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Think DNP Can Be Used Safely? Think Again

CensoredBoardsSuck

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.
-------------------------------------------------------------------------------------------------------------



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.
 
And yet out of the 100s of thousands of people who took prescribed DNP with NO supervision during the 1930s only 8 died:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3550200/table/Tab1/

The cataracts side effect occurred almost EXCLUSIVELY in females and the incidence rate was reported to be 0.1%.
This can easily be countered by having a healthy antioxidant status and/or supplementing with basic vitamins - something not many had access to/were aware of in the 1930s.

As for the death reports despite "safe" dosages of dnp - you will always have outliers when it comes to how people respond to pharmaceuticals.
To suggest that these few individuals represent the fact that DNP cannot be used in a safe manner would be wrong.

I'm not saying that DNP isn't dangerous per se, just that its dangers are blown way out of proportion - statistics don't lie.
 
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.
-------------------------------------------------------------------------------------------------------------



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.

I agree CBS but as a forewarning this type of "cut and paste" evidence is not going to be welcomed on some forums, TID in particular. It seems folk on some forums are perfectly content with limiting posts of this nature to the "experience of vets".

However I've always queried how accurate testimonials can be obtained from DEAD VETS?

Regs
JIM
 
Nice post, I personally think DNP isn't safe but people will come to their own conclusions

Most fat burners in general seem pointless to me unless you are getting on stage for a competition. Just diet if you want to look good on the beach everybody wants to quick fix.
 
I've ran DNP 3 times... On one of those cycles I almost went goodnight. DNP is a horrible drug and should be avoided. Any side you can think of I got it during and after the cycle. Some of the worst nerve pain I've ever felt too.

-Exhausted 24/7
-hot temp
-internal bleeding
-blood in my shit
-rash over half my body right how the middle
-nerve pain in fingers and toes
that's just to name a few

I will never touch this poison again while I live
 
I've ran DNP 3 times... On one of those cycles I almost went goodnight. DNP is a horrible drug and should be avoided. Any side you can think of I got it during and after the cycle. Some of the worst nerve pain I've ever felt too.

-Exhausted 24/7
-hot temp
-internal bleeding
-blood in my shit
-rash over half my body right how the middle
-nerve pain in fingers and toes
that's just to name a few

I will never touch this poison again while I live
Curious, if it was so horrible, why did you run it an extra 2 times?
 
I just dont see it being prudent under any circumstances. Ive always felt the danger is for some the line between therapeutic and lethal dose is too fine and inconsistent. Why take the chance?
 
First time was a very low run just to try DNP at a very low dose.
2nd time was 400 a day for 10 days (worst experience of my life)
3rd I was just a dumbass all honesty each time you run it will be a different experience.
The weight loss is not worth the pain. I can loss just as much with a very strict diet and cardio routine.
 
And yet out of the 100s of thousands of people who took prescribed DNP with NO supervision during the 1930s only 8 died:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3550200/table/Tab1/

The cataracts side effect occurred almost EXCLUSIVELY in females and the incidence rate was reported to be 0.1%.
This can easily be countered by having a healthy antioxidant status and/or supplementing with basic vitamins - something not many had access to/were aware of in the 1930s.

As for the death reports despite "safe" dosages of dnp - you will always have outliers when it comes to how people respond to pharmaceuticals.
To suggest that these few individuals represent the fact that DNP cannot be used in a safe manner would be wrong.

I'm not saying that DNP isn't dangerous per se, just that its dangers are blown way out of proportion - statistics don't lie.

