Endo-Cannabinoids and a new development

[ShaggyFin]

(EDIT: I would like to stress the Cannabis Reuptake Inhibitors are not recreational drugs, they should be viewed more like vitamins to be used only in certain situations. PLEASE READ POST #6 WHICH WILL BE QUOTED AT THE BOTTOM OF THIS POST)

Anyone that came here looking for information on Cancer or Tumor medication, I can not help you. I have personally read anecdotal reports that state because of the mode of action of Cannabinoid Reuptake Inhibitors it helps cancer by helping the body produce more natural Cannabinoids, and others that say they with hurt cancer treatment by not allowing as many Cannabinoids to get out of your brain

But I CAN tell you why I am researching this. My 11 year old brother died from brain swelling that came after a heart attack that was caused by allergies. EndoCannabinoids help with many things that NO OTHER MEDICATION is known to do:
Reduce Brain Swelling (NO OTHER MEDICINE CAN DO THIS, and it is the leading cause of death after stroke, and is the reason my brother died)
Reduce the effect of Brain Trauma (and in some cases when administered late, it even REVERSED the effects. This is according to studies in Israel)
And Even in some cases, bring people out of a Coma

Here is a scholarly article proving that it can help protect your brain, not just cure it:
http://www.sciencemag.org/content/302/5642/84.short

If your loved one is in the hospital because of head trauma or brain swelling, this thread could save their life

The information provided about blood brain barrier boosters should help with people who have a weak heart beat


So. Your brain has natural Cannabinoids that it produces to regulate MANY things, these are called EndoCannabinoids.

Here is a link to the Wiki about EndoCannabinoids function in the brain: http://en.wikipedia.org/wiki/Endocannabinoid_system#Functions_of_the_endocannabinoid_system

I'm not sure if this is proven, but I have heard that there are studies saying that smoking THC and other Cannabinoids makes your brain feel as if it is unnecessary to produce its own Cannabinoids, since you are activating your CB1 receptor on your own.

But there is now a chem out there that is NOT a cannabinoid (I'm not sure what it is) called LY-2183240. What this chem is said to do is this:

Acts both as a potent inhibitor of the reuptake of the endocannabinoid anandamide, and as an inhibitor of fatty acid amide hydrolase (FAAH), the primary enzyme responsible for degrading anandamide. This leads to markedly elevated anandamide levels in the brain, and LY-2183240 has been shown to produce both analgesic and anxiolytic effects in animal models.

So basically,what this does is GETS YOU HIGH ON YOUR OWN CANNABINOIDS. It creates an environment where when a certain Cannabinoid enters the CB1 & CB2 region of the brain, it has to stay there until it DOES SOMETHING. It can't just go back into your blood and get pissed out.

Firstly, it "is a potent inhibitor of the reuptake of the endocannabinoid Anandamine".

Secondly, it stops your body from producing things that EAT Anandamine.

Thirdly, all of these things could slightly effects other Cannabinoids. As your brain is meant for Endocannabinoids, but when you smoke Marijuana, you add to the supply in a way that the brain isn't exactly meant to handle.

Here is what Anandamine is (a natural Cannabinoid that your brain produces: http://en.wikipedia.org/wiki/Anandamide
In 1992, in Raphael Mechoulam's lab, the first such compound was identified as arachidonoyl ethanolamine and named anandamide, a name derived from the Sanskrit word for bliss and -amide. Anandamide is derived from the essential fatty acid arachidonic acid. It has a pharmacology similar to THC, although its chemical structure is different. Anandamide binds to the central (CB1) and, to a lesser extent, peripheral (CB2) cannabinoid receptors, where it acts as a partial agonist. Anandamide is about as potent as THC at the CB1 receptor.[41] Anandamide is found in nearly all tissues in a wide range of animals.[42] Anandamide has also been found in plants, including small amounts in chocolate.

My question is, does anyone think that there is ANY way that using LY-218 could over time create a "Cannabinoid Pocket" in your brain? Kinda like how there is a sea creature that eats Sea Urchens, and through digestion extracts the poison to use in its own needles. But MJ is the Urchen, we are the Animal eating it, and LY-218 is the "step" in adaptation it would take...

What does everyone think?

Also,

Mangoes have become pretty well known over the past year or so for helping Cannabinoids cross the blood brain barrier, so that more THC goes from your blood to your brain in the first place, and faster.

Does anyone know of anything else that has effects like this?

Or effects similar to LY-2183240?

Mangoes:
https://www.google.com/search?newwi...1.0....0...1c.1.28.hp..11.25.2354.c59K2M7YJvM

http://onlinelibrary.wiley.com/doi/10.1111/j.1369-1600.2008.00105.x/full

Natural
Phytocannabinoids
Delta(9)-tetrahydrocannabinol (THC)
Delta(8)-THC
Cannabidiol
Cannabigerol
Cannabichromene
Cannabicyclol
Cannabielsoin
Cannabitriol
Miscellaneous
Endogenous
Endocannabinoids
N-arachidonoylethanolamide (anandamide; CB1-CB2 partial agonist)
2-arachidonoylglycerol (CB1 complete agonist, CB2 agonist)
2-arachidonoylglyceryl ether (noladin ether; CB1 complete agonist)
O-arachinoyl-ethanolamine (virodhamine; CB2 partial agonist, CB1 antagonist, inverse agonist)
N-arachidonyl-dopamine (CB1 agonist)
Docosatetraenoylethanolamide?
Oleamide?
N-Oleoyl dopamine?
Dihomo-linolenoylethanolamide?
Endocannabinoid-related compounds
Fatty acid derivatives
Oleamide
Oleoylethanolamide
2-oleoylglycerol
Stearoylethanolamide
Palmitoylethanolamide
2-palmitoylglycerol
Linoleoylethanolamide
2-linoleoylglycerol
Archidonoyl-aminoacid
Synthetic
Cannabinoid receptor agonists
Classical cannabinoids
Delta (8)-THC (CB1-CB2 agonist)
HU-210 (CB1-CB2 agonist)
AM411 (CB1 agonist)
O-1184 (CB1 agonist, CB2 inverse agonist)
O-1057 (complete CB1-CB2 agonist)
Non-classical cannabinoids
CP-55 940 (complete CB1-CB2 agonist)
JWH-015 (CB2 agonist)
L-768242 (CB2 agonist)
Specific CB-2 receptor agonists
AM-1241
HU-308
L-759633
L-759656
JWH-015
JWH-133
GW405833
Eicosanoids
R-(+)-WIN-55, 212-2 (complete CB1-CB2 agonist)
Aminoalkylindoles
R-(+)-methanandamide
Arachidonoyl-2¢-chloroethylamide
Arachidonylcyclopropylamide
O-1812
2-arylimino-5,6 dihydro-4H-1, 3-thiazines
Arylsulfonamides (CB1 agonists)
Cannabinoid receptor antagonists
Diarylpyrazoles
SR141716A (rimonabant; CB1 antagonist, inverse agonist)
AM251 (CB1 antagonist, inverse agonist)
SR147778 (CB1 antagonist, inverse agonist)
AM281 (CB1 antagonist, inverse agonist)
SR144528 (CB2 antagonist, inverse agonist)
Substituted benzofuranes
LY 320135 (CB1 antagonist)
Aminoalkylidoles
AM 630 (CB2 antagonist, partial CB1 agonist)
Triazole derivatives
LH-21 (CB1 antagonist)


Uptake blockers
AM 404
UCM 707
AM1172
VDM11
VDM13
OMDM1
OMDM2
LY 2183240
LY 2318912
O-2093
Inhibitors of fatty acid amide hydrolase (FAAH)
Carbamate FAAH inhibitors
OL-135
URB 597
URB 532
Bisarylimidazole derivative

WOW. I have been studying THCv for like 2 years, and it is STILL new to me. I just found out it is a Cannabinoid Reuptake inhibitor.

http://en.wikipedia.org/wiki/Endocannabinoid_reuptake_inhibitor
One example of these antagonist compounds which is found in the cannabis plant is THCV (tetrahydrocannabivarin).

