Anabolic Steroid, HGH, IGF, Insulin and Ancillary Profiles

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Insulin

Insulin is a hormone produced in the pancreas which helps to regulate glucose levels in the body. Medically, it is typically used in the treatment of diabetes. Recently, insulin has become quite popular among bodybuilders due to the anabolic effect it can offer. With well-times injections, insulin will help to bring glycogen and other nutrients to the muscle.

In America, regular human insulin is available without a prescription by the name of Humulin R by Eli Lilly and Company. It costs about $20 for a 10 ml vial with a strength of 100 IU per ml. Eli Lilly and Company also produces 5 other insulin formulations, but none of these should be used by bodybuilders. Humulin R is the safest because it takes effect quickly and has the shortest duration of activity. The other insulin formulations remain active for a longer period and can put the user in an unexpected state of hypoglycemia.

Hypoglycemia occurs when blood glucose levels are too low. It is a common and potentially fatal reaction experienced by insulin users. Before an athlete begins taking insulin, it is critical that he understands the warning signs and symptoms of hypoglycemia. The following is a list of symptoms which may indicate a mild to moderate hypoglycemia: hunger, drowsiness, blurred vision, depressive mood, dizziness, sweating, palpitation, tremor, restlessness, tingling in the hands, feet, lips, or tongue, lightheadedness, inability to concentrate, headache, sleep disturbances, anxiety, slurred speech, irritability, abnormal behavior, unsteady movement, and personality changes. If any of these warning signs should occur, an athlete should immediately consume a food or drink containing sugar such as a candy bar or carbohydrate drink. This will treat a mild to moderate hypoglycemia and prevent a severe state of hypoglycemia. Severe hypoglycemia is a serious condition that may require medical attention. Symptoms include disorientation, seizure, unconsciousness, and death.

Insulin is used in a wide variety of ways. Most athletes choose to use it immediately after a workout. Dosages used are usually 1 IU per 10-20 pounds of lean bodyweight. First-time users should start at a low dosage and gradually work up. For example, first begin with 2 IU and then increase the dosage by 1 IU every consecutive workout. This will allow the athlete to safely determine a dosage. Insulin dosages can very significantly among athletes and are dependent upon insulin sensitivity and the use of other drugs. Athletes using growth hormone can thyroid will have higher insulin requirements, and therefore, will be able to handle higher dosages.

Humilin R should be injected subcutaneously only with a U-100 insulin syringe. Insulin syringes are available without a prescription in many states. If the athlete cannot purchase the syringes at a pharmacy, he can mail order them or buy them on the black market. Using a syringe other than a U-100 is dangerous since it will be difficult to measure out the correct dosage. Subcutaneous insulin injections are usually given by pinching a fold of skin in the abdomen area. To speed up the effect of insulin, many athletes will inject their dosage into the thighs or triceps.

Most athletes will bring their insulin with them to the gym. Insulin should be refrigerated, but it is all right to keep it in a gym bag as long as it is kept away from excessive heat. Immediately after a workout, the athlete will inject his dosage of insulin. Within the next fifteen minutes, he should have a carbohydrate drink such as Ultra Fuel by Twinlab. The athlete should consume at least 10 grams of carbohydrates for every 1 IU of insulin injected. Most athletes will also take creatine monohydrate with their carbohydrate drink since the insulin will help to force the creatine into the muscles. An hour or so after injecting insulin, most athletes will eat a meal or consume a protein shake. The carbohydrate drink and meal/protein shake are necessary. Without them, blood sugar levels will drop dangerously low and the athlete will most likely go into a state of hypoglycemia.

Many athletes will get sleepy after injecting insulin. This may be a symptom of hypoglycemia, and an athlete should probably consume more carbohydrates. Avoid the temptation to go to bed since the insulin may take its peak effect during sleep and significantly drop glucose levels. Being unaware of the warning signs during this slumber, the athlete is at a high risk of going into a state of severe hypoglycemia without anyone realizing it. Humulin R usually remains active for only 4 hours with a peak at about two hours after injecting. An athlete would be wise to stay up for the 4 hours after injecting.

Rather than waiting to the end of a workout, many athletes prefer to inject their insulin dosage 30 minutes before their training session is over and then consume a carbohydrate drink immediately following the workout. This will make the insulin more efficient at bringing glycogen to the muscles, but it will also increase the danger of hypoglycemia. Some athletes will even inject a few IUs before lifting to improve their pump. This practice is extremely risky and best left to athletes with experience using insulin. After the injection, they will consume a carbohydrate drink and then have breakfast within the next hour. Some athletes find this application of insulin very beneficial for putting on mass, while others will tend to put on excess fat using insulin in this way.

Insulin use cannot be detected during a drug test. For this reason, along with the fact that it is cheap and readily available, insulin has become a popular drug among the competitive athlete. However, before an athlete attempts to use insulin, he should educate himself and make himself aware of the consequences. One mistake in dosage or diet can be potentially fatal.

Insulin safety

1. Do not use slin alone have a training partner or girlfriend who's not using slin hang around with you from the time you take the slin to about 2.5/4 hrs after.

2. Tell you're partner to look for anything out of the norm for your personality and have a list of questions like your ssn or address etc that they can ask you. Don't joke around, and answer them without ****, because if you cant answer or refuse to answer it could be a sign of hypoglycemia(low blood sugar). Symptoms of hypoglycemia include disorientation, headache, drowsiness, weakness, dizziness, fast heartbeat, sweating, tremor, and nausea.

3. If you cant/wont answer or are feeling the symptoms of hypoglycemia they should be prepared to feed you carbs like pancake syrup, coke, sugary stuff. I bought glucose tablets at walmart. kinda like candy but gets in the blood faster and dissolve quickly. these are for diabetics ask at the pharmacy.

4. Have your partner know that if they suspect low blood sugar and cant convince or force you to consume carbs until your better. CALL 911 and ask for an ambulance and tell the truth to the operator... that they suspect you are in insulin shock and explain when they get there(the ambulance guys not the cops) that you are not diabetic but using insulin for anabolic purposes. Have the type of slin, the dosage and carbs consumed recorded to give the paramedic. They will save your life. Then you refuse transport to the hospital and eat. It might be a good idea to make sure your house is "clean" before every workout just in case the bad thing happens and the cops ask a lot of questions.

5. Why so much preparation for the possible problem?? insulin can kill you in minutes if you go down!!

6. Take the carbs and protein together immediately after injecting the slin(dont take chances trying to time out 15 min after injection). Take the protein with the carbs because the protein is pushed into the muscles with the slin also(creatine too).

7. Before an hour passes you should eat a normal balanced meal(high protein low fat with carbs).

8. Consume another small high protein medium carb low fat meal at 2.5 hours after the injection. Congrats you lived.(keep some gatoraid on hand just to make sure because your not gonna have a lifeline)

9. YAWN... Don't go to sleep within 4/6 hours of using insulin since you can develop hypoglycemia while asleep and not have warning signs

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CYTOMEL - Liothyronine Sodium

Cynomel is a synthetically form of the natural thyroid hormone 3, 5, 3' triiodothyronine, which has all the pharmacologic activities of the natural substance. Clinically, Cynomel had been often utilized in efforts to have treated Hypothyroidism, which is a thyroid insufficiency, as well as other secondary symptoms such as obesity, metabolic disorders, and fatigue. Thyroid hormones had been characteristically believed to have been able to have exerted most of their actions through the control of protein synthesis. When moderate amounts of Thyroid hormones had been administered, they had been able to have increased the synthesis of RNA and protein, which had often been followed by an increased basal metabolic rate; as well as having stimulated the oxidative enzy;;ne systems. This, in turn, had enhanced the release of free fatty acids from adipose tissue, and had increased the intestinal absorption and peripheral utilization of glucose. When higher concentrations had been apparent, this had generally resulted in the decrease of protein synthesis, and in the increase of the breakdown of glycogen, lipids and protein.

The Cynomel compound closely had resembled the natural thyroid hormone, Tricodide-thyronine (L-T3), and under normal circumstances, the thyroid usually had preduced two hormones, L-thyroxine (L-T4) and L4riiodine 4hyronine (L-T3). However, the latter hormone, had been much stronger and more effective of the two, and had been approximately 4 times as potent as L-T4 on a weight basis.

When Cynomel had been administered orally, it had been readily available to the body tissue with approximately 95% of the dose being absorbed within 4 hours from the gastrointestinal tract. The biological half-life of Cynomel had been approximately two and a half days, with the maximal pharmacologic response having occurred within 2 or 3 days. This characteristic had also provided for an early clinical response, as the onset of activity had usually ocatired within a few hours.

Several seff-amninistering athletes had generally claimed that the synthetic compound of Cynomel had been able to have produced the same processes in the body, as if the thyroid had been able to have to produced more of the hormone. Consequently, this entity had allowed Cynomel to have been more effective than the compound of Eutirox or Tiroidine,56 which had been other commercially available L-T4 compounds that had been currently available in Mexico.

Many athletes had taken advantage of these characteristics which had been able to have stimulated the metabolism, which in turn, had resulted in a faster conversion of the macronutrients of carbohydrates, proteins, and fats. B~ybuilders, had been especially interested in increased fatburning (lipolysis) entities of the compound of Cynomel. Cynomel had been often utilized by competing bodybuilders several weeks prior to competition, as it had aided in having maintained an extremely low fat content, without the extremes of a starvation diet. This distinctive feature also had made it very popular amongst female athletes, due to the fact that women generally had slower metabolisms than men. Administration of Cynomel had allegedly allowed for the ridding of bodyfat, without a drastic caloric restriction. This also had perinined many athletes to have been able to have remained on high calorie diets with the added advantage of having maintained a "ripped" appearance. Athletes who had utilized Cytomel over several weeks, often had experienced a decrease in muscle mass, which had been discovered to have been avoidable or at least delayed, by the simultaneous intake of steroidal compounds, and by the consumption of a protein rich diet.

Another advantage which several athletes who had administered low dosages of Cynomel had claimed to have experienced, had been that the simultaneous intake of steroidal compounds had appeared to have become more effective. This possibly may have occurred as a result of the faster conversion of protein. Although some athletes still had utilized the administration of Cynomel, it had not been nearly as popular as it had once appeared to have been. Spiropent, and Ephedrine (the latter is currently not available in Mexico), had emerged to have had employed the same accelerating metabolism effects, with other added advantages such as possible strength and muscle increases. The combination however, of Cynomel and Spiropent, or Ephedrine (the latter is currently not available in Mexico), had allegedly appeared to have had enormously accelerated lipolysis

Doses: 1-5 tablets/ day (25mcg)
Side effects: none "with proper use"
Strength & Mass gains: None
Cutting: Verry good & Excellent fat burner

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DNP - 2,4-Dinitrophenol

DNP (2,4-Dinitrophenol), an industrial chemical with various applications, has gained steady popularity as a fat loss tool. Boasting an astounding 50% increase in metabolic rate, it is able to contribute to reported fat losses of 10-12 pounds in 8 days of use. Classified as an "uncoupler of oxidative phosphorylation" medically, it is quite dangerous as there is no negative feedback system that may deal with overdoses. Specifically, there is no upper limit to the increase in body temperature that may be obtained with its use.

Introduction/History
With summer approaching, competitive bodybuilders and many others are beginning their quest for leanness. Used by the hardcore since Dan Duchaine's reporting of it a couple years ago, DNP (2,4-Dinitrophenol) has managed to steadily gain popularity as a powerful tool for weight loss. Interestingly, DNP was first used to ignite TNT in the early 1900’s. In 1931 a study released by Stanford University declared that DNP was able to cause amazing weight loss; subsequently it found its way into many diet potions and medications; regulation was much less strict during this time than the present, and many of these products were available over the counter. Two years later DNP was banned by the FDA as a dieting agent due to its inclusion in many OTC dietary supplements. The FDA was a new organization at this time and acted in a rather brazen manner, with the absence of any set procedures for taking substances off the market. Granted, there was only a 1% incidence of cataracts over a large population (around 100,000); nonetheless it happened (although interestingly, exclusively women). However, there are now ways to counter this which will be covered thoroughly.
The comparisons to the current drugs used for dieting are astounding, at least in terms of thermogenesis. While the ECA stack has been shown to provide approximately a 3% increase in metabolic rate, DNP can deliver a relatively controlled 50% elevation in resting metabolic rate. The thermogenic aspect of clenbuterol, while sometimes overestimated due to the high CNS stimulation that yields a "wired" feeling, can vary according to prior exposure to various amphetamine-like compounds and certainly is not much greater than that of ECA. DNP does not have the anorectic effects of ephedrine or other thermogenic agents; rather, it tends to increase hunger, particularly appetite for carbohydrates. This problem is easily solved with appetite suppressants, and one may even use ECA itself for this purpose while on DNP.

Molecular Basis for Efficacy
DNP accomplishes the astounding boost in metabolic rate via inhibition of the F0F1 ATP synthase molecule, located in the inner wall of each mitochondrion. While the electron transport chain still functions to pump hydrogen ions into the intermembrane space, the coupling of the proton gradient to ATP production is rendered impossible by DNP. As a result, ATP production is dramatically reduced, and the energy is instead thrown off as heat. This results in an astounding production of heat; when using dinitrophenol, the athlete will radiate so much heat that it is uncomfortable to be within any proximity of them. Luckily, this heat does not fully contribute to body temperature increases, and is instead thrown off from the entire body surface, particularly the head. As a result, adequate doses of DNP will usually only elevate body temperature by about 1-1.5ºC. This is a good thing for your central nervous system and other delicate tissues; if the heat produced by ATP contributed in a more direct matter to body temperature, effective doses for fat loss would cause supraphysiological body temperature increases on a level unwitnessed at this time. Nonetheless, overheating is a very real danger; this and other side effects shall now be addressed.

Risks/Side Effects
Hearing all of these wonderful things probably has you wondering what the side effects and risks are. They are quite formidable and contribute to making DNP one of the most intolerable (though effective) drugs used in bodybuilding. Starting with the most significant, and descending in importance, are the following risks and side effects of DNP use.

Risks:
Overheating - There is no upper limit to DNP's body temperature increase, meaning that one may literally "cook from the inside" if they take too much. Dosage considerations will be given later, but even an overdose of 4-6 times the recommended dosage may be lethal. Much smaller overdoses may result in damage to the brain and/or other body systems.
Carcinogenesis - Phenols in general are reputed to be carcinogenic. Although 2,4-dinitrophenol has never been implicated in a cancer diagnosis, some are nonetheless concerned, and understandably so. In addition to the inherent carcinogenic potential caused by its status as a phenol, production of free radicals and the release of various compounds stored in adipose tissue stores during DNP's rapid oxidation of fat may also potentially be harmful.

Side Effects:
Discomfort and sweating - This is the single most noticeable effect of DNP use, both by the user and those around him/her. Even in the winter, while indoors at ambient temperatures, one may expect his or her shirt to be completely soaked through with sweat. Those with jobs requiring formal or semi-formal apparel are advised to consider other means of fat loss (or a new job, if preferred). Other obvious considerations lie in the areas of social life, personal appearance, etc. and the user must prioritize.
Insomnia - Second in frequency of reports to sweating and discomfort is insomnia; this may be at least partially attributed to discomfort. Possible means of countering this include such supplements as Valerian root or melatonin. Alternatively, one may deal with this via prescription or OTC sleep medications or GHB-A precursors. However, these may be addictive if used on a regular basis and if their use may be avoided, by all means abstain from using them.
Yellow bodily fluids - Some don't notice this, but others find that all of their bodily fluids take on a yellowish appearance. Urine is a darker yellow, and even semen and girl thingyl secretions may be affected. According to current knowledge, this is not known to be harmful in and of itself.
Muscle Soreness - This is yet another thing that may be minimized via cerebral function. Dan Duchaine has recommended using a weight such as to allow no fewer than 15 reps per set of any weight training workout; judging from anecdotal reports and personal experience, this seems to be good advice. Low levels of ATP are a cause of muscle soreness in and of itself; the additional factor of encumbered recovery mechanisms make extreme soreness (and if not careful, catabolism) quite possible.
Allergic Reactions – These are highly individualized but may be summarily discussed. Various reactions are common with DNP use, and approximately 10% of users will be extremely allergic to it. Allergic reactions can include hives, blisters, and/or inexplicable rashes. If you suffer any of these side effects, and they are extremely bothersome, it is the recommendation of the author to cease usage immediately. If so desired, another trial may be made at a later date with a lower dosage, but do not attempt to continue the drug cycle at that point.
Carbohydrate Cravings - To counter this, some methods will be touched on later. As with most diets, willpower is sometimes the single most important factor.


