The aim of this paper is to assess the relevance of somatic evolution by natural selection to our understanding of cancer development. I do so in two steps. In the first part of the paper, I ask to what extent cancer cells meet the formal requirements for evolution by natural selection, relying on Godfrey-Smith’s (2009) framework of Darwinian populations. I argue that although they meet the minimal requirements for natural selection, cancer cells are not paradigmatic Darwinian populations. In the second (...) part of the paper, I examine the most important examples of adaptation in cancer cells. I argue that they are not significant accumulations of evolutionary changes, and that as a consequence natural selection plays a lesser role in their explanation. Their explanation, I argue, is best sought in the previously existing wiring of the healthy cells. (shrink)

In recent years, biologists have increasingly been asking whether the ability to evolve — the evolvability — of biological systems, itself evolves, and whether this phenomenon is the result of natural selection or a by-product of other evolutionary processes. The concept of evolvability, and the increasing theoretical and empirical literature that refers to it, may constitute one of several pillars on which an extended evolutionary synthesis will take shape during the next few years, although much work remains to be done (...) on how evolvability comes about. (shrink)

The book presents a new way of understanding Darwinism and evolution by natural selection, combining work in biology, philosophy, and other fields.

Recent discussions in the philosophy of biology have brought into question some fundamental assumptions regarding evolutionary processes, natural selection in particular. Some authors argue that natural selection is nothing but a population-level, statistical consequence of lower-level events (Matthen and Ariew [2002]; Walsh et al. [2002]). On this view, natural selection itself does not involve forces. Other authors reject this purely statistical, population-level account for an individual-level, causal account of natural selection (Bouchard and Rosenberg [2004]). I argue that each of these (...) positions is right in one way, but wrong in another; natural selection indeed takes place at the level of populations, but it is a causal process nonetheless. (shrink)

Recently, several philosophers have challenged the view that evolutionary theory is usefully understood by way of an analogy with Newtonian mechanics. Instead, they argue that evolutionary theory is merely a statistical theory. According to this alternate approach, natural selection and random genetic drift are not even causes, much less forces. I argue that, properly understood, the Newtonian analogy is unproblematic and illuminating. I defend the view that selection and drift are causes in part by attending to a pair of important (...) distinctions—that between process and product and that between natural selection and fitness. (shrink)

How should the concept of evidence be understood? And how does the concept of evidence apply to the controversy about creationism as well as to work in evolutionary biology about natural selection and common ancestry? In this rich and wide-ranging book, Elliott Sober investigates general questions about probability and evidence and shows how the answers he develops to those questions apply to the specifics of evolutionary biology. Drawing on a set of fascinating examples, he analyzes whether claims about intelligent design (...) are untestable; whether they are discredited by the fact that many adaptations are imperfect; how evidence bears on whether present species trace back to common ancestors; how hypotheses about natural selection can be tested, and many other issues. His book will interest all readers who want to understand philosophical questions about evidence and evolution, as they arise both in Darwin's work and in contemporary biological research. (shrink)

Biologists employ a suggestive metaphor to describe the complexities of molecular interactions within cells and embryos: cytological components are said to be part of “ecosystems” that integrate them in a complex network of relations with many other entities. The aim of this essay is to scrutinize the molecular ecosystem, a metaphor that, despite its longstanding history, has seldom be articulated in detail. I begin by analyzing some relevant analogies between the cellular environment and the biosphere. Next, I discuss the applicability (...) of the molecular ecosystem concept in actual scientific practice. (shrink)

This book offers a philosophy for error-prone humans trying to understand messy systems in the real world.

Two decades ago, the eminent evolutionary biologist George C. Williams and his physician coauthor, Randolph Nesse, formulated the evolutionary medicine research program. Williams and Nesse explicitly made adaptationism a core component of the new program, which has served to undermine the program ever since, distorting its practitioners’ perceptions of evidentiary burdens and in extreme cases has served to warp practitioner’s understandings of the relationship between evolutionary benefits/detriments and medical ones. I show that the Williams and Nesse program more particularly embraces (...) the panselectionist variety of adaptationism (the empirical assumption that non-adaptive evolutionary processes are causally unimportant compared to natural selection), and argue that this has harmed the field. Panselectionism serves to conceal the enormous evidentiary hurdles that evolutionary medicine hypotheses face, making them appear stronger than they are. I use two examples of evolutionary medicine texts, on neonatal jaundice and on asthma, to show that some evolutionary medicine practitioners have allowed their fervent panselectionism to directly shape their recommendations for clinical practice. I argue that this escalation of panselectionism’s influence is inappropriate under Williams’ and Nesse original stated standards, despite being inspired by their program. I also show that the examples’ conflation of clinical and evolutionary considerations is inappropriate even under Christopher Boorse’s controversial evolution-rooted concepts of disease and health. (shrink)

Does natural selection act primarily on individual organisms, on groups, on genes, or on whole species? The question of levels of selection - on which biologists and philosophers have long disagreed - is central to evolutionary theory and to the philosophy of biology. Samir Okasha's comprehensive analysis gives a clear account of the philosophical issues at stake in the current debate.

