The concept of downward causation is frequently used in an explanatory capacity in biology to account for certain regularities and processes. Some philosophers, however, argue that downward causation is metaphysically incoherent, providing three main objections. Underlying these objections is the assumption that entities are connected by compositional hierarchies of levels of organization. In this paper, I introduce the notions of weak and strong compositional relations using examples from evolutionary developmental biology. I argue that downward causation becomes unproblematic (...) if we use features of interventionist theories of causation to explain the causal relations between levels. I show that an interventionist account of downward causation successfully responds to the three central objections to downward causation in the philosophical literature and I clarify the explanatory usefulness of the concept in biology. As such, this paper provides an epistemic solution to demystify downward causation in the context of scientific practice. The solution proposed is compatible with how biologists seem to use a concept of downward causation fruitfully in their work. (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 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)

A common explanatory error in science concerns the conflation of the epistemological roles between two domains. Here we will address a specific case: when explanations of development replace evolutionary explanations or vice versa. Ernst Mayr famously distinguished between proximate and ultimate causal explanations in biology. His view was central to the Modern Synthesis’ exclusion of development from evolutionary theory. Nonetheless, the explanatory role of developmental processes in evolution is a central theme in current theoretical biology which has prompted several revisions (...) of Mayr’s distinction. Here we will review these reviewers to determine whether the integration of development and evolution is based on an appropriate reinterpretation of Mayr’s distinction. In many cases, revisionists suggest an interactionist alternative, in which proximate and ultimate causes interact to produce evolved traits. The most frequent interactionist account relies on the idea of reciprocal causation. We will argue that this perspective is still problematic and that the boundaries between explanatory domains are crossed. Instead, we should rethink Mayr’s distinction by adopting an alternative view of evolutionary causation, the so-called Statisticalist view, which maintains that the only level of causation is the individual level. By ruling out two different levels of causation, this framework is appropriate to avoid fallacious explanations and reconsider reciprocal causation entirely as a proximate phenomenon. We introduce the concept of “statistical reciprocity” to explain the statistical effects of reciprocal causality in populations and outline some ideas of “population ontogenetics” as a prominent framework for unifying development and evolution beyond interactionist positions. (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)

Abstract: A common explanatory error concerns conflating epistemological roles between two domains. Here I deal with a special case: when explanations of development replace evolutionary explanations or vice versa. Ernst Mayr famously distinguished between proximate and ultimate causal explanations in biology. His view was central to keeping development outside the theory of evolution. Nevertheless, the explanatory role of developmental processes in evolution is a central theme in current theoretical biology, which has led to several revisions of Mayr’s distinction. In the (...) following, I will review these reviewers to determine whether the integration of development and evolution is based on an appropriate reinterpretation of Mayr’s distinction. The revisionists often propose an interactionist alternative in which proximate and ultimate causes interact to produce evolved traits. The most common interactionist account relies on the idea of reciprocal causation. I will argue that this perspective is still problematic and that the boundaries between explanatory domains are crossed. Instead, we should rethink Mayr’s distinction by adopting an alternative view of evolutionary causation, the so-called Statisticalist view on natural selection, which claims that the only level of causation is the proximate level. By excluding two different levels of causation, this framework is able to avoid fallacious explanations and fully consider reciprocal causation as a proximate phenomenon. I introduce the concept of “statistical reciprocity” to explain the statistical effects of (proximate) reciprocal causation in ultimate explanations and outline some ideas of “population ontogenetics” as a prominent framework for unifying development and evolution beyond interactionist positions. (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)

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)

