The relationship between 25-hydroxyvitamin D [25(OH)D] levels, physical activity (PA), and depression risk remains underexplored. This study examines how combinations of 25(OH)D and PA influence depression.

We conducted a longitudinal analysis using data from the English Longitudinal Study of Ageing, including cognitively healthy adults aged 50 years and older at baseline. Baseline measurements of PA and 25(OH)D were taken, with depression as the primary outcome. Multivariate Cox proportional hazards models were used, with and without interaction terms. Furthermore, two-sample Mendelian randomization (MR) analyses were performed.

A total of 4146 participants (mean age: 66.0 years; 52.1 % female) were followed for eight years. Multivariate-adjusted hazard ratios (HRs) for depression were 0.71 (95 % CI: 0.61-0.83) for those with high 25(OH)D and PA (P = 0.005), 0.79 (95 % CI: 0.63-0.99) for those younger than 65 (P = 0.042), and 0.65 (95 % CI: 0.53-0.80) for those 65 and older (P = 0.041). A significant interaction between low 25(OH)D and PA was found in the younger group (HR: 1.43, 95 % CI: 1.03-1.99, P = 0.034). High 25(OH)D and PA independently reduced depression risk by 7.2 % and 7.7 %, respectively, with a 23.1 % reduction when combined. Mendelian randomization confirmed these findings.

High 25(OH)D levels are linked to lower depression risk. The combination of high 25(OH)D and PA provides synergistic protection, particularly in older adults, emphasizing the need for vitamin D supplementation and PA in depression prevention.

Late-life depression (LLD), a growing public health challenge in aging societies, profoundly impacts physical and mental health by exacerbating cognitive decline, functional disability, and comorbid chronic diseases. Emerging research highlights vitamin supplementation as a promising adjunctive therapy for LLD, targeting its multifactorial pathogenesis involving mitochondrial dysfunction, neuroinflammation, and oxidative stress. Specific vitamins, including B-complex vitamins (B1, B6, B9, B12), vitamin D, and antioxidants (C, E), demonstrate therapeutic potential through mechanisms ranging from neurotransmitter regulation to mitochondrial function enhancement. For instance, vitamin D modulates serotonin synthesis and calcium signaling, while B vitamins mitigate homocysteine-mediated neurotoxicity and support energy metabolism. Antioxidants counteract neural oxidative damage linked to depressive severity. Clinical studies reveal that vitamin D deficiency (<20 ng/mL) correlates with elevated depression risk, and combined B-vitamin supplementation shows symptom alleviation in nutritionally deficient subgroups. However, evidence remains heterogeneous due to variability in dosing protocols, bioavailability, and population-specific factors like comorbidities. Despite growing evidence, critical gaps persist regarding optimal dosages, bioavailability variations, and long-term outcomes in elderly populations. This review synthesizes current evidence on vitamin-mediated cellular pathways in LLD management, evaluates clinical efficacy across interventions, and proposes personalized nutritional strategies to optimize therapeutic outcomes. By integrating mechanistic insights with clinical data, this analysis aims to guide evidence-based vitamin supplementation protocols for LLD within geriatric care frameworks.

Luteolin is a natural flavonoid compound exists in various fruits and vegetables. Recent studies have indicated that luteolin has variety pharmacological effects, including a wide range of antidepressant properties. Here, we systematically review the preclinical studies and limited clinical evidence on the antidepressant and neuroprotective effects of luteolin to fully explore its antidepressant power. Network pharmacology and molecular docking analyses contribute to a better understanding of the preclinical models of depression and antidepressant properties of luteolin. Seventeen preclinical studies were included that combined network pharmacology and molecular docking analyses to clarify the antidepressant mechanism of luteolin and its antidepressant targets. The antidepressant effects of luteolin may involve promoting intracellular noradrenaline (NE) uptake; inhibiting 5-hydroxytryptamine (5-HT) reuptake; upregulating the expression of synaptophysin, postsynaptic density protein 95, brain-derived neurotrophic factor, B cell lymphoma protein-2, superoxide dismutase, and glutathione S-transferase; and decreasing the expression of malondialdehyde, caspase-3, and amyloid-beta peptides. The antidepressant effects of luteolin are mediated by various mechanisms, including anti-oxidative stress, anti-apoptosis, anti-inflammation, anti-endoplasmic reticulum stress, dopamine transport, synaptic protection, hypothalamic-pituitary-adrenal axis regulation, and 5-HT metabolism. Additionally, we identified insulin-like growth factor 1 receptor (IGF1R), AKT serine/threonine kinase 1 (AKT1), prostaglandin-endoperoxide synthase 2 (PTGS2), estrogen receptor alpha (ESR1), and epidermal growth factor receptor (EGFR) as potential targets, luteolin has an ideal affinity for these targets, suggesting that it may play a positive role in depression through multiple targets, mechanisms, and pathways. However, the clinical efficacy of luteolin and its potential direct targets must be confirmed in further multicenter clinical case-control and molecular targeting studies.

Abnormalities in structural-functional connectivity (SC-FC) coupling have been identified globally in patients with major depressive disorder (MDD). However, investigations have neglected the variability and hierarchical distribution of these abnormalities across different brain regions. Furthermore, the biological mechanisms that underlie regional SC-FC coupling patterns are not well understood.

