For anybody considering or doing DNP....The Facts from Macro and Animal

[curgeo]

This is a post from anabolicfitness.net's Hall of Fame. It seems a lot of people when it starts to get warmer want to get into shape and try DNP to do it. I really don't like the shit as I hated the way it made me feel, but this is about the best info I have ever seen on it. Please read this if you are even THINKING of doing DNP. Again, I don't like the shit and would never do it again.



Animals original post:

Why you might want to use DNP.

Add some DNP to an animals diet. DNP can get metabolism up at least 50% which is conservative as some say
75% This would mean if the animal eats 3000 calories maintenance they are now at 1500 calories a day with no
change in diet! A 2500 calorie a day would leave them with 1250 calories a day. There are 4086 calories in 1lb of
fat and at 3000 calories a day your DNP adjusted calories for the day is 1500. Multiply that x 7 days to give you
10500 calorie deficit which is 2.5 lbs of fat loss for the week. At the 2500 calorie you have a 2.14 lb fat loss. These
are both below what the BO diets claim and you don't have to stop eating!

If your animals weigh around 200lbs their effective dose is 400mg and the max can be as high as 800mg a day.
High fat diets market on the basis that you are going to be able to lose 1.5-2lbs of fat by just changing your diet!

1 gram of fat is 9 calories. There are 454 grams in a 1 pound. This gives you 4086 calories for 1lb of fat. If you
want to lose that 1lb of fat you have to have a 4086 calorie deficit to do it. In other words, you need -4086 calories
in your diet if you want to lose 1 lb of fat. Now, Let's say you are at 3000 cal a day for maintenance. That is 21000
calories a week. You believe the marketing of the post above and think you can lose 1.5lbs of fat. That, my friends,
is 6129 calories which you have to subtract from 21000 which leaves you with 14871 calories for the week or 2124
calories a day. You are going from 3000 to 2124 a day. If you want to lose that great sounding 2 pounds you are
now at 12828 for the week or 1832 calories a day.

Let's be realistic and put you at 2500 maintenance calories. To lose 1.5lb you now need 11371 calories a week or
1624 calories a day or a nearly 900 calorie a day change. To lose the magical 2lb a week you need 9328 calories for
the week or 1333 calories a day or a 1167 calorie change per day! That is rather difficult, but let's add some DNP
which can get you metabolism up at least 50% which would mean you are now at only 1500 calories a day for a
3000 calorie diet with no change in diet! A 2500 calorie a day would leave you with 1250 calories a day.
These are both below what the BO diets claim and you don't have to stop eating!


What you want to keep in mind

Everyone is different.

Don't take it on an empty stomach or it will feel like you have indigestion for most of the day.

I wanted to stress not to just go balls out (5mg/kg) and you should move up gradually on DNP for your first
experience.

If you have an allergic reaction with red spots and itching then stop the DNP and get some Benadryl and then you
should be able to start again.

The type of diet will also affect how you feel, as well as the type of workouts you are doing. These are variables
you also will have to figure out for yourself. The logic of my dieting regimen follows that while you are DNP all
the glycogen/glucose is being scavenged to provide ATP for the mitochondria so you will want to eat a regular diet.
High fat BO is not going to help you build muscle even though DNP is anti-proteolytic (protein sparing)..
Furthermore, when you eat fat it is more likely to go to fat! That is scientifically proven. So if I'm trying to burn
fat, why would I want to eat it right back?

DNP is anti-proteolytic which means it uses carbohydrates or fats exclusively to supply energy for the mitochondria
and does not facilitate muscle breakdown, however, this does not therefore mean DNP is positive for muscle
building. The cells are running on overdrive and they are not going to be looking to make themselves bigger which
requires even more energy.

Everyone is different and other supplements you take will affect your results, but as a whole, most people are not
going to do well or feel well on high fat and DNP. I also have found that taking particular supplements helps with
how will you feel while on the DNP.

I feel better when I don't do huge carbs, however, when I don't do any as in high fat type diets, my workouts suffer
just the same. Each individual has to decide for themselves and put those factors into perspective with what their
goals are and how fast they want to accomplish them and how bad they are willing to feel for the desired weight
loss.

WARNING: DNP will turn everything and anything yellow including skin, clothes, carpet, and hair. I dropped a
capsule in my DNP container and bent over to look for it and my hair touched the edge of the container and my hair
got dyed yellow! My hair did not even touch the DNP, but just the side of the container for about 2 seconds! DNP
for the most part is not removable or bleachable with normal chemicals. It will also track. By that I mean, you think
you have washed it off your hands and you touch something and later you see yellow spots on what you touched. If
you are making caps you need 2 pairs of gloves, at least, as the DNP goes through the first pair due to an atrraction
it has for moisture. DNP sublimes and floats. Due to this sublimation it will land on EVERYTHING if you leave it
out even if there is no air circulation. DNP goes through EVERYTHING including plastic, hdpe plastic, pet plastic,
plastic bags, nitrile and latex gloves. It can be washed out of clothing with hot water and detergents that have
phenolic compounds in them such as Tide. DNP is not solvated by laquer thinner, acetone, paint thinner, or
turpentine or any of the common organic solvents. If you wash your hands immediately after touching DNP with
gamma-butyrolactone, otherwise know as GBL and use to make GHB, and then a detergent such as Dawn
dishwashing soap, the stain will come out for the most part.

I have to say that a certain guru which some people keep quoting is what I feel to be a very unreliable source. I will
give him credit for bringing DNP to the forefront, but I will bet you a million bucks that he has never done it or
mixed it. Here is a quote that bears this out; 'I don't see what the worry is about everything turning yellow? I have no
problems, I just dry it out and cut it with a credit card and cap it.'

That is total BULLSHIT!. Anyone who has used or mixed DNP powder knows that it will get on
EVERYTHING and turn it yellow. It goes through plastic bags. Just today I was sending someone 3g for research
and I put it into a ziploc and 2 hours later I came back and the envelope under the bag was YELLOW! It goes
through 1 laver of rubber gloves. It turns white HDPE bottles yellow. It floats everywhere. I had to put my stuff in a
hood because it got on everything I had sitting out and I had to wash all my glassware and scales before I could use
them again. DNP floats by sublimation which would be known just be reading the safety sheet or the Merck Index..
On the basis of that statement alone I have some real problems believing anything he says on the subject, but
another famouns quote is, 'DNP will raise your body temp high enough to kill you!' This also proves that he has
never done it because as you will find, your body temp only goes up about one degree. Ok, enough about the fake
guru.

Someone just asked me if the shit I sent them was real. Well, if you want a test then rub it on your hands and throw
some on your carpet. When your carpet has to be replaced because NOTHING can remove the yellow and you look
like a total ass because your hands are bright yellow, then you can ask me if it is real!

Mostly people are taking DNP for 1 week at a time because it exhausts you and you sweat a lot, usually that is what
I do, but due to my 'work' with DNP I got a dose while on an ECA week and that combination of DNP-ECA was
like methamphetamine. In fact it was better because it had less side affects. I would venture that DNP-PPACA
would also have the same methamphetamine effects. At this time I do not know, however, whether PPA works on
the same receptor so I would not do them back to back in cycles. ECAY where Y is yohimbine is also a
combination that has meth type benefits. Clen-DNP did not exert any magical meth benefits that I noticed.
Have not taken PPACA or PPACA-DNP or PPACAY.

Tyramine and yohimbine are awesome and someone that I hold using it was getting goosebumps and asked a
pharmacologist what the goosebumps were about. The pharmacologist told him that it meant he was burning a lot
of calories. I love this combination and it is just like meth due to large releases of NA although it only lasts 4 hours
or so.

DNP also 'upgrades' the effects of clen. If you have used clen before and it had/has stopped working, then DNP
will bring back it's glory.

I like to keep the clen and DNP a week apart due to the affects they have on T3 although they work on different
mechanism it is just a precaution to keep from shutting down the T3. You could add Y to it for an added benefit
which will not cause downgrade of anything. Reports on DNP-Y indicate a higher rise in body temperature on this
combination.

Due to the systemic affects of DNP, it affects EVERY cell in the body that has mitochondria, including smooth
(digestive) and muscle and fat as well, you will not see a significant rise in body temp like you see with clen or
ECA. Clen and ECA work primarily on muscle cells and that causes a rise in body temp just as if you were working
out. I don't know why this is such a difficult concept for some to understand, but I was sweating like hell recently,
and I took my temp and it was 95.8. ON DNP!

DNP MECHANISMS

The basics first. DNP is a classified as a chemical poison. It's mode of action is to disrupt the ETC (electron
transport chain) and cause uninhibited exchange of protons. This exchange of protons is what is responsible for
making ADP into ATP. NOTHING can stop the disruption of this process once it starts. DNP works no matter
what! High or low T3 has nothing to do with whether or not DNP affects the mitochondria and burns off extra
energy. DNP gets into the cell and into the mitochondria and causes proton release. No other hormones are needed
or noted.

Even so, it works in much the same way as clen or ECA or PPACA or thyroid. They ALL cause the metabolism to
speed up. These all work via the mitochondria as well, although the non-DNP diet drugs work on the receptors first
and DNP goes directly to the mitochondria, the results are the same which is speeding up the metabolism to burn
fat.

Some other important facts you should know are how ephedrine and beta-3 activation drugs work.
These both cause uncoupling of the ETC chain just like DNP! Ephedrin works part of its magic via beta-3's and
much research has been done looking for a magic beta-3 drug. Why, we have it and it is called DNP! If you are
sitting around and something is making you hotter, you are most likely experiencing an uncoupling of the ETC
chain. No big deal, but DNP just causes a greater effect.
I knew there was a reason that you CANNOT die from DNP usage, at least the doses many are doing. I talked to a
couple people about this but just couldn't find the info to prove it. Ok, so what does DNP do? It uncouples the
ETC or oxidative phosphorylation as was elaborate upon above, allowing electron flow to go unchecked at maximal
rate and resulting in heat production and ATP depletion.

ATP depletion is the key. What condition exists when you have totally exhausted all ATP and no more is being
created? A very good instance we all know about is when you are dead and it is called 'rigor mortis'. Rigor mortis
results because no more ATP is binding to the myosin head of the sarcomere in the muscle fibers.

So what does this have to do with us? No one has ever had rigor mortis on DNP or even severe cramping that has
ever been documented. Furthermore, and to be more specific as to the uncoupler DNP, the electron gradient is
collapsed and it runs unchecked at maximal as I have explained above, but as the gradient continues to increase
electron transport becomes more difficult and the process SLOWS! Additionally, under very large artificially
created electrochemical proton gradients, normal electron flow stops and may even result in
REVERSE electron transport flow!

