It depends on the amount he's dosing Chewey.
If he's up to a therapeutic dose of 1g a day, he should demethylate every 2 weeks to a month.
For maintenance dosing, 1 every 3 months unless there's some rec using going on. Then, more frequently.

:laughtwo: This is valuable information to know, and something I hadn't uncovered yet, so thank you so very much for sharing that Cajun.

*sigh* Let me breathe a minute......... This thread has the potential to turn into a wonderful brainstorming session, if we all let it happen. Cajun's probably the most professionally prepared for what we're attempting here, but we all bring valuable pieces to the table. If we suspend any hesitation and just jump right in we can help each other come to an understanding of what this wonderful medication is doing and find ways to improve the way it's being produced and administered out here in the trenches where so many of us are living. We can offer safe, economical and responsible ways to enhance people's lives with CCO.

And admit it, you love the learning too. :laughtwo: This is like a little slice of heaven to me. I've given myself permission to indulge in my love of immersive learning. Sweet! Thank you all for participating. :circle-of-love:
 
thinking about demethylation

It depends on the amount he's dosing Chewey.
If he's up to a therapeutic dose of 1g a day, he should demethylate every 2 weeks to a month.
For maintenance dosing, 1 every 3 months unless there's some rec using going on. Then, more frequently.



Cajun, if I may?

It makes sense that you set a baseline for things you'd be doing for demethylation - these particular steps carried out on a set schedule until you have the next round of tests done. You restructure the plan based on those results.

- How much is enough? Is there a point of overkill?
- When beginning, and leading up to that 1gram daily dose would you use demethylation practices daily?
- You say every two weeks to a month. For how many days?
 
Let me look into this further and get back to you. You make compelling points. I can see I'll be looking more closely at essential oil makeup today. :laughtwo:

Yeah, the BBB is still something of a mystery to me. I need a deeper understanding of the way it works as well as what happens to cannabinoids when they get into the brain. I feel like there's a piece of the puzzle hidden from view yet.

I'm certain that with brain tumors this is definately something you want, but the bio bomb mix should already be doing this, wouldn't you think? There's so much to learn. This study hall is going to help a lot.

And to throw another spanner in the works...

I've been trying to find which oils are highest in long-chain triglycerides/fatty acids and according to the Wikipedia article on fatty acids (so I'm not sure how accurate it is) LCFAs can't cross the blood-brain barrier! So does this mean using an oil high in LCFAs would be problematic for a brain tumor? Or does the brain tumor develop it's own blood supply and subsequently there's no problem?

There's too many variables!
 
Let me try to clarify the gist of my question, because it goes to a bit of a larger issue I've been pondering lately concerning the cannabinoid transport mechanism. So we know from Cajun that any particular illness is dosed best as close as possible to the illness. I think the example Cajun gave was that you wouldn't try to heal your foot by dosing oro-mucosally or sub-lingually. An extreme example, for sure, but it does get to the heart of the matter. And additionally what receptors should the cannabinoids best bind to in order to heal? So this is what occurs to me.

CB1 receptors are mainly found in the CNS, and largely congregated in the brain, while CB2 receptors are spread out much more in the overall body immune system. So if we are trying to heal issues related to stress, anxiety, insomnia, PTSD, neuropathic pain, neuropsychiatric diseases, etc., you would want to dose such that the cannabinoids would easily cross the BBB and target the CNS receptors, right? Maybe? But treating diseases that occur largely in the abdominal/thoracic areas would be best dosed rectally perhaps? We know this is often the recommendation of clinicians working to heal such diseases as liver and prostate cancers, even metastatic ones that are now creating tumors in bone marrow, lymph nodes, lungs, etc. Does this mean we are targeting the CB2 receptors to heal these conditions? Or are the CB1 receptors in the brain/CNS involved as well? Which would suggest crossing the BBB would be important for all diseases.

Okay, so maybe the above is a little simplistic of an analysis, and largely the result of my musings while hiking to the nearest Starbucks during coffee break time at work. But research has reported that we now have a better understanding of the cannabinoid signaling system (Marijuana: Current Concepts, Graydanus, Graydanus, Hawver & Merrick; Front Public Health, NIH, 2013 Oct 10; 1:42), which is leading to research involving the effect of cannabis on the above mentioned diseases. I just wish I had a better understanding of the signaling system, myself, and how it interacts with the endocannabinoid system. And where in the body.

