how bad actually is clen for ur heart?

[jimmyinkedup]

Rebuttal for 1)
There is a wealth of studies out there showing the myotoxicity of clen and myocyte apoptosis. It has to do with increased sympathetics to the heart. Clen being a sympathomemetic drug, increases this stimulation. Also, as ive said before and seems to be overlooked, ALL of the studies posted for the support of clen being cardio protective is done on a DAMAGED heart. Much different than a healthy heart. In a healthy heart, combined with the increased muscle growth capacity (on cycle), and once again ive said this already *to those PREDISPOSED* this can cause issues, and probably is a large reason for the increasing deaths using Clen (at a younger age, combined with training, and high natural test/AAS cycle test levels)

http://onlinelibrary.wiley.com/doi/1...mus.20407/full
http://onlinelibrary.wiley.com/doi/1...02549/abstract
http://onlinelibrary.wiley.com/doi/1...04.027482/full

Also, high levels of catecholamines is known to be cardio toxic, and with clen being a mimic of them and also increasing the release of catecholamines, you can induce that high levels of clen *in a healthy heart* can be cardiotoxic. Cardiotoxic = kills heart cells
so, no nail in the coffin b/c those studies were done on a failing heart. Healthy heart is totally different.

Rebuttal for 2)
Yes, enlargement of the heart can cause problems. Asthmatics usually dont take a oral B2 drug b/c of the potential cardio issues. Its an inhaler which increases the selectivity of the drug because it has to pass through the lungs before going systemic. So trying to compare heart hypertrophy between asthmatics vs clen users isnt really a good comparison.
Also, the MOA of clen, its not that good of a bronchodialtor. Asthmatics dont use long acting b2 agonists due to the sides of constant use, they are used in combination with other drugs that are basically immunosuppressive which helps calm the overactive nature of asthma. The main b2 agonists used by asthmatics are short acting, aka rescue inhaler. And there are plenty of studies showing the dangers of abuse of those inhalers (even though its local contact with the lungs, too much goes systemic.. and clen is systemic by nature sooo...).
Clen isnt even legal in the US. So what does that tell you about the benefits it has for bronchodialiting? if it was that good, it would be used more. But there are other drugs, and its long acting, and isnt that great of a dialaitor. It has better 'fat burning' properties due to b3 activation, along with some b1 activation. The amount of b1 activation is different between people, and in those (as ive said before) that are predisposed to it, can have some problems. And i would bet that those problems are augmented with those on a AAS cycle due to the 'muscle growth benefits' of the AAS, that those problems would present alot faster.



Still waiting on info about the 'Nonsense' swifto.... Please tell me what im saying is wrong.

Fuksake Lemon - you know what aggrivates me - when the point of the argument is to be right rather than to pass along accurate info. I am stubborn - hell im real stubborn -but people are going to read this and possibly believe some of the crap you are writing as fact and IMO you are doing it to back up your orginal post simply so you can be right. WTF -isnt it about clen and learning? Ok so im not going to point by point rip apart your post here - i'll just keep it very basic.

#1 - First off stop using fvcking propaganda to support your contention. Increasing deaths using clen - there are what two case studies. Fvck i could prob find more case studies on fat soluable vitamin overdoses resulkting in death or some BS like that. Stop that BS. Anyway so let me get this straight - clen causes heart cell death according to you via catecholamines. This purported effect on catecholamines is the same in everyone - damaged heart or not. So basically you are saying that they give a medication that kills heart cells to peole who have damged hearts? Huh ? Or are you saying it only kills heart cell in healthy hearts via catecholamines , but in damaged hearts it doesnt kill them even though the same exact catecholamine effects would occur. Is this real life???

#2 I dont care WHY asthmatics take b2 agonists - the point is they take them - they lead active lives - and they aften take them high frequency - long duration (like a lifetime). In one sentence you say imnhalers increase selectivity - then you say the meds they administer go systemic...which is it ? Also please stop with the BS that long acting oral b2 agonist arent taken for asthma. Should I list the oral long acting or extended release b2 agonists available: ie fomoterol ,modified relase salbutamol , bambuterol,etc. Shall I contnue there are a couple more as well? Should we discuss indacaterol , a new catgory of b2 agonist , ultra long acting? I aslo find it ironic that these "cardic dangerous meds" are not only used in asthma treatment by millions but they are also used to treat COPD as well. Imagine that giving a drug that "dangerously enlarges the heart" and "kills heart cells" to someone with a pulmonary disease. WTF Lemon ? If you are going to base an argument to support a contention thats fine , but dont spread inaccurate info as far as drugs , theiur usage , their method of administration, etc to support your argument just so you can appear "right".

To All:
*Look if you think clen is dangerous - dont take it.
*If you want to use it with caution dosage and duration of course play a role. Also cycling usage may be prudent- ie: 2 weeks on -2 weeks off.
*If you want to use EXTRA caution take it with an ace inhibitor (if not prescription then hawthorne berry supp).
*You should always monitor BP at all times - off cycle , on cycle , clen - no clen. It may be the single most prudent preventive measure we can do in this lifestyle (prob in any lifestyle to be honest)

Ill say this - if I was forced to choose -id use clen over T3 when it comes to adverse cardiac effects. Id use it over DNP for overall safety. Hell based on Lemons catecholamine BS it safer than ephedrine.
Of course we need to keep in mind we are using it in conjunction with AAS - its easy to pick clen and villify it - easier than taking an honest look at all the substances we use and what they can or could do and make the decision to use or not on the same criteria by which we judge clen as "unsafe" or "dangerous". Trust me you start applying the criteria used by those to say clen is dangerous or deadly to other substances we use you would no be touching several of them (like almost all) or at the very least you would be forced to be honest and say yeah i know but i choose to use them anyway. Clen - just like most anything - in the abscence of prexisting condition (like untreated hypertension) or serious medical pre disposition - used prudently is fine imo.

[Lemonada8]

Fuksake Lemon - you know what aggrivates me - when the point of the argument is to be right rather than to pass along accurate info. I am stubborn - hell im real stubborn -but people are going to read this and possibly believe some of the crap you are writing as fact and IMO you are doing it to back up your orginal post simply so you can be right. WTF -isnt it about clen and learning? Ok so im not going to point by point rip apart your post here - i'll just keep it very basic.

#1 - First off stop using fvcking propaganda to support your contention. Increasing deaths using clen - there are what two case studies. Fvck i could prob find more case studies on fat soluable vitamin overdoses resulkting in death or some BS like that. Stop that BS. Anyway so let me get this straight - clen causes heart cell death according to you via catecholamines. This purported effect on catecholamines is the same in everyone - damaged heart or not. So basically you are saying that they give a medication that kills heart cells to peole who have damged hearts? Huh ? Or are you saying it only kills heart cell in healthy hearts via catecholamines , but in damaged hearts it doesnt kill them even though the same exact catecholamine effects would occur. Is this real life???