If you have never heard of THCv, here is what it is.
http://en.wikipedia.org/wiki/THCV

Before I found out it was a reuptake inhibitor I knew it was a dietary supplement, as well as many times stronger than THC. But this blows my mind. It makes other Cannabinoids STRONGER basically.

Endocannabinoids play an important role in every day things, as well as important things like your ability to get pregnant. So do not take Endo-Cannabinoid reuptake inhibitors as if they are Marijuana replacements. They should be used as a tool for brain building (like a once a month boost maybe) just to tell your brain "Hey, those natural Cannabinoids are good for you" so it keeps making them.

ALSO, VERY IMPORTANT. Cannabinoid Reuptake Inhibitors are UNDERSTUDIED. So I would suggest not eating a variety of foods while on them. Ex: When you use MAOI, which is another form of inhibitor that CAN effect cannabis, but is not specifically selective of cannabinoids, is safe for humans to ingest. But because of the effects it has on your immune system you can get headaches, or even die if you eat or drink: Chocolate, Cheese or Alcohol. Simply because these things are toxic to our system, until our bodies break it down. So BE CAREFUL.

Here are the things EndoCannabinoids regulate, and these are the ONLY situations they could possibly be viewed useful in. THEY ARE NOT RECREATIONAL DRUGS.

http://en.wikipedia.org/wiki/Endocannabinoid_system#Functions_of_the_endocannabinoid_system

