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Achilles Heel Of Cancer Found - Its Addiction To Fat

Discussion in 'Scientific Studies' started by haidut, Apr 10, 2016.

  1. haidut

    haidut Member

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    The public propaganda message has always been that cancer cells are addicted to glucose. As a result of that belief, one of the so-called "new wave" therapies in the treatment of cancer is to "starve" the cancer cells of glucose and hope that they die on their own. This usually has disastrous consequences, and accelerates cancer growth.
    As Ray has written many times, and I posted a study about that recently, cancer cells are actually addicted to fat instead of glucose.
    Cancer Cells Addicted To Fat And Use Fat Oxidation For Survival
    They are simply unable to properly metabolize glucose, similar to cells in people with diabetes. Cancer cells thrive on fat instead and will break down muscle to convert it into glucose and then convert a good portion of that glucose to fat to oxidize it. Whatever glucose they don't metabolize turns into lactic acid due to the excessively reductive environment in cancer patients.
    This study goes a step further and describes that BOTH exogenous fat supplies and endogenous (de novo) fat synthesis are absolutely crucial for the survival and growth of cancer cells. The supply of exogenous fat to cells depends largely on the enzyme endothelial lipase (LIPG) and the endogenous synthesis depends largely on the enzyme fatty acid synthase (FAS). The activity of LIPG is controlled by the gene family FoxA.
    Endothelial lipase - Wikipedia, the free encyclopedia
    Fatty acid synthase - Wikipedia, the free encyclopedia

    As a side note, I find it quite interesting that FAS apparently merges with the estrogen receptor in some cancer types, and maybe all of them. Another example of the role of estrogen in promoting and even initiating cancer.
    "...In some cancer cell lines, this protein has been found to be fused with estrogen receptor alpha (ER-alpha), in which the N-terminus of FAS is fused in-frame with the C-terminus of ER-alpha.[4]"

    Blocking one or the other enzyme retards tumor growth, while blocking both completely eliminates it - i.e. tumors cannot grow without a steady supply of fat.
    The study used doxycycline as a well-known FoxA inhibitor, so this is yet another study that shows doxycycline is well-known in scientific circles as a tumor treatment. It also describes an important pathway through which doxycycline inhbits tumor growth. In addition, the more specific fat metabolism inhibitors used in this study were C75 (inhibitor of FAS) and Orlistat (LIPG inhibitor) to completely block tumor growth. Look at Figure 5 in the study, the results are quite impressive.
    While I don't know much about C75, aspirin and niacinamide are two well known inhibitors of FAS and Peat has mentioned them before.
    Lactate vs. CO2 in wounds, sickness, and aging; the other approach to cancer
    "..."Cancer metabolism" or stress metabolism typically involves an excess of the adaptive hormones, resulting from an imbalance of the demands made on the organism and the resources available to the organism. Excessive stimulation depletes glucose and produces lactic acid, and causes cortisol to increase, causing a shift to the consumption of fat and protein rather than glucose. Increased cortisol activates the Randle effect (the inhibition of glucose oxidation by free fatty acids), accelerates the breakdown of protein into amino acids, and activates the enzyme fatty acid synthase, which produces fatty acids from amino acids and pyruvate, to be oxidized in a "futile cycle," producing heat, and increasing the liberation of ammonia from the amino acids. Ammonia suppresses respiratory, and stimulates glycolytic, activity."
    "...The enzyme, fatty acid synthase (FAS), normally active in the liver and fat cells and in the estrogen-stimulated uterus, is highly active in cancers, and its activity is an inverse indicator of prognosis. Inhibiting it can cause cancer cells to die, so the pharmaceutical industry is looking for drugs that can safely inhibit it. This enzyme is closely associated with the rate of cell proliferation, and its activity is increased by both cortisol and estrogen."
    "...Aspirin protects cells in many ways, interrupting excitotoxic processes by blocking nitric oxide and prostaglandins, and consequently it inhibits cell proliferation, and in some cases inhibits glycolysis, but the fact that it can inhibit FAS (Beynen, et al., 1982) is very important in understanding its role in cancer."

