The chapter explores whether, or to what extent, recent work in experimental philosophy puts pressure on the idea that the concept of causation is ‘egalitarian’. Causal selection – where experimental subjects tend to rate the causal strength of (for example) a norm-violator more strongly than a non-norm-violator – is a well established phenomenon, and is in prima facie tension with an egalitarian conception of causation; it also, indirectly, puts prima facie pressure on the idea that causation is (...) a worldly phenomenon whose obtaining is independent of facts about norms. The chapter explores both the various psychological mechanisms and the broadly pragmatic approaches to explaining causal selection. It argues that the answer to the question whether or not the concept of causation is egalitarian is currently significantly empirically underdetermined, and suggests some avenues for further investigation. (shrink)

Among the factors necessary for the occurrence of some event, which of these are selectively highlighted in its explanation and labeled as causes — and which are explanatorily omitted, or relegated to the status of background conditions? Following J. S. Mill, most have thought that only a pragmatic answer to this question was possible. In this paper I suggest we understand this ‘causal selection problem’ in causal-explanatory terms, and propose that explanatory trade-offs between abstraction and stability can (...) provide a principled solution to it. After sketching that solution, it is applied to a few biological examples, including to a debate concerning the ‘causal democracy’ of organismal development, with an anti-democratic (though not a gene-centric) moral. (shrink)

Causal selection is the task of picking out, from a field of known causally relevant factors, some factors as elements of an explanation. The Causal Parity Thesis in the philosophy of biology challenges the usual ways of making such selections among different causes operating in a developing organism. The main target of this thesis is usually gene centrism, the doctrine that genes play some special role in ontogeny, which is often described in terms of information-bearing or programming. (...) This paper is concerned with the attempt of confronting the challenge coming from the Causal Parity Thesis by offering principles of causal selection that are spelled out in terms of an explicit philosophical account of causation, namely an interventionist account. I show that two such accounts that have been developed, although they contain important insights about causation in biology, nonetheless fail to provide an adequate reply to the Causal Parity challenge: Ken Waters's account of actual-difference making and Jim Woodward's account of causal specificity. A combination of the two also doesn't do the trick, nor does Laura Franklin-Hall's account of explanation (in this volume). We need additional conceptual resources. I argue that the resources we need consist in a special class of counterfactual conditionals, namely counterfactuals the antecedents of which describe biologically normal interventions. (shrink)

Among the factors necessary for the occurrence of some event, which of these are selectively highlighted in its explanation and labeled as causes-and which are explanatorily omitted, or relegated to the status of background conditions? Following J. S. Mill, most have thought that only a pragmatic answer to this question was possible. In this paper I suggest we understand this ‘causal selection problem’ in causal-explanatory terms, and propose that explanatory trade-offs between abstraction and stability can provide a (...) principled solution to it. After sketching that solution, it is applied to a few biological examples. (shrink)

Causal selection is the task of picking out, from a field of known causally relevant factors, some factors as elements of an explanation. The Causal Parity Thesis in the philosophy of biology challenges the usual ways of making such selections among different causes operating in a developing organism. The main target of this thesis is usually gene centrism, the doctrine that genes play some special role in ontogeny, which is often described in terms of information-bearing or programming. (...) This paper is concerned with the attempt of confronting the challenge coming from the Causal Parity Thesis by offering principles of causal selection that are spelled out in terms of an explicit philosophical account of causation, namely an interventionist account. I show that two such accounts that have been developed, although they contain important insights about causation in biology, nonetheless fail to provide an adequate reply to the Causal Parity challenge: Ken Waters's account of actual-difference making and Jim Woodward's account of causal specificity. A combination of the two also doesn't do the trick, nor does Laura Franklin-Hall's account of explanation (in this volume). We need additional conceptual resources. I argue that the resources we need consist in a special class of counterfactual conditionals, namely counterfactuals the antecedents of which describe biologically normal interventions. (shrink)

Binding specificity is a centrally important concept in molecular biology, yet it has received little philosophical attention. Here I aim to remedy this by analyzing binding specificity as a causal property. I focus on the concept’s role in drug design, where it is highly prized and hence directly studied. From a causal perspective, understanding why binding specificity is a valuable property of drugs contributes to an understanding of causal selection—of how and why scientists distinguish between causes, (...) not just causes from noncauses. In particular, the specificity of drugs is precisely what underwrites their value as experimental interventions on biological processes. (shrink)

