According to one large family of views, scientific explanations explain a phenomenon (such as an event or a regularity) by subsuming it under a general representation, model, prototype, or schema (see Bechtel, W., & Abrahamsen, A. (2005). Explanation: A mechanist alternative. Studies in History and Philosophy of Biological and Biomedical Sciences, 36(2), 421–441; Churchland, P. M. (1989). A neurocomputational perspective: The nature of mind and the structure of science. Cambridge: MIT Press; Darden (2006); Hempel, C. G. (1965). Aspects of scientific (...) explanation. In C. G. Hempel (Ed.), Aspects of scientific explanation (pp. 331–496). New York: Free Press; Kitcher (1989); Machamer, P., Darden, L., & Craver, C. F. (2000). Thinking about mechanisms. Philosophy of Science, 67(1), 1–25). My concern is with the minimal suggestion that an adequate philosophical theory of scientific explanation can limit its attention to the format or structure with which theories are represented. The representational subsumption view is a plausible hypothesis about the psychology of understanding. It is also a plausible claim about how scientists present their knowledge to the world. However, one cannot address the central questions for a philosophical theory of scientific explanation without turning one’s attention from the structure of representations to the basic commitments about the worldly structures that plausibly count as explanatory. A philosophical theory of scientific explanation should achieve two goals. The first is explanatory demarcation. It should show how explanation relates with other scientific achievements, such as control, description, measurement, prediction, and taxonomy. The second is explanatory normativity. It should say when putative explanations succeed and fail. One cannot achieve these goals without undertaking commitments about the kinds of ontic structures that plausibly count as explanatory. Representations convey explanatory information about a phenomenon when and only when they describe the ontic explanations for those phenomena. (shrink)

Science depends on judgments of the bearing of evidence on theory. Scientists must judge whether an observation or the result of an experiment supports, disconfirms, or is simply irrelevant to a given hypothesis. Similarly, scientists may judge that, given all the available evidence, a hypothesis ought to be accepted as correct or nearly so, rejected as false, or neither. Occasionally, these evidential judgments can be made on deductive grounds. If an experimental result strictly contradicts a hypothesis, then the truth of (...) the data deductively entails the falsity of the hypothesis. In the great majority of cases, however, the connection between evidence and hypothesis is non-demonstrative, or inductive. In particular, this is so whenever a general hypothesis is inferred to be correct on the basis of the available data, since the truth of the data will not deductively entail the truth of the hypothesis. It always remains possible that the hypothesis is false even though the data are correct. (shrink)

It has been argued that implicit biases are operative in philosophy and lead to significant epistemic costs in the field. Philosophers working on this issue have focussed mainly on implicit gender and race biases. They have overlooked ideological bias, which targets political orientations. Psychologists have found ideological bias in their field and have argued that it has negative epistemic effects on scientific research. I relate this debate to the field of philosophy and argue that if, as some studies suggest, the (...) same bias also exists in philosophy then it will lead to hitherto unrecognised epistemic hazards in the field. Furthermore, the bias is epistemically different from the more familiar biases in respects that are important for epistemology, ethics, and metaphilosophy. (shrink)

Whereas an inference (deductive as well as inductive) is usually viewed as being valid in virtue of its argument form, the present paper argues that scientific reasoning is material inference, i.e., justified in virtue of its content. A material inference is licensed by the empirical content embodied in the concepts contained in the premises and conclusion. Understanding scientific reasoning as material inference has the advantage of combining different aspects of scientific reasoning, such as confirmation, discovery, and explanation. This approach explains (...) why these different aspects (including discovery) can be rational without conforming to formal schemes, and why scientific reasoning is local, i.e., justified only in certain domains and contingent on particular empirical facts. The notion of material inference also fruitfully interacts with accounts of conceptual change and psychological theories of concepts. (shrink)

This essay analyzes and develops recent views about explanation in biology. Philosophers of biology have parted with the received deductive-nomological model of scientific explanation primarily by attempting to capture actual biological theorizing and practice. This includes an endorsement of different kinds of explanation (e.g., mathematical and causal-mechanistic), a joint study of discovery and explanation, and an abandonment of models of theory reduction in favor of accounts of explanatory reduction. Of particular current interest are philosophical accounts of complex explanations that appeal (...) to different levels of organismal organization and use contributions from different biological disciplines. The essay lays out one model that views explanatory integration across different disciplines as being structured by scientific problems. I emphasize the philosophical need to take the explanatory aims pursued by different groups of scientists into account, as explanatory aims determine whether different explanations are competing or complementary and govern the dynamics of scientific practice, including interdisciplinary research. I distinguish different kinds of pluralism that philosophers have endorsed in the context of explanation in biology, and draw several implications for science education, especially the need to teach science as an interdisciplinary and dynamic practice guided by scientific problems and explanatory aims. (shrink)

