In a recent publication Tom Douglas and Katrien Devolder have proposed a new account of genetic parenthood, building on the work of Heidi Mertes. Douglas and Devolder’s account aims to solve, among other things, the question of who are the genetic parents of an individual created through somatic cell nuclear transfer (i.e. cloning): (a) the nuclear DNA provider or (b) the progenitors of the nuclear DNA provider. Such a question cannot be answered by simply appealing to the folk (...) account of genetic parenthood, according to which the genetic parents of an individual are those individuals who produced the egg and sperm, respectively, which fused to create the embryo. It cannot be so as in cloning there is no fertilization as such. In this article I critically examine Douglas and Devolder’s new account of genetic parenthood and demonstrate that it is vulnerable to counterexamples that exploit the lack of a condition specifying that genetic parents should cause a child’s coming into existence. (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)

Causation has multiple distinct meanings in genetics. One reason for this is meaning slippage between two concepts of the gene: Mendelian and molecular. Another reason is that a variety of genetic methods address different kinds of causal relationships. Some genetic studies address causes of traits in individuals, which can only be assessed when single genes follow predictable inheritance patterns that reliably cause a trait. A second sense concerns the causes of trait differences within a population. Whereas some (...) single genes can be said to cause population-level differences, most often these claims concern the effects of many genes. Polygenic traits can be understood using heritability estimates, which estimate the relative influences of genetic and environmental differences to trait differences within a population. Attempts to understand the molecular mechanisms underlying polygenic traits have been developed, although causal inference based on these results remains controversial. Genetic variation has also recently been leveraged as a randomizing factor to identify environmental causes of trait differences. This technique—Mendelian randomization—offers some solutions to traditional epidemiological challenges, although it is limited to the study of environments with known genetic influences. (shrink)

The article proposes to further develop the ideas of the Extended Evolutionary Synthesis by including into evolutionary research an analysis of phenomena that occur above the organismal level. We demonstrate that the current Extended Synthesis is focused more on individual traits (genetically or non-genetically inherited) and less on community system traits (synergetic/organizational traits) that characterize transgenerational biological, ecological, social, and cultural systems. In this regard, we will consider various communities that are made up of interacting populations, and for which the (...) individual members can belong to the same or to different species. Examples of communities include biofilms, ant colonies, symbiotic associations resulting in holobiont formation, and human societies. The proposed model of evolution at the level of communities revises classic theorizing on the major transitions in evolution by analyzing the interplay between community/social traits and individual traits, and how this brings forth ideas of top-down regulations of bottom-up evolutionary processes (collaboration of downward and upward causation). The work demonstrates that such interplay also includes reticulate interactions and reticulate causation. In this regard, we exemplify how community systems provide various non-genetic ‘scaffoldings’, ‘constraints’, and ‘affordances’ for individual and sociocultural evolutionary development. Such research complements prevailing models that focus on the vertical transmission of heritable information, from parent to offspring, with research that instead focusses on horizontal, oblique and even reverse information transmission, going from offspring to parent. We call this reversed information transfer the ‘offspring effect’ to contrast it from the ‘parental effect’. We argue that the proposed approach to inheritance is effective for modelling cumulative and distributed developmental process and for explaining the biological origins and evolution of language. (shrink)

A phenome occurs through the many pathways of the complex net of interaction between the phenome and its environment; therefore researching and understanding how it arises requires investigation into many possible causes that are in constant interaction with each other. The most comprehensive investigations in biology are the ones in which many biologists from different sub-areas—evolutionary biology, developmental biology, molecular biology, physiology, genetics, epigenetics, ecology—have collaborated. Still, biologists do not always need to collaborate or look for the most comprehensive explanations. (...) A more standard investigation in biology occurs within a single subarea, and uses well-defined experiments with very specific conditions. This paper is about causation and related explanation in plant phenome research and its relevance to Aristotle’s Theory of Four Causes. I argue that there are causes which resemble Aristotle’s formal, material, and efficient causes in phenotype explanation and occurrence; but causes which resemble Aristotle’s final causes occur in phenotype explanation only, not in the occurrence. (shrink)

I use a contrastive theory of causal explanation to analyze the notion of a genetic trait. The resulting definition is relational, an implication of which is that no trait is genetic always and everywhere. Rather, every trait may be either genetic or non-genetic, depending on explanatory context. I also outline some other advantages of connecting the debate to the wider causation literature, including how that yields us an account of the distinction between genetic traits (...) and genetic dispositions. (shrink)

