​Introduction

​

Defined by ICD-10, Conduct disorders (CD) are a group of psychiatric conditions characterised by constant patterns of anti-social, aggressive and defiant behaviour in childhood. These often significantly contradict age-appropriate social expectations.[1] Despite being heavily under-researched, the prevalence of CD in school children is nearly 3%, and up to 60% of adults with a mental disorder had CD or oppositional defiant disorder (a common precursor to CD) in their childhood.[2]

     Diagnosis of CD is largely clinical, based on symptoms and behavioural displays. Subtypes of the disorder are classed on certain characteristics, such as the age of symptom onset, and the presence or absence of limited prosocial emotions. Limited prosocial emotions commonly include shallow displays of positive feelings as well as limited remorse, guilt and empathy, and are referred to as callous-unemotional (CU) traits.[2,3]

     If symptoms of CD persist past eighteen, the diagnosis is then defined as antisocial personality disorder (ASPD).[4] Typically presenting as a pattern of socially irresponsible, reckless and exploitative behaviour, ASPD is a chronic condition, though typically improves with advancing age.[5]

     Management of CD involves specialist services such as Child and Adolescent Mental Health Services (CAMHS) and psychosocial interventions including carer training, child-focused programs or multimodal interventions.[6] Treatment is effective, but high drop out rates and low funding limits its reach.[7] While medications such as risperidone can be used for short-term episodes or treatment of concurrent disorders, there are no long-term pharmacological treatments currently licensed in the UK for CD.[8]

     Children with lifetime psychiatric disorders like CD are significantly more likely to commit violent crimes,[9] and are at a much higher risk of developing other mental health problems.[10] As they progress into adulthood, they are vulnerable to numerous problems such as contracting infectious diseases, other health problems, substance abuse, homelessness and difficulties in daily life.[11] Therefore, due to the risk posed to themselves and others, would it be beneficial to identify those more likely to develop CD in childhood, to ensure early intervention and minimise any potential harm?
     I believe that genetic testing should not be used to identify children more at risk for CD, and
in this essay I consider the scientific basis and some key ethical implications of this question.

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Using genetic testing to predict children more at risk of developing CD

​

     Conduct disorders are very complex, with both genetics and environmental factors playing a strong role in its development. Studies have shown that there are some genes which may be linked to CD related phenotypes, though they have not yet been confirmed due to the complex and unknown aetiology of the disorders.[12] Retrospective studies have estimated heritability of CD ranging from 40-70% and prospective reports of CD symptoms in children have estimated heritability to be between 40-50% in both boys and girls.[13] 

     Though to date no genes have been definitively identified as being associated with or causative of CD, Gene-wide association studies (GWAS) have identified certain single-nucleotide polymorphisms (SNPs) that may have a significant association with CD symptoms.[13] 

     Two of the significant SNPs were found to be in the gene C1QTNF7.[13] The gene is predicted to allow protein binding14, and while it is thought to influence neurodevelopment and behaviour [15,16], its exact involvement with CD still remains unclear.[13] 

     Both other significant SNPs found were intergenic. The first is found on the edge of the gene LOC642791, located on chromosome 11. This pseudogene is similar to a functional gene elongation factor 1-alpha (EF1A).[13] EF1A is vital for protein synthesis, as well as promoting viral replication and regulating the actin cytoskeleton.[17] The second, found on chromosome 13, is around 13 kb from its nearest gene - LOC647298.13 As a pseudogene of a heat shock protein 1 (HSP1)13, it is responsible for regulating HSP1 in its roles in chaperoning, thermotolerance, apoptosis and immunology.[18] 

     Despite this GWAS suggesting potential associations with these genes and CD symptomology, failure to replicate and lack of further research or knowledge of the genes’ exact functions, makes it difficult to draw accurate conclusions as to the importance of these genes on the development of CD.[13] 

     Some genes have also been potentially shown to be associated with CD development. Monoamine oxidase A (MAOA) is a gene responsible for the breakdown of neurotransmitters and thus, mood regulation. Known as the “warrior gene”, MAOA has been linked to aggressive behaviours, and certain alleles have been thought to have some influence on antisocial behaviours, psychopathy and criminal violence (all of which are associated with CD).[19] Despite this, it is still unknown what role MAOA has in the development of CD. While there is enough evidence to suggest a potential link between the two, more research is needed to definitively conclude if there is a direct association between the two. 