DNP-Related Fatalities
Fatalities from the intake of DNP, whether accidental or suicidal, have been reported since the turn of the twentieth century (Table 1). To date, there have been 62 published deaths attributed to DNP (Fig. 1). The largest publication of 36 deaths due to DNP was published in 1919 [6]. This was a study into the deaths in munition factories in Paris due to occupational exposure to DNP. It highlights the improvements made in the factory to prevent further deaths through simple measures such as ventilation, personal protective equipment and better hygiene. This combined with changes in legislation brought the death rate down from 16.3 per 10,000 t of DNP handled/produced to 1.2 per 10,000 t.
During the 1930s, reported DNP-related fatalities were all individuals who had taken it for weight loss [46, 47, 51, 56, 57, 61, 67, 71]. After the 1930s, there have only been two fatalities in the remainder of the twentieth century [15, 68]. One related to deliberate ingestion of DNP [68] and the other was where an individual accidentally ingested a liquid he thought to be grape juice, but in fact contained derivatives of DNP [15]. This further decline in fatalities may reflect the labelling of DNP as ‘extremely dangerous and not fit for human consumption’ by the US Food and Drug Administration in 1938.
Over the last decade, from 2001 to 2010, there have been 12 deaths related to exposure to DNP. These fatalities have been linked to deliberate overdose [4, 22, 69], accidental toxicity associated with use by bodybuilders or for weight loss [21, 28,7275] and accidental occupational exposure [33]. This resurgence in reported fatalities may reflect the increased availability of DNP over the internet, marketed particularly towards bodybuilders.
Preceding death, the patient is often profoundly hyperthermic and there may be associated methaemoglobinaemia. Death is usually secondary to massive cardiovascular collapse. There have been frequent reports of a rapid (within minutes) onset of generalised rigidity after death [6, 11]. This profound muscle rigidity has also been seen to happen before death making mechanical ventilation very difficult [21]. This early onset of generalised rigidity after death has been attributed to the release of calcium from the cytosol due to the depletion of ATP [22].
Ingestion is currently the most common route of exposure to the drug leading to death. The lowest published lethal human oral dose of DNP is 4.3 mg/kg [76]; the doses reported in the published acute and suicidal fatalities range from 2.8 g to an estimated 5 g. The highest reported dose taken in acute overdose associated with survival was a woman who took 2.4 g with no complications [70].

http://link.springer.com/article/10.1007/s13181-011-0162-6/fulltext.html
 
^^^ pretty much backs up everything I said :)

Here is another interesting paper that compared dnp to thyroid medication and other obesity drugs with the conclusion that dnp was the safer/more effective option:
http://www.ncbi.nlm.nih.gov/pubmed/18089946#

That paper also cites a lot the early research into dnp (interesting read to those who have access to it).
It also recommends looking into the mechanisms of dnp further when it comes to battling the obesity crisis, which is EXACTLY what researchers are doing right now.
 
^^^ pretty much backs up everything I said :)

Here is another interesting paper that compared dnp to thyroid medication and other obesity drugs with the conclusion that dnp was the safer/more effective option:
http://www.ncbi.nlm.nih.gov/pubmed/18089946#

That paper also cites a lot the early research into dnp (interesting read to those who have access to it).
It also recommends looking into the mechanisms of dnp further when it comes to battling the obesity crisis, which is EXACTLY what researchers are doing right now.


Where does it say dnp is safer than thyroid hormone? That's a ridiculous statement!
 
Where does it say dnp is safer than thyroid hormone? That's a ridiculous statement!

Please read my post again.

I CLEARLY said safer/more effective - I'm assuming you know that a forward slash means "or".

The paper showed it to be safer than some other obesity drugs of the time (2007) that caused serious heart problems and more effective than t3, which was catabolic - unlike dnp:
"In contrast to the use of thyroid extract (also in common use at the time to treat obesity), DNP did not promote urinary nitrogen excretion, so the assumption was made that weight loss could be attributed to a specific loss of fat (47)."
 
What would you guys say about the dudes running T3 and T4 to lose weight who have an otherwise perfect thyroid function???? I'd never touch DNP, and even T3/T4 seem pretty fucking scary to me.
 
And yet out of the 100s of thousands of people who took prescribed DNP with NO supervision during the 1930s only 8 died:

You're assuming all DNP related deaths have been reported. They have not.

