Category Archives: THC (Delta-9-Tetrahydrocannabinol)

Nabilone for the treatment of paraneoplastic night sweats: a report of four cases.

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“Night sweats are one of many symptoms experienced by patients with advanced cancer. Persistent night sweats tend to decrease quality of life through interference with sleep… night sweats represent one of the symptoms that displays a tendency not to improve as patients with advanced cancer approach end of life…

This paper serves to report on the successful management of four patients suffering from persistent paraneoplastic night sweats using the synthetic orally administered cannabinoid nabilone…”

http://www.ncbi.nlm.nih.gov/pubmed/18715188

Anandamide hydrolysis: a new target for anti-anxiety drugs?

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“The major psychoactive constituent of cannabis, Delta(9)-tetrahydrocannabinol, affects emotional states in humans and laboratory animals by activating brain cannabinoid receptors. A primary endogenous ligand of these receptors is anandamide, the amide of arachidonic acid with ethanolamine. Anandamide is released in selected regions of the brain and is deactivated through a two-step process consisting of transport into cells followed by intracellular hydrolysis. Pharmacological blockade of the enzyme fatty acid amide hydrolase (FAAH), which is responsible for intracellular anandamide degradation, produces anxiolytic-like effects in rats without causing the wide spectrum of behavioral responses typical of direct-acting cannabinoid agonists. These findings suggest that anandamide contributes to the regulation of emotion and anxiety, and that FAAH might be the target for a novel class of anxiolytic drugs.”

http://www.ncbi.nlm.nih.gov/pubmed/14604824

A role for cannabinoid CB1 receptors in mood and anxiety disorders.

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“Mood and anxiety disorders, the most prevalent of the psychiatric disorders, cause immeasurable suffering worldwide. Despite impressive advances in pharmacological therapies, improvements in efficacy and side-effect profiles are needed. The present literature review examines the role that the endocannabinoid system may play in these disorders and the potential value of targeting this system in the search for novel and improved medications.

Cannabis and its major psychoactive component (-)-trans-delta9-tetrahydrocannabinol, have profound effects on mood and can modulate anxiety and mood states. Cannabinoid receptors and other protein targets in the central nervous system (CNS) that modulate endocannabinoid function have been described. The discovery of selective modulators of some of these sites that increase or decrease endocannabinoid neurotransmission, primarily through the most prominent of the cannabinoid receptors in the CNS, the CB1 receptors, combined with transgenic mouse technology, has enabled detailed investigations into the role of these CNS sites in the regulation of mood and anxiety states. Although data point to the involvement of the endocannabinoid system in anxiety states, the pharmacological evidence seems contradictory: both anxiolytic- and anxiogenic-like effects have been reported with both endocannabinoid neurotransmission enhancers and blockers.

Due to advances in the development of selective compounds directed at the CB1 receptors, significant progress has been made on this target. Recent biochemical and behavioural findings have demonstrated that blockade of CB1 receptors engenders antidepressant-like neurochemical changes (increases in extracellular levels of monoamines in cortical but not subcortical brain regions) and behavioural effects consistent with antidepressant/antistress activity in rodents.”

http://www.ncbi.nlm.nih.gov/pubmed/16148437

Endocannabinoid system dysfunction in mood and related disorders.

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“The endocannabinoid (EC) system is widely distributed throughout the brain and modulates many functions. It is involved in mood and related disorders, and its activity may be modified by exogenous cannabinoids. This article examines the therapeutic potential of cannabinoids in psychiatric disorders.

We propose (hypothesize) that the EC system, which is homoeostatic in cortical excitation and inhibition, is dysfunctional in mood and related disorders. Anandamide, tetrahydrocannabinol (THC) and cannabidiol (CBD) variously combine antidepressant, antipsychotic, anxiolytic, analgesic, anticonvulsant actions, suggesting a therapeutic potential in mood and related disorders. Currently, cannabinoids find a role in pain control. Post mortem and other studies report EC system abnormalities in depression, schizophrenia and suicide. Abnormalities in the cannabinoid-1 receptor (CNR1) gene that codes for cannabinoid-1 (CB1) receptors are reported in psychiatric disorders. However, efficacy trials of cannabinoids in psychiatric disorders are limited but offer some encouragement.

