In this paper I argue that the extent to which a human trait is genetically caused can causally depend upon whether the trait is categorized within human genetics as genetically caused. This makes the kind genetically caused trait an interactive kind. I demonstrate that this thesis is both conceptually coherent and empirically plausible. I outline the core rationale of this thesis and demonstrate its conceptual coherence by drawing upon Waters’ (2007) analysis of genetic causation. I add empirical plausibility to the (...) thesis by describing a hypothetical but empirically plausible mechanism by which the fact that obesity is categorized as genetically caused within human genetics increases the extent to which obesity is in fact genetically caused. (shrink)

People disagree about the causes of social inequality and how to most effectively intervene in them. These may seem like empirical questions for social scientists, not philosophers. However, causal explanation itself depends on broadly normative commitments. From this it follows that (moral) philosophers have an important role to play in determining those causal explanations. I examine the case of causal explanations of poverty to demonstrate these claims. In short, philosophers who work to reshape our moral expectations also work, on the (...) back end, to restructure acceptable causal explanations—and hence solutions—for social inequality. Empirical and normative inquiry, then, are a two-way street. (shrink)

Instances of explanatory reduction are often advocated on metaphysical grounds; given that the only real things in the world are subatomic particles and their interaction, we have to try to explain everything in terms of the laws of physics. In this paper, we show that explanatory reduction cannot be defended on metaphysical grounds. Nevertheless, indispensability arguments for reductive explanations can be developed, taking into account actual scientific practice and the role of epistemic interests. Reductive explanations might be indispensable to address (...) some epistemic interest answering a specific explanation-seeking question in the most accurate, adequate and efficient way. Just like explanatory pluralists often advocate the indispensability of higher levels of explanation pointing at the pragmatic value of the explanatory information obtained on these higher levels, we argue that explanatory reduction—traditionally understood as the contender of pluralism—can be defended in a similar way. The pragmatic value reductionist, lower level explanations might have in the biomedical sciences and the social sciences is illustrated by some case studies. (shrink)

Keller explains the persistence of the nature/nurture debate by a chronic ambiguity in language derived from classical and behavioral genetics. She suggests that the more precise vocabulary of modern molecular genetics may be used to rephrase the underlying questions and hence provide a way out of this controversy. I show that her proposal fits into a long tradition in which other authors have wrestled with the same problem and come to similar conclusions. - Review of 'The mirage of a space (...) between nature and nurture' by Evelyn Fox Keller, Duke University Press, 2010, ISBN 9780822347316. (shrink)

Philosophers and historians of biology have argued that genes are conceptualized differently in different fields of biology and that these differences influence both the conduct of research and the interpretation of research by audiences outside the field in which the research was conducted. In this paper we report the results of a questionnaire study of how genes are conceptualized by biological scientists at the University of Sydney, Australia. The results provide tentative support for some hypotheses about conceptual differences between different (...) fields of biological research. (shrink)

A central idea of developmental systems theory is ‘parity’ or ‘symmetry’ between genes and non-genetic factors of development. The precise content of this idea remains controversial, with different authors stressing different aspects and little explicit comparisons among the various interpretations. Here I characterise and assess several influential versions of parity.

We argue that Madole & Harden's distinction between shallow versus deep genetic causes can bring some clarity to causal claims arising from genome-wide association studies (GWASs). However, the authors argue that GWAS only finds shallow genetic causes, making GWAS commensurate with the environmental studies they hope to supplant. We also assess whether their distinction applies best to explanations or causes.