     Importantly, studies have shown that the combination of MAOA alleles and certain environmental factors may have a strong impact on the display of antisocial behaviours.[18] For example, a study done in 2002 found that amongst males who had been maltreated, those with the MAOA-L variant were more likely to engage in antisocial behaviours, compared with those possessing the MAOA-H variant.[20] Another study suggests that low MAOA activity was a potential risk factor for CD development in boys, but only in the presence of a negative childhood environment.[21] These findings have been replicated, as multiple studies have shown that MAOA only increases the risk of aggression, fraudulent behaviours, crime and antisocial behaviours in the presence of certain negative environmental factors, such as early life stress, social exclusion and peer delinquency.[19]

     While the impact MAOA has on displays of aggressive behaviours has been well researched, it is important to note that there is still very little research around its direct relationship to the development of CD specifically. Furthermore, as most of the research done typically focused on males, there is little evidence to suggest if these results would be replicated in females. 

     In addition to genetics, environmental factors play a huge role in the development of CD.[22] For example, low parental education has been associated with emotional and behavioural problems in children, and children exposed to domestic violence and other adverse events have shown to lead to externalising behaviour problems in later life.[23] A national survey done by ONS in 2004 showed that the prevalence of CD in children who were being looked after, were abused or were on child protection/ safeguarding registers was almost 40%.[24] Substance abuse during pregnancy has also been shown to result in long-term neurodevelopmental and cognitive deficits including behavioural problems, both of which are associated with CD.[23] 

     Though the prevalence of CD and ASPD differs between men and women, there has been some controversy as to what influence, if any, sex has in the development of CD. Some studies have found a qualitative difference in the way environmental and genetic factors influence CD development between the sexes, but others have not found any significant differences.[22] 

     As mentioned previously, interactions between genes and environmental factors have been shown to impact CDs. Some genetic predispositions for CD can contribute to the seeking out of certain types of higher-risk environments. Equally, some environmental factors can lead to changes within genes associated with CD, as well as change the importance of these genetic factors.[12] 

     Overall, it has been shown that genetic and environmental factors play a strong role in the development of CD. Individual genes and environments have been thought to be associated with CD. But, due to the polygenic nature of CD paired with the interplay between genetic and environmental factors,[23] it is not currently possible to exactly identify who has an increased risk of developing CD. Additionally, while many genes have been linked to specific traits of CD, such as aggression or antisocial behaviour, none have yet been identified to be causative of CD itself.

​

A potential screening process

​

     With these genes having been identified as potential risk factors for CD trait development, as well as the known environmental risk factors, it may be possible to screen children to determine how likely they are to develop CD. Identifying these children may allow us to intervene earlier, to minimise harm caused. But should we?

​

Implementing the screening program 

     The term ‘conduct disorder’ covers a wide range of conditions and therefore trying to create a screening program for this specifically is not possible. A more probable solution would be to try and screen for children more at risk for violent behaviour traits, specifically for those that may lead to harm to themselves and the general public. 

     Though numerous environmental factors have been thought to be associated with aggressive traits, some key ones include childhood maltreatment and children in care or being ‘looked after’.[22-24] Other common risk factors include parents with CD/other mental health disorders, [25] and a pre-existing mental health condition like ADHD.[2] 

     Polygenic risk scores (PRS) are currently used as a research tool to estimate heritability, infer genetic overlap between traits and to predict phenotypes using a person's genetic profile. This is done via aggregating SNPs across the genome,and combining knowledge gathered from pre-existing GWAS.[26] Children who are known to have been exposed to these environmental risk factors could theoretically have a DNA sample obtained, and from this, a PRS for CD development could be ascertained. Then, if it is thought that the child has a high risk of displaying aggressive traits or developing CD, they would be considered a ‘positive test’. And thus, we could start interventions early, such as close monitoring for displays of violence, screening for other mental health conditions, and psychosocial interventions. 

