Can't Pee ??

Hyde

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It is an RC and very weak ....... I skipped today, I think I can go every other day.
According to WebMd, once you have built up a few initial 10mg doses it says standard dosing indeed becomes eod for maintenance.
 
Rocket3015

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Today I dropped my Caffeine down by 200mg today I will see what happens
 
Rocket3015

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5mg of Tadalafil EOD has fixed all problems and I'm getting better pumps in the gym !!
 
HIT4ME

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5mg of Tadalafil EOD has fixed all problems and I'm getting better pumps in the gym !!
This is interesting and would go against the caffeine theory, I think, at least at first. Given I am no expert here I am just thinking theoretically, but I would have thought caffeine ---> increased acetylcholine release ----> increased NO.

Of course, Tadalafil reduces NO break down through PDE inhibition, so this means (at least through this mechanism) that increased NO may be solving your issue. This, at first, made me think that increase Acetylecholine was not the issue, and thus caffeine was in the clear.

But I found this : https://www.sciencedirect.com/science/article/abs/pii/S0014299901012778

Which is in rats, and may just be confirmation bias, but this seems to indicate that NO has a role in inhibiting acetylcholine release (at least in rat bladders) - but this would make sense as it would form a negative feedback loop to maintain homeostasis.

Acetylcholine increases NO, and as NO builds up it signals to stop releasing acetylcholine.

So, back to the theory, it is possible that:

Caffeine is increasing Acetylcholine.

Acetylcholine is signaling the bladder that it has to release.

Acetylcholine is also sending the signal to increase NO but you don't have the capability to release enough NO and have maxed out, so not enough is left to reduce the acetylcholine release through the negative feedback loop.

Tadalafil inhibits PDE so NO isn't getting broken down, which allows it to stick around for longer, which reduces the release of acetylcholine and solves the problem.

If course, I don't know sh1t and I am probably just making this all up.

But it seems like overdoing caffeine is being covered up by using other substances potentially.

And, don't get me wrong, far from anti-caffeine. I have many posts on here talking about how little it affects me, even at a gram. But more recently I have dropped it by 80-90% of my previous consumption levels and I honestly feel way better without it. I actually have MORE energy (probably because of better sleep) but placebo/nocebo is a thing too.

Caffeine on a day with less than normal sleep, then, yeah, it makes me awesome in that situation.

This would also have some implications for other things, like why is everyone putting caffeine in pump products? Maybe there is a way to help reduce the negatives of some stimulants with NO products?
 
Rocket3015

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Next week I am out of town on business, so no PWO or Tadalafil, when I come back I am going to resume the PWO with out any additional Caffeine and no Tadalafil and see what happens............
 
HIT4ME

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Next week I am out of town on business, so no PWO or Tadalafil, when I come back I am going to resume the PWO with out any additional Caffeine and no Tadalafil and see what happens............
Honestly, just found that caffeine itself inhibits PDE. To what extent I don't know...but if that is the case, then everything is too intermingled to really say. So, yeah, I know nothing. Don't listen to me :)
 
Rocket3015

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Honestly, just found that caffeine itself inhibits PDE. To what extent I don't know...but if that is the case, then everything is too intermingled to really say. So, yeah, I know nothing. Don't listen to me :)
I appreciate all the work you have put into this !!
 
jswain34

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I think youre overcomplicating things a bit Hit. Or maybe im under complicating things. Caffeine = sympathomimetic. Sympathetic nervous system = no pee, so you dont wanna stop to piss instead of running from that (edit: lion, HGP, whatever you’re running from). But its also a bladder irritant.

Cialis = increased cGMP = increased NO like you said = decreased smooth muscle contraction in the prostate = decreased resistance for the pee to get through as it exits the bladder.
 
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Rocket3015

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I think youre overcomplicating things a bit Hit. Or maybe im under complicating things. Caffeine = sympathomimetic. Sympathetic nervous system = no pee, so you dont wanna stop to piss instead of running from that. But its also a bladder irritant.

Cialis = increased cGMP = increased NO like you said = decreased smooth muscle contraction in the prostate = decreased resistance for the pee to get through as it exits the bladder.
Simple ...
 
HIT4ME

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I think youre overcomplicating things a bit Hit. Or maybe im under complicating things. Caffeine = sympathomimetic. Sympathetic nervous system = no pee, so you dont wanna stop to piss instead of running from that (edit: lion, HGP, whatever you’re running from). But its also a bladder irritant.

Cialis = increased cGMP = increased NO like you said = decreased smooth muscle contraction in the prostate = decreased resistance for the pee to get through as it exits the bladder.
Yeah, so this is somewhat along the lines of my initial stance. Just for, possibly, my own education - I believe NO increases cGMP, not the other way around?

But part of the issue here is that caffeine has a lot of seemingly contradictory effects. For instance, doesn't coffee usually increase your urgency? I know that I often have to piss like a race horse in the morning after drinking a large amount of caffeine....moreso than just drinking the same amount of fluid. Plus, if coffee is a PDE inhibitor, then, it too will increase NO and thus increase cGMP. To what extent, who knows.

Still, I think the caffeine from the pre- may be pushing over limits and may be getting covered up/counteracted by the PDEi.

On the other hand, perhaps, it is a case of Benign Prostatic Hypertrophy, which is common in old men like Rocket and PDEi's are beneficial in that.

