Elsewhere, I defend the “causal interactionist population concept” (CIPC). Here I further defend the CIPC by showing how it clarifies another concept that biologists grapple with, namely, environment. Should we understand selection as ranging only over homogeneous environments or, alternatively, as ranging over any habitat area we choose to study? I argue instead that the boundaries of the population dictate the range of the environment, whether homogeneous or heterogeneous, over which selection operates. Thus, understanding (...) the concept of population helps us to understand concepts of selective environment, exemplifying the importance of the CIPC to other concepts and debates. (shrink)

Biologists and philosophers have offered differing concepts of biological race. That is, they have offered different candidates for what a biological correlate of race might be; for example, races might be subspecies, clades, lineages, ecotypes, or genetic clusters. One thing that is striking about each of these proposals is that they all depend on a concept of population. Indeed, some authors have explicitly characterized races in terms of populations. However, including the concept of population into concepts (...) of race raises three puzzles, all having to do with time. In this paper, I extend the causal interactionist population concept (CIPC) by introducing some simple assumptions about how to understand populations through time. These assumptions help to shed light on the three puzzles, and in the process show that if we want to understand races in terms of populations, we will need to revise our concept(s) of race. (shrink)

In this paper, I plan to show that the use of a specific population concept—Millstein’s Causal Interactionist Population Concept (CIPC)—has interesting and counter-intuitive ramifications for discussions of the reality of biological race in human beings. These peculiar ramifications apply to human beings writ large and to individuals. While this in and of itself may not be problematic, I plan to show that the ramifications that follow from applying Millstein’s CIPC to human beings complicates specific (...) biological racial realist accounts—naïve or otherwise. I conclude with the notion that even if biological races do exist—by fulfilling all of the criteria needed for Millstein’s population concept (which, given particular worries raised by Gannett (Synthese 177:363–385, 2010), and Winther and Kaplan (Theoria 60:54–80, 2013) may not)—the lower-bound limit for the scope of biological racial realism is at the level of populations, and as such they cannot say anything about whether or not individual organisms themselves have races. (shrink)

This paper aims to illustrate one of the primary goals of the philosophy of biology⎯namely, the examination of central concepts in biological theory and practice⎯through an analysis of the concepts of population and metapopulation in evolutionary biology and ecology. I will first provide a brief background for my analysis, followed by a characterization of my proposed concepts: the causal interactionist concepts of population and metapopulation. I will then illustrate how the concepts apply to six cases that (...) differ in their population structure; this analysis will also serve to flesh out and defend the concepts a bit more. Finally, I will respond to some possible questions that my analysis may have raised and then conclude briefly. (shrink)

Darwinian evolution is a population-level phenomenon. This paper deals with a structural population concept within the framework of generalized Darwinism, resp. within a generalized theory of evolution. According to some skeptical authors, GD is in need of a valid population concept in order to become a practicable research program. Populations are crucial and basic elements of any evolutionary explanation—biological or cultural—and have to be defined as clearly as possible. I suggest the “causal interactionist (...) population concept”, by R. Millstein for this purpose, and I will try to embed the approach into a generalized evolutionary perspective by mathematically formalizing its key definitions. Using graph-theory, populations as described in the CIPC can serve as proper clusters of evolutionary classification based on the rates of interactions between their elements. I will introduce the concept of a cohesion index as a measurement of possible population candidates within a distribution of elements. The strength of this approach lies in its applicability and interactions are relatively easy to observe. Furthermore, problems of clustering tokens via typicality, e.g. their similarity in intrinsic key characteristics, can be avoided, because CIPC is a external approach. However, some formal problems and conceptual ambiguities occur within a simple version of this CI, which will be addressed in this paper as well as some possible applications. (shrink)

In “‘Population’ is Not a Natural Kind of Kinds,” Jacob Stegenga argues against the claim that the concept of “population” is a natural kind and in favor of conceptual pluralism, ostensibly in response to two papers of mine (Millstein 2009, 2010). Pluralism is often an attractive position in the philosophy of science. It certainly is a live possibility for the concept of population in ecology and evolutionary biology, and I welcome the opportunity to discuss the (...) topic further. However, I argue that the case for conceptual pluralism has not yet been made. In what follows, I first clarify the issues at stake before taking up the topic of conceptual pluralism and responding to Stegenga’s criticisms of the causal interactionist population concept. (shrink)

