DNP Question

[Gstack80]

If you run DNP by its self will you run into the problem of losing lean muscle mass. Im 5 weeks into my cycle and I put on 15 pounds of muscle and lose 6 pounds of fat. After im done Im going to run DNP to lose some body fat but I dont want to lose the hard earn muscle I've put on. Will I run into the problem of losing muscle on DNP?

 

[dfein]

I'm on DNP right now (only 2nd day), but I can basically tell you that any form of weight loss is going to make your body lose muscle except for steroids. People claim clenbuterol will make you lose fat and gain muscle at the same time but I have not seen this to be true. I kind of think clen is overrated. The best way to minimize muscle loss is to use anabolics while use cutting drugs. I have heard Trenbolone is #1, but you will go bald

 

[Conciliator]

If you run DNP by its self will you run into the problem of losing lean muscle mass.

You shouldn't be losing much muscle, if at all. In contract to things like thyroid, DNP does not appear to be catabolic. Here are four references from the research, with quotes:

Harper JA, Dickinson K and Brand MD (2001) Mitochondrial uncoupling as a target for drug development for the treatment of obesity. Obesity Rev, 2, 255265

In contrast to the use of thyroid extract (also in common use at the time to treat obesity), DNP did not promote urinary nitrogen excretion, so the assumption was made that weight loss could be attributed to a specific loss of fat (47).

Bell, Jacques. 1939. Etude biologique des produits dinitres chez l'homme. Medecine. 19:749-54.

2. This increase of the metabolism is due mostly to an increase in the combustion of the fat and a little to combustion of carbohydrates.
3. Dinitrophenol does not attack cell tissue albumin and does not determine the fat loss to the expense of the muscles, contrary to thyroxine.
...
Finally, thyroxine causes a nitrogen malnutrition: it burns the muscle and fatigues the heart. Dinitrophenol-lysidine, to the contrary, causes a lipid-glycemic loss: it is the elimination of reserve materials without attacking visceral and muscle tissue.

Simkins S 1937 Dinitrophenol and desiccated thyroid in the treatment of obesity. JAMA 108:21102119.

The extra energy of metabolism is derived mainly from fat and practically not at all from protein or carbohydrate. Consequently, dinitrophenol in therapeutic dosage produces no breakdown of significant amounts of body protein, even with patients on an inadequate protein intake. This is in marked contrast with the very consdierable increase in nitrogen excretion observed in patients undergoing treatment with thyroid. The fat is used completely and satisfactorily broken down, as no ketone bodies are found in urine. There is a no hyperlipidemia or constant change in the fixed and fatty acids of the blood.

Cutting WC, Tainter ML. Metabolic actions of dinitrophenol with the use of balanced and unbalanced diets. J Am Med Assoc 1933; 101: 20992102.

Dinitrophenol, used in doses of therapeutic range, caused increases in metabolism of the usual magnitude irrespective of the type of diet. The nitrogen excretion was never greater than the intake, even when the subjects lost as much as 5 pounds in body weight during one week. From this it seemed probable that there was no actual tissue breakdown during these short periods of heightened metabolism, but that the loss of weight was due to the utilization of stored carbohydrate or fat. This does not mean, of course, that tissue breakdown would not occur if the drug should be given over longer periods, but probably when materials other than protein are available these are utilized first. Thus the assumption might be made that, as long as the protein intake is adequate, any reduction in body weight is not primarily at the expense of the tissue proteins.
...
3.The subjects excreted less nitrogen than they ingested, yet there were definite losses of body weight. Therefore, body proteins probably were not broken down. The output of urinary organic acid was not increased, thus indicating that the fats were completely burned without giving rise to acidosis.

 

[Conciliator]

People claim clenbuterol will make you lose fat and gain muscle at the same time but I have not seen this to be true.

It is true. Anticatabolic effects have been shown numerous times in humans, corroborating the animal data.

For example, this study in obese women found that after 8 weeks of EC administration (a general adrenergic agonist), the EC group lost 9.9 lbs more body fat and 6.2 lbs less fat-free mass. "These findings provide evidence that promotion of fat loss and preservation of FFM during weight reduction may also be achieved pharmacologically in humans."

This more extensive study stated "We conclude that the ephedrine/caffeine combination is effective in improving and maintaining weight loss, further it has lean body mass saving properties."

This paper was pretty explicit, titled "Clenbuterol increases lean muscle mass but not endurance in patients with chronic heart failure." They found that "Clenbuterol was well tolerated and led to a significant increase in both lean mass and the lean/fat ratio."

