# How not to mess up on dnp faq



## K1 (Jan 11, 2013)

– By CandyRoids

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 TOXNET

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™, Caltag® & Zymed® Brands | Life Technologies 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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## thatguydoc (Mar 20, 2013)

This is a wealth of knowledge as I am about to start my first cycle of dnp fairly soon. Thanks


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## Ironbuilt (Mar 20, 2013)

Thanks k1 .. This will help a recent thread discussion brutha. I sweat just reading this about dnp.  But do it right and it rocks.


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## Rory (Mar 20, 2013)

Dnp and tren is a God send...


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## Thunder46 (Mar 20, 2013)

Thanks K1 this info was greatly needed on this forum


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## omegachewy (Mar 20, 2013)

Needed this. Thanks mate.


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## bigpoppie (Jun 12, 2013)

Thanx for the awesome info. The only thing I still don't know is how to cycle it. Time on? Time off?


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## basskiller (Jun 12, 2013)

geocities is no longer.. so here are some of what was on that site  


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

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

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

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

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

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

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

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

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

 Drugs which activate K channels: pinacidil, cromakalim.

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

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

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

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

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

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

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

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

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

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

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

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

 2. This increase of the metabolism is due mostly to an increase in the combustion of the fat and a little to combustion of carbohydrates.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

 Finally, thyroxine causes a nitrogen malnutrition: it burns the muscle and fatigues the heart. Dinitrophenol-lysidine, to the contrary, causes a lipid-glycemic loss: it is the elimination of reserve materials without attacking visceral and muscle tissue.
 As for physical exercise, it seems to act exactly like dinitro therapy. Marcowitz, in his communication to the Academy of Medicine of Toronto on October 9, 1934, based on 90 cases of obesity, having followed this treatment during a period of 16 months, concludes that its action may be succinctly described in saying that the effects on the organism are similar to those of physical exercises.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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


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## basskiller (Jun 12, 2013)

Here's the proof as to WHY having a HIGH CARB intake while on DNP(if Kcal's are kept the same) is BETTER.

Before I start, Stew, Macro, Cockedzl, Andy etc...
 THIS IS AN APPROXIMATION since all bodily processess
 are ineffective andtend to entropy.(become chaotic) 

Ok, Lets Use Bodybuilder 1 and Bodybuilder 2. 

Bodybuilder 1 eats 2000Kcal/day composed of 60% carbs,
 30% protein, 10% fat 

Bodybuilder 2 eats 2000Kcal/day composed of 40% fat/30%
 protein/ 30% carbs (Basically a zone-type diet) 

Now: 

Carbs convert to glucose with 100% efficiency
 Protein converts to glucose with 58% efficiency and the
 rest is ketones.
 Fat converts to glucose at 10% and the rest are ketones. 

Ketones btw=Fats 

DNP, btw BURNS DIETARY FAT BEFORE STORED FAT.
 REMEMBER that fact!!!!! 

So, 

Bodybuilder 1 produces the following by-products: 

60% carbs / 2000Kcal= 1200Kcal/4Kcal/g=300g glucose(carbs)
 30% protein/2000Kcal= 600Kcal/4Kcal/g=150g protein,
 *0.58%= 87g glucose and 63g ketones.
 10% Fat/ 2000Kcal= 200Kcal/9Kcal/g= 22.g * 0.1%= 0.2g
 glucose and 2g Ketones. 

So, total for bodybuilder 1: 

Total Glucose: 387.2g glucose
 Total Ketones: 65g Ketones 

Bodybuilder 2 produces the following by-products: 

30% carbs/ 2000Kcal= 600/4= 150g glucose
 30% protein/ 2000 Kcal = 600/4 = 150g protein * 0.58%= 87g
 glucose and 67g ketones
 40% Fat/ 2000Kcal = 800/9Kcal/g= 88.9g Fat = 8.9g glucose
 and 80g ketones. 

Total glucose: 245.9g glucose
 Total Ketones: 147g Ketones 


 NOW, LETS COMPARE 

HIGHER CARB: 

Total glucose: 387.2g glucose
 Total Ketones: 65g Ketones 

HIGHER FAT: 

Total glucose: 245.9g lucose
 Total Ketones: 147g Ketones 

WHAT DOES DNP ULTIMATELY DO? Render the conversion of
 glucose to ATP into HEAT PRODUCTION. 

So, bodybuilder 1: Carbs= Heat
 Ketones= 65g*7Kcal/g= 455Kcal 

And, Bodybuilder 2: Carbs= Heat
 Ketones= 147g*7Kcal/g= 1017.5Kcal 

(Ketones btw=oxidized fatty acids that yield 7Kcal/gram) 

NOW, can you see the MASSIVE DIFFERENCE!!!!!! 

Bodybuilder1 WILL CREATE an EXTRA 562.5Kcal
 deficit just by macro-nutrient manipulation.
 Thats approx. 124% more calories dissipated than
 bodybuilder 2. That means MORE ADIPOSE TISSUE
 BURNT FOR FUEL. 

Therefore, following a high-carb diet while on DNP will increase
 adipose tissue burning through caloric dissipation. 

Godspeed


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## basskiller (Jun 12, 2013)

All you need to know about DNP 

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


 POSTED BY A WELL KNOWN DNP EXPERT

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

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

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



 HISTORY:

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

 MECHANISM OF ACTION:

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

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


 DOSES AND CYCLE RECOMMENDATIONS:

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

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


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

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

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

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

 For competitors:

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


 DIETARY RECOMMENDATIONS:

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

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

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

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




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

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

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

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

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

 SIDE EFFECTS:

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

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

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

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

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

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

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

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

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

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

 Dry/ sore throat- I don’t know the cause of this one, but it is pretty common among users and seems to manifest itself the most during sleep and may contribute to the insomnia.

 Allergies/ dermatitis- this is relatively rare. I’ve been in contact with nearly 500 people who have used DNP and I would estimate about 30-40 of them have experienced allergic reactions to DNP. The allergies manifest themselves first as phantom itches (itching without any rashes or redness) around the torso in some people. It will later develop into rashes and or hives around the body and possibly spread to the face, neck, lips, and scalp area in severe cases. Any over the counter or prescription allergy medication (anti histamine) will cure the allergies. Also if you’re allergic to DNP it doesn’t mean you can’t use it in the future. Allergies to DNP seem to have a tolerance factor. It first gets worse, then better with successive cycles. So if you are allergic, stop immediately and start again 7-10 days later and repeat until you are no longer allergic to DNP anymore. Allergies are also dose and length dependent.

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


 PREVENTION/ CONTRAINDICATIONS:

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

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

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

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

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

 6. If allergies arise take some allergy medication and if that isn’t strong enough then stop the doses for at least 10 days before restarting.

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

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

 SUPPLEMENTATION:

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

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

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



 CONCLUSION

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


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## basskiller (Jun 12, 2013)

DNP GURU SIN "MANUAL"

DNP Manual  

DNP

 By

 Monte E. “DNP Guru”


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



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

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



 HISTORY:

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

 MECHANISM OF ACTION:

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

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


 DOSES AND CYCLE RECOMMENDATIONS:

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

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


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

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

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

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

 For competitors:

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


 DIETARY RECOMMENDATIONS:

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

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

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

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

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

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

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

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

 SIDE EFFECTS:

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

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

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

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

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

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

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

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

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

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

 Dry/ sore throat- I don’t know the cause of this one, but it is pretty common among users and seems to manifest itself the most during sleep and may contribute to the insomnia.

 Allergies/ dermatitis- this is relatively rare. I’ve been in contact with nearly 500 people who have used DNP and I would estimate about 30-40 of them have experienced allergic reactions to DNP. The allergies manifest themselves first as phantom itches (itching without any rashes or redness) around the torso in some people. It will later develop into rashes and or hives around the body and possibly spread to the face, neck, lips, and scalp area in severe cases. Any over the counter or prescription allergy medication (anti histamine) will cure the allergies. Also if you’re allergic to DNP it doesn’t mean you can’t use it in the future. Allergies to DNP seem to have a tolerance factor. It first gets worse, then better with successive cycles. So if you are allergic, stop immediately and start again 7-10 days later and repeat until you are no longer allergic to DNP anymore. Allergies are also dose and length dependent.

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


 PREVENTION/ CONTRAINDICATIONS:

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

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

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

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

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

 6. If allergies arise take some allergy medication and if that isn’t strong enough then stop the doses for at least 10 days before restarting.

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

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

 SUPPLEMENTATION:

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

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

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

 Ephedrine--this can cause increased mobilization of fatty acid from the adipose cells to get them into the blood where they will be used for energy and burned. In short, ephedrine puts the fat in a place where DNP can burn it.

 CONCLUSION

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

 Good Luck

 The Guru


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## basskiller (Jun 12, 2013)

Here's the DNP article that George cut short on Elite. So for anyone who was pissed off because off the fact that someone could get hurt by only reading the first half and thinking that they know enough to do DNP, here's the whole article:

 The 7-day DNP Fat Loss Inferno Cycle -- A Special Report only for Platinum Members!
 Bros,

 Here is a special report I wrote just for you to say thanks for going Platinum. I hope you enjoy it. Also, a special thanks to Fonz and Macro for their input. Please feel free to post your comments.

 Yours in sport,
 George

 Boasting an astounding 50% increase in metabolic rate, DNP is the most effective fat burner that bodybuilders are using today to melt away the last amounts of diet resilient fat on their physiques. For comparison purposes, the ECA stack, which is also a highly effective fat loss tool, produces only a 3% increase in metabolic rate. Athletes reporting fat losses of 10-12 pounds in 8 days of use have further added to the DNP mystique. However, DNP is also the deadliest substance used in bodybuilding - so deadly, that it has killed athletes including one member of Elite Fitness.

 In this issue of Elite Fitness News, I?ll tell you more about DNP, share the precautions you should take if you decide to use it, and give you the reasons why you should avoid it in favor of other diet drugs and supplements that are not nearly so dangerous.
 DNP or 2,4-Dinitrophenol, (Pronounced die ni'tro fe' nolz) is an industrial chemical with various applications such as making dyes, wood preservatives, explosives, insect control substances, other chemicals, and as a photographic developer. Sold under several trade names, including Caswell No. 392, Sulfo Black B, and Nitro Kleenup, DNP has recently gained steady popularity as a fat loss tool.

 DNP was used in diet pills in the 1930s, but was banned for this use in 1938. Classified as an "uncoupler of oxidative phosphorylation," medically, DNP is quite dangerous. You see, the body has no negative feedback system that may deal with overdoses. Specifically, there is no upper limit to the increase in body temperature that may be obtained with DNP?s use.

 The following article combines several theories to form what is perhaps the single best way to cycle DNP for maximum fat-loss benefits. As I mentioned earlier, DNP can be deadly and I would never use it myself nor would I ever recommend that anyone ingest it. The casual use of DNP for dieting is ridiculous. Hearing reports of athletes using DNP before trying a Cyclical Ketogenic Diet, legal diet supplements, and medically supervised weight loss drugs is crazy. Here are a few links to effective weight loss supplements, drugs, and strategies that are much safer than DNP and are certainly a much better alternative for all but the most elite bodybuilders.

 "Seven Diet Drugs for Perfect Definition...

 ...and how to get them quickly and legally. "

 <http://www.elitefitness.com/articledata/efn/070201.html>

 That said, if an athlete makes the personal decision to use DNP, it is possible to take precautions to maximize its benefits and minimize the potential risks.

 The 7-day DNP fat loss inferno cycle:

 The 7-day DNP fat loss inferno cycle involves a moderate to high dosage of DNP for fat burning. The DNP fat loss inferno involves a 7-day on, 7-day off approach with four distinct phases. Most athletes using DNP follow this type of cycle. The phases are as follows:

 Phase 1: The 3-day Carb-Depletion Phase.
 Phase 2: The 1-day Thyroxine (T3) Re-normalization Phase.
 Phase 3: The 14-day DNP Inferno Phase.
 Phase 4: The 2-day Post-DNP Phase.

 Phase 1. The 3-day Carb-depletion phase
 Phase One has a three-day duration and begins the four days preceding the ingestion of DNP. The purpose of this phase is to deplete muscle-glycogen content by restricting carbohydrates. This is achieved through a Ketogenic style diet.

 Kcals should be restricted to 10-12 times bodyweight in lbs. And carbohydrates should be restricted to less than 60g/day. Protein is consumed at 1 gram per pound of bodyweight or higher and the remaining dietary calories should come from fat.

 This phase lasts exactly 3 days, and will reduce muscle-glycogen levels so that the body is forced to rely on fat as fuel more readily when you start your DNP cycle.

 Phase 2 The 1-day Thyroxine (T3) Re-normalization Phase
 This is a new concept for DNP dieting. During the past three days, the athlete has restricted carbohydrates and as a direct consequence T4-T3 conversion is slowed down resulting in reduced T3 levels. This is bad for the DNP phase, as you need enough active T3 to last throughout the entire 7-day on DNP phase.

 Day four of the DNP cycle involves a mega-carbohydrate meal at mid-afternoon (4-6PM) designed to create a massive insulin spike and re-normalize T4-T3. This concept has been extrapolated from ketogenic diets and has been shown to dramatically increase serum concentrations of T3.

 Day 4 involves Keto eating until the Mega-carb meal. Then in the late afternoon, at least circa 250g of carbohydrates must be consumed to create an insulin spike. Any sugar (fructose, sucrose, maltose etc.) is fair game. Fructose in particular is good because it primarily re-fills liver glycogen which is directly involved in T4-T3 conversion. (Empty liver glycogen signals the thyroid to decrease T4-T3 conversion).

 As a side-note, a 250g carb-meal after three days of Keto dieting creates a more pronounced insulin spike than would a 250g carb-meal after three days of normal eating.

 Kcals during Phase 2 should be kept at 15X Bodyweight in lbs. Macro-nutrient break-downs can be calculated by the athlete. The only carb intake on day 4 should be the 250g carb-meal.

 Phase 3 The 14-Day DNP Phase

 The first two days of actual DNP consumption are the most important to follow correctly. During Days 1 and 2 of the actual DNP portion of the cycle, it must be determined if the athlete will have an allergic reaction to DNP.

 Day 1: 200 mg of DNP is ingested
 Day 2: 200 mg of DNP is ingested

 At this point the dieter should be able to assess if an allergic reaction has occurred. A DNP-stimulated allergic reaction will lead to swelling in as little as 1 to 2 days time. Approximately 10% of athletes will have such a reaction. The unfortunate few who experience this type of a reaction must terminate the cycle immediately. Benadryl or Ketotifen (Anti-histamines) can be used to treat mild symptoms. Obviously a doctor should be consulted should the symptoms prove more severe.

 Day 3: Dieters making it to day 3 of the DNP phase have the option of increasing their dosage. The normal dosage for beginners is 400mg DNP/day. Even an amount this small should provide outstanding results. A word of caution. DO NOT TAKE MORE, if you are not experienced with DNP-use. More advanced users may chose to go higher based on past experience.
 The 400mg/day dosage is maintained from Day 3 through Day 9(Exactly 7 days). The last dose is taken on Day 9.

 Supplementation and Nutritional Protocol for a DNP cycle:

 1. An ECA stack is beneficial while on a DNP cycle as it as it acts as an anorectant. DNP raises Neuro-peptide Y levels in the brain, which is directly linked to increased hunger. Consuming 75-100mg total of ephedrine alkaloids/day should be sufficient to suppress appetite. PPA (Nor-ephedrine) should NOT be used as it causes lethargy when combined with DNP.

 2. Anti-oxidants. Due to the DNP induced rapid combustion of fats, free-radical production skyrockets up-wards. To combat this, anti-oxidants must be used. Anti-oxidants are the single most important supplement to take on a DNP cycle.

 a) Fat-soluble Anti-O: Vitamin E: 1000mgs/day
 b) Water-soluble Anti-O: Vitamin C: 2-3g/day
 c) Alpha Lipoic acid: 600-1000mgs/day

 Dual-anti-oxidant: BOTH fat & water-soluble actually re-cycles other anti-oxidants.

 3. Glycerol: Although optional, glycerol is often consumed at 15ml's 3X/day. Glycerol increases hydration for many athletes.
 No additional supplements are really required other than these three. All the rest you have read in various DNP articles are more for peace of mind than improved functionality. I consider them overkill.

 4. Water: Not a supplement, but an absolute necessity.
 DNP causes sweating and can be incredibly dehydrating. Dehydration is the NUMBER ONE cause of most DNP problems and deaths. Excessive dehydration results in over-heating. Dieters who do not replenish fluids properly while on a DNP cycle could die. The consensus among athletes is that at least two gallons of water must be consumed daily.

