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Cancer Cells Addicted To Fat And Use Fat Oxidation For Survival

haidut

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Ray has written several times that while cancer cells use glucose for their normal activities they use fat to evade apoptosis and increase metastasis. Thus, according to Ray, using substances that block fat oxidation can be therapeutic. Niacinamide and aspirin are some of the most beneficial ones. Aspirin also suppresses fatty acid synthase (FAS), which is upregulated in virtually all types of cancer.
Note that one of the drugs used to suppress leukemia growth is etomoxir - a drug that acts very similarly to the drug mildronate that Ray has written about before. Mildronate is also used to treat heart failure and also works by suppressing fatty acid oxidation. Finally, another drug the scientists also found to be effective - orlistat - is available OTC in the US under the brand name Alli.


http://phys.org/news/2010-01-leukemia-c ... -cell.html

"..."The leukemia cells' appetite for fat seems to be formidable," Taegtmeyer said. "More importantly, fat oxidation seems to promote leukemia cell survival. Conversely, shutting off fat oxidation makes the cells vulnerable to self-destruction. If these initial results hold up, inhibitors of fat oxidation may become a new way to treat leukemia patients."

"...In normal cells, the processing of fatty acids in the cell's power-generating mitochondria leads to production of ATP, a molecule that serves as the major source of energy for the cell. The researchers showed that fatty acid oxidation in leukemia cell mitochondria drives cellular oxygen consumption and inhibits the activity of proteins that are vital to apoptosis, the programmed death of defective cells that begins in the mitochondria."

"...For energy generation, leukemia cells rely on glycolysis, the processing of a glucose molecule in the cellular cytoplasm that produces two molecules of ATP and two of pyruvate. Pyruvate, in turn, is converted to energy by the Krebs Cycle, a series of chemical reactions inside the mitochondria. In a series of lab experiments, the researchers demonstrated that etomoxir, a drug used to treat heart failure, inhibits the growth of leukemia cells in culture in a dose-dependent manner. They also found that etomoxir sensitizes leukemia cells to drugs that cause apoptosis. The fatty acid synthase/lipase inhibitor orlistat also sensitized leukemia cells to programmed cell death. Etomoxir treats heart failure by switching the heart's energy supply from fatty acids to pyruvate, which is more efficiently converted to energy by the mitochondria."

"...Our findings suggest that mitochondrial function and resistance to apoptosis in leukemia cells are intimately linked with the entry of fatty acids into mitochondria," said first author Ismael Samudio, M.D., a fellow in Stem Cell Transplantation and Cellular Therapy. "For many years it has been apparent that leukemia cells are addicted to glucose for the generation of cellular energy (ATP). Now our results suggest that leukemia cells are addicted to fatty acids for the function of the Krebs cycle and the prevention of cell death."
 
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LucH

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haidut said:
https://raypeatforum.com/forums/posts/97258/ Cancer cells use fat oxidation for survival
Thanks for pointing at this process. :hattip
I didn't know the "details". I knew cancer could be set in remission by cutting excess sugar, with a paleo diet, but only for a moment. Cancer cells would then adapt themselves and carburate with lipids.
NB: tumor must be "taken" off (eradication).

Here is another source I found to confirm.
Excerpt from "cell mrtabolism"
Limiting Supplies of Fatty Acids to Limit Cancer Cell Proliferation
Since FAs are essential for cancer cell proliferation, limiting their availability could provide a therapeutic strategy. From the perspective of lipid metabolism, limiting FA availability could be achieved in several ways: (1) blocking FA synthesis, (2) increasing FA degradation via oxidation, (3) diverting FAs to storage, or (4) decreasing FA release from storage (Figure 2). Limiting FAs through these mechanisms could be accomplished in isolation or in a combinatorial manner. Using this as a framework, we review evidence relevant to this model.
http://www.sciencedirect.com/science/ar ... 3113002076
 
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haidut

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LucH said:
https://raypeatforum.com/forums/posts/97261/ (1) blocking FA synthesis, (2) increasing FA degradation via oxidation, (3) diverting FAs to storage, or (4) decreasing FA release from storage (Figure 2).

Good find, thanks.

Using your quote I added some substances known to act upon the 4 methods listed:

(1) blocking FA synthesis (aspirin), (2) increasing FA degradation via oxidation (caffeine), (3) diverting FAs to storage (insulin), or (4) decreasing FA release from storage (aspirin, niacinamide) (Figure 2).
 
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Fletcher

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haidut said:
(1) blocking FA synthesis (aspirin), (2) increasing FA degradation via oxidation (caffeine), (3) diverting FAs to storage (insulin), or (4) decreasing FA release from storage (aspirin, niacinamide).

So would Solban be helpful for someone suffering from cancer? If so any idea on what type of dose would be a good starting point?
 

Parsifal

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LucH said:
haidut said:
post 97258 Cancer cells use fat oxidation for survival
Thanks for pointing at this process. :hattip
I didn't know the "details". I knew cancer could be set in remission by cutting excess sugar, with a paleo diet, but only for a moment. Cancer cells would then adapt themselves and carburate with lipids.
NB: tumor must be "taken" off (eradication).

Here is another source I found to confirm.
Excerpt from "cell mrtabolism"
Limiting Supplies of Fatty Acids to Limit Cancer Cell Proliferation
Since FAs are essential for cancer cell proliferation, limiting their availability could provide a therapeutic strategy. From the perspective of lipid metabolism, limiting FA availability could be achieved in several ways: (1) blocking FA synthesis, (2) increasing FA degradation via oxidation, (3) diverting FAs to storage, or (4) decreasing FA release from storage (Figure 2). Limiting FAs through these mechanisms could be accomplished in isolation or in a combinatorial manner. Using this as a framework, we review evidence relevant to this model.
http://www.sciencedirect.com/science/ar ... 3113002076
IIRC Peat said that cancer was not fueling on carbs but on proteins and fats turning it into carbs by glucogenesis.
Gerson's diet is cutting proteins down when there is cancer for that purpose.
 
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haidut

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Fletcher said:
post 101429
haidut said:
(1) blocking FA synthesis (aspirin), (2) increasing FA degradation via oxidation (caffeine), (3) diverting FAs to storage (insulin), or (4) decreasing FA release from storage (aspirin, niacinamide).

So would Solban be helpful for someone suffering from cancer? If so any idea on what type of dose would be a good starting point?

SolBan is for topical purpose only. But the ingredients in it (aspirin, niacinamide, caffeine) listed above can be taken orally. There are plenty of studies and articles by Peat about each of these substances' effect on cancer. In combination they are probably synergistic.
 
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Peatit

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IIRC Peat said that cancer was not fueling on carbs but on proteins and fats turning it into carbs by glucogenesis.
Gerson's diet is cutting proteins down when there is cancer for that purpose.
If I understood correctly, according to Peat, cancer cells turn protein to sugar when there's not enough of it in the diet then use sugar to glycolysis and also to synthesize fatty acids as oxidants (electron acceptors) in the absence of oxygen, in order for the cell to regenerate NAD+ to be able to continue glycolysis to survive.
 

Jsaute21

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Has anyone ever used Mildronate? What are affects from a cognitive standpoint? Looks interesting.
 
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