The relationship between antioxidant vitamins and mental disorders: a meta-analysis

Abstract

Background: mental disorders are associated with oxidative stress. Antioxidant vitamins A, C and E exhibit antioxidant properties. Nevertheless, the association between antioxidant vitamins and mental disorders remains ambiguous. Methods: this meta-analysis compared the levels of dietary and blood vitamins A, C, and E between patients with attention deficit hyperactivity disorder (ADHD), autism spectrum disorder (ASD), depression, and schizophrenia (SZ) and healthy controls. Furthermore, a Mendelian randomization (MR) post-meta-analysis approach was employed to explore the causal relationships between these antioxidant vitamins and mental health conditions. Results: dietary analysis indicated that patients with depression exhibited a significantly lower intake of vitamin A (SMD: −0.13; 95% CI: −0.21, −0.05; and P < 0.01), vitamin C (SMD: −0.18; 95% CI: −0.24, −0.13; and P < 0.01), vitamin E (SMD: −0.16; 95% CI: −0.28, −0.04; and P = 0.01), and carotenoids (SMD: −0.17; 95% CI: −0.20, −0.14; and P < 0.01) compared with controls. Blood analysis revealed that patients with depression had decreased blood levels of vitamin A (SMD = −0.18; 95% CI: −0.29, −0.06; and P < 0.01), vitamin C (SMD = −0.52; 95% CI: −0.94, −0.10; and P = 0.01), and vitamin E (SMD = −0.77; 95% CI: −1.39, −0.16; and P = 0.01). Similarly, patients with SZ demonstrated a reduced blood level of vitamin C (SMD = −0.85; 95% CI: −1.49, −0.21; and P = 0.01) and vitamin E (SMD = −0.92; 95% CI: −1.21, −0.62; and P < 0.01). However, no significant differences were found in the dietary or blood antioxidant vitamins in patients with ADHD and ASD. MR post-meta-analysis identified a causal relationship between SZ and vitamin C. Conclusions: patients with depression had lower levels of dietary and blood vitamins A, C, and E. Similarly, patients with SZ had reduced blood levels of vitamins C and E.

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1. Introduction

Mental disorders are syndromes characterized by clinically significant disturbances in an individual's cognition, emotion regulation, or behavior.¹ The spectrum of mental disorders is extensive. The most prevalent include depression and bipolar disorder (BD) in the category of affective disorders, autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) in the category of neurodevelopmental disorders, schizophrenia (SZ) in the category of thought disorders and so on.² These disorders have the capacity to compromise cognitive and affective functions, disrupt daily living and social interactions, and present substantial challenges to patients, families, and society at large.³ The incidence of mental disorders is increasing rapidly on a global scale, thus rendering the prevention and treatment of these conditions a significant public health issue.⁴

The etiology of mental disorders is multifaceted. Neuroinflammation and oxidative stress have been identified as significant contributing factors to the development of mental disorders.⁵ Therefore, the implementation of antioxidant interventions (e.g., N-acetylcysteine, sulforaphane, α-lipoic acid, L-carnitine, etc.) has become a key strategy for the treatment and prevention of psychiatric disorders.⁶ Notably, vitamins A, C, and E are natural antioxidants. These vitamins have the capacity to reduce oxidative stress and safeguard the structure and function of neurons and other cells.⁷ Concurrently, antioxidant vitamins exhibit certain anti-inflammatory effects. They can reduce neuroinflammation by inhibiting the release of pro-inflammatory cytokines and increasing the expression of anti-inflammatory cytokines.⁸ Furthermore, antioxidant vitamins have been shown to promote nerve growth and repair, enhance neuroplasticity in the brain, and improve neurotransmitter synthesis and metabolism, thereby maintaining a healthy nervous system.^9,10 The preceding evidence suggests a potential association between antioxidant vitamins and mental disorders.

Several studies have demonstrated an association between antioxidant vitamins and mental disorders, indicating that antioxidant vitamin supplementation can ameliorate mental symptoms.^11–13 However, other studies have not obtained similar findings.^14–16 Therefore, we performed a meta-analysis of all relevant studies to explore the association and causal relationship between antioxidant vitamins and mental disorders by assessing the differences in dietary intake and blood levels of antioxidant vitamins between patients with mental disorders and controls. This investigation has important implications for the control and prevention of mental disorders.

2. Materials and methods

2.1 Search methodology and data sources

This meta-analysis was conducted in strict accordance with the PRISMA guidelines and was registered in PROSPERO (ID: CRD42024627906). To explore the effects of vitamins A, C and E on mental disorders, we conducted a comprehensive search of several electronic databases, including PubMed, Cochrane Library, EMBASE, Web of Science, and China National Knowledge Infrastructure (CNKI), for all relevant articles in both English and Chinese published from the inception of these databases to July 4, 2025. The search terms included vitamin A, retinol, vitamin C, ascorbic acid, vitamin E, tocopherol, carotenoids, ADHD, hyperkinetic syndrome, attention-deficit/hyperactivity disorder, autism spectrum disorder, ASD, depression, schizophrenia, and bipolar disorder. These terms were linked using Boolean logic algorithms to filter and identify eligible studies. The specific literature search strategies are shown in Table S1.

