Consider the following two (hypothetical) generic causal claims: “Living in a neighborhood with many families with children increases purchases of bicycles” and “living in an affluent neighborhood with many families with children increases purchases of bicycles.” These claims not only differ in what they suggest about how bicycle ownership is distributed across different neighborhoods (i.e., “the data”), but also have the potential to communicate something about the speakers’ values: namely, the prominence they accord to affluence in representing and making decisions (...) about the social world. Here, we examine the relationship between the level of granularity with which a cause is described in a generic causal claim (e.g., neighborhood vs. affluent neighborhood) and the value of the information contained in the causal model that generates that claim. We argue that listeners who know any two of the following can make reliable inferences about the third: 1) the level of granularity at which a speaker makes a generic causal claim, 2) the speaker’s values, and 3) the data available to the speaker. We present results of four experiments (N=1,323) in the domain of social categories that provide evidence in keeping with these predictions. (shrink)

Change is the fundamental idea of evolution. Explaining the extraordinary biological change we see written in the history of genomes and fossil beds is the primary occupation of the evolutionary biologist. Yet it is a surprising fact that for the majority of evolutionary research, we have rarely studied how evolution typically unfolds in nature, in changing ecological environments, over space and time. While ecology played a major role in the eventual acceptance of the population genetic viewpoint of evolution in the (...) synthetic era (circa 1918-1956), it held a lesser role in the development of evolutionary theory until the 1980s, when we began to systematically study the evolutionary dynamics of natural populations in space and time. As a result, early evolutionary theory was initially constructed in an abstract vacuum that was unrepresentative of evolution in nature. The subtle synthesis between ecology with evolutionary biology (eco-evo synthesis) over the past 40 years has progressed our knowledge of natural selection dynamics as they are found in nature, thus revealing how natural selection varies in strength, direction, form, and, more surprisingly, level of biological organization. Natural selection can no longer be reduced to lower levels of biological organization (i.e., individuals, selfish genes) over shorter timescales but should be expanded to include adaptation at higher levels and over longer timescales. Long-term and/or emergent evolutionary phenomena, such as multilevel selection or evolvability, have thus become tenable concepts within an evolutionary biology that embraces ecology and spatiotemporal change. Evolutionary biology is currently suspended at an intermediate stage of scientific progress that calls for the organization of all the recent knowledge revealed by the eco-evo synthesis into a coherent and unified theoretical framework. This is where philosophers of biology can be of particular use, acting as a bridge between the subdisciplines of biology and inventing new theoretical strategies to organize and accommodate the recent knowledge. Philosophers have recommended transitioning away from outdated philosophies that were originally derived from physics within the philosophical zeitgeist of logical positivism (i.e., monism, reductionism, and monocausation) and toward a distinct philosophy of biology that can capture the natural complexity of multifaceted biological systems within diverse ecosystems—one that embraces the emerging philosophies of pluralism, emergence, and multicausality. Therefore, I see recent advances in ecology, evolutionary biology, and the philosophy of biology as laying the groundwork for another major biological synthesis, what I refer to as the Second Synthesis because, in many respects, it is analogous to the aims and outcomes of the first major biological synthesis (but is notably distinct from the inorganic and contrived progressive movement known as the extended evolutionary synthesis). With the general development of a distinctive philosophy of science, biology has rightfully emerged as an autonomous science. Thus, while the first synthesis legitimized biology, the Second Synthesis autonomized biology and afforded biology its own philosophy, allowing biology to finally realize its full scientific potential. (shrink)

This paper addresses the question of what constitutes an apt interpreted model for the purpose of analyzing causation. I first collect universally adopted aptness principles into a basic account, flagging open questions and choice points along the way. I then explore various additional aptness principles that have been proposed in the literature but have not been widely adopted, the motivations behind their proposals, and the concerns with each that stand in the way of universal adoption. I conclude that the remaining (...) work of articulating aptness for a SEM analysis of causation is tied up with issue to do with modality, ontology, and mereology. Continuing this work is therefore likely to shed light on the relationship between these areas and causation more generally. (shrink)

These preprints were automatically compiled into a PDF from the collection of papers deposited in PhilSci-Archive in conjunction with the PSA 2018.