The explanatory role of natural selection is one of the long-term debates in evolutionary biology. Nevertheless, the consensus has been slippery because conceptual confusions and the absence of a unified, formal causal model that integrates different explanatory scopes of natural selection. In this study we attempt to examine two questions: (i) What can the theory of natural selection explain? and (ii) Is there a causal or explanatory model that integrates all natural selection explananda? For the first question, we argue that (...) five explananda have been assigned to the theory of natural selection and that four of them may be actually considered explananda of natural selection. For the second question, we claim that a probabilistic conception of causality and the statistical relevance concept of explanation are both good models for understanding the explanatory role of natural selection. We review the biological and philosophical disputes about the explanatory role of natural selection and formalize some explananda in probabilistic terms using classical results from population genetics. Most of these explananda have been discussed in philosophical terms but some of them have been mixed up and confused. We analyze and set the limits of these problems. (shrink)

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

I want to exhibit the deeper metaphysical reasons why some common ways of describing the causal role of genes in development and evolution are problematic. Specifically, I show why using the concept of information in an intentional sense in genetics is inappropriate, even given a naturalistic account of intentionality. Furthermore, I argue that descriptions that use notions such as programming, directing or orchestrating are problematic not for empirical reasons, but because they are not strictly causal. They are intentional. By contrast, (...) other notions that are part of the received view in genetics and evolutionary theory are defensible if understood correctly, in particular the idea that genes are the main replicators in evolution. The paper concludes that dropping all intentional or intentionally laden concepts does not force us to accept the so-called causal parity thesis, at least not in its stronger form. (shrink)

Genetic differences can lead to phenotypic differences either directly or indirectly (via causing differences in external environments, which then affect phenotype). This possibility of genetic effects being mediated by environmental influences is often used by scientists and philosophers to argue that heritability is not a very helpful causal or explanatory notion. In this paper it is shown that these criticisms are based on serious misconceptions about methods of behavior genetics.

The rediscovery of Mendel's laws a century ago launched the science that William Bateson called "genetics," and led to a new view of evolution combining selection, particulate inheritance, and the newly characterized phenomenon of "mutation." This "mutationist" view clashed with the earlier view of Darwin, and the later "Modern Synthesis," by allowing discontinuity, and by recognizing mutation (or more properly, mutation-and-altered-development) as a source of creativity, direction, and initiative. By the mid-20th century, the opposing Modern Synthesis view was a prevailing (...) orthodoxy: under its influence, "evolution" was redefined as "shifting gene frequencies," that is, the sorting out of pre-existing variation without new mutations; and the notion that mutation-and-altered-development can exert a predictable influence on the course of evolutionary change was seen as heretical. Nevertheless, mutationist ideas re-surfaced: the notion of mutational determinants of directionality emerged in molecular evolution by 1962, followed in the 1980s by an interest among evolutionary developmental biologists in a shaping or creative role of developmental propensities of variation, and more recently, a recognition by theoretical evolutionary geneticists of the importance of discontinuity and of new mutations in adaptive dynamics. The synthetic challenge presented by these innovations is to integrate mutation-and-altered-development into a new understanding of the dual causation of evolutionary change--a broader and more predictive understanding that already can lay claim to important empirical and theoretical results--and to develop a research program appropriately emphasizing the emergence of variation as a cause of propensities of evolutionary change. (shrink)

According to the proponents of Developmental Systems Theory and the Causal Parity Thesis, the privileging of the genome as “first among equals” with respect to the development of phenotypic traits is more a reflection of our own heuristic prejudice than of ontology - the underlying causal structures responsible for that specified development no more single out the genome as primary than they do other broadly “environmental” factors. Parting with the methodology of the popular responses to the Thesis, this paper offers (...) a novel criterion for ‘causal primacy’, one that is grounded in the ontology of the unique causal role of dispositional properties. This paper argues that, if the genome is conceptualised as realising dispositional properties that are “directed toward” phenotypic traits, the parity of ‘causal roles’ between genetic and extra-genetic factors is no longer apparent, and further, that the causal primacy of the genome is both plausible and defensible. (shrink)