 5. EAT FRUIT while on your DNP cycle.

 Fruit for some reason has been found to greatly reduce the lethargy associated with a DNP cycle. It also has a high water content, therefore it helps to keep the dieter hydrated. Watermelon is an obvious recommendation.

 6. Dietary intake: There are several schools of thought on this matter, but sticking to the old standard always works.
 Kcals should be kept anywhere from 10-15X Bodyweight in lbs. Macro-nutrient break-downs should be kept at around 20% fat, 30% protein and 50% carbs. (Changing the ratios in favor of more carbs and protein w/ less fat will result in a more fat loss but nothing special. Also, remember that more carbohydrates means more heat.)

 Take for example the 220 lb (100 kg) bodybuilder. He would consume anywhere from 2200 to 3300Kcal /day (Depending on his appetite control).  



WHAT NOT TO DO on a DNP cycle.

 a) Do not under any circumstances consume alcohol or ANY type of diuretic while on a DNP cycle. Alcohol and diuretics will dehydrate you and can cause SERIOUS problems.
 b) Do not remain in a hot environment without replenishing fluid loss due to perspiration. This too can also cause SERIOUS problems.
 c) Do not begin with a high dosage of DNP if you are a novice. This is just asking for a trip to the ICU.

 The half-life of 2,4 Dinitrophenol is 36 hours. So, after 36 hours, there is only 50% of the DNP remaining in your system. Therefore, 72 hours later 25% remains. Then 12.5% remains after 108 hours. After 5 days (120 hours), there's roughly 9% of the DNP left in your body that you had on Day 9. This DNP concentration is low-enough to allow you to begin Phase 4 of the cycle -- the 2-day Post-DNP phase -- without compromising glycogen synthesis rates. Kcals during Days 10-14 should remain the same as during days 3-9.

 Phase 4: The 2 day Post DNP Phase.

 The whole purpose of this phase is to get muscle-glycogen levels back to normal. The Ketogenic carb-up can be used as a sort of template for this phase.

 After Phases two and three, muscle-glycogen levels are depressed and need to be replenished.

 Day 15: Carb-intake should be 7g/Kg of LBM (lean body mass = bodyweight minus body fat.) So assuming a 220 lb bodybuilder has 0% body fat, lol, he would consume 700 g of Carbs. Protein-intake remains at 1g/lb and fat is restricted as low as possible.
 The focus on day 1 should be on High-GI foods like Fat-free Ice-cream and all the other non-fat high sugar desserts. Calories should be around 4000 for the 220-lb bodybuilder -- in other words, 18X bodyweight in lbs.

 Drastically restricting fat is CRITICAL here, as the body is still burning fat for fuel as you replenish your glycogen stores. In essence, the dieter is still losing fat while carbing up.

 Day 16: Muscle-glycogen has increased, so carb-intake should be decreased from day one?s 7g/Kg to only 5g/Kg of LBM. That would be 500g for our 220-lb bodybuilder. Protein is 1g/lb again. Fat remains as low as possible. Kcals for the dieter are reduced to 3000 Kcal range, or around 14X Bodyweight in lbs. The focus of Day 2 should be low-GI foods like vegetables, milk, lean meats etc.

 Additional Precautions:

 Dieters feeling extremely nauseated or who vomit during a cycle should discontinue use immediately and not restart for at least 36 hours.

 Dieters should carry a pocket thermometer at all times. If body temperature rises above 102 Fahrenheit then the dosage should be lowered or the cycles should be terminated. Additionally, the dieter should take a very cold bath to lower the temperature.
 In addition to water, V8 juice should be consumed. Drinking gallons of water depletes the body of electrolytes pretty badly predisposing the dieter to shock, nausea, lethargy, and even death. V8 is the best for replenishing electrolytes as it contains 950mg of potassium per 8oz compared to Gatorade?s 35mg of potassium in 8oz.

 Massive amounts of fruits and sweets should be consumed if one becomes nauseated or vomits - i.e. force feed yourself.
 Dieters should never allow themselves to become overheated on a DNP cycle. Always stay next to a fan and keep the air conditioner on. Do not attempt a DNP cycle if you work out doors in a warm climate or another warm environment like a kitchen. Even at low doses this can build up and be potentially dangerous.

 There are two versions of DNP - regular and crystalline. Know which one you are taking. When taking the crystalline DNP caps, never take more than 200mg at once if you've never used it before. Even if you are used to it, it is still much safer to spread the dosage throughout the day. Crystalline DNP is much faster acting and can rapidly elevate temperature.

 Post-Steroid Cycle Use of DNP

 One of the primary causes of muscle breakdown after a steroid cycle is suppressed TSH. Anabolic steroids suppress TSH, which in turn lowers T3 and T4 production by the thyroid gland. The reduction in TSH is one reason that anabolic steroids are such excellent muscle builders.

 Soon after the completion of a steroid cycle, TSH up-regulates, which in turn super-stimulates the thyroid. This excess stimulation causes the thyroid to produce above normal levels of T3 and T4. This increase in thyroid hormones is highly catabolic and is the main reason why people lose muscle post-cycle.

 Athletes have learned that they need to restrict T3 production post cycle to prevent muscle loss. A novel approach to achieving this goal is the use of DNP. About 80% of the body?s endogenous T3 is produced from the metabolically inactive T4 to the metabolically active T3. The de-iodinase enzyme is responsible for this conversion. It literally cleaves off an iodine molecule.
 By ingesting 200mg DNP/day, the athlete can correct the over stimulated Thyroid, returning T3 levels back to normal. DNP directly blocks the production of T3 from T4 via the de-iodinase enzyme.

 As a bonus, the reduction in your ATP stores because of the DNP is counter acted by an increase in the oxidation of triglycerides as an energy source. The benefit is the elimination of any potential fat-gain from the low post-cycle testosterone levels. And as DNP is non-hormonal, it has no effect on HPTA recovery.

 After cessation of DNP use post-cycle, the athlete will reap the benefits of the "Anabolic Rebound Effect" which further lends credence to the use of DNP as a post-cycle ancillary for the elimination of any post-cycle muscular losses.

 Macro?s DNP Supplements

 200mg alpha lipoic acid 3x a day with meals
 1200-1500mg magnesium in 2-3 divided doses.
 2-3000mg vitamin C
 1200IU of vitamin E
 200mcg of selenium.
 1000-2000mg of calcium (can?t take it with the magnesium, though. Take it before bed)
 Melatonin if you can?t sleep and it is also one of the best and cheapest anti-oxidants.
 50mg of zinc a day
 one iron tab as hemoglobin is a protein as well.
 A potassium gluconate tab or two a day
 Taurine at 3g a day.
 Glutamine at 15g-20g a day .
 1 table spoon glycerol 3 x a day
 at least 2 gallons of water
 a fan to point at your head while sleeping- or at work- basically anytime you can point a fan at you
 500mg grapeseed extract
 300mg cranberry extract
 600-900mg of green tea
 a good mulit vitamin
 EC+1g of tyrosine 3x per day and 20mg of yohimbine topically 2x per day- for added energy and fat burning effects


----------



## basskiller (Jun 12, 2013)

DNP Research 101: 2,4 DNP usage to combat post-cycle muscle catabolism/fat gain 

This is a little excerpt from my research into the various
 applications of DNP.

 One of the main problems that affect post-cycle muscle
 catabolism is T3(thyroxine) levels within the blood-stream.
 As we all well know T3 works through PROTEOLYTIC
 pathways.
 Steroids suppress TSH which in turn lowers T3 and T4
 production in the thyroid gland.
 This reduction in TSH is one of the reasons why steroids
 are such efficient muscle builders.

 What happens POST-CYCLE???

 TSH up-regulates, which in turn super-stimulates the thyroid
 into producing above normal levels of T3 and T4.

 This increase in thyroid hormones is VERY catabolic and is
 the main reason why people lose muscle post-cycle.

 What to do then?

 Simple. 200mg DNP/day will literally correct the problem.

 Symptom: Excessive production of T3 and T4 from the
 thyroid gland.
 Note: 80% of the bodies endogeneous T3 is produced
 from the conversion of the metabolically inactive T4
 to the metabolically active T3 via the de-iodinase enzyme
 which basically "cleaves" off an iodine molecule.
 THIS IS KEY!!!

 DNP on the other hand DIRECTLY BLOCKS the production
 of T3 from T4 via the de-iodinase enzyme.

 Ingestion of 200mg DNP day will then SUPPRESS the
 OVER-STIMULATED thyroid gland back to normal
 physiological levels, therefore DRASTICALLY
 reducing thyroid hormone induced post-cycle muscle
 catabolism because T3 levels have been REDUCED
 to normal physiological levels.


 As a bonus, the reduction in your ATP stores because
 of the DNP is COUNTER-ACTED by an increase
 in the oxidation of triglycerides as an energy source,
 therefore eliminating any potential fat-gain from
 low post-cycle testosterone levels.

 DNP is also NON-HORMONAL, therefore it has no effect
 on HPTA recovery.

 Fact is, after cessation of DNP use post-cycle you will also reap
 the benefits of the "Anabolic Rebound Effect" which further
 lends credence to the use of DNp as a post-cycle ancilliary for
 the elimination of any post-cycle muscular losses.

 Fonz


----------



## basskiller (Jun 12, 2013)

Feel Good while on DNP
 A Post by Animal
 [Note: No editorial changes have been made except for font settings. Actual
 post in italics.]
 As you may already know you should be taking the following per day.
 1200-1500mg magnesium in 2 divided doses.
2-3000mg vitamin C.
1200IU of vitamin E
 200mcg of selenium.
 1000-2000mg of calcium (can't take it with the magnesium, though. Take it
 before bed)
 Melatonin if you can't sleep and it is also one of the best anti-oxidants.  

I felt like shit when I went above 400mg and sweat profusely on 600mg and
 800mg which lasted for 2 days. I weigh around 95kg (210).  

Here is what I am taking:
 600mg of DNP which would be 6mg/kg which is well above the recommended 3-
 5mg.
 You have to divide it into two doses of 300mg 12 hours apart.
 After you hit your 600mg limit you don't take the next 300mg for 36 HOURS
 >From the first dose!
 So, if I took the first dose at 6AM on Sunday morning and the second 300
 mg at 6PM Sunday night, the 3rd dose would not be until 6PM on Monday evening.
 The fourth dose would again follow 12 hours from the 3rd which would be
 at 6AM on Tuesday morning.  

I am also taking ECA with this just for fun although at only 2 x a day for
 the ECA.
 How am I not sweating all over the place and not feeling like shit and/or
 dehydrating in the middle of summer while going on hour or longer rides
 in 85 plus heat?. Let me tell you again that I hated the way this shit made
 me feel.
 YOU HAVE TO TAKE GLYCEROL AND PYRUVATE!
 I don't know if you can take one without the other because I was using the
 glycerol (G) and pyruvate (P) to enhance endurance and stem dehydration
 which I am very prone to. I think, however, that you will have to do them
 both as there is a synergistic benefit. I have taken G alone and while you
 have more water to hold on to, you just seem to sweat more. The G-P let
 me drink ½ my normal volume of water on a ride and that is what made me
 try the DNP ECA experiment.  

Glycerol dose. YOU ONLY NEED 1 TABLESPOON 3 TIMES A DAY! One in the morning,
 one in the afternoon and one right before bed. Fuck that shit where those
 idiot researchers tell you to take 1 gram for every kg bodyweight. They
 are idiots and obviously have never taken it or asked the athletes how they
 feel. Let me tell you, you feel like shit! You feel bloated and sometimes
 get a headache and you piss A LOT! 1 tablespoon 3 times a day comes out
 to ½ what they recommend to take 2 hours before an event. The glycerol keeps
 your muscles hydrated and limits the sweating. It will fight the dehydrating
 effects of the ECA. As we know, DNP is carbohydrate specific and glycerol
 also is a carb source that can't go to fat. Glycerol also increases power
 output which may be an added benefit of the type of carb source it is. (Don't
 quote me or call me on this carb source because I don't really care what
 you think. All I know is that it works and I don't have the time to look
 up the frigin' mechanisms)  

Before I explain the P, let me tell you that glycerol and glycerin are the
 same damn thing! A good recipe for taking your glycerol is 1 packet of Kool-
 aid, 1/8 cup sugar, 1 T glycerol and 32-4oz of water. The glycerol makes
 the kool-aid taste like OJ because there are alcohols and fermentation products
 in the OJ which the glycerol mimics.  

Pyruvate dose. 2-5grams a day. Start out at 900mg or so 3 times a day and
 go up from there. I am at 1.5mg 2-3 times a day and if you don't work your
 way up it will give you gas and the runs.
 As I mentioned above, I think the P is working synergistically to hold on
 to the water in your muscles. Additionally, it is an energy source and/or
 it is manipulating the Krebs Cycle intermediates (?) and allows for a different
 energy production pathway without going through the whole rigamorole. (Again,
 I don't care what you think or what the exact mechanisms are. I know it
 changes/manipulates an ATP/energy pathway and decreases lactic acid output
 and if it ain't the Krebs cycle I don't really give a fuck. It works.)  

Now you have a recipe on how to feel good on an overdose of DNP! To recap
 you need:
 3 Tablespoons glycerol 3x a day.
 1g Pyruvate 3x a day.
 DNP at 36 hour intervals.
 If you start to feel bad, just drink some sugared pop or take some glucose
 or maltodextrin with your psuedo-OJ mix.
 The only drawback is that you will still smell rather bad and will emit
 a vinegar type odor although you won't be sweating all over everything.
 If you notice you are starting to sweat more it is time for another glycerol
 dose.  


 I believe that adding dihydroxyacetone (DHA) could also improve this, but
 I don't know where to get it.  

Resistance is futile! You will be assimilated into AAS!


----------



## basskiller (Jun 12, 2013)

Why you might want to use DNP.  

Add some DNP to an animals diet. DNP can get metabolism up at least 50% which is conservative as some say
 75% This would mean if the animal eats 3000 calories maintenance they are now at 1500 calories a day with no
 change in diet! A 2500 calorie a day would leave them with 1250 calories a day. There are 4086 calories in 1lb of
 fat and at 3000 calories a day your DNP adjusted calories for the day is 1500. Multiply that x 7 days to give you
 10500 calorie deficit which is 2.5 lbs of fat loss for the week. At the 2500 calorie you have a 2.14 lb fat loss. These
 are both below what the BO diets claim and you don't have to stop eating!  

If your animals weigh around 200lbs their effective dose is 400mg and the max can be as high as 800mg a day.
 High fat diets market on the basis that you are going to be able to lose 1.5-2lbs of fat by just changing your diet!  

1 gram of fat is 9 calories. There are 454 grams in a 1 pound. This gives you 4086 calories for 1lb of fat. If you
 want to lose that 1lb of fat you have to have a 4086 calorie deficit to do it. In other words, you need -4086 calories
 in your diet if you want to lose 1 lb of fat. Now, Let's say you are at 3000 cal a day for maintenance. That is 21000
 calories a week. You believe the marketing of the post above and think you can lose 1.5lbs of fat. That, my friends,
 is 6129 calories which you have to subtract from 21000 which leaves you with 14871 calories for the week or 2124
 calories a day. You are going from 3000 to 2124 a day. If you want to lose that great sounding 2 pounds you are
 now at 12828 for the week or 1832 calories a day.  

Let's be realistic and put you at 2500 maintenance calories. To lose 1.5lb you now need 11371 calories a week or
 1624 calories a day or a nearly 900 calorie a day change. To lose the magical 2lb a week you need 9328 calories for
 the week or 1333 calories a day or a 1167 calorie change per day! That is rather difficult, but let's add some DNP
 which can get you metabolism up at least 50% which would mean you are now at only 1500 calories a day for a
 3000 calorie diet with no change in diet! A 2500 calorie a day would leave you with 1250 calories a day.
 These are both below what the BO diets claim and you don't have to stop eating!  


 What you want to keep in mind  

Everyone is different.  

Don't take it on an empty stomach or it will feel like you have indigestion for most of the day.  

I wanted to stress not to just go balls out (5mg/kg) and you should move up gradually on DNP for your first
 experience.  

If you have an allergic reaction with red spots and itching then stop the DNP and get some Benadryl and then you
 should be able to start again.  

The type of diet will also affect how you feel, as well as the type of workouts you are doing. These are variables
 you also will have to figure out for yourself. The logic of my dieting regimen follows that while you are DNP all
 the glycogen/glucose is being scavenged to provide ATP for the mitochondria so you will want to eat a regular diet.
 High fat BO is not going to help you build muscle even though DNP is anti-proteolytic (protein sparing)..
 Furthermore, when you eat fat it is more likely to go to fat! That is scientifically proven. So if I'm trying to burn
 fat, why would I want to eat it right back?  