Memory[edit]
Mice treated with tetrahydrocannabinol (THC) show suppression of long-term potentiation in the hippocampus, a process that is essential for the formation and storage of long-term memory.[25] These results concur with anecdotal evidence suggesting that smoking Cannabis impairs short-term memory[26] Consistent with this finding, mice without the CB1 receptor show enhanced memory and long-term potentiation indicating that the endocannabinoid system may play a pivotal role in the extinction of old memories. In contrast, a recent study found that the high-dose treatment of rats with the synthetic cannabinoid HU-210 over several weeks resulted in stimulation of neural growth in the rats' hippocampus region, a part of the limbic system playing a part in the formation of declarative and spatial memories.[27] Taken together, these findings suggest that the effects of endocannabinoids on memory are dependent on what type of neurons are being targeted (excitatory vs. inhibitory) and the location of these networks in the brain.
Role in hippocampal neurogenesis[edit]
In the adult brain, the endocannabinoid system facilitates the neurogenesis of hippocampal granule cells.[27][28] In the subgranular zone of the dentate gyrus, multipotent neural progenitors (NP) give rise to daughter cells that, over the course of several weeks, mature into granule cells whose axons project to and synapse onto dendrites on the CA3 region.[29] NPs in the hippocampus have been shown to possess FAAH and express CB1 and utilize 2-AG.[28] Intriguingly, CB1 activation by endogenous or exogenous cannabinoids promote NP proliferation and differentiation; this activation is absent in CB1 knockouts and abolished in the presence of antagonist.[27][28]
Induction of synaptic depression[edit]
The inhibitory effects of cannabinoid receptor stimulation on neurotransmitter release have caused this system to be connected to various forms of depressant plasticity. A recent study conducted with the bed nucleus of the stria terminalis found that the endurance of the depressant effects was mediated by two different signaling pathways based on the type of receptor activated. 2-AG was found to act on presynaptic CB1 receptors to mediate retrograde short-term depression (STD) following activation of L-type calcium currents, while anandamide was synthesized after mGluR5 activation and triggered autocrine signalling onto postsynapic TRPV1 receptors that induced long-term depression (LTD). Similar post-synaptic receptor dependencies were found in the striatum, but here both effects relied on presynaptic CB1 receptors.[11] These findings provide the brain a direct mechanism to selectively inhibit neuronal excitability over variable time scales. By selectively internalizing different receptors, the brain may limit the production of specific endocannabinoids to favor a time scale in accordance with its needs.
Appetite[edit]
Evidence for the role of the endocannabinoid system in food-seeking behavior comes from a variety of cannabinoid studies. Emerging data suggests that THC acts via CB1 receptors in the hypothalamic nuclei to directly increase appetite.[30] It is thought that hypothalamic neurons tonically produce endocannabinoids that work to tightly regulate hunger. The amount of endocannabinoids produced is inversely correlated with the amount of leptin in the blood.[31] For example, mice without leptin not only become massively obese but express abnormally high levels of hypothalamic endocannabinoids as a compensatory mechanism.[7] Similarly, when these mice were treated with an endocannabinoid inverse agonists, such as rimonabant, food intake was reduced.[7] When the CB1 receptor is knocked-out in mice, these animals tend to be leaner and less hungry than wild-type mice. A related study examined the effect of THC on the hedonic value of food and found enhanced dopamine release in the nucleus accumbens and increased pleasure-related behavior after administration of a sucrose solution.[32] A related study found that endocannabinoids affect taste perception in taste cells [33] In taste cells, endocannabinoids were shown to selectively enhance the strength of neural signaling for sweet tastes, whereas leptin decreased the strength of this same response. While there is need for more research, these results suggest that cannabinoid activity in the hypothalamus and nucleus accumbens is related to appetitive, food-seeking behavior.[30]
Energy balance & metabolism[edit]
The endocannabinoid system has been shown to have a homeostatic role by controlling several metabolic functions, such as energy storage and nutrient transport. It acts on peripheral tissues such as adipocytes, hepatocytes, the gastrointestinal tract, the skeletal muscles and the endocrine pancreas. It has also been implied in modulating insulin sensitivity. Through all of this, the endocannabinoid system may play a role in clinical conditions, such as obesity, diabetes, and atherosclerosis, which may also give it a cardiovascular role.[34]
Stress response[edit]
While the secretion of glucocorticoids in response to stressful stimuli is an adaptive response necessary for an organism to respond appropriately to a stressor, persistent secretion may be harmful. The endocannabinoid system has been implicated in the habituation of the hypothalamic-pituitary-adrenal axis (HPA axis) to repeated exposure to restraint stress. Studies have demonstrated differential synthesis of anandamide and 2-AG during tonic stress. A decrease of anandamide was found along the axis that contributed to basal hypersecretion of corticosterone; in contrast, an increase of 2-AG was found in the amygdala after repeated stress, which was negatively correlated to magnitude of the corticosterone response. All effects were abolished by the CB1 antagonist AM251, supporting the conclusion that these effects were cannabinoid-receptor dependent.[35] These findings show that anandamide and 2-AG divergently regulate the HPA axis response to stress: while habituation of the stress-induced HPA axis via 2-AG prevents excessive secretion of glucocorticoids to non-threatening stimuli, the increase of basal corticosterone secretion resulting from decreased anandamide allows for a facilitated response of the HPA axis to novel stimuli.
Exploration, social behavior, and anxiety[edit]
Prolonged, systemic exposure to cannabinoids has often been associated with anti-social effects. To investigate this theory, a cannabinoid receptor-knockout mouse study examined the effect that these receptors play on exploratory behavior. Researchers selectively targeted glutamatergic and GABAergic cortical interneurons and studied results in open field, novel object, and sociability tests. Eliminating glutamaterigic cannabinoid receptors led to decreased object exploration, social interactions, and increased aggressive behavior. In contrast, GABAergic cannabinoid receptor-knockout mice showed increased exploration of objects, socialization, and open field movement.[36] These contrasting effects reveal the importance of the endocannabinoid system in regulating anxiety-dependent behavior. Results suggest that glutamatergic cannabinoid receptors are not only responsible for mediating aggression, but produce an anxiolytic-like function by inhibiting excessive arousal: excessive excitation produces anxiety that limited the mice from exploring both animate and inanimate objects. In contrast, GABAergic neurons appear to control an anxiogenic-like function by limiting inhibitory transmitter release. Taken together, these two sets of neurons appear to help regulate the organism's overall sense of arousal during novel situations.
Immune function[edit]
Evidence suggests that endocannabinoids may function as both neuromodulators and immunomodulators in the immune system. Here, they seem to serve an autoprotective role to ameliorate muscle spasms, inflammation, and other symptoms of multiple sclerosis and skeletal muscle spasms.[1] Functionally, the activation of cannabinoid receptors has been demonstrated to play a role in the activation of GTPases in macrophages, neutrophils, and BM cells. These receptors have also been implicated in the proper migration of B cells into the marginal zone (MZ) and the regulation of healthy IgM levels.[37] Interestingly, some disorders seem to trigger an upregulation of cannabinoid receptors selectively in cells or tissues related to symptom relief and inhibition of disease progression, such as in that rodent neuropathic pain model, where receptors are increased in the spinal cord microglia, dorsal root ganglion, and thalmic neurons.[9]
Multiple sclerosis[edit]
Historical records from ancient China and Greece suggest that preparations of Cannabis Indica were commonly prescribed to ameliorate multiple sclerosis-like symptoms such as tremors and muscle pain. Modern research has confirmed these effects in a study on diseased mice, wherein both endogenous and exogenous agonists showed ameliorating effects on tremor and spasticity. It remains to be seen whether pharmaceutical preparations such as dronabinol have the same effects in humans.[38][39] Due to increasing use of medical Cannabis and rising incidence of multiple sclerosis patients who self-medicate with the drug, there has been much interest in exploiting the endocannabinoid system in the cerebellum to provide a legal and effective relief.[26] In mouse models of multiple sclerosis, there is a profound reduction and reorganization of CB1 receptors in the cerebellum.[40] Serial sections of cerebellar tissue subjected to immunohistochemistry revealed that this aberrant expression occurred during the relapse phase but returned to normal during the remitting phase of the disease.[40] Other studies suggest that CB1 agonists promote the survival of oligodendrocytes in vitro in the absence of growth and trophic factors; in addition, these agonist have been shown to promote mRNA expression of myelin lipid protein. (Kittler et al., 2000; Mollna-Holgado et al., 2002). Taken together, these studies point to the exciting possibility that cannabinoid treatment may not only be able to attenuate the symptoms of multiple sclerosis but also improve oligodendrocyte function (reviewed in Pertwee, 2001; Mollna-Holgado et al., 2002). 2-AG stimulates proliferation of a microglial cell line by a CB2 receptor dependent mechanism, and the number of microglial cells is increased in multiple sclerosis.[41]
Female reproduction[edit]
The developing embryo expresses cannabinoid receptors early in development that are responsive to anandamide secreted in the uterus. This signaling is important in regulating the timing of embryonic implantation and uterine receptivity. In mice, it has been shown that anandamide modulates the probability of implantation to the uterine wall. For example, in humans, the likelihood of miscarriage increases if uterine anandamide levels are too high or low.[42] These results suggest that intake of exogenous cannabinoids (e.g. marijuana) can decrease the likelihood for pregnancy for women with high anandamide levels, and alternatively, it can increase the likelihood for pregnancy in women whose anandamide levels were too low.[43][44]
Autonomic nervous system[edit]
Peripheral expression of cannabinoid receptors led researchers to investigate the role of cannabinoids in the autonomic nervous system. Research found that the CB1 receptor is expressed presynaptically by motor neurons that innervate visceral organs. Cannabinoid-mediated inhibition of electric potentials results in a reduction in noradrenaline release from sympathetic nervous system nerves. Other studies have found similar effects in endocannabinoid regulation of intestinal motility, including the innervation of smooth muscles associated with the digestive, urinary, and reproductive systems.[10]
Analgesia[edit]
At the spinal cord, cannabinoids suppress noxious-stimulus-evoked responses of neurons in the dorsal horn, possibly by modulating descending noradrenaline input from the brainstem.[10] As many of these fibers are primarily GABAergic, cannabinoid stimulation in the spinal column results in disinhibition that should increase noradrenaline release and attenuation of noxious-stimuli-processing in the periphery and dorsal root ganglion. The endocannabinoid most researched in pain is palmitoylethanolamide . Palmitoylethanolamide is a fatty amine related to anandamide, but saturated and although initially it was thought that palmitoylethanolamide would bind to the CB1 and the CB2 receptor, later it was found that the most important receptors are the PPAR-alpha receptor, the TRPV receptor and the GRP55 receptor. Palmitoylethanolamide has been evaluated for its analgesic actions in a great variety of pain indications and found to be safe and effective. Basically these data are proof of concept for endocannabinoids and related fatty amines to be therapeutically useful analgesics; palmitoylethaanolamide is available under the brandnames Normast and PeaPure as neutraceuticals.
Thermoregulation[edit]
Anandamide and N-arachidonoyl dopamine (NADA) have been shown to act on temperature-sensing TRPV1 channels, which are involved in thermoregulation.[45] TRPV1 is activated by the exogenous ligand capsaicin, the active component of chili peppers, which is structurally similar to endocannabinoids. NADA activates the TRPV1 channel with an EC50 of approximately of 50 nM. The high potency makes it the putative endogenous TRPV1 agonist.[46] Anandamide has also been found to activate TRPV1 on sensory neuron terminals, and subsequently cause vasodilation.[10] TRPV1 may also be activated by methanandamide and arachidonyl-2'-chloroethylamide (ACEA).[1]
Sleep[edit]
Increased endocannabinoid signaling within the central nervous system promotes sleep-inducing effects. Intercerebroventricular administration of anandamide in rats has been shown to decrease wakefulness and increase slow-wave sleep and REM sleep.[47] Administration of anandamide into the basal forebrain of rats has also been shown to increase levels of adenosine, which plays a role in promoting sleep and suppressing arousal.[48] REM sleep deprivation in rats has been demonstrated to increase CB1 receptor expression in the central nervous system.[49] Furthermore, anandamide levels possess a circadian rhythm in the rat, with levels being higher in the light phase of the day, which is when rats are usually asleep or less active, since they are nocturnal.

 

[ShaggyFin]

If you think you can help in a discussion about Cannabinoids, Endocannabinoids and the brain, please come over here:
http://www.bluelight.ru/vb/threads/696549-Endo-Cannabinoids-and-a-new-development

Also,
What is LY-2183240?? Is it a Cannabinoid or what is it?

 

[freehugs]

Awesome info mang!
As far as I know, your body doesn't produce THC, and seeing as how THC is the compound that gets you high, I doubt that you would be getting high off your own supply, so to speak, after taking LY-2183240. God I use too many commas.

