A crucial question for a process view of life is how to identify a process and how to follow it through time. The genidentity view can contribute decisively to this project. It says that the identity through time of an entity X is given by a well-identified series of continuous states of affairs. Genidentity helps address the problem of diachronic identity in the living world. This chapter describes the centrality of the concept of genidentity for David Hull and proposes an (...) extension of Hull’s view to the ubiquitous phenomenon of symbiosis. Finally, using immunology as a key example, it shows that the genidentity view suggests that the main interest of a process approach is epistemological rather than ontological and that its principal claim is one of priority, namely that processes precede and define things, and not vice versa. (shrink)

Griffiths and Russell D. Gray (1994, 1997, 2001) have argued that the fundamental unit of analysis in developmental systems theory should be a process – the life cycle – and not a set of developmental resources and interactions between those resources. The key concepts of developmental systems theory, epigenesis and developmental dynamics, both also suggest a process view of the units of development. This chapter explores in more depth the features of developmental systems theory that favour treating processes as fundamental (...) in biology and examines the continuity between developmental systems theory and ideas about process in the work of several major figures in early 20th century biology, most notable C.H Waddington. (shrink)

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)

The traditional practice of establishing morphological types and investigating morphological organization has found new support from evolutionary developmental biology (evo-devo), especially with respect to the notion of body plans. Despite recurring claims that typology is at odds with evolutionary thinking, evo-devo offers mechanistic explanations of the evolutionary origin, transformation, and evolvability of morphological organization. In parallel, philosophers have developed non-essentialist conceptions of natural kinds that permit kinds to exhibit variation and undergo change. This not only facilitates a construal of species (...) and higher taxa as natural kinds, but also broadens our perspective on the diversity of kinds found in biology. There are many different natural kinds relevant to the investigative and explanatory aims of evo-devo, including homologues and developmental modules. (shrink)

Evo-devo is a multidisciplinary field that investigates the interplay between evolutionary and developmental processes and brings together different kinds of explanatory strategies. This chapter examines the structure of paradigmatic explanations in evo-devo (e.g., the explanation of the origin of an evolutionary novelty) and raises philosophical questions about explanation in evo-devo. Much research in evo-devo is concerned with studying the developmental mechanisms that constrain and facilitate phenotypic evolution, which suggests that a distinctive feature of evo-devo is that it constructs mechanistic explanations. (...) In this chapter, I discuss three major challenges for thinking about evo-devo as providing mechanistic explanations. First, an explanation of an evolutionary novelty consists of several mechanistic explanations, rather than being a single one. Second, developmental mechanisms are ontogenetically and phylogenetically dynamic and thus difficult to individuate. Third, an explanation of an evolutionary novelty also has a non-mechanistic, historical part. Finally, I discuss whether evo-devo’s emphasis on mechanistic explanation promotes explanatory integration or results in a reductionist view of evolution. (shrink)

Philosophers of biology typically pose questions about individuation by asking “what is an individual?” For example, we ask, “what is an individual species”, “what is an individual organism”, and “what is an individual gene?” In the first part of this chapter, I present my account of the gene concept and how it is used in investigative practices in order to motivate a more pragmatic approach. Instead of asking “what is a gene?”, I ask: “how do biologists individuate genes?”, “for what (...) purposes?”, and “do their practices of individuating genes serve these purposes?" In the second part of this chapter, I propose that we use this approach when analyzing concepts of organisms and biological individuals. Following philosophical pragmatism, I argue that we should abstain from attempts to situate individuation of Darwinian individuals or of holobionts in a philosophy of nature. Instead, we should analyze practices of individuating organisms in terms of three-place relations between the world, ideas, and human purposes and actions. I conclude with three lessons: an ontological, an epistemological, and a meta-philosophical lesson, which I suggest, apply to philosophy of science generally and to philosophy and metaphysics at large. (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 edited collection showcases some of the best recent research in the philosophy of science. It comprises of thematically arranged papers presented at the 5th conference of the European Philosophy of Science Association (EPSA15), covering a broad variety of topics within general philosophy of science, and philosophical issues pertaining to specific sciences. The collection will appeal to researchers with an interest in the philosophical underpinnings of their own discipline, and to philosophers who wish to study the latest work on the (...) themes discussed. (shrink)

