Sex Hormone Binding Globulin [SHBG]

[BBC3]

I STILL don't see the value in the discussion, WHEN YOU DON'T KNOW THE RATE OF HORMONE METABOLISM...!!!!!!

And the ONLY WAY to KNOW the RATE of T Metabolism as PRODUCTION VALUES - Is to place a SPIGOT at the top of the testicle.!!!

So here I go - BUT WITH MORE FOCUS..:

Pertaining to SHBG as well as TESTOSTERONE or ANY OTHER Hormone it carries for that matter, you must KNOW (3) Things...:

(1) Production Rates (of WHAT and FROM WHERE)
(2) Usage Rates (time involved with receptor) & Conversion Rates (Back & forth Hormone changes)
(3) Elimination Rates/Clearance (Liver, Kidneys, & Enzymes)

*** These are Minimal and LAST I HEARD you can't Document ANY of this in action.

1. Lets see who can tell me whether SHBG is Calculated based on as "Free" or UNINVOLVED, or is the count just however SHBG they can see no matter what state?

2. Please list for me exactly WHICH Hormones SHBG involves with, and HOW this VARIES from the hormones which Albumin involves with?

3. Who can explain the calculation method for SHBG in blood serum?

Somebody teach me something....

 

[BBC3]

Thats good stuff, but I will have to get back to you here with an attempt at laymonizing or debunking...

Since the SHBG androgen sites are essentially SATURATED once endogenous TT reached 500 ng/dl, someone's SHBG value have LITTLE or NO INFLUENCE on exogenous AAS levels while cycling.

So could/should a mates SHBG LEVEL alter the response to cycling?
(such as warrant a change in dosing)

NO!!

Why? Because SHBG is essentially "SATURATED" while cycling.

So the "extra AAS" has only THREE possible destinations once released from the parenteral DEPOT.

Included are:

1) intercellular/extracellular binding
2) free "floating" within serum
3) bound to ALBUMIN

Because at TT levels of even 1000 ng/dl LESS THAN 1% of albumin sites are "occupied" the majority of that cycled anabolic will become BOUND TO ALBUMIN, (albumin can NOT saturate it's sites regardless of the "AAS level")

 

[BBC3]

I was tossing out a epitome of Conundrum so to speak, as that even the POINT you speak of is genetic INCLINATION. Short of DISEASE which is rare in this case. That IS an interesting observation. But I will also point out I have seen plenty of fat guys that are pretty chilled with weak beards too..

Hair Growth also has something to do with metabolism, people with hyperthyroidism almost never grow much if any facial hair. Of course, TSH increases SHBG as well so there might because of that over active metabolism be less DHT. And an overproduction of adrenaline/histamine would lower DHT.

 

[BBC3]

I think estrogen doubling is more likely to cause mental illness. Or at least hormone imbalance high to the estrogen side at a minimum. Me thinks medical science will soon see estrogen as BOTH the beginning as well as the END of healTHY LIFE...

While Jim is often full of Shitz-N-Giggles. I think he is fair game and bringing forth some good venue. YOU have admitted to running 5 miles per day and keeping your diet and non-existant at the same time. YOU are an anomaly in BEHAVIOR as less than 0.1% of general population given your demographic status... There is only so far you can push things before something goes wrong. I HAPPEN TO PREFER THE SIDE OF INDULGENCE.. .. We are BOTH aware of this risk. We are BOTH in denial of the POSSIBILITY of OCCURRENCE...! I just so happen to stick with the MAJORITY in my behavior... At least in some aspects. There are "minimum requirements" on the PLANET I HALE FROM..

A psychiatric illness would not cause his estrogen to double.

It stands to reason that a man who does not respond subjectively to ham-handed, single hormone replacement likely has a more complicated hormonal issue verus a thinking problem.

Either way, if you really want to "chase a ghost" then chasing "brain fog" will have you spinning in more circles than hormones ever will. The brain is a black box, and anti-depressant medications are all shots in the dark.

Bottom line: This isn't a mental health board. This is a progressive hormone related board and the OP wants his hormones discussed. So, piss off, Dr. Offtopic. Nobody in this thread appreciates your continual trolling, insults and derailing of the conversation.

Can't you handle leaving us alone?

 

[BBC3]

Re: LEF's Take on Low SHBG

Thats some good input. I find it interesting as it FEELS like "educated" anecdotal observation (which YOU KNOW I LOVE), but more importantly, from someone with some BB experience as it relates. I also find your use of the word "CRUSH" interesting...

I just don't even begin to understand how SHBG can get near "ZERO", but then again, I don't understand how a VERY SMALL percentage of Pro BB's can amass and retain that much muscle either...

