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Fat Loss/Cutting without using AAS

DrJMW

New member
I have been experimenting with a combination of meds to aid/speed up fat loss. I have come to the following conclusion:

1. HGH is a must--if it works for you, then substitute Trans-D Tropin. The point being is that elevated HGH levels is the base of the pyramid. It will optimize your thyroid, preserve muscle tissue, and increase lipolysis.

2. Yohimburn--This is necessary to block Alpha-2 receptors. It is much more efficient than oral Yohimbe.

3. Captopril--over the long-term, this blood pressure med helps to literally eliminate Alpha-2 receptors.

Quick review: The alpha-2 receptors are the "pain in the ass" on the fat cell; the cause of "stubborn" fat. They are stimulated by almost everything, including estrogen and insulin. We can now block and eliminate these alpha-2 receptors. The problem with Clen and ECA is that, while stimulating Beta receptors, the fat cell's response is to increase alpha-2 receptors.

4. Glucophage--This is necessary to improve insulin resistance.

You will not grow from this cycle, but you will lose fat. For diet, I suggest keeping carbs as low as possible without feeling weak and faint. For workout, cardio and cyclical training, keeping heartrate up throughout the workout.

Any comments welcome. For further details, drop me an email. DrJMW
 
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T3,clenbuterol,ALA...

I'd like to hear what your opinion is on using T3,clenbuterol,ALA, and arimidex/liquidex as well.
Trying to lose those love-handles is a real bitch.

Right now, I am trying to follow the Tha One CrumCake Diet:

Crum-Diet
 
with respect to HGH.. think that this is more important in older individuals.. though it obviously can be helpful

with respect to glucophage.. it would seem that ALA may be a good, perhaps better substitute.
 
Re: T3,clenbuterol,ALA...

soflaguy said:
I'd like to hear what your opinion is on using T3,clenbuterol,ALA, and arimidex/liquidex as well.
Trying to lose those love-handles is a real bitch.

None of these meds deals with the alpha-2 receptor problem. Yohimburn in conjunction with Captopril will eliminate the alpha-2 receptors. Once they are reduced, then the beta-receptors take over--then T3, clen and ECA would be effective. ALA may turn out to be a good substitute for glucophage--it is already approve for patient use in Germany. The antiestrogens are weaker than yohimbe in blocking alpha-2 receptors.

Trans-D Tropin works in many people, but not in all. If you can afford HGH, then go for it. HGH will optimize the thyroid, eliminating the need for T3, and optimize lipolysis. Obese people have low HGH/IGF-1 levels to begin with.

Captopril is not like Femara. Femara reduces estrogen levels, which is one less thing to stimulate alpha-2 receptors. Captopril actually ELIMINATES alpha-2 receptors--something to do with the inhibition of Angiotensin conversion. It needs to be taken long-term (over three months to get full effect)
 
Damn good post doc.The late great Dan Duchaine touched on Captopril's activity in A2 elimination.I may have to look into some captopril,as I am always borderline hypertensive anyway,and the use of this could be well suited to lower vasopressin release from the pituitary while running androgenics,no?
 
Here are some writings on Captopril that I have saved on my hard drive. They came from Dirty Dieting.

----------------------------------------------------------------------

ALPHA-2 ADRENOCEPTOR DOWN-REGULATION

by Michalovich Dharkam Greutstein

UNDERSTANDING THE PROBLEMS

One class of receptors, once activated, will make the fat cell shrink. The other class of receptors when activated will make the fat cell bigger and prevent it from shrinking. This is the balance between the good and the bad receptors which will determine how fat you are. Furthermore, those good and bad receptors are not equally spread on each fat cells. Some cells contain more good receptors and so are easily shrunk by a diet. But many fat cells contain more bad than good receptors. This is why some fat deposits are very hard to lose. Which means you will never get lean in those areas unless you reduce the number of the bad "Dirty" receptors.