Manipulationism holds that information about the results of interventions is of utmost importance for scientific practices such as causal assessment or explanation. Specifically, manipulation provides information about the stability, or invariance, of the relationship between X and Y: were we to wiggle the cause X, the effect Y would accordingly wiggle and, additionally, the relation between the two will not be disrupted. This sort of relationship between variables are called 'invariant empirical generalisations'. The paper focuses on questions about causal assessment (...) and analyses the status of manipulation. It is argued that manipulationism is trapped in a dilemma. If manipulationism is read as providing a conceptual analysis of causation, then it fails to provide a story about the methods for causal assessment. If, instead, manipulationism is read as providing a method for causal assessment, then it is at an impasse concerning causal assessment in areas where manipulations are not performed. Empirical generalisations are then reassessed, in such a way that manipulation is not taken as methodologically fundamental. The paper concludes that manipulation is the appropriate tool for some scientific contexts, but not for all. (shrink)

Both philosophers and psychologists have argued for the existence of distinct kinds of explanations, including teleological explanations that cite functions or goals, and mechanistic explanations that cite causal mechanisms. Theories of causation, in contrast, have generally been unitary, with dominant theories focusing either on counterfactual dependence or on physical connections. This paper argues that both approaches to causation are psychologically real, with different modes of explanation promoting judgments more or less consistent with each approach. Two sets of experiments isolate the (...) contributions of counterfactual dependence and physical connections in causal ascriptions involving events with people, artifacts, or biological traits, and manipulate whether the events are construed teleologically or mechanistically. The findings suggest that when events are construed teleologically, causal ascriptions are sensitive to counterfactual dependence and relatively insensitive to the presence of physical connections, but when events are construed mechanistically, causal ascriptions are sensitive to both counterfactual dependence and physical connections. The conclusion introduces an account of causation, an "exportable dependence theory," that provides a way to understand the contributions of physical connections and teleology in terms of the functions of causal ascriptions. (shrink)

Engineering failure investigations seek to reconstruct the actual causes of major engineering failures. The investigators need to establish the existence of certain past events and the actual causal relationships that these events bear to the failures in question. In this paper, I examine one method for reconstructing the actual causes of failure events, which I call "feature dependence". The basic idea of feature dependence is that some features of an event are informative about the features of its causes; therefore, the (...) investigators can use the features of a known failure event to reconstruct details of its causes. I make explicit the structure of feature dependence and the evidential basis of its key premises, and show how feature dependence works in the investigation of the American Airlines Flight 191 accident. (shrink)

This chapter examines the relationship between laws and mechanisms as approaches to characterising generalizations and explanations in science. I give an overview of recent historical discussions where laws failed to satisfy stringent logical criteria, opening the way for mechanisms to be investigated as a way to explain regularities in nature. This followed by a critical discussion of contemporary debates about the role of laws versus mechanisms in describing versus explaining regularities. I conclude by offering new arguments for two roles for (...) laws that mechanisms cannot subsume, one epistemically optimistic and one pessimistic, both broadly Humean. Do note that this piece is not primarily Hume exegesis; it is more of a riff in the key of Hume. (shrink)

Various scientists and philosophers have heavily criticized what they see as problematic forms of ‘nutritional reductionism’ or ‘nutritionism’ whereby studying food–health interactions at the level of isolated food components produces largely misguided science and misleading interpretations. However, the exact target of these diverse criticisms remains elusive, and its implications are overstated, which may hinder scientific understanding. To better identify the types of flaws supposedly hindering reductionist research, we disentangle three types of reductionist claims to better determine what the debate is (...) about and to propose ways to move it forward. We then present a qualified defence of the reductionist programme that hinges on the ability to identify nutritional causes that make a difference, which we illustrate through central examples in the history of nutrition. This defence is taken further by using insights from the philosophy of mechanisms to analyse how the field of nutritional ecology offers a synthetic framework to explain, generate, and test predictions about nutrient–organism interactions, which is premised on the biological mechanisms of nutrient-specific appetite regulation. The result, which we call ‘synthetic reductionism’, avoids many, though perhaps not all, of the challenges raised by anti-reductionists, and also highlights the potential of reductionism to identify nutritional difference makers. (shrink)

This chapter examines the status of inference to the best explanation in naturalistic metaphysics. The methodology of inference to the best explanation in metaphysics is studied from the perspective of contemporary views on scientific explanation and explanatory inferences in the history and philosophy of science. This reveals serious shortcomings in prevalent attempts to vindicate metaphysical "explanationism" by reference to similarities between science and naturalistic metaphysics. This critique is brought out by considering a common gambit of methodological unity: (1) Both metaphysics (...) and science employ inference to the best explanation. (2) One has no reason to think that if explanationism is truth-conducive in science, it is not so in metaphysics. (3) One has a positive reason to think that if explanationism is truth-conducive in science, it is also so in metaphysics. (shrink)

