Sleep is a fundamental physiological process essential for maintaining physical health, cognitive function, emotional regulation, and overall well-being throughout the human lifespan, including in the geriatric population. [1, 2, 3] Restorative sleep supports cellular repair, metabolic homeostasis, memory consolidation, neurocognitive performance, and psychological resilience. Optimal sleep quality is closely linked to enhanced cognition and mental health outcomes [1, 2, 3]. Despite its importance, global sleep quality has declined in recent decades, with a rising prevalence of disorders such as insomnia, obstructive sleep apnoea, restless legs syndrome, and chronic sleep deprivation [4, 5].

Although physiological changes in sleep occur with normal ageing, insomnia is disproportionately prevalent in the geriatric population and should not be regarded as an inevitable consequence of ageing. Rather, it is a multifactorial condition influenced by neurobiological changes, psychosocial stressors, comorbidities, polypharmacy, and environmental factors [6]. Sleep disturbance in older adults is associated with increased morbidity and mortality, reduced quality of life—particularly amongst institutionalised individuals—and substantial healthcare costs. It also increases the risk of falls, functional decline, and loss of independence [6].

Ageing is characterised by progressive alterations in sleep architecture, including reduced slow-wave sleep, increased sleep fragmentation, prolonged sleep latency, and decreased sleep efficiency [7]. Consequently, many older adults report dissatisfaction with sleep, making it one of the most common health complaints in this age group [8, 9]. Sleep disruption is further linked to adverse lifestyle behaviours and chronic conditions, including smoking, alcohol consumption, diabetes mellitus, hypertension, obesity, psychological stress, depressive symptoms, and cognitive decline [10]. Clinical management remains challenging, as long-term use of sedative-hypnotics carries substantial risks of cognitive impairment, daytime somnolence, impaired coordination, and falls [8].

Recent research has highlighted the role of micronutrients in sleep regulation, particularly zinc. Zinc is an essential trace element involved in enzymatic, structural, and regulatory processes throughout the body [11]. Within the central nervous system, zinc functions as a neuromodulator, supporting synaptic transmission, neuronal plasticity, and regulation of neurotransmitters such as gamma-aminobutyric acid (GABA), glutamate, serotonin, and melatonin—all critical for sleep–wake regulation [12, 13]. Zinc also modulates circadian rhythms and neuronal signalling pathways involved in sleep initiation and maintenance, with accumulating evidence supporting its role in sleep physiology [13].

Clinical and observational studies suggest that zinc supplementation may be associated with improved sleep quality across age groups [5, 14]. Systematic reviews have reported beneficial associations with sleep latency and efficiency [5]. The geriatric population is particularly susceptible to zinc deficiency due to inadequate dietary intake, impaired absorption, chronic inflammation, systemic illness, and polypharmacy [15]. Subclinical deficiency is common and often underrecognised in this age group. Reduced serum zinc levels have been associated with poor sleep quality, frequent nocturnal awakenings, and insomnia [5, 15]. Zinc deficiency may further exacerbate neuroinflammation, oxidative stress, and dysregulation of neuroendocrine pathways, thereby negatively influencing sleep and mental health outcomes [15].

Sleep disturbances in older adults have profound implications for mental health. Chronic insomnia is associated with depression, anxiety, cognitive impairment, and increased risk of neurodegenerative disorders. Psychiatric conditions may further disrupt sleep, perpetuating a bidirectional cycle that complicates clinical management. Zinc deficiency has also been linked to mood disorders, impaired cognition, and heightened susceptibility to psychological stress, suggesting a biologically plausible connection between zinc status, sleep regulation, and mental health outcomes.

Despite growing interest in zinc's role in sleep and mental health, evidence specifically addressing the geriatric population remains limited [5, 16]. Understanding the associations between zinc status, sleep regulation, insomnia, and mental health is essential for developing targeted preventive and therapeutic strategies. This study therefore aims to evaluate the associations between serum zinc levels, sleep quality, insomnia severity, and mental health outcomes in geriatric patients attending a tertiary care centre, with the goal of identifying modifiable factors to support sleep and overall well-being in this vulnerable group.

