When does a model explain? When does it promote understanding? A dominant approach to scientific explanation is the interventionist view. According to this view, when X explains Y, intervening on X can produce, prevent or alter Y in some predictable way. In this paper, I argue for two claims. First, I reject a position that many interventionist theorists endorse. This position is that to explain some phenomenon by providing a model is also to understand that phenomenon. While endorsing the interventionist (...) view, I argue that explaining and understanding are distinct scientific achievements. Second, I defend a novel theory of scientific understanding. According to this view, when some model M promotes understanding, M makes available a distinctive mental state. This state is of the same psychological kind as when we grasp events in a narrative as bearing on some ultimate conclusion. To conclude, I show that, given this view, mechanistic explanations often provide a powerful source of understanding that many causal-historical models lack. This paper will be of interest to both philosophers of science and epistemologists engaged in the topics of explanation and understanding. (shrink)

Change is the fundamental idea of evolution. Explaining the extraordinary biological change we see written in the history of genomes and fossil beds is the primary occupation of the evolutionary biologist. Yet it is a surprising fact that for the majority of evolutionary research, we have rarely studied how evolution typically unfolds in nature, in changing ecological environments, over space and time. While ecology played a major role in the eventual acceptance of the population genetic viewpoint of evolution in the (...) synthetic era (circa 1918-1956), it held a lesser role in the development of evolutionary theory until the 1980s, when we began to systematically study the evolutionary dynamics of natural populations in space and time. As a result, early evolutionary theory was initially constructed in an abstract vacuum that was unrepresentative of evolution in nature. The subtle synthesis between ecology with evolutionary biology (eco-evo synthesis) over the past 40 years has progressed our knowledge of natural selection dynamics as they are found in nature, thus revealing how natural selection varies in strength, direction, form, and, more surprisingly, level of biological organization. Natural selection can no longer be reduced to lower levels of biological organization (i.e., individuals, selfish genes) over shorter timescales but should be expanded to include adaptation at higher levels and over longer timescales. Long-term and/or emergent evolutionary phenomena, such as multilevel selection or evolvability, have thus become tenable concepts within an evolutionary biology that embraces ecology and spatiotemporal change. Evolutionary biology is currently suspended at an intermediate stage of scientific progress that calls for the organization of all the recent knowledge revealed by the eco-evo synthesis into a coherent and unified theoretical framework. This is where philosophers of biology can be of particular use, acting as a bridge between the subdisciplines of biology and inventing new theoretical strategies to organize and accommodate the recent knowledge. Philosophers have recommended transitioning away from outdated philosophies that were originally derived from physics within the philosophical zeitgeist of logical positivism (i.e., monism, reductionism, and monocausation) and toward a distinct philosophy of biology that can capture the natural complexity of multifaceted biological systems within diverse ecosystems—one that embraces the emerging philosophies of pluralism, emergence, and multicausality. Therefore, I see recent advances in ecology, evolutionary biology, and the philosophy of biology as laying the groundwork for another major biological synthesis, what I refer to as the Second Synthesis because, in many respects, it is analogous to the aims and outcomes of the first major biological synthesis (but is notably distinct from the inorganic and contrived progressive movement known as the extended evolutionary synthesis). With the general development of a distinctive philosophy of science, biology has rightfully emerged as an autonomous science. Thus, while the first synthesis legitimized biology, the Second Synthesis autonomized biology and afforded biology its own philosophy, allowing biology to finally realize its full scientific potential. (shrink)

This paper addresses the question of what constitutes an apt interpreted model for the purpose of analyzing causation. I first collect universally adopted aptness principles into a basic account, flagging open questions and choice points along the way. I then explore various additional aptness principles that have been proposed in the literature but have not been widely adopted, the motivations behind their proposals, and the concerns with each that stand in the way of universal adoption. I conclude that the remaining (...) work of articulating aptness for a SEM analysis of causation is tied up with issues to do with modality, ontology, and mereology. Continuing this work is therefore likely to shed light on the relationship between these areas and causation more generally. (shrink)