WOW. I have been studying THCv for like 2 years, and it is STILL new to me. I just found out it is a Cannabinoid Reuptake inhibitor.

http://en.wikipedia.org/wiki/Endocannabinoid_reuptake_inhibitor
One example of these antagonist compounds which is found in the cannabis plant is THCV (tetrahydrocannabivarin).

If you have never heard of THCv, here is what it is.
http://en.wikipedia.org/wiki/THCV

Before I found out it was a reuptake inhibitor I knew it was a dietary supplement, as well as many times stronger than THC. But this blows my mind. It makes other Cannabinoids STRONGER basically.

Grr if only breeders would use landrace Sativas more as their base genes, then we would have a lot more THCV. Those damn indicas and their cannabinoids profiles.

 

[ShaggyFin]

WOW (again) http://en.wikipedia.org/wiki/AM404

AM404, also known as N-arachidonoylaminophenol,[1] is an active metabolite of paracetamol (acetaminophen), responsible for all or part of its analgesic action

AM-404 is created in the body when you take Tylenol, so taking Tylenol helps Cannabinoids work... Just WOW.

Edit: Found more about AM404
Apparently it can actually make the CB1 receptor STONGER and help you learn to not be afraid of things.

http://www.nature.com/npp/journal/v30/n3/abs/1300655a.html
While the administration of the CB1 agonist WIN 55,212-2 did not appear to affect extinction, administration of AM404, an inhibitor of eCB breakdown and reuptake, led to dose-dependent enhancements in extinction. In addition to showing decreased fear 1 and 24 h after extinction training, AM404-treated animals showed decreased shock-induced reinstatement of fear. Control experiments demonstrated that the effects of AM404 could not be attributed to alterations in the expression of conditioned fear, locomotion, shock reactivity, or baseline startle, as these parameters seemed unchanged by AM404. Furthermore, coadministration of rimonabant with AM404 blocked this enhancement of extinction, suggesting that AM404 was acting to increase CB1 receptor activation during extinction training.

Awesome info mang!
As far as I know, your body doesn't produce THC, and seeing as how THC is the compound that gets you high, I doubt that you would be getting high off your own supply, so to speak, after taking LY-2183240. God I use too many commas.



Grr if only breeders would use landrace Sativas more as their base genes, then we would have a lot more THCV. Those damn indicas and their cannabinoids profiles.

Yeah, I read something saying that it re-uptake inhibitors "shouldn't" make you feel high. But Anecdotal reports on Chems R Us say that it does mildly get you high on its own, but is better in combo with actual Cannabinoids.

And I am a MMJ patient, so I will be smoking mine ON Cannabis (If I can get a re-uptake inhibitor) , lol

Also,
I personally want to go to Africa and use landrace to breed a very strong THCv strain to bring back.

http://voices.yahoo.com/the-mango-marijuana-effect-medicinal-patients-8551501.html
The mango has just been recently discovered to be a perfect ally for marijuana smokers, both recreational and medicinal, around the globe. This is because myrcene terpenes are found in mangos which are also coexistent in cannabis and marijuana. Myrcene is an organic compound most commonly used in the fragrance industry because of the sweet aroma is produces. This is why plants containing myrcene terpenes such as mango's, lemon grass, cannabis, and hops have a sweet odor. The chemical myrcene (specifically the terpenes within it) helps the psychoactive ingredients in marijuana travel faster and more efficiently through the blood brain barrier ultimately increasing, strengthening, and even lengthening the '‹Å"high' feeling.

So, theoretically... If we find the right chem or plant extract, we could basically get a complete "high"and never waste a hit of Cannabis... Just mix the right fruit alkaloid powder in your drink, and take a reuptake inhibitor and a tylenol...

Has anyone ever tried this? Because I want to

http://en.wikipedia.org/wiki/Myrcene

It is a component of the essential oil of several plants including bay, ylang-ylang, wild thyme, parsley,[3] and hops.[4][5] It is produced mainly semi-synthetically from myrcia, from which it gets its name. It is a key intermediate in the production of several fragrances.

The most common source I can find online is Lemon Grass, and of Course we know of Mangoes.

You can extract it from Lemon Grass yourself using a tutorial here: http://www.ehow.com/how_8682821_extract-myrcene-lemongrass.html

You can buy pre-extracted Lemon Grass on Amazon.

Add Lemon Grass extract to Mango juice.

Tylenol is available at the store.

Here is a list of Reuptake inhibitors:
OL-135
URB 597
URB 532
AM 404
UCM 707
AM1172
VDM11
VDM13
OMDM1
OMDM2
LY 2183240
LY 2318912
O-2093


So...

Mango Juice + Lemon Grass Extract + Tylenol + Nicacin + Any Reuptake Inhibitor... Plus a bowl of Medical Marijuana.

I'm going to try this as soon as possible.

http://voices.yahoo.com/lame-brain-niacin-deficiency-3364798.html?cat=5

Niacin is also apparently very helpful with crossing the Blood Brain Barrier, so can help you get higher when you take about 100mg 3x a day. I wouldn't suggest mixing too much niacin with any inhibitors though, as niacin is strange, and does multiple things.

Do you toss and turn before going to sleep? Are you depressed or down in the dumps? Maybe you're forgetful, anxious, get easily distracted? Do any of these ring a bell or have you forgotten the first question already? Did you just glance back to the beginning to refresh your memory?
All of these things can be symptoms of niacin deficiency.

Niacin can also put 'spark' back into your life. Red blood cells that are rich in oxygen produce a negative electric charge; this is their 'spark'. These blood cells repel each other due to the negative electric charge so on their trek through the capillaries to the brain they must go single file. Lack of oxygen can cause them to lose their charge; they all gather around each other and create a barrier from being bunched up. This barrier keeps oxygen out of the brain and leads to the symptoms mentioned above. Go ahead, scan the top to remind yourself what they were. The good news is that niacin gives red blood cells their spark back.

Niacin also helps lower cholesterol and triglycerides, two blood fats that cause clogged arteries, and also helps eliminate the slugging effect (caused by those red blood cells losing their spark and huddling up together).

Niacin is key to lowering fatigue and joint stiffness. Niacin deficiency is known as pellagra, but until symptoms reach a certain stage (dementia, skin rash and diarrhea) it's rarely diagnosed or even caught. Other symptoms of mild pellagra include; fatigue, bloating, joint problems, depression, intestinal problems and irritability.

Taking 50 -100 milligrams up to 3 or 4 times a day can reduce and in many cases eliminate these symptoms. Be sure to check your label if you decide to supplement niacin. Most niacin supplements are sold as niacinamide which has little effect on lowering blood fats. Look for a supplement that contains niacin in its purest form or try to get adequate amounts in your diet.

Niacin is one of the B complex vitamins so it's relatively easy to get them all together in certain foods. Liver is one of the best sources of the B complex vitamins but it's understandable that not many people like liver. You can also get these nutrients in other meats as well. Tuna is another good source and so are nuts and seeds. These are generally good sources because they aren't over processed which can destroy vitamin content. You can also eat more whole grains, peas, and beans to get B vitamins. One of the best sources of B complex vitamins is brewers yeast.

