Discussion

This study examined the associations between demographic characteristics, biochemical and hematologic marker levels, and the odds of taste problems. Age, race, specifically, Non-Hispanic Whites and Black race, less than a high school education, and household income were sociodemographic factors associated with taste problems. Among biochemical markers, serum albumin, percentage of monounsaturated and saturated fatty acids, and serum copper levels were associated with taste problems. Hematologic markers were not associated with self-reported taste problems.

Increasing age has been widely described as being associated with taste problems. A study using NHANES 2011–2012 described that the prevalence of self-reported taste problems increased from approximately 19 % in adults aged 40 and older to 27 % in those aged 80 and older [1]. This age-related decline in gustatory function, termed presbygeusia, appears to be a physiological phenomenon that occurs even in the absence of comorbidities or medication effects [3], 4].

Several factors have been described that may contribute to age-related taste alterations. These include structural changes in taste buds, reduced number and altered morphology of taste receptor cells, decrease in saliva composition and salivary flow, which can lead to dry mouth, changes in the central nervous system, including age-related neuronal decline affecting gustatory processing, and dysbiosis of the oral microbiome. Other important contributors include polypharmacy, zinc deficiency, and oral/systemic diseases [1].

Objective testing confirms that individuals older than 60 years have significantly higher taste thresholds, with the most pronounced increases in detection thresholds occurring for sour and bitter tastes [14]. Taste loss in older adults has been linked to poor quality of life due to reduced appetite, nutritional imbalance, increased susceptibility to diseases, and diminished quality of life [15]. Further, smell and taste disorders can also serve as early signs of neurodegenerative disease, including dementia and Parkinson’s disease, and are associated with increased mortality [3], 4].

The association between race and taste problems is complex. Non-Hispanic White and Black populations have been reported to have a greater genetic diversity in bitter taste receptor genes (TAS2R38), which may contribute to higher odds of taste problems in them. Other risk factors like diet (heavy alcohol use), smoking, polypharmacy, and cardiovascular disease can lead to taste impairment in this group [16], [17], [18], [19], [20]. Lower education levels and annual household income are associated with higher smoking rates, poor nutrition, and greater occupational chemical exposures, which can in turn cause dysgeusia [2], 18], [21], [22], [23]. Both factors have previously been reported as independently associated with self-reported taste problems in population-based studies. In an NHANES 2011–2012 analysis of adults aged 40 and older, lower education was an independent risk factor for self-reported taste alteration after adjusting for health behaviors and chemosensory-related conditions, while family income at or below 110 % of the poverty threshold was an independent predictor of smell alteration [1]. A subsequent NHANES 2013–2014 cross-sectional study confirmed that low educational attainment and low family income were independently associated with higher prevalence of chemosensory impairment, and a JAMA Otolaryngology study of 7,340 NHANES participants further corroborated that individuals with subjective perception of taste loss had lower education levels and family income compared to those without taste loss [23], 24].

Several interconnected pathways likely underlie these associations. Lower socioeconomic status is linked to a greater burden of chronic diseases and polypharmacy, both established causes of taste dysfunction, with drug use and zinc deficiency accounting for approximately 21.7 % and 14.5 % of taste disorders, respectively [2], 25]. Higher prevalence of oral diseases such as dental caries, periodontal disease, and untreated oral pathology in this group of individuals may impair gustatory function [26]. Individuals with lower education are also more likely to be exposed to environmental toxins such as cadmium and lead through occupational settings, and higher blood cadmium levels have been linked to increased risk of chemosensory impairment, although we did not observe a significant association with blood cadmium levels [27]. Higher smoking rates among lower socioeconomic groups further contribute, as tobacco smoke directly damages taste receptor cells [22], 27]. Finally, reduced healthcare access may limit evaluation and management of taste complaints, as only approximately 20 % of the estimated 19.4 million Americans with smell and/or taste abnormalities discuss the problem with a healthcare provider [22].

The mechanism by which lower levels of saturated fatty acids cause taste problems likely involves reduced stimulation of lingual fat taste receptors (CD36 and GPR120), whose expression is directly regulated by levels of dietary fat. Low saturated fatty acid levels can also lead to deficiency of fat-soluble vitamins essential for taste bud cell membrane integrity and receptor function [28], [29], [30], [31]. Conversely, higher levels of monounsaturated fatty acids may lead to dysgeusia through chronic overstimulation and resulting downregulation of the lingual fat taste receptors. This, in turn, can reduce Ca2+ signaling in taste bud cells, blunting taste sensation [32], [33], [34]. Additionally, excessive Monounsaturated fatty acid levels can potentially alter the lipid raft composition of taste bud cell membranes. This can affect fat receptor trafficking and disrupt downstream ERK1/2-MAPK signaling cascades that relay taste signals from the lingual taste receptors to the sensory nerve endings [29], 35].

Albumin deficiency-related taste dysfunction is likely due to the fact that albumin is a carrier for zinc, which is critical for taste bud cell turnover. Therefore, hypoalbuminemia reduces zinc bioavailability and raises taste detection thresholds [36]. Additionally, low albumin reflects underlying protein-energy malnutrition and systemic inflammation, which both independently impair taste bud regeneration and salivary gland function [37], [38], [39]. Finally, elevated serum copper negatively impacts zinc bioavailability, which imbalances the Cu/Zn ratio, in turn, lower zinc levels are associated with increased taste recognition thresholds [40]. High copper levels also generate reactive oxygen species that damage taste bud cells and salivary proteins that are crucial for taste [41], 42].

Clinical and research implications

The findings highlight the importance of routine taste dysfunction screening, especially in older adults, Non-Hispanic White and Black individuals, and those with lower education and annual income. They also suggest that measurement of serum fatty acid concentration, serum albumin, and copper levels may aid in understanding the pathophysiology of dysgeusia. Addressing modifiable risk factors such as polypharmacy, smoking, occupational chemical exposures, and limited access to dental and medical care in underserved populations may reduce the prevalence of taste dysfunction . As our study was retrospective, causal inferences cannot be drawn from it. Future prospective research studies are needed to investigate whether the findings of this study are causally linked to taste dysfunction, particularly stratified by severity and evidence of objective taste abnormalities. In addition to that, studies should examine the role of sociodemographic factors to see if they are causally linked to taste dysfunction.

Strengths and limitations

This study had several strengths. One of these was the use of NHANES data, providing a large, nationally representative sample, promoting the generalization of the findings to the U.S. Population. Another strength was that including both demographic characteristics and biochemical markers made the study comprehensive in the exploration of factors associated with taste dysfunction.

However, several limitations should also be recognized. The observational design of this study does not allow us to establish directionality, meaning that taste dysfunction may itself alter dietary intake and nutritional status, rather than solely resulting from them. Further, taste problems were self-reported which lends itself to recall bias. Also, people might have experienced mild taste loss that wasn’t reported and wouldn’t have been recognized without objective testing methods, like whole-mouth gustatory testing. Finally, while the analysis was adjusted for many covariates, there were many unmeasured factors, such as medication, oral hygiene status, smoking history, dietary intake, BMI, height and weight. These could be incorporated in future studies to further adjust the analysis and improve accuracy.