Thread: DNP price, what do you pay?
06-02-2004, 02:50 PM #1
DNP price, what do you pay?
i've been searching for DNP for a couple months now and am having a hard time coming up with it but i finally found a guy selling it. The only problem is that he's trying to sell it to me for $9 per 200mg cap. Is this a gym price? Cause i've heard of guys paying about .90 cents per cap. I'd like to know what you're all paying just to know for sure so i can try and negotiate with this guy.............thanks a lot!!
06-02-2004, 03:28 PM #2
$9 a cap, thats way to ****ing hi bro, i got mine for $3 p/c
sounds like you found a source froma website. stay away cos they are probably scammers
06-02-2004, 04:00 PM #3Senior Member
- Join Date
- Dec 2003
£ 1.20 in uk each 200mg tabs. the price u are talkin about is not hi... its fockin hi!!!
06-02-2004, 04:01 PM #4New Member
- Join Date
- May 2004
06-02-2004, 05:05 PM #5
ive only seen it on lists for $2 per cap, but i have never used it so i haven't gone bargin shopping for it
06-02-2004, 05:06 PM #6
no, its not from a website, its a guy from the gym. I am skeptical just because i've been screwed before so what i'm gonna do is try and talk to him about giving the money to a third party or something and doing the cycle, and if it turns out to be legit, then he'll get his money. I mean if its for real, what does the guy have to lose right? Anyways, i'll tell him i know its a high price and try to negotiate as well.
06-02-2004, 05:08 PM #7
i got it on two lists
one is $.90 and one is $2 per 200mg cap
06-02-2004, 05:18 PM #8
06-02-2004, 05:20 PM #9
dollar a cap. I think all the hype about DNP being dangerous is a little over done. I know people that have run it around 3 weeks at 200-400 mg with very good results, and very few side effects. They did it RIGHT however.
06-02-2004, 05:27 PM #10
It kills heart cells. Thats not hype!!!! I have seen published in a medical study!!
06-02-2004, 05:28 PM #11Originally Posted by Anhydro78
06-02-2004, 06:38 PM #12
man i wish i just had this stuff on my list for even $2 a cap. Well i should be talkin to this guy again within the next couple of days so we'll see what happens. Thanx for the help guys
06-02-2004, 06:42 PM #13
$1 a cap. Wouldn't touch it but thats what I can get it for. Only for competitors IMO, not for the layman.
06-02-2004, 06:45 PM #14Associate Member
- Join Date
- Mar 2002
If you pay $9/cap, I'd have to say you're one of the dumbest people on earth. They're only $1 each.
06-02-2004, 06:47 PM #15Originally Posted by supirman45
Yeah because if you make your own at $1 a cap thats a 500% mark up. Tell that guy to go **** hisself.
06-02-2004, 07:29 PM #16Associate Member
- Join Date
- Mar 2002
Don't even have to make your own at $1/cap... you can buy them ready made for that price.
06-02-2004, 07:30 PM #17
No I am saying if you make your own it comes to 20 cents a cap, thats why I said it is a 500% mark up. 9 dollars from one would be a 900% mark up.
06-02-2004, 08:42 PM #18Originally Posted by 1badcamaro
Caps start at $1 and go down from there.
Powder....... a fraction of that (very small fraction).
Originally Posted by Anhydro78
2. DNP isn't as dangerous as people make it out to be, and remember everyone's different. Clen and ephedrine, two of those safer drugs make be feel much worse then DNP.
Originally Posted by Anhydro78
Originally Posted by Lozgod
06-02-2004, 08:47 PM #19Originally Posted by SV-1
Note the disclaimer..........IMO, and I said I as in me, lozgod, myself, wouldn't use it.
06-02-2004, 10:22 PM #20
06-02-2004, 10:49 PM #21
06-02-2004, 10:51 PM #22
06-02-2004, 10:58 PM #23Originally Posted by Lozgod
Department of Medical Physiology, Internal Medicine, Faculty of Health Sciences, University of Stellenbosch, South Africa.
Thyroid hormone has important cardiovascular effects, and abnormalities of its production cause cardiovascular morbidity. The role of both excessive and insufficient thyroid hormone production in the pathogenesis of clinical cardiac diseases can be deduced from thyroid hormone-induced molecular changes. Thyroid hormone regulates the expression of myocardial genes regulating the handling of calcium, which affects both systolic and diastolic myocardial function. Thyroid hormone also has indirect and direct effects on peripheral vascular smooth muscle tone, and alters the coupling of the left ventricle and arterial system.
