NIH Workshop Report: sensory nutrition and disease

Abstract

In November 2019, the NIH held the “Sensory Nutrition and Disease” workshop to challenge multidisciplinary researchers working at the interface of sensory science, food science, psychology, neuroscience, nutrition, and health sciences to explore how chemosensation influences dietary choice and health. This report summarizes deliberations of the workshop, as well as follow-up discussion in the wake of the current pandemic. Three topics were addressed: A) the need to optimize human chemosensory testing and assessment, B) the plasticity of chemosensory systems, and C) the interplay of chemosensory signals, cognitive signals, dietary intake, and metabolism. Several ways to advance sensory nutrition research emerged from the workshop: 1) refining methods to measure chemosensation in large cohort studies and validating measures that reflect perception of complex chemosensations relevant to dietary choice; 2) characterizing interindividual differences in chemosensory function and how they affect ingestive behaviors, health, and disease risk; 3) defining circuit-level organization and function that link and interact with gustatory, olfactory, homeostatic, visceral, and cognitive systems; and 4) discovering new ligands for chemosensory receptors (e.g., those produced by the microbiome) and cataloging cell types expressing these receptors. Several of these priorities were made more urgent by the current pandemic because infection with sudden acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the ensuing coronavirus disease of 2019 has direct short- and perhaps long-term effects on flavor perception. There is increasing evidence of functional interactions between the chemosensory and nutritional sciences. Better characterization of this interface is expected to yield insights to promote health, mitigate disease risk, and guide nutrition policy.

Nutrigenomic Regulation of Sensory Plasticity

“…Varying levels of sucrose in the diet also affect taste plasticity in mammals, reviewed recently in 21,23,24 . In particular, a recent study found that rats exposed to 30% sucrose for 4-5 weeks presented lower responses of the chorda tympani nerve a branch of the facial nerve that innervates the front ½ of the tongue to sweet stimuli 32 .…”

“…In fact, correcting the activity of the sweet taste neurons or by preventing the chromatin and transcriptional remodeling by OGT and PRC2, protects animals from diet-induced obesity by restoring normal meal size 27,30,35 . Although the consequences of diet-induced taste plasticity in mammals are still not understood, the anticorrelation between taste function and BMl, as well as the importance of sensory factors in satiation and satiety, suggest that this phenomenon could contribute to deregulated eating and obesity in humans 23,82,99,100 . Consistent with this idea and the fly data, we found that rat OGT x MTF2 DEGs were associated with obesity, waist-to-hip ratio, and cancer in humans.…”

The genetics of eating behaviors: research in the age of COVID-19

“…This research was conducted during the COVID-19 pandemic (September 3, 2020-June 5, 2021). Because cardinal symptoms of COVID-19 are loss of taste, smell, and chemesthesis (e.g., the burn of chili pepper or the cool of menthol) (Parma, et al, 2020), it was important to establish whether participants had an active infection, or had been sick and lost their sense of taste or smell, because these senses affect food enjoyment (Hannum & Reed, 2021; Reed, et al, 2020). We therefore evaluated COVID-19 history using modified survey questions originally designed by members of the Global Consortium for Chemosensory Research (Parma, et al, 2020).…”

Crème de la Créature: Dietary Influences on Behavior in Animal Models

“…Supplementation of the standard chow diet with sugars like sucrose or fructose in the drinking water (ranging from 10 to 55%) has similar effects to the high fat diet over longer exposures, including higher calorie intake, fasting blood glucose, insulin, and leptin levels, and fat stores, but no changes in high-density cholesterol levels (Jurdak et al, 2008 ; Beilharz et al, 2014 ; la Fleur et al, 2014 ; Kothari et al, 2017 ). Many different behaviors have been phenotyped in response to dietary manipulations in rodents, including feeding and reward, cognition, chemosensation and sleep; below we focus primarily on the first two, as the relationship between diet and chemosensory plasticity (Peng et al, 2019 ; May et al, 2020 ; Reed et al, 2020 ) and diet and sleep (Frank et al, 2017 ) have been recently reviewed.…”