     Psychosocial interventions target a range of different aspects, all with the aim of modifying these risk factors to improve prognosis. For children, treatments include parent management training to improve inter-familial relationships and modify parental risk factors, and child therapies aimed at reducing any aggressive behaviour and improving social skills and emotional dysregulation. Teachers of these children are also shown methods to promote positive behaviour, academic engagement and learning for all children, which has been demonstrated to be useful in helping children with CD cope in school. For teenages, interventions are similar, with a strong focus on preventing criminal offending.[11,27] 

     Most of these interventions are designed to be inexpensive but very effective for improving prognosis of CD, or at the very least minimising negative outcomes in the future.[11] Most, if not all studies determining the effectiveness of these treatments have had positive outcomes. Functional family therapy for teenagers was shown to have recidivism rates of up to 30% lower than control groups, and RCTs showed these therapies resulted in a significant reduction in negative behaviours and an increase in prosocial behaviours in children.[11] 

     And thus, PRS could be used in combination with screening for environmental risk factors to identify children at risk of developing CD. From there, children could be trialed with psychosocial interventions and screened for other frequently co-occurring disorders. This would ensure early intervention to improve prognosis,[11] or at the very least minimise harm. However, there are some issues that must be taken into account when trying to implement such a program. 

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Problems with the screening program 

     Perhaps the biggest problem with this proposal is that the exact causes of CD are still unknown. If a specific gene was definitively identified to be causative of CD, then screening would, theoretically, be simple to do. Children with the gene could be identified at birth or via a DNA sample, and then treatment/preventative measures could be taken, as is the case with numerous genetic disorders already. However, even if someone was identified as having any of the genes associated with CD, the complex interplay between these genes and the person's environment [23] makes it difficult to predict whether they will actually be affected by CD. 

     Additionally, while PRS is valuable in research, it is still not used in diagnostics. This is because it is a relatively novel tool, and there are still issues with defining risk thresholds for certain diseases, as well as its accuracy in predicting phenotypes. More research needs to be done in order to ensure PRS is equally accurate across all races and ethnicities.[28] Furthermore, it is highly possible that due to the expense of PRS, only certain people from higher-income families would be able to afford it, thus worsening health disparities.[29] Various studies and surveys around using PRS for disease identification and prognosis suggest that there were multiple concerns including its potential to lead to racial discrimination, as well as privacy concerns.[30,31] And thus, before integrating PRS into a clinical setting, a lot of important issues must be addressed, such as the cost, the accuracy and its accessibility and equality across all genders, races and ethnicities. 

     Accuracy of diagnostic screening tests are often determined by negative predictive values (NPV) and positive predictive values (PPV), and so it is important to consider these values when designing a screening program.[32] Firstly, prevalence rates are necessary when interpreting these results. But, as the prevalence of CD is vastly different between boys and girls, it proves a challenge to determine how useful a screening tool will be. One potential solution is to have a different screening method for boys and girls, a method many researchers have already used.[33] 

     Another challenge is understanding at what point intervention is deemed necessary. If the threshold for intervention is set lower for the best chance of catching everyone, the number of false positives will inevitably increase, leading to a low PPV. Similarly, if the threshold is set high to reduce the number of false positives, the number of true positives will decrease leading to a higher NPV. So, finding a threshold which ensures the maximum number of people are correctly identified, whilst ensuring false positives are kept to a minimum is difficult, especially with the prevalence discrepancies across the sexes.[33] 

     The economic impact of this screening program must also be analysed. Currently, treating CD is expensive, with a recent study suggesting that by the age of 28 costs for those with CD were around 10 times higher than for those with no other problems, with a mean cost of £70,019. Within this, criminality was the greatest expense, followed by educational provisions, foster care and residential care. Additionally, per family, the psychosocial education programs can cost between £629 to £3839 depending on the type of program.[34] Whilst in an ideal scenario, all children who do ‘test positive’ would undergo some type of psychosocial intervention, or at the very least be screened further using current diagnostic tools, the economic burden of this would be huge, and most likely impossible to fund publically. And thus, the screening program has some major problems, including the accuracy of the PRS, the economic burden of testing and treatment, as well as determining where the threshold for intervention should lie.

