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

The emphasis on the organization of entities and their activities and interactions has been labeled one of the most distinct contributions of mechanistic philosophy. In this paper I discuss the manner in which the organization of entities and their activities and interactions participates in bringing about phenomena. I present a well-known example from molecular biology—the functioning of the genetic switch in phage lambda—and discuss Marco J. Nathan’s notion of causation by concentration. Nathan introduces causation by concentration to (...) account for the irreducible causal role that the concentration ratio between two kinds of proteins possesses in the genetic switch mechanism in phage lambda. I discuss what the irreducibility of this causal role amounts to and provide a mechanistic interpretation of Nathan’s causation by concentration; that is, I explain this irreducible causal role as one organizational feature of this mechanism. The paper concludes that biological mechanisms need a causal pluralist framework [similar to Glennan’s account in, and but slightly modified] where organizational features such as the concentration ratio have a causally relevant role, yet all the causally productive relations occur at the level of entities or individuals. (shrink)

This paper sets out to analyze how causation works by focusing on biology, as represented by epidemiology and by scientific information on how the body works (“physiology”). It starts by exploring the specificity of evolved physiological systems, in which evolutionary, developmental and proximal causes all fit together, and the concept of function is meaningful; in contrast, this structure does not apply in epidemiology (or outside biology). Using these two contrasting branches of biology, I examine the role (...) both of mechanism and of difference making in causation. I find that causation necessarily involves both mechanism and difference making, and that they play complementary roles. Both are seen as ontologically necessary, even if the evidence is not always available for both. Influential monist accounts that focus on one of these, at the expense of ignoring the other, are found to be inadequate on these and on other grounds. Recent attempts to combine them are reviewed, notably that of Russo and Williamson (Int Stud Philos Sci 21:157–170, 2007), and it is argued that their epistemic view requires there to be a source of the different types of evidence that a rational agent would consider, and that this source must be ontic. I then analyze how causal relationships work in evolved physiological systems and in those studied by epidemiology, with a particular focus on how mechanism interacts with input. Finally, I consider this concept of causation from the perspective of everyday language, and of its possible generalisability outside biology. (shrink)

This paper argues that scale-dependence of physical and biological processes offers resistance to reductionism and has implications that support a specific kind of downward causation. I demonstrate how insights from multiscale modeling can provide a concrete mathematical interpretation of downward causation as boundary conditions for models used to represent processes at lower scales. The autonomy and role of macroscale parameters and higher-level constraints are illustrated through examples of multiscale modeling in physics, developmental biology, and systems biology. (...) Drawing on these examples, I defend the explanatory importance of constraining relations for understanding the behavior of biological systems. (shrink)

In this paper, we advocate the idea that an adequate explanation of biological systems requires appealing to organizational closure as an emergent causal regime. We first develop a theoretical justification of emergence in terms of relatedness, by arguing that configurations, because of the relatedness among their constituents, possess ontologically irreducible properties, providing them with distinctive causal powers. We then focus on those emergent causal powers exerted as constraints, and we claim that biological systems crucially differ from other natural systems in (...) that they realize a closure of constraints, i.e. a second-order emergent regime of causation such that the constituents, each of them acting as a constraint, realize a mutual dependence among them, and are collectively able to self-maintain. Lastly, we claim that closure can be justifiably taken as an emergent regime of causation, without admitting that it inherently involves whole-parts causation, which would require to commit to stronger ontological and epistemological assumptions. (shrink)

Despite the productivity of basic cancer research, cancer continues to be a health burden to society because this research has not yielded corresponding clinical applications. Many proposed solutions to this dilemma have revolved around implementing organizational and policy changes related to cancer research. Here I argue for a different solution: a new conceptualization of causation in cancer. Neither the standard molecular biomarker approaches nor evolutionary biology approaches to cancer fully capture its complex causal dynamics, even when considered jointly. (...) These approaches map on to Ernst Mayr’s proximate–ultimate distinction, which is an inadequate conceptualization of causation in biological systems and makes it difficult to connect developmental and evolutionary viewpoints. I propose looking to evolutionary developmental biology to overcome the distinction and integrate the proximate and ultimate causal frameworks. I use the concepts of modularity and evolvability to show how an EvoDevo perspective can be manifested in cancer translational research. This perspective on causation in cancer is better suited for integrating the complexity of current empirical results and can facilitate novel developments in the investigation and clinical treatment of cancer. (shrink)

