Research on the human microbiome has generated 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 enterotype—have been introduced in the scientific literature. Here, I argue that analytical tools and exploratory statistical 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 personalized genomic medicine (PGM). There is a tension between the typologizing inherent in much of this research and the personal in PGM. (shrink)

I explore heterogeneous constructionism, my term for the perspective that science in the making is a process of agents building by combining a diversity of components. Issues addressed include causality and explanation; transcending both realism and relativism; scientists as acting, intervening, and imaginative agents; explanations that span many levels of social practice; counterfactuals in the analysis of causal claims; and practical reflexivity. An analogy from research on the social origins of depression and a sketch from my own experience in socioeconomic (...) modeling are used to motivate and render more concrete the form of heterogeneous constructionism I am advocating. (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)

Genetics is in a postgenomic era, and this article illustrates this epistemological evolution using the debate between developmental criticism and traditional biometric genetics about gene × environment interaction. Quantitative geneticists are blamed for failing to respect the complexity of development; as a response, they claim a defensive position, called isolationist pluralism, which supports the idea that studying development is not their problem. But postgenomics seems to have accepted and integrated some developmental criticisms and the isolationist perspective has been challenged during (...) the last few years. The developmental and quantitative traditions actually represent two different levels of analysis, but biometrics has also a clear developmental explanatory potential as it suggests statistically the existence of mechanical causes. Both traditions work together to go ever further in the knowledge of the phenomena being studied. Postgenomic pluralism, instead of being isolationist, may be considered pragmatic. (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)

Ever since Darwin a great deal of the conceptual history of biology may be read as a struggle between two philosophical positions: reductionism and holism. On the one hand, we have the reductionist claim that evolution has to be understood in terms of changes at the fundamental causal level of the gene. As Richard Dawkins famously put it, organisms are just ‘lumbering robots’ in the service of their genetic masters. On the other hand, there is a long holistic tradition that (...) focuses on the complexity of developmental systems, on the non-linearity of gene– environment interactions, and on multi-level selective processes to argue that the full story of biology is a bit more complicated than that. Reductionism can marshal on its behalf the spectacular successes of genetics and molecular biology throughout the 20th and 21st centuries. Holism has built on the development of entirely new disciplines and conceptual frameworks over the past few decades, including evo-devo and phenotypic plasticity. Yet, a number of biologists are still actively looking for a way out of the reductionism–holism counterposition, often mentioning the word ‘emergence’ as a way to deal with the conundrum. This paper briefly examines the philosophical history of the concept of emergence, distinguishes between epistemic and ontological accounts of it, and comments on conceptions of emergence that can actually be useful for practising evolutionary biologists. (shrink)

Probabilistic phenomena are often perceived as being problematic targets for contrastive explanation. It is usually thought that the possibility of contrastive explanation hinges on whether or not the probabilistic behaviour is irreducibly indeterministic, and that the possible remaining contrastive explananda are token event probabilities or complete probability distributions over such token outcomes. This paper uses the invariance-under-interventions account of contrastive explanation to argue against both ideas. First, the problem of contrastive explanation also arises in cases in which the probabilistic behaviour (...) of the explanandum is due to unobserved causal heterogeneity. Second, it turns out that, in contrast to the case of pure indeterminism, the plausible contrastive explananda under causal heterogeneity are not token event probabilities, but population-level statistical facts. (shrink)

The concept of innateness is used to make inferences between various better-understood properties, like developmental canalization, evolutionary adaptation, heritability, species-typicality, and so on (‘innateness-related properties’). This article uses a recently-developed account of the representational content carried by inheritance systems like the genome to explain why innateness-related properties cluster together, especially in non-human organisms. Although inferences between innateness-related properties are deductively invalid, and lead to false conclusions in many actual cases, where some aspect of a phenotypic trait develops in reliance on (...) a genetic representation it will tend, better than chance, to have many of the innateness-related properties. The account also shows why inferences between innateness-related properties sometimes fail and argues that such inferences are especially misleading when applied to human psychology and behaviour because human psychological development is especially reliant on non-genetic inherited representations. (shrink)

