Obsessive–Compulsive Disorder (OCD) and Vitamin D - many studies

Lower vitamin D linked to more severe OCD in 173 adults - observational June 2026

Vitamin D Deficiency and Obsessive–Compulsive Disorder Severity: A Cross-Sectional Study

Life (MDPI), 14 June 2026, https://doi.org/10.3390/life16061002

Marazziti, D.; Mucci, F.; Gambini, M.; Fazio, E.; Cazzato, L.; Carbone, M.G.; Gurrieri, R.

Summary by Claude - June, 2026

In this cross-sectional, observational study of 306 adult OCD outpatients in Pisa, Italy (173 with serum vitamin D data; 171 with both vitamin D and severity scores), lower 25(OH)D tracked with worse OCD symptoms. The cohort was markedly deficient: mean 25(OH)D was 20.0 ± 13.1 ng/mL, with 60.1% below 20 ng/mL and only 15% sufficient (≥30 ng/mL).

Vitamin D correlated inversely with Yale–Brown Obsessive–Compulsive Scale (Y-BOCS) total score (ρ = −0.26, p = 0.001) and with both obsession and compulsion subscales, and the correlation held after adjusting for age, sex, and bipolar comorbidity. Deficient patients (<20 ng/mL) averaged a Y-BOCS total about 5.5 points higher than non-deficient patients (29.2 vs. 23.7) — a difference the authors call clinically meaningful against the usual 25–35% Y-BOCS reduction defining treatment response. In multivariable regression, lower vitamin D (β = −0.25, p = 0.001) and earlier age at onset (β = −0.28, p = 0.001) were the only independent predictors of severity. The effect looked threshold-like around 20 ng/mL rather than a smooth dose–response (a quadratic term was non-significant, p = 0.711). A lifetime history of suicide attempts (n = 16) neither predicted severity nor moderated the vitamin D association.

What this does not show / limitations: Being cross-sectional, it establishes correlation, not causation — low vitamin D could be a consequence of severe OCD (less time outdoors, poorer diet, chronic stress). There was no healthy control group, so it cannot claim OCD patients are more deficient than the general (also widely deficient) Italian population. Vitamin D was measured by competitive protein-binding assay, less precise than LC-MS/MS. Lab data were retrospectively available (possible selection bias), and the tertiary clinic showed unusually high bipolar comorbidity (29.7%) and a male predominance, limiting generalizability. The full model explained only 13.3% of variance in severity. No interventional data — no one was supplemented.

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Decreased vitamin D levels in obsessive-compulsive disorder patients - 2023

CNS Spectrums , October 2023 , DOI: https://doi.org/10.1017/S1092852921000821 PDF behind a paywall

ObjectiveThe present paper compared vitamin D levels in adult patients with obsessive-compulsive disorder (OCD) and explored possible correlations with patients’ characteristics.

MethodsFifty outpatients with OCD, according to DSM-5 criteria, were included and assessed with the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS) and the Hamilton Rating Scale for Depression (HRDS).

ResultsAll the patients except one showed lower vitamin D levels than normative values (>30 nm/L). Vitamin D values of the whole sample were negatively correlated with Y-BOCS total, compulsion subscale, and some items’ scores, specifically “interference from obsessions,” “distress associated with obsessions,” and “time spent on compulsions”. The same relationships were detected in men, while women showed negative correlations between vitamin D levels and Y-BOCS compulsion subscale and “resistance to compulsions,” “degree of control of compulsions,” “insight” item scores.

ConclusionsOur findings would indicate that vitamin D might be involved in the pathophysiology of OCD, and that it is possibly related to the severity of the disorder and to typical symptoms, with some sex-related peculiarities. Further studies are necessary to support or not our findings and to ascertain the effectiveness of vitamin D supplementation in patients with OCD.

Investıgation of vitamin D levels in obsessive-compulsive disorder - 2022

Indian Journal of Psychiatry 64(4):p 349-353, Jul–Aug 2022. | DOI: 10.4103/indianjpsychiatry.indianjpsychiatry2622

Soyak, Hüda Murat; Karakükcü, Çiğdem1

Background: The impact of vitamin D on obsessive-compulsive disorder (OCD) remains unknown.

