In a now classic paper published in 1991, Alberch introduced the concept of genotype–phenotype (G!P) mapping to provide a framework for a more sophisticated discussion of the integration between genetics and developmental biology that was then available. The advent of evo-devo first and of the genomic era later would seem to have superseded talk of transitions in phenotypic space and the like, central to Alberch’s approach. On the contrary, this paper shows that recent empirical and theoretical advances have (...) only sharpened the need for a different conceptual treat- ment of how phenotypes are produced. Old-fashioned metaphors like genetic blueprint and genetic programme are not only woefully inadequate but positively misleading about the nature of G!P, and are being replaced by an algorithmic approach emerging from the study of a variety of actual G!P maps. These include RNA folding, protein function and the study of evolvable soft- ware. Some generalities are emerging from these disparate fields of analysis, and I suggest that the concept of ‘developmental encoding’ (as opposed to the classical one of genetic encoding) provides a promising computational–theoretical underpinning to coherently integrate ideas on evolvability, modularity and robustness and foster a fruitful framing of the G!P mapping problem. (shrink)

Mehlman and Li offer a framework for approaching the bioethical issues raised by the military use of genomics that is compellingly grounded in both the contemporary civilian and military ethics of medical research, arguing that military commanders must be bound by the two principles of paternal- ism and proportionality. I agree fully. But I argue here that this is a much higher bar than we may fully realize. Just as the principle of proportionality relies upon a thorough assessment of harms (...) caused and military advantage gained, the use of genomic research, on Mehlman and Li’s view, will require an accurate understanding of the connection between genotypes and phenotypes – accurate enough to ameliorate the risk undertaken by our armed forces in being subject to such research. Recent conceptual work in evolutionary theory and the philosophy of biology, however, renders it doubtful that such knowledge is forthcoming. The complexity of the relationship between genotypic factors and realized traits (the so-called ‘G→P map’) makes the estimation of potential military advantage, as well as potential harm to our troops, incredibly challenging. Such fundamental conceptual challenges call into question our ability to ever satisfactorily satisfy the demands of a sufficiently rigorous ethical standard. (shrink)

Noting minimal philosophical attention to the shift of the meanings of “genotype” and “phenotype,” and their distinction, as well as to the variety of meanings that have co-existed over the last hundred years, this note invites readers to join in exploring the implications of shifts that have been left unexamined.

Invasion biologists often suggest that phenotypic plasticity plays an important role in successful plant invasions. Assuming that plasticity enhances ecological niche breadth and therefore confers a fitness advantage, recent studies have posed two main hypotheses: (1) invasive species are more plastic than non-invasive or native ones; (2) populations in the introduced range of an invasive species have evolved greater plasticity than populations in the native range. These two hypotheses largely reflect the disparate interests of ecologists and evolutionary biologists. Because these (...) sciences are typically interested in different temporal and spatial scales, we describe what is required to assess phenotypic plasticity at different levels. We explore the inevitable tradeoffs of experiments conducted at the genotype vs. species level, outline components of experimental design required to identify plasticity at different levels, and review some examples from the recent literature. Moreover, we suggest that a successful invader may benefit from plasticity as either (1) a Jack-of-all-trades, better able to maintain fitness in unfavourable environments; (2) a Master-of-some, better able to increase fitness in favourable environments; or (3) a Jack-and-master that combines some level of both abilities. This new framework can be applied when testing both ecological or evolutionary oriented hypotheses, and therefore promises to bridge the gap between the two perspectives. (shrink)

The history of evolution is a history of development from less to more complex organisms. This growth in complexity of organisms goes hand in hand with a concurrent growth in complexity of environments and of organism-environment relations. It is a concern with this latter aspect of evolutionary development that motivates the present paper. We begin by outlining a theory of organism-environment relations. We then show that the theory can be applied to a range of different sorts of cases, both biological (...) and non-biological, in which objects are lodged or housed within specific environments, or niches. Biological science is interested in types—for example in genotypes, phenotypes, and environment types—in regularities that can serve as the basis for the formulation of laws or general principles. Types, however, can exist only through their corresponding tokens. Our theory of token environments is meant to plug this gap and to provide a first step towards a general theory of causally relevant spatial volumes. (shrink)

In this article, we discuss epistemological limitations relating to the use of ethnoracial categories in biomedical research as devised by the Office of Management and Budget’s institutional guidelines. We argue that the obligation to use ethnoracial categories in genomics research should be abandoned. First, we outline how conceptual imprecision in the definition of ethnoracial categories can generate epistemic uncertainty in medical research and practice. Second, we focus on the use of ethnoracial categories in medical genetics, particularly genomics-based precision medicine, where (...) ethnoracial identity is understood as a proxy for medically relevant differences among individuals. Notably, extensive criticisms have been made already against the genetic interpretation of races, but, nonetheless, the concept of race remains a key element of contemporary genomics. This motivates us to explore possible reasons why such criticisms may have been ineffective in redirecting attention to other (non-race-based) ways of controlling for human variability. We contend that popular arguments against the idea that human races have a genetic basis, though convincing in many respects, are not sufficient to exclude the pragmatic use of race and ethnicity as proxies for genetic variability related to complex phenotypes. Finally, we provide two further arguments to support the idea that ethnoracial categories are unlikely to provide meaningful insights into medical genetics, which implies that even the interpretation of race as a useful tool to stratify disease risk is unwarranted. (shrink)