All that was complicated and here is what it means. The respiration chain has a safety mechanism which allows for
feedback controls to keep you from killing yourself. This is also another reason you will not want to do DNP for
long periods. If you have taken enough as to create a large gradient the flow of electrons your burning of calories
might even STOP! This will happen if you don't eat enough calories and appears to be more detrimental on a high
fat type diet because as you will see below, glucose can ameliorate charge differentials in the mitochondria and at
the cell surface while on DNP.


DNP works NO MATTER WHAT! It uncouples the electron transport train (ETC) and there is nothing you can do
to stop it. Some have said it doesn't work after a small dose or only after taking DNP for 2 days or so. I think they
are the same kind of person who would take a drink of beer and say, 'Oh, I'm not drunk so alcohol doesn't work'!
Alcohol still affects your brain cells and hormone levels and slows down the metabolism. Just because you didn't
drink enough to be drunk doesn't mean nothing happens!

DNP is anti-proteolytic. This means DNP does not break down protein via the mechanism through which DNP
works. DNP is actually better for you than cardio because exercise is PROTEOLYTIC which in itself is another
reason to not be doing a high fat diet. High fat diets and exercise both lower insulin and raise glucagon levels which
cause breakdown of protein. It is a proven fact that 10-20% of energy from exercise comes from AA breakdown as
well as release of glutamine from the cells. DNP burns calories and does not affect hormone levels. Someone said
something about it causing ketosis which is likely if you don't eat any carbs, but DNP is not, by itself going to
affect insulin levels like glucose disposal agents metformin or phenformin.

DNP is not going to be advantageous to muscle building. THIS DOES NOT DISAGREE WITH WHAT I WROTE
ABOVE! It is anti-proteolytic via its mode of action, BUT if there is not enough energy in the cells to build muscle
it ain't gonna happen. Again, diet is key.

DNP is one of the SAFEST drugs you can take!!!!! Why? Am I nuts?! I am basing this on DNP's mode of action.
DNP has one purpose and mechanism and affects nothing else, but the mitochondria. DNP does not affect hormone
levels as do clen, ECA, T3, etc. It has no side affects that you don't expect such as shakes or cramping. Compare
DNP to some of the Drugs the FDA has approved and look at their side effects and then tell me what is safer!
HAHA!

After you read this study you need to ask yourself, need I say more? In the earlier paragraph on the mechanisms of
DNP on the mitochondria I explained the safety mechanism which could keep DNP from being totally depleted of
ATP. Some were saying ATP depletion would result in cell death. The study below illustrates another mechanism
which I didn't know about. The crux of it can be summarized by this sentence: 'The failure to find a reduction in
ATP concentration in either fibre type during prolonged exercise in the face of a progressive increase in the number
of fibers showing little or no glycogen concentration suggests that protective mechanisms exist that prevent an
energy crisis. The nature of these protective mechanisms remains to be elucidated. ' In other words,

When glycogen is gone there is a mechanism which keeps ATP from being depleted which is unknown at present!


Energy metabolism in human slow and fast twitch fibers during prolonged cycle exercise.

Author Ball-Burnett M; Green HJ; Houston ME
Address Department of Kinesiology, University of Waterloo, Ontario, Canada.
Source J Physiol (Lond), 437():257-67 1991 Jun
Abstract

1. The effects of prolonged exercise on energy metabolism in type I and type II muscle fibers in the vastus lateralis
muscle were investigated in six male subjects (20.0 +/- 0.5 years, mean +/- S.E.M.) who performed one-legged
cycling at 61% of maximum O2 consumption (VO2,max; determined with one leg) until fatigue or for a maximum
of 2 h. 2. Analysis of pools of freeze-dried fibers obtained by needle biopsy and separated into specific types by the
myofibrillar ATPase histochemical procedure indicated higher (P less than 0.05) lactate concentrations in type II
fibers compared to type I fibers at 15 min (43.9 +/- 9.7 and 51.2 +/- 9.8 mmol (kg dry wt)-1) and at 60 min (18.2 +/-
4.7 and 25.9 +/- 6.5 mmol (kg dry wt)-1). No differences existed in lactate concentration between fibre types for
pre-exercise (10.0 +/- 1.6 and 13.3 +/- 2.8 mmol (kg dry wt)-1) or post-exercise. 3. Glycogen degradation was most
pronounced in type I fibers. By the end of exercise, glycogen concentration was 82.4 +/- 45 mmol glucosyl units (kg
dry wt)-1 in type I fibers and 175 +/- 62 mmol glucosyl units (kg dry wt)-1 in type II fibers. 4. No significant
changes in ATP and creatine phosphate (CrP) were found in either fibre type with exercise. 5. It is concluded that,
at least for lactate and glycogen, fibre-specific differences are evident in prolonged submaximal exercise. The cause
of the difference probably relates both to the unique energy metabolic characteristics of each fibre type and to the
manner in which they are utilized during the exercise. 6. The failure to find a reduction in ATP concentration in
either fibre type during prolonged exercise in the face of a progressive increase in the number of fibers showing
little or no glycogen concentration suggests that protective mechanisms exist that prevent an energy crisis. The
nature of these protective mechanisms remains to be elucidated.

DNP will make you breathe harder via a mechanism called cellular hypermetabolism. You aren't going to die if you
are breathing hard! DNP works by increasing ventilation and oxygen consumption via hypermetabolism of the cell.
DNP makes you breath hard.


Role of tissue hypermetabolism in stimulation of ventilation by dinitrophenol.
Author Levine S
Source J Appl Physiol, 43(1):72-4 1977 Jul
Abstract

Several authors have hypothesized that tissue hypermetabolism accounts for increases in ventilation (VE) elicited by
2,4-dinitrophenol. However, some data in the literature indicate that stimulation of VE by isomers of dinitrophenol
is unrelated to tissue metabolic rate. To test this latter concept, we compared three different isomers of dinitrophenol
(i.e., 2,4-dinitrophenol (2,4-DNP), 2,5-dinitrophenol (2,5,-DNP), 2,6-dinitrophenol (2,6-DNP) with respect to
stimulation of VE and with respect to stimulation of oxygen consumption (VO2). In all experiments, 3-4 mg/kg of
one dinitrophenol isomer was administered to chloralose anesthetized dogs by intra-arterial infusion. 2,4-DNP
elicited large increments in both VE and VO2, 2,6-DNP elicited moderate increments in both VE and VO2, whereas
2,5-DNP elicited small increments in both VE and VO2. These observations demonstrate a correlation between
ventilatory and metabolic changes affected by isomers of dinitrophenol. Accordingly, these results are consistent
with the hypothesis that ventilatory stimulation by congeners of dinitrophenol is related to tissue hypermetabolism.


How to feel good on 600mg of DNP!

This is not an advertisement because I sell more encapsulated DNP for research than I care to spend time making.
Note: I sell it for 'Research'

The longer I took DNP the more I realized those who had originally recommended DNP use were not looking at the
big picture, and they had most likely never used it or mixed it themselves, and/or were just complete morons!

Myth #1.
You die on DNP from heat related to overdose.
Wrong!
You die from dehydration resulting in heat exhaustion and then heat stroke.

Myth #2.
You can do it on high fat-low carbohydrate type diets.
NO YOU CAN'T!
High fat-low carbohydrate diets are based on keeping your blood sugar and insulin low. DNP will also drive down
your blood sugar, so if you want to have blurry vision due to low blood sugar and feel like hell, you go right ahead.
Glucose also has some beneficial cellular effects when used with DNP..

Myth #3. You will go blind.
Right! If you do high fat-low carbohydrate diets and don't keep your blood sugar up and/or don't take pyruvate.

Myth #4.
You can't work out on DNP.
Yes you can, if you know what you are doing and which I am about to tell you.

As you may already know you, should be taking the following per day.

1200-1500mg magnesium in 2-3 divided doses.
2-3000mg vitamin C.
1200IU of vitamin E
200mcg of selenium.
1000-2000mg of calcium (can't take it with the magnesium, though. Take it before bed)
Melatonin if you can't sleep and it is also one of the best and cheapest anti-oxidants.
50mg of zinc a day
one iron tab as hemoglobin is a protein as well.
A potassium gluconate tab or two a day
Taurine at 3g a day.
Glutamine at 15g a day sublingual or with carb/protein drink.


I think taurine will be most beneficial for cramping and holding onto water. I have worked with some mountain
bikers that were having trouble with cramps and had tried using the proverbial potassium supplementation cure and
it didn't work. I had them take the taurine and magnesium and the cramping went away. Taurine is also give to
people who have leg cramps at night at a dosage of 3-6g a day resulting in total alleviation of the cramps.
Clenbuterol depletes the liver of its taurine supply which changes the osmotic pressure and therefore stops T4-T3
conversion. Taking supplemental taurine can alleviate this.

Glutamine also regulates water, but is a bitch to take and unless you want your small intestine to absorb most of it
you have to take it sublingual. You can fool the body a bit by putting it into your carb/protein drink after you work
out or by taking 2g doses throughout the day. Glutamine ALSO causes a rise in insulin.

IF you are on clenbuterol, pyruvate and glycerol will help you a little, and I don't know why, but I still got some
cramping on clen after an event even on P and G. The latest research I have indicates that the reason clen may
cause cramping is due to TAURINE depletion so by taking the 3g a day taurine you should be able to ameliorate
those effects as well and keep your thyroid levels normal as well.

In addition to the vitamins and minerals you should be taking:

3-6g Pyruvate (P)
3 tablespoons Glycerol (G)

If you can't get the G and P go right to the taurine which may be cheaper as well.
Glycerin (glycerol) is avail in the skin care section of your pharmacy and 4oz is about1-2 dollars or there are larger
versions in white bottles and the brand name is H something. Just buy it from a vet and a gallon is around $20!

I felt like shit when I went above 400mg and sweat profusely on single large doses of 600mg and 800mg which
lasted for 2 days. I weigh around 95kg (210).

The object of the DNP dosing with the glycerol and pyruvate was to test their benefits on what is considered an
overdose of DNP while maintaining my exercise level in the middle of summer.

Here is what I was taking:
600mg of DNP which would be 6mg/kg which is well above the recommended 3-5mg.

DNP is said to have a half life of 36 hours and this is what I have based the following dosing scheme. I also have
anecdotal evidence that DNP can last 48 hours or more. When I took an 800mg dose after 3 days on 300mg a day I
sweat for 48 hours straight and that 800mg was the last dose I took.

You have to divide the 600mg into two doses of 300mg 12 hours apart.
After you hit your 600mg limit you don't take the next 300mg for 36 HOURS from the first dose!
So, if I took the first dose at 6AM on Sunday morning and the second 300 mg dose at 6PM Sunday night, the 3rd
dose would not be until 6PM on Monday evening. The fourth dose would again follow 12 hours from the 3rd which
would be at 6AM on Tuesday morning.

I am also taking EC with this just for fun although at only 2 x a day for the EC to keep energy levels up and lessen
the carb craving that goes with DNP.

