For all those new people asking about Clenbuterol or Fat Loss

[jungle4321]

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

lol

 

[eddymerckx]

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.

You discount the theory but cannot discount that each of the mechanism is well-founded. As far as the statement being premature, in the absence of actual studies, it is reasonable to postulate that, based on established physiologic mechanisms, that there would be a decrease in metabolism. You cannot keep returning to the lack of human studies when you know well and good that the clen studies do not look at metabolism as that is not necessary to the narrow scope of the study (e.g. the one human study you trot out continually)


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. “


Your reliance on ONE flawed human study, of 7 human research subjects--(patients at end stage cardiac failure) is not well placed and downright misleading and scientifically invalid given the nature of the study and the many absolute conflicting studies. Aside from the size of the group, lack of control, lack of placebo, and the fact that the conclusion was that clen may induce cardiac hypertrophy and therefore helpful to left ventricular assist devices for the treatment of end-stage heart failure to reverse or prevent the adverse effects of unloading-induced myocardial atrophy.

Moreover, your entire hypothesis is predicated on the fact that “ No significant change in myocyte size or collagen deposition was seen”---(1) what is significant; (2) the observations were not based on actual post mortem examinations of the cardiac muscle (as was done in all the other mammalian studies); and again, this was short term, not done in the manner in which clen is used illicitly, and the subjects were not comparable to illicit users, save for the fact that they were human (about the only similarity)

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?

again, there has not been any human studies--except the off-point and flawed one you cite. Can you actually suggest that collagen deposition in cardiac muscle cannot adversely impact the net output? See http://ndarc.med.unsw.edu.au/NDARCWeb.nsf/resources/NDARCFact_Drugs2/$file/CLENBUTEROL+NDARC+FACT+SHEET.pdf ( “Collagen is a tough connective tissue that can stiffen the heart muscle, actually reducing cardiac output and possibly producing cardiac arrhythmias. Also, clenbuterol rats suffered from noticeable cardiac-cell degeneration”)

trying to consolidate here...

 

[eddymerckx]

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.

[FONT=&quot]
I think I can be forgiven for a spelling error at 2:30 a.m., but nice rhetorical device to undercut your opponent none-the-less and telling that what is to follow is either off-point or relatively specious.[/FONT]

To address your point, your imply that because is that clen has not been proven to be unsafe for human use and in spite of numerous studies in non human mammals, it is safe. You may take issue with such an inference but it is none-the-less a valid one.

As for DNP, we both know it is being studied now--at least its mechanism is, for a potential weight loss drug. The problem is that while you note the incidence of vision-related adverse occurrence may or may not be statistically significant and may result from some genetic predisposition, and as you note the doses taken then and illicitly now are not comparable, the ration of a therapeutic dose and potentially deadly dose is so small as to warrant the gravest of warning against its use--not to mention the risk of the actual dose from an illicit source is palpable.

[FONT=&quot]Finally, I stand by my supposition that if clen was indeed thought to be effective w/o reasonable risk why is it not marketed as such? The simplest answer is most-likely the correct one: the risk/benefit is not economically nor ethically acceptable.[/FONT]

 

[ThaGeneral]

Thanks for the info guys!! and too bad I pissed eddy off I didn't realize there was so many rules to asking questions! My bad next time i'll be more patient. Anyways I tried my helios this morning (sub-Q) and I am very impressed as of right now I recomend it over liquid or pills.

 

[eddymerckx]

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.

I do not discount the notion about an open discussion but I do find it problematic when the many viewers of this thread will take your conclusions and run with them. neither of us have mentioned the reports of cardiac events and deaths that were attributed to the use of clen--and we both know those reports are of little value scientifically--but there are just too many unknowns for the average--or spring break user to think clen is safe.

