Causation in Biology

Advances in biology, at least over the past two centuries, have mostly relied on theories that were subsequently revised, expanded or eventually refuted using experimental and other means. The field of theoretical biology used to primarily provide a basis, similar to theoretical physics in the physical sciences, to rationally examine the frameworks within which biological experiments were carried out and to shed light on overlooked gaps in understanding. Today, however, theoretical biology has generally become synonymous with computational and mathematical biology. (...) This could in part be explained by a relatively recent tendency in which a "data first", rather than a "theory first", approach is preferred. Moreover, generating hypotheses has at times become procedural rather than theoretical, therefore perhaps inadvertently leading some hypotheses to become perfunctory in nature. This situation leaves our understanding enmeshed in data, which should be disentangled from much noise. Given the many unresolved questions in biology and medicine, big and small, ranging from the problem of protein folding to unifying causative frameworks of complex non-Mendelian human diseases, it seems apt to revive the role of pure theory in the biological sciences. This paper, using the current biomedical literature and historical precedents, makes the case for a "philosophical biology" (philbiology), distinct from but quite complementary to philosophy of biology (philobiology), which would entail biological investigation through philosophical approaches. Philbiology would thus be a reincarnation of theoretical biology, adopting the true sense of the word "theory" and making use of a rich tradition of serious philosophical approaches in the natural sciences. A philbiological investigation, after clearly defining a given biological problem, would aim to propose a set of empirical questions, along with a class of possible solutions, about that problem. Importantly, whether or not the questions can be tested using current experimental paradigms would be secondary to whether the questions are inherently empirical or not. These issues will be illustrated using a range of specific examples. The final goal of a philbiological investigation would be to develop a theoretical framework that can lead observational and/or interventional experimental studies of the defined problem, a framework that is structured, generative and expandable, and, crucially, one that simplifies some aspect(s) of the said problem. (shrink)

I argue that Binkley et al. use causal process tracing in conjunction with a natural trajectory experiment and two natural snapshot experiments in their re-examination of the Kaibab. This shows that Aldo Leopold may have been right about trophic cascade in the Kaibab in the 1920s, i.e., that there are good reasons to think that a loss of predators led to a deer irruption which decreased aspen recruitment. Using the different cause-finding practices in combination can strengthen causal inferences and mitigate (...) the shortcomings that each practice has. (shrink)

One hotly debated philosophical question in the analysis of evolutionary theory concerns whether or not evolution and the various factors which constitute it may profitably be considered as analogous to “forces” in the traditional, Newtonian sense. Several compelling arguments assert that the force picture is incoherent, due to the peculiar nature of genetic drift. I consider two of those arguments here – that drift lacks a predictable direction, and that drift is constitutive of evolutionary systems – and show that they (...) both fail to demonstrate that a view of genetic drift as a force is untenable. I go on to diagnose the reasons for the stubborn persistence of this problem, considering two open philosophical issues and offering some preliminary arguments in support of the force metaphor. (shrink)

Discussions of “chance” and related concepts are found throughout philosophical work on evolutionary theory. By drawing attention to three very commonly-recognized distinctions, I separate four independent concepts falling under the broad heading of “chance”: randomness, epistemic unpredictability, causal indeterminism, and probabilistic causal processes. Far from a merely semantic distinction, however, it is demonstrated that conflation of these obviously distinct notions has an important bearing on debates at the core of evolutionary theory, particularly the debate over the interpretation of fitness, natural (...) selection, and genetic drift. (shrink)

Several authors have used the notion of causal specificity in order to defend non-parity about genetic causes (Waters 2007, Woodward 2010, Weber 2017, forthcoming). Non-parity in this context is the idea that DNA and some other biomolecules that are often described as information-bearers by biologists play a unique role in life processes, an idea that has been challenged by Developmental Systems Theory (e.g., Oyama 2000). Indeed, it has proven to be quite difficult to state clearly what the alleged special role (...) of genetic causes consists in. In this paper, I show that the set of biomolecules that are normally considered to be information-bearers (DNA, mRNA) can be shown to be the most specific causes of protein primary structure, provided that causal specificity is measured over a relevant space of biological possibilities, disregarding physical as well as logically possible states of the causal variables. (shrink)

