Heritability

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 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)

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)

Anxious temperament (AT) in human and non-human primates is a trait-like phenotype evident early in life that is characterized by increased behavioural and physiological reactivity to mildly threatening stimuli1–4. Studies in children demonstrate that AT is an important risk factor for the later development of anxiety disorders, depression and comorbid substance abuse5. Despite its importance as an early predictor of psychopathology, little is known about the factors that predispose vulnerable children to develop AT and the brain systems that underlie its (...) expression. To characterize the neural circuitry associated with AT and the extent to which the function of this circuit is heritable, we studied a large sample of rhesus monkeys phenotyped for AT. Using 238 young monkeys from a multigenerational single-family pedigree, we simultaneously assessed brain metabolic activity and AT while monkeys were exposed to the relevant ethological condition that elicits the phenotype. High-resolution 18F-labelled deoxyglucose positron-emission tomography (FDG–PET) was selected as the imaging modality because it provides semi-quantitative indices of absolute glucose metabolic rate, allows for simultaneous measurement of behaviour and brain activity, and has a time course suited for assessing temperament-associated sustained brain responses. Here we demonstrate that the central nucleus region of the amygdala and the anterior hippocampus are key components of the neural circuit predictive of AT. We also show significant heritability of the AT phenotype by using quantitative genetic analysis. Additionally, using voxelwise analyses, we reveal significant heritability of metabolic activity in AT-associated hippocampal regions. However, activity in the amygdala region predictive of AT is not significantly heritable. Furthermore, the heritabilities of the hippocampal and amygdala regions significantly differ from each other. Even though these structures are closely linked, the results suggest differential influences of genes and environment on how these brain regions mediate AT and the ongoing risk of developing anxiety and depression. Anxiety disorders are among the most common forms of psychopathology6, and frequently begin during childhood and adolescence. Although all children experience acute anxiety, children with AT display extreme behavioural and physiological reactivity to novel stimuli, and in the presence of strangers inhibit their locomotor activity and vocalizations3.. (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)

In "The pitfalls of heritability," a review of Edward O. Wilson’s Consilience Times Literary Supplement, Feb 12, 1999, p33], Jerry Hirsch claims to have convicted Wilson of a "confusion about genetic similarity and difference." In his book, Wilson claims that if we assume that "a mere one thousand genes out of the fifty to a hundred thousand genes in the human genome were to exist in two forms in the population," the probability of any two humans--excluding identical siblings--having the same (...) genotype is vanishingly small. Hirsch points out that a single genotype can be produced in more than one way, thus increasing the likelihood of a single genotype recurring in the human population. Hirsch’s point is fair enough as far it goes, but it does not go nearly far enough. Hirsch has failed to carry out all the relevant calculations needed to determine the probability of two humans having the same genotype. In the realm of Vast numbers ("Very much greater than ASTronomical"--Dennett, 1995, p109), increased likelihood in and of itself tells us nothing. Here, then, are some of the relevant calculations. (shrink)

This paper examines some criticisms that have been made of two standard genetic methodologies: heritability and path analysis. I conclude that the criticisms should be taken seriously, concerning both the accuracy of heritability measures and their significance. In light of the fact that such studies remain prominent in the literature, I consider what possible rationale they can retain consistent with these criticisms. In particular, I consider (1) a role in the identification of high-risk individuals and (2) a heuristic role in (...) the planning of research strategy. (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)

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)

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)

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)

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)

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)

It is impossible to discuss the constructs and in a single coherent essay. The following three rejoinders address each of these exceedingly complex constructs individually, as each relates to the two-path model of sociopathy and psychopathy.

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)

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.

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)

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)

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)

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 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)

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)

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)

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 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)

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 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)

The derivation of heritability from human twin studies involves serious methodological flaws. Heritability is consistently overestimated because of biological confounds of twinning, consistent and often gross underestimation of the environmental variance, and nonadditive genetic influences that can hugely exaggerate heritability values. Despite this bad research design, behaviour geneticists continue to publish results implying that their heritability results are valid.

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)

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)