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



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."



What evidence do you have that shows "this can easily be countered by having a healthy antioxident status"? Ans 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."



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



The FDA doesn't agree with you.



Stats don't lie but they don't always tell the whole tale, especially when all the numbers aren't known.

The FDA isn't always right. They take drugs off the market after having approved them. FDA makes mistakes like anyone else.

Funny, you used statistics to make an argument in another thread. They were good enough to "tell the tale" for you but for MrRippedZilla?
 
You're assuming all DNP related deaths have been reported. They have not.

You forget that Tainter also estimated that 100,000 people used dnp - it could easily be higher than this.
Assuming consistent growth over the 5 years that DNP was available over the counter, the usage number could easily reach 500,000.
So yes - there may very well be more unreported deaths, but there are also more unreported users. In the end, I seriously doubt it would make a difference to the overall usage:death ratio.


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."
I'll concede to the updated statistics that Horner provided.


What evidence do you have that shows "this can easily be countered by having a healthy antioxident status"? Ans 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."

This is where it becomes conflicting since their are studies on both sides of the argument.

Here was some research from the 1950s:
http://www.ncbi.nlm.nih.gov/pubmed/13424619

It showed that the group fed a vitamin c-deficient diet developed cataracts while the group that supplemented with vit c did not.
"In these experiments, it is clear that there is a close relationship between the production of cataract and vitamin-C deficiency."

They weren't aware of this in the 30s (at least not to the full extent) because they hadn't been able to identify the cataractogenic metabolite of DNP - something that the researchers in this study did.
It was identified as 2-amino-p-quinonimine. They found that the hydroxyl- and nitro-radicals of DNP in the p-position were vital to the production of dinitrophenol cataract. In other words, genetics plays a major role.

They also hypothesized as follows:
"This suggests that a genetic predisposition plays an important role in susceptibility to this cataract. This notion is strengthened by the fact that, in spite of extensive experiments of long duration by many authors, it has been found impossible to produce dinitrophenol cataract experimentally in various other species, namely, in rats, rabbits, guinea pigs, and dogs, although Bettman observed dinitrophenol cataract in a special strain of mice."

So its a combination of genetics & antioxidant status - though I confess that is mostly theoretical at this point since studies are mixed.


The FDA doesn't agree with you.

We are on a steroid board and your using the FDA argument? Really?
The FDA thinks steroids are dangerous too, they also banned ephedrine despite YEARS of studies showing it to be safe.
Lets stop here shall we :)

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

Exactly WHERE did I say that effectiveness and safety were the same thing hmm?
I said that the study showed dnp to be SAFER than some compounds (fat loss drugs now banned) and more EFFECTIVE then others (thyroid medication).

Do I really need to give an English lesson on how "/" is used?

Don't blame me for your inability to interpret my posts correctly.
 
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/
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.
.

Really well that comment is an opinion completely void of any credible evidence! I would like to think when those like yourself posts an article to support one component of a debate, they would cite several to justify such an outlandish statement.

This is the type of crap that can be potentially DANGEROUS since many noobs visiting Meso could interpret that statement DNP is "safe" providing one uses high doses of Vitamin E, for it's antioxidant benefit.

Have you any idea what physiologic processes are primarily responsible for DNP deaths?

DNP uncouples oxidative phosphorlation with the net effect being ATP is wasted to generate HEAT/entropy rather than energy used for metabolic processes. And although "antioxidants" such as Vitamin-E reduce free radical formation, the latter has little, if anything, to do with DNP COMPLICATIONS.

So DNP patients cook themselves from a metabolic perspective and that's a KNOWN fact bc hyperthermia is also a well established adverse effect of DNP use even at "therapeutic dosages".

Post any evidence "researchers are studying DNP, a REGISTERED POISON, as a dietary aid, the suggestion is absolutely absurd!

Finally DNP is one of the worst dietary aids a BB could use bc it results in the nonspecific catabolism of ALL potential energy sources, from stored Carbs as Glycogen, Protein as MUSCLE, and Fat from adipose tissue. Additionally a large portion of the "weight loss" noted bc of DNP use is the consequence of total body water loss!

