Question about Clen

[Conciliator]

Also, http://www.chp.gov.hk/files/pdf/grp-v10n2-en-2004052100.pdf of 82 cases of meat poisoning in October 2000 in Hong Kong found the concentration of clenbuterol in pork to be 400 mcg/kg, or 40 mcg per 100g. Based on that, a quarter pound serving would contain 45 mcg and a half pound serving would contain 90 mcg.

 

[ChaseQ]

Also, http://www.chp.gov.hk/files/pdf/grp-v10n2-en-2004052100.pdf of 82 cases of meat poisoning in October 2000 in Hong Kong found the concentration of clenbuterol in pork to be 400 mcg/kg, or 40 mcg per 100g. Based on that, a quarter pound serving would contain 45 mcg and a half pound serving would contain 90 mcg.

Thats insane! I would finally be able to eat my bacon and stay lean![)]

Okay so why and how did pigs in China end up mega dosing Clen?

 

[OhNoYo]

Con, Idk why you think heart's of ppl who are healthy and heart's of ppl who have CHF, let alone a LVAD, are the same, b/c they are not. Not only do they work differently, but they are composed of a different ratio of things, and they even look differently. In terms of the way they work, certain things are going to be better for ppl w/ heart failure when in comparison to ppl who are healthy. For example in the link to the study below which is a similar study we have discussed in relation to the ppl who had CHF + LVAD who were given Clenbuterol up to 720mcg/day, it says verbatim...

"The patients underwent implantation of left ventricular assist devices and were treated with lisinopril, carvedilol, spironolactone, and losartan to enhance reverse remodeling. Once regression of left ventricular enlargement had been achieved, the 2-adrenergic–receptor agonist clenbuterol was administered to prevent myocardial atrophy."

http://nejm.highwire.org/cgi/content/abstract/355/18/1873 (NEJM -- Left Ventricular Assist Device and Drug Therapy for the Reversal of Heart Failure)

...So it says there, plain as day, why they gave Clenbuterol to these ppl for the reason I speculated before, to prevent atrophy. Individuals w/ normal hearts do not have to worry about, myocardium atrophy, so therefore Idk where you get this cardioprotective quality that clen possesses in healthy ppl.

Also, the study you gave in the link below you state that the rats achieved "pathological" LVH rather quickly. That's funny, b/c I read the whole article and the authors state nothing about pathological LVH. Furthermore, I searched for the word "pathological" in pdf article format from and still didn't find it. So, Idk what you're talking about in terms of pathological LVH occurring quickly. I've already went thru this with you. The first part of pathological LVH is actually beneficial to the heart, then it goes downhill w/ time. This may be seen w/ the short duration studies that we have both discussed...

http://circres.ahajournals.org/cgi/reprint/28/2/234.pdf

...In the link below I did you a favor and found some study where they actually did a 6week study upon the effects on Clenbuterol on sheep entitled, "Influence of clenbuterol treatment during six weeks of chronic right ventricular pressure overload as studied with pressure-volume analysis". However, what I wanted to get out of this study is provided below, verbatim...

"There is also a lack of information on the cardiac effects of clenbuterol in large mammalian species. Small animal hearts are different from those of large animals both functionally and at the molecular level. For example, in small animals the cardiac myosin heavy chain constitutes close to 90% of total cardiac myosin heavy chain, whereas in human subjects it constitutes only 10%."

http://jtcs.ctsnetjournals.org/cgi/content/full/122/4/767 (Influence of clenbuterol treatment during six weeks of chronic right ventricular pressure overload as studied with pressure-volume analysis -- Hon et al. 122 (4): 767 -- The Journal of Thoracic and Cardiovascular Surgery)

...OK, so from now on, since we are both aware of large mammalian studies may serve as a better model for Clenbuterol in relation to humans than rodents, it might be wise to stop referencing and citing endless mice/rat studies since Clenbuterol may actually act differently on their hearts than ours. You hate how I sometimes speculate upon things, well wouldn't you stating that Clenbuterol is safe for humans from the numerous rat studies you list be speculation also?

However, here is a study stating in horses, which is a large mammal, how chronic use of Clenbuterol is detrimental to cardiovascular function...

Chronic clenbuterol administration negatively alters cardiac... : Medicine & Science in Sports & Exercise

...Also, below is an article that provide what pretty much concludes Clenbuterol may not be a suitable drug for bodybuilders, b/c low doses do not cause any positive attributes...

