Some prominent scientists and philosophers have stated openly that moral and political considerations should influence whether we accept or promulgate scientific theories. This widespread view has significantly influenced the development, and public perception, of intelligence research. Theories related to group differences in intelligence are often rejected a priori on explicitly moral grounds. Thus the idea, frequently expressed by commentators on science, that science is “self-correcting”—that hypotheses are simply abandoned when they are undermined by empirical evidence—may not be correct in all (...) contexts. In this paper, documentation spanning from the early 1970s to the present is collected, which reveals the influence of scientists’ moral and political commitments on the study of intelligence. It is suggested that misrepresenting findings in science to achieve desirable social goals will ultimately harm both science and society. (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)

For most of human history children have been a byproduct of sex rather than a conscious choice by parents to create people with traits that they care about. As our understanding of genetics advances along with our ability to control reproduction and manipulate genes, prospective parents have stronger moral reasons to consider how their choices are likely to affect their children, and how their children are likely to affect other people. With the advent of cheap and effective contraception, and the (...) emergence of new technologies for in vitro fertilization, embryo selection, and genetic engineering, it is becoming increasingly difficult to justify rolling the genetic dice by having children without thinking about the traits they will have. It is time to face up to the awesome responsibilities that accompany our reproductive choices. (shrink)

There are two ways evolution by natural selection is conceptualized in the literature. One provides a ‘recipe’ for ENS incorporating three ingredients: variation, differences in fitness, and heritability. The other provides formal equations of evolutionary change and partitions out selection from other causes of evolutionary changes such as transmission biases or drift. When comparing the two approaches there seems to be a tension around the concept of heritability. A recent claim has been made that the recipe approach is flawed and (...) should be abandoned. In this article, I show that the tension is only a superficial one. If one uses a concept of heritability strictly in line with the formal equations of evolutionary change, the recipe approach keeps its validity and generality. To demonstrate that the intuitive concept of heritability is not a general one, I use one formulation of the Price equation formulated by Okasha, show that the concept of heritability in his formulation incorporates both the intuitive notion of heritability as a measure of similarity between parent and offspring characters, and a measure of persistence. I advocate for persistence to be incorporated in the concept of heritability used in recipes for ENS in the same way heredity is, show that this is readily attainable and thereby dissolve any point of tension concerning heritability between the recipe and the analytical approach to ENS. 1 Introduction2 Heritability in the Price Equation2.1 Different approaches to heredity and heritability2.2 Heritability: From recipes to the Price equation3 A Problem for the Recipes?4 Reinterpreting Heritability for Recipes5 Conclusion Appendix. (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)

Gene–environment covariance is the phenomenon whereby genetic differences bias variation in developmental environment, and is particularly problematic for assigning genetic and environmental causation in a heritability analysis. The interpretation of these cases has differed amongst biologists and philosophers, leading some to reject the utility of heritability estimates altogether. This paper examines the factors that influence causal reasoning when G–E covariance is present, leading to interpretive disagreement between scholars. It argues that the causal intuitions elicited are influenced by concepts of agency (...) and blame-worthiness, and are intimately tied with the conceptual understanding of the phenotype under investigation. By considering a phenotype-specific approach, I provide an account as to why causal ascriptions can differ depending on the interpreter. Phenotypes like intelligence, which have been the primary focus of this debate, are more likely to spark disagreement for the interpretation of G–E covariance cases because the concept and ideas about its ‘normal development’ relatively ill-defined and are a subject of debate. I contend that philosophical disagreement about causal attributions in G–E covariance cases are in essence disagreements regarding how a phenotype should be defined and understood. This moves the debate from one of an ontological flavour concerning objective causal claims, to one concerning the conceptual, normative and semantic dependencies. (shrink)

Okasha claims at the outset of his book "Evolution and the Levels of Selection" that the Price equation lays bare the fundamentals underlying all selection phenomena. However, the thoroughness of his subsequent analysis of multi-level selection theories leads him to abandon his fundamentalist commitments. At critical points he invokes cost benefit analyses that sometimes favors the Price approach and sometimes the contextual approach, sometimes favors MLS1 and sometimes MLS2. And although he doesn’t acknowledge it, even the Price approach breaks down (...) into a family of alternative equations that parse the causes in different ways, none of which is uniquely correct and none of which achieves the ultimate isolation of effects due to what Okasha believes are the fundamental causes. I argue that his book provides good reason to re-conceive our understanding of evolutionary theorizing in terms of a toolbox view and to stop subjecting the analyses of evolutionary concepts to a universalist standard. (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)

