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#1 (permalink) |
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Senior Member
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Hey guys, i need info on which supplements particularly make DNP more effective? I have read that Glycerol is one, for muscle hydration and pyruvate but im not sure how it helps.
Any other supps you guys think can make the DNP's work better while you're on it? ![]() |
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#4 (permalink) | |
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Senior Member
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Quote:
Like Sadie said, prepare to not sleep, sweat like a mother-f@cker and avoid carbs unless you want to watch sweat drip off your nose. Go run through some of the threads in supplements, alot of good stuff in there. |
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__________________
You can be old or you can be bold, but ever both. I don't use drugs, never have, even if this fictional character posts something stating otherwise, it is not me. I do not know anything about anything. |
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#5 (permalink) |
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Senior Member
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-------------------------------------------------------------------------------- JBDD had this in another thread FROM STEROID .COM Knock yourself out! With all the DNP threads I've seen lately I thought it would be a good idea to post my compilation of DNP info. This is most of the info I used when I was researching DNP (and some new stuff). I'm including everything I have whether I agree with it or not, because there is no one right way to run DNP. Different people react to it very..... well, differently. From the sides they experience, the amount of fat they'll lose at a given dose, when they like to run it, how long they like to run it, the diet that works best for them, etc. If you're thinking about taking DNP then you should read ALL of the following info, and after you've read it all...... READ IT AGAIN! Many boards have DNP-guides, but in essence they are the same 3 guides over and over again; These guides are not only outdated, they tend to over do the supplements thus making it more complicated than needed and they are life-threatening to newbies because they don't elaborate enough on important aspects as the 36-hour half-life (thus the accumalative effect) and the elektrolyte-loss (they just tell you to drink V8 ). Not only that but instead of REALLY BASING THEIRSELVES ON SCIENTIFIC RESEARCH, they just post some PUBMED researches and long quotes out of them (not summarized or put in lay-mans terms), just to impress the reader! And often you have the feeling that they really don't know what they are talking about, also they tend to tell more about its history than its practical use and action (BY KNOW WE ALL KNOW IT WAS USED AS AN EXPLOSIVE, INSECTICIDE, YELLOW PAINT etc.)! They don't elaborate enough on Practical inconveniences as well; The foultasting and dry mouth one gets and the fact that if you are making the caps yourself without precautions it is very likely to cover the room with unremovable (except with TEK) Yellow stains everywhere. The final and most important thing is that this new approach is not only at least as effective at fat loss or even more so, but also countless times more convenient and with countless less horrible sides! A REVOLUTION IS UPON US!! ------------------------------------------------------------------------- The new approach to cycling DNP: DNP has a 36-hour half-life meaning it will build up in your blood and due to it being an exponential 2nd degree math function, after a certain amount of time the accumalative effect will be too small (insignificant) and thus bloodlevels will peak and remain stable... The international Physics formula for Half-life: In physics with: N(0) = dosage at time zero N(t) = dosage left at recent time t(1/2) = half life in seconds/hours/days/years (depending on compound) N(t) = N (0) x (1/2)^(t/t(1/2)) at 200 mg every day the peaklevel will be 540 mg... @ day 6 you will already be over 500 mg...! (but given the margin of error in capping and dosingtimes we take 600 mg as standard!) more info: http://forums.anabolicreview.com/sho...28&postcount=2 So a 20 day cycle @ 200 mg ED, will result in a 540 mg peaklevel which is a very comfortable dose for any healthy grown man! A 20 day cycle will also yield great results, most likely greater than a "horrifying sideful" traditional 8 day cycle @ 400 mg. Most of you who are trying DNP for the first time are not willing to jump in a 20 day cycle right away, so a 10 or 12 day cycle @ 200 mg will be more suitable, just make sure that you carbdeplete 2 days in advance for optimum results in such a short low dose cycle... DNP IS NOT SUITABLE FOR WOMEN AND MORBIDLY OBESE PEOPLE!! -------------------------------------------------------------------------- Beneficial Properties: 1. DNP is both Liver and kidneyfriendly. 2. DNP has anti-catabolic properties. 