In addition to being one of the world's most influential philosophers, Aristotle can also be credited with the creation of both the science of biology and the philosophy of biology. He was the first thinker to treat the investigations of the living world as a distinct inquiry with its own special concepts and principles. This book focuses on a seminal event in the history of biology - Aristotle's delineation of a special branch of theoretical knowledge devoted to the systematic investigation (...) of animals. Aristotle approached the creation of zoology with the tools of subtle and systematic philosophies of nature and of science that were then carefully tailored to the investigation of animals. The papers collected in this volume, written by a pre-eminent figure in the field of Aristotle's philosophy and biology, examine Aristotle's approach to biological inquiry and explanation, his concepts of matter, form and kind, and his teleology. (shrink)

This brilliant and controversial work investigates the relationship between 'individual' and 'scientific' knowledge.

Much recent work on explanation in the interventionist tradition emphasizes the explanatory value of stable causal generalizations—i.e., causal generalizations that remain true in a wide range of background circumstances. We argue that two separate explanatory virtues are lumped together under the heading of `stability’. We call these two virtues breadth and guidance respectively. In our view, these two virtues are importantly distinct, but this fact is neglected or at least under-appreciated in the literature on stability. We argue that an adequate (...) theory of explanatory goodness should recognize breadth and guidance as distinct virtues, as breadth and guidance track different ideals of explanation, satisfy different cognitive and pragmatic ends, and play different theoretical roles in helping us understand the explanatory value of mechanisms. Thus keeping track of the distinction between these two forms of stability yields a more accurate and perspicuous picture of the role that stability considerations play in explanation. (shrink)

How do we know what we "know"? How did we –as individuals and as a society – come to accept certain knowledge as fact? In _Human Knowledge,_ Bertrand Russell questions the reliability of our assumptions on knowledge. This brilliant and controversial work investigates the relationship between ‘individual’ and ‘scientific’ knowledge. First published in 1948, this provocative work contributed significantly to an explosive intellectual discourse that continues to this day.

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 discusses several distinct process theories of causality offered in recent years by Phil Dowe and me. It addresses problems concerning the explication of causal process, causal interaction, and causal transmission, whether given in terms of transmission of marks, transmission of invariant or conserved quantities, or mere possession of conserved quantities. Renouncing the mark-transmission and invariant quantity criteria, I accept a conserved quantity theory similar to Dowe's--differing basically with respect to causal transmission. This paper also responds to several fundamental (...) constructive criticisms contained in Christopher Hitchcock's discussion of both the mark-transmission and the conserved quantity theories. (shrink)

This article examines the multiple realizability thesis within a causal framework. The beginnings of this framework are found in Elliott Sober’s “Multiple Realizability Argument against Reduction,”...

In the last two decades few topics in philosophy of science have received as much attention as mechanistic explanation. A significant motivation for these accounts is that scientists frequently use the term “mechanism” in their explanations of biological phenomena. While scientists appeal to a variety of causal concepts in their explanations, many philosophers argue or assume that all of these concepts are well understood with the single notion of mechanism. This reveals a significant problem with mainstream mechanistic accounts– although philosophers (...) use the term “mechanism” interchangeably with other causal concepts, this is not something that scientists always do. This paper analyses two causal concepts in biology–the notions of “mechanism” and “pathway”–and how they figure in biological explanation. I argue that these concepts have unique features, that they are associated with distinct strategies of causal investigation, and that they figure in importantly different types of explanation. (shrink)

Human microbiome research makes causal connections between entire microbial communities and a wide array of traits that range from physiological diseases to psychological states. To evaluate these causal claims, we first examine a well-known single-microbe causal explanation: of Helicobacter pylori causing ulcers. This apparently straightforward causal explanation is not so simple, however. It does not achieve a key explanatory standard in microbiology, of Koch’s postulates, which rely on manipulations of single-microorganism cultures to infer causal relationships to disease. When Koch’s postulates (...) are framed by an interventionist causal framework, it is clearer what the H. pylori explanation achieves and where its explanatory strengths lie. After assessing this ‘simple’, single-microbe case, we apply the interventionist framework to two key areas of microbiome research, in which obesity and mental health states are purportedly explained by microbiomes. Despite the experimental data available, interventionist criteria for explanation show that many of the causal claims generated by microbiome research are weak or misleading. We focus on the stability, specificity and proportionality of proposed microbiome causal explanations, and evaluate how effectively these dimensions of causal explanation are achieved in some promising avenues of research. We suggest some conceptual and explanatory strategies to improve how causal claims about microbiomes are made. (shrink)