Obtaining DNP and Making Capsules
If, given these considerations, you still are ready to take the plunge and use DNP, you will need to learn how to obtain and/or make your own capsules. DNP is shipped industrially in large metal tins holding a glass jar containing the wet DNP, which is wetted with enough water to total 15-35% of total mass to prevent explosion while in transit. Ample cushioning material around the glass jar is included to further prevent ignition of DNP (it is highly flammable) and the obvious possibility of breaking the jar. Chemical sellers will not sell this chemical to individuals or any other entity without an account. However, if you are resourceful enough to get some, the following are instructions on how to properly prepare capsules.

A) Extreme caution is necessary when making the caps. DNP is bright yellow and will even go through gloves. This stain will not go away for up to 2 weeks. If it does get on your hands or other parts of yoru house, you can usually get it off with 2(3H) Furanone dinitro (butyrolactone). It usually will come out of clothes with laundering.

B) Care is of the utmost importance when measuring out the amount one would need. Dan recommends 5 to 8 mg/kg bodyweight in Dirty Dieting #0, assuming that the person is under 15% BF. He subsequently told me that he was really suffering on 6-8 mg/kg, and that is excessive in his opinion. Note that the calculation is bodyweight, not lean body mass. With the exception of obese persons, this method is sufficiently accurate.

C) Obtain a reliable scale, a Cap M. Quik device, and some size "O" caps ($60-$200 minimum, approximately $10, and $2 respectively). Corn starch, available at the grocery, is also needed. Since DNP ships at about either 15% or 35% water by weight, it is necessary to dry out the material overnight before attempting to deal with it. No matter how dry it looks, this step is absolutely necessary for accurate dosing.

D)The next day, mix 15 grams DNP with 10 grams corn starch, and pound it into a fine powder. Spread resulting mixture into the Cap M. Quik, finish the capping process, and you have 50 caps of 300mg potency. Repeat as above with 10 g DNP and 15 g corn starch in order to make 50 caps of 200mg each, or with 12.5g DNP and 12.5g corn starch to make the same number of 250mg caps.

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DNP - 2,4-Dinitrophenol Continued...

Bear in mind that the preparation process, in the absence of a laboratory equipped with a chemical hood, will destroy the immediate area. It gets in the air, and fine particles will stain everything. Wear clothes that are dispensable, at least 2 pairs of gloves, and a fume mask. Preferably, do this outside on an extremely calm day, or alternatively, place protective covering everything in sight if it is necessary to perform the encapsulation indoors.

Timetable of Effects and Symptoms
The following table describes the condition most users will find themselves in during a typical DNP cycle; it is by no means complete and mainly intended to drive home that users typically look at their best 3-5 days following cessation of DNP use.

Day - Effects

1
None; possibly elevated carbohydrate cravings and/or temperature elevation.
2
T4-T3 conversion has begun to decrease; lethargy possible. Temperature should be elevated, and radiation of heat is noticeable.
3-5
Body temperature is elevated, with all the effects that one expects from DNP use. In addition, water retention usually becomes manifest here.
6-8
Definite water retention, along with other symptoms of use; user most likely feels fatter due to having "flatter" muscles (mainly the result of glycogen depletion) and holding water. Final DNP dose taken in the evening of Day 8.
9-10
DNP is clearing the system slowly. All symptoms are still present.
11-12
Water should be gone by now, or getting there. Mild diuretics will expedite this. The user will probably notice perceived greater cardiovascular and muscular endurance.
13-14
This is when someone tends to look their best. Their glycogen stores are usually compensated at this point and the retained water should be gone.

Dosing Schedule
As touched on previously, getting the right dosage of DNP is rather easy to do although the importance of proper dosage cannot be overstated. It is far better for one to err on the side of too little rather than too much, certainly in the case of the novice who does not know if they are allergic to the substance. As stated before, the commonly used dosage by bodybuilders and other reasonably lean persons is 3-5mg/kg of bodyweight. This would mean that a 100-kilogram bodybuilder would use anywhere from 300-500mg per day. Experienced users commonly are found using up to 800mg/day relatively safely, and beginners sometimes find that they enjoy 3-5 pounds of fat loss per week with as little as 200mg/day. Dosing is highly individualized and most generalizations tend to collapse quite quickly; as a result, none will be attempted. Start on the low end of the scale and see how you react. It is not recommended to take more than 300mg at any one time; a larger man taking 600mg per day should divide the dose into a 5:00PM portion and another portion taken approximately 30 minutes before bedtime. Someone taking 300mg/day could easily take one dose in the evening. The typical cycling program is to do 7 or 8 days on, followed by 7 or 8 off; this should not decrease thyroid output dramatically and makes use of T3 (triiodothyronine, brand name Cytomel) unnecessary in most cases. T4-T3 conversion does decrease dramatically in the liver due to excessive heat; this begins within 24 hours of the first dose. However, there is usually adequate active thyroid hormone to make it through 8 days of using it while maintaining elevated body temperature. After approximately 3-5 days, the user may find themselves with a waking temperature that is no longer elevated, even though they are still using DNP. This is due to the decrease in T3 and may signal the necessity of either the use of exogenous T3 in subsequent cycles or shorter cycles of the drug. In addition, the schedule given works nicely because the user is able to enjoy the anabolic rebound effect on a relatively regular basis. Also, longer cycles might leave the muscle fibers in a state of relative dehydration and "starved" of ATP for too long; both of these readily contribute to catabolism.

Supplementation
While using DNP, supplements can greatly aid both in the effectiveness of the therapy and the comfort of the user. Of particular importance are antioxidants and the following quantities are recommended:

Magnesium (1500mg)*
Vitamin C (3000mg in divided doses)*
Vitamin E (1200 IU in divided doses)*
Glutathione (200mg in divided doses)***)
NAC (various amounts)**
T3 (dose according to personal preference)**
Calcium (2000mg not taken with the Magnesium)
5-HTP (if not on antidepressant medication) (various amounts)****
Meridia, Redux, or Fenfluramine (various amounts)****
Hydroxycitric Acid (particularly in the evenings to curb cravings)****
Pyruvate (2-6g/day in divided doses)
Glycerol (3 tbsp/day in divided doses)
Alpha-Lipoic Acid (500-1000mg daily in divided doses)

Key:

* = Integral component of DNP program
** = Of questionable (although possible) importance)
*** = Of particular importance to women for prevention of cataracts
**** = For the purpose of appetite suppression (may not be needed)

Practical Considerations
Given all of this information, there are nonetheless more things to know before you undertake your first DNP cycle. The following tips and tricks gathered from personal experience and consultations with users are presented for your aid:

Aim a fan at your head at night. Your head is the most precious thing on your body and is a prime site for heat loss. Any air flowing over it will aid in cooling via convection.

Wash your bedding daily. It is a good idea to have some spare pillowcases on hand, if nothing else. Most likely, you will be sweating profusely while you sleep, and this will make your bed smell as enticing as a locker room. Cleanliness is also essential in the prevention of disease, not to mention the fact that you are breathing out DNP "fumes" all night and they collect on your bedding.

Prevention of disease goes beyond washing your clothes, and includes all of the normal precautions that you would make to avoid infection, although in a more exaggerated way. DNP depletes your body of energy needed to battle pathogens and weakens your immune system, leaving you ripe for infection and incapable of fighting off most diseases once they have taken hold.
This is rather intuitive, but be certain to wear loose, light clothing, preferably of a light color.

Proper hydration is necessary – I have personally consumed up to 8 liters of water per day. Glycerol specifically aids in muscle hydration, so its use may be very important, particularly when considering that muscle cells in even a semi-dehydrated state are prime sites for catabolism.

Cardiovascular work while on DNP – This is a strange issue that I have been asked about regularly, but am undecided in the direction to take and generally recommend that the user decide for themselves. My personal preference is to do cardio with a fan focused on me for 30-35 minutes at a relatively high intensity. This is an area for personal preference; barring other considerations, just see if you can handle it or not and go from there. Always be ready to stop if you feel yourself getting extremely overheated or weak.

Diet - One may wonder why this issue receives such limited attention; after all, most methods of fat loss require a restrictive diet of some nature. However, there is no set diet that one must use to achieve good results with dinitrophenol, only certain factors that allow the user to decide intelligently how to eat:

Insulin - DNP blunts the effects of insulin; this is a huge boon for dieters because insulin blocks lipolysis and causes the storage of adipose tissue. This means that carbohydrate intake does not need to be strictly limited, although it should stay reasonable for optimal results.
Body Temperature and Comfort - A general guideline is that the more carbohydrates eaten, the hotter the user will get while on DNP. Similarly, overfeeding also produces extreme heat; any excess calories are thrown off as heat quite readily. For this reason, along with certain hormonal factors, Duchaine espouses an Isometric diet while on DNP, and I have followed this personally with good results.
CKD's - These are extremely impractical while on a cyclical ketogenic diet (CKD), and are especially dangerous. This brings up blood glucose considerations; it is important to try to maintain relatively stable, or at least not severely depressed, blood glucose levels. If this guideline is not followed, the user may experience blurred vision and/or extreme fatigue possibly augmented by fainting or lightheadedness.

Anabolic rebound effect – I still remember the first time I spoke to Dan Duchaine regarding DNP, and he told me about what, at the time, seemed impossible. But I have experienced this phenomenon, and it indeed happens. Possible causes include, but are not limited to, either an anabolic effect from glycogen supercompensation-induced cellular expansion, or due to increased mitochondrial density. Increased mitochondrial density is an adaptive mechanism of the body and takes place surprisingly quickly in the presence of an uncoupler such as DNP (or anything else that inhibits oxidative phosphorylation). Whatever the mechanism of the anabolic rebound effect may be, the user can expect to gain about 5-7 pounds of intramuscular water or muscle and lose about the same amount of subcutaneous and intraperitoneal water within a week after their last DNP dose. This is probably the most pleasant aspect of using DNP; the user not only experiences unrivaled fat loss, but also enjoys a fair amount of hypertrophy without any other supplements or drugs. Muscle retention, and possibly gain, is improved with careful attention to several previously discussed considerations such as proper hydration and intelligent cycling.

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CLENBUTEROL

- is attractive for it's pronounced thermogenic effects as well as mild anabolic properties.

A number of medical reviews have cited its outstanding potential to promote muscle gains as well as fat loss and weight loss. There have been an increasing number of American bodybuilders that are experimenting with this drug.

Many athletes who use Clenbuterol claim that it promotes dramatic strength increases and a very noticeable reduction in body fat and weight loss.
Some athletes claim that they enjoyed significant gains in muscle mass while using clenbuterol. Clenbuterol's most valid application seems to be as a pre-contest, cutting drug. It is not banned by any athletic committee; thus, numerous professional bodybuilders have used it for the last month of contest preparation. Cycles range from 6-12 weeks in length. Side effects include nervousness, tremors of the hands, headaches, and insomnia. The reason although it is fairly anabolic, and it promotes the burning of fatty acids through brown fat burning.

Dosages are normally between 20-120 mcg for bodybuilders that use this.This drug becomes ineffective for its anabolic properties after 18 successive days of use. Brown fat-burning and Weight Loss, will continue past the 18 day period. After 12 weeks, the drug should be discontinued for a couple of months. lthough there is quite a bit of medical literature showing clenbuterol's potential as a bodybuilding drug, most of these studies have been done on animals; very little human data on this issue is available. Therefore, in assessing its effects in humans, you have to rely primarily on empirical and anecdotal evidence. And until recently, there has been little of that available. However, with the recent wide scale use of clenbuterol by athletes, we can now gather quite a bit of evidence on what the real world effects of clenbuterol are in weight trainers.

To say that clenbuterol use is rampant in bodybuilding right now would be an understatement. Thousands and thousands of athletes are using this drug. I personally know a number of pro football players, foreign Olympic athletes, and professional bodybuilders who are using clenbuterol. In addition, I have received feedback from at least 200 other athletes who have experimented with this novel compound. Generally, the feedback from clenbuterol users is that the drug produces dramatic body composition alterations. One Canadian strength coach compared the results he has seen in athletes using clenbuterol to what one might experience while using a stack of Anavar and Halotestin. Within weeks of beginning clenbuterol therapy, many athletes notice a significant strength increase and a dramatic reduction in body fat. The results that occur secondary to clenbuterol administration seem to occur equally in men and women as well as young and old.

The trick to using clenbuterol successfully seems to be avoidin receptor downgrade which occurs rapidly with the use of this beta agonist. In fact, one clinical study s owe at receptor downgrade as much as 50% is experienced after using clenbuterol for as little as 18 days consecutively. This same study showed that attenuation can be avoided if clenbuterol is taken in a 2 day on 2 day off pattern. Athletes using clenbuterol in this manner have reported much greater results than those who use the product continualy which seems to support the theory that attenuation can be at least partially avoided by staggering the dosage. Athletes have also made a habit of cycling clenbuterol in an effort to minimize side effects as well as prevent receptor downgrade. Average cycle length on clenbuterol is 8-10 weeks with a 4-6 week off period.

Doses: 3-7 tablets a day (20mcg)
Side effects: None or minimum
Strength & Mass gains: None
Cutting: Great! + Excellent fat burner

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Ketotifen

I see a lot of newbie people trying to find good info on this so I thought it would be best to put it all in one place. I patched this from a wide range of sources as well as my own experience (also thanks to FONZ). This truly is a wonderdrug for BB.

What Is It?
Ketotifen is very safe antihistamine used extensively in Europe to treat bronchial asthma and allergies. It is also being studied as a treatment for colitis. When used for asthma, weight gain and an increase in appetite are among the most frequent side effects. Ketotifen also protects the cells in the stomach, small intestine and perhaps the rest of the gut from a number of toxins. A number of case studies suggest that it may be helpful treating skin problems such as acne. Ketotifen also reduces edema (swelling and puffiness caused by water retention) around sores.

Ketotifen Studies
German researchers have published data showing that ketotifen lowers tnf-alpha in the test tube. One study used ketotifen in combination with oxymethadone, a steroid like Megace that helps people gain weight, so it is hard to gauge what effect ketotifen had (the study notes a 14% reduction in TNF-alpha levels and weight gains of 11-12 pounds in less than four weeks). A larger placebo controlled study of this combination is underway. The other study used ketotifen by itself in eight patients with elevated TNF-alpha, (but no wasting). Taking ketotifen for 12 weeks, these patients gained an average of six pounds, had increases in their body cell mass and reductions in their TNF-alpha levels.

Side Effects and Toxicity
Ketotifen is virtually non-toxic (although it is not advised for patients with epilepsy). People who took twenty times the recommended dose (in suicide attempts) suffered no serious consequences (other than embarrassment). Its primary side effects seem to be temporary drowsiness, dry mouth,(and other mucuos membranes) appetite stimulation and weight gain.

Dosing and side effects
No studies have been done to find the most effective dose but the German researchers used 4 mg ED. Dan Duchaine (who discovered ketos use for BB) suggested 10mg ED but in my experience this much is not needed and makes u far too sleepy. I find that 3-4mg ED seems ideal. However, much higher doses have been shown to be quite safe with no adverse affects other than increased drowsiness and appetite – it will make u hungry for solid foods. You can take it divided in the day or all at once.

Ketotifen and Clen
Clenbuterol is a beta 2 agonist which has a limited anabolic effect during its first few days of use and afterward is normally used to fight fat. At higher doses, however, it can be catabolic to muscle and it must be cycled on a 2 week on, 2 week of basis or the beta 2 receptors that clen binds to become saturated and down regulate.

Ketotifen’s magic is that it upregulates the beta-receptors including the beta 2s that clen uses. As long as you are taking ketotifen, it will continue to clean these receptors, never allowing them to downregulate – even while on a heavy clen cycle. That means you can continue to take clen indefinitely without having to cycle off to regenerate the receptors. 2-3mg ED can upregulate even severely shut down receptors within a week.

It also means that you don’t need as much clen to get the same benefits. It seems u can take about 30-40% less clen and it be equally effective. FONZ posted that it also increases the number of receptor sites on the surface of the cell, allowing more clen to attach and perhaps this is the reason for the increased efficacy. Ketotifen also seems to lessen the sides of clen including the jitters.

Ketotifen and ECA
Perhaps an even better use for ketotifen is taking it with the ECA stack. While the thermogenic effect of ephedrine is not as potent as clen because it doesn't have a high receptor affinity, and it is not limited to beta-2 receptors. In fact it seems to have a good effect on beta 3 receptors as well, which act as a type of thermogenic messenger and over half of ephedrine effect is from beta-3 stimulation. Clen has almost no effect on beta 3 however. So by keeping the beta 2 receptors up, ketotifen can allow the benefits of continuous beta 2 and beta 3 stimulation from ephedrine.