We enrolled 182 patients with MDD and 157 healthy control participants and quantified the intergroup differences in regional SC-FC coupling. Extreme gradient boosting (XGBoost), support vector machine, and random forest models were constructed to assess the potential of SC-FC coupling as biomarkers for MDD diagnosis and symptom prediction. Then, we examined the link between changes in regional SC-FC coupling in patients with MDD, neurotransmitter distributions, and gene expression.

We observed increased regional SC-FC coupling in the default mode network (t337 = 3.233) and decreased coupling in the frontoparietal network (t337 = -3.471) in patients with MDD compared with healthy control participants. XGBoost (area under the receiver operating characteristic curve = 0.853), support vector machine (area under the receiver operating characteristic curve = 0.832), and random forest (p < .05) models exhibited good prediction performance. The alterations in regional SC-FC coupling in patients with MDD were correlated with the distributions of 4 neurotransmitters (p < .05) and expression maps of specific genes. These enriched genes were implicated in excitatory neurons, inhibitory neurons, cellular metabolism, synapse function, and immune signaling. These findings were replicated on 2 brain atlases.

This work enhances our understanding of MDD and paves the way for the development of additional targeted therapeutic interventions.

Vitamin D receptors (VDRs) are present in almost all cells of the immune system, including B cells, T cells, NK (Natural Killer) cells, dendritic cells, and monocytes, as well as the epithelial cells of many organs such as the intestine, pancreas, prostate, lungs, and cardiomyocytes. In addition, some immune cells, including dendritic cells, macrophages, and B and T cells, can synthesize calcitriol by expressing 1α-hydroxylase. Upon binding to VDRs, vitamin D (Vit D) regulates the expression of genes involved in immune responses, including those encoding for cytokines. It modulates the production of pro-inflammatory cytokines while promoting the synthesis of anti-inflammatory cytokines. Vit D also affects the differentiation and maturation of cells of the immune system. By inhibiting the nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways, Vit D reduces the expression of pro-inflammatory genes. These effects highlight the potential of Vit D as a therapeutic agent in the management of inflammatory diseases, including autoimmune disorders, cardiovascular diseases, diabetes, metabolic syndrome, cancer, neurological diseases, depression, and inflammatory bowel disease.

To investigate the association between serum 25(OH)D and kidney stone disease (KSD) in participants from the UK Biobank.

We used data from the UK Biobank. Our analysis involved Cox proportional hazards models to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) to estimate the association between serum 25(OH)D levels (measured at the time of recruitment) and the risk of KSD, which was determined using hospital records.

This study involved 444,343 participants, with 4,458 cases of KSD identified during an average follow-up period of 12.6 years. Higher 25(OH)D levels were not associated with developing kidney stones in general population model 3 (HR = 0.88 [95% CI 0.77-1.01]). Interestingly, higher serum 25(OH)D concentrations in women over 60 years old were associated with a lower risk of kidney stone disease. The multivariate HRs and 95% CIs for participants who had serum 25(OH)D ≥ 50 nmol/L or ≥ 75 nmol/L, compared with those who were severely deficient (25[OH]D < 25 nmol/L), were 0.74 (0.58-0.95), 0.60 (0.43-0.85) for KSD, respectively (P for trend < 0.01). However, this trend was not statistically significant in the subgroup analysis of serum calcium ion concentration.

High 25(OH)D levels were not associated with a higher incidence of kidney stones if serum calcium levels are within a normal range. The findings alleviate physiological concerns regarding the supplementation of vitamin D alone to raise serum 25(OH)D concentration.

To collect evidence from studies that explored the associations between serum vitamin D (25[OH]D) concentrations/status and the presence of depressive/anxiety symptoms in the ante- and/or postnatal periods (PROSPERO-CRD42023390895).

Studies that assessed serum 25[OH]D concentrations in adult women during the ante/postnatal periods and those that used valid instruments to identify the experience/severity of depressive/anxiety symptoms were included. Independent researchers performed the identification/selection of studies, data extraction, risk of bias (RoB) assessment, and bibliometric analysis steps.

Of the total of 6769 eligible records, 15 cohort studies [high (n = 3), moderate (n = 7), and low (n = 5) RoB], nine cross-sectional studies [moderate (n = 3) and low (n = 6) RoB], and one case-control study [moderate RoB] were included (n = 25). Depression (n = 24) and anxiety (n = 4) symptoms were assessed. A significant difference in antenatal serum 25[OH]D concentrations between the groups of women with and without depression was identified (mean difference: -4.63 ng/mL; 95% confidence interval [95% CI]: -8.88; -0.38). Postnatal serum 25[OH]D concentrations were found to be, on average, -2.36 ng/mL (95% CI: -4.59; -0.14) lower in women with postnatal depression than in those without. Maternal antenatal anxiety was associated with significantly lower concentrations/deficiency of 25[OH]D in only one included study.

Based on very low/low-quality evidence, it was observed that reduced serum 25[OH]D concentrations in the ante- and postnatal period are associated with the presence of ante- and postnatal depressive symptoms, respectively. Low/deficient antenatal serum 25[OH]D concentrations may not be related to the presence of anxiety symptoms before childbirth. Well-designed longitudinal studies are needed to explore the estimated pooled effect of these associations.