3. DNP boosts the immunesystem 4. DNP is Anti-Carcinogenic 5. DNP is non-hormonal and thus fatloss is easier to maintain -------------------------------------------------------------------------- Sides: At such a low dose the most likely sides will be: Sweating (+ feeling hot) Heavy breathing Irregular Sleep Pattern Rashes for some (take an anti-histamine for this, if it lasts discontinue DNP!) Lethargy Decreased Strength Musclecramps (Not likely at all especially at such a dose with enough mineralsupplementation). Increased Hunger (especially Sugar-cravings, Sibutramine totally annihilates this side!) Note: I got "the rash" the first and last part of the second cycle... I never took citadrizine HCL... But by cycle 3 (actually end of cycle 2; so 2,5) I never developed an allergy any more... Still Anti-histamines can aid in fat loss if supplemented with Ephedrine and Yohimbine! All these can be combatted to a certain extent... Practical Sides: DNP will provide a hideous sent of it under your Armpits due to the sweating (especially in the last few days) so always wash under your armpits a couple of times a day and put plenty deodorant under it even before bed (I swear the scent will annoy you in bed). DNP leaves a foul and dry taste in your mouth all day long; I found out that drinking Diet Softdrinks helps against it so sweets always get the taste away, but seeing we want to LOSE weight Diet soda is the best option! (normal softdrinks contain sugar and we WANT TO LOSE WEIGHT best bets: Fanta, Fanta Pomelo, Fanta Cassis, Fanta Lemon, Coca Cola Lemon, Sprite etc. ALL LIGHT!). I finish about 2 bottles a day (Ice cold preferabely also seeing drinking water all day gets tiresome!!). -------------------------------------------------------------------------- Effectivity: All over messgeboards I read that an ECA boosts metabolism by 3%, Clen + T3 20% and DNP 50-75%! I don't know where people get these numbers but it is not true! Fat loss not only has to do with metabolism, but also with many other processes like affecting alpha and betareceptors (why Yohimbine has got such fatloss potential for "love handles"). Increased metabolism also means better proteinsynthesis, which is not always the case with these fatburners! Not to mention a 75%-boost on DNP would not make sense since for instance let's take a 2000 calorie boost (And that would mean a maintenance Caloric Requirement of about 2800 Kcal a day!!, which is very high!) --> giving a maximum of 250 gram pure fat loss a day! That would mean an 8 day cycle would yield a maximum of 2 Kg fatloss (I know the offdays count as well but that would be compensated by glycogen-reserves, increased appetite etc.). The real deal: A degree Fahrenheit increase in BMR on DNP is equal to a 120% boosted Caloric-expense! Practical Effectivity: Now here's the big question...... will it yield the same results fat loss-wise as the shorter higher dose cycles? Yes, not only shall the DNP be more effective, but things like T2 and Yohimbine need longer cycles to work their magic and thus you will have even better results! (also the fat loss will be more gradually from the ancillaries and thus prove easier to maintain that weight). Note: The Scale will lie and so will the mirror! Due to the waterbloat and thus waterweight (The waterbloat is less obvious then with Deca for instance since it "hides" around the middlesection + lovehandles!), also the carbdepletion will make your muscles appear less "pumped". So remember that while "on" you will feel fat and bloated and your muscles will be anything but pumped! Fun thing is 5-7 days after discontinuance you will see the drastic change in the mirror and on the scale! The feeling one gets when coming off is great (no more sweating, dry mouth, clearance of bloat etc.)! -------------------------------------------------------------------------- Weightloss is semi-permanent!: I and many other people have noticed that after a DNP-cycle even after months less than 50% of the weightloss is gained back. (And that is even with crappy training and diet) While common rule in dieting is that the more weight one loses in a short time span, the more likely he/she is to gain all that weight back plus even a bit more fat most of the times (the dreaded YOYO-effect!!). Also this research confirms that 3 obese people (2 men and a women) after long term T3 and DNP supplementation lost a lot of weight and managed TO KEEP IT OFF! http://forums.anabolicreview.com/sho...30&postcount=4 As to so many cases of people not experiencing a drastic rebound with DNP (anything that guarantees under 50% of the weightloss gained back is an effective diet-aid in my opinion) it got me thinking as to WHY... So a simple theory which I came up with: DNP is so dangerous, because it doesn't involve in a feedback system (meaning if there is to much present in the blood there is no way the body can combat that). Also it is non-hormonal (hormonal systems always have a feedback-mechanism). This means that it doesn't affect your body's "setpoint" (which is what your body thinks is your "healthy" weight and thus always wants to return to that point). Some mechanisms in the "setpoint" are still unknown but it mostly has to do with dopamine/adrenaline and the various Neuropeptides (especially B, K and Y that all regulate appetite). The "setpoint" is best adjusted if weightloss is as gradually as possible (phentermine users always get the yo-yo effect meaning all the lost weight + some new fat comes back after discontinuance; not only because fat is lost so rapidly but mainly because