Abstract
BACKGROUND: Previous attempts to characterise the burden of chronic respiratory diseases have focused only on specific disease conditions, such as chronic obstructive pulmonary disease (COPD) or asthma. In this study, we aimed to characterise the burden of chronic respiratory diseases globally, providing a comprehensive and up-to-date analysis on geographical and time trends from 1990 to 2017. METHODS: Using data from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017, we estimated the prevalence, morbidity, and mortality attributable to chronic respiratory diseases through an analysis of deaths, disability-adjusted life-years (DALYs), and years of life lost (YLL) by GBD super-region, from 1990 to 2017, stratified by age and sex. Specific diseases analysed included asthma, COPD, interstitial lung disease and pulmonary sarcoidosis, pneumoconiosis, and other chronic respiratory diseases. We also assessed the contribution of risk factors (smoking, second-hand smoke, ambient particulate matter and ozone pollution, household air pollution from solid fuels, and occupational risks) to chronic respiratory disease-attributable DALYs. FINDINGS: In 2017, 544·9 million people (95% uncertainty interval [UI] 506·9-584·8) worldwide had a chronic respiratory disease, representing an increase of 39·8% compared with 1990. Chronic respiratory disease prevalence showed wide variability across GBD super-regions, with the highest prevalence among both males and females in high-income regions, and the lowest prevalence in sub-Saharan Africa and south Asia. The age-sex-specific prevalence of each chronic respiratory disease in 2017 was also highly variable geographically. Chronic respiratory diseases were the third leading cause of death in 2017 (7·0% [95% UI 6·8-7·2] of all deaths), behind cardiovascular diseases and neoplasms. Deaths due to chronic respiratory diseases numbered 3 914 196 (95% UI 3 790 578-4 044 819) in 2017, an increase of 18·0% since 1990, while
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- 2020
34. The global, regional, and national burden of cirrhosis by cause in 195 countries and territories, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017
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Sepanlou, SG, Safiri, S, Bisignano, C, Ikuta, KS, Merat, S, Saberifiroozi, M, Poustchi, H, Tsoi, D, Colombara, DV, Abdoli, A, Adedoyin, RA, Afarideh, M, Agrawal, S, Ahmad, S, Ahmadian, E, Ahmadpour, E, Akinyemiju, T, Akunna, CJ, Alipour, V, Almasi-Hashiani, A, Almulhim, AM, Al-Raddadi, RM, Alvis-Guzman, N, Anber, NH, Angus, C, Anoushiravani, A, Arabloo, J, Araya, EM, Asmelash, D, Ataeinia, B, Ataro, Z, Atout, MMW, Ausloos, F, Awasthi, A, Badawi, A, Banach, M, Bejarano Ramirez, DF, Bhagavathula, AS, Bhala, N, Bhattacharyya, K, Biondi, A, Bolla, SR, Boloor, A, Borzi, AM, Butt, ZA, Alberto Camera, LLA, Campos-Nonato, IR, Carvalho, F, Dinh-Toi, C, Chung, S-C, Cortesi, PA, Costa, VM, Cowie, BC, Daryani, A, de Courten, B, Demoz, GT, Desai, R, Dharmaratne, SD, Djalalinia, S, Hoa, TD, Dorostkar, F, Drake, TM, Dubey, M, Duncan, BB, Effiong, A, Eftekhari, A, Elsharkawy, A, Etemadi, A, Farahmand, M, Farzadfar, F, Fernandes, E, Filip, I, Fischer, F, Gebremedhin, KBB, Geta, B, Gilani, SA, Gill, PS, Alma Gutierrez, R, Haile, MT, Haj-Mirzaian, A, Hamid, SS, Hasankhani, M, Hasanzadeh, A, Hashemian, M, Hassen, HY, Hay, SI, Hayat, K, Heidari, B, Henok, A, Chi, LH, Hostiuc, M, Hostiuc, S, Hsieh, VC-R, Igumbor, EU, Ilesanmi, OS, Irvani, SSN, Balalami, NJ, James, SL, Jeemon, P, Jha, RP, Jonas, JB, Jozwiak, JJ, Kabir, A, Kasaeian, A, Kassaye, HG, Kefale, AT, Khan, RKMA, Khan, EA, Khater, A, Kim, YJ, Koyanagi, A, La Vecchia, C, Lim, L-L, Lopez, AD, Lorkowski, S, Lotufo, PA, Lozano, R, Abd El Razek, MM, Hue, TM, Manafi, N, Manafi, A, Mansournia, MA, Mantovani, LG, Mazzaglia, G, Mehta, D, Mendoza, W, Menezes, RG, Mengesha, MM, Meretoja, TJ, Mestrovic, T, Miazgowski, B, Miller, TR, Mirrakhimov, EM, Mithra, P, Moazen, B, Moghadaszadeh, M, Mohammadian-Hafshejani, A, Mohammed, S, Mokdad, AH, Montero-Zamora, PA, Moradi, G, Naimzada, MD, Nayak, V, Negoi, I, Trang, HN, Ofori-Asenso, R, Oh, I-H, Olagunju, TO, Padubidri, JR, Pakshir, K, Pana, A, Pathak, M, Pourshams, A, Rabiee, N, Radfar, A, Rafiei, A, Ramezanzadeh, K, Rana, SMM, Rawaf, S, Rawaf, DL, Reiner, RC, Roever, L, Room, R, Roshandel, G, Safari, S, Samy, AM, Sanabria, J, Sartorius, B, Schmidt, MI, Senthilkumaran, S, Shaikh, MA, Sharif, M, Sharifi, A, Shigematsu, M, Singh, JA, Soheili, A, Suleria, HAR, Teklehaimanot, BF, Tesfay, BE, Vacante, M, Vahedian-Azimi, A, Valdez, PR, Vasankari, TJ, Giang, TV, Waheed, Y, Weldegwergs, KG, Werdecker, A, Westerman, R, Wondafrash, DZ, Wondmieneh, AB, Yeshitila, YG, Yonemoto, N, Yu, C, Zaidi, Z, Zarghi, A, Zelber-Sagi, S, Zewdie, KA, Zhang, Z-J, Zhao, X-J, Naghavi, M, Malekzadeh, R, Sepanlou, SG, Safiri, S, Bisignano, C, Ikuta, KS, Merat, S, Saberifiroozi, M, Poustchi, H, Tsoi, D, Colombara, DV, Abdoli, A, Adedoyin, RA, Afarideh, M, Agrawal, S, Ahmad, S, Ahmadian, E, Ahmadpour, E, Akinyemiju, T, Akunna, CJ, Alipour, V, Almasi-Hashiani, A, Almulhim, AM, Al-Raddadi, RM, Alvis-Guzman, N, Anber, NH, Angus, C, Anoushiravani, A, Arabloo, J, Araya, EM, Asmelash, D, Ataeinia, B, Ataro, Z, Atout, MMW, Ausloos, F, Awasthi, A, Badawi, A, Banach, M, Bejarano Ramirez, DF, Bhagavathula, AS, Bhala, N, Bhattacharyya, K, Biondi, A, Bolla, SR, Boloor, A, Borzi, AM, Butt, ZA, Alberto Camera, LLA, Campos-Nonato, IR, Carvalho, F, Dinh-Toi, C, Chung, S-C, Cortesi, PA, Costa, VM, Cowie, BC, Daryani, A, de Courten, B, Demoz, GT, Desai, R, Dharmaratne, SD, Djalalinia, S, Hoa, TD, Dorostkar, F, Drake, TM, Dubey, M, Duncan, BB, Effiong, A, Eftekhari, A, Elsharkawy, A, Etemadi, A, Farahmand, M, Farzadfar, F, Fernandes, E, Filip, I, Fischer, F, Gebremedhin, KBB, Geta, B, Gilani, SA, Gill, PS, Alma Gutierrez, R, Haile, MT, Haj-Mirzaian, A, Hamid, SS, Hasankhani, M, Hasanzadeh, A, Hashemian, M, Hassen, HY, Hay, SI, Hayat, K, Heidari, B, Henok, A, Chi, LH, Hostiuc, M, Hostiuc, S, Hsieh, VC-R, Igumbor, EU, Ilesanmi, OS, Irvani, SSN, Balalami, NJ, James, SL, Jeemon, P, Jha, RP, Jonas, JB, Jozwiak, JJ, Kabir, A, Kasaeian, A, Kassaye, HG, Kefale, AT, Khan, RKMA, Khan, EA, Khater, A, Kim, YJ, Koyanagi, A, La