2,4-DiNitroPhenol [DNP]

Heretic

New Member
Credit to the gods that wrote this... :)

HOW TO NOT FUCK UP DNP:

Since some guys have been playing around and disrespecting DNP and then griping to the forums about the painful results, we need to make this VERY specific and VERY correct so that people won't keep jumping for DNP out of curiosity, or without the willpower they need to operate this respondibly. So here are my experienced guidelines to using it the RIGHT way.

FIRST GUIDLINE: Dosing. Use ONLY 200mg a day for the first four days. I don't care that you don't "feel" anything yet and you wanna bump it up. DNP accumulates in the body, and not "feeling" something means NOTHING. It's there, and it's working (the effect on metabolism begins within two hours of the first dose!). Four days will let you test your tolerance: do you have an allergy? Does it give you a rash? etc.
Only after those four days do you bump it up, by 200mg a day. The average dose is 400-600/day, and more than that gets a little severe. A full gram is the highest dose I've heard anyone use. I've used that much, and it's hell. I like to stay around 600 a day, which is HOT but safe and effective. Take caps even hours apart through the day, ending about 4-5 PM.

SECOND GUIDLINE...How to eat on DNP. This is purely personal experience, because some guys like to carb-deplete *before* using DNP (then eat carbs as usual while on), and other guys like a low-carb approach throughout. Both are fine. Using DNP is the only time that fructose is a desireable cutting carb, because it keeps the liver replentished. That reduces lethargy and spares muscle.
Be aware that eating high-carb foods WILL increase the heat sensation within an hour, and last about 2 hours. That means don't eat carbs before bed unless you want those night sweats to be even WORSE.
Personally, I ate whatever the hell I wanted! IHOP, chinese, fajitas...Yes, I burned hot, but I still lost 1.5 pounds every 2 days. Keep protein HIGH for muscles' sake, and try it yourself.

Foods I suggest including:
Blueberry yogurt. Blueberries are excellent antioxidants, and yogurt cultures help with digestive function, gas, and stool consistency (disgustingly soft stools are common during DNP).
Oregano-based foods. Oregano is perhaps one of the most potent antioxidants around,a nd one spoonful counts as a vegetable serving. See this article
Pineapple - I've found that pineapple helps alleviate those "DNP Blues". The fructose helps, and pineapple enzymes aid in protein digestion.
V8 - one 12-ounce can supplies six servings of veggies, concentrated as an excellent source of antioxidants, lycopene, and recovery of electrolytes.
Oatmeal - high-fiber foods are necessary. You'll find out why around, oh, day 5 or so. Trust me.


THIRD GUIDELINE...Supplements and DNP. I suggest:
ECA - DNP is not a stimulant. To keep energy high and aid in fat loss, use an ECA. Some advisors suggest that regular ephedrine is preferable to norephedrine because of the more direct "hit" of energy.
Prohormones - perfectly fine on DNP. I used 1-AD just to help keep strength and muscle up, and it worked fine. No problems here. You won't GROW muscle on DNP, but it'll help with strength and protection.
Obvious stuff - multivitamin, ZMA, etc.
Biotest PowerDrive - No, I'm not pimping Biotest. But PowerDrive is an excellent pre-workout mixture that actually works. Plus it's low-carb (only 15 calories total), so it won't cause carb-heat in the middle of your workout.

Antioxidants - I'm giving my own personal list, and why I use them:
Alpha Lipoic Acid - aids in fat management and blood sugar, and an excellent antioxidant.
Grape seed extract
Syntrax Radox
Green Tea
Inositol - mood enhancement, antioxidant, and muscle support. 1 gram/3x day
Ellagic acid - protects cell DNA/RNA from damage by free radicals, and may even atack cancerous cells. 400mg/twice a day
Fruit antioxidants - beyond-a-century's powder of high-potency natural fruit anti's. 1 gram, 2-3x day.
Trimethylglyceine - antioxidant, helps move fat and blood lipids into the liver and out of the body. 500mg, 2x day.
Vitamins E and C

Supplements NOT to use:
Any medications that suppress energy. No allergy meds, antidepressants, muscle relaxers, or beta blockers. DNP will have you low as it is; don't worsen your body's energy by taking something that suppresses you further.

DRUGS - Sheesh, you'd think I wouldn't have to mention this, but two idiots in particular (right here on this forum) recently affirmed that some people still just don't get it. NO alcohol (not even "moderate"), NO ecstasy, NO GHB, etc. If you don't have the willpower to forego these habits, DNP is not for you.

Syntrax Swole - a personal discovery. I tried Swole while on DNP...once. Two hours of hell, feeling inside-out.