This article analyzes the view of evolutionary theory as a theory of forces. The analogy with Newtonian mechanics has been challenged due to the alleged mismatch between drift and the other evolutionary forces. Since genetic drift has no direction several authors tried to protect its status as a force: denying its lack of directionality, extending the notion of force and looking for a force in physics which also lacks of direction. I analyse these approaches, and although this strategy finally (...) succeeds, this discussion overlooks the crucial point on the debate between causalists and statisticalists: the causal status of evolutionary theory. (shrink)

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

In 1990 Robert Lickliter and Thomas Berry identified the phylogeny fallacy, an empirically untenable dichotomy between proximate and evolutionary causation, which locates proximate causes in the decoding of ‘ genetic programs’, and evolutionary causes in the historical events that shaped these programs. More recently, Lickliter and Hunter Honeycutt argued that Evolutionary Psychologists commit this fallacy, and they proposed an alternative research program for evolutionary psychology. For these authors the phylogeny fallacy is the proximate/evolutionary distinction itself, which they argue (...) constitutes a misunderstanding of development, and its role in the evolutionary process. In this article I argue that the phylogeny fallacy should be relocated to an error of reasoning that this causal framework sustains: the conflation of proximate and evolutionary explanation. Having identified this empirically neutral form of the phylogeny fallacy, I identify its mirror image, the ontogeny fallacy. Through the lens of these fallacies I attempt to solve several outstanding problems in the debate that ensued from Lickliter and Honeycutt’s provocative article. (shrink)

Neo-Darwinism, through the combination of natural selection and genetics, has made possible an explanation of adaptive phenomena that claims to be devoid of metaphysical presuppositions. What Bergson already deplored and what we explore in this paper is the implicit finalism of such evolutionary explanations, which turn living beings into closed and static systems rather than understanding biological evolution as a process characterized by its interactions and temporal openness. Without denying the heuristic efficiency of the explanation resting upon natural selection, we (...) analyze what it leaves out and what remains to be explored: the unpredictability of the evolutionary process. We will therefore study the role of contingency in evolution, as Stephen J. Gould proposed, but we will also consider the causality specific to the living world that makes it impossible to reduce it to a simple algorithm, as proposed by Daniel Dennett among others, but that it is really a creative causation, or dialectical spiral. (shrink)

The thesis that follows proffers a solution to the mind-matter problem, the problem as to how mind and matter relate. The proposed solution herein is a variant of panpsychism – the theory that all (pan) has minds (psyche) – that we name pansentient monism. By defining the suffix 'psyche' of panpsychism, i.e. by analysing what 'mind' is (Chapter 1), we thereby initiate the effacement of the distinction between mind and matter, and thus advance a monism. We thereafter critically examine the (...) prevalent view, antithetical to a pansentient monism, that mind is not identical to matter but emergent therefrom (Chapter 2). This anti-emergentist critique acts also as a fortification of the Genetic Argument for panpsychism: if mind is not emergent (nor distinct) from matter, mind must always have existed with matter. But what is 'matter'? Chapter 3 investigates what we understand by 'matter', or 'the physical', and exposes it as a highly deficient concept and percept that in concreto points to its identity with that denoted by 'mind'. This also acts as a fortification of the Abstraction Argument for panpsychism, employing a new taxonomy of physicalism and a new taxonomy of the varieties of abstraction. Thus do we reach a monism that is a parsimonious psycho-physical identity theory. But here we face what can be called The Identity Problem for Panpsychism: if our panpsychism is a psycho-physical identity theory, how can it respond to the powerful objections that beset the identity theory of the twentieth century? In Chapter 4 it will be argued that, like emergentism, this psycho-neural identity theory presupposed a deficient concept of 'matter', down to which mind was reduced away, let alone identified. But to identify down phenomena to what is actually an abstraction is to commit failure of explanation. When the theory is amended accordingly, we move from a psycho-neural identity theory to a genuine psycho-physical identity theory that as such can overcome the aforementioned identity problem. Furthermore, as Chapter 5 clarifies, our pansentient monism has, in addition to parsimony, the explanatory power to resolve the problem of mental causation that afflicts both the reductive physicalism of psycho-neural identity theory and the non-reductive physicalism of emergentism, by genuinely identifying physical and mental causation. Jaegwon Kim considers the place of consciousness in a physical world and the nature of mental causation to be the two key components of the mind-matter problem. Through the critical analysis of our prosaic understanding of mind and matter in this thesis, which incorporates the thought of both classical and contemporary thinkers through a novel fusion, it is hoped that both components are addressed and redressed. That is to say that I present this pansentient monism as a plausible, parsimonious, explanatory, and thus, I think, powerful position towards this ever-perplexing mind-matter mystery. -/- [This thesis was passed in January 2019 with viva examination from Galen Strawson and Joel Krueger. (shrink)