A common reductionist assumption is that macro-scale behaviors can be described "bottom-up" if only sufficient details about lower-scale processes are available. The view that an "ideal" or "fundamental" physics would be sufficient to explain all macro-scale phenomena has been met with criticism from philosophers of biology. Specifically, scholars have pointed to the impossibility of deducing biological explanations from physical ones, and to the irreducible nature of distinctively biological processes such as gene regulation and evolution. This paper takes a step back (...) in asking whether bottom-up modeling is feasible even when modeling simple physical systems across scales. By comparing examples of multi-scale modeling in physics and biology, we argue that the “tyranny of scales” problem presents a challenge to reductive explanations in both physics and biology. The problem refers to the scale-dependency of physical and biological behaviors that forces researchers to combine different models relying on different scale-specific mathematical strategies and boundary conditions. Analyzing the ways in which different models are combined in multi-scale modeling also has implications for the relation between physics and biology. Contrary to the assumption that physical science approaches provide reductive explanations in biology, we exemplify how inputs from physics often reveal the importance of macro-scale models and explanations. We illustrate this through an examination of the role of biomechanics modeling in developmental biology. In such contexts, the relation between models at different scales and from different disciplines is neither reductive nor completely autonomous, but interdependent. (shrink)

According to the received view of evolution, only genes are inherited. From this view it follows that only genetically-caused phenotypic variation is selectable and, thereby, that all selection is at bottom genetic selection. This paper argues that the received view is wrong. In many species, there are intergenerationally-stable phenotypic differences due to environmental differences. Natural selection can act on these nongenetically-caused phenotypic differences in the same way it acts on genetically-caused phenotypic differences. Some selection is at bottom nongenetic selection. The (...) argument against the received view involves a reformulation of the concepts of inheritance and heritability. Inherited factors are all those developmental factors responsible for parent–offspring similarity; some inherited factors are genetic and some are not. Heritable variation is intergenerationally-stable phenotypic variation; some such variation is genetically-caused and some is not. The received view and its critics The possibility of nongenetic selection (the lucky butterfly) The reality of nongenetic selection 3.1 Imprinting mechanisms 3.2 Other learning mechanisms 3.3 Other nongenetic mechanisms Genetic and nongenetic inheritance mechanisms Genetic and nongenetic inherited factors Genetic and nongenetic heritability Conclusions + Current address: Dr Matteo Mameli, Research Fellow, King's College, Cambridge, CB2 1ST, United Kingdom, matteo.mameli{at}kings.cam.ac.uk' + u + '@' + d + ''//-->. (shrink)

Methodological reductionists practice ‘wannabe reductionism’. They claim that one should pursue reductionism, but never propose how. I integrate two strains in prior work to do so. Three kinds of activities are pursued as “reductionist”. “Successional reduction” and inter-level mechanistic explanation are legitimate and powerful strategies. Eliminativism is generally ill-conceived. Specific problem-solving heuristics for constructing inter-level mechanistic explanations show why and when they can provide powerful and fruitful tools and insights, but sometimes lead to erroneous results. I show how traditional metaphysical (...) approaches fail to engage how science is done. The methods used do so, and support a pragmatic and non-eliminativist realism. (shrink)

Watson and Crick’s discovery of the structure of DNA led to developments that transformed many biological sciences. But what were the relevant developments and how did they transform biology? Much of the philosophical discussion concerning this question can be organized around two opposing views: theoretical reductionism and layer-cake antireductionism. Theoretical reductionist and their anti-reductionist foes hold two assumptions in common. First, both hold that biological knowledge is structured like a layer cake, with some biological sciences, such as molecular biology cast (...) at lower levels of organization, and others, such as classical genetics, cast at higher levels. Second, both assume that scientific knowledge is structured by theory and that the productivity of scientific research depends on whether the underlying theory identifies the fundamentals upon which the phenomena to be explained and investigated depend. In the first part of this paper, I challenge these assumptions. In the second part, I show how recasting the basic theory of classical genetics made it possible to retool the methodologies of genetics. It was the investigative power of these retooled methodologies, and not the explanatory power of a gene-based theory, that transformed biology. (shrink)

Heritability is routinely interpreted causally. Yet, what such an interpretation amounts to is often unclear. Here, I provide a causal interpretation of this concept in terms of range of causal influence, one of several causal dimensions proposed within the interventionist account of causation. An information-theoretic measure of range of causal influence has recently been put forward in the literature. Starting from this formalization and relying upon Woodward’s analysis, I show that an important problem associated with interpreting heritability causally, namely the (...) locality problem, amounts, at least partly, to a low invariance and low stability between the genotype/environment and the phenotype of individuals. In light of this, I plead for a causal interpretation of heritability that takes the notions of Woodward’s invariance and stability into consideration. In doing so, I defuse naive causal interpretations of heritability. (shrink)