DNP is anti-proteolytic which means it uses carbohydrates or fats exclusively to supply energy for the mitochondria
 and does not facilitate muscle breakdown, however, this does not therefore mean DNP is positive for muscle
 building. The cells are running on overdrive and they are not going to be looking to make themselves bigger which
 requires even more energy.  

Everyone is different and other supplements you take will affect your results, but as a whole, most people are not
 going to do well or feel well on high fat and DNP. I also have found that taking particular supplements helps with
 how will you feel while on the DNP.  

I feel better when I don't do huge carbs, however, when I don't do any as in high fat type diets, my workouts suffer
 just the same. Each individual has to decide for themselves and put those factors into perspective with what their
 goals are and how fast they want to accomplish them and how bad they are willing to feel for the desired weight
 loss.  

WARNING: DNP will turn everything and anything yellow including skin, clothes, carpet, and hair. I dropped a
 capsule in my DNP container and bent over to look for it and my hair touched the edge of the container and my hair
 got dyed yellow! My hair did not even touch the DNP, but just the side of the container for about 2 seconds! DNP
 for the most part is not removable or bleachable with normal chemicals. It will also track. By that I mean, you think
 you have washed it off your hands and you touch something and later you see yellow spots on what you touched. If
 you are making caps you need 2 pairs of gloves, at least, as the DNP goes through the first pair due to an atrraction
 it has for moisture. DNP sublimes and floats. Due to this sublimation it will land on EVERYTHING if you leave it
 out even if there is no air circulation. DNP goes through EVERYTHING including plastic, hdpe plastic, pet plastic,
 plastic bags, nitrile and latex gloves. It can be washed out of clothing with hot water and detergents that have
 phenolic compounds in them such as Tide. DNP is not solvated by laquer thinner, acetone, paint thinner, or
 turpentine or any of the common organic solvents. If you wash your hands immediately after touching DNP with
 gamma-butyrolactone, otherwise know as GBL and use to make GHB, and then a detergent such as Dawn
 dishwashing soap, the stain will come out for the most part.  

I have to say that a certain guru which some people keep quoting is what I feel to be a very unreliable source. I will
 give him credit for bringing DNP to the forefront, but I will bet you a million bucks that he has never done it or
 mixed it. Here is a quote that bears this out; 'I don't see what the worry is about everything turning yellow? I have no
 problems, I just dry it out and cut it with a credit card and cap it.'  

That is total BULLSHIT!. Anyone who has used or mixed DNP powder knows that it will get on
 EVERYTHING and turn it yellow. It goes through plastic bags. Just today I was sending someone 3g for research
 and I put it into a ziploc and 2 hours later I came back and the envelope under the bag was YELLOW! It goes
 through 1 laver of rubber gloves. It turns white HDPE bottles yellow. It floats everywhere. I had to put my stuff in a
 hood because it got on everything I had sitting out and I had to wash all my glassware and scales before I could use
 them again. DNP floats by sublimation which would be known just be reading the safety sheet or the Merck Index..
 On the basis of that statement alone I have some real problems believing anything he says on the subject, but
 another famouns quote is, 'DNP will raise your body temp high enough to kill you!' This also proves that he has
 never done it because as you will find, your body temp only goes up about one degree. Ok, enough about the fake
 guru.  

Someone just asked me if the shit I sent them was real. Well, if you want a test then rub it on your hands and throw
 some on your carpet. When your carpet has to be replaced because NOTHING can remove the yellow and you look
 like a total ass because your hands are bright yellow, then you can ask me if it is real!  

Mostly people are taking DNP for 1 week at a time because it exhausts you and you sweat a lot, usually that is what
 I do, but due to my 'work' with DNP I got a dose while on an ECA week and that combination of DNP-ECA was
 like methamphetamine. In fact it was better because it had less side affects. I would venture that DNP-PPACA
 would also have the same methamphetamine effects. At this time I do not know, however, whether PPA works on
 the same receptor so I would not do them back to back in cycles. ECAY where Y is yohimbine is also a
 combination that has meth type benefits. Clen-DNP did not exert any magical meth benefits that I noticed.
 Have not taken PPACA or PPACA-DNP or PPACAY.  

Tyramine and yohimbine are awesome and someone that I hold using it was getting goosebumps and asked a
 pharmacologist what the goosebumps were about. The pharmacologist told him that it meant he was burning a lot
 of calories. I love this combination and it is just like meth due to large releases of NA although it only lasts 4 hours
 or so.  

DNP also 'upgrades' the effects of clen. If you have used clen before and it had/has stopped working, then DNP
 will bring back it's glory.  

I like to keep the clen and DNP a week apart due to the affects they have on T3 although they work on different
 mechanism it is just a precaution to keep from shutting down the T3. You could add Y to it for an added benefit
 which will not cause downgrade of anything. Reports on DNP-Y indicate a higher rise in body temperature on this
 combination.  

Due to the systemic affects of DNP, it affects EVERY cell in the body that has mitochondria, including smooth
 (digestive) and muscle and fat as well, you will not see a significant rise in body temp like you see with clen or
 ECA. Clen and ECA work primarily on muscle cells and that causes a rise in body temp just as if you were working
 out. I don't know why this is such a difficult concept for some to understand, but I was sweating like hell recently,
 and I took my temp and it was 95.8. ON DNP!  

DNP MECHANISMS  

The basics first. DNP is a classified as a chemical poison. It's mode of action is to disrupt the ETC (electron
 transport chain) and cause uninhibited exchange of protons. This exchange of protons is what is responsible for
 making ADP into ATP. NOTHING can stop the disruption of this process once it starts. DNP works no matter
 what! High or low T3 has nothing to do with whether or not DNP affects the mitochondria and burns off extra
 energy. DNP gets into the cell and into the mitochondria and causes proton release. No other hormones are needed
 or noted.  

Even so, it works in much the same way as clen or ECA or PPACA or thyroid. They ALL cause the metabolism to
 speed up. These all work via the mitochondria as well, although the non-DNP diet drugs work on the receptors first
 and DNP goes directly to the mitochondria, the results are the same which is speeding up the metabolism to burn
 fat.  

Some other important facts you should know are how ephedrine and beta-3 activation drugs work.
 These both cause uncoupling of the ETC chain just like DNP! Ephedrin works part of its magic via beta-3's and
 much research has been done looking for a magic beta-3 drug. Why, we have it and it is called DNP! If you are
 sitting around and something is making you hotter, you are most likely experiencing an uncoupling of the ETC
 chain. No big deal, but DNP just causes a greater effect.
 I knew there was a reason that you CANNOT die from DNP usage, at least the doses many are doing. I talked to a
 couple people about this but just couldn't find the info to prove it. Ok, so what does DNP do? It uncouples the
 ETC or oxidative phosphorylation as was elaborate upon above, allowing electron flow to go unchecked at maximal
 rate and resulting in heat production and ATP depletion.  

ATP depletion is the key. What condition exists when you have totally exhausted all ATP and no more is being
 created? A very good instance we all know about is when you are dead and it is called 'rigor mortis'. Rigor mortis
 results because no more ATP is binding to the myosin head of the sarcomere in the muscle fibers.  

So what does this have to do with us? No one has ever had rigor mortis on DNP or even severe cramping that has
 ever been documented. Furthermore, and to be more specific as to the uncoupler DNP, the electron gradient is
 collapsed and it runs unchecked at maximal as I have explained above, but as the gradient continues to increase
 electron transport becomes more difficult and the process SLOWS! Additionally, under very large artificially
 created electrochemical proton gradients, normal electron flow stops and may even result in
 REVERSE electron transport flow!  

All that was complicated and here is what it means. The respiration chain has a safety mechanism which allows for
 feedback controls to keep you from killing yourself. This is also another reason you will not want to do DNP for
 long periods. If you have taken enough as to create a large gradient the flow of electrons your burning of calories
 might even STOP! This will happen if you don't eat enough calories and appears to be more detrimental on a high
 fat type diet because as you will see below, glucose can ameliorate charge differentials in the mitochondria and at
 the cell surface while on DNP.  


 DNP works NO MATTER WHAT! It uncouples the electron transport train (ETC) and there is nothing you can do
 to stop it. Some have said it doesn't work after a small dose or only after taking DNP for 2 days or so. I think they
 are the same kind of person who would take a drink of beer and say, 'Oh, I'm not drunk so alcohol doesn't work'!
 Alcohol still affects your brain cells and hormone levels and slows down the metabolism. Just because you didn't
 drink enough to be drunk doesn't mean nothing happens!  

DNP is anti-proteolytic. This means DNP does not break down protein via the mechanism through which DNP
 works. DNP is actually better for you than cardio because exercise is PROTEOLYTIC which in itself is another
 reason to not be doing a high fat diet. High fat diets and exercise both lower insulin and raise glucagon levels which
 cause breakdown of protein. It is a proven fact that 10-20% of energy from exercise comes from AA breakdown as
 well as release of glutamine from the cells. DNP burns calories and does not affect hormone levels. Someone said
 something about it causing ketosis which is likely if you don't eat any carbs, but DNP is not, by itself going to
 affect insulin levels like glucose disposal agents metformin or phenformin.  

DNP is not going to be advantageous to muscle building. THIS DOES NOT DISAGREE WITH WHAT I WROTE
 ABOVE! It is anti-proteolytic via its mode of action, BUT if there is not enough energy in the cells to build muscle
 it ain't gonna happen. Again, diet is key.  

DNP is one of the SAFEST drugs you can take!!!!! Why? Am I nuts?! I am basing this on DNP's mode of action.
 DNP has one purpose and mechanism and affects nothing else, but the mitochondria. DNP does not affect hormone
 levels as do clen, ECA, T3, etc. It has no side affects that you don't expect such as shakes or cramping. Compare
 DNP to some of the Drugs the FDA has approved and look at their side effects and then tell me what is safer!
 HAHA!  

After you read this study you need to ask yourself, need I say more? In the earlier paragraph on the mechanisms of
 DNP on the mitochondria I explained the safety mechanism which could keep DNP from being totally depleted of
 ATP. Some were saying ATP depletion would result in cell death. The study below illustrates another mechanism
 which I didn't know about. The crux of it can be summarized by this sentence: 'The failure to find a reduction in
 ATP concentration in either fibre type during prolonged exercise in the face of a progressive increase in the number
 of fibers showing little or no glycogen concentration suggests that protective mechanisms exist that prevent an
 energy crisis. The nature of these protective mechanisms remains to be elucidated. ' In other words,  

When glycogen is gone there is a mechanism which keeps ATP from being depleted which is unknown at present!  


 Energy metabolism in human slow and fast twitch fibers during prolonged cycle exercise.  

Author Ball-Burnett M; Green HJ; Houston ME
 Address Department of Kinesiology, University of Waterloo, Ontario, Canada.
 Source J Physiol (Lond), 437():257-67 1991 Jun
 Abstract  

1. The effects of prolonged exercise on energy metabolism in type I and type II muscle fibers in the vastus lateralis
 muscle were investigated in six male subjects (20.0 +/- 0.5 years, mean +/- S.E.M.) who performed one-legged
 cycling at 61% of maximum O2 consumption (VO2,max; determined with one leg) until fatigue or for a maximum
 of 2 h. 2. Analysis of pools of freeze-dried fibers obtained by needle biopsy and separated into specific types by the
 myofibrillar ATPase histochemical procedure indicated higher (P less than 0.05) lactate concentrations in type II
 fibers compared to type I fibers at 15 min (43.9 +/- 9.7 and 51.2 +/- 9.8 mmol (kg dry wt)-1) and at 60 min (18.2 +/-
 4.7 and 25.9 +/- 6.5 mmol (kg dry wt)-1). No differences existed in lactate concentration between fibre types for
 pre-exercise (10.0 +/- 1.6 and 13.3 +/- 2.8 mmol (kg dry wt)-1) or post-exercise. 3. Glycogen degradation was most
 pronounced in type I fibers. By the end of exercise, glycogen concentration was 82.4 +/- 45 mmol glucosyl units (kg
 dry wt)-1 in type I fibers and 175 +/- 62 mmol glucosyl units (kg dry wt)-1 in type II fibers. 4. No significant
 changes in ATP and creatine phosphate (CrP) were found in either fibre type with exercise. 5. It is concluded that,
 at least for lactate and glycogen, fibre-specific differences are evident in prolonged submaximal exercise. The cause
 of the difference probably relates both to the unique energy metabolic characteristics of each fibre type and to the
 manner in which they are utilized during the exercise. 6. The failure to find a reduction in ATP concentration in
 either fibre type during prolonged exercise in the face of a progressive increase in the number of fibers showing
 little or no glycogen concentration suggests that protective mechanisms exist that prevent an energy crisis. The
 nature of these protective mechanisms remains to be elucidated.  

DNP will make you breathe harder via a mechanism called cellular hypermetabolism. You aren't going to die if you
 are breathing hard! DNP works by increasing ventilation and oxygen consumption via hypermetabolism of the cell.
 DNP makes you breath hard.  


 Role of tissue hypermetabolism in stimulation of ventilation by dinitrophenol.
 Author Levine S
 Source J Appl Physiol, 43(1):72-4 1977 Jul
 Abstract  

Several authors have hypothesized that tissue hypermetabolism accounts for increases in ventilation (VE) elicited by
 2,4-dinitrophenol. However, some data in the literature indicate that stimulation of VE by isomers of dinitrophenol
 is unrelated to tissue metabolic rate. To test this latter concept, we compared three different isomers of dinitrophenol
 (i.e., 2,4-dinitrophenol (2,4-DNP), 2,5-dinitrophenol (2,5,-DNP), 2,6-dinitrophenol (2,6-DNP) with respect to
 stimulation of VE and with respect to stimulation of oxygen consumption (VO2). In all experiments, 3-4 mg/kg of
 one dinitrophenol isomer was administered to chloralose anesthetized dogs by intra-arterial infusion. 2,4-DNP
 elicited large increments in both VE and VO2, 2,6-DNP elicited moderate increments in both VE and VO2, whereas
 2,5-DNP elicited small increments in both VE and VO2. These observations demonstrate a correlation between
 ventilatory and metabolic changes affected by isomers of dinitrophenol. Accordingly, these results are consistent
 with the hypothesis that ventilatory stimulation by congeners of dinitrophenol is related to tissue hypermetabolism.  


 How to feel good on 600mg of DNP!  

This is not an advertisement because I sell more encapsulated DNP for research than I care to spend time making.
 Note: I sell it for 'Research'  

The longer I took DNP the more I realized those who had originally recommended DNP use were not looking at the
 big picture, and they had most likely never used it or mixed it themselves, and/or were just complete morons!  

Myth #1.
 You die on DNP from heat related to overdose.
 Wrong!
 You die from dehydration resulting in heat exhaustion and then heat stroke.  

Myth #2.
 You can do it on high fat-low carbohydrate type diets.
 NO YOU CAN'T!
 High fat-low carbohydrate diets are based on keeping your blood sugar and insulin low. DNP will also drive down
 your blood sugar, so if you want to have blurry vision due to low blood sugar and feel like hell, you go right ahead.
 Glucose also has some beneficial cellular effects when used with DNP..  

Myth #3. You will go blind.
 Right! If you do high fat-low carbohydrate diets and don't keep your blood sugar up and/or don't take pyruvate.  

Myth #4.
 You can't work out on DNP.
 Yes you can, if you know what you are doing and which I am about to tell you.  

As you may already know you, should be taking the following per day.  

1200-1500mg magnesium in 2-3 divided doses.
 2-3000mg vitamin C.
 1200IU of vitamin E
 200mcg of selenium.
 1000-2000mg of calcium (can't take it with the magnesium, though. Take it before bed)
 Melatonin if you can't sleep and it is also one of the best and cheapest anti-oxidants.
 50mg of zinc a day
 one iron tab as hemoglobin is a protein as well.
 A potassium gluconate tab or two a day
 Taurine at 3g a day.
 Glutamine at 15g a day sublingual or with carb/protein drink.  


 I think taurine will be most beneficial for cramping and holding onto water. I have worked with some mountain
 bikers that were having trouble with cramps and had tried using the proverbial potassium supplementation cure and
 it didn't work. I had them take the taurine and magnesium and the cramping went away. Taurine is also give to
 people who have leg cramps at night at a dosage of 3-6g a day resulting in total alleviation of the cramps.
 Clenbuterol depletes the liver of its taurine supply which changes the osmotic pressure and therefore stops T4-T3
 conversion. Taking supplemental taurine can alleviate this.  

Glutamine also regulates water, but is a bitch to take and unless you want your small intestine to absorb most of it
 you have to take it sublingual. You can fool the body a bit by putting it into your carb/protein drink after you work
 out or by taking 2g doses throughout the day. Glutamine ALSO causes a rise in insulin.  