it affects all those "setpoint" features and after discontinuance they will try to regain homeostasis!). DNP has no (significant) role in manipulating the "setpoint" (meaning your body will not feel the urge to gain some weight after discontinuance). Also it competes with T3, meaning after you stop DNP, T3 will peak (instead of like with most diets; will be on low) couple that with the fact that it is not catabolic (actually a bit anti-catabolic for that matter) so your BMR stays rougly the same after the DNP-cycle. And the conclusion confirms the reality --> Fat loss induced by DNP is not likely to come back for a significant part! Note: Most people supplement certain compounds with DNP --> I for instance take Sibutramine, T2, T3 and an ECY which are most likely to be the MAIN cause of the "gained weight afterwards" due to the KNOWN disturbance of some processes in the body's metabolism by these ancillaries. -------------------------------------------------------------------------- First things, First! --> Obtaining DNP 1) Make it yourself! Unless you are an experienced homebrewer I can not advise to do this, DNP stains are impossible to remove (with the exception of with TEKTROL), and the DNP powder is at its cheapest $1 (for small amounts) per gram, considering the fact that you pay $1 for a 200 mg cap on average and you only need a small amount of caps per cycle; it is not worth it... The pro with making it yourself is that you can add all sorts of things in thus minimizing the amount of tabs/caps/powder one has to swallow. I used to make them containing per cap: 200 mg DNP 100 mg Quercetin (anti-histamine and anti-oxidant) 10 mg Sibutramine HCL (Appetite suppresant) 150 mg Magnesium Malate 180 mg Synthetic Vitamin E (Comes down to 400 IE/IU) 5 mg Vitamin B12 5 mg Yohimbine HCL 2) Buying them: As to such a potentially dangerous substance, if over dosed, I wouldn't buy it unless it was from someone who is really well known. There is such a guy and he makes the 200 mg DNP caps with 200 mg Quercetin (Anti-histamine and Anti-oxidant) in them for just $1. If you are a regular on this board and are well respected here, you can ask a mod/vet for his e-mail; Normally i wouldn't post this but it is due to the fact that in case of DNP you have to have a real trusted dealer! -------------------------------------------------------------------------- Usage --> Diet: Lots of Water! and other fluids like DietSodas! A diet while on DNP is nonsense since due to its non-hormonal actions there is no benefit in shifting nutrients. You will get bad sugar-cravings though! (Yohimbine, Ephedrine and especially Sibutramine are effective in combatting this!). Just remember that carbs will get you heated (so after carb intake you will start to feel warm for about 10 minutes, but without carbs you will find everything to taste disgusting!). The 2 gram per lbs of bodyweight protein rule is also nonsense! (DNP is not catabolic at all). Keep your intake of vegetables high (especially any kind of Lettuce, cubecomber etc.) Also Fruits (with the exception of Bananas/strawberries/grapes) do combat a lot of sides (refrigerate some Apples, Oranges, Mangos, Peaches and a Pineapple and you will have a tasty meal that also makes you feel more at ease while "on"). -------------------------------------------------------------------------- Supplementing T2 and T3 or not?: This has been a controversial subject... Let's clear some things up (MALLET will thank me for it!): T3 is NOT catabolic! In certain amounts it is very ANABOLIC.... T2 + T3 help DNP operate at peak efficiency; Maximizing Fat Loss! Especially since the thyroid can shut down, the amounts we supplement are quite anabolic/anti-catabolic (Why I GAINED 4 lbs LBM)! For the people afraid of suppressing their thyroid: Fact is T3 and DNP compete a little, so supplementing T3 on a DNP-cycle would be far less suppresive on TSH than on a T3/Clen or T3-only cycle. Not to mention the fact that getting off DNP would give your Thryroid a boost too so recovering would be easier than from the proposed T3-only cycle... T2 info (there is little info available on such a wonderful substance!): (((((I read most Pubmed researces on Thyroid-metabolites and found this to be the found most important things to know))))) - Potencywise: 400 mcg T2 = 50 mcg T3 - T2 is far less catabolic than T3 even when abused: - T2 is far less supressive on FSH than T3 - 3,5-T2 is more suitable for fat loss than 3,3-T2. - T2 is only active for about an hour. - T2 is most effective when supplemented with T3 (or when natural production of T3 is high). - Although T3 has a long half-life, periodic intervals per day of taking it yields far better results! T2 is best taken as much divided during the day as possible; 3 is a minimum (it is only active for one hour and preferabely with meals since it will burn all the fats/carbos you get in immediately!). T2 unlike T3 is not likely to be catabolic even when abused (as previously mentioned T3 engaged in proper usage is quite anabolic!). T2 is available @ Team LR P.S. Team LR probably uses ethanol (Nail polish remover) as a dissolver so the stuff tastes like crap, right before taking it, put it in an Empty cap (the cap will dissolve within 2 minutes of coming in contact with a liquid so take it just before!). -------------------------------------------------------------------------- Proper supplementation: People tend to use TOO MUCH supplements on DNP. Therefore making it way too complicated and frightening In low dose cycles the described supplements (below) are more than enough! In dosages like 600/800/1000 mg ED Magnesium/Phytochemicals/GSE become essential! 