Abstract
Background
While dietary niacin intake is acknowledged for its beneficial impact on mental health, the precise relationship between dietary niacin intake and suicidal ideation (SI) remains unclear. This study seeks to explore the potential association between the prevalence of SI and dietary niacin intake.
Methods
In this study, the data of 26,224 American adults from NHANES were analyzed. To explore the association between dietary niacin intake and SI, as indicated by Item 9 of the Patient Health Questionnaire-9 (PHQ-9), restricted cubic spline, logistic regression, and stratified analyses were utilized. Furthermore, mediation analyses were performed to explore the role of C-reactive protein (CRP) in the association between SI and dietary niacin intake.
Results
Among the subjects, 970 (3.7%) of them reported experiencing SI. Logistic regression analyses demonstrate a significant inverse association between dietary niacin intake and the prevalence of SI, even after adjusting for potential confounding variables (OR = 0.86, 95% CI: 0.77, 0.96). Subgroup analyses indicate a more pronounced association between SI and dietary niacin intake in individuals with a history of hyperlipidemia. Additionally, a non-linear association and saturation effect were observed between dietary niacin intake and the prevalence of SI, characterized by an L-shaped curve with an inflection point at 26.78 mg/day. Mediation analysis reveales that 3.6% of this association was mediated by CRP.
Conclusion
This study indicates an increased dietary niacin intake associated with a reduced prevalence of SI, underscoring the potential public health and clinical importance of dietary niacin intake.
Keywords: Dietary niacin intake, Suicidal ideation, Chronic inflammation, PHQ-9, Depression
Introduction
Suicide constitutes a significant global public health challenge, contributing to more than 700,000 deaths each year [1]. In addressing this issue, the World Health Organization (WHO) has implemented a strategic initiative aimed at reducing suicide mortality by 33% in each member state from 2013 to 2030 [2]. Within the framework of ideation-to-action models of suicide, SI is identified as a critical antecedent to both suicide attempts and completed suicides [3]. Empirical research indicates that the likelihood of suicide within the first year after the onset of SI is approximately 1.40% of psychiatric patients [4]. Therefore, it is essential to identify modifiable risk factors associated with SI to enhance the efforts in suicide prevention. Although various risk factors, including sociodemographic characteristics, mood disorders, and personality traits [5, 6], have been identified in existing literature, many of these factors are often unmodifiable.
A considerable body of evidence indicate that a poor diet often precedes the onset of diseases and can serve as a risk factor for individuals with psychiatric disorders, in contrast to the general population [7, 8]. Furthermore, targeted dietary interventions can be applied as standard therapeutic approaches, potentially yielding positive effects on psychiatric disorders [9, 10]. Research indicates that the intake of specific nutrients, such as niacin, Vitamin B12, folic acid, Vitamin D, and zinc, may reduce the risk of psychiatric conditions, including depression [11–13].
Niacin, also known as Vitamin B3, is a water-soluble vitamin with numerous health benefits [14]. It can be obtained from various dietary sources, including nuts, fish, and grains, as well as in the form of supplements. As an antioxidant, niacin mitigates oxidative stress by neutralizing free radicals, thereby potentially decelerating the aging process [15]. It plays a significant role in both neuronal death and neuroprotection, which is essential for neuronal development and the normal functioning of the central nervous system (CNS) [16]. Disruptions in the synthesis of niacin metabolites can lead to imbalances in physiological mechanisms, potentially contributing to various neuropsychiatric disorders [17]. However, the association between dietary niacin intake and the prevalence of SI remains unexplored.
This study aims to address this gap by exploring the association between dietary niacin intake and the prevalence of SI in American adults. It was hypothesized that there exists an inverse association between dietary niacin intake and the prevalence of SI. The findings can offer novel insights into the clinical prevention and management of SI.
