Cannabinoids Stop Radiation Therapy Oxidation

Radiation Therapy

Radiation therapy is commonly applied to the cancerous tumor because of its ability to control cell growth. Ionizing radiation works by damaging the DNA of exposed tissue, furthermore, it is believed that cancerous cells may be more susceptible to death by this process as many have turned off their DNA repair machinery during the process of becoming cancerous.  To spare normal tissues (such as skin or organs which radiation must pass through in order to treat the tumor), shaped radiation beams are aimed from several angles of exposure to intersect at the tumor, providing a much larger absorbed dose there than in the surrounding, healthy tissue.  Besides the tumor itself, the radiation fields may also include the draining lymph nodes if they are clinically or radiologically involved with tumor, or if there is thought to be a risk of subclinical malignant spread.  It is necessary to include a margin of normal tissue around the tumor to allow for uncertainties in daily set-up and internal tumor motion.  These uncertainties can be caused by internal movement (for example, respiration and bladder filling) and movement of external skin marks relative to the tumor position.

Radiation oncology is the medical specialty concerned with prescribing radiation, and is distinct from radiology, the use of radiation in medical imaging and diagnosis).  Radiation may be prescribed by a radiation oncologist with intent to cure ("curative") or for adjuvant therapy.  It may also be used as palliative treatment (where cure is not possible and the aim is for local disease control or symptomatic relief) or as therapeutic treatment (where the therapy has survival benefit and it can be curative).  It is also common to combine radiation therapy with surgery, chemotherapy, hormone therapy, Immuno-therapy or some mixture of the four.  Most common cancer types can be treated with radiation therapy in some way.  The precise treatment intent (curative, adjuvant, neoadjuvant, therapeutic, or palliative) will depend on the tumor type, location, and stage, as well as the general health of the patient.  Total body irradiation (TBI) is a radiation therapy technique used to prepare the body to receive a bone marrow transplant.  Brachytherapy, in which a radiation source is placed inside or next to the area requiring treatment, is another form of radiation therapy that minimizes exposure to healthy tissue during procedures to treat cancers of the breast, prostate and other organs.

Radiation therapy has several applications in non-malignant conditions, such as the treatment of trigeminal neuralgia, severe thyroid eye disease, pterygium, pigmented villonodular synovitis, and prevention of keloid scar growth, vascular restenosis , and heterotopic ossification.  The use of radiation therapy in non-malignant conditions is limited partly by worries about the risk of radiation-induced cancers.

Radiation therapy works by damaging the DNA of cancerous cells.  This DNA damage is caused by one of two types of energy, photon or charged particle. This damage is either direct or indirect ionizing the atoms which make up the DNA chain.  Indirect ionization happens as a result of the ionization of water, forming free radicals, notably hydroxyl radicals, which then damage the DNA.  In the older, most common form of radiation therapy, Intensity-modulated radiation therapy (IMRT) (photons), most of the radiation effect is through free radicals.  Because cells have mechanisms for repairing single-strand DNA damage, double-stranded DNA breaks prove to be the most significant technique to cause cell death.  Cancer cells generally are undifferentiated and stem cell-like, they reproduce more, and have a diminished ability to repair sub-lethal damage compared to most healthy differentiated cells.  This single-strand DNA damage is then passed on through cell division, accumulating damage to the cancer cell's DNA, causing them to die or reproduce more slowly.

One of the major limitations of photon radiation therapy is that the cells of solid tumors become deficient in oxygen.  Solid tumors can outgrow their blood supply, causing a low-oxygen state known as hypoxia.  Oxygen is a potent radio-sensitizer, increasing the effectiveness of a given dose of radiation by forming DNA-damaging free radicals.  Tumor cells in a hypoxic environment may be as much as two to three times more resistant to radiation damage than those in a normal oxygen environment.  Much research has been devoted to overcoming hypoxia including the use of high pressure oxygen tanks, blood substitutes that carry increased oxygen, hypoxic cell radiosensitizer drugs such as misonidazole and metronidazole, and hypoxic cytotoxins (tissue poisons), such as tirapazamine.