What exactly do social scientists and biologists say when they make causal claims? This question is one of the central puzzles in philosophy of science. Alexander Reutlinger sets out to answer this question. He aims to provide a theory of causation in the special sciences (that is, a theory causation in the social sciences, the biological sciences and other higher-level sciences). According one recent prominent view, causation is that causation is intimately tied to manipulability and the (...) possibility of intervene. Reutlinger's main negative target is to argue interventionist account of causation is not adequate. Where do interventionist accounts go wrong? Reutlinger argues that the central concept of the interventionist theories – that is, the very concept of an intervention – is tremendously problematic. Reutlinger's main positive claim consists in replacing the interventionist approach by an alternative explication of causation in the special sciences, the comparative variability theory of causation. This alternative preserves many insights of the interventionist account without a commitment to the claim that causation and interventions are intimately tied together. (shrink)

The dominant position in Philosophy of Science contends that downward causation is an illusion. Instead, we argue that downward causation doesn’t introduce vicious circles either in physics or in biology. We also question the metaphysical claim that “physical facts fix all the facts.” Downward causation does not imply any contradiction if we reject the assumption of the completeness and the causal closure of the physical world that this assertion contains. We provide an argument for rejecting this (...) assumption. Furthermore, this allows us to reconsider the concept of diachronic emergence. (shrink)

I explicate the crucial role played by efficient cause in Robert Rosen’s characterization of life, by elaborating on the topic of Aristotelian causality, and exploring the many alternate descriptions of causal and inferential entailments. In particular, I discuss the concepts of functional entailment and immanent causation, and examine how they fit into Robert Rosen’s relational-biology universe of living, anticipatory, and complex systems.

The last two words of the title for this essay are taken from a paper by R. S. Lillie, and the first phrase is also taken by implication from the same source. The study of chemical phenomena in life has progressed far enough so that underlying chemical causes, involved in Professor Lillie's picture of Biological Causation, may in part be discussed in general terms, and apart from the mass of detail known about the agents and processes involved. Moreover, this (...) mass of detail is now great enough so that even though we are far from having a complete or even a comprehensive picture of these causes at least some of the fundamental principles involved in the chemical aspects of biological causation are clearly revealed. (shrink)

We propose that the onset and progressive destructive action of cancer within an individual bears a profound and striking similarity to the onset and progressive human-engendered destruction of global ecosystems and the extinction of entire species. Cancer in the human body and our human role in planetary, especially biotic, degradation are uncannily similar systems. For starters, they are the only two known complex systems where a discrete component changes its normal ecological role and function—turning on and potentially killing its host, (...) and in so doing, itself. Both are “hostile takeovers.” Clearly, humans are integral to both systems. With cancer we are the host and victims of the rogue behavior of what starts out as a normal, healthy, and functionally important part of our bodies. With the biodiversity crisis, we are the part of the system that has changed, expanded, and proven so destructive to the system in which we live. We argue that given that these threats to our bodies and Earth are both essentially ecological diseases, understanding the critical role of ecological interdependencies for avoiding both cancer’s and humankind’s destruction of their respective homes should hopefully promote better stewardship of both by the only animal capable of recognizing the problems—us. (shrink)

I present an alternative account of causation in the biomedical and social sciences according to which the meaning of causal claims is given by their inferential relations to other claims. Specifically, I will argue that causal claims are inferentially related to certain evidential claims as well as claims about explanation, prediction, intervention and responsibility. I explain in some detail what it means for a claim to be inferentially related to another and finally derive some implication of the proposed account (...) for the epistemology, semantics and metaphysics of causation. (shrink)

This paper seeks to demonstrate why the existence of suboptimal design in biology does not offer a reason for Christians to reject the biological case for Intelligent Design. In it, I argue that Christians who critique ID based upon alleged deficiencies within biology fail to imagine the various ways in which a divine designer might bring about certain biological effects. That is, such critics presumably envision a simplistic notion of divine causation—where God either directly brings about every (...) biological effect, or is not involved in any biological effect. Such either or thinking, I maintain, is theologically unnecessary. (shrink)