The goal of this paper is to encourage a reconfiguration of the discussion about typology in biology away from the metaphysics of essentialism and toward the epistemology of classifying natural phenomena for the purposes of empirical inquiry. First, I briefly review arguments concerning ‘typological thinking’, essentialism, species, and natural kinds, highlighting their predominantly metaphysical nature. Second, I use a distinction between the aims, strategies, and tactics of science to suggest how a shift from metaphysics to epistemology might be accomplished. Typological (...) thinking can be understood as a scientific tactic that involves representing natural phenomena using idealizations and approximations, which facilitates explanation, investigation, and theorizing via abstraction and generalization. Third, a variety of typologies from different areas of biology are introduced to emphasize the diversity of this representational reasoning. One particular example is used to examine how there can be epistemological conflict between typology and evolutionary analysis. This demonstrates that alternative strategies of typological thinking arise due to the divergent explanatory goals of researchers working in different disciplines with disparate methodologies. I conclude with several research questions that emerge from an epistemological reconfiguration of typology. (shrink)

The inapplicability of variations on theory reduction in the context of genetics and their irrelevance to ongoing research has led to an anti-reductionist consensus in philosophy of biology. One response to this situation is to focus on forms of reductive explanation that better correspond to actual scientific reasoning (e.g. part–whole relations). Working from this perspective, we explore three different aspects (intrinsicality, fundamentality, and temporality) that arise from distinct facets of reductive explanation: composition and causation. Concentrating on these aspects generates new (...) forms of reductive explanation and conditions for their success or failure in biology and other sciences. This analysis is illustrated using the case of protein folding in molecular biology, which demonstrates its applicability and relevance, as well as illuminating the complexity of reductive reasoning in a specific biological context. (shrink)

In this article, we analyse how researchers use the categories of race and ethnicity with reference to genetics and genomics. We show that there is still considerable conceptual “messiness” (despite the wide-ranging and popular debate on the subject) when it comes to the use of ethnoracial categories in genetics and genomics that among other things makes it difficult to properly compare and interpret research using ethnoracial categories, as well as draw conclusions from them. Finally, we briefly reconstruct some of the (...) biases of reductionism to which geneticists (as well as other researchers referring to genetic methods and explanations) are particularly exposed to, and we analyse the problem in the context of the biologization of ethnoracial categories. Our work constitutes a novel, in-depth contribution to the debate about reporting race and ethnicity in biomedical and health research. First, we reconstruct the theoretical background assumptions about racial ontology which researchers implicitly presume in their studies with the aid of a sample of recent papers published in medical journals about COVID-19. Secondly, we use the typology of the biases of reductionism to the problem of biologization of ethnoracial categories with reference to genetics and genomics. (shrink)

Given immunity’s general role in the organism’s economy—both in terms of its internal environment as well as mediating its external relations—immune theory has expanded its traditional formulation of preserving individual autonomy to one that includes accounting for nutritional processes and symbiotic relationships that require immune tolerance. When such a full ecological alignment is adopted, the immune system becomes the mediator of both defensive and assimilative environmental intercourse, where a balance of immune rejection and tolerance governs the complex interactions of the (...) organism’s ecological relationships. Accordingly, immunology, which historically had affiliated with the biology of individuals, now becomes a science concerned with the biology of communities. With this translocation, the ontological basis of the organism is undergoing a profound change. Indeed, the recent recognition of the ubiquity of symbiosis has challenged the traditional notions of biological individuality and requires a shift in the metaphysics undergirding biology, in which a philosophy of the organism must be characterized by ecological dialectics “all-the-way-down.”. (shrink)

This paper analyzes what it means for philosophy of science to be normative. It argues that normativity is a multifaceted phenomenon rather than a general feature that a philosophical theory either has or lacks. It analyzes the normativity of philosophy of science by articulating three ways in which a philosophical theory can be normative. Methodological normativity arises from normative assumptions that philosophers make when they select, interpret, evaluate, and mutually adjust relevant empirical information, on which they base their philosophical theories. (...) Object normativity emerges from the fact that the object of philosophical theorizing can itself be normative, such as when philosophers discuss epistemic norms in science. Metanormativity arises from the kind of claims that a philosophical theory contains, such as normative claims about science as it should be. Distinguishing these three kinds of normativity gives rise to a nuanced and illuminating view of how philosophy of science can be normative. (shrink)

Schaffner’s model of theory reduction has played an important role in philosophy of science and philosophy of biology. Here, the model is found to be problematic because of an internal tension. Indeed, standard antireductionist external criticisms concerning reduction functions and laws in biology do not provide a full picture of the limits of Schaffner’s model. However, despite the internal tension, his model usefully highlights the importance of regulative ideals associated with the search for derivational, and embedding, deductive relations among mathematical (...) structures in theoretical biology. A reconstructed Schaffnerian model could therefore shed light on mathematical theory development in the biological sciences and on the epistemology of mathematical practices more generally. *Received November 2006; revised March 2009. †To contact the author, please write to: Philosophy Department, University of California, Santa Cruz, 1156 High St., Santa Cruz, CA 95064; e‐mail: [email protected]. (shrink)

This paper analyzes the concept of biodiversity in conservation biology and assesses potential methods for its measurement.