How am I not sweating all over the place and not feeling like shit and/or dehydrating in the middle of summer while
going on hour or longer rides in 85 plus heat?. Let me tell you again that I hated the way DNP made me feel.

YOU HAVE TO TAKE GLYCEROL AND PYRUVATE!
I don't know if you can take one without the other because I was using the glycerol (G) and pyruvate (P) to enhance
endurance and stem dehydration which I am very prone to. I think, however, that you will have to do them both as
there may be a synergistic benefit. I have taken G alone and while you have more water to hold on to, you just seem
to sweat more which is also backed up by the research. The G-P cocktail let me drink « my normal volume of water
on rides and that is what made me try the DNP-ECA experiment.

Glycerol dose. YOU ONLY NEED 1 TABLESPOON 3 TIMES A DAY! One in the morning, one in the afternoon
and one right before bed. Don't listen to the researchers who tell you to take 1 gram for every kg body weight 1-2
hours before and event. They are idiots and obviously have never taken it or asked the athletes how they feel. Let
me tell you, you feel awful taking that much glycerol! You feel bloated and sometimes get a headache and you piss
A LOT! 1 tablespoon 3 times a day comes out to « what they recommend to take 2 hours before an event. The
glycerol keeps your muscles hydrated and limits the sweating. It will fight the dehydrating effects of the ECA. As
we know, DNP is carbohydrate/fat specific and glycerol also is a 3 carbon carbohydrate source that can't go to fat!.
Glycerol also increases power output which may be an added benefit of the type of carb source it is. Glycerol is
converted to glucose in the liver and in the liver is where it stays for the most part and does not, therefore, raise
insulin levels.

Before I explain the pyruvate, let me tell you that glycerol and glycerin are the same thing! A good recipe for taking
your glycerol is 1 packet of Kool-aid, 1/8 cup sugar, 1 tablespoon glycerol and 32-oz of water. The glycerol makes
the kool-aid taste like OJ because there are alcohols and fermentation products in the OJ which the glycerol mimics.

Pyruvate dose. 2-5grams a day. Start out at 900mg or so 3 times a day and go up from there. I am at 1.5g 2-3 times
a day and if you don't work your way up it will give you gas and the runs. As I mentioned above, I think the P is
working synergistically to hold on to the water in your muscles. Additionally, it is another 3 carbon energy source
and/or it is manipulating the Krebs Cycle intermediates and allows for a different energy production pathway.
Pyruvate changes/manipulates an ATP/energy pathway and decreases lactic acid output and if it ain't the Krebs
cycle I don't really care. It works.

Some abstracts on the benefits of pyruvate.

Pyruvate and the heart and glucose and insulin.

Cardiac metabolism and electromechanics of human heart.
Author Prasad K
Source Recent Adv Stud Cardiac Struct Metab, 10():119-37 1975
Abstract

The effects of substrates on the metabolic inhibitor-induced changes in the action potential and contraction of
papillary muscles obtained from patients undergoing corrective open-heart surgery were studied. Anoxia produced a
marked shortening of the action potential duration and a decrease in the resting potential, rate of rise of action
potential, effective refractory period, and contractility. In anoxic muscle, although glucose completely restored the
action potential duration, effective refractory period, and resting potential to control levels, it was unable to
completely restore the contractility to the control level. Substrate depletion and metabolic inhibitors (iodoacetate,
dinitrophenol) produced effects similar to that of anoxia, but at a faster rate. Glucose restored the action potential
and, to a lesser extent, contractility to the control level in dinitrophenol-treated muscle but was ineffective in so
doing the iodoacetate-treated muscle. Pyruvate, however, was effective in restoring the action potential and
contracility in iodoacetate-treated muscle. Pretreatment of the muscle with glucose and, particularly, with glucose
plus insulin prevented the combined effects of anoxia and lack of glucose on the action potential and contractility
for a prolonged period. These results suggest that intravenous infusion of glucose and insulin before and during
surgery might prevent or reduced the effect of anoxia on the electrical and mechanical activity of the heart during
open-heart surgery.

Pyruvate was able to restore the action potential (charge) of cells treated with DNP! Unfortunately, most of you
won't understand what an AP is even if I explained it, but I will tell you that restoring it is signiificant!

Now you have a recipe on how to feel good on an overdose of DNP! To recap you need:
3 Tablespoons glycerol 3x a day.
1g Pyruvate 3x a day.
Taurine at 3g a day.
DNP at 36 hour intervals.

If you start to feel bad, just drink some sugared pop or take some glucose or maltodextrin with your psuedo-OJ mix.
The only drawback is that you will still smell rather bad and will emit a vinegar type odor although you won't be
sweating all over everything. If you notice you are starting to sweat more it is time for another glycerol dose.

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Use of AS during DNP

You can use DNP during an AS cycle although the muscle loss from DNP is minimal, if any, so I don't think this is
the best use of your AS. If, however, you have hit a plateau the DNP for a week will help you break through that
plateau in the subsequent week off. Now, I have experienced this, as have others, but as to whether or not it is from
an upregulation or having a rush of T3 available or a type of overcompensation rebound is unknown, but it is cool
and it happens..

Use of AS after DNP or dieting.

DNP and dieting BOTH stop conversion of T3-T4. T3 is responsible for protein synthesis. If you have been on a
diet for 2 weeks or more your thyroid will be depressed and so will protein synthesis due to low T3. By adding AS
you will be increasing protein synthesis while waiting for your thyroid to come back online so you won't get fat
right after a diet.

Use non-aromatizing AS like equipoise, ganabol, maxigan, trenbolone (finaplix or Anibolan), winny-V. Or you can
use testosterone and an anti-aromatase like cytadren or arimidex. If you want to keep the fat off you HAVE TO use
those anti-aromatazes with the testosterones and d-bols as they are the only ones that stop conversion of testosterone
to estradiol. Estradiol conversion will make you fat, especially around the waist! If you have to use a testosterone
and want to lose fat, I would use cytadren because it increase hormones which cause fat loss as well as increasing
IGF-1 levels! (Bet you didn't know that!) I would, however, not stay on cytadren longer than one month and
dosage is one tab divided into 4 doses per day.

A line from a study showing that estrogen makes you fatter for the non-believers!
Obes Res 1995 Nov;3 Suppl 4:561S-568S
Topical fat reduction.
Greenway FL, Bray GA, Heber D
Department of Medicine, UCLA School of Medicine, Torrance, CA, USA.

The fat on women's thighs is more difficult to mobilize due to increased alpha-2 adrenergic
receptor activity induced by estrogen. Lipolysis can be initiated through adipocyte receptor
stimulation (beta adrenergic) or inhibition (adenosine or alpha-2 adrenergic) or by inhibition of
phosphodiesterase.

While yes, they talk about women and estrogen and fat, the mechanism is still absolute and spans the sexes.
Estrogen makes fat cells resistant to lipolysis. Still want to take that test without and anti-estrogen?


Get to fat burning faster!

This is something you can try after you have used DNP once and know your tolerance and is a DNP manual
exclusive! Your working dose will be around 400mg a day, correct? The first day, however, you are going to take
600mgs in divided doses! It takes DNP a couple days to build up so this won't bother you in the least. On the
second day you will start taking 200mg caps every 8 hours until you are sweating or getting the heat you want. Now
you are at your tolerance dose and you can space it out to the 36 hour dosing.


NEW!
Use a blood buffer to combat free radicals and lactic acid!

Add up to one tablespoon of baking soda, sodium citrate, or potassium citrate to your drink of choice throughout the
day. A mix of the sodium and potassium would be best. Why?
What does DNP and exercise have in common? During high intensity exercise (supramaximal) ATP production is
supplied by anaerobic glycolysis. This increases levels of H+ (protons) both inside and outside the cell via lactate
and results in the feeling of fatique (Hermansen and Osnes; Sahlin) In the past, the use of sodium bicarbonate
(baking soda) has been used and has been shown to decrease acidosis via buffering of the blood. The problem with
baking soda is gastric distress and high salt intake with the recommended dosage of 300mg/kg which is around a
tablespoon of baking soda for most people. Dosage for sodium citrate is 100mg-500mg per kg and did not give
stomach problems to the users. Time to exhaustion was increased 15% which is the same as with baking soda.
Alkalosis (making the blood basic) has been found to increase the rate of lactate and proton release from muscle
into the blood. An increase in muscle pH causes phosphofructokinase inhibition (PFK) which is the controlling
enzyme in glycogen utilization and therefore causes an increase in lactate formation. Those two mechanisms also
will hold true for DNP as DNP releases protons which causes the heat. Get it out of the cell with the citrates.


Testomonial:
Hey animal just thought I'd let you know the great results I had with the DNP. I got tested hydrostatically and I'm at
4.8%. DNP is really the shit. Anyway, a buddy of mine is competing in a month and he's currently at 7% bf(he's
about 190lbs) and he'd like to do it for two weeks. I understand that the lower one's bodyfat % the greater amount
needed (I responded very well to 4mg/kilo but I was also dieting)


Questions I have answered for DNP users

Are all of the losses on DNP fat losses?
You can't ever say ALL in the scientific world, but it is the best we can get!


Animal, you have been a big help already. I've got some questions for ya. I am 195#, and plan on taking 200 mg in
evening and 200mg before bed. I also plan on taking pyruvate and glycerol (via your recommendation). I'll going to
use a 8on/8off cycle.
1) Should I attempt to lift while on dnp?
Sure.

2) What dosage glycerol and pyruvate do you reccommend?
3 tablspoons a day on the G and 3g of the P

3) You said that you experienced an anabolic "burst" directly after coming off of dnp. Could this be contributed to
your muscles reglycogenating themselves?
No, because I didn't really get pumped, but strength went up.

or do you feel that this is genuine protein synthesis?
Yes, or nerve excitation/generation or a return of T3. Let me explain the nerve generation in more detail for a
moment. When you do strength exercises of 5 reps or less you are training the nerves to fire more muscle cells and
to fire those muscle cells in the sequence you want. Now, if we add DNP we are exhausting our muscle cells and
they can't fire as strongly. Result? Your nervous system trains more nerves to fire other muscle cells which had
previously gone un or underused when energy stores were high. You are getting a nerve training session due to
exhaustion! The more I think about it the more it is like those overtraining programs where you overtrain for a week
and you get a rebound. That is what is happening except you are overtraining at the same weights due to the DNP.
Hehe. It is called overcompensation training and I'll take it!


A user:
Found some info 'bout DNP "With even a low dosage, in the area of 3-5 mg/kg of body weight a day, it will rate
your metabolic rate 30%. If this dosage is continued daily, it will raise your metabolism by 50%. At this rate you
can burn about 1 lb. of fat a day."

Animal:
Now, let's think about this for a second. If metabolism can go from 30-50% that means there is a residual amount
left over from the previous dose and therefore the 36hour clearance dosing schedule which I recommend.
Furthermore, when I overdosed on 800mg I sweat for OVER 48 hours so this tells me that the half-life can be even
longer in some circumstances. It is, nonetheless, up to you as to how you want to take it. If every 24 hours is
tolerable for you, then do it.

