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      Beyond a Shared History: A Biosocial Perspective on Sociogenomics and Racism in Germany

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          Abstract

          Recent advances in sociogenomics offer new opportunities to integrate genetic and epigenetic measures into social science research on human lifespan development. Now, German social science cohorts have followed suit with this global trend. We anticipate that the integration of genetic measures into German social science cohorts is likely to be met with hesitation and dismay. Historically, racialized pseudo-science disguised as genetic research was used to justify the political exploitation, oppression, and genocide conducted by colonial and Nazi Germany regimes. In response, German institutions and social sciences actively avoided race-related research. However, avoiding the intersection of socially constructed race and genetics may stall the deconstruction of enduring racial discrimination and the identification of racialized social inequalities. Recent survey studies show that half of the German population still believe in the existence of biologically distinct human “races” and that racism is rampant. This article is aimed at providing a biosocial perspective on sociogenomics and racism in Germany. First, we discuss the biologistic construction of race that became prevalent in colonial and Nazi Germany. We argue that racist legacies are sources of social inequality in contemporary German society. We further review recent human genomic science that clearly demonstrates that there is no biological basis to socially constructed race. Second, we propose a biosocial perspective that integrates how genes “get out of the skin” and racism “gets under the skin”. Transactional genetic effects, which involve human behavior and interactions between people in society, are expected to depend on environmental inequalities tied to systemic racism. We summarize recent sociogenomics studies using polygenic indices and epigenetic profile scores showing that a) genes contribute to complex human traits and b) the expression of genetic variation is affected by socioeconomic and racialized inequality. Finally, we offer a roadmap toward race-critical biosocial research that breaks with the historically informed avoidance of race to reconstruct race-critical concepts, datasets, and scientific systems.

          Zusammenfassung

          Der Beitrag beleuchtet die jüngsten Fortschritte in der Soziogenomik und deren Potenzial, genetische und epigenetische Faktoren in die sozialwissenschaftliche Forschung zur menschlichen Entwicklung zu integrieren. Aus einer neuen biosozialen Perspektive auf Soziogenomik und Rassismus in Deutschland wird die Wechselwirkung zwischen Genen, menschlichem Verhalten, sozialen Interaktionen und Umweltfaktoren, insbesondere systemischem Rassismus, untersucht. Durch die Zusammenfassung aktueller soziogenomischer Studien wird verdeutlicht, dass Gene zu komplexen menschlichen Merkmalen beitragen und dass der Ausdruck genetischer Unterschiede von sozioökonomischen und rassifizierten Ungleichheiten beeinflusst wird. Im Beitrag wird außerdem die historisch vorherrschende biologistische Konstruktion von „Rasse“ im kolonialen und nationalsozialistischen Deutschland behandelt und aufgezeigt, wie dieses Erbe soziale Ungleichheit in der modernen deutschen Gesellschaft beeinflusst. Die aktuellsten Erkenntnisse der Humangenomik werden herangezogen, um eindeutig festzuhalten, dass es keine biologische Grundlage für das Konzept von „Rasse“ gibt. Abschließend bietet der Beitrag einen Ausblick auf rassismus-kritische biosoziale Forschung in Deutschland. Diese Forschung strebt an, Konzepte, Datensätze und wissenschaftliche Systeme rassismus-kritisch zu überprüfen und neu zu gestalten.

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          Most cited references114

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          The Hallmarks of Aging

          Aging is characterized by a progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death. This deterioration is the primary risk factor for major human pathologies, including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases. Aging research has experienced an unprecedented advance over recent years, particularly with the discovery that the rate of aging is controlled, at least to some extent, by genetic pathways and biochemical processes conserved in evolution. This Review enumerates nine tentative hallmarks that represent common denominators of aging in different organisms, with special emphasis on mammalian aging. These hallmarks are: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. A major challenge is to dissect the interconnectedness between the candidate hallmarks and their relative contributions to aging, with the final goal of identifying pharmaceutical targets to improve human health during aging, with minimal side effects. Copyright © 2013 Elsevier Inc. All rights reserved.
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            Principal components analysis corrects for stratification in genome-wide association studies.

            Population stratification--allele frequency differences between cases and controls due to systematic ancestry differences-can cause spurious associations in disease studies. We describe a method that enables explicit detection and correction of population stratification on a genome-wide scale. Our method uses principal components analysis to explicitly model ancestry differences between cases and controls. The resulting correction is specific to a candidate marker's variation in frequency across ancestral populations, minimizing spurious associations while maximizing power to detect true associations. Our simple, efficient approach can easily be applied to disease studies with hundreds of thousands of markers.
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              Clinical use of current polygenic risk scores may exacerbate health disparities

              Polygenic risk scores (PRS) are poised to improve biomedical outcomes via precision medicine. However, the major ethical and scientific challenge surrounding clinical implementation of PRS is that those available today are several times more accurate in individuals of European ancestry than other ancestries. This disparity is an inescapable consequence of Eurocentric biases in genome-wide association studies, thus highlighting that-unlike clinical biomarkers and prescription drugs, which may individually work better in some populations but do not ubiquitously perform far better in European populations-clinical uses of PRS today would systematically afford greater improvement for European-descent populations. Early diversifying efforts show promise in leveling this vast imbalance, even when non-European sample sizes are considerably smaller than the largest studies to date. To realize the full and equitable potential of PRS, greater diversity must be prioritized in genetic studies, and summary statistics must be publically disseminated to ensure that health disparities are not increased for those individuals already most underserved.
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                Author and article information

                Contributors
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                Journal
                KZfSS Kölner Zeitschrift für Soziologie und Sozialpsychologie
                Köln Z Soziol
                Springer Science and Business Media LLC
                0023-2653
                1861-891X
                March 11 2024
                Article
                10.1007/s11577-024-00934-6
                66fc54ad-37a2-4bf2-9f81-ddacd32941c1
                © 2024

                https://creativecommons.org/licenses/by/4.0

                https://creativecommons.org/licenses/by/4.0

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