I posted a few threads on vitamin D and how it may help treat endotoxin-related condition, especially ones affecting the liver.
Vitamin D Is Endotoxin (LPS / TLR4) Antagonist, May Treat LPS-linked Conditions
Endotoxin is perhaps the primary driver of actual liver fibrosis, which (if left unopposed) can lead to liver cancer. This new study found yet another mechanism through which vitamin D inhibits liver cancer development and progression and also concludes that vitamin D may prevent (and even treat) liver fibrosis and cancer.
Research uncovers defender against cancer-promoting liver damage
"...This study also revealed that p62 interacts with the vitamin D receptor, which returns stellate cells to their vitamin A-storing state. When p62 is missing, the receptor can’t do its job, so the cells continue to produce pro-inflammatory signals. “Vitamin D and its analogs may still help prevent cancer in patients with hepatitis or fatty liver disease,” commented Diaz-Meco. “At that stage, enough p62 may still be present in stellate cells for the vitamin D receptor to work.” “Since p62 is so important in preventing liver cancer, we’re now interested in why it disappears in stellate cells,” said Moscat. “We plan to explore that question, which may lead to ways to turn its expression back on, which should block liver cancer progression.”
Vitamin D Is Endotoxin (LPS / TLR4) Antagonist, May Treat LPS-linked Conditions
Endotoxin is perhaps the primary driver of actual liver fibrosis, which (if left unopposed) can lead to liver cancer. This new study found yet another mechanism through which vitamin D inhibits liver cancer development and progression and also concludes that vitamin D may prevent (and even treat) liver fibrosis and cancer.
Research uncovers defender against cancer-promoting liver damage
"...This study also revealed that p62 interacts with the vitamin D receptor, which returns stellate cells to their vitamin A-storing state. When p62 is missing, the receptor can’t do its job, so the cells continue to produce pro-inflammatory signals. “Vitamin D and its analogs may still help prevent cancer in patients with hepatitis or fatty liver disease,” commented Diaz-Meco. “At that stage, enough p62 may still be present in stellate cells for the vitamin D receptor to work.” “Since p62 is so important in preventing liver cancer, we’re now interested in why it disappears in stellate cells,” said Moscat. “We plan to explore that question, which may lead to ways to turn its expression back on, which should block liver cancer progression.”