CONCLUSION:

Research is needed to elucidate the role of the EC system in psychiatric disorders and for clinical trials with THC, CBD and synthetic cannabinoids to assess their therapeutic potential.”

http://www.ncbi.nlm.nih.gov/pubmed/21916860

Endocannabinoid system and mood disorders: Priming a target for new therapies.

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“The endocannabinoid system (ECS), comprising two G protein-coupled receptors (the cannabinoid receptors 1 and 2 [CB1 and CB2] for marijuana’s psychoactive principle ∆(9)-tetrahydrocannabinol [∆(9)-THC]), their endogenous small lipid ligands (namely anandamide [AEA] and 2-arachidonoylglycerol [2-AG], also known as endocannabinoids), and the proteins for endocannabinoid biosynthesis and degradation, has been suggested as a pro-homeostatic and pleiotropic signaling system activated in a time- and tissue-specific way during physiopathological conditions. In the brain activation of this system modulates the release of excitatory and inhibitory neurotransmitters and of cytokines from glial cells. As such, the ECS is strongly involved in neuropsychiatric disorders, particularly in affective disturbances such as anxiety and depression. It has been proposed that synthetic molecules that inhibit endocannabinoid degradation can exploit the selectivity of endocannabinoid action, thus activating cannabinoid receptors only in those tissues where there is perturbed endocannabinoid turnover due to the disorder, and avoiding the potential side effects of direct CB1 and CB2 activation. However, the realization that endocannabinoids, and AEA in particular, also act at other molecular targets, and that these mediators can be deactivated by redundant pathways, has recently led to question the efficacy of such approach, thus opening the way to new multi-target therapeutic strategies, and to the use of non-psychotropic cannabinoids, such as cannabidiol (CBD), which act via several parallel mechanisms, including indirect interactions with the ECS. The state of the art of the possible therapeutic use of endocannabinoid deactivation inhibitors and phytocannabinoids in mood disorders is discussed in this review article.”

http://www.ncbi.nlm.nih.gov/pubmed/23261685

Pot Stirring – ELLE

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“Some are using marijuana as their drug of choice to curb anxiety.”

Marijuana Anxiety Disorders
 

 “A thimbleful is all it takes. After a day’s work, I pinch off a small amount of marijuana and put it in a steel-tooth grinder. The flowers, covered in tiny white diamonds of THC, release a piney scent when crushed. I turn on the TV, and instead of taking a glass of wine with my evening news, I take out my vaporizer and set it on the coffee table.

Outside the walls of my bungalow in Oakland, California, I can hear the rush-hour traffic, but I’ve already changed into my Big Lebowski–style robe and slippers. I tap the ground flakes into a canister that I attach to another piece, this one with a bag on the end, and set both on the vaporizer. I flip the switch, and the bag slowly inflates with plumes of white smoke. Once it’s fully clouded, I attach a mouthpiece to the canister, put this to my lips, and press. On the inhale, the cannabinoids taste like sunned grass. My prescription for anxiety disorder didn’t always begin and end with an herb. But I’ve run through enough pharmaceutical drugs to know that pot dulls my panic better than any pill.”

Read more; http://www.elle.com/beauty/health-fitness/pot-stirring-19727

Marijuana nutrients found to help prevent Alzheimer’s disease

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“A study conducted by scientists at Scripps Research Institute in California has found that, contrary to marijuana’s reputation, the ingredients of the drug can actually fight off the memory-impairing effects of Alzheimer’s disease.The researchers found that the active ingredient in marijuana — delta-9-tetrahydrocannabinol, or THC — is responsible for the positive effect, as it can prevent the breakdown of the neurotransmitter acetylcholine even better than commercially marketed prescription drugs.

The study also showed that THC could completely prevent the enzyme acetylcholinesterase (AchE) from forming amyloid plaques, whereas twice as much donepezil and tacrine — the two drugs approved for Alzheimer’s treatment — only reduced such clumping by 22 and 7 percent, respectively, the researchers reported in the journal Molecular Pharmaceutics. This led the scientists to conclude that a more effective Alzheimer’s drug could be developed in the future.”