Personalized genomics companies (PG; also called ‘direct-to-consumer genetics’) are businesses marketing genetic testing to consumers over the Internet. While much has been written about these new businesses, little attention has been given to their roles in science communication. This paper provides an analysis of the gene concept presented to customers and the relation between the information given and the science behind PG. Two quite different gene concepts are present in company rhetoric, but only one features in the science. To explain (...) this, we must appreciate the delicate tension between PG, academic science, public expectation, and market forces. (shrink)

According to the mainstream narrative about race, all groups have the same innate dispositions and potential, and all disparities—at least those favoring whites—are due to past or present racism. Some people who reject this narrative gravitate toward an alternative, anti-Jewish narrative, which sees recent history in terms of a Jewish/gentile conflict. The most sophisticated promoter of the anti-Jewish narrative is the evolutionary psychologist Kevin MacDonald. MacDonald argues that Jews have a suite of genetic adaptations—including high intelligence and ethnocentrism—and cultural practices (...) that lead them to undermine gentile society to advance their own evolutionary interests. He says that Jewish-designed intellectual movements have weakened gentile identity and culture while preserving Jewish identity and separatism. Cofnas recently argued that MacDonald’s theory is based on “systematically misrepresented sources and cherry-picked facts.” However, Cofnas gave short shrift to at least three key claims: Jews are highly ethnocentric, liberal Jews hypocritically advocate liberal multiculturalism for gentiles/gentile countries but racial purity and separatism for Jews/Israel, and Jews are responsible for liberalism and mass immigration to the United States. The present paper examines these claims and concludes that MacDonald’s views are not supported. (shrink)

Some authors defending the “hereditarian” hypothesis with respect to differences in average IQ scores between populations have argued that the sorts of environmental variation hypothesized by some researchers rejecting the hereditarian position should leave discoverable statistical traces, namely changes in the overall variance of scores or in variance–covariance matrices relating scores to other variables. In this paper, I argue that the claims regarding the discoverability of such statistical signals are broadly mistaken—there is no good reason to suspect that the hypothesized (...) environmental causes would leave detectable traces of the sorts suggested. As there remains no way to gather evidence that would permit the direct refutation of the environmental hypotheses, and no direct evidence for the hereditarian position, it remains the case, I argue, that the hereditarian position is unsupported by current evidence. (shrink)

ABSTRACTIn Darwinian Population and Natural Selection, Peter Godfrey-Smith brought the topic of natural selection back to the forefront of philosophy of biology, highlighting different issues surro...

The point Sesardic (Biol Philos 25: 143–162, 2010) makes about the possibility of distinguishing groups for which there is a lot of within-group variation is not sufficient to rehabilitate a biological concept of race. In this note, I sketch a number of issues that quickly arise once we delve more deeply into the relevant scientific knowledge, concepts, methods, and questions for inquiry.

The crucial problem in the philosophy of psychiatry is to determine under which conditions certain behaviors, mental states, and personality traits should be regarded as symptoms of mental illnesses. Participants in the debate can be placed on a continuum of positions. On the one side of the continuum, there are naturalists who maintain that the concept of mental illness can be explained by relying on the conceptual apparatus of the natural sciences, such as biology and neuroscience. On the other side (...) of the continuum, there are normativists who maintain that the appropriate characterization of the concept of mental illness cannot avoid reference to epistemic, moral and other social values. Although, this article is primarily an introduction to the debate, we stress the importance of the normativist positions. (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)

