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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.
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.
A specific analysis of somatropin 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.
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).724 Anabolic/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.
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