Abstract
Background
Inflammation is crucial in the development of depression. This study aims to examine the potential association between the Neutrophil-Percentage-to-Albumin Ratio(NPAR) and depression symptoms.
Methods
This study adopted a cross-sectional design, involving patients with depression symptoms and those without depression symptoms with comprehensive NPAR data originated from the National Health and Nutrition Examination Survey(NHANES) spanning 2011 to 2018. The research utilized weighted multivariate logistic regression models and multivariate linear regression to investigate the linear relationship between NPAR levels and depression symptoms and its severity scores. The characterization of nonlinear relationships was accomplished by employing fitted smoothing curves. Furthermore, subgroup analyses and interaction assessments were conducted to offer additional insights.
Results
This study involved a total of 10,829 participants, and the prevalence of depression among them was found to be 15.08%. The multiple logistic regression analysis revealed a statistically significant positive association between the continuum of NPAR and depression symptoms[OR:1.03, 95% CI: (1.00, 1.05)], as well as depression severity scores[β: 0.08, 95% CI: (0.04,0.11)]. Stratifying NPAR into quartiles, we found that higher NPAR associated with increased odds of depression symptoms. Furthermore, in subgroup analysis, there were no significant differences in the relationship between NPAR levels and depression symptoms or its severity scores within populations with or without diabetes and cardiovascular diseases. Additionally, the use of a two-stage linear regression model uncovered a non-linear relationship between NPAR and depression symptoms.
Conclusions
Our research indicates that NPAR levels were associated with depression symptoms. To corroborate our findings, larger prospective studies are warranted to elucidate nonlinear associations in greater detail.
Supplementary Information
The online version contains supplementary material available at 10.1186/s12888-024-06178-0.
Keywords: Depression symptoms, Neutrophil-percentage-to-albumin ratio(NPAR), NHANES, Cross-sectional study
Introduction
Depression is a significant mental health condition with a substantial global burden. As per the World Health Organization(WHO), it ranks among the most prevalent mental health issues worldwide, affecting hundreds of millions annually [1]. The primary clinical presentations of depression include enduring feelings of low mood, diminished interest or pleasure, self-criticism, and guilt, significantly impairing the patient’s quality of life and daily functioning [2].
Studies suggest that chronic inflammation may induce neuroinflammation by activating brain immune cells, such as microglia and astrocytes [3]. Under stress, these cells secrete pro-inflammatory cytokines like IL-1, IL-6, and TNF-α, which initiate inflammatory processes in the brain. This inflammation impairs neuronal function, particularly in areas responsible for emotion regulation, such as the limbic system and prefrontal cortex [4]. Moreover, the inflammatory response disrupts the balance of critical neurotransmitters like serotonin and dopamine, potentially leading to depressive symptoms such as mood disturbances, anhedonia, and cognitive deficits [5].
The Neutrophil-Percentage-to-Albumin Ratio(NPAR) integrates neutrophils and albumin, two distinct biomarkers that reflect acute and chronic inflammation, respectively [6]. Compared to single inflammation markers like C-reactive protein or IL-6, NPAR offers a more comprehensive assessment by capturing both acute and persistent inflammatory responses [7]. In a cross-sectional study focused on maintenance hemodialysis(MHD) patients, it was observed that Neutrophil-to-Lymphocyte Ratio(NLR) levels were significantly elevated in groups with more severe depressive symptoms. Multivariable analysis further indicated that NLR was an independent predictor of mild to moderately severe depressive symptoms [8]. Similarly, studies on lung cancer patients have demonstrated a relationship between NLR and depressive symptoms, particularly in advanced-stage cases where elevated NLR levels are associated with systemic inflammation [9].
Although the relationship between inflammation and depression has been widely researched, the application of NPAR in this area is still in its early stages. As a relatively novel inflammatory marker, NPAR has not yet been widely utilized in depression symptoms research. Thus, it offers new perspectives and has the potential to open up new avenues for future investigations. Therefore, the objective of this study is to investigate the associations between NPAR and depression symptoms in a substantial, nationally representative sample.
