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.

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)

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)

This paper argues that the consensus physicalist antireductionism in the philosophy of biology cannot accommodate the research strategy or indeed the recent findings of molecular developmental biology. After describing Wolperts programmatic claims on its behalf, and recent work by Gehring and others to identify the molecular determinants of development, the paper attempts to identify the relationship between evolutionary and developmental biology by reconciling two apparently conflicting accounts of bio-function – Wrights and Nagels (as elaborated by Cummins). Finally, the paper seeks (...) a way of defending the two central theses of physicalist antireductionism in the light of the research program of molecular developmental biology, by sharply reducing their metaphysical force. (shrink)

The issue of downward causation (and mental causation in particular), and the exclusion problem is discussed by taking into account some recent advances in the philosophy of science. The problem is viewed from the perspective of the new interventionist theory of causation developed by Woodward. It is argued that from this viewpoint, a higher-level (e.g., mental) state can sometimes truly be causally relevant, and moreover, that the underlying physical state which realizes it may fail to be such.

It is argued that multiscale approaches are necessary for an explanatory modeling of biological systems. A first step, besides common to the multiscale modeling of physical and living systems, is a bottom-up integration based on the notions of effective parameters and minimal models. Top-down effects can be accounted for in terms of effective constraints and inputs. Biological systems are essentially characterized by an entanglement of bottom-up and top-down influences following from their evolutionary history. A self-consistent multiscale scheme is proposed to (...) capture the ensuing circular causality. Its differences with standard mean-field self-consistent equations and slow-fast decompositions are discussed. As such, this scheme offers a way to unravel the multilevel architecture of living systems and their regulation. Two examples, genome functions and biofilms, are detailed. (shrink)

This paper argues in defense of theanti-reductionist consensus in the philosophy ofbiology. More specifically, it takes issues with AlexRosenberg's recent challenge of this position. Weargue that the results of modern developmentalgenetics rather than eliminating the need forfunctional kinds in explanations of developmentactually reinforce their importance.

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)

I show that the recent account of levels in neuroscience proposed by Craver and Bechtel is unsatisfactory since it fails to provide a plausible criterion for being at the same level and is incompatible with Craver and Bechtel’s account of downward causation. Furthermore, I argue that no distinct notion of levels is needed for analyzing explanations and causal issues in neuroscience: it is better to rely on more well-defined notions such as composition and scale. One outcome of this is that (...) apparent cases of downward causation can be analyzed away. (shrink)

We argue that intelligible appeals to interlevel causes (top-down and bottom-up) can be understood, without remainder, as appeals to mechanistically mediated effects. Mechanistically mediated effects are hybrids of causal and constitutive relations, where the causal relations are exclusively intralevel. The idea of causation would have to stretch to the breaking point to accommodate interlevel causes. The notion of a mechanistically mediated effect is preferable because it can do all of the required work without appealing to mysterious interlevel causes. When interlevel (...) causes can be translated into mechanistically mediated effects, the posited relationship is intelligible and should raise no special philosophical objections. When they cannot, they are suspect. (shrink)

The first part of this paper presents an argument showing that the currently most highly acclaimed interventionist theory of causation, i.e. the one advanced by Woodward, excludes supervening macro properties from having a causal influence on effects of their micro supervenience bases. Moreover, this interventionist exclusion argument is demonstrated to rest on weaker premises than classical exclusion arguments. The second part then discusses a weakening of interventionism that Woodward suggests. This weakened version of interventionism turns out either to be inapplicable (...) to cases of downward causation involving supervening macro properties or to render corresponding causal claims meaningless. In sum, the paper argues that, contrary to what many non-reductive physicalists claim, interventionism does not render non-reductive physicalism immune to the problem of causal exclusion. (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)

Argues for the primacy of the phylogenetic system as the general reference system in biology. This book, first published in 1966, generated significant controversy and opened possibilities for evolutionary biology.

What is Life? This is the question asked by Denis Noble in this very personal and at times deeply lyrical book. Noble is a renowned physiologist and systems biologist, and he argues that the genome is not life itself: to understand what life is, we must view it at a variety of different levels, all interacting with each other in a complex web. It is that emergent web, full of feedback between levels, from the gene to the wider environment, that (...) is life. (shrink)

This paper discusses some issues concerning the relationship between the mental and the physical, including the so-called causal exclusion argument, within the framework of a broadly interventionist approach to causation.

When philosophers defend epiphenomenalist doctrines, they often do so by way of a priori arguments. Here we suggest an empirical approach that is modeled on August Weismann’s experimental arguments against the inheritance of acquired characters. This conception of how epiphenomenalism ought to be developed helps clarify some mistakes in two recent epiphenomenalist positions – Jaegwon Kim’s (1993) arguments against mental causation, and the arguments developed by Walsh (2000), Walsh, Lewens, and Ariew (2002), and Matthen and Ariew (2002) that natural selection (...) and drift are not causes of evolution. A manipulationist account of causation (Woodward 2003) leads naturally to an account of how macro- and micro-causation are related and to an understanding of how epiphenomenalism at different levels of organization should be understood. (shrink)

Many researchers consider cancer to have molecular causes, namely mutated genes that result in abnormal cell proliferation (e.g. Weinberg 1998). For others, the causes of cancer are to be found not at the molecular level but at the tissue level where carcinogenesis consists of disrupted tissue organization with downward causation effects on cells and cellular components (e.g. Sonnenschein and Soto 2008). In this contribution, I ponder how to make sense of such downward causation claims. Adopting a manipulationist account of causation (...) (Woodward 2003), I propose a formal definition of downward causation and discuss further requirements (in light of Baumgartner 2009). I then show that such an account cannot be mobilized in support of non-reductive physicalism (contrary to Raatikainen 2010). However, I also argue that such downward causation claims might point at particularly interesting dynamic properties of causal relationships that might prove salient in characterizing causal relationships (following Woodward 2010). (shrink)

Many researchers consider cancer to have molecular causes, namely mutated genes that result in abnormal cell proliferation (e.g. Weinberg 1998); yet for others, the causes of cancer are to be found not at the molecular level but at the tissue level and carcinogenesis would consist in a disrupted tissue organization with downward causation effects on cells and cellular components (e.g. Sonnenschein & Soto 2008). In this contribution, I ponder how to make sense of such downward causation claims. Adopting a manipulationist (...) account of causation (Woodward 2003), I propose a formal definition of downward causation, and discuss further requirements (in light of Baumgartner 2009). I then show that such an account cannot be mobilized in support of non-reductive physicalism (contrary to Raatikainen 2010). However, I also argue that such downward causation claims might point at particularly interesting dynamic properties of causal relationships that might prove salient in characterizing causal relationships (following Woodward 2010). (shrink)

I present a reconstruction of F.H.C. Crick's two 1957 hypotheses "Sequence Hypothesis" and "Central Dogma" in terms of a contemporary philosophical theory of causation. Analyzing in particular the experimental evidence that Crick cited, I argue that these hypotheses can be understood as claims about the actual difference-making cause in protein synthesis. As these hypotheses are only true if restricted to certain nucleic acids in certain organisms, I then examine the concept of causal specificity and its potential to counter claims about (...) causal parity of DNA and other cellular components. I first show that causal specificity is a special kind of invariance under interventions, namely invariance of generalizations that range over finite sets of discrete variables. Then, I show that this notion allows the articulation of a middle ground in the debate over causal parity. (shrink)