#2 I dont care WHY asthmatics take b2 agonists - the point is they take them - they lead active lives - and they aften take them high frequency - long duration (like a lifetime). In one sentence you say imnhalers increase selectivity - then you say the meds they administer go systemic...which is it ? Also please stop with the BS that long acting oral b2 agonist arent taken for asthma. Should I list the oral long acting or extended release b2 agonists available: ie fomoterol ,modified relase salbutamol , bambuterol,etc. Shall I contnue there are a couple more as well? Should we discuss indacaterol , a new catgory of b2 agonist , ultra long acting? I aslo find it ironic that these "cardic dangerous meds" are not only used in asthma treatment by millions but they are also used to treat COPD as well. Imagine that giving a drug that "dangerously enlarges the heart" and "kills heart cells" to someone with a pulmonary disease. WTF Lemon ? If you are going to base an argument to support a contention thats fine , but dont spread inaccurate info as far as drugs , theiur usage , their method of administration, etc to support your argument just so you can appear "right".

why are you taking this so personal? go for it, rip apart my post point by point. I would actually appreciate that. I can debate w/o getting so angry.

Im not using any propaganda at all, i dont need to. The thing is that my first post was pretty neutral, then you had to come in and say "im wrong", so yea im gonna argue that im right. And i am still neutral on the issue, i am just explaining some mechanisms for how issues arise.
You tell me to look at the big picture, ok You do the same.
The cardiac failure patients recieving Clen, are having LV contractility problems. Clen increases contractility, by 2 mechanisms if you really want to get down to it. 1) is the beta1 agonism, which *like ive said* is different between people and is dose dependent. 2) it is a b2 agonist, so its gonna lower BP, You lower BP you raise HR. Easy as that.
No, increased catecholamines would actually help the person with heart contractility issues but since there would be a higher chance of other activation by them, thats why there are specific drugs that target the certain receptors. Do you even know what a catecholamine is? And ive said before, in high doses in a healthy heart (that being dose dependent, and person specific aka have a predisposition towards cardio issues) have a higher chance for apoptosis, and that being combined with AAS, the hypertrophy ability of the heart would be augmented.
Clen can increase catecholamine release, and continous high levels of them can increase issues.. so a->b->c, a->c. aka its possible that continous clen usage can cause cardio issues.
So 2 case studies huh? so how many case studies have to be done on deaths untill it is 'a legitimate issue'?

Have you ever looked at the studies surrounding LABA (long acting beta agonists), they actually decrease life span and increase deaths associated to asthma. Several meta-analysis's done suggesting this. And quit trying to pull in those other LABA (fomoterol, salbutamol, etc) into the same category as clen. They arent the same. And ALL of them are available as inhalers to where the drug is DIRECTLY put in the lungs, where it is wanted to have the most action. If you take a pill of a LABA, it has to go through the digestive system, liver and blood stream before getting to the lungs which = systemic. Well the lungs is a little part of the body, and wait? dont vessels have B2 receptors on them also? So by the time the drug gets to the lungs, there is less of it available so what to do? take more in the oral form. And that increases other side effects. Along with LABA, there is usually either an anti-muscarinic or an immunosuppresive drug to combat the other issues related with COPD and Asthma. And side effects of those medications? Increased BP and Increased HR.
That is a really simple concept, and kinda makes me question your ability to debate this topic if you cant understand that. Must by why im writing 'crap' and 'inaccurate info', and you have to include insults in your reply.

some readings that may be informative
http://www.iaaf.org/mm/document/imported/42027.pdf
http://www.annals.org/content/144/12/904.short

[jimmyinkedup]

why are you taking this so personal? go for it, rip apart my post point by point. I would actually appreciate that. I can debate w/o getting so angry. Your sole purpose is to be right - not be accurate and you will argue till hell freezes over - slipping in ignorant innacurate statements everyt step of the way - its infuriating.

Im not using any propaganda at all, i dont need to. The thing is that my first post was pretty neutral, then you had to come in and say "im wrong", I merely pointed out that you seemed to be ingnoring the fact that clen is a selective beta agonist - which discounted many of your contentions in that post so yea im gonna argue that im right. Yeah fvck if what you say is accurate - better to try to appear be correct and save face than to be humble and learn somethingAnd i am still neutral on the issue, i am just explaining some mechanisms for how issues arise.
You tell me to look at the big picture, ok You do the same.
The cardiac failure patients recieving Clen, are having LV contractility problems. Clen increases contractility, by 2 mechanisms if you really want to get down to it. 1) is the beta1 agonism, which *like ive said* is different between people and is dose dependent. 2) it is a b2 agonist, so its gonna lower BP, You lower BP you raise HR. Easy as that.
No, increased catecholamines would actually help the person with heart contractility issues but since there would be a higher chance of other activation by them, thats why there are specific drugs that target the certain receptors. Do you even know what a catecholamine is? Nice - real nice - you twatAnd ive said before, in high doses in a healthy heart (that being dose dependent, and person specific aka have a predisposition towards cardio issues) have a higher chance for apoptosis, and that being combined with AAS, the hypertrophy ability of the heart would be augmented.
Clen can increase catecholamine release, and continous high levels of them can increase issues.. so a->b->c, a->c. aka its possible that continous clen usage can cause cardio issues.
So 2 case studies huh? so how many case studies have to be done on deaths untill it is 'a legitimate issue'? the point (which im sure u know) is that there are more case studies reporting death from ...you know what...this sentewnce is so fvcking stupid in the context its being used in im not even going to point out how obviouszly stupid it is- like i sad prob more deaths from fat soluable vitamin overdoses...need i say more?

Have you ever looked at the studies surrounding LABA (long acting beta agonists), they actually decrease life span and increase deaths associated to asthma.right-die from ASTHMA symptoms-not cardiac necrosis or LV hyperatrophy. You have no fvcking ethics whatsoever to stoop to being this misleading Several meta-analysis's done suggesting this. And quit trying to pull in those other LABA (fomoterol, salbutamol, etc) into the same category as clen. They arent the same. And ALL of them are available as inhalers to where the drug is DIRECTLY put in the lungs, where it is wanted to have the most action. If you take a pill of a LABA, it has to go through the digestive system, liver and blood stream before getting to the lungs which = systemic. Well the lungs is a little part of the body, and wait? dont vessels have B2 receptors on them also? So by the time the drug gets to the lungs, there is less of it available so what to do? take more in the oral form. And that increases other side effects. you ignorant twat EVERY med i mentioned is avail and prescribed in pill form as well Along with LABA, there is usually either an anti-muscarinic or an immunosuppresive drug to combat the other issues related with COPD and Asthma. And side effects of those medications? Increased BP and Increased HR.
That is a really simple concept, and kinda makes me question your ability to debate this topic if you cant understand that. Must by why im writing 'crap' and 'inaccurate info', and you have to include insults in your reply.

some readings that may be informative
http://www.iaaf.org/mm/document/imported/42027.pdf
http://www.annals.org/content/144/12/904.short
attention all-if u have asthma - you might die from...u ready.....asthma *L*

See bold.