In The Biopsychosocial Model of Health and Disease, Derek Bolton and Grant Gillett argue that a defensible updated version of the biopsychosocial model requires a metaphysically adequate account of disease causation that can accommodate biological, psychological, and social factors. This present paper offers a philosophical critique of their account of biopsychosocial causation. I argue that their account relies on claims about the normativity and the semantic content of biological information that are metaphysically contentious. Moreover, I suggest that these claims are (...) unnecessary for a defence of biopsychosocial causation, as the roles of multiple and diverse factors in disease causation can be readily accommodated by a more widely accepted and less metaphysically contentious account of causation. I then raise the more general concern that they are misdiagnosing the problem with the traditional version of the biopsychosocial model. The challenge when developing an explanatorily valuable version of the biopsychosocial model, I argue, is not so much providing an adequate account of biopsychosocial causation, but providing an adequate account of causal selection. Finally, I consider how this problem may be solved to arrive at a more explanatorily valuable and clinically useful version of the biopsychosocial model. (shrink)

Causal selection is the cognitive process through which one or more elements in a complex causal structure are singled out as actual causes of a certain effect. In this paper, we report on an experiment in which we investigated the role of moral and temporal factors in causal selection. Our results are as follows. First, when presented with a temporal chain in which two human agents perform the same action one after the other, subjects tend (...) to judge the later agent to be the actual cause. Second, the impact of temporal location on causal selection is almost canceled out if the later agent did not violate a norm while the former did. We argue that this is due to the impact that judgments of norm violation have on causal selection—even if the violated norm has nothing to do with the obtaining effect. Third, moral judgments about the effect influence causal selection even in the case in which agents could not have foreseen the effect and did not intend to bring it about. We discuss our findings in connection to recent theories of the role of moral judgment in causal reasoning, on the one hand, and to probabilistic models of temporal location, on the other. (shrink)

Causal selection has to do with the distinction we make between background conditions and “the” true cause or causes of some outcome of interest. A longstanding consensus in philosophy views causal selection as lacking any objective rationale and as guided, instead, by arbitrary, pragmatic, and non-scientific considerations. I argue against this position in the context of causal selection for disease traits. In this domain, causes are selected on the basis of the type of (...) class='Hi'>causal control they exhibit over a disease of interest. My analysis clarifies the principled rationale that guides this selection and how it involves both pragmatic and objective considerations, which have been overlooked in the extant literature. (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)

Waters’s (2007) actual difference making and Weber’s (2013, 2017) biological normality approaches to causal selection have received many criticisms, some of which miss their target. Disagreement about whether Waters’s and Weber’s views succeed in providing criteria that uniquely singles out the gene as explanatorily significant in biology has led philosophers to overlook a prior problem. Before one can address whether Waters’s and Weber’s views successfully account for the explanatory significance of genes, one must ask whether either view satisfactorily (...) meets the necessary conditions for causal selection in the first place. An adequate defense of causal selection must meet two desiderata. First, there must be an explanatory property that sets some causes apart from others. Second, the property identified must be one that is recognized by biologists as relevant to their domain(s) of inquiry. I argue that both fall short of meeting the second condition. I demonstrate this by showing how many of the biological technologies crucial to experimentation do not fit either view very well. I offer a more adequate proposal that accommodates non-actual and artificial causal variables. A consequence of my view is the following: When analyzing the causal selection practices of biologists, philosophers should consider the explanatory targets relevant to a research program – including ones whose explanans must appeal to biological technologies. I then explain how this proposal can inform the existing debate between Weber (2017) and Griffiths et al. (2015). (shrink)

In their book What Darwin Got Wrong, Jerry Fodor and Massimo Piattelli-Palmarini construct an a priori philosophical argument and an empirical biological argument. The biological argument aims to show that natural selection is much less important in the evolutionary process than many biologists maintain. The a priori argument begins with the claim that there cannot be selection for one but not the other of two traits that are perfectly correlated in a population; it concludes that there cannot be (...) an evolutionary theory of adaptation. This article focuses mainly on the a priori argument. (shrink)

It is an ongoing controversy whether natural selection is a cause of population change, or a mere statistical description of how individual births and deaths accumulate. In this paper I restate the problem in terms of the reference class problem, and propose how the structure of stable equilibrium can provide a solution in continuity with biological practice. Insofar natural selection can be understood as a tendency towards equilibrium, key statisticalist criticisms are avoided. Further, in a modification of the (...) Newtonian-force analogy, it can be suggested that a better metaphor for natural selection is that of an emergent force, similar in nature to entropic forces: with magnitude and direction, but lacking a spatiotemporal origin or point of application. (shrink)

This paper critically reviews and characterizes the student's causal-explanatory understanding; this is done as a step toward explicating the problematic of evolution education as it concerns the cognitive difficulties in understanding Darwin's theory of natural selection. The review concludes that the student's understanding is fundamentally different from Darwin's, for the student understands evolutionary change as necessary individual transformation caused by the transformative action of various physical and behavioral factors. This is in complete contrast to Darwin's (and even the (...) Darwinian's, for that matter) understanding of evolutionary change as a change caused by accumulative selection. Hence, to understand natural selection, the student has to learn to “see” how the accumulative selection causes evolutionary change. (shrink)

