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Inhibiting Lipolysis May Treat / Cure Cancer

Discussion in 'Scientific Studies' started by haidut, Jul 1, 2017.

  1. haidut

    haidut Member

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    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."
     
  2. Marg

    Marg Member

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    Haidut, thanks for all your prolific research in gathering all this incredible knowledge.

    And thanks to Charlie for all the work done presenting this forum platform database, as well as the moderators.
     
  3. johnwester130

    johnwester130 Member

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    so vitamin b1 and niacinamide are the best options for this ?
     
  4. Wagner83

    Wagner83 Member

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    Ketogenic diets as an adjuvant cancer therapy: History and potential mechanism

    A Nutritional Perspective of Ketogenic Diet in Cancer: A Narrative Review. - PubMed - NCBI
    Ketogenic diets: from cancer to mitochondrial diseases and beyond
    [...]
    Ketogenic Diets as Anticancer Approaches

    The modulation of cellular metabolism by carbohydrate depletion via ketogenic diets has been suggested as an important therapeutic strategy to selectively kill cancer cells. One hallmark of nearly all cancer cells is the anomalous metabolic phenotype first described by Otto Warburg [31], which is characterized by a metabolic shift from respiration towards glycolysis, regardless of oxygen availability. In the majority of normal cells with functional mitochondria, pyruvate generated via glycolysis is shuttled to the tricarboxylic acid (TCA) cycle for mitochondrial oxidative metabolism. Cancer cells, on the other hand, use pyruvate mostly in the lactic acid fermentation pathway (Fig. 2). This metabolic phenotype provides several advantages to cancer cells. First, it allows for a more efficient generation of carbon equivalents for macromolecular synthesis than oxidative phosphorylation (OXPHOS), which is suitable for a proliferative phenotype [32]. Second, it bypasses mitochondrial oxidative metabolism and its concurrent production of reactive oxygen species (ROS). This confers a survival advantage since cancer cells display higher steady-state levels of oxidative stress relative to normal cells, which renders them more sensitive to ROS-mediated apoptotic stimuli [33]. Finally, an elevated glycolytic flux promotes acidification of the tumour site, which facilitates tumour invasion and progression [34].
    [...]
    Not Always Good: The Risks of Ketogenic Diets
    Although very helpful in a variety of pathologies, ketogenic diets also have short- and long-term adverse effects, which are easily distinguishable. Short-term side effects include gastro intestinal problems, such as gastro-oesophageal reflux and constipation, acidosis [19], hypoglycaemia [125], dehydration, and lethargy [126]. This group of effects are normally transient and easily managed [127]. On the other hand, long-term side effects include hyperlipidaemia (although with some controversy [6, 7]), hypercholesterolaemia [19], nephrolithiasis [128] and cardiomyopathy [129] (Fig. 5). According to a review of 27 papers describing the adverse effects of the ketogenic diet [130], vomiting and increased serum lipid levels seem to be the most common. In a study including 52 epileptic children treated with the classic ketogenic diet, five patients experienced serious adverse effects [131].

    What do you think about those @haidut and the so called "warburg effect"?
     
  5. Regina

    Regina Member

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    :darts:
     
  6. dookie

    dookie Member

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    @Wagner83

    Cortisol can do some amazing anti-inflammatory things in the short-run. In the long run, it doesn't only catabolize the tumor, but also the skin, muscles, brain, thymus, etc.
     
  7. rmgwm

    rmgwm Member

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    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.
     
  8. jb116

    jb116 Member

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    This idea of fat or even sugar "growing cancer" is constantly misunderstood. It's not about these things growing cancer as if they are direct fertilizers or something like that. The implicit context is "under a deranged metabolism, cancer ultimately subsists on fats." This in no way implies never eat fats or sugar. This is a reminder to keep metabolism up; to keep it healthy. It could also mean, looking at the bigger picture, steer clear of unhealthy fats, maintain good nutrient intake, and be predominantly in oxidative metabolism. This all also implicates that if you happen to find yourself in this unfortunate situation, with this knowledge, one knows to perhaps keep fats to a minimum, no matter the type in order to get out of the deranged metabolism and therefore, hopefully, out of sickness.
     
  9. Wilfrid

    Wilfrid Member

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  10. Xisca

    Xisca Member

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    I have read several times that it could be better to be either high fat or high sugar, but not in the intermediate!

    i would dream we could be an optimised "car" going easily from petrol to gazoil to petrol again....
    going from sugar to fat without using anaerobic glycolisis... and worse, never stay between the 2 in aerobic glycolisis...



    Very good post!
    I fully believe all you said.
     
  11. Xisca

    Xisca Member

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    Winter kills a lot of bug in the garden, but not in the tropics. Some cold is useful sometimes. Thus, i mean alternate states.

    Could it be good to run on sugars most of the time, plus have a winter season burning fat?
    Going from high one diet to high other diet?

    I can relate this to high acid stomach followed by high alkaline duodenum! The middle path does not seem good for everything...

    And in the nervous system, it is all about being able to fluidly pass from one state to another instead of being stuck in one, like activation of the sympathic system.
     
  12. James IV

    James IV Member

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    The only "natural" way to stop lipolysis would be to constantly eat carbohydrate 24 hours a day and never be in a caloric deficit.
     
