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Ran across this. Just thought I'd share.
By: Dr. David Lee Spear
Growth hormone binds to DNA and causes, or stimulates, the DNA to produce more ribosomes. Then GH binds to ribosomes and activates them to turn out IGF-1 molecules. IGF-1 molecules leave the cytoplasm and go into the plasma, thus becoming circulating IGF-1. IGF-1 has a half life of about 20 hours.
IGF-1 and insulin both do very similar things: they both attach to receptors of muscle cells. The receptors are very similar. These receptors are part of the cell membrane structure. GH and insulin both increase the cellular membrane permeability of certain amino acids, to thus facilitate the transfer of those amino acids into the muscle cells into the sarco-plasm.
The amino acids that insulin facilitates to cross are different than the amino acids that IGF-1 helps to cross. The entire array of both of them combined is what is necessary for "proteo-genesis" (new protein for muscles). It is like a double key system in a bank safe: you need both keys, or you can't open the safe. You need ALL the amino acids that IGF-1 helps to cross AND all the amino acids that insulin helps to cross, or you can't have proteo-genesis.
High IGF-1 with low insulin has no anabolic effect because to have new proteo-genesis you need ALL the amino acids helped across by IGF-1 AND of insulin. Low IGF-1 and high insulin also does not help to build muscle because IGF-1 is missing, so the amino acid array is incomplete.
ATP can be formed in ample amounts from glucose, fat, or protein. If IGF-1 synthesis by the liver is markedly reduced during ketosis, as I've theorized, it would have to be the result of specific enzyme changes resulting from low insulin concentrations. Low insulin levels cause widespread metabolic changes throughout the body by changing specific enzyme systems.
In fact, low insulin output, by itself, causes shutdown of proteogenesis, regardless of IGF-1 levels, and is the primary (and maybe the only) cause of the greatly increased output of GH during starvation or keto dieting.
Low insulin also increases fat mobilization, an effect enhanced by elevated GH. So, now I withdraw my prediction of low IGF-1 levels during ketosis, but if they occur, low IGF-1 may be an additive factor in the stimulation of GH output, and in the shutdown of muscle proteogenesis.
Growth hormone goes into the insulin producing cells of the pancreas to greatly increase the output of insulin, so insulin goes way up... unless there is very little carbohydrate... in which case high insulin doesn't happen. If it did, you could go into a hypoglecemia coma, and you could even die. Nobody knows how this happens, but when GH goes into the pancreas, something turns off the pancreas's response to glucose.
Acromegalic Giants all become Type I diabetics eventually, because GH has so overstimulated their insulin producing cells that they have literally burned out. (Type I diabetes means their pancreas doesn't produce any insulin.)
The other effect of GH is that it makes us insulin resistant to glucose concentration. The beauty of this insulin resistance is that it allows us to have a high insulin levels without profound hypoglycemia, and together with the IGF-1 this then gives us a maximum anabolic effect.
But prolonged elevated insulin and insulin resistance could lead us in the wrong direction, and Type II diabetes. So in the week off GH, the very low carbohydrate levels causes very low insulin levels, which hopefully reestablishes normal insulin sensitivity. This restores certain enzyme concentrations back to levels that support the burning of fat, instead of glucose and amino acids (catabolic burning of muscle) to cover the energy requirements.
All this means that we have to cycle... and the cycle is: one week ON growth hormone and carbohydrates, and one week OFF growth hormone and carbohydrates.
Growth hormone, however, causes A.D.H. (Anti-Diuretic Hormone) to go up. ADH is a very potent coronary constrictor which also constricts veins. It is produced starting in the hypothalamus. The nerve endings of certain neurons in the hypothalamus reach into the posterior pituitary, and ADH and oxicitocin come from the posterior pituitary. ADH can go up to 20 times normal levels with fear, or anger, and stress. This can cause coronary constriction within minutes, and this can cause a massive heart attack.
Growth hormone makes ADH go up, and as a direct effect of this, water retention goes up, which causes higher blood pressure. ADH is dose dependent of GH, which is why you have to drop the dose if blood pressure goes up too high, until your circulatory system adjusts to handle it. This is the only bad side effect of an otherwise very good dose of growth hormone.
"Clonidine" is the safest high blood pressure medicine. It causes no side effects, and no impotency of any kind. It is indicated if you have high blood pressure due to ADH.
