is ephedrine bad on the liver?

[Terminator 4]

I want to start taking it and im gonna do masterdrol cycle in 2 weeks so I would like to know if ephedrine causes stress and toxic to the liver?

[iceq22]

nope ephedrine is not toxic

[dinoiii]

Ephedrine and alkaloids are not metabolized in a major way via the liver, however, let's say you have a obese individual that is into weight loss and attempts to use PHs et al as solely a muscle-protectant. It could likely be theorized that if ephedrine contributes to the rapidity here and a fatty-like liver fits into the equation...it could provide a realistic strain.

I don't think it is necessarily a case of liver here though. Andrnergic stimulation on cycle doesn't make the most sound sense.

[Jswoll]

Dino, one quick question for my own knowledge whilst on the subject, the way I understand Ephedrine to work is not selective in its binding (NE that is), and in addition to binding to the beta 2 receptor, it also binds to both alpha receptors, as well as the beta 1 and 3 receptors. Question is, the down regulation caused: the extent, time frame in which it's caused, give me a wider picture than just this, there has to be pro's and cons to using something that's non-selective in it's receptor bindings (as opposed to clen), can you fill me in?


Andrnergic stimulation on cycle doesn't make the most sound sense.
Can I get a little more elaboration?

[dinoiii]

Here is a link to a thread I posted in some time ago about the mechanism of action, et al. of thermogenics vs. thyroid supps. I think some of your answers to MOA or questions may be found there as ephedrine doesn't exactly "receptor-bind" at all.

http://www.discountanabolics.com/forum/showthread.php?t=1559&highlight=thyroid+thermogenics



"ON" cycle is a time frame when you are hopefully eating a lot more and insulin is quite high. Consequently, adrenergic stimulation is sort of the reciprocal of that. Think of epi and norepi to run opposite that of insulin AND WITH glucagon. It is NOT the receptor in a direct way I am concerned with. You decrease efficacy in a state of hypOadrenalism. Again, the point remains - you are hypOadrenergic and it is the same if you were to limit supply of the pre-synaptic nerve endings (see that link I provided above).



As far as down regulation properties are concerned...results of receptor responsiveness directly are accounted for in part by the degree of receptor density. What I am saying is in say beta-adrenergics, the number of receptors (which will vary per person accounting for body composition differences seen across the board) dictates the length of time to that particular down-regulation.

If I understand your question as stated, the only advantages that I could say definitively on non-selectives in this regard needs to be extrapolated from cardiac research, which wouldn't apply directly but allows us to make some inferences. I wouldn't jump on a non-selective being better than selective though in the agonist department prolonging down-regulation. However, a antagonist/agonist on the other hand offers some hope. Some scientific studies have characterized receptor desensitization as primarily due to the phosphorylation of receptors by specific receptor kinases (enzymes that add phosphate groups to other proteins in the cell). However, there are also scientific studies that argue against this as a primary mechanism for all receptors and suggest that alternative explanations are needed.

(1) The fact that some receptors desensitize rapidly (milliseconds to microseconds) argues against phosphorylation being the only way receptors desensitize. Receptor phosphorylation may be a secondary action resulting from other molecular processes that take place first within the cellular receptors themselves.

(2) Also, receptor phosphorylation has been observed to account for only part of the total receptor down-regulation observed after agonist exposure.

(3) In addition, the reduction in desensitization observed when antagonists are combined with agonists suggests that alternative mechanisms are necessary to explain rapid receptor desensitization.

[Jswoll]

Thanks D, that more than answered my question, which is a problem--the MORE part, cause it raises even more questions. That's always good I guess, it keeps me thinking. But I'll think them out do a little research myself see if I can't find the answers then I'll plague you with them if I can't logically answer them. But maybe you can make quick work of this one, T3 up regulating beta2, fact or bs or unkown waiting further study? Appreciate it as always.

-Joe

[dinoiii]

Well to your last question, I think there was lack of response with beta blockers in hypERthyroid cases which was purported to potentially mark the upregulation of beta 1's. Beta 2 saw some studies from rats in this modality, but I am unaware of human studies showing it. Perhaps you could show me if you find it?

[Jswoll]

No, I was going off of the rat studies (looking a various ones over at pubmed) as well, that's why I asked your opinion because off of that only mere speculation can be derived. I was kinda hoping you might have known an on going study that might show some support to one side or another.