The field of the philosophy of biology is flourishing in its aim to evaluate and rethink the view inherited from the previous century ---the Modern Synthesis. Different research areas and theories have come to the fore in the last decades in order to account for different biological phenomena that, in the first instance, fall beyond the explanatory scope of the Modern Synthesis. This thesis is anchored and motivated by this revolt in the philosophy of biology. -/- The central target in (...) this context is the possibility of naturalizing teleology, a classical nightmare for the history of biology itself. This requires, principally, understanding the causes of teleological explanations without assuming an unfashioned backward causation of sorts. As the riddles of teleological explanations are about their temporal dimension, I analyze different temporal scales of biological processes: evolutionary, developmental, and physiological. -/- The first one is the one defended in the context of the Modern Synthesis. As expected, one of the aims of this thesis is to evaluate the adequacy of an evolutionary account of teleological explanation. The scrutiny is negative. Evolutionary explanations in the context of the Modern Synthesis lack the necessary causal roots to naturalize teleology. Concerning the physiological scale, a long tradition pushed up by Kant and the organicist movement in the 20th century allows us to better understand how teleological explanations can be naturalized in physiological process. The key notions in this temporal scale are self-organization and the recursive, looped character of physiological process. While the physiological scale may be suitably accounted by contemporaries views, such as Autonomous Systems Theory, different central teleological phenomena remain unexplained from a purely physiological perspective. In particular, different issues concerning the (adaptive) construction of organism ---such as plasticity, robustness, variation, novelty, inheritance--- deserve an ontogenetic analysis. -/- The principal aim of this thesis is to provide a theory of teleological development that falls beyond the Modern Synthesis' framework and is prompted by different insights from the history of biology. I call it Agential Teleosemantics. It rests on two central pillars. First, that developmental processes, beyond any gene-centered stance, can be understood in informational terms; i.e. developmental processes are about the interaction of developmental resources conveying biological information. The second ingredient is agentivity, namely the idea that development is regulated by an agentive system according to the adaptiveness of the phenotypic outcomes produced. The role of agency in Agential Teleosemantic is equivalent to the role of genes in the Modern Synthesis: it is responsible for explaining the order and the adaptive complexity in the living realm. -/- The second target of this thesis regards the possibility of naturalizing intentional explanations in cognitive science. The central project involved in such an aim is known as teleosemantics. Classical teleosemantics however is etiological: it explains the teleofunctions of representational systems in terms of evolutionary processes. The different disputes in the contemporary philosophy of biology provide two insights to analyze teleosemantics in cognitive science. First, the challenges against the Modern Synthesis must be extended to the evolutionary approach of etiological teleosemantics. Second, as Agential Teleosemantics suggests an alternative source for teleofunctions ---ontogeny, I offer an attempt to integrate Agential Teleosemantics into cognitive science in order to provide an alternative teleosemantic project to understand intentional explanations in cognitive science. (shrink)

The success of a piece of behaviour is often explained by its being caused by a true representation (similarly, failure falsity). In some simple organisms, success is just survival and reproduction. Scientists explain why a piece of behaviour helped the organism to survive and reproduce by adverting to the behaviour’s having been caused by a true representation. That usage should, if possible, be vindicated by an adequate naturalistic theory of content. Teleosemantics cannot do so, when it is applied to simple (...) representing systems (Godfrey-Smith 1996). Here it is argued that the teleosemantic approach to content should therefore be modified, not abandoned, at least for simple representing systems. The new ‘infotel-semantics’ adds an input condition to the output condition offered by teleosemantics, recognising that it is constitutive of content in a simple representing system that the tokening of a representation should correlate probabilistically with the obtaining of its specific evolutionary success condition. (shrink)

