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- 1 note
- 2 New antidepressant drug increases 'brain's own cannabis'
- 3 Deficiency?
- 4 THC synthesis pathway: reference needed
- 5 Percents and times
- 6 This article should be divided
- 7 Cannabinoids and parkinson
- 8 Merge
- 9 Cyclidization
- 10 CBD is psychoactive
- 11 The intro paragraph should be re-written -- too influenced by the weed
- 12 THC-C4
- 13 Other CB sources?
- 14 CBD Contradiction
- 15 Is there a scientific term for butane extracted cannabinoids?
- 16 on the order of over 60 cannabinoid naturally occurring cannabinoid molecules / chemicals in the marijuana plant?
- 17 Cannabidiol Discrepancy
- 18 "The endocannabinoid 2-AG has been found in bovine and human maternal milk."
- 19 Cancer anti-tumor effects of cannabinoids
- 20 " natural occurence"
- 21 endocannabinoids
- 22 Added link to CRUK blog
- 23 Which cannabinoids are shared by Echinacea and Cannabis?
- 24 subsection discussing one US Patent from NIH
- 25 table of "natural cannabinoids"
- 26 Alkylamides and catechins are not cannabinoids
- 27 Re-edited text
- 28 Definition of cannabinoid and ligand functionality
- 29 weak (low) affinities
- 30 intracellular lipid signaling
- 31 Deletion of Cochrane Review conclusions
- 32 Immune system and cannabinoids
in section "Cannabinoids",
- the sentence on reversible binding and stereoselectivity should be explained in more lay terms
- are all of these insoluble in water and soluble in fats, alcohols, etc?
in section "Herbal cannabinoids",
- "21 carbon compounds": do you simply mean that they contain 21 carbon atoms?
Also, the chemical discussion here is written such that it might be general, abo ut all cannabinoids, not just the herbal ones. is this correct or not?
- - Centrx 22:14, 25 May 2004 (UTC)
New antidepressant drug increases 'brain's own cannabis'
Someone with more experience in this subject ought to add information regarding synthetic THC analogues. In particular, THC-V seems interesting because it is 500 times more potent than THC (on the order of LSD's potency). http://www.erowid.org/archive/rhodium/chemistry/thc/index.html
I've heard some talk about "endo-cannabinoid deficiency" as a possible syndrome similar to chronic fatigue (or other symptoms, depending on whom you ask) ... Is this a real working medical hypothesis, or just some wishful thinking by potheads? Google doesn't turn up much on the subject, however that in itself doesn't mean it's not true... Rainman420 06:25, 13 May 2006 (UTC)
It is a real theory put forward by (presumably not pot-head) scientists. Here is a link to the abstract for a review paper in which cannabinoid deficiency syndrome is proposed: []. That said, it is still in an infant theory stage, and needs to be tested. Just as an FYI, a good place to look for information on this kind of thing (as long as it is biomedically related) is PubMed[]. Hope this helps! --MudPhud 18:53, 14 July 2006 (UTC)
THC synthesis pathway: reference needed
The article currently states: " Due to molecular similarity and ease of synthetic conversion, it was originally believed that CBD was a natural precursor to THC. However, it is now known that CBD and THC are produced independently in the cannabis plant. "
Mahlberg and Kim (http://www.hempreport.com/issues/17/malbody17.html) state "Delta 9-tetrahydrocannabinol (THC) is derived from CBD." This is supported by the following reference: Lanyon, V., J. Turner and P. G. Mahlberg. 1981. Quantitative analysis of cannabinoids in the secretory product from capitate-stalked glands of Cannabis sativa L. (Cannabaceae). Bot. Gaz. 142:316-319.