    Aspirin concentrations needed for FAS inhibition are int he range of 2mM, which is achievable by 5g-6g dose of aspirin. Emodin also inhibits FAS. This dose of aspirin matches closely Ray's statements of people with cancer taking 6g+ of aspirin daily.
    Ray Peat, PhD on Nitric Oxide – Functional Performance Systems (FPS)
    "...“Emodin inhibits the formation of nitric oxide, increases mitochondrial respiration, inhibits angiogenesis and invasiveness, inhibits fatty acid synthase (Zhang, et al., 2002), inhibits HER-2 neu and tyrosine phosphorylases (Zhang, et al., 1995, 1999), and promotes cellular differentiation in cancer cells (Zhang, et al., 1995). The anthraquinones, like other antiinflammatory substances, reduce leakage from blood vessels, but they also reduce the absorption of water from the intestine. Reduced water absorption can be seen in a slight
    shrinkage of cells in certain circumstances, and is probably related to their promotion of cellular differentiation.”
    Benefits of Aspirin – Functional Performance Systems (FPS)
    "...Salicylate has been found to be an inhibitor of fatty acid synthesis in isolated rat hepatocytes. Half-maximal inhibition of fatty acid synthesis occurs at approximately 2 mM. The inhibitory effect of salicylate on fatty acid synthesis is not relieve by the addition of acetate, suggesting that salicylate inhibits the conversion of acetate into fatty acids."


    Orlistat does not need any introduction and it is available free OTC in any store like CVS, RiteAid, Wallgreens, etc.
    Orlistat - Wikipedia, the free encyclopedia

    The study used in vivo models but does not mention anything about the in vivo doses of doxycycline, C75, or orlistat used. If someone can find that information that would be great!

    Researchers discover that breast cancer tumor growth is dependent on lipid availability
    "...In an article published in Nature Communications, the researchers report that breast cancer cells need to take up lipids from the extracellular environment in order to continue proliferating. The main protein involved in this process is LIPG, an enzyme found in the cell membrane (the layer that surrounds a cell) and without which tumour cell growth is arrested. Analyses of more than 500 clinical samples from patients with various kinds of breast tumour reveal that 85% have high levels of LIPG expression."

    "...It was already known that cancer cells require extracellular glucose to grow and that they reprogram their internal machinery to produce greater amounts of lipids (fats). The relevance of this study is that it reveals for the first time that tumour cells must import extracellular lipids to grow. "This new knowledge related to metabolism could be the Achilles heel of breast cancer," explains ICREA researcher and IRB Barcelona group leader Roger Gomis, co-leader of the study together with Joan J. Guinovart, director of IRB Barcelona and professor at the University of Barcelona. Using animal models and cancer cell cultures, the scientists have demonstrated that blocking of LIPG activity arrests tumour growth."

    Researchers Slow Breast Cancer Growth by Blocking Fat Import to Cells - Breast Cancer News
    "...Complementing their work with animal experiments, researchers also found the genes controlling the expression of the LIPG protein, FOXA1 and FOXA2. When the team removed the LIPG protein from the cells, their growth is slowed. Noting the same result when blocking FOXA, the researchers also evaluated the types of fats these cells processed when LIPG was absent. They noted that without the protein the cells could metabolize fewer fat types, again suggesting that fat import was crucial for cellular growth."

    FoxA and LIPG endothelial lipase control the uptake of extracellular lipids for breast cancer growth : Nature Communications : Nature Publishing Group
    "...To examine the molecular basis of the contribution of FoxA1 and FoxA2 to BCa growth, we engineered constitutive GFP-luciferase-expressing MCF7 and MDA231 cells with a doxycycline-inducible short-hairpin RNA (sh-RNA) vector targeting either FoxA1 or FoxA2. Doxycycline addition to the cell culture media decreased FoxA expression in both cell lines compared with control cells (ShControl (Dox+) and Sh FoxA1 or Sh FoxA2 (Dox−))(Fig. 1d), with the concomitant expression of tRFP (Supplementary Fig. 1c). Of note, there was no gain of expression of FoxA2 in FoxA1-depleted cells or vice versa (Fig. 1d). Interestingly, cancer cell proliferation was impaired in vitro upon depletion of either FoxA1 or FoxA2 in MCF7 and MDA231 cells, respectively (Supplementary Fig. 1d,e). Similarly, when Balb/c nude mice implanted with xenograft tumours from the above described cellular populations were treated with doxycycline and the short hairpins were induced, striking differences in tumour growth were observed. FoxA1-depleted MCF7 and FoxA2-depleted MDA231 tumour growth was blunted (Fig. 1e and additional controls in Supplementary Fig. 1f. Experimental details in the Supplementary Methods Section). Collectively, these observations confirm that FoxA1 or FoxA2 expression is required for BCa growth."