The concept of innateness is a part of folk wisdom but is also used by biologists and cognitive scientists. This concept has a legitimate role to play in science only if the colloquial usage relates to a coherent body of evidence. We examine many different candidates for the post of scientific successor of the folk concept of innateness. We argue that none of these candidates is entirely satisfactory. Some of the candidates are more interesting and useful than others, but the (...) interesting candidates are not equivalent to each other and the empirical and evidential relations between them are far from clear. Researchers have treated the various scientific notions that capture some aspect of the folk concept of innateness as equivalent to each other or at least as tracking properties that are strongly correlated with each other. But whether these correlations exist is an empirical issue. This empirical issue has not been thoroughly investigated because in the attempt to create a bridge between the folk view and their theories, researchers have often assumed that the properties must somehow cluster. Rather than making further attempts to import the folk concept of innateness into the sciences, efforts should now be made to focus on the empirical questions raised by the debates and pave the way to a better way of studying the development of living organisms. Such empirical questions must be answered before it can be decided whether a good scientific successor – in the form of a concept that refers to a collection of biologically significant properties that tend to co-occur – can be identified or whether the concept of innateness deserves no place in science. (shrink)

Despite several decades of criticism, dichotomous thinking about behavioral development remains widespread and influential. This is particularly true in study of birdsong development, where it has become increasingly common to diagnose songs, elements of songs, or precursors of songs as either innate or learned on the basis of isolation-rearing experiments. The theory of sensory templates has encouraged both the dichotomous approach and an emphasis on structural rather than functional aspects of song development. As a result, potentially important lines of investigation (...) have been overlooked and the interpretation of existing data is often flawed. Evidence for a genetic origin of behavioraldifferencesis frequently interpreted as evidence for the genetic determination of behavioralcharacters. The technique of isolation rearing remains the methodology of choice for many investigators, despite the fact that it offers only a rather crude analysis of the contribution of experience to song development and provides no information at all about genetic contributions to development. The latter could in principle be elucidated by the application of developmental-genetic techniques, but it is unlikely that these can easily be applied to the study of birdsong. Because developmental questions are so often posed in terms of the learned–innate dichotomy, “experience” is taken to be synonymous with “learning” and the possible role of nonobvious contributions to song development has largely been ignored. An alternative approach, based on Daniel Lehrman's interactionist theory of development, permits a more thorough appreciation of the problems that have yet to be addressed, and provides a more secure conceptual foundation for theories of song development. (shrink)

The sociogenomics revolution is upon us, we are told. Whether revolutionary or not, sociogenomics is poised to flourish given the ease of incorporating polygenic scores (or PGSs) as “genetic propensities” for complex traits into social science research. Pointing to evidence of ubiquitous heritability and the accessibility of genetic data, scholars have argued that social scientists not only have an opportunity but a duty to add PGSs to social science research. Social science research that ignores genetics is, some proponents argue, at (...) best partial and likely scientifically flawed, misleading, and wasteful. Here, I challenge arguments about the value of genetics for social science and with it the claimed necessity of incorporating PGSs into social science models as measures of genetic influences. In so doing, I discuss the impracticability of distinguishing genetic influences from environmental influences because of non-causal gene–environment correlations, especially population stratification, familial confounding, and downward causation. I explain how environmental effects masquerade as genetic influences in PGSs, which undermines their raison d’être as measures of genetic propensity, especially for complex socially contingent behaviors that are the subject of sociogenomics. Additionally, I draw attention to the partial, unknown biology, while highlighting the persistence of an implicit, unavoidable reductionist genes versus environments approach. Leaving sociopolitical and ethical concerns aside, I argue that the potential scientific rewards of adding PGSs to social science are few and greatly overstated and the scientific costs, which include obscuring structural disadvantages and cultural influences, outweigh these meager benefits for most social science applications. (shrink)

According to The Bell Curve, Black Americans are genetically inferior to Whites. That's not the only point in Richard Herrnstein and Charles Murray's book. They also argue that there is something called "general intelligence" which is measured by IQ tests, socially important, and 60 percent "heritable" within whites. (I'll explain heritability below.) But the claim about genetic inferiority is my target here. It has been subject to wide-ranging criticism since the book was first published last year. Those criticisms, however, have (...) missed its deepest flaws. Indeed, the Herrnstein/Murray argument depends on conceptual confusions that have been tacitly accepted to some degree by many of the book's sharpest critics. (shrink)

Discussions about the biological bases (or lack thereof) of the concept of race in the human species seem to be never ending. One of the latest rounds is represented by a paper by Neven Sesardic, which attempts to build a strong scientific case for the existence of human races, based on genetic, morphometric and behavioral characteristics, as well as on a thorough critique of opposing positions. In this paper I show that Sesardic’s critique falls far short of the goal, and (...) that his positive case is exceedingly thin. I do this through a combination of analysis of the actual scientific findings invoked by Sesardic and of some philo- sophical unpacking of his conceptual analysis, drawing on a dual professional background as an evolu- tionary biologist and a philosopher of science. (shrink)

