NSAIDs may block antidepressants
2nd May 2011 - Medical Observer
Catherine Hanrahan all articles by this author
COMMON anti-inflammatory drugs may antagonise the effects of antidepressants, scientists have found.
US researchers analysed the effects of ibuprofen and other NSAIDs on citalopram in an animal model of depression and in a human population.
They showed that in 1500 patients with depression who took citalopram over a 12-week period, 55% of those who had taken an NSAID at least once were treatment-resistant to citalopram, compared with 45% who had not taken an NSAID.
The clinical data was supported in a mouse model, where all the NSAIDs and analgesics tested blocked the antidepressant effect of citalopram.
In vitro studies showed the anti-inflammatories antagonised p11, a biochemical marker for depression. This protein was regulated by frontal cortical levels of the cytokines tumour necrosis factor alpha and interferon gamma, which were also abolished by ibuprofen.
Clinical pharmacologist Professor Ric Day, from St Vincent’s Hospital and the University of NSW, said the findings may explain why a large proportion of patients are resistant to antidepressants.
However, Professor Ian Hickie, executive director of the Brain and Mind Research Institute, University of Sydney, said the results were contrary to other cytokine hypothesis studies. “Most people have tended to think the opposite – that cytokines appear to be increased in some people with depression and might be driving… things like sleep disturbance, changed body temperature and lack of energy,” he said.
The clinical data could be confounded if taking NSAIDs indicated medical conditions which made patients less likely to respond to standard treatments, he added.
PNAS 2011, online first
US researchers analysed the effects of ibuprofen and other NSAIDs on citalopram in an animal model of depression and in a human population.
They showed that in 1500 patients with depression who took citalopram over a 12-week period, 55% of those who had taken an NSAID at least once were treatment-resistant to citalopram, compared with 45% who had not taken an NSAID.
The clinical data was supported in a mouse model, where all the NSAIDs and analgesics tested blocked the antidepressant effect of citalopram.
In vitro studies showed the anti-inflammatories antagonised p11, a biochemical marker for depression. This protein was regulated by frontal cortical levels of the cytokines tumour necrosis factor alpha and interferon gamma, which were also abolished by ibuprofen.
Clinical pharmacologist Professor Ric Day, from St Vincent’s Hospital and the University of NSW, said the findings may explain why a large proportion of patients are resistant to antidepressants.
However, Professor Ian Hickie, executive director of the Brain and Mind Research Institute, University of Sydney, said the results were contrary to other cytokine hypothesis studies. “Most people have tended to think the opposite – that cytokines appear to be increased in some people with depression and might be driving… things like sleep disturbance, changed body temperature and lack of energy,” he said.
The clinical data could be confounded if taking NSAIDs indicated medical conditions which made patients less likely to respond to standard treatments, he added.
PNAS 2011, online first
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2nd May 2011
1:49pm