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)

Heritability estimates obtained from genome-wide association studies are much lower than those of traditional quantitative methods. This phenomenon has been called the “missing heritability problem.” By analyzing and comparing GWAS and traditional quantitative methods, we first show that the estimates obtained from the latter involve some terms other than additive genetic variance, while the estimates from the former do not. Second, GWAS, when used to estimate heritability, do not take into account additive epigenetic factors transmitted across (...) generations, while traditional quantitative methods do. Given these two points we show that the missing heritability problem can largely be dissolved. (shrink)

Graphical AbstractThere are four major hypotheses (H1, H2, H3, and H4) as to the source of missing heritability. We propose that estimates obtained from GWAS underestimate heritability by not taking into account non-DNA (epigenetic) sources of heritability. Taking those factors into account (H4) should result in increased heritability estimates.

Genetic explanation of complex human behavior presents an excellent test case for pluralism. Although philosophers agree that successful scientific investigation of behavior is pluralistic, there remains disagreement regarding integration and elimination—is the plurality of approaches here to stay, or merely a waystation on the road to monism? In this paper we introduce an issue taken very seriously by scientists yet mostly ignored by philosophers—the missing heritability problem—and assess its implications for disagreement among pluralists. We argue that the (...) class='Hi'>missing heritability problem, which isn’t going anywhere any time soon, implies that pluralism in behavior genetics is both practically ineliminative and theoretically non-integrative. (shrink)

Lucas Matthews and I substantially revised my SEP entry on Heritability. This version includes discussion of the missing heritability problem and other issues that arise from the use of Genome Wide Association Studies by Behavioral Geneticists.

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)

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)

In the multidisciplinary field of developmental cognitive neuroscience, statistical associations between levels of description play an increasingly important role. One example of such associations is the observation of correlations between relatively common gene variants and individual differences in behavior. It is perhaps surprising that such associations can be detected despite the remoteness of these levels of description, and the fact that behavior is the outcome of an extended developmental process involving interaction of the whole organism with a variable environment. Given (...) that they have been detected, how do such associations inform cognitive-level theories? To investigate this question, we employed a multiscale computational model of development, using a sample domain drawn from the field of language acquisition. The model comprised an artificial neural network model of past-tense acquisition trained using the backpropagation learning algorithm, extended to incorporate population modeling and genetic algorithms. It included five levels of description—four internal: genetic, network, neurocomputation, behavior; and one external: environment. Since the mechanistic assumptions of the model were known and its operation was relatively transparent, we could evaluate whether cross-level associations gave an accurate picture of causal processes. We established that associations could be detected between artificial genes and behavioral variation, even under polygenic assumptions of a many-to-one relationship between genes and neurocomputational parameters, and when an experience-dependent developmental process interceded between the action of genes and the emergence of behavior. We evaluated these associations with respect to their specificity, to their developmental stability, and to their replicability, as well as considering issues of missing heritability and gene–environment interactions. We argue that gene–behavior associations can inform cognitive theory with respect to effect size, specificity, and timing. The model demonstrates a means by which researchers can undertake multiscale modeling with respect to cognition and develop highly specific and complex hypotheses across multiple levels of description. (shrink)

In the year since He Jiankui announced the birth of twin girls whose genes were edited as embryos, reactions and revelations have continued, including the recent announcement that He and two colleagues have been sentenced to jail time and hefty fines. But what of Nana and Lulu, now infants, whose lives and futures are often missing in discussions of He's ethical violations? Their status remains a mystery. Other than learning that they were born prematurely by emergency C-section, we know (...) nothing about their well-being. We know even less about a third gene-edited child said to have been born last summer.Meanwhile, the controversy over He's reckless actions—and the debate about reproductive... (shrink)

