The idea that some characteristics of an organism are explained by the organism's intrinsic nature, whilst others reflect the influence of the environment is an ancient one. It has even been argued that this distinction is itself part of the evolved psychology of the human species. The distinction played an important role in the history of philosophy as the locus of the dispute between Rationalism and Empiricism discussed in another entry in this encyclopedia. This entry, however, focuses on twentieth-century accounts (...) of the innate/acquired distinction. These accounts have for the most part been inspired by the sciences of mind and behaviour. (shrink)

Lorenz proposed in his (1935) articulation of a theory of behavioral instincts that the objective of ethology is to distinguish behaviors that are “innate” from behaviors that are “learned” (or “acquired”). Lorenz’s motive was to open the investigation of certain “adaptive” behaviors to evolutionary theorizing. Accordingly, since innate behaviors are “genetic”, they are open to such investigation. By Lorenz’s light an innate/acquired or learned dichotomy rested on a familiar Darwinian distinction between genes and environments. (...) Ever since Lorenz, ascriptions of innateness have become widespread in the cognitive, behavioral, and biological sciences. The trend continues despite decades of strong arguments that show, in particular, the dichotomy that Lorenz invoked in his theory of behavioral instincts is literally false: no biological trait is the product of genes alone. Some critics suggest that the failure of Lorenz’s account shows that innateness is not well-defined in biology and the practice of ascribing innateness to various biological traits should be dropped from respectable science. Elsewhere (Ariew 1996) I argued that despite the arguments of critics, there really is a biological phenomenon underlying the concept of innateness. On my view, innateness is best understood in terms of C.H. Waddington’s concept of “canalization”, i.e. the degree to which a trait is innate is the degree to which its developmental outcome is canalized. The degree to which a developmental outcome is canalized is the degree to which the developmental process is bound to produce a particular endstate despite environmental fluctuations both in the development’s initial state and during the course of development. The canalization account differs in many ways to the traditional ways that ethologists such as Konrad Lorenz originally understood the concept of innateness. Most importantly, on the canalization account the distinction between innate and acquired is not a dichotomy, as Konrad Lorenz had it, but rather a matter of degree difference that lies along a spectrum with highly canalized development outcomes on the one end and highly environmentally sensitive development outcomes on the other end. Nevertheless, I justified the canalization account on the basis of a set of desiderata or criteria that I suggested falls-out of what seemed uncontroversial about Lorenz’s account of innateness (briefly): innateness is a property of a developing individual, innateness denotes environmental stability, and innate-ascriptions are useful in certain natural selection explanations (more below). From that same set of desiderata I argued (in my 1996) that neither the concept of heritability nor of norms of reactions—two concepts from population genetics—suffice to ground innateness. In this essay, I wish to provide further support of the canalization account in two ways. First, I wish to better motivate the desiderata by revisiting a debate between Konrad Lorenz and Daniel Lehrman over the meaning and explanatory usefulness of innate ascriptions in ethology. Second, I wish to compare my canalization account of innateness with accounts proposed by contemporary philosophers, one by Stephen Stich (1975), another by Elliott Sober (forthcoming), and a third by William Wimsatt (1986). (shrink)

The concept of innateness is used to make inferences between various better-understood properties, like developmental canalization, evolutionary adaptation, heritability, species-typicality, and so on (‘innateness-related properties’). This article uses a recently-developed account of the representational content carried by inheritance systems like the genome to explain why innateness-related properties cluster together, especially in non-human organisms. Although inferences between innateness-related properties are deductively invalid, and lead to false conclusions in many actual cases, where some aspect of a phenotypic trait develops in (...) reliance on a genetic representation it will tend, better than chance, to have many of the innateness-related properties. The account also shows why inferences between innateness-related properties sometimes fail and argues that such inferences are especially misleading when applied to human psychology and behaviour because human psychological development is especially reliant on non-genetic inherited representations. (shrink)