    "...LIPG is an endothelial lipase with phospholipase activity. It is involved in lipoprotein metabolism, and its levels have been associated with testis cancer14, 15, 16. However, to date, LIPG has not been linked to tumour growth. Robust changes in the mRNA expression of LIPG, but not BCL2 or CDH11, were confirmed by qRT-PCR (Fig. 2c). Next, we confirmed that FoxA factors regulate LIPG and its promoter activity (Fig. 2c–e)."

    "...LIPG is a phospholipase located in the cytosol and cellular membrane and has been shown to hydrolyse extracellular phospholipids from high-density lipoprotein that are afterwards incorporated into intracellular lipid species thus providing lipid precursors of cell metabolism17, 18. Thus we questioned whether LIPG regulates essential lipid intake in BCa and whether it is necessary for proliferation. To validate this hypothesis, we genetically downregulated the expression of this protein in MCF7 and MDA231 cells by means of sh-RNA (Fig. 3f and Supplementary Fig. 2c). LIPG depletion blunted BCa cell capacity to proliferate in vitro (Fig. 3f), as previously observed in FoxA-depleted cells (Supplementary Fig. 1d,e), and caused a reduction in invasion and self-renewal properties (Supplementary Fig. 3a–d). Similarly, LIPG-depleted cells were unable to grow tumours in vivo (Fig. 3g)."

    "...Collectively, these results suggest that LIPG shapes lipid metabolism in BCa cells to support cellular growth requirements. Interestingly, FoxA depletion in both MCF7 and MDA231 cells led to a lipid metabolic reprograming similar to LIPG depletion (Supplementary Fig. 4c–e)."

    "...Furthermore, gene expression analysis confirmed FoxA depletion and LIPG expression in the tumour populations at the end point of the tumour growth experiment and the rescue was also confirmed in cell culture (Supplementary Fig. 5b,c). Overall, these results suggest that BCa growth requires exogenous lipid precursors and that these are provided, in part, by LIPG activity."

    "...As previous reports showed that de novo lipid metabolism is necessary for BCa growth3, 22, we next questioned whether this lipid synthesis was sufficient or, instead, whether exogenous sources are also required to support BCa cell growth and proliferation, as suggested by our experimental data. To this end, we inhibited the activity of fatty acid synthase (FAS) in BCa cells by means of the chemical inhibitor C75 (ref. 23). FAS activity is crucial for de novo lipid synthesis in cancer cells3, 22. To test the complementarity of both de novo and/or exogenous lipid supplies, we used a C75 concentration causing a 50% reduction in BCa cell growth in vitro 48h post incubation (Fig. 5d and Supplementary Fig. 5d). Similarly, we tested the contribution of LIPG inhibition by means of treatment with a lipase inhibitor, Orlistat21. A specific dose causing a 50% reduction in the growth of each BCa cell line was further used (Fig. 5d and Supplementary Fig. 5d). Interestingly, concomitant treatment with FAS and LIPG inhibitors caused an additive effect, blunting BCa cell growth (Fig. 5d). Next, we evaluated whether LIPG activity was sufficient to rescue the chemical inhibition of FAS. To this end, we overexpressed WT and inactive LIPG and grew MCF7 and MDA231 cells in the presence or absence of a high dose of C75 (20mgml−1), which blocks cell growth (Supplementary Fig. 5d). Complete blockade of FAS was not rescued by LIPG (Fig. 5e). Collectively, our results suggest that both exogenous lipid precursors provided by means of LIPG activity and de novo lipid synthesis mediated by FAS are necessary for BCa cell growth."