The logic of genetic discovery has changed little over time, but the focus of biology is shifting from simple genotype–phenotype relationships to complex metabolic, physiological, developmental, and behavioral traits. In light of this, the traditional reductionist view of individual genes as privileged difference‐making causes of phenotypes is re‐examined. The scope and nature of genetic effects in complex regulatory systems, in which dynamics are driven by regulatory feedback and hierarchical interactions across levels of organization are considered. This review argues that (...) it is appropriate to treat genes as specific actual difference‐makers for the molecular regulation of gene expression. However, they are often neither stable, proportional, nor specific as causes of the overall dynamic behavior of regulatory networks. Dynamical models, properly formulated and validated, provide the tools to probe cause‐and‐effect relationships in complex biological systems, allowing to go beyond the limitations of genetic reductionism to gain an integrative understanding of the causal processes underlying complex phenotypes. (shrink)

Teleological terms such as "function" and "design" appear frequently in the biological sciences. Examples of teleological claims include: A (biological) function of stotting by antelopes is to communicate to predators that they have been detected. Eagles' wings are (naturally) designed for soaring. Teleological notions were commonly associated with the pre-Darwinian view that the biological realm provides evidence of conscious design by a supernatural creator. Even after creationist viewpoints were rejected by most biologists there remained various grounds for concern about the (...) role of teleology in biology, including whether such terms are: 1. vitalistic (positing some special "life-force"); 2. requiring backwards causation (because future outcomes explain present traits); 3. incompatible with mechanistic explanation (because of 1 and 2); 4. mentalistic (attributing the action of mind where there is none); 5. empirically untestable (for all the above reasons). Opinions divide over whether Darwin's theory of evolution provides a means of eliminating teleology from biology, or whether it provides a naturalistic account of the role of teleological notions in the science. Many contemporary biologists and philosophers of biology believe that teleological notions are a distinctive and ineliminable feature of biological explanations but that it is possible to provide a naturalistic account of their role that avoids the concerns above. Terminological issues sometimes serve to obscure some widely-accepted distinctions. (shrink)

Arguments for an extended evolutionary synthesis often center on the concept of “reciprocal causation.” Proponents argue that reciprocal causation is superior to standard models of evolutionary causation for at least two reasons. First, it leads to better scientific models with more predictive power. Second, it more accurately represents the causal structure of the biological world. Simply put, proponents of an extended evolutionary synthesis argue that reciprocal causation is empirically and explanatorily apt relative to competing causal frameworks. (...) In this paper, I present quantitative survey data from faculty members in biology departments at universities across the United States to evaluate this claim. The survey data indicate that a majority of the participants do not agree (i.e., most either disagree or neither agree nor disagree) that the concept of reciprocal causation confers a larger advantage on research practices. However, a majority of the participants agree that the causal framework of the extended evolutionary synthesis more accurately represents the structure of the biological world. These results demonstrate that the explanatory merits of a conceptual framework and its practical utility can come apart in interesting and informative ways. (shrink)

Recent research in philosophy of science has shown that scientists rely on a plurality of strategies to develop successful explanations of different types of phenomena. In the case of biology, most of these strategies go far beyond the traditional and reductionistic models of scientific explanation that have proven so successful in the fundamental sciences. Concretely, in the last two decades, philosophers of science have discovered the existence of at least two different types of scientific explanation at work in the (...) biological sciences, namely: mechanistic and structural explanations. Despite the growing evidence about the radically different nature of these two types of explanation, no inquiry has been conducted to date to determine the ontological reasons that might underlie these differences, nor the way in which these types of explanations can be systematically related with each other. Here, we aim to cover this gap by connecting this plurality of research strategies with the existence of emergent levels of reality. We argue that the existence of these different—and apparently incompatible—explanatory strategies to account for biological phenomena derives from the existence of “ontological jumps” in nature, which generate different regimes of causation that in turn demand the development of different explanatory frameworks. We identify two of these strategies—mechanistic modelling and network modelling—and connect them to the existence of two ontological regimes of causation. Finally, we relate them with each other in a systematic way. In this vein, our paper provides an ontological justification for the plurality of explanatory strategies that we see in the life sciences. (shrink)

