age of onset

Background: Psychiatric disorders differ in their typical age of onset, but evidence describing onset patterns in small clinical samples from Kerala, India, is limited. This pilot study examined the association between diagnostic group and age of symptom onset and described the interval between symptom onset and first diagnosis. Methods: A cross-sectional observational study was conducted using 50 consecutively sampled patient records from psychiatric outpatient and inpatient services at VPSV Ayurveda College, Kottakkal, Kerala. Diagnoses were based on DSM-5 criteria. Data included age at symptom onset, age at first diagnosis, sex, source of onset information, family psychiatric history, comorbidity, and medical or neurological conditions. Descriptive statistics and non-parametric tests were used; inferential analyses were considered exploratory. Results: Participants included 30 males and 20 females; mean current age was 35.14 ± 15.36 years. Mean age at symptom onset was 26.02 ± 14.83 years (median 25.5; range 1-72), and 28% reported onset before age 18. Age of onset differed across ten diagnostic groups (Kruskal-Wallis H = 28.58, df = 9, p < 0.001). Median onset was earliest in neurodevelopmental disorders (3.5 years) and latest in neurocognitive disorders (66 years). Median onset-to-diagnosis interval was one year (interquartile range 0-4); 14% waited six years or longer. Earlier onset correlated with a longer interval to diagnosis (Spearman ? = -0.350, p = 0.013). No significant sex difference in onset age was observed. Conclusion: The findings suggest distinct onset patterns across diagnostic groups in this clinical sample and indicate that some patients experience prolonged diagnostic delays. Larger, multicentre studies are required to confirm these exploratory results.

Abstract Suicidal thoughts and behaviours (STB) span ideation (SI), attempt (SA), and death (SD), yet the factors distinguishing ideation from attempt remain poorly understood. Genome-wide studies suggest shared yet partially distinct genetic liabilities. However, few analyses have tested the differential contributions of SI-, SA-, and SD-related genetic liability across STB phenotypes, particularly in high-risk mood-disorder populations. We analysed up to 17,622 participants from the Australian Genetics of Depression Study and the Australian Genetics of Bipolar Disorder study, jointly modelling polygenic scores (PGS) for SI, SA, and SD across mutually exclusive STB phenotypes using multinomial regression, alongside dimensional outcomes, age of onset, and the ideation-to-attempt transition. SI-PGS and SA-PGS showed independent and distinct associations: SI-PGS showed reduced odds of SI-only but increased odds of SI + SA, and SA-PGS robustly predicted attempt-related outcomes. Transition models captured the clearest clinical signal: SA-PGS predicted a 23% higher odds of attempt among ideators, with absolute risk differences of 9–12% between the top and bottom deciles—larger than those of the onset models (5–7%). Predictive discrimination improved incrementally (ΔAUC ≈ 0.02–0.03; ΔC ≈ 0.01). SD-PGS showed no robust effects. Sex-stratified analyses yielded broadly consistent findings across sexes. These findings support ideation-to-action models at the genetic level, demonstrating partially distinct polygenic liabilities for ideation and attempt. Although absolute predictive utility remains modest, these results indicate that PGS sharpen the stratification of ideators at risk of attempt, providing incremental value for future integrative risk models that combine genetics with mood disorders and environmental predictors.

Abstract We investigated public beliefs about the extent to which mental disorders are perceived to be part of the true self, that is, the set of traits and behaviors that compose one’s core character. We conducted three quantitative vignette-based studies (total n = 601) in UK general public samples, considering seven disorders (attention deficit hyperactivity disorder (ADHD), anorexia nervosa, autism spectrum disorder (ASD), bipolar disorder, major depressive disorder, schizophrenia, and obsessive-compulsive disorder (OCD)). For each disorder, participants rated how much the disorder reflects the vignette character’s true self, along with perceived causes of the disorders (studies 1 and 2), perceived severity, age of onset, duration, probability of recovery (study 2), and stigmatization (study 3). Disorders differed sharply in the extent to which they were judged to be part of the true self: ADHD, ASD, and OCD received higher true self ratings than major depressive disorder, anorexia nervosa, and schizophrenia, with bipolar disorder intermediate. A disorder was rated more ‘true self’ when it was: perceived as more “biologically” caused; less “psychologically” caused; less severe; and recovery was perceived as less likely. Although the extent of stigmatization also varied across disorders, true self ratings did not predict stigmatization. Our results show that the public thinks about different mental disorders in quite different ways, suggesting that different disorders should not be lumped together when considering attitudes and their consequences.