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

Since the ENCODE project published its final results in a series of articles in 2012, there is no consensus on what its implications are. ENCODE’s central and most controversial claim was that there is essentially no junk DNA: most sections of the human genome believed to be «junk» are functional. This claim was met with many reservations. If researchers disagree about whether there is junk DNA, they have first to agree on a concept of function and how function, given a (...) particular definition, can be discovered. The ENCODE debate centered on a notion of function that assumes a strong dichotomy between evolutionary and non-evolutionary function and causes, prevalent in the Modern Evolutionary Synthesis. In contrast to how the debate is typically portrayed, both sides share a commitment to this distinction. This distinction is, however, much debated in alternative approaches to evolutionary theory, such as the EES. We show that because the ENCODE debate is grounded in a particular notion of function, it is unclear how it connects to broader debates about what is the correct evolutionary frame- work. Furthermore, we show how arguments brought forward in the controversy, particularly arguments from mathematical population genetics, are deeply embedded in their particular disciplinary contexts, and reflect substantive assumptions about the evolution of genomes. With this article, we aim to provide an anatomy of the ENCODE debate that offers a new perspective on the notions of function both sides employed, as well as to situate the ENCODE debate within wider debates regarding the forces operating in evolution. (shrink)

The Aristotelian axiom that function follows form was beautifully instantiated in molecular biology by the discovery of DNA’s structure that immediately suggested how DNA might work as depository and vehicle for genetic information. However, later on molecular biology became infatuated with the gene that became the center of the universe. This gene-centered viewpoint is an obstacle for the emerging field of evo-devo aiming at finding the causal connections between evolution and biological development. Here it is argued that molecular biology (...) must reject the narrow-minded causality associated with the gene-centered view and so it must recover to the spirit of Aristotelian natural history and its four types of causation in order to foster the evo-devo field of research. (shrink)

Evolution never stops. Stress is often a manifestation of competition which seems to drive human gene-culture coevolution. A popular, Dutch account on evolution in everyday life. People often claim that we are thoroughly cultural beings, but culture is based on a series of talents which are a product of directional and stabilizing selection. Culture also presupposes certain psychological characteristics. People adopt and change culture to fit their biopsychological needs.

The mantra that "the best way to predict the future is to invent it" (attributed to the computer scientist Alan Kay) exemplifies some of the expectations from the technical and innovative sides of biomedical research at present. However, for technical advancements to make real impacts both on patient health and genuine scientific understanding, quite a number of lingering challenges facing the entire spectrum from protein biology all the way to randomized controlled trials should start to be overcome. The proposal in (...) this chapter is that philosophy is essential in this process. By reviewing select examples from the history of science and philosophy, disciplines which were indistinguishable until the mid-nineteenth century, I argue that progress toward the many impasses in biomedicine can be achieved by emphasizing theoretical work (in the true sense of the word 'theory') as a vital foundation for experimental biology. Furthermore, a philosophical biology program that could provide a framework for theoretical investigations is outlined. (shrink)

This paper takes a critical stance on Tallis’s separation of causation and agency. While his critique of the causal theory of action and the assumptions about causation underlying different versions of determinism, including the one based on neuroscience is right, his rejection of causation (of all sorts) has implausible consequences. Denying the link between action and causation amounts to overlooking the role action plays in causal inference and in the origin of causal concepts. I suggest that (...) a weaker version of Tallis’ claim, compatible with causation understood as agency, would work better. (shrink)

Genetic engineering technologies are a subclass of the biotechnology family, and are concerned with the use of laboratory-based technologies to intervene with a given organism at the genetic level, i.e., the level of its DNA. This class of technologies could feasibly be used to treat diseases and disabilities, create disease-resistant crops, or even be used to enhance humans to make them more resistant to certain environmental conditions. However, both therapeutic and enhancement applications of genetic engineering raise serious (...) ethical concerns. This paper examines various objections to genetic engineering (as applied to humans) which have been raised in the literature, and presents a new way to frame these issues, and to look for solutions. Specifically, this paper frames genetic engineering technologies within the ‘design turn in applied ethics’ lens and thus situates these technologies as covarying with societal forces. The value sensitive design (VSD) approach to technology design is then appropriated as the conceptual framework in which genetic engineering technologies can be considered so that they can be designed for important human values. By doing so, this paper brings further nuance to the scholarship on genetic engineering technologies by discussing the sociotechnicity of genetic engineering systems rather than framing them as value-neutral tools that either support or constrain values based on how they are used. (shrink)