2.2 Inclusion and exclusion criteria

The following studies were included: (a) study type: cohort study or cross-sectional study or case-control study or Mendelian randomization (MR) study; (b) study population: patients with one or more explicitly mental disorders (ADHD, ASD, BD, depression, and SZ); and (c) outcome metrics: dietary intake and/or blood concentrations of one or more antioxidant vitamins (vitamins A, C, and E, and carotenoids) were provided (with data presented as mean ± standard deviation or convertible to mean ± standard deviation), for analyzing differences between patients with mental disorders (ADHD, ASD, BD, depression, and schizophrenia) and control groups (all included carotenoids were of the provitamin A type. When the number of studies investigating these carotenoids was fewer than 3, the data on these carotenoids were incorporated into the vitamin A group). Additionally, MR studies were included if they provided β or odds ratios (ORs)—together with their corresponding Standard Error (SE) or 95% confidence intervals (95% CIs)—for the causal relationships between antioxidant vitamins and mental disorders.

Studies were excluded if they were (a) case studies, editorials, reviews, and conference abstracts; (b) non-human studies; (c) studies with unavailable data, data with obvious errors, or only abstracts without full text; and (d) multiple similar publications by the same author using the same dataset; only the one with the most detailed methodology description and the most complete data was retained.

2.3 Data extraction

Based on careful review, the key information was extracted as follows: first author, publication year, nationality, age, gender, type of study design, method of dietary assessment, diagnostic criteria, sample source (plasma/serum), sample size, intake of dietary antioxidant vitamins, and blood levels of antioxidant vitamins. The following information was extracted from each eligible MR study: first author, publication year, exposure phenotype, outcome phenotype, and β or ORs along with their corresponding SE in the inverse-variance weighted (IVW) analysis.

2.4 Assessment of literature quality

The quality of the included cohort and case-control studies was evaluated using the Newcastle–Ottawa Scale (NOS).¹⁷ Cross-sectional studies were evaluated for quality using the Agency for Healthcare Research and Quality (AHRQ).¹⁸ A score of less than 6 on the NOS scale was considered to indicate a high risk of bias.¹⁷ The AHRQ instrument consists of 11 items with a score of 1 for “yes” and 0 for “no” or “unclear” answers. Studies were categorized as “high quality” (8–11), “moderate quality” (4–7), and “low quality” (0–3) based on their results.¹⁸

For the MR study literature included in the research, quality assessment was conducted based on the evaluation items outlined in the Strengthening the Reporting of Observational Studies in Epidemiology using Mendelian Randomization (STROBE-MR)¹⁹ and the MR systematic review by Luo et al.²⁰ Assessment was performed across five dimensions: relevance assumption, independence assumption, exclusivity assumption, sample overlap issue, and statistical power. With a total score of 12 points, scores from 0 to 4 were categorized as low quality, 5 to 8 as moderate quality, and 9 to 12 as high quality.

2.5 Statistical analysis

Differences in dietary intake and blood levels of antioxidant vitamins between patients with mental disorders and controls were explored using Stata 18.0 software. Mean ± standard deviation (mean ± SD) was used as the effect analysis statistic and the sample size (n) of each group was documented. The standardized mean difference (SMD) and 95% CI were used to analyze the differences in continuous variables between the two groups.

For MR studies, the ORs and 95% CIs were used to present the antioxidant vitamins on the risk of psychiatric disorders. Moreover, the causal effects of psychiatric disorders on the antioxidant vitamins were presented as β and 95% CIs.

The heterogeneity of the results of each meta-analysis was assessed using the I² test. If I² ≤ 50%, meta-analysis was performed using a fixed-effects model; otherwise, a random-effects model was used. The level of meta-analysis was set at α = 0.05. Sensitivity analyses and subgroup analyses were used to determine the source of heterogeneity. Egger's and Begg's tests were used to assess the presence of publication bias, and publication bias was considered to exist at P < 0.05. To further ascertain the impact of publication bias on the outcomes, meta-analyses for the presence of publication bias employed the trim-and-fill method.²¹

3. Results

3.1 Study description

The study screening process is illustrated in Fig. 1. Ultimately, 109 studies were selected for inclusion in this meta-analysis. However, the search yielded only one study¹²⁹ reporting dietary antioxidant vitamin intake in patients with SZ and one study¹³⁰ reporting blood antioxidant vitamin levels in patients with BD. Furthermore, no studies on the dietary intake of antioxidant vitamins in BD patients were retrieved. Due to the limited number of literature reports, the meta-analysis of patients with BD was not conducted; meanwhile, the meta-analysis of dietary antioxidant vitamins in patients with SZ was also not conducted. Consequently, these two studies were excluded from the present analysis. Finally, 107 literature studies were included in the meta-analysis. Two of these studies simultaneously reported the differences between dietary intake and blood levels.^34,59 The detailed information of the studies is summarized in Tables 1 and 2. The results of the quality assessment of the studies are presented in Tables S2–S4.

Fig. 1 Flow diagram of the literature search and selection.

Table 1 Characteristics of studies included in the analysis of dietary antioxidant vitamin intake

