| 1. |
- Forouzanfar, Mohammad H, et al.
(författare)
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Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks in 188 countries, 1990-2013 : a systematic analysis for the Global Burden of Disease Study 2013.
- 2015
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Ingår i: The Lancet. - 0140-6736 .- 1474-547X. ; 386:10010, s. 2287-2323
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The Global Burden of Disease, Injuries, and Risk Factor study 2013 (GBD 2013) is the first of a series of annual updates of the GBD. Risk factor quantification, particularly of modifiable risk factors, can help to identify emerging threats to population health and opportunities for prevention. The GBD 2013 provides a timely opportunity to update the comparative risk assessment with new data for exposure, relative risks, and evidence on the appropriate counterfactual risk distribution.METHODS: Attributable deaths, years of life lost, years lived with disability, and disability-adjusted life-years (DALYs) have been estimated for 79 risks or clusters of risks using the GBD 2010 methods. Risk-outcome pairs meeting explicit evidence criteria were assessed for 188 countries for the period 1990-2013 by age and sex using three inputs: risk exposure, relative risks, and the theoretical minimum risk exposure level (TMREL). Risks are organised into a hierarchy with blocks of behavioural, environmental and occupational, and metabolic risks at the first level of the hierarchy. The next level in the hierarchy includes nine clusters of related risks and two individual risks, with more detail provided at levels 3 and 4 of the hierarchy. Compared with GBD 2010, six new risk factors have been added: handwashing practices, occupational exposure to trichloroethylene, childhood wasting, childhood stunting, unsafe sex, and low glomerular filtration rate. For most risks, data for exposure were synthesised with a Bayesian meta-regression method, DisMod-MR 2.0, or spatial-temporal Gaussian process regression. Relative risks were based on meta-regressions of published cohort and intervention studies. Attributable burden for clusters of risks and all risks combined took into account evidence on the mediation of some risks such as high body-mass index (BMI) through other risks such as high systolic blood pressure and high cholesterol.FINDINGS: All risks combined account for 57·2% (95% uncertainty interval [UI] 55·8-58·5) of deaths and 41·6% (40·1-43·0) of DALYs. Risks quantified account for 87·9% (86·5-89·3) of cardiovascular disease DALYs, ranging to a low of 0% for neonatal disorders and neglected tropical diseases and malaria. In terms of global DALYs in 2013, six risks or clusters of risks each caused more than 5% of DALYs: dietary risks accounting for 11·3 million deaths and 241·4 million DALYs, high systolic blood pressure for 10·4 million deaths and 208·1 million DALYs, child and maternal malnutrition for 1·7 million deaths and 176·9 million DALYs, tobacco smoke for 6·1 million deaths and 143·5 million DALYs, air pollution for 5·5 million deaths and 141·5 million DALYs, and high BMI for 4·4 million deaths and 134·0 million DALYs. Risk factor patterns vary across regions and countries and with time. In sub-Saharan Africa, the leading risk factors are child and maternal malnutrition, unsafe sex, and unsafe water, sanitation, and handwashing. In women, in nearly all countries in the Americas, north Africa, and the Middle East, and in many other high-income countries, high BMI is the leading risk factor, with high systolic blood pressure as the leading risk in most of Central and Eastern Europe and south and east Asia. For men, high systolic blood pressure or tobacco use are the leading risks in nearly all high-income countries, in north Africa and the Middle East, Europe, and Asia. For men and women, unsafe sex is the leading risk in a corridor from Kenya to South Africa.INTERPRETATION: Behavioural, environmental and occupational, and metabolic risks can explain half of global mortality and more than one-third of global DALYs providing many opportunities for prevention. Of the larger risks, the attributable burden of high BMI has increased in the past 23 years. In view of the prominence of behavioural risk factors, behavioural and social science research on interventions for these risks should be strengthened. Many prevention and primary care policy options are available now to act on key risks.FUNDING: Bill & Melinda Gates Foundation.