Fisher’s 1918 paper accomplished two distinct goals: unifying discrete Mendelian genetics with continuous biometric phenotypes and quantifying the variance components of variation in complex human characteristics. The former contributed to the foundation of modern quantitative genetics; the latter was adopted by social scientists interested in the pursuit of Galtonian nature-nurture questions about the biological and social origins of human behavior, especially human intelligence. This historical divergence has produced competing notions of the estimation of variance ratios referred to as heritability. Jay (...) Lush showed that they could be applied to selective breeding on the farm, while the early twin geneticists used them as a descriptive statistic to describe the degree of genetic determination in complex human traits. Here we trace the early history of the heritability coefficient now used by social scientists. (shrink)

This paper examines a novel notion of causality, namely, fuzzy-set-theoretic causality. Over the last decade, a number of conceptual models of causality, in the language of fuzzy-set theory, have appeared in the scientific literature and have been applied to empirical research. They have circulated widely from one scientific discipline to another, weaving a unifying thread through them. However, they have received no philosophical attention. In this paper, I will discuss the value and limitations of this type of model and will (...) read into its application several dimensions of philosophical significance. (shrink)

Philosophers of science have developed an account of causal-mechanical explanation that captures regularity, but this account neglects variation. In this article I amend the philosophy of mechanisms to capture variation. The task is to explicate the relationship between regular causal mechanisms responsible for individual development and causes of variation responsible for variation in populations. As it turns out, disputes over this relationship have rested at the heart of the nature–nurture debate. Thus, an explication of the relationship between regular causal mechanisms (...) and causes of variation and between individual development and variation offers both the necessary amendment to the philosophy of mechanisms and the resources to mediate the dispute. (shrink)

We reconstruct genetic determinism as a reductionist thesis to the effect that the molecular properties of cells can be accounted for to a great extent by their genetic outfit. The non-reductionist arguments offered at this molecular level often use the relationship between structure and function as their point of departure. By contrast, we develop a non-reductionist argument that is confined to the structural characteristics of biomolecules; no appeal to functions is made. We raise two kinds of objections against the reducibility (...) claim underlying genetic determinism. First, some conceptual distinctions at the protein level cannot be captured on a genetic basis. A one-to-many relationship between DNA sequences and proteins emerges from them. Second, the relationship between genes and proteins is characterized by explanatory loops or reciprocal explanatory dependence. The presence of proteins is explained by the transcription from corresponding DNA sequences, and the latter is in turn accounted for by the action of proteins. By contrast, a reductive account requires a unidirectional explanatory dependence. (shrink)

This essay examines the origin of genotype-environment interaction, or G×E. "Origin" and not "the origin" because the thesis is that there were actually two distinct concepts of G×E at this beginning: a biometric concept, or \[G \times E_B\], and a developmental concept, or \[G \times E_D \]. R. A. Fisher, one of the founders of population genetics and the creator of the statistical analysis of variance, introduced the biometric concept as he attempted to resolve one of the main problems in (...) the biometric tradition of biology - partitioning the relative contributions of nature and nurture responsible for variation in a population. Lancelot Hogben, an experimental embryologist and also a statistician, introduced the developmental concept as he attempted to resolve one of the main problems in the developmental tradition of biology - determining the role that developmental relationships between genotype and environment played in the generation of variation. To argue for this thesis, I outline Fisher and Hogben's separate routes to their respective concepts of G × E; then these separate interpretations of G × E are drawn on to explicate a debate between Fisher and Hogben over the importance of G × E, the first installment of a persistent controversy. Finally, Fisher's \[G \times E_B\] and Hogben's \[G \times E_D \] are traced beyond their own work into mid-2Oth century population and developmental genetics, and then into the infamous IQ Controversy of the 1970s. (shrink)

This paper argues that research on normative issues in the life sciences will benefit from a tighter integration of philosophy of science. We examine research on ethical, legal and social issues in the life sciences (“ELSI”) and discuss three illustrative examples of normative issues that arise in different areas of the life sciences. These examples show that important normative questions are highly dependent on epistemic issues which so far have not been addressed sufficiently in ELSI, RRI and related areas of (...) research. Accordingly, we argue for the integration of research on the epistemic aspects of the relevant areas of science into ELSI research to provide a better basis for addressing normative questions. (shrink)

Pluralism is often put forth as a counter-position to reductionism. In this essay, I argue that reductionism and pluralism are in fact consistent. I propose that there are several potential goals for reductions and that the proper form of a reduction should be considered in tandem with the goal that it aims to achieve. This insight provides a basis for clarifying what version of reductionism are currently defended, for explicating the notion of a fundamental level of explanation, and for showing (...) how one can be both a reductionist and a pluralist. (shrink)

Can a heritability value tell us something about the weight of genetic versus environmental causes that have acted in the development of a particular individual? Two possible questions arise. Q1: what portion of the phenotype of X is due to its genes and what portion to its environment? Q2: what portion of X’s phenotypic deviation from the mean is a result of its genetic deviation and what portion a result of its environmental deviation? An answer to Q1 provides the full (...) information about X’s development, while an answer to Q2 leaves out a large portion unexplained—that portion which corresponds to the phenotypic mean. Q1 is unanswerable, but I show it is nevertheless legitimate under certain quantitative genetics models. With regard to Q2, opinions in the philosophical and biological literature differ as to its legitimacy. I argue that not only is it legitimate, but in particular, under a few simplifying assumptions, it allows for a quantitative probabilistic answer: for normally distributed quantitative traits with no G-E correlation or statistical G × E interaction, we can assess the probability that X’s genes had a greater effect than its environment on its deviation from the mean population value. This probability is expressed as a function the heritability and the individual’s phenotypic value; we can also provide a quantitative probabilistic answer to Q2 for an arbitrary individual where the probability is a function only of heritability. (shrink)