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

The nominal ground that entwines human beings and animal behaviours is unwilling to admit moral valuing as a non-human act. Just to nail it down explicitly, two clauses ramify the moral conscience of human beings as follows: a) Can non-humans be moral beings?, b) Unconscious animal behaviours go beyond any moral judgments. My approach aims to rebuff these anthropomorphic clauses by justifying animals’ moral beings and animals’ moral behaviours from a meta-ethical stance. A meta-ethical outlook may enable an analysis of (...) ethical and normative views through the limit of moral motives and reasoning. Animals’ sense of moral motives and their apparatus of getting involved in moral acts cannot be compared with human actions. In human moral engagement, we abide by moral paradigmatic theories and their diversified attitudes that could have conceptual and linguistic use in our societal discourses. However, animals’ intentional apparatus may have the propensity to choose an act following the moral consequences (care, utility, responsibility, etc.) in their life-forms. (shrink)

If each of the subtypes of autism is defined simply as constituted by a set of symptoms, then the criteria for its observation are straightforward, although, of course, some of those symptoms themselves might be hard to observe definitively. Compare with telling whether or not someone is bleeding: while it might be hard to tell if someone is bleeding internally, we know what it takes to find out, and when we have the right access and instruments we can settle the (...) issue. But matters are not so simple for the autism subtypes. For one thing, how do we settle which symptoms to group together under one heading? One key difference between “autism disorder” and “Asperger’s disorder” is that the former exhibit language delays (sometimes extreme), whereas the latter do not. But is that a sign of genuinely distinct conditions or is that an artifact of the distinct groups of subjects that Leo Kanner and Hans Asperger worked with? And in general, although there are certainly types of behavior that are taken to be indicative of autism, none by itself is taken by diagnosticians to be either necessary or sufficient for a definitive diagnosis for any of the autism subtypes. What is the diagnostician to do? This is not merely an academic issue, as many parents can attest. Are we in a situation, then, that each practitioner has his or her own “pet” signs that are the “real keys” to the diagnosis? That would suggest that the term “autistic” might meet the fate of the outdated term “neurotic,” which turned out to be a pseudo-scientific term for an inexact clumping together of unrelated phenomena. The assumption amongst specialists seems to be that we will reach the point with "autism" that we have with "water": there will be a root essence to autism whose presence or absence settles a diagnosis. If that is to be the case, however, we have to settle the level of application of the concept. Does the term apply to people who exhibit particular behaviors? Or is it possible to exhibit “autistic” behaviors without actually being autistic, because autism is instead a particular feature of the mind (as, for example, in Baron-Cohen’s “impaired theory of mind module” theory, discussed below) which usually but not necessarily has behavioral effects? Or is autism located instead in the brain, perhaps in damage to key areas, which in turn would typically have an effect on modules of the mind? Or perhaps autism is located in genetics or biology, so that some people with damage to the brain caused by accidents so that they exhibit autistic symptoms would not actually be autistic. Conversely, supposing one had an “autistic brain” but showed none of (or not a sufficient number of) the symptoms, would one not be autistic? The assumption is that the genotypes and phenotypes will line up neatly, but if they do not, what happens to the concept “autistic?” (There is an analogy in the philosophy of sex and gender: androgen insensitive individuals tend to self-identify as female and have outward female traits, but have XY chromosomes—should we go with chromosomes or self-identity in assigning sex category?) Finally, the implications for these complications for diagnosis and categorization, with the attendant social and medical implications is discussed. The typical assumption of the medical profession is that autism cannot be “cured.” That assumes that autism is not simply the symptoms. However, at the same time, the tests used to diagnose ASDs work simply from the symptoms (for example, Baron-Cohen’s Sally/Anne test, which ASD children of a certain age almost all fail, but which practically no ASD adult fails). This implies an inherent confusion over the status of the concept. I conclude that attempts to make sense of some true or accurate summary of what it is to be autistic (such as one would find in the DSM) are almost certainly misguided and will vanish into history along with “neurotic.” But as with racial terms, which are similarly shifting and perverse, the term has already passed into the public sphere and will have a lasting and dangerous influence beyond its short scientific shelf-life. (shrink)

Recent trends in psychiatry involve a transition from categorical to dimensional frameworks, in which the boundary between health and pathology is understood as a difference in degree rather than as a difference in kind. A major tenet of dimensional approaches is that no qualitative distinction can be made between health and pathology. As a consequence, these approaches tend to characterize such a threshold as pragmatic or conventional in nature. However, dimensional approaches to psychopathology raise several epistemological and ontological issues. First, (...) we review major sources of evidence usually recruited in support of the dimensional trend (focusing on clinical observation and biological data), and we show that these are connected to different conceptualizations of how dimensional traits extend across health and pathology. Second, we criticize two unquestioned assumptions that stand at the core of the dimensional trend: a) that there is continuity from health to pathology at the symptomatic level; b) that such continuity reflects an underlying continuity in the genetic liability for pathological conditions. Third, we argue against the idea of a conventional threshold by showing that such a view implies a linear relationship between the genotype and the phenotype. Fourth, drawing on epigenetics and developmental biology, we offer a characterization of mental disorders as stable and dynamic constellations of multi-level variables that differ qualitatively from ‘healthy states’. We conclude by showing that our account has several theoretical advantages over both categorical and dimensional approaches. Notably, it provides crucial insights into psychological development over time and individual differences, with major implications in terms of intervention and clinical decision-making. (shrink)

