clen or eca?

[macman1234]

was wondering what's better.

[420]

Ive never taken clen but my Gf has. Gf took both and she prefers ECA.

[L3]

clen is more selective towards the receptors, but can only be taken for 2 week intervals at a time ie. 2 on 2 off 2 on

eca can be taken for longer periods of time, people on the board advocate 3 days on 1 day off protocol

[spankmonkey]

clen is more selective towards the receptors, but can only be taken for 2 week intervals at a time ie. 2 on 2 off 2 on

eca can be taken for longer periods of time, people on the board advocate 3 days on 1 day off protocol


Conflicting data on this point is there not? Never cycled clen this way start and run through til done. You may not notice the effects but that does not mean it is not working?

[Amoral]

Conflicting data on this point is there not?

Pulled this off another board. Sorry if this is a repost...only discusses the 2on/2off procedure and does not address ECA...


written by:
suchaman from MM

Let me just start by saying that this is the single most misunderstood compound in use for athletics and bodybuilding today. Most of the information out there is ½ truths and conjecture. Ok…having said that, I’m going to make an effort to dispel some myths and give everyone a better understanding of Clen.

First, lets plow quickly through some of the basics:

Clenbuterol (Clen) is a beta-2 agonist/antagonist bronchodialator. What this means, is that it stimulates your beta-2 receptors. And this in turn stimulates you (clen has stimulant effects which will make you feel….well…stimulated). All of this serves to increase your body temperature a bit, increase your basal metabolic rate, and decrease your appetite (Int J Obes Relat Metab Disord. 1994 Jun;18(6):429-33.). Clen also can decrease insulin sensitivity (Am J Physiol Endocrinol Metab. 2002 Jul;283(1):E146-53.).

Clen is a very effective repartitioning agent, and this is what it’s most often used for. What this means is that it will increase your ratio of Fat Free Mass (FFM) to Fat Mass, by decreasing your Fat and possibly increasing your FFM (J Appl Physiol. 2001 Nov;91(5):2064-70). Want me to quantify that a bit? In one study, horses given a reasonable dose of clen (slightly over 1mcg/lb) and excercised for 20mins, 3x a week ( I suppose they were Mentzer disciples) had significant decreases in %fat (-17.6%) and fat mass (-19.5%) at week 2, which was similar to Clen given to horses who didn’t excretes; however, the exercised group had a different FFM response, which significantly increased (+4.4%) at week 6. Week 6! Clen and clen + exercise produce roughly the same results for the first 2 weeks! Remember the old 2 weeks-on/2weeks-off schedule? It’s officially dead and buried. If you want the quasi-anabolic effect from the clen, it’ll take more than 2weeks on (6 weeks apparently). And in fact, since clen alone is similar to clen + exercise for those first 2 weeks...why would you ever use a 2on/2off protocol? Keep in mind that animal responses to beta-agonist/antagonists differ a bit from ours…but you get the picture. 2on/2off? Ha ha...

Clen has a biphastic elimination, which means that it is technically reduced in your body in 2 different stages. This isn’t particularly important, as a recent study has shown that for most intents and purposes, clen concentrations in the body decline with a ½ life (approximately) equivalent to 7-9.2hours and again up to as much as 35 hours later(J Anal Toxicol. 2001 May-Jun;25(4):280-7. and J Vet Pharmacol Ther. 2004 Apr;27(2):71-7. and J Pharmacobiodyn. 1985 May;8(5):385-91. ). If you’re really interested, though, clen technically declines biphastically at 10 and then 36 hours. But really, in our little world, where we use ½ life to tell us when to take our next dose, who the hell is going to take clen, then a dose 10 hours later, then a dose 36 hours later. We’ll stick with the earlier 7-9 hour ½ life for dosing purposes, and take our clen every 3.5-4.5 hours that we’re awake, stopping early enough to still be able to get to bed. Clen can, in some people, cause insomnia (and as with all stimulants, can cause anxiety in some).