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| 2. |
- Vos, Theo, et al.
(författare)
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Global, regional, and national incidence, prevalence, and years lived with disability for 301 acute and chronic diseases and injuries in 188 countries, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013
- 2015
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Ingår i: The Lancet. - 1474-547X .- 0140-6736. ; 386:9995, s. 743-800
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Tidskriftsartikel (refereegranskat)abstract
- Background Up-to-date evidence about levels and trends in disease and injury incidence, prevalence, and years lived with disability (YLDs) is an essential input into global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013), we estimated these quantities for acute and chronic diseases and injuries for 188 countries between 1990 and 2013. Methods Estimates were calculated for disease and injury incidence, prevalence, and YLDs using GBD 2010 methods with some important refinements. Results for incidence of acute disorders and prevalence of chronic disorders are new additions to the analysis. Key improvements include expansion to the cause and sequelae list, updated systematic reviews, use of detailed injury codes, improvements to the Bayesian meta-regression method (DisMod-MR), and use of severity splits for various causes. An index of data representativeness, showing data availability, was calculated for each cause and impairment during three periods globally and at the country level for 2013. In total, 35 620 distinct sources of data were used and documented to calculated estimates for 301 diseases and injuries and 2337 sequelae. The comorbidity simulation provides estimates for the number of sequelae, concurrently, by individuals by country, year, age, and sex. Disability weights were updated with the addition of new population-based survey data from four countries. Findings Disease and injury were highly prevalent; only a small fraction of individuals had no sequelae. Comorbidity rose substantially with age and in absolute terms from 1990 to 2013. Incidence of acute sequelae were predominantly infectious diseases and short-term injuries, with over 2 billion cases of upper respiratory infections and diarrhoeal disease episodes in 2013, with the notable exception of tooth pain due to permanent caries with more than 200 million incident cases in 2013. Conversely, leading chronic sequelae were largely attributable to non-communicable diseases, with prevalence estimates for asymptomatic permanent caries and tension-type headache of 2.4 billion and 1.6 billion, respectively. The distribution of the number of sequelae in populations varied widely across regions, with an expected relation between age and disease prevalence. YLDs for both sexes increased from 537.6 million in 1990 to 764.8 million in 2013 due to population growth and ageing, whereas the age-standardised rate decreased little from 114.87 per 1000 people to 110.31 per 1000 people between 1990 and 2013. Leading causes of YLDs included low back pain and major depressive disorder among the top ten causes of YLDs in every country. YLD rates per person, by major cause groups, indicated the main drivers of increases were due to musculoskeletal, mental, and substance use disorders, neurological disorders, and chronic respiratory diseases; however HIV/AIDS was a notable driver of increasing YLDs in sub-Saharan Africa. Also, the proportion of disability-adjusted life years due to YLDs increased globally from 21.1% in 1990 to 31.2% in 2013. Interpretation Ageing of the world's population is leading to a substantial increase in the numbers of individuals with sequelae of diseases and injuries. Rates of YLDs are declining much more slowly than mortality rates. The non-fatal dimensions of disease and injury will require more and more attention from health systems. The transition to non-fatal outcomes as the dominant source of burden of disease is occurring rapidly outside of sub-Saharan Africa. Our results can guide future health initiatives through examination of epidemiological trends and a better understanding of variation across countries.
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| 3. |
- Naghavi, Mohsen, et al.