Methods
Study population
NHANES is a research study conducted in the United States with the objective of gathering extensive information on the nutritional and health condition of the entire U.S. population.The sampling technique employed is both sophisticated and rigorous, guaranteeing that the acquired data is representative of the entire nation [10]. This study employed consecutive NHANES dataset cycles spanning from 2011 to 2018. The research protocol was scrutinized and received permission from the National Center for Health Statistics(NCHS) Research Ethics Review Board. Before their participation, all subjects gave informed consent. At the outset, a substantial total of 39,156 participants were included.
Subsequently, individuals with missing data on Neutrophil-Percentage-to-Albumin Ratio(NPAR), depression symptoms, demographic variables, those under 18 years old, as well as those with incomplete information on smoking, blood pressure, cardiovascular disease, diabetes history were excluded. The final sample consisted of 10,829 participants (Fig. 1).
Fig. 1.
Flow chart of study participants selection
Study variables
Assessment of depression symptoms
Depression symptoms data for NHANES participants were collected through questionnaire responses. The Patient Health Questionnaire-9(PHQ-9), a widely used self-assessment tool for depressive syndrome, consists of nine items, such as low mood, poor sleep, diminished interest, fatigue, reduced appetite, psychomotor retardation, low self-esteem, impaired concentration, and suicidal ideation, with each question being scored on a scale ranging from 0 to 3 [11]. The overall score is calculated by combining the scores of all elements. Scores are categorized as follows: 0 to 4 indicates no depression, 5 to 9 suggests mild depression, 10 to 14 reflects moderate depression, and 15 or above signifies severe depression [12], and a PHQ-9 score of ≥ 10 is recommended as the threshold to define the presence of depressive symptoms [13].
Measurement of indicators of NPAR
The neutrophil percentage was determined using the Beckman Coulter DxH 900 Automated Hematology Analyzer (Beckman Coulter, Brea, CA, USA), a highly accurate device that evaluates the amounts of different types of white blood cells in the blood. Furthermore, the concentration of albumin was determined using the Beckman UniCel® DxC 660i Synchron Access.
The NPAR was calculated using the formula: Neutrophil percentage (as a proportion of total white blood cell count) (%) × 100 divided by Albumin concentration (g/dL) [14].
Covariates
Covariates comprised age, gender, race and ethnicity, education level, marital status, Income to Poverty Ratio, smoking status, history of hypertension, history of diabetes, history of cardiovascular disease, alanine aminotransferase(ALT), aspartate aminotransferase(AST), total cholesterol.
Age is divided into three stages: 20–44 years representing young adults, 45–59 years as middle-aged, and 60 years and above as older adults [15].
Total cholesterol was measured using an enzymatic method, ALT was determined by kinetic rate method, and AST was measured using an enzymatic rate method.
Smoking status was classified as having smoked a minimum of 100 cigarettes over a lifetime.
Diabetes mellitus was defined through inquiries such as “Has your doctor diagnosed you with diabetes mellitus?” or by meeting specific biochemical criteria, including an HbA1c ≥ 6.5%, fasting blood glucose level ≥ 7.0 mmol/L, or random blood glucose level ≥ 11.1 mmol/L or taking diabetic pills to lower blood sugar. Meeting any of these criteria constituted a diagnosis of diabetes.
Hypertension was defined as the mean of three consecutive systolic blood pressure readings of 140 mmHg or higher, or three consecutive diastolic readings of 90 mmHg or higher. A medical history of cardiovascular disease(CVD) was confirmed based on positive answers to a doctor’s diagnosis of myocardial infarction, angina pectoris, coronary artery disease, congestive heart failure, or stroke.
The detailed procedures for measuring these variables are publicly available on the official website: www.cdc.gov/nchs/nhanes/.