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)

People more frequently select norm-violating factors, relative to norm- conforming ones, as the cause of some outcome. Until recently, this abnormal-selection effect has been studied using retrospective vignette-based paradigms. We use a novel set of video stimuli to investigate this effect for prospective causal judgments—i.e., judgments about the cause of some future outcome. Four experiments show that people more frequently select norm- violating factors, relative to norm-conforming ones, as the cause of some future outcome. We show that the (...) abnormal-selection effects are not primarily explained by the perception of agency (Experiment 4). We discuss these results in relation to recent efforts to model causal judgment. (shrink)

Since the ENCODE project published its final results in a series of articles in 2012, there is no consensus on what its implications are. ENCODE’s central and most controversial claim was that there is essentially no junk DNA: most sections of the human genome believed to be «junk» are functional. This claim was met with many reservations. If researchers disagree about whether there is junk DNA, they have first to agree on a concept of function and how function, given a (...) particular definition, can be discovered. The ENCODE debate centered on a notion of function that assumes a strong dichotomy between evolutionary and non-evolutionary function and causes, prevalent in the Modern Evolutionary Synthesis. In contrast to how the debate is typically portrayed, both sides share a commitment to this distinction. This distinction is, however, much debated in alternative approaches to evolutionary theory, such as the EES. We show that because the ENCODE debate is grounded in a particular notion of function, it is unclear how it connects to broader debates about what is the correct evolutionary frame- work. Furthermore, we show how arguments brought forward in the controversy, particularly arguments from mathematical population genetics, are deeply embedded in their particular disciplinary contexts, and reflect substantive assumptions about the evolution of genomes. With this article, we aim to provide an anatomy of the ENCODE debate that offers a new perspective on the notions of function both sides employed, as well as to situate the ENCODE debate within wider debates regarding the forces operating in evolution. (shrink)

The evolution of the human mind through natural selection mandates that our conscious experiences are causally potent in order to leave a tangible impact upon the surrounding physical world. Any attempt to construct a functional theory of the conscious mind within the framework of classical physics, however, inevitably leads to causally impotent conscious experiences in direct contradiction to evolution theory. Here, we derive several rigorous theorems that identify the origin of the latter impasse in the mathematical properties of ordinary (...) differential equations employed in combination with the alleged functional production of the mind by the brain. Then, we demonstrate that a mind--brain theory consistent with causally potent conscious experiences is provided by modern quantum physics, in which the unobservable conscious mind is reductively identified with the quantum state of the brain and the observable brain is constructed by the physical measurement of quantum brain observables. The resulting quantum stochastic dynamics obtained from sequential quantum measurements of the brain is governed by stochastic differential equations, which permit genuine free will exercised through sequential conscious choices of future courses of action. Thus, quantum reductionism provides a solid theoretical foundation for the causal potency of consciousness, free will and cultural transmission. (shrink)

This paper brings together Thompson's naive action explanation with interventionist modeling of causal structure to show how they work together to produce causal models that go beyond current modeling capabilities, when applied to specifically selected systems. By deploying well-justified assumptions about rationalization, we can strengthen existing causal modeling techniques' inferential power in cases where we take ourselves to be modeling causal systems that also involve actions. The internal connection between means and end exhibited in naive action (...) explanation has a modal strength like that of distinctively mathematical explanation, rather than that of causal explanation. Because it is stronger than causation, it can be treated as if it were merely causal in a causal model without thereby overextending the justification it can provide for inferences. This chapter introduces and demonstrate the usage of the Rationalization condition in causal modeling, where it is apt for the system(s) being modeled, and to provide the basics for incorporating R variables into systems of variables and R arrows into DAGs. Use of the Rationalization condition supplements causal analysis with action analysis where it is apt. (shrink)

My account of the causal role of consciousness in a physical world is modeled on Dretske’s celebrated explanation of the causal role of beliefs (something that Dretske himself never offered). First, behavior must be understood as a (broadly individuated) process that begins with some external stimulus causing some neurological event C, and ends with causing a bodily movement M (e.g., the Kennedy assassination is a process that begins with Oswald pulling the trigger at 12:30pm CST on November 23 (...) in 1963 in Dallas, Texas, but only ends half an hour later when Kennedy is pronounced dead at 1 pm CST). The internal neurological event C causes bodily movement M, but only by virtue of being recruited by natural selection to represent the instantiation of some external property F when properly stimulated under normal circumstances. But the reason why C causes M lies in the fact that C represents the instantiation of the external property F. I withdraw my hand from a hot surface because the activation of nociceptive specific neurons in my parietal lobe (together with the activation of neuronal patterns in my motor cortices) was recruited by natural selection to represent the tissue damage in my hand. The activation of nociceptive specific neurons causes my hand to withdraw but for the reason that it represents tissue data at the time that I felt pain in my hand. (shrink)

