Sex Hormone Binding Globulin [SHBG]

Re: Calling out the low SHBG guys

You and your docs are chasing SHBG ghosts, rest assured nothing will be found which is uniformly treatable.

But hey at least something is being DONE, right?

Oh yea why can't people read reference ranges.

Because your Hgb-A1c is NORMAL! It's NOT "HIGH" fella.
 
Re: Calling out the low SHBG guys

The doctor said it was in the range so it was normal :D How should i interpret it ?

The only half decent thing I've ever read about low SHBG is in reference to insulin resistance. While your A1C is in range that does NOT mean you aren't showing signs of insulin resistance. My A1c was far lower than your at my worst and every other marker of IR was elevated. Guess what happened when I lost weight and no longer was IR?
 
Re: Calling out the low SHBG guys

Obesity and a sedentary lifestyle both are strongly associated with IR and both of which were effectively "treated" by Idster.

Now that's a lifestyle change most doctors dream about for their patients, unfortunately it's not found in a pill physicians can prescribe!

Congrats mate!
 
Re: Calling out the low SHBG guys

Prediabetes is a diagnosis made for those patients with a FASTING BLOOD SUGAR which is consistently above the normal 100mg/DL range.

Consequently since the Hgb-A1c is reflective of chronic exposure to glucose SOME have suggested it may be used as a replacement for FBS.

Nevertheless until Hgb-A1c levels for prediabetes is well ESTABLISHED, FSB remains the diagnostic gold standard IMO.

That being said those with upper limit Hgb A1c levels although NORMAL are indeed likely to develop or have IR/prediabetes.

But really does that matter?

If your overweight and lead a sedentary lifestyle CHANGE that which may shorten your lifespan or kill you!
 
Re: Calling out the low SHBG guys

Question 1:
my FBG was consistently in 80-90 range. Over last week I am measuring morning FBG at home using strips, and I am getting increasing readings: 101, 107, 112. No changes in diet. What can be the cause of it?
Question 2:
how does wine relate to glucose control?
 
Re: Calling out the low SHBG guys

Why are u measuring your BS on a regular basis.

The metabolic byproducts of alcohol increase serum BS absent insulins countering effect.

More importantly almost all alcoholic beverages excepting perhaps distilled spirits have other carbohydrates which raise BS considerably more than the alcohol alone.

Indeed these carbs are the primary reason some regular "beer drinkers" become overweight, exclusive of their sedentary lifestyle.
 
Re: Calling out the low SHBG guys

The presumption that LOW SHBG is the etiologic basis for these complaints is absolute rubbish.

Is there an association between low SHBG and SD?

NOT one that is literature based OR which is consistent with known medical practice.

James you have been arguing there IS a cause and effect relationship between LOW SHBG and SD ever since you entered the halls of Meso and have even told mates with this "condition" they "need to raise their SHBG" as treatmet, WITHOUT any evidence to support this form of "therapy".

Each and every time you leave when asked to prove your point based on the literature and shortly thereafter I'm met with silence.

WELL NOW YOU HAVE ANOTHER CHANCE !!!

These individuals complain of SD yet sexual dysfunction is more often a multi-factorial disorder and as such has many variables which contribute to its presentation simultaneously or in combination.

Consequently it's its fool hearty for you to assume an couched layman whom has never evaluated either of the mates is more adept at making a more accurate diagnosis (which is contradictory to known SHBG function) than those whom have done so.

Jim


Low SHBG simply means more conversion to DHT and Estrogen, more mental effects of Testosterone. I have high Test (>1200) with LOW estrogen (<12) and low SHBG (1.4) and have a very high sex drive and frequent erections so it's a more a matter of amount and ratio for OP. We don't even know where his prolactin is at, his levels of adrenaline, DHT, we have nothing really specific here.
Low SHBG is a good thing as long as you have high Test in general and are keeping active.

OP, with all due respect, what other remedies have you tried. Any dopaminergics ?
 
Re: Calling out the low SHBG guys

No i havent tried anything for the neurotransmitters and those are the only things left that i havent tested, but as it is mentioned earlier in the thread your low SHBG is due to the exogenous Testosterone and probably was normal before you started therapy. My prolactin is normal as well.
 