Statistical analysis
The data analysis was performed utilizing the R statistical computing and graphics software(version 4.1.3) and EmpowerStats, adhering to CDC guidelines.
Categorical variables are shown as proportions, whereas continuous variables are reported as mean(SD) for normal distributions and median(Q1, Q3) for non-normal distributions. To enhance the transparency and robustness of our findings, we conducted both the Box-Tidwell test and VIF analysis. The results indicated no significant statistical interaction effects, confirming a linear relationship between the continuous independent variables and the dependent variable. Additionally, all VIF values ranged between 1 and 2, suggesting minimal multicollinearity among the independent variables.
To evaluate the association between NPAR and depression symptoms, multiple logistic regression was employed to analyze the odds ratios(ORs) and 95% confidence intervals(CIs). And the association between NPAR and depression symptoms severity scores was explored using multiple linear regression(β(95%CI)). Three models were utilized for multivariate analysis: Model 1, without any variable adjustment; Model 2, adjusted for gender, age, and race; and Model 3, adjusted for all covariates. The association between NPAR and depression symptoms was investigated by adjusting for covariates using smoothed curve fitting. Similarly, the same statistical methodologies were applied to subgroups stratified by history of cardiovascular disease and history of diabetes.
Results
Baseline characteristics
The study involved a total of 10,829 adults, and these adults were selected for the study based on specific criteria for inclusion and exclusion. Among those surveyed, 44.86% were male and 55.14% were female. In addition, 15.08% of the individuals reported experiencing symptoms of depression. Table 1 presents the primary attributes of the individuals participating in the investigation, organized into groups based on the degree of depression symptoms. The results revealed that individuals with elevated depression symptom scores tended to be female, lower-income, non-Hispanic Black, have lower education levels, higher NPAR level, be unmarried, smokers, and individuals with diabetes or cardiovascular disease (Table 1).
Table 1.
Baseline characteristics of the study population based on the degree of depression symptoms
| Depression (PHQ-9 score) | Quartile1 (0–4) |
Quartile2 (5–9) |
Quartile3 (10–14) |
Quartile4 (≥ 15) |
p-value | |||
|---|---|---|---|---|---|---|---|---|
| Age(year), % | 0.070 | |||||||
| 20–44 | 2970 (45.21%) | 1083 (41.24%) | 385 (40.31%) | 259 (38.20%) | ||||
| 45–59 | 1533 (23.33%) | 656 (24.98%) | 256 (26.81%) | 210 (30.97%) | ||||
| >=60 | 2067 (31.46%) | 887 (33.78%) | 314 (32.88%) | 209 (30.83%) | ||||
| Gender, % | < 0.001 | |||||||
| Male | 3133 (47.69%) | 1104 (42.04%) | 363 (38.01%) | 258 (38.05%) | ||||
| Female | 3437 (52.31%) | 1522 (57.96%) | 592 (61.99%) | 420 (61.95%) | ||||
| Race and ethnicity, % | < 0.001 | |||||||
| Mexican American | 836 (12.72%) | 358 (13.63%) | 119 (12.46%) | 73 (10.77%) | ||||
