Ask Dr Rand McClain

[Rand McClain DO]

Here is my question to Dr. McClain: if I stop taking my prescribed dose of rhGH Genotropin at 0.3mg E.D. right before I go to bed (been on for one month straight so far), how long will it take for my Human Growth Hormone serum and IGF-1 level serum to go back to my normal baseline which is >5ng/mL (rhGH serum) and 78 ng/mL (IGF-1)? One week, two weeks? I want to know how long it will take since I have a growth hormone deficiency.

Thank you!

Hi Amacher,
Of course, everyone is different, but the pituitary usually picks up where it left off pretty quickly. I refer to it as similar to a gas powered engine as opposed to a diesel. The length of time using HGH and one's age plays a very large role in the speed at which you regain your "normal" function. However, you state your baseline is 78 ng/mL and you are diagnosed with GH deficiency. Since you have deficiency (78 ng/mL is definitely low for IGF-1 compared to what you were likely producing at 20 years old which would be closer to 300 to 350 ng/mL), to regain that "baseline" shouldn't take very long, and won't make that much difference to you whether we see 68 or 88 ng/mL, because this is a relatively low IGF-1. Things to consider when evaluating your "optimum" level of IGF-1 would include whether you are a vegan or vegetarian, have diabetes or other metabolism issues, and your age. To more directly answer your question, yes, likely weeks rather than months if you are otherwise healthy and don't have a diagnosis of GH deficiency. This can be accelerated through the use of secretagogues now such as ibutamoren, GHRP-2 and 6, Ipamorelin, and sermorelin.

 

[Rand McClain DO]

Dr. McClain,
Do you test E2 or estradiol sensitive? Recently I tested both simultaneously and had a 34 e2 but a 19 sensitive estradiol.
Is this typical and appropriate?

Also,
Ive done 2 courses of 7 months of low dose accutane to clear my skin. Once in 2010 and another in 2017. It's the only thing that clears my oily skin that tends to break out and sometimes includes painful cystic acne. Low dose meaning 20mg daily and this last run, the fiballroom 2 months were @40mg daily.
However, now 9 months post run, the oily skin and blemishes have come back...to a lesser degree.
Most importantly, I've always had issues with zits/cystic type acne on the neck and the back of the head along the hairline and a few inches above. This is the one thing I wish I could permanently change or take care of...it's a real bitch. Any suggestions?

Hi HanginOn,
I use E2 (estradiol), sensitive for just that reason. Once I received a report with both and the E2 was 64 pg/mL while the E2, sensitive was 16 pg/mL on the same draw. This is typical because the simple E2 is not precise enough in the low range likely because the test was originally used mainly for women who have average levels in a much higher range of titers.
Accutane is the best I know of for cystic, persistent and scarring acne vulgaris and also works well for acne rosacea. What I have seen typically is that one course of 4-6 months will provide relief either for life or at least 10 years. It sounds like you may be better off buying lots of Carmex and bearing use of a full dose which is determined to be a range based upon your weight. Also, prior to starting your Accutane or between courses, you can consider using doxycyline (an antibiotic) to help clear the milder cases of acne.

 

[Deleted member 16042]

Dr McClain,

I have been having high PSA (5.9-7.2 with free PSA % at 20-25%) and am due for another PSA w Free PSA blood draw in about a week. I've been considering the next steps as there's too much uncertainty for me and don;t just want to keep repeating PSA every 90 days as my PCP wishes. I read your previous post about your PCA and you mentioned oncoblot, however this is not available to me. From what I have found I think my next logical steps are 4K score and then 3T MRI prior to biopsy. Do you have any other recommendations at this point in the game?

 

[Rand McClain DO]

Hi Dr McClain -

I discovered this site recently, thanks for all that you do (MI YouTube videos you did are awesome).

Im in unknown waters .. am I on the right track:

32, 14 years of weight training and martial arts, natural and always had a grasp of tracking diet and periodizing training. As the career (sales) years kicked in, stress goes up a bit but the last few years everything feels heavy, I'm lethargic, and the low T typical symptoms continue ... Up about 10lbs in a year (195 from 185) without any major diet changes. Feeling fluffy and less muscular, weaker, and less sexual drive.

Question:
Am I on the right track with trying HCG Monotherapy before jumping into T (I'm getting married in Feb ‘19, kids are in the plans)? I had blood done at one clinic (they told me not to fast strangely so my cholesterol #'s are off) only for them to try and sell me on every drug under the sun. Adios to them and thankfully new clinic (Defy) seems to care about their patients / great experience so far, but various folks ( other forums) are getting in my head about their opinions hence why I'm asking this here.

