Why Legalizing Pot Is Good for the Planet

Why Legalizing Pot Is Good for the Planet

Marijuana cultivation can stress the environment, but regulation is difficult when its legal status isn’t clear. Photo credit: Shutterstock

Marijuana cultivation can stress the environment, but regulation is difficult when its legal status isn’t clear. Photo credit: Shutterstock

The movement to legalize marijuana use and cultivation is picking up steam across the U.S. In California medical marijuana has been legal since 1996, while recreational use—though still not legal—is widely accepted with possession of small amounts a minor misdemeanor. Since then, multiple other states have followed on California’s footsteps in legalizing the popular plant or at least decriminalizing it.

But it’s still technically a banned drug at the federal level. So rules governing its use, distribution and growing are uneven, and unevenly enforced. And, according to a new scientific study, that’s not good for the environment.

A team of scientists from the Nature Conservancy, California Department of Fish and Wildlife, and University of California Berkeley published a study this week, High Time for Conservation: Adding the Environment to the Debate on Marijuana Liberalization, in the journal Bioscience, explaining the ways in which a consistent national policy on pot could benefit the environment.

“The policy debate, which has focused on the public health and criminal outcomes of liberalization, has largely neglected another notable source of societal harm arising from widespread marijuana use: the environmental harm associated with its commercial-scale cultivation,” it says.

Its main point: growing marijuana has a series of negative environmental impacts that are worsened by black market and semi-legal growing, which make regulations harder to enact and enforce. By making it fully legal, regulations could be enacted governing its cultivation to mitigate these impacts. It points out that even in California, where 60-70 percent of the pot consumed in the U.S. is grown, black market production flourishes.

“Like all forms of agriculture, marijuana cultivation has implications for natural resources that should be part of the current and future policy discussion,” the report explains. “However, regulation designed to mitigate environmental harm is more difficult to implement for marijuana cultivation than for other agricultural activities because of its unique and evolving legal status. Although many U.S. states are legalizing recreational and medical marijuana possession and use, it remains illegal at the federal level, putting the industry in a semi-legal gray area in these states. This status separates marijuana from fully legal agricultural commodities and greatly complicates regulation of the industry.”

“The combination of limited water resources, a water-hungry crop, and illegal cultivation in sensitive ecosystems means that marijuana cultivation can have environmental impacts that are disproportionately large given the area under production,” it concludes.

High Time for Conservation enumerates ways in which marijuana cultivation stresses the environment, stresses that could be more easily managed with complete legalization.

#1. 

Growing pot is extremely water-intensive, a major issue in a drought-stricken state like California. Outdoor-grown marijuana in California’s north coast region requires about twice as much water as the region’s other major irrigated crop, wine grapes. “We’re only starting to get a handle on these numbers,” said one of the study’s co-authors, Berkeley ecohydrologst Sally Thompson. “This is criminal activity, so it’s dangerous to monitor the impact. But even if the numbers are off, we are still talking about significant quantities of water.” Meanwhile, indoor cultivation is an energy hog; it “can require extensive energy inputs with potentially negative effects on climate,” the study says.

#2. 

That water use can impact endangered species. “Compared with more established forms of agriculture on the north coast, where abundant winter stream flow is sometimes captured and stored locally in ponds or tanks for later summer use, marijuana cultivation is typically irrigated with summer and fall surface water diversions directly from headwater streams and springs,” the report points out. “These diversions are localized in smaller, sensitive watersheds that are hotspots of biodiversity—and particularly aquatic biodiversity. Surface water diversions for marijuana cultivation have been documented to significantly reduce or eliminate already low stream flow during California’s Mediterranean-type dry summer season, particularly during drought years, and therefore threaten the survival of rare and endangered salmonids, amphibians and other animals.”

#3. 

