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Slin with dnp

Thebigone

New member
Kilo Klub Member
Joined
Oct 28, 2009
Messages
3,621
I read the article here about it but was a bit confused. I also read an article Author L. Rea wrote about it with dnp and adding muscle and it just sounded crazy. He recommened way too much slin,etc.. If your doing a mild dnp run. Like 250mg/day for 2weeks is it benefital at all to add some slin? I only have log. Im thinking maybe 5iu pwo 4x per week. It seems as if it would help keep you fuller and not be so flat on it but i cant see how it would help aid in fatloss. Muscle preservation yes but not fatloss. Those who have used slin with dnp how did it turn out and what slin dose did you do. Get more hypo feeling than normal?
 

The Scientist

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Registered
Joined
Nov 13, 2008
Messages
117
My results

Hi TheBigOne...

I tried the dnp/insulin cycle for 20 days like Alri outlined it...as part of a Absolute Anabolic phase.

My results was around 10 pounds but l know l could have gain more if my diet was better planned with no fats.

It was not that unconvertible due to the reason that it cancelled each others nasty side effects out half way trough the endocrine system...

This all is just a way to duplicate a form of IGF 1, next time l will rather buy IGF 1...
 

Thebigone

New member
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Joined
Oct 28, 2009
Messages
3,621
Im not looking to gain any muscle. Maybe shed a bodyfat % or 2. I was thinking maybe 5iu log in the a.m. and pwo 4x per week and thats it. Just enough to stay full(hopefully) on the low dose dnp cycle and stay anabolic. Can you go hypo easier on DNP with slin?
 

majsi98

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Registered
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Jul 30, 2006
Messages
188
Come on ... do you really feel you should take DNP to go down 2 percentages on the bodyfat scale? Now I don't want to play the smart ass guy but I think you can achieve that through cardio + diet only..
 

muscledoc1

Active member
Kilo Klub Member
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Jul 10, 2007
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Interesting....can some one please post the ALRI dnp/insulin article?
 

Thebigone

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Come on ... do you really feel you should take DNP to go down 2 percentages on the bodyfat scale? Now I don't want to play the smart ass guy but I think you can achieve that through cardio + diet only..
I dont know. to me thats just like saying "do you really feel you should take test to add 5lbs of "solid"muscle. Meaning,... "solid muscle" and "pure fat" are both underrated as many think its easily accomplishable when its mainly water most of the time.
 

Thebigone

New member
Kilo Klub Member
Joined
Oct 28, 2009
Messages
3,621
Interesting....can some one please post the ALRI dnp/insulin article?
Truncated Insulin and Bug Spray = The Poor Mans IGF-1 ?
In the world of the Chemically enhanced athlete exists the really strange truth
that someone somewhere has tried it, whatever "it" may be. AAS (anabolic/androgenic
steroids)? Yup. Growth Factors? Duh! Bug spray? Oddly enough, yes...and insulin to
complete the stack. Why?
Picture an average athlete gaining 20 LBS of lean tissue mass while losing half
that amount in adipose tissue without the use of any AAS. Hmmm? Big deal? Have you
seen what 20 lbs of lean meat looks like in the grocery store? Now cut away 1 0 lbs of
fat and rethink that big deal idea.
Thankfully many athletes have realized that maximum progress occurs due to
working with instead of against the body's physiological Action/Reaction Factors.
This means a planned protocol that correctly anticipates and responds to the body's
negative reactions to chemically induced positive actions. Anything else simply
becomes a matter of attempting to maintain a degree of the positive gains achieved
through progressive dosages while negative side-effects mount to a chronic level yet
unknown. Ponder that as you read on.


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.
145
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.)
146
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.
 

mexbeast

Active member
Kilo Klub Member
Joined
Feb 22, 2009
Messages
1,017
i have always wonder if there's any truth to alri's theories? this one is very very interesting!!!
 

greenpatch

New member
Registered
Joined
Jul 15, 2010
Messages
196
insulin =fat plus more

Truncated Insulin and Bug Spray = The Poor Mans IGF-1 ?
In the world of the Chemically enhanced athlete exists the really strange truth
that someone somewhere has tried it, whatever "it" may be. AAS (anabolic/androgenic
steroids)? Yup. Growth Factors? Duh! Bug spray? Oddly enough, yes...and insulin to
complete the stack. Why?
Picture an average athlete gaining 20 LBS of lean tissue mass while losing half
that amount in adipose tissue without the use of any AAS. Hmmm? Big deal? Have you
seen what 20 lbs of lean meat looks like in the grocery store? Now cut away 1 0 lbs of
fat and rethink that big deal idea.
Thankfully many athletes have realized that maximum progress occurs due to
working with instead of against the body's physiological Action/Reaction Factors.
This means a planned protocol that correctly anticipates and responds to the body's
negative reactions to chemically induced positive actions. Anything else simply
becomes a matter of attempting to maintain a degree of the positive gains achieved
through progressive dosages while negative side-effects mount to a chronic level yet
unknown. Ponder that as you read on.


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.
145
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.)
146
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.
ok th dude tht got me into this game was a aas user for over 20 year alway talking listen to me i know what i,m doing,very helpful in all area.in short he died last year from humulin,and even he w ldnt touch DNR so if he died from this but refuses to use DNR .people plz read inbetween th line be good and b safe.
 

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