This study explores psychiatrists’ perceptions of Attention-Deficit Hyperactivity Disorder (ADHD) through the lens of evolutionary psychiatry, a growing field that reframes mental disorders in the context of adaptation and survival. Evolutionary theories suggest that traits associated with ADHD, such as impulsivity, hypercuriosity and novelty-seeking, may have been adaptive in ancestral environments, though they manifest as maladaptive in structured modern contexts.

A bespoke 10-item questionnaire was developed to assess psychiatrists’ attitudes following a presentation on evolutionary perspectives of ADHD by an expert. The questionnaire allowed rating in 5-point Likert fashion and was followed by a free text box for qualitative analysis. Basic descriptive statistics and One-Way ANOVA pairwise comparisons between groups was used to test for statistical significance. A p value of <0.05 was deemed statistically significant.

Forty-two participants, including 21 consultants and 19 psychiatry trainees completed the questionnaire. All participants rated their comprehension of the presentation as high/very high. Most strongly agreed that the information presented could improve psychiatry and therapeutic outcomes. However, consultants with more than 10 years of experience were less likely than trainees to report optimism about the practical applications of evolutionary frameworks. Qualitative feedback emphasized the relevance of evolutionary perspectives in clinical practice, particularly in reducing stigma and enhancing therapeutic engagement with patients and families.

While the results from this study were positive, limitations include the small sample size and lack of prepresentation baseline data. However, this study has formed part of the first step in investigating the perceptions and attitudes of psychiatrists on evolutionary perspectives on ADHD.

Few studies have examined attention-deficit/hyperactivity disorder (ADHD) symptoms in middle- and older-aged adults. We aim to examine the phenotypic expression of ADHD symptoms in these age groups.

This study comprised a random sample (N = 1,562) from the US Health and Retirement Study 2016, a representative US sample aged 50 years and over. ADHD symptoms were assessed based on the Adult ADHD Self-Report Scale.

In the primary analysis, 10 competing confirmatory factor analytic models of ADHD symptoms in middle- and older-aged adults were compared. The best-fitting model was hierarchical with a general ADHD factor at the apex and underneath symptom factors of inattention, hyperactivity, and impulsivity (ꭓ2 = 319.34, df = 91.71, P = 0.00, TLI = 0.98, CFI = 0.96, RMSEA = 0.04, 95% CI = 0.04–0.05). In complementary analyses, this model was a satisfactory fit to the data: (1) in individuals without a history of cognitive impairment or dementia, and when the general ADHD factor was specified to load on (2) cognitive function, (3) depressive symptoms (which showed adequate fit), and (4) ADHD polygenic scores, (5) in middle- and older-aged adults, and (6) when weighted to represent the US population.

These results imply a hierarchical representation of ADHD symptoms in middle- and older-aged adults consisting of a general factor at the apex with neurocognitive and genetic correlates and underneath symptom factors of inattention, hyperactivity, and impulsivity. Collectively, this model offers a novel framework to study the mechanisms of ADHD symptoms in middle- and older-aged adults and points to treatment targets.

Previous studies have estimated the lifetime incidence, age of onset and prevalence of mental disorders, but none have used nationwide data covering both primary and secondary care, even though mental disorders are commonly treated in primary care. We aimed to determine lifetime incidence, age-specific incidence, age of onset and service utilization for diagnosed mental disorders.

This register-based cohort study followed the entire population of Finland from 2000 to 2020. We estimated the cumulative incidence of diagnosed mental disorders with the Aalen–Johansen estimator, accounting for competing risks such as death and emigration. We also calculated age-specific incidence and 12-month service utilization as of 31 December 2019, providing diagnosis-, age- and gender-specific estimates.

We followed 6.4 million individuals for 98.5 million person-years. By age 100, lifetime incidence of any diagnosed mental disorder was 76.7% (95% CI, 76.6–76.7) in women and 69.7% (69.6–69.8) in men; in psychiatric secondary care, it was 39.7% (39.6–39.8) and 31.5% (31.4–31.6). At age 75, stricter estimates for non-organic disorders (ICD-10: F10–F99) were 65.6% (65.5–65.7) for women and 60.0% (59.9–60.1). Anxiety disorders (F40–F48) had the highest cumulative incidence. Median age of onset of non-organic mental disorders was 24.1 (interquartile range, 14.8–43.3 years) in women and 20.0 (interquartile range, 7.3–42.2 years) in men. Service utilization within 12 months was 9.0% for women and 7.7% for men.

Most, though not all, individuals experience at least one type of mental disorder, often during youth. Capturing the overall occurrence of mental disorders requires including both primary and secondary care data.

Self-injurious behaviors (SIB) are common in autistic people. SIB is mainly studied as a broad category, rather than by specific SIB types. We aimed to determine associations of distinct SIB types with common psychiatric, emotional, medical, and socio-demographic factors.

Participants included 323 autistic youth (~50% non−/minimally-speaking) with high-confidence autism diagnoses ages 4–21 years. Data were collected by the Autism Inpatient Collection during admission to a specialized psychiatric inpatient unit (www.sfari.org/resource/autism-inpatient-collection/). Caregivers completed questionnaires about their child, including SIB type and severity. The youth completed assessments with clinicians. Elastic net regressions identified associations between SIB types and factors.

