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Cheap, safe drug kills most cancers

Cheap, safe drug kills most cancers

New Scientist has received an unprecedented amount of interest in this story from readers. If you would like up-to-date information on any plans for clinical trials of DCA in patients with cancer, or would like to donate towards a fund for such trials, please visit the site set up by the University of Alberta and the Alberta Cancer Board. We will also follow events closely and will report any progress as it happens.

It sounds almost too good to be true: a cheap and simple drug that kills almost all cancers by switching off their “immortality”. The drug, dichloroacetate (DCA), has already been used for years to treat rare metabolic disorders and so is known to be relatively safe.

It also has no patent, meaning it could be manufactured for a fraction of the cost of newly developed drugs.

Evangelos Michelakis of the University of Alberta in Edmonton, Canada, and his colleagues tested DCA on human cells cultured outside the body and found that it killed lung, breast and brain cancer cells, but not healthy cells. Tumours in rats deliberately infected with human cancer also shrank drastically when they were fed DCA-laced water for several weeks.

DCA attacks a unique feature of cancer cells: the fact that they make their energy throughout the main body of the cell, rather than in distinct organelles called mitochondria. This process, called glycolysis, is inefficient and uses up vast amounts of sugar.

Until now it had been assumed that cancer cells used glycolysis because their mitochondria were irreparably damaged. However, Michelakis’s experiments prove this is not the case, because DCA reawakened the mitochondria in cancer cells. The cells then withered and died (Cancer Cell, DOI: 10.1016/j.ccr.2006.10.020).

Read the rest of the article at the link above.

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62 Responses to Cheap, safe drug kills most cancers

  1. Awesome news. I have some relatives suffering from cancer that I’ll pass this onto.

  2. This is terrific! Let’s pray that it isn’t just a false hope.

  3. I encourage everyone to submit this to the Drudge Report to increase public awareness:

    Cancer Cure

    http://www.newscientist.com/ch.....ncers.html

    You can submit news tips to the Drudge Report on the lower right of their homepage in the tip submission box. If enough people tip them off they report on it.

  4. Please God, let it be so.

  5. I’m sort of in awe. I didn’t think I’d live to see the day, and now I really hope I will.

    Now I just hope a Parkinson’s cure is imminent.

  6. Didn’t Wells or some other ID bigshot suggest this a while back? As I recall he suggested it as ID inspired research saying that it would see all parts of the cell as a designed whole rather than chance mutations strung together by evolution.

  7. Interesting finding here:

    http://www.wipo.int/pctdb/en/i.....LAY=STATUS

    The Canadian discoverers on 11/04/06 applied for a patent on the treatment protocol.

    Update: This was an international application. The U.S. application was filed on 11/04/05 but isn’t published. There’s a stink emerging from this. The international patent application was filed exactly one year later because there’s a grace period of one year from date of disclosure to international filing. There is no grace period from disclosure to filing in the U.S. The stink is that this research was kept hushed up from at least November 2005 when the U.S. patent was filed to just recently when it went public.

  8. DCAa causes liver cancer in rats and nerve and heart damage. I wonder whether it will lead to substancial increases in the rate of aging also. If one is dying of cancer, it will be a price worth paying.

    “Based upon the pathologic examination, DCA induced observable signs of toxicity in the nervous system, liver and myocardium. However, treatment related neoplastic lesions were observed only in the liver.”

  9. idnet

    Those side effects haven’t been reported in humans at therapeutic doses except for some neuropathy (pain, numbness) in a MELAS clinical study. DCA is metabolized to oxalate (a nerve toxin) and in the presence of adequate thiamine (vitamin B1) to other metabolites. Thiamine stores are rapidly depleted and the metabolism of oxalate slows down. Co-administration of thiamine supplements drastically lowers the oxalate build-up.

    Toxicological Sciences 14: 327–37, 1990 via http://www.lewrockwell.com/sardi/sardi68.html

  10. Hey, can DCA halt materialistic naturalism? That is the cancer of society… ;)

    I have also wondered what effect “dual action cleanse” would have on evolutionists. My guess is that is that they are so FoS that they will just disappear…

  11. From memory, the scientist who first suggested DCA, did so in the 30′s. They said he didn’t know what he was talking about.

    Evolutionists say that the reason kids should be taught Darwinism is so that cures can be found in the lab. Well, how many cures HAVEN’T been found because of this nonsense theory? How many lives could have been spared if the scientific community had listened in the 1930′s?

  12. Kevin Trudeau (“Natural Cures” fame) talks about how (some) cancers cannot surivive in an oxygen-rich environment. And that is the reasoning behind intravenous peroxide drips.

    However not enough money can be made by employing that method so it’s not popular in the USA.

  13. The study you are all getting so excited about was done on isolated cell lines (cultures). To extrapolate from a study such as that to treating cancer in human beings is too big a jump and very dangerous. Dichloracetate (DCA) and other haloacetates are toxic chemicals affecting all types of cells, not just cancerous ones. The authors of the recent article, have published last year another article in which they have shown the DCA relieves hypertension by inducing apoptosis (cell death) in normal vascular cells by the same mechanism that kills cancerous cells. Clearly, DCA is not as selective as the authors make it to be, based on their own previous findings to the contrary.

