Should We Be Managing Estradiol and Hematocrit in Men on Testosterone Replacement?

[J. Keith Nichols MD]

What would you say is an E2? The reason I ask this is because, and please don't take this the wrong way, many doctors have a bias. If your patient says doc I have itchy nips or I am bloated or cry at the drop of a hat. Do you say - oh no that is not from E2?

I tend to agree with the part regarding reasonable e2 control. I've personally seen my lipid panels respond favorably to controlled e2 in range and unfavorably to low e2.

I believe the Dr. is saying that at 1500-2000 TT his patients aren't seeing high e2. That would be because of the 12 hour half life of the cream. More of it is converting to dht compared to longer half life injectables. Also that 1500-2000 TT is 5 hours after application. That doesn't really compare to 1500 TT on test cypiomate imo. I'd imagine on the cream you are well down to physiological levels once you go to sleep. This is just what I've gathered. Someone correct me if I'm wrong.

Your answer is #40

 

[johndoesmith]

I have not seen what you are referring to in hundreds and hundreds of patients. With the method of delivery I have outlined I have NEVER had E2 levels that of "Premenstal women". I have not to date had to prescribe AIs for E2 excess. You have been programed inappropriately to worry and focus on your E2 levels. An expert doesn't titrate to labs, he titrates and adjust to symptoms. I have never myself or in ANY of my patients experienced "massive side effects". Focus on optimizing your free T, free T3, DHEA, Vit D3, appropriate diet, exercise, and supplements, and don't block your E2. The reason this is so foreign to you is it is just not how you have read it should be done on various websites and forums that continue to propagate false information.

Respectfully, I don't feel that you've actually read most of my post. I have never taken an AI, and like I said before, I suffered LOW E2 myself. I do not experience effects of high E2(Dr. Saya can confirm, I am a patient of his) nor do I "block" my E2.

I also remember you said you don't even test E2, so how can you confirm you've never seen this in your patients?

I really feel as though you are picking parts of my post to essentially tear me down as a scapegoat for overzealous use of AI in the industry. You seem to have missed(or I didn't make it clear enough) that I said an expert titrates based on symptoms and labs.

I am not propagating false information, and many here can elaborate on their >70 E2 levels and symptoms(vince carter??).

I am not intending to incite an argument, I just simply asked some questions, and seemingly upset you. Still not sure what you mean by "blocking" E2 btw, generally an aromatase inhibitor is used, which does not block estrogen, but rather its production.

Again, I have never used an AI and I suffered from low E2. Not sure why you insinuate I have.

 

[J. Keith Nichols MD]

What would you say is an E2? The reason I ask this is because, and please don't take this the wrong way, many doctors have a bias. If your patient says doc I have itchy nips or I am bloated or cry at the drop of a hat. Do you say - oh no that is not from E2?

This thread is very informative. Love hearing feedback from different doctors. Dr. Nichols is there a cutoff that you feel is too high of a dose or free t levels that are too high or do you just believe in increasing until all symptoms are gone? Also looking forward to hearing what you have to say about shbg. I know you said you have things to share on that as well.

I appreciate your question and thanks for opening up another can of worms in SHBG. I can provide you with the literature about how important SHBG is to your health. I treat the entire person so it is quite difficult when we focus on trying to cure all ones ills with T alome. I also look into coexisting medical illnesses which may impact a persons health and wellbeing, I look at psychosocial issues which may be contributing to symptoms (some of my patients work at 2 jobs basically 7 days a week to make ends meet and no amount of T or thyroid is going to cure their fatigue). Some have serious relationship issues which no amount of T is going to repair. So I focus on the whole person including their diet and exercise regimens. So once we look at all othe factors that can impact a their wellbeing and discus that, then we begin optimizing their hormones. I obtain a baseline T , and begin T (I also initiate thyroid, DHEA, Vit D3, pregnenolone , etc..). If I have All their hormones in a optimal range and their free T 50 or greater with no improvement then I would look to other issues such as adrenal fatigue etc.... I just have not run into that patient yet. When you increase T, you increase E2 , which increases SHBG which is all good. I cringe when I see people trying to "increase my T by lowering my SHBG". SHBG is good. I overcome a increase in SHBG by increasing T dosage. Maybe since I am just a simple boy from Georgia I follow a KISS (keep it simple stupid) mentality. By addressing the whole person, optimizing free T and not being afraid of a number, not blocking E2 or SHBG, and optimizing free T 3, I have just not run into the problems I read about on this and other websites. Trying to do too much all at once and over complicating the process just confuses the patient. If we just initially focus on the most important issues (T, thyroid, DHEA, diet, exercise, melatonin, pregnenolone, supplements, Vit D, and not blocking E2, medical comorbidities , and psychosocial issues) and optimize those, then I have not had a issue with lack of improvement.

