Many researchers have claimed that the emotion of disgust functions to protect us from disease. Although there have been several discussions of this hypothesis, none have yet reviewed the evidence in its entirety. The authors derive 14 hypotheses from a disease-avoidance account and evaluate the evidence for each, drawing upon research on pathogen avoidance in animals and empirical research on disgust. In all but 1 case, the evidence favors a disease-avoidance account. It is suggested that disgust is evoked by objects/people that possess particular types of prepared features that connote disease. Such simple disgust are directly disease related, are acquired during childhood, and are able to contaminate other objects/people. The complex disgust, which emerge later in development, may be mediated by several emotions. In these cases, violations of societal norms that may subserve a disease-avoidance function, notably relating to food and sex, act as reminders of simple disgust elicitors and thus generate disgust and motivate compliance. The authors find strong support for a disease-avoidance account and suggest that it offers a way to bridge the divide between concrete and ideational accounts of disgust.

Stigmatization is characterized by chronic social and physical avoidance of a person(s) by other people. Infectious disease may produce an apparently similar form of isolation—disease avoidance—but on symptom remission this often abates. We propose that many forms of stigmatization reflect the activation of this disease-avoidance system, which is prone to respond to visible signs and labels that connote disease, irrespective of their accuracy. A model of this system is presented, which includes an emotional component, whereby visible disease cues directly activate disgust and contamination, motivating avoidance, and a cognitive component, whereby disease labels bring to mind disease cues, indirectly activating disgust and contamination. The unique predictions of this model are then examined, notably that people who are stigmatized evoke disgust and are contaminating. That animals too show avoidance of diseased conspecifics, and that disease-related stigma targets are avoided in most cultures, also supports this evolutionary account. The more general implications of this approach are then examined, notably how it can be used to good (e.g. improving hygiene) or bad (e.g. racial vilification) ends, by yoking particular labels with cues that connote disease and disgust. This broadening of the model allows for stigmatization of groups with little apparent connection to disease.

Little is known about when or how different disgust elicitors are acquired. In Study 1, parents of children (0-18 years old) rated how their child would react to 22 disgust elicitors. Different developmental patterns were identified for core, animal, and sociomoral elicitors, with core elicitors emerging first. In Study 2, children (2-16 years old) were exposed alone and then with their parent to a range of elicitors derived from Study 1. Self-report, behavioral, and facial expression data were obtained along with measures of contagion, conservation, and contamination. Convergent evidence supported the developmental patterns reported in Study 1. Evidence for parent-child transmission was also observed, with parents of young children emoting more disgust to their offspring and showing greater behavioral avoidance. Moreover, child reactivity to animal and sociomoral elicitors and contamination correlated with parental responsiveness. Finally, young children who failed to demonstrate contagion and conservation knowledge were as reactive to core elicitors and contamination as children of the same age who demonstrated such knowledge. These findings are interpreted within an evolutionary framework in which core disgust responses are acquired early to promote avoidance of pathogens.

Olfaction's unique cognitive architecture, the apparently inconsistent evidence favoring imagery, and its difficulty of evocation have led some to conclude that there is no capacity for olfactory imagery. Using three streams of evidence, we examine the validity of this claim. First, self-reports of olfactory imagery can resemble those obtained for actual perception. Second, imagining an odor can produce effects similar to actual perception. Third, olfactory perception and memory-based images can interact. A model of olfactory imagery is then presented that utilizes the same systems employed in actual perception, with similar constraints. This model is consistent with olfaction's unique information-processing capacities and can account for previous experimental inconsistencies on the basis of difficulty of evocation, a consequence of unstable access to semantic information. In sum, the evidence presented here is favorable to the existence of an olfactory imagery capacity.