  14. Personally I’ve always been of the opinion that there needs to be a “Bletchley Park” for DNA. Gather as many mathematicians, engineers, and biologists as you can and sick them on the problem of “decoding” DNA. After all, if we truly understood how everything worked millions of lives could be saved…never mind all the possible tech implementations.

  15. Glycolysis produces lactate and if cancerous cells are using mainly glycolysis for energy then there should be elevated levels of lactate in the blood of cancer patients.

    As far as I know high lactate levels are not associated with cancer. It may be that the number of cells affected are too small that they cannot affect blood lactate levels to any substantial amount.

  16. SRivlin

    The study you are all getting so excited about was done on isolated cell lines (cultures). To extrapolate from a study such as that to treating cancer in human beings is too big a jump and very dangerous.

    It was also done on rats infected with human cancers.

    Dichloracetate (DCA) and other haloacetates are toxic chemicals affecting all types of cells, not just cancerous ones.

    Most things are toxic. The LD50 of DCA is 2500-5000mg/kg. The therapeutic dose is 25-100mg/kg. DCA is more toxic than aspirin but not a whole lot more. It has been used for many years to treat a variety of illnesses.

    The authors of the recent article, have published last year another article in which they have shown the DCA relieves hypertension by inducing apoptosis (cell death) in normal vascular cells by the same mechanism that kills cancerous cells. Clearly, DCA is not as selective as the authors make it to be, based on their own previous findings to the contrary.

    Got link?

  17. jerry

    From eMedicine:

    [Lactic acidosis] Type B1 occurs in association with systemic disease such as renal and hepatic failure, diabetes, and malignancy

  18. Dave,

    Glycolysis produces lactate. Excess glycolysis would produce higher than normal levels of lactate and is usually associated with impaired aerobic metabolism except for intensive exercise when the aerobic system is not impaired but is starting to approach maximum. So I was speculating that if this glycolysis was wide spread it would show up as lactate in the blood because excessive lactate has no place to go but the blood stream. I was surprised by the reference to glycolysis since my work requires and understanding of energy metabolism. There are a couple references to higher lactate levels and cancer in google but not a lot. Lactate is easy to measure and it would seem to be a good marker for cancer but it is not currently used as such.

    The interesting thing is that the aerobic metabolism of the cell is not impaired since it comes back when the drug is administered acording to your write up.

    So what causes the glycolysis to proceed at high rates when normally the cell will choose mainly aerobic metabolism using fats as an energy source at low metabolic requirements. I was curious. And what caused the drug to reverse the trend.

    A lot of people will kill for anything that inhibits glycolysis. That is what the blood doping in sports like cycling and distance running is all about.

  19. So what causes the glycolysis to proceed at high rates

    According to the article the mitochondria in cancer cells are inoperative. Normal sugar metabolism takes place in mitochondria. Mitochondria are also responsible for monitoring the cell for proper operation and initiating apoptosis at the appropriate time. Whatever inhibits operation of the mitochondria in a cancer cell is nullified by DCA then the mitochondria start back up, find the cell is not operating properly, and initiate apoptosis.

    One reason DCA isn’t completely effective is cancers usually don’t have a good blood supply (lack of oxygen delivered from blood is why they can’t use aerobic sugar metabolism). The same blood that delivers oxygen also delivers DCA.

  20. DS:
    One reason DCA isn’t completely effective is cancers usually don’t have a good blood supply (lack of oxygen delivered from blood is why they can’t use aerobic sugar metabolism). The same blood that delivers oxygen also delivers DCA.

    This suggests that they need to find a way to get the DCA to the cancer other than via blood- ie direct injection (when possible).

  21. This interests me because my mother had cancer, as did her father. My father had cancer and so did one of my sisters (she died at 3 from a brain tumor).

    I just try to eat right- I take many supplements including “broccoli sprout extract”- and stay away from carcinogens.

    IOW I understand that epigenetics is as importatnt to our lives as genetics…

  22. Joseph,

    I believe the blood system is the only viable method for delivering anything to cells. There are interstitial fluids but getting something there is very local and if it is to spread would do so via the blood system. The way to each cell is through the blood and the network of capillaries.

    Dave,

    Aerobic metabolism only takes place in the mitochondria and this process is the result of several steps in the Krebs cycle and what is called the Electron transfer process. The fuel for most of energy for this aerobic process during normal body activity is fat and to a lesser extent a carbohydrate called pyruvate. At high metabolic rates pyruvate becomes the main source of fuel for the muscles’ production of energy in the mitochondria but I do not know what happens in other cells. Pyruvate is more efficient than fats so cells tend to use it if it is available. This process in the mitochondria is what uses oxygen and is therefore called aerobic. It is our main source of energy and is why we must breathe.

