# STEROIDS FORUM > ANABOLIC STEROIDS - QUESTIONS & ANSWERS > EDUCATIONAL THREADS >  All you need to know about DNP

## CYCLEON

This is what some of you are asking about - Ive used it quite a bit and its great but you need to be informed, as with all AAS. this spells it out pretty well by one of the better experts on the subject IMO. I dont agree with him on every thing, 4 example I think a little t3 is quite usefull during a cycle, but in all its one of the best "manuals" around. CYC


POSTED BY A WELL KNOWN DNP EXPERT

This is an educational article covering different aspects of DNP and is intended only to educate the reader about DNP. This article is far from comprehensive, but it should provide a good background to get the reader started on learning about DNP. If any of this information is unclear please feel free to contact me by email: 

In this article I will attempt to cover the following topics regarding DNP: 

History 
Mechanism of Action 
Dose and Cycle Recommendations 
Dietary Recommendations 
Side effects/ risks 
Prevention/ Contraindications 
Recommended supplements with DNP 



HISTORY: 

DNP stands for 2,4-dinitrophenol. This is a chemical that was once used in the early 20th century to ignite dynamite and cast a yellow dye on wood and other handcrafts. A few years later demographical statistics showed that employees who worked with DNP everyday tended to lose weight, often rapidly. One fall out from this was a study conducted by Stanford University in 1920 showing that the ingestion of DNP does in fact cause weight loss. This prompted physicians to prescribe DNP to obese patients of that era. DNP was on the market for 2 decades as a weight loss drug and was eventually taken off the market and banned for human consumption by the FDA because there was a report of cataract formation among female users of this drug which turned out to be false. This chemical is still deemed too dangerous by the FDA to allow it to come back to the pharmaceutical marketplace. Over the decades of research on DNP, scientists have never shown it to have the ability to cause cancer or any other mutations despite the fact that its a phenol and that most phenolic compounds are carcinogenic. DNP is now only used as a research chemical and as a pesticide in a few states that still approve of its use. It is not illegal to own DNP, but it is illegal to market it for personal consumption. 

MECHANISM OF ACTION: 

DNP exerts its effects within the cell, more specifically within the membrane of the mitochondria. The advantage of intracellular mechanisms of action such as this is that a tolerance to DNP cannot develop. To make a long story short, DNP makes the process of ATP formation very inefficient. Why is this important? Because ATP is the energy unit needed to drive all our biochemical reactions in our body that is necessary to keep us alive. The cells in our body constantly need energy (ATP) to stay alive. The amount of ATP needed to keep a person alive depends on his/her basal metabolic rate. By making ATP formation inefficient, a persons basal metabolic rate can increase indefinitely, but for practical uses, basal metabolic rate can safely increase by 30-50% without putting ones life in danger. It is not unheard of for people to lose up to one pound of pure fat per day while on DNP. 

If youre not familiar with ATP, its what the Calories that are stored in carbs, fats, and proteins are eventually turned into. In other words, the energy that is stored in the macromolecules are transferred to the ATP molecule, but DNP disrupts this process. Instead of making ATP from macromolecules in the presence of DNP, the potential energy is just turned into heat. This is very significant because ATP levels in the body will quickly diminish and cells want to replenish that storage by breaking down more fats, carbs, etc. As you can see, a patter quickly develops where ATP levels will constantly be below normal and the body will always be trying to burn more fats, carbs, and proteins to help replenish the ATP levels. This is no different than doing aerobic exercises such as jogging, biking, etc, except while on DNP, the body is doing the aerobic exercise non stop 24 hours a day. 


DOSES AND CYCLE RECOMMENDATIONS: 

DNP is not a drug for everyone, definitely not the beginner who just wants to lose a couple of pounds to look better with the shirt off Without proper education on its use, DNP can be deadly. 

There are 2 forms of DNP currently on the market, pure crystalline (100% dry) DNP, and powdered DNP (usually 5-10% moisture). The crystalline version is stronger and more effective, but more caution needs to be used while using it. It acts much faster, and the side effects also subside faster as well. 


I recommend between 2-6mg/kg-bw per day for crystalline DNP and 4-10mg/kg-bw for powdered DNP. A beginner should always start off at the low end to assess tolerance. Trying this for the first time 2 weeks before a competition can be disastrous. A 220lb man is 100kg exactly. This means that if he is a first time user of crystalline DNP then he should take 200mg per day. I suggest staying with this dose for at least 3 days to keep it safe, then slowly increase the dosage. 400mg/day can be used, but never take it all at once. Always split up the doses as far as possible, so for 400mg/day that would mean taking 1 200mg capsule every 12 hours. Only on rare occasions should someone attempt 600mg/day with the crystalline capsules unless its used by a very experienced user and all the vital signs are closely monitored. 

Cycle length depends largely on the individual. At first it was thought that a DNP cycle should be limited to 10 days at the most because the thyroids shuts down and t4 to t3 conversion in the liver becomes nil, however, this is not the case. 10 days is a very arbitrary number. A person taking 200mg/day would have almost completely normal thyroid function at day 10 whereas if s/he took 600mg/day, t3 would be non existent after 3 days. While the t3 hormone plays a very large role in determining fat loss, it should not be a big concern while on DNP because the fat burning capabilities of DNP will more than compensate for the suppressed t3 levels. An advantage to suppressed t3 levels is that the body will burn much less muscle while still burning fat on DNP. Normal t3 and thyroid function is restored within a week of stopping DNP. 

Ok, so how long should you do it? I suggest playing around with it and just go by how your body feels. It is not a bad idea to just take 2-3mg/kg-bw for 3-4 weeks. This causes less side effects and will have the same overall effect, but it will just take a bit longer. After you get used to 2-3mg/kg-bw, then another option is to up the dose by 1 cap and carrying that out for as long as your body can handle it because fatigue and a host of other side effects will eventually overtake you. If 2 caps/day is still too mild then repeat the above step with 3 caps per day spread out into 8-hour intervals. 

Because of some water retention caused by DNP, users typically find that they look their best 4-7 days after finishing their cycle when the water has normalized. 

For competitors: 

Take the last DNP capsule 8 days prior to the competition date. Carb deplete after 3 days after the last cap. Carb load immediately 2 days prior to competition and stop fluid intake. This should allow for excellent glycogen super compensation within the muscles for a fuller look. 


DIETARY RECOMMENDATIONS: 

1. Carb deplete for 3 days prior to DNP because DNP will take a good 2-3 days to deplete the body's glycogen stores before it can efficiently burn stored fat. 

2. Once on DNP eat an isocaloric diet (33% prot, 33% fat, 33% carbs) and keep the calories at around maintenance level. Restricting carbs will put the body in a state of hypoglycemia and can be dangerous to the health and also the mental well being. DNP also mimics insulin in that it shuttles glucose into the cells in the absence of glucose. This is great for fat burning, but when carb intake is too low the blood glucose can be at dangerously low levels as well. a more experienced user can switch up this ratio a bit. Either way it won't make a huge difference because it's mostly about the total calorie consumption. 

