TRT in men with low SHBG

[Wheat Thins]

Ive been messaging back and forth with james about our problems with this for a couple years, and I think I got an email from the site automatically cause Im subscribed to this thread, but Im having what I see as slow but actual progress with an adrenal exhaustion program at drlam.com. I think our low t and low shbg among other health problems, as well as lack of response to TRT programs, is caused by weak adrenals.

Also, I might as well throw this out here, odd as it sounds: did anyone here with low shbg and low t problems masturbate daily or more for a long period of time? I did and Im convinced it destroyed my adrenals and caused these problems, james says he did it too but doesnt really think it caused the problems

 

[coolcat20]

I never did/have

 

[BBC3]

You are LOOKING at the right path IMO.. But ADEX is not the solution. Perhaps you were only speculating a scenario for numbers example...? First, Why would anyone need HIGH TT numbers, or any for that matter. This only tells what is ciculating at a moment, and not what the ACTUAL TRANSFER RATE IS - BOTH IN & OUT... The circulating amounts can be nothing more than a BUFFER LEVEL.... Consider that - WHY would anyone NEED Excess in ciruclation. ALL THAT WOULD TELL ONE IS THAT THERE IS MORE NOT BEING USED!??!?

I dont disagree that there is "organ stain" due to excess exogenous hormone application.... I believe in CLEARANCE for sure. Other systems "balancing/counteracting" - perhaps...

Consider that SHBG is ANOTHER CIRUCLATING SERUM COUNT with no accountable method to observe the transfer rate. So is SHBG low because:
a) The body is not making more - either as a CONTROL OR Physical deficiency. - Maybe..
b) The body is metabolizing is extremely quickly - due to EXCESSIVE HORMONE METABOLISM RATES - possibly the proof that LOW SHBG men are in fact metabolizing excessive amounts of hormones, and (A) above is CONTROLLING AS WELL...
c) We still have not determined how SHBG is MEASURED in SERUM. Is it with a hormone attached, without, OR BOTH. CAN IT BE DIFFENTIATED the SATURATION LEVELS of SHBG. OR how much of it is involved with a hormone at any given moment.??

d) AND FINALLY (and a bit of more new thought). Do other hormones (which ones?) involved themselves with SHBG? Meaning, I think we know that a derivative hormone can go on past the initial receptor site at which it was generated, to AGAIN interact with another receptor. So is SHBG the vehicle of transfer for this action? If so, it would seem that excessive DERIVATIVE activity (E2, etc..) could potentially interfere with availability?

I am just not thinking SHBG is ever a cause (short of liver damage), but moreso a symptom of a condition to which is misunderstood.... That is, I am leaning toward. I am speculating there is not a "Low-T Male" out there without low SHBG.... But consider strickly the definition of the middle aged Low-T Male for that statement.

James, you are aware that I am proposing that Low TT counts has nothing to do with actual metabolism rates, and that Low'T sufferers are experiencing symptoms due strictly to estrogen related metabolism bottlenecking, thus starving Androgen receptors to whatever degree. I also propose that the estrogen interaction at the receptors in the body as a whole is reducing available androgen receptors, and therefore the CAUSE - Excess estrogens having a two-fold reaction. YOUR COMPLAINT, or observation, is that Low SHBG subjects can not achieve high TT surplus in blood serum counts, while I am proposing this is MOOT. THE POINT IS, HAVE YOU CONSIDERED WHAT THE EFFECTS ARE WHEN YOU ARE SUPPING THE SYN-T? So are they Low TT, or Low desired androgen responses, OR ARE THEY EXCESSIVE ESTROGEN RESULTS....?!

I believe that a lot of us with low shbg probably did not need testosterone replacement in the first place. Take my initial bloodwork for example.
Total T of 300
E2 of 74
Ok this seems low for a 21 yr old male, but at that time I did not know my shbg was 9.6. If my dr would have prescribed adex to get the e2 down to a safe level, my total t probably would have went up to 500 or so and with a low shbg that would have been great. I would have a free t as high as most men with a total t over 800. Here is my theory, a lot of us with super low shbg attempt trt at a dosage that is just too high and it puts to much stress on our thyroid and adrenals. I feel that a frequent low dose of testosterone such as eod or e3d along with an AI to monitor e2 levels would be sufficient. If your shbg is low like 12 or less, you do not need a total t level of 800. That would actually be way too high and you would have an overload of free t as well as free estrogens. So maybe we should all quit worrying about having super high total t numbers and shoot for a total t of 400-600, or whatever level would put your free t in the 180-250 range on shippens chart and see if that makes a difference. I personally am trying this and will post my results in the future.