Vecchia, C, Lim, L-L, Lopez, AD, Lorkowski, S, Lotufo, PA, Lozano, R, Abd El Razek, MM, Hue, TM, Manafi, N, Manafi, A, Mansournia, MA, Mantovani, LG, Mazzaglia, G, Mehta, D, Mendoza, W, Menezes, RG, Mengesha, MM, Meretoja, TJ, Mestrovic, T, Miazgowski, B, Miller, TR, Mirrakhimov, EM, Mithra, P, Moazen, B, Moghadaszadeh, M, Mohammadian-Hafshejani, A, Mohammed, S, Mokdad, AH, Montero-Zamora, PA, Moradi, G, Naimzada, MD, Nayak, V, Negoi, I, Trang, HN, Ofori-Asenso, R, Oh, I-H, Olagunju, TO, Padubidri, JR, Pakshir, K, Pana, A, Pathak, M, Pourshams, A, Rabiee, N, Radfar, A, Rafiei, A, Ramezanzadeh, K, Rana, SMM, Rawaf, S, Rawaf, DL, Reiner, RC, Roever, L, Room, R, Roshandel, G, Safari, S, Samy, AM, Sanabria, J, Sartorius, B, Schmidt, MI, Senthilkumaran, S, Shaikh, MA, Sharif, M, Sharifi, A, Shigematsu, M, Singh, JA, Soheili, A, Suleria, HAR, Teklehaimanot, BF, Tesfay, BE, Vacante, M, Vahedian-Azimi, A, Valdez, PR, Vasankari, TJ, Giang, TV, Waheed, Y, Weldegwergs, KG, Werdecker, A, Westerman, R, Wondafrash, DZ, Wondmieneh, AB, Yeshitila, YG, Yonemoto, N, Yu, C, Zaidi, Z, Zarghi, A, Zelber-Sagi, S, Zewdie, KA, Zhang, Z-J, Zhao, X-J, Naghavi, M, and Malekzadeh, R
- Abstract
BACKGROUND: Cirrhosis and other chronic liver diseases (collectively referred to as cirrhosis in this paper) are a major cause of morbidity and mortality globally, although the burden and underlying causes differ across locations and demographic groups. We report on results from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017 on the burden of cirrhosis and its trends since 1990, by cause, sex, and age, for 195 countries and territories. METHODS: We used data from vital registrations, vital registration samples, and verbal autopsies to estimate mortality. We modelled prevalence of total, compensated, and decompensated cirrhosis on the basis of hospital and claims data. Disability-adjusted life-years (DALYs) were calculated as the sum of years of life lost due to premature death and years lived with disability. Estimates are presented as numbers and age-standardised or age-specific rates per 100 000 population, with 95% uncertainty intervals (UIs). All estimates are presented for five causes of cirrhosis: hepatitis B, hepatitis C, alcohol-related liver disease, non-alcoholic steatohepatitis (NASH), and other causes. We compared mortality, prevalence, and DALY estimates with those expected according to the Socio-demographic Index (SDI) as a proxy for the development status of regions and countries. FINDINGS: In 2017, cirrhosis caused more than 1·32 million (95% UI 1·27-1·45) deaths (440 000 [416 000-518 000; 33·3%] in females and 883 000 [838 000-967 000; 66·7%] in males) globally, compared with less than 899 000 (829 000-948 000) deaths in 1990. Deaths due to cirrhosis constituted 2·4% (2·3-2·6) of total deaths globally in 2017 compared with 1·9% (1·8-2·0) in 1990. Despite an increase in the number of deaths, the age-standardised death rate decreased from 21·0 (19·2-22·3) per 100 000 population in 1990 to 16·5 (15·8-18·1) per 100 000 population in 2017. Sub-Saharan Africa had the highest age-standardised death rate among GBD super-regions fo
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- 2020
35. Global, regional, and country-specific lifetime risks of stroke, 1990 and 2016
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Feigin V, Nguyen G, Cercy K, Johnson C, Alam T, Parmar P, Abajobir A, Abate K, Abd-Allah F, Abejie A, Abyu G, Ademi Z, Agarwal G, Ahmed M, Akinyemi R, Al-Raddadi R, Aminde L, Amlie-Lefond C, Ansari H, Asayesh H, Asgedom S, Atey T, Ayele H, Banach M, Banerjee A, Barac A, Barker-Collo S, Barnighausen T, Barregard L, Basu S, Bedi N, Behzadifar M, Bejot Y, Bennett D, Bensenor I, Berhe D, Boneya D, Brainin M, Campos-Nonato I, Caso V, Castaneda-Orjuela C, Rivas J, Catala-Lopez F, Christensen H, Criqui M, Damasceno A, Dandona L, Dandona R, Davletov K, de Courten B, deVeber G, Dokova K, Edessa D, Endres M, Faraon E, Farvid M, Fischer F, Foreman K, Forouzanfar M, Gall S, Gebrehiwot T, Geleijnse J, Gillum R, Giroud M, Goulart A, Gupta R, Hachinski V, Hamadeh R, Hankey G, Hareri H, Havmoeller R, Hay S, Hegazy M, Hibstu D, James S, Jeemon P, John D, Jonas J, Jozwiak J, Kalani R, Kandel A, Kasaeian A, Kengne A, Khader Y, Khan A, Khang Y, Khubchandani J, Kim D, Kim Y, Kivimaki M, Kokubo Y, Kolte D, Kopec J, Kosen S, Kravchenko M, Krishnamurthi R, Kumar G, Lafranconi A, Lavados P, Legesse Y, Li Y, Liang X, Lo W, Lorkowski S, Lotufo P, Loy C, Mackay M, Abd El Razek H, Mahdavi M, Majeed A, Malekzadeh R, Malta D, Mamun A, Mantovani L, Martins S, Mate K, Mazidi M, Mehata S, Meier T, Melaku Y, Mendoza W, Mensah G, Meretoja A, Mezgebe H, Miazgowski T, Miller T, Ibrahim N, Mohammed S, Mokdad A, Moosazadeh M, Moran A, Musa K, Negoi R, Nguyen M, Nguyen Q, Nguyen T, Tran T, Ningrum D, Norrving B, Noubiap J, O'Donnell M, Olagunju A, Onuma O, Owolabi M, Parsaeian M, Patton G, Piradov M, Pletcher M, Pourmalek F, Prakash V, Qorbani M, Rahman M, Rai R, Ranta A, Rawaf D, Rawaf S, Renzaho A, Robinson S, Sahathevan R, Sahebkar A, Salomon J, Santalucia P, Santos I, Sartorius B, Schutte A, Sepanlou S, Shafieesabet A, Shaikh M, Shamsizadeh M, Sheth K, Sisay M, Shin M, Shiue I, Silva D, Sobngwi E, Soljak M, Sorensen R, Sposato L, Stranges S, Suliankatchi R, Tabares-Seisdedos R, Tanne D, Nguyen C, Thakur J, Thrift A, Tirschwell D, Topor-Madry R, Tran B, Nguyen L, Truelsen T, Tsilimparis N, Tyrovolas S, Ukwaja K, Uthman O, Varakin Y, Vasankari T, Venketasubramanian N, Vlassov V, Wang W, Werdecker A, Wolfe C, Xu G, Yano Y, Yonemoto N, Yu C, Zaidi Z, Zaki M, Zhou M, Ziaeian B, Zipkin B, Vos T, Naghavi M, Murray C, Roth G, GBD 2016 Lifetime Risk