Study	Country	Age (years)	Sample size		Dietary assessment	Diagnostic criteria of the disease	Antioxidant vitamins
			Case	Control
AHRQ, Agency for Healthcare Research and Quality; ASSQ, Autism Spectrum Screening Questionnaire; BDHQ, Brief Diet History Questionnaire; BDI, Beck Depression Inventory; BDI-II, Beck Depression Inventory-II; CATRS-10, Conners’ Adult ADHD Rating Scales–Self-Report: Short Version (10-item); CES-D, Center for Epidemiologic Studies Depression Scale; CES-DC, Center for Epidemiologic Studies Depression Scale for Children; DASS-21, Depression, Anxiety and Stress Scale-21; DSM, Diagnostic and Statistical Manual of Mental Disorders; DSM-5, Diagnostic and Statistical Manual of Mental Disorders, 5th Edition; DSM-IV, Diagnostic and Statistical Manual of Mental Disorders, 4th Edition; FFQ, food frequency questionnaire; GDS, Geriatric Depression Scale; ICD-10, International Classification of Diseases, 10th Revision; NOS, Newcastle–Ottawa Scale; PHQ, Patient Health Questionnaire; PHQ-9, Patient Health Questionnaire-9; SCID-I, Structured Clinical Interview for DSM Disorders-I (Research Version).
ADHD
Kim, Y. 2011 ^22	Korea	10–12	9	98	24 h recall method	CATRS-10	Vitamins A and C
Salvat, H. 2022 ^23	Iran	5–13	100	100	FFQ	DSM-5	Vitamins A, C, and E
Koc, S. 2023 ^24	Turkey	6–17	169	221	24 h recall method	DSM-5	Vitamins A, C, and E
Chen, J. R. 2004 ^25	China	4–12	58	52	3 d diet record	DSM-IV	Vitamins A, C, and E
Nasim, S. 2019 ^26	Iran	6–13	36	32	FFQ	DSM-IV	Vitamins A, C, and E
ASD
Metwally, A. M. 2024 ^27	Egypt	3–12	285	224	3 d diet record	DSM-5	Vitamins A and C
Lockner, D. W. 2008 ^28	America	3–5	20	20	3 d diet record	—	Vitamins A, C, and E
Tsujiguchi, H. 2023 ^29	Japan	7–12	62	643	BDHQ	ASSQ	Retinol, β-carotene, α-tocopherol, and vitamin C
Tsujiguchi, H. 2020 ^30	Japan	7–15	82	1026	BDHQ	ASSQ	Retinol, β-carotene, α-tocopherol, and vitamin C
Malhi, P. 2017 ^31	India	4–10	63	50	3 d diet record	DSM-IV	Vitamins A and C
Moludi, J. 2019 ^32	Iran	6–13	29	30	FFQ	DSM	Vitamin C
Herndon, A. C. 2009 ^33	America	1–8	46	31	3 d diet record	ADOS-G	Vitamins A, C, and E
Sun, C. 2013 ^34	China	4–6	53	53	3 d diet record	DSM-IV	Vitamins A, C, and E
Zimmer, M. H. 2012 ^35	America	4–12	22	22	FFQ	ADOS	Vitamin A
Marí-Bauset, S. 2015 ^36	Spain	6–9	40	113	3 d diet record	ADOS-G	Vitamins A, C, and E
Barnhill, K. 2018 ^37	America	2–8	86	57	3 d diet record	DSM-IV	Vitamins A, C, and E
Dazıroğlu, M. E. C. 2024 ^38	Turkey	6–18	38	38	3 d diet record	—	Vitamins A, C, and E
Castro, K. 2016 ^39	Brazil	4–16	49	49	3 d diet record	DSM-IV	Vitamins A and C
Liu, X. 2016 ^40	China	3–7	154	73	3 d diet record	DSM-5	Vitamin A
Li, Y. 2019 ^41	China	4–9	48	42	3 d diet record	DSM-5	Vitamin A
Mobarakeh, K. A. 2025 ^42	Iran	5–15	100	108	FFQ	DSM-5	Vitamin E
Depression
Rubio-López, N. 2016 ^43	Spain	6–9	147	563	3 d diet record	CES-DC	Vitamins A, C, and E
Prohan, M. 2014 ^44	Iran	18–25	30	30	FFQ	BDI-II	Vitamins C and E, α-carotene, and β-carotene
Kaner, G. 2015 ^45	Turkey	18–60	29	30	24 h recall method	DSM-IV	Vitamins A, C, and E
Wang, A. 2021 ^46	America	≥18	2334	23 561	24 h recall method	PHQ-9	Vitamin C
Lin, S. 2021 ^47	America	≥18	329	3776	24 h recall method	PHQ-9	α-Carotene, and β-carotene
Li, D. 2022 ^48	America	42–52	746	2308	FFQ	CES-D	Vitamins C and E, and α-carotene
German, L. 2011 ^49	Palestine	≥60	53	59	24 h recall method	GDS	Vitamins C and E
Li, R. 2021 ^50	China	≥55	447	1418	FFQ	GDS	Vitamins A, C, and E, and β-carotene
Chen, W. 2021 ^51	Bahrain	20–60	96	96	FFQ	ICD-10	Vitamins A, C, and E, and β-carotene
De Oliveira, N. G. 2019 ^52	Japan	≥60	18	23	BDHQ	GDS	Vitamins A, C, and E
Purnomo, J. 2012 ^53	Bahrain	20–60	21	37	FFQ	ICD-10	Vitamins A and C
Park, S. H. 2019 ^54	Brazil	50–69	56	122	24 h recall method	BDI	Vitamins A and C
Thao Thi Thu, N. 2017 ^55	Australia	≥40	437	1197	FFQ	CES-D10	Vitamins C and E, retinol, and β-carotene
Yoon, S.-I. 2023 ^56	Korea	19–39	39	76	3 d diet record	CES-D	Vitamins A, C, and E
Payne, M. E. 2012 ^57	America	≥60	144	134	FFQ	DSM-IV	Vitamins C and E, α-carotene, and β-carotene
Vahid, F. 2023 ^58	Iran	20–80	100	77	FFQ	DASS-21	Vitamins A, C, and E, and β-carotene
Beydoun, M. A. 2013 ^59	America	20–85	195	1603	24 h recall method	PHQ	Vitamins C and E, α-carotene, and β-carotene
Park, J. Y. 2010 ^60	Korea	20–21	65	65	3 d diet record	CES-D	Vitamins A, C, and E, and β-carotene
Oldra, C. M. 2020 ^61	Korea	19–64	159	241	24 h recall method	PHQ-9	Vitamin C
Park, S. J. 2018 ^62	America	≥47	170	2768	24 h recall method	PHQ-9	Vitamins A and C, and retinol
Hu, B. 2022 ^63	Iran	≥18	15 901	15 938	24 h recall method	SCID-I	Vitamin A
Mohtadinia, J. 2015 ^64	Iran	18–59	30	30	FFQ	SCID-I	Vitamins A, C, and E
Tasnim, T. 2023 ^65	Bangladesh	≥65	88	20	24 h recall method	GDS	Vitamins A, C, and E
Li, H. 2024 ^66	Singapore	45–74	3173	10 539	FFQ	GDS-15	Vitamins C and E, α-carotene, and β-carotene
Bakir, B. 2023 ^67	Turkey	19–29	48	174	24 h recall method	HADS	Vitamins A, C, and E, and retinol
Di, L. 2019 ^68	America	42–52	740	2022	FFQ	CES-D	α-Carotene and β-carotene
Seo, Y. 2018 ^69	Korea	19–64	246	10 345	FFQ	—	Vitamins A and C, and retinol
Park, S. J. 2021 ^70	Korea	45–69	487	1703	FFQ	BDI-II, CES-D	α-Carotene and β-carotene
Khayyatzadeh, S. S. 2021 ^71	Iran	12–18	255	733	FFQ	BDI	Vitamins A, C, and E, β-carotene, and α-carotene
Ge, H. 2020 ^72	America	18–80	1545	15 856	24 h recall method	PHQ-9	α-Carotene and β-carotene
Farhadnejad, H. 2020 ^73	Iran	15–18	151	148	FFQ	DASS-21	Vitamins C and E, and β-carotene
Ferriani, L. O. 2022 ^74	Brazil	35–74	616	14 121	FFQ	CIS-R	Vitamins A, C, and E
Nanri, A. 2010 ^75	Japan	21–67	186	335	BDHQ	CES-D	Vitamins C and E

