Inhibiting Lipolysis May Treat / Cure Cancer

[Sol]

@Wagner83 Have a look at Artemisinin, it seems to be very effective especially for leukemia.

 

[haidut]

Or we can also read from Warburg himself what he also said about the connection between tumor and glucose.
And especially at the point number 8 from the link below:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2140820/pdf/519.pdf

Thank you so much for this! I think it needs to be a sticky on the forum for all the people who keep believing that starving the cancer of glucose can kill it. So, 90 years ago Warburg knew it cannot be done yet we are still hearing from medical gurus about the latest "breakthrough" treatment designed to limit glucose supply to the tumor!! Not sure how much worse can things get in mainstream medicine...
"...Different from the question of checking tumor growth is the problem of killing off tumor cells in living animals. Tumor cells obtain the oxygen necessary for respiration from the blood circulation. Consequently they can exist without glucose. Even if it were possible to remove the blood-sugar entirely in living animals, the life of the tumor would not be threatened. To support this statement, we kept tumor animals at very low blood-sugar content in insulin convulsions for hours, and then measured the metabolism of pieces of tumor so treated. We found respiration and fermentation nearly normal, a proof that the main part of the tumor cells was intact."

Hey @Wagner83 I think you asked about glucose restriction in one of these posts, so this should interest you.
Hey @charlie can we make this somehow a sticky? or maybe @Amazoniac can add it to the quotes section.

 

[charlie]

Hey @charlie can we make this somehow a sticky?

Sticky'd here in the Scientific Studies section. If anyone can think of any other way to promote it lemme know.

 

[haidut]

OK thanks, would that have to be combined with a no fat diet to be fully effective or would a low fat diet work better (as the body would not have to produce its own fats) ? Have you had acquaintances who treated themselves with the drugs you mentioned and recovered? Atm someone I know has leukemia and is undergoing chemotherapy.

I have received a few reports from people who have been declared to be in "indefinite remission" (not even sure what that means) with a combination of orlistat (mentioned in a few of the studies I posted), aspirin and niacinamide. I think one had lymphoma, another one had breast cancer, and one had prostate cancer. From what I understand, they do eat fat but just try to limit PUFA intake. With the recent studies on caprylic acid and other SFA completely destroying tumors, I think it is another confirmation that it is just the PUFA that needs to be avoided in cancer patients, not all fat. But regardless of the type of fat, orlistat would block most of the fat absorption anyways.

 

[Wagner83]

Thank you so much for this! I think it needs to be a sticky on the forum for all the people who keep believing that starving the cancer of glucose can kill it. So, 90 years ago Warburg knew it cannot be done yet we are still hearing from medical gurus about the latest "breakthrough" treatment designed to limit glucose supply to the tumor!! Not sure how much worse can things get in mainstream medicine...
"...Different from the question of checking tumor growth is the problem of killing off tumor cells in living animals. Tumor cells obtain the oxygen necessary for respiration from the blood circulation. Consequently they can exist without glucose. Even if it were possible to remove the blood-sugar entirely in living animals, the life of the tumor would not be threatened. To support this statement, we kept tumor animals at very low blood-sugar content in insulin convulsions for hours, and then measured the metabolism of pieces of tumor so treated. We found respiration and fermentation nearly normal, a proof that the main part of the tumor cells was intact."

Hey @Wagner83 I think you asked about glucose restriction in one of these posts, so this should interest you.
Hey @charlie can we make this somehow a sticky? or maybe @Amazoniac can add it to the quotes section.

Haha what a joke! Thanks.

I have received a few reports from people who have been declared to be in "indefinite remission" (not even sure what that means) with a combination of orlistat (mentioned in a few of the studies I posted), aspirin and niacinamide. I think one had lymphoma, another one had breast cancer, and one had prostate cancer. From what I understand, they do eat fat but just try to limit PUFA intake. With the recent studies on caprylic acid and other SFA completely destroying tumors, I think it is another confirmation that it is just the PUFA that needs to be avoided in cancer patients, not all fat. But regardless of the type of fat, orlistat would block most of the fat absorption anyways.

