Juicing Cannabis

kesaber

Well-Known Member
I've seen a bunch of clips on the juicing of raw cannabis and it's benefits and I was wondering if anyone knew the answers to a few questions.

Is there a difference between juicing fan leaves and juicing bud? Does it matter what stage the leaves are in? Early veg vs Veg vs flower? I was thinking of keeping a mother plant under an LED light that I regularly defoliated so I can juice it. Is there a stage where I would more benefit or am I missing out on any nutrients by doing it this way?
 

qwizoking

Well-Known Member
Well theres between those 3
Cannabis leaves do not contain but trace levels of cannabinoids. So juicing them realistically wouldnt provide any medical benefits a bottle of chlorophyll would.
Which can upset your stomach

Leaves in flower that have frost "ripen" before the buds do, and you will have a higher ratio of "activated" or decarbed cannabinoids. To hit receptors, cross into the brain and feel most of the medical effects it must be decarbed.

Early flowering leaves with frost will produce very minimal effects as it cant hit receptors but can still modulate the immue system and to a lesser extent reduce inflammation.

In my medical opinion, to get the relief you desire, you need decarbed herb.
 

kesaber

Well-Known Member
Well theres between those 3
Cannabis leaves do not contain but trace levels of cannabinoids. So juicing them realistically wouldnt provide any medical benefits a bottle of chlorophyll would.
Which can upset your stomach

Leaves in flower that have frost "ripen" before the buds do, and you will have a higher ratio of "activated" or decarbed cannabinoids. To hit receptors, cross into the brain and feel most of the medical effects it must be decarbed.

Early flowering leaves with frost will produce very minimal effects as it cant hit receptors but can still modulate the immue system and to a lesser extent reduce inflammation.

In my medical opinion, to get the relief you desire, you need decarbed herb.
Are you a medical expert?

I have been reading/watching some of Dr. Courtney's work and he seems to believe the THC in it's acidic form may provide more benefit than after it is de-carbed. I am obviously no expert on the matter, in fact far from it, but I can say in my experience of juicing a large amount of vegetative leaves I felt an immediate increase in my level of happiness and my energy level was through the roof. I felt as if I had just drank four cups of coffee. I was under the impression that these were medicinal affects. I am not looking to get high. What are your thoughts on that?
 

qwizoking

Well-Known Member
Thc and cbd both get you high while providing benefits.
To name a few of the most popular, gabba, opiate, 5ht, cb1 cb2 "cb3" and "cb4" receptors..

These receptors that get you high are the same ones that provide relief. Hit gabba like xanax and alcohol do, you have reduced anxiety yes and also impaired short term memory and well you feel good. Your natural cannabinoid system regulates hunger, reward, etc. You get the idea..obviously this is a very compacted explanation

its impossible to hit receptors and get certain effects and not others, to reduce pain but not feel sedated..or improve apetite without the effects that also come from cb1 being hit

If not decarbed the cannabinoids just go right down the toilet, literally. There are a few receptor sites that can still be hit. But not really, or to the extent it could. Even if there were huge "site densities" the carboxyl group almost flips the compound from non polar to polar, its quickly excreted and has a harder time binding to receptors. This is called a compounds distribution coefficient and alters how the drug is picked up and processed in the body. Changing the structure of the molecule changes how well it binds to receptors.. realistically the brain has to get involved . Thats not to say though that certain effects cant be felt

I dont know if i like the term expert, makes me feel weird.. but yes i am. Have worked in "drug design" and creating delivery systems, have had the opportunity to work on some new upcoming synthetic cannabinoid products. A fancy pharmacist i am
 

kesaber

Well-Known Member
That all sounds great, but I was hoping I could take advantage of your knowledge to answer specific questions I had.

1) How do you feel about Dr. Courtney saying there is more medical benefit in the THC acid then after it has been de-carbed?

2) Why did I feel such fast and intense relief after juicing the fan leaves from mid-late veg. I felt happier, almost euphoric, and I had a ton of energy. I don't know if it lasted longer than smoking a joint, but it was definitely more intense for longer and I don't recall have any kind of abdominal pain during that time.

Thanks for your time
 

qwizoking

Well-Known Member
Well hope i helped, i tried to keep it short and sweet while but combined a couple older posts

1) How do you feel about Dr. Courtney saying there is more medical benefit in the THC acid then after it has been de-carbed?

