Lysergic Acid Diethylamide (LSD) and the Heart: Exploring the Potential Impacts of LSD on Cardiovascular Function

Summary

This review examines how LSD affects the heart and blood vessels. While some evidence suggests LSD might protect against heart disease by reducing inflammation and blood clots, acute use can dangerously raise heart rate and blood pressure, and cause blood vessel constriction. Regular low-dose use raises concerns about potential valve damage. More research is needed to understand the full cardiovascular safety of LSD before it can be considered for medical use.

Background

LSD is an ergot-derived psychedelic agent that acts on dopaminergic, adrenergic, and serotonergic pathways. While acute ingestion causes tachycardia and hypertension, speculative evidence suggests potential cardioprotective effects through chronic peripheral antagonism of 5-HT2A receptors.

Objective

This review explores the mechanisms by which LSD may influence cardiovascular health, examining both potential cardioprotective effects and adverse cardiovascular impacts across different dosing patterns and exposure durations.

Results

LSD demonstrates dose-dependent cardiovascular effects: acute high-dose usage causes tachycardia, hypertension, and potentially dangerous vasospasm; chronic peripheral antagonism of 5-HT2A receptors theoretically reduces platelet aggregation and smooth muscle proliferation; however, chronic microdosing raises concerns about 5-HT2B receptor activation and valvular heart disease risk.

Conclusion

LSD exhibits complex and contradictory cardiovascular effects that require further investigation. While chronic peripheral antagonism may provide cardioprotective benefits, risks of acute vasospasm at high doses and potential valvular pathology with microdosing warrant caution. Clinical trials and detailed epidemiological studies are needed to clarify LSD’s cardiovascular safety profile.
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