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. 2024 Jul 22;78(10):580–587. doi: 10.1111/pcn.13712

Adverse childhood experiences exacerbate peripheral symptoms of autism spectrum disorder in adults

Kazuki Okumura 1,2,†, Tsutomu Takeda 1,3,†, Takashi Komori 1, Michihiro Toritsuka 1,3, Kazuhiko Yamamuro 1, Ryohei Takada 1, Minobu Ikehara 1, Kohei Kamikawa 1, Yuki Noriyama 1, Yuki Nishi 1, Rio Ishida 1,3, Yoshinori Kayashima 1, Takahira Yamauchi 1, Nakao Iwata 3, Manabu Makinodan 1,3,4,✉
PMCID: PMC11804926  PMID: 39037014

Abstract

Aim

Adverse childhood experiences are potentially traumatic events with long‐lasting effects on the health and well‐being of patients with autism spectrum disorder (ASD). It is important to clarify which types of long‐lasting autism‐related symptoms are influenced by childhood experiences to design future intervention studies. However, few studies have examined the association between childhood experiences and autistic symptoms in large samples of adults with ASD and individuals with typical development (TD). In this study, we evaluate the effects of adverse childhood experiences on multiple ASD phenotypes among both individuals with ASD and those with TD.

Method

We combined questionnaire evaluations; Childhood Abuse and Trauma Scale, the Japanese version of the Autism‐Spectrum Quotient, Conners' Adult ADHD Rating Scale, the Japanese version of the Impact of Event Scale‐Revised, and the Japanese version of the Adolescent/Adult Sensory Profile.

Results

Individuals with ASD and those with TD (n = 205 and 104, respectively) were included. There were significant correlations between the extent of adverse childhood experiences and severity of attention‐deficit/hyperactivity disorder symptoms, posttraumatic stress disorder symptoms, and hypersensitivity in both participants with ASD and those with TD. By contrast, ASD core symptoms showed no significant correlation with adverse childhood experiences in either group. These results remained consistent after adjusting for age, sex, and the estimated intelligence quotient.

Conclusion

These findings suggest the need for a detailed disentanglement of ASD‐related core and peripheral symptoms of adverse childhood experiences, which may help to appropriately set outcomes for future early interventions for the childhood experiences of individuals with ASD.

Keywords: adverse childhood experiences, attention‐deficit/hyperactivity disorder, autism spectrum disorder, sensory hypersensitivity

Adverse childhood experiences (ACEs), or maltreatment, are stressful and potentially traumatic events during childhood or adolescence that can be associated with a variety of long‐term unfavorable psychosocial and biological health outcomes in later life. 1 , 2 , 3 , 4 , 5 These experiences include abuse (emotional, physical, and sexual), neglect (emotional and physical), witnessing domestic violence, parental marital discord, and living with household members who are substance abusers, mentally ill, or criminals. 6 The extra cost caused by ACEs, estimated at 1.1% to 6.0% of the nation's gross domestic products, is a substantial financial burden on society, even in developed European countries, 7 which needs to be addressed. Many previous studies have found an association between ACEs and psychiatric symptoms or disorders, such as depression, anxiety, posttraumatic stress disorder (PTSD), attention‐deficit/hyperactivity disorder (ADHD), substance use disorder, 8 , 9 , 10 , 11 , 12 and enduring abnormalities in the nervous, endocrine, and immune systems of abused children and adults. 13