Total T - 543 ng/DL
Free T - 7.9 ng/DL or 1.5%
SHGB - 53.9 nmol/L (57 is upper limit)
FSH - 3.3 mIU/mL
LH - 1.2L mIU/ML
E2 - 18 pg/ML (I can't say if it was a sensitive test or not)
VitD - low
DHEA - under 250

Everything else (blood, thyroid, PSA, etc in range)

The PA and I chatted, seems my SHGB is high and doesn't want to try Clomid (that could raise SHGB?). We concluded a secondary type issue, my E2 has room to increase with elevated T as a hopeful result of HCG Monotherapy. Being LH was already low (don't recall concussions or anything but did hit my head / stiches at 8yo followed by life of dirt bike wrecking and karate matches), he felt this was a simple place to start before going at lengths of T etc.. 3 small doses weekly to limit E increase, various minerals etc to clean some things up and perhaps lower SHGB (I hear nettle is good too). Anastrozole he said to use if I feel symptoms of high E in next few weeks, but don't need to start day 1.

Is HCG mono a short term hope or sustainable?

The Rx

BEGIN HCG 350 iu SQ Three times weekly to increase testosterone free
BEGIN Anastrozole 0.125 mg twice weekly as needed per E2 symptoms (reviewed with Pt.)
BEGIN DHEA 25 mg one by mouth every night
BEGIN Fish Oil 2grams every day for HDL support
BEGIN Zinc Picolinate 50mg One by mouth every day to reduce SHBG and E2/Raise DHT
BEGIN magnesium glycinate 400mg One every day to Decrease SHBG
BEGIN Boron 10mg every day to aid in Test levels and decrease SHBG
BEGIN Milk Thistle 500mg One every day for liver support
BEGIN Vitamin D 5000IU QD

Follow up 8weeks with limited labs Testosterone Free and Total, LH, Estradiol, SHBG, Vitamin D, Cholesterol Panel, CBC, CMP

I okay or worse case scenarios to be aware of?!

Many thanks, sorry for the novel!

Mike

Hi Mike (Sully09),
First, you are in good hands with Defy Medical. I actually founded Defy along with one of the current owners and Dr. Saya is very knowledgeable and competent. There is more than one way to skin a cat, so we may vary in our preferences for different Rx's and protocols, but yours listed above looks good. If I understand what you present correctly, use of HCG is ideal since your success is promising given the likelihood that your hypogonadism is (appears) secondary, and, your plans to have children are right around the corner. How long this will be useful to you depends upon how long your testicles provide you relief from T deficiency symptoms and signs, but eventually, if you live long enough, odds are that primary hypogonadism will occur. My advice would be to follow the suggested protocol and evaluate the results. If positive, ride the wave of HCG use for as long as it provides a solution to the T deficiency signs and symptoms and fertility.

 

[Rand McClain DO]

Dr McClain,

I have been having high PSA (5.9-7.2 with free PSA % at 20-25%) and am due for another PSA w Free PSA blood draw in about a week. I've been considering the next steps as there's too much uncertainty for me and don;t just want to keep repeating PSA every 90 days as my PCP wishes. I read your previous post about your PCA and you mentioned oncoblot, however this is not available to me. From what I have found I think my next logical steps are 4K score and then 3T MRI prior to biopsy. Do you have any other recommendations at this point in the game?

Hi Blackhawk,
I am still not convinced that PSA is a valuable screening tool. Even the supposed inventor of the PSA test believes it should not be used as such (https://www.nytimes.com/2010/03/10/opinion/10Ablin.html). The only group the adheres to its use still is the AUA. There are too many false negatives and perhaps even worse, false positives, that make it unreliable certainly at best. Unnecessary biopsies are the result of false positives and biopsies are invasive and are accompanied by considerable risk. Passing a large stool the morning of the test (any massage of the prostate gland) can elevate PSA assays. Unfortunately, the ONCOblot was purchased by a Chinese company that has left the US market behind. BUT, a US company is working on a replacement that will use antibodies with a reflex to Western Blot that will end up being cheaper and easier to use. Meanwhile, we are studying the use of nagalase assays to evaluate for cancer presence, but nagalase can show positive with certain viruses too so while a negative test would be great and valuable, a positive nagalase would be inconclusive. At this point, I recommend a multi-parametric MRI of the prostate (at least it's feet first) which can show lesions typically as small as 5mm or even 3mm using a facililty that can process the slices in Holland. From there, depending upon size of any (IF any) lesion, and its location, you can decide whether to biopsy, watchfully wait, or "treat" with various non-surgical options. BTW, one assay, the PCA-3, can test specifically for a certain type of PCA, but it is not all inclusive. Lastly, most athletes will tell you that it takes about 10,000 practice swings to get proficient at something. The DRE (digital rectal exam) is considered the standard for prostate screening. Seriously? How many urologists, proctologists, or any doctors have performed DRE's 10,000 times?....

