Database Query Results : Vitamin D3, ,

VitD3, Vitamin D3: Click to Expand ⟱
Features: Promote calcium and phosphorus absorption
- Major VITAL study stated Vit D did not reduce invasive cancer, but Secondary Analysis stated reduces the incidence of metastatic cancer at diagnosis.
- Amount needed may depend on your BMI.
- Vitamin D deficiency, as determined by serum 25(OH)D concentrations of less than 30 ng/mL,
- Target achieving 80 ng/mL
- Reduces oxidative stress (ROS)
- Nrf2 plays a key role in protecting cells against oxidative stress; this is modulated by vitamin D
- Vit D supplementation may not be compatible with pro-oxidant therapy?

The minimal level is considered to be 30 ng/mL (50 nmol/L).
- One recommendation is to get your level up to around 125 ng/ml
- Chemo depletes Vitamin D levels so 10,000 IUs daily? – ask your doctor first.

After correction of vitamin D deficiency through loading doses of oral vitamin D (or safe sun exposure), adequate maintenance doses of vitamin D3 are needed. This can be achieved in approximately 90% of the adult population with vitamin D supplementation between 1000 to 4000 IU/day, 10,000 IU twice a week, or 50,000 IU twice a month [10,125]. On a population basis, such doses would allow approximately 97% of people to maintain their serum 25(OH)D concentrations above 30 ng/mL [19,126]. Others, such as persons with obesity, those with gastrointestinal disorders, and during pregnancy and lactation, are likely to require doses of 6,000 IU/day.

Vitamin D, particularly its active form 1,25-dihydroxyvitamin D (calcitriol), exerts multiple biological effects that may influence cancer development and progression.
Calcitriol has been reported to induce cell cycle arrest (often at the G0/G1 phase) and promote pro-apoptotic mechanisms in various cancer cell types.

Inhibition of Angiogenesis:
Some studies indicate that vitamin D can reduce the expression of pro-angiogenic factors, thereby potentially limiting the blood supply to tumors, which is necessary for tumor growth and metastasis.

Effects on the Wnt/β-catenin Pathway:
The Wnt/β-catenin signaling pathway, often dysregulated in several cancers (for example, colorectal cancer), may be modulated by vitamin D.
Calcitriol has been shown in some models to inhibit β-catenin signaling, which is associated with decreased cell proliferation and tumor progression.
Vitamin D may interact with other signaling pathways, including the PI3K/AKT/mTOR pathway, which is involved in cell survival and proliferation.
Scientific Papers found: Click to Expand⟱
1496- SFN,  VitD3,    Association between histone deacetylase activity and vitamin D-dependent gene expressions in relation to sulforaphane in human colorectal cancer cells
- in-vitro, CRC, Caco-2
eff↑, data suggest that colon cancer cells respond to dietary components differently under different conditions.
VDR↑, in proliferating Caco-2 cells, D + SFN (P < 0.04) increased VDR expression and decreased CYP27B1
CYP11A1↓,
HDAC↓, Histone deacetylase (HDAC) inhibitor activity was assessed using HDAC I/II assay that measured global changes in acetylation status.

4067- VitB12,  VitB6,  VitD3,    Plants, Plants, and More Plants: Plant-Derived Nutrients and Their Protective Roles in Cognitive Function, Alzheimer's Disease, and Other Dementias
- Review, AD, NA
*cognitive↑, A diet rich in vitamin B and antioxidants can benefit the cognitive functions of individuals as shown in randomized clinical trials

4050- VitB12,  VitD3,  VitE,    Nutrient intake, nutritional status, and cognitive function with aging
- Review, AD, NA
neuroP↑, evidence to support the critical role of several B vitamins in particular, but also of vitamin D, antioxidant vitamins (including vitamin E), and omega-3 fatty acids, which are preferentially taken up by brain tissue.

