Extreme transpiration from venlafaxine (serotonin?)

[palmanita]

I'm currently on 300mg/d of venlafaxine and with the summer finally arriving these days, the already annoying increase of transpiration has become really extreme. Even when I just sit there and do nothing physical at all, drops of sweat are running down my forehead and neck, and the lightest sleeveless shirt becomes wet in probably less than half an hour. I don't feel hot at all, there is so much transpiration that for example my forehead feels quite cold.. good when I have a headache but so uncomfortable overall and socially irritating.

With 150mg/d a couple of years ago it was annoying too but not so bad as now. Was one of the main reasons for discontinuation though (the other has been feeling lethargic and physically weak - as I have adult ADD and get methylphenidate now, this isn't a problem anymore).

Problem is, I need some strong pharmacological antidepressant currently and probably for a long time. I even speculated about venlafaxine being dependence-forming, creating kind of PAWS in addition to the usual discontinuation shit. But this is another topic.

So:
- Is the serotonin itself responsible for the transpiration, or might switching the chemical help? If so, which one has the least incidence of this side effect?
- I know that anticholinergics reduce transpiration (or is this wrong?). Could a pheriperal one like butyl-scopolamine help?
- Or bupropion, being a nicotinergic antagonist? Would help me to reduce smoking but probably incompatible with Concerta? (a better one would be memantine, also helping with tolerance but unfortunately off-label, most docs don't prescribe it that way)

Thanks!

 

[Solipsis]

Adrenergic actions of antidepressants are implicated in causing ADIES, with adrenergic antidepressants like venlafaxine and bupropion having a higher propensity. Both alpha and beta blockers can help improve ADIES by blocking adrenergic output. Alfa blockers can cause dizziness and lightheadedness, and beta-blockers can cause bradycardia.2 Serotonergic antagonists like cyprohepatidine reduce sweating by 5-HT2a blockade in the hypothalamic region. However, all of these medications require regular administration. Sweat glands are unique in that their sympathetic postganglionic innervation, being cholinergic, can be blocked with anticholinergics like benztropine

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3931183/

cause with SSRI's: Serotonergic effect on hypothalamus or spinal cord

Yeah weird, the norepinephrine reuptake inhibition is ignored for venlaxafine here:

http://www.sweathelp.org/pdf/Drug-induced hyperhidrosis and hypohidrosis - Cheshire.pdf

But I guess there could be adrenergic involvement in addition..

 

[Jabberwocky]

I'm currently on 300mg/d of venlafaxine and with the summer finally arriving these days, the already annoying increase of transpiration has become really extreme. Even when I just sit there and do nothing physical at all, drops of sweat are running down my forehead and neck, and the lightest sleeveless shirt becomes wet in probably less than half an hour. I don't feel hot at all, there is so much transpiration that for example my forehead feels quite cold.. good when I have a headache but so uncomfortable overall and socially irritating.

With 150mg/d a couple of years ago it was annoying too but not so bad as now. Was one of the main reasons for discontinuation though (the other has been feeling lethargic and physically weak - as I have adult ADD and get methylphenidate now, this isn't a problem anymore).

Problem is, I need some strong pharmacological antidepressant currently and probably for a long time. I even speculated about venlafaxine being dependence-forming, creating kind of PAWS in addition to the usual discontinuation shit. But this is another topic.

So:
- Is the serotonin itself responsible for the transpiration, or might switching the chemical help? If so, which one has the least incidence of this side effect?
- I know that anticholinergics reduce transpiration (or is this wrong?). Could a pheriperal one like butyl-scopolamine help?
- Or bupropion, being a nicotinergic antagonist? Would help me to reduce smoking but probably incompatible with Concerta? (a better one would be memantine, also helping with tolerance but unfortunately off-label, most docs don't prescribe it that way)

Thanks!

Pretty much ALL SSRI antidepressants cause hyperhidrosis (excessive sweating). It is due to serotonin. If you are susceptible, -- pretty much ALL serotonergic prescription meds and recreational drugs will cause it.

Some people adapt, some don't.

 

[cr33py]

You would also have other unpleasant side effects while on an anticholinergic. I have even seen people on topiramate just for the sweating when it becomes extreme.

 

[Limpet_Chicken]

The butylbromide of scopolamine/hyoscine (same drug, hyoscine is the newer name, from Hyoscyamus, the genus in which are found the henbane plants) is a quaternary ammonium, and as such charged permanently, so it doesn't pass the BBB, its restricted to the PNS and ENS. I take it myself for some rather nasty GI issues of some sort, and I've never noticed any side effects at all, other than if its already there, intensifying drymouth, but even so its only noticeable if already having bad drymouth.