Obesity and type 2 diabetes arise from a set of complex gene–environment interactions. Explanations for the heritability of these syndromes and the environmental contribution to disease susceptibility are addressed by the “thrifty genotype” and the “thrifty phenotype” hypotheses. Here, the merits of both models are discussed and elements of them are used to synthesize a “thrifty epigenotype” hypothesis. I propose that: (1) metabolic thrift, the capacity for efficient acquisition, storage and use of energy, is an ancient, complex trait, (2) (...) the environmentally responsive gene network encoding this trait is subject to genetic canalization and thereby has become robust against mutational perturbations, (3) DNA sequence polymorphisms play a minor role in the aetiology of obesity and type 2 diabetes—instead, disease susceptibility is predominantly determined by epigenetic variations, (4) corresponding epigenotypes have the potential to be inherited across generations, and (5) Leptin is a candidate gene for the acquisition of a thrifty epigenotype. BioEssays 30:156–166, 2008. © 2008 Wiley Periodicals, Inc. (shrink)

This article illustrates in which sense genetic determinism is still part of the contemporary interactionist consensus in medicine. Three dimensions of this consensus are discussed: kinds of causes, a continuum of traits ranging from monogenetic diseases to car accidents, and different kinds of determination due to different norms of reaction. On this basis, this article explicates in which sense the interactionist consensus presupposes the innate?acquired distinction. After a descriptive Part 1, Part 2 reviews why the innate? (...) class='Hi'>acquired distinction is under attack in contemporary philosophy of biology. Three arguments are then presented to provide a limited and pragmatic defense of the distinction: an epistemic, a conceptual, and a historical argument. If interpreted in a certain manner, and if the pragmatic goals of prevention and treatment (ideally specifying what medicine and health care is all about) are taken into account, then the innate?acquired distinction can be a useful epistemic tool. It can help, first, to understand that genetic determination does not mean fatalism, and, second, to maintain a system of checks and balances in the continuing nature?nurture debates. (shrink)

This article illustrates in which sense genetic determinism is still part of the contemporary interactionist consensus in medicine. Three dimensions of this consensus are discussed: kinds of causes, a continuum of traits ranging from monogenetic diseases to car accidents, and different kinds of determination due to different norms of reaction. On this basis, this article explicates in which sense the interactionist consensus presupposes the innate?acquired distinction. After a descriptive Part 1, Part 2 reviews why the innate? (...) class='Hi'>acquired distinction is under attack in contemporary philosophy of biology. Three arguments are then presented to provide a limited and pragmatic defense of the distinction: an epistemic, a conceptual, and a historical argument. If interpreted in a certain manner, and if the pragmatic goals of prevention and treatment are taken into account, then the innate?acquired distinction can be a useful epistemic tool. It can help, first, to understand that genetic determination does not mean fatalism, and, second, to maintain a system of checks and balances in the continuing nature?nurture debates. (shrink)

In 1965, Konrad Lorenz grounded the innate–acquired distinction in what he believed were the only two possible sources of information that can underlie adaptedness: phylogenetic and individual experience. Phylogenetic experience accumulates in the genome by the process of natural selection. Individual experience is acquired ontogenetically through interacting with the environment during the organism’s lifetime. According to Lorenz, the adaptive information underlying innate traits is stored in the genome. Lorenz erred in arguing that genetic adaptation is (...) the only means of accumulating information in phylogenetic experience. Cultural adaptation also occurs over a phylogenetic time scale, and cultural tradition is a third source from which adaptive information can be extracted. This paper argues that genetic adaptation can be distinguished from individual and cultural adaptation in a species like Homo sapiens, in which even adaptations with a genetic component require cultural inputs and scaffolding to develop and be expressed. Examination of the way in which innateness is used in science suggests that scientists use the term, as Lorenz suggested, to designate genetic adaptations. The search for innate traits plays an essential role in generating hypotheses in ethology and psychology. In addition, designating a trait as innate establishes important facts that apply at the information-processing level of description. (shrink)

This article aims to explore the relationship between neutralization and “as if” consciousness in Husserl’s phenomenology, in particular, from its convergence in intuitions concerning phantasy. Starting from a critique of a line of interpretation that, in its attempt to approach phenomenologically to an “aesthetic consciousness”, homologates the neutrality modification with the Epoché, the article seeks to expose the methodological function that the modalization of belief fulfills in the project of Ideas I, as well as highlighting the growing importance that phantasy (...) and the “as if” consciousness will acquire in the subsequent development of Husserl’s phenomenology. (shrink)

