Can anyone tell me if Alin's DNP is powder or Crystaline?

[Juice Freak]

Just wondering if someone could let me know whether Alin's dnp is powder or crystal because it does not say on the site. Just curious I am well versed with DNP and love it but need to know for proper dosing. Cheers.

 

[big_byrd52]

powder

 

[Juice Freak]

Awesome bro, thanks for the help.

 

[bigbaldbulldog]

When ordering his DNP, what is his dosage and how much would a 225lb man need at 10%bf ? i hear between 200-300 mcgs or is it mgs? My good buddy tells me 14 days on 14 days off then again and i should look super ripped and drop about 3-5% bf

 

[Big Ed]

IMO t3 some anti e's and cardio will give you the same results and will be much less toxic. JMO

 

[big_byrd52]

BBB, ull need 400mcg. 14 days is a long time on it! u can do it, but u will feel like death by about day 5 and be really weak-- i mean anything, not just in the gym. if u can handle it then go for it. just go as long as u can stand it, about 7-10 day. then take the break and maybe use some clen in between and then another run and u will be set.

 

[GENE]

i think this is from animals board

ATP-Sensitive Potassium Ion 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 depolarises 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.

· Increase in blood glucose --> increase in glucose metabolism --> increase in intracell ATP --> inhibition of KATP channel.
· 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 (opening) results in lessened calcium influx and smooth muscle relaxation.

· KATP channel BLOCKED --> vascular tone increases.
· KATP channel ACTIVATED --> vascular tone decreases.

Besides being regulated by intracellular signals, potassium channels may also be regulated by membrane potential. Thus, in excitable cells in the heart, muscle, and nervous system, voltage-gated potassium channels are activated during an action potential; the activities of these potassium channels determine to a large extent the shape of the action potential, hence the strength of the signaling.

· KATP BLOCKED --> more strength
· KATP ACTIVATED --> less strength

Drugs which block KATP channels: tolbutamide, glyburide, glibenclamide.

Drugs which activate KATP channels: Prostaglandin E2 and I2, adenosine, lemakalim.

Drugs which activate K channels: pinacidil, cromakalim.

Mitochondria also contain a K+ channel that causes rapid K+ uptake when open [5].

DNP
What happens when someone takes the decoupler dinitrophenol (DNP)? Blood glucose will result in increased metabolism, but the level of ATP in the cell does not increase! In fact, it is depleted. So in this case, the KATP channel is not inhibited, and it stays open. Calcium is not taken into the cell, and insulin is not released. The person taking DNP has in effect given himself temporary diabetes.
Insulin is needed to facilitate the uptake of glucose into cardiac, skeletal, and adipose tissue, and to convert glucose to glycogen in the liver. It is anti-proteolytic and protects against the various ailments commonly seen in diabetics, such as vision problems and polyneuropathy. Not coincidentally, the same problems can result from ingesting DNP.

This is why, when one takes DNP, one also needs to take exogenous insulin.

Since the KATP channel remains open, vascular and muscular tone relax. Probably blood pressure will decrease. Strength will diminish.

It would seem that an antidote for DNP might be anything that causes the KATP channel to close, for example the drug glibenclamide.

References
1. Noma A. 1983. Nature 305: 147.
2. Noma A, Takano M. 1991. The ATP-sensitive K+ channel. Jpn J Physiol 41(1):77-87.
3. Civelek VN, Deeney JT, et al. 1996. Temporal sequence of metabolic and ionic events in glucose-stimulated clonal pancreatic-cells. Biochem. J. 315: 1015-1019. Boston University Medical Center.
4. Nichols, C.G. and Lederer, W.J. 1991. ATP-sensitive potassium channels in the cardiovascular system. American Journal of Physiology 261:H1675-H1686.
5. Paucek, P, Mironova, G, et al. 1992 "Reconstitution and partial purification of the glibenclamide-sensitive, ATP-dependent K+ channel from rat liver and beef heart mitochondria," J. Biol. Chem. 267, 26062.
6. Nakamura S. 1989. Glucose reverses DNP induced changes in action potentials. Cardiovascular Res. 23(4):286-294.
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Biological Study of Dinitro Drugs in Humans
By Dr. Jacques Bell
Bell, Jacques. 1939. Etude biologique des produits dinitres chez l'homme. Medecine. 19:749-54.
Translation © 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.
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, Wood and 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. He remarks 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.

