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)

In recent years the notion of biological specificity has attracted significant philosophical attention. This paper focuses on host specificity, a kind of biological specificity that has not yet been discussed by philosophers, and which concerns the extent to which a species is selective in the range of other species it exploits for feeding and/or reproduction. Host specificity is an important notion in ecology, where it plays a variety of theoretical roles. Here I focus on the role of host specificity in (...) biological control, a field of applied ecology that deals with the suppression of pests through the use of living organisms. Examining host specificity and its role in biological control yields several valuable contributions to our understanding of biological specificity. In particular, I argue that host specificity cannot be fully understood in terms of Woodward’s well-known account of causal specificity. To adequately account for host specificity, we need a notion of causal specificity that takes into consideration the extent to which a variable’s effects are similar to one another – a dimension not captured in Woodward’s account. In addition, the literature on host specificity in biological control highlights certain aspects in which causally specific relationships can be practically valuable that have not yet been addressed in philosophical discussions of specificity. That literature also reveals that in certain contexts specificity can hinder rather than foster effective control, thus leading to a nuanced assessment of the practical value of specific causes. (shrink)

In this article, I consider the term “environment” in various claims and models by evolutionists and ecologists. I ask whether “environment” is amenable to a philosophical explication, in the same way some key terms of evolutionary theorizing such as “fitness,” “species,” or more recently “population” have been. I will claim that it cannot. In the first section, I propose a typology of theoretical terms, according to whether they are univocal or equivocal, and whether they have been the object of formal (...) or conceptual attempts of clarification. “Environment” will appear to be in a position similar to “population,” yet almost no extant attempt has been made to make sense of its meaning and reference. In the second section, I will present several theoretical claims or issues that refer to “environment” in apparently very diverse ways, but always supposing a contrastive term, which is not always the same. The third section directly considers models in evolution and in ecology, and asks “where” in them is the environment term. The fourth section proposes that “environment” refers to a distinction between a varying and an invariant term, but shows that this does not exhaust its meaning, which requires making more conceptual differences. Then, I take on the suggestion that there might be two “environment” terms, one in ecology and one in evolution, but show that is not the case. Finally I center on the specific notion of “complex environment,” which is the object of several research programs, and propose a typology of “complex environments” across theories. (shrink)

The past few years have seen several novel information-theoretic measures of causal emergence developed within the scientific community. In this paper I will introduce one such measure, called ‘effective information’, and describe how it is used to argue for causal emergence. In brief, the idea is that certain kinds of complex system are structured such that an intervention characterised at the macro-level will be more informative than one characterised at the micro-level, and that this constitutes a form of causal emergence. (...) Having introduced this proposal, I will then assess the extent to which it is genuinely ‘causal’ and/or ‘emergent’, and argue that it supports only an epistemic form of causal emergence that is not as exciting as it first seems. (shrink)

The notion of a genetic program has been widely criticized by both biologists and philosophers. But the debate has revolved around a narrow conception of what programs are and how they work, and many criticisms are linked to this same conception. To remedy this, I outline a modern and more apt idea of a program that possesses many of the features critics thought missing from programs. Moving away from over-simplistic conceptions of programs opens the way to a more fruitful interplay (...) of ideas between the complexity of biology and our most complex engineering discipline. (shrink)

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

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)

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)

How should we reason in science? Jan Sprenger and Stephan Hartmann offer a refreshing take on classical topics in philosophy of science, using a single key concept to explain and to elucidate manifold aspects of scientific reasoning. They present good arguments and good inferences as being characterized by their effect on our rational degrees of belief. Refuting the view that there is no place for subjective attitudes in 'objective science', Sprenger and Hartmann explain the value of convincing evidence in terms (...) of a cycle of variations on the theme of representing rational degrees of belief by means of subjective probabilities (and changing them by Bayesian conditionalization). In doing so, they integrate Bayesian inference—the leading theory of rationality in social science—with the practice of 21st century science. Bayesian Philosophy of Science thereby shows how modeling such attitudes improves our understanding of causes, explanations, confirming evidence, and scientific models in general. It combines a scientifically minded and mathematically sophisticated approach with conceptual analysis and attention to methodological problems of modern science, especially in statistical inference, and is therefore a valuable resource for philosophers and scientific practitioners. (shrink)

