Race and ethnicity are closely related, contentious concepts that have been abused and misinterpreted through history, but have a vast potential for good, at least in the health sciences. This article is not intending to elaborate on the conceptual foundations of race and ethnicity; I have addressed that elsewhere and summarized my stance in the glossary reprinted below in the Appendix. The terminology used here follows the glossary. Assuming that the conceptual foundations of my stance are reasonable, the questions addressed (...) here focus on public health and its primary health science, epidemiology, in a European context. The questions are simple ones:1.In epidemiology and public health what are we trying to achieve when we use the concepts of race and ethnicity?2.What would we lose by rejecting these concepts?3.If we do not reject them, how do we put the concepts into operation to help achieve our goals?4.What practical actions can result from the application of these concepts in order to improve the health and well-being of populations? (shrink)

In this book van Fraassen develops an alternative to scientific realism by constructing and evaluating three mutually reinforcing theories.

Common monogenic genetic diseases, ones that have unexpectedly high frequencies in certain populations, have attracted a great number of conflicting evolutionary explanations. This paper will attempt to explain the mystery of why two particularly extensively studied common genetic diseases, Tay Sachs disease and cystic fibrosis, remain evolutionary mysteries despite decades of research. I review the most commonly cited evolutionary processes used to explain common genetic diseases: reproductive compensation, random genetic drift (in the context of founder effect), and especially heterozygote advantage. (...) The latter process has drawn a particularly large amount of attention, having so successfully explained the elevated frequency of sickle cell anemia in malaria-endemic areas. However, the empirical evidence for heterozygote advantage in other common genetic diseases is quite weak. I introduce and illustrate the significance of a hierarchy of genetic disease phenomena found within the genetic disease explanations, which include the phenomena: single mutation variants of a common genetic disease, single genetic diseases, and classes of diseases with related phenotypic effects. I demonstrate that some of the confusion over the explanations of common genetic diseases can be traced back to confusions over which phenomena are being explained. I proceed to briefly evaluate the existing evidence for two common human genetic diseases: Tay Sachs disease and cystic fibrosis. The above considerations will ultimately shed light on why these diseases’ evolutionary explanations remain so deeply unresolved after so such a great volume of research. (shrink)

The Morris water maze has been put forward in the philosophy of neuroscience as an example of an experimental arrangement that may be used to delineate the cognitive faculty of spatial memory (e.g., Craver and Darden, Theory and method in the neurosciences, University of Pittsburgh Press, Pittsburgh, 2001; Craver, Explaining the brain: Mechanisms and the mosaic unity of neuroscience, Oxford University Press, Oxford, 2007). However, in the experimental and review literature on the water maze throughout the history of its use, (...) we encounter numerous responses to the question of “what” phenomenon it circumscribes ranging from cognitive functions (e.g., “spatial learning”, “spatial navigation”), to representational changes (e.g., “cognitive map formation”) to terms that appear to refer exclusively to observable changes in behavior (e.g., “water maze performance”). To date philosophical analyses of the water maze have not been directed at sorting out what phenomenon the device delineates nor the sources of the different answers to the question of what. I undertake both of these tasks in this paper. I begin with an analysis of Morris’s first published research study using the water maze and demonstrate that he emerged from it with an experimental learning paradigm that at best circumscribed a discrete set of observable changes in behavior. However, it delineated neither a discrete set of representational changes nor a discrete cognitive function. I cite this in combination with a reductionist-oriented research agenda in cellular and molecular neurobiology dating back to the 1980s as two sources of the lack of consistency across the history of the experimental and review literature as to what is under study in the water maze. (shrink)

An astonishing volume and diversity of evidence is available for many hypotheses in the biomedical and social sciences. Some of this evidence—usually from randomized controlled trials (RCTs)—is amalgamated by meta-analysis. Despite the ongoing debate regarding whether or not RCTs are the ‘gold-standard’ of evidence, it is usually meta-analysis which is considered the best source of evidence: meta-analysis is thought by many to be the platinum standard of evidence. However, I argue that meta-analysis falls far short of that standard. Different meta-analyses (...) of the same evidence can reach contradictory conclusions. Meta-analysis fails to provide objective grounds for intersubjective assessments of hypotheses because numerous decisions must be made when performing a meta-analysis which allow wide latitude for subjective idiosyncrasies to influence its outcome. I end by suggesting that an older tradition of evidence in medicine—the plurality of reasoning strategies appealed to by the epidemiologist Sir Bradford Hill—is a superior strategy for assessing a large volume and diversity of evidence. (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)

While the concepts of race and ethnicity have been abused historically, they are potentially invaluable in epidemiology and public health. Epidemiology relies upon variables that help differentiate populations by health status, thereby refining public health and health care policy, and offering insights for medical science. Race and ethnicity are powerful tools for doing this. The prerequisite for their responsible use is a society committed to reducing inequalities and inequities in health status. When this condition is met, it is irresponsible not (...) to utilize these concepts. (shrink)

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)