This is what Im proposing to be the optimal DNP diet (for a high dose short cycle(s) and the end of a low dose extended cycle only): 

50% carbs, 35% protein, 15% fat. Its not a misprint; carbs are essential for DNP to work properly. Keep in mind that its only the percentage that changes and not the total calories. From this point it will get a bit complicated, but read over it a few times and you will get the gist of it. Ill also try to keep it as simple as possible.

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## CYCLEON

50% carbs, 35% protein, 15% fat. Its not a misprint; carbs are essential for DNP to work properly. Keep in mind that its only the percentage that changes and not the total calories. From this point it will get a bit complicated, but read over it a few times and you will get the gist of it. Ill also try to keep it as simple as possible. 

When fatty acids are broken down they need to be fed into an energy cycle for a complete break down so that more can be broken down later. The beginning of this cycle is called the citric acid cycle. Fats enter the citric acid cycle as a 2-carbon molecule called acetate and to start off this cycle it needs to bind to another 2-carbon molecule called oxaloacetate. Without enough oxaloacetate this cycle cannot proceed. With little oxaloacetate this cycle is slowed down, thus fat burning is slowed down. Where does oxaloacetate come from? Several sources, but the main one is from pyruvate, the end product of the first step of glucose (carbohydrate) metabolism. Without enough glucose in the blood, fat burning becomes very inefficient. 

This is not to say the more carbs we eat the more pyruvate we can generate, therefore the more fat is burned. We only need adequate levels of pyruvate to supply the citric acid cycle of the necessary starting material for fat to enter, and then it will eventually proceed to be completely oxidized in the electron transport chain. 

Dont worry about eating too many carbs while on DNP because these carbs cannot be stored and are immediately used for fuel to try to replenish cellular ATP. While keeping the calorie level at maintenance level, it would be most beneficial to eat about 55% calories from carbs, 35% protein and 10% fat (mostly unsaturated). It may be optimal for fat burning to raise the carbs a bit more, but the protein should be high enough so that muscle catabolism is kept at a minimum when DNP creates the huge calorie deficit in the body. 

The least effective form of dieting while on a DNP cycle is a fat diet, or ketogenic diet, but the high amounts of fat helps to slow gastric emptying, so you feel more satisfied for a longer period of time. This is one reason why I first recommended the isocaloric diet to beginners who may have trouble controlling their appetite while on DNP. 

SIDE EFFECTS: 

Heat- you will feel very hot while taking this. It is very similar to jogging a slow pace all day long, so be prepared to sweat a little. In some people a lot of sweat is not too uncommon. Body temperature will rise to about 101 degrees and sustain there. This is not too out of the ordinary. This increase in core body temperature causes a vasodilation effect throughout the body to help cool you off. However, evaporative cooling with the aid of vasodilation will not be effective when the surrounding environment does not allow for proper cooling. For example, being out in the summer sun when its 90 degrees and high humidity can cause you to rapidly overheat to dangerous levels. Avoid hot environments at all costs. Stay indoors if you choose to use it in the summer and only go outside briefly when its absolutely necessary. Dehydration can cause the body to not regulate temperature properly and rapidly overheat as well. Drink 1-3 gallons of water daily depending on DNP dose. 

Water retention- this is very closely associated with heat. When the vasodilation occurs due to the rise in body temperature, blood vessels expand, causing an increase in blood volume and subsequent water retention. Also, an increased blood volume leads to decreased pressure, which would lead the body to try to store more sodium and cause even more water retention. All the water retention will subside within a week after stopping the DNP dosage, but often sooner than that. Popular diuretics are not very effective against DNP induced water retention because these diuretics mainly focus on one aspect of diuresis and that is suppression of the anti diuretic hormone (ADH), but the cause of water retention from DNP is independent of ADH. While diuretics will get rid of some naturally stored water, it isnt getting rid of enough water that would make a competitor presentable on stage and would put the user in jeopardy of death or serious health complications due to potassium depletion. 

Lethargy- This is the biggest problem associated with DNP and is somewhat associated with the insomnia that I will cover later. As you have learned DNP depletes the body of ATP and without ATP you have no energy. It literally feels like youre jogging a marathon all day long without a break. Of course the extent of the lethargy will depend on the dose, but it is not uncommon for people to be almost bed ridden. Walking to the kitchen to get food will be a chore. Even eating the food can become very laborious. This will subside within 24-36 hours of stopping the doses. 

Insomnia- sleeping will be very difficult for some people, not because of the familiar central nervous stimulation experienced with ephedrine and caffeine supplementation, but because it gets so damned hot. Many people including myself find it very difficult to sleep when were sweating in our beds. The best way to combat this is to sleep with 2 fans from both sides of the bed and the air conditioner cranked up. Obviously if you have a significant other that you sleep with then it would be wise to sleep in separate beds for parts of the cycle. 

Shortness of breath/ rapid breathing- this is common when the dose is at the upper limits. The breathing will seem like youre jogging even while youre sitting down and doing nothing. It will seem like you can never catch your breath. Doing anything active will make you even more out of breath and this can become dangerous. When breathing becomes irregular, you should avoid doing any aerobic or strenuous activities. This means no working out (not like youll have any energy to do so anyway). 

Dehydration- a very serious side effect. If hydration levels are not adequate it can predispose the body to severe overheating and possibly death. Water needs to be replenished on the order of 1-3 gallons per day. 

Electrolyte depletion- this is caused by excessive water and salt loss through sweating. Drinking water will replace fluids, but not electrolytes. Best way to replenish salts is to drink v8 juice. This can lead to a host of other problems if not remedied including excessive lethargy, low blood pressure, poor cardiac function, nausea, diarrhea 

Nausea- This is a common side effect that afflicts roughly around 30% of the users. There could be several causes to this: dehydration, electrolyte imbalance, low blood pH, and other unknown (by me) mechanisms. 

Diarrhea- possibly due to electrolyte imbalance and undissolved DNP that passes onto the large intestine causing osmotic imbalances. If this becomes too problematic the only thing to do is just to decrease the dosage or stop completely. 

Headache- largely due to dehydration. In most people, forcing down a liter of fluids will alleviate the headaches. 

Dry/ sore throat- I dont know the cause of this one, but it is pretty common among users and seems to manifest itself the most during sleep and may contribute to the insomnia. 

Allergies/ dermatitis- this is relatively rare. Ive been in contact with nearly 500 people who have used DNP and I would estimate about 30-40 of them have experienced allergic reactions to DNP. The allergies manifest themselves first as phantom itches (itching without any rashes or redness) around the torso in some people. It will later develop into rashes and or hives around the body and possibly spread to the face, neck, lips, and scalp area in severe cases. Any over the counter or prescription allergy medication (anti histamine) will cure the allergies. Also if youre allergic to DNP it doesnt mean you cant use it in the future. Allergies to DNP seem to have a tolerance factor. It first gets worse, then better with successive cycles. So if you are allergic, stop immediately and start again 7-10 days later and repeat until you are no longer allergic to DNP anymore. Allergies are also dose and length dependent. 

