steroid500
New Member
So guys, since there wasn’t many replies or insights given on my question regarding using an ACE inhibitor to facilitate fat loss, I have been so kind to donate my body to research on this topic. I will be keeping a log of everything that happens for the next 3 month cycle. To fully grasp the mentality and thinking behind this study, there is a lot of background information, both on myself and the drugs to be used that needs to be discussed.
Myself: I am 23 yr old, been body building and lifting since I was 16. I started naturally and slowly progressed though the various supplements at GNC, up to andro and graduated to gear when I turned 21. Once I got on the sauce, my weight sky rocketed from 190 to 250 (albeit over a course of a couple cycles). I have always had a small spare tire and fat deposits on my chest (not gyno related). I started dieting down at the beginning of August, and dropped from 250lbs to 230 by the end of September just by diet and exercise alone. Maintenance caloric intake is approx 4500 cals, and I am currently running a 2100 cal deficit on that (2400 calories per day) M-F. Diet is sever ketogenic, with carbohydrate intake set to 35g/day, protein at 400g/day and fat 60g/day. Sat-Sun I gylcogen reload by eating normally (no caloric restrictions) and whole grains. I also allow myself to drink a couple beers if I want (however, once I start taking and ACEi, this will have to stop with no exceptions). Exercise is as follows: M-F: arc trainer for 30min in the afternoon, weight loss program, level 6 kept at approx 160-170 rpms. Weight training for 60min in the evening focusing on one body part per day. Sat-Sun: walking on treadmill, 15 deg incline, for 60 min at 3.5-4.0 mph. Currently, I am 2 months out of 3 of my 5th cycle. This cycle is a cutter type cycle consisting of 500mg test e, 400mg eq. For month 1 and 3, I have also stacked in T-3 with the usual taper up/taper down protocol to 100mcg. Combined with my diet and exercise routine, this has dropped me to where I am currently at, at 220lb, approx 10%bf (guesstimation).
The ACEi cycle I am running will begin at the beginning of month 3 of my current steroid cycle and continue through my PCT. Exercise will remain the same intensity and amount throughout, however during the beginning stages of my PCT, I will bump my caloric intake up to ~3000-3500 cals to facilitate better recovery and hold on to my muscle mass. This cycle will consist of 50mg Captopril, 20mg yohimbe, 12mg Albuterol (spread evenly throughout the day). The captopril will be tapered up to 50mg to test my tolerance. The Albuterol will be taken as in a 2week on, 1 week off fashion, tapered up, with benedryl taken throughout the off week to clean receptors,. Cycle length is projected to be 3 months, which will take me into February 2009.
Reasoning and pharmacology: Before I delve into this, I just want to make it known that a lot of this information is from Dan Duchaine’s dirty dieting newsletter. Without it to peak my interest, I would not have even thought of researching this on my own.
Humans are programmed to store fat in preparation for times of famine (fuckin evolution). In the body, fat cells have two types of receptors on them. These receptors respsond differently to hormones and tell the fat cells to either shrink, or enlarge. These receptors are the Alpha-2 adrenoreceptor (in actuality, there are many alpha-2 receps, and the one we are most interested in, in regards to fat loss is the alpha-2 subtype a. For simplicity I will just call them alpha-2.) and the Beta-2 adrenoreceptors. You see, there are many lines of defense the body has to losing weight. It sees fat as an insurance policy and will do everything possible to prevent getting this policy revoked. Insulin is the first defensive move the body has, however when running a ketogenic diet, insulin drops off and this defensive mechanism is defeated, so the body calls on the next line: Alpha-2 adrenoreceptors.
Alpha-2’s tell the cells to hold on to fat. Once the insulin defense is defeated, the alpha-2s kick in. These receptors increase in density and sensitivity in the major fat deposit areas. You can see where there is the most density by looking in the mirror, where you have fat, you also have the highest density.
