T3 without anabolics? Something else?

[tnick7]

I've read mixed opinions. The general consensus is T3 shouldn't be run without anabolics because it will burn too much muscle.

How necessary are anabolics alongside a low dose of T3?

I'm considering running a low dose (tapered up then back down 25-100mcg) in a few months time on a cut (for around 4-6 weeks), but not too keen on running anabolics alongside it (don't want to waste anabolics on a cut). Is this a gamble that's not worth taking? Would running something like hdrol @ 75-100mg alongside it be enough to preserve muscle? I'm still not sure I may run Test prop and T3 as a recomp instead, but kinda want my first run with test to be on a bulk!

I've previously used EC, which I have never been overly impressed with. I want to avoid clen, not interested after reading the studies showing cardiac necrosis.

If not T3, anything else? (Not DNP, usnic acid, want to keep things fairly safe )

Thanks guys in advanced

 

[russy_russ]

I ran liquid T3 at 100mcgs daily with just an anticat and worked fine.

 

[tnick7]

I ran liquid T3 at 100mcgs daily with just an anticat and worked fine.

Anticat? (Anticatabolic?)

What did you use? How was the fat loss?

Thanks

 

[tnick7]

Shameless bump on original question(s)

 

[Prometherion]

I'm interested to know as well.


Hey tnick, where you been? Haven't seen you in a while.

 

[tnick7]

I'm interested to know as well.


Hey tnick, where you been? Haven't seen you in a while.

Busy with studies! Got a break now so I'm back for a bit!

 

[crazyfool405]

if you do T3, Clen should be a good choice if you dont want to run any orals.

but there is a risk of muscle loss when you run it alone.

usnic acid is fairly safe especially when used with an antioxident, but dont exceed much more then 80MG perday. thats when problems arise.

hope this helps.

 

[russy_russ]

I had a bottle of post cycle support left over and glutamine. I noticed ~1-2 lbs loss per week. However, I noticed more that I was leaning out. So, don't be discouraged by the scale.

I'm running T3 with clen right now, and it's working great.

 

[tnick7]

if you do T3, Clen should be a good choice if you dont want to run any orals.

but there is a risk of muscle loss when you run it alone.

usnic acid is fairly safe especially when used with an antioxident, but dont exceed much more then 80MG perday. thats when problems arise.

hope this helps.

Thanks Crazy.

I've read something about chromosome damage with usnic acid so between that and hearing its not all that effective I'd rather avoid it.

I'm also very skeptical about running clen. I'd prefer to run hdrol and take and let me lipids and liver values take a small hit than run clen. What do you reckon? Will the hdrol suffice in preventing muscle loss?

 

[crazyfool405]

Thanks Crazy.

I've read something about chromosome damage with usnic acid so between that and hearing its not all that effective I'd rather avoid it.

I'm also very skeptical about running clen. I'd prefer to run hdrol and take and let me lipids and liver values take a small hit than run clen. What do you reckon? Will the hdrol suffice in preventing muscle loss?

of course Hdrol is ok,

i dont know much about chromosome damage and usnic acid, but its definetly effective in wasting calories, which would actually be quite great on a bulk.

if your eating a surplus and putting on both muscle and fat, but a little more fat then you want, without cutting calories you can use usnic acid to waste them and continue to grow with no effect on muscle gain in theory, and just waste the calories that arent really needed.

 

[citystreets]

can anyone pin point how exactly clen cause heart necrosis? Im thinking anything that raises your blood pressure enough would be just as bad. Such as hdrol?

 

[russy_russ]

can anyone pin point how exactly clen cause heart necrosis? Im thinking anything that raises your blood pressure enough would be just as bad. Such as hdrol?

Can you show scientific data that links necrosis of the heart to clenbuterol use? I really do not believe that clenbuterol will cause unprogrammed death of a cell. Cheifly, the cause of this would be a myocardial infarction in which case a user should not administer clenbuterol if he/she has preexisting heart conditions.