Chen KD and Alway SE. A physiological level of clenbuterol does not prevent atrophy or loss of force in skeletal muscle of old rats. J Appl Physiol 89: 606–612, 2000.

...Con, we both can argue on here til our fingers fall off, but until you show me HUMAN studies where it concludes Clenbuterol is cardioprotective to the general population, I'm not buying it. I was wrong and you were correct claiming Clenbuterol and other beta2 agonists have body partioning effects, however, I still feel that you are wrong stating that Clenbuterol is cardioprotective for all human popluations, Clenbuterol can be used safely for months on end w/ slowly increasing 20mg/wk, and that Clenbuterol is a safe and effective bodybuilding drug. I'm glad that in one of your newer posts you state that 4-12wks is better to use Clenbuterol than in comparison to many months, so maybe you're starting to refute some of your claims. Do you recommend pyramiding this if ppl choose to do this to possibly cause upregulation when lowering doses when going in down-pyramid fashion so the side effects upon discontinuation won't be so pronounced? Also, as for Clenbuterol being safe AND effective, I feel it can be safe OR effective in that w/ low doses it is safe BUT NOT that effective, and in high doses it is effective BUT NOT safe.

 

[OhNoYo]

Also, http://www.chp.gov.hk/files/pdf/grp-v10n2-en-2004052100.pdf of 82 cases of meat poisoning in October 2000 in Hong Kong found the concentration of clenbuterol in pork to be 400 mcg/kg, or 40 mcg per 100g. Based on that, a quarter pound serving would contain 45 mcg and a half pound serving would contain 90 mcg.

I stand corrected then, so I apologize for this... BUT feel rly sorry ppl who got sick eat'n BIG JUICY STEAKS! :drooling:

 

[OhNoYo]

Your question was the typo "do you know EXACTLY as to how Clen in high doses causes cardiac myocytes?" Of course, that makes no sense. I took it to mean, "do you know how clen causes cardiac myocyte apoptosis," like you were talking about at the end of your previous post. My answer for apoptosis is correct. You're asking about something completely different, about how it might play a contributing role in MI. So no, it doesn't contradict me, since I wasn't talking about that.
Why on earth would it be "ignorant" to argue that clenbuterol causes beta-2 AR downregulation in the heart? Are you serious? lol
What mechanism of action do these drugs work through? Do those MOAs produce rapid desensitization? Or do they continue to work with relatively steady dosing? Ask yourself those questions and you'll have your answer. I think you're smart enough to do that on your own.

That said, take a look at the use of vasopressors. The UpToDate physicians reference states "Tachyphylaxis*—*Responsiveness to these drugs can decrease over time due to tachyphylaxis. Doses must be constantly titrated to adjust for this phenomenon and for changes in the patient's clinical condition." When we look at one of the study references, we read the following: "This study demonstrated that significant hemodynamic tolerance to dobutamine develops after three days of continuous infusion. We suggest that the most appropriate manner of dealing with this attenuation of effect is simply to increase the dose until the desired hemodynamic effect is attained."
Why would TRT physicians need to "consistently up the dose"?
Yes, many things, including most drugs, will cause adverse events in excess. You're being asinine to focus on the fact that it's a possibility and not on the fact that there's a dose response, that the doses humans take are lower than the threshold dose, and that at those lower doses there's still significant anabolic effects.
No, I did not agree with you. I explained how, yet again, you were misunderstanding something that you posted.

Yes, you are correct as I was not thinking correctly w/ over-reading the word "apoptosis" (programmed cell death) and instead just picturing in my head ischemic death. So, I do apologize for that. I'm sorry, Con, but when I saw Clenbuterol in terms of causing myocyte death, I immediately pictured in my head ischemia as in what occurs in myocardial infarctions, since there has been such ancedotal evidence regarding clen and MI. So, once again, I apologize.

 

[Conciliator]

Con, Idk why you think heart's of ppl who are healthy and heart's of ppl who have CHF, let alone a LVAD, are the same, b/c they are not.

I don't think they're the same.

In terms of the way they work, certain things are going to be better for ppl w/ heart failure when in comparison to ppl who are healthy.

The fact that clenbuterol administration may be more beneficial for people with heart failure doesn't entail that it's going to detrimental to people who have healthy hearts.