4077- VitB6,  FA,  VitB12,  VitD3,  VitE  Vitamin Supplementation as an Adjuvant Treatment for Alzheimer’s Disease
- Review, AD, NA
*antiOx↑, Vitamins are potent antioxidants and therefore can be used as an adjuvant therapy for the treatment of AD.
*cognitive↑, Among B vitamins, pyridoxine (B6), folic acid (B9), and cobalamin (B12) have shown to have potential in managing symptoms of AD.
*homoC↓, vitamin B6, B9 and B12 have shown to decrease the level of homocysteine, thereby helping in the control of this modifiable risk-factor for AD
*Risk↓, Low levels of vitamin B6 have been implicated in the pathogenesis of AD.
*Risk↓, Low level of serum folate is another predictor for AD
*Risk↓, The plasma levels of vitamin B12 were also found to be deficient in cases of AD
*other↝, Elevated plasma level of homocysteine is an important risk factor for gray matter atrophy
*Dose↝, 0.8mg B9, 20mg B6 and 0.5mg B12, over a period of 2 years has been demonstrated to decrease homocysteine induced gray matter atrophy
*Risk↓, The analysis of current literature on the relationship between vitamin D deficiency and AD revealed a direct relation between decreased serum level of vitamin D and AD
*Risk↓, decreased levels of plasma vitamin E is associated with increased risk of neurodegenerative disorders like AD and Mild Cognitive Impairment (MCI)

4055- VitB6,  VitD3,    Vitamin B6 and vitamin D deficiency co-occurrence in geriatric memory patients
- Study, AD, NA
*Risk↓, Vitamin B6 deficiency was the most common (37.5%), followed by vitamin D deficiency (36.8%).
*cognitive↑, The coexistence of these vitamin deficiencies has a significant association with cognitive performance, indicating the clinical importance of monitoring and supplementation.

3921- VitD3,  RES,    Vitamin D Combined with Resveratrol Prevents Cognitive Decline in SAMP8 Mice
- in-vivo, AD, NA
*cognitive↑, The combination of VD and RSV significantly increased time spent in target quadrant and the number of crossing via MWM test
*Aβ↓, In hippocampus, the combined intervention significantly reduced soluble Aβ42 level and BACE1 protein expression
*BACE↓,
*p‑tau↓, combined treatment significantly reduced phosphorylation of tau at serine404 and p-p53, as well as enhanced p-CREB protein expression
*p‑CREB↑,
*p‑NF-kB↓, The combination also significantly reduced GFAP and p-NFκB p65 in both hippocampus and cortex
*neuroP↑, combined intervention might exert greater neuroprotective effects in SAMP8 mice,

4350- VitD3,    Vitamin D: Evidence-Based Health Benefits and Recommendations for Population Guidelines
- Review, Var, NA - Review, AD, NA
Risk↓, evidence that vitamin D can reduce the risk of cancer incidence and mortality rates is robust.
angioG↓, Vitamin D reduces angiogenesis around tumors, which is required to deliver nutrients to the tumors
TumMeta↓, and it reduces metastasis into the surrounding stromal tissue, which is generally required for mortality.
AntiCan↑, 9 of the 54 patients in the p53-immunoreactive group treated with vitamin D had a relapse or death during 5 years of follow-up, compared to 14 of 26 in the placebo group
*cognitive↑, Adequate 25(OH)D concentrations are associated with improved cognitive function [105,106] and mood stability [107], particularly in vulnerable populations.
*Mood↑, Vitamin D supplementation has shown promise in enhancing mood and reducing depressive symptoms, with studies indicating improved clinical outcomes in patients receiving vitamin D alongside antidepressants

4320- VitD3,    Unraveling the molecular mechanisms of vitamin deficiency in Alzheimer's disease pathophysiology
- Review, AD, NA
*Calcium↝, Vitamin D regulates calcium and phosphorus levels, essential for healthy bone mineralization
*cognitive↑, regulating cognitive genes and removes Aβ plaques
*Aβ↓,
*Inflam↓, Its anti-inflammatory properties lower neuroinflammation, while VDR gene variation may affect an individual's risk of cognitive decline and AD
*Risk↓,
*other↝, vitamin D interacts with genes like APP, PSEN1, PSEN2, and APOE, which are responsible for the pathology of AD