Less SHBG = stronger motivation/nervous system, higher libido, more brain effects of testosterone, and more lean/dry muscle growth as long as estrogen is in proper ratio. Hence why Proviron is used - to crush SHBG.

Most pro'BB's crush SHBG to zero = Dry vascular look, improves composition/solidity

 

[corageon]

I was tossing out a epitome of Conundrum so to speak, as that even the POINT you speak of is genetic INCLINATION. Short of DISEASE which is rare in this case. That IS an interesting observation. But I will also point out I have seen plenty of fat guys that are pretty chilled with weak beards too..

Good point, I have as well; seen some fat lards with kitty whiskers growing outta their chin.. and above their lip.
There is some genetic inclination definitely, but many people maintain that what we eat "changes our genetics", and what I have to say to that is - Yes to some degree, but even a 40% "change" to our genetic coding or so called mRNA's, does not come easily after hundreds of years of the same diet/physical/cultural habits.

 

[James23]

From "Sex Hormone Binding Globulin and the Assessment of Androgen Status":

Hormone carriers exist predominantly in the unbound form, providing a large excess of unfilled steroid binding sites. Over 80% of the SHBG population is unbound in females and over 40% is unbound in males. The other principle testosterone and estrogen carrier, albumin, circulates unbound 99% of the time.[6] Changes in the total hormone concentration produce relatively minor changes in the size of the free fraction because excess carrier protein binding sites modulate extreme variations in hormone concentrations.


In other words, in healthy males, SHBG exceeds the level of SHBG bound testosterone by a ratio of approximately 3:2. This allows the SHBG to buffer extreme variations in hormone concentrations, a buffer that is not maintained in men who are SHBG deficient.

 

[Dr JIM]

Well James since this is your first citation I will overlook the fact you failed to post ENTIRE REFERENCE (Authors, Journal, Volume, Series AND page numbers) including their CONCLUSION rather than yours) You see clown that's THE customary practice. Hey if unsure check out one of the studies DOCs cites.

Now lets look at what is known clown!
1) Although both SHBG and ALBUMIN bind roughly 50% of male androgens the amount either one binds is proportional to the androgen level itself to a point.

2) Consequently once TT levels approximate somewhere between 500-800 SHBG is saturated at a max of EIGHTY PERCENT (100% is NOT possible because of ligand interference)

3) Once the TT level exceeds the SHBG threshold any additional TT WILL be bound to ALBUMIN

4) James if you half a brain you would KNOW the reasons the "percent SHBG saturation" mentioned exceeds that of albumin! It's because SHBG binds androgen much more tightly AND the QUANTITY of ALBUMIN GREATLY EXCEEDS SHBG.

5) Finally FOOL the buffering which occurs at the interstitial/capillary level is the function of ALBUMIN and NOT SHBG because SHBG binds androgen so tightly it does not even begin to off load androgen until the TT is MAINTAINED at a threshold level LOWER than 300ng/dl. Moreover a lowering of SHBG is UNEQUIVOCALLY associated with INCREASED FREE TT LEVELS!

6) So what if SHBG is low! There is no disease process associated with this endpoint (unlike a HIGH SHBG) because ALBUMIN serves the same function.
OR DID YOU OVERLOOK YOUR ARTICLES STATEMENT WHICH I MOST CERTAINLY AGREE WITH:

"Changes in total hormone concentrations produce relatively MINOR changes in FREE TESTOSTERONE because CARRIER PROTEINS (that's plural James) modulate extreme variations in hormonal concentrations".

So James as a research scientist yourself how does it feel to bastardize the conclusion of colleagues, because I KNOW YOUR CONCLUSION DOESN'T EVEN APPROXIMATE THEIRS! FOOL!!!

 

[James23]

1.) The article says that 40% of SHBG, alone, is unbound in healthy males.

2.) If SHBG levels meant "nothing," then why would they fluctuate at all?

3.) Inadequate SHBG for a given level of testosterone, especially exogenous testosterone, typically leads to excessive free testosterone and aromatization, as seen in women with PCOS.

4.) Strong binding is only possible with SHBG. Albumin weakly binds testosterone and cannot adequately substitute for a low level of SHBG.

5.) Your conclusion is patently inane, as it posits that SHBG is worthless to the body and only significant when in excessive quantity but meaningless when insufficient in quantity. This is a gross misunderstanding of the complete role of the protein, and you may be wise to read the paper posted by Dr. Scally a few posts back that challenges the "free hormone hypothesis" that you learned about a few decades ago, Dr. Dinosaur.

 

[Dr JIM]

1) So what 40% of circulating SHBG is bound vs unbound what difference does that make? (The % binding depends upon the TT level, but Iv'e already mentioned that IN MY LAST POST!!!)