Individuals w/ normal hearts do not have to worry about, myocardium atrophy, so therefore Idk where you get this cardioprotective quality that clen possesses in healthy ppl.

When I first stated that beta-2 agonism was cardioprotective, I quoted a study that explained that it has an anti-apoptotic effect. Secondary to that is the fact that it improves heart function in several animal and human models.

Also, the study you gave in the link below you state that the rats achieved "pathological" LVH rather quickly. That's funny, b/c I read the whole article and the authors state nothing about pathological LVH. Furthermore, I searched for the word "pathological" in pdf article format from and still didn't find it. So, Idk what you're talking about in terms of pathological LVH occurring quickly

It's not funny, it just goes to show that you can't connect the dots. The study found an increase in myocardial hydroxyproline content. The study didn't say it, but that's collagen. And study also didn't say it, but that's a fundamental aspect of pathological hypertrophy. To quote that 2006 review, "An interest in the effects of increased collagen on left ventricular (LV) diastolic function was sparked in the late 1970s and early 1980s by the following seminal studies: Bing et al. [16] reported an increase in myocardial hydroxyproline in hypertrophied LV... Since then there have been numerous studies with experimental...or genetic...hypertension to indicate a strong relationship between increased LV collagen concentration and chamber stiffness [2,18].... Finally, in the athlete with a significant increase in LV mass and presumably physiologic hypertrophy, diastolic function is normal at rest and enhanced during exercise [22,23]. This physiologic hypertrophy is in contrast to hypertensive patients who typically have significant diastolic dysfunction despite an increase in LV mass that is less than that occurring in athletes [24]. In view of the fact that collagen concentration is increased in humans with systemic hypertension [14] and that diastolic abnormalities in hypertensive patients are not related to increases in LV mass [25], it is reasonable to assume that hypertension-related diastolic dysfunction is the result of excessive myocardial collagen."

 

[Conciliator]

"There is also a lack of information on the cardiac effects of clenbuterol in large mammalian species. Small animal hearts are different from those of large animals both functionally and at the molecular level. For example, in small animals the cardiac myosin heavy chain constitutes close to 90% of total cardiac myosin heavy chain, whereas in human subjects it constitutes only 10%."

http://jtcs.ctsnetjournals.org/cgi/content/full/122/4/767 (Influence of clenbuterol treatment during six weeks of chronic right ventricular pressure overload as studied with pressure-volume analysis -- Hon et al. 122 (4): 767 -- The Journal of Thoracic and Cardiovascular Surgery)

Wow, talk about being intellectual dishonest. You cherry picked this statement when what the study in this "large mammal" found that clenbuterol improved heart function in a model of pulmonary hypertension. Let's look at a big quote from the paper:

However, Liggett and coworkers,Go 14 and previously Milano and colleagues,Go 15 have shown in transgenic mice that increased ß2-adrenergic receptor expression and activity is in fact beneficial to ventricular function. Liggett and colleaguesGo 14 showed that this is true as long as the level of receptor overexpression does not exceed that for spontaneous activation, which in their experiment was between 150 and 350 times the background ß2-adrenergic receptor expression. Furthermore, they have also demonstrated that the hearts tolerated enhanced contractile function caused by 60-fold ß2-adrenergic receptor overexpression without detriment for a period of at least 1 year. Our current results in sheep are in direct agreement with their findings, suggesting that not only the beneficial effects of ß2-adrenergic receptor stimulation on ventricular function in mice is reproducible in the large animal species but also that clenbuterol is able to modulate an otherwise pathologic hypertrophy process into one that is more physiologic in nature, as illustrated by the improved systolic function and the 26.1% greater wall thickness/end-diastolic volume ratio(Table 2Go).

You hate how I sometimes speculate upon things, well wouldn't you stating that Clenbuterol is safe for humans from the numerous rat studies you list be speculation also?

What you're doing is making unfounded speculation. What I'm doing is informed extrapolation. There's a big difference.

However, here is a study stating in horses, which is a large mammal, how chronic use of Clenbuterol is detrimental to cardiovascular function...

Chronic clenbuterol administration negatively alters cardiac... : Medicine & Science in Sports & Exercise

I've seen this paper. My response is that 1) the dose was still 5 times higher than a human usually ever takes (4.8 mcg/kg) and 2) this subsequent research suggests that horses tend to accumulate higher concentrations of clenbuterol in their hearts than other species do. To quote the paper, "To relate the concentrations in the equine to other species, comparisons of the ratio of CLB concentration in tissue with that in plasma was used to demonstrate some comparisons between species. This comparison suggests that the horse had relatively higher concentrations in the myocardium and other tissues at much lower administered doses."