The scientific study of living organisms is permeated by machine and design metaphors. Genes are thought of as the ‘‘blueprint’’ of an organism, organisms are ‘‘reverse engineered’’ to discover their functionality, and living cells are compared to biochemical factories, complete with assembly lines, transport systems, messenger circuits, etc. Although the notion of design is indispensable to think about adaptations, and engineering analogies have considerable heuristic value (e.g., optimality assumptions), we argue they are limited in several important respects. In particular, the (...) analogy with human-made machines falters when we move down to the level of molecular biology and genetics. Living organisms are far more messy and less transparent than human-made machines. Notoriously, evolution is an opportunistic tinkerer, blindly stumbling on ‘‘designs’’ that no sensible engineer would come up with. Despite impressive technological innovation, the prospect of artificially designing new life forms from scratch has proven more difficult than the superficial analogy with ‘‘programming’’ the right ‘‘software’’ would suggest. The idea of applying straightforward engineering approaches to living systems and their genomes— isolating functional components, designing new parts from scratch, recombining and assembling them into novel life forms—pushes the analogy with human artifacts beyond its limits. In the absence of a one-to-one correspondence between genotype and phenotype, there is no straightforward way to implement novel biological functions and design new life forms. Both the developmental complexity of gene expression and the multifarious interactions of genes and environments are serious obstacles for ‘‘engineering’’ a particular phenotype. The problem of reverse-engineering a desired phenotype to its genetic ‘‘instructions’’ is probably intractable for any but the most simple phenotypes. Recent developments in the field of bio-engineering and synthetic biology reflect these limitations. Instead of genetically engineering a desired trait from scratch, as the machine/engineering metaphor promises, researchers are making greater strides by co-opting natural selection to ‘‘search’’ for a suitable genotype, or by borrowing and recombining genetic material from extant life forms. (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)

It has become somewhat of a platitude to call Aristotle the first epigenesist insofar as he thought form and structure emerged gradually from an unorganized, amorphous embryo. But modern biology now recognizes two senses of “epigenesis”. The first is this more familiar idea about the gradual emergence of form and structure, which is traditionally opposed to the idea of preformationism. But modern biologists also use “epigenesis” to emphasize the context-dependency of the process itself. Used in this sense development is not (...) simply the unfolding of a pre-determined sequence of changes specified in advance by the organism’s genotype. It is also sensitive to inputs from the internal and external environment, which help determine in real-time which of the many potential developmental pathways are actualized during the process. Within this paradigm developing embryos are viewed as dynamic and responsive systems that react to inputs from the internal and external environment ‘on the fly’. In this paper I argue that, while Aristotle was an epigenesist in the first sense, he would have rejected epigenesis in the more modern sense. First, Aristotle’s model of choice for a developing embryo is the automaton that executes a set of preset movements (GA 734b9-13, 741b7-15). The automatons he has in mind are not dynamic AI systems capable of modifying their behaviour on the fly in response to environmental cues but completely deterministic mechanisms whose movements are fixed by their original design. Second, given Aristotle’s views about the different kinds of causal powers there are, it looks like only intentional agents endowed with actual decision-making powers could be capable of the sort of plasticity at the core of a more dynamic epigenesis. For that kind of epigenesis requires powers for alternative outcomes, and Aristotle is explicit that such powers require rational desires (προαίρεσις) that control which of those alternatives to bring about. If I am right, then he could not have made sense of the idea of a developing embryo (as a non-intentional system) making adjustments to its phenotype on the fly in response to emerging problems and opportunities, given the conceptual resources available to him. (shrink)

Discussions about the biological bases (or lack thereof) of the concept of race in the human species seem to be never ending. One of the latest rounds is represented by a paper by Neven Sesardic, which attempts to build a strong scientific case for the existence of human races, based on genetic, morphometric and behavioral characteristics, as well as on a thorough critique of opposing positions. In this paper I show that Sesardic’s critique falls far short of the goal, and (...) that his positive case is exceedingly thin. I do this through a combination of analysis of the actual scientific findings invoked by Sesardic and of some philo- sophical unpacking of his conceptual analysis, drawing on a dual professional background as an evolu- tionary biologist and a philosopher of science. (shrink)

How micro- and macroevolutionary evolutionary processes produce phenotypic change is without question one of the most intriguing and perplexing issues facing evolutionary biologists. We believe that roadblocks to progress lie A) in the underestimation of the role of the environment, and in particular, that of the interaction of genotypes with environmental factors, and B) in the continuing lack of incorporation of development into the evolutionary synthesis. We propose the integration of genetic, environmental and developmental perspectives on the evolution of the (...) phenotype in the form of the concept of the developmental reaction norm (DRN) The DRN represents the set of multivariate ontogenies that can be produced by a single genotype when it is exposed to environmental variation. It encompasses: 1) the processes that alter the phenotype throughout the ontogenetic trajectory, 2) the recognition that different aspects of the phenotype are (and must be) correlated and 3) the ability of a genotype to produce phenotypes in different environments. This perspective necessitates the explicit study of character expression during development, the evaluation of associations between pairs or groups of characters (e.g., multivariate allometries), and the exploration of reaction norms and phenotypic plasticity. We explicitly extend the concept of the DRN to encompass adjustments made in response to changes in the internal environment as well. Thus, ‘typical’ developmental sequences (e.g., cell fate determination) and plastic responses are simply manifestations of different scales of ‘environmental’ effects along a continuum. We present: (1) a brief conceptual review of three fundamental aspects of the generation and evolution of phenotypes: the changes in the trajectories describing growth and differentiation (ontogeny), the multivariate relationships among characters (allometry), and the effect of the environment (plasticity); (2) a discussion of how these components are merged in the concept of the developmental reaction norm; and (3) a reaction norm perspective of major determinants of phenotypes: epigenesis, selection and constraint. (shrink)

Organisms that share the capability of storing information about experiences in the past have an actively generated background resource on which they can compare and evaluate more recent experiences in order to quickly or even better react than in previous situations. This is an essential competence for all reaction and adaptation purposes of living organisms. Such memory/learning skills can be found from akaryotes up to unicellular eukaryotes, fungi, animals and plants, although until recently, it had been mentioned only as a (...) capability of higher animals. With the rise of epigenetics, the context-dependent marking of experiences at both the phenotype and the genotype level is an essential perspective to understand memory and learning in all organisms. Both memory and learning depend on a variety of successful communication processes within the whole organism. (shrink)