Thoughts, or any links to further sources of information?

I would suggest that treatment should be based more on what you're trying to treat as opposed to where you're trying to treat it. If you look up Sharon Kelly you can find videos about her using cannabis oil to treat her cancer. She went with the suppository style method to treat lung cancer, if the route of administration was relevant to the location I would have thought that smoking/vaping would have been the way to go.

My impression is that in treating cancer you really want the cannabinoids to reach the cancer cells and induce apoptosis. In other diseases you may be trying to modify the immune system through the endocannabinoid system in which case you may not be targeting individual cells. However, these are just my thoughts, I have no evidence to back any of them up so I'm happy to be corrected!

I would expect these factors to be of greater importance when determining the route of administration, no?
 
I would suggest that treatment should be based more on what you're trying to treat as opposed to where you're trying to treat it. If you look up Sharon Kelly you can find videos about her using cannabis oil to treat her cancer. She went with the suppository style method to treat lung cancer, if the route of administration was relevant to the location I would have thought that smoking/vaping would have been the way to go.

My impression is that in treating cancer you really want the cannabinoids to reach the cancer cells and induce apoptosis. In other diseases you may be trying to modify the immune system through the endocannabinoid system in which case you may not be targeting individual cells. However, these are just my thoughts, I have no evidence to back any of them up so I'm happy to be corrected!

I would expect these factors to be of greater importance when determining the route of administration, no?

My understanding is that smoking/vaping as a dosing method is not able to achieve the concentration of cannabinoids necessary to achieve healing when dealing with cancer. Plus smoking is very efficient at bridging the blood brain barrier which would result in a higher level of euphoria than with, say, suppositories.

From what I have learned here, it seems both the location of the illness and the type of illness come into play when considering the right dosing method. For instance, CCO suppositories for prostate/liver/lung cancer, and tacking for brain tumors and perhaps esophageal cancer. And smoking is better to treat PTSD where bridging the BBB is important. At least that's how it looks to me based on what I've learned. No direct experience with treating anything yet, so I could be wrong.
 
And to throw another spanner in the works...

I've been trying to find which oils are highest in long-chain triglycerides/fatty acids and according to the Wikipedia article on fatty acids (so I'm not sure how accurate it is) LCFAs can't cross the blood-brain barrier! So does this mean using an oil high in LCFAs would be problematic for a brain tumor? Or does the brain tumor develop it's own blood supply and subsequently there's no problem?

There's too many variables!

Tumors do develop their own blood supply, but you raise a good point about the LCFAs not being able to cross the blood-brain barrier and how that might impact carrier oil choice. I don't recall coming across any mention of a specific oil choice for brain tumors. circuit was treating a brain tumor. Hmmmmm.... I believe he was using coconut oil, but I'm not certain. It's on my list of things to chase down.

The pleasures of a virtual space. I found a 3-hr video of a campfire on the riverbank.

image9550.jpeg


I can load it onto the iPad and listen to instructional videos I'm taking notes from on the phone. It feels for all the world like I'm sitting out along some river. :laughtwo: Yes, I've a very healthy imagination. Lol!
 
It depends on the amount he's dosing Chewey.
If he's up to a therapeutic dose of 1g a day, he should demethylate every 2 weeks to a month.
For maintenance dosing, 1 every 3 months unless there's some rec using going on. Then, more frequently.

Hi Cajun,

When you quote the times given above, lets say, every two weeks to a month. What exactly does that mean? Should he follow the demethylate program for a single day during that time period?

He is smoking a fair amount as it helps him lots
 
thoughts of an obsessive researcher

It just hit me that what I personally need to understand is the benefits of having the cannabinoids in the

- Central Nervous System (on that side of the blood-brain barrier)
- Circulatory Sstem
- Lymphatic System

Also, once in those systems do the cannabinoids remain within those systems or do they migrate throughout the three systems seeking out cells?

I don't know if that made sense to you guys, but it did to me. :laughtwo:

Considering that THC is not very effective at attaching to receptors it suggests more opportunity for locating tumor cells. Of course the other components obviously play an important role in the attachment.....

Slow down Susan. One rabbit hole at a time girl. :laughtwo:

I better catch at least a couple hours of sleep. Lol! Carry on. :battingeyelashes: :love:
 
Tumors do develop their own blood supply, but you raise a good point about the LCFAs not being able to cross the blood-brain barrier and how that might impact carrier oil choice. I don't recall coming across any mention of a specific oil choice for brain tumors. circuit was treating a brain tumor. Hmmmmm.... I believe he was using coconut oil, but I'm not certain. It's on my list of things to chase down.

