Formulations of the essential commitment of the etiological theory of functions have varied significantly, with some individual authors' formulations even varying from one place to another. The logical geography of these various formulations is different from what is standardly assumed; for they are not stylistic variants of the same essential commitment, but stylistic variants of two non-equivalent versions of the etiological theory. I distinguish these “strong” and “weak” versions of the etiological theory (which differ with respect to the role of (...) selection in their definitions of function), draw out their respective implications, and argue that the weak version is to be preferred to the strong. (shrink)

Learning information about the etiology of one's beliefs can reduce the justification a thinker has for those beliefs. Learning information about the etiology of one's desires, emotions, or concepts can similarly have a debunking effect. In this chapter, I develop a unified account of etiological debunking that applies across these different kinds of cases. According to this account, etiological debunking arguments work by providing reason to think that there is no satisfying explanation of how it is that some (...) part of our mental life is fitting. The role that etiological information plays is to help to rule out (or render less plausible) potential explanations, given our background views about the world. This account suggests several potential morals for epistemology, the philosophy of mind, and metaethics. (shrink)

The etiological account of function defines a part’s/trait’s function as whatever that part/trait does and was selected for doing. Some philosophers have tried to employ this as an account of biological interests, claiming that to benefit an organism is to promote its etiological functioning and to harm it is to inhibit such functioning. I argue that etiological functioning is not a good account of biological interests. I first describe the history of theories of biological interests, explaining the special role that (...) etiological accounts of function have played within such theories. Second, I explain the problems with allowing etiological accounts of function to play this role and consider objections to my line of argument. Finally, I consider the theoretical alternatives to etiological function accounts of interests and assess their advantages and disadvantages. (shrink)

Kinds that share historical properties are dubbed “historical kinds” or “etiological kinds,” and they have some distinctive features. I will try to characterize etiological kinds in general terms and briefly survey some previous philosophical discussions of these kinds. Then I will take a closer look at a few case studies involving different types of etiological kinds. Finally, I will try to understand the rationale for classifying on the basis of etiology, putting forward reasons for classifying phenomena on the basis (...) of diachronic features, thereby making a provisional case for considering at least some etiological kinds to be natural kinds. (shrink)

The etiology of a perceptual belief can seemingly affect its epistemic status. There are cases in which perceptual beliefs seem to be unjustified because the perceptual experiences on which they are based are caused, in part, by wishful thinking, or irrational prior beliefs. It has been argued that this is problematic for many internalist views in the epistemology of perception, especially those which postulate immediate perceptual justification. Such views are unable to account for the impact of an experience’s (...) class='Hi'>etiology on its justificational status, McGrath, Siegel, and Vahid ). Our understanding of what we have been told can also be affected by, for example, wishful thinking or irrational background beliefs. I argue that testimonial beliefs based on such states of understanding can thus be rendered unjustified. This is problematic not only for internalist immediate justification views of testimony, but also for some externalist views, such as the form of proper functionalism endorsed by Burge, and Graham. The testimonial version of the argument from etiology, unlike the perceptual variant, does not rest on the controversial hypothesis that perception is cognitively penetrable. Furthermore, there is a stronger case for the claim that testimonial justification can be undermined by etiological effects since, I argue, testimonial beliefs can be based on the background mental states which affect our understanding of what is said, and our states of understanding are rationally assessable. (shrink)

In this paper, I develop and motivate a novel formulation of the safety condition in terms of etiological proper function. After testing this condition against the most pressing objections to safety-theoretic accounts of knowledge in the literature, my conclusion will be the following: once safety is suitably understood in terms of etiological proper function, it stands a better chance as the right anti-Gettier condition on knowledge.

Theory of illness causation is an important issue in all biomedical sciences, and solid etiological explanations are needed in order to develop therapeutic approaches in medicine and preventive interventions in public health. Until now, the literature about the theoretical underpinnings of illness causation research has been scarce and fragmented, and lacking a convenient summary. This interdisciplinary book provides a convenient and accessible distillation of the current status of research into this developing field, and adds a personal flavor to the discussion (...) by proposing the etiological stance as a comprehensive approach to identify modifiable causes of illness. (shrink)