[text=Bold]Excessive levels of thyroid hormone results in an increased cardiac output as well as increased cardiac work efficiency, but reduced cardiac reserve, and potential long term damage [/bold].
Amiodarone therapy for cardiac rhythm can cause both hyper- and hypothyroidism. Amiodarone-induced thyrotoxicosis (AIT) can be due to either excessive thyroid hormone production (type I AIT) or thyroid hormone release due to an inflammatory condition (type II AIT). Classification of AIT is helpful in guiding therapy. Amiodarone causes changes in the thyroid function tests of euthyroid patients on therapy--it inhibits the conversion of T(4) and T(3), which results in decreased T(3) and slightly increased T(4) serum levels in euthyroid patients. Baseline thyroid functions should therefore be determined before starting amiodarone therapy, and at 6-monthly intervals thereafter.
06-02-2004, 11:00 PM #24Originally Posted by chrisAdams
06-02-2004, 11:01 PM #25
Not clen either eh???
Myotoxic effects of clenbuterol in the rat heart and soleus muscle.
Burniston JG, Ng Y, Clark WA, Colyer J, Tan LB, Goldspink DF.
Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool L3 2ET, United Kingdom. firstname.lastname@example.org
Myocyte-specific necrosis in the heart and soleus muscle of adult male Wistar rats was investigated in response to a single subcutaneous injection of the anabolic beta(2)-adrenergic receptor agonist clenbuterol. Necrosis was immunohistochemically detected by administration of a myosin antibody 1 h before the clenbuterol challenge and quantified by using image analysis. Clenbuterol-induced myocyte necrosis occurred against a background of zero damage in control muscles. In the heart, the clenbuterol-induced necrosis was not uniform, being more abundant in the left subendocardium and peaking 2.4 mm from the apex. After position (2.4 mm from the apex), dose (5 mg clenbuterol/kg), and sampling time (12 h) were optimized, maximum cardiomyocyte necrosis was found to be 1.0 +/- 0.2%. In response to the same parameters (i.e., 5 mg of clenbuterol and sampled at 12 h), skeletal myocyte necrosis was 4.4 +/- 0.8% in the soleus. These data show significant myocyte-specific necrosis in the heart and skeletal muscle of the rat. Such irreversible damage in the heart suggests that clenbuterol may be damaging to long-term health.
06-02-2004, 11:02 PM #26Originally Posted by Lozgod
06-02-2004, 11:03 PM #27
06-02-2004, 11:04 PM #28
here's another one relating heart damage (in this case hypertrophy) to high t3 levels.
Hyperthyroidism causes mechanical insufficiency of myocardium with possibly increased SR Ca2+-ATPase activity.
Takeuchi K, Minakawa M, Otaki M, Odagiri S, Itoh K, Murakami A, Yaku H, Kitamura N.
Department of Cardiac Surgery, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655 Japan. email@example.com
Hyperthyroidism is known to affect multiple organ functions, and thyroid hormone has been known to improve myocardial function in a failing heart. The purpose of this study is to elucidate the functional and metabolic effects of thyroid hormone on myocardium in a rat model exposed to long-term excess thyroid hormone, particularly focusing on the SR Ca(2+)-ATPase (SERCA2) function. 3,5,3'-Triiodo-L-thyronine (T3), or the vehicle, was subcutaneously given for 4 weeks (T3 and control [C] group). Bolus I.V. Thapsigargin (TG) was used to test the SERCA2 function (C-TG and T3-TG) in Langendorff perfused heart. Myocardial functions such as LV-developed pressure (LVDP; mmHg), +/- dP/dt (mmHg/s), tau (ms), and oxygen consumption (MVO(2); ml/min/g wt) were measured. SERCA2 and GLUT4 protein level were also evaluated by Western immunoblotting. Left ventricle to body weight (LV/BW) ratio was significantly higher in the T3 group. Both negative dP/dt and tau were significantly decreased by TG. It is interesting that the decrement of negative dP/dt and tau attained by TG was significantly larger in the hyperthyroid group (T3-TG) than in a normal heart (C-TG). SERCA2 and GLUT4 protein levels were not significantly different between control and the T3 group. We conclude that prolonged exposure to thyroid hormone causes hypertrophy of the myocardium and an augmentation of the SR Ca(2+) ATPase activity. Care must be taken in hyperthyroid heart during the ischemia-reperfusion process where the SRECA2 function is inhibited.