Do evolutionary processes such as selection and random drift cause evolutionary change, or are they merely convenient ways of describing or summarizing it? Philosophers have lined up on both sides of this question. One recent defense (Reisman and Forber 2005) of the causal status of selection and drift appeals to a manipulability theory of causation. Yet, even if one accepts manipulability, there are still reasons to doubt that genetic drift, in particular, is genuinely causal. We will address two challenges to (...) treating drift as causal within a manipulation framework. We will argue that both challenges ultimately fail, but that they raise interesting and subtle issues about the nature of causation and the differences between selection and drift. ‡Thanks to audiences at the ‘PBDB1' Conference and the 2006 PSA Meeting for valuable feedback. †To contact the authors, please write to: Patrick Forber, Tufts University, Philosophy Department, Miner Hall, Medford, MA 02155; e-mail: [email protected]. (shrink)

Reconstructing the Past seeks to clarify and help resolve the vexing methodological issues that arise when biologists try to answer such questions as whether human beings are more closely related to chimps than they are to gorillas. It explores the case for considering the philosophical idea of simplicity/parsimony as a useful principle for evaluating taxonomic theories of evolutionary relationships. For the past two decades, evolutionists have been vigorously debating the appropriate methods that should be used in systematics, the field that (...) aims at reconstructing phylogenetic relationships among species. This debate over phylogenetic inference, Elliott Sober observes, raises broader questions of hypothesis testing and theory evaluation that run head on into long standing issues concerning simplicity/parsimony in the philosophy of science. Sober treats the problem of phylogenetic inference as a detailed case study in which the philosophical idea of simplicity/parsimony can be tested as a principle of theory evaluation. Bringing together philosophy and biology, as well as statistics, Sober builds a general framework for understanding the circumstances in which parsimony makes sense as a tool of phylogenetic inference. Along the way he provides a detailed critique of parsimony in the biological literature, exploring the strengths and limitations of both statistical and nonstatistical cladistic arguments. (shrink)

In _ Psychiatry in the Scientific Image, _Dominic Murphy looks at psychiatry from the viewpoint of analytic philosophy of science, considering three issues: how we should conceive of, classify, and explain mental illness. If someone is said to have a mental illness, what about it is mental? What makes it an illness? How might we explain and classify it? A system of psychiatric classification settles these questions by distinguishing the mental illnesses and showing how they stand in relation to one (...) another. This book explores the philosophical issues raised by the project of explaining and classifying mental illness. Murphy argues that the current literature on mental illness -- exemplified by the Diagnostic and Statistical Manual of Mental Disorders -- is an impediment to research; it lacks a coherent concept of the mental and a satisfactory account of disorder, and yields too much authority to commonsense thought about the mind. He argues that the explanation of mental illness should meet the standards of good explanatory practice in the cognitive neurosciences, and that the classification of mental disorders should group symptoms into conditions based on the causal structure of the normal mind. (shrink)

Maladapting Minds discusses a number of reasons why philosophers of psychiatry should take an interest in evolutionary explanations of mental disorders and, more generally, in evolutionary thinking. First of all, there is the nascent field of evolutionary psychiatry. Unlike other psychiatrists, evolutionary psychiatrists engage with ultimate, rather than proximate, questions about mental illnesses. Being a young and youthful new discipline, evolutionary psychiatry allows for a nice case study in the philosophy of science. Secondly, philosophers of psychiatry have engaged with evolutionary (...) theory because evolutionary considerations are often said to play a role in defining the concept of mental disorder. The basic question here is: Can the concept of mental disorder be given an objective definition, or is it rather a normative concept? Thirdly and finally, evolutionary thinking in psychiatry has often been a source of inspiration for a philosophical view on human nature. Thus evolutionary psychiatrists have suggested, for example, that man's vulnerability to mental disorders may well be one of the defining features of our species. -/- Written by leading authors in philosophy, psychiatry, biology and psychology, this volume illustrates that many debates in contemporary philosophy of psychiatry are profoundly influenced by evolutionary approaches to mental disorders. Conversely, it also reveals how philosophers can help contribute to the burgeoning field of evolutionary psychiatry. It is important reading for a wide range of readers interested in mental health care and philosophy. (shrink)

Somatic mutation plays a key role in transforming normal cells into cancerous cells. The analysis of cancer progression therefore requires the study of how point mutations and chromosomal mutations accumulate in cellular lineages. The spread of somatic mutations depends on the mutation rate, the number of cell divisions in the history of a cellular lineage, and the nature of competition between different cellular lineages. We consider how various aspects of tissue architecture and cellular competition affect the pace of mutation accumulation. (...) We also discuss the rise and fall of somatic mutation rates during cancer progression. BioEssays 26:291–299, 2004. © 2004 Wiley Periodicals, Inc. (shrink)