Maternal postpartum depressive and anxiety symptoms are risk factors for subsequent maternal and child mental health problems. Little is known about the potential role of antepartum vitamin D and C-reactive protein (CRP) in the etiology of maternal postpartum affective symptoms. We investigated associations between antepartum vitamin D status and postpartum depressive and anxiety symptoms and whether antepartum CRP mediated these associations.

In 2483 participants of the Amsterdam Born Children and their Development prospective cohort, maternal serum vitamin D and CRP were measured at a median of 13 weeks' gestation. Vitamin D status was defined as deficient (≤29.9 nM), insufficient (30-49.9 nM), sufficient (50-79.9 nM), or normal (≥80 nM). Maternal depressive symptoms (Center for Epidemiologic Studies-Depression) and anxiety (State-Trait Anxiety Inventory) were assessed 3 months postpartum.

After adjustments for confounders, vitamin D deficiency was only associated with increased postpartum anxiety symptoms ( B = 0.17, 95% confidence interval [CI] = 0.03-0.30, p = .017) compared to normal vitamin D levels (≥80 nM). In women not taking vitamin D supplementation ( n = 2303), vitamin D deficiency was associated with increased postpartum depressive and anxiety symptoms ( B = 0.14, 95% CI = 0.03-0.28, p = .045; and B = 0.17, 95% CI = 0.03-0.32, p = .015). Antepartum CRP did not mediate these links.

We found some evidence that antepartum vitamin D deficiency was associated with increased postpartum affective symptoms, especially in women not taking vitamin D supplementation. Clinical trials should determine whether vitamin D supplementation can reduce the risk for postpartum affective disorders.

Vitamin D, obtained from diet or synthesized internally as cholecalciferol and ergocalciferol, influences bodily functions through its most active metabolite and the vitamin D receptor. Recent research has uncovered multiple roles for vitamin D in the central nervous system, impacting neural development and maturation, regulating the dopaminergic system, and controlling the synthesis of neural growth factors. This review thoroughly examines these connections and investigates the consequences of vitamin D deficiency in neurological disorders, particularly neurodegenerative diseases. The potential benefits of vitamin D supplementation in alleviating symptoms of these diseases are evaluated alongside a discussion of the controversial findings from previous intervention studies. The importance of interpreting these results cautiously is emphasised. Furthermore, the article proposes that additional randomised and well-designed trials are essential for gaining a deeper understanding of the potential therapeutic advantages of vitamin D supplementation for neurological disorders. Ultimately, this review highlights the critical role of vitamin D in neurological well-being and highlights the need for further research to enhance our understanding of its function in the brain.

Growing evidence points to the pivotal role of vitamin D in the pathophysiology and treatment of major depressive disorder (MDD). However, there is a paucity of longitudinal research investigating the effects of vitamin D supplementation on the brain of MDD patients.

We conducted a double-blind randomized controlled trial in 46 MDD patients, who were randomly allocated into either VD (antidepressant medication + vitamin D supplementation) or NVD (antidepressant medication + placebos) groups. Data from diffusion tensor imaging, resting-state functional MRI, serum vitamin D concentration, and clinical symptoms were obtained at baseline and after an average of 7 months of intervention.

Both VD and NVD groups showed significant improvement in depression and anxiety symptoms but with no significant differences between the two groups. However, a greater increase in serum vitamin D concentration was found to be associated with greater improvement in depression and anxiety symptoms in VD group. More importantly, neuroimaging data demonstrated disrupted white matter integrity of right inferior fronto-occipital fasciculus along with decreased functional connectivity between right frontoparietal and medial visual networks after intervention in NVD group, but no changes in VD group.

These findings suggest that vitamin D supplementation as adjunctive therapy to antidepressants may not only contribute to improvement in clinical symptoms but also help preserve brain structural and functional connectivity in MDD patients.

On March 28, 2024, the Council of Experts "High-dose vitamin D (Devilam) in the practice of obstetrician-gynecologist, gynecologist and endocrinologist" was held in Moscow with the participation of leading experts gynecologists, endocrinologists and obstetricians-gynecologists, during which new possibilities for the use of high-dose vitamin D in patients of various ages who need correction of existing vitamin D deficiency or insufficiency.

Objectives. To assess levels of 25(OH)D among adolescents with symptoms of pica in northern Sudan. Methods. A cross-sectional study was conducted in North Sudan. Questionaries were used to collect adolescents' sociodemographics. The enzyme-linked immunosorbent assay was used to measure 25(OH)D level. Results. Of the 344 adolescents enrolled, 161 (46.8%) and 183 (53.2%) were male and female, respectively and 103 (29.9%) had symptoms of pica. The median (IQR) of 25(OH)D level was significantly lower in adolescents with symptoms of pica. Multiple linear regression analysis showed that while age (coefficient = 1.1, P = .023) was positively associated with 25(OH)D level, female sex (coefficient = -7.5, P < .001), and pica symptoms (coefficient = -3.5, P = .032) were negatively associated with 25(OH)D level. Conclusion. Adolescents with symptoms of pica had lower 25(OH)D levels. Adolescents with symptoms of pica have to be assessed for vitamin D status.