Resumen: Se discute las consecuencias de ajustar el diseño de investigaciones sociales al formato de las ciencias naturales. Se propone que el costo es la esterilidad de los intentos. Siendo la sociedad un sistema en desarrollo, la observación de hechos según las reglas del laboratorio o del experimento conducen a la invisibilidad del objeto y a un extravío del observador; lo que se escurre es el sentido de la investigación y en su reemplazo queda solo un hábito de precisión técnica. (...) En vez, se sugiere volver a la ciencia social según su impronta historicista y totalista: el contexto es todo y origen de las preguntas. El método son los caminos para producir las respuestas. La ciencia comienza antes y sigue después de este, en la relación sociología/sociedad. Ahí es cuando la investigación toma su sentido, que lleva a esa sociedad a esa pregunta: a investigarse.: This essay discusses the consequences of fitting social research designs to the format of natural sciences. It argues that the cost is null for trying. Being society a system in development, the observation of facts according to lab rules or experiments lead to the invisibility of the subject matter and loosing track to the observer; what is lost is the sense of research and its replacement is just technical precision habits. Instead it suggests going back the social science based on historical and totality roots: the context is everything and the origin of questions. The method is the road to produce answers. Science began before and continues after it, in the relationship between sociology and society. There is when research acquires its meaning, that leads that society to that question: to question itself. (shrink)

This book is the third of a three-volume set on the innate mind. It provides an assessment of nativist thought and definitive reference point for future inquiry. Nativists have long been interested in a variety of foundational topics relating to the study of cognitive development and the historical opposition between nativism and empiricism. Among the issues here are questions about what it is for something to be innate in the first place; how innateness is related to such things (...) as heritability, genetic information, and theories of cognitive development; the status of arguments both for and against nativism; and how best to understand the role of genes in development and inheritance. These issues are all explored in one way or another in this book. But the book also looks to the future. Alongside state-of-the-art discussions of such established nativist concerns as language, number, spatial cognition, and social cognition, this book examines nativist work in a variety of areas where detailed nativist exploration is relatively new, including cultural learning, creativity, economic choice, culture, and morality. The expansion of nativist theorizing into all these new areas shows both the power and the promise of nativist approaches, and points the way to the future. (shrink)

This book is the third of a three-volume set on the innate mind. It provides an assessment of nativist thought and definitive reference point for future inquiry. Nativists have long been interested in a variety of foundational topics relating to the study of cognitive development and the historical opposition between nativism and empiricism. Among the issues here are questions about what it is for something to be innate in the first place; how innateness is related to such things (...) as heritability, genetic information, and theories of cognitive development; the status of arguments both for and against nativism; and how best to understand the role of genes in development and inheritance. These issues are all explored in one way or another in this book. But the book also looks to the future. Alongside state-of-the-art discussions of such established nativist concerns as language, number, spatial cognition, and social cognition, this book examines nativist work in a variety of areas where detailed nativist exploration is relatively new, including cultural learning, creativity, economic choice, culture, and morality. The expansion of nativist theorizing into all these new areas shows both the power and the promise of nativist approaches, and points the way to the future. (shrink)

This book is the third of a three-volume set on the innate mind. It provides an assessment of nativist thought and definitive reference point for future inquiry. Nativists have long been interested in a variety of foundational topics relating to the study of cognitive development and the historical opposition between nativism and empiricism. Among the issues here are questions about what it is for something to be innate in the first place; how innateness is related to such things (...) as heritability, genetic information, and theories of cognitive development; the status of arguments both for and against nativism; and how best to understand the role of genes in development and inheritance. These issues are all explored in one way or another in this book. But the book also looks to the future. Alongside state-of-the-art discussions of such established nativist concerns as language, number, spatial cognition, and social cognition, this book examines nativist work in a variety of areas where detailed nativist exploration is relatively new, including cultural learning, creativity, economic choice, culture, and morality. The expansion of nativist theorizing into all these new areas shows both the power and the promise of nativist approaches, and points the way to the future. (shrink)

