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Anti-depressant medication use and C-reactive protein: results from two population-based studies
Mark Hamer1, G D Batty, Michael G Marmot
1Department of Epidemiology and Public Health, University College London, London, UK. m.hamer@ucl.ac.uk
Insights
Antidepressant use, particularly tricyclic antidepressants, is linked to higher inflammation markers. This suggests a potential pathway for increased cardiovascular disease risk, independent of mental health conditions.
Area of Science:
- Cardiovascular Health
- Psychopharmacology
- Inflammation Research
Background:
- Antidepressant medications are widely prescribed.
- A potential link exists between antidepressant use and cardiovascular disease (CVD).
- Systemic inflammation may mediate this association.
Purpose of the Study:
- To investigate the association between antidepressant use and C-reactive protein (CRP), a marker of systemic inflammation.
- To explore if inflammation is a potential pathway linking antidepressant use to CVD.
- To examine this association in two independent population-based studies.
Main Methods:
- Utilized data from the Scottish Health Surveys (SHS) and the Whitehall II study.
- Assessed antidepressant use based on the British National Formulary.
- Measured C-reactive protein (CRP) levels in blood samples.
- Employed multivariate logistic regression and longitudinal analysis.
Main Results:
- Tricyclic antidepressant (TCA) users showed a higher risk of elevated CRP (OR=1.52).
- Selective serotonin reuptake inhibitor (SSRI) users did not show a significant association with elevated CRP (OR=1.07).
- Longitudinal analysis confirmed an association between antidepressant use and subsequent CRP levels.
Conclusions:
- Antidepressant use is associated with elevated systemic inflammation.
- This inflammation is independent of mental illness symptoms and cardiovascular comorbidities.
- Systemic inflammation may represent a mechanism by which antidepressants increase CVD risk.
Abstract:
The use of anti-depressant medication has been linked to cardiovascular disease (CVD). We examined the association between anti-depressant medication use and a marker of low grade systemic inflammation as a potential pathway linking anti-depressant use and CVD in two population based studies. Data were collected in a representative sample of 8131 community dwelling adults (aged 47.4±15.9 years, 46.7% male) from the Scottish Health Surveys (SHS). The use of anti-depressant medication was coded according to the British National Formulary and blood was drawn for the measurement of C-reactive protein (CRP). In a second study, we attempted to replicate our findings using longitudinal data from the Whitehall II study (n=4584, aged 55.5±5.9 years, mean follow-up 5.5 years). Antidepressants were used in 5.6% of the SHS sample, with selective serotonin reuptake inhibitors (SSRIs) being the most common. There was a higher risk of elevated CRP (>3 mg/L) in users of tricyclic antidepressant (TCA) medication (multivariate adjusted odds ratio (OR)=1.52, 95% CI, 1.07-2.15), but not in SSRI users (multivariate adjusted OR=1.07, 95% CI, 0.81-1.42). A longitudinal association between any antidepressant use and subsequent CRP was confirmed in the Whitehall cohort. In summary, the use of anti-depressants was associated with elevated levels of systemic inflammation independently from the symptoms of mental illness and cardiovascular co-morbidity. This might be a potential mechanism through which antidepressant medication increases CVD risk. Further data are required to explore the effects of dosage and duration of antidepressant treatment.
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