One of the foundational problems of biochemistry concerns the conceptualisation of the relationship between the composition, structure and function of macromolecules like proteins. Part of the recent philosophical literature displays a reductionist bias, that is, the endorsement of a form of microstructuralism mirroring an out-dated biochemical conceptualisation. We shall argue that such microstructuralist approaches are ultimately committed to a potentialist form of micro-predeterminism whereby the macrostructure and function of proteins is accounted for solely in terms of the intrinsic properties and (...) potentialities of the components of the primary structure as if they were self-contained or essentially immutable entities. We shall instead suggest that a conceptualisation of the relationship between proteins’ composition, structure and function consistent with contemporary biochemical practice should account also for the causal role of the cellular, organismal and environmental relations in protein development. The analysis of the folding process we propose suggests that microstructure-laden reductionist approaches are ontologically indefensible. Rather than a potentialist form of micro-predeterminism, our analysis ultimately supports a relational-construction-based view of protein development and potentialities formation, which requires an indispensable analysis of the dynamical interplay between the micro-level of the parts and the macro-level of the relational structures of their systems. (shrink)

ABSTRACT Dealing primarily with implications rather than foundations, and focusing downstream at the expense of upstream prevention, mainstream bioethics is at a toxic watershed. Through an extended analysis of the Environmental Genome Project (EGP), we offer new tools from the philosophy of science and from critical epidemiology to help bioethics to move ahead. Our aim in this paper is not to resolve the moral and conceptual problems we reveal, but rather to outline ways to prevent such problems from arising in (...) future research. (shrink)

I begin by examining how genetics drivesschizophrenia research, and raise both familiar andrelatively novel criticisms of the evidence putativelysupporting the genetic basis of schizophrenia. Inparticular, I call attention to a set of concernsabout the effects of placentation on concordance ratesof schizophrenia in monozygotic twins, which furtherweakens the case for schizophrenia''s so-called stronggenetic component. I then underscore two criticalpoints. First, I emphasize the importance of takingseriously considerations about the complexity of bothontogenesis and the development of hereditarydiseases. The recognition of developmentalconstraints and (...) supports is crucial, for attention todevelopment exposes the naivete of too many models ofgene action in the aetiology of disease. Secondly, Iattend to those schizophreniologists who ignoremethodological criticisms and thus presume a geneticbasis for schizophrenia, and then seek the schizophrenic genotype lacking an adequatephenotype. In response I attempt to demonstrate thenecessity of a sustained effort at characterizing thephenotype of schizophrenia as an enabling conditionfor the whole enterprise of psychiatric genetics – andfor psychiatry itself. Without the organism-levelphenotype, research at the level of genes will remainunproductive – assuming of course that research at thegenetic level is appropriate at all. (shrink)

In the social constructionist literature, little has been said about what it means for social factors to cause X in such a way that X would count as causally socially constructed. In this paper, I argue that being caused by social factors – and thus being causally socially constructed – is best defined in terms of a contrastive counterfactual notion of causation. Unlike some plausible alternatives, this definition captures what is at stake in actual social constructionist debates. It makes transparent (...) which factors the truth of a causal constructionist claim may depend on. By doing so, it sheds light on what the disagreements over whether X is causally socially constructed may turn on. It also helps us to see under which condition the claim that X is socially causally constructed is compatible with the claim that X is caused by biological factors. (shrink)

Extrapolation from a well-understood base population to a less-understood target population can fail if the base and target populations are not sufficiently similar. Differences between laboratory mice and humans, for example, can hinder extrapolation in medical research. Mice that carry a partial or complete human physiological system, known as humanized mice, are supposed to make extrapolation more reliable by simulating a variety of human diseases. But what justifies our belief that these mice are similar enough to their human counterparts to (...) simulate human disease? I argue that, unless three requirements are met in the process of humanizing mice, very little does. My requirements are not meant to provide necessary and sufficient conditions that guarantee a particular outcome. Instead, they serve as a heuristic for guiding scientific judgments involving extrapolation. In developing each requirement, I engage with philosophical issues concerning the nature of model-based science and the mechanistic approach (and its limits) to making generalizations in the life sciences. (shrink)

Synthetic biology research is often described in terms of programming cells through the introduction of synthetic genes. Genetic material is seemingly attributed with a high level of causal responsibility. We discuss genetic causation in synthetic biology and distinguish three gene concepts differing in their assumptions of genetic control. We argue that synthetic biology generally employs a difference-making approach to establishing genetic causes, and that this approach does not commit to a specific notion of genetic program or genetic control. Still, we (...) suggest that a strong program concept of genetic material can be used as a successful heuristic in certain areas of synthetic biology. Its application requires control of causal context, and may stand in need of a modular decomposition of the target system. We relate different modularity concepts to the discussion of genetic causation and point to possible advantages of and important limitations to seeking modularity in synthetic biology systems. (shrink)