 

[kenseth17cd]

I do believe that if the low shbg itself was resolved, the low testosterone would probably resolve itself and in all actuality due to having such a low shbg as (9.6), I was not defeicient in testosterone at all. I believe that back 5 yrs ago a total t level of 300 or so would be sufficient with such a low shbg level and if a diagnosis of my low shbg was found and cured at that time, total t would rise as well as shbg. So basically I feel we need to find out what causes the low shbg and it will solve our problems. But as of now its really unclear what causes the low shbg. I was insulin resistant, but by diet and exercise I have corrected that problem, however I still have low shbg. So my solution is to attempt frequent low dose trt and try to maintain a total t level that puts my free t in the 180-250 range on shippens chart. By doing this and keeping e2 levels on the lower end of normal, it should reduce the amount of free estrogens in our body. This is the only solution I have at this moment but would love to hear what others suggest.

 

[James23]

I agree with WheatThins on one point -- I used to (try to) masturbate daily when I was a teenager. It wasn't always rewarding. I'd need to wait a day or two in between.

Now, however, if I masturbate and it feels good -- I do so for anywhere from an hour to an hour and a half straight. I only orgasm after getting bored of the rush. This was also the case as a teenager. Since I could only masturbate, at most, once per day, I'd restrain myself to make it last as long as possible. Eventually, 30 minutes escalated to 60, etc. It also may have had something to do with dial-up modems and how long it took to download porn back in the 90's.

Regarding the adrenal exhaustion argument, though, my argument is this:

1. Masturbating daily is not excessive, especially if you are doing so because you have the urge to do so. Healthy boys and men are capable of masturbating multiple times per day. Even OLD men.
2. My adrenals appear to be superhuman, rather than exhausted. My DHEA-S, an andrenal hormone, is always elevated above normal range. With or without medication.
3. Costisol is mid-range to high on every lab. If my adrenals were exhausted, cortisol would be low.
4. According to Dr. Eugene Shippen, it is typical for those with secondary hypogonadism to experience elevated adrenal output. The adrenals attempt to "compensate" for the testosterone deficiency.

Anecdotally, all I know is that men with low SHBG never get their sex drives back even if every other hormone appears to be optimized. It therefore stands to reason that SHBG, being the master transport protien/hormonal regulator and signaling hormone of its own NEEDs to be in balance with the rest of the system.

Low SHBG is genetic. According to one study, 30-60% of SHBG of variation in SHBG level is pre-determined by specific genes. Coinidentally, those of us at the bottom of the scale happen to have approximately half of what we'd need to be within the normal range.

Low SHBG has a causal relationship to insulin resistance. It was once assumed that high insulin resulted in low SHBG due to some sort of inhibition, but later studies have concluded that it is the low SHBG itself that causes muscle tissue to resist glycogen intake. SHBG-R receptors exist on adipose tissue, heart tissue and muscle.

SHBG regulates the passage of testosterone through the blood brain barrier and also into cerebospinal fluid. Consider that one!

I am speculating there is not a "Low-T Male" out there without low SHBG.... But consider strickly the definition of the middle aged Low-T Male for that statement.

There are plenty of those. Most men that have primary hypogonadism also have either high SHBG or normal SHBG. I don't know of any cases of old men having low SHBG for any reason other than insulin resistance.

When FT, T, and E2 change but SHBG does not -- we know it is being suppressed.

 

[James23]

Also, FWIW:

On a completely vegan and low-calorie diet (big mistake) I was able to raise my SHBG to a whopping 19 pg/mL.

This may further prove to some that it is not related to cortisol or other hormones.

 

[James23]

I don't know what this "frequent low-dose" TRT is that people keep talking about with relation to low SHBG.

Using daily Androgel is pretty frequent, is it not? It's also easy to control the dose. That never seems to have worked for anyone. I don't know why T-injections would make any more sense.