Mental disorders are intricate and multifaceted and encompass social, economic, environmental, and biological factors. This study aimed to explore the potential association between vitamin D deficiency and anxiety and depression symptoms in adults, considering the role of the vitamin D receptor gene polymorphism FokI (rs2228570). This was a population-based cross-sectional study with stratified and cluster sampling, evaluating anxiety symptoms (AS) and depression symptoms (DS) in 1637 adults. Vitamin D levels were measured using electrochemiluminescence and were considered deficient when < 20 ng/mL in a healthy population or < 30 ng/mL in at-risk groups. Genotyping was performed using real-time polymerase chain reaction with TaqMan probes. The prevalence rates of AS, DS, and vitamin D deficiency were 23.5%, 15.8%, and 30.9%, respectively. No direct association was observed between vitamin D deficiency and AS or DS. However, interaction analysis revealed a combined effect of vitamin D deficiency and FokI for DS but not for AS. Individuals with vitamin deficiency and one or two copies of the altered allele of the FokI exhibited a higher prevalence of DS than individuals homozygous for the wild-type allele and vitamin D sufficiency. The interaction between vitamin D deficiency and the FokI polymorphism was associated with DS.

Macrophage autophagy dysfunction aggravates liver injury by activating inflammasomes, which can cleave pro-IL-1β to its active, secreted form. We investigated whether the vitamin D/vitamin D receptor (VDR) axis could up-regulate macrophage autophagy function to inhibit the activation of inflammasome-dependent IL-1β during cholestasis. Paricalcitol (PAL; VDR agonist) was intraperitoneally injected into bile duct-ligated mice for 5 days. Up-regulation of VDR expression by PAL reduced liver injury by reducing the oxidative stress-induced inflammatory reaction in macrophages. Moreover, PAL inhibited inflammasome-dependent IL-1β generation. Mechanistically, the knockdown of VDR increased IL-1β generation, whereas VDR overexpression exerted the opposite effect following tert-butyl hydroperoxide treatment. The inflammasome antagonist glyburide, the caspase-1-specific inhibitor YVAD, and the reactive oxygen species (ROS) scavenger N-acetyl-l-cysteine (NAC) blocked the increase in Vdr shRNA-induced IL-1β production. Interestingly, up-regulation of VDR also enhanced macrophage autophagy. Autophagy reduction impaired the up-regulation of VDR-inhibited macrophage inflammasome-generated IL-1β, whereas autophagy induction showed a synergistic effect with VDR overexpression through ROS-p38 mitogen-activated protein kinase (MAPK) pathway. This result was confirmed by p38 MAPK inhibitor, MAPK activator, and ROS inhibitor NAC. Collectively, PAL triggered macrophage autophagy by suppressing activation of the ROS-p38 MAPK pathway, which, in turn, suppressed inflammasome-generated cleaved, active forms of IL-1β, eventually leading to reduced inflammation. Thus, triggering the VDR may be a potential target for the anti-inflammatory treatment of cholestatic liver disease.

Objective: the aim of this study is to evaluate the relationship between serum vitamin D and B12 levels, nutritional levels, depression, and anxiety in adult cancer patients before and after chemotherapy. Methods: a case-controlled study was carried out on 44 patients who were diagnosed with cancer and applied to the Chemotherapy Unit for treatment (patient group, PG) and 44 volunteer individuals (control group, CG) with similar characteristics to the age and gender-matched patient group but with no diagnosis of cancer. Results: the average age of individuals in PG is 52.50 ± 12.21 years and for those in CG is 52.84 ± 10.98 years. Serum D and B12 levels in the first cure in individuals in PG are higher than in the last treatment (p > 0.05). It was determined that vitamin C taken with a daily diet reduces the risk of cancer (OR: 0.920, 95 % CI: 0.899-0.942, p = 0.042). No correlation was found between depression and anxiety scores of both groups and serum vitamin D and B12 levels (p > 0.05). It was determined that the Beck Anxiety Inventory (BAI) score increased with decrease in body mass index (BMI) (β = 0.311, p = 0.040) and serum vitamin B12 level (β = -0.406, p = 0.006). In addition, it was found that the increase in the Patient-Generated Subjective Global Assessment (PG-SGA) score, which reflects the nutritional status of cancer patients, worsened the level of anxiety (β = 0.389, p = 0.009). Conclusions: as stated in the findings of the study, chemotherapy treatment mediated the development of anxiety in cancer patients by changing the vitamin B12 levels and anthropometric characteristics with its negative effect on nutritional status. It should be ensured that cancer patients treated with chemotherapy follow a healthy and balanced diet plan that is suitable for their needs and has adequate vitamin and mineral content.

Vitamin D is a lipid-soluble vitamin that can be found in some foods. It is also produced endogenously (in the presence of ultraviolet light), transported through the blood to the targets organs and this is the reason to consider vitamin D as a hormone. It is known that vitamin D has genomic and non-genomic effects. This review is focused mainly on the vitamin D receptors, the importance of vitamin D as a neuromodulator, the role of vitamin D in the pathophysiology of devastating neurological disorders such as Alzheimer's disease, multiple sclerosis, amyotrophic lateral sclerosis, Parkinson's disease and the benefit of vitamin D and its derivates in alleviating these disorders.

