need Clen advice for cutting

[3J]

Lol opinions very

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well, seeing as how i get people in shape for a living and have an extensive background on hormones and steroids... i'd say mine weighs a little heavier

out of all the compounds we use, dnp is by far the most dangerous... anything that you want to do with dnp can be done with diet and training... without the risk of life

its your body, you only get one

educate before you medicate

 

[Poohbear513]

well, seeing as how i get people in shape for a living and have an extensive background on hormones and steroids... i'd say mine weighs a little heavier

out of all the compounds we use, dnp is by far the most dangerous... anything that you want to do with dnp can be done with diet and training... without the risk of life

its your body, you only get one

educate before you medicate

Lol ! Okay I see so ur a personal train that makes u a expert lol !! I can get a certificate in bout 2 weeks !! I do agree exercise and diet are most important things !! But if we r talking about compounds dnp is no more dangerous than t3 or clen at all !! To much of anything can kill u all of them should be use with caution and common sense !!

Thanks

I will be all day if u need anymore help

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[3J]

lol "certified".. youre damn right about that.. those certifications dont mean shit..

but 13 years of studying hormones, steroids, compounds, and nutrition do..

im not your golds gym personal trainer brother... i contest prep pro level athletes...

and your claim that dnp is no more dangerous than clen or t3 tells me how little you know about it..

dnp is an actual poison.. a pesticide that was banned due to its ruining the bald eagle population (eggs were being laid with too thin of shells)

and where do you get dnp from?? ugls.. you dont know if the dosage is correct.. some n00bie makes a mistake and dies from it.. it has happened many times...

the only other drug i can think of that is dangerous is methyl tren... thats about it..

clen and t3 will not kill you.. its very hard to overdose on either because you have to take so much.. but dnp, just a little too much and youre done..

so please do your research and weigh out your options the next time you wanna run dnp

i will never condone the use of it

 

[Poohbear513]

Really clen isn't dangerous but I some from pep company in liquid form

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[Poohbear513]

I have been using roids probably longer than u have been a live so like I said opinions very like assholes everybody has one

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[3J]

Really clen isn't dangerous but I some from pep company in liquid form

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in comparison to dnp?? lol.. come on man...


yea if someone gets clen and runs 200mcg right off the bat, sure... but an er doc can use beta blocking drugs to reverse that..

can you reverse dnp poisoning??

like i said, most dangerous compound you can ever use in our world

 

[Poohbear513]

Clen will bust ur heart overdosed !! Now t3 want kill but fuck u up for life and will be meds til u die lol

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[3J]

using roid and studying them are two very different things...

thats like you saying im 50 and i have been driving for 34 years, and youve only been driving for 10, but youre a formula one driver and i sit at an office desk...

your argument doesn't really take you anywhere brother..

I have been using roids probably longer than u have been a live so like I said opinions very like assholes everybody has one

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overdosing on any of those compounds come with complications... but in comparison to dnp none can equate

Clen will bust ur heart overdosed !! Now t3 want kill but fuck u up for life and will be meds til u die lol

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fyi, this is a debate.. im not bashing on you brother.. i respect you as a person.. we just dont agree on something

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how dangerous is dnp??? here is a study on NON-ORAL EXPOSURE to dnp... people die

[FONT=&quot][h=2]ABSTRACT[/h]Objective: To report clinical features and treatment of 16 cases of acute 2,4-dinitrophenol poisoning. Methods: A total of 16 patients suffering from acute poisoning due to non-oral exposure to 2,4-dinitrophenol were sent to our hospital. Two died within 3 h after admission, while the other 14 responded to supportive treatment and hemoperfusion. Clinical features and treatment of the patients were retrospectively analyzed and presented. Results: Fourteen patients recovered and were discharged after four to six weeks of treatment. No obvious poisoning sequelae were found in the three-month follow-up. Conclusions: Non-oral exposure to 2,4-dinitrophenol is toxic. Hemoperfusion and glucocorticoid treatments may be efficient measures to prevent mortality, but this requires further study.