The use of pesticides on marijuana plantations pollute watersheds and is a threat to wildlife. “Pesticides, used heavily in black-market cultivation on public lands, make their way into terrestrial food chains, posing significant risks to mammalian and avian predators,” says the report.  More than 80 percent of dead Pacific fishers in the region were found to have been exposed to rodenticides used to control rats in black-market marijuana cultivation, it points out. And “The heavy use of pesticides, herbicides, fertilizers and petroleum fuels in both semi-legal and black-market cultivation can also contaminate watersheds.”

#4. 

The built infrastructure of marijuana cultivation can present a threat to the surrounding environment. “Land terracing, road construction and forest clearing for both semi-legal and black-market marijuana plantations remove native vegetation and increase erosion,” write the authors. “Erosion increases fine-sediment loading into streams, damaging spawning and rearing habitat for salmon and trout, such as federally endangered coho salmon.”

#5. 

Humans leave their mark on the ecosystem too, an impact likely to be exacerbated by trying to avoid detection in black-market growing. Trespassing and camping on public or tribal lands for months at a time, they poach wildlife for both sport and sustenance. In addition, “Nonbiodegradable trash and human excrement are commonly dumped around black-market marijuana cultivation sites on public and tribal lands.”

The report says that the “clandestine nature of the business” makes it hard to get a grasp on the facts surrounding marijuana production in California and that semi-legal status “greatly complicates local authority to regulate the medical market and sets the industry apart from traditional agriculture.” Further, the conflict between state and federal standards “encourages secrecy and invisibility among producers for both the semi-legal medical and black markets, leading to lower levels of voluntary compliance with existing environmental regulation.”

The report authors suggest that as legalization spreads, some of the tax revenues collected by the states should be aimed at preventing and mitigating the environmental impacts of cultivation.

“In order to overcome barriers to participation, however, incentive strategies will likely only be feasible where the legal status of production is clarified,” they say. “The current levels of ambiguity and secrecy surrounding the industry impede the revelation of associated environmental impacts, as well as the creation and implementation of solutions. ”

Source: ecowatch.com

The Cannabis Cure For Cancer

The Cannabis Cure For Cancer

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This quick overview of the science backs up the assertion that every cancer patient and every oncologist should put medical marijuana on their treatment maps.

There should be no more confusion about whether or not marijuana is effective for cancer patients. Medical marijuana is chemotherapy, natural style, for cancer patients. The two forms of hemp oil, one with THC and CBD and the other CBD alone (which is pretty much legal everywhere) provide the body with chemo-therapeutics without the danger and staggering side effects. There are many chapters in my book about cancer patients using marijuana, but in this one we present a quick overview of the science that backs up the assertion that every cancer patient and every oncologist should put medical marijuana on their treatment maps.

What you will see in this article is reference to many scientific studies that are all viewable on governmental sites. The United States government is pathetic in its dishonesty about medical marijuana both believing in it and holding patents for its medical use and claiming at the same time that it has no medical use. The federal government and still many states would rather throw innocent people in jail for using medical marijuana than be honest about how much it can help people recover from cancer and other diseases.

Below are summaries to just some of the scientific research out there that sustains the belief that medical marijuana will help people cure their cancer.

One of the most exciting areas of current research in the cannabinoid field is the study of the potential application of these compounds as antitumor drugs. CBD represents the first nontoxic exogenous agent that can significantly decrease Id-1 expression in metastatic breast cancer cells leading to the down-regulation of tumor aggressiveness.[1],[2] The CBD concentrations effective at inhibiting Id-1 expression correlated with those used to inhibit the proliferative and invasive phenotype of breast cancer cells. Of the five cannabinoids tested: cannabidiol, cannabigerol, cannnabichromene; cannabidiol-acid and THC-acid, it was found that cannabidiol is the most potent inhibitor of cancer cell growth. Taken together, these data might set the bases for a cannabinoid therapy for the management of breast cancer.[3]