2-10 gram Potassium Gluconoate ED ECY (E/C/Y/G/A @ 25/200/5/40/75 mg) 2x Vitamin C @ 500 mg 2x Vitamin E @ 400 IU 3x 400 mcg T2 3x 15 mcg T3 Optional: Ketotifen or Benadryl (preferabely on hand!) Melatonin (preferabely on hand!) R-ALA Magnesium (very useful in higher dosages like 400 mg DNP or more!) Taurine @ 500 mg ED ECY (E/C/Y/G/A @ 25/200/5/40/75 mg): Ephedrine/Cafeine/Yohimbine/Guggelsterones/Acetyl-L-carnitine @ 25/200/5/40/75 mg! (should contain SYNTHETIC guggelsterones and SYNTHETIC yohimbine both available at ********). Usage: To combat Lethargy, Curb Appetite and Cravings, to free fatty acid for better fatburning and for better fatburning in "stubborn fat". T2 + T3: Fatloss, preventing lethargy and maybe even anabolism/anti-catabolism Vitamin C & Vitamin E: Basically all the Anti-oxidants you need: A Watersoluble and a Fatsoluble one! due to their activity-span take twice a day! Potassium Gluconoate: You loose alot of minerals through sweating! The elektrolytes you have to replace are Sodium and Potassium (in Latin Natrium and Kalium), sodium is relatively easy to get through ones diet (tablesalt is sodiumchloride/natriumchloride). Potassium is a little harder to get (Still Potassium is present in a lot of vegetables). 10 grams a day of Potassium Gluconoate is best (actually 10 grams is way overkill especially since that would mean 1,6 gram of Potassiumsupplementation a day for a 200 mg cycle). 2 grams is more than enough... Potassium Gluconoate will keep strength up and battle muscle cramps! Potassium gluconoate (16% Potassium) is $20 per 3 lbs at ********! Ketotifen or Benadryl (Ketotifen is much more potent): As Anti-histamine (for Allergies) As sleeping Aid (take before bed!) Upgrading the Fatcell receptors Keeping the ECY effective (during longer runs like 30 days) Melatonin: Anti-oxdidant + Sleeping Aid. Taurine Compensate Taurine Levels in Liver... Magnesium or R-ala As Anti-Oxidant! Obtaining supplements: ******** for all the bulkpowders for the ECY (and all the other supplements) animalkits for Vitamin E powder -------------------------------------------------------------------------- DNP for PCT: Will elaborate on that later! -------------------------------------------------------------------------- Funny Note: Hitler gave it to his troops invading russia to keep them warm during Russia's infamous winters! -------------------------------------------------------------------------- Phytochemicals Story! Morin, Luteolin, Quercetin, Kaempferol and Reservatol are especially good at supressing Sugars from being metabolized (not to mention their life-extentioning abilities and positive effects on Lipid Levels and Cardiac Function). Fisetin, Myrecetin, Baicalein, Galangin are far less effective (In That order --> with the most effective one mentioned first and the least effective one mentioned last). Epigallocachin, Epicatechin, Hesperetin, Taxifolin, Rutin, Flavonol, Flavone didn't do anything at all.... About Phytochemicals: Li BH, Tian WX. Inhibitory effects of flavonoids on animal fatty acid synthase. J Biochem. 2004 Jan;135(1):85-91 Grapeseedextract inhibits fatcells from growing instead of inhibiting sugars being metabolized like the other phytochemicals! About GrapeSeedExtract: Moreno DA, Ilic N, Poulev A, Brasaemle DL, Fried SK, Raskin I. Inhibitory effects of grape seed extract on lipases. Nutrition. 2003 Oct;19(10):876-9. Reservatol: Which frees a lot of fatty acids from stubborn fat, makes fatcells more sensitive for Adrenaline, imitates caloric restriction and actually kills fatcells to a degree! Not to mention its sex-boosting properties, its lifespan enhancing ability and the fact that it pumps your muscles full of Anti-oxidants especially in a PWO-shake to make recovery easy and thus produce an anabolic enviroment! About Reservatol!: Picard F, Kurtev M, Chung N, Topark-Ngarm A, Senawong T, Machado De Oliveira R, Leid M, McBurney MW, Guarente L. Sirt1 promotes fat mobilization in white adipocytes by repressing PPAR-gamma. Nature. 2004 Jun 17;429(6993):771-6 Konrad Howitz, Kevin Bitterman, Haim Cohen, Dudley Lamming, Siva Lavu, Jason Wood, Robert Zipkin, Phuong Chung, Anne Kisielewski, Li-Li Zhang, Brandy Scherer, David Sinclair. Small molecule activators of sirtuins extend Saccharomyces cerevisiae lifespan. Nature 24 August 2003. Molecules Discovered That Extend Life In Yeast, Human Cells; Group Of Compounds Found In Red Wine, Vegetables Simulate Benefit Of Low-calorie Diet. Science Daily, 25-8-2003 That's why I wondered a cap containing a Fatinhibitor like Orlistat (or maybe an even more effective one in the future) and a Glucose-inhibitor like the mentioned Flavonides and GrapeSeedExtract should make the eating of Fast Food/Junk Food perfectly acceptable! Greets Kingofmasters http://patft.uspto.gov/netacgi/nph-P...S=PN/4,673,691 United States Patent 4,673,691 Bachynsky June 16, 1987 Human weight loss inducing method Abstract A human weight reduction method in which 2,4-dinitrophenol and a thyroid hormone preparation are administered to the patient. The