Yellow vision- This is even more rare than allergies. Ive only known about 15 people who have experienced this out of all the people I have come in contact with who have used DNP in the past. It seems to be most apparent when you look at a white surface and yellow spots will appear on the white that you see. Im not sure what exactly causes this, but it doesnt seem to harm anything and goes away within 1-2 days of stopping the doses.

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## CYCLEON

PREVENTION/ CONTRAINDICATIONS: 

1. Never start your first cycle with an optimal dose. Always play it safe and start low. 

2. Never use DNP if youre going to be in a hot environment for an extended period of time. 

3. Never take any diuretics while on DNP. This includes excessive alcohol. While mild diuretics like alcohol will make you much more uncomfortable and hotter, a harsh diuretic like lasix will kill you when taken with DNP. 

4. If oral temperature rises to 103 then discontinue use until temp is completely down to normal. 

5. Do not attempt to work out very intensely. When its hard to find the energy to go to work, dont push yourself thinking you can get a good workout in. Long cardio sessions can be especially harmful for your health. It would also raise cortisol levels through the roof and will be very catabolic to muscle. Dont sweat the cardio when on DNP because DNP will make you burn fat. Stay away from the treadmill! 

6. If allergies arise take some allergy medication and if that isnt strong enough then stop the doses for at least 10 days before restarting. 

7. Watch your electrolytes. Carry a bottle of v8 juice with you. One 8-ounce serving of v8 has 900mg of potassium compared to 35mg of potassium in 8 ounces of Gatorade. Aim for 3000-5000mg of potassium (not all from v8) per day. Fresh meats and vegetables also have a lot of potassium in them. Sodium is very important too, but is usually not hard to get in the diet. Magnesium can be obtained from supplementation. 

8. Hydration. I cant emphasize this enough. Not only will proper hydration levels make you feel better and prevent overheating, but it will also make the cycle more effective at burning fat. 

SUPPLEMENTATION: 

Antioxidantsone of the most effective will be the fat soluble vitamin E. I recommend 800 to 1000 iu of vitamin E per day of the cycle to combat the host of free radical damage caused by increased fat oxidation. 

Glycerolthis can be important to help maintain muscle hydration and prevent catabolism. It comes in liquid and can be bought over the counter. Take 3-4 tablespoons per day. 

Potassium citrateif blood acidity becomes a problem then potassium citrate can help buffer the acid. About 2-3 grams will be very effective, but 1 gram will do the trick as well. 



CONCLUSION 

DNP is the most effective fat burner and perhaps the most complicated drug in the bodybuilding community and should not be taken to lightly by average dieters striving to lose a couple of pounds. The side effects are serious and numerous, but if used correctly, none of the side effects are permanent. Despite these numerous side effects people still use it because it works when nothing else will. I hope this article sufficiently educated you on DNP. If you choose to use it please do so with caution and use this and other literature as a guide to help you on your way to a new physique. 

Good Luck and Be Safe

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## CYCLEON

more studies from "back when" - helpfully dreged up by John_U over at BSS


ATP-Sensitive Potassium Ion Channels 
Some of the following is speculative. Caveat lector.] 
Ion channels are membrane proteins that control the flux of ions across an otherwise impermeable cell membrane. Potassium (K) channels were first decribed by Noma [1] in 1983, and later in 1991 the ATP-sensitive K channel (KATP) was described by the same researcher [2]. Potassium channels determine cell membrane potential. 

KATP channels exist in most excitable cells. They are regulated by the intracellular level of ATP as well as by various nucleotide diphosphates, pH and lactate concentrations. The activity of KATP channels is inhibited by increasing the intracellular ATP concentration. Closure of these channels in response to glucose metabolism depolarises the cell, stimulating voltage-dependent electrical activity, and calcium ion (Ca) entry. In the pancreatic beta cells, an increase in blood sugar level leads to an elevated ATP/ADP ratio, which in turn inhibits KATP channels, so as to alter the membrane potential and cause insulin release. It is accompanied by increases in respiratory rate, pyridine and flavin nucleotide reduction state, and intracellular pH [3]. 
Thus, the KATP channel couples nutrient metabolism to the membrane potential. 

· Increase in blood glucose --> increase in glucose metabolism --> increase in intracell ATP --> inhibition of KATP channel. 
· Channel CLOSED: cell depolarized, Ca++ uptake, insulin exocytosis. 

KATP channels play an important role in the control of vascular tone [4]. Polarization following potassium channel activation (opening) results in lessened calcium influx and smooth muscle relaxation. 

· KATP channel BLOCKED --> vascular tone increases. 
· KATP channel ACTIVATED --> vascular tone decreases. 

Besides being regulated by intracellular signals, potassium channels may also be regulated by membrane potential. Thus, in excitable cells in the heart, muscle, and nervous system, voltage-gated potassium channels are activated during an action potential; the activities of these potassium channels determine to a large extent the shape of the action potential, hence the strength of the signaling. 

· KATP BLOCKED --> more strength 
· KATP ACTIVATED --> less strength 

Drugs which block KATP channels: tolbutamide, glyburide, glibenclamide. 

Drugs which activate KATP channels: Prostaglandin E2 and I2, adenosine, lemakalim. 

Drugs which activate K channels: pinacidil, cromakalim. 

Mitochondria also contain a K+ channel that causes rapid K+ uptake when open [5]. 

DNP 
What happens when someone takes the decoupler dinitrophenol (DNP)? Blood glucose will result in increased metabolism, but the level of ATP in the cell does not increase! In fact, it is depleted. So in this case, the KATP channel is not inhibited, and it stays open. Calcium is not taken into the cell, and insulin is not released. The person taking DNP has in effect given himself temporary diabetes. 
Insulin is needed to facilitate the uptake of glucose into cardiac, skeletal, and adipose tissue, and to convert glucose to glycogen in the liver. It is anti-proteolytic and protects against the various ailments commonly seen in diabetics, such as vision problems and polyneuropathy. Not coincidentally, the same problems can result from ingesting DNP. 

This is why, when one takes DNP, one also needs to take exogenous insulin. 

Since the KATP channel remains open, vascular and muscular tone relax. Probably blood pressure will decrease. Strength will diminish. 

It would seem that an antidote for DNP might be anything that causes the KATP channel to close, for example the drug glibenclamide. 

