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    Default Growth Hormone. HGH. Human Growth Hormone Fat Loss

    Every bodybuilder has heard of human Growth Hormone (GH), even if very few have actually used the drug. GH is one of the most potent and expensive drugs in the bodybuilders' chemical arsenal.1 Despite the expense involved in acquiring GH, it is almost universally used by professional and elite amateur bodybuilders. The success achieved over the last thirty years by bodybuilders has not gone unnoticed, as anti-aging medicine has grown from a cottage industry to a recognized sub-specialty.2

    GH promotes muscle hypertrophy and fat loss, the ideal one-two combination for bodybuilders or anyone concerned about their physical appearance.2 Though GH is an anabolic hormone, chemically, it differs greatly from anabolic steroids. Anabolic steroids are based upon testosterone, being ringed molecules that dissolve well in oil. GH is a protein composed of 191 amino acids.3 The amino acids are linked in a specific order, like a chain, but the molecule is bunched up as though the chain was balled together rather than laid straight. GH does not dissolve well in oil; instead it dissolves in water.

    When used as a drug, GH is dissolved in water, and then injected under the skin several times a week. It travels quickly through the system, affecting nearly every type of cell in the body (fat, muscle, heart, bone, etc).

    Though access to GH as a drug is restricted to a select few people, every healthy person has a supply of the hormone. GH is produced and stored in a specialized gland located near the base of the brain called the pituitary gland.4 It would be wonderful if the pituitary would respond to verbal commands and release GH at any level desired. That would allow everyone to lower body fat, increase muscle size and reduce recovery time.

    Scientists continue to study human growth hormone production and release, as the role of the hormone in aging and other conditions becomes evident. Like other endocrine hormones, GH release is controlled by a feedback system - under some conditions it is stimulated, under others it is blocked. GH release is rather complex, especially when compared to testosterone. Testosterone is controlled using a fairly simple "negative feedback system" involving a three part axis - hypothalamus (a portion of the brain), the pituitary gland and the testes.5 When the testes are not stimulated, blood levels of testosterone are low. This is sensed by the hypothalamus, causing it to release gonadotropin releasing hormone (GnRH). GnRH travels to the pituitary, stimulating the release of luteinizing hormone (LH) into the bloodstream. LH travels to the testes, stimulating production of testosterone, raising blood levels. When testosterone levels rise, the hypothalamus senses the change, shutting off the release of GnRH. This is turn shuts down the release of LH from the pituitary and testosterone release from the testes is reduced until blood levels fall and the cycle is repeated. This triad (GnRH - LH - testosterone) is relatively simple in that each of the hormones is directly linked with the others.

    GH is much different, and unfortunately, much more complex. The control of testosterone is relatively simple in that one hormone (testosterone) from one organ (testes) is monitored. When low levels of testosterone are sensed by the hypothalamus, word is sent chemically to the pituitary and a signaling hormone is released that stimulates the testes to produce more. When too much testosterone is present, that is sensed by the hypothalamus and word is passed to the pituitary, which stops releasing the signaling hormone and the testes go into a rest mode.

    GH affects more than one organ and is stimulated by more than one signaling hormone. So researchers were left to wonder, how is GH release controlled? To this date, that question has not been fully answered, but a fairly clear picture has been developed.

    The pituitary gland is the primary source for GH in the body. Being a protein hormone, GH is stored in special cells in the pituitary gland, contained in tiny hormone filled bubbles.4 When these cells are stimulated, the hormone bubbles connect to a faucet shaped structure on the cell surface (a very, very small faucet, so small only that a few molecules can escape at a time) and they squirt out a spray of GH.6 Think of a squirt gun - when the trigger is pulled, it pushes on a water bladder and some of the water is squirted out of the muzzle.