A user:
That's not what I've noticed. At present I'v even gained some weight. I'm 98 kg now. I don't look a bit harder but
maybe I shouldn't expect that after only 4 days.
You WILL hold onto to water! You WILL be depleting carbs from the muscle that will make you look flat! Most
WILL NOT notice the benefits until a week or two later upon cessation of DNP. Some see benefits right away, but
they appear to already have a bodyfat below 10%.

A speculator wrote:
For a person that is highly active and on a calorie restricted diet, DNP will deplete ATP within a matter of days.
When this happens your body temperature will go back to normal. The only thing you can do at this point is
supplement with in the dosage area of about 150 mcg/day."

Animal:
Believe me, you will feel wasted (tired) and LOSE muscle on the regimen and the liver does not control oxidative
phosphorylation in every cell. You will still be hot regardless of your T3 levels.


Question:
Won't the conversion of T4-T3 come back and function again after discontinuing DNP administration?
Animal
Yes, and as long as you do some carbs at 600g a day for three days after.

Or do I have to look to get T3 as well?
Animal
Not really, if ATP was being ever totally depleted you would be cramping. Lack of ATP generation happens when
you are what? DEAD!!!!!! It is called rigomortis and if people who write right about DNP had an education or an
inkling about body chemistry and process they would know this! Total ATP depletion resulting in death of the cell
is not possible. There is some safety mechanism and I imagine it is via the fat cells, but you will not deplete your
ATP unless you are an anorexic or dead.

User:
And isn't a total lack of ATP what we want, so we can start burning fat instead of ATP?
Animal:
Wrong and this is not your fault, but again those who claim to be experts who are dispensing such disinformation.
Once the ATP to ADP and to AMP is changed below a certain amount the cell gets it energy from another source
which would be the fat. You are looking to burn the glycogen and then the fat is used. This does not mean ATP is
gone!

Why is thermogenesis stopped if there isn't any ATP?
Animal:
Read above and it is never stopped. DNP NEVER stops working unless the proton gradient is severely altered.
Even in such a case, parts of the mitochondria can have one direction of proton gradient while another section can
have a DIFFERENT proton flow!

User:
Is this why you want a break after one week? To load up with ATP so thermogenesis can start again?
Animal:
No, so you don't feel like shit all the time and so you can get the liver converting T4-T3 again

Is a one-week-break enough? Or maybe too short if I'm in a hurry.
You could do DNP for 2 weeks or more if you want.

Wouldn't it be enough just to discontinue the DNP-cycle to let the liver start converting T4 to T3?
That is why you stop after a week!

Where are ATP-molecules stored?
In and/around the mitochondria and in the cytosol of the cell and ATP is attached to certain enzymes waiting for
activation.

How much ATP do we have in storage?
That is a major calculation and I haven't looked for an answer, but I don't think it is important as you can never get
rid of all of it.

A speculator:
"The administration of DNP, at a dose of 3.5 mg per kilo, increases the total production of heat by about 40%, from
the 3rd or 4th day. This increase of the metabolism is due MOSTLY to an increase in the combustion of the fat and
a LITTLE to combustion of carbohydrates."
Any comments on this?

Animal:
Again, you are seeing a residual affect. The molecules that the mitochondria use for production of ATP can come
from carbs or fat, but the important part is that it is not from muscle.

Another fact found in the same report as above:
"In prolonging the administration of the medication, one observes an increase of the tolerance of carbohydrates."
Does this mean we get increased insulin-sensitivity?
That is a weird sentence and I don't know what it means, but I think it means you will be more receptive to carbs.
You now have increased your insulin sensitivity and this could explain the DNP users' craving for carbs while using
DNP.
..
So when I eat carbs (I've noticed that I start to sweat then) the body starts burning fat?
No, the body burns excess ATP and food intake itself is thermogenic.

Why simple sugars? That means I should walk around eating candy all day?
Candy is not really a simple sugar as it usually has fat or fructose with it.
You want a simple sugar every so often to get some insulin rise and some fructose will help recarb the liver as
fructose is about 4 times better at recarbing the liver than glucose. Glucose is, BTW, 2 times at good at recarbing
muscle when compared to fructose.

What happens with the carbs?
They are burned and insulin release and helps change charge on the cells.

Insulin is secreted. I've noticed that. (If it wouldn't I'd go glucose-high-'n-crazy.) Do I store carbs as glycogen?
AHAHA! So much for the speculators that say you have to do insulin!
You won't have time to make glycogen and the glucose will go right to ATP production.

What about cataracts and skin lesions?
That is a long term chronic dose situation and why you take pyruvate.

Have you noticed anything?
Yes, your sweat smells bad, but no lesions. Another reason you want simple sugars or insulin is that DNP starts to
make your vision blurry if you are on a low carb diet.

Animals' Analysis of someone else's recommendations:

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

Animal:
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 fucked 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.

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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.

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.

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
(opening) results in lessened calcium influx and smooth muscle relaxation.

o KATP channel BLOCKED -> vascular tone increases.

o 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.

o KATP BLOCKED -> more strength

o 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 uncoupler 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.
(Animal; another study shows that insulin internalization is also affected so taking insulin is useless)

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.

Animal;
Why all this is a good story we do have to look at what he said in the beginning as in caveat lector. While his
speculation on KATP channels and the need for insulin is understood-, his mechanisms are a bit incorrect. DNP
causes an internalization of the receptor so you now have a cell that is desensitized to insulin and all the insulin in
the world will not help that. Second, the KATP channels can be controlled with pyruvate.

Studies

DNP causes insulin insensitivity by preventing internalization of the receptor.

Insulin internalization into monocytes is decreased in patients with type II diabetes mellitus.
Author Trischitta V; Gullo D; Squatrito S; Pezzino V; Goldfine ID; Vigneri R
Source J Clin Endocrinol Metab, 62(3):522-8 1986 Mar
Abstract

We studied the internalization of [125I]insulin into circulating human monocytes, a cell type widely used for insulin

binding studies. The internalization of [125I]insulin was assessed by both an acid extraction technique, which
removes surface-bound insulin but not intracellular insulin, and by a trypsinization technique, which removes cell
surface-bound hormone. After 5 h of incubation at 22 C, over 40% of the total cell-associated [125I]insulin was
internalized into monocytes of normal subjects. This internalization was temperature dependent; the fraction of
internalized hormone was progressively decreased when the incubation temperature was reduced from 37 to 4 C.
Treatment of monocytes with increasing concentrations of 2,4-dinitrophenol also decreased [125I]insulin
internalization, whereas dansylcadaverine, an inhibitor of transglutaminase, had no effect. Analysis by gel filtration
of the internalized labeled hormone after 4 h of incubation at 22 C indicated that 50-60% of the label was degraded
insulin, but detectable intact insulin was still present. Internalization of insulin was then studied in monocytes from
eight obese patients (161% of ideal body weight) with type II diabetes mellitus. After 4 h of incubation at 22 C, the
specific total monocyte-associated [125I]insulin was decreased compared to that in cells from 7 normal subjects
[6.02 +/- 0.38% (+/- SE) vs. 3.91 +/- 0.31% of the total; P less than 0.001]. Moreover, the percentage of hormone
that was internalized was also decreased from 41.4 +/- 1.2% of the total to 28.9 +/- 1.8% (P less than 0.001). In 20
nondiabetic obese subjects, specific cell-associated [125I]insulin was reduced to 3.9 +/- 0.3% (P less than 0.001).
However, compared to that in normal subjects, the percentage of hormone that was internalized was not decreased
(39.7 +/- 3.51% of the total). The present findings indicate that human circulating monocytes internalize
[125I]insulin; this process is temperature and energy dependent; and monocytes from obese type II diabetic patients
have a significantly decreased ability to internalize insulin. This decreased internalization may play a role in the
cellular resistance to insulin that occurs in these patients.

DNP enhances binding of insulin to the receptor, but does not internalized it.

The effect of phenformin and other adenosine triphosphate (ATP)-lowering agents on insulin binding to IM-9
human cultured lymphocytes.
Author Vigneri R; Maddux B; Goldfine ID
Source J Cell Biochem, 24(2):177-86 1984
Abstract

In the present study, we investigated the mechanism by which the antidiabetic drug phenformin increases insulin
binding to its receptors in IM-9 human cultured lymphocytes. After a 24-hr preincubation, phenformin induced a
twofold increase in specific 125I-insulin binding, and removal of phenformin was followed 6 hr later by a return in
binding to control levels. This effect of phenformin on insulin binding was not a consequence of either inhibition of
cell growth, changes in cellular cyclic adenosine monophosphate (AMP) levels, or changes in guanosine
triphosphate (GTP) content. Since phenformin is known to inhibit various aspects of cellular energy metabolism, the
relationship between 125I-insulin binding and energy metabolism in IM-9 cells was investigated. The
phenformin-induced increase in insulin binding to IM-9 cells was related to a time- and dose-dependent decrease in
ATP levels. Other agents that lowered ATP levels, including antimycin, dinitrophenol, and 2-deoxyglucose, also
raised insulin binding. These studies indicated, therefore, that phenformin enhances insulin binding to receptors on
IM-9 cells and that this effect on insulin receptors may be related to alterations in metabolic functions that are
reflected by a lowering of ATP levels.

DNP blocks all internalization so is more insulin going to help? No.

Evidence for two independent pathways of insulin-receptor internalization in hepatocytes and hepatoma cells.
Author McClain DA; Olefsky JM
Address Department of Medicine, Veterans Administration Medical Center, San Diego 92161.
Source Diabetes, 37(6):806-15 1988 Jun
Abstract


A study of insulin-receptor internalization and recycling was undertaken in primary cultures of rat hepatocytes and a
human hepatoma cell line (HepG2). Receptors were quantitated by measuring 125I-insulin binding to partially
purified soluble receptor preparations from untreated cells (total receptors) and trypsinized cells (intracellular
receptors). In resting HepG2 cells, exposure to insulin results in internalization of insulin receptors, the rate and
extent of which is dependent on the insulin concentration. However, receptors do not accumulate inside the cell in
proportion to the higher rates of internalization at high concentrations of insulin. This lack of accumulation is
explained by much higher recycling rates after exposure to high concentrations of insulin. Similar results were noted
for primary cultures of rat hepatocytes. These results imply qualitatively different fates for receptors internalized
after exposure to different concentrations of insulin. To further investigate the possibility of different pathways for
insulin-receptor internalization and processing, cells in low (1 ng/ml) or high (100 ng/ml) concentrations of insulin
were exposed to drugs or treatments known to affect receptor metabolism. Hypotonic shock and hypokalemia,
which arrest coated-pit formation, blocked internalization of insulin and insulin receptors at low concentrations of
insulin but allowed internalization in response to high concentrations of insulin. The lysosomotropic drugs
monensin and chloroquine caused intracellular accumulation of insulin and its receptors internalized at low
concentrations of insulin but had a relatively smaller effect on receptors internalized at high concentrations of
insulin. All internalization is blocked by 2,4-dinitrophenol. We conclude that high doses of insulin lead to
insulin-receptor internalization and recycling through a pathway that is functionally distinct from the pathway taken
by receptors internalized by low (physiologic) concentrations of insulin. The pharmacologic experiments raise the
possibility that the high-dose pathway, unlike the low-dose pathway, may proceed independently of coated pits and
endosomal acidification.