1. La Therapeutique dinitree (J.-B. Bailliere et Fils, editeurs, 1937).

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Concerning Two Cases of Cataract Caused by Dinitrophenol
By Jean Sedan (Marseille)
Sedan, Jean. 1939. A propos de deux cas de cataracte par phenols dinitres. Annales d'Oculistes. 176:191.
Translation © 1996 Robert Ames

The implementation of the treatment for obesity by dinitrophenol dates only from 1933, the year when it was suddenly and rapidly put in the limelight by the work of the Americans Tainter, Mehrtens and Cutting.

These authors have established that the ingestion of dinitrophenol accelerates metabolism, causing a marked elevation in temperature. It seemed that dinitrophenol was a specially effective treatment for obesity. In 1936, Horner estimated that in the first 15 months following the appearance of the medication in the market, one hundred thousand persons used it to lose weight.

Incidents and accidents multiplied and appeared sufficiently serious that the American Medical Association warned the public against the dangers of unsupervised treatment.

Here we discuss only the case of cataracts, which Horner had said that it occurs in one case in 1000 treatments. At the end of this report we will note the principle bibliographic references concerning the American literature devoted to the subject and which is of a great value, but we wish to emphasize how the European work and especially French are on the other hand still rare and even exceptional.

One can say that it is by the work of Onfray and Gilbert Dreyfus presented to the Congress of the S.F.O. [Societe Francaise des Oculistes?] in 1937 that French opthamologists had their attention drawn to the subject. This remarkably precise work is enriched by two observations of which one is due to Doctor A. Gallois, of Besancon. We frequently reference this, for it contains in addition to minutely observed details, important physio-pathogenic considerations and a complete history of the subject.
Apart from this work, we should also to point out the observations of Van de Hoeve and Polak-Daniels published in Holland in 1936, as well as the French summaries and reviews of Halbron on cataracts and of Laignel-Lavastine on dinitrophenol intoxication.

Finally, we emphasize the interest of the work of Vogt on the cataracts caused by dinitrophenol in Switzerland and of G. Ciotola of those caused by alphadinitrophenol in Italy, both published in 1937. The same year, Stein and Crevecoeur pointed out that in their opinion this affectation was, when all is said and done, quite rare if one thinks of the enormous dissemination of dinitro treatment. This was also the opinion of Andre Mayer, based on the fact that despite the considerable number of intoxications by dintrophenol observed in munitions factories, no cases of cataracts have been noted.

Finally, in 1938, Carlotti and Rivoire de Nice presented a case of cataract by dintrophenyl-lysidine which developed "with almost lightning-like rapidity."
* * *
It was possible for us to observe two very demonstrative cases. In one there was an arrest of development of opacity after the patient stopped taking dinitrophenol, which is more than a rarity, a real exception in the pathological history of dinitrophenol cataracts.

OBSERVATION I. -- Mme. K... Lea, 32 years old presented herself to me in December 1937 with a marked lowering of the vision of both eyes, which began a few weeks earlier, developing extremely fast and was all the more disturbing since she works at a very visual profession in the editing of a newspaper and as she is especially partial to this pleasant and remunerative position. I noticed a beginning of bilateral cataract appearing striated and fleecy which is found almost constantly in the description of toxic lens opacities of this kind. The opacity is situated mainly at the level of the equator of the lens, but also involves the posterior part of the central mass. The vision is only 4/10 in the right and 5/10 in the left, these two acuities correctable to 7/10 O.D.G. -- 2.50.

Mme K... thus learned that she was rapidly becoming myopic.
The most minute research were done in view of identifying a possible cause of this bilateral cataract. All the blood and urine tests were negative. Very complete clinical examinations by Doctor P..., referring physician, point to the same conclusion that it is impossible to relieve Mmme. K...'s pathological process at all.
It is then that I thought of asking her about the possibility of a dinitrophenol anti-obesity treatment, even though the corpulence of my client did not seem excessive. She told me then of having taken two pills each day of 0.30 grams of dinitrophenol in series of ten days with a rest of 15 days, for the past year and a half.
She had, without the least dietary restriction, lost 19 kilograms out of 87 [42 pounds out of 191]. It was at that point that she began complaining about her vision.

I wasn't aware of the topic at that time except by the short summaries of American works, but I didn't hesitate to warn her against what I considered to be the real origin of her sickness.
Very anxious about her state, she was easily convinced and stopped that therapy suddenly and definitively.

