Clenbuterol Vs. Sodium Usinate / Usnic Acid [Forum Archive]

Quote:

Originally Posted by LAM

I had great results with UA on a unclean diet, although I'm not sure what the difference is between UA and sodium usinate. I'm getting ready to run a DNP cycle in about 5 weeks.

I know with UA the main health risk is liver failure due to a complete shutdown of oxidative phosphorylation but a safe dosage elimintates that threat. And with DNP dehydration is the number cause of death.

I remember reading the text of that article about that 28 year old girl whose liver failed due to UA. Of course they forget to site in the text that she was taking 3x the recommended dose of the fat burner that contained UA, go figure why her liver failed.

Quote:

Low Dose Clen Induces Cardiac Apoptosis
It's been known for some time that clenbuterol at high doses causes cardiac necrosis. This study in animals shows that doses of 1 mcg/kg BW induce apoptosis (programmed cell death) in heart tissue. Humans not uncommonly ingest this much clen. For instance, in a 220 lb (100 kg) bodybuilder this translates to 100 mcg. The CEM store sells clen at a concentration of 200 mcg/ml! Other UG labs sell it at similar concentrations, ranging from 100 to 200 mcg per ml.

J Appl Physiol. 2004 Dec 10; [Epub ahead of print] Related Articles, Links

{beta}2-Adrenergic receptor stimulation in vivo induces apoptosis in the rat heart and soleus muscle.

Burniston JG, Tan LB, Goldspink DF.

Research Institute for Sports and Exercise Sciences, Liverpool John Moores University, Liverpool, United Kingdom.

High doses of the beta2-adrenergic receptor (AR) agonist, clenbuterol, can induce necrotic myocyte death in the heart and slow-twitch skeletal muscle of the rat. However, it is not known if this agent can also induce myocyte apoptosis and whether this would occur at a lower dose than previously reported for myocyte necrosis. Male Wistar rats were given single subcutaneous injections of clenbuterol. Immunohistochemistry was used to detect myocyte specific apoptosis (detected on cryosections using a caspase 3 antibody and confirmed using annexin V, single-strand DNA labelling and TUNEL). Myocyte apoptosis was first detected at 2 h, and peaked 4 h after clenbuterol administration. The lowest dose of clenbuterol to induce cardiomyocyte apoptosis was 1 microg kg(-1), with peak apoptosis (0.35 +/- 0.005 %; P<0.05) occurring in response to 5 mg kg(-1) . In the soleus, peak apoptosis (5.8 +/- 2 %; P<0.05) was induced by the lower dose of 10 microg kg(-1). Cardiomyocyte apoptosis occurred throughout the ventricles, atria and papillary muscles. However, this damage was most abundant in the left ventricular subendocardium at a point 1.6 mm, that is, approximately one-quarter of the way from the apex towards the base. beta-AR antagonism (involving propranolol, bisoprolol or ICI 118,551) or reserpine was used to show that clenbuterol-induced myocardial apoptosis was mediated through neuromodulation of the sympathetic system and the cardiomyocyte beta1-AR, whereas in the soleus direct stimulation of the myocyte beta2-AR was involved. These data show that when administered in vivo, beta2-AR stimulation by clenbuterol is detrimental to cardiac and skeletal muscles even at low doses, by inducing apoptosis through beta1- and beta2-AR, respectively.