| Other Hispanic | 639 (9.73%) | 267 (10.17%) | 101 (10.58%) | 103 (15.19%) | ||||
| Non-Hispanic White | 2738 (41.67%) | 1078 (41.05%) | 407 (42.62%) | 311 (45.87%) | ||||
| Non-Hispanic Black | 1309 (19.92%) | 585 (22.28%) | 220 (23.04%) | 127 (18.73%) | ||||
| Other Race | 1048 (15.95%) | 338 (12.87%) | 108 (11.31%) | 64 (9.44%) | ||||
| Education level, % | < 0.001 | |||||||
| Less than 9th grade | 390 (5.94%) | 220 (8.38%) | 84 (8.80%) | 93 (13.72%) | ||||
| 9-11th grade | 676 (10.29%) | 369 (14.05%) | 170 (17.80%) | 129 (19.03%) | ||||
| High school graduate or GED or equivalent | 1431 (21.78%) | 651 (24.79%) | 230 (24.08%) | 168 (24.78%) | ||||
| Some college or AA degree | 2186 (33.27%) | 876 (33.36%) | 325 (34.03%) | 214 (31.56%) | ||||
| College graduate or above | 1887 (28.72%) | 510 (19.42%) | 146 (15.29%) | 74 (10.91%) | ||||
| Marital status, % | < 0.001 | |||||||
| Married | 3395 (51.67%) | 1167 (44.44%) | 339 (35.50%) | 221 (32.60%) | ||||
| Widowed | 456 (6.94%) | 221 (8.42%) | 96 (10.05%) | 62 (9.14%) | ||||
| Divorced | 671 (10.21%) | 346 (13.18%) | 156 (16.34%) | 138 (20.35%) | ||||
| Separated | 184 (2.80%) | 117 (4.46%) | 63 (6.60%) | 40 (5.90%) | ||||
| Never married | 1303 (19.83%) | 547 (20.83%) | 217 (22.72%) | 146 (21.53%) | ||||
| Living with partner | 561 (8.54%) | 228 (8.68%) | 84 (8.80%) | 71 (10.47%) | ||||
| Income to poverty ratio | 3.22 (1.68, 5.00) | 2.33 (1.21, 4.25) | 1.71 (0.97, 3.69) | 1.48 (0.89, 2.65) | < 0.001 | |||
| Somking behavior, % | < 0.001 | |||||||
| Yes | 2718 (41.37%) | 1271 (48.40%) | 541 (56.65%) | 425 (62.68%) | ||||
| No | 3852 (58.63%) | 1355 (51.60%) | 414 (43.35%) | 253 (37.32%) | ||||
| Hypertension, % | 0.128 | |||||||
| Yes | 1211 (18.43%) | 544 (20.72%) | 200 (20.94%) | 138 (20.35%) | ||||
| No | 5359 (81.57%) | 2082 (79.28%) | 755 (79.06%) | 540 (79.65%) | ||||
| Diabetes, % | < 0.001 | |||||||
| Yes | 1141 (17.37%) | 585 (22.28%) | 239 (25.03%) | 177 (26.11%) | ||||
| No | 5429 (82.63%) | 2041 (77.72%) | 716 (74.97%) | 501 (73.89%) | ||||
| History of CVD, % | < 0.001 | |||||||
| Yes | 592 (9.01%) | 377 (14.36%) | 158 (16.54%) | 148 (21.83%) | ||||
| No | 5978 (90.99%) | 2249 (85.64%) | 797 (83.46%) | 530 (78.17%) | ||||
| ALT(U/L) | 20.00 (16.00, 28.00) | 20.00 (15.00, 28.00) | 20.00 (14.00, 29.00) | 20.00 (15.00, 28.00) | 0.608 | |||
| AST(U/L) | 22.00 (19.00, 27.00) | 22.00 (18.00, 27.00) | 21.00 (18.00, 26.00) | 21.00 (18.00, 27.00) | 0.130 | |||
| Total cholesterol(mg/dL) | 189.00 (164.00, 217.00) | 188.00(162.00, 218.00) | 191.00(165.00, 223.00) | 190.00(162.00, 222.00) | 0.428 | |||
| NPAR | 13.60 (12.09, 15.28) | 13.90 (12.30, 15.52) | 14.00 (12.07, 15.90) | 14.11 (12.67, 16.10) | < 0.001 |
Association between NPAR and depression symptoms and its severity scores
