Griffiths and Stotz’s Genetics and Philosophy: An Introduction offers a very good overview of scientific and philosophical issues raised by present-day genetics. Examining, in particular, the questions of how a “gene” should be defined and what a gene does from a causal point of view, the authors explore the different domains of the life sciences in which genetics has come to play a decisive role, from Mendelian genetics to molecular genetics, behavioural genetics, and evolution. In this review, I highlight what (...) I consider as the two main theses of the book, namely: genes are better conceived as tools; genes become causes only in a context. I situate these two theses in the wider perspective of developmental systems theory. This leads me to emphasize that Griffiths and Stotz reflect very well an on going process in genetics, which I call the “epigenetization” of genetics, i.e., the growing interest in the complex processes by which gene activation is regulated. I then make a factual objection, which is that Griffiths and Stotz have almost entirely neglected the perspective of ecological developmental biology, and more precisely recent work on developmental symbioses, and I suggest that this omission is unfortunate in so far as an examination of developmental symbioses would have considerably strengthened Griffiths and Stotz’s own conclusions. (shrink)

A number of areas of biology raise questions about what is of value in the natural environment and how we ought to behave towards it: conservation biology, environmental science, and ecology, to name a few. Based on my experience teaching students from these and similar majors, I argue that the field of environmental ethics has much to teach these students. They come to me with pent-up questions and a feeling that more is needed to fully engage in their subjects, and (...) I believe some exposure to environmental ethics can help focus their interests and goals. I identify three primary areas in which environmental ethics can con- tribute to their education. The first is an examination of who (or what) should be considered to be part of our moral community (i.e., the community to whom we owe direct duties). Is it humans only? Or does it include all sentient life? Or all life? Or ecosystems considered holistically? Often, readings implicitly assume one or more of these answers; the goal is to make the student more sensitive to these implicit claims and to get them to think about the different reasons that support them. The second area, related to the first, is the application of the different answers concerning the extent of the ethical community to real environmental issues and problems. Students need to be aware of how the different answers concerning the moral community can imply conflicting answers for how we should act in certain cases and to think about ways to move toward conflict resolution. The third area in which environmental ethics can contribute is a more conceptual one, focusing on central concepts such as biodiversity, sustainability, species, and ecosystems. Exploring and evaluating various meanings of these terms will make students more reflective and thoughtful citizens and biologists, sensitive to the implications that different conceptual choices make. (shrink)

What is the relationship between pain and the body? I claim that pain is best explained as a type of personal experience and the bodily response during pain is best explained in terms of a type of mechanical neurophysiologic operation. I apply the radical philosophy of identity theory from philosophy of mind to the relationship between the personal experience of pain and specific neurophysiologic mechanism and argue that the relationship between them is best explained as one of type identity. Specifically, (...) pain is a specific type of personal experience identical to a specific type of allostatic stress response comprised of interdependent nervous, endocrine and immune mechanical operations. (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)

Evo-Devo exhibits a plurality of scientific “cultures” of practice and theory. When are the cultures acting—individually or collectively—in ways that actually move research forward, empirically, theoretically, and ethically? When do they become imperialistic, in the sense of excluding and subordinating other cultures? This chapter identifies six cultures – three /styles/ (mathematical modeling, mechanism, and history) and three /paradigms/ (adaptationism, structuralism, and cladism). The key assumptions standing behind, under, or within each of these cultures are explored. Characterizing the internal structure of (...) the cultures is necessary for understanding how they collaborate or compete, and how they are fragmented or integrated, in the rich interdisciplinary /trading zone/ (Galison 1997) of Evo-Devo. Evo-Devo is an important example of how science can progress through a radical plurality of perspectives and cultures. (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)

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)

In recent years, a ''change in attitude'' in particle physics has led to our understanding current quantum field theories as effective field theories (EFTs). The present paper is concerned with the significance of this EFT approach, especially from the viewpoint of the debate on reductionism in science. In particular, I shall show how EFTs provide a new and interesting case study in current philosophical discussion on reduction, emergence, and inter-level relationships in general.

Richard Levins’ distinction between aggregate, composed and evolved systems acquires new significance as we recognize the importance of mechanistic explanation. Criteria for aggregativity provide limiting cases for absence of organization, so through their failure, can provide rich detectors for organizational properties. I explore the use of failures of aggregativity for the analysis of mechanistic systems in diverse contexts. Aggregativity appears theoretically desireable, but we are easily fooled. It may be exaggerated through approximation, conditions of derivation, and extrapolating from some conditions (...) of decomposition illegtimately to others. Evolved systems particularly may require analyses under alternative complementary decompositions. Exploring these conditions helps us to better understand the strengths and limits of reductionistic methods. (shrink)

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)

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.

