The following factors increase some people's susceptibility to airsickness:

- Fatigue, stress, and anxiety, are some factors that can increase susceptibility to motion sickness of any type.

- The use of alcohol, drugs, and medications may also contribute to airsickness.

- Additionally, airsickness is more common in women (especially during menstruation or pregnancy), young children, and individuals prone to other types of motion sickness.

- Although airsickness is uncommon among experienced pilots, it does occur with some frequency in student pilots.

Travelers who are susceptible to motion sickness can minimize symptoms by:

- Choosing a window seat with a view of the ground or of lower clouds, such that motion can be detected. This will not work if the plane is flown in the clouds for a long duration.

- Choosing seats with the smoothest ride in regards to pitch (the seats over the wings in an airplane). (This may not be sufficient for sensitive individuals who need to see ground movement)

- Sitting facing forward while focusing on distant objects rather than trying to read or look at something inside the airplane.

- Eating dry crackers, olives or suck on a lemon, to dry out the mouth, lessening nausea.

- Drinking a carbonated beverage.

One common suggestion is to simply look out of the window of the moving vehicle and to gaze towards the horizon in the direction of travel. This helps to re-orient the inner sense of balance by providing a visual reaffirmation of motion.

In the night, or in a ship without windows, it is helpful to simply close one's eyes, or if possible, take a nap. This resolves the input conflict between the eyes and the inner ear. Napping also helps prevent psychogenic effects (i.e. the effect of sickness being magnified by thinking about it).

Fresh, cool air can also relieve motion sickness slightly, although it is likely this is related to avoiding foul odors which can worsen nausea.

While playing computer games, and mainly in first-person shooter games, some cases of simulation sickness can be resolved by changing the field of view in the game. Some games have a default setting which places a player's vision a small distance ahead of the actual object controlled, which will most likely trigger simulation sickness.

The most common hypothesis for the cause of motion sickness is that it functions as a defense mechanism against neurotoxins. The area postrema in the brain is responsible for inducing vomiting when poisons are detected, and for resolving conflicts between vision and balance. When feeling motion but not seeing it (for example, in a ship with no windows), the inner ear transmits to the brain that it senses motion, but the eyes tell the brain that everything is still. As a result of the discordance, the brain will come to the conclusion that the individual is hallucinating and further conclude that the hallucination is due to poison ingestion. The brain responds by inducing vomiting, to clear the supposed toxin. Treisman's indirect argument has recently been questioned via an alternative direct evolutionary hypothesis, as well as modified and extended via a direct poison hypothesis. The direct evolutionary hypothesis essentially argues that there are plausible means by which ancient real or apparent motion could have contributed directly to the evolution of aversive reactions, without the need for the co-opting of a poison response as posited by Treisman. Nevertheless, the direct poison hypothesis argues that there still are plausible ways in which the body's poison response system may have played a role in shaping the evolution of some of the signature symptoms that characterize motion sickness.

An alternative theory, also known as the Nystagmus Hypothesis, has been proposed based on stimulation of the vagus nerves resulting from the stretching or traction of extra-ocular muscles co-occurring with eye movements caused by vestibular stimulation. There are three critical aspects to the theory: first is the close linkage between activity in the vestibular system, i.e., semicircular canals and otolith organs, and a change in tonus among various of each eye's six extra-ocular muscles. Thus, with the exception of voluntary eye movements, the vestibular and oculomotor systems are thoroughly linked. Second is the operation of Sherrington's Law describing reciprocal inhibition between agonist-antagonist muscle pairs, and by implication the stretching of extraocular muscle that must occur whenever Sherrington's Law is made to fail, thereby causing an unrelaxed (contracted) muscle to be stretched. Finally there is the critical presence of afferent output to the Vagus nerves as a direct result of eye muscle stretch or traction. Thus, 10th nerve stimulation resulting from eye muscle stretch is proposed as the cause of motion sickness. The theory explains why labyrinthine defective individuals are immune to motion sickness; why symptoms emerge when undergoing various body-head accelerations; why combinations of voluntary and reflexive eye movements may challenge the proper operation of Sherrington's Law, and why many drugs that suppress eye movements also serve to suppress motion sickness symptoms.