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

[Vettester Chris]

Dr. Nichols, so glad you joined, welcome to the EM community!

You have noted the importance of optimizing one's Free T3 serum levels as part of an effective HRT protocol. I concur wholeheartedly with that, and I think too many physicians and patients tend to overlook the importance of how thyroid hormone, FT3 in particular, can impact the overall program.

I am curious, when gauging the efficacy of T3 treatment, are you factoring other areas like Reverse T3, iron, ferritin, etc., to help ensure T3 productivity is optimal and not pooling? Also, do you have different protocols designed for patients that are diagnosed with TPO or TgAb autoimmune?

I know this thread is more-so focused on the E2 discussion, so if needed we can always expand to a new thread that could cover this topic? I don't know how simple or complex you view T3 optimization when treating your patients?

 

[Dr Justin Saya MD]

Off the current topic, but since you mentioned it I'll address. I actually treat females as well and have been since day 1. Unfortunately there is indeed data on increased coagulability with oral estradiol (and yes of course we know the story with Premarin/Prempro, etc...preaching to the choir there).

https://www.ncbi.nlm.nih.gov/m/pubmed/11341495/#fft

"oral estradiol (2mg) changed markers of coagulation towards hypercoagulability, and increased serum CRP concentrations."

This from ACOG (American College of Obstetricians and Gynecologists):

"In most investigations of the relationship of venous thromboembolism and menopausal HT, the route of hormone administration has been primarily oral. It has been proposed that orally administered estrogen may exert a prothrombotic effect through the hepatic induction of some of these substances (18–23). The prothrombotic effect is possibly related to high concentrations of estrogen in the liver due to the “first-pass” effect. Studies that compared oral and transdermal ET have demonstrated that transdermally administered estrogen has little or no effect in elevating prothrombotic substances and may have beneficial effects on proinflammatory markers, including C-reactive protein, prothrombin activation peptide, and antithrombin activity. Also, in contrast to oral ET, transdermal ET also may have a suppressive effect on tissue plasminogen activator antigen and plasminogen activator inhibitor activity (23–29).

The Estrogen and Thromboembolism Risk study, a multicenter case–control study of thromboembolism among postmenopausal women aged 45–70 years, demonstrated an odds ratio for venous thromboembolism in users of oral and transdermal estrogen to be 4.2 (95% CI, 1.5–11.6) and 0.9 (95% CI,0.4–2.1), respectively, when compared with nonusers (10). Transdermal estrogen had no increased risk compared with nonusers. Similar results were reported elsewhere (30–35) and of particular importance, in women who were stratified for weight (36) and the presence of prothrombotic mutations (37).

Several nonoral delivery systems presently are available for the administration of estradiol. These include transdermal estradiol patches, ethanolic estradiol-containing gels and sprays, and the vaginal (ring) delivery system. Topical vaginal creams and tablets prescribed for treatment of local urogenital atrophic changes have low levels of systemic absorption but have no detectable effect on coagulation proteins or incidence of venous thromboembolism. Both transdermal (patches or gels) and vaginal (ring) delivery bypass the gastrointestinal conversion of estradiol to estrone with less increase of triglyceride levels, clotting factors, and globulins (38). The vaginal ring containing estradiol acetate for systemic treatment, shown to be effective in the management of vasomotor symptoms, is not associated with an increased risk of venous thromboembolism (38–40). The practicing gynecologist should be aware that other less mainstream estrogen delivery methods, including transbuccal lozenges and troches, are widely used throughout the United States. These alternatives, which are meant to dissolve in the mouth and bypass the enterohepatic circulation, are available as single agents or in combination with other hormones and are fashioned by compounding pharmacies. Data on the safety and efficacy of compounded troches and lozenges are limited. Although widely prescribed, these less mainstream estrogen delivery methods have not been subjected to significant scientific scrutiny."

Since this relates to females only (as no males will be taking any estradiol, let alone oral vs transdermal), we'll not sidetrack the thread any further on that topic.

 

[Dr Justin Saya MD]

Dr Nichols- you've mentioned many times in the thread "50 years of TRT data" when discussing and bolstering your positions, but let's make sure we're in agreement here:

The OVERWHELMING majority of the TRT data "over the past 50 years" is related to antiquated TRT regimens that are not similar to regimens that either of us prescribe [and that's a good thing as those regimens...i.e. low dose transdermals (androgel), q2week T cyp injections (or even worse q3-4week) - virtually always result in failure]. In other words, there ISN'T data from the past 50 years of patients with sustained levels you are describing with your patients of Total T 1500-2000, free T 40-50, estradiol 75 (as you state yours is...or in that vicinity for other patients) for prolonged periods of time (again we're talking potentially decades of TRT treatment). You also stated not checking DHT levels, which I would highly recommend with the transdermal 150mg BID directly to the scrotum as those DHT levels are almost certainly to be VERY high. Same goes for free T3 levels 4-7 as you mentioned, a free T3 of 7 is WELL within hyperthyroid range. There is no data of the safety of patients with a prolonged free T3 of 7, but there certainly are mountains of data on the risk with the hyperthyroid population. Main point being, the "50 years of data" is apples to oranges with the type of regimens that you're describing and, thus, is not relevant. In other words, you are in uncharted waters and please don't let the (inapplicable) 50 years of data give a false impression of patient safety considerations.