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SPIRONOTHIAZ- Spironolactone/Hydrochlorthiazide

Spironothiazide is a diuretic. it is a combination of a potassium sparing diuretic, spironolactone (see also aldactone) and a thiazide. Thiazides, from their type, are similar to loop diuretics (see also Lasix). The main difference from loop diuretics is that thiazides lead to a lower release of calcium and have a less pronounced
and less drastic dehydrating effect.

Spironothiazide combines an aldosterone antagonist (see also Aldactone) with the stronger thiazid diuretic, making it a favorite and effective remedy for many competing body-builders to reduce excessive water. The advantage of this combina-tion, on the one hand, is that potassium reabsorption by the spironolactone can be compensated by the thiazide. This usually leads to a suspension of the potassium-linked side effects.

On the other hand, a good overall effect can also be obtained at lower dosages. Thus many use it as an alternative to the stronger and higher risk furosemides (Lasix). Spironothiazide is usually taken by athletes during the last days before a competition. Generally a dosage of 2-3 tablets of 50mg per day is taken and divided into 2-3 indi-vidual doses. The side effects are mostly caused by the expected imbalances in the fluids and electrolytes. These can manifest them-selves in muscle cramps, irregular pulse rate (especially at an increased potassium level) and dizziness.

In men, due to the antiandrogenic
characteristics of spironolactone, gynecomastia and impotence are also possible but unlikely due to the short intake (see also Aldactone). As a preventive measure, the additional adminis-tration of potassium should be avoided and the period of intake should be as short as possible. Spironothiazide must be prescribed and is usually difficult to find on the black market since most athletes get prescriptions from their physicians. Fifty tablets of 50/50 mg cost approximately $40 on the black market

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What is Clenbuterol?

Clenbuterol is a beta-2 agonist and is used in many countries as a broncodilator
for the treatment of asthma. Because of it's long half life, clenbuterol is not
FDA approved for medical use. It is a central nervous system stimulant and acts
like adrenaline. It shares many of the same side effects as other CNS stimulants
like ephedrine. Contrary to popular belief, Clenbuterol has a half life of 35
hours and not 48 hours.

Dosing and Cycling

Clenbuterol comes in 20mcg tablets, although it is also available in syrup, pump
and injectable form. It's also available as a powder in some areas. Doses are
very dependent on how well the user responds to the side effects, but somewhere
in the range of 4-8 tablets per day for men and 2-4 tablets a day for women is
most common. Clenbuterol loses its thermogenic effects after around 8 weeks when
body temperature drops back to normal. Its anabolic/anti-catabolic properties
fade away at around the 18 day mark. Taking the long half life into
consideration, the most effective way of cycling clen is 2 weeks on/ 2 weeks off
for no more than 12 weeks. Ephedrine or Yohimbine can be used in the off weeks.

Clenbuterol vs Ephedrine vs DNP

Ephedrine will raise metabolic levels by about 2-3 percent and 200mg of DNP
raises metabolic levels by about 30 percent. Clenbuterol raises metabolic levels
about 10 percent and it can raise body temperature several degrees.

DNP is by far the most effective fat burner but many people will never use it
because of the risks associated with it. It also offers no anti-catabolic
benefit. Although it does have anti-catabolic effect, ephedrine's short
half-life prevents it from being all that effective.

As far as side effects, Clenbuterol's are certainly milder than DNP's, and some
would even say milder than an ECA stack. There is no ECA-style crash on
Clenbuterol and many users find it easier on the prostate and sex drive. This
may in part be due to the fact that Clen is generally used for only 2 weeks at a
time.

Side effects

NAUSEA
NERVOUSNESS
DIZZINESS
DROWSINESS
DRY MOUTH
FACIAL FLUSHING
HEADACHE
HEARTBURN
INCREASED BLOOD PRESSURE
INCREASED SWEATING
INSOMNIA
LIGHTHEADEDNESS
MUSCLE CRAMPS
TREMORS
VOMITING
CHEST PAIN

The most significant side effects are muscle cramps, nervousness, headaches, and
increased blood pressure.

Muscle cramps can be avoided by drinking 1.5-2 gallons of water and consuming
bananas and oranges or supplementing with potassium tablets at 200-400mg a
day taken before bed on an empty stomach. Taurine at 3-5grams is a necessity in
minimizing cramps.

Headaches can easily be avoided with Tylenol Extra Strength taking at the first
signs of a headache.

Common Uses

Post-Cycle Therapy: Clen is used post cycle to aid in recovery. It allows the
user to continue eating large amounts of food, without worrying about adding
body fat. It also helps the user maintain more of his strength as well as his
intensity in the gym. Diet: Roughly the same as on cycle.

Fat loss: The most popular use for Clen, it also increases muscle hardness,
vascularity, strength and size on a caloric deficit. For the most significant
fat loss, Clen can be stacked with T3. Diet: A high protein(1.5g per lb of
bodyweight), moderate carb(0.5g to 1g per lb of bodyweight), low fat diet(0.25g
per lb of bodyweight) seems to work best with Clen.

Alternative to Steroids: Clenbuterol has mild steroid-like properties and can be
used by non-AS using bodybuilder to increase LBM as well as strength and muscle
hardness. Diet: A moderate carb, high protein, moderate fat diet work well.

Stimulant/Performance Enhancement: It can be used as a stimulant, but an ECA
stack may be a better choice because of it's much shorter half-life. Diet: To
take full advantage of the stimulatory effects of Clen, carbohydrates must be
included in the diet. Ketogenic diets do not work well in this case.

Precautions: Is Clen for you?

The same precautions that apply to Ephedrine must be applied to Clen, although
some people find ECA stacks are harsher than Clen. It should not be stacked
with other CNS stimulants such as Ephedrine and Yohimbine. These combinations
are unnecessary and potentially dangerous. Caffeine can be used in moderation
before a workout for an extra quick. burst of energy.

A word on Ketotifen

Ketotifen is safe antihistamine used extensively some European countries to
treat asthma and allergies. It can up regulate beta-2-receptors that Clen down
regulates. Basically, it allows users to extend their use of Clen for 6-8 weeks
at a time. 2-3mg a day is ideal, 10mg as found in "superclen" can make users
extremely drowsy. It also increases the effectiveness of Clen so doses must be
adjusted accordingly. The downfall of this drug is its ability to induce
extreme hunger is some people, which is not a desirable state to be in when
dieting.

Cycling Clenbuterol

Most users that report bad side effects and discontinue use are those who use
high doses right at the start of the cycle. The worst side effects occur within
the first 3-4 days of use.

A first time user should not exceed 40mcg the first day. Increase by one tab
until the side effects are not tolerable

Example of a first cycle:

Day1: 20mcg
Day2: 40mcg
Day3: 60mcg
Day4: 80mcg
Day5: 80mcg(Note: Increase the dose only when the side effects are tolerable)
Day6-Day12: 100mcg
Day13: 80 mcg (Tapering is not necessary, but it helps some users get back to
normal gradually)
Day14: 60 mcgs
Day15: off
Day16: off
Day 17: ECA/ NYC stack

Example of a second cycle:

Day1: 60mcg
Day2: 80mcg
Day3: 80mcg
Day4: 100mcg
Day5: 100mcg
Day6-Day12: 120mcg
Day13: 100 mcg
Day14: 80 mcgs
Day15: off
Day16: off
Day 17: ECA/ NYC stack

What else do I need to know?

Taurine MUST be used with Clen at 3-5g daily. Clenbuterol depletes taurine
levels in the liver which stops the conversion of T4 to T3 in the liver.
Taurine allows the user to avoid the dreaded rebound effect and painful muscle
cramps. It's a must with Clen.

Clenbuterol should not be taken too close to a workout. It can interfere with
your breathing and complete ruin your workout. When doing cardio, it's
advisable to stay at a consistent pace and avoid HIIT style routines.

Do not take Clen Past 4pm and drink plenty of water; 1.5-2 gallons a day.
Q: Will Clenbuterol show up on a drug test?

A: Only if you are being tested by a body that bans it. This is generally
international competition such as the Olympics. Employment, doctors physicals, military does NOT test for this


Drug Approximate Detection Time in Urine:
Alcohol 1-2 days
Amphetamines (crystal, Ice, crank, methamphetamines) 5-7 days
Barbituates Short-Acting (ie. secobarbital) 1-2 days
Barbituates Long-Acting (ie. phenobarbital) 2-3 weeks
Benzodiazepines (Librium®,Valium®,Serax,Xanax®) 2-30 days
Cannabinoids (THC,Marijuana) 20-90 days
Clenbuterol 2-4 days
Cocaine (Crack) 3-5 days
Codeine 2-5 days
Euphorics (MDMA, Ecstasy) 3-7 days
LSD 1-4 days
Methadone 3-5 days
Methaqualone (Quaalude) l-14 days
Opiates (heroin, Vicode, morphine, codeine) 2-7 days
Phencyclidine (PCP, Angel Dust) 1-30 days
Phenobarbital 10-20 days
Propoxyphene (Darvon) 1-3 days
Psilocybin (mushrooms) 3-5
Steroids (anabolic) oral 14 days

Courtousy of BIG ANDY & SWOLE

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Steroid Profiles from our old sticky

By BigGuns

below is a link to a site with good info on steroid profiles.

http://www.united-pharmacy.com/profiles.asp

Note: they also sell them, but I STRONGLY recommend you do not buy from them. Odds are...at best you will lose your money...at worst you get a new shiny pair of silver bracelets (and i'm sure Ironman would agree). The reason I'm posting this link is because it has very good profiles of different steroids i.e. what they are, what they do, etc. Just click on which one you want and learn about it.

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Thyroid Hormone for Weight Loss: Physiologic and Metabolic Effects


by Karl Hoffman

Introduction


It has been over 100 years since the discovery by Magnus-Levy that thyroid hormones play a central role in energy homeostasis, and 75 years since the hormones were first used for weight loss. Despite this great length of time, the precise mechanisms by which thyroid hormones exert their calorigenic effect are not completely characterized, and still actively debated. Despite numerous clinical studies having shown that the administration of thyroid hormone induces weight loss, it is not currently indicated as a weight loss agent. This is probably due to the number of side effects observed during thyroid hormone use at the relatively high doses used in the majority of obesity treatment studies. These deleterious effects include cardiac problems such as tachycardia and atrial arrhythmias, loss of muscle mass as well as fat, increased bone resorption and muscle weakness. Nevertheless, thyroid hormones, particularly triiodothyronine (T3) are a mainstay in the arsenal of drugs used by bodybuilders for fat loss. The widespread underground use of T3 warrants an understanding of its mechanism of action, as well as a knowledge of how it is most effectively and safely used, with an eye to minimizing side effects.



Thyroid Function and Physiology


Before jumping right into a discussion of the use of thyroid hormone for fat loss, a little review of thyroid function and physiology might be in order. The thyroid gland secretes two hormones of interest to us, thyroxine (T4) and triiodothyronine (T3). T3 is considered the physiologically active hormone, and T4 is converted peripherally into T3 by the action of the enzyme deiodinase. The bulk of the body's T3 (about 80%) comes from this conversion. The secretion of T4 is under the control of Thyroid Stimulating Hormone (TSH) which is produced by the pituitary gland. TSH secretion is in turn controlled through release of Thyrotropin Releasing Hormone which is produced in the hypothalamus. This is analogous to testosterone production, where GnRH from the hypothalamus causes the pituitary to release LH, which in turn stimulates the testes to produce testosterone.

In addition to T3, it has recently been recognized that there exist two additional active metabolites of T3: 3,5 and 3,3' diiodothyronines, which we will collectively call T2. Studies have shown that 3,3'-T2 may be more effective in raising resting metabolic rate when hypothyroid subjects are treated with T3, than when normal (euthyroid) subjects are given T3. Therefore in normal subjects 3,5-T2 may be the principal active metabolite of T3 (1)

Like the hypothalamic-pituitary-gonadal axis, the thyroid gland is under negative feedback control. When T3 levels go up, TSH secretion is suppressed. This is the mechanism whereby exogenous thyroid hormone suppresses natural thyroid hormone production. There is a difference though between the way anabolic steroids suppress natural testosterone production and the way T3 suppresses the thyroid. With steroids, the longer and heavier the cycle is, the longer your natural testosterone is suppressed. This is not the case with exogenous thyroid hormone.

An early study that looked at thyroid function and recovery under the influence of exogenous thyroid hormone was undertaken by Greer (2). He looked at patients who were misdiagnosed as being hypothyroid and put on thyroid hormone replacement for as long as 30 years. When the medication was withdrawn, their thyroids quickly returned to normal.

Here is a remark about Greer's classic paper from a later author:


"In 1951, Greer reported the pattern of recovery of thyroid function after stopping suppressive treatment with thyroid hormone in euthyroid [normal] subjects based on sequential measurements of their thyroidal uptake of radioiodine. He observed that after withdrawal of exogenous thyroid therapy, thyroid function, in terms of radioiodine uptake, returned to normal in most subjects within two weeks. He further observed that thyroid function returned as rapidly in those subjects whose glands had been depressed by several years of thyroid medication as it did in those whose gland had been depressed for only a few days" (3)

These results have been subsequently verified in several studies.(3)(4) So contrary to what has been stated in the bodybuilding literature, there is no evidence that long term thyroid supplementation will somehow damage your thyroid gland. Nevertheless, most bodybuilders will choose to cycle their T3 (or T4 which in most cases works just as well) as part of a cutting strategy, since T3 is catabolic with respect to muscle just as it is with fat. As previously mentioned, long term T3 induced hyperthyroidism is also catabolic to bone as well as muscle.

The proviso about T4 vs T3 for weight loss alluded to above needs some elaboration. There have been a number of studies that have shown that during starvation, or when carbohydrate intake is reduced to approximately 25 to 50 grams per day, levels of deiodinase decline, hindering the conversion of T4 to the physiologically active T3.(5) From an evolutionary standpoint this makes sense: during periods of starvation the body, teleologically speaking, would like to reduce its basal metabolic rate to preserve fat and especially muscle stores. However, a recent study demonstrating the effectiveness and safety of the ketogenic diet for weight loss recorded no change in circulating T3 levels.(6) So this issue not completely settled. Nevertheless, persons contemplating thyroid supplementation during ketogenic dieting might prefer T3 over T4 since the bulk of the research does suggest a decline in the peripheral conversion of T4 to T3 during low carb dieting.

Now that we have reviewed a little about thyroid function, let's consider just how it is that thyroid hormone exerts its fat burning effects.



Increased Oxidative Energy Metabolism


Thyroid hormone has long been recognized as a major regulator of the oxidative metabolism of energy producing substrates (food or stored substrates like fat, muscle, and glycogen) by the mitochondria. The mitochondria are often called the "cell's powerhouses" because this is where foodstuffs are turned into useful energy in the form of ATP. T3 and T2 increase the flux of nutrients into the mitochondria as well as the rate at which they are oxidized, by increasing the activities of the enzymes involved in the oxidative metabolic pathway. The increased rate of oxidation is reflected by an increase in oxygen consumption by the body.

T3 and T2 appear to act by different mechanisms to produce different results. T2 is believed to act on the mitochondria directly, increasing the rate of mitochondrial respiration, with a consequent increase in ATP production. T3 on the other hand acts at the nuclear level, inducing the transcription of genes controlling energy metabolism, primarily the genes for so-called uncoupling proteins, or UCP (see below). The time course of these two actions is quite different. T2 begins to increase mitochondrial respiration and metabolic rate immediately. T3 on the other hand requires a day or longer to increase RMR since the synthesis of new proteins, the UCP, is required (1).

There are a number of putative mechanisms whereby T2 is believed to increase mitochondrial energy production rates, resulting in increased ATP levels. These include an increased influx of Ca++ into the mitochondria, with a resulting increase in mitochondrial dehydrogenases. This in turn would lead to an increase in reduced substrates available for oxidation. An increase in cytochrome oxidase activity has also been observed. This would hasten the reduction of O2, speeding up respiration. These and a number of other proposed mechanisms for the action of T2 are reviewed by Lannie et al.(7)

What is the fate of the extra ATP produced during hyperthyroidism? There are a number of ways by which the increased ATP promotes an increase in metabolic activity, including the following:

Increased Na+/K+ATPase. This is the enzyme responsible for controlling the Na/K pump, which regulates the relative intracellular and extracellular concentrations of these ions, maintaining the normal transmembrane ion gradient. Sestoft(7) has estimated this effect may account for up to to 10% of the increased ATP usage.


