Think DNP Can Be Used Safely? Think Again

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Master
10+ Year Member
It's the time of year when bodybuilders start looking for ways to shed body fat and the interest for many invariably turns to DNP. There are articles on the internet that suggest DNP can be used safely if you're smart about it. Nothing could be further from the truth. DNP is a poison that has lead to cataracts, renal failure and deaths due to hyperthermia. It has an extremely narrow therapeutic index, i.e. the dose of DNP required to induce weight loss is very close to its lethal dose. In addition, its effects are unpredictable. A dose that was well tolerated in a previous cycle might not be tolerated on the next. As the use of DNP continues to gain in popularity, the death rate will continue to climb. There is no safe dose of DNP.

The first two studies below note the dosage of DNP in which deaths have occurred. These dosages are the same dosages currently being advertised as safe and the ones most often used by bodybuilders.
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According to the U.S. Department of Health and Human Services, deaths have occurred in people who ingested 3--46 mg of dinitrophenols per kg of body weight per day (3-46 mg/kg/day) for short periods or 1--4 mg/kg/day for long periods.

Reports of DNP poisoning related to weight loss appear to be becoming more common. McFee et al. (13) reported the death of a 22-year-old male 16 h after his last DNP dose, estimated at 600 mg/day over four days for weight loss.



Journal of Analytical Toxicology, Vol. 30, April 2006

Case Report
Two Deaths Attributed to the Use of 2,4-Dinitrophenol
Estuardo J. Miranda 1, lain M. Mclntyre 2, Dawn R. Parker 2, Ray D. Gary 2, and Barry K. Logan TM


We report the cases of two individuals, one in Tacoma, WA, and
the second in San Diego, CA, whose deaths were attributed to
ingestion of 2,4-dinitrophenol (2,4-DNP). 2,4-DNP has historically
been used as a herbicide and fungicide. By uncoupling
mitochondrial oxidative phosphorylation, the drug causes a
marked increase in fat metabolism that has led to its use to aid
weight loss. Both cases reported here involved its use for this
purpose. Features common to both cases included markedly
elevated body temperature, rapid pulse and respiration, yellow
coloring of the viscera at autopsy, history of use of weight loss or
body building supplements, and presence of a yellow powder at
the decedent's residence. Because of its acidic nature, the drug is
not detected in the basic drug fraction of most analytical protocols,
but it is recovered in the acid/neutral fraction of biological extracts
and can be measured by high-performance liquid chromatography
or gas chromatography-mass spectrometry. The concentration
of 2,4-DNP in the admission blood samples of the two deaths
reported here were 36.1 and 28 rag/L, respectively. Death in both
cases was attributed to 2,4-DNP toxicity. Review of information
available on the internet suggests that, although banned,
2,4-DNP is still illicitly promoted for weight loss.
Introduction


[In the paper below, McFee et al. reported the death of a 22-year-old male 16 h after his last DNP dose, estimated at 600 mg/day over four days.]

Vet Hum Toxicol. 2004 Oct;46(5):251-4.
Dying to be thin: a dinitrophenol related fatality.
McFee RB1, Caraccio TR, McGuigan MA, Reynolds SA, Bellanger P.

Abstract
2, 4-dinitrophenol (DNP) was originally used as an explosive and later introduced in the 1930's to stimulate metabolism and promote weight loss. It's also a component of pesticides still available globally. Concerns about hyperpyrexia lead to DNP being banned as a dietary aid in 1938. A 22-y-old male presented to the Emergency Department (ED) with a change in mental status 16 h after his last dose of DNP. On admission he was diaphoretic and febrile with an oral temperature of 102 F, but lucid and cooperative. He became agitated and delirious. Intravenous midazolam was initiated with mechanical cooling. Pancuronium was administered later and the patient was intubated. Over the next hour the patient became bradycardic, then asystolic, and despite resuscitative efforts, died. Advertisements claim DNP safe at the dose our patient ingested. It is widely available and with the potential to cause severe toxicity is an understudied public health concern.



