Are evolutionary hypotheses for motion sickness "just-so" stories?1

Abstract

Vertebrates have evolved rapidly conditionable nausea and vomiting reflexes mediated by gut and brainstem receptors, clearly as a defense against neurotoxin ingestion. In 1977 Treisman proposed that sensory orientation linkages to emetic centers evolved for the same reason, and that motion sickness was an accidental byproduct. It was an “adaptationist” explanation for motion sickness, since it assumed that evolution has shaped all phenotypic traits for survival advantage. Treisman's “poison” theory is plausible, and frequently cited as the accepted scientific explanation for motion sickness. However, alternative explanations have been proposed. The creation of hypotheses is an essential part of science – provided they are testable. This paper reviews the evidence for the Poison theory and several other adaptationist explanations. These hypotheses are certainly not “just-so stories”, but supporting evidence is equivocal, and contradictory evidence exists Parsimony suggests an alternative “pluralistic” view: The vertebrate reticular formation maintains oxygenated blood flow to the brain, discriminates unexpected sensory stimuli- including postural disturbances, and detects and expels ingested neurotoxins. The three systems share neuroarchitectural elements but normally function independently. Brainstem sensory conflict neurons normally discriminate brief postural disturbances, but can be abnormally stimulated during prolonged passive transport (e.g. by boat, beginning about 150–200 generations ago). Sensory conflict signals cross couple into the neurotoxin expulsion and avoidance system, producing an arguably maladaptive emetic phenotype.