Not all people conform to socially constructed norms, nor should they have to. Neurodiversity, the natural variation in human brains and cognition, is fundamental to understanding human behavior, yet neurodivergent individuals in academia are often stigmatized, undervalued, or pressured to mask their differences. This position statement, authored predominantly by neurodivergent scholars, explores how aligning the values of the neurodiversity movement with practices of Open Scholarship (OSch) can foster greater research integrity, rigor, social responsibility and justice, diversity, equity, inclusivity, and accessibility in academia. We review systemic barriers faced by neurodivergent researchers—from disclosure dilemmas and hidden curriculum expectations to intersectional disadvantages—and identify how OSch principles (transparency, accessibility, collaboration) can help mitigate these challenges. Drawing on lived experiences and current research, we propose concrete reforms, including adopting universal design in scholarly communication, promoting participatory research methods, and enacting supportive policies (e.g., flexible work arrangements, inclusive codes of conduct). By leveraging shared values of openness and neuro-inclusion, academia can become more just and epistemically equitable. Our recommendations chart a path toward an academic culture where neurodivergent scholars can thrive openly, to the benefit of scientific rigor and social justice alike.

Phan, J. M., Middleton, S. L., Azevedo, F., Iley, B. J., Grose‐Hodge, M., Tyler, S. L., Kapp, S.K., Yeung, S.K., Shaw, J.J., Hartmann, H. & FORRT. (2025). Bridging neurodiversity and open scholarship: how shared values can guide best practices for research integrity, social justice, and principled education. Journal of Social Issues, 81(4), e70035. https://doi.org/10.1111/josi.70035

Autistic individuals disproportionately experience obesity, cardiovascular disease, diabetes, and a range of other adverse health outcomes, relative to both the general population and those with other developmental conditions. These individuals also disproportionately experience Post-Traumatic Stress Disorder (PTSD). Many of these conditions emerge during adolescence and young adulthood (age 15–30). This study analyzed Medicaid claims data (2008–2019) from autistic (n = 627,586; M age = 17.15 [3.55]) and non-autistic (n = 1,223,161; M age 19.35 [4.56]) adolescent and young adults. Using logistic regression and adjusting for demographic and clinical characteristics, this study: (1) evaluated associations between the presence of autism, obesity, and other health co-morbidities using the Adolescent and Young Adult (AYA) Hope Comorbidity Index; and (2) tested PTSD as a moderator in these associations. Compared with non-autistic beneficiaries, autistic beneficiaries demonstrated 2.12 (95% CI: 2.09, 2.15) and 2.12 (95% CI: 2.09, 2.16) times the odds of having obesity and other health comorbidities, respectively. PTSD moderated these associations such that autism status was more strongly associated with obesity and health co-morbidities among those without a PTSD diagnosis compared to those with a PTSD diagnosis. Autistic adolescents and young adults experience higher rates of obesity, health co-morbidities, and PTSD relative to their non-autistic counterparts. Future work is needed to explore measurement of stress and trauma beyond PTSD diagnoses and elucidate the precise association between stress and trauma with adverse health outcomes in this population.

Hotez, E., Tsevat, R.K., Tao, S.,Phan, J.M., Smith, P., Shen, T., Ventimiglia, J., Rivera, L., Kissner, H., Croen, L.A., & Shea, L. (2025). Autism, obesity, and PTSD among adolescents and young adults: An analysis of national Medicaid claims data. Journal of Autism and Developmental Disorders. https://doi.org/10.1007/s10803-025-06881-1