The manifest appearance of function and purpose in living systems is responsible for the prevalence of apparently teleological explanations of organismic structure and behavior in biology. Although the attribution of function and purpose to living systems is an ancient practice, teleological notions are largely considered ineliminable from modern biological sciences, such as evolutionary biology, genetics, medicine, ethology, and psychiatry, because they play an important explanatory role. Historical and recent examples of teleological claims include the following: The chief function (...) of the heart is the transmission and pumping of the blood through the arteries to the extremities of the body. (Harvey 1616 [1928: 49]) The Predator Detection hypothesis remains the strongest candidate for the function of stotting [by gazelles]. (Caro 1986: 663) The geographic range of human malaria is much wider than the range of the sickle-cell gene. As it happens, other antimalarial genes take over the protective function of the sickle-cell gene in … other warm parts. (Diamond 1994: 83) Despite the substantial amount of data we now have on theropod dinosaurs, more information is necessary in order to determine the likelihood that early feathers served an adaptive function in visual display as opposed to other proposed adaptive functions such as thermoregulation. (Dimond et al. 2011: 62) The ubiquity of claims such as these raises the question: how should apparently teleological notions in biology be understood? Most post-Darwinian approaches attempt to naturalize teleology in biology, in opposition to nineteenth-century viewpoints which grounded it theologically. Nevertheless, biologists and philosophers have continued to question the legitimacy of teleological notions in biology. For instance, Ernst Mayr (1988), identified four reasons why teleological notions remain controversial in biology, namely that they are: vitalistic (positing some special ‘life-force’); requiring backwards causation (because goal-directed explanations seem to use future outcomes to explain present traits); incompatible with mechanistic explanation (because of 1 and 2); mentalistic (attributing the action of mind where there is none). A fifth complaint is that they are not empirically testable (Allen & Bekoff 1995). The current philosophical literature offers both Darwinian and non-Darwinian accounts of teleology in biology that aim to avoid these concerns. In this article, we hope to bring some clarity to the contemporary debates over the role of teleological notions in biology by sketching a taxonomy of the various accounts of biological function on offer (see Allen & Bekoff 1995 for a more comprehensive taxonomy that forms the basis of this presentation). We primarily focus on naturalistic accounts of biological function, since this is where we see the most lively and productive current debates (see, e.g., Garson 2016 for an extended survey). We also briefly discuss the notion of goal-directedness in section 2. (shrink)

My project in this paper is to extend the interventionist analysis of causation to give an account of causation in psychology. Many aspects of empirical investigation into psychological causation fit straightforwardly into the interventionist framework. I address three problems. First, the problem of explaining what it is for a causal relation to be properly psychological rather than merely biological. Second, the problem of rational causation: how it is that reasons can be causes. Finally, I look at (...) the implications of an interventionist analysis for the idea that an inquiry into psychological causes must be an inquiry into causal mechanisms. I begin by setting out the main ideas of the interventionist approach. (shrink)

Existing accounts of mechanistic causation are not suited for understanding causation in biological and neural mechanisms because they do not have the resources to capture the unique causal structure of control heterarchies. In this paper, we provide a new account on which the causal powers of mechanisms are grounded by time-dependent, variable constraints. Constraints can also serve as a key bridge concept between the mechanistic approach to explanation and underappreciated work in theoretical biology that sheds light on (...) how biological systems channel energy to actively respond to the environment in adaptive ways, perform work, and fulfill the requirements to maintain themselves far from equilibrium. We show how the framework applies to several concrete examples of control in simple organisms as well as the nervous system of complex organisms. (shrink)

Inferences like these are known as extrapolations.