Behaving presents an overview of the recent history and methodology of behavioral genetics and psychiatric genetics, informed by a philosophical perspective. Kenneth F. Schaffner addresses a wide range of issues, including genetic reductionism and determinism, "free will," and quantitative and molecular genetics. The latter covers newer genome-wide association studies that have produced a paradigm shift in the subject, and generated the problem of "missing heritability." Schaffner also presents cases involving pro and con arguments for genetic testing for IQ (...) and for Attention Deficit Hyperactivity Disorder. Schaffner examines the nature-nurture controversy and Developmental Systems Theory using C. elegans or "worm" studies as a test case, concluding that genes are special and provide powerful tools, including "deep homology," for investigating behavior. He offers a novel account of biological knowledge emphasizing the importance of models, mechanisms, pathways, and networks, which clarifies how partial reductions provide explanations of traits and disorders. The book also includes examinations of personality genetics and of schizophrenia and its etiology, alongside interviews with prominent researchers in the area, and discusses debates about psychosis that led to changes in the DSM-5 in 2013.Schaffner concludes by discussing additional philosophical implications of the genetic analyses in the book, some major worries about "free will," and arguments pro and con about why genes and DNA are so special. Though genes are special, newer perspectives presented in this book will be needed for progress in behavioral genetics- perspectives that situate genes in complex multilevel prototypic pathways and networks. With a mix of optimism and pessimism about the state of the field and the subject, Schaffner's book will be of interest to scholars in the history and philosophy of science, medicine, and psychiatry. (shrink)

Throughout evolution, there has been interaction and exchange between RNA pools in the environment, and DNA and RNA pools of eukaryotic organisms. Metagenomic and metatranscriptomic sequencing of invertebrate hosts and their microbiota has revealed a rich evolutionary history of RNA virus shuttling between species. Horizontal transfer adapted the RNA pool for successful future interactions which lead to zoonotic transmission and detrimental RNA viral pandemics like SARS‐CoV2. In eukaryotes, noncoding RNA (ncRNA) is an established mechanism derived from prokaryotes to defend against (...) viral attack through innate immunity and regulation of host‐derived mRNA. Transgenerational inheritance of ncRNA is evidence for feedforward adaptive immunity and epigenetically encoded environmental change across generations, which may explain the ‘‘missing heritability’’ of common disease. Causal graph theory and the Price Equation can model epigenetic inheritance involving dynamic internal and external RNA pools. Experimental designs should include metatranscriptomic analyses to understand how ncRNA responds to rapidly changing environmental conditions, within and between organisms, and across generations. (shrink)

Psychological dualism (or dualism herein) purports that there is a complementary, non-material/physical, mind-active component associated with a living organism. Thus mind would not simply be an expression of brain function as confidently believed by neuroscience (and science in general). As earlier work has suggested that confidence can be brushed aside by considering some accepted unusual behaviors. One simple dualism-consistent example is terminal lucidity in which people return to psychological coherence shortly before death despite having been lost to “dull, unconscious, or (...) mentally ill” conditions, in some cases for years. Arguably framing these challenges to materialism, though, is genetics’ unfolding “missing heritability” crisis in which many expected DNA origins have not been found despite extensive searches. An associated soul-consistent explanation is that instead of DNA origins these innate characteristics reflect continuity associated with the earlier lives of incarnating souls (and of course with this some other particular explanations). Herein arguments for the existence of souls are considered for the very surprising case of multiple soul residency in a single organism. Discussions on this possibility focus on the stunning experiences of some heart transplant patients, and also the very difficult condition of Multiple Personality (or Dissociative Identity) Disorder. These two phenomena pose very difficult challenges for materialism (and brain function), and on the other hand are suggestive of the influences of additional souls. Finally, some of the implications of these extraordinary possibilities are briefly considered. (shrink)

Science’s theory of evolution purports to explain life and its historical dynamics in a physics/material-only fashion. But this entails a broad reliance on DNA (deoxyribonucleic acid) for inheritance (and thus blueprints), which appears to be implausible for a number of unusual innate behaviors. The immediate unfolding challenge, though, is that the inheritance role is conveniently testable via searches for the DNA origins of a number of human behavioral and health tendencies, and despite enormous efforts those searches have thus far largely (...) failed (i.e., the “absolutely beyond belief” missing heritability problem). This existing case for DNA’s inadequacies will be briefly reviewed herein. The subsequent main analysis considers some big challenges facing DNA associated with some evolutionary dynamics—the acquisition of color vision in primates; instinctive behaviors including the egg-laying practices of emerald jewel wasps; kin selection; and our natural religious beliefs. Together these challenges strongly suggest that the acceptance of DNA as the (complete) language of life was premature. The haphazard and ambiguous nature of DNA/genetic specifications is very unlikely to have provided a vehicle for the exacting blueprints required for the many instinctive behaviors or capacities. Life appears to be more complex than biologists believe. Two possible alternative explanations are briefly considered in the wake of these discussions. Finally, does anyone—beginning with academics—care about this unfolding foundational failure? (shrink)