Autism spectrum disorder (ASD) is a heterogeneous cluster of etiologically and phenotypically complex neurodevelopmental disorders characterized by social and emotional problems. 14 , 15 In the 1950s, the hypothesis that an emotionally distant nurturing environment contributes to the development of ASD gained significant attention, but was refuted by the proponent Leo Kanner himself in 1957. 16 In contrast, recent genetic studies, including twin studies, suggest that genetic factors are important in the development of ASD. 17 Children with ASD have been reported to face significantly more ACEs than their peers, 18 and their mental health worsened as the number of ACEs increased. 19 In a recent study, trauma was listed among the top five mental health research priorities for adults with autism. 20 Higher autistic symptoms among women in the general population are associated with an increased risk of developing PTSD symptoms, partially due to increased exposure to childhood abuse. 21 ADHD symptoms are common in children with ASD, 15 and the stronger the ADHD symptoms, the greater the prevalence of comorbid psychiatric symptoms. 22 Thus, it is hypothesized that peripheral symptoms of ASD, compared with ASD core symptoms, could be exacerbated by ACEs, to which ACEs might contribute more than genetic factors. Although the efficacy of early intervention in ASD is controversial, and the impact of conflicts of interest has been suggested, 23 , 24 it is important to clarify which types of long‐lasting autism‐related symptoms are influenced by childhood experiences to design future intervention studies. However, few studies have examined the association between childhood experiences and autistic symptoms in large samples of adults with ASD and individuals with typical development (TD). Here, we first investigated whether ACEs are associated with ASD core symptoms and, subsequently, ACEs are associated with multiple ASD peripheral phenotypes, including ADHD symptoms, PTSD symptoms, and sensory hypersensitivity in a large sample of adults with ASD and participants with TD.

Methods

Psychological examinations

All psychological examinations were conducted by an experienced psychologist. The Mini‐International Neuropsychiatric Interview (MINI) was used to screen for psychiatric disorders. 25 The Autism Diagnostic Observation Schedule Second Edition (ADOS‐2), the gold‐standard tool for ASD assessment, was used to confirm ASD diagnosis. R.I., a qualified psychologist, administers ADOS‐2 for research. The Child Abuse and Trauma Scale (CATS) was used to assess the degree of ACEs. 26 The CATS questionnaire consists of 38 self‐rated items and retrospectively assesses the frequency of adverse event experiences in childhood and adolescence in five categories: sexual abuse, physical abuse, emotional abuse, neglect, and others. To assess the core symptoms of ASD, we used a self‐administered questionnaire called the Japanese version of the Autism‐Spectrum Quotient (AQ‐J). 27 , 28 The full intelligence quotient (IQ) was estimated using the Wechsler Adult Intelligence Scale short form (third or fourth edition) with “similarities” and “symbol search” subsets. 29 The severity of ADHD symptoms was measured using the self‐reported Conners' Adult ADHD Rating Scale (CAARS) with 66 items. This is currently the international standard for the questionnaire‐based assessment of ADHD. 30 The Japanese version of the Impact of Event Scale‐Revised (IES‐R) was used to evaluate PTSD symptoms, including intrusion (eight items), avoidance (eight items), and hyperarousal (six items). 31 , 32 Total and subscale scores were calculated, with higher scores reflecting greater severity. Symptoms of sensory hypersensitivity were assessed using the Japanese version of the Adolescent/Adult Sensory Profile (AASP), a self‐report of behavioral responses to everyday sensory experiences. 33 , 34 The AASP contains quadrant scores: low registration, sensation seeking, sensory sensitivity, and sensation avoiding. Concerning sensory stimuli reactivity, the quadrant scores can be classified into two categories: passive (low registration and sensory sensitivity) and active (sensation seeking and sensation avoiding). 35

Participants

Between December 2016 and February 2023, we recruited high‐functioning adults with ASD and control participants with TD aged at least 18 years. Adults with ASD were outpatients recruited from the Department of Psychiatry, Nara Medical University Hospital. They were initially screened by two or more trained psychiatrists or psychologists to meet the diagnosis of ASD based on the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM‐5). Subsequently, only patients classified as having ASD using the ADOS‐2 were included in the ASD group. The comorbidities of psychiatric disorders are listed in Table S1, and four participants with ASD had epilepsy. The TD group included only participants with no history of psychiatric, neurological, or developmental disorders; no MINI diagnosis; and an AQ‐J score <26. 28 To avoid the effects of intellectual disability, individuals with an estimated full IQ <70 were excluded from both the ASD and TD groups. The study was approved by the Nara Medical University Ethics Committee (No. 1319), and written informed consent was obtained from all participants, which conforms to the provisions of the Declaration of Helsinki. In addition, participants' smoking, drinking, and educational histories were included in the questionnaire.

