This paper suggests and discusses an answer to the following question: What distinguishes causal from non-causal or coincidental co-occurrences? The answer derives from Elizabeth Anscombe’s idea that causality is a highly abstract concept whose meaning derives from our understanding of specific causally productive activities, and from her rejection of the assumption that causality can be informatively understood in terms of actual or counterfactual regularities.Keywords: Elizabeth Anscombe; Causality; Explanation; Inhibition.

Many contemporary race scholars reject the biological reality of race.Elsewhere I have argued that they have been too quick to do so. Part ofthe reason is that they have overlooked the possibility that races canbe defined cladistically. Since the publication of the cladistic raceconcept, a number of questions and objections have been raised. My aimin this paper is to address these objections.

With In Search of Mechanisms, Carl F. Craver and Lindley Darden offer both a descriptive and an instructional account of how biologists discover mechanisms. Drawing on examples from across the life sciences and through the centuries, Craver and Darden compile an impressive toolbox of strategies that biologists have used and will use again to reveal the mechanisms that produce, underlie, or maintain the phenomena characteristic of living things. They discuss the questions that figure in the search for mechanisms, characterizing the (...) experimental, observational, and conceptual considerations used to answer them, all the while providing examples from the history of biology to highlight the kinds of evidence and reasoning strategies employed to assess mechanisms. At a deeper level, Craver and Darden pose a systematic view of what biology is, of how biology makes progress, of how biological discoveries are and might be made, and of why knowledge of biological mechanisms is important for the future of the human species. (shrink)

This paper critiques the new mechanistic explanatory program on grounds that, even when applied to the kinds of examples that it was originally designed to treat, it does not distinguish correct explanations from those that blunder. First, I offer a systematization of the explanatory account, one according to which explanations are mechanistic models that satisfy three desiderata: they must 1) represent causal relations, 2) describe the proper parts, and 3) depict the system at the right ‘level.’ Second, I argue that (...) even the most developed attempts to fulfill these desiderata fall short by failing to appropriately constrain explanatorily apt mechanistic models. -/- *This paper used to be called "The Emperor's New Mechanisms". (shrink)

This paper defends a counterfactual account of explanation, according to which successful explanation requires tracing patterns of counterfactual dependence of a special sort, involving what I call active counterfactuals. Explanations having this feature must appeal to generalizations that are invariant--stable under certain sorts of changes. These ideas are illustrated by examples drawn from physics and econometrics.

This paper attempts to elucidate three characteristics of causal relationships that are important in biological contexts. Stability has to do with whether a causal relationship continues to hold under changes in background conditions. Proportionality has to do with whether changes in the state of the cause “line up” in the right way with changes in the state of the effect and with whether the cause and effect are characterized in a way that contains irrelevant detail. Specificity is connected both to (...) David Lewis’ notion of “influence” and also with the extent to which a causal relation approximates to the ideal of one cause–one effect. Interrelations among these notions and their possible biological significance are also discussed. (shrink)

I defend an account of explanatory depth according to which explanations in the non-fundamental sciences can be deeper than explanations in fundamental physics.

Biologists studying complex causal systems typically identify some factors as causes and treat other factors as background conditions. For example, when geneticists explain biological phenomena, they often foreground genes and relegate the cellular milieu to the background. But factors in the milieu are as causally necessary as genes for the production of phenotypic traits, even traits at the molecular level such as amino acid sequences. Gene-centered biology has been criticized on the grounds that because there is parity among causes, the (...) “privileging” of genes reflects a reductionist bias, not an ontological difference. The idea that there is an ontological parity among causes is related to a philosophical puzzle identified by John Stuart Mill: what, other than our interests or biases, could possibly justify identifying some causes as the actual or operative ones, and other causes as mere background? The aim of this paper is to solve this conceptual puzzle and to explain why there is not an ontological parity among genes and the other factors. It turns out that solving this puzzle helps answer a seemingly unrelated philosophical question: what kind of causal generality matters in biology? (shrink)

The point Sesardic (Biol Philos 25: 143–162, 2010) makes about the possibility of distinguishing groups for which there is a lot of within-group variation is not sufficient to rehabilitate a biological concept of race. In this note, I sketch a number of issues that quickly arise once we delve more deeply into the relevant scientific knowledge, concepts, methods, and questions for inquiry.

