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)

Most psychological research aims to uncover generalizations about the mind that hold across subjects. Philosophical discussions of scientific explanation have focused on such generalizations, but in doing so, have often overlooked an important phenomenon: variation. Variation is ubiquitous in psychology and many other domains, and an important target of explanation in its own right. Here I characterize explananda that concern individual differences and formulate an account of what it takes to explain them. I argue that the notion of actual difference (...) making, the only causal concept in the literature that explicitly addresses variation, cannot be used to ground such an account. Instead, I propose a view on which explaining individual differences involves identifying causes that could be intervened on to reduce the variability in the population. This account provides criteria of success for explaining variation and deepens our understanding of causal explanation. (shrink)

Recent philosophical work has explored the distinction between causal and non-causal forms of explanation. In this literature, topological explanation is viewed as a clear example of the non-causal variety–it is claimed that topology lacks temporal information, which is necessary for causal structure. This paper explores the distinction between topological and causal forms of explanation and argues that this distinction is not as clear cut as the literature suggests. One reason for this is that some explanations involve both topological and causal (...) information. In these “borderline” cases scientists explain some outcome by appealing to the causal topology of the system of interest. These cases help clarify a type of topological explanation that is genuinely causal, but that differs from standard topological and interventionist accounts 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)

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)

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)

Jacques Monod (1971) argued that certain molecular processes rely critically on the property of chemical arbitrariness, which he claimed allows those processes to “transcend the laws of chemistry”. It seems natural, as some philosophers have done, to interpret this in modal terms: a biological relationship is chemically arbitrary if it is possible, within the constraints of chemical “law”, for that relationship to have been otherwise than it is. But while modality is certainly important for understanding chemical arbitrariness, understanding its biological (...) role also requires an account of the concrete causal-functional features that distinguish arbitrary from non-arbitrary phenomena. In this paper I elaborate on this under-emphasised aspect by offering a general account of these features: arbitrary relations are instantiated by mechanisms that involve molecular adapters, which causally couple two properties or processes which would otherwise be uncorrelated. Additionally, adapters work by acting as intermediate rather than cooperating causes. (shrink)

The concept of causal specificity is drawing considerable attention from philosophers of biology. It became the rationale for rejecting (and occasionally, accepting) a thesis of causal parity of developmental factors. This literature assumes that attributing specificity to causal relations is at least in principle a straightforward (if not systematic) task. However, the parity debate in philosophy of biology seems to be stuck at a point where it is not the biological details that will help move forward. In this paper, I (...) take a step back to reexamine the very idea of causal specificity and its intended role in the parity dispute in philosophy of biology. I contend that the idea of causal specificity across variations as currently discussed in the literature is irreducibly twofold in nature: it is about two independent components that are not mutually entailed. I show this to be the source of prior complications with the notion of specificity itself that ultimately affect the purposes for which it is often invoked, notably to settle the parity dispute. (shrink)

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

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)

Several prominent debates in biology, such as those surrounding adaptationism, group selection, and punctuated equilibrium, have focused on disagreements about the relative importance of a cause in producing a phenomenon of interest. Some philosophers, such as John Beatty have expressed scepticism about the scientific value of engaging in these controversies, and Karen Kovaka has suggested that their value might be limited. In this paper, I challenge that scepticism by giving a novel analysis of relative significance controversies, showing that there are (...) three forms they can take. I argue that these controversies can have significant epistemic upshots, in that they help scientists form predictions about new instances of the phenomenon of interest. Finally, using two historical examples, I show how engaging in these controversies can improve our understanding of causal relationships. (shrink)

This work addresses biological explanations and aims to provide a philosophical account which brings together logical-procedural and historical-processual aspects when considering molecular pathways. It is argued that, having molecular features as explananda, a particular non-classical logical language – Zsyntax – can be used to formally represent, in terms of logical theorems, types of molecular processes, and to grasp how we get from one molecular interaction to another, hence explaining why a given outcome occurs. Expressing types of molecular biology processes in (...) terms of the Zsyntax language allows us to represent causal interactions by taking into account their context-sensitivity, and amounts to partly reviving the spirit of the so-called received view of explanation – which aimed to capture scientific explanatory accounts in terms of their logical structure and their appealing to nomological relations. Such a partial revival is pursued by invoking here non-classical deductions and empirical generalisations, which are called to provide the epistemic norms to explain the behavior of molecular pathways. (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)

Living organisms act as integrated wholes to maintain themselves. Individual actions can each be explained by characterizing the mechanisms that perform the activity. But these alone do not explain how various activities are coordinated and performed versatilely. We argue that this depends on a specific type of mechanism, a control mechanism. We develop an account of control by examining several extensively studied control mechanisms operative in the bacterium E. coli. On our analysis, what distinguishes a control mechanism from other mechanisms (...) is that it relies on measuring one or more variables, which results in setting constraints in the control mechanism that determine its action on flexible constraints in other mechanisms. In the most basic arrangement, the measurement process directly determines the action of the control mechanism, but in more complex arrangements signals mediate between measurements and effectors. This opens the possibility of multiple responses to the same measurement and responses based on multiple measurements. It also allows crosstalk, resulting in networks of control mechanisms. Such networks integrate the behaviors of the organism but also present a challenge in tailoring responses to particular measurements. We discuss how integrated activity can still result in differential, versatile, responses. (shrink)