Alpha-2 Receptors: The Enemy

You have heard of them before. Their exact name is alpha-2 receptors for simplification). They are not the first line of defene for our fat cells. The first line of defense among the bad receptors are insulin receptors. But once you go on a low calorie diet, especially the BodyOpus diet, your insulin level will go down. There will not be enough of that hormone to prevent fat cells from shrinking. Once the body realizes its first line of defense is out of order it calls upon the second line of defense: it increases the responsiveness of each alpha-2 receptor. From a dieter's point of view, this means he will then be unable to lose fat where a high density of alpha-2 receptors can be found.

Alpha-2 Receptor Densities

It is easy to figure out where the alpha-2 receptors are the most dense just by looking at someone. This is exactly where their fat accumulates. You see, alpha-2 receptors not only prevent fat loss but they also promote fat gains. They are like magnets, attracting and retaining fat. Alpha-2 receptors are found in very high densities below the skin (subcutaneously). We can distinguish two main patterns of alpha-2 distributions:

1. In most women and in some men with a female type body fat distribution, alpha-2 receptors are found in high density mostly on the subcutaneous fat of the butt and of the legs.

2. In most men and in some women (those neither showing a specific lower body fat accumulation), most of the alpha-2 receptors are located equally all over the subcutaneous fat of the body.

Subcutaneous vs Intramuscular Fat

The subcutaneous fat is the fat located between the skin and the muscles. This is the fat that if carried in excess will make you look fat in a mirror. Intramuscular fat on the other hand is the fat that we find inside the muscles. You can have plenty of intramuscular fat and not look fat. In fact, if one only carries intramuscular fat with virtually no subcutaneous fat, he will look big and lean even though he really is fat.

In reality, most people will carry more subcutaneous fat than intramuscular fat. This is bad enough, but as you go on a diet, things turn ugly. As we said above, the subcutaneous fat contains the most alpha-2 receptors (around twice as much) when compared to intramuscular fat. So when you go on a diet, you will lose intramuscular fat twice as easily as subcutaneous fat. In front of a mirror, this is a catastrophe: by losing intramuscular fat, your muscles will appear smaller. But since little subcutaneous fat will be lost, you will not look much leaner. In fact, you will only see a smaller (but not leaner) version of yourself. All this because of those damned alpha-2 receptors.

To sum it up; people with much of their bodyfat as subcutaneous fat will lost fat but in the wrong place and so will not appear leaner where they want to. Alpha-2 adrenoceptors are the main culprit. Before being able to combat those receptors, we first have to understand which factors increase alpha-2 numbers on our fat cells.

When the Betas Control the Alphas

We have said above that there were two big classes of receptors on fat cells; the good ones and the bad ones. So far we have talked of the bad ones. The good ones are called beta receptors. Like alpha-2 receptors, they are found on the fat cells. When activated, these beta receptors will try to shrink the fat cells. But they will only succeed if the alpha-2 receptors are not found in too high quantity in those cells. You see, alpha-2 receptors have exactly the opposite effects of beta receptors. As both are activated by the same hormones (adrenaline and noradrenaline), if a higher quantity of alpha-2 receptors are found, beta receptor effects will be overwhelmed and no fat loss will occur in those receptors. Beta receptors will only induce fat loss on fat cells with low alpha-2 density. That is the area where it is easy to lose fat while on a diet (mostly intramuscular fat).

As if things were not bad enough, each time beta receptors are activated, two signals are sent to the fat cells:

1. To either increase the number of alpha-2 receptors or their responsiveness or both.

2. To either decrease the number of beta receptors or their responsiveness or both.

This means that within a few days you will have a stronger alpha-2 response to the hormones which are supposed to make you leaner (remember adrenaline and noradrenaline) and a weaker beta response. That is bad, really bad. You now understand why will have to get dirty!

Playing Russian Roulette With Low-Calories Diets and Alpha-2 Receptors

A second factor which controls alpha-2 receptors on fat cells is the diet itself. As your calorie intake goes down, so will the level of insulin in your blood. As we said above this will increase the responsiveness of each alpha-2 receptor in the short run. This is bad but not terribly bad as it will also increase both the number and the responsiveness of the good receptors (beta receptors). But after a few days of dieting, most people will get lucky. The number of alpha-2 receptors will decrease a little. Some people will be unlucky though, as either their number of alpha-2 receptors will go up or the responsiveness of each alpha-2 receptor will increase. Even worse, in some people both the number and the responsiveness of the alpha receptors will increase. We all know who they are; those who cannot lose ft no matter what (that is until now). So the impact of dieting on alpha-2 receptors looks more like Russian Roulette than a science. And even on the luckiest, the favorable effects of diets on alpha-2 receptors will be mild.