References
1. Noma A. 1983. Nature 305: 147. 
2. Noma A, Takano M. 1991. The ATP-sensitive K+ channel. Jpn J Physiol 41(1):77-87. 
3. Civelek VN, Deeney JT, et al. 1996. Temporal sequence of metabolic and ionic events in glucose-stimulated clonal pancreatic-cells. Biochem. J. 315: 1015-1019. Boston University Medical Center. 
4. Nichols, C.G. and Lederer, W.J. 1991. ATP-sensitive potassium channels in the cardiovascular system. American Journal of Physiology 261:H1675-H1686. 
5. Paucek, P, Mironova, G, et al. 1992 "Reconstitution and partial purification of the glibenclamide-sensitive, ATP-dependent K+ channel from rat liver and beef heart mitochondria," J. Biol. Chem. 267, 26062. 
6. Nakamura S. 1989. Glucose reverses DNP induced changes in action potentials. Cardiovascular Res. 23(4):286-294.
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Biological Study of Dinitro Drugs in Humans 
By Dr. Jacques Bell 
Bell, Jacques. 1939. Etude biologique des produits dinitres chez l'homme. Medecine. 19:749-54. 
Translation © 1996 Robert Ames
There is a fundamental difference between biological experimentation with dinitrophenol in humans and what was done in the laboratories of physiologists. These last are essentially interested in hyperthermia (Andre Mayer, Leon Binet, etc.). Yet, in medicine, the doses of dinitrophenol employed do not determine any elevation of temperature. The physiological effects, observed in these conditions, differ considerably from those made by the experimenter. It is thus for example that the animal in hyperthermia presents a polypnoea [rapid, shallow breathing], a hyperglycemia, a hypoglobulinemia that one does not observe with therapeutic doses; it is because experimental hyperthermia is essentially a combustion of carbohydrates, while therapeutic hypermetabolism is mainly a combustion of lipids, as is shown by the lowering of respiratory quotient. 
One shouldn't be surprised at these differences. The clinician uses strychnine as a tonic; the experimenter employs it to cause convulsions. The clinician uses adrenaline, at titrated doses, to produce a manageable hypertension; the physiologist, with massive doses causes acute edema of the lung. 
Yet, to base the clinical use of adrenaline or of strychnine on acute edema of the lung or experimental convulsions, constitutes an obvious error. It is the same for dinitrophenol. 
In France, besides, one uses almost exclusively dinitrophenyl-lysidine, which, according to the same terms of the study made by Professor Pouchet, "is easy to purify by crystallization, to easily modify the first of its components from the point of view of toxicity, dissolves easily in water, and, by addition of the methylglyoxalidine (lysidine) group, favors energetically the elimination of waste." 

After Professor Pouchet, we have, in our thesis [1], demonstrated the superiority of this last product; in what follows, it is by comparison with him that we will study the biology of the dinitro drugs. 
We shall see, in order: 
I. Their action on the basal metabolism,
II. Their visceral action,
III. Their nutritional action.

I. ACTION ON BASAL METABOLISM 
After the experimental research of Magne, Mayer and Plantefol, in animals, the experiments of Cutting and Tainter has confirmed, in humans, that dinitrophenol is a drug which strongly increases the metabolism, exaggerating the oxidation process of the organism by direct action on the cellular metabolism. These authors have observed a rise of close to 20% after one hour, being able to attain 70% in ten hours and a tendency to return to normal at 24 hours if the administration of the medicine is not continued. 
This increase is not due to a sympathetic deregulation. The dinitro treatment respects the autonomic nervous system, in an inverse way from thyroxine, which, at slimming doses, determines rapidly some tremors, insomnia, and a mental instability of the type "basedowien." [a thyroid illness where one secretes too much thyroid hormones] 

In the thyroid illnesses, or the thyroid treatments, there is an inverse connection between the level of the basal metabolism and that of blood cholesterol, this being as much lower as the metabolism is higher. One doesn't observe similar phenomena in the course of dinitro treatment. 

This fact indicates that the changes caused in the blood cholesterol in the course of thyroid treatment are directly linked with the thyroid medication and not at all to do with the elevation of the metabolism which is responsible for the reduction of obesity. Dinitrophenol has almost no action on the blood cholesterol. (Grant and Schube). 

An attentive exploration of the nutritional changes in the course of dinitro treatment, in the cases of five obese women, has shown the following facts: 

1. The administration of dinitrophenol, at a dose of 3.5 mg per kilo, increases the total production of heat by about 40%, from the 3rd or 4th day. 

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. 

II. VISCERAL ACTION 
Dinitro treatment respects the liver, the kidneys, the cardio-vascular system and the blood. 

This innocuity for the principal visceral functions is without doubt one of the main reasons for the distribution of this therapy. 
Tainter, Stockton and Cutting have reported a series of cases in which one had measured the plasma bile index and determined the test of Van de Bergh. Their analyses demonstrate, beyond a doubt, that the liver does not suffer any damage in the course of dinitro treatment. 

Experimental studies on animals do not show toxic effects of dinitrophenol on the kidney (Taitner, Cutting, Wood and Proescher). Anatomical-pathological examinations of animals, even those which died from a massive dose of dinitrophenol, do not reveal any important anatomical changes, except a small degree of cytolysis. Clinical documents are not abundant, but, on the whole, do not seem to demonstrate that dinitrophenol is toxic for the kidneys. 

As T.L. Schulte and M.L. Tainter wrote, "it doesn't seem that dinitrophenol at usual clinical doses is likely to harm the kidneys." 
Dinitrophenol is remarkable for its absence of effect on the cardio-vascular system. Even when the basal metabolism is found elevated to significant levels, there is no change in the rhythm of the pulse (Rosenblum). 

On this point, dinitrophenol differs from all the other metabolic accelerants known. It is an observation that all the clinicians, today, have had occasion to make. 

All the clinicians know that, contrary to thyroxine, dinitrophenol is absolutely devoid of toxicity for the heart. 

The research of Professor Loeper and of his students has demonstrated the physiological and clinical importance of myocardiac glycogen. Extensive studies by P.N. Taussig have shown that dinitrophenol does not reduce cardiac glycogen at all and that, on this point, it differs completely from thyroxine. 

III. ACTION ON NUTRITION 
The influence of dinitro therapy on nutrition has been the object of a very important clinical study. 

"One does not observe variations in the elimination of chlorine; eliminated phosphorus varies sometimes more, sometimes less, the elimination of sulphur increases slightly, especially in the form of sulphur conjugates, urines show a small increase of total nitrogen and of urea." (Prof. Pouchet). 

It is a well known fact that the administration of thyroid extract or hyperthyroidism is accompanied by an increased secretion of calcium and of phosphorus. This calcium and phosphorus in the urine are not due to the acceleration of metabolism, as one does not observe these facts either during fever, nor in the course of leukemias which raise the metabolism (J.C. Aub, N.B. Bauer, C.I. Heath, Alright, Bauer and Aub). 

Thyroxine reduces bone density. 
With dinitrophenol, nothing of the sort is observed. The experiments of Clarence L. Robbins show that dinitrophenol, in spite of the elevation of the metabolism that it produces, does not cause any increase of the loss of calcium or of phosphorus. An increase of 37% in the basal metabolism, caused by the ingestion of dinitrophenol, does not lead to modification in the excretion of these elements. 

In normal individuals, when one administers dinitrophenol during a short period, it produces a small elevation of reduced substances in the blood after fasting (although one would not be able to call this hyperglycemia). When one administers the medication over a longer period, this phenomenon is not produced and there is a marked elevation of the tolerance to carbohydrates. 

In diabetics, following treatments of short duration, the results are variable, the tolerance to glucose being as often increased as it is decreased, with parallel changes in the fasting blood sugar level. But, in prolonging the administration of the medication, one observes an increase of the tolerance of carbohydrates. Anyway, in basing himself on the study of 32 cases of diabetes, Simkins concludes that dinitrophenol is not toxic for diabetics. He remarks that this observation goes counter to some assertions that have been a little prematurely advanced. 

