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While Paxil Causes Fragile X and Vaccines cause Autism and Cancer, FDA Hides:

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March 27, 2024, 12:55:24 pm Mark says: Shocked Shocked Shocked Shocked  When Hamas spokesman Abu Ubaida began a speech marking the 100th day of the war in Gaza, one confounding yet eye-opening proclamation escaped the headlines. Listing the motives for the Palestinian militant group's Oct. 7 massacre in Israel, he accused Jews of "bringing red cows" to the Holy Land.
December 31, 2022, 10:08:58 am NilsFor1611 says: blessings
August 08, 2018, 02:38:10 am suzytr says: Hello, any good churches in the Sacto, CA area, also looking in Reno NV, thanks in advance and God Bless you Smiley
January 29, 2018, 01:21:57 am Christian40 says: It will be interesting to see what happens this year Israel being 70 years as a modern nation may 14 2018
October 17, 2017, 01:25:20 am Christian40 says: It is good to type Mark is here again!  Smiley
October 16, 2017, 03:28:18 am Christian40 says: anyone else thinking that time is accelerating now? it seems im doing days in shorter time now is time being affected in some way?
September 24, 2017, 10:45:16 pm Psalm 51:17 says: The specific rule pertaining to the national anthem is found on pages A62-63 of the league rulebook. It states: “The National Anthem must be played prior to every NFL game, and all players must be on the sideline for the National Anthem. “During the National Anthem, players on the field and bench area should stand at attention, face the flag, hold helmets in their left hand, and refrain from talking. The home team should ensure that the American flag is in good condition. It should be pointed out to players and coaches that we continue to be judged by the public in this area of respect for the flag and our country. Failure to be on the field by the start of the National Anthem may result in discipline, such as fines, suspensions, and/or the forfeiture of draft choice(s) for violations of the above, including first offenses.”
September 20, 2017, 04:32:32 am Christian40 says: "The most popular Hepatitis B vaccine is nothing short of a witch’s brew including aluminum, formaldehyde, yeast, amino acids, and soy. Aluminum is a known neurotoxin that destroys cellular metabolism and function. Hundreds of studies link to the ravaging effects of aluminum. The other proteins and formaldehyde serve to activate the immune system and open up the blood-brain barrier. This is NOT a good thing."
http://www.naturalnews.com/2017-08-11-new-fda-approved-hepatitis-b-vaccine-found-to-increase-heart-attack-risk-by-700.html
September 19, 2017, 03:59:21 am Christian40 says: bbc international did a video about there street preaching they are good witnesses
September 14, 2017, 08:06:04 am Psalm 51:17 says: bro Mark Hunter on YT has some good, edifying stuff too.
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Author Topic: While Paxil Causes Fragile X and Vaccines cause Autism and Cancer, FDA Hides:  (Read 425 times)
Meek_n_Mild
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« on: January 02, 2012, 03:15:54 pm »

National Cancer Institute study: MJ shrinks cancer tumors in mice without harming NORMAL TISSUE

I do not recommend using drugs to alter mental states without a doctor's recommendation.
However, that said, I wanted to share a very real murine study accomplished with intention to see if the herb mj affected the growth of cancer in mice. This is the result of that study. Most website try to tell you that herbal remedies cause cancer and DNA damage. I believe the truth is very different -- that abuse of chemicals can cause DNA damage in general but that in the world of medicine, even the most potent poisons may have healing effects under the right conditions. Consider digitalis, penicillin, and even cyanide, which itself has medical uses.

Please don't hate on Dr. Paul too much over his stance on mj. He knows the awful truth, as a doctor, about many prevalent pharmaceuticals and how those are, without a doubt, killing you and me.
Just remember this article if you know someone with difficult cancer, especially a metasta-whatevered (late stage?) or lymphatic cancer.
MJ is like chemotherapy but many times milder on the human body. Otherwise you would see all types of MJ deaths, which simply do not happen as most people have a lot to do aside from smoke pot.

