Preface by Daniel C. Dennett Beginning with a general theory of function applied to body organs, behaviors, customs, and both inner and outer representations, ...

Christopher Boorse’s Biostatistical Theory of Health has been the main contender among naturalistic accounts of health for the last 40 years. Yet, a recent criticism of this theory, presented by Elselijn Kingma, identifies a dilemma resulting from the BST’s conceptual linking of health and statistical typicality. Kingma argues that the BST either cannot accommodate the situation- specificity of many normal functions or cannot account for many situation-specific diseases. In this article, we expand upon with Daniel Hausman’s response to Kingma’s dilemma. (...) We propose that recalling Boorse’s specification that health is an intrinsic property of its bearers and explicating this intrinsic property in relation to the concept of homeostasis can illuminate how proponents of naturalistic accounts of health should deal with the situation- specificity of normal functions. We argue that beyond what Boorse and Hausman have delineated, the situation- specificity of normal function cannot be fully captured in a simple dichotomy between normal and abnormal environment or between relevant and irrelevant situations. By bringing homeostasis to the fore of the analysis of health, we set out a richer picture of what the various situations that affect living organisms’ functional performance can be. Accordingly, we provide a broader classification of these various situations which, we contend, better accounts for the main intuitions that philosophers of medicine have sought to accommodate than previous naturalistic theories of health. (shrink)

Causal selection is the task of picking out, from a field of known causally relevant factors, some factors as elements of an explanation. The Causal Parity Thesis in the philosophy of biology challenges the usual ways of making such selections among different causes operating in a developing organism. The main target of this thesis is usually gene centrism, the doctrine that genes play some special role in ontogeny, which is often described in terms of information-bearing or programming. This paper is (...) concerned with the attempt of confronting the challenge coming from the Causal Parity Thesis by offering principles of causal selection that are spelled out in terms of an explicit philosophical account of causation, namely an interventionist account. I show that two such accounts that have been developed, although they contain important insights about causation in biology, nonetheless fail to provide an adequate reply to the Causal Parity challenge: Ken Waters's account of actual-difference making and Jim Woodward's account of causal specificity. A combination of the two also doesn't do the trick, nor does Laura Franklin-Hall's account of explanation (in this volume). We need additional conceptual resources. I argue that the resources we need consist in a special class of counterfactual conditionals, namely counterfactuals the antecedents of which describe biologically normal interventions. (shrink)

This paper attempts to elucidate three characteristics of causal relationships that are important in biological contexts. Stability has to do with whether a causal relationship continues to hold under changes in background conditions. Proportionality has to do with whether changes in the state of the cause “line up” in the right way with changes in the state of the effect and with whether the cause and effect are characterized in a way that contains irrelevant detail. Specificity is connected both to (...) David Lewis’ notion of “influence” and also with the extent to which a causal relation approximates to the ideal of one cause–one effect. Interrelations among these notions and their possible biological significance are also discussed. (shrink)

Woodward's long awaited book is an attempt to construct a comprehensive account of causation explanation that applies to a wide variety of causal and explanatory claims in different areas of science and everyday life. The book engages some of the relevant literature from other disciplines, as Woodward weaves together examples, counterexamples, criticisms, defenses, objections, and replies into a convincing defense of the core of his theory, which is that we can analyze causation by appeal to the notion of manipulation.

The void is deadly. If you were cast into a void, it would cause you to die in just a few minutes. It would suck the air from your lungs. It would boil your blood. It would drain the warmth from your body. And it would inflate enclosures in your body until they burst}.

Synthetic biology research is often described in terms of programming cells through the introduction of synthetic genes. Genetic material is seemingly attributed with a high level of causal responsibility. We discuss genetic causation in synthetic biology and distinguish three gene concepts differing in their assumptions of genetic control. We argue that synthetic biology generally employs a difference-making approach to establishing genetic causes, and that this approach does not commit to a specific notion of genetic program or genetic control. Still, we (...) suggest that a strong program concept of genetic material can be used as a successful heuristic in certain areas of synthetic biology. Its application requires control of causal context, and may stand in need of a modular decomposition of the target system. We relate different modularity concepts to the discussion of genetic causation and point to possible advantages of and important limitations to seeking modularity in synthetic biology systems. (shrink)