Dinitrophenyl-lysidine at therapeutic doses therefore has an action on the organism which is completely physiological. This action has been demonstrated in obesity where it has been compared to the actions of thyroid medication and physical exercise. 

The existence of obesities of glandular origin, especially by thyroid insufficiency, has resulted in the use of thyroxine in numerous subjects. 

"This wasn't without inconveniences, sometimes grave, characterized especially by cardiac and nervous troubles; the effective dose of thyroxine is, in fact, very close to the toxic dose. Further, we has frequently seen these accidents persisting after the administration even of a single dose, which leads to the impossibility of stopping them immediately by a simple suspension of the medication. Yet, from the point of view of its specific action on the basal metabolism, dinitrophenol offers this precious advantage that the cessation of its use at the slightest appearance of signs indicating an imminence of intoxication results immediately in the arrest of those symptoms." (Professor Pouchet). 

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. 
As for physical exercise, it seems to act exactly like dinitro therapy. Marcowitz, in his communication to the Academy of Medicine of Toronto on October 9, 1934, based on 90 cases of obesity, having followed this treatment during a period of 16 months, concludes that its action may be succinctly described in saying that the effects on the organism are similar to those of physical exercises. 

The fact is besides established by physiologists, since dinitrophenol raises thermogenesis and not the metabolic quotient. 

All the clinicians know actually that dinitro medication is irreplaceable in cases of monstrous obesities which prevent all exercise. It can be used in the obese for whom occupations, life style or cardiac troubles do not permit physical exercises. It is indispensible for the grossly obese in cases of abdominal operations and immobilization due to illness (inflammation of fallopian tubes, appendicitis, etc.) for which there is an urgency to obtain a reduction of subcutaneous fat. 

But this clinical use has not been able to be extended other than when the experimental research pursued on humans, with a dinitro drug free from impurities, has been able to demonstrate the biological effects of it in a very precise way. 

1. La Therapeutique dinitree (J.-B. Bailliere et Fils, editeurs, 1937). 

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Concerning Two Cases of Cataract Caused by Dinitrophenol
By Jean Sedan (Marseille)
Sedan, Jean. 1939. A propos de deux cas de cataracte par phenols dinitres. Annales d'Oculistes. 176:191. 
Translation © 1996 Robert Ames

The implementation of the treatment for obesity by dinitrophenol dates only from 1933, the year when it was suddenly and rapidly put in the limelight by the work of the Americans Tainter, Mehrtens and Cutting. 

These authors have established that the ingestion of dinitrophenol accelerates metabolism, causing a marked elevation in temperature. It seemed that dinitrophenol was a specially effective treatment for obesity. In 1936, Horner estimated that in the first 15 months following the appearance of the medication in the market, one hundred thousand persons used it to lose weight. 

Incidents and accidents multiplied and appeared sufficiently serious that the American Medical Association warned the public against the dangers of unsupervised treatment. 

Here we discuss only the case of cataracts, which Horner had said that it occurs in one case in 1000 treatments. At the end of this report we will note the principle bibliographic references concerning the American literature devoted to the subject and which is of a great value, but we wish to emphasize how the European work and especially French are on the other hand still rare and even exceptional. 

One can say that it is by the work of Onfray and Gilbert Dreyfus presented to the Congress of the S.F.O. [Societe Francaise des Oculistes?] in 1937 that French opthamologists had their attention drawn to the subject. This remarkably precise work is enriched by two observations of which one is due to Doctor A. Gallois, of Besancon. We frequently reference this, for it contains in addition to minutely observed details, important physio-pathogenic considerations and a complete history of the subject. 
Apart from this work, we should also to point out the observations of Van de Hoeve and Polak-Daniels published in Holland in 1936, as well as the French summaries and reviews of Halbron on cataracts and of Laignel-Lavastine on dinitrophenol intoxication. 

Finally, we emphasize the interest of the work of Vogt on the cataracts caused by dinitrophenol in Switzerland and of G. Ciotola of those caused by alphadinitrophenol in Italy, both published in 1937. The same year, Stein and Crevecoeur pointed out that in their opinion this affectation was, when all is said and done, quite rare if one thinks of the enormous dissemination of dinitro treatment. This was also the opinion of Andre Mayer, based on the fact that despite the considerable number of intoxications by dintrophenol observed in munitions factories, no cases of cataracts have been noted. 

Finally, in 1938, Carlotti and Rivoire de Nice presented a case of cataract by dintrophenyl-lysidine which developed "with almost lightning-like rapidity." 
* * *
It was possible for us to observe two very demonstrative cases. In one there was an arrest of development of opacity after the patient stopped taking dinitrophenol, which is more than a rarity, a real exception in the pathological history of dinitrophenol cataracts. 

OBSERVATION I. -- Mme. K... Lea, 32 years old presented herself to me in December 1937 with a marked lowering of the vision of both eyes, which began a few weeks earlier, developing extremely fast and was all the more disturbing since she works at a very visual profession in the editing of a newspaper and as she is especially partial to this pleasant and remunerative position. I noticed a beginning of bilateral cataract appearing striated and fleecy which is found almost constantly in the description of toxic lens opacities of this kind. The opacity is situated mainly at the level of the equator of the lens, but also involves the posterior part of the central mass. The vision is only 4/10 in the right and 5/10 in the left, these two acuities correctable to 7/10 O.D.G. -- 2.50. 

Mme K... thus learned that she was rapidly becoming myopic. 
The most minute research were done in view of identifying a possible cause of this bilateral cataract. All the blood and urine tests were negative. Very complete clinical examinations by Doctor P..., referring physician, point to the same conclusion that it is impossible to relieve Mmme. K...'s pathological process at all. 
It is then that I thought of asking her about the possibility of a dinitrophenol anti-obesity treatment, even though the corpulence of my client did not seem excessive. She told me then of having taken two pills each day of 0.30 grams of dinitrophenol in series of ten days with a rest of 15 days, for the past year and a half. 
She had, without the least dietary restriction, lost 19 kilograms out of 87 [42 pounds out of 191]. It was at that point that she began complaining about her vision. 

I wasn't aware of the topic at that time except by the short summaries of American works, but I didn't hesitate to warn her against what I considered to be the real origin of her sickness. 
Very anxious about her state, she was easily convinced and stopped that therapy suddenly and definitively. 

I had the opportunity to see her in March, July and October 1938 and I noticed with great interest the complete arrest in the development of these catacts, which accompanied in very precise fashion the progressive and total disappearance of myopia to the extent that although it was possible to note an appreciable modification in the lens opacities, the visual acuity was spontaneously returned to 7/10 (uncorrected) at the end of October 1938. 

We add that Mme. K..., doubly happy, very far from regaining weight in spite of the renunciation of dinitrophenol, had lost another 5 kilos by a very strict nutritional discipline complemented with rigorous gymnastic practices and the introduction into her life of a new intoxification, certainly less dangerous than the preceeding -- tea. 

In this case, the role played by the toxin in the opacification of the lens seems to us demonstrated in an almost experimental fashion by the disappearance of the myopia at the moment of the cessation of the intoxification and even more by the incontestable and enduring stabilization of the state of opacities that maintained itself for six months. In contrast, the development was very sudden in a month before the application of this measure. It is presumed that only the precocity of the requested medical consultation and of the medical diagnostic given, has permitted a stop in the development of this toxic cataract -- a completely unusual phenomenon. 