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

Among the many causes of an event, how do we distinguish the important ones? Are there ways to distinguish among causes on principled grounds that integrate both practical aims and objective knowledge? Psychologist Tania Lombrozo has suggested that causal explanations “identify factors that are ‘exportable’ in the sense that they are likely to subserve future prediction and intervention” (Lombrozo 2010, 327). Hence portable causes are more important precisely because they provide objective information to prediction and intervention as practical aims. However, (...) I argue that this is only part of the epistemology of causal selection. Recent work on portable causes has implicitly assumed them to be portable within the same causal system at a later time. As a result, it has appeared that the objective content of causal selection includes only facts about the causal structure of that single system. In contrast, I present a case study from systems biology in which scientists are searching for causal factors that are portable across rather than within causal systems. By paying careful attention to how these biologists find portable causes, I show that the objective content of causal selection can extend beyond the immediate systems of interest. In particular, knowledge of the evolutionary history of gene networks is necessary for correctly identifying causal patterns in these networks that explain cellular behavior in a portable way. (shrink)

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 first book length-work on Afa Ajura and translation of his complete poems_ This is the first English translation of and commentary on the collected poems of Alhaj Yūsuf Ṣāliḥ Ajura, a northern Ghanaian orthodox Islamic scholar, poet, and polemicist known as Afa Ajura, or “scholar from Ejura.” The poems, all handwritten in Arabic script, mainly in the Ghanaian language of Dagbani and also Arabic, explore the author’s socio‑religious beliefs. In the accompanying introduction, the translator examines the diverse themes of (...) the poems and how they challenge Tijāniyyah Sufi clerics and traditional practices such as idol worship. (shrink)

It has been argued that supervenience generates unavoidable confounding problems for interventionist accounts of causation, to the point that we must choose between interventionism and supervenience. According to one solution, the dilemma can be defused by excluding non-causal determinants of an outcome as potential confounders. I argue that this solution undermines the methodological validity of causal tests. Moreover, we don’t have to choose between interventionism and supervenience in the first place. Some confounding problems are effectively circumvented by experimental designs routinely (...) employed in science. The remaining confounding issues concern the physical interpretation of variables and cannot be solved by choosing between interventionism and supervenience. (shrink)

Invariance is one of several dimensions of causal relationships within the interventionist account. The more invariant a relationship between two variables, the more the relationship should be considered paradigmatically causal. In this paper, I propose two formal measures to estimate invariance, illustrated by a simple example. I then discuss the notion of invariance for causal relationships between non-nominal (i.e., ordinal and quantitative) variables, for which Information theory, and hence the formalism proposed here, is not well suited. Finally, I propose how (...) invariance could be qualified for such variables. (shrink)

In cases in which many causes together bring about an effect, it is common to select some as particularly important. Philosophers since Mill have been pessimistic about analyzing this reasoning because of its variability and the multifarious causal and pragmatic details of how it works. I argue Mill was right to think these details matter but wrong that they preclude philosophical analysis of causal selection. I show that analyzing the pragmatic details of scientific debates about the important causes of the (...) Bhopal Gas Tragedy can illuminate causal reasoning about disasters and shed new light on causality and causal selection. (shrink)

