Please Scroll Down to See Forums Below endojuicedr
Banned
First of all it's catabolic so you have to use it on aas or you will lose a good amount of muscle. Secondly, I believe it's more dangerous than dee-en-pee(which is not catabolic), messing with your thyroid is no joke.
who has used cytomel and recovered no problem?
- Thread starter aaron10121
- Start date
aaron10121
New member
8 wks out from comp... have decided not to take the plunge. will keep the t3 and pass along. i am just too nervous and i really think my diet and cardio will get me to where i need to be. too concerned with my health later on to take chance.
downunder hunter
New member
looks like we got a runnin battle in two threads.
Again, you didnt answer my question! Are you talking from experience or just talking out of your ass and regurgitating shit that you read on the net?
You are right though it can be dangerous if not used correctly, To say its worse that DNP but is ridicolous
Last edited:
endojuicedr
Banned
Time for school:
Quote:
Harper JA, Dickinson K and Brand MD (2001) Mitochondrial uncoupling as a target for drug development for the treatment of obesity. Obesity Rev, 2, 255–265
In contrast to the use of thyroid extract (also in common use at the time to treat obesity), DNP did not promote urinary nitrogen excretion, so the assumption was made that weight loss could be attributed to a specific loss of fat (47).
Quote:
Bell, Jacques. 1939. Etude biologique des produits dinitres chez l'homme. Medecine. 19:749-54.
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.
...
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.
Quote:
Simkins S 1937 Dinitrophenol and desiccated thyroid in the treatment of obesity. JAMA 108:2110–2119.
The extra energy of metabolism is derived mainly from fat and practically not at all from protein or carbohydrate. Consequently, dinitrophenol in therapeutic dosage produces no breakdown of significant amounts of body protein, even with patients on an inadequate protein intake. This is in marked contrast with the very consdierable increase in nitrogen excretion observed in patients undergoing treatment with thyroid. The fat is used completely and satisfactorily broken down, as no ketone bodies are found in urine. There is a no hyperlipidemia or constant change in the fixed and fatty acids of the blood.
Quote:
Cutting WC, Tainter ML. Metabolic actions of dinitrophenol with the use of balanced and unbalanced diets. J Am Med Assoc 1933; 101: 2099–2102.
Dinitrophenol, used in doses of therapeutic range, caused increases in metabolism of the usual magnitude irrespective of the type of diet. The nitrogen excretion was never greater than the intake, even when the subjects lost as much as 5 pounds in body weight during one week. From this it seemed probable that there was no actual tissue breakdown during these short periods of heightened metabolism, but that the loss of weight was due to the utilization of stored carbohydrate or fat. This does not mean, of course, that tissue breakdown would not occur if the drug should be given over longer periods, but probably when materials other than protein are available these are utilized first. Thus the assumption might be made that, as long as the protein intake is adequate, any reduction in body weight is not primarily at the expense of the tissue proteins.
...
3.The subjects excreted less nitrogen than they ingested, yet there were definite losses of body weight. Therefore, body proteins probably were not broken down. The output of urinary organic acid was not increased, thus indicating that the fats were completely burned without giving rise to acidosis.
This should make it very clear that T3 is much more catabolic, as far as arguing sides and dangers almost all of the problems with DNP have come from misdosage combined with misuse. It is very rare to find a UGL that doses their DNP correctly. I won't speak anymore about this subject since it is not allowed here, I'm not trying to promote one over the other but I do like to point things out when people are parroting incorrect information.
Quote:
Harper JA, Dickinson K and Brand MD (2001) Mitochondrial uncoupling as a target for drug development for the treatment of obesity. Obesity Rev, 2, 255–265
In contrast to the use of thyroid extract (also in common use at the time to treat obesity), DNP did not promote urinary nitrogen excretion, so the assumption was made that weight loss could be attributed to a specific loss of fat (47).
Quote:
Bell, Jacques. 1939. Etude biologique des produits dinitres chez l'homme. Medecine. 19:749-54.
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.
...
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.
Quote:
Simkins S 1937 Dinitrophenol and desiccated thyroid in the treatment of obesity. JAMA 108:2110–2119.
The extra energy of metabolism is derived mainly from fat and practically not at all from protein or carbohydrate. Consequently, dinitrophenol in therapeutic dosage produces no breakdown of significant amounts of body protein, even with patients on an inadequate protein intake. This is in marked contrast with the very consdierable increase in nitrogen excretion observed in patients undergoing treatment with thyroid. The fat is used completely and satisfactorily broken down, as no ketone bodies are found in urine. There is a no hyperlipidemia or constant change in the fixed and fatty acids of the blood.
Quote:
Cutting WC, Tainter ML. Metabolic actions of dinitrophenol with the use of balanced and unbalanced diets. J Am Med Assoc 1933; 101: 2099–2102.
Dinitrophenol, used in doses of therapeutic range, caused increases in metabolism of the usual magnitude irrespective of the type of diet. The nitrogen excretion was never greater than the intake, even when the subjects lost as much as 5 pounds in body weight during one week. From this it seemed probable that there was no actual tissue breakdown during these short periods of heightened metabolism, but that the loss of weight was due to the utilization of stored carbohydrate or fat. This does not mean, of course, that tissue breakdown would not occur if the drug should be given over longer periods, but probably when materials other than protein are available these are utilized first. Thus the assumption might be made that, as long as the protein intake is adequate, any reduction in body weight is not primarily at the expense of the tissue proteins.
...
3.The subjects excreted less nitrogen than they ingested, yet there were definite losses of body weight. Therefore, body proteins probably were not broken down. The output of urinary organic acid was not increased, thus indicating that the fats were completely burned without giving rise to acidosis.
This should make it very clear that T3 is much more catabolic, as far as arguing sides and dangers almost all of the problems with DNP have come from misdosage combined with misuse. It is very rare to find a UGL that doses their DNP correctly. I won't speak anymore about this subject since it is not allowed here, I'm not trying to promote one over the other but I do like to point things out when people are parroting incorrect information.