The unfolding problems with science’s materialist understanding of life are obviously noteworthy in and of themselves, but the associated potential support for dualistic/religious beliefs is particularly significant. Beyond a number of behavioral conundrums, the general problem facing the scientific molecular-only vision is the unfolding missing heritability (or DNA origins)—problem. Given our innate dualistic/religious understanding of life and its presumed—but increasingly questionable—DNA basis, it is argued here that this combination offers a straightforward preliminary argument supporting the basic dualism common (...) to religions. With this as a backdrop, a focus herein will be placed on experiences of transcendence (or unified consciousness or enlightenment) associated with religious/mystical practices. With such real-life transformations, there is the possibility of glimpsing the ultimate goal associated with religious practices. An introduction will be provided via the independent Unity experience given in Jacque Lusseyran’s And There Was Light. Next, a sequence of similar experiences associated with Buddhist practices is given. A suggested framework then connects such experiences to the religious/dualistic element, a soul, and with this a potential new avenue for discussions on meaning. A modern framing of these discussions is found in comparisons between traditional Buddhism, and its contemporary science-influenced, Western peer. Sam Harris’ Waking Up is utilized in part as a guide to the latter. It is not unlikely that other spiritual or religious traditions are facing analogous detours in our science-led, meaning-deprived, and increasingly superficial era. (shrink)

We argue that the physics of complex materials and self-organizing processes should be made central to the biology of form. Rather than being encoded in genes, form emerges when cells and certain of their molecules mobilize physical forces, effects, and processes in a multicellular context. What is inherited from one generation to the next are not genetic programs for constructing organisms, but generative mechanisms of morphogenesis and pattern formation and the initial and boundary conditions for reproducing the specific traits of (...) a taxon. There is no inherent antagonism between this “physicalist” perspective and genetics, since physics acts on matter, and gene products are essential material components of living systems whose variability affects the systems’ parameters. We make this notion concrete by summarizing the concept of “dynamical patterning modules” (DPMs; Newman and Bhat, Phys Biol 5:1–14, 2008; Int J Dev Biol 53:693–705, 2009), an explicit physico-genetic framework for the origin and evolution of multicellular form in animals, as well as (when differences in interaction toolkit genes and applicable physical processes are taken into account) in multicellular plants (Hernández-Hernández et al., Int J Dev Biol 56:661–674, 2012). DPMs provide the missing link between development and evolution by revealing how genes acting in concert with physics can generate and transform morphology in a heritable fashion. (shrink)

Recent findings in epigenetics have been attracting much attention from social scientists and bioethicists because they reveal the molecular mechanisms by which exposure to socioenvironmental factors, such as pollutants and social adversity, can influence the expression of genes throughout life. Most surprisingly, some epigenetic modifications may also be heritable via germ cells across generations. Epigenetics may be the missing molecular evidence of the importance of using preventive strategies at the policy level to reduce the incidence and prevalence of common (...) diseases. But while this “policy translation” of epigenetics introduces new arguments in favor of public health strategies and policy-making, a more “clinical translation” of epigenetics is also emerging. It focuses on the biochemical mechanisms and epigenetic variants at the origin of disease, leading to novel biomedical means of assessing epigenetic susceptibility and reversing detrimental epigenetic variants. In this paper, we argue that the impetus to create new biomedical interventions to manipulate and reverse epigenetic variants is likely to garner more attention than effective social and public health interventions and therefore also to garner a greater share of limited public resources. This is likely to happen because of the current biopolitical context in which scientific findings are translated. This contemporary neoliberal “regime of truth,” to use a term from Michel Foucault, greatly influences the ways in which knowledge is being interpreted and implemented. Building on sociologist Thomas Lemke's Foucauldian “analytics of biopolitics” and on literature from the field of science and technology studies, we present two sociological trends that may impede the policy translation of epigenetics: molecularization and biomedicalization. These trends, we argue, are likely to favor the clinical translation of epigenetics—in other words, the development of new clinical tools fostering what has been called “personalized” or “precision” medicine. In addition, we argue that an overemphasized clinical translation of epigenetics may further reinforce this biopolitical landscape through four processes closely related to neoliberal pathways of thinking: the internalization and isolation of socioenvironmental determinants of health and increased opportunities for commodification and technologicalization of health care interventions. (shrink)