  13. Vinero

    Vinero Member

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    Vitamin E also lowers free fatty acids.
    "Besides antagonizing some of the end effects of the toxic fatty acids, vitamin E inhibits lipolysis, lowering the concentration of free fatty acids (the opposite of estrogen’s effect), and it also binds to, and inactivates, free fatty acids."
     
  14. Nokoni

    Nokoni Member

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    Yeah but nothing kicks FFA like niacinamide. Put 1/4 tsp in palm, dampen other hand, rub hands together, spread on skin. If you're rockin' lots of FFA, you're about to get HUNGRY. It's actually a good test for high FFA levels.

    Wife doing low-carb, sees me applying. Is that good, can I try? Sure, here you go. Oh BTW, it might make you hungry (chuckles quietly to self). She comes home from work, man that hunger was PAINFUL. Lol. Good times :)
     
  15. lollipop

    lollipop Guest

    Veeerrryy interesting @Don. Now I want to try :):
     
  16. Nokoni

    Nokoni Member

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    Highly recommended. Just have a sandwich and a coke standing by :)
     
  17. OP
    haidut

    haidut Member

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    Starving the cancer of sugar is not a new idea. It has been tried over and over again over the last 5 decades. There is even a special chemical they use - 2-deoxy-glucose (2-DG).
    2-Deoxy-D-glucose - Wikipedia
    "...2-DG is uptaken by the glucose transporters of the cell. Therefore, cells with higher glucose uptake, for example tumor cells, have also a higher uptake of 2-DG. Since 2-DG hampers cell growth, its use as a tumor therapeutic has been suggested, and in fact, 2-DG is in clinical trials [3] A recent clinical trial showed 2-DG can be tolerated at a dose of 63 mg/kg/day, however the observed cardiac side-effects (prolongation of the Q-T interval) at this dose and the fact that a majority of patients' (66%) cancer progressed casts doubt on the feasibility of this reagent for further clinical use.[4] However, it is not completely clear how 2-DG inhibits cell growth. The fact that glycolysis is inhibited by 2-DG, seems not to be sufficient to explain why 2-DG treated cells stop growing [5]"

    As you can see from the Wiki article and the referenced studies, 2-DG is ineffective and is cardiotoxic. It is not a bad idea as it targets cancer metabolism and not genes, but you can't fool the cancer by providing a non-metabolizable glucose analog. The cancer will simply adapt and then upregulate cortisol production to consume muscle and skin and convert them into glucose through gluconeogenesis. Most people with advanced cancer have something called "ectopic Cushing syndrome" which is how the tumor increases cortisol production to consume tissues.
    So far, inhibiting fat availability does not seem to lead to anything bad because the tumor cells are so reliant on fat they quickly die when fat supply is cut off. Cancer is NOT addicted to sugar it is addicted to fat. It simply wastes sugar through glycolysis to generate lactic acid which is the most potent endogenous angiogenesis promoter (VEGF) and thus helps tumor vascularization for growth. And then whatever sugar does enter the Krebs cycle get shunted into fat synthesis through upregulating the enzyme citrate synthase.
    Enhanced citrate synthase activity in human pancreatic cancer. - PubMed - NCBI
    "...RESULTS: The average of citrate synthase activity in human pancreatic ductal carcinoma is significantly higher comparing with adjacent nonneoplastic tissue: 40.2 +/- 27.2 and 18.3 +/- 13.6 nmole/min/mg protein, respectively (P = 0.001). The lactate dehydrogenase and glucose 6-phosphate dehydrogenase activity in human pancreatic ductal carcinoma were also higher than in adjacent nonneoplastic tissues. CONCLUSION: It is likely that enhanced citrate synthase activity contributes to the conversion of glucose to lipids in pancreatic cancer providing substrate for membrane lipids synthesis."

    Activating PDH (and/or inhibiting PDK) to reduce lactic acid production, and inhibiting the enzyme fatty acid synthase (FAS) (and/or fatty acid transport/oxidation, or lipolysis) quickly regresses even the most aggressive cancers. Thiamine, biotin, DCA, thyroid and methylene blue can do the former pretty well and drugs like aspirin (FAS inhibitor, lipolysis inhibitor, FAO inhibitor), Mildronate (carnitine synthesis inhibitor, FAO inhibitor), quinones (FAS inhibitors), niacinamide (lipolysis inhibitor), orlistat (FAS inhibitor) can do the latter. Obviously, a combination of the above therapies would be even more effective and adding something like a serotonin antagonist may even initiate spontaneous regression as the tumor is highly sensitive to signals that excessive growth is no longer needed. The anti-serotonin drugs are one such signal.
     
  18. dfspcc20

    dfspcc20 Member

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    Can confirm. Little bit of niacinamide mixed in water splashed on the face makes my skin feel amazingly smooth. I've never been one to get cravings, but doing this makes me crave sugary fruit almost immediately. Guess that means my FFA is usually high, esp in the mornings.
     
  19. Nokoni

    Nokoni Member

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    I've noticed that adding a roughly equal amount of thiamine to the niacinamide enhances the effect, and, from Haidut's post above yours, now I know why. The thiamine is slightly sticky so after it has dried on my skin I come back with a bit more water and go over the same areas to get further penetration and make it less sticky. Also, I tried mixing with vodka (ethanol and water) but didn't notice any increase in the effect so I went back to water because it's so easy.

    And it really does make the skin nice.
     
  20. Wagner83

    Wagner83 Member

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    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.
     
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