Aim: Studies suggest that vitamin D deficiency may be associated with neuropsychiatric diseases. The purpose of this study is to investigate vitamin D levels in those diagnosed with OCD. In addition, the relation between OCD symptom severity and serum vitamin D level is investigated.

Methods: About 174 patients newly diagnosed with OCD and 170 healthy volunteers were included in the study. Yale–Brown Obsessive Compulsive Scale (YBOCS) was used to assess the severity of OCD symptoms. Serum vitamin D levels of the two groups were compared.

Results: The serum vitamin D levels of the OCD group were found to be significantly lower than the control group. Serum vitamin D levels were negatively correlated with the obsession, compulsion, and total scale scores measured in YBOCS but there was no correlation between the serum vitamin D levels and illness duration of OCD patients.

Conclusions: To the best of our knowledge, this is one of the first studies to investigate vitamin D levels in newly diagnosed adult OCD patients without comorbidities. Although our findings suggest that vitamin D may play a role in the pathophysiology of OCD, further studies are needed to support our findings.

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Compare OCD and ADHD prevalence

Claude AI - June 2026

OCD

In US adults, lifetime prevalence is about 2.3% and 12-month prevalence about 1.2%, based on the National Comorbidity Survey Replication. That works out to roughly 1 in 40 people affected at some point in life. Globally, estimates run somewhat higher: a recent analysis of the World Mental Health surveys across 10 countries found a combined lifetime prevalence of 4.1% and a 12-month prevalence of 3.0%, though older meta-analyses pooled global prevalence closer to 1.6–2%. One consistent feature is that the 12-month figure is nearly as high as the lifetime figure, suggesting OCD tends to be persistent and chronic once it develops. It's also more common in women than men in adulthood, and more than 80% of cases begin by early adulthood.

ADHD

Prevalence depends heavily on age group:

In US children (ages 3–17), an estimated 7 million, or about 11.4%, have ever been diagnosed with ADHD per 2022 national survey data. Current diagnosis (rather than ever-diagnosed) is around 10.5%, roughly 6.5 million children. Boys are diagnosed at more than twice the rate of girls, and state-level estimates vary widely, from about 6% to 16%.

In US adults, an estimated 15.5 million (6.0%) have a current diagnosis of ADHD. Globally, adult figures depend on definition: a recent synthesis estimated about 6.8% for symptomatic adult ADHD and 2.6% for persistent adult ADHD (which requires confirmed childhood onset), with prevalence declining across the adult lifespan.

A few caveats worth noting: the US childhood ADHD numbers reflect diagnosed cases from parent surveys, which tend to run higher than research-based prevalence estimates and have risen substantially over recent decades. OCD figures come from structured diagnostic interviews, so the two conditions aren't measured by identical methods, which makes direct head-to-head comparison imperfect.

Bibliography: Vitamin D and Obsessive-Compulsive Disorder

Claude AI - June 2026

The bulk of the evidence — at least seven case-control/cross-sectional studies plus a 2024 OCD-specific meta-analysis (pooled SMD = -0.603, p < 0.001) — shows OCD patients, both adult and pediatric, tend to have lower serum 25(OH)D than controls, with vitamin D inversely correlated with symptom severity (Y-BOCS/CY-BOCS); however, several pediatric studies found the difference non-significant, so the literature is best described as "positive-leaning but mixed."
There is NO randomized controlled trial of vitamin D supplementation in OCD itself; the strongest interventional evidence comes from the adjacent chronic tic disorder (CTD) literature — including a 2025 dose-comparison RCT and Li et al. 2019 — which shows vitamin D3 reduces tic severity, plus a closely related PANDAS literature.
A genuine literature gap exists: no study has examined VDR gene polymorphisms directly in OCD, and there is no dedicated maternal/prenatal vitamin D → offspring OCD study (only adjacent ASD/ADHD/schizophrenia work). Mechanistic plausibility (serotonergic TPH2, dopaminergic tyrosine hydroxylase, glutamatergic/NMDA, neuroinflammation, basal ganglia, PANDAS autoimmunity) is strong but indirect.

