A 2007 Harvard Medical School study shows Marijuana cuts lung cancer tumor growth in half.

A 2007 Harvard Medical School study shows Marijuana cuts lung cancer tumor growth in half.


Spain Study Confirms Hemp Oil Cures Cancer without Side Effects


The medical science is strongly in favor of THC laden hemp oil as a primary cancer therapy, not just in a supportive role to control the side effects of chemotherapy.

The International Medical Veritas Association (IMVA) is putting hemp oil on its cancer protocol. It is a prioritized protocol list whose top five items are magnesium chloride, iodine, selenium,Alpha Lipoic Acid and sodium bicarbonate. It makes perfect sense to drop hemp oil right into the middle of this nutritional crossfire of anti cancer medicines, which are all available without prescription.

Hemp oil has long been recognised as one of the most versatile and beneficial substances known to man. Derived from hemp seeds (a member of the achene family of fruits) it has been regarded as a superfood due to its high essential fatty acid content and the unique ratio of omega3 to omega6 and gamma linolenic acid (GLA) – 2:5:1. Hemp oil, is known to contain up to 5% of pure GLA, a much higher concentration than any other plant, even higher than spirulina. For thousands of years, the hemp plant has been used in elixirs and medicinal teas because of its healing properties and now medical science is zeroing in on the properties of its active substances.

Both the commercial legal type of hemp oil and the illegal THC laden hemp oil are one of the most power-packed protein sources available in the plant kingdom. Its oil can be used in many nutritional and transdermal applications. In other chapters in my Winning the War on Cancer book we will discuss in-depth about GLA and cancer and also the interesting work of Dr. Johanna Budwig. She uses flax seed oil instead of hemp oil to cure cancer – through effecting changes in cell walls – using these omega3 and omega6 laden medicinal oils.

Actually there is another way to use medical marijuana without smoking the leaf. According to Dr. Tod H. Mikuriya, “The usual irritating and toxic breakdown products of burning utilized with smoking are totally avoided with vaporization. Extraction and inhaling cannabinoid essential oils below ignition temperature of both crude and refined cannabis products affords significant mitigation of irritation to the oral cavity, and tracheobronchial tree from pyrollytic breakdown products.[iii]

Rick Simpson, the man in the documentary below, has been making hemp oil and sharing it with friends and neighbors without charging for it. In small doses, he says, it makes you well without getting you high. “Well you can’t deny your own eyes can you?” Simpson asks. “Here’s someone dying of cancer and they’re not dying anymore. I don’t care if the medicine comes from a tomato plant, potato plant or a hemp plant, if the medicine is safe and helps and works, why not use it?” he asks.

When a person has cancer and is dying this question reaches a critical point. The bravery of Rick Simpson from Canada in showing us how to make hemp oil for ourselves offers many people a hope that should be increasingly appreciated as money dries up for expensive cancer treatments. We are going to need inexpensive medicines in the future and there is nothing better than the ones we can make reasonably cheaply ourselves.

For most people in the world it is illegal so the choice could come down to breaking the law or dying. There is no research to indicate what advantages oral use of hemp oil vs. vaporization but we can assume that advantage would be nutritional with oral intake. Dr. Budwig Below work would sustain this point of view especially for cancer patients.

The Science

According to Dr. Robert Ramer and Dr. Burkhard Hinz of the University of Rostock in Germany medical marijuana can be an effective treatment for cancer.[v] Their research was published in the Journal of the National Cancer Institute Advance Access on December 25th of 2007 in a paper entitled Inhibition of Cancer Cell Invasion by Cannabinoids via Increased Expression of Tissue Inhibitor of Matrix Metalloproteinases-1.

The biggest contribution of this breakthrough discovery, is that the expression of TIMP-1 was shown to be stimulated by cannabinoid receptor activation and to mediate the anti-invasive effect of cannabinoids. Prior to now the cellular mechanisms underlying this effect were unclear and the relevance of the findings to the behavior of tumor cells in vivo remains to be determined.

Marijuana cuts lung cancer tumor growth in half, a 2007 Harvard Medical School study shows.[vi] The active ingredient in marijuana cuts tumor growth in lung cancer in half and significantly reduces the ability of the cancer to spread, say researchers at Harvard University who tested the chemical in both lab and mouse studies.

This is the first set of experiments to show that the compound, Delta-tetrahydrocannabinol (THC), inhibits EGF-induced growth and migration in epidermal growth factor receptor (EGFR) expressing non-small cell lung cancer cell lines. Lung cancers that over-express EGFR are usually highly aggressive and resistant to chemotherapy. THC that targets cannabinoid receptors CB1 and CB2 is similar in function to endocannabinoids, which are cannabinoids that are naturally produced in the body and activate these receptors.