 

[James23]

I'll throw this out there one more time:

Lyophilized HUMAN SERUM SEX HORMONE BINDING GLOBULIN SHBG Purified Human Biomarkers Proteins Enzymes Plasma Antigens Suppliers Producers Manufacturers

 

[BBC3]

The only thing here I am going to give is the perplexion I have remaining with high SHBG males who also have TRUE low T symptoms. I speculate they will be younger for the most part. I also speculate it has to do with genetic propensity. Regardless, ciruclating SHBG has yet to be accurately defined here, and with consideration for serum counts related to hormones, it says a whole lot of the same which is nothing. NORMAL in ranges means NORMAL. This means there is not a problem. I feel some scales need lowering on bottom end. There are many different scenarios and combinations of homone profiles that play out in labs and the only way to try to make sense of them is to measure the REAL physical effects. The problem REMAINS that the Real physical effect are often DUE TO INTENTIONAL BEHAVIOR of the part of the subject EVEN when considering the physical manifestations that COULD Present as a medical effect or symptom. IE If the testicals are soft and small, is it the chicken of the egg? Is it a normal resonse or an underlying cause. The only way to see for sure would be to observe a physically prime active candidate who suddenly falls into a condition presenting the issues, with no explanation other than an injury or health problem. Otherwise, we are just observing the logical and natural end road for many that we discuss here. Make NO MISTAKE. These conditions do not manifest overnight in most of us, and we worked hard lying in bed eating twikies for a LONG TIME to get here.

BUT I DO BELIEVE THAT LOW SHBG WILL CORROLATE MORE WITH LOW T MALES and not other causes. I also think it should corrolate more positively with time extended in age, in conjunction with the time spent in a non changing sedentary state.

I agree I think blood sugar and insuling play a role. To what degree I dont even speculate.

But to be clear. I am referring to the mainstream LOW T Male. This is the man they are advertisind to on TV today. This is the middle aged sedentary male who is overweight. This is also the younger males that fall into this catagory due to lack of activity, or too much body fat - and all as a conglomeration resulting related to TIME vs. degrees of these factors.

First the concept of hypogonadism as Primary, or failure of the testicles. IMO does not exist in this group for the most part. Secondary, or brain related, would be moreso the classification, but not due to disease or physical trama in most cases - AS CLAIMED. Really, how many low T men out there are not just a bunch of sedentary fat asses!?!? So I would propose that the LOW T Male is NOT EVEN AN ILLNESS, but a normal response by the body to given stimulus.

REAL cases of primary hypo are probably hard to come by. And how would you qualify that anyway. Its all fantasy if you subscribe to the FACT that serum counts are worthless. And most are indeed the mysterious LowT Males. Further, and with regard to secondary, how do you even qualifiy a TRUE brain malfunction? Short of a pituitary tumor?? Or a condition resulting with symptoms following an illness that can be directly related. So the "Low-T Male" conveniently EXPLAINS the current conditions of men in society today, and thus provides explaination for sympoms with no REAL MEASURABLE Physical trauma. Sure a set of nuts is small, does that discern between and injury to THEM, or a proper shutdown response to conditions? Sure the brain does not appear to be producing a certain level of LH or FSH. but how does this discern between normal reposnse and a brain injury - short of a tumor???!! IT does not!! SIMPLY PUT, The whole world can not have a medical condition of type I or II hypogonadism. But if you took them all to the lab and did bloodwork, there is not a single sedentary male that will document TT levels out of the 3-500 range - T SPECULATIVELY GUARANTEE. Studies are skewed for starters in that the only folks interesting in this kind of testing are somewhat, or have been active, and not complete slobs - else they would not be interested. Yet still, many studies come back with many sufferers...

The world has not racked their nutz in tighties for too long, and our brains are not melting from radiation. Hypogonadism has become an illness that is conveniently serving a bunch of lazy bastards. The TRUTH is that they are low T males, and thus have a condition which is a normal response to extended stimulus.

I agree with WheatThins on one point -- I used to (try to) masturbate daily when I was a teenager. It wasn't always rewarding. I'd need to wait a day or two in between.

Now, however, if I masturbate and it feels good -- I do so for anywhere from an hour to an hour and a half straight. I only orgasm after getting bored of the rush. This was also the case as a teenager. Since I could only masturbate, at most, once per day, I'd restrain myself to make it last as long as possible. Eventually, 30 minutes escalated to 60, etc. It also may have had something to do with dial-up modems and how long it took to download porn back in the 90's.