Re: Calling out the low SHBG guys

Now were using replacement neurotransmitters as SHBG therapy. Well how about Haldol then, lol!
 
Re: Calling out the low SHBG guys

No i havent tried anything for the neurotransmitters and those are the only things left that i havent tested, but as it is mentioned earlier in the thread your low SHBG is due to the exogenous Testosterone and probably was normal before you started therapy. My prolactin is normal as well.

This is correct.

In men who respond to TRT with low SHBG, invariably they have normal SHBG expression prior to the TRT, where as men with low SHBG have SHBG that does not change no matter how the hormonal environment in the body changes.

One interesting consideration is that studies have shown that SHBG's binding affinity is genetically determined and can be up to over 2x higher in certain individuals. One man's "low" is another man's "normal."

I have high Test (>1200) with LOW estrogen (<12) and low SHBG (1.4)

Most men with TT of > 1200 ng/dl will have serious estrogen issues. If E2 is still low with SHBG so low, then you have a larger issue at play and the SHBG that your body produces is CORRECT for your situation due to low aromatization.
 
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Re: Calling out the low SHBG guys

I was initially seen by a junior registrar endo, I was given a TRT trial from him due to my complaint of low T symptoms and 'borderline' testosterone serum levels, he carried out no further investigation and seemed to show little knowledge of the importance of low SHGB and high Estrogen. I requested to be seen by a senior consultant.

As said above, this consultant has stopped my T therapy and is going through the process of trying to identify a possible 'primary' condition that is causing the low T and low SHGB...

Dexamethasone suppression came back as normal.

Now that my HTPA has recovered, my doctor has requested a full bloodwork set to get baseline numbers a follows ;

Group tests
-urea & electrolytes
-liver group
-bone group
-glucose

others
-testosterone (serum)
-SHGB
-LH & FSH
-E2
-Prolactin
-DHEA
-CRP
-Feritin
-Andiare ? Andiore? Andire? Ardiare? (cannot read handwriting)

Haematology
-Full blood count
-PV

Immunology
-ANA
-ANCA
-C3 & C4

Maybe I should start a new thread and update with my low shgb investigations?

Yes. Please start a thread!

I am disappointed in that list. I do not see anything on that list that makes much sense other that CRP and DHEA-S, both of which I expect to come back either within the high end of the normal range or slightly elevated.

Be sure to ask him what ailments he is trying to uncover.
 
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Re: Calling out the low SHBG guys

This is correct.

In men who respond to TRT with low SHBG, invariably they have normal SHBG expression prior to the TRT, where as men with low SHBG have SHBG that does not change no matter how the hormonal environment in the body changes.

One interesting consideration is that studies have shown that SHBG's binding affinity is genetically determined and can be up to over 2x higher in certain individuals. One man's "low" is another man's "normal."

I still tend to think it's more complicated than SHBG, something along the way that is affected. Like estrogen, or some neural network.
There's a lot of people with low SHBG who have no negative effects.
 
Re: Calling out the low SHBG guys

There's a lot of people with low SHBG who have no negative effects.

No, there aren't. You are referring to men with normal SHBG who suppress it with TRT.

Low SHBG means that SHBG is low no matter what, and these men typically do not respond to TRT.
 
Re: Calling out the low SHBG guys

No, there aren't. You are referring to men with normal SHBG who suppress it with TRT.

Low SHBG means that SHBG is low no matter what, and these men typically do not respond to TRT.

Do you know of any studies to support this view?
 
Re: Calling out the low SHBG guys

Now DOC James has yet to post a single study which supports his "views" and I really doubt that your calling him to task will make a damn bit if difference.

There are many men whom are not on TRT and have low SHBG without any ill effects, (Dr S has seen them as have I) the only difference, they are not mentally deranged and think about their SHBG level on a second by second basis as James obviously does!
 
Re: Calling out the low SHBG guys

Jim, you look like a complete ass to the afflicted men who are reading this thread and trying to share information. No one is listening to you, and for what it's worth, I'd say you are trolling us at this point. You don't seem to understand half of what is going on here. I am asking you nicely to leave this thread. You seem obsessed with following me around.


Do you know of any studies to support this view?

No. I do not believe ED and low SHBG have ever been studied together. If they have, it is in the context of a low SHBG related disease like Metabolic Syndrome.

