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This article analyses in what way Swiss academic institutions have had a favourable or unfavourable influence on changing research practices by following developments in four scientific areas – Bose-Einstein Condensates, Evolutionary Developmental Biology, Large-Scale Assessments in education research and Computerised Corpus Linguistics. Based on empirical evidence, we argue that overall a number of institutional conditions have had a positive influence on the decisions of scientists to dare a switch to a new scientific field. One finds, however, also differences in the working of these institutional conditions leading to quicker or slower developments of the four selected scientific areas.

Our primary aim is to discuss the variability that exists in the operationalization of race/ethnicity in research on genetic and biological markers. We employ Stuart Hall’s “floating signifiers” of race approach to explain the ambiguous manner in which researchers discuss the links between race and genetics.

We examine articles that use race/ethnicity and genetic or biological markers between 2000 and 2013 within three prominent genetic journals. We focused on original, empirical articles only. We utilize various race/ethnic-related search terms to obtain our sample and to categorize how terms were used.

A total of 336 articles fit our search criteria. The number of articles mentioning race/ethnicity and genetic or biological information increased over the time. A significant percentage of publications base their research on whites only. When discussions of race are included in studies, scientists often use multiple categories of race/ethnicity without much explanation.

We omit non-research articles and commentary for each journal, which could contain important discussions regarding race and genetics. This work highlights how race/ethnicity can vary in application and interpretation.

Our discussion of race/ethnicity as “floating signifiers” adds a layer of complexity to the longstanding debate regarding the importance of race/ethnicity in genetic research. The “floating” nature of race/ethnicity underlines how subjective the characterizations of samples are and how possible interpretations of results for groups can impact health disparities research. Given the increased use of genetic data by social scientists, there is a need for more cross-disciplinary discussions on the race–gene relationship.

This mixed-methods study reports on an outreach clinics program designed to deliver genetic services to medically underserved communities in Wisconsin.

We show the geographic distribution, funding patterns, and utilization trends for outreach clinics over a 20-year period. Interviews with program planners and outreach clinic staff show how external and internal constraints limited the program’s capacity. We compare clinic operations to the conceptual models guiding program design.

Our findings show that state health officials had to scale back financial support for outreach clinic activities while healthcare providers faced increasing pressure from administrators to reduce investments in charity care. These external and internal constraints led to a decline in the overall number of patients served. We also find that redistribution of clinics to the Milwaukee area increased utilization among Hispanics but not among African-Americans. Our interviews suggest that these patterns may be a function of shortcomings embedded in the planning models.

Planning models have three shortcomings. First, they do not identify the mitigation of health disparities as a specific goal. Second, they fail to acknowledge that partners face escalating profit-seeking mandates that may limit their capacity to provide charity services. Finally, they underemphasize the importance of seeking trusted partners, especially in working with communities that have been historically marginalized.

There has been little discussion about equitably leveraging genetic advances that improve healthcare quality and efficacy. The role of State Health Agencies in mitigating disparities in access to genetic services has been largely ignored in the sociological literature.

Heritability studies attempt to estimate the contribution of genes (vs. environments) to variation in phenotypes (or outcomes of interest) in a given population at a given time. This chapter scrutinizes heritability studies of adverse health phenotypes, emphasizing flaws that have become more glaring in light of recent advances in the life sciences and manifest most visibly in epigenetics.

Drawing on a diverse body of research and critical scholarship, this chapter examines the veracity of methodological and conceptual assumptions of heritability studies.

The chapter argues that heritability studies are futile for two reasons: (1) heritability studies suffer from serious methodological flaws with the overall effect of making estimates inaccurate and likely biased toward inflated heritability, and, more importantly (2) the conceptual (biological) model on which heritability studies depend – that of identifiably separate effects of genes versus the environment on phenotype variance – is unsound. As discussed, contemporary bioscientific work indicates that genes and environments are enmeshed in a complex (bidirectional, interactional), dynamic relationship that defies any attempt to demarcate separate contributions to phenotype variance. Thus, heritability studies attempt the biologically impossible. The emerging research on the importance of microbiota is also discussed, including how the commensal relationship between microbial and human cells further stymies heritability studies.