http://www.cancer.gov/cancertopics/pdq/cam/cannabis/healthprofessional/page4


Laboratory/Animal/Preclinical Studies

Antitumor Effects
Appetite Stimulation
Analgesia


Cannabinoids are a group of 21-carbon–containing terpenophenolic compounds produced uniquely by Cannabis sativa and Cannabis indica species.[1,2] These plant-derived compounds may be referred to as phytocannabinoids. Although delta-9-tetrahydrocannabinol (THC) is the primary psychoactive ingredient, other known compounds with biologic activity are cannabinol, cannabidiol (CBD), cannabichromene, cannabigerol, tetrahydrocannabivarin, and delta-8-THC. CBD, in particular, is thought to have significant analgesic and anti-inflammatory activity without the psychoactive effect (high) of delta-9-THC.
Antitumor Effects

One study in mice and rats suggested that cannabinoids may have a protective effect against the development of certain types of tumors.[3] During this 2-year study, groups of mice and rats were given various doses of THC by gavage. A dose-related decrease in the incidence of hepatic adenoma tumors and hepatocellular carcinoma was observed in the mice. Decreased incidences of benign tumors (polyps and adenomas) in other organs (mammary gland, uterus, pituitary, testis, and pancreas) were also noted in the rats. In another study, delta-9-THC, delta-8-THC, and cannabinol were found to inhibit the growth of Lewis lung adenocarcinoma cells in vitro and in vivo .[4] In addition, other tumors have been shown to be sensitive to cannabinoid-induced growth inhibition.[5-8]

Cannabinoids may cause antitumor effects by various mechanisms, including induction of cell death, inhibition of cell growth, and inhibition of tumor angiogenesis and metastasis.[9-11] Cannabinoids appear to kill tumor cells but do not affect their nontransformed counterparts and may even protect them from cell death. These compounds have been shown to induce apoptosis in glioma cells in culture and induce regression of glioma tumors in mice and rats. Cannabinoids protect normal glial cells of astroglial and oligodendroglial lineages from apoptosis mediated by the CB1 receptor.[12]

The effects of delta-9-THC and a synthetic agonist of the CB2 receptor were investigated in hepatocellular carcinoma (HCC).[13] Both agents reduced the viability of hepatocellular carcinoma cells in vitro and demonstrated antitumor effects in hepatocellular carcinoma subcutaneous xenografts in **** mice. The investigations documented that the anti-HCC effects are mediated by way of the CB2 receptor. Similar to findings in glioma cells, the cannabinoids were shown to trigger cell death through stimulation of an endoplasmic reticulum stress pathway that activates autophagy and promotes apoptosis. Other investigations have confirmed that CB1 and CB2 receptors may be potential targets in non-small cell lung carcinoma[14] and breast cancer.[15]

In an in vivo model using severe combined immunodeficient mice, subcutaneous tumors were generated by inoculating the animals with cells from human non-small cell lung carcinoma cell lines.[16] Tumor growth was inhibited by 60% in THC-treated mice compared with vehicle-treated control mice. Tumor specimens revealed that THC had antiangiogenic and antiproliferative effects. However, research with immunocompetent murine tumor models has demonstrated immunosuppression and enhanced tumor growth in mice treated with THC.[17,18]

In addition, both plant-derived and endogenous cannabinoids have been studied for anti-inflammatory effects. A mouse study demonstrated that endogenous cannabinoid system signaling is likely to provide intrinsic protection against colonic inflammation.[19] As a result, a hypothesis that phytocannabinoids and endocannabinoids may be useful in the risk reduction and treatment of colorectal cancer has been developed.[20-23]
Appetite Stimulation

Many animal studies have previously demonstrated that delta-9-THC and other cannabinoids have a stimulatory effect on appetite and increase food intake. It is believed that the endogenous cannabinoid system may serve as a regulator of feeding behavior. The endogenous cannabinoid anandamide potently enhances appetite in mice.[24] Moreover, CB1 receptors in the hypothalamus may be involved in the motivational or reward aspects of eating.[25]
Analgesia