The theoretical heuristic of assuming distinct alleles (or genotypes) for alternative phenotypes is the foundation of the paradigm of evolutionary explanation we call the Modern Synthesis. In modeling the evolution of sociality, the heuristic has been to set altruism and selfishness as alternative phenotypes under distinct genotypes, which has been dubbed the “phenotypic gambit.” The prevalence of the altruistic genotype that is of lower evolutionary fitness relative to the alternative genotype for non-altruistic behavior in populations is the basis (...) of the “paradox of altruism.” I show in this article that the assumption of contrasting genotypes for altruism and selfishness in our “phenotypic gambit” is inconsistent with the empirical data when viewed in the light of today’s post-Mendelian understanding of gene expression. I demonstrate that however nuanced and sophisticated the models may have become today, they are still rooted in that fundamentally problematic assumption. I then offer a genetic conception of altruism that best fits the field data. (shrink)

Der berühmte Ameisenmann E.O. Wilson war schon immer einer meiner Helden - nicht nur ein hervorragender Biologe, sondern eine der winzigen und verschwindenden Minderheit von Intellektuellen, die es zumindest wagt, die Wahrheit über unsere Natur anzudeuten, die andere nicht verstehen oder, soweit sie es verstehen, aus politischen Gründen unermüdlich vermeiden. Leider beendet er seine lange Karriere auf äußerst schäbige Weise als Partei eines ignoranten und arroganten Angriffs auf die Wissenschaft, der zumindest teilweise durch die religiöse Inbrunst seiner Harvard-Kollegenmotiviertist. Es zeigt (...) die abscheulichen Folgen, wenn Universitäten Geld von religiösen Gruppen annehmen, Wissenschaftszeitschriften von großen Namen so bewundert sind, dass sie eine ordnungsgemäße Peer Review vermeiden und wenn Egos außer Kontrolle geraten dürfen. Es führt uns in die Natur der Evolution, die Grundlagen der wissenschaftlichen Methodik, wie Mathematik mit Wissenschaft zusammenhängt, was eine Theorie ausmacht, und sogar, welche Einstellungen zu Religion und Großzügigkeit angemessen sind, wenn wir uns unaufhaltsam dem Zusammenbruch der industriellen Zivilisation nähern. Ich fand Abschnitte in 'Conquest' mit dem üblichen prägnanten Kommentar (obwohl nichts wirklich Neues oder Interessantes, wenn man seine anderen Werke gelesen hat und auf biologie im Allgemeinen ist) in der oftgestylten Prosa, die sein Markenzeichen ist, aber war ziemlich überrascht, dass der Kern des Buches seine Ablehnung inklusiver Fitness (die seit über 50 Jahren ein Standbein der Evolutionsbiologie ist) zugunsten der Gruppenauswahl ist. Man nimmt an, dass von ihm kommen und mit den articles er bezieht sich auf veröffentlicht von sich selbst und Harvard Mathematik Kollege Nowak in großen Peer-Review-Zeitschriften wie Nature, muss es ein wesentlicher Fortschritt sein,, trotz der Tatsache, dass ich wusste, Gruppenauswahl wurde fast überall abgelehnt, da mit jeder großen Rolle in der Evolution. Ich habe zahlreiche Rezensionen im Netz gelesen und viele haben gute Kommentare, aber die, die ich am meisten sehen wollte, war, dass von renommierten Wissenschaftsautor und Evolutionsbiologe Richard Dawkins. Im Gegensatz zu den meisten von Fachleuten, die in Zeitschriften nur für diejenigen mit Zugang zu einer Universität zur Verfügung stehen, ist es leicht im Netz verfügbar, obwohlanscheinend, entschied er sich, es nicht in einer Zeitschrift zu veröffentlichen, da es angemessen abscheulich ist. Leider findet man eine vernichtende Ablehnung des Buches und den acerbic Kommentar über einen wissenschaftlichen Kollegen, den ich je von Dawkins gesehen habe -- über alles in seinem vielen Austausch mit dem verstorbenen und unbeklagten Demagogen und Pseudowissenschaftler Stephan Jay Gould. Obwohl Gould für seine persönlichen Angriffe auf seinen Harvard-Kollegen Wilson berüchtigt war, stellt Dawkins fest, dass ein Großteil von "Conquest" einen unbequem an Goulds häufige Verfehlungen in "bland, unfocussed ecumenicalis" erinnert. Dasselbe gilt mehr oder weniger für Wilsons populäres Schreiben, einschließlich seines jüngsten Buches "The Meaning of Human Existence" – eine weitere schamlose Eigenwerbung seiner diskreditierten Ideen zu Inklusiver Fitness (IF). Dawkins weist darauf hin, dass das berüchtigte 2010-Papier von Nowak, Tarnita und Wilson in Nature von über 140 Biologen, die einen Brief unterzeichnet haben, fast überall abgelehnt wurde und dass es in Wilsons Buch kein Wort darüber gibt. Auch in den folgenden 4 Jahren mit Artikeln, Vorträgen und mehreren Büchern haben sie dies nicht korrigiert. Es gibt keine andere Wahl, als Dawkins trenchant Kommentar zuzustimmen: "Für Wilson nicht zu zugeben, dass er für sich selbst gegen die große Mehrheit seiner professionellen Kollegen spricht - es schmerzt mich, dies von einem lebenslangen Helden zu sagen -- ein Akt mutwilligen Arroganz." Angesichts von Nowaks späterem Verhalten muss man ihn auch einbeziehen. Ich habe das Gefühl, dass einer der fassungslosen Menschen, die man im Fernsehen sieht, interviewt wird, nachdem der nette Mann von nebenan, der seit 30 Jahren alle Kinder babysitten, als Serienmörder entlarvt wird. Dawkins weist auch darauf hin (wie er und andere seit vielen Jahren), dass inklusive Fitness mit dem Neo-Darwinismus (d.h. logischerweise folgt) entsteht und nicht abgelehnt werden kann, ohne die Evolution selbst abzulehnen. Wilson erinnert uns erneut an Gould, der Kreationisten von der einen Seite seines Mundes anprangerte, während er ihnen Trost spendete, indem er endlosen ultraliberalen marxistisch gefärbten Kauderwelsch über Spandrels, unterbrochenes Gleichgewicht und Evolutionspsychologie von der anderen ausspeist. Die Unbestimmtheit und mathematische Opazität (für die meisten von uns) der Mathematik der Gruppen- oder Mehrebenenauswahl ist genau das, was die Sanftmütigen ihnen ermöglichen wollen, dem rationalen Denken in ihren endlosen antiwissenschaftlichen Gerüchten und (in der Wissenschaft) postmodernen Wortsalate zu entkommen. Schlimmer noch, Wilsons "Eroberung" ist ein schlecht durchdachtes und schlampig geschriebenes Durcheinander voller Nonsequiturs, vager Streifzüge, Verwirrungen und Inkohärenz. Eine gute Bewertung, die einige davon im Detail ist, dass von Absolvent Gerry Carter, die Sie im Netz finden können. Wilson hat auch nichts mit unserem gegenwärtigen Verständnis der Evolutionspsychologie (EP) zu tun (siehe z.B. die letzten 300 Seiten von Pinkers 'The Better Angels of our Nature'). Wenn Sie eine seriöse Buchlänge Bericht über die soziale Evolution und einige relevante EP von einem Experten wollen, siehe 'Principles of Social Evolution' von Andrew F.G. Bourke, oder ein nicht ganz so ernster und zugegebenermaßen fehlerhafter und irrender Bericht, aber ein Muss,das Robert Trivers dennoch lesen muss—'The Folly of Fools: The Logic of Deceit and Self-Deception in Human Life' und ältere, aber immer noch aktuelle und durchdringende Werke wie 'The Evolutionof Cooperation':Revised Edition by Robert Axelrod and 'The Biology ofMoral Systems' von Richard Alexander. (shrink)

