Diagnosis of autism falls under the remit of psychiatry. Recognition that psychiatrists could be autistic is recent. Psychiatrists are the second largest specialty group in Autistic Doctors International, a peer support group for autistic doctors.

To explore the experiences of autistic psychiatrists in relation to recognising themselves and others as autistic.

This was a qualitative study using loosely structured interviews and an interpretive phenomenological analysis.

Eight autistic senior psychiatrists based in the UK participated. One had a childhood diagnosis, two had been diagnosed in adulthood and the remainder self-identified as autistic as adults. Recognition of autism followed diagnosis of their children or encounters with autistic patients. Barriers to self-recognition included lack of autism training, the deficit-based diagnostic criteria and stereotypical views of autism. Recognising that they were autistic led to the realisation that many colleagues were also likely to be autistic, particularly in neurodevelopmental psychiatry. All participants reported the ability to quickly recognise autistic patients and to develop a good rapport easily, once they were aware of their own autistic identity. Difficulties recognising patients as autistic occurred before self-recognition when they shared autistic characteristics and experiences. ‘If we don't recognise ourselves as autistic how on earth can we diagnose patients accurately?’

Autistic psychiatrists face multiple barriers to recognising that they are autistic. Lack of self-recognition may impede diagnostic accuracy with autistic patients. Self-recognition and disclosure by autistic psychiatrists may be facilitated by reframing the traditional deficit-based view of autism towards a neurodiversity-affirmative approach, with consequent benefits for autistic patients.

Physical health conditions are more common in individuals with autism. Some, like epilepsy, have considerable evidence supporting their increased prevalence, but many diseases lack literature to make strong conclusions.

To investigate the prevalence of physical health comorbidities in autism.

We undertook a nested cross-sectional study, using a sample from the National Centre for Mental Health database. It included participants from England and Wales who reported a clinician-made diagnosis of autism (n = 813), and a control sample without autism or mental illness (n = 2781). Participants had provided a medical history at enrolment. Analysis was carried out by binomial logistic regressions controlling for age, gender, smoking status, and antipsychotic and mood stabiliser use. A subanalysis of individuals with concurrent intellectual disability (n = 86) used binomial logistic regression with the same control variables.

Many physical health conditions were significantly more common in autism. Sixteen out of 28 conditions showed increased odds, with the highest odds ratios observed for liver disease, chronic obstructive pulmonary disease, kidney disease, osteoporosis and rheumatoid arthritis. A subanalysis demonstrated a similar pattern of physical health in individuals with autism with and without concurrent intellectual disability. Some conditions, including osteoporosis, hyperthyroidism, head injury and liver disease, had larger odds ratios in individuals with concurrent intellectual disability.

Physical health conditions occur more commonly in individuals with autism, and certain conditions are further increased in those with concurrent intellectual disability. Our findings contribute to prior evidence, including novel associations, and suggest that people with autism are at greater risk of physical health problems throughout adulthood.

Previous observational epidemiological studies have suggested that coffee consumption during pregnancy may affect fetal neurodevelopment. However, results are inconsistent and may represent correlational rather than causal relationships. The present study investigated whether maternal coffee consumption was observationally associated and causally related to offspring childhood neurodevelopmental difficulties (NDs) in the Norwegian Mother, Father and Child Cohort Study.

The observational relationships between maternal/paternal coffee consumption (before and during pregnancy) and offspring NDs were assessed using linear regression analyses (N = 58694 mother-child duos; N = 22 576 father-child duos). To investigate potential causal relationships, individual-level (N = 46 245 mother-child duos) and two-sample Mendelian randomization (MR) analyses were conducted using genetic variants previously associated with coffee consumption as instrumental variables.

We observed positive associations between maternal coffee consumption and offspring difficulties with social-communication/behavioral flexibility, and inattention/hyperactive-impulsive behavior (multiple testing corrected p < 0.005). Paternal coffee consumption (negative control) was not observationally associated with the outcomes. After adjusting for potential confounders (smoking, alcohol, education and income), the maternal associations attenuated to the null. MR analyses suggested that increased maternal coffee consumption was causally associated with social-communication difficulties (individual-level: beta = 0.128, se = 0.043, p = 0.003; two-sample: beta = 0.348, se = 0.141, p = 0.010). However, individual-level MR analyses that modelled potential pleiotropic pathways found the effect diminished (beta = 0.088, se = 0.049, p = 0.071). Individual-level MR analyses yielded similar estimates (heterogeneity p = 0.619) for the causal effect of coffee consumption on social communication difficulties in maternal coffee consumers (beta = 0.153, se = 0.071, p = 0.032) and non-consumers (beta = 0.107, se = 0.134, p = 0.424).

Together, our results provide little evidence for a causal effect of maternal coffee consumption on offspring NDs.

