This paper evaluates and criticises the developmental systems conception of evolution and develops instead an extension of the gene's eye conception of evolution. We argue (i) Dawkin's attempt to segregate developmental and evolutionary issues about genes is unsatisfactory. On plausible views of development it is arbitrary to single out genes as the units of selection. (ii) The genotype does not carry information about the phenotype in any way that distinguishes the role of the genes in development from that other factors. (...) (iii) There is no simple and general causal criterion which distinguishes the role of genes in development and evolution. (iv) There is, however, an important sense in which genes but not every other developmental factor represent the phenotype. (v) The idea that genes represent features of the phenotype forces us to recognise that genes are not the only, or almost the only, replicators. Many mechanisms of replication are involved in both development and evolution. (vi) A conception of evolutionary history which recognises both genetic and non-genetic replicators, lineages of replicators and interactors has advantages over both the radical rejection of the replicator/interactor distinction and the conservative restriction of replication to genetic replication. (shrink)

Whatever we take “life” to mean, it must involve an attempt to describe the objective reality beyond scientists’ biases. Traditionally, this is thought to involve comparing our scientific categories to “natural kinds.” But this approach has been tainted with an implicit metaphysics, inherited from Aristotle, that does not fit biological reality. In particular, we must accept that biological categories will never be specifiable in terms of necessary and sufficient conditions or shared underlying physical structures that produce clean boundaries. Biology blurs (...) all lines and failure to embrace this unique feature has blocked attempts to reach consensus on the meaning of “life.” Thus, while the three classical accounts all fall short of offering a complete definition, their advocates fail to realize that they share the same view of life’s ultimate, functional hallmark: its uniquely rich adaptive capacity. I develop an account of life as adaptive capacity that sidesteps debates about the relative importance of specific mechanisms and the precise location of boundaries to bring the three classical accounts together under a shared conceptual framework. (shrink)

An increasing number of biologists are expressing discontent with the prevailing theory of neo-Darwinism. In particular, the tendency of neo-Darwinians to adopt genetic determinism and atomistic notions of both genes and organisms is seen as grossly unfair to the body of developmental theory. One faction of dissenteers, the Process Structuralists, take their inspiration from the rational morphologists who preceded Darwin. These neo-rationalists argue that a mature biology must possess universal laws and that these generative laws should be sought within organismal (...) development. Such a rational biology will only be possible once the neo-Darwinian paradigm, with its reliance on inherently stochastic processes, is overthrown.To facilitate this revolution, process structuralism launches a broad attack on the theoritical adequacy of its opponent. It is charged that neo-Darwinism is untestable and therefore its hypotheses are nothing more than adaptive stories. Further, the lamentable tendencies toward genetic determinism and atomism by modern biologists is seen as the inescapable consequences of adopting the neo-Darwinian outlook. (shrink)

This book focuses on the emerging scientific discipline of astrobiology, exploring the humanistic issues of this multidisciplinary field. To be sure, there are myriad scientific questions that astrobiologists have only begun to address. However, this is not a purely scientific enterprise. More research on the broader social and conceptual aspects of astrobiology is needed. Just what are our ethical obligations toward different sorts of alien life? Should we attempt to communicate with life beyond our planet? What is “life” in the (...) most general sense? The current volume addresses these questions by looking at different perspectives from philosophers, historians, theologians, social scientists, and legal scholars. It sets a benchmark for future work in astrobiology, giving readers the groundwork from which to base the continuous scholarship coming from this ever-growing scientific field. (shrink)

Recently, Fred Gifford attempted to explicate the meaning of the term genetic as applied to phenotypic traits. He takes as his primary goal the explication of how the term is used and tries to avoid conclusions about how it should be used. He proposes two independent criteria (DF and PI) which together capture much of what biologists mean when they describe traits as genetic. Although Gifford's approach is extremely insightful in many ways, I argue that his analysis is not sufficiently (...) critical concerning the adequacy of common usage.In particular, while DF is a perfectly legitimate and useful measure of heritability in populations, it is not necessarily a genetic one and should not be labeled as such. PI on the other hand, although very intuitive, depends on an extremely problematic distinction between causes and mere conditions (e.g., genes and epigenetic factors). Both criteria will be highly relative and both, via what I term the new problem of genetics, will inspire contradictory analyses based on the same data. (shrink)

