Researchers at QIMR Berghofer and King's College London have analysed genetic data on anxiety symptoms in 693,869 people of European ancestry, revealing new insights into the genetic pathways involved in the condition.
Published in Nature Human Behaviour , the study has found the largest number of genetic associations with anxiety to date. By linking genetic data to severity of symptoms rather than the yes/no category of a clinical diagnosis, it brings new understanding to the biological continuum behind anxiety that
can range from healthy stress responses to debilitating disorder.
Anxiety disorders are the most prevalent mental health conditions worldwide and rates are rising. Symptoms vary in their intensity and type throughout the population, reflecting the evolutionary function that fear and worry serve by enabling vigilance and caution in response to potential threats.
The new research is a genome wide association study (GWAS) and analyses the DNA of many people - in this case nearly 700,000 - to identify which genetic differences occur more often in those who experience more severe anxiety symptoms.
Professor Thalia Eley, Professor of Developmental Behavioural Genetics at Institute of Psychiatry, Psychology & Neuroscience (IoPPN) King's College London and lead author on the study said: "Despite the public health impact of anxiety, progress in the understanding of its genetics lags behind other major mental health conditions. Given the high and rising rates of anxiety, especially in young adults, it is more important than ever to improve our ability to identify and understand sources of risk. We hope our findings encourage a new wave of large-scale analyses to accelerate our progress in understanding the genetic architecture of anxiety."
The study identified 74 locations in the genome where genetic differences were linked to anxiety symptoms. Around half of these have been reported in previous anxiety GWAS, but the remainder (39 of the loci) were novel.
Beyond identifying the largest number of anxiety-associated loci to date, the results provide support for the role of certain genes in anxiety, such as PCLO and SORCS3. Many of the implicated genes are particularly active in brain tissue and are involved in how nerve cells communicate with each other. The analysis also found that common genetic variation explains around 6% of the differences in anxiety symptom severity between people, leaving substantial room for environmental influences, gene-environment interactions, and undetected genetic effects.
Dr Megan Skelton, Research Fellow at IoPPN, King's College London and first author on the study said: "This is an exciting step forward in understanding how anxiety risk can be influenced by biological processes. It's important to highlight that even someone with a very high genetic risk might not develop anxiety, and someone with a low genetic risk could. Genetic influences work alongside and interplay with life experiences, social contexts, and psychological factors to shape individual risk. The rise we're seeing in anxiety rates points to environmental factors, and understanding genetic risk can help us to identify who may be most vulnerable to those factors, ultimately contributing to more
effective prevention and treatment strategies."
The study also calculated polygenic scores for anxiety, which summarise each individual's genetic risk. The scores were created using the European-ancestry GWAS results, in separate samples of people from European, African and South Asian populations, and explained 1.2% to 2.9% of the variance in anxiety symptom severity. The polygenic risk score results provide some support for shared genetic influences across these groups, but ancestry-specific GWAS remain necessary to identify population-specific genetic risk. At present, there are not enough datasets available with information on both anxiety symptoms and genetics in people with African or South Asian ancestry to run statistically meaningful GWAS.
There was a broad range of significant genetic correlations of anxiety with both mental and physical health conditions, including depression, irritable bowel syndrome, chronic pain, coronary artery disease, endometriosis and migraine.
Dr Brittany Mitchell , Team Head of The Complex Trait Genomics group at QIMR Berghofer and co-first author on the study said: "These correlations highlight the interconnection between mental
and physical health. Importantly, while some shared genetic variants may increase risk for both a physical health condition and more severe anxiety symptoms, it's also true that living with chronic pain or illness can contribute to anxiety symptoms. Our findings don't reveal causation or the direction of effect, but they do open up important questions for future research."
The study was an output of the Psychiatric Genomics Consortium, which is a group of scientists that focus on meta- and mega-analyses of psychiatric genetic studies. This phase of work by the Consortium was partially funded by the US National Institute for Health (NIH). The researchers were supported by a range of bodies including the Wellcome Trust, the Medical Research Council (MRC), the National Institute for Health and Care Research (NIHR) Maudsley Biomedical Research Centre and the Australian National Health and Medical Research Council.
'Genome-wide analyses of quantitative generalised anxiety symptom severity' by Skelton, M. et al (2026) was published in Nature Human Behaviour. https://doi.org/10.1038/s41562-026-02476-7
This media release was kindly produced and distributed by the team at King's College London.