[FONT=&quot]Moreover, and to the casual reader, I do not pretend to be any sort of expert on clen, anatomy, or bio-physiology--I am a freakin' tax attorney--so take what you read here and do your own research, ask your own physician, or just opt to either accept the body you have or change it through slow, steady, and well-reasoned training---there is no quick fix or substitute for the aforementioned--period. [/FONT]

I will end my contributions with the above---

 

[Conciliator]

You discount the theory but cannot discount that each of the mechanism is well-founded. As far as the statement being premature, in the absence of actual studies, it is reasonable to postulate that, based on established physiologic mechanisms, that there would be a decrease in metabolism. You cannot keep returning to the lack of human studies when you know well and good that the clen studies do not look at metabolism as that is not necessary to the narrow scope of the study (e.g. the one human study you trot out continually)

I'm not discounting the theory. I'm saying that you haven't presented a shred of evidence to support it. There's no reason for anyone reading this to believe it occurs. You are now relying on the argument that "each of the mechanisms is well-founded." That's nothing but an argumentum ad populum. It's an appeal to common knowledge, an "everyone knows this." That's a fallacy. You're stretching things and I think you know it. You're making statements of fact when you should be saying "might". It's far from "well-founded" that the doses of clen that humans take will deplete hepatic taurine to a sufficient extent that T4->T3 conversion will be imparied to a sufficient extent that metabolic rate will drop to a degree that's practically significant. Let's see the references. If you don't have them, that's fine. Let's just be very clear that this is a tenuous theory of yours that you haven't provided a shred of evidence for.

According to your theory, taurine supplementation would prevent it anyway, right?

Your reliance on ONE flawed human study, of 7 human research subjects--(patients at end stage cardiac failure) is not well placed and downright misleading and scientifically invalid given the nature of the study and the many absolute conflicting studies. Aside from the size of the group, lack of control, lack of placebo, and the fact that the conclusion was that clen may induce cardiac hypertrophy and therefore helpful to left ventricular assist devices for the treatment of end-stage heart failure to reverse or prevent the adverse effects of unloading-induced myocardial atrophy.

I didn't rely on one human study, did I? Don't put up a straw man. I also posted a study in lambs, in which 400mcg/day "significantly decreased collagen concentration because myofibrillar proteins were preferentially produced." I also provided a second study in humans where "It was concluded that clenbuterol could inhibit partially the proliferation of intramuscular collagens in denervated skeletal muscle." There are a handful of studies showing cardiac collagen deposition in animals, but they are are all at extremely high doses of clen. Even then, there is animal research like this where they found that "left ventricular concentration of collagen and morphology was normal as were the expression of SERCA2a and PLB mRNA. CONCLUSION: These results suggest that clenbuterol-induced hypertrophy is 'physiological' in terms of its function, extracellular structure and gene expression."

You even go so far as to discount your own study, which corroborated all of these others. It found that 10mcg/day, a dose relevant to therapeutic doses in humans, was insufficent to produce significant collagen deposition. You simply do not have any good evidence to be making statements of fact that "damage to your heart has probably already occured." No, not at all. Damage to your heart is probably very unlikely, in light of the evidence to the contrary, both in humans and in animals taking relevant doses.

 

[Conciliator]

Moreover, your entire hypothesis is predicated on the fact that “ No significant change in myocyte size or collagen deposition was seen”---(1) what is significant; (2) the observations were not based on actual post mortem examinations of the cardiac muscle (as was done in all the other mammalian studies); and again, this was short term, not done in the manner in which clen is used illicitly, and the subjects were not comparable to illicit users, save for the fact that they were human (about the only similarity)

What is significant? Do you understand what statistical significance is? It means that the study failed to show that the differences were large enough to be due to anything more than just change. It means the study failed to find a statistical difference in collagen deposition between placebo and 1, 10, and even 100 mcg/day.

I don't see how you think you're making a point saying that "this was short term, not done in the manner in which clen is used illicitly." No, they took vastly higher doses, for a much longer period of time... things that would exaggerate the effects on collagen deposition, if they existed. Does the study prove that clenbuterol doesn't increase the cardic collagen content in bodybuilders? Definitely not. But it certainly rebuts that presumption, especially when taken in light of all the other studies showing no effect.

again, there has not been any human studies--except the off-point and flawed one you cite. Can you actually suggest that collagen deposition in cardiac muscle cannot adversely impact the net output? See http://ndarc.med.unsw.edu.au/NDARCWeb.nsf/resources/NDARCFact_Drugs2/$file/Clenbuterol+NDARC+FACT+SHEET.pdf ( “Collagen is a tough connective tissue that can stiffen the heart muscle, actually reducing cardiac output and possibly producing cardiac arrhythmias. Also, Clenbuterol rats suffered from noticeable cardiac-cell degeneration”)

You again provide an excerpt from a paper that is unreferenced and that is neither academic nor peer reveiwed. I agree that collagen deposition can adversely affect net output. However, considering that the evidence doesn't support the contention of collagen deposition in humans, it's unfounded to take it one step further and make statements of fact that "Thus, the heart is not stronger, but actually degrades the actual muscle fibers and reduces cardiac output."