The dual role of microbial communities as either beneficial/functional or harmful/pathogenic involves two issues concerning causality in physiology and medicine, etiology of disease, and the notion of function in biology. Causal explanation formulated by the germ theory of disease and the Koch postulates connects the existence of a specifically identified microbe to disease by the isolation and identification of a pathogen from an organism with the disease and the successful infection of a healthy individual. Similarly, microbiome research in medicine centers (...) on taxonomic composition in correlation with physiological conditions and germ-free mice experimentations to establish causal connections. However, because the microbiome is an ecological community, it lacks the specificity of identification assumed in the germ theory. Furthermore, the ecological aspects within and between microbiomes such as background conditions, microbial interactions, and interdependence, are treated as confounding. Looking at ecological studies, the causal explanations are less specific regarding complex systems with their processes of interactions. This article makes the following two points: One is that microbiome causality in the host should be understood similarly to the microbiome causality in an ecosystem. The second is that if considering a microbiome’s causality in the host as an ecosystem, its etiological explanation needs to be revisited to include a heterogeneous and mutual notion of interactions. Finally, according to the second point, the notion of function in ecology with its relevant notion of causality should be considered accordingly. (shrink)

The question of whether cultural transmission is faithful has attracted significant debate over the last 30 years. The degree of fidelity with which an object is transmitted depends on 1) the features chosen to be relevant, and 2) the quantity of details given about those features. Once these choices have been made, an object is described at a particular grain. In the absence of conventions between different researchers and across different fields about which grain to use, transmission fidelity cannot be (...) evaluated because it is relative to the choice of grain. In biology, because a genotype-to-phenotype mapping exists and transmission occurs from genotype to genotype, a privileged grain of description exists that circumvents this ‘grain problem.’ In contrast, in cultural evolution, the genotype–phenotype distinction cannot be drawn, rendering claims about fidelity dependent upon researchers’ choices. Thus, due to a lack of unified conventions, claims about fidelity transmission are difficult to evaluate. (shrink)

The history of developmental biology is interwoven with debates as to whether mechanistic explanations of development are possible or whether alternative explanatory principles or even vital forces need to be assumed. In particular, the demonstrated ability of embryonic cells to tune their developmental fate precisely to their relative position and the overall size of the embryo was once thought to be inexplicable in mechanistic terms. Taking a causal perspective, this Element examines to what extent and how developmental biology, having turned (...) molecular about four decades ago, has been able to meet the vitalist challenge. It focuses not only on the nature of explanations but also on the usefulness of causal knowledge – including the knowledge of classical experimental embryology – for further scientific discovery. It also shows how this causal perspective allows us to understand the nature and significance of some key concepts, including organizer, signal and morphogen. This title is also available as Open Access on Cambridge Core. (shrink)

In this paper I argue that the extent to which a human trait is genetically caused can causally depend upon whether the trait is categorized within human genetics as genetically caused. This makes the kind genetically caused trait an interactive kind. I demonstrate that this thesis is both conceptually coherent and empirically plausible. I outline the core rationale of this thesis and demonstrate its conceptual coherence by drawing upon Waters’ (2007) analysis of genetic causation. I add empirical plausibility to the (...) thesis by describing a hypothetical but empirically plausible mechanism by which the fact that obesity is categorized as genetically caused within human genetics increases the extent to which obesity is in fact genetically caused. (shrink)

