clen isn't a roid

you guys tell them to PM the natty crew lel

Weeks Bruh. This is easy research. You could find this info yourself.

clen made my have kegel cramps will pooping.

saying clen isn't a roid is like saying michael jackson is white.
but i mean chemically speaking it doesn't fall into the category as steroid no, but holy its pretty close

clen definitely more closely related to ephedrine than any steroid because of its thermogenic properties

But I feel you most people who run a cycle run clen at the end to cut

This post was edited by ug_warrior(xtc) on Aug 17 2015 05:22pm

except balla

they often post to troll or some arrogant comment

cant deny that

Nothing truer has ever been said. Balla doesn't troll though, he's a good guy.

yaaaa. feeling id be trolled mostly here
I did do research
wanted first hand experience from guys who have used it
and what cycles and amounts they did.
thx anyways

Then 600 in 2 weeks from now

.... he was trolling



wot
it's not at all pretty close lol. nowhere near in fact.
Just bc a given substance is used/abused by bodybuilders doesn't mean they all fall into the category of steroids
So your analogy is a bit vacuous. Saying clen isn't a roid is tantamount to saying the sky isn't red. No tergiversation.



@OP 2 weeks on/off is fine. Or you could run it straight through a for upward of 4ish weeks by taking some ketotifen alongside it (at least for portions) which would help sustain adequate beta-2 adrenergic receptor expression.
You could also MAYBE get this effect via benadryl but it's not as studied, or at least documented in humans. Just theorycrafting predicated on its ability to inhibit phospholipase c.. or well, more likely via antagonizing the h1 receptor that's Gq coupled and thereby impede its activation, may sustain more Gs coupling through the beta-2 adrenergic receptor. I've also read random posts from people talking about phospholipid methylation via beta-2 agonism and thereby that causing subsequent downregulation via phospholipases.. but I've never been able to identify a study (or group of studies) tying that together. Because it's known that membrane/receptor methylation actually increases coupling of the beta-2 receptor to its major effector, cAMP. So that contention doesn't make much sense to me unless anyone has a more concrete study to show. Sorry for the nuance.