06-02-2004, 11:05 PM #29
06-02-2004, 11:09 PM #30
06-02-2004, 11:14 PM #31
Me personally I love life too much to take risks like that. I am convinced that AAS's can be used safely, thats why I am an advocate of getting lab work before, during, and after cycles. It's also why I know what my HDL, LDL, Triglycerides, Liver values, BUN levels, etc. I am not convinced that DNP is safe. So I, me, lozgod, myself, not anyone else, <----, K**** L***** M********, will not use it.
06-02-2004, 11:21 PM #32Senior Member
- Join Date
- Jul 2003
06-02-2004, 11:22 PM #33
First of please dont even compare people that decide to change their physical apperance or performance with hormones to those that decide to use DNP . Its people like DNP users that give validity to any claims that STEROIDS ARE DANGEROUS!!! SH!t!!! And that we as a population cant make safe,informed desicions for ourselves. So the goverment has to bullsh!t!!!!!!!!!!!!!!!!!
I cant believe that this is being openly discussed like its perfectly safe. And anyone claiming that it is dangerous is being flamed. Appointed Mods and vets should have more sence than this!!!!!!!!!!!!!!!
You guys want some reading material here it is!!!!!!!!!!!!
06-02-2004, 11:24 PM #34
Heres what your own site has to say about it.
The substance; 2, 4-Dinitrophenol has many other brand names such as, 1 Hydroxy-2,4-dinitrophenol, Solfo Black, Nitrophen, Aldifen, and Chemox are just a few and is among many things, a metabolic stimulant. That is it's popularity here in our world, it burns fat like no other. Let me just tell you of it's other uses before I continue. First, it is a toxic dye, chemically related to Trinitrophenol (Picric Acid), second, it is found in insecticides, wood preservatives, herbicides, explosives, and is also a hazardous material. Third, it is used in science to couple or attach to DNA molecules. All of this should tell you that it is not a run-of-the-mill metabolic stimulant, like Clenbuterol or Triacana or Ephedrine or any other for that matter. Here is DNP 's tox faq's from the international chemical safety cards to you give an idea of what it is considered to be; Combustible. Gives off irritating or toxic fumes (or gases) in a fire. Risk of fire and explosion. DO NOT expose to friction or shock. MAY BE ABSORBED! Redness. Roughness. Yellow staining on the skin. PHYSICAL STATE; APPEARANCE: YELLOW CRYSTALS ROUTES OF EXPOSURE: The substance can be absorbed into the body by inhalation, through the skin and by ingestion. PHYSICAL DANGERS: Dust explosion possible if in powder or granular form, mixed with air. INHALATION RISK: Evaporation at 20°C is negligible; a harmful concentration of airborne particles can, however, be reached quickly. CHEMICAL DANGERS: May explosively decompose on shock, friction, or concussion. May explode on heating. Shock-sensitive compounds are formed with alkalis, ammonia and most metals. The substance decomposes on heating producing toxic gases including nitrogen oxides. EFFECT OF SHORT-TERM EXPOSURE: The substance may cause effects on metabolism, resulting in very high body temperature. Exposure may result in death. EFFECTS OF LONG TERM OR REPEATED EXPOSURE: Repeated or prolonged contact with skin may cause dermatitis. The substance may have effects on the peripheral nervous system. The substance may have effects on the eyes, resulting in cataracts. Boiling point: sublimes °C, Melting point: 112°C, Relative density (water = 1): 1.68. Solubility in water, g/100 ml at 54.5°C: 0.14. Relative vapor density (air = 1): 6.36. This product is handled and shipped in a 15% solution of water, making it a paste, so that it will not explode due to shock or friction.
DNP is an uncoupling agent that inhibits the flow of electrons and the pumping of H+ ions for ATP synthesis. Fifty years ago it was used for weight loss, however, in 1938 the FDA removed it from the counter, as it caused cataracts and even sometimes death. If electron transport does not produce ATP, then much more sugar must be metabolized for energy needs. Very low production of ATP would be lethal. In oxidative phosphorylation, the flow of electrons from NADH (the reduced form of NAD+, oxidized from NAD. This enzyme is important in accepting electrons in the course of metabolic reactions. When NAD+ gives up it's electron, it is converted to it's reduced form NADH) and FADH2 (the reduced form of FAD) to oxygen results in the pumping of H+ from the matrix to the inner membrane space of the mitochondria. This gradient of H+ can produce ATP by flowing through ATP synthetase in the mitochondrial inner membrane. Dinitrophenol disrupts the H+ gradient reducing ATP synthesis. Under these conditions, much of the food that we eat could not be used for ATP synthesis and we lose weight. However, too much inhibitor and we could make too little ATP for life. The difference between weight loss and death is only a small concentration change in dinitrophenol, making the drug dangerous. Simply put, this means that while eating your normal diet, you will have somewhere between 20% and 40% reduction of calories.
