The value is in the relationship. Consider Total T to be the well. The answer to your question is that IT CUTS BOTH WAYS, but only to an extent lesser than we are thinking these days. While SHBG may be one indication of how much free T is available, relationally speaking, it is still only a player in the sympony. While on the surface it would appear that only the Free T is active. This is true only to the extent of how much free T does your body need.
I consider SHBG to be a thermostat that is getting feedback from BOTH
the ACTUAL PRODUCTION RATE OF THE TESTICLES IN RELATION TO DHT
AND E2 ACTION ON THE BODY. Forget about whether or not you are supplementing testosterone
for a moment. You have (3) primary reasons the testicles meter production. (a) physical damage, (b) natural regulation by the body as genetic predisposed saturations of e2, and/or DHT
occur, and (c) Exogenous supplementation. While ANY ONE of these factors can tell the boys to make more or less, one thing is constant, and that is the ever changing SHBG measurement
. If the testicles are producing less testosterone for any one of those reasons, then the well is low. So the body now limits production of SHBG in order to make more Free Testosterone available in order to compensate. Consider the testicles are primary organs indeed. I believe there has been way too much overspeculation as to this, and this is the fact plain and simple, and applicable to a majority of all instances involving.
In my example the Hypothalmus would be the Central Contral unit, and the Pituitary would be vector, or connecting wires to the testicles.
KEEP IN MIND FOR THESE EXAMPLES THAT THEY COULD ALL VARY DEPENDING UPON ACTUAL FUNCTION OF EACH PARTICULAR SYSTEM INCLUSIVE OF OTHERS NOT MENTIONED, ENZYMES, ETC.....
Example #1: Testicles just aren't up to snuff due to injury or natural failure. Your body is most likely going to lower SHBG in order to compensate, thus giving you the same end result which is genetically mandated levels of E2, and/or DHT.
Example #2: You are a middle aged male with body fat percentages approaching 20-30%. Your preponderance of E2 is going to shut down T production in order to limit available testosterone. Hence now your quickly responding, SHBG will again lower in order to compensate for the lack of testosterone available overall, so that the fatty tissue's learned and hardened demand for E2 can be still met.
Example #3 You are a natural body builder. Same as the above scenerio except involving DHT
to trigger this time. You body again lowers the well (TOTAL T) in order to keep you from drowning yourself in DHT
. You again wind up with a lower SHBG to compensate.
Example #4: You are supplementing Exogenous Testosterone for whatever reason. Your feedback from E2 and DHT
receptors will again regulate the boys. This is the most obvious, yet convoluted situation. Your prepoderance of Total T as you fill the well with firehose of Exogenous T shuts down the testicles as you supply enough T to start an E2 and DHT
world wide party at any level of SHBG. So you say now, " why would you have a low SHBG in this situation?" SImply put, the nuts are clearly the chicken and not the egg. They
are producing no testosterone so SHBG goes down again.
When I mentioned consideration for the actual functionality of individual systems I apply it as such. Consider that there are variations that can be added to the above situations, and a multiture of other situations all together that will change SHBG to high instead of low, to achieve the same result, only by means of less Free T by SHBG modulation rather that a total reduction in T. The bottom line is that in the end, you are always going to find the necessary amounts of Free T that your body requires, depending on genetics, receptor presence and capability, other potential system interactions, etc... If the body truely cant make the Free T that it needs to operate to its desired levels of DHT
and E2, then something is truely fucked and this is a rare bird considering our application is AAS
and Age onset HYpogonad here.
The value of the measurement of both Total T and Free T is this. If active testosterone accounts for only about 2% of the total T count. Then how much T do you really even need? Lets say you are young with a total T of 1200 and free T levels at 1.5%, would this not be exactly the same effective end result Total T of 600 and Free T of 3%??
Some of the ideas above are a bit radical in nature. CONSIDER THAT SHBG COUNT MAY NOT BE PROPORTIONATE TO FREE T LINEARLY, OR IF AT ALL. This could be proven in the fact that Free T rarely rises about 3.5%. The actual presetation of the physical measurements of T, free T, and SHBG are misleading to say the least. If SHBG can range up to 40 or 50 and be workable, then why would a SHBG count drop down to 12 not effect a Free t of 25% or more. It is because SHBG is more of an assistant to the availability of Free T, and not a determining factor.
