Journalists deal a blow to DCA (so they think)

Journalists deal a blow to DCA (so they think)

[ Response to: Unapproved cancer therapy DCA makes some tumours worse (ANNE McILROY) ]

The Globe and Mail reports that DCA has been shown ineffective in colorectal cancer and even worse, it has been shown to protect certain cancerous cells.

http://www.theglobeandmail.com/life/health/unapproved-cancer-therapy-dca-makes-some-tumours-worse/article1806516/

The article made it to the Associated Press as well:

http://www.rdmag.com/News/FeedsAP/2010/11/life-sciences-unapproved-cancer-therapy-dca-makes-some-tumours-w/

The state of science reporting is truly depressing and distressing to say the least.  The lack of scientific literacy makes room for such errant reporting.  The article is filled with conjecture and supposition with very little reference to the actual article.

Very few people have actually read the journal post, and fewer still can understand it.  Just the same, here it is:

http://www.martincwiner.com/wp-content/uploads/2010/11/DCAColorectalTumorHypoxia.pdf

The article says that under hypoxic conditions (low oxygen) conditions that DCA is proven to be ineffective. 

No kidding.

DCA is a drug that restores mitochondrial function.  The mitochondria are responsible for cell aptopsis (cell suicide) in cancer.  When they are restored to normal function, they are able to recognize that the cell is in an errant state and kill the cell.  Mitochondria rely on oxygen to work.  The mechanism by which they produce energy for a cell is called none other than oxidative phosphorylation (ie, it requires oxygen).

At the core of a dense tumour there is almost no oxygen at all.  Indeed, it’s unlikely DCA could even be delivered to the core of a deeply dense tumour where there is insufficient blood vessel perfusion.  If DCA was administered to cells where there was no oxygen available, it would be equivalent to fixing an engine but still being out of gas — the engine still wouldn’t turn over.

The ‘protective’ effect DCA supposedly offers hypoxic cancer cells could be explained by restored mitochondrial function which is able to provide cellular energy with the little oxygen available, whereas the mitochondria aren’t functioning well enough to effect aptopsis.  By continued analogy, DCA might fix the engine enough to allow it to turn over with the pint of gas in the tank, but the engine would stall before being able to arrive at the destination: aptopsis.

What the researchers fail to ask is: what is occurring at the surface of the tumour where there is sufficient oxygen?  Is it possible that DCA is able to reach the cells on the surface and effect aptopsis there?  If so, then DCA could work it’s way in slowly from the outside in… it a far gentler and safer way than most common anti-cancer treatments.

In fact, many common cancer treatments kill cancers too rapidly causing a rapid decline in overall health of the patient opening the patient to further cancers or eventual worsening of tumour in question.

Dr. Brenda Coomber et al out at the University of Guelph have managed only to underscore the vital need for a full clinical trial of DCA to answer the questions posed here an in other places as to the efficacy and safety of DCA in broad spectrum use against many forms of cancer.

If journalists who aren’t versed in science would like to publish articles about said subject, might I suggest they direct their attention to the fact that DCA is not likely to receive funds to make its way through a full clinical trial.  Regrettably DCA is as common as table salt and is not patentable.  Journalists need to focus on why profit trumps caring in medical research.

14 thoughts on “Journalists deal a blow to DCA (so they think)

  1. There is one more research on DCA and colorectal cancer available, this one is from University of Leeds: http://www.nature.com/bjc/journal/v102/n12/full/6605701a.html
    They used few cell lines to investigate DCA’s impact on colorectal cancer cells. One line was the same as the line examined by researchers from Guelph. The most interesting fact is that in both researches they examined what’s happening with SW480 cells treated with DCA under hypoxic and normoxic conditions and results are different. According to Leeds research there is no difference in cell proliferation between hypoxia and normoxia. Guelph states something different.. What should one think about it? Who’s right, who’s wrong? Or maybe the problem is that i just can’t understand reports well? What’s your opinion Martin?

    P.S. Sorry for my english skills, i hope it’s understandable

  2. Your english is just fine.

    The difference between the two papers hinges critically on the difference between hypoxia and anoxia. The paper you present above, hereinafter ‘the British paper’ compares hypoxia to normoxia. The paper I review in this post, hereinafter ‘the Guelph paper’ compares anoxia to normoxia. The British paper incubates at 1% oxygen which sounds low, but in actuality is 5% of normal oxygen. Perhaps just enough to allow the mitochondria to effect apoptosis. The Guelph paper incubates at less than 0.1% oxygen. Under such a situation it’s likely the mitochondria didn’t have enough oxygen(hence energy) to effect apoptosis.

