Clen safe for heart failure?

Brat

PiNCHe GRiNGa!
Thought this was interesting...part in italics made me laugh...

http://news.yahoo.com/s/hsn/20060421/hl_hsn/asthmadrugmighthelpfightheartfailure

Asthma Drug Might Help Fight Heart Failure
By Amanda Gardner
HealthDay Reporter Fri Apr 21, 7:09 PM ET

FRIDAY, April 21 (HealthDay News) -- Body builders sometimes turn, illicitly, to the asthma drug clenbuterol to help them bulk up, but now researchers say the drug might also help heart failure patients stay strong without the need for heart transplant.

The first U.S. study of the drug found it was safe in a small number of heart failure patients. The drug was also found to increase skeletal muscle mass and strength, although there was no significant change in heart function.

The trial, which is a precursor to bigger trials, is an example of how far doctors will go to find solutions to the growing problem of heart failure.

And like many other avenues of research, the promise is still a faint one.

"We've learned the hard way that any pharmacological intervention in this very fragile group of patients needs to be studied very cautiously and thoroughly," cautioned Dr. Ann Bolger, a spokeswoman for the
American Heart Association and professor of medicine at the University of California, San Francisco. "Something that looks to be positive early on may not still be positive later on."

The end step for many heart failure patients is a heart transplant. But with a worldwide shortage of organ donors, many patients have to survive on heart pumps. Is there a way to avoid both heart pumps and transplants? Possibly, the experts say.

"The idea is to one day develop strategies to promote cardiac recovery while patients are supported with a heart pump. That would obviate the need for heart transplants," said Dr. Simon Maybaum, medical director of the Center for Advanced Cardiac Therapy and the Cardiac Transplant and Assist Device Program at Montefiore Medical Center and Albert Einstein College of Medicine in New York City. "This is a growing area of research, and both novel pharmacological agents and cellular therapy [stem cells] will be studied. This research is crucial since because of the critical lack of organs for patients with end-stage heart failure."

Maybaum was lead author of the study, which was presented recently at a meeting of the International Society of Heart and Lung Transplantation in Madrid, Spain.

"We're looking for ways to make the transition off the pump and potentially go forward from there," Bolger added. "We need more tools to save lives."

Studies done by one British center found that clenbuterol resulted in significant improvement in cardiac function in patients with heart pumps awaiting heart transplants. In fact, the pumps could be taken out in more than half of the patients, meaning they no longer were in need of transplant. Those studies used doses 20 times those typically used by asthma patients and athletes.

Clenbuterol is not approved in the United States and, in fact, has a checkered history: Some people fell ill after eating livestock that had been treated with the drug.

Maybaum, however, managed to obtain permission from the U.S.
Food and Drug Administration to conduct a small pilot study using high-dose clenbuterol.

There were two parts to the study: The first tested high-dose clenbuterol in heart pump patients. The second focused on whether the drug in lower doses would improve muscle function and quality of life in heart failure patients without heart pumps (those with milder heart failure). Seven patients completed the study.

Clenbuterol did increase skeletal muscle mass and strength, and was safe at the doses given -- 10 to 15 times that usually taken by asthmatics and athletes. There was no significant change in heart function. However, Maybaum pointed out that the study was not designed to look at this.

Data from the second part of the study is still blinded to researchers, and therefore not yet available.

The next step will be to conduct a multi-center trial in the United States to try to replicate the British findings with heart pump patients.

However, some experts voiced major concerns.

"Patients in heart failure have a pretty broad spectrum of responses to all kinds of therapies, so we have to be very careful. In some situations, this type of drug can be very dangerous with respect to arrhythmias, blood pressure changes and even stroke," Bolger said. "Medications that seem to give the heart an extra boost sometimes make patients feel better, but increase early mortality."

On the other hand, Bolger added, muscle-building strategies including physical fitness, have already been shown to benefit heart failure patients.

Even the study authors were cautious about the odds of success.

"Whenever there are such novel results which have the potential to dramatically affect such a difficult disease process, we go into the research with a mixture of excitement and skepticism," Maybaum acknowledged. "We're optimistic that we will find solution, but we're not sure which one will bear out. We will definitely live in an era where we will be able to repair the heart as opposed to replace it."
 
I can imagine they were fractional of the dosage of recreational use.

i can see the idea tho,

as cardiac output increases with stimulation of beta adrenergic receptors

dont quite know how it causes anabolism tho!

if your not sensetive to clen then i dont see how it can be bad for your heart!

the only problem is when it drives the heart rate to over 100bpm resting rate(the body constantly on a tredmill)

innevitably this will put increased stress on the heart and may cause damage either by enlarging or actual damage to the heart

i wouldnt touch clen because my heart goes nuts after a couple coffees so id hate to see what clen would do.


that would be dangerous
 
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"and was safe at the doses given -- 10 to 15 times that usually taken by asthmatics and athletes."

They were using higher doseage than "recreational" with no change in heart function. So is it just someone's guess somewhere along the way that clen can cause heart problems or is it a fact. Maybe it's kinda like the myth that T3 use will shut you down for life.
 
after taking clenbuteral this final time, i have heart palpations frequently, even tried going to a cardiologist to check it out....

and beforehand i experienced none.... just my experience
 
Wow, science is so confusing. Look at these studies (brought to my attention by ready2exploed on another board that I will not mention) showing clen is detrimental to the heart:

Myotoxic effects of clenbuterol in the rat heart and soleus muscle.