Consider the following two (hypothetical) generic causal claims: “Living in a neighborhood with many families with children increases purchases of bicycles” and “living in an affluent neighborhood with many families with children increases purchases of bicycles.” These claims not only differ in what they suggest about how bicycle ownership is distributed across different neighborhoods (i.e., “the data”), but also have the potential to communicate something about the speakers’ values: namely, the prominence they accord to affluence in representing and making decisions (...) about the social world. Here, we examine the relationship between the level of granularity with which a cause is described in a generic causal claim (e.g., neighborhood vs. affluent neighborhood) and the value of the information contained in the causal model that generates that claim. We argue that listeners who know any two of the following can make reliable inferences about the third: 1) the level of granularity at which a speaker makes a generic causal claim, 2) the speaker’s values, and 3) the data available to the speaker. We present results of four experiments (N=1,323) in the domain of social categories that provide evidence in keeping with these predictions. (shrink)

We often hear how scientists have discovered that a certain human trait – or a trait of another type of organism – is innate, genetic, heritable, inherited, naturally selected etc. All these claims have something in common: they all declare a trait to have significant organism internal (for instance genetic) causes that are present in the organism at its birth. I call claims like these “nativist claims”. Nativist claims are important. They shape our overall understanding of what we are, what (...) we can do and what is good for us. They also impact our practical decision making. For instance, we know that certain types of genes increase the risk of certain diseases, and increasingly this has an effect on healthcare practices. Many people believe that in the matter of children’s education we should consider the fact that many cognitive abilities are highly heritable. Associations between genetics and aggressive behavior have been taken to be alleviating circumstances in criminal sentencing. It is therefore important to correctly understand the content and implications of nativist claims. In this doctoral thesis I analyze, by philosophical means, the content of different kinds of nativist claim. What does it mean that some psychological tendency is innate? What does it mean that intelligence is 50% heritable? How (if at all) do genes come to carry information about the traits of an organism – they are nothing like the information carriers familiar to us, such as newspapers, e-mails, secret codes, and audio files. This thesis emphasizes two things. Firstly, I demonstrate, that in different scientific contexts these words ('innate', 'genetically caused' etc.) can mean very different things. Therefore, the implications of a given nativist claim in one scientific context can be remarkably different from another nativist claim’s implications in some other scientific context. Secondly, I explain how the development of innate, heritable and genetically caused traits can be determined in different and often unexpected ways by our environment and experiences. I demonstrate that the content of a concept that is considered innate by cognitive scientists can be determined by what the organism that possesses the concept has experienced. I also show that even a trait which is 100% heritable can at the same time be a socially constructed trait. (shrink)

Various scientists and philosophers have heavily criticized what they see as problematic forms of ‘nutritional reductionism’ or ‘nutritionism’ whereby studying food–health interactions at the level of isolated food components produces largely misguided science and misleading interpretations. However, the exact target of these diverse criticisms remains elusive, and its implications are overstated, which may hinder scientific understanding. To better identify the types of flaws supposedly hindering reductionist research, we disentangle three types of reductionist claims to better determine what the debate is (...) about and to propose ways to move it forward. We then present a qualified defence of the reductionist programme that hinges on the ability to identify nutritional causes that make a difference, which we illustrate through central examples in the history of nutrition. This defence is taken further by using insights from the philosophy of mechanisms to analyse how the field of nutritional ecology offers a synthetic framework to explain, generate, and test predictions about nutrient–organism interactions, which is premised on the biological mechanisms of nutrient-specific appetite regulation. The result, which we call ‘synthetic reductionism’, avoids many, though perhaps not all, of the challenges raised by anti-reductionists, and also highlights the potential of reductionism to identify nutritional difference makers. (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)

Humean accounts of laws are often contrasted with governing accounts, and recent developments have added pragmatic versions of Humeanism. This paper offers Mitchell's pragmatist, perspectival account of laws as a third option. The differences between these accounts come down to the role of modality. Mitchell's bottom-up account allows for subtle gradations of modal content to be conveyed by laws. The perspectival character of laws is not an accident or something to be eventually eliminated - it is part of how this (...) modal content is conveyed. I conclude with a discussion of the metaphysical commitments in Humeanism as requiring a perspectiveless view of the manifold from outside, and how Mitchell's situated account is better able to account for the substantive notion of possibility involved in scientific laws. (shrink)

Causal dispositionalism developed in metaphysics of science offers a useful tool to conceptualize shallow causes in behaviour genetics, in a way such that (a) it accounts for complex aetiology and heterogeneity of effects, and (b) genetic causal contribution can be considered to be explanatory. Genes are thus causal powers that make a difference.

