DNP and insulin at the same time? whaaa?

[lookingforanedge]

Would love a copy of that book too...anyone know where to grab a copy?

 

[bruiser]

So basically everyone is saying you gotta be on aas or something to keep looking muscular while on dnp.

but the aas/slin you're using, isn't it going to waste. People say you don't gain muscle while on dnp.

 

[TNH]

So basically everyone is saying you gotta be on aas or something to keep looking muscular while on dnp.

but the aas/slin you're using, isn't it going to waste. People say you don't gain muscle while on dnp.

You won't gain muscle. The AAS is to hold onto muscle (even though DNP is protein sparing, I do it just to be safe). The slin is there to keep yourself somewhat full (the DNP flattens you out big time).

 

[bruiser]

You won't gain muscle. The AAS is to hold onto muscle (even though DNP is protein sparing, I do it just to be safe). The slin is there to keep yourself somewhat full (the DNP flattens you out big time).

Okay, so what cycle would you suggest with dnp?(enough to hold onto muscle) And im sorry but there is no point in running slin unless you're looking to gain serious muscle. "keeping yourself somewhat full" isn't worth the risk of taking slin.

I was under the impression that with slin you're more likely to gain muscle and no fat while taking dnp.

 

[TNH]

Okay, so what cycle would you suggest with dnp?(enough to hold onto muscle) And im sorry but there is no point in running slin unless you're looking to gain serious muscle. "keeping yourself somewhat full" isn't worth the risk of taking slin.

I was under the impression that with slin you're more likely to gain muscle and no fat while taking dnp.

It depends on the individual. A lean 270lb guy is going to need more than me. I personally just take about 25mg of tren per day, sometimes with 150mg of test per week.

As far as using slin, I guess that varies from person to person too.
I am comfortable using it whenever, just like aspirin... only dangerous if you take too much.

 

[Myck]

From 'Building The Perfect Beast' (Arthur Rea)

For a moment imagine the freaky potential insulin would possess for lean tissue growth if it did not inhibit fat loss while remaining anabolic to muscle tissue? Yup, a poor mans IGF-1 would be the result!

DNP (2,4 DINITROPHENOL)

This was truly reported as being chemical exercise. Normally the mitochondria
process that converts ADP (adenosine diphosphate) into ATP (adenosine triphosphate) is about 60% efficient, which means there is a great deal of energy wasted. Those who have read the creatine section ahead of this are well aware of our good friend ATP.

When we exercise, this process accelerates and raises our metabolic rate. (More calories are burned as a result) The process is called oxidative phosphorylation. Since ATP is the high-energy chemical our bodies utilize for intense training, anything that compromises this process will make cellular mitochondria work harder and expend more energy as heat. (Body temperature rises).

DNP is an oxidative phosphorylation uncoupler. It makes the process only about 40% efficient by uncoupling a high-energy phosphate molecule from ATP and therefore turning ATP into ADP. To maintain an adequate supply of ATP, the body must step-up production. For this reason metabolism is significantly increased and an incredible amount of calories are burned. During this accelerated metabolic state, and due to the need for ATP production, most of the calories come from fatty acids (adipose/fat tissue). So little or no muscle is lost (With adequate protein intake).

Users experienced elevated body temperatures and perspiration even while
sitting around. Simply stated, metabolic rates elevate 100-200% in only a few hours.

Sounds great, but DNP can be deadly. It has even been used as a component of bug spray. Since increased energy is dissipated as body heat, too high of a dosage of DNP for to long of a period can actually COOK ORGANS! No joke, I mean medium well done. I cannot stress enough how dangerous the use of this chemical can be.

The body usually possesses receptors or pathways to shut down as a means of survival from the potential life threatening dangers and damage of most chemicals. In the case of DNP there are none.

The issue of body temperature is of interest here and is a relevant point to
discuss further. Clenbuterol and ephedrine are fairly easy to chart for effective results by checking body temperature. However, DNP is much different in this sense. When an athlete (or anyone) used DNP, increased respiration, heart rate, and skin dilation occurred. Thus heat is quickly dissipated. This means that a person using DNP could feel warm but a thermometer can fail to show an increase in body temperature. According to available literature, in most cases a body temperature of near 100 degrees indicates a metabolic rate of about twice normal. It also means that the individual is in the very near the danger zone. This is wholly unnecessary, and it is the low cellular ATP level induced by high dosage DNP use that was most dangerous.