Stress has been well-documented to have a significant role in the etiopathogenesis of bruxism. Activation of the hypothalamic-pituitary-adrenal axis (HPA) and subsequent release of corticosteroids lead to increased muscle activity. Neurological studies have demonstrated that chronic stress exposure induces neurodegeneration of important neuronal structures and destabilization of the mesocortical dopaminergic pathway. These disruptions impair the abilities to counteract the overactivity of the HPA axis and disinhibit involuntary muscle activity, while at the same time, there is activation of the amygdala. Recent evidence shows that overactivation of the amygdala under stressful stimuli causes rhythmic jaw muscle activity by over activating the mesencephalic and motor trigeminal nuclei. The present review aimed to discuss the negative effects of certain vitamin and mineral deficiencies, such as vitamin D, magnesium, and omega-3 fatty acids, on the central nervous system. It provides evidence on how such insufficiencies may increase stress sensitivity and neuromuscular excitability and thereby reduce the ability to effectively respond to the overactivation of the sympathetic nervous system, and also how stress can in turn lead to these insufficiencies. Finally, the positive effects of individualized supplementation are discussed in the context of diminishing anxiety and oxidative stress, neuroprotection and in the reversal of neurodegeneration, and also in alleviating/reducing neuromuscular symptoms.

Depression is a mental disorder triggered by the interaction of social, psychological and biological factors that have an important impact on an individual's life. Despite being a well-studied disease with several established forms of treatment, its prevalence is increasing, especially among older adults. New forms of treatment and prevention are encouraged, and some researchers have been discussing the effects of vitamin D (VitD) on depression; however, the exact mechanism by which VitD exerts its effects is not yet conclusive. In this study, we aimed to discuss the possible mechanisms underlying the association between VitD and depression in older adults. Therefore, we conducted a systematic search of databases for indexed articles published until 30 April 2021. The primary focus was on both observational studies documenting the association between VitD and depression/depressive symptoms, and clinical trials documenting the effects of VitD supplementation on depression/depressive symptoms, especially in older adults. Based on pre-clinical, clinical and observational studies, it is suggested that the maintenance of adequate VitD concentrations is an important issue, especially in older adults, which are a risk population for both VitD deficiency and depression. Nevertheless, it is necessary to carry out more studies using longitudinal approaches in low- and middle-income countries to develop a strong source of evidence to formulate guidelines and interventions.

In the last few years, vitamin D functions have been studied progressively, and along with their main role in regulating calcium homeostasis, the potential function in the nervous system and the link between different psychiatric disorders and vitamin D deficiency have been revealed. The discovery of vitamin D receptors in multiple brain structures, like the hippocampus, led to the hypothesis that vitamin D deficiency could be responsible for treatment resistance in psychiatric diseases. The aim of this study was to analyze the current knowledge in the literature regarding vitamin D deficiency among individuals afflicted with psychiatric disorders and assess the potential therapeutic benefits of vitamin D supplementation. A systematic search was conducted on the PubMed database for articles published in the last five years (2016-2022) in English, focusing on human subjects. Results show that vitamin D deficiency has implications for numerous psychiatric disorders, affecting mood and behavior through its influence on neurotransmitter release, neurotrophic factors, and neuroprotection. It also plays a role in modulating inflammation, which is often elevated in psychiatric disorders. In conclusion, vitamin D deficiency is prevalent and has far-reaching implications for mental health. This review underscores the importance of exploring the therapeutic potential of vitamin D supplementation in individuals with psychiatric disorders and highlights the need for further research in this complex field.

In recent years, there has been a significant increase in depression, which is related to, among other things, the COVID-19 pandemic. Depression can be fatal if not treated or if treated inappropriately. Depression is the leading cause of suicide attempts. The disease is multifactorial, and pharmacotherapy often fails to bring satisfactory results. Therefore, increasingly more importance is attached to the natural healing substances and nutrients in food, which can significantly affect the therapy process and prevention of depressive disorders. A proper diet is vital to preventing depression and can be a valuable addition to psychological and pharmacologic treatment. An inadequate diet may reduce the effectiveness of antidepressants or increase their side effects, leading to life-threatening symptoms. This study aimed to review the literature on the pathogenesis of the development and treatment of depression, with particular emphasis on dietary supplements and the role of nutrition in the prevention and treatment of depressive disorders.

Vitamin D is a fat-soluble vitamin that has multiple biological effects on the body. Recent findings have also linked vitamin D deficiency to a range of neuropsychiatric disorders. The aim of this review article is to provide insight into the metabolism of vitamin D and its effect on the body, especially on the brain, and to recognize the role of vitamin D in some neuropsychiatric disorders. Vitamin D is well-known as a neuroactive steroid that modulates brain functions and development. There is strong evidence to show that optimal vitamin D levels are important to protect against neuropsychiatric disorders. Vitamin D has also been proposed to alter neurotransmitter pathways in the central nervous system. Abnormalities in these neurotransmitters have been implicated in various neuropsychiatric diseases, such as schizophrenia, Parkinson's disease, and depression. Vitamin D also has some reported neurosteroid-like actions, including regulation of calcium homeostasis, clearance of amyloid-peptide, and antioxidant and anti-inflammatory effects, as well as possible protection against the neurodegenerative mechanisms associated with Alzheimer's disease and autism. Vitamin D is an important modulator of brain development and has many functions in the brain. Several studies found that vitamin D has a protective role in neuropsychiatric disorders, and its supplementation decreases the development of these disorders and lowers their symptoms. Therefore, evidence shows that early intervention to maintain vitamin D concentrations at sufficiently high levels is crucial to slow, prevent, or improve neurocognitive decline.