Well not to attack the other person. But in my opinion, thats not the case. with certain conditions it could provide a greater degree of relief relative to side effects. But thats far from saying thca has more medical benefit. Overall alot fewer ailments could be treated.


2) Why did I feel such fast and intense relief after juicing the fan leaves from mid-late veg. I felt happier, almost euphoric, and I had a ton of energy. I don't know if it lasted longer than smoking a joint, but it was definitely more intense for longer and I don't recall have any kind of abdominal pain during that time.

Well..a portion could be psychological, dont underestimate your mind..also during this process some could have been decarbed, wether chemically or through heat..

But for a compound to have "drug likeness" it must have a polar surface area (psa) under 60 angstroms in order to cross the blood brain barrier and reach receptors......the higher the number the more polar it is. Your blood being polar the barrier being fatty... it must be able to travel in blood and non polar enough to cross the barrier and get back out, this all has huge implications in pharmacology
.. in the polar acid form(thca) has a psa of 66...meaning you will feel certain effects from cbd as the cb2 receptors are located throughout the body and don't require a reduction in polarity..no bb barrier to cross. However most medical use results from activation of one of the cb receptors in the brain, specifically with cbd the "cb3" "cb4" opiate activity etc and indirect pathways being medically limiting...

a psa under 60 is optimum but some of the compound will cross up to a psa about 70. thca at 66 will cross but not efficiently and taking higher doses..this would be a huge waste of product however..especially since it takes relatively high doses to get high anyway, compare to most pharmaceuticals having a therapeutic window 1-20mg..... after decarbing it drops to a psa of 30 easilly passing through and staying in our body a good while, there are side effects of this bioaccumulation in heavy users, but thats another subject.
cbda is more polar than thc with a psa of 77 and cbd about 40..will not cross if not decarbed

Cbd is more polar than the other cannabinoids. Cbc cbg thc and propyls'- thcv etc all have near identical psa's


So if you ingested enough you would not recieve the sedative properties of cbd but possibly felt the more uplifting thc and it heloed with abdominal pain.
Back to psychological, consider
thc has a logp of about 7
In practice optimum colonic absorption is 1.32, intestinal is 1.35, oral 1.8, Cns 2, percutaneous at 2.6 and sublingual 5.5. Neither form of thc is efficiently absorbed without carriers etc. The lower the number the higher the polarity. Youll see that loosely, the more non polar (as in decarbed thc) the faster it is absorbed
 

qwizoking

Well-Known Member
This is incredibly long..if you feel like reading, more power to you


Intestinal Motility and Irritable Bowel Syndrome: The CB1 cannabinoid receptor has specifically been found to inhibit motility of the intestine in a variety of laboratory and farm animals. The effect is specific, indicating that endogenous cannabinoids to be responsible for regulating smooth muscle tone in the intesting, and therateof peristalsis.

Rosell et al[iv] first demonstrated that cannabinoids inhibit contractions of the small intestine in the rat. Pertwee et al[v] established the presence of cannabinoid (CB1) receptors within the guinea-pig intestine, Kazuhisa et al[vi] established the presence of enzymes which break down anandamide (the endogenous cannabinoid CB1-agonist) within the small intestine, and in rats Katayama et al[vii] also found "a high content of anandamide hydrolase in small intestine". The smooth muscle-relaxant properties of cannabinoids are so well established that preparations of guinea-pig intestine are routinely used as an in vitro screening tool to testthe potencyand function of novel cannabinoids[viii][ix].

Shook & Burks[x] found that THC reduced the frequency of intestinal contractions, and reduced the flow of food in the small intestine, without altering

cannabidiol) exert an inhibitory effect on GI transit and motility in rats". Cadas et al[xi] reported that a gut enzyme (vasoactive intestinal peptide) may regulate the precursor chemical to anandamide (which activates cannabinoid CB1 receptors) and N-palmitoylethanolamine (which activates a CB2-like receptor subtype), suggesting that endogenous cannabinoids may play a role in regulating theactivityofthe gut.