A major debate in the philosophy of biology centers on the question of how we should understand the causal structure of natural selection. This debate is polarized into the causal and statistical positions. The main arguments from the statistical side are that a causal construal of the theory of natural selection's central concept, fitness, either (i) leads to inaccurate predictions about population dynamics, or (ii) leads to an incoherent set of causal commitments. In this (...) essay, I argue that neither the predictive inaccuracy nor the incoherency arguments successfully undermine the causal account of fitness. 1 Introduction2 The Importance of Trait Fitness3 Trait Fitness is not a Silver Bullet4 The Fundamental Incoherency Argument5 Car Racing and Trait Fitness Reversals6 Population Subdivisions and Evolution7 The STP and the Argument for the Incoherency of the Causal Account of Fitness8 Conclusions. (shrink)

A major debate in the philosophy of biology centers on the question of how we should understand the causal structure of natural selection. This debate is polarized into the causal and statistical positions. The main arguments from the statistical side are that a causal construal of the theory of natural selection's central concept, fitness, either (i) leads to inaccurate predictions about population dynamics, or (ii) leads to an incoherent set of causal commitments. In this (...) essay, I argue that neither the predictive inaccuracy nor the incoherency arguments successfully undermine the causal account of fitness. 1 Introduction2 The Importance of Trait Fitness3 Trait Fitness is not a Silver Bullet4 The Fundamental Incoherency Argument5 Car Racing and Trait Fitness Reversals6 Population Subdivisions and Evolution7 The STP and the Argument for the Incoherency of the Causal Account of Fitness8 Conclusions. (shrink)

I propose a new account of homology, according to which homology is a correspondence of developmental mechanisms due to common ancestry, formally defined as an isomorphism of causal graphs over lineages. The semiformal definition highlights the role of homology as a higher-order principle unifying evolutionary models and also provides definite meanings to concepts like constraints, evolvability, and novelty. The novel interpretation of homology suggests a broad perspective that accommodates evolutionary developmental biology and traditional population genetics as distinct but (...) complementary approaches to understand evolution, prompting further empirical and theoretical research. (shrink)

In this paper, I will conduct three interrelated analyses. First, I will develop an analysis of various concepts in the history of biology that used to refer to individual-level phenomena but were then reinterpreted by the Modern Synthesis in terms of populations. Second, I argue that a similar situation can be found in contemporary biological theory. While different approaches reflect on the causal role of developing organisms in evolution, proponents of the Modern Synthesis avoid any substantial change by reinterpreting (...) and explaining individual-level phenomena from a population perspective. Finally, I will approach this debate by advocating the statistical reading of natural selection, which holds that explanations by natural selection are statistical. I will argue that the above historical conceptual reinterpretations belong to a new explanatory strategy developed by the Modern Synthesis based on population thinking. The reinterpretation of concepts at the individual level is part of the explanatory framework of the Modern Synthesis and the empty role of development within this framework. Moreover, the statistical perspective adopted here allows for the integration of two explanatory models: population-statistical and individual-causal. Finally, I will argue that this pluralistic framework can help to define the explanatory scope of the different biological approaches in order to achieve a coherent integration of development into evolution without rejecting population thinking. (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’ (...) 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 views of linguistic analysts and objectivists are explored with regard to the question of interactionism. It is argued that the admission of a logical difference between explanation by cause and explanation by motive cannot disqualify causal explanations of human action, cannot be construed as challenging the competence of science, and cannot count against interactionism. It is also argued that objectivist programs for eliminating mentalistic concepts either implicitly admit interactionism or cannot distinguish relevantly between interactionism and parallelism.

