There is no clear evidence that depression is caused by low serotonin levels, research suggests.

The new review, which analysed existing studies, suggests the condition is not likely caused by a chemical imbalance, and calls into question what antidepressants do.

Researchers say their findings are important as studies show that as many as 85-90% of the public believes that depression is caused by low serotonin or a chemical imbalance.

Most antidepressants are selective serotonin reuptake inhibitors (SSRIs), and were originally said to work by correcting abnormally low serotonin levels.

There is no other accepted way by which antidepressants affect the symptoms of depression.

Lead author Joanna Moncrieff, a professor of psychiatry at UCL is a consultant psychiatrist at North East London NHS Foundation Trust (NELFT).

She said: ‘It is always difficult to prove a negative, but I think we can safely say that after a vast amount of research conducted over several decades, there is no convincing evidence that depression is caused by serotonin abnormalities, particularly by lower levels or reduced activity of serotonin.

‘The popularity of the “chemical imbalance” theory of depression has coincided with a huge increase in the use of antidepressants.

‘Prescriptions for antidepressants have risen dramatically since the 1990s, with one in six adults in England and 2% of teenagers now being prescribed an antidepressant in a given year.’

‘Many people take antidepressants because they have been led to believe their depression has a biochemical cause, but this new research suggests this belief is not grounded in evidence.’

Professor Moncrieff added: ‘Thousands of people suffer from side effects of antidepressants, including the severe withdrawal effects that can occur when people try to stop them, yet prescription rates continue to rise.

‘We believe this situation has been driven partly by the false belief that depression is due to a chemical imbalance.

‘It is high time to inform the public that this belief is not grounded in science.’

The umbrella review looked at all relevant studies that have been published in the most important fields of research on serotonin and depression.

In total, these involved tens of thousands of participants.

One of the findings was that research that compared levels of serotonin and its breakdown products in the blood or brain fluids did not find a difference between people diagnosed with depression and healthy people.

The authors also looked at studies where serotonin levels were artificially lowered in hundreds of people.

These studies have been cited as demonstrating that a serotonin deficiency is linked to depression.

But a review of the research available in 2007 and a sample of recent studies found that lowering serotonin in this way did not produce depression in hundreds of healthy volunteers.

Other studies looked at the effects of stressful life events and found that the more stressful life events a person had experienced, the more likely they were to be depressed.

One early study found a relationship between stressful events, the type of serotonin transporter gene a person had and the chance of depression.

However, larger, more comprehensive studies suggest this was a false finding.

These findings led the authors to conclude that there is ‘no support for the hypothesis that depression is caused by lowered serotonin activity or concentrations’.

Some evidence suggests that believing low mood is caused by a chemical imbalance leads people to have a pessimistic outlook on the likelihood of recovery, and the possibility of managing moods without medical help.

According to the research, there is also evidence from other studies that people who used antidepressants had lower levels of serotonin in their blood.

The scientists say this indicates that some evidence was consistent with the possibility that long-term antidepressant use reduces serotonin concentrations.

This may imply that the increase in serotonin that some antidepressants produce in the short term could lead to compensatory changes in the brain that produce the opposite effect in the long term.

Professor Moncrieff said: ‘We do not understand what antidepressants are doing to the brain exactly, and giving people this sort of misinformation prevents them from making an informed decision about whether to take antidepressants or not.’

The researchers caution that anyone considering withdrawing from antidepressants should seek the advice of a health professional.

The findings are published in Molecular Psychiatry.

A spokesman for the Royal College of Psychiatrists said: ‘Antidepressants will vary in effectiveness for different people, and the reasons for this are complex, which is why it’s important that patient care is based on each individual’s needs and reviewed regularly.

‘Continued research into treatments for depression is important to help us better understand how medications work as well as their effectiveness.

‘Medication should be available for anyone who needs it. We would not recommend for anyone to stop taking their antidepressants based on this review, and encourage anyone with concerns about their medication to contact their GP.’

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