 

[AbsoluteZ3R0]

Dr Nichols, is this you? http://www.t1institute.com/health-and-wellness-Nichols.php

 

[J. Keith Nichols MD]

What would you say is an E2? The reason I ask this is because, and please don't take this the wrong way, many doctors have a bias. If your patient says doc I have itchy nips or I am bloated or cry at the drop of a hat. Do you say - oh no that is not from E2?

Respectfully, I don't feel that you've actually read most of my post. I have never taken an AI, and like I said before, I suffered LOW E2 myself. I do not experience effects of high E2(Dr. Saya can confirm, I am a patient of his) nor do I "block" my E2.

I also remember you said you don't even test E2, so how can you confirm you've never seen this in your patients?

I really feel as though you are picking parts of my post to essentially tear me down as a scapegoat for overzealous use of AI in the industry. You seem to have missed(or I didn't make it clear enough) that I said an expert titrates based on symptoms and labs.

I am not propagating false information, and many here can elaborate on their >70 E2 levels and symptoms(vince carter??).

I am not intending to incite an argument, I just simply asked some questions, and seemingly upset you. Still not sure what you mean by "blocking" E2 btw, generally an aromatase inhibitor is used, which does not block estrogen, but rather its production.

Again, I have never used an AI and I suffered from low E2. Not sure why you insinuate I have.

apologies if you felt insulted in any way. We have all been programmed to focus on E2. If no studies show benefit in blocking (lowering) E2 why would we want to lower it ? If no studies show harm in raising E2 with T why would in need to measure it? If a patient were to experience symptoms of E2 excess then I would treat with a AI until symptoms resolvemthen discontinue. I also treat many women in my practice so the importance of E2 is one of my personal interests. If we know from the literature that E2 improves cognition, protects against Alzheimer's disease, decreases visceral body fat, maintains bone strength, is apoptotic to prostate cancer cells, protects against heart attacks and strokes, improves our lipid profiles, among many other benefits then why do we want to block it? It is hard to move away from what we have been programmed to think for so long. Vergel also understands the importance of E2. My E2 is 75. If you have no symptoms of E2 excess then leave it alone and quit worrying about if because it is only providing you with benefits

 

[J. Keith Nichols MD]

What would you say is an E2? The reason I ask this is because, and please don't take this the wrong way, many doctors have a bias. If your patient says doc I have itchy nips or I am bloated or cry at the drop of a hat. Do you say - oh no that is not from E2?

Dr Nichols, is this you? http://www.t1institute.com/health-and-wellness-Nichols.php

Yes it is. Website being updated as well. My profile picture here is most recent taken a few weeks ago

 

[johndoesmith]

apologies if you felt insulted in any way. We have all been programmed to focus on E2. If no studies show benefit in blocking (lowering) E2 why would we want to lower it ? If no studies show harm in raising E2 with T why would in need to measure it? If a patient were to experience symptoms of E2 excess then I would treat with a AI until symptoms resolvemthen discontinue. I also treat many women in my practice so the importance of E2 is one of my personal interests. If we know from the literature that E2 improves cognition, protects against Alzheimer's disease, decreases visceral body fat, maintains bone strength, is apoptotic to prostate cancer cells, protects against heart attacks and strokes, improves our lipid profiles, among many other benefits then why do we want to block it? It is hard to move away from what we have been programmed to think for so long. Vergel also understands the importance of E2. My E2 is 75. If you have no symptoms of E2 excess then leave it alone and quit worrying about if because it is only providing you with benefits

I am not saying to just lower E2 when it's not a problem, but I am saying that in those who DO have symptoms and it IS a problem, lowering E2 can help! There are SO many here who can attest to this.