Key Findings

Direction of evidence. Across adult and pediatric case-control studies, the consistent signal is lower 25(OH)D in OCD and an inverse correlation between 25(OH)D and OCD symptom severity. The largest and best-powered adult studies (Soyak & Karakükçü/Abraham, n=174 vs 170; Marazziti et al., n=50) are clearly positive. Several pediatric studies (Yazıcı 2018; Çelik 2016 PANDAS) found lower vitamin D in cases but the difference did not reach statistical significance, while Esnafoğlu & Yaman 2017 (pediatric) was strongly positive.

Evidence tiers (strongest to weakest):1. Meta-analysis — One OCD-specific meta-analysis (Othman et al., Bangladesh J Medicine 2024) reports a significant pooled reduction; the Balandeh 2021 meta-analysis covers OCD vitamins broadly but was more cautious on vitamin D specifically.2. RCTs — None in OCD. RCT-level evidence exists only in chronic tic disorders (a condition highly comorbid with OCD).3. Observational (case-control/cross-sectional) — The main body of evidence; ~7 studies.4. Mechanistic / case reports — Strong biological rationale plus a single illustrative adult case report.

Tier 1 — Meta-analyses and systematic reviews

1. Othman Z, Zakaria WNA, Wijaya A. "Exploring the Relationship between Vitamin D Levels and Obsessive-Compulsive Disorder: A Comprehensive Meta-analysis and Systematic Review." Bangladesh Journal of Medicine. 2024;35:156-166 (Universiti Sains Malaysia). This is the most directly relevant quantitative synthesis. Pooling six studies, it found "a noteworthy reduction in vitamin D levels among individuals with OCD compared to controls (SMD = -0.603, 95% CI = -0.8001 to -0.4053, p < 0.001, I² = 50.86%; Q statistic p = 0.093)." Conclusion: vitamin D may play a role in OCD pathogenesis. This is the single strongest piece of OCD-specific quantitative evidence — though published in a lower-profile journal and should be weighted accordingly.

2. Balandeh E, Karimian M, Behjati M, Mohammadi AH. "Serum Vitamins and Homocysteine Levels in Obsessive-Compulsive Disorder: A Systematic Review and Meta-Analysis." Neuropsychobiology. 2021;80(6):502-515. doi:10.1159/000514075. PMID: 33744893. PRISMA-based, searched Scopus/PubMed/Google Scholar/Web of Science. Found significant reductions in vitamin B12, vitamin E, and folate-related markers and elevated homocysteine in OCD. Notably, a later paper interprets Balandeh as concluding the available literature "does not allow to clearly determine a higher susceptibility of OCD patients to vitamin D deficiency than the general population" — i.e., more cautious than the 2024 meta-analysis on vitamin D specifically. Worth flagging this nuance for balance.

3. Adjacent meta-analysis (tic disorders): "Vitamin D status and tic disorder: a systematic review and meta-analysis of observational studies." Frontiers in Pediatrics. 2023;11:1173741. Concluded children with tic disorders have lower vitamin D than healthy children (relevant because OCD and tics are highly comorbid and share basal-ganglia circuitry). Authors caution about design/diagnostic limitations of included studies.

Tier 2 — Intervention/RCT evidence (none in OCD; all in adjacent tic disorders)

4. "Efficacy of high-dose vs. low-dose vitamin D₃ supplementation in children with chronic tic disorders: a randomized controlled trial." Nutrition Journal. 2025;24 (doi:10.1186/s12937-025-01112-w). RCT, n=83 children aged 4-15 with CTDs; high-dose (5,000 IU/day) vs low-dose (1,000 IU/day) vitamin D3 for 3 months. Both groups showed significant improvement in tic severity (YGTSS) and rises in 25(OH)D (p < 0.05); high-dose was significantly superior. Low-dose group YGTSS fell from 27.19 ± 8.54 to 24.00 ± 4.52; 25(OH)D rose from 20.22 ± 6.13 to 26.81 ± 6.00 ng/mL. This is the highest-tier interventional evidence in any OCD-adjacent condition.