 

[Rand McClain DO]

Hi Dr Mcclain
I have a question regarding DHT. When i inject 100 mgs of testosterone cypionate per week, the following few days my dht goes well over 150, i know the day after the injection it does. A week later just before my next injection my dht is 90 ( range 35-80 ). When my total T ( natural) is only 340, my dht is 38. Would it make sense to inject smaller amounts of T every monday and thursday at 45 mgs in order to reduce those high spikes in DHT ? Would doing so cut down the chances of hair loss and prostate issues? I somehow believe that it is the day after and the following few days after an injection when DHT spikes above the high level of normal when all the negative dht side effect can occur.. what is your opinion? Im thinking smaller/ frequent T injections would reduce those high dht spikes?
what is your opinion on using very low dose finasteride, breaking a 1mg tab in half (.5 ) and using finasteride at small dosages every monday wed and friday in order to reduce dht but minimize possible finasteride side effects by lowering dht too low?
thank you

Hi lexer,
Not sure if I answered your question, but it appears that at some point I hadn't. Sorry to you and others whose questions I haven't answered. I screwed up initially answering questions without tying them to each other (question with answer) so I frankly got lost in what had and hadn't been answered. Please feel free to "double up" on a question if it goes too long without an answer. My bad. As for the DHT, yes, presumably (and as witnessed in practice), by reducing the average titer of T you will reduce your average titer of DHT. This reduction appears NOT to be linear either as the body tends to "overreact" to higher levels than more moderate levels, particularly when above "normal" range. DHT will further or exacerbate hair loss IF such (like MPB) is in your genes, but if not, then no. DHT definitely contributes to BPH so reducing DHT should slow the benign growth of the prostate. Using finasteride to punctuate your T dosing such that it blocks a spike is a good strategy for reducing the leverage your body places on T to convert to DHT. Spikes in T after injecting T Cyp or Enanthate usually occur ROUGHLY 2.5 days after injection so taking your finasteride, say, 24 hours after your injections may effectively smooth out your titer of DHT. You could also try to bury your DHT using more finasteride more frequently. You may not notice any SE's from doing so and if you did, you could discontinue the finasteride and expect normalization of signs, symptoms and assays within two weeks. However, 5-alpha reductase can inhibit more than conversion of T to DHT so simply be aware that more is impacted that just DHT.

 

[Rand McClain DO]

Hi Doctor Mcclain,

Legalities aside, are there any androgens besides testosterone that you believe would be beneficial as an adjunct to testosterone for therapeutic purposes?

That's a loaded question for many more reasons than legalities. There are so many, not just androgens, but steroids that have therapeutic value. To which therapeutic purpose(s) are you referring? For simple anabolic purposes, two anabolic steroids that are legal in the US are nandrolone and oxandrolone, and both appear to be safe and effective at increasing muscle mass, and, oxandrolone, at both increasing muscle mass and decreasing fat mass (intra-abdominal fat). For wasting disorders, they are both remarkable at helping to not only resist wasting but reverse it. There are other anabolic steroids that are legal and branded such as anadrol, halotestin and winstrol but I do not see their being prescribed for therapeutic purposes because they are other options better suited for, eg, treating pernicious anemia which is an indication for anadrol. Again, it depends upon what you call therapeutic purposes, because, eg, winstrol is a DHT derivative anabolic steroid indicated for angioedema. Every bodybuilder and many track professionals know that it works wonders at squeezing out the last bit of third-spaced (unnecessary) water prior to a show or meet so that every cross-striation (earned) is more visible and every step lighter without the unnecessary water, respectively.

 

[Rand McClain DO]

thanks a lot doc !
*DO you think i could take dutasteride while taking low dosage of arimidex to lower oestradiol ? because despite getting sides effect with finasteride i get poor result with it in terms of hair regrowth and maintenance .