The temperature or heat issue is secondary by comparison. Most reported
users of DNP ingested a daily dosage of 6-8 mg per kilogram of body weight.
Realistically speaking, I can say from personal experience that this is not only an uncomfortable experience, but dangerous and unnecessary as well. My experience has been that 3-5mg/kg daily provided better results and did so even without a calorie decrease. Personally I felt a body temperature of 99.5-99.7 degrees was preferable also.

Before going on, I would like to say a few related points. Now we know that the mitochondrial process of converting ADP into ATP is called oxidative phosphorylation and that the process is normally 60% efficient. We know DNP is an oxidative phosphorylation uncoupler that will reduce the process efficiency to 40% and that this burns fat while raising metabolic rates 100-200% while increasing body temperature.

(We also know misuse can cook our guts!).

*So now we have insulin and its "anabolic to muscle and fat" alike qualities and DNP that increases calorie expenditure primarily from fat stores. It would seem that we have applied Action/Reaction Factors correctly to create an increase in lean tissue mass at the expense of adipose tissue stores. But here is where it gets really interesting...

Warning: More Science Geek Stuff Interesting

Studies Sometimes Validate What We Have learned

*Rapid stimulation of glucose transport by mitochondria! uncoupling depends in part on cytosolic Ca2+ and cPKC Z A Khayat, T Tsakiridis, A Ueyama, R Somwar, A Kiip AMERICAN JOURNAL OF PHYSIOLOGY, 275(6 Pt 1):C1487~C1497 1998


2,4-Dinitrophenoi (DNP) uncouples the mitochondria! oxidative chain from ATP
production, preventing oxidative metabolism, The consequent increase in energy demand is, however, contested by cells increasing glucose uptake to produce ATP via glycolysis. In skeletal muscle cells, DNP rapidly doubles glucose transport, reminiscent of the effect of insulin. However, glucose transport stimulation by DNP does not require insulin receptor substrate-1 phosphorylation and is wortmanniti insensitive.

Overnight treatment with 4-phorbol 12-myristate 13-acetate down-regulated
cPKC isoforms alpha, beta, and gamma and partially inhibited (45.0 +/- 3.6%) DNPbut not insulin-stimulated glucose uptake. Consistent with this, the PKC inhibitor bisindolyimaleimide I blocked PKC enzyme activity at the plasma membrane (100%) and inhibited DNP-stimulated 2-[3H]deoxyglucose uptake (61.2 +/- 2.4%) with no effect on the stimulation of glucose transport by insulin. Finally, the selective PKCbeta inhibitor LY-379196 partially inhibited DNP effects on glucose uptake (66.7 +/-1.6%). The results suggest interfering with mitochondria! ATP production acts on a signal transduction pathway independent from that of insulin and partly mediated by Ca2+ and cPKCs, of which PKC-beta likely plays a significant role.

So now we know that insulin is not the only mediator of glucose transport into muscle cells. We also have validated the increase in potential muscle glycogen synthesis during the employment of DNP is about twice that of insulin. Hmmm, not getting it yet? Be patient. You will in a minute.

*Effects of cellular ATP depletion on glucose transport and insulin signaling in 3T3-L1 adipocytes
E Heart, J Kang, C K Sung
American Journal of Physiology - Endocrinology and Metabolism , 280(3):E428-E435 2001

Glucosamine induced insulin resistance in 3T3-L1 adipocytes (fat cells), which
was associated with a 15% decrease in cellular ATP content. To study the role of ATP depletion in insulin resistance, researchers employed sodium azide (NaN3) and dinitropheno! (DNP), which affect mitochondrial oxidative phosphorylation, to achieve a similar 15% ATP depletion.

Unlike glucosamine, NaN3 and DNP markedly increased basal glucose
transport, and the increased basal glucose transport was associated with increased GLUT-1 content in the plasma membrane without changes in total GLUT-1 content.