More ! = better. Yes, E2 is an ESSENTIAL hormone for all, I am NOT denying that.

Measuring E2 is of utmost importance, and I do not think anyone here will disagree with this.

My E2 was <10pg/ml before TRT, so I am no stranger to it's importance, please remember that. I almost entirely attribute all of my symptoms of hypogonadism to low E2.

 

[J. Keith Nichols MD]

What would you say is an E2? The reason I ask this is because, and please don't take this the wrong way, many doctors have a bias. If your patient says doc I have itchy nips or I am bloated or cry at the drop of a hat. Do you say - oh no that is not from E2?

This thread is very informative. Love hearing feedback from different doctors. Dr. Nichols is there a cutoff that you feel is too high of a dose or free t levels that are too high or do you just believe in increasing until all symptoms are gone? Also looking forward to hearing what you have to say about shbg. I know you said you have things to share on that as well.

Answer #43. Thanks for the question

 

[Dr Justin Saya MD]

If you have no symptoms of E2 excess then leave it alone

Well said Dr Nichols and this could perhaps summarize the entire estradiol discussion. I will say, however, from my experience of treating over 10 thousand patients I have seen my fair share who unfortunately do have symptoms and respond favorably to CONSERVATIVE aromatase inhibition. Many of these can even be somewhat predicted, albeit not with 100% accuracy (most notably obese patients, those with very high baseline E:T ratios, and those with baseline low SHBG). You did note that you treat (or would treat) when symptoms are present, which I feel puts you on the right side of the fence on that one for sure.

On the topic of possible longterm risks of elevated E2 in males, as we all know there is not strong data one way or the other. I'll post below a couple study links that I mentioned on the forum a few days ago on a different thread regarding E2 and Carotid IMT. What I found interesting about the first study was that they did NOT administer oral estradiol (which you rightly pointed out previously would provide useless comparisons as ORAL estrogens, synthetic or bioidentical, can increase coagulability independent of actual E2 levels)...they administered parenteral estradiol which means that the data should hold true for actual serum E2 levels as opposed to the route of delivery. Your input and alternative views are welcome and appreciated as they contribute to scholarly discussion. Curious if you are a follower or mentee of Dr Neal Rouzier? Your position on some of these topics are very similar. The copy/paste from the other thread is below. All the best.


"There are no valid studies of safety/risks of elevated E2 levels for men ON TRT with upper physiologic range T levels, so we do the best with the info we have. There are a few studies (not men on TRT mind you) that did suggest a possible trend in increased carotid atherosclerosis (increased IMT as an indicator for increased cardiovascular disease) with increases in FREE estradiol levels. "

https://academic.oup.com/jcem/article-lookup/doi/10.1210/jc.2006-0932

http://circ.ahajournals.org/content/109/17/2074.long#sec-7

Just noticed the link for the parenteral estradiol study was broken, so I've included citation below.

Parenteral estrogen versus combined androgen deprivation in the treatment of metastatic prostatic cancer: part 2. Final evaluation of the Scandinavian Prostatic Cancer Group (SPCG) Study No. 5.
Randomized controlled trial
Hedlund PO, et al. Scand J Urol Nephrol. 2008.

 

[Vince Carter]

I would go with my friend JDS here, uncontrolled estrogen was rather detrimental to my personal and professional life and would on occasion manifest itself on this forum...just PMS'ish, too easily angered, inability to deal with relatively minor stressors, getting in to skirmishes at work, hard to tolerate "people", night sweats/overly hot in bed and then later at night overly cold, it was a terrible spot, for me, to have the uncontrolled E.
But I think we're all dancing around the same thing in different terms or ways of expressing it and it's not to drive down E to some prejudged number, or to let it run high and unrestricted, with negative symptoms. I think we're all saying treat the negative symptom that may be present in the individual. Let me add that in those bad times for me I was running 50/60/70 and as high as 88, unexplained aromatase, and was to a point only using EOD (50mg) and then daily CYP (28mg) but I run 12-15 SHBG constantly, even when the E was high so SHBG did not follow E in my case, but I feel that I had/have a parallel with Free T and Free E in my body that still presents some negative symptoms even with Anastrozole @ .25mg M/W/F. I'm subjectively doing a little bit better on symptoms with .25mg EOD and my LC/MS/MS E2 @ about 15-20.