    "...In this context, a high-fat diet was shown to rescue the absence of a critical intracellular lipase, Monoacylglycerol lipase, for cancer pathogenesis given cancer cells ability to uptake lipids from the extracellular compartment was functional19. Herein, we showed that this rescue mechanism is not functional in BCa cells in the absence of FoxA2 or LIPG. In support of this notion, it is worth noting that extracellular LIPG activity releases fatty acids from high-density lipoprotein phospholipids and these acids are further employed for intracellular lipid production in the human hepatic cell line HepG2 (refs 28, 29)"

    "...In conclusion, BCa cells are dependent on a mechanism to supply precursors derived from extracellular sources for intracellular lipid production, and LIPG fulfills this function. Therefore, LIPG stands out as an important component of the lipid metabolic adaptations that BCa cells, and not normal tissue, must undergo to support high proliferation rates. Our results also suggest that de novo lipid synthesis is necessary but not sufficient to support lipid production for BCa tumour growth. Accordingly, recent clinical studies demonstrate the association between lipids and lipoproteins in circulation and risk of BCa in women with extensive mammographic density. This observation implies that interventions aimed to reduce them may have effect on BCa risk30. All together, these observations make LIPG activity an Achilles heel of luminal and, more importantly, of triple negative/basal-like breast tumours, for which limited therapeutic options are currently available."
     
  2. Nighteyes

    Nighteyes Member

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    Very interesting set of studies - thanks you for that.
     
  3. mhm

    mhm Member

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    Georgi, might this explain (at least in part) the anti-cancer virtues of fasting in your opinion?
     
  4. DrJ

    DrJ Member

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    Sorry if dumb question, but how does a receptor merge with another receptor? Does it have to do that they are just watching something like a 'macro' effect and theorize a receptor model in some 'black box' beyond the observation capabilities of their instruments, and conclude the effects of a supposed set of receptors is becoming the same? Is there some physical/chemical basis for explaining merging receptors? Is there some root paper explaining receptor theory? I can't seem to find how this all got started, but the talk of receptors is in all modern research I attempt to read...
     
  5. OP
    haidut

    haidut Member

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    I think the short term beneficial effects of fasting on cancer are likely due to that effect - i.e. lowering fat contents of cells, considering most of that fat is PUFA. But chronically fasting will elevate cortisol, which not only destroys your muscle mass but also promotes FAS. So, people who diet usually lose mostly water and muscle mass and end up worse then they are, even without having cancer. Fasting chronically leads to cachexa in cancer patients much earlier than it would have occurred at normal calorie intake.
     
  6. OP
    haidut

    haidut Member

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    You bring up some very good points. I am also not aware of any root study explaining the receptors. If you find such an artifact please do post here as so many people would be interested in reading it.
    As far as the merging part - given that a receptor is simply a protein inside the cell, proteins can merge with other proteins quite easily and make larger proteins (peptides). The implication of the FAS merging with ER is that both promote each other's activity, so a FAS+ER super-receptor would probably make the cell even more prone to fat synthesis and growth.
     
  7. PakPik

    PakPik Member

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    Yet another way PUFAs are excellent tumor promoters. Some researchers found PUFAs, but not SFAs, are positively correlated to plasma Endothelial Lipase. Same thing for the PUFA/SFA ratio, the higher, the more Endothelial Lipase:

    Paradoxical association between total dietary PUFA intake and plasma endothelial lipase protein levels in humans
    Paulo Bispo, Pedro O. Rodrigues, Narcisa M. Bandarra, Firmina Lebre and Augusta Marques

    Background: Although a large number of epidemiological and clinical studies have consistently showed that the substitution of dietary SFA by PUFA contributed for decrease CVD risk, e.g. by lowering LDL-c and/or TAG blood levels, a reduction on HDL-c is also commonly observed. Furthermore, well defined molecular mechanisms can help to explain the role of PUFA on ApoBrich lipoproteins metabolism. The lowering of HDL-c levels observed in some studies, are less well understood.

    Methods: The sample population represented by 81 consecutive walk-in adults from both genders. Blood was sampled after an overnight fast and analyzed for glucose, triacylglycerols (TAG), total cholesterol (Total-c), HDL-c, ApoA1, Apo B or hs-CRP. Endothelial lipase (EL) (n=57), and insulin by mELISA. Dietary intake was obtained by face-to-face interviews using a semi-quantitative food frequency questionnaire, validated for the Portuguese population. Descriptive, bivariate and partial correlations were determined.
    Results: By bivariate analysis, the PUFA/SFA ratio showed a negative correlation with the HDL-c levels (p< 0.05) and, although in the borderline of statistical significance, with Total-c and HDLc/ApoA1 ratio. In addition, the PUFA/SFA ratio correlated positively with fasting insulin levels (p<0.05). Total dietary PUFA and the PUFA/SFA ratio correlated positively with the plasma endothelial lipase (EL) levels (p< 0.05), that remained significant after multi-adjust for age, BMI, total fat and carbohydrates in diet, alcohol consumption, fasting insulin or hs-CRP levels.