    Glycolysis is what is referred to as the anaerobic system because it does not use oxygen to produce energy and only takes place in the cystolic fluids outside the mitochondria and uses glucose/glycogen (chains of glucose molecules) for its fuel. Glucose is the sugar you are referring to when you call it sugar metabolism. The output of glycolysis is pyruvate which converts to lactate quickly if not used by the mitochondria for fuel for aerobic metabolism. Thus, if the mitochondria is being shut down somehow then the cell can use only glycolysis for energy production to survive and will flood the cell and if there are enough of them eventually the blood system with lactate.

    There are other consequences of glycolysis such as the production of hydrogen ions which lower the pH of the cell and actually inhibits glycolysis which would mean that if the mitochondria are shut down there should be limited energy production for the cell and the cell should eventually die. So that the cells are thriving without the mitochondria seems unusual and the way to kill them is to restore the mitochondria also seems a contradiction. I will be interested in how this happens.

    I sell lactate testing equipment and was not aware of this connection of lactate with cancer. So I was curious about the process that was described in the initial post. My ears go up immediately when I see the term glycolyisis. Lactate is a hot topic in some medical areas and there are extensive testing programs investigating high lactate levels with HIV, sepsis and some other conditions but I had not heard about a connection of cancer with higher lactate levels. So I am curious about why not.

    As I said that maybe in the beginning the number of cells that are cancerous may be too small to produce enough lactate to show up as a measurable difference in the blood. Lactate is in the blood and is produced by the red blood cells since they have no mitochondria. I will try to ask some people. I know research is going on trying to find markers for cancer’s early detection.

    There are doctors and maybe some physiologists who read this site who may have more information on this.

  23. Dave,

    First, here’s the link you requested:

    Dichloroacetate Prevents and Reverses Pulmonary Hypertension by Inducing Pulmonary Artery Smooth Muscle Cell Apoptosis
    M. Sean McMurtry, Sebastien Bonnet, Xichen Wu, Jason R.B. Dyck, Alois Haromy, Kyoko Hashimoto, Evangelos D. Michelakis
    Circ Res. 2004 Oct 15;95(8):830-40

    Second, I responded yesterday to Jerry’s comment regarding the glycolytic energy metabolism in cancerous cells and why lactate appears not to increase in the blood of cancer patients, but my response was never posted, thus I will repeat it again here.

    Even if cancerous cells are relying exclusively on glycolysis for their energy production (without the participation of mitochondria in the process) and even if the main product of such metabolism is lactate, any healthy tissue surrounding the cancer and most other tissues that receive blood that contains lactate (liver, heart, brain, lungs, kidneys, etc.) will immediately metabolize lactate oxidatively such that any trace of an increase in lactate production is wiped out immediatley. Much has been changed in our understanding of energy metabolism over the past 20 years and lactate is no longer perceived as simply an end-product of anaerobic energy metabolism.

  24. Joseph

    Radiation targets tumors and doesn’t depend on blood supply. DCA isn’t a complete cure but it might be the most effective, cheapest, and least debilitating chemotherapy drug found so far. Other chemotherapy drugs, radiation, and surgery would still be used but likely to a lesser extent. The lesser extent could alleviate a lot of pain & suffering concomitant with current treatment regimens.

    We really need clinical studies for this. The “stink” I talked of in an earlier comment is that DCA’s efficacy as a cancer killer was known about in 2005 when UofA filed for a U.S. patent on the treatment protocol. Clinical testing could have been finished by now since this drug was already approved for use in other diseases.

  25. Here’s some recent scientific articles that indicate DCA itself to be carcinogenic and could explain the skepticism that some may have regarding its anti-cancer activity:

    Hassoun E, Kariya C, Williams FE. Dichloroacetate-induced developmental toxicity and production of reactive oxygen species in zebrafish embryos. J Biochem Mol Toxicol. 2005;19(1):52-8.

    Bull RJ, Sasser LB, Lei XC. Interactions in the tumor-promoting activity of carbon tetrachloride, trichloroacetate, and dichloroacetate in the liver of male B6C3F1 mice. Toxicology. 2004 Jul 1;199(2-3):169-83.

    Pereira MA, Wang W, Kramer PM, Tao L. Prevention by methionine of dichloroacetic acid-induced liver cancer and DNA hypomethylation in mice. Toxicol Sci. 2004 Feb;77(2):243-8. Epub 2003 Dec 2.

    Hassoun EA, Ray S. The induction of oxidative stress and cellular death by the drinking water disinfection by-products, dichloroacetate and trichloroacetate in J774.A1 cells. Comp Biochem Physiol C Toxicol Pharmacol. 2003 Jun;135(2):119-28.

    Carter JH, Carter HW, Deddens JA, Hurst BM, George MH, DeAngelo AB. A 2-year dose-response study of lesion sequences during hepatocellular carcinogenesis in the male B6C3F(1) mouse given the drinking water chemical dichloroacetic acid. Environ Health Perspect. 2003 Jan;111(1):53-64.

  26. Joseph

    I drink a 28 ounce pot or two of green tea every day plus take this vitamin supplement.

