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  1. #31
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    Androgenic 100
    Anabolic 100
    Standard Testosterone (Standard)
    Chemical Names 4-androsten-3-one-17beta-ol, 17beta-hydroxy-androst-4-en-3-one
    Estrogenic Activity moderate
    Progestational Activity low
    Description:

    Sustanon 250 is an oil-based injectable testosterone blend that contains four different testosterone esters: testosterone propionate (30 mg); testosterone phenylpropionate (60 mg); testosterone isocaproate (60 mg); and testosterone decanoate (100 mg). Sustanon® is designed to provide a fast yet extended release of testosterone, usually requiring injections once every 3 to 4 weeks in a clinical setting. This is an improvement from standard testosterones such as cypionate or enanthate, which provide a shorter duration of activity. As with all testosterone products, Sustanon 250 is a very strong anabolic drug with pronounced androgenic activity. It is most commonly used in bulking cycles, providing exceptional gains in strength and muscle mass. A shorter-acting version of Sustanon, called Sustanon 100, is also made in certain areas (see:Sustanon 100).
    History:

    Sustanon 250 first appeared on international drug markets during the early 1970’s. It was developed by the international pharmaceutical giant Organon (now Merck/MSD), also responsible for such steroids as Durabolin®, Deca-Durabolin®, and Andriol®. Sustanon 250 was designed to offer a therapeutic advantage over existing single esters of testosterone, which need to be injected more frequently (cited advantages in hormone stability are probably not valid). In spite of this advantage, however, Sustanon 250 has never been approved for sale in the United States, although around the world it is one of the most popular brands of testosterone available. The lack of U.S. availability is probably due to the high costs associated with the FDA approval process and the availability of other somewhat comparable agents.
    Over the past 25 years, Sustanon 250 has probably been the most sought-after injectable testosterone among athletes. It must be emphasized, however, that this is not due to an unusual potency of this testosterone combination (esters really only affect the release of testosterone). This is simply due to the fact that a stack of four different testosterone compounds is a very good selling point; it is perceived to have more value. In most instances you will actually get a lot more for your money with testosterone enanthate or cypionate. The advantages to be found in Sustanon 250 are for the medical user only. If you were tied to your doctor for regular injections, then Sustanon 250 would allow you to visit him or her less frequently. This equates to a clear improvement in patient comfort. But if you are a bodybuilder injecting the drug every week, blood levels will build to the same extremes with either type of testosterone, and the added expense is probably not warranted.
    How Supplied:

    Sustanon 250 is widely available in human and (select) veterinary drug markets. Packaging volume may vary by country and manufacturer; the majority of products are supplied as 1 mL glass ampules.


    Structural Characteristics:

    Sustanon 250 contains a mixture of four testosterone compounds, which where modified with the addition of carboxylic acid esters (propionic, propionic phenyl ester, isocaproic, and decanoic acids) at the 17-beta hydroxyl group. Esterified forms of testosterone are less polar than free testosterone, and are absorbed more slowly from the area of injection. Once in the bloodstream, the ester is removed to yield free (active) testosterone. Esterified forms of testosterone are designed to prolong the window of therapeutic effect following administration, allowing for a less frequent injection schedule compared to injections of free (unesterified) steroid. Sustanon 250 is designed to provide a rapid peak in testosterone levels (24-48 hours after injection), and maintain physiological concentrations for approximately 21 days.586 Each 250 mg ampule provides 176mg of testosterone.

    Figure 1. Serum testosterone levels after a single injection of Sustanon 250. Source: Clinical Endocrinology (1984) 21, 97-107
    Side Effects (Estrogenic):

    Testosterone is readily aromatized in the body to estradiol (estrogen). The aromatase (estrogen synthetase) enzyme is responsible for this metabolism of testosterone. Elevated estrogen levels can cause side effects such as increased water retention, body fat gain, and gynecomastia. Testosterone is considered a moderately estrogenic steroid. An anti-estrogen such as clomiphene citrate or tamoxifen citrate may be necessary to prevent estrogenic side effects. One may alternately use an aromatase inhibitor like Arimidex® (anastrozole), which more efficiently controls estrogen by preventing its synthesis. Aromatase inhibitors can be quite expensive in comparison to anti-estrogens, however, and may also have negative effects on blood lipids.
    Estrogenic side effects will occur in a dose-dependant manner, with higher doses (above normal therapeutic levels) of Sustanon 250 more likely to require the concurrent use of an anti-estrogen or aromatase inhibitor. Since water retention and loss of muscle definition are common with higher doses of testosterone, this drug is usually considered a poor choice for dieting or cutting phases of training. Its moderate estrogenicity makes it more ideal for bulking phases, where the added water retention will support raw strength and muscle size, and help foster a stronger anabolic environment.
    Side Effects (Androgenic):

    Testosterone is the primary male androgen, responsible for maintaining secondary male sexual characteristics. Elevated levels of testosterone are likely to produce androgenic side effects including oily skin, acne, and body/facial hair growth. Men with a genetic predisposition for hair loss (androgenetic alopecia) may notice accelerated male pattern balding. Those concerned about hair loss may find a more comfortable option in nandrolone decanoate, which is a comparably less androgenic steroid. Women are warned of the potential virilizing effects of anabolic/androgenic steroids, especially with a strong androgen such as testosterone. These may include deepening of the voice, menstrual irregularities, changes in skin texture, facial hair growth, and clitoral enlargement.
    In androgen-responsive target tissues such as the skin, scalp, and prostate, the high relative androgenicity of testosterone is dependant on its reduction to dihydrotestosterone (DHT). The 5-alpha reductase enzyme is responsible for this metabolism of testosterone. The concurrent use of a 5-alpha reductase inhibitor such as finasteride or dutasteride will interfere with site-specific potentiation of testosterone action, lowering the tendency of testosterone drugs to produce androgenic side effects. It is important to remember that anabolic and androgenic effects are both mediated via the cytosolic androgen receptor. Complete separation of testosterone’s anabolic and androgenic properties is not possible, even with total 5-alpha reductase inhibition.
    Side Effects (Hepatotoxicity):

    Testosterone does not have hepatotoxic effects; liver toxicity is unlikely. One study examined the potential for hepatotoxicity with high doses of testosterone by administering 400 mg of the hormone per day (2,800 mg per week) to a group of male subjects. The steroid was taken orally so that higher peak concentrations would be reached in hepatic tissues compared to intramuscular injections. The hormone was given daily for 20 days, and produced no significant changes in liver enzyme values including serum albumin, bilirubin, alanine-amino-transferase, and alkaline phosphatases.587
    Side Effects (Cardiovascular):

    Anabolic/androgenic steroids can have deleterious effects on serum cholesterol. This includes a tendency to reduce HDL (good) cholesterol values and increase LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a direction that favors greater risk of arteriosclerosis. The relative impact of an anabolic/androgenic steroid on serum lipids is dependant on the dose, route of administration (oral vs. injectable), type of steroid (aromatizable or non-aromatizable), and level of resistance to hepatic metabolism. Anabolic/androgenic steroids may also adversely affect blood pressure and triglycerides, reduce endothelial relaxation, and support left ventricular hypertrophy, all potentially increasing the risk of cardiovascular disease and myocardial infarction.
    Testosterone tends to have a much less dramatic impact on cardiovascular risk factors than synthetic steroids. This is due in part to its openness to metabolism by the liver, which allows it to have less effect on the hepatic management of cholesterol. The aromatization of testosterone to estradiol also helps to mitigate the negative effects of androgens on serum lipids. In one study, 280 mg per week of testosterone ester (enanthate) had a slight but not statistically significant effect on HDL cholesterol after 12 weeks, but when taken with an aromatase inhibitor a strong (25%) decrease was seen.588 Studies using 300 mg of testosterone ester (enanthate) per week for 20 weeks without an aromatase inhibitor demonstrated only a 13% decrease in HDL cholesterol, while at 600 mg the reduction reached 21%.589 The negative impact of aromatase inhibition should be taken into consideration before such drug is added to testosterone therapy.
    Due to the positive influence of estrogen on serum lipids, tamoxifen citrate or clomiphene citrate are preferred to aromatase inhibitors for those concerned with cardiovascular health, as they offer a partial estrogenic effect in the liver. This allows them to potentially improve lipid profiles and offset some of the negative effects of androgens. With doses of 600 mg or less of testosterone per week, the impact on lipid profile tends to be noticeable but not dramatic, making an anti-estrogen (for cardioprotective purposes) perhaps unnecessary. Doses of 600 mg or less per week have also failed to produce statistically significant changes in LDL/VLDL cholesterol, triglycerides, apolipoprotein B/C-III, C-reactive protein, and insulin sensitivity, all indicating a relatively weak impact on cardiovascular risk factors.590 When used in moderate doses, injectable testosterone esters are usually considered to be the safest of all anabolic/androgenic steroids.
    To help reduce cardiovascular strain it is advised to maintain an active cardiovascular exercise program and minimize the intake of saturated fats, cholesterol, and simple carbohydrates at all times during active AAS administration. Supplementing with fish oils (4 grams per day) and a natural cholesterol/antioxidant formula such as Lipid Stabil or a product with comparable ingredients is also recommended.
    Side Effects (Testosterone Suppression):