Methods
Data sources
Cross-sectional data were collected from National Health and Nutrition Examination Survey (NHANES), which is administered by National Center for Health Statistics (NCHS) to explore the nutritional and physical health of the non-institutionalized American population [18]. Although the data from NHANES are still collected in a biennial cycle, they are continuously updated. The stratified multi-stage probabilistic sampling design employed by NHANES ensures a relatively high representativeness among the enrolled subjects. All survey methodologies and protocols utilized in NHANES have received approval from the ethical review committee of NCHS.
Study population
In this study, the data from the two cycles of NHANES 1999–2018 were subjected to a retrospective analysis. Subjects aged 18 years old or older (n = 59,204) were included. Based on the exclusion criteria, individuals lacking data on SI (n = 27,880), those without the information of dietary niacin intake (n = 1,008), pregnant females (n = 599), and those missing the data on BMI and other covariates (n = 3,493) were excluded to ensure data reliability and completeness for multivariable analysis. Consequently, the final sample consisted of 26,224 subjects, as depicted in Fig. 1.
Fig. 1.
Flowchart of the sample selection from the 1999–2018 NHANES
Evaluation of dietary niacin intake
Dietary niacin intake was explored on two distinct occasions as part of NHANES. The first took place in person, and the second was conducted through a phone call. Owing to substantial data deficiencies identified during the second round of interviews, the analysis for this study relied solely on the dietary information obtained during the initial session [19]. Specifically, dietary niacin intake was defined based on the data collected during the first visit only. This approach was chosen to ensure consistency and completeness of the data on dietary niacin intake, as the second visit had a higher rate of information missing.
Evaluations on SI
SI was evaluated through an analysis on responses to Item 9 of PHQ-9, inquiring: “Over the past two weeks, how often have you engaged in self-harm or considered that it would be preferable to die?” Subjects who scored 1 to 3 were categorized as experiencing SI, whereas those who scored zero were categorized as not experiencing SI [20]. Consistent with the evaluation of dietary niacin intake, the evaluation of SI was conducted on the data collected during the initial visit.
Covariates
Drawing on prior research [20] and utilizing variables supplied by NHANES, covariates of interest, including sociodemographic variables, physical examination outcomes, and self-reported health data, were identified as potential confounding factors. Trained interviewers gathered self-reported health information, such as medical history, smoking status, and alcohol abuse, during interviews conducted at the Mobile Examination Center (MEC) and in subjects’ homes. The sociodemographic variables encompassed marital status, education level, age, poverty-to-income ratio (PIR), gender, and race. Physical examination data, encompassing BMI and blood pressure, were gathered by trained health technicians at MEC. Furthermore, blood samples were procured at MEC to assess levels of creatinine, total cholesterol (TC), CRP, albumin, and LDL-C. The criteria for diagnosing hypertension, hyperlipidemia, and diabetes, adhered to previously established definitions [21]. The incidence of stroke, cancer, and coronary heart disease (CHD) was ascertained based on self-reported diagnoses. The first eight questions of PHQ-8, excluding Item 9, were utilized to calculate a depression score, as referenced in source [22]. A threshold score of ≥ 10 was employed to identify the presence of depressive symptoms. Subjects with PHQ-8 ≥ 10 or those currently taking antidepressant medication were diagnosed with depressive disorder.
Boruta algorithm
The results of feature selection through the Boruta algorithm are depicted in Fig. 2. After conducting 500 iterations, it was determined that the seventeen variables the most strongly associated with SI were race, alcohol abuse, gender, BMI, physical activity levels, age, smoking status, hyperlipidemia, stroke, CHD, PIR, education level, albumin, creatinine, marital status, dietary niacin intake, and cancers.
Fig. 2.