Biologists studying complex causal systems typically identify some factors as causes and treat other factors as background conditions. For example, when geneticists explain biological phenomena, they often foreground genes and relegate the cellular milieu to the background. But factors in the milieu are as causally necessary as genes for the production of phenotypic traits, even traits at the molecular level such as amino acid sequences. Gene-centered biology has been criticized on the grounds that because there is parity among causes, the (...) “privileging” of genes reflects a reductionist bias, not an ontological difference. The idea that there is an ontological parity among causes is related to a philosophical puzzle identified by John Stuart Mill: what, other than our interests or biases, could possibly justify identifying some causes as the actual or operative ones, and other causes as mere background? The aim of this paper is to solve this conceptual puzzle and to explain why there is not an ontological parity among genes and the other factors. It turns out that solving this puzzle helps answer a seemingly unrelated philosophical question: what kind of causal generality matters in biology? (shrink)

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

Much of the philosophical literature on causation has focused on the concept of actual causation, sometimes called token causation. In particular, it is this notion of actual causation that many philosophical theories of causation have attempted to capture.2 In this paper, we address the question: what purpose does this concept serve? As we shall see in the next section, one does not need this concept for purposes of prediction or rational deliberation. What then could the purpose be? We will argue (...) that one can gain an important clue here by looking at the ways in which causal judgments are shaped by people‘s understanding of norms. (shrink)

It has long been known that people’s causal judgments can have an impact on their moral judgments. To take a simple example, if people conclude that a behavior caused the death of ten innocent children, they will therefore be inclined to regard the behavior itself as morally wrong. So far, none of this should come as any surprise. But recent experimental work points to the existence of a second, and more surprising, aspect of the relationship between causal judgment and moral (...) judgment. It appears that the relationship can sometimes go in the opposite direction. That is, it appears that our moral judgments can sometimes impact our causal judgments. (Hence, we might first determine that a behavior is morally wrong and then, on that basis, arrive at the conclusion that it was the cause of various outcomes.). (shrink)

We propose a new definition of actual causes, using structural equations to model counterfactuals. We show that the definition yields a plausible and elegant account of causation that handles well examples which have caused problems for other definitions and resolves major difficulties in the traditional account.

Woodward's long awaited book is an attempt to construct a comprehensive account of causation explanation that applies to a wide variety of causal and explanatory claims in different areas of science and everyday life. The book engages some of the relevant literature from other disciplines, as Woodward weaves together examples, counterexamples, criticisms, defences, objections, and replies into a convincing defence of the core of his theory, which is that we can analyse causation by appeal to the notion of manipulation.

Thirty years after Lewis's paper, this book brings together some of the most important recent work connecting—or, in some cases, disputing the connection ...

Among the many philosophers who hold that causal facts1 are to be explained in terms of—or more ambitiously, shown to reduce to—facts about what happens, together with facts about the fundamental laws that govern what happens, the clear favorite is an approach that sees counterfactual dependence as the key to such explanation or reduction. The paradigm examples of causation, so advocates of this approach tell us, are examples in which events c and e— the cause and its effect— both occur, (...) but: had c not occurred, e would not have occurred either. From this starting point ideas proliferate in a vast profusion. But the remarkable disparity among these ideas should not obscure their common foundation. Neither should the diversity of opinion about the prospects for a philosophical analysis of causation obscure their importance. For even those philosophers who see these prospects as dim—perhaps because they suffer post-Quinean queasiness at the thought of any analysis of any concept of interest—can often be heard to say such things as that causal relations among events are somehow “a matter of” the patterns of counterfactual dependence to be found in them. (shrink)

The biological sciences employ a concept of normality that must be distinguished from statistical or value concepts. The concept of normality is presupposed in the standard explications of biological functions, and it is crucial to the strategy of explanation by approximations in, for example, physiology. Nevertheless, this concept of normality does not seem to be captured in the language of physics. Thus attempts at explaining the methodological relationship between the biological sciences and the physical sciences by concentrating only on the (...) concept of biological function cannot go very far. An analysis of the concept of normality is also necessary. (shrink)

Recent work in psychology and experimental philosophy has shown that judgments of actual causation are often influenced by consideration of defaults, typicality, and normality. A number of philosophers and computer scientists have also suggested that an appeal to such factors can help deal with problems facing existing accounts of actual causation. This article develops a flexible formal framework for incorporating defaults, typicality, and normality into an account of actual causation. The resulting account takes actual causation to be both graded and (...) comparative. We then show how our account would handle a number of standard cases. 1 Introduction2 Causal Models3 The HP Definition of Actual Causation4 The Problem of Isomorphism5 Defaults, Typicality, and Normality6 Extended Causal Models7 Examples7.1 Omissions7.2 Knobe effects7.3 Causes versus background conditions7.4 Bogus prevention7.5 Causal chains7.6 Legal doctrines of intervening causes7.7 Pre-emption and short circuits8 Conclusion. (shrink)

A central idea of developmental systems theory is ‘parity’ or ‘symmetry’ between genes and non-genetic factors of development. The precise content of this idea remains controversial, with different authors stressing different aspects and little explicit comparisons among the various interpretations. Here I characterise and assess several influential versions of parity.