Thank God Meso is loaded with experienced, rational mates like JIMMY INK, WunderP, DemonD, B66 and many more, on this thread alone, who are willing to impart their well reasoned insight.

regs
jim



 
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CBS you have never used DNP, learn something about it or ask somebody with experience...............


You ever have the clap, Sworder? I have not, but I still know it hurts when you pee. You, apparently, aren't capable of knowing that without first acquiring the clap.

Of all the stupid comments I've seen on Meso, you just made the top five. Bravo!
 
Harper JA, Dickinson K and Brand MD (2001) Mitochondrial uncoupling as a target for drug development for the treatment of obesity. Obesity Rev, 2, 255–265
"In contrast to the use of thyroid extract (also in common use at the time to treat obesity), DNP did not promote urinary nitrogen excretion, so the assumption was made that weight loss could be attributed to a specific loss of fat (47)."

Bell, Jacques. 1939. Etude biologique des produits dinitres chez l'homme. Medecine. 19:749-54.
"2. This increase of the metabolism is due mostly to an increase in the combustion of the fat and a little to combustion of carbohydrates.
3. Dinitrophenol does not attack cell tissue albumin and does not determine the fat loss to the expense of the muscles, contrary to thyroxine.
...
Finally, thyroxine causes a nitrogen malnutrition: it burns the muscle and fatigues the heart. Dinitrophenol-lysidine, to the contrary, causes a lipid-glycemic loss: it is the elimination of reserve materials without attacking visceral and muscle tissue."

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

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

Cutting WC, Tainter ML. Metabolic actions of dinitrophenol with the use of balanced and unbalanced diets. J Am Med Assoc 1933; 101: .
"Dinitrophenol, used in doses of therapeutic range,caused increases in metabolism of the usual magnitude irrespective of the type of diet. The nitrogen excretion was never greater than the intake, even when the subjects lost as much as 5 pounds in body weight during one week. From this it seemed probable that there was no actual tissue breakdown during these short periods of heightened metabolism, but that the loss of weight was due to the utilization of stored carbohydrate or fat. This does not mean, of course, that tissue breakdown would not occur if the drug should be given over longer periods, but probably when materials other than protein are available these are utilized first. Thus the assumption might be made that, as long as the protein intake is adequate, any reduction in body weight is not primarily at the expense of the tissue proteins.
...
3.The subjects excreted less nitrogen than they ingested, yet there were definite losses of body weight. Therefore, body proteins probably were not broken down. The output of urinary organic acid was not increased, thus indicating that the fats were completely burned without giving rise to acidosis."
 
Harper JA, Dickinson K and Brand MD (2001) Mitochondrial uncoupling as a target for drug development for the treatment of obesity. Obesity Rev, 2, 255–265
"In contrast to the use of thyroid extract (also in common use at the time to treat obesity), DNP did not promote urinary nitrogen excretion, so the assumption was made that weight loss could be attributed to a specific loss of fat (47)."

Bell, Jacques. 1939. Etude biologique des produits dinitres chez l'homme. Medecine. 19:749-54.
"2. This increase of the metabolism is due mostly to an increase in the combustion of the fat and a little to combustion of carbohydrates.
3. Dinitrophenol does not attack cell tissue albumin and does not determine the fat loss to the expense of the muscles, contrary to thyroxine.
...
Finally, thyroxine causes a nitrogen malnutrition: it burns the muscle and fatigues the heart. Dinitrophenol-lysidine, to the contrary, causes a lipid-glycemic loss: it is the elimination of reserve materials without attacking visceral and muscle tissue."

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

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

Cutting WC, Tainter ML. Metabolic actions of dinitrophenol with the use of balanced and unbalanced diets. J Am Med Assoc 1933; 101: .
"Dinitrophenol, used in doses of therapeutic range,caused increases in metabolism of the usual magnitude irrespective of the type of diet. The nitrogen excretion was never greater than the intake, even when the subjects lost as much as 5 pounds in body weight during one week. From this it seemed probable that there was no actual tissue breakdown during these short periods of heightened metabolism, but that the loss of weight was due to the utilization of stored carbohydrate or fat. This does not mean, of course, that tissue breakdown would not occur if the drug should be given over longer periods, but probably when materials other than protein are available these are utilized first. Thus the assumption might be made that, as long as the protein intake is adequate, any reduction in body weight is not primarily at the expense of the tissue proteins.
...
3.The subjects excreted less nitrogen than they ingested, yet there were definite losses of body weight. Therefore, body proteins probably were not broken down. The output of urinary organic acid was not increased, thus indicating that the fats were completely burned without giving rise to acidosis."