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Table 2 Characteristics of studies included in the analysis of blood levels of antioxidant vitamins

Study	Country	Age (years)	Sample size		Sample source	Antioxidant vitamins	Diagnostic criteria of disease
			Case	Control
AHRQ, Agency for Healthcare Research and Quality; CCMD-3, Chinese Classification of Mental Disorders, 3rd Edition; DSM-III, Diagnostic and Statistical Manual of Mental Disorders, 3rd Edition; DSM-4, Diagnostic and Statistical Manual of Mental Disorders, 4th Edition; DSM-5, Diagnostic and Statistical Manual of Mental Disorders, 5th Edition; GDS-15, 15-item Geriatric Depression Scale; HRSD, Hamilton Rating Scale for Depression; ICD-10, International Classification of Diseases, 10th Revision; NOS, Newcastle–Ottawa Scale; PHQ-9, Patient Health Questionnaire-9.
ADHD
Verlaet, A. A. J. 2019 ^76	Belgium	6–12	57	69	Plasma	Retinol, α-tocopherol, γ-tocopherol, and β-carotene	DSM-5
Li, H.-H. 2020 ^77	China	6–9	82	106	Serum	Retinol	DSM-5
Li, H. 2022 ^78	China	4–12	34	34	Serum	Vitamins A and E	DSM-5
Lan, H. 2022 ^79	China	9–11	30	30	Serum	Vitamins A and E	DSM-5
Guo, L. 2021 ^80	China	6–12	40	60	Serum	Vitamins A and E	DSM-5
SZ
Telo, S. 2016 ^81	Turkey	20–70	80	40	Plasma	Vitamin E	DSM-4
Cheng, X. 1995 ^82	China	20–50	56	42	Serum	Vitamins A and E	DSM-5
McCreadie, R. 2000 ^83	England	14–44	30	30	Plasma, serum	Vitamins A and E	DSM-4
Zhang, X. 1995 ^84	China	20–50	56	42	Serum	Vitamin E	DSM-5
Young, J. 2007 ^85	England	16–60	16	17	Serum	Vitamin C	DSM-4
Kilicgun, H. 2016 ^86	Turkey	19–40	30	30	Serum	Vitamin E	DSM-5
Wang, S. 2001 ^87	China		98	60	Serum	Vitamin E	CCMD-3
Suboticanec, K. 1990 ^88	Yugoslavia	37–49	35	35	Plasma	Vitamin C	DSM-III
D'Souza, B. 2003 ^89	India	29–68	14	18	Plasma	Vitamin E	—
						Vitamin C
Dadheech, G. 2006 ^90	India	18–60	58	40	Plasma	Vitamin E	DSM-4
ASD
Krajcovicova-Kudlackova, M. 2009 ^91	Slovakia	5–18	24	77	Plasma	Vitamins A, C, and E, and β-carotene	—
Tan, Y. 2020 ^92	China	2–6	71	71	Serum	Vitamin C	DSM-V
Feng, J. 2023 ^93	China	40–68	181	205	Serum	Vitamin A	DSM-V
Guo, M. 2018 ^94	China	3–7	33	32	Serum	Retinol	DSM-V
Wang, L. 2020 ^95	China	4–14	31	30	Serum	Vitamins A and E	—
Zou, M. 2024 ^96	China	2–7	120	110	Serum	Vitamins A and E	DSM-V
Lin, X. 2022 ^97	China	6–9	67	134	Plasma	Vitamins A and E	DSM-V
Sun, C. 2013 ^34	China	4–6	53	53	Serum	Vitamin A	DSM-V
Gulati, S. 2024 ^98	India	2–18	119	52	Serum	Vitamin E	DSM-V
Sweetman, D. U. 2019 ^99	Ireland	2–18	74	72	Serum	Vitamin A	DSM-IV
Cheng, B. 2021 ^100	China	2–7	323	180	Serum	Retinol	DSM-V
Guo, M. 2019 ^101	China	3–7	332	197	Serum	Retinol	DSM-V
Guo, M. 2020 ^102	China	2–7	274	97	Serum	Vitamin A	DSM-V
Zhu, J. 2020 ^103	China	2–6	743	302	Serum	Vitamin A	DSM-V
Adams, J. B. 2011 ^104	America	5–16	55	44	Plasma	Vitamins A, C, and E, and β-carotene	DSM
Depression
Bajpai, A. 2014 ^105	China	6–9	60	40	Serum	Vitamin C	DSM-V
Khanzode, S. D. 2003 ^106	India	≥18	62	40	Serum	Vitamin C	DSM-IV
Feng, N. 2023 ^107	China	45–55	33	94	Serum	Vitamins A, C, and E	DSM-IV
Lindqvist, D. 2017 ^108	America	≥18	50	55	Serum	Vitamin C	DSM-IV
Bal, N. 2012 ^109	Turkey	≥18	42	38	Serum	Vitamin C	DSM-IV
Zhang, W. 2024 ^110	America	≥18	545	6719	Serum	α-Carotene and β-carotene	PHQ-9
Lee, S. M. 2023 ^111	Korea	≥20	815	2498	Serum	Vitamins A and E	PHQ-9