In another human study, they gave high dose clenbuterol (up to 720 mcg) for three months. There wasn't a control group, but they found that "clenbuterol therapy increased skeletal muscle mass and strength."

This study, titled "Oral albuterol dosing during the latter stages of a resistance exercise program" found that "A higher lean body mass trend also occurred with albuterol from weeks 10-13."

Finally, this study give albuterol for 12 weeks to boys with muscular dystrophy. Outcome measurements included lean body mass and fat mass. They found that "Lean body mass was significantly higher for subjects following albuterol treatment compared to placebo treatment, while fat mass was significantly lower."

While there is definitely more evidence in animals showing anabolic/anti-catabolic effects from beta-agonists, there is plenty of evidence supporting the existence of the same effect in human skeletal muscle.

 

[Conciliator]

The best way to minimize muscle loss is to use anabolics while use cutting drugs.

That's one way. You can also use other anti-catabolic drugs while lifting heavy, making sure to keep protein intake high, and ensuring that the caloric deficit is not too low.

I have heard Trenbolone is #1, but you will go bald

Tren (and other androgens) will accelerate baldness only in those who are genetically susceptible to androgenic alopecia (i.e. those who will eventually go bald anyway).

 

[dfein]

720mcg is way too high though. The funny thing is that if you look at some medical articles, you will find some people have "overdosed" on 120mcg of Clenbuterol. I take 200mcg daily and I don't feel like my muscles have got any bigger. It does make my heart beat fast and it makes me sweat. It makes me breathe better too. For asthma medicine, it works quite well. My weight has not changed much. I spent money on it, so I'm just going to continue to use it until I finish it, but I don't intend on buying it again. I honestly think that to get the benefits from it, you have to use an insane dose which is perhaps life threatening.

 

[Conciliator]

720mcg is way too high though.

A dose is only "high" relative to sensitivity. They didn't just start the guys on 720mg/day. They slowly titrated to that dose over 41 weeks. That means the dose increased LESS than 20 mcg/wk. Most bodybuilders will go up 20 mcg every day or two. The people in this study were using LOWER doses relative to their sensitivity than the average bodybuilder. The important thing is that as their tolerance for clen grew, their dose was slowly raised to compensate.

The funny thing is that if you look at some medical articles, you will find some people have "overdosed" on 120mcg of Clenbuterol.

There's nothing odd about that. If you take 120mcg all at once, without having used clen and become desensitized to it, it's going to have very strong effects.

I take 200mcg daily and I don't feel like my muscles have got any bigger.

Muscle grows at such an incredibly slow rate, you're kidding yourself if you think you're going to notice a difference in the rate of growth.

My weight has not changed much.

Well that shows you're not eating enough to grow, so even if you could notice notice a difference in the rate of growth, you're not eating enough to support that growth.

I honestly think that to get the benefits from it, you have to use an insane dose which is perhaps life threatening.

No, you don't. You just have to use a dose slightly higher than the dose that maintains homeostasis with your current degree of sensitivity.

 

[dfein]

A dose is only "high" relative to sensitivity. They didn't just start the guys on 720mg/day. They slowly titrated to that dose over 41 weeks. That means the dose increased LESS than 20 mcg/wk. Most bodybuilders will go up 20 mcg every day or two. The people in this study were using LOWER doses relative to their sensitivity than the average bodybuilder. The important thing is that as their tolerance for clen grew, their dose was slowly raised to compensate.

Even titrated, 720 mcg sounds lethal to me. It sounds like to me that it was only tolerable to these patients because they were experiencing heart failure and it was actually helpful. I don't know of any bodybuilder ever using 700mcg of clenbuterol. 200mcg daily to me accelerates my heart markedly, and I'm on my 2nd month.

Muscle grows at such an incredibly slow rate, you're kidding yourself if you think you're going to notice a difference in the rate of growth.

Well that shows you're not eating enough to grow, so even if you could notice notice a difference in the rate of growth, you're not eating enough to support that growth.

I have noticed practically no change at all since using it. Food should not have anything to do with it because clenbuterol increases feed efficiency. Even severely malnourished rats had increased protein content at the expense of fat loss. All of them increased in weight despite eating little food. They even found recently that clenbuterol increases muscle size in rats independent of myostatin blockade. This was something in a dose like 200 mcg PER KG.

 

[jasthace]

You shouldn't be losing much muscle, if at all. In contract to things like thyroid, DNP does not appear to be catabolic. Here are four references from the research, with quotes:

..

Just as T3 depletes Muscle ATP stores ,so dos DNP.
This has a weakening effect and may cause the muscle to become flat and smaller will have a negative effect on performance.