If you believe research performed in the 1930"S on DNP, (especially when you SELECTIVELY mis-apply a quote to support BS) some likely supported by it's manufacturers, is evidence based compared to contemporary standards using isotopically labeled substrates, TRY AGAIN, LAMO!
 
Uncoupling oxidative phosphorylation is exactly how DNP works to reduce body weight/fat. It's not always a bad thing apparently:

MILD MITOCHONDRIAL UNCOUPLING AND BENEFICIAL EFFECTS OF DNP

Considerable evidence indicates that reactive oxygen species (ROS) are centrally implicated in a number of chronic and acute disorders. Of special interest is the case of several neurological diseases in which ROS participate in neuronal damage triggered by various types of insult. Among these conditions are Alzheimer’s, Parkinson’s and Huntington’s diseases, amyotrophic lateral sclerosis and AIDS dementia complex (for reviews, see 12, 13). Other acute insults leading to massive brain cell death that have been related to oxidative damage include hypoglycemia, neurological trauma, stroke, ischemia/reperfusion and epilepsy (12, 13).

The mitochondrial respiratory chain is the major source of intracellular ROS production under physiological and in many pathological conditions (14). ROS formation results from
monoelectronic reduction of oxygen, generating the super- oxide anion instead of water, which is increased under conditions of high electrochemical gradient across the mito- chondrial membrane (14). This suggests that mild mito- chondrial uncoupling, with a corresponding decrease in electrochemical gradient, might prevent excessive ROS for- mation and cellular oxidative damage in certain pathological conditions.

It has recently been demonstrated that rats treated intraperitoneally with DNP showed significant protection against brain damage caused by striatal injection of the N-methyl-D-aspartate (NMDA) receptor agonist quinolinic acid (15). Overactivation of NMDA receptors (by excessive glutamate or other agonists) leads to excitotoxic neuronal damage, involving increased intracellular calcium levels and increased mitrochondrial ROS production (16). Interestingly, rats administered DNP either 1 h before or 3 h following quinolinic acid infusion developed lesions that were 25% smaller than control animals (15). The mechanism of neuroprotection by DNP was subsequently found to be related to the decrease in mitochondrial Ca2þ levels and in ROS formation (17). These findings indicate that DNP confers protection against acute brain injury involving excitotoxic pathways by mechanisms that maintain mitochondrial function.

Another recent study showed that intraperitoneal admin- istration of DNP reduces the infarct volume by approximately 40% in a model of focal ischemia-reperfusion injury in rat brains (18). Interestingly, overexpression of human uncoup- ling protein 2 (UCP-2) in mice has been shown to reduce brain damage after experimental stroke and traumatic brain injury (19), suggesting that mitochondrial uncoupling might play a role in the prevention of damage. That same study also showed that neuronal death induced by oxygen and glucose deprivation in cultured cortical neurons was reduced in the presence of DNP under conditions that caused mild mito- chondrial uncoupling. In a different experimental paradigm, intraperitoneal injection of DNP in rats was shown to improve mitochondrial function, to attenuate oxidative damage and to increase white matter sparing in the contused spinal cord (20), suggesting that this might constitute a novel approach for the treatment of spinal cord contusion damage. Taken together, these studies suggest that, contrary to the uncontrolled and deleterious mitochondrial uncoupling that takes place in the presence of high concentrations of DNP, mild uncoupling induced by low doses of DNP may actually be beneficial in terms of reducing oxidative neuronal damage in different pathological conditions.