Evolutionary theory is formulated in terms of individuals that carry heritable information and are subject to selective pressures. However, individuality itself is a trait that had to evolve - an individual is not an indivisible entity, but a result of evolutionary processes that necessarily begin at the lower level of hierarchical organisation. Traditional approaches to biological individuality focus on cooperation and relatedness within a group, division of labour, policing mechanisms and strong selection at the higher level. Nevertheless, despite considerable theoretical (...) progress in these areas, a full dynamical first-principles account of how new types of individuals arise is missing. To the extent that individuality is an emergent trait, the problem can be approached by recognising the importance of individuating mechanisms that are present from the very beginning of the transition, when only lower-level selection is acting. Here we review some of the most influential theoretical work on the role of individuating mechanisms in these transitions, and demonstrate how a lower-level, bottom-up evolutionary framework can be used to understand biological complexity involved in the origin of cellular life, early eukaryotic evolution, sexual life cycles and multicellular development. Some of these mechanisms inevitably stem from environmental constraints, population structure and ancestral life cycles. Others are unique to specific transitions - features of the natural history and biochemistry that are co-opted into conflict mediation. Identifying mechanisms of individuation that provide a coarse-grained description of the system's evolutionary dynamics is an important step towards understanding how biological complexity and hierarchical organisation evolves. In this way, individuality can be reconceptualised as an approximate model that with varying degrees of precision applies to a wide range of biological systems. (shrink)

As Achim Rosemann and colleagues rightly suggest in their article “Heritable Genome Editing in Global Context: National and International Policy Challenges,” in this issue of the Hastings Center Report, the scientific, ethical, and governance challenges associated with heritable genome editing are global in scope. Both the genetic interventions and the social and moral judgments about human identity and integrity associated with them will affect all humanity. Yet the worries, problems, and solutions that the study illuminates reflect only a partial picture (...) of those challenges. That is to be expected from a study of this sort: the “stakeholders” who were consulted are a limited group and as such are bound to provide a particular, limited picture. One of the important contributions that such a study can make is in providing a picture of what problems particular kinds of experts see as the primary problems and how the framing of those problems may displace other questions and perspectives, especially when such parochial framings of problems are elevated to the level of the “global.” Rosemann et al. do not explain how participants were identified as stakeholders or, indeed, how the study identified the stakes. This is a missed opportunity, and it points toward a set of questions that themselves need to be asked about how the stakeholders—and the stakes—of global governance of heritable genome editing are identified. (shrink)

The opening chapter of this work is a comprehensive “Historical Overview of the Hereditary Puzzle.” Goldie Morgentaler's analysis of theories of heredity before Mendel will interest students of biological science. She admits that “resurrecting such theories without contamination from subsequent knowledge often requires an imaginative leap.” Very true. There have been such profound advances in the science of genetics since that time, with the avalanche of discoveries during the past half century, that much of the previous thought now falls in (...) the realm of philosophical fantasy.These early concepts were those to which Charles Dickens was exposed for most of his life. His literary reaction to them is exhaustively analyzed in the subsequent two parts of the book. The first of these is entitled “Heredity and the Individual,” and the second is “The Public Face of Heredity.” The latter includes interesting discussion of class and race, with analyses of the last three novels. These indicate that Dickens's views on heredity changed during his later life, perhaps influenced by Darwin, whose work he had read … and vice versa.The author is to be admired for her detailed knowledge of Dickens's works and his characters. For a reviewer who has been steeped in evidence‐based medicine and science for most of his career, it seems that much of the speculation regarding heredity in the nineteenth century is tenuous and far‐fetched. While Dickens engaged the topic of heredity many times, he appears to have followed the general trend of that era by showing little consistency in his views. This is not surprising in light of the paucity of scientific evidence at that time.While the title implies a study of Dickens and heredity, the substance covers a much wider field, with ventures into ethics, morality, religion, psychology, philosophy, sociology, and more. The appended notes tell of assiduous research and concentration. To the pragmatic reader it sometimes appears that Morgentaler makes observations and draws conclusions that are more profound than Dickens himself might have achieved, or admitted. This is, of course, a common diversion in revisionist studies of well‐known authors and other celebrities.It is inevitable that the perennial question of the relative strength of nature and nurture must have prominence in this study. In his earlier novels Dickens implied support for the notion that goodness and virtue were heritable traits allied to beauty and good physical appearance. Morgentaler returns repeatedly to this question in many aspects. In her final chapter she points out that Dickens's views changed, paradoxically, after The Origin of Species was published, toward the end of his life. He then gave less weight to the influence of heredity. She has, perhaps, missed an opportunity of recording that Dickens noticed hereditary factors in alcoholism and longevity. In the case of Jenny Wren's family, Mr. Cleaver was “like his own father, a weak wretched trembling creature, falling to pieces, never sober” . The Wardle family in Pickwick Papers showed familial longevity in that “only one member hasn't lived to eighty‐five, and he was beheaded by one of the Henrys.”The relationship of some of the discussion to heredity is profound, often remote, even cryptic. To those who are hybrids of a scientific historian and an obsessive Dickens aficionado, this work will be absorbing. Unfortunately for the author and the publisher, such hybrids are probably rare—but I hope not extinct. To the pure scientist this work might be an uphill exercise. The production of the book is faultless. (shrink)