Feature selection process for suicidal ideation based on Boruta’s algorithm(A) and the value evolution of Z-score in the screening process (B). In A, the horizontal axis represents the variable name and the vertical axis represents the Z-values of each variable. In B, the horizontal axis represents the number of iterations, and the vertical axis represents the change in Z-values during the screening process. The blue boxes and lines correspond to the minimum, average, and maximum Z-scores for a shadow feature. The green boxes and lines represent the confirmed variables
Statistical analysis
Dietary niacin intake was stratified into quartiles as follows: Q1: <15.2 mg/d, Q2: 15.2-22.0 mg/d, Q3: 22.0-31.0 mg/d, and Q4: >31.0 mg/d. The association between dietary niacin intake and the prevalence of SI was analyzed with 95% CI and OR derived from multivariable logistic regression models. The Boruta algorithm was employed for variable selection, leading to the development of three distinct models: Model 1 (unadjusted), Model 2 (adjusted for age and gender) and Model 3 (comprehensively adjusted for race, alcohol abuse, age, BMI, physical activities, hyperlipidemia, gender, smoking status, CHD, education level, stroke, creatinine levels, PIR, albumin levels, marital status, depression disorder, and cancers). The association between dietary niacin intake and the prevalence of SI was evaluated through interactions and subgroup analyses across a range of variables to account for heterogeneity. Furthermore, the non-linear association between SI and dietary niacin intake was explored with RCS curves. Subsequently, the proportion of mediating effects attributable to CRP was quantified through mediation analyses utilizing the mediation package. Relevant data were analyzed with Free Statistics software and R software.
Results
Subjects’ characteristics
Table 1 provides a detailed overview of primary characteristics of the study cohort. Among the 26,224 subjects, 970 (3.7%) of them reported experiencing SI, with a mean age of 49.6 years old, and females comprising 49.8% of them. Those reporting SI were more likely to live alone and exhibited lower levels of PIR, albumin and education. This subgroup also showed a higher prevalence of comorbid conditions, such as diabetes, stroke, hypertension, CHD, depression, and hyperlipidemia, alongside increased CRP and BMI. Additionally, dietary niacin intake was significantly lower among subjects with SI (Fig. 3), with all differences being statistically significant (p < 0.05).
Table 1.
Characteristics of the study population based on suicidal ideation
| Characteristic | Total (n = 26224) | Non-suicidal ideation (n = 25254) | Suicidal ideation (n = 970) | P value |
|---|---|---|---|---|
| Age | 49.6 ± 17.7 | 49.6 ± 17.7 | 49.6 ± 16.9 | 0.911 |
| Gender, % | < 0.001 | |||
| Male | 13,165 (50.2) | 12,732 (50.4) | 433 (44.6) | |
| Female | 13,059 (49.8) | 12,522 (49.6) | 537 (55.4) | |
| Race, % | < 0.001 | |||
| Mexican American | 4218 (16.1) | 4036 (16) | 182 (18.8) | |
| Other Hispanic | 2520 (9.6) | 2364 (9.4) | 156 (16.1) | |
| Non-Hispanic White | 11,857 (45.2) | 11,469 (45.4) | 388 (40) | |
| Non-Hispanic Black | 5336 (20.3) | 5156 (20.4) | 180 (18.6) | |
| Other Race | 2293 (8.7) | 2229 (8.8) | 64 (6.6) | |