Sue, coconut oil makes sense for brain tumors, as it is a MCFA. I also just checked my notes from Cajun's cancer thread, and LCFAs were recommended for prostate cancer. Makes sense to me, as there doesn't seem to be a need for the brain to be involved to treat that cancer. In fact, it's better if it isn't, to reduce the psychoactive effect.
 
thoughts of an obsessive researcher

It just hit me that what I personally need to understand is the benefits of having the cannabinoids in the

- Central Nervous System (on that side of the blood-brain barrier)
- Circulatory Sstem
- Lymphatic System

Also, once in those systems do the cannabinoids remain within those systems or do they migrate throughout the three systems seeking out cells?

I don't know if that made sense to you guys, but it did to me. :laughtwo:

Makes perfect sense to me. That is THE question in my mind that we need to get a handle on. It's at the heart of the issue about how and where in the body do you treat for various illnesses and cancer types.


Considering that THC is not very effective at attaching to receptors it suggests more opportunity for locating tumor cells. Of course the other components obviously play an important role in the attachment.....

Sue, did you mean CBD? THC seems to bind relatively easily to both CB1 and CB2 receptors, per Medicinal use of cannabis: History and current status by Harold Kalant, (Pain Res Manage Vol 6 No 2 Summer 2001). The following table is from that paper:

Cannabinoid_Receptor_Table.jpg


But I also wonder if the cannabinoids also travel freely to cancer sights. They must to some degree, else how would CBD be so effective in it's own right, beyond just a modulator of THC?

Cannabinoid Signaling... from the earlier paper I referenced. That plays a role in here somewhere. Supposedly scientists understand it. I need to find out what they understand.
 
My understanding is that smoking/vaping as a dosing method is not able to achieve the concentration of cannabinoids necessary to achieve healing when dealing with cancer. Plus smoking is very efficient at bridging the blood brain barrier which would result in a higher level of euphoria than with, say, suppositories.

From what I have learned here, it seems both the location of the illness and the type of illness come into play when considering the right dosing method. For instance, CCO suppositories for prostate/liver/lung cancer, and tacking for brain tumors and perhaps esophageal cancer. And smoking is better to treat PTSD where bridging the BBB is important. At least that's how it looks to me based on what I've learned. No direct experience with treating anything yet, so I could be wrong.

Having looked back at our posts I think we are saying similar things in different ways! Admittedly, I didn't know whether vaping could be used for treating cancer in any shape or form, I was just trying to use it as a (very poor) example.

Sue, coconut oil makes sense for brain tumors, as it is a MCFA. I also just checked my notes from Cajun's cancer thread, and LCFAs were recommended for prostate cancer. Makes sense to me, as there doesn't seem to be a need for the brain to be involved to treat that cancer. In fact, it's better if it isn't, to reduce the psychoactive effect.

However here I see something I don't quite get. On one hand tacking is for brain tumors and on the other hand MCFAs are for brain tumors? Can you tack using CCO in a carrier oil? Or is it just different users suggesting different methods for treating the same condition?

I've been spending a lot of time trying to understand what's going on with these carrier oils. I'm not sure if you guys find the same thing happens but when I start searching for something I open a bunch of tabs then start going through them, then find something else interesting to search for in one of them, open a bunch of new tabs, forget why I opened the first bunch of tabs, close them, realise there was something important in one of them, go back for ages trying to find it again, and so on so I'm not sure how much of this I can put together right now... (Is there a facepalm emoticon?!)

Anyway, I've been looking at lipospheres (not to be confused with liposomes) and in particular Piperene-Pro-Nano-Lipospheres. If you search for "Advanced Piperine-Pro-Nano Lipospheres for Enhancing the Oral Bioavailability of Cannabidiol" you can find some research showing that the lipospheres on their own increased the AUC and Cmax of CBD. The piperene increased those even further as this appears to be a cytochrome inhibitor which may be worth just taking with the cannabis oil like apigenin and amentoflavone (assuming it doesn't interact with any medications). This patent I believe is linked to the research and states:

Results:

1.1 The results indicate that in rats the Piperine-PNL elevated the bioavailability of CBD by 6 fold (Table 13, Fig. 15). The contribution of the Piperine component was 2 fold increased bioavailability due to its phase-II metabolism inhibition.

