Regulations Concerning Cannabis & Conflicting Cannnabinoid Research

The rules and regulations concerning cannabis do not coincide with the research into the plant and its inherent pharmacological properties. When an institution of authority identifies a substance as a “poison” or “medicine” through the influential force that is rhetoric or propaganda, the stigma then predisposes individuals to unite in confirmation of the former or the latter, rather than conceding to the existence or manifestation of both. 
THE RULES

Cannabis, or Marijuana is classified as a Schedule I controlled substance under the Controlled Substances Act (CSA).  As a Schedule I drug, marijuana is classified under the following criteria:
A. The drug has a high potential for abuse.
B. The drug has no currently accepted medical use in treatment in the United States
C. There is a lack of accepted safety for use of the drug under medical supervision
Having this classification attached to the plant, includes Cannabis with heroin, lysergic acid diethylamide (LSD), and methaqualone (Quaaludes).
Federal law assigns every drug to a schedule which purports to determine the drugs medicinal value verses its potential for abuse. Because marijuana is classified as a Schedule I drug, the law provides that does not have an acceptable medicinal value because it has no medical value while being highly addictive.
Physicians may exercise their right to free speech by recommending the use of marijuana under the First Amendment; however federal law does not make exclusions for a doctor to “prescribe” marijuana.
Regardless of state laws to the contrary, there is no such thing as “medical” marijuana under Federal law. The U.S. Federal government has also prohibited Cannabis under the Interstate Commerce Clause. Additionally, under the Supremacy Clause, any state law in conflict with federal law is not valid.
Federal Marijuana Sentencing Law & Federal Sentencing Guidelines for Marijuana Offenses
The sentencing guidelines allocate a range for suggested sentences based on several mitigating or aggravating factors including: the quantity of cannabis involved in the offense and the defendant’s criminal record. Every marijuana conviction under Federal law can potentially result in imprisonment
For any federal sentence imposed that requires imprisonment, the defendant must serve a minimum of 85% of that sentence before early parole or “good time” is considered.
Larger amount of marijuana typically come with harsher minimum mandatory sentences. For instance, cultivation of 100 plants or the possession of 100 kg or more results in a five year minimum mandatory prison sentence under federal law. 
The minimum mandatory sentence is doubled for this offense if the defendant has any prior conviction for felony drug charges. The cultivation of 1000 plants or possession of 1,000 kilograms of Cannabis produces a ten-year minimum mandatory sentence. An offender with a prior conviction for any drug offense will result in a twenty-year minimum mandatory sentence. With two prior felony drug convictions, the defendant faces a life sentence.
How can our leaders conceivably testify without perjuring themselves, that cannabis has no medicinal value while at the same time they hold a patent that describes in great detail so many of the demonstrated medicinal qualities of Cannabis?
Even with Prohibition in Effect, The United States Federal Government Owns a patent on Cannabis…
United States Patent #  6,630,507
Hampson ,   et al.
Filing date: Feb 2, 2001
Issue date: Oct 7, 2003
Application number: 09/674,028               
Cannabinoids have been found to have antioxidant properties, unrelated to NMDA receptor antagonism. This new found property makes cannabinoids useful in the treatment and prophylaxis of wide variety of oxidation associated diseases, such as ischemic, age-related, inflammatory and autoimmune diseases. The cannabinoids are found to have particular application as neuroprotectants, for example in limiting neurological damage following ischemic insults, such as stroke and trauma, or in the treatment of neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease and HIV dementia. Nonpsychoactive cannabinoids, such as cannabidoil, are particularly advantageous to use because they avoid toxicity that is encountered with psychoactive cannabinoids at high doses useful in the method of the present invention. A particular disclosed class of cannabinoids useful as neuroprotective antioxidants is formula (I) wherein the R group is independently selected from the group consisting of H, CH.sub.3, and COCH.sub.3. ##STR1##
 “The prestige of government 
has undoubtedly been lowered considerably 
by the Prohibition law. 
 For nothing is more destructive 
of respect for the government and 
the law of the land
 than passing laws which cannot be enforced”
Albert Einstein
The Medical and Scientific Research
I would like to share with you some of the existing research between cannabis and cancers of the immune system (leukemia/lymphoma). This information is specific to Jurkat leukemia cell lines… which is a CD4+ T-cell Acute Lymphoblastic Leukemia… This is the same lineage discovered in Mykayla’s leukemia. Brave Mykayla’s specific type of cancer has a large volume of proven science behind cannabis being an effective treatment because scientists discovered that immune system cells have a SPECIFIC cb2 receptor on them that cause apoptosis (cell death)
Δ9-Tetrahydrocannabinol-Induced Apoptosis in Jurkat Leukemia T Cells Is Regulated by Translocation of Bad to Mitochondria
abstract
THC induces apoptosis in Jurkat (t-cell acute lymphoblastic leukemia) cells via three different mechanisms. (1) THC binds to CB1 and CB2, and leads to ceramide synthesis by serine palmitoyltransferase. (2) Ceramide enters the mitochondria and results in cytochrome c leakage into the cytosol. (3) Cytochrome c combines with Apaf-1, caspase 9, and forms the apoptosome. (4) The apoptosome converts procaspase 3 to active caspase 3, resulting in apoptosis. THC also activates the extrinsic pathway (caspases 8 and 10), and inhibits Raf/Mek/Erk pathway. The inhibition of the cell survival pathway leads to dephosphorylation of Bad, and translocation of this Bcl-2 protein into the mitochondria, and subsequently to apoptosis.
Targeting cannabinoid receptors to treat leukemia: Role of cross-talk between extrinsic and intrinsic pathways in Δ9-tetrahydrocannabinol (THC)-induced apoptosis of Jurkat cells
abstract
 