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’ (...) 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. 1 Introduction2 Biological Population, Broad and Narrow3 Difficulties with Narrow Biological Population Conditions3.1 Against the genealogical condition3.2 Against the conspecificity condition3.3 Against the proximity condition3.4 Against the typology condition4 Causal Connectivity5 Massively Multidimensional Population Constructs6 Population Uniqueness and Natural Selection6.1 Statisticalism and its discontents6.2 Price at what price?7 Conclusion. (shrink)

One contentious debate in the philosophy of biology is that between the statisticalists and causalists. The former understand core evolutionary concepts like fitness and selection to be mere statistical summaries of underlying causal processes. In this view, evolutionary changes cannot be causally explained by selection or fitness. The causalist side, on the other hand, holds that populations can change in response to selection—one can cite fitness differences or driftability in causal explanations of evolutionary change. But, on the causalist (...) side, it is often not clear how, precisely, one should understand these causes. Thus, much more could be said about what sort of causes fitness and driftability are. In this paper, I borrow Dretske's distinction between structuring and triggering causes and I suggest that fitness and driftability are structuring causes of evolution. (shrink)

In this important book, Ellery Eells explores and refines philosophical conceptions of probabilistic causality. In a probabilistic theory of causation, causes increase the probability of their effects rather than necessitate their effects in the ways traditional deterministic theories have specified. Philosophical interest in this subject arises from attempts to understand population sciences as well as indeterminism in physics. Taking into account issues involving spurious correlation, probabilistic causal interaction, disjunctive causal factors, and temporal ideas, Professor Eells advances the (...) analysis of what it is for one factor to be a positive causal factor for another. A salient feature of the book is a theory of token level probabilistic causation in which the evolution of the probability of a later event from an earlier event is central. This will be a book of crucial significance to philosophers of science and metaphysicians; it will also prove stimulating to many economists, psychologists, and physicists. (shrink)

Causal inference is perhaps the most important form of reasoning in the sciences. A panoply of disciplines, ranging from epidemiology to biology, from econometrics to physics, make use of probability and statistics to infer causal relationships. The social and health sciences analyse population-level data using statistical methods to infer average causal relations. In diagnosis of disease, probabilistic statements are based on population-level causal knowledge combined with knowledge of a particular person’s symptoms. For the physical (...) sciences, the Salmon-Dowe account develops an analysis of causation based on the notion of process and interaction. In artificial intelligence, the development of graphical methods has leant impetus to a probabilistic analysis of causality. The biological sciences use probabilistic methods to look for evolutionary causes of the state of a current species and to look for genetic causal factors. This variegated situation raises at least two fundamental philosophical issues: about the relation between causality and probability, and about the interpretation of probability in causal analysis. In this book we bring philosophers and scientists together to discuss the relation between causality and probability, and the applications of these concepts within the sciences. (shrink)

The relationship between individual and population health is partially built on the broad dichotomization of medicine into clinical medicine and public health. Potential drawbacks of current views include seeing both individual and population health as absolute and independent concepts. I will argue that the relationship between individual and population health is largely relative and dynamic. Their interrelated dynamism derives from a causally defined life course perspective on health determination starting from an individual’s conception through growth, development and (...) participation in the collective till death, all seen within the context of an adaptive society. Indeed, it will become clear that neither individual nor population health is identifiable or even definable without informative contextualization within the other. For instance, a person’s health cannot be seen in isolation but must be placed in the rich contextual web such as the socioeconomic circumstances and other health determinants of where they were conceived, born, bred, and how they shaped and were shaped by their environment and communities, especially given the prevailing population health exposures over their lifetime. We cannot discuss the “what” and “how much” of individual and population health until we know the cumulative trajectories of both, using appropriate causal language. (shrink)

The main aim of this paper is to provide some probabilistic notions on causality proposed to be applied to the nomic statements which intend to give account of the indeterministic processes within the domain of a scientific theory. In general, such statements are, in more or less extent, idealized statements which rest on a variety of unrealistic suppositions. I try to show how the probability distribution over the final states of an indeterministic process changes accordingly as the nomic statement in (...) question is de-idealized by means of addition of the causally relevant factors. In order to illustrate the study I take few nomic statements from population genetics. Besides, in the course, I attempt to contrast the ideas embraced here with some of the notions of Humphreys´ ontic conceptions of causality and explanation, which are contrary to the epistemic view adopted here about those subjects. (shrink)

This book covers the overlap between informatics, computer science, philosophy of causation, and causal inference in epidemiology and population health research. Key concepts covered include how data are generated and interpreted, and how and why concepts in health informatics and the philosophy of science should be integrated in a systems-thinking approach. Furthermore, a formal epistemology for the health sciences and public health is suggested. -/- Causation in Population Health Informatics and Data Science provides a detailed guide of (...) the latest thinking on causal inference in population health informatics. It is therefore a critical resource for all informaticians and epidemiologists interested in the potential benefits of utilising a systems-based approach to causal inference in health informatics. (shrink)

