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

LSD acts primarily on 5-HT2A receptors in the brain and periphery, producing psychedelic effects. Although acute ingestion raises heart rate and blood pressure, and large recreational doses can cause cardiovascular or cerebrovascular events, chronic peripheral antagonism of 5-HT2A receptors may reduce atherosclerosis and thrombosis by decreasing platelet aggregation and vascular smooth muscle cell proliferation. Central sympathetic stimulation from microdosing LSD may also reduce chronic inflammation, a contributor to cardiovascular disease, through anti-inflammatory effects and increased cortical synaptogenesis.

Study at a glance

Abstract

Lysergic acid diethylamide (LSD) is an ergot-derived psychedelic agent that produces perceptual and psychic effects of heightened sensations by acting on the dopaminergic, adrenergic, and serotonergic pathways in the brain and periphery, with 5-hydroxytryptamine 2A (5-HT2A) as the primary target molecule. Its action on these receptors in the central nervous system is comparatively well studied with respect to the psychedelic effects; however, there is speculative evidence of cardioprotective effects in the current literature attributed to the usage of this substance, even though acute ingestion causes tachycardia and hypertension, just like other psychedelics. Larger recreational doses of the drug can lead to cardiovascular and cerebrovascular incidents, but chronic peripheral antagonism of 5-HT2A receptors by the drug reduces atherosclerotic and thrombotic processes due to a reduction in platelet aggregation and vascular smooth muscle cell proliferation. Central sympathetic stimulation caused by micro-dosing of LSD imparts anti-inflammatory effects and increases cortical synaptogenesis, leading to reduced chronic inflammation implicated in causing cardiovascular diseases.