Bertrand Russell once pointed out that modern science doesn’t deal with causal laws and that assuming otherwise is not only wrong but such thinking is erroneously thought to do no harm. However, looking into the scientific practice of simulation or experimentation reveals a general causal comprehension of physical processes. In this paper I trace causal experiences to the existence of innate causal capacity by which we organize sensory information. This capacity, I argue, is something we have (...) got in virtue of natural selection as can be seen from experiments with intelligent animals like crows and chimpanzees. So understanding the empirical world is impossible without the use of causal categories. The reason why Russell believed that modern science does not refer to causal laws is, I think, because he argued that the laws of mathematical physics give us a non-causal description of reality. In contrast to such a claim I hold that theoretical laws are prescriptive rules of description rather than descriptions themselves. (shrink)

Many have argued that there is no reason why natural selection should cause directional increases in measures such as body size or complexity across evolutionary history as a whole. In this paper I argue that this conclusion does not hold for selection for adaptations to environmental variability, and that, given the inevitability of environmental variability, trends in adaptations to variability are an expected feature of evolution by natural selection. As a concrete instance of this causal structure, (...) I outline how this may be applied to a trend in phenotypic plasticity. (shrink)

Sober [2011] argues that some causal statements are a priori true and that a priori causal truths are central to explanations in the theory of natural selection. Lange and Rosenberg [2011] criticize Sober's argument. They concede that there are a priori causal truths, but maintain that those truths are only ‘minimally causal’. They also argue that explanations that are built around a priori causal truths are not causal explanations, properly speaking. Here we criticize (...) both of Lange and Rosenberg's claims. (shrink)

The selected effects or ‘etiological’ theory of Proper function is a naturalistic and realist account of biological teleology. It is used to analyse normativity in philosophy of language, philosophy of mind, philosophy of medicine and elsewhere. The theory has been developed with a simple and intuitive view of natural selection. Traits are selected because of their positive effects on the fitness of the organisms that have them. These ‘selected effects’ are the Proper functions of the traits. Proponents argue that (...) this analysis of biological teleology has the unique advantage that the selected effect function of a trait is also a causal explanation of the trait: the trait exists because it performs this function. We show, however, that selected effect functions as currently defined explain the existence of traits only under highly restrictive assumptions about evolutionary dynamics. In many common scenarios in which traits evolve by natural selection, selected effect functions do not explain those traits. This is because definitions of selected effect function extract from any evolutionary scenario only the information that would be explanatorily relevant in the simple evolutionary scenario implicit in those definitions. When applied to more complex scenarios selected effect functions omit the key information that is explanatorily relevant in those scenarios. The assumptions required for selected effect functions to be explanatory are particularly unlikely to hold in the domain that its proponents care most about - the evolution of representation. A more adequate selected effects theory of Proper functions may be possible, but will require much greater attention to the structure of actual evolutionary explanations. (shrink)

In 'Fiction and Fictionalism', Mark Sainsbury has recently dubbed “Selection Problem” a serious trouble for Meinongian object theories. Typically, Meinongianism has been phrased as a kind of realism on nonexistent objects : these are mind-independent things, not mental simulacra, having the properties they have independently from the activity of any cognitive agent. But how can one single out an object we have no causal acquaintance with, and which is devoid of spatiotemporal location, picking it out from a pre-determined, (...) mind-independent set ? In this paper, I set out a line of response by distinguishing different ways in which a thing may not exist. I show that the selection problem (a) does not arise for past, currently nonexistent objects ; (b) may not arise also for future existents (provided one massages naïve intuitions a bit) ; and (c) even for mere possibilia ; but (d) is a real snag for purely fictional objects, such as Holmes or Gandalf. As for (d), I propose a solution that forces Meinongianism to introduce a kind of ontological dependence of purely fictional nonexistents upon existents. The strategy complicates the intuitively simple, naïve Meinongian framework a bit, but looks quite promising. (shrink)