A crucial question for a process view of life is how to identify a process and how to follow it through time. The genidentity view can contribute decisively to this project. It says that the identity through time of an entity X is given by a well-identified series of continuous states of affairs. Genidentity helps address the problem of diachronic identity in the living world. This chapter describes the centrality of the concept of genidentity for David Hull and proposes an (...) extension of Hull’s view to the ubiquitous phenomenon of symbiosis. Finally, using immunology as a key example, it shows that the genidentity view suggests that the main interest of a process approach is epistemological rather than ontological and that its principal claim is one of priority, namely that processes precede and define things, and not vice versa. (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)

This paper aims to clarify the consequences of new scientific and philosophical approaches for the practical-theoretical framework of modern developmental biology. I highlight normal development, and the instructive-permissive distinction, as key parts of this framework which shape how variation is conceptualised and managed. Furthermore, I establish the different dimensions of biological variation: the units, temporality and mode of variation. Using the analytical frame established by this, I interpret a selection of examples as challenges to the instructive-permissive distinction. These examples include (...) the phenomena of developmental plasticity and transdifferentiation, the role of the microbiome in development, and new methodological approaches to standardisation and the assessment of causes. Furthermore, I argue that investigations into organismal development should investigate the effects of a wider range of kinds of variation including variation in the units, modes and temporalities of development. I close by examining various possible opportunities for producing and using normal development free of the assumptions of the instructive-permissive distinction. These opportunities are afforded by recent developments, which include new ways of producing standards incorporating more natural variation and being based on function rather than structure, and the ability to produce, store, and process large quantities of data. (shrink)

We describe an approach to measuring biological information where ‘information’ is understood in the sense found in Francis Crick’s foundational contributions to molecular biology. Genes contain information in this sense, but so do epigenetic factors, as many biologists have recognized. The term ‘epigenetic’ is ambiguous, and we introduce a distinction between epigenetic and exogenetic inheritance to clarify one aspect of this ambiguity. These three heredity systems play complementary roles in supplying information for development. -/- We then consider the evolutionary significance (...) of the three inheritance systems. Whilst the genetic inheritance system was the key innovation in the evolution of heredity, in modern organisms the three systems each play important and complementary roles in heredity and evolution. -/- Our focus in the earlier part of the paper is on ‘proximate biology’, where information is a substantial causal factor that causes organisms to develop and causes offspring to resemble their parents. But much philosophical work has focused on information in ‘ultimate biology’. Ultimate information is a way of talking about the evolutionary design of the mechanisms of development and inheritance. We conclude by clarifying the relationship between the two. Ultimate information is not a causal factor that acts in development or heredity, but it can help to explain the evolution of proximate information, which is. (shrink)

This paper articulates an account of causation as a collection of information-theoretic relationships between patterns instantiated in the causal nexus. I draw on Dennett’s account of real patterns to characterize potential causal relata as patterns with specific identification criteria and noise tolerance levels, and actual causal relata as those patterns instantiated at some spatiotemporal location in the rich causal nexus as originally developed by Salmon. I develop a representation framework using phase space to precisely characterize causal relata, including their degree (...) of counterfactual robustness, causal profiles, causal connectivity, and privileged grain size. By doing so, I show how the philosophical notion of causation can be rendered in a format that is amenable for direct application of mathematical techniques from information theory such that the resulting informational measures are causal informational measures. This account provides a metaphysics of causation that supports interventionist semantics and causal modeling and discovery techniques. (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)

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)

Griffiths et al. (2015) have proposed a quantitative measure of causal specificity and used it to assess various attempts to single out genetic causes as being causally more specific than other cellular mechanisms, for example, alternative splicing. Focusing in particular on developmental processes, they have identified a number of important challenges for this project. In this discussion note, I would like to show how these challenges can be met.

