I think the literature suggests that effexor is mostly serotonergic (mostly, due to desvenlafaxine, which is much more adrenergic, being a metabolite) at lower doses, maybe below 150mg. But don't quote me on that! Some people have had great success with various forms of anxiety, as well as depression, with effexor.
So Cymbalta and Pristiq have adrenergic action at much lower doses than effexor. I may be wrong, but if pristiq is still on patent, that might be largely why people are given cymbalta, or higher doses of effexor (that is, as far as I know, tapered up to)
The effexor/pristiq withdrawal are somewhat notorious, as it would seem. There was a study that determined opioidergic activity in it. Hang on a bit..
So I could see why this would be. This study relates noradrenergic activity to analgesia:
https://link.springer.com/article/10.1007/s40263-014-0151-9
More evidence:
https://www.sciencedirect.com/science/article/pii/S0014299914003550
This means that SNRIs, mostly NRI activity, fights neuropathic pain indepdent from opioid receptor activation.
https://www.karger.com/Article/Abstract/345035
For example, if someone is critically injured, the "fight-or-flight" response occurs, and a shock period, though I'm not knowledgeable of the specifics. But this shock period may then render pain reduced? Any other advanced neuro people want to weigh in?
If i recall, cymbalta is actually FDA-approved for neuropathic pain, which means a lot.
So it doesn't really matter how it happens. If its effective and safe and prescribed in a reasonable manner by a doctor, then good.