4187- VitD3,    Protective effects of vitamin D on neurophysiologic alterations in brain aging: role of brain-derived neurotrophic factor (BDNF)
- in-vivo, NA, NA
*BDNF↑, Vitamin D supplementation significantly mitigated the observed aging-related reduction in brain BDNF level and activities of AChE and antioxidant enzymes and elevation in malondialdehyde level and caspase-3 activity compared to control groups.
*MDA↓,
*Casp3↓,

4186- VitD3,    The Association of Vitamin D, Nerve Growth Factor (NGF), Brain-Derived Neurotrophic Factor (BDNF), and Glial Cell-Derived Neurotrophic Factor (GDNF) with Development in Children
- Study, NA, NA
*BDNF∅, There was no association of vitamin D with NGF, GDNF, or BDNF levels.

4185- VitD3,    Effects of vitamin D supplementation on neuroplasticity in older adults: a double-blinded, placebo-controlled randomised trial
- Study, NA, NA
*other↑, After 10 weeks, mean 25(OH)D levels increased from 46 to 81 nmol/L in the vitamin D group with no change in the placebo group.
*BDNF∅, There was no effect of vitamin D on muscle power, function or BDNF.

4184- VitD3,    Neuroplasticity-related effects of vitamin D relevant to its neuroprotective effects: A narrative review
- Review, NA, NA
*BDNF↑, A cross-sectional study in older adults (≥ 60 years, n = 576) found an association between vitamin D levels and serum BDNF, with higher vitamin D levels associated with higher serum BDNF concentrations and cognitive performance
*cognitive↑,

4183- VitD3,  Ex,    Combined Exercise and Vitamin D on Brain-Derived Neurotrophic Factor
- Review, NA, NA
*BDNF↑, Certain types of physical exercise have been shown to markedly (threefold) increase BDNF synthesis in the human brain, a phenomenon that is partly responsible for exercise-induced neurogenesis and improvements in cognitive function [42].
*Inflam↓, In addition to its effects on gene expression, vitamin D may also modulate BDNF levels through its anti-inflammatory properties
*other↝, , research has suggested that vitamin D may interact with other molecules implicated in BDNF regulation, such as serotonin and dopamine.

4182- VitD3,    The association between vitamin D and BDNF on cognition in older adults in Southern Brazil
- Study, AD, NA
*cognitive↑, we observed a direct and positive effect of vitamin D on cognitive function (Coef: 0.06; 95%CI: 0.02 to 0.11; p < 0.001) and serum BDNF concentration (Coef: 21.55; 95%CI: 9.92 to 33.17; p = 0.002),
*BDNF↑,

4086- VitD3,    The beneficial role of vitamin D in Alzheimer's disease
- Review, AD, NA
*Mood↑, Patients with AD have a high prevalence of vitamin D deficiency, which is also associated with low mood and impaired cognitive performance in older people.
*cognitive↑,
*eff↑, Calcitriol, 1αα,25-dihydroxyvitamin D3, is best used for AD because of its active form of vitamin D3 metabolite and its receptor in the central nervous system.

115- VitD3,    Vitamin D3 triggers antitumor activity through targeting hedgehog signaling in human renal cell carcinoma Vitamin D3 Inhibits Hedgehog Signaling and Proliferation in Murine Basal Cell Carcinomas
- in-vivo, RCC, NA - in-vivo, BCC, NA
HH↓,
GLI2↓,
Shh↓,
Gli1↓,

2369- VitD3,    Long Non-coding RNA MEG3 Activated by Vitamin D Suppresses Glycolysis in Colorectal Cancer via Promoting c-Myc Degradation
- in-vitro, CRC, DLD1 - in-vitro, CRC, RKO
MEG3↑, MEG3 can be activated by vitamin D and vitamin D receptor (VDR).
Glycolysis↓, overexpression of MEG3 significantly inhibited glycolysis
lactateProd↓, as well as lactate production in CRC cells
LDHA↓, inhibited c-Myc target genes involved in the glycolysis pathway such as lactate dehydrogenase A
PKM2↓, pyruvate kinase muscle 2, and hexokinase 2
HK2↓,

