I posted this awhile back with its own thread....
I found this on another forum (edited for irrelevant content).
Bromocriptine still effective taken with clen and vice versa?
joe (2002-09-14 01:15:49 1953936499)
After reading cyborg I have the question is bromo still effective for weight loss taken with clen or eca? I am currently using both.
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Cy Willson (2002-09-14 16:31:42 1953936636)
Yes, I mentioned this. It's best to use as an adjunct to beta-2 agonists but be sure to monitor BP and heart rate.
HHH to Cy (2002-09-14 18:39:01 1953936678)
In Lyle McDonald's e-book about Bromocriptine he said not to take it with clen or an eca stack?????
Cy (2002-09-14 19:17:31 1953936685)
Yes, and once again, as I said in the column, there are some who believe that blood pressure or heart rate will increase too much if a beta 2 agonist or the eca combo and bromocriptine are taken concurrently. However, this is simply one of the "label cautions" you'd see from the manufacturer and in most cases, the person will be fine. In fact, I promise you that a very high % of the combos bodybuilders use are cautioned against by their producers. It's more of a liability issue than anything else. Since, as you know, there is going to be someone out there who experiences a severe headache with this combo or any number of indicative factors that should be a strong signal to discontinue usage, but instead decides to keep on with their regular dosage. I guess a good example is simply those who are on MAOI's. Well, ephedrine isn't to be used with them and yet I've seen more than I can count use ephedrine/caffeine while being on an MAOI and remain perfectly fine. It's something that I'd only advise to those who know what they're doing.
Blade (2002-09-15 13:17:46 1953936850)
This is incorrect, Cy. All beta-agonist (or sympathomimetics) block the effects of Bromocriptine. Refer to the FDA's review, pg 75-76, at
http://www.fda.gov/ohrms/dockets/ac...scpt/3408t2.pdf (Takes forever to download) But considering that Bromo fixes the drop in metabolic rate, fat burning etc, you don't really need EC anymore.
Cy Willson (2002-09-15 20:53:24 1953936929)
You know, perhaps it's just because I haven't consumed a decent amount of carbs today but I'm now remembering why I don't post any longer and rarely view the forum (aside from classes being back in session). It's as if people feel the need to challenge me or something. I don't have a problem with discussions with those who know what they are talking about or at least have some evidence but I do get peeved when I get shit like "Cy, you're wrong" cuz this says so. First, you have things very backwards. Bromocriptine ONLY reduces the amount of norepinephrine(which isn't a beta 2 agonist in the first place, but I'll go on) and not vice versa! Now, I'm sure you're thinking that since ephedrine in particular causes a localized release of norepinephrine, that using bromocriptine concurrently will therefore reduce ephedrine's effects. Oh, well in that aspect you're 100% correct! Guess what though? This has asbolutely nothing to do with beta 2 agonism. Norepinephrine only stimulates alpha and cardiac beta receptors or beta-1 receptors. So, if anything this is beneficial, since the increase in heart rate and blood pressure won't be as dramatic, therefore making the combo safer. Now when you apply this argument to selective beta 2 agonists, it has even less application, even in the improved safety aspect, so I don't know where you're getting this info from but it's ridiculous. I skimmed over the article which was essentially a discussion and being as I don't have time to go over 300 some odd pages, I'm guessing you just misconstrued what the people were saying. I'm hoping that's all it was, otherwise I'd be very shocked that those men would state something false like that.
Blade (2002-09-17 05:51:22 1953937480)
First, I apologize if it came off as a challenge to you, it was not intended and I should perhaps have rephrased it to: "this seems to be inaccurate". Second, do not make any presumptions regarding my knowledge or my line of reasoning - although I presented a conflicting view from yours doesn't necessarily imply that you know everything and I'm just stupid to think otherwise... I'm not really sure by what mechanism sympathomimetics (such as the EC stack) block the effects of Bromocriptine, but it seems to be either via the beta-adrenoceptors (B3 in some studies) or via the dopamine2 receptor itself. B-agonists seem to suppress leptin release from adipocytes, and also to reverse Bromocriptine induced tachycardia (via beta-adrenoceptor desensitization). I can only speculate as I don't really have the time to dig further into the literature, but Lyle McDonald also stated that EC blocks Bromocriptine's effects - and I trust that guy knows what he's talking about in this regard. A few studies: Can J Physiol Pharmacol 2000 Mar;78(3):260-5 Lahlou S et al. Effects of long-term pretreatment with isoproterenol on bromocriptine-induced tachycardia in conscious rats. Am J Physiol Cell Physiol 2002 Jul;283(1):C244-50 Cammisotto PG, Bukowiecki LJ Mechanisms of leptin secretion from white adipocytes. Proc Natl Acad Sci U S A 2001 Dec 4;98(25):14720-5 Mastronardi CA et al. Lipopolysaccharide-induced leptin release is neurally controlled.
