When is Bioavailable T Too Low?

My doctor claims bioavailable T is the most important indicator and that mine is low enough to consider supplementation. He says to start with one full tube of Testim 1%, then recheck my levels after 4 weeks. Here are my lab results he’s going off of.

Testosterone Total 462 (range 250-1100)
Testosterone Free 62.4 (range 46-224)
Bioavailable Testosterone 133.7 (range 110-575)

Is this bioavailable T actually low?
All other hormones have been checked in other recent labs, and have been in the normal range.

I would be glad you have a doctor that is willing to treat you with somewhat low bioavailable T, and low Free T. Most doctors nowadays would say, “Your Total T is mid range, there’s nothing wrong…”
You don’t mention E2 or SHBG. What are those results, if you have them?
Also maybe TSH, Free T4, and Free or Total T3?

I’ll throw in a couple of pennies here.

First off, how you feel and function is more important than what your numbers are. So how do you feel and function? Morning wood? Energy levels? Mood? Libido? In other words, do you have any of the symptoms of low testosterone?

Was your bioavailable testosterone calculated or assayed? Calculated values can easily be off by as much as 30%.

Also, calling anything within the reference range “normal” is misleading. Reference ranges are nothing more than the numbers required to encompass 80% of recorded values. They are NOT based on random samples of the total population. They’re based on guys who have a reason to get their testosterone levels tested. “Normal” men do not get their testosterone tested.

It would also give a better picture of the situation if you included relevant information like your age and fat percentage and how you got into all of this in the first place.

Lastly, there’s way too much focus on testosterone as if it was the only thing that matters. Testosterone is only a messenger. It doesn’t actually do anything until it binds to an androgen receptor. Since estradiol can also bind to androgen receptors (and render them useless), it is essential to also measure estradiol (E2) levels.

Here are the full lab results from my most recent lab, and some other recent relevant labs below…

Thyroxine- Free 1.1 (range 0.8-1.8)
TSH .81 (range .40-4.5)
Testosterone Total 462 (range 250-1100)
Testosterone Free 62.4 (range 46-224)
Bioavailable Testosterone 133.7 (range 110-575)

The below lab is from April. For some reason my Total T was much higher, even though my symptoms were the same. I have never used AAS.

Total T 917 (range 250-1100)
Free T 127.6 (range 46-224)
Bioavail T 262.4 (range 110-575)
DHEA 219 (range 110-370)
Free T3 335 (range 230-420)

Here’s more results, including LH and FSH from blood drawn in 10/07
FSH 4.3 (range 1.6-18.1)
LH 5.3 (range 2-18)
Total T 669 (range 270-1070)
Free T 26.6 (range 12.4-40.0)
Insulin like GR 218 (range 109-289)

To answer some of the questions in the above posts, I’m not sure if my levels were calculated or assayed. How do I find that out?
My symptoms are depression and fatigue for several years, but most importantly, the inability to recover from exercise. Any type of exercise. I am 33, and have no identifiable health problems, and am not a pound overweight. I have already tried sensible things like vitamins, Cortef, Armour thyroid, treatment for depression, without any improvement. My doctor is basically out of options. And while he is open-minded, I fear he knows nothing about things like injections vs. gel, T shut down, testosterone side effects, etc. What should I ask him to do next, and what other labs should I request, like E2 levels? Any help is appreciated.

If I were you…

Get a complete physical with all the blood work that goes with it. Then if possible, have the estradiol test added. Be sure to describe the symptoms (no recovery, depression) before he orders the blood work.

Even if I didn’t have symptoms, a complete physical is a good idea anyway.

I had the same symptoms, BUT my testosterone was evidently low in all categories.

The reason that doctors and others go into analysis paralysis over “Well there’s this much free and this much total and this much ‘bioavailable’” is that they don’t understand physical chemistry or the biochemistry of this.

The only, repeat only, testosterone value that itself is clear in meaning is free testosterone.

The others are the product, so to speak, of the free concentration and other things, and do not add any information about the biological effect of the testosterone, but only – if already knowing the free amount – add information about the amount of SHBG, serum albumin, and other substances weakly binding testosterone, none of which has any effect on outcome.

For example, if you have a given free T level both in an earlier test and now, but now you have half or double the SHBG levels, approximately speaking you will now have half or double the total testosterone.

The doctor, and most who don’t understand the chemistry, will think that oh, this must biologically be very different.

