How should the concept of evidence be understood? And how does the concept of evidence apply to the controversy about creationism as well as to work in evolutionary biology about natural selection and common ancestry? In this rich and wide-ranging book, Elliott Sober investigates general questions about probability and evidence and shows how the answers he develops to those questions apply to the specifics of evolutionary biology. Drawing on a set of fascinating examples, he analyzes whether claims about intelligent design (...) are untestable; whether they are discredited by the fact that many adaptations are imperfect; how evidence bears on whether present species trace back to common ancestors; how hypotheses about natural selection can be tested, and many other issues. His book will interest all readers who want to understand philosophical questions about evidence and evolution, as they arise both in Darwin's work and in contemporary biological research. (shrink)

In Studying Human Behavior, Helen E. Longino enters into the complexities of human behavioral research, a domain still dominated by the age-old debate of “nature versus nurture.” Rather than supporting one side or another or attempting..

John Dupr explores recent revolutionary developments in biology and considers their relevance for our understanding of human nature and society. He reveals how the advance of genetic science is changing our view of the constituents of life, and shows how an understanding of microbiology will overturn standard assumptions about the living world.

Everyone has heard the claim, "Correlation does not imply causation." What might sound like a reasonable dictum metastasized in the twentieth century into one of science's biggest obstacles, as a legion of researchers became unwilling to make the claim that one thing could cause another. Even two decades ago, asking a statistician a question like "Was it the aspirin that stopped my headache?" would have been like asking if he believed in voodoo, or at best a topic for conversation at (...) a cocktail party rather than a legitimate target of scientific inquiry. Scientists were allowed to posit only that the probability that one thing was associated with another. This all changed with Judea Pearl, whose work on causality was not just a victory for common sense, but a revolution in the study of the world. (shrink)

Phenotypic plasticity integrates the insights of ecological genetics, developmental biology, and evolutionary theory. Plasticity research asks foundational questions about how living organisms are capable of variation in their genetic makeup and in their responses to environmental factors. For instance, how do novel adaptive phenotypes originate? How do organisms detect and respond to stressful environments? What is the balance between genetic or natural constraints (such as gravity) and natural selection? The author begins by defining phenotypic plasticity and detailing its history, including (...) important experiments and methods of statistical and graphical analysis. He then provides extended examples of the molecular basis of plasticity, the plasticity of development, the ecology of plastic responses, and the role of costs and constraints in the evolution of plasticity. A brief epilogue looks at how plasticity studies shed light on the nature/nurture debate in the popular media. (shrink)

Behaving presents an overview of the recent history and methodology of behavioral genetics and psychiatric genetics, informed by a philosophical perspective. Kenneth F. Schaffner addresses a wide range of issues, including genetic reductionism and determinism, "free will," and quantitative and molecular genetics. The latter covers newer genome-wide association studies that have produced a paradigm shift in the subject, and generated the problem of "missing heritability." Schaffner also presents cases involving pro and con arguments for genetic testing for IQ and for (...) Attention Deficit Hyperactivity Disorder. Schaffner examines the nature-nurture controversy and Developmental Systems Theory using C. elegans or "worm" studies as a test case, concluding that genes are special and provide powerful tools, including "deep homology," for investigating behavior. He offers a novel account of biological knowledge emphasizing the importance of models, mechanisms, pathways, and networks, which clarifies how partial reductions provide explanations of traits and disorders. The book also includes examinations of personality genetics and of schizophrenia and its etiology, alongside interviews with prominent researchers in the area, and discusses debates about psychosis that led to changes in the DSM-5 in 2013.Schaffner concludes by discussing additional philosophical implications of the genetic analyses in the book, some major worries about "free will," and arguments pro and con about why genes and DNA are so special. Though genes are special, newer perspectives presented in this book will be needed for progress in behavioral genetics- perspectives that situate genes in complex multilevel prototypic pathways and networks. With a mix of optimism and pessimism about the state of the field and the subject, Schaffner's book will be of interest to scholars in the history and philosophy of science, medicine, and psychiatry. (shrink)

Behavior genetics is a controversial science. For decades, scholars have sought to understand the role of heredity in human behavior and life-course outcomes. Recently, technological advances and the rapid expansion of genomic databases have facilitated the discovery of genes associated with human phenotypes such as educational attainment and substance use disorders. To maximize the potential of this flourishing science, and to minimize potential harms, careful analysis of what it would mean for genes to be causes of human behavior is needed. (...) In this paper, we advance a framework for identifying instances of genetic causes, interpreting those causal relationships, and applying them to advance causal knowledge more generally in the social sciences. Central to thinking about genes as causes is counterfactual reasoning, the cornerstone of causal thinking in statistics, medicine, and philosophy. We argue that within-family genetic effects represent the product of a counterfactual comparison in the same way as average treatment effects (ATEs) from randomized controlled trials (RCTs). Both ATEs from RCTs and within-family genetic effects are shallow causes: They operate within intricate causal systems (non-unitary), produce heterogeneous effects across individuals (non-uniform), and are not mechanistically informative (non-explanatory). Despite these limitations, shallow causal knowledge can be used to improve understanding of the etiology of human behavior and to explore sources of heterogeneity and fade-out in treatment effects. (shrink)

