Use of medication for treatment of ADHD (or its historical precursors) has been debated for more than forty years. Reasons for the ongoing differences of opinion are analyzed by exploring some of the arguments for and against considering ADHD a mental disorder. Relative to two important DSM criteria — that a mental disorder causes some sort of harm to the individual and that a mental disorder is the manifestation of a dysfunction in the individual — ADHD’s classification as a mental (...) disorder is found to be contentiously value-laden. The disagreements spill over to reasoning regarding appropriate management, because justification for a drug prescription is in part predicated on the idea that the drugs manage mental disorders. These debates do not appear to be nearing resolution, so individuals offering advice, or trying to decide whether ADHD drugs are appropriate for themselves or their children, may find it helpful to compare the values underlying various perspectives with their own. (shrink)

In this book the author explores the shifting philosophical boundaries of modern medical knowledge and practice occasioned by the crisis of quality-of-care, especially in terms of the various humanistic adjustments to the biomedical model.

If dispositions are conceived as properties of systems that refer to possible causal relations, dispositions can be used in singular causal explanations. By means of these dispositional explanations, we can explain behavior B of a system x by (i) referring to a situation of type S that triggered B, given that x has a disposition D to do B in S, or (ii) by referring to a disposition D of x to do B in S, given that x is in (...) a situation of type S. Dispositional explanations are adequate and indispensable explanations: they can explain behavior B without explicitly referring to the underlying causal basis in x that constitutes a disposition to do B. Radical Behaviorist explanations are a sort of dispositional explanations, but the dispositional model is not restricted to these explanations. The dispositional model is compatible with, or can be applied to, several research programs. (shrink)

Carl Craver investigates what we are doing when we sue neuroscience to explain what's going on in the brain.

We argue that intelligible appeals to interlevel causes (top-down and bottom-up) can be understood, without remainder, as appeals to mechanistically mediated effects. Mechanistically mediated effects are hybrids of causal and constitutive relations, where the causal relations are exclusively intralevel. The idea of causation would have to stretch to the breaking point to accommodate interlevel causes. The notion of a mechanistically mediated effect is preferable because it can do all of the required work without appealing to mysterious interlevel causes. When interlevel (...) causes can be translated into mechanistically mediated effects, the posited relationship is intelligible and should raise no special philosophical objections. When they cannot, they are suspect. (shrink)

The world is complex, but acknowledging its complexity requires an appreciation for the many roles context plays in shaping natural phenomena. In _Unsimple Truths, _Sandra Mitchell argues that the long-standing scientific and philosophical deference to reductive explanations founded on simple universal laws, linear causal models, and predict-and-act strategies fails to accommodate the kinds of knowledge that many contemporary sciences are providing about the world. She advocates, instead, for a new understanding that represents the rich, variegated, interdependent fabric of many levels (...) and kinds of explanation that are integrated with one another to ground effective prediction and action. Mitchell draws from diverse fields including psychiatry, social insect biology, and studies of climate change to defend “integrative pluralism”—a theory of scientific practices that makes sense of how many natural and social sciences represent the multi-level, multi-component, dynamic structures they study. She explains how we must, in light of the now-acknowledged complexity and contingency of biological and social systems, revise how we conceptualize the world, how we investigate the world, and how we act in the world. Ultimately _Unsimple Truths _argues that the very idea of what should count as legitimate science itself should change. (shrink)

Explanatory pluralism has been defended by several philosophers of history and social science, recently, for example, by Tor Egil Førland in this journal. In this article, we provide a better argument for explanatory pluralism, based on the pragmatist idea of epistemic interests. Second, we show that there are three quite different senses in which one can be an explanatory pluralist: one can be a pluralist about questions, a pluralist about answers to questions, and a pluralist about both. We defend the (...) last position. Finally, our third aim is to argue that pluralism should not be equated with “anything goes”: we will argue for non-relativistic explanatory pluralism. This pluralism will be illustrated by examples from history and social science in which different forms of explanation (for example, structural, functional, and intentional explanations) are discussed, and the fruitfulness of our framework for understanding explanatory pluralism is shown. (shrink)

The paper argues for a pragmatic account of genetic explanation. This is to say that when a disease or other trait is termed genetic, the reasons for singling out genes as causes over other, also necessary, genetic and nongenetic conditions are not wholly theoretical but include pragmatic dimensions. Whether the explanation is the presence of a trait in an individual or differences in a trait among individuals, genetic explanations are context-dependent in three ways: they are relative to a causal background (...) of genetic and nongenetic factors; they are relative to a population; and they are relative to the present state of knowledge. Criteria like causal priority, nonstandardness, and causal efficacy that purport to distinguish objectively between genetic causes and nongenetic conditions either incorporate pragmatic elements or fail for other reasons. When the pragmatic dimensions of genetic explanations are recognized, we come to understand the current phenomenon of geneticization to be a reflection of increased technological capacities to manipulate genes in the laboratory, and potentially the clinic, rather than theoretical progress in understanding how diseases and other traits arise. This calls into question the value of the search for theoretical definitions of designations like genetic disease or genetic susceptibility as directives for action. (shrink)