FOURTH GUIDELINE...working out on DNP. Keep lifting short, 30-40 minutes. DNP works very well, causing your body to use 150% or more the calories per action you'd normally use. That means DON'T try to repeat your usual workouts. Drop to moderate weights, 8-12 reps, not to failure, and with plenty of walking rest between sets. You are NOT going to grow muscle on DNP, so don't use your usual heavy routine. Since DNP can cause light-headedness and heat dizzyness, you have my permission to skip squats in favor of leg presses this time.

Cardio is a controversial one. My advice - do NOT do cardio on high doses of DNP (600mg or more). It's dangerous and counterproductive. Below that amount, some cardio is fine, but keep it to 20 minutes and not at full-gallop. Remember, DNP will drain water from your quickly, causing you to leech out minerals, vitamins, and salts. Don't overdo it.

During exercise, consume at least 1 liter of water per 30 minutes of work, whether you're thirsty or not. DNP is evil in the way it blunts thirst, while at the same time doing the cruel trick of bloating your body with water WHILE dehydrating you from water in your organs. MAKE yourself drink. Always folllow DNP exercise with antioxidants, carbs, and this is a good time to use your multivitamin.

Don't feel embarrassed about poor workouts. Just this morjning I did a workout with a whopping nine sets (wimp!) before calling it quits. Listen to your body, and let it tell you when enough's enough; don't guage workouts by what you *usually* can do otherwise.

Here's my research. This is AMAZING! Not only has not a single test found it to be carcinogenic, but test after tyest after test find that DNP actually ATTACKS cancer cells, and helps anti-cancer medications work better, and helps anti-leukemia medications work without destroying cell DNA, and suppresses tumor growth by 20-50%. The summaries are all right here, friends. Karma me up!

DNP is Ames negative, and does not promote tumors. See for yourself at http://toxnet.nlm.nih.gov/

http://www.epa.gov/ttn/atw/hlthef/dinitrop.html (2,4-Dinitrophenol | Technology Transfer Network Air Toxics Web site | US EPA) reports on health risks. While there have not been human studies, animal studies found no cancers caused by DNP administration. It is considered a toxin because it causes nausea, sweating, and weight loss.

Cyberiron.com reports on halth risks from external exposue. In other words, don?t get it in your eyes, or on your skin if you?re allergic. Pretty elementary stuff.

http://www.ebec2000.com/abstracts/056.htm This animal study documents a 64% increase in metabolism. "These findings confirm that DNP effectively increases metabolic rate..." Duh.

Biosource A PDF file about an antidote to DNP.

http://www.boehringer-ingelheim.es/...glesa/cap13.htm finds that DNP did not activate liver enzymes (MAT) associated with liver damage

"Comparative study of toxicity of 4-nitrophenol and 2,4-dinitrophenol in newborn and young rats." Koizumi M, Yamamoto Y, Ito Y, Takano M, Enami T, Kamata E, Hasegawa R. Division of Risk Assessment, National Institute of Health Sciences, 1-18-1 Kamiyoga, Setagaya-ku, Tokyo 158-8501, Japan. This study found that DNP can induce death in overdosed amounts, but that up to that point no toxicity was evident, nor were there any abnormalities in physical development.

"Phenol toxicity and conjugation in human colonic epithelial cells." Pedersen G, Brynskov J, Saermark T. Dept of Medical Gastroenterology, Herlev University Hospital, Copenhagen, Denmark.. This study found that DNP has a toxic effect on cells of the colon, with "toxic" defined in two ways: first, it interfered with metabolism (this we know?it?s the intended effect of DNP users!) and second, it interfered with bowel inflammation (not a health risk. This is caused by osmotic effect, with the worst results being softened stools and gas).

"Mechanisms of bacterial resistance to macrolide antibiotics." Nakajima Y. Division of Microbiology, Hokkaido College of Pharmacy, 7-1 Katsuraoka-cho, Otaru, Hokkaido 047-0264, Japan. This study found that antibiotic-resistant bacteria could be thwarted with DNP. "the extent of the accumulated drug in a resistant cell increases as much as that in a susceptible cell in the presence of an uncoupling agent such as?2,4-dinitrophenol (DNP)."

"Absence of Crabtree effect in human melanoma cells adapted to growth at low pH: reversal by respiratory inhibitors." Burd R, Wachsberger PR, Biaglow JE, Wahl ML, Lee I, Leeper DB. Departments of Radiation Oncology, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA. Check this out?DNP actually helps make melanoma tumors easier to attack by increasing ratio of oxygen consumption to lactic acid production, while glycolysis remains the same. "Therefore, tumor acute acidification and oxygenation can be achieved by exposure?"


