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Clen and Early Death?

I HAVE ABSOLUTELY NO REASON TO LIE. I COULD GIVE TWO SHITS IF YOU CAN GET CLEN FROM YOUR DOC OR NOT.

you are lying because if the DEA and FDA say a drug is not for human consumption a doctor cant prescribe it because its not available for prescription, how can it be filled? it cant. your a liar trying to save face.

NEver before did I say that she had been prescibed anything within the last few months. I said that she had it in her medicine cabinet and her doc had prescibed it to her.

nice try back pedaling on your initial story liar, unless the prescription was from the early 90's.

your a liar and your story is fabricated. this is the usa, doctors cant do whatever they like - nice try on that one asshole, thats why they get busted for legally prescribing oxycontin to people in large amounts. but they can do what they like. you have no clue and are a lying prick. keep referencing me as some kid too, i love when im 100% right and some asshole tries and argues a point which is a lie. your dumb and a liar too. good combination.

im done here. your too stupid to even get the point that you were 100% proven wrong by actual DEA statements. get it, proven wrong. thanks for the fun, this has been nothing but hilarious watching you try and back up a complete lie.


heres a study you can stick up your ass liar:
this one has been around for awhile. try and do your own research dickhead, as i proved you wrong with the prescription availability i shouldnt even fucking post this for a lying jerkoff like you, but because i like to prove idiots wrong, heres some food for thought.

here you go. it was done on rats but the dosage is nearly the same as human consumption.

Low Dose Clen Induces Cardiac Apoptosis (cell death of heart cells)
Originaly posted by nandi on CM board.

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.
 
also, are there any studies that show that the heart tissue can rejuvinate itself?
ill search
 
SwolK said:
i found a few articles that say that clen acutually helped patients with heart failure

http://www.behavemed.com/info/news/GStone060426.asp

this is true, though you need to read the fine print, it did so by sustaining left ventricle muscle (preventing atropy) during chronic LVAD therapy. other studies have found it to not be effective in this aspect.


1: J Heart Lung Transplant. 2006 Sep;25(9):1084-90. Links
Effect of clenbuterol on cardiac and skeletal muscle function during left ventricular assist device support.George I, Xydas S, Mancini DM, Lamanca J, DiTullio M, Marboe CC, Shane E, Schulman AR, Colley PM, Petrilli CM, Naka Y, Oz MC, Maybaum S.
Department of Surgery, Division of Cardiothoracic Surgery, Columbia College of Physicians and Surgeons, New York, New York 10032, USA. [email protected]

BACKGROUND: High-dose clenbuterol (a selective beta2-adrenergic agonist) has been proposed to promote myocardial recovery during left ventricular assist device (LVAD) support, but its effects on cardiac and skeletal muscle are largely unknown. METHODS: Seven subjects with heart failure (5 ischemic, 2 non-ischemic) were started on oral clenbuterol 5 to 46 weeks post-LVAD implantation and up-titrated to daily doses of 720 microg. The following procedures were performed at baseline and after 3 months of therapy: echocardiography at reduced support (4 liters/min); cardiopulmonary exercise testing; body composition analysis; and quadriceps maximal voluntary contraction (MVC). Myocardial histologic analysis was measured at device implantation and explantation. RESULTS: There were no serious adverse events or arrhythmias. Creatine phosphokinase (CPK) was elevated in 4 subjects, with no clinical sequelae. No change in ejection fraction was seen. End-diastolic dimension increased significantly (4.73 +/- 0.67 vs 5.24 +/- 0.66; p < 0.01), despite a trend toward increased LV mass. Body weight and lean mass increased significantly (75.5 +/- 17.9 vs 79.2 +/- 25.1 kg, 21.1 +/- 8.9 vs 23.6 +/- 9.7 kg, respectively; both p < 0.05). Exercise capacity did not change, but MVC improved significantly from 37.0 +/- 15.7 to 45.8 +/- 20.6 kg (p < 0.05). No significant change in myocyte size or collagen deposition was seen. CONCLUSIONS: Cardiac function did not improve in this cohort of LVAD patients treated with high-dose clenbuterol. However, clenbuterol therapy increased skeletal muscle mass and strength and prevented the expected decrease in myocyte size during LVAD support. Further study will clarify its potential for cardiac and skeletal muscle recovery.


however in a normal, non atrophied system, the indications are for apoptosis.


what it does indicate is that clenbuterol does have potential for use in preventing atrophy.
 
macrophage69alpha said:
this is true, though you need to read the fine print, it did so by sustaining left ventricle muscle (preventing atropy) during chronic LVAD therapy. other studies have found it to not be effective in this aspect.


1: J Heart Lung Transplant. 2006 Sep;25(9):1084-90. Links
Effect of clenbuterol on cardiac and skeletal muscle function during left ventricular assist device support.George I, Xydas S, Mancini DM, Lamanca J, DiTullio M, Marboe CC, Shane E, Schulman AR, Colley PM, Petrilli CM, Naka Y, Oz MC, Maybaum S.
Department of Surgery, Division of Cardiothoracic Surgery, Columbia College of Physicians and Surgeons, New York, New York 10032, USA. [email protected]

BACKGROUND: High-dose clenbuterol (a selective beta2-adrenergic agonist) has been proposed to promote myocardial recovery during left ventricular assist device (LVAD) support, but its effects on cardiac and skeletal muscle are largely unknown. METHODS: Seven subjects with heart failure (5 ischemic, 2 non-ischemic) were started on oral clenbuterol 5 to 46 weeks post-LVAD implantation and up-titrated to daily doses of 720 microg. The following procedures were performed at baseline and after 3 months of therapy: echocardiography at reduced support (4 liters/min); cardiopulmonary exercise testing; body composition analysis; and quadriceps maximal voluntary contraction (MVC). Myocardial histologic analysis was measured at device implantation and explantation. RESULTS: There were no serious adverse events or arrhythmias. Creatine phosphokinase (CPK) was elevated in 4 subjects, with no clinical sequelae. No change in ejection fraction was seen. End-diastolic dimension increased significantly (4.73 +/- 0.67 vs 5.24 +/- 0.66; p < 0.01), despite a trend toward increased LV mass. Body weight and lean mass increased significantly (75.5 +/- 17.9 vs 79.2 +/- 25.1 kg, 21.1 +/- 8.9 vs 23.6 +/- 9.7 kg, respectively; both p < 0.05). Exercise capacity did not change, but MVC improved significantly from 37.0 +/- 15.7 to 45.8 +/- 20.6 kg (p < 0.05). No significant change in myocyte size or collagen deposition was seen. CONCLUSIONS: Cardiac function did not improve in this cohort of LVAD patients treated with high-dose clenbuterol. However, clenbuterol therapy increased skeletal muscle mass and strength and prevented the expected decrease in myocyte size during LVAD support. Further study will clarify its potential for cardiac and skeletal muscle recovery.


however in a normal, non atrophied system, the indications are for apoptosis.


what it does indicate is that clenbuterol does have potential for use in preventing atrophy.
thanks for clearing some of that up
how does Alcar(sp?) prevent heart damage?
 
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