Increased Ca++-dependent ATPase. The intracellular concentration of calcium must be kept lower than the extracellular concentration to maintain normal cellular function. ATP is required to pump out excess calcium. It has been estimated that 10% of a cell's energy expenditure is used just to maintain Ca++ homeostasis. (1)


Substrate cycling. Hyperthyroidism induces a futile cycle of lipogenesis/lipolysis in fat cells. The stored triglycerides are broken down into free fatty acids and glycerol, then reformed back into triglycerides again. This is an energy dependent process that utilizes some of the excess ATP produced in the hyperthyroid state (8). Futile cycling has been estimated to use approximately 15% of the excess ATP created during hyperthyroidism (8)


Increased Heart Work. This puts perhaps the greatest single demand on ATP usage, with increased heart rate and force of contraction accounting for up to 30% to 40% of ATP usage in hyperthyroidism (9)



Mitochondrial Uncoupling


As mentioned, the mitochondria are often characterized as the cell's powerhouse. They convert foodstuffs into ATP, which is used to fuel all the body's metabolic processes. Much research suggests that T3, like another much more potent agent DNP, has the ability to uncouple oxidation of substrates from ATP production. T3 is believed to increase the production of so called uncoupling proteins. Uncoupling protein (UCP) is a transporter family that is present in the mitochondrial inner membrane, and as its name suggests, it uncouples respiration from ATP synthesis by dissipating the transmembrane proton gradient as heat. Instead of useful ATP being produced from energy substrates, heat is generated instead. There are conflicting studies about the importance of T3 induced uncoupling. Animal studies have demonstrated an actual increase in ATP production commensurate with increased oxygen consumption as we discussed above. Other studies in humans have shown that in fact uncoupling in skeletal muscle does occur. This would contribute to T3 induced thermogenesis, with a resulting increase in basal metabolic rate.(10)

To make up for the deficit in ATP production (as well as provide fuel for the extra ATP production discussed above) more substrates must be burned for fuel, resulting in fat loss. Unfortunately, along with the fat that is burned, some protein from muscle is also catabolized for energy. This is the downside of T3 use, and the reason many people choose to use an anabolic steroid or prohormone during a T3 cycle to help preserve muscle mass. Studies have shown this to be an effective strategy (11). (Muscle glycogen is also more rapidly depleted, and less efficiently stored during hyperthyroidism. This may account for some of the muscle weakness generally associated with T3 use.)

Countering T3 induced muscle loss with AAS or prohormones makes sense from a physiological viewpoint as well. Thyroid hormone muscle protein breakdown is mainly mediated via the so-called ubiquitin-proteasome pathway. (12). (There are several independent metabolic pathways of protein breakdown in the body. For instance, another pathway, the lysosomal pathway, is responsible for the accelerated rate of muscle protein breakdown during and after exercise.) Testosterone administration has been shown to decrease ubiquitin-proteasome activity. (13) So AAS specifically target the muscle protein breakdown process stimulated by T3.

What may not be an effective strategy to maintain muscle mass during a T3 cycle is the use of exogenous growth hormone (GH). Studies have shown that when GH and T3 are administered concurrently, the increased nitrogen retention normally associated with GH use is abolished. This has been attributed to the observation that T3 increases levels of insulin like growth factor binding protein, reducing the bioavailability of igf-1 (14). Nevertheless, GH has fat burning properties independent of igf-1, so using GH with T3 would act additively to speed fat burning, but with little if any preservation of lean body mass. So again, if GH is used in conjunction with T3, anabolic steroid/prohormone use would be indicated.



Andregenic Receptor Modulation


Administration of T3 has been shown to upregulate the so-called beta 2 adrenergic receptor in fat tissue. What is the significance of this effect for fat loss? Before fat can be used as fuel, it must be mobilized from the fat cells where it is stored. An enzyme called Hormone Sensitive Lipase (HSL) is the rate-controlling enzyme in lipolysis, or fat mobilization. The body produces two catecholamines, epinephrine and norepinephrine, which bind to the beta 2 receptor and activate HSL. The upregulation of the beta 2 receptor due to T3 results in an increased ability of catecholamines to activate HSL, leading to increased lipolysis.

Bodybuilders often use drugs like clenbuterol, which bind to the beta 2 receptors and activate them in the same way as the body's endogenous catecholamines. The use of clenbuterol along with T3 can produce an additive lipolytic effect: T3 increases the number of receptors, while clenbuterol binds to the receptors activating HSL and increasing lipolysis. Since clenbuterol itself downregulates the beta 2 receptor, most bodybuilders use clenbuterol in a two week on/ two week off cycle, the rationale being that this minimizes downregulation and allows receptor recovery. Another option is to use the antihistamine ketotifen concurrently with the clenbuterol. Studies have shown that ketotifen attenuates the beta 2 receptor downregulation caused by clenbuterol (15). Moreover, research in AIDS patients has shown that ketotifen blocks the production of the proinflammatory and catabolic cytokine TNF-alpha (16). This may be of relevance to bodybuilders since there is evidence showing TNF lowers both testosterone and IGF-1 levels quite significantly (17) (18), while strenuous exercise elevates TNF levels. (19)

Besides increasing beta 2 receptor density in adipose tissue, T3 upregulates this receptor in human skeletal muscle (12). This has some very intriguing if somewhat speculative implications for the combined use of clenbuterol and T3. Animal studies have shown that catecholamines, particularly clenbuterol, inhibit Ca++ dependent skeletal muscle proteolysis (20). Like the lysosomal and ubiquitin-proteasome pathways discussed above, Ca++ regulated proteolysis is yet another way for the body to degrade muscle protein. Again the implications are enticing: Increased beta 2 receptor density from T3 use, coupled with the beta 2 agonist clenbuterol, could slow this pathway of muscle catabolism.

Another adrenergic receptor important to lipolysis is the alpha 2 receptor, which impedes fat mobilization by counteracting the effects of the beta 2 receptor. There are some conflicting studies about the effects of T3 on the alpha 2 receptor, with studies showing either a downregulation (21) or no effect (22). If T3 does in fact downregulate alpha 2 receptors, this would further aid lipolysis.

Studies in rats have shown that inducing hyperthyroidism increases the lipolytic beta 3 receptor density in white adipose tissue by 70% (23). Beta 3 receptors are abundant in human white adipose tissue as well, and if T3 administration has the same effect in humans, this could could contribute significantly to T3 induced fat loss. This might also argue for taking a currently available beta 3 agonist such as octopamine along with T3 and perhaps clenbuterol.



Decreased Phosphodiesterase Expression


In hyperthyroid patients as well as in normal subjects given T3, levels of the enzyme phosphodiesterase are lowered in fat cells (20). When lipolytic hormones like epinephrine (adrenaline) bind to the beta 2 receptor described above, they initiate a signaling cascade mediated by the so called “second messenger” cyclic AMP (cAMP). cAMP in turn acts on other cellular enzymes to initiate and maintain lipolysis. The original signal is terminated when cAMP is degraded by the enzyme phosphodiesterase. Clearly, maintaining elevated cAMP levels, by lowering phosphodiesterase concentrations with T3, will prolong lipolysis.

As an aside, caffeine is thought to exert at least a portion of its lipolytic action by lowering phosphodiesterase in fat cells. Interestingly, Viagra and Cialis are also phosphodiesterase inhibitors but their action seems to be limited to relaxing vascular smooth muscles.



Increased Growth Hormone Secretion


In vitro, animal, and human studies have all demonstrated that T3 administration increases growth hormone production. (24)(25) Since GH is calorigenic aside from any increase in igf-1, elevated GH may contribute to some of the fat burning associated with T3 administration. This effect may obviate the need for the use of expensive recombinant HGH, as mentioned above.



Decreased Insulin Secretion


Insulin is well known as a lipogenic hormone. It promotes fat storage by facilitating the uptake of fatty acids by adipocytes, and reducing lipid oxidation in muscle tissue. Several studies have shown that thyroid hormone is associated with glucose intolerance resulting from decreased glucose stimulated insulin secretion (26).

This defect in insulin secretion is believed to result from an increase in the rate of apoptosis (programmed cell death) of pancreatic beta cells as a direct effect of thyroid hormone excess.(27) This process is reversible, since when thyroid hormone is withdrawn the rate of beta cell replication increases until homeostasis returns. However, there are conflicting studies regarding the effects of T3 on insulin. For example, Dimitriadis et al (28) showed a decrease in glucose stimulated insulin secretion, consistent with (25), but an increase in basal insulin. They also observed increased insulin clearance, with a compensatory increase in basal insulin secretion.

So if in fact the hyperthyroid state is associated with lower insulin levels, this could explain a portion of hyperthyroid stimulated lipolysis. The obvious downside here is that insulin is also an anabolic hormone. Basal insulin concentration is thought to limit the action of the ubiquitin-proteasome degradative pathway of muscle protein breakdown (29). Of course supplementing with insulin during T3 use would be counterproductive. However, as mentioned above, anabolic steroids inhibit ubiquitin-proteasome activity, so their use could counter any loss in muscle anabolism resulting from a drop insulin levels.

[tribal]

Thyroid Hormone for Weight Loss: Physiologic and Metabolic Effects - Continued

The Future


As mentioned at the beginning of this article, a major roadblock in the adoption of T3 by the medical community as an antiobesity agent is its deleterious effect on the heart. Recent research has identified two isoforms of the thyroid hormone receptor, TRalpha and TRbeta. The TRalpha-form may preferentially regulate the heart rate, and an experimental agent, GC-1, has been developed that selectively binds the TRbeta receptor, with minimal effects on the heart (30). The distribution and actions of TRalpha and TRbeta throughout the body are not yet well characterized. However should it turn out that TRalpha is specific to the heart, then drugs like GC-1 may turn out to be effective fat burning agents with a much safer profile that T3 or T4.

One alleged “futuristic” agent that is here now is T2, or 3,5-Di-iodo-L-thyronine, the T3 metabolite discussed above. Unfortunately, this product does not live up to its hype. It has been claimed to be as or more effective that T3 for fat burning with minimal suppression of endogenous thyroid production. Regarding the relative effectiveness of T2 as a lipolytic agent, and its effect on TSH, this topic was thoroughly covered in a recent article by Bryan Haycock in Muscle Monthly.

All of my research into this subject has led me to the same conclusion reached by Mr. Haycock. That is, T2 is only slightly less suppressive of TSH than is T3, and only packs a portion of the lipolytic punch of T3, with no ability to increase the expression of the UCPs, which is a major determinant of the action of thyroid hormone.



Summary


We have discussed a number of ways by which T3, and its active metabolite T2 act to increase resting energy expenditure. Also discussed were some drawbacks of T3 use, such as cardiac stress, as well as the potential loss of muscle mass. It is ironic that the latter may be of more concern to many bodybuilders that the other more serious potential impacts on health. Nevertheless, used moderately and for short periods (a couple of months or less) in people with no preexisting cardiovascular disease T3 has a relatively safe medical profile, compared to other lipolytic agents like DNP. Perhaps most importantly we have presented substantial evidence that even the long-term use of supraphysiological levels of T3 does not damage the thyroid gland.


References:

(1) Endocrinology 2002 Feb;143(2):504-10 Are the effects of T3 on resting metabolic rate in euthyroid rats entirely caused by T3 itself? Moreno M, Lombardi A, Beneduce L, Silvestri E, Pinna G, Goglia F, Lanni A.

(2)(Greer,M. N Engl J Med 244:385, 1951)

(3)N Engl J Med 1975 Oct 2;293(14):681-4 Recovery of pituitary thyrotropic function after withdrawal of prolonged thyroid-suppression therapy. Vagenakis AG, Braverman LE, Azizi F, Portinay GI, Ingbar SH.

(4) J Clin Endocrinol Metab 1975 Jul;41(1):70-80 Patterns off recovery of the hypothalamic-pituitary-thyroid axis in patients taken of chronic thyroid therapy. Krugman LG, Hershman JM, Chopra IJ, Levine GA, Pekary E, Geffner DL, Chua Teco GN

(5) Int J Obes 1983;7(2):123-31 The effect of a low-calorie diet alone and in combination with triiodothyronine therapy on weight loss and hypophyseal thyroid function in obesity. Koppeschaar HP, Meinders AE, Schwarz F.

(6) Am J Med 2002 Jul;113(1):30-6 Effect of 6-month adherence to a very low carbohydrate diet program. Westman EC, Yancy WS, Edman JS, Tomlin KF, Perkins CE.

(7) J Endocrinol Invest 2001 Dec;24(11):897-913 Control of energy metabolism by iodothyronines.
Lanni A, Moreno M, Lombardi A, de Lange P, Goglia F

(8) Clin Endocrinol (Oxf) 1980 Nov;13(5):489-506 Metabolic aspects of the calorigenic effect of thyroid hormone in mammals. Sestoft L.

(9)Annu Rev Nutr 1995;15:263-91 Thermogenesis and thyroid function. Freake HC, Oppenheimer JH.

(10) J Clin Invest 2001 Sep;108(5):733-7 Effect of triiodothyronine on mitochondrial energy coupling in human skeletal muscle. Lebon V, Dufour S, Petersen KF, Ren J, Jucker BM, Slezak LA, Cline GW, Rothman DL, Shulman GI.

(11)J Clin Endocrinol Metab 1999 Jan;84(1):207-12 Testosterone administration preserves protein balance but not muscle strength during 28 days of bed rest. Zachwieja JJ, Smith SR, Lovejoy JC, Rood JC, Windhauser MM, Bray GA.

(12) Genome Res 2002 Feb;12(2):281-91 In vivo regulation of human skeletal muscle gene expression by thyroid hormone. Clement K, Viguerie N, Diehn M, Alizadeh A, Barbe P, Thalamas C, Storey JD, Brown PO, Barsh GS, Langin D.

(13) J Clin Endocrinol Metab 2003 Jan;88(1):358-62 Related Articles, Links Differential anabolic effects of testosterone and amino Acid feeding in older men. Ferrando AA, Sheffield-Moore M, Paddon-Jones D, Wolfe RR, Urban RJ.

(14) J Hepatol 1996 Mar;24(3):313-9 Effects of long-term growth hormone (GH) and triiodothyronine (T3) administration on functional hepatic nitrogen clearance in normal man. Wolthers T, Grofte T, Moller N, Vilstrup H, Jorgensen JO.

(15) Cardiovasc Res 1998 Oct;40(1):211-22 Terbutaline-induced desensitization of human cardiac beta 2-adrenoceptor-mediated positive inotropic effects: attenuation by ketotifen. Poller U, Fuchs B, Gorf A, Jakubetz J, Radke J, Ponicke K, Brodde OE.

(16) Eur J Clin Pharmacol 1996;50(3):167-70 Ketotifen in HIV-infected patients: effects on body weight and release of TNF-alpha. Ockenga J, Rohde F, Suttmann U, Herbarth L, Ballmaier M, Schedel I.

(17)Endocrinology 1998 Jun;139(6):2863-8 Tumor necrosis factor-alpha inhibits leydig cell steroidogenesis through a decrease in steroidogenic acute regulatory protein expression. Mauduit C, Gasnier F, Rey C, Chauvin MA, Stocco DM, Louisot P, Benahmed M.

(18) Growth Horm IGF Res 2001 Aug;11(4):250-60 Tissue-specific regulation of IGF-I and IGF-binding proteins in response to TNFalpha. Lang CH, Nystrom GJ, Frost RA.

(19) Exerc Immunol Rev 2001;7:18-31 Exercise and cytokines with particular focus on muscle-derived IL-6. Pedersen BK, Steensberg A, Fischer C, Keller C, Ostrowski K, Schjerling P.

(20) Am J Physiol Endocrinol Metab 2001 Sep;281(3):E449-54 Catecholamines inhibit Ca(2+)-dependent proteolysis in rat skeletal muscle through beta(2)-adrenoceptors and cAMP. Navegantes LC, Resano NM, Migliorini RH, Kettelhut IC

(21) J Clin Endocrinol Metab 2002 Feb;87(2):630-4 Regulation of human adipocyte gene expression by thyroid hormone Viguerie N, Millet L, Avizou S, Vidal H, Larrouy D, Langin D.