Causation has multiple distinct meanings in genetics. One reason for this is meaning slippage between two concepts of the gene: Mendelian and molecular. Another reason is that a variety of genetic methods address different kinds of causal relationships. Some genetic studies address causes of traits in individuals, which can only be assessed when single genes follow predictable inheritance patterns that reliably cause a trait. A second sense concerns the causes of trait differences within a population. Whereas some single genes can (...) be said to cause population-level differences, most often these claims concern the effects of many genes. Polygenic traits can be understood using heritability estimates, which estimate the relative influences of genetic and environmental differences to trait differences within a population. Attempts to understand the molecular mechanisms underlying polygenic traits have been developed, although causal inference based on these results remains controversial. Genetic variation has also recently been leveraged as a randomizing factor to identify environmental causes of trait differences. This technique—Mendelian randomization—offers some solutions to traditional epidemiological challenges, although it is limited to the study of environments with known genetic influences. (shrink)

The theory of concepts advanced in the dissertation aims at accounting for a) how a concept makes successful practice possible, and b) how a scientific concept can be subject to rational change in the course of history. Traditional accounts in the philosophy of science have usually studied concepts in terms only of their reference; their concern is to establish a stability of reference in order to address the incommensurability problem. My discussion, in contrast, suggests that each scientific concept consists of (...) three components of content: 1) reference, 2) inferential role, and 3) the epistemic goal pursued with the concept's use. I argue that in the course of history a concept can change in any of these three components, and that change in one component—including change of reference—can be accounted for as being rational relative to other components, in particular a concept's epistemic goal.This semantic framework is applied to two cases from the history of biology: the homology concept as used in 19th and 20th century biology, and the gene concept as used in different parts of the 20th century. The homology case study argues that the advent of Darwinian evolutionary theory, despite introducing a new definition of homology, did not bring about a new homology concept (distinct from the pre-Darwinian concept) in the 19th century. Nowadays, however, distinct homology concepts are used in systematics/evolutionary biology, in evolutionary developmental biology, and in molecular biology. The emergence of these different homology concepts is explained as occurring in a rational fashion. The gene case study argues that conceptual progress occurred with the transition from the classical to the molecular gene concept, despite a change in reference. In the last two decades, change occurred internal to the molecular gene concept, so that nowadays this concept's usage and reference varies from context to context. I argue that this situation emerged rationally and that the current variation in usage and reference is conducive to biological practice.The dissertation uses ideas and methodological tools from the philosophy of mind and language, the philosophy of science, the history of science, and the psychology of concepts. (shrink)

This article argues for the explanatory autonomy of psychology drawing on cases from the multilevel modeling practice. This is done by considering a multilevel linear model in personality and social psychology, and discussing its philosophical implications for the reductionism debate in philosophy of psychology. I argue that this practice challenges the reductionist position in philosophy of psychology, and supports the explanatory autonomy of psychology.

These preprints were automatically compiled into a PDF from the collection of papers deposited in PhilSci-Archive in conjunction with the PSA 2018.

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)

Ongoing empirical discoveries in molecular biology have generated novel conceptual challenges and perspectives. Philosophers of biology have reacted to these trends when investigating the practice of molecular biology and contributed to scientific debates on methodological and conceptual matters. This article reviews some major philosophical issues in molecular biology. First, philosophical accounts of mechanistic explanation yield a notion of explanation in the context of molecular biology that does not have to rely on laws of nature and comports well with molecular discovery. (...) Second, reductionism continues to be debated and increasingly be rejected by scientists. Philosophers have likewise moved away from reduction toward integration across fields or integrative explanations covering several levels of organization. Third, although the gene concept has undergone substantial transformation and even fragmentation, it still enjoys widespread use by molecular biologists, which has prompted philosophers to understand the empirical reasons for this. At the same time, it has been argued the notion of ‘genetic information’ is largely an empty metaphor, which generates the illusion of explanatory understanding without offering an adequate explanation of molecular and developmental mechanisms. (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)

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)

This article discusses the work of George Udny Yule in relation to the evolutionary synthesis and the biometric-Mendelian debate. It has generally been claimed that (i.) in 1902, Yule put forth the first account showing that the competing biometric and Mendelian programs could be synthesized. Furthermore, (ii.) the scientific figures who should have been most interested in this thesis (the biometricians W. F. Raphael Weldon and Karl Pearson, and the Mendelian William Bateson) were too blinded by personal animosity towards each (...) other to appreciate Yule's proposal. This essay provides a detailed account of (i.), maintaining that Yule's 1902 proposal is better understood as a reduction, not a synthesis of the two programs. The results of this analysis are then used to evaluate (ii.), where I will instead argue that Bateson and the biometricians had good reasons to avoid endorsing Yule's account. (shrink)

We reconsider the Nagelian theory of reduction and argue that, contrary to a widely held view, it is the right analysis of intertheoretic reduction. The alleged difficulties of the theory either vanish upon closer inspection or turn out to be substantive philosophical questions rather than knock-down arguments.