Hillig and Mahlberg (2004 http://www.amjbot.org/cgi/content/full/91/6/966) state that "Cannabigerol (CBG) is the direct precursor of cannabichromene (CBC), cannabidiol (CBD), and 9-tetrahydrocannabinol (THC) (Taura et al., 1995 , 1996 ; Morimoto et al., 1997)." This does not explicitly state that CBD is never a precursor to THC. Perhaps the cited material does make that statement, but if that is the case, then it should be explained in the article, with appropriate citation. Chondrite 20:45, 6 August 2006 (UTC)
Percents and times
This article said that HU-210 is 100-800 times as powerful as THC. the HU-210 article says it's 100-800 percent more powerful! Which is it? I brought this article in line with the "main" one (i.e., HU-210), but couldn't find any confirmation one way or the other in independent sources. Then again, I'm not a biochemist. Anyone? --tgeller 05:10, 11 October 2006 (UTC)
i've read that it was sold on a pharaceutical research chemical website and it said it was 100x as potent i believe. yes, here is the link: http://www.marijuana.org/mydna10-12-05.htm
This article should be divided
This article is too long. It mainly deals with natural compounds of the cannabis plant and many of the compounds mentioned in the Table of natural cannabinoids does not bind to the cannabinoid receptors. In the scientific literature the term cannabinoid includes all chemicals that bind to the cannabinoid receptors (natural and synthetic cannabinoids, cannabinoid agonists and antagonists, like rimonabant). Synthetic cannabinoids are much more potent than natural ones. Synthetic cannabinoids are important research tools and many of them have been shown to have therapetic potential and are in drug development, which makes them more interesting and important than natural cannabinoids. I suggest that this article will be divited into sections:
- Natural cannabinoids (of the cannabis plant)
- Synthetic cannabinoids
--Tanevala 15:28, 19 November 2006 (UTC)
Go for it, SqueakBox 18:15, 19 November 2006 (UTC)
- Readable prose at Cannabinoid is approximately 20K, and so by article size guidelines it should not be split. There's plenty of room to expand the article before a split is needed. Chondrite 17:12, 20 November 2006 (UTC)
Cannabinoids and parkinson
I Oppose the merge on the grounds that cannabinoids are a sufficiently large category of drug to warrant their own article separate from the endocanainoid system. --Selket Talk 22:37, 16 February 2007 (UTC)
If this is the page to discuss the merging-I oppose
if someone wants to point out the lack of valid point in legislature (what would be the only reason for merging I can think of) then there are (I assume) articles dealing with this specific issue Okyea 01:48, 20 March 2007 (UTC)
I OPPOSE the cannabinoids themselves should be LINKED to the endogenous system page yes but merged, definitely not. Too large and sufficiently different in content (i assume based on knowledge of the system i have not checked the article)
Opposed- This article is about chemicals not systems. Ccroberts 04:55, 5 May 2007 (UTC)
I Oppose the merge for the reasons already stated - there's far too much non-overlapping information. St3vo 18:44, 12 October 2007 (UTC)
I oppose it also, even though they are closely linked in scope. Perhaps a for further information tag should be placed. Rhetth 05:10, 23 October 2007 (UTC)
- Great idea. I put a "Details" link in the lead of the "Endocannabinoid" section and summed up the Endocannabinoid System article as well as I could. Does that satisfy everyone re: the proposed merge?St3vo 19:57, 23 October 2007 (UTC)
What is meant by the second column in the table of natural cannabinoids. What are they meant to illustrate? Whats up with the unpaired oxygen? Is it negativly charged or what?