In this paper, I argue that causal theories of memory are typically committed to two independent, non-mutually entailing theses. The first thesis pertains to the necessity of appropriate causation in memory, specifying a condition token memories need to satisfy. The second pertains to the explanation of memory reliability in causal terms and it concerns memory as a type of mental state. Post-causal theories of memory can reject only the first (weak post-causalism) or both (strong post-causalism) theses. Upon this backdrop, (...) I examine Werning’s (2020) causalist argument from probabilistic correlation. I argue that it doesn’t establish the necessity of appropriate causation and thus it can only target strong post-causalist theories. I end up by presenting some general considerations, suggesting that memories may not always be causally linked to past experiences. (shrink)

Whereas many philosophers take backwards causation to be impossible, the few who maintain its possibility either take it to be absent from the actual world or else confined to theoretical physics. Here, however, I argue that backwards causation is not only actual, but common, though occurring in the context of our social institutions. After juxtaposing my cases with a few others in the literature and arguing that we should take seriously the reality of causal cases in these contexts, (...) I consider several objections. These objections involve whether the cases should be reinterpreted, whether they are properly within the institution, whether they involve necessitation or else Cambridge changes, whether and how they involve changing the past, and whether this should call us to question institutional reality. I end by suggesting that it is a virtue of our institutions that they allow backwards causation, that this is a kind of technology that they are often built to incorporate. (shrink)

In many spheres, the law takes the legal concept of causation to correspond to the folk concept (the correspondence assumption). Courts, including the US Supreme Court, tend to insist on the "common understanding" and that which is "natural to say" (Burrage v. United States) when it comes to expressions relating to causation, and frequently refuse to clarify the expression to juries. As recent work in psychology and experimental philosophy has uncovered, lay attributions of causation are susceptible to (...) a great number of unexpected factors, some of which seem rather peripheral to causation. One of those is the norm effect (Knobe & Fraser, 2008): Agents who, in acting as they do, break a salient norm, are more likely to be considered as having caused a certain consequence than when they do not violate a norm. According to some (e.g., Alicke, 1992) this constitutes a bias. According to others (e.g., Sytsma, 2020), the folk concept of causation is sensitive to normative factors, and there’s nothing wrong with that. In this paper, we explore the question whether the norm effect should be considered a bias from the legal perspective on the one hand, and from the psychological perspective on the other. To do this, we test whether norms which are nonpertinent to the consequences or outright silly also impact causation judgements. The data from two preregistered experiments (total N=593) clearly show they do. This, we argue, makes the bias interpretation plausible from the psychological perspective, and both plausible and problematic from the legal perspective. It also shows that the law should abstain from unreflectively assuming conceptual correspondence between legal and ordinary language concepts. (shrink)

The standard objection to dualist theories of mind is that they seemingly cannot account for the obvious fact that mental phenomena cause our behaviour. On the plausible assumption that all our behaviour is physically necessitated by entirely physical phenomena, there appears to be no room for dualist mental causation. Some argue that dualists can address this problem by making minimal adjustments in their ontology. I argue that no such adjustments are required. Given recent developments in philosophy of causation, (...) it is plausible that mental phenomena cause behaviour in standard dualist ontologies. (shrink)

Which country, politician, or policy is more of a cause of the Covid-19 pandemic death toll? Which of the two factories causally contributed more to the pollution of the nearby river? A wide-ranging portion of our everyday thought and talk, and attitudes rely on a graded notion of causation. However, it is sometimes highlighted that on most contemporary accounts, causation is on-off. Some philosophers further question the legitimacy of talk of degrees of causation and suggest that we (...) avoid it. Some hold that the notion of degrees of causation is an illusion. In this paper, I’ll argue that causation does come in degrees. (shrink)