Regulatory Toxicology and Pharmacology 48 (2007) 115–1
Dinitrophenol and obesity: An early twentieth-century regulatory dilemma
Eric Colman

Abstract

In the early 1930s, the industrial chemical dinitrophenol found widespread favor as a weight-loss drug, due principally to the work of Maurice Tainter, a clinical pharmacologist from Stanford University. Unfortunately the compound’s therapeutic index was razor thin and it was not until thousands of people suffered irreversible harm that mainstream physicians realized that dinitrophenol’s risks outweighed its benefits and abandoned its use. Yet, it took passage of the Food, Drug, and Cosmetic Act in 1938 before federal regulators had the ability to stop patent medicine men from selling dinitrophenol to Americans lured by the promise of a drug that would safely melt one’s fat away.


Cyril MacBryde, a physiologist from Washington University School of Medicine, reported ‘‘alarming functional changes’’ indicative of liver, heart, and muscle toxicity in his obese patients treated with small doses of dinitrophenol (MacBryde and Taussig, 1935).

But some physicians continued to believe that the drug was a reasonable therapeutic option for obese patients recalcitrant to dietary intervention when used in the properdose and under the care of a knowledgeable physician. Even this position, however, became untenable when young women taking therapeutic doses of dinitrophenol under the supervision of physicians started going blind (Horner et al., 1935). If the estimate of one San Francisco ophthalmologist is accurate, during a two and a half year span, as many as 2500 Americans may have lost their sight due to what became known as ‘‘dinitrophenol cataracts’’ (Horner, 1936).



Australas J Dermatol. 2014 Nov 4. doi: 10.1111/ajd.12237. [Epub ahead of print]
Cutaneous drug toxicity from 2,4-dinitrophenol (DNP): Case report and histological description.
Le P1, Wood B, Kumarasinghe SP.

Abstract
The use of 2,4-dinitrophenol (DNP) has regained popularity as a weight loss aid in the last two decades due to increased marketing to bodybuilders and the increasing availability of this banned substance via the Internet. 2,4-DNP is a drug of narrow therapeutic index and toxicity results in hyperthermia, diaphoresis, tachycardia, tachypnoea and possible cardiac arrest and death. Skin toxicity from 2,4-DNP has not been reported since the 1930s. We report a case of a 21-year-old bodybuilding enthusiast who presented with a toxic exanthem after taking 2,4-DNP, and describe the first skin biopsy findings in a case of 2,4-DNP toxicity.
 
CBS is deflecting, he doesn't even want to answer what he considers "safe" to mean..

The tone may have calmed down for a bit. I'll give him some time to do so since we don't all work on the same clock
What you've listed seems are harm reduction measures to reduce the significant risks associated with DNP. That's all good but if this is an argument for the safety of DNP, it is not very convincing...

But by your definition it is impossible For DNP to be safe bc it's a non-medical use so no amount of convincing or no matter the strength of the argument your mind is set.
 
I don't define non-medical use of drugs in terms of being safe. I define it in terms of risk. It's a much more effective way to educate/inform without the appearance of bias.

So the whole premise of this thread is irrelevant by this standard. The title should then read "Think DNP can be used without risk" or something along those lines.



What's wrong with existing definitions as they are commonly used?

Ironically, CBS isn't the one using avoidance of death as proof of DNP safety.

Which is sillier? Citing death as proof of DNP danger? Or citing avoidance of death as proof of DNP safety?

No he isnt but ironically he's using death as proof of lack of safety. Which is it?


Safe suggests absence of risk. Unsafe suggests presence of risk. Risk exists on a continuum. The degree of risk and nature of risks varies with different drugs.

Trying to defend the non-medical use of any drug as safe hasn't been a very effective strategy. That's why I prefer discussing it in terms of associated risks.

And the risks of DNP are higher than almost any other compound we talk about here but it's benefits in terms of fat loss are also higher than any compound we talk about here. Taking safety out of the equation and focusing on risk, the risk of death as shown by the statistics and the risk of cataracts to males is very minor compared to the benefits of raising my metabolism by anywhere from 10-40% depending on the dosage used and losing 2-3lbs of actual fat a week, and losing a great amount of fat in such a short period of time is worth it to me personally which I why I choose to use DNP.
 