 

The ethics of the screening program 

     The impact on the patient must also be analysed, and this can be done by considering the framework of the Four pillars of Medical Ethics - autonomy, beneficence, non-maleficence and justice.[35] 

     The principle of autonomy [35] raises a significant dilemma. Is it possible for these patients to make informed decisions for themselves? 

     Testing must be done on children, and unless the child is over sixteen or falls under gillick competency, someone with parental responsibility must consent for them. If this is deemed unsuitable, then a court can overrule the decision to ensure the best interests for the child.[36] This begs the question as to whether this proposal would be in the best interests of the child. 

     As mentioned previously, one major benefit would be that children who are at a high risk of displaying aggressive behaviours and developing CD are caught earlier, leading to improved prognosis and minimising negative outcomes in the future.[11] However, due to the inaccuracies of PRS28, the exact causative genes of CD being unknown,[13] and the fact that these associated genes are very common in the general population [21] it is almost definite that a lot of children picked up would be false positives. They would therefore be subjected to numerous further tests and treatments they would not necessarily need. This would have major impacts on their psychological well-being, not to mention have a massive impact on their family and disrupt their daily life. Not only does this suggest that it would not be in the best interest of the child, unnecessary treatment of children goes against the principles of non-maleficence and beneficence. It also contradicts the principle of justice, as the economic impact of this unnecessary treatment would mean that those who actually do need treatment may not get it due to limited funding, as well as increased waiting times.[7] 

     Reviewing the environmental factors of anyone deemed high risk by the PRS before commencing treatment may alleviate some economic burden whilst simultaneously increasing the number of children who actually are true positives. However, this method still does rely on the PRS accurately estimating probability, which is currently untrue. 

     Another concern is the impact this may have on the wider population. Screening in this way can lead to the incorrect assumption that everyone with CD are aggressive and commit violent crimes, which is not the case. In fact, studies have found that many children with CD improved, and did not go onto being diagnosed with ASPD in adulthood. Furthermore, it has been shown that whilst most may be arrested at a young age, as they grow older their arrest rates decline. Most older adults with ASPD are arrested for conduct offenses such as public drunkenness rather than violent crimes.[5] Indeed, this assumption of violence will undoubtedly open up discrimination and stigmatization, leading to more harm than benefits, thus contradicting multiple ethical principles.[35] 

     One potential method of reducing these concerns is to carry out the screening test after a child has displayed violent behaviours. This may reduce the amount of false positives, whilst still ensuring true positives are caught, thus allowing for the benefits whilst mitigating some of the negative consequences such as harmful assumptions and unnecessary testing. However, this raises a major concern. Telling a child that they have abnormalities that may lead them to displaying violent phenotypes could lead to the self-fulfilling prophecy - a psychosocial phenomenon whereby a person’s expectations about a situation comes true due to their own behavioural changes. This is because the prediction will guide how they act, leading to the predicted outcome being more likely to occur.[37] Therefore, carrying out the screening test after displays of violent behaviours may lead to more harm in the long run, once again contradicting multiple ethical principles.[35] 

     In order to try and bypass the self-fulfilling prophecy, results of the screening test could only be disclosed to the parents, allowing them to decide what treatments or interventions are feasible. Whilst this may be acceptable for young children who would not understand what CD means, it contradicts the principle of autonomy for children with capacity to consent.[36] 

     Moreover, telling parents their child has an increased risk of displaying violent behaviours opens up a wide array of problems. If parents choose to prevent this by using harsh discipline on their child, it could actually exacerbate the problem according to the social cognitive information-processing model of aggression. Harsh parenting environments actually reinforce children to employ the same aggressive behaviours to deal with problems,[38] as they perceive the behaviour as reasonable and a correct method of solving problems. Negative comments from parents towards children already exhibiting aggressive behaviours can make it harder for children to develop positive problem-solving methods, including ways to effectively manage aggression as they grow older. And thus, rather than benefiting the child, disclosing the results from this screening test could actually exacerbate the problem and increase aggression levels.[39] This contradicts the fundamental point of screening. 