    All anabolic/androgenic steroids when taken in doses sufficient to promote muscle gain are expected to suppress endogenous testosterone production. Testosterone is the primary male androgen, and offers strong negative feedback on endogenous testosterone production.Testosterone-based drugs will, likewise, have a strong effect on the hypothalamic regulation of natural steroid hormones. Without the intervention of testosterone-stimulating substances, testosterone levels should return to normal within 1-4 months of drug secession. Note that prolonged hypogonadotrophic hypogonadism can develop secondary to steroid abuse, necessitating medical intervention.
    The above side effects are not inclusive. For more detailed discussion of potential side effects, see the Steroid Side Effects section of this book.
    Administration (General):

    Testosterone propionate is often regarded as a painful injection. This is due to the very short carbon chain of the propionic acid ester, which can be irritating to tissues at the site of injection. Many sensitive individuals choose to stay away from this steroid completely, their bodies reacting with a pronounced soreness and low-grade fever that may last for a few days after each injection.
    Administration (Men):

    To treat androgen insufficiency, the prescribing guidelines for Sustanon® 250 call for a dosage of 250 mg every 3 weeks. Although active in the body for a longer time, Sustanon 250 is usually injected every 7 to 10 days for muscle-building purposes. This schedule will allow for the higher doses most commonly applied by athletes, and more stable elevations in hormone level. The usual dosage among male athletes is in the range of 250-750 mg per injection, taken in cycles 6 to 12 weeks in length. This level is sufficient for most users to notice exceptional gains in muscle size and strength.
    Sustanon 250 is usually incorporated into bulking phases of training, when added water retention will be of little consequence, the user more concerned with raw mass than definition. Some do incorporate this drug into cutting cycles as well, but typically in lower doses (125- 250 mg every 7-10 days) and/or when accompanied by an aromatase inhibitor to keep estrogen levels under control. Sustanon 250 is a very effective anabolic drug, and is often used alone with great benefit. Some, however, find a need to stack it with other anabolic/androgenic steroids for a stronger effect, in which case an additional 200-400 mg per week of boldenone undecylenate, methenolone enanthate, or nandrolone decanoate should provide substantial results with no significant hepatotoxicity. Testosterone is ultimately very versatile, and can be combined with many other anabolic/androgenic steroids to tailor the desired effect.
    Some bodybuilders have been known to use excessively high dosages of this drug (1,000 mg per week or more), although this practice is generally not advised. At dosages above 750 mg per week, water retention will likely account for more of the additional weight gain than new muscle tissue. The practice of “megadosing” is inefficient (not to mention potentially dangerous), especially when we take into account the typical high cost of Sustanon 250. Such use is usually not justified outside of aggressive bodybuilding regimens.
    Administration (Women):

    Sustanon 250 is rarely used with women in clinical medicine. When applied, it is most often used to induce masculinization in female to male transsexuals. Sustanon 250 is not recommended for women for physique- or performance-enhancing purposes due to its strong androgenic nature, tendency to produce virilizing side effects, and slow-acting characteristics (making blood levels difficult to control).
    Availability:

    Sustanon remains a popular testosterone product in many countries outside of the United States. The vast majority of products in western markets are made by or under license from Organon (now Merck/MSD), though many “clone” products are also manufactured in less regulated markets of Asia.

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    Growth Hormone Description:

    As its name suggests, human growth hormone is an important mediator of the human growth process. This hormone is produced endogenously by the anterior pituitary gland, and exists at especially high levels during childhood. Its growth-promoting effects are broad, and can be separated into three distinct areas: bone, skeletal muscle, and internal organs. It also supports protein, carbohydrate, lipid, and mineral metabolism, and can stimulate the growth of connective tissues. Although vital to early development, human growth hormone is produced throughout adulthood. Its levels and biological role decline with age, but continue to support metabolism, muscle tissue growth/maintenance, and the management (reduction) of adipose tissue throughout life. Somatropin specifically describes pharmaceutical human growth hormone that was synthesized with the use of recombinant DNA technology. Somatropin (rhGH) is biologically equivalent to human growth hormone (hGH) of pituitary origin.
    In a medical setting, somatropin is used to help treat a variety of health conditions. It is most notably prescribed in cases of childhood growth disorders that are characterized by insufficient growth hormone production. While usually not fully corrective, somatropin use is often capable of substantially increasing the linear growth rate and overall height before further growth is halted in adolescence. This medication is also used to accelerate growth in children that were born small and failed to catch up by the age of two. Other uses include the treatment of short bowel syndrome, growth failure due to renal insufficiency, muscle wasting associated with HIV infection, and adult growth hormone deficiency.
    Growth Hormone (somatropin) is also sometimes prescribed to healthy men and women who are aging. Growth hormone levels tend to decline as we get older, and many physicians believe that its supplementation to more youthful levels can help slow some of the damage of aging. Given its beneficial metabolic effects on muscle mass, strength, energy, cell regeneration, and fat loss, there are many supporters of this use, even if hGH may not specifically retard the aging process. Note that in order to prescribe hGH for adult hormone deficiency in the U.S., the patient must have a diagnosed pituitary disease or history of childhood GH deficiency. It is specifically illegal according to Federal law to prescribe growth hormone for any off-label use, which includes anti-aging and bodybuilding purposes.717
    Somatropin may be given by either subcutaneous or intramuscular injection. During clinical studies, the pharmacokinetic properties of somatropin following both methods of use were determined. When given by subcutaneous injection, somatropin has a similar but moderately higher level of bioavailability (75% vs. 63%). The rate of drug metabolism following both routes was also very similar, with somatropin displaying a half-life of approximately 3.8 hours and 4.9 hours after subcutaneous and intramuscular injection, respectively. Baseline hormone levels are usually reached between 12 hours and 18 hours following injection, with the slower times seen with intramuscular use. Given the delayed rise in IGF-1 levels, however, which can remain elevated 24 hours after hGH injection, the metabolic activity of human growth hormone will outlast its actual levels in the body. Although drug absorption is acceptable by both methods of use, daily subcutaneous administration is generally regarded as the preferred method of using somatropin.
    A specific analysis of growth hormone activity shows a hormone with a diverse set of effects. It is anabolic to skeletal muscle, shown to increase both the size and number of cells (processes referred to as hypertrophy and hyperplasia, respectively). The hormone also seems to have growth-promoting effects on all organs of the body excluding the eyes and brain. Somatropin has a diabetogenic effect on carbohydrate metabolism, which means that it causes blood sugar levels to rise (a process normally associated with diabetes). Excessive administration of somatropin over time may induce a state of type-2 (insulin resistant) diabetes. This hormone also supports triglyceride hydrolysis in adipose tissue, and may reduce body fat stores. Coinciding with this tends to be a reduction in serum cholesterol. The drug also tends to reduce levels of potassium, phosphorous, and sodium, and may cause a decrease in levels of the thyroid hormone triiodothyronine (T3). The latter effect marks a reduction in thyroid-supported metabolism, and can interfere with the effectiveness of extended therapy with somatropin.
    Growth hormone has both direct and indirect effects. On the direct side, the hGH protein attaches to receptors in muscle, bone, and adipose tissues, sending messages to support anabolism and lipolysis (fat loss). Growth hormone also directly increases glucose synthesis (gluconeogenesis) in the liver, and induces insulin resistance by blocking its activity in target cells. The indirect effects of growth hormone are largely mediated by IGF-1 (insulin-like growth factor), which is produced in the liver and virtually all other tissues in response to growth hormone. IGF-1 is also anabolic to both muscle and bone, augmenting growth hormone’s activity. IGF-1, however, also has effects that are strongly antagonistic to growth hormone. This includes increased lipogenesis (fat retention), increased glucose consumption, and decreased gluconeogenesis. The synergistic and antagonists effects of these two hormones combine to form the character of hGH. Likewise, they also dictate the effects of somatropin administration, which include the support lipolysis, increased serum glucose levels, and reduced insulin sensitivity.
    Growth Hormone is considered to be a controversial anabolic and performance-enhancing drug in the realm of bodybuilding and athletics. The main issue of debate is the exact level of potential benefit this substance carries. While studies with HIV+ patients in a wasting state tend to support potentially strong anabolic and anticatabolic properties, studies demonstrating these same effects in healthy adults and athletes are lacking. During the 1980s, a large body of myth surrounded discussions of hGH in bodybuilding circles, which may have been fueled by the high cost of the drug and its very name (“growth hormone”). It was once thought to be the most powerful anabolic substance you could buy. Today, recombinant human growth hormone is much more affordable and readily obtained. Most experienced individuals now tend to agree that it is the fat-loss-promoting properties of somatropin that are most obvious. The drug can support muscle growth, strength gains, and increased athletic performance, but its effects are generally milder than those of anabolic/androgenic steroids. For a highly advanced athlete or bodybuilder, however, somatropin can help push body and performance further than might have been possible with steroids alone.
    History:
    The first human growth hormone preparations to be used in medicine were made from pituitary extracts of human origin. These are now commonly referred to as cadaver growth hormone preparations. Approximately 1 mg of hGH (a 1 day dose) could be obtained from each cadaver. The first successful treatment with human cadaver GH was reported in 1958.718 Soon after these medicines were introduced to market, and were sold in the U.S. until 1985. The Food and Drug Administration banned them that year after they had been linked to the development of Creutzfeldt-Jakob’s disease (CJD), a highly degenerative and ultimately fatal brain disorder, in a number of patients. The disease can be transmitted from one person to another under exceptional circumstances (usually blood transfusion or organ implantation are involved), and was likely caused by the extraction of hGH from infected cadavers. CJD has a very slow incubation period, and has been diagnosed anywhere from 4 to 30 years after therapy with growth hormone of cadaver origin. As of 2004 estimates, at least 26 patients that received cadaver GH drugs in the United States have been diagnosed with the disease.719 The overall incidence of this disease is less than 1%, as approximately 6,000 patients are documented to have received the medication.
    The FDA approved the first synthetic human growth hormone drug in 1985. Synthesis produced a pure hormone without biological contamination, eliminating the possibility of CJD transmission. The drug approved was called somatrem (Protropin), and was based on a manufacturing technology developed by Genentech in 1979.720 Somatrem came at an important time given the removal of cadaver GH by the FDA that same year. This hormone is actually a slight variant of the hGH protein, but displays the same biological properties of the natural hormone. Protropin was initially very successful being it was the first synthetic GH product. By 1987, however, Kabi Vitrum (Sweden) had published methods for the production of pure synthetic somatropin with the exact amino acid sequence of endogenous growth hormone.721 It was also discovered that the unnatural structure of somatrem causes a much higher incidence of antibody reactions in patients, which can reduce drug efficacy.722Somatropin would come to be viewed as a more reliable drug, and would dominate the global market within several years. Today, although somatrem products are still sold, somatropin retains the vast majority of hGH sales worldwide.
    How Supplied:
    Somatropin is most commonly supplied in multi-dose vials containing a white lyophilized powder that requires reconstitution with sterile or bacteriostatic water before use. Dosage may vary widely from 1mg to 24mg or more per vial. Somatropin is also available as a stabile pre-mixed solution (Nutropin AQ) that is biologically equivalent to reconstituted somatropin.
    Structural Characteristics:
    Somatropin is human growth hormone protein manufactured by recombinant DNA technology. It has 191 amino acid residues and a molecular weight of 22,125 daltons. It is identical in structure to human growth hormone of pituitary origin.
    Storage:
    Do not freeze. Follow package insert for storage information. Refrigeration (2º to 8ºC, 35º to 46º F) may be required before and after reconstitution.
    Side Effects (General):
    The most common adverse reactions to somatropin therapy are joint pain, headache, flu-like symptoms, peripheral edema (water retention), and back pain. Less common adverse reactions include inflammation of mucous membranes in the nose (rhinitis), dizziness, upper respiratory infection, bronchitis, tingling or numbness on the skin, reduced sensitivity to touch, general edema, nausea, sore bones, carpal tunnel syndrome, chest pain, depression, gynecomastia, hypothyroidism, and insomnia. The abuse of somatropin may cause diabetes, acromegaly (a visible thickening of the bones, most notably the feet, forehead, hands, jaw, and elbows), and enlargement of the internal organs. Due to the growth promotion effects of human growth hormone, this drug should not be used by individuals with active or recurring cancer.
    Side Effects (Impaired glucose tolerance):
    Somatropin may reduce sensitivity to insulin and raise blood sugar levels. This may occur in individuals without preexisting diabetes or impaired glucose tolerance.
    Side Effects (Injection site):
    The subcutaneous administration of somatropin may cause redness, itching, or lumps at the site of injection. It may also cause a localized decrease of adipose tissue, which may be compounded by the repeated administration at the same site of injection.
    Administration:
    Somatropin is designed for subcutaneous or intramuscular administration. One milligram of somatropin is equivalent to approximately 3 International Units (3 IU). When used to treat adult onset growth hormone deficiency, the drug is commonly applied at a dosage of .005/mg/kg per day to .01mg/kg per day. This equates to roughly 1 IU to 3 IU per day for person of approximately 180-220 lbs. A long-term maintenance dosage is established after reviewing the patient’s IGF-1 levels and clinical response over time.
    When used for physique- or performance-enhancing purposes, somatropin is usually administered at a dosage between 1 IU and 6 IU per day (2-4 IU being most common). The drug is commonly cycled in a similar manner to anabolic/androgenic steroids, with the length of intake generally being between 6 weeks and 24 weeks. The anabolic effects of this drug are less apparent than its lipolytic (fat loss) properties, and generally take longer periods of time and higher doses to manifest themselves.
    Other drugs are commonly used in conjunction with somatropin in order to elicit a stronger response. Thyroid drugs (usually T3) are particularly common given the known effects of somatropin on thyroid levels, and may significantly enhance fat loss during therapy. Insulin is also commonly used with somatropin. Aside from countering some of the effects somatropin has on glucose tolerance, insulin can increase receptor sensitivity to IGF-1, and reduce levels of IGF binding protein-1, allowing for more IGF-1 activity723 (growth hormone itself also lowers IGF binding protein levels).724Anabolic/androgenic steroids are also commonly taken with somatropin, in an effort to maximize potential muscle-building effects. Anabolic steroids may also further increase free IGF-1 levels via a lowering of IGF binding proteins.725 Note that the stacking of somatropin with thyroid drugs and/or insulin is usually approached with great care and caution, given that these are particularly strong medications with potentially serious or life threatening acute side effects.
    Availability:
    Somatropin is produced by many different drug companies, and is distributed in virtually all developed countries. The most common brand names include Serostim (Serono), Saizen (Serono), Humatrope (Eli Lilly), Norditropin (novo nodisk), Omnitrope (Sandoz), and Genotropin (Pharmacia). Be aware that growth hormone products are extremely high value targets for drug counterfeiting operations. By this author’s estimation, the majority of products sold on the black market are in fact not real growth hormone preparations.