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What exactly is a genetic disease? For a phrase one hears on a daily basis, there has been surprisingly little analysis of the underlying concept. Medical doctors seem perfectly willing to admit that the etiology of disease is typically complex, with a great many factors interacting to bring about a given condition. On such a view, descriptions of diseases like cancer as geneticseem at best highly simplistic, and at worst philosophically indefensible. On the other hand, there is clearly some practical (...) value to be had by classifying diseases according to theirpredominant cause when this can be accomplished in a theoretically satisfactory manner. The question therefore becomes exactly how one should go about selecting a single causal factor among many to explain the presence of disease. When an attempt to defend such causal selection is made at all, the standard accounts offered (Koch's postulates, Hill's epidemiological criteria, manipulability) are all clearly inadequate. I propose, however, an epidemiological account of disease causation which walks the fine line between practical applicability and theoretical considerations of causal complexity and attempts to compromise between patient-centered and population-centered concepts of disease. The epidemiological account is the most basic framework consistent with our strongly held intuitions about the causal classification of disease, yet it avoids the difficulties encountered by its competitors. (shrink)

Why is the academy in general, and philosophy in particular, not more involved in the fight against the creationist threat? And why, when a response is offered, is it so curiously ineffective? I argue, by using an analogy with the battle against the Black Knight from the movie Monty Python and the Holy Grail, that the difficulty lies largely in a failure to see the nature of the problem clearly. By modifying the analogy, it is possible to see both why (...) large sections of the academy have remained unmoved and also why many of the reactions to the threat have been so unsuccessful. Finally, I offer some very broad suggestions as to how to modify our approach in light of this new perspective. (shrink)

Modern medicine emphasizes treatment of the sick. It is often said that the widespread genetic testing soon to follow the completion of the Human Genome Project will usher in a new era of preventive medicine. Such changes require new ways of thinking, however. For example, there may be nothing clinically wrong with a healthy patient who requests genetic testing, even if the tests reveal disease genes. Since all individuals have genetic skeletons in their closets, it is important to be careful (...) not to confuse having disease genes with having the diseases that they cause. Unfortunately, many in the public have adopted a kind of genetic determinism that sees genes as destiny: for example, having the gene associated with colon cancer means they will develop colon cancer. Physicians tend to be more careful, yet even they are not immune to subtle versions of genetic determinism. One example of this is the uncritical categorization of certain diseases as “genetic”. In fact, an adequate concept of genetic disease is extremely difficult to come by. The simplest notion would require a 1:1 correspondence between a disease and its genes, but this is the exception rather than the rule. For example, cystic fibrosis (CF) is often put forward as a good example of a genetic disease, since it seems to result from mutations in a single gene, CFTR. Even in this case, however, the exact relationship between CFTR mutations and disease is not clear, as virtually every possible combination of sweat chloride test results, genetic test results, and symptoms has been observed.[1] If a patient presents with the classic symptoms of CF and is found to have a mutation in the CFTR gene, the physician might understandably infer that the mutation caused the disease. But if an asymptomatic patient is tested and it is discovered that he or she has a CFTR mutation, it is unclear what this means. The doctor might tell the patient the gene is abnormal and that he or she is likely to develop pulmonary problems, etc., but it’s not really known whether even this qualified prognosis is true.. (shrink)

What exactly is a genetic disease? For a phrase one hears on a daily basis, there has been surprisingly little analysis of the underlying concept. Medical doctors seem perfectly willing to admit that the etiology of disease is typically complex, with a great many factors interacting to bring about a given condition. On such a view, descriptions of diseases like cancer as genetic seem at best highly simplistic, and at worst philosophically indefensible. On the other hand, there is clearly some (...) practical value to be had by classifying diseases according to their predominant cause when this can be accomplished in a theoretically satisfactory manner. The question therefore becomes exactly how one should go about selecting a single causal factor among many to explain the presence of disease. When an attempt to defend such causal selection is made at all, the standard accounts offered (Koch's postulates, Hill's epidemiological criteria, manipulability) are all clearly inadequate. I propose, however, an epidemiological account of disease causation which walks the fine line between practical applicability and theoretical considerations of causal complexity and attempts to compromise between patientcentered and population-centered concepts of disease. The epidemiological account is the most basic framework consistent with our strongly held intuitions about the causal classification of disease, yet it avoids the difficulties encountered by its competitors. (shrink)

Proposal in Brief : I have been invited by Michael Ruse, editor of the Cambridge Studies in Philosophy and Biology series for Cambridge University Press, to submit a book proposal on the Philosophy of Developmental Biology. This is both a great honor and a magnificent opportunity for a relatively junior professor, especially since the field is new - done well, this book could help set the basic parameters of an emerging discipline.