AUC (h*ng/mL) Cmax (ng/niL)
90±21 39±8 CBD
300±95 (*) 137±43 (*) CBD-PNL
570±23 (*" ) 170±13 (*) CBD-Piperine-PNL

This got me thinking about all these different methods and routes of administration as well as how cancer can metastesize.

From what I understand, all of these different routes of administration are at least partly to improve bioavailability, correct? I mean, suppositories and tacking both try to bypass the first pass metabolism of the liver so in the end they try to get the various compounds in to the bloodstream directly just at different locations?

The LCFA carrier oils are also meant to improve the bioavailability, however, assuming you get the compounds to be transported with or in the same way as the carrier oil in to the lymphatic system then this route would also have some effect on the lymphatic system which I believe is one path that cancer can metastesize. Having said that, I assume there are receptors there which means you may need a larger dose as some of the cannabinoids may bind there before entering the bloodstream.

I also only just found out that the lymphatic system appears to extend to the brain (I believe it was only just discovered recently).

Anyway, what I'm trying to get at is that perhaps using carrier oils and getting the compounds (cannabinoids/terpenes/etc.) in to the lymphatic system can serve two purposes, improved oral bioavailability and a better chance of cannabinoids connecting with cancer cells moving through the lymphatic system. It may be worth including some properly prepared oral cannabis oil with other protocols "just in case". To be clear, I am not suggesting it should replace something that's working, only compliment it.

This may be a good usage case for PsyCro's extraction method as it seems to be efficient with yields and capable of treatment in it's own right. I'm not sure if it even needs any further processing such as this liposphere concept, perhaps the extraction method does something so that the compounds are more efficiently transported to the lymphatic system as opposed to a CCO added to a carrier oil?

I wish I could put together a more coherent and well referenced post, I do have more information that's difficult to refer to but for now perhaps I can bounce this off the more experienced minds around here and see what they think! Hopefully I'll have more information to add soon and can improve on it then...
 
We don't have to get all the information into one post fookinel. :laughtwo:

Good morning all. I'm loving the discussion. Lots to feed the brain on as I run around with first-of-the-month chores with the daughter. This is my busiest day of the month, so I may be more scarce than I care to be.

SlowToke, my statement about the binding affinity of THC was gleaned from Dr. Ethan Russo's talk for the Society of Cannabis Clinicians last December.

Minor Cannabinoids and Cannabis Terpenoids

Dr. Russo's a board-certified neurologist and psychopharmacology researcher, and former Chairman of the International Association for Cannabinoid Medicines. At 27:00 into the video he says that THC is a "low potency agonist at both CB1 and CB2 receptors. He went on to explain that although that may seem counterproductive it's because too much would overwhelm the system. In his words

"This is a homeostatic system. It needs a gentle nudge. It doesn't need a full-blown push."

It set me to thinking about how some doctors treating patients with cannabis are coming to the conclusion that a better therapeutic level might be somewhere in the 300mg a day dose instead of the one gram a day everyone's pushing for and straining resources to reach.

I still haven't watched all of this one. I keep taking too many notes. :laughtwo:

I'd have posted the video here, but I can't seem to make that work today. If someone else can get it posted I'd appreciate it. The video is just overflowing with pertinent information.
 
Let's see if I can post it...

Minor Cannabinoids and Cannabis Terpenoids on Vimeo

Ok. Cool!

Sue, yes, I know of Mr. Russo. Kind of hard to study this stuff without running into him repeatedly! Thanks for the clarification on the receptor issue. I'll have to wait until tonight or this weekend to watch the video. These videos eat up my available data like wild, so unfortunately I'll have to wait until I'm home on my network.
 
Having looked back at our posts I think we are saying similar things in different ways! Admittedly, I didn't know whether vaping could be used for treating cancer in any shape or form, I was just trying to use it as a (very poor) example.

However here I see something I don't quite get. On one hand tacking is for brain tumors and on the other hand MCFAs are for brain tumors? Can you tack using CCO in a carrier oil? Or is it just different users suggesting different methods for treating the same condition?

I've been spending a lot of time trying to understand what's going on with these carrier oils. I'm not sure if you guys find the same thing happens but when I start searching for something I open a bunch of tabs then start going through them, then find something else interesting to search for in one of them, open a bunch of new tabs, forget why I opened the first bunch of tabs, close them, realise there was something important in one of them, go back for ages trying to find it again, and so on so I'm not sure how much of this I can put together right now... (Is there a facepalm emoticon?!)