 

[Conciliator]

...Also, below is an article that provide what pretty much concludes Clenbuterol may not be a suitable drug for bodybuilders, b/c low doses do not cause any positive attributes...
Chen KD and Alway SE. A physiological level of clenbuterol does not prevent atrophy or loss of force in skeletal muscle of old rats. J Appl Physiol 89: 606–612, 2000.

This study is questionable in my mind because it contradicts a lot of other papers. A possible explanation for the different finding may be that they used a novel slow-release pellet to administer the clenbuterol. Other studies have given injections to ensure an accurate administration of the drug. Several studies that have shown anabolic effects from very low doses of other beta-2 agonists. http://physrev.physiology.org/cgi/content/full/88/2/729 (This extensive review) references the paper, saying "Chen and Alway (85) found that clenbuterol administered to rats at a low dose of 10 µg·kg–1·day–1 had only modest effects on slow-twitch skeletal muscle and no discernable effect on fast-twitch skeletal muscles. In contrast, newer generation ?-agonists such as formoterol and salmeterol when administered to rats daily via intraperitoneal injection at very low doses (µg/kg) can still elicit significant anabolic responses in fast and slow muscles of the rat (389). A study from our laboratory indicates that formoterol administration to rats at a dose of only 1 µg·kg–1·day–1 can still elicit muscle hypertrophy in both fast- and slow-twitch skeletal muscles (389)."

I'm glad that in one of your newer posts you state that 4-12wks is better to use Clenbuterol than in comparison to many months, so maybe you're starting to refute some of your claims.

I'm not refuting any of my claims. I simply responded to the study protocol (that went up to 720 mcg) and said that I didn't think the slow titration to that dose was particularly dangerous. As for what I've acutally recommended, it's never been close to that protocol.

Do you recommend pyramiding this if ppl choose to do this to possibly cause upregulation when lowering doses when going in down-pyramid fashion so the side effects upon discontinuation won't be so pronounced?

I do recommend pyramiding down. I don't think it's essential, but I do think it's a good idea to prevent withdrawal symptoms.

Also, as for Clenbuterol being safe AND effective, I feel it can be safe OR effective in that w/ low doses it is safe BUT NOT that effective, and in high doses it is effective BUT NOT safe.

You should read this study from start to finish. That's exactly what it addressed. You know the famous study showing cardiomyocyte apoptosis at a threshold level of 1 mcg/kg? Well this is a subsequent paper by the same authors. They answer that it can be safe and effective. Also, if this is your position, you'd have to say that all of the studies I posted earlier showing an anabolic effect in humans were unsafe (since they were effective). Are you sure you want to take that position?

 

[OhNoYo]

I don't think they're the same.
The fact that clenbuterol administration may be more beneficial for people with heart failure doesn't entail that it's going to detrimental to people who have healthy hearts.
When I first stated that beta-2 agonism was cardioprotective, I quoted a study that explained that it has an anti-apoptotic effect. Secondary to that is the fact that it improves heart function in several animal and human models.
It's not funny, it just goes to show that you can't connect the dots. The study found an increase in myocardial hydroxyproline content. The study didn't say it, but that's collagen. And study also didn't say it, but that's a fundamental aspect of pathological hypertrophy. To quote that 2006 review, "An interest in the effects of increased collagen on left ventricular (LV) diastolic function was sparked in the late 1970s and early 1980s by the following seminal studies: Bing et al. [16] reported an increase in myocardial hydroxyproline in hypertrophied LV... Since then there have been numerous studies with experimental...or genetic...hypertension to indicate a strong relationship between increased LV collagen concentration and chamber stiffness [2,18].... Finally, in the athlete with a significant increase in LV mass and presumably physiologic hypertrophy, diastolic function is normal at rest and enhanced during exercise [22,23]. This physiologic hypertrophy is in contrast to hypertensive patients who typically have significant diastolic dysfunction despite an increase in LV mass that is less than that occurring in athletes [24]. In view of the fact that collagen concentration is increased in humans with systemic hypertension [14] and that diastolic abnormalities in hypertensive patients are not related to increases in LV mass [25], it is reasonable to assume that hypertension-related diastolic dysfunction is the result of excessive myocardial collagen."

