Heritability

Fisher’s 1918 paper accomplished two distinct goals: unifying discrete Mendelian genetics with continuous biometric phenotypes and quantifying the variance components of variation in complex human characteristics. The former contributed to the foundation of modern quantitative genetics; the latter was adopted by social scientists interested in the pursuit of Galtonian nature-nurture questions about the biological and social origins of human behavior, especially human intelligence. This historical divergence has produced competing notions of the estimation of variance ratios referred to as heritability. Jay (...) Lush showed that they could be applied to selective breeding on the farm, while the early twin geneticists used them as a descriptive statistic to describe the degree of genetic determination in complex human traits. Here we trace the early history of the heritability coefficient now used by social scientists. (shrink)

Gene centrism is the idea that genes have a privileged causal role in the ontogeny of phenotypes. It has traditionally been defended on the grounds that genetic causation is a special kind of causation. According to this viewpoint, genes are special causal agents because they carry the information to build the organism. The recent trend in the philosophy of biology is to replace informational concepts with causal ones. Specific influence of genes in the production of RNA and proteins has received (...) much attention. However, the history of genetics shows that gene centrism concerns not only the most proximate effects of genes, but also higher level phenotypes and the kind of specificity required to justify gene centrism must extend beyond proteins and RNAs. The missing heritability problem implies that it is no easy task to find specific causal relations between genomes and phenotypes. It seems to be the case that thousands of genes somehow influence variation in any complex trait and genomic findings offer no clear-cut mechanistic explanation. Thus, causal specificity concepts currently employed in philosophy are inadequate for answering the substantive problem of genotype-phenotype relations. (shrink)

Reichenbach’s early solution to the scientific problem of how abstract mathematical representations can successfully express real phenomena is rooted in his view of coordination. In this paper, I claim that a Reichenbach-inspired, ‘layered’ view of coordination provides us with an effective tool to systematically analyse some epistemic and conceptual intricacies resulting from a widespread theorising strategy in evolutionary biology, recently discussed by Okasha (2018) as ‘endogenization’. First, I argue that endogenization is a form of extension of natural selection theory that (...) comprises three stages: quasi-axiomatisation, functional extension, and semantic extension. Then, I argue that the functional extension of one core principle of natural selection theory, namely, the principle of heritability, requires the semantic extension of the concept of inheritance. This is because the semantic extension of ‘inheritance’ is necessary to establish a novel form of coordination between the principle of heritability and the extended domain of phenomena that it is supposed to represent. Finally, I suggest that – despite the current lack of consensus on the right semantic extension of ‘inheritance’ – we can fruitfully understand the reconceptualization of ‘inheritance’ provided by niche construction theorists as the result of a novel form of coordination. (shrink)

ITA: In questo articolo analizzerò la differenza tra il concetto di ereditarietà e quello di ereditabilità. In primo luogo, evidenzierò come i due concetti derivino storicamente da differenti tradizioni nello studio della variabili-tà fenotipica e del rapporto genotipo-fenotipo. Secondariamente, illustrerò gli aspetti teorici e metodologici alla base dei due concetti, che sono peraltro collegati a differenti aree delle scienze biologiche. Infine, spigherò brevemente come si sia recentemente tentato, con molte difficoltà, di connettere lo studio dei meccanismi dell’ereditarietà allo studio dell’ereditabilità. (...) Nel discutere le questioni di cui sopra, farò riferimento a tratti psi-cologici come l’intelligenza dal momento che è proprio dallo studio di questo tipo di tratti che sono emersi i maggiori problemi teorici e metodologici, nonché le controversie più intense. -/- ENG: In this paper, I analyse the distinction between heredity and heritability. First, I highlight that the two con-cepts derive from different historical traditions in the study of phenotypic variability and of the genotype-phenotype relationship. Second, I illustrate the theoretical and methodological aspects connected to the two concepts, which are traditionally associated with different areas of biological research. Then, I focus on recent attempts aimed at connecting with each other the analysis of heredity and of heritability. In my discussion, I shall often refer to human psychological traits such as intelligence. Indeed, most theoretical and methodological dis-cussions have emerged with respect to the study of these traits. (shrink)