dinitrophenol is administered in dosages sufficient to elevate the patient's body temperature, typically 250 mg every other day. The thyroid hormone preparation preferably contains 3,5,3'-triiodothyronine and is administered in dosages sufficient to substantially maintain the patient's serum T3 concentration originally present at treatment onset. Inventors: Bachynsky; Nicholas (1110 Pine Cir., Sea Brook, TX 77586) Assignee: Bachynsky; Nicholas (Sea Brook, TX) Appl. No.: 668501 Filed: November 5, 1984 Current U.S. Class: 514/567; 514/909 Intern'l Class: A61K 031/195 Field of Search: 514/728,909,567 References Cited [Referenced By] U.S. Patent Documents 4087554 May., 1978 Haydock et al. 514/728. Other References Chem. Abst. 66:82758c (1967)--Rossini et al. Chem. Abst. 71:27671x (1969)--Tomita et al. Chem. Abst. 77:109780v (1972)--Tiller et al. Chem. Abst. 82:25791q (1975)--Wahl et al. Chem. Abst. 88:167300b (1978)--Kaplan et al. Chem. Abst. 89:191455x (1978)--Organesyan et al. Chem. Abst. 100:168805y (1984)--Sydykov. Chem. Abst. 102:56608w (1985)--Langer. Simkins, S., "Dinitrophenol and Desiccated Thyroid in the Treatment of Obesity," JAMA 108, pp. 2110-2117 and 2193-2199 (1937). Tainter, M. L. et al., "Dinitrophenol in the Treatment of Obesity," JAMA 105, pp. 332-336 (1935). Tiller, F. W. et al., "The Effects of Noradrenaline and 2,4-Dinitrophenol on the Oxygen Consumption of Different-Aged Rats After Treatment with Triiodothyronine or Methylthiouracil," Arch. Int. Pharmacodyn. 198, pp. 377-384 (1972) (With Translation). Wahl, R. et al., "Influence of Various Drugs on the Adsorption of Thyroid Hormones to Liver Mitochondria," Z. Naturforsch, 29, pp. 608-617 (1974) (With Translation). Schimmel, M. et al., "Thyroidal and Peripheral Production of Thyroid Hormones," Annals of Internal Medicine 87, pp. 760-768 (1977). Arena, Jay M., Poisoning, pp. 86 and 92 (Charles C. Thomas, Springfield, Ill. (1978). Cazeneuve, P. et al., "Sur les effets produits par l'ingestion et l'infusion intra-veineuse de trois colorants jaunes, derives de la houille," C.R. Acad. Sci. 101, pp. 1167-1169 (1885). Brobeck, J. R., "Food Intake as a Mechanism of Temperature Regulation," Yale Journal of Biology and Medicine 20, pp. 545-552 (1948). Cutting, W. C. et al., "Actions and Uses of Dinitrophenol," JAMA 101, pp. 193-195 (1933). Diechmann, W. B. et al., Symptomatology and Therapy of Toxicological Emergencies, pp. 452-453 (Academic Press, New York 1964). Counsel on Pharmacy and Chemistry, "Dinitrophenol Not Acceptable for N.N.R.," JAMA 105, pp. 31-33 (1935). Horner, W. D., "Cataract Following Dinitrophenol Treatment for Obesity," Archives of Opthalmology 16, pp. 447-461 (1936). Negherbon, W. O., Handbook of Toxicology, vol. 3, pp. 303-308, (W. B. Saunders Co., Philadelphia 1959). Perkins, R. G. "A Study of the Munitions Intoxications in France," Public Health Reports 34, pp. 2335-2374 (1919). Sims, E. A. H. et al., "Endocrine and Metabolic Effects of Experimental Obesity in Man," Recent Progress in Hormone Research 29, pp. 457-496 (1973). Spector, W. S., Handbook of Toxicology, vol. 1, p. 118, (W. B. Saunders Co., Philadelphia, 1956). Tainter, M. L. et al., "A Case of Fatal Dinitrophenol Poisoning," JAMA 102, pp. 1147-1149 (1934). Physician's Desk Reference, 37th ed., pp. 1896-1897 (1983). Primary Examiner: Robinson; Douglas W. Attorney, Agent or Firm: Pravel, Gambrell, Hewitt & Kimball Claims I claim: 1. A method of inducing weight loss in a patient, comprising the steps of: (a) administering 2,4-dinitrophenol or salt thereof at a rate ranging from about 60 to about 250 mg/day; and (b) concurrently administering 3,5,3'-triiodothyronine to the patient at a rate ranging from about 25 to about 100 mcg/day. 2. The method of claim 1, wherein said 3,5,3'-triiodothyronine is substantially free of thyroxine. 3. The method of claim 1, wherein said 3,5,3'-triiodothyronine administration is at a rate ranging from about 50 to about 100 mcg/day. 4. The method of claim 1, wherein said dinitrophenol is administered at said rate with dosages given only on alternate days. 5. The method of claim 1, wherein said dinitrophenol is administered at said rate with primary dosages given on alternate days and smaller, supplemental dosages given on the days immediately subequent to said alternate days. 6. The method of claim 1, wherein 2,4-dinitrophenol is administered. 7. A method of inducing weight loss in a patient, comprising the steps of: (a) administering 2,4-dinitrophenol to the patient at a rate ranging from about 125 to about 250 mg/day; and (b) concurrently administering 3,5,3'-triiodothyronine substantially free of thyroxine to the patient at a rate ranging from about 50 to about 100 mcg/day. 8. The method of claim 7, wherein said dinitrophenol and said 3,5,3'-triiodothyronine are administered at initial rates of about 250 mg of said dinitrophenol every other day and about 50 mcg 3,5,3'-triiodothyronine per day, and following 2-12 weeks of said administration at said initial rates, are administered at subsequent rates of about 250 mg of said dinitrophenol every other day alternated with about 125 mg of said dinitrophenol on subsequent days and about 100 mcg 3,5,3'-triiodothyronine per day. Description This invention relates to a method of inducing weight loss in patients by the concurrent administration of 2,4-dinitrophenol