Consider SHBG as if it were merely a "trademark" or signpost on T available for use that this T has been marked for use.. While the drop to 12 on the SHBG measurement may indeed corrolate with more Free T. The actual number's rammifications could be considered almost impotent in relation to the actual Free T required to service the body. This rate of measurement for SHBG is hence proven of little value as presented, by the fact that it ellicits little to no VISIBLE change in the Free T percentage, while at the same time the small percentage movements effect on the body is MASSIVE. All of this is simply proves that the body can only use so much DHT
or E2 depending on active and available receptors. AND IT DONT TAKE MUCH.... So now why do we have natural levels of 900 in Total T when clearly we only need 40 of them so to speak? I would claim that it is primarily a physical relation to blood volume composition as it relates to the mass of the body serviced, with also some consideration for the bodies inherent design of redundancy that protects out critical systems.. The baseline would be the fact that we all have about the same total blood volume circulating regardless of our size. There simply has to be enough T floating around to be available
to make the small, yet critical conversion. Consider the actual physical measurement of SHBG. You are gonna have to put plenty of T out to deliver to all the areas where this limited hormone can activate it. You may only need 2%, but that is a large area to cover. Which finally brings us back around to testicular production of T. If the body only needs 2% of Total T to be free, Then would it not make sense that the actual slowdown of T production for any of the above listed reasons would require quite a considerable reduction in Total T to have an effect. Consider that you are living in an incideous feedback loop that is not only constantly trying to correct its self to a "known Stasis", it is trying to prevent problems as well. The older you get (high fat composition), or the more changes you make to a said "normal" system (working out adding on piles of muscle), the more you have perverted this norm. This is causing mass systemwide confusion as the body tries to adjust. The end result is the spiraling action in the direction that best solves the problems with the corruption of the natural design of the system, while at the same time mitigates the problems associated with still living at natural design levels that are now arrising due to the mounting factors now making this natural optimal profile no longer acceptable.
In short, my Total T levels were 350 when diagnosed Hypogonadal. My free T however, was 3.5 percent. Did I ever really have a problem. Sure, I am middle aged and fat, so my Total testosterone well has been naturally reduced to a mere 350. After all my body does not want to beat its self senseless with all the E2 I was generating from this high amount of fatty tissue. But didn't I potentially have the same effective Free testosterone as I might have has at a younger Total T level of 600 or higher,, if my Free T were only 1.5 or 2% when younger? So why did my body crank Free T up? Didn't that leave me right back where I was? No. The chicken is the Testicles. A significant reduction of Total T was MANDITORY considering that it only takes 2% to function. My body would now be in a condition of E2 onslaught if my Total T were to remain high.. Just how impacting can even a .25% move on available Free T be?? Consider a Total T level of 2000. What then does a 2% level of Free T mean?? Probably your ass if it stayed there long enough!!!
But at Total T of 350, the percentage means squat more than a best attempt. Then what benefit has all this provided? Not too much really. The body is pretty astute in compenstation methods. My body is now trying to get Free T back up to meet the still remaining demand for known stasis, or perhaps even a now inadvertantly reduced DHT
level that is too low. THIS IS SIMPLY THE PROOF THAT THE TESTICLES ARE THE CHICKEN. "Normal" stasis now demands that the Free testosterone still be available. This two will dwindle with time, the increase in Free T is merely the second response by the body to provide previous AND LEARNED levels of available T. As the field of production and availability narrow, the game gets tougher and tighter. STASIS MUST BE FOUND. Misproportions of muscle to fat are only fuel to this fire making it worse further keeping the original harmony an impossibility, and we are left only with mitigating factors.
I'm done. Someone correct me where I missed....
Originally Posted by chemman
Can anyone explain the value of measuring/analyzing total testosterone when it appears that total testosterone appears to be a function of the amount of SHBG present rather than HPTA output? I have read on another forum where Bill Roberts explains the rationale behind this more clearly.
Here's the link: T-Nation.com | When is Bioavailable T Too Low? - Page 1
So when you have a person in a situation like mine where Total testosterone is decent (476) and free T is out of range low, does this indicate hypogonadism? Some would say that the problem is high SHBG. But based on the above thinking, it looks like SHBG is relatively static and isn't the real problem. Granted I don't have a SHBG lab (yet), but it is most likely high.
Also, do feedback loops work on SHBG bound hormones or free?
Thanks in advance for your input.