This perspective piece addresses critical challenges in oxytocin-based interventions for autism, drawing on neurodivergent perspectives to highlight key issues in research relevance and inclusivity. Although oxytocin has been posited to modulate social and routinized behaviors in autistic individuals, empirical findings on its efficacy remain inconsistent. We argue that these behavioral targets may reflect neurotypical biases, often disregarding autistic individuals' perspectives, thereby limiting intervention acceptability and efficacy. Past research has frequently excluded marginalized autistic populations, such as individuals with intellectual disabilities or gender-diverse identities, exacerbating generalizability issues. This piece advocates for a reorientation of research objectives in autism, proposing a shift from modifying core autistic behaviors towards enhancing quality of life through participatory research. By integrating autistic perspectives into study design and outcome selection, researchers can avoid deficit-oriented frameworks and instead prioritize socially valid outcomes, such as reducing anxiety and improving adaptive functioning. Further, the perspective piece critiques the reliance on animal models, which often lack translational validity due to autism's complex social and communicative dimensions. In closing, we underscore the importance of inclusive, reproducible autism research practices that align with the lived experiences and priorities of autistic individuals. Embracing participatory research, alongside rigorous methodological adjustments, can foster advancements that effectively support the well-being of the autistic community.

Phan, J. M., Dwyer, P., Elsherif, M. M., Friedel, E., & Kapp, S. K. (2025). Oxytocin in autism: Rethinking treatment and research through a neurodivergent perspective. Psychoneuroendocrinology, 171, 107220. https://doi.org/10.1016/j.psyneuen.2024.107220

Activational effects of the reproductive neuroendocrine system may explain why some youths with ADHD are at greater risk for exacerbated ADHD symptoms (hyperactivity, inattention, impulsivity) during adolescence. For youths diagnosed with ADHD, first signs of ADHD symptoms become noticeable by multiple reporters (e.g., teachers, parents) when children enter schools, typically around kindergarten. The current study examined possible sex differences in ADHD, impairment, and comorbidity due to pubertal effects, as the role of pubertal development in ADHD is understudied. ADHD symptoms, depressive symptoms, impairment, and pubertal stage were assessed annually by multiple reporters in a well-characterized clinical sample of 849 children over eight years. Ages ranged from 7 to 18 years (38.16% girls). Multilevel models indicated that boys had higher levels of hyperactivity, impulsivity, and inattention than girls, but that girls had higher levels of impairment than boys. Inattention symptoms did not show marked maturation changes. Hyperactivity and impulsivity declined as youth aged and impairment increased as youth aged. Lastly, depressive symptoms largely increased as youth aged and were higher amongst youth at later pubertal stages. Put together, aging and pubertal development are associated with improved ADHD symptoms but not for youth with high impairment. Findings from this study contributes to understanding the role that aging, pubertal status, and pubertal development plays in ADHD, impairment, and comorbidity in children and adolescents.

Eng, A. G., Phan, J. M., Shirtcliff, E. A., Eisenlohr-Moul, T. A., Goh, P. K., & Martel, M. M. (2023). Aging and pubertal development differentially predict symptoms of ADHD, depression, and impairment in children and adolescents: An eight-year longitudinal study. Research on Child and Adolescent Psychopathology, 51(6), 819-832. https://doi.org/10.1007/s10802-023-01030-7

Adolescents experience profound neuroendocrine changes, including hormone “coupling” between cortisol, testosterone, and dehydroepiandrosterone. Emerging research has only begun to elucidate the role of hormone coupling, its genetic and environmental etiology, and the extent to which coupling is impacted by gender, puberty, and family context. We included measures on parent and child mental health, parenting stress, and family conflict of 444 twin pairs and their parents across two timepoints, when youth were on average 8 and 13 years old, respectively. Structural equation models examined the impact of family context effects on coupling during adolescence. Biometric twin models were then used to probe additive genetic, shared, and non-shared environmental effects on hormone coupling. Hormones were more tightly coupled for females than males, and coupling was sensitive to parental depression and co-twin psychopathology symptoms and stress exposure in females. The association between family context and coupling varied across specific neuroendocrine measures and was largely distinct from pubertal maturation. Biometric models revealed robust shared and non-shared environmental influences on coupling. We found that family antecedents modify the strength of coupling. Environmental influences account for much of the variation on coupling during puberty. Gender differences were found in genetic influences on coupling.