(författare)
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Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013
- 2015
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Ingår i: The Lancet. - 1474-547X .- 0140-6736. ; 385:9963, s. 117-171
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Tidskriftsartikel (refereegranskat)abstract
- Background Up-to-date evidence on levels and trends for age-sex-specifi c all-cause and cause-specifi c mortality is essential for the formation of global, regional, and national health policies. In the Global Burden of Disease Study 2013 (GBD 2013) we estimated yearly deaths for 188 countries between 1990, and 2013. We used the results to assess whether there is epidemiological convergence across countries. Methods We estimated age-sex-specifi c all-cause mortality using the GBD 2010 methods with some refinements to improve accuracy applied to an updated database of vital registration, survey, and census data. We generally estimated cause of death as in the GBD 2010. Key improvements included the addition of more recent vital registration data for 72 countries, an updated verbal autopsy literature review, two new and detailed data systems for China, and more detail for Mexico, UK, Turkey, and Russia. We improved statistical models for garbage code redistribution. We used six different modelling strategies across the 240 causes; cause of death ensemble modelling (CODEm) was the dominant strategy for causes with sufficient information. Trends for Alzheimer's disease and other dementias were informed by meta-regression of prevalence studies. For pathogen-specifi c causes of diarrhoea and lower respiratory infections we used a counterfactual approach. We computed two measures of convergence (inequality) across countries: the average relative difference across all pairs of countries (Gini coefficient) and the average absolute difference across countries. To summarise broad findings, we used multiple decrement life-tables to decompose probabilities of death from birth to exact age 15 years, from exact age 15 years to exact age 50 years, and from exact age 50 years to exact age 75 years, and life expectancy at birth into major causes. For all quantities reported, we computed 95% uncertainty intervals (UIs). We constrained cause-specific fractions within each age-sex-country-year group to sum to all-cause mortality based on draws from the uncertainty distributions. Findings Global life expectancy for both sexes increased from 65.3 years (UI 65.0-65.6) in 1990, to 71.5 years (UI 71.0-71.9) in 2013, while the number of deaths increased from 47.5 million (UI 46.8-48.2) to 54.9 million (UI 53.6-56.3) over the same interval. Global progress masked variation by age and sex: for children, average absolute diff erences between countries decreased but relative diff erences increased. For women aged 25-39 years and older than 75 years and for men aged 20-49 years and 65 years and older, both absolute and relative diff erences increased. Decomposition of global and regional life expectancy showed the prominent role of reductions in age-standardised death rates for cardiovascular diseases and cancers in high-income regions, and reductions in child deaths from diarrhoea, lower respiratory infections, and neonatal causes in low-income regions. HIV/AIDS reduced life expectancy in southern sub-Saharan Africa. For most communicable causes of death both numbers of deaths and age-standardised death rates fell whereas for most non-communicable causes, demographic shifts have increased numbers of deaths but decreased age-standardised death rates. Global deaths from injury increased by 10.7%, from 4.3 million deaths in 1990 to 4.8 million in 2013; but age-standardised rates declined over the same period by 21%. For some causes of more than 100 000 deaths per year in 2013, age-standardised death rates increased between 1990 and 2013, including HIV/AIDS, pancreatic cancer, atrial fibrillation and flutter, drug use disorders, diabetes, chronic kidney disease, and sickle-cell anaemias. Diarrhoeal diseases, lower respiratory infections, neonatal causes, and malaria are still in the top five causes of death in children younger than 5 years. The most important pathogens are rotavirus for diarrhoea and pneumococcus for lower respiratory infections. Country-specific probabilities of death over three phases of life were substantially varied between and within regions. Interpretation For most countries, the general pattern of reductions in age-sex specifi c mortality has been associated with a progressive shift towards a larger share of the remaining deaths caused by non-communicable disease and injuries. Assessing epidemiological convergence across countries depends on whether an absolute or relative measure of inequality is used. Nevertheless, age-standardised death rates for seven substantial causes are increasing, suggesting the potential for reversals in some countries. Important gaps exist in the empirical data for cause of death estimates for some countries; for example, no national data for India are available for the past decade.
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| 4. |
- Wang, Haidong, et al.
(författare)
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Estimates of global, regional, and national incidence, prevalence, and mortality of HIV, 1980-2015 : the Global Burden of Disease Study 2015.