Beta-2s are also found in fat cells and tell the cells to release fat. Both alpha and beta receps are stimulated by adrenaline and noradrenaline, however, when alpha-2s have more density than the beta-2s, the beta-2s catabolic effect is far outweighed by the alpha-2s, and thus the body holds on to the fat. This is why it is easy to lose fat in some places than others, it all has to do with alpha/beta density ratios. To make matters worse, once beta-2s are stimulated and begin the fat releasing process, the body signals the fat cells to either increase alpha-2 density or responsiveness, or decrease beta-2 density or responsiveness.
Exercise has no effect on reducing alpha-2 density or lowering their responsiveness. And with the low insulin levels from the ketogenic diet, there is actually an up regulation of the alpha-2 cells. This is why some people cannot lose weight no matter how hard they try, or why woman cannot lose weight in the hips/thighs/buttocks area, simply because the alpha-2 density is way too high.
It is a proven fact (although I am not sure as to the mechanism-couldn’t find how) that estrogen regulates alpha-2 receptors. Give a woman birth control, and she puts on weight on her hips and butt. Don’t give a woman estrogen after menopause, and watch her lose weight. Lowering estrogen in men is easy, just use and AI, and since I am a man, I will only talk how it affects men (sorry ladies, I’m not hating, just that I don’t understand you! Lol) Why an AI and not nolva or clomid? We know that both nolva and clomid are both agonists and antagonists. They prevent estrogen binding in the nipples, but promote binding in fat cell. We need to get rid of the root of the problem (estrogen) by using an AI.
We also know from experience that testosterone up regulates alpha-2s. When bulking using AAS, we put on a lot of mass, both muscle and fat, and the fat gets harder to lose. Obviously we don’t want to lower our testosterone level, so a strong androgen like masteron (which actually acts like an anti estrogen) should be used.
Angiotensin II is a peptide hormone for the expression of the alpha-2s. Without it, alpha-2s cannot form in fat cells (ahh…now hes getting somewhere…) Receptors are constantly being regenerated in all the cells. If we take away the hormone that says “build alpha-2s” the old ones will eventually die, leaving no alpha-2 receptors. Angiotensin II only acts on receptors that are of subtype a, and on cells that are rich in alpha-2 and Angiotensin II receptors. Fat cells are rich in both of these receptors!
Ok, that’s the background, now I will delve into the drugs of choice and how they affect these alpha-2s.
Yohimbe: this blocks the alpha-2 receptors. However, it is not discriminating to the alpha-2a’s, and blocks them all. That is why there are the negative side effects like raised heart rate, bp, etc. When alpha-2s become blocked, the body responds by increasing their level or responsiveness. which is why we get diminishing returns on yohimbe when taken for a long duration.
Captopril: Angoitensin II is an active hormone derived from the precursor Angiotensin I. Captopril prevents this conversion into Angiotensin II. This drug is originally designed to combate hypertension, so if you are already hypertensive, I would not do this. Of course, if we are using AAS, this drug will be good since AAS causes a rise in bp. This drug also prevents the formation of aldosterone, a hormone which promotes water retention. That being said, within the first couple weeks of beginning therepy, there will be a large water weight loss . A long term side effect of captopril that has been documented is weight loss! However, this drug is not instantaneous, and it will take approx 2 weeks for the receptors to start to “die” off. A lower than maintenance caloric diet is needed and there is still another line of defense the body has to prevent fat loss. But, with administration, it will cause you to lose weight in place you have never been able before in great strides.
Albuterol: Like clen, albuterol is a beta-2 agonist. And as described earlier, beta-2 receptors are our friends when it comes to weight loss. If we stimulate them, we cause the fat cells to release fat stores into the blood stream. I chose albuterol over clen for a couple reasons. 1) its not nearly as harsh, as I have taken clen before and had some very nasty sides. 2) it doesn’t cause heart cell apoptosis…always a good thing. And 3) it is also anti-catabolic.
This brings me back to my stack. To reiterate, it is:
Captopril 50mg/day
Yohimbe 20mg/day
Albuterol 4mg, 3x/day
I wish I would have stumbled on this earlier so I could have stacked it with gear, but doing it off cycle will give a good base as to what could be achieved with this stack. As I said, I will keep track of my progress, possibly with pictures to boot so you guys can follow along. Any comments? Concerns? Questions? Anticipated first day is November 23, that is if my captopril comes in on time.