and 3,5,3'-triiodothyronine. BACKGROUND OF THE INVENTION Obesity is a common problem. Simply stated, obesity is an excess accumulation of adipose tissue which contains fat stored in the form of triglycerides. The number of cells in the body is determined at least by late adolescence and while the number of adipocyte cells may increase, it does not decrease. Thus, weight gain can result from an enlargement of adipocyte cells or an increase in their number. Typically, obese individuals have hypertrophic cells and the severely obese have an increase in adipose cell number as well as hypertrophy. An obese patient only reduces the fat in his cells when he loses weight. Further, he may not ever lose the tendency to gain weight. Body weight is regulated by an endogenous body mechanism. Physiological and neurological properties establish and maintain a given weight. Briefly stated, glycerol which is released during hydrolysis of triglycerides and adipose tissue is widely believed to regulate caloric intake and metabolism. Others have postulated that caloric intake is affected by both body temperature and environmental temperature. In addition, cell size and number affect energy regulation. Weight gain cannot be predicted solely on the amount of calories ingested. In normal persons, thermogenesis is an adaptive mechanism which increases the metabolic rate after overeating. While a normal person will experience an increase in thermogenesis following increased caloric intake, the obese either has a substantially decreased thermogenic mechanism or lacks this particular mechanism entirely. The use of dinitrophenol to treat obesity is known. Dinitrophenol is known to elevate the body temperature and produces a marked increase in caloric metabolism. However, ingestion of massive amounts of dinitrophenol causes toxicity by the uncoupling of oxidative phosphorylation in the mitochondria of cells. Because of this toxicity, excessive amounts can result in profuse diaphoresis, fever, thirst, tachycardia and respiratory distress which can lead to hyperpyrexia, profound weight loss, respiratory failure and death. The minimum fatal human oral dose is estimated at one to three grams (approximately 20-30 mg/kg). In methods heretofore known to using dinitrophenol to induce weight loss, while initial daily dosages have usually been much less than the toxic amount, about 100-250 mg, as the treatment progressed the patient normally developed a tolerance for dinitrophenol and the dosage was increased to obtain the same results. This increased dosage led to an increased frequency of toxic symptoms and general disuse of dinitrophenol in inducing weight loss. It has also been known to use drugs with thyroid hormone activity for the treatment of obesity. However, as described in Physicians' Desk Reference, Medical Economics Co. Inc., (Oradell, N.J.), 37th Ed. (1983), in euthyroid patients, it is well established that doses within the daily hormonal requirements are ineffective for weight reduction. However, larger doses may produce serious or even life-threatening manifestations of toxicity. SUMMARY OF THE INVENTION The present invention avoids the necessity of increased dosages of dinitrophenol and the concomitant toxicity problems associated therewith as treatment progresses while obtaining improved results. It has been discovered that the use of dinitrophenol induces hypothyroidism which can be prevented by concurrently administering thyroid hormone preparation with the dinitrophenol. Briefly, the present invention is a method of inducing weight loss in patients, including the steps of administering dinitrophenol to the patient in an amount sufficient to clinically increase thermogenesis of the patient, and concurrently administering a thyroid hormone preparation to the patient in an amount sufficient to substantially maintain the serum concentration of 3,5,3'-triiodothyronine of the patient originally present at treatment onset. DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENT It has been discovered that the ingestion of dinitrophenol induces hypothyroidism. Athough it is not fully understood, it is believed that the normal thyroid gland produces both thyroxine (referred to herein as T4) and 3,5,3'-triiodothyronine (referred to herein as T3). However, approximately eighty percent of the serum T3 present in the body is produced by the extrathyroidal monodeiodination of T4 to T3. When dosages of dinitrophenol are taken, hypothyroidism is induced, not by a reduction in activity of the thyroid, but by a reduction of the rate of extrathyroidal conversion of T4 to T3. While both T4 and T3 are biologically active, T3 is much more active than T4. Thus, the reduction in serum T3 concentration induced by taking dinitrophenol substantially offsets the metabolic effect of the dinitrophenol. By analogy, the reduction in serum T3 concentration is similar to that observed in fasting patients. Typically, normal serum T3 concentration ranges from about 70 to about 200 ng/dl. It has further been discovered that deficient serum T3 concentrations resulting from administration of dinitrophenol can be restored to normal concentrations by concurrently administering a thyroid hormone preparation therewith. In practicing the method of this invention, dinitrophenol is administered to the patient. The metabolically active