  27. S.Rivlin

    Yet DCA is still approved for use in other diseases…

  28. Dave,

    Could you provide me with the list of diseases in which DCA is approved as treatment and the appropriate links?

    Thanks.

  29. It’s approved as an investigational drug in the U.S. The most interest has been in Congenital Lactic Acidosis. It’s been used to treat lactic acidosis in severe malaria. It’s used to treat systemic monochloroacetate poisoning. It’s also been used to treat lactic acidemia in severe burn victims and in treating lactic acidosis associated with NRTI therapy.

    There are probably more but I got sick of looking. Why couldn’t you find these for yourself? I ban people for making me do research they should be doing for themselves. Consider yourself warned.

  30. Dave,

    Sorry for asking you to provide a link. You did the same yesterday when you asked me for a link. I promise not to ask you for links anymore. Nevertheless, I hope you’ll allow an exchange of information to continue on your blog, even if, at times, the information does not necessarily agree with your own position.

    As to the use of DCA: it is not an approved drug. It has been used in a clinical trial (congenital Lactic Acidosis), in severe malaria and in poisening. The malaria study was done in Thiland, not in the US. The poisening of monochloroacetate, for which the third study used DCA, is not a disease. In all these studies, the aim was to reduce the levels of lactic acid in the blood with the assumption that the lactic acid is the problem. This is an old concept that has been proven to be wrong many years ago. Lactic acid is simply an indicator that energy metabolism is not functioning normally, but by itself is not a toxic substance. On the contrary, it could be an essential and crucial energy substrate on its own.
    That is probably why the Gainsvill group that did the clinical trial with DCA on congenital lactic acidosis found a decrease in lactate levels and an increase in pH, but no improvement in the neurological prognosis.

  31. Where did I say it’s approved for routine use in the United States? It’s approved in the U.S. for investigative use in humans thus there is no obstacle to going directly to administering it to humans in a clinical study for cancer treatment.

  32. Dave,

    Unfortunately that vitamin compound is not veggie friendly. But if it works for you. With that and the green tea you obviously understand the importance of preventative maintenance that we our ourselves.

    My point about the DCA delivery method, ie via blood, is that it is non-invasive. But what if we went in to the cancer and coated the thing with DCA? Or injected the DCA directly into it?

    Or has that been done?

    (we coat a wart and it dissolves)

    With that method perhaps we could them restrict the flow of DCA to the immediate cancerous area.

  33. Early this morning (just after midnight) I saw Kevin Trudeau on TV promoting his new books- “More Cures Revealed” and one about losing weight. In the “More Cures” infomercial he stated that Canadians have used linseed oil to cure breast cancer! Allegedly it works much better than chemo.

    He also said that such a treatment was illegeal in the USA…

  34. Joseph, with Trudeau’s record, I hope you’re taking his words with a pound of salt or so.

  35. What record?

    Does he have a CD? :)

  36. S. Rivlin,

    Aren’t you curious as to why cancer cells use only glycolysis for energy and how the aerobic metabolism in the cell is suppressed? You claim you are an expert on energy metabolism so I thought you might have some knowledge or opinions on this. From my little reading on this since this subject came up it seems there is no accepted reason as to what causes this phenomena.

    My understanding of glycolysis is that it cannot go on unabated because it generates hydrogen ions which lower the pH and then that inhibits glycolysis. It would also seem to require large amouunts of glucose to fuel all the cellular energy needs because of the relatively low output of ATP per glucose molecule. However, my main understanding of this is based on what happens in a muscle cell during intense exercise.

    I would be interested in your comments on this. It is the first I heard about this issue relevant to cancer even though I am involved in selling machines that measure lactate and people often relate their interest in measuring lactate. No one has ever brought it up though HIV, malaria, sepsis, several veterinary issues and some other diseases have been frequently discussed.

    I am just curious as to why aerobic metabolism is shut down and how can glycolysis go on unabated when apparently the mitochondria are healthy.

  37. “I am just curious as to why aerobic metabolism is shut down and how can glycolysis go on unabated when apparently the mitochondria are healthy.” –jerry

    Jerry, I’m no expert on the matter, but I have been generally been given two plausible explanations which are not mutually exclusive. First, apoptotic pathways are closely associated with mitochondria, so shutting the mitochondria down is one avenue (among many cancers use) to avoid programmed cell death, which is otherwise an effective natural defense against cancer. Second, the oxygen dispersal in tumors is not that efficient–it’s poor in tissue in general–particularly in the central region of larger tumors, so glycolis is the only viable option. Depending on the the cancer, it can’t continue unabated, and some larger tumors will actually start to die from the core out, probably partially b/c of the pH issue. Unfortunately, the outer layers can still survive, along with metastatic off-shoot tumors, etc. I’m hoping this drug works out, but unfortunately we’ve cured cancer in rodents a hundred times over, and the results just haven’t translated to humans. I *think* this is because life-history differences put very different pressures on humans vs. rodents in terms of cancer safeguards. There are many more safeguard systems in place in humans than in rodents b/c they live longer and deal with more damage over time. Once the cancer has broken through those natural human defenses, it means that it is probably a much nastier beast than a rodent cancer, which can be more easily induced.