"New insights in the cellular processing of platinum antitumor compounds, using fluorophore-labeled platinum complexes and digital fluorescence microscopy."
Molenaar C, Teuben JM, Heetebrij RJ, Tanke HJ, Reedijk J. Department of Molecular Cell Biology, Leiden University Medical Centre, The Netherlands. DNP is used as a control in tests of antitumor cells because it does NOT bind to cell DNA, nor promote tumors, yet its staining abilities enable tracking of the uptake of antitumor drugs.

Specific inhibition of breast cancer cells by antisense poly-DNP-oligoribonucleotides and targeted apoptosis." Ru K, Taub ML, Wang JH. Department of Biochemistry, State University of New York, Buffalo 14260-3000, USA Are you ready for this? DNP actually INHIBITS (!!!) breast cancers! Yes, not only does it NOT promote cancers, it?s being recognized as a cancer-fighter/blocker. "Two membrane-permeable and RNase-resistant antisense poly-2'-O-(2,4-dinitrophenyl)-oligoribonucleotides (poly-DNP-RNAs) have been synthesized as inhibitors of human breast cancer?fluorescence assay indicates that the targeted antisense inhibition by poly-DNP-RNAs leads to apoptosis of SK-Br-3 cells but does not affect nontumorigenic MCF-10A cells. The control poly-DNP-RNAs with random or sense nucleotide sequence are completely inactive." Plain English? DNP can be synthesized as an anti-cancer compound, because tests show that it blocks mutagens but does NOT affect non-mutagenic (healthy) cells, and has no RNA effects on them.

"Heat shock protein induction by certain chemical stressors is correlated with their cytotoxicity, lipophilicity and protein-denaturing capacity." Neuhaus-Steinmetz U, Rensing L. Institute of Cell Biology, Biochemistry and Biotechnology, NW II University of Bremen, Germany. The thermic effect of DNP induces protein synthesis (heat shock protein, or HSP, synthesis). In fact, it?s quite GOOD at it: "ASA, DNP and CCCP induced HSP at lower concentrations than substances with a similar lipophilicity?"

"Comparative effects of the metabolic inhibitors 2,4-dinitrophenol and iodoacetate on mouse neuroblastoma cells in vitro." Andres MI, Repetto G, Sanz P, Repetto M.
National Institute of Toxicology, Seville, Spain. In this study, DNP?s observed effect was an increase in metabolism (duh!), while the other toxins compared to it had harmful in vitro effects but no increase in metabolism.

"Inhibition of uncoupled respiration in tumor cells. A possible role of mitochondrial Ca2+ efflux." Gabai VL.Medical Radiology Research Center, Russian Academy of Medical Sciences, Obninsk. DNP not only does not cause tumors, but it inhibited their respiration by 20-25% compared to controls.

"Amsacrine-induced lesions in DNA and their modulation by novobiocin and 2,4-dinitrophenol." Shibuya ML, Buddenbaum WE, Don AL, Utsumi H, Suciu D, Kosaka T, Elkind MM. Department of Radiology and Radiation Biology, Colorado State University, Fort Collins 80523. In this study, researchers found that DNP abrogates?or disrupts?cytotoxicity in hamsters (using cancerous cells). They expected to find that DNP would interfere with anticancer treatments, but instead found that DNP increased their effects. They state, though, that they cannot claim a proven effect of DNP on anticancer treatments yet, although they do agree that treatment with DNP actually enhanced the effects of the DNA regenerative therapy of anticancer chemotherapy.

"Induction of endonucleolytic DNA cleavage in human acute myelogenous leukemia cells by etoposide, camptothecin, and other cytotoxic anticancer drugs: a cautionary note." Kaufmann SH. Oncology Center, Johns Hopkins Hospital, Baltimore, Maryland 21205. The authors warn that certain anti-leukemia drugs resulted in "extensive DNA degradation." BUT (good ol? DNP to the rescue!), "Preincubation with dinitrophenol abolished the effect?"

"[Dependence of the nature of the action of metabolic inhibitors on ribosomal RNA synthesis in Ehrlich ascites carcinoma cells on cell integrity]" [Article in Russian] Akhlynina TV, Buzhurina IM, Panov MA, Rozovskaia IA, Chernaia NG. DNP actually inhibits the synthesis of RNA in carcinoma cells. In other words, it helps cancerous cells commit suicide by neutering themselves. "Ribosomal RNA (rRNA) synthesis in the intact Ehrlich ascite carcinoma cells is selectively inhibited by papaverin (ED50 = 0.01 mM), 2,4-dinitrophenol (DPN; ED50 = 5 microM), and actinomycin D (ED50 = 0.1 microgram/ml)."