In this paper I argue that the ontological interpretation of the concepts of reduction and emergence is often misleading in the philosophy of science and should nearly always be eschewed in favor of an epistemological interpretation. As a paradigm case, an example is drawn from the philosophy of chemistry to illustrate the drawbacks of “ontological reduction” and “ontological emergence,” and the virtues of an epistemological interpretation of these concepts.

This paper outlines a critique of the use of the genetic variance–covariance matrix (G), one of the central concepts in the modern study of natural selection and evolution. Specifically, I argue that for both conceptual and empirical reasons, studies of G cannot be used to elucidate so-called constraints on natural selection, nor can they be employed to detect or to measure past selection in natural populations – contrary to what assumed by most practicing biologists. I suggest that the search for (...) a general solution to the difficult problem of identifying causal structures given observed correlation’s has led evolutionary quantitative geneticists to substitute statistical modeling for the more difficult, but much more valuable, job of teasing apart the many possible causes underlying the action of natural selection. Hence, the entire evolutionary quantitative genetics research program may be in need of a fundamental reconsideration of its goals and how they correspond to the array of mathematical and experimental techniques normally employed by its practitioners. (shrink)

Okasha, in Evolution and the Levels of Selection, convincingly argues that two rival statistical decompositions of covariance, namely contextual analysis and the neighbour approach, are better causal decompositions than the hierarchical Price approach. However, he claims that this result cannot be generalized in the special case of soft selection and argues that the Price approach represents in this case a better option. He provides several arguments to substantiate this claim. In this paper, I demonstrate that these arguments are flawed and (...) argue that neither the Price equation nor the contextual and neighbour partitionings sensu Okasha are adequate causal decompositions in cases of soft selection. The Price partitioning is generally unable to detect cross-level by-products and this naturally also applies to soft selection. Both contextual and neighbour partitionings violate the fundamental principle of determinism that the same cause always produces the same effect. I argue that a fourth partitioning widely used in the contemporary social sciences, under the generic term of ‘hierarchical linear model’ and related to contextual analysis understood broadly, addresses the shortcomings of the three other partitionings and thus represents a better causal decomposition. I then defend this model against the argument that because it predicts that there is some organismal selection in some specific cases of segregation distortion then it should be rejected. I show that cases of segregation distortion that intuitively seem to contradict the conclusion drawn from the hierarchical linear model are in fact cases of multilevel selection 2 while the assessment of the different partitionings are restricted to multilevel selection 1. (shrink)

Genetic determinism can be described as the attribution of the formation of traits to genes, where genes are ascribed more causal power than what scientific consensus suggests. Belief in genetic determinism is an educational problem because it contradicts scientific knowledge, and is a societal problem because it has the potential to foster intolerant attitudes such as racism and prejudice against sexual orientation. In this article, we begin by investigating the very nature of belief in genetic determinism. Then, we investigate whether (...) knowledge of genetics and genomics is associated with beliefs in genetic determinism. Finally, we explore the extent to which social factors such as gender, education, and religiosity are associated with genetic determinism. Methodologically, we gathered and analyzed data on beliefs in genetic determinism, knowledge of genetics and genomics, and social variables using the “Public Understanding and Attitudes towards Genetics and Genomics” instrument. Our analyses of PUGGS responses from a sample of Brazilian university freshmen undergraduates indicated that belief in genetic determinism was best characterized as a construct built up by two dimensions or belief systems: beliefs concerning social traits and beliefs concerning biological traits; levels of belief in genetic determination of social traits were low, which contradicts prior work; associations between knowledge of genetics and genomics and levels of belief in genetic determinism were low; and social factors such as age and religiosity had stronger associations with beliefs in genetic determinism than knowledge. Although our study design precludes causal inferences, our results raise questions about whether enhancing genetic literacy will decrease or prevent beliefs in genetic determinism. (shrink)

Fisher’s ‘fundamental theorem of natural selection’ is notoriously abstract, and, no less notoriously, many take it to be false. In this paper, I explicate the theorem, examine the role that it played in Fisher’s general project for biology, and analyze why it was so very fundamental for Fisher. I defend Ewens (1989) and Lessard (1997) in the view that the theorem is in fact a true theorem if, as Fisher claimed, ‘the terms employed’ are ‘used strictly as defined’ (1930, p. (...) 38). Finally, I explain the role that projects such as Fisher’s play in the progress of scientific inquiry. (shrink)

