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)

The standard perception of the dichotomy between population thinking and essentialism (typological thinking) in evolutionary economics descends from the golden age of the neo-Darwinian Synthesis. Over the last few decades the received view on population thinking has been seriously challenged in biology and its philosophy. First, the strong version of population thinking that banishes essentialism witnessed important tensions stemming from the ontological status of species. These tensions have been amplified by the demise of positivism and the rise of a (...) new essentialism in philosophy of science. Second, the soft version that transforms the opposition between population thinking and essentialism to the dichotomy between ultimate and proximate causation has led to contradictory interpretations regarding the locus of ultimate causes. Taking stock of the previous discussion the paper addresses the limits to population thinking in the socio-economic realm. The upshot is that without denying the important achievements made by the application of population thinking in sub-disciplines like industrial dynamics and economic anthropology, the idea to generalize these applications into the whole socio-economic realm is problematic. The aforementioned achievements cannot come to grips with the structural aspects of capitalism, its different periods (e.g. the contemporary finance-led capitalism) and its geographical varieties. The resulting gap points to the importance of structural analysis (essentialism) and evolutionary political economy. The latter is distinguished from the rest of evolutionary economics by its project to go beyond the surface of economic phenomena and to critically analyze their underlying social structures. (shrink)

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)

Exceptions are often cited as a counterargument against formal causation. Against this I argue that Aristotle explicitly allows for exceptions to essences in his biological writings, and that he has a means of explaining them through formal causation – though this means that he has to slightly elaborate on his general case theory from the Posterior Analytics, by supplementing it with a special case application in the biological writings. Specifically for Aristotle an essential predication need not be a (...) universal predication. Rather an essential predication is where a property belongs essentially to a species or genus. This essential predication serves a causal and explanatory role, and is not dependent on a corresponding universal predication. (shrink)

A phenome occurs through the many pathways of the complex net of interaction between the phenome and its environment; therefore researching and understanding how it arises requires investigation into many possible causes that are in constant interaction with each other. The most comprehensive investigations in biology are the ones in which many biologists from different sub-areas—evolutionary biology, developmental biology, molecular biology, physiology, genetics, epigenetics, ecology—have collaborated. Still, biologists do not always need to collaborate or look for (...) the most comprehensive explanations. A more standard investigation in biology occurs within a single subarea, and uses well-defined experiments with very specific conditions. This paper is about causation and related explanation in plant phenome research and its relevance to Aristotle’s Theory of Four Causes. I argue that there are causes which resemble Aristotle’s formal, material, and efficient causes in phenotype explanation and occurrence; but causes which resemble Aristotle’s final causes occur in phenotype explanation only, not in the occurrence. (shrink)

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)

The fracture in the emerging discipline of biosemiotics when the code biologist Marcello Barbieri claimed that Peircian biosemiotics is not genuine science raises anew the question: What is science? When it comes to radically new approaches in science, there is no simple answer to this question, because if successful, these new approaches change what is understood to be science. This is what Galileo, Darwin and Einstein did to science, and with quantum theory, opposing interpretations are not merely about what theory (...) is right, but what is real science. Peirce's work, as he acknowledged, is really a continuation of efforts of Schelling to challenge the heritage of Newtonian science for the very good reason that the deep assumptions of Newtonian science had made sentient life, human consciousness and free will unintelligible, the condition for there being science. Pointing out the need for such a revolution in science has not succeeded as a defence of Peircian biosemiotics, however. In this paper, I will defend the scientific credentials of Peircian biosemiotics by relating it to the theoretical biology of the bio-mathematician, Robert Rosen. Rosen's relational biology, focusing on anticipatory systems and giving a place to final causes, should also be seen as a rigorous development of the Schellingian project to conceive nature in such a way that the emergence of sentient life, mind and science are intelligible. Rosen has made a very strong case for the characterization of his ideas as a real advance not only in science, but in how science should be understood, and I will argue that it is possible to provide a strong defence of Peircian biosemiotics as science through Rosen's defence of relational biology. In the process, I will show how biosemiotics can and should become a crucial component of anticipatory systems theory. (shrink)

In this paper, I defend the agent/patient distinction against critics who argue that causal interactions are symmetrical. Specifically, I argue that there is a widespread type of causal interaction between distinct entities, resulting in a type of ontological asymmetry that provides principled grounds for distinguishing agents from patients. The type of interaction where the asymmetry is found is when one of the entities undergoes a change in kind, structure, powers, or intrinsic properties as a result of the interaction while the (...) other does not. Interactions of this type are widespread in molecular biology and chemistry. I focus specifically on (i) the actions of enzymes on substrates and (ii) water molecules breaking the bonds of polarized molecules. Finally, I respond to objections by laying out and to a limited extent defending three commitments of my account: emergent entities and powers, realism about chemical kinds or structures, and the assumption of the agent/patient distinction in functional attributions in biology. (shrink)