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    Increlex is a brand name for mecasermin, which is human insulin-like growth factor-1 (IGF-1) manufactured by recombinant DNA technology (rhIGF-1). IGF-1 is the primary mediator of the growth promoting effects of human growth hormone. As such, mecasermin also can stimulate the growth of bone, muscle, and internal organs. Its effects on skeletal muscle are also strongly hyperplasic, meaning it causes an increase in cell number. Unlike hGH, however, mecasermin has very strong insulin-like effects. It can support growth by increasing the uptake of amino acids, glucose, and fatty acids, but lowers blood sugar levels so efficiently that it can induce severe hypoglycemia if too high a dosage is taken. The increased uptake of fatty acids also means that mecasermin may promote lipogenesis, or an increase in the storage of body fat.This agent is of interest to bodybuilders and athletes for its potential to support the growth of skeletal muscle and connective tissue.
    Increlex is most commonly prescribed for the treatment of severe primary IGF-1 deficiency (Primary IGFD). This disease is characterized by a failure to produce normal levels of IGF-1 due to insufficiencies in the growth hormone / IGF-1 axis (usually involving GH receptor, signaling pathway, or IGF-1 gene defects). Such patients typically have normal or even high levels of growth hormone, but their bodies do not respond to it with the sufficient production of IGF-1. Mecasermin may also be used for the treatment of patients who have developed antibodies to growth hormone therapy. In both instances the patient is not GH deficient, but does not respond properly to growth hormone therapy, making IGF-1 an effective alternative medication¹. Given its differing effects on metabolism, however, mecasermin is not considered to be a medical substitute for hGH therapy, and retains a narrow field of FDA approved uses.
    History:
    The U.S. Food and Drug Administration approved Mecasermin in August 2005. It is sold under the brand name Increlex, manufactured by Tercica Inc. of Brisbane, California. Tercica licenses this technology from Genentech, which was the first company to sell a synthetically manufactured human growth hormone product in the United States (Protropin). Tercica’s rhIGF-1 is produced by a similar recombinant DNA technology. The process involves inserting the gene encoding for the human IGF-1 protein into E. coli bacteria, which then synthesize the protein. In October 2006, Tercia licensed the European rights to Increlex to the specialties pharmaceutical firm Ipsen. Ipsen received approval to market Increlex in the European Union in August 2007.
    How Supplied:
    Mecasermin (Increlex) is supplied in 4mL multi-dose vials containing 10 mg/mL.
    Structural Characteristics:
    Mecasermin is human IGF-1 protein manufactured by recombinant DNA technology. It consists of a string of 70 amino acids and has a molecular weight of 7,649 daltons. Its amino acid sequence is identical to that of endogenous human IGF-1.
    Storage:
    Do not freeze. Refrigeration (2º to 8ºC, 35º to 46º F) required before and after reconstitution.
    Side Effects (Hypoglycemia):
    The most common adverse reaction to mecasermin therapy is hypoglycemia, which occurred on at least one occasion in 42% of patients receiving the drug during clinical trials. Approximately 7% of patients noticed severe hypoglycemia, and 5% noticed hypoglycemic seizure or loss of consciousness. Signs of mild to moderate hypoglycemia include 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, one should immediately consume a food or drink containing simple sugars such as a candy bar or carbohydrate drink. Signs of severe hypoglycemia include disorientation, seizure, and unconsciousness. Severe hypoglycemia can lead to death and requires immediate emergency medical attention. Note that in some cases the symptoms of hypoglycemia can be mistaken for drunkenness.
    Mecasermin should never be taken before sleep or in higher than recommended doses. A meal or snack must be consumed within 20 minutes (before or after) of administration.
    Side Effects (Injection site):
    The subcutaneous administration of mecasermin may cause bruising at the site of injection. It may also cause a localized increase of adipose tissue, which may be compounded by the repeated administration at the same site of injection. Rotation of the injection sites is recommended.
    Side Effects (General):
    Other potential adverse reactions to mecasermin therapy include joint pain, growth of the tonsils, snoring, headache, dizziness, convulsions, vomiting, ear pain, hearing loss, and hypertrophy of the thymus gland. Mild elevations in serum AST, ALT, and LDH levels were found in a significant number of patients, but they were not associated with hepatotoxicity. Mecasermin can stimulate the growth of internal organs. Kidney and spleen hypertrophy was particularly pronounced in the first years of long-term therapy in clinical trials, without declining renal function. Elevations in cholesterol and triglycerides were also observed, but remained within the upper limit of normal values. Evidence of heart enlargement was observed in a few patients, but this appeared without any apparent clinical significance. The overall relationship between mecasermin use and cardiac changes has not yet been fully assessed. Thickening of facial soft tissues was observed in several patients, and should be monitored during therapy. The abuse of mecasermin may cause acromegaly, which is characterized by a visible thickening of the bones, most notably the feet, forehead, hands, jaw, and elbows. Due to the growth promotion effects of hIGF-1, this drug should not be used by individuals with active or recurring cancer.
    Administration:
    Increlex is intended for subcutaneous administration. The initiation of therapy involves close monitoring of blood glucose levels until a proper maintenance dose is established. The recommended starting dose is .04 to .08 mg/kg (40 to 80 mcg/kg) twice daily. The dose may be increased by .04 mg/kg per injection, reaching a maximum of .12 mg/kg twice daily. Doses greater than .12 mg/kg are not advised due to potential hypoglycemic effects. Mecasermin should always be administered within 20 minutes (before or after) a meal or snack.
    Mecasermin is not widely used for physique- or performance-enhancing purposes. Common protocols of administration have not yet been established. Due to the potential for severe hypoglycemia, maximum doses among bodybuilders and athletes are not likely to measurably exceed those supplied by therapeutic guidelines. This drug will most likely by taken in cycles lasting no longer than 8-12 weeks in an effort to minimize unwanted organ growth or fat gain.