The outcomes of multivariate logistic regression studies, utilizing three models, are displayed in Table 2. A robust positive connection was discovered between NPAR and the likelihood of depression symptoms, consistently significant across all three models. With full adjustment, for each incremental unit increase in NPAR, the odds of an individual developing depression symptoms rose by 3%[OR: 1.03, CI: 1.00, 1.05]. When NPAR was divided into quartiles, individuals in the highest quartile(Q4) exhibited a considerably higher probability of experiencing depression symptoms compared to those in the lowest quartile(Q1), with a 0.23-fold higher likelihood[OR: 1.23, 95% CI: 1.01, 1.49](Table 2). And the outcomes of multivariate linear regression studies, also utilizing three models, are displayed in Table 3. We observed that for each unit increase in NPAR, depression symptom scores increased by 0.08 units[β: 0.08, 95% CI: 0.04, 0.11]. When dividing NPAR into quartiles, participants in Q4, compared to those in Q1, showed a 0.65-unit increase in depression symptoms scores for each unit increase in NPAR[β: 0.65, 95% CI: 0.40, 0.90](Table 3). And we conducted a data analysis of NPAR and calculated its quartile values as follows: the Q1 is 12.08, Q2 is 13.74, and Q3 is 15.50. Furthermore, the ranges for the NPAR quartiles are as follows: Min to Q1: 0.86 to 12.08; Q1 to Q2: 12.08 to 13.74; Q2 to Q3: 13.74 to 15.50; Q3 to Max: 15.50 to 36.10.
Table 2.
Association between NPAR and depression symptoms(OR(95%CI))
| Exposure | Model 1[OR(95%CI)] | Model 2[OR(95%CI)] | Model 3[OR(95%CI)] | ||||||
|---|---|---|---|---|---|---|---|---|---|
|
Continuous NPAR |
1.05(1.02, 1.08) | 1.05(1.02, 1.07) | 1.03(1.00, 1.05) | ||||||
| NPAR classification | |||||||||
| Quartile 1 | Reference | Reference | Reference | ||||||
| Quartile 2 | 0.92(0.73, 1.16) | 0.92(0.73, 1.17) | 0.92(0.72, 1.18) | ||||||
|
Quartile 3 Quartile 4 |
0.95(0.76, 1.18) 1.44(1.19, 1.74) |
0.94(0.75, 1.17) 1.40(1.15, 1.70) |
0.92(0.74, 1.15) 1.23(1.01, 1.49) |
Table 3.
Association between NPAR and depression symptoms severity scores(β(95%CI))
| Exposure | Model 1[β(95%CI)] | Model 2[β(95%CI)] | Model 3[β(95%CI)] | ||||||
|---|---|---|---|---|---|---|---|---|---|
|
Continuous NPAR |
0.13(0.09, 0.16) | 0.12(0.08, 0.15) | 0.08(0.04, 0.11) | ||||||
| NPAR classification | |||||||||
| Quartile 1 | Reference | Reference | Reference | ||||||
| Quartile 2 | 0.01(-0.24, 0.26) | 0.01(-0.24, 0.26) | 0.04(-0.20, 0.28) | ||||||
|
Quartile 3 Quartile 4 |
0.13(-0.12, 0.38) 0.99(0.74, 1.25) |
0.11(-0.15, 0.36) 0.93(0.67, 1.18) |
0.08(-0.16, 0.32) 0.65(0.40, 0.90) |
Model 1: no covariates were adjusted. Model 2: age, gender, and race were adjusted. Model 3:age, gender, race, education level, marital status, income to poverty ratio, smoking behavior, hypertension, diabetes, history of CVD, ALT, AST, Total cholesterol were adjusted
Furthermore, in the subgroup analysis, no significant associations were found between NPAR levels and depression symptoms or depression severity scores within populations with or without diabetes(P > 0.05) and cardiovascular diseases(P > 0.05)(Table 4)(Table 5).
Table 4.
Associations between NPAR and depression symptoms stratified by cardiovascular disease and DM status(OR(95%CI))
| Subgroup | OR(95%CI) | P-interaction | ||||
|---|---|---|---|---|---|---|
| CVD | 0.905 | |||||
| Yes | 1.04(0.98, 1.10) | |||||
| No | 1.04(1.02, 1.07) | |||||
| DM | 0.450 | |||||
| Yes | 1.06(1.00, 1.12) | |||||
| No | 1.04(1.01, 1.07) |
Table 5.
