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)

Kerry et al. criticize our discussion of causal knowledge in evidence-based medicine (EBM) and our assessment of the relevance of their dispositionalist ontology for EBM. Three issues need to be addressed in response: (1) problems concerning transfer of causal knowledge across heterogeneous contexts; (2) how predictions about the effects of individual treatments based on population-level evidence from RCTs are fallible; and (3) the relevance of ontological theories like dispositionalism for EBM.

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.

Many philosophers are skeptical about the scientific value of the concept of biological information. However, several have recently proposed a more positive view of ascribing information as an exercise in scientific modeling. I argue for an alternative role: guiding empirical data collection for the sake of theorizing about the evolution of semantics. I clarify and expand on Bergstrom and Rosvall’s suggestion of taking a “diagnostic” approach that defines biological information operationally as a procedure for collecting empirical cases. The more recent (...) modeling-based accounts still perpetuate a theory-centric view of scientific concepts, which motivated philosophers’ misplaced skepticism in the first place. (shrink)

An astonishing volume and diversity of evidence is available for many hypotheses in the biomedical and social sciences. Some of this evidence—usually from randomized controlled trials (RCTs)—is amalgamated by meta-analysis. Despite the ongoing debate regarding whether or not RCTs are the ‘gold-standard’ of evidence, it is usually meta-analysis which is considered the best source of evidence: meta-analysis is thought by many to be the platinum standard of evidence. However, I argue that meta-analysis falls far short of that standard. Different meta-analyses (...) of the same evidence can reach contradictory conclusions. Meta-analysis fails to provide objective grounds for intersubjective assessments of hypotheses because numerous decisions must be made when performing a meta-analysis which allow wide latitude for subjective idiosyncrasies to influence its outcome. I end by suggesting that an older tradition of evidence in medicine—the plurality of reasoning strategies appealed to by the epidemiologist Sir Bradford Hill—is a superior strategy for assessing a large volume and diversity of evidence. (shrink)

The aim of this paper is to determine whether and to what extent Woodward’s interventionist theory of causation is variable relative. In an influential review, Strevens has accused Woodward’s account of a damaging form of variable relativity, according to which obviously false causal claims can be made true by choosing a depleted variable set. Following McCain, I show that Strevens’ objection doesn’t succeed. However, Woodward also wants to avoid another kind of variable relativity, according to which it can be true (...) that X is a cause of Y in one set of background conditions, but false in another. I show that Woodward’s account is problematically overpermissive, unless there are restrictions on the values that certain variables can take. I formulate a modified account that makes these restrictions explicit, then use it to argue that Woodward’s attempt to avoid relativity to background conditions is misguided. On the best interpretation of the interventionist theory, causal claims are assessed relative to a particular kind of variable set. Thus, I conclude that the theory should be understood as variable relative, in a specific, unproblematic sense. (shrink)

The aim of this virtual special issue is to bring together philosophical and historical perspectives to address long-standing issues in the interpretation, utility, and impacts of quantitative genetics methods and findings. Methodological approaches and the underlying scientific understanding of genetics and heredity have transformed since the field's inception. These advances have brought with them new philosophical issues regarding the interpretation and understanding of quantitative genetic results. The contributions in this issue demonstrate that there is still work to be done integrating (...) old and new methodological and conceptual frameworks. In some cases, new results are interpreted using assumptions based on old concepts and methodologies that need to be explicitly recognised and updated. In other cases, new philosophical tools can be employed to synthesise historical quantitative genetics work with modern methodologies and findings. This introductory article surveys three general themes that have dominated philosophical discussion of quantitative genetics throughout history: (1) how methodologies have changed and transformed our knowledge and interpretations; (2) whether or not quantitative genetics can offer explanations relating to causation and prediction; and (3) the importance of defining the phenotypes under study. We situate the contributions in this virtual special issue within a historical framework addressing these three themes. (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)

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)

Against the neo-Darwinian assumption that genetic factors are the principal source of variation upon which natural selection operates, a phenotype-first hypothesis strikes us as revolutionary because development would seem to constitute an independent source of variability. Richard Watson and his co-authors have argued that developmental memory constitutes one such variety of phenotypic variability. While this version of the phenotype-first hypothesis is especially well-suited for the late metazoan context, where animals have a sufficient history of selection from which to draw, appeals (...) to developmental memory seem less plausible in the evolutionary context of the early metazoans. I provide an interpretation of Stuart Newman’s account of deep metazoan phylogenesis that suggests that spandrels are, in addition to developmental memory, an important reservoir of phenotypic variability. I conclude by arguing that Gerd Müller’s “side-effect hypothesis” is an illuminating generalization of the proposed non-Watsonian version of the phenotype-first hypothesis. (shrink)