“The beauty of this study is that we are showing that a substance of abuse, if used prudently, may offer a new road to therapy against lung cancer,” said Anju Preet, Ph.D., a researcher in the Division of Experimental Medicine. Acting through cannabinoid receptors CB1 and CB2, endocannabinoids (as well as THC) are thought to play a role in variety of biological functions, including pain and anxiety control, and inflammation.

Researchers reported in the August 15, 2004 issue of Cancer Research, the journal of the American Association for Cancer Research, that marijuana’s constituents inhibited the spread of brain cancer in human tumor biopsies.[vii] In a related development, a research team from the University of South Florida further noted that THC can also selectively inhibit the activation and replication of gamma herpes viruses. The viruses, which can lie dormant for years within white blood cells before becoming active and spreading to other cells, are thought to increase one’s chances of developing cancers such as Kaposi’s Sarcoma, Burkitt’s lymphoma and Hodgkin’s disease.[viii]

In 1998, a research team at Madrid’s Complutense University discovered that THC can selectively induce programmed cell death in brain tumor cells without negatively impacting surrounding healthy cells. Then in 2000, they reported in the journal Nature Medicine that injections of synthetic THC eradicated malignant gliomas (brain tumors) in one-third of treated rats, and prolonged life in another third by six weeks.[ix]

Led by Dr. Manuel Guzman the Spanish team announced they had destroyed incurable brain cancer tumors in rats by injecting them with THC. They reported in the March 2002 issue of “Nature Medicine” that they injected the brains of 45 rats with cancer cells, producing tumors whose presence they confirmed through magnetic resonance imaging (MRI). On the 12th day they injected 15 of the rats with THC and 15 with Win-55,212-2 a synthetic compound similar to THC.[x]

Researchers at the University of Milan in Naples, Italy, reported in the Journal of Pharmacology and Experimental Therapeutics that non-psychoactive compounds in marijuana inhibited the growth of glioma cells in a dose-dependent manner, and selectively targeted and killed malignant cells through apoptosis. “Non-psychoactive CBD produce[s] a significant anti-tumor activity both in vitro and in vivo, thus suggesting a possible application of CBD as an antineoplastic agent.”[xi]

The first experiment documenting pot’s anti-tumor effects took place in 1974 at the Medical College of Virginia at the behest of the U.S. government. The results of that study, reported in an Aug. 18, 1974, Washington Post newspaper feature, were that marijuana’s psychoactive component, THC, “slowed the growth of lung cancers, breast cancers and a virus-induced leukemia in laboratory mice, and prolonged their lives by as much as 36 percent.”[xii]

Funded by the National Institute of Health to find evidence that marijuana damages the immune system, found instead that THC slowed the growth of three kinds of cancer in mice — lung and breast cancer, and a virus-induced leukemia. The DEA quickly shut down the Virginia study and all further cannabis/tumor research even though the researchers “found that THC slowed the growth of lung cancers, breast cancers and a virus-induced leukemia in laboratory mice, and prolonged their lives by as much as 36 percent.”

“Antineoplastic Activity of Cannabinoids,” an article in a 1975 Journal of the National Cancer Institute reports, “Lewis lung adenocarcinoma growth was retarded by the oral administration of tetrahydrocannabinol (THC) and cannabinol (CBN)” — two types of cannabinoids, a family of active components in marijuana. “Mice treated for 20 consecutive days with THC and CBN had reduced primary tumor size.”

Marijuana relieves pain that narcotics like morphine and OxyContin
have hardly any effect on, and could help ease suffering from
illnesses such as multiple sclerosis, diabetes and cancer.[xiii]

According to Devra Davis in her book Secret History of the War on Cancer, 1.5 million lives have been lost because Americans failed to act on existing knowledge about the environmental causes of cancer. It is impossible to calculate the added deaths from suppressed ‘cancer cures’ but we do know of the terrible suffering of hundreds of thousands of people who have been jailed for marijuana use.

Hemp oil with THC included has the making of a primary cancer treatment, which even alone seems to have a great chance of turning the tide against cancer tumors. It has the added advantage of safety, ease of use, lack of side effects and low cost if one makes it oneself. Surrounded by other medicinal anti-cancer substances in a full protocol it’s hard to imagine anyone failing and falling in their war on cancer.

THC should be included in every cancer protocol.

Sodium bicarbonate is another excellent anti tumor substance that reduces tumors but is much more difficult to administer than THC hemp oil. Cannabinoids are able to pass through all barriers in the body like Alpha Lipoic Acid so simple oral intake is sufficient. With bicarbonate we need intravenous applications and often even this is not sufficient, often we have to use catheters and few doctors in the world are willing to administer this way.