You may now be wondering just what kind of dose would be effective, but not harmful. A dose of 2mg/kg/day (or two mgs per kg of body weight per day) would be an effective dose, causing the loss of about 5 to 10 pounds in a 10 to 14 day period, maybe less. So, a person weighing 200 lbs would weigh about 91 kgs, so 2mgs per kg of body weight would be the equivalent of 182 mgs of DNP per day, but since it typically comes in 200 mg capsules, you would take one cap per day. Since DNP has this inhibiting effect, glycolosis is inhibited as well, causing a diabetic effect due to the conversion of glucose without insulin , so you may have heard that people take insulin with DNP. This will counter act the symptoms of lethargy and lack of energy due to DNP's use.
Finding DNP, this may be a little difficult as there are only two manufacturers of it. Sigma and Springfield scientific, though they do not generally sell to the public, it is still available. If you cannot find someone with capsules, you may try to get some bulk (somewhere around $20.00 - $30.00 per lb I think), but since this is considered a hazardous material, it cannot be conveniently or inconspicuously shipped (which for consumption is a felony), however, it is possible. However, to get use of the bulk/raw form, you will need to make your own capsules, which is a meticulous process.
06-02-2004, 11:25 PM #35
here you go!!!!!!!!!!!!!!
courtesy of EliteFitness Platinum
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. "
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.
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
06-02-2004, 11:27 PM #36
Chris Adams...your rebuttal?????
06-02-2004, 11:29 PM #37
Read this one this is the most intresting one.
Dinitrophenol (2,4-Dinitrophenol, DNP )
NOTHING IN THE TEXT ABOVE SHOULD BE CONSTRUED AS ENCOURAGEMENT TO TAKE PRESCRIPTION MEDICATION WITHOUT SUPERVISION. CONSULT YOUR DOCTOR.
Common Name: 2,4-Dinitrophenol
CAS Number: 51-28-5
DOT Number: UN 1320
Date: July, 1989
2,4-Dinitrophenol can effect you when breathed in and by passing through your skin.
2,4-Dinitrophenol can cause reproductive damage. Handle with extreme caution.
2,4-Dinitrophenol is a FLAMMABLE LIQUID and a FIRE HAZARD.
Contact can irritate the skin. Long term exposure may cause dermatitis.
2,4-Dinitrophenol can irritate the eyes, and may cause clouding of the eye lenses (cataracts).
Breathing 2,4-Dinitrophenol can irritate the nose and throat.
High or repeated exposure can affect the nervous system causing nausea, vomiting, abdominal pain, convulsions and even death.
2,4-Dinitrophenol may damage the liver and kidneys.
2,4-Dinitrophenol is a yellow crystalline (sand-like) solid but is often found in a solution. It is used in dyes, photo developers, explosives, and as a preservative of lumber.
REASON FOR CITATION
2,4-Dinitrophenol is on the Hazardous Substance List because it is cited by EPA and DOT.
HOW TO DETERMINE IF YOU ARE BEING EXPOSED
Exposure to hazardous substances should be routinely evaluated. This may include collecting personal and area air samples. You can obtain copies of sampling results from your employer. You have a legal right to this information under OSHA 1910.20.
If you think you are experiencing any work-related health problems, see a doctor trained to recognize occupational diseases. Take this Fact Sheet with you.
WORKPLACE EXPOSURE LIMITS
No occupational exposure limits have been established for 2,4- Dinitrophenol. This does not mean that this substance is not harmful. Safe work practices should always be followed.
It should be recognized that 2,4-Dinitrophenol can be absorbed through your skin, thereby increasing your exposure.
2,4-Dinitrophenol may be a teratogen in humans. All contact with this chemical should be reduced to the lowest possible level.
WAYS OF REDUCING EXPOSURE
Where possible, enclose operations and use local exhaust ventilation at the site of chemical release. If local exhaust ventilation or enclosure is not used, respirators should be worn.
Post hazard and warning information in the work area. In addition, as part of an ongoing education and training effort, communicate all information on the health and safety hazards of 2,4-Dinitrophenol to potentially exposed workers.