Understanding the mechanism of cannabinoid-induced analgesia has been increased through the study of cannabinoid receptors, endocannabinoids, and synthetic agonists and antagonists. The CB1 receptor is found in both the central nervous system (CNS) and in peripheral nerve terminals. Similar to opioid receptors, increased levels of the CB1 receptor are found in regions of the brain that regulate nociceptive processing.[26] CB2 receptors, located predominantly in peripheral tissue, exist at very low levels in the CNS. With the development of receptor-specific antagonists, additional information about the roles of the receptors and endogenous cannabinoids in the modulation of pain has been obtained.[27,28]

Cannabinoids may also contribute to pain modulation through an anti-inflammatory mechanism; a CB2 effect with cannabinoids acting on mast cell receptors to attenuate the release of inflammatory agents, such as histamine and serotonin, and on keratinocytes to enhance the release of analgesic opioids has been described.[29-31]

References

   1. Adams IB, Martin BR: Cannabis: pharmacology and toxicology in animals and humans. Addiction 91 (11): 1585-614, 1996.  [PUBMED Abstract]

   2. Grotenhermen F, Russo E, eds.: Cannabis and Cannabinoids: Pharmacology, Toxicology, and Therapeutic Potential. Binghamton, NY: The Haworth Press, 2002.

   3. National Toxicology Program .: NTP toxicology and carcinogenesis studies of 1-trans-delta(9)-tetrahydrocannabinol (CAS No. 1972-08-3) in F344 rats and B6C3F1 mice (gavage studies). Natl Toxicol Program Tech Rep Ser 446 (): 1-317, 1996.  [PUBMED Abstract]

   4. Bifulco M, Laezza C, Pisanti S, et al.: Cannabinoids and cancer: pros and cons of an antitumour strategy. Br J Pharmacol 148 (2): 123-35, 2006.  [PUBMED Abstract]

   5. Sánchez C, de Ceballos ML, Gomez del Pulgar T, et al.: Inhibition of glioma growth in vivo by selective activation of the CB(2) cannabinoid receptor. Cancer Res 61 (15): 5784-9, 2001.  [PUBMED Abstract]

   6. McKallip RJ, Lombard C, Fisher M, et al.: Targeting CB2 cannabinoid receptors as a novel therapy to treat malignant lymphoblastic disease. Blood 100 (2): 627-34, 2002.  [PUBMED Abstract]

   7. Casanova ML, Blázquez C, Martínez-Palacio J, et al.: Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors. J Clin Invest 111 (1): 43-50, 2003.  [PUBMED Abstract]

   8. Blázquez C, González-Feria L, Alvarez L, et al.: Cannabinoids inhibit the vascular endothelial growth factor pathway in gliomas. Cancer Res 64 (16): 5617-23, 2004.  [PUBMED Abstract]

   9. Guzmán M: Cannabinoids: potential anticancer agents. Nat Rev Cancer 3 (10): 745-55, 2003.  [PUBMED Abstract]

  10. Blázquez C, Casanova ML, Planas A, et al.: Inhibition of tumor angiogenesis by cannabinoids. FASEB J 17 (3): 529-31, 2003.  [PUBMED Abstract]

  11. Vaccani A, Massi P, Colombo A, et al.: Cannabidiol inhibits human glioma cell migration through a cannabinoid receptor-independent mechanism. Br J Pharmacol 144 (Cool: 1032-6, 2005.  [PUBMED Abstract]

  12. Torres S, Lorente M, Rodríguez-Fornés F, et al.: A combined preclinical therapy of cannabinoids and temozolomide against glioma. Mol Cancer Ther 10 (1): 90-103, 2011.  [PUBMED Abstract]

  13. Vara D, Salazar M, Olea-Herrero N, et al.: Anti-tumoral action of cannabinoids on hepatocellular carcinoma: role of AMPK-dependent activation of autophagy. Cell Death Differ 18 (7): 1099-111, 2011.  [PUBMED Abstract]

  14. Preet A, Qamri Z, Nasser MW, et al.: Cannabinoid receptors, CB1 and CB2, as novel targets for inhibition of non-small cell lung cancer growth and metastasis. Cancer Prev Res (Phila) 4 (1): 65-75, 2011.  [PUBMED Abstract]