Targeting cannabinoid receptors has recently been shown to trigger apoptosis and offers a novel treatment modality against malignancies of the immune system. However, the precise mechanism of apoptosis in such cancers has not been previously addressed. In this study, we used human Jurkat leukemia cell lines with defects in intrinsic and extrinsic signaling pathways to elucidate the mechanism of apoptosis induced by Δ9-tetrahydrocannabinol (THC). We observed that Jurkat cells deficient in FADD or caspase-8 were partially resistant to apoptosis, while dominant-negative caspase-9 mutant cells were completely resistant to apoptosis. Use of caspase inhibitors confirmed these results. Furthermore, overexpression of Bcl-2 rendered the cells resistant to THC at early time points but not upon prolonged exposure. THC treatment led to loss of Δψm, in both wild-type and FADD-deficient Jurkat cells thereby suggesting that THC-induced intrinsic pathway was independent of FADD. THC treatment of wild-type Jurkat cells caused cytochrome c release, and cleavage of caspase-8, -9, -2, -10, and Bid. Caspase-2 inhibitor blocked THC-induced caspase-3 in wild-type Jurkat cells but not loss of Δψm. Together, these data suggest that the intrinsic pathway plays a more critical role in THC-induced apoptosis while the extrinsic pathway may facilitate apoptosis via cross-talk with the intrinsic pathway.
Targeting CB2 cannabinoid receptors as a novel therapy to treat malignant lymphoblastic disease:
abstract
Fig. 7.The current study demonstrates that targeting CB2 receptors to induce apoptosis may constitute a novel approach to treating malignancies of the immune system. The advantage in using CB2 receptor agonists is that they do not exhibit psychoactive properties. Also, because CB2 receptors are expressed exclusively on immune cells, use of CB2 receptor agonists will not be toxic to non-immune cells. Thus, further research on CB2 receptor agonists to target transformed immune cells could lead to discovery of a new class of highly selective anticancer agents
Cannabidiol-Induced Apoptosis in Human Leukemia Cells: A Novel Role of Cannabidiol in the Regulation of p22phox and Nox4 Expression
abstract
https://i0.wp.com/molpharm.aspetjournals.org/content/70/3/897/F4.large.jpgIn the current study, we examined the effects of the nonpsychoactive cannabinoid, cannabidiol, on the induction of apoptosis in leukemia cells. Exposure of leukemia cells to cannabidiol led to cannabinoid receptor 2 (CB2)-mediated reduction in cell viability and induction in apoptosis. Furthermore, cannabidiol treatment led to a significant decrease in tumor burden and an increase in apoptotic tumors in vivo. From a mechanistic standpoint, cannabidiol exposure resulted in activation of caspase-8, caspase-9, and caspase-3, cleavage of poly(ADP-ribose) polymerase, and a decrease in full-length Bid, suggesting possible cross-talk between the intrinsic and extrinsic apoptotic pathways. The role of the mitochondria was further suggested as exposure to cannabidiol led to loss of mitochondrial membrane potential and release of cytochrome c. It is noteworthy that cannabidiol exposure led to an increase in reactive oxygen species (ROS) production as well as an increase in the expression of the