- 2016
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Ingår i: The lancet. HIV. - : Elsevier. - 2352-3018. ; 3:8, s. e361-e387
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Timely assessment of the burden of HIV/AIDS is essential for policy setting and programme evaluation. In this report from the Global Burden of Disease Study 2015 (GBD 2015), we provide national estimates of levels and trends of HIV/AIDS incidence, prevalence, coverage of antiretroviral therapy (ART), and mortality for 195 countries and territories from 1980 to 2015.METHODS: For countries without high-quality vital registration data, we estimated prevalence and incidence with data from antenatal care clinics and population-based seroprevalence surveys, and with assumptions by age and sex on initial CD4 distribution at infection, CD4 progression rates (probability of progression from higher to lower CD4 cell-count category), on and off antiretroviral therapy (ART) mortality, and mortality from all other causes. Our estimation strategy links the GBD 2015 assessment of all-cause mortality and estimation of incidence and prevalence so that for each draw from the uncertainty distribution all assumptions used in each step are internally consistent. We estimated incidence, prevalence, and death with GBD versions of the Estimation and Projection Package (EPP) and Spectrum software originally developed by the Joint United Nations Programme on HIV/AIDS (UNAIDS). We used an open-source version of EPP and recoded Spectrum for speed, and used updated assumptions from systematic reviews of the literature and GBD demographic data. For countries with high-quality vital registration data, we developed the cohort incidence bias adjustment model to estimate HIV incidence and prevalence largely from the number of deaths caused by HIV recorded in cause-of-death statistics. We corrected these statistics for garbage coding and HIV misclassification.FINDINGS: Global HIV incidence reached its peak in 1997, at 3·3 million new infections (95% uncertainty interval [UI] 3·1-3·4 million). Annual incidence has stayed relatively constant at about 2·6 million per year (range 2·5-2·8 million) since 2005, after a period of fast decline between 1997 and 2005. The number of people living with HIV/AIDS has been steadily increasing and reached 38·8 million (95% UI 37·6-40·4 million) in 2015. At the same time, HIV/AIDS mortality has been declining at a steady pace, from a peak of 1·8 million deaths (95% UI 1·7-1·9 million) in 2005, to 1·2 million deaths (1·1-1·3 million) in 2015. We recorded substantial heterogeneity in the levels and trends of HIV/AIDS across countries. Although many countries have experienced decreases in HIV/AIDS mortality and in annual new infections, other countries have had slowdowns or increases in rates of change in annual new infections.INTERPRETATION: Scale-up of ART and prevention of mother-to-child transmission has been one of the great successes of global health in the past two decades. However, in the past decade, progress in reducing new infections has been slow, development assistance for health devoted to HIV has stagnated, and resources for health in low-income countries have grown slowly. Achievement of the new ambitious goals for HIV enshrined in Sustainable Development Goal 3 and the 90-90-90 UNAIDS targets will be challenging, and will need continued efforts from governments and international agencies in the next 15 years to end AIDS by 2030.
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| 5. |
- Brunner, Benedikt, et al.
(författare)
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Macroalgae maintain growth outside their observed distributions: Implications for biodiversity-ecosystem functioning at landscape scales
- 2023
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Ingår i: Journal of Ecology. - 0022-0477 .- 1365-2745. ; 111:6, s. 1362-1373
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Tidskriftsartikel (refereegranskat)abstract
- The spatial insurance hypothesis states that at landscape scales with environmental variability between different places, biodiversity increases ecosystem functioning if species respond asynchronously to environmental variation, and they are highest functioning in places where they dominate the relative abundance. Under this hypothesis, observed species turnover between places in a landscape with environmental variation might suggest that species diversity is an important driver of landscape-scale ecosystem functioning. However, the spatial insurance implicitly assumes that species found in one place in the landscape will not be able to maintain high functioning in other places. Given this assumption of the spatial insurance hypothesis, we would predict that species' functioning in monoculture should decline if transplanted to a different place on an environmental gradient, away from where they naturally dominate. If this is the case, we would expect that the loss of one species in one place of the environmental gradient could not be compensated through the establishment of another species in that place. We tested this prediction using a model system of marine macroalgae on intertidal rocky shores on the Swedish west coast. We performed a reciprocal transplant experiment with adult individuals of four fucoid seaweeds that dominate the standing stock biomass at different depths on these shores and monitored their relative growth rate over 2 months. Counter to the assumptions made by the spatial insurance hypothesis, growth rates for three of the four species showed limited responses to being transplanted to different depth zones. Spatial insurance may, hence, play a minor role in sustaining landscape ecosystem functioning in this and other systems. Synthesis. The functional consequences of species loss at landscape scales may not be as obvious as observational studies and ecological models suggest. Consequently, natural patterns of species turnover should not be used directly to argue for the role of biodiversity at landscape scales. Instead, how species may or may not be able to compensate for the loss of other species is a critical aspect if we are to understand how changes in biodiversity at the landscape scale affect ecosystem functioning.