| Education level, % | < 0.001 | |||
| Less than high school | 6460 (24.6) | 6081 (24.1) | 379 (39.1) | |
| High school or above | 19,752 (75.4) | 19,162 (75.9) | 590 (60.9) | |
| Marital, % | < 0.001 | |||
| Married/living with partner | 16,620 (63.4) | 16,122 (63.8) | 498 (51.3) | |
| Separated/divorced/widowed | 4914 (18.7) | 4662 (18.5) | 252 (26) | |
| Never married | 4690 (17.9) | 4470 (17.7) | 220 (22.7) | |
| Physical activity, % | 0.595 | |||
| Low | 21,765 (83.0) | 20,935 (82.9) | 830 (83.9) | |
| High | 4459 (17.0) | 4319 (17.1) | 140 (16.1) | |
| Alcohol status, n% | 0.194 | |||
| Current or ever, % | 18,883 (72.1) | 18,203 (72.2) | 680 (70.2) | |
| Never | 7312 (27.9) | 7024 (27.8) | 288 (29.8) | |
| Smoking status, n% | < 0.001 | |||
| Current or ever, % | 11,987 (45.7) | 11,445 (45.3) | 542 (55.9) | |
| Never | 16,792 (64.1) | 16,251 (64.4) | 541 (56) | |
| Hypertension, % | < 0.001 | |||
| Yes | 9397 (35.9) | 8972 (35.6) | 425 (44) | |
| No | 16,977 (64.9) | 16,435 (65.2) | 542 (56.9) | |
| Diabetes, % | < 0.001 | |||
| Yes | 3825 (14.6) | 3621 (14.3) | 204 (21) | |
| No | 22,384 (85.4) | 21,618 (85.7) | 766 (79) | |
| Hyperlipidemia, % | 0.005 | |||
| Yes | 18,795 (71.7) | 18,061 (71.5) | 734 (75.7) | |
| No | 7429 (28.3) | 7193 (28.5) | 236 (24.3) | |
| CHD, % | < 0.001 | |||
| Yes | 1065 (4.1) | 996 (3.9) | 69 (7.1) | |
| No | 25,159 (95.9) | 24,258 (96.1) | 901 (92.9) | |
| Stroke | < 0.001 | |||
| Yes | 918 (3.5) | 842 (3.3) | 76 (7.8) | |
| No | 25,306 (96.5) | 24,412 (96.7) | 894 (92.2) | |
| Cancer, % | 0.068 | |||
| Yes | 2479 (9.5) | 2371 (9.4) | 108 (11.1) | |
| No | 23,745 (90.5) | 22,883 (90.6) | 862 (88.9) | |
| Depression disorder, % | < 0.001 | |||
| Yes | 2196 (8.4) | 1643 (6.5) | 553 (57) | |
| No | 24,028 (91.6) | 23,611 (93.5) | 417 (43) | |
| Body mass index, kg/m2 | 29.2 ± 6.9 | 29.1 ± 6.8 | 30.0 ± 7.7 | < 0.001 |
| Albumin, g/dl | 42.6 ± 3.3 | 42.6 ± 3.3 | 42.1 ± 3.7 | < 0.001 |
| Creatinine, umol/L | 80.7 ± 39.6 | 80.7 ± 39.8 | 79.9 ± 35.2 | 0.514 |
| PIR | 2.55 ± 1.63 | 2.59 ± 1.63 | 1.73 ± 1.39 | < 0.001 |
| CRP | 0.20 (0.08, 0.46) | 0.20 (0.08, 0.46) | 0.23 (0.08, 0.62) | 0.018 |
| Dietary niacin intake, mg/d | 25.2 ± 15.4 | 25.2 ± 15.3 | 23.7 ± 16.2 | < 0.001 |
CHD coronary heart disease, PIR family income-to-poverty ratio, WBC white blood cell
Values are mean±SD or number (%), P < 0.05 was deemed significant
Fig. 3.
Dietary niacin intake levels in participants with or without suicidal ideation
SI and dietary niacin intake
Table 2 displays the findings from the logistic regression analysis investigating the association between dietary niacin intake and SI. To improve the interpretability of ORs, the exposure variable was subjected to a logarithmic transformation when it was analyzed as a continuous variable. In Model 3, after adjusting for confounding variables, dietary niacin intake was found to be associated with a reduced prevalence of SI (OR: 0.86, 95% CI: 0.77–0.96). Furthermore, when dietary niacin intake was categorized into quartiles, the comprehensively adjusted Model 3 revealed that, compared to those in the lowest Q1, the adjusted OR for individuals in Q3 and Q4 were 0.81 (95% CI: 0.68–0.98) and 0.83 (95% CI: 0.66–0.99), respectively.
Table 2.