A prevalent narrative locates the discovery of the statistical phenomenon of regression to the mean in the work of Francis Galton. It is claimed that after 1885, Galton came to explain the fact that offspring deviated less from the mean value of the population than their parents did as a population-level statistical phenomenon and not as the result of the processes of inheritance. Arguing against this claim, we show that Galton did not explain regression towards mediocrity statistically, and did not (...) give up on his ideas regarding an inheritance process that caused offspring to revert to the mean. While the common narrative focuses almost exclusively on Galton’s statistics, our arguments emphasize the anthropological and biological questions that Galton addressed. Galton used regression towards mediocrity to support the claim that some biological types were more stable than others and hence were resistant to evolutionary change. This view had implications concerning both natural selection and eugenics. The statistical explanation attributed to Galton appeared later, during the biometrician-mutationist debate in the early 1900s. It was in the context of this debate and specifically by the biometricians, that the development of the statistical explanation was originally attributed to Galton. (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 recent debate over the causal foundations of evolutionary theory pits those who believe that natural selection causally explains long-term, adaptive population change against those who do not. In this paper, I argue that this debate – far from being an invention of several articles in 2002 – dates from our very first engagements with evolution as a quantified, statistical science. Further, when we analyze that history, we see that a pivotal figure in the early use of statistical methodology in (...) evolutionary theory, W.F.R. Weldon, changes his mind about precisely the central claim at issue. I close by drawing some morals which I think the case can offer for the contemporary debate going forward. (shrink)

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

Recent philosophical work on causation has focused on distinctions across types of causal relationships. This paper argues for another distinction that has yet to receive attention in this work. This distinction has to do with whether causal relationships have “material continuity,” which refers to the reliable movement of material from cause to effect. This paper provides an analysis of material continuity and argues that causal relationships with this feature are associated with a unique explanatory perspective, are studied with distinct causal (...) investigative methods, and provide different types of causal control over their effects. (shrink)

Although the definition of ‘signal’ has been controversial for some time within the life sciences, current approaches seem to be converging toward a common analysis. This powerful framework can satisfactorily accommodate many cases of signaling and captures some of its main features. This paper argues, however, that there is a central feature of signals that so far has been largely overlooked: its special causal role. More precisely, I argue that a distinctive feature of signals is that they are minimal causes. (...) I explain this notion, suggest some strategies for identifying its instances and defend its relevance by means of conceptual and empirical considerations. (shrink)

The Central Dogma of molecular biology, which holds that DNA makes protein and not the other way around, is as influential as it is controversial. Some believe the Dogma has outlived its usefulness, either because it fails to fully capture the ins-and-outs of protein synthesis (Griffiths and Stotz, 2013; Stotz, 2006), because it turns on a confused notion of information (Sarkar, 2004), or because it problematically assumes the unidirectional flow of information from DNA to protein (Gottlieb, 2001). This paper evaluates (...) an underexplored defense of the Dogma, which relies on the assumption that the Dogma and the Inheritance of Acquired Traits, a principle which dates as far back as Jean Baptiste-Lamarck, are incompatible principles (Smith, 1993; Judson, 1979; Dawkins, 1970; Cobb, 2017; Wilkins, 2002; Graur, 2018). By appealing to empirical evidence in molecular science, I argue that this apparent incompatibility is indeed merely apparent. I conclude by briefly demonstrating how these considerations bear on the topic of conceptual pluralism in the philosophy of science (Stencel and Proszewska, 2018; Lu and Bourrat, 2018). (shrink)

The concept of information and its relation to biosemiotics is a major area of contention among biosemioticians. Biosemioticians influenced by von Uexküll, Sebeok, Bateson and Peirce are critical of the way the concept as developed in information science has been applied to biology, while others believe that for biosemiotics to gain acceptance it will have to embrace information science and distance biosemiotics from Peirce’s philosophical work. Here I will defend the influence of Peirce on biosemiotics, arguing that information science and (...) biosemiotics as these were originally formulated are radically opposed research traditions. Failure to appreciate this will undermine the challenge of biosemiotics and other anti-reductionist traditions to mainstream science with its reductionist ambition to explain everything through physics. However, for this challenge to be successful, it will be necessary to respond to criticisms of Peircian ideas, jettisoning ideas that are no longer defensible and integrating ideas allied to his anti-reductionist agenda. Here I will argue that the natural philosophy of Gilbert Simondon, offering a searching critique of the application of the new concept of information and cybernetics to the life and human sciences, provides the means to defend and advance Peirce’s core ideas and thereby defend post-reductionist biosemiotics. (shrink)