2368- VitD3,    Vitamin D3 supplementation shapes the composition of gut microbiota and improves some obesity parameters induced by high-fat diet in mice
- in-vivo, Obesity, NA
*Weight↓, VD3 supplementation reduced body weight and the levels of TG, TC, HDL-C, TNF-α, IL-1β and LPS, and increased ZO-1 in HFD-fed mice
*TNF-α↓,
*IL1β↓,
LPS↓,
*ZO-1↑,
*GutMicro↑, increased α-diversity, reduced F/B ratio and altered microbiota composition by increasing relative abundance of Bacteroidetes, Proteobacteria, Desulfovibrio, Dehalobacterium, Odoribacter, and Parabacteroides and reducing relative abundance of Firmic

2367- VitD3,    Vitamin D activates FBP1 to block the Warburg effect and modulate blast metabolism in acute myeloid leukemia
- in-vivo, AML, NA
FBP1↑, VD3-induced FBP1 overexpression might be a novel therapeutic target to block the “Warburg Effect” to reduce energy production in AML blasts.
Warburg↓,
Glycolysis↓,
lactateProd↓, functional lactate assay showed the significant reduction of the lactate concentration in MV4–11 cells after 1,25VD3 treatment

2366- VitD3,    Vitamin D3 decreases glycolysis and invasiveness, and increases cellular stiffness in breast cancer cells
- in-vitro, BC, MCF-7
Glycolysis↓, We find that VD3 treatment significantly down-regulates glycolytic enzymes and genes and decreases glucose uptake - for both lowly metastatic MCF-7 and highly metastatic MDA-MB-231 (MB231) breast cancer cells.
tumCV↓, VD3 also significantly decreases cell viability by inducing apoptosis
Apoptosis↑,
mTOR↓, consistent with decreased expression of mammalian target of rapamycin (mTOR),
AMPK↑, increases 5' adenosine monophosphate-activated protein kinase (AMPK) activation
EMT↓, presumably a consequence of reversal of the epithelial to mesenchymal transition
E-cadherin↑, increased E-cadherin, and F-actin, and reduced vimentin expression
F-actin↑,
Vim↓,

2365- VitD3,    Vitamin D Affects the Warburg Effect and Stemness Maintenance of Non- Small-Cell Lung Cancer Cells by Regulating the PI3K/AKT/mTOR Signaling Pathway
- in-vitro, Lung, A549 - in-vitro, Lung, H1975 - in-vivo, NA, NA
Glycolysis↓, vitamin D inhibited glycolysis and stemness maintenance in A549 and NCI-H1975 cells.
Warburg↓, vitamin D attenuated the expression of metabolism-related enzymes associated with the Warburg effect (GLUT1, LDHA, HK2, and PKM2).
GLUT1↓,
LDHA↓,
HK2↓,
PKM2↓,
OCT4↓, In addition, vitamin D down-regulated the expression of stemness-related genes (Oct-4, SOX-2, and Nanog) and the expression of PI3K, AKT, and mTOR.
SOX2↓,
Nanog↓,
PI3K↓,
Akt↓,
mTOR↓,

2171- VitD3,    Vitamin D and the Immune System
- Analysis, Nor, NA
eff↑, beneficial effects of supplementing vitamin D deficient individuals with autoimmune disease may extend beyond the effects on bone and calcium homeostasis.
Dose↝, Cod liver oil, a rich source of vitamin D has also been employed as a treatment for tuberculosis as well as for general increased protection from infections
eff↝, seasonal infections varied, and were lowest in the summer and highest in the winter, the association of lower serum vitamin D levels and infection held during each season
eff↑, ll have reported an association of lower vitamin D levels and increased rates of infection
eff↑, above 40nmol