Read up on left vs right side heart failure on top of systolic vs diastolic dysfunction so you can better understand the overall aspects of LVH and heart failure b/c increased collagen synthesis in the myocardium isn't the KNOW ALL AND SAY ALL in developing heart failure. On top of this, its extremely arrogant of you to put words into the researchers mouths, when they said nothing about "pathological" LVH in the study, Sir.

 

[OhNoYo]

Wow, talk about being intellectual dishonest. You cherry picked this statement when what the study in this "large mammal" found that clenbuterol improved heart function in a model of pulmonary hypertension. Let's look at a big quote from the paper:

What you're doing is making unfounded speculation. What I'm doing is informed extrapolation. There's a big difference.
I've seen this paper. My response is that 1) the dose was still 5 times higher than a human usually ever takes (4.8 mcg/kg) and 2) this subsequent research suggests that horses tend to accumulate higher concentrations of clenbuterol in their hearts than other species do. To quote the paper, "To relate the concentrations in the equine to other species, comparisons of the ratio of CLB concentration in tissue with that in plasma was used to demonstrate some comparisons between species. This comparison suggests that the horse had relatively higher concentrations in the myocardium and other tissues at much lower administered doses."

Con, I didn't cherry pick anything. The technique used in the study on the sheep is in NO way, shape, or form meant to mimic ANYTHING even closely related to what happens in normal human physiology in healthy subjects. This (yet again) comes back to how is Clenbuterol cardioprotective in normal, healthy human subjects. First, you state how it is b/c it was in studies regarding ppl w/ heart failure. Then I state how they used the Clenbuterol to retain normal myocardium size and how its common knowledge healthy ppl don't need to worry about myocardium retention size Clenbuterol is NOT cardioprotective. Now you bring up some bullshit about it has cardioprotective qualities b/c it prevents apoptosis. In high doses, we both know this is NOT the case. Also, below is an excellent review for you to read before you go throwing around the word "apoptosis", since you need a better understanding of what the word actually means in pertinence to myocytes...

The Mitochondrial Death Pathway and Cardiac Myocyte Apoptosis -- Crow et al. 95 (10): 957 -- Circulation Research

Also, below is a study I found for you that supports your claim of cardioprotective qualities by preventing apoptosis, BUT IN FAILING HEARTS ONLY, abstract is verbatim...

"Abstract
Beta-adrenergic receptor (AR) subtypes are archetypical members of the G protein-coupled receptor (GPCR) superfamily. Whereas both beta1AR and beta2AR stimulate the classic G(s)-adenylyl cyclase-3',5'-adenosine monophosphate (cAMP)-protein kinase A (PKA) signaling cascade, beta2AR couples to both G(s) and G(i) proteins, activating bifurcated signaling pathways. In the heart, dual coupling of the beta2AR to G(s) and G(i) results in compartmentalization of the G(s)-stimulated cAMP signal, thus selectively affecting plasma membrane effectors (such as L-type Ca(2+) channels) and bypassing cytoplasmic target proteins (such as phospholamban and myofilament contractile proteins). More important, the beta2AR-to-G(i) branch delivers a powerful cell survival signal that counters apoptosis induced by the concurrent G(s)-mediated signal or by a wide range of assaulting factors. This survival pathway sequentially involves G(i), G(beta)(gamma), phosphoinositide 3-kinase, and Akt. Furthermore, cardiac-specific transgenic overexpression of betaAR subtypes in mice results in distinctly different phenotypes in terms of the likelihood of cardiac hypertrophy and heart failure. These findings indicate that stimulation of the two betaAR subtypes activates overlapping, but different, sets of signal transduction mechanisms, and fulfills distinct or even opposing physiological and pathophysiological roles. Because of these differences, selective activation of cardiac beta2AR may provide catecholamine-dependent inotropic support without cardiotoxic consequences, which might have beneficial effects in the failing heart."

Beta-adrenergic signaling in the heart: dual coupl... [Sci STKE. 2001] - PubMed result

...so beta2 agonists MIGHT have positive effects to heart failure, which we have pretty much established anyway. However, since what was spoke about in the study above, normal functioning hearts don't have to worry about, so Clenbuterol is NOT cardioprotective. On top of that, since Clenbuterol indirectly activates beta1 agonists, I will again go to the review regarding apoptosis, in what it says, verbatim...