Degradation of insulin by human fibroblasts: effects of inhibitors of pinocytosis and lysosomal activity.
Author Kooistra T; Lloyd JB
Source Int J Biochem, 17(7):805-11 1985
Abstract
The role of the pinosome-lysosome pathway in the degradation of 125I-labelled bovine insulin by cultured human
fibroblasts was examined by comparing the effects of various known inhibitors of pinocytosis and lysosomal
degradation on the uptake and degradation of 125I-labelled polyvinylpyrrolidone, formaldehyde-denatured bovine
serum albumin and bovine insulin by these cells. Fibroblasts incubated with polyvinylpyrrolidone steadily
accumulate this substrate, whereas incubations with insulin or denatured albumin led to the progressive appearance
in the culture medium of [125I]iodotyrosine. Inhibitors of pinocytosis (bacitracin, colchicine and monensin),
metabolic inhibitors (2,4-dinitrophenol and NaF), lysosomotropic agents (chloroquine and NH4Cl) and an inhibitor
of cysteine-proteinases (leupeptin) decreased the rate of uptake of polyvinylpyrrolidone and denatured albumin very
similarly, but only bacitracin had an effect on the processing of insulin. Chloroquine, NH4Cl and leupeptin strongly
inhibited the digestion of denatured albumin, but not of insulin. The different responses to the modifiers, with
polyvinylpyrrolidone and denatured albumin on the one hand and insulin on the other, suggest that insulin
degradation can occur by a non-lysosomal pathway. The very strong inhibitory effect of bacitracin on insulin
processing by fibroblasts may point to an important role of plasma membrane proteinases in insulin degradation.


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.

Here is the scare story that is going around on cataract. I raise this because of the connection with this problem and
insulin and the previous story. I was starting to see spots and when I took insulin they went away. The myopia
stops when DNP is discontinued. Note, that this was a chronic user below.

Subject: DNP and Cataracts

MDGADPC has kindly sent me a photocopy from the French journal Annales des Oculistes, concerning the effects
of DNP on the eyes. Since this paper may be of some general interest, I have translated it and attach it below.

For those who may be unaware, DNP or dinitrophenol is a toxic compound which was used for weight loss in the
1930's. It was withdrawn from the market as a result of severe side effects, including deaths, but recently it has been
suggested that it could have a role in the contest preparation of elite bodybuilders.

One point to consider in the text below is that cataracts may develop 6 to 12 months after the DNP treatment is
completed.
Note: the intake of DNP was chronic and continuous.

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

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.
Note: 100,000 people used it.
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
Francaisedes 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
Hollandin 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 alpha dinitrophenol 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.
Note: Because they were not intoxicated with it continuously.

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.
Note: That is a long time!

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.
Note: She lost a lot of weight, too!

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 cataracts, 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. 114-128).

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.

Copyright 1995-97 Deja News, Inc. All rights reserved.


DNP and GHB?

What are you talking about? Not really GHB, but gamma-butyrolactone (GBL)! I am also about to tell you how
they will never be able to shut down GBL sales. GBL is non-toxic and is used as acetone free nail polish remover.
GBL will take the ink stains off almost anything. I was pouring some into a bottle and it got down the side on the
label and the color was gone, running down the side. You can remove ink stains from white shirts, etc. If somebody
wants to sell GBL, all they have to do is make some bottles that say, 'Acetone free nail polish' or 'Ink remover' A
friends kid spilled puffy paint on the carpet. It was red on a white carpet to boot! We tried everything to get it out;
acetone, laquer thinner, rubbing alcohol and so on. I remembered the ink and decided to try GBL. Guess what?
There is no stain!

So what does that have to do with DNP? DNP is what? A DYE!!! And a very unique one in that it is not soluble
in anything. I wanted to test it so I made transfered some caps into a bottle with my bare hands. Now I have bright
yellow dots and marks all over my finger tips. I rubbed it in for fun and let it set in for about 10 minutes. I took
GBL on a rag and start to wipe at some of the yellow marks. I hope this works or I am going to be wearing gloves
for about 3 days. It worked! All the marks were gone in 5 minutes and the rag now had yellow marks all over it.
The most interesting this I found was that there was no transference of the DNP back off the rag while the GBL is
still wet. It is also great that you don't have to wash your hands with it.

Previously I had been using detergents, like TIDE, to try and remove the yellow, because it had phenol in it. That
didn't work too well so then I switched to the Tektrol which is used to sterilize hospitals and it has 10% phenol in it.
The Tektrol worked better, but the higher level of phenol is tough on your skin, and Tektrol can't touch GBL in
effectiveness. No yellow is left at all! If you have it stained deep via not trying to remove the dye fast enough or
have it in your fingernails, you may need to use the 'Palmolive method' where you soak your fingertips in the GBL
until the DNP is gone.

Lyle McDonalds little self experiment.
(Animal: Kinda silly and some theories are incorrect like the need for T3, but it is interesting reading)

My second realization about DNP is that, as I expected, it makes you lethargic as hell. DNP works by depleting
Type I fibers of ATP so you have no energy for anything low intensity (although training is generally not affected
assuming that you can drag your ass to the gym in the first place). I just felt shitty. Also, DNP does not blunt
hunger like ECA. But, again, at 50% increase in BMR, eating a couple hundred more calories is no big deal.
(Note: That is why you can take ECA on it. DNP also removes ATP from ALL cells)

So, like the dumbass I am, I figured I'd see what taking the ECA stack would do to me. My biggest fear was
raising body temp too high. ECA/Clen and DNP work through independent mechanisms and I wondered if the body
temp increases would be synergistic or not. I don't think they were but it was an interesting experience.

The net effect of DNP is a depressant although it's not through central nervous system modulation. ECA is a major
CNS stimulant. Also, to be a real dumbfuck, I added some yohimbe fuel to keep alpha receptors in check since
ECA has some alpha agonist activity as well (NB: overstimulating alpha agonists has a major, major side effect. It
makes your dick not work. I found this out the hard (err, soft) way. Just be warned).
(Animal; unfortunately he doesn't know his yohimbine mechs and that it takes nearly a month for the 'dick raising'
benefits of yohimbine to take effect.)

Ok, I was feeling really bad by Thursday. DNP stays in your system (according to Robert Ames) for 36 hours so
I'm not convinced that dosing schedule of every 24 hours is ideal as there is a 12 hour period when you have twice
the recommended dose active in your body. But, this makes a nice failsafe to avoid nasty side effects: nobody can
take DNP more than 5 days straight because you get tired of feeling like total shit all the time. It's possible that
dosing every 36 hours would allow you to take it indefinitely but this isn't necessarily a good thing as the negative
effects of constant ATP depletion (like cataracts which apparently occurs from ATP depletion in your eyes) would
increase with time. So a dose every 24 might be ideal.

Anyway, like I said, I had lots o'DNP and some ECA in my system Thursday. And I was drinking a lot of diet coke
so caffeine intake was massive. And I was severely dehydrated from sweating so much and DNP blunts your thirst
mechanism. All of this added up to giving me a resting heart rate of 132 (that's not a typo) beats per minute. I didn't
get my blood pressure measured but I"m sure it was high. I'm surprised I didn't have a fucking stroke. I probably
deserved to have one just for being a dumbass (nature's way of thinning the herd. Darwinism at work for you).
(his heart rate was from the ECA. DNP doesn't raise it.)

So, the body composition record.
Day Date Wt Pec Abs SI Thigh Sum3 BF% FM FFM
---------------------------------------------------------
Mon 12/30 156 3 22 13 6 31 8.5 13.3 142.7
Fri 1/3 151 3 18 12 6 27 7.6 11.4 139.6

Holy Shit! With minimal dieting (hell, no dieting), maybe 30' total of cardio (warm-up and cool down before
weights), about 2.5 hours total of weight training this week, I still dropped almost 2 lbs of bodyfat. Now, the
decrease in lean body mass is somewhat worrisome but I attribute most of it to dehydration. Since I was stronger on
Friday than on Monday (same workout, heavier poundages, same reps), I don't feel that I lost any of the small
amount of LBM I have. I don't really look like I lost that much fat but, seeing as most of what I've got is smack dab
on my midsection, I'm not too surprised. This is where the biggest change in skinfolds happened anyway which is
fine with me. I'm still not quite to cut abs, but I'm getting there.
(Animal Note: dehydration is why you take the glycerol, furthermore, if you muscles and cells are void of glycogen
you WILL test lower because glycogen holds a lot of water.)

So, here's the plan for the next few weeks. I really don't want to do another cycle of DNP just yet (esp since I don't
have that much and haven't had time to figure out where to get more). So, I figure it this way. I know I canuse
Bodyopus with some ass kicking training in the gym to put on a decent amount of LBM each week with minimal fat
gain. So, I figure on doing a week or three of Bodyopus training at above maintenance calories to put on a pound or
two of lean with maybe .5 lbs of fat. Then, I can use DNP or dieting to cut down for a week or two and sort of stair
step down in body fat while increasing in muscle mass. I had considered doing 1 week of mass training
with Bodyopus alternated with 1 week of dieting with DNP and isocaloric but I'm not sure the body can switch
gears like that so quickly. We'll see.


Here is another one and let me add that pyruvate could be added instead of alpha-lipoic for reasons that I'm not
going to go into yet.

Diabetes, Glucose And Muscle Energy

Although the general recommended supplemental dose of alpha-lipoic acid is 50 mg daily, much higher doses have
been medically approved in Germany to treat adult-onset diabetes and diabetic complications. This use dates back to
1970, when researchers at the University of Pennsylvania reported that alpha-lipoic acid increased the burning of
glucose, or blood sugar.

More recently, doctors at the Rostock-Sudstadt Clinic in Germany have reported that 600 mg of alpha-lipoic acid
daily significantly reduces symptoms of diabetic neuropathy or nerve damage.5 Other experiments have shown that
alpha-lipoic acid increases the sugar-burning activity of insulin and reduces insulin-resistance. These findings are
significant because insulin resistance is a major underlying cause of adult-onset diabetes and a prominent factor in
coronary heart disease and obesity.6

Most of the body's glucose is burned in muscle cells to produce energy. The role of alpha-lipoic acid in generating
energy may have been best illustrated in the recent treatment of a 33-year-old Italian woman with a genetic defect
interfering with her production of adenosine triphosphate (ATP), which acts as an energy-storage molecule in cells.
As a child, the woman had been thin, weak and intolerant of exercise. By her early 20s, she had developed
eye-muscle disorders and droopy eyelids. In her early 30s, she had weak arm and leg muscles. A biopsy and other
tests confirmed that her muscle cells were producing inadequate levels of ATP.