Stroke, Roth, G, Feigin, V, Nguyen, G, Cercy, K, Johnson, C, Alam, T, Parmar, P, Abajobir, A, Abate, K, Abd-Allah, F, Abejie, A, Abyu, G, Ademi, Z, Agarwal, G, Ahmed, M, Akinyemi, R, Al-Raddadi, R, Aminde, L, Amlie-Lefond, C, Ansari, H, Asayesh, H, Asgedom, S, Atey, T, Ayele, H, Banach, M, Banerjee, A, Barac, A, Barker-Collo, S, Bärnighausen, T, Barregard, L, Basu, S, Bedi, N, Behzadifar, M, Béjot, Y, Bennett, D, Bensenor, I, Berhe, D, Boneya, D, Brainin, M, Campos-Nonato, I, Caso, V, Castañeda-Orjuela, C, Rivas, J, Catalá-López, F, Christensen, H, Criqui, M, Damasceno, A, Dandona, L, Dandona, R, Davletov, K, de Courten, B, Deveber, G, Dokova, K, Edessa, D, Endres, M, Faraon, E, Farvid, M, Fischer, F, Foreman, K, Forouzanfar, M, Gall, S, Gebrehiwot, T, Geleijnse, J, Gillum, R, Giroud, M, Goulart, A, Gupta, R, Hachinski, V, Hamadeh, R, Hankey, G, Hareri, H, Havmoeller, R, Hay, S, Hegazy, M, Hibstu, D, James, S, Jeemon, P, John, D, Jonas, J, Jóźwiak, J, Kalani, R, Kandel, A, Kasaeian, A, Kengne, A, Khader, Y, Khan, A, Khang, Y, Khubchandani, J, Kim, D, Kim, Y, Kivimaki, M, Kokubo, Y, Kolte, D, Kopec, J, Kosen, S, Kravchenko, M, Krishnamurthi, R, Anil Kumar, G, Lafranconi, A, Lavados, P, Legesse, Y, Li, Y, Liang, X, Lo, W, Lorkowski, S, Lotufo, P, Loy, C, Mackay, M, Abd El Razek, H, Mahdavi, M, Majeed, A, Malekzadeh, R, Malta, D, Mamun, A, Mantovani, L, Martins, S, Mate, K, Mazidi, M, Mehata, S, Meier, T, Melaku, Y, Mendoza, W, Mensah, G, Meretoja, A, Mezgebe, H, Miazgowski, T, Miller, T, Ibrahim, N, Mohammed, S, Mokdad, A, Moosazadeh, M, Moran, A, Musa, K, Negoi, R, Nguyen, M, Nguyen, Q, Nguyen, T, Tran, T, Anggraini Ningrum, D, Norrving, B, Noubiap, J, O'Donnell, M, Olagunju, A, Onuma, O, Owolabi, M, Parsaeian, M, Patton, G, Piradov, M, Pletcher, M, Pourmalek, F, Prakash, V, Qorbani, M, Rahman, M, Rai, R, Ranta, A, Rawaf, D, Rawaf, S, Renzaho, A, Robinson, S, Sahathevan, R, Sahebkar, A, Salomon, J, Santalucia, P, Santos, I, Sartorius, B, Schutte, A, Sepanlou, S, Shafieesabet, A, Shaikh, M, Shamsizadeh, M, Sheth, K, Sisay, M, Shin, M, Shiue, I, Silva, D, Sobngwi, E, Soljak, M, Sorensen, R, Sposato, L, Stranges, S, Suliankatchi, R, Tabarés-Seisdedos, R, Tanne, D, Tat Nguyen, C, Thakur, J, Thrift, A, Tirschwell, D, Topor-Madry, R, Tran, B, Nguyen, L, Truelsen, T, Tsilimparis, N, Tyrovolas, S, Ukwaja, K, Uthman, O, Varakin, Y, Vasankari, T, Venketasubramanian, N, Vlassov, V, Wang, W, Werdecker, A, Wolfe, C, Xu, G, Yano, Y, Yonemoto, N, Yu, C, Zaidi, Z, El Sayed Zaki, M, Zhou, M, Ziaeian, B, Zipkin, B, Vos, T, Naghavi, M, Murray, C, Department of Public Health, Clinicum, Neurologian yksikkö, 10922180 - Schutte, Aletta Elisabeth, Feigin, Valery L, Nguyen, Grant, Cercy, Kelly, Johnson, Catherine O, Ahmed, Muktar B, Roth, Gregory A, and GBD 2016 Lifetime Risk of Stroke Collaborators
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Male ,Percentile ,Nutrition and Disease ,Disease ,030204 cardiovascular system & hematology ,Global Health ,Socioeconomic Factor ,Global Burden of Disease ,0302 clinical medicine ,prevention ,Voeding en Ziekte ,Cause of Death ,Global health ,Stroke ,POPULATION ,Cause of death ,Aged, 80 and over ,education.field_of_study ,Incidence (epidemiology) ,Incidence ,Medicine (all) ,11 Medical And Health Sciences ,General Medicine ,Middle Aged ,lifetime risk ,stroke ,3142 Public health care science, environmental and occupational health ,3. Good health ,GBD 2016 Lifetime Risk of Stroke Collaborators ,Female ,BURDEN ,Life Sciences & Biomedicine ,Research Article ,Human ,Adult ,Risk ,Population ,Global Burden of Disease (GBD) ,03 medical and health sciences ,Medicine, General & Internal ,Age Distribution ,General & Internal Medicine ,medicine ,Humans ,Life Science ,Point estimation ,cardiovascular diseases ,Sex Distribution ,education ,VLAG ,Aged ,Science & Technology ,HYPERTENSION ,business.industry ,medicine.disease ,Socioeconomic Factors ,business ,030217 neurology & neurosurgery ,RC ,Demography - Abstract
Background: The lifetime risk of stroke has been calculated in a limited number of selected populations. We sought to estimate the lifetime risk of stroke at the regional, country, and global level using data from a comprehensive study of the prevalence of major diseases.Methods: We used the Global Burden of Disease (GBD) Study 2016 estimates of stroke incidence and the competing risks of death from any cause other than stroke to calculate the cumulative lifetime risks of first stroke, ischemic stroke, or hemorrhagic stroke among adults 25 years of age or older. Estimates of the lifetime risks in the years 1990 and 2016 were compared. Countries were categorized into quintiles of the sociodemographic index (SDI) used in the GBD Study, and the risks were compared across quintiles. Comparisons were made with the use of point estimates and uncertainty intervals representing the 2.5th and 97.5th percentiles around the estimate.Results: The estimated global lifetime risk of stroke from the age of 25 years onward was 24.9% (95% uncertainty interval, 23.5 to 26.2); the risk among men was 24.7% (95% uncertainty interval, 23.3 to 26.0), and the risk among women was 25.1% (95% uncertainty interval, 23.7 to 26.5). The risk of ischemic stroke was 18.3%, and the risk of hemorrhagic stroke was 8.2%. In high-SDI, high-middle–SDI, and low-SDI countries, the estimated lifetime risk of stroke was 23.5%, 31.1% (highest risk), and 13.2% (lowest risk), respectively; the 95% uncertainty intervals did not overlap between these categories. The highest estimated lifetime risks of stroke according to GBD region were in East Asia (38.8%), Central Europe (31.7%), and Eastern Europe (31.6%), and the lowest risk was in eastern sub-Saharan Africa (11.8%). The mean global lifetime risk of stroke increased from 22.8% in 1990 to 24.9% in 2016, a relative increase of 8.9% (95% uncertainty interval, 6.2 to 11.5); the competing risk of death from any cause other than stroke was considered in this calculation.Conclusions: In 2016, the global lifetime risk of stroke from the age of 25 years onward was approximately 25% among both men and women. There was geographic variation in the lifetime risk of stroke, with the highest risks in East Asia, Central Europe, and Eastern Europe. (Funded by the Bill and Melinda Gates Foundation.)