Associations between NPAR and depression symptoms severity scores stratified by cardiovascular disease and DM status(β(95%CI))
| Subgroup | β(95%CI) | P-interaction | ||||
|---|---|---|---|---|---|---|
| CVD | 0.845 | |||||
| Yes | 0.10(-0.04, 0.23) | |||||
| No | 0.11(0.06, 0.16) | |||||
| DM | 0.367 | |||||
| Yes | 0.15(0.05, 0.25) | |||||
| No | 0.10(0.05, 0.16) |
age, gender, race, education level, marital status, income to poverty ratio, smoking behavior, hypertension, diabetes, history of CVD, ALT, AST, Total cholesterol were adjusted. In the subgroup analyses, the model is not adjusted for the stratification variable itself
We applied a generalized model with smooth curve fitting to verify the non-linear relationship between NPAR and depression symptoms. The results confirmed a non-linear association between NPAR and depression symptoms (Fig. 2).
Fig. 2.
The association between NPAR and depression
Discussion
In an investigation involving 10,829 individuals, we identified a nonlinear association between NPAR and depression symptoms and its severity scores. Subgroup analysis and interaction tests indicated no significant differences in the relationship between NPAR levels and depression symptoms based on the presence of diabetes or cardiovascular disease. Our findings suggest that NPAR may serve as a potential marker for the likelihood of depression symptoms, although the direction of causality remains unclear. Notably, this study represents the first cross-sectional investigation specifically exploring the potential link between NPAR and depression symptoms among U.S. adults. However, due to the study design, we are unable to determine whether elevated NPAR leads to depression symptoms or if depression symptoms influence NPAR levels.
Chronic inflammation has been firmly linked to a spectrum of chronic ailments, including cardiovascular disease [16], diabetes [17], and cancer [18]. And chronic inflammation has gained considerable attention in recent years for its potential involvement in the pathophysiology of depression [19].
Studies have demonstrated that individuals with depression often exhibit increased levels of pro-inflammatory cytokines, including interleukin-1(IL-1), interleukin-6(IL-6), and tumor necrosis factor-alpha(TNF-α) [20]. These cytokines can cross the blood-brain barrier and trigger neuroimmune responses in the central nervous system, leading to neuroinflammation, which directly causes neuronal damage [21].
Additionally, pro-inflammatory cytokines activate the tryptophan-kynurenine metabolic pathway, diverting tryptophan from the 5-hydroxytryptamine(5-HT) production pathway toward kynurenine metabolism [22]. Since tryptophan is a precursor of 5-HT, this shift results in reduced 5-HT synthesis, contributing to depressive symptoms [23]. Moreover, kynurenine and its metabolites, such as quinolinic acid(QUIN), exhibit neurotoxic effects by triggering N-methyl-D-aspartate(NMDA) receptors, resulting in excitotoxicity, further exacerbating neuronal damage and death, particularly in brain regions responsible for mood regulation, such as the hippocampus and prefrontal cortex [24].
Chronic inflammation is also closely linked to dysregulation of the hypothalamic-pituitary-adrenal(HPA) axis. Pro-inflammatory cytokines like IL-6 and TNF-α can stimulate the HPA axis, resulting in excessive cortisol release [25]. Prolonged elevated cortisol levels can have detrimental effects on the brain, particularly the hippocampus, leading to decreased neuronal plasticity and structural damage, ultimately impairing mood regulation and cognitive function [26].
