In this important book, Ellery Eells explores and refines philosophical conceptions of probabilistic causality. In a probabilistic theory of causation, causes increase the probability of their effects rather than necessitate their effects in the ways traditional deterministic theories have specified. Philosophical interest in this subject arises from attempts to understand population sciences as well as indeterminism in physics. Taking into account issues involving spurious correlation, probabilistic causal interaction, disjunctive causal factors, and temporal ideas, Professor Eells advances the analysis of what (...) it is for one factor to be a positive causal factor for another. A salient feature of the book is a theory of token level probabilistic causation in which the evolution of the probability of a later event from an earlier event is central. This will be a book of crucial significance to philosophers of science and metaphysicians; it will also prove stimulating to many economists, psychologists, and physicists. (shrink)

Metagenomics is an emerging microbial systems science that is based on the large-scale analysis of the DNA of microbial communities in their natural environments. Studies of metagenomes are revealing the vast scope of biodiversity in a wide range of environments, as well as new functional capacities of individual cells and communities, and the complex evolutionary relationships between them. Our examination of this science focuses on the ontological implications of these studies of metagenomes and metaorganisms, and what they mean for common (...) sense and philosophical understandings of multicellularity, individuality and organism. We show how metagenomics requires us to think in different ways about what human beings are and what their relation to the microbial world is. Metagenomics could also transform the way in which evolutionary processes are understood, with the most basic relationship between cells from both similar and different organisms being far more cooperative and less antagonistic than is widely assumed. In addition to raising fundamental questions about biological ontology, metagenomics generates possibilities for powerful technologies addressed to issues of climate, health and conservation. We conclude with reflections about process-oriented versus entity-oriented analysis in light of current trends towards systems approaches. (shrink)

Presents a synoptic, compact, and accessible exposition of this influential and interesting sector of twentieth-century American philosophy.

Standard microbial evolutionary ontology is organized according to a nested hierarchy of entities at various levels of biological organization. It typically detects and defines these entities in relation to the most stable aspects of evolutionary processes, by identifying lineages evolving by a process of vertical inheritance from an ancestral entity. However, recent advances in microbiology indicate that such an ontology has important limitations. The various dynamics detected within microbiological systems reveal that a focus on the most stable entities (or features (...) of entities) over time inevitably underestimates the extent and nature of microbial diversity. These dynamics are not the outcome of the process of vertical descent alone. Other processes, often involving causal interactions between entities from distinct levels of biological organisation, or operating at different time scales, are responsible not only for the destabilisation of pre-existing entities, but also for the emergence and stabilisation of novel entities in the microbial world. In this article we consider microbial entities as more or less stabilised functional wholes, and sketch a network-based ontology that can represent a diverse set of processes including, for example, as well as phylogenetic relations, interactions that stabilise or destabilise the interacting entities, spatial relations, ecological connections, and genetic exchanges. We use this pluralistic framework for evaluating (i) the existing ontological assumptions in evolution (e.g. whether currently recognized entities are adequate for understanding the causes of change and stabilisation in the microbial world), and (ii) for identifying hidden ontological kinds, essentially invisible from within a more limited perspective. We propose to recognize additional classes of entities that provide new insights into the structure of the microbial world, namely “processually equivalent” entities, “processually versatile” entities, and “stabilized” entities. (shrink)

Causation is everywhere in the world: it features in every science and technology. But how much do we understand it? Mumford and Anjum develop a new theory of causation based on an ontology of real powers or dispositions. They provide the first detailed outline of a thoroughly dispositional approach, and explore its surprising features.

