Tracy Kent Teague

Background: One in 4 young adults has prediabetes, and improving diet is a key step to lowering the risk of diabetes. Existing standard-of-care diet approaches show short-term efficacy but lack long-term effectiveness, including in young adults. Greater fiber intake is associated with a reduced risk of diabetes; however, fiber is not well targeted using existing interventions. Many young adults may be reluctant to consume fiber given the coexistence with digestible carbohydrates and concerns over gastrointestinal effects. Targeting these factors more explicitly may improve uptake and lower diabetes risk, and doing so via a mobile health (mHealth) intervention may be particularly responsive to young adult demands. Objective: This study aims to establish and preliminarily test the feasibility of a highly innovative and scalable mHealth-based intervention to improve fiber intake among young adults with prediabetes. Methods: This single-arm feasibility study includes 2 phases to preliminarily test an mHealth-based fiber intervention (phase 1) and elucidate factors that impact sustained behavior change and fiber intake after intervention end using ecological momentary assessment (EMA; phase 2). The intervention is 3 months in length and features daily EMAs with responsive text–based coping messages to target key predictors of fiber intake. EMAs will also be paired with brief (ie, 1c , and insulin resistance (Homeostatic Model Assessment of Insulin Resistance) will be assessed. After the postintervention time point, participants will continue with daily EMAs to assess factors associated with sustained fiber intake. Diet will be assessed using Automated Self-Administered 24-hour dietary recalls at the baseline and postintervention time point and after the phase 2 EMA. Results: This study was initiated in July 2025. As of March 2026, the mHealth intervention content is being built, with app completion and trial enrollment both slated to begin in April 2026. Conclusions: The results of this study will provide pivotal evidence on the utility of a fiber-focused intervention delivered via mHealth with biofeedback and home-delivered foods to lower the risk of diabetes in young adults with prediabetes.

Neuroimaging and blood-based biomarkers are increasingly utilized to identify long-term effects of concussion and contact-sport exposure (CSE), but female athletes are underrepresented in this work, despite potential sex-related differences. Early research indicates that widely used oral contraceptives (OCs) influence brain structure and function and concussion-related biomarkers. This study investigated whether current oral contraceptive (OC) use moderates associations of concussion history and CSE with magnetic resonance imaging (MRI) measures and brain injury biomarkers in female athletes. Part of a larger cross-sectional study, 68 collegiate-aged female athletes (30 OC users, 38 with no hormonal contraceptive use [NoHC]), completed interviews to retrospectively determine the number of prior concussions (last injury at least 6 months before study enrollment) and years of CSE. Serum glial fibrillary acidic protein, neurofilament light, and total tau levels were measured, along with hippocampal volume, cortical thickness, and Neurite Orientation Dispersion and Density Imaging metrics. Linear regression and Bayesian multilevel modeling tested interactions between OC use and concussion history or CSE on outcomes. Number of prior concussions was negatively associated with hippocampal volumes and cortical thickness. OC use moderated relationships between CSE and cortical thickness, isotropic volume fraction (ISO), and intracellular volume fraction, and between concussion history and orientation dispersion index (ODI). OC users had lower tau levels than the NoHC group. Exploratory models suggested OC pill formulation may moderate associations of concussion history and/or CSE with outcomes and directly affect cortical thickness, ODI, and ISO. These results suggest OC use deserves consideration as an influencing factor in future research and personalized treatment for female athletes.

A subset of major depressive disorder (MDD) is characterized by immune system dysfunction, but the intracellular origin of these immune changes remains unclear. Here we tested the hypothesis that abnormalities in endoplasmic reticulum (ER) stress, inflammasome activity and mitochondrial biogenesis contribute to the development of systemic inflammation in MDD. RT-qPCR was used to measure mRNA expression of key organellar genes from peripheral blood mononuclear cells (PBMCs) isolated from 186 MDD and 67 healthy control (HC) subjects. The comparative C_T (2^-ΔΔCT) method was applied to quantify mRNA expression using GAPDH as the reference gene. After controlling for age, sex, BMI, and medication status using linear regression models, expression of the inflammasome (NLRC4 and NLRP3) and the ER stress (XBP1u, XBP1s, and ATF4) genes was found to be significantly increased in the MDD versus the HC group. Sensitivity analyses excluding covariates yielded similar results. After excluding outliers, expression of the inflammasome genes was no longer statistically significant but expression of the ER stress genes (XBP1u, XBP1s, and ATF4) remained significant and the mitochondrial biogenesis gene, MFN2, was significantly increased in the MDD group. NLRC4 and MFN2 were positively correlated with serum C-reactive protein concentrations, while ASC trended significant. The altered expression of inflammasome activation, ER stress, and mitochondrial biogenesis pathway components suggest that dysfunction of these organelles may play a role in the pathogenesis of MDD.