In this paper I argue that it is finally time to move beyond the Nagelian framework and to break new ground in thinking about epistemic reduction in biology. I will do so, not by simply repeating all the old objections that have been raised against Ernest Nagel’s classical model of theory reduction. Rather, I grant that a proponent of Nagel’s approach can handle several of these problems but that, nevertheless, Nagel’s general way of thinking about epistemic reduction in terms of (...) theories and their logical relations is entirely inadequate with respect to what is going on in actual biological research practice. (shrink)

On the basis of distinctions between those properties of entities that can be defined without reference to other entities and those that (in different ways) cannot, this note argues that non-trivial forms of frequency-dependent selection of entities should be interpreted as selection occurring at a level higher than that of those entities. It points out that, except in degenerately simple cases, evolutionary game-theoretic models of selection are not models of individual selection. Similarly, models of genotypic selection such as heterosis cannot (...) be legitimately interpreted as models of genic selection. The analysis presented here supports the views that: (i) selection should be viewed as a multi-level process; (ii) upper-level selection is ubiquitous; (iii) kin selection should be viewed as a type of group selection rather than individual selection; and (iv) inclusive fitness is not an individual property. (shrink)

Fisher’s ‘fundamental theorem of natural selection’ is notoriously abstract, and, no less notoriously, many take it to be false. In this paper, I explicate the theorem, examine the role that it played in Fisher’s general project for biology, and analyze why it was so very fundamental for Fisher. I defend Ewens and Lessard in the view that the theorem is in fact a true theorem if, as Fisher claimed, ‘the terms employed’ are ‘used strictly as defined’. Finally, I explain the (...) role that projects such as Fisher’s play in the progress of scientific inquiry. (shrink)

Fred Sanger, the inventor of the first protein, RNA and DNA sequencing methods, has traditionally been seen as a technical scientist, engaged in laboratory bench work and not interested at all in intellectual debates in biology. In his autobiography and commentaries by fellow researchers, he is portrayed as having a trajectory exclusively dependent on technological progress. The scarce historical scholarship on Sanger partially challenges these accounts by highlighting the importance of professional contacts, institutional and disciplinary moves in his career, spanning (...) from 1940 to 1983. This paper will complement such literature by focusing, for the first time, on the transition of Sanger’s sequencing strategies from degrading to copying the target molecule, which occurred in the late 1960s as he was shifting from protein and RNA to DNA sequencing, shortly after his move from the Department of Biochemistry to the Laboratory of Molecular Biology, both based in Cambridge (UK). Through a reinterpretation of Sanger’s papers and retrospective accounts and a pioneering investigation of his laboratory notebooks, I will claim that sequencing shifted from the working procedures of organic chemistry to those of the emergent molecular biology. I will also argue that sequencing deserves a history in its own right as a practice and not as a technique subordinated to the development of molecular biology or genomics. My proposed history of sequencing leads to a reappraisal of current STS debates on bioinformatics, biotechnology and biomedicine. (shrink)

This article is a systematic critical survey of work done in the philosophy of biology within the logical empiricist tradition, beginning in the 1930s and until the end of the 1950s. It challenges a popular view that the logical empiricists either ignored biology altogether or produced analyses of little value. The earliest work on the philosophy of biology within the logical empiricist corpus was that of Philipp Frank, Ludwig von Bertalanffy, and Felix Mainx. Mainx, in particular, provided a detailed analysis (...) of biology in the 1930s and 1940s in his contribution to the logical empiricists’ Encyclopedia of Unified Science. However, the most important contributions to the philosophy of biology were those of Joseph Henry Woodger and Ernest Nagel. Woodger is primarily remembered for deploying the axiomatic method in biology but he also used semiformal methods for the analysis of many biological problems. While Woodger’s axiomatic work was often derided by some later philosophers of biology (e.g., David Hull and Michael Ruse), this article defends both the biological and the philosophical significance of some of that work, for instance, those aspects that led to the recognition of the conceptual complexity of mereology and temporal identity in biological systems. Woodger’s semiformal analyses were even more important, for instance, his explication of the concepts of the Bauplan and of innateness. Nagel’s importance lies in his analyses of reduction and emergence in the context of all empirical sciences and his use of these analyses in a careful exploration of biological problems. While Nagel’s model of reduction was generally rejected by philosophers of science in the 1970s and 1980s, particularly for biological contexts, it has recently been sympathetically reconstructed by many commentators; this article defends its continued relevance for the philosophy of biology. (shrink)

This paper analyzes the development of evolutionary theory in the period from 1918 to 1932. It argues that: (i) Fisher's work in 1918 constituted a not fully satisfactory reduction of biometry to Mendelism; (ii) there was a synthesis in the 1920s but that this synthesis was mainly one of classical genetics with population genetics, with Haldane's The Causes of Evolution being its founding document; (iii) the most important achievement of the models of theoretical population genetics was to show that natural (...) selection sufficed as a mechanism for evolution; and (iv) Haldane formulated a prospective evolutionary theory in the 1920s whereas Fisher and Wright formulated retrospective theories of evolutionary history. (shrink)