IF you are on clenbuterol, pyruvate and glycerol will help you a little, and I don't know why, but I still got some
 cramping on clen after an event even on P and G. The latest research I have indicates that the reason clen may
 cause cramping is due to TAURINE depletion so by taking the 3g a day taurine you should be able to ameliorate
 those effects as well and keep your thyroid levels normal as well.  

In addition to the vitamins and minerals you should be taking:  

3-6g Pyruvate (P)
 3 tablespoons Glycerol (G)  

If you can't get the G and P go right to the taurine which may be cheaper as well.
 Glycerin (glycerol) is avail in the skin care section of your pharmacy and 4oz is about1-2 dollars or there are larger
 versions in white bottles and the brand name is H something. Just buy it from a vet and a gallon is around $20!  

I felt like shit when I went above 400mg and sweat profusely on single large doses of 600mg and 800mg which
 lasted for 2 days. I weigh around 95kg (210).  

The object of the DNP dosing with the glycerol and pyruvate was to test their benefits on what is considered an
 overdose of DNP while maintaining my exercise level in the middle of summer.  

Here is what I was taking:
 600mg of DNP which would be 6mg/kg which is well above the recommended 3-5mg.  

DNP is said to have a half life of 36 hours and this is what I have based the following dosing scheme. I also have
 anecdotal evidence that DNP can last 48 hours or more. When I took an 800mg dose after 3 days on 300mg a day I
 sweat for 48 hours straight and that 800mg was the last dose I took.  

You have to divide the 600mg into two doses of 300mg 12 hours apart.
 After you hit your 600mg limit you don't take the next 300mg for 36 HOURS from the first dose!
 So, if I took the first dose at 6AM on Sunday morning and the second 300 mg dose at 6PM Sunday night, the 3rd
 dose would not be until 6PM on Monday evening. The fourth dose would again follow 12 hours from the 3rd which
 would be at 6AM on Tuesday morning.  

I am also taking EC with this just for fun although at only 2 x a day for the EC to keep energy levels up and lessen
 the carb craving that goes with DNP.  

How am I not sweating all over the place and not feeling like shit and/or dehydrating in the middle of summer while
 going on hour or longer rides in 85 plus heat?. Let me tell you again that I hated the way DNP made me feel.  

YOU HAVE TO TAKE GLYCEROL AND PYRUVATE!
 I don't know if you can take one without the other because I was using the glycerol (G) and pyruvate (P) to enhance
 endurance and stem dehydration which I am very prone to. I think, however, that you will have to do them both as
 there may be a synergistic benefit. I have taken G alone and while you have more water to hold on to, you just seem
 to sweat more which is also backed up by the research. The G-P cocktail let me drink « my normal volume of water
 on rides and that is what made me try the DNP-ECA experiment.  

Glycerol dose. YOU ONLY NEED 1 TABLESPOON 3 TIMES A DAY! One in the morning, one in the afternoon
 and one right before bed. Don't listen to the researchers who tell you to take 1 gram for every kg body weight 1-2
 hours before and event. They are idiots and obviously have never taken it or asked the athletes how they feel. Let
 me tell you, you feel awful taking that much glycerol! You feel bloated and sometimes get a headache and you piss
 A LOT! 1 tablespoon 3 times a day comes out to « what they recommend to take 2 hours before an event. The
 glycerol keeps your muscles hydrated and limits the sweating. It will fight the dehydrating effects of the ECA. As
 we know, DNP is carbohydrate/fat specific and glycerol also is a 3 carbon carbohydrate source that can't go to fat!.
 Glycerol also increases power output which may be an added benefit of the type of carb source it is. Glycerol is
 converted to glucose in the liver and in the liver is where it stays for the most part and does not, therefore, raise
 insulin levels.  

Before I explain the pyruvate, let me tell you that glycerol and glycerin are the same thing! A good recipe for taking
 your glycerol is 1 packet of Kool-aid, 1/8 cup sugar, 1 tablespoon glycerol and 32-oz of water. The glycerol makes
 the kool-aid taste like OJ because there are alcohols and fermentation products in the OJ which the glycerol mimics.  

Pyruvate dose. 2-5grams a day. Start out at 900mg or so 3 times a day and go up from there. I am at 1.5g 2-3 times
 a day and if you don't work your way up it will give you gas and the runs. As I mentioned above, I think the P is
 working synergistically to hold on to the water in your muscles. Additionally, it is another 3 carbon energy source
 and/or it is manipulating the Krebs Cycle intermediates and allows for a different energy production pathway.
Pyruvate changes/manipulates an ATP/energy pathway and decreases lactic acid output and if it ain't the Krebs
 cycle I don't really care. It works.  

Some abstracts on the benefits of pyruvate.  

Pyruvate and the heart and glucose and insulin.  

Cardiac metabolism and electromechanics of human heart.
 Author Prasad K
 Source Recent Adv Stud Cardiac Struct Metab, 10():119-37 1975
 Abstract  

The effects of substrates on the metabolic inhibitor-induced changes in the action potential and contraction of
 papillary muscles obtained from patients undergoing corrective open-heart surgery were studied. Anoxia produced a
 marked shortening of the action potential duration and a decrease in the resting potential, rate of rise of action
 potential, effective refractory period, and contractility. In anoxic muscle, although glucose completely restored the
 action potential duration, effective refractory period, and resting potential to control levels, it was unable to
 completely restore the contractility to the control level. Substrate depletion and metabolic inhibitors (iodoacetate,
 dinitrophenol) produced effects similar to that of anoxia, but at a faster rate. Glucose restored the action potential
 and, to a lesser extent, contractility to the control level in dinitrophenol-treated muscle but was ineffective in so
 doing the iodoacetate-treated muscle. Pyruvate, however, was effective in restoring the action potential and
 contracility in iodoacetate-treated muscle. Pretreatment of the muscle with glucose and, particularly, with glucose
 plus insulin prevented the combined effects of anoxia and lack of glucose on the action potential and contractility
 for a prolonged period. These results suggest that intravenous infusion of glucose and insulin before and during
 surgery might prevent or reduced the effect of anoxia on the electrical and mechanical activity of the heart during
 open-heart surgery.  

Pyruvate was able to restore the action potential (charge) of cells treated with DNP! Unfortunately, most of you
 won't understand what an AP is even if I explained it, but I will tell you that restoring it is signiificant!  

Now you have a recipe on how to feel good on an overdose of DNP! To recap you need:
 3 Tablespoons glycerol 3x a day.
 1g Pyruvate 3x a day.
 Taurine at 3g a day.
 DNP at 36 hour intervals.  

If you start to feel bad, just drink some sugared pop or take some glucose or maltodextrin with your psuedo-OJ mix.
 The only drawback is that you will still smell rather bad and will emit a vinegar type odor although you won't be
 sweating all over everything. If you notice you are starting to sweat more it is time for another glycerol dose.  

====================================================================
 ====================================================================
 +++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++++  

Use of AS during DNP  

You can use DNP during an AS cycle although the muscle loss from DNP is minimal, if any, so I don't think this is
 the best use of your AS. If, however, you have hit a plateau the DNP for a week will help you break through that
 plateau in the subsequent week off. Now, I have experienced this, as have others, but as to whether or not it is from
 an upregulation or having a rush of T3 available or a type of overcompensation rebound is unknown, but it is cool
 and it happens..  

Use of AS after DNP or dieting.  

DNP and dieting BOTH stop conversion of T3-T4. T3 is responsible for protein synthesis. If you have been on a
 diet for 2 weeks or more your thyroid will be depressed and so will protein synthesis due to low T3. By adding AS
 you will be increasing protein synthesis while waiting for your thyroid to come back online so you won't get fat
 right after a diet.  

Use non-aromatizing AS like equipoise, ganabol, maxigan, trenbolone (finaplix or Anibolan), winny-V. Or you can
 use testosterone and an anti-aromatase like cytadren or arimidex. If you want to keep the fat off you HAVE TO use
 those anti-aromatazes with the testosterones and d-bols as they are the only ones that stop conversion of testosterone
 to estradiol. Estradiol conversion will make you fat, especially around the waist! If you have to use a testosterone
 and want to lose fat, I would use cytadren because it increase hormones which cause fat loss as well as increasing
 IGF-1 levels! (Bet you didn't know that!) I would, however, not stay on cytadren longer than one month and
 dosage is one tab divided into 4 doses per day.  

A line from a study showing that estrogen makes you fatter for the non-believers!
 Obes Res 1995 Nov;3 Suppl 4:561S-568S
 Topical fat reduction.
 Greenway FL, Bray GA, Heber D
 Department of Medicine, UCLA School of Medicine, Torrance, CA, USA.  

The fat on women's thighs is more difficult to mobilize due to increased alpha-2 adrenergic
 receptor activity induced by estrogen. Lipolysis can be initiated through adipocyte receptor
 stimulation (beta adrenergic) or inhibition (adenosine or alpha-2 adrenergic) or by inhibition of
 phosphodiesterase.  

While yes, they talk about women and estrogen and fat, the mechanism is still absolute and spans the sexes.
 Estrogen makes fat cells resistant to lipolysis. Still want to take that test without and anti-estrogen?  


 Get to fat burning faster!  

This is something you can try after you have used DNP once and know your tolerance and is a DNP manual
 exclusive! Your working dose will be around 400mg a day, correct? The first day, however, you are going to take
 600mgs in divided doses! It takes DNP a couple days to build up so this won't bother you in the least. On the
 second day you will start taking 200mg caps every 8 hours until you are sweating or getting the heat you want. Now
 you are at your tolerance dose and you can space it out to the 36 hour dosing.  


 NEW!
 Use a blood buffer to combat free radicals and lactic acid!  

Add up to one tablespoon of baking soda, sodium citrate, or potassium citrate to your drink of choice throughout the
 day. A mix of the sodium and potassium would be best. Why?
 What does DNP and exercise have in common? During high intensity exercise (supramaximal) ATP production is
 supplied by anaerobic glycolysis. This increases levels of H+ (protons) both inside and outside the cell via lactate
 and results in the feeling of fatique (Hermansen and Osnes; Sahlin) In the past, the use of sodium bicarbonate
 (baking soda) has been used and has been shown to decrease acidosis via buffering of the blood. The problem with
 baking soda is gastric distress and high salt intake with the recommended dosage of 300mg/kg which is around a
 tablespoon of baking soda for most people. Dosage for sodium citrate is 100mg-500mg per kg and did not give
 stomach problems to the users. Time to exhaustion was increased 15% which is the same as with baking soda.
 Alkalosis (making the blood basic) has been found to increase the rate of lactate and proton release from muscle
 into the blood. An increase in muscle pH causes phosphofructokinase inhibition (PFK) which is the controlling
 enzyme in glycogen utilization and therefore causes an increase in lactate formation. Those two mechanisms also
 will hold true for DNP as DNP releases protons which causes the heat. Get it out of the cell with the citrates.  


 Testomonial:
 Hey animal just thought I'd let you know the great results I had with the DNP. I got tested hydrostatically and I'm at
 4.8%. DNP is really the shit. Anyway, a buddy of mine is competing in a month and he's currently at 7% bf(he's
 about 190lbs) and he'd like to do it for two weeks. I understand that the lower one's bodyfat % the greater amount
 needed (I responded very well to 4mg/kilo but I was also dieting)  


 Questions I have answered for DNP users  

Are all of the losses on DNP fat losses?
 You can't ever say ALL in the scientific world, but it is the best we can get!  


 Animal, you have been a big help already. I've got some questions for ya. I am 195#, and plan on taking 200 mg in
 evening and 200mg before bed. I also plan on taking pyruvate and glycerol (via your recommendation). I'll going to
 use a 8on/8off cycle.
 1) Should I attempt to lift while on dnp?
 Sure.  

2) What dosage glycerol and pyruvate do you reccommend?
 3 tablspoons a day on the G and 3g of the P  

3) You said that you experienced an anabolic "burst" directly after coming off of dnp. Could this be contributed to
 your muscles reglycogenating themselves?
 No, because I didn't really get pumped, but strength went up.  

or do you feel that this is genuine protein synthesis?
 Yes, or nerve excitation/generation or a return of T3. Let me explain the nerve generation in more detail for a
 moment. When you do strength exercises of 5 reps or less you are training the nerves to fire more muscle cells and
 to fire those muscle cells in the sequence you want. Now, if we add DNP we are exhausting our muscle cells and
 they can't fire as strongly. Result? Your nervous system trains more nerves to fire other muscle cells which had
 previously gone un or underused when energy stores were high. You are getting a nerve training session due to
 exhaustion! The more I think about it the more it is like those overtraining programs where you overtrain for a week
 and you get a rebound. That is what is happening except you are overtraining at the same weights due to the DNP.
 Hehe. It is called overcompensation training and I'll take it!  


 A user:
 Found some info 'bout DNP "With even a low dosage, in the area of 3-5 mg/kg of body weight a day, it will rate
 your metabolic rate 30%. If this dosage is continued daily, it will raise your metabolism by 50%. At this rate you
 can burn about 1 lb. of fat a day."  

Animal:
 Now, let's think about this for a second. If metabolism can go from 30-50% that means there is a residual amount
 left over from the previous dose and therefore the 36hour clearance dosing schedule which I recommend.
 Furthermore, when I overdosed on 800mg I sweat for OVER 48 hours so this tells me that the half-life can be even
 longer in some circumstances. It is, nonetheless, up to you as to how you want to take it. If every 24 hours is
 tolerable for you, then do it.  

A user:
 That's not what I've noticed. At present I'v even gained some weight. I'm 98 kg now. I don't look a bit harder but
 maybe I shouldn't expect that after only 4 days.
 You WILL hold onto to water! You WILL be depleting carbs from the muscle that will make you look flat! Most
 WILL NOT notice the benefits until a week or two later upon cessation of DNP. Some see benefits right away, but
 they appear to already have a bodyfat below 10%.  

A speculator wrote:
 For a person that is highly active and on a calorie restricted diet, DNP will deplete ATP within a matter of days.
 When this happens your body temperature will go back to normal. The only thing you can do at this point is
 supplement with in the dosage area of about 150 mcg/day."  

Animal:
 Believe me, you will feel wasted (tired) and LOSE muscle on the regimen and the liver does not control oxidative
 phosphorylation in every cell. You will still be hot regardless of your T3 levels.  


 Question:
 Won't the conversion of T4-T3 come back and function again after discontinuing DNP administration?
 Animal
 Yes, and as long as you do some carbs at 600g a day for three days after.  

Or do I have to look to get T3 as well?
 Animal
 Not really, if ATP was being ever totally depleted you would be cramping. Lack of ATP generation happens when
 you are what? DEAD!!!!!! It is called rigomortis and if people who write right about DNP had an education or an
 inkling about body chemistry and process they would know this! Total ATP depletion resulting in death of the cell
 is not possible. There is some safety mechanism and I imagine it is via the fat cells, but you will not deplete your
 ATP unless you are an anorexic or dead.  

User:
 And isn't a total lack of ATP what we want, so we can start burning fat instead of ATP?
 Animal:
 Wrong and this is not your fault, but again those who claim to be experts who are dispensing such disinformation.
 Once the ATP to ADP and to AMP is changed below a certain amount the cell gets it energy from another source
 which would be the fat. You are looking to burn the glycogen and then the fat is used. This does not mean ATP is
 gone!  

Why is thermogenesis stopped if there isn't any ATP?
 Animal:
 Read above and it is never stopped. DNP NEVER stops working unless the proton gradient is severely altered.
 Even in such a case, parts of the mitochondria can have one direction of proton gradient while another section can
 have a DIFFERENT proton flow!  

User:
 Is this why you want a break after one week? To load up with ATP so thermogenesis can start again?
 Animal:
 No, so you don't feel like shit all the time and so you can get the liver converting T4-T3 again  

Is a one-week-break enough? Or maybe too short if I'm in a hurry.
 You could do DNP for 2 weeks or more if you want.  

Wouldn't it be enough just to discontinue the DNP-cycle to let the liver start converting T4 to T3?
 That is why you stop after a week!  

Where are ATP-molecules stored?
 In and/around the mitochondria and in the cytosol of the cell and ATP is attached to certain enzymes waiting for
 activation.  

How much ATP do we have in storage?
 That is a major calculation and I haven't looked for an answer, but I don't think it is important as you can never get
 rid of all of it.  

A speculator:
 "The administration of DNP, at a dose of 3.5 mg per kilo, increases the total production of heat by about 40%, from
 the 3rd or 4th day. This increase of the metabolism is due MOSTLY to an increase in the combustion of the fat and
 a LITTLE to combustion of carbohydrates."
 Any comments on this?  

Animal:
 Again, you are seeing a residual affect. The molecules that the mitochondria use for production of ATP can come
 from carbs or fat, but the important part is that it is not from muscle.  