In this chapter, I am concerned with the concept of Intra-individual Genetic Hetereogeneity (IGH) and its potential influence on biodiversity estimates. Definitions of biological individuality are often indirectly dependent on genetic sampling -and vice versa. Genetic sampling typically focuses on a particular locus or set of loci, found in the the mitochondrial, chloroplast or nuclear genome. If ecological function or evolutionary individuality can be defined on the level of multiple divergent genomes, as I shall argue is the case in IGH, (...) our current genetic sampling strategies and analytic approaches may miss out on relevant biodiversity. Now that more and more examples of IGH are available, it is becoming possible to investigate the positive and negative effects of IGH on the functioning and evolution of multicellular individuals more systematically. I consider some examples and argue that studying diversity through the lens of IGH facilitates thinking not in terms of units, but in terms of interactions between biological entities. This, in turn, enables a fresh take on the ecological and evolutionary significance of biological diversity. (shrink)

The model of human intelligence that is most widely adopted derives from psychometrics and behavioral genetics. This standard approach conceives intelligence as a general cognitive ability that is genetically highly heritable and describable using quantitative traits analysis. The paper analyzes intelligence within the debate on natural kinds and contends that the general intelligence conceptualization does not carve psychological nature at its joints. Moreover, I argue that this model assumes an essentialist perspective. As an alternative, I consider an HPC theory of (...) intelligence and evaluate how it deals with essentialism and with intuitions coming from cognitive science. Finally, I highlight some concerns about the HPC model as well, and conclude by suggesting that it is unnecessary to treat intelligence as a kind in any sense. (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)

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)

In evolutionary models of indirect reciprocity, reputation mechanisms can stabilize cooperation even in severe cooperation problems like the prisoner’s dilemma. Under certain circumstances, conditionally cooperative strategies, which cooperate iff their partner has a good reputation, cannot be invaded by any other strategy that conditions behavior only on own and partner reputation. The first point of this paper is to show that an evolutionary version of backward induction can lead to a breakdown of this kind of indirectly reciprocal cooperation. Backward induction, (...) however, requires strategies that count and then cease to cooperate in the last, last but one, last but two, … game they play. These strategies are unlikely to exist in natural settings. We then present two new findings. (1) Surprisingly, the same kind of breakdown is also possible without counting. Strategies using rare golden opportunities for defection can invade conditional cooperators. This can create further golden opportunities, inviting the next wave of opportunists, and so on, until cooperation breaks down completely. (2) Cooperation can be stabilized against these opportunists, by letting an individual’s initial reputation be inherited from that individual’s parent. This ‘inclusive reputation’ mechanism can cope with any observably opportunistic strategy. Offspring of opportunists who successfully exploited a conditional cooperator cannot repeat their parents’ success because they inherit a bad reputation, which forewarns conditional cooperators in later generations. (shrink)

In this paper I use a case study—the discovery of the chaperon function exerted by proteins in the various steps of the hereditary process—to re-discuss the question whether the nucleic acids are the sole repositories of relevant information as assumed in the information theory of heredity. The evidence I here present of a crucial role for molecular chaperones in the folding of nascent proteins, as well as in DNA duplication, RNA folding and gene control, suggests that the family of proteins (...) acting as molecular chaperones provides information that is complementary to that stored in the nucleic acids, and equally important. A re-evaluation of the role of proteins in the hereditary process is in order away from the gene-centric approach of the information theory of heredity, to which neo-Darwinian evolutionists adhere. (shrink)

Many things evolve: species, languages, sports, tools, biological niches, and theories. But are these real instances of natural selection? Current assessments of the proper scope of Darwinian theory focus on the broad similarity of cultural or non-organic processes to familiar central instances of natural selection. That similarity is analysed in terms of abstract functional descriptions of evolving entities (e.g. replicators, interactors, developmental systems etc). These strategies have produced a proliferation of competing evolutionary analyses. I argue that such reasoning ought not (...) to be employed in arbitrating debates about whether particular phenomena count as instances of natural selection. My argument is based on hierarchical functional descriptions of natural selection. I suggest that natural selection ought not to be thought of as a single process but rather as a series of processes which can be analysed in terms of a hierarchy of functional descriptions (in much the same way as many people think of cognition). This, in turn, casts doubt on the idea that it is possible in principle to settle debates about whether particular phenomena count as instances of natural selection. (shrink)

Behavioural phenotypes have been explained by genetic and environmental factors (E) and their interaction. Here we suggest a rethinking of the E factor. Passively incurred environmental influences (E pass) and actively copied information and behaviour (E act) may be distinguished at shared and non-shared level. We argue that E act underlies mutation and selection and is the base of gene-independent heritability.