To explore the cross-sectional and longitudinal association between vitamin D and depressive symptoms across early adolescence.

This longitudinal study included 1607 early adolescents [mean (s.d.) age, 12.49 years; 972 (60.5%) males] from the Chinese Early Adolescents Cohort, recruited from a middle school in Anhui Province and followed up annually (2019-2021). Serum 25(OH)D levels were measured in both 2019 and 2021. Self-reports on depression were assessed at each of three time points from 2019 to 2021.

In the whole sample, higher baseline serum 25(OH)D levels were linked with a lower risk of cumulative incident depression within two-year follow-ups (adjusted RR = 0.97, 95% CI 0.94-0.99) and the increasing trajectory of depression symptoms across the three waves (adjusted RR = 0.97, 95% CI 0.95-0.99). Baseline vitamin D deficiency (VDD) (adjusted RR = 1.50, 95% CI 1.10-2.05) were associated with an increased risk for the increasing trajectory of depression symptoms across the three waves. Remitted VDD was positively related to one dichotomous depression symptoms across three waves (adjusted OR 2.15, 95% CI 1.15-4.01). The above-mentioned significant association was also found in males. Additionally, baseline VDD (adjusted OR 1.59, 95% CI 1.04-2.44) and persistent VDD (adjusted OR 1.58, 95% CI 1.02-2.60) were linked to an increased risk of having two dichotomous depression symptoms only in males.

Our results highlight a prospective association between baseline vitamin D and depression risk in early adolescents. Additionally, a male-specific association between vitamin D and depression risk was observed. Our findings support a potential beneficial effect of vitamin D supplementation in reducing depression risk in early adolescents.

Depression is an important public health burden, its risk of occurrence is associated with vitamin D deficiency and may also increase with age, while serum vitamin D levels are closely related to age.

The purpose of this study was to evaluate whether vitamin D and age are associated with depression after adjustment for each other.

We extracted data from NHANES 2013-2018, including demographic characteristics, depression level, vitamin D level, physical activity, and body measures. A total of 15,156 adults aged 20 years or older (mean age 49.81 ± 17.67 years, 7301 males and 7855 females) were included. Depression was screened by PHQ-9. Vitamin D deficiency was defined by a serum vitamin D level < 30nmol/L. We performed binary logistic regression models to analyze the association between vitamin D, age and depression, respectively.

Vitamin D levels were negatively associated with depression (P < 0.001). Vitamin D had a significant effect on depression (OR = 0.776, 95%CI: 0.682-0.884, P < 0.001), the effect remained significant after adjusted for confounding variables (OR = 0.761, 95%CI: 0.663-0.874, P < 0.001). Age was positively associated with depression (P < 0.001) and had a significant effect on depression (OR = 1.079, 98%CI: 1.032-1.128, P = 0.001), the effect remained significant after adjusted for confounding variables (OR = 1.092, 95%CI: 1.040-1.146, P < 0.001). Age and vitamin D levels were positively correlated (P < 0.001), and older age had a significant effect on vitamin D level (OR = 1.526, 95%CI: 1.416-1.645, P < 0.001), the effect remained significant after adjusted for confounding variables (OR = 1.371, 95%CI: 1.263-1.487, P < 0.001). In addition, the prevalence of depression was higher in females (2312/7855, 29.43%) than in males (1571/7301, 21.52%), and the difference was statistically significant (P < 0.001).

Vitamin D deficiency and older age are both associated with higher risk of depression, while older age is a protective factor for vitamin D deficiency.

Sunlight contains ultraviolet B (UVB) radiation that triggers the production of vitamin D by skin. Vitamin D has widespread effects on brain function in both developing and adult brains. However, many people live at latitudes (about > 40 N or S) that do not receive enough UVB in winter to produce vitamin D. This exploratory study investigated the association between the age of onset of bipolar I disorder and the threshold for UVB sufficient for vitamin D production in a large global sample.

Data for 6972 patients with bipolar I disorder were obtained at 75 collection sites in 41 countries in both hemispheres. The best model to assess the relation between the threshold for UVB sufficient for vitamin D production and age of onset included 1 or more months below the threshold, family history of mood disorders, and birth cohort. All coefficients estimated at P ≤ 0.001.

The 6972 patients had an onset in 582 locations in 70 countries, with a mean age of onset of 25.6 years. Of the onset locations, 34.0% had at least 1 month below the threshold for UVB sufficient for vitamin D production. The age of onset at locations with 1 or more months of less than or equal to the threshold for UVB was 1.66 years younger.

UVB and vitamin D may have an important influence on the development of bipolar disorder. Study limitations included a lack of data on patient vitamin D levels, lifestyles, or supplement use. More study of the impacts of UVB and vitamin D in bipolar disorder is needed to evaluate this supposition.

This study aimed to evaluate the association of vitamin D with sleep quality during the COVID-19 pandemic and the influence of daily sunlight on this association.

