I don't see anything re DHA reducing longevity, so it should be safe, but I also doubt that it would act the way you think it will -- as a "C4" explosive that oxidizes a cancer cell, because the research you linked to also used a DGAT inhibitor "that prevents the formation of lipid droplets." They investigated several, in fact, which improved the results via peroxidation.
According to the paper DHA by itself had strong tumor inhibitory effects, both in vitro and in vivo with mice. The DGAT inhibitor simply enhanced the effect of DHA -
https://www.cell.com...t/S1550-4131(21[/url])00233-3?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1550413121002333%3Fshowall%3Dtrue
Mice were injected with HCT-116 cancer cells 2 weeks after initiation of either diet, i.e., at a time when mice of both groups were consuming the same daily amounts of food. The development of acidosis in these tumors was verified using a pHLIP peptide as an in vivo acid sensor. A highly specific accumulation of Alexa647-conjugated pHLIP peptide could be detected, whereas a control pH-insensitive peptide (K-pHLIP conjugated to Alexa568) failed to label tumors (Figure S13B). A significant tumor growth delay was observed in mice fed the DHA-rich diet (versus OA-rich diet) (Figure 6H), together with a significant prolongation of mouse survival (Figures 6I and S13C). Importantly, while the DHA-rich diet per se very significantly delayed tumor growth, DGAT1i further delayed tumor growth in mice fed the DHA-rich diet, but not the OA-rich diet (Figures 6H and 6I). GC-FID measurements of FA accumulated into tumors confirmed a net increase in n-3 PUFAs as FFAs, PL, and NL for the mice fed the DHA-rich diet (versus OA-rich diet) (Figure 6J). Of note, in the tumors of mice fed the OA-rich diet, most n-6 PUFAs consisted in LA (C18:2) that is much less peroxidable than n-3 EPA (C20:5) and DHA (C22:6), the two most enriched PUFAs in the tumors of mice fed the fish oil-based diet (Figure S13D).
A DGAT inhibitor is probably unnecessary to trigger ferroptosis in DHA fed cancer if Carbon 60 is used to contact the UCP2 pores of cancer in order to set off uncontrolled oxidative processes within those cancer cells.
Interestingly mice fed olive oil did not experience the ferroptopic effects fish oil/DHA fed mice did.
Another potential way to use Carbon C60 as an “oxidative detonator” is combining it with iron. Cancer cells require higher levels of iron to function than normal cells. But if iron is exposed to oxidation the reaction is toxic to cancer.
For example artemesia annua AKA sweet wormwood damages cancer cells by triggering oxidative reactions with the iron stores of cancer cells. This reaction with iron then destroys the cancer cells that were using iron.
This might mean that an iron chelation like IP6 should not be used before using C60 since one would want cancer cells to have plenty of iron stores BEFORE C60 triggers oxidation of the cancer cells.
One would also not want to use an antioxidant like glutathione with the C60 protocol because you would want the oxidative reaction of cancer cells to contact any iron that is nearby. It may not be necessary for people to supplement with iron before using C60 since most people have ferritin levels over 150.
For those with low iron stores with ferritin below 100 it might be advisable to take an iron supplement of 20 mgs 24 hours before using C60. But they shouldn’t supplement with iron more than couple of days a year since the body has no natural way of removing excess iron.
Edited by Kelvin, 13 November 2022 - 08:55 PM.
