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Palmitic Acid (palmitate) Dramatically Inhibits Liver Cancer Progression

Discussion in 'Scientific Studies' started by haidut, Jun 16, 2017.

  1. haidut

    haidut Member

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    I posted a thread yesterday showing that palmitic acid is a strong inhibitor of fatty acid oxidation, perhaps more effective than established drugs like Mildronate. Palmitic acid also seems to be able to double oxidative metabolism when used in relatively low doses.
    Palmitic Acid (palmitate) Is A Fatty Acid Oxidation Inhibitor More Powerful Than Mildronate
    Palmitic Acid (palmitate) Strongly Increases Oxidative Metabolism

    Inhibitors of FAO are the next wave of drugs for cancer and diabetes, and Peat has wrote for decades about their therapeutic effects. As I posted in that other thread, the effects of palmitate on FAO are not specific to heart but also seem to extend to liver, as the study below shows. As a result, palmitate may be a viable therapeutic option for liver (and probably most other) cancers as well. As the study says, most other FAO inhibitors have pretty serious side effects and this is yet another aspect where palmitate shines due to it being devoid of such side effects.
    Perhaps the most amazing finding of the study below was the ability of palmitic acid to suppress liver cancer progression when used in a dose so low, most people working in drugs development would probably consider a homeopathic effect :) Palmitate was effective in an oral HED of just 1.5mg/kg, which is an amount easily obtainable from food sources like coconut/palm oil or from endogenous synthesis from sucrose/fructose.
    Finally, the study authors tested palmitate on other cancer types including gastric and colon and also found it to be effective.

    Saturated Free Fatty Acid Sodium Palmitate-Induced Lipoapoptosis by Targeting Glycogen Synthase Kinase-3β Activation in Human Liver Cells
    Functional lipidomics: palmitic acid impairs hepatocellular carcinoma development by modulating membrane fluidity and glucose metabolism. - PubMed - NCBI

    "...Heightened lipogenesis has been recognised as an important early hallmark of the rewired metabolism of cancerous cells.(1-2) Of all the lipogenic enzymes in the fatty acid synthesis pathway, most efforts have been focussed on pharmacologically inhibiting ACC, FASN or SREBPs to devise novel therapeutic strategies for metabolically treating and preventing cancer.(3-5) These compounds have shown significant antitumor activities with concomitant suppression of fatty acid synthesis, whereas they have also exhibited unsatisfactory pharmacokinetics or unexpected side-effects like weight loss or even target-related toxicities. Hence, there are urgent needs for the discoveries of specific lipid signatures and additional optimal therapeutic targets in cancer."

    "...Tumor-bearing mice were randomized into four groups (n=8) five days later, and each group was closely matched before treatment. The mice were treated with C16:0 (10.26 mg/kg) per day via gavage. Positive control group received 2.2 mg/kg of intraperitoneal cisplatin twice a week while negative control group received 9 g/l NaCl solution daily. Antitumor effects of C16:0 (5.13 mg/kg) in combination with cisplatin (1.1 mg/kg) on HCC were also examined. Tumor volumes were evaluated every 3 days."

    "...To explore the role of C16:0-containing GPs, we firstly performed cell proliferation experiments by treating HCC cells with C16:0 of different concentrations (0, 50, 100, 200 µM). The growth of Hep3B and 97L cells were inhibited gradually while cell proliferation of high metastatic LM3 was suppressed remarkably with C16:0 supply, in a dosage dependent manner (Fig. 2A). To exclude the lipotoxic effect of C16:0 accumulation in HCC cells, we evaluated proliferation of nontransformed hepatic cell line L02 with the same treatment condition. Interestingly, proliferation rate of L02 remained unchanged when cells exposed to C16:0 (Fig. 2A). Meanwhile, induction of oleic acid (C18:1) or stearic acid (C18:0) did not inhibit cell proliferation in LM3 cells (Supporting Fig. S2A, B), indicating selectively inhibition role of C16:0 on metastatic HCC cell growth."

    "...We further examined cell growth of colon cancer cell lines and gastric cancer cell lines to prove that the growth suppression role of C16:0 is not universal even for cancer cells. Exposure of SW480 and SW620 cells to C16:0 severely suppressed cell proliferation (Supporting Fig. S3A, B). When exposed gastric cancer cell lines (eg. AGS and BGC-823) to C16:0, cell growth were inhibited; however, the metastatic cell line HGC-27 remained unchanged (Supporting Fig. S3C-E). These experiments indicated that C16:0 exhibited varying degrees of inhibition roles in different cancer cell lines."