Regarding the adrenal exhaustion argument, though, my argument is this:

1. Masturbating daily is not excessive, especially if you are doing so because you have the urge to do so. Healthy boys and men are capable of masturbating multiple times per day. Even OLD men.
2. My adrenals appear to be superhuman, rather than exhausted. My DHEA-S, an andrenal hormone, is always elevated above normal range. With or without medication.
3. Costisol is mid-range to high on every lab. If my adrenals were exhausted, cortisol would be low.
4. According to Dr. Eugene Shippen, it is typical for those with secondary hypogonadism to experience elevated adrenal output. The adrenals attempt to "compensate" for the testosterone deficiency.

Anecdotally, all I know is that men with low SHBG never get their sex drives back even if every other hormone appears to be optimized. It therefore stands to reason that SHBG, being the master transport protien/hormonal regulator and signaling hormone of its own NEEDs to be in balance with the rest of the system.

Low SHBG is genetic. According to one study, 30-60% of SHBG of variation in SHBG level is pre-determined by specific genes. Coinidentally, those of us at the bottom of the scale happen to have approximately half of what we'd need to be within the normal range.

Low SHBG has a causal relationship to insulin resistance. It was once assumed that high insulin resulted in low SHBG due to some sort of inhibition, but later studies have concluded that it is the low SHBG itself that causes muscle tissue to resist glycogen intake. SHBG-R receptors exist on adipose tissue, heart tissue and muscle.

SHBG regulates the passage of testosterone through the blood brain barrier and also into cerebospinal fluid. Consider that one!



There are plenty of those. Most men that have primary hypogonadism also have either high SHBG or normal SHBG. I don't know of any cases of old men having low SHBG for any reason other than insulin resistance.

When FT, T, and E2 change but SHBG does not -- we know it is being suppressed.

 

[seahawk888]

My total test is 525, My free test is 83.1. I have shrunken testicles do to excessive steroid use and now I suffer from ed even after 3 months of 1000 iu's of hcg and an additional 2 months with clomid and taximofed.I still have shrunken testicles and Ed. How can I have Hypogonadism if my t levels are in range? Are my adrenals low? Would secondary Hypogonadism and low adrenals make any sense? Through your experience what is your observation?

The only thing here I am going to give is the perplexion I have remaining with high SHBG males who also have TRUE low T symptoms. I speculate they will be younger for the most part. I also speculate it has to do with genetic propensity. Regardless, ciruclating SHBG has yet to be accurately defined here, and with consideration for serum counts related to hormones, it says a whole lot of the same which is nothing. NORMAL in ranges means NORMAL. This means there is not a problem. I feel some scales need lowering on bottom end. There are many different scenarios and combinations of homone profiles that play out in labs and the only way to try to make sense of them is to measure the REAL physical effects. The problem REMAINS that the Real physical effect are often DUE TO INTENTIONAL BEHAVIOR of the part of the subject EVEN when considering the physical manifestations that COULD Present as a medical effect or symptom. IE If the testicals are soft and small, is it the chicken of the egg? Is it a normal resonse or an underlying cause. The only way to see for sure would be to observe a physically prime active candidate who suddenly falls into a condition presenting the issues, with no explanation other than an injury or health problem. Otherwise, we are just observing the logical and natural end road for many that we discuss here. Make NO MISTAKE. These conditions do not manifest overnight in most of us, and we worked hard lying in bed eating twikies for a LONG TIME to get here.

BUT I DO BELIEVE THAT LOW SHBG WILL CORROLATE MORE WITH LOW T MALES and not other causes. I also think it should corrolate more positively with time extended in age, in conjunction with the time spent in a non changing sedentary state.

I agree I think blood sugar and insuling play a role. To what degree I dont even speculate.

But to be clear. I am referring to the mainstream LOW T Male. This is the man they are advertisind to on TV today. This is the middle aged sedentary male who is overweight. This is also the younger males that fall into this catagory due to lack of activity, or too much body fat - and all as a conglomeration resulting related to TIME vs. degrees of these factors.

First the concept of hypogonadism as Primary, or failure of the testicles. IMO does not exist in this group for the most part. Secondary, or brain related, would be moreso the classification, but not due to disease or physical trama in most cases - AS CLAIMED. Really, how many low T men out there are not just a bunch of sedentary fat asses!?!? So I would propose that the LOW T Male is NOT EVEN AN ILLNESS, but a normal response by the body to given stimulus.