I had the opportunity to see her in March, July and October 1938 and I noticed with great interest the complete arrest in the development of these catacts, which accompanied in very precise fashion the progressive and total disappearance of myopia to the extent that although it was possible to note an appreciable modification in the lens opacities, the visual acuity was spontaneously returned to 7/10 (uncorrected) at the end of October 1938.

We add that Mme. K..., doubly happy, very far from regaining weight in spite of the renunciation of dinitrophenol, had lost another 5 kilos by a very strict nutritional discipline complemented with rigorous gymnastic practices and the introduction into her life of a new intoxification, certainly less dangerous than the preceeding -- tea.

In this case, the role played by the toxin in the opacification of the lens seems to us demonstrated in an almost experimental fashion by the disappearance of the myopia at the moment of the cessation of the intoxification and even more by the incontestable and enduring stabilization of the state of opacities that maintained itself for six months. In contrast, the development was very sudden in a month before the application of this measure. It is presumed that only the precocity of the requested medical consultation and of the medical diagnostic given, has permitted a stop in the development of this toxic cataract -- a completely unusual phenomenon.

We emphasize that the treatment had included plainly excessive doses and that however the opacification only appeared late in the treatment. On this topic remember that in the discussion which followed the expose made to the S.F.O. in 1937 by MM. Onfray and Gilbert Dreyfus-Arruga, who had occasion to observe and operate in America [illegible] ... don't generally appear except at the end of many months and even sometimes six to twelve months after the cessation of treatment. These late-developing cataracts are almost always bilateral.

OBSERVATION II.
[Not included. Summary: A 32 year old woman weighing 90 kg. (198 pounds) began taking dinitrophenol on February 1st, 1937. She began with 9 to 10 pills daily, each being 30 mg. of DNP. After a week she increased the dose to 12 pills / day (360 mg.). At this dosage she lost 800 grams per week, or 10 kg. (22 pounds) in three months, without changing her diet. She stopped taking DNP for four months and then began again. So she took 32.4 grams of DNP in the first 90 days and the same amount in the second course. American reports indicated that cataracts had resulted from doses as small as 100 mg. per day for a total of 40 grams.

On June 10th 1938, after several days in a very sunny seaside resort, the patient began to lose vision in her left eye, and on July 12th, the other eye was affected. By August 1st she was unable to see to drive. By September she was blind.
Fortunately, surgery produced favorable results.]

It is necessary, indeed, to publicize cases in order to attract the attention of physicians and of the French public to the danger of intoxification by dinitrophenol. The fact that we have been able to stabilize, if not make regress one cataract of this class by stopping all toxic ingestion is but another reason which compels us to make it known.

These arguments and our observations are so needed to challenge the imagination and influence young women against harmful weight loss techniques that the work appears discouraging.

Indeed, in ending, we repeat the unlikely remark that our second patient made to us upon taking leave following the success of her first operation: "And now, Doctor, do not oppose my taking of dinitrophenol since I no longer risk having cataracts."
References