2) UNDERLINE my post where I said SHBG levels meant nothing?

3) Absolute GARBAGE James, HOW and WHY you concoct such nonsense without supportive data is beyond reason. I'll ask you for the third time "do you have even a vague understanding of aromatase kinetics", NOT!

4) Strong binding is a function of SHBG, really are you my parrot, lol!

Albumin is an adequate surrogate carrier for "low SHBG" because that's exactly what happens when SHBG is low otherwise FTT levels would reach astronomical levels which does NOT occur. In fact a TT value above 4% has not been reported in the literature TO DATE.

In fact ALL OF THIS "LOW SHBG" CRAP YOU SPEW HAS NOT BEEN DOCUMENTED TO CAUSE THE AILMENTS YOU DESCRIBE THROUGHOUT THIS GARBAGE FILLED "LOW SHBG" thread. The thread you initiated may I add.

5) Finally YOUR conclusion is baseless James and most certainly is not based on medical science, OR the citation YOU HAVE POSTED AS EVIDENCE!

Lastly why is it you fail to cite the entire reference including the: COMPLETE ABSTRACT, AUTHORS, JOURNAL YEAR, VOLUME and SERIES all of which is customary practice? PUT UP OR SHUT UP CLOWN [)]
(But then again ANYONE who has been following your drivel on LOW SHBG KNOWS the latter WON'T HAPPEN)

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[James23]

It's not my job to be your tutor. I can't waste my time bringing you up to speed with modern endocrinology. If you don't know what we're talking about, then please leave the discussion. You are nothing but a troll.

From the same paper:

Decreased SHBG, concomitant with normal to just slightly elevated total testosterone, results in greater peripheral androgen activity, as seen in disorders such as hirsutism, severe acne, virilism, and features of polycystic ovarian disease.5,8 Management of these diseases often involves either suppressing
androgen synthesis or stimulating SHBG synthesis via estrogen supplements.

Assorted sources:

"Decreased SHBG levels lower total testosterone levels because unbound testosterone is more subject to degradation or conversion into estrogen by aromatase enzymes, which are found in many tissues but particularly in bodyfat."

"The research on mice and human cell cultures shows we should replace simple sugars (like table sugar, glucose and fructose) with complex ones, like starches, found in grains, fruits, legumes (peas and beans), and other vegetables, if we want to keep the fires going in bed.

That’s because when the simple sugars go to the liver to be metabolized, the excess is stored as fats. All that work for cells synthesizing fats, deactivates the SHBG (sex hormone binding globulin) gene, plummeting the levels of SHBG protein in the bloodstream."

 

[Dr JIM]

Reference data for you article James!!!!!!

Now wait are you saying you don't have them because youve been plagiarizing some blog opinion? Yep!

Are u saying (but not saying) you didn't ask for this info James before posting someone else's conclusion on Meso as evidence, yep!


Ya see I take umbrage for DOC including his post (on hormonal binding proteins and their functions as intracellular messengers) on the same line, as your garbage.

Why well for a variety of reasons really, but suffice it to say when DOC posts an article he includes that reference information needed for those WHO WANT TO KNOW the scientific facts, unlike you who want credit form some stupid theory they have concocted regardless of credibility, reproducible evidence, patient encounters, DIRECT medical exposure etc.

Nope DOC also included that data to ensure those "dinasours" like me and those wanna be neophytes like yourself remain on a level playing field the only thing required by both parties is a little effort. SO James using the references DOC cited did you even bother to read and review the entire article readily available on Medline.

I mean shit James since your best effort is to use blog posts as references and sources,all on Meso who KNOW YOU also understand the answer to that question is a resounding NOT!!

Well rest assured DOCs article, once again, failed to MENTION or correlate your infamous "low SHBG" junk theory being associated with TRT unresponsiveness.

Lastly posting assorted BLOG sources as evidence to support your garbage is about as foolish and idiotic as the "CONCLUSION" you reached from the "article"
posted using a "TRT or LOW T BLOG!

GARBAGE IN GARBAGE OUT!
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[hardrlz]

Even though the low SHBG is not recognized officially as a TRT non responsiveness cause, and even if it is not one, i dont think its wrong that we are trying to figure out what the main cause is. James is providing useful contribution to this problem and i dont see anything wrong in trying to find a cure by sharing information with others in the same situation. Its not like he is trying to sell a drug or proposing a dangerous practice for curing ourselves. So Dr Jim instead of mocking and denouncing everything try to look from our point of view and see that we are just trying to find out what is wrong with us, not because we believe all doctors are unknowledgeable, but the fact that most of them havent been able to help us so far.