dinitrophenols suitable for use in the invention include 2,4-dinitrophenol and the salts thereof. By the term administration is meant any suitable manner of introducing the medication into the patient's body, including orally (p.o.) and topically. The preferred manner of administering dinitrophenol is orally, as in the form of a tablet or capsule. The amount of dinitrophenol given should be sufficient so that the patient experiences increased body temperature. Preferably, the body temperature is elevated approximately 1.degree. F. The dose of dinitrophenol required to obtain this result varies from patient to patient, depending on factors such as, for example, weight, age, health, environmental conditions, physical activity, nutrition, and psychological state, but will normally be in the range of from about 60 to about 500 mg per day, or about 0.60 to about 5.0 mg/kg of body weight per day. Preferably, the dinitrophenol is administered in daily or alternating daily dosages, insuring that no cumulative effective results, such as excessive thermogenesis. It is essential that the amount of dinitrophenol administered not exceed toxic doses. In a few patients, adverse reactions may occur at dosages of dinitrophenol which are not effective to elevate the body temperature, contraindications including any clinical state in which there is hypermetabolism, such as hyperthyroidism, ongoing infections, and pregnancy, and any other clinical conditions such as heart disease, chronic obstructive pulmonary disease, Addison's disease, liver disorders, or renal failure. Most are safely treated with suitable results from the aforementioned dosages. Concurrently with the administering of the dinitrophenol, or shortly thereafter, a thyroid hormone preparation is administered to the patient. As used herein, the term thyroid hormone preparation includes any suitable preparation which restores the serum T3 concentration, including preparations containing 3,5,3'-triiodothyronine, thyroxine, derivatives thereof or combinations thereof. Preferably, the thyroid hormone preparation contains T3. Because of the varying potency of such preparations, dosages of thyroid harmone preparation are reported herein on a T3 equivalent basis. The thyroid hormone preparation is administered in an amount sufficient to maintain the pretreatment serum T3 concentration in the patient, typically about 70-200 ng/dl in normal patients. Generally, from about 25 to about 200 mcg T3 equivalent per day, or from about 0.3 to about 2.7 mcg T3 equivalent per kilogram of body weight per day, is sufficient. Preferably, the thyroid hormone preparation is administered daily. In an especially preferred embodiment, the thyroid hormone preparation is administered orally with the dinitrophenol. As described above, the rate of extrathyroidal conversion of T4 to T3 may vary as treatment with the dinitrophenol progresses. Thus, it may be necessary to increse or decrease the dosage of the thyroid hormone preparation accordingly. It is preferred that in the practice of the method of this invention, the patient be closely monitored, especially in the initial stages of treatment. Recommended pretreatment and initial treatment protocol includes physical examination, electrocardiogram, and stress electrocardiogram if indicated, complete blood count, urinalysis, thyroid function studies (T3, T4 and reverse T3), serum electrolytes, HDL cholesterol, serum creatinine, blood urea nitrogen, uric acid, calcium, pulmonary function tests and liver function tests including liver enzymes, biliribin, and alkaline phosphatase. In an especially preferred embodiment, the patient is started on initially lower dosage rates of dinitrophenol, about 250 mg every other day, and thyroid hormone preparation, about 25-50 mcg/day on a T3 equivalent basis. After 2-12 weeks of this treatment, if no adverse reactions are noted, the dosage rates may be increased to about 250 mg dinitrophenol alternated daily with about 125 mg, i.e. 250 mg on even-numbered days and 125 mg on odd-numbered days, and to about 100 mcg/day thyroid hormone preparation on a T3 equivalent basis. When the weight goal of the patient is achieved, the administration of the dinitrophenol may be discontinued, and the thyroid hormone preparation continued to maintain the patient's weight. While dietary control need not be strict, weight loss and weight maintenance are facilitated by moderate caloric intake of less than about 1800 calories per day, during and following treatment. This method is illustrated by way of the case histories which follow. Case 1 A white female 31 years of age with a weight in excess of 200 pounds had attempted to loss weight with various diet plans. She had only been able to achieve about a 20-pound loss, and had immediately regained the weight. The patient was nulliparous and had no ongoing medical problems. Upon physical examination, she had a weight of 208.5 pounds, a height of 5 feet, 3 inches, and a blood pressure of 132/80, without any goiter. Laboratory analyses, including complete blood count, liver profile, serum electrolytes, kidney function tests and thyroid function tests, were all within normal limits. Because of her familial history of heart disease, she underwent a stress electrocardiogram which was normal other than early fatigue and calf cramping. The patient was started on CYTOMEL