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After all of my posts and nandi's posts on Fat Loss and captopril, I decided to get back to basics. So, I popped open my pharmacology book and read some more articles about adipose tissue. Interestingly, muscle gain and muscle loss is very analogous to fat gain and fat loss.
Testosterone basically improves protein synthesis in muscle tissue, causing an increase in muscle cell size. HGH, through the IGF-1 and insulin mechanism, causes an increase in muscle cell number. Add in intramuscular fat and muscle glycogen storage, and that is what determines overall muscle group size. We also know that genetics determines all of this (endomorph, mesomorph, ectomorph). We also know, despite public belief, that hormone supplementation will enhance all of these body types.
Now, fat cell size is increased by stimulation of the alpha-2 receptors. We know that insulin and estrogen stimulate these receptors. We know that lots of carbs and fat--dietary in combination with carbs or exogenous--raise insulin and estrogen levels. Obese people tend to have more alpha-2 receptors than beta 3 receptors on each fat cell. Mesos and ectos have a more favorable ratio. Obese people also have the ability to create new adipose cells as a way of preserving fat--remember their genetics dictate that fat reigns, not muscle.
Now, the problem. How do we stimulate Beta 3 receptors? ECA, Clen, NYC stimulate Beta 2 receptors but they are not specific to beta 3 receptors. The other problem is the fat cell responds to beta stimulation by either increasing the number of alpha-2 receptors or by producing new fat cells.
So we need a beta 3 receptor-specific stimulator. The only one that seems to work is HGH. Some may argue that T3 is the answer, but it is the "band-aid on the broken leg." Just think about the side effects and advantages of long-term HGH therapy compared to long-term T3 therapy. Now, after reading all of the posted articles about Captopril, I believe that Captopril may aid in inhibiting denovo [new] fat cell formation, but not really do anything about alpha-2 receptors. Yohimburn/Yohimbine is probably the best alpha-2 receptor blocker.
So, lets assume we put our imaginary test subject on an appropriate diet and weight training program. Let's have them take 5IU HGH 6 days on and one day off. Let's have them take 100mg captopril at bedtime, and apply Yohimburn (www.anabolicfitness.net) as directed. Let's do this for six months.
Here is my hypothesis: They will lose fat and preserve muscle tissue; their blood chemistry will be normal or normalized as a result of therapy. HGH will cause lipolysis, optimize thyroid function, and preseve muscle. Captopril will improve glucose transport, protect kidneys, normalize blood pressure and prevent denovo fat cell synthesis. Yohimburn will block the effects of estrogen and insulin on existing fat cells.
Now, suppose, this person's BF% becomes acceptable and bloods become normal. Suppose they still have some "stubborn fat" areas that are not esthetic. I propose liposuction to treat these areas.
Now, maintenance. As a result of the fat loss, the person's HGH/IGF-1 levels will normalize--so HGH long-term is no longer necessary. The person becomes self maintaining. We now add Glucophage. This drug will continue proper glucose transport and prevent visceral fat gains. We may need to maintain Captopril to prevent denovo fat cell synthesis. We will need to add low dose Testosterone or Oxandrin to maintain adequate Testo levels.
Comments and thoughts are appreciated.
Testosterone basically improves protein synthesis in muscle tissue, causing an increase in muscle cell size. HGH, through the IGF-1 and insulin mechanism, causes an increase in muscle cell number. Add in intramuscular fat and muscle glycogen storage, and that is what determines overall muscle group size. We also know that genetics determines all of this (endomorph, mesomorph, ectomorph). We also know, despite public belief, that hormone supplementation will enhance all of these body types.
Now, fat cell size is increased by stimulation of the alpha-2 receptors. We know that insulin and estrogen stimulate these receptors. We know that lots of carbs and fat--dietary in combination with carbs or exogenous--raise insulin and estrogen levels. Obese people tend to have more alpha-2 receptors than beta 3 receptors on each fat cell. Mesos and ectos have a more favorable ratio. Obese people also have the ability to create new adipose cells as a way of preserving fat--remember their genetics dictate that fat reigns, not muscle.
Now, the problem. How do we stimulate Beta 3 receptors? ECA, Clen, NYC stimulate Beta 2 receptors but they are not specific to beta 3 receptors. The other problem is the fat cell responds to beta stimulation by either increasing the number of alpha-2 receptors or by producing new fat cells.
So we need a beta 3 receptor-specific stimulator. The only one that seems to work is HGH. Some may argue that T3 is the answer, but it is the "band-aid on the broken leg." Just think about the side effects and advantages of long-term HGH therapy compared to long-term T3 therapy. Now, after reading all of the posted articles about Captopril, I believe that Captopril may aid in inhibiting denovo [new] fat cell formation, but not really do anything about alpha-2 receptors. Yohimburn/Yohimbine is probably the best alpha-2 receptor blocker.
So, lets assume we put our imaginary test subject on an appropriate diet and weight training program. Let's have them take 5IU HGH 6 days on and one day off. Let's have them take 100mg captopril at bedtime, and apply Yohimburn (www.anabolicfitness.net) as directed. Let's do this for six months.
Here is my hypothesis: They will lose fat and preserve muscle tissue; their blood chemistry will be normal or normalized as a result of therapy. HGH will cause lipolysis, optimize thyroid function, and preseve muscle. Captopril will improve glucose transport, protect kidneys, normalize blood pressure and prevent denovo fat cell synthesis. Yohimburn will block the effects of estrogen and insulin on existing fat cells.
Now, suppose, this person's BF% becomes acceptable and bloods become normal. Suppose they still have some "stubborn fat" areas that are not esthetic. I propose liposuction to treat these areas.
Now, maintenance. As a result of the fat loss, the person's HGH/IGF-1 levels will normalize--so HGH long-term is no longer necessary. The person becomes self maintaining. We now add Glucophage. This drug will continue proper glucose transport and prevent visceral fat gains. We may need to maintain Captopril to prevent denovo fat cell synthesis. We will need to add low dose Testosterone or Oxandrin to maintain adequate Testo levels.
Comments and thoughts are appreciated.
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