Phenotypic integration refers to the study of complex patterns of covariation among functionally related traits in a given organism. It has been investigated throughout the 20th century, but has only recently risen to the forefront of evolutionary ecological research. In this essay, I identify the reasons for this late flourishing of studies on integration, and discuss some of the major areas of current endeavour: the interplay of adaptation and constraints, the genetic and molecular bases of integration, the role of phenotypic (...) plasticity, macroevolutionary studies of integration, and statistical and conceptual issues in the study of the evolution of complex phenotypes. I then conclude with a brief discussion of what I see as the major future directions of research on phenotypic integration and how they relate to our more general quest for the understanding of phenotypic evolution within the neo-Darwinian framework. I suggest that studying integration provides a particularly stimulating and truly interdisciplinary convergence of researchers from fields as disparate as molecular genetics, developmental biology, evolutionary ecology, palaeontology and even philosophy of science. (shrink)

Background: One of the all-time questions in evolutionary biology regards the evolution of organismal shapes, and in particular why certain forms appear repeatedly in the history of life, others only seldom and still others not at all. Recent research in this field has deployed the conceptual framework of constraints and natural selection as measured by quantitative genetic methods. Scope: In this paper I argue that quantitative genetics can by necessity only provide us with useful statistical sum- maries that may lead (...) researchers to formulate testable causal hypotheses, but that any inferential attempt beyond this is unreasonable. Instead, I suggest that thinking in terms of coordinates in phenotypic spaces, and approaching the problem using a variety of empirical methods (seeking a consilience of evidence), is more likely to lead to solid inferences regarding the causal basis of the historical patterns that make up most of the data available on phenotypic evolution. (shrink)

An exploration of the nexus between ecology, evolutionary biology and molecular biology, via the concept of phenotypic plasticity.

In addition to considerable debate in the recent evolutionary literature about the limits of the Modern Synthesis of the 1930s and 1940s, there has also been theoretical and empirical interest in a variety of new and not so new concepts such as phenotypic plasticity, genetic assimilation and phenotypic accommodation. Here we consider examples of the arguments and counter- arguments that have shaped this discussion. We suggest that much of the controversy hinges on several misunderstandings, including unwarranted fears of a general (...) attempt at overthrowing the Modern Synthesis paradigm, and some fundamental conceptual confusion about the proper roles of phenotypic plasticity and natural selection within evolutionary theory. (shrink)

The study of phenotypic plasticity has progressed significantly over the past few decades. We have moved from variation for plasticity being considered as a nuisance in evolutionary studies to it being the primary target of investigations that use an array of methods, including quantitative and molecular genetics, as well as of several approaches that model the evolution of plastic responses. Here, I consider some of the major aspects of research on phenotypic plasticity, assessing where progress has been made and where (...) additional effort is required. I suggest that some areas of research, such the study of the quantitative genetic underpinning of plasticity, have been either settled in broad outline or superseded by new approaches and questions. Other issues, such as the costs of plasticity are currently at the forefront of research in this field, and are likely to be areas of major future development. (shrink)

How to use a model organism to study phenotypic integration and constraints on evolution.