 

[sportsfan8724]

Thanks again to both doctors for responding to each other as well as us. A few questions for you both. I'm wondering if maybe the reasons Dr. Nichols sees no one with estradiol issues and Dr. Saya does is maybe because the topical cream Dr. Nichols uses helps increase dht enough that it offsets the increase in estradiol? I know this was briefly mentioned earlier in the thread. Or do you think it's more of the fact Dr. Nichols it's getting the free t in a high enough range that it offsets the estradiol? Maybe it's neither of these maybe it's a bit of both just curious if you doctors had an opinion on that. The next question is a different can of worms but always has had me thinking... when people are going from male to female (gender change) there estradiol levels are going high and also there testosterone is being made low. We don't here of them complaining of fatigue and other symptoms or having strokes or heart attacks. Just curious on your opinions on that. I would just think these would be the people with a ton of complaints and maybe they do ... Always had made me think though that estradiol can't be that bad or would here about it from transgenders. Hopefully that part of my question makes sense.

 

[J. Keith Nichols MD]

Well said Dr Nichols and this could perhaps summarize the entire estradiol discussion. I will say, however, from my experience of treating over 10 thousand patients I have seen my fair share who unfortunately do have symptoms and respond favorably to CONSERVATIVE aromatase inhibition. Many of these can even be somewhat predicted, albeit not with 100% accuracy (most notably obese patients, those with very high baseline E:T ratios, and those with baseline low SHBG). You did note that you treat (or would treat) when symptoms are present, which I feel puts you on the right side of the fence on that one for sure.

On the topic of possible longterm risks of elevated E2 in males, as we all know there is not strong data one way or the other. I'll post below a couple study links that I mentioned on the forum a few days ago on a different thread regarding E2 and Carotid IMT. What I found interesting about the first study was that they did NOT administer oral estradiol (which you rightly pointed out previously would provide useless comparisons as ORAL estrogens, synthetic or bioidentical, can increase coagulability independent of actual E2 levels)...they administered parenteral estradiol which means that the data should hold true for actual serum E2 levels as opposed to the route of delivery. Your input and alternative views are welcome and appreciated as they contribute to scholarly discussion. Curious if you are a follower or mentee of Dr Neal Rouzier? Your position on some of these topics are very similar. The copy/paste from the other thread is below. All the best.


"There are no valid studies of safety/risks of elevated E2 levels for men ON TRT with upper physiologic range T levels, so we do the best with the info we have. There are a few studies (not men on TRT mind you) that did suggest a possible trend in increased carotid atherosclerosis (increased IMT as an indicator for increased cardiovascular disease) with increases in FREE estradiol levels. "

https://academic.oup.com/jcem/article-lookup/doi/10.1210/jc.2006-0932

http://circ.ahajournals.org/content/109/17/2074.long#sec-7

Just noticed the link for the parenteral estradiol study was broken, so I've included citation below.

Parenteral estrogen versus combined androgen deprivation in the treatment of metastatic prostatic cancer: part 2. Final evaluation of the Scandinavian Prostatic Cancer Group (SPCG) Study No. 5.
Randomized controlled trial
Hedlund PO, et al. Scand J Urol Nephrol. 2008.[/QUOT