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| 6. |
- Buschke, F. T., et al.
(författare)
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Random population fluctuations bias the Living Planet Index
- 2021
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Ingår i: Nature Ecology and Evolution. - : Springer Science and Business Media LLC. - 2397-334X. ; 5:8, s. 1145-1152
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Tidskriftsartikel (refereegranskat)abstract
- The Living Planet Index (LPI) is a standardized indicator for tracking population trends through time. Due to its ability to aggregate many time series in a single metric, the LPI has been proposed as an indicator for the Convention on Biological Diversity’s post-2020 Global Biodiversity Strategy. However, here we show that random population fluctuations introduce biases when calculating the LPI. By combining simulated and empirical data, we show how random fluctuations lead to a declining LPI even when overall population trends are stable and imprecise estimates of the LPI when populations increase or decrease nonlinearly. We applied randomization null models that demonstrate how random fluctuations exaggerate declines in the global LPI by 9.6%. Our results confirm substantial declines in the LPI but highlight sources of uncertainty in quantitative estimates. Randomization null models are useful for presenting uncertainty around indicators of progress towards international biodiversity targets. © 2021, The Author(s), under exclusive licence to Springer Nature Limited.
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| 7. |
- Gamfeldt, Lars, 1975, et al.
(författare)
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Scaling-up the biodiversity-ecosystem functioning relationship: the effect of environmental heterogeneity on transgressive overyielding
- 2023
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Ingår i: Oikos. - : Wiley. - 0030-1299 .- 1600-0706. ; 2023:3
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Tidskriftsartikel (refereegranskat)abstract
- Knowledge of how biodiversity sustains ecosystem function comes predominantly from studies focused on small spatial scales. Thus, we know relatively little about the role of biodiversity at larger scales of space and time where habitats become increasingly heterogeneous. Efforts to upscale the relationship between biodiversity and function have yielded inconclusive results. Given that increasing habitat heterogeneity is a ubiquitous consequence of increasing spatial scale, we asked: as habitat heterogeneity increases, can single species continue to maintain ecosystem function? Or, does transgressive overyielding (functioning of species mixture divided by the functioning of the highest functioning single species) change with habitat heterogeneity? We addressed this using a combination of computer simulations, an experiment and a meta-analysis. The three parts followed the same rationale: habitat heterogeneity was increased by aggregating local habitats with different conditions into larger and more heterogeneous landscapes. The computer simulations showed that, on average, transgressive overyielding increased with habitat heterogeneity because monoculture functioning decreased with habitat heterogeneity. We tested this expectation experimentally by varying the strain richness from one to five species across 10800 bacterial communities in five different habitats defined by sub-inhibitory concentrations of antibiotics. On average, the experimental results concurred with the simulations. We tested the generality of this result using a meta-analysis of 26 published experiments that manipulated habitat conditions and species richness. This confirmed that transgressive overyielding tended to increase with habitat heterogeneity but only when species were specialised to different habitats and were not inhibited in mixtures by negative species interactions. This was not the case in several experiments used in our meta-analysis where one species maximised functioning across all habitats, contrary to the assumptions of many ecological models. Our results illustrate the importance of biodiversity at larger spatial scales with more heterogeneity but also highlights contingencies that this pattern depends on.