AM-404, which occurs when you take Tylenol can help you break your cigarette habit (if you have one)
So get higher, and help yourself stop liking cigarettes

Source: unboundmedicine.com

BACKGROUND AND PURPOSE
The fatty acid amide hydrolase inhibitor URB597 can reverse the abuse-related behavioural and neurochemical effects of nicotine in rats. Fatty acid amide hydrolase inhibitors block the degradation (and thereby magnify and prolong the actions) of the endocannabinoid anandamide (AEA), and also the non-cannabinoid fatty acid ethanolamides oleoylethanolamide (OEA) and palmitoylethanolamide (PEA). OEA and PEA are endogenous ligands for peroxisome proliferator-activated receptors alpha (PPAR-α). Since recent evidence indicates that PPAR-α can modulate nicotine reward, it is unclear whether AEA plays a role in the effects of URB597 on nicotine reward. EXPERIMENTAL APPROACH A way to selectively increase endogenous levels of AEA without altering OEA or PEA levels is to inhibit AEA uptake into cells by administering the AEA transport inhibitor N-(4-hydroxyphenyl)-arachidonamide (AM404). To clarify AEA's role in nicotine reward, we investigated the effect of AM404 on conditioned place preference (CPP), reinstatement of abolished CPP, locomotor suppression and anxiolysis in an open field, and dopamine elevations in the nucleus accumbens shell induced by nicotine in Sprague-Dawley rats. KEY

RESULTS
AM404 prevented the development of nicotine-induced CPP and impeded nicotine-induced reinstatement of the abolished CPP. Furthermore, AM404 reduced nicotine-induced increases in dopamine levels in the nucleus accumbens shell, the terminal area of the brain's mesolimbic reward system. AM404 did not alter the locomotor suppressive or anxiolytic effect of nicotine.

CONCLUSIONS AND IMPLICATIONS
These findings suggest that AEA transport inhibition can counteract the addictive effects of nicotine and that AEA transport may serve as a new target for development of medications for treatment of tobacco dependence. LINKED ARTICLES This article is part of a themed section on Cannabinoids in Biology and Medicine. To view the other articles in this section visit British Journal of Pharmacology - Volume 165, Issue 8 - Themed Section: Cannabinoids in Biology and Medicine, Part II. Guest Editors: Itai Bab and Steve Alexander - Wiley Online Library. To view Part I of Cannabinoids in Biology and Medicine visit British Journal of Pharmacology - Volume 163, Issue 7 - Cannabinoids in Biology and Medicine, Part I. Guest Editors: Itai Bab and Steve Alexander - Wiley Online Library.

Don't over due the Tylenol if you try this, just BTW:

In September 2013 an episode of This American Life entitled "Use Only as Directed"[51] surfaced alarming evidence, that "acetaminophen, the active ingredient in Tylenol ... kills the most people [of any over-the-counter drug], according to data from the federal government. Over 150 Americans die each year". This report was accompanied by two pieces of extended research in ProPublica[52][53] showing that the "FDA has long been aware of studies showing the risks of acetaminophen. So has the maker of Tylenol, McNeil Consumer Healthcare, a division of Johnson & Johnson" and "McNeil, the maker of Tylenol, ... has repeatedly opposed safety warnings, dosage restrictions and other measures meant to safeguard users of the drug." This is especially concerning given acetaminophen's narrow safety margin ("the dose that helps is close to the dose that can cause serious harm, according to the FDA").

URB-597:
In pre-clinical laboratory tests researchers found URB597 increased the production of endocannabinoids resulting in measurable antidepressant and analgesic effects.

So this one not only helps keep the EndoCannabinoids there, it helps PRODUCE them

 

[Toz]

If you think you can help in a discussion about Cannabinoids, Endocannabinoids and the brain, please come over here:
http://www.bluelight.ru/vb/threads/696549-Endo-Cannabinoids-and-a-new-development

Also,
What is LY-2183240?? Is it a Cannabinoid or what is it?

No it's acetaminophen v2.0 from the way I see it, lol.

 

[Seyer]

Seriously, edit your posts when youre adding to them.

 

[Toz]

LY-2183240 works as an inhibitor of FAAH. The most similiar pharmaceutical drug used to this is paracetamol/acetaminophen. My guess is that this will get you just as high as tylenol does. I do not believe you can get "high" on your endogenous cannabinoids. They regulate some bodily functions, but while elevating them might provide some pain relief, it will not get you high. Kind of in the same way taking SSRIs will not get you high either.

 

[ShaggyFin]

Endocannabinoids play an important role in every day things, as well as important things like your ability to get pregnant. So do not take Endo-Cannabinoid reuptake inhibitors as if they are Marijuana replacements. They should be used as a tool for brain building (like a once a month boost maybe) just to tell your brain "Hey, those natural Cannabinoids are good for you" so it keeps making them.

ALSO, VERY IMPORTANT. Cannabinoid Reuptake Inhibitors are UNDERSTUDIED. So I would suggest not eating a variety of foods while on them. Ex: When you use MAOI, which is another form of inhibitor that CAN effect cannabis, but is not specifically selective of cannabinoids, is safe for humans to ingest. But because of the effects it has on your immune system you can get headaches, or even die if you eat or drink: Chocolate, Cheese or Alcohol. Simply because these things are toxic to our system, until our bodies break it down. So BE CAREFUL.

Here are the things EndoCannabinoids regulate, and these are the ONLY situations they could possibly be viewed useful in. THEY ARE NOT RECREATIONAL DRUGS.

http://en.wikipedia.org/wiki/Endocannabinoid_system#Functions_of_the_endocannabinoid_system