I may be over- or under-thinking it. I am not sure. But I am pretty confident that I shouldn't be thinking so much about another man's urinary issues :)

Yeah, it's weird, but the potential underlying pathways are pretty interesting...
 
jswain34

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I agree that the physiological mechanisms are interesting and absolutely complex..so much so that im sure to cover it in sufficient detail youd have to write a multipage article about it lol.

The diuretic effects of caffeine (with long-term use of the same or less dosages) has been dispelled I believe. As in you will get a diuretic effect with intermittent dosing but a stable long term dose the effect wears off to the point where caffeine (edit: coffee) provides a similar level of hydration to plain water (I wont lie, I havent looked at this data myself - regurgitating it from some literature review service I follow). With that said, as I mentioned, caffeine metabolites are local bladder irritants which can absolutely lead to an increased urgency. I highly doubt the PDE5 inhibition from caf holds a stick to that of the -fils but once again I cant speak to exact numbers.

If im not mistaken the cGMP leads to changes in NO, if it works similarly to how cAMP affects NO in bronchial smooth muscle anyhow. Beta agonist (albuterol) = increased cAMP = increased NO = bronchial smooth muscle dilation/relaxation.

We’re probably both over and underthinking certain parts and not even aware of half of whats going on, lol.
 
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Rocket3015

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Yeah, so this is somewhat along the lines of my initial stance. Just for, possibly, my own education - I believe NO increases cGMP, not the other way around?

But part of the issue here is that caffeine has a lot of seemingly contradictory effects. For instance, doesn't coffee usually increase your urgency? I know that I often have to piss like a race horse in the morning after drinking a large amount of caffeine....moreso than just drinking the same amount of fluid. Plus, if coffee is a PDE inhibitor, then, it too will increase NO and thus increase cGMP. To what extent, who knows.

Still, I think the caffeine from the pre- may be pushing over limits and may be getting covered up/counteracted by the PDEi.

On the other hand, perhaps, it is a case of Benign Prostatic Hypertrophy, which is common in old men like Rocket and PDEi's are beneficial in that.

I may be over- or under-thinking it. I am not sure. But I am pretty confident that I shouldn't be thinking so much about another man's urinary issues :)

Yeah, it's weird, but the potential underlying pathways are pretty interesting...
Whats this old man crap ??
 
JKVol

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In my experience it’s Yohimbe and AY that cause “weak stream” for me the most. Caffeine and Bronkaid does not do it but caffeine and Y will do it. After 5 seconds or so of peeing it gets better. Reign would kill me down there. Agree that Tadalafil works great for this but I won’t touch Y or AY anymore.
 
HIT4ME

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I agree that the physiological mechanisms are interesting and absolutely complex..so much so that im sure to cover it in sufficient detail youd have to write a multipage article about it lol.

The diuretic effects of caffeine (with long-term use of the same or less dosages) has been dispelled I believe. As in you will get a diuretic effect with intermittent dosing but a stable long term dose the effect wears off to the point where caffeine provides a similar level of hydration to plain water (I wont lie, I havent looked at this data myself - regurgitating it from some literature review service I follow). With that said, as I mentioned, caffeine metabolites are local bladder irritants which can absolutely lead to an increased urgency. I highly doubt the PDE5 inhibition from caf holds a stick to that of the -fils but once again I cant speak to exact numbers.

If im not mistaken the cGMP leads to changes in NO, if it works similarly to how cAMP affects NO in bronchial smooth muscle anyhow. Beta agonist (albuterol) = increased cAMP = increased NO = bronchial smooth muscle dilation/relaxation.

We’re probably both over and underthinking certain parts and not even aware of half of whats going on, lol.
Yeah, I need to study cGMP in a little more depth now, this will take many nights.

As far as the caffeine thing - what's interesting is that I came across a study that showed the vasoconstriction from caffeine was transient and that increased NO from caffeine could, over a longer period, cause vasodilation.

Also, caffeine is known to be an adenosine antagonist and the adenosine sub-receptors are known to have seemingly contradictory effects when activated/deactivated.

Whats this old man crap ??
Did I say "old man" out loud? Oops.
 
Rocket3015

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I tried Albuterol and after (1) dose I could not pee, I may try it again with some Tadalafil and see what happens ???
 
Rocket3015

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Rocket3015

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You mean you don't have enlarged prostate issue? so where do the symptomes come from?
Yes it is an enlarged prostate, but with the addition of the Tadalafil it has "Relaxed" and is back to normal. The Dr. believes something in my PWO "Aggravated" it
 
jswain34

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Look what I found today when I was going through my tox textbook for another reason:

IMG_6621.JPG


IMG_6622.JPG
 
Rocket3015

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Nice !
 
Rostam

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I’m wondering why yohimbine is worsening BPH symptomes. It’s an alpha 2 adrenergic antagonist so it should not contract the sphincter but relax them, no?
 
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jswain34

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Double posted
 
jswain34

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I’m wondering why yohimbine is worsening BPH symptomes. It’s an alpha 2 adrenergic antagonist so it should not contract the sphincter but relax them, no?
Alpha 1s are the receptors you think about when dealing with the urinary tract (found it other places as well).

Alpha 2 receptors are mainly located in the brain stem and regulate sympathetic outflow. When it is agonized it throttles down sympathetic outflow, when it is antagonized it takes the throttle off which is what yohimbine does.
 

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