"Autocatabolism of surface macromolecules shed by human melanoma cells." Bystryn JC, Perlstein J. Cancer Res 1982 Jun;42(6):2232-7. This study finds that DNP helps melanoma cells die (autocatabolize) while other cells are unaffected.

http://www.geocities.com/byggdegstor/dnpforside - tons of research, including medical studies. Excerpts:

DNP does not cause liver damage: "Their analyses demonstrate, beyond a doubt, that the liver does not suffer any damage in the course of dinitro treatment." (Biological Study of Dinitro Drugs in Humans By Dr. Jacques Bell. Bell, Jacques. 1939. Etude biologique des produits dinitres chez l'homme. Medecine. 19:749-54. Translation ? 1996 Robert Ames)

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

"Dinitrophenol has almost no action on the blood cholesterol. (Grant and Schube)."

"it doesn't seem that dinitrophenol at usual clinical doses is likely to harm the kidneys."

"Dinitrophenol is remarkable for its absence of effect on the cardio-vascular system...dinitrophenol is absolutely devoid of toxicity for the heart."

"Dinitrophenol does not attack cell tissue albumin and does not determine the fat loss to the expense of the muscles, contrary to thyroxine."

"dinitrophenol offers this precious advantage that the cessation of its use at the slightest appearance of signs indicating an imminence of intoxication results immediately in the arrest of those symptoms." (Professor Pouchet)."


Interestingly, one medical theory on a health ADVANTAGE of DNP is that the slight increase in thermogenic temperature simulates the fever a body induces during a viral attack. The body increases itsheat to protect organs but kill viruses, and some theorize that DNP can do the same thing, thus killing viruses in the body. In this mechanism, DNP may have an immune-enhancing effect.
 
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Would this be the place to put a DNP log, or should it have its own thread? I've been keeping one with the intent to share but I'm not familiar with the board and posting etiquette here.
 
I see on your profile that you will provide on line coaching that's scary,
you have very little or no knowledge please keep you advice to yourself before you seriously hurt someone.

don’t make stupid comments. front load to get saturation level to where it would be several days in because of its half-life. Stay away from chemicals you know nothing about/don’t do enough research on i guess. Have a spread sheet somewhere i’m going to post some more.

edit: any other kid getting triggered by my post? should i not post my experience let me know in DM[/QUOTE]
 
[OA] 2,4 Dinitrophenol as Medicine

In the sanctity of pure drug discovery, objective reasoning can become clouded when pursuing ideas that appear unorthodox, but are spot on physiologically. To put this into historical perspective, it was an unorthodox idea in the 1950's to suggest that warfarin, a rat poison, could be repositioned into a breakthrough drug in humans to protect against strokes as a blood thinner. Yet it was approved in 1954 as Coumadin((R)) and has been prescribed to billions of patients as a standard of care.

Similarly, no one can forget the horrific effects of thalidomide, prescribed or available without a prescription, as both a sleeping pill and "morning sickness" anti-nausea medication targeting pregnant women in the 1950's. The "thalidomide babies" became the case-in-point for the need of strict guidelines by the U.S. Food & Drug Administration (FDA) or full multi-species teratogenicity testing before drug approval. More recently it was found that thalidomide is useful in graft versus host disease, leprosy and resistant tuberculosis treatment, and as an anti-angiogenesis agent as a breakthrough drug for multiple myeloma (except for pregnant female patients).

Decades of diabetes drug discovery research has historically focused on every possible angle, except, the energy-out side of the equation, namely, raising mitochondrial energy expenditure with chemical uncouplers. The idea of "social responsibility" allowed energy-in agents to be explored and the portfolio is robust with medicines of insulin sensitizers, insulin analogues, secretagogues, SGLT2 inhibitors, etc., but not energy-out medicines.

The primary reason?

It appeared unorthodox, to return to exploring a drug platform used in the 1930s in over 100,000 obese patients used for weight loss. This is over 80-years ago and prior to Dr Peter Mitchell explaining the mechanism of how mitochondrial uncouplers, like 2,4-dinitrophenol (DNP) even worked by three decades later in 1961. Although there is a clear application for metabolic disease, it was not until recently that this platform was explored for its merit at very low, weight-neutral doses, for treating insidious human illnesses and completely unrelated to weight reduction.

