Why Some People Get Motion Sick and Others Don't

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Your friend reads a novel in the backseat for three hours without flinching. You can barely glance at a text message. What's going on — and is there anything you can do about it?

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It's one of life's small injustices. You're white-knuckling through a ferry crossing, trying to breathe through your nose and fixate on the horizon, while the person next to you is happily eating a sandwich and watching YouTube on their phone. They seem genuinely confused when you explain that the boat is making you sick. "Really? I don't feel anything."

If you've ever wondered why motion sickness seems to strike some people mercilessly while leaving others completely untouched, you're asking the right question. And the answer turns out to be more nuanced — and more hopeful — than most people realize.

Motion sickness susceptibility isn't random. It's shaped by a combination of genetics, hormones, how your brain processes sensory information, and how much motion exposure you've had throughout your life. Some of these factors you can't change. But the ones that matter most? Those are trainable.

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Genetics play a real but incomplete role

Let's start with the factor people assume explains everything: DNA.

There is a genuine genetic component to motion sickness. Twin studies — the gold standard for separating genetic influence from environmental influence — have consistently shown that identical twins are significantly more likely to share motion sickness susceptibility than fraternal twins. Estimates of heritability range from 55 to 70 percent, meaning that more than half the variation in motion sickness susceptibility across the population can be attributed to genetic differences.

A large genome-wide association study published in Human Molecular Genetics identified 35 genetic variants associated with motion sickness, many of which are connected to balance, inner ear development, and neurological function. Some variants affect the structure and sensitivity of the vestibular organs themselves — the semicircular canals and otolith organs that detect rotation and acceleration. Others influence neurotransmitter systems, including histamine and acetylcholine pathways (which is why antihistamines like Dramamine work as symptom relief). Still others affect glucose metabolism and oxygen delivery in the brain, which may influence how efficiently the brain processes sensory conflict.

So yes, if your parents got carsick, you're more likely to get carsick too. There's real biology behind it.

But here's the critical nuance that most articles leave out: genetics determine your starting point, not your ceiling. A genetic predisposition to motion sickness means your brain's sensory integration system is more reactive to conflict by default — it doesn't mean it can't be trained to handle conflict better.

Think of it like flexibility. Some people are naturally flexible; others are naturally stiff. But everyone, regardless of their starting point, can improve their flexibility with consistent stretching. The naturally stiff person may never become a contortionist, but they can go from barely touching their toes to reaching the floor. The same principle applies to motion sickness susceptibility. Your genetics set the baseline. Training determines how far you move from it.

This is supported directly by the research: the University of Warwick visuospatial training study specifically recruited participants with high motion sickness susceptibility — people whose genetics and history made them particularly vulnerable — and still achieved a 51 to 58 percent reduction in symptoms through a two-week training protocol. Genetic predisposition didn't prevent improvement. It just meant there was more room to improve.

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Age and hormones shift susceptibility throughout your life

Motion sickness isn't static. Your susceptibility changes across your lifespan, and hormones are one of the biggest reasons why.

Childhood is peak susceptibility

Motion sickness is rare in infants under two — their vestibular systems aren't fully developed yet, so there's less sensory conflict to trigger. It ramps up sharply between ages 2 and 12, peaking around age 9 to 10 in most studies. If you remember getting carsick as a kid, you were in the majority — most children experience it to some degree. Many people "grow out of it" during adolescence as their brains mature and accumulate more motion exposure, but a significant percentage carry it into adulthood.

Women are more susceptible than men

This is one of the most consistent findings in motion sickness research. Women report motion sickness at roughly 2 to 3 times the rate of men across nearly every study population. The gap appears to be driven primarily by hormonal fluctuations, not by differences in vestibular anatomy.

The evidence for hormonal influence is strong. Motion sickness susceptibility fluctuates across the menstrual cycle, typically peaking during menstruation and the late luteal phase when estrogen and progesterone levels are shifting most dramatically. Pregnancy often increases motion sickness — which makes intuitive sense given the massive hormonal changes involved, and may share a mechanism with morning sickness. Hormonal birth control, particularly estrogen-containing pills, can worsen motion sickness in some women. And many women report new or increased motion sickness during perimenopause, when hormonal patterns become erratic.

The hormonal connection doesn't mean women are "stuck with" worse motion sickness. It means their susceptibility may fluctuate more, and they may need to account for timing when planning challenging motion situations. Brain training works regardless of hormonal status — the sensory processing improvements are structural, not hormonal.

