I use caryophyllene and I source it from Copaiba essential oil. I use it sublingually so it can reach my brain and nervous system without my liver metabolising it and making it unusable for the specific target I am targeting which is CB2 receptors. These are expressed across many immune cell types. I also take it in gelatin capsules (5-6 drops) to target more of the body but specifically the gut which is intimately connected to the brain, nervous system and ME/CFS symptoms.
I take before bed and when I get up. I then take it every 3-4 hours or before and after activity. We know when we know if something will trigger your condition so use it like a preventative and PEM preventer by taking before and after. If resting and not doing anything to trigger ME/CFS symptoms take every 3-4 hours.
I did mix with MCT oil to dilute and it worked good. To save money I now just take it pure as I do not mind the taste, 1 maybe 2 drops. After 1-2 minutes so it can absorb under my tongue through the mucosa I take a drink or food to remove the taste. It is in fact a flavour deemed safe for consumption by FDA and EU food safety agency.
I have today read in an old thread that you asked before and I am sorry I did not answer you then. I was dealing with immune activation from the treatment at the time. The immune activation is part of the treatment we may possible go through as our immune system pulls back and is able to recognise any opportunistic infections and functionally attack those. If and when this is experienced I take the copaiba much less so not to get in the way of functional immune activation for about 7-10 days or when it feels like it is subsiding. It can be like a mild increase of ME/CFS and stress (see image below) can be a big trigger while like this so avoid. When I cut back I use before bed and when I wake, then maybe if I feel too bad to manage it. I used CBD a lot at first and it works synergistically with caryophyllene and was necessary at the beginning and infrequent now. I used the CBD sublingually.
Dragonfly CBD Cannabidiol Oil 1000mg 10ml | CBD | Boots
View attachment 48607
Bought this 100ml 6months ago and still have a bit under half left
Amazing non-cannabis cannabinoid: Caryophyllene 3 - YouTube This video covers science and a product made with caryophyllene.
It is shifting between these microglia states the CB2 agonist works, it also affects many other immune cells in a positive way for us (ME/CFS) but I want to keep this short for you, ask questions if you like just do it on any of my threads so I do not invade other peoples.
View attachment 48602
Microglia Polarization From M1 to M2 in Neurodegenerative Diseases - PMC (nih.gov)
Abstract
Microglia-mediated neuroinflammation is a common feature of neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS).
Microglia can be categorized into two opposite types: classical (M1) or alternative (M2), though there’s a continuum of different intermediate phenotypes between M1 and M2, and microglia can transit from one phenotype to another. M1 microglia release inflammatory mediators and induce inflammation and neurotoxicity, while M2 microglia release anti-inflammatory mediators and induce anti-inflammatory and neuroprotectivity. Microglia-mediated neuroinflammation is considered as a double-edged sword, performing both harmful and helpful effects in neurodegenerative diseases. Previous studies showed that balancing microglia M1/M2 polarization had a promising therapeutic prospect in neurodegenerative diseases. We suggest that shifting microglia from M1 to M2 may be significant and we focus on the modulation of microglia polarization from M1 to M2, especially by important signal pathways, in neurodegenerative diseases.
The protective effects of β-caryophyllene on LPS-induced primary microglia M1/M2 imbalance: A mechanistic evaluation | Request PDF (researchgate.net)
Abstract
Aims Neuroinflammation is observed as a routine characterization of neurodegenerative disorders such as dementia, multiple sclerosis (MS) and Alzheimer's diseases (AD). Scientific evidence propounds both of the neuromodulatory and immunomodulatory effects of CB2 in the immune system. β-Caryophyllene (BCP) is a dietary selective CB2 agonist, which deserves the anti-inflammatory and antioxidant effects at both low and high doses through activation of the CB2 receptor. Methods In this study, we investigated the protective effects of a broad range concentration of BCP against LPS-induced primary microglia cells inflammation and M1/M2 imbalance and identifying the portion of the involvement of related signaling pathways on BCP effects using pharmacological antagonists of CB2, PPAR-γ, and sphingomyelinase (SMase).
Key findings The protective effects of BCP on LPS-induced microglia imbalance is provided by the M2 healing phenotype of microglia, releasing the anti-inflammatory (IL-10, Arg-1, and urea) and anti-oxidant (GSH) parameters and reducing the inflammatory (IL-1β, TNF-α, PGE2, iNOS and NO) and oxidative (ROS) biomarkers. Moreover, we showed that BCP exerts its effects through CB2 receptors which overproduction of ceramides by SMase at middle to higher concentrations of BCP reduce the protective activity of BCP and results in the activation of the PPAR-γ pathway. Significance In conclusion, the low concentration of BCP has higher selective anti-inflammatory effects rather than high levels. On this occasion, BCP by modulating the microglia is able to have potential therapeutic effects in neuro-inflammation conditions and microglia cells such as MS and AD.
Taking too much may not be beneficial and many medications use the same enzymes to metabolise so may interact with many common medications.
If anyone is considering taking caryophyllene, caryophyllene oxide and Humulene containing substances please check medications- CYP3A | Phoenix Rising ME/CFS Forums