Despite a large and multifaceted effort to understand the vast landscape of phenotypic data, their current form inhibits productive data analysis. The lack of a community-wide, consensus-based, human- and machine-interpretable language for describing phenotypes and their genomic and environmental contexts is perhaps the most pressing scientific bottleneck to integration across many key fields in biology, including genomics, systems biology, development, medicine, evolution, ecology, and systematics. Here we survey the current phenomics landscape, including data resources and handling, and the progress that (...) has been made to accurately capture relevant data descriptions for phenotypes. We present an example of the kind of integration across domains that computable phenotypes would enable, and we call upon the broader biology community, publishers, and relevant funding agencies to support efforts to surmount today's data barriers and facilitate analytical reproducibility. (shrink)

Is integrative biology a good idea, or even possible? There has been much interest lately in the unifica- tion of biology and the integration of traditionally separate disciplines such as molecular and develop- mental biology on one hand, and ecology and evolutionary biology on the other. In this paper I ask if and under what circumstances such integration of efforts actually makes sense. I develop by example an analogy with Aristotle’s famous four “causes” that one can investigate concerning any object (...) or phenomenon: material (what something is made of), formal (what distinguishes that particular object from others), efficient (how was the object made) and final (why was the object made). The example is provided by ongoing research on different aspects of flowering time in the model system Arabidop- sis, a small weed belonging to the mustard family. I show that understanding how flowering time is controlled is an epistemologically different sort of question from why and how it evolved, and that the two research agendas can be pursued largely independently of each other. Toward the end, I propose that the real goal of integrative biology is to understand the boundary layers between levels of biologi- cal analysis, something to which modern philosophy of science can contribute significantly. (shrink)

Developmental plasticity as the nexus between genetics and ecology.

A phenome occurs through the many pathways of the complex net of interaction between the phenome and its environment; therefore researching and understanding how it arises requires investigation into many possible causes that are in constant interaction with each other. The most comprehensive investigations in biology are the ones in which many biologists from different sub-areas—evolutionary biology, developmental biology, molecular biology, physiology, genetics, epigenetics, ecology—have collaborated. Still, biologists do not always need to collaborate or look for the most comprehensive explanations. (...) A more standard investigation in biology occurs within a single subarea, and uses well-defined experiments with very specific conditions. This paper is about causation and related explanation in plant phenome research and its relevance to Aristotle’s Theory of Four Causes. I argue that there are causes which resemble Aristotle’s formal, material, and efficient causes in phenotype explanation and occurrence; but causes which resemble Aristotle’s final causes occur in phenotype explanation only, not in the occurrence. (shrink)

We attempt to improve the understanding of the notion of agene being `for a phenotypic trait or traits. Considering theimplicit functional ascription of one thing being `for another,we submit a more restrictive version of `gene for talk.Accordingly, genes are only to be thought of as being forphenotypic traits when good evidence is available that thepresence or prevalence of the gene in a population is the resultof natural selection on that particular trait, and that theassociation between that trait and the gene (...) in question isdemonstrably causal. It is therefore necessary to gatherstatistical, biochemical, historical, as well as ecologicalinformation before properly claiming that a gene is for aphenotypic trait. Instead of hampering practical use of the `genefor talk, our approach aims at stimulating much needed researchinto the functional ecology and comparative evolutionary biologyof gene action. (shrink)

A response to Via about the existence (or not) and role of plasticity genes in evolution.

Digital phenotyping will potentially enable earlier detection and prediction of mental illness by monitoring human interaction with and through digital devices. Notwithstanding its promises, it is certain that a person’s digital phenotype will at times be at odds with their first-person testimony of their psychological states. In this paper, we argue that there are features of digital phenotyping in the context of psychiatry which have the potential to exacerbate the tendency to dismiss patients’ testimony and treatment preferences, which can (...) be instances of epistemic injustice. We first explain what epistemic injustice is, and why it is argued to be an extensive problem in health and disability settings. We then explain why epistemic injustice is more likely to apply with even greater force in psychiatric contexts, and especially where digital phenotyping may be involved. Finally, we offer some tentative suggestions of how epistemic injustice can be minimised in digital psychiatry. (shrink)

How we ought to diagnose, categorise and respond to spectrum disabilities such as autism and Attention Deficit/Hyperactivity Disorder (ADHD) is a topic of lively debate. The heterogeneity associated with ADHD and autism is described as falling on various continua of behavioural, neural, and genetic difference. These continua are varyingly described either as extending into the general population, or as being continua within a given disorder demarcation. Moreover, the interrelationships of these continua are likewise often vague and subject to diverse interpretations. (...) -/- In this paper, I explore geneticists' and self-advocates’ perspectives concerning autism and ADHD as continua. These diagnoses are overwhelmingly analysed as falling on a continuum or continua of underlying traits, which supports the notion of “the neurodiversity spectrum”, i.e., a broader swath of human neural and behavioural diversity on which some concentrations of different functioning are diagnosed. I offer a taxonomy of conceptions of the genetic, phenotypic, and endophenotypic dimensionality within and beyond these diagnostic categories, and suggest that the spectrum of neurodiversity is characteristically endophenotypic. (shrink)

In a recent paper, Brandon and Nijhout argue against genic selectionism—the thesis, roughly, that evolutionary processes are best understood from the gene’s-eye point of view—by presenting a case in which genic models of selection allegedly make predictions that conflict with the (correct) predictions of higher-level genotypic selection models. Their argument, if successful, would refute the widely held belief that genic models and higher-level models are predictively equivalent. Here, I argue that Brandon and Nijhout fail to demonstrate that the models make (...) incompatible predictions. (shrink)

Psychiatry has witnessed a new wave of approaches to clinical phenotyping and the study of psychopathology, including the National Institute of Mental Health’s Research Domain Criteria, clinical staging, network approaches, the Hierarchical Taxonomy of Psychopathology, and the general psychopathology factor, as well as a revival of interest in phenomenological psychopathology. The question naturally emerges as to what the relationship between these new approaches is – are they mutually exclusive, competing approaches, or can they be integrated in some way and used (...) to enrich each other? In this opinion piece, we propose a possible integration between clinical staging and phenomenological psychopathology. Domains identified in phenomenological psychopathology, such as selfhood, embodiment, affectivity, etc., can be overlaid on clinical stages in order to enrich and deepen the phenotypes captured in clinical staging (‘high resolution’ clinical phenotypes). This approach may be useful both ideographically and nomothetically, in that it could complement diagnosis, enrich clinical formulation, and inform treatment of individual patients, as well as help guide aetiological, prediction, and treatment research. The overlaying of phenomenological domains on clinical stages may require that these domains are reformulated in dimensional rather than categorial terms. This integrative project requires assessment tools, some of which are already available, that are sensitive and thorough enough to pick up on the range of relevant psychopathology. The proposed approach offers opportunities for mutual enrichment: clinical staging may be enriched by introducing greater depth to phenotypes; phenomenological psychopathology may be enriched by introducing stages of severity and disorder progression to phenomenological analysis. (shrink)