"Apoptosis is an evolutionarily conserved suicide process that plays critical roles in embryonic development and in the homeostasis, remodeling, surveillance, and host defenses of postnatal tissues.7 The pathways that mediate apoptosis are more than one billion years old and are central to such fundamental biological processes as growth, proliferation, differentiation, death, inflammation, and immunity. Hence, apoptosis is essential for life itself. Conversely, dysregulation of apoptosis, resulting in either too little or too much cell death, has been implicated in human disease.8 For example, insufficient apoptosis may contribute to carcinogenesis, whereas excessive apoptosis may be a component in the pathogenesis of stroke, myocardial infarction, and heart failure. It is interesting to speculate why a pathological role for apoptosis has persisted in the face of evolutionary change. One possibility is that the importance of apoptosis in basic biological functions outweighs its potentially detrimental effects. Another likely explanation is that most diseases involving excessive apoptosis occur in postreproductive life.

Cardiac myocytes undergo apoptosis in response to a myriad of stimuli including hypoxia,9 especially followed by reoxygenation,10 acidosis,11 oxidative stress,12 serum deprivation,13,14 glucose deprivation and metabolic inhibition,15,16 ß1-adrenergic agonists,17–19 stretch,20 angiotensin II,21 tumor necrosis factor-,22 Fas ligand,23,24 and anthracyclines.25 In intact animals, cardiac myocyte apoptosis occurs during myocardial infarction,26–29 especially followed by reperfusion,30,31 heart failure32–38 and various cardiomyopathic states,39 myocarditis,40 and transplant rejection.41 The strength of the data differ for these syndromes but are most compelling for ischemia-reperfusion injury and heart failure."

The Mitochondrial Death Pathway and Cardiac Myocyte Apoptosis -- Crow et al. 95 (10): 957 -- Circulation Research

...so, apoptosis is essential for life, so preventing it in healthy hearts might not necessarily be a good thing. Hell, it is known as programmed cell death, so in healthy humans I think the cells know when it is time for them to die. Also in bold, something we BOTH are aware of anyway, beta1 agonist cause apoptosis, since clen has indirect beta1 agonist function, this isn't a good quality for bodybuilders.

Con, though until you bring up some human studies about Clenbuterol being cardioprotective in normal, healthy subjects, then your claim to this is merely speculation, and you know it is! So, until you show me a study which concludes that, you are ONLY speculating, and speculating from animal models which are poor models and from ppl who are diagnosed w/ heart failure, which is a total joke and someone as intelligent as you, you should be ashamed of urself, unless of course you show me some human studies where Clenbuterol is cardioprotective along the lines of being able to give significant results to body composition at low safe doses that you give in your protocol, then I will shut my mouth. But, I really don't see it happening for reasons that case studies + ancedotal evidence refute this.

 

[OhNoYo]

Yes, I really think that, based on the evidence. In contrast, you don't think that, based on hunches and speculation and poor analogies to hypertension, in contradiction to the evidence.
I haven't looked into this specifically. However, it's known that catacholamines are both myotoxic and cause pathological LVH, in contrast to the selective b2-agonism of clenbuterol.
Your reasoning on this is very poor. I hope you don't think you can conclude from this case report that the clenbuterol caused his LVH or that the LVH was pathological. Things other than clenbuterol could have caused the LVH. For example, this study found that 43% of drug-free bodybuilders had "left ventricular dimensions beyond normal ranges (>11 mm)."

It's even a further stretch to say that the LVH was pathological. As the previous reference explains, "A recent review on the athlete’s heart has suggested the differential in pathologic versus physiologic LVH is found in the diastolic function [3]." This case report says nothing to suggest impaired function.

Regarding the dose, I would not call 20mg twice a day a "very small dose, which I find is OK." Early on, I think 40mcg/day is far too high. It's 4-8x higher than I would ever take or recommend taking for initial dosing and it's double what most bodybuilders would take for initial dosing. Please let it register that the absolute dose means essentially nothing. It's the dose relative to sensitivity that has any meaning. I don't know why that concept is so hard for you to comprehend.

A very important piece of information from this case report is that the chest pain "appeared after an episode of emotional stress the day before." Weaker pain that occurred 1 month earlier was also "at the time when the boy was having difficulties at school." The presence of high levels of natural catacholamines during an episode of high stress is very relevant here.

