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Associations of antidepressants and antipsychotics with lipid parameters: Do / genes play a role? A UK population-based study. | LitMetric

AI Article Synopsis

Article Abstract

Background: Dyslipidaemia is an important cardiovascular risk factor for people with severe mental illness, contributing to premature mortality. The link between antipsychotics and dyslipidaemia is well established, while evidence on antidepressants is mixed.

Aims: To investigate if antidepressant/antipsychotic use was associated with lipid parameters in UK Biobank participants and if and genetic variation plays a role.

Methods: Review of self-reported prescription medications identified participants taking antidepressants/antipsychotics. Total, low-, and high-density lipoprotein cholesterol (L/HDL-C) and triglycerides derived from blood samples. and metabolic phenotypes were assigned from genetic data. Linear regression investigated aims, adjusted for key covariates.

Results: Of 469,739 participants, 36,043 took antidepressants (53% female, median age 58, 17% taking cholesterol-lowering medications) and 3255 took antipsychotics (58% female, median age 57, 27% taking cholesterol-lowering medications). Significant associations were found between use of each amitriptyline, fluoxetine, citalopram/escitalopram, sertraline, paroxetine and venlafaxine with higher total cholesterol, LDL-C, and triglycerides and lower HDL-C, compared to participants not taking each medication. Venlafaxine was associated with the worst lipid profile (total cholesterol, adjusted mean difference: 0.21 mmol/L, 95% confidence interval (CI): 0.17 to 0.26,  < 0.001). Antipsychotic use was significantly associated with lower HDL-C and higher triglycerides. In participants taking sertraline, intermediate metabolisers had higher HDL-C (0.05 mmol/L, 95% CI: 0.01 to 0.09,  = 0.007) and lower triglycerides (-0.17 mmol/L, 95% CI: -0.29 to -0.05,  = 0.007), compared to normal metabolisers.

Conclusions: Antidepressants were significantly associated with adverse lipid profiles, potentially warranting baseline and regular monitoring. Further research should investigate the mechanistic pathways underlying the protective effects of the intermediate metaboliser phenotype on HDL-C and triglycerides in people taking sertraline.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10101178PMC
http://dx.doi.org/10.1177/02698811231152748DOI Listing

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