Funny how you choose to repeatedly ignore my summations re the topic which put everything into perspective , show how foolish this fear mongering is in the big picture ,and even offer suggestions for helpful supplementation if u are paranoid. I guess you cant acknowledge that because in some sense it shows the lack of prudence in your entire argument and god forbid u concede that fact and learn something.

Your contribuions and misinformation perpitrated in this thread are right up there with your "winstrol wont do anything in women since they dont have dht receptors" idiotic statement.

[Lemonada8]

back to insults huh? Congrats for really showing who the twat is.

Whats infuriating is someone who thinks they are a complete bad azz on the fvckin internet and doesnt know shit about ANS pharmacology, cardiac remodeling, and whatever other topic is included in this thread.

hmm what did you say, imma pull out the bolded statements.

Your sole purpose is to be right - not be accurate and you will argue till hell freezes over - slipping in ignorant innacurate statements everyt step of the way - its infuriating.
*insult

I merely pointed out that you seemed to be ingnoring the fact that clen is a selective beta agonist - which discounted many of your contentions in that post
*irrelevant due to IVE ALREADY SAID THAT, and the point is that ORAL beta 2 selective is going to hit beta 1 receptors in high enough doses. (go back and read, ive said that already a few times i believe)

Yeah fvck if what you say is accurate - better to try to appear be correct and save face than to be humble and learn something
*insult

Nice - real nice - you twat
*insult, yet you fail to acknowledge that you know what catecholeamines are. You think oh its bad no matter what... Sry nice try but WRONG.

right-die from ASTHMA symptoms-not cardiac necrosis or LV hyperatrophy. You have no fvcking ethics whatsoever to stoop to being this misleading
*insult
btw, its LV hypertrophy, not hyperatrophy. Cardiac cell apoptosis/necrosis doesnt shrink the heart, it enlarges it b/c it become fibrous which, over time if enough occurs, can cause contractility issues.
Yet this is still a 2 way street, cuz clen increases angiogensis so in those fibrous cells it would be getting blood flow somewhat halting that from happening. But like ive said *when in combination with AAS* muscle grows faster than blood vessels, so the rate of angiogensis doesnt keep up with the hypertrophy of the heart you get less bloodflow to the heart, and when it reaches a point in some people it = myocardial infarction aka loss of blood flow.
It works in those needing LV contractility increase, mainly cuz thats due to a natural lack of blood flow and the angiogensis isnt trying to outcompete with the growth of muscle tissue. So like ive said from the start, in a diseased heart its beneficial but a healthy heart it can be problematic, more so if on AAS.
Yes, those deaths are more related to asthma, but are they the same doses as people taking clen? doubtful. You act like they are perfectly safe, yet with extended use it increases death rates.

you ignorant twat EVERY med i mentioned is avail and prescribed in pill form as well
*insult, after failing to understand i NEVER said its not available in pill form, i was pointing out how difference in administeration of the medicine affects the sides. But you didnt see that, you saw " oh its in pill form also not just inhaler i know that".. blah blah blah. Another FAIL on understanding the point, just seeing a argueable point and spewing insults combined with NO REAL INSIGHT. Congrats. So, listen to your own damn advice and *ill use ur quote* "Yeah fvck if what you say is accurate - better to try to appear be correct and save face than to be humble and learn somethin"

Funny how you choose to repeatedly ignore my summations re the topic which put everything into perspective , show how foolish this fear mongering is in the big picture ,and even offer suggestions for helpful supplementation if u are paranoid.havent touched this one... but a herbal ACE inhibitor cant hurt anyways. does it have much of an effect on this issue? doubtful I guess you cant acknowledge that because in some sense it shows the lack of prudence in your entire argument and god forbid u concede that fact and learn something. another insult

Your contribuions and misinformation perpitrated in this thread are right up there with your "winstrol wont do anything in women since they dont have dht receptors" idiotic statementyup that was pretty dumb... but im positive i acknowledged how dumb that statement was in a post later on in that thread. Puts a damper on your "be humble" suggestion, cuz well ive already shown that i am when presented with actual knowledge in a debate/topic. Instead you offer insults..

Put it in perspective huh? well the funny thing is that you cant offer any scientific knowledge in defense of what you are saying, and cant/dont offer a rebuttal in mechanisms on how issues occur. that combined with insults... OoOo just cuz i can talk(type) angrly means im right.
And mis information huh? all you have rebutted me with is insults and attacks, NO MISINFORMATION WHATSOEVER. So what does that leave? i retort with scientific knowledge and u give me insults. FAIL.

Performance-enhancing substances in sport and exercise By Michael S. Bahrke - check out in google books chapter 4.
http://www.fasebj.org/content/16/2/135.full - info about cardiac remodeling
http://www.ncbi.nlm.nih.gov/pubmed/16060696 - if you dont believe what i am saying... here you go, pretty much word for word. And thats with inhaled, what happens when its oral? it has to go systemic before gettin to the lungs, so Increased possibilities of issues.

Inhaled beta2-adrenoceptor agonists: cardiovascular safety in patients with obstructive lung disease.

Although large surveys have documented the favourable safety profile of beta(2)-adrenoceptor agonists (beta(2)-agonists) and, above all, that of the long-acting agents, the presence in the literature of reports of adverse cardiovascular events in patients with obstructive airway disease must induce physicians to consider this eventuality. The coexistence of beta(1)- and beta(2)-adrenoceptors in the heart clearly indicates that beta(2)-agonists do have some effect on the heart, even when they are highly selective. It should also be taken into account that the beta(2)-agonists utilised in clinical practice have differing selectivities and potencies. beta(2)-agonist use has, in effect, been associated with an increased risk of myocardial infarction, congestive heart failure, cardiac arrest and sudden cardiac death. Moreover, patients who have either asthma or chronic obstructive pulmonary disease may be at increased risk of cardiovascular complications because these diseases amplify the impact of these agents on the heart and, unfortunately, are a confounding factor when the impact of beta(2)-agonists on the heart is evaluated. Whatever the case may be, this effect is of particular concern for those patients with underlying cardiac conditions. Therefore, beta(2)-agonists must always be used with caution in patients with cardiopathies because these agents may precipitate the concomitant cardiac disease.

[jimmyinkedup]

back to insults huh? Congrats for really showing who the twat is.

Whats infuriating is someone who thinks they are a complete bad azz on the fvckin internet and doesnt know shit about ANS pharmacology, cardiac remodeling, and whatever other topic is included in this thread.

