Richard J. Stevenson

Disgust as a disease-avoidance mechanism

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.

An Initial Evaluation of the Functions of Human Olfaction

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.

A cognitive remediation programme for adults with Attention Deficit Hyperactivity Disorder.

Objective: This is the first systematic examination of the efficacy of a cognitive remediation programme (CRP) for management of adult Attention Deficit Hyperactivity Disorder (ADHD). The CRP was designed to target problems commonly associated with adult ADHD, namely, attention problems, poor motivation, poor organizational skills, impulsivity, reduced anger control and low self-esteem. Method: In a randomized, controlled trial, a representative sample of adults with ADHD (some medicated, some not) were assigned to either a CRP (n = 22) or a waiting list control (n = 21). The CRP was delivered in an intensive format with eight two-hour, weekly sessions with support people who acted as coaches, and participant workbooks with homework exercises. Results: Participants who completed the CRP reported reduced ADHD symptomatology (effect size (d) = 1.4), improved organizational skills (d = 1.2) and reduced levels of anger (d = 0.5). Clinically significant improvements in ADHD symptomatology (d = 1.4) and organizational skills (d = 1.3) were maintained one year after the intervention. Conclusions: These findings suggest that the CRP provides a practical way of enhancing daily functioning for adults with ADHD.

Olfactory perceptual learning: the critical role of memory in odor discrimination

The major problem in olfactory neuroscience is to determine how the brain discriminates one odorant from another. The traditional approach involves identifying how particular features of a chemical stimulus are represented in the olfactory system. However, this perspective is at odds with a growing body of evidence, from both neurobiology and psychology, which places primary emphasis on synthetic processing and experiential factors--perceptual learning--rather than on the structural features of the stimulus as critical for odor discrimination. In the present review of both psychological and sensory physiological data, we argue that the initial odorant feature extraction/analytical processing is not behaviorally/consciously accessible, but rather is a first necessary stage for subsequent cortical synthetic processing which in turn drives olfactory behavior. Cortical synthetic coding reflects an experience-dependent process that allows synthesis of novel co-occurring features, similar to processes used for visual object coding. Thus, we propose that experience and cortical plasticity are not only important for traditional associative olfactory memory (e.g. fear conditioning, maze learning, and delayed-match-to-sample paradigms), but also play a critical, defining role in odor discrimination.

A mnemonic theory of odor perception.

The psychological basis of odor quality is poorly understood. For pragmatic reason, descriptions of odor quality generally rely on profiling odors in terms of what odorants they bring to mind. It is argued here that this reliance on profiling reflects a basic property of odor perception, namely that odor quality depends on the implicit memories that an odorant elicits. This is supported by evidence indicating that odor quality as well as ones ability to discriminate odors is affected by experience. Developmental studies and cross-cultural research also point to this conclusion. In this article, these findings are reviewed and a model that attempts to account for them is proposed. Finally, the models consistency with both neurophysiological and neuropsychological data is examined.

The longer-term impacts of Western diet on human cognition and the brain.

Animal work over the last three decades has generated a convincing body of evidence that a Western diet - one high in saturated fat and refined carbohydrates (HFS diet) - can damage various brain systems. In this review we examine whether there is evidence for this in humans, using converging lines of evidence from neuropsychological, epidemiological and neuroimaging data. Using the animal research as the organizing principal, we examined evidence for dietary induced impairments in frontal, limbic and hippocampal systems, and with their associated functions in learning, memory, cognition and hedonics. Evidence for the role of HFS diet in attention deficit disorder and in neurodegenerative conditions was also examined. While human research data is still at an early stage, there is evidence of an association between HFS diet and impaired cognitive function. Based upon the animal data, and a growing understanding of how HFS diets can disrupt brain function, we further suggest that there is a causal link running from HFS diet to impaired brain function in humans, and that HFS diets also contribute to the development of neurodegenerative conditions.

Resistance to extinction of conditioned odor perceptions: evaluative conditioning is not unique.

A tasteless odor will smell sweeter after being sampled by mouth with sucrose and will smell sourer after being sampled with citric acid. This tasty-smell effect was found in experiments that compared odor-taste and color-taste pairings. Using odors and colors with minimal taste (Experiment 1), the authors found that repeated experience of odor-taste mixtures produced conditioned changes in odor qualities that were unaffected by intermixed color-taste trials (Experiment 2). An extinction procedure, consisting of postconditioning presentations of the odor in water, had no detectable effect on the changed perception of an odor (Experiments 3 and 4). In contrast, this procedure altered judgments about the expected taste of colored solutions. Evaluative conditioning (conditioned changes in liking) is claimed to be resistant to extinction. However, these results suggest that resistance to extinction in odors is related to the way they are encoded rather than to their hedonic properties.

Higher reported saturated fat and refined sugar intake is associated with reduced hippocampal-dependent memory and sensitivity to interoceptive signals.

Regulation of energy intake depends in part on both memory for prior food intake and internal signals of hunger and satiety. These functions are both mediated by the hippocampus, a brain structure that animal studies have shown to be impaired after maintenance on high fat and refined sugar (HFS) diets. Study 1, using a cross-sectional design, revealed that self-reported HFS diet was associated with poorer performance on hippocampal sensitive memory tasks but not other neuropsychological control measures. Study 2 replicated this finding in two groups selected to differ in HFS intake, additionally showing that this effect is specific to hippocampal functioning and does not extend to measures of prefrontal cortex function. Furthermore, in a laboratory-based test of food intake, the HFS rich diet groups were less accurate in recalling what they had previously eaten and evidenced reduced sensitivity to internal signals of hunger and satiety, relative to a group consuming less HFS rich diets. Together, these findings reveal an association between HFS consumption and poorer hippocampal function in human participants, consistent with findings from animal-based studies. Moreover, our results suggest that this may be related to impaired regulation of energy intake via less accurate tracking of prior food intake and reduced sensitivity to hunger and satiety signals.

Olfactory imagery: A review

Olfactions 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 olfactions 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.

Children's response to adult disgust elicitors: development and acquisition.

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.