-
Happy Birthday ICMag! Been 20 years since Gypsy Nirvana created the forum! We are celebrating with a 4/20 Giveaway and by launching a new Patreon tier called "420club". You can read more here.
-
Important notice: ICMag's T.O.U. has been updated. Please review it here. For your convenience, it is also available in the main forum menu, under 'Quick Links"!
Cannabis biochemistry
- Thread starter BullDogUK
- Start date
BasementBreeder
Member
Please do. I would definitely be interested in it.
W
willyweed
sound's interesting ! bring it on
Green Devil
Member
http://www.amazon.co.uk/gp/search?index=books&linkCode=qs&keywords=1592599478
http://www.worldcat.org/title/biology-of-marijuana-from-gene-to-behavior/oclc/53236248
http://www.amazon.co.uk/gp/search?index=books&linkCode=qs&keywords=0789015080
Some interesting reading for you who can spare a few bucks!
http://www.worldcat.org/title/biology-of-marijuana-from-gene-to-behavior/oclc/53236248
http://www.amazon.co.uk/gp/search?index=books&linkCode=qs&keywords=0789015080
Some interesting reading for you who can spare a few bucks!
Very well, let us begin. I hope you have your smoking equipment at the ready 
Ok so first let's look at how cannabinoids exist in your body once absorbed and how they are processed. Within the cannabis plant, the synthesized cannabinoids exist as acids which require decarboxylation (the loss of one CO2 molecule from the acid) to form the 'active' cannabinoid, we usually achieve this via the application of heat (smoking or cooking) however can also be caused by sunlight, which is why we keep our bud in the dark!
Cannabinoids are hydrophobic compounds, meaning they dissolve poorly (if at all) in water but form solutions easily with other organic molecules such as alcohols, fats (such as the lipids forming cell membranes) etc. This is due to a lack of polarity on the majority of the molecule (i.e. points where a hydrogen bond can be formed between a water molecule and the THC molecule) and results in the accumulation of cannabinoids with other hydrophobic molecules (in the body I imagine cannabinoids pass through the blood system through liposomes). Due to this hydrophobic nature, cannabinoids are stored within adipose tissues after consumption and remain in the body long after use (and remain detectable
)
Quick visual of how hydrophobicity works - the lower image is more favorable in terms of entropy as fewer water molecules are required to form a shell around the hydrophobic molecules.
Cannabinoids, like most xenobiotics (fancy name for chemicals from outside the body), are oxidized in the liver by the cytochrome p450 enzyme family, specifically the CYP2C9 enzyme. As chemicals absorbed via the gut must pass through the liver before entering the rest of the blood stream, cannabinoids absorbed from edibles will be processed before being able to enter the brain whilst inhaled cannabinoids are capable of reaching the brain before being cycled through the liver. Whilst I'm not sure what the exact effect of this might be, it may go some way in explaining some of the differences between eating and inhaling cannabis.
Like most Cytochrome p450 enzymes, CYP2C9 is subject to a high level of variation amongst the population at large meaning unoxidized (and active) cannabinoids may remain in the blood stream for wildly different amounts of time in different individuals. Whilst variations in the cannabinoids receptors and resulting signal pathways are the likely cause of the difference in highs between people, this enzyme variation may explain the difference tolerance to weed between people (disregarding tolerance of course). Other substrates of CYP2C9, which may act to inhibit the oxidation of cannabinoids, include ibuprofen, fluvastatin, prozac and ketamine, the enzyme may also be inhibited by Luvox and sertraline - I wonder if anyone here taking these drugs has noticed any difference in the effect cannabis has on them?
Anyway that's it for now! I will do some research into cannabinoid receptors over the next few days and do another post.
Ok so first let's look at how cannabinoids exist in your body once absorbed and how they are processed. Within the cannabis plant, the synthesized cannabinoids exist as acids which require decarboxylation (the loss of one CO2 molecule from the acid) to form the 'active' cannabinoid, we usually achieve this via the application of heat (smoking or cooking) however can also be caused by sunlight, which is why we keep our bud in the dark!