This article examines how people of color can biologically inherit the deleterious effects of white racism. Drawing primarily on the field of epigenetics, I demonstrate how transgenerational racial disparities are in fact racist disparities that can be manifest physiologically, helping constitute the chemicals, hormones, cells, and fibers of the human body. Epigenetics can be used to demonstrate how white racism can have durable effects on the biological constitution of human beings that are not limited to the specific person who is (...) the target of white racism, but instead extend to that person's offspring. In this way, the field of epigenetics can help philosophers and others understand the transgenerational biological impact of social forces such as white racism. It reveals that the damage done by white racism is more extensive than critical philosophers of race might have realized, and also that interventions against white racism must address not just the economic, geographical, social, and psychological, but also the biological aspects of human existence. In particular, the article examines racist disparities in preterm birth rates and argues that the scope and significance of prenatal care for African American women must be expanded intergenerationally and include wide-scale forms of racial justice. (shrink)

In the early 2000s, Esteban Burchard and his colleagues defended a controversial route to the view that there’s a racial classification of people that’s useful in medicine. The route, which I call ‘Burchard’s route,’ is arguing that there’s a racial classification of people that’s useful in medicine because, roughly, there’s a racial classification with medically relevant genetic differentiation :1170–1175, 2003). While almost all scholars engaged in this debate agree that there’s a racial classification of people that’s useful in medicine in (...) some way, there’s tremendous controversy over whether any racial scheme is useful in medicine because there are medically relevant genetic differences among those races : 564–565, 2016). The goal of this paper will be to show that Burchard’s route is basically correct. However, I will use a slightly different argument than Burchard et al.’s in order to provide a firmer foundation for the thesis, both metaphysically and genetically. I begin by reviewing Burchard’s route and its critics. Second, I present an original argument for establishing Burchard et al.’s conclusion using a Burchard-like route. I call it ‘Spencer’s route’. I reply to major objections along the way, and I end with a summary. (shrink)

It is nowadays a dominant opinion in a number of disciplines (anthropology, genetics, psychology, philosophy of science) that the taxonomy of human races does not make much biological sense. My aim is to challenge the arguments that are usually thought to invalidate the biological concept of race. I will try to show that the way “race” was defined by biologists several decades ago (by Dobzhansky and others) is in no way discredited by conceptual criticisms that are now fashionable and widely (...) regarded as cogent. These criticisms often arbitrarily burden the biological category of race with some implausible connotations, which then opens the path for a quick eliminative move. However, when properly understood, the biological notion of race proves remarkably resistant to these deconstructive attempts. Moreover, by analyzing statements of some leading contemporary scholars who support social constructivism about race, I hope to demonstrate that their eliminativist views are actually in conflict with what the best contemporary science tells us about human genetic variation. (shrink)

We argue that the health sciences make causal claims on the basis of evidence both of physical mechanisms, and of probabilistic dependencies. Consequently, an analysis of causality solely in terms of physical mechanisms or solely in terms of probabilistic relationships, does not do justice to the causal claims of these sciences. Yet there seems to be a single relation of cause in these sciences - pluralism about causality will not do either. Instead, we maintain, the health sciences require a theory (...) of causality that unifies its mechanistic and probabilistic aspects. We argue that the epistemic theory of causality provides the required unification. (shrink)

Race is a prominent category in medicine. Epidemiologists describe how rates of morbidity and mortality vary with race, and doctors consider the race of their patients when deciding whether to test them for sickle‐cell anemia or what drug to use to treat their hypertension. At the same time, critics of racial classification say that race is not real but only an illusion or that race is scientifically meaningless. In this paper, I explain how race is used in medicine as a (...) proxy for genes that encode drug metabolizing enzymes and how a proper understanding of race calls into doubt the practice of treating race as a marker of any medically relevant genetic trait. (shrink)

A strong case has been made for the role and value of mechanistic reasoning in process-oriented sciences, such as molecular biology and neuroscience. This paper shifts focus to assess the role of mechanistic reasoning in an area where it is neither obvious nor expected: population genetics. Population geneticists abstract away from the causal-mechanical details of individual organisms and, instead, use mathematics to describe population-level, statistical phenomena. This paper, first, develops a framework for the identification of mechanistic reasoning where it is (...) not obvious: mathematical and mechanistic styles of scientific reasoning. Second, it applies this framework to demonstrate that both styles are integrated in modern investigations of evolutionary biology. Characteristic of the former, applied population genetic techniques provide statistical evidence for associations between genotype, phenotype, and fitness. Characteristic of the latter, experimental interventions provide causal-mechanical evidence for associations between the very same relationships, often in the same model organisms. The upshot is a richer perspective of how evolutionary biologists build evidence for hypotheses regarding adaptive evolution and a general framework for assessing the scope of mechanistic reasoning across the sciences. (shrink)

The concept of mechanism is analyzed in terms of entities and activities, organized such that they are productive of regular changes. Examples show how mechanisms work in neurobiology and molecular biology. Thinking in terms of mechanisms provides a new framework for addressing many traditional philosophical issues: causality, laws, explanation, reduction, and scientific change.

This article deals with mechanisms conceived as composed of entities and activities. In response to many perplexities about the nature of activities, a number of arguments are developed concerning their epistemic and ontological status. Some questions concerning the relations between cause and causal explanation and mechanisms are also addressed.