In the last couple of years, a few seemingly independent debates on scientific explanation have emerged, with several key questions that take different forms in different areas. For example, the questions what makes an explanation distinctly mathematical and are there any non-causal explanations in sciences (i.e., explanations that don’t cite causes in the explanans) sometimes take a form of the question of what makes mathematical models explanatory, especially whether highly idealized models in science can be explanatory and in virtue (...) of what they are explanatory. These questions raise further issues about counterfactuals, modality, and explanatory asymmetries: i.e., do mathematical and non-causal explanations support counterfactuals, and how ought we to understand explanatory asymmetries in non-causal explanations? Even though these are very common issues in the philosophy of physics and mathematics, they can be found in different guises in the philosophy of biology where there is the statistical interpretation of the Modern Synthesis theory of evolution, according to which the post-Darwinian theory of natural selection explains evolutionary change by citing statistical properties of populations and not the causes of changes. These questions also arise in philosophy of ecology or neuroscience in regard to the nature of topological explanations. The question here is can the mathematical (or more precisely topological) properties in network models in biology, ecology, neuroscience, and computer science be explanatory of physical phenomena, or are they just different ways to represent causal structures. The aim of this special issue is to unify all these debates around several overlapping questions. These questions are: are there genuinely or distinctively mathematical and non-causal explanations?; are all distinctively mathematical explanations also non-causal; in virtue of what they are explanatory; does the instantiation, implementation, or in general, applicability of mathematical structures to a variety of phenomena and systems play any explanatory role? This special issue provides a platform for unifying the debates around several key issues and thus opens up avenues for better understanding of mathematical and non-causal explanations in general, but also, it will enable even better understanding of key issues within each of the debates. (shrink)

The explanatory role of natural selection is one of the long-term debates in evolutionary biology. Nevertheless, the consensus has been slippery because conceptual confusions and the absence of a unified, formal causal model that integrates different explanatory scopes of natural selection. In this study we attempt to examine two questions: (i) What can the theory of natural selection explain? and (ii) Is there a causal or explanatory model that integrates all natural selection explananda? For (...) the first question, we argue that five explananda have been assigned to the theory of natural selection and that four of them may be actually considered explananda of natural selection. For the second question, we claim that a probabilistic conception of causality and the statistical relevance concept of explanation are both good models for understanding the explanatory role of natural selection. We review the biological and philosophical disputes about the explanatory role of natural selection and formalize some explananda in probabilistic terms using classical results from population genetics. Most of these explananda have been discussed in philosophical terms but some of them have been mixed up and confused. We analyze and set the limits of these problems. (shrink)

This paper derives from a broader project dealing with the notion of causal order. I use this term to signify two kinds of parts-whole dependence: Orderly systems have rich, decomposable, internal structure; specifically, parts play differential roles, and interactions are primarily local. Disorderly systems, in contrast, have a homogeneous internal structure, such that differences among parts and organizational features are less important. Orderliness, I suggest, marks one key difference between individuals and collectives. My focus here will be the connection (...) between order and robustness, i.e. functional resilience in the face of internal or environmental perturbations. I distinguish three varieties of robustness. Ordered robustness is grounded in the system’s specific organizational pattern. In contrast, disorderly robustness stems from the aggregate outcome of many similar parts. In between, we find semi-ordered robustness, wherein a messy ensemble of elements is subjected to a selection or stabilization mechanism. I give brief characterizations of each category, discuss examples and remark on the connection between the order/disorder axis and the notions of individual versus collective. (shrink)

Traditionally, Darwin has been grouped with the functionalists because natural selection (an adaptational mechanism) plays the prominent role in shaping organic form. In this paper, I sketch the dichotomy of functionalism versus structuralism and then argue that Darwin cannot be characterized adequately with this dichotomy. I argue that Darwin can incorporate both causal stories because he makes two important modifications to the traditional metaphysical presuppositions. I then offer some brief reflections on the import of Darwin's causal pluralism (...) for the Philosophy of Science. (shrink)

As physical entities that translate symbols into physical actions, computers offer insights into the nature of meaning and agency. • Physical symbol systems, generically known as agents, link abstractions to material actions. The meaning of a symbol is defined as the physical actions an agent takes when the symbol is encountered. • An agent has autonomy when it has the power to select actions based on internal decision processes. Autonomy offers a partial escape from constraints imposed by direct physical influences (...) such as gravity and the transfer of momentum. Swimming upstream is an example. • Symbols are names that can designate other entities. It appears difficult to explain the use of names and symbols in terms of more primitive functionality. The ability to use names and symbols, i.e., symbol grounding, may be a fundamental cognitive building block. • The standard understanding of causality—wiggling X results in Y wiggling—applies to both physical causes (e.g., one billiard ball hitting another) and symbolic causes (e.g., a traffic light changing color). Because symbols are abstract, they cannot produce direct physical effects. For a symbol to be a cause requires that the affected entity determine its own response. This is called autonomous causality. • This analysis of meaning and autonomy offers new perspectives on free will. (shrink)

The neutral and nearly neutral theories of molecular evolution are sometimes characterized as theories about drift alone, where drift is described solely as an outcome, rather than a process. We argue, however, that both selection and drift, as causal processes, are integral parts of both theories. However, the nearly neutral theory explicitly recognizes alleles and/or molecular substitutions that, while engaging in weakly selected causal processes, exhibit outcomes thought to be characteristic of random drift. A narrow focus on (...) outcomes obscures the significant role of weakly selected causal processes in the nearly neutral theory. (shrink)