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    Insulin is peptide hormone produced in the Islets of Langerhans in the pancreas. The release of this hormone in the human body is most closely tied to blood glucose levels, although a number of other factors including pancreatic and gastrointestinal hormones, amino acids, fatty acids, and ketone bodies are also involved. The main biological role of insulin is to promote the intracellular utilization and storage of amino acids, glucose, and fatty acids, while simultaneously inhibiting the breakdown of glycogen, protein, and fat. It is most notably identified with the control of blood sugar levels, and insulin medications are typically prescribed to people with diabetes, a metabolic disorder characterized by hyperglycemia (high blood sugar).While insulin targets many different organs in the body, this hormone is both anabolic and anti-catabolic to skeletal muscle tissue,732 733 734 a fact that explains the inclusion of pharmaceutical insulin in the realm of athletics and bodybuilding.
    The use of insulin to improve performance and body composition can be a little tricky because this hormone can also promote nutrient storage in fat cells.This, however, is an activity of insulin that can be somewhat managed by the user. Athletes have found that a strict regimen of intense weight training and a diet without excess caloric and fat intake can enable insulin to show a much higher affinity for protein and glucose storage in muscle (as opposed to fatty acid storage in adipose) cells. This is especially true in the post-exercise enhanced-absorptive state, where insulin sensitivity in skeletal muscle has been shown to increase significantly over baseline (rested) levels.735 When used during the post-training window, the hormone is, likewise, capable of producing rapid and noticeable muscle gains. The muscles often begin to look fuller (and even sometimes more defined) very soon after initiating insulin therapy, and the overall results of therapy are often described as dramatic.
    The fact that insulin use cannot be detected by urinalysis has ensured it a place in the drug regimens of many athletes and professional bodybuilders. Note that there has been some progress in drug detection, especially with the analogs, but to date regular insulin is still considered a ”safe” drug. Insulin is often used in combination with other “contest safe” drugs like human growth hormone, thyroid medications, and low dose testosterone injections, and together can have a dramatic effect on the user’s physique and performance without fear of a positive urinalysis result. Those who do not have to worry about drug testing, however, often find that insulin combined with anabolic/androgenic steroids can be a very synergistic combination. This is because the two actively support an anabolic state through different mechanisms. Insulin strongly enhances the transport of nutrients into muscle cells and inhibits protein breakdown, and the anabolic steroids (among other things) strongly increase the rate of protein synthesis.
    As mentioned, the usual medical purpose for insulin is to treat different forms of diabetes. More specifically, the human body may not be producing enough insulin (Type-I diabetes), or may not recognize insulin well at the cell site although some level is present in the blood (Type-II diabetes). Type-I diabetics are, therefore, required to inject insulin on a regular basis, as they are left without a sufficient level of this hormone. Along with medication, the individual will need to constantly monitor blood glucose levels and regulate their sugar intake. Together with lifestyle modifications such as regular exercise and developing a balanced diet, insulin dependent individuals can live a healthy and full life. When left untreated, however, diabetes can be a fatal disease.
    History:
    Insulin first became available as a medicine during the 1920s. Credit for the discovery is most appropriately given to Canadian physician Fred Banting and Canadian physiologist Charles Best, who worked together to produce the first insulin preparations, and the world’s first effective treatment of diabetes. Their work stemmed from an idea initially proposed by Banting, who as a young doctor theorized that an active extract could be made from animal pancreases to regulate blood sugar in human patients. He needed help to try and actualize his idea, and he sought out world-renowned physiologist J.J.R. Macleod at the University of Toronto. Macleod, initially less than impressed with the unusual concept (but likely impressed with Banting’s conviction and tenacity), assigned a couple of graduate students to assist him in his work. A coin flip determined who would work with Banting, and he was eventually paired with graduate student Best. Together they made medical history.
    The first insulin preparations they produced were made of crude pancreatic extracts taken from dogs. At one point the supply of laboratory animals was exhausted, and desperate to continue their research, the pair actually began taking stray dogs to supplement their pancreas supply. Shortly after, the two found that they could work with the pancreases of slaughtered cows and pigs, making their work much easier (and ethically acceptable). They successfully treated their first diabetic patient with insulin in January 1922. By August of that year, they had been successful in treating a group of clinical patients, including 15-year-old Elizabeth Hughes, daughter of former presidential candidate Charles Evans Hughes. Elizabeth was diagnosed with diabetes in 1918, and her dramatic fight for life with the disease gained national attention. Elizabeth would be saved by insulin on the doorstep of starvation, as severe calorie restriction was the only remedy known to slow the disease at the time. Banting and Macleod swiftly won the Nobel Prize for their discovery, which was presented to them approximately a year later in 1923. Shortly after, dispute over credit arose, and ultimately Banting shared his prize with Best, and Macleod shared his prize with J. B. Collip, a chemist that assisted in the extraction and purification process.
    After initially declining the assistance in the hopes that they could work out production issues on their own, Banting and his team worked with Eli Lilly & Co. to develop the first mass-produced insulin medicines using their animal extraction techniques. Their production success was extreme and rapid, and the drug became commercially available on a wide scale in 1923, the same year Banting and Macleod won the Nobel prize.That same year, Nordisk Insulinlaboratorium was founded by Danish scientist Augusta Krogh, who desperately wanted to bring back an insulin manufacturing technique to Denmark to treat his wife, who was ill with diabetes.This Denmark firm eventually became Novo Nordisk, the world’s second leading producer of insulin next to Eli Lilly & Co.
    The early insulin medications were fairly impure by today’s standards. They typically contained 40 units of animal insulin per milliliter, in contrast to today’s accepted standard concentration of 100 units. The large doses needed with these early low-concentration drugs were not very comfortable for patients, and injection-site reactions were not uncommon. They also contained significant protein impurities that would sometimes cause allergic reactions in users. Despite these faults, the drugs saved the lives of countless individuals who beforehand were faced with a sure death sentence following a diagnosis of diabetes. Eli Lilly and Novo Nordisk improved the purity of their products in the coming years, but no major improvements in insulin technology developed until the mid-1930s, when the first longer-acting insulin preparations began to surface.
    The first longer-acting drug made use of protamine and zinc to delay the action of insulin in the body, extending the activity curve and reducing the number of daily injections required for many patients. Dubbed Protamine Zinc Insulin (PZI), the preparation would have an effect lasting as long as 24-36 hours. Neutral Protamine Hagedorn (NPH) Insulin, also known as Isophane insulin, followed, reaching market by 1950. This preparation was very similar to PZI insulin except that it could be mixed with regular insulin without disturbing the release curve of the respective insulins. In other words, a regular insulin drug could be mixed in the same syringe with NPH insulin, providing a biphasic release pattern characterized by an early peak effect due to the regular insulin, and an extended action brought on by the NPH.
    In 1951 the Lente insulins began to surface, which included semilente, lente, and ultra-lente preparations. The amount of zinc used in each varied, producing preparations with distinct and long-acting pharmacokinetics. Unlike previous Insulins, this was also achieved without the use of protamine. Many physicians were soon able to successfully switch their patients from NPH insulin over to a single morning dose of Lente insulin, often heralding the release of the new drugs as a big advance in insulin medications (though some would still require an evening dose with a Lente insulin to maintain full control over blood glucose levels during the 24-hour period). Up to this point the insulin drugs made by the large pharmaceutical companies worked very well. No substantial step forward in the development of new insulin delivery technologies would come for another 23 years.
    In 1974, chromatographic purification techniques allowed the manufacture of animal insulin with extremely low impurity levels (less than 1 pmol/l of protein impurities). Novo was the first to release a drug made with this technology, which it called monocomponent (MC) Insulin. Eli Lilly also released a version called “Single Peak” Insulin, likely referring to the single protein peak noticed upon chemical analysis. This advance, though significant, would be short lived. In 1975, Ciba-Geigy produced the first synthetic insulin preparation (CGP 12831). And just three years later, scientists at Genentech were able to produce insulin using modified E. coli bacteria, the first synthetic insulin with an identical amino acid sequence as human insulin (although the animal insulins work fine in humans their structures are slightly different). The U.S. Food and Drug administration approved the first such medicines in 1982, with the acceptance of Humulin R (Regular) and Humulin NPH from Eli Lilly & Co. The name Humulin is a contraction of the words “human” and “insulin”, of course. Novo would follow with semi-synthetic insulins Actrapid HM and Monotard HM.
    The FDA has approved a variety of other insulin drug combinations over the years, including various biphasic insulin blends that use differing amounts of rapid and longer-acting insulins. More recently, we have also seen the FDA approval of Eli Lilly’s rapid-acting insulin analog Humalog. Several other analogs are also now available including Lantus and Apidra from Aventis, and Levemir and Novorapid from Novo Nordisk. A number of additional analogs are also under investigation at this time. With the large variety of different insulin medications approved and sold in the U.S. and other nations, it is important to understand that “insulin” represents an extremely broad class of medicines. As a class, these drugs are likely to continue to expand as new agents are developed and successfully tested. Today, it is estimated that 55 million people use some form of injectable insulin on a regular basis to manage their diabetes, making this an extremely important and lucrative area of human medicine.
    How Supplied:
    Pharmaceutical insulin comes from one of two basic origins, animal or synthetic.With animal source insulin, the hormone is extracted from the pancreas of either pigs or cows (or both) and prepared for medical use. These preparations are further divided into the categories “standard” and “purified”, dependent on the level of purity and non-insulin content of the solution. With such products there is always the slight possibility of pancreatic contaminants making their way into the prepared drug. Specifically called biosynthetic, synthetic insulin is produced by a recombinant DNA procedure similar to the process used to manufacture human growth hormone. The result is a polypeptide hormone consisting of one 21- amino acid “A-chain” coupled by two disulfide bonds with one 30-amino acid “B-chain”. The biosynthetic process will produce a drug free of the pancreatic protein contaminants possible with animal insulin, and that is structurally and biologically identical to human pancreatic insulin. With the innate (remote) risk of contamination involved with animal insulin, coupled with the fact that the structure is (very slightly) different from human insulin, synthetic human insulin drugs dominate the market today. Biosynthetic human insulin/insulin analogs are also the most common insulins of use among athletes,and the main focus of this profile.
    There are a variety of synthetic insulins available, with each possessing unique properties relating to speed of onset, peak and duration of activity, and concentration of dose. This therapeutic variety may allow physicians to tailor a treatment program for insulin-dependant diabetics that allows for the least amount of daily injections and the greatest level of patient comfort. It is important that one should be aware of the individual activity of any insulin drug before attempting its use. Due to the differences between preparations, it is also medically advised that extreme care be taken whenever a physician attempts to switch an insulin-dependant diabetic patient from one form of insulin medication to another.
    Below is a list showing the distinctions between popular forms of biosynthetic insulin.
    Short-acting Insulins:
    Humalog® (Insulin Lispro): Humalog® is a short-acting analog of human insulin, specifically the Lys(B28) Pro(B29) analog of insulin created when the amino acids at positions 28 and 29 are reversed. It is considered equipotent to regular soluble insulin on a unit-to-unit basis, but with more rapid activity.736 The onset of drug action following subcutaneous administration is approximately 15 minutes, and its peak effect is reached in 30 to 90 minutes. It has a total duration of action between 3 and 5 hours.