Doctors at the University of Bologna, Italy, gave the woman 200 mg of alpha-lipoic acid three times daily for
several months. She felt better, and tests showed an increase in her muscle-energy levels. Treatment with
alpha-lipoic acid also resulted in higher energy reserves in her brain, probably by increasing sugar metabolism and
raising ATP production.

Preventing Macular Degeneration

Can the leading cause of blindness in people over 65 be averted by antioxidants? What about zinc, lutein and
vitamin C?
By Michelle Badash

It's been said that the eyes are the first to go. As we get older, one experience we commonly share with others in our
age group is deteriorating vision. "Macular degeneration," an eye disease affecting the central part of the retina,1
has recently been the focus of a lot of research--possibly because so many of us are now approaching the time of
life when our eyes cease to see as well as they used to.

In the United States, macular degeneration is the leading cause of severe loss of vision, even legal blindness, in
people over 65. It affects about 6 percent of Americans between the ages of 65 and 75, and accounts for 14 percent
of all new cases of blindness, with 16,000 cases reported annually.2 Prevalence is slightly higher among women,
while it is rarely found in people of color. Although its causes have not yet been determined, some scientists
speculate that frequent exposure to sunlight and smoking may contribute to the disease's development.

What Is Macular Degeneration?
Macular degeneration occurs when the cells of the macula, which is the central portion of the retina, become
damaged and stop functioning. The retina is a thin layer of light-sensitive tissue that stretches across the back of the
eye. It functions like a screen onto which all visual images are projected. The role of the macula is to view complex
images. It allows us to focus on objects directly in front of us; enables us to see fine detail during activities such as
reading, writing,
sewing and driving; and determines our ability to distinguish color.


There are several types of macular degeneration. One is called juvenile macular dystrophy. It's a fairly rare,
inherited form of the disease that may occur in children or young adults. Another less common form, called pigment
epithelial detachment, is caused by a blister formation under the retina. In general, however, the two most common
forms of macular degeneration are termed "wet" and "dry," and occur primarily after age 60.

Dry: The most prevalent, and less serious, form of macular degeneration
(accounting for approximately 85 percent of all cases) is "dry," characterized by
a gradual loss of central vision. The process may occur over a period of several
years and can affect one or both eyes. The deterioration may be related to
general atrophy or, in certain cases, caused by deposits of drusen, a yellowish
substance that accumulates under the retina.

Typically, the symptoms of this form of macular degeneration include blurriness
when reading, difficulty in seeing objects that are far away, or shape distortion
(such as a tree appearing bent or crooked). Some people may also notice a
dark spot in the center of an object, or find that colors and sizes vary in each eye.

Wet: The "wet" form of macular degeneration is caused by abnormal blood
vessel growth behind the retina that may leak or bleed and cause the retina to
separate from the eye. These abnormal blood vessels are called subretinal
neovascular membranes, and their proliferation results in a rapid loss of vision.
Occasionally, the dry form of macular degeneration may develop into the wet
form.

Although both wet and dry forms drastically diminish visual acuity, neither result
in complete vision loss. Furthermore, peripheral vision is not affected.

At this time, there is no treatment for the dry form of macular degeneration. If the
wet form is detected in its early stages, laser surgeries are recommended in
certain cases; however, it is estimated that within one year up to 50 percent of the
laser lesions may experience regrowth of new blood vessels.3 Laser treatment
seals the abnormal blood vessels to prevent further bleeding and growth--it does
not restore vision. In addition to laser treatment, there are some experimental
forms of surgery that actually remove the abnormal blood vessels. However,
these procedures are still considered quite risky.

Given the fact that macular degeneration causes significant vision loss in
thousands of people each year, and that there are few treatment options, a
pertinent question is: Can supplements help prevent the progression of this
debilitating condition?

For some time, researchers have been investigating the possibility that
antioxidants may be able to combat--or prevent--macular degeneration. Why?
The answer lies in the fascinating physiology of the eye.

How The Eye Works

The eye functions much like a camera. A lens system at the front of the eye
collects and focuses light rays. The iris (the colored part of the eye) acts as an
aperture, and the retina may be compared to film that captures the images.
When light rays reach the retina, they are converted into electrical nerve signals,
then sent through the optic nerve to the brain.

To perform these functions, a host of nutrients are needed to nourish the eye.
For example, antioxidants such as vitamins C and E, beta-carotene and lutein,
as well as zinc, selenium and copper, are all found in the macula. In addition to
providing nourishment, these antioxidants protect against free radicals, which
inevitably form as a result of all the activity generated by the eye. David
Newsome, M.D., of the Tulane University School of Medicine in New Orleans, is
the author of several studies on macular degeneration. He notes, "Where the
oxygen-containing environment is especially rich and the metabolic rate is high,
as in the macula, oxidative free radicals are generated plentifully."4

In addition to the wear and tear of chemical activity, the constant processing of
light, particularly blue and ultraviolet, can cause photo damage to the eye. One
interesting theory is that melanin, which is present in the skin and also
contributes to the color of the eye, helps absorb wavelengths of light and acts as
an antioxidant by protecting against free radical damage. Consequently, people
with green or blue eyes and light skin are more likely to experience macular
degeneration than people with dark eyes or skin. Newsome observes that
melanin may be the protective factor.5

The bottom line is that researchers believe antioxidants may help stave off
some of the harmful oxidative processes that result from the eye's many
chemical reactions. This theory is based on an understanding of how
antioxidants function in other parts of the body, as well as in the eye.

It has been observed in several studies that people who have macular
degeneration tend to have low levels of certain types of antioxidants in their
blood. However, the research gets fuzzy when it tries to pinpoint which
antioxidant is most--or least--beneficial. One study noted that low levels of
lycopene (an antioxidant found in tomatoes) was most strongly linked with the
development of macular degeneration.6

Carotenoid Protection

Another study focused on the positive role that carotenoids seemed to play in
preventing macular degeneration--particularly lutein and zeaxanthin, both found
exclusively in dietary sources such as dark green leafy vegetables (e.g., kale
and spinach).7 Researchers are intrigued by these two carotenoids because
they are important to macula function. The foveal part of the retina (a depression
in the center of the macula) has a yellow pigmentation that is composed
primarily of lutein and zeaxanthin. Given that these carotenoids are present in
large quantities, researchers suspect that their role is significant, although the
mechanism for their functioning has not yet been determined.

It is also unclear whether a cause-and-effect relationship exists between the
dietary intake of carotenoids and their absorption in the body. Interesting clues
suggest that men and women may actually use these carotenoids differently.
One recent study found that men showed a 38 percent higher macular pigment
density than women, despite matching carotenoid blood levels.8 More research
is needed to determine the functions of lutein and zeaxanthin and their potential
role in preventing macular degeneration.

Another nutrient that has garnered interest as a potentially beneficial infection
fighter is the trace mineral zinc. While results concerning antioxidants are still
sketchy, research results from zinc studies are slightly more conclusive.

Zinc is highly concentrated in the retina and tissues surrounding the macula.
More than 100 different enzymes rely on zinc to function, and it is instrumental in
many chemical reactions in the retina.9 As with antioxidants, zinc also helps to
protect cell membranes from free radical damage.

Several studies have found that zinc does seem to provide some protective
benefits against certain types of macular degeneration, most notably the early
stages of dry macular degeneration. However, zinc does not appear to affect the
wet form of macular degeneration. According to a recent study of nine patients
who had the wet form of macular degeneration in one eye, no improvement
occurred when they were given zinc supplements.10

Since macular degeneration generally occurs in the later stages of life, it's
important to consider how dietary factors could contribute to its development. It is
a well-known fact that many elderly people eat diets that are low in antioxidants.
Furthermore, food sources that are rich in zinc, such as meat and seafood, may
also be eaten in reduced amounts for many reasons: They're relatively
expensive; they're more difficult to store; they're subject to spoilage; and they
can be hard to digest. Even if they do eat zinc-rich protein sources, many elderly
people experience reduced output of stomach acid (achlorhydria).
Consequently, their bodies' ability to absorb sufficient levels of zinc, as well as
antioxidants, may be compromised.

Although current research does not provide strong conclusive evidence to
support the potential role of antioxidants and zinc in preventing macular
degeneration, many physicians and ophthalmologists do recommend
supplementing with these nutrients if it is not contraindicated by other health
conditions. In the case of zinc, however, patients must be instructed not to take
more than the recommended levels (50 mg/day) to avoid toxicity and possible
interference with absorption of other trace minerals such as copper. Zinc is also
not advised for patients who are taking blood-thinning medications such as
coumadin .

Last year, a study heralded as a "breakthrough discovery" in macular
degeneration research was published in Science. Study authors discovered a
cluster of genetic mutations believed to cause nearly one-sixth of all macular
degeneration cases.11 These mutations affect a particular gene that if mutated
causes cells to produce a protein that helps destroy the macula.

This is one of the first concrete findings in macular degeneration research.
Further studies are needed to explore how nutritional interventions and other
methods, such as photodynamic therapy, may be combined to treat the disease.

Michelle Badash has 12 years of experience working at a nutrition
research center in Boston. She has written and edited a newsletter
about nutrition research and is also a free-lance writer.

Preventing Macular Degeneration:
Where The Nutrients Are

beta-carotene: Carrots

Copper: Nuts, mushrooms, salmon, lentils, oats

Selenium: Broccoli

Vitamin C: Oranges

Vitamin E: Almonds, wheat germ, sunflower seeds

Zinc: Oysters, wheat bran, sesame seeds, soybeans

Lycopene: Tomatoes

Lutein: Spinach and kale.


REFERENCES

1. "Consumer's Guide to Macular Degeneration."
http://www.eyecare.org/consumer/disease/md.html

2. Ibid.

3. "Wet Age-Related Macular Degeneration." http://
www.iex.net/eol/retinal/wet_amd.html

4. Newsome, D. "The role of antioxidants in macular
degeneration: An update." Ophthalmic Practice, 12(4):
169-71, 1994.

5. Ibid.

6. Mares-Perlman, J.A., et al. "Serum antioxidants and
age-related macular degeneration in a population-based
case-control study." Archives of Ophthalmology, 113(12,
15): 18-23, December 1995.

7. Seddon, J.M., et al. JAMA, 272: 1413-20, 1994.

8. Hammond, B.R., et al. "Sex differences in macular
pigment optical density: Relation to plasma carotenoid
concentrations and dietary patterns." Vision Research,
36(13): 2001-12, July 1996.

