Nonsteroidal anti-inflammatory drugs (NSAIDs) alleviate pain by counteracting the cyclooxygenase (COX) enzyme.
In whole, the NSAIDs prevent the prostaglandins from ever being synthesized, reducing or eliminating the inflammation and resulting pain.
The newer specific COX-inhibitors are not classified together with the traditional NSAIDs, even though they presumably share the same mode of action.
Contrary to NSAIDs, which reduce pain and inflammation by inhibiting COX enzymes, paracetamol has—as early as 2006—been shown to block the reuptake of endocannabinoids,[2][3] which only reduces pain, likely explaining why it has minimal effect on inflammation; paracetamol is sometimes combined with an NSAID (in place of an opioid) in clinical practice to enhance the pain relief of the NSAID, while still receiving the injury/disease modulating effect of NSAID-induced inflammation reduction (which is not received from opioid/paracetamol combinations).
[11][12] Various serotonergic psychedelics, acting as serotonin 5-HT2A receptor agonists, have been found to be powerful and highly potent anti-inflammatory and immunomodulatory agents.
[19][20][21][22] Hence, the psychedelic and anti-inflammatory effects of serotonin 5-HT2A receptor agonists appear to be fully dissociable.
[31][34] A preliminary animal study found that chronic microdosing of LSD did not result in heart structure changes or valvulopathy in rodents.