I have recently been sick, and I was running fevers for many days. During the fevers, I observed that I felt really high, but I had not consumed any cannabis, so I did a bit of research. Guess what, I wasn’t wrong. The sensation, that medical people would call fever delirium, is quite literally a natural high.
Natural cannabinoids are released into the body to give you a fever.
This explains the hot flash experienced after doing a fat dab.
After a dab, I feel so hot, to the point of sweating. Now I understand why.
The blast of THC causes a very temporary reset of our internal thermostat. I will need to take my temperature, directly after inhaling a dab. I always assumed that the hot feeling was imagined, but now I’m betting that I will record an actual spike in body temperature.
If you happen to be doing dabs, check your own temperature. See if there has been an increase.
I do note that only the first dab has a really profound effect, later dabs (after you are already blasted) don’t do it as much.
Now I understand the term “green fever”. Thanks brother 
decrease in temp apparently.
Cannabinoids can possibly bind to chemokine receptors as they have similar homology. The act of a fever or hot sensation is likely due to a direct or indirect activation of TRP receptors. Let me look I actually had a really interesting discovery.
EP3-deficient mice as well as mice selectively deleted of EP3 expression in the brain’s median preoptic nucleus fail to develop fever in response to endotoxin (i.e. bacteria-derived lipopolysaccharide) or the host-derived regulator of body temperature, IL-1β. The ability of endotoxind and IL-1β but not that of PGE2 to trigger fever is blocked by inhibitors of nitric oxide and PG2 EP33-deficient mice exhibit normal febrile responses to stress, interleukin-8, and macrophage inflammatory protein-1beta (MIP-1β). It is suggested that these findings indicate that a) activation of the EP3 receptor suppresses the inhibitory tone that the preoptic hypothalamus has on thermogenic effector cells in the brain; b) endotoxin and IL-1β simulate the production of nitric oxide which in turn causes the production of PGE2 and thereby the EP3-dependent fever-producing; c) other factors such as stress, interleukin 8, and MIP-1β trigger fever independently of EP3; and d) inhibition of the PGE2-EP3 pathway underlies the ability of aspirin and other Nonsteroidal anti-inflammatory drugs to reduce fever caused by inflammation in animals and, possibly, humans.[15][16]
Studies with mice, guinea pig, and human tissues and in guinea pigs indicate that PGE2operates through EP3 to trigger coughresponses. Its mechanism of action involves activation and/or sensitization of TRPV1 (as well as TRPA1) receptors, presumably by an indirect mechanism. Genetic polymorphism in the EP3 receptor (rs11209716[19]), has been associated with ACE inhibitor-induce cough in humans.[20][21] The use of EP3 receptor antagonists may warrant study for the treatment of chronic cough in humans.[22]
All I wanna know is…how does this relate to the thermoregulatory hijacking that is Cannabinoid Hyperemesis Syndrome, and the magical effects of hot water…?
I thought chs was really neem oil toxicity
Where’d you hear that? I haven’t heard of CHS symptoms being attributed to neem toxicity. I know a few people who suffer from it, and this is news to me.
I dont know anything about the subject but I could swear I saw something in an article I skimmed about chs and neem being related.
I could be totally wrong but I remember someone saying it at least lol
I’m definitely not saying it’s not true, just to be clear. I just haven’t seen that data.
I’ve heard asamax blamed as well. I’m really curious about the chs (or cvs) and hot showers too
Haven’t heard that one, either.
Neem and Azadirachtin are lower toxicity, but still affect the nervous system of bugs. It may do the same in humans causing CHS.
It’s why we switched to dormant oil (corn, cotton, canola) as a smothering agent along with alcohol and insecticidal soap when making homemade Green Cleaner for organic grows.
Now I cannot say that I haven’t seen neem and azadirectin being attributed to CHS symptoms, but that article was more sensasotional garbage than anything else.
They put the claims from anonymous readers claiming neem to be the real underlying issue in giant bold block print while the actual information from doctors (which contradicts the uneducated readers’ comments) is buried at the end in normal, small font. This article was designed to sensationalize what appear to be baseless claims.
If neem poisoning were really the culprit, there would likely be increased prevalence in areas where the use of neem consumption is more prevalent, like India, where it has been used in cooking for likely many thousands of years. This is not to say that neem is not toxic, but as the doctor interviewed in the article states, the thermoregulatory symptom of needing to feel hot (shower, dermal rub, capsaicin use, etc.), which happens to be very specific to CHS, is completely missing from the documented cases of neem and azadirectin poisoning.
While I will accept these theories as being possible, they are highly unlikely, and my mind has not been changed. Thanks for sharing the article @RedundantAlexithymia.
Trust me, it is not. Happy to discuss sometime!
That misconception is common though, and fair. I think I’d have had a tough time believing the details of CHS from a third party. It is that strange.
I’ve heard the same thing.
Not sure about the connection between this and CHS, but my theory is that Prostaglandins, and other molecular similar to Endocannabinoids, can promote or inhibit, the fever response, many of these molecules serve dual purposes which are barely understood. I briefly watched a lecture on CHS, let me see if it was posted publicly.