Biology seems to present local and transitory regularities rather than immutable laws. To account for these historically constituted regularities and to distinguish them from mathematical invariants, Montévil and Mossio (Journal of Theoretical Biology 372:179–191, 2015) have proposed to speak of constraints. In this article we analyse the causal power of these constraints in the evolution of biodiversity, i.e., their positivity, but also the modality of their action on the directions taken by evolution. We argue that to fully account (...) for the causal power of these constraints on evolution, they must be thought of in terms of normativity. In this way, we want to highlight two characteristics of the evolutionary constraints. The first, already emphasised as reported by Gould (The structure of evolutionary theory, Harvard University Press, 2002), is that these constraints are both produced by and producing biological evolution and that this circular causation creates true novelties. The second is that this specific causality, which generates unpredictability in evolution, stems not only from the historicity of biological constraints, but also from their internalisation through the practices of living beings. (shrink)

The biological sciences have always proven a fertile ground for philosophical analysis, one from which has grown a rich tradition stemming from Aristotle and flowering with Darwin. And although contemporary philosophy is increasingly becoming conceptually entwined with the study of the empirical sciences with the data of the latter now being regularly utilised in the establishment and defence of the frameworks of the former, a practice especially prominent in the philosophy of physics, the development of that tradition hasn’t received the (...) wider attention it so thoroughly deserves. This review will briefly introduce some recent significant topics of debate within the philosophy of biology, focusing on those whose metaphysical themes (in everything from composition to causation) are likely to be of wide-reaching, cross-disciplinary interest. (shrink)

When a group of processes achieves such closure that a set of states of affairs recurs continually, then the effect of that coherence on the world differs from what would occur in the absence of that closure. Such altered effectiveness is an attribute of the system as a whole, and would have consequences. This indicates that the network of processes, as a unit, has ontological significance. Whenever a network of processes generates continual return to a limited set of states of (...) affairs, the system may function as a “whole”— with respect to appropriate interaction partners. The balance achieved by the processes provides the form of definiteness of a unified agent. The causal powers of such coherent aggregates are indeed just the powers of the “constituents acting in concert”. However, the components act in concert in the specific way they do only because of their inclusion in the closed set of interactions that defines the coherence. This renders the causal powers of the coherence defined by that closure non-redundant, and hence the coherence, as a unit, is ontologically significant. The form of definiteness that provides internal coherence also grounds external efficacy of the societal aggregation. The closure is a structural feature of the coherence — possibly, but not necessarily, apparent in spatial structuring. This approach can provide a unified account that includes quantum microphysics, systems biology, and the philosophy of organism ─ without reducing any of these to another. (shrink)

Disputes about the causal structure of natural selection have implications for teleosemantics. Etiological, mainstream teleosemantics is based on a causalist view of natural selection. The core of its solution to Brentano’s Problem lies in the solution to Kant’s Puzzle provided by the Modern Synthesis concerning populational causation. In this paper, I suggest that if we adopt an alternative, statisticalist view on natural selection, the door is open for two reflections. First, it allows for setting different challenges to etiological teleosemantics (...) that arise if a statisticalist reading of natural selection is right. Second, by providing a different solution to Kant’s Puzzle based on individual causes of evolution, statisticalism promotes a different answer to Brentano’s Problem, what I label as Agential Teleosemantics. (shrink)

Should we think of our universe as law-governed and “clockwork”-like or as disorderly and “soup”-like? Alternatively, should we consciously and intentionally synthesize these two extreme pictures? More concretely, how deterministic are the postulated causes and how rigid are the modeled properties of the best statistical methodologies used in the biological and behavioral sciences? The charge of this entry is to explore thinking about causation in the temporal evolution of biological and behavioral systems. Regression analysis and path analysis are simply (...) explicated with reference to a thought experiment of painting three universes (clockwork, soup, and conscious) useful for imagining our actual universe. Attention to historical, structural, and mechanistic explanatory perspectives broadens the palette of methodologies available for analyzing determinism in, and explanation of, biological and behavioral systems. Each justified methodology provides a partial perspective on complex reality. Is a total explanation of any system ever possible, and what would it require? (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)