These agents, like glucosamine, did not affect the early insulin signaling that is implicated in insulin stimulation of glucose transport. In cells with a severe 40% ATP depletion, basal glucose transport was similarly elevated, and insulin-stimulated glucose transport was similar in cells with 15% ATP depletion.

In these cells, however, early insulin signaling was severely diminished. These
data suggest that cellular ATP depletion by glucosamine, NaN3, and DNP exerts differential effects on basal and insulin-stimulated glucose transport and that ATP depletion per se does not induce insulin resistance in 3T3-L1 adipocytes.

DNP aids in inducing an environment of insulin resistance in adipose sites thus
decreasing the ability for fat cells to get food. So DNP increases calorie expenditure as heat, increases glucose transport into muscle cells but decreases fat cell gluttony. Gee, do you think the combination of the super anabolic insulin and DNP just may be very pro-muscle growth and fat loss?

Closing Thoughts and Other insanity

When athletes have employed the DNP/lnsulin Protocol in the past there has
been a noted dramatic increase in lean tissue mass and a lack of hypoglycemia in almost all cases. This in itself was an exciting issue to research as one of the many negative side effects possible from non-medically supervised administration of insulin in hypoglycemia and coma...and death. (All of which suck)

There are two possible explanations for this:

1. The insulin molecule is experiencing N-terminal truncation when coming into
contact with circulatory DNP. When the N-terminal is removed from IGF-1 the
resulting growth factor is called Des (1-3) IGF-1. The result is an anabolic far
more powerful than even IGF-1 itself. This is true of IGF-2 and other growth
factors including insulin. The possibility strongly suggests that the truncated
insulin molecule would more readily fit into and activate the muscle cell IGF-1
receptors as well.

2. The insulin and IGF-1 receptors themselves are truncated by the presence of DNP. In this case the truncation is effecting the COOH-Terminal response thus altering the hypoglycemic and anabolic effects of insulin positively toward that of IGF-1 in both function and action.

*There are several approaches that have been employed for Insulin and DNP but one of the more effective examples follows. Please do not try this at home. (Even with proper medical supervision and a professional exterminator.)

WARNING!
This is intended as a discussion example only and not meant as a guide for use. DNP and insulin can both be very dangerous chemicals. Insulin use must be medically supervised and DNP has not been a legal supplement since the 20's.

Insulin & Bug Spray Example Protocol

DAY DRUGS

1. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
2.
3. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
4.
5. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
6.
7. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
8.
9. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
10.
11. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
12.
13. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
14.
15. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
16.
17. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
18.
19. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
20.
21. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
22.
23. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
24.
25. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
26.
27. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
28.

• Optional layer: Avandia 2mg 2xd increases muscle cell insulin receptor sensitivity and facilitates an improved IGF-1 profile.

 

[bruiser]

From 'Building The Perfect Beast' (Arthur Rea)

For a moment imagine the freaky potential insulin would possess for lean tissue growth if it did not inhibit fat loss while remaining anabolic to muscle tissue? Yup, a poor mans IGF-1 would be the result!

DNP (2,4 DINITROPHENOL)

This was truly reported as being chemical exercise. Normally the mitochondria
process that converts ADP (adenosine diphosphate) into ATP (adenosine triphosphate) is about 60% efficient, which means there is a great deal of energy wasted. Those who have read the creatine section ahead of this are well aware of our good friend ATP.

When we exercise, this process accelerates and raises our metabolic rate. (More calories are burned as a result) The process is called oxidative phosphorylation. Since ATP is the high-energy chemical our bodies utilize for intense training, anything that compromises this process will make cellular mitochondria work harder and expend more energy as heat. (Body temperature rises).

DNP is an oxidative phosphorylation uncoupler. It makes the process only about 40% efficient by uncoupling a high-energy phosphate molecule from ATP and therefore turning ATP into ADP. To maintain an adequate supply of ATP, the body must step-up production. For this reason metabolism is significantly increased and an incredible amount of calories are burned. During this accelerated metabolic state, and due to the need for ATP production, most of the calories come from fatty acids (adipose/fat tissue). So little or no muscle is lost (With adequate protein intake).