The philosophy of biology literature offers several arguments aimed at showing that information theory is conceptually unsuited to capture the informational talk in molecular biology. Such arguments led to the consensus that, if the informational talk in biology can be defended and explained at all, we need a different strategy. The debate, in fact, developed mostly along this line. However, recent contributions seem to (and even claim to) challenge the consensus and thus to vindicate the role and relevance of information (...) theory to this particular debate. In this paper, I examine the main arguments leading to such a consensus and I analyze the extent to which those recent accounts actually succeed in vindicating the invocation of information theory. I argue that these attempts fail to vindicate the information-theoretic strategy and, therefore, the consensus remains unaffected by them. (shrink)

In ‘Proportionality in Causation, Part I: Theories’, I presented various ways of understanding the idea that causes which are ‘proportional’ to their effects are in some sense preferable. In this companion article, I discuss the principal applications of the resulting theories of proportionality, and the challenges they face.

A much-discussed idea in the causation literature is that it is preferable to invoke causes which are proportional to—neither too general nor too specific for—the effect. This article presents various ways of understanding this idea. In what sense are such causal claims ‘preferable’? And what is it for one event to be ‘proportional’ to another? In a companion article, ‘Proportionality in Causation, Part II: Applications and Challenges’, I discuss the principal applications of the resulting theories of proportionality, and the challenges (...) they face. (shrink)

Social scientists appeal to various “structures” in their explanations including public policies, economic systems, and social hierarchies. Significant debate surrounds the explanatory relevance of these factors for various outcomes such as health, behavioral, and economic patterns. This paper provides a causal account of social structural explanation that is motivated by Haslanger (2016). This account suggests that social structure can be explanatory in virtue of operating as a causal constraint, which is a causal factor with unique characteristics. A novel causal framework (...) is provided for understanding these explanations–this framework addresses puzzles regarding the mysterious causal influence of social structure, how to understand its relation to individual choice, and what makes it the main explanatory (and causally responsible) factor for various outcomes. (shrink)

This article examines the multiple realizability thesis within a causal framework. The beginnings of this framework are found in Elliott Sober’s “Multiple Realizability Argument against Reduction,”...

We argue that Koch’s postulates are best understood within an interventionist account of causation, in the sense described in Woodward. We show how this treatment helps to resolve interpretive puzzles associated with Koch’s work and how it clarifies the different roles the postulates play in providing useful, yet not universal criteria for disease causation. Our paper is an effort at rational reconstruction; we attempt to show how Koch’s postulates and reasoning make sense and are normatively justified within an interventionist framework (...) and more difficult to understand within alternative frameworks for thinking about causation. (shrink)

According to mainstream philosophical views causal explanation in biology and neuroscience is mechanistic. As the term ‘mechanism’ gets regular use in these fields it is unsurprising that philosophers consider it important to scientific explanation. What is surprising is that they consider it the only causal term of importance. This paper provides an analysis of a new causal concept—it examines the cascade concept in science and the causal structure it refers to. I argue that this concept is importantly different from the (...) notion of mechanism and that this difference matters for our understanding of causation and explanation in science. (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)

Both ecologists and statistical physicists use a variety of highly idealized models to study active matter and self-organizing critical phenomena. In this paper, I show how universality classes play a crucial role in justifying the application of highly idealized ‘minimal’ models to explain and understand the critical behaviors of active matter systems across a wide range of scales and scientific fields. Appealing to universality enables us to see why the same minimal models can be used to explain and understand behaviors (...) across these different systems despite drastic differences in the causes and mechanisms responsible for the behaviors of interest. After analyzing these cases in detail, I argue that accounts that focus on identifying common causes or mechanisms in order to explain patterns are unable to accommodate these cases. In contrast, I argue that the justification for using these minimal models is that they are within the same universality class as real systems whose causes and mechanisms are known to be different. I also use these cases to identify several different kinds of explanatory autonomy that have important implications for how scientists ought to approach the modeling of multiscale phenomena. (shrink)

A prominent approach to scientific explanation and modeling claims that for a model to provide an explanation it must accurately represent at least some of the actual causes in the event's causal history. In this paper, I argue that many optimality explanations present a serious challenge to this causal approach. I contend that many optimality models provide highly idealized equilibrium explanations that do not accurately represent the causes of their target system. Furthermore, in many contexts, it is in virtue of (...) their independence of causes that optimality models are able to provide a better explanation than competing causal models. Consequently, our account of explanation and modeling must expand beyond the causal approach. (shrink)