In this chapter we examine the relationship between biological information, the key biological concept of specificity, and recent philosophical work on causation. We begin by showing how talk of information in the molecular biosciences grew out of efforts to understand the sources of biological specificity. We then introduce the idea of ‘causal specificity’ from recent work on causation in philosophy, and our own, information theoretic measure of causal specificity. Biological specificity, we argue, is simple the causal specificity of (...) certain biological processes. This, we suggest, means that causal relationships in biology are ‘informational’ relationships simply when they are highly specific relationships. Biological information can be identified with the storage, transmission and exercise of biological specificity. It has been argued that causal relationships should not be regarded as informational relationship unless they are ‘arbitrary’. We argue that, whilst arbitrariness is an important feature of many causal relationships in living systems, it should not be used in this way to delimit biological information. Finally, we argue that biological specificity, and hence biological information, is not confined to nucleic acids but distributed among a wide range of entities and processes. (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)

The methodological nonreductionism of contemporary biology opens an interesting discussion on the level of ontology and the philosophy of nature. The theory of emergence (EM), and downward causation (DC) in particular, bring a new set of arguments challenging not only methodological, but also ontological and causal reductionism. This argumentation provides a crucial philosophical foundation for the science/theology dialogue. However, a closer examination shows that proponents of EM do not present a unified and consistent definition of DC. Moreover, they (...) find it difficult to prove that higher-order properties can be causally significant without violating the causal laws that operate at lower physical levels. They also face the problem of circularity and incoherence in their explanation. In our article we show that these problems can be overcome only if DC is understood in terms of formal rather than physical (efficient) causality. This breakdown of causal monism in science opens a way to the retrieval of the fourfold Aristotelian notion of causality. (shrink)

A theoretical framework is provided to explore teleonomy as a problem of self-causation, distinct from upward, downward and reticulate causation. Causality theories in biology are often formulated within hierarchy theories, where causation is conceptualized as running up or down the rungs of a ladder-like hierarchy or, more recently, as moving between multiple hierarchies. Research on the genealogy of cosmologies demonstrates that in addition to hierarchy theories, causality theories also depend upon ideas of time. This paper explores (...) the roots and impact of both time and hierarchy thinking on causal reasoning in the evolutionary sciences. Within evolutionary biology, the Neodarwinian synthesis adheres to a linear notion of time associated with linear hierarchies that portray upward causation. Eco-evo-devo schools recognize the importance of downward causation and consequently receive resistance from the standard view because downward causation is sometimes understood as backward causation, considered impossible by adherents of a linear time model. In contrast, downward causation works with a spatial or presential time notion. Hybridization, lateral gene transfer, infective heredity, symbiosis and symbiogenesis require recognition of reticulate causation occurring in both space and time, or spacetime, between distinct and interacting ontological hierarchies. Teleonomy is distinct from these types of causation because it invokes the problem of self-causation. By asking how the focal level in a hierarchy can persist through time, self-causation raises philosophical concerns on the nature of duration, identity and individuality. (shrink)

Symmetries play a major role in physics, in particular since the work by E. Noether and H. Weyl in the first half of last century. Herein, we briefly review their role by recalling how symmetry changes allow to conceptually move from classical to relativistic and quantum physics. We then introduce our ongoing theoretical analysis in biology and show that symmetries play a radically different role in this discipline, when compared to those in current physics. By this comparison, we stress (...) that symmetries must be understood in relation to conservation and stability properties, as represented in the theories. We posit that the dynamics of biological organisms, in their various levels of organization, are not just processes, but permanent (extended, in our terminology) critical transitions and, thus, symmetry changes. Within the limits of a relative structural stability (or interval of viability), variability is at the core of these transitions. (shrink)

The Aristotelian axiom that function follows form was beautifully instantiated in molecular biology by the discovery of DNA’s structure that immediately suggested how DNA might work as depository and vehicle for genetic information. However, later on molecular biology became infatuated with the gene that became the center of the universe. This gene-centered viewpoint is an obstacle for the emerging field of evo-devo aiming at finding the causal connections between evolution and biological development. Here it is argued that molecular (...) biology must reject the narrow-minded causality associated with the gene-centered view and so it must recover to the spirit of Aristotelian natural history and its four types of causation in order to foster the evo-devo field of research. (shrink)

This is an extended review of John Dupré's _Processes of Life_, a collection of essays. It clarifies Dupré's concepts of reductionism and anti-reductionism, and critically examines his associated discussions of downward causation, and both the context sensitivity and multiple realization of categories. It reviews his naturalistic monism, and critically distinguishes between his realism about categories and constructivism about classification. Challenges to his process ontology are presented, as are arguments for his pluralism about scientific categories. None of his main conclusions (...) are rejected; rather it is main arguments for them that are the focus. (shrink)