Beydoun, M. A. 2013 ^59	America	20–85	195	1603	Serum	Retinol, β-carotene, and vitamins C and E	PHQ-9
Xue, Y. 2020 ^112	China	18–35	75	48	Plasma	Vitamin A	DSM-IV
Hamer, M. 2011 ^113	England	≥65	210	797	Plasma	Vitamin C	GDS-15
Maes, M. 2000 ^114	Belgium	≥18	42	36	Serum	Vitamin E	DSM-III
Islam, M. R. 2020 ^115	Bangladesh	≥18	247	248	Serum	Vitamins A, C, and E	DSM-V
Yanik, M. 2004 ^116	Turkey	20–47	21	28	Plasma	Vitamin C	DSM-IV
Al-Fartusie, F. S. 2019 ^117	Iraq	39–60	60	60	Serum	Vitamins A and E	—
M. Gautam, 2012 ^118	India	20–60	40	20	Serum	Vitamins A, C, and E	ICD-10
Narwaria, S. S. 2025 ^119	India	23–44	55	55	Serum	Vitamin C	HRSD
Xu, Q. 2025 ^120	America	≥20	311	3967	Serum	Vitamins A, C, and E	PHQ-9
Cao, Q. 2024 ^121	America	≥20	867	2567	Serum	Vitamin C	PHQ-9

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A total of 8 ^121–128 studies on MR were finally included in this research. The literature quality scores ranged from 9 to 12 points, all of which were classified as high-quality literature. The exposure samples and outcome samples of the included literature were all from European populations. The specific details of the included literature are presented in Table S5.

3.2 Meta-analysis of dietary antioxidant vitamins with mental disorders

3.2.1 Dietary antioxidant vitamin intake in patients with ADHD and ASD. The differences in the dietary intake of antioxidant vitamins A, C, and E between ADHD patients and the control group are shown in Fig. S1. There were no statistically significant differences between the two groups in the intake of dietary vitamin A (SMD = −0.14; 95% CI: −0.28, −0.00; P = 0.05; and I² = 0.00%), vitamin C (SMD = −0.17; 95% CI: −0.59, 0.24; P = 0.42; and I² = 85.54%), and vitamin E (SMD = 0.07; 95% CI: −0.34, 0.49; P = 0.73; and I² = 86.05%).

The differences in the dietary intake of antioxidant vitamins A, C, and E between ASD patients and the control group are shown in Fig. S2. There were no statistically significant differences between the two groups in the intake of dietary vitamin A (SMD = −0.18; 95% CI: −0.38, 0.01; P = 0.07; and I² = 83.77%), vitamin C (SMD = −0.18; 95% CI: −0.38, 0.02; P = 0.08; and I² = 77.75%), and vitamin E (SMD = −0.03; 95% CI: −0.44, 0.37; P = 0.87; and I² = 91.85%).

3.2.2 Dietary antioxidant vitamin intake in patients with depression. The discrepancy in the dietary intake of antioxidant vitamins A, C, and E between depression patients and the control group is illustrated in Table 3. The results indicated that patients with depression had significantly lower intake of vitamin A (SMD: −0.13; 95% CI: −0.21, −0.05; P < 0.01; and I² = 83.32%), vitamin C (SMD: −0.18; 95% CI: −0.24, −0.13; P < 0.01; and I² = 66.88%), vitamin E (SMD: −0.16; 95% CI: −0.28, −0.04; P = 0.01; and I² = 92.41%), and carotenoids (SMD: −0.17; 95% CI: −0.20, −0.14; P < 0.01; and I² = 49.98%) compared to the control group. Sensitivity analyses showed relatively stable results from meta-analyses (no extreme results, Fig. S3). Meanwhile, subgroup analyses were conducted according to country, dietary assessment method, and diagnostic criteria (Table S6). The subgroup analysis results showed that the heterogeneity among subgroups remained high, and the heterogeneity indicators within subgroups did not significantly decrease compared with the overall analysis.