Many researchers consider language to be definitionally unique to humans. However, increasing evidence suggests that language emerged via a series of adaptations to neural systems supporting earlier capacities for visuomotor integration and manual action. This paper reviews comparative neuroscience evidence for the evolutionary progression of these adaptations. An outstanding question is how to mechanistically explain the emergence of new capacities from pre-existing circuitry. One possibility is that human brains may have undergone selection for greater plasticity, reducing the extent to which (...) brain organization is hard-wired and increasing the extent to which it is shaped by socially transmitted, learned behaviors. Mutations that made these new abilities easier or faster to learn would have undergone positive selection, and over time, the neural changes once associated with individual neural plasticity would tend to become heritable, innate, and fixed. Clearly, though, language is not entirely “innate;” it does not emerge without the requisite environmental input and experience. Thus, a mechanistic explanation for the evolution of language must address the inherent trade-off between the evolutionary pressure for underlying neural systems to be flexible and sensitive to environmental input vs. the tendency over time for continually adaptive behaviors to become reliably expressed in an early-emerging, canalized, less flexible manner. (shrink)

This is the third of a three-volume set on The Innate Mind providing a comprehensive assessment of nativist thought and definitive reference point for future inquiry. Together these volumes point the way toward a synthesis that provides a powerful picture of our minds and their place in the natural order.

It is widely recognized that the innate versus acquired distinction is a false dichotomy. Yet many scientists continue to describe certain traits as “innate” and take this to imply that those traits are not acquired, or “unlearned.” This article asks what cognitive role, if any, the concept of innateness should play in the psychological and behavioural sciences. I consider three arguments for eliminating innateness from scientific discourse. First, the classification of a trait as innate is (...) thought to discourage empirical research into its developmental origin. Second, this concept lumps together a number of different biological properties that ought to be treated as distinct. Third, innateness is associated with the outmoded folk biological theory of essentialism. In response to these objections, I consider two attempts to revise the concept of innateness which aim to make it more suitable for scientific explanation and research. One proposal is that innateness can be defined in terms of the biological property of environmental canalization. On this view, a trait is innate to the extent that it is developmentally buffered against a range of different environments. Another proposal is that innateness serves as an explanatory primitive for cognitive science. This view holds that there exist a sharp boundary between psychological and biological explanations and that to identify a trait as innate means that it falls into the latter explanatory domain. This essay ends with some questions for future research. (shrink)

Quantitative genetic studies of human aggressive behavior only partly support the claim of social role theory that individual differences in aggressive behavior are learnt rather than innate. As to its heritable component, future studies on the genetic architecture of aggressive behavior across different contexts could shed more light on the evolutionary origins of male-female versus male-male aggression.

David Papineau (2003; 2005) has discussed the relationship between social learning and the family of postulated evolutionary processes that includes ‘organic selection’, ‘coincident selection’, ‘autonomisation’, ‘the Baldwin effect’ and ‘genetic assimilation’. In all these processes a trait which initially develops in the members of a population as a result of some interaction with the environment comes to develop without that interaction in their descendants. It is uncontroversial that the development of an identical phenotypic trait might depend on an interaction (...) with the environment in one population and not in another. For example, some species of passerine songbirds require exposure to species-typical songs in order to reproduce those songs whilst others do not. Hence we can envisage a species beginning with one type of developmental pathway and evolving the other type. If, however, the successive evolution of these two developmental pathways were a mere coincidence, selection first favoring the ability to acquire the trait and later, quite independently, favoring the ability to develop it autonomously, then this would not be a distinctive kind of evolutionary process, but merely two standard instances of natural selection. George Gaylord Simpson pointed this out in the paper that gave us the term ‘Baldwin effect’ (Simpson, 1953). The real interest of the Baldwin effect and its relatives lies in the mechanisms which might link the evolution of the two developmental pathways, so that acquiring the trait through interaction with the environment makes it more likely that later generations will evolve the ability to acquire the same trait without that interaction. (shrink)