A classic analytic approach to biological phenomena seeks to refine definitions until classes are sufficiently homogenous to support prediction and explanation, but this approach founders on cases where a single process produces objects with similar forms but heterogeneous behaviors. I introduce object spaces as a tool to tackle this challenging diversity of biological objects in terms of causal processes with well-defined formal properties. Object spaces have three primary components: (1) a combinatorial biological process such as protein synthesis that generates objects (...) with parts that are modular, independent, and organized according to an invariant syntax; (2) a notion of “distance” that relates the objects according to rules of change over time as found in nature or useful for algorithms; (3) mapping functions defined on the space that map its objects to other spaces or apply an evaluative criterion to measure an important quality, such as parsimony or biochemical function. Once defined, an object space can be used to represent and simulate the dynamics of phenomena on multiple scales; it can also be used as a tool for predicting higher-order properties of the objects, including stitching together series of causal processes. Object spaces are the basis for a strategy of theorizing, discovery, and analysis in biology: as heuristic idealizations of biology, they help us transform inchoate, intractable problems into articulated, well-structured ones. Developing an object space is a research strategy with a long, successful history under many other names, and it offers a unifying but not overreaching approach to biological theory. (shrink)

In her landmark book, Language, Thought, and Other Biological Categories (Millikan1984),1 Ruth Garrett Millikan utilizes the idea of a biological function to solve philosophical problems associated with the phenomena of language, thought, and meaning. Language and thought are activities of biological organisms, according to Millikan, and we should treat them as such when trying to answer related philosophical questions. Of special interest is Millikan’s treatment of intentionality. Here Millikan employs the notion of a biological function to explain what it is (...) for one thing in nature, a bee dance (43), for example, to be about another, in this case, the location of a nectar source. My concern in this paper is to understand whether Millikan’s account of intentionality adequately explains how humans achieve reference, in language or thought, to individuals and groups in their environment. In bringing her theory of intentional content to bear on human activities, Millikan focuses largely on natural language. Thus, in what follows, I begin by laying out the biology-based principles that underlie Millikan’s theory of content, then proceed with an explanation of how the theory is to apply to natural language. As it appears, Millikan’s account of how content is determined for natural language terms and sentences rests on the determinacy of intentional content at the psychological level. This leads me to take a careful look at what Millikan says about the content of mental representations, in hopes of finding a sufficient basis there for the application of Millikan’s theory of content to natural language. Ultimately, I conclude that Millikan’s theory faces a problem of vacuity. If we approach the theory as a theory of intentional content, intended to explain the nature of reference, the theory is lacking in an extremely important respect: Millikan explains how it could be one of the biological functions of a mental or natural language term to refer, without telling us precisely what in the natural order constitutes the reference relation.. (shrink)

Philosophers of dispositionalism deny the Humean account of causality in terms of constant conjunction, contiguity, temporal priority and contingency. And some of them go further to explain the causal relation not between events or objects, but between properties, in terms of reciprocity, simultaneity, ubiquity, intentionality and holism. But their exposition seems to remain fragmented even though they try to make use of the notions of intentionality and holim. I would inquire reasons why it is piecemeal, by analysing that they employ (...) these notions of intentionality and holism which has been constructed within the dualistic tradition. If one wants to make the dispositional project to be powerful, she should look for the notions of intentionality and holism which are free of the dualistic traits and which have been constructed in the tradition of naturalism. The concept of integrationality may be a candidate for such a task. This conception was coined in Zhongyong under the name of cheng in that there is nothing without cheng, and was developed in one of Sok-hon Ham's thesis that any entity in the world contains "seed" within it to realize objectives shared by all involved. Humans are privileged and distinct from other natures, but there is continuity between them. An example of the integrationality applied to the case of humans would be that realization of myself and realizations of all others are one and not two. I would summarize notions of "cheng" and "seed" by offering the integrationality thesis, that is, that there is integrationality in any entity like dispositions such that the integrationality is a power to realize the embedded objective of it in the context where it interacts with all others. I would claim that integrationality is a metaphysical basis for a way of human thinking, by arguing that it is a necessary part of presupposition for our understanding of the world without which the world is not intelligible. The notion of integrationality is involved empirically as well as conceptually. Empirically, there are numerous reports from physics, biology and information science, which provide with a clue which may well be taken to show the ubiquitous integrationality. But some conceptual considerations would also indicate necessarily toward the same direction. These would include various theses of ontology, epistemology, disposition, modality, naturalized intentionality, fitting and topics like these. I will investigate some of them in order to justify my claim of this paper. (shrink)

