Inhibiting Lipolysis May Treat / Cure Cancer

[Addie1970]

Ok but you have to eat a diet that contains fat, or sugar, both which are known to apparently grow cancer. So what would the solution be? Although it's interesting/good information I'm not sure I understand the takeaway here.

 

[mangoes]

I have been on Fenbendozole for 13 weeks now and feel it is not enough as the phenotype of prostate cancer is different than Joe's cancer. I feel my greatest advantage is blocking FAS (orlistat)and FAO (mildronate) as well as taking the Care Oncology Clinic (started in London in 2013) cocktail. Fenben is a microtubule disrupter like chemo but beta microtubule's, a glucose blocker, and activates the p53 gene in the mitochondria. The COC uses Mebendazole in its cocktail. I follow Jane McLelland's "Metro Map" from the book "how to starve cancer"

I found this study when researching superoxide dismutase and thought you might find it interesting
SOD Mimetics: A Novel Class of Androgen Receptor Inhibitors That Suppresses Castration-Resistant Growth of Prostate Cancer - PubMed
I also see you’re taking mildronate which I saw in another study of lung injury in rats that mildronate can increase SOD activity

 

[Estradiol]

@haidut

Did you ever look Niclosamide? It's a salicylic acid derivative antihelminthic drug. Studied for cancers and looks so Peaty.

 

[Highserotonin90]

If Niacinamide causes me depression is that a sign that sam-e is being consumed and lowers neurotransmitter production?

 

[Jon2547]

I would like to make sense of this. Having heard and read of those who have had success with cancer treatments by lowering sugars this seems at first glance to be wrong. By this I mean, the idea that lowering lipolysis is the key.
This is just one of a thousand anecdotes: My former father in law had a dog with a tumour protuding from his skull. Vet gave the dog three weeks to live. But former father in law went to the internet, took the dog off regular dog food and onto carnivore diet plus saffron and dog went into remission and lived another four years. (And this dog was thriving during the remaining four years of life)

I said all of that to say this: How do we make sense of all of this in light of the testimonials of not only man but also in the animal kingdom?

 

[Highserotonin90]

So does inhibiting FAO necessarily mean blocking lipolysis or can I continue to lose body fat? it seems to me that niacinamide works but slows down lipolysis.

Does LESS Weight Loss/Fat Loss Occur If Inhibiting Lipolysis?

If you're already at your ideal weight, inhibiting lipolysis might be only beneficial, let's say you actually need to lose a bit of weight (and don't want it to take 2 years.) In other words, does inhibiting lipolysis negatively impact fat loss/weight loss?

raypeatforum.com

@Hans

 

[Texon]

So does inhibiting FAO necessarily mean blocking lipolysis or can I continue to lose body fat? it seems to me that niacinamide works but slows down lipolysis.

Does LESS Weight Loss/Fat Loss Occur If Inhibiting Lipolysis?

If you're already at your ideal weight, inhibiting lipolysis might be only beneficial, let's say you actually need to lose a bit of weight (and don't want it to take 2 years.) In other words, does inhibiting lipolysis negatively impact fat loss/weight loss?

raypeatforum.com

@Hans

Simplistically speaking baiting cancer cells with heat-damaged pufas and selenium compounds was the basis for Dr Emmanuel Revici's cancer cure. I call it non-toxic chemotherapy. The cancers went for the damaged fats which were then killed by the SE. He lived to age 101 and had very good success with the protocol. My wife used it to cure stage 2 breast cancer caused by Rx estrogen patches not properly monitored.

 

[Texon]

I posted a number of threads over the last 6 months that show cancer's appetite for fat and how inhibiting fatty acid oxidation or transport into the cell can have dramatic therapeutic results even for highly lethal malignancies like pancreatic cancer.
Triple-Negative Breast Cancers Depend On Fat As Fuel
Cancer Cells Addicted To Fat And Use Fat Oxidation For Survival
Achilles Heel Of Cancer Found - Its Addiction To Fat
Dietary Fat And Its Oxidation Drives Cancer Metastasis
Cancer Addiction To Fat Confirmed; Niacinamide As Possible Treatment
Niacinamide Can Cure Liver (and Maybe Pancreatic) Cancer

Now this new study shows that even inhibiting just lipolysis (hello, again, niacinamide) is enough to kill the cancer stem cells, which are responsible for metastasis. Perhaps just as importantly, it shows that the cancer metabolism is akin to hibernation - i.e. the organism relies on fat to satisfy its energetic needs. Inhibiting this supply of fat quickly kills the cancer stem cells, or wakes up the animal from sleep (in the case of hibernation).

