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)

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)

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.

Manipulablity theories of causation, according to which causes are to be regarded as handles or devices for manipulating effects, have considerable intuitive appeal and are popular among social scientists and statisticians. This article surveys several prominent versions of such theories advocated by philosophers, and the many difficulties they face. Philosophical statements of the manipulationist approach are generally reductionist in aspiration and assign a central role to human action. These contrast with recent discussions employing a broadly manipulationist framework for understanding causation, (...) such as those due to the computer scientist Judea Pearl and others, which are non-reductionist and rely instead on the notion of an intervention. This is simply an appropriately exogenous causal process; it has no essential connection with human action. This interventionist framework manages to avoid at least some of these difficulties faced by traditional philosophical versions of the manipulability theory and helps to clarify the content of causal claims. (shrink)

The reference class problem arises when we want to assign a probability to a proposition (or sentence, or event) X, which may be classified in various ways, yet its probability can change depending on how it is classified. The problem is usually regarded as one specifically for the frequentist interpretation of probability and is often considered fatal to it. I argue that versions of the classical, logical, propensity and subjectivist interpretations also fall prey to their own variants of the reference (...) class problem. Other versions of these interpretations apparently evade the problem. But I contend that they are all “no-theory” theories of probability - accounts that leave quite obscure why probability should function as a guide to life, a suitable basis for rational inference and action. The reference class problem besets those theories that are genuinely informative and that plausibly constrain our inductive reasonings and decisions. I distinguish a “metaphysical” and an “epistemological” reference class problem. I submit that we can dissolve the former problem by recognizing that probability is fundamentally a two-place notion: conditional probability is the proper primitive of probability theory. However, I concede that the epistemological problem remains. (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)

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)

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)

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

I argue that Calcott :481–505, Calcott 2017) mischaracterizes in an important way the notion of causal specificity proposed by Woodward :287–318, Woodward 2010). This leads him to rely too heavily on one single aspect of Woodward’s analysis on causal specificity; propose an information-theoretic measure he calls ‘precision’ which is partly redundant with, but less general than one of the dimensions in Woodward’s analysis of specificity, without acknowledging Woodward’s analysis; and claim that comparing the specificities of two or more causes under (...) what he calls a competitive analysis of causes, does not permit to capture the distinction between permissive and instructive causes. After having restated Woodward’s analysis of causal specificity, I present an information-theoretic measure which, although related to Calcott’s measure, is more general than his and corresponds to the notion of specificity he missed in Woodward's analysis. I then show how this measure can be used, together with mutual causal information, to distinguish permissive from instructive causes in a competitive analysis of causes. (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)