In this paper, I argue that causal theories of memory are typically committed to two independent, non-mutually entailing theses. The first thesis pertains to the necessity of appropriate causation in memory, specifying a condition token memories need to satisfy. The second pertains to the explanation of memory reliability in causal terms and it concerns memory as a type of mental state. Post-causal theories of memory can reject only the first (weak post-causalism) or both (strong post-causalism) theses. Upon this backdrop, (...) I examine Werning’s (2020) causalist argument from probabilistic correlation. I argue that it doesn’t establish the necessity of appropriate causation and thus it can only target strong post-causalist theories. I end up by presenting some general considerations, suggesting that memories may not always be causally linked to past experiences. (shrink)

This paper examines the adequacy of causal graph theory as a tool for modeling biological phenomena and formalizing biological explanations. I point out that the causal graph approach reaches it limits when it comes to modeling biological phenomena that involve complex spatial and structural relations. Using a case study from molecular biology, DNA-binding and -recognition of proteins, I argue that causal graph models fail to adequately represent and explain causal phenomena in this field. The inadequacy of these models is (...) due to their failure to include relevant spatial and structural information in a way that does not render the model non-explanatory, unmanageable, or inconsistent with basic assumptions of causal graph theory. (shrink)

This paper advances the thesis of methodological mechanism, the claim that to be committed to mechanism is to adopt a certain methodological postulate, i.e. to look for causal pathways for the phenomena of interest. We argue that methodological mechanism incorporates a minimal account of understanding mechanisms, according to which a mechanism just is a causal pathway described in the language of theory. In order to argue for this position we discuss a central example of a biological mechanism, the mechanism of (...) cell death, known as apoptosis. We argue that this example shows that our philosophically deflationary account is sufficient in order to have an illuminating account of mechanisms as the concept is used in biology. (shrink)

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

This chapter explores the idea that causal inference is warranted if and only if the mechanism underlying the inferred causal association is identified. This mechanistic stance is discernible in the epidemiological literature, and in the strategies adopted by epidemiologists seeking to establish causal hypotheses. But the exact opposite methodology is also discernible, the black box stance, which asserts that epidemiologists can and should make causal inferences on the basis of their evidence, without worrying about the mechanisms that might underlie their (...) hypotheses. I argue that the mechanistic stance is indeed a bad methodology for causal inference. However, I detach and defend a mechanistic interpretation of causal generalisations in epidemiology as existence claims about underlying mechanisms. (shrink)

Current debates surrounding the virtues and shortcomings of randomization are symptomatic of a lack of appreciation of the fact that causation can be inferred by two distinct inference methods, each requiring its own, specific experimental design. There is a non-statistical type of inference associated with controlled experiments in basic biomedical research; and a statistical variety associated with randomized controlled trials in clinical research. I argue that the main difference between the two hinges on the satisfaction of the comparability requirement, (...) which is in turn dictated by the nature of the objects of study, namely homogeneous or heterogeneous populations of biological systems. Among other things, this entails that the objection according to which randomized experiments fail to provide better evidence for causation because randomization cannot guarantee comparability is mistaken. (shrink)

Between 1653 and 1655 Margaret Cavendish makes a radical transition in her theory of matter, rejecting her earlier atomism in favour of an infinitely-extended and infinitely-divisible material plenum, with matter being ubiquitously self-moving, sensing, and rational. It is unclear, however, if Cavendish can actually dispense of atomism. One of her arguments against atomism, for example, depends upon the created world being harmonious and orderly, a premise Cavendish herself repeatedly undermines by noting nature’s many disorders. I argue that her supposed difficulties (...) with atomism expose a deeper tension in her work between two fundamental metaphysical commitments each of which has substantial philosophical support: her monist theory of the material world (which maintains that there exists just one natural substance which is the single principal cause) and her occasional theory of causation (which requires multiple finite principal causes in nature -- causes that might be considered individual substances). Her monism undermines atomism while her theory of occasional cause seems to rest on a conception of nature that would be especially friendly to atomism. I argue further that we can solve this tension within a Cavendishian framework in such a way as to preserve her theory of causation and her monism, but that this solution depends upon our taking her monism in a particular (and weak) form. I finally note that we can best make sense of her unique and interesting form of monism by acknowledging her social-political motivations in addition to her motivations in natural philosophy. (shrink)