9. "Nutrition and Macular Degeneration." http://www.
eyenet.org//public/faqs/nutrition_faq.html

10. Stur, M., et al. "Oral zinc and the second eye in
age-related macular degeneration." Invest Ophthalmol Vis
Sci, 37(7, 12): 25-35, June 1996.

11. Allikmets, R., et.al. "Mutation of the stargardt disease
gene (ABCR) in age-related macular degeneration."
Science, 277(5333): 1805, Sept. 19, 1997.

================================================== ==================


Brain Function And Memory

Recently, Manas Panigrahi, Ph.D., of the National Institute of Mental Health and Neurosciences, India, described
how alpha-lipoic acid prevented "reperfusion injury" after strokes were induced in a group of laboratory rats.
Reperfusion injury is caused by the production of a large number of free radicals when oxygenated blood is restored
to deprived tissues. In the brain, it typically occurs after a stroke, cerebral hemorrhage or head injury. And in the
heart, it occurs after a heart attack or coronary artery bypass surgery.
(Note: Pyruvate also prevents reperfusion injury and DNP causes release of huge amounts of free radicals)

In an experiment, animals receiving alpha-lipoic acid before a stroke had one-third the death rate of animals who did
notreceive the supplements. The animals getting alpha-lipoic acid also fared substantially better than those receiving
the antioxidant glutathione, according to an article by Panigrahi.8 An experiment on reperfusion injury to the heart
found similar benefits from alpha-lipoic acid.9

Alpha-lipoic acid also seems to protect brain cells against some hazardous chemicals. Two years ago, researchers at
the University of Rochester Medical Center reported that the nutrient prevented the neuron-damaging effects of
excess N-methyl-D-aspartate or NMDA. The researchers wrote that the effect "suggests a possible role of these
endogenous compounds in the treatment of acute and chronic neurological disorders," such as Parkinson's and
Huntington diseases.10

Alpha-lipoic acid might also improve memory in the elderly, if one extrapolates from another animal study.
Researchers at Germany's Central Institute for Mental Health, Mannheim, described how large doses of alpha-lipoic
acid were ineffective with young mice; in aged mice, however, long-term memory improved.

"The lack of any treatment effect in young, treated mice suggests that alpha-lipoic acid compensates age-related,
long-term memory deficits rather than improving memory in general," the researchers wrote.11

AIDS And Cancer

Excessive production of free radicals can promote over-activation of nuclear factor kappa-B (NF-kB),11 a protein
that functions as a nuclear transcription factor and appears to play a role in inflammation, gene changes leading to
cancer, and eplication of the human immunodeficiency virus (HIV). A number of antioxidants block NF-kB. In a
cell-culture study, Yuichiro J. Suzuki, Ph.D., of the University of California, Berkeley, found that cells bathed in
alpha-lipoic acid could inhibit the activation of NF-kB and, subsequently, HIV replication.12

Conclusion

The properties of alpha-lipoic acid are strikingly similar to other antioxidants, as is its essential role in cellular
energy production along with Co-Q10 and carnitine. What makes alpha-lipoic stand out, however, is its remarkable
versatility. Packer has at various times described it as the "metabolic," "universal" and "ideal" antioxidant. Coming
from a leading scientist, instead of an advertising copywriter, such words are particularly meaningful.

Although recognition of alpha-lipoic acid as a potent antioxidant is relatively recent, the pace of research on this
nutrient has increased since the late 1980s. According to Packer, alpha-lipoic acid supplements are easily absorbed
and may be preferable to the major dietary source of the nutrient, which is red meat. Alpha-lipoic acid supplements
have been approved and used for the treatment of diabetic neuropathy in Germany, and experience suggests that it is
safe and only rarely poses
side effects.

"The therapeutic potential of alpha-lipoic acid is just beginning to be explored," observed Packer, "but this
compound holds great promise."

Jack Challem is based in Aloha, Ore., and has been writing for health magazines for 20 years. He also publishes his
own newsletter, The Nutrition Reporter, which summarizes recent medical journal articles on vitamins.


You WILL breathe harder on DNP.

In taking the pyruvate, glycerin, and taurine; should they be taken at one time during the day, or split up over the
day? Split by 3.

Also, I have been doing aerobic exercise in the morning on an empty stomach. Would you still reccomend this
while on DNP? My thinking is that you would not, but I wanted to ask your opinion. What would your suggestion
be in relation to aerobics in the morning.
While on DNP, that probably wouldn't be the best thing to do, but it really depends on your intensity. Never hurts
to burn some more calories.

I
When you speak of taking the glycerine, taurine, and pyruvate while "on" DNP, do you mean take it only on the
days I take capsules, or take it on the days "in between" in addition to the days I take capsules? You just take the
glycerine while on the DNP. You should be taking taurine all the time already. Pyruvate may help with additional
fat loss in the weeks after DNP, too

Also, how much Taurine is 3g, I don't have a scale.
0 cap holds about 500mg, 00 holds about 750mg
The same problem with pyruvate. 00 holds 300mg and 000 holds 400mg.

Why is it that you say to avoid fructose? I've heard that quite a few times, and was curious why. How important is
this? Fructose resupplies the liver with glycogen first, if the liver is full, then via the pentose phosphate pathway, all
additional fructose goes to fat.

As formaltodextrin, have you ever tried the stuff from proteinfactory.com?
They have a pretty good price at $2.50 a pound.
Should be 1.50 or so which you can get at a beer supply store.

What would your price be on Taurine?
Bulk? I don't have time to cap them.

Anarchy in the USA!.
Do you think it would be a good idea to bike on an empty stomach, THEN take my DNP dose AFTER the ride?
Just don't want to go to the gym at 5:30a.m. and fall out from doing a medium intensity ride. Then one of the
trainers would probobly shit his pants or something.
That would be better as DNP can cause your stomach to burn at times as well.
When you speak of taking the glycerine, taurine, and pyruvate while "on" DNP, do you mean take it only on the
days I take capsules, or take it on the days "in between" in addition to the days I take capsules? You
just take the glycerine while on the DNP. You should be taking taurine
all the time already. Pyruvate may help with additional fat loss in the
weeks after DNP, too

Well, what I meant was this: Should I take the glycerin EVERYDAY while
on the DNP experiment (looking at 4-8wks), or take it only on the days I
take capsules (considering that you say to only take DNP caps EVERY
OTHER day). I ask this because i thought you stated that the half-life
of DNP is 36hrs, if that is the case, i should be TAKING glycerin
everyday, right?
Yes take the glycerin everyday.
>Also, how much Taurine is 3g, I don't have a scale.
>0 cap holds about 500mg, 00 holds about 750mg
>The same problem with pyruvate. 00 holds 300mg and 000 holds 400mg.
Is capping Taurine the ONLY way to take it? I know that Phosphagen HP
has taurine in it, and it is just in powder. Can it be thrown into a
protein/carb drink? That is what I meant when I asked about How much
taurine is 1g or 3g. Could the taurine be put into the
glycerine/kool-aid mix? If so, I could take them all at once since each
is taken 3 times daily.
Yea, you could throw them in there and I will measure out how much taurine is in a teaspoon for y
I was also wondering this about the pyruvate because I am planning on
mixing it into a paste w/flax oil. I was wondering how much 3g would
be, or 5g. I was planning on mixing the paste in the morning and just
taking it throughout the day--3 times. Probobly mixing it in with a MRP
or just protein drink. Could the paste sit all day (refrigerated, of
course)?
1 tablespoon of flax will hold about 3g of pyruvate. Any more pyruvate and it gets chunky!
I saw on the 'feeling good' that you reccomend glutamine. How much? I
currently take 10g-15 of glutamine a day. I throw some powder into my
shakes after my workout (an MRP) and before bed (usually just protien
powder & milk or water).
That should be good.
Bulk is what I was asking about. You can see my thoughts on it.
I have to look up what I paid for it, and will tell you when I tell you how much a teaspoon is.
Anarchy in the USA!


Guess I'm burning a lot of cals at the moment.
> What am I gonna need to do when I come off of DNP/t3? Will I need to
> taper off to get my thyroid back online, or will it happen by itself?
> Or is it only low because I am taking DNP? What is the deal here? You> know, I don't want to have to take
thyroid med. for the rest of my
> life!! Whatever you can tell me regarding this would be VERY helpful.
This is why I only like to recommend 1week on DNP. DNP reduces t4-t3 conversion and the thyroid reads that and
increases T4 output so when you stop the DNP you get MORE of your own thryoid for the following week! Now,
when you add T3 your thryoid reads that and reduces T4 output so when you stop the diet you have LOWER T4
which means lower T3.
If you only do it for a week you will be alright and then do a high carb diet for three days at 600g carbs a day and
you will be alright.
This is why I recommend pyruvat. It seems that the pyruvate keeps the conversion going so temp never drops.

> You could drop the glycerol and substitute taurine. >I like the pyr because it is such a good
ant-oxidant >AND it may keep the t4-t3 online.
I've already ordered the pyr. & glycerol, so I'll be using both...how much more effective do
you think adding the taurine be? (How about MCT's like duchaine has reccomended in the past?)
You want to burn fat so I don't know why you would want to take in more. I never noticed any advantage when I
took them in the past with other diets. Taurine will help keep your electrolytes balanced.

> Do you max for the first two days until you start to >sweat and then you can switch to the 36
hour >regimen.
>
Could you clarify this?...does it mean 400mg b/f bed for 2 days then 400mg every 36hrs?..or
split up into 2-200mg doses? If you max is 800 then you do 200 every 6 hours or so.

> And how many days in a row do you suggest taking >it? Only seven to get the thyroid back to
normal if >not on pyruvate.
Seven is the norm and if you are on pyruvate your thyroid will still go down at the end of the second week.
>
If on pyr. (which I'll be) would 10 days be alright or pushing it?
That would be fine

And what do you suggest for training (cardio) and calorie levels?
Eat as normally as you can and depending how much you can bear the sweat cardio can remain normal as well.
thanx for your time...

>>Also, someone mentioned a post you had about "How to use 600mg of DNP
a
I already sent the DNP and the manual is basically a longer form of the 600mg on DNP.