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Results show that Δ9-tetrahydrocannabinol reduces tumor growth, tumor number, and the amount/severity of lung metastases in MMTV-neu mice.[4] Cannabinoids induce ICAM-1, thereby conferring TIMP-1 induction and subsequent decreased cancer cell invasiveness thus inhibits lung cancer invasion and metastasis.[5]

Non-small cell lung cancer (NSCLC) is the leading cause of cancer deaths worldwide. Researchers have observed expression of CB1 (24%) and CB2 (55%) in NSCLC patients. They have also shown that the treatment of NSCLC cell lines (A549 and SW-1573) with CB1/CB2- and CB2-specific agonists Win55,212-2 and JWH-015, respectively, significantly attenuated random as well as growth factor-directed in vitro chemotaxis and chemoinvasion in these cells.[6]

Researchers in lung cancers also reported that they observed significant reduction in focal adhesion complex, which plays an important role in cancer migration. Medical marijuana significantly inhibited in vivo tumor growth and lung metastasis (∼50%).[7]

In research on pancreatic cancer it was found that cannabinoids lead to apoptosis of pancreatic tumor cells via a CB2 receptor and de novo synthesized ceramide-dependent up-regulation of p8 and the endoplasmic reticulum stress–related genes ATF-4 and TRB3. These findings may contribute to set the basis for a new therapeutic approach for the treatment of pancreatic cancer as reported by the National Cancer Institute.

Prostate cancer cells possess increased expression of both cannabinoid 1 and 2 receptors, and stimulation of these results in decrease in cell viability, increased apoptosis, and decreased androgen receptor expression and prostate-specific antigen excretion.[8]

In colorectal carcinoma cell lines, cannabidiol protected DNA from oxidative damage, increased endocannabinoid levels and reduced cell proliferation in a CB(1)-, TRPV1- and PPARγ-antagonists sensitive manner. It is concluded that cannabidiol exerts chemopreventive effect in vivo and reduces cell proliferation through multiple mechanisms.[9]

Ovarian cancer represents one of the leading cause of cancer-related deaths for women and is the most common gynecologic malignancy. Results with medical marijuana support a new therapeutic approach for the treatment of ovarian cancer. It is also conceivable that with available cannabinoids as lead compounds, non-habit forming agents that have higher biological effects could be developed.[10]

Examination of a number of human leukaemia and lymphoma cell lines demonstrate that CB2 cannabinoid receptors expressed on malignancies of the immune system may serve as potential targets for the induction of apoptosis. Also, because CB2 agonists lack psychotropic effects, they may serve as novel anticancer agents to selectively target and kill tumors of immune origin.[11] Plant-derived cannabinoids, includin

mmg Delta9-tetrahydrocannabinol (THC), induce apoptosis in leukemic cells.[12]

Cannabinoid-treated tumors showed an increased number of apoptotic cells. This was accompanied by impairment of tumor vascularization, as determined by altered blood vessel morphology and decreased expression of proangiogenic factors (VEGF, placental growth factor, and angiopoietin. Abrogation of EGF-R function was also observed in cannabinoid-treated tumors.[13] These results support a new therapeutic approach for the treatment of skin tumors.

Hepatocellular carcinoma (HCC) is the third cause of cancer-related death worldwide. When these tumors are in advanced stages, few therapeutic options are available. In this study, the effects of cannabinoids–a novel family of potential anticancer agents–on the growth of HCC was investigated. It was found that Δ(9)-tetrahydrocannabinol (Δ(9)-THC, the main active component of Cannabis sativa) and JWH-015 (a cannabinoid receptor 2 (CB(2)) cannabinoid receptor-selective agonist) reduced the viability of the human HCC cell lines Cannabinoids were able to inhibit tumor growth and ascites in an orthotopic model of HCC xenograft.[14] These findings may contribute to the design of new therapeutic strategies for the management of HCC.