To naturalize the concept of teleological causality in biology it is not enough to avoid assuming backward causation or positing the existence of an inscrutable te- leological essence like the élan vital. We must also specify how the causality of or- ganisms is distinct from the causality of designed artifacts like thermostats or asym- metrically oriented processes like the ubiquitous increase of entropy. Historically, the concept of teleological causality in biology has been based on an analogy to the familiar (...) experience of purposeful action. This is experienced by us as a disposition to achieve a general type of end that is represented in advance, and which regulates the selection of efficient means to achieve it. Inspired by this analogy, to bridge the gap between biology and human agency we describe a simple molecular pro- cess called autogenesis that shows how two linked complementary self-organizing processes can give rise to higher-order relations that resemble purposeful disposi- tions, though expressed in terms of constraints on molecular processes. Because the autogenic model is described in sufficient detail to be empirically realizable, it provides a proof of principle demonstrating a simple form of teleological causality. (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)

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 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)

This chapter introduces the main research schools and paradigms along which the field of evolutionary biology has been developing. Evolutionary thinking was originally founded upon the Neo-Darwinian paradigm that combines the teachings of traditional Darwinism with those of the Modern Synthesis. The Neo-Darwinian paradigm has since further diversified into the Micro-, Meso-, and Macroevolutionary schools, and it has also started to integrate the school of Ecology. Together, these schools establish the paradigm called Ecological Evolutionary Developmental Biology (Eco-Evo-Devo). A final school (...) studies Reticulate Evolution as it occurs by means of symbiosis, symbiogenesis, lateral gene transfer, infective heredity, and hybridization. This chapter reviews the major tenets and points of differentiation that exist between these distinct evolution schools. The chapter ends by looking into how evolution can be defined and how distinct units, levels, and mechanisms underlie theorizing on evolutionary hierarchies and evolutionary causation. The following chapter examines how the different evolution schools are implemented into the symbolic sciences. (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)

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)

The role of reciprocal causation in Extended Evolutionary Synthesis (EES) is controversial. Proponents of EES argue that reciprocal causation is a key innovation, underpinning the necessity of EES. Conversely, critics of the EES maintain that Standard Evolutionary Theory (SET) adequately encompasses the concept of reciprocal causation, challenging the need for EES. This skepticism is rooted in two primary critiques. First, the mischaracterization of causal dynamics within SET by EES advocates leads to a misrepresentation of SET. Second, the (...) oversight of how SET incorporates and acknowledges instances of reciprocal causation leads to claims about the empirical inaptness of SET. As a result, the debate has reached an impasse, with limited progress towards a constructive examination of reciprocal causation’s significance to evolutionary explanations. This paper introduces the scope argument, which examines reciprocal causation through timescales and grain of explanations. This approach revitalizes the debate in two ways. First, reframing the debate in terms of scope clarifies the role of reciprocal causation by allowing research programs to specify targets of explanation. Second, the elements of scope (timescales and grain) elucidate the epistemic advantage of reciprocal causation in the respective research programs in question. (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)

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 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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

In their target article, Lynch, Parke, and O’Malley argue against the quick application of causal, interventionist explanatory frameworks to microbiomes and their purported role in many disparate states, from obesity to anxiety. I think the authors have undersold the force of their argument. A careful consideration of the scope of their claims, made easier by a parallel drawn from the history of explanation in neuroscience, yields a productive pessimism: that causal explanations likely operate at the wrong level of analysis for (...) dynamic, distributed, Quineian entities like the microbiome. That is, we shouldn’t expect causal explanations for microbiomes at all—and this includes the authors’ own “microbiome success story” of C. difficile. Neuroscience, with its own computationally challenging, dynamic entity—the brain—may provide lessons for how to approach something like predictive control over the microbiome. (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)

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)

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)

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)

At the dawn of the computational era, immunology is at a crossroads: Its efforts to frame microbial-host interactions in combative, war-related terms no longer fit the larger picture of immune protection, and its focus on antimicrobial responses barely captures the diverse functions of the immune system, from tissue maintenance to cancer surveillance to development. As the classical view of immune processes becomes increasingly complex, the problem of self, individuality, mind-body interactions, and disease causation have stimulated extensive philosophical comment. Relating (...) these disparate research topics to changing avenues of theoretical studies, philosophy of immunology helps to reframe basic conceptions of the organism from an atomistic, insular entity to one characterized by fluidity, hybridity, and porosity. In addition, highlighting the role of the observer in experimental research, this interdisciplinary field has redefined classical demarcations between science and culture while advancing our understanding of biology as a fundamentally human endeavor. (shrink)