 

[Michael Scally MD]

Svartberg J, Schirmer H, Wilsgaard T, et al. Single-nucleotide polymorphism, rs1799941 in the sex hormone-binding globulin (SHBG) gene, related to both serum testosterone and SHBG levels and the risk of myocardial infarction, type 2 diabetes, cancer and mortality in men: the Tromso Study. Andrology. http://onlinelibrary.wiley.com/doi/10.1111/j.2047-2927.2013.00174.x/abstract

Low testosterone levels are associated with metabolic and cardiovascular disease risk factor, and have been shown to predict type 2 diabetes mellitus (T2DM), myocardial infarction (MI) and all-cause mortality. It is not known if these associations are causal or not. Recently, it has been shown that the serum testosterone levels are associated with single-nucleotide polymorphisms (SNPs), and we therefore studied the associations between one of these SNPs, rs1799941 on the sex hormone-binding globulin (SHBG) gene, and MI, T2DM, cancer and death.

DNA was prepared from men who participated in the fourth survey of the Tromso Study in 1994-1995 and who were registered with the endpoints MI, T2DM, cancer or death and a randomly selected control group. For mortality, the observation time was set from 1994, and for the other endpoints from birth. The endpoint data were completed up to 2010-2013. Genetic analyses were successfully performed in 5309 men, of whom 1454 were registered with MI, 638 with T2DM, 1534 with cancer and in 2226 who had died.

Men with the minor homozygote genotype had significantly higher levels of total testosterone (14.7%) and SHBG (24.7%) compared with men with the major homozygote genotype, whereas free testosterone levels did not differ significantly between the genotypes. The SNP rs1799941 was not significantly associated with MI, T2DM, cancer or mortality.

Thus, our result does not support a causal relationship between total testosterone and SHBG and MI, T2DM, cancer or mortality, suggesting that low testosterone more likely is a marker of poor health.

 

[Dr JIM]

Dadgum DOC where do you come up with this stuff?

(Journal of Andrology, right I know, lol)

Nice post
THX

 

[hardrlz]

James in this thread https://thinksteroids.com/community/threads/134294681 you were discussing the male PCOS version and insulin resistance. Have you been keeping up with managing insulin resistance and how did that work out for u ?

 

[James23]

James in this thread https://thinksteroids.com/community/threads/134294681 you were discussing the male PCOS version and insulin resistance. Have you been keeping up with managing insulin resistance and how did that work out for u ?

I do have insulin issues, and females in my family have a history of PCOS. (My mother and half-sister.) I have been diagnosed with reactive hypoglycemia (RHG.) This is typically due to an excess of insulin that removes too much sugar from the blood. This has been confirmed by a three hour oral glucose tolerance test. (I recommend that everyone with low SHBG have this test done to rule out insulin resistance. Low SHBG is marker for IR.)

According to the OGTT, however, my insulin is classicly low, and even this low amount of insulin takes my blood sugar down the the 50s. Therefore, I am considered overly insulin sensitive rather than insulin resistant. This is yet another area in which modern endocrinology seems to have no answer regarding treatment or management.

 

[James23]

Anybody with low SHBG also have body odor issues?

A few men, myself included, get zero-to-no body odor that directly correlates with the periods of impotence. Normal masculine musk reverts to a pre-pubescent lack of odor, no matter how much sweat is produced or how long it is left to stay.

Since apocrine (fatty) sweat is directly mediated by androgen receptor activity, it seems that this would be a fair indicator of overall androgenic signaling.

 

[hardrlz]

I dont have odor issues, but i have sweating issues. I am sweating too much under the armpit and i have constant stains especially when i am wearing shirts. James i wanted to ask you one more question as well , you said that you have tried eating anti inflammatory or vegan diet i dont remember correctly and that rose you SHBG to 19. Did you try TRT with that level , because 19 seems like a good number. I am asking because currently i am following an anti inflammatory diet and i have been on it for about 2 months, so next week i will test my SHBG and testosterone to see how they are influenced.

 

[BBC3]

OR - Could POSSIBLY all that in those last two posts have ANYTHING possibly to do with the fact that you go psycho on road runs daily for 5 miles at a time and EAT little to nothing.. Just sayin...

I hereby DEMAND and FORMALLY ORDER YOU to take and publish a pic of your legs from the lower thighs down.. I got even money says your knee caps may be the same diameter or larger EVEN than you quad mad area diameter. Prove me wrong. Prove it.. Prove it....

Anybody with low SHBG also have body odor issues?

A few men, myself included, get zero-to-no body odor that directly correlates with the periods of impotence. Normal masculine musk reverts to a pre-pubescent lack of odor, no matter how much sweat is produced or how long it is left to stay.

Since apocrine (fatty) sweat is directly mediated by androgen receptor activity, it seems that this would be a fair indicator of overall androgenic signaling.