We emphasize that the treatment had included plainly excessive doses and that however the opacification only appeared late in the treatment. On this topic remember that in the discussion which followed the expose made to the S.F.O. in 1937 by MM. Onfray and Gilbert Dreyfus-Arruga, who had occasion to observe and operate in America [illegible] ... don't generally appear except at the end of many months and even sometimes six to twelve months after the cessation of treatment. These late-developing cataracts are almost always bilateral. 

OBSERVATION II. 
[Not included. Summary: A 32 year old woman weighing 90 kg. (198 pounds) began taking dinitrophenol on February 1st, 1937. She began with 9 to 10 pills daily, each being 30 mg. of DNP. After a week she increased the dose to 12 pills / day (360 mg.). At this dosage she lost 800 grams per week, or 10 kg. (22 pounds) in three months, without changing her diet. She stopped taking DNP for four months and then began again. So she took 32.4 grams of DNP in the first 90 days and the same amount in the second course. American reports indicated that cataracts had resulted from doses as small as 100 mg. per day for a total of 40 grams. 

On June 10th 1938, after several days in a very sunny seaside resort, the patient began to lose vision in her left eye, and on July 12th, the other eye was affected. By August 1st she was unable to see to drive. By September she was blind. 
Fortunately, surgery produced favorable results.] 

It is necessary, indeed, to publicize cases in order to attract the attention of physicians and of the French public to the danger of intoxification by dinitrophenol. The fact that we have been able to stabilize, if not make regress one cataract of this class by stopping all toxic ingestion is but another reason which compels us to make it known. 

These arguments and our observations are so needed to challenge the imagination and influence young women against harmful weight loss techniques that the work appears discouraging. 

Indeed, in ending, we repeat the unlikely remark that our second patient made to us upon taking leave following the success of her first operation: "And now, Doctor, do not oppose my taking of dinitrophenol since I no longer risk having cataracts." 
References

· ALLEN and BENSON. -- Late development of cataracts following use of dinitrophenol about a year before. JAMA, 1935, V, 105, p. 795. 
· BARKAN, BORLEY, FINE and BETTMAN. -- Operative results in cataracts coincident with dinitrophenol therapy. Cal W. Med. 1936, XXXXIV, p. 360. 
· BENCE, JONES. -- On the rate of passage of crystalloids into and out of the vascular and non-vascular textures of the body. Pr. R. Soc., 1863, London, 14, 400. 
· BOARDMAN. -- Rapidly developing cataracts after dinitrophenol. JAMA, 1935, CV, p. 108. 
· CAMERON, cited by HORNER. -- Arch. of opth. 1936, XVI, p. 452. 
· CARLOTTI and RIVOIRE. -- Sur un cas de cataracte per le Dinitrophenyllyside. Rev. O.N.O., Nov. 1938, p. 622-624. 
· CAZENEUVE and LEPINE. -- Sur les effets produits par l'ingestion et l'injection intraveineuse de trois colorants jaunes derives de la houille. C.R. Ac. Sc. de Paris, 1885, CI, p. 1, 167. 
· CIOTOLA (G.). -- Cataracte par alpha-dinitrophenol. Boll. d'Oc., 16, 1937, p. 531. 
· COGAN D. and COGAN F. -- Dinitrophenol cataract. JAMA, 1935, CV, p. 794. 
· CUTTING, MEHRTENS, TAINTER. -- Dinitrophenol, not acceptable for N.N.R. JAMA. 1935, CV, p. 31. (Important bibliography on the subject). 
· DALLY. -- Du nouveau sur le dinitrophenol. Concours Med. 1935, L, p. 3, 491. 
· EBSTEIN and ROSENBLUM. -- Peripheral neuritis and abortion following dinitrophenol therapy. J. Lab. an Clin. Med. 1935, XX, p. 1, 118. 
· GIBBS-Reichert. -- Am. Chem. J., 1891, XIII, p. 289. 
· GUTZEIT (R.). -- Cure d'obesite et cataracte. Munch. med. Wschr., 2, 1937, p. I.724. 
· HALBRON. -- Les cataractes apres emploi therapeutique du dinitrophenol. Sem. des Hopitaux de Paris, XII, 1937, p. 329. 
· HORNER, JONES, BOARDMAN. -- Cataracts following the use of dinitro. JAMA, 1935, CV, p. 108. 
· HORNER. -- Cataracts after dinitrophenol. Ar. of Opth. 1936, XVI, p. 446-461. 
· HORNER (W.-D.). -- Cataracts following dinitrophenol treatment for obesity. Transact. of the opth. sect. of the Amer. Med. Ass., 1936. 
· KNISKERN. -- Cataract following dinitrophenol. JAMA, 1935, CV, p. 794. 
· KOCH-LEE and TAINTER. -- Dinitrophenol on liver function. Calif. and W. Med., 1935, XXXXIII, p. 337. 
· LAIGNEL-LAVASTINE. -- Soc. Med. des Hopit. de Paris, 1937. 
· LAZAR. -- Cataract following dinitrophenol. JAMA, 1935, CV, p. 794. 
· LEUTSKER. -- Instance of circulatory collapse attributed to dinitrophenol. U.S. Nav. Med. Bull., 1935, XXXIII, p. 394. 
· MAC BRYDE-TAUSIG. -- Functional changes in liver, heart and muscles loss of dextrose tolerance resulting from dinitrophenol. JAMA, 1935, CV, p. 13. 
· MAGNE, MAYER, PLANTEFOL, et al. -- Etude sur l'action du dinitrophenol. An. de Physiol., 1932, CV, p. 12. 
· NADLER. -- Peripheral neuritis caused by prolonged use of dinitrophenol. JAMA, 1935, p. 12. 
· ONFRAY and GILBERT DREYFUS. -- Bull. et Memoires S.F.O., 1937, (I, pp. 114-12. 
· ONETO-GALINO-NATALE. -- Developpement de cataracte aux deux yeux, consequence d'un traitment au dinitrophenol pour amaigrissement. Soc. Argentin. of., 24 Oct. 1937. 
· PERKINS. -- A study of munitions intoxication in France. Pub. Health Rep., 1919, XXXIV, p. 2, 335. 
· RODIN. -- Cataracts following the use of dinitrophenol. Calif. West Med. 44.4, 1936, p. 3. 
· SCHUTES. -- Dinitrophenol. Am. J. Opth., 1935, 18, p. 752. 
· SPAETH (E.-B.). -- Cataractes dues au dinitrophenol avec symptomes de tetanie. Am. J. Opth., Apr. 1936, p. 320-323. 
· STEIN and CREVECOEUR. -- Semaine des Hopitaux de Paris, 15 Dec. 1937. 
· TAINTER, CUTTING and STOCKTON. -- Use of dinitrophenol in nutritional disorders. Am. J. Pub. Health., 1934, XXIV, p. 1045. 
· VAN DER HOEVE and POLAK-DANIELS. -- Cataracte et dinitrophenol. Nederl. Tijdsch. V. Genessk., I, 1936, no. 2, p. 126. 
· VOGT (A.). -- La Cataracte par dinitrophenol en Suisse. Schweiz. Med. Wocst., 76-37, 11 Sep. 1937, p. 873. 
· WHALMAN. -- Dinitrophenol cataract. Am. J. O., Oct. 1936, XIX, p. 885.