The history of research on the genetics of intelligence is fraught with social bias. During the eugenics era, the hereditary theory of intelligence justified policies that encouraged the proliferation of favored races and coercively stemmed procreation by disfavored ones. In the 1970s, Berkeley psychologist Arthur Jensen argued that black students’ innate cognitive inferiority limited the efficacy of federal education programs. The 1994 controversial bestseller The Bell Curve, by Richard J. Herrnstein and Charles Murray, rehashed the claim that race and (...) class disparities stem from immutable differences in inherited intelligence, which could not be eliminated through social interventions. Today most scientists studying the genetics of intelligence distance themselves from this history of social bias by arguing that their research need not investigate intellectual differences between social groups. Rather, they argue, examining the heritability of intelligence can be socially neutral and may even help to reduce social inequities. I argue, however, that research on the genetics of intelligence cannot be socially neutral. Even if we divorce the heritability of intelligence from a eugenicist mission, measuring intelligence remains useful only as a gage of individuals’ appropriate positions in society. Research into the genetics of intelligence ultimately helps to determine individuals’ inherited capacity for particular social positions, even when researchers aim to modify the effects of inheritance. (shrink)

CONJECTURE: Alongside the innate physical sucking reflex for obtaining milk to be digested, decomposed and used all over the body for growth, repair, and energy, there is a genetically determined information-sucking reflex, which seeks out, sucks in, and decomposes information, which is later recombined in many ways, growing the information-processing architecture and many diverse recombinable competences.

Recent findings have provided evidence for the existence of non‐vertebrate acquired immunity. We survey these findings and propose that all living organisms must express both innate and acquired immunity. This is opposed to the paradigm that only vertebrates manifest the two forms of immune mechanism; other species are thought to use innate immunity alone. We suggest new definitions of innate and acquired immunity, based on whether immune recognition molecules are encoded in the inherited genome (...) or are generated through somatic processes. We reason that both forms of immunity are similarly ancient, and have co‐evolved in response to lifestyle, cost‐benefit tradeoffs and symbiosis versus parasitism. However, different species have evolved different immune solutions that are not necessarily genetically related, but serve a similar general function – allowing individuals to learn from their own immune experience; survival of species is contingent on the acquired immune experience of its individuals. (shrink)

S. Oyama’s prominent account of the Parity Thesis states that one cannot distinguish in a meaningful way between nature-based (i.e. gene-based) and nurture-based (i.e. environment-based) characteristics in development because the information necessary for the resulting characteristics is contained at both levels. Oyama as well as P. E. Griffiths and K. Stotz argue that the Parity Thesis has far-reaching implications for developmental psychology in that both nativist and interactionist developmental accounts of psychological capacities that presuppose a substantial nature/nurture dichotomy are inadequate. (...) We argue that well-motivated abandoning of the nature/nurture dichotomy, as advocated in converging versions of the Parity Thesis in biology, does not necessarily entail abandoning the distinction between biologically given abilities necessary for the development of higher psychological capacities and the learning process they enable. Thus, contrary to the claims of the aforementioned authors, developmental psychologists need not discard a substantial distinction between innate (biologically given) characteristics and those acquired by learning, even if they accept the Parity Thesis. We suggest a two-stage account of development: the first stage is maturational and involves interaction of genetic, epigenetic and environmental causes, resulting in the endogenous biological ‘machinery’ (e.g. language acquisition device), responsible for learning in the subsequent stage of the developmental process by determining the organism’s responses to the environment. This account retains the crux of nativism (the endogenous biological structure determines the way the organism learns/responds to an environment) whilst adopting the developmentalist view of biology by characterizing environments as distinctly different in terms of structure and function in two developmental stages. (shrink)

ABSTRACT Ethical and political attitudes are not randomly distributed in a population. Attitudes of family members, for example, tend to be more similar than those of a random sample of the same size. In the fields of social psychology and political science, the historically standard explanation for these attitude distribution patterns was that social and political attitudes are a function of environmental factors like parental socialization and prevailing social norms. This received view is, however, complicated by more recent work in (...) behavioral genetics, which consistently and repeatedly demonstrates that certain ethical and political attitudes dealing with issues like censorship, abortion, capital punishment, and immigration policy have a significant heritability coefficient, to wit, a substantial percentage of attitude variance in a population can be attributed to genetic variance, independent of environmental factors. In this paper, I argue that the genetic influence on our ethical and political attitudes is mediated by what we can agree to be irrelevant and distorting factors that can lead moral reasoning astray. Further, I argue that we should significantly lower our credences in ethical and political attitudes that fall within the domains of belief that involve significant genetic influence. (shrink)