Human microbiome research makes causal connections between entire microbial communities and a wide array of traits that range from physiological diseases to psychological states. To evaluate these causal claims, we first examine a well-known single-microbe causal explanation: of Helicobacter pylori causing ulcers. This apparently straightforward causal explanation is not so simple, however. It does not achieve a key explanatory standard in microbiology, of Koch’s postulates, which rely on manipulations of single-microorganism cultures to infer causal relationships to disease. When Koch’s postulates (...) are framed by an interventionist causal framework, it is clearer what the H. pylori explanation achieves and where its explanatory strengths lie. After assessing this ‘simple’, single-microbe case, we apply the interventionist framework to two key areas of microbiome research, in which obesity and mental health states are purportedly explained by microbiomes. Despite the experimental data available, interventionist criteria for explanation show that many of the causal claims generated by microbiome research are weak or misleading. We focus on the stability, specificity and proportionality of proposed microbiome causal explanations, and evaluate how effectively these dimensions of causal explanation are achieved in some promising avenues of research. We suggest some conceptual and explanatory strategies to improve how causal claims about microbiomes are made. (shrink)

Human microbiome research makes causal connections between entire microbial communities and a wide array of traits that range from physiological diseases to psychological states. To evaluate these causal claims, we first examine a well-known single-microbe causal explanation: of Helicobacter pylori causing ulcers. This apparently straightforward causal explanation is not so simple, however. It does not achieve a key explanatory standard in microbiology, of Koch’s postulates, which rely on manipulations of single-microorganism cultures to infer causal relationships to disease. When Koch’s postulates (...) are framed by an interventionist causal framework, it is clearer what the H. pylori explanation achieves and where its explanatory strengths lie. After assessing this ‘simple’, single-microbe case, we apply the interventionist framework to two key areas of microbiome research, in which obesity and mental health states are purportedly explained by microbiomes. Despite the experimental data available, interventionist criteria for explanation show that many of the causal claims generated by microbiome research are weak or misleading. We focus on the stability, specificity and proportionality of proposed microbiome causal explanations, and evaluate how effectively these dimensions of causal explanation are achieved in some promising avenues of research. We suggest some conceptual and explanatory strategies to improve how causal claims about microbiomes are made. (shrink)

In this lucid portrayal of human behavior, Fred Dretske provides an original account of the way reasons function in the causal explanation of behavior.

This paper examines Wesley Salmon's "process" theory of causality, arguing in particular that there are four areas of inadequacy. These are that the theory is circular, that it is too vague at a crucial point, that statistical forks do not serve their intended purpose, and that Salmon has not adequately demonstrated that the theory avoids Hume's strictures about "hidden powers". A new theory is suggested, based on "conserved quantities", which fulfills Salmon's broad objectives, and which avoids the problems discussed.

Computing is changing the traditional field of Philosophy of Science in a very profound way. First as a methodological tool, computing makes possible ``experimental Philosophy'' which is able to provide practical tests for different philosophical ideas. At the same time the ideal object of investigation of the Philosophy of Science is changing. For a long period of time the ideal science was Physics (e.g., Popper, Carnap, Kuhn, and Chalmers). Now the focus is shifting to the field of Computing/Informatics. There are (...) many good reasons for this paradigm shift, one of those being a long standing need of a new meeting between the sciences and humanities, for which the new discipline of Computing/Informatics gives innumerable possibilities. Contrary to Physics, Computing/Informatics is very much human-centered. It brings a potential for a new Renaissance, where Science and Humanities, Arts and Engineering can reach a new synthesis, so very much needed in our intellectually split culture. This paper investigates contemporary trends and the relation between the Philosophy of Science and the Philosophy of Computing and Information, which is equivalent to the present relation between Philosophy of Science and Philosophy of Physics. (shrink)

What precisely does aristotle mean when he asserts that something is (or comes to be) "for" "the" "sake" "of" something? I suggest that the answer to this question may be found by examining aristotle's position on the problem of reduction in biology, As it arises within his own scientific "and" "philosophical" context. I discuss the role of the concepts of "nature" and "potential" in aristotelian scientific explanation, And reformulate the reduction problem in that light. I answer the main question by (...) establishing that aristotle holds an "irreducibility" thesis in regard to the generation and development of a living organism, And that this thesis is the core of his conception of final causality. I conclude by arguing that aristotle's teleology is fundamentally "empirical" in character, And not an a priori doctrine brought "to" the study of nature. (shrink)

Each Aristotelian science consists in the causal investigation of a specific department of reality. If successful, such an investigation results in causal knowledge; that is, knowledge of the relevant or appropriate causes. The emphasis on the concept of cause explains why Aristotle developed a theory of causality which is commonly known as the doctrine of the four causes. For Aristotle, a firm grasp of what a cause is, and how many kinds of causes there are, is essential for a successful (...) investigation of the world around us. (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)

Causal selection has to do with the distinction we make between background conditions and “the” true cause or causes of some outcome of interest. A longstanding consensus in philosophy views causal selection as lacking any objective rationale and as guided, instead, by arbitrary, pragmatic, and non-scientific considerations. I argue against this position in the context of causal selection for disease traits. In this domain, causes are selected on the basis of the type of causal control they exhibit over a disease (...) of interest. My analysis clarifies the principled rationale that guides this selection and how it involves both pragmatic and objective considerations, which have been overlooked in the extant literature. (shrink)