Clenbuterol can also cause a down-regulation in testicular androgen receptors and in pulmonary, cardiac and central nervous system beta-adrenergic receptors(J Anim Physiol Anim Nutr (Berl). 2004 Apr;88(3-4):94-100.)…possibly making steroids less effective while you are on clen, but definitely making clen less effective as time goes on and you keep taking it. To counteract this, you can take some ketotifen or periactim every 3rd or 4th week that you remain on clen. Both of these are prescription anti-histimines, so they’ll make you drowsy (take before bedtime). Basically, the way both of these work is to reduce beta-2 receptor activity.

A lot of people claim that clen is quite anti-catabolic and/or anabolic. This hasn’t been confirmed in human studies (Ann Pharmacother. 1995 Jan;29(1):75-7.). And the doses given to the animals in these studies where clen is shown to be very anti catabolic or highly anabolic are so absurdly high that no human could ever take them (1mg/kg of bodyweight and higher). The best you can hope for is the very mild anabolic effects I cited earlier.

Oh yeah…I guess I should get around to the proper dosing of clen. My recommendations are the same for both men and women. You’ll need to take 20mcgs upon rising, and then repeat that same dose again later in the day, and then once again in that day (if you find you can tolerate the effects). So you’ll start with 20mcgs, and then repeat that dose 2 more times that same day if you can tolerate it (side effects will determine this…hand shaking, sweating, etc…classic stimulant sides). Then you can start increasing the dose gradually. Personally, I wouldn’t work my way up to more than 200mcg/day. 60-120mcg/day is an average dose.

Also, bear in mind that clen isn’t great for your heart, and can cause some issues there (enlargement of ventricles, etc…) but most studies showing clen to cause heart problems are with animals, and even though the dosing is similar to what humans take (in some studies) it’s important to remember that animals have more beta-2 receptors and they cause certain event chains that humans’ beta-2 receptors may not. Clen causes cardiac hypertrophy to some degree, in some cases. Again though, many studies showing more significant heart problems are with mg dosing. We humans take clen in mcg doses.

If we want to duplicate the “therapeutic” levels of clen in the more conservative studies, we’d be taking just over 1mcg/lb of bodyweight. I’d suggest a bit less, though.

Performance issues with clen also vary. Some studies show reduced exercise (cardiovascular) performance with clen (Med Sci Sports Exerc. 2002 Dec;34(12):1976-85.), while some show that clen can alleviate exercise induced asthma (Respiration. 1987;51(3):205-13.)! Sometimes you feel like a nut…sometimes you don’t, I guess. What this means, to me, is that you’ll need to figure out how clen affects your performance individually.

Which brings me to the issue of cramps while on clen. I don’t get them. My friends don’t get them. Most of us are athletes who use clen during the season as well as the off season, and one of my friends even claims that it gives him more “wind” (cardiovascular stamina). Take on enough water every day and you should be fine. If you’re really concerned, you can take some extra minerals and taurine, since clen depletes taurine (Adv Exp Med Biol. 1996;403:233-45) as do most if not all beta-agonists. I don’t take anything more than my usual vitamins and minerals.

Well…there it is…pretty much all I know about clen. I hope this answers some questions and clears up some misconceptions.

Hooker also states if you want to just stay on Clenbuterol, you can take 50mgs of Benadryl every night for a week (say...1 week per month), and you'll keep your beta-2 receptors fresh. Instead of coming off the clen, that is.

There appear to be conflicting opinions about this...so take it as a grain of salt...

[Amoral]

The cost between ECA and Clen is pretty big to the comparable results seen by both. ECA should work fine if you get your cardio and diet in check just as fine, or better, than Clen.

Comments by ECA users can be seen here:

http://www.canadabodybuilding.com/forums/showthread.php?t=3660

[gsxr750]

ECA actually works better on fat loss the longer you're on it. The energizing effects go away but it continues to burn fat.

"Industry Insider Vol. 8:
Brown Fat and the Myth of ECA Cycling
by: Gerhard Waitz
January, 2001 © Iron Magazine Online L.L.C.



Since I started writing most of the Industry Insider columns for Ironmag some 4 months ago after the departure of a previous writer, I've spent quite a bit of my spare time reviewing a lot of the literature currently available on the internet pertaining to bodybuilding. To be honest, during the time before I was approached by Ironmag to write for them, I didn't really think bodybuilders had much time for computers and internet surfing. While I still believe many real bodybuilders have better things to do than surf the 'net, I still believe they turn to the internet as a source of up to date information that isn't written for beginner bodybuilders who most often purchase printed magazines like Muscle & Fitness.