This paper explores the analytical relevance of Foucault's notion of biopower in the context of regulating and managing non-human lives and populations, specifically those animals that are the focus of livestock breeding based on genetic techniques. The concept of biopower is seen as offering theoretical possibilities precisely because it is concerned with the regulation of life and of populations. The paper approaches the task of testing the 'analytic mettle' of biopower through an analysis of four policy documents concerned with farm (...) animal genetics: the UK's National Scrapie Plan (2003); the UK National Action Plan on Farm Animal Genetic Resources (2006); the Agriculture and Environment Biotechnology Committee's report on Animals and Biotechnology (2002); and the Farm Animal Welfare Council's report on the Welfare Implications of Animal Breeding and Breeding Technologies in Commercial Agriculture (2004). Of interest is whether and how the four policy case studies articulate a form of biopower in relation to human-livestock animal relations in the context of genetic approaches to livestock breeding, and how biopower is variably expressed in relation to the different policy issues addressed. In concluding, the paper considers the overall applicability and relevance of biopower in the context of regulating animal lives within livestock breeding, highlighting both possibilities and limitations, and offers suggestions for taking forward research on livestock populations from a neo-Foucaultian perspective. (shrink)

In this article, I focus on two problematic aspects of British health-promotion campaigns regarding feeding children, particularly regarding breastfeeding and obesity. The first of these is that health-promotion campaigns around “lifestyle” issues dehumanize mothers with their imagery or text, stemming from the ongoing undervaluing and objectification of mothers and women. Public health-promotion instrumentalizes mothers as necessary components in achieving its aims, while at the same time undermining their agency as persons and interlocutors by tying “mother” to particular images. This has (...) a double effect: first, it excludes mothers who do not fit the campaign picture of a mother; second, it encloses those who do fit the picture into an objectified image of motherhood that is defined by and subject to the dominant white, heteropatriarchal gaze. The second problem is that campaigns place unjustified demands on mothers, which stem from a misinterpretation of the maternal duty to benefit. I argue that nutrition-related health concerns regarding children are improperly framed as individual failures of maternal duty, rather than as failures of a system to function correctly. These arguments ultimately support shifting the focus of responsibility for issues around childhood nutrition away from mothers and back toward policymakers. (shrink)

The recent explosion of interest in epigenetics is often portrayed as the dawning of a scientific revolution that promises to transform biomedical science along with developmental and evolutionary biology. Much of this enthusiasm surrounds what we call the epigenetic switch hypothesis, which regards certain examples of epigenetic inheritance as an adaptive organismal response to environmental change. This interpretation overlooks an alternative explanation in terms of coevolutionary dynamics between parasitic transposons and the host genome. This raises a question about whether epigenetics (...) researchers tend to overlook transposon dynamics more generally. To address this question, we surveyed a large sample of scientific publications on the topics of epigenetics and transposons over the past fifty years. We found that enthusiasm for epigenetics is often inversely related to interest in transposon dynamics across the four disciplines we examined. Most surprising was a declining interest in transposons within biomedical science and cellular and molecular biology over the past two decades. Also notable was a delayed and relatively muted enthusiasm for epigenetics within evolutionary biology. An analysis of scientific abstracts from the past twenty-five years further reveals systematic differences among disciplines in their uses of the term epigenetic, especially with respect to heritability commitments and functional interpretations. Taken together, these results paint a nuanced picture of the rise of epigenetics and the possible neglect of transposon dynamics, especially among biomedical scientists. (shrink)