NAD(P)H oxidases Nox4 and p22phox. Furthermore, cannabidiol-induced apoptosis and reactive oxygen species (ROS) levels could be blocked by treatment with the ROS scavengers or the NAD(P)H oxidase inhibitors. Finally, cannabidiol exposure led to a decrease in the levels of p-p38 mitogen-activated protein kinase, which could be blocked by treatment with a CB2-selective antagonist or ROS scavenger. Together, the results from this study reveal that cannabidiol, acting through CB2 and regulation of Nox4 and p22phox expression, may be a novel and highly selective treatment for leukemia.
Cannabinoid receptor-mediated regulation of intracellular calcium by Δ9-tetrahydrocannabinol in resting T cells
abstract
Cannabinoids exhibit broad immune modulating activity by targeting many cell types within the immune system, including T cells, which exhibit sensitivity, as evidenced by altered activation, proliferation, and cytokine expression. As a result of the critical role calcium plays in T cell function coupled with previous findings demonstrating disruption of the calcium-regulated transcription factor, nuclear factor of activated T cells, by cannabinoid treatment, the objective of the present investigation was to perform an initial characterization of the role of the cannabinoid receptors in the regulation of the intracellular calcium concentration ([Ca2+]i) by Δ9-tetrahydrocannabinol (Δ9-THC) in T lymphocytes. Here, we demonstrate that Δ9-THC robustly elevates [Ca2+]i in purified murine splenic T cells and in the human peripheral blood acute lymphoid leukemia (HPB-ALL) human T cell line but only minimally elevates [Ca2+]i in Jurkat E6-1 (dysfunctional cannabinoid receptor 2-expressing) human T cells. Removal of extracellular calcium severely attenuated the Δ9-THC-mediated rise in [Ca2+]i in murine splenic T cells and HPB-ALL cells. Pretreatment with cannabinoid receptor antagonists, SR144528 and/or SR141716A, led to an attenuation of Δ9-THC-mediated elevation in [Ca2+]i in splenic T cells and HPB-ALL cells but not in Jurkat E6-1 cells. Furthermore, pretreatment of HPB-ALL cells with SR144528 antagonized the small rise in [Ca2+]i elicited by Δ9-THC in the absence of extracellular calcium. These findings suggest that Δ9-THC induces an influx of extracellular calcium in resting T cells in a cannabinoid receptor-dependent manner.
Cannabinoids: potential anticancer agents
 abstract
Cannabinoids — the active components of Cannabis sativa and their derivatives — exert palliative effects in cancer patients by preventing nausea, vomiting and pain and by stimulating appetite. In addition, these compounds have been shown to inhibit the growth of tumour cells in culture and animal models by modulating key cell-signalling pathways. Cannabinoids are usually well tolerated, and do not produce the generalized toxic effects of conventional chemotherapies. So, could cannabinoids be used to develop new anticancer therapies?
 

“Prohibition… goes beyond the bounds of reason in that it attempts to control mans’ appetite through legislation and makes a crime out of things that are not even crimes… A prohibition law strikes a blow at the very principles upon which our Government was founded.”

CannaDad

 

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