Lemon it is impossible to get anywhere with you other than "you are right" When you say something and someone corrects you - you merely say oh well it doesnt matter because xyz. If you make a claim that you use to form a key part of your argument and then someone proves it inaccurate - you say yeah but so what because blah blah blah. Its all one jusitfication after another - all about you being "right" instead of about what is ultimately, in the big picture of this discussion, correct. I hoenstly wonder if you even read the responses to your posts entirely - if you did you surely would not say some of the fooish things you do (ie: your comments re: my knowledge of catecholamines), It goes to a point of 2 case studies becomeing "the increasing number of deaths from clen" and studies showing astmatics that use long acting b2 agonist die of (drumroll please) ........asthma. For christs sake. Its just ridiculous. Look at the study you just posted - its retarded - it says that those with copd and asthma need to be careful with taking b2 agonist because the DISEASE amplifies the impact b2 agonists have on the heart. Christ between that statement there and the last line you quoted you virtually shot 1/2 the agruiments you made in this thread right in the foot! You cant argue science with someone when everytime you prove a main point they make untrue they totally change the relevance of said contention or point. It to the point you are so wrapped up in being right you dont even realize when you contradict yourself later on in the discussion! What was once a significant point in your argument then becomes insiginificant. Its ridiculous.
I'll be honest - i dont care what you think. I stand firmly by my contentions, im going to re post the cliffs right now -them im out. I cannot , nor will I agrue with you any longer. Not because i feel I lack the intelectual ability to do so , but because I feel it is an exercise in fultitilty given the way you change the foundations of your contentions or supporting points once they are proven wrong. As a result of that the argument/discuassion would never end. It would only end for you if you left thinking you were right and everyone said so.

Cliffs:
To All:
*Look if you think clen is dangerous - dont take it.
*If you want to use it with caution dosage and duration of course play a role. Also cycling usage may be prudent- ie: 2 weeks on -2 weeks off.
*If you want to use EXTRA caution take it with an ace inhibitor (if not prescription then hawthorne berry supp).
*You should always monitor BP at all times - off cycle , on cycle , clen - no clen . It may be the single most prudent preventive measure we can do in this lifestyle (prob in any lifestyle to be honest)

Ill say this - if I was forced to choose -id use clen over T3 when it comes to adverse cardiac effects. Id use it over DNP for overall safety. Hell based on Lemons catecholamine BS it safer than ephedrine.
Of course we need to keep in mind we are using it in conjunction with AAS - its easy to pick clen and villify it - easier than taking an honest look at all the substances we use and what they can or could do and make the decision to use or not on the same criteria by which we judge clen as "unsafe" or "dangerous". Trust me you start applying the criteria used by those to say clen is dangerous or deadly to other substances we use you would no be touching several of them (like almost all) or at the very least you would be forced to be honest and say yeah i know but i choose to use them anyway. Clen - just like most anything - in the abscence of prexisting condition (like untreated hypertension) or serious medical pre disposition - used prudently is fine imo.

Try to argue those cliffs lemon. (rhetorical device there)

[Lemonada8]

w/e. Ur 'cliffs' are just saying how to use precaution while using clen. Nothing more. I was putting up mechanisms on how clen can be dangerous and you wanted to argue.
and my catecholeamine BS? what is that? that high amounts lead to heart damage? and that clen mimics them? and increases the release of them? and how in a failing heart that they can be good because there isnt enough stimulation hence a failing heart? .... but its my BS tho right?
Thats what makes me think you really dont know what is goin on there.

so please point out where i contradict myself... or are you just saying that? and where i am 'wrong' with facts? or are you just saying that also?

The coexistence of beta(1)- and beta(2)-adrenoceptors in the heart clearly indicates that beta(2)-agonists do have some effect on the heart, even when they are highly selective. It should also be taken into account that the beta(2)-agonists utilised in clinical practice have differing selectivities and potencies. beta(2)-agonist use has, in effect, been associated with an increased risk of myocardial infarction, congestive heart failure, cardiac arrest and sudden cardiac death.

Thats even before COPD and asthma was mentioned... So Hmm... Drumroll..... must be even in people w/o those conditions.. mind blowing huh?

so you think asthma and copd are the only things playing a part in heart issues with b2 drugs? and that nothing about the b2 has to do with affects on the heart?.... i know ur not going to, and i dont feel continueing this arguement... but look at b2 agonists on normal healthy hearts. There are more issues b/c its excessive to the heart/body.

and there are alot more than 2 case studies out there, but since you are only goin with the ones that end in death.. w/e


and what did you show was inaccurate? nothing. you came back with insults and attitude. and you put up precautionary measures while using clen...

You want to argue sematics and minimal points, where i am putting up mechanisms on HOW clen can be damaging to the heart but you want to argue with that.

That and I never made an opinionated stance on usage, then u tried to clear out "broscience" but I come back with studies disproving ur claim u retort with insults. So don't try to go scientific if u can't handle it

[jimmyinkedup]

Clinical Trail
Randomized, double-blind, placebo-controlled, parallel-group study
352 people
1 year long
100mcg /day
Salmeterol (long acting selective b2 agoinist-just like clen)
No clinically significant changes in cardiac function or increases in cardiovascular adverse effects.
http://chestjournal.chestpubs.org/co...3/642.abstract
Blow Me.....

[Lemonada8]

Clinical Trail
352 people
1 year long
100mcg /day
Salmeterol (long acting b2 agoinist-just like clen)
No clinically significant changes in cardiac function or increases in cardiovascular adverse effects.
http://chestjournal.chestpubs.org/co...3/642.abstract
Blow Me.....

It was inhaled....
and it's not clen.
Blow yourself

[Huge_Brah]

Of course we need to keep in mind we are using it in conjunction with AAS

What if you just want to use clen by itself? I guess it would be safer?

[jimmyinkedup]

It was inhaled....
and it's not clen.
Blow yourself

Pretty appropraite you put dancing man gifs at the bottom of several of your posts - you are quite the tap dancer....

[jimmyinkedup]

It was inhaled....
and it's not clen.
Blow yourself

Here a good clinical for you.
Doulble Blind Study
Controlled release albuterol versus sustained-release theophylline
124 people
12 weeks
Only one patient in the study stopped treatment because of an adverse effect. This patient had tremor during albuterol administration. All other adverse events were tolerated or resolved during treatment. Controlled-release albuterol proved to be a safe and effective alternative vs sustained-release theophylline for management of patients with asthma.
http://www.sciencedirect.com/science...9167499090102A


Oh and stop with the BS studies showing dangerous effects in ashtmatics - the potential for increase in asthma related deaths with patients taking LABA is sudden bronchial inflammation and sensativity - it has absolutely nothing tio do with effects on the heart. So save the BS and stop misleading people so you can appear "right" - like i said patients with asthma taking LABA have an increased chance of dying from asthma - earthshattering huh .....