Keywords: 2,4-Dinitrophenol; Poisoning; Therapeutics; Hemoperfusion; Glucocorticoid
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[h=2]1. INTRODUCTION[/h]Dinitrophenols (C6-H4-N2-O4; Chemical Abstracts Service (CAS) No. 25550-58-7) are highly toxic chemicals with six isomeric compounds. They are widely used in dyes, developers, drugs, indicators, insecticides, and in the preservation of wood. 2,4-Dinitrophenol (2,4-DNP) (CAS No. 51-28-5), the most toxic compound, is a yellow, combustible crystalline solid that has a musty odor and is poorly soluble in water. It was used as an oral weight control drug in the 1930s, because it clearly increased the body’s basal metabolic rate, but was soon banned for this purpose by the Food and Drug Administration (FDA) because of serious adverse effects such as hyperthermia, cataracts, and even death (Tainter et al., 1934). In recent years, some illegal weight control drugs with 2,4-DNP can be purchased and poisoning events, even deaths, because of ingestion have been reported in some countries (Kurt et al., 1986).
Since 2,4-DNP is a crystalline solid and is barely soluble in water, poisoning accidents are rare with normal protective measures other than deliberate ingestion. In this study, we report 16 patients with acute 2,4-DNP poisoning through occupational exposure due to ignorance of the risk of poisoning.
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[3J]

[h=2]Abstract[/h][h=3][FONT=&quot]2,4-Dinitrophenol (DNP) is reported to cause rapid loss of weight, but unfortunately is associated with an unacceptably high rate of significant adverse effects. DNP is sold mostly over the internet under a number of different names as a weight loss/slimming aid. It causes uncoupling of oxidative phosphorylation; the classic symptom complex associated with toxicity of phenol-based products such as DNP is a combination of hyperthermia, tachycardia, diaphoresis and tachypnoea, eventually leading to death. Fatalities related to exposure to DNP have been reported since the turn of the twentieth century. To date, there have been 62 published deaths in the medical literature attributed to DNP. In this review, we will describe the pattern and pathophysiology of DNP toxicity and summarise the previous fatalities associated with exposure to DNP.

[FONT=&quot]Keywords: Dinitrophenol, Weight loss, Toxicity, Fatality[/FONT]

Organ Systems Affected by Therapeutic Use[/h][h=1][FONT=&quot]There is a small margin between the beneficial effects and the toxic effects of DNP. The most common side effect reported with the therapeutic use of DNP is a rash [6, 36–38]. This rash can be maculo-papular, urticarial, angio-oedematous or a severe exfoliative dermatitis [39–41]. There is often accompanying pruritis and subsequent desquamation [39, 41, 42]. Prolonged peripheral neuritis has been reported, often affecting the hands and feet and associated with skin changes [11, 43, 44]. A common complaint is that of yellow discoloration of the skin, sclera and urine [45–48]. This same yellow discoloration is often seen at autopsy and has been confused with jaundice due to reports of liver damage [36, 45, 49–52].
T wave and ST segment abnormalities have been noted and some of the earlier autopsied case reports recorded heart muscle damage [46, 50, 53]. Gastroenteritis and anorexia have been reported in high doses [11, 36]. Acute kidney injury, as evidenced by acute tubular necrosis, has been found at autopsy and also reported in two other cases [46, 54, 55]. Confusion, agitation, convulsion and coma are the most common neurological effects reported [50, 56, 57].
Agranulocytosis and neutropaenia have been associated with the therapeutic use of DNP [36, 37, 45, 47,58–61]. Cataracts can develop quickly after the use of DNP, usually leading to a permanent decrease in vision to light–dark perception in days to months [62–65]. Permanent deafness has been reported at doses considered to be therapeutic [66].

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[/h][h=3]Intentional Overdose[/h][h=1][FONT=&quot]The average time to presentation in the reported cases of acute or suicidal overdose is 7–8 h and the average time of death is 14 h [4, 15, 22, 51, 56, 67–69]. The onset of symptoms was reported as early as 3 h and 30 min after the overdose [56]. The usual complaint of the patient is that of profuse sweating [46]. The initial fever is not associated with a change in heart rate or blood pressure, but tachycardia, tachypnoea, shock, confusion, convulsions, cardiovascular collapse and pulseless electrical activity are the eventual consequence of the fatal, deliberate overdose, regardless of treatment [4, 15, 22, 51, 56, 67–69]. However, there has been at least one case of survival following deliberate overdose in an 18-year-old female who developed typical features of DNP toxicity [tachycardia of 144 beats per minute, tachypnoea of 38–40 breaths per minute and hyperthermia of 39.7°C (103.4°F)] [70]. She was managed conservatively with intravenous fluids and ice packs to maintain her temperature below 38.3°C (101°F) and was discharged less than 48 h following admission to hospital with no adverse effects at the time of discharge. Ingestion of DNP was confirmed by analysis of gastric lavage contents.