Miss R. Meager; III.—The Uniqueness of a Work of Art, Proceedings of the Aristotelian Society, Volume 59, Issue 1, 1 June 1959, Pages 49–70, https://doi.org/10.

Conception has a prominent role to play in Thomas Reid’s philosophy of mind, as is apparent from his Essays on the Intellectual Powers of Man (EIP henceforth). The present investigation concerns Reid’s explanation of how objects (be they real or nonexistent) are conceived. According to him, conception functions in two different ways: it is either an ingredient in another act of thinking, such as perception or memory, or it is exercised by itself, sometimes about objects that do not (and will (...) never) exist. Fictional objects can be remembered, but to do so the mind needs an initial, independent grip on them, which can only be achieved by an exercise of “bare conception”. (shrink)

Cet article propose une voie d’issue pour sortir de l’antinomie dans laquelle se trouvent souvent les défenseurs de la liberté académique, celle du libéralisme ou du « républicanisme » d’État, et donc de la penser autrement que comme un cas particulier de la liberté d’expression tout en évitant d’en faire le privilège d’un corps social (les universitaires) dont le peuple serait exclu. La philosophie de Spinoza nous permet de redéfinir la liberté académique comme une modalité de la liberté de penser, (...) et plus précisément de la liberté de philosopher, et nous offre un cadre utile pour comprendre le rôle des universités publiques dans le développement de la puissance de penser des masses citoyennes et leur centralité dans la conservation d’un État démocratique. (shrink)

It is commonly believed that people become selfish and turn to looting, price gouging, and other immoral behaviour in emergencies. This has been the basis for an argument justifying extraordinary measures in emergencies. It states that if emergencies are not curtailed, breakdown of moral norms threaten (‘the moral black hole’). Using the example of natural disasters, we argue that the validity of this argument in non-antagonistic situations, i.e. situations other than war and armed conflict, is highly questionable. Available evidence suggests (...) that people in such emergencies typically do not display panic reactions or exaggerated selfishness, and that phenomena such as looting and price gouging are rare. Furthermore, a version of the moral-black-hole argument based on the mere possibility of a moral black hole occurring runs into problems similar to those of Pascal’s Wager. We conclude that we should be wary against applying the moral-black-hole argument to non-antagonistic cases. (shrink)

Language is a cognitively demanding human trait, but it is also a fundamentally cooperative enterprise that rests on the motivation to share information. Great apes possess many of the cognitive prerequisites for language, but largely lack the motivation to share information. Callitrichids (including marmosets and tamarins) are highly vocal monkeys that are more distantly related to humans than great apes are, but like humans, they are cooperative breeders and all group members help raising offspring. Among primates, this rearing system is (...) correlated with proactive prosociality, which can be expressed as motivation to share information. We therefore propose that the unique coincidence of these two components in humans set the stage for language evolution: The cognitive component inherited from our great ape-like ancestors, and the motivational one added convergently as a result of cooperative breeding. We evaluate this scenario based on a review of callitrichd vocal communication and show that furthermore, they possess many of the mechanistic elements emphasized by the mirror system hypothesis of language evolution. We end by highlighting how more systematic phylogenetic comparisons will enable us to further promote our understanding of the role of cooperative breeding during language evolution. (shrink)

Occupational health remains neglected in developing countries because of competing social, economic and political challenges. Ethical issues in the workplace related to the hazards and risks of becoming infected by Leishmania (Leishmania) mexicana, through the bite of naturally infected sand flies, is another area of concern that has been neglected as well. We report here the results of reviewing two entomological field studies carried out in our research center from 2003 to 2006. Eight students from our School of Biology were (...) invited to catch sand flies. A total of six of the eight (75%) developed a typical clinical picture of Localized Cutaneous Leishmaniasis (LCL) caused by L. (L.) mexicana. In this article we identify the ethical issues related to these kinds of studies and propose some guidelines for conducting them. (shrink)

