| 1. |
- Kassebaum, Nicholas J., et al.
(författare)
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Global, regional, and national disability-adjusted life-years (DALYs) for 315 diseases and injuries and healthy life expectancy (HALE), 1990-2015 : a systematic analysis for the Global Burden of Disease Study 2015
- 2016
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Ingår i: The Lancet. - 0140-6736 .- 1474-547X. ; 388:10053, s. 1603-1658
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Tidskriftsartikel (refereegranskat)abstract
- Background Healthy life expectancy (HALE) and disability-adjusted life-years (DALYs) provide summary measures of health across geographies and time that can inform assessments of epidemiological patterns and health system performance, help to prioritise investments in research and development, and monitor progress toward the Sustainable Development Goals (SDGs). We aimed to provide updated HALE and DALYs for geographies worldwide and evaluate how disease burden changes with development. Methods We used results from the Global Burden of Diseases, Injuries, and Risk Factors Study 2015 (GBD 2015) for all-cause mortality, cause-specific mortality, and non-fatal disease burden to derive HALE and DALYs by sex for 195 countries and territories from 1990 to 2015. We calculated DALYs by summing years of life lost (YLLs) and years of life lived with disability (YLDs) for each geography, age group, sex, and year. We estimated HALE using the Sullivan method, which draws from age-specific death rates and YLDs per capita. We then assessed how observed levels of DALYs and HALE differed from expected trends calculated with the Socio-demographic Index (SDI), a composite indicator constructed from measures of income per capita, average years of schooling, and total fertility rate. Findings Total global DALYs remained largely unchanged from 1990 to 2015, with decreases in communicable, neonatal, maternal, and nutritional (Group 1) disease DALYs off set by increased DALYs due to non-communicable diseases (NCDs). Much of this epidemiological transition was caused by changes in population growth and ageing, but it was accelerated by widespread improvements in SDI that also correlated strongly with the increasing importance of NCDs. Both total DALYs and age-standardised DALY rates due to most Group 1 causes significantly decreased by 2015, and although total burden climbed for the majority of NCDs, age-standardised DALY rates due to NCDs declined. Nonetheless, age-standardised DALY rates due to several high-burden NCDs (including osteoarthritis, drug use disorders, depression, diabetes, congenital birth defects, and skin, oral, and sense organ diseases) either increased or remained unchanged, leading to increases in their relative ranking in many geographies. From 2005 to 2015, HALE at birth increased by an average of 2.9 years (95% uncertainty interval 2.9-3.0) for men and 3.5 years (3.4-3.7) for women, while HALE at age 65 years improved by 0.85 years (0.78-0.92) and 1.2 years (1.1-1.3), respectively. Rising SDI was associated with consistently higher HALE and a somewhat smaller proportion of life spent with functional health loss; however, rising SDI was related to increases in total disability. Many countries and territories in central America and eastern sub-Saharan Africa had increasingly lower rates of disease burden than expected given their SDI. At the same time, a subset of geographies recorded a growing gap between observed and expected levels of DALYs, a trend driven mainly by rising burden due to war, interpersonal violence, and various NCDs. Interpretation Health is improving globally, but this means more populations are spending more time with functional health loss, an absolute expansion of morbidity. The proportion of life spent in ill health decreases somewhat with increasing SDI, a relative compression of morbidity, which supports continued efforts to elevate personal income, improve education, and limit fertility. Our analysis of DALYs and HALE and their relationship to SDI represents a robust framework on which to benchmark geography-specific health performance and SDG progress. Country-specific drivers of disease burden, particularly for causes with higher-than-expected DALYs, should inform financial and research investments, prevention efforts, health policies, and health system improvement initiatives for all countries along the development continuum.
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| 2. |
- Magnusson, Cecilia, et al.
(författare)
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Migration and autism-spectrum disorder : population-based study
- 2012
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Ingår i: British Journal of Psychiatry. - : Royal College of Psychiatrists. - 0007-1250 .- 1472-1465. ; 201:2, s. 109-115
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Tidskriftsartikel (refereegranskat)abstract
- Background: Migration has been implicated as a risk factor for autism, but evidence is limited and inconsistent. Aims: To investigate the relationship between parental migration status and risk of autism spectrum disorder, taking into consideration the importance of region of origin, timing of migration and possible discrepancies in associations between autism subtypes. Method: Record-linkage study within the total child population of Stockholm County between 2001 and 2007. Individuals with high- and low-functioning autism were defined as having autism spectrum disorder with and without comorbid intellectual disability, and ascertained via health and habilitation service registers. Results: In total, 4952 individuals with autism spectrum disorder were identified, comprising 2855 children with high-functioning autism and 2097 children with low-functioning autism. Children of migrant parents were at increased risk of low-functioning autism (odds ratio (OR) = 1.5, 95% CI 1.3-1.7); this risk was highest when parents migrated from regions with a low human development index, and peaked when migration occurred around pregnancy (OR=2.3, 95% CI 1.7-3.0). A decreased risk of high-functioning autism was observed in children of migrant parents, regardless of area of origin or timing of migration. Parental age, income or obstetric complications did not fully explain any of these associations. Conclusions: Environmental factors associated with migration may contribute to the development of autism presenting with comorbid intellectual disability, especially when acting in utero. High- and low-functioning autism may have partly different aetiologies, and should be studied separately.