Another fact found in the same report as above:
 "In prolonging the administration of the medication, one observes an increase of the tolerance of carbohydrates."
 Does this mean we get increased insulin-sensitivity?
 That is a weird sentence and I don't know what it means, but I think it means you will be more receptive to carbs.
 You now have increased your insulin sensitivity and this could explain the DNP users' craving for carbs while using
 DNP.
 ..
 So when I eat carbs (I've noticed that I start to sweat then) the body starts burning fat?
 No, the body burns excess ATP and food intake itself is thermogenic.  

Why simple sugars? That means I should walk around eating candy all day?
 Candy is not really a simple sugar as it usually has fat or fructose with it.
 You want a simple sugar every so often to get some insulin rise and some fructose will help recarb the liver as
 fructose is about 4 times better at recarbing the liver than glucose. Glucose is, BTW, 2 times at good at recarbing
 muscle when compared to fructose.  

What happens with the carbs?
 They are burned and insulin release and helps change charge on the cells.  

Insulin is secreted. I've noticed that. (If it wouldn't I'd go glucose-high-'n-crazy.) Do I store carbs as glycogen?
 AHAHA! So much for the speculators that say you have to do insulin!
 You won't have time to make glycogen and the glucose will go right to ATP production.  

What about cataracts and skin lesions?
 That is a long term chronic dose situation and why you take pyruvate.  

Have you noticed anything?
 Yes, your sweat smells bad, but no lesions. Another reason you want simple sugars or insulin is that DNP starts to
 make your vision blurry if you are on a low carb diet.  

Animals' Analysis of someone else's recommendations:  

Comment
 After 7 days, DNP dislodges T4 off the carrier proteins, allowing the T4 to be excreted rapidly.  

Animal:
 THIS IS A FUNCTION OF THE PRESENCE OF ATP. END OF DISCUSSION! This has been proven with
 many people who have used pyruvate which provides an easily usable energy source. Most users only stay on it 7
 days so the point would be moot. Since you have depleted the carbs from the liver you are changing the ability of
 the liver to change T4 to T3. This happens with ANY diet within 7 days. With DNP you have inhibition of
 conversion via heat (small factor I believe) and via glycogen depletion. This loss of water due to glycogen
 depletion changes the osmolarity of the liver cells and inhibits the conversion of T4-T3. Now, with the concomitant
 loss of water you have a loss of charge which is what we are trying to control with the taurine dosing..  

Comment
 I have used T3, and recorded the average elevated body temperature at day 4 on DNP. After 7 days, the temp will
 decline, so I use T3 2X a day to restore the elevation.  

Animal.
 Really? Most people, including myself, hardly notice any temperature change. I used T3 at 50mcg up to 100mcg on
 day 5 and never felt worse or more run down than any other DNP experiments I have done.  

Comment:
 It really doesn't matter how much or how long for the T3, because though excessive-looking, T3 blood level will be
 normal.  

Animal:
 This is NOT true because people have had their thyroid tested while on DNP and their thyroid levels were sky high.
 Excess thyroid can be responsible for what when calorie deprived? Muscle breakdown. Carbs are gone due to
 DNP. Your cells are going to be looking to scavenge energy so they are not going to have any protein synthesis
 because this requires energy. You are going to be in ketosis which is producing glucagon which is responsible for
 protein breakdown. You will, therefore, have no insulin which is responsible for anabolism of glycogen. You will
 have no blood sugar or liver glycogen left. Now what is going to happen?! Muscle breakdown. DNP is carb/fat
 specific and since there is no glycogen/glucose circulating due to high fat-low carbohydrate diet, where is the energy
 coming from? Ketones can't be made into carbs and about the only source of carbs you are going to have is the
 glycerol molecule which results from fat breakdown which is minimal. Now throw your excess T3 on there.
 Hmmm? Sounds like a recipe for muscle breakdown to me.  

Comment:
 Besdies, you'll get sick before you have to worry of being on T3 so long. Trust me, children: DNP for 7 days, and 7
 off. You'll be much healthier.  

Reply.
 I totally disagree! Many of us have permanently lowered body temps due to clen-T3 usage which many of the same
 moron gurus recommended even when using clen for 2-3 weeks. The thyroid is going to see excess T3 in the blood
 and do you think it is going to want to produce more T4 and T3 on its own? This is what I really don't like about
 doing the T3, here. Yea, it is only for a week, but 2 weeks on clen which is not even T3 has fucked up many of us,.
 If your theory panned out then why couldn't we do 1 week AS cycles or why have all the 2x2x2 cycles fallen into
 the pit of futility? I know we are talking different receptors, but they all still function via the negative feedback
 system.  

Auxillary  

(Consultation question)
 After this Clen, DNP, and high fat diet experience I'm hoping to be down to around 7%BF. Which would leave me
 at about 165-170lbs. That is too small for me. I want to go on a cycle after that and try to put on a good 20lbs. I
 have a great diet for my cycle, so I know if I dont make the 20lbs gain I want its not because of nutrition. ( A
 problem i seem to always have). I wanted to know your thoughts on a cycle that I could really put on a good 20lbs.
 I know how much of your gains you keep depends on what you do prevent losses ( example: Clomid, and something
 to regulate cortisone levels, along with others, I have a gains keeper formula I plan to use). but If I do this I want to
 keep the majority of my gains. That's why I wanted to include primo since you usually keep what you gain from
 primo.  

Answer
 Yea, but you don't gain much and Eq or ganabol would be better as would fina.  

Can you think of a good combo to add to primo for permanent MASS gains?????
 Answer
 Test (Tp, Tc, Te) or a trenbolone (fina, anibolan, parabolan). D-bol then fina always works nicely, too.  

Maybe deca and sustanon or deca and omandren????
 Answer:
 Wouldn't go with deca and sus and omna are more or less the same.  

Any other s??? ? I have heard if you want to keep gains tests are not good to use
 (enthanate, cyp etc.)
 Answer:
 BS. You have to know how to come off and not overtrain as you are coming off. Think about it. You have gotten
 stronger which is a result of nerve training. Now if you lift and let your muscles recover longer when off the AS
 you won't lose your size!  

.. Do I have to take insulin while on DNP if I am taking equipoise and finaplix?
 Answer:
 No, not really and not if you are going to stay on only for a week at about 400mg or less DNP dose.  

Do I have to take cytomel, clen or ECA stack while on DNP?
 Answer:
 I would take EC, but do the others after being careful to note that Clen and T3 will suppress your natural T3.
 Would be better to throw in tyramine and yohimbine or mazindol.  

I have quite a bit of clen, and cytomel, but no ephedrine.
 Answer:
 You can sub in PPA or adipokinetix or pyruvate or nicotine or mazindol.
 ( I have never had a problem doing nicotine as a chew or as cigars and then quitting, but this is obviously not for all)  

I didn't understand if you said whether or not to start with a low dosage of DNP or not.
 Answer:
 I would if you have never done it before just to see what your tolerance is.  

Question:
 Also, you told me that I should not take cytomel while I am using> the DNP but to use it after the DNP. I was
 under the impression that DNP suppresses the thyroid and that I should use the cytomel while using the DNP so I
 will keep burning fat. Would you please explain this to me?  

Answer:
 DNP alters the blood and liver glucose levels and THIS is what keeps the liver from converting T4-T3. If you eat
 normally this won't happen so drastically and T3 will return to normal soon after stopping DNP. Now, if you have
 low Blood sugar levels and you add T3 you are going to lose muscle as well as is seen in people that are on low
 calorie diets who supplement T3. T3 without the right energy and hormones stores is disastrous to muscle.  

Other dieting stuff  

ketotifen and upgrade of clen receptors, but you need 10 1mg tabs of ketotifen a day which will make you hungry
 and sleepy.  

I was thinking of the efficacy or more like the 'sense of adding t3 toDNP.
 Well, if you are adding-T3 you are going to have a lot of T4 AND T3 floating around and the thyroid is going to
 read that as an exess and shut down T3 and T4 production.  


 Other cycles for DNP use  

Why not do DNP in even smaller doses like that of ephedrine up to 100mg or so?. It will speed up the metabolism
 and cause a loss of weight without all the discomfort and t4-t3 conversion shutdown. Furthermore, by speeding up
 the metabolism it may help upgrade steriod receptors and clen receptors with much less discomfort for the user.  

DNP seems to upgrade clen receptor sites as well as steroid receptor sites.
 The rebound for the AS upgrade is only known from anecdotal feedback from myself and others, but if you increase
 the metabolism of the cell it only stands to reason that you are going to decrease the time it takes to regenerate the
 receptor sites. The ATP depletion and opening of ATP channels is also likely to be playing a part in these benefits
 as well, but that is research that probably won't be done. So the channel part in the upgrade is just speculation.  

Some may need to build-up the dose to start. I had to do it for 3 days and then do 800mg before I started to sweat
 like a pig for 2 days! Now moderate doses of 200mg make me sweat although not to the same extent, but at least I
 know I've taken it. Kinda like bee stings. You don't have any allergic reaction until one sting and then you get the
 benefits (problems) from one sting. I do know of a case with a women that had similiar results and said it wasn't
 working and even talked to w8 about it, but then she ordered more so this has to be what the problem was/is.  


 Response to someone that was throwing up and nauseated from DNP use.  

You have low blood sugar!
 This is a classic symptom which can occur with diabetics who use too much insulin. When I use too much insulin
 and then ride too soon after I would see spots. DNP caused me to see spots as well. DNP depletes all your blood
 sugar and glycogen first and this will give you low blood sugar, nausea, etc. That is why you want to get your
 insulin up with glucose once or twice a day on DNP and DO NOT do high fat diets on DNP. W8 will disagree with
 me on this, but when you look at the actions happening at the liver you will realize that high fat diets just extenuates
 the slowdown of T4 to T3 conversion.  


 Q: But when I'm off I'm gonna keep carbs almost non-existant to burn more fat, and take Adipokinetix to avoid a
 rebound off of the DNP.
 A: DNP stops conversion of T4-T3 due to carb depletion so you may not want to do that although the Adipo is
 good. DNP, Adipo, clen, ECA, DNP would be a good way to go or do the clen right before a week of DNP, but
 only for a week.  


 Q: IM OFF MY CYCLE IN AWEEK. THEN IM GONNA TAKE CLOMID, PS,NOLVADEX, TO AVOID A
 LOSS INGAINS. THEN ITS CUTTING TIME.
 A: Nolvadex and clomid are redundant, do one or the other. PS sucks, but if you already have it, then use it.  

==================================================================================
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 ===========================================  

Good things about DNP:  

Biological Study of Dinitro Drugs in Humans
 By Dr. Jacques Bell
 Translation Copyright 1996 Robert Ames  

There is a fundamental difference between biological experimentation with dinitrophenol in humans and what was
 done in the laboratories of physiologists. These last are essentially interested in hyperthermia (Andre Mayer,Leon
 Binet, etc.). Yet, in medicine, the doses of dinitrophenol employed do not determine any elevation of temperature.
 The physiological effects, observed in these conditions, differ considerably from those made by the experimenter. It
 is thus for example that the animal in hyperthermia presents a polypnoea [rapid, shallow breathing], a
 hyperglycemia, a hypoglobulinemia that one does not observe with therapeutic doses; it is because experimental
 hyperthermia is essentially a combustion of carbohydrates, while therapeutic hypermetabolism is
 mainly a combustion of lipids, as is shown by the lowering of respiratory quotient.  

One shouldn't be surprised at these differences. The clinician uses strychnine as a tonic; the experimenter employs it
 to cause convulsions. The clinician uses adrenaline, at titrated doses, to produce a manageable hypertension; the
 physiologist, with massive doses causes acute edema of the lung.  

Yet, to base the clinical use of adrenaline or of strychnine on acute edema of the lung or experimental convulsions,
 constitutes an obvious error. It is the same for dinitrophenol.  

In France, besides, one uses almost exclusively dinitrophenyl-lysidine, which, according to the same terms of the
 study made by Professor Pouchet, "is easy to purify by crystallization, to easily modify the first of its components
 from the point of view of toxicity, dissolves easily in water, and, by addition of the methylglyoxalidine
 (lysidine)group, favors energetically the elimination of waste."  

After Professor Pouchet, we have, in our thesis [1], demonstrated the superiority of this last product; in what
 follows, it is by comparison with him that we will study the biology of the dinitro drugs.  

We shall see, in order:  

I. Their action on the basal metabolism,
 II. Their visceral action,
 III. Their nutritional action.  

I. ACTION ON BASAL METABOLISM  

After the experimental research of Magne, Mayer and Plantefol, in animals, the experiments of Cutting and Tainter
 has confirmed, in humans, that dinitrophenol is a drug which strongly increases the metabolism, exaggerating the
 oxidation process of the organism by direct action on the cellular metabolism. These authors have observed a rise of
 close to 20% after one hour, being able to attain 70% in ten hours and a tendency to return to normal at 24 hours if
 the administration of the medicine is not continued.  

This increase is not due to a sympathetic deregulation. The dinitro treatment respects the autonomic nervous system,
 in an inverse way from thyroxine, which, at slimming doses, determines rapidly some tremors, insomnia, and a
 mental instability of the type "basedowien." [a thyroid illness where one secretes too much thyroid hormones]  

In the thyroid illnesses, or the thyroid treatments, there is an inverse connection between the level of the basal
 metabolism and that of blood cholesterol, this being as much lower as the metabolism is higher. One doesn't observe
 similar phenomena in the course of dinitro treatment.
 This fact indicates that the changes caused in the blood cholesterol in the course of thyroid treatment are directly
 linked with the thyroid medication and not at all to do with the elevation of the metabolism which is responsible for
 the reduction of obesity. Dinitrophenol has almost no action on the blood cholesterol. (Grant and Schube).  

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

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

2. This increase of the metabolism is due mostly to an increase in the combustion of the fat and a little to
 combustion of carbohydrates.  

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

II. VISCERAL ACTION  

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

This innocuity for the principal visceral functions is without doubt one of the main reasons for the distribution of
 this therapy.  

Tainter, Stockton and Cutting have reported a series of cases in which one had measured the plasma bile index and
 determined the test of Van de Bergh. Their analyses demonstrate, beyond a doubt, that the liver does not suffer any
 damage in the course of dinitro treatment.  

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

As T.L. Schulte and M.L. Tainter wrote, "it doesn't seem that dinitrophenol at usual clinical doses is likely to harm
 the kidneys."  

Dinitrophenol is remarkable for its absence of effect on the cardio-vascular system. Even when the basal
 metabolism is found elevated to significant levels, there is no change in the rhythm of the pulse (Rosenblum).  

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

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

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

III. ACTION ON NUTRITION  

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

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

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

Thyroxine reduces bone density.  

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

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

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

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

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

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

Finally, thyroxine causes a nitrogen malnutrition: it burns the muscle and fatigues the heart.
 Dinitrophenol-lysidine, to the contrary, causes a lipid-glycemic loss: it is the elimination of reserve materials
 without attacking visceral and muscle tissue.  

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

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

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

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

Studies to ponder which helps you see where my answers have come from.  

Here is why you need to eat a regular diet:  

Subject: DNP, Insulin, and ATP-sensitive Potassium channels  

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

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

o Increase in blood glucose -> increase in glucose metabolism -> increase in intracellular ATP -> inhibition of
 KATP channel.  

o Channel CLOSED: cell depolarized, Ca++ uptake, insulin exocytosis.  

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

o KATP channel BLOCKED -> vascular tone increases.  

o KATP channel ACTIVATED -> vascular tone decreases.  

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

o KATP BLOCKED -> more strength  

o KATP ACTIVATED -> less strength  

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

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

Drugs which activate K channels: pinacidil, cromakalim.  

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

DNP  

What happens when someone takes the uncoupler dinitrophenol (DNP)? Blood glucose will result in increased
 metabolism, but the level of ATP in the cell does not increase! In fact, it is depleted. So in this case, the KATP
 channel is not inhibited, and it stays open. Calcium is not taken into the cell, and insulin is not released. The person
 taking DNP has in effect given himself temporary diabetes.
 (Animal; another study shows that insulin internalization is also affected so taking insulin is useless)  

Insulin is needed to facilitate the uptake of glucose into cardiac, skeletal, and adipose tissue, and to convert glucose
 to glycogen in the liver. It is anti-proteolytic and protects against the various ailments commonly seen in diabetics,
 such as vision problems and polyneuropathy. Not coincidentally, the same problems can result from ingesting DNP.  

This is why, when one takes DNP, one also needs to take exogenous insulin.Since the KATP channel remains open,
 vascular and muscular tone relax. Probably blood pressure will decrease. Strength will diminish.  