Users experienced elevated body temperatures and perspiration even while
sitting around. Simply stated, metabolic rates elevate 100-200% in only a few hours.

Sounds great, but DNP can be deadly. It has even been used as a component of bug spray. Since increased energy is dissipated as body heat, too high of a dosage of DNP for to long of a period can actually COOK ORGANS! No joke, I mean medium well done. I cannot stress enough how dangerous the use of this chemical can be.

The body usually possesses receptors or pathways to shut down as a means of survival from the potential life threatening dangers and damage of most chemicals. In the case of DNP there are none.

The issue of body temperature is of interest here and is a relevant point to
discuss further. Clenbuterol and ephedrine are fairly easy to chart for effective results by checking body temperature. However, DNP is much different in this sense. When an athlete (or anyone) used DNP, increased respiration, heart rate, and skin dilation occurred. Thus heat is quickly dissipated. This means that a person using DNP could feel warm but a thermometer can fail to show an increase in body temperature. According to available literature, in most cases a body temperature of near 100 degrees indicates a metabolic rate of about twice normal. It also means that the individual is in the very near the danger zone. This is wholly unnecessary, and it is the low cellular ATP level induced by high dosage DNP use that was most dangerous.

The temperature or heat issue is secondary by comparison. Most reported
users of DNP ingested a daily dosage of 6-8 mg per kilogram of body weight.
Realistically speaking, I can say from personal experience that this is not only an uncomfortable experience, but dangerous and unnecessary as well. My experience has been that 3-5mg/kg daily provided better results and did so even without a calorie decrease. Personally I felt a body temperature of 99.5-99.7 degrees was preferable also.

Before going on, I would like to say a few related points. Now we know that the mitochondrial process of converting ADP into ATP is called oxidative phosphorylation and that the process is normally 60% efficient. We know DNP is an oxidative phosphorylation uncoupler that will reduce the process efficiency to 40% and that this burns fat while raising metabolic rates 100-200% while increasing body temperature.

(We also know misuse can cook our guts!).

*So now we have insulin and its "anabolic to muscle and fat" alike qualities and DNP that increases calorie expenditure primarily from fat stores. It would seem that we have applied Action/Reaction Factors correctly to create an increase in lean tissue mass at the expense of adipose tissue stores. But here is where it gets really interesting...

Warning: More Science Geek Stuff Interesting

Studies Sometimes Validate What We Have learned

*Rapid stimulation of glucose transport by mitochondria! uncoupling depends in part on cytosolic Ca2+ and cPKC Z A Khayat, T Tsakiridis, A Ueyama, R Somwar, A Kiip AMERICAN JOURNAL OF PHYSIOLOGY, 275(6 Pt 1):C1487~C1497 1998


2,4-Dinitrophenoi (DNP) uncouples the mitochondria! oxidative chain from ATP
production, preventing oxidative metabolism, The consequent increase in energy demand is, however, contested by cells increasing glucose uptake to produce ATP via glycolysis. In skeletal muscle cells, DNP rapidly doubles glucose transport, reminiscent of the effect of insulin. However, glucose transport stimulation by DNP does not require insulin receptor substrate-1 phosphorylation and is wortmanniti insensitive.

Overnight treatment with 4-phorbol 12-myristate 13-acetate down-regulated
cPKC isoforms alpha, beta, and gamma and partially inhibited (45.0 +/- 3.6%) DNPbut not insulin-stimulated glucose uptake. Consistent with this, the PKC inhibitor bisindolyimaleimide I blocked PKC enzyme activity at the plasma membrane (100%) and inhibited DNP-stimulated 2-[3H]deoxyglucose uptake (61.2 +/- 2.4%) with no effect on the stimulation of glucose transport by insulin. Finally, the selective PKCbeta inhibitor LY-379196 partially inhibited DNP effects on glucose uptake (66.7 +/-1.6%). The results suggest interfering with mitochondria! ATP production acts on a signal transduction pathway independent from that of insulin and partly mediated by Ca2+ and cPKCs, of which PKC-beta likely plays a significant role.