Reduction and reductionism have been central philosophical topics in analytic philosophy of science for more than six decades. Together they encompass a diversity of issues from metaphysics and epistemology. This article provides an introduction to the topic that illuminates how contemporary epistemological discussions took their shape historically and limns the contours of concrete cases of reduction in specific natural sciences. The unity of science and the impulse to accomplish compositional reduction in accord with a layer-cake vision of the sciences, the (...) seminal contributions of Ernest Nagel on theory reduction and how they strongly conditioned subsequent philosophical discussions, and the detailed issues pertaining to different accounts of reduction that arise in both physical and biological science (e.g., limit-case and part-whole reduction in physics, the difference-making principle in genetics, and mechanisms in molecular biology) are explored. The conclusion argues that the epistemological heterogeneity and patchwork organization of the natural sciences encourages a pluralist stance about reduction. (shrink)

Among the many causes of an event, how do we distinguish the important ones? Are there ways to distinguish among causes on principled grounds that integrate both practical aims and objective knowledge? Psychologist Tania Lombrozo has suggested that causal explanations “identify factors that are ‘exportable’ in the sense that they are likely to subserve future prediction and intervention” (Lombrozo 2010, 327). Hence portable causes are more important precisely because they provide objective information to prediction and intervention as practical aims. However, (...) I argue that this is only part of the epistemology of causal selection. Recent work on portable causes has implicitly assumed them to be portable within the same causal system at a later time. As a result, it has appeared that the objective content of causal selection includes only facts about the causal structure of that single system. In contrast, I present a case study from systems biology in which scientists are searching for causal factors that are portable across rather than within causal systems. By paying careful attention to how these biologists find portable causes, I show that the objective content of causal selection can extend beyond the immediate systems of interest. In particular, knowledge of the evolutionary history of gene networks is necessary for correctly identifying causal patterns in these networks that explain cellular behavior in a portable way. (shrink)

We describe an approach to measuring biological information where ‘information’ is understood in the sense found in Francis Crick’s foundational contributions to molecular biology. Genes contain information in this sense, but so do epigenetic factors, as many biologists have recognized. The term ‘epigenetic’ is ambiguous, and we introduce a distinction between epigenetic and exogenetic inheritance to clarify one aspect of this ambiguity. These three heredity systems play complementary roles in supplying information for development. -/- We then consider the evolutionary significance (...) of the three inheritance systems. Whilst the genetic inheritance system was the key innovation in the evolution of heredity, in modern organisms the three systems each play important and complementary roles in heredity and evolution. -/- Our focus in the earlier part of the paper is on ‘proximate biology’, where information is a substantial causal factor that causes organisms to develop and causes offspring to resemble their parents. But much philosophical work has focused on information in ‘ultimate biology’. Ultimate information is a way of talking about the evolutionary design of the mechanisms of development and inheritance. We conclude by clarifying the relationship between the two. Ultimate information is not a causal factor that acts in development or heredity, but it can help to explain the evolution of proximate information, which is. (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 article compares causal and constitutive explanation. While scientific inquiry usually addresses both causal and constitutive questions, making the distinction is crucial for a detailed understanding of scientific questions and their interrelations. These explanations have different kinds of explananda and they track different sorts of dependencies. Constitutive explanations do not address events or behaviors, but causal capacities. While there are some interesting relations between building and causal manipulation, causation and constitution are not to be confused. Constitution is a synchronous and (...) asymmetric relation between relata that cannot be conceived as independent existences. However, despite their metaphysical differences, the same key ideas about explanation largely apply to both. Causal and constitutive explanations face similar challenges (such as the problems of relevance and explanatory regress) and both are in the business of mapping networks of counterfactual dependence—i.e. mechanisms—although the relevant counterfactuals are of a different sort. In the final section the issue of developmental explanation is discussed. It is argued that developmental explanations deserve their own place in taxonomy of explanations, although ultimately developmental dependencies can be analyzed as combinations of causal and constitutive dependencies. Hence, causal and constitutive explanation are distinct, but not always completely separate forms of explanation. (shrink)