     To summarise, there are a wide range of ethical principles with screening children to predict the risk of CD development, including consent, the four principles, parental behaviour towards the child, and the psychosocial phenomenon of the self-fulfilling prophecy.

​

Conclusion

​

     Conduct disorders (CD) are a group of psychiatric disorders where violent and harmful behaviour to both the individual and others is common.[1] A conduct diagnosis often leads to a diagnosis of Antisocial Personality Disorder (ASPD) in adulthood. Research has identified multiple genes and environmental risk factors potentially associated with CD development Thus, theoretically, we could use Polygenic Risk Scores (PRS) to pick up children who are at a higher risk of displaying violent or aggressive phenotypes linked to conduct disorders in the future. This could lead to early intervention to improve CD prognosis, and mitigate any negative future outcomes. Despite these advantages, the biological basis of the screening program is very new, and more research needs to be done in order to improve the accuracy of the screening test, especially with regards to using PRS diagnostically and causative genes of CD. 

     In conclusion, I believe that the disadvantages outweigh the advantages with regards to genetically testing children to predict CD. Whilst the idea is promising, the ethical and accuracy issues would ultimately cause more harm to the child and the wider society. However, continuing research into this area is vital to give a deeper insight into the causes of CD and ASPD. Understanding this is key to enable development of novel treatments. I believe this will be more beneficial than using a screening test to try and predict violent phenotypes, and thus a child’s risk of developing CD.

​Works Cited

1.  NICE. Conduct disorders in children and young people: What is it? NICE. Published April 2023. Accessed November 23, 2025. 

2. https://cks.nice.org.uk/topics/conduct-disorders-in-children-young-people/background -information/definition/ 

3. 2. Fairchild G, Hawes DJ, Frick PJ, et al. Conduct disorder. Nature Reviews Disease Primers. 2019;5(1). doi:https://doi.org/10.1038/s41572-019-0095-y 

4. 3. Deng J, Wang M, Shou Y, Gao Y. Core features of callous–unemotional traits: Network analysis of the inventory of callous–unemotional traits in offender and community samples. Journal of Clinical Psychology. 2020;77(6):1487-1498. doi:https://doi.org/10.1002/jclp.23090 

5. 4. Black DW. Antisocial personality disorder: current evidence and challenges. World Psychiatry. 2025;24(2):271-272. doi:https://doi.org/10.1002/wps.21321 5. Black D. The natural history of antisocial personality disorder. The Canadian Journal of Psychiatry. 2015;60(7):309-314. doi:https://doi.org/10.1177/070674371506000703 6. NICE. Conduct disoders in children and young people: Scenario: Managing suspected conduct disorders. NICE. Published April 2023. Accessed June 23, 2025. https://cks.nice.org.uk/topics/conduct-disorders-in-children-young-people/manageme nt/managing-suspected-conduct-disorders/ 

6. 7. Poldrack RA, Monahan J, Imrey PB, et al. Predicting Violent Behavior: What Can Neuroscience Add? Trends in Cognitive Sciences. 2017;22(2):111-123. doi:https://doi.org/10.1016/j.tics.2017.11.003 

7. 8. NICE. Recommendations | Antisocial behaviour and conduct disorders in children and young people: recognition and management | Guidance | NICE. 

8. www.nice.org.uk. Published March 27, 2013. Accessed June 24, 2025. https://www.nice.org.uk/guidance/cg158/chapter/Recommendations#pharmacological -interventions 

9. 9. Coker KL, Smith PH, Westphal A, Zonana HV, McKee SA. Crime and Psychiatric Disorders Among Youth in the US Population: An Analysis of the National Comorbidity Survey–Adolescent Supplement. Journal of the American Academy of Child & Adolescent Psychiatry. 2014;53(8):888-898.e2. 

10. doi:https://doi.org/10.1016/j.jaac.2014.05.007 

11. 10. Romeo R, Knapp M, Scott S. Economic cost of severe antisocial behaviour in children - and who pays it. British Journal of Psychiatry. 2006;188(6):547-553. doi:https://doi.org/10.1192/bjp.bp.104.007625 

12. 11. Scott S. An update on interventions for conduct disorder. Advances in Psychiatric Treatment. 2018;14(1):61-70. doi:https://doi.org/10.1192/apt.bp.106.002626 12. Salvatore JE, Dick DM. Genetic influences on conduct disorder. Neuroscience & Biobehavioral Reviews. 2019;91:91-101. 