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- 2018
36. Global, regional, and national burden of stroke, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016
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Johnson, CO, Nguyen, M, Roth, GA, Nichols, E, Alam, T, Abate, D, Abd-Allah, F, Abdelalim, A, Abraha, HN, Abu-Rmeileh, NM, Adebayo, OM, Adeoye, AM, Agarwal, G, Agrawal, S, Aichour, AN, Aichour, I, Aichour, MTE, Alahdab, F, Ali, R, Alvis-Guzman, N, Anber, NH, Anjomshoa, M, Arabloo, J, Arauz, A, Ärnlöv, J, Arora, A, Awasthi, A, Banach, M, Barboza, MA, Barker-Collo, SL, Bärnighausen, TW, Basu, S, Belachew, AB, Belayneh, YM, Bennett, DA, Bensenor, IM, Bhattacharyya, K, Biadgo, B, Bijani, A, Bikbov, B, Bin Sayeed, MS, Butt, ZA, Cahuana-Hurtado, L, Carrero, JJ, Carvalho, F, Castañeda-Orjuela, CA, Castro, F, Catalá-López, F, Chaiah, Y, Chiang, PPC, Choi, JYJ, Christensen, H, Chu, DT, Cortinovis, M, Damasceno, AAM, Dandona, L, Dandona, R, Daryani, A, Davletov, K, De Courten, B, De la Cruz-Góngora, V, Degefa, MG, Dharmaratne, SD, Diaz, D, Dubey, M, Duken, EE, Edessa, D, Endres, M, Faraon, EJA, Farzadfar, F, Fernandes, E, Fischer, F, Flor, LS, Ganji, M, Gebre, AK, Gebremichael, TG, Geta, B, Gezae, KE, Gill, PS, Gnedovskaya, EV, Gómez-Dantés, H, Goulart, AC, Grosso, G, Guo, Y, Gupta, R, Haj-Mirzaian, A, Hamidi, S, Hankey, GJ, Hassen, HY, Hay, SI, Hegazy, MI, Heidari, B, Herial, NA, Hosseini, MA, Hostiuc, S, Irvani, SSN, Islam, SMS, Jahanmehr, N, and Javanbakht, M
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Neurology & Neurosurgery - Abstract
© 2019 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license Background: Stroke is a leading cause of mortality and disability worldwide and the economic costs of treatment and post-stroke care are substantial. The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) provides a systematic, comparable method of quantifying health loss by disease, age, sex, year, and location to provide information to health systems and policy makers on more than 300 causes of disease and injury, including stroke. The results presented here are the estimates of burden due to overall stroke and ischaemic and haemorrhagic stroke from GBD 2016. Methods: We report estimates and corresponding uncertainty intervals (UIs), from 1990 to 2016, for incidence, prevalence, deaths, years of life lost (YLLs), years lived with disability (YLDs), and disability-adjusted life-years (DALYs). DALYs were generated by summing YLLs and YLDs. Cause-specific mortality was estimated using an ensemble modelling process with vital registration and verbal autopsy data as inputs. Non-fatal estimates were generated using Bayesian meta-regression incorporating data from registries, scientific literature, administrative records, and surveys. The Socio-demographic Index (SDI), a summary indicator generated using educational attainment, lagged distributed income, and total fertility rate, was used to group countries into quintiles. Findings: In 2016, there were 5·5 million (95% UI 5·3 to 5·7) deaths and 116·4 million (111·4 to 121·4) DALYs due to stroke. The global age-standardised mortality rate decreased by 36·2% (−39·3 to −33·6) from 1990 to 2016, with decreases in all SDI quintiles. Over the same period, the global age-standardised DALY rate declined by 34·2% (−37·2 to −31·5), also with decreases in all SDI quintiles. There were 13·7 million (12·7 to 14·7) new stroke cases in 2016. Global age-standardised incidence declined by 8·1% (−10·7 to −5·5) from 1990 to 2016 and decreased in all SDI quintiles except the middle SDI group. There were 80·1 million (74·1 to 86·3) prevalent cases of stroke globally in 2016; 41·1 million (38·0 to 44·3) in women and 39·0 million (36·1 to 42·1) in men. Interpretation: Although age-standardised mortality rates have decreased sharply from 1990 to 2016, the decrease in age-standardised incidence has been less steep, indicating that the burden of stroke is likely to remain high. Planned updates to future GBD iterations include generating separate estimates for subarachnoid haemorrhage and intracerebral haemorrhage, generating estimates of transient ischaemic attack, and including atrial fibrillation as a risk factor. Funding: Bill & Melinda Gates Foundation
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- 2019
37. Global, regional, and national burden of stroke, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016.
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Grosso G., Rafiei A., Rahim F., Rahimi K., Rahimi-Movaghar V., Rahman M., Rahman M.A., Reis C., Remuzzi G., Renzaho A.M.N., Ricci S., Roberts N.L.S., Robinson S.R., Roever L., Roshandel G., Sabbagh P., Safari H., Safari S., Safiri S., Sahebkar A., Salehi Zahabi S., Samy A.M., Santalucia P., Santos I.S., Santos J.V., Santric Milicevic M.M., Sartorius B., Sawant A.R., Schutte A.E., Sepanlou S.G., Shafieesabet A., Shaikh M.A., Shams-Beyranvand M., Sheikh A., Sheth K.N., Shibuya K., Shigematsu M., Shin M.-J., Shiue I., Siabani S., Sobaih B.H., Sposato L.A., Sutradhar I., Sylaja P.A., Szoeke C.E.I., Te Ao B.J., Temsah M.-H., Temsah O., Thrift A.G., Tonelli M., Topor-Madry R., Tran B.X., Tran K.B., Truelsen T.C., Tsadik A.G., Ullah I., Uthman O.A., Vaduganathan M., Valdez P.R., Vasankari T.J., Vasanthan R., Venketasubramanian N., Vosoughi K., Vu G.T., Waheed Y., Weiderpass E., Weldegwergs K.G., Westerman R., Wolfe C.D.A., Wondafrash D.Z., Xu G., Yadollahpour A., Yamada T., Yatsuya H., Yimer E.M., Yonemoto N., Yousefifard M., Yu C., Zaidi Z., Zamani M., Zarghi A., Zhang Y., Zodpey S., Feigin V.L., Vos T., Murray C.J.L., Johnson C.O., Nguyen M., Roth G.A., Nichols E., Alam T., Abate D., Abd-Allah F., Abdelalim A., Abraha H.N., Abu-Rmeileh N.M., Adebayo O.M., Adeoye A.M., Agarwal G., Agrawal S., Aichour A.N., Aichour I., Aichour M.T.E., Alahdab F., Ali R., Alvis-Guzman N., Anber N.H., Anjomshoa M., Arabloo J., Arauz A., Arnlov J., Arora A., Awasthi A., Banach M., Barboza M.A., Barker-Collo S.L., Barnighausen T.W., Basu S., Belachew A.B., Belayneh Y.M., Bennett D.A., Bensenor I.M., Bhattacharyya K., Biadgo B., Bijani A., Bikbov B., Bin Sayeed M.S., Butt Z.A., Cahuana-Hurtado L., Carrero J.J., Carvalho F., Castaneda-Orjuela C.A., Castro F., Catala-Lopez F., Chaiah Y., Chiang P.P.-C., Choi J.-Y.J., Christensen H., Chu D.-T., Cortinovis M., Damasceno A.A.M., Dandona L., Dandona R., Daryani A., Davletov K., De Courten B., De la Cruz-Gongora V., Degefa M.G., Dharmaratne S.D., Diaz D., Dubey M., Duken E.E., Edessa D., Endres M., Faraon E.J.A., Farzadfar F., Fernandes E., Fischer F., Flor L.S., Ganji M., Gebre A.K., Gebremichael T.G., Geta B., Gezae K.E., Gill P.S., Gnedovskaya E.V., Gomez-Dantes H., Goulart A.C., Guo Y., Gupta R., Haj-Mirzaian A., Hamidi S., Hankey G.J., Hassen H.Y., Hay S.I., Hegazy M.I., Heidari B., Herial N.A., Hosseini M.A., Hostiuc S., Irvani S.S.N., Islam S.M.S., Jahanmehr N., Javanbakht M., Jha R.P., Jonas J.B., Jozwiak J.J., Jurisson M., Kahsay A., Kalani R., Kalkonde Y., Kamil T.A., Kanchan T., Karch A., Karimi N., Karimi-Sari H., Kasaeian A., Kassa T.D., Kazemeini H., Kefale A.T., Khader Y.S., Khalil I.A., Khan E.A., Khang Y.