This dissertation begins by addressing the question of when a causal model is apt for deciding questions of actual causation with respect to some target situation. I first provide relevant background about causal models, explain what makes them promising as a tool for analyzing actual causation, and motivate the need for a theory of aptness as part of such an analysis (Chapter 1). I then define what it is for a model on a given interpretation to be accurate of, that (...) is, say only true things about, some target situation. This involves a systematization of various representational principles mentioned and/or discussed throughout the literature into a method of interpretation, which I propose be taken as standard (Chapter 2). Next, I explain and address two reasons for which accuracy as I’ve defined it is insufficient for aptness. The first reason – already discussed in the literature – is the problem of structural isomorphs. In response, I propose the aptness condition of Explicit Partial Mediation (Chapter 3). The second reason – which has yet to be noticed – is the problem of the indeterminacy of accuracy. As I demonstrate, a model is accurate of a target situation only relative to a set of background possibilities – what I call a modal profile. It follows that a model represents a situation only relative to some modal profile or other. I go on to discuss the ramifications of this observation for a theory of actual causation in terms of models. I argue that the relativity be taken at face value and built into our metaphysical account of causation, resulting in a view that I call causal relativism (Chapter 4). I explore one advantage of this view in detail: that the resulting account can defend the principle of strong proportionality against several objections (Chapter 5). Finally, I apply the earlier discussion of aptness to attempts to provide a semantics of counterfactuals in terms of causal models – an interventionist semantics. I show how just as a similarity semantics relies on an opaque notion of similarity, an interventionist semantics relies on an analogous notion of aptness. The challenge of articulating aptness thus undermines the claim that an interventionist semantics avoids representational problems inherent in a similarity semantics (Chapter 6). I close with a recap and suggestions for future research (Chapter 7). -/- . (shrink)

This paper argues that the interventionist account of causation faces a dilemma concerning macroscopic causation – i.e., causation by composite objects. Interventionism must either require interventions on a composite object to hold the behavior of its parts fixed, or allow such interventions to vary the behavior of those parts. The first option runs the risk of making wholes causally excluded by their parts, while the second runs the risk of mistakenly ascribing to wholes causal abilities that belong to their parts (...) only. Using as starting point Baumgartner’s well-known argument that interventionism leads to causal exclusion of multiply realized properties, I first show that a similar interventionist exclusion argument can be mounted against the causal efficacy of composite objects. I then show that Woodward’s (2015) updated interventionist account (explicitly designed to address exclusion worries) avoids this problem, but runs into an opposite issue of over-inclusion: it grants to composites causal abilities that belong to their parts only. Finally, I examine two other interventionist accounts designed to address Baumgartner’s argument, and show that when applied to composites, they too fall on one horn (exclusion) or the other (over-inclusion) of the dilemma. I conclude that the dilemma constitutes an open and difficult issue for interventionism. (shrink)

In this paper I argue that the extent to which a human trait is genetically caused can causally depend upon whether the trait is categorized within human genetics as genetically caused. This makes the kindgenetically caused traitan interactive kind. I demonstrate that this thesis is both conceptually coherent and empirically plausible. I outline the core rationale of this thesis and demonstrate its conceptual coherence by drawing upon Waters’ (2007) analysis of genetic causation. I add empirical plausibility to the thesis by (...) describing a hypothetical but empirically plausible mechanism by which the fact that obesity is categorized as genetically caused within human genetics increases the extent to which obesity is in fact genetically caused. (shrink)