Studying guinea-pigs & rats, Coutts et al[xii] report "Activation of cannabinoid CB(1) receptors inhibits gastrointestinal motility, propulsion, and transit, whereas selective antagonism of these receptors has the opposite effects, suggesting the presence of endocannabinoid tone." Lopez-Redondo

transmission occurred by reversible activation of both presynaptic and postsynaptic CB1

synaptic transmission can also be reversibly depressed by cannabinoids." In mice, Pinto et al[xiv] found endogenous and exogenous CB1-receptor

"endocannabinoids acting on myenteric CB1 receptors tonically inhibit colonic propulsion in mice.", Izzo et al[xv] concluded "inflammation of the gut increases the potency of cannabinoid agonists possibly by'up-regulating' CB(1) receptor expression; in addition, endocannabinoids, whose turnover is increased in inflamed gut, might tonically inhibit intestinal motility", finding CB2 receptor antagonists did notreverse the effect[xvi], and Mancinelli et al[xvii] concluded "cannabinoids perform a neuromodulatory role in varioustracts of gastrointestinal system".

Ueda et al[xviii] established the presence of anandamide hydrolase· an enzyme which breaks down endogenous cannabinoids, in the rat, as well as other enzymes inhibiting its activity, suggesting close regulation of endocannabinoid levels in the gut. They noted "The anandamide hydrolase and synthase activities were detected in a variety of rat organs, and liver showed by far the highest activities. A high anandamide hydrolase activity was also detected in small intestine but only after the homogenate was precipitated with acetone to remove endogenous lipids inhibiting theenzyme activity."

In an in vitro study of human tissue preparations, Croci et al[xix] reported "These results provide functional evidence of the existence of prejunctional cannabinoid CB1-receptors in the human ileum longitudinal smooth muscle. Agonist activation of these receptors prevents responses to electrical field stimulation, presumably by inhibiting acetylcholine release. SR 141716 is a potent and competitive antagonist ofcannabinoid CB1 receptors naturally expressed in thehuman gut."

Tyler et al[xx] found CB1 agonists inhibited, and CB1 antagonists increased, small intestinal secretion, concluding "cannabinoids may have therapeutic potential for diarrhea unresponsive to available therapies." However, after finding humans using cannabis produced more voluminous diarrhoea when challenged with cholera or E.Coli, Nalin et al[xxi] warned "Cannabis use may be an important factor predisposing to severe diarrhoea." Izzo et al[xxii] found SR141716A (CB1 antagonist) increased, whereas WIN 55,212-2 (CB1 agonist) decreased, defaecation, gastrointestinal transit and fluid accumulation. Winn et al[xxiii] found "Ten new delta6a,10a-THC analogs

antihypertensives, and hypnotics and as antisecretory, antiulcer, and antidiarrheal agents."

Turker et al[xxiv] found an antihistaminic and anti-inflammatory activity of THC in intestinal tissue. Kulkarni-Narla et al[xxv] noted "Cannabis has been used for centuries in the medicinal treatment of gastrointestinal disorders. Endogenous cannabinimimetic substances such as 2-arachidonylglycerol have been isolated from gut homogenates and CB1-cannabinoid binding sites have been identified in small intestine."

Gastric Emptying & Motility: Pertwee[xxvi] noted "Cannabinoid receptor agonists delay gastric emptying in humans as well as in rodents and probably also inhibit human gastric acid secretion", Landi et al[xxvii]

mechanisms in gastrointestinal transit delay by specific agonists". Izzo et al[xxviii] concluded "cannabinoid agonists delay gastric emptying through activation of cannabinoid CB1 receptors, while the endogenous cannabinoid system does not seem to modulate gastric motility", whilst Krowicki et al[xxix] found "THC evoked long-lasting decreases in intragastric pressure and pyloric contractility. ... gastric motor... effects ofperipherally administered delta9-THC seem to be mediated through cannabinoid CB1 receptors".