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| 8. |
- Hagan, James
(författare)
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Compensation alters estimates of the number of species required to maintain ecosystem functioning across an emersion gradient: A case study with intertidal macroalgae
- 2024
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Ingår i: Functional Ecology. - 0269-8463 .- 1365-2435. ; 38:2, s. 338-349
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Tidskriftsartikel (refereegranskat)abstract
- Whether more species are required to maintain ecosystem functioning as spatial scale increases or across environmental gradients has frequently been studied by examining whether different species drive ecosystem functioning in different sites. However, this approach does rule out the counterfactual scenario where a few species could potentially maintain ecosystem functioning across sites as this requires examining which species can (or cannot) compensate for the loss of others. Here, I used an observational study and a field-based transplant experiment to examine the effects of species loss on biomass productivity in an intertidal marine macroalgal system. I calculated the number of species required to maintain biomass productivity across four depth zones reflecting a water emersion gradient using two commonly used observational approaches. Then, I combined hypothetical simulated extinction scenarios with field-based transplant data of relative growth rates of all species across the four depth zones to explore how the number of species required to maintain biomass productivity across depth zones changed under counterfactual scenarios where species compensated for species loss. The observational analyses suggested that between three and four species were required to maintain productivity across the depth zones. The simulated extinction scenarios did not. Rather, decreases in biomass productivity due to the loss of some species (e.g. Fucus spiralis, Ascophyllum nodosum) were easily compensated by other species (e.g. Fucus vesiculosus). However, for some species like F. vesiculosus, the extinction simulations suggested that compensation would be unlikely. Commonly used observational approaches may overestimate the number of species required to maintain ecosystem functioning across environmental gradients and spatial scales. Read the free Plain Language Summary for this article on the Journal blog.
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| 9. |
- Hagan, James, 1993
(författare)
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Connections between biodiversity and ecosystem functioning in large-scale natural ecosystems
- 2023
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Billions of years of evolution have given us a planet that supports a remarkable diversity of life. Estimates for the number of Eukaryotic species frequently number in the millions and the Prokaryotes are much more diverse than that. This biodiversity makes up the ecosystems that we, as humans, rely on to sustain almost every aspect of our lives. But, despite our reliance on these biodiverse ecosystems, we are eroding them at an alarming rate through habitat destruction, overexploitation and our transformation of the climate. Indeed, some estimates suggest that the rate at which species are going extinct is as high as previous mass extinction events that have sporadically occurred throughout earth’s history. How will this loss of biodiversity affect the functioning of ecosystems that we rely on? How much biodiversity do we need for healthy ecosystems? These are some of the questions that researchers began to address in the early 1990’s. Based on hundreds of experimental manipulations of biodiversity, there is a general scientific consensus that biodiverse ecosystems tend to be more stable and more productive than depauperate ones. However, much of this work has taken place in artificial, experimental systems and at small scales of space and time. Thus, several questions remain. For example, if small-scale experiments show that biodiversity is important for ecosystem functioning, will the effects be the same at large scales? If ten species are required to maximise ecosystem functioning in a one square meter experimental grass patch, how many are required in a whole meadow, or in a landscape with many meadows? In my thesis, I attempt to extend our knowledge so we can better understand the consequences of biodiversity loss in natural systems and at larger scales of space and time. In Paper I, I re-examined experimental work on biodiversity and ecosystem functioning from the last 30 years through the lens of community assembly theory. The aim was to understand what these experiments may tell us about how biodiversity loss will impact ecosystem functioning in natural ecosystems. My analysis showed that there are probably many cases where the results of experiments will not easily transfer to natural ecosystems. Rather than studying the community of species present in a local place, as is done in the experiments, I argue that we should instead focus on the pool of species present in the whole landscape, and the processes that govern the composition of local communities. Many experiments performed over the last 30 years have shown that a high-diversity community of species is only rarely higher functioning