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a question for people who know abotu DNP.

would the reults of DNP be the same (to a certain degree) if someone at 25% body fat took it and someone at 15% body fat took it, if they did the same sort of training and diet?!?!
Thanx!
 
LeeJunFan said:
ok, I already drink about 2 gallons of water a day anyway so that shouldn't be much of a problem, should I just take multi-vitamins to get my vit. E and vit. C or should I get them on their own?



p.s. what's Quercetin, is it similar to Benadryl?

Thanx!!!!

It has anti-histaminic properties(broad Spectrum) like Benadryl except it doesn't make you drowsy.
 
so let me get this straight, it's:

-600mg of R-ALA a day (doesn't matter whether with carbs or not as long as I get the 600mg?)
-1200IU's of Vit. E a day (what are IU's)
-1000mg of Vit. C a day
-3000mgs of Quercetin a day

Thanx!
 
LeeJunFan said:
so let me get this straight, it's:

-600mg of R-ALA a day (doesn't matter whether with carbs or not as long as I get the 600mg?)
-1200IU's of Vit. E a day (what are IU's)
-1000mg of Vit. C a day
-3000mgs of Quercetin a day

Thanx!

1200 IU's = 1200 International Units

Used when dosaging Alpha-Tocopherol, the synthetic form of Vitamin E.
 
lejunfan:

the essentials of dnp (for someone who just has to use the bloody stuff) is:

correct dose. small frequent doses are far better than the 200/400/600mg doses some idiots take at once

good hydration. glycerol at about 20ml with 500mL of water 3x a day (so long as you dont have a heart condition) will aid in staying hydrated. drinking a lot of cool water throughout the day is the other obvious neccessity.

correct electrolytes. dont sweat too much (stay in cool conditions) or piss too much (dont drink 12L of water on day 1 out of fear) and take an electrolyte replacement (buy from pharmacy, they taste awful, but...get over it) every, say, second day. avoid drinking all the V8 juice that every moron says to drink, it can bump your potassium way too high.

less-sedating antihistamine (eg fexofenadine at about 180mg a day) go to your pharmacy, ask for it. these are for daytime, they are effective, but wont make you drowsy

sedating antihistamine (eg promethazine at about 50mg a day) for use at night to help you sleep. get from pharmacy. they will make you drowsy, they will fuck up quality sleep, they will dry out your mucous membranes in the throat, nose etc making them dry and uncomfortable.

vitamin C, a few grams a day. take as much as you want really, you just piss out any excess

vitamin E take the reccommended dose, or a bit above if youre paranoid. just so you know, one IU of vitamin E is just one mg of vitamin E. its nowhere near as complicated as other members make it out to be. sheesh.

id skip the ala. i think its bullshit. most important is to stay cool, hydrated, well dosed, and have normal electrolytes. these are the danger factors. the rest are as nothing compared to them.

cheers
 
GoldenDelicious said:
lejunfan:

the essentials of dnp (for someone who just has to use the bloody stuff) is:

correct dose. small frequent doses are far better than the 200/400/600mg doses some idiots take at once

good hydration. glycerol at about 20ml with 500mL of water 3x a day (so long as you dont have a heart condition) will aid in staying hydrated. drinking a lot of cool water throughout the day is the other obvious neccessity.

correct electrolytes. dont sweat too much (stay in cool conditions) or piss too much (dont drink 12L of water on day 1 out of fear) and take an electrolyte replacement (buy from pharmacy, they taste awful, but...get over it) every, say, second day. avoid drinking all the V8 juice that every moron says to drink, it can bump your potassium way too high.

less-sedating antihistamine (eg fexofenadine at about 180mg a day) go to your pharmacy, ask for it. these are for daytime, they are effective, but wont make you drowsy

sedating antihistamine (eg promethazine at about 50mg a day) for use at night to help you sleep. get from pharmacy. they will make you drowsy, they will fuck up quality sleep, they will dry out your mucous membranes in the throat, nose etc making them dry and uncomfortable.

vitamin C, a few grams a day. take as much as you want really, you just piss out any excess

vitamin E take the reccommended dose, or a bit above if youre paranoid. just so you know, one IU of vitamin E is just one mg of vitamin E. its nowhere near as complicated as other members make it out to be. sheesh.

id skip the ala. i think its bullshit. most important is to stay cool, hydrated, well dosed, and have normal electrolytes. these are the danger factors. the rest are as nothing compared to them.

cheers

Big mistake in not taking the R-ALA. You forget that DNP blocks insulin. That's why it works on everybody. It keeps the (Na)2+ (Sodium) and
(K)+ (Potassium) channels simultaneously open which no other drug can do,.