Accumulating evidence indicates that aging is, at least in part, linked to changes in mitochondrial metabolism and ROS formation. In this regard, it has been proposed that, similar to calorie restriction (21), mild mitochondrial uncoupling could increase lifespan by reduction of oxidative stress (14). Although more studies are certainly warranted to determine
whether this might be the case in higher organisms, it is interesting to note that DNP administration has recently been shown to prolong the lifespan of both Drosophila melanogaster and Saccharomyces cerevisiae (22, 23).

http://onlinelibrary.wiley.com/stor...sv&s=a34b96fbfb28c1a85d1ce5ecb86f797c5464bdc0
 
If you believe research performed in the 1930"S on DNP, some likely supported by it's manufacturers, is evidence based compared to contemporary standards using isotopically labeled substrates, TRY AGAIN, LAMO!

Well Jimbo, according to your previous post this one is an OPINION

Post up some research proving your claims or you're as full of shit you try to make everyone else out to be :)

Edit* don't forget the 2001 study at the top. Is that too from the 1930s? Or has the research changed since then? Apparently they found similar results as they did back then...
 
Let me put it to you this way: the studies performed mean more to me than your unsupported OPINION. Substantiate your OPINION with FACTS or you're just another BROSCIENCE peddler
 
Uncoupling oxidative phosphorylation is exactly how DNP works to reduce body weight/fat. It's not always a bad thing apparently:

MILD MITOCHONDRIAL UNCOUPLING AND BENEFICIAL EFFECTS OF DNP

Considerable evidence indicates that reactive oxygen species (ROS) are centrally implicated in a number of chronic and acute disorders. Of special interest is the case of several neurological diseases in which ROS participate in neuronal damage triggered by various types of insult. Among these conditions are Alzheimer’s, Parkinson’s and Huntington’s diseases, amyotrophic lateral sclerosis and AIDS dementia complex (for reviews, see 12, 13). Other acute insults leading to massive brain cell death that have been related to oxidative damage include hypoglycemia, neurological trauma, stroke, ischemia/reperfusion and epilepsy (12, 13).

The mitochondrial respiratory chain is the major source of intracellular ROS production under physiological and in many pathological conditions (14). ROS formation results from
monoelectronic reduction of oxygen, generating the super- oxide anion instead of water, which is increased under conditions of high electrochemical gradient across the mito- chondrial membrane (14). This suggests that mild mito- chondrial uncoupling, with a corresponding decrease in electrochemical gradient, might prevent excessive ROS for- mation and cellular oxidative damage in certain pathological conditions.

It has recently been demonstrated that rats treated intraperitoneally with DNP showed significant protection against brain damage caused by striatal injection of the N-methyl-D-aspartate (NMDA) receptor agonist quinolinic acid (15). Overactivation of NMDA receptors (by excessive glutamate or other agonists) leads to excitotoxic neuronal damage, involving increased intracellular calcium levels and increased mitrochondrial ROS production (16). Interestingly, rats administered DNP either 1 h before or 3 h following quinolinic acid infusion developed lesions that were 25% smaller than control animals (15). The mechanism of neuroprotection by DNP was subsequently found to be related to the decrease in mitochondrial Ca2þ levels and in ROS formation (17). These findings indicate that DNP confers protection against acute brain injury involving excitotoxic pathways by mechanisms that maintain mitochondrial function.

Another recent study showed that intraperitoneal admin- istration of DNP reduces the infarct volume by approximately 40% in a model of focal ischemia-reperfusion injury in rat brains (18). Interestingly, overexpression of human uncoup- ling protein 2 (UCP-2) in mice has been shown to reduce brain damage after experimental stroke and traumatic brain injury (19), suggesting that mitochondrial uncoupling might play a role in the prevention of damage. That same study also showed that neuronal death induced by oxygen and glucose deprivation in cultured cortical neurons was reduced in the presence of DNP under conditions that caused mild mito- chondrial uncoupling. In a different experimental paradigm, intraperitoneal injection of DNP in rats was shown to improve mitochondrial function, to attenuate oxidative damage and to increase white matter sparing in the contused spinal cord (20), suggesting that this might constitute a novel approach for the treatment of spinal cord contusion damage. Taken together, these studies suggest that, contrary to the uncontrolled and deleterious mitochondrial uncoupling that takes place in the presence of high concentrations of DNP, mild uncoupling induced by low doses of DNP may actually be beneficial in terms of reducing oxidative neuronal damage in different pathological conditions.

