Tag: acid

All About DCA A Natural Holistic Cancer Cure

Dichloroacetic acid

From Wikipedia, the free encyclopedia
Dichloroacetic acid
Identifiers
CAS number 79-43-6  Yes
PubChem 6597
ChemSpider 10771217  Yes
UNII 9LSH52S3LQ  Yes
DrugBank DB08809
KEGG C11149  Yes
MeSH Dichloroacetate
ChEBI CHEBI:36386  Yes
ChEMBL CHEMBL13960  Yes
RTECS number AG6125000
Jmol-3D images Image 1
Properties
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 ethanol, diethyl ether[1]
Acidity (pKa) 1.35[1]
Thermochemistry
Std enthalpy of
formation ΔfHo298		 -496.3 kJ·mol-1[1]
Hazards
MSDS MSDS (jtbaker)
R-phrases R35 R50
S-phrases (S1/2) S26 S45 S61
NFPA 704
NFPA 704.svg
1
3
0
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 It is an acid, an analogue of acetic acid, in which two of the three hydrogenatoms of the methyl group have been replaced by chlorine atoms.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]

Contents

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[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]

A 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 neuropathy, neurotoxicity, and gait disturbance.[4][34]

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

[edit]Neuropathy

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]

[edit]Carcinogenicity

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).

[edit]Self-medication

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]

[edit]References

  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.
  21. ^ “Small molecule offers big hope against cancer” , by Ryan Smith. From ExpressNews, a University of Alberta publication. Published January 16, 2007. Accessed 15 February 2007.
  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.
  42. ^ Oishi K, Yoshioka M, Ozawa R, Yamamoto T, Oya Y, Ogawa M, Kawai M (2003). “Dichloroacetate treatment for adult patients with mitochondrial disease”. Rinsho Shinkeigaku 43 (4): 154–61. PMID 12892050.
  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 2574579. PMID 18665889.
  44. ^ Caldwell JC, Keshava N (September 2006). “Key issues in the modes of action and effects of trichloroethylene metabolites for liver and kidney tumorigenesis” . Environ. Health Perspect.114 (9): 1457–63. PMC 1570066. PMID 16966105.
  45. ^ Pearson, Helen (2007). “Cancer patients opt for unapproved drug”. Nature 446 (7135): 474–475. doi:10.1038/446474a .PMID 17392750.
  46. ^ Interview: Would you try an untested cancer drug? , New Scientist, August 15, 2007
  47. ^ Andrea Sands (March 18, 2007). “Experts caution against patients compiling own data on unapproved cancer drug” . Edmonton Journal.

[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.

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    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.”

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    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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All About Astragalus, The Cancer Fighter

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(NaturalNews) Astragalus is a traditional Chinese medicinal herb that has been around for over 4,000 years. Astragalus is an adaptogenic, nontoxic herb and plant extract that helps the body resist the damaging effects of stress while restoring normal physiological function. Astragalus aids adrenal function, digestion, metabolism, combats fatigue and increases stamina. Astragalus is very effective in helping people with AIDS and has even proven to have an anti-tumor effect and can increase the efficacy of chemotherapy.

A native plant of China, astragalus is officially known as astragalus membranaceus: AKA Milk Vetch Root and Huang Qi. Astragalus is a perennial plant that grows up to 4 feet tall. The root of the plant has a sweet taste and contains choline, flavonoids, amino acids-gamma aminobutyric acid, canavanine, beta-sitosterol, saponins (astragalosides) and oil. The primary actions of astragalus are adaptogenic and immunomodulating. The secondary actions are anti-inflammatory, anti-viral, cardiotonic, diuretic and hepatoprotective.

Medicinal Use

Astragalus is an herb that has actions in nearly all of the body systems. It is used to treat chronic colds, Epstein Barr Virus, HIV and candida by preventing infection recurrence. Astragalus stimulates bone marrow blood cells while enhancing deep immune strength. Studies show that the polysaccharides in astragalus increase phagocytosis (the engulfing of microorganism invaders by the immune system), increase production of immunoglobulins and macrophages and modulate the pituitary-adrenal cortical activity. Astragalus protects the kidneys and lungs from damage from autoantibody complexes, regulates sweating, decreases fatigue and increases tolerance to stress.

