here is an interesting read on androgenic compounds and cutting
Guide to Losing Fat While "On"
Some interesting stuff but i believe some of it to not be accurate:
Your Guide to Losing Fat While "On"
by Cy Willson
So you wanna drop some fat and you wanna' do it at breakneck speed, huh? What's that? You also want to retain all your muscle mass while greatly reducing calories? Man, you want it all, don't you? Well, it can be done, if you take the proper precautions.
We all know the danger of a super strict diet: potential muscle loss. Who wants to look ripped if you have to lose a lot of hard-earned muscle to get there? Of course, you could go on a sensible diet and slowly drop the fat, but hey, where's the fun in that? Besides, we're in a hurry here!
Many people choose to use steroids while on a severe diet to stave off any possible muscle loss. But which ones and how much? And how should you eat while "on"? Our junior guru Cy Willson has the answers for you. And don't worry, if steroids aren't your bag, he'll also provide some legal alternatives to help you rapidly drop the fat while keeping the muscle.
The Real Anabolic Diet
At one time or another, everyone involved in bodybuilding decides to shed the fat and "see what's under there." With those that use anabolic steroids, this effort has always included the use of drugs that have gained a reputation for their so-called "hardening effect."
Most have attributed this "hardening effect" to a simple reduction in water retention. For example, Joe Blow is using 1,000 mg of Testosterone enanthate per week along with 50 mg per day of methandrostenolone for a course of six to eight weeks. He stops using those two drugs on the ninth week and switches to androgens which cause less water retention. This lack of water retention is the effect referred to as "hardening," right? Actually, I don't think that's the entire story.
True, the reduction in water does play a role. However, I also think certain steroids are much more potent than others in terms of reducing adipose tissue and/or inhibiting the uptake of triglycerides into adipose tissue. Think about it: androgens vary in terms of their anabolic effects upon muscle tissue, so why would this be any different in terms of their effects on the reduction of adipose tissue?
I'll go over my reasoning behind this in the body of my article, as well as provide a list of drugs that are best suited for a fat loss phase. I'll also include a diet plan that will greatly accelerate the reduction of adipose tissue.
Don't worry, I'll also include a "steroid alternative" section which will consist of prohormone usage for those of you who don't like to worry about DEA agents, phone taps, and undercover officers dressed like fitness bunnies, which only paranoid bastards like me worry about anyway.
The AR (Androgen Receptor)
There are many mechanisms behind the ability of androgens to reduce body fat. However, one key determinant of the amount of adipose tissue reduced is that particular androgen's ability to bind to the AR.
I need to mention that most androgens interact with both AR and GR (Glucocorticoid Receptors). We'll touch on that later. For now, let me explain why it matters how well an androgen binds to the AR in terms of reducing adipose tissue. Most of you know that ARs are present in tissue such as muscle. This is one of the mechanisms behind their ability to induce muscular hypertrophy. Now what does this have to do with body fat? Simple, AR's are present in adipose tissue as well. (1)
What does this mean? Well, it's been shown that the higher the density of ARs, the more that lipid uptake is inhibited. (2) It's also been shown that androgens that bind avidly to the AR cause an increase or upregulation of AR in adipocytes. (1) I think the greater the androgen binds to the AR, the more upregulation of AR in adipocytes occurs. This would lead to a significant reduction in subcutaneous adipose tissue. (3)
Notice that I specifically mentioned subcutaneous adipose tissue (fat right beneath the skin) and not visceral adipose tissue (fat around the internal organs). Why did I bother to differentiate between the two? Simple. For the most part, we bodybuilders are concerned only with subcutaneous adipose tissue. Visceral fat doesn't have much of an effect on a person's appearance. For that reason, we're only concerning ourselves with subcutaneous adipose tissue.
Now, what other mechanisms of action can account for the effects seen with those steroids that bind tightly to the AR? Well, those that bind tightly to the AR will decrease LPL (Lipoprotein Lipase), which is an enzyme that causes lipid accumulation. (4) They may also decrease Acetyl-CoA Carboxylase and Fatty Acid Synthetase.(5)
Another interesting note is that androgens have been shown to increase adenyl cylclase as well. This is the enzyme which is responsible for the conversion of cytoplasmic ATP into cyclic AMP. Increasing its concentrations is a good thing, in other words.
The Glucocorticoid Receptor (GR)
There are certain androgens that can interact with GRs and this may very well be another mechanism behind their ability to induce a loss of adipose tissue. The mechanism? Well, the binding of cortisol to the GR can cause an increase in LPL. (6,7,8) This isn't what we want if we're trying to drop body fat, as LPL causes lipid accumulation. So, certain androgens may prevent lipid accumulation through this mechanism.
Some androgens may do one of two things ? or possibly even both ? in order to lower LPL levels in adipose tissue. That is, they may bind to the GR and thus prevent cortisol from binding and increasing LPL activity, or they may downregulate the number of GRs in adipose tissue. (9, 10, 11)
Microsomal Receptors (MR)
The last mechanism involves the presence of the AR in subcellular fractions. To be more specific, the AR has been identified in microsomal portions of the cell. So what does this mean? Certain androgens are able to bind to the AR in microsomes and carry out a posttranscriptional effect. In fact, it appears that out of all the available androgens, stanozolol (Winstrol) is able to bind to this receptor while all others (with the possible exception of danazol) are not.
If you couple this with the idea that the AR is present in the subcellular fractions of adipose tissue ? or the microsomes to be more specific ? this can account for its ability to induce fat loss. (12,13,14)