Statistical analyses

First, we performed descriptive statistics stratified by the ASD and TD groups; continuous variables were displayed as means and SDs, dichotomous variables as counts and proportions, and between‐group differences compared using Welch's t test and χ2 tests. Differences in psychological test scores between the two groups were compared in ANCOVA models adjusted for age, sex, and estimated IQ. We then performed simple and multivariate linear regression analyses for each group, with the CATS total score as the independent variable and each of the other psychological test scores as the dependent variable. In the multivariate models, we adjusted for age and sex as covariates in model 1 and estimated IQ as an additional covariate in model 2. All statistical analyses were performed using R version 4.2.1, and P < 0.05 was considered statistically significant.

Results

Of the participants with available CATS scores who met the inclusion criteria, 205 from the ASD group and 104 from the TD group were included in the analysis. Autism core symptoms measured by the AQ total score were significantly higher in the ASD group than in the TD group (31.1 ± 7.3 vs 14.7 ± 5.3) (P < 0.001, Table 1). Age and percentage of smokers did not differ significantly between the two groups; however, there were more men, fewer drinkers, fewer people with higher education (≥13 years), and a lower estimated IQ in the ASD group than in the TD group (Table 1).

Table 1.

Basic characteristics in each group

Variables ASD, n = 205 TD, n = 104 P‐value †
AQ total score, mean (SD) 31.1 (7.3) 14.7 (5.3) <0.001
Age, mean (SD) 27.7 (7.1) 28.9 (6.4) 0.128
Men, n (%) 151 (74%) 57 (55%) 0.001
Current smoker, n (%) 20 (9.8%) 13 (12%) 0.587
Habitual drinker, n (%) 91 (44%) 72 (69%) <0.001
Education ≥13 years, n (%) 144 (70%) 90 (87%) 0.003
Estimated full IQ, mean (SD) 99.4 (14.0) 106.9 (10.9) <0.001
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†

P‐values were calculated using Welch's t test or Pearson χ 2 test.

Abbreviations: ASD, autism spectrum disorder; AQ, Autism‐Spectrum Quotient; IQ: intelligence quotient; TD, typical development.

ACEs (CATS scores)

Compared with the TD group, the ASD group had a significantly higher variance (F(204, 103) = 3.77, 95% confidence interval [CI], 2.67–5.23, P < 0.001) and higher mean (45.0 ± 28.8 vs 19.8 ± 14.8, P < 0.001) of the CATS total score (Fig. 1a). All CATS subscales including “sexual abuse” (0.66 ± 1.85 vs 0.11 ± 0.50, P < 0.001), “neglect” (10.7 ± 5.3 vs 7.3 ± 3.8, P < 0.001), “punishment” (15.8 ± 11.3 vs 6.0 ± 5.9, P < 0.001), “emotional abuse” (10.6 ± 8.0 vs 3.8 ± 4.4, P < 0.001), and “others” (7.3 ± 6.2 vs 2.6 ± 3.5, P < 0.001) were also significantly higher in the ASD group (Fig. S1). These associations remained significant even after adjusting for age, sex, and estimated IQ (Table S2).

Fig. 1.

Fig. 1

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(a) Density plot of the Child Abuse and Trauma Scale (CATS) total score. Compared with the group with typical development (TD), the group with autism spectrum disorder (ASD) had a higher mean and variance of the CATS total score, i.e. ASD was associated with more adverse childhood experiences (ACEs). (b) However, when stratified by ASD diagnosis, the total CATS score was not significantly associated with the severity of ASD core symptoms as assessed by the Autism‐Spectrum Quotient (AQ) total score in the univariate linear regression models. These results suggest that innate ASD characteristics may be associated with ACEs, but ACEs are not associated with the worsening of core ASD symptoms.

However, linear regression analyses stratified by diagnostic groups showed no significant association between the CATS total score and the AQ‐J total score, neither in the ASD group (β = 0.00 [95% CI, −0.04 to 0.03], P = 0.9) nor in the TD group (β = 0.02 [95% CI, −0.05 to 0.09]) (P = 0.6, Fig. 1b). All other subscales of the AQ, except “local details” in the ASD group, were also not significantly associated with the CATS total score (Fig. S2, Table S3).