Finally, the kid had hyperhomocysteinemia and markers of a prothrombotic state, both of which would predispose him to an MI. While the clen may very well have contributed, there's no way to know for sure. What we do know is that this paper does nothing to support a link between LVH and the MI. Rather, the authors suggest that "Hyperhomocysteinemia causes endothelial dysfunction which might facilitate thrombosis or promote coronary artery spasm resulting from the action of clenbuterol."

Unless they have a congential heart defect, particularly hypercardiomyopathy, 17 year old's just don't have myocardial infarctions (MI), unless of course something like drugs caused it. In this case, it is Clenbuterol. You state the Clenbuterol may have caused it but no one knows for sure b/c of the hyperhomocysteinemia plus prothrombatic states, but whose not to say that Clenbuterol couldn't have caused that as well? Below is a case study I think you may find intriguing regarding how a synephrine containing OTC supplement may have caused an MI. There hypothesis was that it may have triggered coronary spasm which caused a blood clot to form. The Clenbuterol in the 17 year old's case may have caused the same thing, perhaps?...

STEMI in a 24-Year-Old Man after Use of a Synephrine-Containing Dietary Supplement

 

[OhNoYo]

Your question was the typo "do you know EXACTLY as to how Clen in high doses causes cardiac myocytes?" Of course, that makes no sense. I took it to mean, "do you know how clen causes cardiac myocyte apoptosis," like you were talking about at the end of your previous post. My answer for apoptosis is correct. You're asking about something completely different, about how it might play a contributing role in MI. So no, it doesn't contradict me, since I wasn't talking about that.
Why on earth would it be "ignorant" to argue that clenbuterol causes beta-2 AR downregulation in the heart? Are you serious? lol
What mechanism of action do these drugs work through? Do those MOAs produce rapid desensitization? Or do they continue to work with relatively steady dosing? Ask yourself those questions and you'll have your answer. I think you're smart enough to do that on your own.

That said, take a look at the use of vasopressors. The UpToDate physicians reference states "Tachyphylaxis*—*Responsiveness to these drugs can decrease over time due to tachyphylaxis. Doses must be constantly titrated to adjust for this phenomenon and for changes in the patient's clinical condition." When we look at one of the study references, we read the following: "This study demonstrated that significant hemodynamic tolerance to dobutamine develops after three days of continuous infusion. We suggest that the most appropriate manner of dealing with this attenuation of effect is simply to increase the dose until the desired hemodynamic effect is attained."
Why would TRT physicians need to "consistently up the dose"?
Yes, many things, including most drugs, will cause adverse events in excess. You're being asinine to focus on the fact that it's a possibility and not on the fact that there's a dose response, that the doses humans take are lower than the threshold dose, and that at those lower doses there's still significant anabolic effects.
No, I did not agree with you. I explained how, yet again, you were misunderstanding something that you posted.

It is ignorant and pointless to compare beta1 and beta2 receptors in the heart of ppl w/ CHF compared to ppl who have normal, healthy hearts in regards to respected drug MOA b/c the receptors are different in distribution and number. This is one of the things I keep trying to get at when you keep giving studies about how great Clenbuterol is in ppl w/ severe CHF (sometimes along w/ LVAD), then using that to bridge over to how it is cardioprotective to ALL HUMANS, when it is NOT! Read the article below and for future reference either understand what I'm talking about, or plz not take my statements out of context...

Beta2-adrenergic receptor redistribution in heart ... [Science. 2010] - PubMed result

...As for the TRT dose being increased, it was a generic comment being compared to what you explain to be such a great thing, which is increasing clen dose to prolong its body partioning effects. Think of someone who first takes TRT and starts to notice some body composition effects at first, but then they stop, and it he wants to see more in terms of positive body composition. You think the doctors is going to keep upping his TRT dose to get him where he wants? I just meant this to be a general comment, where do things end and where should the line be drawn in terms of side effects vs effectiveness?

 

[OhNoYo]

Con, although the link provided below is not a study, I feel that it is essential material in relation to what we have been discussing regarding Clenbuterol. The information in the link states that Clenbuterol may trigger powerful growth factors for ppl that have CHF + LVAD! Con, do you know what those powerful growth factors are and how they would possibly reverse the effects of the horrible negative consequence of CHF, Sir?...

http://www.msnbc.msn.com/id/19033358/ns/health-heart_health/ (Banned drug may help treat heart failure - Heart health- msnbc.com)