This cross-sectional, population-based study among adults stratified by multistage probability cluster sampling was conducted from October to December 2020 in the Iron Quadrangle region of Brazil. The outcome was sleep quality, evaluated by the Pittsburgh Sleep Quality Index. Vitamin D (25-hydroxyvitamin D) concentrations were determined by indirect electrochemiluminescence and a deficiency was classified as 25(OH)D < 20 ng/mL. To assess sunlight, the average daily sunlight exposure was calculated and was classified as insufficient when less than 30 min/d. Multivariate logistic analysis was used to estimate the association between vitamin D and sleep quality. A directed acyclic graph was used to select minimal and sufficient sets of adjustment variables for confounding from the backdoor criterion.

In a total of 1709 individuals evaluated, the prevalence of vitamin D deficiency was 19.8% (95% CI, 15.5-24.9%), and the prevalence of poor sleep quality was 52.5% (95% CI, 48.6-56.4%). In multivariate analysis, vitamin D was not associated with poor sleep quality in individuals with sufficient sunlight. Moreover, in individuals with insufficient sunlight, vitamin D deficiency was associated with poor sleep quality (odds ratio [OR], 2.02; 95% CI, 1.10-3.71). Furthermore, each 1-ng/mL increase in vitamin D levels reduced the chance of poor sleep quality by 4.2% (OR, 0.96; 95% CI, 0.92-0.99).

Vitamin D deficiency was associated with poor sleep quality in individuals with insufficient exposure to sunlight.

Depression is classified as one of the most common mental disorders. Its prevalence has recently increased, becoming a growing public health threat. This review focuses on clarifying the role and importance of individual nutrients in the diet and the impact of nutrient deficiencies on the risk of depression. Deficiencies in nutrients such as protein, B vitamins, vitamin D, magnesium, zinc, selenium, iron, calcium, and omega-3 fatty acids have a significant impact on brain and nervous system function, which can affect the appearance of depressive symptoms. However, it is important to remember that diet in itself is not the only factor influencing the risk of or helping to treat depression. There are many other aspects, such as physical activity, sleep, stress management, and social support, that also play an important role in maintaining mental health. The data review observed that most of the available analyses are based on cross-sectional studies. Further studies, including prospective cohort, case-control studies, are recommended to draw more reliable conclusions.

Stress is considered as a major cause of depression. C-Jun N-terminal kinase (JNK) is a member of the stress-induced mitogen activated protein (MAP) kinase family which is often activated through phosphorylation. Clinical studies and animal experiments have found that abnormal phosphorylation/activation of JNK exists in the occurrence of various psychiatric diseases. Recently, several studies linked JNK kinase activity to depression. However, whether excessive activation of JNK activity is directly responsible for the occurrence of depression and the underlying mechanisms remain unclear. Here, we constructed a conditional transgenic mouse which is specifically expressing MKK7-JNK1 (CAJNK1) in the central nervous system. CAJNK1 mice showed activation of JNK and lead to depression-like behavior in mice. Transcriptome analysis indicates reduced expression of synaptic-associated genes in CAJNK1 mice brains. Consistently, we found abnormal dendritic spine development and PSD95 downregulation in CAJNK1 hippocampal neurons. Our studies provide compelling evidence that activation of JNK as an intrinsic factor leading to depression-like behavior in mice provides direct clues for targeting the JNK activity as a potential therapeutic strategy for depression.

Association between vitamin D levels and the occurrence of depression are not always consistent. The present cohort study aimed to determine this association in older adults, using a method for measuring vitamin D levels which is more accurate than those used in previous studies.

Participants were 3447 individuals aged 40-74 years without depressive symptoms at baseline who participated in the 5-year follow-up survey. The baseline investigation, including a self-administered questionnaire survey and blood collection, was conducted in 2011-2013. Plasma 25-hydroxyvitamin D (25[OH]D) levels were measured, and divided into overall quartiles summed up by sub-quartiles and stratified by age, sex, and season. The outcome was depressive symptoms determined by the CES-D (11-item, cut-off score of 6/7) 5 years later. Covariates were demographics, lifestyles, baseline CES-D score, and disease history.

Mean plasma 25(OH)D levels were 58.0 nmol/L in men and 45.7 in women (P < 0.0001), and cumulative incidences of depressive symptoms were 249/1577 (15.8 %) in men and 313/1870 (16.7 %) in women (P = 0.4526). The lower 25(OH)D quartile group had higher adjusted ORs in men and women combined (P for trend = 0.0107) and women (P for trend = 0.0003), but not in men. Adjusted ORs of the lowest quartile group were significantly higher than the highest group in men and women combined (OR = 1.39, 95 % CI: 1.06-1.81) and women (OR = 1.89, 95 % CI: 1.31-2.72).

Depressive symptoms were self-reported.

Low vitamin D levels were associated with a high risk of depressive symptoms, especially in women. Women are thus considered a major target for preventing vitamin D deficiency to address depression.

The pathophysiological mechanism of cognitive impairments of bipolar disorder (BD) has not yet been completely revealed. It is well known that Vitamin D and physical activity (PA) are associated with BD. However, specific links between Vitamin D and cognitive deficits in BD are still unclear.