Table 3 Meta-analysis of dietary antioxidant vitamin intake in patients with depression and controls

Vitamins	Number of studies	SMD (95% CI)	P	I ^2 (%)
Vitamin A	27	−0.13 (−0.21, −0.05)	<0.01	83.32
Vitamin C	33	−0.18 (−0.24, −0.13)	<0.01	66.88
Vitamin E	26	−0.16 (−0.28, −0.04)	0.01	92.41
Carotenoids	28	−0.17 (−0.20, −0.14)	<0.01	49.98

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Publication bias was assessed for each meta-analysis result using Begg's test and Egger's test, which indicated that publication bias existed in the studies on dietary vitamin A intake in patients with depression (P < 0.05), while no publication bias was observed in the remaining studies (P > 0.05) (Table S7). To address the potential issue of publication bias, the trim-and-fill method was employed for further analysis. For studies on dietary vitamin A intake in patients with depression, statistical significance was observed before applying the trim-and-fill method (SMD = −0.13; 95% CI: −0.21, −0.05; and P < 0.05). After incorporating data from eight imputed studies via the trim-and-fill method and re-analyzing all studies in the meta-analysis, statistical significance was lost (SMD = −0.06; 95% CI: −0.15, 0.02; and P > 0.05).

3.3 Meta-analysis of blood levels of antioxidant vitamins with mental disorders

3.3.1 Blood levels of antioxidant vitamins in patients with ADHD and ASD. The meta-analysis revealed a statistically significant difference in blood vitamin A levels between ADHD patients and controls (SMD = −0.52; 95% CI: −1.02, −0.01; P = 0.04; and I² = 89.79%), with lower levels observed in ADHD patients. In contrast, no significant difference was found for vitamin E (SMD = 0.11; 95% CI: −0.10, 0.32; P = 0.31; and I² = 26.89%) (Fig. S4). Sensitivity analysis showed that the significant difference in vitamin A levels was driven by four studies,^76–78,80 and the significance disappeared upon removal of any one of these studies (Fig. S5). No significant publication bias was detected for vitamin A (P > 0.05) (Table S7).

The meta-analysis showed a significant difference in blood vitamin A levels between ASD patients and controls (SMD = −0.85; 95% CI: −1.67, −0.03; P = 0.04; and I² = 99.14%), with lower levels in ASD patients. No significant differences were observed for vitamin C (SMD = 0.43; 95% CI: −0.13, 0.98; P = 0.13; and I² = 82.86%) or vitamin E (SMD = −0.16; 95% CI: −0.50, 0.18; P = 0.36; and I² = 81.91%) (Fig. S6). Sensitivity analysis revealed that the significant difference in vitamin A levels was driven by seven studies, with significance loss upon removal of any one study.^{34,94,95,100–102,104} (Fig. S7). No significant publication bias was detected for vitamin A (P > 0.05) (Table S7).

3.3.2 Blood levels of antioxidant vitamins in patients with depression. The meta-analysis results on the differences in antioxidant vitamins A, C, and E levels in the blood between patients with depression and controls showed that the differences in blood levels of vitamin A (SMD = −0.18; 95% CI: −0.29, −0.06; P < 0.01; and I² = 85.39%), vitamin C (SMD = −0.52; 95% CI: −0.94, −0.10; P = 0.01; and I² = 98.19%), and vitamin E (SMD = −0.77; 95% CI: −1.39, −0.16; P = 0.01; and I² = 99.09%) were statistically significant, with lower levels of vitamins A, C, and E observed in patients with depression compared to controls (Fig. 2).

Fig. 2 Forest plot of antioxidant vitamin levels in the blood of patients with depression and controls. A: Vitamin A; B: vitamin C; and C: vitamin E.

Sensitivity analysis indicated that the meta-analysis results were relatively stable, with no extreme results observed (Fig. S8). Given the high heterogeneity in the analysis of blood levels of vitamins A, C, and E, subgroup analyses were conducted based on country and diagnostic criteria (Table S8). The subgroup analysis results showed that heterogeneity remained high across subgroups, with no significant reduction in heterogeneity indices within subgroups compared to the overall analysis.

Publication bias was assessed for each meta-analysis result using Begg's test and Egger's test, which indicated that publication bias existed in the studies on blood vitamin E levels in patients with depression (P < 0.05), while no publication bias was observed in the remaining studies (P > 0.05) (Table S7). To address the potential issue of publication bias, the trim-and-fill method was employed for further analysis. For studies on blood vitamin E levels in patients with depression, statistical significance was observed before applying the trim-and-fill method (SMD = −0.77; 95% CI: −1.39, −0.16; and P < 0.05). After incorporating data from three imputed studies via the trim-and-fill method and re-analyzing all studies in the meta-analysis, statistical significance was lost (SMD = −0.18; 95% CI: −0.99, 0.63; and P > 0.05).

3.3.3 Blood levels of antioxidant vitamins in patients with SZ. The meta-analysis revealed no significant difference in blood vitamin A (SMD = −0.37; 95% CI: −0.85, 0.11; P = 0.13; and I² = 66.62%) levels between SZ patients and controls, but significant differences were observed for vitamin C (SMD = −0.85; 95% CI: −1.49, −0.21; P = 0.01; and I² = 82.98%) and vitamin E (SMD = −0.92; 95% CI: −1.21, −0.62; P < 0.01; and I² = 74.02%), with lower levels in SZ patients (Fig. 3).