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

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

Two decades of critique have sensitized historians and philosophers of science to the inadequacies of conventional dichotomies between theory and practice, thereby prompting the search for new ways of writing about science that are less beholden than the old ways to the epistemological mores of theoretical physics, and more faithful to the actual practices not only of physics but of all the natural sciences. The need for alternative descriptions seems particularly urgent if one is to understand the place of theory (...) (and, in parallel, the role of modeling) in contemporary molecular biology, a science where, until now, no division between theory and experiment has obtained, and where distinctions between representing and intervening, and more generally, between basic and applied science, are daily becoming more blurred. Indeed, the very division between theory and experiment threatens to slight the extensive and sophisticated theoretical analyses (and even modeling) on which experimental work in contemporary molecular biology so often depends. My aim in this paper is to find a way of talking about theoretical practices in biology that is directly rooted in the mix of conceptual and material work that biologists do. As an example of such theoretical practices, I choose for the focus of my analysis the development of a model for gene regulation out of the experimental work of Eric Davidson and his colleagues at Cal Tech. (shrink)

This paper examines the discourses and practices of pedigree livestock breeding, focusing on beef cattle and sheep in the UK, concentrating on an under-examined aspect of this—the deselection and rejection of some animals from future breeding populations. In the context of exploring how animals are valued and represented in different ways in relation to particular agricultural knowledge-practices, it focuses on deselecting particular animals from breeding populations, drawing attention to shifts in such knowledge-practices related to the emergence of “genetic” techniques in (...) livestock breeding which are arguably displacing “traditional” visual and experiential knowledge’s of livestock animals. The paper situates this discussion in the analytical framework provided by Foucault’s conception of “biopower,” exploring how interventions in livestock populations aimed at the fostering of domestic animal life are necessarily also associated with the imperative that certain animals must die and not contribute to the future reproduction of their breed. The “geneticization” of livestock breeding produces new articulations of this process associated with different understandings of animal life and the possibilities of different modes of intervention in livestock populations. Genetic techniques increasingly quantify and rationalize processes of selection and deselection, and affect how animals are perceived and valued both as groups and as individuals. The paper concludes by emphasizing that the valuation of livestock animals is contested, and that the entanglement of “traditional” and “genetic” modes of valuation means that there are multiple layers of valuation and (de)selection involved in breeding knowledge-practices. (shrink)

In cases in which many causes together bring about an effect, it is common to select some as particularly important. Philosophers since Mill have been pessimistic about analyzing this reasoning because of its variability and the multifarious causal and pragmatic details of how it works. I argue Mill was right to think these details matter but wrong that they preclude philosophical analysis of causal selection. I show that analyzing the pragmatic details of scientific debates about the important causes of the (...) Bhopal Gas Tragedy can illuminate causal reasoning about disasters and shed new light on causality and causal selection. (shrink)

The themes, problems and challenges of developmental systems theory as described in Cycles of Contingency are discussed. We argue in favor of a robust approach to philosophical and scientific problems of extended heredity and the integration of behavior, development, inheritance, and evolution. Problems with Sterelny's proposal to evaluate inheritance systems using his `Hoyle criteria' are discussed and critically evaluated. Additional support for a developmental systems perspective is sought in evolutionary studies of performance and behavior modulation of fitness.

This paper questions the prevailing historical understanding that scientific racism “retreated” in the 1950s when anthropology adopted the concepts and methods of population genetics and race was recognized to be a social construct and replaced by the concept of population. More accurately, a “populational” concept of race was substituted for a “typological one”—this is demonstrated by looking at the work of Theodosius Dobzhansky circa 1950. The potential for contemporary research in human population genetics to contribute to racism needs to be (...) considered with respect to the ability of the typological-population distinction to arbitrate boundaries between racist society and nonracist, even anti-racist, science. I point out some ethical limits of “population thinking” in doing so. (shrink)