  15. Nasser MW, Qamri Z, Deol YS, et al.: Crosstalk between chemokine receptor CXCR4 and cannabinoid receptor CB2 in modulating breast cancer growth and invasion. PLoS One 6 (9): e23901, 2011.  [PUBMED Abstract]

  16. Preet A, Ganju RK, Groopman JE: Delta9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo. Oncogene 27 (3): 339-46, 2008.  [PUBMED Abstract]

  17. Zhu LX, Sharma S, Stolina M, et al.: Delta-9-tetrahydrocannabinol inhibits antitumor immunity by a CB2 receptor-mediated, cytokine-dependent pathway. J Immunol 165 (1): 373-80, 2000.  [PUBMED Abstract]

  18. McKallip RJ, Nagarkatti M, Nagarkatti PS: Delta-9-tetrahydrocannabinol enhances breast cancer growth and metastasis by suppression of the antitumor immune response. J Immunol 174 (6): 3281-9, 2005.  [PUBMED Abstract]

  19. Massa F, Marsicano G, Hermann H, et al.: The endogenous cannabinoid system protects against colonic inflammation. J Clin Invest 113 (Cool: 1202-9, 2004.  [PUBMED Abstract]

  20. Patsos HA, Hicks DJ, Greenhough A, et al.: Cannabinoids and cancer: potential for colorectal cancer therapy. Biochem Soc Trans 33 (Pt 4): 712-4, 2005.  [PUBMED Abstract]

  21. Liu WM, Fowler DW, Dalgleish AG: Cannabis-derived substances in cancer therapy--an emerging anti-inflammatory role for the cannabinoids. Curr Clin Pharmacol 5 (4): 281-7, 2010.  [PUBMED Abstract]

  22. Malfitano AM, Ciaglia E, Gangemi G, et al.: Update on the endocannabinoid system as an anticancer target. Expert Opin Ther Targets 15 (3): 297-308, 2011.  [PUBMED Abstract]

  23. Sarfaraz S, Adhami VM, Syed DN, et al.: Cannabinoids for cancer treatment: progress and promise. Cancer Res 68 (2): 339-42, 2008.  [PUBMED Abstract]

  24. Mechoulam R, Berry EM, Avraham Y, et al.: Endocannabinoids, feeding and suckling--from our perspective. Int J Obes (Lond) 30 (Suppl 1): S24-8, 2006.  [PUBMED Abstract]

  25. Fride E, Bregman T, Kirkham TC: Endocannabinoids and food intake: newborn suckling and appetite regulation in adulthood. Exp Biol Med (Maywood) 230 (4): 225-34, 2005.  [PUBMED Abstract]

  26. Walker JM, Hohmann AG, Martin WJ, et al.: The neurobiology of cannabinoid analgesia. Life Sci 65 (6-7): 665-73, 1999.  [PUBMED Abstract]

  27. Meng ID, Manning BH, Martin WJ, et al.: An analgesia circuit activated by cannabinoids. Nature 395 (6700): 381-3, 1998.  [PUBMED Abstract]

  28. Walker JM, Huang SM, Strangman NM, et al.: Pain modulation by release of the endogenous cannabinoid anandamide. Proc Natl Acad Sci U S A 96 (21): 12198-203, 1999.  [PUBMED Abstract]

  29. Facci L, Dal Toso R, Romanello S, et al.: Mast cells express a peripheral cannabinoid receptor with differential sensitivity to anandamide and palmitoylethanolamide. Proc Natl Acad Sci U S A 92 (Cool: 3376-80, 1995.  [PUBMED Abstract]

  30. Ibrahim MM, Porreca F, Lai J, et al.: CB2 cannabinoid receptor activation produces antinociception by stimulating peripheral release of endogenous opioids. Proc Natl Acad Sci U S A 102 (Cool: 3093-8, 2005.  [PUBMED Abstract]

  31. Richardson JD, Kilo S, Hargreaves KM: Cannabinoids reduce hyperalgesia and inflammation via interaction with peripheral CB1 receptors. Pain 75 (1): 111-9, 1998.  [PUBMED Abstract]
« Last Edit: January 02, 2012, 03:20:03 pm by Meek_n_Mild » Report Spam   Logged

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