This paper discusses the representation and explanation of relationships between phenomena that are important in psychiatric contexts. After a general discussion of complexity in the philosophy of science, I distinguish zooming-out approaches from zooming-in approaches. Zooming-out has to do with seeing complex mental illnesses as abstract models for the purposes of both explanation and reduction. Zooming-in involves breaking complex mental illnesses into simple components and trying to explain those components independently in terms of specific causes. Connections between existing practice and (...) zooming-out are drawn, and zooming-in is criticised. (shrink)

I describe two traditions of philosophical accounts of evidence: one characterizes the notion in terms of signs of success, the other characterizes the notion in terms of conditions of success. The best examples of the former rely on the probability calculus, and have the virtues of generality and theoretical simplicity. The best examples of the latter describe the features of evidence which scientists appeal to in practice, which include general features of methods, such as quality and relevance, and general features (...) of evidence, such as patterns in data, concordance with other evidence, and believability of the evidence. Two infamous episodes from biomedical research help to illustrate these features. Philosophical characterization of these latter features—conditions of success—has the virtue of potential relevance to, and descriptive accuracy of, practices of experimental scientists. (shrink)

I distinguish three theses associated with the new mechanistic philosophy – concerning causation, explanation and scientific methodology. Advocates of each thesis are identified and relationships among them are outlined. I then look at some recent work on natural selection and mechanisms. There, attention to different kinds of New Mechanism significantly affects of what is at stake.

After a decade of intense debate about mechanisms, there is still no consensus characterization. In this paper we argue for a characterization that applies widely to mechanisms across the sciences. We examine and defend our disagreements with the major current contenders for characterizations of mechanisms. Ultimately, we indicate that the major contenders can all sign up to our characterization.

Most psychological research aims to uncover generalizations about the mind that hold across subjects. Philosophical discussions of scientific explanation have focused on such generalizations, but in doing so, have often overlooked an important phenomenon: variation. Variation is ubiquitous in psychology and many other domains, and an important target of explanation in its own right. Here I characterize explananda that concern individual differences and formulate an account of what it takes to explain them. I argue that the notion of actual difference (...) making, the only causal concept in the literature that explicitly addresses variation, cannot be used to ground such an account. Instead, I propose a view on which explaining individual differences involves identifying causes that could be intervened on to reduce the variability in the population. This account provides criteria of success for explaining variation and deepens our understanding of causal explanation. (shrink)

We do not all make choices, reason, interpret our experience, or respond to our environment in the same way. A recent surge of scientific interest has thrust these individual differences into the spotlight: researchers in cognitive psychology and neuroscience are now devoting increasing attention to cognitive variation. The philosophical dimensions of this research, however, have yet to be systematically explored. Here I make an initial foray by considering how cognitive variation is characterized. I present a central dilemma facing descriptions of (...) individual differences, discuss several distinctions used to categorize variation, and show that these distinctions require further elaboration. Finally, by canvassing several philosophical topics for which the characterization of cognitive variation may have significant implications, I argue that philosophers should take note of how and why our minds differ. (shrink)

Griffiths and Russell D. Gray (1994, 1997, 2001) have argued that the fundamental unit of analysis in developmental systems theory should be a process – the life cycle – and not a set of developmental resources and interactions between those resources. The key concepts of developmental systems theory, epigenesis and developmental dynamics, both also suggest a process view of the units of development. This chapter explores in more depth the features of developmental systems theory that favour treating processes as fundamental (...) in biology and examines the continuity between developmental systems theory and ideas about process in the work of several major figures in early 20th century biology, most notable C.H Waddington. (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)

This contribution claims that the two fundamental notions of causation at work in the health sciences are manipulative and mechanistic, and investigates what kinds of evidence matter for the assessment of causal relations. This article is a development of our 2007 article, ‘Plurality of Causality’, where we argue for a pluralistic account of causation with an eye to econometrics and a single medical example. The present contribution has a wider focus, and considers the notion of evidence within a whole range (...) of disciplines belonging to the health sciences. Section 1 addresses the relations between kinds of evidence and causal accounts, and it is shown how different notions of causation can be employed in various medical cases. Section 2 calls attention to issues crucial for any adequate epistemological theory of causation, such as the distinctions between types and tokens, observational and experimental regimes, explanation and prediction. Lastly, the notion of context is articulated, highlighted in its role in the assessment of causal links. All these issues are tackled in the framework of what we label a ‘bottom–up’ epistemology. (shrink)