Causal relations among components and activities are intentionally misrepresented in mechanistic explanations found routinely across the life sciences. Since several mechanists explicitly advocate accurately representing factors that make a difference to the outcome, these idealizations conflict with the stated rationale for mechanistic explanation. We argue that these idealizations signal an overlooked feature of reasoning in molecular and cell biology—mechanistic explanations do not occur in isolation—and suggest that explanatory practices within the mechanistic tradition share commonalities with model-based approaches prevalent in (...) population biology. (shrink)

The inapplicability of variations on theory reduction in the context of genetics and their irrelevance to ongoing research has led to an anti-reductionist consensus in philosophy of biology. One response to this situation is to focus on forms of reductive explanation that better correspond to actual scientific reasoning (e.g. part–whole relations). Working from this perspective, we explore three different aspects (intrinsicality, fundamentality, and temporality) that arise from distinct facets of reductive explanation: composition and causation. Concentrating on these aspects (...) generates new forms of reductive explanation and conditions for their success or failure in biology and other sciences. This analysis is illustrated using the case of protein folding in molecular biology, which demonstrates its applicability and relevance, as well as illuminating the complexity of reductive reasoning in a specific biological context. (shrink)

In many biological experiments, due to gene-redundancy or distributed backup mechanisms, there are no visible effects on the functionality of the organism when a gene is knocked out or down. In such cases there is apparently no counterfactual dependence between the gene and the phenotype in question, although intuitively the gene is causally relevant. Due to relativity of causal relations to causal models, we suggest that such cases can be handled by changing the resolution of the causal model that represents (...) the system. By decreasing the resolution of our causal model, counterfactual dependencies can be established at a higher level of abstraction. By increasing the resolution, stepwise causal dependencies of the right kind can serve as a sufficient condition for causal relevance. Finally, we discuss how introducing a temporal dimension in causal models can account for causation in cases of non-modular systems dynamics. (shrink)

The problem of natural teleology in biology has traditionally focused on reconciling Aristotle’s efficient and final causation. In this paper, however, I emphasize the importance of formal causation in natural teleological explanations and suggest that undermining its legitimacy is a backdoor route to undermining natural teleology itself. Formal causation, I argue, represents the “phenotype” of an object, to use a familiar word from genetics. This means that formal causes specify not only intrinsic “genotypic” qualities of an (...) object but also a range of environments in which the object is “properly” to inhabit. Such environmental specificity is possible through conscious activity, but is not found anywhere in non-conscious nature. Das Problem der natürlichen Teleologie ist traditionellerweise darin gesehen worden, Aristoteles’ Wirkursache und seine Finalursache miteinander zu vereinbaren. Dagegen betone ich in diesem Aufsatz die Bedeutung der formalen Verursachung in natürlichen teleologischen Erklärungen. Wenn man ihre Legitimität untergräbt, so lege ich nahe, untergräbt man gleichsam durch die Hintertür natürliche Teleologie als solche. Ich argumentiere, dass formale Verursachung den „Phänotyp“ eines Objekts darstellt, um ein geläufiges Wort aus der Genetik zu verwenden. Dies bedeutet, dass formale Ursachen nicht nur intrinsische „genotypische“ Eigenschaften eines Objekts spezifizieren, sondern auch eine Bandbreite von Umgebungen, in denen das Objekt „im eigentlichen Sinn“ angesiedelt sein sollte. Diese Spezifizierung der Umgebung ist durch bewusste Aktivität möglich, findet sich aber nirgendwo in der nicht-bewussten Natur. (shrink)

Many models of evolution are implicitly causal processes. Features such as causal feedback between evolutionary variables and evolutionary processes acting at multiple levels, though, mean that conventional causal models miss important phenomena. We develop here a general theoretical framework for analyzing evolutionary processes drawing on recent approaches to causal modeling developed in the machine-learning literature, which have extended Pearls do-calculus to incorporate cyclic causal interactions and multilevel causation. We also develop information-theoretic notions necessary to analyze causal information dynamics in (...) our framework, introducing a causal generalization of the Partial Information Decomposition framework. We show how our causal framework helps to clarify conceptual issues in the contexts of complex trait analysis and cancer genetics, including assigning variation in an observed trait to genetic, epigenetic and environmental sources in the presence of epigenetic and environmental feedback processes, and variation in fitness to mutation processes in cancer using a multilevel causal model respectively, as well as relating causally-induced to observed variation in these variables via information theoretic bounds. In the process, we introduce a general class of multilevel causal evolutionary processes which connect evolutionary processes at multiple levels via coarse-graining relationships. Further, we show how a range of fitness models can be formulated in our framework, as well as a causal analog of Prices equation, clarifying the relationships between realized/probabilistic fitness and direct/indirect selection. Finally, we consider the potential relevance of our framework to foundational issues in biology and evolution, including supervenience, multilevel selection and individuality. Particularly, we argue that our class of multilevel causal evolutionary processes, in conjunction with a minimum description length principle, provides a conceptual framework in which identification of multiple levels of selection may be reduced to a model selection problem. (shrink)