    "...Then we investigated the in vivo antitumor effect of C16:0 in nude mice bearing LM3 cell carcinoma xenografts. Tumor growths were observed and the macroscopic images were shown as isolated tumors (Fig. 3A). C16:0 treatment alone (10.26 mg/kg/day) or cisplatin alone (1.1 mg/kg) caused hugely suppression of tumor growth in both size and weight, while combined therapy of the two further reduced the tumor volume slightly compared to C16:0 or cisplatin alone, which statistically differed from those of their negative control (P<0.05; Fig. 3B,C)."

    "...The total number and grade of lung metastatic lesions in C16:0 treatment group was much lower than those in controls (P<0.05) (Fig. 3H). These results show the antitumor effects of C16:0 on in vivo tumor growth and metastasis of HCC xenografts."
     
  2. milk_lover

    milk_lover Member

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    This is great news, haidut! Thanks for posting those awesome studies!

    I don't like the taste of CO as it gives me weird symptoms.. But I certainly do love my juices and coke/pepsi.. which way you think is superior to provide us with enough palmitic acid, external sources or internal sources from sugar conversion to palmitic acid?
     
  3. OP
    haidut

    haidut Member

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    Well, getting palmitic acid directly is probably more effective as de-novo lipogenesis is not a major source in humans as we posted before. You need to consume 500g+ of carbs daily to start producing palmitate from carbs.
     
  4. Makaveli

    Makaveli Member

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    Are there any adverse reactions to too much palmitic acid?
     
  5. OP
    haidut

    haidut Member

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    Other than contributing to weight gain in very high amounts (50g - 60g daily) I am not aware of any bad effects.
     
  6. raypeatclips

    raypeatclips Member

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    Could these benefits be achieved by absorbing coconut oil topically as per one of your other threads?
     
  7. ecstatichamster

    ecstatichamster Member

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    I wonder if this would slow down other cancers as well.
     
  8. Mufasa

    Mufasa Member

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    Would methyl palmitate have similar effects?
     
  9. OP
    haidut

    haidut Member

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    Sure, it may work even better as it would prolong the half life.
     
  10. OP
    haidut

    haidut Member

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    Well, it worked on liver, gastric and colon cancers. In the DeFibron thread I also posted studied of positive effects on leukemia and a few other cancers. So, I don't see why it would not work on all of them as the increased FAS and FAO are common features of all cancers studied so far.
     
  11. OP
    haidut

    haidut Member

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    Yes, and given its powerful inhbition of NF-kB it may be even better than just plain palmitate.
     
  12. amaranthine

    amaranthine Member

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    @haidut your posts on palmitic acid interested me and I looked it up and found this: http://www.nature.com/nature/journal/v541/n7635/full/nature20791.html

    "Palmitic acid or a high-fat diet specifically boosts the metastatic potential of CD36+ metastasis-initiating cells in a CD36-dependent manner."

    What do you think about it? According to wiki palmitic acid is the fat with the strongest effect to cause metastasis
     
  13. OP
    haidut

    haidut Member

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    See below.
    Palmitic Acid Is Androgen Agonist, Increases Androgen Synthesis, Decreases Cortisol

    Also, something about that study is suspicious. They say that palmitic acid increased metastases in 10% of mice but when you look at the section on Materials & Methods, palmitic acid is not mentioned at all as being given to the animals. There is only discussion about high fat diet, which is about 60% PUFA.
    "...High-fat diet experiments were performed by feeding the mice with a 60/Fat Research diet (TD.06414, Harlan) for 7 days before inoculating the mice with the tumour cells and thereafter. Normal diet was used for control groups. For doxycycline treatment, mice were treated continuously with 50μg ml–1 of fresh doxycycline in light-protected drinking water that contained 5% sucrose. Glucose levels were measured once a week at a controlled time by using a glucometer (BAYER, ContourRnext)."

    So, I am not sure if the palmitic acid was even given in vivo or the effect from high fat diet was ascribed to palmitic acid blindly due to its effects on CD36+ cells. If somebody emails the authors of that study to get an answer that would be great.
     
  14. Danmcakes

    Danmcakes Member

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    Just wondering, which study are all of those paragraphs taken from? I can't seem to find it.
     
  15. DaveFoster

    DaveFoster Member

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    Fully hydrogenated coconut oil (or refined CO) both lack flavor.
     
  16. Broken man

    Broken man Member

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    Hello, I find some palmitic acid but the vendor told me that its not for oral use, that its toxic. So is palmitic acid for human use something special ? Please what I should look for?
     
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