Blood Molecules May Signal Anxiety, Depression and Stress in Deaf Adults

Deaf adults face a psychological burden that hearing populations rarely have to think about. Communication barriers, social stigma, reduced access to healthcare, and daily practical challenges stack up in ways that can quietly erode mental well-being. Now, a team of researchers in Jordan has added an intriguing biological dimension to this picture. In one of the first studies of its kind, they report that two molecules circulating in the blood — brain-derived neurotrophic factor, or BDNF, and the fat-derived hormone adiponectin — track closely with levels of anxiety, depression, and stress in deaf adults. The stronger the psychological distress, the lower the concentrations of these molecules tended to be, a relationship that held even after accounting for age, sex, and body mass index.

The study, published in Frontiers in Behavioral Neuroscience, recruited 204 deaf adults aged 18 to 45 years in Amman, all of whom had congenital, profound bilateral hearing loss and used sign language as their primary means of communication. The researchers, led by Rand Alsharq of Applied Science Private University and Abeer Ahmad Bahathig of Northern Border University, went to considerable lengths to make the research genuinely accessible. Consent forms, questionnaires, and the entire psychological assessment were delivered in Jordanian Sign Language by certified interpreters, and all communication during the study was conducted exclusively in sign language. That methodological care matters, because psychological research in deaf populations has long been hampered by instruments that were never designed or validated for sign language users.

To measure psychological distress, the team used the Depression, Anxiety, and Stress Scale-21, a widely used 21-item questionnaire that yields separate scores for each of the three emotional states. Body composition was assessed with bioelectrical impedance analysis, providing detailed measurements of body fat percentage, visceral fat, lean mass, and skeletal muscle. Blood samples were drawn, centrifuged, and frozen, then analyzed with enzyme-linked immunosorbent assays to quantify serum concentrations of BDNF and adiponectin. The result was an unusually rich dataset linking psychology, metabolism, and molecular biology in a population that has been almost entirely overlooked in this literature.

The headline finding is striking. Serum BDNF levels showed strong inverse correlations with all three measures of distress: a correlation coefficient of −0.632 with anxiety, −0.732 with depression, and −0.795 with stress, all statistically significant at p < 0.001. In plain terms, the participants with the least BDNF in their blood reported the most severe psychological symptoms, and the relationship was remarkably tight. Adiponectin told a similar but weaker story, with inverse correlations of −0.422 for anxiety, −0.344 for depression, and −0.446 for stress. Because correlation alone cannot rule out confounding, the researchers then ran multiple linear regression models adjusted for age, sex, and body mass index. BDNF emerged as an independent negative predictor of all three outcomes, with standardized coefficients of −0.48 for anxiety, −0.55 for depression, and −0.62 for stress, and the full models explained between 36 and 42 percent of the variance in psychological scores.

Adiponectin, by contrast, survived the statistical adjustment only for anxiety (β = −0.19, p = 0.03) and stress (β = −0.21, p = 0.02). Its association with depression, while present in the raw correlations, lost statistical significance once demographic factors and body composition were taken into account. That attenuation is itself informative. It suggests that the apparent link between adiponectin and depressive symptoms in this sample is largely carried by factors such as adiposity, which is known to suppress circulating adiponectin. BDNF, meanwhile, appears to be the more robust molecular signature of psychological distress in this population, standing on its own regardless of body size.

Understanding why these molecules matter requires a brief tour of their biology. BDNF is a member of the neurotrophin family, a group of proteins that support the survival, growth, and connectivity of neurons. It is highly expressed in the hippocampus and prefrontal cortex, regions central to emotion regulation, and it underpins synaptic plasticity — the cellular machinery of learning, memory, and adaptive responses to stress. Chronic inflammation and prolonged psychological stress are known to suppress BDNF expression, impairing neuroplasticity and destabilizing emotional regulation. Decades of research have linked reduced BDNF concentrations to major depressive disorder, anxiety disorders, and stress-related conditions, particularly during acute episodes. The new study extends this framework to deaf adults, a group whose chronic exposure to communication stressors may plausibly feed into the same neurobiological pathway.