In human volunteers, Bateman[xxx] reported "Despite significant change in pulse rate and psychological parameters consistent with cannabis activity there was no significant effect on the pattern of gastric emptying. It is therefore suggested that an anti-emetic action of delta-9-tetrahydrocannabinol does not involvea change in gastric emptying",

Gastric Acid Secretion & Ulcers: Studying the effects of cannabinoids on gastric acid secretions, Adami et al[xxxi] found "gastric antisecretory effects of cannabinoids in the rat are mediated by suppression of vagal drive to the stomach through activation of CB(1) receptors" Izzo et al[xxxii] noted "The digestive tract contains endogenous cannabinoids (anandamide and 2-arachidonylglycerol) and cannabinoid CB1 receptors can be found on myenteric and submucosal nerves. Activation of CB1 receptors inhibits gastrointestinal motility, intestinal secretion and gastric acid secretion" and conclude "The enteric location of CB1 receptors could provide new strategies for the managementof gut disorders."

Corruzzi et al[xxxiii] concluded

anaesthetized rat is mediated by specific cannabinoid receptors. Moreover, the antagonism of WIN 55,212-2-induced effects by the selective CB1 receptor antagonists SR141716A and LY320135 together with the ineffectiveness of both the CB2 receptor agonist JWH-015 and the CB2 receptor antagonist SR144528 indicate that CB1 receptor subtypes are predominantlyinvolved in the antisecretory effect of WIN 55,212-2". In humans, Nalin et al[xxxiv] found "smoking of cannabis greater than 2 days a week waslinked with low (stomach) acid output"

Germano et al[xxxv] reported "The cannabinoid receptor agonist WIN 55,212-2... reduced gastric ulceration. The protective effect of WIN 55,212-2 was counteracted by the cannabinoid CB1 receptor antagonist SR141716A... These results indicate that the antiulcer effect of the cannabinoid receptor agonist(s) is mediated by cannabinoid CB1 receptors." De Souza[xxxvi] found acute and long-term cannabis treatment reduced the rate of gastriculceration in rats subjected to restraint-induced stress.

Summary - Cannabinoids and the GI Tract: While I am not aware of any published results from controlled human studies of medical use of cannabis in the treatment of conditions such as gastric ulcers or irritable bowel syndrome, there appears to be sufficient animal evidence of the potential efficacy of cannabis in reducing intestinal spasms, ulceration and gastric acid secretion to merit further research into this and related indications.

Any symptomatic relief obtained from smoking cannabis, or use via inhalers or sublingual sprays, would occur far more rapidly than with oral preparations.
 

kesaber

Well-Known Member
This is incredibly long..if you feel like reading, more power to you


Intestinal Motility and Irritable Bowel Syndrome: The CB1 cannabinoid receptor has specifically been found to inhibit motility of the intestine in a variety of laboratory and farm animals. The effect is specific, indicating that endogenous cannabinoids to be responsible for regulating smooth muscle tone in the intesting, and therateof peristalsis.

Rosell et al[iv] first demonstrated that cannabinoids inhibit contractions of the small intestine in the rat. Pertwee et al[v] established the presence of cannabinoid (CB1) receptors within the guinea-pig intestine, Kazuhisa et al[vi] established the presence of enzymes which break down anandamide (the endogenous cannabinoid CB1-agonist) within the small intestine, and in rats Katayama et al[vii] also found "a high content of anandamide hydrolase in small intestine". The smooth muscle-relaxant properties of cannabinoids are so well established that preparations of guinea-pig intestine are routinely used as an in vitro screening tool to testthe potencyand function of novel cannabinoids[viii][ix].

Shook & Burks[x] found that THC reduced the frequency of intestinal contractions, and reduced the flow of food in the small intestine, without altering

cannabidiol) exert an inhibitory effect on GI transit and motility in rats". Cadas et al[xi] reported that a gut enzyme (vasoactive intestinal peptide) may regulate the precursor chemical to anandamide (which activates cannabinoid CB1 receptors) and N-palmitoylethanolamine (which activates a CB2-like receptor subtype), suggesting that endogenous cannabinoids may play a role in regulating theactivityofthe gut.

Studying guinea-pigs & rats, Coutts et al[xii] report "Activation of cannabinoid CB(1) receptors inhibits gastrointestinal motility, propulsion, and transit, whereas selective antagonism of these receptors has the opposite effects, suggesting the presence of endocannabinoid tone." Lopez-Redondo

transmission occurred by reversible activation of both presynaptic and postsynaptic CB1

synaptic transmission can also be reversibly depressed by cannabinoids." In mice, Pinto et al[xiv] found endogenous and exogenous CB1-receptor

"endocannabinoids acting on myenteric CB1 receptors tonically inhibit colonic propulsion in mice.", Izzo et al[xv] concluded "inflammation of the gut increases the potency of cannabinoid agonists possibly by'up-regulating' CB(1) receptor expression; in addition, endocannabinoids, whose turnover is increased in inflamed gut, might tonically inhibit intestinal motility", finding CB2 receptor antagonists did notreverse the effect[xvi], and Mancinelli et al[xvii] concluded "cannabinoids perform a neuromodulatory role in varioustracts of gastrointestinal system".