The field of the philosophy of biology is flourishing in its aim to evaluate and rethink the view inherited from the previous century ---the Modern Synthesis. Different research areas and theories have come to the fore in the last decades in order to account for different biological phenomena that, in the first instance, fall beyond the explanatory scope of the Modern Synthesis. This thesis is anchored and motivated by this revolt in the philosophy of biology. -/- The central target in (...) this context is the possibility of naturalizing teleology, a classical nightmare for the history of biology itself. This requires, principally, understanding the causes of teleological explanations without assuming an unfashioned backward causation of sorts. As the riddles of teleological explanations are about their temporal dimension, I analyze different temporal scales of biological processes: evolutionary, developmental, and physiological. -/- The first one is the one defended in the context of the Modern Synthesis. As expected, one of the aims of this thesis is to evaluate the adequacy of an evolutionary account of teleological explanation. The scrutiny is negative. Evolutionary explanations in the context of the Modern Synthesis lack the necessary causal roots to naturalize teleology. Concerning the physiological scale, a long tradition pushed up by Kant and the organicist movement in the 20th century allows us to better understand how teleological explanations can be naturalized in physiological process. The key notions in this temporal scale are self-organization and the recursive, looped character of physiological process. While the physiological scale may be suitably accounted by contemporaries views, such as Autonomous Systems Theory, different central teleological phenomena remain unexplained from a purely physiological perspective. In particular, different issues concerning the (adaptive) construction of organism ---such as plasticity, robustness, variation, novelty, inheritance--- deserve an ontogenetic analysis. -/- The principal aim of this thesis is to provide a theory of teleological development that falls beyond the Modern Synthesis' framework and is prompted by different insights from the history of biology. I call it Agential Teleosemantics. It rests on two central pillars. First, that developmental processes, beyond any gene-centered stance, can be understood in informational terms; i.e. developmental processes are about the interaction of developmental resources conveying biological information. The second ingredient is agentivity, namely the idea that development is regulated by an agentive system according to the adaptiveness of the phenotypic outcomes produced. The role of agency in Agential Teleosemantic is equivalent to the role of genes in the Modern Synthesis: it is responsible for explaining the order and the adaptive complexity in the living realm. -/- The second target of this thesis regards the possibility of naturalizing intentional explanations in cognitive science. The central project involved in such an aim is known as teleosemantics. Classical teleosemantics however is etiological: it explains the teleofunctions of representational systems in terms of evolutionary processes. The different disputes in the contemporary philosophy of biology provide two insights to analyze teleosemantics in cognitive science. First, the challenges against the Modern Synthesis must be extended to the evolutionary approach of etiological teleosemantics. Second, as Agential Teleosemantics suggests an alternative source for teleofunctions ---ontogeny, I offer an attempt to integrate Agential Teleosemantics into cognitive science in order to provide an alternative teleosemantic project to understand intentional explanations in cognitive science. (shrink)

The Culpable Control Model assumes that causal judgments are irrational: a negative evaluative reaction to an agent would lead individuals to overestimate his causal contribution to a harm. However, the extent to which these judgments deviate from criteria of rationality remains unclear. The two present studies aimed at investigating conditions under which this effect occurs. Participants red a vignette in which the evaluative reaction was operationalized through the agent’s motives (blameworthy, laudable). We also varied the causal link between the agent’s (...) action and the outcome (strong, weak, preempted). In both studies, we found that negative motives influenced causal judgments when a strong action-outcome link could be established. In Study 2, we replicated the effect of motives on causal judgment in the weak link condition. However, participants consistently judged the agent as less causal when the link was weak (vs. strong), regardless of the agent’s motives. These findings show that both the presence and the strength of the actual causal link between the action and the outcome moderate the detrimental effect of negative evaluative reactions on causal judgments. Thus, common sense causal judgments seem to deviate relatively little from the criteria of rationality. (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)

This paper aims to clarify the nature of understanding in medicine. The first part describes in more detail what it means to understand something and links a type of understanding (i.e., objectual understanding) to explanations. The second part proceeds to investigate what objectual understanding of a disease (i.e., biomedical understanding) requires by considering the case of scurvy from the history of medicine. The main hypothesis is that grasping a mechanistic explanation of a condition is necessary for a biomedical understanding of (...) that condition. The third part of the paper argues that biomedical understanding is necessary, but not sufficient for understanding in a clinical context (i.e., clinical understanding). The hypothesis is that clinical understanding combines biomedical understanding of a _disease_ or pathological condition with understanding _illness,_ which involves some degree of personal understanding of the patient. It is argued that, in many cases, clinical understanding necessitates adopting a particular second-personal stance and using cognitive resources _in addition_ to those involved in biomedical understanding. (shrink)

