Pubmed (TDAH) du 03/06/26
1. Arslan G, Karaçul FE. Childhood Adversity, ADHD Symptoms, Shame, and Well-Being in College Students. Psychol Rep. 2026: 332941261457385.
Childhood adversity is consistently associated with long-term psychological challenges, most notably impaired self-regulatory capacities and lower levels of subjective well-being (SWB). The present study examined the associations among adverse childhood experiences (ACEs), shame (internal and external), ADHD symptoms, and SWB. It was hypothesized that (i) ADHD symptoms and internal/external shame would sequentially mediate the relationship between ACEs and SWB, and (ii) ADHD symptoms would mediate the association between ACEs and shame. Participants were 496 college students (68% female, 32% male), aged 18-47 years (M = 20.79, SD = 2.96), recruited from a public university in Türkiye. Participants completed self-report measures assessing ACEs, ADHD symptoms, shame, and SWB. Results showed that individuals with higher ACEs reported significantly greater internal and external shame, more ADHD symptoms, and lower SWB. Internal shame-but not ADHD symptoms-significantly mediated the association between ACEs and SWB. External shame showed a weaker, marginally significant effect. ADHD symptoms did not significantly mediate the relationship between ACEs and shame. Findings highlight internal shame as a key psychological mechanism linking early adversity to lower subjective well-being.
Lien vers le texte intégral (Open Access ou abonnement)
2. Bandini L, Vinceti B, Urbano T, Plazzi G, Filippini T, Vinceti M. The impact of maternal vitamin D levels during pregnancy and risk of autism spectrum disorder and attention deficit hyperactivity disorder diagnosis and symptoms in offspring: a systematic review and dose-response meta-analysis. Eur Child Adolesc Psychiatry. 2026.
INTRODUCTION: Autism Spectrum Disorder (ASD) and Attention Deficit Hyperactivity Disorder (ADHD) have a complex etiology involving both genetic and environmental factors, with mechanisms still unclear. In this review, we investigated the association between maternal 25-hydroxyvitamin D status during pregnancy and the risk of diagnosis and symptoms of ASD and ADHD in offspring in developmental age. METHODS: We searched online databases up to February 13, 2026. We conducted a quantitative meta-analysis by comparing the exposure categories and using a dose-response approach across the entire exposure range. RESULTS: We included 15 eligible studies: 8 related to ASD and ASD symptoms, 5 related to ADHD and ADHD symptoms, and 2 to both. Comparing high versus low maternal vitamin D status, we found an inverse association with both lower ASD risk (RR = 0.91; 95% CI 0.87-0.96) and ADHD risk (RR = 0.90; 95% CI 0.82-0.99). In the dose-response pooled analysis, ASD risk linearly decreased by 9% for every 10 nmol/L increase in maternal serum vitamin D levels. Higher vitamin D levels were also inversely associated with ADHD symptoms, though estimates were statistically imprecise due to the limited number of studies. CONCLUSIONS: Higher vitamin D status during pregnancy appears to be linearly associated with a reduced risk of ASD and ADHD diagnoses and symptoms in offspring, with no evidence of thresholds across the investigated exposure range. These findings suggest the opportunity to assess vitamin D levels during pregnancy, and to consider its supplementation in deficiency cases, to support fetal brain development and promote neuroprotection.
Lien vers le texte intégral (Open Access ou abonnement)
3. de Melo IH, Franca G. High functioning, yet high suffering – the need to incorporate invisible struggles in adult ADHD diagnostic assessment/criteria. Front Psychiatry. 2026; 17: 1813029.
Current DSM-5 diagnostic criteria for adult Attention-Deficit/Hyperactivity Disorder (ADHD) rely predominantly on externally observable signs and measurable functional impairment. While prior literature has criticized the child-centric and male-centric biases embedded in this framework, less attention has been given to its sign-centric and impairment-centric orientation. In this perspective article, we argue that this emphasis creates a critical diagnostic blind spot: adults who maintain high academic, occupational, or social performance through compensatory strategies and masking, yet experience substantial internal suffering. For these individuals, impairment is not absent but concealed beneath sustained effort, perfectionistic overcompensation, and chronic self-monitoring. The resulting psychological burden, emotional exhaustion, anxiety, shame, cognitive fatigue, and diminished quality of life often remain invisible within behavior-based diagnostic systems. We contend that current criteria capture the end-products of ADHD (observable behaviors and overt dysfunction) while neglecting the upstream processes shaping lived experience. Phenomena such as mind-wandering, internal restlessness, time blindness, sensory over-responsivity, and effortful self-regulation are clinically meaningful yet insufficiently represented in formal criteria. Moreover, compensatory mechanisms and masking, despite their relevance to clinical presentation and diagnostic accuracy, are not systematically assessed. We propose a process-based expansion of adult ADHD assessment that incorporates subjective cognitive phenomena, explicit evaluation of masking and compensatory strategies, and recognition of subjective distress and effort-to-output imbalance as diagnostically relevant dimensions. Such a paradigm shift would enhance diagnostic sensitivity, reduce misdiagnosis and underrecognition – particularly among high-functioning adults and women – and promote more equitable access to appropriate care. Recognizing invisible struggles is essential to capturing the full heterogeneity and lived reality of adult ADHD.