Direct damage to cancer cell DNA occurs through high-LET (linear energy transfer) charged particles such as proton, boron, carbon or neon ions which have an antitumor effect which is independent of tumor oxygen supply because these particles act mostly via direct energy transfer usually causing double-stranded DNA breaks.  Due to their relatively large mass, protons and other charged particles have little lateral side scatter in the tissue;  the beam does not broaden much, stays focused on the tumor shape and delivers small dose side-effects to surrounding tissue.  They also more precisely target the tumor using the Bragg peak effect.  This procedure reduces damage to healthy tissue between the charged particle radiation source and the tumor and sets a finite range for tissue damage after the tumor has been reached.  In contrast, with IMRT using uncharged particles (photons), its energy is deposited differently such that it is still damaging healthy cells when it exits the body.  This exiting damage is not therapeutic, can increase treatment side effects, and increases the probability of secondary cancer induction.    This difference is very important in cases where the close proximity of other organs makes any stray ionization very damaging (example: head and neck cancers). This x-ray exposure is especially bad for children, due to their growing bodies, and they have a thirty percent  chance of a second malignancy after five years post initial treatment.

The amount of radiation used in photon radiation therapy is measured in gray (Gy), and varies depending on the type and stage of cancer being treated.  For curative cases, the typical dose for a solid epithelial tumor ranges from ( 60 to 80 Gy),  while lymphomas are treated with ( 20 to 40 Gy).
Preventative (adjuvant) doses are typically around ( 45 – 60 Gy in 1.8 – 2 Gy )  fractions  (for Breast, Head, and Neck cancers) .   Many other factors are considered by radiation oncologists when selecting a dose, including whether the patient is receiving chemotherapy,  whether radiation therapy is being administered before or after surgery, and the degree of success of surgery.
Delivery parameters of a prescribed dose are determined during treatment planning.   Treatment planning is generally performed on dedicated computers using specialized treatment planning software.  The planner will try to design a plan that delivers a uniform prescription dose to the tumor and minimizes dose to surrounding healthy tissue.

Different cancers respond differently to radiation therapy

The response of a cancer to radiation is described by its radio-sensitivity.  Highly radiosensitive cancer cells are rapidly killed by modest doses of radiation.  These include leukemias, most lymphomas and germ cell tumors. The majority of epithelial cancers are only moderately radiosensitive, and require a significantly higher dose of radiation (60-70Gy) to achieve a radical cure.  Some types of cancer are notably radioresistant, that is, much higher doses are required to produce a radical cure than may be safe in clinical practice.  Renal cell cancer and melanoma are generally considered to be radio-resistant

Before treatment, a CT scan is performed to identify the tumor and surrounding normal structures.  The patient is then sent for a simulation so that molds can be created to be used during treatment.  The patient receives small skin marks to guide the placement of treatment fields.
The response of a tumor to radiation therapy is also related to its size.  For complex reasons, very large tumors respond less well to radiation than smaller tumors or microscopic disease.  Various strategies are used to overcome these  effects.
Medicine has used radiation therapy as a treatment for cancer for more than 100 years, with its earliest roots traced from the discovery of x-rays in 1895 by Wilhelm Röntgen.

The field of radiation therapy began to grow in the early 1900's largely due to the groundbreaking work of Nobel Prize-winning scientist Marie Curie (1867–1934), who discovered the radioactive elements polonium and radium in 1898. This began a new era in medical treatment and research.   Radium was used in various forms until the mid-1900's, when cobalt and casium units came into use.  Medical linear accelerators have been used too as sources of radiation since the late 1940's.
With Godfrey Hounsfield’s invention of computed tomography (CT) in 1971, three-dimensional planning became a possibility and created a shift from 2-D to 3-D radiation delivery.