Our ordinary causal concept seems to fit poorly with how our best physics describes the world. We think of causation as a time-asymmetric dependence relation between relatively local events. Yet fundamental physics describes the world in terms of dynamical laws that are, possible small exceptions aside, time symmetric and that relate global time slices. My goal in this paper is to show why we are successful at using local, time-asymmetric models in causal explanations despite this apparent mismatch with fundamental (...) physics. In particular, I will argue that there is an important connection between time asymmetry and locality, namely: understanding the locality of our causal models is the key to understanding why the physical time asymmetries in our universe give rise to time asymmetry in causal explanation. My theory thus provides a unified account of why causation is local and time asymmetric and thereby enables a reply to Russell’s famous attack on causation. (shrink)

What would it be for a process to happen backwards in time? Would such a process involve different causal relations? It is common to understand the time-reversal invariance of a physical theory in causal terms, such that whatever can happen forwards in time can also happen backwards in time. This has led many to hold that time-reversal symmetry is incompatible with the asymmetry of cause and effect. This article critiques the causal reading of time reversal. First, I argue that the (...) causal reading requires time-reversal-related models to be understood as representing distinct possible worlds and, on such a reading, causal relations are compatible with time-reversal symmetry. Second, I argue that the former approach does, however, raise serious sceptical problems regarding the causal relations of paradigm causal processes and as a consequence there are overwhelming reasons to prefer a non-causal reading of time reversal, whereby time reversal leaves causal relations invariant. On the non-causal reading, time-reversal symmetry poses no significant conceptual nor epistemological problems for causation. _1_ Introduction _1.1_ The directionality argument _1.2_ Time reversal _2_ What Does Time Reversal Reverse? _2.1_ The B- and C-theory of time _2.2_ Time reversal on the C-theory _2.3_ Answers _3_ Does Time Reversal Reverse Causal Relations? _3.1_ Causation, billiards, and snooker _3.2_ The epistemology of causal direction _3.3_ Answers _4_ Is Time-Reversal Symmetry Compatible with Causation? _4.1_ Incompatibilism _4.2_ Compatibilism _4.3_ Answers _5_ Outlook. (shrink)

Many philosophical theories of causation are egalitarian, rejecting a distinction between causes and mere causal conditions. We sought to determine the extent to which people's causal judgments discriminate, selecting as causes counternormal events—those that violate norms of some kind—while rejecting non-violators. We found significant selectivity of this sort. Moreover, priming that encouraged more egalitarian judgments had little effect on subjects. We also found that omissions are as likely as actions to be judged as causes, and that counternormative selectivity appears (...) to apply equally to actions and omissions. (shrink)

The reduction of grounding to causation, or each to a more general relation of which they are species, has sometimes been justified by the impressive inferential capacity of structural equation modelling, causal Bayes nets, and interventionist causal modelling. Many criticisms of this assimilation focus on how causation is inadequate for grounding. Here, I examine the other direction: how treating grounding in the image of causation makes the resulting view worse for causation. The distinctive features of causal (...) modelling that make this connection appealing are distorted beyond use by forcing them to fit onto grounding. The very inferential strength that makes causation attractive is only possible because of a narrow construal of what counts as a causal relation; as soon as that broadens, the inferential capacity markedly diminishes. Making causation suitable for application to grounding spoils what was appealing about causation for this task in the first place. However, grounding need not appeal to causation: causal modelling does not have exclusive claim to structural equation modeling or other formal techniques of modelling structure. I offer a case in favour of a different kind of metaphysical frugality, which tend towards narrow, more restrictive construals of relations like causation or grounding, because then each relation behaves more homogenously. This more homogenous behavior delivers stronger inferential power per relation even though there may be more relations to which one is committed. (shrink)

In this paper I present an argument in favour of a parental duty to use preimplantation genetic diagnosis (PGD). I argue that if embryos created in vitro were able to decide for themselves in a rational manner, they would sometimes choose PGD as a method of selection. Couples, therefore, should respect their hypothetical choices on a principle similar to that of patient autonomy. My thesis shows that no matter which moral doctrine couples subscribe to, they ought to conduct the (...) PGD procedure in the situations when it is impossible to implant all of the created embryos and if there is a significant risk for giving birth to a child with a serious condition. (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)