Blade (2002-09-17 08:57:31 1953937495)
Also, in the FDA proceedings on Bromocriptine use in diabetics, Dr Cincotta of Ergo Science stated: "The key exclusion criteria for the adjunct therapy studies included...or individuals on the following medications:insulin, sympathomimetics because they interact with our mechanism of action and actually block the effect of our drug" Do a search on Cincotta and bromocriptine at Medline, and you get a bunch of studies showing the mechanisms responsible for this statement.
Cy Willson (2002-09-17 11:52:35 1953937526)
Let me get this straight, you say it's mediated via the beta 3 receptor, yet you cite references which have nothing do with that. If you knew much of anything you'd understand that we humans have next to zero BAT as adults and thus have very few beta 3 receptors. This is not the main mech of action of ephedrine or any beta agonist in terms of fat loss. Next you insult me by citing a a few studies that are nothing more than abstracts which contain a beta agonist and bromocriptine in the same paragraph. That first concluded that "These results show that 15-day isoproterenol pretreatment not only abolished but reversed bromocriptine-induced tachycardia to bradycardia, an effect that is mainly related to further cardiac beta-adrenoceptor desensitization rather than to impairment of autonomic regulation of the heart. They suggest that, in normal conscious rats, the central tachycardia of bromocriptine appears to predominate and to mask the bradycardia of this agonist at peripheral dopamine D2 receptors." Well, if you were as informed as you claim you'd understand that this provides no evidence other than an effect on cardiac receptors (beta 1) which has nothing to do with beta 2 or beta 3 receptors!
Then you cite a study with leptin (which has been ditched) and beta agonists. I must have missed the groundbreaking part where you provide evidence that bromocriptine negates the lipolytic effects of a beta 2 agonist. To top things off, it's all rat research.
Last, I don't care who says what, if they don't have at least decent evidence, I don't blindly believe something they say. I can't believe you'd simply just "believe" what another person says without them having any evidence. I'm sorry but I'm not some 15 year kid whom you can trick by citing some studies after a statement and expect to wow me. Those studies demonstrate your research ability, which is poor. Oh and how about YOU look on medline and find ONE study that conclusively demonstrates in humans, hell even mammals, that deals with bromocriptine negating the effects of a beta 2 agonist. This is the last time I'm responding to this crap. Do me a favor and take a look at a physiology text some time instead of going over medline and concluding false arguments.
I'm certainly not perfect and will regularly admit when I'm wrong but this is certainly not the case.
Blade (2002-09-18 14:52:55 1953937913)
No, you're absolutely right - I don't know the exact interaction mechanisms of Bromocriptine and sympathomimetics which would block Bromo's effect. One can only speculate, and I also stated that I really didn't have time to look into the research but presented a few studies that might provide some "reasonable doubt". I'm somewhat surprised at your reaction, I certainly didn't intend to offend you personally - so what gives you the right to direct personal insults at someone whose only crime is having a different opinion? I never take what someone says at face value, but instead try to find the underlying research and mechanisms for that statement. If one of the scientists responsible for the research and development of Ergocet (brand name for Bromocriptine) states in an FDA hearing that sympathomimetics block the effects of Bromo, I find it a lot more credible than the personal opinion of some self-appointed guru on the Internet. From a more fundamental standpoint, bromocriptine obviates the need for EC while dieting - that and the "reasonable doubt" makes me more inclined to use Bromocriptine by itself. Now try eating some carbs or something...
Moonpiephil (2002-09-18 16:41:24 1953937937)
Ok, I've watched enough of this so I'll act as a quick mediator. Blade- Cy is correct and he was trying to explain to you that the lipolytic actions of beta 2 agonists are due not to indirect-acting sympathomimetic action but due to the molecule actually binding to the beta 2 receptors and activating cAMP production which are called "direct-acting sympathomimetics. Sympathomimetic action by definition merely means that you have a substance that mimics the actions of or even facilitates the release of norepinephrine and epinephrine. Now what you're confusing is "direct-acting" and indirect-acting sympathomimetics. These are two different classes. The literature has clearly established that bromocriptine and similar dopamine agonists can negate the effects of indirect-acting sympathomimetic compounds (i.e., amphetamine, PPA, methamphetamine, etc.) , but not direct-acting sympathomimetics (i.e., clenbuterol, albuterol, metaproterenol, isoetharine, etc.) Now where this gets confusing is the fact that ephedrine actually has characteristics of both an indirect-acting and direct-acting sympathomimetic but since it binds avidly to the beta 2 receptor itself, and that is the mechanism of action behind its' lipolytic actions, that would mean bromocriptine wouldn't really negate its' effects. It's easy to see where the confusion was. Oh and although I'm not a "self-appointed guru" but I do possess a Ph.D. in Physiology and Biophysics so I think that qualifies me in this discussion.
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