Astragalus protects against oxidative damage by increasing mitochondrial function without increasing the mitochondrial oxygen consumption. In the liver, astragalus is a mild choleretic and also increases repairs in chronic viral hepatitis while reducing inflammation and othersymptoms. Astragalus also lengthens telomeres for longevity(TA 65 is a very pricey extract made from Astragalus that is touted to reduce all the effects of aging and mimics pretty much all the benefits of the inexpensive herb form of astragalus). Astragalus even increases motility of human sperm.

Astragalus is considered to be a cardiac tonic.In the cardiovascular system, the saponins in astragalus inhibit lipid peroxidation in the myocardium and one study using patients with angina revealed that cardiac output increased after two weeks of treatment. Astragalus strengthens left ventricular function and reduces free radical damage in patients after a heart attack and increases super oxide dismutase activity in cardiac muscle.

Astragalus: the unsung cancer fighter

Studies at the University of Houston have shown that astragalus can improve immune function in cancer patients by increasing T-cell counts. Astragalus increases the ability of NK cells and T-cells to kill cancer cells while switching on the anti-tumor activity of Interleukin-2. Inchemotherapy treatmentsastragalus provides anti-neoplastic activity anddecreasesimmunosupression. Astragalus reduces the consequences with both chemo and radiation of fatigue,weight loss, anemia, nausea and loss of strength while increasing WBC production for leucopenia (a common side effect of immunosuppressive therapy), thereby decreasing life-threatening infections.

Even though this incredible herb is listed on the Botanical Herbs Board Exams and in theCompendium of Pharmacological Actions of Medicinal Plants and Their Constituents, naming the benefits of astragalus can bring a warning letter from both the FDA and FTC, as Dr. Andrew Weil found out when he listed the benefits of taking astragalus to prevent the swine flu. So don’t expect to see any of this information on a vitamin or herb label. Despite what modern medicine and the FDA says, healing did occur long before pharmaceuticals were invented. True health comes by good foods, minerals, herbs, fasting and cleansing. Astragalus is a good guy for natural health!

Sources:

Compendium of Pharmacological Actions of Medicinal Plants and Their Constituents, Compiled and copyrighted by Eric Yarnell, ND Actions of Medicinal Plants 2007 Eric Yarnell, ND

Zhang CZ, Wang SX, Zhang Y, Chen JP, Liang XM. “In vitro estrogenic activities of Chinese medicinal plants traditionally used for the management of menopausal symptoms.” J Ethnopharmacol 2005;98(3):295-300.

Nutrition 740 notes Spring 2006, Dr. Mona Morstein, SCNM

http://www.cancertutor.com/WarBetween/War_Cure_Rates.htmlhttp://cms.herbalgram.org/herbclip/pdfs/121581-151.pdf

About the author:
Craig Stellpflug is a Cancer Nutrition Specialist, Lifestyle Coach and Neuro Development Consultant at Healing Pathways Medical Clinic, Scottsdale, AZ. With 17 years of clinical experience working with both brain disorders and cancer, Craig has seen first-hand the devastating effects of vaccines and pharmaceuticals on the human body and has come to the conclusion that a natural lifestyle and natural remedies are the true answers to health and vibrant living. You can find his daily health blog atwww.blog.realhealthtalk.comand his articles and radio show archives atwww.realhealthtalk.com

Learn more:http://www.naturalnews.com/035924_astragalus_cancer_prevention.html#ixzz1vathSZRH

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Absolutely know the the Truth about the Shroud of Turin

By:Daniel J Leach

Many claim that The Shroud of Turin is Jesus Christ but the  Knights Templar claim that this is Jacques de Molay.  I myself would like to think that this is Jesus Christ but with my research and understanding of history tend to lead me to believe that this is indeed Jacques de Molay and not Jesus Christ.

Geoffroi de Charny (the French Knight who died at the 1356 battle of Poitiers) and his wife Jeanne de Vergy are the first reliably recorded owners of the Turin Shroud. This Geoffroi participated in a failed crusade under Humbert II of Viennois in the late 1340s.[26] He is sometimes confused with Templar Geoffroi de Charney.[27]

This Section Copied from: http://blog.templarhistory.com/2010/03/the-templars-and-the-shroud-of-turin/

Any discussion of the Shroud of Turin is bound to be controversial. Those who view this sacred and holy relic fall into two camps, those that believe it to be the undisputed earthly evidence of a Christ risen and those who believe it to be a medieval forgery.