    Conclusions: Total dietary PUFA, but not SFA, positively associated with plasma EL mass, put forward a putative mechanism by which PUFA may contribute for lowering HDL-c levels in humans. Additionally, the PUFA Vs.SFA showed opposite associations with the HDL-c/ApoA1 ratio, a proxy of HDL particles size and composition.
     
  8. Philomath

    Philomath Member

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    Obesity induced rapid melanoma progression is reversed by orlistat treatment and dietary intervention: Role of adipokines
    http://www.moloncol.org/article/S1574-7891(14)00282-8/pdf

    "...Obese mice were administered orally with orlistat (10 mg/kg on every alternate day)
    which would be roughly .71mg/kg or 60mg for an 80kg person- if my conversion math is correct. (((mouse_dose) * 3) / 42)


    "...Orlistat treatment decreased not only body weight (Figure 2Aa and Ba) but also tumor progression, in terms of volume and weight, in both the HFD models as compared to untreated counter parts (Figure 2Abec and Bbec). Further to assess the impact of controlling diet on melanoma progression in obese mice, HFD mice were shifted from high fat to normal chow. Consistent with findings in orlistat treated HFD mice, switch from high fat diet to normal diet led to normalization of body weight and serum chemistry profile in par with that of ND mice which was accompanied by decreased tumor volume and weight (Table 1; Figure 2Aaec). Also, fat mass of these mice was reduced significantly as compared to the control group (Supplementary Figure 2Ab). Interestingly, the normalization in obese parameters and reduction in tumor parameters were much more effective and pronounced when dietary intervention was combined with orlistat treatment"
     
  9. OP
    haidut

    haidut Member

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    Thanks a lot! The conversion is correct and this is pretty good news as that dose of orlistat is easily achievable with OTC supplements sold in many drug stores in the USA.
     
  10. tyw

    tyw Member

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    As far as I'm concerned, receptors are simply sites on an interface (eg: cell membrane) which can be modulated by electromagnetic activity. eg: a specific set of proteins / lipids / lipoproteins which have a specific E/M resonance, and which can have energy given to or subtracted from them.

    In normal conditions, this energetic exchange must happen through specific carrier molecules. A hormone would be nothing but a specific type of molecule with a specific set of proteins that can interact in a specific way with the receptor proteins on a cell membrane.

    "Merging" of receptors (which is all detected by fluorescence -- ie: the E/M force) is then nothing more than a conformational degradation in the structure of the receptor, which will cause it to be able to uptake signals from compounds other than the specific compounds that it was originally meant to interact with.

    "Estrogenic" really just means: Able to interact electromagnetically with the proteins responsible for the observed "estrogen cascade effect" .

    In Breast Cancer cells, we find that 50Hz fields will directly result in sensitivity to "estrogenic resonance", and lack of sensitivity to "anti-estrogenic compounds" like melatonin:

    - Signal transduction of the melatonin receptor MT1 is disrupted in breast cancer cells by electromagnetic fields. - PubMed - NCBI
    - Electromagnetic fields alter the expression of estrogen receptor cofactors in breast cancer cells. - PubMed - NCBI

    Obviously we are dealing with receptors here, and at the low field intensities used, it is not likely that the change in the receptors is due to a direct energetic insult. Instead, changes in receptor structure must be due to fundamental signalling resonances brought about by 50Hz ELF-EMF exposure.

    But the E/M force is very specific. No effect on Toll-like receptors with similar frequencies -- Extremely low frequency electromagnetic field exposure does not modulate toll-like receptor signaling in human peripheral blood mononuclear cells

    But some very key systems are affected -- http://www.hindawi.com/journals/bmri/2015/237183/

    We found that genome-wide methylation in GC-2 cells decreased at magnetic intensity of 1 mT and increased at 3 mT exposure to 50 Hz ELF-EMF compared with the control. Taken together, these data suggest that DNA hypomethylation may be an important epigenetic event in the process of 50 Hz ELF-EMF exposure on GC-2 cells. Although our results need to be confirmed in animal and human study, it appears that there is a direct relationship between DNA hypomethylation and 50 Hz ELF-EMF exposure

    And systemic effects can be hugely complex -- An Approach to Induction of Heat Shock Proteins by Electromagnetic Wave-Activated Transient Receptor Potential Channels in Living Cells | Ito | Journal of Biochemistry and Molecular Biology Research

    upload_2016-6-16_7-51-44.png



    Therefore, even if we know how and where the E/M force affects receptor activity, we will still be a long way off from actually being able to monitor it is real-time, and even less so to be able to have specific measures to affect it.