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## J-Dogg

WoW thats the most I read in a long time.

Thanks for the great info, I enjoyed it.

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## Dr.Evil

can i edit a part on the electrolyte depletion?

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## 03733+$

WOW THANKS FOR THE N-FO GREAT POST!!

______________________________________

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## demetri

Anyone out there know how to make DNP ? I've heard that it's not that hard to make just a little dangerous.

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## solid90062

Why try to make it when it can be bought cheaply? And I would think consumption of THIS product by a novice chemist would be very dangerous.

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## demetri

I have a couple more dumb questions. Since DNP interferes with ATP it will cause a drop in strengh while you are on it right. Does it also affect the muscle cell volume and the overall look and feel of the muscle?

I'm looking for a good fat burner as I don't have much success with Clen or EFC stack (years of hard coffee drinking might have something to do with that), but I don't want to sacrifice much muscle.

I've read some info on making caps, but since DNP ship moist would there be any problems disolving into a liquid and drinking it? This would make it easier to spread it out over the day. I'm concerned about taking too much at once as I'm not the average 100 kg bodybuiler and just a little squirt.

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## Andy13

> _Originally posted by demetri_ 
> *Anyone out there know how to make DNP? I've heard that it's not that hard to make just a little dangerous.*



lol...

2,4 dinitro-chloro-benzene can be made into DNP by heating with NaOH solution...

the chloro compound used to be dirt cheap to get since it didn't cost an arm and a leg to send...
Now (apparently) things have changed..

Andy

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## VaDeR_1138

I have a question can you take clen & T-3 with DNP or is the DNP enough? and if so how would you stack\cycle the three and should you ad an ECA stack on the off weeks of clen? thank you in advance for your advise. VaDeR_1138

P.S. great post CYC very informative!

P.P.S. I am 22 years old 5'8" 235lbs (fat) trying to lose a lot of unwanted fat. Any advise would be greatly appreciated

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## VaDeR_1138

[QUOTE]_Originally posted by CYCLEON_ 
[B]more studies from "back when" - helpfully dreged up by John_U over at BSS


ATP-Sensitive Potassium Ion Channels 
Some of the following is speculative. Caveat lector.] 
Ion channels are membrane proteins that control the flux of ions across an otherwise impermeable cell membrane. Potassium (K) channels were first decribed by Noma [1] in 1983, and later in 1991 the ATP-sensitive K channel (KATP) was described by the same researcher [2]. Potassium channels determine cell membrane potential. 

What is the longest one can stay on DNP ? 

Awesome post by the way very informative.

VaDeR_1138

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## armwrestler22

great post, maybe should be a sticky

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## Ambulance

Dr Evil, why edit...is there something cycleon and you need to debate about? Let us know your outlook on the electrolites bro

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## Cycleon

actually he did edit it to reflect the thinking that was intended

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## LightWeightBaby

Very good article, explains DNP very well.

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## wannaberipped23

Couple questions on making the DNP - will it combust after drying it out? Whats the purpose of mixing it with corn starch? Why do you "pound" it into a fine powder - i thought it was already so fine that it could be dispersed into the air real easily??? 

Just wondering, and making sure I dont Screw with this stuff,.... or else i know all the consequenses

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## powerlifter

Cycleon - excellent source of hard to find info - lots of misinformation out there

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## iNvid

very good read

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## hatchblack

good read....wants to make me consider DNP vs. Clen ...?

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## iNvid

> good read....wants to make me consider DNP vs. Clen...?


Totally different things. Its like comparing corvette vs a civic heh.

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## NCWrestler

Can anyone verify that the 2,4-dinitrophenol being sold at the chemical supplier www.sciencelab.com is the same exact 2,4-dinitrophenol used in the pills?

So, I could purchase this material, weigh it out for pills or a drink and take it straight from the package?

I hear about people processing TNT and other chemicals to make DNP ... in the sizes they offer, the prices seem better to just buy it in bulk straight from a chemical supplier like sciencelab.com

Any advice?

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## Alexander the Graet

thanks for the info!

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## goldenFloyd

i am very interested in the long-term effects. The studies you cite seem to indicate a low level of toxicity for the kidneys, liver, and cardio-vascular system... indicating there is no increase in pulse levels which is unique among metabolic accelerators. I am worried about this information because it was studied in 1939 (referring to Bell, Jacques. 1939. Etude biologique des produits dinitres chez l'homme. Medecine. 19:749-54.)... do you think this still holds true and are there more current studies on this? I understand that back then it was actually administered as a fat loss agent, which would prompt more clinical studies of DNP for this purpose, but are there more current ones that might analyze more the effects of DNP on cancer and the cardio-vascular system?

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## fejaouk

[QUOTE=CYCLEON]Water retention- this is very closely associated with heat. When the vasodilatation occurs due to the rise in body temperature, *blood vessels expand, causing an increase in blood volume and subsequent water retention.* Also, an increased blood volume leads to decreased pressure, which would lead the body to try to store more sodium and cause even more water retention. All the water retention will subside within a week after stopping the DNP dosage, but often sooner than that. Popular diuretics are not very effective against DNP induced water retention because these diuretics mainly focus on one aspect of diuresis and that is suppression of the anti diuretic hormone (ADH), but the cause of water retention from DNP is independent of ADH. While diuretics will get rid of some naturally stored water, it isnt getting rid of enough water that would make a competitor presentable on stage and would put the user in jeopardy of death or serious health complications due to potassium depletion. [QUOTE]

I dont know if this is a mistype, but its not correct. Vasodilatation will cause a drop in blood pressure (CO = L x M, BP = CO x Systemic Vascular Resistance-SVR), but not a drop in blood volume. Blood volume is only affected by other factors like hypovolaemic shock or in the case of DNP the movement of fluids. As far as I can understand about DNP, the increase in core body temperature will cause vasodilatation, excess sweating and fluid shifts within the body. Also due to the excess sweating caused by DNP this will cause loss of fluids from the interstitial and circulatory system. This drop in circulating volume (due to movement of fluid out of the circulatory system and not vasodilation) and cardiac output and loss of vascular tone, is recognised by the baroreceptors in the atrium, vena cava and the carotid sinus and also by the medulla oblongata. The cells of the Juxta glomerular apparatus stimulate the release of Renin that splits Angiotensinogen into Angiotensin (I), it is then converted into Angiotensin (II) under the influence of A.C.E (angiotensinogen converting enzyme). Angiotensin (II) causes the secretion of Aldosterone from the adrenal gland allowing Na (sodium) and water to be retained to increase circulating volume, which will be exhibited by decreased urine output. The retention of sodium is important as water will always follow sodium. Sodium performs three vital body functions. 