This article examines and rejects the claim that 'innateness is canalization'. Waddington's concept of canalization is distinguished from the narrower concept of environmental canalization with which it is often confused. Evidence is presented that the concept of environmental canalization is not an accurate analysis of the existing concept of innateness. The strategy of 'biologicizing the mind' by treating psychological or behavioral traits as if they were environmentally canalized physiological traits is criticized using data from developmental psychobiology. (...) It is concluded that identifying innateness with environmental canalization can only result in adding unhelpful associations from 'folkbiology' to the relatively precise idea of canalization. (shrink)

Griffiths and Machery (2008) argue that innateness is a ?folk biological? notion, which, as such, has no useful reconstruction in contemporary biology. If this is so, not only is it wrong to identify the vernacular notion with the precise theoretical concept of canalization, but worse, it would appear that many of the putative scientific claims for particular competences and capacities being innate are simply misplaced. The present paper challenges the core substantive claim of Griffiths and Machery's position, namely, (...) that innateness understood on canalization lines as environment-independent development (somehow and to some degree) is a confused, outmoded notion. It will be contended that the modality-independence of language offers a prima facie case against Griffiths and Machery's general position. (shrink)

The phenomenon of ‘canalization’ ‐ the genetic capacity to buffer developmental pathways against mutational or environmental perturbations ‐ was first characterized in the late 1930s and early 1940s. Despite enormous subsequent progress in understanding the nature of the genetic material and the molecular basis of gene expression, there have been few attempts to interpret the classical work on canalization in molecular genetic terms. Some recent findings, however, bear on one form of canalization, ‘genetic (...) canalization’, the stabilization of development against mutational effects. These data indicate that co‐expressed paralogous genes can function as mutual ‘back‐up’ elements in developmental processes. Paralogues, however, are far from the only basis of canalization: other genetic sources can be readily envisaged and some of these are described here. The evolutionary questions about genetic canalization and the mechanistic questions about developmental instability that still need to be addressed are also briefly discussed. (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)

Behavioral genetics and cultural evolution have both revolutionized our understanding of human behavior – largely independent of each other. Here, we reconcile these two fields under a dual inheritance framework, offering a more nuanced understanding of the interaction between genes and culture. Going beyond typical analyses of gene–environment interactions, we describe the cultural dynamics that shape these interactions by shaping the environment and population structure. A cultural evolutionary approach can explain, for example, how factors such as rates of innovation and (...) diffusion, density of cultural subgroups, and tolerance for behavioral diversity impact heritability estimates, thus yielding predictions for different social contexts. Moreover, when cumulative culture functionally overlaps with genes, genetic effects become masked, unmasked, or even reversed, and the causal effects of an identified gene become confounded with features of the cultural environment. The manner of confounding is specific to a particular society at a particular time, but a WEIRD (western, educated, industrialized, rich, and democratic) sampling problem obscures this boundedness. Cultural evolutionary dynamics are typically missing from models of gene-to-phenotype causality, hindering generalizability of genetic effects across societies and across time. We lay out a reconciled framework and use it to predict the ways in which heritability should differ between societies, between socioeconomic levels, and other groupings within some societies but not others, and over the life course. An integrated cultural evolutionary behavioral genetic approach cuts through the nature–nurture debate and helps resolve controversies in topics such as IQ. (shrink)

The idea that innateness can be understood in terms of genetic coding or genetic programming is discussed. I argue that biology does not provide any support for the view that the whole-organism features of interest to nativists in psychology and linguistics are genetically coded for. This provides some support for recent critical and deflationary treatments of the concept of innateness.