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[/h][h=2]DNP-Related Fatalities[/h][h=1][FONT=&quot]Fatalities from the intake of DNP, whether accidental or suicidal, have been reported since the turn of the twentieth century (Table 1). To date, there have been 62 published deaths attributed to DNP (Fig. 1). The largest publication of 36 deaths due to DNP was published in 1919 [6]. This was a study into the deaths in munition factories in Paris due to occupational exposure to DNP. It highlights the improvements made in the factory to prevent further deaths through simple measures such as ventilation, personal protective equipment and better hygiene. This combined with changes in legislation brought the death rate down from 16.3 per 10,000 t of DNP handled/produced to 1.2 per 10,000 t.
During the 1930s, reported DNP-related fatalities were all individuals who had taken it for weight loss [46,47, 51, 56, 57, 61, 67, 71]. After the 1930s, there have only been two fatalities in the remainder of the twentieth century [15, 68]. One related to deliberate ingestion of DNP [68] and the other was where an individual accidentally ingested a liquid he thought to be grape juice, but in fact contained derivatives of DNP [15]. This further decline in fatalities may reflect the labelling of DNP as ‘extremely dangerous and not fit for human consumption’ by the US Food and Drug Administration in 1938.
Over the last decade, from 2001 to 2010, there have been 12 deaths related to exposure to DNP. These fatalities have been linked to deliberate overdose [4, 22, 69], accidental toxicity associated with use by bodybuilders or for weight loss [21, 28, 72–75] and accidental occupational exposure [33]. This resurgence in reported fatalities may reflect the increased availability of DNP over the internet, marketed particularly towards bodybuilders.
Preceding death, the patient is often profoundly hyperthermic and there may be associated methaemoglobinaemia. Death is usually secondary to massive cardiovascular collapse. There have been frequent reports of a rapid (within minutes) onset of generalised rigidity after death [6, 11]. This profound muscle rigidity has also been seen to happen before death making mechanical ventilation very difficult [21]. This early onset of generalised rigidity after death has been attributed to the release of calcium from the cytosol due to the depletion of ATP [22].
Ingestion is currently the most common route of exposure to the drug leading to death. The lowest published lethal human oral dose of DNP is 4.3 mg/kg [76]; the doses reported in the published acute and suicidal fatalities range from 2.8 g to an estimated 5 g. The highest reported dose taken in acute overdose associated with survival was a woman who took 2.4 g with no complications [70].
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[/h][h=2]Options for Management[/h][h=1][FONT=&quot]There is no specific antidote for DNP poisoning and all management strategies are based on case reports and expert opinions, but the key to the management of DNP poisoning lies in early recognition and a high index of suspicion [46]. Patients who have acutely overdosed on DNP in any form should be observed for at least 12 h, as no patient has been recorded to be asymptomatic beyond 10 h after an acute overdose [4]. During this time, their body temperature, cardiac rhythm, heart rate and oxygen saturation should be carefully monitored.
Although there are no previous reports of its use, in line with the previously published American Academy of Clinical Toxicology/European Association of Poisons Centres and Clinical Toxciologists position statements on the use of oral activated charcoal, we would recommend consideration of a single dose of activated charcoal in those individuals who present within an hour of ingestion. Previous autopsies have reported a yellow coloured fluid in the intestines of some cases; there is no evidence that this fluid contains DNP rather than staining following ingestion. Therefore, at this time although there is no evidence to support the use of multi-dose activated charcoal and/or whole bowel irrigation, we feel that the potential benefit outweighs the potential risk. External decontamination, if appropriate, should be undertaken by washing to reduce dermal exposure. Based on the underlying pathophysiological principles and previous experience, it would be advisable to avoid the use of salicylates as it may worsen the DNP-related toxidrome [77, 78]. Aggressive fluid resuscitation should be initiated, using cooled fluids in those with hyperthermia.
