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For all those new people asking about Clenbuterol or Fat Loss
- Thread starter eddymerckx
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Wow, the walking clen encyclopedia sure knows a lot of shit. OMEGA you better have something good...
Re: For all those new people asking about Clenbuterol
Just to offer the most cited studies (but not the most recent as my Pub Med account is not working---liberated from your home site:
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. [email protected]
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 MEDLIN
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.
__________________
Just to offer the most cited studies (but not the most recent as my Pub Med account is not working---liberated from your home site:
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. [email protected]
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 MEDLIN
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.
__________________
now, for Achems Razor: If clen was this magic and safe fat loss pill (as DNP was touted on the '30s...before it rendered many women blind) why is it not marketed as such in any country?
no, it sounds like a competitor trying to sell clen....all we need is to see the parents of some knucklehead who suffered a stroke or heart attack because junior tried to lose his/her beer gut in time for spring break by taking increasing doses of clen....and put the spotlight back on those evil performance enhancing drugs.....
ryno9000
New member
Wow, really? In the United States? That's interesting. Kind of a sick world we live in, considering a large % of the country was doing the "I lost everything I have and can't afford to eat so I am moving out to california in hopes of picking fruit" diet during the 30's.
that is actually where most of it happened--California---but the upside was if you are blind more people may buy your apples for 5 cents
Monday, Jun. 29, 1936
Again, Dinitrophenol
One hundred Los Angeles women were known to be blind or partly so with cataracts last week as result of taking dinitrophenol to reduce. That drug, whose weight-reducing properties were first cautiously utilized by San Francisco doctors (TIME, July 31, 1933), is illegally and secretly sold in California under the following names: Nitromet, Dinitrolac, Nitra-phen, Dinitriso, Formula 281, Dinitrose, Noxben-ol, Re-du, Aldinol, Dinitrenal, Pre-scription No. 17, Slim, Dinitrole, Tabolin, Redusols. Against them Los Angeles Health Officer John Larrabee Pomeroy last week initiated an elimination drive.
Besides cataracts, dinitrophenol depletes white corpuscles of the blood, causes polyneuritis, is responsible for seven known deaths. Last week in the American Medical Association Journal two Cleveland physicians declared it may also cause heart disease.
http://www.time.com/time/magazine/article/0,9171,770212,00.html.
Conciliator
Banned
Re: For all those new people asking about Clenbuterol
This is a proposed mechanism of action, which I appreciate. However, it's far from evidence. Do you have any references that these steps occur in humans? I don't think I've ever heard anyone report a reduction in thyroid levels after a cycle of clenbuterol. Unless there's some decent evidence that these steps occur in humans, or even direct evidence in animals that clenbuterol suppresses metabolism, I think it's very premature for you to be making statements of fact like "on the off days, your metabolism rebounds into a slower range" and that "you have a net lowering of your metabolism."
Your link doesn't work. Further, this quote is far from an authoratative excerpt. I found the whole text, and it looks like an article on tainted meat from a student in an animal science class. It has no references. The excerpt immediately preceding the one you posted should make you question the accuracy of the whole paper: "Athletes generally take a 20 mcg dose 3 times a day for 2 days then go off it for 2 days. They repeat this cycle for 6-8 weeks." If you have any actual evidence that clenbuterol causes a reduction in metabolic rate upon cessation, please post it.
Yes, I will definitely argue that the "the studies that proved such were not on humans" and "with doses exponentially higher than that which would be used in humans." I've already posted research IN HUMANS, in which three months of very high doses of clen resulted in no significant change in collagen deposition. Why do you discount that? Even the last study you posted only found a significant increase in the area fraction of collagen in the myocardium when the dose was raised to 1000 mcg/kg. It referenced another paper that suggested that 10 mcg/kg in rats was equivalent to the therapeutic dose for humans. But at 10mcg/kg, the change in collagen was insignificant. Further, that dose provided "a model of clenbuterol-induced hypertrophy in the absence of myocyte death." In light of the evidence I've seen, your statement of fact to a clenbuterol user that "damage to your heart has probably already occurred" appears to be grossly premature.
I've already addressed cardiomyocyte toxicity and necrosis here in this thread.
Also, I didn't see you respond to this: do you have any references for your claimn that there is a degredation in cardiac output, especially in humans or at doses relevant to human use?
This is a proposed mechanism of action, which I appreciate. However, it's far from evidence. Do you have any references that these steps occur in humans? I don't think I've ever heard anyone report a reduction in thyroid levels after a cycle of clenbuterol. Unless there's some decent evidence that these steps occur in humans, or even direct evidence in animals that clenbuterol suppresses metabolism, I think it's very premature for you to be making statements of fact like "on the off days, your metabolism rebounds into a slower range" and that "you have a net lowering of your metabolism."
Your link doesn't work. Further, this quote is far from an authoratative excerpt. I found the whole text, and it looks like an article on tainted meat from a student in an animal science class. It has no references. The excerpt immediately preceding the one you posted should make you question the accuracy of the whole paper: "Athletes generally take a 20 mcg dose 3 times a day for 2 days then go off it for 2 days. They repeat this cycle for 6-8 weeks." If you have any actual evidence that clenbuterol causes a reduction in metabolic rate upon cessation, please post it.
Yes, I will definitely argue that the "the studies that proved such were not on humans" and "with doses exponentially higher than that which would be used in humans." I've already posted research IN HUMANS, in which three months of very high doses of clen resulted in no significant change in collagen deposition. Why do you discount that? Even the last study you posted only found a significant increase in the area fraction of collagen in the myocardium when the dose was raised to 1000 mcg/kg. It referenced another paper that suggested that 10 mcg/kg in rats was equivalent to the therapeutic dose for humans. But at 10mcg/kg, the change in collagen was insignificant. Further, that dose provided "a model of clenbuterol-induced hypertrophy in the absence of myocyte death." In light of the evidence I've seen, your statement of fact to a clenbuterol user that "damage to your heart has probably already occurred" appears to be grossly premature.
I've already addressed cardiomyocyte toxicity and necrosis here in this thread.
Also, I didn't see you respond to this: do you have any references for your claimn that there is a degredation in cardiac output, especially in humans or at doses relevant to human use?
Conciliator
Banned
Occam's Razor?
I don't think anyone thinks that clen is magic or completely safe. I think that's a fallacious straw man. Rather, I think clen has utility for mobilizing fat when there's a large caloric deficit. It's useful at low BF percentages when there's little fat left to mobilize. It also has utility as an anti-catabolic during dieting. Magic? No.
DNP, on the other hand, is about as close to magic as you can get. Can it cause cataracts? Yes. Of the estimated 500,000 people who took DNP in the 1930's, there were 164 case reports of cataracts, according to Horner's extensive 1941 review. They're rare, but are one of DNP's most serious risks. There appears to be a genetic factor causing suscpetibility. There's also reason to think that antioxidant supplemention might prevent their occurance (even though uncouplers reduce mitochondrial oxidative stress). That's because DNP induced cataracts are caused by a rare, second-order metabolite of DNP that is a cataractogenic semiquinone.
The main problem with DNP is that people don't know how to use it properly. Like clen, doses need to be carefully titrated and kept relatively low. Take too much, like most bodybuilders do, and you'll add undue risks and side effects.
Conciliator
Banned
I sound like a competitor trying to sell clen? I hope I sound more educated than that
. I'm not selling anything, I'm just a bodybuilding enthusiast.As for saving the children, I don't think anything should stand in the way of objective discussion about the facts, even if it means calling into question some of the dangers that are used for scare tactics. Hopefully we learned something from steroids and the disingenuous anti-steroid propaganda.
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