I defend a radical interpretation of biological populations—what I call population pluralism—which holds that there are many ways that a particular grouping of individuals can be related such that the grouping satisfies the conditions necessary for those individuals to evolve together. More constraining accounts of biological populations face empirical counter-examples and conceptual difficulties. One of the most intuitive and frequently employed conditions, causal connectivity—itself beset with numerous difficulties—is best construed by considering the relevant causal relations as ‘thick’ (...) class='Hi'>causal concepts. I argue that the fine-grained causal relations that could constitute membership in a biological population are huge in number and many are manifested by degree, and thus we can construe population membership as being defined by massively multidimensional constructs, the differences between which are largely arbitrary. I end by showing that positions in two recent debates in theoretical biology depend on a view of biological populations at odds with the pluralism defended here. (shrink)

The causal premise of the evolutionary debunking argument contends that human moral beliefs are explained by the process of natural selection. While it is universally acknowledged that such a premise is fundamental to the debunker’s case, the vast majority of philosophers focus instead on the epistemic premise that natural selection does not track moral truth and the resulting skeptical conclusion. Recently, however, some have begun to concentrate on the causal premise. So far, the upshot of this (...) small but growing literature has been that the causal premise is likely false due to the seemingly persuasive evidence that our moral beliefs are in fact not the result of natural selection. In this paper, I argue that this view is mistaken. Specifically, I advocate the Innate Biases Model, which contends that there is not only compelling evidence for an evolved cognitive capacity for acquiring norms but also for the existence of an evolutionarily instilled set of cognitive biases that make it either more or less likely that we adopt certain moral beliefs. (shrink)

Donald Davidson’s causal theory of actions states that actions must be rationalized and caused by a belief-desire-pair. One problem of such a causal theory are cases of deviant causal chains. In these cases, the rationalized action is not caused in the right way but via a deviant causal chain. It therefore intuitively seems to be no action while all conditions of the causal theory are met. I argue that the problem of deviant causal chains (...) can be solved by adding a teleofunctionalist condition. This condition requires that the belief-desire pair that rationalizes an action must cause that action in a selection-historically normal way. I try to show that this additional condition drops counterintuitive cases of deviant causal chains out of the class of actions while being flexible enough to classify such cases as actions in which causal detours are intuitively permissible. (shrink)

An influential argument due to Elliott Sober, subsequently strengthened by Denis Walsh and Joel Pust, moves from plausible premises to the bold conclusion that natural selection cannot explain the traits of individual organisms. If the argument were sound, the explanatory scope of selection would depend, surprisingly, on metaphysical considerations concerning origin essentialism. I show that the Sober-Walsh-Pust argument rests on a flawed counterfactual criterion for explanatory relevance. I further show that a more defensible criterion for explanatory relevance recently (...) proposed by Michael Strevens lends support to the view that natural selection can be relevant to the explanation of individual traits. (shrink)

The conflation of two fundamentally distinct issues has generated serious confusion in the philosophical and biological literature concerning the units of selection. The question of how a unit of selection of defined, theoretically, is rarely distinguished from the question of how to determine the empirical accuracy of claims--either specific or general--concerning which unit(s) is undergoing selection processes. In this paper, I begin by refining a definition of the unit of selection, first presented in the philosophical literature (...) by William Wimsatt, which is grounded in the structure of natural selection models. I then explore the implications of this structural definition for empirical evaluation of claims about units of selection. I consider criticisms of this view presented by Elliott Sober--criticisms taken by some (for example, Mayo and Gilinsky 1987) to provide definitive damage to the structuralist account. I shall show that Sober has misinterpreted the structuralist views; he knocks down a straw man in order to motivate his own causal account. Furthermore, I shall argue, Sober's causal account is dependent on the structuralist account that he rejects. I conclude by indicating how the refined structural definition can clarify which sorts of empirical evidence could be brought to bear on a controversial case involving units of selection. (shrink)

Christie, Brusse, et al. argue that selected effects are insufficient to explain the prevalence of traits when selection is heterogeneous. One could object that it’s useful to ground functions in selected effects so long as selected effects are necessary to explain the prevalence of traits. This raises a challenging question: what justifies singling out selected effects from other factors that are necessary to explain the prevalence of traits when selection is heterogeneous? I consider three answers: selected effects are (...) the only factors that explain the prevalence of traits and (a) can plausibly ground functions; (b) enable biological generalization; and (c) enable representational explanation. I argue that none of these answers is satisfactory. Only the third answer might be able to justify singling out any selected effects at all (when selection is heterogeneous): the small share of selected effects that ground representations of causal particulars. Thus, I agree with Christie, Brusse, et al. that heterogeneous selection is a serious problem for selected effects theories of function. (shrink)