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

Animal;
 Why all this is a good story we do have to look at what he said in the beginning as in caveat lector. While his
 speculation on KATP channels and the need for insulin is understood-, his mechanisms are a bit incorrect. DNP
 causes an internalization of the receptor so you now have a cell that is desensitized to insulin and all the insulin in
 the world will not help that. Second, the KATP channels can be controlled with pyruvate.  

Studies  

DNP causes insulin insensitivity by preventing internalization of the receptor.  

Insulin internalization into monocytes is decreased in patients with type II diabetes mellitus.
 Author Trischitta V; Gullo D; Squatrito S; Pezzino V; Goldfine ID; Vigneri R
 Source J Clin Endocrinol Metab, 62(3):522-8 1986 Mar
 Abstract  

We studied the internalization of [125I]insulin into circulating human monocytes, a cell type widely used for insulin  

binding studies. The internalization of [125I]insulin was assessed by both an acid extraction technique, which
 removes surface-bound insulin but not intracellular insulin, and by a trypsinization technique, which removes cell
 surface-bound hormone. After 5 h of incubation at 22 C, over 40% of the total cell-associated [125I]insulin was
 internalized into monocytes of normal subjects. This internalization was temperature dependent; the fraction of
 internalized hormone was progressively decreased when the incubation temperature was reduced from 37 to 4 C.
 Treatment of monocytes with increasing concentrations of 2,4-dinitrophenol also decreased [125I]insulin
 internalization, whereas dansylcadaverine, an inhibitor of transglutaminase, had no effect. Analysis by gel filtration
 of the internalized labeled hormone after 4 h of incubation at 22 C indicated that 50-60% of the label was degraded
 insulin, but detectable intact insulin was still present. Internalization of insulin was then studied in monocytes from
 eight obese patients (161% of ideal body weight) with type II diabetes mellitus. After 4 h of incubation at 22 C, the
 specific total monocyte-associated [125I]insulin was decreased compared to that in cells from 7 normal subjects
 [6.02 +/- 0.38% (+/- SE) vs. 3.91 +/- 0.31% of the total; P less than 0.001]. Moreover, the percentage of hormone
 that was internalized was also decreased from 41.4 +/- 1.2% of the total to 28.9 +/- 1.8% (P less than 0.001). In 20
 nondiabetic obese subjects, specific cell-associated [125I]insulin was reduced to 3.9 +/- 0.3% (P less than 0.001).
 However, compared to that in normal subjects, the percentage of hormone that was internalized was not decreased
 (39.7 +/- 3.51% of the total). The present findings indicate that human circulating monocytes internalize
 [125I]insulin; this process is temperature and energy dependent; and monocytes from obese type II diabetic patients
 have a significantly decreased ability to internalize insulin. This decreased internalization may play a role in the
 cellular resistance to insulin that occurs in these patients.  

DNP enhances binding of insulin to the receptor, but does not internalized it.  

The effect of phenformin and other adenosine triphosphate (ATP)-lowering agents on insulin binding to IM-9
 human cultured lymphocytes.
 Author Vigneri R; Maddux B; Goldfine ID
 Source J Cell Biochem, 24(2):177-86 1984
 Abstract  

In the present study, we investigated the mechanism by which the antidiabetic drug phenformin increases insulin
 binding to its receptors in IM-9 human cultured lymphocytes. After a 24-hr preincubation, phenformin induced a
 twofold increase in specific 125I-insulin binding, and removal of phenformin was followed 6 hr later by a return in
 binding to control levels. This effect of phenformin on insulin binding was not a consequence of either inhibition of
 cell growth, changes in cellular cyclic adenosine monophosphate (AMP) levels, or changes in guanosine
 triphosphate (GTP) content. Since phenformin is known to inhibit various aspects of cellular energy metabolism, the
 relationship between 125I-insulin binding and energy metabolism in IM-9 cells was investigated. The
 phenformin-induced increase in insulin binding to IM-9 cells was related to a time- and dose-dependent decrease in
 ATP levels. Other agents that lowered ATP levels, including antimycin, dinitrophenol, and 2-deoxyglucose, also
 raised insulin binding. These studies indicated, therefore, that phenformin enhances insulin binding to receptors on
 IM-9 cells and that this effect on insulin receptors may be related to alterations in metabolic functions that are
 reflected by a lowering of ATP levels.  

DNP blocks all internalization so is more insulin going to help? No.  

Evidence for two independent pathways of insulin-receptor internalization in hepatocytes and hepatoma cells.
 Author McClain DA; Olefsky JM
 Address Department of Medicine, Veterans Administration Medical Center, San Diego 92161.
 Source Diabetes, 37(6):806-15 1988 Jun
 Abstract  


 A study of insulin-receptor internalization and recycling was undertaken in primary cultures of rat hepatocytes and a
 human hepatoma cell line (HepG2). Receptors were quantitated by measuring 125I-insulin binding to partially
 purified soluble receptor preparations from untreated cells (total receptors) and trypsinized cells (intracellular
 receptors). In resting HepG2 cells, exposure to insulin results in internalization of insulin receptors, the rate and
 extent of which is dependent on the insulin concentration. However, receptors do not accumulate inside the cell in
 proportion to the higher rates of internalization at high concentrations of insulin. This lack of accumulation is
 explained by much higher recycling rates after exposure to high concentrations of insulin. Similar results were noted
 for primary cultures of rat hepatocytes. These results imply qualitatively different fates for receptors internalized
 after exposure to different concentrations of insulin. To further investigate the possibility of different pathways for
 insulin-receptor internalization and processing, cells in low (1 ng/ml) or high (100 ng/ml) concentrations of insulin
 were exposed to drugs or treatments known to affect receptor metabolism. Hypotonic shock and hypokalemia,
 which arrest coated-pit formation, blocked internalization of insulin and insulin receptors at low concentrations of
 insulin but allowed internalization in response to high concentrations of insulin. The lysosomotropic drugs
 monensin and chloroquine caused intracellular accumulation of insulin and its receptors internalized at low
 concentrations of insulin but had a relatively smaller effect on receptors internalized at high concentrations of
 insulin. All internalization is blocked by 2,4-dinitrophenol. We conclude that high doses of insulin lead to
 insulin-receptor internalization and recycling through a pathway that is functionally distinct from the pathway taken
 by receptors internalized by low (physiologic) concentrations of insulin. The pharmacologic experiments raise the
 possibility that the high-dose pathway, unlike the low-dose pathway, may proceed independently of coated pits and
 endosomal acidification.  

Degradation of insulin by human fibroblasts: effects of inhibitors of pinocytosis and lysosomal activity.
 Author Kooistra T; Lloyd JB
 Source Int J Biochem, 17(7):805-11 1985
 Abstract
 The role of the pinosome-lysosome pathway in the degradation of 125I-labelled bovine insulin by cultured human
 fibroblasts was examined by comparing the effects of various known inhibitors of pinocytosis and lysosomal
 degradation on the uptake and degradation of 125I-labelled polyvinylpyrrolidone, formaldehyde-denatured bovine
 serum albumin and bovine insulin by these cells. Fibroblasts incubated with polyvinylpyrrolidone steadily
 accumulate this substrate, whereas incubations with insulin or denatured albumin led to the progressive appearance
 in the culture medium of [125I]iodotyrosine. Inhibitors of pinocytosis (bacitracin, colchicine and monensin),
 metabolic inhibitors (2,4-dinitrophenol and NaF), lysosomotropic agents (chloroquine and NH4Cl) and an inhibitor
 of cysteine-proteinases (leupeptin) decreased the rate of uptake of polyvinylpyrrolidone and denatured albumin very
 similarly, but only bacitracin had an effect on the processing of insulin. Chloroquine, NH4Cl and leupeptin strongly
 inhibited the digestion of denatured albumin, but not of insulin. The different responses to the modifiers, with
 polyvinylpyrrolidone and denatured albumin on the one hand and insulin on the other, suggest that insulin
 degradation can occur by a non-lysosomal pathway. The very strong inhibitory effect of bacitracin on insulin
 processing by fibroblasts may point to an important role of plasma membrane proteinases in insulin degradation.  


 References:
 1. Noma A. 1983. Nature 305: 147.
 2. Noma A, Takano M. 1991. The ATP-sensitive K+ channel. Jpn J Physiol 41(1):77-87.
 3. Civelek VN, Deeney JT, et al. 1996. Temporal sequence of metabolic and ionic events in glucose-stimulated
 clonal
 pancreatic-cells. Biochem. J. 315: 1015-1019. Boston University Medical Center.
 4. Nichols, C.G. and Lederer, W.J. 1991. ATP-sensitive potassium channels in the cardiovascular system. American
 Journal
 of Physiology 261:H1675-H1686.
 5. Paucek, P, Mironova, G, et al. 1992 "Reconstitution and partial purification of the glibenclamide-sensitive,
 ATP-dependent
 K+ channel from rat liver and beef heart mitochondria," J. Biol. Chem. 267, 26062.
 6. Nakamura S. 1989. Glucose reverses DNP induced changes in action potentials. Cardiovascular Res.
 23(4):286-294.  

Here is the scare story that is going around on cataract. I raise this because of the connection with this problem and
 insulin and the previous story. I was starting to see spots and when I took insulin they went away. The myopia
 stops when DNP is discontinued. Note, that this was a chronic user below.  

Subject: DNP and Cataracts  

MDGADPC has kindly sent me a photocopy from the French journal Annales des Oculistes, concerning the effects
 of DNP on the eyes. Since this paper may be of some general interest, I have translated it and attach it below.  

For those who may be unaware, DNP or dinitrophenol is a toxic compound which was used for weight loss in the
 1930's. It was withdrawn from the market as a result of severe side effects, including deaths, but recently it has been
 suggested that it could have a role in the contest preparation of elite bodybuilders.  

One point to consider in the text below is that cataracts may develop 6 to 12 months after the DNP treatment is
 completed.
 Note: the intake of DNP was chronic and continuous.  

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

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

These authors have established that the ingestion of dinitrophenol accelerates metabolism, causing a marked
 elevation in temperature. It seemed that dinitrophenol was a specially effective treatment for obesity. In 1936,
 Horner estimated that in the first 15 months following the appearance of the medication in the market, one hundred
 thousand persons used it to lose weight.
 Note: 100,000 people used it.
 Incidents and accidents multiplied and appeared sufficiently serious that the American Medical Association warned
 the public against the dangers of unsupervised treatment.  

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

One can say that it is by the work of Onfray and Gilbert Dreyfus presented to the Congress of the S.F.O. [Societe
 Francaisedes Oculistes?] in 1937 that French opthamologists had their attention drawn to the subject. This
 remarkably precise work is enriched by two observations of which one is due to Doctor A. Gallois, of Besancon.
 We frequently reference this, for it contains in addition to minutely observed details, important physio-pathogenic
 considerations and a complete history of the subject.  

Apart from this work, we should also to point out the observations of Van de Hoeve and Polak-Daniels published in
 Hollandin 1936, as well as the French summaries and reviews of Halbron on cataracts and of Laignel-Lavastine on
 dinitrophenol intoxication.  

Finally, we emphasize the interest of the work of Vogt on the cataracts caused by dinitrophenol in Switzerland and
 of G.Ciotola of those caused by alpha dinitrophenol in Italy, both published in 1937. The same year, Stein and
 Crevecoeur pointed out that in their opinion this affectation was, when all is said and done, quite rare if one thinks
 of the enormous dissemination of
 dinitro treatment. This was also the opinion of Andre Mayer, based on the fact that despite the considerable number
 of intoxications by dintrophenol observed in munitions factories, no cases of cataracts have been noted.
 Note: Because they were not intoxicated with it continuously.  

Finally, in 1938, Carlotti and Rivoire de Nice presented a case of cataract by dintrophenyl-lysidine which developed
 "with almost lightning-like rapidity."  

It was possible for us to observe two very demonstrative cases. In one there was an arrest of development of opacity
 after the patient stopped taking dinitrophenol, which is more than a rarity, a real exception in the pathological
 history of dinitrophenol cataracts.  

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

Mme K... thus learned that she was rapidly becoming myopic.  

The most minute research were done in view of identifying a possible cause of this bilateral cataract. All the blood
 and urine tests were negative. Very complete clinical examinations by Doctor P..., referring physician, point to the
 same conclusion that it is impossible to relieve Mmme. K...'s pathological process at all.  


 It is then that I thought of asking her about the possibility of a dinitrophenol anti-obesity treatment, even though the
 corpulence of my client did not seem excessive. She told me then of having taken two pills each day of 0.30 grams
 of dinitrophenol in series of ten days with a rest of 15 days, for the past year and a half.
 Note: That is a long time!  

She had, without the least dietary restriction, lost 19 kilograms out of 87 [42 pounds out of 191]. It was at that point
 that she began complaining about her vision.
 Note: She lost a lot of weight, too!  

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

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


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

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

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

OBSERVATION II.  

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

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

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

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

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

REFERENCES  

ALLEN and BENSON. Late development of cataracts following use of dinitrophenol about a year before. JAMA,
 1935,
 V, 105, p. 795. BARKAN, BORLEY, FINE and BETTMAN. Operative results in cataracts coincident with
 dinitrophenol
 therapy. Cal W. Med. 1936, XXXXIV, p. 360.  

BENCE, JONES. On the rate of passage of crystalloids into and out of the vascular and non-vascular textures of
 the body.
 Pr. R. Soc., 1863, London, 14, 400.  

BOARDMAN. Rapidly developing cataracts after dinitrophenol. JAMA, 1935, CV, p. 108.  

CAMERON, cited by HORNER. Arch. of opth. 1936, XVI, p. 452. CARLOTTI and RIVOIRE. Sur un cas de
 cataracte per le Dinitrophenyllyside. Rev. O.N.O., Nov. 1938, p. 622-624. CAZENEUVE and LEPINE. Sur les
 effets
 produits par l'ingestion et l'injection intraveineuse de trois colorants jaunes derives de la houille. C.R. Ac. Sc. de
 Paris, 1885,
 CI, p. 1, 167. CIOTOLA (G.). Cataracte par alpha-dinitrophenol. Boll. d'Oc., 16, 1937, p. 531.  

COGAN D. and COGAN F. Dinitrophenol cataract. JAMA, 1935, CV, p. 794.  

CUTTING, MEHRTENS, TAINTER. Dinitrophenol, not acceptable for N.N.R. JAMA. 1935, CV, p. 31.
 (Important
 bibliography on the subject).  

DALLY. Du nouveau sur le dinitrophenol. Concours Med. 1935, L, p. 3, 491.  

EBSTEIN and ROSENBLUM. Peripheral neuritis and abortion following dinitrophenol therapy. J. Lab. an Clin.
 Med.
 1935, XX, p. 1, 118. GIBBS-Reichert. Am. Chem. J., 1891, XIII, p. 289. GUTZEIT (R.). Cure d'obesite et
 cataracte.
 Munch. med. Wschr., 2, 1937, p. I.724.  

HALBRON. Les cataractes apres emploi therapeutique du dinitrophenol. Sem. des Hopitaux de Paris, XII, 1937,
 p. 329.
 HORNER, JONES, BOARDMAN. Cataracts following the use of dinitro.  

JAMA, 1935, CV, p. 108.  

HORNER. Cataracts after dinitrophenol. Ar. of Opth. 1936, XVI, p. 446-461.  

HORNER (W.-D.). Cataracts following dinitrophenol treatment for obesity. Transact. of the opth. sect. of the
 Amer. Med.
 Ass., 1936.  

KNISKERN. Cataract following dinitrophenol. JAMA, 1935, CV, p. 794.  

KOCH-LEE and TAINTER. Dinitrophenol on liver function. Calif. and W. Med., 1935, XXXXIII, p. 337.  

LAIGNEL-LAVASTINE. Soc. Med. des Hopit. de Paris, 1937.  

LAZAR. Cataract following dinitrophenol. JAMA, 1935, CV, p. 794. LEUTSKER. Instance of circulatory
 collapse
 attributed to dinitrophenol. U.S. Nav. Med. Bull., 1935, XXXIII, p. 394. MAC BRYDE-TAUSIG. Functional
 changes in
 liver, heart and muscles loss of dextrose tolerance resulting from dinitrophenol. JAMA, 1935, CV, p. 13.  

MAGNE, MAYER, PLANTEFOL, et al. Etude sur l'action du dinitrophenol. An. de Physiol., 1932, CV, p. 12.  

NADLER. Peripheral neuritis caused by prolonged use of dinitrophenol. JAMA, 1935, p. 12.  

ONFRAY and GILBERT DREYFUS. Bull. et Memoires S.F.O., 1937, (I, pp. 114-128).  

ONETO-GALINO-NATALE. Developpement de cataracte aux deux yeux, consequence d'un traitment au
 dinitrophenol
 pour amaigrissement. Soc. Argentin. of., 24 Oct. 1937.  