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)

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

The paper addresses the question of whether heritability can be useful in establishing genetics as an explanation for an individual’s display of some trait or behavior. After reviewing the fundamental philosophical challenge to heritability—that heritability is a population level measure—an argument is presented for rethinking the role heritability occupies in both causal and explanatory claims. It is argued that heritability can be useful for genetically based explanations of individual traits, if the conditions for proper genetic explanation are modestly reconceived, and (...) the measure is seen as an evidential tool which conforms to standard methods for determining causal factors. (shrink)

Genetic determinism labels the morally problematical claim that some socially significant traits, traits we care about, such as sexual orientation, gender roles, violence, alcoholism, mental illness, intelligence, are largely the results of the operation of genes and not much alterable by environment, learning or other human intervention. Genetic determinism does not require that genes literally fix these socially significant traits, but rather that they constrain them within narrow channels beyond human intervention. In this essay we analyze genetic determinism in light (...) of what is now known about the inborn error of metabolism phenylketonuria , which has for so long been the poster child ‘simple’ argument in favor of some form of genetic determinism. We demonstrate that this case proves the exact opposite of what it has been proposed to support and provides a strong refutation of genetic determinism in all its guises. (shrink)

Many psychometricians and behavioral geneticists believe that high heritability of IQ test scores within racial groups coupled with environmental hypotheses failing to account for the differences between the mean scores for groups lends plausibility to explanations of mean differences in terms of genetic factors. I show that heritability estimates and the statistical analysis of variance on which they are based have limited relevance in exposing genetic and environmental factors operating within any single group or population. I begin with agricultural investigations, (...) where replication of genetic types and control over environmental factors are possible, and highlight the difficulties of moving from AOV of observed traits to investigation of measurable genetic factors. The difficulties can only be exacerbated for human data sets, which are equivalent to a crop trial in which each variety is replicated in only one or two of the locations. (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)

The idea that some characteristics of an organism are explained by the organism's intrinsic nature, whilst others reflect the influence of the environment is an ancient one. It has even been argued that this distinction is itself part of the evolved psychology of the human species. The distinction played an important role in the history of philosophy as the locus of the dispute between Rationalism and Empiricism discussed in another entry in this encyclopedia. This entry, however, focuses on twentieth-century accounts (...) of the innate/acquired distinction. These accounts have for the most part been inspired by the sciences of mind and behaviour. (shrink)

The debate about the levels of selection has been one of the most controversial both in evolutionary biology and in philosophy of science. Okasha’s book makes the sort of contribution that simply will not be able to be ignored by anyone interested in this field for many years to come. However, my interest here is in highlighting some examples of how Okasha goes about discussing his material to suggest that his book is part of an increasingly interesting trend that sees (...) scientists and philosophers coming together to build a broadened concept of “theory” through a combination of standard mathematical treatments and conceptual analyses. Given the often contentious history of the relationship between philosophy and science, such trend cannot but be welcome. (shrink)

This article illustrates in which sense genetic determinism is still part of the contemporary interactionist consensus in medicine. Three dimensions of this consensus are discussed: kinds of causes, a continuum of traits ranging from monogenetic diseases to car accidents, and different kinds of determination due to different norms of reaction. On this basis, this article explicates in which sense the interactionist consensus presupposes the innate?acquired distinction. After a descriptive Part 1, Part 2 reviews why the innate?acquired distinction is under attack (...) in contemporary philosophy of biology. Three arguments are then presented to provide a limited and pragmatic defense of the distinction: an epistemic, a conceptual, and a historical argument. If interpreted in a certain manner, and if the pragmatic goals of prevention and treatment (ideally specifying what medicine and health care is all about) are taken into account, then the innate?acquired distinction can be a useful epistemic tool. It can help, first, to understand that genetic determination does not mean fatalism, and, second, to maintain a system of checks and balances in the continuing nature?nurture debates. (shrink)