5. Li HH, Xu ZD, Wang B, Feng JY, Dong HY, Jia FY. "Clinical improvement following vitamin D3 supplementation in children with chronic tic disorders." Neuropsychiatr Dis Treat. 2019;15:2443-2450. doi:10.2147/NDT.S212322. PMID: 31933522. 120 children with CTDs + 140 controls; 36 of the CTD children received vitamin D3 (300 IU/kg/day, max 5000 IU/day) for 3 months. CTD children had significantly lower baseline 25(OH)D, inversely correlated with tic severity; supplementation significantly improved YGTSS total/motor/phonic/impairment and CGI-SI scores with no adverse reactions. (This is the study Vitamin D Life already references.)

6. Mechanistic animal intervention: "Effects and mechanisms of vitamins A and D on behavior associated with Tourette syndrome in rats" (Frontiers, 2025, PMC12476997). IDPN-induced TS-like rat model; vitamins A (3 mg/kg/d) and D (10 µg/kg/d) by gavage for 8 weeks reduced stereotyped/head-twitch behavior, implicating striatal dopamine regulation and vitamin D modulation of neuroinflammation.

Note on a frequently-cited "OCD vitamin D RCT": Several secondary/web sources (and a 2025 systematic-review protocol on medRxiv/JMIR) cite "Lee et al. (2019)" or attribute to Marazziti a finding that "vitamin D supplementation significantly improved OCD symptoms in a small cohort." These claims appear to be secondary mischaracterizations; Marazziti 2023 was observational (no supplementation arm). No primary OCD supplementation RCT could be verified. Henry should treat any "OCD supplementation trial" claim with caution pending a primary citation.

Tier 3 — Observational case-control / cross-sectional studies

ADULT POPULATIONS

7. Marazziti D, Barberi FM, Fontenelle L, Buccianelli B, Carbone MG, Parra E, Palermo S, Massa L, Tagliarini C, Della Vecchia A, Mucci F, Arone A, Dell'Osso L. "Decreased vitamin D levels in obsessive-compulsive disorder patients." CNS Spectrums. 2023 Oct;28(5):606-613. doi:10.1017/S1092852921000821 (Epub 2021). PMID: 34551844. Italy; 50 adult OCD outpatients (DSM-5), assessed with Y-BOCS and HRSD. All but one patient (49/50, 98%) had vitamin D below the normative >30 ng/mL threshold. Vitamin D inversely correlated with Y-BOCS total, the compulsion subscale, and specific items (interference from obsessions, distress, time spent on compulsions), with sex-specific patterns.

IMPORTANT CAVEATS: no recruited control group (comparison was to a normative cutoff); 38/50 had ≥1 psychiatric comorbidity and 34/50 were on ≥1 psychotropic — significant confounders. A "14.58 nmol/L" mean circulating online for this paper is a misattribution from the same group's bipolar study; the precise OCD mean is in paywalled text.

8. Dahal T, Abraham J. "Examination of vitamin D status in individuals with obsessive-compulsive disorder." Indian Journal of Clinical Anatomy and Physiology. 2024;11(3):164-169. doi:10.18231/j.ijcap.2024.035. ~174 newly diagnosed adult OCD patients (no comorbidities) vs 170 healthy controls. OCD serum vitamin D significantly lower than controls; significant negative correlation between 25(OH)D and Y-BOCS obsession, compulsion, and total scores (no correlation with illness duration). This study appears to share its dataset/description very closely with the Soyak & Karakükçü report below (identical n=174/170 and correlation pattern) — likely the same underlying Turkish cohort; flag possible duplication before listing as independent.