Accumulating evidence indicates that aging is, at least in part, linked to changes in mitochondrial metabolism and ROS formation. In this regard, it has been proposed that, similar to calorie restriction (21), mild mitochondrial uncoupling could increase lifespan by reduction of oxidative stress (14). Although more studies are certainly warranted to determine
whether this might be the case in higher organisms, it is interesting to note that DNP administration has recently been shown to prolong the lifespan of both Drosophila melanogaster and Saccharomyces cerevisiae (22, 23).

http://onlinelibrary.wiley.com/stor...sv&s=a34b96fbfb28c1a85d1ce5ecb86f797c5464bdc0

Oh so in this instance using MICE, RATS, and other invertebrates is GTG. Your a walking CONTRADICTION DD, LOL

Your next topic the moon is made of cheese!
 
Let me put it to you this way: the studies performed mean more to me than your unsupported OPINION. Substantiate your OPINION with FACTS or you're just another BROSCIENCE peddler

Bla, bla, bla, I havent the time to argue with idiots but the take home message should be DNP does NOT SELECTIVELY catabolize FAT, but also consumes, and may even prefer, PROTEIN and CARBS.

An excellent dietary aid for any BB no doubt, LMAO!
 
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Really well that comment is an opinion is completely void of any credible evidence! I would like to think when those like yourself posts an article to support one component of a debate, they would cite several to justify such an outlandish comment.

This is the type of crap that can be potentially DANGEROUS since many noobs visiting Meso could interpret that statement DNP is "safe" providing one uses high doses of Vitamin E, for it's antioxidant benefit.

I have no idea whether you did it on purpose or not, but here is my original post that you attempted to quote:

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.

You conveniently forgot to include the part I highlighted in bold - making it sound like I was suggesting antioxidants make DNP use safe.
AT NO POINT DID I MAKE ANY SUCH SUGGESTION.


I suggested antioxidant status has an impact on the cataracts side effect, NOT regarding the potential for death.
I also mentioned in a later post a study from the 1950s (reference I couldn't find) that clearly showed some evidence for my statement regardining antioxidatns for the cataracts side effect - I also admitted that the overall body of evidence was mixed.

Is this a common thing on meso - the inability of members to read posts properly?

Post any evidence a "researchers are studying DNP, a REGISTERED POISON, as a dietary aid, the suggestion is absolutely absurd!

And here is another example of how INCREDIBLE you are Dr Jim at reading what you want to read and closing your eyes for the rest.

I said that the MECHANISMS of dnp were being studied, not DNP itself and here it is:
http://www.sciencemag.org/content/early/2015/02/25/science.aaa0672.abstract

But I suppose you think its just a coincidence that they are looking into mitochondrial uncoupling for fat loss and DNP just HAPPENS to do the exact thing?
Yes just a coincidence, how absurd indeed!


Finally DNP is one of the worst dietary aids a BB could use bc it's use results in the catabolism of ALL potential energy sources, from stored Carbs as Glycogen, Protein as MUSCLE, and Fat from adipose tissue.

And now its your turn Jim, where is your evidence for this incorrect statement?
Because the EVIDENCE suggests that dnp is very much anti-catabolic especially compared to other options, like thyroid medication.

The rest of your post is the scientific equivalent of "dnp is poison bro!"

Yes, it's a metabolic poison in that it interferes with energy production, making it less efficient.
This is EXACTLY what makes it the most effective fat burner available.
This poisonous effect also has a host of BENEFITS, which I will quote Conciliator:

"benefits...including a reduction in mitochondrial free radical formation, improved mitochondrial stability, neuroprotection, protection in several models of cell injury (e.g. ischemia/reperfusion, contusion), slowing of telomeric senescence (e.g. extension of lifespan with DNP has now been shown in three different species), etc."
 