Is Neo-Aristotelian hylomorphism compatible mechanistic science? In this essay I forge a rapprochement between Neo-Aristotelian hylomorphism and the "new mechanist philosophy" in biology, neuroscience, and psychology by drawing attention to their shared commitments concerning multilevel organization, mechanisms, and teleology. Significantly, the new mechanists endorse organization realism (a touchstone of hylomorphism). Similarly, Neo-Aristotelian hylomorphism is committed to the reality of mechanisms or causal powers that produce, underlie, or maintain the behavior of (i) phenomena that are constituted through the (ii) spatial, (...) temporal, and active organization of their (iii) component entities and (iv) component activities (the four hallmarks of the new mechanist philosophy). In the course of the essay I address potential disagreements between these two positions pertaining to emergence, downward causation, and teleology. I conclude that Neo-Aristotelian hylomorphism should not been seen as fundamentally opposed to mechanisms; rather, hylomorphism provides a rigorous ontological framework that complements the insights of the new mechanist philosophy of biology, neuroscience and psychology. (shrink)

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

In 1961, Ernst Mayr published a highly influential article on the nature of causation in biology, in which he distinguished between proximate and ultimate causes. Mayr argued that proximate causes (e.g. physiological factors) and ultimate causes (e.g. natural selection) addressed distinct ‘how’ and ‘why’ questions and were not competing alternatives. That distinction retains explanatory value today. However, the adoption of Mayr’s heuristic led to the widespread belief that ontogenetic processes are irrelevant to evolutionary questions, a belief that has (...) (1) hindered progress within evolutionary biology, (2) forged divisions between evolutionary biology and adjacent disciplines and (3) obstructed several contemporary debates in biology. Here we expand on our earlier (Laland et al. in Science 334:1512–1516, 2011) argument that Mayr’s dichotomous formulation has now run its useful course, and that evolutionary biology would be better served by a concept of reciprocal causation, in which causation is perceived to cycle through biological systems recursively. We further suggest that a newer evolutionary synthesis is unlikely to emerge without this change in thinking about causation. (shrink)

This paper proposes an extended version of the interventionist account for causal inference in the practical context of biological mechanism research. This paper studies the details of biological mechanism researchers’ practices of assessing the evidential legitimacy of experimental data, arguing why quantity and variety are two important criteria for this assessment. Because of the nature of biological mechanism research, the epistemic values of these two criteria result from the independence both between the causation of data generation and the (...) class='Hi'>causation in question and between different interventions, not techniques. The former independence ensures that the interventions in the causation in question are not affected by the causation that is responsible for data generation. The latter independence ensures the reliability of the final mechanisms not only in the empirical but also the formal aspects. This paper first explores how the researchers use quantity to check the effectiveness of interventions, where they at the same time determine the validity of the difference-making revealed by the results of interventions. Then, this paper draws a distinction between experimental interventions and experimental techniques, so that the reliability of mechanisms, as supported by the variety of evidence, can be safely ensured in the probabilistic sense. The latter process is where the researchers establish evidence of the mechanisms connecting the events of interest. By using case studies, this paper proposes to use ‘intervention’ as the fruitful connecting point of literature between evidence and mechanisms. (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)

Chance comes into plays at many levels of the explanation of the evolutionary process; but the unity of sense of this category is problematic. The purpose of this talk is to clarify the meaning of chance at various levels in evolutionary theory: mutations, genetic drift, genetic revolutions, ecosystems, macroevolution. Three main concepts of chance are found at these various levels: luck (popular concept), randomness (probabilistic concept), and contingency relative to a given theoretical system (epistemological concept). After identifying which concept(s) of (...) chance fit(s) with these levels, the question is raised whether these concepts can be reduced to a smaller number, and whether chance in evolutionary theory has a subjective or an objective sense. (shrink)