9. Soyak HM, Karakükçü Ç. "Investigation of vitamin D levels in obsessive-compulsive disorder." Indian Journal of Psychiatry. 2022;64(4):349. (One of Henry's two known studies.) 174 newly diagnosed OCD vs 170 controls. OCD vitamin D significantly lower; strong negative correlations with Y-BOCS: obsession r = -0.693, compulsion r = -0.633, total r = -0.705 (all p < 0.001).

No correlation with illness duration. Vitamin D insufficiency and deficiency significantly more frequent in OCD (p < 0.001). One of the strongest single positive datasets.

10. "Evaluation of Vitamin B12, Folic Acid, Ferritin and Vitamin D Levels in Obsessive Compulsive Disorder." Journal of Contemporary Medicine, 2023 (Turkey). Retrospective, 50 OCD (12F/38M) vs 50 healthy controls. Serum VitB12 (p < 0.001), folic acid (p = 0.004) and vitamin D (p = 0.001) all significantly lower in OCD; no difference in ferritin. Positive for vitamin D.

11. "Deep clinical phenotyping of patients with obsessive-compulsive disorder" (Translational Psychiatry, 2023; s41398-023-02368-8). Large German FDP-OCD screening cohort. Found suboptimal vitamin D in 75% of OCD patients and folic acid deficiency in 21%, alongside elevated streptococcal (46%) and antinuclear antibodies (36%); detected probable/possible "organic" (mostly autoimmune) OCD in ~16%. Supports a vitamin-D/autoimmune subgroup hypothesis.

PEDIATRIC POPULATIONS

12. Esnafoğlu E, Yaman E. "Vitamin B12, folic acid, homocysteine and vitamin D levels in children and adolescents with obsessive compulsive disorder." Psychiatry Research. 2017;254:232-237. 52 child/adolescent OCD patients vs 30 controls. Significantly lower vitamin B12 and vitamin D, and higher homocysteine in OCD (all p < 0.001). Strongly positive pediatric study; authors conclude vitamin D deficiency "may be a risk factor for development of OCD."

13. Yazıcı KU, Percinel Yazıcı I, Ustundag B. "Vitamin D levels in children and adolescents with obsessive compulsive disorder." Nordic Journal of Psychiatry. 2018;72(3):173-178. Turkey; child/adolescent OCD vs controls. Vitamin D lower in OCD (15.88 ± 6.96 ng/mL vs 18.21 ± 13.24 ng/mL) but NOT statistically significant (p = .234); calcium, phosphate, ALP not different. Negative correlation between 25(OH)D-3 and CY-BOCS obsession scores. NULL on the primary comparison — flag honestly. Described as the first study of vitamin D in OCD patients without comorbidity.

14. Çelik G, Taş D, Tahiroğlu A, Avcı A, Yüksel B, Çam P. "Vitamin D Deficiency in Obsessive-Compulsive Disorder Patients with Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS): A Case Control Study." Noro Psikiyatri Arşivi. 2016;53:33-37. 33 OCD-with-PANDAS patients vs 20 healthy controls. NO significant difference in mean serum 25(OH)D between groups; BUT vitamin D deficiency was significantly more frequent in patients (48.5% vs 20.0%, p = 0.038), and OCD patients with vitamin D deficiency had higher rates of comorbid ADHD (87.5% vs 52.6%, p = 0.027). PTH positively correlated with Y-BOCS scores. MIXED result. First study linking immune-related pediatric OCD to vitamin D metabolism.

Maternal / prenatal vitamin D and offspring risk

No dedicated maternal-vitamin-D → offspring-OCD study exists. The closest evidence:

