| Features: Promote calcium and phosphorus absorption | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Vitamin D3 (Cholecalciferol) - 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 - Vitamin D may modulate oxidative stress markers. (ROS) - Nrf2 plays a key role in protecting cells against oxidative stress; this is modulated by vitamin D - Vitamin D has antioxidant and anti-inflammatory regulatory effects; whether supplementation alters response to specific chemotherapy regimens remains context-dependent and not firmly established. - excess Vit D can raise calcium and cause harm Vitamin D deficiency is generally defined as serum 25(OH)D <20 ng/mL (50 nmol/L), though some guidelines consider ≥30 ng/mL sufficient. - One recommendation is to get your level up to around 125 ng/ml (however not supported by consensus clinical trial evidence). - Chemo depletes Vitamin D levels so 10,000 IUs daily? – ask your doctor first. Typical maintenance dosing for most adults is 800–2000 IU/day; higher doses may be used short-term under medical supervision when correcting deficiency. 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.
Time-Scale Flag (TSF): P / R / G
Clinical trial data suggest vitamin D supplementation effects may be attenuated in individuals with obesity, potentially due to pharmacokinetic and inflammatory differences.
|
| Source: |
| Type: |
| Cytochrome c ** The term "release of cytochrome c" ** an increase in level for the cytosol. Small hemeprotein found loosely associated with the inner membrane of the mitochondrion where it plays a critical role in cellular respiration. Cytochrome c is highly water-soluble, unlike other cytochromes. It is capable of undergoing oxidation and reduction as its iron atom converts between the ferrous and ferric forms, but does not bind oxygen. It also plays a major role in cell apoptosis. The term "release of cytochrome c" refers to a critical step in the process of programmed cell death, also known as apoptosis. In its new location—the cytosol—cytochrome c participates in the apoptotic signaling pathway by helping to form the apoptosome, which activates caspases that execute cell death. Cytochrome c is a small protein normally located in the mitochondrial intermembrane space. Its primary role in healthy cells is to participate in the electron transport chain, a process that helps produce energy (ATP) through oxidative phosphorylation. Mitochondrial outer membrane permeability leads to the release of cytochrome c from the mitochondria into the cytosol. The release of cytochrome c is a pivotal event in apoptosis where cytochrome c moves from the mitochondria to the cytosol, initiating a chain reaction that leads to programmed cell death. On the one hand, cytochrome c can promote cancer cell survival and proliferation by regulating the activity of various signaling pathways, such as the PI3K/AKT pathway. This can lead to increased cell growth and resistance to apoptosis, which are hallmarks of cancer. On the other hand, cytochrome c can also induce apoptosis in cancer cells by interacting with other proteins, such as Apaf-1 and caspase-9. This can lead to the activation of the intrinsic apoptotic pathway, which can result in the death of cancer cells. Overexpressed in Breast, Lung, Colon, and Prostrate. Underexpressed in Ovarian, and Pancreatic. |
| 1740- | VitD3, | Vitamin D and Cancer: An Historical Overview of the Epidemiology and Mechanisms |
| - | Review, | Var, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:167 Target#:77 State#:% Dir#:2
wNotes=0 sortOrder:rid,rpid