 

[theGirlWithBlueHair]

Pretty much ALL SSRI antidepressants cause hyperhidrosis (excessive sweating). It is due to serotonin. If you are susceptible, -- pretty much ALL serotonergic prescription meds and recreational drugs will cause it.

Some people adapt, some don't.

It's more likely that he is getting hyperhidrosis from the increased noradrenergic activity from the venlafaxine. It's an extremely potent NRI.

You would also have other unpleasant side effects while on an anticholinergic. I have even seen people on topiramate just for the sweating when it becomes extreme.

It would be nice if topiramate worked for withdrawal-induced hyperhidrosis... -_-

 

[Limpet_Chicken]

I didn't think venlafaxine had much at all in the way of 5HT effects, isn't it a selective NRI?

 

[theGirlWithBlueHair]

It's considered an SNRI, with dopamine reuptake inhibition in the higher dosage range. But it's noradrenergic effects are the most pronounced. But it does block the serotonin transporter.

 

[palmanita]

I didn't think venlafaxine had much at all in the way of 5HT effects, isn't it a selective NRI? / It's an extremely potent NRI.

Do you have a source for that? The usual opinion afaik is that it's SERT > NET >> DAT, and having a higher ratio than Cymbalta (9:1 SERT to NET). If it indeed is so potent on NE then I'll switch to another one. With the methylphenidate already being relatively potent in increasing NE levels I don't need any more (so unfortunate that isopropylphenidate pills are still so far away).

Will MPH & venlafaxine synergize or might the venla even reduce MPH's NE effects by competing for the receptors and reducing the inverse agonism of MPH?

The butylbromide of scopolamine/hyoscine (same drug, hyoscine is the newer name, from Hyoscyamus, the genus in which are found the henbane plants) is a quaternary ammonium, and as such charged permanently, so it doesn't pass the BBB, its restricted to the PNS and ENS.

So CNS activity is required to reach the sweating glands?

I'm currently taking 100mg of trazodone for sleep. Could try to replace it with an anticholinergic tricyclic and possibly reduce the venlafaxine dosage then as well.
Another option would then be Propanolol or carisoprodol, hopefully also lowering my naturally high heartbeat (usually at least 85-105 even at rest).

How potent is memantine as an anticholinergic? If it's potent enough and I could somehow manage to get it again, it'd be a promising option slowing down tolerance to both MPH and buprenorphine ...

 

[Limpet_Chicken]

Propranolol is only good, or rather, useable at all for physical symptoms, it does nothing to alleviate the rotten feeling. Clonidine, or tizaidine would be a better bet IMO.

And no the sweat glands are exposed to the periphery and
can be affted by quats like hyoscine butylbromide, idea is to preSvent the stuff getting to the CNS where it can fuckwith e.g memory.

 

[palmanita]

Thanks for your response, yeah - I've missed clonidine. Could indeed be the best choice and it has the plus of helping with some downsides from the MPH too. And it used to reliably cancel panic attacks.

In the meantime I'll give Buscopan a try.
It's just weird that sometimes I do have a dry mouth together with the hyperhydrosis.

But - now how about venlafaxine? Is it really more of a NRI than SNRI?

 

[theGirlWithBlueHair]

It's both. It's serotonergic effects are stronger. But it's a potent norepinphrine reuptake inhibtor as well, at high dosages. At 150mg of the xr, the first time I took it in a while, I got marked stimulation and mydriasis. I took a lot of it once, as well and was up for 24 hours, consistent with the pro-vigilance effects of noradrenergic activity, which was immediately terminated with pregabalin which blocks calcium channels - which decreases norephinephrine release.

What dose do you take?

I take a very high dose of IR bupropion and I get no noticeable noradrenergic effects from it, but with venlafaxine I get very apparent noradrenergic and dopaminergic effects at high dosages, consistent with its activity as a SNDRI.

 

[palmanita]

Currently 300mg but I'm thinking about going down to 150mg again, if the difference to 300mg consists mainly of more NE and a bit of DA or even switching to a different, more selective SSRI. For dopamine I'm on Concerta which already feels kinda dirty by itself after experiencing the more selective isopropylphenidate.. (Yes, venlafaxine causes slight stimulation at 75mg and mydriasis at 150mg for me too. But can't a huge increase of 5-HT alone cause mydriasis? As some weird side effect it exacrebates my attention deficit dose-dependently when it should do the opposite..)