We often hear how scientists have discovered that a certain human trait – or a trait of another type of organism – is innate, genetic, heritable, inherited, naturally selected etc. All these claims have something in common: they all declare a trait to have significant organism internal (for instance genetic) causes that are present in the organism at its birth. I call claims like these “nativist claims”. Nativist claims are important. They shape our overall understanding of what we are, what (...) we can do and what is good for us. They also impact our practical decision making. For instance, we know that certain types of genes increase the risk of certain diseases, and increasingly this has an effect on healthcare practices. Many people believe that in the matter of children’s education we should consider the fact that many cognitive abilities are highly heritable. Associations between genetics and aggressive behavior have been taken to be alleviating circumstances in criminal sentencing. It is therefore important to correctly understand the content and implications of nativist claims. In this doctoral thesis I analyze, by philosophical means, the content of different kinds of nativist claim. What does it mean that some psychological tendency is innate? What does it mean that intelligence is 50% heritable? How (if at all) do genes come to carry information about the traits of an organism – they are nothing like the information carriers familiar to us, such as newspapers, e-mails, secret codes, and audio files. This thesis emphasizes two things. Firstly, I demonstrate, that in different scientific contexts these words ('innate', 'genetically caused' etc.) can mean very different things. Therefore, the implications of a given nativist claim in one scientific context can be remarkably different from another nativist claim’s implications in some other scientific context. Secondly, I explain how the development of innate, heritable and genetically caused traits can be determined in different and often unexpected ways by our environment and experiences. I demonstrate that the content of a concept that is considered innate by cognitive scientists can be determined by what the organism that possesses the concept has experienced. I also show that even a trait which is 100% heritable can at the same time be a socially constructed trait. (shrink)

People disagree about the causes of social inequality and how to most effectively intervene in them. These may seem like empirical questions for social scientists, not philosophers. However, causal explanation itself depends on broadly normative commitments. From this it follows that (moral) philosophers have an important role to play in determining those causal explanations. I examine the case of causal explanations of poverty to demonstrate these claims. In short, philosophers who work to reshape our moral expectations also work, on the (...) back end, to restructure acceptable causal explanations—and hence solutions—for social inequality. Empirical and normative inquiry, then, are a two-way street. (shrink)

A phenome occurs through the many pathways of the complex net of interaction between the phenome and its environment; therefore researching and understanding how it arises requires investigation into many possible causes that are in constant interaction with each other. The most comprehensive investigations in biology are the ones in which many biologists from different sub-areas—evolutionary biology, developmental biology, molecular biology, physiology, genetics, epigenetics, ecology—have collaborated. Still, biologists do not always need to collaborate or look for the most comprehensive explanations. (...) A more standard investigation in biology occurs within a single subarea, and uses well-defined experiments with very specific conditions. This paper is about causation and related explanation in plant phenome research and its relevance to Aristotle’s Theory of Four Causes. I argue that there are causes which resemble Aristotle’s formal, material, and efficient causes in phenotype explanation and occurrence; but causes which resemble Aristotle’s final causes occur in phenotype explanation only, not in the occurrence. (shrink)

This paper explores some issues about the choice of variables for causal representation and explanation. Depending on which variables a researcher employs, many causal inference procedures and many treatments of causation will reach different conclusions about which causal relationships are present in some system of interest. The assumption of this paper is that some choices of variables are superior to other choices for the purpose of causal analysis. A number of possible criteria for variable choice are described and defended within (...) a broadly interventionist approach to causation. (shrink)

This paper explores the interpretation and use of polygenic risk scores (PRSs). We argue that PRSs generally do not directly embody causal information. Nonetheless, they can assist us in tracking other causal relationships concerning genetic effects. Although their purely predictive/correlational use is important, it is this tracking feature that contributes to their potential usefulness in other applications, such as genetic dissection, and their use as controls, which allow us, indirectly, to "see" more clearly the role of environmental variables.

This paper defends an interventionist treatment of mechanisms and contrasts this with Waskan (forthcoming). Interventionism embodies a difference-making conception of causation. I contrast such conceptions with geometrical/mechanical or “actualist” conceptions, associating Waskan’s proposals with the latter. It is argued that geometrical/mechanical conceptions of causation cannot replace difference-making conceptions in characterizing the behavior of mechanisms, but that some of the intuitions behind the geometrical/mechanical approach can be captured by thinking in terms of spatio-temporally organized difference-making information.

This paper responds to recent criticisms of the idea that true causal claims, satisfying a minimal “interventionist” criterion for causation, can differ in the extent to which they satisfy other conditions—called stability and proportionality—that are relevant to their use in explanatory theorizing. It reformulates the notion of proportionality so as to avoid problems with previous formulations. It also introduces the notion of conditional independence or irrelevance, which I claim is central to understanding the respects and the extent to which upper (...) level explanations can be “autonomous”. (shrink)

This essay advocates a “functional” approach to causation and causal reasoning: these are to be understood in terms of the goals and purposes of causal thinking. This approach is distinguished from accounts based on metaphysical considerations or on reconstruction of “intuitions.”.