So, the ONLY way to control blood sugar fluctuations is with R-ALA, when eating carbs. Also, you forget that R-ALA recycles both Vit. E and Vit. C after they have both destroyed the free radicals generated vby the rapid oxidation of FFA's. So, instead of being excreted, Vit. E and Vit.C get thrown back into the mix.

Apart from that, R-ALA increases intra-cellular Glutahione levels by 50-70%, which is DEFINATELY a good thing to have on your side while on DNP, as all the free radicals generated by the rapid fat oxidation is attacking the cells at an accelerated rate. This compromises the immune system somewhat so increasing intra-cellular glutathione is a good idea(R-ALA is fat soluble, apart from water soluble so it can enter the cell membrane)
 
Fonz said:
Big mistake in not taking the R-ALA. You forget that DNP blocks insulin.
justify this statement. i would like a study of decent quality, and not just the abstracts that you try to pass off as convincing evidence to the uninitiated. i contest that DNP blocks the action of insulin.

Fonz said:
That's why it works on everybody.
justify this statement also. i disagree. the reason that dnp works is through its retardation of oxidative phosphorilation on the mitochondrial cell wall, not through any action on insulin.

Fonz said:
It keeps the (Na)2+ (Sodium) and
(K)+ (Potassium) channels simultaneously open which no other drug can do,.
i love these statements. perhaps you should look up the action of a few neurotoxins before you assert that dnp is the only agent which opens sodium and potassium channels.

Fonz said:
So, the ONLY way to control blood sugar fluctuations is with R-ALA, when eating carbs.
really? so using a low GI carbohydrate such as fructose in lieu of higher GI carbs wont achieve the same effect? has the rationale of eating fruit rather than white bread slipped your mind? (or did it stay still while your mind was slipping? i suspect the latter)

Fonz said:
Also, you forget that R-ALA recycles both Vit. E and Vit. C after they have both destroyed the free radicals generated vby the rapid oxidation of FFA's. So, instead of being excreted, Vit. E and Vit.C get thrown back into the mix.
of course the daily ingestion of both of these very cheap agents is insufficient to accomplish the purpose of mopping up a few free radicals. if you want to recyle, fonz, stick to saving aluminium cans. leave other peoples drug therapy out of it.

Fonz said:
Apart from that, R-ALA increases intra-cellular Glutahione levels by 50-70%, which is DEFINATELY a good thing to have on your side while on DNP, as all the free radicals generated by the rapid fat oxidation is attacking the cells at an accelerated rate.
wow that sounds really nifty and complicated. you must be very smart. i love the way you skirt around the subject at hand but dont actually explain anything in such a way that everyone reading it understands. what was it that einstein said again? if you cant explain something simply, you probably dont understand it well enough? yeah, sounds like it

Fonz said:
This compromises the immune system somewhat
really? how? please back the statement up with high quality evidence, as usual. to be a bot more precise, anything derived from the back of a cereal box IS NOT HIGH QUALITY

Fonz said:
so increasing intra-cellular glutathione is a good idea(R-ALA is fat soluble, apart from water soluble so it can enter the cell membrane)
wow. sounds coooooooooool

fonz, when you get the itch to reply to things that you dont really understand, just repeat to yourself, over and over: "it is better for me to say nothing, and have people assume i am stupid, rather than open my mouth and remove all doubt"

now excuse me while i clean my shoes from all the bullshit that plopped on them while i was reading your post
 