Exercise and Alpha-2 Receptors

Exercise does not seem to help get rid of alpha-2 receptors. In fact, if exercise has an impact on alpha-2 receptors on fat cells it would tend to be an up-regulation. But most studies show no impact at all. This has a direct consequence especially for women (but this also applies to men). We said that the major reason why women have a hard time losing fat on the butt is because the density of alpha-2 receptors on that body part is too high. Furthermore, we just saw that exercise will not help to down-regulate alpha-2 receptors.

Conclusion: Don't waste your time doing endless repetition with a light weight on butt blaster or doing high rep lunges. This might burn off a few calories but it will not solve the problem. This is also true for men doing endless repetitions of sit ups for abdominals to fight subcutaneous fat on the stomach. I know this will not prevent you from doing it but at least now you understand why you get nothing out of it!
 
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Here's part two of the article.

------------------------------------------------

ANGIOTENSIN II:

by Michalovich Dharkam Greutstein

The Permissive Substance

Angiotensin II is a polypeptide which is required for the expression of some (but not all) alpha-2 receptors. This means that without angiotensin II, alpha-2 receptors cannot be developed in some cells. As a result, if we somehow get rid of angiotensin II which is naturally produced by the body, the normal renewal of the alpha-2receptors will not happen. You have to understand that there is a constant renewal of the receptors in any cell. By blocking the formation of a specific receptor type in a cell (for example alpha-2 receptors), after a while there will not be any alpha-2 receptors in this cell. The old receptors will "die" and we will have prevented the new generation of receptors from replacing the old ones.

Viola. No more alpha-2 receptors. The big issue is whether this action of angiotensin II takes place in fat cells. Angiotensin II only acts on alpha-2 receptors which respond to two conditions:

* It seems to have the most effect on alpha-2 receptors of the 'a' subtype. This is good as it is specifically these receptors which are found on the fat cells. So, the first condition is filled.

* Angiotension II only acts on cells which are rich in both alpha 2 receptors and angiotensin II receptors. That is where we get lucky. We already know that fat cells are very rich in alpha-2 receptors. Scientists also have known for some time that fat cells are very rich angiotensin II receptors.

The key point to remember here is that on fat cells, angiotensin II is needed for alpha-2 receptors to be normally renewed. If we somehow prevent the formation of angiotensin II we will cause major troubles in the renewal of alpha-2 receptors exactly where we want it: on fat cells.

So all you have to do is to impair the production of antiotensin II and allow time to do the rest of the work for you. Within a few weeks the number of alpha-2 receptors will fall. Easy and effective.

Let Me Introduce The Hero of The Day: Captopril

I will not waste time on explaining how Captopril works. The trade name for this molecule can be Capoten, by Bristol-Meyers. Technically, it is a converting enzyme inhibitor. Let's just say that it is very effective at preventing the formation of angiotensin II. Captopril has no direct effect on alpha-2 receptors. It is only because it prevents the formation of angiotensin II that it will (indirectly) reduce the number of alpha-2 receptors.

How to Use Captopril

Captopril is a drug meant to combat hypertension. If you already suffer from hypotension, you will have some trouble with it. A first key rule is to start slowly 25 mg (half of a pill) daily is a good start. Once you get used to it, you can increase the doses from one to two 50 mg per day. The second side effect you will see with Captopril is you feel like you want to sleep after you swallow a pill. So, it is bst to take it before bedtime and not first thing in the morning. Another side effect you going to see quickly
is the loss of water. This is because Captopril prevents the formation of a hormone (aldosterone) which promotes water retention. So, by reducing the secretion of aldosterone, Captopril will force you to urinate more often. Don't worry though, the diuretic effect of Captopril is only mild.