The cumulative impact of enhancement technologies may alter the human species in the very long-term future. In this article, I will start showing how radical genetic enhancements may accelerate the conversion into a novel species. I will also clarify the concepts of ‘biological species’, ‘transhuman’ and ‘posthuman’. Then, I will summarize some ethical arguments for creating a transhuman or posthuman species with a substantially higher level of well-being than the human one. In particular, I will present what I shall (...) call the Principle of the Best Interests of Posthumanity, which states that the enhancement of the human and transhuman species must be directed towards the creation of a posthuman existence that is substantially more valuable than its predecessors. I suggest that human extinction may be considered, within that principle, as one of the best interests of posthumanity. Finally, I will develop three objections that make that principle unattractive and that show that pursuing a full-blown programme of posthuman evolution is ethically flawed. (shrink)

Genetically engineered (GE) insects, such as the GE OX513A Aedes aegypti mosquitoes, have been designed to suppress their wild-type populations so as to reduce the transmission of vector-borne diseases in humans. Apart from the ecological and epidemiological uncertainties associated with this approach, such biotechnological approaches may be used by individual governments or the global community of nations to avoid addressing the underlying structural, systemic causes of those infections... We discuss here key ethical questions raised by the use of GE mosquitoes, (...) with the aim of fostering discussion between the public, researchers, policy makers, healthcare organizations, and regulatory agencies at the local, national, and international levels. We affect that goal by outlining a procedural approach to decision-making about the use of the “biotechnology” that goes beyond “community engagement.” The protocol we advocate for entails informed deliberations and decision-making at the community level. It is designed to ensure that the voices of the marginalized and vulnerable groups that would be disproportionately affected by the decision are heard during the community-wide discussions. Moreover, we make the case that the values embedded in the risk assessment should be identified so that the community can make an informed decision about the use of GE insects. In addition, we advocate for the involvement of a variety of actors whose responsibility would be to ensure that the community has the opportunity to make an informed decision based on deliberations about the use of the “biotechnology.”. (shrink)

How we ought to diagnose, categorise and respond to spectrum disabilities such as autism and Attention Deficit/Hyperactivity Disorder (ADHD) is a topic of lively debate. The heterogeneity associated with ADHD and autism is described as falling on various continua of behavioural, neural, and genetic difference. These continua are varyingly described either as extending into the general population, or as being continua within a given disorder demarcation. Moreover, the interrelationships of these continua are likewise often vague and subject to diverse (...) interpretations. -/- In this paper, I explore geneticists' and self-advocates’ perspectives concerning autism and ADHD as continua. These diagnoses are overwhelmingly analysed as falling on a continuum or continua of underlying traits, which supports the notion of “the neurodiversity spectrum”, i.e., a broader swath of human neural and behavioural diversity on which some concentrations of different functioning are diagnosed. I offer a taxonomy of conceptions of the genetic, phenotypic, and endophenotypic dimensionality within and beyond these diagnostic categories, and suggest that the spectrum of neurodiversity is characteristically endophenotypic. (shrink)

We propose that all actual causes are simultaneous with their direct effects, as illustrated by both everyday examples and the laws of physics. We contrast this view with the sequential conception of causation, according to which causes must occur prior to their effects. The key difference between the two views of causation lies in differing assumptions about the mathematical structure of time.

I provide a comprehensive metaphysics of causation based on the idea that fundamentally things are governed by the laws of physics, and that derivatively difference-making can be assessed in terms of what fundamental laws of physics imply for hypothesized events. Highlights include a general philosophical methodology, the fundamental/derivative distinction, and my mature account of causal asymmetry.

In a recent paper I argued that agent causation theorists should be compatibilists. In this paper, I argue that compatibilists should be agent causation theorists. I consider six of the main problems facing compatibilism: (i) the powerful intuition that one can't be responsible for actions that were somehow determined before one was born; (ii) Peter van Inwagen's modal argument, involving the inference rule (β); (iii) the objection to compatibilism that is based on claiming that the ability to do (...) otherwise is a necessary condition for freedom; (iv) "manipulation arguments," involving cases in which an agent is manipulated by some powerful being into doing something that he or she would not normally do, but in such a way that the compatibilist's favorite conditions for a free action are satisfied; (v) the problem of constitutive luck; and (vi) the claim that it is not fair to blame someone for an action if that person was determined by forces outside of his or her control to perform that action. And in the case of each of these problems, I argue that the compatibilist has a much more plausible response to that problem if she endorses the theory of agent causation than she does otherwise. (shrink)