than the highest functioning single species (i.e. monoculture). In Paper II, I used a set of theoretical simulations, an experiment in a bacteria-based model system, and a synthesis of previously published experiments to show that this may be because experiments have been performed in relatively homogeneous environments. When environmental heterogeneity increased, we found that the functioning of diverse species mixtures increased relative to the highest functioning monocultures. But, despite the general trend observed in Paper II, there were many experiments in the synthesis where a single species in monoculture was highest functioning across the range of environmental conditions. This contradicted many theoretical models for the effect of biodiversity on ecosystem functioning. Thus, in Paper III, I wanted to study species along an environmental gradient to see if we would obtain similar results. I did this using a transplant experiment with four common species of marine seaweeds on Swedish rocky shores. These species occupy relatively distinct depth zones on the shores, which are characterised by different environmental conditions. I thus hypothesised that the four species would grow best at the depth where they are most common. Counter to my predictions, the experiment showed that only one species responded strongly to being transplanted to a different depth zone. For Paper IV, I took the results obtained from Paper III and attempted to model what would happen to the biomass production of the seaweed communities if each of the four species went extinct. I found that the biomass production of these rocky shore communities would probably only be strongly affected if one of the seaweed species (Fucus vesiculosus) went extinct. This is because the four species showed high productivity outside of the depth zones where they are naturally found and, therefore, may be able to compensate for the loss of any of the other species. Arguably the most direct way to calculate an effect of biodiversity on ecosystem functioning is to compare a mixture of interacting species to a null expectation where species do not interact based on species’ functioning in monoculture. However, in natural systems, this is generally not possible because we rarely have natural monocultures. In Paper V, I developed a Bayesian analytical pipeline to impute missing monoculture data which enables comparisons of mixtures and monocultures in natural ecosystems. Combined with a previously developed statistical partition, I was able to show that a combination of local-scale species interactions, local-scale dominance by a few high functioning species and spatial niche partitioning all contributed to a positive effect of biodiversity on ecosystem functioning in two, natural marine ecosystems. Based on these five papers, I conclude that the hundreds of experiments that have been done to date provide useful but imprecise information about how biodiversity loss may affect the functioning of natural ecosystems. To understand the ecosystem-level effects of biodiversity loss more thoroughly, we will need to carefully study how biodiversity is changing across multiple scales of space and time and use methods that can detect the consequences of these changes. Papers IV and V suggest avenues for how this may be done.
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| 10. |
- Hagan, James, et al.
(författare)
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We should not necessarily expect positive relationships between biodiversity and ecosystem functioning in observational field data
- 2021
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Ingår i: Ecology Letters. - : Wiley. - 1461-023X .- 1461-0248. ; 24:12, s. 2537-2548
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Tidskriftsartikel (refereegranskat)abstract
- Our current, empirical understanding of the relationship between biodiversity and ecosystem function is based on two information sources. First, controlled experiments which show generally positive relationships. Second, observational field data which show variable relationships. This latter source coupled with a lack of observed declines in local biodiversity has led to the argument that biodiversity-ecosystem functioning relationships may be uninformative for conservation and management. We review ecological theory and re-analyse several biodiversity datasets to argue that ecosystem function correlations with local diversity in observational field data are often difficult to interpret in the context of biodiversity-ecosystem function research. This occurs because biotic interactions filter species during community assembly which means that there can be a high biodiversity effect on functioning even with low observed local diversity. Our review indicates that we should not necessarily expect any specific relationship between local biodiversity and ecosystem function in observational field data. Rather, linking predictions from biodiversity-ecosystem function theory and experiments to observational field data requires considering the pool of species available during colonisation: the local species pool. We suggest that, even without local biodiversity declines, biodiversity loss at regional scales-which determines local species pools-may still negatively affect ecosystem functioning.
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