Memory[edit]
Mice treated with tetrahydrocannabinol (THC) show suppression of long-term potentiation in the hippocampus, a process that is essential for the formation and storage of long-term memory.[25] These results concur with anecdotal evidence suggesting that smoking Cannabis impairs short-term memory[26] Consistent with this finding, mice without the CB1 receptor show enhanced memory and long-term potentiation indicating that the endocannabinoid system may play a pivotal role in the extinction of old memories. In contrast, a recent study found that the high-dose treatment of rats with the synthetic cannabinoid HU-210 over several weeks resulted in stimulation of neural growth in the rats' hippocampus region, a part of the limbic system playing a part in the formation of declarative and spatial memories.[27] Taken together, these findings suggest that the effects of endocannabinoids on memory are dependent on what type of neurons are being targeted (excitatory vs. inhibitory) and the location of these networks in the brain.
Role in hippocampal neurogenesis[edit]
In the adult brain, the endocannabinoid system facilitates the neurogenesis of hippocampal granule cells.[27][28] In the subgranular zone of the dentate gyrus, multipotent neural progenitors (NP) give rise to daughter cells that, over the course of several weeks, mature into granule cells whose axons project to and synapse onto dendrites on the CA3 region.[29] NPs in the hippocampus have been shown to possess FAAH and express CB1 and utilize 2-AG.[28] Intriguingly, CB1 activation by endogenous or exogenous cannabinoids promote NP proliferation and differentiation; this activation is absent in CB1 knockouts and abolished in the presence of antagonist.[27][28]
Induction of synaptic depression[edit]
The inhibitory effects of cannabinoid receptor stimulation on neurotransmitter release have caused this system to be connected to various forms of depressant plasticity. A recent study conducted with the bed nucleus of the stria terminalis found that the endurance of the depressant effects was mediated by two different signaling pathways based on the type of receptor activated. 2-AG was found to act on presynaptic CB1 receptors to mediate retrograde short-term depression (STD) following activation of L-type calcium currents, while anandamide was synthesized after mGluR5 activation and triggered autocrine signalling onto postsynapic TRPV1 receptors that induced long-term depression (LTD). Similar post-synaptic receptor dependencies were found in the striatum, but here both effects relied on presynaptic CB1 receptors.[11] These findings provide the brain a direct mechanism to selectively inhibit neuronal excitability over variable time scales. By selectively internalizing different receptors, the brain may limit the production of specific endocannabinoids to favor a time scale in accordance with its needs.
Appetite[edit]
Evidence for the role of the endocannabinoid system in food-seeking behavior comes from a variety of cannabinoid studies. Emerging data suggests that THC acts via CB1 receptors in the hypothalamic nuclei to directly increase appetite.[30] It is thought that hypothalamic neurons tonically produce endocannabinoids that work to tightly regulate hunger. The amount of endocannabinoids produced is inversely correlated with the amount of leptin in the blood.[31] For example, mice without leptin not only become massively obese but express abnormally high levels of hypothalamic endocannabinoids as a compensatory mechanism.[7] Similarly, when these mice were treated with an endocannabinoid inverse agonists, such as rimonabant, food intake was reduced.[7] When the CB1 receptor is knocked-out in mice, these animals tend to be leaner and less hungry than wild-type mice. A related study examined the effect of THC on the hedonic value of food and found enhanced dopamine release in the nucleus accumbens and increased pleasure-related behavior after administration of a sucrose solution.[32] A related study found that endocannabinoids affect taste perception in taste cells [33] In taste cells, endocannabinoids were shown to selectively enhance the strength of neural signaling for sweet tastes, whereas leptin decreased the strength of this same response. While there is need for more research, these results suggest that cannabinoid activity in the hypothalamus and nucleus accumbens is related to appetitive, food-seeking behavior.[30]
Energy balance & metabolism[edit]
The endocannabinoid system has been shown to have a homeostatic role by controlling several metabolic functions, such as energy storage and nutrient transport. It acts on peripheral tissues such as adipocytes, hepatocytes, the gastrointestinal tract, the skeletal muscles and the endocrine pancreas. It has also been implied in modulating insulin sensitivity. Through all of this, the endocannabinoid system may play a role in clinical conditions, such as obesity, diabetes, and atherosclerosis, which may also give it a cardiovascular role.[34]
Stress response[edit]
While the secretion of glucocorticoids in response to stressful stimuli is an adaptive response necessary for an organism to respond appropriately to a stressor, persistent secretion may be harmful. The endocannabinoid system has been implicated in the habituation of the hypothalamic-pituitary-adrenal axis (HPA axis) to repeated exposure to restraint stress. Studies have demonstrated differential synthesis of anandamide and 2-AG during tonic stress. A decrease of anandamide was found along the axis that contributed to basal hypersecretion of corticosterone; in contrast, an increase of 2-AG was found in the amygdala after repeated stress, which was negatively correlated to magnitude of the corticosterone response. All effects were abolished by the CB1 antagonist AM251, supporting the conclusion that these effects were cannabinoid-receptor dependent.[35] These findings show that anandamide and 2-AG divergently regulate the HPA axis response to stress: while habituation of the stress-induced HPA axis via 2-AG prevents excessive secretion of glucocorticoids to non-threatening stimuli, the increase of basal corticosterone secretion resulting from decreased anandamide allows for a facilitated response of the HPA axis to novel stimuli.
Exploration, social behavior, and anxiety[edit]
Prolonged, systemic exposure to cannabinoids has often been associated with anti-social effects. To investigate this theory, a cannabinoid receptor-knockout mouse study examined the effect that these receptors play on exploratory behavior. Researchers selectively targeted glutamatergic and GABAergic cortical interneurons and studied results in open field, novel object, and sociability tests. Eliminating glutamaterigic cannabinoid receptors led to decreased object exploration, social interactions, and increased aggressive behavior. In contrast, GABAergic cannabinoid receptor-knockout mice showed increased exploration of objects, socialization, and open field movement.[36] These contrasting effects reveal the importance of the endocannabinoid system in regulating anxiety-dependent behavior. Results suggest that glutamatergic cannabinoid receptors are not only responsible for mediating aggression, but produce an anxiolytic-like function by inhibiting excessive arousal: excessive excitation produces anxiety that limited the mice from exploring both animate and inanimate objects. In contrast, GABAergic neurons appear to control an anxiogenic-like function by limiting inhibitory transmitter release. Taken together, these two sets of neurons appear to help regulate the organism's overall sense of arousal during novel situations.
Immune function[edit]
Evidence suggests that endocannabinoids may function as both neuromodulators and immunomodulators in the immune system. Here, they seem to serve an autoprotective role to ameliorate muscle spasms, inflammation, and other symptoms of multiple sclerosis and skeletal muscle spasms.[1] Functionally, the activation of cannabinoid receptors has been demonstrated to play a role in the activation of GTPases in macrophages, neutrophils, and BM cells. These receptors have also been implicated in the proper migration of B cells into the marginal zone (MZ) and the regulation of healthy IgM levels.[37] Interestingly, some disorders seem to trigger an upregulation of cannabinoid receptors selectively in cells or tissues related to symptom relief and inhibition of disease progression, such as in that rodent neuropathic pain model, where receptors are increased in the spinal cord microglia, dorsal root ganglion, and thalmic neurons.[9]
Multiple sclerosis[edit]
Historical records from ancient China and Greece suggest that preparations of Cannabis Indica were commonly prescribed to ameliorate multiple sclerosis-like symptoms such as tremors and muscle pain. Modern research has confirmed these effects in a study on diseased mice, wherein both endogenous and exogenous agonists showed ameliorating effects on tremor and spasticity. It remains to be seen whether pharmaceutical preparations such as dronabinol have the same effects in humans.[38][39] Due to increasing use of medical Cannabis and rising incidence of multiple sclerosis patients who self-medicate with the drug, there has been much interest in exploiting the endocannabinoid system in the cerebellum to provide a legal and effective relief.[26] In mouse models of multiple sclerosis, there is a profound reduction and reorganization of CB1 receptors in the cerebellum.[40] Serial sections of cerebellar tissue subjected to immunohistochemistry revealed that this aberrant expression occurred during the relapse phase but returned to normal during the remitting phase of the disease.[40] Other studies suggest that CB1 agonists promote the survival of oligodendrocytes in vitro in the absence of growth and trophic factors; in addition, these agonist have been shown to promote mRNA expression of myelin lipid protein. (Kittler et al., 2000; Mollna-Holgado et al., 2002). Taken together, these studies point to the exciting possibility that cannabinoid treatment may not only be able to attenuate the symptoms of multiple sclerosis but also improve oligodendrocyte function (reviewed in Pertwee, 2001; Mollna-Holgado et al., 2002). 2-AG stimulates proliferation of a microglial cell line by a CB2 receptor dependent mechanism, and the number of microglial cells is increased in multiple sclerosis.[41]
Female reproduction[edit]
The developing embryo expresses cannabinoid receptors early in development that are responsive to anandamide secreted in the uterus. This signaling is important in regulating the timing of embryonic implantation and uterine receptivity. In mice, it has been shown that anandamide modulates the probability of implantation to the uterine wall. For example, in humans, the likelihood of miscarriage increases if uterine anandamide levels are too high or low.[42] These results suggest that intake of exogenous cannabinoids (e.g. marijuana) can decrease the likelihood for pregnancy for women with high anandamide levels, and alternatively, it can increase the likelihood for pregnancy in women whose anandamide levels were too low.[43][44]
Autonomic nervous system[edit]
Peripheral expression of cannabinoid receptors led researchers to investigate the role of cannabinoids in the autonomic nervous system. Research found that the CB1 receptor is expressed presynaptically by motor neurons that innervate visceral organs. Cannabinoid-mediated inhibition of electric potentials results in a reduction in noradrenaline release from sympathetic nervous system nerves. Other studies have found similar effects in endocannabinoid regulation of intestinal motility, including the innervation of smooth muscles associated with the digestive, urinary, and reproductive systems.[10]
Analgesia[edit]
At the spinal cord, cannabinoids suppress noxious-stimulus-evoked responses of neurons in the dorsal horn, possibly by modulating descending noradrenaline input from the brainstem.[10] As many of these fibers are primarily GABAergic, cannabinoid stimulation in the spinal column results in disinhibition that should increase noradrenaline release and attenuation of noxious-stimuli-processing in the periphery and dorsal root ganglion. The endocannabinoid most researched in pain is palmitoylethanolamide . Palmitoylethanolamide is a fatty amine related to anandamide, but saturated and although initially it was thought that palmitoylethanolamide would bind to the CB1 and the CB2 receptor, later it was found that the most important receptors are the PPAR-alpha receptor, the TRPV receptor and the GRP55 receptor. Palmitoylethanolamide has been evaluated for its analgesic actions in a great variety of pain indications and found to be safe and effective. Basically these data are proof of concept for endocannabinoids and related fatty amines to be therapeutically useful analgesics; palmitoylethaanolamide is available under the brandnames Normast and PeaPure as neutraceuticals.
Thermoregulation[edit]
Anandamide and N-arachidonoyl dopamine (NADA) have been shown to act on temperature-sensing TRPV1 channels, which are involved in thermoregulation.[45] TRPV1 is activated by the exogenous ligand capsaicin, the active component of chili peppers, which is structurally similar to endocannabinoids. NADA activates the TRPV1 channel with an EC50 of approximately of 50 nM. The high potency makes it the putative endogenous TRPV1 agonist.[46] Anandamide has also been found to activate TRPV1 on sensory neuron terminals, and subsequently cause vasodilation.[10] TRPV1 may also be activated by methanandamide and arachidonyl-2'-chloroethylamide (ACEA).[1]
Sleep[edit]
Increased endocannabinoid signaling within the central nervous system promotes sleep-inducing effects. Intercerebroventricular administration of anandamide in rats has been shown to decrease wakefulness and increase slow-wave sleep and REM sleep.[47] Administration of anandamide into the basal forebrain of rats has also been shown to increase levels of adenosine, which plays a role in promoting sleep and suppressing arousal.[48] REM sleep deprivation in rats has been demonstrated to increase CB1 receptor expression in the central nervous system.[49] Furthermore, anandamide levels possess a circadian rhythm in the rat, with levels being higher in the light phase of the day, which is when rats are usually asleep or less active, since they are nocturnal.