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| 3. |
- Rai, Dheeraj
(författare)
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Environmental risk factors for autism spectrum disorders
- 2013
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Aims: Two overarching hypotheses were tested in this thesis- first, that the environmental factors studied during pregnancy or the time preceding birth would be associated with a higher risk of autism spectrum disorders (ASD) in the offspring; and second, that these risk factors and/or their magnitude of associations may be different for autism spectrum disorders with and without intellectual disability (ID). Methods: Studies I-IV were case-control studies nested within a population-based cohort of all children 0 to 17 years old, living in Stockholm County between the years 2001 to 2007 (n=589,114). ASD cases, identified using multisource case-ascertainment, were matched by age and sex to 10 living non-ASD controls. Prospectively collected information on exposures and potential confounders was ascertained by record linkage with relevant registers, and timed to the prenatal period. Exposures included measures of parental socioeconomic status (Study I), migration (Study II), life events (Study III) and parental depression and maternal antidepressant use during pregnancy (Study IV). For Study III, an additional cohort in England (maximum n = 11554) was used to study the risk of offspring ASD in relation to a combined maternal exposure to up to 42 common and rare life events, as well as their perceived impact upon the mother during pregnancy and early life. Results: In Study I, measures of a lower parental socioeconomic status – specifically, lower household income, and unskilled, manual or unclassified occupations were associated with a higher risk of ASD. The associations were similar in ASD with or without ID. In Study II, maternal migration had divergent relationships with ASD with and without ID- showing heightened risks for ASD with ID and reduced ones for ASD without ID. This study found that associations of migration with autism varied by the geographical region of origin of the mother, by the human development of the region of origin, and the timing of migration in relation to pregnancy. In Study III, no evidence for a relationship between stressful life events during pregnancy and a heightened risk of ASD was found, using data from the two population-based studies in Sweden and England respectively. In Study IV, a higher risk of ASD was associated with a prenatal history of maternal depression, but did not appear to be associated with paternal depression. In a smaller sample, when maternal antidepressant use was simultaneously studied, the associations of maternal depression with ASD appeared to be confined to the group of women who reported taking antidepressants during pregnancy. The associations were higher for ASD without ID, and were not observed for ASD with ID. Conclusion: In three of the four studies there was evidence of a relationship between the prenatal factors studied and a higher risk of autism spectrum disorders. In two studies, the timing of the event (migration, antidepressant use or severe depression during pregnancy) was indicative of pregnancy related exposures, highlighting the importance of considering environmental factors acting in utero in the pathways to autism. The marked differences in risks for autism with and without intellectual disability with exposures in two studies highlight the value of studying these categories separately, since they may have different determinants.
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| 4. |
- Reed, Zoe E., et al.
(författare)
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Mapping the genetic and environmental aetiology of autistic traits in Sweden and the United Kingdom
- 2021
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Ingår i: JCPP Advances. - : John Wiley & Sons. - 2692-9384. ; 1:3
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Tidskriftsartikel (refereegranskat)abstract
- Background: Autistic traits are influenced by both genetic and environmental factors, and are known to vary geographically in prevalence. But to what extent does their aetiology also vary from place to place?Methods: We applied a novel spatial approach to data on autistic traits from two large twin studies, the Child and Adolescent Twin Study in Sweden (CATSS; N = 16,677, including 8307 twin pairs) and the Twins Early Development Study in the UK (TEDS; N = 11,594, including 5796 twin pairs), to explore how the influence of nature and nurture on autistic traits varies from place to place.Results: We present maps of gene- and environment- by geography interactions in Sweden and the United Kingdom (UK), showing geographical variation in both genetic and environmental influences across the two countries. In Sweden genetic influences appear higher in the far south and in a band running across the centre of the country. Environmental influences appear greatest in the south and north, with reduced environmental influence across the central band. In the UK genetic influences appear greater in the south, particularly in more central southern areas and the southeast, the Midlands and the north of England. Environmental influences appear greatest in the south and east of the UK, with less influence in the north and the west.Conclusions: We hope this systematic approach to identifying aetiological interactions will inspire research to examine a wider range of previously unknown environmental influences on the aetiology of autistic traits. By doing so, we will gain greater understanding of how these environments draw out or mask genetic predisposition and interact with other environmental influences in the development of autistic traits.
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