Explanatory pluralism is the view that the best form and level of explanation depends on the kind of question one seeks to answer by the explanation, and that in order to answer all questions in the best way possible, we need more than one form and level of explanation. In the first part of this article, we argue that explanatory pluralism holds for the medical sciences, at least in theory. However, in the second part of the article we show that (...) medical research and practice is actually not fully and truly explanatory pluralist yet. Although the literature demonstrates a slowly growing interest in non-reductive explanations in medicine, the dominant approach in medicine is still methodologically reductionist. This implies that non-reductive explanations often do not get the attention they deserve. We argue that the field of medicine could benefit greatly by reconsidering its reductive tendencies and becoming fully and truly explanatory pluralist. Nonetheless, trying to achieve the right balance in the search for and application of reductive and non-reductive explanations will in any case be a difficult exercise. (shrink)

In the contemporary biomedical literature, every disease is considered genetic. This extension of the concept of genetic disease is usually interpreted either in a trivial or genocentrist sense, but it is never taken seriously as the expression of a genetic theory of disease. However, a group of French researchers defend the idea of a genetic theory of infectious diseases. By identifying four common genetic mechanisms (Mendelian predisposition to multiple infections, Mendelian predisposition to one infection, and major gene and polygenic predispositions), (...) they attempt to unify infectious diseases from a genetic point of view. In this article, I analyze this explicit example of a genetic theory, which relies on mechanisms and is applied only to a specific category of diseases, what we call “a regional genetic theory.” I have three aims: to prove that a genetic theory of disease can be devoid of genocentrism, to consider the possibility of a genetic theory applied to every disease, and to introduce two hypotheses about the form that such a genetic theory could take by distinguishing between a genetic theory of diseases and a genetic theory of Disease. Finally, I suggest that network medicine could be an interesting framework for a genetic theory of Disease. (shrink)

The pivotal problem of comorbidity research lies in the psychometric foundation it rests on, that is, latent variable theory, in which a mental disorder is viewed as a latent variable that causes a constellation of symptoms. From this perspective, comorbidity is a (bi)directional relationship between multiple latent variables. We argue that such a latent variable perspective encounters serious problems in the study of comorbidity, and offer a radically different conceptualization in terms of a network approach, where comorbidity is hypothesized to (...) arise from direct relations between symptoms of multiple disorders. We propose a method to visualize comorbidity networks and, based on an empirical network for major depression and generalized anxiety, we argue that this approach generates realistic hypotheses about pathways to comorbidity, overlapping symptoms, and diagnostic boundaries, that are not naturally accommodated by latent variable models: Some pathways to comorbidity through the symptom space are more likely than others; those pathways generally have the same direction (i.e., from symptoms of one disorder to symptoms of the other); overlapping symptoms play an important role in comorbidity; and boundaries between diagnostic categories are necessarily fuzzy. (shrink)

The paper addresses the question of whether heritability can be useful in establishing genetics as an explanation for an individual’s display of some trait or behavior. After reviewing the fundamental philosophical challenge to heritability—that heritability is a population level measure—an argument is presented for rethinking the role heritability occupies in both causal and explanatory claims. It is argued that heritability can be useful for genetically based explanations of individual traits, if the conditions for proper genetic explanation are modestly reconceived, and (...) the measure is seen as an evidential tool which conforms to standard methods for determining causal factors. (shrink)

Instances of explanatory reduction are often advocated on metaphysical grounds; given that the only real things in the world are subatomic particles and their interaction, we have to try to explain everything in terms of the laws of physics. In this paper, we show that explanatory reduction cannot be defended on metaphysical grounds. Nevertheless, indispensability arguments for reductive explanations can be developed, taking into account actual scientific practice and the role of epistemic interests. Reductive explanations might be indispensable to address (...) some epistemic interest answering a specific explanation-seeking question in the most accurate, adequate and efficient way. Just like explanatory pluralists often advocate the indispensability of higher levels of explanation pointing at the pragmatic value of the explanatory information obtained on these higher levels, we argue that explanatory reduction—traditionally understood as the contender of pluralism—can be defended in a similar way. The pragmatic value reductionist, lower level explanations might have in the biomedical sciences and the social sciences is illustrated by some case studies. (shrink)

We discuss the latent variables construct, particularly in regard to the following: that latent variables are considered as the sole explanatory factor of a disorder; that pragmatic concerns are ignored; and that the relationship of these variables to biological markers is not addressed. Further, we comment on the relationship between bridge symptoms and causality, and discuss the proposal in relationship to other constructs (endophenotypes, connectionist-inspired networks).