brand of liothyronine sodium (manufactured by Smith, Kline and French), 50 mcg/day p.o., and on 2,4-dinitrophenol, 250 mg every other day p.o. On the 19th day of medication, the patient had normal vital signs and the dosages were increased to 100 mcg/day liothyronine, and 250 mg/day dinitrophenol alternated every other day with 125 mg/day. The patient was subsequently maintained on these dosages and returned for follow-up examinations approximately every 3 weeks. The weight loss history is seen in Table 1. After 241 days of medication, the patient has achieved her weight goal of 135 pounds. Administration of the dinitrophenol was discontinued and the patient was maintained on liothyronine, 100 mcg/day p.o. No weight gain was subsequently observed. TABLE 1 ______________________________________ ----------Day----------Weight (lbs) ______________________________________ ----------1 -----------208 1/2 ----------19 ----------202 1/2 ----------35 ----------196 1/2 ----------49 ----------189 1/2 ----------69 ----------184 ----------92 ----------175 ----------113 ---------167 ----------134 ---------160 ----------155 ---------152 1/2 ----------180 ---------148 ----------206 ---------146 ----------241 ---------135 ______________________________________ Case 2 A male 40 years of age with a weight of approximately 250 pounds had attempted to lose weight with a variety of diet plans and diet medications. Success had been limited to 5-10 pound weight losses, with immediate regain. On physical examination, the patient has a height of 5 feet, 10 inches, a weight of 255 pounds and a blood pressure of 160/100. Complete blood count, SMAC, serum electrolytes, thyroid function tests, glucose tolerance tests and stress electrocardiogram were normal. The patient was started on liothyronine, 50 mcg/day p.o., and on dinitrophenol, 250 mg every other day p.o. After two weeks, the blood pressure returned to normal (130/80), and the dosages were increased to 100 mcg/day liothyronine and 250 mg dinitrophenol alternated daily with 125 mg. The weight loss history is presented in Table 2. Once the weight goal of 167 pounds had been achieved, the patient was taken off the dinitrophenol administration and the 100 mcg/day liothyronine medication was maintained. The patient was instructed to restrict caloric intake to approximately 1800 calories per day. No subsequent weight gain was observed. TABLE 2 ______________________________________ ----------Day----------Weight (lbs) ______________________________________ ----------1 -----------255 ----------14 ----------241 ----------30 ----------232 ----------44 ----------227 ----------65 ----------220 ----------76 ----------214 ----------97 ----------208 ----------125 ---------203 ----------153 ---------197 3/4 ----------181 ---------193 ----------209 ---------189 ----------279 ---------178 ----------321 ---------167 ______________________________________ Case 3 A white male 38 years of age with a weight of approximately 342 pounds had made numerous attempts to lose weight "with all methods" without any success. Upon physical examination, the patient had a weight of 352 pounds, a height of 5 feet, 11 inches and a blood pressure of 150/110. Other than a slight enlargement of the heart on X-ray and +3 pitting edema, the physical examination was unremarkable. Laboratory analysis initially revealed a blood sugar of 372 with a glycohemoglobin of 14.3 (normal 4.4-8.2). The remaining tests, including stress electrocardiogram, were within normal limits. The patient was started on liothyronine, 50 mcg/day p.o., and dinitrophenol, 250 mg every other day, and was instructed to restrict his caloric intake to approximately 1800 calories per day. On the 59th day of treatment, the dosages were increased to 100 mcg/day liothyronine, and 250 mg/day dinitrophenol alternated every day with 125 mg. The patient's weight loss history is presented in Table 3. Following treatment, the dinitrophenol administration was discontinued and the patient was maintained on liothyronine, 100 mcg/day p.o. and instructed to maintain his caloric intake to approximately 1800 calories per day. No subsequent weight gain was observed. TABLE 3 ______________________________________ ----------Day----------Weight (lbs) ______________________________________ ----------1 -----------354 ----------24 ----------333 ----------38 ----------314 ----------59 ----------317 ----------80 ----------297 1/4 ----------101 ---------288 ----------122 ---------275 ----------143 ---------260 1/2 ----------164 ---------254 ----------185 ---------243 1/2 ----------206 ---------246 ----------227 ---------235 1/2 ----------248 ---------234 ----------269 ---------229 ----------290 ---------222 ______________________________________ The above cases illustrate the effectiveness of the method with obese patients unable to reduced their weight by conventional methods. Having described any weight loss method above, many variations in the details thereof will occur to those skilled in the art. It is intended that all such variations which fall within the scope and spirit of the appended claims be embraced thereby. DNP FAQ-also a cut and paste FROM ANIMAL'S MANUAL) 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 BULL****!. 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 **** 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 tri |