Nope, it’s not: the hormonal effect of the testosterone will be the same. All that has been learned is that there’s now half or twice as much SHBG.

(The only biological difference will be the SHBG itself has some slight signalling effect on cells, so the amount of that would be varying. But binding to the androgen receptor will be the same so long as free T is the same, totally regardless of changes to “total” or “bioavailable.”)

These additional figures taken are not the slightest more relevant than taking, for example, total body testosterone, if there was such a thing.

In that case, when at 20% bf there would be, for same free testosterone, about twice as much testosterone in the body as when at 10% bf. Ooooo, twice as much testosterone!

But exactly the same effect. The added measurement only adds confusion (if expecting it to mean anything) not information, or rather not any information except that bodyfat isn’t the same level anymore.

In other words, pay no attention to anything but the free T, with regard to testosterone values.

Thanks for the info Bill. I guess the next question is, based on my 3 lab results from the last year, and my symptoms, is my Free T low enough to treat?

It would depend on the doctor you find.

Some have the attitude, If it’s in the normal range, then prescribing is inappropriate.

Some have the attitude that optimizing your condition is worth doing and that means being at least in the middle.

There are doctors who, particularly if you had complaints that seemed related to low T, would consider it appropriate to bump your value up.

You might well be able to get your value up by other means, though, such as taking a low dose of an aromatase inhibitor such as letrozole, if you can acquire it. A quarter of a 2.5 mg tab four or five times per week should be enough.

It might even get your free T above the top of the normal range – that has been seen in the literature (though with a differing dosing protocol of a single whole 2.5 mg tab once per week, which is probably not as good a method though it surely would have better patient compliance.)

The advantage of this approach is that it doesn’t further shut down your natural production, as taking exogenous testosterone will do. This approach does not produce dependence, whereas taking exogenous T on an every-week basis does.

…are you suggesting that he take a ‘heavy’ AI such as Letrozole, especially without even knowing his actual E2 levels. Is that such a good idea? Just curious…hebs

Sounds a bit of overkill to me …

With regards to using this stuff on a cycle, unless you are extremely gyno prone, or need to reduce estrogen levels to virtually nothing (for a bodybuilding contest or whatever), it�??s going to be too powerful for most people.

Male and female competitors typically use it to get the last bits of estrogen related water retention out of them during the final weeks of contest preparation. But when used on a typical cycle, Letro is generally overkill unless a ripped look with zero water and estrogen is desired or if the user is prone to gyno.

[quote]hebsie wrote:
…are you suggesting that he take a ‘heavy’ AI such as Letrozole, especially without even knowing his actual E2 levels. Is that such a good idea?

Just curious…hebs[/quote]

I don’t know why you are calling the dose I recommend, about 1/6th or 1/7th the usual recommendation, “heavy,” nor if you mean the compound is “heavy” in any way or compared to other aromatase inhibitors, why you would say that. The side effect profile is zip at low effective doses, unlike Arimidex.

It’s a lot less intrusive than further inhibiting the HPTA. That’s why I mentioned it as an option.

Sxracer, have you really looked into and found problems with men with low testosterone using it a low dose as means of boosting testosterone? I am guessing you have not.

It seems you are extrapolating opinions from steroid cycle considerations rather than results from the actual sort of situation being discussed.

No Bill … I did not.
I can see your reasoning at LOW doseages.
I was always told to stay away from this stuff as an AI, but never looked into the T boostong side. Although if I remember correctly, A-dex and Amorasin are also noted as increasing T production as well.

I guess the real issue here was low free T.
If E2 is in check, isn’t SHBG the culprit 99% of the time ??

What you say on SHBG has indeed been said and written countless times.

The problem is that it’s not so. SHBG does not consume or in any way use up testosterone; it is merely (along with having some cell signalling properties of its own) a transport mechanism. Having more of that transport does not reduce free T.

The amount actually bound to SHBG is also so tiny that any period of reducing SHBG does not release significant testosterone nor does any period of increasing SHBG soak it up, so to speak. At for example 1000 ng/dL of T bound to SHBG, since there are only about 5 liters of blood, the grand total of T bound to SHBG would work out as only about 50,000 nanograms… fifty thousand BILLIONTHS of a gram, or put in other ways 50 millionths of a gram or 1/20th of one milligram.

You can see that there is not some vast depot sucking up or releasing lots of testosterone.