The problem of downward causation is that an intuitive response to an intuitive picture leads to counterintuitive results. Suppose a mental event, m1, causes another mental event, m2. Unless the mental and the physical are completely independent, there will be a physical event in your brain or your body or the physical world as a whole that underlies this event. The mental event occurs at least partly in virtue of the physical event’s occurring. And the same goes for m2 (...) [2] and p2. Let’s not worry about what exactly “underlying” or “in virtue of” means here. Here’s the picture. m1 -----> m2 | | p1 -----> p2 The horizontal arrows represent causation, and the vertical lines represent underlying, whatever that may be. There’s some reason to think that the only way m1 can bring about m2 is by bringing about p2. You can’t convince someone of something through mental telepathy. You need to interact with the physical world, perhaps by saying something and so making some noise, or by pointing and getting them to turn their head and see. What goes for the case of two people goes for the case of one person as well. Superstition aside, there is no purely mental energy that floats free of the merely physical workings of the brain. If m1 brings about m2 by bringing about p2, then m1 brings about p2. This is downward causation. But wait. Doesn’t p1 bring about p2? Isn’t that what the bottom arrow represents? Maybe m1 and p1 work together to bring about p2. There are little holes in the physical causal structure that need to be filled by mental events. You don’t need a sweeping metaphysical thesis about the causal closure of the physical to find this implausible. Maybe p2 is overdetermined. (shrink)

The problem of mental causation is discussed by taking into account some recent developments in the philosophy of science. The problem is viewed from the perspective of the new interventionist theory of causation developed by Woodward. The import of the idea that causal claims involve contrastive classes in mental causation is also discussed. It is argued that mental causation is much less a problem than it has appeared to be.

In The Biopsychosocial Model of Health and Disease, Derek Bolton and Grant Gillett argue that a defensible updated version of the biopsychosocial model requires a metaphysically adequate account of disease causation that can accommodate biological, psychological, and social factors. This present paper offers a philosophical critique of their account of biopsychosocial causation. I argue that their account relies on claims about the normativity and the semantic content of biological information that are metaphysically contentious. Moreover, I suggest that these (...) claims are unnecessary for a defence of biopsychosocial causation, as the roles of multiple and diverse factors in disease causation can be readily accommodated by a more widely accepted and less metaphysically contentious account of causation. I then raise the more general concern that they are misdiagnosing the problem with the traditional version of the biopsychosocial model. The challenge when developing an explanatorily valuable version of the biopsychosocial model, I argue, is not so much providing an adequate account of biopsychosocial causation, but providing an adequate account of causal selection. Finally, I consider how this problem may be solved to arrive at a more explanatorily valuable and clinically useful version of the biopsychosocial model. (shrink)

There have recently been a number of strong claims that normative considerations, broadly construed, influence many philosophically important folk concepts and perhaps are even a constitutive component of various cognitive processes. Many such claims have been made about the influence of such factors on our folk notion of causation. In this paper, we argue that the strong claims found in the recent literature on causal cognition are overstated, as they are based on one narrow type of data about a (...) particular type of causal cognition; the extant data do not warrant any wide-ranging conclusions about the pervasiveness of normative considerations in causal cognition. Of course, almost all empirical investigations involve some manner of ampliative inference, and so we provide novel empirical results demonstrating that there are types of causal cognition that do not seem to be influenced by moral considerations. (shrink)

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)

Causation is a macroscopic phenomenon. The temporal asymmetry displayed by causation must somehow emerge along with other asymmetric macroscopic phenomena like entropy increase and the arrow of radiation. I shall approach this issue by considering ‘causal inference’ techniques that allow causal relations to be inferred from sets of observed correlations. I shall show that these techniques are best explained by a reduction of causation to structures of equations with probabilistically independent exogenous terms. This exogenous probabilistic independence imposes (...) a recursive order on these equations and a consequent distinction between dependent and independent variables that lines up with the temporal asymmetry of causation. (shrink)

I propose a new formalist account of legal (/proximate) causation – one that holds legal causation to be a matter of amoral, descriptive fact. The account starts with a metaphysical relation, akin to but distinct from common-sense causation, and it argues that legal causation aligns exactly with that relation; it is unified and principled.

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

This paper examines a promising probabilistic theory of singular causation developed by David Lewis. I argue that Lewis' theory must be made more sophisticated to deal with certain counterexamples involving pre-emption. These counterexamples appear to show that in the usual case singular causation requires an unbroken causal process to link cause with effect. I propose a new probabilistic account of singular causation, within the framework developed by Lewis, which captures this intuition.