Dr. Weeks’ Comment: My friend Frank Shallenberger, M.D. wrote this piece for his newsletter and sent it to me to share. It is well worth the read. for more info see www.thedcasite.com
Can this inexpensive, essentially harmless chemical actually cure cancer?
Dichloroacetic acid or DCA is a chemical that does not exist in nature. Molecularly, however, it is similar to the stuff you put on salads – vinegar. Doesn’t sound like much does it? However, recently there has been some very fascinating research that suggests that DCA might be a useful treatment for cancer. In fact, the authors of a study published only a few years ago in the journal Cancer Cell summarized their impression of DCA as a “promising selective anti-cancer agent.” I believe that DCA should be taken seriously. That’s why I presented a paper on it at the recent annual meeting of the International Organization of IPT (Insulin Potentiation Therapy) Physicians in Miami. This is the gist of what I presented there.
The whole story of DCA starts with an amazing observation that two time Nobel Prize for Medicine winner Dr. Otto Warburg made eighty years ago. Dr. Warburg discovered that cancer cells had a very confusing attribute. Unlike normal cells, cancer cells are extremely inefficient in their ability to use oxygen to produce energy. Even when they are surrounded by oxygen, for some inexplicable reason they still can’t use it with any level of efficiency at all.
So because they are so inept at using oxygen, they choose to make their energy in a process that does not use oxygen called anaerobic metabolism. But anaerobic metabolism is 19 times less efficient in the production of energy than oxygen metabolism (aerobic metabolism). Cancer cells need enormous amounts of energy, so why in the world would they want to do that? This is a question that has baffled researchers for decades. There must be some advantage to cancer cells for being such inefficient oxygen users, but what in the world could it be? Now thanks to the research around DCA, we may know the answer.
It has to do with something called apoptosis. Apoptosis is a strange word that describes a very simple concept – the concept of controlled cell death. Just as every living thing has a defined lifespan, so also do our individual cells. They can only live so long, and then they have to die and be replaced by a new cell. Think of it. If we did not have some kind of limit on cell growth built into our cells, we would grow uncontrollably, and would soon be just big, useless blobs.
So all of our cells have a system in them that determines when it is time to die, and then initiates the destruction mode. This process is referred to as apoptosis.
But cancer cells have found a way around apoptosis. This is what allows them to grow without any controls. In fact, it is precisely the lack of apoptosis that make a cancer cell a cancer cell. Or to put it another way. If a cancer cell had to go through apoptosis like every other cell, it would have the growth restraints that normal cells have, and would no longer be a problem. That’s where DCA comes in. DCA is able to induce apoptosis in cancer cells. And as you might have guessed by now, it has to do with how efficiently cells are able to use oxygen.
In order for a cell to efficiently use oxygen it has to be able to convert a molecule called pyruvate into something called acetyl coenzyme A. Unless pyruvate is converted into acetyl coenzyme A, the cell’s ability to use oxygen will be very compromised.
This important conversion is controlled by an enzyme system called pyruvate dehydrogenase or PDH for short. As long as PDH is working well, pyruvate will be converted to acetyl coenzyme A, and oxygen metabolism will proceed efficiently. But here’s the problem.
PDH is inhibited by another enzyme called PDH kinase. So when PDH kinase is activated, PDH can’t work, and the conversion of pyruvate into acetyl coenzyme A is inhibited. So the end result of PDH kinase is to decrease the efficient utilization of oxygen. And here’s why all of this is important.
Apoptosis is controlled by oxygen utilization. The better a cell utilizes oxygen, the more efficiently it is able to initiate apoptosis. The less efficiently a cell uses oxygen, the less able it is to start and complete the apoptosis process. And that is precisely the advantage that cancer cells have by choosing not to use oxygen even when plenty of it is around. It allows them to grow without restraint. And that’s where DCA comes in.
DCA is a potent inhibitor of PDH kinase. So when a cancer cell is exposed to DCA, PDH kinase no longer works to inhibit PDH. That causes the cell to use oxygen more efficiently, and ends up causing it to die through the apoptosis process. In essence, it changes a cancer cell that has no growth restrictions into a more normal cell that does.
Recently, researchers at the University of Ottawa in Canada under the direction of Dr. Sebastien Bonnet performed some incredible experiments using DCA.
They took some standard laboratory lung cancer cells, breast cancer cells, and brain cancer cells. They also used normal lung, artery, and connective tissue cells to compare them to. Then they tested the cells to see how efficiently they were using oxygen. As expected, the cancer cells used oxygen much less efficiently than the normal cells.
Then they exposed all of the cells to DCA. The normal cells were not affected at all. Why should they be? They were already using oxygen efficiently. The cancer cells however had a dramatic shift. So dramatic that within only 48 hours, their oxygen utilization was completely normal! This goes entirely against the prevailing wisdom that cancer cells have permanently defective oxygen utilization, and that this characteristic cannot be reversed.
They also looked at the effect of DCA on the production of lactic acid in cancer cells. Because cancer cells do not use oxygen efficiently, they end up producing excessive amounts of lactic acid. This excessive production of lactic acid is what helps cancer cells to spread. But because DCA improved oxygen utilization so effectively in the cancer cells, their production of lactic acid decreased to that of normal cells. This is a significant blow to the ability of cancers to spread.