Thanks for this, now the issue is trying to convince people with very serious conditions that I, an ignorant lad, have ideas that should be tried no matter what the doc says.. The chemotherapy is done btw.

 

[Koveras]

I have received a few reports from people who have been declared to be in "indefinite remission" (not even sure what that means) with a combination of orlistat (mentioned in a few of the studies I posted), aspirin and niacinamide. I think one had lymphoma, another one had breast cancer, and one had prostate cancer. From what I understand, they do eat fat but just try to limit PUFA intake. With the recent studies on caprylic acid and other SFA completely destroying tumors, I think it is another confirmation that it is just the PUFA that needs to be avoided in cancer patients, not all fat. But regardless of the type of fat, orlistat would block most of the fat absorption anyways.

More evidence for orlistat

Orlistat Reduces Proliferation and Enhances Apoptosis in Human Pancreatic Cancer Cells (PANC-1). - PubMed - NCBI
BACKGROUND/AIM:
Pancreatic cancer is a disease with very poor prognosis, and none of currently available pharmacotherapies have proven to be efficient in this indication. The aim of this study was to analyze the expression of fatty acid synthase (FASN) gene as a potential therapeutic target in proliferating human pancreatic cancer cells (PANC-1), and verify if orlistat, originally developed as an anti-obesity drug, inhibits PANC-1 proliferation.

MATERIALS AND METHODS:
The effects of orlistat on gene expression, lipogenesis, proliferation and apoptosis was studied in PANC-1 cell culture.

RESULTS:
Expression of FASN increased during proliferation of PANC-1. Inhibition of FASN by orlistat resulted in a significant reduction of PANC-1 proliferation and enhanced apoptosis of these cells.

CONCLUSION:
This study showed, to our knowledge for the first time, that orlistat exhibits significant antitumor activity against PANC-1 cells. This implies that orlistat analogs with good oral bioavailability may find application in pharmacotherapy of pancreatic cancer.

 

[bdawg]

More evidence for orlistat

Orlistat Reduces Proliferation and Enhances Apoptosis in Human Pancreatic Cancer Cells (PANC-1). - PubMed - NCBI
BACKGROUND/AIM:
Pancreatic cancer is a disease with very poor prognosis, and none of currently available pharmacotherapies have proven to be efficient in this indication. The aim of this study was to analyze the expression of fatty acid synthase (FASN) gene as a potential therapeutic target in proliferating human pancreatic cancer cells (PANC-1), and verify if orlistat, originally developed as an anti-obesity drug, inhibits PANC-1 proliferation.

MATERIALS AND METHODS:
The effects of orlistat on gene expression, lipogenesis, proliferation and apoptosis was studied in PANC-1 cell culture.

RESULTS:
Expression of FASN increased during proliferation of PANC-1. Inhibition of FASN by orlistat resulted in a significant reduction of PANC-1 proliferation and enhanced apoptosis of these cells.

CONCLUSION:
This study showed, to our knowledge for the first time, that orlistat exhibits significant antitumor activity against PANC-1 cells. This implies that orlistat analogs with good oral bioavailability may find application in pharmacotherapy of pancreatic cancer.

I thought FASN was related to saturated fat (palmitate) synthesis

 

[Hugh Johnson]

Preliminary reports indicate that patients who were able to continue the ketogenic diet therapy for over 3 months

Holy survivorship bias, Fatman!

 

[Hugh Johnson]

I thought FASN was related to saturated fat (palmitate) synthesis

Yeah, but I would hypothesize you need to have fatty acids in the first place to desaturate them. Besides, if the cancer cell can use SFA, but not sugar, the story is consistent.