In the end all cancer treatments that are not promoted by mainstream oncology are illegal. No licensed doctor is going to claim that are curing cancer with sodium bicarbonate though they will treat people with cancer explaining they are balancing pH or some other metabolic profile with this common emergency room medicine found also most kitchens of the world. More than several states have passed laws making medical marijuana legal but the federal government will not relax and let people be free to choose their treatments even if their lives depend on it.

Davis notes that the cowardice of research scientists, who publish thoroughly referenced reports but pull their punches at the end, by claiming that more research needs to be done before action can be taken. Statements like these are exploited by industry that buys time to make much more money. It is a deliberate attempt that creates wholesale public doubt from small data gaps and remaining scientific uncertainties.

They have done that with everything right up to and including sunlight. Everything is thought to be dangerous except the pharmaceutical drugs which are the most dangerous substances of all. Stomach wrenching chemotherapy and the death principle of radiation are legal yet safe THC laden hemp oil is not.

It is legal for doctors to attack people with their poisons but you can go to jail for trying to save yourself or a loved one from cancer with the oil of a simple garden weed. Our civilization has put up with this insanity but there is a great price being paid. In a mad medical world people die that need not and this is a terrible sadness that has destroyed the integrity and ethics of modern medicine.

The science for the use of hemp oil is credible, specific fact-based, and is documented in detail.[xiv] There is absolutely no reason to not legalize medical marijuana and create an immediate production and distribution of THC hemp oil to cancer patients. Unfortunately we live in a world populated with governments and medical henchmen who would rather see people die cruel deaths then have access to a safe and effect cancer drug.

Meanwhile the Food and Drug Administration approved Genentech’s best-selling drug, Avastin, as a treatment for breast cancer, in a decision, according to the New York Times, “that appeared to lower the threshold somewhat for approval of certain cancer drugs. The big question was whether it was enough for a drug temporarily to stop cancer from worsening — as Avastin had done in a clinical trial — or was it necessary for a drug to enable patients to live longer, which Avastin had failed to do. Oncologists and patient advocates were divided, in part because of the drug’s sometimes severe side effects.”[xv]

The differences between Avastin and hemp oil are huge. First Avastin will earn Genentech hundreds of millions where THC hemp oil will earn no one anything. Second there are no severe or even mild side effects to taking hemp oil and lastly it is not a temporary answer but a real solution. Certainly hemp oil will ensure a longer life.


Learn more with Books about the healing power of Cannabis:

 Too High to Fail: Cannabis and the New Green Economic Revolution  Marijuana Gateway to Health: How Cannabis Protects Us from Cancer and Alzheimer’s Disease  Understanding Marijuana: A New Look at the Scientific Evidence

All About DCA A Natural Holistic Cancer Cure

Dichloroacetic acid

From Wikipedia, the free encyclopedia
Dichloroacetic acid
CAS number 79-43-6  Yes
PubChem 6597
ChemSpider 10771217  Yes
DrugBank DB08809
KEGG C11149  Yes
MeSH Dichloroacetate
ChEBI CHEBI:36386  Yes
RTECS number AG6125000
Jmol-3D images Image 1
Molecular formula C2H2Cl2O2
Molar mass 128.94 g mol−1
Appearance Colorless liquid
Density 1.5634 g/cm3 (20 °C)
Melting point 9-11 °C, 282-284 K, 48-52 °F
Boiling point 194 °C, 467 K, 381 °F
Solubility in water miscible
Solubility miscible with ethanoldiethyl ether[1]
Acidity (pKa) 1.35[1]
Std enthalpy of
-496.3 kJ·mol-1[1]
MSDS MSDS (jtbaker)
R-phrases R35 R50
S-phrases (S1/2) S26 S45 S61
NFPA 704
NFPA 704.svg
Related compounds
Related chloroacetic acids Chloroacetic acid
Trichloroacetic acid
Related compounds Acetic acid
Difluoroacetic acid
Dibromoacetic acid
 Yes (verify) (what is: Yes/?)
Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)
Infobox references

Dichloroacetic acid, often abbreviated DCA, is the chemical compound with formulaCHCl2COOH. It is an acid, an analogue of acetic acid, in which two of the three hydrogenatoms of the methyl group have been replaced by chlorine atoms. The salts and esters of dichloroacetic acid are called dichloroacetates. Salts of DCA have been studied as potential drugs because they inhibit the enzyme pyruvate dehydrogenase kinase.[citation needed]



[edit]Chemistry and occurrence

The chemistry of dichloroacetic acid is typical for halogenated organic acids. It is a member of the chloroacetic acids family. The dichloroacetate ion is produced when the acid is mixed with water. As an acid with a pKa of 1.35,[1] pure dichloroacetic acid is verycorrosive and extremely destructive to tissues of the mucous membranes and upper respiratory tract.[2]

DCA does not occur in nature. It is a trace product of the chlorination of drinking water and is produced by the metabolism of various chlorine-containing drugs or chemicals.[3] DCA is typically prepared by the reduction of trichloroacetic acid.

