How Motion Sickness Rewires Your Body's Chemistry
The secret to understanding motion sickness may lie not in the inner ear, but in the complex hormonal symphony it triggers within our bodies.
Imagine setting sail on a calm sea, only to be overcome by a wave of nausea, cold sweat, and dizziness. For centuries, this experience was shrouded in mystery. Today, scientists are unraveling this puzzle by examining what happens deep inside our bodies during motion sickness—a complex hormonal storm that reveals our body's profound confusion between perceived and actual motion.
At its core, motion sickness is not merely a fleeting discomfort but a physiological crisis triggered by a fundamental mismatch in sensory information. Your brain relies on three primary systems to navigate the world: the vestibular system in your inner ear (tracking movement and balance), your visual system (what you see), and proprioceptive receptors (sensing your body's position in space)1 5 .
Inner ear balance mechanism detecting motion and spatial orientation
Eyes providing information about stationary vs. moving environments
Body sensors detecting position and movement of limbs and torso
The most widely accepted theory, the sensory conflict theory, explains that motion sickness occurs when these systems report contradictory information to the brain1 5 . When you're reading in a moving car, for instance, your eyes (focused on a stationary page) tell your brain you're still, while your vestibular system detects the vehicle's motion. This neural mismatch activates a cascade of physiological responses, many of which are governed by the body's endocrine and nervous systems.
What's particularly fascinating is that this conflict doesn't just cause momentary discomfort. It can trigger a full-blown stress response involving multiple communication pathways between the brain and body, including anatomical connections through nerves like the vagus nerve, and hormonal signals released into the bloodstream4 .
When sensory conflict occurs, it doesn't just cause dizziness—it sends your body into a state of alarm, activating a complex hormonal cascade. Several key players have been identified in this physiological drama:
This primary stress hormone, released by the adrenal glands, shows dramatic shifts during motion sickness. In one study of student pilots, cortisol levels skyrocketed from average baseline measurements to over 29,000 pg·mL⁻¹ following a nauseogenic test8 . This indicates a powerful activation of the HPA axis (hypothalamic-pituitary-adrenal axis), the body's central stress response system.
This hormone, also known as antidiuretic hormone, is strongly linked to nausea and vomiting responses. Research suggests it may play a pivotal role in motion sickness, with higher baseline levels potentially predicting poorer adaptation to provocative motion8 .
Often called the "hunger hormone," ghrelin also appears involved in the motion sickness response. Elevated pre-exposure levels have been observed in individuals who struggle to adapt to motion stimuli, suggesting it may serve as a potential biomarker for susceptibility8 .
Recent research has revealed an intriguing connection between motion sickness and the gut-brain axis4 . The vagus nerve, which serves as a direct communication highway between the brain and gastrointestinal tract, may play a crucial role in conveying the distress signals that lead to nausea and vomiting. This bidirectional communication means that our gut feelings during motion sickness are more than just metaphor—they represent a real neurobiological conversation between our brain and digestive system.
To understand precisely how motion sickness affects our hormonal balance, let's examine a revealing 2025 study conducted with student pilots suffering from incapacitating airsickness8 .
The researchers designed a comprehensive study to track physiological changes during a standardized airsickness rehabilitation program:
The Coriolis Stress Test itself is a standardized procedure that typically involves rotating participants in a chair while they perform specific head movements—a reliable method for inducing motion sickness in laboratory conditions.
The findings revealed a compelling narrative of physiological adaptation and stress:
| Hormone/Biomarker | Initial CST Response | Final CST Response | Significance |
|---|---|---|---|
| Cortisol | Dramatic peak in all subjects (avg. 6288 to 29,861 pg·mL⁻¹) | Peak observed only in the one rehabilitation failure case | Indicates high stress during sickness; normalizes with successful adaptation |
| Vasopressin | Higher in the single fail-case participant | Not reported | May predict individual adaptation capacity |
| Ghrelin | Higher in the single fail-case participant | Not reported | Potential biomarker for susceptibility |
| 15-F2t-isoprostane | Elevated in all participants | Significantly reduced after rehabilitation | Suggests oxidative stress decreases with adaptation |
All participants initially vomited during the Coriolis Stress Test, yet after rehabilitation, the same test provoked no symptoms in six of the seven pilots. The hormonal data told a parallel story: the successful adapters showed normalized cortisol responses, while the single "fail case" continued to exhibit dramatic cortisol spikes—from 10,040 to 63,050 pg·mL⁻¹ during the final test8 .