Many accounts of scientific modelling assume that models can be decomposed into the contributions made by their accurate and inaccurate parts. These accounts then argue that the inaccurate parts of the model can be justified by distorting only what is irrelevant. In this paper, I argue that this decompositional strategy requires three assumptions that are not typically met by our best scientific models. In response, I propose an alternative view in which idealized models are characterized as holistically distorted representations that (...) are justified by allowing for the application of various modelling techniques. (shrink)

Renormalization group (RG) methods are an established strategy to explain how it is possible that microscopically different systems exhibit virtually the same macro behavior when undergoing phase-transitions. I argue – in agreement with Robert Batterman – that RG explanations are non-causal explanations. However, Batterman misidentifies the reason why RG explanations are non-causal: it is not the case that an explanation is non- causal if it ignores causal details. I propose an alternative argument, according to which RG explanations are non-causal explanations (...) because their explanatory power is due to the application mathematical operations, which do not serve the purpose of representing causal relations. (shrink)

What are ceteris paribus laws? Which disciplines appeal to cp laws and which semantics, metaphysical underpinning, and epistemological dimensions do cp law statements have? Firstly, we give a short overview of the recent discussion on cp laws, which addresses these questions. Secondly, we suggest that given the rich and diverse literature on cp laws a broad conception of cp laws should be endorsed which takes into account the different ways in which laws can be non-universal . Finally, we provide an (...) overview of the special issue on that basis and describe the individual contributions to the special issue according to the issues they address: the range of applications of cp laws as well as the semantics, metaphysics, and epistemology pertaining to cp law statements. (shrink)

In their influential paper “Ceteris Paribus, There is No Problem of Provisos”, Earman and Roberts (Synthese 118:439–478, 1999) propose to interpret the non-strict generalizations of the special sciences as statistical generalizations about correlations. I call this view the “statistical account”. Earman and Roberts claim that statistical generalizations are not qualified by “non-lazy” ceteris paribus conditions. The statistical account is an attractive view, since it looks exactly like what everybody wants: it is a simple and intelligible theory of special science laws (...) without the need for mysterious ceteris paribus conditions. I present two challenges to the statistical account. According to the first challenge, the statistical account does not get rid of so-called “non-lazy” ceteris paribus conditions. This result undermines one of the alleged and central advantages of the statistical account. The second challenge is that the statistical account, qua general theory of special science laws, is weakened by the fact that idealized law statements resist a purely statistical interpretation. (shrink)

In their Every Thing Must Go, Ladyman and Ross defend a novel version of Neo- Russellian metaphysics of causation, which falls into three claims: (1) there are no fundamental physical causal facts (orthodox Russellian claim), (2) there are higher-level causal facts of the special sciences, and (3) higher-level causal facts are explanatorily emergent. While accepting claims (1) and (2), I attack claim (3). Ladyman and Ross argue that higher-level causal facts are explanatorily emergent, because (a) certain aspects of these higher-level (...) facts (their universality) can be captured by renormalization group (RG) explanations, and (b) RG explanations are not reductive explanations. However, I argue that RG explanation should be understood as reductive explanations. This result undermines Ladyman and Ross’s RG-based argument for the explanatory emergence of higher-level causal facts. (shrink)

This paper describes one style of functional analysis commonly used in the neurosciences called task-bound functional analysis. The concept of function invoked by this style of analysis is distinctive in virtue of the dependence relations it bears to transient environmental properties. It is argued that task-bound functional analysis cannot explain the presence of structural properties in nervous systems. An alternative concept of neural function is introduced that draws on the theoretical neuroscience literature, and an argument is given to show that (...) this alternative concept of may help to overcome the explanatory limitations of task-bound functional analysis. (shrink)

How are scientific explanations possible in ecology, given that there do not appear to be many—if any—ecological laws? To answer this question, I present and defend an account of scientific causal explanation in which ecological generalizations are explanatory if they are invariant rather than lawlike. An invariant generalization continues to hold or be valid under a special change—called an intervention—that changes the value of its variables. According to this account, causes are difference-makers that can be intervened upon to manipulate or (...) control their effects. I apply the account to ecological generalizations to show that invariance under interventions as a criterion of explanatory relevance provides interesting interpretations for the explanatory status of many ecological generalizations. Thus, I argue that there could be causal explanations in ecology by generalizations that are not, in a strict sense, laws. I also address the issue of mechanistic explanations in ecology by arguing that invariance and modularity constitute such explanations. (shrink)