GoldenDelicious said:
justify this statement. i would like a study of decent quality, and not just the abstracts that you try to pass off as convincing evidence to the uninitiated. i contest that DNP blocks the action of insulin.

justify this statement also. i disagree. the reason that dnp works is through its retardation of oxidative phosphorilation on the mitochondrial cell wall, not through any action on insulin.

i love these statements. perhaps you should look up the action of a few neurotoxins before you assert that dnp is the only agent which opens sodium and potassium channels.

really? so using a low GI carbohydrate such as fructose in lieu of higher GI carbs wont achieve the same effect? has the rationale of eating fruit rather than white bread slipped your mind? (or did it stay still while your mind was slipping? i suspect the latter)

of course the daily ingestion of both of these very cheap agents is insufficient to accomplish the purpose of mopping up a few free radicals. if you want to recyle, fonz, stick to saving aluminium cans. leave other peoples drug therapy out of it.

wow that sounds really nifty and complicated. you must be very smart. i love the way you skirt around the subject at hand but dont actually explain anything in such a way that everyone reading it understands. what was it that einstein said again? if you cant explain something simply, you probably dont understand it well enough? yeah, sounds like it

really? how? please back the statement up with high quality evidence, as usual. to be a bot more precise, anything derived from the back of a cereal box IS NOT HIGH QUALITY

wow. sounds coooooooooool

fonz, when you get the itch to reply to things that you dont really understand, just repeat to yourself, over and over: "it is better for me to say nothing, and have people assume i am stupid, rather than open my mouth and remove all doubt"

now excuse me while i clean my shoes from all the bullshit that plopped on them while i was reading your post



I hate embarrasing people, but you leave me no choice. You're talking to one of the four people who have the most knowledge regarding DNP. You're an amateur compared to me.

Anyways:

Question #1:

"justify this statement. i would like a study of decent quality, and not just the abstracts that you try to pass off as convincing evidence to the uninitiated. i contest that DNP blocks the action of insulin."

1: Proc Natl Acad Sci U S A. 1989 May;86(9):3209-13. Related Articles, Links


Tyrosine phosphorylation of the insulin receptor is not required for receptor internalization: studies in 2,4-dinitrophenol-treated cells.

Backer JM, Kahn CR, White MF.

Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02215.

The relation between insulin-stimulated autophosphorylation of the insulin receptor and internalization of the receptor was studied in Fao rat hepatoma cells. Treatment of Fao cells with 2,4-dinitrophenol for 45 min depleted cellular ATP by 80% and equally inhibited insulin-stimulated receptor autophosphorylation, as determined by immunoprecipitation of surface-iodinated or [32P]phosphate-labeled cells with anti-phosphotyrosine antibody. In contrast, internalization of the insulin receptor and internalization and degradation of 125I-labeled insulin by 2,4-dinitrophenol-treated cells were normal. These data show that autophosphorylation of the insulin receptor is not required for the receptor-mediated internalization of insulin in Fao cells and suggest that insulin receptor recycling is independent of autophosphorylation.

PMID: 2470095 [PubMed - indexed for MEDLINE]


Go back to Pharmacy School kid. You just got owned. The reason why 2,4 dinitrophenol works is because it depletes cellular ATP. The energy is the released off as heat. However, DEPLETION of ATP by 2,4 dinitrophenol(DNP) INHIBITED insulin-stimulated receptor auto-phosphorylation. This means that the insulin-dependant transporters WERE NOT ABLE TO translocate to the outside of the cell membrane. Which means DNP BLOCKS INSULIN MEDIATED RECEPTORS. It does not let the insulin dependent transporters do their job. It blocks them.

And as said in the last sentence, INSULIN RECEPTOR RECYCLING is INDEPENDENT of autophosphorylation. This means that when DNP blocks ATP production, INSULIN DOES NOT attach itself to its receptors outside the cell, because they have translocated inside, due to the DNP.