Griffiths et al. (2015) have proposed a quantitative measure of causal specificity and used it to assess various attempts to single out genetic causes as being causally more specific than other cellular mechanisms, for example, alternative splicing. Focusing in particular on developmental processes, they have identified a number of important challenges for this project. In this discussion note, I would like to show how these challenges can be met.

The recent literature on causality has seen the introduction of several distinctions within causality, which are thought to be important for understanding the widespread scientific practice of focusing causal explanations on a subset of the factors that are causally relevant for a phenomenon. Concepts used to draw such distinctions include, among others, stability, specificity, proportionality, or actual-difference making. In this contribution, I propose a new distinction that picks out an explanatorily salient class of causes in biological systems. Some select causes (...) in complex biological systems, I argue, have the property of enabling coherent causal control of these systems. Examples of such control variables include hormones and other signaling molecules, e.g., TOR (target of rapamycin), morphogens or the products of homeotic selector genes in embryonic pattern formation. I propose an analysis of this notion based on concepts borrowed from causal graph theory. (shrink)

We propose a formal framework for interpretable machine learning. Combining elements from statistical learning, causal interventionism, and decision theory, we design an idealised explanation game in which players collaborate to find the best explanation for a given algorithmic prediction. Through an iterative procedure of questions and answers, the players establish a three-dimensional Pareto frontier that describes the optimal trade-offs between explanatory accuracy, simplicity, and relevance. Multiple rounds are played at different levels of abstraction, allowing the players to explore overlapping causal (...) patterns of variable granularity and scope. We characterise the conditions under which such a game is almost surely guaranteed to converge on a optimal explanation surface in polynomial time, and highlight obstacles that will tend to prevent the players from advancing beyond certain explanatory thresholds. The game serves a descriptive and a normative function, establishing a conceptual space in which to analyse and compare existing proposals, as well as design new and improved solutions. (shrink)

We propose a formal framework for interpretable machine learning. Combining elements from statistical learning, causal interventionism, and decision theory, we design an idealisedexplanation gamein which players collaborate to find the best explanation(s) for a given algorithmic prediction. Through an iterative procedure of questions and answers, the players establish a three-dimensional Pareto frontier that describes the optimal trade-offs between explanatory accuracy, simplicity, and relevance. Multiple rounds are played at different levels of abstraction, allowing the players to explore overlapping causal patterns of (...) variable granularity and scope. We characterise the conditions under which such a game is almost surely guaranteed to converge on a (conditionally) optimal explanation surface in polynomial time, and highlight obstacles that will tend to prevent the players from advancing beyond certain explanatory thresholds. The game serves a descriptive and a normative function, establishing a conceptual space in which to analyse and compare existing proposals, as well as design new and improved solutions. (shrink)

In their paper “How Causal are Microbiomes? A Comparison with the Helicobacter pylori Explanation of Ulcers,” Lynch, Parke, and O’Malley successfully argue that certain causal attributions made to the microbiome have not satisfied Koch’s postulates nor the interventionist framework. However, their argument involves an implicit assumption that cases such as H. pylori are sufficiently similar to cases involving the microbiome, such that causal attributions to both should be evaluated according to the same causal framework. Our commentary targets this assumption. First, (...) we introduce the historical circumstances that led to the formulation of Koch’s postulates in order to differentiate the case of the microbiome from that of infectious bacteria. Then, we introduce the concept of the holobiont, the idea that hosts and their symbionts should be conceptualized as a metaphysical and biological unit. Finally, using the holobiont concept, we argue that Koch’s postulates and the interventionist framework are ill-equipped to handle the microbiome. We conclude by suggesting that a revision of what counts as microbiological causality within the holobiont is justified. (shrink)

Most psychological research aims to uncover generalizations about the mind that hold across subjects. Philosophical discussions of scientific explanation have focused on such generalizations, but in doing so, have often overlooked an important phenomenon: variation. Variation is ubiquitous in psychology and many other domains, and an important target of explanation in its own right. Here I characterize explananda that concern individual differences and formulate an account of what it takes to explain them. I argue that the notion of actual difference (...) making, the only causal concept in the literature that explicitly addresses variation, cannot be used to ground such an account. Instead, I propose a view on which explaining individual differences involves identifying causes that could be intervened on to reduce the variability in the population. This account provides criteria of success for explaining variation and deepens our understanding of causal explanation. (shrink)