A more long term side effect of Captopril which is well documented by medical studies is weight loss. Well, here we are. Of course, this weight loss could be due to muscle loss- but this is not the case. In fact, Captopril if anything has an anabolic effect on the muscles. This was the reason we started using it. If you think we just made a brilliant discovery, let me tell you it all started by mistake.

The True Captopril Story

I first spotted Captopril for its potentially anabolic properties. A woman with an eating disorder asked me to recommend a drug which would give her muscles but without any virilization. I knew her well as I already helped her with her diet. I figured it was the right occasion to test Captopril I did not change her diet which is supposed to be a bit below maintenance as she will have periodic high calorie intake due to her eating disorder. For some reason, I was unable to see her for two to two and a half months. When I saw her again, she told me she was till taking Captopril as her only drug. She did gain a little bit of muscle but not much. But what struck me the most is the fact she had lost fat in areas where she had been unable to significantly lose fat before. She told me she did not change her diet nor did she have less binge eating phases.

At first, I was not that happy as I was expecting the anabolic effect to be stronger. So I went back to the medical library to figure out the mechanisms by which Captopril allowed her to lose fat where so many drugs and diets failed. That is how I found the relation between Captropril and alpha-2 receptors.

It did not take long before I had the occasion to try Captopril again. This time was on a high level bodybuilder competitor. He was able to get lean everywhere but on his legs. This was due to genetics, as his mother had exactly the same fat pattern as he did. He tried many drugs without success, including strong androgens like Permastril. It did help a bit but it was not enough to bring him up from his usual 4th-5th place finishes up to first place. He was a perfect guinea pig as he had several months before his competition. Of course, he was using drugs but he kept using the same ones at the same dosages. To make long story short, for the first time in his life he was able to see his leg definition the day of the competition.

These two examples illustrate how effective Captopril is at helping to get rid of those alpha-2 receptors in real life and not just in theory.

Limitations of Captopril

* Captopril is not an instantaneous cosmetically gratifying drug. Remember, the alpha-2 down regulation will take at least two months before becoming significant.

* You have to follow a lower than maintenance diet to see good results in terms of fat loss. We said that alpha-2 receptors prevent normal fat loss. It does not mean that you will automatically get lean just because you will have reduced the number of alpha-2 receptors. It only means that diet-induced fat loss will be easier (does not mean easy). It will have a permissive effect on fat loss by allowing you to lose fat where it was not possible before.

* The last limitation is that there is still a line of defense for the fat cells. We said that a low calorie diet reduces insulin and its anti-lipolytic effects. By doing that, it triggers the second big line of defense for the fat cells: the alpha-2 receptors. By partially removing the alpha-2 line of defense, we trigger a new one constituted by antilipolytic receptors called peptide YY located on fat cells too. It means that reducing alpha-2 receptor level will allow you to lose more fat than it would have been naturally possible, but it does not mean you will be able to get rid of all your fat.

But, Captopril will permit you to take a big step forward in the right direction.
 
Here's the last part.

--------------------------------------------

Some Proposed Stacks To Get The Most Out of Captopril

by M. Dharkam Greutstein


Non-androgenic Advanced Stack:

* Captopril 50mg a day
* Yohimbine 10 mg a day

Non-androgenic advanced stack:

* Captopril 50-100 mg a day

* Yohimbine 10-20 mg a day

* Clenbuterol (3 to 6, 20 mcg a day)

* Ephedrine + caffeine can be substituted for clenbuterol

* A thyroid cream + an aminophylline cream applied on the area you want to get rid of.

If you do not have access to a thyroid cream, you can make one. Get 1/2 of cytomel. Crunch it and mix it with DMSO. Apply the aminophylline cream first and then the home made thyroid cream.

Androgen Stack:

To the above stack add an aromatase inhibitor (one and a half cytadren taken in 3 divided dosages throughout the day is a cost effective formula) + strong androgen such as Masteron. For muscle mass, keep your favorite anabolic stack.

In any case, take the clen and the yohimbine before working out on an empty stomach.