How does microbiota research impact our understanding of biological individuality? We summarize the interdisciplinary summer school on "Microbiota, Symbiosis and Individuality: Conceptual and Philosophical Issues" (July 2019), which was supported by a European Research Council starting grant project "Immunity, DEvelopment, and the Microbiota" (IDEM). The summer school centered around interdisciplinary group work on four facets of microbiota research: holobionts, individuality, causation, and human health. The conceptual discussion of cutting-edge empirical research provided new insights into microbiota and highlights the (...) value of incorporating into meetings experts from other disciplines, such as philosophy and history of science. (shrink)

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

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

[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.

Contemporary evolutionary biology comprises a plural landscape of multiple co-existent conceptual frameworks and strenuous voices that disagree on the nature and scope of evolutionary theory. Since the mid-eighties, some of these conceptual frameworks have denounced the ontologies of the Modern Synthesis and of the updated Standard Theory of Evolution as unfinished or even flawed. In this paper, we analyze and compare two of those conceptual frameworks, namely Niles Eldredge’s Hierarchy Theory of Evolution (with its extended ontology of evolutionary entities) and (...) the Extended Evolutionary Synthesis (with its proposal of an extended ontology of evolutionary processes), in an attempt to map some epistemic bridges (e.g. compatible views of causation; niche construction) and some conceptual rifts (e.g. extra-genetic inheritance; different perspectives on macroevolution; contrasting standpoints held in the “externalism–internalism” debate) that exist between them. This paper seeks to encourage theoretical, philosophical and historiographical discussions about pluralism or the possible unification of contemporary evolutionary biology. (shrink)

The usual way of discussing normativity and naturalism is by running through a standard range of issues: the relations of fact and value, objectivity, reason and emotion, is and ought, and the so-called ‘naturalistic fallacy’. This is a naturalism that is virtually silent on nature. I outline an alternative approach that relates normativity to our nature as living beings, for whom specific things are good or bad for us. Our nature as evaluative beings is shown to be rooted in and (...) emergent from this biological normativity. There is also significant downward causation, such that our brain-bodies are continually modified by our experience and thoughts. Cultures, as emergent from the affordances of our brain-bodies, create further extensive, irreducible sources of normativity, albeit ones which do not wholly escape biological normativity and can impact back on it. (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)

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)

Functional robustness refers to a system’s ability to maintain a function in the face of perturbations to the causal structures that support performance of that function. Modularity, a crucial element of standard methods of causal inference and difference-making accounts of causation, refers to the independent manipulability of causal relationships within a system. Functional robustness appears to be at odds with modularity. If a function is maintained despite manipulation of some causal structure that supports that function, then the relationship between (...) that structure and function fails to be manipulable independent of other causal relationships within the system. Contrary to this line of reasoning, I argue that functional robustness often attends feedback control, rather than failures of modularity. Feedback control poses its own challenges to causal explanation and inference, but those challenges do not undermine modularity—and indeed, modularity is crucial to grappling with them. (shrink)

The widespread mistrust of metaphysics-the main obstacle to the unification of physics and philosophy-is based on the myth that metaphysical claims cannot be falsified or verified, because they are supposedly true independently of empirical knowledge. This is not true of metaphysical naturalism, whose approach is to critically reflect on the theories and findings of all the empirical disciplines and abstract from them a theory about such general features of reality that no single empirical discipline can be the authority on. (...) class='Hi'>Causation is such a feature, since its instances include anything from planetary motions to particle interactions, chemical reactions, biological functions, and closing a door. Consequently, a general account of causation is beyond any particular empirical discipline. Metaphysical naturalism takes a meta-perspective on the results of the empirical sciences and attempts to figure out how it fits together in a coherent whole, e.g. by offering a general account of causation. General accounts of this kind are falsifiable in so far as the theories are falsifiable from which they are generalizations. The paper also discusses some fundamental metaphysical principles implicitly assumed by the sciences generally, and why they imply that unification is methodologically virtuous. (shrink)