Niche Construction Theory has been gaining acceptance as an explanatory framework for processes in biological and human evolution. Human cultural niche construction, in particular, is suggested as a basis for understanding many phenomena that involve human genetic and cultural evolution. Herein I assess the ability of the cultural niche construction framework to meet this explanatory role by looking into several NCT-inspired accounts that have been offered for two important episodes of human evolution, and by examining the contribution of NCT to (...) the elucidation of two “primary examples” mentioned often in the NCT literature. The result, I claim, is rather disappointing: While NCT may serve as a descriptive framework for these phenomena, it cannot be said to explain them in any substantive sense. Especially disturbing is NCT’s failure to account for differing developments in very similar situations, and to facilitate evaluation and discrimination between divergent and contradictory causal accounts of particular phenomena. I argue that these problems are inherent, and they render NCT unsuitable to serve as an explanatory framework for human phenomena. NCT’s value, at least as related to human phenomena, is therefore descriptive and heuristic rather than explanatory. In conclusion, I discuss and reject comparisons made between NCT and the theory of natural selection, and examine several potential sources of NCT’s explanatory weakness. (shrink)

A notion of delegated causality is introduced here. This subtle kind of causality is dual to interventional causality. Delegated causality elucidates the causal role of dynamical systems at the “edge of chaos”, explicates evident cases of downward causation, and relates emergent phenomena to Gödel’s incompleteness theorem. Apparently rich implications are noticed in biology and Chinese philosophy. The perspective of delegated causality supports cognitive interpretations of self-organization and evolution.

In the postgenomic era, interactions between organism and environment are central in disciplines such as epigenetics, medical physiology, and immunology. Particularly in the more "applied" medical fields, an emphasis lies on interactions of the organism with other organisms, that is, other living things. There is, however, a growing amount of research investigating the impact of abiotic triggers on the immune system. While the distinction between biota and abiota features heavily in other contexts, its status is not explicit within immunology. Do (...) immunologists distinguish living from nonliving triggers? In this article, I will carve out whether and in which ways the biotic/abiotic distinction operates in immunology. I will look into responses to biotic and abiotic stressors in plant and invertebrate model species and ask how and why they are conceptually separated. I will trace the reasons by investigating the disciplinary situatedness of immune phenomena and the import of vertebrate immunology when conceptualizing immune responses in other model organisms. I will then investigate how the convergence of biotic and abiotic stress responses in plants and invertebrates adds to the recent philosophical programs advocating an ecological perspective on immune systems. (shrink)

The discovery of RNA interference in 1998 has made a lasting impact on biological research. Identifying the regulatory role of small RNAs changed the modes of molecular biological inquiry as well as biologists' understanding of genetic regulation. This article examines the early years of small RNA biology's success story. I query which factors had to come together so that small RNA research came into life in the blink of an eye. I primarily look at scientific repertoires as facilitators of rapid (...) scientific change. I show that for a short period of time, between the years 1998 and 2002, different model organism communities, investigative strategies, technological innovations, and research interests could be successfully aligned to take small RNA research off the ground. I discuss how the keystone discoveries were situated in specific experimental traditions and what strategies were employed to establish these discoveries as more general phenomena. Providing thus a practice-based approach of rapid scientific change, I ask how to relate the change in propositional bits of scientific knowledge with changes in scientific practice. (shrink)

Biologists and philosophers often use the language of determination in order to describe the nature of developmental phenomena. Accounts in terms of determination have often been reductionist. One common idea is that DNA is supposed to play a special explanatory role in developmental explanations, namely, that DNA is a developmental determinant. In this article we try to make sense of determination claims in developmental biology. Adopting a manipulationist approach, we shall first argue that the notion of developmental determinant is causal. (...) We suggest that two different theses concerning developmental determination can be articulated: determination of occurrence and structural determination. We shall argue that, while the first thesis is problematic, the second, opportunely qualified, is feasible. Finally, we shall argue that an analysis of biological causation in terms of determination cannot account for entangled dynamics. Characterising causal entanglement as a particular kind of interactive causation whereby difference-making causes ascribable to different levels of biological organisation influence a particular ontogenetic outcome, we shall, via two illustrative examples, diagnose some potential limits of a reductionist, molecular and intra-level understanding of biological causation. (shrink)