Kenneth C. Schaffner's paper is an important contribution to the literature on behavioral genetics and on genetics in general. Schaffner has a long record of injecting real molecular biology into philosophical discussions of genetics. His treatments of the reduction of Mendelian to molecular genetics first drew philosophical attention to the problems of detail that have fuelled both anti-reductionism and more sophisticated models of theory reduction. An injection of molecular detail into discussions of genetics is particularly necessary at the present time, (...) when so many philosophers seem happy to discuss the philosophical and ethical implications of molecular biology using gene concepts derived from evolutionary biology ). Schaffner has long advocated the view that the philosophy of biology should be more than the philosophy of evolution. This paper shows how radically a picture of gene action derived from molecular biology undercuts the popular picture associated with a more evolutionary view of genes as units of heredity or as ‘difference-makers’ mediated by the ‘black box’ of development. (shrink)

Advocates of an ‘extended evolutionary synthesis’ have claimed that standard evolutionary theory fails to accommodate epigenetic inheritance. The opponents of the extended synthesis argue that the evidence for epigenetic inheritance causing adaptive evolution in nature is insufficient. We suggest that the ambiguity surrounding the conception of the gene represents a background semantic issue in the debate. Starting from Haig’s gene-selectionist framework and Griffiths and Neumann-Held’s notion of the evolutionary gene, we define senses of ‘gene’, ‘environment’, and ‘phenotype’ in a way (...) that makes them consistent with gene-centric evolutionary theory. We argue that the evolutionary gene, when being materialized, need not be restricted to nucleic acids but can encompass other heritable units such as epialleles. If the evolutionary gene is understood more broadly, and the notions of environment and phenotype are defined accordingly, current evolutionary theory does not require a major conceptual change in order to incorporate the mechanisms of epigenetic inheritance. _1_ Introduction _2_ The Gene-centric Evolutionary Theory and the ‘Evolutionary Gene’ _2.1_ The evolutionary gene _2.2_ Genes, phenotypes, and environments _3_ Epigenetic Inheritance and the Gene-Centred Framework _3.1_ Treating the gene as the sole heritable material? _3.2_ Epigenetics and phenotypic plasticity _4_ Conclusion. (shrink)

Genome-wide association studies of human complex traits have provided us with new estimates of heritability. These estimates foreground the question of genetic causation. After having presen...

We develop an account of laboratory models, which have been central to the group selection controversy. We compare arguments for group selection in nature with Darwin's arguments for natural selection to argue that laboratory models provide important grounds for causal claims about selection. Biologists get information about causes and cause-effect relationships in the laboratory because of the special role their own causal agency plays there. They can also get information about patterns of effects and antecedent conditions in nature. But to (...) argue that some cause is actually responsible in nature, they require an inference from knowledge of causes in the laboratory context and of effects in the natural context. This process, cause detection, forms the core of an analogical argument for group selection. We discuss the differing roles of mathematical and laboratory models in constructing selective explanations at the group level and apply our discussion to the units of selection controversy to distinguish between the related problems of cause determination and evaluation of evidence. Because laboratory models are at the intersection of the two problems, their study is crucial for framing a coherent theory of explanation for evolutionary biology. (shrink)

A high heritability estimate usually corresponds to a situation in which trait variation is largely caused by genetic variation. However, in some cases of gene-environment covariance, causal intuitions about the sources of trait difference can vary, leading experts to disagree as to how the heritability estimate should be interpreted. We argue that the source of contention for these cases is an inconsistency in the interpretation of the concepts ‘genotype’, ‘phenotype’, and ‘environment’. We propose an interpretation of these terms under which (...) trait variance initially caused by genetic variance is subsumed into a heritability for all cases of gene-environment covariance. (shrink)