Griffiths and Stotz’s Genetics and Philosophy: An Introduction offers a very good overview of scientific and philosophical issues raised by present-day genetics. Examining, in particular, the questions of how a “gene” should be defined and what a gene does from a causal point of view, the authors explore the different domains of the life sciences in which genetics has come to play a decisive role, from Mendelian genetics to molecular genetics, behavioural genetics, and evolution. In this review, I highlight what (...) I consider as the two main theses of the book, namely: genes are better conceived as tools; genes become causes only in a context. I situate these two theses in the wider perspective of developmental systems theory. This leads me to emphasize that Griffiths and Stotz reflect very well an on going process in genetics, which I call the “epigenetization” of genetics, i.e., the growing interest in the complex processes by which gene activation is regulated. I then make a factual objection, which is that Griffiths and Stotz have almost entirely neglected the perspective of ecological developmental biology, and more precisely recent work on developmental symbioses, and I suggest that this omission is unfortunate in so far as an examination of developmental symbioses would have considerably strengthened Griffiths and Stotz’s own conclusions. (shrink)

A causal approach to biological information is outlined. There are two aspects to this approach: information as determining a choice between alternative objects and information as determining the construction of a single object. The first aspect has been developed in earlier work to yield a quantitative measure of biological information that can be used to analyze biological networks. This article explores the prospects for a measure based on the second aspect and suggests some applications for such a measure. These two (...) aspects are not suggested to exhaust all the facets of biological information. (shrink)

In 2015, Tomasetti and Vogelstein published a paper in Science containing the following provocative statement: “… only a third of the variation in cancer risk among tissues is attributable to environmental factors or inherited predispositions. The majority is due to “bad luck,” that is, random mutations arising during DNA replication in normal, noncancerous stem cells.” The paper—and perhaps especially this rather coy reference to “bad luck”—became a flash point for a series of letters and reviews, followed by replies and yet (...) further counterpoints. In this paper, I critically assess Tomasetti and Vogelstein's argument, discuss the meaning of “luck” (or, better: “chance”) in the context of the debate, and use this case study to address larger questions about methodological criteria for causal explanations of population level patterns in biomedicine. (shrink)

Cancer is not one, but many diseases, and each is a product of a variety of causes acting (and interacting) at distinct temporal and spatial scales, or “levels” in the biological hierarchy. In part because of this diversity of cancer types and causes, there has been a diversity of models, hypotheses, and explanations of carcinogenesis. However, there is one model of carcinogenesis that seems to have survived the diversification of cancer types: the multi-stage model of carcinogenesis. This paper examines the (...) history of the multistage theory, and uses the theory as a case study in the limits and goals of unification as a theoretical virtue, comparing and contrasting it with “integrative” research. (shrink)

Cancer is not one, but many diseases, and each is a product of a variety of causes acting at distinct temporal and spatial scales, or ‘‘levels’’ in the biological hierarchy. In part because of this diversity of cancer types and causes, there has been a diversity of models, hypotheses, and explanations of carcinogenesis. However, there is one model of carcinogenesis that seems to have survived the diversification of cancer types: the multi-stage model of carcinogenesis. This paper examines the history of (...) the multistage theory, and uses the theory as a case study in the limits and goals of unification as a theoretical virtue, comparing and contrasting it with ‘‘integrative’’ research. (shrink)

The status of genes as bearers of semantic content remains very much in dispute among philosophers of biology. In a series of papers, Nicholas Shea has argued that his ‘infotel’ theory of semantics vindicates the claim that genes carry semantic content. On Shea’s account, each organism is associated with a ‘developmental system’ that takes genetic representations as inputs and produces whole-organism traits as outputs. Moreover, at least in his most recent work on the topic, Shea is explicit in claiming that (...) these genetic representations are ‘read in ontogenetic time, in the course of individual development’. Here I argue that a close examination of the process of reading, in Shea’s sense, reveals that acts of reading do not actually occur over the course of developmental time at all. To make this vivid, I contrast the process of reading for Shea with another type of developmental process that is widely seen as a form of reading directed on inherited genes, and which certainly does occur over the course of developmental time, namely, gene expression. I suggest that this error in Shea’s thinking can be traced back to an equivocation on Shea’s part in the meaning of ‘reads’, and also to a reliance on an invalid principle regarding the transference of representational content from one token gene to another. The issues at play are bound up with questions about causation and in particular about causation over time. Thus, having first presented my arguments in a way that doesn’t depend on any particular theory of causation, I then make use of Kenneth Waters’ framework of difference-making causation to conceptually sharpen and shed further light on matters. I conclude by discussing a consequence of the fact that acts of reading do not occur in development. 1 Introduction2 Reading for Shea3 Gene Expression as Reading4 Are Genetic Representations Read in Development? Part 15 The Manipulability Theory of Causation and Difference-Making Causation6 Are Genetic Representations Read in Development? Part 27 Conclusion. (shrink)