[Lemonada8]

lol this is gettin pathetic.
no sh!t that patients with asthma have a higher chance of dying of asthma, did i every say no to that? nope.
and albuterol is a SABA, controlled release means it has something that is blocking it from the receptor untill its degraded from the true drug, similar to the ester on test.
and comparing albuterol to theophyline? not even the same drug class
why are you trying to argue that oral beta 2 selective (no matter how selective) WILL have some cross stimulation on beta 1 receptors?
Im not misleading at all, like ive said in my posts, with a normal heart the negatives will be greater than in a failing heart b/c of overstimulation in those predisposed to heart issues.

would you rather me put up links of people who had to go the ER for heart issues after taking clen? is that more relevant (that you claim im spreading false info, when you are doing the same thing *according to your reasonings* ) but you wanna appear right... Hmm...

if you would have went with that roughly 10% of inhaled drugs are used at the lungs, the rest goes sytemic that would be a better arugement then post supporting facts with inhaled versions. but you prolly didnt know that.
or that when you lower BP you raise HR anyways. And that the increased working of the heart induces hypertrophy.
and how when combined with AAS (cuz that builds muscle) well the heart is a muscle so it could have a combined effect with cardiac hypertropy.
but you dont wanna argue mechanisms, but say its dangerous and provide ways to take precautions. I have no arguement with that. but dont try to argue mechanisms and HOW the heart would get potential issues.

ill just go back to the study already posted by someone else, saying clen increased heart size by 26%
http://cardiovascres.oxfordjournals....37/1/115.short

or this one..
http://journals.lww.com/acsm-msse/Ab...tively.13.aspx
"After treatment, CLENEX and CLEN demonstrated significantly higher left ventricular internal dimension (LVD) at end diastole (+23.7 ± 4.8%; +25.6 ± 4.1%), LVD at end systole (+29.2 ± 8.7%; +40.1 ± 7.9%), interventricular septal wall thickness (IVS) at end diastole (+28.9 ± 11.0%; +30.7 ± 7.0%), IVS at end systole (+29.2 ± 8.7%; +40.1 ± 7.9%), and left ventricular posterior wall systolic thickness (+43.1 ± 14.%; +45.8 ± 14.1%). CLENEX and CLEN had significantly increased aortic root dimensions (+29.9 ± 6.1%; +24.0 ± 1.7%), suggesting increased risk of aortic rupture"
clenex is clen plus exercise

and that goes back to the statement of 'those predisopsed to heart issues... )

Its not scare tatics if its correct info. Ive already said that its dose dependent on those HEALTHY people using clen if there are going to be heart issues.
and the fact its used in DAMAGED hearts to help increase contractility and repair... pretty simple idea if you know clinical pharmacology.

but ill end it with, yes it can be dangerous. insome more than others. I wasnt trying to say dont use it, or do use it.. just putting out HOW heart problems can arise.

almost forgot my dancin dude. :-)

[jimmyinkedup]

Albuterol Study
Pretty interesting for several reasons.
Shows increase in lbm , decrease in bodyfat , mentions potential prudence of "pulsing" ie 2 weeks on / 2 weeks off to prevent receptor downregulation.
Oh also of note - A cardiologist participated in the study - 3 participants displayed elevated heart rates. it was determined that they were within normal range. 24 weeks total - no cartdic issues other than the above metioned observed.
http://www.parentprojectmd.org/site/...pdf?docID=2861
I will admit this isnt the most relevant study I have posted related to this debate (but of course it does have some relevance) but for those interested its a great read with some good info on how b2 agonists promote anabolism. Some I knew about others they mention here I did not. Its pretty interesting.

[jimmyinkedup]

lol this is gettin pathetic.
no sh!t that patients with asthma have a higher chance of dying of asthma, did i every say no to that? nope.
and albuterol is a SABA, controlled release means it has something that is blocking it from the receptor untill its degraded from the true drug, similar to the ester on test.
and comparing albuterol to theophyline? not even the same drug class
why are you trying to argue that oral beta 2 selective (no matter how selective) WILL have some cross stimulation on beta 1 receptors?
Im not misleading at all, like ive said in my posts, with a normal heart the negatives will be greater than in a failing heart b/c of overstimulation in those predisposed to heart issues.

would you rather me put up links of people who had to go the ER for heart issues after taking clen? is that more relevant (that you claim im spreading false info, when you are doing the same thing *according to your reasonings* ) but you wanna appear right... Hmm...

if you would have went with that roughly 10% of inhaled drugs are used at the lungs, the rest goes sytemic that would be a better arugement then post supporting facts with inhaled versions. but you prolly didnt know that.
or that when you lower BP you raise HR anyways. And that the increased working of the heart induces hypertrophy.
and how when combined with AAS (cuz that builds muscle) well the heart is a muscle so it could have a combined effect with cardiac hypertropy.
but you dont wanna argue mechanisms, but say its dangerous and provide ways to take precautions. I have no arguement with that. but dont try to argue mechanisms and HOW the heart would get potential issues.

ill just go back to the study already posted by someone else, saying clen increased heart size by 26%
http://cardiovascres.oxfordjournals....37/1/115.short

or this one..
http://journals.lww.com/acsm-msse/Ab...tively.13.aspx
"After treatment, CLENEX and CLEN demonstrated significantly higher left ventricular internal dimension (LVD) at end diastole (+23.7 ± 4.8%; +25.6 ± 4.1%), LVD at end systole (+29.2 ± 8.7%; +40.1 ± 7.9%), interventricular septal wall thickness (IVS) at end diastole (+28.9 ± 11.0%; +30.7 ± 7.0%), IVS at end systole (+29.2 ± 8.7%; +40.1 ± 7.9%), and left ventricular posterior wall systolic thickness (+43.1 ± 14.%; +45.8 ± 14.1%). CLENEX and CLEN had significantly increased aortic root dimensions (+29.9 ± 6.1%; +24.0 ± 1.7%), suggesting increased risk of aortic rupture"
clenex is clen plus exercise

and that goes back to the statement of 'those predisopsed to heart issues... )

Its not scare tatics if its correct info. Ive already said that its dose dependent on those HEALTHY people using clen if there are going to be heart issues.
and the fact its used in DAMAGED hearts to help increase contractility and repair... pretty simple idea if you know clinical pharmacology.

but ill end it with, yes it can be dangerous. insome more than others. I wasnt trying to say dont use it, or do use it.. just putting out HOW heart problems can arise.

almost forgot my dancin dude. :-)

You do not appear to understand what im saying at all. This is very clear by your posts. You remind me of one of those book smart people with liitle to no common sense or interpretation skills of others points when you are soley focused on proving yours. Some of the things you say clearly demonstrate the fact hat you have blinders on to the point that you even forget things you posted that my posts correct. Anyway - Lets look at those 2 studies - i dont have the full study on the rats - do you? Cause I have no idea based on the abstract how much clen was injected into them so calculating HED is impossible. The next study the dosage is 2.4mcg/kg 2x/day. Thats almost 500mcg of clen /day for a 220lb man. WTF ?
Again - is this real life ????