In this paper, I offer one example of conceptual change. Specifically, I contend that the discovery that viruses could cause cancer represents an excellent example of branch jumping, one of Thagard’s nine forms of conceptual change. Prior to about 1960, cancer was generally regarded as a degenerative, chronic, non-infectious disease. Cancer causation was therefore usually held to be a gradual process of accumulating cellular damage, caused by relatively non-specific component causes, acting over long periods of time. Viral infections, on (...) the other hand, were generally understood to be acute processes, whereby single, specific and necessary causal agents acted alone to produce disease. However, during the 1960s and 1970s, a number of cancers were discovered to have an infectious aetiology. Of particular note were two—Burkitt’s lymphoma and cervical cancer—which I will discuss in detail later in this piece. Together, these discoveries led, in the short term, to a tentative aetiological reclassification of some types of cancer as infectious diseases and, in the longer term, to a full-blown reclassification of cancer as an aetiological disease branch in its own right. This process of reclassification forms the empirical basis for my concluding remarks on the influence of classification upon causation in medicine. Through this, I aim to demonstrate that conceptual change, far from being a purely abstract concern of the philosopher of science, is of substantial import to scientific practitioners. (shrink)

The anti-reductionist character of the recent philosophy of biology and the dynamic development of the science of emergent properties prove that the time is ripe to reintroduce the thought of Aristotle, the first advocate of a “top-down” approach in life-sciences, back into the science/philosophy debate. His philosophy of nature provides profound insights particularly in the context of the contemporary science of evolution, which is still struggling with the questions of form, teleology, and the role of chance in evolutionary processes. (...) However, although Aristotle is referenced in the evolutionary debate, a thorough analysis of his theory of hylomorphism and the classical principle of causality which he proposes is still needed in this exchange. Such is the main concern of the first part of the present article which shows Aristotle’s metaphysics of substance as an open system, ready to incorporate new hypothesis of modern and contemporary science. The second part begins with the historical exploration of the trajectory from Darwin to Darwinism regarded as a metaphysical position. This exploration leads to an inquiry into the central topics of the present debate in the philosophy of evolutionary biology. It shows that Aristotle’s understanding of species, teleology, and chance – in the context of his fourfold notion of causality – has a considerable explanatory power which may enhance our understanding of the nature of evolutionary processes. This fact may inspire, in turn, a retrieval of the classical theology of divine action, based on Aristotelian metaphysics, in the science/theology dialogue. The aim of the present article is to prepare a philosophical ground for such project. (shrink)

Many believe that a suitably programmed computer could act for its own goals and experience feelings. I challenge this view and argue that agency, mental causation and qualia are all founded in the unique, homeostatic nature of living matter. The theory was formulated for coherence with the concept of an agent, neuroscientific data and laws of physics. By this method, I infer that a successful action is homeostatic for its agent and can be caused by a feeling - which (...) does not motivate as a force, but as a control signal. From brain research and the locality principle of physics, I surmise that qualia are a fundamental, biological form of energy generated in specialized neurons. Subjectivity is explained as thermodynamically necessary on the supposition that, by converting action potentials to feelings, the neural cells avert damage from the electrochemical pulses. In exchange for this entropic benefit, phenomenal energy is spent as and where it is produced - which precludes the objective observation of qualia. (shrink)

Many enthusiasts of theistic evolution willingly accept Aquinas’s distinction between primary and secondary causes, to describe theologically “the mechanics” of evolutionary transformism. However, their description of the character of secondary causes in relation to God’s creative action oftentimes lacks precision. To some extent, the situation within the Thomistic camp is similar when it comes to specifying the exact nature of secondary and instrumental causes at work in evolution. Is it right to ascribe all causation in evolution to creatures—acting as (...) secondary and instrumental causes? Is there any space for a more direct divine action in evolutionary transitions? This article offers a new model of explaining the complexity of the causal nexus in the origin of new biological species, including the human species, analyzed in reference to both the immanent and transcendent orders of causation. (shrink)

Niche construction is a concept that captures a wide array of biological phenomena, from the environmental effects of metabolism to the creation of complex structures such as termite mounds and beaver dams. A central point in niche construction theory is that organisms do not just passively undergo developmental, ecological, or evolutionary processes, but are also active participants in them Evolution: From molecules to men, Cambridge University Press, Cambridge, 1983; Laland KN, Odling-Smee J, Feldman MW, In: KN Laland and T Uller (...) Evolutionary causation: Biological and philosophical reflections, MIT Press, Cambridge, MA, 2019). In this paper, we distinguish between two fundamentally different ways in which organisms are active participants: as agents and as contributors. Roughly, organisms act as agents when niche constructing effects are a result of a goal-directed behavior over which the organisms have some degree of control. Organisms act as contributors when the niche constructing effects do not arise from a goal to perform the constructive activity. As illustrative examples we discuss plants altering leaf-morphology to optimize light exposure as reported by Sultan and bacteria creating novel niches through excreting energy-rich metabolites. The difference between agential and contributional niche construction is important for understanding the different ways organisms can actively participate in development, ecology, and evolution. Additionally, this distinction can increase our understanding of how the capacity of agency is distributed across the tree of life and how agency influences developmental and evolutionary processes. (shrink)