Associations between dietary niacin intake and suicidal ideation
| subgroups | Model1 | Model2 | Model3 | |||
|---|---|---|---|---|---|---|
| OR (95%CI) | P-value | OR (95%CI) | P-value | OR (95%CI) | P-value | |
| Ln (niacin intake) | 0.76 (0.68, 0.84) | < 0.001 | 0.78 (0.70, 0.88) | < 0.001 | 0.86 (0.77 ~ 0.96) | 0.008 |
| niacin intake (category) | ||||||
| Q1 | 1(Ref) | 1(Ref) | 1(Ref) | |||
| Q2 | 0.82 (0.69, 0.97) | 0.021 | 0.83 (0.70, 0.99) | 0.035 | 0.89 (0.75 ~ 1.06) | 0.203 |
| Q4 | 0.69 (0.58, 0.83) | < 0.001 | 0.71 (0.60, 0.86) | < 0.001 | 0.81 (0.68 ~ 0.98) | 0.030 |
| Q4 | 0.69 (0.57, 0.82) | < 0.001 | 0.73 (0.60, 0.88) | 0.001 | 0.83 (0.66 ~ 0.99) | 0.048 |
| P for trend | < 0.001 | < 0.001 | 0.035 | |||
Model 1: None covariates were adjusted; Model 2: gender and age were adjusted; Model 3, gender, age, race, drinking, BMI, smoking, physical activities, CHD, hyperlipidemia, stroke, PIR, education level, marital status, albumin, creatinine, depression disorder, and cancer were adjusted
Non-linear association
After adjusting for all variables, a non-linear association between dietary niacin intake and SI was identified, as illustrated in Fig. 4. Specifically, an L-shaped association was observed, with an inflection point at 26.78 mg/day. Below this threshold, dietary niacin intake exhibited a significant effect size of 0.81, whereas above this level, the effect size was not statistically significant (refer to Table 3).
Fig. 4.
Restricted cubic spline fitting for the association between dietary niacin intake and suicidal ideation. (A) No adjustment for covariates. (B) Adjusted for age, and gender. (C) Adjusted for gender, age, race, drinking, BMI, smoking, physical activities, CHD, hyperlipidemia, stroke, PIR, education level, marital status, albumin, creatinine and cancer
Table 3.
Threshold effect analysis of dietary niacin intake and suicidal ideation using the two-piecewise linear regression model
| dietary niacin intake | Adjusted OR (95% CI) | P value |
|---|---|---|
| Fitting by the standard linear model (ln niacin intake increment) | 0.86 (0.77 ~ 0.96) | 0.008 |
| Fitting by the two-piecewise linear model | ||
| Inflection point | 26.78 | |
| dietary niacin < 26.78(ln niacin intake increment) | 0.81 (0.69 ~ 0.95) | 0.008 |
| dietary niacin > 26.78(ln niacin intake increment) | 1.37 (0.94 ~ 2.01) | 0.102 |
| Log likelihood ratio | 0.011 | |
Gender, age, race, drinking, BMI, smoking, physical activities, CHD, hyperlipidemia, stroke, PIR, education level, marital status, albumin, creatinine, depression disorder, and cancer were adjusted
Subgroup analyses
A stratified multivariate logistic regression analysis was conducted to examine the association between dietary niacin intake and SI across various population subgroups (see Fig. 5). The interaction test indicated no statistically significant differences in the association between SI and dietary niacin intake concerning gender, diabetes, BMI, age, hypertension, CHD, cancers, and stroke. Furthermore, the association between dietary niacin intake and SI was more pronounced among individuals with a history of hyperlipidemia.
Fig. 5.
Association between dietary niacin intake and suicidal ideation in various subgroups
Mediation analysis
The mediation model and its associated pathways are illustrated in Fig. 6. The results suggest that CRP partially mediates the association between dietary niacin intake and SI, accounting for approximately 3.6% of the total effect, as detailed in Table 4.
Fig. 6.
