Given the resurgence of scientific studies on the etiology of homosexuality in the wake of the AIDS epidemic, this article considers the effects these studies had on contemporaneous queer filmmakers. By using the subject of criminality as a way to talk about homosexual causality, queer films of the 1990s illustrate that contemporary scientific studies on homosexuality were historically and politically situated in relation to cultural anxieties about other forms of deviance. This article focuses on films that dissect the hetero-normative (...) tendency to amalgamate forms of deviance in order to distinguish between the diseased and the healthy. Such products of New Queer Cinema highlight this amalgamation of criminality and homosexuality in order to challenge demands by the LGBT community of the 1980s and 1990s for “more positive images” in film. This article argues that queer filmmakers have manipulated the image of the queer criminal to usurp the medical tendency to biologize and pathologize the notion of queer transgression. In such a way, queer films that enthusiastically dramatize the queer outlaw perpetuate myths about homosexuality in order to dissect and discredit them. (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)
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.
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)
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 (see Markie (2005, 2006, 2013), McGrath (2013), Siegel (2012, 2013), and Vahid (2014)). -/- 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 (1993), and Graham (2010). 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)
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)
This paper examines the debate over the human immunodeficiency virus (HIV) as the cause of acquired immunodeficiency syndrome (AIDS) from an historical perspective. The changing criteria for proving the link between putative pathological agents and diseases are discussed, beginning with Robert Koch's research on anthrax in the late nineteenth century. Various versions of 'Koch's postulates' are analyzed in relation to the necessity and sufficiency arguments of logical reasoning. In addition, alterations to Koch's postulates are delineated, specifically those required by the (...) discovery of rickettsiae and viruses in the early twentieth century and by the immunological testing developed after midcentury to demonstrate the links between elusive viral agents and two diseases, hepatitis B and infectious mononucleosis. From this perspective, an examination of the AIDS debate is constructed. Molecular biologist Peter Duesberg's argument that HIV is not the cause of AIDS is analyzed in light of his contention that a version of Koch's postulates has not been satisfied. Additional research findings through 1990 relating to the etiology of AIDS are also noted. (shrink)
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.
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)
In 1905 two different etiologic agents for syphilis were proposed in Berlin, one, the Cytorrhyctes luis, by John Siegel, the other, Spirochaete pallida, by Fritz Schaudinn. Both scientists were pupils of Franz Eilhard Schulze, and were outsiders to the Berlin medical establishment. Both belonged to the same thought collective, used the same thought style, and started from the same supposition that the etiologic agent of syphilis must be a protist. Both used the same morphological approach, the same microscopes and the (...) same stains. Both presented their findings in the same societies, used the same rhetoric, published in the same journals, used the same arguments to criticise each other's shortcomings. Both were backed by powerful institutions and enlisted the support of prestigious patrons. Within half a year, the scientific community at large had in its overwhelming majority accepted Schaudinn's results and rejected those of Siegel. Social forces thus cannot be shown to have played any role in deciding the issue. Ludwik Fleck's suggestion that 'appropriate influence' and a 'proper measure of publicity throughout the thought collective' would have been sufficient for Siegel's ideas to win the day is untenable. (shrink)
Examining the language and paradigms of science as rhetorical, that is, arising from the sociocultural forces that shape ideology, reveals androcentric assumptions that tend to thwart democratic public policy as well as effective methodology. This paper applies some recent feminist critiques of the biological sciences to the current research on the possible hormonal and genetic factors contributing to homosexuality, clarifying how this research perpetuates hierarchical binaries and suggesting ways to reconceptualize human sexuality through revised research protocols.