This article examines eight “gaps” in order to clarify why the quantitative genetics methods of partitioning variation of a trait into heritability and other components has very limited power to show anything clear and useful about genetic and environmental influences, especially for human behaviors and other traits. The first two gaps should be kept open; the others should be bridged or the difficulty of doing so should be acknowledged: 1. Key terms have multiple meanings that are distinct; 2. Statistical patterns (...) are distinct from measurable underlying factors; 3. Translation from statistical analyses to hypotheses about measurable factors is difficult; 4. Predictions based on extrapolations from existing patterns of variation may not match outcomes; 5. The partitioning of variation in human studies does not reliably estimate the intended quantities; 6. Translation from statistical analyses to hypotheses about the measurable factors is even more difficult in light of the possible heterogeneity of underlying genetic or environmental factors; 7. Many steps lie between the analysis of observed traits and interventions based on well-founded claims about the causal influence of genetic or environmental factors; 8. Explanation of variation within groups does not translate to explanation of differences among groups. At the start, I engage readers’ attention with three puzzles that have not been resolved by past debates. The puzzles concern generational increases in IQ test scores, the possibility of underlying heterogeneity, and the translation of methods from selective breeding into human genetics. After discussing the gaps, I present each puzzle in a new light and point to several new puzzles that invite attention from analysts of variation in quantitative genetics and in social science more generally. The article’s critical perspectives on agricultural, laboratory, and human heritability studies are intended to elicit further contributions from readers across the fields of history, philosophy, sociology, and politics of biology and in the sciences. (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)

Exploring whether clades can reproduce leads to new perspectives on general accounts of biological development and individuation. Here we apply James Griesemer's general account of reproduction to clades. Griesemer's account of reproduction includes a requirement for development, raising the question of whether clades may bemeaningfully said to develop. We offer two illustrative examples of what clade development might look like, though evaluating these examples proves difficult due to the paucity of general accounts of development. This difficulty, however, is instructive about (...) what a general account of development should look like and how it may usefully be applied to research problems (further suggesting a means for evaluating general accounts of development). Reproduction also requires individuation of parent and offspring. We argue that there is no special problem of individuating older and younger clades. The vagaries involved with determining when clades begin, mature, and end are precisely the same as those that arise when the same questions are asked of cells, organisms, or species. Though the question of clade reproduction and selection may still be open, the process of discovery presents new insights into old problems. (shrink)

The notion of innateness is widely used, particularly in philosophy of mind, cognitive science and linguistics. Despite this popularity, it remains a controversial idea. This is partly because of the variety of ways in which it can be explicated and partly because it appears to embody the suggestion that we can determine the relative causal contributions of genes and environment in the development of biological individuals. As these causes are not independent, the claim is metaphysically suspect. This paper argues that (...) there is a plausible reconstruction of the notion of innateness. This involves defining it sufficiently broadly to cover most of the current usages as well as making it an informational rather than a causal property. This has two consequences. Firstly, innateness becomes a matter of degree. Secondly, we have to abandon the idea, originally proposed by ethologists, that innate traits are necessarily the products of genetic information. (shrink)

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

In a widely acclaimed study from 2002, researchers found a case of gene-environment interaction for a gene controlling neuroenzymatic activity (low vs. high), exposure to childhood maltreatment, and antisocial personality disorder (ASPD). Cases of gene-environment interaction are generally characterized as evincing a genetic predisposition; for example, individuals with low neuroenzymatic activity are generally characterized as having a genetic predisposition to ASPD. I first argue that the concept of a genetic predisposition fundamentally misconstrues these cases of gene-environment interaction. This misconstrual will (...) be diagnosed, and then a new concept—interactive predisposition—will be introduced. I then show how this conceptual shift reconfigures old questions and raises new questions for genetic screening. Attempts to screen embryos or fetuses for the gene associated with low neuroenzymatic activity with an eye towards selecting against the low-activity variant fall prey to the myth of pre-environmental prediction; attempts to screen newborns for the gene associated with low neuroenzymatic activity with an eye towards early intervention will have to face the interventionist’s dilemma. (shrink)