REAL cases of primary hypo are probably hard to come by. And how would you qualify that anyway. Its all fantasy if you subscribe to the FACT that serum counts are worthless. And most are indeed the mysterious LowT Males. Further, and with regard to secondary, how do you even qualifiy a TRUE brain malfunction? Short of a pituitary tumor?? Or a condition resulting with symptoms following an illness that can be directly related. So the "Low-T Male" conveniently EXPLAINS the current conditions of men in society today, and thus provides explaination for sympoms with no REAL MEASURABLE Physical trauma. Sure a set of nuts is small, does that discern between and injury to THEM, or a proper shutdown response to conditions? Sure the brain does not appear to be producing a certain level of LH or FSH. but how does this discern between normal reposnse and a brain injury - short of a tumor???!! IT does not!! SIMPLY PUT, The whole world can not have a medical condition of type I or II hypogonadism. But if you took them all to the lab and did bloodwork, there is not a single sedentary male that will document TT levels out of the 3-500 range - T SPECULATIVELY GUARANTEE. Studies are skewed for starters in that the only folks interesting in this kind of testing are somewhat, or have been active, and not complete slobs - else they would not be interested. Yet still, many studies come back with many sufferers...

The world has not racked their nutz in tighties for too long, and our brains are not melting from radiation. Hypogonadism has become an illness that is conveniently serving a bunch of lazy bastards. The TRUTH is that they are low T males, and thus have a condition which is a normal response to extended stimulus.

 

[hardasnails1973]

My total test is 525, My free test is 83.1. I have shrunken testicles do to excessive steroid use and now I suffer from ed even after 3 months of 1000 iu's of hcg and an additional 2 months with clomid and taximofed.I still have shrunken testicles and Ed. How can I have Hypogonadism if my t levels are in range? Are my adrenals low? Would secondary Hypogonadism and low adrenals make any sense? Through your experience what is your observation?

Clomid can push up SHBG resulting in drop of free T levels. Free T levels are not an accurate reading. One needs to look at the SHBG. If shbg is 35-40 then TT 525 may not be enough. Again then you need to examine the estrogen levels as well.

YOu did way too much LH stmulation it caused a down regulation possible resulting in low T of 250-350

 

[coolcat20]

Hope and pray that the low SHBG stems from elevated cortisol, elevated insulin or subclinical hypothyroidism.

Otherwise, the only way to treat low SHBG is to replace or stimulate SHBG production. SHBG is available in research form, but not as an approved medication (at least not in the USA.)

Caffeine (350mg/day+), estrogens, and T3 induced hyperthyroidism have been shown in studies to increase SHBG where it is deficient.

Maybe it is a Cortisol problem and maybe that could be why i urinate so much and struggle to sleep (cant relax)

These tests were at 9 am but i hadnt slept and had woke up at 5pm the day before... so it was basically my night time.

TSH 6.9 Miu/L (.020-6.00)

Free T4 15.9 Pmol/L (10.0-25.0)

SHBG: 16 (13-71)

Prolaction 257 (0-550)

Oestradiol (extractn) 132 pmol/L (<150)

Testosterone 8.9 nmol/L (8.0-30)


Cortisol 246 nmol/L (Random cortisol is dependent on time of sample: 0900h cortisol 150 - 600 nmol/L 2400h (midnight) cortisol <50 nmol/L)

Cortisol after short synacthen test: 495 nmol/L


Now i asked the endo if it mattered how id slept or if i did at all before i got my cortisol checked and he said no, but in the brackets next to my reading it states "Random cortisol is dependent on time of sample" does that mean my Cortisol level of 246 should really be compared within the midnight range? so under 50 - witch it isnt.

 

[BBC3]

To be clear, I am no formal expert. I am only taking "guesses" based on information I get, and trying to provide some new context of thought.

The only thing I can tell you for sure, is that hormone serum counts, or any serum count for that matter is NOTHING MORE than a snapshot of whats in the blood at the moment. And I DO mean moment with regard to testosterone. All the serum count tells you is basically what the current amount in the blood is. I have a feeling this is first genetic, then age and condition impacted. The serum count gives NO DIRECT indication of the processing rate of these hormones, or how fast one is metabolizing them. So you have to consider 2 sides to the story. The production end, and the elimination end. I have only begun to give the elimination side consideration, and I think it deserves great overlooked merit. Consider if hormones travel on protiens in the blood, how are you going to turnover new ones, if the old ones are still present.?!?! There is also the concept of the lifespan of various hormone derivatives (estrogen from FT, androgens from Free T etc...). WHich appears to be a mystery all together.