I provide this:
Clinical Trail
Randomized, double-blind, placebo-controlled, parallel-group study
352 people
1 year long
100mcg /day
Salmeterol (long acting selective b2 agoinist-just like clen)
No clinically significant changes in cardiac function or increases in cardiovascular adverse effects.
http://chestjournal.chestpubs.org/co...3/642.abstract


And you are gonna continue to argue. WTF is your problem? You wanna argue HOW it may happpen when im showing you it doesnt *L* You are saying this effect may take plkace - im saying so the fvck what if it does it doesnt to the extent that these claims of cardiac damage or LV hyopertrophy are occuring. Are there some people that may have prexisiting conditions -sure - but that can be said for anything.

I provide a year long, 350+ person randomized, double-blind, placebo-controlled, parallel-group study;
with a substance that is the same as clen , identical MOA ,with a relaistic daily dose for our purposes.

You ulitmately refer to a rat study with iv dosage of unknown quanitity and a study with 4x the dosage most would use.

Yeah but its not about being right for you is it ?

Just stop ...wtf is it with you? This is how BS propaganda gets started in these circles - people like you focusing on potential this and possibly that and ignoring the real freaking world. It like being afraid of getting stung by a bee and ignoring the freaking train its landed on thats headed right for you.

Conversely I post my opinion , support it (with prob the absolute best study i have ever seen on LA selective b2 agonists - bar none-post#87) , and out of respect for others offer what i consider helpful advice no matter where you stand on this topic.

Ahh one more thing I have to say I do as well , I allow myself to get into back and forth pissings contest with arrogant immature fvcks thst post dancing men at the end of their posts to be smartasses. I need to work on that.

[Lemonada8]

the study about the rats.
http://cardiovascres.oxfordjournals..../37/1/115.full
Groups II (n = 8) and VI (n = 8) were injected s.c. with clenbuterol (a gift from Boehringer Ingelheim, UK) once daily at a dose of 2 μg/g body weight
free full text...

and comparing clen to salmeterol is like comparing tamox and clomid. They are in the same class but have different actions.
If they were identical, then why dont people take salmeterol for weight control? why isnt clen legal or salmeterol illegeal?

and you wanna argue that beta agonists dont have a part in cardiac hypertrophy? thats a basic standard.

You constantly think i have a stance on this, i DONT FVCKIN CARE! i wanted to talk mechanisms but since it had a 'negative' outlook b/c i say "this is how issues can arise"... you wanna argue that its just fine and dandy to take it and those issues are false... so continue to argue to look "right" and make it look safe when the orginal question was HOW bad is it for the heart... Im posting HOW heart issues can arise. but you want to disagree with me...

heres another study:
http://www.ncbi.nlm.nih.gov/pubmed/20577844
"Together these data show that clenbuterol acts to induce mild cardiac hypertrophy in cardiac myocytes via paracrine signalling involving fibroblast-derived IGF-1."

Hmm, doesnt AAS increase IGF-1? so wouldnt being on cycle, perhaps, increase the risk of cardiac issues?

another:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1828609/
this study shows how its Type 2 fibers that are increased in size. And you can add in that type 2 are usually grown larger during AAS cycles which would result in more hypertrophy

http://www.ncbi.nlm.nih.gov/pubmed/7586459
Clenbuterol 2 micrograms.g body wt-1.d-1 was administered subcutaneously for a period
The hypertrophy was more pronounced for hindlimb skeletal muscle (21% to 35% for GPS), and the effects of this relatively high dose of clenbuterol on the heart were less marked (18% to 20% hypertrophy)

http://www.ncbi.nlm.nih.gov/pubmed/6818359
in horses
clenbuterol (0.8 microgram/kg) appears to be effective in reducing non-elastic resistance of the lung, however intravenous administration to an animal with pre-existing cardiovascular or cardiopulmonary disease should be avoided.


http://www.ncbi.nlm.nih.gov/pmc/arti...h0160-1048.pdf
here you go, Receptor affinitys for beta agonists.
b1 n b2 n b3 n
Clenbuterol -6.62 0.03 5 -7.90 0.05 5 -5.35 0.07 7
Salmeterol -5.73 0.03 11 -9.26 0.06 10 -6.33 0.10 8

higher affinity for beta 1 receptor, less affinity for beta 2,3 for clen compared to salmeterol.
more information available in the study.
it does have a higher affinity for beta 2, which ive said all along. BUT it will cross activate beta 1, and that depends on the person. but it all will equal in cardiac hypertrophy. along with other 'muscle building' events that we do, if it has any part(partially debatable) but nonetheless it would increase that effect.

here u go, clen causing problems when people using it. yes i bet you can find more studies on 'a fat person ODing on fat soluable vitamins", but it doesnt make it any less viable.
http://www.ncbi.nlm.nih.gov/pubmed/16127201
http://www.ncbi.nlm.nih.gov/pubmed/9715231
http://www.ncbi.nlm.nih.gov/pubmed/12555590
http://www.ncbi.nlm.nih.gov/pubmed/17393901 - case study and liteature review...

And you can induce many other studies when you consider the 'hyperstimulation' of the heart and how that can cause issues.

why try to argue that clen enhance muscle building? It does, in several studies it shows that it increases muscle mass.

So still catecholamine BS huh? They increase sympathetics on the heart, clen mimics this and increases the release of them. Or you gonna say that increased SNS is fine for the heart?

http://www.ncbi.nlm.nih.gov/pubmed/7791106
These results indicate that activation of beta-2 adrenoceptors facilitates the SNS-evoked release of CA from the dog adrenal medulla under the condition in which beta-1 adrenoceptors are blocked, and they suggest that activation of beta-1 adrenoceptors inhibits the beta-2 adrenoceptor-mediated facilitation process of adrenal CA release.
Clen is a beta 2 agonist right?

http://www.ncbi.nlm.nih.gov/pubmed/2835688
These results suggest that the release of adrenal catecholamines is locally modulated by a positive feedback mechanism through activation of beta-2 adrenoceptors.


I am starting propaganda, then you are going with propaganda in the oppsite sense. you are bringing in different drugs, saying they are similar and that the hypertrophic effects dont happen. Thats like using apples in a arguement about oranges, when down to the nuts and bolts it doesnt really apply.

SO quit arguing, and trying to disclaim my posts by saying 'im saying ur posts are right" b/c the only part i am saying that is right is that its dangerous and precautions should be taken. THats it, dont try to assume that i think ALL your post is right.


Here u go


as for being a " arrogant immature fvcks" , you would fit the defination for " arrogant immature fvck MOD"
did i ever post a usage opinion? NO!

[Lemonada8]

What if you just want to use clen by itself? I guess it would be safer?