Ueda et al[xviii] established the presence of anandamide hydrolase· an enzyme which breaks down endogenous cannabinoids, in the rat, as well as other enzymes inhibiting its activity, suggesting close regulation of endocannabinoid levels in the gut. They noted "The anandamide hydrolase and synthase activities were detected in a variety of rat organs, and liver showed by far the highest activities. A high anandamide hydrolase activity was also detected in small intestine but only after the homogenate was precipitated with acetone to remove endogenous lipids inhibiting theenzyme activity."

In an in vitro study of human tissue preparations, Croci et al[xix] reported "These results provide functional evidence of the existence of prejunctional cannabinoid CB1-receptors in the human ileum longitudinal smooth muscle. Agonist activation of these receptors prevents responses to electrical field stimulation, presumably by inhibiting acetylcholine release. SR 141716 is a potent and competitive antagonist ofcannabinoid CB1 receptors naturally expressed in thehuman gut."

Tyler et al[xx] found CB1 agonists inhibited, and CB1 antagonists increased, small intestinal secretion, concluding "cannabinoids may have therapeutic potential for diarrhea unresponsive to available therapies." However, after finding humans using cannabis produced more voluminous diarrhoea when challenged with cholera or E.Coli, Nalin et al[xxi] warned "Cannabis use may be an important factor predisposing to severe diarrhoea." Izzo et al[xxii] found SR141716A (CB1 antagonist) increased, whereas WIN 55,212-2 (CB1 agonist) decreased, defaecation, gastrointestinal transit and fluid accumulation. Winn et al[xxiii] found "Ten new delta6a,10a-THC analogs

antihypertensives, and hypnotics and as antisecretory, antiulcer, and antidiarrheal agents."

Turker et al[xxiv] found an antihistaminic and anti-inflammatory activity of THC in intestinal tissue. Kulkarni-Narla et al[xxv] noted "Cannabis has been used for centuries in the medicinal treatment of gastrointestinal disorders. Endogenous cannabinimimetic substances such as 2-arachidonylglycerol have been isolated from gut homogenates and CB1-cannabinoid binding sites have been identified in small intestine."

Gastric Emptying & Motility: Pertwee[xxvi] noted "Cannabinoid receptor agonists delay gastric emptying in humans as well as in rodents and probably also inhibit human gastric acid secretion", Landi et al[xxvii]

mechanisms in gastrointestinal transit delay by specific agonists". Izzo et al[xxviii] concluded "cannabinoid agonists delay gastric emptying through activation of cannabinoid CB1 receptors, while the endogenous cannabinoid system does not seem to modulate gastric motility", whilst Krowicki et al[xxix] found "THC evoked long-lasting decreases in intragastric pressure and pyloric contractility. ... gastric motor... effects ofperipherally administered delta9-THC seem to be mediated through cannabinoid CB1 receptors".

In human volunteers, Bateman[xxx] reported "Despite significant change in pulse rate and psychological parameters consistent with cannabis activity there was no significant effect on the pattern of gastric emptying. It is therefore suggested that an anti-emetic action of delta-9-tetrahydrocannabinol does not involvea change in gastric emptying",

Gastric Acid Secretion & Ulcers: Studying the effects of cannabinoids on gastric acid secretions, Adami et al[xxxi] found "gastric antisecretory effects of cannabinoids in the rat are mediated by suppression of vagal drive to the stomach through activation of CB(1) receptors" Izzo et al[xxxii] noted "The digestive tract contains endogenous cannabinoids (anandamide and 2-arachidonylglycerol) and cannabinoid CB1 receptors can be found on myenteric and submucosal nerves. Activation of CB1 receptors inhibits gastrointestinal motility, intestinal secretion and gastric acid secretion" and conclude "The enteric location of CB1 receptors could provide new strategies for the managementof gut disorders."