Whereas many philosophers take backwards causation to be impossible, the few who maintain its possibility either take it to be absent from the actual world or else confined to theoretical physics. Here, however, I argue that backwards causation is not only actual, but common, though occurring in the context of our social institutions. After juxtaposing my cases with a few others in the literature and arguing that we should take seriously the reality of causal cases in these contexts, (...) I consider several objections. These objections involve whether the cases should be reinterpreted, whether they are properly within the institution, whether they involve necessitation or else Cambridge changes, whether and how they involve changing the past, and whether this should call us to question institutional reality. I end by suggesting that it is a virtue of our institutions that they allow backwards causation, that this is a kind of technology that they are often built to incorporate. (shrink)

Since Aristotle the central question in biology was the origin of organic form; a question put in the backyard by neo-Darwinism that considers organic form as a side effect of the interactions between genes and their products. On the other hand, the fashionable notion of self-organization also fails to provide a true causal explanation for organic form. For Aristotle form is both a cause and the principle of intelligibility and this coupled to the classical concepts of potentiality and actuality (...) provides a rational framework,currently embodied in the contemporary concept of ‘attractor’, for understanding the origin of organic form. (shrink)

The anti-reductionist character of the recent philosophy of biology and the dynamic development of the science of emergent properties prove that the time is ripe to reintroduce the thought of Aristotle, the first advocate of a “top-down” approach in life-sciences, back into the science/philosophy debate. His philosophy of nature provides profound insights particularly in the context of the contemporary science of evolution, which is still struggling with the questions of form species), teleology, and the role of chance in evolutionary (...) processes. However although Aristotle is referenced in the evolutionary debate, a thorough analysis of his theory of hylomorphism and the classical principle of causality which he proposes is still needed in this exchange. Such is the main concern of the first part of the present article which shows Aristotle’s metaphysics of substance as an open system, ready to incorporate new hypothesis of modern and contemporary science. The second part begins with the historical exploration of the trajectory from Darwin to Darwinism regarded as a metaphysical position. This exploration leads to an inquiry into the central topics of the present debate in the philosophy of evolutionary biology. It shows that Aristotle’s understanding of species teleology and chance – in the context of his fourfold notion of causality – has a considerable explanatory power which may enhance our understanding of the nature of evolutionary processes. This fact may inspire, in turn, a retrieval of the classical theology of divine action, based on Aristotelian metaphysics, in the science/theology dialogue. The aim of the present article is to prepare a philosophical ground for such project. (shrink)

Homology is a biological sameness relation that is purported to hold in the face of changes in form, composition, and function. In spite of the centrality and importance of homology, there is no consensus on how we should understand this concept. The two leading views of homology, the genealogical and developmental accounts, have significant shortcomings. We propose a new account, the hierarchical-dependency account of homology, which avoids these shortcomings. Furthermore, our account provides for continuity between special, general, and serial homology.

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)

It is widely thought that there is an important argument to be made that starts with premises taken from the science of physics and ends with the conclusion of physicalism. The standard view is that this argument takes the form of a causal argument for physicalism. Roughly: physics tells us that the physical realm is causally complete, and so minds (among other entities) must be physical if they are to interact with the world as we think they do. In what (...) follows, I raise problems for this view. After an initial review of the causal argument, I begin my case by showing that the totality of physical truths do not deductively entail the causal completeness of the physical realm, using a double-prevention scenario and causation by omission to show that nonphysical causes of physical effects would not need to violate physical conservation laws. I then move on to raise problems for an inductive argument for causal completeness by drawing on the neo-Russellian view that there is no causation in fundamental physics, and so causation must itself be a realized or derived entity. I conclude by suggesting that the underlying problem is that the causal argument has fallen out of touch with the sophisticated understanding that philosophers have developed of the role of causation within physics. (shrink)