"Maternal Effects as Causes of Risk for Obsessive-Compulsive Disorder" (Frontiers in Psychiatry, PMC8023336). Swedish national register study; 7,184 of the birth cohort (0.87%) diagnosed with OCD. Discusses maternal/in-utero effects (including vitamin D's protective role in MS as analogy) as a framework for OCD risk, but does not directly measure maternal vitamin D and offspring OCD.
Strong adjacent evidence for OTHER psychiatric outcomes: Sucksdorff M, et al. "Maternal Vitamin D Levels and the Risk of Offspring Attention-Deficit/Hyperactivity Disorder." J Am Acad Child Adolesc Psychiatry. 2021;60(1):142-151 (doi:10.1016/j.jaac.2019.11.021) — Finnish nationwide case-control (1,067 cases/1,067 controls); continuously decreasing vitamin D was associated with offspring ADHD (aOR 1.45, 95% CI 1.15-1.81; lowest vs highest quintile aOR 1.53, 95% CI 1.11-2.12). And Bandini L, Vinceti B, Urbano T, Plazzi G, Filippini T, Vinceti M. Eur Child Adolesc Psychiatry, published online June 3, 2026 (doi:10.1007/s00787-026-03059-7) — dose-response meta-analysis of 15 studies: "Comparing high versus low maternal vitamin D status, we found an inverse association with both lower ASD risk (RR = 0.91; 95% CI 0.87-0.96) and ADHD risk (RR = 0.90; 95% CI 0.82-0.99)." Plus Sourander et al. on maternal vitamin D and offspring schizophrenia. These establish biological precedent but are NOT OCD outcomes. Flag as an open research gap and a potential Vitamin D Life "needed study" note.

VDR gene polymorphisms

No study has directly examined VDR gene polymorphisms (FokI/rs2228570, BsmI/rs1544410, TaqI/rs731236, ApaI/rs7975232) in OCD patients vs controls. This is a genuine literature gap (confirmed by targeted PubMed/Scholar searching). VDR polymorphism case-control studies exist for childhood autism (e.g., Han Chinese cohort, n=201 ASD vs 200 controls, PMC5821970; and PMC5615256), adolescent anxiety/depression (Fok1/Apa1, central Italy, PMC11276141), PCOS, multiple sclerosis, and others — but none in OCD. OCD genetic association studies have instead focused on serotonergic (SLC6A4/5-HTTLPR), catecholaminergic (COMT, MAO-A), and GWAS loci (DNM3, PTPRD, GRID2, DLGAP1). Henry could flag VDR-in-OCD as an explicitly untested hypothesis and candidate for new research.

Mechanistic studies linking vitamin D to OCD-relevant neurobiology

Serotonergic (strongest mechanistic thread): Patrick RP, Ames BN. "Vitamin D hormone regulates serotonin synthesis. Part 1: relevance for autism." FASEB J. 2014;28(6):2398-2413; and "Part 2: relevance for ADHD, bipolar disorder, schizophrenia, and impulsive behavior." FASEB J. 2015;29(6):2207-2222. Vitamin D (calcitriol) transcriptionally activates TPH2 (brain serotonin synthesis) via a vitamin D response element (VDRE) and represses TPH1 outside the blood-brain barrier. Directly relevant given serotonin's central role in OCD and SSRIs as first-line treatment.
Dopaminergic/catecholaminergic: 1,25(OH)2D3 regulates tyrosine hydroxylase, the rate-limiting enzyme for dopamine/norepinephrine synthesis; vitamin D protects dopaminergic neurons against neuroinflammation/oxidative stress (Lima et al., "Vitamin D protects dopaminergic neurons against neuroinflammation and oxidative stress in hemiparkinsonian rats," J Neuroinflammation 2018;15:249). Relevant to basal-ganglia/dopamine models of OCD and tics.
Glutamatergic / NMDA / calcium: Brewer et al. (J Neurosci. 2001;21(1):98) showed vitamin D hormone confers neuroprotection via downregulation of L-type calcium channels; vitamin D modulates NMDA/AMPA receptors and excitotoxicity (Frontiers in Neuroscience 2021, PMC8492967). OCD has a well-documented glutamatergic component. (Caveat: at supraphysiologic doses vitamin D3 can promote excitotoxicity via glutamatergic over-activation — PMC8196622 — so the relationship is dose-dependent, not monotonic.)
Neuroinflammation/iNOS: Vitamin D inhibits inducible nitric oxide synthase (iNOS), reduces microglial activation and pro-inflammatory cytokines; vitamin D deficiency reduces neuroprotection — proposed as an OCD-relevant pathway.
Basal ganglia: "The Role of Vitamin D in Basal Ganglia Diseases" (PMID 36424745) — systematic review of 60 studies; vitamin D deficiency common across basal-ganglia disorders (causality established only for Parkinson's). OCD is fundamentally a cortico-striato-thalamo-cortical (basal ganglia) disorder.