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

In this work I propose a theory of evolution as a process of unfolding. This theory is based on four logically concatenated principles. The principle of evolutionary order establishes that the more complex cannot be generated from the simpler. The principle of origin establishes that there must be a maximum complexity that originates the others by logical deduction. Finally, the principle of unfolding and the principle of actualization guarantee the development of the evolutionary process from the simplest to the most (...) complex. These logical principles determine the existence of a virtual ideological matrix that contains the sequence of the preformed and folded morphogenetic fields. In this manner, the evolutionary process consists of the sequential unfolding and actualization of these fields, which is motorized by a process of teleologization carried out by the opening consciousness of the forms included in the fields of the ideological matrix. This theory leads to a radical change of perspective regarding the materialist worldview, and places life at the center of the evolutionary process as an activity carried out by a consciousness that seeks to fulfill a purpose by actualizing its own potentialities. (shrink)

Has science already answered the fundamental questions about the concepts of Life, Cosmos and Evolution? Has science not relegated these fundamental questions by following up on more immediate, “useful” and practical endeavors that ultimately ensure that the wheel of capitalism keeps spinning in its frantic search for material and economic progress? There is something terribly wrong with the current theory of evolution, understood as the Darwinian theory with its successive versions and extensions. The concept of natural selection, the cornerstone of (...) Darwinism, is logically inconsistent. This has been demonstrated in some of my latest academic publications. The entire conceptual framework of Darwinism is inadequate. Organisms do not compete with each other for the survival of the fittest. The fundamental relationship in Nature is not competition or confrontation, but interconnectivity, complementarity, and relational meaningfulness. A new theory of evolution is necessary to explain how it is possible that organisms as simple as bacteria, protozoa and diatoms could have generated organisms as complex as primates, and among them, the human being, a being capable of feeling and thinking, of suffering and enjoying, a being capable of having ideals and purposes. A theory that explains how it is possible that this being so complex, rich, and to some extent still unknown, has emerged from a single cell, an egg-cell, lacking all the capacities, riches and depths of human existence. Such a theory already exists. (shrink)

This paper challenges the common assumption that some phenotypic traits are quantitative while others are qualitative. The distinction between these two kinds of traits is widely influential in biological and biomedical research as well as in scientific education and communication. This is probably due to both historical and epistemological reasons. However, the quantitative/qualitative distinction involves a variety of simplifications on the genetic causes of phenotypic variability and on the development of complex traits. Here, I examine three cases from the life (...) sciences that show inconsistencies in the distinction: Mendelian traits, Mendelian diseases, and polygenic mental disorders. I show that these traits can be framed both quantitatively and qualitatively depending, for instance, on the methods through which they are investigated and on specific epistemic purposes. This suggests that the received view of quantitative and qualitative traits has a limited heuristic power—limited to some local contexts or to the specific methodologies adopted. Throughout the paper, I provide directions for framing phenotypes beyond the quantitative/qualitative distinction. I conclude by pointing at the necessity of developing a principled characterisation of what phenotypic traits, in general, are. (shrink)