However, the link between excess E2 and ED has been established through studies, and SHBG is the primary determinant of the T:E2 ratio in non-obese men. It is through this inference that we suggest that total estrogens are elevated in cases of inadequate SHBG, which may trump attempts to control E2 to restore erectile function.

The last study that I posted was a study where oxandrolone decreased SHBG and create erectile dysfunction in the men being treated, even though T levels were stable.

There is a drug in the GTx's pipeline designed for prostate cancer, that is the first ever drug created to control free testosterone by increasing SHBG. It works as an estrogen agonist in liver tissue to increase SHBG expression.

It appears to be extremely effective, unlike anything ever released. In Phase II trials, SHBG increased by an average of 446% at the 1000 mg dose. It is also LH suppressive, so would need to be used off-label (but isn't every ancillary that we use here?) and taken along with exogenous testosterone. For men who are already suppressing LH with T injections, it's certainly something to keep an eye on. I would even suggest applying to be a part of the clinical trials, if you live near the researchers.
 
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Re: Labs say low free T but high Bioavailable T. Why?

Sex hormone-binding globulin (SHBG) is the high-affinity plasma transport protein for androgens and estrogens, and it modulates the amounts of free or nonprotein- bound sex steroids that can access their target tissues. The presence of human SHBG within cells raises the obvious question of whether it promotes the internalization and actions of sex steroids, or dampens their effects by restricting steroid access to their nuclear receptors. These questions were explored in a series of experiments that lead researchers to conclude that the presence of human SHBG within specific cell types, such as PCT epithelial cells, accentuates the uptake of androgens and serves as a reservoir for androgens that can be accessed by the AR, and that this may be especially important under conditions where the supply of androgens is limited.


Hong E-J, Sahu B, Janne OA, Hammond GL. Cytoplasmic Accumulation of Incompletely Glycosylated SHBG Enhances Androgen Action in Proximal Tubule Epithelial Cells. Mol Endocrinol:me.2010-0483. Cytoplasmic Accumulation of Incompletely Glycosylated SHBG Enhances Androgen Action in Proximal Tubule Epithelial Cells -- Hong et al., 10.1210/me.2010-0483 -- Molecular Endocrinology

Human sex hormone-binding globulin (SHBG) accumulates within the cytoplasm of epithelial cells lining the proximal convoluted tubules of mice expressing human SHBG transgenes. The main ligands of SHBG, testosterone and its metabolite, 5{alpha}-dihydrotestosterone (DHT), alter expression of androgen-responsive genes in the kidney. To determine how intracellular SHBG might influence androgen action, we used a mouse proximal convoluted tubule (PCT) cell line with characteristics of S1/S2 epithelial cells in which human SHBG accumulates. Western blotting revealed that SHBG extracted from PCT cells expressing a human SHBG cDNA (PCT-SHBG) is 5-8 kDa smaller than the SHBG secreted by these cells, due to incomplete N-glycosylation and absence of O-linked oligosaccharides. PCT-SHBG cells sequester [3H]DHT more effectively from culture medium than parental PCT cells, and the presence of SHBG accentuates androgen-dependent activation of a luciferase reporter gene, as well as the endogenous kidney androgen-regulated protein (Kap) gene. After androgen withdrawal, androgen-induced Kap mRNA levels in PCT-SHBG cells are maintained for more than 2 wk vs 2 d in parental PCT cells. Transcriptome profiling after testosterone or DHT pretreatments, followed by 3 d of steroid withdrawal, also demonstrated that intracellular SHBG enhances androgen-dependent stimulation (e.g. Adh7, Vcam1, Areg, Tnfaip2) or repression (e.g. Cldn2 and Osr2) of many other genes in PCT cells. In addition, nuclear localization of the androgen receptor is enhanced and retained longer after steroid withdrawal in PCT cells containing functional SHBG.

Thus, intracellular SHBG accentuates the uptake of androgens and sustains androgens access to the androgen receptor, especially under conditions of limited androgen supply.

HEY DR SCALLY

Just read through all of those studies, thanks for posting, so in your opinion would it be more detrimental to total androgen receptor activation to lower SHBG or raise it?