Can heritability estimates provide causal information? This paper argues for an affirmative answer: since a non-nil heritability estimate satisfies certain characteristic properties of causation (i.e., association, manipulability, and counterfactual dependence), it increases the probability that the relation between genotypic variance and phenotypic variance is (at least partly) causal. Contrary to earlier proposals in the literature, the argument does not assume the correctness of any particular conception of the nature of causation, rather focusing on properties that are characteristic of (...) causal relationships. The argument is defended against Lewontin's (1974) locality objection and Kaplan and Turkheimer's (2021) recent critique of Genome-Wide Association Studies (GWAS). (shrink)

Heritability is routinely interpreted causally. Yet, what such an interpretation amounts to is often unclear. Here, I provide a causal interpretation of this concept in terms of range of causal influence, one of several causal dimensions proposed within the interventionist account of causation. An information-theoretic measure of range of causal influence has recently been put forward in the literature. Starting from this formalization and relying upon Woodward’s analysis, I show that an important problem associated with interpreting heritability causally, (...) namely the locality problem, amounts, at least partly, to a low invariance and low stability between the genotype/environment and the phenotype of individuals. In light of this, I plead for a causal interpretation of heritability that takes the notions of Woodward’s invariance and stability into consideration. In doing so, I defuse naive causal interpretations of heritability. (shrink)

Presenting a look at the human mind's capacity while criticizing artificial intelligence, the author makes suggestions about classical and quantum physics and ..

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)

A high heritability estimate usually corresponds to a situation in which trait variation is largely caused by genetic variation. However, in some cases of gene-environment covariance, causal intuitions about the sources of trait difference can vary, leading experts to disagree as to how the heritability estimate should be interpreted. We argue that the source of contention for these cases is an inconsistency in the interpretation of the concepts ‘genotype’, ‘phenotype’, and ‘environment’. We propose an interpretation of these terms (...) under which trait variance initially caused by genetic variance is subsumed into a heritability for all cases of gene-environment covariance. (shrink)

Conditionals whose antecedent and consequent are not somehow internally connected tend to strike us as odd. The received doctrine is that this felt oddness is to be explained pragmatically. Exactly how the pragmatic explanation is supposed to go has remained elusive, however. This paper discusses recent philosophical and psychological work that attempts to account semantically for the apparent oddness of conditionals lacking an internal connection between their parts.

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)

Available corpora for Argument Mining differ along several axes, and one of the key differences is the presence (or absence) of discourse markers to signal argumentative content. Exploring effective ways to use discourse markers has received wide attention in various discourse parsing tasks, from which it is well-known that discourse markers are strong indicators of discourse relations. To improve the robustness of Argument Mining systems across different genres, we propose to automatically augment a given text with discourse markers such that (...) all relations are explicitly signaled. Our analysis unveils that popular language models taken out-of-the-box fail on this task; however, when fine-tuned on a new heterogeneous dataset that we construct (including synthetic and real examples), they perform considerably better. We demonstrate the impact of our approach on an Argument Mining downstream task, evaluated on different corpora, showing that language models can be trained to automatically fill in discourse markers across different corpora, improving the performance of a downstream model in some, but not all, cases. Our proposed approach can further be employed as an assistant tool for better discourse understanding. (shrink)

Can a heritability value tell us something about the weight of genetic versus environmental causes that have acted in the development of a particular individual? Two possible questions arise. Q1: what portion of the phenotype of X is due to its genes and what portion to its environment? Q2: what portion of X’s phenotypic deviation from the mean is a result of its genetic deviation and what portion a result of its environmental deviation? An answer to Q1 provides the (...) full information about X’s development, while an answer to Q2 leaves out a large portion unexplained—that portion which corresponds to the phenotypic mean. Q1 is unanswerable, but I show it is nevertheless legitimate under certain quantitative genetics models. With regard to Q2, opinions in the philosophical and biological literature differ as to its legitimacy. I argue that not only is it legitimate, but in particular, under a few simplifying assumptions, it allows for a quantitative probabilistic answer: for normally distributed quantitative traits with no G-E correlation or statistical G × E interaction, we can assess the probability that X’s genes had a greater effect than its environment on its deviation from the mean population value. This probability is expressed as a function the heritability and the individual’s phenotypic value; we can also provide a quantitative probabilistic answer to Q2 for an arbitrary individual where the probability is a function only of heritability. (shrink)