Several authors have argued that causes differ in the degree to which they are ‘specific’ to their effects. Woodward has used this idea to enrich his influential interventionist theory of causal explanation. Here we propose a way to measure causal specificity using tools from information theory. We show that the specificity of a causal variable is not well-defined without a probability distribution over the states of that variable. We demonstrate the tractability and interest of our proposed measure by measuring the (...) specificity of coding DNA and other factors in a simple model of the production of mRNA. (shrink)

Perceptual constancy has played a significant role in philosophy of perception. It figures in debates about direct realism, color ontology, and the minimal conditions for perceptual representation. Despite this, there is no general consensus about what constancy is. I argue that an adequate account of constancy must distinguish it from three distinct phenomena: mere sensory stability through proximal change, perceptual categorization of a distal dimension, and stability through irrelevant proximal change. Standard characterizations of constancy fall short in one or more (...) of these respects. I develop an account of constancy that overcomes these problems. The account has two parts: an analysis of constancy mechanisms, and an analysis of the conditions under which a constancy capacity is exercised. I then employ this account to evaluate whether constancy is a necessary condition for perceptual representation, as some have conjectured. I argue that explanatory practice in perceptual psychology fails to support this view. Rather, it fits better with the weaker principle that representation requires specific tracking of a distal dimension. (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)

Goldman (1967) proposed that a subject s knows p if and only if p is appropriately causally connected to s’s believing p. He later on abandoned this theory (Goldman, 1976). The main objection to the theory is that the causal connection required by Goldman is compatible with certain problematic forms of luck. In this paper we argue that Goldman’s causal theory of knowledge can overcome the luck problem if causation is understood along interventionist lines. We also show that the modified (...) theory leads to the correct results in contexts involving other prominent forms of epistemic luck and compare it with other accounts on the market. (shrink)

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

I respond to recent criticism of my analysis of the permissive-instructive distinction and outline problems with the alternative analysis on offer. Amongst other problems, I argue that the use of formal measures is unclear and unmotivated, that the distinction is conflated with others that are not equivalent, and that no good reasons are provided for thinking the alternative model or formal measure tracks what biologists are interested in. I also clarify my own analysis where it has been misunderstood or ignored.

This paper develops axiomatic foundations for a probabilistic-interventionist theory of causal strength. Transferring methods from Bayesian confirmation theory, I proceed in three steps: I develop a framework for defining and comparing measures of causal strength; I argue that no single measure can satisfy all natural constraints; I prove two representation theorems for popular measures of causal strength: Pearl's causal effect measure and Eells' difference measure. In other words, I demonstrate these two measures can be derived from a set of plausible (...) adequacy conditions. The paper concludes by sketching future research avenues. (shrink)

This article proposes two conditions to assess whether an entity at a level of description is a unit of selection qua interactor. These two conditions make it possible to (1) distinguish biologically relevant entities from arbitrary ones and (2) distinguish units that can _potentially_ enter a selection process from those that have already done so. I show that the classical approaches used in the literature on units and levels of selection do not fare well with respect to either or both (...) of these desiderata. (shrink)

It is often thought that non-junk or coding DNA is more significant than other cellular elements, including so-called junk DNA. This is for two main reasons: because coding DNA is often targeted by historical or current selection, it is considered functionally special and because its mode of action is uniquely specific amongst the other actual difference makers in the cell, it is considered causally special. Here, we challenge both these presumptions. With respect to function, we argue that there is previously (...) unappreciated reason to think that junk DNA is significant, since it can alter the cellular environment, and those alterations can influence how organism-level selection operates. With respect to causality, we argue that there is again reason to think that junk DNA is significant, since it too is remarkably causally specific. As a result, something is missing from the received view of significance in molecular biology—a view which emphasizes specificity and neglects something we term ‘reach’. With the special case of junk DNA in mind, we explore how to model and understand the causal specificity, reach, and corresponding efficacy of difference makers in biology. The account contains implications for how evolution shapes the genome, as well as advances our understanding of multi-level selection. (shrink)

Philosophical discussions of information and specificity in biology are now commonplace, but no consensus exists about whether the privileging of genetic causation in investigation and explanation...