The serum levels of vitamin D were measured. The cognitive performances of 102 first-diagnosed and drug-naïve BD patients were evaluated for analysis. The repeatable battery for the assessment of neuropsychological status (RBANS) and the Stroop Color-Word test was used in this study. PA was collected by international physical activity questionnaire.

Patients with BD had high levels of serum vitamin D. Furthermore, immediate and delayed memory was negatively associated with vitamin D levels in patients' group. The serum levels of vitamin D in patients with low PA were positively associated with memory. However, increased PA attenuated the protective effect of vitamin D on executive cognition.

It is concluded that the increased levels of vitamin D were observed in the serum of patients with BD. Thus, it is found that more PA is less beneficial to cognition of patients with BD than longer resting.

Depression is one of the leading health problems, and >300 million people have a major depressive disorder and this number is getting increasing. Depression complicates the management of existing chronic diseases and the management of complications that may arise. A person's mental state can affect their food preferences, and food preferences can also affect their mental state. In this paper, depression and eating behavior, diet quality, folic acid, vitamin B12, vitamin B6, vitamin D, omega-3 fatty acids, magnesium, selenium, zinc and copper, prebiotics and probiotics are discussed. Research on the subject emphasizes that diet quality may also affect the occurrence of depression. However, studies also indicated that dietary nutrients such as folic acid, vitamin B12, vitamin B6, omega-3 fatty acids, zinc, selenium, and magnesium might be associated with the risk of depression.

Meta-analyses of interventional and observational studies investigating the efficacy and the relationship between vitamin D and depression provided inconsistent results. The current umbrella meta-analysis was conducted to assess the available evidence and provide a conclusive outcome in this regard. The following international databases were systematically searched till March 2022: PubMed, Scopus, Embase, Web of Science, and Google Scholar. Random-effects model was carried out to calculate the pooled point estimates and their respective 95 % confidence intervals (CI). Ten meta-analyses of randomised controlled trials (RCTs) revealed significant reduction in depression symptoms comparing participants on vitmain D supplements to those on placebo (Pooled standardised mean difference: - 0.40; 95 % CI: - 0.60, - 0.21, p < 0.01: I² = 89.1 %, p < 0.01). Four meta-analyses of cohort studies (with one having two subgroups) revealed that participants with lower levels of serum vitamin D were at increased odds of depression than those with higher levels of serum vitamin D (Pooled odds ratio: 1.60; 95 % CI: 1.08, 2.36, p < 0.01; I² = 91.3 %, p < 0.01). The present umbrella meta-analysis confirms the potential benefits of vitamin D supplementation and higher serum vitamin D levels in reducing the development and symptoms of depression.

Vitamin D is a secosteroid hormone exerting neurosteroid-like properties. Its well-known nuclear hormone receptor, and recently proposed as a mitochondrial transcription factor, vitamin D receptor, acts for its primary functions. The second receptor is an endoplasmic reticulum protein, protein disulfide isomerase A3 (PDIA3), suggested to act as a rapid response. Vitamin D has effects on various systems, particularly through calcium metabolism. Among them, the nervous system has an important place in the context of our subject. Recent studies have shown that vitamin D and its receptors have numerous effects on the nervous system. Neurodegeneration is a long-term process. Throughout a human life span, so is vitamin D deficiency. Our previous studies and others have suggested that the out-come of long-term vitamin D deficiency (hypovitaminosis D or inefficient utilization of vitamin D), may lead neurons to be vulnerable to aging and neurodegeneration. We suggest that keeping vitamin D levels at adequate levels at all stages of life, considering new approaches such as agonists that can activate vitamin D receptors, and utilizing other derivatives produced in the synthesis process with UVB are crucial when considering vitamin D-based intervention studies. Given most aspects of vitamin D, this review outlines how vitamin D and its receptors work and are involved in neurodegeneration, emphasizing Alzheimer's disease.

Glaucoma has currently become the second leading cause of blindness in the world. Serum vitamin B12 level has been found to be involved in the development and progression of glaucoma. We performed the present study to confirm this association.

This cross-sectional study included 594 participants aged 40 years and older in the National Health and Nutrition Examination Survey (NHANES) from 2005 to 2008. Retinal imaging was performed using the Ophthalmic Digital Imaging system (Retinography) to assess the retina for the presence of features of glaucomatous lesions. Logistic regression models were used to assess the association between dietary vitamin intake and glaucoma.

After screening, 594 subjects were finally included. Among all vitamin intakes, we observed significant differences between the two groups for vitamin B12 intake (5.93 vs. 4.77 mg, p = 0.033). According to the logistic regression results, the intake of vitamin B12 was significantly positively associated with glaucoma (model 1: OR = 1.078, 95% CI = 1.019-1.141; model 2: OR = 1.092, 95% CI = 1.031-1.158; model 3: OR = 1.092, 95% CI = 1.029-1.158). After performing a quantile regression, we observed a significant positive association between vitamin B12 intake and incident glaucoma in the fourth quartile (model 1: OR = 1.133, 95% CI = 1.060-1.210; model 2: OR = 1.141, 95% CI = 1.072-1.215; model 3: OR = 1.146, 95% CI = 1.071-1.226).

Therefore, the above results, high-dose intake of vitamin B12 may promote the development of glaucoma.