I have no idea whether you did it on purpose or not, but here is my original post that you attempted to quote:



You conveniently forgot to include the part I highlighted in bold - making it sound like I was suggesting antioxidants make DNP use safe.
AT NO POINT DID I MAKE ANY SUCH SUGGESTION.


I suggested antioxidant status has an impact on the cataracts side effect, NOT regarding the potential for death.
I also mentioned in a later post a study from the 1950s (reference I couldn't find) that clearly showed some evidence for my statement regardining antioxidatns for the cataracts side effect - I also admitted that the overall body of evidence was mixed.

Is this a common thing on meso - the inability of members to read posts properly?



And here is another example of how INCREDIBLE you are Dr Jim at reading what you want to read and closing your eyes for the rest.

I said that the MECHANISMS of dnp were being studied, not DNP itself and here it is:
http://www.sciencemag.org/content/early/2015/02/25/science.aaa0672.abstract

But I suppose you think its just a coincidence that they are looking into mitochondrial uncoupling for fat loss and DNP just HAPPENS to do the exact thing?
Yes just a coincidence, how absurd indeed!




And now its your turn Jim, where is your evidence for this incorrect statement?
Because the EVIDENCE suggests that dnp is very much anti-catabolic especially compared to other options, like thyroid medication.

The rest of your post is the scientific equivalent of "dnp is poison bro!"

Yes, it's a metabolic poison in that it interferes with energy production, making it less efficient.
This is EXACTLY what makes it the most effective fat burner available.
This poisonous effect also has a host of BENEFITS, which I will quote Conciliator:

"benefits...including a reduction in mitochondrial free radical formation, improved mitochondrial stability, neuroprotection, protection in several models of cell injury (e.g. ischemia/reperfusion, contusion), slowing of telomeric senescence (e.g. extension of lifespan with DNP has now been shown in three different species), etc."

Ripped, Jim is pretty good at seeing what he WANTS to see and not what's actually there. He'll put words into your mouth then argue against something you never said. I can link you to the thread where this happened last week. He took my statement about carbohydrates/glucose being rarely stored as fat and argued I had said fatty acids cannot be broken down to form glucose. Be careful with this wily character indeed
 
Ripped, Jim is pretty good at seeing what he WANTS to see and not what's actually there. He'll put words into your mouth then argue against something you never said. I can link you to the thread where this happened last week. He took my statement about carbohydrates/glucose being rarely stored as fat and argued I had said fatty acids cannot be broken down to form glucose. Be careful with this wily character indeed

I've noticed from previous arguments I've had on other boards that this trait is very common among people who know that they are losing the debate.
The minute they realise that someone is debating pretty well against them, they resort to misquoting, misinterpretation, etc in the hope that viewers are too stupid to look back and follow the thread accurately.

Its weirdly satisfying to know someone is having to resort to such measures :)
 
Exactly WHERE did I say that effectiveness and safety were the same thing hmm?
I said that the study showed dnp to be SAFER than some compounds (fat loss drugs now banned) and more EFFECTIVE then others (thyroid medication).

Do I really need to give an English lesson on how "/" is used?

Don't blame me for your inability to interpret my posts correctly.

The forward slash is not used in formal English. Now that that's out of the way, we'll look at your inappropriate use of the forward slash.

The forward slash is sometimes used informally as a substitute for the word "or," and you say that's how you were using it.

Your statement is below. You were comparing DNP to thyroid hormone, with "other obesity drugs" thrown in as an afterthought.


"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"

If the forward slash was used to make a comparison as you claim, your statement actually reads "...the conclusion that dnp was the safer [OR] more effective option."

The statement "the conclusion that dnp was the safer or more effective option" doesn't make sense as the reader is left wondering whether DNP is safer than thyroid hormone, or whether DNP more effective than thyroid hormone.

But your intent wasn't to use a grammatically ambiguous statement in order to give the reader a choice. Your intent was to mislead the reader into believing that the study's author said DNP was both safer AND more effective than thyroid hormone.

Now that we've established that you don't know how to properly use punctuation to articulate your points, we're still left with the fact that you have not provided evidence that supports your assertion that DNP is safer than thyroid hormone OR ANY OTHER anti-obesity drug.

CBS
 
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