13. doi:https://doi.org/10.1016/j.neubiorev.2016.06.034 

14. 13. Dick DM, Aliev F, Krueger RF, et al. Genome-wide association study of conduct disorder symptomatology. Molecular Psychiatry. 2011;16(8):800-808. 

15. doi:https://doi.org/10.1038/mp.2010.73 

16. 14. NCBI. C1QTNF7 C1q and TNF related 7 [Homo sapiens (human)] - Gene - NCBI. Nih.gov. Published November 25, 2025. Accessed November 25, 2025. https://www.ncbi.nlm.nih.gov/gene/114905

17. 15. Diamant I, Clarke DB, Evangelista J, Lingam N, Ma’ayan A. Harmonizome 3.0: integrated knowledge about genes and proteins from diverse multi-omics resources. Nucleic Acids Research. 2025;53(D1):D1016-D1028. 

18. doi:https://doi.org/10.1093/nar/gkae1080 

19. 16. Rouillard AD, Gundersen GW, Fernandez NF, et al. The harmonizome: a collection of processed datasets gathered to serve and mine knowledge about genes and proteins. Database. 2016;2016:baw100. doi:https://doi.org/10.1093/database/baw100 

20. 17. Jakobsson ME, Małecki J, Falnes PØ. Regulation of eukaryotic elongation factor 1 alpha (eEF1A) by dynamic lysine methylation. RNA Biology. 2018;15(3):314-319. doi:https://doi.org/10.1080/15476286.2018.1440875 

21. 18. Malik JA, Lone R. Heat shock proteins with an emphasis on HSP 60. Molecular Biology Reports. 2021;48(10):6959-6969. 

22. doi:https://doi.org/10.1007/s11033-021-06676-4 

23. 19. Kolla NJ, Bortolato M. The Role of Monoamine Oxidase a in the Neurobiology of aggressive, antisocial, and Violent behavior: a Tale of Mice and Men. Progress in Neurobiology. 2020;194(1):101875. 

24. doi:https://doi.org/10.1016/j.pneurobio.2020.101875 

25. 20. Caspi A, McClay J, Moffitt TE, et al. Role of Genotype in the Cycle of Violence in Maltreated Children. Science (New York, NY). 2002;297(5582):851-854. doi:https://doi.org/10.1126/science.1072290 

26. 21. Foley DL, Eaves LJ, Wormley B, et al. Childhood Adversity, Monoamine Oxidase A Genotype, and Risk for ConductDisorder. Archives of General Psychiatry. 2004;61(7):738. doi:https://doi.org/10.1001/archpsyc.61.7.738 

27. 22. Wesseldijk LW, Bartels M, Vink JM, et al. Genetic and environmental influences on conduct and antisocial personality problems in childhood, adolescence, and adulthood. European Child & Adolescent Psychiatry. 2017;27(9):1123-1132. doi:https://doi.org/10.1007/s00787-017-1014-y 

28. 23. Tesli N, Jaholkowski P, Haukvik UK, et al. Conduct disorder - a comprehensive exploration of comorbidity patterns, genetic and environmental risk factors. Psychiatry Research. 2024;331:115628. 

29. doi:https://doi.org/10.1016/j.psychres.2023.115628 

30. 24. National Institute for Health and Care Excellence. Antisocial behaviour and conduct disorders in children and young people: recognition and management. PubMed. Published online 2017. Accessed November 23, 2025. 

31. https://pubmed.ncbi.nlm.nih.gov/32073810/ 

32. 25. Dean K, Stevens H, Mortensen PB, Murray RM, Walsh E, Pedersen CB. Full Spectrum of Psychiatric Outcomes Among Offspring With Parental History of Mental Disorder. Archives of General Psychiatry. 2010;67(8):822. 

