Taste and Smell Clinic

A good sense of smell is essential for physical and mental health, and social wellbeing; however, across the globe, regardless of the setting, national public health agendas never consider smell health. This review aims to summarise the wide-reaching impact of smell health in public health. Narrative review of the literature has been undertaken by leading opinion figures in the field of olfactory health. The sense of smell should be promoted as an essential pillar of health, as it enables good nutrition and cognitive and psychological well-being. To improve smell health internationally, a focus on education and awareness, research and targeted public health policies is needed. We recommend developing smell health educational programmes and awareness campaigns, introducing smell screening and developing and implementing smell health policies across sectors of society. Efforts are needed to ensure equity, diversity and inclusivity for all people, particularly given the current demographic as those seeking help are typically not from a diverse cross-section of the community.

A healthy olfactory cleft is critical to normal olfactory function. The aim of this study was to explore the differential orthonasal and retronasal olfactory functions in patients with olfactory cleft (OC) obstructions including a combination of OC syndrome, chronic rhinosinusitis with or without nasal polyps (CRSwNP or CRSsNP), and respiratory adenomatoid epithelial hamartoma (REAH). Patients (n = 93) presenting to an ENT clinic with OC obstruction underwent nasal endoscopy, chemosensory event-related potential (ERP) recordings, and radiologic assessment, and were subsequently diagnosed with OC syndrome, CRSsNP with OC syndrome, CRSwNP in the OC, REAH, and CRSwNP with REAH. Orthonasal and retronasal function were assessed using the complete Sniffin’ Sticks test and a set of 30 powders, respectively. Orthonasal function was lower in patients with REAH and CRSwNP+REAH compared to CRSwNP in OC patients. Retronasal function was similarly diminished in REAH compared to CRSwNP in OC. Patients with OC syndrome alone had higher orthonasal scores than those with CRSsNP plus OC syndrome and CRSwNP in OC but not statistically different retronasal function. There was no significant difference in orthonasal or retronasal scores in REAH patients based on concurrent CRSwNP. REAH corresponded with greater orthonasal and retronasal olfactory loss compared to other olfactory cleft obstructions, indicating a greater effect on the olfactory mucosa beyond disrupting airflow. The difference between CRS and OC syndrome is more pronounced orthonasally than retronasally.

ABSTRACTBackgroundOlfactory impairment (OI) is associated with poor ageing outcomes. While cross‐sectional studies found a high prevalence of OI among patients with neurodegenerative diseases, the temporal relationship remains unclear. This meta‐analysis aims to synthesise the longitudinal association of OI with cognitive decline (CD).MethodsPubMed, Embase and Web of Science were searched through August 9, 2024 for longitudinal studies reporting on self‐reported and objectively measured OI in adults, in association with CD, measured using validated methods. The outcome of interest was incident CD. Independent authors extracted data, assessed for bias and graded the strength of evidence. A mixed‐effects meta‐analysis with subgroup, sensitivity and bias analyses was conducted. The population‐attributable fraction (PAF) of OI‐associated CD was calculated.ResultsThis study included 48 articles and 37,783 participants. OI patients had a 2.06‐fold greater risk of any CD (risk ratio [RR] = 2.06; 95% CI = 1.87‒2.26, I2 = 0%), compared to individuals with normal olfaction. Patients with severe OI had a higher risk of any CD (RR = 2.60; 95% CI = 2.12‒3.20, I2 = 0%) than patients with moderate OI (RR = 1.51; 95% CI = 1.23‒1.85, I2 = 0%). The risk of any CD increased by 18% per 10% decrease in olfactory score (RR = 1.18; 95% CI = 1.14‒1.22, I2 = 24%) and by 15% per point decrement on the Sniffin’ Sticks Odor Identification Test (RR = 1.15; 95% CI = 1.11‒1.18, I2 = 0%). These results remained robust to supplementary analyses. The PAF of OI‐associated incident CD was 18%.ConclusionOI may increase the risk of CD, with poorer olfaction linked to greater risks. OI should be assessed as a potential cognitive screening tool, and cognitive screening should be considered in patients with long‐standing OI.

Abstract Chronic pain is a global epidemic that disproportionately affects Black, Indigenous, and other people of color as well as individuals of lower socioeconomic status. Unfortunately, the mechanisms that cause and sustain disparities in pain outcomes remain underexamined. This review highlights recent insights into epigenetics as a uniquely suited biological mechanism linking environmental stressors and pain disparities. Emerging evidence suggests that epigenetic modification of genes in pathways involved in stress dysregulation and neuroinflammation may play a central role in racial pain disparities and internalized stigma. These findings indicate that differential environmental exposure (ie, chronic stress) induces epigenetic changes (mediators) that explain pain disparities. Another putative mechanism by which differential epigenetic modifications contribute to pain disparities is epigenetic age acceleration. Emerging evidence suggests that epigenetic age acceleration mediates the relationship between lower socioeconomic status (household income, food insecurity, and neighborhood deprivation) and worse pain outcomes. Epigenetic modifications are dynamic and reversible, leaning toward pharmacological and nonpharmacological interventions. Logically, these will contribute to tailored interventions for pain management and equity in pain management. Finally, we cannot ignore that social and structural forces are the root causes of pain disparities. Thus, there is a need for policy changes addressing these forces.