Cannabinoids are hydrophobic compounds, meaning they dissolve poorly (if at all) in water but form solutions easily with other organic molecules such as alcohols, fats (such as the lipids forming cell membranes) etc. This is due to a lack of polarity on the majority of the molecule (i.e. points where a hydrogen bond can be formed between a water molecule and the THC molecule) and results in the accumulation of cannabinoids with other hydrophobic molecules (in the body I imagine cannabinoids pass through the blood system through liposomes). Due to this hydrophobic nature, cannabinoids are stored within adipose tissues after consumption and remain in the body long after use (and remain detectable
)Quick visual of how hydrophobicity works - the lower image is more favorable in terms of entropy as fewer water molecules are required to form a shell around the hydrophobic molecules.
Cannabinoids, like most xenobiotics (fancy name for chemicals from outside the body), are oxidized in the liver by the cytochrome p450 enzyme family, specifically the CYP2C9 enzyme. As chemicals absorbed via the gut must pass through the liver before entering the rest of the blood stream, cannabinoids absorbed from edibles will be processed before being able to enter the brain whilst inhaled cannabinoids are capable of reaching the brain before being cycled through the liver. Whilst I'm not sure what the exact effect of this might be, it may go some way in explaining some of the differences between eating and inhaling cannabis.
Like most Cytochrome p450 enzymes, CYP2C9 is subject to a high level of variation amongst the population at large meaning unoxidized (and active) cannabinoids may remain in the blood stream for wildly different amounts of time in different individuals. Whilst variations in the cannabinoids receptors and resulting signal pathways are the likely cause of the difference in highs between people, this enzyme variation may explain the difference tolerance to weed between people (disregarding tolerance of course). Other substrates of CYP2C9, which may act to inhibit the oxidation of cannabinoids, include ibuprofen, fluvastatin, prozac and ketamine, the enzyme may also be inhibited by Luvox and sertraline - I wonder if anyone here taking these drugs has noticed any difference in the effect cannabis has on them?
Anyway that's it for now! I will do some research into cannabinoid receptors over the next few days and do another post.
Dingofriar
Member
Rite on bulldog... Keep up the good research... Subd. Q;-)
W
willyweed
nice little read thanks, look forward to the next
Well done man, good to see you amking your mark 
Hi Bulldog, couple of quick Q's if you don't mind.
You say that we require decarboxylation to take place, and that we can achieve that via sunlight, however we also avoid achieving this with sunlight. Would you mind clarifying that a little please, it seems a little contradictory at first reading.
You say that chemicals absorbed via the gut must pass through the liver, does this mean eating consumables may be more damaging than smoking or at least vaping? Or would this act as a protective measure for the liver? Are you aware of any studies that have been conducted on this?
In my youth, there was a common practice of using vodka in a bong to pass the smoke through. Most claimed it got them higher. Since you say that "Cannabinoids are hydrophobic compounds, meaning they dissolve poorly (if at all) in water but form solutions easily with other organic molecules such as alcohols, " would the alcohol actually have reduced the effect of the smoke rather than enhanced it?
You say that we require decarboxylation to take place, and that we can achieve that via sunlight, however we also avoid achieving this with sunlight. Would you mind clarifying that a little please, it seems a little contradictory at first reading.
You say that chemicals absorbed via the gut must pass through the liver, does this mean eating consumables may be more damaging than smoking or at least vaping? Or would this act as a protective measure for the liver? Are you aware of any studies that have been conducted on this?
In my youth, there was a common practice of using vodka in a bong to pass the smoke through. Most claimed it got them higher. Since you say that "Cannabinoids are hydrophobic compounds, meaning they dissolve poorly (if at all) in water but form solutions easily with other organic molecules such as alcohols, " would the alcohol actually have reduced the effect of the smoke rather than enhanced it?
Adze
Member
GMT,
There is some interesting information concerning decarboxylation of specific cannabinoids in this: http://www.theweedblog.com/cannabinoid-profiles-thc-thca-thcv-cbd-cbg-cbn-cbc-and-terpenes/
There is some interesting information concerning decarboxylation of specific cannabinoids in this: http://www.theweedblog.com/cannabinoid-profiles-thc-thca-thcv-cbd-cbg-cbn-cbc-and-terpenes/
Hey GMT, thanks for the questions!