The advent of new imaging technologies, including magnetic resonance imaging (MRI) in the 1970's and positron emission tomography (PET) in the 1980's, has moved radiation therapy from 3-D conformal to intensity-modulated radiation therapy (IMRT) and to image-guided radiation therapy (IGRT) tomography.   These advances allowed radiation oncologists to better see and target tumors, which have resulted in better treatment outcomes, more organ preservation and fewer side effects.

Historically, the three main divisions of radiation therapy are external beam radiation therapy (EBRT or XRT) or teletherapy, brachytherapy or sealed source radiation therapy, and systemic radioisotope therapy or unsealed source radiotherapy.  The differences relate to the position of the radiation source;  external is outside the body, brachytherapy uses sealed radioactive sources placed precisely in the area under treatment, and systemic radioisotopes are given by infusion or oral ingestion that is delivered immediately after surgical removal of the cancer.  

  1. external beam radiation therapy or teletherapy
  2. brachytherapy or sealed source radiation therapy
  3. systemic radioisotope therapy or unsealed source radiotherapy

Radiation therapy is a type of cancer treatment that uses beams of intense energy to kill cancer cells. Radiation therapy most often gets its power from X-rays, but the power can also come from protons or other types of energy.
The term "radiation therapy" most often refers to external beam radiation therapy.  During this type of radiation, the high-energy beams come from a machine outside of your body that aims the beams at a precise point on your body.  During a different type of radiation treatment called brachytherapy (brak-e-THER-uh-pee), radiation is placed inside your body.

Radiation therapy damages cells by destroying the genetic material that controls how cells grow and divide. While both healthy and cancerous cells are damaged by radiation therapy, the goal of radiation therapy is to destroy as few normal, healthy cells as possible.

Cannabinoids stop radiation therapy oxidation

Marijuana is a very special natural medicine that increases our chances of beating cancer, though contemporary oncologists are mostly interested in it for its ability to mitigate the nasty side effects of chemo and radiation therapy.  They would never think of it as an important part of the actual treatment of cancer.
Marijuana is obviously useful for many more disorders than most doctors and the government realize.  It is a front-line medicinal for radiation exposure. 
Doctors who truly care about their patients would do better to take a serious look at what is available in the field of complementary and alternative medicine (CAM), and advocate forcefully for clinical trials to further test the potential of the most promising less-toxic treatments.

Cancer treatment:  radiation therapy.  Administer  cannabinoids in subjects who have been exposed to radiation therapy and other oxidative processes.
It is the sum total of every chemical and radiation assault against your DNA at the cellular level, inside the nucleus of your cells, what you do not see.  This oxidation  damage causes mutations in cells that lead to abnormal cell growth and cancer.
Cannabinoids protect cells from this oxidation.  X-rays and all forms of radiation therapy (even sunlight) cause oxidation.

Medical marijuana is now a cutting-edge medicine -- one that has been around the block in the world of medicine and was especially popular in pharmacies until it was made illegal starting in 1913 just after the Federal Reserve Act was passed.  The same interests that took control of the money supply took control of the pharmaceutical industry.  These fast growing companies needed to make inexpensive drugs and pain medications illegal so they could legally get away with murder from the use of more dangerous synthetic drugs.

Receptor mechanism and antiemetic activity of structurally-diverse cannabinoids against radiation-induced emesis in the least shrew.

Darmani NA, Janoyan JJ, Crim J, Ramirez J.
Source
Department of Basic Medical Sciences, College of Osteopathic Medicine of the Pacific, Western University of Health Sciences, 309 East Second Street, Pomona, CA 91766, USA. ndarmani@westernu.edu