This paper is on the problem of causal selection and comments on Collingwood's classic paper "The so-called idea of causation". It discusses the relevance of Collingwood’s control principle in contemporary life sciences and defends that it is not the ability to control, but the willingness to control that often biases us towards some rather than other causes of a phenomenon. Willingness to control is certainly only one principle that influences causal selection, but it is an important (...) one. It shows how norms make causes. (shrink)

Many philosophical theories of causation are egalitarian, rejecting a distinction between causes and mere causal conditions. We sought to determine the extent to which people's causal judgments discriminate, selecting as causes counternormal events—those that violate norms of some kind—while rejecting non-violators. We found significant selectivity of this sort. Moreover, priming that encouraged more egalitarian judgments had little effect on subjects. We also found that omissions are as likely as actions to be judged as causes, and that counternormative selectivity (...) appears to apply equally to actions and omissions. (shrink)

Neither Aristotle nor Aquinas assumes the reality of the evolution of species. Their systems of thought, however, remain open to the new data, offering an essential contribution to the ongoing debate between scientific, philosophical, and theological aspects of the theory of evolution. After discussing some key issues of substance metaphysics in its encounter with the theory of evolution (hylomorphism, transformism of species, teleology, chance, the principle of proportionate causation), I present a Thomistic response to its major hypotheses. Concerning the philosophy (...) of Aquinas, I trace what might be seen as a preliminary description of natural selection in his commentary on Aristotle's Physics. Turning toward theology, besides addressing the topics that were referred to in the past—such as: Aquinas’ reading of Genesis, his account of creation as dependence in being, secondary and instrumental causality, and univocal/equivocal predication of God—I bring into discussion Thomas’ concept of the perfection of the universe, which has been virtually unused in this context. (shrink)

Contents: Danuta Ługowska, Incommensurability of Paradigms Exemplified by the Differences Between the Western and Eastern European Image of the Human Person ; Maria-Magdalena Weker, Light, Body and Soul – the Issues Fundamental for Theories of Vision. A Historical Survey ; Dariusz Kucharski, The Conception of Sensory Perception and Scientific Research. (The Theory of Sign within Philosophy of G. Berkeley and T. Reid) ; Grzegorz Bugajak, Causality and Determinism in Physics ; Anna Lemańska, Truth in Mathematics ; Anna Latawiec, Troubles with (...) the Philosophy of Medicine ; Adam Świeżyński, Values, Axiological Experience, and Scientific Research ; Grzegorz Bugajak, Fears of Science. Nature and Human Actions ; Adam Świeżyński, Some Remarks on the Human Search for Sense in the Context of Human Actions. (shrink)

I have defended the idea that the passage of time can be thought of as a local phenomenon, as the succession of causal diamonds along timelike curves, in relativistic spacetimes. This idea has been criticized by Craig Callender and Oliver Pooley. In this paper, I articulate my view in more detail than I have hitherto and defend it from their criticisms.

I argue that verbal models should be included in a philosophical account of the scientific practice of modelling. Weisberg (2013) has directly opposed this thesis on the grounds that verbal structures, if they are used in science, only merely describe models. I look at examples from Darwin's On the Origin of Species (1859) of verbally constructed narratives that I claim model the general phenomenon of evolution by natural selection. In each of the cases I look at, a particular scenario (...) is described that involves at least some fictitious elements but represents the salient causal components of natural selection. I pronounce the importance of prioritising observation of scientific practice for the philosophy of modelling and I suggest that there are other likely model types that are excluded from philosophical accounts. (shrink)

Two major clarifications have greatly abetted the understanding and fruitful expansion of the theory of natural selection in recent years: the acknowledgment that interactors, not replicators, constitute the causal unit of selection; and the recognition that interactors are Darwinian individuals, and that such individuals exist with potency at several levels of organization (genes, organisms, demes, and species in particular), thus engendering a rich hierarchical theory of selection in contrast with Darwin’s own emphasis on the organismic level. (...) But a piece of the argument has been missing, and individuals at levels distinct from organisms have been denied potency (although granted existence within the undeniable logic of the theory), because they do not achieve individuality with the same devices used by organisms and therefore seem weak by comparison. We show here that different features define Darwinian individuality across scales of size and time. In particular, species-individuals may develop few emergent features as direct adaptations. The interactor approach works with emergent fitnesses, not with emergent features; and species, as a consequence of their different mechanism for achieving individuality (reproductive exclusivity among subparts, that is, among organisms), express many effects from other levels. Organisms, by contrast, suppress upwardly cascading effects, because the organismic style of individuality (by functional integration of subparts) does not permit much competition or differential reproduction of parts from within. Species do not suppress the operation of lower levels; such effects therefore become available as exaptations conferring emergent fitness—a primary source of the different strength that species achieve as effective Darwinian individuals in evolution. (shrink)