I'm going to pass this thread over to further discussion with you and the fellas...you've certainly sparked lively discussion.

 

[J. Keith Nichols MD]

Dr. Nichols, so glad you joined, welcome to the EM community!

You have noted the importance of optimizing one's Free T3 serum levels as part of an effective HRT protocol. I concur wholeheartedly with that, and I think too many physicians and patients tend to overlook the importance of how thyroid hormone, FT3 in particular, can impact the overall program.

I am curious, when gauging the efficacy of T3 treatment, are you factoring other areas like Reverse T3, iron, ferritin, etc., to help ensure T3 productivity is optimal and not pooling? Also, do you have different protocols designed for patients that are diagnosed with TPO or TgAb autoimmune?

I know this thread is more-so focused on the E2 discussion, so if needed we can always expand to a new thread that could cover this topic? I don't know how simple or complex you view T3 optimization when treating your patients?

Thyroid optimization is as important to my practice and patients wellbeing as testosterone. We what some may call "Agressively" treat with amour thyroid and aim for a free T 3 level of 4-5 or more if necessary. The most difficult problem is always the patients family MD. This of course supppresses the TSH which makes their MD think we are making them hyperthyroid which is absolutely not true. I take a very simple approach in our health and wellness program. We optimize DHEA, Vit D, Trestosterone, use pregnenolone and melatonin, treat PCOS, and really stress the importance of optimizing thyroid. We at times will use it BID for those that have afternoon fatigue or needing to decrease their body fat (weight loss) to improve their insulin resistance. We simply measure TSH (meaningless) , T4, and T3 and use a KISS (keep it simple stupid ) approach. Luckily by not over complicating matters and confusing patients we are having excellent success. We have as many women come in per week as men for thyroid management and PCOS management as we do men. We once again treat the symptoms and not the number with thyroid. Here are some excellent articles by Tammas Kelly that will help understand that high dose Thyroid is not dangerous and does not cause the same complications as endogenous hyperthyroidism
1. Elevated levels of circulating thyroid hormones do not cause the medical sequalae of hyperthyroidism
2. An examination of myth: a favorable cardiovascular risk benefit analysis of high dose thyroid for affective disorder
3. Long term augmentation with T3 in refractory major depression
Sincerely
Keith

 

[Gianluca]

Thanks for your reply, and I apologize for my misspelling of your last name

I don't have any medical conditions beside a mild sleep apnea, that I'm trying to fix, and adrenal fatigue. I'm a 6"3 tall per about 190lb, I just use T injections, HCG and a small dose of AI, all my other hormones are fine beside cortisol which has been low as I mentioned before, Doc Justin Saya is actually the doctor I'm under the care of,so he could confirm that, and I'm actually really looking forward to discuss with him about Free Estrogen soon, as I'm positive keeping that on track will improve my TRT, and like you previously said about the actual focus on FT rather than TT, as a low SHBG guy, I do believe, we, always referring to the SHBG club, should be focusing on FE rather than TE

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]

Off the current topic, but since you mentioned it I'll address. I actually treat females as well and have been since day 1. Unfortunately there is indeed data on increased coagulability with oral estradiol (and yes of course we know the story with Premarin/Prempro, etc...preaching to the choir there).

https://www.ncbi.nlm.nih.gov/m/pubmed/11341495/#fft

"oral estradiol (2mg) changed markers of coagulation towards hypercoagulability, and increased serum CRP concentrations."

This from ACOG (American College of Obstetricians and Gynecologists):

"In most investigations of the relationship of venous thromboembolism and menopausal HT, the route of hormone administration has been primarily oral. It has been proposed that orally administered estrogen may exert a prothrombotic effect through the hepatic induction of some of these substances (18–23). The prothrombotic effect is possibly related to high concentrations of estrogen in the liver due to the “first-pass” effect. Studies that compared oral and transdermal ET have demonstrated that transdermally administered estrogen has little or no effect in elevating prothrombotic substances and may have beneficial effects on proinflammatory markers, including C-reactive protein, prothrombin activation peptide, and antithrombin activity. Also, in contrast to oral ET, transdermal ET also may have a suppressive effect on tissue plasminogen activator antigen and plasminogen activator inhibitor activity (23–29).