It is not the intention of this web site to cast doubt on or support the authenticity of the shroud, but rather to show its possible relationship to the Knights Templar. We receive many letters from angry people who wish to enter into lengthy debates about carbon 14 reliability. We are aware of new evidence that puts the reliability of carbon 14 dating in question, so please refrain from telling us of the findings or directing us to URLs that make the claims.

There are two theories that relate to the Templars having been involved with the Shroud, one, which would support the authenticity of the Shroud and another, which would refute it.

In 1204 the Crusaders sacked the city of Constantinople. Among them were the Knights Templar, whom some scholars contend took the Burial shroud of Jesus from the city. To support this theory, author Ian Wilson who wrote the book “The Shroud of Turin: Burial Cloth Of Jesus?” makes the claim that the head that the Templars were accused of worshipping was none other than that of Jesus. His belief is that the Shroud when folded depicted the head of Christ and was referred to as the “Mandylion.” There is a painted panel at Templecombe in England that shows a bearded head like that, which is depicted on the Mandylion.

In their two books, “The Hiram Key” and “The Second Messiah,” authors Christopher Knight and Robert Lomas paint a contrasting picture to the Mandylion theory. The authors theorize that the image on the Shroud of Turin is in fact that of the last Grand Master of the order, Jacques de Molay, who was tortured some months before his execution in 1307. The image on the shroud certainly does fit the description of de Molay as depicted in medieval wood cuts, a long nose, hair shoulder length and parted in the center, a full beard that forked at its base, not to mention the six-foot frame. De Molay was said to be quite tall.

However, many have criticized the theory on the basis that the Templar rule of order forbade the Templars from growing their hair long. What critics of the theory overlook is that during DeMolay’s seven years in prison it is highly unlikely that he would have been afforded such luxuries as good grooming.

Knight and Lomas claim that the shroud figured in the Templars rituals of figurative resurrection and that DeMolay’s tortured body was wrapped in a shroud, which the Templars kept after his death. Lomas and Knight further believe that lactic acid and blood from DeMolay’s tortured body mixed with frankincense (used to whiten the cloth) etching his image into the shroud.

When the shroud was first put on display in 1357 (50 years after the disbanding of the order) by the family of Geoffrey de Charney who was also burned at the stake with de Molay, the first people viewing the shroud recognized the image to be that of Christ.

The authors theorize that Jacques de Molay may have been tortured in a manner similar to Christ as a mockery. Certainly then, the wounds suffered by de Molay where the same as those of Jesus Christ on the Cross.

Today it is commonly believed by many, through carbon dating, that the shroud dates to the late 13th century and not to the date of Christ’s supposed crucifixion. It is interesting that the church revealed these carbon dating results on October 13th, 1989, which is the same day the Templars were arrested by Church and State. According to the authors:

“Carbon dating has conclusively shown that the Shroud of Turin dates from between 1260 and 1380, precisely as we would expect if it were the image of Jacques de Molay. There is no other known theory that fits the scientifically established facts. Through experimentation, we know that the figure on the Shroud was on a soft bed of some kind, which strongly suggests that the victim was not dead and was expected to recover.”

The Second Messiah pg. 161 – Christopher Knight and Robert Lomas

Regardless of whether the findings of Ian Wilson or Knight and Lomas are correct, it is evident that this most holy and venerated relic has found its way into the Templar mythos.

Lynn Picknet and Clive Prince, authors of “Turin Shroud: In Whose Image?” present another theory of interest on the matter. Readers will recognize the authors from the book, “The Templar Revelation.” In the authors’ earlier book the duo claim that Leonardo Da Vinci who created an early photographic technique manufactured the image on the shroud of Turin.

Stephanie Pappas
Live Science
Thu, 05 Apr 2012 17:01 CDT
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Shroud of Turin

© Public domain
Full-length negative photograph of the Shroud of Turin.

A hoax or a miracle? The Shroud of Turin has inspired this question for centuries. Now, an art historian says this piece of cloth, said to bear the imprint of the crucified body of Jesus Christ, may be something in between.

According to Thomas de Wesselow, formerly of Cambridge University, the controversial shroud is no medieval forgery, as a 1989 attempt at radiocarbon dating suggests. Nor is the strange outline of the body on the fabric a miracle, de Wesselow writes in his new book, The Sign: The Shroud of Turin and the Secret of the Resurrection (Dutton Adult, 2012). Instead, de Wesselow suggests, the shroud was created by natural chemical processes – and then interpreted by Jesus’ followers as a sign of his resurrection.