Question #2

The rationale behind using low GI carbs is to REDUCE the SPEED and amplitude of the insulin RELEASE from the pancreas. Because the higher the transient insulogenic surge, the higher the heat production, as your body is more rapidly trying to produce ATP. The opposite stands for low GI carbs. As the speed and amplitude of the insulogenic spike is slower and smaller, the heat production is going to be lower, because the body is then trying to produce ATP at a musch slower rate.

See, Heat production due to DNP is a function of the Glycaemic Index of the meal, the amount of macronutrients consumed(and calories), and the amount of DNP in your system. The more DNP in your system, the more ATP will be blocked, and therfore more heat will be released to the surroundings.

Sorry GD, but this is more my little realm...we're in the realm of calculus and partial differentiation involving three substrates(Prots, carbs, fats), and the amount of heat generated by a meal with a certain amount of these substartes, taking into account the Glycaemic index, and the ATP blocking speed due to the DNP in your system at the present time. I already wrote an equation(very detailed in fact) about 2 hyears ago, detailing EXACTLY how much heat could be generated by DNP depending on a whole host of variables.


Now do everybody a big favor and go back to READING more about DNP. You're knowledge regarding it is downright PRIMITIVE.

And to make you GO AWAY:

"i love these statements. perhaps you should look up the action of a few neurotoxins before you assert that dnp is the only agent which opens sodium and potassium channels?"

Cyanide does the exact same thing. It blocks ATP production. But is much more deadly. As it is able to block it completely at lower dosages than DNP. And since the body only has about 1% of ATP reserve at any given time, death can result in minutes from the complete blockage of ATP by Cyanide.

Just call me Dr. Fonz :)
 
before i begin, i would like to point out that you left most of my questions and assertations unanswered, which is of course, your usual style of arguing. how...selective of you. :rolleyes:

Fonz said:
I hate embarrasing people, but you leave me no choice.
so why do you do it to yourself, over and over and over again? ;)

Fonz said:
You're talking to one of the four people who have the most knowledge regarding DNP.
i get the feeling im jus talking to one of your personalities. :mix: do you mind if i talk to the real fonz, split personality number 1?

Fonz said:
You're an amateur compared to me.
er, no. im a professional, end of story. you on the other hand, take a bit more than a single word to describe. narcissistic? deluded? hmm?

Fonz said:
Anyways:

Question #1:

"justify this statement. i would like a study of decent quality, and not just the abstracts that you try to pass off as convincing evidence to the uninitiated. i contest that DNP blocks the action of insulin."

1: Proc Natl Acad Sci U S A. 1989 May;86(9):3209-13. Related Articles, Links


Tyrosine phosphorylation of the insulin receptor is not required for receptor internalization: studies in 2,4-dinitrophenol-treated cells.

Backer JM, Kahn CR, White MF.

Joslin Diabetes Center, Department of Medicine, Brigham and Women's Hospital, Boston, MA 02215.

The relation between insulin-stimulated autophosphorylation of the insulin receptor and internalization of the receptor was studied in Fao rat hepatoma cells. Treatment of Fao cells with 2,4-dinitrophenol for 45 min depleted cellular ATP by 80% and equally inhibited insulin-stimulated receptor autophosphorylation, as determined by immunoprecipitation of surface-iodinated or [32P]phosphate-labeled cells with anti-phosphotyrosine antibody. In contrast, internalization of the insulin receptor and internalization and degradation of 125I-labeled insulin by 2,4-dinitrophenol-treated cells were normal. These data show that autophosphorylation of the insulin receptor is not required for the receptor-mediated internalization of insulin in Fao cells and suggest that insulin receptor recycling is independent of autophosphorylation.

PMID: 2470095 [PubMed - indexed for MEDLINE]


Go back to Pharmacy School kid. You just got owned. The reason why 2,4 dinitrophenol works is because it depletes cellular ATP. The energy is the released off as heat. However, DEPLETION of ATP by 2,4 dinitrophenol(DNP) INHIBITED insulin-stimulated receptor auto-phosphorylation. This means that the insulin-dependant transporters WERE NOT ABLE TO translocate to the outside of the cell membrane. Which means DNP BLOCKS INSULIN MEDIATED RECEPTORS. It does not let the insulin dependent transporters do their job. It blocks them.