The Estrogen and Thromboembolism Risk study, a multicenter case–control study of thromboembolism among postmenopausal women aged 45–70 years, demonstrated an odds ratio for venous thromboembolism in users of oral and transdermal estrogen to be 4.2 (95% CI, 1.5–11.6) and 0.9 (95% CI,0.4–2.1), respectively, when compared with nonusers (10). Transdermal estrogen had no increased risk compared with nonusers. Similar results were reported elsewhere (30–35) and of particular importance, in women who were stratified for weight (36) and the presence of prothrombotic mutations (37).

Several nonoral delivery systems presently are available for the administration of estradiol. These include transdermal estradiol patches, ethanolic estradiol-containing gels and sprays, and the vaginal (ring) delivery system. Topical vaginal creams and tablets prescribed for treatment of local urogenital atrophic changes have low levels of systemic absorption but have no detectable effect on coagulation proteins or incidence of venous thromboembolism. Both transdermal (patches or gels) and vaginal (ring) delivery bypass the gastrointestinal conversion of estradiol to estrone with less increase of triglyceride levels, clotting factors, and globulins (38). The vaginal ring containing estradiol acetate for systemic treatment, shown to be effective in the management of vasomotor symptoms, is not associated with an increased risk of venous thromboembolism (38–40). The practicing gynecologist should be aware that other less mainstream estrogen delivery methods, including transbuccal lozenges and troches, are widely used throughout the United States. These alternatives, which are meant to dissolve in the mouth and bypass the enterohepatic circulation, are available as single agents or in combination with other hormones and are fashioned by compounding pharmacies. Data on the safety and efficacy of compounded troches and lozenges are limited. Although widely prescribed, these less mainstream estrogen delivery methods have not been subjected to significant scientific scrutiny."

Since this relates to females only (as no males will be taking any estradiol, let alone oral vs transdermal), we'll not sidetrack the thread any further on that topic.

Would you like to comment on the Danish, elite, epat, or associated studies ?

 

[J. Keith Nichols MD]

Thanks for your reply, and I apologize for my misspelling of your last name

I don't have any medical conditions beside a mild sleep apnea, that I'm trying to fix, and adrenal fatigue. I'm a 6"3 tall per about 190lb, I just use T injections, HCG and a small dose of AI, all my other hormones are fine beside cortisol which has been low as I mentioned before, Doc Justin Saya is actually the doctor I'm under the care of,so he could confirm that, and I'm actually really looking forward to discuss with him about Free Estrogen soon, as I'm positive keeping that on track will improve my TRT, and like you previously said about the actual focus on FT rather than TT, as a low SHBG guy, I do believe, we, always referring to the SHBG club, should be focusing on FE rather than TE

You need to do everything you can to decrease your insulin resistance. Low carb diet, exercise, optimize T, DHEA, metformin, and thyroid especially. Anything you can do to lower your insulin resistance will raise your SHBG. There's alway HGH if you can afford it.

 

[meanbreen]

You need to do everything you can to decrease your insulin resistance. Low carb diet, exercise, optimize T, DHEA, metformin, and thyroid especially. Anything you can do to lower your insulin resistance will raise your SHBG. There's alway HGH if you can afford it.

Dr. Nichols, would you say that treating low T3 could have the effect of increasing SHBG? This is only anecdotal, but I saw my own SHBG increase substantially after taking NDT for a few months to increase my T3 (I didn't feel much difference with the increased T3 so discontinued that treatment, though I am considering trying again since my T3 is 3.1) but have not seen anyone else report this effect.

 

[MikeXL]

If no studies show benefit in blocking (lowering) E2 why would we want to lower it ?

I don't believe that this has been studied directly. So this is a lack of data. Not a reason to not lower E2

If no studies show harm in raising E2 with T why would in need to measure it?

I don't believe that this has been studied well. Same thought as above

As to the treason to lower it, there seems to be something disconcerting about E2 levels way out of normal range. Wouldn't common sense seem to say since we don't have the data one way or the other let's go middle of the road ?

 

[GEORGE TOULIATOS]

https://anabolic.org/the-effects-of-steroids-on-bone-marrow-and-erythropoiesis-2/

 

[J. Keith Nichols MD]

https://anabolic.org/the-effects-of-steroids-on-bone-marrow-and-erythropoiesis-2/

Erythrocytosis does not lead to polycythemia Vera. it is artlicles like these that cause such unnecessary confusion.

 

[J. Keith Nichols MD]

Would you like to comment on the Danish, elite, epat, or associated studies ?

I could spend the next 2 days discussing why ACOG makes their recommendations and how the world ended with the WHI. You least time consuming approach is to simply ask...Can you provide me with one single RCT where oral estradiol caused a increase in heart attacks, strokes, or DVTs? I just am asking for one. There have been multiple RCTs utilizing oral E2 instead of Premarin since the WHI and none have caused harm. I listed a few for you. Medical societies continuing to associate the adverse effects of Premarin to Estradiol I can't explain when the studies are there for them to read as well.