Older adults sometimes develop new susceptibility

Vestibular function gradually declines with age, beginning as early as the 40s. The hair cells in the semicircular canals and otolith organs slowly deteriorate, reducing the precision of vestibular signals. This can lead to new motion sickness in people who were never previously susceptible, or a return of childhood motion sickness that had seemingly been outgrown. Age-related vestibular decline is also why falls become more common in older adults — the same system that maintains balance during stillness is the one that processes motion.

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Your sensory "style" might be the biggest modifiable factor

Beyond genetics and hormones, there's a factor that researchers believe plays an enormous role in motion sickness susceptibility — and unlike DNA or hormones, it's highly trainable. It's called visual dependence.

Every person's brain balances three sensory inputs — visual, vestibular, and proprioceptive — differently. Some people are "visually dominant," meaning their brain assigns disproportionate weight to what their eyes report when constructing a sense of spatial orientation. Others are "vestibularly dominant," relying more on inner ear signals. Most people fall somewhere along the spectrum.

Visually dominant people are significantly more susceptible to motion sickness.

The logic is straightforward. If your brain trusts your eyes above all else, then any situation where visual input conflicts with vestibular input hits you harder. Reading in a car? Your eyes say "still," and your brain believes them — so when your inner ear insists you're moving, the contradiction is jarring. Your brain can't reconcile the two, because it has overcommitted to the visual signal.

Vestibularly dominant people, by contrast, have brains that weight inner ear signals more heavily. For them, the same reading-in-car conflict is less severe — their brain is already primed to trust the vestibular system's motion report, so the conflicting visual "you're still" signal gets partially overridden rather than creating a full-blown contradiction.

Visual dependence can be measured using rod-and-frame tests and posturography assessments. And — here's the encouraging part — it can be shifted through training.

The visuospatial exercises used in the Warwick study and in vestibular rehabilitation programs work, in part, by rebalancing the sensory weighting. They train the brain to build stronger internal spatial models and to integrate vestibular input more effectively, reducing over-reliance on visual cues. In essence, they move a visually dependent person toward the center of the spectrum — not by weakening their visual processing, but by strengthening the vestibular and spatial processing that was being underutilized.

Your sensory processing style is not fixed, and changing it directly reduces susceptibility. This is arguably the most actionable finding in motion sickness research.

For a detailed look at how sensory conflict creates the nausea response, see our article on the science behind motion sickness. For exercises that target visual dependence and visuospatial processing specifically, see our guide to vestibular exercises you can do at home.

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Experience and exposure history make a bigger difference than most people realize

There's a reason sailors, pilots, and astronauts rarely suffer from chronic motion sickness: they've accumulated thousands of hours of motion exposure, and their brains have adapted.

Habituation — the reduction of a response through repeated exposure — is one of the most robust phenomena in neuroscience. It applies to almost every sensory and reflexive system in the body, and the vestibular system is no exception. A brain that has been exposed to motion-related sensory conflict many times learns, gradually, that the conflict isn't dangerous. The nausea response weakens. The threshold for triggering it rises.

This has a straightforward implication for everyday motion sickness: people who avoid their triggers tend to maintain or worsen their susceptibility, while people who encounter them regularly tend to improve.

If you always drive instead of riding as a passenger, always sit in the front seat, always avoid boats, always skip the VR headset — you're protecting yourself in the short term, but you're also preventing the habituation that would reduce your sensitivity long-term. Your brain never gets the practice it needs.

This creates a frustrating cycle:

• You avoid motion because it makes you sick
• Because you avoid motion, your brain never adapts
• Because your brain never adapts, motion keeps making you sick
• So you avoid it more

The way to break the cycle is structured, progressive exposure — which is exactly what brain training provides. Rather than throwing yourself into a challenging motion situation and hoping for the best (which usually ends badly and reinforces avoidance), a structured program creates small, controlled doses of sensory conflict that your brain can process and adapt to. Each session pushes the boundary slightly further, in a way that's uncomfortable but manageable.

The "just get used to it" advice your uncle gives you contains a genuine kernel of neuroscience. He's describing habituation. Where he's wrong is in the method — random, uncontrolled exposure is slow, unpredictable, and often aversive enough to make people quit. Structured training achieves the same neurological result in days or weeks instead of months or years.

For more on how this approach can create permanent improvement, read our article on whether motion sickness can be cured permanently.

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Psychological and situational factors amplify susceptibility

Beyond the biological and experiential factors, several psychological and environmental elements can make motion sickness significantly worse — or better.