To my current understanding the last study you posted made it seem that test bound to SHBG was more beneficial to androgen receptor activation than its unbound counterpart. Correct?

Following this it would be more beneficial to have a higher SHBG assuming that an equally higher percentage of protein bound test is transported through cell walls by increase Megalin. Due to this limiting factor IMO it would still be more beneficial to overall androgen receptor activation to increase the free test level ratio to TT.

I would be interested to see a study that compared lean muscle mass of mice that did not express SHBG with those that do normally.

I think that would give me a more conclusive answer.
 
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Re: Calling out the low SHBG guys

GTx-758, ERa Agonist, Reduces Both Serum Free Testosterone(T) and Serum PSA in Men With Advanced and Castrate Resistant Prostate Cancer
GTx-758, ERa Agonist, Reduces Both Serum Free Testosterone(T) and Serum PSA in Men With Advanced and Castrate Resistant Prostate Cancer -- Coss et al. 34 (3): SAT-319 -- Endocrine Reviews

Introduction: Androgen deprivation therapy (ADT) improves disease-free survival in men with advanced prostate cancer. Primary ADT with LHRH analogs lowers serum total testosterone (T) by reducing testicular androgen production, thereby lowering serum total and serum free T. Estrogen-based ADT induces sex hormone binding globulin (SHBG) expression resulting in proportionally greater reductions in serum free T. Primary ADT patients achieving lower serum T levels, and men with CRPC undergoing secondary hormonal therapy to further reduce T, experience better prostate cancer outcomes.

Objectives: Herein we compare the effects GTx-758 (an oral, selective estrogen receptor alpha (ER?) agonist) versus leuprolide on total T, free (unbound) serum T, SHBG and PSA levels in men with advanced prostate cancer.

Methods: In Phase II studies, men with advanced prostate cancer (n=164) received 1000 mg or 2000 mg GTx-758 daily or Lupron Depot® (4 month), while men with CRPC (n=7) received 2000 mg GTx-758 daily while on ADT. Serum concentrations of total T, free T, PSA and SHBG were determined at baseline and during treatment.

Results: The ADT naïve ITT population receiving GTx-758 demonstrated a mean reduction in serum total T from baseline of 54±52 and 72±43% for the 1000 and 2000 mg doses, respectively, compared to 93±2.8% reduction in the Lupron treated arm at Day 21. However, mean PSA reductions from baseline at Day 21 were 55±47 and 60±32% for the 1000 and 2000 mg doses of GTx-758, respectively, compared to 38±24% in Lupron treated patients. GTx-758 treatment resulted in 55 and 51% greater reduction in serum free T per unit reduction in serum total T relative to Lupron in the 1000 mg and 2000 mg arms, respectively, at Day 21. Reductions in serum free T coincided with mean increases in SHBG of 399±186 and 439±165% for 1000 mg and 2000 mg GTx-758 groups, respectively, compared to 5±14% in Lupron treated patients at Day 28. SHBG inductions were highly correlated with reductions in %Free T([free T/total T]X100) in both ADT naïve and CRPC prostate cancer patients (p<0.001).

Conclusions: Although GTx-758 and LHRH ADT, both reduce total serum T and PSA levels in ADT naïve advanced prostate cancer patients, SHBG induction rapidly reduced %free T to a greater degree in only the GTx-758 treated patients. GTx-758 therapy also demonstrated efficacy in men with CRPC, with similar reductions in %free T and PSA observed. The ability of GTx-758 to reduce free T demonstrates a unique and effective mechanism to treat men with advanced prostate cancer and CRPC.
 
Re: SHBG - Free & Bioavailable Testosterone

Its funny - I have a soapbox around here.... But you bring up again the notion of
"Bioavailable". I don't recall precisely how I ultimately discerned "medical science's" interpretation and FORMAL description of this. But it seems like they were basically referring to Free T as "bioavailable' in the RECENT past. I could be wrong. My past posts on this can be found to prove or disprove me here.

It's long be MY NOTION that Free T is MERELY "Proof of life", as PROOF that EXCESS testosterone exists in SURPLUS. And that the ONLY VALUABLE TESTOSTERONE is BOUND TESTOSTERONE which MUST be BOUND in order to be delivered to action as cell/tissue. This is MY laymonizing REVIEW and ASSUMED Approach which I have been operating under to TRY/ATTEMPT to inject LOGIC to MEDICAL SCIENCE - where is seems to all the sudden fly out an invisible window.