 

[Dr Justin Saya MD]

I could spend the next 2 days discussing why ACOG makes their recommendations and how the world ended with the WHI. You least time consuming approach is to simply ask...Can you provide me with one single RCT where oral estradiol caused a increase in heart attacks, strokes, or DVTs? I just am asking for one. There have been multiple RCTs utilizing oral E2 instead of Premarin since the WHI and none have caused harm. I listed a few for you. Medical societies continuing to associate the adverse effects of Premarin to Estradiol I can't explain when the studies are there for them to read as well.

As I mentioned above, the female oral estradiol discussion is completely off topic of this thread (and this forum in general), so we will not sidetrack the other salient discussion points here.

We BOTH agree that the WHI data that has been mistakenly extrapolated to include estradiol (as opposed to equine estrogens) is beyond flawed...that's indisputable. Thus, we both believe bioidentical estradiol to be safer and more effective.

My position is that TRANSDERMAL estradiol is equally as effective and safer than oral estradiol treatment, primarily due to the absence of first-pass metabolism through the liver. Your position seems to be opposite. We can agree to disagree on that one.

The other topics discussed above are of much more relevance to this forum and the members.

 

[J. Keith Nichols MD]

Dr Nichols- you've mentioned many times in the thread "50 years of TRT data" when discussing and bolstering your positions, but let's make sure we're in agreement here:

The OVERWHELMING majority of the TRT data "over the past 50 years" is related to antiquated TRT regimens that are not similar to regimens that either of us prescribe [and that's a good thing as those regimens...i.e. low dose transdermals (androgel), q2week T cyp injections (or even worse q3-4week) - virtually always result in failure]. In other words, there ISN'T data from the past 50 years of patients with sustained levels you are describing with your patients of Total T 1500-2000, free T 40-50, estradiol 75 (as you state yours is...or in that vicinity for other patients) for prolonged periods of time (again we're talking potentially decades of TRT treatment). You also stated not checking DHT levels, which I would highly recommend with the transdermal 150mg BID directly to the scrotum as those DHT levels are almost certainly to be VERY high. Same goes for free T3 levels 4-7 as you mentioned, a free T3 of 7 is WELL within hyperthyroid range. There is no data of the safety of patients with a prolonged free T3 of 7, but there certainly are mountains of data on the risk with the hyperthyroid population. Main point being, the "50 years of data" is apples to oranges with the type of regimens that you're describing and, thus, is not relevant. In other words, you are in uncharted waters and please don't let the (inapplicable) 50 years of data give a false impression of patient safety considerations.

I'm going to pass this thread over to further discussion with you and the fellas...you've certainly sparked lively discussion.