This paper attempts to elucidate three characteristics of causal relationships that are important in biological contexts. Stability has to do with whether a causal relationship continues to hold under changes in background conditions. Proportionality has to do with whether changes in the state of the cause “line up” in the right way with changes in the state of the effect and with whether the cause and effect are characterized in a way that contains irrelevant detail. Specificity is connected both to (...) David Lewis’ notion of “influence” and also with the extent to which a causal relation approximates to the ideal of one cause–one effect. Interrelations among these notions and their possible biological significance are also discussed. (shrink)

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)

Leading philosophical accounts presume that Thomas H. Morgan’s transmission theory can be understood independently of experimental practices. Experimentation is taken to be relevant to confirming, rather than interpreting, the transmission theory. But the construction of Morgan’s theory went hand in hand with the reconstruction of the chief experimental object, the model organism Drosophila melanogaster . This raises an important question: when a theory is constructed to account for phenomena in carefully controlled laboratory settings, what knowledge, if any, indicates the theory’s (...) relevance to phenomena outside highly controlled settings? The answer, I argue, is found within the procedural knowledge embedded within laboratory practice. †To contact the author, please write to: Minnesota Center for Philosophy of Science, University of Minnesota, Department of Philosophy, 831 Heller Hall, 271 19th Ave., University of Minnesota, Minneapolis, MN 55455‐0310; e‐mail: [email protected]. (shrink)

Philosophers’ traditional emphasis on theories, theoretical modeling, and explanation misguides research in philosophy of science. Articulating and applying core theories is part of scientific practice, but it is not the essence of scientific practice. Insofar as science has an essence, it is to systematically investigate and learn about what is not yet understood. This lecture analyzes genetics to articulate a broad-practice-centered approach to philosophy of science. It concludes by arguing that this approach can lead to richer, deeper, and more useful (...) philosophies of science, philosophies that can better inform science policy and the public’s understanding of science. (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)

We do not all make choices, reason, interpret our experience, or respond to our environment in the same way. A recent surge of scientific interest has thrust these individual differences into the spotlight: researchers in cognitive psychology and neuroscience are now devoting increasing attention to cognitive variation. The philosophical dimensions of this research, however, have yet to be systematically explored. Here I make an initial foray by considering how cognitive variation is characterized. I present a central dilemma facing descriptions of (...) individual differences, discuss several distinctions used to categorize variation, and show that these distinctions require further elaboration. Finally, by canvassing several philosophical topics for which the characterization of cognitive variation may have significant implications, I argue that philosophers should take note of how and why our minds differ. (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)

In this paper we consider mechanistic explanations for biologic malfunctions. Drawing on Lipton’s work on difference making, we offer three reasons why one should distinguish i) mechanistic features that only make a difference to the malfunction one aims to explain, from ii) features that make a difference to both the malfunction and normal functioning. Recognition of the distinction is important for a) repair purposes, b) mechanism discovery, and c) understanding. This analysis extends current mechanistic thinking, which fails to appreciate the (...) distinction. We illustrate our contribution with a case on sleeping disorders as arising from disruptions of circadian rhythms. (shrink)

In the Meno, Phaedo, and Phaedrus, Plato outlines the controversial thesis of a priori knowledge that all learning is a form of recollection—anamnesis. He uses this as an argument for the immortality of the soul via reincarnation. Because of this latter claim, the thesis is widely mocked by contemporary evolutionarily-informed materialists. But we can safely reject the metaphysical claim without abandoning the insight of the epistemological one. And indeed, modern evolutionary theory can explain how learning—at least of the sort that (...) depends on certain a priori concepts—can be a kind of recollection. Through this metaphor, natural selection is a process by which information about the world is transmitted across time. When we learn by reasoning about a priori knowledge, then, we in an important sense rely on information in our genomes—if not our souls—information acquired by the process of natural selection—if not conscious acquisition. Thinking of a priori knowledge with the metaphor of anamnesis elucidates two essential features of the relationship between epistemology and ontology. First, it emphasizes that there is necessarily a time-delay between our a priori knowledge and the universe to which it bears a relationship, if any. Second, it clarifies that a priori knowledge is knowledge that enhances reproductive fitness—which could well be because it reflects ontology faithfully, but could as easily be a kind of innate nominalism. (shrink)