In one approach to classifying island phenomena, there is a group that answers to the following description. ADJUNCT ISLAND CONDITION If an XP is in an adjunct position, nothing may move out of it. In the inﬂuential approach to this condition in Huang, “adjunct” position is deﬁned in terms that reference argument structure and its reﬂection in phrasemarker geometry. This deﬁnition groups together subject phrases and modifying phrases, contrasting them with phrases in “complement” position. The subsequent bounding theories in Lasnik (...) and Saito and Chomsky build on this basic idea, but attempt to spread it to a wide variety of island effects, including those characterized by early versions of Chomsky’s Subjacency condition. Central to their approaches is the notion of “lexical governor,” which is responsible for making the complement/non-complement cut — only phrases that are governed by a suitably lexical Xo are “complements,” and the island conditions are deﬁned, then, over all the others. This part of the system has fallen into disuse partly, I suspect, because characterizing the “lexical” versus “non-lexical” distinction never found itself grounded in something more general, and partly because it became unwieldy in the increasing richness of post-Pollock representations of phrase-markers. This paper adopts the view that there is an island condition like that in, which groups together subjects and adjuncts, but it does not attempt to deﬁne these phrases on the basis of a “lexical governor.” Instead, let us adopt a characterization of “adjunct” that is wholly geometric: An adjunct is a phrase whose sister is also a phrase and whose mother is not its projection. This will put together “subject” phrases and modiﬁer phrases under the standard assumption that these are both necessarily sisters to phrases rather than heads. Thus it will single out the boxed phrases in. (shrink)
This article elaborates on Putnam's ''discrete behavioral states'' model of dissociative identity disorder (Putnam, 1997) by proposing the involvement of the orbitalfrontal cortex in the development of DID and suggesting a potential neurodevelopmental mechanism responsible for the development of multiple representations of self. The proposed ''orbitalfrontal'' model integrates and elaborates on theory and research from four domains: the neurobiology of the orbitalfrontal cortex and its protective inhibitory role in the temporal organization of behavior, the development of emotion regulation, the development (...) of the self, and experience-dependent reorganizing neocortical processes. The hypothesis being proposed is that the experience-dependent maturation of the orbitalfrontal cortex in early abusive environments, characterized by discontinuity in dyadic socioaffective interactions between the infant and the caregiver, may be responsible for a pattern of lateral inhibition between conflicting subsets of self-representations which are normally integrated into a unified self. The basic idea is that the discontinuity in the early caretaking environment is manifested in the discontinuity in the organization of the developing child's self. (shrink)
Phillips & Silverstein (P&S, 2003) propose that NMDA-receptor dysfunction may be the fundamental neurobiological mechanism underlying and associating impaired holistic perception and cognitive coordination with schizophrenic psychopathology. We discuss how the P&S hypothesis shares different aspects of the weak central coherence account of autism from both theoretical and experimental perspectives. Specifically, we believe that neither those persons with autism nor those with schizophrenia integrate visuo-perceptual information efficiently, resulting in incongruous internal representations of their external world. However, although NMDA-hypofunction may be (...) responsible for perceptual impairments in schizophrenia and possibly autism, we suggest that it is highly unlikely that NMDA-hypofunction is specifically responsible for the autistic behavioral symptomology, as described by P&S in their target article. (shrink)
Several million people are treated with neuroleptic medications in North America each year. A large percentage of these patients develop a chronic neurologic disorder-tardive dyskinesia-characterized by abnormal movements of the voluntary muscles. Most cases are permanent and there is no known treatment. Evidence has been accumulating that the neuroleptics also cause damage to the highest centers of the brain, producing chronic mental dysfunction, tardive dementia and tardive psychosis. These drug effects may be considered a mental equivalent of tardive dyskinesia. Relevant (...) data are derived from human autopsies, brain imaging , neurophysical tests, and clinical research. That the neuroleptics can damage higher brain centers is confirmed by their known neurotoxicity and neurophysiological impact, animal autopsies, and a comparison to diseases that mimic neuroleptic effects, such as Huntington's chorea and lethargic encephalitis. Patients and the public should be informed of the danger of both tardive dyskinesia and tardive dementia. The mental health professions should severely limit the use of neuroleptics and develop safer and better alternatives to these dangerous substances. (shrink)
The doctrine of agent-causation has been suggested by many interested in defending libertarian theories of free action to provide the conceptual apparatus necessary to make the notion of incompatibility freedom intelligible. In the present essay the conceptual viability of the doctrine of agent-causation will be assessed. It will be argued that agent-causation is, insofar as it is irreducible to event-causation, mysterious at best, totally unintelligible at worst. First, the arguments for agent-causation made by such eighteenth-century luminaries as Samuel Clarke and (...) Thomas Reid will be considered alongside the defenses of agent-causation proffered in this century by C.A. Campbell, Roderick Chisholm, and Richard Taylor. It will be shown that the case for agent-causation made by these figures is ultimately unconvincing. Two defenses of agent-causation made within the past ten years will then be taken up for examination and critique. First, Timothy O'Connor's attempt at advancing an unrefined and unrepentant doctrine of agent-causation will be shown to suffer from the same maladies as its predecessors. Next, Randolph Clarke's causal agent-causal theory of free action, which seeks a via media between agent-causal theories of free action and causal theories of action, is examined. Clarke's theory is an attempt at providing an account of how both events and agents qua substances can be the codeterminants of free actions. Despite the improvement of Clarke's theory over more conventional agent-causal theories of free action, it will be shown that agent-causation makes his theory more cumbersome than it needs to be. Clarke is able to get as much mileage out of a causal indeterminacy theory of action that does not require him to posit obscure agent-causes. Finally, a sketch of an alternative theory of free action will be offered. While it may suffer from its own conceptual deficiencies, it may not suffer from the same conceptual problems as agent-causal theories of free action. (shrink)