Wear protective work clothing.
Wash thoroughly immediately after exposure to 2,4- Dinitrophenol and at the end of the workshift.
This Fact Sheet is a summary source of information of all potential and most severe health hazards that may result from exposure. Duration of exposure, concentration of the substance and other factors will affect your susceptibility to any of the potential effects described below.
HEALTH HAZARD INFORMATION
Acute Health Effects
The following acute (short-term) health effects may occur immediately or shortly after exposure to 2,4-Dinitrophenol:
2,4-Dinitrophenol can irritate the skin and eyes.
Breathing 2,4-Dinitrophenol can irritate the nose and throat.
Exposure to 2,4-Dinitrophenol cause fatigue, thirst, sweating, headache and weakness. It may also cause anxiety and excitement.
Chronic Health Effects
The following chronic (long-term) health effects can occur at some time after exposure to 2,4-Dinitrophenol and can last for months or years:
2,4-Dinitrophenol may cause mutations (genetic changes) in living cells. Whether or not it poses a cancer or reproductive hazard needs further study.
2,4-Dinitrophenol has not been tested for its ability to cause cancer in animals.
2,4-Dinitrophenol may damage the developing fetus.
2,4-Dinitrophenol has not been tested for its ability to adversely affect reproduction.
Other Long-Term Effects
Exposure to 2,4-Dinitrophenol can cause dermatitis. Clouding of the eye lenses (cataracts) may occur after a long exposure.
High or repeated exposure can effect the nervous system causing nausea, vomiting, diarrhea, abdominal pain, headache, anxiety, weakness, convulsions and even death.
2,4-Dinitrophenol may damage the liver and kidneys.
If symptoms develop or overexposure is suspected, the following may be useful:
Liver and kidney function tests.
Exam of the eyes.
Evaluation by a qualified allergist, including careful exposure history and special testing, may help diagnose skin allergy.
Any evaluation should include a careful history of past and present symptoms with an exam. Medical tests that look for damage already done are not a substitute for controlling exposure.
Request copies of your medical testing. You have a legal right to this information under OSHA 1910.20.
WORKPLACE CONTROLS AND PRACTICES
Unless a less toxic chemical can be substituted for a hazardous substance, ENGINEERING CONTROLS are the most effective way of reducing exposure. The best protection is to enclose operations and/or provide local exhaust ventilation at the site of chemical release. Isolating operations can also reduce exposure. Using respirators or protective equipment is less effective than the controls mentioned above, but is sometimes necessary.
In evaluating the controls present in your workplace, consider: (1) how hazardous the substance is, (2) how much of the substance is released into the workplace and (3) whether harmful skin or eye contact could occur. Special controls should be in place for highly toxic chemicals or when significant skin, eye, or breathing exposures are possible.
In addition, the following control are recommended:
Where possible, automatically transfer 2,4-Dinitrophenol from drums or other storage containers to process containers.
Before entering a confined space where 2,4-Dinitrophenol may be present, check to make sure that an explosive concentration does not exist.
Good WORK PRACTICES can help to reduce hazardous exposures. The following work practices are recommended:
Workers whose clothing has been contaminated by 2,4- Dinitrophenol should change into clean clothing promptly.
Contaminated work clothes should be laundered by individuals who have been informed of the hazards of exposure to 2,4- Dinitrophenol.
Eye wash fountains should be provided in the immediate work area for emergency use.
If there is the possibility of skin exposure, emergency shower facilities should be provided.
On skin contact with 2,4-Dinitrophenol, immediately wash or shower to remove the chemical. At the end of the workshift, wash any areas of the body that may have contacted 2,4- Dinitrophenol, whether or not known skin contact has occurred.
Do not eat, smoke, or drink where 2,4-Dinitrophenol is handled, processed, or stored, since the chemical can be swallowed. Wash hands carefully before eating or smoking.
For dust powder use a vacuum or a wet method to reduce dust during clean-up. DO NOT DRY SWEEP.
PERSONAL PROTECTIVE EQUIPMENT
WORKPLACE CONTROLS ARE BETTER THAN PERSONAL PROTECTIVE EQUIPMENT. However, for some jobs (such as outside work, confined space entry, jobs done only once in a while, or jobs done while workplace controls are being installed), personal protective equipment may be appropriate.
The following recommendations are only guidelines and may not apply to every situation.
Avoid skin contact with 2,4-Dinitrophenol. Wear protective gloves and clothing. Safety equipment suppliers/manufacturers can provide recommendations on the most protective glove/clothing material for your operation.