And the risks of DNP are higher than almost any other compound we talk about here but it's benefits in terms of fat loss are also higher than any compound we talk about here. Taking safety out of the equation and focusing on risk, the risk of death as shown by the statistics and the risk of cataracts to males is very minor compared to the benefits of raising my metabolism by anywhere from 10-40% depending on the dosage used and losing 2-3lbs of actual fat a week, and losing a great amount of fat in such a short period of time is worth it to me personally which I why I choose to use DNP.
If the cost/benefit ratio is acceptable to you, that is fine. I'm not arguing otherwise. And no one can tell me the cost/benefit ratio should be acceptable to me either. It's a subjective determination.

Don't think I'm judging you. I know ways to lose 2-3 lbs bodyfat/week that may be riskier and I'd happily accept the cost/benefit ratio.
 
CBS is deflecting, he doesn't even want to answer what he considers "safe" to mean..

I have no reason to deflect. I've posted my evidence and you people have been unable to find anything that refutes it.

Safe = No side effects?

No drug is without side effects.

Safe = Using without permanent and irreversible damage?

No one has provided evidence showing that the risk of permanent harm or irreversible damage can be mitigated.

Safe = avoiding death?

No one has provided evidence showing that the risk of death can be mitigated.
 
I'm going to ask CBS this for the final time:

Do you TRULY believe that the evidence you provided in your original post is an ACCURATE representation of DNP?

On a side note, it is NOT up to us to prove that the risk of permanent harm/damage can be mitigated or that the risk of death can be mitigated.
Your the one claiming that they cannot, nothing you have used as evidence so far shows that permanent harm/damage or death is inevitable.
 
Many of the people who are dying do so bc of hyperthermia. How does one do this? Don't run it in the summer months or extremely hot climates, drink extra fluids and electrolytes to maintain hydration, minimize amount of exercise performed (no long duration sweaty intense cardio etc), monitor body temps closely and adjust dosage as necessary or come off if unable to control, if body temps get high take an ice bath, out cold damp towels on your forehead, underarms, Palma etc. If hospitalized don't hesitate to provide info to the emergency room staff (some of the deaths came about bc the doctor's had no idea what they were treating so they chased symptoms instead of formulated a plan), and some other methods.

This is pure speculation. There is no evidence to suggest any of those measures will prevent complications. They seem like prudent steps to take but there's no reason to believe they will be successful. It's worth pointing out that mechanical cooling has been unsuccessful in ERs. The only thing on that list that has been shown effective is letting the ER staff know about the use of DNP, but that does nothing to prevent complications.
 
If the cost/benefit ratio is acceptable to you, that is fine. I'm not arguing otherwise. And no one can tell me the cost/benefit ratio should be acceptable to me either. It's a subjective determination.

Don't think I'm judging you. I know ways to lose 2-3 lbs bodyfat/week that may be riskier and I'd happily accept the cost/benefit ratio.

Of course we are all tree to choose our path and I would never force my choices on you or anyone else. My choices are mine and mine alone.

I don't believe you are judging anyone. Even if you were it's your right to have opinions. My question now is do you think enough evidence was presented to warrant the original claim from the OP, namely that there is no safe dose of DNP and that it cannot be ran safely or with minimal risk? Not asking what you believe about the issue but specifically was enough evidence presented here in this thread?
 
- Do you TRULY believe that the evidence you provided in your original post is an ACCURATE representation of DNP?

The evidence I provided in my OP is an accurate evaluation of the risks associated with DNP use. There is at least a 1% chance that users will develop cataracts and according to Horner, the risk is likely far higher. There is also a risk of mortality. How high, I don't know and neither do you. But it does happen and that makes DNP unique among pharmaceuticals. One of the charts from the link you posted shows mortality rate follows the frequency of exposure to DNP. When people are exposed, mortality goes up. When people aren't exposed, mortality goes down. That cannot be disputed.