This article argues that the basic account of mechanism and mechanistic explanation, involving sequential execution of qualitatively characterized operations, is itself insufficient to explain biological phenomena such as the capacity of living organisms to maintain themselves as systems distinct from their environment. This capacity depends on cyclic organization, including positive and negative feedback loops, which can generate complex dynamics. Understanding cyclically organized mechanisms with complex dynamics requires coordinating research directed at decomposing mechanisms into parts and operations with research using computational (...) models to recompose mechanisms and determine their dynamic behavior. This coordinated endeavor yields dynamic mechanistic explanations. (shrink)

We address three fundamental questions: What does it mean for an entity to be living? What is the role of inter-organismic collaboration in evolution? What is a biological individual? Our central argument is that life arises when lineage-forming entities collaborate in metabolism. By conceiving of metabolism as a collaborative process performed by functional wholes, which are associations of a variety of lineage-forming entities, we avoid the standard tension between reproduction and metabolism in discussions of life – a tension particularly evident (...) in discussions of whether viruses are alive. Our perspective assumes no sharp distinction between life and non-life, and does not equate life exclusively with cellular or organismal status. We reach this conclusion through an analysis of the capabilities of a spectrum of biological entities, in which we include the pivotal case of viruses as well as prions, plasmids, organelles, intracellular and extracellular symbionts, unicellular and multicellular life-forms. The usual criterion for classifying many of the entities of our continuum as non-living is autonomy. This emphasis on autonomy is problematic, however, because even paradigmatic biological individuals, such as large animals, are dependent on symbiotic associations with many other organisms. These composite individuals constitute the metabolic wholes on which selection acts. Finally, our account treats cooperation and competition not as polar opposites but as points on a continuum of collaboration. We suggest that competitive relations are a transitional state, with multi-lineage metabolic wholes eventually outcompeting selfish competitors, and that this process sometimes leads to the emergence of new types or levels of wholes. Our view of life as a continuum of variably structured collaborative systems leaves open the possibility that a variety of forms of organized matter – from chemical systems to ecosystems – might be usefully understood as living entities. (shrink)

The philosophical theory of scientific explanation proposed here involves a radically new treatment of causality that accords with the pervasively statistical character of contemporary science. Wesley C. Salmon describes three fundamental conceptions of scientific explanation--the epistemic, modal, and ontic. He argues that the prevailing view is untenable and that the modal conception is scientifically out-dated. Significantly revising aspects of his earlier work, he defends a causal/mechanical theory that is a version of the ontic conception. Professor Salmon's theory furnishes a robust (...) argument for scientific realism akin to the argument that convinced twentieth-century physical scientists of the existence of atoms and molecules. To do justice to such notions as irreducibly statistical laws and statistical explanation, he offers a novel account of physical randomness. The transition from the "reviewed view" of scientific explanation to the causal/mechanical model requires fundamental rethinking of basic explanatory concepts. (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.

In this sequence of philosophical essays about natural science, the author argues that fundamental explanatory laws, the deepest and most admired successes of modern physics, do not in fact describe regularities that exist in nature. Cartwright draws from many real-life examples to propound a novel distinction: that theoretical entities, and the complex and localized laws that describe them, can be interpreted realistically, but the simple unifying laws of basic theory cannot.

It is tempting to analyse causality in terms of just one of the indicators of causal relationships, e.g., mechanisms, probabilistic dependencies or independencies, counterfactual conditionals or agency considerations. While such an analysis will surely shed light on some aspect of our concept of cause, it will fail to capture the whole, rather multifarious, notion. So one might instead plump for pluralism: a different analysis for a different occasion. But we do not seem to have lots of different concepts of cause (...) – just one eclectic notion. The resolution of this conundrum, I think, requires us to accept that our causal beliefs are generated by a wide variety of indicators, but to deny that this variety of indicators yields a variety of concepts of cause. This focus on the relation between evidence and causal beliefs leads to what I call epistemic causality. Under this view, certain causal beliefs are appropriate or rational on the basis of observed evidence; our notion of cause can be understood purely in terms of these rational beliefs. Causality, then, is a feature of our epistemic representation of the world, rather than of the world itself. This yields one, multifaceted notion of cause. (shrink)

