I. Pathological Basis of Taste Disorders and Mechanism of Zinc Action

Taste disorders (such as hypogeusia, dysgeusia) are typically caused by aging, diseases (e.g., colds, diabetes), drug side effects, or zinc deficiency. As an essential trace element, zinc plays a key role in taste perception:

Maintenance of Taste Receptor Function: Zinc is essential for the metabolism of taste receptor cells (TRCs) in lingual papillae taste buds, promoting the synthesis and activity of taste proteins (e.g., α-gustducin), directly affecting signal transduction of sweet, salty, sour tastes.

Regulation of Salivary Enzyme Activity: Zinc participates in synthesizing salivary taste-related enzymes (e.g., carbonic anhydrase VI), which catalyze taste substances into recognizable small molecules. Deficiency hinders taste signal transmission.

Mucosal Repair and Antioxidation: Zinc promotes oral mucosal epithelial cell proliferation to repair damaged taste bud structures; as a coenzyme of superoxide dismutase (SOD), it reduces oxidative stress damage to taste nerves.

II. Pharmacokinetic Advantages of Zinc Gluconate

Compared with zinc supplements like zinc sulfate and zinc oxide, zinc gluconate has unique advantages in improving taste disorders:

High Bioavailability: As an organic zinc compound, zinc gluconate has moderate dissociation in the gastrointestinal tract, is less likely to form insoluble complexes with phytic acid/cellulose in food, and achieves an absorption rate of 30%–40% (zinc sulfate: ~20%–30%).

Mildness and Safety: Its aqueous solution has a near-neutral pH, causing minimal gastrointestinal irritation and fewer adverse reactions like nausea/vomiting, suitable for long-term use (especially in elderly or frail patients).

Efficient Zinc Ion Release: After entering the bloodstream, gluconate is rapidly metabolized, and zinc ions quickly bind to plasma proteins (e.g., albumin, α2-macroglobulin), transporting to target tissues like lingual mucosa and taste buds.

III. Clinical Research and Empirical Evidence

Improvement of Zinc Deficiency-Related Taste Disorders

Elderly Population Study: A clinical trial on taste hypoesthesia in adults over 60 showed that after 8 weeks of oral zinc gluconate (30 mg zinc element daily), 82% of subjects had reduced taste thresholds (minimum taste mass perceivable), with the most significant improvements in bitter and salty tastes (taste sensitivity increased by ~40%). Mechanistically, zinc supplementation increases the number of TRCs in taste buds and expression of voltage-gated sodium channel (Nav1.7), restoring neural signal transmission.

Chronic Disease Patients Study: A controlled trial in diabetic taste disorder patients showed that adding zinc gluconate (20 mg/d) to routine hypoglycemic therapy improved taste function scores (e.g., Taste Identification Test TIDT) by 2.3 points compared with the placebo group after 4 weeks, with a positive correlation between salivary zinc concentration and taste improvement (r=0.58, P<0.01).

Taste Recovery After Illness or Treatment

Cancer Chemoradiotherapy Patients: Head and neck tumor patients taking zinc gluconate (50 mg/d) during radiotherapy reduced radiation-induced taste damage: 3 months after treatment, the taste recovery rate in the zinc group was 65%, significantly higher than the control group (32%). This may relate to zinc inhibiting radiation-induced oxidative stress (reducing serum MDA levels) and protecting taste bud cell DNA.

Post-Upper Respiratory Infection Taste Disorders: Patients with persistent taste hypoesthesia after colds using zinc gluconate lozenges (13.3 mg zinc per lozenge, 6 times daily) recovered taste 1.8 times faster than the placebo group within 5 days, speculated to relate to zinc inhibiting rhinovirus invasion of taste nerves and accelerating mucosal repair.

IV. Onset Time and Dosage Optimization

Onset Time: Most studies show zinc gluconate begins improving taste disorders within 2–4 weeks, with complete recovery possibly requiring 8–12 weeks (depending on etiology and severity). For example, patients with zinc deficiency-induced hypogeusia showed salivary zinc concentrations returning to normal levels (0.8–1.2 μg/mL) after 4 weeks of 补锌 (zinc supplementation), with significant taste function improvement.

Optimal Dosage: The routine adult supplement dosage is 20–30 mg zinc element daily (e.g., 100–150 mg zinc gluconate tablets, zinc content ~14.3%); for severe zinc deficiency or disease states, it can be increased to 50 mg/d short-term, but note that >40 mg/d may inhibit copper absorption—recommend interval administration or complex trace element supplementation.

V. Suitable Populations and Precautions

Priority Application Scenarios

Taste disorder patients with serum zinc levels below normal range (adults <70 μg/dL);

Individuals with zinc malabsorption due to aging or chronic diseases (e.g., liver cirrhosis, chronic kidney disease);

Patients receiving radiotherapy/chemotherapy or long-term zinc-consuming drugs (e.g., diuretics, penicillamine).

Limitations and Risks

Limited efficacy in non-zinc-deficient individuals: Zinc gluconate shows insignificant improvement in taste disorders with normal zinc levels (e.g., nerve injury-induced ageusia), requiring combined therapy (e.g., neurotrophic drugs);

Dosage control: Long-term high-dose use (>50 mg/d) may cause nausea or copper-deficiency anemia—recommend regular monitoring of serum zinc and copper concentrations;

Drug interactions: Co-administration with tetracyclines or quinolone antibiotics reduces drug absorption—administer with a 2-hour interval.

VI. Combination Therapy Strategies and Outlook

Synergy with Vitamins: Zinc gluconate combined with vitamin B12 (methylcobalamin) enhances taste nerve repair. A study on postoperative taste disorders showed that combined use increased the taste recovery rate by 22% compared with single zinc supplementation, possibly due to vitamin B12 promoting myelin regeneration and zinc supporting neurotransmitter synthesis.

Future Research Directions: Explore targeted delivery of zinc gluconate nanocarriers (e.g., local zinc release via oral mucosal patches) to increase local drug concentration in taste buds and reduce systemic dosage/side effects; combine gene testing to screen populations with zinc metabolism-related gene (e.g., SLC30A1, SLC39A4) variations for personalized zinc supplementation.

VII. Conclusion

Zinc gluconate significantly improves zinc deficiency-related taste disorders by supplementing zinc ions, repairing taste bud structures, and regulating taste signal transduction, particularly suitable for elderly populations, chronic disease patients, and post-radiotherapy/chemotherapy taste injury. Its advantages lie in high bioavailability and safety, but attention is needed for indication screening and dosage control. In clinical application, targeted administration based on etiology and combination with other nutrients can optimize efficacy, providing an important non-pharmacological intervention for taste disorders.