Since I'm on 600mg of pregabalin too against social and general anxiety, if more NE means dampened efficiency from that then I have one more reason for switching the AD.

Interesting that you didn't get noradrenergic effects from bupropion. This drug is complex with all the active metabolites.. maybe NE builds up more when taking the ER formula, and/or daily with accumulating metabolites? From a single dose I didn't feel much, just a light strange feeling. Continued dosing wasn't spectacular too. But when I catched a cold and took 50mg ER dextromethorphan HBr (the maximal dosage is 150mg/d and there is no contra-indication like with SSRIs) at night for some days - also a dosage I usually wouldn't feel anything besides coughing less - the combo became a strong stimulant not completely unlike moderatly dosed 3-MMC with a tiny dissociative effect added just that it lasted all day long

 

[theGirlWithBlueHair]

yeah I take 150mg every 6 hours for the first 3 and then 4 hours for the last dose, and I take the 600mg dosage (it's not contraindicated for me as I am on two anticonvulsant medications - one for migraines and one for pain). Interesting, what pharmacological mechanism do you think is responsible for for the stimulant effects you get when combining the two?

 

[Pallyress]

Isn't venlafaxine a SNRI, rather than a SSRI? Methylphenidate also Inhibit reuptake of noradrenaline.

Wiki says Noradrenaline makes you sweat. https://en.m.wikipedia.org/wiki/Sympathetic_nervous_system

I don't understand ehy you are doubled up on N from both meds if your are combating anxiety. I don't know it in debt, but will it not basically jazz it way up, and make the relative more skewed comparez with dopamime/serotonin?

 

[theGirlWithBlueHair]

Venlafaxine is an SNDRI..

You are correct about your last point. That is a hell of a lot of norepinephrine :/ I wouldn't want to be on that combo every day. It sounds fun to combine recreationally, though.

Propranolol is only good, or rather, useable at all for physical symptoms, it does nothing to alleviate the rotten feeling. Clonidine, or tizaidine would be a better bet IMO.

And no the sweat glands are exposed to the periphery and
can be affted by quats like hyoscine butylbromide, idea is to preSvent the stuff getting to the CNS where it can fuckwith e.g memory.

Propranolol or any beta blocker would only make the sweating worse. It's actually a common side effect of them. By blocking the beta adrenergic receptors, it leaves the alpha adrenergic receptors entirely unopposed, and they are free to be activated by norepinphrine and epinephrine. This isn't a good thing to recommend. The alpha blockers or alpha 2 agonists would be work.

 

[Pallyress]

Yikes. That meds combination must be difficult to get off.

Also, I read the entire tread, realising my post said what everyone already had concluded lonh before. Captain Obvious at your service!

OP: my experience with prescribed methylphenidate was that it felt dirty and gave me a lot of general anxiety. I also crashed when it wore off, and in the morning I felt like my body eas filled with shattered glass. I would huddle up im a fetal position until meds kicked in.

Swapping to Vyvanse removed these side effects, I had less issues on my second day on vyvanse, than in my fifht month on methylphenidate. It's very smoot in comparison..

Perhaps you have already tried it, but if anxiety is an issue it might be worth giving it a go. It helped me a lot. Hardly touched anxiety pills after I changed, even if I battle ptsd.

 

[theGirlWithBlueHair]

I've read a lot on ADD/ADHD forum and the general consensus is that NDRIs are generall unpleasant and have awful comedowns. Amphetamines seem to be always preferred.

But that seems to be contradicted when it comes to recreational drugs. Cocaine has quite a good reputation compared to methamphetamine for some reason even though amphetamine and methamphetamine are better/safer drugs.

 

[Nagelfar]

But that seems to be contradicted when it comes to recreational drugs. Cocaine has quite a good reputation compared to methamphetamine for some reason even though amphetamine and methamphetamine are better/safer drugs.

Except for when it comes to long term neurotoxicity versus neuroprotection, but one has to remember that cocaine has quite the effect on 5-HTT as well. Sigma affinities between it and amphetamines also differ.

 

[theGirlWithBlueHair]

Yeah, but SRIs are mostly considered to be dysphoric.

I would say the devastating/lethal effects on the heart by cocaine are worse than the long term neurotoxicity of amphetamines.

You're right about the sigma receptor. That does add to the recreational effects.