Philosophers of science have developed an account of causal-mechanical explanation that captures regularity, but this account neglects variation. In this article I amend the philosophy of mechanisms to capture variation. The task is to explicate the relationship between regular causal mechanisms responsible for individual development and causes of variation responsible for variation in populations. As it turns out, disputes over this relationship have rested at the heart of the nature–nurture debate. Thus, an explication of the relationship between regular causal mechanisms (...) and causes of variation and between individual development and variation offers both the necessary amendment to the philosophy of mechanisms and the resources to mediate the dispute. (shrink)

I argue for the thesis that causal evidence is context-dependent. The same causal claim may be warranted by the same piece of evidence in one context but not another. I show this in particular for the type of causal evidence characteristic of the manipulability theory defended by Woodward (Making things happen: a theory of causal explanation. Oxford University Press, Oxford, 2003). My thesis, however, generalises to other theories—and at the end of the paper I outline the generalization to counterfactual theories. (...) The paradigmatic form of causal evidence in the manipulability theory is provided by tests of the functional invariance of the relation between putative cause and effect under interventions (on the putative cause). I show that such evidence exhibits at least two kinds of context-relativity: personal, or epistemic; and situational, or objective. (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)

A central idea of developmental systems theory is ‘parity’ or ‘symmetry’ between genes and non-genetic factors of development. The precise content of this idea remains controversial, with different authors stressing different aspects and little explicit comparisons among the various interpretations. Here I characterise and assess several influential versions of parity.

Making sense of why something succeeded or failed is central to scientific practice: it provides an interpretation of what happened, i.e. an hypothesized explanation for the results, that informs scientists’ deliberations over their next steps. In philosophy, the realism debate has dominated the project of making sense of scientists’ success and failure claims, restricting its focus to whether truth or reliability best explain science’s most secure successes. Our aim, in contrast, will be to expand and advance the practice-oriented project sketched (...) by Arthur Fine in his work on the Natural Ontological Attitude. An important obstacle to articulating a positive program, we suggest, has been overlooking how scientists adopt standardized rules and procedures in order to define and operationalize meanings for success and failure relative to their situated goals. To help fill this gap, we introduce two new ideas, design specifications and track records, and show how they advance our ability to make sense of scientific modeling practices while maintaining a deflationary stance toward the realism debate. (shrink)

This paper develops axiomatic foundations for a probabilistic-interventionist theory of causal strength. Transferring methods from Bayesian confirmation theory, I proceed in three steps: I develop a framework for defining and comparing measures of causal strength; I argue that no single measure can satisfy all natural constraints; I prove two representation theorems for popular measures of causal strength: Pearl's causal effect measure and Eells' difference measure. In other words, I demonstrate these two measures can be derived from a set of plausible (...) adequacy conditions. The paper concludes by sketching future research avenues. (shrink)

It is widely agreed that an artwork having certain non-aesthetic properties explains its having a certain aesthetic property. One interesting feature of such an explanation is its selectivity—it cites only some of the non-aesthetic properties on which the presence of the aesthetic property depends. Hence a question arises as to what distinguishes the selected non-aesthetic properties from the unselected ones. I answer this question by proposing a selection principle modeled on Laura Franklin-Hall’s selection principle for causal explanation, according to which (...) an explanation selects a package of factors that maximizes the ratio of delivery to cost. (shrink)

We argue that Madole & Harden's distinction between shallow versus deep genetic causes can bring some clarity to causal claims arising from genome-wide association studies (GWASs). However, the authors argue that GWAS only finds shallow genetic causes, making GWAS commensurate with the environmental studies they hope to supplant. We also assess whether their distinction applies best to explanations or causes.