Both cholangiocarcinoma cell lines and surgical specimens from cholangiocarcinoma patients expressed cannabinoid receptors. THC inhibited cell proliferation, migration and invasion, and induced cell apoptosis. THC also decreased actin polymerization and reduced tumor cell survival in anoikis assay. pMEK1/2 and pAkt demonstrated the lower extent than untreated cells. Consequently, THC is potentially used to retard cholangiocarcinoma cell growth and metastasis.[15]

Smoking marijuana might decrease the smoker’s risk for bladder cancer, a new study shows. Retrospectively analyzing a large database of patients, researchers at Kaiser Permanente in California found that patients who reported cannabis use were 45% less likely to be diagnosed with bladder cancer than patients who did not smoke at all.

THC is a potent inducer of apoptosis, even at 1 x IC(50) (inhibitory concentration 50%) concentrations and as early as 6 hours after exposure to the drug. These effects were seen in leukemic cell lines (CEM, HEL-92, and HL60) as well as in peripheral blood mononuclear cells.[16] Cannabinoids represent a novel class of drugs active in increasing the life span in  mice carrying Lewis lung tumors and decreasing primary tumor size.[17]

Research has also found a cannabidiol-driven impaired invasion of human cervical cancer (HeLa, C33A) and human lung cancer cells (A549) that was reversed by antagonists to both CB(1) and CB(2) receptors as well as to transient receptor potential vanilloid 1 (TRPV1). The decrease of invasion by cannabidiol appeared concomitantly with up regulation of tissue inhibitor of matrix metalloproteinases-1 (TIMP the findings provide a novel mechanism underlying the anti-invasive action of cannabidiol and imply its use as a therapeutic option for the treatment of highly invasive cancers.[18]

A new anticancer quinone (HU-331) was synthesized from cannabidiol. It shows significant high efficacy against human cancer cell lines in vitro and against in vivo tumor grafts in nude mice. Two non-psychotropic cannabinoids, cannabidiol (CBD) and cannabidiol-dimethylheptyl (CBD-DMH), induced apoptosis in a human acute myeloid leukemia (AML) HL-60 cell line.[19]

Other studies show a synthetic and potent cannabinoid receptor agonist, investigated in hepatoma HepG2 cells and a possible signal transduction pathway that is proposed, indicates a potential positive role in liver cancer.[20] Cannabinoids have been found to counteract intestinal inflammation and colon cancer.[21]

The control of the cellular proliferation has become a focus of major attention as opening new therapeutic possibilities for the use of cannabinoids as potential antitumor agents.[22] Cannabinoid treatment inhibits angiogenesis of gliomas in vivo.[23] Remarkably, cannabinoids kill glioma cells selectively and can protect non-transformed glial cells from death. These and other findings reviewed here might set the basis for a potential use of cannabinoids in the management of gliomas. Other confirming studies may provide the basis for a new therapeutic approach for the treatment of malignant gliomas.[24]

In Summary

Cannabinoids are found to exert their anti-cancer effects in a number of ways and in a variety of tissues.

  • Triggering cell death, through a mechanism called apoptosis
  • Stopping cells from dividing
  • Preventing new blood vessels from growing into tumours
  • Reducing the chances of cancer cells spreading through the body, by stopping cells from moving or invading neighbouring tissue
  • Speeding up the cell’s internal ‘waste disposal machine’ – a process known as autophagy – which can lead to cell death

All these effects are thought to be caused by cannabinoids locking onto the CB1 and CB2 cannabinoid receptors.  Almost daily we are seeing new or confirming evidence that Cannibinoids can be used to great benefit in cancer treatment of many types.


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[1] Crosstalk between chemokine receptor CXCR4 and cannabinoid receptor CB2 in modulating breast cancer growth and invasion. Nasser MW; et al; PLoS One. 2011;6(9):e23901. doi: 10.1371/journal.pone.0023901. Epub 2011 Sep 7;  http://www.ncbi.nlm.nih.gov/pubmed/21915267 .