Study Design and Setting This cross-sectional observational study was conducted at F.H. Medical College and Hospital, Agra, India encompassing both the outpatient and inpatient departments catering to geriatric patients, from April 2025 to March 2026. Ethical approval was obtained from the Institutional Ethics Committee (IEC) of F.H. Medical College and Hospital, Agra, prior to the commencement of the study. Written informed consent was obtained from all participants after explaining the study objectives, procedures, potential risks, and benefits. Study Population The study population comprised geriatric patients aged ≥60 years attending the study site. Participants were included irrespective of gender, comorbidities, or socioeconomic status, provided they met the predefined inclusion and exclusion criteria and provided voluntary written informed consent. Inclusion and Exclusion Criteria Patients aged 60 years or older attending the outpatient or inpatient departments of the study centre, who were willing to provide written informed consent and agreed to undergo serum zinc measurement and complete sleep and mental health assessments, were included. Patients with known chronic liver or renal disease affecting zinc metabolism, those currently receiving zinc supplements or medications known to interfere with serum zinc levels, individuals with severe cognitive impairment or psychiatric conditions precluding reliable questionnaire completion, those with acute critical illness requiring intensive care, and those unwilling or unable to provide informed consent were excluded from the study. Sampling and Sample Size A convenience sample of 40 participants was enrolled during the study period based on feasibility and resource constraints The sample size was calculated using the singl population proportion formula n = Z²PQ / d² Where: Z = 1.96 at a 95% confidence level P = 73.3% (0.733), representing the prevalence of poor sleep quality among older adults reported in the reference study by Afzali et al. [8] Q = 1 − P = 0.267 d = 14% (0.14) as the absolute precision Calculation: n = (1.96² × 0.733 × 0.267) / (0.14²) n = 38.3 The calculated sample size was 38 participants, which was rounded up to 40 participants. Final Sample Size = 40 participants. Data Collection Demographic and clinical data, including age, gender, and comorbidities, were systematically recorded. Fasting venous blood samples (5 mL) were collected in trace element-free tubes by trained phlebotomists. Serum zinc concentrations were measured using atomic absorption spectrophotometry (AAS) on a calibrated instrument following standard laboratory protocols. Participants were classified as having low serum zinc (<70 µg/dL), normal serum zinc (70–120 µg/dL), or high serum zinc (>120 µg/dL) in accordance with established reference ranges [28]. Sleep quality, insomnia severity, depressive symptoms, and anxiety were assessed using the following validated instruments, all of which are freely available for non-commercial academic and clinical research use with appropriate citation of the original source: Pittsburgh Sleep Quality Index (PSQI) [29]: A 19-item self-rated questionnaire assessing overall sleep quality over the preceding month. Scores range from 0 to 21; a global score >5 indicates poor sleep quality. The PSQI demonstrates good internal consistency (Cronbach's α = 0.83) and has been validated in older adult populations. Insomnia Severity Index (ISI) [30]: A 7-item scale evaluating the nature, severity, and impact of insomnia. Scores range from 0 to 28; scores of 0–7 indicate no clinically significant insomnia, 8–14 subthreshold insomnia, 15–21 moderate insomnia, and 22–28 severe insomnia. Internal consistency is good (α = 0.74). Geriatric Depression Scale-15 (GDS-15) [31]: A 15-item yes/no questionnaire designed to screen for depression in older adults. Scores range from 0 to 15; a score ≥5 is suggestive of depression (sensitivity 92%, specificity 89%). Generalised Anxiety Disorder Scale-7 (GAD-7) [32]: A 7-item scale for assessing anxiety severity. Scores range from 0 to 21; scores of 5–9 indicate mild anxiety, 10–14 moderate anxiety, and ≥15 severe anxiety. The scale demonstrates excellent internal consistency (α = 0.92). The GDS-15 is in the public domain, while the PSQI, ISI, and GAD-7 are copyright-protected but may be used free of charge for non-commercial academic and clinical research with appropriate citation of the original source. All collected data were anonymised and securely stored to maintain participant confidentiality. Statistical Analysis Data were analysed using SPSS version 28.0 (IBM Corp., Armonk, NY, USA). Continuous variables were expressed as mean ± standard deviation (SD), and categorical variables as frequencies and percentages. The prevalence of low serum zinc, poor sleep quality, insomnia, depression, and anxiety was calculated. Comparisons between participants with low and non-low serum zinc were performed using independent samples t-tests. Associations between serum zinc levels and sleep and mental health scores were assessed using Pearson correlation coefficients. Assumptions of normality and homogeneity of variance were evaluated prior to parametric testing. A p-value <0.05 (two-tailed) was considered statistically significant.