ITA: In questo articolo analizzerò la differenza tra il concetto di ereditarietà e quello di ereditabilità. In primo luogo, evidenzierò come i due concetti derivino storicamente da differenti tradizioni nello studio della variabili-tà fenotipica e del rapporto genotipo-fenotipo. Secondariamente, illustrerò gli aspetti teorici e metodologici alla base dei due concetti, che sono peraltro collegati a differenti aree delle scienze biologiche. Infine, spigherò brevemente come si sia recentemente tentato, con molte difficoltà, di connettere lo studio dei meccanismi dell’ereditarietà allo studio dell’ereditabilità. (...) Nel discutere le questioni di cui sopra, farò riferimento a tratti psi-cologici come l’intelligenza dal momento che è proprio dallo studio di questo tipo di tratti che sono emersi i maggiori problemi teorici e metodologici, nonché le controversie più intense. -/- ENG: In this paper, I analyse the distinction between heredity and heritability. First, I highlight that the two con-cepts derive from different historical traditions in the study of phenotypic variability and of the genotype-phenotype relationship. Second, I illustrate the theoretical and methodological aspects connected to the two concepts, which are traditionally associated with different areas of biological research. Then, I focus on recent attempts aimed at connecting with each other the analysis of heredity and of heritability. In my discussion, I shall often refer to human psychological traits such as intelligence. Indeed, most theoretical and methodological dis-cussions have emerged with respect to the study of these traits. (shrink)

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

This article defends the notion of downward causation, relating it to a notion of conditional independence.

Cancer research is experiencing ‘paradigm instability’, since there are two rival theories of carcinogenesis which confront themselves, namely the somatic mutation theory and the tissue organization field theory. Despite this theoretical uncertainty, a huge quantity of data is available thanks to the improvement of genome sequencing techniques. Some authors think that the development of new statistical tools will be able to overcome the lack of a shared theoretical perspective on cancer by amalgamating as many data as possible. We think instead (...) that a deeper understanding of cancer can be achieved by means of more theoretical work, rather than by merely accumulating more data. To support our thesis, we introduce the analytic view of theory development, which rests on the concept of plausibility, and make clear in what sense plausibility and probability are distinct concepts. Then, the concept of plausibility is used to point out the ineliminable role played by the epistemic subject in the development of statistical tools and in the process of theory assessment. We then move to address a central issue in cancer research, namely the relevance of computational tools developed by bioinformaticists to detect driver mutations in the debate between the two main rival theories of carcinogenesis. Finally, we briefly extend our considerations on the role that plausibility plays in evidence amalgamation from cancer research to the more general issue of the divergences between frequentists and Bayesians in the philosophy of medicine and statistics. We argue that taking into account plausibility-based considerations can lead to clarify some epistemological shortcomings that afflict both these perspectives. (shrink)

The aim of this paper is to provide a theoretical framework to understand how multicellular systems realize functionally integrated physiological entities by organizing their intercellular space. From a perspective centered on physiology and integration, biological systems are often characterized as organized in such a way that they realize metabolic self-production and self-maintenance. The existence and activity of their components rely on the network they realize and on the continuous management of the exchange of matter and energy with their environment. One (...) of the virtues of the organismic approach focused on organization is that it can provide an understanding of how biological systems are functionally integrated into coherent wholes. Organismic frameworks have been primarily developed by focusing on unicellular life. Multicellularity, however, presents additional challenges to our understanding of biological systems, related to how cells are capable to live together in higher-order entities, in such a way that some of their features and behaviors are constrained and controlled by the system they realize. Whereas most accounts of multicellularity focus on cell differentiation and increase in size as the main elements to understand biological systems at this level of organization, we argue that these factors are insufficient to provide an understanding of how cells are physically and functionally integrated in a coherent system. In this paper, we provide a new theoretical framework to understand multicellularity, capable to overcome these issues. Our thesis is that one of the fundamental theoretical principles to understand multicellularity, which is missing or underdeveloped in current accounts, is the functional organization of the intercellular space. In our view, the capability to be organized in space plays a central role in this context, as it enables (and allows to exploit all the implications of) cell differentiation and increase in size, and even specialized functions such as immunity. We argue that the extracellular matrix plays a crucial active role in this respect, as an evolutionary ancient and specific (non-cellular) control subsystem that contributes as a key actor to the functional specification of the multicellular space and to modulate cell fate and behavior. We also analyze how multicellular systems exert control upon internal movement and communication. Finally, we show how the organization of space is involved in some of the failures of multicellular organization, such as aging and cancer. (shrink)