We characterize access to empirical objects in biology from a theoretical perspective. Unlike objects in current physical theories, biological objects are the result of a history and their variations continue to generate a history. This property is the starting point of our concept of measurement. We argue that biological measurement is relative to a natural history which is shared by the different objects subjected to the measurement and is more or less constrained by biologists. We call symmetrization the theoretical (...) and often concrete operation which leads to considering biological objects as equivalent in a measurement. Last, we use our notion of measurement to analyze research strategies. Some strategies aim to bring biology closer to the epistemology of physical theories, by studying objects as similar as possible, while others build on biological diversity. (shrink)

[DRAFT] Paper presented at Congress for Doctoral Researchers in Philosophy, Tampere University, 25.–27.10. 2021. The Paper strives to flesh out Gilbert Simondon's notion of information as a multifaced process (transduction-modulation-organization) from the viewpoint of living (/biological) beings.

Essentialism in philosophy is the position that things, especially kinds of things, have essences, or sets of properties, that all members of the kind must have, and the combination of which only members of the kind do, in fact, have. It is usually thought to derive from classical Greek philosophy and in particular from Aristotle’s notion of “what it is to be” something. In biology, it has been claimed that pre-evolutionary views of living kinds, or as they are sometimes (...) called, “natu-ral kinds”, are essentialist. This static view of living things presumes that no tran-sition is possible in time or form between kinds, and that variation is regarded as accidental or inessential noise rather than important information about taxa. In contrast it is held that Darwinian, and post-Darwinian, biology relies upon varia-tion as important and inevitable properties of taxa, and that taxa are not, therefore, kinds but historical individuals. Recent attempts have been made to undercut this account, and to reinstitute essentialism in biological kind terms. Others argue that essentialism has not ever been a historical reality in biology and its predecessors. In this chapter, I shall outline the many meanings of the notion of essentialism in psychology and social science as well as science, and discuss pro- and anti-essentialist views, and some recent historical revisionism. It turns out that nobody was essentialist to speak of in the sense that is antievolutionary in biology, and that much confusion rests on treating the one word, “essence” as meaning a single notion when in fact there are many. I shall also discuss the philosophical implica-tions of essentialism, and what that means one way or the other for evolutionary biology. Teaching about evolution relies upon narratives of change in the ways the living world is conceived by biologists. This is a core narrative issue. (shrink)

We take the potentialities that are studied in the biological sciences (e.g., totipotency) to be an important subtype of biological dispositions. The goal of this paper is twofold: first, we want to provide a detailed understanding of what biological dispositions are. We claim that two features are essential for dispositions in biology: the importance of the manifestation process and the diversity of conditions that need to be satisfied for the disposition to be manifest. Second, we demonstrate that the concept (...) of a disposition (or potentiality) is a very useful tool for the analysis of the explanatory practice in the biological sciences. On the one hand it allows an in-depth analysis of the nature and diversity of the conditions under which biological systems display specific behaviors. On the other hand the concept of a disposition may serve a unificatory role in the philosophy of the natural sciences since it captures not only the explanatory practice of biology, but of all natural sciences. Towards the end we will briefly come back to the notion of a potentiality in biology. (shrink)

According to the new mechanistic approach, an acting entity is at a lower mechanistic level than another acting entity if and only if the former is a component in the mechanism for the latter. Craver and Bechtel :547–563, 2007. doi:10.1007/s10539-006-9028-8) argue that a consequence of this view is that there cannot be causal interactions between acting entities at different mechanistic levels. Their main reason seems to be what I will call the Metaphysical Argument: things at different levels of a mechanism (...) are related as part and whole; wholes and their parts cannot be related as cause and effect; hence, interlevel causation in mechanisms is impossible. I will analyze this argument in more detail and show under which conditions it is valid. This analysis will reveal that interlevel causation in mechanisms is indeed possible, if we take seriously the idea that the relata of the mechanistic level relation are acting entities and accept a slightly modified notion of a mechanistic level that is highly plausible in the light of the first clarification. (shrink)

Much contemporary debate on the nature of mechanisms centers on the issue of modulating negative causes. One type of negative causability, which I refer to as “causation by absence,” appears difficult to incorporate into modern accounts of mechanistic explanation. This paper argues that a recent attempt to resolve this problem, proposed by Benjamin Barros, requires improvement as it overlooks the fact that not all absences qualify as sources of mechanism failure. I suggest that there are a number of additional (...) types of effects caused by absences that need to be incorporated to account for the diversity of causal connections in the biological sciences. Furthermore, it is argued that recognizing natural variability in mechanisms, such as attenuation, leads to some interesting line-drawing issues for contemporary philosophy of mechanisms. (shrink)