Contemporary debates about the nature of semantic reference have tended to focus on two competing approaches: theories which emphasize the importance of descriptive information associated with a referring term, and those which emphasize causal facts about the conditions under which the use of the term originated and was passed on. Recent empirical work by Machery and colleagues suggests that both causal and descriptive information can play a role in judgments about the reference of proper names, with findings of (...) cross-cultural variation in judgments that imply differences between individuals with respect to whether they favor causal or descriptive information in making reference judgments. We extend this theoretical and empirical line of inquiry to views of the reference of natural and nominal kind concepts, which face similar challenges to those concerning the reference of proper names. In two experiments, we find evidence that both descriptive and causal factors contribute to judgments of concept reference, with no reliable differences between natural and nominal kinds. Moreover, we find evidence that the same individuals’ judgments can rely on both descriptive and causal information, such that variation between individuals cannot be explained by appeal to a mixed population of “pure descriptive theorists” and “pure causal theorists.” These findings suggest that the contrast between descriptive and causal theories of reference may be inappropriate; intuitions may instead support a hybrid theory of reference that includes both causal and descriptive factors. We propose that future research should focus on the relationship between these factors, and describe several possible frameworks for pursuing these issues. Our findings have implications for theories of semantic reference, as well as for theories of conceptual structure. (shrink)

This article examines three aspects of the problem of understanding Benjamin Libet’s idea of conscious will causally interacting with certain neural activities involved in generating overt bodily movements. The first is to grasp the notion of cause involved, and we suggest a definition. The second is to form an idea of by what neural structure(s) and mechanism(s) a conscious will may control the motor activation. We discuss the possibility that the acts of control have to do with levels of supplementary (...) motor area activity and with the activation of populations of excitatory and inhibitory interneurons. The third aspect is to conceive of the main features of Libet’s proposed conscious mental field (CMF). We consider both an ontological and an epistemological interpretation of the CMF being nonphysical. In an attempt to refute the idea that Libet’s dualist mind–brain interactionism would violate the law of conservation of energy, we suggest that a CMF may alter the probability of the ion-channel gating by influencing structures of a size to which quantum mechanics needs to be applied. We argue that given the suggested definition of cause, and given the epistemological interpretation of the CMF being nonphysical, nothing would necessarily rule out that an element of a CMF, conscious will, may causally interact with neural activities in the brain. This defense of the idea of conscious will being causally efficacious has a bearing not only on the understanding of the mind–brain relation but also on the free will debate. (shrink)

Causal cognition – how we perceive, represent and reason about causal events – are fundamental to the human mind, but it has rarely been approached in its cultural specificity. Here, we investigate this core concept among Wichi people, an indigenous group living in Chaco Forest. We focus on the Wichi, because their epistemological orientations and explanatory frameworks about ecosystem differ importantly from those documented among most Western majority-culture populations. We asked participants to reason about causes of events (...) that involve the hunhat lheley (inhabitants of the earth: humans, non-human animals, plants and spiritual beings) and other entities of their ecosystem (e.g., lagoon). We find a native ontological framework that encompasses three interacting organizing principles. This new evidence highlights ways in which native categories guide causal reasoning. Our research challenge long-held assumptions that dichotomies – nature-culture or natural-supernatural – are universal features of the human mind. (shrink)

This is the second of two volumes of essays in commemoration of Alan Turing; it celebrates his intellectual legacy within the philosophy of mind and cognitive science. A distinguished international cast of contributors focus on the relationship beteen a scientific, computational image of the mind and a common-sense picture of the mind as an inner arena populated by concepts, beliefs, intentions, and qualia. Topics covered include the causal potency of folk- psychological states, the connectionist reconception of learning and (...) class='Hi'>concept formation, the understanding of the notion of computation itself, and the relation between philosophical and psychological theories of concepts. (shrink)