* according to you ; the gynecomastia caused by finasteride is more due to the Low DHT or the high oestradiol ?


*IS there any interaction between an AI and a DHT blocker ?
*don't you think aromasin could be a better choice than arimidex ?

* I have read a study about the use of tamoxifen while taking biclutamide / finasteride , to prevent the growth of gynecomastia . IS long term tamoxifen a safe option ?

SOrry for all the questions and my poor english . You are really one of my inspiration in the medical field !

Hi eudes,
There is no contraindication taking dutasteride with anastrozole (Arimidex). You may indeed get better results with dutasteride than finasteride. Gynecomastia is not driven by DHT but rather estrogen. If you take a 5-alpha reductase inhibitor such as finasteride or dutasteride and you begin to get gynecomastia (assuming no other changes to your protocol), then the presumption is that while less T is being converted to DHT, that very same T, if you will, is now available to be, and is being, converted to estrogen. This is the only "interaction" between the use of either of these meds - ie, their effect on the substrate, T, from which they, DHT and estrogen, are made. Long-term tamoxifen safe? Safer than having estrogen activity too high, but there are studies showing tamoxifen is carcinogenic (not well publicized I believe because for someone with estrogen sensitive cancer it can be a life saver, and that hurdle needs to be crossed with tamoxifen sometimes being the only practical option). I prefer use of either an AI like anastrozole or a suicide inhibitor of estrogen like exemestane (Aromasin). To me, these two are for medical/clinical purposes essentially interchangeable, but exesmestane is usually more expensive.

 

[eudes]

thanks a lot doctor for taking your time to anwser my question
I wish i could live in the US to make an appointment with you . Do you make skype consultation ?
So my main issue is to keep my hair by using dutasteride while at the same time getting rid of the gynecomastia caused by it .
I took several blood test and before finasteride my oestradiol were 20 pg/ ml , and while on it it increases to 60 pg/ ml !
I am unlucky because the studies said that finasteride / dutasteride increase E2 by 20-30 %
* SO i will need to take an aromatase inhibitor to keep the oestradiol in the normal range . However i am worried about the impact on the lipid and on the hair of the arimidex if I take this medication on the long terms .

* I was thinking about taking 0.25 mg arimidex EOD and trying to reach the 20 pg/ ml range , AND taking a 1 month course of raloxifen( which is better to tamoxifen according to studies ) to " shrink" the gynecomastia lump .

thanks a lot doctor .

 

[Fernando Almaguer]

Hi Dr. Rand McClain!

I think this is an awesome and valuable thread to be on thanks for answering questions. Also, I have seen your YouTube videos with muscle insider or something like that and I learned a lot! Very valuable videos and priceless knowledge.

With that said: I hear some talk about AIs causing osteoporosis in men. Is this something easily achieved or would it take a large amount for a very long time or a small amount over a long period of time?

 

[galaxy]

Hi Dr Rand in a YouTube video by muscle Insider a couple years ago you mentioned two things that I was wondering if you had the same views on.

1) you mentioned that you weren't a fan of Subq injections.

2) you mentioned that you weren't a fan of combining Hcg and testosterone in one injection.

Thanks

 

[Rand McClain DO]

Hi Dr Rand in a YouTube video by muscle Insider a couple years ago you mentioned two things that I was wondering if you had the same views on.

1) you mentioned that you weren't a fan of Subq injections.

2) you mentioned that you weren't a fan of combining Hcg and testosterone in one injection.

Thanks

Hi Galaxy, one of the main reasons for not "endorsing" sub Q injections of T was because it was relatively new (at least in terms of being main stream). I (arguably, we) just didn't have enough data/feedback, and, I had seen some pretty bad case of sub Q injections gone bad - mainly large blebs, sometimes infected, from injecting too much T under the skin. More recently, I have seen more cases of individuals using either strict sub Q injections or sort of a hydrid of a sub Q and IM combined using a short (5/8") needle to inject. In addition, these successful cases are using smaller, more frequent injections to overcome the issue with creating the bleb under the skin where there is less vasculature extant to absorb/remove the T. My only quandry with this is that the whole purpose of an esterified T is to make dosing (an invasive procedure with a needle) less frequent, more safe, and more convenient. Why not consider an appropriate dose of a gel or cream if one is going to dose daily, eg? But, for those who don't mind the extra work, the fact that one is more frequently dosing smaller amounts AND the T is esterified makes for a more stable titer of T. This can make some people feel better than when the titer varies much more so with weekly injections (though rarely do patients notice a difference in my experience as long as the titer is high enough to be therapeutic) and it can reduce or even eliminate the need for estrogen control. This obviation for the need for an estrogen "blocker" such as an AI or an actual receptor blocker is, to me, the best reason for more frequent dosing of an ester of T whether via sub Q, IM, or hybrid.
As for combining T with HCG, I am still not a fan for the simple reason that combining an aqueous with an oil-based solution is asking for and often results in a problem. The two do not mix and the injection site often develops a "mouse" - a red, raised area that can develop into an infection/abscess.