Traditionally a scientific theory is viewed as based on universal laws of nature that serve as axioms for logical deduction. In analyzing the logical structure of evolutionary biology, Elisabeth Lloyd argues that the semantic account is more appropriate and powerful. This book will be of interest to biologists and philosophers alike.

In this consensus report by a diverse group of academics who conduct and/or are concerned about social and behavioral genomics (SBG) research, the authors recount the often‐ugly history of scientific attempts to understand the genetic contributions to human behaviors and social outcomes. They then describe what the current science—including genomewide association studies and polygenic indexes—can and cannot tell us, as well as its risks and potential benefits. They conclude with a discussion of responsible behavior in the context of SBG research. (...) SBG research that compares individuals within a group according to a “sensitive” phenotype requires extra attention to responsible conduct and to responsible communication about the research and its findings. SBG research (1) on sensitive phenotypes that (2) compares two or more groups defined by (a) race, (b) ethnicity, or (c) genetic ancestry (where genetic ancestry could easily be misunderstood as race or ethnicity) requires a compelling justification to be conducted, funded, or published. All authors agree that this justification at least requires a convincing argument that a study's design could yield scientifically valid results; some authors would additionally require the study to have a socially favorable risk‐benefit profile. (shrink)

In this book, Neven Sesardic defends the view that it is both possible and useful to measure the separate contributions of heredity and environment to the explanation of human psychological differences. He critically examines the view - very widely accepted by scientists, social scientists and philosophers of science - that heritability estimates have no causal implications and are devoid of any interest. In a series of clearly written chapters he introduces the reader to the problems and subjects the arguments to (...) close philosophical scrutiny. His conclusion is that anti-heritability arguments are based on conceptual confusions and misunderstandings of behavioural genetics. His book is a fresh and compelling intervention in a very contentious debate. (shrink)

(Journal of Philosophy, 1988, 85:303-318).

Explores the political forces underlying shifts in thinking about the respective influence of heredity and environment in shaping human behavior, and the feasibility and morality of eugenics.

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...

Darwin's ideas on variation, heredity, and development differ significantly from twentieth-century views. First, Darwin held that environmental changes, acting either on the reproductive organs or the body, were necessary to generate variation. Second, heredity was a developmental, not a transmissional, process; variation was a change in the developmental process of change. An analysis of Darwin's elaboration and modification of these two positions from his early notebooks (1836-1844) to the last edition of the /Variation of Animals and Plants Under Domestication/ (1875) (...) complements previous Darwin scholarship on these issues. Included in this analysis is a description of the way Darwin employed the distinction between transmission and development, as well as the conceptual relationship he saw between heredity and variation. This paper is part of a larger project comparing commitments regarding variation during the latter half of the nineteenth century. (shrink)

August Weismann is famous for having argued against the inheritance of acquired characters. However, an analysis of his work indicates that Weismann always held that changes in external conditions, acting during development, were the necessary causes of variation in the hereditary material. For much of his career he held that acquired germ-plasm variation was inherited. An irony, which is in tension with much of the standard twentieth-century history of biology, thus exists – Weismann was not a Weismannian. I distinguish three (...) claims regarding the germ-plasm: (1) its continuity, (2) its morphological sequestration, and (3) its variational sequestration. With respect to changes in Weismann’s views on the cause of variation, I divide his career into four stages. For each stage I analyze his beliefs on the relative importance of changes in external conditions and sexual reproduction as causes of variation in the hereditary material. Weismann believed, and Weismannism denies, that variation, heredity, and development were deeply intertwined processes. This article is part of a larger project comparing commitments regarding variation during the latter half of the nineteenth century. (shrink)

This paper explores the interpretation and use of polygenic risk scores (PRSs). We argue that PRSs generally do not directly embody causal information. Nonetheless, they can assist us in tracking other causal relationships concerning genetic effects. Although their purely predictive/correlational use is important, it is this tracking feature that contributes to their potential usefulness in other applications, such as genetic dissection, and their use as controls, which allow us, indirectly, to "see" more clearly the role of environmental variables.