The cataracts side effect occurred almost EXCLUSIVELY in females and the incidence rate was reported to be 0.1%.

Horner updated the incidence of cataracts in 1941 from 0.1% to close to 1%, and suggested that even that was much too low due to under reporting.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1315023/pdf/taos00060-0454.pdf

"In a paper published in 1937100 I estimated that the
incidence of cataract in patients who had taken dinitrophenol
was probably between 0.1 per cent. and 1 per cent., and that
the total number of patients so affected would range between
60 and 100.

There are only a few reports of extensive clinical studies of
dinitro-bodies to be found in the literature. The data available
show that Tainter, Stockton, and Cutting24 (1935) reported
1 case in 170 treated patients; Hill90 (1936), 1 in 68;
Simkins41 (1937), 1 in 159; MAhlWn121 (1938), 1 in 66 of
Berglund's 73 cases who received dinitro-ortho-cresol. These
average 0.86 per cent.,
which is within the estimate previously
given. Since the interval between the discontinuance
of the drug and the occurrence of cataract may be as long
as one year, some of the patients treated in these four series
may have acquired cataracts at a later time. This figure is,
therefore, more likely to be minimum than maximum. My

previous estimate of the number of persons affected proved
much too low. I have recently collected a total of 177 cases
from the literature up to January, 1941. Of these, 164 followed
the use of dinitrophenol, whereas 13 had been taking
dinitro-ortho-cresol. These figures are probably again too
low.
It is certain that additional cases have occurred which
have failed to be reported in the medical journals. Other
cases may have been presented as case reports before local
medical societies. Since relatively few of the proceedings of
the latter are published, such patients are lost sight of."

This can easily be countered by having a healthy antioxidant status and/or supplementing with basic vitamins - something not many had access to/were aware of in the 1930s.

What evidence do you have that shows "this can easily be countered by having a healthy antioxident status"? And why do you believe they weren't aware of this in the 1930s?

Horner again:

"Tainter and Borley 32 could not produce cataracts in
animals that were suffering from deficiencies of vitamin A,
B2, or C by feeding them dinitrophenol in maximum tolerated

doses. This potentiality was investigated in order to determine
whether possible vitamin deficiency in patients undergoing
weight reduction with dinitrophenol might predispose
the lens to cataract formation."

"H. Barkan, Borley, Fine and Bettman,94 in discussing the
etiology of dinitro-cataracts, refer to the role of vitamin C in
normal and cataractous lenses. While cevitamic acid was

used by Josephson81 in the treatment of an early case of
dinitrophenol cataract, a specific relationship to vitamin C is

unproved. Barkan and others suggest the possibility of a
disturbance of the nutrition of the lens or an altered pH
toward the acid side as a potential factor. No estimation of
the pH of dinitrophenol cataract has, to my knowledge, appeared
in the literature."

As for the death reports despite "safe" dosages of dnp - you will always have outliers when it comes to how people respond to pharmaceuticals.

Indeed, but with the exception of anaphylaxis, abuse, overdose, etc., people don't die from the therapeutic effect of prescription drugs.

To suggest that these few individuals represent the fact that DNP cannot be used in a safe manner would be wrong.

The FDA doesn't agree with you.

I'm not saying that DNP isn't dangerous per se, just that its dangers are blown way out of proportion - statistics don't lie.

Stats don't lie but they don't always tell the whole tale, especially when all the numbers aren't known.
 
Last edited:
Please read my post again.

I CLEARLY said safer/more effective - I'm assuming you know that a forward slash means "or".

The paper showed it to be safer than some other obesity drugs of the time (2007) that caused serious heart problems and more effective than t3, which was catabolic - unlike dnp:
"In contrast to the use of thyroid extract (also in common use at the time to treat obesity), DNP did not promote urinary nitrogen excretion, so the assumption was made that weight loss could be attributed to a specific loss of fat (47)."


Then you shouldn't have included the word 'safe' at all. More effective DOES NOT imply safer.
 
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