Human microbiome research makes causal connections between entire microbial communities and a wide array of traits that range from physiological diseases to psychological states. To evaluate these causal claims, we first examine a well-known single-microbe causal explanation: of Helicobacter pylori causing ulcers. This apparently straightforward causal explanation is not so simple, however. It does not achieve a key explanatory standard in microbiology, of Koch’s postulates, which rely on manipulations of single-microorganism cultures to infer causal relationships to disease. When Koch’s postulates (...) are framed by an interventionist causal framework, it is clearer what the H. pylori explanation achieves and where its explanatory strengths lie. After assessing this ‘simple’, single-microbe case, we apply the interventionist framework to two key areas of microbiome research, in which obesity and mental health states are purportedly explained by microbiomes. Despite the experimental data available, interventionist criteria for explanation show that many of the causal claims generated by microbiome research are weak or misleading. We focus on the stability, specificity and proportionality of proposed microbiome causal explanations, and evaluate how effectively these dimensions of causal explanation are achieved in some promising avenues of research. We suggest some conceptual and explanatory strategies to improve how causal claims about microbiomes are made. (shrink)

Experiments are commonly thought to have epistemic privilege over simulations. Two ideas underpin this belief: first, experiments generate greater inferential power than simulations, and second, simulations cannot surprise us the way experiments can. In this article I argue that neither of these claims is true of experiments versus simulations in general. We should give up the common practice of resting in-principle judgments about the epistemic value of cases of scientific inquiry on whether we classify those cases as experiments or simulations, (...) per se. To the extent that either methodology puts researchers in a privileged epistemic position, this is context sensitive. (shrink)

Human microbiome research makes causal connections between entire microbial communities and a wide array of traits that range from physiological diseases to psychological states. To evaluate these causal claims, we first examine a well-known single-microbe causal explanation: of Helicobacter pylori causing ulcers. This apparently straightforward causal explanation is not so simple, however. It does not achieve a key explanatory standard in microbiology, of Koch’s postulates, which rely on manipulations of single-microorganism cultures to infer causal relationships to disease. When Koch’s postulates (...) are framed by an interventionist causal framework, it is clearer what the H. pylori explanation achieves and where its explanatory strengths lie. After assessing this ‘simple’, single-microbe case, we apply the interventionist framework to two key areas of microbiome research, in which obesity and mental health states are purportedly explained by microbiomes. Despite the experimental data available, interventionist criteria for explanation show that many of the causal claims generated by microbiome research are weak or misleading. We focus on the stability, specificity and proportionality of proposed microbiome causal explanations, and evaluate how effectively these dimensions of causal explanation are achieved in some promising avenues of research. We suggest some conceptual and explanatory strategies to improve how causal claims about microbiomes are made. (shrink)

Human microbiome research makes causal connections between entire microbial communities and a wide array of traits that range from physiological diseases to psychological states. To evaluate these causal claims, we first examine a well-known single-microbe causal explanation: of Helicobacter pylori causing ulcers. This apparently straightforward causal explanation is not so simple, however. It does not achieve a key explanatory standard in microbiology, of Koch’s postulates, which rely on manipulations of single-microorganism cultures to infer causal relationships to disease. When Koch’s postulates (...) are framed by an interventionist causal framework, it is clearer what the H. pylori explanation achieves and where its explanatory strengths lie. After assessing this ‘simple’, single-microbe case, we apply the interventionist framework to two key areas of microbiome research, in which obesity and mental health states are purportedly explained by microbiomes. Despite the experimental data available, interventionist criteria for explanation show that many of the causal claims generated by microbiome research are weak or misleading. We focus on the stability, specificity and proportionality of proposed microbiome causal explanations, and evaluate how effectively these dimensions of causal explanation are achieved in some promising avenues of research. We suggest some conceptual and explanatory strategies to improve how causal claims about microbiomes are made. (shrink)