[2] Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells; McAllister SD et al; Mol Cancer Ther. 2007 Nov;6(11):2921-7;

[3] Delta9-tetrahydrocannabinol inhibits cell cycle progression in human breast cancer cells through Cdc2 regulation; Caffarel MM et al; Cancer Res; 2006 Jul 1;66(13):6615-21;

[4] Cannabinoids: a new hope for breast cancer therapy? Caffarel MM et al; Cancer Treat Rev.: 2012 Nov; 38(7):911-8. doi: 10.1016/j.ctrv.2012.06.005. Epub 2012 Jul 7;

[5] Cannabidiol inhibits lung cancer cell invasion and metastasis via intercellular adhesion molecule-1. Ramer R et al; FASEB J.; 2012 Apr;26(4):1535-48. doi: 10.1096/fj.11-198184. Epub 2011 Dec 23;

[6] Cannabinoid receptors, CB1 and CB2, as novel targets for inhibition of non-small cell lung cancer growth and metastasis; Preet A, et al; Cancer Prev Res (Phila). 2011 Jan; 4(1):65-75. doi: 10.1158/1940-6207.CAPR-10-0181. Epub 2010 Nov 19;

[7] Δ9-Tetrahydrocannabinol inhibits epithelial growth factor-induced lung cancer cell migration in vitro as well as its growth and metastasis in vivo; A Preetet al; Oncogene; (2008) 27,339–346; doi:10.1038/sj.onc.1210641; published online 9 July 2007;

[8] The role of cannabinoids in prostate cancer: Basic science perspective and potential clinical applications; Juan A. Ramos and Fernando J. Bianco; Indian J Urol. 2012 Jan-Mar; 28(1): 9–14;.doi:10.4103/0970-1591.94942;

[9] Chemopreventive effect of the non-psychotropic phytocannabinoid cannabidiol on experimental colon cancer. Aviello G et al; ;J Mol Med (Berl); 2012 Aug;90(8):925-34. doi: 10.1007/s00109-011-0856-x. Epub 2012;  Jan 10.;

[10] Cannabinoid receptors as a target for therapy of ovarian cancer. Farrukh Afaq; et al;, Proc Amer Assoc Cancer Res, Volume 47, 2006;

[11] Targeting CB2 cannabinoid receptors as a novel therapy to treat malignant lymphoblastic disease. McKallip RJ et al; Blood. 2002 Jul 15;100(2):627-34.;

[12] Delta9-tetrahydrocannabinol-induced apoptosis in Jurkat leukemia T cells is regulated by translocation of Bad to mitochondria. Jia W et al; Mol Cancer Res.; 2006 Aug;4(8):549-62;

[13] Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors. Casanova ML et al: J Clin Invest. 2003 Jan;111(1):43-50;

[14] Anti-tumoral action of cannabinoids on hepatocellular carcinoma: role of AMPK-dependent activation of autophagy. Vara D et al; Cell Death Differ; 2011 Jul;18(7):1099-111. doi: 10.1038/cdd.2011.32. Epub 2011 Apr 8.;

[15] The dual effects of delta(9)-tetrahydrocannabinol on cholangiocarcinoma cells: anti-invasion activity at low concentration and apoptosis induction at high concentration. Leelawat Set al;Cancer Invest. 2010 May;28(4):357-63. doi: 10.3109/07357900903405934;

[16] Cannabis-induced cytotoxicity in leukemic cell lines: the role of the cannabinoid receptors and the MAPK pathway; Powles T et al; Blood;.2005 Feb 1;105(3):1214-21; Epub 2004 Sep 28.;

[17] In vivo effects of cannabinoids on macromolecular biosynthesis in Lewis lung carcinomas; Friedman MA; Cancer Biochem Biophys. 1977;2(2):51-4.;

[18] Cannabidiol inhibits cancer cell invasion via upregulation of tissue inhibitor of matrix metalloproteinases-1; Ramer Ret al; Biochem Pharmacol; 2010 Apr 1;79(7):955-66. doi: 10.1016/j.bcp.2009.11.007. Epub 2009 Nov 13;