  3. I have spent a bit of time studying DCA and its’ mechanism of action, and frankly, the literature has me confused because it is routinely contradicts itself.

    Literature that addresses its’ effect on cancer describe it as an inhibitor of pyruvate dehydrogenase, other literature, including a pharmacological journal describe it as a stimulator of pyruvate dehydrogenase. These have an opposite effect on mitochondrial function.

    Warberg believed that reactivating mitochondrial function would cure cancer, however, I am not convinced.

    There are a whole class of chemicals that work by inhibiting ATP production that manage to destroy cancerous cells quite effectively, these include Paw Paw, mitocans, methylglyoxal, bromopyruvate, methyl jasmonate, brop, arsenic trioxide, etc. to name a few. 3-bromopyruvate (an inhibitor of hexokinase II) when delivered intra-arterially can utterly destroy (cure) advanced liver cancers with a single one-hour treatment. Thus agents that inhibit mitochondrial function (not stimulate) have been shown to cure cancer too.

    Will DCA cure certain varieties of cancer? I believe it will. Does it work by “reactivating” the mitochondria? I have serious doubts. Until our scientists can agree on what DCA actually does to the mitochondria, we must all have our doubts.

    But big Pharma wants expensive treatments to market, not cures, especially cheap ones. I don’t expect any non-patentable medicine to make it to main-stream medical science short of government intervention. Given that Canada has socialized medicine, it seems that it could save quite a bit of money by using cheap cures, rather than expensive treatments. But it is also been my experience that politicians care more about money (their own) than people. Thus, big Pharma will always find allies in our government that will find some way to slow or stop the advance of medical science to preserve their own financial well-being.

  4. Yes I know that Dr. Ko was let go by Johns Hopkins. I watched that case carefully from the moment it began to unfold. The fight should never have happened, but it did. Unfortunately Dr. Ko gave the school grounds to dismiss her because she claimed to have a her own lab when she applied for, and received a $500,000 grant from the Susan B. Komen foundation to continue her research.
    Though the issue has been shrouded in a lot of mystery, I can tell you generally what happened. Dr. Geschwind recieved an e-mail (as did hundreds of others) detailing how an intra-arterial infusion of an energetic inhibitor could rapidly target and kill (within minutes) cells that were reproducing while leaving non-reproducing cells unharmed. Dr. Geschwind then went to Dr. Petersen’s lab to discuss potential chemicals that might be used as a proof-in-principle for this mechanism.
    Though Pedersen gave Ko the credit of choosing 3-bromopyruvate, citing her previous work in nemotodes, Pedersen also had experience in studying its’ effects on trypanosomes, just three years earlier. So what is the truth here? I am not sure. Ko, Geschwind and Pedersen have all filed patents on the concept (as have many others), including one that they have filed together. So maybe they have made up (Pedersen and Ko were never estranged).
    Eventually, I think, the full truth of this ugly chapter in history will be revealed.

  5. The broader point you make is well taken. I don’t think capitalism and science mix well. At the best of times they form a cloudy colloid and at the worst they kill the experimenter.

  6. In your latest sentence ” If journalists who aren’t versed in science would like to publish articles about said subject, might I suggest they direct their attention to the fact that DCA is not likely to receive funds to make its way through a full clinical trial. Regrettably DCA is as common as table salt and is not patentable. Journalists need to focus on why profit trumps caring in medical research.”, DCA can be replaced by 3-BP and the story is identical. The scientific results on inhibition of growth of tumor cells by 3-BP were peer reviewed, found sound and published. No funding, no clinical research, no progress. Why ?

  7. I’m assuming your ‘Why?’ is rhetorical. Indeed, why not add to the list high potency intravenous vitamin C? There are several other non patentable agents which are ignored by the pharmaceutical industry. 3-Bromopyruvate effected a cure of liver cancer whereas DCA has only demonstrated reduction (in general). However, 3-Bromopyruvate is in worse shape than DCA because it has never been used in humans and is thus ineligible for ‘off label’ prescription. What can I tell you? Please pass along links to the petition and to the http://www.martincwiner.com/dca to as many people as you can. If you can think of any other ways to promote the cause, I’m all ears.

  8. As we experience for DCA, a new open system for drug development is needed. You may find a proposal here http://stm.sciencemag.org/content/5/171/171cm1.abstract (“An End to the Myth: There Is No Drug Development Pipeline”) as “A new map is presented for creating an open, collaborative, and coordinated system for drug development.” and also an Italian summary (to be translated by Google) at http://www.lescienze.it/news/2013/02/07/news/nuovo_modello_sviluppo_farmaci-1497681/.

  9. Feel free to post comments here on the DCA page. If you’d like I can create a post called “General DCA Discussion” and allow comments on it.

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