188.8.131.52 14:39, 2 March 2007 (UTC)
It's just the carbon-oxygen backbone (the connectivity) of the molecules to illustrate the cyclization pattern. Real chemical structures are give for the compounds itself. Cacycle 03:01, 20 March 2007 (UTC)
CBD is psychoactive
Anything that crosses the BBB is psychoactive. CBD certainly does. In the same paragraph that the article says it doesn't the article reads "Medically, it appears to relieve convulsion, inflammation, anxiety, and nausea. CBD has a greater affinity for the CB2 receptor than for the CB1 receptor. It is perceived to have more effect on the body." So how is not psychoactive? All of the other cannabinoids are too. —Preceding unsigned comment added by 184.108.40.206 (talk) 01:35, 12 September 2007 (UTC)
- Nearly everything that crosses the blood-brain barrier is NOT psychoactive. I suggest that you read the article psychoactive drug. Only anxiety effects would count as psychoactive effects, but this is nothing that you could easily notice, and definitely not the kind of psychoactivity of THC. Almost all cannabinoids are not known to be psychoactive. Cacycle 02:21, 12 September 2007 (UTC)
- CBD is most certainly a psychoactive compound. It is currently being studied as an alternative treatment for schizophrenia, having antipsychotic properties, and as antipsychotics are considered to be psychoactive, CBD certainly must be as well. Any compound which has a measurable effect on the brain by binding to neurotransmitter receptor sites is psychoactive. CBD binds with CB1 and CB2 sites as an antagonist, directly competing with endocannabinoids(created by the body) as well as delta-9 THC(edit: further reading shows this is not precisely true, it is an indirect antagonist, but the reasoning holds true). Any substance which binds to a receptor site directly interferes with the brain's ordinary functioning, however small or large the effect, by either agonistic activity, antagonistic activity, or simply blocking of that receptor's ordinary function. That is the definition of a psychoactive drug, or at least what is taught in pharmacology/related classes in university. To put it another way; although there is a temptation to define 'psychoactive' as a property of euphoric or hallucinogenic drugs, this is a definition derived from pop-culture, not science, and is incorrect for a scientific article on the subject. Finally, the actual wiki page on the CBD compound lists it as a psychoactive drug, and this small entry is in direct contradiction with the primary article.HarleArmistice (talk) 15:40, 14 December 2009 (UTC)
The intro paragraph should be re-written -- too influenced by the weed
When I read the intro paragraph, I think that cannabinoids refer to the reefer, and that isn't entirely correct. Unless there's some major opposition, I'm going to re-write it to reflect the edogenous and exogenous nature of the chemical. Rhetth 05:13, 23 October 2007 (UTC)
Is THC-C4, the analogue of THC with a four carbon chain instead of five, be agonistic, antagonistic or not active at all? —Preceding unsigned comment added by 220.127.116.11 (talk) 03:59, 21 December 2007 (UTC)
Other CB sources?
- I don't believe that's true; to my knowledge, the only natural source of phytocannabinoids is cannabis (see Di Marzo, et al. 1998). However, many cannabinoid compounds such as anandamide and THC are also active at TRPV1, the receptor for capsaicin (the chemical responsible for the "spice" of hot peppers such as the jalapeño). Does that help? St3vo (talk) 22:00, 13 February 2008 (UTC)
- TRPV1 is not considered part of the eCB system, but rather the endovanilloid system. That said, the systems overlap quite a bit in distribution and ligands (in fact, the first endogenous TRPV1 ligand was the endocannabinoid anandamide). For a good review, see Starowicz, Nigam, and Di Marzo, 2007. St3vo (talk) 16:56, 29 February 2008 (UTC)
Medically, it appears to relieve convulsion, inflammation, anxiety, and nausea. CBD has a greater affinity for the CB2 receptor than for the CB1 receptor. It is perceived to have more effect on the body."
Yet in the cannabidiol article, it says that it does not bind to either receptor.
Is there a scientific term for butane extracted cannabinoids?
- It does not matter how cannabinoids are extracted, they do not change their structure. You just get less other contaminants in your complex mixture. Cacycle (talk) 23:11, 15 May 2008 (UTC)
That's not true. Isocannabinoid molecules look completely different than cannabinoids and I believe they have a different psychoactive effect. —Preceding unsigned comment added by CosmologyProfessor (talk • contribs) 06:30, 16 May 2008 (UTC)
on the order of over 60 cannabinoid naturally occurring cannabinoid molecules / chemicals in the marijuana plant?