In sum, the evidence for collagen deposition is much like the evidence for cardiomyocyte apoptosis. It is found at high doses in some animals. It is not found at low doses. Nor is it found even at high doses in some animal studies. The few human studies corroborate the low-dose animal studies, showing no effect. If you want to talk about conceivable dangers like collagen deposition, that's fine. Clenbuterol might have negative effects in this regard. I'm not saying it's impossible. The evidence just doesn't support statements of fact to the contrary, which you should refain from. The problem I have is you making statements that are unsupported and much stronger than the underlying evidence warrants.

 

[Conciliator]

To address your point, your imply that because is that clen has not been proven to be unsafe for human use and in spite of numerous studies in non human mammals, it is safe. You may take issue with such an inference but it is none-the-less a valid one.

Huh? When did I ever say clen "is safe"? To the contrary, I talked about undue risks and side effects that are undoubtedly present at high doses.

As for DNP, we both know it is being studied now--at least its mechanism is, for a potential weight loss drug. The problem is that while you note the incidence of vision-related adverse occurrence may or may not be statistically significant and may result from some genetic predisposition, and as you note the doses taken then and illicitly now are not comparable, the ration of a therapeutic dose and potentially deadly dose is so small as to warrant the gravest of warning against its use--not to mention the risk of the actual dose from an illicit source is palpable.

This is almost unintelligible, but I think I get the gist. I do, however, have to disagree that "the ratio of a therapeutic dose and potentially deadly dose is so small as to warrant the gravest of warning against its use." It has a low therapeutic index, yes, and care must be taken, but it's not that low. For example, I take a moderate dose of 300-400 mg/day of actual DNP. The lethal dose has been estimated to be somewhere between 1500-3000mg. I've got to make quite a big mistake to take 15-30 capsules in a day instead of my usual 3-4. With a modicum of care in titrating the dose, monitoring body temperature, and keeping the dose low, the risk of overdose is negligible.

Do you know how many case reports of fatal overdose there were in the all of the 1930's, when hundrends of thousands of people took DNP over the counter? Three. Not three thousand, not three hundred, just three. Unfortunately, I can guarantee that the mortality rate in recent times (among bodybuilders, for example) is much higher. This is undoubtedly due to the careless and excessive dosages that are frequently seen as users try to push the envelope and maximize fat loss. The high dose "inferno cycle" (sold at Elite, no less) is a most atrocious dosing protocol. That IS the problem with overdose. Fortunately, longer, lower-dose cycles are becoming more and more popular.

Finally, I stand by my supposition that if clen was indeed thought to be effective w/o reasonable risk why is it not marketed as such? The simplest answer is most-likely the correct one: the risk/benefit is not economically nor ethically acceptable.

As a general fat burner, I agree with you. Clen sucks. It doesn't do much to help you create a caloric deficit. Unless major dieatry changes are made with it, it's not going to do much. However, that's not to say it doesn't have untility in more specific circumstances, such as when there's a large caloric deficit or an already low BF percentage. I think clen and DNP complement each other very well, for a number of reasons. For a basic "fat burner," though, I think 99% of people will do much better with the EC stack than with clen.

 

[OneBreath]

This thread is titled "For all those NEW people asking about clen....".

Mastering the art of Google and posting studies doesn't really touch on the above. Its great food for thought and we human minds love to add ridiculous amounts of knowledge to our primitive minds. However, none goes to answering the simple question of "do these noobs need clen?". The answer to that question is probably no.

If they are serious about one day competing, then down the road perhaps that answer changes. But for those reading this now, all of those studies posted doesn't mean its fine to take clen. The thread just got sidetracked into a technical discussion.

 

[slat1]

I'm not a big fan of clen. I get the same results just keeping my diet ultra tight. Plus, the new research linking it to cancer is interesting.