DNP works by uncoupling oxidative phosphorylation, which increases the body's temperature and metabolic rate (1). Synthesis of fatty acid in adipose tissue requires cooperation of mitochondria! and cytoplasmic enzymes. Mitochondria release energy from food molecules and transform energy into useable form via the production of ATP. ATP is the primary carrier of energy within your cells, and most cells die quickly in the absence of it. ATP in turn powers your muscles. What does DNP have to do with all this? DNP depletes your muscle's ATP (4), thus requiring your mitochondria to convert more energy from food molecules, and thus create more ATP to replace what was lost. This makes your body use more energy to do anything, from walking the dog to benching 315Ibs. In addition, since cellular levels of all these metabolites depend on the efficiency of mitochondrial energy conversion, a mitochondrial proton leak via uncoupling proteins (UCPs) could modulate Fatty Acid synthesis (8). Paradoxically, DNP inhibits muscle contraction, even though it accelerates the ATPase activity of isolated myosin (13). ATPase is the enzyme that causes ATP molecules to release the energy they store, and myosin is a protein that (along with actin) is responsible for both muscular contraction and relaxation.

Anabolic Facts - DNP 2,4-dinitrophenol - complete description

 

[Conciliator]

Even titrated, 720 mcg sounds lethal to me.

Reality is unconcerned with how things sound to you. Titration to 700+ mcg is not lethal, by definition of titration. With increasing desensitization and andrenergic receptor downregulation, you could go even higher. Again, by definition of titration.

It sounds like to me that it was only tolerable to these patients because they were experiencing heart failure and it was actually helpful.

The tolerability has nothing to do with the heart failure. It has to do with slow titration over 41 weeks. Tachyphylaxis from clenbuterol is a well known phenomenon.

I don't know of any bodybuilder ever using 700mcg of clenbuterol.

That's because most titrate up over two, maybe four weeks, not forty-one weeks. If you were to titrate up to 700 mcg in just a couple of weeks, you'd probably have serious problems. It's pretty simple.

I have noticed practically no change at all since using it.

As was said before, muscle grows at such an incredibly slow rate, you're kidding yourself if you think you're going to notice a difference in the rate of growth. Say that naturally you're able to gain half a pound of muscle per week. That's hard enough to "notice" in the short term as it is. You think you'd be able to notice it if you added clen and increased growth 50%? Are you going to be able to notice an additional rate of gain of 1 lb per month? Hell no. That's why there's statistical analysis and well controlled studies to look at this stuff, because personal anecdote is essentially worthless. To top it all off, clen is typically used when people are dieting. When you're dieting, you're doing good to just maintain the muscle you have and not lose anything. You think you're going to notice if you're losing less than if you hadn't taken clen? Again. no. You're deluding yourself if you think that your uncontrolled anecdote has more value than several controlled studies that are in consensus. Adrenergic agonists clearly promote both protein synthesis and lipolysis.

Food should not have anything to do with it because clenbuterol increases feed efficiency. Even severely malnourished rats had increased protein content at the expense of fat loss. All of them increased in weight despite eating little food. They even found recently that clenbuterol increases muscle size in rats independent of myostatin blockade. This was something in a dose like 200 mcg PER KG.

Yes, clenbuterol is a strong repartitioning agent and you can fuel protein synthesis with your own fatty acids from adipose. However, that doesn't make you a bigger person. It makes you a leaner person. If you want to notice an increase in size, rather than a substitution of body fat for body protein, you're going to have to eat more.

 

[Conciliator]

Just as T3 depletes Muscle ATP stores ,so dos DNP.

T3 and DNP work through different mechanisms of action. If you read the references I posted above, you'll note the stark contrast between the two. Also, DNP does not deplete ATP at the therapetic doses used in humans. This was examined in a 2007 study by Rohas et al at Harvard Medical School. As they explain in their conclusion, "Mild, but chronic, treatment with mitochondrial uncouplers should cause increased energy expenditure and oxygen consumption while causing little or no change in ATP levels." They found that this was because of PGC-1 signaling and an increase in mitochondrial expression. They went so far as to say in the abstract that "In light of this compensatory system that limits the toxicity of mild uncoupling, the use of chemical uncoupling of mitochondria as a means of treating obesity should be re-evaluated."

This has a weakening effect and may cause the muscle to become flat and smaller will have a negative effect on performance.

Flat and smaller muscles aren't due to a reduction in ATP levels. It has to do with a reduction in glycogen and its accompanying water.