Dr Saya,
Another Pandora's box to open up.
Lets start with thyroid. We were all taught that giving too much thyroid would cause a person to become hyperthyroid and develop all the complications of Graves' disease. You just diagnosed hyperthyroidism in a patient with a free T 3 of 7 without knowing anything about them. You were able to do this by looking at a number. That's how we were both taught along with everyone else. Don't suppress the TSH and keep the T4 and T3 in a normal range or else they would be hyperthyroid. Well what we thought would occur has not occurred with high dose thyroid treatment. I have provided you with the articles in a previous post by Tammas Kelly and I would strongly recommend you read them as they are a fascinating read. The recent literature dispels all that we we taught regarding hyperthyroidism. High dose thyroid treatment is one of the most studied augmentations for refractory depression. High dose thyroid is also included in the major treatment guidelines for bipolar disorder. Armour thyroid has 9mcg of T3 in I grain (60 mg) and the average dose we use ranges from 2-3 grains but can be more. I personally take 2 grains twice a day and my free T 3 is over 5 and I'm not hyperthyroid. So if a patient is taking 3 grains then they are getting 27mcgs of T3. The dosages used in HDT can go up to 150mcg...Wow!!!. These patients are not becoming hyperthyroid and developing all the morbidities and mortalities of Graves' disease. They prescribe it as we would a NSAID and don't even worry about the levels. Once again wow!!! This is because it is now known that exogenous HDT is not the same as endogenous hyperthyroidism (Graves' disease). There is a autoimmune component to Graves' disease that does not occur with High dose thyroid therapy. High dose thyroid is also used to treat thyroid cancer without any of the complications people with actual Graves' disease have. You can remove the thyroid of someone with Graves' disease and they still have complications. Once again they have a autoimmune component. So this fear of thyroid is unwarranted and not supported by the literature. So a free T 3 level of 7 is not hyperthyroidism. Any hormone can have side effects and if a patient develops increased sweating or increased heart rate then the dosage is simply lowered. Isn't this why we all continue to try and learn and grow so that we can keep a open mind and sometimes learn that the way we were first taught may not be correct? Shouldn't our patients demand that of us? I also feared thyroid until I learned better and my patients thank us for it. I can't tell you how many "fibromyalgia" patients have had their symptoms resolve with High T and and thyroid treatment. So point is this, the fears we had with making people hyperthyroid and having all the complications of people with Graves' disease are unwarranted.
DHT? Why should I care what my DHT levels are? If my hair is not falling out then why should I be concerned? If my hair or my patient was losing hair then I would treat with the appropriate meds and switch to injections. That has not occurred yet but if it did that is how I would approach. I don't need to know my DHT levels if I am doing great and having no symptoms no more than I need to know my E2 levels when I am doing great with no symptoms
TRT. We can't ignore 5 decades of increasing a mans E2 with IM testosterone without adverse effects. We know the adverse effects of having low T. We know the spike in T after a injection and how that causes more issues with E2 excess than a transdermal route. Have you ever given yourself a injection of T cyp 200mg and measured you T levels hourly throughout that day and then daily for the next week? We have just for the hell of it to see what happened. Your head would blow up if i told you the T values the first day especially. It seems you are still caught up in the numbers such as 1500 and feel that is somehow dangerous just like the thyroid values. Remember that those values are based on the avg of a population and they aren't going out and measuring the levels of only the most healthy and fit. By the time we are 50 and above it becomes the avg of a population of sick people and the number is decided on by a pathologist in a lab that is not out in the world treating people. So would you rather your numbers be normal or optimal? Would our patients rather us treat a number on a piece of paper or their symptoms? The art of medicine has been lost in that we treat numbers and not a patients symptoms and then when we get uncomfortable with the number we then decide it must be something else .
I'm not sure it was probably best for me to join the forum in that I have been quietly treating patients and spending months of the year traveling and learning new information and finding that the way I had previously learned certain things were wrong or could be improved. I wasn't looking to treat thyroid when I started. I would have told you you were crazy if said I would be treating PCOS and menopausal women. I now think know why I am not running into a lot of the problems that I read about on this forum with regard to HRT. I am actually optimizing T and thyroid as by treating a patients symptoms without fearing a number and thank goodness I was willing to try every method myself until i found a program where we don't run into the E2 issues so many people seem to have.

 

[Dr Justin Saya MD]

Dr Saya,
Another Pandora's box to open up.
Lets start with thyroid. We were all taught that giving too much thyroid would cause a person to become hyperthyroid and develop all the complications of Graves' disease. You just diagnosed hyperthyroidism in a patient with a free T 3 of 7 without knowing anything about them. You were able to do this by looking at a number. That's how we were both taught along with everyone else. Don't suppress the TSH and keep the T4 and T3 in a normal range or else they would be hyperthyroid. Well what we thought would occur has not occurred with high dose thyroid treatment. I have provided you with the articles in a previous post by Tammas Kelly and I would strongly recommend you read them as they are a fascinating read. The recent literature dispels all that we we taught regarding hyperthyroidism. High dose thyroid treatment is one of the most studied augmentations for refractory depression. High dose thyroid is also included in the major treatment guidelines for bipolar disorder. Armour thyroid has 9mcg of T3 in I grain (60 mg) and the average dose we use ranges from 2-3 grains but can be more. I personally take 2 grains twice a day and my free T 3 is over 5 and I'm not hyperthyroid. So if a patient is taking 3 grains then they are getting 27mcgs of T3. The dosages used in HDT can go up to 150mcg...Wow!!!. These patients are not becoming hyperthyroid and developing all the morbidities and mortalities of Graves' disease. They prescribe it as we would a NSAID and don't even worry about the levels. Once again wow!!! This is because it is now known that exogenous HDT is not the same as endogenous hyperthyroidism (Graves' disease). There is a autoimmune component to Graves' disease that does not occur with High dose thyroid therapy. High dose thyroid is also used to treat thyroid cancer without any of the complications people with actual Graves' disease have. You can remove the thyroid of someone with Graves' disease and they still have complications. Once again they have a autoimmune component. So this fear of thyroid is unwarranted and not supported by the literature. So a free T 3 level of 7 is not hyperthyroidism. Any hormone can have side effects and if a patient develops increased sweating or increased heart rate then the dosage is simply lowered. Isn't this why we all continue to try and learn and grow so that we can keep a open mind and sometimes learn that the way we were first taught may not be correct? Shouldn't our patients demand that of us? I also feared thyroid until I learned better and my patients thank us for it. I can't tell you how many "fibromyalgia" patients have had their symptoms resolve with High T and and thyroid treatment. So point is this, the fears we had with making people hyperthyroid and having all the complications of people with Graves' disease are unwarranted.
DHT? Why should I care what my DHT levels are? If my hair is not falling out then why should I be concerned? If my hair or my patient was losing hair then I would treat with the appropriate meds and switch to injections. That has not occurred yet but if it did that is how I would approach. I don't need to know my DHT levels if I am doing great and having no symptoms no more than I need to know my E2 levels when I am doing great with no symptoms
TRT. We can't ignore 5 decades of increasing a mans E2 with IM testosterone without adverse effects. We know the adverse effects of having low T. We know the spike in T after a injection and how that causes more issues with E2 excess than a transdermal route. Have you ever given yourself a injection of T cyp 200mg and measured you T levels hourly throughout that day and then daily for the next week? We have just for the hell of it to see what happened. Your head would blow up if i told you the T values the first day especially. It seems you are still caught up in the numbers such as 1500 and feel that is somehow dangerous just like the thyroid values. Remember that those values are based on the avg of a population and they aren't going out and measuring the levels of only the most healthy and fit. By the time we are 50 and above it becomes the avg of a population of sick people and the number is decided on by a pathologist in a lab that is not out in the world treating people. So would you rather your numbers be normal or optimal? Would our patients rather us treat a number on a piece of paper or their symptoms? The art of medicine has been lost in that we treat numbers and not a patients symptoms and then when we get uncomfortable with the number we then decide it must be something else .
I'm not sure it was probably best for me to join the forum in that I have been quietly treating patients and spending months of the year traveling and learning new information and finding that the way I had previously learned certain things were wrong or could be improved. I wasn't looking to treat thyroid when I started. I would have told you you were crazy if said I would be treating PCOS and menopausal women. I now think know why I am not running into a lot of the problems that I read about on this forum with regard to HRT. I am actually optimizing T and thyroid as by treating a patients symptoms without fearing a number and thank goodness I was willing to try every method myself until i found a program where we don't run into the E2 issues so many people seem to have.