 

[crazyfool405]

Can you show scientific data that links necrosis of the heart to clenbuterol use? I really do not believe that clenbuterol will cause unprogrammed death of a cell. Cheifly, the cause of this would be a myocardial infarction in which case a user should not administer clenbuterol if he/she has preexisting heart conditions.

i dont think it causes heart necrosis, but i know it causes left ventricular hypertrophy, or an enlarged heart, but these are in huge doses i believe.

 

[Conciliator]

Can you show scientific data that links necrosis of the heart to clenbuterol use?

This is the study that gets the most publicity among bodybuilders: Invalid Link Removed The very first sentence of the abstract reads "High doses of ... clenbuterol can induce necrotic myocyte death in the heart and slow-twitch skeletal muscle of the rat."

 

[Conciliator]

can anyone pin point how exactly clen cause heart necrosis? Im thinking anything that raises your blood pressure enough would be just as bad. Such as hdrol?

The study I linked to above explains the mechanism of action. Beta-2 agonism in the heart actually cardioprotective. It's often missed, but the abstract says "...clenbuterol-induced myocardial apoptosis was mediated through neuromodulation of the sympathetic system and the cardiomyocyte beta 1-adrenoreceptor..." So it wasn't beta-2 agonism in the heart that caused the apoptosis. As the paper explains, "available information suggests that b2-AR stimulation is antiapoptotic and that it may even be beneficial to the failing heart." Rather, what induced apoptosis was excessive beta-1 agonism from the local release of noradrenaline in response to the clen. They conclude:

Taking all our experimental observations together, the most likely mechanism for clenbuterol-induced toxicity on cardiac myocytes appears to be an injurious effect, not directly via the cardiomyocyte b2-AR, but indirectly via stimulation of the b2-AR of presynaptic nerve terminals, which consequently augments the release of noradrenaline (30). This observation that b2-AR activation in vivo can induce apoptosis does not negate the putative antiapoptotic effects of b2-AR stimulation in vitro (7, 46, 47, 49) but instead shows that the antiapoptotic effect of b2-AR stimulation is relatively small and easily overwhelmed by the concomitant indirect b1-AR stimulation that occurs in vivo.

The problem is when excessive doses of clen are taken, because this causes the release of norepinephrine from presynaptic nerve terminals. The norepinephrine can then cause undesirable cardiovascular effects (and possible heart damage). Moral of the story: keep your doses of clen low. You can still get a profound lipolytic (fat loss) effect from a low dose, while reducing your risk of adverse events.

The question now is whether humans have the same ratio of beta-2 agonism to presynaptic noradrenaline release (and beta-1 agonism). IMO, if humans really experienced significant beta-1 agonism, you'd expect the heart rate to rise much more than it does. Yet this is not what you see with moderate dosages of clen. Rats are not humans and extrapolations here are really questionable in my mind.

The study in rats showed a threshold level for cardiomyocyte apoptosis at 1 mcg/kg. For a 200 lb bodybuilder, that would be about 91 mcg/day, which is well within common dosages. Nonetheless, one could easily run a cycle below this threshold level. I think an important point is that doses are increased in light of desensitization. Extrapolating from the study, apoptosis would occur in a 200lb bodybuilder if he took 91 mcg on day 1. Most would agree that's very excessive so early on. Now if we're talking about day 10, things are much different, since beta-2 AR downregulation will mean the higher dose is effectively a lower one, with much less impact.

Lastly, take into consideration that taurine is cardioprotective and often taken along with clen. It may change the threshold level, even if directly applicable to humans.

 

[steveironman]

clen is the way to go imo ...along with increased bmr comes increased rate of protein systhesis thus the anti catbolic properties ..just keep diet clean but with adequate protein. Clen by nature naturally preferntial to burning bodyfat (b/c of thermogenic properties lypolisis is stimulated) ..t3 is indiscriminate and the thyroid hormore increse bmr to a point where fat and muscle are burned...esp w/o anabolics. The real danfger in clen is when running with AAS at higher doses(of both) for a longer duration. Use clen and then every week of so for 3 nights in a row take 50-75mgs benadryl as u build a tolerance to it (clen) and the benadryl will clear recpetors to keep clen effective ...JMO...