PERKINS. A study of munitions intoxication in France. Pub. Health Rep., 1919, XXXIV, p. 2, 335.  

RODIN. Cataracts following the use of dinitrophenol. Calif. West Med. 44.4, 1936, p. 3.  

SCHUTES. Dinitrophenol. Am. J. Opth., 1935, 18, p. 752. SPAETH (E.-B.). Cataractes dues au dinitrophenol
 avec
 symptomes de tetanie. Am. J. Opth., Apr. 1936, p. 320-323.  

STEIN and CREVECOEUR. Semaine des Hopitaux de Paris, 15 Dec. 1937.  

TAINTER, CUTTING and STOCKTON. Use of dinitrophenol in nutritional disorders. Am. J. Pub. Health., 1934,
 XXIV,
 p. 1045. VAN DER HOEVE and POLAK-DANIELS. Cataracte et dinitrophenol.  

Nederl. Tijdsch. V. Genessk., I, 1936, no. 2, p. 126.  

VOGT (A.). La Cataracte par dinitrophenol en Suisse. Schweiz.  

Med. Wocst., 76-37, 11 Sep. 1937, p. 873.  

WHALMAN. Dinitrophenol cataract. Am. J. O., Oct. 1936, XIX, p. 885.  

Copyright 1995-97 Deja News, Inc. All rights reserved.  


 DNP and GHB?  

What are you talking about? Not really GHB, but gamma-butyrolactone (GBL)! I am also about to tell you how
 they will never be able to shut down GBL sales. GBL is non-toxic and is used as acetone free nail polish remover.
 GBL will take the ink stains off almost anything. I was pouring some into a bottle and it got down the side on the
 label and the color was gone, running down the side. You can remove ink stains from white shirts, etc. If somebody
 wants to sell GBL, all they have to do is make some bottles that say, 'Acetone free nail polish' or 'Ink remover' A
 friends kid spilled puffy paint on the carpet. It was red on a white carpet to boot! We tried everything to get it out;
 acetone, laquer thinner, rubbing alcohol and so on. I remembered the ink and decided to try GBL. Guess what?
 There is no stain!  

So what does that have to do with DNP? DNP is what? A DYE!!! And a very unique one in that it is not soluble
 in anything. I wanted to test it so I made transfered some caps into a bottle with my bare hands. Now I have bright
 yellow dots and marks all over my finger tips. I rubbed it in for fun and let it set in for about 10 minutes. I took
 GBL on a rag and start to wipe at some of the yellow marks. I hope this works or I am going to be wearing gloves
 for about 3 days. It worked! All the marks were gone in 5 minutes and the rag now had yellow marks all over it.
 The most interesting this I found was that there was no transference of the DNP back off the rag while the GBL is
 still wet. It is also great that you don't have to wash your hands with it.  

Previously I had been using detergents, like TIDE, to try and remove the yellow, because it had phenol in it. That
 didn't work too well so then I switched to the Tektrol which is used to sterilize hospitals and it has 10% phenol in it.
 The Tektrol worked better, but the higher level of phenol is tough on your skin, and Tektrol can't touch GBL in
 effectiveness. No yellow is left at all! If you have it stained deep via not trying to remove the dye fast enough or
 have it in your fingernails, you may need to use the 'Palmolive method' where you soak your fingertips in the GBL
 until the DNP is gone.  

Lyle McDonalds little self experiment.
 (Animal: Kinda silly and some theories are incorrect like the need for T3, but it is interesting reading)  

My second realization about DNP is that, as I expected, it makes you lethargic as hell. DNP works by depleting
 Type I fibers of ATP so you have no energy for anything low intensity (although training is generally not affected
 assuming that you can drag your ass to the gym in the first place). I just felt shitty. Also, DNP does not blunt
 hunger like ECA. But, again, at 50% increase in BMR, eating a couple hundred more calories is no big deal.
 (Note: That is why you can take ECA on it. DNP also removes ATP from ALL cells)  

So, like the dumbass I am, I figured I'd see what taking the ECA stack would do to me. My biggest fear was
 raising body temp too high. ECA/Clen and DNP work through independent mechanisms and I wondered if the body
 temp increases would be synergistic or not. I don't think they were but it was an interesting experience.  

The net effect of DNP is a depressant although it's not through central nervous system modulation. ECA is a major
 CNS stimulant. Also, to be a real dumbfuck, I added some yohimbe fuel to keep alpha receptors in check since
 ECA has some alpha agonist activity as well (NB: overstimulating alpha agonists has a major, major side effect. It
 makes your dick not work. I found this out the hard (err, soft) way. Just be warned).
 (Animal; unfortunately he doesn't know his yohimbine mechs and that it takes nearly a month for the 'dick raising'
 benefits of yohimbine to take effect.)  

Ok, I was feeling really bad by Thursday. DNP stays in your system (according to Robert Ames) for 36 hours so
 I'm not convinced that dosing schedule of every 24 hours is ideal as there is a 12 hour period when you have twice
 the recommended dose active in your body. But, this makes a nice failsafe to avoid nasty side effects: nobody can
 take DNP more than 5 days straight because you get tired of feeling like total shit all the time. It's possible that
 dosing every 36 hours would allow you to take it indefinitely but this isn't necessarily a good thing as the negative
 effects of constant ATP depletion (like cataracts which apparently occurs from ATP depletion in your eyes) would
 increase with time. So a dose every 24 might be ideal.  

Anyway, like I said, I had lots o'DNP and some ECA in my system Thursday. And I was drinking a lot of diet coke
 so caffeine intake was massive. And I was severely dehydrated from sweating so much and DNP blunts your thirst
 mechanism. All of this added up to giving me a resting heart rate of 132 (that's not a typo) beats per minute. I didn't
 get my blood pressure measured but I"m sure it was high. I'm surprised I didn't have a fucking stroke. I probably
 deserved to have one just for being a dumbass (nature's way of thinning the herd. Darwinism at work for you).
 (his heart rate was from the ECA. DNP doesn't raise it.)  

So, the body composition record.
 Day Date Wt Pec Abs SI Thigh Sum3 BF% FM FFM
 ---------------------------------------------------------
 Mon 12/30 156 3 22 13 6 31 8.5 13.3 142.7
 Fri 1/3 151 3 18 12 6 27 7.6 11.4 139.6  

Holy Shit! With minimal dieting (hell, no dieting), maybe 30' total of cardio (warm-up and cool down before
 weights), about 2.5 hours total of weight training this week, I still dropped almost 2 lbs of bodyfat. Now, the
 decrease in lean body mass is somewhat worrisome but I attribute most of it to dehydration. Since I was stronger on
 Friday than on Monday (same workout, heavier poundages, same reps), I don't feel that I lost any of the small
 amount of LBM I have. I don't really look like I lost that much fat but, seeing as most of what I've got is smack dab
 on my midsection, I'm not too surprised. This is where the biggest change in skinfolds happened anyway which is
 fine with me. I'm still not quite to cut abs, but I'm getting there.
 (Animal Note: dehydration is why you take the glycerol, furthermore, if you muscles and cells are void of glycogen
 you WILL test lower because glycogen holds a lot of water.)  

So, here's the plan for the next few weeks. I really don't want to do another cycle of DNP just yet (esp since I don't
 have that much and haven't had time to figure out where to get more). So, I figure it this way. I know I canuse
 Bodyopus with some ass kicking training in the gym to put on a decent amount of LBM each week with minimal fat
 gain. So, I figure on doing a week or three of Bodyopus training at above maintenance calories to put on a pound or
 two of lean with maybe .5 lbs of fat. Then, I can use DNP or dieting to cut down for a week or two and sort of stair
 step down in body fat while increasing in muscle mass. I had considered doing 1 week of mass training
 with Bodyopus alternated with 1 week of dieting with DNP and isocaloric but I'm not sure the body can switch
 gears like that so quickly. We'll see.  


 Here is another one and let me add that pyruvate could be added instead of alpha-lipoic for reasons that I'm not
 going to go into yet.  

Diabetes, Glucose And Muscle Energy  

Although the general recommended supplemental dose of alpha-lipoic acid is 50 mg daily, much higher doses have
 been medically approved in Germany to treat adult-onset diabetes and diabetic complications. This use dates back to
 1970, when researchers at the University of Pennsylvania reported that alpha-lipoic acid increased the burning of
 glucose, or blood sugar.  

More recently, doctors at the Rostock-Sudstadt Clinic in Germany have reported that 600 mg of alpha-lipoic acid
 daily significantly reduces symptoms of diabetic neuropathy or nerve damage.5 Other experiments have shown that
 alpha-lipoic acid increases the sugar-burning activity of insulin and reduces insulin-resistance. These findings are
 significant because insulin resistance is a major underlying cause of adult-onset diabetes and a prominent factor in
 coronary heart disease and obesity.6  

Most of the body's glucose is burned in muscle cells to produce energy. The role of alpha-lipoic acid in generating
 energy may have been best illustrated in the recent treatment of a 33-year-old Italian woman with a genetic defect
 interfering with her production of adenosine triphosphate (ATP), which acts as an energy-storage molecule in cells.
 As a child, the woman had been thin, weak and intolerant of exercise. By her early 20s, she had developed
 eye-muscle disorders and droopy eyelids. In her early 30s, she had weak arm and leg muscles. A biopsy and other
 tests confirmed that her muscle cells were producing inadequate levels of ATP.  

Doctors at the University of Bologna, Italy, gave the woman 200 mg of alpha-lipoic acid three times daily for
 several months. She felt better, and tests showed an increase in her muscle-energy levels. Treatment with
 alpha-lipoic acid also resulted in higher energy reserves in her brain, probably by increasing sugar metabolism and
 raising ATP production.  

Preventing Macular Degeneration  

Can the leading cause of blindness in people over 65 be averted by antioxidants? What about zinc, lutein and
 vitamin C?
 By Michelle Badash  

It's been said that the eyes are the first to go. As we get older, one experience we commonly share with others in our
 age group is deteriorating vision. "Macular degeneration," an eye disease affecting the central part of the retina,1
 has recently been the focus of a lot of research--possibly because so many of us are now approaching the time of
 life when our eyes cease to see as well as they used to.  

In the United States, macular degeneration is the leading cause of severe loss of vision, even legal blindness, in
 people over 65. It affects about 6 percent of Americans between the ages of 65 and 75, and accounts for 14 percent
 of all new cases of blindness, with 16,000 cases reported annually.2 Prevalence is slightly higher among women,
 while it is rarely found in people of color. Although its causes have not yet been determined, some scientists
 speculate that frequent exposure to sunlight and smoking may contribute to the disease's development.  

What Is Macular Degeneration?
 Macular degeneration occurs when the cells of the macula, which is the central portion of the retina, become
 damaged and stop functioning. The retina is a thin layer of light-sensitive tissue that stretches across the back of the
 eye. It functions like a screen onto which all visual images are projected. The role of the macula is to view complex
 images. It allows us to focus on objects directly in front of us; enables us to see fine detail during activities such as
 reading, writing,
 sewing and driving; and determines our ability to distinguish color.  


 There are several types of macular degeneration. One is called juvenile macular dystrophy. It's a fairly rare,
 inherited form of the disease that may occur in children or young adults. Another less common form, called pigment
 epithelial detachment, is caused by a blister formation under the retina. In general, however, the two most common
 forms of macular degeneration are termed "wet" and "dry," and occur primarily after age 60.  

Dry: The most prevalent, and less serious, form of macular degeneration
 (accounting for approximately 85 percent of all cases) is "dry," characterized by
 a gradual loss of central vision. The process may occur over a period of several
 years and can affect one or both eyes. The deterioration may be related to
 general atrophy or, in certain cases, caused by deposits of drusen, a yellowish
 substance that accumulates under the retina.  

Typically, the symptoms of this form of macular degeneration include blurriness
 when reading, difficulty in seeing objects that are far away, or shape distortion
 (such as a tree appearing bent or crooked). Some people may also notice a
 dark spot in the center of an object, or find that colors and sizes vary in each eye.  

Wet: The "wet" form of macular degeneration is caused by abnormal blood
 vessel growth behind the retina that may leak or bleed and cause the retina to
 separate from the eye. These abnormal blood vessels are called subretinal
 neovascular membranes, and their proliferation results in a rapid loss of vision.
 Occasionally, the dry form of macular degeneration may develop into the wet
 form.  

Although both wet and dry forms drastically diminish visual acuity, neither result
 in complete vision loss. Furthermore, peripheral vision is not affected.  

At this time, there is no treatment for the dry form of macular degeneration. If the
 wet form is detected in its early stages, laser surgeries are recommended in
 certain cases; however, it is estimated that within one year up to 50 percent of the
 laser lesions may experience regrowth of new blood vessels.3 Laser treatment
 seals the abnormal blood vessels to prevent further bleeding and growth--it does
 not restore vision. In addition to laser treatment, there are some experimental
 forms of surgery that actually remove the abnormal blood vessels. However,
 these procedures are still considered quite risky.  

Given the fact that macular degeneration causes significant vision loss in
 thousands of people each year, and that there are few treatment options, a
 pertinent question is: Can supplements help prevent the progression of this
 debilitating condition?  

For some time, researchers have been investigating the possibility that
 antioxidants may be able to combat--or prevent--macular degeneration. Why?
 The answer lies in the fascinating physiology of the eye.  

How The Eye Works  

The eye functions much like a camera. A lens system at the front of the eye
 collects and focuses light rays. The iris (the colored part of the eye) acts as an
 aperture, and the retina may be compared to film that captures the images.
 When light rays reach the retina, they are converted into electrical nerve signals,
 then sent through the optic nerve to the brain.  

To perform these functions, a host of nutrients are needed to nourish the eye.
 For example, antioxidants such as vitamins C and E, beta-carotene and lutein,
 as well as zinc, selenium and copper, are all found in the macula. In addition to
 providing nourishment, these antioxidants protect against free radicals, which
 inevitably form as a result of all the activity generated by the eye. David
 Newsome, M.D., of the Tulane University School of Medicine in New Orleans, is
 the author of several studies on macular degeneration. He notes, "Where the
 oxygen-containing environment is especially rich and the metabolic rate is high,
 as in the macula, oxidative free radicals are generated plentifully."4  

In addition to the wear and tear of chemical activity, the constant processing of
 light, particularly blue and ultraviolet, can cause photo damage to the eye. One
 interesting theory is that melanin, which is present in the skin and also
 contributes to the color of the eye, helps absorb wavelengths of light and acts as
 an antioxidant by protecting against free radical damage. Consequently, people
 with green or blue eyes and light skin are more likely to experience macular
 degeneration than people with dark eyes or skin. Newsome observes that
 melanin may be the protective factor.5  

The bottom line is that researchers believe antioxidants may help stave off
 some of the harmful oxidative processes that result from the eye's many
 chemical reactions. This theory is based on an understanding of how
 antioxidants function in other parts of the body, as well as in the eye.  

It has been observed in several studies that people who have macular
 degeneration tend to have low levels of certain types of antioxidants in their
 blood. However, the research gets fuzzy when it tries to pinpoint which
 antioxidant is most--or least--beneficial. One study noted that low levels of
 lycopene (an antioxidant found in tomatoes) was most strongly linked with the
 development of macular degeneration.6  

Carotenoid Protection  

Another study focused on the positive role that carotenoids seemed to play in
 preventing macular degeneration--particularly lutein and zeaxanthin, both found
 exclusively in dietary sources such as dark green leafy vegetables (e.g., kale
 and spinach).7 Researchers are intrigued by these two carotenoids because
 they are important to macula function. The foveal part of the retina (a depression
 in the center of the macula) has a yellow pigmentation that is composed
 primarily of lutein and zeaxanthin. Given that these carotenoids are present in
 large quantities, researchers suspect that their role is significant, although the
 mechanism for their functioning has not yet been determined.  

It is also unclear whether a cause-and-effect relationship exists between the
 dietary intake of carotenoids and their absorption in the body. Interesting clues
 suggest that men and women may actually use these carotenoids differently.
 One recent study found that men showed a 38 percent higher macular pigment
 density than women, despite matching carotenoid blood levels.8 More research
 is needed to determine the functions of lutein and zeaxanthin and their potential
 role in preventing macular degeneration.  

Another nutrient that has garnered interest as a potentially beneficial infection
 fighter is the trace mineral zinc. While results concerning antioxidants are still
 sketchy, research results from zinc studies are slightly more conclusive.  

Zinc is highly concentrated in the retina and tissues surrounding the macula.
 More than 100 different enzymes rely on zinc to function, and it is instrumental in
 many chemical reactions in the retina.9 As with antioxidants, zinc also helps to
 protect cell membranes from free radical damage.  