So now we know that insulin is not the only mediator of glucose transport into muscle cells. We also have validated the increase in potential muscle glycogen synthesis during the employment of DNP is about twice that of insulin. Hmmm, not getting it yet? Be patient. You will in a minute.

*Effects of cellular ATP depletion on glucose transport and insulin signaling in 3T3-L1 adipocytes
E Heart, J Kang, C K Sung
American Journal of Physiology - Endocrinology and Metabolism , 280(3):E428-E435 2001

Glucosamine induced insulin resistance in 3T3-L1 adipocytes (fat cells), which
was associated with a 15% decrease in cellular ATP content. To study the role of ATP depletion in insulin resistance, researchers employed sodium azide (NaN3) and dinitropheno! (DNP), which affect mitochondrial oxidative phosphorylation, to achieve a similar 15% ATP depletion.

Unlike glucosamine, NaN3 and DNP markedly increased basal glucose
transport, and the increased basal glucose transport was associated with increased GLUT-1 content in the plasma membrane without changes in total GLUT-1 content.

These agents, like glucosamine, did not affect the early insulin signaling that is implicated in insulin stimulation of glucose transport. In cells with a severe 40% ATP depletion, basal glucose transport was similarly elevated, and insulin-stimulated glucose transport was similar in cells with 15% ATP depletion.

In these cells, however, early insulin signaling was severely diminished. These
data suggest that cellular ATP depletion by glucosamine, NaN3, and DNP exerts differential effects on basal and insulin-stimulated glucose transport and that ATP depletion per se does not induce insulin resistance in 3T3-L1 adipocytes.

DNP aids in inducing an environment of insulin resistance in adipose sites thus
decreasing the ability for fat cells to get food. So DNP increases calorie expenditure as heat, increases glucose transport into muscle cells but decreases fat cell gluttony. Gee, do you think the combination of the super anabolic insulin and DNP just may be very pro-muscle growth and fat loss?

Closing Thoughts and Other insanity

When athletes have employed the DNP/lnsulin Protocol in the past there has
been a noted dramatic increase in lean tissue mass and a lack of hypoglycemia in almost all cases. This in itself was an exciting issue to research as one of the many negative side effects possible from non-medically supervised administration of insulin in hypoglycemia and coma...and death. (All of which suck)

There are two possible explanations for this:

1. The insulin molecule is experiencing N-terminal truncation when coming into
contact with circulatory DNP. When the N-terminal is removed from IGF-1 the
resulting growth factor is called Des (1-3) IGF-1. The result is an anabolic far
more powerful than even IGF-1 itself. This is true of IGF-2 and other growth
factors including insulin. The possibility strongly suggests that the truncated
insulin molecule would more readily fit into and activate the muscle cell IGF-1
receptors as well.

2. The insulin and IGF-1 receptors themselves are truncated by the presence of DNP. In this case the truncation is effecting the COOH-Terminal response thus altering the hypoglycemic and anabolic effects of insulin positively toward that of IGF-1 in both function and action.

*There are several approaches that have been employed for Insulin and DNP but one of the more effective examples follows. Please do not try this at home. (Even with proper medical supervision and a professional exterminator.)

WARNING!
This is intended as a discussion example only and not meant as a guide for use. DNP and insulin can both be very dangerous chemicals. Insulin use must be medically supervised and DNP has not been a legal supplement since the 20's.

Insulin & Bug Spray Example Protocol

DAY DRUGS

1. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
2.
3. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
4.
5. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
6.
7. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
8.
9. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
10.
11. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
12.
13. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
14.
15. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
16.
17. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
18.
19. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
20.
21. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
22.
23. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
24.
25. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
26.
27. Humulin-R 8-10 iu 3xd/DNP 4-5mg/kg Daily
28.

• Optional layer: Avandia 2mg 2xd increases muscle cell insulin receptor sensitivity and facilitates an improved IGF-1 profile.

wow, damn.....
So um... this means Ill still gain muscle and no fat right? lol sorry ....