 

[Conciliator]

if your eating a surplus and putting on both muscle and fat, but a little more fat then you want, without cutting calories you can use usnic acid to waste them and continue to grow with no effect on muscle gain in theory, and just waste the calories that arent really needed.

Huh? In theory, taking an uncoupler would ramp up AMPK and inhibit mTOR and protein synthesis. What do you mean "no effect on muscle gain in theory"?

It's far from clear what effect "wasting calories" with an uncoupler would have on a bulk. Reduced fat gain with the same muscle gain is hardly an expected outcome.

 

[AUTO]

dont run clen with t3.

 

[Conciliator]

clen is the way to go imo ...along with increased bmr comes increased rate of protein systhesis thus the anti catbolic properties

Increased BMR doesn't entail increased protein synthesis and anticatabolism. If that were the case, things that increase BMR the most, like DNP, would be the most anti-catabolic. That's just not the case. The reason clen is anabolic/anti-catabolic appears to be due to beta-2 agonism in muscle cells and a resultant activation of Akt and mTOR. For more information, Invalid Link Removed.

..just keep diet clean but with adequate protein. Clen by nature naturally preferntial to burning bodyfat (b/c of thermogenic properties lypolisis is stimulated)

Clenbuterol stimulates lipolysis directly though beta-adrenergic agonism in fat cells. It's not indirectly through thermogenesis.

The real danfger in clen is when running with AAS at higher doses(of both) for a longer duration. Use clen and then every week of so for 3 nights in a row take 50-75mgs benadryl as u build a tolerance to it (clen) and the benadryl will clear recpetors to keep clen effective ...JMO...

Ketotifen has been shown many times to upregulate beta-2 receptors. Just do a pubmed search on ketotifen and tachyphylaxis. It works well to take clen in the mornings and keto at night, before bed, since ketotifen has a sedative-hypnotic effect.

As far as I know, no research has shown that benadryl also prevents beta adrenergic desensitization. Both ketotifen and benadryl are H1 antagonists, leading many to assume they have similar effects in this regard, but they're very different molecules belonging to different classes of antihistamine. I don't think the mechanism of action behind beta receptor upregulation has been elucidated. Based on that, I'd recommend taking ketotifen, which has a proven effect.

 

[Conciliator]

I've read something about chromosome damage with usnic acid so between that and hearing its not all that effective I'd rather avoid it.

Usnic acid is also clearly heptoxic, as several case reports show. Personally, I'd much rather take DNP, which has risks of its own, but is not hepatotoxic.

I'm also very skeptical about running clen.

I think clen is often underestimated and misunderstood. It is true that it does little to help you create a caloric deficit. Clen increases metabolic rate a small amount and doesn't generally suppress hunger. However, clen is profoundly fat mobilizing. It sends a lipolytic signal to fat cells so that free fatty acids are released into your bloodstream. This has two important effects that I can think of. One is its beneficial effect on partitioning. An increase in FFA concentrations from clen would result in insulin resistance. This is beneficial when dieting. Glucose and protein are spared, lipogenesis (fat creation) is inhibited, and fat is used preferentially for fuel.

Two, the greatly enhanced lipolysis allows you to sustain a greater caloric deficit. There's a point you reach when dieting where the ability of fat to supply your body with energy is maxed out. If you cut calories even further, body proteins will be used and you'll lose muscle. This point decreases as you get leaner and have less fat to mobilize. Clen raises the point greatly, so much more fat is available and you can sustain a greater caloric defict. If you don't cut calories, then clen isn't going to do much. If you create a big caloric deficit, though, I think clen can help a ton. This is why I think clen complements DNP so well. It mobilizes a great deal of fat that can be burned by the large caloric deficit created by the DNP.

Lastly, clen is an adrenergic agonist. This has anabolic effects in muscle cells. We know from research that even EC, which is much weaker than clen, greatly prevents the loss of muscle during a diet. This is believed to be due to a mild anabolic effect (since it doesn't appear to limit catabolism). Unfortunately, most guys in the gym are in a very poor position to evaluate clen's mild anabolic effects. When you're dieting, you're doing great to just maintain muscle mass, let alone gain anything. I think those who don't lose muscle while taking clen would have lost muscle without it. And I think those who do lose muscle while taking clen would have lost even more without it. If EC has been proven to be protein sparing (I have references for anyone interested), then clen is definitely protein sparing.