Abstract
Xenobiotic cannabinoid CB1/CB2-receptor agonists appear to possess broad-spectrum antiemetic activity since they prevent vomiting produced by a variety of emetic stimuli including the chemotherapeutic agent cisplatin, serotonin 5-HT3-receptor agonists, dopamine D2/D3-receptor agonists and morphine, via the stimulation of CB1-receptors. The purpose of this study was to evaluate whether structurally-diverse cannabinoids [Delta9-THC, (delta-9-tetrahydrocannabinol); (Delta8-THC, delta-8-tetrahydrocannabinol); WIN55,212-2, (R (+)-[2,3-dihydro-5-methyl-3-[(morpholinyl)), methyl] pyrolol [1,2,3-de]-1,4 benzoxazinyl]-(1-naphthalenyl) methenone mesylate); and CP55,940, ((-)-3-[2-hydroxy-4-(1,1-dimethylheptyl]-4-[3-hydroxypropyl] cyclohexane-1-ol)), can prevent radiation-induced emesis. Exposure to total body radiation (0, 5, 7.5 and 10 Gy) caused robust emesis in the least shrew (Cryptotis parva) in a dose-dependent manner (ED50=5.99 (5.77-6.23) Gy) and all animals vomited at the highest tested dose of radiation. In addition, the radiation exposure reduced locomotor behaviors to a significant but mild degree in a non-dose-dependent fashion up to one hour post-treatment. Radiation-induced emesis (10 Gy) was blocked in a dose-dependent manner by the CB1/CB2-receptor agonists with the following ID50 potency order: CP55,940 (0.11 (0.09-0.12) mg/kg)>WIN55,212,2 (3.65 (3.15-4.23) mg/kg)=Delta8-THC (4.36 (3.05-6.22) mg/kg)>Delta9-THC (6.76 (5.22-8.75) mg/kg).


Although the greater antiemetic potency and efficacy of Delta8-THC relative to its isomer Delta9-THC is unusual as the latter cannabinoid possesses higher affinity and potency for cannabinoid receptors in functional assays, the current data support the results of a clinical study in children suggestive of complete protection from emesis by Delta8-THC. This effect has not been clinically observed for Delta9-THC in cancer patients receiving chemo- or radiation-therapy. Cannabinoids prevented the induced emesis via the stimulation of cannabinoid CB1-receptors because the CB1 (SR141716A)and not the CB2 (SR144528)--receptor antagonist reversed both the observed reduction in emesis frequency and shrew emesis protection afforded by either Delta9-THC or CP55,940 against radiation-induced emesis.  These findings further suggest that the least shrew can be utilized as a versatile and inexpensive small animal model to rapidly screen the efficacy of investigational antiemetics for the prevention of radiation-induced emesis.

All research leads us to the undeniable conclusion that marijuana is the premier cancer medicine mankind has been looking for and finally has found.  The problem is that there are special interests whose main interest is that real cures for cancer are never discovered.  Actually it is a mistake to think in terms of cure;  it is better to think in terms of effective treatment,  for cancer is a very complicated phenomena with multiple and often concurrent causes.  Treatments need to touch down on many if not all the causes to affect a permanent cure.
THC has been approved by the Food and Drug Administration because medical science confirms its use in a broad variety of clinical situations.   Specifically a THC-containing drug called Marinol is FDA approved though it does not come close to the  effectiveness of natural cannabinoids.  Synthetic copies of natural substances rarely if ever maintain the same pharmacological effects as the original.    We know this to be especially true in the case of cannabis and the copies, the pharmaceutical companies manufacture to replicate cannabinoids.  The copies are never as good as the natural drugs. 

Instead of recommending cannabis for the symptoms of radiation therapy—doctors should be recommending cannabis for the treatment of the CANCER itself!  The cannabis along with other treatments is what will cure the cancer

Recommendation:

Indica x Sativa hybrid (rich in CBD, CBG, CBN, THC)
Whole plant extracts

References


1. Harrison LB, Chadha M, Hill RJ, Hu K, Shasha D (2002). "Impact of tumor hypoxia and anemia on radiation therapy outcomes". Oncologist 7 (6): 492–508. doi:10.1634/theoncologist.7-6-492. PMID 12490737. http://theoncologist.alphamedpress.org/cgi/pmidlookup?view=long&pmid=12490737.
2. Curtis RE, Freedman DM, Ron E, Ries LAG, Hacker DG, Edwards BK, Tucker MA, Fraumeni JF Jr. (eds). New Malignancies Among Cancer Survivors: SEER Cancer Registries, 1973–2000. National Cancer Institute. NIH Publ. No. 05-5302. Bethesda, MD, 2006.
3. http://www.helmholtz-muenchen.de/fileadmin/ISS/PDF/Risikoanalyse/Georgetown/Robison.pdf
4. CK Bomford, IH Kunkler, J Walter. Walter and Miller’s Textbook of Radiation therapy (6th Ed), p311
5. “Radiosensitivity” on GP notebook http://www.gpnotebook.co.uk/simplepage.cfm?ID=2060451853
6. “Radiation therapy- what GPs need to know” on patient.co.uk http://www.patient.co.uk/showdoc/40002299/
7. a b c Camphausen KA, Lawrence RC. "Principles of Radiation Therapy" in Pazdur R, Wagman LD, Camphausen KA, Hoskins WJ (Eds) Cancer Management: A Multidisciplinary Approach. 11 ed. 2008.
8. a b "University of Alabama at Birmingham Comprehensive Cancer Center, History of Radiation Oncology" (from the Wayback Machine). Archived from the original on 2008-01-05. http://web.archive.org/web/20080105043216/http://www3.ccc.uab.edu/show.asp?durki=68504.
9. http://www.rtanswers.com/aboutus/history.aspx
10. Vaidya J. "TARGIT (TARGeted Intraoperative radiation therapy)". http://www.targit.org.uk. Retrieved 2009-09-27.
11. http://www.astro.org/PressRoom/PressKit/AnnualMeeting/documents/Timmerman.pdf
12. http://www.rtanswers.com/treatmentinformation/treatmenttypes/stereotacticradiation.aspx
13. Bucci M, Bevan A, Roach M (2005). "Advances in radiation therapy: conventional to 3D, to IMRT, to 4D, and beyond.". CA Cancer J Clin 55 (2): 117–34. doi:10.3322/canjclin.55.2.117. PMID 15761080. http://caonline.amcancersoc.org/cgi/content/full/55/2/117.
14. Galvin JM, Ezzell G, Eisbrauch A, et al. (Apr 2004). "Implementing IMRT in clinical practice: a joint document of the American Society for Therapeutic Radiology and Oncology and the American Association of Physicists in Medicine". Int J Radiat Oncol Biol Phys. 58 (5): 1616–34. doi:10.1016/j.ijrobp.2003.12.008. PMID 15050343.
15. Intensity Modulated Radiation Therapy
16. Brain tumor patient 'unaware' treatment was available on NHS
17. Gerbaulet A et al. (2005). "Cervix carcinoma". In Gerbaulet A, Pötter R, Mazeron J, Limbergen EV. The GEC ESTRO handbook of brachytherapy. Belgium: ACCO.
18. Ash D et al. (2005). "Prostate cancer". In Gerbaulet A, Pötter R, Mazeron J, Limbergen EV. The GEC ESTRO handbook of brachytherapy. Belgium: ACCO.
19. Van Limbergen E et al. (2005). "Breast cancer". In Gerbaulet A, Pötter R, Mazeron J, Limbergen EV. The GEC ESTRO handbook of brachytherapy. Belgium: ACCO.
20. Van Limbergen E et al. (2005). "Skin cancer". In Gerbaulet A, Pötter R, Mazeron J, Limbergen EV. The GEC ESTRO handbook of brachytherapy. Belgium: ACCO.
21. a b Gerbaulet A et al. (2005). "General aspects". In Gerbaulet A, Pötter R, Mazeron J, Limbergen EV. The GEC ESTRO handbook of brachytherapy. Belgium: ACCO.
22. a b Stewart AJ et al. (2007). "Radiobiological concepts for brachytherapy". In Devlin P. Brachytherapy. Applications and Techniques. Philadelphia: LWW.
23. Yashar, C; Blair, S; Wallace, A; Scanderbeg, D (2009). “Initial Clinical Experience with the Strut-Adjusted Volume Implant Brachytherapy Applicator for Accelerated Partial Breast Irradiation.” Brachytherapy 8: 367–372.
24. Sartor O (2004). "Overview of samarium sm 153 lexidronam in the treatment of painful metastatic bone disease". Rev Urol 6 Suppl 10: S3–S12. PMC 1472939. PMID 16985930.
25. Fda Approves First Radiopharmaceutical Product To Treat Non-Hodgkin’S Lymphoma
26. Tositumomab and Iodine I 131 Tositumomab – Product Approval Information – Licensing Action
27. http://www.rtanswers.com/treatmentinformation/cancertypes/breast/possiblesideeffects.aspx
28. Hall, Eric J. (2000). Radiobiology for the radiologist. Philadelphia: Lippincott Williams Wilkins. p. 351. ISBN 0781726492, 9780781726498.
29. O. Gutfeld, M. Wygoda, L. Shavit & T. Grenader : Fertility After Adjuvant External Beam Radiotherapy For Stage I Seminoma . The Internet Journal of Oncology. 2007 Volume 4 Number 2
30. Meek AG (1998). "Breast radiation therapy and lymphedema.". Cancer 83 (12 Suppl American): 2788–97. doi:10.1002/(SICI)1097-0142(19981215)83:12B+<2788::AID-CNCR27>3.0.CO;2-I. PMID 9874399.
31. Taylor CW, Nisbet A, McGale P, Darby SC (Dec 2007). "Cardiac exposures in breast cancer radiation therapy: 1950s–1990s". Int J Radiat Oncol Biol Phys. 69 (5): 1484–95. doi:10.1016/j.ijrobp.2007.05.034. PMID 18035211.
32. Nieder C, Milas L, Ang KK (2000). "Tissue tolerance to reirradiation.". Semin Radiat Oncol 10 (3): 200–9. doi:10.1053/srao.2000.6593. PMID 11034631.
33. Bogdanich, Walt; Ruiz, Rebecca R. (25 February 2010). "Missouri Hospital Reports Errors in Radiation Doses". The New York Times. http://www.nytimes.com/2010/02/25/us/25radiation.html. Retrieved 26 February 2010.