Thats what i would go with, or use during PCT to help keep gains and not gain any estro-releated weight (due to low hormone levels)
i wouldnt use it on a cycle, unless there were no issues before. So for a first time, i wouldnt use on a cycle.
but thats my opinion.
Take precautions, listen to your body, dont start huge thinkin you can back off, start small and go upward *in regards to doses*

[jimmyinkedup]

ATTENTION EVERYONE : aerobic exercise and strength training cause Ventricular Hypertrophy.....as a result of this it is presumed by some to be dangerous and shoud not be undertaken . Thats akin to this debate. WTF ?

Aparently clinical significance ( ie real world relevance) is out the window and its down to who can post the most studies - of course we are ignoring the participants , the method of administration , the dosage , the duration and any other relevant points that woukd go against Lemons contentions. The point here is for him to be correct - not provide accurate real world data. Ignore the fact hat the only study I saw on humans that beared this effect was at 4-5x the dosage of clen we would use. Ignore the fact that although Lemon want to try to make the comparison between clen and salmeterol foolish - it is in fact very prudent . The clinical significance of the numbers he psosted to illustrate a difference amounts to virtually nothing. The clinical trial i posted is the single best study i have ever seen re: the long term use of long acting selective beta agonists. Its methods and so on could be considered the benchmark standard for reliablity and credibility. Its extremely relevant to anyone with an interest in the truth ...of course to someone trying to prove a point and appear correct at any cost - eh not so much.

To address the original point of this entire thread: How bad is clen for your heart - not nearly as bad as Lemon is trying to make it out to be in his ego driven attempt to be correct . Should we exercise prudence when using it - of course ( i even pointed out ways to do so if one is so inclined)- we should exercise prudence when using anything. If anything the 3 #'s Lemon posted as far as recpetor agonism differences between clen and salmeterol did anything they showed the prudence of the analogy and demonstrated mcg / mcg the dosages of said compunds would be virtually eqivalent for comparision purposes. The dosage amount in the study translates to our dsoing of clen. If a long acting selective beta agonist ( with no clinically significant diff in agonism than clen) can be used every day for a year with "No clinically significant changes in cardiac function or increases in cardiovascular adverse effects" . I thnk we have a pretty good answer- esp given our relative short durations of usage and commonly accepted on/off protocol. Of course if you prefer you can rely on horse and rat studies with ridiculous dosages and IV route of administration to come to your conclusion. Oh wait there is the one strudy on humans as well - but of course that is at 4-5x the normal dose for our purposes.
Gimme a fvcking break - fear mongering in the name of I need to be right bvllshit.... AND immature smartass danncing men ......fvck me.....

[Swifto]

the study about the rats.
http://cardiovascres.oxfordjournals..../37/1/115.full
Groups II (n = 8) and VI (n = 8) were injected s.c. with clenbuterol (a gift from Boehringer Ingelheim, UK) once daily at a dose of 2 μg/g body weight
free full text...

and comparing clen to salmeterol is like comparing tamox and clomid. They are in the same class but have different actions.
If they were identical, then why dont people take salmeterol for weight control? why isnt clen legal or salmeterol illegeal?

and you wanna argue that beta agonists dont have a part in cardiac hypertrophy? thats a basic standard.

You constantly think i have a stance on this, i DONT FVCKIN CARE! i wanted to talk mechanisms but since it had a 'negative' outlook b/c i say "this is how issues can arise"... you wanna argue that its just fine and dandy to take it and those issues are false... so continue to argue to look "right" and make it look safe when the orginal question was HOW bad is it for the heart... Im posting HOW heart issues can arise. but you want to disagree with me...

heres another study:
http://www.ncbi.nlm.nih.gov/pubmed/20577844
"Together these data show that clenbuterol acts to induce mild cardiac hypertrophy in cardiac myocytes via paracrine signalling involving fibroblast-derived IGF-1."

Hmm, doesnt AAS increase IGF-1? so wouldnt being on cycle, perhaps, increase the risk of cardiac issues?

another:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1828609/
this study shows how its Type 2 fibers that are increased in size. And you can add in that type 2 are usually grown larger during AAS cycles which would result in more hypertrophy

http://www.ncbi.nlm.nih.gov/pubmed/7586459
Clenbuterol 2 micrograms.g body wt-1.d-1 was administered subcutaneously for a period
The hypertrophy was more pronounced for hindlimb skeletal muscle (21% to 35% for GPS), and the effects of this relatively high dose of clenbuterol on the heart were less marked (18% to 20% hypertrophy)

http://www.ncbi.nlm.nih.gov/pubmed/6818359
in horses
clenbuterol (0.8 microgram/kg) appears to be effective in reducing non-elastic resistance of the lung, however intravenous administration to an animal with pre-existing cardiovascular or cardiopulmonary disease should be avoided.


http://www.ncbi.nlm.nih.gov/pmc/arti...h0160-1048.pdf
here you go, Receptor affinitys for beta agonists.
b1 n b2 n b3 n
Clenbuterol -6.62 0.03 5 -7.90 0.05 5 -5.35 0.07 7
Salmeterol -5.73 0.03 11 -9.26 0.06 10 -6.33 0.10 8

higher affinity for beta 1 receptor, less affinity for beta 2,3 for clen compared to salmeterol.
more information available in the study.
it does have a higher affinity for beta 2, which ive said all along. BUT it will cross activate beta 1, and that depends on the person. but it all will equal in cardiac hypertrophy. along with other 'muscle building' events that we do, if it has any part(partially debatable) but nonetheless it would increase that effect.

here u go, clen causing problems when people using it. yes i bet you can find more studies on 'a fat person ODing on fat soluable vitamins", but it doesnt make it any less viable.
http://www.ncbi.nlm.nih.gov/pubmed/16127201
http://www.ncbi.nlm.nih.gov/pubmed/9715231
http://www.ncbi.nlm.nih.gov/pubmed/12555590
http://www.ncbi.nlm.nih.gov/pubmed/17393901 - case study and liteature review...

And you can induce many other studies when you consider the 'hyperstimulation' of the heart and how that can cause issues.

why try to argue that clen enhance muscle building? It does, in several studies it shows that it increases muscle mass.

So still catecholamine BS huh? They increase sympathetics on the heart, clen mimics this and increases the release of them. Or you gonna say that increased SNS is fine for the heart?

http://www.ncbi.nlm.nih.gov/pubmed/7791106
These results indicate that activation of beta-2 adrenoceptors facilitates the SNS-evoked release of CA from the dog adrenal medulla under the condition in which beta-1 adrenoceptors are blocked, and they suggest that activation of beta-1 adrenoceptors inhibits the beta-2 adrenoceptor-mediated facilitation process of adrenal CA release.
Clen is a beta 2 agonist right?

http://www.ncbi.nlm.nih.gov/pubmed/2835688
These results suggest that the release of adrenal catecholamines is locally modulated by a positive feedback mechanism through activation of beta-2 adrenoceptors.


