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Psychiatric Medication Use Associated with Increased Risk and Accelerated Progression of ALS

Psychiatric Medication Use Associated with Increased Risk and Accelerated Progression of ALS

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A Swedish study links the use of common psychiatric medications to an increased risk of ALS and faster disease progression, suggesting early psychiatric symptoms may be related to ALS development.

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Recent research from Sweden has revealed that the use of common psychiatric medications—such as anxiolytics (anti-anxiety drugs), hypnotics and sedatives, and antidepressants—is linked to a heightened risk of developing amyotrophic lateral sclerosis (ALS), as well as worse outcomes following diagnosis. A nationwide study led by Karolinska Institutet analyzed health data spanning from 2015 to 2023, including over a thousand ALS cases and thousands of controls, along with sibling and spousal comparisons.

The study found that individuals prescribed anxiolytics had a 34% increased likelihood of being diagnosed with ALS. Hypnotics and sedatives were associated with a 21% increased risk, and antidepressants correlated with a 26% increase. Notably, patients who were already diagnosed with ALS and had a history of using these medications faced a 52% higher risk of death or invasive ventilation. The hazard was even higher for antidepressant users, who had a 72% increased risk.

Furthermore, prediagnostic use of antidepressants was linked to a faster decline in functional ability, as measured by ALS functional rating scales. The researchers suggest that these findings might reflect a complex relationship where psychiatric symptoms or disorders could either be early signs of ALS or share underlying mechanisms with motor neuron degeneration. Possible biological factors such as dysregulation of the hypothalamic-pituitary-adrenal axis, neuroinflammation, and glial activation are areas identified for further investigation.

The study underscores the importance of carefully monitoring psychiatric medication use among populations at risk and considering the potential implications for ALS development and progression. While the findings do not establish causality, they highlight a significant association that warrants further scientific exploration—possibly illuminating new insights into ALS pathology and early detection strategies.

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