Using functional genomics, we identified stearoyl-CoA desaturase (SCD), an enzyme that controls synthesis of unsaturated fatty acids, as essential in breast and prostate cancer cells. SCD inhibition altered cellular lipid composition and impeded cell viability in the absence of exogenous lipids. SCD inhibition also altered cardiolipin composition, leading to the release of cytochrome C and induction of apoptosis. Furthermore, SCD was required for the generation of poly-unsaturated lipids in cancer cells grown in spheroid cultures, which resemble those found in tumour tissue. We also found that SCD mRNA and protein expression is elevated in human breast cancers and predicts poor survival in high-grade tumours. Finally, silencing of SCD in prostate orthografts efficiently blocked tumour growth and significantly increased animal survival.​

Inhibition of fatty acid desaturation is detrimental to cancer cell survival in metabolically compromised environments

For every human tumor line examined, except MCF7 cells, viability could be rescued by the addition of exogenous lipids (Fig. 7D). Moreover, treatment with SCD1 inhibitor phenocopied O2 deprivation in RCC10, U2S1, and HEK293 cells, which could be rescued by the addition of oleic acid (Fig. 7F). These results demonstrate that cell death under SO limitation is not specific to Tsc2−/− MEFs and confirm that desaturated lipids are a critically limiting nutrient for hypoxic cell survival in multiple human cancer cell types. We suggest that cells exposed to low O2 rely on lipids in the serum to support growth. Under tumor-like stress, many cancer cells fail to appropriately attenuate growth and proliferation via mutations in mTOR-dependent and -independent pathways and therefore exhibit cell death because they are unable to coordinate protein and lipid synthesis due to a deficiency in desaturated lipids​

Dysregulated mTORC1 renders cells critically dependent on desaturated lipids for survival under tumor-like stress

 

[GAF]

More evidence for orlistat

Orlistat Reduces Proliferation and Enhances Apoptosis in Human Pancreatic Cancer Cells (PANC-1). - PubMed - NCBI

On the right column of the page of the above 2017 study is a reference from 2005 about orlistat and breast cancer. 12 long years ago.

Pathetic, but not surprising.

 

[haidut]

On the right column of the page of the above 2017 study is a reference from 2005 about orlistat and breast cancer. 12 long years ago.

Pathetic, but not surprising.

It actually goes back at least 60 years ago. There are Russian studies from the 1950s showing beneficial effects of lipolysis and fat oxidation inhibition for infections, sepsis, and "cysts". The political biases arising from the cold war in biology (as per that famous book) made sure that no advances in medicine achieved by the enemy were assimilated into Western clinical practice after the demise of the USSR. But even in Western medicine, there are a ton of studies from the 1980s on the beneficial effects of niacinamide on tumor conditions. They just never progressed from animal studies or human case studies into clinical practice of human trials. Why would they? I think at this point you probably realize that clinical trials are nothing but a financial venture. They don't even care if the drug is better than placebo. As long as it is about 5%+ better than placebo, the FDA will approve it and money will flow. And in the case of Xarelto, the FDA approved it even after it became public knowledge that the trials were fraudulent. Needless to say, that is probably not the only fraudulent trial for a potentially lethal drug.
https://raypeatforum.com/community/...in-for-preventing-strokes-trial-halted.20293/

 

[Jackson Chung]

Haidut,

Thanks for the information. Very well researched. Slowly I've been learning more and more about Peat's ideas. My opinion is that the man is brilliant.

I've also been reading your research and again very good work.

That being said, I think it may be a good idea to combine ideas to come up with a "Protocol".

I've been in the alternative health field for about 7 years, made a lot of mistakes but I have had quite a few successes. Just wondering what your opinion of cancertutor.com is? My initial opinion is the website owner (Webster Kher) does have a lot of solid ideas.

just a disclaimer I am not a doctor and what is say is just my opinion and I am not giving medical advice...

Here is what my protocol would look like: What do you think?