[edit]Therapeutic use

Owing to the highly corrosive action of the acid, only the salts of dichloroacetic acid are used therapeutically, including its sodium and potassium salts, sodium dichloroacetate and potassium dichloroacetate.

[edit]Lactic acidosis

The dichloroacetate ion stimulates the activity of the enzyme pyruvate dehydrogenase by inhibiting the enzyme pyruvate dehydrogenase kinase.[4] Thus, it decreases lactateproduction by shifting the metabolism of pyruvate from fermentation towards oxidation in the mitochondria. This property has led to trials of DCA for the treatment of lactic acidosisin humans.[5][6][7][8]

randomized controlled trial in children with congenital lactic acidosis found that while DCA was well tolerated, it was ineffective in improving clinical outcomes.[6] A separate trial of DCA in children with MELAS (a syndrome of inadequate mitochondrial function, leading to lactic acidosis) was halted early, as all 15 of the children receiving DCA experienced significant nerve toxicity without any evidence of benefit from the medication.[7] A randomized controlled trial of DCA in adults with lactic acidosis found that while DCA lowered blood lactate levels, it had no clinical benefit and did not improve hemodynamicsor survival.[8]

Thus, while early case reports and pre-clinical data suggested that DCA might be effective for lactic acidosis, subsequent controlled trials have found no clinical benefit of DCA in this setting. In addition, clinical trial subjects were incapable of continuing on DCA as a study medication owing to progressive toxicities.

[edit]Potential cancer applications

Cancer cells generally express increased glycolysis, because they rely on anaerobic respiration that occurs in the cytosol (lactic acid fermentation) rather than oxidative phosphorylation in the mitochondria for energy (the Warburg effect), as a result of hypoxia that exists in tumors and malfunctioning mitochondria.[9][10] Usually dangerously damaged cells kill themselves via apoptosis, a mechanism of self-destruction that involves mitochondria, but this mechanism fails in cancer cells.

A phase I study published in January 2007 by researchers at the University of Alberta, who had tested DCA on human[11] cancer cells grown in mice, found that DCA restored mitochondrial function, thus restoring apoptosis, allowing cancer cells to self-destruct and shrink the tumor.[12]

These results received extensive media attention, beginning with an article in New Scientist titled “Cheap, ‘safe’ drug kills most cancers”.[11] Subsequently, the American Cancer Society and other medical organizations have received a large volume of public interest and questions regarding DCA.[13] Clinical trials in humans with cancer have not been conducted in the USA and are not yet final in Canada, emphasizing the need for caution in interpreting the preliminary results.[13][14]

[edit]Results of phase II clinical trials

In in vitro studies, Evangelos Michelakis of University of Alberta found that in tissue samples from 49 patients, DCA caused depolarization of mitochondria in GBM tissue but not in healthy brain tissue.[15]

Five palliative patients with primary GBM were entered into a phase II trial. Three had not responded to several chemotherapies; two were newly diagnosed. After surgical removal of tumor mass, they were treated with DCA and chemotherapy.[15]

Of the five patients tested, one died after three months. The surviving four were followed for 15 months. Their Karnofsky scores were unchanged in two cases, and decreased by 10 points in two patients.[15]

DCA was associated with tumor regression and had a good safety profile. DCA side effects were minimal.[15]

Michelakis is proceeding with phase three human studies with private funding from philanthropic groups and individuals. DCA’s legal status as a discovery is public domain because it was made or discovered as far back as 1864[16] and has been used in the treatment of canine and human lactic acidosis, some who presented at the beginning of treatment with cancer.

