Heritability

This paper discusses the widespread use of heritability calculations in recent behaviour research including behaviour genetics. In the sequel, a radical criticism concerning the basic axioms of the underlying, more general concept itself is presented. The starting point for testing the proclaimed universal validity of this concept stems from a fictitious yet realistic example taken from learning research. The theoretical result, based on the application of the conventional reasoning in this field, states that developmental processes — and learning is only (...) one specific case out of an immense number of similar behavioural mechanisms — can neither be adequately described nor causally explained with sufficient reliability within the context of the heredity paradigm. On the contrary, an inherent inconsistency of the concept itself when applied to behaviour processes is demonstrated. Finally, a conceptual alternative involving a systems-theoretical approach to the problem is presented: In such a perspective it is the concept of cognition which represents the adequate explanatory theorem - a theorem in which quantitative processing of information from the environment is clearly revealed to belong to a subordinate level of living organization. (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)

Most behavioural genetic studies focus on genetic and environmental influences on inter-individual phenotypic differences at the population level. The growing collection of intensive longitudinal data in social and behavioural science offers a unique opportunity to examine genetic and environmental influences on intra-individual phenotypic variability at the individual level. The current study introduces a novel idiographic approach and one novel method to investigate genetic and environmental influences on intra-individual variability by a simple empirical demonstration. Person-specific non-shared environmental influences on intra-individual variability (...) of daily school feelings were estimated using time series data from twenty-one pairs of monozygotic twins over two consecutive weeks. Results showed substantial inter-individual heterogeneity in person- specific non-shared environmental influences. The current study represents a first step in investigating environmental influences on intra-individual variability with an idiographic approach, and provides implications for future behavioural genetic studies to examine developmental processes from a microscopic angle. (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)

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)

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)

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)

Inbreeding introduced by R. Bakewell (1725-1795) in England for creating new animal races, was opposed by animal breeders on the Continent on religious grounds, and was soon introduced in sheep breeding for wool production in Moravia. In 1790-1840 the protagonists repeatedly rejected 'the spectre of inbreeding' and included consanguineous matching in scientific breeding. In 1836 they even formulated the research question of heredity and next year proposed the inductive method for its investigation. The achievements of sheep breeders instigated German breeders (...) to reject the dogma of the constancy of race and to elaborate the theory of individual potency. Treating heredity as the force under the influence of environment they could not solve the enigma. The question formulated in 1836 was explained in 1865 by Gregor Mendel. His theory was not perceived by animal breeders as well as by biologists up to the end of the century. (shrink)

In a previous study, using experimental metapopulations of the flour beetle, Tribolium castaneum, we investigated phase III of Wright's shifting balance process (Wade and Griesemer 1998). We experimentally modeled migration of varying amounts from demes of high mean fitness into demes of lower mean fitness (as in Wright's characterization of phase III) as well as the reciprocal (the opposite of phase III). We estimated the meta-populational heritability for this level of selection by regression of offspring deme means on the weighted (...) parental deme means.Here we develop a Punnett Square representation of the inheritance of the group mean to place our empirical findings in a conceptual context similar to Mendelian inheritance of individual traits. The comparison of Punnett Squares for individual and group inheritance shows how the latter concept can be rigorously defined and extended despite the lack of explicitly formulated, simple Mendelian laws of inheritance at the group level. Whereas Wright's phase III combines both interdemic selection and meta-populational inheritance, our formulation separates the issue of meta-populational heritability from that of interdemic selection. We use this conceptual context to discuss the controversies over the levels of selection and the units of inheritance. (shrink)

The difference in formulation of the question of heredity on a different level of knowledge in Brno in the 1830s and after 1850 is discussed in this article. In order to solve the problem the most important source is forshown in the new philosophy of plant physiology and in physics. Mendel was pleased to have met excellent teachers of both these fields. This explanation is an example of Mirko Grmek's thesis: 'l'histoire des sciences est le laboratoire de l'épistomologie'.

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)

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)

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 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.

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 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)

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)

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)

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)

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)

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)

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)

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.

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)

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)

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)

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)

Heriditary, innate, genetical are three different concepts of which the meanings are different but, since obviously related, are often used one for the other, for they are all three used in opposition to acquired or what is called environmental factors. What is acquired is linked to the environment: what is not innate (hereditary, genetical, ...) is acquired and what is acquired cannot be so but through the environment. Thus,innate (hereditary, genetical, ...) andacquired correspond to the usual opposition betweeninside andoutside.This is (...) an abstract, if rather caricatural not untrue, description of the use of these concepts in modern biology, especially after August Weismann (1834–1914) who emphasized the distinction betweensoma andgermen. (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)

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)

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)