Among philosophers, controversy over the notion of drift in population genetics is ongoing. This is at least partly because the notion of drift has an ambiguous usage among population geneticists. My goal in this paper is to explicate the causal dimension of drift, to say what causal influences are responsible for the stochasticity in population genetics models. It is commonplace for population genetics to oppose the influence of selection to that of drift, and to (...) consider how the dynamics of populations are altered when each has greater or lesser influence. I define the causes that are referred to as drift when researchers speak this way. Introduction Populations and Variant Types The Cause–Effect Ambiguity of Drift Non-directional Factors in Population Genetics How N ev Is Used in Population Genetics Causal Conceptions of Drift 6.1 The Millstein/Beatty conception of drift 6.2 Rosenberg and Bouchard: Drift as initial conditions NINPICs 7.1 Why drift is instituted by NINPICs 7.2 How NINPICS work 7.3 NINPICs and random sampling 7.4 Independent sampling and effective population size 7.5 Variance in progeny number 7.6 Population effects of NINPICs NINPICs and the Stochastic Character of Selection Theory Conclusion Appendix CiteULike Connotea Del.icio.us What's this? (shrink)

A distinction is drawn between property causation and token causation. According to the former, a positive causal factor in a population raises the probability of its effects within "background contexts". The latter, which concerns "actual physical connections" between token events, is not explicated here although its distinctness from the first concept and its importance are discussed. The applicability of both is illustrated by two currently controversial issues in evolutionary theory -- the units of selection controversy and the (...) use of parsimony as an inference rule in phylogenetic reconstruction. (shrink)

I define a concept of causal probability and apply it to questions about the role of probability in evolutionary processes. Causal probability is defined in terms of manipulation of patterns in empirical outcomes by manipulating properties that realize objective probabilities. The concept of causal probability allows us see how probabilities characterized by different interpretations of probability can share a similar causal character, and does so in such way as to allow new inferences about relationships (...) between probabilities realized in different chance setups. I clarify relations between probabilities and properties defined in terms of them, and argue that certain widespread uses of computer simulations in evolutionary biology show that many probabilities relevant to evolutionary outcomes are causal probabilities. This supports the claim that higher-level properties such as biological fitness and processes such as natural selection are causal properties and processes, contrary to what some authors have argued. (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)

What exactly is a genetic disease? For a phrase one hears on a daily basis, there has been surprisingly little analysis of the underlying concept. Medical doctors seem perfectly willing to admit that the etiology of disease is typically complex, with a great many factors interacting to bring about a given condition. On such a view, descriptions of diseases like cancer as geneticseem at best highly simplistic, and at worst philosophically indefensible. On the other hand, there is clearly some (...) practical value to be had by classifying diseases according to theirpredominant cause when this can be accomplished in a theoretically satisfactory manner. The question therefore becomes exactly how one should go about selecting a single causal factor among many to explain the presence of disease. When an attempt to defend such causal selection is made at all, the standard accounts offered (Koch's postulates, Hill's epidemiological criteria, manipulability) are all clearly inadequate. I propose, however, an epidemiological account of disease causation which walks the fine line between practical applicability and theoretical considerations of causal complexity and attempts to compromise between patient-centered and population-centered concepts of disease. The epidemiological account is the most basic framework consistent with our strongly held intuitions about the causal classification of disease, yet it avoids the difficulties encountered by its competitors. (shrink)

The goal of research in social epidemiology is not simply conceptual clarification or theoretical understanding, but more importantly it is to contribute to, and enhance the health of populations (and so, too, the people who constitute those populations). Undoubtedly, understanding how various individual risk factors such as smoking and obesity affect the health of people does contribute to this goal. However, what is distinctive of much on-going work in social epidemiology is the view that analyses making use of individual-level variables (...) is not enough. In the spirit of Durkheim and Weber, S. Leonard Syme makes this point by writing that just “as bad water and food may be harmful to our health, unhealthful forces in our society may be detrimental to our capacity to make choices and to form opinions” conducive to health and well-being. Advocates of upstream (distal) causes of adverse health outcomes propose to identify the most important of these “unhealthful forces” as the fundamental causes of adverse health outcomes. However, without a clear, theoretically precise and well-grounded understanding of the characteristics of fundamental causes, there is little hope in applying the statistical tools of the health sciences to hypotheses about fundamental causes, their outcomes, and policies intended to enhance the health of populations. This paper begins the process of characterizing the social epidemiological concept of fundamental cause in a theoretically respectable and robust way. (shrink)