The book aims to offer a contribution to the historiographical and conceptual reconfiguration of the evolutionary revolution in the light of the centuries-old tenets of the Aristotelian biological tradition. Darwin’s breakthrough constitutes a thorough overturning of the fixist, essentialist and teleological framework created by Aristotle, a framework still dominant in the 17th Century world of Harvey and Ray, as well as Galileo, and then hegemonic until Linnaeus and Cuvier. This change is exemplified in the morphological analysis of useless parts, such (...) as the sightless eyes of moles, already discussed by Aristotle, and which Darwin used almost like a crowbar to unhinge the systematic recourse to final causes. This is an ancient teleological heritage present in various forms in the concept of natural selection, but by then confined within an eminently historical framework open to randomness. Un contributo alla riconfigurazione storiografica e concettuale della rivoluzione evoluzionistica alla luce della tenuta plurisecolare della tradizione biologica aristotelica. La svolta di Darwin si delinea quale puntuale rovesciamento dell'impianto fissista, essenzialista e teleologico coniato da Aristotele, ancora dominante nel Seicento di Harvey e di Ray, nonostante Galileo, e poi egemone fino a Linneo e Cuvier. Svolta esemplificata dall'analisi morfologica delle parti inutili, come gli occhi ciechi della talpa, tematizzate già da Aristotele, e che Darwin usò quale grimaldello per scardinare il ricorso sistematico alle cause finali. Antica eredità teleologica presente in varie forme nel concetto di selezione naturale, ma ormai calata entro una griglia eminentemente storica e aperta alla casualità. (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)

According to a once influential view of selection, it consists of repeated cycles of replication and interaction. It has been argued that this view is wrong: replication is not necessary for evolution by natural selection. I analyze the nine most influential arguments for this claim and defend the replication–interaction conception of selection against these objections. In order to do so, however, the replication–interaction conception of selection needs to be modified significantly. My proposal is that replication is not the copying of (...) an entity, the replicator, but the copying of a property. Thus, we can have a replication process without there being a replicator that is being copied. (shrink)

Commentary on Bergstrom and Rosvall, ‘The transmission sense of information’, Biology and Philosophy. In response to worries that uses of the concept of information in biology are metaphorical or insubstantial, Bergstrom and Rosvall have identified a sense in which DNA transmits information down the generations. Their ‘transmission view of information’ is founded on a claim about DNA’s teleofunction. Bergstrom and Rosvall see their transmission view of information as a rival to semantic accounts. This commentary argues that it is complementary. The (...) idea that DNA is transmitting information down the generations only makes sense if it is carrying a message, that is to say if it has semantic content. (shrink)

Inheritance and variation were a major focus of Charles Darwin’s studies. Small inherited variations were at the core of his theory of organic evolution by means of natural selection. He put forward a developmental theory of heredity (pangenesis) based on the assumption of the existence of material hereditary particles. However, unlike his proposition of natural selection as a new mechanism for evolutionary change, Darwin’s highly speculative and contradictory hypotheses on heredity were unfruitful for further research. They attempted to explain many (...) complex biological phenomena at the same time, disregarded the then modern developments in cell theory, and were, moreover, faithful to the widespread conceptions of blending and so-called Lamarckian inheritance. In contrast, Mendel’s approaches, despite the fact that features of his ideas were later not found to be tenable, proved successful as the basis for the development of modern genetics. Mendel took the study of the transmission of traits and its causes (genetics) out of natural history; by reducing complexity to simple particulate models, he transformed it into a scientific field of research. His scientific approach and concept of discrete elements (which later gave rise to the notion of discrete genes) also contributed crucially to the explanation of the existence of stable variations as the basis for natural selection. © Springer Science+Business Media B.V. 2010. (shrink)