13181_2011_162_Fig1_HTML.jpg


Please consider a few things before you answer this question:
- the overall statistics that I PROVIDED on dnp related deaths along with the doses at which it occurred vs your 2 or 3 case studies. This is known as STRONG OPPOSING research since it proves that your overstating the danger dramatically.

The numbers of deaths from DNP are likely to be underrepresented in the literature, just as the number of users who developed cataracts are likely to be underrepresented. Your estimate of the total number of DNP users is unsupported. There is simply no way to know that. Guesstimating the number of DNP users and then using that to estimate the number of users versus deaths is not strong opposing evidence, it's speculation.


- the fact that you highlighted one physiologists opinion that dnp is toxic to the liver, heart, etc when the ATSDR toxicological profile says otherwise. More OPPOSING research.

The papers that reported physiological changes based their findings on the results of autopsy. Not in lab animals, in humans. ATSDR used the same references that we've been discussing.

Regardless, from ATSDR:

"Data also exist regarding death, systemic effects of acute-, intermediate-, and chronic-duration exposure, and immunologic and neurologic effects in humans after oral exposure to 2,4-DNP. The systemic effect categories for which some data were located were respiratory, cardiovascular, gastrointestinal, hematological, musculoskeletal, hepatic, renal, endocrine, dermal, ocular, body weight, metabolic, and other (hearing). The ocular effects consisted of cataract formation after acute-, intermediate- or chronic-duration oral exposure to 2,4-DNP"

"In other fatal cases, cloudy swelling, pyknosis, and necrosis in the renal tubules, edema in interstitial tissue, distention of capillary and arterial loops in the glomernlus, and hemorrhage were seen in the kidneys of a woman who took 7 mg/kg/day 2,4-DNP as the sodium salt for 5 days (Poole and Haining 1934); marked destruction of the epithelium lining the renal tubules with hemorrhage into the glomernli was found in the kidneys of a woman who took an indeterminate dose of 2,4-DNP for 1 week (Lattimore 1934); and hemorrhagic nephritis was found in the kidneys of a young girl who took 1.03 mg/kg/day 2,4-DNP for 46 days (Goldman and Haber 1936)."

"Upon autopsy and histological examination, hyperemic and hemorrhagic lungs, degeneration of renal tubules and liver cells, segmentation and fragmentation of cardiac muscles, and hemorrhagic spleen, stomach mucosa, spinal cord, pons, and medulla were found (Poole and Haining 1934)."

"Autopsy revealed marked segmentation and fragmentation of the cardiac muscles. A psychiatric patient was given sodium 2, 4-DNP in an experimental study to determine whether 2,4-DNP would be beneficial in treating depression (Masserman and Goldsmith 1934)."

- the fact that I SPECIFICALLY explained a 1950s study showing the impact vit c has on cataracts. More OPPOSING research.

You posted a single study on guinea pigs. That's hardly convincing. You also conceded that it was "mostly theoretical at this point since studies are mixed."

Again, from ATSDR

"Cataracts in animals after oral exposure have been demonstrated only in a special strain of mice, in vitamin C deficient guinea pigs, and in chicks and ducks and were transient and/or histologically different from the human cataracts (Bettman 1946; Ogino and Yasukura 1957; Robbins 1944). Hence, the animal data indicate that animals may be much less sensitive and may not respond in the same manner to 2,4-DNP as do humans."

- the significant amount of data doc provided.

He provided studies on efficacy and I'm not disputing that. He posted nothing that suggests the risks associated with DNP use can ameliorated.
 
If the number of deaths in the literature and number of cases of cataracts are under reported it goes without saying that the number of users of DNP is also under reported.
 
On a side note, it is NOT up to us to prove that the risk of permanent harm/damage can be mitigated or that the risk of death can be mitigated.
Your the one claiming that they cannot
, nothing you have used as evidence so far shows that permanent harm/damage or death is inevitable.