When people make judgments about the effects of a perturbation on populations of species in a food web, their judgments exhibit the dissipation effect: a tendency to judge that effects of the perturbation weaken or dissipate as they spread out through the food web from the locus of the perturbation. In the present research evidence for two more phenomena is reported. Terminal locations are points in the food web with just a single connection to the rest of the web. Judged (...) changes tended to be higher for species at terminal locations than for species the same distance from the perturbation but at nonterminal locations. Branches are points in the web where a route splits into two or more routes. Judged changes tended to be lower for species following branching points than for species the same distance from the perturbation but not following branching points. It is proposed that the findings can be explained as effects of a mental model employing concepts of influence and resistance. Under this model a perturbation is a change in energy level at a point in the system that acts as an influence affecting the rest of the system. The basic concepts in this model are domain‐general and on that basis it is predicted that the dissipation effect should be found in judgments of any physical system to which notions of influence and resistance can be applied. (shrink)

This article offers an analysis of ecologist Charles Elton’s “functional” concept of the niche and of the notion of function implicitly associated with it. It does so in part by situating Elton’s niche concept within the broader context of the “functionalist-interactionist” approach to ecology he introduced, and in relation to his views on the relationship between ecology and evolution. This involves criticizing the common claim that Elton’s idea of species as fulfilling functional roles within ecological communities committed (...) him to an idea of communities as units of selection. While such a claim implicitly attributes to Elton an understanding of function along the lines of the selected-effects theory of function advocated by many biologists and philosophers of biology, Elton’s use of the niche concept, I maintain, involves an understanding of function more along the lines of alternative nonselectionist theories such as the causal-role, goal-contribution, and organizational theories. I also briefly discuss how ecologists after Elton also tend to have typically adopted a nonselectionist understanding of the function concept, similar to his. (shrink)

Advances in the empirical sectors of biology are beginning to reveal evolvability as a major evolutionary process. Yet evolvability’s theoretical role is still intensely debated. Since its inception nearly thirty years ago, the evolvability research front has put a strong emphasis on the non-genetic mechanisms that influence the short-term evolvability of individuals within populations by causing phenotypic heterogeneity, such as developmental trait plasticity, phenotypic plasticity, modularity, the G-P map, robustness, and/or epigenetic variation. However, genetic evolvability mechanisms such as mutation or (...) recombination have a deeper history in evolutionary thought that is often overlooked by those in the evolvability research front, with recent evidence suggesting that species switch to genetic evolvability mechanisms when short-term evolvability strategies fail to relieve selective pressures. For this reason, a causal distinction must be made between genetic evolvability and the more recently emphasized non-genetic (or evo-devo) evolvability to allow for its maturation as a central explanatory concept. I conclude by arguing that the anachronisms of the scientific process are the main culprit behind recent divisions in biology and likely beyond. To streamline theoretical progress, we need to build a new science with new underlying philosophies like restricted pluralism. (shrink)

The present paper deals with the tools that can be used to represent causation and to reason about it and, specifically, with their diversity. It focuses on so-called “causal probabilities”—that is, probabilities of effects given one of their causes—and critically surveys a recent paper in which Joyce argues that the values of these probabilities do not depend on one’s conception of causation. I first establish a stronger independence claim: I show that the very definition of causal probabilities is (...) independent of one’s conception of causation. Second, I investigate whether causal probabilities indeed take the same values under their different possible definitions. (shrink)

In biology and philosophy of biology, discussing the notion of interaction leads to an examination of interactionism, which is, broadly speaking, the view that rejects gene-centrism and gene determinism and instead emphasizes the fact that traits of organisms are always the result of genes and environments. It has long been asserted that the nature-nurture problem requires an interactionist solution of sorts, the so-called interactionist consensus. This consensus, however, has been deemed insufficient and challenged by several authors triggering an (...) extension of the debate among contestants and defenders. Unfortunately, part of the problem is that the views on causation that would ground claims about interactionism are not always made explicit in this debate, which renders those views somewhat complicated to assess. Moreover, it seems to be assumed that causal complexity excludes the possibility of characterizing, distinguishing, or comparing among causal contributions. By turning to a detailed survey of the origin of the debate and to some developments in the philosophy of causation, we will contend that this view is unwarranted, and that much of the debate around interactionism is based on the drawing of this conclusion. We also examine implications of this analysis for the project to develop a framework based on the notion of inter-identities. (shrink)

