@Mauritio said in Vitamin A and D deficiency increases liver cancer:

o for anyone thinking vitamin A and D are poisons maybe ingest some Vitamin E at least.

I’d like to point out some inadequacy to remind:

High levels of vitamin E alpha (only one dimer) affect retinol binding protein (RBP). Excessive vitamin E could increase the concentration of vitamin A in liver by inhibiting RBP synthesis in hepatocytes.
We need 20-25 mg vitamin E per day, according to Chris Masterjohn. So I won’t take 400 UI every day but every 72 hours (+/ 2x/wk.), 3x if inflammation. There is U-shape effect with retinol:
An excess of vitamin A (or a vitamin D deficiency) prevents the formation of heterodimers: essentially homodimers (RXR-RXR) will be formed, leaving the VDR unoccupied and inactive. Zoëhlo (Pharmacologist). A deficit in Fe Zn Vit E or protein can exhaust the carriage, the storage and the use of vitamin A.
Useful links: Vitamin A is one of the Keys to a Tolerant Immune System? (in French, translator needed)
https://mirzoune-ciboulette.forumactif.org/t721-vitamine-a-la-cle-dun-systeme-immunitaire-tolerant#6555 Vitamin A works as an estrogen antagonist
The greatest use of vitamin A is at the level of production of pregnenolone, progesterone and the other steroid hormones associated with youth.
“Vitamin A is for the production of pregnenolone, progesterone, and the other youth-associated steroids”.
http://raypeat.com/articles/articles/alzheimers2.shtml

interesting find - if u target a main 2% subset of melanoma cells the tumor goes in most cases without destroying the other part. if some are left theres potential for the regression to return
(does doxycyline help these ones get destroyed when combined with inhibitors?)

https://www.pnas.org/doi/10.1073/pnas.1009069108

we revealed that established tumor lesions can be efficiently eradicated by targeted elimination of the less than 2% subset of melanoma cells with the CD20+ high molecular weight melanoma-associated antigen (HMW-MAA)+ phenotype without targeting the tumor cell mass, whereas targeted elimination of any minor subset is less effective.
These data provide a strategy for improving the biological therapy of melanomas and, moreover, for redesigning current drug development paradigms used in the treatment of cancer.

HMW-MAA+ cells gave rise to melanomas upon transplantation, whereas sorted HMW-MAA− cells from the same melanoma did not.
indicating that these cells exhibit melanoma-initiating capacities.
T cells with redirected specificity for CD20 eradicated established melanoma lesions in four out of five melanoma biopsies, although the targeted cells represented less than 2% of melanoma cells.
It is noteworthy that transplanted tumors of patient 5, in which no CD20+ melanoma cells were detected, could not be eradicated by a CD20-redirected T-cell attack.

Where tumors were eradicated, no tumor relapse occurred during the observation period of >36 wk.
Because no tumor relapse was observed in any case during the >36 wk observation period, such melanoma eradication is obviously long lasting
We conclude that CD20 is not functionally crucial but marks a specific cell population. The unexpected observation, however, is that targeting the minor CD20+ melanoma cell population is as effective as targeting the majority of tumor cells. A caveat for a broad therapeutic application is that obviously some melanomas, in our cohort one out of five patients, do not harbor CD20+ melanoma cells

The observation that the specific elimination of a minor subset of tumor cells results in eradication of established melanoma lesions is crucial for the understanding of the biology of melanoma. Continuous melanoma growth obviously requires the presence of a minor population of cells, which displays the CD20+ HMW-MAA+ phenotype;Elimination of these cells is obviously required to eradicate the melanoma irrespective of the bulk of tumor cells

High sodium chloride intake decreases betaine-homocysteine S-methyltransferase expression in guinea pig liver and kidney

"Betaine-homocysteine S-methyltransferase (BHMT) is the only enzyme known to catabolize betaine. In addition to being a substrate for BHMT, betaine also functions as an osmoprotectant that accumulates in the kidney medulla under conditions of high extracellular osmolarity. The mechanisms that regulate the partitioning of betaine between its use as a methyl donor and its accumulation as an osmoprotectant are not completely understood. The aim of this study was to determine whether BHMT expression is regulated by salt intake. This report shows that guinea pigs express BHMT in the liver, kidney, and pancreas and that the steady-state levels of BHMT mRNA in kidney and liver decrease 68% and 93% in guinea pigs consuming tap water containing high levels of salt compared with animals provided untreated tap water. The animals consuming the salt water also had ∼50% less BHMT activity in the liver and kidney, and steady-state protein levels decreased ∼30% in both organs. Pancreatic BHMT activity and protein levels were unaffected by the high salt treatment. The complex mechanisms involved in the downregulation of hepatic and renal BHMT expression in guinea pigs drinking salt water remain to be clarified, but the physiological significance of this downregulation may be to expedite the transport and accumulation of betaine into the kidney medulla under conditions of high extracellular osmolarity."

@KettleBelCanto Haidut is too good for Chaz, he'd be more suited as Trump's personal physician