 

[Rand McClain DO]

Hi Dr. Rand McClain!

I think this is an awesome and valuable thread to be on thanks for answering questions. Also, I have seen your YouTube videos with muscle insider or something like that and I learned a lot! Very valuable videos and priceless knowledge.

With that said: I hear some talk about AIs causing osteoporosis in men. Is this something easily achieved or would it take a large amount for a very long time or a small amount over a long period of time?

Hi Fernando,
Thank you and thank Nelson for this! And, for the videos, the credit goes to Dave "Mad Max" Bourlet (btw, we are now on Jay Cutler's channel/website) For my part, I am more than happy to help if I can.
I do not see how an AI would lead to osteoporosis in a typical male. If one were not replacing or have enough T then, even then, I find it hard to see how an AI might contribute to osteoporosis because one would already have low T and by extension low E, so an AI would either not be reducing E by much or boosting T by blocking its conversion to E. If a male has enough T and is doing just about anything that is weight bearing, he should be preventing osteoporosis. Doctors tend to focus on estrogen, particularly with women, when treating or discussing osteoporosis, but T helps prevent it as well.

 

[Rand McClain DO]

thanks a lot doctor for taking your time to anwser my question
I wish i could live in the US to make an appointment with you . Do you make skype consultation ?
So my main issue is to keep my hair by using dutasteride while at the same time getting rid of the gynecomastia caused by it .
I took several blood test and before finasteride my oestradiol were 20 pg/ ml , and while on it it increases to 60 pg/ ml !
I am unlucky because the studies said that finasteride / dutasteride increase E2 by 20-30 %
* SO i will need to take an aromatase inhibitor to keep the oestradiol in the normal range . However i am worried about the impact on the lipid and on the hair of the arimidex if I take this medication on the long terms .

* I was thinking about taking 0.25 mg arimidex EOD and trying to reach the 20 pg/ ml range , AND taking a 1 month course of raloxifen( which is better to tamoxifen according to studies ) to " shrink" the gynecomastia lump .

thanks a lot doctor .

Hi eudes, you are very welcome. I can Skype with you if you like.
Regarding your concern for your lipids, as long as you are not OVERsuppressing your estrogen, you should have no negative effect on your HDL. You can avoid gynecomastia (estrogen related) by keeping your E within normal limits, and keeping it so, will not negatively affect your lipids.
One consideration: if you are 30 years old or older, and you have no signs of male pattern baldness yet, it is unlikely you will develop it and therefore you may have less concern for modulating your DHT downward. Remember that Receding Hairline is also genetic, but not affected by excess DHT, so use of a 5-alpha reductase inhibitor to attempt to treat this would be relatively fruitless.
Taking Raloxifen while taking Arimidex will reduce the efficacy of Arimidex somewhat (about 13% if I remember correctly), and theoretically after about 4 days of Arimidex, you would not benefit from an E receptor blocker like Raloxifen. BUT, I will say that, clinically, I have seen benefit in the treatment of acute onset gynecomastia using tamoxifen, even when using Arimidex to keep E levels optimal, so I would consider sticking with your plan if your gynecomastia is newly developed. While it may shrink completely if new, I find that often what gynecomastia is diminished can be enough to make it no longer a nuisance, but that some breast tissue still remains. When removing gynecomastia, I regularly find, say, a golf ball sized tissue mass once excised, yet upon palpation presurgically, I felt the presence of, say, a marble sized mass.