There are many ways of attaching two objects together: for example, they can be connected, linked, tied or bound together; and the connection, link, tie or bind can be made of chain, rope, or cement. Every one of these binding methods has been used as a metaphor for causation. What is the real significance of these metaphors? They express a commitment to a certain way of thinking about causation, summarized in the following thesis: ‘In any concrete situation, there is an (...) objective fact of the matter as to whether two events are in fact bound by the causal relation. It is the aim of philosophical inquiry to analyze this objective relation.’ Through a variety of examples, I hope to cast doubt on this seemingly innocuous thesis. The problem lies not with the word ‘objective’, but with the word ‘the’. The goal of a philosophical account of causation should not be to capture the causal relation, but rather to capture the many ways in which the events of the world can be bound together. 1 The metaphors 2 Unpacking the metaphors 3 Theories of causation 4 The two assassins 5 The birth control pills 6 The smoker-protector gene 7 The bicycle thief 8 Further examples 8.1 Indeterminism 8.2 Probability-lowering causes 8.3 Parts vs wholes 8.4 Symmetric overdetermination 8.5 Delayers 8.6 Causation by omission 8.7 Double prevention/disconnection 8.8 Preemptive prevention 8.9 Quantitative variables 9 Conclusion. (shrink)

In this paper I offer an analysis of causation based upon a theory of mechanisms-complex systems whose internal parts interact to produce a system's external behavior. I argue that all but the fundamental laws of physics can be explained by reference to mechanisms. Mechanisms provide an epistemologically unproblematic way to explain the necessity which is often taken to distinguish laws from other generalizations. This account of necessity leads to a theory of causation according to which events are causally related when (...) there is a mechanism that connects them. I present reasons why the lack of an account of fundamental physical causation does not undermine the mechanical account. (shrink)

We argue that the health sciences make causal claims on the basis of evidence both of physical mechanisms, and of probabilistic dependencies. Consequently, an analysis of causality solely in terms of physical mechanisms or solely in terms of probabilistic relationships, does not do justice to the causal claims of these sciences. Yet there seems to be a single relation of cause in these sciences - pluralism about causality will not do either. Instead, we maintain, the health sciences require a theory (...) of causality that unifies its mechanistic and probabilistic aspects. We argue that the epistemic theory of causality provides the required unification. (shrink)

After clarifying the probabilistic conception of causality suggested by Good (1961-2), Suppes (1970), Cartwright (1979), and Skyrms (1980), we prove a sufficient condition for transitivity of causal chains. The bearing of these considerations on the units of selection problem in evolutionary theory and on the Newcomb paradox in decision theory is then discussed.

We currently have on offer a variety of different theories of causation. Many are strikingly good, providing detailed and plausible treatments of exemplary cases; and all suffer from clear counterexamples. I argue that, contra Hume and Kant, this is because causation is not a single, monolithic concept. There are different kinds of causal relations imbedded in different kinds of systems, readily described using thick causal concepts. Our causal theories pick out important and useful structures that fit some familiar cases—cases we (...) discover and ones we devise to fit. (shrink)

The concept of mechanism is analyzed in terms of entities and activities, organized such that they are productive of regular changes. Examples show how mechanisms work in neurobiology and molecular biology. Thinking in terms of mechanisms provides a new framework for addressing many traditional philosophical issues: causality, laws, explanation, reduction, and scientific change.

After a decade of intense debate about mechanisms, there is still no consensus characterization. In this paper we argue for a characterization that applies widely to mechanisms across the sciences. We examine and defend our disagreements with the major current contenders for characterizations of mechanisms. Ultimately, we indicate that the major contenders can all sign up to our characterization.

Compares classic and contemporary theories of genetics and evolution and explores the role of teleological thought in biology.

In recent years, there has been a philosophical cottage industry producing arguments that our concept of causation is not univocal: that there are in fact two concepts of causation, corresponding to distinct species of causal relation. Papers written in this tradition have borne titles like “Two Concepts of Cause” and “Two Concepts of Causation”. With due apologies to Charles Dickens, I hereby make my own contribution to this genre.

Precis of my book by this title, for a symposium.