Philosophers of biology and biologists themselves for the most part assume that the concept of kin is progenerative: what makes two individuals kin is a direct or indirect function of reproduction. Derivatively, kinship might likewise be presumed to be progenerative in nature. Yet a prominent view of kinship in contemporary cultural anthropology is a kind of constructivism or performativism that rejects such progenerativist views. This paper critically examines an influential line of thinking used to critique progenerativism and support performativism that cites cross-cultural diversity in what I will call kinmaking. I challenge several key assumptions made in moving from this appeal to ethnography to conclusions about kinship and progeneration, arguing that closer scrutiny of both the ethnographic record and inferences that draw on it in fact support progenerative views of kinmaking.
Communication can arise when the interests of speaker and listener diverge if the cost of signaling is high enough that it aligns their interests. But what happens when the cost of signaling is not sufficient to align their interests? Using methods from experimental economics, we test whether theoretical predictions of a partially informative system of communication are borne out. As our results indicate, partial communication can occur even when interests do not coincide.
This paper examines the complex research landscape of contemporary suicidology from a philosophy of science perspective. I begin by unpacking the methods, concepts, and assumptions of some of the prominent approaches to studying suicide causation, including psychological autopsy studies, epidemiological studies, biological studies, and qualitative studies. I then analyze the different ways these approaches partition the causes of suicide, with particular emphasis on the ways they conceptualize the domain of mental disorder. I argue that these different ways of partitioning the causal space and conceptualizing mental disorder result in incommensurabilities between the approaches. These incommensurabilities restrict the degrees to which the different approaches can be integrated, thus lending support to explanatory pluralism in the study of suicide causation. They also shed light on some of the philosophical underpinnings of the disagreement between mainstream suicidology and the emerging area of critical suicidology.
Some biologists and philosophers of biology claim selection can “create” novel traits. Others claim creativity is to be found only in development. I here endorse the former claim, but take seriously and address the concerns that underlie the latter. My discussion of these issues is informed by recent work that champions the “return of the organism” to mainstream evolutionary biology, and I suggest how population and organismal perspectives on trait origins can be reconciled.
Although concepts of disease have received much scrutiny, the benefits of distinguishing between theoretical and clinical disease-and what is meant by those terms-may not be as readily apparent. One way of characterizing the distinction between theoretical and clinical conceptions of disease is by relying on Boorse's biostatistical theory (BST) for a conception of theoretical disease. Clinical disease could then be defined as theoretical disease that is diagnosed. Explicating this distinction provides a useful extension of the BST. The benefits of this approach are clearly and non-normatively demarcating disease from non-disease, while allowing for values and purpose to determine what criteria are used in clinical practice to represent a disease's underlying dysfunction. Through discussion of a variety of medical conditions, including polycystic ovary syndrome and type 2 diabetes mellitus, I explore how the relationship between BST-based theoretical and clinical disease could make sense of various features of clinical practice and medical theory. It could do this by lending focus to a nuanced understanding of the pathophysiological defects present in disease and the means by which they are assessed. This could contribute to making sense of revised nosologies and diagnostic criteria.
Some interpreters claim Kant distinguishes between organisms and living things. I argue this claim is under-determined by the textual evidence. Once this is recognized, it becomes a real possibility that Kant's various remarks about the essential properties of living things generalize to organisms as such. This, in turn, generates a puzzle. Kant repeatedly claims that the capacity for representation is essential to the nature of a living thing. If he does not distinguish between living things and organisms, then how might the capacity for representation be essential to the latter? Drawing on the writings of Kant and his contemporaries, I reconstruct a framework within which representational capacities might conceivably be thought to play this role. On this view, what distinguishes an organism from mechanically explicable products of nature is its capacity for endogenous behavior that is instinctual and representationally mediated.
In this article I critically evaluate the thesis that DNA is an ontologically distinctive developmental cause. I shall critically analyse different versions of the latter thesis by taking into consideration concrete developmental cases. I shall argue that DNA is neither a developmental determinant nor an ontologically distinctive developmental cause. Instead, I shall argue that mechanistic analysis shows that DNA's causal role in development depends on the higher robustness of the developmental processes in which it exerts its causal capacities. The focus on process and developmental system implies a metaphysical shift: rather than attributing to DNA molecules biochemically unique properties, I suggest that it might be better to think about DNA's causal role in development in terms of the causal capacities that DNA molecules manifest in a rich developmental milieu. I shall also suggest that my position is distinct both from the view advocating the instrumental primacy of DNA-centric biology and developmental constructionism. It is different from the former because it provides a substantial answer to the question of what makes DNA causally central in developmental processes. Finally, I argue that evolutionary considerations pose an important challenge to developmental constructionism.
Contingency-theorists have put forth differing accounts of evolutionary contingency. The bulk of these accounts abstractly refer to certain causal structures in which an evolutionarily contingent outcome is supposedly embedded. For example, an outcome is evolutionarily contingent if it is at the end of a 'path-dependent' or 'causally dependent' causal chain. However, this paper argues that many of these proposals fail to include a desideratum - the notion of biological evitability or that evolutionary outcomes could have been otherwise - that for good theoretical reasons ought to be part of an account of evolutionary contingency. Although an inclusion of this desideratum might seem obvious enough, under some existing accounts, an outcome can be contingent yet inevitable all the same. In my diagnosis of this issue, I develop the idea of trajectory propensity to highlight the fact that there are plausible biological scenarios in which causal structures, alone, fail to exhaustively determine the biological evitability of evolutionary forms. In the second half of the paper, I present two additional desiderata of an account of evolutionary contingency and, subsequently, proffer a novel account of evolutionary contingency as non-trivial objective probability, which overcomes the shortcomings of some previous proposals. According to this outcome-based account, contingency claims are probabilistic statements about an evolutionary outcome's objective probability of evolution within a specifically defined modal range: an outcome, O, is evolutionarily contingent in modal range, R, to the degree of objective probability, P (where P is in between 1 and 0).