It’s one of those things that sounds logical but actually has no measured factual basis and when examined closely, not only isn’t logical at all but is absolutely contrary to facts such as chemical equilbrium equations and chemical potential.

What SHBG does do is that it provides a reservoir, tiny as it is, such that T can be added to a small volume of blood such as that entering the testes without the transport being limited by the extremely low water solubility of T. And also there must be some biological reason for why SHBG itself has cell signalling properties, but why that is I don’t know, about all I know on it is that it exists (Once I knew more specifically what it did but have since forgotten.)

But in terms of how test results can come out, yes, the way that one can have good or high total T while having low free T is from having high SHBG.

It’s not that the high SHBG causes the low free T though. Rather it’s completely the other way around: the low free T is the direct outcome of the HPTA function, and would be the same regardless of SHBG amount, but as the amount of T bound to SHBG is a product, so to speak, of both free T and amount of SHBG, high SHBG causes a given free T amount to yield a higher total T value.

If one makes the mistake of taking total T as a valid predictor in its own right, and ignores that free T is what should be looked at, then the high SHBG combined with the wrong assumption leads to the wrong conclusion that things are OK.

Whereas looking at the free T alone and ignoring the other values, as they are only consequences of free T and levels of other things, avoids coming to wrong conclusions.

Wow … that was a lot of info.

So you are saying do NOT worry about SHBG, and focus on Free t. What if it takes me a total T of say 1400, (Range of 342-1030) to get my free T in the top 1/3 of Free T range, is that considered OK ??

I think my Doc would cut back doseage at high total T level, and be happy with medicore Free T just to cover his A$$.

I thought Proviron helped free T by binding with SHBG, and thus increasing Free T levels.

[quote]sxracer wrote:
Wow … that was a lot of info.

So you are saying do NOT worry about SHBG, and focus on Free t. [/quote]
Yes.

That would be fine. A given doctor might well think it was “supraphysiological” but it would be absolutely fine in every way, and equivalent to having the same free T and merely average total T. It would just be a question of having more SHBG, not actually having more binding of T to receptors.

It’s entirely likely.

That’s been written many times, but as shown by the calculation on how little T actually is bound to SHBG, clearly if every single bit was released and not ever reabsorbed, that release wouldn’t be a drop in the bucket compared to natural rate of production of T (which is on the order of 10 milligrams per day very roughly speaking, and obviously variable but normally on that order.)

That concept either comes from mistaken thinking – “reducing SHBG has GOT to free up the testosterone, so free T must increase!” – or maybe there have been blood tests done where the analytical method counting Proviron as being testosterone: that is another possibility, I don’t know.

In fact Proviron inhibits testosterone production, by the way, even at doses as low as 50 mg/day. There is a literature study showing that, though it’s not one that turns up by a Medline search and I don’t by now know where it was.

[quote]Bill Roberts wrote:
hebsie wrote:
…are you suggesting that he take a ‘heavy’ AI such as Letrozole, especially without even knowing his actual E2 levels. Is that such a good idea?

Just curious…hebs

I don’t know why you are calling the dose I recommend, about 1/6th or 1/7th the usual recommendation, “heavy,” nor if you mean the compound is “heavy” in any way or compared to other aromatase inhibitors, why you would say that. The side effect profile is zip at low effective doses, unlike Arimidex.

It’s a lot less intrusive than further inhibiting the HPTA. That’s why I mentioned it as an option.[/quote]

…understood. I totally missed the actual (low) dosing part last night, thanks…hebs

If I remember correctly … Proviron is stated as binding to SHBG so the T will not. It does not actually reduce SHBG, but rather occupies it, hence giving better Free T #'s.

Make sense ???

It makes sense when necessary facts are not being considered, but when you consider the facts I presented above I think you will see it is in fact irrelevant.

Or let me make an analogy: A lot more T is stored (dissolved) in bodyfat than is present in the blood. But does losing a pound of bodyfat result in an anabolic surge?

No. And if it happened it would not be an ongoing effect, but only a temporary effect (however, it’s so small as to be utterly negligible, less than injecting a milligram of testosterone would be.)

The amount of T that could be “driven off” of SHBG is even more trivial – I calculated an example maximum possible amount above – and likewise even if were important (which it’s not) it would be a momentary effect. It would not be an ongoing source of T, just a surge of a few micrograms.

Make sense?

Just because theories get repeated by many authors doesn’t mean the theories must be right. Some of them aren’t.