It is known that mitochondrial uncouplers specifically target the entire organelle's physiology non-genomically. It has been known for years that many neuromuscular and neurodegenerative diseases are associated with overt production of reactive oxygen species (ROSs), a rise in isoprostanes (biomarker of mitochondrial ROSs in urine or blood) and poor calcium (Ca(2+)) handing. It has also been known that mitochondrial uncouplers lower ROS production and Ca(2+) overload.

There is evidence that elevation of isoprostanes precedes disease onset, in Alzheimer's Disease (AD). It is also curious, why so many neurodegenerative diseases of known and unknown etiology start at mid-life or later, such as Multiple Sclerosis (MS), Huntington Disease (HD), AD, Parkinson Disease, and Amyotrophic Lateral Sclerosis (ALS).

Is there a relationship to a buildup of mutations that are sequestered over time due to ROSs exceeding the rate of repair?

If ROS production were managed, could disease onset due to aging be delayed or prevented?

Is it possible that most, if not all neurodegenerative diseases are manifested through mitochondrial dysfunction?

Although DNP, a historic mitochondrial uncoupler, was used in the 1930s at high doses for obesity in well over 100,000 humans, and so far, it has never been an FDA-approved drug. This review will focus on the application of using DNP, but now, repositioned as a potential disease-modifying drug for a legion of insidious diseases at much lower and paradoxically, weight neutral doses.

DNP will be addressed as a treatment for "metabesity", an emerging term related to the global comorbidities associated with the over-nutritional phenotype; obesity, diabetes, nonalcoholic steatohepatitis (NASH), metabolic syndrome, cardiovascular disease, but including neurodegenerative disorders and accelerated aging. Some unexpected drug findings will be discussed, such as DNP's induction of neurotrophic growth factors involved in neuronal heath, learning and cognition.

For the first time in 80's years, the FDA has granted (to Mitochon Pharmaceutical, Inc., Blue Bell, PA, USA) an open Investigational New Drug (IND) approval to begin rigorous clinical testing of DNP for safety and tolerability, including for the first ever, pharmacokinetic profiling in humans.

Successful completion of Phase I clinical trial will open the door to explore the merits of DNP as a possible treatment of people with many truly unmet medical needs, including those suffering from HD, MS, PD, AD, ALS, Duchenne Muscular Dystrophy (DMD), and Traumatic Brain Injury (TBI).

Geisler JG. 2,4 Dinitrophenol as Medicine. Cells 2019;8. 2,4 Dinitrophenol as Medicine
 
I think ppl talking about half lives of dnp, saturation doses, and frontloading massive doses of this drug need to think about the fact that everyones body dont act exactly the same and metabolize drugs at exactly the same rate like u can punch numbers in a calculator and come up with the exact measurment of how many mgs is in there system. One person might be able to take 1500mgs the first day and be fine dosing a smaller dose after that. But another person might die from that exact same protocol. Its irresponsible to post shit like that knowing its getting read by ppl that are new to the drug and might try what u are saying and wind up hurting themselves or even dying. Dnp already burns fat faster than anything else you're gonna do at a lower safe dose. Its a huge shortcut to your goal even at a safe dose. No need to risk your life to save a couple days time in reaching your target weight. New ppl to dnp should start at a low dose and stay at that same dose for a week b4 upping it and gauging how your body handles the drug. Then u can slowly raise it and experiment with what u can handle. Nobody's body is the same so dont think a chart or a calculator can tell u how your body is metabolizing a drug becuz it cant. Its a tool to use to help u along your way but its not an exact measurment of whats in u. Your levels could be much higher or much lower depending on your body and many other factors. Fear mongering and misinformation of this drug causes ppl to either never wanna touch this awesome drug but also causes ppl to be reckless and not respect the actual dangers that this drug poses. Basically all drugs can be helpful or harmful depending on how u use them. Be safe and educate yourselves with dnp so we dont lose access to this drug any more than we already have ppl.
 
I think ppl talking about half lives of dnp, saturation doses, and frontloading massive doses of this drug need to think about the fact that everyones body dont act exactly the same and metabolize drugs at exactly the same rate like u can punch numbers in a calculator and come up with the exact measurment of how many mgs is in there system. One person might be able to take 1500mgs the first day and be fine dosing a smaller dose after that. But another person might die from that exact same protocol. Its irresponsible to post shit like that knowing its getting read by ppl that are new to the drug and might try what u are saying and wind up hurting themselves or even dying. Dnp already burns fat faster than anything else you're gonna do at a lower safe dose. Its a huge shortcut to your goal even at a safe dose. No need to risk your life to save a couple days time in reaching your target weight. New ppl to dnp should start at a low dose and stay at that same dose for a week b4 upping it and gauging how your body handles the drug. Then u can slowly raise it and experiment with what u can handle. Nobody's body is the same so dont think a chart or a calculator can tell u how your body is metabolizing a drug becuz it cant. Its a tool to use to help u along your way but its not an exact measurment of whats in u. Your levels could be much higher or much lower depending on your body and many other factors. Fear mongering and misinformation of this drug causes ppl to either never wanna touch this awesome drug but also causes ppl to be reckless and not respect the actual dangers that this drug poses. Basically all drugs can be helpful or harmful depending on how u use them. Be safe and educate yourselves with dnp so we dont lose access to this drug any more than we already have ppl.
Very true give this guy a cookie
 