All protective clothing (suites, gloves, footwear, headgear) should be clean, available each day, and put on before work.
Wear splash-proof chemical goggles and face shield when working with liquid, unless full facepiece respiratory protection is worn.
Wear dust-proof goggles and face shield when working with powders or dust, unless full facepiece respiratory protection is worn.
IMPROPER USE OF RESPIRATORS IS DANGEROUS.
Such equipment should only be used if the employer has a written program that takes into account workplace conditions, requirements for worker training, respirator fit testing and medical exams, as described in OSHA 1910.134.
Engineering controls must be effective to ensure that exposure to 2,4-Dinitrophenol does not occur.
Where the potential exists for exposure to 2,4-Dinitrophenol, use a MSHA/NIOSH approved supplied-air respirator with a full facepiece operated in the positive pressure mode or with a full facepiece, hood, or helmet in the continuous flow mode, or use a MSHA/NIOSH approved self-contained breathing apparatus with a full facepiece operated in pressure-demand or other positive pressure mode.
Common Name: 2,4-Dinitrophenol
DOT Number: UN 1599 (Dinitrophenol solution); UN 0076 (Dry or
wetted with less than 15% water); UN 1320
(Dinitrophenol, wet with at least 15% water) DOT
Emergency Guide codes: 57,36,46
CAS Number: 51-28-5
Hazard rating NJDOH NFPA
Flammability 3 Not Rated
Reactivity 0 Not Rated
POISONOUS GASES ARE PRODUCED IN FIRE CONTAINERS MAY EXPLODE IN FIRE
SOLID DINITROPHENOL MAY EXPLODE
Hazard Rating Key: 0=minimal; 1=slight; 2=moderate; 3=serious;
Dried out material may explode.
Vapor explosion hazard indoors, outdoors and in sewers.
2,4-Dinitrophenol is a FLAMMABLE LIQUID (depending upon carrier solvent) or an explosive solid.
Flood with water, if water is not available ,use dry chemical or dirt.
POISONOUS GASES ARE PRODUCED IN FIRE, including Nitrogen Oxides.
CONTAINERS MAY EXPLODE IN FIRE.
FIRE MAY RESTART AFTER IT HAS BEEN EXTINGUISHED.
use water spray to keep fire-exposed containers cool.
If employees are expected to fight fires, they must be trained and equipped as stated in OSHA 1910.156.
SPILLS AND EMERGENCIES
If 2,4-Dinitrophenol is spilled or leaked, take the following steps:
Restrict persons not wearing protective equipment from area of spill or leak until clean-up is complete.
Remove all ignition sources.
Ventilate area after clean-up is complete.
Collect powdered material in the most convenient and safe manner and deposit in sealed containers.
Keep 2,4-Dinitrophenol out of a confined space, such as a sewer, because of the possibility of an explosion, unless the sewer is designed to prevent the build-up of explosive concentrations.
It may be necessary to contain and dispose of 2,4- Dinitrophenol as a HAZARDOUS WASTE. Contact your Department of Environmental Protection (DEP) or your regional office of the federal Environmental Protection Agency (EPA) for specific recommendations.
FOR LARGE SPILLS AND FIRES call your fire department immediately.
HANDLING AND STORAGE
Prior to working with 2,4-Dinitrophenol you should be trained on its proper handling and storage.
Keep 2,4-Dinitrophenol wet or treat it as an explosive. Dried out material may explode if exposed to heat, flame or shock.
Store in tightly closed containers in a cool, well-ventilated area away from LIGHT.
2,4-Dinitrophenol is incompatible with STRONG OXIDIZERS (such as CHLORINE, BROMINE and FLUORINE, STRONG BASES, ACID CHLORIDES and ACID ANHYDRIDES).
Immediately flush with large amounts of water for at least 15 minutes, occasionally lifting upper and lower lids. Seek medical attention (immediately).
Quickly remove contaminated clothing. Immediately wash contaminated skin with large amounts of (soap and) water.
Remove the person from exposure.
Begin rescue breathing if breathing has stopped and CPR if heart action has stopped.
Transfer promptly to a medical facility.
Flash Point: Not Found
Water Solubility: Slightly soluble
OTHER COMMONLY USED NAMES
Chemical Name: 1-Hydroxy-2,4-Dinitrobenzene
Other Names and Formulations:
Alpha Dinitrophenol; Aldifen; Fenoxyl Carbon N.
Not intended to be copied and sold for commercial purposes.
