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.

Although referred to in passing in several places, there have been few attempts to specify the functions of the human olfactory system. This article presents an initial effort at identifying and categorizing these functions, using 3 sources of information as a guide: 1) losses experienced by anosmic participants; 2) olfactory function in other mammals; and 3) capacity, namely, whether the human olfactory system can support the suggested function and whether there is evidence that it does. Three major classes of function were identified, relating to Ingestion (Detection/identification prior to ingestion; Detection of expectancy violations; Appetite regulation; Breast orientation and feeding), Avoiding environmental hazards (Fear related; Disgust related), and Social communication (Reproductive [inbreeding avoidance, fitness detection in prospective mates]; Emotional contagion [fear contagion, stress buffering]). These suggested functions were then examined with respect to 1) issues of ecological validity in human olfactory research; 2) their impact on olfactory loss; and 3) their general and specific implications for the study of human olfaction.

This study investigated the relationship between perception of an odour when smelled and the taste of a solution to which the odour is added as a flavorant. In Experiment 1 (E1) sweetness, sourness, liking and intensity ratings were obtained for 20 odours. Taste ratings were then obtained for sucrose solutions to which the odours had been added as flavorants. Certain odours were found to enhance tasted sweetness while others suppressed it. The degree to which an odour smelled sweet was the best predictor of the taste ratings. These findings were extended in Experiment 2 (E2), which included a second tastant, citric acid, and employed four odours from E1. The most sweet smelling odour, caramel, was found to suppress the sourness of citric acid and, as in E1, to enhance the sweetness of sucrose. Again, odours with low sweetness suppressed the sweetness of tasted sucrose. The study demonstrated that the effects of odours on taste perception are not limited to sweetness enhancement and apply to sour as well as sweet tastes. The overall pattern of results is consistent with an explanation of the taste properties of odours in terms of prior flavour–taste associations.

There is strong epidemiological evidence that poor diet is associated with depression. The reverse has also been shown, namely that eating a healthy diet rich in fruit, vegetables, fish and lean meat, is associated with reduced risk of depression. To date, only one randomised controlled trial (RCT) has been conducted with elevated depression symptoms being an inclusion criterion, with results showing that a diet intervention can reduce clinical levels of depression. No such RCTs have been performed in young adults. Young adults with elevated levels of depression symptoms and who habitually consume a poor diet were randomly allocated to a brief 3-week diet intervention (Diet Group) or a habitual diet control group (Control Group). The primary and secondary outcome measures assessed at baseline and after the intervention included symptoms of depression (Centre for Epidemiological Studies Depression Scale; CESD-R; and Depression Anxiety and Stress Scale– 21 depression subscale; DASS-21-D), current mood (Profile of Mood States), self-efficacy (New General Self-Efficacy Scale) and memory (Hopkins Verbal Learning Test). Diet compliance was measured via self-report questionnaires and spectrophotometry. One-hundred-and-one individuals were enrolled in the study and randomly assigned to the Diet Group or the Control Group. Upon completion of the study, there was complete data for 38 individuals in each group. There was good compliance with the diet intervention recommendations assessed using self-report and spectrophotometry. The Diet group had significantly lower self-reported depression symptoms than the Control Group on the CESD-R (p = 0.007, Cohen’s d = 0.65) and DASS-21 depression subscale (p = 0.002, Cohen’s d = 0.75) controlling for baseline scores on these scales. Reduced DASS-21 depression subscale scores were maintained on follow up phone call 3 months later (p = .009). These results are the first to show that young adults with elevated depression symptoms can engage in and adhere to a diet intervention, and that this can reduce symptoms of depression. The findings provide justification for future research into the duration of these benefits, the impacts of varying diet composition, and their biological basis.