-H., Khubchandani J., Kim D., Kim Y.J., Kisa A., Kivimaki M., Koyanagi A., Krishnamurthi R.K., Anil Kumar G., Lafranconi A., Lewington S., Li S., Lo W.D., Lopez A.D., Lorkowski S., Lotufo P.A., Mackay M.T., Majdan M., Majdzadeh R., Majeed A., Malekzadeh R., Manafi N., Mansournia M.A., Mehndiratta M.M., Mehta V., Mengistu G., Meretoja A., Meretoja T.J., Miazgowski B., Miazgowski T., Miller T.R., Mirrakhimov E.M., Mohajer B., Mohammad Y., Mohammadoo-Khorasani M., Mohammed S., Mohebi F., Mokdad A.H., Mokhayeri Y., Moradi G., Morawska L., Moreno Velasquez I., Mousavi S.M., Muhammed O.S.S., Muruet W., Naderi M., Naghavi M., Naik G., Nascimento B.R., Negoi R.I., Nguyen C.T., Nguyen L.H., Nirayo Y.L., Norrving B., Noubiap J.J., Ofori-Asenso R., Ogbo F.A., Olagunju A.T., Olagunju T.O., Owolabi M.O., Pandian J.D., Patel S., Perico N., Piradov M.A., Polinder S., Postma M.J., Poustchi H., Prakash V., Qorbani M., Grosso G., Rafiei A., Rahim F., Rahimi K., Rahimi-Movaghar V., Rahman M., Rahman M.A., Reis C., Remuzzi G., Renzaho A.M.N., Ricci S., Roberts N.L.S., Robinson S.R., Roever L., Roshandel G., Sabbagh P., Safari H., Safari S., Safiri S., Sahebkar A., Salehi Zahabi S., Samy A.M., Santalucia P., Santos I.S., Santos J.V., Santric Milicevic M.M., Sartorius B., Sawant A.R., Schutte A.E., Sepanlou S.G., Shafieesabet A., Shaikh M.A., Shams-Beyranvand M., Sheikh A., Sheth K.N., Shibuya K., Shigematsu M., Shin M.-J., Shiue I., Siabani S., Sobaih B.H., Sposato L.A., Sutradhar I., Sylaja P.A., Szoeke C.E.I., Te Ao B.J., Temsah M.-H., Temsah O., Thrift A.G., Tonelli M., Topor-Madry R., Tran B.X., Tran K.B., Truelsen T.C., Tsadik A.G., Ullah I., Uthman O.A., Vaduganathan M., Valdez P.R., Vasankari T.J., Vasanthan R., Venketasubramanian N., Vosoughi K., Vu G.T., Waheed Y., Weiderpass E., Weldegwergs K.G., Westerman R., Wolfe C.D.A., Wondafrash D.Z., Xu G., Yadollahpour A., Yamada T., Yatsuya H., Yimer E.M., Yonemoto N., Yousefifard M., Yu C., Zaidi Z., Zamani M., Zarghi A., Zhang Y., Zodpey S., Feigin V.L., Vos T., Murray C.J.L., Johnson C.O., Nguyen M., Roth G.A., Nichols E., Alam T., Abate D., Abd-Allah F., Abdelalim A., Abraha H.N., Abu-Rmeileh N.M., Adebayo O.M., Adeoye A.M., Agarwal G., Agrawal S., Aichour A.N., Aichour I., Aichour M.T.E., Alahdab F., Ali R., Alvis-Guzman N., Anber N.H., Anjomshoa M., Arabloo J., Arauz A., Arnlov J., Arora A., Awasthi A., Banach M., Barboza M.A., Barker-Collo S.L., Barnighausen T.W., Basu S., Belachew A.B., Belayneh Y.M., Bennett D.A., Bensenor I.M., Bhattacharyya K., Biadgo B., Bijani A., Bikbov B., Bin Sayeed M.S., Butt Z.A., Cahuana-Hurtado L., Carrero J.J., Carvalho F., Castaneda-Orjuela C.A., Castro F., Catala-Lopez F., Chaiah Y., Chiang P.P.-C., Choi J.-Y.J., Christensen H., Chu D.-T., Cortinovis M., Damasceno A.A.M., Dandona L., Dandona R., Daryani A., Davletov K., De Courten B., De la Cruz-Gongora V., Degefa M.G., Dharmaratne S.D., Diaz D., Dubey M., Duken E.E., Edessa D., Endres M., Faraon E.J.A., Farzadfar F., Fernandes E., Fischer F., Flor L.S., Ganji M., Gebre A.K., Gebremichael T.G., Geta B., Gezae K.E., Gill P.S., Gnedovskaya E.V., Gomez-Dantes H., Goulart A.C., Guo Y., Gupta R., Haj-Mirzaian A., Hamidi S., Hankey G.J., Hassen H.Y., Hay S.I., Hegazy M.I., Heidari B., Herial N.A., Hosseini M.A., Hostiuc S., Irvani S.S.N., Islam S.M.S., Jahanmehr N., Javanbakht M., Jha R.P., Jonas J.B., Jozwiak J.J., Jurisson M., Kahsay A., Kalani R., Kalkonde Y., Kamil T.A., Kanchan T., Karch A., Karimi N., Karimi-Sari H., Kasaeian A., Kassa T.D., Kazemeini H., Kefale A.T., Khader Y.S., Khalil I.A., Khan E.A., Khang Y.-H., Khubchandani J., Kim D., Kim Y.J., Kisa A., Kivimaki M., Koyanagi A., Krishnamurthi R.K., Anil Kumar G., Lafranconi A., Lewington S., Li S., Lo W.D., Lopez A.D., Lorkowski S., Lotufo P.A., Mackay M.T., Majdan M., Majdzadeh R., Majeed A., Malekzadeh R., Manafi N., Mansournia M.A., Mehndiratta M.M., Mehta V., Mengistu G., Meretoja A., Meretoja T.J., Miazgowski B., Miazgowski T., Miller T.R., Mirrakhimov E.M., Mohajer B., Mohammad Y., Mohammadoo-Khorasani M., Mohammed S., Mohebi F., Mokdad A.H., Mokhayeri Y., Moradi G., Morawska L., Moreno Velasquez I., Mousavi S.M., Muhammed O.S.S., Muruet W., Naderi M., Naghavi M., Naik G., Nascimento B.R., Negoi R.I., Nguyen C.T., Nguyen L.H., Nirayo Y.L., Norrving B., Noubiap J.J., Ofori-Asenso R., Ogbo F.A., Olagunju A.T., Olagunju T.O., Owolabi M.O., Pandian J.D., Patel S., Perico N., Piradov M.A., Polinder S., Postma M.J., Poustchi H., Prakash V., and Qorbani M.
- Abstract
Background: Stroke is a leading cause of mortality and disability worldwide and the economic costs of treatment and post-stroke care are substantial. The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) provides a systematic, comparable method of quantifying health loss by disease, age, sex, year, and location to provide information to health systems and policy makers on more than 300 causes of disease and injury, including stroke. The results presented here are the estimates of burden due to overall stroke and ischaemic and haemorrhagic stroke from GBD 2016. Method(s): We report estimates and corresponding uncertainty intervals (UIs), from 1990 to 2016, for incidence, prevalence, deaths, years of life lost (YLLs), years lived with disability (YLDs), and disability-adjusted life-years (DALYs). DALYs were generated by summing YLLs and YLDs. Cause-specific mortality was estimated using an ensemble modelling process with vital registration and verbal autopsy data as inputs. Non-fatal estimates were generated using Bayesian meta-regression incorporating data from registries, scientific literature, administrative records, and surveys. The Socio-demographic Index (SDI), a summary indicator generated using educational attainment, lagged distributed income, and total fertility rate, was used to group countries into quintiles. Finding(s): In 2016, there were 5.5 million (95% UI 5.3 to 5.7) deaths and 116.4 million (111.4 to 121.4) DALYs due to stroke. The global age-standardised mortality rate decreased by 36.2% (-39.3 to -33.6) from 1990 to 2016, with decreases in all SDI quintiles. Over the same period, the global age-standardised DALY rate declined by 34.2% (-37.2 to -31.5), also with decreases in all SDI quintiles. There were 13.7 million (12.7 to 14.7) new stroke cases in 2016. Global age-standardised incidence declined by 8.1% (-10.7 to -5.5) from 1990 to 2016 and decreased in all SDI quintiles except the middle SDI group. There were 80.1 million (74.1
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- 2019
38. Brown adipose tissue thermogenesis in polycystic ovary syndrome.
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Henry B.A., Shorakae S., Jona E., de Courten B., Lambert G.W., Lambert E.A., Phillips S.E., Clarke I.J., Teede H.J., Henry B.A., Shorakae S., Jona E., de Courten B., Lambert G.W., Lambert E.A., Phillips S.E., Clarke I.J., and Teede H.J.