Now you're asking me to prove a negative. You should know that's impossible. I didn't say permanent harm/damage or death is inevitable, those are your words. I posted the risks of DNP use. All I can do is report the risks. I can't prove that the risk of cataract CAN'T be mitigated, that's absurd. I can only point out the fact that there is no evidence showing it can be mitigated. You're the one saying I've overestimated the risks, and that those risks can be mitigated. And you're the one saying DNP can be used safely. That makes you the positive claimant. The onus is on you to support your assertions that the risk of permanent harm/damage can be mitigated or that the risk of death can be mitigated.
 
Now you're asking me to prove a negative. You should know that's impossible. I didn't say permanent harm/damage or death is inevitable, those are your words. I posted the risks of DNP use. All I can do is report the risks. I can't prove that the risk of cataract CAN'T be mitigated, that's absurd. I can only point out the fact that there is no evidence showing it can be mitigated. You're the one saying I've overestimated the risks, and that those risks can be mitigated. And you're the one saying DNP can be used safely. That makes you the positive claimant. The onus is on you to support your assertions that the risk of permanent harm/damage can be mitigated or that the risk of death can be mitigated.

You posted the risks of DNP use but you also made the claim there is no safe dose to which insufficient evidence has been presented to substantiate that claim. You posted a couple case studies and someone's opinion.
 
The evidence I provided in my OP is an accurate evaluation of the risks associated with DNP use.

The numbers of deaths from DNP are likely to be underrepresented in the literature, just as the number of users who developed cataracts are likely to be underrepresented. Your estimate of the total number of DNP users is unsupported. There is simply no way to know that. Guesstimating the number of DNP users and then using that to estimate the number of users versus deaths is not strong opposing evidence, it's speculation.

So you believe that citing 2 or 3 case studies is an accurate evalutation of the risks associated with DNP use hmmm...

Interesting that you have read the toxicology report yet never bothered to mention this:

"There were no deaths, however, in a number of clinical and experimental studies in which obese or normal subjects were given 2,4-DNP or its sodium salt at oral dosages of 1.2-4.3 mg/kg/day 2,4-DNP for ≤14 days (Castor and Beierwaltes 1956; Cutting et al. 1934; Cutting and Tainter 1933; MacBryde and Taussig 1935; Stockton and Cutting 1934; Tainter et al. 1935b). "

Or this:
"Several clinical studies regarding the effects of 2,4-DNP or its sodium salt in obese and non-obese humans taking the drug for an intermediate duration at doses of 3.5-5.27 mg/kg/day 2,4-DNP have reported no deaths from this treatment (Cutting et al. 1934; Grant
and Schube 1934; Looney and Hoskins 1934; MacBryde and Taussig 1935; Simkins 1937a, 1937b; Tainter et al. 1934a, 1935b)."


Accurate representation?
My ass :)

Huh...so my estimate at the total number of dnp users being higher is pure speculation, but then what do we call your presumption that the death & cataract rates must be higher?
How about...speculation?

The papers that reported physiological changes based their findings on the results of autopsy. Not in lab animals, in humans. ATSDR used the same references that we've been discussing.

Regardless, from ATSDR:

"Data also exist regarding death, systemic effects of acute-, intermediate-, and chronic-duration exposure, and immunologic and neurologic effects in humans after oral exposure to 2,4-DNP. The systemic effect categories for which some data were located were respiratory, cardiovascular, gastrointestinal, hematological, musculoskeletal, hepatic, renal, endocrine, dermal, ocular, body weight, metabolic, and other (hearing). The ocular effects consisted of cataract formation after acute-, intermediate- or chronic-duration oral exposure to 2,4-DNP"

"In other fatal cases, cloudy swelling, pyknosis, and necrosis in the renal tubules, edema in interstitial tissue, distention of capillary and arterial loops in the glomernlus, and hemorrhage were seen in the kidneys of a woman who took 7 mg/kg/day 2,4-DNP as the sodium salt for 5 days (Poole and Haining 1934); marked destruction of the epithelium lining the renal tubules with hemorrhage into the glomernli was found in the kidneys of a woman who took an indeterminate dose of 2,4-DNP for 1 week (Lattimore 1934); and hemorrhagic nephritis was found in the kidneys of a young girl who took 1.03 mg/kg/day 2,4-DNP for 46 days (Goldman and Haber 1936)."