1. Fat oxidation inhibition: Niacinamide 500 - 1000 mg/day. Also increases NAD+ ratio and therefore improves mitochondrial function
2. Glucose support: Vitamin B1 (inhibits glycolysis as per Peat at around 400 mg), Vitamin B2, Vitamin B6 and Biotin (unsure of the doses, but I would think your Energin supplement is enough?)
3. Lower stress hormones: Steady supply of sugar & protein (OJ, Milk)
4. Support immune system (Beta-Glucans, AHCC, mushroom based immune stimulants)
5. Lower microbial load (carrot salad, tetracyclines, etc...)
6. Support thyroid and lower estrogen: Vitamins A, D, E and K
7. Protective steroids: Progesterone, Pregnenone, Thyroid, DHEA
8. Other protective substances: Aspirin, caffeine, quinones, cascara
9. Red light and or sunlight
10. Minerals: Mg, Ca, K, Na, Cu, Zn and other trace minerals (Cr, Mn, Se). While avoiding heavy metals
11. Avoid PUFA and use saturated fats whenever possible (coconut oil, chocolate which are both anti-cancer)
12. Increase CO2 levels (bag breathing, high altitude)

 

[haidut]

Haidut,

Thanks for the information. Very well researched. Slowly I've been learning more and more about Peat's ideas. My opinion is that the man is brilliant.

I've also been reading your research and again very good work.

That being said, I think it may be a good idea to combine ideas to come up with a "Protocol".

I've been in the alternative health field for about 7 years, made a lot of mistakes but I have had quite a few successes. Just wondering what your opinion of cancertutor.com is? My initial opinion is the website owner (Webster Kher) does have a lot of solid ideas.

just a disclaimer I am not a doctor and what is say is just my opinion and I am not giving medical advice...

Here is what my protocol would look like: What do you think?

1. Fat oxidation inhibition: Niacinamide 500 - 1000 mg/day. Also increases NAD+ ratio and therefore improves mitochondrial function
2. Glucose support: Vitamin B1 (inhibits glycolysis as per Peat at around 400 mg), Vitamin B2, Vitamin B6 and Biotin (unsure of the doses, but I would think your Energin supplement is enough?)
3. Lower stress hormones: Steady supply of sugar & protein (OJ, Milk)
4. Support immune system (Beta-Glucans, AHCC, mushroom based immune stimulants)
5. Lower microbial load (carrot salad, tetracyclines, etc...)
6. Support thyroid and lower estrogen: Vitamins A, D, E and K
7. Protective steroids: Progesterone, Pregnenone, Thyroid, DHEA
8. Other protective substances: Aspirin, caffeine, quinones, cascara
9. Red light and or sunlight
10. Minerals: Mg, Ca, K, Na, Cu, Zn and other trace minerals (Cr, Mn, Se). While avoiding heavy metals
11. Avoid PUFA and use saturated fats whenever possible (coconut oil, chocolate which are both anti-cancer)
12. Increase CO2 levels (bag breathing, high altitude)

Thanks for the nice words!
I think the protocol you listed would be a great idea to have as a separate thread. So, if you want to start one and then keep editing that post as new studies come out I think a lot of people would be very grateful. It would also draw a lot of attention to that thread through Google. I would consider also adding things like cyproheptadine (for serotonin blockade) and anti-prolactin drugs like bromocriptine/lisuride. See below.
The Serotonin Receptor 5-HT2B Is Required For Cancer; Can Be Blocked
LSD-derivatives Like Bromocriptine Can Fully Cure Breast Cancer
Cyproheptadine Is An Estrogen Antagonist, May Treat Breast Cancer

In terms of blocking lipolysis, anti-adrenaline drugs like clonidine and even beta blockers may also be helpful in cases where aspirin/niacinamide are not enough on their own. Fatty acid oxidation inhibitors would be hugely beneficial. Again, aspirin and niacinamide are some of the milder ones available OTC but mentioning things like Mildronate and other clinically used drugs would be helpful as an extra choice for intractable cases. Lowering NO would also be big, and this is where arginine depletion with L-NAME would come into play, as would niacinamide and even agmatine.
I think this would be great as a start and then we can add to it as new information becomes available. The forum admins (@charlie) can even make it into a sticky or move it into the Wiki section if people think it is valuable information.