A biological function is supposed to be performed adequately, and hence may fail to do so: this is dysfunction. This raises two questions. One is how to make explicit the way in which function can be discriminated from dysfunction without confusing dysfunction with non-function. The second question is how what is “right” and “wrong” can be legitimated by natural regulatory norms. A function can be viewed as a quality to which at least one variable with a definite set of values (...) is associated. Accordingly, function and dysfunction are the same quality of the same trait, but differ in the values associated to this variable. Dysfunction occurs when the associated set of values does not match this normal state. Biological systems have the epistemic singularity that their existence is the consequence of two distinct causal regimes, the so-called “proximate” and “ultimate” causes, whose convergence defines a system’s prescriptive normality. Each cause imposes restrictive rules that limit the possible ways these systems can putatively exist. When a system is insensitive to ultimate cause, it is determined by proximate causation alone, and hence escapes its own prescriptive norms. In conclusion: The normality of a biological system is defined by the convergence of proximate and ultimate causes. A function is a variable-associated quality whose values are defined relative to the norms of the system. Dysfunction occurs when the set of values of the same variable does not match the normality of the system, which can occur when the system is insensitive to ultimate causation. (shrink)

Background on probability and evolution -- Laying the foundation. Population-environment systems ; Causal probability and empirical practice ; Irrelevance of fitness as a causal property of token organisms ; Roles of environmental variation in selection -- Reconstructing evolution and chance. Populations in biological practice: Pragmatic yet real ; Real causation in pragmatic population-environment systems ; Fitness concepts in measurement and modeling ; Chance in population-environment systems ; The input measure problem for MM-CCS chance -- Conclusion.

I defend a theory of mental representation that satisfies naturalistic constraints. Briefly, we begin by distinguishing (i) what makes something a representation from (ii) given that a thing is a representation, what determines what it represents. Representations are states of biological organisms, so we should expect a unified theoretical framework for explaining both what it is to be a representation as well as what it is to be a heart or a kidney. I follow Millikan in explaining (i) in terms (...) of teleofunction, explicated in terms of natural selection. -/- To explain (ii), we begin by recognizing that representational states do not have content, that is, they are neither true nor false except insofar as they both “point to” or “refer” to something, as well as “say” something regarding whatever it is they are about. To distinguish veridical from false representations, there must be a way for these separate aspects to come apart; hence, we explain (ii) by providing independent theories of what I call f-reference and f-predication (the ‘f’ simply connotes ‘fundamental’, to distinguish these things from their natural language counterparts). -/- Causal theories of representation typically founder on error, or on what Fodor has called the disjunction problem. Resemblance or isomorphism theories typically founder on what I’ve called the non-uniqueness problem, which is that isomorphisms and resemblance are practically unconstrained and so representational content cannot be uniquely determined. These traditional problems provide the motivation for my theory, the structural preservation theory, as follows. F-reference, like reference, is a specific, asymmetric relation, as is causation. F-predication, like predication, is a non-specific relation, as predicates typically apply to many things, just as many relational systems can be isomorphic to any given relational system. Putting these observations together, a promising strategy is to explain f-reference via causal history and f-predication via something like isomorphism between relational systems. -/- This dissertation should be conceptualized as having three parts. After motivating and characterizing the problem in chapter 1, the first part is the negative project, where I review and critique Dretske’s, Fodor’s, and Millikan’s theories in chapters 2-4. Second, I construct my theory about the nature of representation in chapter 5 and defend it from objections in chapter 6. In chapters 7-8, which constitute the third and final part, I address the question of how representation is implemented in biological systems. In chapter 7 I argue that single-cell intracortical recordings taken from awake Macaque monkeys performing a cognitive task provide empirical evidence for structural preservation theory, and in chapter 8 I use the empirical results to illustrate, clarify, and refine the theory. (shrink)