I'll take them in reverse order because of reasons:
- Using vodka in a bong? I've never heard of that! But yes I imagine that if it had any effect at all it would be to reduce the overall amount of cannabinoids that you were actually getting in the smoke. As far as I can tell (not much research on this topic!) the purpose of a water pipe, besides cooling the smoke, is to filter out some of the contaminants in your smoke, which may be polar and thus water soluble.
- Cannabinoids passing through the liver are not going to cause any damage; the liver acts as the main site of the processing of much of what you absorb through the gut as blood from the gut must pass through the hepatic portal vein and the liver before entering the rest of the bloodstream. Hepatocytes (liver cells) produce large quantities of enzymes involved in the conversion of non-polar molecules into polar molecules that can be more readily excreted by the body (http://en.wikipedia.org/wiki/Xenobiotic_metabolism if you want some more info on that).
- Yes I'm sorry that is quite contradictory sounding! What I mean is that you do not want the decarboxylation of your bud's cannabinoids occurring before you intend it to happen as once decarboxylation has occurred the cannabinoid molecules can begin to degrade (i.e. THC may degrade into CBN)
http://www.clinchem.org/content/46/11/1846.full.pdf - Degradation of cannabinoids in hair follicles is largely due to solar UV radiation.
I'll take them in reverse order because of reasons:
- Using vodka in a bong? I've never heard of that! But yes I imagine that if it had any effect at all it would be to reduce the overall amount of cannabinoids that you were actually getting in the smoke. As far as I can tell (not much research on this topic!) the purpose of a water pipe, besides cooling the smoke, is to filter out some of the contaminants in your smoke, which may be polar and thus water soluble.
- Cannabinoids passing through the liver are not going to cause any damage; the liver acts as the main site of the processing of much of what you absorb through the gut as blood from the gut must pass through the hepatic portal vein and the liver before entering the rest of the bloodstream. Hepatocytes (liver cells) produce large quantities of enzymes involved in the conversion of non-polar molecules into polar molecules that can be more readily excreted by the body (http://en.wikipedia.org/wiki/Xenobiotic_metabolism if you want some more info on that).
- Yes I'm sorry that is quite contradictory sounding! What I mean is that you do not want the decarboxylation of your bud's cannabinoids occurring before you intend it to happen as once decarboxylation has occurred the cannabinoid molecules can begin to degrade (i.e. THC may degrade into CBN)
http://www.clinchem.org/content/46/11/1846.full.pdf - Degradation of cannabinoids in hair follicles is largely due to solar UV radiation.
Oh and as someone prescribed Setraline I can tell you that I think setraline (also known as zoloft in the US) has bigger drawbacks :-S
I'm meant to be calming and make you feel less depressed but basically it really screws you up, if you miss taking it then it messes with your sleep, you can easily sleep 16 hours in a day when your body is missing the setraline, according to the packet it may cause sexual and fertility issues and it may cause thoughts of suicide along with many other things,
I'm sort of off it at the moment and even being stoned all the time is easier than setraline, setraline makes you even more docile and the weed also helps me deal with my OCD better.
(PS. I've been feeling more stoned for less time while on setraline, but that coincides with me changing from eating to vaping)
I'm meant to be calming and make you feel less depressed but basically it really screws you up, if you miss taking it then it messes with your sleep, you can easily sleep 16 hours in a day when your body is missing the setraline, according to the packet it may cause sexual and fertility issues and it may cause thoughts of suicide along with many other things,
I'm sort of off it at the moment and even being stoned all the time is easier than setraline, setraline makes you even more docile and the weed also helps me deal with my OCD better.
(PS. I've been feeling more stoned for less time while on setraline, but that coincides with me changing from eating to vaping)
I'm also prescribed sertraline which doesn't help at all with my insomnia and quite often makes me very twitchy and restless which cannabis really helps with but I've never noticed any difference in the high or the length of high so I was really just wondering if anyone else, perhaps on a higher dosage, has noticed anything? (thus the questions 
)
)Hello everyone! 