ADHD symptoms (CAARS scores)

Compared with the TD group, the ASD group had significantly more severe ADHD symptoms, as assessed by all CAARS items (Fig. 2, Table S4). In particular, for the “CAARS H: ADHD index,” the ASD group had a mean value of 67.7 ± 13.1, which was significantly higher than the TD group's mean value of 44.4 ± 6.6 (P < 0.001). After stratified by group, linear regression models showed that in the ASD group, higher CATS total score was significantly associated with higher scores of all CAARS items, including the “CAARS H: ADHD index” (β = 0.18 [95% CI, 0.12–0.24], P < 0.001) (Fig. 2, Table S5). As for the TD group, only “CAARS D: self‐concept” (β = 0.16 [95% CI, 0.06–0.25], P = 0.001), “CAARS E: DSM‐IV, inattentive” (β = 0.10 [95% CI, 0.01–0.19], P = 0.038), and “CAARS H: ADHD index” (β = 0.09 [95% CI, 0.01–0.18], P = 0.033) showed a significant positive correlation with the CATS total score, similar to the ASD group (Fig. 2, Table S5). These associations remained unchanged after adjusting for age, sex, and the estimated IQ (Table S5).

Fig. 2.

Fig. 2

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Above: density plots of Conners' Adult ADHD Rating Scale (CAARS) scores. The autism spectrum disorder (ASD) group had higher CAARS scores than the group with typical development (TD). Below: linear regression analyses stratified into the ASD and TD groups, showing that adverse childhood experiences are associated with higher CAARS scores independent of ASD diagnosis. ADHD, attention‐deficit/hyperactivity disorder; CATS, Child Abuse and Trauma Scale.

PTSD symptoms (IES‐R scores)

PTSD symptoms were significantly higher in the ASD group than in the TD group when assessed by the IES‐R total score (37.0 ± 21.3 vs 8.8 ± 11.5, P < 0.001), and all subscales of the IES‐R were consistently higher in the ASD group (Fig. 3, Table S6). In the linear regression model, a higher CATS total score was significantly and independently associated with higher IES‐R total scores in both the ASD (β = 0.33 [95% CI, 0.24–0.43], P < 0.001) and TD (β = 0.23 [95% CI, 0.09–0.38], P = 0.002) (Fig. 3) groups. All subscales of the IES‐R were significantly correlated with the CATS total score, except for the “IES‐R hyperarousal” in the adjusted models of the TD group (Fig. 3, Table S7).

Fig. 3.

Fig. 3

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Above: density plots of Impact of Event Scale‐Revised (IES‐R) scores. The autism spectrum disorder (ASD) group had higher IES‐R scores than the typical development (TD) group. Below: linear regression analyses stratified into the ASD and TD groups, showing that adverse childhood experiences are associated with higher IES‐R scores independent of ASD diagnosis. CATS, Child Abuse and Trauma Scale.

Sensory processing (AASP scores)

Compared with the TD group, the ASD group had significantly high scores in the sensitivity symptoms measured by the AASP, including “low registration” (39.5 ± 10.1 vs 24.5 ± 6.1, P < 0.001), “sensory sensitivity” (42.9 ± 11.7 vs 30.2 ± 7.7, P < 0.001), and “sensation avoiding” (43.8 ± 11.2 vs 30.0 ± 7.9, P < 0.001), whereas the ASD group had significantly low scores in “sensation seeking” (35.6 ± 8.1 vs 38.5 ± 7.4, P = 0.002) (Fig. 4). These associations were significant even after adjusting for potential confounders, including age, sex, and estimated IQ (Table S8). Linear regression models stratified into the TD and ASD groups showed that higher values of low registration (ASD: β = 0.08 [95% CI, 0.04–0.13], P < 0.001; TD: β = 0.11 [95% CI, 0.03–0.19], P = 0.007), sensory sensitivity (ASD: β = 0.13 [95% CI, 0.08–0.18], P < 0.001; TD: β = 0.17 [95% CI, 0.08–0.27], P < 0.001), and sensation avoiding (ASD: β = 0.09 [95% CI, 0.04–0.14], P < 0.001; TD: β = 0.15 [95% CI, 0.04–0.25], P = 0.005) were all significantly associated with higher CATS total scores in both groups (Fig. 4). Interestingly, sensation seeking was positively correlated with the CATS total score in the ASD group (β = 0.07 [95% CI, 0.03–0.10], P < 0.001) (Fig. 4). Conversely, in the TD group, there was no significant relationship between sensation seeking and CATS total score (β = −0.01 [95% CI, −0.10 to 0.09], P > 0.9) (Fig. 4). These associations remained unchanged after adjustment for potential confounders (Table S9).

