A large Australian study suggests that atypical depression is genetically, metabolically and clinically distinct, with poorer response to SSRIs and SNRIs.
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Psychiatric disorders share genetic variants that cluster into five main factors. Understanding shared biology could improve treatment, but more diverse genetic data urgently needed.
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Recent research suggests that lower IQ and cognitive performance link to higher alcohol use disorder risk, but education and societal factors can amplify or reduce this vulnerability, not genetics alone.
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This study used Mendelian randomisation to test potential causal relationships between depression and 137 traits. Depression liability was linked to somatic diseases, inflammation, suicide risk, insomnia, lower cognitive function and functional impairments, though findings require validation.
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This twin study of nearly 14,000 UK adolescents found that body dissatisfaction at age 16 was linked to eating disorder symptoms at 21 and depression at 26. Comparing twins helped researchers show these were likely causal relationships, not just correlations, though genetics also played a substantial role.
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How often do people with eating disorders switch diagnoses, recover, or relapse? This large Danish study follows more than 10,000 people over nearly a decade, uncovering patterns of remission and genetic vulnerability that could help shape more personalised care.
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Self-harm is common among adolescents and a strong predictor of suicide risk. A major new cohort study in the British Journal of Psychiatry explores how genetic risk and brain differences might explain who’s most at risk, and why.
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A big new study suggests that certain genetic traits—like insomnia risk and neuroticism—may make depression harder to treat, while protective traits include education and cognitive ability.
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Why do people who were maltreated as children face higher risks of both mental and physical illness? A new Mendelian randomisation study suggests that metabolic markers — like triglycerides and blood sugar — may be part of the chain connecting adversity to later multimorbidity.
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Psychiatric disorders are highly heritable, but are the genes we identify in GWAS the same ones our medications target? This new study digs into the overlap and raises questions about how we develop treatments.
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