Illustrative case report

"The Possible Role of Vitamin D and Autoimmunity in the Etiology of Obsessive-Compulsive Disorder" (PMC9597067). 35-year-old woman, OCD with Y-BOCS 30, anti-TPO positive and 25(OH)D deficient (9.75 ng/mL). Vitamin D replacement + fluoxetine → symptom remission; relapse coincided with falling vitamin D (8.9 ng/mL) and rising anti-TPO/Y-BOCS; re-supplementation (to 45.2 ng/mL) → remission again. Anecdotal but a clean longitudinal "vitamin-D-tracks-symptoms" illustration.

Recommendations to Vitamin D Life

For building out Vitamin D Life OCD coverage, organize by tier:

Lead with the 2024 OCD-specific meta-analysis (Othman et al., SMD = -0.603) as the headline quantitative finding, but pair it with Balandeh 2021's more cautious conclusion and the Bond/EMTICS 2022 counterintuitive tic result so the page is balanced and credible. Honesty about mixed/null findings (Yazıcı 2018 non-significant; Çelik 2016 mixed; Bond 2022 negative-direction) will strengthen the page's evidence-based reputation.
Create distinct sub-sections: (a) Adult case-control; (b) Pediatric case-control; (c) PANDAS/PANS; (d) Tourette/tic disorders (including the only RCT-tier evidence); (e) Mechanisms; (f) Open gaps (VDR polymorphisms, maternal/prenatal OCD, OCD-specific RCT).
Flag the absence of any OCD supplementation RCT as the single most important research gap. The tic-disorder RCTs (Nutrition Journal 2025; Li 2019) are the best available interventional proxy and should be presented as "adjacent evidence," not as OCD trials. Correct the circulating "Lee 2019" / "Marazziti supplementation" misattributions.
Note two data-quality issues for accuracy: (i) Soyak & Karakükçü 2022 and Dahal/Abraham 2024 appear to describe the same n=174/170 cohort — verify before listing as independent. (ii) The "14.58 nmol/L" figure attached online to Marazziti's OCD paper is a misattribution from the group's bipolar study.

Thresholds that would change these recommendations: If a placebo-controlled OCD supplementation RCT is published showing Y-BOCS reduction, vitamin D would move from "associated biomarker" to "candidate adjunctive treatment." If a Mendelian-randomization or VDR-polymorphism study in OCD appears, the causal interpretation would firm up considerably. Until then, the honest framing is: robust cross-sectional association, plausible mechanism, but unproven causation and untested as a treatment in OCD specifically.

Caveats

Association ≠ causation. Every OCD vitamin D study is observational; reverse causation (OCD behaviors → less sun exposure/poorer diet → lower vitamin D) is unaddressed in most. Confounding by comorbidity and psychotropic medication is explicit in Marazziti.
Heterogeneity and small samples. Most studies are single-center, Turkish or Italian, with modest n; assay methods and deficiency cutoffs vary (e.g., pediatric "deficiency" defined as <15 or <30 ng/mL in different papers).
Publication/geographic bias. Positive findings cluster in a few Turkish groups; the meta-analytic heterogeneity (I² ≈ 51%) and the contradictory EMTICS tic result counsel caution.
Mechanistic studies are extrapolated from autism, ADHD, Parkinson's, and animal/in-vitro models — not from OCD tissue directly. The serotonin-TPH2 mechanism is compelling but inferred, and the vitamin-D/glutamate relationship is dose-dependent rather than simply protective.
The 2024 Othman meta-analysis is published in a lower-profile journal (Bangladesh Journal of Medicine); its pooled estimate should be weighted accordingly relative to the more conservative Karger/Neuropsychobiology synthesis.