Xu Eileen Y, Grimes Poppy Z, Kwong Alex S F, Lawrie Stephen M, Whalley Heather C
Division of Psychiatry, University of Edinburgh, Edinburgh, United Kingdom.
MRC Integrative Epidemiology Unit, University of Bristol, Bristol, United Kingdom.
medRxiv. 2025 Jul 8:2025.07.08.25331098. doi: 10.1101/2025.07.08.25331098.
Understanding adolescent depression risk is vital for mitigating its long-term adverse effects. Though polygenic risk scores (PRS) explain increasing proportions of heritable risk, environmental risk remains challenging to quantify, hindering prediction. Existing prediction models often examine environmental risk in isolation, and vary in the number of predictors used - ranging from 8 to 800+ variables, limiting generalisability. Here, we develop a model predicting adolescent depression symptoms (depRS) from a review of key environmental risk factors and assess depRS and PRS prediction of lifetime depression at 2-year follow-up. Using data from the Adolescent Brain Cognitive Development study (N=7 029), we generated PRS in European, African, American Admixed and East Asian ancestries from a recent trans-ancestry genome-wide study of major depression. We trained depRS using Elastic Net regression with 10-fold cross-validation to predict follow-up depression symptoms (age 11-13 years) from 23 baseline predictors (age 9-11 years), identified from systematic reviews with meta-analyses of risk factors. Parental depression, abuse, sleep duration and dieting emerged as top predictors of depression symptoms; depRS explained 16.9% of overall variance. depRS showed better-than-chance classification of parent-reported (AUC=0.68; 95% CI 0.63-0.72) lifetime depression at follow-up, associating with greater depression odds (OR=1.73; 95% CI: 1.57-1.91) than PRS (OR=1.42; 95% CI: 1.25-1.62). Combining depRS and PRS maximised accuracy (AUC=0.70; 95% CI 0.65-0.78). Though external validation of depRS across geographically and gender diverse cohorts is needed to assess generalisability, findings highlight sleep and dieting as potential targets for mitigating risk and demonstrate the utility of genetic scores in models predicting adolescent depression.
了解青少年抑郁症风险对于减轻其长期不良影响至关重要。尽管多基因风险评分(PRS)解释了越来越大比例的遗传风险,但环境风险的量化仍然具有挑战性,这阻碍了预测。现有的预测模型通常单独研究环境风险,并且所使用的预测变量数量各不相同——从8个到800多个变量不等,这限制了模型的通用性。在此,我们通过对关键环境风险因素的综述开发了一个预测青少年抑郁症状的模型(depRS),并在2年随访时评估depRS和PRS对终生抑郁症的预测。利用青少年大脑认知发展研究的数据(N = 7029),我们从最近一项跨种族全基因组重度抑郁症研究中生成了欧洲、非洲、美国混血和东亚血统的PRS。我们使用弹性网络回归和10折交叉验证训练depRS,以从23个基线预测变量(9至11岁)预测随访时的抑郁症状(11至13岁),这些预测变量是通过对风险因素进行荟萃分析的系统综述确定的。父母抑郁、虐待、睡眠时间和节食成为抑郁症状的首要预测因素;depRS解释了总体方差的16.9%。depRS在随访时对父母报告的终生抑郁症的分类表现优于随机水平(AUC = 0.68;95%CI 0.63 - 0.72),与PRS相比,其抑郁症几率更高(OR = 1.73;95%CI:1.57 - 1.91)(OR = 1.42;95%CI:1.25 - 1.62)。将depRS和PRS相结合可使准确性最大化(AUC = 0.70;95%CI 0.65 - 0.78)。尽管需要在地理和性别多样化的队列中对depRS进行外部验证以评估其通用性,但研究结果突出了睡眠和节食作为减轻风险的潜在目标,并证明了基因评分在预测青少年抑郁症模型中的效用。