I am beginning to have the notion that estrogen is the Primary cause of "LowT" symptoms in men. Perhaps we are not Low T at all. Perhaps we are really all HIGH E!?!? WHat if E is remaining in the blood or at the receptors with a much longer lifespan than Androgens? Perhpas a generated E molecule can go on to involved with different receptors over and over till certain conditions are met?!? Why would the testicles need to make any more TT.? How many times can an E molecule go on to interact (interfere/compete) with receptors that may otherwise produce androgens? How much albumin and SHBG (blood transport proteins) are they "hogging" So consider that Male Low T symptoms (1) may not be caused by a TT deficiency, (2) may not even be caused by excess E activity creating an E based reverse feedback type shutdown, but (3) may just be flat out interfering the TT metabolism by their sheer presence, both dominating blood volume and competing at the receptors which may otherwise generate androgens. The indication is that there has been no physical trauma to the testicles or brain, so what else could it be. Whats worse is that receptors are occupied, just by the wrong hormones. SO why would the body need to make anymore? The real question now would be; do estrogens have a longer lifespan, or is it just an over abundance by estrogen generating factors? But for guys not that overweight, this hypothesis would tend to indicate estrogens do have a longer life, and perhaps just an accumulation of controlling dominance over time. Its an incideous concept that elludes to a loosing game corrolating with time and abundance of estrogen activity.


I dont think there even is a condition of secondary or primary hypgonaism that really exists, short of a Failure/malfunction due to illness or physical trauma. What it really seems to be is a normal reponse to conditions. You cant really say whats going on with you without a whole lot of date and time collecting it. Consider this, you could have a T levels you cited whether you were "burning" 1 mg/day of TT, or 10mgs/day. I do think that the higher the number there is an exponentially higher TRUE RATE OF METABOLISM. But if you truely have shrunken testicles, this may prove false. Then again, there is just a simple genetic predisposition of what you blood will carry in RESERVE. The one clarity this rabble run I have been on here seems to elude is, WHY IS IT THAT GUYS IN SHAPE tend to have higher TT levels? This may also indicate estrogens have a much longer lifespan active in the body. They are essential yet Men just dont need that much I would think. THerefore they may be fundamentally protected due to both their IMPORTANCE and their HISTORICAL Lack of generating factors. AND whilst we are living in a FAT ROMAN WORLD which no longer requires this mechanism..... Through most of history MAN has been hunting to survive and lean, not sitting on the couch eating twinkies. How many generations do we evolve in a century? Right. HOW many does a snake!! And you can go get one from the pet store tomorrow, throw him in a field, AND HE WILL HUNT!!!! Our estrogens are now SHOOTING DUCKS......

If I were you. I personally think HCG is an awful idea for our purposes. Its estrogenic, and even only really intended as a PHYSICAL SHOCK TREATMENT post testosterone cessation at best. You have not given yourself a fair shot. I would suggest iNTERMITTENT 2 week runs of tamox every 2 months while training and weight loss. Thus you would techically be blocking the estrogen activity, while generating androgen activity, with no extended agonistic effects from the SERM. I would further even speculate alternating between clomid and tamox for every two months when you run that 2 weeks in order to switch up the agonistic effects possible. The fact that Low T symptoms are EVENTUALLY occurring in guys that are not all that fat, would also indicaite there may even be a LEARNING or cumulative receptor affinity with TIME. This is irreparable without tissue change. Tissue change has got to be slow. While I state that the human body is a DEMAND BASED ENVIROMENT, I am not totally disclaiming that abundace by excess supply does not encourage development. It has to. Unless you are/were shredded, you must have had plenty of T on hand for estrogen development if there is anything at all to propensity for development simply by availability is abundance of hormones... Also, A lot of time passes in a typical mid twenties or early thirties steroid user's run. Comming out we would not be the same regardless. We are older. So good luck. And keep in mind I KNOW NOTHING. So I am not diagnosing or prescribing by any means. Just some though to feed on...