Myself: I am 23 yr old, been body building and lifting since I was 16. I started naturally and slowly progressed though the various supplements at GNC, up to andro and graduated to gear when I turned 21. Once I got on the sauce, my weight sky rocketed from 190 to 250 (albeit over a course of a couple cycles). I have always had a small spare tire and fat deposits on my chest (not gyno related). I started dieting down at the beginning of August, and dropped from 250lbs to 230 by the end of September just by diet and exercise alone. Maintenance caloric intake is approx 4500 cals, and I am currently running a 2100 cal deficit on that (2400 calories per day) M-F. Diet is sever ketogenic, with carbohydrate intake set to 35g/day, protein at 400g/day and fat 60g/day. Sat-Sun I gylcogen reload by eating normally (no caloric restrictions) and whole grains. I also allow myself to drink a couple beers if I want (however, once I start taking and ACEi, this will have to stop with no exceptions). Exercise is as follows: M-F: arc trainer for 30min in the afternoon, weight loss program, level 6 kept at approx 160-170 rpms. Weight training for 60min in the evening focusing on one body part per day. Sat-Sun: walking on treadmill, 15 deg incline, for 60 min at 3.5-4.0 mph. Currently, I am 2 months out of 3 of my 5th cycle. This cycle is a cutter type cycle consisting of 500mg test e, 400mg eq. For month 1 and 3, I have also stacked in T-3 with the usual taper up/taper down protocol to 100mcg. Combined with my diet and exercise routine, this has dropped me to where I am currently at, at 220lb, approx 10%bf (guesstimation).
The ACEi cycle I am running will begin at the beginning of month 3 of my current steroid cycle and continue through my PCT. Exercise will remain the same intensity and amount throughout, however during the beginning stages of my PCT, I will bump my caloric intake up to ~3000-3500 cals to facilitate better recovery and hold on to my muscle mass. This cycle will consist of 50mg Captopril, 20mg yohimbe, 12mg Albuterol (spread evenly throughout the day). The captopril will be tapered up to 50mg to test my tolerance. The Albuterol will be taken as in a 2week on, 1 week off fashion, tapered up, with benedryl taken throughout the off week to clean receptors,. Cycle length is projected to be 3 months, which will take me into February 2009.
Reasoning and pharmacology: Before I delve into this, I just want to make it known that a lot of this information is from Dan Duchaine’s dirty dieting newsletter. Without it to peak my interest, I would not have even thought of researching this on my own.
Humans are programmed to store fat in preparation for times of famine (fuckin evolution). In the body, fat cells have two types of receptors on them. These receptors respsond differently to hormones and tell the fat cells to either shrink, or enlarge. These receptors are the Alpha-2 adrenoreceptor (in actuality, there are many alpha-2 receps, and the one we are most interested in, in regards to fat loss is the alpha-2 subtype a. For simplicity I will just call them alpha-2.) and the Beta-2 adrenoreceptors. You see, there are many lines of defense the body has to losing weight. It sees fat as an insurance policy and will do everything possible to prevent getting this policy revoked. Insulin is the first defensive move the body has, however when running a ketogenic diet, insulin drops off and this defensive mechanism is defeated, so the body calls on the next line: Alpha-2 adrenoreceptors.
Alpha-2’s tell the cells to hold on to fat. Once the insulin defense is defeated, the alpha-2s kick in. These receptors increase in density and sensitivity in the major fat deposit areas. You can see where there is the most density by looking in the mirror, where you have fat, you also have the highest density.
Beta-2s are also found in fat cells and tell the cells to release fat. Both alpha and beta receps are stimulated by adrenaline and noradrenaline, however, when alpha-2s have more density than the beta-2s, the beta-2s catabolic effect is far outweighed by the alpha-2s, and thus the body holds on to the fat. This is why it is easy to lose fat in some places than others, it all has to do with alpha/beta density ratios. To make matters worse, once beta-2s are stimulated and begin the fat releasing process, the body signals the fat cells to either increase alpha-2 density or responsiveness, or decrease beta-2 density or responsiveness.