Fig. 3 Forest plot of antioxidant vitamin levels in the blood of patients with SZ and controls. A: Vitamin A; B: vitamin C; and C: vitamin E.

Sensitivity analysis indicated that the meta-analysis results were relatively stable, with no extreme results observed (Fig. S9). Due to high heterogeneity, subgroup analyses based on country and diagnostic criteria were performed (Table S9), but heterogeneity remained high within subgroups, with no significant reduction compared to the overall analysis.

Publication bias was assessed for studies on blood levels of vitamins C and E in patients with SZ using Begg's test and Egger's test, which indicated that publication bias existed in the subset of studies focusing on blood vitamin C levels (P < 0.05), while no publication bias was observed in those focusing on blood vitamin E levels (P > 0.05) (Table S7). To address the potential issue of publication bias, the trim-and-fill method was employed for further analysis of the vitamin C subset. For these vitamin C studies, statistical significance was observed before applying the trim-and-fill method (SMD = −0.34; 95% CI: −0.54, −0.13; and P < 0.05). After incorporating data from three imputed studies using the trim-and-fill method and re-analyzing all vitamin C studies in the meta-analysis, statistical significance was lost (SMD = −0.16; 95% CI: −0.34, 0.03; and P > 0.05).

3.4 Meta-analysis of the causal relationship between antioxidant vitamins and mental disorders

We conducted a meta-analysis of MR studies investigating the associations between vitamins A, C, E and two conditions (depression and SZ). The primary IVW analysis showed no significant associations in the following specific comparisons: between vitamin A and depression (OR = 0.98, 95% CI: 0.89, 1.08, P = 0.71; I² = 90.48%), vitamin C and SZ (OR = 0.95, 95% CI: 0.86, 1.06, P = 0.38; I² < 0.01%), vitamin E and SZ (OR = 0.94, 95% CI: 0.81, 1.10, P = 0.45; I² = 43.26%), and vitamin E and depression (OR = 0.95, 95% CI: 0.88, 1.02, P = 0.16; I² = 47.63%) (Table S10). However, a statistically significant association was observed between vitamin C and depression (OR = 1.04, 95% CI: 1.01, 1.07, P = 0.01; I² = 0.46%). Nevertheless, sensitivity analysis indicated that this result was influenced by one study,¹²⁸ and the statistical significance of the association disappeared upon removal of this study (Fig. S10).

In the meta-analysis of MR studies exploring the relationships between depression, SZ, and vitamins A, C, and E, the results of the primary IVW analysis revealed no significant associations between depression and vitamin A (β = −0.00, 95% CI: −0.01, 0.00, P = 0.30; I² < 0.01%), vitamin C (β = −0.03, 95% CI: −0.07, 0.00, P = 0.08; I² = 84.30%), or vitamin E (β = 0.01, 95% CI: −0.02, 0.04, P = 0.45; I² = 86.81%), nor between SZ and vitamin E (β = 0.00, 95% CI: −0.00, 0.01, P = 0.13; I² = 93.30%) (Table S11). However, a statistically significant effect of SZ on vitamin C was observed (β = 0.00, 95% CI: 0.00, 0.01, P < 0.01; I² < 0.01%). Sensitivity analyses demonstrated that the meta-analysis results were relatively stable, with no extreme outcomes identified (Fig. S11). Additionally, no publication bias was detected via Egger's test (P = 0.96) and Begg's test (P = 1.00).

4. Discussion

In recent years, the potential role of antioxidant vitamins in the development and progression of psychiatric disorders has garnered widespread attention. This meta-analysis systematically elucidates the differences in dietary intake and blood levels of antioxidant vitamins between patients with psychiatric disorders (ADHD, ASD, depression, and SZ) and healthy controls.

ADHD and ASD patients showed no significant differences in antioxidant vitamin intake or blood levels compared with healthy controls. In contrast, patients with depression exhibited significant abnormalities in both aspects: their dietary intake of antioxidant vitamins was significantly lower than that of healthy controls, which is consistent with previous studies,^131,132 and their blood levels of antioxidant vitamins were significantly reduced. This high consistency between dietary intake and blood levels further supports the view proposed by Jerome Sarris et al.¹³³ that “dietary patterns may affect the pathogenesis of depression by regulating oxidative stress levels”. Patients with SZ also had reduced antioxidant vitamin levels, manifested as significant vitamin deficiency in the blood. Taken together, patients with depression and SZ generally exhibit lower levels of antioxidant vitamins. Deficiencies in vitamins C and E, in particular, may impair neuroprotective mechanisms and exacerbate neuronal damage,¹³⁴ whereas no such differences are observed in patients with ADHD or ASD. This disease-specific discrepancy may be related to the clinical characteristics of different mental disorders: for example, anorexia and dietary monotony often associated with depression may lead to insufficient intake of antioxidant vitamins, which in turn affects the condition through a vicious cycle of oxidative stress and neuroinflammation,¹³⁵ and vitamin deficiency in SZ patients may be related to metabolic side effects caused by the long-term use of antipsychotics.¹³⁶