This paper challenges the common assumption that some phenotypic traits are quantitative while others are qualitative. The distinction between these two kinds of traits is widely influential in biological and biomedical research as well as in scientific education and communication. This is probably due to both historical and epistemological reasons. However, the quantitative/qualitative distinction involves a variety of simplifications on the genetic causes of phenotypic variability and on the development of complex traits. Here, I examine three cases from the life (...) sciences that show inconsistencies in the distinction: Mendelian traits, Mendelian diseases, and polygenic mental disorders. I show that these traits can be framed both quantitatively and qualitatively depending, for instance, on the methods through which they are investigated and on specific epistemic purposes. This suggests that the received view of quantitative and qualitative traits has a limited heuristic power—limited to some local contexts or to the specific methodologies adopted. Throughout the paper, I provide directions for framing phenotypes beyond the quantitative/qualitative distinction. I conclude by pointing at the necessity of developing a principled characterisation of what phenotypic traits, in general, are. (shrink)

An important function of scientific diagrams is to identify causal relationships. This commonly relies on contrasts that highlight the effects of specific difference-makers. However, causal contrast diagrams are not an obvious and easy to recognize category because they appear in many guises. In this paper, four case studies are presented to examine how causal contrast diagrams appear in a wide range of scientific reports, from experimental to observational and even purely theoretical studies. It is shown that causal contrasts can be (...) expressed in starkly different formats, including photographs of complexly visualized macromolecules as well as line graphs, bar graphs, or plots of state spaces. Despite surface differences, however, there is a measure of conceptual unity among such diagrams. In empirical studies they generally serve not only to infer and communicate specific causal claims, but also as evidence for them. The key data of some studies is given nowhere except in the diagrams. Many diagrams show multiple causal contrasts in order to demonstrate both that an effect exists and that the effect is specific -- that is, to narrowly circumscribe the phenomenon to be explained. In a large range of scientific reports, causal contrast diagrams reflect the core epistemic claims of the researchers. (shrink)

I critically assess two widely cited evolutionary biological arguments for two versions of the ‘Extended Mind Thesis’ (EMT): namely, an argument appealing to Dawkins’s ‘Extended Phenotype Thesis’ (EPT) and an argument appealing to ‘Developmental Systems Theory’ (DST). Specifically, I argue that, firstly, appealing to the EPT is not useful for supporting the EMT (in either version), as it is structured and motivated too differently from the latter to be able to corroborate or elucidate it. Secondly, I extend and defend Rupert’s (...) argument that DST also fails to support or elucidate the EMT (in either version) by showing that the considerations in favour of the former theory have no bearing on the truth of the latter. I conclude by noting that the relevance of this discussion goes beyond the debate surrounding the EMT, as it brings out some of the difficulties of introducing evolutionary biological considerations into debates in psychology and philosophy more generally. (shrink)

Causal assessment is the problem of establishing whether a relation between (variable) X and (variable) Y is causal. This problem, to be sure, is widespread across the sciences. According to accredited positions in the philosophy of causality and in social science methodology, invariance under intervention provides the most reliable test to decide whether X causes Y. This account of invariance (under intervention) has been criticised, among other reasons, because it makes manipulations on the putative causal factor fundamental for the causal (...) methodology; consequently, the argument goes, the account is ill-suited to those contexts where manipulations are not performed, for instance, the social sciences. The article aims to extend the account of invariance (under intervention), in a way that manipulations on the putative causal factors are not methodologically fundamental, and yet invariance remains key for causal assessment both in experimental and non-experimental contexts. (shrink)

Recent philosophical work on causation has focused on distinctions across types of causal relationships. This paper argues for another distinction that has yet to receive attention in this work. This distinction has to do with whether causal relationships have “material continuity,” which refers to the reliable movement of material from cause to effect. This paper provides an analysis of material continuity and argues that causal relationships with this feature are associated with a unique explanatory perspective, are studied with distinct causal (...) investigative methods, and provide different types of causal control over their effects. (shrink)