[edit]Concerns about pre-trial use

Following its initial publication, The New Scientist later editorialized, “The drug may yet live up to its promise as an anti-cancer agent – clinical trials are expected to start soon. It may even spawn an entirely new class of anti-cancer drugs. For now, however, it remains experimental, never yet properly tested in a person with cancer. People who self-administer the drug are taking a very long shot and, unlikely as it may sound, could even make their health worse.”[17]

In 2010, it was found that for human colorectal tumours grown in mice, under hypoxic conditions, DCA decreased rather than increased apoptosis, resulting in enhanced growth of the tumours.[18] These findings suggest that at least in some cancer types DCA treatment could be detrimental to patient health, highlighting the need for further testing before it can be considered a safe and effective cancer treatment.[18]

[edit]Planned and ongoing clinical trials

DCA is non-patentable as a compound, though a patent has been filed for its use in cancer treatment.[19] Research by Evangelos Michelakis has received no support from the pharmaceutical industry.[20] Concerns have been raised that without strong intellectual property protection, the financial incentive for drug development is reduced, and therefore obtaining sufficient funds to conduct clinical trials presents difficulty.[11][13][14][21] However, other sources of funding exist; previous studies of DCA have been funded by government organizations such as the National Institutes of Health, the Food and Drug Administration, the Canadian Institutes of Health Researchand by private charities (e.g. the Muscular Dystrophy Association). Recognizing anticipated funding challenges, Michelakis’s lab took the unorthodox step of directly soliciting online donations to fund the research.[22] After 6 months, his lab had raised over $800,000, enough to fund a small Clinical Phase 2 study. Michelakis and Archer have applied for a patent on the use of DCA in the treatment of cancer.[19][23]

On 24 September 2007, the Department of Medicine of Alberta University reported that after the trial funding was secured, both the Alberta local ethics committee and Health Canada approved the first DCA clinical trial for cancer.[24] This initial trial was relatively small with enrollment of up to 50 patients. The trial was completed in August 2009.[25] In May 2010 the team published a press release[26]stating no conclusions could be drawn as a result of the trial. A paper describing the results was published[27] but not linked from the press release. Only five patients had been treated with the drug during the trial.

In May 2011, online reports[28] suggested that the Alberta group had released new data which the media “had not reported”. However, this appeared to be caused by confusion between dates (the previous update was May 2010[29]) and cancer charities moved quickly to counter these rumours,[30][31] which were subsequently covered in New Scientist magazine.[32]

The use of this compound as an anti-cancer agent has been patented.[33]

[edit]Side effects

Reports in the lay press after the 2007 University of Alberta announcement claim that dichloroacetate “has actually been used safely in humans for decades”,[34] DCA is generally well tolerated, even in children.[35] Short-term, infused, bolus doses of DCA at 50 mg/kg/day have been well tolerated.[36]

At sustained, higher doses(generally 25 mg/kg/day taken orally, or greater), there is increased risk of several reversible toxicities, especially peripheral neuropathyneurotoxicity, and gait disturbance.[4][34]

Studies have also shown that it can be carcinogenic in male B6C3F1 mice at high doses.[37]


A clinical trial where DCA was given to patients of MELAS (a form of genetically inherited lactic acidosis) at 25 mg/kg/day was ended prematurely due to excessive peripheral nerve toxicity.[38] Dichloroacetate can also have anxiolytic or sedative effects.[3]

Animal studies suggest that the neuropathy and neurotoxicity during chronic dichloroacetate treatment may be partly due to depletion of thiamine, and thiamine supplementation in rats reduced these effects.[39] However, more recent studies in humans suggest that peripheral neuropathy is a common side effect during chronic DCA treatment, even with coadministration of oral thiamine.[40][41] An additional study reported that 50 mg/kg/day DCA treatment resulted in unsteady gait and lethargy in two patients, with symptoms occurring after one month for one patient and two months for the second. Gait disturbance and consciousness were recovered with cessation of DCA, however sensory nerve action potentials did not recover in one month.[42]

It has been reported that animals and patients treated with DCA have elevated levels of delta-aminolevulinic acid (delta-ALA) in the urine. A study published in 2008 suggests that this product may be the cause of the neurotoxic side effect of DCA by blocking peripheralmyelin formation.[43]


Long term use (three years or more) of high doses (> 77 mg/kg/day) of DCA has been shown to increase risk of liver cancer in mice.[37]Studies of the trichloroethylene (TCE) metabolites dichloroacetic acid (DCA), trichloroacetic acid (TCA), and chloral hydrate suggest that both DCA and TCA are involved in TCE-induced liver tumorigenesis and that many DCA effects are consistent with conditions that increase the risk of liver cancer in humans.[44] It should be noted here that the maximum recommended dose for cancer treatment is 20mg/kg/day (less than 1/3rd of the 77mg/kg/day shown to increase liver cancer risk in mice).