Identifying the necessary and sufficient conditions for individuating and classifying diseases is a matter of great importance in the fields of law, ethics, epidemiology, and of course, medicine. In this paper, I first propose a means of achieving this goal, ensuring that no two distinct disease-types could correctly be ascribed to the same disease-token. I then posit a metaphysical ontology of diseases—that is, I give an account of what a disease is. This is essential to providing the most effective means (...) of interfering with disease processes. Following existing work in the philosophy of medicine and epidemiology (primarily Christopher Boorse; Caroline Whitbeck; Alexander Broadbent), philosophy of biology (Joseph LaPorte; D.L. Hull), conditional analyses of causation (J.L. Mackie; David Lewis), and recent literature on dispositional essentialism (Stephen Mumford and Rani Anjum; Alexander Bird), I endorse a dispositional conception of disease. Following discussion of various conceptions of disease-identity, their relations to the clinical and pathological effects of the diseases in question, and how diseases are treated, I conclude (i) that diseases should be individuated by their causes, and (ii) that diseases are causal processes best seen as simultaneously acting sequences of mutually manifesting dispositions. (shrink)

Much of the current research in regenerative medicine concentrates on stem-cell therapy that exploits the regenerative capacities of stem cells when injected into different types of human tissues. Although new therapeutic paths have been opened up by induced pluripotent cells and human mesenchymal cells, the rate of success is still low and mainly due to the difficulties of managing cell proliferation and differentiation, giving rise to non-controlled stem cell differentiation that ultimately leads to cancer. Despite being still far from becoming (...) a reality, these studies highlight the role of physical and biological constraints (e.g., cues and morphogenetic fields) placed by tissue microenvironment on stem cell fate. This asks for a clarification of the coupling of stem cells and microenvironmental factors in regenerative medicine. We argue that extracellular matrix and stem cells have a causal reciprocal and asymmetric relationship in that the 3D organization and composition of the extracellular matrix establish a spatial, temporal, and mechanical control over the fate of stem cells, which enable them to interact and control (as well as be controlled by) the cellular components and soluble factors of microenvironment. Such an account clarifies the notions of stemness and stem cell regeneration consistently with that of microenvironment. (shrink)

The problem of biological memory led Russell to propose the existence of mnemic causation, a mechanism by which past experience influences current thought directly, that is, without the need for a material intermediary in the form of a neural "memory trace." Russell appears to have been inspired by German biologist Richard Semon's concept of mnemic homophony, which conveys memory to consciousness on the basis of similarity between current and past circumstances. Semon, however, in no way denied a role (...) for stable neural structures or "engrams" in the memory process. In contrast to Russell, contemporary biologist Rupert Sheldrake provides a viable theory of memory by remaining true to Semon's original idea and expanding it beyond personal memory to the collective memory of species, encompassing not only mental but developmental memory. (shrink)

In a recent remarkable article, Froese (2023) presents his Irruption Theory to explain how motivations can make a behavioral difference in motivated activity. In this opinion article, we review the main tenets of Froese’s theory, and highlight its difficulty in overcoming the randomness challenge it supposedly solves, that is, the issue of how adaptive behavior can arise in the face of material underdetermination. To advance our understanding of motivated behavior in line with Froese’s approach, we recommend that future work should (...) endorse a multilevel pluralistic approach to causation and explanation in which motivations could genuinely play an irreducible role. Additionally, in line with the life-mind continuity thesis, we suggest that the best place to look for the interplay between motivations and nonmotivational physical, biological, and dynamical factors, may be at the level of the continuous feeling of being an embodied, living organism. (shrink)