LY-2183240 works as an inhibitor of FAAH. The most similiar pharmaceutical drug used to this is paracetamol/acetaminophen. My guess is that this will get you just as high as tylenol does. I do not believe you can get "high" on your endogenous cannabinoids. They regulate some bodily functions, but while elevating them might provide some pain relief, it will not get you high. Kind of in the same way taking SSRIs will not get you high either.

According to all the anecdotal reports I can find, it gets you high in the sense of general optimism. Due to: Lack of headaches, Regulated Sleep, etc.

And I am not suggesting that anyone use it by itself to get them high.

ALSO

Read more: http://healthland.time.com/2012/10/29/how-cannabinoids-may-slow-brain-aging

The latest review, published in Philosophical Transactions of the Royal Society B, suggests that activating the brain’s cannabinoid system may trigger a sort of anti-oxidant cleanse, removing damaged cells and improving the efficiency of the mitochrondria, the energy source that powers cells, ultimately leading to a more robustly functioning brain.



Activation of cannabinoid receptors can also reduce brain inflammation in several different ways, which may in turn suppress some of the disease processes responsible for degenerative brain diseases such as Alzheimer’s.



Other studies covered in the review showed that mice bred to lack the cannabinoid receptors have better memories early in life but have more rapid cognitive decline as they age, including inflammation in the hippocampus, a key region for memory. “This finding suggests that, at some point during aging, cannabinoid activity helps maintain normal cognitive functions in mice,” says Daniele Piomelli, professor of neurobiology, anatomy and biological chemistry at the University of California – Irvine, who was not associated with the study.


WHY IS THERE NOT A THREAD ABOUT PEOPLE WHO HAVE TAKEN THCV????

If anyone would like to grow a Marijuana Strain with a BUILT IN Cannabinoid Reuptake Inhibitor, I suggest THIS (But it is also a CB1 receptor antagonist, so it semi-blocks the CB1 receptor, and focuses on the CB2 receptor, which is rare:

Malawi Gold, This is the strain I want to grow next.

It contains VERY high amounts of THCv. If you are looking for a strain that is more popular that has THCv, here are some more:

Jack the Ripper
Blackberry
Bakhye Shamonie
Pineapple Purps
Mataro blue
Durban Poison


THCV is:

anti-epileptic (eases seizures)
Dietary
It has also been reported to stimulate bone growth
effective not only at reducing symptoms of Parkinson's disease, but also for slowing the progression of the disease

Authors reported that although THCV administration did not significantly affect food intake or body weight gain in any of the models, it did produce several metabolically beneficial effects, including reduced glucose intolerance, improved glucose tolerance, improved liver triglyceride levels, and increased insulin sensitivity.

Researchers concluded: “Based on these data, it can be suggested that THCV may be useful for the treatment of the metabolic syndrome and/or type 2 diabetes (adult onset diabetes), either alone or in combination with existing treatments.

THCV was also found to increase the animals’ sensitivity to insulin while also protecting the cells that produce insulin, allowing them to work better and for longer.

Tetrahydrocannabivarin (THCV) is prevalent in certain South African and Southeast Asian strains of Cannabis. It is an antagonist of THC at CB1 receptors and attenuates the psychoactive effects of THC.

 

[freehugs]

WHY IS THERE NOT A THREAD ABOUT PEOPLE WHO HAVE TAKEN THCV????

If anyone would like to grow a Marijuana Strain with a BUILT IN Cannabinoid Reuptake Inhibitor, I suggest THIS:

http://www.aceseeds.org/malawifemeng.php This is the strain I want to grow next.

It contains VERY high amounts of THCv. If you are looking for a strain that is more popular that has THCv, here are some more:

Jack the Ripper
Blackberry
Bakhye Shamonie
Pineapple Purps
Mataro blue
Durban Poison


THCV is:

anti-epileptic (eases seizures)
Dietary
It has also been reported to stimulate bone growth
effective not only at reducing symptoms of Parkinson's disease, but also for slowing the progression of the disease

Authors reported that although THCV administration did not significantly affect food intake or body weight gain in any of the models, it did produce several metabolically beneficial effects, including reduced glucose intolerance, improved glucose tolerance, improved liver triglyceride levels, and increased insulin sensitivity.

Researchers concluded: “Based on these data, it can be suggested that THCV may be useful for the treatment of the metabolic syndrome and/or type 2 diabetes (adult onset diabetes), either alone or in combination with existing treatments.

THCV was also found to increase the animals’ sensitivity to insulin while also protecting the cells that produce insulin, allowing them to work better and for longer.

Tetrahydrocannabivarin (THCV) is prevalent in certain South African and Southeast Asian strains of Cannabis. It is an antagonist of THC at CB1 receptors and attenuates the psychoactive effects of THC.

I think the strain with the highest THCv content is the landrace Malawi Gold

 

[ShaggyFin]

I think the strain with the highest THCv content is the landrace Malawi Gold

The link I added was to a Malawi land race

Update:

I ordered some Tylenol, Niacin & Lemon Grass.