 

[jasthace]

DNP does not deplete ATP at the therapeutic doses used in humans. This was examined in a 2007 study by Rohas et al at Harvard Medical School. As they explain in their conclusion, "Mild, but chronic, treatment with mitochondrial uncouplers should cause increased energy expenditure and oxygen consumption while causing little or no change in ATP levels." They found that this was because of PGC-1 signaling and an increase in mitochondrial expression. They went so far as to say in the abstract that "In light of this compensatory system that limits the toxicity of mild uncoupling, the use of chemical uncoupling of mitochondria as a means of treating obesity should be re-evaluated."

Definition of a therapeutic dose?
The information I have read suggests that DNP does deplete muscle ATP stores.By way of preventing/inhibiting the production of ATP in favour of heat production.i.e loss of efficiency
So it seems an issues of debate
In living cells, DNP acts as a proton ionophore, an agent that can shuttle protons (hydrogen ions) across biological membranes. It defeats the proton gradient across mitochondria and chloroplast membranes, collapsing the proton motive force that the cell uses to produce most of its ATP chemical energy. Instead of producing ATP, the energy of the proton gradient is lost as heat.

Flat and smaller muscles aren't due to a reduction in ATP levels. It has to do with a reduction in glycogen and its accompanying water.

It is common knowledge that , increased creatine phosphate storage supports muscle tissue hydration, making muscles fuller and stronger ('volumised').Muscle cells use this phosphorylated form of creatine to store energy. Normal metabolism can not produce energy as quickly as a muscle cell can use it, so an extra storage source is needed. The phosphate group can be quickly transferred to ADP to regenerate the ATP necessary for muscle contraction. Hydrolysis of creatine phosphate to creatine releases
A good example of a product that will produce fuller harder stronger muscle through means of increased creatine phosphate stores and muscle hydraton is Oxandrolone{anavar}.
Most steroids increase muscle glycogen stores but anavar also increase Creatine phostate stores.

 

[Conciliator]

Definition of a therapeutic dose?

A therapeutic dose in vivo is a dose equivalent to the doses used by humans for weight loss. ]A therapeutic dose in vitro is a concentration equivalent to the concentration found in humans taking DNP for weight loss. A therapeutic dose is in contrast to a toxic dose, which results in injury or death. Obviously, if you use a dose that will kill an organism or a cell, it will deplete ATP levels, as well as do all sorts of other things that therapeutic doses will not.

The information I have read suggests that DNP does deplete muscle ATP stores.By way of preventing/inhibiting the production of ATP in favour of heat production.i.e loss of efficiency
So it seems an issues of debate

No, it's not an issue of debate. DNP makes ATP production less efficient. If metabolism remained constant, that would result in a reduciton in ATP levels. But metabolism does not remain constant. It increases in order to compensate for the inefficiency and maintain ATP levels. That's the whole purpose of the paper published by the Harvard group. They found that both in vitro and in vivo, the cell/organism would quickly adapt to the inefficiency of energy production, "causing little or no change in ATP levels." It's not an issue of debate when you look at the relevant context.

In living cells, DNP acts as a proton ionophore, an agent that can shuttle protons (hydrogen ions) across biological membranes. It defeats the proton gradient across mitochondria and chloroplast membranes, collapsing the proton motive force that the cell uses to produce most of its ATP chemical energy. Instead of producing ATP, the energy of the proton gradient is lost as heat.

Ok, so you can [ame="http://en.wikipedia.org/wiki/Dinitrophenol"]2,4-Dinitrophenol - Wikipedia, the free encyclopedia@@AMEPARAM@@/wiki/Fileintrophenol.svg" class="image"><img alt="" src="http://upload.wikimedia.org/wikipedia/commons/thumb/2/24/Dintrophenol.svg/120px-Dintrophenol.svg.png"@@AMEPARAM@@commons/thumb/2/24/Dintrophenol.svg/120px-Dintrophenol.svg.png[/ame]. This says nothing about the net effect of protonophores on ATP levels. It talks about the mechanism through which protonophores affect ATP production.

Muscle cells use this phosphorylated form of creatine to store energy. Normal metabolism can not produce energy as quickly as a muscle cell can use it, so an extra storage source is needed. The phosphate group can be quickly transferred to ADP to regenerate the ATP necessary for muscle contraction. Hydrolysis of creatine phosphate to creatine releases

Ok, you can plagiarize a http://muscle.ucsd.edu/musintro/energy.shtml (UCSD website) as well.