Human microbiome research makes causal connections between entire microbial communities and a wide array of traits that range from physiological diseases to psychological states. To evaluate these causal claims, we first examine a well-known single-microbe causal explanation: of Helicobacter pylori causing ulcers. This apparently straightforward causal explanation is not so simple, however. It does not achieve a key explanatory standard in microbiology, of Koch’s postulates, which rely on manipulations of single-microorganism cultures to infer causal relationships to disease. When Koch’s postulates (...) are framed by an interventionist causal framework, it is clearer what the H. pylori explanation achieves and where its explanatory strengths lie. After assessing this ‘simple’, single-microbe case, we apply the interventionist framework to two key areas of microbiome research, in which obesity and mental health states are purportedly explained by microbiomes. Despite the experimental data available, interventionist criteria for explanation show that many of the causal claims generated by microbiome research are weak or misleading. We focus on the stability, specificity and proportionality of proposed microbiome causal explanations, and evaluate how effectively these dimensions of causal explanation are achieved in some promising avenues of research. We suggest some conceptual and explanatory strategies to improve how causal claims about microbiomes are made. (shrink)

The so-called “Baldwin Effect” has been studied for years in the fields of Artificial Life, Cognitive Science, and Evolutionary Theory across disciplines. This idea is often conflated with genetic assimilation, and has raised controversy in trans-disciplinary scientific discourse due to the many interpretations it has. This paper revisits the “Baldwin Effect” in Baldwin’s original spirit from a joint historical, theoretical and experimental approach. Social Heredity – the inheritance of cultural knowledge via non-genetic means in Baldwin’s term – is also taken (...) into consideration. I shall argue that the Baldwin Effect can occur via social heredity without necessity for genetic assimilation. Computational experiments are carried out to show that when social heredity is permitted with high fidelity, there is no need for the assimilation of acquired characteristics; instead the Baldwin Effect occurs as promoting more plasticity to facilitate future intelligence. The role of mind and intelligence in evolution and its implications in an extended synthesis of evolution are briefly discussed. (shrink)

Human microbiome research makes causal connections between entire microbial communities and a wide array of traits that range from physiological diseases to psychological states. To evaluate these causal claims, we first examine a well-known single-microbe causal explanation: of Helicobacter pylori causing ulcers. This apparently straightforward causal explanation is not so simple, however. It does not achieve a key explanatory standard in microbiology, of Koch’s postulates, which rely on manipulations of single-microorganism cultures to infer causal relationships to disease. When Koch’s postulates (...) are framed by an interventionist causal framework, it is clearer what the H. pylori explanation achieves and where its explanatory strengths lie. After assessing this ‘simple’, single-microbe case, we apply the interventionist framework to two key areas of microbiome research, in which obesity and mental health states are purportedly explained by microbiomes. Despite the experimental data available, interventionist criteria for explanation show that many of the causal claims generated by microbiome research are weak or misleading. We focus on the stability, specificity and proportionality of proposed microbiome causal explanations, and evaluate how effectively these dimensions of causal explanation are achieved in some promising avenues of research. We suggest some conceptual and explanatory strategies to improve how causal claims about microbiomes are made. (shrink)

The role of genetic relatedness in social evolution has recently come under critical attention. These arguments are here critically analyzed, both theoretically and empirically. It is argued that when the conceptual structure of the theory of natural selection is carefully taken into account, genetic relatedness can be seen to play an indispensable role in the evolution of both facultative and advanced eusociality. Although reviewing the empirical evidence concerning the evolution of eusociality reveals that relatedness does not play a role in (...) the initial appearance of helper phenotypes, this follows simply from the fact that natural selection – of which relatedness is a necessary component – does not play a causal role in the origin of any traits. Further, separating two logically distinct elements of causal explanation – necessity and sufficiency – explains why the debate lingers on: although relatedness plays a necessary role in the evolution of helping and advanced eusociality, relatedness alone is not sufficient for their appearance. Therefore, if the relatedness variable in a given data set is held at a uniformly high value, then it indeed may turn out that other factors occupy a more prominent role. However, this does not change the fact that high relatedness functions as a necessary background condition for the evolution of advanced eusociality. (shrink)