What sizes do you make caps in?
100-400mg sizes
I am currently taking 600mg/day, and was thinking about upping the dose. Would I go to 700 or 800?
800 as it is not a great rise percentage wise.
Since I ordered from you before, what will the price be per cap for 100 caps?
Would you find out how much a 1/2 gal of glycerin would cost me
shipped?? JOKER won't get off his ass and find out about some for me (his bro-in-law is a vet).
I can ship up to four pounds PM for under $6 so « gal would weigh about 3 plus whatever else you order.
This stuff is great! Using it, I have lost over 20lbs in 3wks. I got sick (with a cold) and stopped, but am planning
on starting it again after the symptoms subside.
Good to hear.
For the recarb pd you told me about (to use after basal temp decreases), how important is it to stay away from
fructose during that pd? You can use it, but you only want so much of it and if youdrink soft drinks and juice it will
work.
I had Hell getting that many carbs (600g) in a day without resorting to stuff like sweetened cereal and soft
drinks/juices. Actually, once I just ate "normal" for 3 days with no DNP and my temp came back up.
I know that fructose is stored b4 any other sugar b/c of its structure, but is that really that bad? A carb is a carb,
whether it comes from glucose or fructose, right?
No, because if the liver is fully carbed then all subsequent fructose goes directly to fat.
If I am burning as many calories as I do on DNP, what does it matter where the carbs come from. If they ARE
deposited in the liver/muscle, won't they just be broken down when the body needs sugar?
Yes.
I could be way off here, so enlighten me. What is the deal? Will SOME fructose hurt me very much in order to
keep my blood sugar up?
No, but you are trying to keep your liver carbed up.
Not RELYING on it, but having some (in things like juice, soft drinks, sports drinks, etc., and for taking creatine--I
use powerade mix to get carbs for the insulin spike).
If you have around 300-400 cal a day from fructose you will be ok.
What is the deal with the poisons produced in the body from use of DNP?
It's free radicals.
We actually talked about it in my Biochem class the other day, and my prof said that things like cyanide and azide
are produced in the body during use of DNP.
I'd like to come in and tell him a thing or two! Since when does the body produce it's own cyanide! HAHA! Ask
him what the mechanism is for that one!
I kinda thought that this was the major reason for such high doses of antioxidants.
Yes.

Macro added some stuff:

posted 12-03-00 09:21 PM
MIGHT I ADD SOMETHING

I COULD NOT FIND MY ORIGINAL POST ON DNP, THOUGH ANIMALS ARTICLE, WHICH I BELIEVE HE HAS COPYRIGHTED, COVERS MOST OF THE SAME CONTENT.
HERE ARE SOME OTHER POSTS- THAT MIGHT BE OF INTEREST
IF YOU HAVE ANY SPECIFIC QUESTIONS POST THEM
GOVERNMENT ANALYSIS OF DNP AND MACRO'S COMMENTS
you will find my comments in ALL CAPS

What are dinitrophenols?
(Pronounced die ni'tro fe' nolz)
Dinitrophenols are a class of manufactured chemicals that do not occur naturally in the environment. There are six different dinitrophenols.
The most commercially important dinitrophenol, 2,4-dinitrophenol (DNP), is a yellow solid with no smell. It is used in making dyes, wood preservatives, explosives, insect control substances, and other chemicals, and as a photographic developer.
DNP DOES SMELL-VERY STRONG- KIND OF LIKE CHERRY WOOD
It was used in diet pills in the 1930s but was banned for this use in 1938. It may be sold under several trade names, including Caswell No. 392, Sulfo Black B, and Nitro Kleenup. Use of trade names is for identification only and does not imply endorsement by the Agency for Toxic Substances and Disease Registry, the Public Health Service, or the U.S. Department of Health and Human Services.
What happens to dinitrophenols when they enter the environment?
DNP enters the air, water, and soil during its manufacture and use.
It may be formed from reaction of other chemicals in the air.
DNP may also enter the environment through landfill and storage tank leaks, or accidental spills during manufacture or transport.
It dissolves slightly in water, and does not easily evaporate to air.
It can be broken down slowly in water and soil by small organisms or by reacting with other chemicals.
DNP sticks to particles in water, which will cause it to eventually settle to the bottom sediment.
DNP also sticks to some types of soil particles, which may prevent it from moving very deep into the soil with rainwater.
DNP probably does not build up significantly in fish.
How might I be exposed to dinitrophenols?
Breathing contaminated workplace air where it is manufactured or used.
Breathing contaminated air from DNP-containing waste sites, waste incineration, or automobile exhaust.
Touching contaminated soil or water near DNP-containing waste sites.
Ingesting contaminated soil or water near DNP-containing waste sites.
DONT FORGET ENCAPUSLATING AND CONSUMING IT

How can dinitrophenols affect my health?
Most of the information on the health effects of dinitrophenols comes from old studies of patients who were prescribed diet pills containing dinitrophenol before it was banned.
Deaths have occurred in people who ingested 3-46 milligrams of dinitrophenols per kilogram of body weight per day (3-46 mg/kg/day) for short periods, or 1-4 mg/kg/day for long periods. WHILE THIS MAY BE TRUE THEY DIED FROM DEHYDRATION, HYPERTHERMIA, AND STARVATION/EXTREME LOW BLOOD SUGAR, ETC..- ALL OF WHICH CAN BE AVOIDED WITH PROPER NUTRITION, SUPPLEMENTS AND EATING- DONT FORGET THOSE CARBS. Also, people who breathed air containing 40 mg dinitrophenols per cubic meter of air (40 mg/m3) for long periods have died.
The amount of dinitrophenols ingested that causes harmful effects varies among people. Increased basal metabolic rate (the rate that you use energy at complete rest)- MAKES YOU LOSE FAT, increased sweating- DEHYDRATES YOU- WHY YOU TAKE GLYCEROL AND 2 GALLONS OF WATER MIN., a feeling of warmth, weight loss-WHY MOST PEOPLE TAKE IT, and increased heart rate-THIS IS NOT TRUE-EXCEPT IN CASES WHERE LOW BLOOD SUGAR RESULTS IN THE RELEASE OF GLUCAGON,ETC.., breathing rate-INCREASED RESPIRATION IS A NORMAL FUNCTION OF INCREASED METABOLISM, and body temperature have been observed in people who swallowed as little as 1 mg/kg/day or as much as 46 mg/kg/day for short or long periods of time.
Ingesting 2-4 mg/kg/day DNP for short or long periods has caused cataracts in some people-ONE PERSON-THEY HAVE ONE ANECDOTAL CASE- WHICH REMARKABLY, WHEN COMPARED TO THE DNP INGESTING POPULATION, IS THE SAME AS AMONG THE GENERAL POPULATION-STILL WE TAKE EXTRA ANTIOXIDENTS- JUST IN CASE, while ingesting 1-4 mg/kg/day for short or long periods has caused skin rashes and decreases in white blood cells.-I HAVE SEEN NO RESEARCH THAT POINTS THIS OUT BUT SKIN RASHES WERE PROBABLY DUE TO LESS FATTY ACIDS FOR SKIN MAINTANANCE AND SOME ALLERGIC REACTIONS
How likely are dinitrophenols to cause cancer?
The Department of Health and Human Services (DHHS), the International Agency for Research on Cancer (IARC), and the EPA have not classified dinitrophenols for carcinogenicity. FOR GOOD REASON DNP HAS BEEN SHOWN TO NOT BE CARCINOGENIC
There are no studies available in people or animals on the carcinogenic effects of dinitrophenols.
WELL AREN'T WE LITTLE LIARS- THERE HAVE BEEN CANCER STUDIES IN ANIMALS 6 MONTHS AT HIGH EXPOSURE LEVELS IN MICE- NO CARCINOMAS
Is there a medical test to show whether I've been exposed to dinitrophenols?
Tests are available that measure the amount of DNPs or their breakdown products in blood, urine, and samples of tissue from the body. However, these tests may require special equipment and may not be available in your doctor's office.
Has the federal government made recommendations to protect human health?
The EPA recommends that not more than 70 parts of dinitrophenols per billion parts of water (70 ppb) be present in lakes or streams used for swimming.
The EPA lists DNPs as hazardous air pollutants (HAP) under the Clean Air Act. The EPA also requires that discharges or spills into the environment of 10 pounds or more be reported.
SOME EXTRA POINTS DNP IS ANTI PROTEOLYTIC- MUSCLE SPARING-
DNP IS STILL DANGEROUS IF TAKEN INCORRECTLY AND/OR WITHOUT THE PROPER PREPARATIONS. ITS USE IS NOT AN UNDERTAKING THAT SHOULD BE ENTERED INTO WITHOUT CONSIDERABLE KNOWLEDGE AND RESEARCH- KNOWLEDGE IS POWER.
heres a short list of supplements
feel free to add any other antioxidents
200mg alpha lipoic acid 3x a day with meals
1200-1500mg magnesium in 2-3 divided doses.
2-3000mg vitamin C.
1200IU of vitamin E
200mcg of selenium.
1000-2000mg of calcium (can’t take it with the magnesium, though. Take it before bed)
Melatonin if you can’t sleep and it is also one of the best and cheapest anti-oxidants.
50mg of zinc a day
one iron tab as hemoglobin is a protein as well.
A potassium gluconate tab or two a day
Taurine at 3g a day.
Glutamine at 15g-20g a day .
1 table spoon glycerol 3 x a day
at least 2 gallons of water
a fan to point at your head while sleeping- or at work- basically anytime you can point a fan at you
personally I take a lot of supplements
i usually exceed those dosages and I take other antioxidents
including about
500mg grapeseed extract
300mg cranberry extract
600-900mg of green tea
and a good mulit vitamin-twinlab dualtabs
BTW- EC+1g of tyrosine 3x per day and 20mg of yohimbine topically 2x per day- for added energy and fatburning effects
DNP WHY IS THE LD-50 SO LOW
all of the mortality studies that have been done with dnp have been done on animals. LD50 is the dose that is considered to be lethal to 50% of the population. However, when one looks at the studies and the inferences that people, including duchaine, have made, you will find that such inferences are completely erroneous. They have based their dosing and life threatening parameters of DNP ingestion on studies done on organisms incapable of changing their behaviour to cope with the effects of DNP.
Here is some of the reasons why.
can you tell a rat he needs to triple or quadruple his water consumption?
even if the water is available will a rat force himself to drink it? like a human could
do rats take glycerol?
do they take antioxidents?
do they have fans to point at their heads?
can they lower the dosage if they feel its too strong for them?
can they turn up the AC?
can you see some of the fallacies of such studies-if not I will be sure to continue.


PEACE

MP

 

[muscleup]

well I read the first paragraph......Seems intersting. One day I will read it all.

Thanks

 

[rtnhrtnh]

Disgustingly massive repost, but it's a good idea to flag it for attention right now. Props.

 

[CRsteve]

Click click, saved to favorites. I was going to comment on it last time it was posted in the other DNP thread, but now is as good a time as any. Suggested read to all, even if DNP isn't on your list of near-future supps. (it's not on mine, but I'm curious).

 

[bicepts101]

real good post...i read up untill the testimonials....real nice info...ide like to hears macros comments on it though

 

[curgeo]

I put macros comments as of when that post was written in bold. This was a very fine article by both him and animal.

 

[curgeo]

a bump for those that may not have seen it already!

 

[OMEGA]

curgeo lol

funny screen name

 

[curgeo]

Curious George was already taken. Came over to check on me huh?....LOL

 

[OMEGA]

yes I did

I think Curgeo is cool