"Upon autopsy and histological examination, hyperemic and hemorrhagic lungs, degeneration of renal tubules and liver cells, segmentation and fragmentation of cardiac muscles, and hemorrhagic spleen, stomach mucosa, spinal cord, pons, and medulla were found (Poole and Haining 1934)."

"Autopsy revealed marked segmentation and fragmentation of the cardiac muscles. A psychiatric patient was given sodium 2, 4-DNP in an experimental study to determine whether 2,4-DNP would be beneficial in treating depression (Masserman and Goldsmith 1934)."
O dear...
The primary cause of death from dnp is hyperthermia.
Hyperthermia itself causes all of the organ failure/damage notes that you mentioned - that's why all of it has been spotted in fatal cases and NOT in alive users.

In other words, all of this only occurs with TOXIC OVERDOSE. Toxic doses are in no way representative of what occurs at therapeutic doses - the toxicology report uses ALOT of extreme cases to illustrate some of the risks that are not present in the original clinical trials.

For example:
Poole and Haining 1934 - a woman who took 7mg/kg for 5 days.
Goldman and Haber 1936 - This was an obese woman who took 3.97 mg/kg/day for 35 days. She had been taking DNP intermittently for 1 year before she became ill. She had agranulocytosis, mild anemia, marked albuminuria. I do not believe that this wasn't a toxic overdose and its pretty obvious that cases like this are rare, atypical examples - none of these sort of symptoms are present in the original clinical trials.

Also from the same toxicology report:
"Tests for liver function, such as icteric index (a measure of serum bilirubin), the Van den Bergh test, and the bromsulphalein retention test, in other case reports and clinical studies of people exposed orally found no evidence of impaired damage (Anderson et al. 1933; Masserman and Goldsmith 1934; Simkins 1937a, 1937b). "

Again, you will only find these sort of effects in those who took toxic doses OR rare, atypical cases - if you find the original clinical trials for dnp using normal, healthy individuals none of these effects occurred.


So no - the evidence you provided is NOT an accurate evaluation of the risks associated with dnp. The fact that you believe it is shows just how uneducated you are when it comes to this compound.

Your OP is an illustration of what can happen in EXTREME, RARE cases - nothing more, nothing less.
 
You posted the risks of DNP use but you also made the claim there is no safe dose to which insufficient evidence has been presented to substantiate that claim. You posted a couple case studies and someone's opinion.

Yes, and saying there is NO safe dose should be seen as a claim of opinion because such a claim is unjustifiable. Logic and reason can only be applied to that which exists, not to that which doesn't exist. I cannot possibly prove there is no safe dosage as that would require me to be omniscient. If you don't agree with my opinion, show me the safe dosage. Don't ask me to prove something that is impossible. My statement should be taken as a challenge to prove me wrong.
 
Out of curiosity if it comes in a pill would it be a safer option to open the capsule. And weigh the millagrams? I have no experience with this. But I would assume that it would be safer to open weigh and recap?
 
Yes, and saying there is NO safe dose should be seen as a claim of opinion because such a claim is unjustifiable. Logic and reason can only be applied to that which exists, not to that which doesn't exist. I cannot possibly prove there is no safe dosage as that would require me to be omniscient. If you don't agree with my opinion, show me the safe dosage. Don't ask me to prove something that is impossible. My statement should be taken as a challenge to prove me wrong.

So you get side step saying what you really want to say, that which can't be proven by the way, and wash your hands of the responsibility that comes with making your claim simply by saying "My statement should be taken as a challenge to prove me wrong." And admitting you can't prove there is no safe dosage? A natural born Houdini.

Once again, with only 62 reported deaths up until 2011, out of hundreds of thousands of users, it's pretty clear your case studies are well outside the norm. It's like demonizing dairy bc part of the population is lactose intolerant.
 