This paper aims to clarify the nature of understanding in medicine. The first part describes in more detail what it means to understand something and links a type of understanding (i.e., objectual understanding) to explanations. The second part proceeds to investigate what objectual understanding of a disease (i.e., biomedical understanding) requires by considering the case of scurvy from the history of medi- cine. The main hypothesis is that grasping a mechanistic explanation of a condi- tion is necessary for a biomedical (...) understanding of that condition. The third part of the paper argues that biomedical understanding is necessary, but not sufficient for understanding in a clinical context (i.e., clinical understanding). The hypothe- sis is that clinical understanding combines biomedical understanding of a disease or pathological condition with understanding illness, which involves some degree of personal understanding of the patient. It is argued that, in many cases, clinical understanding necessitates adopting a particular second-personal stance and using cognitive resources in addition to those involved in biomedical understanding. (shrink)

Social scientists appeal to various “structures” in their explanations including public policies, economic systems, and social hierarchies. Significant debate surrounds the explanatory relevance of these factors for various outcomes such as health, behavioral, and economic patterns. This paper provides a causal account of social structural explanation that is motivated by Haslanger (2016). This account suggests that social structure can be explanatory in virtue of operating as a causal constraint, which is a causal factor with unique characteristics. A novel causal framework (...) is provided for understanding these explanations–this framework addresses puzzles regarding the mysterious causal influence of social structure, how to understand its relation to individual choice, and what makes it the main explanatory (and causally responsible) factor for various outcomes. (shrink)

Cancer biology features the ascription of normal functions to parts of cancers. At least some ascriptions of function in cancer biology track local normality of parts within the global abnormality of the aberration to which those parts belong. That is, cancer biologists identify as functions activities that, in some sense, parts of cancers are supposed to perform, despite cancers themselves having no purpose. The present paper provides a theory to accommodate these normal function ascriptions—I call it the Modeling Account of (...) Normal Function (MA). MA comprises two claims. First, normal functions are activities whose performance by the function-bearing part contributes to the self-maintenance of the whole system and, thereby, results in the continued presence of that part. Second, MA holds that models of system-level activities that are (partly) constitutive of self-maintenance are improved by including a representation of the relevant function-bearing part and by making reference to the activity/activities that part performs which contribute(s) to those system-level activities. I contrast MA with two other accounts that seek to explicate the ascription of normal functions in biology, namely, the organizational account and the selected effects account. Both struggle to extend to cancer biology. However, I offer ecumenical readings which allow them to recover some ascriptions of normal function to parts of cancers. So, though I contend that MA excels in this respect, the purpose of this paper is served if it provides materials for bridging the gap between cancer biology, philosophy of cancer, and the literature on function. (shrink)

The epidemiologist Bradford Hill famously argued that in epidemiology, specificity of association (roughly, the fact that an environmental or behavioral risk factor is associated with just one or at most a few medical outcomes) is strong evidence of causation. Prominent epidemiologists have dismissed Hill’s claim on the ground that it relies on a dubious `one-cause one effect’ model of disease causation. The paper examines this methodological controversy, and argues that specificity considerations do have a useful role to play in causal (...) inference in epidemiology. More precisely, I argue that specificity considerations help solve a pervasive inferential problem in contemporary epidemiology: the problem of determining whether an exposure-outcome correlation might be due to confounding by a social factor. This examination of specificity has interesting consequences for our understanding of the methodology of epidemiology. It highlights how the methodology of epidemiology relies on local tools designed to address specific inference problems peculiar to the discipline, and shows that observational causal inference in epidemiology can proceed with little prior knowledge of the causal structure of the phenomenon investigated. I also argue that specificity of association cannot (despite claims to the contrary) be entirely explained in terms of Woodward’s well-known concept of “one-to-one” causal specificity. This is because specificity as understood by epidemiologists depends on whether an exposure (or outcome) is associated with a `heterogeneous’ set of variables. This dimension of heterogeneity is not captured in Woodward’s notion, but is crucial for understanding the evidential import of specificity of association. (shrink)

Both ecologists and statistical physicists use a variety of highly idealized models to study active matter and self-organizing critical phenomena. In this paper, I show how universality classes play a crucial role in justifying the application of highly idealized ‘minimal’ models to explain and understand the critical behaviors of active matter systems across a wide range of scales and scientific fields. Appealing to universality enables us to see why the same minimal models can be used to explain and understand behaviors (...) across these different systems despite drastic differences in the causes and mechanisms responsible for the behaviors of interest. After analyzing these cases in detail, I argue that accounts that focus on identifying common causes or mechanisms in order to explain patterns are unable to accommodate these cases. In contrast, I argue that the justification for using these minimal models is that they are within the same universality class as real systems whose causes and mechanisms are known to be different. I also use these cases to identify several different kinds of explanatory autonomy that have important implications for how scientists ought to approach the modeling of multiscale phenomena. (shrink)