    Novolog® (Insulin Aspart): Novolog is a short-acting analog of human insulin created when the amino acid proline at position B28 is replaced with aspartic acid. The onset of drug action following subcutaneous administration is approximately 15 minutes, and its peak effect is reached in 1-3 hours. It has a total duration of action between 3 and 5 hours. It has similar pharmacokinetics to Insulin Lispro.
    Insulin lispro or aspart are usually used as a supplement to a longer acting insulin product, providing a fast-acting medication that can be taken before or immediately after meals to mimic the body’s natural insulin response. Many athletes believe that their short window of effect makes they ideal insulin medications for physique- or performance-enhancing purposes, as most of its action can be concentrated in the post-training enhanced-nutrient-uptake window.
    Humulin®-R “Regular” (insulin Inj): Identical to human insulin. Also sold as Humulin-S® (Soluble) in some markets, this product consists of zinc-insulin crystals dissolved in clear fluid. There is nothing added to slow the release of this product, so it is generically referred to as soluble human Insulin. This drug works rapidly and has a short duration of effect.The onset of drug action following subcutaneous administration is 20-30 minutes, and its peak effect is reached in 1-3 hours. It has a total duration of action between 5 and 8 hours. Together with Humalog, these two forms of insulin are the most popular (almost exclusive) choices among athletes and bodybuilders for physique- or performance-enhancement purposes.
    Intermediate- and Long-acting Insulins:
    Humulin®-N, NPH (insulin isophane): A crystalline suspension of insulin with protamine and zinc to delay its release and extend its action. Insulin isophane is considered intermediate length insulin. The onset of drug action following subcutaneous administration is approximately 1-2 hours, and its peak effect is reached in 4-10 hours. It has a total duration of activity lasting more than 14 hours. This type of insulin is not commonly used for physique- or performance-enhancement purposes.
    Humulin®-L, Lente (medium zinc suspension): A crystalline suspension of insulin with zinc to delay its release and extend its action. Humulin-L is considered an intermediate length insulin. The onset of drug action following subcutaneous administration is approximately 1-3 hours, and its peak effect is reached in 6-14 hours. It has a total duration of activity lasting more than 20 hours. This type of insulin is not commonly used for physique- or performance-enhancement purposes.
    Humulin®-U, Ultralente (prolonged zinc suspension): A crystalline suspension of insulin with zinc to delay its release and extend its action. Humulin-U is considered a long-acting insulin. The onset of drug action following subcutaneous administration is approximately 6 hours, and its peak effect is reached in 14-18 hours. It has a total duration of activity lasting 18-24 hours.This type of insulin is not commonly used for physique- or performance-enhancement purposes.
    Lantus (insulin glargine): A long-acting analog of human insulin. Insulin glargine is created when the amino acid asparagine at position A21 is replaced by glycine, and two arginines are added to the C-terminus of the insulin B chain. The onset of drug action following subcutaneous administration is approximately 1-2 hours, and the drug is considered to have no significant peak (it is designed to have a very stable release pattern throughout the duration of activity). Insulin glargine lasts between 20-24 hours in the body following subcutaneous injection. This type of insulin is not commonly used for physique- or performance-enhancement purposes.
    Biphasic Insulins:
    Humulin® Mixtures: These are mixtures of regular soluble insulin for a fast onset of action, and a long- or intermetiate-acting insulin for a prolonged effect. These are labeled by the mixture percentage, commonly 10/90, 20/80, 30/70, 40/60, and 50/50. Mixtures using Humalog as the rapid-acting insulin are also available.
    Warning: Concentrated Insulin
    The most common forms of insulin come in a concentration of 100 IU of hormone per milliliter. These are identified as “U-100” preparations in the U.S. and many other regions. In addition to this, however, there are also concentrated forms of insulin available for patients that require higher doses and a more economical or comfortable option to U-100 preparations. In the U.S., products containing as much as 5 times the normal concentration, or 500 IU per milliliter, are also sold. These are identified as “U-500” preparations, and are available by prescription only. It can be extremely dangerous or life threatening to replace a U-100 insulin product with a U-500 product without making the necessary dosing adjustments to compensate for the greater drug concentration. Given the general difficulty in accurately measuring athletic doses (2-15 IU) with a drug of such high concentration, U-100 preparations are used almost exclusively for physique- and performance-enhancing purposes.
    Side Effects (Hypoglycemia):
    Hypoglycemia is the primary danger with the use of insulin. This is a dangerous condition that occurs when blood glucose levels fall too low. It is a common and potentially fatal reaction experienced at some time or another by most medical and nonmedical insulin users, so it needs to be taken seriously. It is, therefore, critical to understand the warning signs of hypoglycemia. The following is a list of symptoms that may indicate 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, one should immediately consume a food or drink containing simple sugars such as a candy bar or carbohydrate drink.This will hopefully raise blood glucose levels sufficiently enough to ward off mild to moderate hypoglycemia. There is always a possibility of severe hypoglycemia, which is very serious and requires immediate emergency medical attention. Symptoms of this include disorientation, seizure, unconsciousness, and death. Note that in some cases the symptoms of hypoglycemia are mistaken for drunkenness.
    It is also very important to note that you may notice a tendency to get sleepy after injecting insulin. This is an early symptom of hypoglycemia, and a clear sign the user should be consuming more carbohydrates. One should absolutely avoid the temptation to go to sleep at this point, as the insulin may take its peak effect during rest, and blood glucose levels could be left to drop significantly. Unaware of this condition during sleep, the athlete may be at a high risk for going into a state of severe hypoglycemia. The serious dangers of such a state have already been discussed, and unfortunately consuming more carbohydrates during sleep will not be an option. Those experimenting with insulin would, therefore, be wise to always stay awake for the duration of the drug’s effect, and also avoid using insulin in the early evening to ensure the drug will not be inadvertently active when retiring for the night. It is also important to make sure others are aware of your use of the drug so that they may inform emergency medical technicians should you lose consciousness or the ability to inform others of your condition due to hypoglycemia. This information can spare valuable (perhaps life saving) time in helping medical professionals establish a diagnosis and provide supportive treatment.
    Side Effects (Lipodystrophy):
    The subcutaneous administration of insulin may cause a localized increase in adipose tissue at the site of injection. This may be compounded by the repeated administration of insulin at the same site of injection.
    Side Effects (Allergy to Insulin):
    In a small percentage of users, the administration of insulin may cause a localized allergy. This may include irritation, swelling, itching, and/or redness at the site of injection. This often subsides as therapy continues. In some instances it may be due to an allergy to an ingredient, or in the case of animal insulin, a protein contaminant. Less common, but potentially more serious, is a systemic allergic reaction to insulin administration. This may include a rash on the whole body, wheezing, shortness of breath, fast pulse, sweating, and/or a reduction in blood pressure. In rare instances this may be life threatening. Any adverse reaction should be reported to a medical authority.
    Administration (General):
    Given that there are varying forms of insulin available for medical use with differing pharmacokinetic patterns, as well as products with different drug concentrations, it is extremely important that the user be familiar with the dosage and actions of any specific insulin preparation they intend to use so that peak-effect, total time of effect, total dosage, and carbohydrate intake can be closely monitored. Rapid-acting insulin preparations (Novolog, Humalog, and Humulin-R) are the most popular choices for physique- or performance-enhancing purposes, and the subject of the dosing information presented in this book. It is also important to stress that before one considers using insulin they should also become very familiar with using a glucometer. This is a medical device that can give you a quick and accurate reading of your blood glucose level. This device can be indispensable in helping one manage and optimize their insulin/carbohydrate intake.
    Administration (Short-acting Insulin):
    Short acting forms of insulin (Novolog, Humalog, Humulin-R) are designed for subcutaneous injection. Following subcutaneous injection, the injection site should be left alone and not rubbed, to prevent the drug from releasing into circulation too quickly. It is also advised to rotate subcutaneous injection sites regularly to avoid the localized buildup of subcutaneous fat that may develop due to the lipogenic properties of this hormone (see Adverse Reactions: Lipodystrophy). The medical dosage will vary depending on the individual requirements of the patient. Furthermore, changes in such things as diet, activity level, or work/sleep schedule may affect the required insulin dose. Although not recommended medically, it is possible to administer some short-acting insulins via intramuscular injection. This, however, may create more variability (and potential risk) with regard to drug dissipation and hypoglycemic effect.
    Insulin dosages can vary slightly among athletes, and are often dependent upon factors like body weight, insulin sensitivity, activity level, diet, and the use of other drugs. Most users choose to administer insulin immediately after a workout, which is the most opportunistic time of the day to use this drug. Among bodybuilders, dosages of regular insulin (Humulin-R) used are usually in the range of 1IU per 15-20 pounds of lean bodyweight; 10IU is perhaps the most common dosage. This amount may be adjusted downward slightly for users of the more rapid-acting Humalog and Novolog preparations, which provide a higher and faster peak effect. First-time cautious users usually ignore bodyweight guidelines, and instead start at a low dosage with the intention of gradually working up to a normal dosage. For example, on the first day of insulin therapy one may begin with a dose as low as 2 IU. Each consecutive post-workout application this dosage might be increased by 1IU, until the user determines a comfortable range. Many feel this is safer and much more tailored to the individual than simply calculating and injecting a dose, as some find they tolerate slightly more or less insulin than weight guidelines would dictate. Athletes using growth hormone in particular often have slightly higher insulin requirements, as HGH therapy is shown to both lower secretion of, and induce cellular resistance to, insulin.
    One must also remember that it is very important to consume carbohydrates for several hours following insulin use. One should generally follow the rule-of-thumb of ingesting at least 10-15 grams of simple carbohydrates per IU of insulin injected (with a minimum immediate intake of 100 grams regardless of dose).This is timed 10 to 30 minutes after subcutaneous injection of Humulin-R, or immediately after using Novolog or Humalog.The use of a carbohydrate replacement drink is often used as a fast carbohydrate source. Properly cautious insulin users will always have a source for simple sugars on-hand in case an unexpected drop in glucose levels is noticed. Many athletes will also take creatine monohydrate with their carbohydrate drink, since the insulin may help force more creatine into the muscles. 30-60 minutes after injecting insulin, one should also eat a good meal and consume a protein shake. The carbohydrate drink and meal/protein shake are absolutely necessary, as without them blood sugar levels may drop dangerously low and the athlete may enter a state of hypoglycemia (see Adverse Reactions: Hypoglycemia). Carbohydrates and proteins are continually provided in sufficient amounts to meet glucose requirements throughout the entire window of insulin effect.
    Administration (Intermediate-acting, Long-acting, and Biphasic Insulins):
    Intermediate-acting, long-acting, and biphasic insulins are designed for subcutaneous injection. Intramuscular injection will cause the drug to be released too rapidly, potentially resulting in hypoglycemia. Following subcutaneous injection, the injection site should be left alone and not rubbed, to prevent the drug from releasing into circulation too quickly. It is also advised to rotate subcutaneous injection sites regularly to avoid the localized buildup of subcutaneous fat due to the lipogenic properties of this hormone (see Adverse Reactions: Lipodystrophy). The medical dosage will vary depending on the individual requirements of the patient. Furthermore,changes in such things as diet, activity level, or work/sleep schedule may affect the required insulin dose. Intermediate-acting, long-acting, and biphasic insulins are not widely used for physique- or performance-enhancing purposes due to their longer acting nature, which makes them poorly suited for concentrating the nutrient partitioning effect of insulin during the short post-workout enhanced-nutrient-uptake window.
    Availability:
    U-100 insulins may be dispensed from pharmacies in the United States without a prescription. This is so that an insulin-dependent diabetic will have easy access to this life-saving medication. Concentrated (U-500) insulin is sold by prescription only. In most regions of the world, high medical use of the drug leads to easy access and low prices on the black market.