The lipolysis pathway sustains normal and transformed stem cells in adult <i>Drosophila</i>
Eliminating cancer stem cells: an interview with CCR’s Steven Hou | Center for Cancer Research

"...Cancer stem cells, or CSCs, are usually localized to a storage niche surrounded by a dense cellular environment, which may make them less accessible to the sugar and amino acid nutrition from the body’s circulatory system. Most normal cells rely on sugar and amino acids for their energy supply with lipolysis (fat) playing only a minor role in their survival. Our results show that CSCs are metabolically unique. Like hibernating animals, they mainly rely on lipid reserves for their energy supply, and blocking a process called COPI/Arf1-mediated lipolysis can starve them to death. We also discovered that CSC-like stem cells were more sensitive than normal stem cells to Arf1 inhibition. So we think that by selectively blocking lipolysis, we may be able to kill CSCs without severe side effects. Further, targeting the COPI/Arf1 complex or the lipolysis pathway appear to be novel approaches for eliminating CSCs."

Can Behenic Acid (C22:0) Levels be a Prognostic Factor in Glial Tumors? - PubMed - NCBI
"...BACKGROUND: Inhibition of fatty acid synthase leads to apoptosis in cancers, which leads to high levels of fatty acid synthesis. This indicates that cancer cells depend on fatty acid in order to survive. In this study, we investigated whether or not there was a relationship between the glial tumor grade and free fatty acid level of tumor tissue."

Simplistically speaking baiting cancer cells with heat-damaged pufas and selenium compounds was the basis for Dr Emmanuel Revici's cancer cure. I call it non-toxic chemotherapy. The cancers went for the damaged fats which were then killed by the SE. He lived to age 101 and had very good success with the protocol. My wife used it to cure stage 2 breast cancer caused by Rx estrogen patches not properly monitored. When I asked his grand niece what he took for maintenance she said occasional use of separate zinc and selenium products. She also said he was a master of never being stressed even during extreme persecution my the medical mafia. She also said he was a junk food junkie lol.

 

[Motorneuron]

So does inhibiting FAO necessarily mean blocking lipolysis or can I continue to lose body fat? it seems to me that niacinamide works but slows down lipolysis.

Does LESS Weight Loss/Fat Loss Occur If Inhibiting Lipolysis?

If you're already at your ideal weight, inhibiting lipolysis might be only beneficial, let's say you actually need to lose a bit of weight (and don't want it to take 2 years.) In other words, does inhibiting lipolysis negatively impact fat loss/weight loss?

raypeatforum.com

@Hans

Amazing question

 

[cs3000]

Starving an animal with a tumor increases the stress hormones, providing free fatty acids and amino acids, and accelerates the tumor's growth (Sauer and Dauchy, 1987); it's impossible to "starve a tumor," by the methods often used. Preventing the excessive breakdown of protein and reducing the release of fatty acids from fat cells would probably cause many cancer cells to die, despite the availability of glucose, because of lactate's toxic effects, combined with the energy deficit caused by the respiratory defect that causes their aerobic glycolysis

ray peat: "Cancer cells use glucose and the amino acid glutamine primarily for synthetic purposes, and use fats as their energy source;the growth stimulating effect of the "essential fatty acids" (Sueyoshi and Nagao, 1962a; Holley, et al., 1974) shows that depriving a tumor of those fats retards its growth.
the great energetic inefficiency of the cancer metabolism, which causes it to produce a large amount of heat and to cause systemic stress, failure of immunity, and weight loss, is because it synthesizes fat from glucose and amino acids, and then oxidizes the fat as if it were diabetic."

https://www.jstage.jst.go.jp/article/kjm1952/11/4/11_4_223/_pdf

In their previous work Sueyoshi and Nagao(1) reported that the consumption of linoleic acid by tumor tissue is much greater than that of the normal muscle.
This is probably due to the great need of linoleic acid by the tumor tissue for its growth. Based on this suggestion, one might expect the inhibitory effect of the withdrawal of linoleic acid from the diet for the growth of the tumor.