The promise of DCA as a cheap, effective and safe treatment for cancer generated a great deal of public interest. Many people turned to self-medication.[45][46]

Doctors warned of potential problems if people attempt to try DCA outside a controlled clinical trial. “If it starts going badly, who is following you before it gets out of control? By the time you realize your liver is failing, you’re in big trouble”, said Laura Shanner, Associate Professor of Health Ethics at the University of Alberta.[47]


  1. a b c d Haynes, William M., ed. (2011). CRC Handbook of Chemistry and Physics (92nd ed.). CRC Press.ISBN 1439855110.
  2. ^ J.T. Baker MSDS
  3. a b Stacpoole P, Henderson G, Yan Z, James M (1998).“Clinical pharmacology and toxicology of dichloroacetate”.Environ Health Perspect 106 Suppl 4: 989–994.doi:10.2307/3434142 . JSTOR 3434142 . PMC 1533324.PMID 9703483.
  4. a b Stacpoole PW (1989). “The pharmacology of dichloroacetate”. Metabolism 38 (11): 1124–1144.doi:10.1016/0026-0495(89)90051-6 . PMID 2554095.
  5. ^ Stacpoole P, Lorenz A, Thomas R, Harman E (1988). “Dichloroacetate in the treatment of lactic acidosis”. Ann Intern Med 108 (1): 58–63. PMID 3337517.
  6. a b Stacpoole P, Kerr D, Barnes C, Bunch S, Carney P, Fennell E, Felitsyn N, Gilmore R, Greer M, Henderson G, Hutson A, Neiberger R, O’Brien R, Perkins L, Quisling R, Shroads A, Shuster J, Silverstein J, Theriaque D, Valenstein E (2006). “Controlled clinical trial of dichloroacetate for treatment of congenital lactic acidosis in children”. Pediatrics 117 (5): 1519–1531. doi:10.1542/peds.2005-1226 . PMID 16651305.
  7. a b Kaufmann P, Engelstad K, Wei Y, Jhung S, Sano M, Shungu D, Millar W, Hong X, Gooch C, Mao X, Pascual J, Hirano M, Stacpoole P, DiMauro S, De Vivo D (2006). “Dichloroacetate causes toxic neuropathy in MELAS: a randomized, controlled clinical trial”. Neurology 66 (3): 324–330.doi:10.1212/01.wnl.0000196641.05913.27 .PMID 16476929.
  8. a b Stacpoole P, Wright E, Baumgartner T, Bersin R, Buchalter S, Curry S, Duncan C, Harman E, Henderson G, Jenkinson S (1992). “A controlled clinical trial of dichloroacetate for treatment of lactic acidosis in adults. The Dichloroacetate-Lactic Acidosis Study Group”. N Engl J Med 327 (22): 1564–1569.doi:10.1056/NEJM199211263272204 . PMID 1435883.
  9. ^ Xu R, Pelicano H, Zhou Y, Carew J, Feng L, Bhalla K, Keating M, Huang P (2005). “Inhibition of glycolysis in cancer cells: a novel strategy to overcome drug resistance associated with mitochondrial respiratory defect and hypoxia”. Cancer Res 65(2): 613–21. PMID 15695406.
  10. ^ Kim JW, Dang CV (2006). “Cancer’s molecular sweet tooth and the Warburg effect” . Cancer Res. 66 (18): 8927–8930.doi:10.1158/0008-5472.CAN-06-1501 . PMID 16982728.
  11. a b c “Cheap, ‘safe’ drug kills most cancers” . New Scientist. 2007-01-17. Retrieved 2007-01-17.
  12. ^ Bonnet, Sébastien; Archer, Stephen L.; Allalunis-Turner, Joan; Haromy, Alois; Beaulieu, Christian; Thompson, Richard; Lee, Christopher T.; Lopaschuk, Gary D. et al. (2007). “A Mitochondria-K+ Channel Axis Is Suppressed in Cancer and Its Normalization Promotes Apoptosis and Inhibits Cancer Growth”. Cancer Cell 11 (1): 37–51.doi:10.1016/j.ccr.2006.10.020 . PMID 17222789.
  13. a b c “DCA: Cancer Breakthrough or Urban Legend?”  FromABC News, 5 February 2007. Accessed 15 February 2007.
  14. a b “No Wonder Drug” , letter to New Scientist from Ralph Moss Lemont. Published February 3, 2007. Accessed 16 February 2007.
  15. a b c d Michelakis, E. D.; Sutendra, G.; Dromparis, P.; Webster, L.; Haromy, A.; Niven, E.; Maguire, C.; Gammer, T. L. et al. (2010). “Metabolic Modulation of Glioblastoma with Dichloroacetate” . Sci Transl Med 2 (31): 31ra34–31ra34.doi:10.1126/scitranslmed.3000677 . PMID 20463368.
  16. ^ T. E. (Thomas Edward) Thorpe. A Dictionary of Applied Chemistry. Vol. 3. Page 9 of 189 at http://www.ebooksread.com/authors-eng/t-e-thomas-edward-thorpe/a-dictionary-of-applied-chemistry-volume-3-hci/page-9-a-dictionary-of-applied-chemistry-volume-3-hci.shtml
  17. ^ “Editorial: Gambling with your life” , New Scientist, 31 March 2007
  18. a b Shahrzad, Siranoush; Lacombe, Kristen; Adamcic, Una; Minhas, Kanwal; Coomber, Brenda L. (November 2010). “Sodium dichloroacetate (DCA) reduces apoptosis in colorectal tumor hypoxia”. Cancer Letters 297 (1): 75–83.doi:10.1016/j.canlet.2010.04.027 . PMID 20537792.