NEW JERSEY DEPARTMENT OF HEALTH
Right to Know Program
CN 368, Trenton, NJ 08625-0368
2,4-Dinitrophenol is a yellowish crystalline solid and is the most important of the six possible dinitrophenol forms. It is used mostly as an intermediate to make dyes, photochemicals, pest control agents, wood preservatives, and explosives. It may enter the environment from industrial discharges, spills, or possibly as a breakdown product of certain pesticides containing 2,4- Dinitrophenol moieties.
ACUTE (SHORT-TERM) ECOLOGICAL EFFECTS
Acute toxic effects may include the death of animals, birds, or fish, and death or low growth rate in plants. Acute effects are seen two to four days after animals or plants come in contact with a toxic chemical substance.
2,4-Dinitrophenol has high acute toxicity to aquatic life and to birds. Insufficient data are available to evaluate or predict the short-term effects of 2,4-Dinitrophenol to plants or land animals.
CHRONIC (LONG-TERM) ECOLOGICAL EFFECTS
Chronic toxic effects may include shortened lifespan, reproductive problems, lower fertility, and changes in appearance or behavior. Chronic effects can be seen long after first exposure(s) to a toxic chemical.
2,4-Dinitrophenol has moderate chronic toxicity to aquatic life. Insufficient data are available to evaluate or predict the long- term effects of 2,4-Dinitrophenol to plants, birds, or land animals.
2,4-Dinitrophenol is moderately soluble in water. Concentrations of between 1 to 1,000 milligrams will mix with a liter of water.
DISTRIBUTION AND PERSISTENCE IN THE ENVIRONMENT
2,4-Dinitrophenol is slightly persistent in water, with a half-life of between 2 to 20 days. The half-life of a pollutant is the amount of time it takes for one-half of the chemical to be degraded. About 98.75% of 2,4-Dinitrophenol will eventually end up in water; about 0.65% will end up in terrestrial soil; and about 0.6% will end up in aquatic sediments.
BIOACCUMULATION IN AQUATIC ORGANISMS
Some substances increase in concentration, or bioaccumulate, in living organisms as they breathe contaminated air, drink contaminated water, or eat contaminated food. These chemicals can become concentrated in the tissues and internal organs of animals and humans.
The concentration of 2,4-Dinitrophenol found in fish tissues is expected to be somewhat higher than the average concentration of 2,4-Dinitrophenol in the water from which the fish was taken. SUPPORT DOCUMENT: AQUIRE Database, ERL-Duluth, U.S.EPA.
06-02-2004, 11:30 PM #38
First of all, this was taken from the merck index, and the later one from osha.. I suggest you go there and look up all the dangers and precautions they have listed for water.
Why are you on a crusade against DNP ? Have you experienced these effects first hand? Are you dead? Do you have cataracts? Has it exploded in your face?
Originally Posted by Anhydro78
Last edited by chrisAdams; 06-02-2004 at 11:32 PM.
06-02-2004, 11:31 PM #39
2,4-Dinitrophenol is used in the manufacture of dyes, wood preservatives, and as a pesticide. The acute (short-term) effects of 2,4-dinitrophenol in humans through oral exposure are nausea, vomiting, sweating, dizziness, headaches, and loss of weight. Chronic (long-term) oral exposure to 2,4-dinitrophenol in humans has resulted in the formation of cataracts and skin lesions, weight loss, and has caused effects on the bone marrow, central nervous system (CNS), and cardiovascular system. Limited or no information is available on the developmental, reproductive, or carcinogenic effects of 2,4-dinitrophenol in humans. EPA has not classified 2,4-dinitrophenol for carcinogenicity.
Please Note: The main sources of information for this fact sheet are EPA's Integrated Risk Information System (IRIS), which contains information on the oral chronic toxicity of 2,4-dinitrophenol and the RfD, and the the Agency for Toxic Substances and Disease Registry's (ATSDR's) Toxicological Profile for Dinitrophenols.