Understandably, few sociologists have the time or interest to be informed about the methodological and theoretical underpinnings of heritability studies or to keep pace with the incredible advances in genetics and epigenetics over the last several years. The present chapter aims to provide interested scholars with information about heritability and heritability estimates of adverse health outcomes in light of recent advances in the biosciences.

Attempts to establish a biological basis for classifying human races into definable groups, arranged hierarchically from most advanced to least advanced, have a long and sordid history. From the days of the Spanish Inquisition, to the colonization of North and South America, the beginnings of the slave trade, to more recent claims about inborn racial differences in intelligence and personality, racists have tried to find biological differences that would separate the various races and provide a justification for social and economic exploitation. Biologically, races have been equated with subspecies as defined in the general biological literature. But the evidence from modern, molecular genetics, indicates that humans do not form the same kinds of distinguishable sub-groups common to other animal, especially mammalian, species. Biologically, human populations are 99% similar genetically, and the various visible characteristics that have traditionally been used to distinguish one “race” from another, do not correlate with any other characters of importance. Humans have evolved as a single lineage with many local populations that have always been in reproductive contact with each other. Thus, human sub-populations have not diverged to the extent that is found in other species, such as chimpanzees.

Regression analyses of compensatory educational programs have been criticized on the grounds that the pupils were not randomly selected. Specifically, it has been argued that a spurious deleterious effect of the treatment will be observed when the selection procedure systematically puts lower-ability students into the treatment group and higher-ability students into the control group.

We evaluate this argument via a simple test score model: pretest score and posttest score are fallible measures of underlying true ability and the true treatment effect is zero. Posttest is regressed on pretest and a treatment dummy. The spurious effect arises when selection of subjects for treatment is explicit on the basis of true ability, but not when it is explicit on the basis of pretest score.

This study analyzes the rise of genome instability in the life sciences and traces the problematic of instability as it relates to the sociology of health. Genome instability is the study of how genomes change and become variable between generations and within organisms over the life span. Genome instability reflects a significant departure from the Platonic genome imagined during the Human Genome Project. The aim of this chapter is to explain and analyze research on copy number variation and somatic mosaicism to consider the implications of these sciences for sociologists interested in genomics.

This chapter draws on two multi-sited ethnographies of contemporary biomedical science and literature in the sociology of health, science, and biomedicine to document a shift in thinking about the genome from fixed and universal to highly variable and influenced by time and context.

Genomic instability has become a framework for addressing how genomes change and become variable between generations and within organisms over the life span. Instability is a useful framework for analyzing changes in the life sciences in the post-genomic era.

Genome instability requires life scientists to address how differences both within and between individuals articulate with shifting disease categories and classifications. For sociologists, these findings have implications for studies of identity, sociality, and clinical experience.

This is the first sociological analysis of genomic instability. It identifies practical and conceptual implications of genomic instability for life scientists and helps sociologists delineate new approaches to the study of genomics in the post-genomic era.

This chapter explores the rise in genetic approaches to health disparities at the turn of the twenty-first century.

Analysis of public health policies, genome project records, ethnography of project leaders and leading genetic epidemiologists, and news coverage of international projects demonstrates how the study of health disparities and genetic causes of health simultaneously took hold just as the new field of genomics and matters of racial inequality became a global priority for biomedical science and public health.

As the U.S. federal government created policies to implement racial inclusion standards, international genome projects seized the study race, and diseases that exhibit disparities by race. Genomic leaders made health disparities research a central feature of their science. However, recent attempts to move toward analysis of gene-environment interactions in health and disease have proven insufficient in addressing sociological contributors to health disparities. In place of in-depth analyses of environmental causes, pharmacogenomics drugs, diagnostics, and inclusion in sequencing projects have become the frontline solutions to health disparities.

The chapter argues that genetic forms of medicalization and racialization have taken hold over science and public health around the world, thereby engendering a divestment from sociological approaches that do not align with the expansion of genomic science. The chapter thus contributes to critical discussions in the social and health sciences about the fundamental processes of medicalization, racialization, and geneticization in contemporary society.