Adiponectin is a different beast altogether. Secreted by adipose tissue, it is best known as an anti-inflammatory, insulin-sensitizing, cardioprotective hormone — levels typically fall as body fat rises. But growing evidence points to a neuroprotective role as well, acting through pathways involving inflammation, oxidative stress, and neurotrophic signaling, including direct interactions with BDNF itself. Lower adiponectin has been reported in people with mood, anxiety, and stress-related disorders, and meta-analyses have generally found reduced levels in depression, although the literature is not unanimous. The Jordanian findings sit comfortably within this emerging picture, while adding the caveat that in deaf adults the adiponectin signal may be substantially mediated by body composition.

The study also documented a heavy burden of psychological distress in its own right. Moderate depression was the single most common severity category, affecting 40.2 percent of participants, with a further 19.1 percent in the severe range. Moderate anxiety was the most frequent anxiety category at 34.8 percent, and 38.2 percent of participants reported moderate stress. Sex differences emerged in the upper tail of the distributions: deaf women were significantly overrepresented in the very severe anxiety category and in the moderate, severe, and very severe stress categories, although depression severity did not differ between the sexes. The female participants also carried significantly more body fat on average — 43.9 percent, above the normal acceptable range — which the authors suggest may partly explain their elevated vulnerability, given the well-documented links between excess adiposity and emotional distress.

The authors are careful about what the study can and cannot show. As a cross-sectional design, it captures a single moment in time and cannot establish whether low BDNF and adiponectin cause psychological distress, whether distress depletes these molecules, or whether both are driven by some third factor. Physical activity was not assessed, and this is no small omission: exercise can acutely raise circulating BDNF and, with repeated training, enhance BDNF-related neuroplasticity through lactate signaling and the PGC-1α/FNDC5 pathway, so unmeasured variation in activity could have shaped the results. Diet, too, may influence both biomarkers. The sign language version of the DASS-21, while culturally and linguistically adapted by a certified researcher, has not yet been independently psychometrically validated in deaf adults. These limitations temper but do not erase the central finding, which the authors describe as the first demonstration that BDNF and adiponectin may serve as biomarkers of psychological distress in the deaf population.

The implications reach beyond biomarker hunting. If impaired neuroplasticity and inflammatory pathways genuinely contribute to the psychological burden carried by deaf adults, then interventions that boost these molecular systems — tailored nutrition, structured exercise, or targeted mental healthcare delivered in sign language — could offer a route to measurable relief. The authors call for prospective longitudinal studies to untangle causal direction and to test whether lifestyle interventions aimed at raising BDNF and adiponectin can alleviate distress in this population. For a community whose mental health needs have long been underserved and understudied, the idea that a simple blood test might one day help identify those at greatest risk is a small but genuinely hopeful step forward.

Subject of Research: Associations between serum BDNF and adiponectin and psychological distress in deaf adults

Article Title: Association of serum brain-derived neurotrophic factor and adiponectin with anxiety, depression, and stress in deaf adults: a cross-sectional study

Article References: Alsharq, R., AL-Dalaeen, A., Saleh, E., Batarseh, N., & Bahathig, A. A. (2026). Association of serum brain-derived neurotrophic factor and adiponectin with anxiety, depression, and stress in deaf adults: a cross-sectional study. Frontiers in Behavioral Neuroscience, 20, Article 1955159. https://doi.org/10.3389/fnbeh.2026.1955159

Image Credits: AI Generated

DOI: 10.3389/fnbeh.2026.1955159

Keywords: BDNF, adiponectin, deaf adults, anxiety, depression, stress, psychological distress, biomarkers, neuroplasticity, cross-sectional study, Jordan, mental health