Perceptual dogmatism is a prominent theory in epistemology concerning the relationship between perceptual experience and reasonable belief. It holds that, in the absence of counterevidence, it is reasonable to believe what your perceptual experience tells you. Thus, if you are not aware of your experience’s casual history, then it doesn’t matter. Critics object that the causal history does matter: when a perceptual experience is caused in certain ways, it is unreasonable to trust what it tells you. These objections regularly (...) appeal to cognitive penetration and biased searches for evidence. Given the myriad accounts of what covert attention is, one wonders (at least I wondered) if biased patterns of covert attention could raise a new objection to dogmatism. I argue that, while covert selection might raise various problems for dogmatism, none of them are new. This is good news for dogmatism, because the fewer distinct problems it faces, the more likely it can resolve them all. (shrink)

Which way does causation proceed? The pattern in the material world seems to be upward: particles to molecules to organisms to brains to mental processes. In contrast, the principles of quantum mechanics allow us to see a pattern of downward causation. These new ideas describe sets of multiple levels in which each level influences the levels below it through generation and selection. Top-down causation makes exciting sense of the world: we can find analogies in psychology, in the formation of (...) our minds, in locating the source of consciousness, and even in the possible logic of belief in God. (shrink)

Recent discussion of mechanism has suggested new approaches to several issues in the philosophy of science, including theory structure, causal explanation, and reductionism. Here, I apply what I take to be the fruits of the 'new mechanical philosophy' to an analysis of a contemporary debate in evolutionary biology about the role of natural selection in speciation. Traditional accounts of that debate focus on the geographic context of genetic divergence--namely, whether divergence in the absence of geographic isolation is possible (...) (or significant). Those accounts are at best incomplete, I argue, because they ignore the mechanisms producing divergence and miss what is at stake in the biological debate. I argue that the biological debate instead concerns the scope of particular speciation mechanisms which assign different roles to natural selection at various stages of divergence. The upshot is a new interpretation of the crux of that debate--namely, whether divergence with gene flow is possible (or significant) and whether the isolating mechanisms producing it are adaptive. (shrink)

Abstract : This research work examined how major macro economic variables in Nigeria such as Gross Domestic Product (GDP), Gross Fixed Capital Formation (GFCF) and National Savings (NS) reacted to International Monetary Fund (IMF) conditionality from 1986 to 2016. Many policy makers and researchers have questioned the benefits of IMF credit facilities to developing nations. This work therefore seeks to evaluate the impact of IMF conditionality like Reduction in Government Expenditure (TGE), Devaluation of Local Currencies (RER), and Trade openness (TO) (...) on the Identified Macro Economic Variable in Nigeria. The data for the analysis were sourced from the data bank of World Bank. Granger causality test and ordinary Least Square (OLS) method were used to test the formulated hypotheses. The result revealed that IMF conditionality has significant effect on GDP, GFCF and NS of Nigeria. Devaluation of local currency is the greatest IMF conditionality that exerts great negative influence on economic growth of Nigeria. The work recommends among others that: instead of currency devaluation, protectionist policies via guided liberalization should be promoted combined with the use of fiscal policy in order to encourage local production and usage of locally produced goods. TGE that showed significant positive effect on GDP, GFCF and NS is an indication that government can positively influence the economic positions of Nigeria with the use of fiscal policy. (shrink)

Is all explanations causal explanation? Puzzles about barometer readings "explain" storms and shadow lengths "explaining" flagpole heights make it attractive to think so. Wesley Salmon (1984) has endorsed this causal thesis. One way to test this thesis is to assess the explanatory import of pseudo-processes. I do so by discussing the concept of heritability, which measures a pseudo-process, and one role it played in the theory of natural selection: explaining response to selection. This will show, not (...) just that heritability has heuristic or predictive utility, but that it can be explanatory. Possible responses to this case are also discussed. (shrink)

In temporal binding, the temporal interval between one event and another, occurring some time later, is subjectively compressed. We discuss two ways in which temporal binding has been conceptualized. In studies showing temporal binding between a voluntary action and its causal consequences, such binding is typically interpreted as providing a measure of an implicit or pre-reflective “sense of agency”. However, temporal binding has also been observed in contexts not involving voluntary action, but only the passive observation of a cause-effect (...) sequence. In those contexts, it has been interpreted as a top-down effect on perception reflecting a belief in causality. These two views need not be in conflict with one another, if one thinks of them as concerning two separate mechanisms through which temporal binding can occur. In this paper, we explore an alternative possibility: that there is a unitary way of explaining temporal binding both within and outside the context of voluntary action as a top-down effect on perception reflecting a belief in causality. Any such explanation needs to account for ways in which agency, and factors connected with agency, have been shown to affect the strength of temporal binding. We show that principles of causal inference and causal selection already familiar from the literature on causal learning have the potential to explain why the strength of people’s causal beliefs can be affected by the extent to which they are themselves actively involved in bringing about events, thus in turn affecting binding. (shrink)