Cannabinoids stop radiation therapy oxidation


Marijuana is a very special natural medicine that increases our chances of beating cancer, though contemporary oncologists are mostly interested in it for its ability to mitigate the nasty side effects of chemo and radiation therapy.  They would never think of it as an important part of the actual treatment of cancer.
Marijuana is obviously useful for many more disorders than most doctors and the government realize.  It is a front-line medicinal for radiation exposure. 
Doctors who truly care about their patients would do better to take a serious look at what is available in the field of complementary and alternative medicine (CAM), and advocate forcefully for clinical trials to further test the potential of the most promising less-toxic treatments.


Cancer treatment:  radiation therapy.  Administer  cannabinoids in subjects who have been exposed to radiation therapy and other oxidative processes.
It is the sum total of every chemical and radiation assault against your DNA at the cellular level, inside the nucleus of your cells, what you do not see.  This oxidation  damage causes mutations in cells that lead to abnormal cell growth and cancer.
Cannabinoids protect cells from this oxidation.  X-rays and all forms of radiation therapy (even sunlight) cause oxidation.


Medical marijuana is now a cutting-edge medicine -- one that has been around the block in the world of medicine and was especially popular in pharmacies until it was made illegal starting in 1913 just after the Federal Reserve Act was passed.  The same interests that took control of the money supply took control of the pharmaceutical industry.  These fast growing companies needed to make inexpensive drugs and pain
medications illegal so they could legally get away with murder from the use of more dangerous synthetic drugs.


Receptor mechanism and antiemetic activity of structurally-diverse cannabinoids against radiation-induced emesis in the least shrew.