Major depressive disorder (MDD) is associated with interoceptive processing dysfunctions, but the molecular mechanisms underlying this dysfunction are poorly understood. This study combined brain neuronal-enriched extracellular vesicle (NEEV) technology and serum markers of inflammation and metabolism with Functional Magnetic Resonance Imaging (fMRI) to identify the contribution of gene regulatory pathways, in particular micro-RNA (miR) 93, to interoceptive dysfunction in MDD. Individuals with MDD (n = 41) and healthy comparisons (HC; n = 35) provided blood samples and completed an interoceptive attention task during fMRI. EVs were separated from plasma using a precipitation method. NEEVs were enriched by magnetic streptavidin bead immunocapture utilizing a neural adhesion marker (L1CAM/CD171) biotinylated antibody. The origin of NEEVs was validated with two other neuronal markers - neuronal cell adhesion molecule (NCAM) and ATPase Na+/K+ transporting subunit alpha 3 (ATP1A3). NEEV specificities were confirmed by flow cytometry, western blot, particle size analyzer, and transmission electron microscopy. NEEV small RNAs were purified and sequenced. Results showed that: (1) MDD exhibited lower NEEV miR-93 expression than HC; (2) within MDD but not HC, those individuals with the lowest NEEV miR-93 expression had the highest serum concentrations of interleukin (IL)-1 receptor antagonist, IL-6, tumor necrosis factor, and leptin; and (3) within HC but not MDD, those participants with the highest miR-93 expression showed the strongest bilateral dorsal mid-insula activation during interoceptive versus exteroceptive attention. Since miR-93 is regulated by stress and affects epigenetic modulation by chromatin re-organization, these results suggest that healthy individuals but not MDD participants show an adaptive epigenetic regulation of insular function during interoceptive processing. Future investigations will need to delineate how specific internal and external environmental conditions contribute to miR-93 expression in MDD and what molecular mechanisms alter brain responsivity to body-relevant signals.

A subset of major depressive disorder (MDD) is characterized by immune system dysfunction, but the intracellular origin of these immune changes remains unclear. Here we tested the hypothesis that abnormalities in the endoplasmic reticulum (ER) stress, inflammasome activity and mitochondrial biogenesis contribute to the development of systemic inflammation in MDD. RT-qPCR was used to measure mRNA expression of key organellar genes from peripheral blood mononuclear cells (PBMCs) isolated from 186 MDD and 67 healthy control (HC) subjects. The comparative C_T (2^−ΔΔCT) method was applied to quantify mRNA expression using GAPDH as the reference gene. After controlling for age, sex, BMI, and medication status using linear regression models, expression of the inflammasome (NLRC4 and NLRP3) and the ER stress (XBP1u, XBP1s, and ATF4) genes was found to be significantly increased in the MDD versus the HC group. After excluding outliers, expression of the inflammasome genes was no longer statistically significant but expression of the ER stress genes (XBP1u, XBP1s, and ATF4) and the mitochondrial biogenesis gene, MFN2, was significantly increased in the MDD group. ASC and MFN2 were positively correlated with serum C-reactive protein concentrations. The altered expression of inflammasome activation, ER stress, and mitochondrial biogenesis pathway components suggest that dysfunction of these organelles may play a role in the pathogenesis of MDD.

Major depressive disorder (MDD) is associated with interoceptive processing dysfunctions, but the molecular mechanisms underlying this dysfunction are poorly understood. This study combined brain Neuronal-Enriched Extracellular Vesicle (NEEV) technology and serum markers of inflammation and metabolism with Functional Magnetic Resonance Imaging (fMRI) to identify the contribution of gene regulatory pathways, in particular micro-RNA (miR) 93, to interoceptive dysfunction in MDD. Individuals with MDD (n = 44) and healthy comparisons (HC; n = 35) provided blood samples and completed an interoceptive attention task during fMRI. EVs were separated from plasma using a precipitation method. NEEVs were enriched by magnetic streptavidin bead immunocapture utilizing a neural adhesion marker (CD171) biotinylated antibody. NEEV specificities were confirmed by flow cytometry, western blot, particle size analyzer, and transmission electron microscopy. NEEV small RNAs were purified and sequenced. Results showed that: (1) MDD exhibited lower NEEV miR-93 expression than HC; (2) within MDD but not HC, those individuals with the lowest NEEV miR-93 expression had the highest serum concentrations of interleukin (IL)-1 receptor antagonist, IL-6, tumor necrosis factor, and leptin; and (3) within HC but not MDD, those participants with the highest miR-93 expression showed the strongest bilateral dorsal mid-insula activation. Since miR-93 is regulated by stress and affects epigenetic modulation by chromatin re-organization, these results suggest that healthy individuals but not MDD participants show an adaptive epigenetic regulation of insular function during interoceptive processing. Future investigations will need to delineate how specific internal and external environmental conditions contribute to miR-93 expression in MDD and what molecular mechanisms alter brain responsivity to body-relevant signals.

This randomized controlled pilot trial shows, for the first time, that 8 wk of structured, progressive exercise training lowers serum endothelin-1 (ET-1) and improves positive psychological coping in young women with significant early-life psychosocial stress. Furthermore, the observed associations among changes in psychological attributes, ET-1, and systolic blood pressure signify a potential interplay between positive psychology and cardiovascular disease risk among women with adverse childhood experiences.