Exercise has no effect on reducing alpha-2 density or lowering their responsiveness. And with the low insulin levels from the ketogenic diet, there is actually an up regulation of the alpha-2 cells. This is why some people cannot lose weight no matter how hard they try, or why woman cannot lose weight in the hips/thighs/buttocks area, simply because the alpha-2 density is way too high.
It is a proven fact (although I am not sure as to the mechanism-couldn’t find how) that estrogen regulates alpha-2 receptors. Give a woman birth control, and she puts on weight on her hips and butt. Don’t give a woman estrogen after menopause, and watch her lose weight. Lowering estrogen in men is easy, just use and AI, and since I am a man, I will only talk how it affects men (sorry ladies, I’m not hating, just that I don’t understand you! Lol) Why an AI and not nolva or clomid? We know that both nolva and clomid are both agonists and antagonists. They prevent estrogen binding in the nipples, but promote binding in fat cell. We need to get rid of the root of the problem (estrogen) by using an AI.
We also know from experience that testosterone up regulates alpha-2s. When bulking using AAS, we put on a lot of mass, both muscle and fat, and the fat gets harder to lose. Obviously we don’t want to lower our testosterone level, so a strong androgen like masteron (which actually acts like an anti estrogen) should be used.
Angiotensin II is a peptide hormone for the expression of the alpha-2s. Without it, alpha-2s cannot form in fat cells (ahh…now hes getting somewhere…) Receptors are constantly being regenerated in all the cells. If we take away the hormone that says “build alpha-2s” the old ones will eventually die, leaving no alpha-2 receptors. Angiotensin II only acts on receptors that are of subtype a, and on cells that are rich in alpha-2 and Angiotensin II receptors. Fat cells are rich in both of these receptors!
Ok, that’s the background, now I will delve into the drugs of choice and how they affect these alpha-2s.
Yohimbe: this blocks the alpha-2 receptors. However, it is not discriminating to the alpha-2a’s, and blocks them all. That is why there are the negative side effects like raised heart rate, bp, etc. When alpha-2s become blocked, the body responds by increasing their level or responsiveness. which is why we get diminishing returns on yohimbe when taken for a long duration.
Captopril: Angoitensin II is an active hormone derived from the precursor Angiotensin I. Captopril prevents this conversion into Angiotensin II. This drug is originally designed to combate hypertension, so if you are already hypertensive, I would not do this. Of course, if we are using AAS, this drug will be good since AAS causes a rise in bp. This drug also prevents the formation of aldosterone, a hormone which promotes water retention. That being said, within the first couple weeks of beginning therepy, there will be a large water weight loss . A long term side effect of captopril that has been documented is weight loss! However, this drug is not instantaneous, and it will take approx 2 weeks for the receptors to start to “die” off. A lower than maintenance caloric diet is needed and there is still another line of defense the body has to prevent fat loss. But, with administration, it will cause you to lose weight in place you have never been able before in great strides.
Albuterol: Like clen, albuterol is a beta-2 agonist. And as described earlier, beta-2 receptors are our friends when it comes to weight loss. If we stimulate them, we cause the fat cells to release fat stores into the blood stream. I chose albuterol over clen for a couple reasons. 1) its not nearly as harsh, as I have taken clen before and had some very nasty sides. 2) it doesn’t cause heart cell apoptosis…always a good thing. And 3) it is also anti-catabolic.
This brings me back to my stack. To reiterate, it is:
Captopril 50mg/day
Yohimbe 20mg/day
Albuterol 4mg, 3x/day
I wish I would have stumbled on this earlier so I could have stacked it with gear, but doing it off cycle will give a good base as to what could be achieved with this stack. As I said, I will keep track of my progress, possibly with pictures to boot so you guys can follow along. Any comments? Concerns? Questions? Anticipated first day is November 23, that is if my captopril comes in on time.
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