2,4-Dinitrophenol is used in the manufacture of dyes and wood preservatives, as a pesticide, and as an indicator for the detection of potassium and ammonium ions. (1,6)
During the 1930s, 2,4-dinitrophenol was used as a diet pill, but this use was stopped in 1938. (1)
Sources and Potential Exposure
Exposure to 2,4-dinitrophenol occurs from pesticide runoff to water and from releases to the air from manufacturing plants. (1)
Assessing Personal Exposure
2,4-Dinitrophenol can be measured in the blood, urine, and tissues of exposed persons. (1)
Health Hazard Information
Acute oral exposure to high levels of 2,4-dinitrophenol in humans has resulted in increased basal metabolic rate, nausea, vomiting, sweating, dizziness, headache, loss of weight, and other symptoms. (1,2)
2,4-Dinitrophenol is considered to have high acute toxicity, based on short-term animal tests in rats and mice. (3)
Chronic Effects (Noncancer):
Chronic oral exposure to 2,4-dinitrophenol in humans and animals has resulted in the formation of cataracts and skin lesions and has caused effects on the bone marrow, CNS, and cardiovascular system. (1,2)
The Reference Dose (RfD) for 2,4-dinitrophenol is 0.002 milligrams per kilogram body weight per day (mg/kg/d) based on cataract formation in humans. The RfD is an estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure to the human population (including sensitive subgroups), that is likely to be without appreciable risk of deleterious noncancer effects during a lifetime. It is not a direct estimator of risk but rather a reference point to gauge the potential effects. At exposures increasingly greater than the RfD, the potential for adverse health effects increases. Lifetime exposure above the RfD does not imply that an adverse health effect would necessarily occur. (4)
EPA has low confidence in the study on which the RfD was based since this study only describes anecdotal data; low confidence in the database since the supporting database is meager; and, consequently, low confidence in the RfD. (4)
EPA has not established a Reference Concentration (RfC) for 2,4-dinitrophenol. (4)
Case reports of women taking 2,4-dinitrophenol orally for weight loss suggest that it may affect the female reproductive system, but the limited information is inconclusive. (1)
One study reported an increased incidence of stillborn animals and increased pup mortality in the offspring of animals exposed to 2,4-dintrophenol by gavage. (1)
No information is available on the carcinogenic effects of 2,4-dinitrophenol in humans. (1)
One study reported that 2,4-dinitrophenol did not promote tumor development in mice. (1,5)
EPA has not classified 2,4-dinitrophenol for potential carcinogenicity. (4)
The chemical formula for 2,4-dinitrophenol is C6H4N2O5 and the molecular weight is 184.11 g/mol. (6)
The vapor pressure for 2,4-dinitrophenol is 1.42 × 10-7 mm Hg at 25 °C, and its log octanol/water partition coefficient (logKow) is 1.91. (7)
2,4-Dinitrophenol exists as yellowish crystals, is slightly soluble in water, and is volatile with steam. (6)
The odor threshold for 2,4-dinitrophenol is not available.
To convert concentrations in air (at 25 °C) from ppm to mg/m3: mg/m3 = (ppm) × (molecular weight of the compound)/(24.45). For 2,4-dinitrophenol: 1 ppm = 7.53 mg/m3.
Health Data from Oral Exposure
LD50 (Lethal Dose50)--A calculated dose of a chemical in water to which exposure for a specific length of time is expected to cause death in 50% of a defined experimental animal population.
The health values cited in this factsheet were obtained in December 1999.
a Health numbers are toxicological numbers from animal testing or risk assessment values developed by EPA.
b Regulatory numbers are values that have been incorporated in Government regulations, while advisory numbers are nonregulatory values provided by the Government or other groups as advice.
c The LOAEL is from the critical study used as the basis for the EPA RfD.
Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for Dinitrophenols. Public Health Service, U.S. Department of Health and Human Services, Atlanta, GA. 1995.
National Research Council. Drinking Water and Health. Volume 4. National Academy Press, Washington, DC. 1982.
U.S. Department of Health and Human Services. Registry of Toxic Effects of Chemical Substances (RTECS, online database). National Toxicology Information Program, National Library of Medicine, Bethesda, MD. 1993.
U.S. Environmental Protection Agency. Integrated Risk Information System (IRIS) on 2,4-Dinitrophenol. National Center for Environmental Assessment, Office of Research and Development, Washington, DC. 1999.
U.S. Department of Health and Human Services. Hazardous Substances Databank (HSDB, online database). National Toxicology Information Program, National Library of Medicine, Bethesda, MD. 1993.
The Merck Index. An Encyclopedia of Chemicals, Drugs, and Biologicals. 11th ed. Ed. S. Budavari. Merck and Co. Inc., Rahway, NJ. 1989.
U.S. Environmental Protection Agency. Assessment Tools for the Evaluation of Risk (ASTER, online database). Environmental Research Laboratory, Duluth, MN. 1993.
06-02-2004, 11:31 PM #40Originally Posted by Anhydro78
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