The philosophy of biology literature offers several arguments aimed at showing that information theory is conceptually unsuited to capture the informational talk in molecular biology. Such arguments led to the consensus that, if the informational talk in biology can be defended and explained at all, we need a different strategy. The debate, in fact, developed mostly along this line. However, recent contributions seem to (and even claim to) challenge the consensus and thus to vindicate the role and relevance of information (...) theory to this particular debate. In this paper, I examine the main arguments leading to such a consensus and I analyze the extent to which those recent accounts actually succeed in vindicating the invocation of information theory. I argue that these attempts fail to vindicate the information-theoretic strategy and, therefore, the consensus remains unaffected by them. (shrink)

Slightly modified excerpt from the section 13.4 Zusammenfassung und Ausblick (translated into englisch): This chapter is based on an analysis of ethical debates on epigenetics and genome editing, debates, in which ethical arguments relating to future generations and justice play a central role. The analysis aims to contextualize new developments in genetic engineering, such as genome and epigenome editing, ethically. At the beginning, the assumptions of "genetic determinism," on which "genetic essentialism" is based, of "epigenetic determinism" as well as "genetic" (...) and "epigenetic exceptionalism" are analyzed and critically discussed. The remarks on the ethical discourse on epigenetics show that the notion of "epigenetic determinism" can sometimes be discerned not only in popular scientific discourse but also in ethical discourse. Ethical debates on epigenetics, however, have distanced themselves from this deterministic understanding. As a result, the focus in the ethical discourse on epigenetics shifts from responsibility for one's own health and that of subsequent generations to justice. What is meant here is justice, for example, in terms of access to healthy environmental conditions, regardless of whether these contribute to health with or without epigenetic agency. An analysis of the discourse on genome editing reveals that it is primarily germline interventions that are being ethically examined, with a concentration on the aspect of inheritance. The question is whether this is accompanied by an implicit "genetic determinism" or even a "genetic essentialism": the determinism could lie in the centrality of the aspect of heritability, since only genetic information is inherited. Does the aspect of heritability and genome modification play a more decisive role in debates on genome editing than the safety issue? Is the problem of embryos and their potential offspring not being able to consent to germline intervention given such a high priority because it is a genetic intervention? Under such a premise of "strong genetic determinism" supplemented by "epigenetic determinism," not only genome editing but also epigenome editing would be ethically relevant precisely because it too would have an influence on the genome. How this influence of genome editing and epigenome editing is ethically evaluated in each case therefore depends initially on whether the assumptions of "genetic" and "epigenetic determinism" are advocated. These assumptions are increasingly viewed critically in ethical discourse because they cannot be confirmed from a scientific perspective. In popular scientific debates in particular, however, they seem to persist, which ultimately also influences the public discussion. Since a broad public discussion is required especially on genome editing, a reflective approach to the various "-isms" analyzed in this chapter is central. DOI: 10.5771/9783748927242. (shrink)

There is a tension between, on the one hand, the view that natural selection refers to individual-level causes, and on the other hand, the view that it refers to a population-level cause. In this article, I make the case for the individual-level cause view. I respond to recent claims made by McLoone that the individual-level cause view is inconsistent. I show that if one were to follow his arguments, any causal claim in any context would have to be regarded as (...) vindicating a form of population-level cause view. I show why this is implausible and how a consistent individual-level cause position can be held within the interventionist account of causation. Finally, I argue that there is one sense in which natural selection might be said to refer to population-level causes of evolutionary change. The upshot is that, as noted by others, natural selection can be regarded as referring to a population-level cause in the context of frequency-dependent selection and other situations of fitness-altering interactions between the individuals of a population. But whether this statement is true will depend on the empirical case investigated, not some a priori conceptual distinction. Thus, even though situations of frequency dependence might be ubiquitous, it is orthogonal to the conceptual question of whether frequency-independent natural selection—McLoone’s target—refers to individual- or population-level causes. (shrink)

The interventionist account provides us with several notions permitting the qualification of causal relationships. In recent years, there has been a push toward formalizing these notions using information theory. In this paper, I discuss one of them, namely causal specificity. The notion of causal specificity is ambiguous as it can refer to at least two different concepts. After having presented these, I show that current attempts to formalize causal specificity in information theoretic terms have mostly focused on one of these (...) two concepts. I then propose and apply a new information-theoretic measure which captures the other concept. (shrink)

The question of whether cultural transmission is faithful has attracted significant debate over the last 30 years. The degree of fidelity with which an object is transmitted depends on 1) the features chosen to be relevant, and 2) the quantity of details given about those features. Once these choices have been made, an object is described at a particular grain. In the absence of conventions between different researchers and across different fields about which grain to use, transmission fidelity cannot be (...) evaluated because it is relative to the choice of grain. In biology, because a genotype-to-phenotype mapping exists and transmission occurs from genotype to genotype, a privileged grain of description exists that circumvents this ‘grain problem.’ In contrast, in cultural evolution, the genotype–phenotype distinction cannot be drawn, rendering claims about fidelity dependent upon researchers’ choices. Thus, due to a lack of unified conventions, claims about fidelity transmission are difficult to evaluate. (shrink)