Thanks so much for the post hopefully I can continue the conversion and further the debate. In addition to treating men, I treat just as many women on a daily basis so I am dealing with PCOS, peri menopause, menopause, and young post hysterectomy patients. Quite franklin, us men go through nothing compared to these poor women. Imagine if we were all castrated and no one would help us.
With regard to some of your points. I agree that men with high baseline E2 have been should to have a high I cide ce of cardiovascular disease. Makes perfect sense. If you look at the BMI and other risks factors in these me you see exactly
why they have cardiovascular disease. The high E2 is just a bystander and not responsible for their cardiovascular disease but a result of the obesity. It's the obesity and other conditions that kill them (HTN, CAD, dyslipidemia, etc..) but estrogen gets blamed.
Unfortunately, you do not see the cardioprotective effects of E2 unless it is given orally. IM estradurin is not oral estradiol and you could fully predict that it would not provide the cardioprotective effects that oral E2 does. It is the first pass effect that provides the cardioprotective benefits of oral estradiol. The NIH and all major European studies now use for the most part only oral estradiol as that is the only way to get all the benefits of estrogen. No RCT to date has shown oral estradiol to cause a increase in heart attacks, strokes, or DVTs. Mechanism of delivery is especially important with E2. Are we to ignore all the studies since the WHI (Premarin not E2) including the JAMA, EPAT, CORA, WEST, KEEPS, and DANISH trials with oral E2. So you point out that oral (synthetic or bioidentical) can increase coaguability, but the actual studies show now increase in adverse events with oral E2. I women greater than 60'years of age or greater than 10 years out of menopause when given Premarin (CEE) there were 30 additional adverse events out of 30,000 women. In women younger than 60 years of age even Premarin was cardioprotective. None of the adverse effects seen with Premarin have been seen with oral estradiol to date. So if oral estradiol causes a increase in coaguability leading to adverse events such as DVTs etc...the please provide me with that study and I will absolutely change my opinion.
You can't extrapolate the effects of Premarin or IM Estradurin to oral estradiol. Look at the interventional studies as listed above and see what actually happens when you give oral estradiol. Don't assume all estrogens are the same or even the effects based on mechanism of delivery are the same. Look at what happens when they are give. I can bring a womans blood levels of estrogen up with various forms of estrogen but based on the literature I strongly disagree that blood levels only are what matters. It is obtaining the proper blood levels using the right dosage, right estrogen E2, and proper route of delivery (oral) to achieve proper protection.
With regard to AIs I would definitely treat if a patient presented with symptoms of excess. I am so fortunate I guess That we just don't see it with how the T is administered in our practice.
With regard to no long term studies on increased E2 in males, I have to respectfully disagree. We have been raising men's E2 (H/Hct as well) with IM testosterone for over 50 years. Think about it. For over half a century we have been increasing E2 with T and have not seen any increase in cardiovascular mortality. In fact, we see improvement. How do we just ignore the last 50 years of T studies?
You do have studies that show the harm in blocking estrogen in men (NEJM). I have to see patients now but I would love to continue this conversion by providing some actual patient labs and their symptoms and asking you and our colleagues what they would do with "the lab values" in these men and how they would treat.














A

 

[J. Keith Nichols MD]

Thanks again to both doctors for responding to each other as well as us. A few questions for you both. I'm wondering if maybe the reasons Dr. Nichols sees no one with estradiol issues and Dr. Saya does is maybe because the topical cream Dr. Nichols uses helps increase dht enough that it offsets the increase in estradiol? I know this was briefly mentioned earlier in the thread. Or do you think it's more of the fact Dr. Nichols it's getting the free t in a high enough range that it offsets the estradiol? Maybe it's neither of these maybe it's a bit of both just curious if you doctors had an opinion on that. The next question is a different can of worms but always has had me thinking... when people are going from male to female (gender change) there estradiol levels are going high and also there testosterone is being made low. We don't here of them complaining of fatigue and other symptoms or having strokes or heart attacks. Just curious on your opinions on that. I would just think these would be the people with a ton of complaints and maybe they do ... Always had made me think though that estradiol can't be that bad or would here about it from transgenders. Hopefully that part of my question makes sense.

Excellent point my friend. The reason no increase in cardiovascular events is that oral E2 has not show in any interventional trial to cause them. Women prior to menopause have high E2 levels, but it is only after menopause when they lose the protective effects of estrogen that they begin dying of heart attacks and strokes.