This is going to have to be a briefer post than I'd like due to final exams rearing their ugly head and me having to get my nose stuck into Dyskeratosis and Alzheimer's rather than weed
Most of the information used is taken from a review paper in the British Journal of Pharmacology by R.G. Pertwee in 2008 named The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: tetrahydrocannabinol, cannabidiol and tetrahydrocannabivarin which I certainly give my virtual thumbs up to.
So let's get to it! In the body cannabinoids interact with a pre-existing group of receptors of which two, CB1 and CB2, have been identified thus far. These receptors exist to facilitate the endocannabinoid pathways found in all/most organisms of the deuterostome superphylum and seem to have evolved in the ancestors of modern-day sea-squirts. I'll do another post on endocannabinoids another time however the CB receptors seem to be primarily located in immune-related tissues and the periphieral and central nervous systems with CB1 receptors being far more common in the central nervous system and CB2 being more common in immune tissues. The receptors are by no means limited to these areas and have been identified in liver, lung, kidney and endothelial cells (making up the interior of your blood vessels).
The cannabinoid receptors are part of a receptor superfamily known as 7TM g protein-coupled receptors meaning they consist of 7 linked helices each spanning the cell membrane, linked to another protein or protein complex. Upon activation of the receptor by the cannabinoid (we refer to this as the ligand) a change in the shape of the receptor (conformational change) results in the gprotein becoming detached or activated in some other way, resulting in the initiation of a signal within the cell. Whilst (as far as I can tell) no complete structure has been determined we do have a few fragments of some of the helices and loops involved in the structure:
Loops 6-7 of CB1 with water excluded (orange surface shows atomic surface, underlying colours show amino acids and their hydrophobicity).
The precise effects of each cannabinoid is determined by the affinity with which it is capable of binding to the receptor as a ligand. A higher affinity results in the binding of the molecule to the receptor for a longer period of time, perhaps leading to the differential effects.
Here's some pretty pictures of cannabinoids themselves so you can see how shape affects affinity:
Cheers for reading and catch you in a few days when I manage to drag myself into doing some more fun reading!
This is going to have to be a briefer post than I'd like due to final exams rearing their ugly head and me having to get my nose stuck into Dyskeratosis and Alzheimer's rather than weed
Most of the information used is taken from a review paper in the British Journal of Pharmacology by R.G. Pertwee in 2008 named The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: tetrahydrocannabinol, cannabidiol and tetrahydrocannabivarin which I certainly give my virtual thumbs up to.
So let's get to it! In the body cannabinoids interact with a pre-existing group of receptors of which two, CB1 and CB2, have been identified thus far. These receptors exist to facilitate the endocannabinoid pathways found in all/most organisms of the deuterostome superphylum and seem to have evolved in the ancestors of modern-day sea-squirts. I'll do another post on endocannabinoids another time however the CB receptors seem to be primarily located in immune-related tissues and the periphieral and central nervous systems with CB1 receptors being far more common in the central nervous system and CB2 being more common in immune tissues. The receptors are by no means limited to these areas and have been identified in liver, lung, kidney and endothelial cells (making up the interior of your blood vessels).
The cannabinoid receptors are part of a receptor superfamily known as 7TM g protein-coupled receptors meaning they consist of 7 linked helices each spanning the cell membrane, linked to another protein or protein complex. Upon activation of the receptor by the cannabinoid (we refer to this as the ligand) a change in the shape of the receptor (conformational change) results in the gprotein becoming detached or activated in some other way, resulting in the initiation of a signal within the cell. Whilst (as far as I can tell) no complete structure has been determined we do have a few fragments of some of the helices and loops involved in the structure:
Loops 6-7 of CB1 with water excluded (orange surface shows atomic surface, underlying colours show amino acids and their hydrophobicity).
The precise effects of each cannabinoid is determined by the affinity with which it is capable of binding to the receptor as a ligand. A higher affinity results in the binding of the molecule to the receptor for a longer period of time, perhaps leading to the differential effects.
Here's some pretty pictures of cannabinoids themselves so you can see how shape affects affinity:
Cheers for reading and catch you in a few days when I manage to drag myself into doing some more fun reading!
