T Nation

Tribex+test.ent =more free test ?

I use a gram of test + 400 mg of deca+ 30 mg dbol - would adding tribex result in more free testosterone or does that apply to endogenous t exclusively ?

Any other options for freeing up the good stuff ?

You need more T ??? Is this a joke ?

No, I do not believe Tribex would help here.

You also should not think of SHBG is being harmful to free testosterone levels. It is not.
How much testosterone is bound to SHBG? About 30 MICROGRAMS. Thirty millionths of a gram.

Even if it were being “used up,” that would be insignificant. But it is not being used up… rather, it is being momentarily stored safely (in a manner where the liver is far less able to metabolize the testosterone, whereas free testosterone is extremely vulnerable to metabolism), transported elsewhere to the body, and released.

This is good, not bad.

In the case of injectable testosterone esters, your free testosterone levels are independent of how much SHBG you have, but are the result of the total amount of free testosterone dissolved in fat in the body, and the partition coefficient between free testosterone in serum and fat (which is a fixed chemical property.) Not on SHBG. The amount stored there is tiny, and as mentioned, is not used up: it is not a loss.

Can you elaborate on the dissolved in fat/partition coefficent? I thought that free T and SHBG were inversely associated.

No, there is no evidence (that I have ever seen) that increasing SHBG causes free T to decrease, and it also makes zero sense since, as mentioned, the amount of T actually bound to SHBG is trivial relative to the total amount of T in the body, and relative to daily production; and furthermore, the T bound to SHBG is not lost! It is just there temporarily while being transported and comes right off, no loss.

However, one can be deceived by the fact that the body responds to low T by increasing SHBG, and vice versa. If one confuses cause and effect, it could appear that high SHBG causes low testosterone.

As for the partition coefficient, Mr Euclid pointed out some time ago that things equal to each other are equal to the same. In this case, at equilibrium, which is approximately the case, the chemical potential of testosterone (not the ester, but testosterone) in fat is equal to the chemical potential of free testosterone in the blood. The chemical potential is the same also for testosterone bound to SHBG, and for testosterone bound to the AR, and all other possible states of testosterone. Given the concentration of testosterone in any of these states, the concentration in the other states follows directly from the partition coefficient. If we know one of these values – for example, concentration of free testosterone in the blood – all the other concentrations (or chemical potentials) follow and you do not need to know the amounts of each other substance: does not affect the equation. The body regulates testosterone levels according to free testosterone, and rate of metabolic elimination is entirely or at least mostly according to that: it really is all you need to know with regard to the effect of testosterone in the body.

And reducing SHBG would, at best, transiently release a few micrograms of testosterone. A one-shot deal at the moment you did it, not a lasting effect. And how much testosterone is a few micrograms? Nothing worth mentioning, especially for a one-shot deal. That’s all you would accomplish.

Oh, and the reason I brought up the partition coefficient between free testosterone in fat and in the blood, is because most of the testosterone is in the fat, and the biggest effect (in terms of where the injection goes) from an injection is that the fat becomes some percent saturated with testosterone. (Actually, it is always quite a low percentage.) The concentration in the blood will be the concentration in fat divided by this partition coefficient, which is a physical constant for the substance (not affected, for example, by amount of SHBG.)

Bill, can you comment on the following paper: They suggest that higher SHBG decreases the available androgen to act on the prostate, potentially lowering the risk of prostate cancer.

Tymchuk, C. N., S. B. Tessler, et al. (1998). “Effects of diet and exercise on insulin, sex hormone-binding globulin, and prostate-specific antigen.” Nutr Cancer 31(2): 127-31

As of yet, after reading your post, I have read only the abstract, not the full paper. However, it does not seem from the abstract that they made any effort, or claimed to, to determine if the hypothesis that increasing SHBG would decrease testosterone. It appears in the abstract only as a hypothesis.

So it is not evidence that it is so.

It is a hypothesis which has appeared in the literature many times, partly because of the correlative reason, and also probably because to those not particularly versed in chemical equilibria or who have not thought about the problem too much, it seems to make sense that if something binds testosterone, it must reduce levels of free testosterone.

Looking at the clinical data showing a strong correlation where higher free androgen levels are correlated with lower SHBG and vice versa, one might conclude (I believe wrongly) that SHBG levels control androgen levels. However, it has never been demonstrated that cause and effect works in that direction in this situation, it does not make sense for reasons I’ve pointed out, and it IS demonstrated that cause and effect does work in the other direction, which also perfectly well explains the correlation. Namely, if you increase free androgen levels, for example by injecting androgen, SHBG levels go down. This indicates that the body reduces SHBG levels when androgen levels increase, and vice versa. So the cause and effect is the reverse of what this paper is hypothesizing.

Very interesting. Would you say that with IGF-1 and its binding proteins, the equilibrium would be analagous? That is, that increasing BP-1, for instance, decreases free IGF-1, but this isn’t cause and effect?
Thanks for your time, as always.

I am not familiar with the case with IGF-1. In general, what I described is true with regard to binding proteins, but there can be exceptions. If higher amounts of a binding protein result in faster elimination from the body, then indeed, more binding protein can reduce free levels.

For example, if I recall correctly, serum albumin very efficiently delivers diazepam
to the liver: the equilibrium in the liver is different than elsewhere in the body, because the pH is a little different and the conformation of the protein changes, “unloading” the diazepam for metabolism
and excretion.

I have no knowledge if something like that goes on with IGF-1 or not, though.