[OA] [DNP] Nonalcoholic Fatty Liver Disease as a Nexus of Metabolic and Hepatic Diseases

However, it is possible to create compounds that will specifically, directly, and safely increase hepatic mitochondrial energy expenditure. We previously demonstrated the efficacy of low doses of the mitochondrial protonophore, 2,4-dinitrophenol (DNP), in preventing steatosis in high-fat-fed rats, with decreased PKCε activation and improved hepatic insulin signaling and hepatic insulin action (Samuel et al., 2004).

Though DNP has been used clinically in the past, this compound is not safe for clinical use due to the low therapeutic index. If DNP is modified with a methyl-ester (ME), it remains inactive until activated within hepatocytes. This increases the therapeutic index of DNP-ME 50-fold over DNP.

DNP-ME increased hepatic mitochondrial fat oxidation by ∼60% and reversed hypertriglyceridemia, hepatic and peripheral insulin resistance, and hyperglycemia in rat models of NAFLD and T2D (Perry et al., 2013). DNP-ME did not alter cellular energy charge, nor did it lead to activation of AMPK; its actions are likely due purely to the induced energy inefficiency of the mitochondria exclusively in liver.

Furthermore, correction of liver and muscle insulin resistance was associated with marked reductions in liver and skeletal muscle DAG content with decreased activation of PKCε and PKCθ, respectively. The latter improvements in muscle DAG-PKCθ activity could be attributed to DNP-ME increased in hepatic fat oxidation, leading to reduced VLDL production, reduced plasma triglycerides, and decreased fat delivery to skeletal muscle. Importantly, these improvements occurred independently of any changes in body weight, inflammatory mediators, FGF-21, adiponectin, or hepatic ceramide content (Perry et al., 2013).

Similar effects were seen with a second liver-targeted mitochondrial uncoupling agent, controlled release mitochondrial protonophore (CRMP) (Perry et al., 2015b). Combining DNP into a cellulose-based matrix extends the time required for absorption, resulting in relatively stable plasma DNP concentrations after oral administration. CRMP increases the therapeutic index by 500-fold and, as with DNP, lowers hepatic and muscle lipid (DAG) content and improves insulin hepatic and peripheral sensitivity in numerous rodent models of NAFLD/NASH (Perry et al., 2015b).

While CRMP is not “liver specific” by design, the first-pass hepatic uptake largely confines its actions to the liver. CRMP increased the rate of hepatic tricarboxylic cycle flux without changing whole-body energy balance or mitochondrial activity in other tissues. Like DNP-ME, the reductions in plasma triglyceride and improvement in skeletal muscle activity were attributed to CRMP-induced increases in hepatic mitochondrial fatty acid oxidation, resulting in decreased VLDL production and hypertriglyceridemia and reduced delivery and uptake of fat by the skeletal muscle. In rats fed an MCD diet, CRMP treatment reduced hepatic inflammation and reversed hepatic fibrosis.

CRMP has also recently been shown to reverse hepatic steatosis and hepatic and peripheral insulin resistance in an A-ZIP/F1 mouse model of severe lipodystrophy (Abulizi et al., 2017). CRMP also decreased several markers of liver inflammation and the unfolded protein response in this lipodystrophic mouse. Furthermore, CRMP, like DNP-ME, reversed hepatic insulin resistance and diabetes with reductions in hepatic DAG-PKCε activity and hepatic acetyl-CoA content, offering further support for the roles of these metabolites in causing hepatic insulin resistance and increased hepatic gluconeogenesis, respectively, in T2D.

Taken together, these studies offer proof of concept in support of the development of novel liver-targeted mitochondrial uncoupling agents for the treatment of NAFLD, NASH, and T2D.