Japanese agricultural scientist Toyama Kametaro's report about the Mendelian inheritance of silkworm cocoon color in Studies on the Hybridology of Insects (1906) spurred changes in Japanese silk production and thrust Toyama and his work into a scholarly exchange with American entomologist Vernon Kellogg. Toyama's work, based on research conducted in Japan and Siam, came under international scrutiny at a time when analyses of inheritance flourished after the "rediscovery" of Mendel's laws of heredity in 1900. The hybrid silkworm studies in Asia (...) attracted the attention of Kellogg, who was concerned with how experimental biology would be used to study the causes of natural selection. He challenged Toyama's conclusions that Mendelism alone could explain the inheritance patterns of silkworm characters such as cocoon color because they had been subject to hundreds of years of artificial selection, or breeding. This examination of the intersection of Japanese sericulture and American entomology probes how practical differences in scientific interests, societal responsibilities, and silkworm materiality were negotiated throughout the processes of legitimating Mendelian genetics on opposite sides of the Pacific. The ways in which Toyama and Kellogg assigned importance to certain silkworm properties show how conflicting intellectual orientations arose in studies of the same organism. Contestation about Mendelism took place not just on a theoretical level, but the debate was fashioned through each scientist's rationale about the categorization of silkworm breeds and races and what counted as "natural." This further mediated the acceptability of the silkworm not as an experimental organism, but as an appropriately "natural" insect with which to demonstrate laws of inheritance. All these shed light on the challenges that came along with the use of agricultural animals to convincingly articulate new biological principles. (shrink)

Political imputations in science are notoriously a tricky business. I addressed this issue in the context of the nature–nurture debate in the penultimate chapter of my book Making Sense of Heritability (Cambridge U. P. 2005). Although the book mainly dealt with the logic of how one should think about heritability of psychological differences, it also discussed the role of politics in our efforts to understand the dynamics of that controversy. I first argued that if a scholar publicly defends a certain (...) view (say, hereditarianism) in the debate about IQ, race and genetics this fact alone cannot justify attributing a political motivation to that person. But then later I suggested that the pressure of political correctness could explain some peculiarities of the contemporary controversy about the heritability of group differences in IQ. Several reviewers of my book raised a tu quoque objection. Am I not doing here the same thing that I condemn others for? (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)

Many natural and biological phenomena can be depicted as networks. Theoretical and empirical analyses of networks have become prevalent. I discuss theoretical biases involved in the delineation of biological networks. The network perspective is shown to dissolve the distinction between regulatory architecture and regulatory state, consistent with the theoretical impossibility of distinguishing a priori between “program” and “data”. The evolutionary significance of the dynamics of trans-generational and inter-organism regulatory networks is explored and implications are presented for understanding the evolution of (...) the biological categories development-heredity; plasticity-evolvability; and epigenetic-genetic. (shrink)

An important historical relation that has hardly been addressed is the influence of Prosper Lucas's Treatise on Natural Inheritance on the development of Charles Darwin's concepts related to inheritance. In this article we trace this historical connection. Darwin read Lucas's Treatise in 1856. His reading coincided with many changes concerning his prior ideas on the transmission and expression of characters. We consider that this reading led him to propose a group of principles regarding prepotency, hereditary diseases, morbid tendencies and atavism; (...) following Lucas, he called these principles: laws of inheritance. (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)

The dichotomy between Nature and Nurture, which has been dismantled within the framework of development, remains embodied in the notions of plasticity and evolvability. We argue that plasticity and evolvability, like development and heredity, are neither dichotomous nor distinct: the very same mechanisms may be involved in both, and the research perspective chosen depends to a large extent on the type of problem being explored and the kinds of questions being asked. Epigenetic inheritance leads to transgenerationally extended plasticity, and developmentally-induced (...) heritable epigenetic variations provide additional foci for selection that can lead to evolutionary change. Moreover, hereditary innovations may result from developmentally induced large-scale genomic repatterning events, which are akin to Goldschmidtian “systemic mutations”. The epigenetic mechanisms involved in repatterning can be activated by both environmental and genomic stress, and lead to phylogenetic as well as ontogenetic changes. Hence, the effects and the mechanisms of plasticity directly contribute to evolvability. (shrink)

In recent years, biologists have increasingly been asking whether the ability to evolve — the evolvability — of biological systems, itself evolves, and whether this phenomenon is the result of natural selection or a by-product of other evolutionary processes. The concept of evolvability, and the increasing theoretical and empirical literature that refers to it, may constitute one of several pillars on which an extended evolutionary synthesis will take shape during the next few years, although much work remains to be done (...) on how evolvability comes about. (shrink)