So my analysis of your labs would be as follows...:

(1) you have a high end TT level in serum. This indicates a HIGHLY DYNAMIC DEMAND Situation. and ONLY this. This could mean as used for androgens, estrogens, or OTHER/unclear... The flip side or "proof" I would be hanging my hat on (when not in my ass - LOL) is that a modern "Low-T" patient is NOT "Low-T" at all. He just has different demand profile for END USAGE. Perhaps estrogens as fat activity turn over much less T to E's as example hypothesis thought.. (as an example of the case I present). But the point being a high TT number would be reflective of a high POTENTIAL DEMAND or "Burn RATE", meaning that high supplys are REGULARLY REQUIRED - and as a result of the BIOLOGICAL DEMAND BASE IN PLACE (The body in question).

(2) My Primary Argument surrounding this, and which I am attempting to support is that NO ONE can tell the RATE at which T is metabolized..! Its not possible with considerations of various supply points, and the myriad of conversions, finally also considering elimination and the factors associated. Short of placing a SPIGOT on the testicles with a METER which counts production - its not possible ( i can argue that to whatever degree anyone likes and hold water).

(3) So the POINT, was that the "low-T" diagnosed patient is NOT LOW T, by definition of hypogonadism type II (or pituitary directed if i recall), but IN FACT producing EXACTLY what his body is DEMANDING. So in your case, the high TT count would mean either good TT conversion, but not every moment, but AT LEAST proof of high rates at time thus SUSPECTING good androgenic type male activity.

(4) I believe one of these articles attached talks about Albumin bound TT (the half of the 98% BOUND which is NOT the half bound to SHBG). They are NOW saying that perhaps this albumin bound TT has biological value, but since its 'weakly bound".. L........ M...........A..........O...........! But how could I not help. So now they are admitting some bound T has value- BUT WITH CAVEAT..?!?!?!? But I am thinking the reason for the distinction of the term "bioavailable might be held to the "Protect and Release" premise POSSIBLY. ( I stretch here as I have come back to this at end of thoughts...)

(5) Keep in mind. The way I understand common medical science's approach to explaining the VALUE of testosterone with relations to metabolic activity in men is as follows (could be wrong). But, I have interpreted science to say that testosterone is not "lost forever" because it became bound, BUT its being held in CAPTIVITY and for PROTECTIVE PURPOSE. So that when the call comes, the Bound T becomes FREE, and THEN is POTENT AVAILABLE FREE T... With that sentence UTTERED, While it does kinda sound like the same thing I am arguing (as blood proteins 'effectively delivering T to cells" - IT IS NOT. Because this premise assumes the Bound T is FIRST RELEASED and then USED where needed.. My HYPOTHESIS/Premise is that the Binding of the T to SHBG or Albumin is in FACT REQUIRED FOR DELIVERY as the PROTEIN IS THE MODE OF DELIVERY INTO THE CELL..

(6) Why in the FUK would a fundamental hormone in the body all be "locked up and unavailable - Thus pointing to the poor medical argument that "one must have Free T to have Good available T". This is worthy or RIDICULE Indeed...

(7) Would it not be logical to then assume that T is produced by the testicles PRIMARILY, enters general circulation, and where it is THEN Picked up/interacted with BLOOD PROTEIN for cellular metabolism where DEMANDED..?!? THUS - FREE T MUST ONLY be what is left over when demand lessens. Whether Free T has any value remains unclear to ME in my LAYMAN'S constructive analysis. Perhaps Free T interacts NEUROLOGICALLY as affecting EMOTION and other functions of the body which are psychological and on a dime. I WONDER does a person with a low FT count have DIMINISHED EMOTIONAL CAPACITY...!?!! I wonder does a man's "RYLE" have limits, or not effectively increase without ("Roid rage", "young stuff", "lead in pencil" - whatever your preference). This is just an example of some thought process. Perhaps FT is worthless leftover. Perhaps it is as scientifically stated currently, and indeed just some generalized "freeing of T for use". But I find it amuUUUZZzing to see science tending toward common logic as I present here and in past....

