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alpha-yohimbine long term?

Cosmonaut

Cosmonaut

New member
I just have a couple of question about the long term effects on the alpha2 and beta2 adrenergic receptors (AR's) specifically.

Wouldn't alpha-yohimbine sensitize the effects of a2-AR's and cause greater fat storage in the long run? I am assuming if there is antagonism of these receptors then they should upregulate?

Also, if someone has already downregulated beta-2-AR, would using alpha-yohimbine cause even greater far storage in the long run since you have down-regulated beta2-AR and up-regulated alpha2-AR?

Any help would be appreciated.

Thanks
 
great question... its great to see more specific questions concerning supplements... unfortunately i cant answer this question... it would make since but from my limited knowledge on the subject i dont think u can indirectly up-regulate the a2-AR...definitely dont take my word on it though...
 
No clue, sorry. I'm currently using Yohimbine HCL and just ordered a bottle of AlphaBurn... I wonder if Cosmonaut's question also applies to Yohimbine HCL...
 
i would think if you cycle everything you should be fine and your body correct itself, but your asking long term use, i wouldnt use anything permanently.

bump, dsade?
 
I think this stuff is bad news and should not be used...."my"personal opinion and what research is out there. cost-to-risk ratio eww
 
Cosmonaut said:
I just have a couple of question about the long term effects on the alpha2 and beta2 adrenergic receptors (AR's) specifically.

Wouldn't alpha-yohimbine sensitize the effects of a2-AR's and cause greater fat storage in the long run? I am assuming if there is antagonism of these receptors then they should upregulate?

Also, if someone has already downregulated beta-2-AR, would using alpha-yohimbine cause even greater far storage in the long run since you have down-regulated beta2-AR and up-regulated alpha2-AR?

Any help would be appreciated.

Thanks
Click to expand...

Can't answer the a2 upregulation question. I can say though, that as far as I know, the a2 receptor is responsible for decreasing the output of catecholamines (norE and E bind to the a2 receptor after being released into the synaptic cleft, and this binding downregulates norE/E release...they bind to the beta receptors on the postsynaptic terminal, and alpha receptors on the presynaptic terminal). The idea is that by blocking the a2 receptor, you can help prevent downregulation of catecholamine release.
 
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