OVERVIEW. The concept of emergence – which I define as the (diachronic) construction of functional structures in complex systems that achieve a (synchronic) focus of systematic behaviour as they constrain the behaviour of individual components – plays a crucial role in debates in philosophical reflection on science as a whole (the question of reductionism) as well as in the fields of biology (the status of the organism), social science (the practical subject), and cognitive science (the cognitive subject).1 In this essay (...) I examine how the philosophy of Deleuze and that of Deleuze and Guattari2 can help us see some of the most important implications of the debate on the status of the organism, as well as prepare the ground for a discussion of the practical and cognitive subject. (shrink)

Scientists, philosophers, and even the lay public commonly accept that schizophrenia stems from a biological or internal ‘dysfunction.’ However, this assessment is typically accompanied neither by well-defined criteria for determining that something is dysfunctional nor empirical evidence that schizophrenia satisfies those criteria. In the following, a concept of biological function is developed and applied to a neurobiological model of schizophrenia. It concludes that current evidence does not warrant the claim that schizophrenia stems from a biological dysfunction, and, in fact, that (...) unusual neural structures associated with schizophrenia may have functional or adaptive significance. The fact that current evidence is ambivalent between these two possibilities (dysfunction versus adaptive function) implies that schizophrenia researchers should be much more cautious in using the ‘dysfunction’ label than they currently are. This has implications for both psychiatric treatment as well as public perception of mental disorders. (shrink)

Since the late 1990s, the characterization of complete DNA sequences for a large and taxonomically diverse set of species has continued to gain in speed and accuracy. Sequence analyses have indicated a strikingly baroque structure for most eukaryotic genomes, with multiple repeats of DNA sequences and with very little of the DNA specifying proteins. Much of the DNA in these genomes has no known function. These results have generated strong interest in the factors that govern the evolution of genome architecture. (...) While adaptationist ‘just so’ stories have been offered, recent theoretical analyses based on mathematical population genetics strongly suggest that non-adaptive processes dominate genome architecture evolution. This article critically synthesizes and develops these arguments, explicating a core argument along with several variants. It provides a critical assessment of the evidence that supports these arguments’ premises. It also analyses adaptationist responses to these arguments and notes potential problems with the core argument. These theoretical analyses continue the molecular reinterpretation of evolution initiated by the neutral theory in 1968. The article ends by noting that some of these arguments can also be extended to evolution at higher levels of organization which raises questions about adaptationism in general. This remains a puzzle because there is probably little reason to doubt that many organismic features are genuine adaptations. 1 Introduction2 Preliminaries: Senses of Adaptationism3 Genome Architecture3.1 Surprises of early eukaryotic genetics3.2 Genome structure, post-20014 The Case against Adaptationism4.1 Just so stories versus population genetics4.2 The core argument4.3 Three variants of the core argument4.4 Examples: Non-adaptive features of the genome5 Adaptationist Responses6 Concluding Remarks. (shrink)

Selectionist evolutionary theory has often been faulted for not making novel predictions that are surprising, risky, and correct. I argue that it in fact exhibits the theoretical virtue of predictive capacity in addition to two other virtues: explanatory unification and model fitting. Two case studies show the predictive capacity of selectionist evolutionary theory: parallel evolutionary change in E. coli, and the origin of eukaryotic cells through endosymbiosis.

The presence of gene–environment statistical interaction and correlation in biological development has led both practitioners and philosophers of science to question the legitimacy of heritability estimates. The paper offers a novel approach to assess the impact of GxE and rGE on the way genetic and environmental causation can be partitioned. A probabilistic framework is developed, based on a quantitative genetic model that incorporates GxE and rGE, offering a rigorous way of interpreting heritability estimates. Specifically, given an estimate of heritability and (...) the variance components associated with estimates of GxE and rGE, I arrive at a probabilistic account of the relative effect of genes and environment. (shrink)

In this article, we use the theory of Information Ethics to argue that deceased people have a prima facie moral right to privacy in the context of health data research, and that this should be reflected in regulation and guidelines. After death, people are no longer biological subjects but continue to exist as informational entities which can still be harmed/damaged. We find that while the instrumental value of recognising post-mortem privacy lies in the preservation of the social contract for health (...) research, its intrinsic value is grounded in respect for the dignity of the post-mortem informational entity. However, existing guidance on post-mortem data protection is available only in the context of genetic studies. In comparing the characteristics of genetic data and other health-related data, we identify two features of DNA often given as arguments for this genetic exceptionalism: relationality and embodiment. We use these concepts to show that at the appropriate Level of Abstraction, there is no morally relevant distinction between posthumous genetic and other health data. Thus, genetic data should not automatically receive special moral status after death. Instead we make a plea for ‘contextual exceptionalism’. Our analysis concludes by reflecting on a real-world case and providing suggestions for contextual factors that researchers and oversight bodies should take into account when designing and evaluating research projects with health data from deceased subjects. (shrink)

