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I did a great deal of reading on IGF-1 this weekend--web searches, medical abstracts and journals, stuff like that. First, a short review.
Growth hormone (GH), the most abundant hormone secreted by the pituitary gland, is the primary hormone responsible for growth in mammals, accelerating lipolysis (fat metabolism) and protein synthesis. GH secretion is markedly blunted in obesity, but the reason for the decrease is not known. Other factors besides obesity diminish growth hormone secretion, including aging, nutritional status and exercise.
A variety of factors appear to be involved in decreased GH secretion of obese individuals. Whatever the cause, the defect of GH secretion in obesity appears to be secondary, since it is completely reversed by the normalization of body weight.
Growth hormone markedly improves body composition in both GH deficient and non-deficient adults. In experiments on elderly and obese subjects, fat free mass was increased and body fat reduced. And in studies on calorie restriction, GH treated subjects lose more weight.
PART 1: NORMAL GROWTH HORMONE FUNCTION
THE SOMATOTROPHIC AXIS
Overview.
Growth hormone (GH), also known as somatotrophin, is released from somatotroph cells in the pituitary gland. It is primarily released in pulses that take place during the early hours of sleep.
Growth hormone secretion. Production of growth hormone is modulated by many factors, including stress, exercise, nutrition, sleep and growth hormone itself. However, its primary controllers are two hypothalamic hormones:
Growth hormone releasing hormone (GHRH), a peptide that stimulates the synthesis and secretion of GH, and
Somatostatin (SRIH), a peptide that inhibits GH release.
Insulin-like growth factor. The half life of GH in humans is only about 25 minutes, just long enough to stimulate its uptake into the liver, where it is converted to growth factors. The most important of these growth factors is insulin-like growth factor (IGF-1), which forms a negative feed back loop with GH. High IGF-1 levels lead to decreased secretion of GH, by suppressing lactotrophic cells and stimulating the release of SRIH from the hypothalamus.
Many neurotransmitters (e.g. norepinephrine, epinephrine, and acetylcholine) and neuropeptides (opioid peptides and galanin) also stimulate and inhibit GH secretion. Peptides exert their effects on GH secretion indirectly through GHRH and SRIH.
Direct and indirect effects. GH acts directly by interacting with specific growth hormone receptors (GHRs) which are widely distributed throughout the body. Fat cells (adipocytes), for example, have growth hormone receptors, and growth hormone stimulates them to break down
Graphic: Colorado State University
triglyceride and suppresses their ability to take up and accumulate circulating lipids. GH can also interact with the GH-binding protein (GHBP), a truncated form of GHR. GHBPs in plasma form complexes with some of the GH in the blood, modulating the action of GH at the receptor level.
Growth and metabolism.
Bone and muscle growth. Indirect effects of GH are mediated primarily through insulin-like growth factor (IGF-1). A majority of the growth promoting effects of growth hormone is actually due to IGF-1 acting on its target cells. IGF-1 stimulates chondrocytes (cartilage cells), resulting in bone growth. IGF-1 also promotes muscle growth by stimulating the differentiation and proliferation of myloblasts, amino acid uptake and protein synthesis in muscle and other tissues. IGF-1 circulates largely bound to IGF binding protein-3 (IGFBP-3) and acid-labile subunit (ALS), in a complex which allows IGF-1 to remain in circulation for a longer period of time.
Protein, lipid and carbohydrate metabolism. GH affects protein, lipid and carbohydrate metabolism both directly, and indirectly through IGF-1.
Protein. Stimulates protein synthesis, increases amino acid uptake, and decreases oxidation of proteins.
Fat. Enhances fat utilization by stimulating triglyceride breakdown and adipocyte oxidation.
Carbohydrate. Suppresses the ability of insulin to stimulate the uptake of glucose in peripheral tissues and enhances glucose synthesis in the liver.
IGF-1 bound to IGFBP-3 and the ALS subunit above is important. Long R3 IGF-1 has a very similiar effect as this IGF-1 complex. So, there is a way around the lack of IGFBP-3 levels (genetically and environmentally determined). So, I have a new hypothesis. Suppose we restore one's Testosterone to high-normal via using Test Gel, Test sublingual Tabs, or Injectible Testos. Suppose we restore one's HGH levels. Now, suppose we add in Long R3 IGF-1 as previously discussed. If I am correct, we can transform the obese person with low Testos. and low HGH levels into a lean and healthy individual. Those with normal or high-normal Testos and HGH levels may benefit from only having to use IGF-1. Can you imagine only having to do a size/strength cycle with Long R3 IGF-1? No suppression of the HPTA. No estrogenic or prolactin/progesteronic sides and no DHT sides. Just some thoughts.