By: Dr. David Lee Spear
Growth hormone binds to DNA and causes, or stimulates, the DNA to produce more ribosomes. Then GH binds to ribosomes and activates them to turn out IGF-1 molecules. IGF-1 molecules leave the cytoplasm and go into the plasma, thus becoming circulating IGF-1. IGF-1 has a half life of about 20 hours.
IGF-1 and insulin both do very similar things: they both attach to receptors of muscle cells. The receptors are very similar. These receptors are part of the cell membrane structure. GH and insulin both increase the cellular membrane permeability of certain amino acids, to thus facilitate the transfer of those amino acids into the muscle cells into the sarco-plasm.
The amino acids that insulin facilitates to cross are different than the amino acids that IGF-1 helps to cross. The entire array of both of them combined is what is necessary for "proteo-genesis" (new protein for muscles). It is like a double key system in a bank safe: you need both keys, or you can't open the safe. You need ALL the amino acids that IGF-1 helps to cross AND all the amino acids that insulin helps to cross, or you can't have proteo-genesis.
High IGF-1 with low insulin has no anabolic effect because to have new proteo-genesis you need ALL the amino acids helped across by IGF-1 AND of insulin. Low IGF-1 and high insulin also does not help to build muscle because IGF-1 is missing, so the amino acid array is incomplete.
ATP can be formed in ample amounts from glucose, fat, or protein. If IGF-1 synthesis by the liver is markedly reduced during ketosis, as I've theorized, it would have to be the result of specific enzyme changes resulting from low insulin concentrations. Low insulin levels cause widespread metabolic changes throughout the body by changing specific enzyme systems.
In fact, low insulin output, by itself, causes shutdown of proteogenesis, regardless of IGF-1 levels, and is the primary (and maybe the only) cause of the greatly increased output of GH during starvation or keto dieting.
Low insulin also increases fat mobilization, an effect enhanced by elevated GH. So, now I withdraw my prediction of low IGF-1 levels during ketosis, but if they occur, low IGF-1 may be an additive factor in the stimulation of GH output, and in the shutdown of muscle proteogenesis.
Growth hormone goes into the insulin producing cells of the pancreas to greatly increase the output of insulin, so insulin goes way up... unless there is very little carbohydrate... in which case high insulin doesn't happen. If it did, you could go into a hypoglecemia coma, and you could even die. Nobody knows how this happens, but when GH goes into the pancreas, something turns off the pancreas's response to glucose.
Acromegalic Giants all become Type I diabetics eventually, because GH has so overstimulated their insulin producing cells that they have literally burned out. (Type I diabetes means their pancreas doesn't produce any insulin.)
The other effect of GH is that it makes us insulin resistant to glucose concentration. The beauty of this insulin resistance is that it allows us to have a high insulin levels without profound hypoglycemia, and together with the IGF-1 this then gives us a maximum anabolic effect.
But prolonged elevated insulin and insulin resistance could lead us in the wrong direction, and Type II diabetes. So in the week off GH, the very low carbohydrate levels causes very low insulin levels, which hopefully reestablishes normal insulin sensitivity. This restores certain enzyme concentrations back to levels that support the burning of fat, instead of glucose and amino acids (catabolic burning of muscle) to cover the energy requirements.
All this means that we have to cycle... and the cycle is: one week ON growth hormone and carbohydrates, and one week OFF growth hormone and carbohydrates.
Growth hormone, however, causes A.D.H. (Anti-Diuretic Hormone) to go up. ADH is a very potent coronary constrictor which also constricts veins. It is produced starting in the hypothalamus. The nerve endings of certain neurons in the hypothalamus reach into the posterior pituitary, and ADH and oxicitocin come from the posterior pituitary. ADH can go up to 20 times normal levels with fear, or anger, and stress. This can cause coronary constriction within minutes, and this can cause a massive heart attack.
Growth hormone makes ADH go up, and as a direct effect of this, water retention goes up, which causes higher blood pressure. ADH is dose dependent of GH, which is why you have to drop the dose if blood pressure goes up too high, until your circulatory system adjusts to handle it. This is the only bad side effect of an otherwise very good dose of growth hormone.
"Clonidine" is the safest high blood pressure medicine. It causes no side effects, and no impotency of any kind. It is indicated if you have high blood pressure due to ADH.