If you do a google search for "60 cannabinoids", over one hundred and fifty thousand article hits appear, many claiming that marijuana has 'over 60 cannabinoids' (unique chemicals to the cannabis plant in nature) and anywhere from 200 to 400 other chemical ingredients. The article here doesn't touch on anywhere near that many, or even mention the order of how many natural cannabinoids exist in the plant, the list if very small in comparison even with the synthetics counted among them. Have they all been classified? I doubt the synergistic activity of each one with the other has been studied in a way that is thorough enough to say they all lack psychoactive effect except THC. CBN, CBD & THCV have been shown to have a psychoactive effect when present in the brain with THC, for example. Though my main concern is the lack of the number given in the article in comparison to the number easily found through sources. Maybe it is so long as to require a 'list of cannabinoids' article? 18.104.22.168 (talk) 12:29, 25 October 2008 (UTC)
Under the Cannabidiol heading, there is a statement that:
Cannabidiol has no affinity for CB1 and CB2 receptors but acts as an indirect antagonist of cannabinoid agonists.
Yet shortly afterwards, a contradicting statement of:
CBD has a greater affinity for the CB2 receptor than for the CB1 receptor.
- I assume might be if we take the second writing of 'receptor' that what is instead meant is the indirect means of antagonism for CB2 is greater. Nagelfar (talk) 09:35, 25 December 2010 (UTC)
"The endocannabinoid 2-AG has been found in bovine and human maternal milk."
Perhaps a route to making a synthetic 2-AG agonist for weening human babies off of their mother's milk without the disconnect of a physical rejection. Toward the purposes of where there's perception that the primal life stage harbors the creation of psychological issues by such otherwise innocuous type of forced detachment pre-verbally and that such has a real existence in that school of therapy, and this type of empirical experimentation done for a help at proof to those theories in deep rooted psychology I possibly see as a reasoning for their delving into and undertaking. (where neuropsychology takes from neurobiology) Nagelfar (talk) 09:32, 25 December 2010 (UTC)
Cancer anti-tumor effects of cannabinoids
There have been a number of studies that have been performed with cannabinoids that have demonstrated potent anti-cancer effects. This 'Nature' review by Dr. Manuel Guzmán covers a number of them: http://americanmarijuana.org/Guzman-Cancer.pdf Shouldn't this be covered in this article? 22.214.171.124 (talk) 01:31, 12 April 2011 (UTC)
" natural occurence"
I have a combination of Latico-Bodig and Lou Gehrig's disease. My rilutek was increased from 30 mg to 50 mg because I inherited both diseases from my father (I took a gene test). I also am on my endocannabinoids which are providing new motor neurons through neuro-genesis through CB1s. I used to be on medical marijuana and never got stoned. I had these diseases since 2006 and was rediagnosed in April of 2012 finding a dangerous result when the neurologist did a electro-conductor test on my left leg. I take tai chi and kung fu and have a Chinese foot massage once a week. My endocannabinoids are healing my left foot and in the mean-time with my rilutek tremendously slowing down these diseases. I also lift weights three times a week and take yohimbe and levitra so I can have sex with my wife. I am Bisaya and my wife in Micronesian. I was born in Tampa, Florida and my wife was born in Oakland. I am a Baha'i by faith. — Preceding unsigned comment added by Hechavez (talk • contribs) 01:00, 31 May 2012 (UTC)
I've added a link to a blog authored by my organisation (Cancer Research UK) in the 'Further Reading' section, summarising the state of evidence wrt cannabis and cannabinoids. I suspect this may ruffle a few feathers but it is entirely evidence-based and, I hope, a useful addition to the page. If this violates any rules, feel free to amend, clarify or even delete :) — Preceding unsigned comment added by HenryScow (talk • contribs) 09:49, 26 July 2012 (UTC)
I've tagged this statement A significant number of cannabinoids are found in both Cannabis and Echinacea plants because it is not clear. Does it mean 'between the two, though shared by neither', or 'the two plants contain many of the same cannabinoids'?