Anxiety and anticipation

If you expect to get motion sick, you're more likely to get motion sick. This isn't just psychosomatic — anticipatory anxiety triggers the autonomic nervous system, increasing nausea sensitivity and reducing your brain's tolerance for sensory conflict. Research shows that people with higher trait anxiety consistently score higher on motion sickness susceptibility questionnaires. The "I know this is going to make me sick" thought becomes a self-fulfilling prophecy.

The flip side is also true: confidence reduces susceptibility. As you build evidence through training that you can handle motion without getting sick, the anxiety component diminishes, which further reduces your symptoms. This is one of the underappreciated benefits of a structured training program — it doesn't just improve your sensory processing, it also breaks the psychological pattern of dread and avoidance.

Sleep deprivation, dehydration, and hunger

These three compound your baseline susceptibility more than most people realize:

• Sleep deprivation slows your brain's ability to resolve sensory conflicts — when you're tired, processing is less efficient and the nausea response fires more easily
• Dehydration affects blood pressure regulation and vestibular function; even mild dehydration measurably worsens symptoms
• An empty stomach increases nausea sensitivity; a light, bland meal before a motion situation is more effective than most people expect

Strong smells — car exhaust, diesel fumes, food odors, perfume — can also trigger or amplify symptoms. If you're already in a state of sensory conflict, an unexpected or unpleasant smell can push you over the edge.

Control matters more than anything situational

This is one of the most fascinating findings in motion sickness research: drivers almost never get carsick. The reason is that when you control the vehicle, your brain has advance knowledge of every upcoming motion. You initiate the turns. You initiate the braking. There's no prediction error, so there's no sensory conflict. The moment you hand the keys to someone else and become a passenger, the same road that felt fine a minute ago can start making you sick — because now the motions are unpredictable.

This principle extends beyond driving. On boats, people who are steering or actively engaged in tasks experience less seasickness than idle passengers. In VR, experiences where the user controls the locomotion cause less sickness than on-rails experiences where motion is imposed. Any time you can increase your sense of control or predictability in a motion situation, you reduce the sensory conflict that triggers symptoms.

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The factors you can change matter more than the ones you can't

Here's the empowering takeaway from all of this: the most impactful determinants of motion sickness susceptibility are the trainable ones.

You can't change your genetics. You can't fully control your hormones. You can't stop aging.

But you can retrain your sensory processing style — shifting from visual dependence toward better vestibular integration. You can build habituation through structured exposure. You can break the anxiety-avoidance cycle by proving to yourself that motion doesn't have to mean misery. And you can manage the situational factors — sleep, hydration, control — that amplify your baseline susceptibility.

The research is consistent: even people with strong genetic predisposition, even women at peak hormonal susceptibility, even people who have been severely motion sick their entire lives — can meaningfully reduce their susceptibility through targeted training. The Warwick study didn't screen out the most susceptible participants. It specifically recruited them. And it still worked.

Your susceptibility isn't your identity. It's a starting point.

Take the free Motion Relief assessment →

Find out where you fall on the susceptibility spectrum. The assessment measures your specific triggers, severity, and processing style — then creates a personalized 14-day training plan based on your starting point. Under 3 minutes, completely free.

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Sources cited in this article:

• Hromatko, I. & Tkalčić, M. (2003). "The effects of traveling speed and gender on the incidence and intensity of motion sickness." Review of Psychology, 10(2), 105–110.
• Golding, J.F. (2006). "Predicting individual differences in motion sickness susceptibility by questionnaire." Personality and Individual Differences, 41(2), 237–248.
• Hromatko, I. et al. (2006). "The genetic contribution to individual differences in motion sickness susceptibility." Behavior Genetics, 36, 947 (Abstract).
• Flanagan, M.B. et al. (2005). "Sex differences in visually induced motion sickness." Aviation, Space, and Environmental Medicine, 76(12), 1109–1115.
• Smyth, J. et al. (2021). "A novel method for reducing motion sickness susceptibility through training visuospatial ability — A two-part study." Applied Ergonomics, 90, 103264.
• Lackner, J.R. (2014). "Motion sickness: more than nausea and vomiting." Experimental Brain Research, 232(8), 2493–2510.
• Reason, J.T. & Brand, J.J. (1975). Motion Sickness. Academic Press.

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This article is part of our Complete Guide to Training Your Brain to Prevent Motion Sickness. Motion Relief's training program is based on peer-reviewed visuospatial and vestibular research. It is not a substitute for medical advice — if you experience persistent vertigo, sudden hearing loss, or new-onset dizziness unrelated to motion, please consult a healthcare provider.