Posted on 09/09/2013 1:05:35 PM PDT by Teófilo
PING!
The RCC has always been a friend of tyranny.
Including legal drugs makes this interesting and provocative. More people are harmed by legal than illegal drugs now.
Maybe the pope should take on BigPharma.
Assuming that all the article is true, it still isn’t working
I attended a funeral service Saturday for a friend’s kid who was a user.
Drugs have devastated the town they live in. Evil results, but evil results despite our drug control.
I’ve concluded there is a group of people who are predisposed to abuse drugs or alcohol. Prohibition didn’t change the group of alcoholics. Drug control hasn’t changed the group of addicts. Both groups ruin their lives. Both do it despite the laws, the militarization of police, the incarceration of a generation, the rampant crime and murder that has shifted overseas to control the supply of drugs that responds to the demand in our country.
I don’t like it, but there it is. I no longer support it, or incarceration for recreational use. At some point, if someone wants to drink themselves to death, they do. If they want to blot out all reality and pain in their lives through drug use, they do.
It might be money better spent to send special forces to hunt down and kill the cartels that grow, ship and smuggle drugs to us. But even then, it won’t stop the problems.
Please, explain.
~Theo
Legalizing drugs does not legitimize drugs. The legal prohibition of drugs drive the price up and causes the high profits which make traffickers so vicious. The Holy Father is spot on about drugs being a moral issue, but he is wrong to delegate those moral issues to secular governments.
What many people don’t seem to understand is that outright legalization would not only mean that the traffickers down south would become legitimate businessmen, but that Big Pharma, Big Tobacco, and every beer and rum maker would also be free to produce and market their own “safer” brands.
It is true that many people would just go ahead and kill themselves by drowning in their drug of choice. But things like marijuana - today’s marijuana is not the 60’s weed - cocaine, heroin, and methamphetamine as well designer drugs and of course, diverted pharmaceuticals used inappropriately create their own demand, enslaving their users forever.
Put in another way: entropy happens, and it will happen whether we attempt to control it or not. But we don’t have to help entropy, not when a human soul is at stake.
+JMJ,
~Theo
-— I dont like it, but there it is. I no longer support it, or incarceration for recreational use ——
St. Thomas believed that vices, as bad as prostitution, could be tolerated.legally, if the vice resulting from criminalization outweighed the vice resulting from toleration.
I agree that we seem to have reached that point with respect to the drug war.
Really? Google "Molly" and say, Madonna, Hollywood, concert, rap and see what you get.
In the minds of our kids drugs are already legitimate, legal or not.
+JMJ,
~Theo
“not when a human soul is at stake.”
And yet rock bottom does lead a human soul to seek Christ.
What is at stake is the body...
Now that CO and WA have legalized mj, do you support their 10th Amendment authority to carry out the policy?
I *tolerate* their 10th Amendment authority to legislate on this issue, yes.
+JMJ,
~Theo
Many times it does, yes.
What is at stake is the body...
Which is the temple of the Holy Spirit.
+JMJ,
~Theo
“Which is the temple of the Holy Spirit. “
... but only for believers. Those who need Christ are different.
Autoimmunity. 2006 Mar;39(2):143-51.
Hadassah University Hospital, Department of Bone Marrow Transplantation & Cancer Immunotherapy, POB 12000, Jerusalem, 91120, Israel.
Cannabidinoids are components of the Cannabis sativa (marijuana) plant that have been shown capable of suppressing inflammation and various aspects of cell-mediated immunity. Cannabidiol (CBD), a non-psychoactive cannabidinoid has been previously shown by us to suppress cell-mediated autoimmune joint destruction in an animal model of rheumatoid arthritis. We now report that CBD treatment significantly reduces the incidence of diabetes in NOD mice from an incidence of 86% in non-treated control mice to an incidence of 30% in CBD-treated mice. CBD treatment also resulted in the significant reduction of plasma levels of the pro-inflammatory cytokines, IFN-gamma and TNF-alpha. Th1-associated cytokine production of in vitro activated T-cells and peritoneal macrophages was also significantly reduced in CBD-treated mice, whereas production of the Th2-associated cytokines, IL-4 and IL-10, was increased when compared to untreated control mice. Histological examination of the pancreatic islets of CBD-treated mice revealed significantly reduced insulitis. Our results indicate that CBD can inhibit and delay destructive insulitis and inflammatory Th1-associated cytokine production in NOD mice resulting in a decreased incidence of diabetes possibly through an immunomodulatory mechanism shifting the immune response from Th1 to Th2 dominance.