 

[Jackson Chung]

Thank you for the response Haidut. I agree that a thread should be started, however I am a bit new haha. I would not be offended if you took my "Protocol" (I'm sure you probably have something better!) and put it in a thread that is permanent. I can then respond from there.

I think what would be a great idea is to first research the mechanisms of cancer i.e. how it derives energy, evades the immune systems, replicates, etc...For each of those mechanisms I propose a therapy. From my experience a combination that is synergic works great. It would also be nice if people gave feedback on the protocol.

I understand lots of people must contact you, I would be delighted to hear of any miracles you have come across!

Also have you guys ever thought of having meet ups? I think a lot more can get accomplished that way.

 

[Wagner83]

Thanks for the nice words!
I think the protocol you listed would be a great idea to have as a separate thread. So, if you want to start one and then keep editing that post as new studies come out I think a lot of people would be very grateful. It would also draw a lot of attention to that thread through Google. I would consider also adding things like cyproheptadine (for serotonin blockade) and anti-prolactin drugs like bromocriptine/lisuride. See below.
The Serotonin Receptor 5-HT2B Is Required For Cancer; Can Be Blocked
LSD-derivatives Like Bromocriptine Can Fully Cure Breast Cancer
Cyproheptadine Is An Estrogen Antagonist, May Treat Breast Cancer

In terms of blocking lipolysis, anti-adrenaline drugs like clonidine and even beta blockers may also be helpful in cases where aspirin/niacinamide are not enough on their own. Fatty acid oxidation inhibitors would be hugely beneficial. Again, aspirin and niacinamide are some of the milder ones available OTC but mentioning things like Mildronate and other clinically used drugs would be helpful as an extra choice for intractable cases. Lowering NO would also be big, and this is where arginine depletion with L-NAME would come into play, as would niacinamide and even agmatine.
I think this would be great as a start and then we can add to it as new information becomes available. The forum admins (@charlie) can even make it into a sticky or move it into the Wiki section if people think it is valuable information.

In the past you told me two people you knew about were on ondansetron (and possibly niacinamide) and in "indefinite remission". I'm not sure about milk (goat milk?). Besides moderators and administrators, I don't think one can edit his own posts past a few hours. You said clonidine had a pretty harsh rebound effect on adrenaline so duration of treatment would probably matter too. As for aginine, wouldn't arginine restriction through diet help more? What harm can arginine do if it's very low in the diet? Wouldn't things like L-NAME increase iNOS in the long run?

 

[haidut]

In the past you told me two people you knew about were on ondansetron (and possibly niacinamide) and in "indefinite remission". I'm not sure about milk (goat milk?). Besides moderators and administrators, I don't think one can edit his own posts past a few hours. You said clonidine had a pretty harsh rebound effect on adrenaline so duration of treatment would probably matter too. As for aginine, wouldn't arginine restriction through diet help more? What harm can arginine do if it's very low in the diet? Wouldn't things like L-NAME increase iNOS in the long run?

Niacinamide is already listed but ondansetron is probably a good addition. I am just suggesting what he can do if we wants to start a section on "cancer protocol". But if he cannot edit his posts then I guess making a Wiki section would be the only option. Arginine restriction from diet is nearly impossible as it is in pretty much every protein, even gelatin. L-NAME is currently in clinical trials in Europe for cancer, and another beneficial side effect is that it lowers FAO (as do other NO inhibitors like MB and niacinamide). My goal is not to argue what is the best but simply to add pro-metabolic things to that protocol that have evidence for them, especially from human trials. I don't think iNOS will increase in from lowering NO. That is why it is called (i)nducible-NOS - i.e. it gets triggered by various agents such as endotoxin and lactic acid. So, there is no rationale to increase iNOS in a feedback mechanism as it would be akin to increasing sensitivity to a known metabolic toxin (NO) if its levels decrease. Why would that happen? The eNOS expression may increase from chronically low NO levels but I am less sure on that (maybe @Travis can shed some light). Be that as it may, for a person with cancer I'd say their last worry would be upregulating iNOS/eNOS by lowering NO. Lowering stress signals like NO is much more important for bringing them back to health.