Sometimes it’s reasonable to reduce confidence in a proposition in response to gaining etiological information. Suppose, for example, a theist learns that her theism is ‘due to’ her religious upbringing. There is a clear range of cases where it would be reasonable for her to respond by slightly decreasing her confidence in God’s existence. So long as reasonability and justification are distinct, this reasonability claim would appear consistent with the thesis that this kind of etiological information cannot, all by itself, (...) affect one’s justification. In what follows, I argue that this is mistaken. For, even if reasonability and justification are distinct, the reasonability of decreasing confidence in response to etiological information must be explained in terms of a decrease in justification. The argument to follow threatens not only the stronger thesis that etiological information never defeats justification but the substantially weaker thesis, advocated by various authors, that justification is defeated by etiological information in only a limited range of circumstances. I go on to show how the arguments en route to this conclusion have much wider epistemological ramifications. (shrink)

There is a common assumption that evolutionary explanations of religion undermine religious beliefs. Do etiological accounts similarly affect the rationality of religious practices? To answer this question, this paper looks at two influential evolutionary accounts of ritual, the hazard-precaution model and costly signaling theory. It examines whether Cuneo’s account of ritual knowledge as knowing to engage God can be maintained in the light of these evolutionary accounts. While the evolutionary accounts under consideration are not metaphysically incompatible with the idea that (...) religious rituals engage God, they cast doubt on whether many, if not all, rituals can do this successfully. (shrink)

In this article, I will reconstruct the monocausal model and argue that modern 'multifactorial diseases' are not monocausal by definition. 'Multifactorial diseases' are instead defined according to a constitutive disease model. On closer analysis, infectious diseases are also defined using the constitutive model rather than the monocausal model. As a result, our classification models alone cannot explain why infectious diseases have a universal etiology while chronic and noncommunicable diseases lack one. The explanation is instead provided by the nineteenth-century germ (...) theorists. (shrink)

Aristotle’s biological teleology is rooted in an epigenetic account of reproduction. As such, it is best interpreted by consequence etiology. I support this claim by citing the capacity of consequence etiology’s key distinctions to explain Aristotle’s opposition to Empedocles. There are implications for the relation between ancient and modern biology. The analysis reveals that in an important respect Darwin’s account of adaptation is closer to Aristotle’s than to Empedocles’s. They both rely on consequence etiological considerations to evade attributing (...) the purposiveness of organisms to chance. Two implications follow: Darwinian explanations of adaptation are as teleological as Aristotle’s, albeit differently; and these differences show how deeply resistant Aristotle’s version of biological teleology is to descent from a common ancestor. (shrink)

Teleosemantics is a naturalistic research programme in the philosophy of mind and language. Its ambition is to achieve a reduction, first, of mental content to teleological function; second, of teleological function to non-teleological notions. This article explores the second step, particularly as envisaged by Millikan’s etiological theory of function.

Models of illness causation play a crucial role in medicine and public health. In their recent paper on this topic, Michael Kelly, Rachel Kelly, and Federica Russo state that the integration of social, biological, and behavioral causes in one and the same etiologic mechanism remains to be clarified. In particular, they think that current models of illness causation do not appreciate "the truly integrated nature of bio-social-behavioral pathogenesis". In brief, Kelly, Kelly, and Russo suggest that two levels of explanation are (...) at work in medicine and public health, biological and social; that integration is difficult because of resistance to including social determinants of disease in both the... (shrink)

People sometimes try to call others’ beliefs into question by pointing out the contingent causal origins of those beliefs. The significance of such ‘Etiological Challenges’ is a topic that has started attracting attention in epistemology. Current work on this topic aims to show that Etiological Challenges are, at most, only indirectly epistemically significant, insofar as they bring other generic epistemic considerations to the agent’s attention. Against this approach, we argue that Etiological Challenges are epistemically significant in a more direct and (...) more distinctive way. An Etiological Challenge prompts the agent to assess whether her beliefs result from practices of indoctrination, and whether she should reduce confidence in those beliefs, given the anti-reliability of indoctrination as a method of belief-acquisition. Our analysis also draws attention to some of the ways in which epistemic concerns interact with political issues—e.g. relating to epistemic injustice, identity-based discrimination, and segregation—when we’re thinking about the contingent causal origins of our beliefs. (shrink)

It is argued there are features which distinguish causal conditions from necessary or sufficient conditions in general; that causal conditions are those which serve our instrumental interests, i.e., interests in producing or preventing states of affairs. It is further argued that the context of our instrumental interests determines what causal condition is designated as "the cause" in scientific contexts. It is argued that this is true of the health sciences in particular and the particular instrumental interests characteristic of the health (...) sciences are further shown to govern the choice of what causal condition of a disease is accorded the status of etiologic agent. (shrink)

Millikan's account of how we acquire our most basic concepts might be clarified by a better ontological taxonomy, especially one that distinguishes between natural kinds on the one hand and wholes composed of parts on the other. The two have a different causal basis, which is important because once classification goes beyond the stage of naive induction, it becomes fundamentally etiological.