| Rehabilitation Outcome | Number of Participants | Percentage | Cortisol Response Post-Rehab |
|---|---|---|---|
| Successful Adaptation | 6 | 86% | Normalized, no significant peak |
| Failed Adaptation | 1 | 14% | Remained elevated (10,040-63,050 pg·mL⁻¹) |
The implications of these findings are substantial for understanding motion sickness:
The persistent cortisol spike in the single participant who failed rehabilitation suggests this hormone may serve as a biological marker for predicting adaptation success8 .
By measuring objective hormonal changes, researchers gained deeper insight into the physiological underpinnings of motion sickness adaptation8 .
The study highlights remarkable individual differences in motion sickness susceptibility and adaptation capacity8 .
The hormonal disruptions of motion sickness create far-reaching physiological consequences beyond the immediate discomfort. Elevated cortisol, while adaptive in short bursts, can impair cognitive function when sustained. Research on cybersickness (a form of motion sickness induced by virtual reality) has shown that the condition can significantly impair working memory performance for extended periods—in some cases up to 90 minutes after the motion exposure has ended.
This cognitive impairment likely results from the dual impact of stress hormones on prefrontal cortex function and the competition for cognitive resources as the brain struggles to resolve sensory conflicts. Furthermore, the presence of oxidative stress biomarkers like 15-F2t-isoprostane in motion sickness sufferers suggests that the condition may create a temporary state of cellular stress throughout the body8 .
| System Affected | Effects | Duration |
|---|---|---|
| Endocrine System | Elevated cortisol, vasopressin, and ghrelin | Can persist for hours after stimulus removal |
| Cognitive Function | Impaired working memory, reduced concentration | Up to 90 minutes post-exposure, sometimes longer |
| Autonomic Nervous System | Increased salivation, cold sweating, pallor | Typically during exposure and shortly after |
| Oxidative Stress | Elevated 15-F2t-isoprostane | Reduces with successful adaptation |
Motion sickness doesn't just affect your stomach—it impairs cognitive functions including:
The physical manifestations of motion sickness include:
Understanding hormonal changes in motion sickness requires specialized tools and methods. Here are some key approaches and reagents used in this research:
A standardized rotational procedure used to reliably induce motion sickness in laboratory settings8 .
A highly sensitive biochemical technique used to measure precise concentrations of hormones in blood plasma8 .
Extremely precise methods for measuring hormone concentrations, detecting even minute changes8 .
Specialized equipment including rotating chairs and VR systems for standardized motion stimuli1 .
The study of hormonal changes in motion sickness opens exciting avenues for both understanding and treating this ancient malady. Recent research exploring the gut-brain connection suggests that the gut microbiome and enteroendocrine cells may play previously unappreciated roles in motion sickness susceptibility and symptom manifestation4 . This aligns with the observed changes in ghrelin, a gut-derived hormone, in motion sickness sufferers.
As we increasingly encounter novel motion environments—from virtual reality to space travel—understanding the hormonal dimensions of motion sickness becomes increasingly crucial. Future research may lead to personalized anti-motion sickness interventions based on an individual's hormonal profile, or medications that specifically target the neuroendocrine pathways most involved in the condition.
What remains clear is that motion sickness is far more than a simple inconvenience—it represents a profound disruption of our body's homeostatic systems, a storm that rages not in the sea or on the road, but within the very chemistry of our bodies. As research continues to unravel its complexities, we move closer to taming this storm, potentially bringing relief to the millions affected by this condition in their travels, work, and leisure.