Some social scientists and philosophers (e.g., James Coleman and Jon Elster) claim that all social facts are best explained by means of a micro-explanation. They defend a micro-reductionism in the social sciences: to explain is to provide a mechanism on the individual level. The first aim of this paper is to challenge this view and defend the view that it has to be substituted for an explanatory pluralism with two components: (1) structural explanations of P-, O- and T-contrasts between social (...) facts are more efficient than the competing micro-explanations; and (2) whether a plain social fact (as opposed to a contrast) is best explained in a micro-explanation or a structural explanation depends on the explanatory interest. The second aim of the paper is to show how this explanatory pluralism is compatible with ontological individualism. This paper is motivated by our conviction that explanatory pluralism as defended by Frank Jackson and Philip Pettit is on the right track, but must be further elaborated. We want to supplement their contribution, by (1) introducing the difference between explanations of facts and explanations of contrasts; (2) giving examples from the social sciences, instead of mainly from the natural sciences or common sense knowledge; and (3) emphasizing the pragmatic relevance of explanations on different levels –social, psychological, biological, etc. – which is insufficiently done by Jackson and Pettit. (shrink)

Recent pleas for more heterodoxy in explaining economic action have been defending a pluralism for economics. In this article, I analyse these defences by scrutinizing the pluralistic qualities in the work of one of the major voices of heterodoxy, Tony Lawson. This scrutiny will focus on Lawson's alternatives concerning ontology and explanation to mainstream economics. Subsequently, I will raise some doubts about Lawson's pluralism, and identify questions that will have to be addressed by heterodox economists in order to maintain the (...) claim of pluralism. (shrink)

ABSTRACTExplanatory pluralism has been defended by several philosophers of history and social science, recently, for example, by Tor Egil Førland in this journal. In this article, we provide a better argument for explanatory pluralism, based on the pragmatist idea of epistemic interests. Second, we show that there are three quite different senses in which one can be an explanatory pluralist: one can be a pluralist about questions, a pluralist about answers to questions, and a pluralist about both. We defend the (...) last position. Finally, our third aim is to argue that pluralism should not be equated with “anything goes”: we will argue for non‐relativistic explanatory pluralism. This pluralism will be illustrated by examples from history and social science in which different forms of explanation are discussed, and the fruitfulness of our framework for understanding explanatory pluralism is shown. (shrink)

This paper focuses on the causation of diseases, particularly on the idea of a “genetic cause” taking Alzheimer’s Disease (AD) as an example. We (1) provide some historical information and a synopsis of the current knowledge on the etiology and pathogenesis of AD, (2) analyse some conceptual problems related to the notion of “genetic disease” (3) elaborate on the alleged (genetic) cause of AD, and (4) place the discussion on the cause of AD in a broader philosophical context, paying attention (...) to a constructivist perspective, the notions of causal connection and causal selection, and to some practical and normative consequences of our analysis. We conclude (a) that AD is not a specific disease entity with one specific cause, (b) that the idea of a single (sufficient) cause can still function as a heuristic tool in AD research and practice, and (c) that a “belief” in causation can go together with the notions of multicausality and probability. (shrink)

This paper deals with the "functions of intentional explanations" of actions (IEAs), i.e., explanations that refer to intentional states (beliefs, desires, etc.) of the agent. IEAs can have different formats. We consider these different formats to be instruments that enable the explainer to capture different kinds of information. We pick out two specific formats, i.e. "contrastive" and "descriptive", which will enable us to discuss the functions of IEAs. In many cases the explanation is contrastive, i.e. it makes use of one (...) or more contrasts between real intentional states and ideal intentional states (ideal from the point of view of the explainer). In many other cases IEAs have a descriptive (covering-law) format. The aim of this paper is to analyze the functions the two kinds of explanations can have. We will show that certain functions are better served by one rather than the other format. This leads to pluralism with respect to formats. We argue that both formats are necessary and that their functions are complementary. (shrink)

This paper focuses on the causation of diseases, particularly on the idea of a "genetic cause" taking Alzheimer's Disease as an example. We provide some historical information and a synopsis of the current knowledge on the etiology and pathogenesis of AD, analyse some conceptual problems related to the notion of "genetic disease", elaborate on the alleged cause of AD, and place the discussion on the cause of AD in a broader philosophical context, paying attention to a constructivist perspective, the notions (...) of causal connection and causal selection, and to some practical and normative consequences of our analysis. We conclude that AD is not a specific disease entity with one specific cause, that the idea of a single cause can still function as a heuristic tool in AD research and practice, and that a "belief" in causation can go together with the notions of multicausality and probability. (shrink)