Research on the human microbiome has gen- erated a staggering amount of sequence data, revealing variation in microbial diversity at the community, species (or phylotype), and genomic levels. In order to make this complexity more manageable and easier to interpret, new units—the metagenome, core microbiome, and entero- type—have been introduced in the scientific literature. Here, I argue that analytical tools and exploratory statisti- cal methods, coupled with a translational imperative, are the primary drivers of this new ontology. By reducing the (...) dimensionality of variation in the human microbiome, these new units render it more tractable and easier to interpret, and hence serve an important heuristic role. Nonetheless, there are several reasons to be cautious about these new categories prematurely ‘‘hardening’’ into natural units: a lack of constraints on what can be sequenced metagenomically, freedom of choice in taxonomic level in defining a ‘‘core microbiome,’’ typological framing of some of the concepts, and possible reification of statistical constructs. Finally, lessons from the Human Genome Project have led to a translational imperative: a drive to derive results from the exploration of microbiome variation that can help to articulate the emerging paradigm of per- sonalized genomic medicine (PGM). There is a tension between the typologizing inherent in much of this research and the personal in PGM. (shrink)

In reworking a variety of biological concepts, Developmental Systems Theory (DST) has made frequent use of parity of reasoning. We have done this to show, for instance, that factors that have similar sorts of impact on a developing organism tend nevertheless to be invested with quite different causal importance. We have made similar arguments about evolutionary processes. Together, these analyses have allowed DST not only to cut through some age-old muddles about the nature of development, but also to effect a (...) long-delayed reintegration of development into evolutionary theory. Our penchant for causal symmetry, however (or 'causal democracy', as it has recently been termed), has sometimes been misunderstood. This paper shows that causal symmetry is neither a platitude about multiple influences nor a denial of useful distinctions, but a powerful way of exposing hidden assumptions and opening up traditional formulations to fruitful change. (shrink)

Most psychological research aims to uncover generalizations about the mind that hold across subjects. Philosophical discussions of scientific explanation have focused on such generalizations, but in doing so, have often overlooked an important phenomenon: variation. Variation is ubiquitous in psychology and many other domains, and an important target of explanation in its own right. Here I characterize explananda that concern individual differences and formulate an account of what it takes to explain them. I argue that the notion of actual difference (...) making, the only causal concept in the literature that explicitly addresses variation, cannot be used to ground such an account. Instead, I propose a view on which explaining individual differences involves identifying causes that could be intervened on to reduce the variability in the population. This account provides criteria of success for explaining variation and deepens our understanding of causal explanation. (shrink)

Brain damage may doubly dissociate cognitive modules, but the practice of revealing dissociations is predicated on modularity being true (T. Shallice, 1988). This article questions the utility of assuming modularity, as it examines a paradigmatic double dissociation of reading modules. Reading modules illustrate two general problems. First, modularity fails to converge on a fixed set of exclusionary criteria that define pure cases. As a consequence, competing modular theories force perennial quests for purer cases, which simply perpetuates growth in the list (...) of exclusionary criteria. The first problem leads, in part, to the second problem. Modularity fails to converge on a fixed set of pure cases. The second failure perpetuates unending fractionation into more modules. (shrink)

Nineteenth-century medical advances were entwined with a conceptual innovation: the idea that many cases of disease which were previously thought to have diverse causes could be explained by the action of a single kind of cause, for example a certain bacterial or parasitic infestation. The focus of modern epidemiology, however, is on chronic non-communicable diseases, which frequently do not seem to be attributable to any single causal factor. This paper is an effort to resolve the resulting tension. The paper criticises (...) the monocausal model of disease, so successful in the nineteenth century. It also argues that a multifactorial model of disease can only be satisfactory if it amounts to more than a mere rejection of the monocausal model. A third alternative, the contrastive model, is proposed and defended on the grounds that it links the notions of disease and of general explanation, while avoiding the philosophical naiveties and practical difficulties of the monocausal model. (shrink)

The question of the influence of genes on behavior raises difficult philosophical and social issues. In this paper I delineate what I call the Developmentalist Challenge (DC) to assertions of genetic influence on behavior, and then examine the DC through an indepth analysis of the behavioral genetics of the nematode, C. elegans, with some briefer references to work on Drosophila. I argue that eight "rules" relating genes and behavior through environmentally-influenced and tangled neural nets capture the results of developmental and (...) behavioral studies on the nematode. Some elements of the DC are found to be sound and others are criticized. The essay concludes by examining the relations of this study to Kitcher's antireductionist arguments and Bechtel and Richardson's decomposition and localization heuristics. Some implications for human behavioral genetics are also briefly considered. (shrink)