This needs to be made clear, and more information is needed which is the reason for the tag. Which cannabinoids do they share? If none, how many cannabinoids does each plant offer to make up the "significant number"? Personally, I would love to know. Thanks. petrarchan47tc 20:15, 3 January 2013 (UTC)
- For now, I removed the "are found in both" statement and the tag. petrarchan47tc 20:27, 3 January 2013 (UTC)
subsection discussing one US Patent from NIH
I deleted the section discussing one patent. There are over 200 issued patents in the US alone covering cannabinoids. http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO2&Sect2=HITOFF&p=1&u=%2Fnetahtml%2FPTO%2Fsearch-bool.html&r=0&f=S&l=50&TERM1=cannabinoid&FIELD1=ABTX&co1=AND&TERM2=&FIELD2=&d=PTXT
table of "natural cannabinoids"
the article discusses phyocannabinoids and another one on endocannabinoids, then at the bottom, a "Table of natural cannabinoids". The table is not sourced (is it copied from somewhere?) and it is not clear what is phyto- and what is endo-. I think perhaps this table should go, as wikipedia is not a textbook.... what do you think? Jytdog (talk) 01:59, 21 April 2013 (UTC)
Alkylamides and catechins are not cannabinoids
The term cannabinoid is reserved for those natural olivetol based products occurring so far only in cannabis, as well as for their endogenous and synthetic analogs with considerable affinities to cb receptors. Catechins and alkylamides are therefor not cannabinoids. They can be named more appropriately cannabimimetics or cannabinomimetics, as they mimic the effects of cannabinoids, but are not exclusively functionally or chemically related to the cannabinoids in hemp.(Osterluzei (talk) 11:58, 25 December 2013 (UTC))
OK, I have reedited the text without deleting most of it. We have to be a little more professional about these terms we use. And I have come up with pertinent expression that are appropriate to the subject matter. I have taken some of the conceptual ideas from the German language entries on the topic. I will watch this from now on like a hawk. Some statements about solubility etc. actually do not belong in here, but I have nevertheless left them in; the don't need any citations (e.g. the sky is blue). If someone has to make more edits, who has the qualifications to do so, please correct me.
- It really doesn't matter whether you have personal knowledge in the subject if your changes can't be supported by WP:RS. One always needs to include a reference to a recognized reliable source when adding to or changing an article in this way.~ RS uses "phytocannabinoids", so we are obligated to do the same. petrarchan47tc
The entries must be restructured anyway. My references were fine, you can read the full text at research gate. I would adapt them to other language entries. Or at least use the expression "cannabinoids from other plants", rather than repeating the text on the classical cannabinoids. General statements about solubilities of phytocannabinoids as this is one here do not make sense, since tea catechins are also listed as phytocannabinoids and they are very well soluble in water without forming phenolates. Or then use as in the German version: Cannabinoidmimetika aus anderen Pflanzen (cannabinoidmimetics from other plants, and define on which receptor they are cannabinoids to displace the notion that a cup of tea will get us high; that binding affinity is very low even towards cb2.... and suspect). In the German version, the disposition is acceptable. I still think cannabimimetics is the better term.