We are on the same side of the spectrum when it comes to "normalizing" vs "optimizing", but our definitions and tolerance for risk for our patients appears fundamentally different.

The concern with free T3 levels (as you stated up to 7) comes not from sticker shock with the comparable reference ranges, but from real world experience seeing fitness athletes, bodybuilders, etc taking high doses with the resultant high levels and most DO in fact have various hyperthyroid symptoms- I have counseled and helped many as patients (elevated HR, sweating, grinding teeth, jitteriness/anxiousness, insomnia, etc). Further, IMO, if one is increasing HR drastically with elevated thyroid levels (higher HR = more workload for heart) AND you are not concerned when blood viscosity (HCT) increases to higher levels (more viscous blood = more workload for heart)...higher HR + thicker blood = double whammy for cardiac workload, especially longterm.

Not monitoring DHT, especially with the route of administration being high doses to the scrotum...you mentioned hair, what about the prostate? You also mentioned if a male had high DHT symptoms (of which you only mention hair...again think about prostate) that you would prescribe the appropriate medication. Not finasteride I hope, especially without monitoring DHT levels.

Not monitoring E2, but would treat temporarily with an AI if patient had high E2 symptoms- again flying blind. How would you know how aggressive or conservative to be with the AI without first checking E2 levels.

You mentioned you have not run into a patient yet that needed HCG. Don't take his the wrong way, but that would give the impression that you have a comparatively very small patient population at this point or a VERY select group of patients. Fertility, testicular atrophy, etc haven't been important considerations for ANY of your patients?

We are of similar ideologies in some ways (I am FAR from the traditional PCP, urologist, endocrinologist that prescribes useless and antiquated protocols), but at the same time have some important differences in opinion. I am not here to tell you your approaches are incorrect, as you are not to mine, but I do feel that you are taking the ideology of "treat symptoms not JUST numbers" (which I agree with) to the extreme by not even bothering to check some of the relevant levels. In my opinion, BOTH numbers and symptoms need to be taken into consideration to have the overall picture, otherwise you're charting a course with only half of the data available to you.

 

[J. Keith Nichols MD]

We are on the same side of the spectrum when it comes to "normalizing" vs "optimizing", but our definitions and tolerance for risk for our patients appears fundamentally different.

The concern with free T3 levels (as you stated up to 7) comes not from sticker shock with the comparable reference ranges, but from real world experience seeing fitness athletes, bodybuilders, etc taking high doses with the resultant high levels and most DO in fact have various hyperthyroid symptoms- I have counseled and helped many as patients (elevated HR, sweating, grinding teeth, jitteriness/anxiousness, insomnia, etc). Further, IMO, if one is increasing HR drastically with elevated thyroid levels (higher HR = more workload for heart) AND you are not concerned when blood viscosity (HCT) increases to higher levels (more viscous blood = more workload for heart)...higher HR + thicker blood = double whammy for cardiac workload, especially longterm.