And as said in the last sentence, INSULIN RECEPTOR RECYCLING is INDEPENDENT of autophosphorylation. This means that when DNP blocks ATP production, INSULIN DOES NOT attach itself to its receptors outside the cell, because they have translocated inside, due to the DNP.

a couple of things.

the first thing id like to clear up is that translocation the way youre talking about it happens in star trek, but thats about it.

secondly, i told you to get a decent quality source, not your usual half understood medline abstract. sorry mate, but you just dont understand it, and it doesnt help your argument since the content of that article is not what you are talking about. im not going to bother explaining the role of insulin in fat loss in this instance because id get better results explaining it to my dog.

all i can say is stop, take a look at what you said in the context of what we are talking about, meditate for a couple of hours, and maybe youll see why youre off the mark. (i suspect not, but anyway)

anyway bud i have owned you that many times it amazing. hell if you were worth anything i would have sold you. but you aint.

Fonz said:
Question #2

The rationale behind using low GI carbs is to REDUCE the SPEED and amplitude of the insulin RELEASE from the pancreas. Because the higher the transient insulogenic surge, the higher the heat production, as your body is more rapidly trying to produce ATP. The opposite stands for low GI carbs. As the speed and amplitude of the insulogenic spike is slower and smaller, the heat production is going to be lower, because the body is then trying to produce ATP at a musch slower rate.
thats a very interesting angle youre taking. you make a point supporting what i am saying, then act as if it was what you were saying all along. brilliant!

oh i just thought id mention: there is no such thing as anything insulogenic. youre making up words. also, any such 'insulogic' parameter in the body does not move with any speed. its a body, not a raceway. lastly the body is not 'trying' to produce atp more slowly. it is a process retarded by the dnp.

anyway i get the feeling youre a bit lost, so ill move on the the next slab of steamy bullshit..

Fonz said:
See, Heat production due to DNP is a function of the Glycaemic Index of the meal, the amount of macronutrients consumed(and calories), and the amount of DNP in your system. The more DNP in your system, the more ATP will be blocked, and therfore more heat will be released to the surroundings.
um, no it isnt. and no, im not going to spend 10 minutes typing to explain why. your whole response is reminiscant of your...ahem...'article' on 'glucose uptake after a meal'. and dont get me started on that piece of garbage

Fonz said:
Sorry GD, but this is more my little realm...we're in the realm of calculus and partial differentiation involving three substrates(Prots, carbs, fats), and the amount of heat generated by a meal with a certain amount of these substartes, taking into account the Glycaemic index, and the ATP blocking speed due to the DNP in your system at the present time. I already wrote an equation(very detailed in fact) about 2 hyears ago, detailing EXACTLY how much heat could be generated by DNP depending on a whole host of variables.
er no, drugs are my area. and there are a few id like to see YOU on. mostly psych drugs. lithium springs to mind (no pun intended)

anyway could you get this formula for me? is it as good as your glucose article? if so ill get a bag of potato chips and a coffee...

Fonz said:
Now do everybody a big favor and go back to READING more about DNP. You're knowledge regarding it is downright PRIMITIVE.
what im really looking forward to reading is your book ;)

i have a question though. how are you going to make a pop-up book viewable on the internet? you do know that computer monitors dont fold up, dont you?

Fonz said:
And to make you GO AWAY:

GoldenDeliciousTheFonzAssRapist said:
"i love these statements. perhaps you should look up the action of a few neurotoxins before you assert that dnp is the only agent which opens sodium and potassium channels?"

Fonz said:
It keeps the (Na)2+ (Sodium) and
(K)+ (Potassium) channels simultaneously open which no other drug can do,.

Fonz said:
Cyanide does the exact same thing.

Fonz said:
Just call me Dr. Fonz :)

sure thing Dr fonz. Sure thing ;)
 
While we're on the subject of DNP, how does it work exactly? I thought it worked by changing the proton gradient on the electron transport chain, making ATP synthesis much less effective, requiring more glucose to make the same amount of ATP. is that true or false?
 
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