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)

Diseases of complex origin have a component of quantitative genetics that contributes to their susceptibility and phenotypic variability. However, after several studies, a major part of the genetic component of complex phenotypes has still not been found, a situation known as “missing heritability.” Although there have been many hypotheses put forward to explain the reasons for the missing heritability, its definitive causes remain unknown. Complex diseases are caused by multiple intermediate phenotypes involved in their pathogenesis and, very (...) often, each one of these intermediate phenotypes also has a component of quantitative inheritance. Here we propose that at least part of the missing heritability can be explained by the genetic component of intermediate phenotypes that is not detectable at the level of the main complex trait. At the same time, the identification of the genetic component of intermediate phenotypes provides an opportunity to identify part of the missing heritability of complex diseases. (shrink)

The reductionistic vision of evolutionary theory, "the gene's eye view of evolution" is the dominant view among evolutionary biologists today. On this view, the gene is the only unit with sufficient stability to act as a unit of selection, with individuals and groups being more ephemeral units of function, but not of selection. This view is argued to be incorrect, on several grounds. The empirical and theoretical bases for the existence of higher-level units of selection are explored, and alternative analyses (...) discussed critically. The success of a multi-level selection theory demands the recognition and development of a multi-level genetics. The way to accomplish this is suggested. The genotype/phenotype distinction also requires further analysis to see how it applies at higher levels of organization. This analysis provides a way of defining genotype and phenotype for cultural evolution, and a treatment of the innate-acquired distinction which are both generalizeable to analyze problems of the nature and focus of scientific change. (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 complex behaviors are genetically hardwired. Based on previous findings on genetic control of mating and other behaviors in invertebrate and mammalian systems, I suggest that genetic control of complex behaviors is modular: first, dedicated genes specify different behavioral patterns; secondly, separable genetic networks govern distinct behavioral components. I speculate that modular genetic encoding of complex behaviors may in part reflect modularity in brain development and function.Editor's suggested further reading in BioEssays From songs to synapses: Molecular (...) mechanisms of birdsong memory Abstract. (shrink)

Charney describes several mechanisms that will bias estimates of heritability in unpredictable directions. In addition, the mechanisms described by Charney explain the puzzling fact that research in human-behavior genetics routinely reports higher heritabilities than animal studies do. However, I argue that the concept of heritability has no real place in human research anyway.

Suicidal behavior is an interesting blank space in Keller & Miller's (K&M's) population genetical account on explaining the existence and persistence of common, harmful, heritable mental disorders. I argue that suicidal behavior is yet another of these disorders. It may well be consistent with all three evolutionary models considered by K&M. (Published Online November 9 2006).

Gyngell and colleagues consider that the recent Nuffield Council report does not go far enough: heritable genome editing is not just justifiable in a few rare cases; instead, there is a moral imperative to undertake it. We agree that there is a moral argument for this, but in the real world it is mitigated by the fact that it is not usually possible to ensure a better life. We suggest that a moral imperative for HGE can currently only be concluded (...) if one first buys into an overly deterministic view of a genome sequence, and the role of variation within in it, in the aetiology of the disease: most diseases cannot simply be attributed to specific genetic variants that we could edit away. Multiple, poorly understood genetic and environmental factors interact to influence the expression of diseases with a genetic component, even well understood ‘monogenic’ disorders. Population-level genome analyses are now demonstrating that many genetic ’mutations' are much less predictive than previously thought 1. Furthermore, HGE might introduce new risks just as it reduces old ones; or remove protections not yet clearly delineated. (shrink)

Interpreting heritability estimates through the lens of cultural evolution presents two broad and interlinking problems for educational behavior genetics. First, the problem of interpreting high heritability of educational phenotypes as indicators of the genetic basis of traits, when these findings also reflect cultural homogeneity. Second, the problem of extrapolating from genetic research findings in education to policy and practice recommendations.

Skills cannot be divided into the innate and the acquired. Also, genetic effects may not come into play until well after early childhood, and evocative gene-environment correlations are to be expected. Special talents are common in autism and warrant more detailed study, but whether they have the same meaning as talents in nonautistic individuals is not known.

Understanding Human Conduct: The Innate and Acquired Meaning of Life develops the Consciousness-Meaning (CM) model, which aims to explain why most human beings are able to lead a meaningful life without undergoing an existentialist life crisis.