During the last two decades the role of quantitative genetics in evolutionary theory has expanded considerably. Quantitative genetic-based models addressing long term phenotypic evolution, evolution in multiple environments (phenotypic plasticity) and evolution of ontogenies (developmental trajectories) have been proposed. Yet, the mathematical foundations of quantitative genetics were laid with a very different set of problems in mind (mostly the prediction of short term responses to artificial selection), and at a time in which any details of the genetic machinery were virtually (...) unknown. In this paper we discuss what a model is in population biology, and what kind of model we need in order to address the complexities of phenotypic evolution. We review the assumptions of quantitative genetics and its most recent accomplishments, together with the limitations that such assumptions impose on the modelling of some aspects of phenotypic evolution. We also discuss three alternative appr oaches to the theoretical description of evolutionary trajectories (nonlinear dynamics, complexity theory and optimization theory), and their respective advantages and limitations. We conclude by calling for a new theoretical synthesis, including quantitative genetics and not necessarily limited to the other approaches here discussed. (shrink)

After introducing the new field of cultural evolution, we review a growing body of empirical evidence suggesting that culture shapes what people attend to, perceive and remember as well as how they think, feel and reason. Focusing on perception, spatial navigation, mentalizing, thinking styles, reasoning (epistemic norms) and language, we discuss not only important variation in these domains, but emphasize that most researchers (including philosophers) and research participants are psychologically peculiar within a global and historical context. This rising tide of (...) evidence recommends caution in relying on one’s intuitions or even in generalizing from reliable psychological findings to the species, Homo sapiens. Our evolutionary approach suggests that humans have evolved a suite of reliably developing cognitive abilities that adapt our minds, information-processing abilities and emotions ontogenetically to the diverse culturally-constructed worlds we confront. (shrink)

Metaphors play a crucial role in both science in particular and human discourse in gen- eral. Plato’s story of the cave—about people shackled to a wall and incapable of perceiv- ing the world as it really is—has stimulated thinking about epistemology and the nature of reality for more than two millennia. But metaphors can also be misleading: being too taken with Plato’s story has cost philosophers endless discussions about how to access the world “as it is,” until Kant showed us (...) that it is just not going to happen, ever. (shrink)

The concept of reaction norms plays a crucial role in connecting molecular and evolutionary biology.

The idea of phenotypic novelty appears throughout the evolutionary literature. Novelties have been defined so broadly as to make the term meaningless and so narrowly as to apply only to a limited number of spectacular structures. Here I examine some of the available definitions of phenotypic novelty and argue that the modern synthesis is ill equipped at explaining novelties. I then discuss three frameworks that may help biologists get a better insight of how novelties arise during evolution but warn that (...) these frameworks should be considered in addition to, and not as potential substitutes of, the modern synthesis. †To contact the author, please write to: Departments of Ecology and Evolution and Philosophy, Stony Brook University, Stony Brook, NY 11794; e‐mail: [email protected]. (shrink)

The concepts of reaction norms and phenotypic plasticity help us better understand what a biological trait is.

The transformational pace of modern education, healthcare, business management systems, etc., requires new approaches for prompt and reliable personality assessment. Phenotypology is one of such theories and it claims of the discovered interconnections of a person’s psychological and psychophysical characteristics on the basis of individual features of his/her phenotype. The article aim is to present some validation results for the Phenotypology hypotheses as a possible tool for personality assessment. In order to verify connections between phenotypic treats and individual behavior, (...) we conducted the study when respondents were differentiated according to some anthropometric (facial) peculiarities and characterological features. The results were quantified and analyzed using the mathematical-statistical linear regression. The research output contains the rationale for the conclusion that there are no statistically significant correlations between some phenotypic body features and such individual psychological characteristics as aggressiveness, impetuosity, pedantry, passivity, etc. In particular, the validity of using of appropriate phenotypologic representations to predict the examined character traits was studied. The obtained results disproved the possibility to use directly the phenotypic approach for reliable characterological profiling. Though, the study outcome is tentative due to some limitations on generality. It is necessary to continue verification of the Phenotypology hypotheses with a broader experimental sample with the inclusion of various ethnic and racial groups’ representatives. However, until then, based on actual findings, the practical application of the Phenotypology statements is doubtful, at least for the purposes of character diagnosis and personality assessment. (shrink)

Many have argued that there is no reason why natural selection should cause directional increases in measures such as body size or complexity across evolutionary history as a whole. In this paper I argue that this conclusion does not hold for selection for adaptations to environmental variability, and that, given the inevitability of environmental variability, trends in adaptations to variability are an expected feature of evolution by natural selection. As a concrete instance of this causal structure, I outline how this (...) may be applied to a trend in phenotypic plasticity. (shrink)

The Modern Synthesis (MS) is the current paradigm in evolutionary biology. It was actually built by expanding on the conceptual foundations laid out by its predecessors, Darwinism and neo-Darwinism. For sometime now there has been talk of a new Extended Evolutionary Synthesis (EES), and this article begins to outline why we may need such an extension, and how it may come about. As philosopher Karl Popper has noticed, the current evolutionary theory is a theory of genes, and we still lack (...) a theory of forms. The field began, in fact, as a theory of forms in Darwin’s days, and the major goal that an EES will aim for is a unification of our theories of genes and of forms. This may be achieved through an organic grafting of novel concepts onto the foundational structure of the MS, particularly evolvability, phenotypic plasticity, epigenetic inheritance, complexity theory, and the theory of evolution in highly dimensional adaptive landscapes. (shrink)