I am starting propaganda, then you are going with propaganda in the oppsite sense. you are bringing in different drugs, saying they are similar and that the hypertrophic effects dont happen. Thats like using apples in a arguement about oranges, when down to the nuts and bolts it doesnt really apply.

SO quit arguing, and trying to disclaim my posts by saying 'im saying ur posts are right" b/c the only part i am saying that is right is that its dangerous and precautions should be taken. THats it, dont try to assume that i think ALL your post is right.


Here u go


as for being a " arrogant immature fvcks" , you would fit the defination for " arrogant immature fvck MOD"
did i ever post a usage opinion? NO!

Nice research, but unless you can show me how "unsafe" Clenbuterol is using smaller initial doses of 5-10mcg/ED and tirating up those two doses as well, for a period of 2-10 weeks, using ketotifen to prevent/limit desensitisation or not, your research is bullshit.

Jimmy has posted one of the most comprehensive year long cycles at a dose most bb'ers would call on the high side (100mcg) and what was the conclusion again?

As thats what this comes down too.

[Lemonada8]

So by taking precautionary measures to minimize issues makes my research bs?
That actually shows its correct and that it can be dangerous so being smart about usage is recommended.

Nice try tho

[Swifto]

So by taking precautionary measures to minimize issues makes my research bs?
That actually shows its correct and that it can be dangerous so being smart about usage is recommended.
Nice try tho

Are you joking?

So your sole point here is to state thats "its dangerous", Jimmy is exactly right, but well done for answwering the question as I thought you would.

This isnt about safe practical usage of Clen anymore, you've tried to twist it into proving "clen is dangerous".

Vitamin C is dangerous as well. So shall I stop suggesting its use as an anti-oxident and to lower serum cortisol pre and post WO?

You've posted countless animal studies (I'm not saying they have no application here) but when the dose and level of sensitivity is taken into account and translated to humans, nothing you have posted proves "clen is dangerous" to humans when the dose is administered how we (bb'ers) use it.

[Lemonada8]

Yes that was my sole point. Like I've been saying I was trying to show mechanisms on HOW it can be dangerous by inducing hypertrophy.
That combined with normal hypertrophy by working out and aas usage that it could have more severe problems in those predisposed.
I said nothing on usage, agreed with the precautionary measures and that if used intelligently that it wouldn't be nearly as bad as it could be if used recklessly.

[Swifto]

Yes that was my sole point. Like I've been saying I was trying to show mechanisms on HOW it can be dangerous by inducing hypertrophy.
That combined with normal hypertrophy by working out and aas usage that it could have more severe problems in those predisposed.
I said nothing on usage, agreed with the precautionary measures and that if used intelligently that it wouldn't be nearly as bad as it could be if used recklessly.

You have lost site of the appliaction here. So you're wasting your time googling Clen's effects on animals given large doses and not taking sensitivity into account.

No one was arguing its not optimal at large doses, its not. It probably is dangerous in large "reckless" doses, again, so is vitamin C.

Resistanc training can cause abnormal heart dimensions. For example, this study found that 43% of drug-free bodybuilders had "left ventricular dimensions beyond normal ranges."

So does that mean its unsafe to train? Same with aerobic exercise.

Thats the route your going down.

[Swifto]

To quote this study(full) done on rodents (I know, not ideal),

"Clenbuterol treatment of failing rat hearts, alone or in combination with mechanical
unloading, improves LV function at the whole-heart and cellular levels by affecting cell morphology,
excitation–contraction coupling, and myofilament sensitivity to calcium. This study supports the use
of this drug in the strategy to enhance recovery in HF patients treated with LVADs and also begins to
elucidate some of the possible cellular mechanisms responsible for the improvement in LV function.".

Dose was "2mg/kg" (a boat load) for "7 days".... Guess what... Read the above again.

[Swifto]

I'd just like to add something here...

Clen increases BP, lypolysis, is anabolic in muscle, increases CNS stimulation, protein synthesis and reduces protein degradation with no impact on the HPTA. This is why its used by bb'ers during bodyfat cutting phases. Its an excellent repartioning agent. Seems ideal right?

Well not exactly. It can be dangerous in large doses or when the dose is tirated too fast. This is displayed in various side effects, including and not limited too, tachycardia, hypokalemia, arrhythmia, increased HR, muscle cramps, and muscle tremors. Case reports include bb'ers who present with myocardial infarction and end-stage renal disease. Which are far more serious.

Clen IS given to heart failure patients around the world, which seems slightly ironic given the sides I have just listed right? Yeah, I agree.

Well, Tamoxifen has been known to cause cancer's as its a carcinogen, but is also the most widely prescibed anti-cancer drug given to women experiencing breast cancer. Again, seems stupid right? Well not really considering the facts. There have been plenty of studies (10years+,, using 10,000+ patients across many cultures) on Tamoxifen at doses of 20mg/ED and the outcome of sides is "not significant". The total dose over the given peroid is what matters here.

My point is that these cases are rare compared to the whole picture. Just like the deaths associated with fat soluable vitamins, paracetemol and other OTC herbs, compounds and vitamins. Anything is dangerous given enough time. Peanuts are fatal to some, does that mean they're lethal to all of us? No.

I think Clen is safe, adequate measures are taken. As I have said before the dose is relevant to sensitivity. So if you begin on 40mcg/ED, you're at a far higher risk than someone starting on 10mcg, even if you end up on the same dose after X amount of days. Get it?

My advice:

Start at 5-10mcg/ED and work up, slowly. Dont be afraid to use the same dose for a few days.

Tirate the dose in 5-10mcg incriments.

I would not exceed 80-100mcg. Scally states "60mcg".

Use Ketotifen 1-2mg pre-bed.

If you experience sides, lower the dose or stop.

[Lemonada8]

^ agree with precautions above

along with monitoring BP, another thing that is easy to monitor is resting heart rate (first waking, then throughout the day during 'rest' periods to get a more accurate reading)
if it is gettin upwards of 90+ then lower the dose.
Also, if possible, watch it during working out also. Using the max HR equation (220-age) as your 'max' is a good start. If it is getting close to this during your workouts then lower your dose, but you can also pay attention to how you are feeling at the time.

dont increase your dose really fast either, or dont start too high thinking you can always come down, its better to take more over time when the 'effects' are starting to diminish. or take a break, constant beta receptor activation can lead to downregulation hence the 2 week on/2 week off and use of ketotifen to help minimize this

[RangersLTW]

Good post lem thats how I understand all my studies on clen....but to each his own...swifto and jimmy always make for good reads and great info...i'm sure dec is right in some ways also(never seen that guy before?)...but I'm never own nor do I post much.....

Clen has to have dose related issues no one has same effects on drugs...

[RangersLTW]

No one will know the truth without a healthy patients and CHF patients using clen a doing wedge pressure test...like a PA cath

[RangersLTW]

Swifto I usually click on ur page and just read ur post haha...thats how I get most of my knowledge...not kidding either