[19] Gamma-irradiation enhances apoptosis induced by cannabidiol, a non-psychotropic cannabinoid, in cultured HL-60 myeloblastic leukemia cells. Gallily R et al; Leuk Lymphoma.:2003 Oct;44(10):1767-73;

[20] Apoptosis induced in HepG2 cells by the synthetic cannabinoid WIN: involvement of the transcription factor PPARgamma. Giuliano Met et al; Biochimie;. 2009 Apr;91(4):457-65. doi: 10.1016/j.biochi.2008.11.003. Epub 2008 Nov 27.

[21] Cannabinoids in intestinal inflammation and cancer. Izzo AA1, Camilleri M.; Pharmacol Res; 2009 Aug;60(2):117-25. doi: 10.1016/j.phrs.2009.03.008. Epub 2009 Mar 18;

[22] Involvement of cannabinoids in cellular proliferation; López-Rodríguez ML et al; Mini Rev Med Chem; 2005 Jan;5(1):97-106

[23] Hypothesis: cannabinoid therapy for the treatment of gliomas? Velasco G et al; Neuropharmacology;.2004 Sep;47(3):315-23;

[24] Anti-tumoral action of cannabinoids: involvement of sustained ceramide accumulation and extracellular signal-regulated kinase activation; Galve-Roperh; Nat Med.; 2000 Mar;6(3):313-9;

Article Originally Published Here

Blocking Brain’s ‘Internal Marijuana’ May Trigger Early Alzheimer’s Deficits, Study Shows

Blocking Brain’s ‘Internal Marijuana’ May Trigger Early Alzheimer’s Deficits, Study Shows

A new study led by investigators at the Stanford University School of Medicine has implicated the blocking of endocannabinoids — signaling substances that are the brain’s internal versions of the psychoactive chemicals in marijuana and hashish — in the early pathology of Alzheimer’s disease.

A substance called A-beta — strongly suspected to play a key role in Alzheimer’s because it’s the chief constituent of the hallmark clumps dotting the brains of people with Alzheimer’s — may, in the disease’s earliest stages, impair learning and memory by blocking the natural, beneficial action of endocannabinoids in the brain, the study demonstrates. The Stanford group is now trying to figure out the molecular details of how and where this interference occurs. Pinning down those details could pave the path to new drugs to stave off the defects in learning ability and memory that characterize Alzheimer’s.

In the study, published June 18 in Neuron, researchers analyzed A-beta’s effects on a brain structure known as the hippocampus. In all mammals, this midbrain structure serves as a combination GPS system and memory-filing assistant, along with other duties.

“The hippocampus tells us where we are in space at any given time,” said Daniel Madison, PhD, associate professor of molecular and cellular physiology and the study’s senior author. “It also processes new experiences so that our memories of them can be stored in other parts of the brain. It’s the filing secretary, not the filing cabinet.”

Surprise finding

Applying electrophysiological techniques to brain slices from rats, Madison and his associates examined a key hippocampal circuit, one of whose chief elements is a class of nerve cells called pyramidal cells. They wanted to see how the circuit’s different elements reacted to small amounts of A-beta, which is produced throughout the body but whose normal physiological functions have until now been ill-defined.

A surprise finding by Madison’s group suggests that in small, physiologically normal concentrations, A-beta tamps down a signal-boosting process that under certain conditions increases the odds that pyramidal nerve cells will transmit information they’ve received to other nerve cells down the line.

When incoming signals to the pyramidal tract build to high intensity, pyramidal cells adapt by becoming more inclined to fire than they normally are. This phenomenon, which neuroscientists call plasticity, is thought to underpin learning and memory. It ensures that volleys of high-intensity input — such as might accompany falling into a hole, burning one’s finger with a match, suddenly remembering where you buried the treasure or learning for the first time how to spell “cat” — are firmly stored in the brain’s memory vaults and more accessible to retrieval.