One of the most common questions I see on the world wide web's new bodybuilding population involves the ECA stack and fat burning. Most likely through printed magazines or mass market bodybuilding sites aimed at beginner bodybuilders like Musclemag.com or Elite Fitness (two sites I now avoid completely) I find the theories of cycling ECA with some odd "cycling patterns". Some bodybuilders favor a two day on, two day off cycle; others say that receptor downgrade occurs after 2 weeks; and still other's quote longer times of 2 months. Well they're all wrong. Yes the notion that you have to cycle ECA or it's fat burning effects will dwindle to nothing are simply not true.

To understand why it's not necessary to design elaborate (and ineffective) cycles for ECA, one must look at it's primary ingredient, ephedrine (the herbal forms being ma huang or sida cordefolia) and how it works.

Ephedrine works by stimulating the release of noradrenaline, which stimulates all the adrenergic receptors. The stimulant side effects subside because they are primarily mediated by the beta-1 and beta-2 receptors, which downregulate during chronic use. Previous thought was that catecholamines mobilize energy-rich lipids by stimulating lipolysis in fat cells and thermogenesis in brown adipose tissue and skeletal muscle. Originally, these effects were believed to be only mediated by (beta)1- and (beta)2-adrenergic receptors. However there is also an additional adrenergic receptor, (beta)3, that is involved as well. Pharmacologically, the (beta)3-adrenergic receptor differs from the (beta)1- and (beta)2-adrenergic receptors in two important ways (2): it has a lower affinity for catecholamines, and it resists desensitization (i.e., down-regulation).

In the past scientists screened drugs for their thermogenic potential, and during tests on non-selective adrenergic drugs like ephedrine, some studies showed that the thermogenic effect of ephedrine was maintained and even increased with long term use. It was found that agonists for post-synaptic adrenoceptors were found to be much less effective in chronically enhancing thermogenesis and fat losses than sympathetic stimulants capable of increasing the synaptic levels of noradrenaline. As we all know studies done have shown that that a combination of ephedrine (20 mg) and caffeine (200 mg) taken orally three times a day in combination with a low calorie diet improves weight loss for 24 weeks. However what is not noted in most articles or literature about ECA is that the combination can maintain or slightly improve weight loss during treatment from the time after 26 weeks.

This discovery led to further studies in the hopes of uncovering an undiscovered receptor involved in noradrenaline-induced thermogenesis. The scientists found that even after blocking all the known adrenergic receptors non-selective drugs like ephedrine still caused a significant thermogenic effect. Eventually, this led to the discovery of the beta 3 receptor that, as mentioned above is more resistant to downregulation than the other beta receptors. This is why the thermogenic effect of ECA is maintained so well during long term use. This discovery effectively shows that cycling of ECA is simply wrong.

Now I'm going to explain just why the thermogenic effects of ECA actually increase with long term use. I really only need two words. Brown Fat.

Brown fat (adipose) tissue is sometimes mistaken for a type of gland, which it resembles more than white adipose tissue. It varies in color from dark red to tan, reflecting lipid content. Its lipid reserves are depleted when the animal is exposed to a cold environment, and the color darkens. In contrast to white fat, brown fat is richly vascularized and has numerous unmyelinated nerves which provide sympathetic stimulation to the adipocytes. Brown fat is of particular importance in cold environments, and animals that hibernate, because it has the ability to dissipate stored energy as heat. In contrast to other cells, including white adipocytes, brown adipocytes express mitochondrial uncoupling protein, which gives the cell's mitochondria an ability to uncouple oxidative phosphorylation and utilize substrates to generate heat rather than ATP. Exposure to cold leads to sympathetic stimulation of brown adipocyte via norepinephrine binding to beta- adrenergic receptors. As in white fat, sympathetic stimulation promotes hydrolysis of triglyceride, with release of fatty acids and glycerol. However, within brown adipocytes, most fatty acids are immediately oxidized in mitochondria and, because of the uncoupling protein, a large amount of heat is produced. This process is part of what is called non-shivering thermogenesis.