Not monitoring DHT, especially with the route of administration being high doses to the scrotum...you mentioned hair, what about the prostate? You also mentioned if a male had high DHT symptoms (of which you only mention hair...again think about prostate) that you would prescribe the appropriate medication. Not finasteride I hope, especially without monitoring DHT levels.

Not monitoring E2, but would treat temporarily with an AI if patient had high E2 symptoms- again flying blind. How would you know how aggressive or conservative to be with the AI without first checking E2 levels.

You mentioned you have not run into a patient yet that needed HCG. Don't take his the wrong way, but that would give the impression that you have a comparatively very small patient population at this point or a VERY select group of patients. Fertility, testicular atrophy, etc haven't been important considerations for ANY of your patients?

We are of similar ideologies in some ways (I am FAR from the traditional PCP, urologist, endocrinologist that prescribes useless and antiquated protocols), but at the same time have some important differences in opinion. I am not here to tell you your approaches are incorrect, as you are not to mine, but I do feel that you are taking the ideology of "treat symptoms not JUST numbers" (which I agree with) to the extreme by not even bothering to check some of the relevant levels. In my opinion, BOTH numbers and symptoms need to be taken into consideration to have the overall picture, otherwise you're charting a course with only half of the data available to you.

Firtsly, those are not hyperthyroid symptoms. Secondly, you concerns are not borne out in the medical literature. I still refer you to Dr Kelly's articles. Until you are of the understanding that exogenous HDT is not the same as endogenous hyperthyroidism and does not have the same morbidities and mortalities then we are just spinning our wheels here. When the medical community is using thyroid dosages for other disorder 5-10x the amount we are utilizing then I have to wonder why you are seeing all of the adverse effects you report that most others are not? Can you please provide evidence increased Cadiac load with thyroid and Hct causing harm in any study to date or is that just "your opinion".

Since T increases DHT and we know T does not cause prostate cancer can you tell me why i should be concerned for my prostate? In all the men on testosterone withou measuring DHT levels there is no increase in prostate cancer. The
PCPT (prostate cancer prevention trial) raises a new debate on finasteride.

If i am having symptoms of E2 excess and I know I am only going to take a AI until sympoms resolve can you tell me why I need to know a level. Since I am taking the AI for symptoms are you saying that I should measure a number and then reduce E2 to another number? If so, what are those numbers? Once again, it appears you are more caught up in following numbers that don't change treatment. I'm not sure what you mean by being aggressive or conservative. If I am going to take anastrazole 2x per week until symptoms resolve why would I need to know a number?

I'm not treating 20 year olds we discuss fertility and testicular atrophy with all patients they are not interested in hcg as one of patients said "my wife has never told me the next day, honey your testicles were so good last night". They are more concerned about a strong firm consistent erection day to day. I honestly feel you are over complicating the process leading men to chase numbers and become number focused instead of just trusting the process and feeling better. I think you are correct though I have a select population of patients that trust in what we are doing and That's why they do so well.

 

[Dr Justin Saya MD]

Since T increases DHT and we know T does not cause prostate cancer can you tell me why i should be concerned for my prostate? In all the men on testosterone withou measuring DHT levels there is no increase in prostate cancer. The
PCPT (prostate cancer prevention trial) raises a new debate on finasteride.

If i am having symptoms of E2 excess and I know I am only going to take a AI until sympoms resolve can you tell me why I need to know a level. Since I am taking the AI for symptoms are you saying that I should measure a number and then reduce E2 to another number? If so, what are those numbers? Once again, it appears you are more caught up in following numbers that don't change treatment. I'm not sure what you mean by being aggressive or conservative. If I am going to take anastrazole 2x per week until symptoms resolve why would I need to know a number?

Does elevated DHT not contribute to BPH?

How much anastrozole are you going to prescribe without knowing their levels? E2 levels can easily crash in a week or two with inappropriate dosing.

Do we only monitor hypertension when patients are having symptoms of severe hypertension (headaches, kidney damage, visual disturbances)...and then do we treat BLINDLY without following BP measurements? Or do we just assume their BP is okay when the symptoms of severe hypertension resolve?

Do we treat diabetes only based on symptoms so that when their polyuria, visual disturbances, neuropathies improve we sound the horns of success...or do we monitor their fasting blood glucose, HgB A1C, fasting insulin, etc?

Again you are falling on the lines of an "extremist" when it comes to the symptom first ideology. The TRUTH is often found not at the extremes, but somewhere in the middle. I agree we are spinning our wheels and see no point in further debate, but feel compelled to convey to you, as per our Hippocratic oath as physicians, that in my own opinion and experience I find some of the treatment details you've noted to be risky and borderline reckless. Take it for what it's worth, both of our opinions are known.