FInally I am speculating that all hormonal stimulation from serms is derived at the action at the receptor, rather than some magical direct effect on the brain as many have cited for years. With the increased hormone counts primarily from the blockade action, and not so much from stimulation of production AT ANY RATE. The positive comes from the androgen activity now allowed at sites which had otherwise been controlled by excess estogens. But its about PRESENCE. When you take it away, stasis will return to whatever conditions are if not changed. There is no stimulation, only temporary relief, and at what cost? Its about what we are is what we eat. OR DO.

The scariest part of all, is that once you realize that SERUM COUNTS can tell us nothing, unless measured in short (5 min) intervals, or long (6 month) intervals; THEN WHAT THE FUCK IS MEDICAL SCIENCE FOUNDING ALL THEIR CANCER RESEARCH ON? And how are they measuring the results. Consider the action of an AI may even lower estrogen SERUM COUNTS from 150 to 20, WHEN ALL ALONG THE SAME AMOUNT COULD BE TRANSFERRED/METABOLISED AT THE RECEPTORS THE WHOLE TIME.!!!! Now thats messed up. Medical does know the reality, but I ganders they have been "experimenting" for the past 2 decades. But what else is there? CUT REMOVE DESTROY? Dont get sick. There is no CURE. Only Mitigation. Choose you poison wisely NOW, or be forced to choose it later...

My total test is 525, My free test is 83.1. I have shrunken testicles do to excessive steroid use and now I suffer from ed even after 3 months of 1000 iu's of hcg and an additional 2 months with clomid and taximofed.I still have shrunken testicles and Ed. How can I have Hypogonadism if my t levels are in range? Are my adrenals low? Would secondary Hypogonadism and low adrenals make any sense? Through your experience what is your observation?

 

[James23]

chris_az,

Have you made any progress with your low SHBG and high E2 issue? It has been 9 years.

 

[Yankee232]

Very old thread, but I'm going to bump it as I've found others like me.

Low SHBG male here as well, usually runs 12-13. Test never above 270 even on Androgel. My libido isn't awful, and I still maintain decent erections without Androgel. My liver seems fine, had tons of TSH and T4 tests done for thyroid and all look good.

Anyone made any progress on the SHBG front?

 

[InfoFront]

For the most part, you can only raise your SHBG if you have significant insulin resistance, and correct it. The rest of us just have to deal with it. EOD subQ injections are the closest thing we have to a standard treatment.

 

[Tyler81]

I don't know what this "frequent low-dose" TRT is that people keep talking about with relation to low SHBG.

Using daily Androgel is pretty frequent, is it not? It's also easy to control the dose. That never seems to have worked for anyone. I don't know why T-injections would make any more sense.

Actually Testim/Androgel is the ONLY form of TRT that worked for me decently well. And I have low SHBG (13).

 

[James23]

Actually Testim/Androgel is the ONLY form of TRT that worked for me decently well. And I have low SHBG (13).

What I meant here is that people continually espouse low dose injectable therapy for low SHBG. Meanwhile, topical DAILY administration is theoretically the best. Even better than Androgel would be Striant, or any of the drugs that are applied TWICE DAILY. If you check out some my other posts, you'll see that I mention Androgel to be the best candidate. However, it did not work for me. Androgel was my very first therapy when I was 21.

 

[Tyler81]

I tried Striant it did not work well for me. The levels spike too high and they arent smooth like the transdermals. I've tried literally every form of TRT: Androderm patch, Testim, Androgel, Test eth, Test cyp, Striant, Testopel pellets, Test prop.

Of those therapies the best was TWICE daily dosing of the transdermals like you say;
5gram gel (am, pm) at the same time everyday.

When the gels absorbed for me that regime kept my levels stable and i felt decent.

 

[James23]

I tried Striant it did not work well for me. The levels spike too high and they arent smooth like the transdermals. I've tried literally every form of TRT: Androderm patch, Testim, Androgel, Test eth, Test cyp, Striant, Testopel pellets, Test prop.

Of those therapies the best was TWICE daily dosing of the transdermals like you say;
5gram gel (am, pm) at the same time everyday.

When the gels absorbed for me that regime kept my levels stable and i felt decent.

Have you noticed any DHT spikes within lab results with this method?

My primary concern with topicals is MPB due to a higher 5-AR concentration in the skin. If it weren't for this detail, I would stick with transdermal administration.