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)

Heritability estimates obtained from genome-wide association studies are much lower than those of traditional quantitative methods. This phenomenon has been called the “missing heritability problem.” By analyzing and comparing GWAS and traditional quantitative methods, we first show that the estimates obtained from the latter involve some terms other than additive genetic variance, while the estimates from the former do not. Second, GWAS, when used to estimate heritability, do not take into account additive epigenetic factors transmitted across generations, while traditional quantitative (...) methods do. Given these two points we show that the missing heritability problem can largely be dissolved. (shrink)

On the classical account of evolution by natural selection found in Lewontin and many subsequent authors, ENS is conceived as involving three key ingredients: phenotypic variation, fitness differences, and heredity. Through the analysis of three problem cases involving heredity, I argue that the classical conception is substantially flawed, showing that heredity is not required for selection. I consider further problems with the classical account of ENS arising from conflations between three distinct senses of the central concept of ‘fitness’ and offer (...) an alternative to the classical conception of ENS involving the interaction of distinct evolutionary mechanisms. (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)

Polygenic score (PGS) computations assume an additive model of gene action because associations between phenotypes and alleles at different loci are compounded, ignoring interactions between alleles or loci let alone between genotype and environment. Consequently, PGSs are subject to the same objections that invalidated traditional heritability analyses in the 1970s. Thus, PGSs should not be used in the social sciences.

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)

We argue that heritability estimates cannot be used to make informed judgments about the populations from which they are drawn. Furthermore, predicting changes in heritability from population changes is likely impossible, and of limited value. We add that the attempt to separate human environments into cultural and non-cultural components does not advance our understanding of the environmental multiplier effect.

The method in human genetics of ascribing causal responsibility to genotype by the use of heritability estimates has been heavily criticized over the years. It has been argued that these estimates are rarely valid and do not serve the purpose of tracing genetic causes. Recent contributions strike back at this criticism. I present and discuss two opposing views on these matters represented by Richard Lewontin and Neven Sesardic, and I suggest that some of the disagreement is based on differing concepts (...) of genetic causation. I use the distinction of structuring and triggering causes to help clarifying the basis for the opposing views. (shrink)

The critics of "hereditarianism" often claim that any attempt to explain human behavior by invoking genes is confronted with insurmountable methodological difficulties. They reject the idea that heritability estimates could lead to genetic explanations by pointing out that these estimates are strictly valid only for a given population and that they are exposed to the irremovable confounding effects of genotype-environment interaction and genotype-environment correlation. I argue that these difficulties are greatly exaggerated, and that we would be wrong to regard them (...) as presenting a fundamental obstacle to the search for genetic explanations. I also show that, to the extent they are cogent, these objections may prove to be even more damaging to the "environmentalist" standpoint. (shrink)

Contemporary Debates in Philosophy of Science contains sixteen original essays by leading authors in the philosophy of science, each one defending the affirmative or negative answer to one of eight specific questions, including: Are there laws of social science? Are causes physically connected to their effects? Is the mind a system of modules shaped by natural selection? Brings together fresh debates on eight of the most controversial issues in the philosophy of science. Questions addressed include: “Are there laws of social (...) science?”; “Are causes physically connected to their effects?”; “Is the mind a system of modules shaped by natural selection?” Each question is treated by a pair of opposing essays written by eminent scholars, and especially commissioned for the volume. Lively debate format sharply defines the issues, and paves the way for further discussion. Will serve as an accessible introduction to the major topics in contemporary philosophy of science, whilst also capturing the imagination of professional philosophers. (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)

Many cases of gene‐environment interaction, or , are misconstrued as evincing a genetic predisposition. I diagnose this misconstrual and then introduce a new concept— interactive predisposition —to correct for the mistake. I conclude by examining how recent debates over screening for individual predispositions are related to older debates about group differences between populations , drawing on the lessons of the latter to inform the former. †To contact the author, please write to: Department of Philosophy, University of Utah, Salt Lake City, (...) UT 84112; e‐mail: [email protected]. (shrink)

In 1875 Francis Galton was the first to study twins as a test of the relative strength of heredity and environment. This paper examines Galton's work on twins, using his surviving working papers. It shows that his enquiry was larger and more systematic than previously realized. Galton issued several hundred questionnaires to parents of twins, with the aim of establishing how far the similarities and differences between twins were affected by their life experiences. The paper also discusses Galton's study in (...) relation to his understanding of the physiology of twinning and his theory of heredity. The modern concept of monozygotic twins had not yet been established, and the similarity between Galton's work and modern twin studies should not be overstated. While Galton's work was important as a pioneering study, in some respects his conclusions went beyond his evidence. The paper finally examines whether Galton's twin studies influenced his position on the links between social class, heredity and social mobility, and surveys the evidence for his views on these issues. (shrink)