This special issue of Human Biology, titled “Perspectives in Embodiment Theory,” brings together researchers who use a variety of lenses within the field of human biology to celebrate the plurality and wide applicability of embodiment. This special issue works to cross disciplinary boundaries to create more nuanced understandings of embodiment, plasticity, and experience in humans.

This article reviews literature in human epigenetic research as a case study in order to examine and critique the dominant framework of embodiment as unidirectional or bidirectional and mechanistically driven. The authors identify three major critiques to this approach: (1) the treatment of epigenetic traits as a mechanism of embodiment, rather than as multidirectional components of a dynamic and ongoing embodiment process; (2) a tendency to view changing epigenetic traits as both the cause and the solution for embodied social inequalities rather than examining the need for systemic change; and (3) a loss of the complexity of varied lived experiences within epigenetic studies. The authors suggest weaving in humanistic frameworks and expanding toward a multidirectional definition of embodiment in the field as a way forward.

Existing research supports both embodiment of stress through epigenetics and epigenetic impacts on dental development. This article proposes two models for embodiment of stress in dental development: the stress-delay model, with increased stress during development producing delays in dental development, and the inflammation-acceleration model, with increased stress producing faster dental development through inflammatory pathways. These models were tested on dental development scores from the New Mexico Decedent Image Database, using (a) nonaccidental death (homicide, suicide, and natural) as proxy for elevated stress exposure during life and (b) cadaver body mass index (BMI) percentile as proxy for living BMI. Sex was treated as a positive control because typically dental development is faster in females than in males. Nonaccidental death and male sex were both associated with slower dental development; however, manner of death was significant only for 7 of 32 (22%) of teeth. Mean BMI percentile was highest for natural death and lowest for homicide. These findings support the stress-delay model and accord with existing studies that found limited evidence that embodied effects on dental development are sufficiently large to affect estimates of age.

Posttraumatic stress disorder (PTSD) is a common and debilitating psychiatric disorder that may occur in individuals exposed to traumatic events such as accidents, interpersonal violence, war, combat, or natural disasters. Additionally, PTSD has been implicated in the development of a variety of chronic conditions, including cardiovascular and metabolic diseases, suggesting the biological alterations associated with the disorder can manifest as chronic diseases in those suffering from PTSD. The biological underpinnings of the disorder are not well understood. Gene expression studies can illuminate the complex physiology of PTSD reflecting the embodiment of trauma, that is, the process in which traumatic experiences in our social environments could potentially manifest in our body by genomic mechanisms. To date, gene expression studies that examine the whole transcriptome are scarce and limited to single-time-point assessments. Here we applied a transcriptome-wide gene expression screen with RNA-seq to whole blood samples from predominantly African American community-dwelling participants to elucidate the gene expression signatures associated with the development of PTSD. The study participants (N = 72) comprised a trauma-exposed subsample of participants enrolled in a longitudinal, prospective cohort study of adults living in Detroit, Michigan. PTSD was assessed in a structured telephone interview, and whole blood samples were taken both before and after trauma exposure. Among the 72 study participants, 10 had PTSD at baseline and 21 developed it during the study. We found 45 differentially expressed genes associated with PTSD development with an estimated log₂-fold change > 1.5 at a nominal p-value of <0.05. Six genes (PAX6, TSPAN7, PXDN, VWC2, SULF1, and NFATC4) were also ubiquitously expressed in all brain regions. Longitudinal sampling provides a promising mean to elucidate the pathophysiology underlying the embodiment of trauma.

This article historically situates human biology research by engaging with feminist science and technology scholars to show plasticity, how a key mechanism of embodiment, is used to re/produce sex and gender binaries in anthropological research and beyond. It first defines embodiment and demonstrates its reliance on plasticity and then reviews how and why plasticity has been taken up in human biology research. The article then engages with the works of feminist, trans, and queer scholars who have examined the connections among embodiment, plasticity, and the creation of Western binarized sex and gender. Further, the article presents how the re/production of a sex and gender binary is entwined with the justification of racial hierarchies through plasticity. While deterministic frameworks are often the most criticized in biology for harmful racist and sexist understandings of race and gender, plasticity and gene × environment interaction frameworks are not without fault. Even with large shifts in scientific understanding—in this case, from determinism to plasticity—science, in particular human biology, can still be a tool to create and maintain racist, patriarchal, cis- and heteronormative systems. The author concludes with recommendations and possible pathways forward for embodiment and plasticity research in human biology, suggesting that human biology research should engage with feminist science and technology critiques to be mindful of how our concepts might be re/producing harm.