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Objective: Polycystic ovary syndrome (PCOS) is associated with increased obesity with a greater propensity to weight gain and a lack of sustainable lifestyle interventions. Altered brown adipose tissue (BAT) thermogenesis is a potential contributor to obesity in PCOS. BAT activity and modulation have not been studied in PCOS. This observational study explored BAT thermogenesis and its associations in women with and without PCOS. Participants and methods: Cutaneous temperature was recorded from supraclavicular (indicator of BAT activity) and upper arm regions using dataloggers (SubCue, Calgary, Canada) in a cross-sectional substudy, nested within a randomized control trial, of community-recruited premenopausal women with (n = 47, Rotterdam diagnostic criteria) and without (n = 11) PCOS. Result(s): Complete temperature data were available in 44 PCOS (mean age: 30.0 +/- 6.2, mean BMI: 29.3 +/- 5.5) and 11 non-PCOS (mean age: 33.0 +/- 7.0, mean BMI: 25 +/- 3) women. Women with PCOS had lower supraclavicular skin temperature compared to controls overall (33.9 +/- 0.7 vs 34.5 +/- 1, P < 0.05) and during sleep (34.5 +/- 0.6 vs 35.2 +/- 0.9, P < 0.001). In the PCOS group, supraclavicular skin temperature overall and over sleep and waking hours correlated inversely with testosterone (r = -0.41 P < 0.05, r = -0.485 P < 0.01 and r = -0.450 P < 0.01 respectively). Testosterone levels explained approximately 15%, 30% and 20% of the variability in supraclavicular skin temperature overall and over sleep and waking hours in women with PCOS, respectively. Conclusion(s): Women with PCOS have lower BAT activity compared to controls. BAT thermogenesis is negatively associated with androgen levels in PCOS.Copyright © 2018 John Wiley & Sons Ltd
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- 2019
39. Metabolic syndrome and its associations with components of sarcopenia in overweight and obese older adults.
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Shore-Lorenti C., Ebeling P.R., Scott D., Mesinovic J., McMillan L.B., De Courten B., Shore-Lorenti C., Ebeling P.R., Scott D., Mesinovic J., McMillan L.B., and De Courten B.
- Abstract
Ageing, obesity and the metabolic syndrome (MetS) may all contribute to poor muscle health (sarcopenia). This study aimed to determine the cross-sectional associations between MetS (International Diabetes Federation classification) and sarcopenia (revised EuropeanWorking Group on Sarcopenia in Older People definition) in 84 overweight and obese older adults. Components of sarcopenia included muscle strength (hand grip and leg extension), physical performance (stair climb test and short physical performance battery (SPPB), including gait speed and repeated chair stands time), muscle mass (appendicular lean mass (ALM), dual-energy X-ray absorptiometry), muscle size (peripheral quantitative computed tomography-determined calf and forearm cross-sectional area (CSA)) and muscle quality (muscle density and strength normalised to lean mass). Waist circumference was associated with greater muscle size, but poorer leg extension strength, chair stands and stair climb time, gait speed, SPPB scores and muscle quality measures (all p < 0.05). MetS was positively associated with ALM and forearm muscle CSA, and negatively associated with muscle quality measures and chair stands time (all p < 0.05). MetS is associated with larger muscle size, yet poorer muscle quality in overweight and obese older adults. Assessments of muscle function and quality should be considered for obese older adults and those with MetS.Copyright © 2019 by the authors. Licensee MDPI, Basel, Switzerland.
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- 2019
40. Sarcopenia and type 2 diabetes mellitus: A bidirectional relationship.
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Mesinovic J., Scott D., Ebeling P.R., De Courten B., Zengin A., Mesinovic J., Scott D., Ebeling P.R., De Courten B., and Zengin A.
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The incidence and prevalence of metabolic and musculoskeletal diseases are increasing. Type 2 diabetes mellitus (T2DM) is characterized by insulin resistance, inflammation, advanced glycation end-product accumulation and increased oxidative stress. These characteristics can negatively affect various aspects of muscle health, including muscle mass, strength, quality and function through impairments in protein metabolism, vascular and mitochondrial dysfunction, and cell death. Sarcopenia is a term used to describe the age-related loss in skeletal muscle mass and function and has been implicated as both a cause and consequence of T2DM. Sarcopenia may contribute to the development and progression of T2DM through altered glucose disposal due to low muscle mass, and also increased localized inflammation, which can arise through inter-and intramuscular adipose tissue accumulation. Lifestyle modifications are important for improving and maintaining mobility and metabolic health in individuals with T2DM and sarcopenia. However, evidence for the most effective and feasible exercise and dietary interventions in this population is lacking. In this review, we discuss the current literature highlighting the bidirectional relationship between T2DM and sarcopenia, highlight current research gaps and treatments, and provide recommendations for future research.Copyright © 2019 Mesinovic et al.
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- 2019
41. Effect of 16-weeks vitamin D replacement on calcium-phosphate homeostasis in overweight and obese adults.
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Scott D., Mesinovic J., Mousa A., Wilson K., Scragg R., Plebanski M., de Courten M., de Courten B., Naderpoor N., Scott D., Mesinovic J., Mousa A., Wilson K., Scragg R., Plebanski M., de Courten M., de Courten B., and Naderpoor N.
- Abstract
This randomised placebo-controlled trial aimed to determine the effect of 16-weeks cholecalciferol supplementation on calcium-phosphate homeostasis and bone mineral density (BMD) in overweight and obese adults. Fifty-four vitamin D-deficient (25OHD<50 nmol/L), overweight and obese adults (mean age 32 +/- 8.5 years) were included in the trial. Participants were randomly assigned to receive either a bolus oral dose of 100,000 IU cholecalciferol followed by 4000 IU cholecalciferol/d or a matching placebo for 16 weeks. Before and after the intervention, serum calcium, phosphate, 25-hydroxyvitamin D [25(OH)D], intact parathyroid hormone (iPTH) and C-terminal plasma fibroblast growth factor-23 (cFGF-23) concentrations were measured. Whole-body BMD was assessed using dual-energy X-ray absorptiometry (DXA) and diet and sun exposure were assessed using self-administered questionnaires. There were no significant differences in baseline characteristics between the vitamin D and placebo group. After 16-weeks of vitamin D supplementation, mean changes in 25(OH)D concentration were higher in the vitamin D group (57 nmol/L 95% CI 49, 65) compared with placebo (2 nmol/L 95% CI -4, 8), P < 0.001. Additionally, iPTH concentrations declined in the vitamin D group (-1.19 pmol/L 95% CI -1.9, -0.47) compared with placebo (0.14 pmol/L 95% CI -0.49, 0.77), P = 0.006. There were no significant differences in calcium, phosphate, iPTH and cFGF-23 concentrations and whole-body BMD between vitamin D and placebo at follow-up. Inverse correlations were observed between mean change in serum iPTH and cFGF-23 in the vitamin D group only (r=-0.41, P = 0.029). In individuals with greater vitamin D deficiency at baseline (25(OH)D < 30 nmol/L), there was a significant increase in mean whole-body BMD (0.01 g/cm2, 95% CI 0.001, 0.025) however, the mean change in BMD was not different between vitamin D and placebo groups in this sub-group analysis. We conclude that cholecalciferol supplementation for 16 we
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- 2019
42. Depression and diabetes distress in adults with type 2 diabetes: results from the Australian National Diabetes Audit (ANDA) 2016.
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Zoungas S., de Courten B., Nanayakkara N., Pease A., Ranasinha S., Wischer N., Andrikopoulos S., Speight J., Zoungas S., de Courten B., Nanayakkara N., Pease A., Ranasinha S., Wischer N., Andrikopoulos S., and Speight J.