Metaphors of adorning, crafting, water flowing downward, and growing sprouts appear in the Analects , the Mencius , and the Xunzi 荀子. They express and guide thinking about what there is in human nature to cultivate and how it is to be cultivated. The craft metaphor seems to imply that our nature is of the sort that must be disciplined and reshaped to achieve goodness, while the adorning, water, and sprout metaphors imply that human nature has an inbuilt directionality toward (...) the ethical that should be protected or nurtured. I argue that all the metaphors capture different aspects of human nature and how one must work with these aspects. There is much in contemporary psychology and neuroscience to suggest that the early Confucians were on the right track. It is also argued that they point to a fruitful conception of ethical development that is relational and holistic. (shrink)

Abstract Gene-selectionists define fundamental terms in non-standard ways. Genes are determinants of difference. Phenotypes are defined as a gene’s effects relative to some alternative whereas the environment is defined as all parts of the world that are shared by the alternatives being compared. Environments choose among phenotypes and thereby choose among genes. By this process, successful gene sequences become stores of information about what works in the environment. The strategic gene is defined as a set of gene tokens that combines (...) ‘actor’ tokens responsible for an effect with ‘recipient’ tokens whose replication is thereby enhanced. This set of tokens can extend across the boundaries of individual organisms, or other levels of selection, as these are traditionally defined. Content Type Journal Article Pages 1-19 DOI 10.1007/s10539-012-9315-5 Authors David Haig, Department of Organismic and Evolutionary Biology, Harvard University, 26 Oxford Street, Cambridge, MA 02138, USA Journal Biology and Philosophy Online ISSN 1572-8404 Print ISSN 0169-3867. (shrink)

Showcasing original arguments for well-defined positions, as well as clear and concise statements of sophisticated philosophical views, this volume is an ...

If one investigates a process that has several causes but assumes that it has only one cause, one risks ruling out important causal factors. Three mechanisms account for this mistake: either the significance of the single cause under test is masked by noise contributed by the unsuspected and uncontrolled factors, or the process appears only when two or more causes interact, or the process appears when there are present any of a number of sufficient causes which are not mutally exclusive. (...) In ecology and evolutionary biology, experiments usually test single factor hypotheses, and many scientists apparently believe that hypotheses incorporating several factors are so much more difficult to test that to do so would not be practical. We discuss several areas in ecology and evolutionary biology in which the presupposition of simple causation has apparently impeded progress. We also examine a more mature field, the study of atherosclerosis, in which single factor studies did significantly delay progress towards understanding what now appears to be a multifactor process. The problem has three solutions: either factorial experiments, dynamic models that make quantitative predictions, response-surface methods, or all three. In choosing a definition for ‘cause’, we make a presupposition that profoundly influences subsequent observations and experimental designs. Alternative definitions of causation should be considered as contributing to potential cures for research problems. (shrink)

Developmental Systems Theory (DST) emphasises the importance of non-genetic factors in development and their relevance to evolution. A common, deflationary reaction is that it has long been appreciated that non-genetic factors are causally indispensable. This paper argues that DST can be reformulated to make a more substantive claim: that the special role played by genes is also played by some (but not all) non-genetic resources. That special role is to transmit inherited representations, in the sense of Shea (2007: Biology and (...) Philosophy, 22, 313-331). Formulating DST as the claim that there are non-genetic inherited representations turns it into a striking, empirically-testable hypothesis, driving the sort of investigations that are only now beginning to appear in the scientific literature. DST’s characteristic rejection of a gene vs. environment dichotomy is preserved, but without dissolving all potentially explanatory distinctions into an interactionist causal soup, as some have alleged. (shrink)