There are several important criticisms against the unificationist model of scientific explanation: Unification is a broad and heterogeneous notion and it is hard to see how a model of explanation based exclusively on unification can make a distinction between genuine explanatory unification from cases of ordering or classification. Unification alone cannot solve the asymmetry and irrelevance problems. Unification and explanation pull in different directions and should be decoupled, because for good scientific explanation extra ad explanandum information is often required. I (...) am presenting a possible solution to those problems, by focusing on an often overlooked but important element of how theoretic unification is achieved—the conceptual frameworks of theories. The core conceptual assumptions behind theories are decisive for discriminating between explanatory and non-explanatory unification. The conceptual framework is also flexible enough to balance the tension between informativeness and maximum systematization in constructing explanatory inferences. A short case study of orthogenetic and Darwinian explanations in paleontology is presented as an illustration of how my addition to the unificationist model is applicable to a historical debate between rival explanations. (shrink)

The debate between the dynamical and the statistical interpretations of natural selection is centred on the question of whether all explanations that employ the concepts of natural selection and drift are reducible to causal explanations. The proponents of the statistical interpretation answer negatively, but insist on the fact that selection/drift arguments are explanatory. However, they remain unclear on where the explanatory power comes from. The proponents of the dynamical interpretation answer positively and try to reduce selection/drift arguments to some of (...) the most prominent accounts of causal explanation. In turn, they face the criticism raised by statisticalists that current accounts of causation have to be violated in some of their core conditions or otherwise used in a very loose manner in order to account for selection/drift explanations. We propose a reconciliation of both interpretations by conveying evolutionary explanations within the unificationist model of scientific explanation. Therefore, we argue that the explanatory power in natural selection arguments is a result of successful unification of individual- and population-level facts. A short case study based on research on sympatric speciation will be presented as an example of how population- and individual-level facts are unified to explain the morphological mosaic of bill shape in island scrub jays. (shrink)

A long-standing debate on the causality of levels in biological explanations has divided philosophers into two camps. The reductionist camp insists on the causal primacy of lower, molecular levels, while the critics point out the inescapable shifting, reciprocity, and circularity of levels across biological explanations. We argue, however, that many explanations in biology do not exclusively draw their explanatory power from detailed insights into inter-level interactions; they predominantly require identifying the adequate levels of biological complexity to be explained. Moreover, the (...) main explanatory strategies grounding both theoretical and experimental approaches to one of the central debates in contemporary biology, i.e., on the origin of life, are primarily and sometimes exclusively driven by issues concerning the levels of biochemical complexity, and these only subsequently frame more substantial and detailed accounts of inter-level biochemical interactions. (shrink)

This article reviews the causal exclusion argument and confronts it with some recently proposed refutations based on the interventionist account of causation. I first show that there are several technical and interpretative difficulties in applying the interventionist account to the exclusion issue. Different ways of accommodating the two to one another are considered and all are shown to leave the issue without a fully satisfactory resolution. Lastly, I argue that, on the most consistent construal, the interventionist approach can provide grounds (...) for thinking that higher-level causal notions are as legitimate as lower-level causal notions, but it does not provide grounds for postulating inter-level causal interactions. (shrink)

Interventionism is a theory of causation with a pragmatic goal: to define causal concepts that are useful for reasoning about how things could, in principle, be purposely manipulated. In its original presentation, Woodward’s interventionist definition of causation is relativized to an analyzed variable set. In Woodward, Woodward changes the definition of the most general interventionist notion of cause, contributing cause, so that it is no longer relativized to a variable set. This derelativization of interventionism has not gathered much attention, presumably (...) because it is seen as an unproblematic way to save the intuition that causal relations are objective features of the world. This paper first argues that this move has problematic consequences. Derelativization entails two concepts of unmediated causal relation that are not coextensional, but which nonetheless do not entail different conclusions about manipulability relations within any given variable set. This is in conflict with the pragmatic orientation at the core of interventionism. The paper then considers various approaches for resolving this tension but finds them all wanting. It is concluded that interventionist causation should not be derelativized in the first place. Various considerations are offered rendering that conclusion acceptable. (shrink)