- Researchers found 74 genome locations linked to anxiety symptoms, 39 newly identified
- The study analysed genetic data from 693,869 people of European ancestry
- Genetic variation explains about 6% of anxiety symptom severity differences
Researchers have identified 74 locations in the genome where genetic differences were linked to anxiety symptoms, 39 of which were newly linked with anxiety, showing the largest number anxiety-related genetic associations. Researchers, led by those at King's College London and QIMR Berghofer Medical Research Institute in Australia, analysed genetic data on anxiety symptoms in 6,93,869 people of European ancestry. The genome wide association study (GWAS) identified which genetic differences occur more often in people with more severe anxiety symptoms. A GWAS is a research method that helps identify genetic variants linked to a trait or disease.
The findings, published in the journal Nature Human Behaviour, show the largest number of genetic associations with anxiety identified to date, the team said.
By linking genetic data to severity of symptoms rather than a 'yes' or 'no' category of a clinical diagnosis, the study brings a new understanding to the biological continuum behind anxiety that can range from healthy stress responses to debilitating disorder, they said.
First author Megan Skelton, research fellow at King's College London, said, "This is an exciting step forward in understanding how anxiety risk can be influenced by biological processes. It's important to highlight that genetics interplay with life experiences, social contexts, and psychological factors to shape individual risk." The result meant that one with a high genetic risk may not develop anxiety, while one with a low genetic risk could, Skelton said.
"The rise in anxiety rates points to environmental factors, as genetics don't change much across generations, so reducing anxiety in the population will require these factors to be addressed," the first author said.
Skelton added that at the same time, understanding genetic risk can help identifying those more sensitive to environmental influences, eventually contributing to more effective prevention and treatment strategies.
The study's results also 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 involved in how nerve cells communicate with each other.
The researchers also found that common genetic variation explains around six per cent of the differences in anxiety symptom severity between people, leaving substantial room for environmental influences, gene-environment interactions, and undetected genetic effects, they said.
Lead author Thalia Eley, professor of developmental behavioural genetics at King's College London, 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," Eley said.
"We hope our findings encourage a new wave of large-scale analyses to accelerate our progress in understanding the genetic architecture of anxiety," the lead author said.
The study also found 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.
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