This all sounds great, but do these DCA effects actually cause cancer cells to go into apoptosis cell death as advertised? Yes. When Dr. Bonnet’s team exposed the various cancer cells to DCA they found out that the cells grow about 1/6th as fast as they ordinarily would have. And when they counted the number of cells that were exposed to DCA they discovered that there were 600% fewer cells. In other words, these cancer cells exposed to DCA were dividing and growing at a much slower rate, and were dying at a much fast rate – rates that are typical of normal cells!
They also measured something else called “survivin”. Survivin is a molecule that cancer cells make that indicates how well they are able to resist the process of apoptosis. It also indicates how aggressive they are. The more survivin a cancer makes, the less likely it is going to undergo apoptosis and die, and the more aggressive it is. Not surprisingly, the team found that when cancer cells are exposed to DCA, their ability to make survivin decreases dramatically to about 1/10th of what they normally make.
But despite these fantastic results, they are all “in vitro” tests. That means that they were conducted in a test tube, not in an animal. Things can easily happen in test tubes that have little or no effect in actual living biological systems. So the next step was to see if DCA was able to create the same kinds of effects in living animals.
They took a group of lab rats, and implanted cancers into them. One group received no treatment at all. Another group received DCA, but not right away. The researchers wanted to see the effect of DCA on cancers that were already well established. So in this group they did not give them any DCA until after the cancer had been allowed to grow for two weeks. Then they gave them DCA in their drinking water for three weeks. Here’s what they found.
At the end of six weeks, the cancers in the no treatment group were almost ten times larger than the DCA treated animals. And there was no lag effect to DCA treatment. It worked right away. The tumor growth in the DCA rats stopped immediately as soon as they received the DCA. And this cessation of growth persisted to the end of the experiment 3 weeks later.
The researchers then completed a second experiment that was different. In this experiment, they waited a full 10 weeks before they administered the DCA. This time the cancers had taken an even greater hold before they began treatment. They followed the animals for two weeks. Again, immediately the cancers stopped growing in the DCA treated group. And by the end of the two weeks, the cancers were actually smaller. They were acting like normal cells act. Sound good so far? It even gets better.
When they examined the rate of apoptosis in the cancers that were in the rats treated with DCA, they found that there were almost no cells at all that were still able to resist apoptosis. This was true even after only two weeks. And as expected, only 1/6th of the cancer cells were still producing survivin.
But what about toxicity. Surely a treatment as effective as that must be very toxic to healthy cells. According to Dr. Bonnet, all these great effects occurred “without affecting non-cancerous cells, or eliciting systemic toxicity.”
My dear readers, I think this is fantastic news. Here is a substance that has no toxicity, works immediately, is cheap (about $20/week), and is taken orally so that it is easy for any patient or doctor to use. And it has dramatic effects on cancer cells causing them to change their metabolism back to aerobic metabolism, which in turn controls their growth through the apoptosis process. Certainly you will soon be hearing all about DCA and this incredible study on the network shows right? Probably not. At least not a word so far, and Dr. Bonnet’s research was published four years ago.
In fact if you hear anything about DCA let me now predict that despite this and other studies and case reports it will probably be negative. Imagine how Big Pharma and the other powers that be must feel about an $80 a month treatment for cancer that might complete with their $20,000 per month therapies. You can expect the standard, “It may be somewhat effective, but it is still unproven, and should never be used.” Why? Because DCA has two almost insurmountable strikes against it: It is cheap, and it is not patentable.
But the fact is that DCA is not new to the medical world. It has been given to children with mitochondrial disorders for the past thirty years to reduce their output of lactic acid. So we know a lot about how it works clinically in children. Additionally, in one study it was used in adult onset diabetics for over six months. So we also know how it works in adults. There really should be no complaints at all against the use of DCA to treat patients with cancer. But again, the problem remains: it is not patentable, and therefore little or no follow up research is likely to be done on DCA.
But, last I looked, it is still a free country. And the FDA does allow patients to import DCA for their own personal use. Of course make no mistake about it. If a patient elects to do that, they definitely need to be under the guidance of a physician who knows how to properly use and dose DCA.
Additionally, I do not see DCA as a stand alone therapy for cancer. There is just not enough data on how effective it is in humans with advanced cancers to completely rely on it. But I do believe that it can be used in conjunction with other effective cancer therapies such as IPT.
So if you are a patient, and you are interested in DCA, please contact one of the physicians listed in the referral site for the International Organization of IPT (Insulin Potentiation Therapy) Physicians: http://www.iptforcancer.com. These physicians have been thoroughly trained and certified in IPT. And they are also proficient in the other essential aspects of cancer therapy such as detoxification, revitalization, and immune enhancement. Physicians or patients who would like to get a recording of my lecture on DCA can get it at this same web site.
No doubt there will be more that will be coming out on the use on DCA for cancer. And as that happens, you can bet that I will be reporting it all back to you.
Bonnet S, Archer SL, Allalunis-Turner J, Haromy, et al. A mitochondria-K+ channel axis is suppressed in cancer and its normalization promotes apoptosis and inhibits cancer growth. Cancer Cell. 2007 Jan;11(1):37-5
Gatenby RA, Gillies RJ. Why do cancers have high aerobic glycolysis? Nat Rev Cancer. 2004 Nov;4(11):891-9.