The influence of zinc deficiency on taste disorders in selected medical aspects

It has been proven that the absorption of zinc taken orally is 25–66%. The absorption process takes place in the small intestine and especially in two of its sections: the jejunum and the ileum. Zinc is present in all tissues and body fluids, including blood cells, pancreas, retina, prostate, kidneys, lungs, skin, liver, brain, gastrointestinal tract, choroid of the eye and heart, as well as muscles and bones, where the highest content was recorded [18,19]. Zinc transport occurs in serum due to the presence of proteins such as albumin (57%), α2-globulin (40%), transferrin and amino acids (3%). The content of zinc in serum is less than 2% of its total content. The vast majority, as much as 95%, of the total content is intracellular zinc found, among other sites, in the cytosol and organelles such as nuclei and vesicles [20]. There are studies stating that there are cellular mechanisms that condition the right amount of zinc and prevent its excessive accumulation [18]. Zinc is imported into the cell by 14 protein members belonging to a family of zinc importers (ZIP- Zrt- and Irt-like proteins), while the export takes place thanks to the presence of 10 protein members belonging to the zinc exporter family (ZnT). ZIP and ZnT are also responsible for regulating the presence of zinc in the Golgi apparatus, endoplasmic reticulum, and mitochondria. Intracellular zinc homeostasis is caused by metallothioneins (MTs)—constituting a zinc cell buffer due to the ability to bind to 7 zinc ions each [21]. Associated with the cell membrane are zincosomes in the form of vesicles that have the ability to absorb zinc and release it when needed [18].

Taste disorder is a common complaint reported by patients with diabetes type I [22,23,24] and type II [25,26]. It has been shown that one of the potential factors responsible for the occurrence of taste disturbances is zinc deficiency [12,27,28]. Patients with type II diabetes have lower concentrations of zinc in their serum compared to healthy people [29,30].

Matsugasumi et al. concluded that the ability to taste sour or bitter was significantly associated with serum zinc concentration in patients with type 2 diabetes and taste disturbances. It has been proven that serum zinc levels in patients with type 2 diabetes improved as a result of an educational program lasting 2 weeks. Continuing, both taste ability (for sour and bitter taste) and glycemic control were significantly related to serum zinc concentrations. It was proven that the improvement in glycemic control after 2 weeks of hospitalization was accompanied by an improvement in serum zinc concentration and in taste perception. However, no direct causal relationship between taste sharpness and serum zinc concentration has been demonstrated [31]. Chang et al. claimed that the ability of taste buds to perceive sour taste is selectively dependent on the sensitivity of genetically identified cells to zinc ions [32]. However, the research of Uchida et al. confirms that the transient receptor potential associated with bitter taste [33] is regulated by zinc ions[34].

One of the most common side effects in patients with head and neck cancers treated with an external beam of radiotherapy as the only form of therapy or in combination with chemotherapy is dysgeusia [35]. Changes in taste and tongue pain caused by radiation therapy usually begin to improve between three weeks and two months after the end of treatment. Improvement can take a year. The taste potential may not fully return to its pre-treatment state, especially if the salivary glands are damaged [36]. Radiation therapy and chemotherapy, by affecting the taste buds of the tongue and the mucous membrane of the nasal cavity, can cause taste disorders. Additional factors that may contribute to the change in taste are the bitter taste of chemotherapy, low oral hygiene, infections, and mucositis [37].

The Mossman and Henkin study, in which patients with taste disturbances have been treated by zinc supplementation after completing radiation therapy to the head and neck, showed that the threshold for detecting and recognizing taste was lowered [38].

Chi et al. showed that zinc-based therapy resulted in a reduced incidence of radiotherapy-induced dysgeusia. However, dysgeusia zinc treatment after radiotherapy had minimal therapeutic effect [39]. The consequence of chemoradiotherapy of head and neck cancers may be a decrease in the importance of zinc in the process of taste perception. This can be explained by the mechanism of combining sulfhydryl groups of some chemotherapeutic agents with zinc and its chelation. As a result, there is a reduced amount of zinc and direct destruction of the DNA of progenitor cells of taste buds [40,41,42,43]. This suggests that zinc has a protective potential against the improper consequences of radiotherapy occurring in taste bud cells, thereby reducing the incidence of radiotherapy-induced dysgeusia [39].

Tian et al. conducted a systematic search of three databases and included five double-blind randomized controlled trials that included a total of 352 patients undergoing chemotherapy taking either zinc sulfate or placebo. In a meta-analysis, they assessed the effect of zinc intake on the occurrence, onset, and severity of oral mucositis. Zinc intake has been shown to have no significant effect on the occurrence, onset, or worsening of mucositis caused by chemotherapy [44].

A characteristic issue in the context of the occurrence of taste disturbances is that the highest frequency of this disorder is among the older age group. With age, the percentage of people complaining of disorders in the proper perception of taste stimuli increases [45,46].

Serum zinc levels in patients with taste disturbances were quantified to demonstrate an association between zinc deficiency and age. The mean-minimum serum zinc concentration in older adults did not differ significantly from the other age groups (< 49 years of age and 50 to 64 years). However, zinc concentrations below 69 mg/dl were observed in 33% of the elderly—a much higher percentage than for those aged 49 years or younger. This result suggests that zinc deficiency may be an important factor in dysgeusia in older adults [47].

In the study conducted by Heckmann et al. patients with idiopathic taste disorder were examined. The zinc gluconate group (140 mg/day, equivalent to 20 mg/day of the element) consisted of 26 people aged 41–82 years; the average age was 61.1 years. The control group included 24 people receiving placebo (age range 47–78 years; average age 61.0 years). The therapy lasted 3 months. As a result of zinc therapy, there was a significant improvement in taste perception [48].

Stewart-Knox et al. assessed taste acuity among healthy, older people. It consisted of patients being treated with elemental zinc (15 mg or 30 mg as zinc gluconate) or placebo for six months. In the results, the ability to feel salty taste was significantly higher in the group taking zinc in the amount of 30 mg. However, the sensory threshold for salty tastes may be age-related. There were no differences in the perception of sweet, sour, or bitter taste among the patients studied. There were also no differences in taste in patients treated with zinc 15 mg [49].

Halitosis, defined as an unpleasant smell from the oral cavity, may co-occur together with taste disorders in the course of periodontitis and xerostomia. The main cause of halitosis is the bacterial metabolism of amino acids [50]. Volatile sulfur compounds such as hydrogen sulfide, methyl mercaptan, and dimethyl sulfide formed as a result of bacteria are responsible for the formation of unpleasant odor from the mouth. Large amounts of hydrogen sulfide and methyl mercaptan as a result of the processing of cysteine, methionine, or serum proteins are produced by anaerobic bacteria such as Porphyromonas gingivalis, Treponema denticola, Prevotella intermedia, Fusobacterium nucleatum, and Eubacterium [51,52].

In a study conducted by Suzuki et al., the ability of zinc ions to directly bind to hydrogen sulfide gas was compared to other metal ions. Nine metal chlorides and six metal acetates were tested. The minimum concentration needed to inhibit hydrogen sulfide oxidation was determined using the serial dilution method. The inhibitory effect of zinc ions on the growth of six strains of oral bacteria related to volatile sulfur compounds (VSCs) and three strains unrelated to VSC production were also investigated. It was proved that aqueous zinc solutions inhibited the volatilization of hydrogen sulfide almost completely. In contrast, the effect of zinc ions on the growth of bacteria in the mouth was strain dependent [53].