A good example of a product that will produce fuller harder stronger muscle through means of increased creatine phosphate stores and muscle hydraton is Oxandrolone{anavar}. Most steroids increase muscle glycogen stores but anavar also increase Creatine phostate stores.

An even better example of something that increases creatine phosphate levels is... tah-dah... creatine. Some of the earliest research on DNP was performed by Corneille Heymans and coworkers in Ghent, Belgium from 1928 into the early 1930's. They found a decrease in both muscle glycogen and PCr. You could say that flatter muscles are due to reductions not in ATP levels, but in glycogen and PCr, both of which are known to affect hydration and muscle size.

 

[jasthace]

DNP makes ATP production less efficient. If metabolism remained constant, that would result in a reduction in ATP levels. But metabolism does not remain constant. It increases in order to compensate for the inefficiency and maintain ATP levels.

Yeah that's pretty cool alright

Ok, so you can plagiarize wikipedia. Ok, you can plagiarize a http://muscle.ucsd.edu/musintro/energy.shtml (UCSD website) as well.

Lol
You must have done mega memory

Some of the earliest research on DNP was performed by Corneille Heymans and coworkers in Ghent, Belgium from 1928 into the early 1930's. They found a decrease in both muscle glycogen and PCr. You could say that flatter muscles are due to reductions not in ATP levels, but in glycogen and PCr, both of which are known to affect hydration and muscle size.

Wouldn't this decrease in PCr stores in muscle not have a direct effect on muscle hydration/fullness effecting muscle size?

Not that that is unacceptable in a diet.These things are easily reversed with muscle hypertrophy once an adequate diet is reintroduced.

 

[mikeylikesit]

Conciliator, I sent you a PM a few days ago regarding DNP and would like to know if you could please reply.
I am sorry, I didn't mean to highjack the thread by any means, but I have no other way to ask you to reply.
Thanks

 

[CuriousInAlabama]

I weigh 220 lbs...I am a female and want to use DNP to help me lose weight. How many mg's would anyone recommend per day (safely).

 

[bigrobbie]

I weigh 220 lbs...I am a female and want to use DNP to help me lose weight. How many mg's would anyone recommend per day (safely).

Safely and DNP being used in the same sentence just doesnt feel right...LOL! Have you studied

up on DNP? Want to make sure you understand what you are going to be putting in your body. I

would urge you to be very careful w/ DNP, study all the risks and sides.

 

[CuriousInAlabama]

Yes I have read tons of material on DNP but I do appreciate you asking. The only thing I'm unsure of is how much to take each day and when is the best time to take it. I'm not going to be soley dependent on the DNP but would like it to basically jump start my weight loss; I know I can't stay on it forever but I am hoping it will help me shed the first 20 to 30 lbs.

 

[bigrobbie]

Yes I have read tons of material on DNP but I do appreciate you asking. The only thing I'm unsure of is how much to take each day and when is the best time to take it. I'm not going to be soley dependent on the DNP but would like it to basically jump start my weight loss; I know I can't stay on it forever but I am hoping it will help me shed the first 20 to 30 lbs.

Different opinions on mg intake...200mg e.d. seems to be the norm for a woman with your body

weight, but I have read different things. I worry you haven't researched enough, simply because

you are asking for dosage...I can say I have read of DNP harming womens reproductive system,

T3, Clen, a cardio and weight routine added to a very clean, strict diet should give you the same

results without the potential of getting sick...I can't give you solid advise because I am afraid of

DNP. I'm not trying to rain on your parade, don't get me wrong, I just can't give any advise other

than stay away from the DNP. More harm than good (I'm sure I'll get flamed for saying this, but

I can take it...LOL!)

 

[CuriousInAlabama]

No, everyone is entitled to their opinion and as far as reproductive system, that's not a worry. I have 2 kids and I had a partial hysterectomy last year......me having more kids hasn't been an option since 1997! I have read a lot on DNP but I just have not found something definitive as far as the mg's for me; I was thinking 200 to 300 mg per day? I do understand there are risks but that's so with anything you consume and for the most part I've only read that has taken place when someone abused DNP by taking an excessive amount thinking more = better.....I do understand that it takes time and that it stays in your system and to not really expect results to start until about the 4th day. The other option I was considering was an HCG/500 calorie diet per day but have been told by most that I would be wasting my money on the HCG (it's $600 for 40 days) that it's the 500 calorie diet alone that will cause the drastic weight loss and would be very dangerous also. I know that chemicals are not solely the answer. I do understand that I need to change my life/eating habits but I honestly just want something to kick start my weight loss……I have tried many many diets only to fail. I think I could handle sweating and a raised body temperature.