Burniston JG, Ng Y, Clark WA, Colyer J, Tan LB, Goldspink DF.

Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool L3 2ET, United Kingdom. hhsjburn@livjm.ac.jp

Myocyte-specific necrosis in the heart and soleus muscle of adult male Wistar rats was investigated in response to a single subcutaneous injection of the anabolic beta(2)-adrenergic receptor agonist clenbuterol. Necrosis was immunohistochemically detected by administration of a myosin antibody 1 h before the clenbuterol challenge and quantified by using image analysis. clenbuterol-induced myocyte necrosis occurred against a background of zero damage in control muscles. In the heart, the clenbuterol-induced necrosis was not uniform, being more abundant in the left subendocardium and peaking 2.4 mm from the apex. After position (2.4 mm from the apex), dose (5 mg clenbuterol/kg), and sampling time (12 h) were optimized, maximum cardiomyocyte necrosis was found to be 1.0 +/- 0.2%. In response to the same parameters (i.e., 5 mg of clenbuterol and sampled at 12 h), skeletal myocyte necrosis was 4.4 +/- 0.8% in the soleus. These data show significant myocyte-specific necrosis in the heart and skeletal muscle of the rat. Such irreversible damage in the heart suggests that clenbuterol may be damaging to long-term health.

PMID: 12381771 [PubMed - indexed for MEDLINE]

==================================

Characterization of adrenoceptor involvement in skeletal and cardiac myotoxicity Induced by sympathomimetic agents: toward a new bioassay for beta-blockers.

Tan LB, Burniston JG, Clark WA, Ng Y, Goldspink DF.

Academic Unit of Molecular Vascular Medicine, University of Leeds, England.

Excessive levels of catecholamines have long been known to be cardiotoxic, but less well known are their toxic effects on skeletal muscle. By using an antimyosin monoclonal antibody and quantitative methods to measure the extent of myocyte necrosis, and by employing modulators of adrenoceptors (ARs), including clenbuterol, bupranolol, propranolol, bisoprolol, atenolol, ICI-118551, phenoxybenzamine, prazosin, and yohimbine, the involvement of ARs in isoproterenol-induced myotoxicity was characterized. In the myocardium, the toxic effects were predominantly mediated via the beta(1)-ARs. In the soleus muscle, it was almost solely via the beta(2)-ARs. Myotoxicity was also observed in the myocardium when challenged with the beta(2)-AR agonist clenbuterol. This was found to be mediated via sympathetic presynaptic beta(2)-ARs, leading to enhanced release of norepinephrine. This effect was abolished by prior treatment with reserpine. The skeletal muscle was found to be more sensitive to the myotoxic effects than cardiac muscle at lower doses of beta-AR agonists. These experiments introduce a new way of assaying beta-AR antagonists by classifying them according to their ability to prevent catecholamine-induced myotoxicity. Further research along these lines may deepen understanding of which beta-blockers work best in heart failure therapy.

PMID: 12658052 [PubMed - indexed for MEDLINE]

=====================================

Dose-dependent separation of the hypertrophic and myotoxic effects of the beta(2)-adrenergic receptor agonist clenbuterol in rat striated muscles.

Burniston JG, Clark WA, Tan LB, Goldspink DF.

Research Institute for Sport & Exercise Sciences, Liverpool John Moores University, Webster Street, Liverpool L3 2ET, UK.

Muscle growth in response to large doses (milligrams per kilogram) of beta(2)-adrenergic receptor agonists has been reported consistently. However, such doses may also induce myocyte death in the heart and skeletal muscles and hence may not be safe doses for humans. We report the hypertrophic and myotoxic effects of different doses of clenbuterol. Rats were infused with clenbuterol (range, 1 mug to 1 mg.kg(-1)) for 14 days. Muscle protein content, myofiber cross-sectional area, and myocyte death were then investigated. Infusions of >/=10 mug.kg(-1).d(-1) of clenbuterol significantly (P < 0.05) increased the protein content of the heart (12%-15%), soleus (12%), plantaris (18%-29%), and tibialis anterior (11%-22%) muscles, with concomitant myofiber hypertrophy. Larger doses (100 mug or 1 mg) induced significant (P < 0.05) myocyte death in the soleus (peak 0.2 +/- 0.1% apoptosis), diaphragm (peak 0.15 +/- 0.1% apoptosis), and plantaris (peak 0.3 +/- 0.05% necrosis), and significantly increased the area fraction of collagen in the myocardium. These data show that the low dose of 10 mug.kg(-1).d(-1) can be used in rats to investigate the anabolic effects of clenbuterol in the absence of myocyte death. Muscle Nerve, 2006.

PMID: 16411205 [PubMed - in process]

================================

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.
 
I've read the original study as well as the other ones. It's pretty hard to know for sure with so much conflicting advice.
 
inked1 said:
why can't taking T3 permantly shut down your thyroid?
Because it doesn't. I mean I'm sur it's possible if you are just the unlucky one, but research shows that even after prolonged high doses of thyroid hormones, usually due to misdiagnosis that the thyroid springs back to regular function very quickly.
 
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