  38. great_ape

    I keep hearing this claim that we’ve found many drugs that work wonderfully in mice but not in humans. Now you use the flippant phrase we’ve cured cancer in rodents a hundred times over. I checked the examples of cures in mice Gorkski gave (immunotherapy and antiangiogenic therapy) and these were nothing at all like DCA in either method or result.

    What this sounds like to me is the equivalent of the Darwinian’s “overwhelming evidence” that evolution is true when there’s actually no real evidence at all that chance & necessity turned mice into men.

    Of course you’ve been posting here a long time so I’ll give you the benefit of doubt and ask that you give me just ten examples out of those “hundred” times we’ve “cured” cancer in rodents. I bet you can’t come up with one instance that can be reasonably called a cure.

  39. Yikes. 25 examples is a steep order. A lot of this stuff doesn’t see the light of day so it’s not so easy to dig up the details. I know that sounds like a major cop-out, but it’s the truth. Many are anecdotal examples I hear about, but anecdotes you hear at a cancer center have a bit more credibility than elsewhere. I attend talks on so-called “translational research”, or the process of getting things from the lab bench and into the hands of physicians. The phrase “cured cancer a hundred times over in mice” is a running joke heard among the jaded old-timers in attendance. The last such talk I heard involved genetically manipulating or “training” T-cells so that they targeted prostate cancer cells more efficiently. Worked great in mice and in culture. A company, I forget which, went ahead with an initial human trial and it failed. I tried using pubmed to pull up similar examples, but I admittedly had difficulty finding the proper search terms; there are many technical ways to say “cured cancer in mice,” and you’re right, some people use the term “cured” more loosely than others. Do a google search, though, for ["mouse" & "cure" & "cancer"] and many hits come up for popscience articles that can be traced back to the legitimate research article. (unfortunately you have to wade through many spins on the same research) None of these work the way DCA does, but that wasn’t my point. The point is that if different approaches have previously shown promise in mice but not in men, it is reasonable to temper one’s enthusiasm when news of mouse cures comes out, whatever the mechanism. I’m all for clinical trials for DCA, and I hope as much as anyone else that this drug will be different. We all have people who are close to us that are dying or have already died of cancer. Folks in research are no exception. And if they’re anything like me, most cancer researchers have exposed themselves to so many toxic agents and radioactivity in the lab that we’re especially hoping for some sort of magic bullet to come along.

  40. Great Ape,

    Thank you for the response. I have another question if you have time to answer. If the cell can get glucose for glycolysis why cannot it not also get oxygen for respiration? Glycogen should run out fairly quickly if nothing but glycolysis is going on and has no way for resupply via the blood system.

    I find this a fascinating discussion since if the mitochondria are shut down some how, what did it and what could open them up again. I have little knowledge on cancer but this seems such as obvious area of research and if so how much has been done.

    My business sells lactate analyzers primarily for exercise physiology and veterinary emergency medicine and I know research in exercise physiology has been fairly intense on what affects the use of anaerobic vs aerobic energy metabolism and how they interact and why does the cell decide to choose one versus the other. If DCA inhibits glycolysis, does it do so by shutting down some part of the glycolytic process or does it somehow stimulate the mitochondria.

    An aside, about a year and a half ago, I read sort of a polemic article that said it was nearly impossible to get a grant to do cancer research unless it was gene related and that some obvious areas are just not funded very well. If your cancer research friends have any idea of what percentage of cancer research is gene related versus other areas, I would be interested.

  41. great_ape

    It’s urban legend. We haven’t cured cancer a hundred times over in mice. It wouldn’t be hard to find. Trained t-cells, also called immunotherapy, is one of two examples Gorski gave. I looked it up. It worked to some extent on some very specific cancers. It was also hideously expensive to the point of being impractical for widespread use. Most cancers don’t present anything remotely recognizable as non-self to the immune system and mice immune systems are a lot different than human because they only live for few weeks. The hoops that had to jumped through to coax an immune response were many and high. Mitochondria on the other hand, which is how DCA works, are the same in mice and men. And every cancer cell has mitochondria. I’ve been reading about cancer research for 40 years and I’ve never heard of anything like this. It would be the kind of quackery I’d dismiss in a minute if it was some stupid herbal cure or megadose of vitamins but this is from a real team of scientists at a real university studying DCA for another real medical application and they happened to stumble onto its efficacy in killing tumor cells and figured out it does it through a mechanism that makes good sense. I wouldn’t be making a big deal out of it otherwise since it’s pretty off-topic for ID. The only way this is related to ID is the same way global warming is related to ID – it’s an example of how greed and ego stifle science that threatens to upset applecarts. This is particularly egregious because no one is suffering and dying over ID being ignored so as not to endanger the evolutionary biology gravy train.