Holism and emergence are coherent notions. The paper points to the classes of emergent phenomena -- such as autocatalysis -- that are taken as commonplace phenomena in biological sciences. Thus it questions the Democritean credo, “wholes are completely determined by their parts” (in some of its forms, called mereological determinism), that has become a dogma of contemporary philosophy. A living thing requires the ability to initiate, mediate and terminate processes that produce products that make up the whole. Autocatalysis is one (...) such mechanism, and its action at the level of the whole produces effects on the parts such that the properties, manifested by the parts in the absence of the whole engaged in autocatalysis, are altered. For these reasons, some writers suggest that autocatalysis is a law of organization and that it is emergent. It also appears that this is a case of downward causation -- one that clearly occurs in nature. If this is not a case of downward causation on Kim’s terms, then biological systems that are claimed to be emergent do not need to involve downward causation in his sense. The author thinks that this constitutes downward causation in an important sense -- the causal properties of the whole drive the behavior of the parts. Another set of examples comes from chaos dynamics. Relying on this evidence, the author challenges the Democritean credo (and mereological determinism) and shifts the onus of proof. (shrink)

Physics underlies all complexity, including our own existence: how is this possible? How can our own lives emerge from interactions of electrons, protons, and neutrons? This book considers the interaction of physical and non-physical causation in complex systems such as living beings, and in particular in the human brain, relating this to the emergence of higher levels of complexity with real causal powers. In particular it explores the idea of top-down causation, which is the key effect allowing the (...) emergence of true complexity and also enables the causal efficacy of non-physical entities, including the value of money, social conventions, and ethical choices. (shrink)

A comprehensive treatment of the concept of causation in evolutionary biology that makes clear its central role in both historical and contemporary debates. Most scientific explanations are causal. This is certainly the case in evolutionary biology, which seeks to explain the diversity of life and the adaptive fit between organisms and their surroundings. The nature of causation in evolutionary biology, however, is contentious. How causation is understood shapes the structure of evolutionary theory, and historical (...) and contemporary debates in evolutionary biology have revolved around the nature of causation. Despite its centrality, and differing views on the subject, the major conceptual issues regarding the nature of causation in evolutionary biology are rarely addressed. This volume fills the gap, bringing together biologists and philosophers to offer a comprehensive, interdisciplinary treatment of evolutionary causation. Contributors first address biological motivations for rethinking evolutionary causation, considering the ways in which development, extra-genetic inheritance, and niche construction challenge notions of cause and process in evolution, and describing how alternative representations of evolutionary causation can shed light on a range of evolutionary problems. Contributors then analyze evolutionary causation from a philosophical perspective, considering such topics as causal entanglement, the commingling of organism and environment, and the relationship between causation and information. Contributors John A. Baker, Lynn Chiu, David I. Dayan, Renée A. Duckworth, Marcus W Feldman, Susan A. Foster, Melissa A. Graham, Heikki Helanterä, Kevin N. Laland, Armin P. Moczek, John Odling-Smee, Jun Otsuka, Massimo Pigliucci, Arnaud Pocheville, Arlin Stoltzfus, Karola Stotz, Sonia E. Sultan, Christoph Thies, Tobias Uller, Denis M. Walsh, Richard A. Watson. (shrink)

The aim of this dissertation is to provide an analysis of central concepts in philosophy of science from the perspective of current molecular and developmental research. Each chapter explores the ways in which particular phenomena or discoveries in molecular biology influences our philosophical understanding of the nature of scientific knowledge. The introductory prologue draws some general connections between the various threads, which revolve around two central themes: causation and explanation. Chapter Two identifies a particular type of causal relation (...) which is widespread across the sciences, but cannot be straightforwardly accommodated by extant accounts of causation and causal explanation. Chapter Three explores how the form of redundant causality identified in the previous chapter plays an important role in causal explanation, by making the effect stable and robust. Chapter Four offers a novel perspective on the debate over biological reductionism by distinguishing between different paradigms of molecular explanation. Chapter Five provides a philosophical analysis of the so-called "Developmental Synthesis" of evolutionary and developmental biology, and suggests a general account of scientific unification grounded in the notion of explanatory relevance. Chapter Six offers an account of dispositional properties inspired by mechanisms of gene regulation, according to which dispositions are not properties of entities, but properties that describe the behavior of abstract idealized models. Finally, Chapter Seven scrutinizes the concept of the molecular ecosystem, a metaphor frequently employed by biologists to describe cellular interactions, but seldom articulated in detail. (shrink)