I think a lot of people misunderstand clen, when it's most beneficial, and what it does exactly. It reminds me of when people say "creatine just fills your muscles with water". No, it does a lot more than that.

 

[tnick7]

Usnic acid is also clearly heptoxic, as several case reports show. Personally, I'd much rather take DNP, which has risks of its own, but is not hepatotoxic.
I think clen is often underestimated and misunderstood. It is true that it does little to help you create a caloric deficit. Clen increases metabolic rate a small amount and doesn't generally suppress hunger. However, clen is profoundly fat mobilizing. It sends a lipolytic signal to fat cells so that free fatty acids are released into your bloodstream. This has two important effects that I can think of. One is its beneficial effect on partitioning. An increase in FFA concentrations from clen would result in insulin resistance. This is beneficial when dieting. Glucose and protein are spared, lipogenesis (fat creation) is inhibited, and fat is used preferentially for fuel.

Two, the greatly enhanced lipolysis allows you to sustain a greater caloric deficit. There's a point you reach when dieting where the ability of fat to supply your body with energy is maxed out. If you cut calories even further, body proteins will be used and you'll lose muscle. This point decreases as you get leaner and have less fat to mobilize. Clen raises the point greatly, so much more fat is available and you can sustain a greater caloric defict. If you don't cut calories, then clen isn't going to do much. If you create a big caloric deficit, though, I think clen can help a ton. This is why I think clen complements DNP so well. It mobilizes a great deal of fat that can be burned by the large caloric deficit created by the DNP.

Lastly, clen is an adrenergic agonist. This has anabolic effects in muscle cells. We know from research that even EC, which is much weaker than clen, greatly prevents the loss of muscle during a diet. This is believed to be due to a mild anabolic effect (since it doesn't appear to limit catabolism). Unfortunately, most guys in the gym are in a very poor position to evaluate clen's mild anabolic effects. When you're dieting, you're doing great to just maintain muscle mass, let alone gain anything. I think those who don't lose muscle while taking clen would have lost muscle without it. And I think those who do lose muscle while taking clen would have lost even more without it. If EC has been proven to be protein sparing (I have references for anyone interested), then clen is definitely protein sparing.

I think a lot of people misunderstand clen, when it's most beneficial, and what it does exactly. It reminds me of when people say "creatine just fills your muscles with water". No, it does a lot more than that.

Thanks Conciliator. You've provided some great info in this thread!

So to conclude, in your opinion, the risks of cardiac necrosis can be greatly reduced by keeping the dose of clen under the threashold (1mc/kg) and tapering up?

I hear so many different methods of running clen, 2weeks on/2off, 4weeks straight, 2days on 1 off etc. What in your opinion is the best way to run it?

What is your opinion on T3 alongside clen?

Thanks

 

[russy_russ]

Clen will downregulate the beta-2 receptors after about 2 weeks which diminishes its effect significantly. Some people stop taking it for 2 weeks, while often taking benadryl during this time off. You can run clen for 4-6 weeks with ketotifen generally taken after the 2nd week.

 

[crazyfool405]

Huh? In theory, taking an uncoupler would ramp up AMPK and inhibit mTOR and protein synthesis. What do you mean "no effect on muscle gain in theory"?

It's far from clear what effect "wasting calories" with an uncoupler would have on a bulk. Reduced fat gain with the same muscle gain is hardly an expected outcome.

i didnt think it would have any effect on protein syntesis, i never read that on usnic acid.

reduced calories from them being wasted but still a surplus will still result in some gains no? along with less fat?

obviously i got to read a little more on usnic acid.

 

[WeightShift]

I'm glad somebody is finally giving Clen is fair chance at the spotlight. People love to talk about cardiovascular hypertrophy and necrosis but fail to remember that those studies were on animals who have much more concentrated amounts of beta-2 receptors and at doses that exceed 1:1 lb/mcg ratio.

I get more side-effects from an ECA stack than clen.