“People in the past did not view images as just the mundane things that we see them as today. They were potentially alive. They were seen as sources of power,” de Wesselow told LiveScience. The image of Jesus found on the shroud would have been seen as a “living double,” he said. “It seemed like they had a living double after his death and therefore it was seen as Jesus resurrected.”

Believing the shroud

As de Wesselow is quick to admit, this idea is only a hypothesis. No one has tested whether a decomposing body could leave an imprint on shroud-style cloth like the one seen on the shroud. A 2003 paper published in the journal Melanoidins in Food and Health, however, posited that chemicals from the body could react with carbohydrates on the cloth, resulting in a browning reaction similar to the one seen on baked bread. (De Wesselow said he knows of no plans to conduct an experiment to discover if this idea really works.)

Perhaps more problematic is the authenticity of the shroud itself. Radiocarbon dating conducted in 1988 estimated the shroud to medieval times, between approximately A.D. 1260 and 1390. This is also the same time period when records of the shroud begin to appear, suggesting a forgery.

Critics have charged that the researchers who dated the shroud accidentally chose asample of fabric added to the shroud during repairs in the medieval era, skewing the results. That controversy still rages, but de Wesselow is convinced of the shroud’s authenticity from an art history approach.

“It’s nothing like any other medieval work of art,” de Wesselow said. “There’s just nothing like it.”

Among the anachronisms, de Wesselow said, is the realistic nature of the body outline. No one was painting that realistically in the 14th century, he said. Similarly, the body image is in negative (light areas are dark and vice versa), a style not seen until the advent of photography centuries later, he said.

“From an art historian’s point of view, it’s completely inexplicable as a work of art of this period,” de Wesselow said.

Resurrection: spiritual or physical?

If de Wesselow’s belief in the shroud’s legitimacy is likely to rub skeptics the wrong way, his mundane explanation of how the image of Jesus came to be is likely to ruffle religious feathers. According to de Wesselow, there’s no need to invoke a miracle when simple chemistry could explain the imprint. It’s likely, he says, that Jesus’ female followers returned to his tomb to finish anointing his body for burial three days after his death. When they lifted the shroud to complete their work, they would have seen the outline of the body and interpreted it as a sign of Jesus’ spiritual revival.

From there, de Wesselow suspects, the shroud went on tour around the Holy Land, providing physical proof of the resurrection to Jesus’ followers. When the Bible talks about people meeting Jesus post-resurrection, de Wesselow said, what it really means is that they saw the shroud. He cites the early writings of Saint Paul, which focus on a spiritual resurrection, over the gospels of Mark, Matthew, Luke and John, which were written later and invoke physical resurrection.

“The original conception of the resurrection was that Jesus was resurrected in a spiritual body, not in his physical body,” de Wesselow said.

These ideas are already receiving pushback, though de Wesselow says he’s yet to get responses from people who have read his entire book. Noted skeptic Joe Nickell toldMSNBC’s Alan Boyle that de Wesselow’s ideas were “breathtakingly astonishing,” and not in a good way; Nickell has argued on multiple occasions that the shroud’s spotty historical record and too-perfect image strongly suggest a counterfeit.

On the other end of the religious spectrum, former high-school teacher and Catholic religious speaker David Roemer believes in Jesus’ resurrection, but not the shroud’s authenticity. The image is too clear and the markings said to be blood aren’t smeared as they would be if the cloth had covered a corpse, Roemer told LiveScience.

“When you get an image this detailed, it means it was done by some kind of a human being,” Roemer said.

Unlike many “shroudies,” as believers are deprecatingly called, Roemer suspects the shroud was deliberately created by Gnostic sects in the first or second century. A common religious explanation for the markings is that a flash of energy or radiation accompanied Christ’s resurrection, “burning” his image onto the cloth.

If anything is certain about de Wesselow’s hypothesis, it’s that it is not likely to settle the shroud controversy. Scientific examinations of the delicate cloth are few and far between – and so are disinterested parties. Roemer, for example, recently arrived at a scheduled talk at a Catholic church in New York only to find the talk had been canceled when the priest learned of Roemer’s shroud skepticism. (The Catholic Church has no official position on the shroud’s authenticity.)

Meanwhile, de Wesselow said, people who aren’t driven by faith to accept the cloth as real generally don’t care about the shroud at all.

“The intellectual establishment, if you like, is not interested in shroud science,” he said. “It regards it as fringe and it’s not interested.”

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