Lien vers le texte intégral (Open Access ou abonnement)
4. Lu W, He X, Lei P, Liu Y, Zhan X, Ma Q, Yan B, Ma X, Yang J, Gao Y. Dissecting the shared genetic architecture between testosterone traits and attention-deficit/hyperactivity disorder. Eur Child Adolesc Psychiatry. 2026.
Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder with sex differences, possibly linked to testosterone; however, the relationship remains unclear. This study aimed to clarify the genetic correlation and polygenic overlap between ADHD and testosterone traits, identify shared genomic loci, and investigate the underlying biological mechanisms through functional annotation. Genomic data on ADHD and three testosterone traits (total testosterone [TT], bioavailable testosterone [BT], and sex hormone-binding globulin [SHBG]) were obtained from publicly accessible genome-wide association studies. Employing the MiXeR bivariate causal mixture model, we quantified the polygenic overlap between ADHD and these testosterone traits. Subsequently, we applied the conjunctional false discovery rate (conjFDR) method to identify genomic loci and performed functional annotation with the Functional Mapping and Annotation tool to aid biological interpretation. Using MiXeR, we found negative correlations between TT and ADHD, and SHBG and ADHD, but a positive correlation between BT and ADHD. Over one-third of testosterone-associated variants were predicted to affect ADHD. Using the conjFDR approach, we identified 22-51 genomic loci shared between testosterone traits and ADHD, including MCM9 and MANBA. Functional enrichment analysis highlighted the predominant involvement of these mapped genes in signal transduction pathways, synapses, cell differentiation, and neurogenesis. In conclusion, we reported a substantial polygenic overlap between ADHD and testosterone traits, identified multiple shared genomic loci implicating common biological mechanisms, and highlighted the association of glutamatergic synapses and neurogenesis with ADHD and testosterone levels.
Lien vers le texte intégral (Open Access ou abonnement)
5. Malcon L, Gomes Silva A, Bezerra Falcão A, Bonganhi de Bem É, Grevet F, Wagner F, Duarte I, Barbedo L, Schneider M, Rohde LA, Hoffmann M, Caye A. Efficacy of Extended Time on Exams for College Students and Applicants With Attention-Deficit/Hyperactivity Disorder: Protocol for a Randomized, Counterbalanced Crossover and Within-Subject Trial. JMIR Res Protoc. 2026; 15: e80271.
BACKGROUND: Extended time on academic exams is one of the most frequently granted accommodations for students with attention-deficit/hyperactivity disorder. However, there is a lack of empirical evidence supporting its effectiveness, particularly in the college population. OBJECTIVE: This study aimed to assess the efficacy and specificity of extended test time as an accommodation for college and college-prospective students with attention-deficit/hyperactivity disorder. METHODS: This study will use a randomized, counterbalanced crossover and within-subject experimental design, using convenience sampling to recruit participants. All participants will undergo clinical and neuropsychological assessments to confirm their diagnostic status and cognitive performance. Following these assessments, participants will be randomized to sequentially complete 3 versions of a test modeled on the Brazilian National High School Exam under standard time conditions, with 25% extra time and with 50% extra time. RESULTS: The study was funded in February 2023. Data collection started in August 2023. As of March 2026, we have enrolled 103 participants. Data analysis was initiated in March 2026, and no projected timeline for the publication of results is currently available. CONCLUSIONS: The study will be the first of its kind outside the United States and one of the first to investigate the effectiveness of extended testing time at different dosages in the college population. Findings will provide insights into the impact of extended time accommodations in a distinct academic system, addressing gaps in previous research, such as different intervention doses and predictors of effectiveness. TRIAL REGISTRATION: ClinicalTrials.gov NCT06063382; https://clinicaltrials.gov/study/NCT06063382. INTERNATIONAL REGISTERED REPORT IDENTIFIER (IRRID): DERR1-10.2196/80271.