(8) So in my world your high corresponding FT would also indicate that you are either (a) using some serious hormones and regularly, OR (b) in flux AT THE MOMENT - as primary thoughts. What I am saying is that a serum count of a blood draw is worthless with two exceptions. (a) Long term to denote and track trends/long term change (every six months or year), OR (B) if samples collected on CLOSE INTERVAL, and say every 3 minutes for few hours. Or every few minutes for an hour during and post a workout, OR EVEN having to think mentally or endure JOB related stress. This is the only way to validate the difference in these numbers - But NO ONE WANTS to know really. Is more like it... Science dont care cause $ dont care, and actually discourages. Hence - ARE YOU STATISTICALLY NORMAL. Yes you are, but with SLIGHT variation at best. You could come back and argue that you have had this blood work three years running and similar. I COULD respond - YES, I believe it. And the reason for the high FT in conjunction with the high TT, is that each time you were tested in a "Loading Phase" where T was being actively produced at the RATE required to satisfy the RECEPTOR DEMAND which requires the delivery VIA Blood protein (shbg or Albumin). But if you are using the produced T effectively or not, It could simply be an elimination issue where you are dumping too fast, who knows. But it would make sense that a high hormone usage of BOUND T at cellular tissue receptors in a healthy individual would MOST LIKELY correlate with times of high Free T, or EXCESS PRODUCED T which DID NOT get taken into protein bonding. This could related to many factors. And right down to are you working out, controlling calories in different manners and timings, and did all of the sudden you ran out of calories to METABOLIZE, thus the demand for T production ceased abruptly. (T can not be used without a calorie to facilitate would be part of my hypothesis - in most cellular conditions). Growth, WORK, or general maintenance REQUIRED CALORIES (Food), else we die. T is a SERVICING PRINCIPLE of this function. The end goal is that we EAT to LIVE - Right?? It also happen to be PRIMARY. HOW WE LIVE Pertains to Testosterone. There is NO chicken or egg there.

(9) With some reference to SHBG. I initially began my inquiry into this as "just how is SHBG Calculated in Blood serum". So - So they count the SHBG whichis attached to a hormone (it works with others too ya know) INCLUDED in this calculation?? The initial result of my enquiry pretty much climaxed with SHBG being determined as calculated in MOLAR expression, which is a nightmare with exponential factoring involved which really makes it complicated for anyone short of a STATISTICIAN with a SERIOUS math background to apply a real ANALYSIS for correlation purpose. So while this is away from the issue of the half of blood bound T which is albumin related, it is at the same time pertinent. (and doesnt ANYONE find if FUNNY that all anyone talks about round here, OR in medical science is RELEVANCE to TT as bound to SHBG, and not Albumin..!??!?) LOL. Quaint indeed...!

(10) So you post a value of SHBG at 26... So what does / could this mean, and with consideration of the other factors you provide. Some say that LOW SHBG (12-13) is associated with TRT patients many times, and that application of further exogenous T only LOWERS this number. You can look to the high side folks (SHBG 65 and up) and then wonder why so high? Is this "androgen resistance" (or whatever the fuck they currently coin). Perhaps an indication of Primary type I hypogonadism where the testicles are not making T, and thus an excess SHBG available. Or EVEN perhaps a receptor RECEIPT PROBLEM where T is attaching to blood protein, and plenty of it (again real counts unclear), but the tissue CAN'T uptake for metabolism. COULD this possibly be an indication of INSULIN SUPPLY MALFUNCTION, thus even with food available, NO FIRE can burn in the cell if FUEL/Calories cant be effectively delivered. So the body would drive up SHBG in CONFUSION attempting to pick up more T, while the Brain still limits as safety catch knowing the shizzle is present in blood and on deck.???! OR - could it even be a deficiency of calories as restrictive diet, poor diet, poor intestinal/digestive function/failure, or lack of another processing component/enzyme to readily convert FOOD-to Calories- TO FUEL to burn. And with further dissection as to WHAT TYPE CALORIE meaning is a body failing to metabolize a protein to a carb when and where required for some reason. But high SHBG guys have high and low TT values and the kicker being whatever REAL physical SYMPTOMS remaining UNRESOLVED MEDICALLY - and for no apparent reason other than the failure of medicine to acknowledge hormones in mainstream science...! You can further start to apply FT to the above SHBG based analysis and get more indepth - all leading to a closer resolution ALL FAILING as the Bottle neck - we cant count TT production endogenously. So YOU focus on YOUR symptoms and deliver them to the RIGHT HELP.. Is all you can do. and read posts like these and THINK... THINK.. THINK.. Yes it hurts bad. I dont like it many days.:D;)