The interventionist account of causation offers a criterion to distinguish causes from non-causes. It also aims at defining various desirable properties of causal relationships, such as specificity, proportionality and stability. Here we apply an information-theoretic approach to these properties. We show that the interventionist criterion of causation is formally equivalent to non-zero specificity, and that there are natural, information-theoretic ways to explicate the distinction between potential and actual causal influence. We explicate the idea that the description of causes should be (...) proportional to that of their effects. Then we draw a distinction between two ideas in the existing literature, the range of invariance of a causal relationship and its stability. The range of invariance is related to specificity and range of causal values. Stability concerns the effect of additional variables on the relationship between some focal pair of cause and effect variables. We show how to distinguish and measure the direct influence of background variables on the effect variable, and their influence on the relationship between the focal cause and the effect variable. Finally, we discuss the limitations of the information-theoretic approach, and offer prospects for complementary approaches. (shrink)

This dissertation aims to determine the optimal level of granularity for the variables used in probabilistic causal models. These causal models are useful for generating explanations in a number of scientific contexts. In Chapter 1, I argue that there is rarely a unique level of granularity at which a given phenomenon can be causally explained, thereby rejecting various causal exclusion arguments. In Chapter 2, I consider several recent proposals for measuring the explanatory power of causal explanations, and show that these (...) measures fail to track the comparative depth of explanations given at different levels of granularity. In Chapter 3, I offer a pragmatic account of how to partition the measure space of a causal variable so as to optimally explain its effect. My account uses the decision-theoretic notion of value of information, and indexes the relative depth of an explanation to a particular agent faced with a particular decision problem. Chapter 4 applies this same decisiontheoretic framework to answer the epistemic question of how to discover constitutive relationships in nature. In Chapter 5, I describe the formal details of the relationship between random variables that are meant to be coarse-grained and fine-grained representations of the same type of phenomenon. I use this formal framework to rebut a popular argument for the view that special science probabilities can be objective chances. Chapter 6 discusses challenges related to the causal interpretation of Bayes nets that use imprecise rather than precise probabilities. (shrink)

Everyone has heard of ‘epigenetics’, but the term means different things to different researchers. Four important contemporary meanings are outlined in this paper. Epigenetics in its various senses has implications for development, heredity, and evolution, and also for medicine. Concerning development, it cements the vision of a reactive genome strongly coupled to its environment. Concerning heredity, both narrowly epigenetic and broader ‘exogenetic’ systems of inheritance play important roles in the construction of phenotypes. A thoroughly epigenetic model of development and evolution (...) was Waddington’s aim when he introduced the term ‘epigenetics’ in the 1940s, but it has taken the modern development of molecular epigenetics to realize this aim. In the final sections of the paper we briefly outline some further implications of epigenetics for medicine and for the nature/nurture debate. (shrink)

In their considered reviews both Thomas Pradeu and Lindell Bromham introduce important topics not sufficiently covered in our book. Pradeu asks us to enlarge on the epigenetic and ecological context of genes, particularly in the form of symbioses. We use the relationship between eukaryotes and their symbiotic organisms as a welcome opportunity to clarify our concept of the developmental niche, and its relationship to the developmental system. Bromham’s comments reveal that she is primarily interested in identifying macroevolutionary patterns. From her (...) vantage point eco-evo-devo, the study of phenotypic plasticity, epigenetic and exogenetic inheritance, have not yet demonstrated the need for any revolutionary change in evolutionary thought. For us they highlight the extent to which proximate developmental mechanisms can inform ultimate biology. (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)