1741- VitD3,    Vitamin D Deficiency: Effects on Oxidative Stress, Epigenetics, Gene Regulation, and Aging
- Review, Var, NA
*Inflam↓, Vitamin D is one of the key controllers of systemic inflammation, oxidative stress
*antiOx↑, Vitamin D is also a potent anti-oxidant
*eff↑, Excess Sun Exposure Does Not Cause Hypervitaminosis D
*ROS↓, When vitamin D status is adequate, many of the intracellular oxidative stress-related activities are downregulated.
*NRF2↑, The intracellular Nrf2 level is inversely correlated with the accumulation of mitochondrial ROS [51,60] and the consequent escalation of oxidative stress.
*GPx↑, Vitamin D also upregulates the expression of glutathione peroxidase that converts the ROS molecule H2O2 to water
*Dose↝, adequate maintenance doses of vitamin D3 are needed. This can be achieved in approximately 90% of the adult population with vitamin D supplementation between 1000 to 4000 IU/day, 10,000 IU twice a week, or 50,000 IU twice a month
Dose↑, Others, such as persons with obesity, those with gastrointestinal disorders, and during pregnancy and lactation, are likely to require doses of 6,000 IU/day

1740- VitD3,    Vitamin D and Cancer: An Historical Overview of the Epidemiology and Mechanisms
- Review, Var, NA
Risk↓, An analysis of 25(OH)D-cancer incidence rates suggests that achieving 80 ng/mL vs. 10 ng/mL would reduce cancer incidence rates by 70 ± 10%.
eff↑, In 1936, Peller reported that people who developed skin cancer from light exposure, such as from their occupation, had lower rates of internal cancers
eff↑, low rates(internal cancer) in three southwest states and high rates in approximately 15 northeast states
Risk↓, Inverse correlations were found for 11 cancers with respect to solar UVB doses for white Americans and several types of cancer for black Americans
Risk↓, It reported an 82% lower risk of breast cancer for 25(OH)D concentration >60 ng/mL versus <20 ng/mL
ChemoSen↑, Sensitization to Apoptosis, Combined Action with Chemotherapy and Radiotherapy
RadioS↑,
Cyt‑c↑, it favors the release of cytochrome C from mitochondria and the activation of caspases 3 and 9 that lead to apoptosis promoted by a variety of signals
Casp3↑,
Casp9↑,
hTERT↓, by downregulation of telomerase reverse transcriptase (hTERT) via the induction of miR-498
eff↑, In addition, 1,25-(OH)2D3 and metformin have additive/synergistic antiproliferative and proapoptotic effects in colon carcinoma and other types of cells, which are modulated but not hampered by TP53 status
E-cadherin↑, 1,25-(OH)2D3 upregulates an array of intercellular adhesion molecules that are constituents of adherens junctions and tight junctions, including E-cadherin, occludin, claudin-2 and -12, and ZO-1 and -2
CLDN2↑,
ZO-1↑,
Snail↓, 1,25-(OH)2D3 inhibits SNAIL1 and ZEB1 expression in non-small cell lung carcinoma cells
Zeb1↓,
Vim↓, vimentin downregulation
VEGF↓, 1,25-(OH)2D3 alone and more strongly in combination with cisplatin suppresses VEGF activity in ovarian cancer cells
NK cell↑, 1,25-(OH)2D3 is an enhancer of innate immune reactions against infections and tumor cells by activating the responsive cells (macrophages, natural killer (NK) cells, and neutrophils)
Risk↓, vitamin D deficiency promotes gut permeability, colon mucosa bacterial infiltration, and translocation of intestinal pathogens. These effects lead to changes in immune cell populations and gut inflammation, and cancer—an overall condition that is im
eff↑, Combination with immunotherapy

1739- VitD3,    Effect of Vitamin D3 Supplements on Development of Advanced Cancer
- Trial, Var, NA
AntiCan↑, vitamin D3 may reduce the risk of developing advanced cancer among adults without a diagnosis of cancer at baseline; this protective effect is apparent for those who have normal but not elevated body mass index.
Dose↝, Vitamin D3 (cholecalciferol, 2000 IU/d) and marine omega-3 fatty acids (1 g/d) supplements.
Risk↓, people who took vitamin D supplements with those who took a placebo for at least 3 years; people who took vitamin D supplements had a 13% lower risk of dying from cancer than those who took a placebo
TumCP↓, , inhibition of cancer cell proliferation, and anti-inflammatory, immunomodulatory, proapoptotic, and antiangiogenic effects.
Inflam↓,
eff∅, There was no association of omega-3 fatty acid supplementation with advanced cancer, nor was there an interaction by omega-3 treatment arm