"Phytocannabinoids (also called natural cannabinoids, herbal cannabinoids, and classical cannabinoids)", is not a correct statement. I have nothing against the term "phytocannabinoids" per se, although it lends to confusion when mentioned in connection with a tea beverage! Alkylamides and catechins are not classical cannabinoids! And the table chemical structures to the right is only displaying the cannabinoids from cannabis (these are the classical cannabinoids). Also the alkylamides of echinacae are not concentrated in the stems, just certain types of those alkylamides. The highest concentrations of alkylamides can be found in the roots and the flowers of the plant. The achenes are indeed a plant part where these compounds overall can be found in high concentrations. Only the "C11 diene-diynes were highest in vegetative stems". To conclude that most of the alkylamides can be found in the stems is thus wrong. That article reflects relative concentrations. The authors of these texts often don't read the articles. Also only some alkylamides show affintities to cb2. As it is now it looks like all those alkylamides described by the Bauer Wagner group are cannabinoids. That is not a correct statement. Also about this paragraph: All-natural cannabinoids are derived from their respective 2-carboxylic acids (2-COOH) by decarboxylation (catalyzed by heat, light, or alkaline conditions). OK, let's stop playing semantics, but this statement above then is not correct. It only refers to some of the classical cannabinoids. Not all natural cannabinoids are derived from their respective 2-carboxylic acids (and that is why I have these reservations). For example a more recent research on cannabinoids has also found non-phenolic type sesquiterpenes to be "dietary cannabinoids". So, for these the above statement is certainly not correct as a general statement about "herbal cannabinoids". So, I go along with you to call anything a cannabinoid that binds to the cb1 or cb2 receptor even tea catechins. But still, a revision will be required. It is interesting, more recent researcher of dietary cannabinoids, such as Prof. Gertsch from the ETH Zürich also uses cannabinoid in the title of a research paper on beta-caryophyllene, but in the text itself he uses "cannabimimetic effects in vivo". I therefore view cannabimimetic as the better term. Overall, the English language entry on cannabinoids is not good at all, I find. Because of the reasons mentioned above. I would think Prof. Gertsch from the ETH would likely side with you to call all these substances cannabinoids but as a consequence other statements need to go. Let me consult with him and ask about that. Wouldn't you agree? By the way, it also wrong to list Sativex among the synthetic cannabinoids. THC and CBD, as it says in the text, are isolated from Cannabis. So these are natural cannabinoids, but in that notion of "natural and herbal", they were viewed as synthetics.
(Osterluzei (talk) 02:48, 28 December 2013 (UTC))
OK. Introduced citations, where they were needed. And did not affect the overall content. I think the structure is much better now. Most of the entries on phytocannabinoids only related to the classical cannabinoids, and so I avoided confusion through a logical disposition. Most papers still consider the non-cannabis cannabinoids cannabinomimetics, but I went along with the general term for cannabinoids. It looks much better now...Don't revert this to the old version, please, otherwise one loses needed citations! (Osterluzei (talk) 06:02, 28 December 2013 (UTC))
Definition of cannabinoid and ligand functionality
The article starts "Cannabinoids are a class of diverse chemical compounds that activate cannabinoid receptors..." so it sounds like the substance has to be a agonist if it's about activating and not blocking or dampening the receptors like antagonists does. But many cannabinoids are antagonists on the cannabinoid receptor so shouldn't the definition say something else than "activate cannabinoid receptors".--Custoo (talk) 21:40, 14 February 2014 (UTC)
weak (low) affinities
The affinities of the two recently discovered cb1 and cb2 ligands yangonin and EGCG are very weak for either the cb1 and cb2 receptor, in comparison with the traditional cannabinoids and endocannabinoids. In the case of yangonin, I have to read the literature more carefully. I believe, it has not been determined yet whether yangonin is indeed an agonist.(Osterluzei (talk) 14:24, 18 March 2014 (UTC))
intracellular lipid signaling
Deletion of Cochrane Review conclusions
Nothing in MEDRS says that we only use the single most recent review, and you will find precious few articles in Wikipedia that do that. In fact, WP:NPOV, which is POLICY, requires that we present "fairly, proportionately, and, as far as possible, without bias, all of the significant views that have been published by reliable sources on a topic."
- The problem is that you tried to use an older review to refute findings from a more recent one. That is the opposite of how science works. petrarchan47คุก 05:15, 9 October 2015 (UTC)
Immune system and cannabinoids
I am planning on making as many edits as I possibly can to better this article and I have read the missing components needed to improve it. I hope my contributions are sufficient, but feel free to critique my contributions of some of the research I have found. Please make sure you leave a detailed notice as to why revisions are made to some of the edits I will be doing. In particular, I will be making a new sub section pertaining to how cannabinoids react or interact with the Th1 and Th2 immunological pathways. Also, I will be posting information on research done and the derived results.
- Exciting! Please make sure you source per WP:MEDRS - reviews in the biomedical literature or statements by major health authorities; please also make sure the content is precise; cannabinoids are a broad class of compounds. Jytdog (talk) 04:25, 2 May 2016 (UTC)
Here is the content promised above; it was added in this dif.