Cummins (1982) argues that etiological considerations are not onlyinsufficient butirrelevant for the determination offunction. I argue that his claim of irrelevance rests on a misrepresentation of the use of functions in evolutionary explanations. I go on to suggest how accepting anetiological constraint on functional analysis might help resolve some problems involving the use of functional explanations.

Institutions generate cooperative benefits that explain why they exist and persist. Therefore, their etiological function is to promote cooperation. The function of a particular institution, such as money or traffic regulations, is to solve one or more cooperation problems. We go on to argue that the teleological function of institutions is to secure values by means of norms. Values can also be used to redesign an institution and to promote social change. We argue, however, that an adequate theory of institutions (...) should not be ‘moralized’ in that they should not be defined in terms of the values they are supposed to promote. (shrink)

The aim of teleosemantics is to give a scientifically respectable, or ‘naturalistic’ theory of mental content. In the debates surrounding the scope and merits of teleosemantics a lot has been said about the concept of indication (or carrying information). The aim of this paper is to focus on the other key concept of teleosemantics: biological function. It has been universally accepted in the teleosemantics literature that the account of biological function one should use to flesh out teleosemantics is that of (...) etiological function. My claim is that if we replace this concept of function with an alternative one (that we have independent reasons to accept) and if we also restrict the scope of teleosemantics, we can arrive at an account of biologizing mental content that is much less problematic than the previous attempts. (shrink)

INTRODUCTION The appeal to teleological principles of explanation within the body of natural science has had an unfortunate history. ...

In this paper I offer a theory of what makes certain influences on visual experiences by prior mental states (including desires, beliefs, moods, and fears) reduce the justificatory force of those experiences. The main idea is that experiences, like beliefs, can have rationally assessable etiologies, and when those etiologies are irrational, the experiences are epistemically downgraded.

A fundamental aspect of human beings is that they learn. The process of learning and what is learned are impacted by a number of factors, both cognitive and social; that is, humans are boundedly rational. Cognitive and social limitations interact, making it difficult to reason about how to provide information to impact what humans know, believe, and do. Herein, we use a multi‐agent dynamic‐network simulation system, Construct, to conduct such reasoning. In particular, we ask, What media should be used to (...) provide information to most impact what people know, believe, and do, given diverse social structures? All simulated agents are boundedly rational both at the cognitive and social level, and so are subject to factors such as literacy, education, and the breadth of their social network. We find that there is no one most effective intervention; rather, to be effective, messages and the media used to spread the message need to be selected for the population being addressed. Typically, a multimedia campaign is critical. (shrink)

It can be shown that considerable common ground exists between indigenous or traditional theories of contagious disease in Africa, and modern medicine, whether human or veterinary. Yet this is not recognized because of the generally low regard in which the medically trained – whether African or expatriate – hold African traditional medicine. This attitude seems to result from the assumption that African health beliefs are based on witchcraft and related “supernatural” thinking. I argue that this may not be so in (...) the important domain of diseases biomedically classified as contagious; such diseases tend to be understood naturalistically. An accurate understanding of how Africans traditionally interpret contagious diseases of humans and livestock is the foundation for the design and implementation of more effective health programs. (shrink)

We reply to Artiga and Martinez’s claim according to which the organizational account of cross-generation functions implies a backward looking interpretation of etiology, just as standard etiological theories of function do. We argue that Artiga and Martinez’s claim stems from a fundamental misunderstanding about the notion of “closure”, on which the organizational account relies. In particular, they incorrectly assume that the system, which is relevant for ascribing cross-generation organizational function, is the lineage. In contrast, we recall that organizational closure (...) refers to a relational description of a network of mutual dependencies, abstracted from time, in which production relations are irrelevant. From an organizational perspective, ascribing a function to an entity means locating it in the abstract system that realizes closure. In particular, the position of each entity within the relational system conveys an etiological explanation of its existence, because of its dependence on the effects exerted by other entities subject to closure. Because of the abstract relational nature of closure, we maintain that the organizational account of functions does not endorse a backward looking interpretation of etiology. As a consequence, it does not fall prey of epiphenomenalism. (shrink)