Table 1: Demographic Characteristics

A total of 40 geriatric patients were enrolled, with a mean age of 72.3 ± 6.1 years (range: 60–88 years); 55% were female and 45% were male [Table 1].

Table 2: Serum Zinc Distribution

Low serum zinc (<70 µg/dL) was identified in 40% (n=16) of participants [Table 2]. The mean serum zinc level across the entire cohort was 74.3 ± 13.1 µg/dL. The high prevalence of zinc deficiency reflects the nutritional vulnerability of older adults to micronutrient inadequacy.

Given that only one participant had elevated serum zinc (>120 µg/dL), this individual was grouped with the normal zinc category to form a 'non-low' zinc group (n=24) for subsequent comparative analysis, ensuring statistical meaningfulness.

Table 3: Sleep Quality, Insomnia, and Mental Health Outcomes (Whole Sample)

Sleep disturbance was highly prevalent in this cohort, with 80% of participants demonstrating poor sleep quality (PSQI >5) and 35% meeting the threshold for moderate-to-severe insomnia [Table 3]. Depressive symptoms (GDS-15 ≥5) were identified in 45% of participants, while clinically significant anxiety (GAD-7 ≥10) was present in 10%. These findings indicate a substantial burden of sleep and mood disturbances in this geriatric sample.

Table 4: Pearson Correlation Between Serum Zinc and Outcome Measures

*p < 0.05; statistically significant.

Serum zinc demonstrated a statistically significant moderate negative correlation with PSQI (r = −0.45, p = 0.004) and ISI (r = −0.39, p = 0.010), indicating that lower serum zinc was associated with poorer sleep quality and greater insomnia severity [Table 4]. A weaker but statistically significant negative correlation was observed with depressive symptoms (GDS-15: r = −0.31, p = 0.049). The association with anxiety (GAD-7: r = −0.28, p = 0.070) did not reach statistical significance, representing a non-significant trend.

Table 5: Comparison of Outcomes by Zinc Status (Low vs non-low)

*p < 0.05; statistically significant.

Participants with low serum zinc had significantly higher PSQI scores (11.2 ± 2.8 vs 9.0 ± 2.9, p = 0.010), greater insomnia severity (ISI: 15.1 ± 4.6 vs 12.5 ± 5.2, p = 0.042), and more pronounced depressive symptoms (GDS-15: 6.2 ± 2.5 vs 4.6 ± 2.3, p = 0.020) compared to the non-low zinc group [Table 5]. Anxiety scores were elevated in the low zinc group but the difference did not reach statistical significance (GAD-7: 6.1 ± 3.0 vs 4.6 ± 2.5, p = 0.060).

The principal findings of this study indicate that zinc deficiency is prevalent in the geriatric population and is significantly associated with poorer sleep quality, greater insomnia severity, and higher depressive scores. These findings are consistent with the emerging body of literature [5, 13, 15, 16] on the role of micronutrient status in sleep and mental health in older adults.

The high prevalence of poor sleep quality (80%) and depressive symptoms (45%) in our sample is consistent with published epidemiological estimates [9, 16]. Fernandes et al. reported sleep disorder prevalence rates of 23–34% in geriatric populations, with higher rates observed in hospitalised or institutionalised cohorts [16]. Similarly, zinc deficiency was found in 40% of our participants, reflecting the well-documented vulnerability of older adults to micronutrient inadequacy attributable to reduced dietary intake, impaired gastrointestinal absorption, polypharmacy, and chronic inflammatory states [5, 15].