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    Protropin (Somatrem) Description:

    Somatrem is a synthetically manufactured form of human growth hormone (hGH). It is actually a variant of endogenous hGH protein, containing the same sequence of 191 amino acids, but with the addition of an extra amino acid, methionine. For this reason somatrem is commonly described as methionyl human growth hormone. As an hGH medication, somatrem supports the growth of bone, skeletal muscle, connective tissues, and internal organs. It also plays a role in protein, carbohydrate, lipid, and mineral metabolism. In a medical setting, somatrem is used to treat children with growth failure caused by endogenous growth hormone deficiency. When administered as a long-term treatment before linear growth is stopped due to closed epiphyses, the drug may impart a significant positive effect on linear growth. Somatrem is considered to be therapeutically equivalent to growth hormone of pituitary origin. As an hGH drug, somatrem is valued by bodybuilders and athletes for its ability to promote fat loss and muscle and connective tissue growth.
    Although somatrem is considered equivalent to human growth hormone, it is not a natural protein to the human body. This may increase the chance for developing antibodies to growth hormone during treatment. The antibodies work by binding with the growth hormone molecule, interfering with its ability to bind receptors and exert activity. In one clinical investigation, 2/3rd of the children treated with somatrem developed antibodies to growth hormone after one year.726 In a similarly configured investigation involving the administration of somatropin for one year, only 1 in 7 patients produced serum antibodies to growth hormone.727 It is important to note that in both studies the antibody reactions were not strong, and did not appear to substantially diminish the ability of the drugs to be therapeutically effective. Diminishment activity (as determined by antibody levels) appears in an very small percentage (<1%) of patients taking somatrem. Still, the correct 191 amino acid configuration of somatropin is considered more desirable to use.
    History:
    Somatrem was approved for sale in the U.S. in 1985. It was the first synthetic growth hormone medication available worldwide, produced via a manufacturing process called Inclusion Body Technology.728 The technology involves inserting the DNA encoding for the hGH protein into escherichia coli (E.coli) bacteria, which assemble and synthesize the pure protein. Prior to the advent of synthetic growth hormone, hGH was made into a medication only by extracting the natural protein from human corpses. Biological or cadaver hGH, as it was called, was banned in the U.S. in 1985 due to the high prevalence of a rare neurological disease in patients. Somatrem was approved for sale that same year, giving Genentech a short monopoly on the growth hormone market. Within several years, however, other biotechnology companies began selling a form of hGH that was identical to the endogenous protein, called somatropin. Although somatrem remains available in a number of markets including the United States, somatropin is much more widely distributed.
    How Supplied:
    Somatrem is most commonly supplied in multi-dose vials containing a white lyophilized powder that requires reconstitution with sterile or bacteriostatic water before use. Dosage may vary from 1mg to 10 mg per vial.
    Structural Characteristics:
    Somatrem is a polypeptide (methionyl human growth hormone) manufactured by recombinant DNA technology. It has 192 amino acid residues and a molecular weight of 22,256 daltons.
    Storage:
    Do not freeze. Refrigeration (2º to 8ºC, 35º to 46º F) required before and after reconstitution.
    Side Effects (General):
    The most commonly reported adverse reactions to somatrem therapy include carpal tunnel syndrome, increased growth of nevi (moles and birthmarks), gynecomastia, and pancreatitis. Note that the side effects of somatrem will generally mirror those of somatropin therapy. The abuse of somatrem may cause diabetes, acromegaly (a visible thickening of the bones, most notably the feet, forehead, hands, jaw, and elbows), and enlargement of the internal organs. Due to the growth promotion effects of human growth hormone, this drug should not be used by individuals with active or recurring cancer.
    Side Effects (Impaired glucose tolerance):
    Somatrem may reduce sensitivity to insulin and raise blood sugar levels. This may occur in individuals without preexisting diabetes or impaired glucose tolerance.
    Side Effects (Injection site):
    The subcutaneous administration of somatrem may cause redness, itching, or lumps at the site of injection. It may also cause a localized decrease of adipose tissue, which may be compounded by the repeated administration at the same site of injection.
    Administration:
    Somatrem is given by subcutaneous or intramuscular injection. One milligram of somatrem is equivalent to approximately 3 International Units (3IU). When used to treat children with growth failure due to growth hormone deficiency, the drug is applied at a dosage up to .04/mg/kg per day. This equates to a maximum of roughly 10IU per day for a person of approximately 180 lbs. A long-term maintenance dosage is established after reviewing the patient’s IGF-1 levels and clinical response over time, and may be substantially lower than 10IU.
    When used for physique- or performance-enhancing purposes, somatrem is usually administered at a dosage between 1IU and 6 IU per day (2-4 IU being most common). The drug is commonly cycled in a similar manner to anabolic/androgenic steroids, with the length of intake generally being between 6 weeks and 24 weeks. The anabolic effects of this drug are less apparent than its lipolytic (fat loss) properties, and generally take longer periods of time and higher doses to manifest themselves.
    Availability:
    Somatrem is available in the United States under the Protropin brand name which is distributed by Roche. In Europe and most nations the vast majority of hGH is the correct 191 amino acid sequence somatropin. Somatrem can be found in some markets, however, most commonly in Asia, where it tends to sells for a substantially lower price than somatropin