Kerry et al. criticize our discussion of causal knowledge in evidence-based medicine (EBM) and our assessment of the relevance of their dispositionalist ontology for EBM. Three issues need to be addressed in response: (1) problems concerning transfer of causal knowledge across heterogeneous contexts; (2) how predictions about the effects of individual treatments based on population-level evidence from RCTs are fallible; and (3) the relevance of ontological theories like dispositionalism for EBM.

A wide range of gene knockout experiments shows that functional stability is an important feature of biological systems. On this backdrop, we present an argument for higher‐level causation based on counterfactual dependence. Furthermore, we sketch a metaphysical picture providing resources to explain the metaphysical nature of functional stability, higher‐level causation, and the relevant notion of levels. Our account aims to clarify the role empirical results and philosophical assumptions should play in debates about reductionism and higher‐level causation. It thereby contributes to (...) the development of a philosophical foundation for systems biology. †To contact the authors, please write to: CSMN/IFIKK, University of Oslo, Box 1020 Blindern, N‐0315, Oslo, Norway; e‐mail: [email protected] , [email protected]. (shrink)

We propose a new definition of actual causes, using structural equations to model counterfactuals. We show that the definition yields a plausible and elegant account of causation that handles well examples which have caused problems for other definitions and resolves major difficultiesn in the traditional account.

Gene–environment covariance is the phenomenon whereby genetic differences bias variation in developmental environment, and is particularly problematic for assigning genetic and environmental causation in a heritability analysis. The interpretation of these cases has differed amongst biologists and philosophers, leading some to reject the utility of heritability estimates altogether. This paper examines the factors that influence causal reasoning when G–E covariance is present, leading to interpretive disagreement between scholars. It argues that the causal intuitions elicited are influenced by concepts of agency (...) and blame-worthiness, and are intimately tied with the conceptual understanding of the phenotype under investigation. By considering a phenotype-specific approach, I provide an account as to why causal ascriptions can differ depending on the interpreter. Phenotypes like intelligence, which have been the primary focus of this debate, are more likely to spark disagreement for the interpretation of G–E covariance cases because the concept and ideas about its ‘normal development’ relatively ill-defined and are a subject of debate. I contend that philosophical disagreement about causal attributions in G–E covariance cases are in essence disagreements regarding how a phenotype should be defined and understood. This moves the debate from one of an ontological flavour concerning objective causal claims, to one concerning the conceptual, normative and semantic dependencies. (shrink)

In the past century, nearly all of the biological sciences have been directly affected by discoveries and developments in genetics, a fast-evolving subject with important theoretical dimensions. In this rich and accessible book, Paul Griffiths and Karola Stotz show how the concept of the gene has evolved and diversified across the many fields that make up modern biology. By examining the molecular biology of the 'environment', they situate genetics in the developmental biology of whole organisms, and reveal how the molecular (...) biosciences have undermined the nature/nurture distinction. Their discussion gives full weight to the revolutionary impacts of molecular biology, while rejecting 'genocentrism' and 'reductionism', and brings the topic right up to date with the philosophical implications of the most recent developments in genetics. Their book will be invaluable for those studying the philosophy of biology, genetics and other life sciences. (shrink)

In many biological experiments, due to gene-redundancy or distributed backup mechanisms, there are no visible effects on the functionality of the organism when a gene is knocked out or down. In such cases there is apparently no counterfactual dependence between the gene and the phenotype in question, although intuitively the gene is causally relevant. Due to relativity of causal relations to causal models, we suggest that such cases can be handled by changing the resolution of the causal model that represents (...) the system. By decreasing the resolution of our causal model, counterfactual dependencies can be established at a higher level of abstraction. By increasing the resolution, stepwise causal dependencies of the right kind can serve as a sufficient condition for causal relevance. Finally, we discuss how introducing a temporal dimension in causal models can account for causation in cases of non-modular systems dynamics. (shrink)

This paper combines the ancient idea that causes necessitate their effects with Angelika Kratzer’s semantics of modality. On the resulting view, causal claims quantify over restricted domains of possible worlds determined by two contextually determined parameters. I argue that this view can explain a number of otherwise puzzling features of the way we use and evaluate causal language, including the difference between causing an effect and being a cause of it, the sensitivity of causal judgements to normative facts, and the (...) semantics of causal disagreements. (shrink)