Koonin argues that CRISPR-Cas systems present the best-known case in point for Lamarckian evolution because they satisfy his proposed criteria for the specific inheritance of acquired adaptive characteristics. We see two interrelated issues with Koonin’s characterization of CRISPR-Cas systems as Lamarckian. First, at times he appears to confuse an account of the CRISPR-Cas system with an account of the mechanism it employs. We argue there is no evidence for the CRISPR-Cas system being “Lamarckian” in any sense. Second, it is unclear (...) whether the mechanism is more “Lamarckian” than many other forms of genetic change already well-characterized in Darwinian terms. We present three conceptually distinct senses in which the mechanism of IAC may be considered Lamarckian and argue that only the strongest sense of goal-directed IAC would be difficult to accommodate in a Darwinian account. As the CRISPR-Cas mechanism does not qualify as “Lamarckian” in this strong sense, we argue there is no conceptual value in calling it “Lamarckian”. Finally, we suggest that CRISPR-Cas systems do hold the potential for genuinely non-Darwinian, directed evolution in a way that Koonin did not discuss, involving their potential use as a human gene-editing tool. (shrink)

The global pandemic needs to mark a turning point for the peoples of Aotearoa New Zealand. How can we make sure that our culturally diverse nation charts an equitable and sustainable path through and beyond this new world? In a less affluent future, how can we ensure that all New Zealanders have fair access to opportunities? One challenge is to preserve the sense of common purpose so critical to protecting each other in the face of Covid-19. How can we centre (...) what we have learnt about resilience within Māori and wider Pacific communities in our reforms? How can public understanding of Covid-19 science create a platform for the future social valuing of expertise? How can we ensure that the impact of Covid-19 in New Zealand results in a more sustainable, and inclusive workforce–for instance by expanding our perceptions of the value of our workers through promoting digital inclusion? To meet these challenges, we must reimagine our existing traditions of thought, breathing new life into perennial concepts and debates. Our paper indicates some of the ways that Philosophy is central to this collective reimagining, highlighting solutions to be found across our rich philosophical traditions. (shrink)

Microbial model systems have a long history of fruitful use in fields that include evolution and ecology. In order to develop further insight into modelling practice, we examine how the competitive exclusion and coexistence of competing species have been modelled mathematically and materially over the course of a long research history. In particular, we investigate how microbial models of these dynamics interact with mathematical or computational models of the same phenomena. Our cases illuminate the ways in which microbial systems and (...) equations work as models, and what happens when they generate inconsistent findings about shared targets. We reveal an iterative strategy of comparative modelling in different media, and suggest reasons why microbial models have a special degree of epistemic tractability in multimodel inquiry. (shrink)

In this paper, I discuss the recent discovery of alleged arsenic bacteria in Mono Lake, California, and the ensuing debate in the scientific community about the validity and significance of these results. By situating this case in the broader context of projects that search for anomalous life forms, I examine the methodology and upshots of challenging biochemical constraints on living things. I distinguish between a narrower and a broader sense in which we might challenge or change our knowledge of life (...) as the result of such a project, and discuss two different kinds of projects that differ in their potential to overhaul our knowledge of life. I argue that the arsenic bacteria case, while potentially illuminating, is the kind of constraint-challenging project that could not—in spite of what was said when it was presented to the public—change our knowledge of life in the deeper sense. (shrink)

Francesco Redi’s seventeenth-century experiments on insect generation are regarded as a key contribution to the downfall of belief in spontaneous generation. Scholars praise Redi for his experiments demonstrating that meat does not generate insects, but condemn him for his claim elsewhere that trees can generate wasps and gallflies. He has been charged with rejecting spontaneous generation only to change his mind and accept it, and in the process, with failing as a rigorous experimental philosopher. In this paper I defend Redi (...) from both of these charges. In doing so, I draw some broader lessons for our understanding of spontaneous generation. ‘Spontaneous generation’ does not refer to a single theory, but rather a landscape of possible views. I analyze Redi’s theoretical commitments and situate them within this landscape, and argue that his error in the case of insects from plants is not as problematic as previous commentators have said it is. In his research on gall insects Redi was addressing a different question from that of his experiments on insect generation—the question was not “Can insects come from nonliving matter?,” but rather, “Can insects come from living organisms which are not their parents?” In the latter case, he gave an answer which we now know to be false, but this was not due to any failure in his rigor as an experimental philosopher. (shrink)