Fig. 4.

Fig. 4

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Above: density plots of Adolescent/Adult Sensory Profile (AASP) scores. Compared with the typical development (TD) group, the autism spectrum disorder (ASD) group had higher AASP scores for “low registration,” “sensory sensitivity,” and “sensation avoiding,” and lower scores for “sensation seeking.” Below: in the ASD group, a higher Child Abuse and Trauma Scale (CATS) total score was associated with higher all AASP scores. In contrast, in the TD group, the CATS total score was significantly associated with low registration, sensory sensitivity, and sensation avoiding, as well as ASD, but not with sensation seeking.

Discussion

To the best of our knowledge, this is the first study to show that ACEs are significantly associated with the intensity of ADHD, PTSD, and sensory hypersensitivity symptoms, independent of ASD diagnosis and the severity of ASD core symptoms, in a large sample, including both adults with ASD and individuals with TD. As in previous studies, 18 the ASD group had more ACEs than the TD group in this study (Fig. 1a, Fig. S1, Table S2); however, it was unclear whether each ASD‐related clinical symptom was attributable to the presence or absence of an innate ASD pathophysiology or acquired ACEs. Interestingly, the results of this study showed that the core symptoms of ASD assessed using the AQ‐J were not significantly associated with ACEs in either the ASD or TD group (Fig. 1b, Fig. S2, Table S3), thus not supporting the hypothesis that ACEs exacerbate the core symptoms of ASD. By contrast, peripheral symptoms comorbid with ASD, including PTSD, ADHD, and sensory hypersensitivity symptoms, were consistently and significantly associated with ACEs in the ASD and TD groups. These results suggest that placing children in better environments may not change their ASD core symptoms. However, it may improve their clinically problematic peripheral symptoms, even in children with ASD who are more likely to have ACEs.

ADHD symptoms are among the most common complications of ASD. They are reported to be present in approximately 14% to 78% of children with ASD 36 and 40% of adults with ASD. 37 , 38 In contexts unrelated to ASD, a large body of evidence suggests that ACEs could worsen ADHD symptoms. 39 , 40 Conversely, ADHD may be a risk factor for subsequent ACEs. 41 Similar to these previous studies, our findings show significantly more ADHD symptoms in the ASD group (Fig. 2, Table S4), and ACEs were positively correlated with the severity of ADHD symptoms in the ASD and TD groups (Fig. 2, Table S5). Since the range of ACEs scores differed between the ASD and TD groups, we could not directly compare the impact of ACEs on ADHD symptoms between the two groups. However, the current results suggest that the influence of ACEs must be considered in future ASD research concerning ADHD symptoms as well as among individuals with TD.

PTSD symptoms, including avoidance, hyperarousal, and intrusion, are also known to be common complications in ASD. 42 Similar to the results of this study (Fig. 3, Table S6), a higher prevalence of PTSD symptoms was reported in the ASD group than in the TD group. 43 Consistent with previous studies reporting that ACEs predict PTSD symptoms, 11 , 44 our study showed that ACEs were associated with PTSD severity in both the ASD and TD groups (Fig. 3, Table S7). Similarly, due to the different ranges of CATS scores, we could not compare the effects of ACEs on PTSD symptoms between the ASD and TD groups. Nevertheless, our findings suggest that the influence of ACEs should be considered in future studies examining PTSD symptoms complicated by ASD.