These intense bursts of incoming signals are the exception, not the rule. Pyramidal nerve cells constantly receive random beeps and burps from upstream nerve cells — effectively, noise in a highly complex, electrochemical signaling system. This calls for some quality control. Pyramidal cells are encouraged to ignore mere noise by another set of “wet blanket” nerve cells called interneurons. Like the proverbial spouse reading a newspaper at the kitchen table, interneurons continuously discourage pyramidal cells’ transmission of impulses to downstream nerve cells by steadily secreting an inhibitory substance — the molecular equivalent of yawning, eye-rolling and oft-muttered suggestions that this or that chatter is really not worth repeating to the world at large, so why not just shut up.

Passing along the message

But when the news is particularly significant, pyramidal cells squirt out their own “no, this is important, you shut up!” chemical — endocannabinoids — which bind to specialized receptors on the hippocampal interneurons, temporarily suppressing them and allowing impulses to continue coursing along the pyramidal cells to their follow-on peers.

A-beta is known to impair pyramidal-cell plasticity. But Madison’s research team showed for the first time how it does so. Small clusters consisting of just a few A-beta molecules render the interneuron’s endocannabinoid receptors powerless, leaving inhibition intact even in the face of important news and thus squashing plasticity.

While small A-beta clusters have been known for a decade to be toxic to nerve cells, this toxicity requires relatively long-term exposure, said Madison. The endocannabinoid-nullifying effect the new study revealed is much more transient. A possible physiological role for A-beta in the normal, healthy brain, he said, is that of supplying that organ’s sophisticated circuits with yet another, beneficial layer of discretion in processing information. Madison thinks this normal, everyday A-beta mechanism run wild may represent an entry point to the progressive and destructive stages of Alzheimer’s disease.

Exactly how A-beta blocks endocannabinoids’ action is not yet known. But, Madison’s group demonstrated, A-beta doesn’t stop them from reaching and binding to their receptors on interneurons. Rather, it interferes with something that binding ordinarily generates. (By analogy, turning the key in your car’s ignition switch won’t do much good if your battery is dead.)

Exposure to marijuana over minutes or hours is different: more like enhancing everything indiscriminately, so you lose the filtering effect.

Madison said it would be wildly off the mark to assume that, just because A-beta interferes with a valuable neurophysiological process mediated by endocannabinoids, smoking pot would be a great way to counter or prevent A-beta’s nefarious effects on memory and learning ability. Smoking or ingesting marijuana results in long-acting inhibition of interneurons by the herb’s active chemical, tetrahydrocannabinol. That is vastly different from short-acting endocannabinoid bursts precisely timed to occur only when a signal is truly worthy of attention.

“Endocannabinoids in the brain are very transient and act only when important inputs come in,” said Madison, who is also a member of the interdisciplinary Stanford Bio-X institute. “Exposure to marijuana over minutes or hours is different: more like enhancing everything indiscriminately, so you lose the filtering effect. It’s like listening to five radio stations at once.”

Besides, flooding the brain with external cannabinoids induces tolerance — it may reduce the number of endocannabinoid receptors on interneurons, impeding endocannabinoids’ ability to do their crucial job of opening the gates of learning and memory.

The study’s lead author was postdoctoral scholar Adrienne Orr, PhD. Other co-authors were postdoctoral scholars Jesse Hanson, PhD (now at Genentech) and Dong Li, PhD; and former undergraduate Adam Klotz, now a student at Stanford’s Graduate School of Business. The study was funded by the National Institute for Mental Health (grant MH065541), the Harold and Leila Y. Mathers Charitable Foundation and Elan Pharmaceuticals.

Information about Stanford’s Department of Molecular and Cellular Physiology, which also supported this work, is available at http://mcp.stanford.edu/.

Editors note: Original press release can be found here. 