 

[user_joe]

You are wrong. It is applied bid and levelsare still optimal "by the time you go to sleep". If I measured you 10 hours after application your free T will still be 30-50. Once again, if you are having a consistent morning erection your T is going to be in a optimal range. You are making a total assumption not based on actual medical data. How does that "not compare to a level of 1500 TT on test cypionate "? These opinions are which are not based on medical facts or what is seen in medical practice is what confuses those looking for information on HRT. I am in no way trying to be offensive but I think we should all focus on how we communicate by considering a quote by Hippocrates the father of medicine. "There are in effect two things, science and opinion: the former begets knowledge, the later ignorance" We should focus on what the medical literature supports. What study shows that increasing E2 with T is harmful? What study shows that decreasing E2 is beneficial?

im not sure if you read it the way I meant it. Not in the medical field here. Just a patient.

With a half life of 12 hours your T levels must decline on the later half of a 24 day, right? Lab ranges usually peak around 1200 TT. I'm assuming you would be at or under that level before the next application. Doesn't mean it's suboptimal.

If you injected say 250mg test cypionate divided into 7 morning injections you'd likely see 1500 TT, but it doesn't vary much. Average TT over the week is higher.

Im saying that because of the very slow release you see more e2 conversion with long esters than faster releasing methods. Is that incorrect? It would explain why those on creams see less or no symptoms we associate with elevated e2 and see higher e2 levels.


The 250 example is from personal experience. I dosed my ai too low, and elevated e2 made me. just plain hostile. 1-2 days after doubling the AI dose I was fine. Ultimately I just lowered my T dose.

Your patients that that insist on injecting, what's a successful regimen with no AI look like?

 

[sportsfan8724]

He has them applying it twice a day if I understand correctly. That's why they say high free t all day and night. I'm curious too his opinions on frequency and dosing if doing injections is the only option your Dr can provide us. I think I'm his practice though he has no one on injections because he said after switching to the cream he uses no one has wanted to go back to injections. I gathered that he was only stating IF they wanted injections he wouldn't refuse them. Again just my interpretation I'm sure he can clear that up. But yeah like you I would be interested to hear how he would do injections based trt if the patient prefers it.

 

[Gianluca]

I'm another example like Vince Carter, I'm a low SHBG guy and it doesn't matter if my Tot E2 is high my SHBG just doesn't follow, I have been really thought through my TRT from start till now and E2 seems to be what the issue is, when I'm about 50 I really start to feel "crazy" agitated etc, last summer I couldn't handle the heat and I was constantly face bloated and lethargic moody at all time, beside I realized even when e2 have been lower then 40/50, I would complain about some water retention hot flashes etc...

Doc Nicholas what is your take on low SHBG guy and estrogen? I just understood that Low SHBG guys, beside a higher FT may also have an elevated F Estadiol

of course I understand by now that you would treat with an AI someone making my complains, although I thought you have been a bit too laud at the beginning about the fact to not treating E2

 

[J. Keith Nichols MD]

im not sure if you read it the way I meant it. Not in the medical field here. Just a patient.

With a half life of 12 hours your T levels must decline on the later half of a 24 day, right? Lab ranges usually peak around 1200 TT. I'm assuming you would be at or under that level before the next application. Doesn't mean it's suboptimal.

If you injected say 250mg test cypionate divided into 7 morning injections you'd likely see 1500 TT, but it doesn't vary much. Average TT over the week is higher.

Im saying that because of the very slow release you see more e2 conversion with long esters than faster releasing methods. Is that incorrect? It would explain why those on creams see less or no symptoms we associate with elevated e2 and see higher e2 levels.


The 250 example is from personal experience. I dosed my ai too low, and elevated e2 made me. just plain hostile. 1-2 days after doubling the AI dose I was fine. Ultimately I just lowered my T dose.

Your patients that that insist on injecting, what's a successful regimen with no AI look like?