Vmartinex18, please do see WP:MEDHOW for formatting refs; including the PMID in citations is really, really important for helping other editors look at, and access your sourcing. You don't have to use the citation templates but they are easier in some ways. But even if you hand-format citations, please include the PMID. For the 1st ref below it is PMID 10843702. (the Wikipedia software automatically formatted that link; I didn't have to do anything but type). If you then click on that link and go to pubmed, you find a) there is a free fulltext version of the article available which is getting to be the case more and more often, and b) if you look under "Publication Types, MeSH Terms, Substances, Grant Support" (down below the abstract - click on it to expand it) you see that this is a "research" paper. If it were a review, it would say "Review" there. This distinction is really important - see Wikipedia:Identifying_reliable_sources_(medicine)#Definitions. Reviews are secondary sources (and we prefer recent ones, from the past five years per WP:MEDDATE which is further down WP:MEDRS.
The sources you used here are really, really old. Everything should be in the last five years or so, especially in an actively researched field like this.
On top of that, this content makes broad claims about "cannabinoids" and above I had warned you to be try to be really specific. Change a few atoms on a compound and you can get really different activities; please make claims about the class of "cannabinoids" with great care and base them on very strong sources. (if you don't know what I mean by "strong sources" please ask). Thanks.
- Cannabinoids & The Immune System
The immune system is responsible for mediating the life, death, and differentiation of cells in order to provide protection to a biological system. On a cellular level, this is accomplished by the monitoring and balancing Th1 and Th2 response, which are categorized as two immunological pathways. The Th1 pathway is claimed to be responsible for protection against infections. Cannabinoids, categorized as a diverse set of chemical compounds that affect cannabinoid receptors, inhibit the Th1 response, therefore are classified as immune inhibitor; but the inhibition of the Th1 response allows the promotion of the Th2. Th1 pathways are responsible for generating essential defenders against pathogens, tuberculosis, Leishmania, and Legionnaire’s disease, which are known as free radicals. Therefore, the use of cannabis should be avoided when the Th1 pathway is needed to protects someone who has any of these diseases. In contrast, many autoimmune diseases have been correlated to an excessive Th1 immune response, such as multiple sclerosis, arthritis, Crohn’s disease, and diabetes 
- Interactions with Cytochrome P450
Cannabinoids have been linked to affecting the pharmacokinetics of other drugs. Cytochrome P450 isoenzymes are associated with metabolizing not only clinical drugs, but a multitude of cannabinoids as well. More specifically, cannabinoids are inhibitors of the enzyme P450. There are benefits pertaining to the cannabinoid inhibition of cytochrome P450. The production of pro-carcinogens from tobacco smoke cause cancer mutations to the P450 but if the P450 enzyme were to be inhibited by the cannabinoids it would minimize the smoking mutation caused by tobacco carcinogens since the carcinogens will not be able to bind and cause mutational changes to cytochrome P450. Many pharmaceuticals drugs are metabolized by way of the P450 enzyme. Therefore, when several unfortunate drug interactions occur it can eventually lead to drug toxicities if not metabolized by P450 due to an inhibition. There are six P450 isozymes: CYP1A2, CYP2C19, CYP2C9, CYP2D6, CYP2E1, and CYP3A4 that have been linked to drug metabolizing. These enzymes are considered heme-containing membrane proteins located in endoplasmic reticulum of many tissues. Rapid metabolization of drugs lead to a decrease in efficacy, but a drug with active metabolites is associated with increases in potency or toxicity due to enzyme induction. Therefore, inhibition of cytochrome P450 can affect drug potency. When an enzyme chooses between two drug inhibitors, the deciding factor pertaining to whether or the inhibiting drug will remove depends on the potency. In other words, predomination of the inhibitor is potency dependent. Thus, the less potent competing drug will be metabolized less frequently causing an increase in serum levels; thus leading to a significant possibility for toxicicity.
- 08:43, 2 May 2016 (UTC)