This essay explores the relation between nature and culture and analyses it from the perspective of contemporary evolutionary theory. Both animals and humans are conceived of as attaining both natural and cultural features that interact with each other on a number of levels of varying complexity: nature as cultural, nature as influenced by culture, culture as natural, and culture as influenced by nature. “Nature as cultural” is meant to express a decoupling of behavioral/phenotypic changes of an organism from its genetic (...) determination. “Nature as influenced by culture” is the idea of niche construction, wherein such decoupled changes can causally feedback to genetic reality, thereby influencing the evolutionary features of downstream species. “Culture as natural” portrays how cultural structures of humans and animals persist through the generations, accumulate incurred changes, and evolve in analogous ways to biological natural selection. “Culture as influenced by nature” is the notion that the cultural/linguistic capacities of animals and humans have evolutionarily emerged from precultural history. All this is meant to evaluate the viability of constructing a nature/culture divide. The conclusion is made that the divide seems arbitrary within and between human and animal life when considering how the differences between the natural and cultural dynamics of humans and animals are modelled as differences of degree, not kind. A potential approach in using the concept of consciousness to recontextualize a nature/culture divide in terms of the possession of consciousness is proposed at the end. (shrink)

In the fall of 1990 I had just began my doc- toral studies at the University of Connecticut. Freshly arrived from Italy, I came to the United States to work with Carl Schlichting on something to do with phenotypic plastic- ity. I spent most of that semester discussing with other graduate students what I thought was a momentous paper by Mary Jane West- Eberhard (1989) in the Annual Review of Ecol- ogy and Systematics. That paper, entitled Phe- notypic Plasticity and (...) the Origins of Diversity, was a (quite lengthy) forerunner of the (also quite bulky) book I am reviewing now. Like the paper, this volume has the potential to be momentous in the development of our ideas on phenotypic evolution. (shrink)

Driven by technological innovations, newborn screening (NBS) panels have been expanded and the development of genomic NBS pilot programs is rapidly progressing. Decisions on disease selection for NBS are still based on the Wilson and Jungner (WJ) criteria published in 1968. Despite this uniform reference, interpretation of the WJ criteria and actual disease selection for NBS programs are highly variable. A systematic literature search [PubMED search “Wilson” AND “Jungner”; last search 16.07.22] was performed to evaluate the applicability of the WJ (...) criteria for current and future NBS programs and the need for adaptation. By at least two reviewers, 105 publications (systematic literature search, N = 77; manual search, N = 28) were screened for relevant content and, finally, 38 publications were evaluated. Limited by the study design of qualitative text analysis, no statistical evaluation was performed, but a structured collection of reported aspects of criticism and proposed improvements was instead collated. This revealed a set of general limitations of the WJ criteria, such as imprecise terminology, lack of measurability and objectivity, missing pediatric focus, and absent guidance on program management. Furthermore, it unraveled specific aspects of criticism on clinical, diagnostic, therapeutic, and economical aspects. A major obstacle was found to be the incompletely understood natural history and phenotypic diversity of rare diseases prior to NBS implementation, resulting in uncertainty about case definition, risk stratification, and indications for treatment. This gap could be closed through the systematic collection and evaluation of real-world evidence on the quality, safety, and (cost-)effectiveness of NBS, as well as the long-term benefits experienced by screened individuals. An integrated NBS public health program that is designed to continuously learn would fulfil these requirements, and a multi-dimensional framework for future NBS programs integrating medical, ethical, legal, and societal perspectives is overdue. (shrink)

I argue that the Conceptual Ethics and Conceptual Engineering framework, in its pragmatist version as recently defended by Thomasson (2017, 2020), provides a means of articulating and defending the conventionalist interpretation of projects of conceptual extension (e.g. the extended mind, the extended phenotype) in biology and psychology. This promises to be illuminating in both directions: it helps to make sense of, and provides an explicit methodology for, pragmatic conceptual extension in science, while offering further evidence for the value and (...) fruitfulness of the conceptual ethics/engineering framework itself, in particular with respect to conceptual change within science, which has thus-far received little attention in the literature on conceptual ethics/engineering. (shrink)

Precision Medicine is driven by the idea that the rapidly increasing range of relatively cheap and efficient self-tracking devices make it feasible to collect multiple kinds of phenotypic data. Advocates of N = 1 research emphasize the countless opportunities personal data provide for optimizing individual health. At the same time, using biomarker data for lifestyle interventions has shown to entail complex challenges. In this paper, we argue that researchers in the field of precision medicine need to address the performative dimension (...) of collecting data. We propose the fun-house mirror as a metaphor for the use of personal health data; each health data source yields a particular type of image that can be regarded as a ‘data mirror’ that is by definition specific and skewed. This requires competence on the part of individuals to adequately interpret the images thus provided. (shrink)

Hybridization by introgression (“hybridization”) is a complex topic in conservation. Many conservation decision-makers are concerned about hybridization by introgression because it may threaten species persistence or local phenotypes, among other potential long-term problems. While attitudes have changed towards hybridization as a conservation threat, there are still concerns about hybridization as a problem, particularly if the hybridization was anthropogenically mediated. I propose that these concerns are overblown and that it is misguided to focus on whether hybridization is unintentionally human-mediated. I argue (...) that practitioners should still consider the effects of hybridization on conservation, but the reasons should concern the long-term environmental consequences, such as ecological function and social and cultural that hybridization has, rather than whether humans “caused” the hybrid. I propose a series of steps to think differently about these cases. (shrink)