PulseExploreJournal ClubDebatesTrendingResearchersJournals
Instagram
HomeExploreJournal ClubTrending
Synapse
⌘+K
Synapse
February 2, 20260 citationsOpen Access

Botanic Cannabinoids and the Endocannabinoid System: A Mechanistic Model for Motion Sickness Intervention

View Full Paper
DDDavid A Dawson

Key Points

  • The paper aims to explore how botanic cannabinoids can intervene in motion sickness via the endocannabinoid system.
  • Review of existing literature on motion sickness and cannabinoids
  • Theoretical modeling of cannabinoid effects on the endocannabinoid system
  • Identification of phytochemical candidates for intervention
  • Proposes that cannabinoids may normalize anandamide levels and enhance CB1 receptor function
  • Suggests that cannabinoid modulation can attenuate vestibular hyperactivation and improve gastric rhythm
  • Identifies potential biomarkers to evaluate the effectiveness of cannabinoid interventions in clinical studies

Abstract

Motion sickness is a highly prevalent condition characterized by nausea, vomiting, and autonomic symptoms triggered by sensory conflict between the vestibular and visual systems. Current pharmacological treatments, including anticholinergics and antihistamines, often produce undesirable side effects such as sedation and dry mouth, and do not address the underlying neurophysiological dysregulation. The endocannabinoid system is a key neuromodulator of stress responses, emesis control, and homeostatic balance. Evidence from parabolic flight studies indicates that motion-susceptible individuals exhibit reduced circulating anandamide levels and downregulation of CB1 receptor expression, suggesting that hypoactivity of the endocannabinoid system contributes to symptom development. This theoretical paper proposes that targeted modulation of the ECS via botanic cannabinoids—such as Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD)—and selected terpenes may restore ECS tone, attenuate vestibular hyperactivation, normalize gastric rhythm, and reduce motion-induced nausea. We outline a mechanistic model for cannabinoid intervention, discuss key phytochemical candidates, and identify biomarker-driven endpoints for future clinical studies.

Ask AI
Helpful
Bookmark
Share
View Full Paper

Cite This Study

David A Dawson (2025) studied this question.

synapsesocial.com/papers/6980fdc7c1c9540dea80f6bahttps://doi.org/10.5281/zenodo.18409538
Ask AI
Helpful
Bookmark
Share
View Full Paper