Read more: http://www.naturalnews.com/020667_Marijuana_Alzheimers_drugs.htm

Marijuana and Alzheimer’s – How Marijuana Outperforms Drugs for Alzheimer’s Disease

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“Marijuana and Alzheimer’s – Alzheimer’s Help without Nasty Drug-Induced Side Effects.”

marijuanaplants 235x147 Marijuana and Alzheimers How Marijuana Outperforms Drugs for Alzheimer’s Disease

“The war on drugs has most people believing there is no legitimate argument for marijuana, causing it to be highly looked down upon and illegal under federal law throughout the United States. But there is an exceptionally large body of research pointing to the positive impact marijuana can have on various health ailments, with recent research revealing a link between marijuana and Alzheimer’s – showing that THC, the psychoactive component of marijuana, may be beneficial for Alzheimer’s patients.

As published in the journal Molecular Pharmacology, a Skaggs Institute for Chemical Biology study shows that Δ9-tetrahydrocannabinol (THC) both “competitively inhibits the enzyme acetylcholinesterase (AChE) as well as prevents AChE-induced amyloid β-peptide (Aβ) aggregation.” In other words, cannabinoid molecules found in cannabis could halt the progression of Alzheimer’s disease.”

Read more by  : http://naturalsociety.com/marijuana-and-alzheimers-outperforms-harmful-drugs/

“A Molecular Link Between the Active Component of Marijuana and Alzheimer’s Disease Pathology” – Free full text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2562334/

Cannabidiol affects the expression of genes involved in zinc homeostasis in BV-2 microglial cells.

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“Cannabidiol (CBD) has been shown to exhibit anti-inflammatory, antioxidant and neuroprotective properties. Unlike Δ(9)-tetrahydrocannabinol (THC), CBD is devoid of psychotropic effects and has very low affinity for both cannabinoid receptors, CB(1) and CB(2). We have previously reported that CBD and THC have different effects on anti-inflammatory pathways in lipopolysaccharide-stimulated BV-2 microglial cells, in a CB(1)/CB(2) independent manner. Moreover, CBD treatment of BV-2 cells, was found to induce a robust change in the expression of genes related to oxidative stress, glutathione deprivation and inflammation. Many of these genes were shown to be controlled by Nrf2 and ATF4 transcription factors. Using the Illumina MouseRef-8 BeadChip platform, DAVID Bioinformatics and Ingenuity Pathway Analysis, we identified functional sets of genes and networks affected by CBD. A subset of genes was found to be regulated by the metal responsive element (MRE)-binding transcription factor-1 (MTF-1) and is shown to be related to zinc homeostasis. We found that CBD upregulates the expression of the mRNAs for metallothionein 2 (Mt2), N-myc-downstream regulated gene 1 and matrix metalloproteinase 23 as well as of the zinc transporters ZnT1/Slc30a1 and Zip4/Slc39a4 but downregulates the expression of the mRNA for the zinc transporter Zip10/Slc39a10 as well as for the zinc finger protein 472. Among these genes, ZnT1, Mt2 and the zinc transporters ZIPs are known to function together to control the intracellular zinc concentration. These results show that CBD, but much less so THC, affects the expression of genes involved in zinc homeostasis and suggest that the regulation of zinc levels could have an important role through which CBD may exert its antioxidant and anti-inflammatory effects.”

http://www.ncbi.nlm.nih.gov/pubmed/22178458

WIN55212-2 attenuates amyloid-beta-induced neuroinflammation in rats through activation of cannabinoid receptors and PPAR-γ pathway.

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“Cannabinoids have been shown to exert neuroprotective effects in a plethora of neurodegenerative conditions. Over the past decade, some studies demonstrate that cannabinoids can interact with nuclear peroxisome proliferator-activated receptors (PPARs). We investigated protective properties of WIN55212-2 (WIN, a non-selective cannabinoid receptor agonist) in beta-amyloid (Aβ)-induced neurodegeneration in rat hippocampus and possible involvement of PPAR-gamma (PPAR-γ).

WIN administration significantly improved memory function…

Our findings indicate that WIN exerts neuroprotective and anti-inflammatory actions against Aβ damage through both CB₁ and CB₂ receptors. Of great note, both direct and CB₁-mediated increase in PPAR-γ signaling also contributes to WIN-induced neuroprotection.”

http://www.ncbi.nlm.nih.gov/pubmed/22634229