I am going to start a Niacin regimen, like 250mg a day to promote blood flow, which will help THC and other things in my blood cross to my brain.

Then I will take Tylenol 1+ times a week, so that my brain has a little AM-404 in it frequently, so that it knows to keep its natural Cannabinoids, as well as the ones I add to it.

Then I will buy some Mangoes and a Juicer, so that I can drink a bowl of Mango juice in the morning, to help Cannabinoids cross my blood brain barrier.

And I will make a lemon grass extract, and add a little to my mango juice every morning. Which should boost the effects of the Mangoes.

And I am a medical MJ patient, so I can compare and contrast my highs.

Update 2:

Thinking about getting something like LY-218, here is some research
http://www.ncbi.nlm.nih.gov/pubmed/20838777 This says that mice were being given 30mg/Kg so I'm thinking this is on the weaker side in terms of potency and compared to synthetic cannabinoids. Wiki answers says that it can be dissolved in Ethanol.

As near as makes no difference inactive so far, smoked a decent joint's worth of blend and there is definitely *something* it's really not pronounced, same slightly sweaty face you get from smoking, chest feels tight and I feel sleepy and everything has a funny look about it, but not stoned, it's very slight. I did get a rough bout of nausea that subsided as quickly as it came on, as well.

I'll give it another shot later, possibly work as a potentiator for other 'noids like I've read.

NOTE: I have a severe, synth 'noid tolerance, I've smoked grams of the pure powder in less than a day. Take heed of knothing's post below and watch out, there could be a number of reasons why this is inactive to me, and mixing them is incredibly stupid. Tread lightly, 'noids are active at MILLIGRAM dosage levels, I'll continue to post up my findings.

After having smoked a fair bit of this now, I've come to the conclusion that while on it's own, it's pretty weak, after having smoked numerous joints and a couple waterfalls, I'm barely more than slightly buzzed, definitely feeling it, but it's nowhere near as potent as other varieties of noid.

That being said, I decided to see if it would work as a potentiator, so I scraped up some 5F blend from my tray, on it's own, it wouldn't have been enough to produce any results, the smallest amount, just enough for a thin layer, then a decent chunk of LY, less than I've been smoking on it's own. The LY definitely potentiated the 5F, it created a very smooth, natural type high, which was actually pretty strong, from basically nothing, as both would've produced close to no effects on their own.

Overall verdict is, I can see this being used in blends to give it a bit of extra oomf, on it's own, so far it's pretty lacklustre, I do feel slightly stoned, but I'm still at a certain level of sober where it just feels like an annoyance, I've went awkward the way I do on other noids, and trying to focus on things is slightly harder, but apart from some other slight, possibly placebo effects I feel nothing.

the problem I have with this one is authenticity,

a legitimate medical supplier like cayman charges $46 for 10mg while the supplier I got this from in China charged $20 for 1000mg (1G),

a bit fishy to say the least. chin

I had a really difficult time trying to duplicate the lab results other published studies achieved.

 

[ShaggyFin]

No it's acetaminophen v2.0 from the way I see it, lol.

What dose of Acetaminophen do you have to take to get a good dose of AM404?

And what is an active dose of LY-2183240????

 

[freehugs]

The link I added was to a Malawi land race

Update:

I ordered some Tylenol, Niacin & Lemon Grass.

I am going to start a Niacin regimen, like 250mg a day to promote blood flow, which will help THC and other things in my blood cross to my brain.

Then I will take Tylenol 1+ times a week, so that my brain has a little AM-404 in it frequently, so that it knows to keep its natural Cannabinoids, as well as the ones I add to it.

Then I will buy some Mangoes and a Juicer, so that I can drink a bowl of Mango juice in the morning, to help Cannabinoids cross my blood brain barrier.

And I will make a lemon grass extract, and add a little to my mango juice every morning. Which should boost the effects of the Mangoes.

And I am a medical MJ patient, so I can compare and contrast my highs.

Thats what I get for not clicking the link haha. I'm going to have to remove it though since it is sourcing, there are definitely other sites with info on Malawi Gold that don't sell the seeds as well.

I'm excited to see how your experimenting goes though! Have you taken niacin before? If not prepare for your skin to get very flushed.

 

[omnipresenthuman]

To quote Jesse Pinkman, 'Yeah, Science!'

 

[ShaggyFin]

Thats what I get for not clicking the link haha. I'm going to have to remove it though since it is sourcing, there are definitely other sites with info on Malawi Gold that don't sell the seeds as well.

I'm excited to see how your experimenting goes though! Have you taken niacin before? If not prepare for your skin to get very flushed.

Oh, sorry. I didn't know vendor rules applied to seed, in my mind that was different. I won't post any more though.

I have taken Niacin before, trying to detox, I took way too much and it was like a sun burn all over my body that itched.

I took 250 mg of Niacin today, and plan on taking that for about a week before I try a Tylenol.

To quote Jesse Pinkman, 'Yeah, Science!'

I still have like 2-3 seasons of this to watch (no idea), and now that it's over, I'm glad I saved so much to watch.

 

[Arnold]

The endocannabinoid most researched in pain is palmitoylethanolamide . Palmitoylethanolamide is a fatty amine related to anandamide, but saturated and although initially it was thought that palmitoylethanolamide would bind to the CB1 and the CB2 receptor, later it was found that the most important receptors are the PPAR-alpha receptor, the TRPV receptor and the GRP55 receptor. Palmitoylethanolamide has been evaluated for its analgesic actions in a great variety of pain indications and found to be safe and effective. Basically these data are proof of concept for endocannabinoids and related fatty amines to be therapeutically useful analgesics; palmitoylethaanolamide is available under the brandnames Normast and PeaPure as neutraceuticals.

Has anyone ever used PEA, Palmitoylethanolamide , for pain management or depression?
Any good or bad or just a waste of time due to minimal effects?

It's a missing link for a few people imo.

 

[purplehaze147]

Wonder if a cyclodextrin could capture anandamide. The cyclodextrin family is glucose units in the form of a ring (most basic definition). They make molecules that are water insoluble, such as steroids, soluble, while also increasing bioavailability and protecting the molecule from enzymes. This may work, I'd bet. Butanol (i have to think on that, probably a better solvent) edit isoamyl alcohol final answer (It can be a banana perfume worst case and all the pigs in town will smell your ready and will be after dat ass) 99% purity solution and 1:1 molar ratio w/ slight excess cyclodextrin, then wash off with water and collect aqueous part. A larger cyclodextrin like gamma would be better than alpha or beta, maybe another odd one would be best.

 

[Twisted_Chemist]

Paracetamol/acetaminophen is made from Aniline or based of it. All drugs that are part of that family have been known to be very toxic. If this drug is part of that family I would very cautious on using it. Paracetamol/acetaminophen is the number one drug people OD on in the world.

 

[A9254DF]

I always wondered if there are any cannabinoids that work to clear the receptors and therefore clear your tollerence? Sounds like an odd idea but really I thought of it by being on opiate replacement therapy where there are obviously drugs like naloxone or going in the other direction is naltrexone.
Is there anything that works in a similar way but on the cannabinoid receptors?
It would be so useful for me to be able to just kick the receptors clean to lower tolerance to cannabinoids so that my prescribed quantity works like it did when I was like 14 years old.
No, im not just trying to get more high coz it feels nice, I am trying to make the very expensive medication I buy in this country work more efficiently and therefore need to buy less of it.