· ALLEN and BENSON. -- Late development of cataracts following use of dinitrophenol about a year before. JAMA, 1935, V, 105, p. 795.
· BARKAN, BORLEY, FINE and BETTMAN. -- Operative results in cataracts coincident with dinitrophenol therapy. Cal W. Med. 1936, XXXXIV, p. 360.
· BENCE, JONES. -- On the rate of passage of crystalloids into and out of the vascular and non-vascular textures of the body. Pr. R. Soc., 1863, London, 14, 400.
· BOARDMAN. -- Rapidly developing cataracts after dinitrophenol. JAMA, 1935, CV, p. 108.
· CAMERON, cited by HORNER. -- Arch. of opth. 1936, XVI, p. 452.
· CARLOTTI and RIVOIRE. -- Sur un cas de cataracte per le Dinitrophenyllyside. Rev. O.N.O., Nov. 1938, p. 622-624.
· CAZENEUVE and LEPINE. -- Sur les effets produits par l'ingestion et l'injection intraveineuse de trois colorants jaunes derives de la houille. C.R. Ac. Sc. de Paris, 1885, CI, p. 1, 167.
· CIOTOLA (G.). -- Cataracte par alpha-dinitrophenol. Boll. d'Oc., 16, 1937, p. 531.
· COGAN D. and COGAN F. -- Dinitrophenol cataract. JAMA, 1935, CV, p. 794.
· CUTTING, MEHRTENS, TAINTER. -- Dinitrophenol, not acceptable for N.N.R. JAMA. 1935, CV, p. 31. (Important bibliography on the subject).
· DALLY. -- Du nouveau sur le dinitrophenol. Concours Med. 1935, L, p. 3, 491.
· EBSTEIN and ROSENBLUM. -- Peripheral neuritis and abortion following dinitrophenol therapy. J. Lab. an Clin. Med. 1935, XX, p. 1, 118.
· GIBBS-Reichert. -- Am. Chem. J., 1891, XIII, p. 289.
· GUTZEIT (R.). -- Cure d'obesite et cataracte. Munch. med. Wschr., 2, 1937, p. I.724.
· HALBRON. -- Les cataractes apres emploi therapeutique du dinitrophenol. Sem. des Hopitaux de Paris, XII, 1937, p. 329.
· HORNER, JONES, BOARDMAN. -- Cataracts following the use of dinitro. JAMA, 1935, CV, p. 108.
· HORNER. -- Cataracts after dinitrophenol. Ar. of Opth. 1936, XVI, p. 446-461.
· HORNER (W.-D.). -- Cataracts following dinitrophenol treatment for obesity. Transact. of the opth. sect. of the Amer. Med. Ass., 1936.
· KNISKERN. -- Cataract following dinitrophenol. JAMA, 1935, CV, p. 794.
· KOCH-LEE and TAINTER. -- Dinitrophenol on liver function. Calif. and W. Med., 1935, XXXXIII, p. 337.
· LAIGNEL-LAVASTINE. -- Soc. Med. des Hopit. de Paris, 1937.
· LAZAR. -- Cataract following dinitrophenol. JAMA, 1935, CV, p. 794.
· LEUTSKER. -- Instance of circulatory collapse attributed to dinitrophenol. U.S. Nav. Med. Bull., 1935, XXXIII, p. 394.
· MAC BRYDE-TAUSIG. -- Functional changes in liver, heart and muscles loss of dextrose tolerance resulting from dinitrophenol. JAMA, 1935, CV, p. 13.
· MAGNE, MAYER, PLANTEFOL, et al. -- Etude sur l'action du dinitrophenol. An. de Physiol., 1932, CV, p. 12.
· NADLER. -- Peripheral neuritis caused by prolonged use of dinitrophenol. JAMA, 1935, p. 12.
· ONFRAY and GILBERT DREYFUS. -- Bull. et Memoires S.F.O., 1937, (I, pp. 114-12.
· ONETO-GALINO-NATALE. -- Developpement de cataracte aux deux yeux, consequence d'un traitment au dinitrophenol pour amaigrissement. Soc. Argentin. of., 24 Oct. 1937.
· PERKINS. -- A study of munitions intoxication in France. Pub. Health Rep., 1919, XXXIV, p. 2, 335.
· RODIN. -- Cataracts following the use of dinitrophenol. Calif. West Med. 44.4, 1936, p. 3.
· SCHUTES. -- Dinitrophenol. Am. J. Opth., 1935, 18, p. 752.
· SPAETH (E.-B.). -- Cataractes dues au dinitrophenol avec symptomes de tetanie. Am. J. Opth., Apr. 1936, p. 320-323.
· STEIN and CREVECOEUR. -- Semaine des Hopitaux de Paris, 15 Dec. 1937.
· TAINTER, CUTTING and STOCKTON. -- Use of dinitrophenol in nutritional disorders. Am. J. Pub. Health., 1934, XXIV, p. 1045.
· VAN DER HOEVE and POLAK-DANIELS. -- Cataracte et dinitrophenol. Nederl. Tijdsch. V. Genessk., I, 1936, no. 2, p. 126.
· VOGT (A.). -- La Cataracte par dinitrophenol en Suisse. Schweiz. Med. Wocst., 76-37, 11 Sep. 1937, p. 873.
· WHALMAN. -- Dinitrophenol cataract. Am. J. O., Oct. 1936, XIX, p. 885

 

[big_byrd52]

very interesting. finally some scientific studies to back the dnp and insulin cycle from way back.

 

[Juice Freak]

I'm not familiar with this insulin/DNP theory, how would you use these two together and would you not lose less fat by combining insulin into the mix?