Background Eating disorder treatment is most successful when delivered at first onset, underscoring the importance of early intervention. Genetic factors may contribute to earlier onset, but molecular genetic research into symptom onset and severity remains limited. Aims We investigated: (a) age at onset of behavioural symptoms and low weight, including sex and gender differences; and (b) the single-nucleotide polymorphism (SNP)-based heritability and cross-trait polygenic associations of symptoms, onset, and severity. Method Participants ( n = 24 973) of genetically derived European ancestry were from the National Institute for Health and Care Research BioResource, including the Genetic Links to Anxiety and Depression Study, the Eating Disorders Genetics Initiative UK and the COVID-19 Psychiatry and Neurological Genetics study. Symptoms were assessed with the ED100K questionnaire. We described sex-stratified onset of binge eating, low weight, self-induced vomiting, laxatives, diuretics, excessive exercise, and fasting. SNP-based heritability was estimated with genome-wide complex trait analysis using genomic-relatedness-based restricted maximum-likelihood. We tested associations with 26 polygenic scores (PGS), which were calculated using SBayesRC. Results Symptom median onset ranged from 16 to 20 years: vomiting (16 years), fasting and excessive exercise (17 years), binge eating (18 years), laxatives (19 years), diuretics (20 years) and low weight (20 years). Males were disproportionately likely to report adult onset. In females, behavioural symptoms and low weight showed substantial heritability (SNP-based h 2 = 0.31–0.78), but age at onset and cognitive symptoms were less heritable. PGS analyses identified distinct pathways: in females, higher childhood obesity PGS was linked to earlier binge eating onset (approximately 7 months), and higher educational attainment PGS to earlier low weight onset (approximately 6 months). Conclusions Eating disorder symptoms begin in adulthood as frequently as adolescence, challenging stereotypes and underscoring investment needed in adult services, particularly for males. Although behavioural symptoms and low weight were strongly heritable, age at onset and cognitive symptoms showed limited genetic contribution. Symptom-level PGS analyses highlight distinct biological and developmental pathways. Larger sample sizes and more accurate phenotyping are needed.

زمینه: درمان اختلالات خوردن زمانی بیشترین موفقیت را دارد که در اولین بروز علائم ارائه شود و این امر اهمیت مداخله زودهنگام را برجسته می‌کند. عوامل ژنتیکی ممکن است به شروع زودتر بیماری کمک کنند، اما پژوهش‌های ژنتیک مولکولی درباره شروع و شدت علائم همچنان محدود است. اهداف: ما بررسی کردیم: (الف) سن شروع علائم رفتاری و وزن پایین، از جمله تفاوت‌های جنسیتی و جنسیتی؛ و (ب) وراثت‌پذیری مبتنی بر تک‌نوکلئوتید پلی‌مورفیسم (SNP) و ارتباطات پلی‌ژنتیکی بین صفات مختلف علائم، شروع و شدت. روش: شرکت‌کنندگان (n = 24 973) با تبار اروپایی مشتق‌شده ژنتیکی از بانک زیستی مؤسسه ملی پژوهش سلامت و مراقبت، شامل مطالعه Genetic Links to Anxiety and Depression، ابتکار ژنتیک اختلالات خوردن بریتانیا و مطالعه COVID-19 Psychiatry and Neurological Genetics بودند. علائم با پرسشنامه ED100K ارزیابی شد. ما سن شروع پرخوری، وزن پایین، استفراغ القایی، مصرف ملین‌ها، دیورتیک‌ها، ورزش بیش از حد و روزه‌داری را به تفکیک جنسیت توصیف کردیم. وراثت‌پذیری مبتنی بر SNP با تحلیل صفات پیچیده در کل ژنوم با استفاده از حداکثر درست‌نمایی محدودشده مبتنی بر ارتباط ژنومی برآورد شد. ارتباط با ۲۶ نمره پلی‌ژنتیکی (PGS) که با SBayesRC محاسبه شد، بررسی گردید. نتایج: میانه سن شروع علائم بین ۱۶ تا ۲۰ سال بود: استفراغ (۱۶ سال)، روزه‌داری و ورزش بیش از حد (۱۷ سال)، پرخوری (۱۸ سال)، ملین‌ها (۱۹ سال)، دیورتیک‌ها (۲۰ سال) و وزن پایین (۲۰ سال). مردان به طور نامتناسبی احتمال بیشتری داشت که شروع بیماری در بزرگسالی را گزارش کنند. در زنان، علائم رفتاری و وزن پایین وراثت‌پذیری قابل توجهی نشان دادند (وراثت‌پذیری مبتنی بر SNP h2 = 0.31–0.78)، اما سن شروع و علائم شناختی وراثت‌پذیری کمتری داشتند. تحلیل‌های PGS مسیرهای متمایزی را شناسایی کرد: در زنان، نمره پلی‌ژنتیکی چاقی دوران کودکی بالاتر با شروع زودتر پرخوری (حدود ۷ ماه) و نمره پلی‌ژنتیکی تحصیلات بالاتر با شروع زودتر وزن پایین (حدود ۶ ماه) مرتبط بود. نتیجه‌گیری: علائم اختلالات خوردن به همان اندازه که در نوجوانی آغاز می‌شوند، در بزرگسالی نیز شروع می‌شوند؛ این امر کلیشه‌ها را به چالش می‌کشد و بر لزوم سرمایه‌گذاری در خدمات بزرگسالان، به ویژه برای مردان، تأکید می‌کند. اگرچه علائم رفتاری و وزن پایین وراثت‌پذیری بالایی داشتند، اما سن شروع و علائم شناختی سهم ژنتیکی محدودی نشان دادند. تحلیل‌های PGS در سطح علائم، مسیرهای زیستی و رشدی متمایزی را برجسته می‌سازد. به حجم نمونه‌های بزرگ‌تر و فنوتیپ‌گذاری دقیق‌تر نیاز است.