There is a tension between, on the one hand, the view that natural selection refers to individual-level causes, and on the other hand, the view that it refers to a population-level cause. In this article, I make the case for the individual-level cause view. I respond to recent claims made by McLoone that the individual-level cause view is inconsistent. I show that if one were to follow his arguments, any causal claim in any context would have to be regarded as (...) vindicating a form of population-level cause view. I show why this is implausible and how a consistent individual-level cause position can be held within the interventionist account of causation. Finally, I argue that there is one sense in which natural selection might be said to refer to population-level causes of evolutionary change. The upshot is that, as noted by others, natural selection can be regarded as referring to a population-level cause in the context of frequency-dependent selection and other situations of fitness-altering interactions between the individuals of a population. But whether this statement is true will depend on the empirical case investigated, not some a priori conceptual distinction. Thus, even though situations of frequency dependence might be ubiquitous, it is orthogonal to the conceptual question of whether frequency-independent natural selection—McLoone’s target—refers to individual- or population-level causes. (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)

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)

We often hear how scientists have discovered that a certain human trait – or a trait of another type of organism – is innate, genetic, heritable, inherited, naturally selected etc. All these claims have something in common: they all declare a trait to have significant organism internal (for instance genetic) causes that are present in the organism at its birth. I call claims like these “nativist claims”. Nativist claims are important. They shape our overall understanding of what we are, what (...) we can do and what is good for us. They also impact our practical decision making. For instance, we know that certain types of genes increase the risk of certain diseases, and increasingly this has an effect on healthcare practices. Many people believe that in the matter of children’s education we should consider the fact that many cognitive abilities are highly heritable. Associations between genetics and aggressive behavior have been taken to be alleviating circumstances in criminal sentencing. It is therefore important to correctly understand the content and implications of nativist claims. In this doctoral thesis I analyze, by philosophical means, the content of different kinds of nativist claim. What does it mean that some psychological tendency is innate? What does it mean that intelligence is 50% heritable? How (if at all) do genes come to carry information about the traits of an organism – they are nothing like the information carriers familiar to us, such as newspapers, e-mails, secret codes, and audio files. This thesis emphasizes two things. Firstly, I demonstrate, that in different scientific contexts these words ('innate', 'genetically caused' etc.) can mean very different things. Therefore, the implications of a given nativist claim in one scientific context can be remarkably different from another nativist claim’s implications in some other scientific context. Secondly, I explain how the development of innate, heritable and genetically caused traits can be determined in different and often unexpected ways by our environment and experiences. I demonstrate that the content of a concept that is considered innate by cognitive scientists can be determined by what the organism that possesses the concept has experienced. I also show that even a trait which is 100% heritable can at the same time be a socially constructed trait. (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)

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)

U svojoj inačici filozofije biologije Neven Sesardić izvodi dalekosežne moralne i političke posljedice određenih genetičkih istraživanja. On pretpostavlja da su uočene razlike u kvocijentu inteligencije između crnih i bijelih studenata urođene i da one ne mogu biti objašnjene niti promijenjene bilo kakvim utjecajem iz okoliša. Na toj osnovi on razvija teoriju o genetski određenoj inferiornosti crne rase. Teorija tvrdi da su svi podaci o društvenim i ekonomskim nedostatcima crne rase učinak njihovog lošeg biološkog nasljeđa, a ne društvene segregacije ili rasne (...) diskriminacije. Prema tome, bilo koja politika usmjerena na smanjivanje ili eliminiranje društvenih i ekonomskih razlika između siromašnih i bogatih ljudi, kao što je politika pozitivne diskriminacije, osuđena je na propast. U ovom se članku suprotstavljam Sesardićevu filozofskom tumačenju genetike i njegovim izvodima koji se tiču politike i društva. Pokazujem da mnogi relevantni genetičari ne prihvaćaju takvo filozofsko tumačenje i njegove političke posljedice. Suprotno Sesardićevoj tvrdnji da su svi environmentalisti zaraženi ljevičarskom političkom ideologijom, pokazujem da njih njihova znanstvena istraživanja, a ne apriorna politička uvjerenja, navode na odbacivanje jednostranih hereditarističkih filozofskih tumačenja i njihove političke primjene. Posebno sam usmjeren na povijest ropstva u Americi i na aktualne izvještaje o rasnoj diskriminaciji kao na važne elemente društvenog okoliša koji ne mogu biti zanijekani u bilo kojem ozbiljnom pokušaju objašnjavanja klasnih i rasnih odnosa u suvremenoj Americi. (shrink)