Neuropharmacology. 2008 Jan;54(1):244-9. Epub 2007 Jul 17.
Department of Bone Marrow Transplantation and Cancer Immunotherapy, Hadassah Hebrew University Hospital, Jerusalem 91120, Israel. lolaw@hadassa.org.il
We have previously reported that cannabidiol (CBD) lowers the incidence of diabetes in young non-obese diabetes-prone (NOD) female mice. In the present study we show that administration of CBD to 11-14 week old female NOD mice, which are either in a latent diabetes stage or with initial symptoms of diabetes, ameliorates the manifestations of the disease. Diabetes was diagnosed in only 32% of the mice in the CBD-treated group, compared to 86% and 100% in the emulsifier-treated and untreated groups, respectively. In addition, the level of the proinflammatory cytokine IL-12 produced by splenocytes was significantly reduced, whereas the level of the anti-inflammatory IL-10 was significantly elevated following CBD-treatment. Histological examination of the pancreata of CBD-treated mice revealed more intact islets than in the controls. Our data strengthen our previous assumption that CBD, known to be safe in man, can possibly be used as a therapeutic agent for treatment of type 1 diabetes.
Pre-Clinical Research | December 14, 2010
Drs. Rajesh and Partha Mukhopadhyay contributed equally to this article. This study was supported by the Intramural Research Program of the NIH/NIAAA (to Dr. Pacher) and NIDA Grant DA9789 (to Dr. Mechoulam). Dr. Horváth is a recipient of a Hungarian Research Council Scientific Research Fund Fellowship (NKTH-OTKA-EU, MB08-80238). Dr. Veves receives funding from Novartis for an investigator-initiated research grant, unrelated to this study. Dr. Mechoulam is a consultant for GW Pharmaceuticals, United Kingdom, which is not involved in this publication and is unaware of it. All other authors have reported that they have no relationships to disclose.Reprint requests and correspondence: Dr. Pál Pacher, Section on Oxidative Stress Tissue Injury, Laboratory of Physiological Studies, National Institutes of Health/NIAAA, 5625 Fishers Lane, MSC-9413, Bethesda, Maryland 20892-9413
American College of Cardiology Foundation
Objectives In this study, we have investigated the effects of cannabidiol (CBD) on myocardial dysfunction, inflammation, oxidative/nitrative stress, cell death, and interrelated signaling pathways, using a mouse model of type I diabetic cardiomyopathy and primary human cardiomyocytes exposed to high glucose.
Background Cannabidiol, the most abundant nonpsychoactive constituent of Cannabis sativa (marijuana) plant, exerts anti-inflammatory effects in various disease models and alleviates pain and spasticity associated with multiple sclerosis in humans.
Methods Left ventricular function was measured by the pressure-volume system. Oxidative stress, cell death, and fibrosis markers were evaluated by molecular biology/biochemical techniques, electron spin resonance spectroscopy, and flow cytometry.
Results Diabetic cardiomyopathy was characterized by declined diastolic and systolic myocardial performance associated with increased oxidative-nitrative stress, nuclear factor-κB and mitogen-activated protein kinase (c-Jun N-terminal kinase, p-38, p38α) activation, enhanced expression of adhesion molecules (intercellular adhesion molecule-1, vascular cell adhesion molecule-1), tumor necrosis factor-α, markers of fibrosis (transforming growth factor-β, connective tissue growth factor, fibronectin, collagen-1, matrix metalloproteinase-2 and -9), enhanced cell death (caspase 3/7 and poly[adenosine diphosphate-ribose] polymerase activity, chromatin fragmentation, and terminal deoxynucleotidyl transferase dUTP nick end labeling), and diminished Akt phosphorylation. Remarkably, CBD attenuated myocardial dysfunction, cardiac fibrosis, oxidative/nitrative stress, inflammation, cell death, and interrelated signaling pathways. Furthermore, CBD also attenuated the high glucose-induced increased reactive oxygen species generation, nuclear factor-κB activation, and cell death in primary human cardiomyocytes.