(22) Metabolism 1987 Nov;36(11):1031-9 Alpha 2- and beta-adrenergic receptor binding and action in gluteal adipocytes from patients with hypothyroidism and hyperthyroidism. Richelsen B, Sorensen NS

(23) Br J Pharmacol 2000 Feb;129(3):448-56 Regulation of beta 1- and beta 3-adrenergic agonist-stimulated lipolytic response in hyperthyroid and hypothyroid rat white adipocytes. Germack R, Starzec A, Perret GY

(24) Braz J Med Biol Res 1994 May;27(5):1269-72 Role of thyroid hormone in the control of growth hormone gene expression. Volpato CB, Nunes MT.

(25) Am J Physiol 1999 Aug;277(2 Pt 1):E370-9 Related Articles, Links Low-dose T(3) improves the bed rest model of simulated weightlessness in men and women. Lovejoy JC, Smith SR, Zachwieja JJ, Bray GA, Windhauser MM, Wickersham PJ, Veldhuis JD, Tulley R, de la Bretonne JA.

(26) Life Sci 2002 Jul 19;71(9):1059-70 Evidence for a deficient pancreatic beta-cell response in a rat model of hyperthyroidism. Fukuchi M, Shimabukuro M, Shimajiri Y, Oshiro Y, Higa M, Akamine H, Komiya I, Takasu N.

(27) Diabetologia 2002 Jun;45(6):851-5 Thyroxine induces pancreatic beta cell apoptosis in rats.
Jorns A, Tiedge M, Lenzen S.

(28) Am J Physiol 1985 May;248(5 Pt 1):E593-601 Effect of thyroid hormone excess on action, secretion, and metabolism of insulin in humans.= Dimitriadis G, Baker B, Marsh H, Mandarino L, Rizza R, Bergman R, Haymond M, Gerich J

(29) Curr Opin Clin Nutr Metab Care 2000 Jan;3(1):67-71 Effects of insulin on muscle tissue.
Wolfe RR.

(30) J Steroid Biochem Mol Biol 2001 Jan-Mar;76(1-5):31-42 Selective modulation of thyroid hormone receptor action. Baxter JD, Dillmann WH, West BL, Huber R, Furlow JD, Fletterick RJ, Webb P, Apriletti JW, Scanlan TS.

[RRAdam]

More info on igf-1

To understand how IGF-1 works you have to understand how muscles grow. The ability of muscle tissue to constantly regenerate in response to activity makes it unique. It’s ability to respond to physical/mechanical stimuli depends greatly on what are called satellite cells. Satellite cells are muscle precursor cells. You might think of them as "pro-muscle" cells. They are cells that reside on and around muscle cells. These cells sit dormant until called upon by growth factors such as IGF-1. Once this happens these cells divide and genetically change into cells that have nuclei identical to those of muscle cells. These new satellite cells with muscle nuclei are critical if not mandatory to muscle growth.
Without the ability to increase the number of nuclei, a muscle cell will not grow larger and its ability to repair itself is limited. The explanation for this is quite simple. The nucleus of the cell is where all of the blue prints for new muscle come from. The larger the muscle, the more nuclei you need to maintain it. In fact there is a "nuclear to volume" ratio that cannot be overridden. Whenever a muscle grows in response to functional overload there is a positive correlation between the increase in the number of myonuclei and the increase in fiber cross sectional area (CSA). When satellite cells are prohibited from donating new nuclei, overloaded muscle will not grow (Rosenblatt,1992 & 1994; Phelan,1997). So you see, one important key to unnatural muscle growth is the activation of satellite cells by growth factors such as IGF-1.
IGF-1 stimulates both proliferation (an increase in cell number) and differentiation (a conversion to muscle specific nuclei) in an autocrine-paracrine manner, although it induces differentiation to a much greater degree. This is in agreement with the Dual Effector theory. In fact, you can inject a muscle with IGF-1 and it will grow! Studies have shown that , when injected locally, IGF-1 increases satellite cell activity, muscle DNA content, muscle protein content, muscle weight and muscle cross sectional area (Adams,1998).
On the very cutting edge of research scientists are now discovering the signaling pathway by which mechanical stimulation and IGF-1 activity leads to all of the above changes in satellite cells, muscle DNA content, muscle protein content, muscle weight and muscle cross sectional area just outlined above. This research is stemming from studies done to explain cardiac hypertrophy. It involves a muscle enzyme called calcineurin which is a phosphatase enzyme activated by high intracellular calcium ion concentrations (Dunn, 1999). Note that overloaded muscle is characterized by chronically elevated intracellular calcium ion concentrations. Other recent research has demonstrated that IGF-1 increases intracellular calcium ion concentrations leading to the activation of the signaling pathway, and subsequent muscle fiber hypertrophy (Semsarian, 1999; Musaro, 1999). I am by no means a geneticist so I hesitated even bringing this new research up. In summary the researchers involved in these studies have explained it this way, IGF-1 as well as activated calcineurin, induces expression of the transcription factor GATA-2, which accumulates in a subset of myocyte nuclei, where it associates with calcineurin and a specific dephosphorylated isoform of the transcription factor nuclear factor of activated T cells or NF-ATc1. Thus, IGF-1 induces calcineurin-mediated signaling and activation of GATA-2, a marker of skeletal muscle hypertrophy, which cooperates with selected NF-ATc isoforms to activate gene expression programs leading to increased contractile protein synthesis and muscle hypertrophy. Did you get all that?

[RRAdam]

PGF2a



Prostoglandin Factor 2 alpha(PGF2) is not a hormone at all, but can have some interesting effects of the muscle building process, fat loss and endocrine system. This drug is used agriculture to syncrinize ovulation and induce labor or abortions. It must absolutly stay out of contact with females!!!!! It is easily trandermaly absorbed. In the male bodybuilder it can have many benifits.
1. Anabolic: In site specific IM injections it cuases muscle size and definition to increase, it is especialy useful in getting stubborn nonresponding muscles to grow, even after treatment is over. I see it less as an anabolic and more a anti-catabolic, precontest, this stuff will save pounds of tissue.People have reported loss in strength due to pain, though I have never experienced it.
-for this purpose I recomend 10-60 iu 5-8 times a day, starting at the lower dose/frequency working SLOWLY up to max.
2. Fat loss: This stuff kills fat cells on contact!!! Don't beleive me, go look it up. Only compound I can think of that actually does this. Fat cells die, actually dissolve, releasing fatty acids into the blood streem, so you gotta due cartio right after(or T3,clen) On T3 you can actually save Lean tissue by using this as frequently as possible. It can be used transdermal(check Lab for recipe) or sub-cue right where you need it. I accually carved out a six pack in a week this way. Put it right in the where want cuts to form.
3. Endocrine:I just read a whole buch of old german studies that recently were translated that showed certain Prostoglandins increased LH. The study also showed increased adrogen activity on the inter-celluar basis. I will do more research for you all on this and report back later.
Sounds like the perfect drug right? Wrong! This **** has got more sides than a giga-gon(let me know who got that), I've seen this **** kill a horse, 20some minutes after injection. It causes asthma attacks to a degree in everybody(sometimes aysimtomatic), contractions of smooth muscle(diareaha), intense injection site pain, fever, and genneral feeling of "**** this sucks".

-------------------------------------------------------------------------

Prostaglandin F2{alpha} stimulates growth of skeletal muscle cells via an NFATC2-dependent pathway.
- Horsley V, Pavlath GK
J Cell Biol 2003 Apr 14;161(1):111-118.

Skeletal muscle growth requires multiple steps to form large multinucleated muscle cells. Molecules that stimulate muscle growth may be therapeutic for muscle loss associated with aging, injury, or disease. However, few factors are known to increase muscle cell size. We demonstrate that prostaglandin F2alpha (PGF2alpha) as well as two analogues augment muscle cell size in vitro. This increased myotube size is not due to PGF2alpha-enhancing cell fusion that initially forms myotubes, but rather to PGF2alpha recruiting the fusion of cells with preexisting multinucleated cells. This growth is mediated through the PGF2alpha receptor (FP receptor). As the FP receptor can increase levels of intracellular calcium, the involvement of the calcium-regulated transcription factor nuclear factor of activated T cells (NFAT) in mediating PGF2alpha-enhanced cell growth was examined. We show that NFAT is activated by PGF2alpha, and the isoform NFATC2 is required for PGF2alpha-induced muscle cell growth and nuclear accretion, demonstrating the first intersection between prostaglandin receptor activation and NFAT signaling. Given this novel role for PGF2alpha in skeletal muscle cell growth, these studies raise caution that extended use of drugs that inhibit COX receptors, such as nonsteroidal antiinflammatory drugs, may be deleterious for muscle growth

[RRAdam]

pgf2a cont'd

WARNING:

What I am going to reveal is true for men ONLY. Women will not get any "benefit" from what I will describe below. Further, no women should EVER touch this drug which will induce a very severe pain in their ovaries. As
men do not have ovaries, this is something that will not happen to them. Ill side effect most probably will occour in males as well.

PGF2 and anabolism.

Many studies have demonstrated an anabolic effect of PGF2 in skeletal muscles of both humans and animals. Paradoxically, PGF2 usage is still reserved to a bodybuilding elite and no one is willing to
divulge the precious secret edge. One of the most remarkable effects of PGF2 is that it mediates the
major part of the anabolic effects of insulin. By using PGF2, you can use far less insulin and get a
far stronger muscle building effect.

PGF2 and weak bodyparts.

The cardinal rule of PGF2 is to inject as far away as possible from the intestine. You see, PGF2 induces a very strong contraction of the intestine and the bladder (both smooth muscles). The major candidate as a site of injection was the front shoulders. But by repeating injections in
the shoulders, bodybuilders soon ended up with grossly overdeveloped front delts. They looked like walking monkeys. The rest of their body was growing too, but not as fast as the muscles closest to the sites of
injections. What this means is that if one wants to develop a weak muscle, just inject PGF2 locally and watch
the muscle grow. We are talking about a real muscle growth and not an artificial swelling like Synthol or Esiclene would induce. Calves are a muscle of choice. In fact, even if your calves failed to grow no matter how much ******* and training you administered, PGF2 will solve your problem.
After a single cycle of PGF2, unresponsive calves start to respond to both training and *******s
even if they never did before.

The localized growth induced by PGF2 may appear magical, but there is a simple explanation. The
life cycle of the injected PGF2 is terribly short (minutes). Most of it will be destroyed in your lungs.
If you hit your right calf for example, this muscle will be exposed to a maximal concentration of
PGF2. As the prostaglandin rapidly leaks out of the calf and passes into the blood, it will quickly
reach the lungs where most of it will be destroyed. What is left of the PGF2 will be dispatched
evenly though your whole body. It means that the other muscles will be exposed to far less of the
anabolic effects of PGF2. So unless you want to make a weak point grow, you should rotate the
sites of injections frequently which as we will see is not a problem.

PGF2 is not to be confused with steroids.

You've probably realized by now that PGF2 produces growth in a radically different way from
*******s -- although I do not exclude that part of the anabolic actions of androgens are mediated by a
local release of PGF2. The way PGF2 should be used is therefore radically different from that of
androgens. ******* use is comparitively comfortable. You inject or swallow them once in a while and wait
for the growth to occur. This is not the case with PGF2. Their main drawback is precisely their
difficulty of administration. *******s once injected survive several days in your body. PGF2 will last
only several minutes though their stimulatory actions on anabolism will be far longer lasting
(hours). It means that frequent injections are compulsory for significant effect. Ideally this would be five times per day,30 minutes after meals. You will also notice that once you have injected PGF2, the muscle which received it gets sore almost immediately. If the muscle was already sore from training, that painful sensation may
become very intense. You definitely do not want to repeat injections at the very same location,
hence the necessity for rotation. By the same token, you will notice that you cannot inject in a
muscle and then train this muscle. PGF2 is algesic (a pain mediator). Therefore, the timing of
injections is key. You should wait for at least 2 to 3 days after you have trained a muscle to inject
it. Then you will have to wait for 24 hours before training this muscle. If your muscle is already
sore, It is advised not to use it as a site of injection as long as it hurts if it is to be used at all.

You will also learn that it is more comfortable to hit the outer part of the muscle than the inner part.
For example, it is less painful to hit the outer head of the triceps than the inner head that touches
your lats. Some bodyparts such as the biceps, the back, etc. are especially sensitive to the pain
sensation PGF2 will induce.

What about fat: PGF2 vs DNP?

We are told that DNP is the strongest thermogenic (temperature elevating) drug available. I dispute
this statement. Inject PGF2, wait for ten minutes and you will sweat profusely. In fact, your body
temperature will rise so much that you may feel very cold while a witness will get scared as you
feel so hot. By elevating your body temperature, PGF2 will burn up your fat at an accelerated rate.
Furthermore, unlike muscle cells, fat cells do not like to be exposed to PGF2. As a result, they die.
Mark this well: unlike a classical diet which makes each fat cell shrink, PGF2 kills fat cells. With
PGF2, you can say goodbye to your excess adipose tissue.

What about stacking *******s with PGF2?

If PGF2 is so powerful, why not stack it along with *******s for maximal effect? It looks like a neat
idea until you try. PGF2 potentiates the effects of androgens on muscles most likely by increasing
androgen receptor level. *******s also increase the effects of PGF2 probably by increasing the
density of muscle PGF2 receptors. You will end up with a combination that is too powerful.

Within two or three days on PGF2, you will notice that your muscles get very tight. You cannot find
harder muscles than muscles from a PGF2 user. It looks and feels great until you try to train. Within
three to four reps even with an empty bar, your muscles will get so pumped that you will not be able
to move. In fact, your training poundage are likely to drop severely. I have witnessed someone going
from 3 reps at 500 pounds in the incline bench press, to failing at 6 reps at 130 after a week of
(serious) PGF2 administration plus *******s. Do not worry though, your muscles will grow and you
will be able to resume heavy training once PGF2 is stopped. This pumping effect is too exaggerated
if you take *******s along with PGF2. So it is best to use the prostaglandins to grow when you're off
the *******s.

Is PGF2 safe?

The answer is clearly no, but neither is the use of *******s, insulin, Clenbuterol, etc. By the way,
PGF2 is absolutely invisible at any drug test. What kind of side effects to expect? The first ones -- if
we except the elevation of temperature -- are that it will empty your guts of whatever they contain.
So make sure you have unrestricted use of a bathroom. This is going to last around 20 minutes.
What you do not want is to inject PGF2 into a vein! Learn to do the aspiration test. PGF2 is to be
injected intramuscularly with an insulin needle if you are lean enough. This is going to hurt like hell
and for a very long time (up to an hour) if you inject into a vein. You also may feel as if you had
some kind of cold in your throat. It is due to the vasoconstricting effect PGF2 has in your lungs.
Vomiting is a reported side effect but I have never heard of it in men.

Dosages.

You should start with a pretty low dosage (a half milligram) and see what happens. From there,
build up VERY slowly. Then, the sky is the limit. You can inject what is normally needed for several
cows and survive but believe me, you do not want to go through this. Do not forget to keep the vials
refrigerated. If you are new to PGF2, for simplicity choose the natural form and not an analog. PGF2
analogs have several advantages over straight PGF2 in that they have a longer half life and less
side effects, but some of them have no anabolic properties while others are more potent than
straight PGF2. Do not take a chance on that.

To sum up, I would like to paraphrase what Dan Duchaine has said about ******* users...

PGF2 users: Healthy, who knows? Big and lean, yes!

Re: PGF2A + Esiclene + Winstrol



Prostaglandins

Among the most potent growth factors produced locally in the muscles are the prostaglandins. These quasi-hormones use fats as their raw materials. Several classes of prostaglandins exist. We will mainly focus on the most potent one, namely the prostaglandin F2 alpha or PGF2 for short. If you apply PGF2 to a muscle cell, you are going to trigger a very strong anabolic response. PGF2 has been used by veterinarians for years not only to get animals pregnant but also to make them grow. A few daredevils figured out that if it was making animals more muscular, it would make bodybuilders bigger too. This was a big leap of faith as many drugs produce wonderful effects in animals only to fail miserably in bodybuilders. Clenbuterol is a good example of this: ultra potent in animals, deceptive in humans. Amazingly enough, this time it worked wonders.

WARNING:

What I am going to reveal is true for men ONLY. Women will not get any benefit from what I will describe below. Further, no women should EVER touch this drug which will induce a very severe pain in their ovaries. As men do not have ovaries, this is something that will not happen to them.

PGF2 and anabolism.