Explaining the supervenience of the moral on the natural is, perhaps, the central metaphysical challenge for the non-naturalist. However, Scanlon (2014) and Fogal and Risberg (2020) have developed a strategy which purports to explain supervenience rather simply. Fogal and Risberg call it the 'Divide and Conquer' strategy. The key idea is to postulate explanatory moral principles linking the natural and the moral. The moral principles are metaphysically necessary, so trivially supervene on the natural. All other moral facts are determined by (...) the necessary moral principles and the natural facts, so they supervene on the natural too. -/- I argue that there are two versions of the Divide and Conquer strategy and both fail. The first strategy doesn’t give an adequate explanation of supervenience because it doesn't properly identify what makes a difference to the holding of supervenience. The second perhaps does give an adequate explanation of supervenience, but only by introducing something similarly puzzling that needs explanation. -/- Consequently, non-naturalists need additional metaphysical machinery to develop their view -- just appealing to moral principles or metaphysical laws won't do the job. (shrink)

Engineering failure investigations seek to reconstruct the actual causes of major engineering failures. The investigators need to establish the existence of certain past events and the actual causal relationships that these events bear to the failures in question. In this paper, I examine one method for reconstructing the actual causes of failure events, which I call "feature dependence". The basic idea of feature dependence is that some features of an event are informative about the features of its causes; therefore, the (...) investigators can use the features of a known failure event to reconstruct details of its causes. I make explicit the structure of feature dependence and the evidential basis of its key premises, and show how feature dependence works in the investigation of the American Airlines Flight 191 accident. (shrink)

I develop and defend a maximizing theory of moral motivation: I claim that consequentialists should recommend only those desires, emotions, and dispositions that will make the outcome best. I advance a conservative account of the motives that are possible for us; I say that a motive is an alternative if and only if it is in our psychological control. The resulting theory is less demanding than its competitors. It also permits us to maintain many of the motivations that we value (...) most, including our love for those most important to us. I conclude that we are closer to meeting morality’s demands on our character than has been appreciated. (shrink)

In this paper I develop a concept of behavioural ecological individuality. Using findings from a case study which employed qualitative methods, I argue that individuality in behavioural ecology should be defined as phenotypic and ecological uniqueness, a concept that is operationalised in terms of individual differences such as animal personality and individual specialisation. This account make sense of how the term “individuality” is used in relation to intrapopulation variation in behavioural ecology. The concept of behavioural ecological individuality can sometimes be (...) used to identify individuals. It also shapes research agendas and methodological choices in behavioural ecology, leading researchers to account for individuals as sources of variation. Overall, this paper draws attention to a field that has been largely overlooked in philosophical discussions of biological individuality and highlights the importance of individual differences and uniqueness for individuality in behavioural ecology. (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)

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)

Behavioral economists have proposed that people are subject to an IKEA effect, whereby they attach greater value to products they make for themselves, like IKEA furniture, than to otherwise indiscernible goods. Recently, cognitive psychologist Tom Stafford has suggested there may be an epistemic analog to this, a kind of epistemic IKEA effect. In this paper, I use Stafford’s suggestion to defend a certain thesis about epistemic value. Specifically, I argue that there is a distinctive epistemic value in being an active (...) producer of epistemic goods, like true belief, as opposed to just a passive recipient of such goods, and that because of this it can be rationally permissible to sacrifice truth in a certain way for the sake of this other value. In particular, it is rationally permissible for an epistemic agent to prefer a belief set that contains fewer overall truths but more truths obtained through the agent’s own intellectual labor, in something like the way that a practical agent might prefer furniture they have made through their own manual labor to inherently superior furniture made by someone else. In making my case, I draw on Ernest Sosa’s discussion of causation and praxical epistemic values, and Jennifer Lackey’s testimony-based criticism of the credit view of knowledge. After defending my thesis about epistemic value, I further clarify it by connecting it to the focus of Stafford’s discussion, conspiracy theorists. (shrink)