Alexander Rosenberg recently claimed (1997) that developmental biology is currently being reduced to molecular biology. cite several concrete biological examples that are intended to impugn Rosenberg's claim. I first argue that although Laubichler and Wagner's examples would refute a very strong reductionism, a more moderate reductionism would escape their attacks. Next, taking my cue from the antireductionist's perennial stress on the importance of spatial organization, I describe one form an empirical finding that refutes this moderate reductionism would take. Finally, I (...) point out an actual example, anterior-posterior axis determination in the chick, that challenges the reductionist's belief that all developmental regularities can be explained by molecular biology. In short, I argue that Rosenberg's position can be saved from Laubichler and Wagner's criticisms and putative counter-examples, but it would not survive a different kind of counter-example. (shrink)

A standard norm of reaction (NoR) is a graphical depiction of the phenotypic value of some trait of an individual genotype in a population as a function of an environmental parameter. NoRs thus depict the phenotypic plasticity of a trait. The topological properties of NoRs for sets of different genotypes can be used to infer the presence of (non-linear) genotype-environment interactions. While it is clear that many NoRs are adaptive, it is not yet settled whether their evolutionary etiology should be (...) explained by selection on the mean phenotypic trait values in different environments or whether there are specific genes conferring plasticity. If the second alternative is true the NoR is itself an object of selection. Generalized NoRs depict plasticity at the level of populations or subspecies within a species, species within a genus, or taxa at higher levels. Historically, generalized NoRs have routinely been drawn though rarely explicitly recognized as such. Such generalized NoRs can be used to make evolutionary inferences at higher taxonomic levels in a way analagous to how standard NoRs are used for microevolutionary inferences. (shrink)

This paper discusses the individuation of characters for the use asunits by geneticists at the beginning of the 20th century. Thediscussion involves the Presence and Absence Hypothesis as a case study. It issuggested that the gap between conceptual consideration and etiological factorsof individuating of characters is being handled by way of mutual adjustment.Confrontation of a suggested morphological unit character with experimentresults molded the final boundaries of it.

Slightly modified excerpt from the section 13.4 Zusammenfassung und Ausblick (translated into englisch): This chapter is based on an analysis of ethical debates on epigenetics and genome editing, debates, in which ethical arguments relating to future generations and justice play a central role. The analysis aims to contextualize new developments in genetic engineering, such as genome and epigenome editing, ethically. At the beginning, the assumptions of "genetic determinism," on which "genetic essentialism" is based, of "epigenetic determinism" as well as "genetic" (...) and "epigenetic exceptionalism" are analyzed and critically discussed. The remarks on the ethical discourse on epigenetics show that the notion of "epigenetic determinism" can sometimes be discerned not only in popular scientific discourse but also in ethical discourse. Ethical debates on epigenetics, however, have distanced themselves from this deterministic understanding. As a result, the focus in the ethical discourse on epigenetics shifts from responsibility for one's own health and that of subsequent generations to justice. What is meant here is justice, for example, in terms of access to healthy environmental conditions, regardless of whether these contribute to health with or without epigenetic agency. An analysis of the discourse on genome editing reveals that it is primarily germline interventions that are being ethically examined, with a concentration on the aspect of inheritance. The question is whether this is accompanied by an implicit "genetic determinism" or even a "genetic essentialism": the determinism could lie in the centrality of the aspect of heritability, since only genetic information is inherited. Does the aspect of heritability and genome modification play a more decisive role in debates on genome editing than the safety issue? Is the problem of embryos and their potential offspring not being able to consent to germline intervention given such a high priority because it is a genetic intervention? Under such a premise of "strong genetic determinism" supplemented by "epigenetic determinism," not only genome editing but also epigenome editing would be ethically relevant precisely because it too would have an influence on the genome. How this influence of genome editing and epigenome editing is ethically evaluated in each case therefore depends initially on whether the assumptions of "genetic" and "epigenetic determinism" are advocated. These assumptions are increasingly viewed critically in ethical discourse because they cannot be confirmed from a scientific perspective. In popular scientific debates in particular, however, they seem to persist, which ultimately also influences the public discussion. Since a broad public discussion is required especially on genome editing, a reflective approach to the various "-isms" analyzed in this chapter is central. DOI: 10.5771/9783748927242. (shrink)

Philosophical discussion of molecular and developmental biology began in the late 1960s with the use of genetics as a test case for models of theory reduction. With this exception, the theory of natural selection remained the main focus of philosophy of biology until the late 1970s. It was controversies in evolutionary theory over punctuated equilibrium and adaptationism that first led philosophers to examine the concept of developmental constraint. Developmental biology also gained in prominence in the 1980s as part of a (...) broader interest in the new sciences of self-organization and complexity. The current literature in the philosophy of molecular and developmental biology has grown out of these earlier discussions under the influence of twenty years of rapid and exciting growth of empirical knowledge. Philosophers have examined the concepts of genetic information and genetic program, competing definitions of the gene itself and competing accounts of the role of the gene as a developmental cause. The debate over the relationship between development and evolution has been enriched by theories and results from the new field of 'evolutionary developmental biology'. Future developments seem likely to include an exchange of ideas with the philosophy of psychology, where debates over the concept of innateness have created an interest in genetics and development. (shrink)