Interactionism has emerged as a promising approach to moral character in the wake of the situationist challenge and the character-situation debate. This paper will consider whether interactionism is troubled by a familiar problem from the philosophy of mind: the coupling-constitution or causal-constitution fallacy. In relation to character, this issue pertains to whether the external factors featured in interactionist models are partly constitutive of the agent’s character, or whether they merely play a causal role. In contrast to some (...) other interactionist theorists, I argue that interactionism doesn’t need to make distinctions regarding causation and constitution, and would be better off without attempting to do so. Making such claims would only add metaphysical baggage to interactionism that won’t aid in its goal of providing an empirically adequate moral psychology of character. Interactionists are thus better off evading the C-C fallacy challenge, rather than attempting to meet it head-on. (shrink)

The kernel of this volume is an English translation of Jan Łukasiewicz’s classic work on the concept of cause (1906). It is the starting point for analytical considerations on causality of two generations of philosophers belonging to the tradition of the Lvov-Warsaw School.

We start this paper by arguing that causality should, in analogy with force in Newtonian physics, be understood as a theoretical concept that is not explicated by a single definition, but by the axioms of a theory. Such an understanding of causality implicitly underlies the well-known theory of causal nets and has been explicitly promoted by Glymour. In this paper we investigate the explanatory warrant and empirical content of TCN. We sketch how the assumption of directed cause–effect relations (...) can be philosophically justified by an inference to the best explanation. We then ask whether the explanations provided by TCN are merely post-facto or have independently testable empirical content. To answer this question we develop a fine-grained axiomatization of TCN, including a distinction of different kinds of faithfulness. A number of theorems show that although the core axioms of TCN are empirically empty, extended versions of TCN have successively increasing empirical content. (shrink)

In the last two decades few topics in philosophy of science have received as much attention as mechanistic explanation. A significant motivation for these accounts is that scientists frequently use the term “mechanism” in their explanations of biological phenomena. While scientists appeal to a variety of causal concepts in their explanations, many philosophers argue or assume that all of these concepts are well understood with the single notion of mechanism. This reveals a significant problem with mainstream mechanistic accounts– although (...) philosophers use the term “mechanism” interchangeably with other causal concepts, this is not something that scientists always do. This paper analyses two causal concepts in biology–the notions of “mechanism” and “pathway”–and how they figure in biological explanation. I argue that these concepts have unique features, that they are associated with distinct strategies of causal investigation, and that they figure in importantly different types of explanation. (shrink)

This article explores the conceptions of spirituality in a large and representative sample of the general population in the Netherlands. Spirituality is described mostly in cognitive terms, especially in the form of general references to a transcendent reality. Experiential expressions are used in more than a quarter of the descriptions. Important patterns in the descriptions are: spirituality as the transcendent God, spirituality as inwardness, and spirituality as mental health. In the sample, 21% distance themselves from spirituality; among people with (...) a secular outlook this percentage is 35%. We paid special attention to differences in conceptions of spirituality between people inside and outside institutional religious contexts and between people who self-identify as ‘spiritual’ and those who do not. (shrink)

Recent discussions in the philosophy of biology have brought into question some fundamental assumptions regarding evolutionary processes, natural selection in particular. Some authors argue that natural selection is nothing but a population-level, statistical consequence of lower-level events (Matthen and Ariew [2002]; Walsh et al. [2002]). On this view, natural selection itself does not involve forces. Other authors reject this purely statistical, population-level account for an individual-level, causal account of natural selection (Bouchard and Rosenberg [2004]). I argue that (...) each of these positions is right in one way, but wrong in another; natural selection indeed takes place at the level of populations, but it is a causal process nonetheless. (shrink)

This commentary argues that one specific but central concept in Lewis's theory, circular causality, is fundamentally flawed and should be discarded – first, because it does not make theoretical sense, and, second, because it leads to problems in practice, such as confounding the interaction between different systems with the relationship between different levels of analysis of a single system.