We report three experiments investigating whether people’s judgments about causal relationships are sensitive to the robustness or stability of such relationships across a range of background circumstances. In Experiment 1, we demonstrate that people are more willing to endorse causal and explanatory claims based on stable (as opposed to unstable) relationships, even when the overall causal strength of the relationship is held constant. In Experiment 2, we show that this effect is not driven by a causal generalization’s actual scope of (...) application. In Experiment 3, we offer evidence that stable causal relationships may be seen as better guides to action. Collectively, these experiments document a previously underappreciated factor that shapes people’s causal reasoning: the stability of the causal relationship. (shrink)

This paper aims to clarify the nature of understanding in medicine. The first part describes in more detail what it means to understand something and links a type of understanding (i.e., objectual understanding) to explanations. The second part proceeds to investigate what objectual understanding of a disease (i.e., biomedical understanding) requires by considering the case of scurvy from the history of medicine. The main hypothesis is that grasping a mechanistic explanation of a condition is necessary for a biomedical understanding of (...) that condition. The third part of the paper argues that biomedical understanding is necessary, but not sufficient for understanding in a clinical context (i.e., clinical understanding). The hypothesis is that clinical understanding combines biomedical understanding of a _disease_ or pathological condition with understanding _illness,_ which involves some degree of personal understanding of the patient. It is argued that, in many cases, clinical understanding necessitates adopting a particular second-personal stance and using cognitive resources _in addition_ to those involved in biomedical understanding. (shrink)

Philosophy of epidemiology has recently emerged as a distinct branch of philosophy. The field will surely benefit from pluralism, reflected in the broad range of topics and perspectives in this special issue. Here, I argue that a healthy pluralistic field of philosophy of epidemiology has social responsibilities that require the field as a whole to engage actively with research on social determinants of health and health disparities. Practicing epidemiologists and the broader community of public health scientists have gradually acknowledged that (...) much of their attention ought to be paid to these, i.e. inequitable between-population health variations that largely reflect the world’s inequitable distribution of resources and social conditions. The paper illustrates how and why health disparities and social determinants of health, through no ill will, become de facto secondary concerns in Alex Broadbent’s field-defining Philosophy of Epidemiology, showing the ease with which these topics can be incidentally sidelined. As means for philosophy of epidemiology to meet its social responsibility obligations, I suggest philosophy of epidemiology expand its attention to two particular lines research. First, the paper discusses Geoffrey Rose’s concept of “causes of incidence”—causes of disparities between populations—and argues for the importance of engaging with these causes. Second, the paper argues for the value of engaging with Bruce Link and Jo Phelan’s “fundamental causes” model of how flexible social resources serve as buffers from harms, generating a plethora of shifting and locally-contingent health effects. (shrink)

Mooreans claim that intrinsic goodness is a conceptual primitive. Fitting-attitude theorists object: they say that goodness should be defined in terms of what it is fitting for us to value. The Moorean view is often considered a relic; the fitting-attitude view is increasingly popular. I think this unfortunate. Though the fitting-attitude analysis is powerful, the Moorean view is still attractive. I dedicate myself to the influential arguments marshaled against Moore’s program, including those advanced by Scanlon, Stratton-Lake and Hooker, and Jacobson; (...) I argue that they do not succeed. (shrink)

I develop and defend a maximizing theory of moral motivation: I claim that consequentialists should recommend only those desires, emotions, and dispositions that will make the outcome best. I advance a conservative account of the motives that are possible for us; I say that a motive is an alternative if and only if it is in our psychological control. The resulting theory is less demanding than its competitors. It also permits us to maintain many of the motivations that we value (...) most, including our love for those most important to us. I conclude that we are closer to meeting morality’s demands on our character than has been appreciated. (shrink)

Establishing the effectiveness of medical treatments is one of the most important aspects of medical practice. Bradford Hill's viewpoints play an important role in inferring causality in medicine,...

In this paper I develop a concept of behavioural ecological individuality. Using findings from a case study which employed qualitative methods, I argue that individuality in behavioural ecology should be defined as phenotypic and ecological uniqueness, a concept that is operationalised in terms of individual differences such as animal personality and individual specialisation. This account make sense of how the term “individuality” is used in relation to intrapopulation variation in behavioural ecology. The concept of behavioural ecological individuality can sometimes be (...) used to identify individuals. It also shapes research agendas and methodological choices in behavioural ecology, leading researchers to account for individuals as sources of variation. Overall, this paper draws attention to a field that has been largely overlooked in philosophical discussions of biological individuality and highlights the importance of individual differences and uniqueness for individuality in behavioural ecology. (shrink)