 

[eudes]

Hi eudes, you are very welcome. I can Skype with you if you like.
Regarding your concern for your lipids, as long as you are not OVERsuppressing your estrogen, you should have no negative effect on your HDL. You can avoid gynecomastia (estrogen related) by keeping your E within normal limits, and keeping it so, will not negatively affect your lipids.
One consideration: if you are 30 years old or older, and you have no signs of male pattern baldness yet, it is unlikely you will develop it and therefore you may have less concern for modulating your DHT downward. Remember that Receding Hairline is also genetic, but not affected by excess DHT, so use of a 5-alpha reductase inhibitor to attempt to treat this would be relatively fruitless.
Taking Raloxifen while taking Arimidex will reduce the efficacy of Arimidex somewhat (about 13% if I remember correctly), and theoretically after about 4 days of Arimidex, you would not benefit from an E receptor blocker like Raloxifen. BUT, I will say that, clinically, I have seen benefit in the treatment of acute onset gynecomastia using tamoxifen, even when using Arimidex to keep E levels optimal, so I would consider sticking with your plan if your gynecomastia is newly developed. While it may shrink completely if new, I find that often what gynecomastia is diminished can be enough to make it no longer a nuisance, but that some breast tissue still remains. When removing gynecomastia, I regularly find, say, a golf ball sized tissue mass once excised, yet upon palpation presurgically, I felt the presence of, say, a marble sized mass.

thanks a lot doctor , that would be great if I could have a skype consultation with you .
I am 25 yo and unfortunately I have both receding hairline and crown thinning .
Even if it the receding hairline is genetic , i have seen quite a lot of result in the internet for the receding hairline with the use of dutasteride .
And unfortunately too the gynecomastia lump might be the size of a marble .
*So , this is sure that the gynecomastia process with the use of 5 ar inhibitor ( finasteride / dutasteride ) is caused by the excess oestradiol And not the low DHT or maybe higher prolactin level ?
This is the same process as the gyno cause by testosterone cycle ?
* I am just trying to set up a regimen to maintain my hair while avoiding the excess E2 side effect . And trying to be healthy for my lipid .

Again thanks for taking your time to answer those questions . because here in france , if you start taking about TRT / E2 management / finasteride / arimidex ... Doctor will call you crazy , and they are not formed to deal with those issue . We are still in the " old school " way of dealing with th hormonal topic . Endocrinologist are mainly formed to treat diabete / thyroid .
t

 

[Fernando Almaguer]

Thanks for your time Dr. Rand McClain !

 

[galaxy]

Great thanks so much Dr. McClain

 

[Rand McClain DO]

thanks a lot doctor , that would be great if I could have a skype consultation with you .
I am 25 yo and unfortunately I have both receding hairline and crown thinning .
Even if it the receding hairline is genetic , i have seen quite a lot of result in the internet for the receding hairline with the use of dutasteride .
And unfortunately too the gynecomastia lump might be the size of a marble .
*So , this is sure that the gynecomastia process with the use of 5 ar inhibitor ( finasteride / dutasteride ) is caused by the excess oestradiol And not the low DHT or maybe higher prolactin level ?
This is the same process as the gyno cause by testosterone cycle ?
* I am just trying to set up a regimen to maintain my hair while avoiding the excess E2 side effect . And trying to be healthy for my lipid .

Again thanks for taking your time to answer those questions . because here in france , if you start taking about TRT / E2 management / finasteride / arimidex ... Doctor will call you crazy , and they are not formed to deal with those issue . We are still in the " old school " way of dealing with th hormonal topic . Endocrinologist are mainly formed to treat diabete / thyroid .
t

Can't say for sure if the culprit is estrogen or prolactin, but, again, by blocking conversion from T to DHT, there is more T available for conversion to E, and you note that this is indeed what you saw with your assays. Yes, low DHT, in and of itself, does not drive gynecomastia. A T cycle, if not done properly controlling estrogen can cause gynecomastia, the process simply being the conversion of T to excess estrogen. Hope this does and happy to help.

 

[eudes]

Can't say for sure if the culprit is estrogen or prolactin, but, again, by blocking conversion from T to DHT, there is more T available for conversion to E, and you note that this is indeed what you saw with your assays. Yes, low DHT, in and of itself, does not drive gynecomastia. A T cycle, if not done properly controlling estrogen can cause gynecomastia, the process simply being the conversion of T to excess estrogen. Hope this does and happy to help.

thanks again doc .
So the final word , according to you in order to prevent the gynecomastia caused by finasteride/dutasteride , one should use an aromatase inhibitor rather than a SERM ?
Using proper dosing of arimidex to keep the E2 on the normal range .
I have read that one side of arimidex is hair thinning ; Is it caused if you reduce your E2 too much ?
The normal range for you is 15-20 pg/ml ?