The kin selection theory has recently been criticised on the basis of claiming that genetic relatedness does not play a causal role in the social evolution among individuals of insect societies. We outline here a line of criticism of this view by demonstrating two things. First, there are strong conceptual, theoretical and empirical reasons to think that close genetic relatedness has been necessary for the rise of the helper castes of social insects. And second, once we understand how causal explanation (...) itself results from an interplay of two logically distinct elements, necessity and sufficiency, we can also understand the scenarios in which relatedness does not seem to play a causal role for evolution of helper castes. The result of this analysis is that we should be more careful about the way we frame the empirical data on the evolution of social behaviour. (shrink)

In this paper we defend the view that mechanisms are underpinned by networks of difference-making relations. First, we distinguish and criticise two different kinds of arguments in favour of an activity-based understanding of mechanism: Glennan’s metaphysics- first approach and Illari and Williamson’s science-first approach. Second, we present an alternative difference-making view of mechanism and illustrate it by looking at the history of the case of scurvy prevention. We use the case of scurvy to argue that evidence for a mechanism just (...) is evidence for difference-making relations. (shrink)

In psychiatry, many scientists desire to move from a classification system based on symptoms toward a system based on biological causes. The idea is that psychiatric diseases should be redefined such that each disease would be associated with specific biological causes. This desire is intelligible because causal disease models often facilitate understanding and identification of new ways to intervene in disease processes. In its attempt to move from syndromal to specific etiological definitions, psychiatry follows the trend of general medicine.Current psychiatric...

Biologists and philosophers often use the language of determination in order to describe the nature of developmental phenomena. Accounts in terms of determination have often been reductionist. One common idea is that DNA is supposed to play a special explanatory role in developmental explanations, namely, that DNA is a developmental determinant. In this article we try to make sense of determination claims in developmental biology. Adopting a manipulationist approach, we shall first argue that the notion of developmental determinant is causal. (...) We suggest that two different theses concerning developmental determination can be articulated: determination of occurrence and structural determination. We shall argue that, while the first thesis is problematic, the second, opportunely qualified, is feasible. Finally, we shall argue that an analysis of biological causation in terms of determination cannot account for entangled dynamics. Characterising causal entanglement as a particular kind of interactive causation whereby difference-making causes ascribable to different levels of biological organisation influence a particular ontogenetic outcome, we shall, via two illustrative examples, diagnose some potential limits of a reductionist, molecular and intra-level understanding of biological causation. (shrink)

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)

In this paper we offer a minimal characterisation of the concept of mechanism in biomedicine, according to which a mechanism is a theoretically described causal pathway. We argue that this conceptionan be drawn from scientific practice, as illustrated by how a central biological and biomedical mechanism, the mechanism of apoptosis, was first identified and characterised. We will use the example of cytological and biochemical theoretical descriptions of the mechanism of apoptosis to draw lessons about the meaning of the concept of (...) mechanism in biomedical contexts and to contrast our preferred account of mechanism with some prominent accounts within the philosophical literature. The main outcome of our discussion will be that commitment to mechanism is first and foremost a methodological stance. (shrink)