    So tell me, since this was discovered and documented over a year ago (the discoverers filed for a patent on the process in November 2005), and it’s a drug that is already approved in the U.S. as an investigational drug for use in human trials, and has been used in human trials for many years (unsuccessfully but still it’s approved for use because the side effects are minimal) then why has no clinical trial for cancer begun yet? You can prattle on all you want about a hundred cancer cures in mice but the cold hard fact remains this is promising, human trials can begin immediately, yet none have for over a year.

  42. jerry

    I’d guess the reason glucose can get delivered where oxygen is in short supply is because glucose is a small molecule directly dissolved in plasma whereas oxygen (in large quantities) must be carried by red blood cells instead of just dissolved in the plasma. Red blood cells and large quantities of oxygen can’t migrate by osmosis and/or diffusion through intercellular plasma the way I presume glucose can.

  43. I just want to take a moment to thank Dave, Jerry, SRivlin and Great_Ape for the discussion. It is amazing what can be openly discussed without reverting to personal attacks. (also I almost forgot what an open discussion was)

    Thanks guys- please continue…

  44. zach on ATBC mentions this

    http://www.mskcc.org/mskcc/html/12544.cfm

    The reason zach can’t post here is because he can’t read. We are looking for examples of the claim that we’ve cured cancer 100 times over in mice but those cures fail to work in humans. The example he cites hasn’t failed in humans. However, as I wrote in a comment above about immunotherapies, it is still limited to a few types of cancers and is hideously expensive as it requires harvesting immune cells from each cancer patient, genetically engineering those cells to recognize the cancer, then replacing them.

    Thanks for trying zach. If you ever get a clue maybe I’ll let you return here but until you do you’ll have to remain sniping stupidly from the sidelines.

  45. Showing only that I’m interested layman, and not a scientist, I was astonished to read in the link provided:

    DCA attacks a unique feature of cancer cells: the fact that they make their energy throughout the main body of the cell, rather than in distinct organelles called mitochondria. This process, called glycolysis, is inefficient and uses up vast amounts of sugar.

    Something as astonishing yet basic as that, and in all the main stream media reports, in the past, I’ve never known that at all.

    That aspect should provide several avenues, I think, of potential attack, even if this drug is ultimately unsuccessful.

    I wonder if anyone else in the field of research has used that approach.

    I wonder what Michael Behe thinks?

  46. j.parker

    Something as astonishing yet basic as that, and in all the main stream media reports, in the past, I’ve never known that at all.

    I suspect this is where the ego protection is coming into play and why cancer researchers are ignoring or downplaying it. The discovers aren’t cancer researchers. They were investigating DCA as a drug to help people recover from heart surgery.

    Otto Warburg was awarded a Nobel Prize in 1931 for his discovery that cancer cells, unlike normal cells, rely on anaerobic metabolism (glycolysis) for energy production.

    The cancer research community, from what I understand, believed or assumed the anaerobic metabolism was because cancer cell mitochondria were irreparably damaged. In my understanding mitochondria take an anaerobic glycolysis byproduct (pyruvate) and extract energy from it in what’s called the Krebs cycle but that can be done only in the presence of oxygen. If the mitochondria aren’t working for some reason (heavy exercise stops them from working because there isn’t enough oxygen being delivered to the cell) the only energy source is glycolysis which isn’t nearly as efficient as the Krebs cycle and causes excess lactic acid to build up. DCA has long been known effective in treating severe lactic acidosis caused by severe malaria, burns, congenital lactic acidosis and some others.

    Mitochondria are also know be involved in apoptosis (programmed cell death) but I’m not sure how long their role in apoptosis has been known. I found literature going back at least 10 years talking about mitochondria mediated apoptosis.

    Evidently, judging from the DCA response, cancer cell mitochondria aren’t irreparably damaged but are rather just dormant and DCA wakes them up. Upon waking they discover the cell isn’t working right and initiate the self-destruct mechanism.

    It appears DCA is a magic bullet unlike anything else ever discovered. The “ho hum, we’ve cured cancer a hundred times in rats” response from the cancer research community goes absolutely beyond belief. It’s only been a matter of two weeks since this discovery was made public in a cancer research journal. The discoverers kept it close to the vest for at least the past year when they filed for a U.S. patent on the process. No private sources wanted to fund a clinical trial because I believe (and I used to work in the patent business so I have some expertise here) the patent won’t be issued and/or won’t hold up in court if it is isssued. Thus any private investment won’t earn any return. The discoverers have by now become frustrated at the lack of any source of funding for clinical trials and getting desperate enough to set up a website begging for money.

  47. Should someone also be looking into what starts the process of the mito “shutting down” (becoming dormant)? And treat that?

    Or do we already know that it is some mutational “overload” which “directs” the mito to “sleep”.

    And perhaps that peroxide drip just floods the system with so much oxygen that it “kick starts” the mito, which starts to work normally, which in turn kills the cancer.

  48. Dave,

    The main fuels for aerobic metabolism are fat and pyruvate. Fats or pyruvate enter the Krebs cycle and then the bi products enter the electron chain and produce most of the ATP. Fats metabolize slower than pyruvate which is why during heavy exercise most of the fuel is pyruvate. If pyruvate runs out, the cell must use fats so the exercise has to slow down.