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)

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)

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)

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)

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)

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)

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)

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)

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)

This is a contribution to the encyclopedia of systems biology on reduction.

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)

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)

Reduction and reductionism have been central philosophical topics in analytic philosophy of science for more than six decades. Together they encompass a diversity of issues from metaphysics and epistemology. This article provides an introduction to the topic that illuminates how contemporary epistemological discussions took their shape historically and limns the contours of concrete cases of reduction in specific natural sciences. The unity of science and the impulse to accomplish compositional reduction in accord with a layer-cake vision of the sciences, the (...) seminal contributions of Ernest Nagel on theory reduction and how they strongly conditioned subsequent philosophical discussions, and the detailed issues pertaining to different accounts of reduction that arise in both physical and biological science (e.g., limit-case and part-whole reduction in physics, the difference-making principle in genetics, and mechanisms in molecular biology) are explored. The conclusion argues that the epistemological heterogeneity and patchwork organization of the natural sciences encourages a pluralist stance about reduction. (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)

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)

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)

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)

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)

I begin by examining how genetics drivesschizophrenia research, and raise both familiar andrelatively novel criticisms of the evidence putativelysupporting the genetic basis of schizophrenia. Inparticular, I call attention to a set of concernsabout the effects of placentation on concordance ratesof schizophrenia in monozygotic twins, which furtherweakens the case for schizophrenia''s so-called stronggenetic component. I then underscore two criticalpoints. First, I emphasize the importance of takingseriously considerations about the complexity of bothontogenesis and the development of hereditarydiseases. The recognition of developmentalconstraints and (...) supports is crucial, for attention todevelopment exposes the naivete of too many models ofgene action in the aetiology of disease. Secondly, Iattend to those schizophreniologists who ignoremethodological criticisms and thus presume a geneticbasis for schizophrenia, and then seek the schizophrenic genotype lacking an adequatephenotype. In response I attempt to demonstrate thenecessity of a sustained effort at characterizing thephenotype of schizophrenia as an enabling conditionfor the whole enterprise of psychiatric genetics – andfor psychiatry itself. Without the organism-levelphenotype, research at the level of genes will remainunproductive – assuming of course that research at thegenetic level is appropriate at all. (shrink)

There have been two different schools of thought on the evolution of dominance. On the one hand, followers of Wright [Wright S. 1929. Am. Nat. 63: 274–279, Evolution: Selected Papers by Sewall Wright, University of Chicago Press, Chicago; 1934. Am. Nat. 68: 25–53, Evolution: Selected Papers by Sewall Wright, University of Chicago Press, Chicago; Haldane J.B.S. 1930. Am. Nat. 64: 87–90; 1939. J. Genet. 37: 365–374; Kacser H. and Burns J.A. 1981. Genetics 97: 639–666] have defended the view that dominance (...) is a product of non-linearities in gene expression. On the other hand, followers of Fisher [Fisher R.A. 1928a. Am. Nat. 62: 15–126; 1928b. Am. Nat. 62: 571–574; Bürger R. 1983a. Math. Biosci. 67: 125–143; 1983b. J. Math. Biol. 16: 269–280; Wagner G. and Burger R. 1985. J. Theor. Biol. 113: 475–500; Mayo O. and Reinhard B. 1997. Biol. Rev. 72: 97–110] have argued that dominance evolved via selection on modifier genes. Some have called these “physiological” versus “selectionist,” or more recently [Falk R. 2001. Biol. Philos. 16: 285–323], “functional,” versus “structural” explanations of dominance. This paper argues, however, that one need not treat these explanations as exclusive. While one can disagree about the most likely evolutionary explanation of dominance, as Wright and Fisher did, offering a “physiological” or developmental explanation of dominance does not render dominance “epiphenomenal,” nor show that evolutionary considerations are irrelevant to the maintenance of dominance, as some [Kacser H. and Burns J.A. 1981. Genetics 97: 639–666] have argued. Recent work [Gilchrist M.A. and Nijhout H.F. 2001. Genetics 159: 423–432] illustrates how biological explanation is a multi-level task, requiring both a “top-down” approach to understanding how a pattern of inheritance or trait might be maintained in populations, as well as “bottom-up” modeling of the dynamics of gene expression. (shrink)

Academia is subdivided into separate disciplines, most of which are quite discrete. In this review I trace the interactions between two of these disciplines: biology and philosophy of biology. I concentrate on those topics that have the most extensive biological content: function, species, systematics, selection, reduction and development. In the final section of this paper I touch briefly on those issues that biologists and philosophers have addressed that do not have much in the way of biological content.

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)

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)