Recently, the “gut-brain axis” has received considerable attention for its role in the interaction between gut microbiota and brain function. Dysbiosis of the gut microbiota is closely linked to increased systemic inflammation. Research indicates that a compromised intestinal barrier allows harmful bacterial endotoxins, such as lipopolysaccharides(LPS), to enter the bloodstream, provoking systemic inflammatory responses [27]. This dysregulation of gut microbiota is thought to contribute to the pathophysiology of depression, particularly by aggravating neuroinflammation and disrupting neurotransmitter metabolism [28].
Furthermore, chronic inflammation induces oxidative stress, compounding neuronal damage [29]. During inflammatory processes, the production of large amounts of reactive oxygen species(ROS) and free radicals leads to the damage of neuronal DNA, proteins, and cell membranes, resulting in neuronal death [30]. This oxidative stress is closely associated with neuronal atrophy, brain structural damage, and cognitive decline observed in patients with depression [31].
As a combined measure of neutrophils and albumin levels, the Neutrophil-to-Albumin Ratio(NPAR) functions as a dual biological marker [32], drawing increasing attention for its potential clinical significance in inflammation-related disorders [33]. Neutrophils play a crucial role in managing infections, injury, and inflammation, contributing to these processes by producing reactive oxygen species(e.g., superoxide) and promoting cytokine release, which helps sustain inflammatory responses [34]. In patients with chronic depression, elevated neutrophil levels may indicate a persistent inflammatory state [35]. Concurrently, low albumin levels are indicative of potential malnutrition, a condition often observed in individuals with long-standing depressive disorders [36]. Albumin, acting as an antioxidant, neutralizes free radicals and mitigates oxidative stress. A reduction in albumin levels may weaken antioxidant defenses, exacerbate neuroinflammation, and worsen the progression of depression [37]. In such cases, malnutrition and inflammation frequently coexist, exacerbating the severity of the illness. An increased NPAR may suggest a strong link between depression and chronic inflammation. Although studies have shown NPAR’s potential as a biomarker for inflammation-related conditions such as cardiovascular disease and diabetes [38], there is currently no conclusive evidence supporting its widespread use in clinical practice for depression and depression symptoms. This study explores the potential of monitoring NPAR to provide valuable insights into the identification and assessment of depression symptoms, which could aid in the development of tailored nutritional and pharmacological interventions.
Our study presents several limitations that warrant consideration. Primarily, due to its cross-sectional nature, we were unable to determine temporal causation, and the lack of long-term follow-up limited our ability to discern prolonged effects. Additionally, the observational nature of the research limited our ability to establish a causal link between NPAR levels and depression symptoms. Although we have made efforts to account for different relevant confounding variables, there is still a possibility of residual confounding, as certain crucial factors may not have been taken into consideration. Lastly, reliance on self-reported data in certain segments of the NHANES survey introduces the possibility of recall bias or inaccuracies, which may influence the reliability of our findings. Therefore, further prospective investigations are necessary to authenticate the results of our study, specifically concerning the prognostic significance of NPAR in depression symptoms.
Conclusion
In the general population, a notable association exists between NPAR and depression symptoms and its severity scores. We propose NPAR as a potential biomarker for depression symptoms in the U.S. adult population. Nevertheless, these conclusions warrant validation through subsequent prospective investigations.
Ethics statement
This study received approval from the NCHS Ethics Review Board. Written informed consent was obtained from all participants.
Electronic supplementary material
Below is the link to the electronic supplementary material.
Author contributions
YTZ designed the research. YTZ and ZCF collected and analyzed the data. YTZ wrote the initial draft, and ZCF revised it. All authors contributed to and approved the final version of the manuscript.
Funding
This study received no funding.
Data availability
Availability of Data and Materials: The survey data are publicly accessible online for researchers and data users worldwide (www.cdc.gov/nchs/nhanes/).
Declarations
Ethics approval and consent to participate
Not applicable.
Consent for publication
Not applicable.
Clinical trial number
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Data Availability Statement
Availability of Data and Materials: The survey data are publicly accessible online for researchers and data users worldwide (www.cdc.gov/nchs/nhanes/).