 

[steveironman]

Increased BMR doesn't entail increased protein synthesis and anticatabolism. If that were the case, things that increase BMR the most, like DNP, would be the most anti-catabolic. That's just not the case. The reason clen is anabolic/anti-catabolic appears to be due to beta-2 agonism in muscle cells and a resultant activation of Akt and mTOR. For more information, [
Clenbuterol stimulates lipolysis directly though beta-adrenergic agonism in fat cells. It's not indirectly through thermogenesis.
Ketotifen has been shown many times to upregulate beta-2 receptors. Just do a pubmed search on ketotifen and tachyphylaxis. It works well to take clen in the mornings and keto at night, before bed, since ketotifen has a sedative-hypnotic effect.

As far as I know, no research has shown that benadryl also prevents beta adrenergic desensitization. Both ketotifen and benadryl are H1 antagonists, leading many to assume they have similar effects in this regard, but they're very different molecules belonging to different classes of antihistamine. I don't think the mechanism of action behind beta receptor upregulation has been elucidated. Based on that, I'd recommend taking ketotifen, which has a proven effect.

Thanks for the info ..i learned a few things/and theories (dont wanna debate study results and how and whys-clen reacts diff in diff animals rats-raises cortisol ..horses lowers it.....etc ...a lot of speculation to transfer meahanisms to humans ....anyway) 1 thing i will say for sure..the benadryl does work from personal experience..ketotifen may be most effective i n...but its easier and cheaper just to pick up benedryl from pharmacy otc ...and it def work...pretty easy to see when this works as anyone that has experienced clen and tolerance build up ...if you try the bendryl you will find your effects def return at much lower dosages post benedryl.....

 

[russy_russ]

Ketotifen allows the user to take clen 4-6 weeks continuously.. while cycling 2 weeks on / 2 weeks off with benadryl..

 

[steveironman]

Ketotifen allows the user to take clen 4-6 weeks continuously.. while cycling 2 weeks on / 2 weeks off with benadryl..

hmmm not the case with me at all i go fri sat sun pm with benadryl ....not cycle on off 2 weeks....etc ....clen def works at lower dosages..no doubt in my personal experince. U May wanna give that atry of hey if the ketotifen is orking for you and you dont mind the $ and accessability thing then stick with what works for you...

Concicliator ...you seem to have extensive clen knowledge ...which do you prefer when your run clen ?....

 

[tnick7]

Thanks Conciliator. You've provided some great info in this thread!

So to conclude, in your opinion, the risks of cardiac necrosis can be greatly reduced by keeping the dose of clen under the threashold (1mc/kg) and tapering up?

I hear so many different methods of running clen, 2weeks on/2off, 4weeks straight, 2days on 1 off etc. What in your opinion is the best way to run it?

What is your opinion on T3 alongside clen?

Thanks

Bump in case Conciliator checks back in

 

[Mr.50]

Conciliator,

Any info on how to take clen without it decreasing aerobic efficiancy? Everytime I take it my aerobic performance (boxing) suffers cause it just seems to crank up my heart rate too much (or some such other effect).

I have had good success with clen topical combined with a good transdermal carrier!

Mr.50

 

[crazyfool405]

this is straight from dave palumbo

and ive been searching and i couldnt find info on this action by usnic acid.

Dave do uncouplers effect protein synthesis? by inhibiting mTOR? specifically usnic acid?
….Absolutely not! Uncouplers merely cause potential energy that was gonna be used to make ATP get released from the cells as heat.

 

[russy_russ]

Conciliator,

Any info on how to take clen without it decreasing aerobic efficiancy? Everytime I take it my aerobic performance (boxing) suffers cause it just seems to crank up my heart rate too much (or some such other effect).

I have had good success with clen topical combined with a good transdermal carrier!

Mr.50

I've noticed the same thing while olympic lifting. I have to drink tons more water and take longer breaks between sets.

 

[Conciliator]

this is straight from dave palumbo

and ive been searching and i couldnt find info on this action by usnic acid.