	Regulation of osmolarity
	Influences cell permeability
	Helps regulate acid base balance

In response to stimulation of osmoreceptors and baroreceptors A.D.H is released by the posterior pituitary gland, this allows more water to be retained by increasing the permeability of the distal tubules of the kidney, without A.D.H the kidney tubules are almost impermeable to water and thus the action of Aldosterone would be fruitless without it. A bit of a long winded answer, however I hope it helps.

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## xith

Have any of you actually taken DNP ? I finally have some and i've been reading about it, and it sounds a little scary. There are tons of things you can do to protect yourself, but I want to hear some stories about people who've actually done it and what they went through. Also, there was nothing said about if its addictive or not..

Thanks for any replies.

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## Aboot

> Have any of you actually taken DNP ? I finally have some and i've been reading about it, and it sounds a little scary. There are tons of things you can do to protect yourself, but I want to hear some stories about people who've actually done it and what they went through. Also, there was nothing said about if its addictive or not..
> 
> Thanks for any replies.


There's several DNP journals on here, just do a search. Here's one:

http://forums.steroid.com/showthread...&highlight=DNP

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## sonnydjoe

I'm just wondering .......

Lets say I found a chemsupply co. overseas who is willing to ship/sell!!!

Would I have anything to worry about when it came time for it to come into port...... such as Customs/feds/dea ect. ?????

because I'm under the impression that as long as its not in Cap's it's perfectly OK.....

Please shed some light for a newbie

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## devil1

another great dnp thread!!

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## arigby

Sorry i am new to this website and for some reason i ended up here.I am actuely looking for some advise on bulking up on muscle ive been working out for a year and have been out of action for 3 months due to a facture i want to gain muscle what should i take,how long do i take them.Im new to all this your help would be much appreciated.

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## magic32

> I have a couple more dumb questions. Since DNP interferes with ATP it will cause a drop in strengh while you are on it right. 
> OF COURSE!
> *YOU'LL BE TOO TIRED TO LIFT MUCH OF ANYTHING, SO BE SURE TO USE A CNS STIM.*
> 
> Does it also affect the muscle cell volume and the overall look and feel of the muscle?
> *NO.*
> 
> I'm looking for a good fat burner as I don't have much success with Clen or EFC stack (years of hard coffee drinking might have something to do with that).
> *THAT'S A GOOD ASSESSMENT.
> ...


---------------




> *VaDeR_1138 -*
> What is the longest one can stay on DNP?


This is largely contingent upon your protocol, but still amounts to the time it takes for you to effectively reach the stage of severe poisoning, after which even the staunchest user will necessarily succumb.

-----------------

*This stuff is bad news fellas, ask/pm any DNP experienced guy and he'll tell you the same:
Goose
Gear
Nark
Marcus
etc.*

*It's a lot of info, but it's still info on a poison!*

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## naturalsux

thanks for bumping this magic32.

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## 2475

Like

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## shroom911

*Second warning, next time you will be banned.*

http://forums.steroid.com/showthread.php?t=355865

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## nah man

one of the best write ups ive seen.

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## killagorilla187

I heard of many users not eating many carbs and still dropping alot of Lbs on this.

You need that many carbs to burn fat on dnp ?

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## Housemoney

> i heard of many users not eating many carbs and still dropping alot of lbs on this.
> 
> You need that many carbs to burn fat on dnp?


bump...

I'm taking dnp and cant find a consensus...

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## Iron_Pig

the feds and dea will do nothing customs can and will take it they catch it.





> I'm just wondering .......
> 
> Lets say I found a chemsupply co. overseas who is willing to ship/sell!!!
> 
> Would I have anything to worry about when it came time for it to come into port...... such as Customs/feds/dea ect. ?????
> 
> because I'm under the impression that as long as its not in Cap's it's perfectly OK.....
> 
> Please shed some light for a newbie

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## Krztoff2202

Good read

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## elcrisp76

> Anyone out there know how to make DNP? I've heard that it's not that hard to make just a little dangerous.


Making it would be a little difficult for anyone without a fully equipped lab at their disposal.. 

But why would you make it.. It's cheap as chips! i just got a FREE 50 gram sample from a Chinese company which I capped myself.. I had to pay for postage, and have permanently stained yellow hands, but at least i know exactly the dosage I'm putting into my body.. That equates to 250 x 200mg caps... for the price of a capping kit and postage (only 50 grams of postage at that)

Oh did i mention it was free? I actually found one site that was charging $150 for 15 caps whilst looking for the stuff!! 

It's a shame that people can be so stupid with this type of a compound that they need to ban it.. As long as that is the case, there will always be dodgy operators who will charge as MUCH as they can get away with, often for underdosed products. Find a source and cap it yourself, but make sure to research the hell out of the stuff first - you don't want to be the next casualty!

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## kaigab

I think the safest way is to buy the powder (it's not difficult to find a source), have it tested by a lab and then prepare your own pills.

Maybe i am too cautious, but i don't feel calm to eat pills of this stuff made by somenone else..if for any reason the dose is wrong you risk death.

Otherwise just stick with T3/Clen .

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## big_k

I almost ordered DNP Salt (1,2 Dinitrophenol Sodium) I don't know if it would of been detrimental...but I didn't want to find out!


Besides that, I'm having a hard time finding concrete laws for it with regards to importing. Because I really need this potent fertilizer for my melon farm.  :Wink/Grin:

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## Jeet Kune Do

> I almost ordered DNP Salt (1,2 Dinitrophenol Sodium) I don't know if it would of been detrimental...but I didn't want to find out!
> 
> 
> Besides that, I'm having a hard time finding concrete laws for it with regards to importing. Because I really need this potent fertilizer for my melon farm.


Its legal as a dye for clothing and such. Not for human consumption. Its fine as a testing chem for animals as well. So its not hard to find. But if a cop see's you taking them, asks what it is, you tell him DNP, he knows what it is, gets a blood test and arrests you, you may get a slap on the wrists for consuming a toxic chemical/attempting suicide. Lol.

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## craftsmen998

> Making it would be a little difficult for anyone without a fully equipped lab at their disposal.. 
> 
> But why would you make it.. It's cheap as chips! i just got a FREE 50 gram sample from a Chinese company which I capped myself.. I had to pay for postage, and have permanently stained yellow hands, but at least i know exactly the dosage I'm putting into my body.. That equates to 250 x 200mg caps... for the price of a capping kit and postage (only 50 grams of postage at that)
> 
> Oh did i mention it was free? I actually found one site that was charging $150 for 15 caps whilst looking for the stuff!! 
> 
> It's a shame that people can be so stupid with this type of a compound that they need to ban it.. As long as that is the case, there will always be dodgy operators who will charge as MUCH as they can get away with, often for underdosed products. Find a source and cap it yourself, but make sure to research the hell out of the stuff first - you don't want to be the next casualty!


I agree with everything said. capping it yourself allows you to a) control how much cap and 2) you can add some stuff to it. 

The first time I capped I used cornstarch with "0" caps. it was almost a 2:1 ratio starch to DNP for 200mg. Then I added taurine to the second batch. not enough for the day, but it made me feel like i was making it a bit better. 

do your research and be smart.

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