An analysis of arguments for pain eliminativism reveals two significant points of divergence between assumptions underlying biomedical research on pain and assumptions typically endorsed by eliminativist accounts. The first concerns the status of the term 'pain,' which is a description of a phenomenon, rather than an explanatory construct. The second concerns reductive explanation: pain is explained causally, in terms of mechanisms or factors that produce or determine it, rather than by identifying it with a physical structure, process or mechanism. These discrepancies undermine several arguments for pain eliminativism.
The ENCODE project has made important new estimates of human genome functionality, now revising the percentage considered functional to more than 80%, which is in stark contrast to the received view, which estimated that less than 10% of the conserved parts of the human genome are functional. ENCODE's unorthodox use of the notion of biological function has stirred the so-called ENCODE controversy, involving conflicting views about the correct notion of function in postgenomics. The debate hinges on the traditional philosophical contrast between the causal role (CR) and selected effects (SE) approaches. In this paper, we examine the ENCODE controversy in terms of the distinction between function monism and pluralism. We propose to apply a weak etiological account to genomic function ascriptions. In this approach, we can ascribe a function to a genomic structure of an organism if and only if performing the function persists in causally contributing to the organism's and its ancestors' fitness. In comparison to the strong etiological (i.e., the selected effects) approach, the present account does not require there to be selection for the structure in question. This is a monistic approach that enables us to avoid the main difficulties of CR, as well as SE's overdependence on natural selection, while still preserving an evolutionary-constrained notion of biological functions. Our proposal is much more moderate in accommodating the estimates of the functionality of the human genome than both ENCODE's proposal itself and the views of the critics relying on a version of the SE account of functions.
How is scientific data used to represent phenomena and as evidence for claims about phenomena? In this paper, I propose that a specific type of claims-evidential claims - is involved in data practices to define and restrict the representational and evidential content of a dataset. I present an account of data practices in the epidemiology of the exposome based on the notion of evidential claims, which helps unpack the approaches, assumptions and warrants that connect different stages of research. I identify three different strategies to generate different types of evidential claims in this case. The macro strategy, which individuates the dataset that serves as the initial evidential space for research. The micro strategy, which is used to generate evidential claims about the microscopic and individual component of target phenomena. The association strategy, that uses evidence from the other strategies to identify a dataset as representation of the different levels and relations of exposure and disease. Differentiating between these strategies sheds light on the multi-faceted landscape of biomedical research on environment and health; and the roles of data and evidence in the process of inquiry.
In the months before and after the final surrender of Nazi Germany on 8 May 1945, British aviation medicine specialists were sent to the European continent to learn the progress that German aviation medicine had made since September 1939. For the medical officers at the Royal Air Force Institute of Aviation Medicine at Farnborough in Hampshire, the dilemma over whether the medical data from the Nazi aviation medicine experiments at Dachau concentration camp should be exploited presented profound moral and ethical problems. Their deliberations paralleled those of the 1945-46 Nuremberg Trial, which revealed the crimes that were committed under the Nazi regime. At the same time, the British medical establishment debated the morality of publishing the Nazi medical research to serve humanity. This article shows that on the basis of British wartime and post-war research, and determinations that were made by the British Advisory Committee for the Investigation of German Medical War Crimes, by 1948 the RAF IAM had essentially rejected the results of the Nazi aviation medicine experiments on scientific and ethical grounds.
The paper argues that transfer of assumptions, concepts, models and metaphors from a variety of Lamarckisms played a significant role in the endeavors to constitute psychology as a scientific discipline. It deals with such efforts in the second half of the nineteenth century and until early twentieth century in Britain and in France. The paper discusses works by Herbert Spencer, John Hughlings-Jackson, Théodule Ribot and Sigmund Freud. It argues that certain crucial facets of their work as discipline-founders could and should be looked upon as resulting from such transfer of/from Lamarckisms. Specifically it looks at the constitutive roles of notions of hierarchical order, parallelism, self, memory and collectivity.
Ecology arguably has roots in eighteenth-century natural histories, such as Linnaeus's economy of nature, which pressed a case for holistic and final-causal explanations of organisms in terms of what we'd now call their environment. After sketching Kant's arguments for the indispensability of final-causal explanation merely in the case of individual organisms, and considering the Linnaean alternative, this paper examines Kant's critical response to Linnaean ideas. I argue that Kant does not explicitly reject Linnaeus's holism. But he maintains that the indispensability of final-causal explanation depends on robust modal connections between types of organism and their functional parts; relationships in Linnaeus's economy of nature, by contrast, are relatively contingent. Kant's framework avoids strong metaphysical assumptions, is responsive to empirical evidence, and can be fruitfully compared with some contemporary approaches to biological organization.