Dave do uncouplers effect protein synthesis? by inhibiting mTOR? specifically usnic acid?
….Absolutely not! Uncouplers merely cause potential energy that was gonna be used to make ATP get released from the cells as heat.

Dave is apparently unaware of the body of research showing that uncouplers are potent activators of AMPK. Same goes for AMPK and its effects on mTOR and protein synthesis. He also sells usnic acid, so I'd say he's biased.

1. Maybe he can explain why in Invalid Link Removed, DNP increased AMPK more than any of the other six conditions they tested.
   
2. Maybe he can explain why in Invalid Link Removed, they stated that "treatment of L6 cells with DNP (0.5 mM)... increased AMPK activity by 3.5-fold" and also that "AMPK is activated in conditions that raise the cellular AMP/ATP ratio (8). DNP disrupts ATP production by the mitochondria thus elevating this ratio."
   
3. Maybe he can explain why in Invalid Link Removed, they found that "stimulation with DNP produced a 2.2-fold increase in AMPK phosphorylation (P < 0.01)." The whole purpose of the paper was to examine how much of DNP's effects were due to AMPK activation. A foundational principal is yhat DNP activates AMPK.
   
4. Maybe he can explain why in the introduction to Invalid Link Removed, the authors talk about why researchers use DNP specifically for activation of AMPK: "Accordingly, investigators have used chemical substances, most notably... (AICAR), which, after uptake and phosphorylation, acts like 5'-AMP to directly activate AMPK, or, to a lesser extent, dinitrophenol (DNP), which uncouples oxidative phosphorylation and thereby increases endogenous 5'-AMP levels to activate AMPK, as partial surrogates for exercise in stimulating Glut4 translocation/glucose transport in skeletal muscle preparations."
   
5. Maybe he can explain why the abstract of Invalid Link Removed described 2,4-dinitrophenol (DNP) as a "known activator of AMPK".
   
6. Maybe he can explain why the abstract of Invalid Link Removed states that known AMPK stimuli include "AICAR, rotenone (a Complex I inhibitor), dinitrophenol (a mitochondrial uncoupler), muscle contraction, and sorbitol (producing hyperosmolar shock)." In the full text, they explain that DNP is "a chemical mitochondrial uncoupler which reduces cellular ATP levels and activates AMPK."
   
7. Maybe he can explain why Invalid Link Removed says that "Not surprisingly, AMPK can also be activated by metabolic poisons that inhibit ATP production via oxidative phosphorylation, such as ... dinitrophenol,41–43"
   
8. Maybe he can explain why in the large table on page 5482 of Invalid Link Removed they list dinitropheol and overexpression of natural uncoupling proteins as "stresses that activate AMPK"
   
9. Finally, maybe he can explain Invalid Link Removed, where they found that DNP increased AMPK 5.6-fold. They also found that site Thr2446 on mTOR decreases the activity of mTOR and that "nutrient deprivation, DNP, and AICAR all activate AMPK and stimulate phosphorylation of Thr2446". In other words, DNP activates AMPK, and AMPK inhibits mTOR.

So what's your guess? Is Dave just ignorant of the effects that uncouplers have on cellular energy regulation? Is he just ignorant of the research on AMPK? Or is he lying to you because he doesn't want you to have a reason not to buy Lipolyze from him? My vote is that he's ignorant, not a liar. He needs to learn that uncouplers do a lot more than "merely cause potential energy to get released as heat." They have a profound effect on numerous signalling enzymes involved in cellular energy regulation.

 

[crazyfool405]

Dave is apparently unaware of the body of research showing that uncouplers are potent activators of AMPK. Same goes for AMPK and its effects on mTOR and protein synthesis. He also sells usnic acid, so I'd say he's biased.

1. Maybe he can explain why in Invalid Link Removed, DNP increased AMPK more than any of the other six conditions they tested.
   
2. Maybe he can explain why in Invalid Link Removed, they stated that "treatment of L6 cells with DNP (0.5 mM)... increased AMPK activity by 3.5-fold" and also that "AMPK is activated in conditions that raise the cellular AMP/ATP ratio (8). DNP disrupts ATP production by the mitochondria thus elevating this ratio."
   