Seizures should be controlled with benzodiazepines. These may also be needed to control severely agitated patients, as their agitation will add to the hyperthermic state which may lead to circulatory collapse. External cooling measures with ice or cooling blankets should be initiated to control hyperpyrexia [11, 70,79–81]. If benzodiazepines do not control agitation or seizures, then paralysis, intubation and ventilation should be considered. Dantrolene and ice baths have been used to control the severe hyperthermic state [46, 82]. There is the possibility for the use of external cooling devices, such as those used to induce therapeutic hypothermia following an out of hospital cardiac arrest, to rapidly reduce temperature; however, there have been no previous reports of using these devices in patients with DNP toxicity. Dantrolene has previously been recommended to manage the hyperthermia associated with the use of DNP. There is no evidence to support this recommendation, but it has been used successfully in a single case report [34, 82].
Intravenous vasopressors and/or inotropes should be considered accompanied with invasive arterial monitoring if fluid therapy fails to maintain the blood pressure. Cardiopulmonary resuscitation was performed in some of the cases of DNP overdose and in one case for up to an hour [69], but has never led to a return of spontaneous circulation. Halothane should be avoided as possible synergistic hyperthermia may cause deterioration and death [29].
Methaemoglobinaemia should always be suspected and tested for. Levels exceeding 30% should be treated with intravenous methylthioninium chloride (methylene blue), but treatment may be started at lower serum methaemoglobin levels in the presence of other signs of shock and tissue hypoperfusion.
The use of continuous veno-venous haemofiltration (CVVH) has been recommended to manage hyperkalaemia and hyperthermia associated with DNP overdose [4, 83]. However, there are no published cases in which CVVH or similar therapies have been used in DNP poisoning.
Propranolol has been studied in dogs poisoned by DNP and a significant reduction in lactate levels was recorded [25], but its clinical use in humans cannot be recommended due to the inhibitory effect on glucose production and unknown effect on mortality. High-dose insulin and glucose may have a beneficial effect through facilitation of glycolysis, but there is no animal or human data to support this treatment modality at this time [84]. However, glucose administration alone may be useful since glycolysis would be the main source of ATP production in DNP-poisoned cells [85].
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[/h][h=2]Summary[/h][h=1][FONT=&quot]DNP has been available for over a century, initially in the manufacture of munitions, due to its explosive properties. From the 1930s onwards, there has been interest in its properties to increase the underlying metabolic rate, leading to an associated weight loss. Following a number of deaths in the 1930s, the US Food and Drug Administration determined that DNP was ‘extremely dangerous and not fit for human consumption’. There were very few reported deaths since the late 1930s, until the last decade. It appears that there has been increasing interest and availability of DNP-containing products on the internet. Whilst these appear to be largely targeted towards bodybuilders to try and reduce fat and improve muscle bulk, there have been a number of deaths related to its use for more general weight loss. The primary toxicity seen with DNP is similar to that seen with other phenol-based products and is a combination of hyperthermia, tachycardia, diaphoresis and tachypnoea with associated cardiovascular collapse/cardiac arrest and death. There is no specific management for individuals with DNP-related toxicity; it is imperative that the temperature is brought down as rapidly and as soon as possible to try and reduce systemic toxicity and/or death. Currently, DNP remains freely available on the internet, with both detailed ‘regimens’ for its use and about the potential for acute toxicity and death on the internet seller websites. It is likely that some individuals, despite these warnings, will continue to purchase and use DNP-containing products to aid with weight loss, with the potential risk of acute toxicity and/or death.
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there you go... read up brother.. this is science, not broscience

 

[Poohbear513]

Okay u win since u feel so strongly about it !! But I'm 52 and probably forgot more than most people will ever know !! Plus I didn't get out of a book I lived it !!

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[3J]

Okay u win since u feel so strongly about it !! But I'm 52 and probably forgot more than most people will ever know !! Plus I didn't get out of a book I lived it !!

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and no one can take that away from you... but your personal experiences vs scientific study... scientific study triumphs every time

if youre just working off your own experience, things easily fall in the category of bro science... hence your opinion that dnp is as dangerous as clen or t3..

again, not trying to be a dick.. just trying to state facts about the dangers of the compound

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in other words, is there a "safe" way to use dnp... yes, but the margin of error and the risk is much much higher.. and the juice is not worth the squeeze