Many studies have demonstrated an anabolic effect of PGF2 in skeletal muscles of both humans and animals. Paradoxically, PGF2 usage is still reserved to a bodybuilding elite and no one is willing to divulge the precious secret edge. One of the most remarkable effects of PGF2 is that it mediates the major part of the anabolic effects of insulin. By using PGF2, you can use far less insulin and get a far stronger muscle building effect.
PGF2 and weak bodyparts. The cardinal rule of PGF2 is to inject as far away as possible from the intestine. You see, PGF2 induces a very strong contraction of the intestine and the bladder (both smooth muscles). The major candidate as a site of injection was the front shoulders. But by repeating injections in the shoulders, bodybuilders soon ended up with grossly overdeveloped front delts. They looked like walking monkeys. The rest of their body was growing too, but not as fast as the muscles closest to the sites of injections. What this means is that if you want to develop a weak muscle, just inject PGF2 locally and watch the muscle grow. We are talking about a real muscle growth and not an artificial swelling like Synthol or Esiclene would induce. Calves are a muscle of choice. In fact, even if your calves failed to grow no matter how much steroid and training you administered, PGF2 will solve your problem. After a single cycle of PGF2, unresponsive calves start to respond to both training and steroids even if they never did before.The localized growth induced by PGF2 may appear magical, but there is a simple explanation. The life cycle of the injected PGF2 is terribly short (minutes). Most of it will be destroyed in your lungs. If you hit your right calf for example, this muscle will be exposed to a maximal concentration of PGF2. As the prostaglandin rapidly leaks out of the calf and passes into the blood, it will quickly reach the lungs where most of it will be destroyed. What is left of the PGF2 will be dispatched evenly though your whole body. It means that the other muscles will be exposed to far less of the anabolic effects of PGF2. So unless you want to make a weak point grow, you should rotate the sites of injections frequently which as we will see is not a problem.

PGF2 is not to be confused with steroids. You've probably realized by now that PGF2 produces growth in a radically different way from steroids -- although I do not exclude that part of the anabolic actions of androgens are mediated by a local release of PGF2. The way PGF2 should be used is therefore radically different from that of androgens. Steroid use is rather comfortable. You inject or swallow them once in a while and wait for the growth to occur. This is not the case with PGF2. Their main drawback is precisely their difficulty of administration. Steroids once injected survive several days in your body. PGF2 will last only several minutes though their stimulatory actions on anabolism will be far longer lasting (hours). It means that frequent injections are compulsory. Ideally this would be five times per day, 30 minutes after meals.
You will also notice that once you have injected PGF2, the muscle which received it gets sore almost immediately. If the muscle was already sore from training, that painful sensation may become very intense. You definitely do not want to repeat injections at the very same location, hence the necessity for rotation. By the same token, you will notice that you cannot inject in a muscle and then train this muscle. PGF2 is algesic (a pain mediator). Therefore, the timing of injections is key. You should wait for at least 2 to 3 days after you have trained a muscle to inject it. Then you will have to wait for 24 hours before training this muscle. If your muscle is already sore, I advise against using it as a site of injection as long as it hurts. You will also learn that it is more comfortable to hit the outer part of the muscle than the inner part. For example, it is less painful to hit the outer head of the triceps than the inner head that touches your lats. Some bodyparts such as the biceps, the back, etc. are especially sensitive to the pain sensation PGF2 will induce.

Is PGF2 safe?

The answer is clearly no, but neither is the use of steroids, insulin, Clenbuterol, etc. By the way, PGF2 is absolutely invisible at any drug test. What kind of side effects to expect? The first ones -- if we except the elevation of temperature -- are that it will empty your guts of whatever they contain. So make sure you have unrestricted use of a bathroom. This is going to last around 20 minutes. What you do not want is to inject PGF2 into a vein! Learn to do the aspiration test. PGF2 is to be injected intramuscularly with an insulin needle if you are lean enough. This is going to hurt like hell and for a very long time (up to an hour) if you inject into a vein. You also may feel as if you had some kind of cold in your throat. It is due to the vasoconstricting effect PGF2 has in your lungs. Vomiting is a reported side effect but I have never heard of it in men.

Dosages.

The lowest possible "effective" dose should be used You should start with a low dosage no higher than (a half milligram) and see what happens. From there, build up VERY slowly. Then, the sky is the limit. You can inject what is normally needed for several cows and survive but believe me, you do not want to go through this and it is potentially deadly. Do not forget to keep the vials refrigerated. If you are new to PGF2, for simplicity choose the natural form and not an analog. PGF2 analogs have several advantages over straight PGF2 in that they have a longer half life and less side effects, but some of them have no anabolic properties while others are more potent than straight PGF2. Do not take a chance on that.

[RRAdam]

pgf2a part 3

PGF2 analogues

Just as testosterone has analogues such as nandrolone, so do prostaglandins. The analogues are an attempt to solve the problems caused by the original hormone or substance. Steroid molecules such as nandrolone or trenbolone were developed in the hope they would induce more favorable actions (anabolism) while producing less side effects (virilization) compared to testosterone. Researchers designed PGF2 analogues in order to address the three main problems inherent to PGF2. First: to increase its very short life cycle, second: to lessen the incidence of the numerous side effects associated with PGF2 usage, third: to ease prostaglandin usage by developing oral versions.
As with testosterone some analogues proved useless while others do have some interesting properties, at least in the test tube. I am not going to tell you which analogue is the best. The truth is that I don't know. I only have experience with the real thing. This may be disappointing but I am not going to lie just to look better.
Aspirin as an anti-prostaglandin
Aspirin or aspirin-like substances have the potential to reduce some of the side effects such as pain associated with PGF2 administration. However I tend to consider that the use of aspirin along with PGF2 weakens the overall anabolic effects without effectively fighting the side effects. This is true for the aspirin you can find in medication as well as the aspirin hidden in some ephedrine-caffeine stacks. I suggest that you avoid both of them. Several hypotheses could be advanced about the inhibiting effects of aspirin. Some research has shown that aspirin could block prostaglandin receptors. It may also impair the conversion of PGF2 to PGE2 which seems important for a maximal muscle building effect. I know that PGE2 is considered as a muscle enemy in the bodybuilding magazines, but the fact is that several studies have pointed out its usefulness in the bodybuilding process as a growth agent for the muscles. One last hypothesis is that PGF2 stimulates the subsequent natural release of muscle PGF2 or PGE2 which could further enhance the anabolic process. Aspirin would prevent this secondary anabolic secretion.
Preventing the local growth by rotating the sites of injections I consider the local growth induced by PGF2 as a side effect. As I said last month, it is due to a weakness of PGF2 (a very rapid degradation) rather than a magical effect. Unless you want to bring up a specific weak point, you should constantly rotate the sites of injections. One more restriction is that it is easy, for example, to inject PGF2 in some body part like the front shoulders but far harder in the inner side of the biceps. You should also make sure to avoid hitting too close to the intestine which exacerbates the gastro-intestinal discomfort caused by PGF2. Though close to the intestine, the front legs are a rather interesting and "easy" site of injections. You just may feel your quads "better" as you walk. I would suggest you mark all the possible injection sites you have in order to structure your injection pattern. If you have weak points, they should be hit more often than your strong bodyparts. No injecting your right calf will make your left calve grow to the same extent. Same thing with the gastronemius and the soleus. Hitting one will mostly make the injected muscle grow with a lesser stimulation for the nearby muscles. So for the calves only, we have at least 15 possible sites of injections. One on the upper, outer soleus, one for the lower, outer soleus and one for the lower inner part of the soleus. One or two for the front calves depending on your degree of development. For the gastronemius, you have both the upper and lower part of the outer side as well as the upper and lower parts of the inner/rear part. Of course, you can multiply that by two as you hopefully have 2 calves. I consider that you have the same number of sites on the upper legs. Avoid the abs, the lower back and maybe the forearms. Your triceps hold at least 6 sites and at least 4 for your biceps. Your shoulders have at least 12. If you are not too sensitive, you can manage 12 more on your chest. It is a total of at least 64 sites (excluding the back) to choose from every day.If you are not sure about the muscle locations, check with an anatomy chart to avoid hitting a tendon or a bone. Note carefully which side of the body you last hit so that you can shift from the right to the left and from the left to the right with each injection. If a friend of yours is willing to help you with the injections, it will increase the potential number of injection sites by adding your whole upper back and helping the right handed persons with their right side of their upper body (and the opposite for the left handed persons). You will always find a helping hand in the gym.The main problem with the rotation is to inject into muscles that you are not about to train or muscles that you trained recently. This is why training each bodypart seriously only once a week will ease our use of PGF2. Light pumping sessions should not interfere with the PGF2 rotation schedule as the mild pain should be bearable. In fact, during a light workout, having a soreness-like mild pain should help you feel the muscle contraction better and should enhance your focus on the trained muscles.As I said last month, you should wait for at least two to three days after training to inject PGF2 because of its pain promoting effect. This length of time depends upon the degree of trauma inflicted to the trained muscles. If your training was really traumatic (by including plenty of heavy negative reps), you may have to wait longer. But PGF2 users do not have to traumatize their muscles to get results. In fact, thanks to the muscle pump you will obtain with the light weights, you will not have to go too heavy. Your workouts are more likely to be non-traumatic, allowing you to inject after only two days after the workout.I also advised to stop injecting into a muscle 24 hours before retraining it. This means that you have a three day window of opportunity for a single muscle per week to soak it up with PGF2.

Here is a one week schedule example. It assumes that your upper body is lagging a bit compared to your legs and is therefore trained a bit more. The first muscle is the bodypart of the day and should be trained hard (but avoid overly traumatic techniques such as pure negative reps and super heavy weights). The second and sometimes third muscles are meant to be trained in a light high rep fashion for around 5 sets each. In the least column, the muscles receiving PGF2 are mentioned. You will note that even though there are days off training, it is best to administer PGF2 everyday. Again, this is due to the short life cycle of PGF2 which makes it necessary to repeat injections frequently.




Day Muscle of the day Pumping muscles of the day Muscles in which PGF2 can be administered for the day
Monday Back Chest Chest*, Arms
Tuesday Legs Shoulders Shoulders*, Arms
Wesnesday Chest Back Shoulders, Arms
Thursday Rest Rest Shoulders, Back.
Friday Arms Legs Back, legs*.
Saturday Shoulders Back, Chest Back*, legs, chest*
Sunday Rest Rest Legs, Chest
* Inject after training rather than before.
The dosage issue
Most readers are interested in an "ideal" dosage schedule. Unfortunately, such a miraculous schedule does not exist. Steroids have been used for decades, yet no one is able to come up with a one fits all, fail-safe schedule. Though some claim to know exactly how to use steroids and how to stack them, this is a lie. The same applies to PGF2. The ideal schedule does not exist. It is up to you to figure out which one suits you best. I can give you some guidelines but I am more able to tell you how not to use it than to prescribe its use. As mentioned last month, I suggest to start with half a milligram. At that dosage, not much should occur. Better to be safe than sorry. If everything goes well, go up to a milligram the next time. See what is happening. If you are fine, try 2 milligrams. I think you understand how to build up your dosage during the first days of your very first cycle. There is normally 25 mg of PGF2 per 5 milliliters. At 1 ml. (therefore 5 mg.), you should start to be able to tell the drug is working. I suggest not to go above 2 ml. per injection. If you are using 1 ml. five times a day, it means one vial a day (two if you use 2 ml.s). 5 ml. is the most I have ever heard with a single injection, but I consider it as a huge dosage. Maybe in 5 to 10 years, it will sound like a sissy dosage, but only time will help us determine an upper limit.
Lowering the required dosage One easy way to reduce the PGF2 dosage (and therefore the side effects) while optimizing the anabolic response is to administer PGF2 while insulin secretion is high. This means at meal time -- or more precisely after a meal. Insulin can trigger the muscle secretion of PGF2. This is probably how it produces anabolism. But insulin does not stop here: it increases the muscle sensitivity to the anabolic effects of PGF2. This is why you can reduce your PGF2 dosage if it is used at meal time or administered with insulin or an insulin booster. The dosages mentioned above already take into account the beneficial synergetic action of insulin on PGF2.

How often?

Due to its short life cycle, PGF2 has to be administered as often as possible for optimal effect. This makes it very uncomfortable to use but as I mentioned in the introduction, it is a potent yet not ideal drug to use. As most bodybuilders eat at least five times, it means that there are five opportunities per day for PGF2 administration. Of course this assumes that you have plenty of free time. Not everybody is a pro bodybuilder and you may not need (or want) to reach their degree of muscularity or to act like them. Administered only twice or three times a day along with your major meals, PGF2 will still perform its magic. I would not recommend less than twice a day. During week ends, you may have more time and so you may be able to increase the injection frequency. You can resume your twice a day schedule as you go back to work on Monday.
Just understand that the more often you inject PGF2, the longer time your muscles will be exposed to this anabolic substance. Let's assume the anabolic stimulation of a single PGF2 administration lasts for two hours. Of course, this figure depends upon the dosage: the higher the dose, the longer it lasts, as it will take more time for our body to degrade the prostaglandins. If you inject only twice a day, you will generate a total of four hours of intense anabolism per 24 hours. It means that 20 hours during the day are wasted. If you inject 5 times a day, you create 10 hours of intense anabolism per 24 hours.
Is this a strength or a weakness of PGF2 over steroids? You are exposed to steroids 24 hours per day (assuming you use injectables over orals). So, again steroids are more comfortable to use. But you may have noticed that the levels of most of our endogenous hormones fluctuate throughout the day. It prevents our muscles from downregulating their anabolic responses to the growth stimulating hormones. This is one of main the problem associated with the constant delivery of steroids. The time off PGF2 inherent in its short life cycle helps fight the tendency toward reduced anabolic response as time goes by. It is therefore a source of discomfort but also an advantage as far as results are concerned.
I am going to propose two schedules as examples. One will be for beginners who want to build up some lean muscles. The other is for more advanced bodybuilders who want to fill the gap between two steroid cycles.
The beginner schedule Inject PGF2 ex. (half a ml.) 30 minutes after the noon lunch. Inject the whole half a ml. at only one place. Your lunch should be high in proteins and carbs while low in fats. Make sure you have a serving of weight gainers at hand during the next two hours. This has two purposes. First, some people report a hypoglycemia-like feeling after PGF2. Of course this side effect should be countered. Eating a liquid meal generally makes them feel better. Second, whenever anabolism is elevated, so should be protein feeding frequency. Repeat a similar procedure after the evening meal. Change the side of injection. For the most daring, adding an insulin booster before the meals may be a good idea. ex. Glipizide (2.5 mg) but Glibenclamide (the insulin booster of reference) has been shown to lessen the incidence of side effects of PGF2 especially on the intestine. For Glibenclamide, start with the 1.25 mg pills and build up to the 2.5 mg. This makes it a smart stack to enhance anabolism while reducing side effects. Of course, you should be extra careful about the potential hypoglycemia so make sure you ingest some carbs every 30 minutes for the next two hours when it is time for the weight gainers. I suggest that you increase your creatine intake according to your PGF2 dosage as prostaglandins like most other anabolic substances accelerate the wasting of creatine. Go with at least 10 grams of creatine per day.

The advanced schedule

This is not a pro schedule. It should rather fit most of the readers' needs for muscles. As you taper off your steroid intake, slowly build up your PGF2 intake first in terms of dosage, then in terms of frequency. The animal studies suggest that PGF2 tends to depress testosterone secretion. But the PGF2 users usually get very "horny", which is a good sign, especially at the end of a steroid cycle. And do not discount the general hardening properties of PGF2 which amazingly is not restricted to skeletal muscles. Frequency of administration as well as dosage should be increased compared to beginners. You also have the choice between insulin injections and oral insulin boosters. Sticking with the oral booster may be wiser until you get more comfortable with the control of your glycemia. This is especially true as PGF2 will enhance the hypoglycemic effects of insulin. Wake up and have a liquid meal followed by a more solid meal within 30 minutes. Use that period for an insulin shot (start low with 5 UI and build up to no more than 15 UI per meal) or for oral Glipizide (2.5 to 5 mg). Prefer a long acting insulin to a short one. Wait for 15 minutes before your PGF2 (always start low and build up as you feel more comfortable). Repeat this procedure at lunch. Keep the liquid meal for after the lunch in case you feel hypoglycemia. Another reason to prefer Glipizide at that time is that you may get tired of the frequent injections. Repeat this procedure after training. You can use another PGF2 injection a bit before bedtime still with a meal but without the insulin or the booster. Some people who bad-mouth the prostaglandins argue that prostaglandins depress GH secretion. This is funny as the scientific literature points out the opposite. GH should be liberated overnight.
As you use more PGF2 than in the beginner cycle, go with at least 15 grams of creatine over 24 hours.