No single factor relates to all SIB types. SIB types have unique sets of associations. Consistent with previous work, more repetitive motor movements and lower adaptive skills are associated with most types of SIB; female sex is associated with hair/skin pulling and self-rubbing/scratching. More attention-deficit/hyperactivity disorder symptoms are associated with self-rubbing/scratching, skin picking, hair/skin pulling, and inserts finger/object. Inserts finger/object has the most medical condition associations. Self-hitting against surface/object has the most emotion dysregulation associations.

Specific SIB types have unique sets of associations. Future work can develop clinical likelihood scores for specific SIB types in inpatient settings, which can be tested with large community samples. Current approaches for SIB focus on the behavior functions, but there is an opportunity to further develop interventions by considering the specific SIB type in assessment and treatment. Identifying factors associated with specific SIB types may aid with screening, prevention, and treatment of these often-impairing behaviors.

Emerging evidence suggests a co-occurrence of attention-deficit hyperactivity disorder (ADHD) and immune response-related conditions. However, it is unclear whether there is a causal relationship between ADHD and immune response.

We investigated the associations between ADHD traits, common variant genetic liability to ADHD, and serum C-reactive protein (CRP) levels in childhood and adulthood, using data from the Avon Longitudinal Study of Parent and Children. Genetic correlation was estimated using linkage-disequilibrium score regression. Two-sample Mendelian randomization (MR) was conducted to test potential causal effects of ADHD genetic liability on serum CRP as an indicator of systemic inflammation, as well as the genetically proxied levels of specific plasma cytokines.

There was little evidence to suggest association between ADHD and CRP in childhood and adulthood. ADHD genetic liability was associated with a higher serum CRP at ages 9 (β = 0.02, 95% confidence interval [CI] = 0, 0.03), 15 (β = 0.04; 95% CI = 0.02, 0.06), and 24 years (β = 0.03; 95% CI = 0.01, 0.05). There was evidence of genetic correlations between ADHD and CRP ($ {r}_g $ = 0.27; 95% CI = 0.19, 0.35). Evidence of a bidirectional effect of genetic liability to ADHD and CRP was found by two-sample MR (ADHD-CRP: βIVW= 0.04, 95% CI = 0.01, 0.07; CRP-ADHD: ORIVW = 1.09, 95% CI = 1.01, 1.17).

Further work is necessary to understand the biological pathways linking ADHD genetic liability and CRP and gain insights into understanding how they might contribute in the links between ADHD and later-life adverse physical and mental health outcomes.

There is increasing evidence that childhood Attention-Deficit Hyperactivity Disorder (ADHD) elevates the risk of later Bipolar Spectrum Disorder (BD). However, it remains unclear whether different trajectories of ADHD symptoms confer differential risk for BD.

Data from the Avon Longitudinal Study of Parents and Children were available from 7811 children at age 8 years, 7435 at 10, 6798 at 13, and 1217 at 21–23 years. ADHD symptoms were assessed at 8, 10, and 13 years with the Development and Well-Being Assessment. Clinically significant hypomanic symptoms (CSHS) at 21–23 years were assessed using the Hypomania Symptom Checklist (HCL-32). Group trajectories of ADHD and its subtypes were estimated using latent class growth analysis. The prospective associations between different ADHD trajectories and CSHS were tested using logistic regression analysis.

Persistently high, increasing, remitting, and persistently low ADHD symptom trajectories were identified for the three ADHD-related categories. Individuals with persistently high and increasing levels of ADHD symptoms had increased odds of CSHS compared to persistently low class. Sensitivity analyses validated these results. In separate analyses, persistently high levels of hyperactivity and inattentive, and increasing levels of inattentive symptoms were also independently associated with CSHS.

Young people with a longitudinal pattern of high and increasing ADHD symptoms are at higher risk for developing CSHS in young adulthood compared to individuals with low symptom patterns. These two trajectories in childhood and adolescence may represent distinct phenotypic risk profiles for subsequently developing BD and be clinically significant targets for prevention and treatment of BD.

To refine the knowledge on familial transmission, we examined the (shared) familial components among neurodevelopmental problems (i.e. two attention-deficit/hyperactivity–impulsivity disorder [ADHD] and six autism spectrum disorder [ASD] subdomains) and with aggressive behavior, depression, anxiety, and substance use.

Data were obtained from a cross-sectional study encompassing 37 688 participants across three generations from the general population. ADHD subdomains, ASD subdomains, aggressive behavior, depression, anxiety, and substance use were assessed. To evaluate familial (co-)aggregation, recurrence risk ratios (λR) were estimated using Cox proportional hazards models. The (shared) familiality (f2), which is closely related to (shared) heritability, was assessed using residual maximum likelihood-based variance decomposition methods. All analyses were adjusted for sex, age, and age2.

The familial aggregation and familiality of neurodevelopmental problems were moderate (λR = 2.40–4.04; f2 = 0.22–0.39). The familial co-aggregation and shared familiality among neurodevelopmental problems (λR = 1.39–2.56; rF = 0.52–0.94), and with aggressive behavior (λR = 1.79–2.56; rF = 0.60–0.78), depression (λR = 1.45–2.29; rF = 0.43–0.76), and anxiety (λR = 1.44–2.31; rF = 0.62–0.84) were substantial. The familial co-aggregation and shared familiality between all neurodevelopmental problems and all types of substance use were weak (λR = 0.53–1.57; rF = −0.06–0.35).

Neurodevelopmental problems belonging to the same disorder were more akin than cross-disorder problems. That said, there is a clear (shared) familial component to neurodevelopmental problems, in part shared with other psychiatric problems (except for substance use). This suggests that neurodevelopmental disorders, disruptive behavior disorders, and internalizing disorders share genetic and environmental risk factors.