Yes, I agree we're close on our thoughts, but I wanted to clarify that the it's not just the illness, but also the location of the illness. You're post might have implied that, but it wasn't obvious to me. Concerning your brain tumor thought, that's a good point. I'll have to circle back with Circuit to get a clarification. And your right about the open tabs! It's easy to get lost!

You've got some excellent thoughts in the rest of you post... I will need a little time to digest it, but thanks for sharing all the information! :thumb:
 
We don't have to get all the information into one post fookinel. :laughtwo:

Okay, point taken :)

It set me to thinking about how some doctors treating patients with cannabis are coming to the conclusion that a better therapeutic level might be somewhere in the 300mg a day dose instead of the one gram a day everyone's pushing for and straining resources to reach.

I've heard this as well, suggestions that the 1 gram/day may not really be needed. Of course I don't need to point out that bioavailability needs to be considered :)
 
I've heard this as well, suggestions that the 1 gram/day may not really be needed. Of course I don't need to point out that bioavailability needs to be considered :)

I wish when researchers start suggesting dose strengths that they would be more specific about what conditions they are referring to. Will this dose work as well for cancer as it does for PSTD or some other condition? Who knows? In fact, it seems that fighting actual cancer, as apposed to treating the conventional treatment side effects, seems to be rarely discussed, outside of clinician discussions. At least from what I can find. Another result of prohibition, I suppose. At any rate, I'll remain skeptical until a number of folks take one for the team and treat an aggressive stage IV cancer with less than 1g CCO per day to see what happens.

I assume that they're being taken orally and not as a suppository?

Yes, that's right. Sorry I wasn't more clear.

Hey Sue, I watched about half of Russo's talk on cannabinoids/terpenes last night before I had to crash. Good Stuff! I need to go back to the beginning and start taking notes!
 
So to add a bit more on to my last post on the previous page, I'll provide some more information for people's thoughts...

This pages states:

In the summer of 2015, a US laboratory performed some of the first tests ever known to be conducted, on cannabidiol absorption into human intestinal cells. The results were astonishing. Utilizing a mixture of hemp oil, black tea and select lipids, and processed with a patent-pending technological method, resulted in intestinal tissue CBD permeability 325% higher than CBD mixed with black tea and water. And when that same mixture of hemp oil, black tea and select lipids, and processed with the patent-pending technological method is compared to the absorption of CBD and water alone, the absorption levels into the human intestinal cells rose to a 499% improvement.

Unfortunately I don't know what that "patent-pending" technology is and can't find it yet. Could it be sonication? Some other method of creating lipospheres?

This page suggests that linoleic acid (C18:2) is better than oleic acid (C18:1), which is better than linolenic acid (C18:3) in terms of bioavailability of halofantrine. Linoleic acid is found in high amounts in oils like some safflower oil, some sunflower oil, grape seed oil, and probably some others. Oleic acid is found in high amounts in olive oil, high oleic safflower oil, high oleic sunflower oil, peanut oil, and probably some others. Interestingly, flaxseed oil is lower in the two better fatty acids and is high in linolenic acid. However, I believe different compounds are more bioavailable with different carriers, so just because linoleic acid was best for halofantrine it doesn't mean that linoleic acid is best for all compounds.

To touch on that further, this page suggests that olive oil resulted in the highest amount in the lymphatic system. There is also a link on that page to the full text version and the full text version has more information about the composition of the fats used in the test. It shows that corn oil is much higher in linoleic acid and that olive oil is much higher in oleic acid yet olive oil was better (which illustrates that while linoleic acid may be best for halofantrine it may not always be best).

Combining this information with how PsyCro's method uses olive oil I've decided to combine the CCO with olive oil and lecithin to get the person I'm trying to help started on CCO sooner rather than later! The olive oil is easy to get, it should be able to be slightly heated to help mix with the lecithin, and will hopefully significantly improve oral bioavailability (ideally I want it to be as bioavailable as a suppository which I can't seem to get them to try). I may also see if I can stagger the doses of CCO away from other medications to allow for other supplements like apegenin and/or piperine for competitive inhibition.

Finally, just to annoy SweetSue and try to get everything in to one post :) This page is a patent that discusses microemulsions and gives an example of one for use with ibuprofen...
 
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