  19. a b “CTV.ca: Researchers launch website on new cancer research” . CTV News.
  20. ^ “CTV.ca: Small molecule offers hope for cancer treatment” . CTV News. Retrieved 21 April 2012.
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  22. ^ Official University of Alberta DCA Site
  23. ^ A Method of Treating Cancer Using Dichloroacetate , Application to the European Patent Office, 19 October 2006
  24. ^http://www.dca.med.ualberta.ca/Home/Updates/letter_092407.pdf , 24 September 2007
  25. ^ The Safety and Efficacy of DCA for the Treatment of Brain Cancer , ClinicalTrials.gov identifier: NCT00540176
  26. ^ Outlook 2008 , Tufts Center for the Study of Drug Development
  27. ^ Michelakis, ED; Sutendra, G; Dromparis, P; Webster, L; Haromy, A; Niven, E; Maguire, C; Gammer, TL et al. (2010). “Metabolic modulation of glioblastoma with dichloroacetate”.Science translational medicine 2 (31): 31ra34–31ra34.doi:10.1126/scitranslmed.3000677 . PMID 20463368.
  28. ^ The Cure for Cancer Has Been Found and is Purposely Being Ignored  – Technorati blog (accessed 16/05/2011)
  29. ^ DCA Research Team publishes results of Clinical Trials  – University of Alberta website
  30. ^ Potential cancer drug DCA tested in early trials  – Cancer Research UK science blog
  31. ^ @CR_UK tweet  – tweeted 16/05/11
  32. ^ Cancer drug resurfaces and threatens false optimism  – New Scientist, 16 May 2011
  33. ^ US 8071645 , Newell, M. Karen; Newell, Evan & Villalobos-Menuey, Elizabeth, “Systems and methods for treating human inflammatory and proliferative diseases and wounds, with fatty acid metabolism inhibitors and/or glycolytic inhibitors”
  34. a b Picard, André (2007-01-17). “Long-used drug shows new promise for cancer” . Toronto: The Globe and Mail. Retrieved 2007-01-17.
  35. ^ Pearson H; Kurtz, TL; Han, Z; Langaee, T (2008). “Role of dichloroacetate in the treatment of genetic mitochondrial diseases”. Adv Drug Deliv Rev. 60 (13,14): 1478–1487.doi:10.1016/j.addr.2008.02.014 . PMID 18647626.
  36. ^ Agbenyega T, Planche T, Bedu-Addo G, Ansong D, Owusu-Ofori A, Bhattaram VA, Nagaraja NV, Shroads AL, Henderson GN, Hutson AD, Derendorf H, Krishna S, Stacpoole PW (2003). “Population kinetics, efficacy, and safety of dichloroacetate for lactic acidosis due to severe malaria in children”. J Clin Pharmacol. 43 (4): 386–396.doi:10.1177/0091270003251392 . PMID 12723459.
  37. a b DeAngelo AB, Daniel FB, Stober JA, Olson GR (1991). “The carcinogenicity of dichloroacetic acid in the male B6C3F1 mouse”. Fundam Appl Toxicol. 16 (2): 337–347.doi:10.1016/0272-0590(91)90118-N . PMID 2055364.
  38. ^ Kaufmann P, Engelstad K, Wei Y et al. (2006). “Dichloroacetate causes toxic neuropathy in MELAS: a randomized, controlled clinical trial”. Neurology 66 (3): 324–330. doi:10.1212/01.wnl.0000196641.05913.27 .PMID 16476929.
  39. ^ Stacpoole P, Harwood H, Cameron D, Curry S, Samuelson D, Cornwell P, Sauberlich H (1990). “Chronic toxicity of dichloroacetate: possible relation to thiamine deficiency in rats”.Fundam Appl Toxicol 14 (2): 327–37. doi:10.1016/0272-0590(90)90212-3 . PMID 2318357.
  40. ^ Kurlemann G, Paetzke I, Moller H, Masur H, Schuierer G, Weglage J, Koch HG (1995). “Therapy of complex I deficiency: peripheral neuropathy during dichloroacetate therapy”. Eur J Pediatr 154 (11): 928–32. doi:10.1007/BF01957508 .PMID 8582409.
  41. ^ Spruijt L, Naviaux RK, McGowan KA, Nyhan WL, Sheean G, Haas RH, Barshop BA (2001). “Nerve conduction changes in patients with mitochondrial diseases treated with dichloroacetate”. Muscle Nerve 24 (7): 916–24.doi:10.1002/mus.1089 . PMID 11410919.
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  43. ^ Felitsyn, N; McLeod, C; Shroads, AL; Stacpoole, PW; Notterpek, L (2008). “The heme precursor delta-aminolevulinate blocks peripheral myelin formation”Journal of Neurochemistry 106 (5): 2068–2079. doi:10.1111/j.1471-4159.2008.05552.x . PMC 2574579PMID 18665889.
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  46. ^ Interview: Would you try an untested cancer drug? , New Scientist, August 15, 2007
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[edit]External links

