A Reply to Cook and Oreskes on Climate Science Consensus Messaging

In their replies to our paper (Pearce et al., 2017), both Cook and Oreskes agree with our central point: that deliberating and mobilizing policy responses to climate change requires thinking beyond public belief in a scientific consensus. However, they both continue to defend consensus messaging, either because of ‘the dangers of neglecting to communicate the scientific consensus’ (Cook, 2017, p. 1) or because ‘“no consensus”…remains… a contrarian talking point’ (Oreskes, 2017, p. 1). Both highlight previously conducted market research by fossil fuel companies which suggested that scientific uncertainty provided a political weapon in fighting regulation, concluding that incorrect public perceptions of the scientific consensus weaken support for policy action (Oreskes, 2017, p. 2)

Abundance in the Anthropocene

Numerous attempts have been made to understand the Anthropocene in relation to overwhelming species and habitat loss. However, amidst these losses ecological niches have emerged and been taken as signs of resilience and hope: from mushrooms that flourish in damaged forests to urban wildlife in brownfield sites. This article offers an alternative conception of abundance, which addresses the sociological and conceptual challenges posed when abundance is a characteristic of so-called pests, parasites and pathogens. The article draws together research from three case studies: bed bugs, hookworms and antibiotic resistant microbes, all of which have become intimately entangled with particular human communities as other lifeforms have declined. Through contrasting these cases we elucidate how the affordances of abundant lifeforms, including the dangers they pose to other forms of life, are entwined with failed ‘technofixes’, colonial legacies and contemporary inequalities. In doing so we situate abundance as a constitutive element of the Anthropocene that requires as sustained an ethical engagement as questions of species loss. We conclude by arguing that further ethical attention needs to be paid to finding ways of ‘being alongside’ life that is difficult to live with, but is becoming intimately re-entangled with human worlds. In doing so, we complicate existing theoretical work that has drawn hope from multispecies abundance and entanglement

The Sustainable Path to a Circular Bioeconomy

This is the final version. Available on open access from Elsevier via the DOI in this recordCircular bioeconomy is gaining prominence in academic, policy, and industry contexts, linking circular economy and bioeconomy agendas in service of sustainability. However, it is at risk of developing in narrow, unsustainable ways. A sustainable path to circular bioeconomies must embrace diverse expert and stakeholder input, multiple solutions, and noneconomic value.European Union Horizon 2020University of NottinghamEngineering and Physical Sciences Research Council (EPSRC)Biotechnology and Biological Sciences Research Council (BBSRC)Economic and Social Research Council (ESRC)University of ManchesterResearch EnglandHub for Biotechnology in the Built Environment, Newcastle Universit

Beyond counting climate consensus

Several studies have been using quantified consensus within climate science as an argument to foster climate policy. Recent efforts to communicate such scientific consensus attained a high public profile but it is doubtful if they can be regarded successful. We argue that repeated efforts to shore up the scientific consensus on minimalist claims such as ‘humans cause global warming’ are distractions from more urgent matters of knowledge, values, policy framing and public engagement.  Such efforts to force policy progress through communicating scientific consensus misunderstand the relationship between scientific knowledge, publics and policymakers. More important is to focus on genuinely controversial issues within climate policy debates where expertise might play a facilitating role. Mobilising expertise in policy debates calls for judgment, context and attention to diversity, rather than deferring to formal quantifications of narrowly scientific claims

Impact of primary kidney disease on the effects of empagliflozin in patients with chronic kidney disease: secondary analyses of the EMPA-KIDNEY trial

Background: The EMPA KIDNEY trial showed that empagliflozin reduced the risk of the primary composite outcome of kidney disease progression or cardiovascular death in patients with chronic kidney disease mainly through slowing progression. We aimed to assess how effects of empagliflozin might differ by primary kidney disease across its broad population. Methods: EMPA-KIDNEY, a randomised, controlled, phase 3 trial, was conducted at 241 centres in eight countries (Canada, China, Germany, Italy, Japan, Malaysia, the UK, and the USA). Patients were eligible if their estimated glomerular filtration rate (eGFR) was 20 to less than 45 mL/min per 1·73 m2, or 45 to less than 90 mL/min per 1·73 m2 with a urinary albumin-to-creatinine ratio (uACR) of 200 mg/g or higher at screening. They were randomly assigned (1:1) to 10 mg oral empagliflozin once daily or matching placebo. Effects on kidney disease progression (defined as a sustained ≥40% eGFR decline from randomisation, end-stage kidney disease, a sustained eGFR below 10 mL/min per 1·73 m2, or death from kidney failure) were assessed using prespecified Cox models, and eGFR slope analyses used shared parameter models. Subgroup comparisons were performed by including relevant interaction terms in models. EMPA-KIDNEY is registered with ClinicalTrials.gov, NCT03594110. Findings: Between May 15, 2019, and April 16, 2021, 6609 participants were randomly assigned and followed up for a median of 2·0 years (IQR 1·5–2·4). Prespecified subgroupings by primary kidney disease included 2057 (31·1%) participants with diabetic kidney disease, 1669 (25·3%) with glomerular disease, 1445 (21·9%) with hypertensive or renovascular disease, and 1438 (21·8%) with other or unknown causes. Kidney disease progression occurred in 384 (11·6%) of 3304 patients in the empagliflozin group and 504 (15·2%) of 3305 patients in the placebo group (hazard ratio 0·71 [95% CI 0·62–0·81]), with no evidence that the relative effect size varied significantly by primary kidney disease (pheterogeneity=0·62). The between-group difference in chronic eGFR slopes (ie, from 2 months to final follow-up) was 1·37 mL/min per 1·73 m2 per year (95% CI 1·16–1·59), representing a 50% (42–58) reduction in the rate of chronic eGFR decline. This relative effect of empagliflozin on chronic eGFR slope was similar in analyses by different primary kidney diseases, including in explorations by type of glomerular disease and diabetes (p values for heterogeneity all >0·1). Interpretation: In a broad range of patients with chronic kidney disease at risk of progression, including a wide range of non-diabetic causes of chronic kidney disease, empagliflozin reduced risk of kidney disease progression. Relative effect sizes were broadly similar irrespective of the cause of primary kidney disease, suggesting that SGLT2 inhibitors should be part of a standard of care to minimise risk of kidney failure in chronic kidney disease. Funding: Boehringer Ingelheim, Eli Lilly, and UK Medical Research Council