Explainable artificial intelligence (XAI) aims to help people understand black box algorithms, particularly of their outputs. But what are these explanations and when is one explanation better than another? The manipulationist definition of explanation from the philosophy of science offers good answers to these questions, holding that an explanation consists of a generalization that shows what happens in counterfactual cases. Furthermore, when it comes to explanatory depth this account holds that a generalization that has more abstract variables, is broader in (...) scope and/or more accurate is better. By applying these definitions and contrasting them with alternative definitions in the XAI literature I hope to help clarify what a good explanation is for AI. (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)

Interventionism is a theory of causation with a pragmatic goal: to define causal concepts that are useful for reasoning about how things could, in principle, be purposely manipulated. In its original presentation, Woodward’s interventionist definition of causation is relativized to an analyzed variable set. In Woodward, Woodward changes the definition of the most general interventionist notion of cause, contributing cause, so that it is no longer relativized to a variable set. This derelativization of interventionism has not gathered much attention, presumably (...) because it is seen as an unproblematic way to save the intuition that causal relations are objective features of the world. This paper first argues that this move has problematic consequences. Derelativization entails two concepts of unmediated causal relation that are not coextensional, but which nonetheless do not entail different conclusions about manipulability relations within any given variable set. This is in conflict with the pragmatic orientation at the core of interventionism. The paper then considers various approaches for resolving this tension but finds them all wanting. It is concluded that interventionist causation should not be derelativized in the first place. Various considerations are offered rendering that conclusion acceptable. (shrink)

Cognitive science is unusual in that cognitive scientists have dramatic disagreements about the extension of their object of study, cognition. This paper defends a novel analysis of the scientific concept of cognition: that cognition is the sensitive management of an agent’s behavior. This analysis is “modular,” so that its extension varies depending on how one interprets certain of its constituent terms. I argue that these variations correspond to extant disagreements between cognitive scientists. This correspondence is evidence that the proposed analysis (...) models the contemporary understanding of cognition among scientists, without artificially resolving questions that are currently considered open. (shrink)

Epidemiological explanation often has a “black box” character, meaning the intermediate steps between cause and effect are unknown. Filling in black boxes is thought to improve causal inferences by making them intelligible. I argue that adding information about intermediate causes to a black box explanation is an unreliable guide to pragmatic intelligibility because it may mislead us about the stability of a cause. I diagnose a problem that I call wishful intelligibility, which occurs when scientists misjudge the limitations of certain (...) features of an explanation. Wishful intelligibility gives us a new reason to prefer black box explanations in some contexts. (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)

Behavioral economists have proposed that people are subject to an IKEA effect, whereby they attach greater value to products they make for themselves, like IKEA furniture, than to otherwise indiscernible goods. Recently, cognitive psychologist Tom Stafford has suggested there may be an epistemic analog to this, a kind of epistemic IKEA effect. In this paper, I use Stafford’s suggestion to defend a certain thesis about epistemic value. Specifically, I argue that there is a distinctive epistemic value in being an active (...) producer of epistemic goods, like true belief, as opposed to just a passive recipient of such goods, and that because of this it can be rationally permissible to sacrifice truth in a certain way for the sake of this other value. In particular, it is rationally permissible for an epistemic agent to prefer a belief set that contains fewer overall truths but more truths obtained through the agent’s own intellectual labor, in something like the way that a practical agent might prefer furniture they have made through their own manual labor to inherently superior furniture made by someone else. In making my case, I draw on Ernest Sosa’s discussion of causation and praxical epistemic values, and Jennifer Lackey’s testimony-based criticism of the credit view of knowledge. After defending my thesis about epistemic value, I further clarify it by connecting it to the focus of Stafford’s discussion, conspiracy theorists. (shrink)

In this dissertation I develop a pluralist theory of actual causation. I argue that we need to distinguish between total, path-changing, and contributing actual causation. The pluralist theory accounts for a set of example cases that have raised problems for extant unified theories and it is supported by considerations about the various functions of causal concepts. The dissertation also analyses the context-sensitivity of actual causation. I show that principled accounts of causal reasoning in legal inquiry face limitations and I argue (...) that the context-sensitivity of actual causation is best represented by a distinction between default and deviant states in causal models. (shrink)

