BackgroundThe association of gustatory dysfunction (GD) with quality of life (QOL) and cognition in older adults is understudied. Our objective was to study the prevalence of GD in the community and explore impacts and associated factors.MethodsA prospective, multi‐institutional, pre‐corona virus disease (COVID) cohort of adults aged 50 years and older had smell and taste testing using “Sniffin’ Sticks” (TDI) and “Taste Strips.” The impact of GD on mood, QOL, and social interaction was assessed through visual analog scales. Subjects completed the Questionnaire of Olfactory Disorders, Patient Health Questionnaire 9, Mini‐Mental State Examination (MMSE), Montreal Cognitive Assessment, and the DeJong scale of loneliness.ResultsA total of 48 patients, average age of 54.7 years, were enrolled. Thirty‐two percent experienced GD on taste strips, and 62% experienced olfactory dysfunction (OD) on TDI. Almost 30% (29.5%) had both GD and OD. GD and OD correlated with worsened cognitive function on MMSE (r = 0.392 and 0.05, p = 0.018 and 0.003). Subjects with both GD and OD had worse MMSE than either alone (p = 0.003). Dry mouth and difficult chewing correlated with GD (r = −0.37 and −0.31, p = 0.10 and 0.37). Self‐reported GD and OD were correlated (r = 0.46, p = 0.001), as were psychophysical GD and OD (r = 0.394, p = 0.008). GD did not correlate with other metrics.ConclusionThirty‐two percent of subjects experienced GD on psychophysical testing, yet most are unaware without impacts on daily life. However, GD correlates with worsened cognitive function. Taste testing may play a role in screening of neurocognitive decline, and multisensory dysfunction may indicate of worsened cognitive states.

The differential rates of opioid tolerances raise the question of discrete underlying mechanisms. While opioid tolerance is strongly linked to the development of dependence, there is a dissociation between the two phenomena in the gut as tolerance does not develop to chronic opioid-induced constipation, but diarrhea still manifests upon withdrawal. Here, we find that tolerance develops to inhibition of small intestinal motility after one day of morphine exposure, and is more rapid compared to spinally-mediated antinociception and constipation in chronic morphine-treated mice. This tolerance can be reversed by protein kinase C (PKC) inhibition but not by β-arrestin-2 deletion. Similarly, morphine tolerance develops to inhibition of neuronal excitability in ileum myenteric neurons independently of β-arrestin-2 and is attenuated by inhibiting PKC. These findings reveal a potential mechanism for differences in the rates of tolerances to opioids and implicate myenteric neurons of the ileum as the primary cause for opioid-induced withdrawal effects

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