I use some recent formal work on measuring causation to explore a suggestion by James Woodward: that the notion of causal specificity can clarify the distinction in biology between permissive and instructive causes. This distinction arises when a complex developmental process, such as the formation of an entire body part, can be triggered by a simple switch, such as the presence of particular protein. In such cases, the protein is said to merely induce or "permit" the developmental process, whilst the (...) causal "instructions" for guiding that process are already prefigured within the cells. I construct a novel model that expresses in a simple and tractable way the relevant causal structure of biological development and then use a measure of causal specificity to analyse the model. I show that the permissive-instructive distinction cannot be captured by simply contrasting the specificity of two causes as Woodward proposes, and instead introduce an alternative, hierarchical approach to analysing the interaction between two causes. The resulting analysis highlights the importance of focusing on gene regulation, rather than just the coding regions, when analysing the distinctive causal power of genes. (shrink)

Supporters of the autonomy of higher-level causation (or explanation) often appeal to proportionality, arguing that higher-level causes are more proportional than their lower-level realizers. Recently, measures based on information theory and causal modeling have been proposed that allow one to shed new light on proportionality and the related notion of specificity. In this paper we apply ideas from this literature to the issue of higher vs. lower-level causation (and explanation). Surprisingly, proportionality turns out to be irrelevant for the question of (...) whether higher-level causes (or explanations) can be autonomous; specificity is a much more informative notion for this purpose. (shrink)

Contrastive neuroimaging is often taken to provide evidence about the localization of cognitive functions. After canvassing some problems with this approach, I offer an alternative: neuroimaging gives evidence about regions of the brain that bear difference-making relationships to psychological processes of interest. I distinguish between the specificity and what I call the systematicity of a difference-making relationship, and I show how at least some neuroimaging experiments can give evidence for systematic difference-making.

A striking characteristic of the highly successful techniques in molecular biology is that they are derived from natural systems. RNA interference, for example, utilises a mechanism that evolved in eukaryotes to destroy foreign nucleic acid. Other examples include restriction enzymes, the polymerase chain reaction, green fluorescent protein and CRISPR-Cas. I propose that biologists exploit natural molecular mechanisms for their effectors’ activity and biological specificity. I also show that the developmental trajectory of novel techniques in molecular biology, such as RNAi, is (...) four characteristic phases. The first phase is discovery of a biological phenomenon, typically as curiosity driven research. The second is identification of the mechanism’s trigger, the effector and biological specificity. The third is the application of the technique. The final phase is the maturation and refinement of the molecular biology technique. The development of new molecular biology techniques from nature is crucial for biological research. These techniques transform scientific knowledge and generate new knowledge. (shrink)

I extend work from Krakauer et al. (2020), who propose a conception of individuality as the capacity to propagate information through time. From this conception, they develop information-theoretic measures. I identify several shortcomings with these measures—in particular, that they are associative rather than causal. I rectify this shortcoming by deriving a causal information-theoretic measure of individuality. I then illustrate how this measure can be implemented and extended in the context of evolutionary transitions in individuality.

Debates concerning the units and levels of selection have persisted for over fifty years. One major question in this literature is whether units and levels of selection are genuine, in the sense that they are objective features of the world, or merely reflect the interests and goals of an observer. Scientists and philosophers have proposed a range of answers to this question. This Element introduces this literature and proposes a novel contribution. It defends a realist stance and offers a way (...) of delineating genuine levels of selection by invoking the notion of a functional unit. (shrink)

Heritability is routinely interpreted causally. Yet, what such an interpretation amounts to is often unclear. Here, I provide a causal interpretation of this concept in terms of range of causal influence, one of several causal dimensions proposed within the interventionist account of causation. An information-theoretic measure of range of causal influence has recently been put forward in the literature. Starting from this formalization and relying upon Woodward’s analysis, I show that an important problem associated with interpreting heritability causally, namely the (...) locality problem, amounts, at least partly, to a low invariance and low stability between the genotype/environment and the phenotype of individuals. In light of this, I plead for a causal interpretation of heritability that takes the notions of Woodward’s invariance and stability into consideration. In doing so, I defuse naive causal interpretations of heritability. (shrink)

A causal approach to biological information is outlined. There are two aspects to this approach: information as determining a choice between alternative objects and information as determining the construction of a single object. The first aspect has been developed in earlier work to yield a quantitative measure of biological information that can be used to analyze biological networks. This article explores the prospects for a measure based on the second aspect and suggests some applications for such a measure. These two (...) aspects are not suggested to exhaust all the facets of biological information. (shrink)