Evidence‐based medicine (EBM) proponents have argued that mechanistic evidence concerning medical treatments should be considered secondary to evidence derived from randomized controlled trials (RCTs). One common criticism of RCTs is that they often do not yield results that are generalizable to clinical practice, and that for clinical practice application, mechanistic evidence is needed. However, proponents of EBM have argued that mechanistic reasoning is often unreliable and thus not very useful. Here we suggest an important role of mechanistic explanation that has (...) been left out of this discussion entirely, namely, its importance in a patient’s decision of whether or not to take certain drugs. We argue that in certain cases, knowing how a treatment works is just as important for the patient as knowing whether it does. In this paper, we explore how and why giving patients mechanistic information can be an important factor in obtaining informed consent for medical treatment, focusing on the example case of hormonal contraceptives. (shrink)

This paper distinguishes three concepts of "race": bio-genomic cluster/race, biological race, and social race. We map out realism, antirealism, and conventionalism about each of these, in three important historical episodes: Frank Livingstone and Theodosius Dobzhansky in 1962, A.W.F. Edwards' 2003 response to Lewontin (1972), and contemporary discourse. Semantics is especially crucial to the first episode, while normativity is central to the second. Upon inspection, each episode also reveals a variety of commitments to the metaphysics of race. We conclude by interrogating (...) the relevance of these scientific discussions for political positions and a post-racial future. (shrink)

Support for the biological concept of race declined slowly but steadily during the second half of the twentieth century. However, debate about the validity of the race concept has recently been reignited. Genetic-clustering studies have shown that despite the small proportion of genetic variation separating continental populations, it is possible to assign some individuals to their continents of origin, based on genetic data alone. Race naturalists have interpreted these studies as empirically confirming the existence of human subspecies, and by extension (...) biological races. However, the new racial naturalism is not convincing. The continental clusters appealed to by race naturalists are arbitrary and superficial groupings, which should not be elevated to subspecies status. Moreover, the criteria applied to humans are not consistent with those used to define subspecies in nonhuman animals, and no rationale has been given for this differential treatment. (shrink)

Confusions about the place of race in medicine result in part from a failure to recognize the plurality of race concepts. Recognition that the ordinary concept of race is not identical to the racialist concept of race makes it possible to ask whether there might be a legitimate place for the deployment of concepts of race in medical contexts. Two technical race concepts are considered. The concept of social race is the concept of a social group that is taken to (...) be a racialist race. It is apt for use in examining and addressing the medical effects of discrimination. The populationist concept of race represents race as a kind of biological population. It makes it possible to frame the question whether biological race is a factor in disease susceptibility and drug responsiveness. It is apt for use in determining whether biological race is a medically significant category. (shrink)

This essay unpacks a seeming paradox: a concept used to formulate, promote, and legitimate oppressive ideologies—a concept used to formulate mistaken, because they were typological, biological theories about human diversity—is, it seems, the same concept that now promises to deliver wonderful, socially sensitized, innovative results in social and genetic epidemiology. But how could that be? How could scientists expect a concept as problematic as ordinary race to deliver useful scientific results? I propose that there is a process for retranslating Ballungen (...) race concepts in appropriate ways to make them fit and work within social scientific and bioscientific contexts. (shrink)

Approaches to explanation -- Causal and explanatory relevance -- The kairetic account of /D making -- The kairetic account of explanation -- Extending the kairetic account -- Event explanation and causal claims -- Regularity explanation -- Abstraction in regularity explanation -- Approaches to probabilistic explanation -- Kairetic explanation of frequencies -- Kairetic explanation of single outcomes -- Looking outward -- Looking inward.

Targeting high-risk populations for public health interventions is a classic tool of public health promotion programs. This practice becomes thornier when racial groups are identified as the at-risk populations. I present the particular ethical and epistemic challenges that arise when there are low-risk subpopulations within racial groups that have been identified as high-risk for a particular health concern. I focus on two examples. The black immigrant population does not have the same hypertension risk as US-born African Americans. Similarly, Finnish descendants (...) have a far lower rate of cystic fibrosis than other Caucasians. In both cases the exceptional nature of these subpopulations has been largely ignored by the designers of important public health efforts, including the recent US government dietary recommendations. I argue that amending the publicly-disseminated risk information to acknowledge these exceptions would be desirable for several reasons. First, recognizing low-risk subpopulations would allow more efficient use of limited resources. Communicating this valuable information to the subpopulations would also promote truth-telling. Finally, presenting a more nuanced empirically-supported representation of which groups are at known risk of diseases (not focusing on mere racial categories) would combat harmful biological race essentialist views held by the public. (shrink)

This paper defends the concept of racialization against its critics. As the concept has become increasingly popular, questions about its meaning and value have been raised, and a backlash against its use has occurred. I argue that when “racialization” is properly understood, criticisms of the concept are unsuccessful. I defend a definition of racialization and identify its companion concept, “racialized group.” Racialization is often used as a synonym for “racial formation.” I argue that this is a mistake. Racial formation theory (...) is committed to racial ontology, but racialization is best understood as the process through which racialized – rather than racial – groups are formed. “Racialization” plays a unique role in the conceptual landscape, and it is a key concept for race eliminativists and anti-realists about race. (shrink)