Sensory sensitivity is one of the hallmark symptoms of ASD, with suggested effects on core symptoms such as social communication. 45 Our cohort also had significantly higher sensory sensitivity symptoms in the ASD group than in the TD group (Fig. 4, Table S8). Unlike the core symptoms of ASD as measured by the AQ, sensory hypersensitivity symptoms were associated with ACEs in both groups (Fig. 4, Table S9). Given the cross‐sectional design, this study cannot clarify the direction of causality. Three possibilities therefore exist: first, ACEs may exacerbate subsequent sensory symptoms; second, sensory hypersensitivity may affect the subjective perception of ACEs; and, third, confounding factors may create a pseudocorrelation between sensory hypersensitivity and ACEs. The fact that hypersensitivity symptoms have a strong genetic component in ASD supports the second possibility. 46 However, as ACEs have actually been reported to be associated with altered pain thresholds, 47 , 48 the influence of environmental factors on sensory sensitivity symptoms in ASD should also be carefully considered. Identification of confounding factors is difficult based on the results of this study alone, but it is possible that those could be ADHD/PTSD symptoms observed to be associated with ACEs in the current study.

Several biological mechanisms are expected to underlie the results of the present study. Across species, it has been suggested that adversity occurring early in life has a greater impact on neurobiological and psychiatric outcomes than adversity in adulthood. 49 , 50 , 51 This means that organisms in the early developmental stages may be prone to long‐lasting neurobiological scars caused by environmental factors. ACEs affect brain functions, including emotional and cognitive functions, possibly through changes in the brain, neuroendocrine system, inflammation, and epigenetics. 52 , 53 , 54

Multiple lines of evidence suggest that ACEs can lead to long‐term structural and functional changes in the brain. 55 Previous studies have shown that ACEs are associated with structural and functional abnormalities in brain regions, such as the prefrontal cortex (PFC), amygdala, and hippocampus, as well as their connections. 56 , 57 , 58 , 59 , 60 , 61 Since the PFC plays an important role in executive function, and PFC dysfunction and impaired executive function is a hallmark of ADHD, 62 , 63 these impairments may contribute to the observed association between ACEs and ADHD symptoms. In addition, the amygdala, which connects to the hippocampus and medial PFC, is related to threat processing and emotion regulation. Thus, ACE‐induced changes in the amygdala may increase PTSD symptoms. 64

ACEs are also associated with the activation of the hypothalamic–pituitary–adrenal axis, which plays an important role in the stress response, and basal levels of the stress hormone cortisol in saliva and hair have been shown to be elevated. 65 , 66 However, some recent systematic reviews have indicated inconsistent findings on these associations, possibly because of differences in the types of adversities studied or research contexts. 67 , 68 Researchers found that people with ACEs have a blunter cortisol response to psychosocial stressors and smaller effect sizes than those without ACEs. 69 Reduced cortisol responses to psychosocial stressors have also been demonstrated in patients with PTSD, 70 , 71 , 72 suggesting that cortisol responsiveness is a potential mechanism linking ACEs and PTSD symptoms. 54

This study has several limitations. First, this was a cross‐sectional study, and causality could not be proven. Symptom scores are not repeated measures but only single‐point measures. Second, the main exposure, the severity of ACEs assessed using the CATS score, was based on a self‐administered questionnaire at the time of study participation and requires careful interpretation. The possibility of recall bias cannot be ruled out because many of the participants in the ASD group had visited a psychiatrist for a social life problem. In both groups, we examined the association with symptoms involving psychosocial difficulties. It is also possible that some cognitive or sensory traits were a common cause of the worsening of both CATS and various symptom scores. However, this association was independent of ASD characteristics. Third, the participants in the ASD and TD groups were not randomly sampled from the general population and, therefore, may contain some bias. Fourth, the current study did not assess depressive or anxiety symptoms, which are clinically common comorbidities of ASD, because we were interested in long‐lasting traits rather than dynamic psychological states. Finally, this study did not reveal any biological changes.