    There is a term in marathons called hitting the wall which means the muscles have run very low in glycogen or glucose and thus glycolysis can not proceed very fast and pyruvate cannot be produced in any quantities. Thus, the runner has to start metabolizing mostly fats and run slower because of the slower metabolising rate of fat.

    Glycolysis is relatively inefficient because it only produces 2 or 3 ATP per glucose molecule but it does it so fast that it actually produces more per unit of time than aerobic metabolism so one can go faster but only for a short time because of low Ph resulting from an hydrogen ion build up which accompanys glycolysis and will eventually inhibit and then shut down glycolysis. Also intense exercise uses glycogen very quickly so it will run out and the person has to slow down or stop. There is not an endless supply of glycogen in the body so when you run out it takes time to resupply. In the Tour de France the cyclists spend time after the race taking glucose intervenously to hasten the resupply for the next day.

    Glucose is smaller than hemoglobin so your explanation may be a possibility but both are tiny compared to a cell and the cells need more nutrients than just glucose and oxygen. You would think something like this would be written up some place and maybe it is in some technical part of a text book.

    Great Ape or anyone to the rescue.

  49. Jerry

    I believe hemoglobin stays inside the red blood cells whereas glucose is dissolved in the plasma. Hemoglobin is huge compared to glucose, by the way, but both are tiny compared to an RBC.

    A bit of trivia – red blood cells are the only cells in your body without DNA. In mammals they are stripped of their nucleus and organelles upon maturity in order to make them smaller so they can get though smaller capillaries and thus closer to the cells they service.

  50. Dave,

    II am glad to see natural selection at work for mammals. No one would have ever designed something like that.

    Are there other animal classes besides mammals for which this is true for their rbc’s?

    Rbc’s have no mitochondria either which also would be a residing place for that version of the DNA. I have a question, How similar is the mitochondria DNA compared to the regular cell’s DNA? I assume it is the same as the mother’s since it is inherited only from the mother. But is it exactly the same as the mother’s except for possible mutations?

    It might be interesting to list major differences between classes such as this some place on the site or start a thread discussing differences. For example, Darwinists tend to hide the nature of the oxygen transport system of birds which is much more efficient than reptiles and mammals and is unique and very different. It is a necessary system for flight but not one that would have evolved after they took up flying and why should it happen before hand.

    Maybe you should ignore this request since it is off topic and answer it some other time.

    By the way do all classes get cancer? Is there a percentage difference between them? I never thought much of it but I know our mammal pets get cancer all the time.

  51. Another bit of trivia:

    Begin with slide 1004, a smear of normal canine blood. (If you’re a cat person, try slide 1001, normal feline blood, instead.) I’ve put these two formed elements first because they have some things in common: in mammals they’re not true cells, but are derived from true cells. They lack a nucleus and organelles and have limited, specific functions.

    The most common formed element is the erythrocyte, or “red blood cell” (RBC). Despite the common term, this is not a cell at all, although it’s derived from true cells. The RBC is the mature stage of development of a cell line in which the nucleus (present in earlier forms) has been lost.

  52. Dave, thanks for the informative and thought provoking reply; the same resistance to any paradigm shift appears at work!

  53. Jerry,

    Dave’s answer above concerning hemoglobin is as good as any I have regarding oxygen vs. glucose dispersal in tumors. Remember also, though, that the mitochondria->apoptosis connection is also a strong motivation for glycolysis–even if enough oxygen did penetrate the tissue.

    I’m not sure about the DCA mechanism–it’s only recently on my radar screen–so I won’t venture a guess there, but I do know a few things about the mitochondrial genome…

    “…How similar is the mitochondria DNA compared to the regular cell’s DNA?” –jerry

    The human mitochondria is a tiny 16,000 bp compared to an approximately 3 billion bases (haploid) and 6 billion (diploid) bases of nuclear DNA. The human mitochondria contains something like 27 genes. I won’t belabor the issue–I’m sure it has come up here before–but many aspects of the mitochondrial genome are reminiscent of bacteria (origin of replication, circular genome, etc) Also, the mitochondria appears to have gotten smaller over time as genes have moved from the mitochondrial genome to the nucleus. The forces driving this relocation is unknown but it appears to be a general trend across many species.

    “How similar is the mitochondria DNA compared to the regular cell’s DNA? I assume it is the same as the mother’s since it is inherited only from the mother. But is it exactly the same as the mother’s except for possible mutations?” –jerry

    What little is there in the mitoch. is different in the way it’s organized, replicated etc. Mitochondria are mostly maternally inherited although there have been occasional reports of paternal transmission via sperm. There is also heteroplasmy, wherein people have pools of different mitochondria with different patterns of mutations. In general, however, a single person has a pretty homogeneous set of mitochondria genomes (aside from mutations that accumulate during their lifetimes), presumably due to “bottleneck” effects during repeated transmissions. As of a few years ago, the mitochondria have been a hot topic concerning regional selection (for cold weather tolerance, etc.)as some of the patterns of mitochondrial variation
    are difficult to account for by neutral population genetics means.