Growth hormone (GH), the most abundant hormone secreted by the pituitary gland, is the primary hormone responsible for growth in mammals, accelerating lipolysis (fat metabolism) and protein synthesis. GH secretion is markedly blunted in obesity, but the reason for the decrease is not known. Other factors besides obesity diminish growth hormone secretion, including aging, nutritional status and exercise.
A variety of factors appear to be involved in decreased GH secretion of obese individuals. Whatever the cause, the defect of GH secretion in obesity appears to be secondary, since it is completely reversed by the normalization of body weight.
Growth hormone markedly improves body composition in both GH deficient and non-deficient adults. In experiments on elderly and obese subjects, fat free mass was increased and body fat reduced. And in studies on calorie restriction, GH treated subjects lose more weight.
PART 1: NORMAL GROWTH HORMONE FUNCTION
THE SOMATOTROPHIC AXIS
Overview.
Growth hormone (GH), also known as somatotrophin, is released from somatotroph cells in the pituitary gland. It is primarily released in pulses that take place during the early hours of sleep.
Growth hormone secretion. Production of growth hormone is modulated by many factors, including stress, exercise, nutrition, sleep and growth hormone itself. However, its primary controllers are two hypothalamic hormones:
Growth hormone releasing hormone (GHRH), a peptide that stimulates the synthesis and secretion of GH, and
Somatostatin (SRIH), a peptide that inhibits GH release.
Insulin-like growth factor. The half life of GH in humans is only about 25 minutes, just long enough to stimulate its uptake into the liver, where it is converted to growth factors. The most important of these growth factors is insulin-like growth factor (IGF-1), which forms a negative feed back loop with GH. High IGF-1 levels lead to decreased secretion of GH, by suppressing lactotrophic cells and stimulating the release of SRIH from the hypothalamus.
Many neurotransmitters (e.g. norepinephrine, epinephrine, and acetylcholine) and neuropeptides (opioid peptides and galanin) also stimulate and inhibit GH secretion. Peptides exert their effects on GH secretion indirectly through GHRH and SRIH.
Direct and indirect effects. GH acts directly by interacting with specific growth hormone receptors (GHRs) which are widely distributed throughout the body. Fat cells (adipocytes), for example, have growth hormone receptors, and growth hormone stimulates them to break down
Graphic: Colorado State University
triglyceride and suppresses their ability to take up and accumulate circulating lipids. GH can also interact with the GH-binding protein (GHBP), a truncated form of GHR. GHBPs in plasma form complexes with some of the GH in the blood, modulating the action of GH at the receptor level.
Growth and metabolism.
Bone and muscle growth. Indirect effects of GH are mediated primarily through insulin-like growth factor (IGF-1). A majority of the growth promoting effects of growth hormone is actually due to IGF-1 acting on its target cells. IGF-1 stimulates chondrocytes (cartilage cells), resulting in bone growth. IGF-1 also promotes muscle growth by stimulating the differentiation and proliferation of myloblasts, amino acid uptake and protein synthesis in muscle and other tissues. IGF-1 circulates largely bound to IGF binding protein-3 (IGFBP-3) and acid-labile subunit (ALS), in a complex which allows IGF-1 to remain in circulation for a longer period of time.
Protein, lipid and carbohydrate metabolism. GH affects protein, lipid and carbohydrate metabolism both directly, and indirectly through IGF-1.
Protein. Stimulates protein synthesis, increases amino acid uptake, and decreases oxidation of proteins.
Fat. Enhances fat utilization by stimulating triglyceride breakdown and adipocyte oxidation.
Carbohydrate. Suppresses the ability of insulin to stimulate the uptake of glucose in peripheral tissues and enhances glucose synthesis in the liver.
IGF-1 bound to IGFBP-3 and the ALS subunit above is important. Long R3 IGF-1 has a very similiar effect as this IGF-1 complex. So, there is a way around the lack of IGFBP-3 levels (genetically and environmentally determined). So, I have a new hypothesis. Suppose we restore one's Testosterone to high-normal via using Test Gel, Test sublingual Tabs, or Injectible Testos. Suppose we restore one's HGH levels. Now, suppose we add in Long R3 IGF-1 as previously discussed. If I am correct, we can transform the obese person with low Testos. and low HGH levels into a lean and healthy individual. Those with normal or high-normal Testos and HGH levels may benefit from only having to use IGF-1. Can you imagine only having to do a size/strength cycle with Long R3 IGF-1? No suppression of the HPTA. No estrogenic or prolactin/progesteronic sides and no DHT sides. Just some thoughts.