Beta-3 receptor sites are found predominantly in brown adipose tissue. We know that rats and mice have large areas of fat that are exclusively made of brown fat to help them regulate their body temperature, in the interscapular region and the axillae, and minor amounts are found near the thymus and in the dorsal midline region of the thorax and abdomen. During maturation, in non-hibernating animals, brown adipose tissue is metabolically less active, although cold exposure can activate it. Newborn human babies have distinct areas of brown fat. Adult humans though don't have a lot of distinct brown fat. However the key with brown adipose tissue in adults, is that it is scattered about the more common white fat in a diffuse manner - especially around the viscera, and that each of these small deposits of brown fat actually adds up to a large amount. The beta-3 receptor found in brown fat is responsible for burning off fat in the midsection of the body.

Long term use of the ECA stack does lead to beta-2 downregulation. It does not cause rapid desensitization and/or down-regulation of adrenergic receptors, however after about 4 months it will cause the beta-2 receptors on muscle and fat cells will be drawn into the cell membrane to reduce their availability. This is the cause of the loss of stimulatory effects associated with the ECA stack. However, thermogenesis is actually increasing through beta-3 receptor stimulation.

I recommned adjusting your dosing schedule of ECA to every 2 hours during the first 4 months. This will enhance the duration and consistency of beta-adrenergic activity. Don't forget adjust the amount you take each time in order to maintain the total amount taken over the course of a day. It has been demonstrated, that when you infuse beta agonists with short half-lives, you can elicit the anabolic activity, that is similar to the anabolic activity of clenbuterol. Muscle preservation through the use of ephedrine is negigable over long term use. This is most likely the only valid reason for the cycling of ECA. As a fat loss catalyist though, there is no reason.

After four months switch back to your usual 3 times a day dosage. You can continue to burn fat for as long as you use ECA.



References:
Astrup A, Lundsgaard C, Madsen J, Christensen NJ "Enhanced thermogenic responsiveness during chronic ephedrine treatment in man" Am J Clin Nutr 1985, Vol 42 (1), Pg 83-94, PMID: 0004014068.

Dulloo, AG "Ephedrine, xanthines and prostaglandin-inhibitors: actions and interactions in the stimulation of thermogenesis." Int J Obes 1993 Feb, Vol 17 (Suppl 1), Pg S35-40, PMID: 0008384178.

P. Marin, B. Anderson, M. Ottoson, et al, "The Morphology and Metabolism of Intraabdominal Fat in Men," Metabolism 41 (1992) : 1242-1248.

Rosenbaum M, Malbon CC, Hirsch J, Leibel RL. Lack of beta 3-adrenergic effect on lipolysis in human subcutaneous adipose tissue. J Clin Endocrinol Metab 1993 Aug;77(2):352-355

[xxSCHiSMxx]

I prefer ECA over clen. Both work just fine for fat loss, but I can't handle the sides from clen. jitters, insomnia, anxiety ...

[gustavo77]

If you have never used either then go with the ECA. I find the ECA is much more tolerable. The results are good with either though and ultimately, your diet will dictate your results no matter what you take...if something is not working, look at your diet before anything else.

[Praetorian]

Clen is by far a much more potent fat burner than ECA. The body will attenuize to clen after a few weeks but this can be overcome by 1. increasing the dosage slightly, and/or 2. add 1mg of ketotifen per 100 mcg clen before bed to upregulate the beta 2 receptors. Clen is a more specific beta 2 agonist where as ECA effects 1, and 3 as well. The issue with ECA is cortisol release as well as adrenal burnout which will happen if taken for long periods. This basically nullifies the the theory of using it for long periods of time...not smart!
Clen is safer, works better at lower dosages, and has little affect on adrenals if taken in moderate dosages...at these dosages it is not a stimulant..ie cardiac affecting.
P

[45's]

Im running clen right now as we speak, been on for a week. imo that everyone responds to eca/clen differently, just like certain exercises. Myself i love clen but you also have to watch out for cramping which might happen so you should be taking tuarine (supplement) to help ward off the cramping, i love eca but it hits my prostate hard and makes me feel like a 80yr old man trying to take a pee, which feels like a slow tap dripping. You just have to try either one for yourself and see what responds best to you, but remember that more does not mean better....