they did not restrict starches for this study (72% starches - so ~400 human grams of carbs) , and showed adding back linseed oil / linoleic acid increased the tumor weight again (columns 3 and 4 in the image) , 400g starches daily without PUFA = 33% cancer size (column 2)
(linseed oil replacing 20% of the starch in the fat-free diet) -> In 4 days after this diet change the tumor tissue grows so fast that the tumor becomes almost as large as in group I.
^ so shows pufa especially is insane fuel for cancer where starches (glucose) are not

in vivo we get elevation of fatty acids through being at a caloric / carb deficit , which is even more fuel than the glucose being used to get the fatty acids indirectly

Effects of Linoleic Acid on the Growth and Metastasis of Two Human Breast Cancer Cell Lines in Nude Mice and the Invasive Capacity of These Cell Lines in Vitro1

by 6 weeks the MDA-MB-231-cell tumors exhibited an acceleration of growth which was enhanced by the high-LA diet. Mice fed the 12% LA diet had a higher incidence of grossly visible MDA-MB-435 cell pulmonary metastatic nodules than those fed the 2% LA diet (67% versus 33%; P < 0.02), and greater total volumes (62.0 ± 25.9 versus 24.8 ± 9.0 mm3; P < 0.02) per mouse

Linoleic acid suppresses colorectal cancer cell growth by inducing oxidant stress and mitochondrial dysfunction Linoleic acid suppresses colorectal cancer cell growth by inducing oxidant stress and mitochondrial dysfunction
^ PUFA induces mitochondrial dysfunction and oxidative stress. if u overload the cell so much this kills the cell , then pufa is killing cancer cells. and probably generating more cancer from healthier cells by the same mechanism

Linoleic acid enhances angiogenesis through suppression of angiostatin induced by plasminogen activator inhibitor 1 - British Journal of Cancer

LA did not alter cell growth in culture, but increased dietary LA-enhanced tumour growth in an animal model. Our findings suggest that dietary LA impacts multiple steps in cancer invasion and angiogenesis, and that reducing LA in the diet may help slow cancer progression.

We have previously described in vivo metastasis studies in which mice fed diets containing LA at 12% showed increased tumour incidence, frequency, and volume of tumour nodules per mouse, when compared with mice fed diets containing LA at 2.

* Five weeks after starting the mice on a diet of either 2 or 12% LA, PAI-1 serum concentration and subcutaneous tumour size were measured. LA significantly enhanced PAI-1 serum concentration (3.21±0.79 vs 7.60±1.17 ng ml−1, P<0.01) and tumour size (344.1±115 vs 1172.5±266.5 mm3, P<0.01

*** 3x faster cancer tumor growth in 12% PUFA diet vs 2% .
3x faster cancer growth in 25g of fat from PUFA for humans, vs 5g of fat from pufa daily

^ though i have seen beef tallow is harmful in vivo for cancer at 20% of caloric intake, for some reason. even though stearic acid alone has benefit.


https://www.pnas.org/doi/10.1073/pnas.1720113115

Our data support a model in which signals from the tumor microenvironment induce a circuitry of glycolysis, FA synthesis, and oxidation that confers a preferential proliferative advantage to Tregs
Recent studies have established that metabolic restrains, such as glucose restriction, impair the activities of effector T cells in the tumor microenvironment. In the same context, a huge expansion of activated Treg cells in tumor tissues has been described in mice and humans, contributing to the suppression of protective antitumor immunity

https://pubmed.ncbi.nlm.nih.gov/32882923/

Glycolysis is known as the main pathway for ATP production in cancer cells. However, in cancer cells, glucose deprivation for 24 h does not reduce ATP levels, whereas it does suppress lactate production. In this study, metabolic pathways were blocked to identify the main pathway of ATP production in pancreatic ductal adenocarcinoma (PDAC). Blocking fatty acid oxidation (FAO) decreased ATP production by 40% in cancer cells with no effect on normal cells. The effects of calorie balanced high- or low-fat diets were tested to determine whether cancer growth is modulated by fatty acids instead of calories. A low-fat diet caused a 70% decrease in pancreatic preneoplastic lesions compared with the control, whereas a high-fat diet caused a two-fold increase in preneoplastic lesions accompanied with increase of ATP production in the Kras (G12D)/Pdx1-cre PDAC model. The present results suggest that ATP production in cancer cells is dependent on FAO rather than on glycolysis, which can be a therapeutic approach by targeting cancer energy metabolism.

this stuff made me wonder about why there's been efficacy show in in keto cancer trials. Is there some mechanism overwhelming the increase in fatty acid fuel? or Maybe its simply the use of MCT oil in the keto groups which is anti-cancer?

 

[S.Holmes]