Mediated analysis model path diagram. Notes: dietary niacin intake was defined as the independent variable; suicidal ideation as the dependent variable; and CRP as the mediating variable
Table 4.
Mediation analysis of CRP in the association between dietary niacin intake and suicidal ideation
| Independent variable | Mediator | Total effect | Indirect effect | Direct effect | Proportion mediated, % | |||
|---|---|---|---|---|---|---|---|---|
| Coefficient (95% CI) | P value | Coefficient (95% CI) | P value | Coefficient (95% CI) | P value | |||
| Niacin intake | CRP | −0.0257 (−0.0481, −0.011) | < 0.001 | −0.0009 (−0.0015, −0.0003) | 0.006 | −0.0248 (−0.0471, −0.0102) | < 0.001 | 3.6 |
Gender, age, race, drinking, BMI, smoking, physical activities, CHD, hyperlipidemia, stroke, PIR, education level, marital status, albumin, creatinine, depression disorder, and cancer were adjusted
Discussion
In this cross-sectional study comprising 26,224 subjects, an independent association was identified between reduced dietary niacin intake and an elevated prevalence of SI. The association between dietary niacin intake and SI prevalence was delineated by an L-shaped curve, with a threshold determined at 26.78 mg/day. This association was particularly more pronounced in individuals with a history of hyperlipidemia. Additionally, mediation analysis revealed that CRP partially mediates the association between dietary niacin intake and SI.
To the best of our knowledge, this study is the first to explore the association between dietary niacin intake and the prevalence of SI. Historical research from the 1950 s indicates a association between niacin deficiency and conditions, such as benign depression and catatonia, with niacin supplementation reportedly ameliorating symptoms of irritability, depression, and anxiety [23]. More recent findings demonstrate that the treatment with aqueous niacin skin flushing significantly alleviated symptoms of anxiety, depression, and somatic complaints in a cohort of 30 patients experiencing recurrent monophasic depression [24]. Additionally, the data from NHANES 2007–2014 suggest a non-linear inverse association between depression risk and dietary niacin intake [25]. A study conducted in Korea further corroborated these findings, illustrating a negative association between depression and dietary niacin intake [26].
In recent years, scholarly interest in the impact of dietary antioxidants on SI has markedly increased. Strumila et al. [27] found that individuals with low selenium may be at an elevated risk of suicidal tendencies, which could be associated with a higher incidence of suicide attempts. Additionally, the study of Sher [28] underscored the pivotal role of selenium deficiency in the pathophysiology of suicidal behavior among individuals with alcohol abuse. Huang et al. [29] observed a negative association between the composite dietary antioxidant index and both the prevalence of SI and all-cause mortality in American adults. The current study supports these findings, revealing a negative association between dietary niacin intake, as a dietary antioxidant, and the probability of experiencing SI.
The results of this study offer additional insights into the L-shaped association between dietary niacin intake and the prevalence of SI in American adults, suggesting that increased intake may serve as a non-pharmacological preventive strategy. The findings indicate that maintaining a dietary niacin intake of at least 26.78 mg/day may reduce the risk of SI. Given the variability in individual differences and dietary habits, further research is warranted to determine the optimal dietary niacin intake level.
The findings of this study indicate that CRP may serve as a partial mediator in the association between dietary niacin intake and SI, underscoring the significance of monitoring inflammatory markers in individuals with reduced dietary niacin intake. Niacin is extensively documented for its significant anti-inflammatory properties, and increased intake has been associated with reduced levels of inflammatory markers [30]. Therefore, enhancing dietary niacin intake may mitigate the inflammatory response by lowering CRP, which can potentially decrease the incidence of SI, indicating that clinicians should prioritize advocating for a balanced diet in patients with elevated CRP. Adequate supplementation with niacin-rich foods may serve as a preventive measure against SI.