Several studies have found that zinc does seem to provide some protective
 benefits against certain types of macular degeneration, most notably the early
 stages of dry macular degeneration. However, zinc does not appear to affect the
 wet form of macular degeneration. According to a recent study of nine patients
 who had the wet form of macular degeneration in one eye, no improvement
 occurred when they were given zinc supplements.10  

Since macular degeneration generally occurs in the later stages of life, it's
 important to consider how dietary factors could contribute to its development. It is
 a well-known fact that many elderly people eat diets that are low in antioxidants.
 Furthermore, food sources that are rich in zinc, such as meat and seafood, may
 also be eaten in reduced amounts for many reasons: They're relatively
 expensive; they're more difficult to store; they're subject to spoilage; and they
 can be hard to digest. Even if they do eat zinc-rich protein sources, many elderly
 people experience reduced output of stomach acid (achlorhydria).
 Consequently, their bodies' ability to absorb sufficient levels of zinc, as well as
 antioxidants, may be compromised.  

Although current research does not provide strong conclusive evidence to
 support the potential role of antioxidants and zinc in preventing macular
 degeneration, many physicians and ophthalmologists do recommend
 supplementing with these nutrients if it is not contraindicated by other health
 conditions. In the case of zinc, however, patients must be instructed not to take
 more than the recommended levels (50 mg/day) to avoid toxicity and possible
 interference with absorption of other trace minerals such as copper. Zinc is also
 not advised for patients who are taking blood-thinning medications such as
 coumadin .  

Last year, a study heralded as a "breakthrough discovery" in macular
 degeneration research was published in Science. Study authors discovered a
 cluster of genetic mutations believed to cause nearly one-sixth of all macular
 degeneration cases.11 These mutations affect a particular gene that if mutated
 causes cells to produce a protein that helps destroy the macula.  

This is one of the first concrete findings in macular degeneration research.
 Further studies are needed to explore how nutritional interventions and other
 methods, such as photodynamic therapy, may be combined to treat the disease.  

Michelle Badash has 12 years of experience working at a nutrition
 research center in Boston. She has written and edited a newsletter
 about nutrition research and is also a free-lance writer.  

Preventing Macular Degeneration:
 Where The Nutrients Are  

beta-carotene: Carrots  

Copper: Nuts, mushrooms, salmon, lentils, oats  

Selenium: Broccoli  

Vitamin C: Oranges  

Vitamin E: Almonds, wheat germ, sunflower seeds  

Zinc: Oysters, wheat bran, sesame seeds, soybeans  

Lycopene: Tomatoes  

Lutein: Spinach and kale.  


 REFERENCES  

1. "Consumer's Guide to Macular Degeneration."
http://www.eyecare.org/consumer/disease/md.html 

2. Ibid.  

3. "Wet Age-Related Macular Degeneration." http://
www.iex.net/eol/retinal/wet_amd.html 

4. Newsome, D. "The role of antioxidants in macular
 degeneration: An update." Ophthalmic Practice, 12(4):
 169-71, 1994.  

5. Ibid.  

6. Mares-Perlman, J.A., et al. "Serum antioxidants and
 age-related macular degeneration in a population-based
 case-control study." Archives of Ophthalmology, 113(12,
 15): 18-23, December 1995.  

7. Seddon, J.M., et al. JAMA, 272: 1413-20, 1994.  

8. Hammond, B.R., et al. "Sex differences in macular
 pigment optical density: Relation to plasma carotenoid
 concentrations and dietary patterns." Vision Research,
 36(13): 2001-12, July 1996.  

9. "Nutrition and Macular Degeneration." http://www.
 eyenet.org//public/faqs/nutrition_faq.html  

10. Stur, M., et al. "Oral zinc and the second eye in
 age-related macular degeneration." Invest Ophthalmol Vis
 Sci, 37(7, 12): 25-35, June 1996.  

11. Allikmets, R., et.al. "Mutation of the stargardt disease
 gene (ABCR) in age-related macular degeneration."
 Science, 277(5333): 1805, Sept. 19, 1997.  

====================================================================  


 Brain Function And Memory  

Recently, Manas Panigrahi, Ph.D., of the National Institute of Mental Health and Neurosciences, India, described
 how alpha-lipoic acid prevented "reperfusion injury" after strokes were induced in a group of laboratory rats.
 Reperfusion injury is caused by the production of a large number of free radicals when oxygenated blood is restored
 to deprived tissues. In the brain, it typically occurs after a stroke, cerebral hemorrhage or head injury. And in the
 heart, it occurs after a heart attack or coronary artery bypass surgery.
 (Note: Pyruvate also prevents reperfusion injury and DNP causes release of huge amounts of free radicals)  

In an experiment, animals receiving alpha-lipoic acid before a stroke had one-third the death rate of animals who did
 notreceive the supplements. The animals getting alpha-lipoic acid also fared substantially better than those receiving
 the antioxidant glutathione, according to an article by Panigrahi.8 An experiment on reperfusion injury to the heart
 found similar benefits from alpha-lipoic acid.9  

Alpha-lipoic acid also seems to protect brain cells against some hazardous chemicals. Two years ago, researchers at
 the University of Rochester Medical Center reported that the nutrient prevented the neuron-damaging effects of
 excess N-methyl-D-aspartate or NMDA. The researchers wrote that the effect "suggests a possible role of these
 endogenous compounds in the treatment of acute and chronic neurological disorders," such as Parkinson's and
 Huntington diseases.10  

Alpha-lipoic acid might also improve memory in the elderly, if one extrapolates from another animal study.
 Researchers at Germany's Central Institute for Mental Health, Mannheim, described how large doses of alpha-lipoic
 acid were ineffective with young mice; in aged mice, however, long-term memory improved.  

"The lack of any treatment effect in young, treated mice suggests that alpha-lipoic acid compensates age-related,
 long-term memory deficits rather than improving memory in general," the researchers wrote.11  

AIDS And Cancer  

Excessive production of free radicals can promote over-activation of nuclear factor kappa-B (NF-kB),11 a protein
 that functions as a nuclear transcription factor and appears to play a role in inflammation, gene changes leading to
 cancer, and eplication of the human immunodeficiency virus (HIV). A number of antioxidants block NF-kB. In a
 cell-culture study, Yuichiro J. Suzuki, Ph.D., of the University of California, Berkeley, found that cells bathed in
 alpha-lipoic acid could inhibit the activation of NF-kB and, subsequently, HIV replication.12  

Conclusion  

The properties of alpha-lipoic acid are strikingly similar to other antioxidants, as is its essential role in cellular
 energy production along with Co-Q10 and carnitine. What makes alpha-lipoic stand out, however, is its remarkable
 versatility. Packer has at various times described it as the "metabolic," "universal" and "ideal" antioxidant. Coming
 from a leading scientist, instead of an advertising copywriter, such words are particularly meaningful.  

Although recognition of alpha-lipoic acid as a potent antioxidant is relatively recent, the pace of research on this
 nutrient has increased since the late 1980s. According to Packer, alpha-lipoic acid supplements are easily absorbed
 and may be preferable to the major dietary source of the nutrient, which is red meat. Alpha-lipoic acid supplements
 have been approved and used for the treatment of diabetic neuropathy in Germany, and experience suggests that it is
 safe and only rarely poses
 side effects.  

"The therapeutic potential of alpha-lipoic acid is just beginning to be explored," observed Packer, "but this
 compound holds great promise."  

Jack Challem is based in Aloha, Ore., and has been writing for health magazines for 20 years. He also publishes his
 own newsletter, The Nutrition Reporter, which summarizes recent medical journal articles on vitamins.  


 You WILL breathe harder on DNP.  

In taking the pyruvate, glycerin, and taurine; should they be taken at one time during the day, or split up over the
 day? Split by 3.  

Also, I have been doing aerobic exercise in the morning on an empty stomach. Would you still reccomend this
 while on DNP? My thinking is that you would not, but I wanted to ask your opinion. What would your suggestion
 be in relation to aerobics in the morning.
 While on DNP, that probably wouldn't be the best thing to do, but it really depends on your intensity. Never hurts
 to burn some more calories.  

I
 When you speak of taking the glycerine, taurine, and pyruvate while "on" DNP, do you mean take it only on the
 days I take capsules, or take it on the days "in between" in addition to the days I take capsules? You just take the
 glycerine while on the DNP. You should be taking taurine all the time already. Pyruvate may help with additional
 fat loss in the weeks after DNP, too  

Also, how much Taurine is 3g, I don't have a scale.
 0 cap holds about 500mg, 00 holds about 750mg
 The same problem with pyruvate. 00 holds 300mg and 000 holds 400mg.  

Why is it that you say to avoid fructose? I've heard that quite a few times, and was curious why. How important is
 this? Fructose resupplies the liver with glycogen first, if the liver is full, then via the pentose phosphate pathway, all
 additional fructose goes to fat.  

As formaltodextrin, have you ever tried the stuff from proteinfactory.com?
 They have a pretty good price at $2.50 a pound.
 Should be 1.50 or so which you can get at a beer supply store.  

What would your price be on Taurine?
 Bulk? I don't have time to cap them.  

Anarchy in the USA!.
 Do you think it would be a good idea to bike on an empty stomach, THEN take my DNP dose AFTER the ride?
 Just don't want to go to the gym at 5:30a.m. and fall out from doing a medium intensity ride. Then one of the
 trainers would probobly shit his pants or something.
 That would be better as DNP can cause your stomach to burn at times as well.
 When you speak of taking the glycerine, taurine, and pyruvate while "on" DNP, do you mean take it only on the
 days I take capsules, or take it on the days "in between" in addition to the days I take capsules? You
 just take the glycerine while on the DNP. You should be taking taurine
 all the time already. Pyruvate may help with additional fat loss in the
 weeks after DNP, too  

Well, what I meant was this: Should I take the glycerin EVERYDAY while
 on the DNP experiment (looking at 4-8wks), or take it only on the days I
 take capsules (considering that you say to only take DNP caps EVERY
 OTHER day). I ask this because i thought you stated that the half-life
 of DNP is 36hrs, if that is the case, i should be TAKING glycerin
 everyday, right?
 Yes take the glycerin everyday.
 >Also, how much Taurine is 3g, I don't have a scale.
 >0 cap holds about 500mg, 00 holds about 750mg
 >The same problem with pyruvate. 00 holds 300mg and 000 holds 400mg.
 Is capping Taurine the ONLY way to take it? I know that Phosphagen HP
 has taurine in it, and it is just in powder. Can it be thrown into a
 protein/carb drink? That is what I meant when I asked about How much
 taurine is 1g or 3g. Could the taurine be put into the
 glycerine/kool-aid mix? If so, I could take them all at once since each
 is taken 3 times daily.
 Yea, you could throw them in there and I will measure out how much taurine is in a teaspoon for y
 I was also wondering this about the pyruvate because I am planning on
 mixing it into a paste w/flax oil. I was wondering how much 3g would
 be, or 5g. I was planning on mixing the paste in the morning and just
 taking it throughout the day--3 times. Probobly mixing it in with a MRP
 or just protein drink. Could the paste sit all day (refrigerated, of
 course)?
 1 tablespoon of flax will hold about 3g of pyruvate. Any more pyruvate and it gets chunky!
 I saw on the 'feeling good' that you reccomend glutamine. How much? I
 currently take 10g-15 of glutamine a day. I throw some powder into my
 shakes after my workout (an MRP) and before bed (usually just protien
 powder & milk or water).
 That should be good.
 Bulk is what I was asking about. You can see my thoughts on it.
 I have to look up what I paid for it, and will tell you when I tell you how much a teaspoon is.
 Anarchy in the USA!  


 Guess I'm burning a lot of cals at the moment.
 > What am I gonna need to do when I come off of DNP/t3? Will I need to
 > taper off to get my thyroid back online, or will it happen by itself?
 > Or is it only low because I am taking DNP? What is the deal here? You> know, I don't want to have to take
 thyroid med. for the rest of my
 > life!! Whatever you can tell me regarding this would be VERY helpful.
 This is why I only like to recommend 1week on DNP. DNP reduces t4-t3 conversion and the thyroid reads that and
 increases T4 output so when you stop the DNP you get MORE of your own thryoid for the following week! Now,
 when you add T3 your thryoid reads that and reduces T4 output so when you stop the diet you have LOWER T4
 which means lower T3.
 If you only do it for a week you will be alright and then do a high carb diet for three days at 600g carbs a day and
 you will be alright.
 This is why I recommend pyruvat. It seems that the pyruvate keeps the conversion going so temp never drops.  

> You could drop the glycerol and substitute taurine. >I like the pyr because it is such a good
 ant-oxidant >AND it may keep the t4-t3 online.
 I've already ordered the pyr. & glycerol, so I'll be using both...how much more effective do
 you think adding the taurine be? (How about MCT's like duchaine has reccomended in the past?)
 You want to burn fat so I don't know why you would want to take in more. I never noticed any advantage when I
 took them in the past with other diets. Taurine will help keep your electrolytes balanced.  

> Do you max for the first two days until you start to >sweat and then you can switch to the 36
 hour >regimen.
 >
 Could you clarify this?...does it mean 400mg b/f bed for 2 days then 400mg every 36hrs?..or
 split up into 2-200mg doses? If you max is 800 then you do 200 every 6 hours or so.  

> And how many days in a row do you suggest taking >it? Only seven to get the thyroid back to
 normal if >not on pyruvate.
 Seven is the norm and if you are on pyruvate your thyroid will still go down at the end of the second week.
 >
 If on pyr. (which I'll be) would 10 days be alright or pushing it?
 That would be fine  

And what do you suggest for training (cardio) and calorie levels?
 Eat as normally as you can and depending how much you can bear the sweat cardio can remain normal as well.
 thanx for your time...  

>>Also, someone mentioned a post you had about "How to use 600mg of DNP
 a
 I already sent the DNP and the manual is basically a longer form of the 600mg on DNP.  

What sizes do you make caps in?
 100-400mg sizes
 I am currently taking 600mg/day, and was thinking about upping the dose. Would I go to 700 or 800?
 800 as it is not a great rise percentage wise.
 Since I ordered from you before, what will the price be per cap for 100 caps?
 Would you find out how much a 1/2 gal of glycerin would cost me
 shipped?? JOKER won't get off his ass and find out about some for me (his bro-in-law is a vet).
 I can ship up to four pounds PM for under $6 so « gal would weigh about 3 plus whatever else you order.
 This stuff is great! Using it, I have lost over 20lbs in 3wks. I got sick (with a cold) and stopped, but am planning
 on starting it again after the symptoms subside.
 Good to hear.
 For the recarb pd you told me about (to use after basal temp decreases), how important is it to stay away from
 fructose during that pd? You can use it, but you only want so much of it and if youdrink soft drinks and juice it will
 work.
 I had Hell getting that many carbs (600g) in a day without resorting to stuff like sweetened cereal and soft
 drinks/juices. Actually, once I just ate "normal" for 3 days with no DNP and my temp came back up.
 I know that fructose is stored b4 any other sugar b/c of its structure, but is that really that bad? A carb is a carb,
 whether it comes from glucose or fructose, right?
 No, because if the liver is fully carbed then all subsequent fructose goes directly to fat.
 If I am burning as many calories as I do on DNP, what does it matter where the carbs come from. If they ARE
 deposited in the liver/muscle, won't they just be broken down when the body needs sugar?
 Yes.
 I could be way off here, so enlighten me. What is the deal? Will SOME fructose hurt me very much in order to
 keep my blood sugar up?
 No, but you are trying to keep your liver carbed up.
 Not RELYING on it, but having some (in things like juice, soft drinks, sports drinks, etc., and for taking creatine--I
 use powerade mix to get carbs for the insulin spike).
 If you have around 300-400 cal a day from fructose you will be ok.
 What is the deal with the poisons produced in the body from use of DNP?
 It's free radicals.
 We actually talked about it in my Biochem class the other day, and my prof said that things like cyanide and azide
 are produced in the body during use of DNP.
 I'd like to come in and tell him a thing or two! Since when does the body produce it's own cyanide! HAHA! Ask
 him what the mechanism is for that one!
 I kinda thought that this was the major reason for such high doses of antioxidants.
Yes.


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## basskiller (Jun 12, 2013)

remember.. none of this is mine.. it all came from the geocities site


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## [email protected] (Aug 18, 2013)

can evey one tell me about test 400 pls is it good or bad???
have frist one and my arm is still hurting truth pls people Ty...


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## [email protected] (Aug 18, 2013)

any one help???or bump??


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## Ironbuilt (Aug 18, 2013)

[email protected] said:


> can evey one tell me about test 400 pls is it good or bad???
> have frist one and my arm is still hurting truth pls people Ty...



If this is real please post a new thrread  t400 pip pain and how much u did and where u pinned it AND more information pleaseto get better relplies than in this dnp thread.  You have picture ?  Ib


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