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This study explores the prevalence of, and factors associated with, likely depression and diabetes distress in adults with type 2 diabetes in a large, national sample. Australian National Diabetes Audit data were analysed from adults with type 2 diabetes attending 50 diabetes centres. The Brief Case find for Depression and Diabetes Distress Score 17 were administered to screen for likely depression and diabetes-related distress, respectively. A total of 2,552 adults with type 2 diabetes participated: (mean+/-SD) age was 63+/-13 years, diabetes duration was 12+/-10 years, and HbA1c was 8+/-2%. Twenty-nine percent of patients had likely depression, 7% had high diabetes distress, and 5% had both. Difficulty following dietary recommendations, smoking, forgetting medications, and diabetes distress were all associated with greater odds of depression whereas higher own health rating was associated with lower odds (all p<0.02). Female gender, increasing HbA1c, insulin use, difficulty following dietary recommendations and depression were all associated with greater odds of diabetes distress & older age, higher own health rating and monitoring blood glucose levels as recommended were associated with lower odds (all p<0.04). Depression was associated with sub-optimal self-care, while diabetes distress was associated with higher HbA1c and sub-optimal self-care.
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- 2019
43. Vitamin D supplementation improves waist-to-hip ratio and fasting blood glucose in vitamin D deficient, overweight or obese Asians: A pilot secondary analysis of a randomised controlled trial.
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Scragg R., Mousa A., Naderpoor N., de Courten M.P.J., de Courten B., Scott D., Scragg R., Mousa A., Naderpoor N., de Courten M.P.J., de Courten B., and Scott D.
- Abstract
Recent trials do not support a role for vitamin D supplementation in prevention or treatment of type 2 diabetes mellitus, although effects may differ in Asian populations. In this pilot secondary analysis of a placebo-controlled randomised trial of overweight or obese individuals with low 25-hydroxyvitamin D (25(OH)D < 50 nmol/L), we examined whether vitamin D supplementation improved insulin sensitivity or body composition in participants of Asian ethnicity. Amongst 65 trial participants, 33 reported being of Asian descent (mean +/- SD age 30 +/- 7 years; 67% male). Participants were block randomised to receive vitamin D (n = 14; initial bolus dose of 2500 mug cholecalciferol followed by 100 mug cholecalciferol/d) or placebo (n = 19; identical capsules) for 16 weeks. Primary outcome was change in insulin sensitivity (M-value) assessed by hyperinsulinemic-euglycemic clamp. Secondary outcomes were changes in 25(OH)D (chemiluminescent immunoassay), fasting blood glucose (YSI Stat 2300), and body composition including waist-hip ratio and total body fat percentage (dual-energy X-ray absorptiometry). Questionnaires assessed sun-exposure habits, physical activity, and diet. After the 16-week intervention, 25(OH)D concentrations increased significantly in the vitamin D group with no change in placebo (61.4 +/- 21.1 vs -0.4 +/- 12.7 nmol/L; P < 0.01). Vitamin D group participants demonstrated significant improvements in waist-hip ratio (-0.02 +/- 0.03 vs 0.00 +/- 0.02; P < 0.01) and fasting blood glucose (-0.1 +/- 0.2 vs 0.2 +/- 04 mmol/L; P < 0.04) compared with the placebo group, but changes in insulin sensitivity and other body composition measures did not differ significantly between groups (all P > 0.05). In conclusion, vitamin D supplementation improved waist-hip ratio and fasting blood glucose in overweight and obese Asian-Australians with low vitamin D concentrations. Further research is required to determine whether vitamin D supplementation is potentially more eff
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- 2019
44. Outcomes of people with severe hypoglycaemia requiring prehospital emergency medical services management: a prospective study.
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de Courten B., Earnest A., Smith K., Giannopoulos D., Soldatos G., Zoungas S., Villani M., de Courten B., Earnest A., Smith K., Giannopoulos D., Soldatos G., Zoungas S., and Villani M.
- Abstract
Aims/hypothesis: The aim of this work was to investigate clinical outcomes following severe hypoglycaemia requiring prehospital emergency medical services (EMS) management. Method(s): We carried out a prospective, observational study of adults with diabetes attended by prehospital EMS for management of severe hypoglycaemia between April 2016 and July 2017. Information on precipitants, hospitalisation, length of hospital stay and recurrence was collected at 1 and 3 months following the episode of severe hypoglycaemia. Median and logistic regression models examined predictive factors. Result(s): Five hundred and five adults (61% male, median age 67 years) participated in the study. Fifty-two per cent had type 1 diabetes, 43% type 2 diabetes and 5% were unsure of their diabetes type. Following EMS management of the index episode of severe hypoglycaemia, 50.3% were transported to hospital. Of those transported, 41.3% were admitted to hospital for ongoing management (20.8% of all participants). The following factors predicted hospital admission: older age (OR 1.28 [95% CI 1.02, 1.60] per 10 years), greater number of comorbidities (OR 1.27 [95% CI 1.08, 1.48] per morbidity), moderate-severe injury accompanying the hypoglycaemia (OR 5.24 [95% CI 1.07, 25.8] compared with nil-mild injury) and unknown cause of hypoglycaemia (OR 2.21 [95% CI 1.24, 3.94] compared with known cause). The median (interquartile range) length of hospital stay was 4 (2-7) days. During follow-up, recurrent severe hypoglycaemia attended by prehospital EMS was experienced by 10.7% of participants. Predictive factors of recurrent severe hypoglycaemia in 3 months were decreased HbA1c (OR 1.97 [95% CI 1.27, 3.06] per 10 mmol/mol decrease) and a greater number of antecedent severe hypoglycaemia episodes (OR 1.12 [95% CI 1.03, 1.23] per episode). Conclusions/interpretation: Following an episode of severe hypoglycaemia managed by EMS, one-fifth of participants required hospital admission, more likely in thos
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- 2019
45. Higher glomerular filtration rate is related to insulin resistance but not to obesity in a predominantly obese non-diabetic cohort.
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Soldatos G., de Courten B., Naderpoor N., Lyons J.G., Mousa A., Ranasinha S., de Courten M.P.J., Soldatos G., de Courten B., Naderpoor N., Lyons J.G., Mousa A., Ranasinha S., and de Courten M.P.J.
- Abstract
Glomerular hyperfiltration has been associated with obesity, insulin resistance, and systolic blood pressure (SBP). However, previous studies are limited by confounders such as pre-existing diabetes or hypertension, or have used indirect measures of adiposity and insulin sensitivity (IS). Therefore, we examined the relationship between estimated glomerular filtration rate (eGFR) and IS measured by the hyperinsulinaemic euglycaemic clamp in a healthy population on no medications. We performed oral glucose tolerance test (OGTT) and measured % body fat (DEXA), BMI, blood pressure and M-value (hyperinsulinaemic euglycaemic clamp) in 104 individuals (44 females and 60 males). The majority of the study population (n=89, 85.6%) were classified on their BMI as overweight/obese. eGFR was related to age, BMI, M-value (IS), 2-hour glucose levels post OGTT and white blood cell count (WBC) (all p<0.05); but not to SBP (p=0.1) or fasting glucose levels (p=0.2). After adjustment for gender, BMI, SBP and WBC, the inverse association between eGFR and M-value (p=0.001), and 2-hour glucose post OGTT (p=0.02) persisted. In conclusion, although eGFR has been associated with BMI and blood pressure in previous studies, in our healthy population, eGFR was more closely related to markers of glucose metabolism (IS and 2-hour glucose post OGTT) than to BMI and blood pressure.
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- 2019
46. Effect of vitamin D supplementation on faecal microbiota: A randomised clinical trial.
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Barrett H.L., Mousa A., Arango L.F.G., de Courten B., Nitert M.D., Naderpoor N., Barrett H.L., Mousa A., Arango L.F.G., de Courten B., Nitert M.D., and Naderpoor N.
- Abstract
In animal studies, vitamin D supplementation has been shown to improve gut microbiota and intestinal inflammation. However, limited evidence exists on the effect of vitamin D supplementation on the human gut microbiota. We examined the effect of vitamin D supplementation on faecal microbiota in 26 vitamin D-deficient (25-hydroxyvitamin D (25(OH)D) <=50 nmol/L), overweight or obese (BMI >=25 kg/m2) otherwise healthy adults. Our study was ancillary to a community based double-blind randomised clinical trial, conducted between 2014 and 2016. The participants provided stool samples at baseline and after 100,000 international units (IU) loading dose of cholecalciferol followed by 4000 IU daily or matching placebo for 16 weeks. Faecal microbiota was analysed using 16S rRNA sequencing; V6-8 region. There was no significant difference in microbiome alpha-diversity between vitamin D and placebo groups at baseline and follow-up (all p > 0.05). In addition, no clustering was found based on vitamin D supplementation at follow-up (p = 0.3). However, there was a significant association between community composition and vitamin D supplementation at the genus level (p = 0.04). The vitamin D group had a higher abundance of genus Lachnospira, and lower abundance of genus Blautia (linear discriminate analysis >3.0). Moreover, individuals with 25(OH)D >75 nmol/L had a higher abundance of genus Coprococcus and lower abundance of genus Ruminococcus compared to those with 25(OH)D <50 nmol/L. Our findings suggest that vitamin D supplementation has some distinct effects on faecal microbiota. Future studies need to explore whether these effects would translate into improved clinical outcomes.Copyright © 2019 by the authors. Licensee MDPI, Basel, Switzerland.