3. Maybe he can explain why in Invalid Link Removed, they found that "stimulation with DNP produced a 2.2-fold increase in AMPK phosphorylation (P < 0.01)." The whole purpose of the paper was to examine how much of DNP's effects were due to AMPK activation. A foundational principal is yhat DNP activates AMPK.
   
4. Maybe he can explain why in the introduction to Invalid Link Removed, the authors talk about why researchers use DNP specifically for activation of AMPK: "Accordingly, investigators have used chemical substances, most notably... (AICAR), which, after uptake and phosphorylation, acts like 5'-AMP to directly activate AMPK, or, to a lesser extent, dinitrophenol (DNP), which uncouples oxidative phosphorylation and thereby increases endogenous 5'-AMP levels to activate AMPK, as partial surrogates for exercise in stimulating Glut4 translocation/glucose transport in skeletal muscle preparations."
   
5. Maybe he can explain why the abstract of Invalid Link Removed described 2,4-dinitrophenol (DNP) as a "known activator of AMPK".
   
6. Maybe he can explain why the abstract of Invalid Link Removed states that known AMPK stimuli include "AICAR, rotenone (a Complex I inhibitor), dinitrophenol (a mitochondrial uncoupler), muscle contraction, and sorbitol (producing hyperosmolar shock)." In the full text, they explain that DNP is "a chemical mitochondrial uncoupler which reduces cellular ATP levels and activates AMPK."
   
7. Maybe he can explain why Invalid Link Removed says that "Not surprisingly, AMPK can also be activated by metabolic poisons that inhibit ATP production via oxidative phosphorylation, such as ... dinitrophenol,41–43"
   
8. Maybe he can explain why in the large table on page 5482 of Invalid Link Removed they list dinitropheol and overexpression of natural uncoupling proteins as "stresses that activate AMPK"
   
9. Finally, maybe he can explain Invalid Link Removed, where they found that DNP increased AMPK 5.6-fold. They also found that site Thr2446 on mTOR decreases the activity of mTOR and that "nutrient deprivation, DNP, and AICAR all activate AMPK and stimulate phosphorylation of Thr2446". In other words, DNP activates AMPK, and AMPK inhibits mTOR.

So what's your guess? Is Dave just ignorant of the effects that uncouplers have on cellular energy regulation? Is he just ignorant of the research on AMPK? Or is he lying to you because he doesn't want you to have a reason not to buy Lipolyze from him? My vote is that he's ignorant, not a liar. He needs to learn that uncouplers do a lot more than "merely cause potential energy to get released as heat." They have a profound effect on numerous signalling enzymes involved in cellular energy regulation.

thank you for the studies!!!!

but being that usnic acid is not nearly as effective as DNP nor is the dose used (80mg) for usnic acid any where as potent would it be safe to say that theres very little inhibition or AMPK?

i dont know much about the enzymes and pathways you have spoke about but im willing to learn lol

 

[Conciliator]

thank you for the studies!!!!

but being that usnic acid is not nearly as effective as DNP nor is the dose used (80mg) for usnic acid any where as potent would it be safe to say that theres very little inhibition or AMPK?

Everything is dose-dependent. At a certain dose, usnic acid will uncouple oxidative phosphorylation just as much as DNP. People might usually take lower doses of usnic acid, doses that produce less of an uncoupling effect, but that's a function of the dose. Someone could reduce his dose of DNP for the same effect. Both are uncouplers. Both produce results through the same mechanism of action. The important feature relative to this discussion is that uncouplers (DNP, usnic acid, DNOC, UCP's, etc) lower cellular levels of ATP (despite adaptations that prevent this from occuring to a large extent). This reduction in ATP raises the cellular AMP/ATP ratio and activates AMPK, which is probably also dose-dependent. Take a low dose of usnic acid or a low dose of DNP and AMPK is not going to be activated nearly as much as with a higher dose. The more you take, and the more you tax energy production, the more you're going to activate AMPK. As a master energy regulator, AMPK, in turn, promotes energy producing pathways (e.g. insulin-independant glucose uptake) and inhibits energy consuming pathways (e.g. mTOR and protein synthesis).