The observed inverse associations between serum zinc and PSQI (r = −0.45, p = 0.004) and ISI (r = −0.39, p = 0.010) are biologically plausible. Zinc serves as a cofactor in neurotransmission and neuroendocrine regulation, modulating GABA, glutamate, serotonin, and melatonin pathways critical for sleep initiation and maintenance [12, 13]. Zinc further influences melatonin synthesis, growth hormone secretion, immune function, and antioxidant defence, collectively affecting sleep architecture and mental health [17–20]. These mechanisms provide a strong rationale for the negative correlation observed between zinc deficiency and sleep outcomes in our cohort. These correlations, while statistically significant, were of weak-to-moderate strength and should therefore be interpreted cautiously, particularly given the modest sample size and cross-sectional design [Table 4]. This inference is further supported by the comparison of outcomes according to zinc status, in which participants with low serum zinc had significantly poorer PSQI, ISI, and GDS-15 scores than those with non-low zinc, corroborating the correlation-based findings from an independent analytical approach [Table 5].

Our findings are consistent with previous observational and interventional studies. Afzali et al. reported that zinc supplementation (30 mg/day for 10 weeks) was associated with significantly improved PSQI scores in older adults [8], whilst Haddadian-Khouzani et al. observed similar improvements in sleep quality in haemodialysis patients receiving zinc gluconate supplementation [15]. Luojus et al. reported that serum zinc concentrations were lowest among ageing men who reported short sleep duration (≤6 hours), measured by self-reported habitual sleep duration in a large population-based cohort of 2,570 men (analysed using analysis of covariance across sleep-duration categories rather than a Pearson correlation coefficient), a finding directionally consistent with our observations [26]. Conversely, some studies found no significant association between zinc supplementation and sleep outcomes in younger populations or those without baseline zinc deficiency [22, 23, 24], suggesting that the effect of zinc may be most pronounced in individuals with established deficiency, as seen in our geriatric cohort.

The statistically significant, albeit weak, negative correlation between serum zinc levels and GDS-15 scores (r = −0.31, p = 0.049) [Table 4] is consistent with evidence linking zinc deficiency to mood dysregulation and depressive symptoms, although the modest effect size warrants cautious interpretation. The lack of statistical significance for the GAD-7 correlation (r = −0.28, p = 0.070), which approached the effect size observed for GDS-15, more plausibly reflects insufficient statistical power in a sample of 40 participants than a true absence of association, although a genuinely weaker relationship between zinc status and anxiety compared with depressive symptoms cannot be excluded. These findings suggest that zinc deficiency in older adults may have a more pronounced association with sleep quality, insomnia severity, and depressive symptoms than with anxiety.

Limitations

This study has several important limitations that warrant consideration when interpreting the findings. The sample size was small (n = 40), limiting statistical power and generalisability. The cross-sectional design precludes causal inference, and the observed associations should be interpreted accordingly. The absence of control for potential confounders—including comorbidities, medication use, dietary zinc intake, physical activity, and socioeconomic factors—means that the reported associations may be partially explained by unmeasured variables. Recruitment from a single tertiary care centre limits representativeness, and self-reported questionnaire data may be subject to recall and response bias. Future research should employ larger, multicentre, longitudinal, or randomised interventional designs with appropriate confounder adjustment to confirm these associations and evaluate the therapeutic potential of zinc optimisation in geriatric sleep and mental health management.

This study demonstrates significant inverse associations between serum zinc levels and sleep quality, insomnia severity, and depressive symptoms in geriatric patients, with zinc deficiency prevalent in 40% of participants. These findings support the routine assessment of zinc status in older adults and suggest that targeted nutritional interventions may represent a modifiable strategy to improve sleep and mental health outcomes in this vulnerable population. Larger, longitudinal, and interventional studies are warranted to confirm these associations and evaluate the therapeutic potential of zinc optimisation.

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