There has been a general failure among mental health theorists and social psychologists to understand the etiology of work-engendered depression. Yet the condition is increasingly prevalent in highly industrialized societies, where an exclusionary focus upon work, money, and the things that money can buy has displaced values that traditionally exerted a liberating and humanizing influence. Social critics have called the result an impoverishment of the spirit, a state of cultural bankruptcy, and an incapacity for genuine leisure. From a clinical (...) perspective, the condition has been diagnosed as widespread narcissism and obsessive work. -/- Acedia, a concept developed by the Scholastics, throws clarifying light on the origin of this form of depression. (shrink)

This paper contains a positive development and a negative argument. It develops a theory of function loss and shows how this undermines an objection raised against the etiological theory of function in support of the modal theory of function. Then it raises two internal problems for the modal theory of function.

Modern medicine is often said to have originated with nineteenth century germ theory, which attributed diseases to bacterial contagions. The success of this theory is often associated with an underlying principle referred to as the “doctrine of specific etiology”. This doctrine refers to specificity at the level of disease causation or etiology. While the importance of this doctrine is frequently emphasized in the philosophical, historical, and medical literature, these sources lack a clear account of the types of specificity (...) that it involves and why exactly they matter. This paper argues that nineteenth century germ theory involves two types of specificity at the level of etiology. One type receives significant attention in the literature, but its influence on modern medicine has been misunderstood. A second type is present in this model, but it has been completely overlooked in the extant literature. My analysis clarifies how these types of specificity led to a novel conception of etiology that continues to figure in medicine today. (shrink)

Conscious existence is the product of a neural brain mechanism, which is largely identical with Immanuel Kant's Oneness Function, a service performed by 200 million neurons in the prefrontal lobe, & makes possible our interior cosmos, the record of our interconnected, or general, experience. Essential for us humans is the well-being of our interior cosmos, or Saint Teresa of Avila's interior castle, in all interactions with each other \& the greater environment. Any disorders of our cosmos are liable to make (...) us fall ill, setting our existence on a path of psychosomatic etiology of a large class of mysterious undiagnosed diseases. (shrink)

Uno de los temas recurrentes en la filosofía contemporánea es, sin duda, el de la idea de la nada, si bien, de alguna manera, ha sido tema constante de la filosofía. El doble objeto del juicio de existencia implica la primera otredad intelectual que es, precisamente, el origen de la idea de no-ser.

Scientists disagree about which capacities a functional analysis of consciousness should target. To address this disagreement, I propose that a good functional analysis should target the etiological functions of consciousness. The trouble is that most hypotheses about the etiological origins of consciousness presuppose particular functional analyses. In recent years, however, a small number of scientists have begun to offer evolutionary hypotheses that are relatively theory neutral. I argue that their hypotheses can serve an independent standard for evaluating among theories of (...) consciousness. (shrink)

Scientists disagree about which capacities a functional analysis of consciousness should target. To address this disagreement, I propose that a good functional analysis should target the etiological functions of consciousness. The trouble is that most hypotheses about the etiological origins of consciousness presuppose particular functional analyses. In recent years, however, a small number of scientists have begun to offer evolutionary hypotheses that are relatively theory neutral. I argue that their hypotheses can serve an independent standard for evaluating among theories of (...) consciousness. (shrink)

In this paper I clarify a major affinity between Nietzsche and Spinoza that has been neglected in the literature—but that Nietzsche was aware of—namely a tendency to what I call etiology. Etiologies provide second- order explanations of some opponents’ first-order views, but not in order to decide first-order matters. The example I take up here is Nietzsche’s and Spinoza’s rejections of free will—and especially their etiologies concerning how we wrongly come to think that we may boast of such a (...) capacity. In working through the former (i.e., their rejections of free will) in order to make my central metaphilosophical point regarding the latter (i.e., their accounts of why we generally affirm that we have free will), I shed important new light on Nietzsche’s relation to Spinoza. I also further our understanding of what role such second-order accounts play within each of their larger projects on their own terms. (shrink)

Cognitive science of religion is sometimes portrayed as having no bearing on the theological doctrines of particular religious traditions, such as Christianity. In this paper, I argue that the naturalistic account of the etiology of religious beliefs offered by the cognitive science of religion undermines the important Christian doctrine of the grace of faith, which teaches that the special gift of divine grace is a necessary precondition for coming to faith. This has some far-reaching ramifications for Christian theology. -/- (...) . (shrink)