Corruzzi et al[xxxiii] concluded

anaesthetized rat is mediated by specific cannabinoid receptors. Moreover, the antagonism of WIN 55,212-2-induced effects by the selective CB1 receptor antagonists SR141716A and LY320135 together with the ineffectiveness of both the CB2 receptor agonist JWH-015 and the CB2 receptor antagonist SR144528 indicate that CB1 receptor subtypes are predominantlyinvolved in the antisecretory effect of WIN 55,212-2". In humans, Nalin et al[xxxiv] found "smoking of cannabis greater than 2 days a week waslinked with low (stomach) acid output"

Germano et al[xxxv] reported "The cannabinoid receptor agonist WIN 55,212-2... reduced gastric ulceration. The protective effect of WIN 55,212-2 was counteracted by the cannabinoid CB1 receptor antagonist SR141716A... These results indicate that the antiulcer effect of the cannabinoid receptor agonist(s) is mediated by cannabinoid CB1 receptors." De Souza[xxxvi] found acute and long-term cannabis treatment reduced the rate of gastriculceration in rats subjected to restraint-induced stress.

Summary - Cannabinoids and the GI Tract: While I am not aware of any published results from controlled human studies of medical use of cannabis in the treatment of conditions such as gastric ulcers or irritable bowel syndrome, there appears to be sufficient animal evidence of the potential efficacy of cannabis in reducing intestinal spasms, ulceration and gastric acid secretion to merit further research into this and related indications.

Any symptomatic relief obtained from smoking cannabis, or use via inhalers or sublingual sprays, would occur far more rapidly than with oral preparations.
It seems that I may not have necessarily relayed the information I read properly.

After reading what you wrote and doing a small amount of my own research I have no found anything that says THCa is better as a medicine. In fact, Dr. William Courtney himself, the man who promotes juicing raw cannabis, agrees and says the plant must be de-carboxylated for it to bring out it's true medicinal properties. Instead, he promotes juicing cannabis as a dietary essential saying that although it may not cure cancer, it may assist in preventing it by giving your body the necessary nutrients it needs. He says that while you gain certain benefits from decarboxylating it you also lose out on many benefits such including bone remodeling and help with inflammation.

This is the first video I saw on the matter and it is relatively short.

 

kesaber

Well-Known Member
I almost forgot my original question. To get the benefit does this video claim, would I be able to juice leaves from late in the vegetative stage? Even if you don't get the maximum benefit I would have to worry about harvesting and starting over, nor would I have to worry about getting a second tent for a perpetual cycle. It also means I would feel better about using an LED light and not spending a ton on electricity. Would it be that much better for me to allow it to flower before juicing them? Is juicing in veg a waste of time? Does anyone still have a reason why juicing cannabis in general is a waste of time? Any information on this would be greatly appreciated?
 

paindog

Member
Thank you kwizoking, that was a great review of the relevant research for us gut sufferers to dig deeper into. just wish I had studied science! Any hope somebody is working on a more efficient medicine for us suffering with ibs and crohns etcetera than stuffing joints into our faces constantly?
A pill that had all the benefits of weed for my symptoms but was much longer lasting than smoking and enabled me to choose which days/when I got wasted would be great. I miss smoking for fun rather than needing it for relief! Mate if you could design that drug and engineer some yeast to pump it out you could help a lot of people be less miserable! (possibly make a little cash too, seeing how many people struggle with it. The stats on working hours lost to ibs in the USA is crazy!)

I have so far found certain pheno's of chemdog to be the best medicine for my guts. Unfortunately I lost those genetics and am currently working on a big pheno hunt at the moment:
Cheese-dog by Connoisseur genetics
Chem-dog by Cali- connect
Headband ". "
Lovedawg by bodhi seeds
Cheese candy by Delicious seeds
All in my system at various stages.