  • International Chemical Safety Card 0868
  • CTV.ca News Staff (16 January 2007). “Small molecule offers hope for cancer treatment” . CTV.ca Website (CTV television network). Retrieved 2007-01-31.
  • DCA Research Information Website  (University of Alberta)
  • Wait for Clinical Trials , New Scientist, 24 February 2007
  • Potential cancer drug DCA tested in early trials , by Cancer Research UK
  • Interviewing Drs. Akbar and Humaira Khan about DCA
  • Cancer Biology – Cramping Tumors  Economist, January 18, 2007
  • Official University of Alberta DCA (dichloroacetate) Website , The University of Alberta Discovery. March 15, 2007
  • Dichloroacetate Orders

    Telephone Orders: 1-347-535-4322 (New York area)
    We are VERY busy, if you get the answering machine leave your name and phone number, we will call you back.

    UPDATE we now have DCA in capsules
    333 mg per capsule, Click To Buy DCA

    60 Day DCA Treatment Kit is now available in the DCA Store

    What’s New With Dichloroacetate?

    February 2012 Video added “Using a Scale to Measure DCA
    August 31, 2011 Doctor Flavin, M.D. read his letter Doctor Flavin’s letter
    March 20, 2011 Read how one person beat cancer using DCA.
    May 12, 2010 Latest Positive DCA Clinical Trials and More! Visit the University of Alberta  (the university site is currently down, try this link to read about the doctor )

    Recent Medical Research at a Canadian University has confirmed that scientists do understand the cause of cancer. The dying off of old cells to be replaced by new cells is a normal part of our cellular lifecycle and keeps us well. It seems that in cancerous cells, our body has forgotten how to tell the aged cells how to die off and be replaced by healthy new cells. This process is governed by the mitochondria and is known as “cell death” or “apoptosis”. In a cancer cell, the mitochondria has lost the ability to direct the cell to die off – the sick cell becomes “immortal”, spreading and making the person increasingly unwell. Recent Medical trials using Pure DCA have proven this compound can reactivate the mitochondria restoring the cell’s original function of “apoptosis” enabling shrinkage in tumor size and mass. Testimonials have shown reversal in illness, remission, clean health tests, increased health and vitality. Favourable results (scientifically measurable) have been accomplished within days (less than a week) of starting treatment with Pure DCA.

    “Dr. Evangelos Michelakis, a professor at the U of A Department of Medicine, has shown that dichloroacetate (DCA) causes regression in several cancers, including lung, breast, and brain tumors.

    Sodium dichloroacetate offered by PureDCA.com is more than 99% pure. It is made using a sophisticated synthesis process. No organic solvents are used during the production. WE SHIP DCA WORLDWIDE.

    We are working with Doctors around the world but also service individual orders for Pure DCA for those looking for an alternative cancer treatment. You do NOT need a prescription.

    We ship dichloroacetate internationally, with no exceptions. We are a reliable source of sodium dichloroacetate (Pure DCA). Buy sodium dichloroacetate.

    Below you can find a description of the main sections of this website.

    Pure DCA Store

    • Buy DCA Online or by Telephone
    • Pure DCA Powder is available in 3 sizes: 20 grams, 50 grams, and 100 grams
    • Pure DCA in Capsules (333mg)
    • Pure Powdered Thiamine (Vitamin B1)
    • Pure NAC Powder (N-Acetyle L-Cysteine)
    • Medicinal dosing scales also available

    Pure DCA Information
    The main facts about sodium dichloroacetate, pure DCA

    Frequently Asked Questions

    Contact Us

    Dichloroacetate has been used in recent human trials and was found to shrink tumors. These trials were done by a university and their results have been published for anyone to read about the dichloroacetate cancer connection. The link to the universities dichloroacetate  study.

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