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- 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.