Putting the concept of biological embedding in historical perspective (original) (raw)
Related papers
Psychoneuroendocrinology, 2019
Individuals of lower socioeconomic position (SEP) carry a heavier burden of disease and morbidity and live shorter lives on average compared with their more advantaged counterparts. This has sparked research interest in the processes and mechanisms via which social adversity gets biologically embedded. The present study directly compares the empirical worth of two candidate mechanisms: Allostatic Load (AL) and the Epigenetic Clock(s) for advancing our understanding of embodiment using a sub-sample of 490 individuals from the Irish Longitudinal Study (TILDA) who were explicitly selected for this purpose based on their inter-generational life course social class trajectory. A battery of 14 biomarkers representing the activity of 4 different physiological systems: Immunological, Cardiovascular, Metabolic, and Renal was used to construct the AL score. Biomarkers were dichotomised into high and low risk groups according to sex-specific quartiles of risk and summed to create a count ranging from 0-14. Three measures of epigenetic age acceleration were computed according to three sets of age-associated Cytosine-phosphate-Guanine (CpG) sites described by Horvath, Hannum and Levine. AL was strongly socially patterned across a number of measures of SEP, while the epigenetic clocks were not. AL partially mediated the association between measures of SEP and an objective measure of physiological functioning: performance on the Timed Up and Go (TUG test). We conclude that AL may represent the more promising candidate for understanding the pervasive link between SEP and health.
A different kind of association between socio-histories and health
The British journal of sociology, 2015
In the last 15 years, genetics researchers have developed new molecular genomic technologies for analysing human differences at the level of DNA. This was soon followed by an explosion of studies that aimed to find genetic explanations for the differential health outcomes between individuals and groups by examining association between DNA and disease. Meanwhile, other geneticists have used the new molecular technologies to examine DNA differences between individuals and groups to build theories about migration, language, and ancestry in human history. Many of these studies have organized DNA differences into groups that oftentimes correspond to institutionallyestablished racial categories as they currently exist in the USA. Some of this new research has rekindled debates about the relationship between biology and race in many fields, including sociology. In tandem with this new research on DNA differences is an explosion of social scientific research critiquing the revitalization of research on biological differences by race. Troy Duster is the originator of and inspiration for much of this critical research (Duster 2003, originally published in 1990). More significantly, Duster has in this BJS article assembled the findings of the research referred to below to show how these different fragments come together to make a coherent story about the 'creeping molecularization' (personal communication) of race in very different realms. Many have critiqued what Duster calls the creeping molecularization of race in genetics research because it threatens to reinvigorate the belief that human social classification systems like race have a biological, 'natural' basis. Some of these social scientific studies described the new genetic classificatory research as examples of a 'genetic reinscription of race' (
The Developmental Origins of Health Inequality
In this chapter, I review recent evidence on the developmental origins of health inequality. I discuss the origins of the education-health gradient, the long-term costs caused by early life adversity, and how early life experiences affect the biology of the body. Additionally, I provide complementary evidence on enrichment interventions which can at least partially compensate for these gaps. I highlight emerging lines of scientific inquiry which are likely to have a significant impact on the field. I argue that, while the evidence that early life conditions have long-term effects is now uncontroversial, the literature needs to be expanded both in a theoretical and empirical direction. On the one hand, a model linking early life origins to ageing needs to be developed; on the other hand, a better understanding of the mechanisms À both biological and socioeconomic À is required, in order to design more effective interventions.
We have known for quite some time that disadvantaged individuals suffer from poorer health outcomes and lower life spans than the advantaged. The disadvantaged do not perform as well on educational tests than their wealthier peers. In some situations, racial discrimination intersects with poverty to worsen these outcomes for minorities. With the notion that poverty becomes implanted in an individual's genes and brain, science helps explain how these disparate lifespans and variations in cognitive outcomes come to be. This Article collectively refers to these scientific theories as embodied inequality. Embodied inequality explains why it is so difficult for individuals to escape the effects of socioeconomic disadvantage.
Social inequalities in health: Biological, cognitive and learning theory perspectives
2000
Increasing social inequalities in health have been ascribed to unequal distribution of resources, and to exposure factors. We propose that these differences also may be explained by principles from cognitive stress theory. There seems to be consensus in the stress literature that the stress response is not predicted from the external situation. The acquired expectancies to stimuli and response outcome
How Race Becomes Biology: Embodiment of Social Inequality
The current debate over racial inequalities in health is arguably the most important venue for advancing both scientific and public understanding of race, racism, and human biological variation. In the United States and elsewhere, there are well-defined inequalities between racially defined groups for a range of biological outcomes—cardiovascular disease, diabetes, stroke, certain cancers, low birth weight, preterm delivery, and others. Among biomedical researchers, these patterns are often taken as evidence of fundamental genetic differences between alleged races. However, a growing body of evidence establishes the primacy of social inequalities in the origin and persistence of racial health disparities. Here I summarize this evidence and argue that the debate over racial inequalities in health presents an opportunity to refine the critique of race in three ways: (1) to reiterate why the race concept is inconsistent with patterns of global human genetic diversity; (2) to refocus attention on the complex, environmental influences on human biology at multiple levels of analysis and across the lifecourse; and (3) to revise the claim that race is a cultural construct and expand research on the sociocultural reality of race and racism. Drawing on recent developments in neighboring disciplines, I present a model for explaining how racial inequality becomes embodied—literally—in the biological well-being of racialized groups and individuals. This model requires a shift in the way we articulate the critique of race as bad biology.
Social-biological transitions: how does the social become biological?
Longitudinal and Life Course Studies, 2013
The present discussion paper sets forward a model within the life course perspective of how the social becomes biological. The model is intended to provide a framework for thinking about such questions as how does social class get into the molecules, cells and tissues of the body to produce social class differences in life expectancy and cause of death? A categorisation of social exposures and biological processes is suggested; and some principles governing their interrelations proposed. The paper ends by suggesting two public health applications of this approach.