We outline a number of ethical objections to genetic technologies aimed at enhancing human capacities and traits. We then argue that, despite the persuasiveness of some of these objections, they are insufficient to stop the development and use of genetic enhancement technologies. We contend that the inevitability of the technologies results from a particular guiding worldview of humans as masters of the human evolutionary future, and conclude that recognising this worldview points to new directions for ethical thinking about genetic enhancement (...) technologies. (shrink)

According to the proponents of Developmental Systems Theory and the Causal Parity Thesis, the privileging of the genome as “first among equals” with respect to the development of phenotypic traits is more a reflection of our own heuristic prejudice than of ontology - the underlying causal structures responsible for that specified development no more single out the genome as primary than they do other broadly “environmental” factors. Parting with the methodology of the popular responses to the Thesis, this paper offers (...) a novel criterion for ‘causal primacy’, one that is grounded in the ontology of the unique causal role of dispositional properties. This paper argues that, if the genome is conceptualised as realising dispositional properties that are “directed toward” phenotypic traits, the parity of ‘causal roles’ between genetic and extra-genetic factors is no longer apparent, and further, that the causal primacy of the genome is both plausible and defensible. (shrink)

The theory of evolution by natural selection is, perhaps, the crowning intellectual achievement of the biological sciences. There is, however, considerable debate about which entity or entities are selected and what it is that fits them for that role. This article aims to clarify what is at issue in these debates by identifying four distinct, though often confused, concerns and then identifying how the debates on what constitute the units of selection depend to a significant degree on which of these (...) four questions a thinker regards as central. (shrink)

In robustness analysis, hypotheses are supported to the extent that a result proves robust, and a result is robust to the extent that we detect it in diverse ways. But what precise sense of diversity is at work here? In this paper, I show that the formal explications of evidential diversity most often appealed to in work on robustness – which all draw in one way or another on probabilistic independence – fail to shed light on the notion of diversity (...) relevant to robustness analysis. I close by briefly outlining a promising alternative approach inspired by Horwich’s (1982) eliminative account of evidential diversity. (shrink)

In the face of causal complexity, scientists reconstitute phenomena in order to arrive at a more simplified and partial picture that ignores most of the 'bigger picture.' This paper will distinguish between two modes of reconstituting phenomena: one moving down to a level of greater decomposition (toward organizational parts of the original phenomenon), and one moving up to a level of greater abstraction (toward different differences regarding the phenomenon). The first aim of the paper is to illustrate that phenomena are (...) moving targets, i.e., they are not fixed once and for all, but are adapted, if necessary, on the basis of the preferred perspective adopted for pragmatic reasons. The second aim is to analyze in detail the second mode of reconstituting phenomena. This includes an exposition of the kind of pragmatic-pluralistic picture resulting from the fact that phenomena are reconstituted by a move up to a level of greater abstraction. (shrink)

This paper is on the problem of causal selection and comments on Collingwood's classic paper "The so-called idea of causation". It discusses the relevance of Collingwood’s control principle in contemporary life sciences and defends that it is not the ability to control, but the willingness to control that often biases us towards some rather than other causes of a phenomenon. Willingness to control is certainly only one principle that influences causal selection, but it is an important one. It shows how (...) norms make causes. (shrink)

How does a complex organism develop from a relatively simple, homogeneous mass? The usual answer is: through the execution of species-specific genetic instructions specifying the development of that organism. Commentators are sometimes sceptical of this usual answer, but of course not all commentators. Some biologists refer to master control genes responsible for the activation of all the genes responsible for every aspect of organismal development; and some philosophers, most notoriously Rosenberg, buy this claim hook, line, and sinker. Here I explore (...) both the seeming plausibility of the usual position, and also its ultimate inadequacy. (shrink)