Causalism is the thesis that natural selection can cause evolution. A standard argument for causalism involves showing that a hypothetical intervention on some population-level property that is identified with natural selection will result in evolution. In a pair of articles, one of which recently appeared in the pages of this journal, Jun Otsuka has put forward a quite different argument for causalism. Otsuka attempts to show that natural selection can cause evolution by considering a hypothetical intervention on an individual-level property. (...) Specifically, Otsuka identifies natural selection with the causal relationship between a trait and fitness, claims an intervention on the strength of this relationship can cause evolution, then concludes that natural selection can cause evolution. Below I describe why Otsuka’s argument for causalism is unconvincing. Central to my criticism is that Otsuka’s argument works only if one adopts an indefensible account of natural selection, according to which natural selection can occur in the absence of trait or fitness variation. I go on to explain why any attempt to demonstrate the truth of causalism via a hypothetical intervention on an individual-level property would appear to require one to adopt an account of natural selection that is inadequate for the same reason. This in turn means the plausibility of causalism does indeed depend on the plausibility of the claim that population-level properties, which supervene on the properties of the individuals in the population, can be causally efficacious. (shrink)

We propose a novel account of the distinction between innate and acquired biological traits: biological traits are innate to the degree that they are caused by factors intrinsic to the organism at the time of its origin; they are acquired to the degree that they are caused by factors extrinsic to the organism. This account borrows from recent work on causation in order to make rigorous the notion of quantitative contributions to traits by different factors in development. We avoid the (...) pitfalls of previous accounts and argue that the distinction between innate and acquired traits is scientifically useful. We therefore address not only previous accounts of innateness but also skeptics about any account. The two are linked, in that a better account of innateness also enables us better to address the skeptics. (shrink)

This is an epistemologically-driven history of the concept of evolution. Starting from its inception, this work will follow the development of this pregnant concept. However, in contradistinction to previous attempts, the objective will not be the identification of the different meanings it adopted through history, but conversely, it will let the concept to be unfolded, to be explicated and to express its own inner potentialities. The underlying thesis of the present work is, therefore, that the path that leads to the (...) development of the concept of evolution is the path that studies the possibilities of the evolution of concepts, and that the historical reconstruction of its conceptual trajectory will shed light into potential and unexploited possibilities. This methodology will provide useful tools and resources for future developments of the concept. For example, it will define the concept of transmutation as a different conceptual trajectory deviating from the one corresponding to evolution, at the onset of the 19th century. Moreover, epigenesis will not be the opposing concept to evolution, but only to simultaneous and instantaneous generation. It will demonstrate that every important system of epigenesis drew upon some kind of formative power to explain development. More importantly, it will show that the problem of preformation cannot be overlooked, and that some kind of virtual preformation must be considered in order to address the problems of generation and development. (shrink)

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

Ernst Mayr’s concept of dual causality in biology with the two forms of causes continues to provide an essential foundation for the philosophy of biology. They are equivalent to functional and evolutionary causes with both required for full biological explanations. The natural sciences can be classified into nomological, historical nomological and historical dual causality, the last including only biology. Because evolutionary causality is unique to biology and must be included for all complete biological explanations, biology is autonomous from the physical (...) sciences. (shrink)

Recent work by Brian Skyrms offers a very general way to think about how information flows and evolves in biological networks — from the way monkeys in a troop communicate, to the way cells in a body coordinate their actions. A central feature of his account is a way to formally measure the quantity of information contained in the signals in these networks. In this paper, we argue there is a tension between how Skyrms talks of signalling networks and his (...) formal measure of information. Although Skyrms refers to both how information flows through networks and that signals carry information, we show that his formal measure only captures the latter. We then suggest that to capture the notion of flow in signalling networks, we need to treat them as causal networks. This provides the formal tools to define a measure that does capture flow, and we do so by drawing on recent work defining causal specificity. Finally, we suggest that this new measure is crucial if we wish to explain how evolution creates information. For signals to play a role in explaining their own origins and stability, they can’t just carry information about acts: they must be difference-makers for acts. (shrink)

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

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)

Mechanisms are said to consist of two kinds of components, entities and activities. In the first half of this chapter, I examine what entities and activities are, how they relate to well-known ontological categories, such as processes or dispositions, and how entities and activities relate to each other (e.g., can one be reduced to the other or are they mutually dependent?). The second part of this chapter analyzes different criteria for individuating the components of mechanisms and discusses how real the (...) boundaries of mechanisms are. (shrink)