In conclusion, this is the first investigation to show within a single study that ACEs are significantly associated with peripheral symptoms of ASD, including ADHD, PTSD, and sensory hypersensitivity, in both ASD and TD. Conversely, ACEs are not associated with ASD core symptoms. The results suggest that, when conducting early intervention for the childhood experiences of children with ASD in the future, there may be little improvement effect on the core symptoms of ASD, while a significant impact on the peripheral symptoms of ASD can be expected. Therefore, consideration should be given in advance to the setting of outcomes. Furthermore, it is important for clinicians to understand that the core symptoms of ASD are not necessarily the fault of the nurturing environment and to ensure that parents are not unfairly blamed. Our findings warrant further research, including longitudinal studies or intervention studies in the early environment, to establish causality and detailed molecular, biological, physiological, and anatomical studies to elucidate the underlying biological mechanisms and temporal relationships of the various comorbid symptoms associated with ASD. These insights may ultimately lead to the identification of novel or refined therapeutic targets and methods for individuals with ASD and may be translated into clinical practice.

Disclosure statement

N.I. received grants from Sumitomo Pharma and Otsuka Pharmaceutical, and speaker honoraria from Sumitomo Pharma, Otsuka Pharmaceutical, Takeda Pharmaceuticals, Viatris, and Meiji Seika Pharma. M.M. received grants from Kyowa Kirin and speaker honoraria from Sumitomo Pharma and MSD.

Author contributions

K.O., T.T., T.K., M.T., K.Y., R.T., M.I., K.K., Y.N., Y.N., Y.K., T.Y., and M.M. recruited participants and examined psychological symptoms. R.I. and Y.K. performed psychological tests. K.O., T.T., N.I., and M.M. analyzed the data and wrote the manuscript.

Funding information

This work was supported by AMED‐PRIME (grant number 21gm6310015h0002 to M.M.), AMED‐CREST (grant numbers 23gm1510009h0002 and 23gm1910004s0301 to M.M.), AMED (grant number 21wm04250XXs0101 to M.M.), AMED (grant number 21uk1024002h0002 to M.M.), and JSPS KAKENHI (grand numbers 23H04173 and 24K02386 to M.M.).

Supporting information

Figure S1. The distribution of Child Abuse and Trauma Scale (CATS) scores for both the autism spectrum disorder (ASD) and typical development (TD) groups are shown by density plots; compared with the TD group, the ASD group tends to have higher mean and higher variance of CATS scores (total score and all subscales, including “sexual abuse,” “neglect,” “punishment,” “emotional abuse,” and “others”).

PCN-78-580-s003.tiff (10.9MB, tiff)

Figure S2. When stratified by the diagnostic groups, there was no significant correlation between Child Abuse and Trauma Scale (CATS) total score and Autism‐Spectrum Quotient (AQ) total score in the autism spectrum disorder (ASD) group or in the typical development (TD) group. All subscales of the AQ, except for “local details” in the ASD group, were not significantly associated with the CATS total score.

PCN-78-580-s001.tiff (9.7MB, tiff)

Data S1. Supporting Information.

PCN-78-580-s002.docx (46.1KB, docx)

Acknowledgments

We are grateful for the cooperation and patience of the patients who made this study possible.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

Figure S1. The distribution of Child Abuse and Trauma Scale (CATS) scores for both the autism spectrum disorder (ASD) and typical development (TD) groups are shown by density plots; compared with the TD group, the ASD group tends to have higher mean and higher variance of CATS scores (total score and all subscales, including “sexual abuse,” “neglect,” “punishment,” “emotional abuse,” and “others”).

PCN-78-580-s003.tiff (10.9MB, tiff)

Figure S2. When stratified by the diagnostic groups, there was no significant correlation between Child Abuse and Trauma Scale (CATS) total score and Autism‐Spectrum Quotient (AQ) total score in the autism spectrum disorder (ASD) group or in the typical development (TD) group. All subscales of the AQ, except for “local details” in the ASD group, were not significantly associated with the CATS total score.

PCN-78-580-s001.tiff (9.7MB, tiff)

Data S1. Supporting Information.

PCN-78-580-s002.docx (46.1KB, docx)

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