Beyond Counting Climate Consensus

© 2017 Informa UK Limited, trading as Taylor & Francis Group. Several studies have been using quantified consensus within climate science as an argument to foster climate policy. Recent efforts to communicate such scientific consensus attained a high public profile but it is doubtful if they can be regarded successful. We argue that repeated efforts to shore up the scientific consensus on minimalist claims such as “humans cause global warming” are distractions from more urgent matters of knowledge, values, policy framing and public engagement. Such efforts to force policy progress through communicating scientific consensus misunderstand the relationship between scientific knowledge, publics and policymakers. More important is to focus on genuinely controversial issues within climate policy debates where expertise might play a facilitating role. Mobilizing expertise in policy debates calls for judgment, context and attention to diversity, rather than deferring to formal quantifications of narrowly scientific claims

Impact of primary kidney disease on the effects of empagliflozin in patients with chronic kidney disease: secondary analyses of the EMPA-KIDNEY trial

Background: The EMPA-KIDNEY trial showed that empagliflozin reduced the risk of the primary composite outcome of kidney disease progression or cardiovascular death in patients with chronic kidney disease mainly through slowing progression. We aimed to assess how effects of empagliflozin might differ by primary kidney disease across its broad population. Methods: EMPA-KIDNEY, a randomised, controlled, phase 3 trial, was conducted at 241 centres in eight countries (Canada, China, Germany, Italy, Japan, Malaysia, the UK, and the USA). Patients were eligible if their estimated glomerular filtration rate (eGFR) was 20 to less than 45 mL/min per 1·73 m2, or 45 to less than 90 mL/min per 1·73 m2 with a urinary albumin-to-creatinine ratio (uACR) of 200 mg/g or higher at screening. They were randomly assigned (1:1) to 10 mg oral empagliflozin once daily or matching placebo. Effects on kidney disease progression (defined as a sustained ≥40% eGFR decline from randomisation, end-stage kidney disease, a sustained eGFR below 10 mL/min per 1·73 m2, or death from kidney failure) were assessed using prespecified Cox models, and eGFR slope analyses used shared parameter models. Subgroup comparisons were performed by including relevant interaction terms in models. EMPA-KIDNEY is registered with ClinicalTrials.gov, NCT03594110. Findings: Between May 15, 2019, and April 16, 2021, 6609 participants were randomly assigned and followed up for a median of 2·0 years (IQR 1·5-2·4). Prespecified subgroupings by primary kidney disease included 2057 (31·1%) participants with diabetic kidney disease, 1669 (25·3%) with glomerular disease, 1445 (21·9%) with hypertensive or renovascular disease, and 1438 (21·8%) with other or unknown causes. Kidney disease progression occurred in 384 (11·6%) of 3304 patients in the empagliflozin group and 504 (15·2%) of 3305 patients in the placebo group (hazard ratio 0·71 [95% CI 0·62-0·81]), with no evidence that the relative effect size varied significantly by primary kidney disease (pheterogeneity=0·62). The between-group difference in chronic eGFR slopes (ie, from 2 months to final follow-up) was 1·37 mL/min per 1·73 m2 per year (95% CI 1·16-1·59), representing a 50% (42-58) reduction in the rate of chronic eGFR decline. This relative effect of empagliflozin on chronic eGFR slope was similar in analyses by different primary kidney diseases, including in explorations by type of glomerular disease and diabetes (p values for heterogeneity all >0·1). Interpretation: In a broad range of patients with chronic kidney disease at risk of progression, including a wide range of non-diabetic causes of chronic kidney disease, empagliflozin reduced risk of kidney disease progression. Relative effect sizes were broadly similar irrespective of the cause of primary kidney disease, suggesting that SGLT2 inhibitors should be part of a standard of care to minimise risk of kidney failure in chronic kidney disease. Funding: Boehringer Ingelheim, Eli Lilly, and UK Medical Research Council