Phylogenetic information is often necessary to distinguish between evolutionary scenarios. Recently, some prominent proponents of evolutionary psychology have acknowledged this, and have claimed that such evidence has in fact been brought to bear on adaptive hypotheses involving complex human psychological traits. Were this possible, it would be a valuable source of evidence regarding hypothesized adaptive traits in humans. However, the structure of the Hominidae family makes this difficult or impossible. For many traits of interest, the closest extant relatives to the (...) human species are too phenotypically different from humans for such methods to provide meaningful data. While phylogenetic information can be useful for testing adaptive hypotheses in humans, these generally involve traits that are (a) not widely shared in the species or (b) fairly widely shared in the Hominidae family, and hence likely of a lower order of complexity than the sorts of traits evolutionary psychology has so far been interested in. (shrink)

The distinction between phenotype and genotype is fundamental to the understanding of heredity and development of organisms. The genotype of an organism is the class to which that organism belongs as determined by the description of the actual physical material made up of DNA that was passed to the organism by its parents at the organism's conception. For sexually reproducing organisms that physical material consists of the DNA contributed to the fertilized egg by the sperm and egg of its two (...) parents. For asexually reproducing organisms, for example bacteria, the inherited material is a direct copy of the DNA of its parent. The phenotype of an organism is the class to which that organism belongs as determined by the description of the physical and behavioral characteristics of the organism, for example its size and shape, its metabolic activities and its pattern of movement. (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)

Standard statistical measures of strength of association, although pioneered by Pearson deliberately to be acausal, nowadays are routinely used to measure causal efficacy. But their acausal origins have left them ill suited to this latter purpose. I distinguish between two different conceptions of causal efficacy, and argue that: 1) Both conceptions can be useful 2) The statistical measures only attempt to capture the first of them 3) They are not fully successful even at this 4) An alternative definition more squarely (...) based on causal thinking not only captures the second conception, it can also capture the first one better too. (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)

Selection explanations explain some non-accidental generalizations in virtue of a selection process. Such explanations are not particulaizable - they do not transfer as explanations of the instances of such generalizations. This is unlike many explanations in the physical sciences, where the explanation of the general fact also provides an explanation of its instances (i.e. standard D-N explanations). Are selection explanations (e.g. in biology) therefore a different kind of explanation? I argue that to understand this issue, we need to see that (...) a standard D-N explanation of some non-accidental generalization (al Fs are Gs) may also ipso facto explain its contrapositive (all non-Gs are non-Fs), but the explanation is particularizable with respect to the former but not to the latter. This can be seen by noting that the Raven Paradox counterexample to the H-D model of confirmation also generates a counterexample to the D-N model of explanation (all ravens are black does not explain why the non-black shoe is a non-raven). In such cases it is natural to take the generalization with the positive predicates to have a particularizable explanation. However, this need not be the case, and in selection explanations it is the generalization with the positive predicates whose explanation is no particularizable. Thus there is no need to suppose that selection explanations are fundamentally different. (shrink)

Edward O. Wilson's forays into human sociobiology have been the target of persistent, vehement attack by his Harvard colleague in evolutionary biology, Richard C. Lewontin. Through examination of existing documents in the case, together with in-depth personal interviews of Wilson, Lewontin, and other biologists, the reasons for Wilson's stance and Lewontin's criticisms are uncovered. It is argued that the dispute is not primarily personally or politically motivated, but involves a conflict between long-term scientific-cum-moral agendas, with the reductionist program as a (...) key issue. It is concluded that it is in the interest of both disputants to keep the controversy alive. (shrink)