Out of curiosity if it comes in a pill would it be a safer option to open the capsule. And weigh the millagrams? I have no experience with this. But I would assume that it would be safer to open weigh and recap?

Weighing wouldn't give you much info alone. The caps weigh more than the DNP present in them bc of fillers used. So a 250mg cap of DNP could very well weigh 300mg bc of the amount of fillers used.
 
Out of curiosity if it comes in a pill would it be a safer option to open the capsule. And weigh the millagrams? I have no experience with this. But I would assume that it would be safer to open weigh and recap?

The safest method would be to buy the powder (it's ridiculously cheap) and cap it yourself.
This way you can ensure that all measurements are accurate - but I warn you that this is a very messy and annoying process.
 
If one wanted to lose a large amount of fat quickly, why would DNP be a better choice than a PSMF combined with drugs that have a dramatic positive effect on nutrient partioning (AAS, GH/peptides)?
 
So you believe that citing 2 or 3 case studies is an accurate evalutation of the risks associated with DNP use hmmm...

Interesting that you have read the toxicology report yet never bothered to mention this:

"There were no deaths, however, in a number of clinical and experimental studies in which obese or normal subjects were given 2,4-DNP or its sodium salt at oral dosages of 1.2-4.3 mg/kg/day 2,4-DNP for ≤14 days (Castor and Beierwaltes 1956; Cutting et al. 1934; Cutting and Tainter 1933; MacBryde and Taussig 1935; Stockton and Cutting 1934; Tainter et al. 1935b). "

Or this:
"Several clinical studies regarding the effects of 2,4-DNP or its sodium salt in obese and non-obese humans taking the drug for an intermediate duration at doses of 3.5-5.27 mg/kg/day 2,4-DNP have reported no deaths from this treatment (Cutting et al. 1934; Grant
and Schube 1934; Looney and Hoskins 1934; MacBryde and Taussig 1935; Simkins 1937a, 1937b; Tainter et al. 1934a, 1935b)."


Accurate representation?
My ass :)

Huh...so my estimate at the total number of dnp users being higher is pure speculation, but then what do we call your presumption that the death & cataract rates must be higher?
How about...speculation?


O dear...
The primary cause of death from dnp is hyperthermia.
Hyperthermia itself causes all of the organ failure/damage notes that you mentioned - that's why all of it has been spotted in fatal cases and NOT in alive users.

In other words, all of this only occurs with TOXIC OVERDOSE. Toxic doses are in no way representative of what occurs at therapeutic doses - the toxicology report uses ALOT of extreme cases to illustrate some of the risks that are not present in the original clinical trials.

For example:
Poole and Haining 1934 - a woman who took 7mg/kg for 5 days.
Goldman and Haber 1936 - This was an obese woman who took 3.97 mg/kg/day for 35 days. She had been taking DNP intermittently for 1 year before she became ill. She had agranulocytosis, mild anemia, marked albuminuria. I do not believe that this wasn't a toxic overdose and its pretty obvious that cases like this are rare, atypical examples - none of these sort of symptoms are present in the original clinical trials.

Also from the same toxicology report:
"Tests for liver function, such as icteric index (a measure of serum bilirubin), the Van den Bergh test, and the bromsulphalein retention test, in other case reports and clinical studies of people exposed orally found no evidence of impaired damage (Anderson et al. 1933; Masserman and Goldsmith 1934; Simkins 1937a, 1937b). "

Again, you will only find these sort of effects in those who took toxic doses OR rare, atypical cases - if you find the original clinical trials for dnp using normal, healthy individuals none of these effects occurred.


So no - the evidence you provided is NOT an accurate evaluation of the risks associated with dnp. The fact that you believe it is shows just how uneducated you are when it comes to this compound.

Your OP is an illustration of what can happen in EXTREME, RARE cases - nothing more, nothing less.


More unsupported nonsense. Continue with your head in the sand. You come about your conclusions based on wishful thinking. We are clear that you have no scientific support for your arguments, they are based on anecdote alone. All will know how you go about making recommendations.
 
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