    We are down to avoidance of non-native E/M fields as much as possible, and maintenance of good cellular signalling (which is directly tied to metabolism -- http://www.basic.northwestern.edu/g-buehler/cellint0.htm), so that cells only choose to respond to the correct / body-native signals.

    .....
     
  11. Mjhl85

    Mjhl85 Member

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    Yea good luck with that avoidance in 2016
     
  12. tyw

    tyw Member

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    It is very possible ;)

    - Basic stuff like not using WiFi (ethernet instead) will cut down your exposure from the 3+ mW/cm^2 range to <0.5mW/cm^2 (at least from your computer).
    - Locating your office and sleep space as far away from emitters like your refrigerator or what not is completely possible.
    - Using a wired headset with microscope for your cellphone calls cuts the EMF exposure to the head region by a huge amount.

    The E/M force drops off exponentially with distance, so it is definitely possible to avoid at least the most potent of exposure. We're talking "definitely harmful" levels 3 feet away from an emitter, to "very low levels" at 10 feet away.

    If you live in a big city, obviously the risk is much higher -- eg: your neighbours WiFi router could be next to your bedroom. Their smartmeter may emit into your living room, etc .... In those situations, avoidance is harder but still doable if you are pedantic about taking an EMF meter and measuring hotspots and safe spots in your living space, and then keep activity to those regions. Office spaces are obviously horrible.

    Obviously, if you're really extreme, head out to the country side away from any cell towers and power lines.

    Has this been a major impact on human health over the last 4 to 5 decades? IMO, yes. Dr Robert Becker would not be happy .....

    ......
     
  13. XPlus

    XPlus Member

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    Ray also said that cancer cells thrive on lactic acid - or was that just in reference to their ideal environment.
     
  14. paymanz

    paymanz Member

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  15. Mjhl85

    Mjhl85 Member

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    Yea apartment living is for the rats! add to that, city aprtmentss. But some of us can't afford anything but, so avoidance at a good level is extremely difficult.
     
  16. Liubo

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  17. OP
    haidut

    haidut Member

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    So, it is high manganese and low iron that contributes to the extreme resilience of the bacteria to radiation. Not genes (surprise, surprise). Interestingly, the recent study about the beneficial effects of Claritin on Lyme disease seem to depend on the same mechanism - Claritin depleted magnanese in the pathogen and this is how it kills it.
    https://raypeatforum.com/community/threads/claritin-for-lyme-disease.5881/#post-214822
    So, manganese seems vital for proper functioning of living organisms and manganese depletion may be a viable anti-bacterial approach while manganese loading may be a viable approach to radiation protection. The beneficial effects of low iron are well known in regards to radiation, so nothing new there.
     
  18. Mito

    Mito Member

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    Manganese is an important cofactor for the enzyme superoxide dismutase (SOD) in the mitochondria. SOD converts superoxide to hydrogen peroxide which can potentially be converted to water. Could this also be the case for bacteria so that a manganese deficiency causes a build up of superoxide in the mitochondria that kills the bacteria?
     
  19. kayumochi

    kayumochi Member

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  20. OP
    haidut

    haidut Member

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    Yes, very possible. This would also suggest that manganese supplementation may not be very good for people with cancer as it would increase anti-oxidant status. There is at least one study that found just that.
    Cell Death and Disease - Manganese superoxide dismutase promotes anoikis resistance and tumor metastasis
    "...Taken together with our previous finding that detached cells evade excessive ROS production by attenuating oxidative metabolism of glucose, we conclude that mammary epithelial cells coordinate their responses to detachment through increasing MnSOD and decreasing ROS generation from mitochondrial glucose oxidation, thereby mitigating anoikis. Anoikis is a barrier to tumor metastasis. Indeed, MnSOD expression is elevated in human breast cancer metastases compared with primary tumors. Expression of MnSOD correlates with histologic tumor grades in human cancer and contributes to cancer cell’s resistance to anoikis. Our study suggests that inhibition of ROS detoxification coupled with stimulation of glucose oxidative metabolism may be an efficient strategy to enhance anoikis and block metastasis."
     
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