Motion sickness, also known as kinetosis, is a common physiological response to real or perceived motion that affects a significant portion of the population. Approximately one in three individuals is highly susceptible, though almost everyone can be affected under extreme conditions. The symptoms, which often include dizziness, nausea, vomiting, and cold sweats, arise when the central nervous system struggles to reconcile conflicting sensory information.
The Sensory Conflict Hypothesis
The most widely accepted explanation for motion sickness is the sensory conflict hypothesis, which posits that symptoms are triggered by a mismatch in signals received by the brain. The brain constantly estimates the body’s motion and position by integrating input from multiple sensory systems, including the eyes and the inner ear’s balance mechanisms. Motion sickness occurs when these sensory inputs deliver contradictory messages, creating a conflict in the brain’s perception of reality.
A common example is reading a book while riding in a car. The eyes are focused on a stationary object, signaling stillness, while the inner ear senses the vehicle’s acceleration and motion. This discrepancy between visual input and inner ear input confuses the central nervous system. Conversely, being below deck on a ship provides a similar conflict, where the eyes see a stationary cabin interior, but the inner ear detects the continuous rocking motion. The brain interprets this unusual sensory pattern as a possible sign of poisoning, triggering the nausea and vomiting response as a defense mechanism.
Defining the Genetic Link
Susceptibility to motion sickness is highly variable among individuals, suggesting an underlying biological predisposition. Research, particularly twin studies, confirms a significant genetic component, meaning the likelihood of experiencing motion sickness can be inherited. Studies comparing identical twins (who share nearly 100% of their genes) to fraternal twins (who share about 50%) show a much higher concordance rate for motion sickness in the identical pairs.
The heritability of motion sickness susceptibility is estimated to be substantial, with some studies suggesting that over 50% of the variation in risk is due to genetic factors. Children whose parents are both susceptible are five times more likely to experience it themselves, providing evidence for a strong familial link. While the sensory conflict is the trigger, a person’s genetic makeup determines their baseline sensitivity to that conflict.
Genes and Biological Pathways
The genetic contribution to motion sickness is complex, involving multiple genes that influence various biological systems. Research, including large genome-wide association studies, has identified over 35 genetic variations, known as single-nucleotide polymorphisms (SNPs), associated with motion sickness susceptibility. These genetic markers are not linked to a single “motion sickness gene” but rather to a combination of genes that affect sensory processing and neurological function.
Many identified genes are involved in the development and function of sensory organs that process motion, such as the inner ear and the eyes. Variations in these genes may lead to subtle differences in how the balance system is structured or how effectively it processes movement signals. Genetic variations also affect neurological pathways involving neurotransmitters like dopamine and histamine, which are key components of the brain’s nausea and vomiting centers. Variations regulating these signaling molecules can create a more reactive central nervous system, quicker to trigger the illness response when presented with conflicting motion signals.
Environmental and Developmental Triggers
While genetics sets the baseline for susceptibility, external and developmental factors modulate how often and how severely motion sickness is experienced. Age is a significant factor: susceptibility is low in infants, peaks in children between two and twelve, and then declines in adulthood. This heightened vulnerability in childhood is thought to be related to the ongoing maturation of the vestibular and central nervous systems, which may not yet efficiently process complex motion information.
Other environmental elements can act as immediate triggers. Hormonal fluctuations, such as those during the menstrual cycle or pregnancy, can temporarily increase susceptibility. Symptoms are more likely to occur with low-frequency, erratic movements, like a turbulent flight or choppy seas, compared to smoother motions. The brain’s ability to adapt to repeated exposure, known as habituation, also varies, demonstrating a gene-environment interaction where repeated travel can lower sensitivity over time.