(Editor notes): Capoten is the most potent of the ACE inhibitors. Unfortunately, it has the most undesirable side effects. There are newer, more benign ACE inhibitors. However, the Alpha-2 down-regulation research has been done only on Capoten. We do not know if the newer drugs will have the same positive effect. For example, because of my kidney disease, Capoten would be a terrible choice for me, so I use Zestril instead. It seems to be reducing my lower body fat, ut it would be interesting to see if there is any better improvement with Capoten. DD
 
HUCKLEBERRY FINNaplex said:
Karma to you Engicream.Dharkam has always been one of my favorite gurus.Looks like captopril may be another serious weapon for endomorphs.

from research I have seen captopril has not delivered

two serious issues:

1. he reccomends aminophylline (a diuretic) topical for fat burning- given the other substances in the stack why add such a mild beta-agonist

2. actually reccomending cytadren as an aromatase inhibitor.. even back then..
 
macrophage69alpha said:


from research I have seen captopril has not delivered

two serious issues:

1. he reccomends aminophylline (a diuretic) topical for fat burning- given the other substances in the stack why add such a mild beta-agonist

2. actually reccomending cytadren as an aromatase inhibitor.. even back then..

How much actual research has been done with Capto in regards to fat loss?I'm just wondering if this is one of those drugs like anastrozole that is proven by US before it is the scientific mainstream?

I agree on the Cytadren,lol.But remember,even back then,only super lotto jackpot winners could afford arimidex,lol.
 
macrophage69alpha said:


from research I have seen captopril has not delivered

two serious issues:

1. he reccomends aminophylline (a diuretic) topical for fat burning- given the other substances in the stack why add such a mild beta-agonist

2. actually reccomending cytadren as an aromatase inhibitor.. even back then..

macro:

do you see any reason NOT to try it, especially as a 23-year-old, a2-rich, yohimburn-worshipping, cutting juicer? high bp runs in my family, but so far i'm actually a bit low and keep low sodium diet. my kidney is fine.
 
DrJMW said:
I have been experimenting with a combination of meds to aid/speed up fat loss. I have come to the following conclusion:

1. HGH is a must--if it works for you, then substitute Trans-D Tropin. The point being is that elevated HGH levels is the base of the pyramid. It will optimize your thyroid, preserve muscle tissue, and increase lipolysis.

2. Yohimburn--This is necessary to block Alpha-2 receptors. It is much more efficient than oral Yohimbe.

3. Captopril--over the long-term, this blood pressure med helps to literally eliminate Alpha-2 receptors.

Quick review: The alpha-2 receptors are the "pain in the ass" on the fat cell; the cause of "stubborn" fat. They are stimulated by almost everything, including estrogen and insulin. We can now block and eliminate these alpha-2 receptors. The problem with Clen and ECA is that, while stimulating Beta receptors, the fat cell's response is to increase alpha-2 receptors.

4. Glucophage--This is necessary to improve insulin resistance.

You will not grow from this cycle, but you will lose fat. For diet, I suggest keeping carbs as low as possible without feeling weak and faint. For workout, cardio and cyclical training, keeping heartrate up throughout the workout.

Any comments welcome. For further details, drop me an email. DrJMW

glucophage improves insulin scensetivity making it possible for your body to use muscle less insulin drive glucose into your cells
 
Re: Re: Fat Loss/Cutting without using AAS

serge said:


glucophage improves insulin scensetivity making it possible for your body to use muscle less insulin drive glucose into your cells

but both into fat- and muscle-cells...
 
Re: Re: Re: Fat Loss/Cutting without using AAS

DaMan said:


but both into fat- and muscle-cells...

one can argue that its the case, but if less insulin is secreted, there should be less chance for the fat storage
 
Re: Re: Re: Re: Fat Loss/Cutting without using AAS

serge said:


one can argue that its the case, but if less insulin is secreted, there should be less chance for the fat storage

why, does it increase slin sensitivity in myocyte tissue only?

i'd have thought it'll have the same effect on adipocytes as well, so less slin = greater insulin sensitivity in both muscle and fat cells, yielding the same effect.

btw how's the femara going?
 
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