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    Androgenic: 500
    Anabolic: 500
    Standard: Nandrolone acetate
    Chemical Name: 17beta-Hydroxyestra-4,9,11-trien-3-one
    Estrogenic Activity: none
    Progestational Activity: moderate
    Description:

    Trenbolone enanthate is an injectable form of the strong anabolic steroid trenbolone. Given the use of an enanthate ester, this drug will exhibit virtually identical pharmacokinetics to testosterone enanthate, providing a peak release of its steroid within the first several days after injection, followed by declining levels for approximately 2 weeks. The base steroid here (trenbolone) is a derivative of nandrolone, and exhibits strong anabolic and androgenic properties. On a milligram for milligram basis it is considerably more potent than testosterone as both an anabolic and androgenic agent, though it does carry a more favorable balance (toward anabolism). Trenbolone is also unable to convert to estrogen, however it does exhibit notable progestational activity, which may mimic estrogenic side effects given the right physiological conditions. Trenbolone enanthate is virtually interchangeable with Parabolan (trenbolone hexahydrobenzylcarbonate), capable of promoting strong gains in lean muscle mass, often with an accompanying increase in relative hardness and definition.
    History:

    Slow-acting trenbolone esters were first studied in 1967, during a series of experiments into synthetic anabolic steroids by Roussel-UCLAF.607 Roussel did not specifically investigate Trenbolone enanthate, although the drug would have remained an obvious possibility once trenbolone was released given the widespread application of steroid esters (including enanthate) by the 1960’s. The drug would not see the light of day for many decades, however, and was only first released for commercial sale in 2004. It was introduced by British Dragon, an underground manufacturer. British Dragon would sell it under the trade name Trenabol, in 200 mg/mL strength.
    Although it was not for sale through pharmacies nor approved for human or veterinary use, Trenabol was widely distributed throughout the world, and became an extremely popular product with athletes and bodybuilders. Much of this had to do with the fact that it was unique, in that it was one of but a few options for injectable trenbolone that used slow-acting esters. At the time of its introduction, trenbolone acetate products were by and large the dominant form of trenbolone, and remain the dominant form of the drug to this day. Although British Dragon was perhaps the largest and most well known underground steroid manufacturer in the world, the company abruptly collapsed at the end of 2006. The brand has since re-emerged under new ownership. Trenbolone enanthate continues to be sold by a number of underground labs, though no registered drug company has yet introduced it to a legitimate drug market.
    How Supplied:

    Trenbolone enanthate is not available as a prescription drug product.


    Structural Characteristics:

    Trenbolone is a modified form of nandrolone. It differs by the introduction of double bonds at carbons 9 and 11, which inhibit aromatization (9-ene), increase androgen-binding affinity,608 and slows its metabolism. The resulting steroid is significantly more potent as both an anabolic and an androgen than its nandrolone base. The trenbolone here is modified with an enanthate ester at the 17-beta hydroxyl group, so that the free steroid is released more slowly from the area of injection.
    Side Effects (Estrogenic):

    Trenbolone is not aromatized by the body, and is not measurably estrogenic. It is of note, however, that this steroid displays significant binding affinity for the progesterone receptor (slightly stronger than progesterone itself ).609 610 The side effects associated with progesterone are similar to those of estrogen, including negative feedback inhibition of testosterone production and enhanced rate of fat storage. Progestins also augment the stimulatory effect of estrogens on mammary tissue growth. There appears to be a strong synergy between these two hormones, such that gynecomastia might even occur with the help of progestins, without excessive estrogen levels. The use of an anti-estrogen, which inhibits the estrogenic component of this disorder, is often sufficient to mitigate gynecomastia caused by progestational anabolic/androgenic steroids. Note that progestational side effects are more common when trenbolone is being taken with other aromatizable steroids.
    Side Effects (Androgenic):

    Although classified as an anabolic steroid, trenbolone is sufficiently androgenic. Androgenic side effects are still common with this substance, and may include bouts of oily skin, acne, and body/facial hair growth. Anabolic/androgenic steroids may also aggravate male pattern hair loss. Women are also warned of the potential virilizing effects of anabolic/androgenic steroids. These may include a deepening of the voice, menstrual irregularities, changes in skin texture, facial hair growth, and clitoral enlargement. Additionally, the 5-alpha reductase enzyme does not metabolize trenbolone,611 so its relative androgenicity is not affected by finasteride or dutasteride.
    Side Effects (Hepatotoxicity):

    Trenbolone is not c-17 alpha alkylated, and is generally not considered a hepatotoxic steroid; liver toxicity is unlikely. This steroid does have a strong level of resistance to hepatic breakdown, however, and severe liver toxicity has been noted in bodybuilders abusing trenbolone.612 Although unlikely, hepatotoxicity cannot be completely excluded, especially with high doses.
    Side Effects (Cardiovascular):

    Anabolic/androgenic steroids can have deleterious effects on serum cholesterol. This includes a tendency to reduce HDL (good) cholesterol values and increase LDL (bad) cholesterol values, which may shift the HDL to LDL balance in a direction that favors greater risk of arteriosclerosis. The relative impact of an anabolic/androgenic steroid on serum lipids is dependant on the dose, route of administration (oral vs. injectable), type of steroid (aromatizable or non-aromatizable), and level of resistance to hepatic metabolism. Due to its non-aromatizable nature and strong resistance to metabolism, trenbolone has a moderate to strong (negative) impact on lipid values and atherogenic risk. Anabolic/androgenic steroids may also adversely affect blood pressure and triglycerides, reduce endothelial relaxation, and support left ventricular hypertrophy, all potentially increasing the risk of cardiovascular disease and myocardial infarction.
    To help reduce cardiovascular strain it is advised to maintain an active cardiovascular exercise program and minimize the intake of saturated fats, cholesterol, and simple carbohydrates at all times during active AAS administration. Supplementing with fish oils (4 grams per day) and a natural cholesterol/antioxidant formula such as Lipid Stabil or a product with comparable ingredients is also recommended.
    Side Effects (Testosterone Suppression):

    All anabolic/androgenic steroids when taken in doses sufficient to promote muscle gain are expected to suppress endogenous testosterone production. Without the intervention of testosterone-stimulating substances, testosterone levels should return to normal within 1-4 months of drug secession. Note that prolonged hypogonadotrophic hypogonadism can develop secondary to steroid abuse, necessitating medical intervention. In experimental studies, trenbolone was determined to be approximately three times stronger at suppressing gonadotropins than testosterone on a milligram for milligram basis.
    The above side effects are not inclusive. For more detailed discussion of potential side effects, see the Steroid Side Effects section.
    Administration (Men):

    Trenbolone enanthate was never approved for use in humans. Prescribing guidelines are unavailable. Common doses for physique- and performance-enhancing purposes fall in the range of 150-300 mg per week, which is usually taken for 6-10 consecutive weeks. This level is sufficient to produce considerable increases in lean muscle mass and strength, which are usually combined with notable fat loss and increased muscle definition. As with all trenbolone injectables, this product is fairly versatile, and can be combined with many other agents depending on the desired results.
    Administration (Women):

    Trenbolone enanthate was never approved for use in humans. Prescribing guidelines are unavailable.This agent is generally not recommended for women for physique- or performance-enhancing purposes due to strong androgenic nature and tendency to produce virilizing side effects.
    Availability:

    Trenbolone enanthate is currently not a prescription drug product. It is made exclusively by underground and export oriented steroid manufacturers only.

  7. #37
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    Exotics
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    Anyone ever heard of this one?
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    Some of these exotics I have never heard of. It makes me wonder where they went to.
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