The Hidden Side-Effects Of Colorado’s Cannabis Boom

The Hidden Side-Effects Of Colorado’s Cannabis Boom

In November 2012, Colorado became the first US state to legalise cannabis. As other states look set to follow suit business may be booming, but there’s a dark side to the ‘silver bullet’ of legalisation.

Ginger mango dew drops, rice crispy and chocolate truffle may all sound more like children’s sweets than cannabis treats, but they’re the entrepreneurial inspirations of Tripp Keber, a man unashamedly looking to cash in on cannabis legalisation. “I’m not here wearing a Bob Marley T-shirt. I do not have dreadlocks in my hair. I’m business.” With everything from marijuana medical centres to cosmetics, food and drinks, it’s easy to see why other states like DC and Illinois are keen to follow Colorado’s suit. According to lobbyist Matt Brown, the city of Aurora in Colorado, “has missed out on hundreds of millions of dollars of investment”, because it didn’t follow Denver’s suit in legalising the drug. But that’s only one side of the story. Aaron Huey, who runs a rehab centre for addicted teens, is fiercely critical of the legalisation. “I never had this number and never at this time of year. This is the first time I’m experiencing this. So is it getting worse? Our numbers say so.” With big alcohol and tobacco companies said to be watching closely and some predicting federal legalisation within ten years, is dope America’s newest big business opportunity?

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New Study: Vaporized Marijuana is a Safe and Effective Pain Treatment

New Study: Vaporized Marijuana is a Safe and Effective Pain Treatment

New Study: Vaporized Marijuana is a Safe and Effective Pain Treatmentby Elizabeth Renter

When we talk about the medicinal benefits of marijuana, those who disapprove of its use tend to roll their eyes. But the fact is, this powerful plant has numerous potential applications in healthcare and pain management in particular. A new study has once again demonstrated that the vilified plant can safely and effectively treat general pain along with the painful symptoms of neuropathy.

Neuropathy is damage to the nervous system – particularly the peripheral nervous system (not including the brain and spinal cord). It is characterized by pain and numbness especially in the hands and feet, and is often the result of diabetes. Neuropathy can also be caused by injuries, toxic exposure, infections, and more.

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This latest study was conducted by researchers at the University of California Davis Medical Center and was published in The Journal of Pain. It was a double-blind, placebo-controlled, crossover study that looked at the effectiveness of using vaporized, inhaled cannabis in 39 participants. These participants were experiencing neuropathic pain despite having tried traditional treatments (like opiate drugs). All participants continued to take their prescribed medications throughout the 4 week study period.

Researchers gave participants doses of cannabis with moderate THC levels (3.53 percent) or low THC levels (1.29 percent). (THC, or tetrahydrocannabinol, is the plant’s primary psychoactive chemical). Some also received a placebo with no THC. They found both doses of cannabis to be effective in reducing pain significantly.

“Both the low and medium doses proved to be salutary analgesics for the heterogeneous collection of neuropathic pain conditions studied. Both active study medications provided statistically significant 30% reductions in pain intensity when compared to placebo,” stated the researchers.

This is far from the first study to illustrate the pain-relieving benefits of cannabis. In fact, cannabis (even in THC-free form, or free of psychoactive effects) has been identified as a powerful pain reliever in more than 80 peer-reviewed studies. Still, the herb is classified as dangerous by the U.S. government.

Why is marijuana still illegal? Opponents of medicinal marijuana (including the federal government) say the research isn’t enough. It isn’t clear what they would like to see in marijuana studies, but it’s beginning to look like they want the impossible. It seems they would rather Americans continue consuming addictive prescription pain medications than use a plant.

According to AlterNet, sales of opiate pain pills have tripled since 1999. Oxycodone (one of the more popular choices on the legal and illegal market) has increased from 8.3 tons in 1997 to a whopping 105 tons in 2011. Overdose deaths are similarly climbing as is the number of people addicted to these substances. To date, no one has died from a marijuana overdose.

Additional Sources:

Norml.org

MedicalNewsToday

Republished from:
Natural Society