 

[Vettester Chris]

Thyroid optimization is as important to my practice and patients wellbeing as testosterone. We what some may call "Agressively" treat with amour thyroid and aim for a free T 3 level of 4-5 or more if necessary. The most difficult problem is always the patients family MD. This of course supppresses the TSH which makes their MD think we are making them hyperthyroid which is absolutely not true. I take a very simple approach in our health and wellness program. We optimize DHEA, Vit D, Trestosterone, use pregnenolone and melatonin, treat PCOS, and really stress the importance of optimizing thyroid. We at times will use it BID for those that have afternoon fatigue or needing to decrease their body fat (weight loss) to improve their insulin resistance. We simply measure TSH (meaningless) , T4, and T3 and use a KISS (keep it simple stupid ) approach. Luckily by not over complicating matters and confusing patients we are having excellent success. We have as many women come in per week as men for thyroid management and PCOS management as we do men. We once again treat the symptoms and not the number with thyroid. Here are some excellent articles by Tammas Kelly that will help understand that high dose Thyroid is not dangerous and does not cause the same complications as endogenous hyperthyroidism
1. Elevated levels of circulating thyroid hormones do not cause the medical sequalae of hyperthyroidism
2. An examination of myth: a favorable cardiovascular risk benefit analysis of high dose thyroid for affective disorder
3. Long term augmentation with T3 in refractory major depression
Sincerely
Keith

Dr. Nichols, thank you for the response. When saying you "aim" for a FT3 serum level of 4 -to-5, is this based on the standardized serum assay with the reference range of 2.0pg/ml - 4.4pg/ml? I believe you said you said you personally administered 2 grains/day (correct me if I'm wrong?), are you able to achieve optimal levels at 2 grains? I have found 2 grains usually achieves 3.5 to 3.6 pg/ml, or around 70% of reference range, but I know everyone metabolizes differently, and optimal levels are different from 1 person to the next person.

Out of curiousity, are you seeing good results with Armour, since the the Activas Pharma acquisition from Forest Labs, back in 2015? There's been a lot of mixed reviews with the new Armour in the various thyroid discussion communities, and I was wondering if you have compared it with other NDT's, regardless if branded or compounded?

I am with you 110% on the TSH subject, which too many physicians use as a primary marker for evaluating and diagnosing thyroid treatment. However, I strongly support monitoring other 'key' markers, such as Reverse T3, iron, ferritin, cortisol, electrolytes, D3. As mentioned in my first post, do you factor areas like Reverse T3 into the equation with thyroid treatment? Also, again, do you take different approach when patients have Hashis TPO or TgAb. Pooling tends to be a frequent obstacle with many here (and other communities), which usually seem attributed from adrenal imbalance, and/or iron & ferritin deficiencies.

At some point (it doesn't have to be this thread), I'd also like your take on women needing thyroid treatment (as you noted the equal ratio of male to female patients), but more- so predicated on cases that are estrogen dominance related, stemming from peri/post menopausal stages. I have read a lot of related info. from Dr. Uzzi Reiss, and figured (like HRT) this subject is vastly misunderstood with the mainstream general physicians and endocrinoligists alike (?), thus the majority of female population with this condition don't get treated even close to adequately.

 

[Jackie Treehorn]

Does elevated DHT not contribute to BPH?

How much anastrozole are you going to prescribe without knowing their levels? E2 levels can easily crash in a week or two with inappropriate dosing.

Do we only monitor hypertension when patients are having symptoms of severe hypertension (headaches, kidney damage, visual disturbances)...and then do we treat BLINDLY without following BP measurements? Or do we just assume their BP is okay when the symptoms of severe hypertension resolve?

Do we treat diabetes only based on symptoms so that when their polyuria, visual disturbances, neuropathies improve we sound the horns of success...or do we monitor their fasting blood glucose, HgB A1C, fasting insulin, etc?

Again you are falling on the lines of an "extremist" when it comes to the symptom first ideology. The TRUTH is often found not at the extremes, but somewhere in the middle. I agree we are spinning our wheels and see no point in further debate, but feel compelled to convey to you, as per our Hippocratic oath as physicians, that in my own opinion and experience I find some of the treatment details you've noted to be risky and borderline reckless. Take it for what it's worth, both of our opinions are known.

I've been following this thread with interest, while biting my tongue at times, and keeping my mouth shut. I for one really appreciate Dr. Saya's thorough and conservative approach to TRT. I don't want my doctor guessing about dosage levels, or not monitoring labs that we all know to be important in a TRT protocol. This is exactly why Dr. Saya is my TRT physician.

 

[Tommy Wall]

And not monitoring DTH for me is strange and why should the optimal level be 1500+ I thought the best is to try to mimic a healthy man´s level. When I was on the "old school protocol" 250 every third week I had a testo rush the first 5 days and couldn´t enter a supermarket without going crazy of women and if something went agaist me I would snap. Not optimal and natural test levels for sure. If my doc asked me "how do you feel" I would reply " oh great" I he would think I was at an optinal level wich of coarse I wasn´t at all.