Samuel VT, Shulman GI. Nonalcoholic Fatty Liver Disease as a Nexus of Metabolic and Hepatic Diseases. Cell metabolism 2018;27:22-41. https://www.sciencedirect.com/science/article/pii/S1550413117304874
 
Curious if anyone knows anything about niclosamide ethanolamine. Its a mitochondrial uncoupler used in studies as a cure for type 2 diabetes and other similar things dnp is used for. But ive read its supposed to be much safer and more effective but i haven't seen any studies on weight loss but im thinking that could possibly be an effect of it as well. Just wondering if anyone has any knowledge about it they can share as it sounds interesting. if we can find something that works as good as dnp for fat loss without or at least less dangers would be a good thing for a lot of ppl.
 
I think ppl talking about half lives of dnp, saturation doses, and frontloading massive doses of this drug need to think about the fact that everyones body dont act exactly the same and metabolize drugs at exactly the same rate like u can punch numbers in a calculator and come up with the exact measurment of how many mgs is in there system. One person might be able to take 1500mgs the first day and be fine dosing a smaller dose after that. But another person might die from that exact same protocol. Its irresponsible to post shit like that knowing its getting read by ppl that are new to the drug and might try what u are saying and wind up hurting themselves or even dying. Dnp already burns fat faster than anything else you're gonna do at a lower safe dose. Its a huge shortcut to your goal even at a safe dose. No need to risk your life to save a couple days time in reaching your target weight. New ppl to dnp should start at a low dose and stay at that same dose for a week b4 upping it and gauging how your body handles the drug. Then u can slowly raise it and experiment with what u can handle. Nobody's body is the same so dont think a chart or a calculator can tell u how your body is metabolizing a drug becuz it cant. Its a tool to use to help u along your way but its not an exact measurment of whats in u. Your levels could be much higher or much lower depending on your body and many other factors. Fear mongering and misinformation of this drug causes ppl to either never wanna touch this awesome drug but also causes ppl to be reckless and not respect the actual dangers that this drug poses. Basically all drugs can be helpful or harmful depending on how u use them. Be safe and educate yourselves with dnp so we dont lose access to this drug any more than we already have ppl.

Very very benefical thank you. Bit of a read lol but much appreciated
 
We have a 25 year old, 45kg, girl who says she only took 2 tablets. The authors admit to not knowing how much DNP was in each tab, which means she never told them and the dose that caused the reaction remains unknown. Caution is advised about taking any of this as fact because we know self-reporting within the literature is notoriously inaccurate. Especially coming from this group - a young woman suffering with body dysmorphia.

If we're going to speculate then, knowing the UK market as I do, I would guess that the dose around 100-250mg per tab. That translates to 4.4-11.1mg/kg. The high end of that range will absolutely generate the reaction seen here. The low end might do if it's the starting point. So despite my skepticism about the self-reported nature of the dose, it absolutely would not surprise me that this dosing range caused that reaction.

The UK for whatever reason is a breeding ground for dumbass DNP users. This seems to fall into that camp based on the limited facts we have. She clearly had no idea that the dose was way too high for her specifically. I don't have sympathy for folks who use potentially dangerous drugs without doing some extensive research to begin with.
She didnt bother reading the directions
 
there is a pretty good dnp excel calculator an old timer made on another forum maybe it would be worthwhile to post it here i haven’t been here in a long time i’ll try an search it out here but google dnp calculator he has the half life formulated in cells and you could play with the doses, but to that question there is a noticeable difference. but that’s only for blasts i really wouldn’t recommend anyone doing blasts i’ve just experiment over the years many times with blasts and its killed literally 6 weeks off a diet before a show.
“Killed literally 6weeks of diet off a show?”
you could have killed yourself and then, I wonder how you would have placed then. I know that this is where people are suppose to come and feel comfortable taking about the experience, and/or about asking questions, however, I feel there is an exception to that rule. Which is dnp, just because you managed to cheat death by using a method that your mind was able to make sense of. Dnp use is not the same the use of AAS. Because of the hightened risk involved(death) it need to be treated with a different level of finesse, respect, and responsibility. Any disregard for those things by an individual, tells me, that person is not ready to deal with the consequence, shall any arise.
 
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30+ shows later, here i am. you mad?
No not at all, I don’t have a beef with you, but I do agree with what everyone has said, all it takes is for one person, to come on here, read about your irresponsible attempt at winning a contest, because they thought they can gamble with your method, and they end up dead. The fact that You remain so cavalier about it is really sad. No one said that you were an idiot, at least not in the beginning, they are all saying that the fact that you went over and above to post irresponsible activity out in the open, is stupid.
 
No not at all, I don’t have a beef with you, but I do agree with what everyone has said, all it takes is for one person, to come on here, read about your irresponsible attempt at winning a contest, because they thought they can gamble with your method, and they end up dead. The fact that You remain so cavalier about it is really sad. No one said that you were an idiot, at least not in the beginning, they are all saying that the fact that you went over and above to post irresponsible activity out in the open, is stupid.

