Antidepressants taken by 8.6m people linked to increased motor neurone disease risk

Antidepressants, taken by around 8.6 million people in the UK, may increase the risk of motor neurone disease (MND) by up to 26 per cent, according to a major study.

Scandinavian researchers also found an increased risk linked to other commonly prescribed drugs, including anxiolytics (used to treat anxiety disorders), sedatives, and sleeping pills.

Motor neurone disease—of which amyotrophic lateral sclerosis (ALS) is the most common form—is a progressive, incurable, muscle-wasting condition that eventually stops a person from being able to move, talk, and even eat. It affects around 5,000 adults in the UK and was famously suffered by physicist Stephen Hawking.

The study suggests that being prescribed any of these medications just twice over a lifetime could increase the risk of developing MND by up to 34 per cent. The elevated risk remained even when the drugs were taken more than five years before diagnosis.

The research, conducted in Sweden, analysed 1,057 patients diagnosed with the disease between January 2015 and July 2023, with an average age of 67. Researchers examined their medication history and followed the patients for an average of 1.33 years after diagnosis.

Each patient was matched with a group of healthy controls to identify differences that could help explain the development of the disease.

Prescribed use of anxiolytics was associated with a 34 per cent increased risk of developing MND. Antidepressants were linked to a 26 per cent rise in risk, while sedatives and sleeping pills were associated with a 21 per cent increase.

Use of antidepressants before diagnosis was also associated with a faster rate of functional decline.

However, other scientists have urged caution in interpreting the findings, suggesting the apparent link may reflect an underlying connection between mental health conditions and MND, rather than a direct effect of the medication.

Professor Ammar Al-Chalabi, a specialist in complex disease genetics at King’s College London, said: “Association is not causation. That is especially important here.

“We already know that some of the genetic variants that nudge people towards schizophrenia, for example, overlap with variants that nudge people towards ALS.

“It may not be use of the medication that increases ALS risk, but that the need for the medication is a signal that someone is already at increased genetic risk.”

The study authors, from several Scandinavian institutions, noted that depression, anxiety, and sleep disturbances have been shown to have detrimental effects on brain cells, resulting in structural changes that occur alongside ALS.

Lead author Dr Charilaos Chourpiliadis said more research is needed to understand the connection fully. However, he added: “Closer monitoring in younger patients with psychiatric symptoms might lead to an earlier ALS diagnosis.”

Dr Brian Dickie, chief scientist at the MND Association, pointed out that the most common genetic risk factor for ALS—a repeat expansion in the C9orf72 gene—is especially prevalent in Scandinavian populations.

“A study in the Swedish population will most likely have a higher proportion of people with this particular genetic form of the disease,” he said.

“Not only would higher use of psychiatric medication be likely, but this genetic form is also linked with faster progression and shorter survival, which could explain the association between psychiatric medication and more aggressive disease.”