Behavioral economists have proposed that people are subject to an IKEA effect, whereby they attach greater value to products they make for themselves, like IKEA furniture, than to otherwise indiscernible goods. Recently, cognitive psychologist Tom Stafford has suggested there may be an epistemic analog to this, a kind of epistemic IKEA effect. In this paper, I use Stafford’s suggestion to defend a certain thesis about epistemic value. Specifically, I argue that there is a distinctive epistemic value in being an active (...) producer of epistemic goods, like true belief, as opposed to just a passive recipient of such goods, and that because of this it can be rationally permissible to sacrifice truth in a certain way for the sake of this other value. In particular, it is rationally permissible for an epistemic agent to prefer a belief set that contains fewer overall truths but more truths obtained through the agent’s own intellectual labor, in something like the way that a practical agent might prefer furniture they have made through their own manual labor to inherently superior furniture made by someone else. In making my case, I draw on Ernest Sosa’s discussion of causation and praxical epistemic values, and Jennifer Lackey’s testimony-based criticism of the credit view of knowledge. After defending my thesis about epistemic value, I further clarify it by connecting it to the focus of Stafford’s discussion, conspiracy theorists. (shrink)

Behavioral economists have proposed that people are subject to an IKEA effect, whereby they attach greater value to products they make for themselves, like IKEA furniture, than to otherwise indiscernible goods. Recently, cognitive psychologist Tom Stafford has suggested there may be an epistemic analog to this, a kind of epistemic IKEA effect. In this paper, I use Stafford’s suggestion to defend a certain thesis about epistemic value. Specifically, I argue that there is a distinctive epistemic value in being an active (...) producer of epistemic goods, like true belief, as opposed to just a passive recipient of such goods, and that because of this it can be rationally permissible to sacrifice truth in a certain way for the sake of this other value. In particular, it is rationally permissible for an epistemic agent to prefer a belief set that contains fewer overall truths but more truths obtained through the agent’s own intellectual labor, in something like the way that a practical agent might prefer furniture they have made through their own manual labor to inherently superior furniture made by someone else. In making my case, I draw on Ernest Sosa’s discussion of causation and praxical epistemic values, and Jennifer Lackey’s testimony-based criticism of the credit view of knowledge. After defending my thesis about epistemic value, I further clarify it by connecting it to the focus of Stafford’s discussion, conspiracy theorists. (shrink)

A central argument for non-reductive accounts of group agency is that complex social entities are capable of exerting causal influence independently of and superseding the causal efficacy of the individuals constituting them. A prominent counter is that non-reductionists run into an insuperable dilemma between identity and redundancy – with identity undermining independent higher-level efficacy and redundancy leading to overdetermination or exclusion. This paper argues that critics of non-reductionism can manage with a simpler and more persuasive reductio strategy called mapping: allow (...) that group agents are causally efficacious in their own right and chart how their causal efficacy is carried out; how it relates to the causal efficacy of individual determiners; how it connects to the causal relevance of background structural factors. The focus exclusively on whether groups are or are not causally efficacious black-boxes implementation, while close attention to how causation is wired increases the visibility of individualist arguments and countenances structure-oriented explanations. (shrink)

Recently, many have argued that there are certain kinds of abstract mathematical explanations that are noncausal. In particular, the irrelevancy approach suggests that abstracting away irrelevant causal details can leave us with a noncausal explanation. In this paper, I argue that the common example of Renormalization Group explanations of universality used to motivate the irrelevancy approach deserves more critical attention. I argue that the reasons given by those who hold up RG as noncausal do not stand up to critical scrutiny. (...) As a result, the irrelevancy approach and the line between casual and noncausal explanation deserves more scrutiny. (shrink)

Causal selection and priority are at the heart of discussions of the causal parity thesis, which says that all causes of a given effect are on a par, and that any justified priority assigned to a given cause results from causal explanatory interests. In theories of causation that provide necessary and sufficient conditions for the truth of causal claims, status as cause is an either/or issue: either a given cause satisfies the conditions or it does not. Consequently, assessments of causal (...) parity and priority require more resources, which can either be additional or part of the causal analysis itself. While adding resources in terms of a theory of causal explanation has been standard, here we develop a unified conceptual analysis that includes a range of different precise causal concepts that allows for assessments of causal priority in terms of different kinds of causal relevance. (shrink)