Thanks for your post. There is always a spike after a IM injection. If you measure your levels 1, 2, 3 ,4 hours and so on after a injection you wll see a most significant spike( all of us that have labs in office have probably done this just to see the values) compared to a lidoderm cream. It is this spike that some believe cause the increased E2 symptoms seen mor frequently with injections. You also don't see the symptoms (or at least I haven't ) such as hostility and irritability with the compounded creams that I did see with the injections
Let me give you a brief history so you can better understand my methods. I went through the miserable experience of low T. I have done pellets, injections, gels, and creams. I have taken on a regular basis AIs in order to keep my estrogen controlled. When I first began practicing I provided my patient with injections and regular AIs (anastrozole 2x weekly) and monitored their estrogen levels and kept their T 1200 to maybe 1500 at most but not many as well as keep their free T 20-30 at most as well. I was following what I read and was taught by those that had been taught by others etc...I was not seeing the consistent results that I wanted in myself or my patients. They were good but not what I would consider optimal. As I began researching more and more and understanding the literature and then seeing that what I was doing was based on accepted principles that didn't always have the literature to support it. As I treated more And more women and the literature associated with them I began to rethink the whole estradiol issue. I saw the studies on how beneficial it was in both men and women. How important it was to so many body systems but especially that it was E2 not T that was responsible for decreasing visceral body fat and vital for sexual function in males. So I slowly and reluctantly started make some changes. I went to a max concentration compounded cream initially applying to chest or inner thighs and I continued the AIs in my patients but discontinued it in myself. I began to slowly allow myself to not fear the T or free T numbers and treated until symptoms resolved (of course optimizing thyroid as well) and optimal. I noticed a significant change in myself. My libido improved, stronger erections, every morning erections, no fatigue or irritability, increased strength and endurance etc...). I was having to apply 11/2 grams bid which brought my levels to 1800 with a free T in the 40s. E2 level 75 with absolutely no symptoms at all. I decided that in order to have even better absorption and use less cream I began applying to the testicles. Dosage was cut in half 3/4 gm bid and levels were 2000 and >50 wirh still no symptoms of E2 excess. Cut dose to 1/2 gm bid and continue that to this day
So, I began same regimen with my patients. Lectured them on the importance of E2 and the potential problems with blocking it. All were switched to testicular application bid and all their dosages were at least cut in half with all of their free Ts kept around 40 or greater. I began not to fear the numbers. I did not and have not had a single issue with a patient complaining of E2 excess so I quit even measuring it. I could not have a happier patient population. Everyone that came in on injections wanted to try it this way because their friend was on it "and doing great". I have not had one ask to go back to injections. I no longer advertise. It is all by word of mouth.
The point to all this is I have tried it all, but once I was willing to take a hard look at the medical literature and a
was just willing to experiment with something different I have been able to make a dramatic change in myself, friends, family, and patients. Injections are great but I just don't have the issues with my
patients now that I used to have

 

[J. Keith Nichols MD]

I'm another example like Vince Carter, I'm a low SHBG guy and it doesn't matter if my Tot E2 is high my SHBG just doesn't follow, I have been really thought through my TRT from start till now and E2 seems to be what the issue is, when I'm about 50 I really start to feel "crazy" agitated etc, last summer I couldn't handle the heat and I was constantly face bloated and lethargic moody at all time, beside I realized even when e2 have been lower then 40/50, I would complain about some water retention hot flashes etc...

Doc Nicholas what is your take on low SHBG guy and estrogen? I just understood that Low SHBG guys, beside a higher FT may also have an elevated F Estadiol

of course I understand by now that you would treat with an AI someone making my complains, although I thought have been a bit too laud at the beginning about the fact to not treating E2

If you don't mind me asking but what other hormones are you on and any other medical conditions? Body weight etc..?

 

[J. Keith Nichols MD]

He has them applying it twice a day if I understand correctly. That's why they say high free t all day and night. I'm curious too his opinions on frequency and dosing if doing injections is the only option your Dr can provide us. I think I'm his practice though he has no one on injections because he said after switching to the cream he uses no one has wanted to go back to injections. I gathered that he was only stating IF they wanted injections he wouldn't refuse them. Again just my interpretation I'm sure he can clear that up. But yeah like you I would be interested to hear how he would do injections based trt if the patient prefers it.

You are absolutely correct. I prefer a man get T anyway he can vs being without it.

 

[J. Keith Nichols MD]

You are absolutely correct. I prefer a man get T anyway he can vs being without it.

if switching back to injection I would try to mimic the patterns seen with the creams. I would do daily low dose or every other day at worst to try and avoid any significant spikes and maintain a optimal level daily