Analysis of someone else?s recommendations:

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


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

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

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

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

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

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

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

Auxillary



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

Answer
Yea, but you don?t gain much and Eq or ganabol would be better as would fina.

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

Maybe deca and sustanon or deca and omandren????
Answer:
Wouldn?t go with deca and sus and omna are more or less the same.

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

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

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

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

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

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

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

Other dieting stuff

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

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

Other cycles for DNP use

Why not do DNP in even smaller doses like that of ephedrine up to 100mg or so?. It will speed up the metabolism and cause a loss of weight without all the discomfort and t4-t3 conversion shutdown. Furthermore, by speeding up the metabolism it may help upgrade steriod receptors and clen receptors with much less discomfort for the user.
DNP seems to upgrade clen receptor sites as well as steroid receptor sites.
The rebound for the AS upgrade is only known from anecdotal feedback from myself and others, but if you increase the metabolism of the cell it only stands to reason that you are going to decrease the time it takes to regenerate the receptor sites. The ATP depletion and opening of ATP channels is also likely to be playing a part in these benefits as well, but that is research that probably won?t be done. So the channel part in the upgrade is just speculation.

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


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

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


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


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


Good things about DNP:

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

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




Part 3
One shouldn't be surprised at these differences. The clinician uses strychnine as a tonic; the experimenter employs it to cause convulsions. The clinician uses adrenaline, at titrated doses, to produce a manageable hypertension; the physiologist, with massive doses causes acute edema of the lung.
Yet, to base the clinical use of adrenaline or of strychnine on acute edema of the lung or experimental convulsions, constitutes an obvious error. It is the same for dinitrophenol.

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

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


We shall see, in order:

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

I. ACTION ON BASAL METABOLISM

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

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

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

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

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

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

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

II. VISCERAL ACTION

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

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

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

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

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

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

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

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

III. ACTION ON NUTRITION

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

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

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

Thyroxine reduces bone density.

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

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

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

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

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

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

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

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

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

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

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

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

All about DNP : Animal's manuel (continued)


Here is why you need to eat a regular diet:

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

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

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

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

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

KATP channels play an important role in the control of vascular tone [4]. Polarization following potassium channel activation