(11) With some more reference to Blood Protein and specifically - ALbumin. WHY IS THE SUBJECT AVOIDED? After all, half the bound T in the body is bound to ALBUMIN.... COULD it be possible that albumin....:
(a) Services a completely different set of tissue/cells/receptors.
(b) Actually works at each and every cell, and in conjunction with SHBG bound T, but albumin bound serving different type receptors on the cell (immune for example)
(c) Albumin crosses certain "biological barriers" (blood /brain for example) BETTER than SHBG, or Even DOES actually service a different set of principles. Perhaps Albumin bound T services more active "Driving systems", like fight/flight, Sympathetic/a-sympathetic CNS specifically, Or perhaps interacts with BONE/Skeletal primarily..?

Here is interesting from Wiki - [ame=http://en.wikipedia.org/wiki/Albumin]Albumin - Wikipedia, the free encyclopedia[/ame] (aint Wiki Awsome!!!);)
The albumins (formed from Latin: albumen[3] "(egg) white; dried egg white") are a family of globular proteins, the most common of which is serum albumin. The albumin family consists of all proteins that are water-soluble, are moderately soluble in concentrated salt solutions, and experience heat denaturation. Albumins are commonly found in blood plasma, and are unique from other blood proteins in that they are not glycosylated. Substances containing albumins, such as egg white, are called albuminoids.

A number of blood transport proteins are evolutionarily related, including serum albumin, alpha-fetoprotein, vitamin D-binding protein and afamin.[4][5][6]


LOOKING ABOVE at the small excerpt, you can denote the relation to EGG. Egg happens to be one of the best workout/energy/GROWTH proteins there is BARR NONE. Raw meat is close. But CONSIDER striated muscle tissue is only part of the animal. The EGG is the WHOLE THING... Further NOTE "water soluble" - Hmmmm.. And also NOTING "Salt".. I'm thinking SODIUM CHANNELS which are critical in CNS activity... Hmmmmm.. Finally NOTING - "Experience Heat Denaturization".. So with that said you EVEN have to wonder if ALBUMIN BOUND T is the T that is primarily used when in a state of STRESS from EITHER Physical Work, or Mental Psychological activity/stress... !!! ??? !! Is it the "first to Go"/be metabolised when UNDER A LOAD. And thus SHBG being the "long term" or "Time Release", the SHBG related T/Hormones which provide the SUSTENANCE for Repair and Growth when the day is done.. YOU HAVE TO WONDER...

Keep in mind all this is based upon my POTENTIALLY ABSURD notion that the only GOOD Testosterone is indeed a BOUND TESTOSTERONE. Thus Free Testosterone ONLY Being left over production for PRIMARY PROTEIN DELIVERY METHOD which again - Free T I believe is spent in seconds once in blood if not picked up by SHBG or Albumin...

So - be it that I am a complete LOON or Medical Messiah - There you go. You NOW have something to CHEW ON... For fun at least..:drooling::)

Finally, EVEN IF SOMEONE COMES ALONG AND TECHNICALLY DEBUNKS EVERY SINGLE WORD I HAVE SAID. There is no way anyone can say I did not make them THINK in different terms. This is my purpose. This is what I Do. And I ENCOURAGE EACH AND EVERY CORRECTION, CHALLENGE, INTERJECTION...

My most recent labs have low free and high bioavailable as follows:

Total T - 978 (range = 241 - 827 ng/dl)
Free T - 10.89 (range = 12.4 - 40.0 pg/ml)
Bioavailable T - 630.0 (range = 110.0 - 575.0 ng/dl)
SHBG = 26.5 (range 13 - 71 nmol/L)

Does anyone know why I have total and free levels above the reference ranges alongside free levels below reference range? My regimen is injecting 36 mg of testosterone cyp. twice a week and 200 units of HCG twice a week.
 
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