Sorry, do you want a hug now or later friend?

@rbj people aren't trying to be a dick u have to realize that young kids could come here an see what u did an think its ok an safe especially when u brag about ur 30+ shows therw are young men out here who will see this an think its ok an its not ur words carry consequences an u should be a little more considerate when u post dangerous things in the most famous steroid forum in the world...its called harm reduction for a reason there is always bop tho
 
[OA] [DNP] Nonalcoholic Fatty Liver Disease as a Nexus of Metabolic and Hepatic Diseases

However, it is possible to create compounds that will specifically, directly, and safely increase hepatic mitochondrial energy expenditure. We previously demonstrated the efficacy of low doses of the mitochondrial protonophore, 2,4-dinitrophenol (DNP), in preventing steatosis in high-fat-fed rats, with decreased PKCε activation and improved hepatic insulin signaling and hepatic insulin action (Samuel et al., 2004).

Though DNP has been used clinically in the past, this compound is not safe for clinical use due to the low therapeutic index. If DNP is modified with a methyl-ester (ME), it remains inactive until activated within hepatocytes. This increases the therapeutic index of DNP-ME 50-fold over DNP.

DNP-ME increased hepatic mitochondrial fat oxidation by ∼60% and reversed hypertriglyceridemia, hepatic and peripheral insulin resistance, and hyperglycemia in rat models of NAFLD and T2D (Perry et al., 2013). DNP-ME did not alter cellular energy charge, nor did it lead to activation of AMPK; its actions are likely due purely to the induced energy inefficiency of the mitochondria exclusively in liver.

Furthermore, correction of liver and muscle insulin resistance was associated with marked reductions in liver and skeletal muscle DAG content with decreased activation of PKCε and PKCθ, respectively. The latter improvements in muscle DAG-PKCθ activity could be attributed to DNP-ME increased in hepatic fat oxidation, leading to reduced VLDL production, reduced plasma triglycerides, and decreased fat delivery to skeletal muscle. Importantly, these improvements occurred independently of any changes in body weight, inflammatory mediators, FGF-21, adiponectin, or hepatic ceramide content (Perry et al., 2013).

Similar effects were seen with a second liver-targeted mitochondrial uncoupling agent, controlled release mitochondrial protonophore (CRMP) (Perry et al., 2015b). Combining DNP into a cellulose-based matrix extends the time required for absorption, resulting in relatively stable plasma DNP concentrations after oral administration. CRMP increases the therapeutic index by 500-fold and, as with DNP, lowers hepatic and muscle lipid (DAG) content and improves insulin hepatic and peripheral sensitivity in numerous rodent models of NAFLD/NASH (Perry et al., 2015b).

While CRMP is not “liver specific” by design, the first-pass hepatic uptake largely confines its actions to the liver. CRMP increased the rate of hepatic tricarboxylic cycle flux without changing whole-body energy balance or mitochondrial activity in other tissues. Like DNP-ME, the reductions in plasma triglyceride and improvement in skeletal muscle activity were attributed to CRMP-induced increases in hepatic mitochondrial fatty acid oxidation, resulting in decreased VLDL production and hypertriglyceridemia and reduced delivery and uptake of fat by the skeletal muscle. In rats fed an MCD diet, CRMP treatment reduced hepatic inflammation and reversed hepatic fibrosis.

CRMP has also recently been shown to reverse hepatic steatosis and hepatic and peripheral insulin resistance in an A-ZIP/F1 mouse model of severe lipodystrophy (Abulizi et al., 2017). CRMP also decreased several markers of liver inflammation and the unfolded protein response in this lipodystrophic mouse. Furthermore, CRMP, like DNP-ME, reversed hepatic insulin resistance and diabetes with reductions in hepatic DAG-PKCε activity and hepatic acetyl-CoA content, offering further support for the roles of these metabolites in causing hepatic insulin resistance and increased hepatic gluconeogenesis, respectively, in T2D.

Taken together, these studies offer proof of concept in support of the development of novel liver-targeted mitochondrial uncoupling agents for the treatment of NAFLD, NASH, and T2D.

Samuel VT, Shulman GI. Nonalcoholic Fatty Liver Disease as a Nexus of Metabolic and Hepatic Diseases. Cell metabolism 2018;27:22-41. Nonalcoholic Fatty Liver Disease as a Nexus of Metabolic and Hepatic Diseases - ScienceDirect

Another rodent DNP study, knowing the difference bt human and rodent hepatic metabolism extrapolation to humans is ill advised in the absence of clinical trials.

Jim
 
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