The prevalence of mental health conditions is high for autistic adults. Yet, the IAPT manual states that referral rates into NHS Talking Therapies Services (NHS-TTS) do not reflect this nationally. Non-adapted treatment has been identified as a key barrier to accessing these services. It is therefore imperative that clinicians adapt to the needs of autistic individuals to make treatment accessible and effective. However, there is limited research in the field, especially for low-intensity cognitive behavioural therapy (LICBT). This service evaluation explores adapted LICBT for autistic adults within Plymouth’s NHS-TTS and Autism Service. It investigated clinical outcomes of adapted group and one-to-one LICBT with 84 participants. It hypothesised that psychometric measures for anxiety and depression would be lowered on treatment completion, whilst exploring whether either intervention showed a greater reduction. Additionally, semi-structured interviews were conducted with six participants from the sample to gather perspectives on what aspects of treatment were favourable or require improvement. A factorial ANOVA revealed that psychometric measures reduced on completion across both interventions, with a greater decrease for one-to-one treatment and the anxiety measure. In addition, four themes and nine subthemes emerged following a thematic analysis, which focus on different aspects of treatment, such as content, structure, interaction, and barriers to engagement. Findings indicated that adapted LICBT was associated with lower anxiety and depression for autistic adults. This consequently has implications for improving the current LICBT provisions being offered to autistic adults within the NHS-TTS.

1. (1) To understand some of the barriers autistic people face accessing an NHS Talking Therapies Service (NHS-TTS) and cognitive behavioural therapy (CBT).

2. (2) To reflect on the importance of adapting practice and CBT for autistic people.

3. (3) To present potential adaptations to low-intensity CBT for autistic adults with anxiety and depression.

Maternal vitamin-D and omega-3 fatty acid (DHA) deficiencies during pregnancy have previously been associated with offspring neurodevelopmental traits. However, observational study designs cannot distinguish causal effects from confounding.

First, we conducted Mendelian randomisation (MR) using genetic instruments for vitamin-D and DHA identified in independent genome-wide association studies (GWAS). Outcomes were (1) GWAS for traits related to autism and ADHD, generated in the Norwegian mother, father, and child cohort study (MoBa) from 3 to 8 years, (2) autism and ADHD diagnoses. Second, we used mother–father–child trio-MR in MoBa (1) to test causal effects through maternal nutrient levels, (2) to test effects of child nutrient levels, and (3) as a paternal negative control.

Associations between higher maternal vitamin-D levels on lower ADHD related traits at age 5 did not remain after controlling for familial genetic predisposition using trio-MR. Furthermore, we did not find evidence for causal maternal effects of vitamin-D/DHA levels on other offspring traits or diagnoses. In the reverse direction, there was evidence for a causal effect of autism genetic predisposition on lower vitamin-D levels and of ADHD genetic predisposition on lower DHA levels.

Triangulating across study designs, we did not find evidence for maternal effects. We add to a growing body of evidence that suggests that previous observational associations are likely biased by genetic confounding. Consequently, maternal supplementation is unlikely to influence these offspring neurodevelopmental traits. Notably, genetic predisposition to ADHD and autism was associated with lower DHA and vitamin-D levels respectively, suggesting previous associations might have been due to reverse causation.

The right inferior frontal gyrus (RIFG) is a potential beneficial brain stimulation target for autism. This randomized, double-blind, two-arm, parallel-group, sham-controlled clinical trial assessed the efficacy of intermittent theta burst stimulation (iTBS) over the RIFG in reducing autistic symptoms (NCT04987749).

Conducted at a single medical center, the trial enrolled 60 intellectually able autistic individuals (aged 8–30 years; 30 active iTBS). The intervention comprised 16 sessions (two stimulations per week for eight weeks) of neuro-navigated iTBS or sham over the RIFG. Fifty-seven participants (28 active) completed the intervention and assessments at Week 8 (the primary endpoint) and follow-up at Week 12.

Autistic symptoms (primary outcome) based on the Social Responsiveness Scale decreased in both groups (significant time effect), but there was no significant difference between groups (null time-by-treatment interaction). Likewise, there was no significant between-group difference in changes in repetitive behaviors and exploratory outcomes of adaptive function and emotion dysregulation. Changes in social cognition (secondary outcome) differed between groups in feeling scores on the Frith-Happe Animations (Week 8, p = 0.026; Week 12, p = 0.025). Post-hoc analysis showed that the active group improved better on this social cognition than the sham group. Dropout rates did not vary between groups; the most common adverse event in both groups was local pain. Notably, our findings would not survive stringent multiple comparison corrections.

Our findings suggest that iTBS over the RIFG is not different from sham in reducing autistic symptoms and emotion dysregulation. Nonetheless, RIFG iTBS may improve social cognition of mentalizing others' feelings in autistic individuals.

Prominent clinical perspectives posit that the interface of autism and (borderline) personality disorder manifests as either a misdiagnosis of the former as the latter or a comorbidity of both. In this editorial, we integrate these disparate viewpoints by arguing that personality difficulties are inherent to the autistic spectrum.