The science of cycling

The length of a PGF2 cycle is generally determined by default. The cycle usually lasts the whole time you want to be off steroids. It means it can go from between 24 hours to two months. Even though bodybuilders welcome a drug that allows them to grow while off steroids, most will get tired of using PGF2 after a while. They are usually happy to switch back to anabolics. A good rule of thumb is therefore to use PGF2 until you get tired of it. Again, there is no magic number here.
Yet many maintain a lighter intake of PGF2 centered around their weak bodypart. A lighter schedule includes one or two injections a day in a weak bodypart such as the calves to help bring them up but without having to go with all the trouble associated with normal PGF2 use.
To conclude, I again would like to quote Dan Duchaine about steroids in USH II:
"Rule #7: Most people who have taken massive amounts of steroids don't get sick, don't die, and don't go crazy.
Rule #8: ... Never assume that you are like 'most people' until you prove it."
This exact same rule apply to PGF2 users. Do not assume that PGF2 use is benign. PGF2 will affect every one of the cells composing your body. You are not immune from a rare, unexpected reaction. Please do not consider PGF2 usage lightly. We would not like to hear from you in the horror story section of a bodybuilding magazine.


Prostaglandins and their Discovery

Prostaglandins are part of a class of substances called eicosanoids. Eicosanoids are a group of substances derived from fatty acids and include prostaglandins, thromboxanes, and leukotrienes, all of which are formed from precursor fatty acids by the incorporation of oxygen atoms into the fatty acid chains. This reaction is called oxygenation and is carried out by cyclo-oxygenase enzymes. Prostaglandins and their metabolites have been found in virtually every tissue in the body.

The discovery of prostaglandins and determination of their structure began in 1930, when Raphael Kurzrok and Charles Lieb, both new York gynecologists, observed that human seminal fluid stimulates contraction of isolated uterine muscle. A few years later in Sweden, Ulf von Euler confirmed this report and noted that human seminal fluid also produces contraction in intestinal smooth muscle and lowers blood pressure when injected into the blood stream. It was Von Euler who came up with the name prostaglandin for this mysterious substance. The name prostaglandin seemed appropriate because he thought it originated in the prostate gland. Today, we know that prostaglandin production is not limited to the prostate, in fact, there is virtually no soft tissue in the body that doesn’t produce them. The name, however, has stuck with us through the years. If Von Euler had known his name for prostaglandins would still be with us into the next millennia, I’m sure he would have chosen to name them "Von Eulers" or "UVEs" instead of prostaglandins. By 1960, several specific prostaglandins had been isolated in pure crystalline form and their structures determined. Because our concern with prostaglandins involves primarily PGF2a, and perhaps PGE2, we will not go into detail about the myriad of other prostaglandins. Just know that prostaglandins are abbreviated "PG". The additional letter and numerical script indicate the type and series. The various types differ in the functional group present in the five-membered ring.

While scientists were studying the structure of these new compounds, other research was being done to determine their role in human physiology and their potential as drugs. Initially these compounds were extremely expensive to synthesize and/or isolate in sufficient quantities for research. In 1969, the price of prostaglandins dropped dramatically with the discovery that the gorgonian sea whip, or sea fan, is a rich source of prostaglandin-like materials. Now however, there is no need to rely on natural sources because chemists have developed highly effective laboratory methods for the synthesis of almost any prostaglandin or prostaglandin analog.

[RRAdam]

pgf2a part 4


Endogenous production from Arachidonic Acid

Prostaglandins (PGs) are not stored in the tissues of your body. PGs are produced in response to some physiological trigger. The starting material for PG synthesis are unsaturated fatty acids that have 20 carbon structures. The fatty acid that is used to make PGF2a is arachidonic acid.

Functions of prostaglandins in the body

Prostaglandins are classified as autocrine (effecting the same cell that produced it), as well as paracrine (effecting adjacent cells), regulators. They do not really fit into the category of hormones, nor are they neurotransmitters, instead they are simply considered as a corollary of the endocrine system.

The following are some of the regulatory functions of prostaglandins in various organs and systems of the body:

Inflammation & Pain. PGs promote many aspects of the inflammatory response. They are involved in the sensation of pain associated with inflammation and vasoconstriction and/or dilation, and the development of fever. PGs, when injected directly into the hypothalamus, induce fever. Anecdotally, the use of PGF2a also induces a rise in body temperature presumably by interacting with the hypothalamus as well.

Reproductive systems. PGs may play a role in ovulation and corpus luteum function in the ovaries and in contraction of the uterus. Excessive PG production may be involved in premature labor, endometriosis, dysmenorrhea (menstrual cramps), and other gynecological disorders. PGs are often given to induce labor.

Gastrointestinal tract. The stomach and intestine produce PGs. PGs are believed to inhibit gastric secretions and influence gastric motility as well as fluid absorption. Drugs such as aspirin that inhibit prostaglandin production can lead to overproduction of gastric secretion. This predisposes the person to gastric ulcers.

Respiratory System. PGs can cause vasoconstriction as well as vasodilation of blood vessels within the lungs, depending on which PGs are being produced. PGs also cause both dilation and constriction of bronchial smooth muscle. PGs as well as other eicosanoids may play a role in asthma.

Blood vessels. Some PGs are vasoconstrictors, others are vasodilators. The overall effect is determined by which PG is present in greater concentration.

Blood clotting. Thromboxanes, also a product of cyclo-oxygenase, are produced by blood platelets. These eicosanoids promote platelet aggregation and vasoconstriction. Prostacyclin, produced by vascular endothelial cells, inhibits platelet aggregation and causes vasodilation.

Kidneys. PGs are produced in the medulla of the kidneys and cause vasodilation, resulting in increased renal blood flow and increased excretion of water and electrolytes in the urine. In particular, high potassium intake has been shown to selectively increase PGF2a excretion in animals.

Protein synthesis. PGs are known to be regulators of protein synthesis in skeletal muscle. PGE2 and PGF2a being involved in protein breakdown and protein synthesis rates respectively. Stretch induced hypertrophy of skeletal muscle is in part regulated by prostaglandins. More on the role of PGs in protein synthesis in later sections.

Adipogenesis. PGF2a directly inhibits adipogenesis. You should not be surprised to hear that yet another prostaglandin serves to induce adipogenesis, namely PGJ2. PGJ2 derivatives function as activating ligands for peroxisome proliferator-activated receptor (PPAR), a nuclear hormone receptor that is central to fat cell proliferation. PGF2 blocks adipogenesis through activation of mitogen-activated protein kinase (the same kinase involved in insulin action), resulting in inhibitory phosphorylation of PPAR. Both mitogen-activated protein kinase activation and PPAR phosphorylation are required for the anti-adipogenic effects of PGF2. So you have PGs within the cell telling the fat cell to divide while at the same time you have other PGs, such as PGF2a, at the outside preventing it from taking place.


Current uses of PGF2a

Humans PGF2a is not currently FDA approved for use in humans. Products containing PGF2a should be considered hazardous to women and must be handled with extreme care. PGF2a is readily absorbed through the skin and may result in birth defects and/or instantaneous abortion. Prostaglandins of use today in humans are of the "E" class and are administered to women for abortion or to induce labor. Prostaglandins are also used for impotence in men. In such case it (PGE1) is injected directly into the penis.

Animals PGF2a has been tested in a wide range of animals from monkeys to horses. In most cases the side effects are increased body temperature, vomiting and diarrhea, bronchial constriction, confusion, loss of coordination, tachycardia, and low blood pressure just to name a few. PGF2a is nontoxic with a serum half life of only minutes.

PGF2a is currently used in animal husbandry to manage breeding. It is used commonly as dinoprost in the form of a tromethamine salt. Upjohn makes a version called Lutalyse? as a sterile solution for subcutaneous and intramuscular injection. It’s purpose is to synchronizing ovulation in cattle by sequential injection of several hormones along with PGF2a. A hormone selected from the group consisting of gonadotropin releasing hormone (GnRH), luteinizing hormone (LH), or human chorionic gonadotropin (hCG) is administered to an open cow during an estrous cycle in order to stimulate follicle development. PGF2a is then administered to initiate corpus luteum regression about five to eight days after administration of the GnRH, LH or hCG. A second dose of GnRH, LH or hCG is then administered concomitantly with the PGF2a injection or up to about three days after the PGF2a injection. This second dose of hormone functions to stimulate the ovulation of a dominant follicle and the cow is then breed within one day of the administration of the second dose of hormone.


The Role of PGF2a in Muscle Growth

After that brief introduction into prostaglandins, we can now begin to discuss more specifically the role of prostaglandins in muscle growth. In a nutshell, mechanical stimulation (i.e. intermittent stretch) results in the production and efflux of two prostaglandins, PGE2 and PGF2a. PGE2 increases protein degradation where as PGF2a increases protein synthesis. Muscle hypertrophy is usually achieved by an increase in protein synthesis as well as a proportionately smaller increase in degradation. The simultaneous release of both PGE2 and PGF2a creates this condition.

It is well known that mechanical stretch, without any electrical activity, is sufficient to induce muscle hypertrophy. Recent studies have shown that the mechanism by which mechanical stretch leads to prostaglandin production and ultimately muscle growth, involves G proteins embedded in the cell membrane. These G proteins increase the amount of cyclo-oxygenase, the enzyme responsible for making prostaglandins from arachidonic acid. Skeletal muscle cyclooxygenase generates PGE2 and PGF2 alpha at a ratio approximately equal to one.

The exact mechanism by which PGF2a increases protein synthesis is not entirely clear. That’s just a spineless way of saying, "I don’t know the exact answer to that!" We are free to speculate though. It may involve short phase protein synthesis and/or long phase protein synthesis.

2 phases of protein synthesis Modulation

Modulation of protein synthesis rates occurs at two levels, the short phase and the long phase. The short phase alteration in protein synthesis rates occurs by altering the activity of existing ribosomes and/or eukaryotic initiation factors (eIFs). This happens within minutes of the appropriate physiological trigger. The long phase modulation of protein synthesis happens by way of increasing the number of myonuclei. This mechanism involves hormones and growth factors such as HGH and IGF-1 bringing about the activation of myogenic stem cells. This can take several days to effect protein synthesis rates. This is a simplified view but for our purposes it is sufficient.

The role of PGF2a in short phase protein synthesis in muscle tissue is speculative at best. In non-muscle tissue, prostaglandins effect calcium fluxes, plasma membrane ionic channel activities, and cyclic nucleotide levels. All of which are important regulators of protein synthesis rates in muscle. PGF2a has been shown to interact with the S6 small ribosomal subunit, increasing its potential to form the ribosomal initiation complex with the large subunits. It is also plausible that PGF2a may effect the activity of eIFs.

Initiation of translation (the binding of mRNA to the ribosomal pre-initiation complex) requires group 4 eukaryotic initiation factors (eIFs). These initiation factors interact with the mRNA in such a way that makes translation (the construction of new proteins from the mRNA strand) possible. Two eIFs, called eIF4A and eIF4B, act in concert to unwind the mRNA strand. Another one called eIF4E binds to what is called the "cap region" and is important for controlling which mRNA strands are translated and also for stabilization of the mRNA strand. Finally, eIF4G is a large polypeptide that acts as a scaffold or framework around which all of these initiation factors and the mRNA and ribosome can be kept in place and proper orientation for translation. There is yet no direct evidence to confirm that PGF2a works through this mechanism however.

Long term modulation of protein synthesis involves the activation of myogenic stem cells or satellite cells. If you recall, when a muscle is stretched it not only produces PGF2a, but also PGE2. PGE2 is a potent inducer of satellite cell proliferation and fusion. This is how existing muscle cells increase the number of nuclei they contain. This is important because in order for a muscle to grow rapidly, it must produce more mRNA. This is done in the nucleus of the muscle cell. The more nuclei you have, the more mRNA you can produce. Within the cell, prostaglandins may also be involved in regulating the number of ribosomes. This could have long term implications on growth and development as well as stretch induced hypertrophy.


The role of other hormones, drugs and diet in the action of PGs.

Because prostaglandins are signaling molecules that get their message across through multi step signal transduction pathways, they are susceptible to modulation by several chemical, hormonal, and dietary factors. I will do my best to shed some light on the subject without bogging you down with meaningless terms and jargon. It is well to remember that the action and interaction of prostaglandins in the human body is complex.

Cortisol

Cortisol effects the production of prostaglandins in muscle tissue by at least two mechanisms. First, cortisol by way of lipocortins, inhibits the action of phospholipase A2. Phospholipase is necessary in order to make arachidonic acid available for PGF2a production. Cortisol also inhibits the production of cyclo-oxygenase mRNA content within cells. As mentioned earlier, cyclo-oxygenase is the enzyme that converts arachidonic acid into prostaglandins. So cortisol inhibits muscle growth by preventing the production of PGF2a in response to training (mechanical stimulation) and eating (insulin action).

Insulin

As eluded to above, insulin stimulated protein synthesis is linked to the production of phospholipases which lead to increased availability of arachidonic acid. This is a two edged sword. Increased availability of arachidonic acid can increase the amount of PGF2a thereby increasing protein synthesis. On the other hand, arachidonic aid directly suppresses GLUT4 production which is the chief glucose transporter in skeletal muscle. High levels of arachidonic acid can reduce glucose transport by up to 50%. It could be that insulin action is more dependant on the cAMP antagonist, cyclic PIP (prostaglandylinositol cyclic phosphate), a proposed second messenger for insulin and alpha-adrenoceptor action, than on PGF2a. PGE2 however is a different story. Prostaglandin E, myo-inositol and one phosphate are components of cyclic PIP. So increased production of PGE2 may increase insulin mediated glucose transport through this mechanism. Taking this into consideration, exogenous PGF2a should not be considered to replace insulin.

Dietary Fatty Acids

Dietary fatty acids significantly effects prostaglandin production. Diets high in omega-3 fatty acids (fish oil, flax oil) decrease prostaglandin production. Diets high in omega-6 fatty acids (corn oil) increase prostaglandin production. Once again you have pros and cons with trying to manipulate PGF2a production with your diet. By increasing omega-3s, you get lower levels of PGF2a and probably a less intense stimulus of protein synthesis immediately after you workout. On the other hand by increasing omega-3s you reduce inflamation, pain, increase GLUT4 content, and a whole host of other factors related to cardiac risk. I don’t think its as clear cut as Dr. Sears (Zone Diet) would have you believe. Trying to manipulate the diet to control prostaglandin kinetics is fraught with complexity making black and white statements difficult to support.

NSAIDs

NSAIDs are non-steroidal anti-inflammatory drugs. An example of such drugs are aspirin, ibuprofen (Motrin), naproxen sodium (Anaprox, Alleve). There are several more but these are the most common to consumers. NSAIDs work by inhibiting the activity of cyclooxygenase. By blocking cyclooxygenase you block prostaglandin production. These drugs have been shown to improve nitrogen balance under conditions of severe physical stress such as after surgery. The effect is abolished when PGE2 is infused linking PGE2 production with the catabolic effect of stress. In the case of PGF2a, the use of NSAIDs also blocks its production in that PGE2 and PGF2a are normally produced in a 1:1 ratio from the same precursor. Using NSAIDS while using exogenous PGF2a may improve the anabolic effect by reducing PGE2 in the presents of elevated PGF2a shifting the ratio towards anabolism.

PGF2a + IGF-1: The ultimate cocktail for localized muscle growth?!

Say good by to lagging body parts forever. It is a special time to be a bodybuilder. With the advent of PGF2a as a localized anabolic agent along with the newly available rhIGF-1 which has also been shown to build muscle where you want it, the future for genetically challenged bodybuilders looks bright indeed. A brief refresher course on locally injected IGF-1. Non-exercised muscle, when injection with 0.9 - 1.9 micrograms/kg/day of rhIGF-1 was shown to mimic the effects of physically loading the muscle. Much the same effect PGF2a but by different mechanisms. With local IGF-1 injections there is an increase in protein content, cross sectional area and DNA content. The increase in muscle DNA is presumed to be a result of increased proliferation and differentiation of satellite cells which donate their nuclei upon fusion with damaged or hypertrophying muscle cells. Take note that the quantities of IGF-1 needed are extremely small, much smaller than studies that have shown relatively poor results from administering IGF-1 systemically which range from 1.0 to 6.9 milligrams/kg/day.

Now add PGF2a to the mix and whalla! You can virtually mimic the mechanical stimulus of training without even picking up a weight. You have PGF2a to accelerate short term protein synthesis by activating ribosomes and/or eIFs and thereby translation, as well as IGF-1 to activate satellite cells to bind and donate additional nuclei to boost the amount of mRNA to be used by the ribosomes. Because the mechanism of action is different, the two compounds should compliment each other delivering results beyond what either one alone could produce.