Sensory functions of organs of the head and neck allow humans to interact with the environment and establish social bonds. With aging, smell, taste, vision, and hearing decline. Evidence suggests that accelerated impairment in sensory abilities can reflect a shift from healthy to pathological aging, including the development of Alzheimer's disease (AD) and other neurological disorders. While the drivers of early sensory alteration in AD are not elucidated, insults such as trauma and infections can affect sensory function. Herein, we review the involvement of the major head and neck sensory systems in AD, with emphasis on microbes exploiting sensory pathways to enter the brain (the "gateway" hypothesis) and the potential feedback loop by which sensory function may be impacted by central nervous system infection. We emphasize detection of sensory changes as first-line surveillance in senior adults to identify and remove potential insults, like microbial infections, that could precipitate brain pathology.

ABSTRACT The intestinal barrier, an indispensable guardian of gastrointestinal health, mediates the intricate exchange between internal and external environments. Anchored by evolutionarily conserved junctional complexes, this barrier meticulously regulates paracellular permeability in essentially all living organisms. Disruptions in intestinal junctional complexes, prevalent in inflammatory bowel diseases and irritable bowel syndrome, compromise barrier integrity and often lead to the notorious “leaky gut” syndrome. Critical to the maintenance of the intestinal barrier is a finely orchestrated network of intrinsic and extrinsic factors that modulate the expression, composition, and functionality of junctional complexes. This review navigates through the composition of key junctional complex components and the common methods used to assess intestinal permeability. It also explores the critical intracellular signaling pathways that modulate these junctional components. Lastly, we delve into the complex dynamics between the junctional complexes, microbial communities, and environmental chemicals in shaping the intestinal barrier function. Comprehending this intricate interplay holds paramount importance in unraveling the pathophysiology of gastrointestinal disorders. Furthermore, it lays the foundation for the development of precise therapeutic interventions targeting barrier dysfunction.

World-wide some 658 million people were infected with coronavirus disease 2019 (COVID-19) and millions suffer from chemosensory impairment associated with long COVID. Current treatments for taste and smell disorders are limited. Involving patients has the potential to catalyze the dynamic exchange and development of new ideas and approaches to facilitate biomedical research and therapeutics. We assessed patients’ perceptions of the efficacy of treatments for chemosensory impairment using an online questionnaire completed by 5,815 people in the US Logistic regression determined variables predictive of reported treatment efficacy for patients aged 18 to 24, 25 to 39, 40 to 60, and 60+ yrs. who were treated with nasal steroids, oral steroids, zinc, nasal rinse, smell training, theophylline, platelet-rich plasma, and Omega 3. The most consistent predictor was age, with the majority of those 40 to 60 and 60+ reporting that nasal steroids, oral steroids, zinc, nasal rinse, and smell training were only slightly effective or not effective at all. Many of these treatment strategies target regeneration and immune response, processes compromised by age. Only those under 40 reported more than slight efficacy of steroids or smell training. Findings emphasize the need to include patients of all ages in clinical trials. Older adults with olfactory impairment are at increased risk for Alzheimer’s disease (AD). We speculate that olfactory impairment associated with long COVID introduces the potential for a significant rise in AD. Long COVID-associated chemosensory impairment increases the urgency for translational and clinical research on novel treatment strategies. Suggestions for high-priority areas for epidemiological, basic, and clinical research on chemosensory impairment follow.

ObjectivesThe aim of this observational cross-sectional study was to determine the endotypic inflammatory pattern of a sample of patients with CRS in Brazil, correlate it with olfactory function, and evaluate the clinical severity of the disease. MethodsIn this cross-sectional study, 73 CRS patients were recruited. Patients were classified into type 2 and non-type 2 endotypic patterns based on IgE and eosinophilia levels. All subjects performed the University of Pennsylvania Smell Identification Test (UPSIT®) and responded to the Sino-Nasal Outcome Test (SNOT-22). ResultsThe majority of patients had type 2 CRS (n=57, 78.1%). Patients with type 2 CRS compared to non-type 2 CRS had a higher prevalence of nasal polyps (93% vs. 12.5%), asthma (40.3% vs. 12.5%), and non-steroidal anti-inflammatory drug exacerbated respiratory disease (NERD, 17.5% vs. 0%). Type 2 patients also had significantly lower UPSIT® and higher SNOT-22, Lund-Kennedy, and Lund-Mackay scores. ConclusionOur study provides evidence that type 2 CRS is associated with a higher prevalence of nasal polyps, asthma, and NERD, as well as decreased olfactory function and worse quality of life scores. These data will contribute to the body of knowledge on CRS and the development of treatments for this disease in Brazil. Level of evidence3.

Nicotine is an addictive drug whose popularity has recently increased, particularly among adolescents, because of the availability of electronic nicotine devices (i.e., "vaping") and nicotine e-liquids containing additives with rich chemosensory properties. Some efforts to understand the role of these additives in nicotine reward suggest that they increase nicotine reward and reinforcement, but the sensory contributions of additives, especially in their vapor forms, are largely untested. Here, to better understand how a fruit-flavored (i.e., strawberry) additive influences nicotine reward and aversion, we used a conditioned place preference (CPP) procedure in which nicotine and a strawberry additive were delivered as a vapor to male and female adolescent mice. We found that nicotine vapor alone can lead to a dose-dependent CPP when using a biased design. The strawberry additive did not produce CPP on its own, and we did not observe an effect of the strawberry additive on nicotine vapor-induced reward. Nevertheless, mice exposed to nicotine plus strawberry additive vapor had higher plasma cotinine concentrations, which did not appear to reflect altered nicotine metabolism. Instead, by directly measuring vapor sampling through respiration monitoring, we uncovered an increase in the amount of sniffing toward strawberry-containing nicotine vapor compared with nicotine vapor alone. Together these data indicate that chemosensory-rich e-liquid additives may enhance the perceived sensory profile of nicotine vapors rather than the reward value per se, which leads to overall increased nicotine exposure.