Have recently wasted an awfully long time on running Cotton Candy by Delicious seeds. I am a massive fan of their cheese candy and bought cotton candy seeds assuming shared heritagefRom the candy name. Should have donem y researc!
Cotton candy produces Very vigorous plants, one tasty skunky pheno was kept as it is a good yielder but I personally found it to have no medical value whatsoever and ended up trading my beautiful buds for crappy commercial schwagg as it was more use to me! Oh to live in a civilized place with dispensaries! Anyway my question is whether you have any advice when selecting strains specifically to treat ibs? I have limited space for pheno hunting just wondered if you had any insight into favourable cannabinoid profiles to treat ibs. Thanks again prof! Props for giving freelyo f your knowledge when it benefits you not. Shame kasaber seems to want a magic cure and disliked your reasoned and rational approach to the evidence!
 

Lord Kanti

Well-Known Member
I threw some sun dried Alien OG with some fresh Blue Dream in with my smoothie. I feel like I have Tiger Balm under the skin of my shoulders now.

I'll also throw in pinched off low level buds when I clean stalks to force flowers up top to thicken. Also consume the pinched off buds from super cropping / FIMing. As I type this I feel a high coming on. Don't count on raw cannabis NOT getting you high. It can, so plan accordingly.

I blended 4.29 g of wet and dry herb and drank half the smoothie. I feel legitimately medicated. My limbs feel like I have anti inflammatory cream rubbed thoroughly Into my skin.

~~~~~~UPDATE~~~~~~

God, it feels like I'm melting away into a tingling mass as I sink into this mattress. The only thing missing is a woman walking on my back.
 
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Bugeye

Well-Known Member
Well hope i helped, i tried to keep it short and sweet while but combined a couple older posts

1) How do you feel about Dr. Courtney saying there is more medical benefit in the THC acid then after it has been de-carbed?

Well not to attack the other person. But in my opinion, thats not the case. with certain conditions it could provide a greater degree of relief relative to side effects. But thats far from saying thca has more medical benefit. Overall alot fewer ailments could be treated.


2) Why did I feel such fast and intense relief after juicing the fan leaves from mid-late veg. I felt happier, almost euphoric, and I had a ton of energy. I don't know if it lasted longer than smoking a joint, but it was definitely more intense for longer and I don't recall have any kind of abdominal pain during that time.

Well..a portion could be psychological, dont underestimate your mind..also during this process some could have been decarbed, wether chemically or through heat..

But for a compound to have "drug likeness" it must have a polar surface area (psa) under 60 angstroms in order to cross the blood brain barrier and reach receptors......the higher the number the more polar it is. Your blood being polar the barrier being fatty... it must be able to travel in blood and non polar enough to cross the barrier and get back out, this all has huge implications in pharmacology
.. in the polar acid form(thca) has a psa of 66...meaning you will feel certain effects from cbd as the cb2 receptors are located throughout the body and don't require a reduction in polarity..no bb barrier to cross. However most medical use results from activation of one of the cb receptors in the brain, specifically with cbd the "cb3" "cb4" opiate activity etc and indirect pathways being medically limiting...

a psa under 60 is optimum but some of the compound will cross up to a psa about 70. thca at 66 will cross but not efficiently and taking higher doses..this would be a huge waste of product however..especially since it takes relatively high doses to get high anyway, compare to most pharmaceuticals having a therapeutic window 1-20mg..... after decarbing it drops to a psa of 30 easilly passing through and staying in our body a good while, there are side effects of this bioaccumulation in heavy users, but thats another subject.
cbda is more polar than thc with a psa of 77 and cbd about 40..will not cross if not decarbed

Cbd is more polar than the other cannabinoids. Cbc cbg thc and propyls'- thcv etc all have near identical psa's


So if you ingested enough you would not recieve the sedative properties of cbd but possibly felt the more uplifting thc and it heloed with abdominal pain.
Back to psychological, consider
thc has a logp of about 7
In practice optimum colonic absorption is 1.32, intestinal is 1.35, oral 1.8, Cns 2, percutaneous at 2.6 and sublingual 5.5. Neither form of thc is efficiently absorbed without carriers etc. The lower the number the higher the polarity. Youll see that loosely, the more non polar (as in decarbed thc) the faster it is absorbed
Thanks for the info! I took down my post in Extracts on THCa as it was based on the Dr. Courtney info and I see you as a better resource.

The people using the THCa stuff I made could be reporting placebo improvements. One person using for anti-spasm control and one applied topically for arthritis. I'm making decarbed extracts this week so they will get those to try and compare as well.

Cheers!
 
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