Despite the fact that ASD, ADHD, and depression are all classified as mental disorders, patients with depression have significantly lower dietary intake of antioxidant vitamins compared to controls, whereas such differences are not observed in ASD or ADHD. We propose that this discrepancy may stem from the distinct pathophysiological mechanisms underlying these different disorders. Depression is closely associated with mitochondrial dysfunction, chronic oxidative stress, and systemic inflammation,¹³⁷ which may exacerbate nutrient depletion and alter dietary patterns due to appetite dysregulation or metabolic dysfunction.¹³⁸ Conversely, ASD and ADHD are neurodevelopmental disorders, whose behavioral symptoms, such as food selectivity in ASD¹³⁹ or impulsivity in ADHD,¹⁴⁰ may obscure true dietary differences. Additionally, studies involving patients with ASD and ADHD frequently focus on pediatric cohorts, where parental reporting biases or age-related metabolic resilience may mitigate observable differences.^141,142 Vitamins A and E, as fat-soluble vitamins, can act on the lipid-phase environment of biological membranes to maintain membrane structural stability and regulate neural development.^143,144 Vitamin C, a water-soluble vitamin, is distributed in the aqueous-phase environment of intracellular fluid, where it scavenges reactive oxygen species (ROS) and assists in substance metabolism.¹⁴⁵ The essential mechanism underlying the actions of these two types of vitamins lies in antioxidation and neuroprotection targeted at different environments. The core pathology of depression and SZ is mostly characterized by excessive central oxidative stress or damage to neural membranes, which is highly associated with the functions of these two categories of vitamins.^146,147 In contrast, the core mechanisms of ASD and ADHD, such as abnormal synaptic connections and impaired dopamine transporter function, have a relatively weak association with the “oxidative damage–vitamin neuroprotection” pathway. Therefore, the vitamin levels in patients with ASD and ADHD generally remain within the normal range.^148–151

Meanwhile, the present study found that patients with SZ exhibited significantly reduced levels of antioxidant vitamins in the blood. However, there is a paucity of dietary data to support this finding. This limitation may be attributed to the fact that patients with SZ often experience cognitive impairments,¹⁵² communication difficulties,¹⁵³ and adverse drug effects,¹⁵⁴ which collectively increase the difficulty of implementing dietary surveys and reduce patient compliance.

Studies on the dietary intake of vitamin A in patients with depression, the blood levels of vitamin E in patients with depression, and the blood levels of vitamin C in patients with SZ exhibited publication bias. After incorporating virtual studies, the statistical significance of the differences disappeared, indicating that negative results may not have been adequately published. Future research needs to reduce bias through prospective design and rigorous documentation.

To address the limitation of insufficient causal inference ability, our team further conducted a meta-analysis following MR. We found that SZ affects vitamin C levels; however, vitamin C levels have no impact on SZ, thus demonstrating a unidirectional causal relationship from SZ to vitamin C. However, our results showed that the regression coefficient for the effect of SZ on vitamin C was <0.01, suggesting that this causal relationship requires further validation in more studies involving diverse populations (or additional GWAS). We were unable to establish causal relationships between vitamin E and SZ, or between vitamins A, C, E and depression. This may be constrained by factors such as an insufficient number of included studies and inter-study heterogeneity; therefore, the possibility of potential causal relationships between them cannot be completely ruled out.

The limitations of this study include: insufficient data on patients with BD, which precludes the drawing of comprehensive conclusions; the predominance of cross-sectional and case-control studies, which makes causal inference difficult; the limited number of available MR studies and the exclusive inclusion of European populations, which may have hindered the identification of true causal relationships between antioxidant vitamins and mental disorders; and the failure to control for confounding factors such as medication use and comorbidities, which may lead to biased results.

Currently, the number of longitudinal cohort studies and intervention trials investigating the relationship between antioxidant vitamins and mental disorders remains limited, and the scale and consistency of existing studies also need to be improved. This has precluded us from conducting a systematic meta-analysis in this field within the present study. Therefore, future research urgently requires more well-designed longitudinal cohort studies and intervention trials to establish the temporal association between antioxidant status and the occurrence or progression of diseases, and to clarify whether supplementation with antioxidant vitamins can alter the clinical outcomes of mental disorders. Additionally, it is necessary to combine metabolomics and genetic testing techniques to deeply elucidate the specific mechanisms by which antioxidant vitamins regulate neuroinflammatory pathways, mitochondrial function, and epigenetic regulation in mental disorders. These efforts will help to further clarify the relationship between antioxidant vitamin deficiency and mental disorders, as well as the underlying mechanisms, thereby providing a more reliable scientific basis for the prevention and intervention of related diseases.

5. Conclusions

Patients with depression had lower levels of dietary and blood vitamins A, C, and E. Similarly, patients with SZ had reduced blood levels of vitamins C and E. However, no significant differences were found in the dietary or blood antioxidant vitamins in patients with ADHD and ASD. MR post-meta-analysis identified a causal relationship between SZ and vitamin C.

Author contributions

H. P. and W. H. X.: data analysis and manuscript writing; M. T. L. and Y. H.: search and review of literature; S. Q. J.: data extraction; and L. X. and H. T. Y.: conceptualization and manuscript writing. All authors have reviewed and approved the final manuscript.

Conflicts of interest

All authors disclosed that there were no financial and personal relationships with other people or organizations that could inappropriately influence (bias) their work.

Data availability

No primary research results, software or code have been included and no new data were generated or analysed as part of this review.

Supplementary information (SI): all supplementary figures and tables are included. See DOI: https://doi.org/10.1039/d5fo03181h.

Acknowledgements

This work was supported by the Health Commission of Jilin Province (2024A008).

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Footnote

† These authors contributed equally to this work.

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