Behavioral genetics and cultural evolution have both revolutionized our understanding of human behavior – largely independent of each other. Here, we reconcile these two fields under a dual inheritance framework, offering a more nuanced understanding of the interaction between genes and culture. Going beyond typical analyses of gene–environment interactions, we describe the cultural dynamics that shape these interactions by shaping the environment and population structure. A cultural evolutionary approach can explain, for example, how factors such as rates of innovation and (...) diffusion, density of cultural subgroups, and tolerance for behavioral diversity impact heritability estimates, thus yielding predictions for different social contexts. Moreover, when cumulative culture functionally overlaps with genes, genetic effects become masked, unmasked, or even reversed, and the causal effects of an identified gene become confounded with features of the cultural environment. The manner of confounding is specific to a particular society at a particular time, but a WEIRD (western, educated, industrialized, rich, and democratic) sampling problem obscures this boundedness. Cultural evolutionary dynamics are typically missing from models of gene-to-phenotype causality, hindering generalizability of genetic effects across societies and across time. We lay out a reconciled framework and use it to predict the ways in which heritability should differ between societies, between socioeconomic levels, and other groupings within some societies but not others, and over the life course. An integrated cultural evolutionary behavioral genetic approach cuts through the nature–nurture debate and helps resolve controversies in topics such as IQ. (shrink)

Lucas Matthews and I substantially revised my SEP entry on Heritability. This version includes discussion of the missing heritability problem and other issues that arise from the use of Genome Wide Association Studies by Behavioral Geneticists.

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)

A survey of innateness in cognitive science, focusing on (1) what innateness might be, and (2) whether concepts might be innate.

This paper advocates a dispositional account of innate cognitive capacities, which has an illustrious history from Plato to Chomsky. The "triggering model" of innateness, first made explicit by Stich ([1975]), explicates the notion in terms of the relative informational content of the stimulus (input) and the competence (output). The advantage of this model of innateness is that it does not make a problematic reference to normal conditions and avoids relativizing innate traits to specific populations, as biological models of innateness are (...) forced to do. Relativization can be avoided in the case of cognitive capacities precisely because informational content is involved. Even though one cannot measure output relative to input in a precise way, there are indirect and approximate ways of assessing the degree of innateness of a specific cognitive capacity. (shrink)

In 1976, the Genetics Society of America published a document entitled “Resolution of Genetics, Race, and Intelligence.” This document laid out the Society’s position in the IQ controversy, particularly that on scientific and ethical questions involving the genetics of intellectual differences between human populations. Since the GSA was the largest scientific society of geneticists in the world, many expected the document to be of central importance in settling the controversy. Unfortunately, the Resolution had surprisingly little influence on the discussion. In (...) 1979, William Provine analyzed the possible factors that decreased the impact of the Resolution, among them scientists’ limited understanding of the relationship between science and ethics. Through the analysis of unpublished versions of the Resolution and exchanges between GSA members, I will suggest that the limited impact of the statement likely depended on a shift in the aims of the GSA due to the controversies that surrounded the preparation of the document. Indeed, the demands of the membership made it progressively more impartial in both scientific and political terms, decreasing its potential significance for a wider audience. Notably, the troubled history of the Resolution raises the question of what can make effective or ineffective the communication between scientists and the public—a question with resonance in past and present discussions on topics of social importance. (shrink)

Biology above the level of the individual organism ? population ecology and genetics, community ecology, biogeography and evolution ? requires the study of intrinsically complex systems. But the dominant philosophies of western science have proven to be inadequate for the study of complexity:(1)The reductionist myth of simplicity leads its advocates to isolate parts as completely as possible and study these parts. It underestimates the importance of interactions in theory, and its recommendations for practice (in agricultural programs or conservation and environmental (...) protection) are typically thwarted by the power of indirect and unanticipated causes rather than by error in the detailed description of their own objects of study.(2)Reductionism ignores properties of complex wholes; the effects of these properties are therefore seen only as noise; this randomness is elevated into an ontological principle which leads to the blocking of investigation and the reification of statistics, so that data reduction and statistical prediction often pass for explanation.(3)The faith in the atomistic nature of the world makes the allocation of relative weights to separate causes the main object of science, and makes it more difficult to study the nature of interconnectedness. (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)

The causal impacts of genes and environment on any one biological trait are inextricably entangled, and consequently it is widely accepted that it makes no sense in singleton cases to privilege either factor for particular credit. On the other hand, at a population level it may well be the case that one of the factors is responsible for more variation than the other. Standard methodological practice in biology uses the statistical technique of analysis of variance to measure this latter kind (...) of causal efficacy. In this paper, I argue that: 1) analysis of variance is in fact badly suited to this role; and. (shrink)