    How do cancer cells shut down the mitochondria? I don’t know, but I’ve encountered some devilishly ingenious schemes cancer uses to overcome other defense systems. Cancer cells in some instances can send out signals to chemically “reprogram” other cells and use them for their own ends. Renegade cells must (and do) solve a number of tricky engineering problems to be so destructive.

  54. Joseph, Jerry, Great_ape, Dave,

    Notwithstanding cancer energy metabolism, the preceeding discussion on glycolysis, glycogen, mitochondria, glucose, pyruvate and other “vegetables” will need much clarification and straightening to make any sense. Much of the pH dogma (lactic acidosis) has been reinvestigated lately due to some new findings that have questioned even our most basic “understanding” of energy metabolism. You are encouraged to read a recent paper in ‘Science’ magazine from 2004 regarding the role of lactate in muscle fatigue. The Danish investigators managed to demonstrate very elegantly that lactic acid has nothing to do with muscle fatigue. On the contrary, the drop in pH actually allows the muscle to contiue to contract (to produce action potential), which it could not do in normal pH.
    There are many types of cancer that do not form big, oxygen-deprived tumors (leukemia), while others form very small tumors that are probably can still receive oxygen. On the other hand, there are some huge, benign tumors that surely do not get any oxygen to their core, yet they survive and continue to grow. I read last week that a 93 lb tumor was removed from the abdomen of a woman.

    As much as we tend to simplify things, they are not always simple. DCA, as I have mentioned earlier in this thread, can induce apoptosis in normal cells, too. In the cancer cells, at least based on the Canadian paper, DCA triggers dormant mitochondria by activating a K+ channel that for some reason is blocked in those cells. Once activated, the mitochondrial process that normally induce apoptosis is activated. Nevertheless, the non-selectivity of DCA and its other, nonrelated effects on energy metabolism in normal cells, must be well understood and documented before it can be even tried as an experimental anti-cancer drug in humans.

  55. Great Ape,

    As always, thank you for the information.

  56. Nevertheless, the non-selectivity of DCA and its other, nonrelated effects on energy metabolism in normal cells, must be well understood and documented before it can be even tried as an experimental anti-cancer drug in humans.

    This drug has already been used on humans in clinical trials. Its side effects are well characterized for use in humans and compared to currently approved chemotherapy drugs are mild and easily tolerated. Which part of that don’t you understand? Please be specific because if you don’t stop peddling misinformation you’re out of here. Final warning.

  57. great_ape

    Remember also, though, that the mitochondria->apoptosis connection is also a strong motivation for glycolysis–even if enough oxygen did penetrate the tissue.

    Have you read the paper published in Cancer Cell?

    http://www.depmed.ualberta.ca/dca/cancer_cell.pdf

    It describes cancer cells as all beginning in an oxygen deprived environment (I’m not sure I understood that part, maybe you can clarify that for me) but goes on to say even if or after they’ve become well vascularized and have plenty of oxygen they still keep normal glucose metabolism shut down. It appears the apotosis link is the key one and abnormal glucose metabolism is simply a side effect of it.

    By the way, your comments have been missed here. I trust you’ve been constructively occupied during your absence?

  58. S. Rivlin,

    You should understand something about lactate since you may not be involved in exercise physiology. There is a point in exercise intensity that is well documented that is called the maximum lactate steady state. At this point an athlete can continue on for anywhere from an hour to slightly longer without stopping (eventually glycogen depletion force the athlete to slow down).

    The lactate levels in the blood and hence the muscles, since they are in equilibrium, do not rise during this exercise and remain relatively constant with small fluctuations. At any point past this intensity, even small amounts, the lactate starts to rise and the athletes will be forced to halt exercise or slow down. The time to exhaustion varies with the conditioning level of the athletes but for everyone there is slow or fast inevitable onset of exhaustion. That is why lactate is of interest in athletic competition.

    No one that knows anything claims anymore that it is the lactate per se which forces the slowdown or the halting of exercise and the best explanation I have seen is the lowering of pH. in the muscles that accompanies glycolysis and lactate production.

    Fatigue is a word with a hundred definitions and it has to be carefully defined within the context of interest. My guess is that you are referring to an article by Pedersen et al.

    I have not seen a reference to it in the exercise physiology literature, I was unaware of it. I will try to get it to see if it hasn’t anything relevant to athletic competition.

    However, what is above has no relevance to the thing in question which is the possibility that DCA could help in cancer treatment.

    I hope you continue to post information that will help us evaluate the potential of DCA and its possible negatives as well as information about energy metabolism in cancer cells. We are all eager to learn here and not so dumb as the people on other blogs hope us to be.

  59. There is another chemical that reduces lactic acid, improves immunity and cellular oxygenation – dimethylglycine, and yes, it has been used by athletes and horses and greyhounds to enhance endurance. It does not, however, ‘wake-up’ mitochondria like DCA does. http://www.dmgdoctor.com

  60. test:

    onetwothree

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