1738- VitD3,    VITAL study: an incomplete picture?
- Trial, Var, NA
AntiCan↑, normal-weight individuals in the vitamin D group showed a lower cancer incidence compared to those in the placebo group
*BioAv↓, decreased bioactivity of vitamin D associated with obesity
Dose↑, 6,000-10,000 IU/day for 8 weeks, followed by maintenance therapy of 3,000-6,000 IU/day

1313- VitD3,  MEL,    The effects of melatonin and vitamin D3 on the gene expression of BCl-2 and BAX in MCF-7 breast cancer cell line
- in-vitro, BC, MCF-7
BAX↑, upregulation of Bax gene
Bcl-2↓,
Bax:Bcl2↑, Bax/BCL-2 ratio was increased significantly
eff↑, treatment with melatonin and vitamin D3 inhibits the proliferation and induced apoptosis in breast cancer cells

1223- VitD3,    Vitamin D3 Treatment Influences PGE2 and TGFβ in Normal and Increased Breast Cancer Risk Women
- Trial, NA, NA
*TGF-β↑, TGFβ2 increase correlated with increase in 25(OH)D. DBP serum levels
*PGE2↓,


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 28

Results for Effect on Cancer/Diseased Cells:
Akt↓,1,   AMPK↑,1,   angioG↓,1,   AntiCan↑,3,   Apoptosis↑,1,   BAX↑,1,   Bax:Bcl2↑,1,   Bcl-2↓,1,   Casp3↑,1,   Casp9↑,1,   ChemoSen↑,1,   CLDN2↑,1,   CYP11A1↓,1,   Cyt‑c↑,1,   Dose↑,2,   Dose↝,2,   E-cadherin↑,2,   eff↑,9,   eff↝,1,   eff∅,1,   EMT↓,1,   F-actin↑,1,   FBP1↑,1,   Gli1↓,1,   GLI2↓,1,   GLUT1↓,1,   Glycolysis↓,4,   HDAC↓,1,   HH↓,1,   HK2↓,2,   hTERT↓,1,   Inflam↓,1,   lactateProd↓,2,   LDHA↓,2,   LPS↓,1,   MEG3↑,1,   mTOR↓,2,   Nanog↓,1,   neuroP↑,1,   NK cell↑,1,   OCT4↓,1,   PI3K↓,1,   PKM2↓,2,   RadioS↑,1,   Risk↓,6,   Shh↓,1,   Snail↓,1,   SOX2↓,1,   TumCP↓,1,   tumCV↓,1,   TumMeta↓,1,   VDR↑,1,   VEGF↓,1,   Vim↓,2,   Warburg↓,2,   Zeb1↓,1,   ZO-1↑,1,  
Total Targets: 57

Results for Effect on Normal Cells:
antiOx↑,2,   Aβ↓,2,   BACE↓,1,   BDNF↑,4,   BDNF∅,2,   BioAv↓,1,   Calcium↝,1,   Casp3↓,1,   cognitive↑,9,   p‑CREB↑,1,   Dose↝,2,   eff↑,2,   GPx↑,1,   GutMicro↑,1,   homoC↓,1,   IL1β↓,1,   Inflam↓,3,   MDA↓,1,   Mood↑,2,   neuroP↑,1,   p‑NF-kB↓,1,   NRF2↑,1,   other↑,1,   other↝,3,   PGE2↓,1,   Risk↓,7,   ROS↓,1,   p‑tau↓,1,   TGF-β↑,1,   TNF-α↓,1,   Weight↓,1,   ZO-1↑,1,  
Total Targets: 32

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