Conclusions Collectively, these results coupled with the excellent safety and tolerability profile of CBD in humans, strongly suggest that it may have great therapeutic potential in the treatment of diabetic complications, and perhaps other cardiovascular disorders, by attenuating oxidative/nitrative stress, inflammation, cell death and fibrosis.
Antitumor Effects
Appetite Stimulation
Analgesia
Cannabinoids are a group of 21-carboncontaining 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 (HCC) 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 invasion and metastasis.[9-12] One review summarizes the molecular mechanisms of action of cannabinoids as antitumor agents.[13] 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.[14]
The effects of delta-9-THC and a synthetic agonist of the CB2 receptor were investigated in HCC.[15] Both agents reduced the viability of HCC cells in vitro and demonstrated antitumor effects in HCC subcutaneous xenografts in nude 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 [16] and breast cancer.[17]
An in vitro study of the effect of CBD on programmed cell death in breast cancer cell lines found that CBD induced programmed cell death, independent of the CB1, CB2, or vanilloid receptors. CBD inhibited the survival of both estrogen receptorpositive and estrogen receptornegative breast cancer cell lines, inducing apoptosis in a concentration-dependent manner while having little effect on nontumorigenic, mammary cells.[18]
CBD has also been demonstrated to exert a chemopreventive effect in a mouse model of colon cancer.[19] In the experimental system, azoxymethane increased premalignant and malignant lesions in the mouse colon. Animals treated with azoxymethane and CBD concurrently were protected from developing premalignant and malignant lesions. In in vitro experiments involving colorectal cancer cell lines, the investigators found that CBD protected DNA from oxidative damage, increased endocannabinoid levels, and reduced cell proliferation.
Another investigation into the antitumor effects of CBD examined the role of intercellular adhesion molecule-1 (ICAM-1).[12] ICAM-1 expression has been reported to be negatively correlated with cancer metastasis. In lung cancer cell lines, CBD upregulated ICAM-1, leading to decreased cancer cell invasiveness.
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.[20] 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.[21,22]
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.[23] As a result, a hypothesis that phytocannabinoids and endocannabinoids may be useful in the risk reduction and treatment of colorectal cancer has been developed.[24-27]
CBD may also enhance uptake of cytotoxic drugs into malignant cells. Activation of the transient receptor potential vanilloid type 2 (TRPV2) has been shown to inhibit proliferation of human glioblastoma multiforme cells and overcome resistance to the chemotherapy agent carmustine.[28] In an in vitro model, CBD increased TRPV2 activation and increased uptake of cytotoxic drugs, leading to apoptosis of glioma cells without affecting normal human astrocytes. This suggests that coadministration of CBD with cytotoxic agents may increase drug uptake and potentiate cell death in human glioma cells. 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.[29] Moreover, CB1 receptors in the hypothalamus may be involved in the motivational or reward aspects of eating.[30] 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.[31] 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.[32,33]
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.[34-36] One study reported that the efficacy of synthetic CB1- and CB2-receptor agonists were comparable with the efficacy of morphine in a murine model of tumor pain.[37] References
Your position is one of respect for the Constitution, something which most Drug Warriors lack.
The Framers of the Constitution of the United States described in its preamble a number of values to be protected by our government...
What is a stake if our personal freedom.
LOL, gotta love the Jesuits.
No one, and I mean absolutely no one, can do to words, what Jesuits can do to words.
Even Satan stands in awe.
What is a stake if our personal freedom. No society is truly free when the members of such a society are slaves to chemicals
Ditto to this.
Druggies don’t live in isolation. Their addiction always impacts others. Taxpayers foot the healthcare bill of poor druggies. Taxpayers pay for social services which are used when druggies neglect & abuse children.
I never see drug legalazation advocates mention how others are negatively by a druggie
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