 

[Texon]

Niacinamide is already listed but ondansetron is probably a good addition. I am just suggesting what he can do if we wants to start a section on "cancer protocol". But if he cannot edit his posts then I guess making a Wiki section would be the only option. Arginine restriction from diet is nearly impossible as it is in pretty much every protein, even gelatin. L-NAME is currently in clinical trials in Europe for cancer, and another beneficial side effect is that it lowers FAO (as do other NO inhibitors like MB and niacinamide). My goal is not to argue what is the best but simply to add pro-metabolic things to that protocol that have evidence for them, especially from human trials. I don't think iNOS will increase in from lowering NO. That is why it is called (i)nducible-NOS - i.e. it gets triggered by various agents such as endotoxin and lactic acid. So, there is no rationale to increase iNOS in a feedback mechanism as it would be akin to increasing sensitivity to a known metabolic toxin (NO) if its levels decrease. Why would that happen? The eNOS expression may increase from chronically low NO levels but I am less sure on that (maybe @Travis can shed some light). Be that as it may, for a person with cancer I'd say their last worry would be upregulating iNOS/eNOS by lowering NO. Lowering stress signals like NO is much more important for bringing them back to health.

@Jackson Chung @Wagner83 I know this is an older thread, and although this has been posted in a thread frequented by @Obi-wan, I thought it might be useful here. This is the most dramatic reversal of cancer I have ever come across particularly with respect to speed of recovery from a very advanced case.
https://www.mycancerstory.rocks

 

[Obi-wan]

@Jackson Chung @Wagner83 I know this is an older thread, and although this has been posted in a thread frequented by @Obi-wan, I thought it might be useful here. This is the most dramatic reversal of cancer I have ever come across particularly with respect to speed of recovery from a very advanced case.
https://www.mycancerstory.rocks

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"

 

[Texon]

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 wonder if it also had something to do with the rest of his supplements, one of which was a cbd oil. I also read today of a lady on his facebook group who had made good progress, but noticed some area that was lacking, so she decided to increase the Fenbenzadole to every day instead of just 3 days a week. Anyway, it sounds like you're on a great protocol.

 

[jondoeuk]

Thank you so much for this! I think it needs to be a sticky on the forum for all the people who keep believing that starving the cancer of glucose can kill it. So, 90 years ago Warburg knew it cannot be done yet we are still hearing from medical gurus about the latest "breakthrough" treatment designed to limit glucose supply to the tumor!! Not sure how much worse can things get in mainstream medicine...
"...Different from the question of checking tumor growth is the problem of killing off tumor cells in living animals. Tumor cells obtain the oxygen necessary for respiration from the blood circulation. Consequently they can exist without glucose. Even if it were possible to remove the blood-sugar entirely in living animals, the life of the tumor would not be threatened. To support this statement, we kept tumor animals at very low blood-sugar content in insulin convulsions for hours, and then measured the metabolism of pieces of tumor so treated. We found respiration and fermentation nearly normal, a proof that the main part of the tumor cells was intact."

Hey @Wagner83 I think you asked about glucose restriction in one of these posts, so this should interest you.
Hey @charlie can we make this somehow a sticky? or maybe @Amazoniac can add it to the quotes section.

We now have a few of OXPHOS inhibitors in trials [1,2] and others are at the preclinical stage [3].

Refs:
1 Abstract CT021: Phase I study of an oxidative phosphorylation inhibitor IM156 in patients with advanced solid tumors
2 https://ascopubs.org/doi/abs/10.1200/JCO.2019.37.15_suppl.3014
3 Gboxin is an oxidative phosphorylation inhibitor that targets glioblastoma