Despite a long history of debates about the heritability of human traits by researchers and other critical commentators, the possible heterogeneity of genetic and environmental factors that underlie patterns in observed traits has not been recognized as a significant conceptual and methodological issue. This article is structured to stimulate a wide range of readers to pursue diverse implications of underlying heterogeneity and of its absence from previous debates. Section 1, a condensed critique of previous conceptualizations and interpretations of heritability studies, (...) consists of three core propositions centered on heterogeneity and six supplementary propositions. Reference is made to agricultural evaluation trials in which a number of different genetically replicable varieties are raised in multiple replicates in one or more locations. In such analyses, the best case for illuminating genetic and environmental factors can be achieved; analyses in human genetics, in contrast, fall far short of the ideal. Section 2 identifies a wide range of questions that invite philosophical, historical, sociological, and scientific inquiry. These are organized under four headings: debate over the conceptual implications of heterogeneity; history of translation of methods from agriculture and laboratory breeding into human genetic analysis; racialized imaginaries in the analysis of differences among groups; and areas of scientific inquiry that may allow more attention to underlying heterogeneity. (shrink)

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)

Estimates of a trait’s heritability can be used to predict the advance through selective breeding in agriculture and the laboratory where researchers can replicate varieties and locations. These conditions do not apply to human populations, yet considerable attention is still given to high heritability and to small effects of family members growing up together relative to differences within families. This article shows that the conventional partitioning of a trait’s variation produces components that cannot be associated reliably with average differences among (...) varieties and locations , let alone underwrite hypotheses about measurable genetic and environmental influences. (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)

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. This two-component argument cannot be sustained when viewed in the light of the conceptual and methodological themes introduced in Taylor . These themes concern the difficulties of moving from the statistical analysis of variance of observed traits (...) to investigation of measurable genetic factors and measurable environmental factors. One such theme is that quantities estimated by an AOV of observed traits cannot be equated with measurable genetic or environmental factors involved in the development of those traits. Once this distinction is clear, the argument that environmental factors have failed to explain the differences lacks weight because it does not consider whether genetic factors have been more successful. This article exposes additional flaws in the lines of thinking associated with the two-component argument, with the distinction between passive, reactive, and active associations between genetic and environmental factors, and with the reciprocal causation models Dickens and Flynn propose in order to reconcile high estimates of heritability and large IQ test score gains between generations. Human heritability estimates are irrelevant in developing explanations of differences across groups or across generations. My critique is directed at opening up more conceptual space for deriving empirically validated models of developmental pathways whose components are heterogeneous and differ among individuals at any one time and over generations. (shrink)

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)

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)

This paper investigates the role of the concept of group heritability in group selection theory, in relation to the well-known distinction between type 1 and type 2 group selection (GS1 and GS2). I argue that group heritability is required for the operation of GS1 but not GS2, despite what a number of authors have claimed. I offer a numerical example of the evolution of altruism in a multi-group population which demonstrates that a group heritability coefficient of zero is perfectly compatible (...) with the successful operation of group selection in the GS2 sense. A diagnosis of why group heritability has wrongly been regarded as necessary for GS2 is suggested. (shrink)

Genetic differences can lead to phenotypic differences either directly or indirectly (via causing differences in external environments, which then affect phenotype). This possibility of genetic effects being mediated by environmental influences is often used by scientists and philosophers to argue that heritability is not a very helpful causal or explanatory notion. In this paper it is shown that these criticisms are based on serious misconceptions about methods of behavior genetics.

The aim of this paper is to outline a typologyof selection processes, and show that differentsub-categories have different explanatorypower. The basis of this typology of selectionprocesses is argued to be the difference ofreplication processes involved in them. Inorder to show this, I argue that: 1.Replication is necessary for selection and 2.Different types of replication lead todifferent types of selection. Finally, it isargued that this typology is philosophicallysignificant, since it contrasts cases ofselection (on the basis of the replicationprocesses involved in them) (...) whereby selectioncauses adaptation – and, therefore, can beused in explanations of the (real or apparent)teleology of Nature – and cases in whichselection lacks such explanatory power. (shrink)