Darmani NA, Janoyan JJ, Crim J, Ramirez J.
Source
Department of Basic Medical Sciences, College of Osteopathic Medicine of the Pacific, Western University of Health Sciences, 309 East Second Street, Pomona, CA 91766, USA. ndarmani@westernu.edu


Abstract
Xenobiotic cannabinoid CB1/CB2-receptor agonists appear to possess broad-spectrum antiemetic activity since they prevent vomiting produced by a variety of emetic stimuli including the chemotherapeutic agent cisplatin, serotonin 5-HT3-receptor agonists, dopamine D2/D3-receptor agonists and morphine, via the stimulation of CB1-receptors. The purpose of this study was to evaluate whether structurally-diverse cannabinoids [Delta9-THC, (delta-9-tetrahydrocannabinol); (Delta8-THC, delta-8-tetrahydrocannabinol); WIN55,212-2, (R (+)-[2,3-dihydro-5-methyl-3-[(morpholinyl)), methyl] pyrolol [1,2,3-de]-1,4 benzoxazinyl]-(1-naphthalenyl) methenone mesylate); and CP55,940, ((-)-3-[2-hydroxy-4-(1,1-dimethylheptyl]-4-[3-hydroxypropyl] cyclohexane-1-ol)), can prevent radiation-induced emesis. Exposure to total body radiation (0, 5, 7.5 and 10 Gy) caused robust emesis in the least shrew (Cryptotis parva) in a dose-dependent manner (ED50=5.99 (5.77-6.23) Gy) and all animals vomited at the highest tested dose of radiation. In addition, the radiation exposure reduced locomotor behaviors to a significant but mild degree in a non-dose-dependent fashion up to one hour post-treatment. Radiation-induced emesis (10 Gy) was blocked in a dose-dependent manner by the CB1/CB2-receptor agonists with the following ID50 potency order: CP55,940 (0.11 (0.09-0.12) mg/kg)>WIN55,212,2 (3.65 (3.15-4.23) mg/kg)=Delta8-THC (4.36 (3.05-6.22) mg/kg)>Delta9-THC (6.76 (5.22-8.75) mg/kg).


Although the greater antiemetic potency and efficacy of Delta8-THC relative to its isomer Delta9-THC is unusual as the latter cannabinoid possesses higher affinity and potency for cannabinoid receptors in functional assays, the current data support the results of a clinical study in children suggestive of complete protection from emesis by Delta8-THC. This effect has not been clinically observed for Delta9-THC in cancer patients receiving chemo- or radiation-therapy. Cannabinoids prevented the induced emesis via the stimulation of cannabinoid CB1-receptors because the CB1 (SR141716A)and not the CB2 (SR144528)--receptor antagonist reversed both the observed reduction in emesis frequency and shrew emesis protection afforded by either Delta9-THC or CP55,940 against radiation-induced emesis.  These findings further suggest that the least shrew can be utilized as a versatile and inexpensive small animal model to rapidly screen the efficacy of investigational antiemetics for the prevention of radiation-induced emesis.


All research leads us to the undeniable conclusion that marijuana is the premier cancer medicine mankind has been looking for and finally has found.  The problem is that there are special interests whose main interest is that real cures for cancer are never discovered.  Actually it is a mistake to think in terms of cure;  it is better to think in terms of effective treatment,  for cancer is a very complicated phenomena with multiple and often concurrent causes.  Treatments need to touch down on many if not all the causes to affect a permanent cure.
THC has been approved by the Food and Drug Administration because medical science confirms its use in a broad variety of clinical situations.   Specifically a THC-containing drug called Marinol is FDA approved though it does not come close to the  effectiveness of natural cannabinoids.  Synthetic copies of natural substances rarely if ever maintain the same pharmacological effects as the original.    We know this to be especially true in the case of cannabis and the copies, the pharmaceutical companies manufacture to replicate cannabinoids.  The copies are never as good as the natural drugs. 