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- 2019
47. Role of serum biomarkers to optimise a validated clinical risk prediction tool for gestational diabetes.
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Teede H.J., Abell S.K., Shorakae S., Boyle J.A., De Courten B., Stepto N.K., Harrison C.L., Teede H.J., Abell S.K., Shorakae S., Boyle J.A., De Courten B., Stepto N.K., and Harrison C.L.
- Abstract
Background: Clinical risk prediction tools for gestational diabetes (GDM) may be enhanced by measuring biomarkers in early pregnancy. Aim(s): To evaluate a two-step GDM risk prediction tool incorporating fasting glucose (FG) and serum biomarkers in early pregnancy. Material(s) and Method(s): High molecular weight (HMW) adiponectin, omentin-1 and interleukin-6 (IL-6) were measured at 12-15 weeks gestation in women with high risk of GDM from a randomised trial using a clinical risk prediction tool. GDM diagnosis (24-28 weeks) was evaluated using 1998 Australian Diabetes in Pregnancy (ADIPS) criteria and newer International Association of the Diabetes and Pregnancy Study Groups (IADPSG) criteria. Associations between biomarkers and development of GDM were examined using multivariable regression analysis. Area under the receiver-operator curve (AUC), sensitivity and specificity were calculated to determine classification ability of each model compared to FG and maternal characteristics. Result(s): HMW adiponectin improved prediction of ADIPS GDM (AUC 0.85, sensitivity 50%, specificity 96.2%, P = 0.04), compared to FG and maternal factors (0.78, 35% and, 98.1%, respectively). HMW adiponectin <1.53 mug/mL further improved the model (AUC 0.87, sensitivity 75%, specificity 88.2%, P = 0.01). HMW adiponectin did not improve prediction of IADPSG GDM (AUC 0.84, sensitivity 64%, specificity 97.9%, P = 0.22) compared to FG and maternal factors (0.79, 56%, 93.8%). Omentin-1 and IL-6 did not significantly improve classification ability for GDM. Conclusion(s): A two-step approach combining FG and HMW adiponectin to a validated clinical risk prediction tool improved sensitivity and predictive ability for ADIPS GDM. Further research is required to enhance GDM prediction using IADPSG criteria for application in clinical practice.Copyright © 2018 The Royal Australian and New Zealand College of Obstetricians and Gynaecologists
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- 2019
48. Geographical variation of diabetic emergencies attended by prehospital Emergency Medical Services is associated with measures of ethnicity and socioeconomic status.
- Author
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de Courten B., Villani M., Earnest A., Smith K., Zoungas S., de Courten B., Villani M., Earnest A., Smith K., and Zoungas S.
- Abstract
Geographical variation of diabetic emergencies attended by prehospital emergency medical services (EMS) and the relationship between area-level social and demographic factors and risk of a diabetic emergency were examined. All cases of hypoglycaemia and hyperglycaemia attended by Ambulance Victoria between 1/01/2009 and 31/12/2015 were tabulated by Local Government Area (LGA). Conditional autoregressive models were used to create smoothed maps of age and gender standardised incidence ratio (SIR) of prehospital EMS attendance for a diabetic emergency. Spatial regression models were used to examine the relationship between risk of a diabetic emergency and area-level factors. The areas with the greatest risk of prehospital EMS attendance for a diabetic emergency were disperse. Area-level factors associated with risk of a prehospital EMS-attended diabetic emergency were socioeconomic status (SIR 0.70 95% CrI [0.51, 0.96]), proportion of overseas-born residents (SIR 2.02 95% CrI [1.37, 2.91]) and motor vehicle access (SIR 1.47 95% CrI [1.08, 1.99]). Recognition of areas of increased risk of prehospital EMS-attended diabetic emergencies may be used to assist prehospital EMS resource planning to meet increased need. In addition, identification of associated factors can be used to target preventative interventions tailored to individual regions to reduce demand.
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- 2019
49. Brown adipose tissue thermogenesis in polycystic ovary syndrome
- Author
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Shorakae, S, Jona, E, de Courten, B, Lambert, GW, Lambert, EA, Phillips, SE, Clarke, IJ, Teede, HJ, Henry, BA, Shorakae, S, Jona, E, de Courten, B, Lambert, GW, Lambert, EA, Phillips, SE, Clarke, IJ, Teede, HJ, and Henry, BA
- Abstract
Objective Polycystic ovary syndrome (PCOS) is associated with increased obesity with a greater propensity to weight gain and a lack of sustainable lifestyle interventions. Altered brown adipose tissue (BAT) thermogenesis is a potential contributor to obesity in PCOS. BAT activity and modulation have not been studied in PCOS. This observational study explored BAT thermogenesis and its associations in women with and without PCOS. Participants and methods Cutaneous temperature was recorded from supraclavicular (indicator of BAT activity) and upper arm regions using dataloggers (SubCue, Calgary, Canada) in a cross-sectional substudy, nested within a randomized control trial, of community-recruited premenopausal women with (n = 47, Rotterdam diagnostic criteria) and without (n = 11) PCOS. Results Complete temperature data were available in 44 PCOS (mean age: 30.0 ± 6.2, mean BMI: 29.3 ± 5.5) and 11 non-PCOS (mean age: 33.0 ± 7.0, mean BMI: 25 ± 3) women. Women with PCOS had lower supraclavicular skin temperature compared to controls overall (33.9 ± 0.7 vs 34.5 ± 1, P < 0.05) and during sleep (34.5 ± 0.6 vs 35.2 ± 0.9, P < 0.001). In the PCOS group, supraclavicular skin temperature overall and over sleep and waking hours correlated inversely with testosterone (r = −0.41 P < 0.05, r = −0.485 P < 0.01 and r = −0.450 P < 0.01 respectively). Testosterone levels explained approximately 15%, 30% and 20% of the variability in supraclavicular skin temperature overall and over sleep and waking hours in women with PCOS, respectively. Conclusion Women with PCOS have lower BAT activity compared to controls. BAT thermogenesis is negatively associated with androgen levels in PCOS.
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- 2019
50. Metabolic Syndrome and Its Associations with Components of Sarcopenia in Overweight and Obese Older Adults
- Author
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Mesinovic, J, McMillan, LB, Shore-Lorenti, C, De Courten, B, Ebeling, PR, Scott, D, Mesinovic, J, McMillan, LB, Shore-Lorenti, C, De Courten, B, Ebeling, PR, and Scott, D
- Abstract
Ageing, obesity and the metabolic syndrome (MetS) may all contribute to poor muscle health (sarcopenia). This study aimed to determine the cross-sectional associations between MetS (International Diabetes Federation classification) and sarcopenia (revised European Working Group on Sarcopenia in Older People definition) in 84 overweight and obese older adults. Components of sarcopenia included muscle strength (hand grip and leg extension), physical performance (stair climb test and short physical performance battery (SPPB), including gait speed and repeated chair stands time), muscle mass (appendicular lean mass (ALM), dual-energy X-ray absorptiometry), muscle size (peripheral quantitative computed tomography-determined calf and forearm cross-sectional area (CSA)) and muscle quality (muscle density and strength normalised to lean mass). Waist circumference was associated with greater muscle size, but poorer leg extension strength, chair stands and stair climb time, gait speed, SPPB scores and muscle quality measures (all p < 0.05). MetS was positively associated with ALM and forearm muscle CSA, and negatively associated with muscle quality measures and chair stands time (all p < 0.05). MetS is associated with larger muscle size, yet poorer muscle quality in overweight and obese older adults. Assessments of muscle function and quality should be considered for obese older adults and those with MetS.
- Published
- 2019
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