Phan, J. M., Van Hulle, C. A., Shirtcliff, E. A., Schmidt, N. L., & Goldsmith, H. H. (2021). Longitudinal effects of family psychopathology and stress on pubertal maturation and hormone coupling in adolescent twins. Developmental Psychobiology, 63(3), 512-528. https://doi.org/10.1002/dev.22028

Parent-child physiological attunement, particularly during stressful situations, appears adaptive as shared stress reactivity may promote dyadic engagement. Romantic partners eventually replace parents as the primary support figure, yet it remains unclear whether romantic partners buffer physiological stress or display physiological attunement as most studies on adults examine attunement during conflict paradigms. The present study examined physiological attunement in 63 emerging adult romantic partner dyads (one partner was the active participant, the other the observer) during the Trier Social Stress Task (TSST). Heart rate (HR) and respiratory sinus arrhythmia (RSA) were continuously monitored across the visit. Repeated saliva samples were assayed for cortisol. Physiological attunement was operationalized as a correlation in biomarkers between the TSST participant and their partner; sex, social support, and physical proximity were examined as moderators. We then compared the biomarker profiles of partnered-TSST participants to individuals who participated in the TSST solo (n = 63) to determine if partner presence buffered stress biomarker reactivity during the TSST. RSA attunement between partners was found but was not further moderated by social support or sex. Adrenocortical attunement was moderated, such that lower social support and increased proximity resulted in higher attunement. HR attunement was higher when the participant was male and when partners were in close physical proximity. Compared to TSST solo, romantic partner presence increased participant cortisol levels and altered HR reactivity, suggesting that emerging adult romantic partners do not buffer physiological stress reactivity. Future research should examine whether physiological attunement and partner presence is protective in more established relationships.

Phan, J. M., R. Dismukes, A., Barnett, N., Miocevic, O., L. Ruttle, P., & Shirtcliff, E. A. (2019). Adrenocortical and autonomic attunement between romantic partners in emerging adulthood. Stress, 22(4), 461-471. https://doi.org/10.1080/10253890.2019.1600502

Laboratory stress tasks such as the Trier Social Stress Test (TSST) have provided a key piece to the puzzle for how psychosocial stress impacts the hypothalamic-pituitary-adrenal axis, other stress-responsive biomarkers, and ultimately wellbeing. These tasks are thought to work through biopsychosocial processes, specifically social evaluative threat and the uncontrollability heighten situational demands. The present study integrated an experimental modification to the design of the TSST to probe whether additional social evaluative threat, via negative verbal feedback about speech performance, can further alter stress reactivity in 63 men and women. This TSST study confirmed previous findings related to stress reactivity and stress recovery but extended this literature in several ways. First, we showed that additional social evaluative threat components, mid-task following the speech portion of the TSST, were still capable of enhancing the psychosocial stressor. Second, we considered stress-reactive hormones beyond cortisol to includedehydroepiandrosterone (DHEA) and testosterone, and found these hormones were also stress-responsive, and their release was coupled with one another. Third, we explored whether gain- and loss-framing incentive instructions, meant to influence performance motivation by enhancing the personal relevance of task performance, impacted hormonal reactivity. Results showed that each hormone was stress reactive and further had different responses to the modified TSST compared to the original TSST. Beyond the utility of showing how the TSST can be modified with heightened social evaluative threat and incentive-framing instructions, this study informs about how these three stress-responsive hormones have differential responses to the demands of a challenge and a stressor.

Phan, J. M., Schneider, E., Peres, J., Miocevic, O., Meyer, V., & Shirtcliff, E. A. (2017). Social evaluative threat with verbal performance feedback alters neuroendocrine response to stress. Hormones and Behavior, 96, 104-115. https://doi.org/10.1016/j.yhbeh.2017.09.007