Adopting the notion of “pragmatic information” as interpreted by Roederer and granted that understanding arises from genuine information processing, I show that Searle’s “Chinese Room Argument” in rejecting the thesis of Strong Artificial Intelligence and his responses to critics are sound and acceptable. The paper is a safe and secure translation of Searle’s argument into a language of information. According to the notion of information that I adopt, information and information processing are exclusive attributes of biological and artificial systems. However, (...) I will show that information-theoretically, biological brains are fundamentally different from their artificial simulations. I will argue that only biological systems, or their duplicates, are genuine information processing systems and thus capable of understanding Chinese. “Understanding”, in my proposal, denotes “phenomenal consciousness” in the context of Chalmers’ thesis of naturalistic dualism. (shrink)

A crucial question for a process view of life is how to identify a process and how to follow it through time. The genidentity view can contribute decisively to this project. It says that the identity through time of an entity X is given by a well-identified series of continuous states of affairs. Genidentity helps address the problem of diachronic identity in the living world. This chapter describes the centrality of the concept of genidentity for David Hull and proposes an (...) extension of Hull’s view to the ubiquitous phenomenon of symbiosis. Finally, using immunology as a key example, it shows that the genidentity view suggests that the main interest of a process approach is epistemological rather than ontological and that its principal claim is one of priority, namely that processes precede and define things, and not vice versa. (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 sets out to analyze how causation works by focusing on biology, as represented by epidemiology and by scientific information on how the body works (“physiology”). It starts by exploring the specificity of evolved physiological systems, in which evolutionary, developmental and proximal causes all fit together, and the concept of function is meaningful; in contrast, this structure does not apply in epidemiology (or outside biology). Using these two contrasting branches of biology, I examine the role both of mechanism and (...) of difference making in causation. I find that causation necessarily involves both mechanism and difference making, and that they play complementary roles. Both are seen as ontologically necessary, even if the evidence is not always available for both. Influential monist accounts that focus on one of these, at the expense of ignoring the other, are found to be inadequate on these and on other grounds. Recent attempts to combine them are reviewed, notably that of Russo and Williamson (Int Stud Philos Sci 21:157–170, 2007), and it is argued that their epistemic view requires there to be a source of the different types of evidence that a rational agent would consider, and that this source must be ontic. I then analyze how causal relationships work in evolved physiological systems and in those studied by epidemiology, with a particular focus on how mechanism interacts with input. Finally, I consider this concept of causation from the perspective of everyday language, and of its possible generalisability outside biology. (shrink)

Genetics is in a postgenomic era, and this article illustrates this epistemological evolution using the debate between developmental criticism and traditional biometric genetics about gene × environment interaction. Quantitative geneticists are blamed for failing to respect the complexity of development; as a response, they claim a defensive position, called isolationist pluralism, which supports the idea that studying development is not their problem. But postgenomics seems to have accepted and integrated some developmental criticisms and the isolationist perspective has been challenged during (...) the last few years. The developmental and quantitative traditions actually represent two different levels of analysis, but biometrics has also a clear developmental explanatory potential as it suggests statistically the existence of mechanical causes. Both traditions work together to go ever further in the knowledge of the phenomena being studied. Postgenomic pluralism, instead of being isolationist, may be considered pragmatic. (shrink)

The presence of gene–environment statistical interaction and correlation in biological development has led both practitioners and philosophers of science to question the legitimacy of heritability estimates. The paper offers a novel approach to assess the impact of GxE and rGE on the way genetic and environmental causation can be partitioned. A probabilistic framework is developed, based on a quantitative genetic model that incorporates GxE and rGE, offering a rigorous way of interpreting heritability estimates. Specifically, given an estimate of heritability and (...) the variance components associated with estimates of GxE and rGE, I arrive at a probabilistic account of the relative effect of genes and environment. (shrink)