Instead of recommending cannabis for the symptoms of radiation therapy—doctors should be recommending cannabis for the treatment of the CANCER itself!  The cannabis along with other treatments is what will cure the cancer


Recommendation:


Indica x Sativa hybrid (rich in CBD, CBG, CBN, THC)
Whole plant extracts


References




1. Harrison LB, Chadha M, Hill RJ, Hu K, Shasha D (2002). "Impact of tumor hypoxia and anemia on radiation therapy outcomes". Oncologist 7 (6): 492–508. doi:10.1634/theoncologist.7-6-492. PMID 12490737. http://theoncologist.alphamedpress.org/cgi/pmidlookup?view=long&pmid=12490737.
2. Curtis RE, Freedman DM, Ron E, Ries LAG, Hacker DG, Edwards BK, Tucker MA, Fraumeni JF Jr. (eds). New Malignancies Among Cancer Survivors: SEER Cancer Registries, 1973–2000. National Cancer Institute. NIH Publ. No. 05-5302. Bethesda, MD, 2006.
3. http://www.helmholtz-muenchen.de/fileadmin/ISS/PDF/Risikoanalyse/Georgetown/Robison.pdf
4. CK Bomford, IH Kunkler, J Walter. Walter and Miller’s Textbook of Radiation therapy (6th Ed), p311
5. “Radiosensitivity” on GP notebook http://www.gpnotebook.co.uk/simplepage.cfm?ID=2060451853
6. “Radiation therapy- what GPs need to know” on patient.co.uk http://www.patient.co.uk/showdoc/40002299/
7. a b c Camphausen KA, Lawrence RC. "Principles of Radiation Therapy" in Pazdur R, Wagman LD, Camphausen KA, Hoskins WJ (Eds) Cancer Management: A Multidisciplinary Approach. 11 ed. 2008.
8. a b "University of Alabama at Birmingham Comprehensive Cancer Center, History of Radiation Oncology" (from the Wayback Machine). Archived from the original on 2008-01-05. http://web.archive.org/web/20080105043216/http://www3.ccc.uab.edu/show.asp?durki=68504.
9. http://www.rtanswers.com/aboutus/history.aspx
10. Vaidya J. "TARGIT (TARGeted Intraoperative radiation therapy)". http://www.targit.org.uk. Retrieved 2009-09-27.
11. http://www.astro.org/PressRoom/PressKit/AnnualMeeting/documents/Timmerman.pdf
12. http://www.rtanswers.com/treatmentinformation/treatmenttypes/stereotacticradiation.aspx
13. Bucci M, Bevan A, Roach M (2005). "Advances in radiation therapy: conventional to 3D, to IMRT, to 4D, and beyond.". CA Cancer J Clin 55 (2): 117–34. doi:10.3322/canjclin.55.2.117. PMID 15761080. http://caonline.amcancersoc.org/cgi/content/full/55/2/117.
14. Galvin JM, Ezzell G, Eisbrauch A, et al. (Apr 2004). "Implementing IMRT in clinical practice: a joint document of the American Society for Therapeutic Radiology and Oncology and the American Association of Physicists in Medicine". Int J Radiat Oncol Biol Phys. 58 (5): 1616–34. doi:10.1016/j.ijrobp.2003.12.008. PMID 15050343.
15. Intensity Modulated Radiation Therapy
16. Brain tumor patient 'unaware' treatment was available on NHS
17. Gerbaulet A et al. (2005). "Cervix carcinoma". In Gerbaulet A, Pötter R, Mazeron J, Limbergen EV. The GEC ESTRO handbook of brachytherapy. Belgium: ACCO.
18. Ash D et al. (2005). "Prostate cancer". In Gerbaulet A, Pötter R, Mazeron J, Limbergen EV. The GEC ESTRO handbook of brachytherapy. Belgium: ACCO.
19. Van Limbergen E et al. (2005). "Breast cancer". In Gerbaulet A, Pötter R, Mazeron J, Limbergen EV. The GEC ESTRO handbook of brachytherapy. Belgium: ACCO.
20. Van Limbergen E et al. (2005). "Skin cancer". In Gerbaulet A, Pötter R, Mazeron J, Limbergen EV. The GEC ESTRO handbook of brachytherapy. Belgium: ACCO.
21. a b Gerbaulet A et al. (2005). "General aspects". In Gerbaulet A, Pötter R, Mazeron J, Limbergen EV. The GEC ESTRO handbook of brachytherapy. Belgium: ACCO.
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