    The released GH enters the circulation, traveling to all the tissues of the body. In some tissues, GH stimulates growth, such as muscle and bone.7,8 In fat cells, GH stimulates the release of stored fat.9 In addition to acting directly as a hormone, GH also stimulates the production of a second anabolic hormone called IGF-1.10 IGF-1 also stimulates muscle growth and bone density, and is believed to be responsible for much of the anabolic effect of GH.1

    GH differs from the example of testosterone at the level of the hypothalamus in that IGF-1 affects both GHRH and somatostatin, explained in detail below. In the example of the testosterone feedback cycle, LH - the signaling hormone released by the pituitary gland, does not act on any other tissues than the testes. GH on the other hand, affects many different tissues. The primary action of LH is the release of testosterone, which is monitored by the hypothalamus. GH increases the production and release of IGF-1. Receptors on the hypothalamus monitor IGF-1, which has been shown to increase somatostatin and decrease GHRH release with a net effect of decreasing GH release from the pituitary gland.11,12

    GH has been described as a promiscuous hormone, in that it reacts to a number of chemical stimuli, much as a promiscuous woman might respond to a number of male suitors.12,13 For many years, GH was believed to be under the control of two hypothalamic hormones - GH releasing hormone (GHRH) and somatostatin. Functionally, these two are opposites, GHRH stimulates the release of GH and somatostatin inhibits GH release.12 This was simple enough to understand. Imagine a car where you have one foot on the brake and the other on the gas at all times. When you press the brake harder, the car stops. If you let up on the brake and step on the gas, the car accelerates forward. IGF-1 appears to step on the brake (increase somatostatin) and let up on the gas (decrease GHRH) at the same time.

    GHRH and somatostatin flip-flop up and down, allowing GH to be released many times a day in a cycle. However, GH seems to respond to environmental factors as well, such as hunger, exercise, arginine, etc. It was later discovered that a separate type of receptor is present on the hypothalamus and pituitary, called the GH secretagogue receptor.14 The natural stimulus for this new receptor appears to be the hormone ghrelin, which is produced by cells in the stomach, small intestine and areas of the brain. Ghrelin signals when the stomach is empty and stimulates hunger and feeding. Though ghrelin increases GH, a fat reducing hormone, it also increases appetite and fat storage. Part of the weight loss success experienced by people who have gastric bypass surgery (weatherman Al Roker, singer Carnie Wilson) is due to a sharp drop in ghrelin levels after the surgery.15

    Other drugs have been developed which also stimulate the GH secretagogue receptor. Pharmaceutical companies have developed several different secretagogues, with positive clinical studies, but no licensed products have been released to the U.S. market at this time.

    Many bodybuilders are aware of the ability of L-arginine to increase GH release.16 L-arginine, when consumed in large amounts (several grams) can increase GH release, but the effect is not universal nor is it consistent. It appears that L-arginine does not directly stimulate GH release; rather it blocks somatostatin release and makes the pituitary gland more sensitive to GHRH. The effects of L-arginine are due in part to one of its metabolites, nitric oxide. Nitric oxide appears to stimulate one of the cellular reactions that take place in the pituitary after GHRH has signaled for GH release. When nitric oxide levels are high, the response to GHRH is greater.17 This may account for some of the conflicting data relating to L-arginine induced GH release. If the conditions do not support GHRH release at the same time, nitric oxide appears to have little effect on GH levels.

    The understanding of GH release goes much deeper, with several pathways and messengers being involved inside the pituitary cells.18 However, these pathways are all subject to the actions taking place at the level of the receptors. Though a few people might find discussions of phospholipase C, IP3 and protein kinase C riveting or the identification of porosomes amazing (actually, it was an amazing discovery), for most the inner workings of the pituitary cells will always remain a black box.

    One would think that the expanded knowledge of the control and release of GH would lead to new treatments for obesity, GH deficiency and aging related disorders. Yet, little has developed along these lines. The primary reason is that there is an ample supply of GH that is safe, effective and well understood. Until a need arises for means of treating pituitary deficiency directly, or the medical community understands that there are many people who have normal GH levels, but desire optimal GH levels, it is unlikely that pharmaceutical companies will devote the resources necessary to develop such drugs. It would be interesting to see what benefits some of the shelved projects, such as the secretagogues might provide to the growing population of healthy, but driven adults in the U.S.
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    Great Post Presser! You have the best Bodybuilding , Anabolic Steroid, HGH, IGF 1 lr3, sarm and peptide type articles around!

    Yes thats called Key word stuffing, lol
    Growth Hormone. HGH. Human Growth Hormone Fat Loss

  3. #3
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    Shameful lol
    Growth Hormone. HGH. Human Growth Hormone Fat Loss

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