Subgroup analyses in this study have uncovered a novel finding that an increased dietary niacin intake was significantly associated with a declined prevalence of SI in individuals with hyperlipidemia. Niacin can exhibit lipid-regulating properties, notably by increasing HDL-C and declining LDL-C [31]. Previous studies have demonstrated a strong association between hyperlipidemia and psychiatric disorders [32, 33]. Consequently, for those with hyperlipidemia, dietary niacin intake may effectively mitigate SI by reducing blood lipid levels. Therefore, dietary niacin intake should be considered as an important factor in preventing SI, especially for the aforementioned population.
The inverse association between dietary niacin intake and SI may be explained by various mechanisms that potentially influence the pathology of SI. A considerable body of research suggests that individuals diagnosed with psychiatric disorders frequently exhibit increased inflammation and oxidative stress, alongside relatively low antioxidants of dietary niacin intake [34–36]. Niacin has been shown to alleviate oxidative stress in endothelial cells through mechanisms, such as enhancing glutathione reduction, inhibiting the production of reactive oxygen species, and increasing NADP [30]. Moderate dietary niacin intake can increase serum 5-HT levels, improve cerebral energy deficits, and exhibit significant antioxidant properties. These effects may represent a biological mechanism underlying its potential role in the prevention of SI. Moreover, research has demonstrated that niacin facilitates the phenotypic transition of macrophages from M1 (pro-inflammatory) phenotype to M2 (anti-inflammatory) phenotype by activating the niacin receptor GPR109A. This process mitigates the inflammatory response and enhances anti-inflammatory mechanisms [37]. Furthermore, niacin attenuates the secretion of pro-inflammatory mediators, such as TNF-α, MCP-1, and IL-6, thereby mitigating the inflammatory response [38]. Nonetheless, additional prospective studies are necessary to substantiate the potential preventive effects of niacin on SI.
This study demonstrates several significant strengths. Firstly, it utilized a nationally representative, large sample of American adults. Secondly, it accounted for both established and potential risk factors associated with SI through appropriate adjustments. However, the study has its limitations: (1) The cross-sectional design restricts the ability to establish causality, rendering the causal association between dietary niacin intake and SI indeterminate. (2) The evaluation on SI primarily depended on the use of questionnaires, a method that may be susceptible to measure errors. (3) This study did not include measurements of serum niacin concentration, leaving it uncertain whether the effect of dietary niacin intake on SI is mediated through serum niacin levels. (4) Acknowledging the potential influence of variables such as presence of gastrointestinal disorders, experiences with substance addiction, and the treatment for suicidal patients, as well as psychological, social, and environmental factors, is crucial in interpreting the results of this study. Future research should take these factors and their potential confounding effects into account, in order to attain a more comprehensive understanding of the association between dietary niacin intake and SI.
Conclusion
This study identified an L-shaped non-linear inverse association between dietary niacin intake and the prevalence of SI in American adults. These findings may have significant implications for the prevention and treatment of SI. Given that diet is a modifiable lifestyle factor, further prospective studies and randomized controlled trials are necessary to explore the safety and efficacy of niacin-rich foods in mitigating the risk of SI.
Acknowledgements
We would like to thank the NHANES database for providing the data source for this study.
Authors’ contributions
HL, JX, BJW, WY, and XQJ– study concept and design; preparation, review and approval of manuscript. SSQ– data collection and interpretation; preparation, review and approval of manuscript.
Funding
This study was supported by the Wenzhou Municipal Science and Technology Bureau (Y20240231 to Jing Xu).
Data availability
The datasets generated and analysis during the current study are available in the NHANES, www.cdc.gov/nchs/NHANEs/.
Declarations
Ethics approval and consent to participate
The study was approved by the National Centre for Health Statistics Research Ethics Review Board, and every participant signed informed consent. The written informed consent of all subjects was obtained following the Declaration of Helsinki.
Consent for publication
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.
Hao Lin and Jing Xu contributed equally to this work.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The datasets generated and analysis during the current study are available in the NHANES, www.cdc.gov/nchs/NHANEs/.