A central argument for non-reductive accounts of group agency is that complex social entities are capable of exerting causal influence independently of and superseding the causal efficacy of the individuals constituting them. A prominent counter is that non-reductionists run into an insuperable dilemma between identity and redundancy – with identity undermining independent higher-level efficacy and redundancy leading to overdetermination or exclusion. This paper argues that critics of non-reductionism can manage with a simpler and more persuasive reductio strategy called mapping: allow (...) that group agents are causally efficacious in their own right and chart how their causal efficacy is carried out; how it relates to the causal efficacy of individual determiners; how it connects to the causal relevance of background structural factors. The focus exclusively on whether groups are or are not causally efficacious black-boxes implementation, while close attention to how causation is wired increases the visibility of individualist arguments and countenances structure-oriented explanations. (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)

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)

Intuitions play an important role in the debate on the causal status of high‐level properties. For instance, Kim has claimed that his “exclusion argument” relies on “a perfectly intuitive … understanding of the causal relation.” We report the results of three experiments examining whether laypeople really have the relevant intuitions. We find little support for Kim's view and the principles on which it relies. Instead, we find that laypeople are willing to count both a multiply realized property and its realizers (...) as causes, and regard the systematic overdetermination implied by this view as unproblematic. (shrink)

When someone masters a skill, their performance looks to us like second nature: it looks as if their actions are smoothly performed without explicit, knowledge-driven, online monitoring of their performance. Contemporary computational models in motor control theory, however, are instructionist: that is, they cast skillful performance as a knowledge-driven process. Optimal motor control theory, as representative par excellence of such approaches, casts skillful performance as an instruction, instantiated in the brain, that needs to be executed—a motor command. This paper aims (...) to show the limitations of such instructionist approaches to skillful performance. We specifically address the question of whether the assumption of control-theoretic models is warranted. The first section of this paper examines the instructionist assumption, according to which skillful performance consists of the execution of theoretical instructions harnessed in motor representations. The second and third sections characterize the implementation of motor representations as motor commands, with a special focus on formulations from OMCT. The final sections of this paper examine predictive coding and active inference—behavioral modeling frameworks that descend, but are distinct, from OMCT—and argue that the instructionist, control-theoretic assumptions are ill-motivated in light of new developments in active inference. (shrink)

This article examines the multiple realizability thesis within a causal framework. The beginnings of this framework are found in Elliott Sober’s “Multiple Realizability Argument against Reduction,”...

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)

Why do we value higher-level scientific explanations if, ultimately, the world is physical? An attractive answer is that physical explanations often cite facts that don’t make a difference to the event in question. I claim that to properly develop this view we need to commit to a type of deterministic chance. And in doing so, we see the theoretical utility of deterministic chance, giving us reason to accept a package of views including deterministic chance.

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)

There have been repeated attempts in the history of comparative biology to provide a mechanistic account of morphological homology. However, it is well-established that homologues can develop from diverse sets of developmental causes, appearing not to share any core causal architecture that underwrites character identity. We address this challenge with a new conceptual model of Character Identity Mechanisms. ChIMs are cohesive mechanisms with a recognizable causal profile that allows them to be traced through evolution as homologues despite having a diverse (...) etiological organization. Our model hypothesizes that anatomical units at different levels of organization—cell types, tissues, and organs—have level-specific ChIMs with different conserved parts, activities, and organization. Relying on a methodology of conceptual engineering, we show how the ChIM concept advances our understanding of the developmental basis of morphological characters, while forging an important link between comparative and mechanistic biology. (shrink)

Racial disparities in health outcomes have recently become a flashpoint in the debate about the value of race as a biological concept. What role, if any, race has in the etiology of disease is a philosophically and scientifically contested topic. In this article, I expand on the insights of the new mechanistic philosophy of science to defend a mechanism discovery approach to investigating epidemiological racial disparities. The mechanism discovery approach has explanatory virtues lacking in the populational approach typically employed in (...) the study of race and biomedicine. The explanatory constraints that form an integral part of the new mechanistic approach enable mechanism discovery to avoid the epistemic and normative shortcomings of the populational approach. The methodology of mechanism discovery can fruitfully be extended to the treatment and reversal of epidemiological racial disparities. (shrink)