Abstract We are seeing an exploding expansion of antisemitic attacks worldwide, raising concerns about their potential impact on biological stress regulation and health. Antisemitism is a historically persistent and structurally embedded form of social exclusion that may contribute to chronic psychosocial stress exposure. Building on research into intergenerational trauma, including neuroendocrine alterations in Holocaust survivors and their descendants, this commentary integrates psychometric, empirical, and conceptual approaches to propose a biologically grounded framework linking antisemitism to endocrine and cardiometabolic processes. Preliminary findings from a pilot study using a Checklist of Antisemitic Perception instrument, in combination with established psychometric measures, indicate an increased psychological burden associated with antisemitic experiences, with clinically relevant symptom levels observed across groups. Mechanistically, chronic stress is mediated by neuroendocrine pathways involving the hypothalamic–pituitary–adrenal axis, autonomic nervous system, and immune regulation, contributing to allostatic load and cardiometabolic risk. Emerging evidence suggests that stress responses are heterogeneous and influenced by individual coping styles, with distinct allostatic set-points and associated neurobiological adaptations, including alterations in striatal glutamatergic signaling. Institutional and discursive contexts may further modulate exposure to antisemitic stressors, as reflected in heterogeneous professional engagement and variations in thematic emphasis within medical discourse. Taken together, these observations support the conceptualization of antisemitism as a chronic stressor with potential biological consequences and highlight the importance of integrating psychometric and biological approaches in future research.
Ettrich et al. (Fri,) studied this question.