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Re: Tolerance is just so low!! SLS

Posted by jay2112 on November 21, 2022, at 17:45:32

In reply to Re: Tolerance is just so low!!, posted by SLS on November 21, 2022, at 7:10:32

> > > I am having so much difficulty tolerating ANY venlafaxine. Even 1/4 of 37.5mg is giving me chest tightness. My tolerance of bupropion is much higher.
> > >
> > > Trying to restart the venlafaxine is proving difficult.
> > >
> > > Linkadge
> >
> > Try just taking the 37.5 and you should feel a bit better within a week or two. Do you have access to any benzo's, clonidine, or propranolol? Those will crumple the norepinephrine uptake. Propranolol, in particular, has made me actually tolerate and do not bad on Effexor. It won't work until you boost the Effexor so it can down-regulate the norepinephrine on it's own.
> These are excellent ideas - except, perhaps. for the clonidine. I have seen clonidine be robustly depressogenic. Of course, this might not be true when added to Effexor when psychiatric side effects emerge.

Thanks, Scott! I often figure that if I get acute effects, there has *got* to be another med to antagonize. I do hear you, moreso now, on the depressing effect of clonidine. It is the strength in which it lowers blood pressure, which we absolutely don't want to get too low...putting our lives in danger. I used to eat it like candy, on 300mg of Effexor, and I felt so blahhh. Mind you, 300mg of Effexor, and I have been up to 450mg's, just turned me into this weird catatonic state. I would sit there and stare at walls.

> > It's like taking a horrible tasting cough medicine, and then you get used of it.
> ...and maybe even like it.
> What are your beliefs regarding Effexor and NE receptor downregulation?
> In the early 1980s, it was considered putative that NE reuptake inhibitors downregulated NE *beta* receptors. At the time, this was believed to be the mechanism of action of tricyclic antidepressants. If this beta downregulation property of NE reuptake inhibitors is still advocated by neuroscientists, a beta-blocker like propranolol might make the most sense to ease into establishing higher dosages of Effexor. I like pindolol as an alternative. Aside from being a NE beta-blocker, it also blocks serotonin 5-HT1a axo-dentritic receptors. Pindolol has been found to accelerate an antidepressant response, and perhaps potentiate it.

I am certainly no expert in this area. My doctor once thought of Pindolol, but at the time, I was doing awesome on Serzone, with 75mg's of Effexor, and added 5ht2 blockade with a small dose of Risperidone. I have never really found my way back, as nefadozone has been taken off the market in Canada.I am on the spectrum, high functioning when medicated properly. One little supplement I find helpful during an "overload/meltdown", is Lecithin, which has choline in it, and is a mild but slightly helpful treatment.

> I get the impression that 150 mg/day is the lowest effective dosage of Effexor. Infequently, 75 mg/day. For me, Effexor does not produce its maximum antidepressant effect until I get to 300 mg/day, although the improvement was only partial. I found this dosage to be easily tolerable once established, despite having side effects after the very first dose of 25 mg. The side effects were of an uncomfortable stimulation. I had a sort of "warmth" and tingling in my head during my de novo treatment with Effexor. None of my subsequent trials of Effexor produced this effect. Also, I never experienced these side effects with Pristiq. Of course, this could have been an artifact of being treated with Effexor previously.

25 mg's of Effexor? Are you talking about the original, immediate release? OMG, I remember taking a 25mg tab, and having the hugest panic attack I *ever* had!! I remember the place...I was just going into a restaurant with a friend. And the *burning, seething* anger!! Yikes!!

> Speaking of side effects - and perhaps the receptivity to treatment - drug reactions are often changed by pre-treatment with another compound. Effexor was always helpful until I switched to it immediately after a trial of vortioxetine (Trintellix). It is a well-known and often-used experimental strategy to elucidate the mechanisms behind neuronal functions in normal versus manipulated biological states. This most often involves assaying receptor states to reveal how they control regional and global brain functions.
Yeah, I honestly have found dropping the dose after a fw weeks, then increasing a few weeks latter, then dropping, to be the only way I can really tolerate Effexor. I know...strange as F*&^$....but whatever gets us through the night, right?

> - Scott


Humans punish themselves endlessly
for not being what they believe they should be.
-Don Miguel Ruiz-




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