Are these compounds going to replace traditional training? Not in the near future. The use of site injectable drugs only reaches the surface musculature. Deeper muscles are only stimulated to grow with traditional training. For strength athletes, strength is dependant on neuromuscular training which is not enhanced by simple muscle hypertrophy without actual lifting in a coordinated fashion. Are these compounds going to replace traditional anabolics? No. The reason is basically the same as with training. Deeper muscle groups are only reached by systemically administered anabolics that are carried throughout the entire body. In addition, androgens are needed to influence genetic expression in favor of whole body skeletal muscle growth. Are these compounds going to change the face of bodybuilding? It is very likely that they will, depending on their availability and cost. I would hope that as competitors become educated about these alternatives that we will no longer see implants in top level competitors. It would also be nice to see people have an option when it comes to pumping their muscles full of "stuff" in hopes that it will improve their symmetry. No doubt the future will bring us even more new and exciting drugs like non-steroidal androgens and compounds that alter the expression of myostatin (GDF . Once again, it is an exciting time in the science of bodybuilding, perhaps now more than any other time since the introduction of testosterone.

[RRAdam]

pgf2a part 5

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Palmer RM. Prostaglandins and the control of muscle protein synthesis and degradation. Prostaglandins Leukot Essent Fatty Acids. 1990 Feb;39(2):95-104

Sadoshima J, Izumo S. The cellular and molecular response of cardiac myocytes to mechanical stress. Annu Rev Physiol 1997;59:551-71

Sadoshima J, Izumo S. Mechanical stretch rapidly activates multiple signal transduction pathways in cardiac myocytes: potential involvement of an autocrine/paracrine mechanism. EMBO J 1993 Apr;12(4):1681-92

Southorn BG, Palmer RM Inhibitors of phospholipase A2 block the stimulation of protein synthesis by insulin in L6 myoblasts. Biochem J. 1990 Sep 15;270(3):737-9.

Thompson MG, Palmer RM Signaling pathways regulating protein turnover in skeletal muscle. Cell Signal. 1998 Jan;10(1):1-11.

Vandenburgh HH, Shansky J, Solerssi R, Chromiak J. Mechanical stimulation of skeletal muscle increases prostaglandin F2 alpha production, cyclooxygenase activity, and cell growth by a pertussis toxin sensitive mechanism. J Cell Physiol 1995 May;163(2):285-94

Wasner HK, Salge U, Gebel M. The endogenous cyclic AMP antagonist, cyclic PIP: its ubiquity, hormone-stimulated synthesis and identification as prostaglandylinositol cyclic phosphate. Acta Diabetol 1993;30(4):220

[RRAdam]

Halotestin
Pharmaceutical Name: Fluoxymesterone
Chemical structure: 9-alpha-fluoro-11-beta-hydroxy-17-alpha-methyl-4-androstene-3-one,17b-ol
Effective dose: 20-30 mg / day orally


With the exception of perhaps anadrol, Halotestin is the single most dangerous steroid to use. Its liver toxicity is unrivaled and you wouldn't be the first person to end up in the hospital with jaundice and dangerously elevated liver values after a hefty cycle of fluoxymesterone. My question has often been simply "Why?". Fluoxymesterone has a low anabolic capacity. The results in mass would be small to non-existent. Qualitatively similar gains as one would book with trenbolone, but tren would go for equal or less money, deliver three times the gains and wouldn't be half as risky to use. Therefor the sole marked use of fluoxymesterone that is actually warranted is that by power- and weightlifters seeking to boost strength while remaining in a set weight class.

In bodybuilding its used near the end of cutting cycles, since in people with an already low body-fat percentage it adds a distinct hardness and definition to the look, although, as stated, better and safer products will achieve similar effects. As with these alternatives fluoxymesterone has absolutely zero estrogenic activity and will thus not add water or fat to the frame in any way.

While a definite increase in aggressiveness and a notable rise in erythrropoesis is noticed with the use of fluoxymesterone, it has been theorized that it actually has very moderate binding to the androgen receptor. Either that or it shows a higher affinity for other receptors. The enzyme aromatase comes to mind because of the effect it has, like a DHT compound would, on muscle hardness. The latter seems like a better explanation. On the one hand there is nothing that would immediately indicate it acting on the androgen receptor, on the other there is very good likeness to other steroids that are mostly AR-mediated. Its my best guess that not all has been said about fluoxymesterone. Its not a very interesting or grateful object of study however due to the high risk and low yield of this particular steroid.

Athletes that may consider its use are endurance athletes that do not get drug tested (as it is quite easy to detect). The stimulating effect on erythropoesis (red blood cell production) and cell respiration, such an athlete would find a good use for the increase in aerobic capacity noticed for this, without adding unnecessary bodyweight to the frame he has to carry. In this aspect it may be good to note that a short cycle of Halotestin with a moderately long cycle of Equipoise may have some merit in this instance. Neither would increase water retention drastically, neither would give explosive gains. But both have positive effects on the VO2 max.

In any case, and whatever the reason of use, 4 weeks is the best duration of use, 6 weeks at the most. As stated before, many athletes, having used fluoxymesterone while not under supervision of a physician, have ended up in the hospital with life-threatening conditions.

Halotestin is taken in mild doses (10-20 mg) every day for short periods of time, 4 weeks, 6 weeks at the very most due to its high level of toxicity. The use of anti-estrogens is not necessary since fluoxymesterone does not aromatize at all. As secondary drugs one may want to consider blood pressure medication such as catepressan to avoid hypertensive conditions. What you will definitely need is a check of liver values on a regular basis if you want to play it safe. I don't normally recommend the use of liver-protectors during a cycle as enhances liver function breaks down a greater amount of your steroid, but in this case you ought to make an exception. Milk thistle, dessicated liver, vitamin B6 and such both during and after a cycle are highly advised. There is no need for clomid of Nolvadex use after a cycle to bring back natural test. Halotestin really only serves a purpose as a bodybuilding drug when the athlete is cutting. Probably in the late stages of a cutting cycle to promote muscle density and hardness, preserve muscle tissue and such. To that effect it may be good to use some Halotestin (20-30 mg/day) the last 4 weeks of a boldenone or methenolone cycle for example, or at the end of a stack with trenbolone. It may make a good stacking partner for stanazolol (Winstrol/Stromba) as well since they serve the same purpose. But frankly in all cases opting for a higher dose of the other drug may be a better choice, both in terms of gains and safety. Boldenone (Equipoise) being the one possible exception. Due to its toxicity Halotestin is not much sought out in stacks.

[RRAdam]

Cheque Drops
Pharmaceutical Name: Mibolerone
Chemical structure: 7-alpha, 17-alpha-dimethyl-19Nor-androst-4-en-3-one,17b-ol
Effective dose: A few drops per day, taken sublingually


This is without a doubt THE most powerful steroid that was ever commercially marketed. Its androgenic potency is slightly less than that of methyltrienolone, but it can still aromatize, adding the benefits of estrogen as well. Unfortunately the only product it was ever marketed as never fully exploited the potential of this drug. It was delivered in microgram amounts in liquid droppers, the intent being to add a few drops to the food of female dogs in heat to keep them under control. Human athletes used a few drops under the tongue before a sporting event or training to increase their aggression levels, but noted little or no anabolic effect from this drug because it was so lowly dosed. Not that there was much room for high doses, because even in these low amounts using it longer than 2 or 3 weeks on end seemed to seriously compromise your liver. Just to demonstrate quite how toxic the compound mibolerone was to humans.

If it was free and safe to use orally, just 5 mg per day would probably give you more anabolic effect than a high-dose stack of several of the strongest products out there. It wasn't that far in potency from methyltrienolone. It possessed the same androgenic binding of trenbolone, even more so because its affinity for binding structures was even more reduced due to its 17-alpha-alkylation. But unlike methyltrienolone, it still allowed for aromatization to testosterone, enhanced by the progestagenic effect that all 19nor compounds seem to possess, which only further enhanced the extreme anabolic effect of mibolerone. Unfortunately because of its 17-alpha-alkylation it also rivaled methyltrienolone (metribolone) in liver toxicity, making it completely unsafe to even use 5 mg a day without killing yourself short term. A much better choice in that regard would have been trestolone (MENT), which is the same as Mibolerone but doesn't possess the toxic 17-alpha-methyl group. Sadly enough, MENT was never commercially marketed despite its well documented use as a male contraceptive (same for Mibolerone as well by the way).

But bodybuilders and other athletes had to make do with low-dosed cheque drops to increase activity. Nonetheless they enjoyed a great popularity. Mostly owed to the late Steroid guru Dan Duchaine. This was one of his many obscure (and usually dangerous) discoveries. The same person that discovered DNP, and extremely hazardous and powerful fatburner. Oddly enough cheque drops were more popular outside of bodybuilding. Boxers, football players and martial artists who fought full contact particularly had a fondness of this product and used it to enhance aggression prior to an important match with great success. It wasn't seldom that when a particularly aggressive incident occurred in boxing, that it was rumoured Mibolerone was the real culprit.

But even that didn't last, cheque drops have all but disappeared and I have yet to come across a legit one, or even an empty packaging from a legit one a long time ago. Which would illustrate what a dinosaur cheque drops have become in such a short time. But for those who really look around, they are still out there and I believe in some countries still used in veterinary medicine. So if you want it bad enough, but like I said, its impossible to use it to its full capacity, so its probably a waste to pursue anyway.

Because its extremely toxic in higher doses and cannot be used longer than 2 weeks on end, there really isn't much to stack with cheque drops. A user will opt to take but a few drops sublingually (under the tongue) prior to an event for which he requires and increase in energy and aggression. But because here too there is the risk of natural testosterone suppression, cheque drops are best used during a cycle with other anabolic steroids. In this nature it stacks with literally everything however, and is both suited for use during bulking as well as cutting, eventhough it doesn't have a direct influence on either. Because it's a non-aromatizing steroid that cannot be used longer than two weeks, the post-cycle use of clomid or Nolvadex is not required. Natural test will only partially be suppressed and should bounce back. If as advised you stacked it with a longer cycle of other steroids, its imperative that you still run them because of these other steroids, not so much for the cheque drops. For those prone to hypertension the use of an anti-hypertensive agent like Catapresan would be advised however. No other ancillaries should be required with this agent.

[RRAdam]

Andriol
Pharmaceutical Name: Testosterone (as Undecanoate)
Chemical structure: androsta-4-en-3-one,17b-ol
Effective dose: 8-16 caps/day orally
Available Doses: 40 mg/ml caps


Andriol is a fairly recently developed steroid. A new attempt at making an orally available testosterone, the first since the very unpopular methyl-testosterone. The delivery system used for andriol is quite novel in itself and shows a lot of promise. If it weren't for a few quirks I'm sure this delivery method could have caught on fast. The crude methyl-testosterone was the first of many oral steroids delivered by way of a 17-alpha-methyl alteration to the base compound. Apart from changing the affinity for a lot a structures, making a steroid with completely different characteristics, the main problem here was that it invoked a level of hepatoxicity. Often minor, sometimes severe (anadrol, Halotestin). This meant that treatment could not be continued for extended periods of time in complete safety. The demand for an oral steroid that can be used for lengthy treatment has been high since the very beginning. First of all its never easy for a doctor to sell his patients on injection protocols (many fear or at least dislike needles) and for the doctor too it would be easier if the patient could take a pill than to have him come back every other week for an injection. So the pressure was on to create a steroid that wouldn't require a 17-alpha-methyl alteration.

The answer was to seek a new way of delivery, that bypassed the liver, so that no alteration was needed to protect the steroid from being deactivated in the liver. That way was found in lymphatic absorption. As with many paths of uptake, this one too is very specific and limited. The lymphatic system is a series of heavily filtered channels intended for the resorption of water. When blood is delivered to a tissue through the arterial system, it is depleted of oxygen and nutrients, and then lead back to the heart by the venous system. Unfortunately only about 85% of the fluid is readily re-absorbed. That means 15% stays behind in the tissue and if that process where to continue day and night, we'd all swell up like Marshmallow man and explode in less than a week. That's why, inside tissues, there is another extended capillary system other than the cardiovascular one. The lymphatic system. This has the sole purpose of draining water from tissue. This is why it mostly only transports water. Its also heavily filtered by lymph nodes throughout the body that will remove almost everything, because the system is easily accessible and if not properly filtered a virus or cancer cell could easily spread throughout the body in this manner. But in the digestive tract it seems the lymph system makes an exception. Lymph fluid is usually clear (since its pure water), but in this area its troubled. That's because it appears to absorb oils and fats as well.

Steroids are made from the prime storage of fat in the body, cholesterol. So there is a definite possibility here. And the lymphatic system, for 75-80%, empties itself in the major duct (ductus thoracicus), which in turn empties itself in the angulus venosus, where the vena jugularis interna (internal jugular vein) and the vena subclavia (vein below the collarbone) meet, right before they enter the heart through a common vein. That means, without having to pass the liver, these fats can be delivered straight to the heart. Now the question is, if indeed it was readily absorbed by the lymphatic system, why alter a steroid at all to survive the liver ? Obviously it doesn't get through to any great extent. That's because it absorbs only actual fats. This carrier therefore targets the solution of the steroid in an oil, so that it will be absorbed with the oil. It also seeks to make the compound more lipophillic so solution is more complete and permanent. As we also learned from injectable steroids, the way to make a compound more lipophillic is by attaching an ester. The longer the ester is, the more lipophillic it makes the steroid. In this case they opted for an undecanoate ester, which has a length of 11 carbons, the longest ester used to date.

In this case we are talking about a testosterone undecanoate. It is dissolved in a type of sterile oil and then sealed inside a cap. As a whole, the dissolved steroid is then easily absorbed by the lymphatic system, prior to passing the liver, and delivered with ease to the heart where it is then sent out across the body. The system itself is ingenious and in theory perfect. Maximal delivery and no hepatoxicity. A potent steroid capable of being used for long treatments. However (I'm sure you saw that one coming) in practice things don't always turn out the way they appear in theory. In studies1 done on both men and women, andriol was shown to be a mild and inconsistent steroid at best. Mild is a problem that is easily solved with higher doses, but inconsistent is another story entirely. It seems that the amount that was delivered and the peak levels of testosterone in the blood as well as the length of activity, differed not only from person to person, but from day to day. That means a different person, from day to day, will get very varying levels of testosterone in the blood. And the differences were not minor.

One subject may have a peak level of 5 ng/mmol while another can have in excess of 50 ng/mmol. What's worse, the same person may get these levels on different days. In terms of its anabolic (ie non-medical) use, that means doses of 8-16 caps per day are being used. That's more than most will inject per week of the shorter cypionate and enanthate esters. Normally 1 cap delivers 40 mg of testosterone undecanoate. An ester releases the steroid in the blood, leaving us with approximately 25 mg of testosterone per cap (it's a long and heavy ester). That's 200-400 mg per day being used, and andriol being as novel as it is, isn't cheap or easy to come by. That makes it, at best, just as uninteresting as methyl-testosterone.

As far as the properties of this steroid go, like a propionate ester or a suspension injection, levels of testosterone, DHT and estrogen are easy to control, which makes this steroid a possibility for use during any time of the year, whether the athlete be cutting or bulking. The water retention is less notable than with longer esters, and if too high is easily controlled with Proviron or Nolvadex. Its pure testosterone, so if delivered in high enough doses, for reasons previously stated, it is of course a good mass builder with all the characteristics of testosterone. No more no less. It is of course a safe (to the liver), controllable oral steroid that can be used for extended periods of time, which does spark the interest of some, but anybody serious about gains will usually find andriol a very poor buy. Great invention for the medical world, but of little to no interest to the serious athlete.

Andriol doesn't have that many uses. When utilized in doses of 8-16 caps per day are used and it can obviously be stacked with most any other steroid. Water retention problems that are common with testosterone are usually controllable enough to warrant use even during cutting phases, and even if not Proviron can be added to maximize its potential. The use of ancillaries is generally not required as its very mild to begin with and most problems can be solved by discontinuing use or lowering the dose. The usual anti-estrogens can be used, but generally with the cost of andriol for what little it does makes it less appealing to invest in the likes of Nolvadex or arimidex. Caps are best spread out throughout the day. Most oral steroids have a 17-alpha-methyl alteration that changes affinity and binding of the steroid, so that a single dose is usually enough. With andriol delivery is swift, peak doses high, but the steroid never outlasts its half-life of 3-5 hours. So it should be taken in three equal doses throughout the day, preferably with meals as lymphatic absorption is promoted in the presence of bile and other secretions in the GI tract.