33. doi:https://doi.org/10.1001/archgenpsychiatry.2010.86 

34. 26. Choi SW, Mak TSH, O’Reilly PF. Tutorial: A guide to performing polygenic risk score analyses. Nature Protocols. 2020;15(9):2759-2772. 

35. doi:https://doi.org/10.1038/s41596-020-0353-1 

36. 27. Gatti U, Grattagliano I, Rocca G. Evidence-based psychosocial treatments of conduct problems in children and adolescents: an overview. Psychiatry, Psychology and Law. 2019;26(2):171-193. doi:https://doi.org/10.1080/13218719.2018.1485523 

37. 28. Frach L, Barkhuizen W, Allegrini AG, et al. Examining intergenerational risk factors for conduct problems using polygenic scores in the norwegian mother, father and

38. child cohort study: Molecular Psychiatry. Molecular Psychiatry. 2024;29. doi:https://doi.org/10.1038/s41380-023-02383-7 

39. 29. Siena LM, Baccolini V, Riccio M, et al. Weighing the evidence on costs and benefits of polygenic risk-based approaches in clinical practice: A systematic review of economic evaluations. The American Journal of Human Genetics. 

40. 2025;112(8):1735-1753. doi:https://doi.org/10.1016/j.ajhg.2025.05.012 30. Deo Mujwara, Kintzle J, Domenico PD, Busby GB, Giordano Bottà. Cost-effectiveness analysis of implementing polygenic risk score in a workplace cardiovascular disease prevention program. Frontiers in Public Health. 2023;11:https://www.frontiersin.org/journals/public-health/articles/10.3389/fpubh.2023 .1139496/full. doi:https://doi.org/10.3389/fpubh.2023.1139496 

41. 31. Swami N, Yamoah K, Mahal BA, Dee EC. The right to be screened: Identifying and addressing inequities in genetic screening. The Lancet Regional Health - Americas. 2022;11:100251. doi:https://doi.org/10.1016/j.lana.2022.100251 

42. 32. Dhamnetiya D, Jha RP, Shalini S, Bhattacharyya K. How to Analyze the Diagnostic Performance of a New Test? Explained with Illustrations. Journal of Laboratory Physicians. 2021;14(1):90-98. doi:https://doi.org/10.1055/s-0041-1734019 

43. 33. Hill LG, Coie JD, Lochman JE, Greenberg MT. Effectiveness of Early Screening for Externalizing Problems: Issues of Screening Accuracy and Utility. Journal of Consulting and Clinical Psychology. 2004;72(5):809-820. 

44. doi:https://doi.org/10.1037/0022-006x.72.5.809 

45. 34. Dretzke J, Frew E, Barlow J, Steward-Brown S, al et. The effectiveness and cost-effectiveness of parent training/education programmes for the treatment of conduct disorder, including oppositional defiant disorder, in children. Health Technol Assess. 2005;9(50). doi:https://doi.org/10.3310/hta9500 

46. 35. Zhu L, Zhang S, Lu Z. Respect for Autonomy: Seeking the Roles of Healthcare Design From the Principle of Biomedical Ethics. HERD: Health Environments Research & Design Journal. 2020;13(3):193758672090850. 

47. doi:https://doi.org/10.1177/1937586720908508 

48. 36. NHS. Children and young people. nhs.uk. Published October 2017. Accessed June 23, 2025. https://www.nhs.uk/tests-and-treatments/consent-to-treatment/children/ 37. Mertens M. The self-fulfilling prophecy in medicine. Theoretical Medicine and Bioethics. 2024;45:363-385. doi:https://doi.org/10.1007/s11017-024-09677-z 38. Pakaslahti L. Children’s and adolescents’ aggressive behavior in context. Aggression and Violent Behavior. 2000;5(5):467-490. 

49. doi:https://doi.org/10.1016/s1359-1789(98)00032-9 

50. 39. Yang Q, Xie R, Zhang R, Ding W. Harsh Childhood Discipline and Developmental Changes in Adolescent Aggressive Behavior: The Mediating Role of Self-Compassion. Behavioral sciences. 2023;13(9):725-725. 

51. doi:https://doi.org/10.3390/bs13090725