Ask Dr Rand McClain

eudes

Member
Hi i am a 24 yo male who is in 7th year of medicine course , and i would like to ask a question to dr rand ;
I have been taking finasteride for 4 years now , and unfortunately my oestradiol level are high.
I would like to know if it is possible to take low dose of armidex to lower my oestradiol to a normal range While being on propecia 1 mg ?
thanks for your work .
 
Hi i am a 24 yo male who is in 7th year of medicine course , and i would like to ask a question to dr rand ;
I have been taking finasteride for 4 years now , and unfortunately my oestradiol level are high.
I would like to know if it is possible to take low dose of armidex to lower my oestradiol to a normal range While being on propecia 1 mg ?
thanks for your work .

That's an easy one. You can certainly use Arimidex to lower your estrogen while taking finasteride.
 
Re: Aspirin and HCG

Dr. McClain,

I have read with concern recent studies supporting the antiandrogenic properties of NSAIDs. See, e.g., "Ibuprofen alters human testicular physiology to produce a state of compensated hypogonadism." I noted with particular interest the further study cited in footnote 34 thereto ("Aspirin inhibits androgen response to chorionic gonadotropin in humans").

My current TRT protocol includes 500 IU HCG, administered SubQ q.3.5d., and among other things I am also currently on aspirin, 81 mg q.d. It was not prescribed by my doctor, but I thought it might be cheap insurance given my age and some of my lipid levels.

The latter study above made me wonder if perhaps I should stop aspirin? Or should I not be concerned because the dose I'm on is only approximately 10% of the dose used in the study (800 mg. b.i.d.)?

I have not seen aspirin or NSAID's affecting endogenous T levels in any of my patients, BUT, I can't say I have been looking for the effect of aspirin or NSAID's. If you are not receiving the benefits you are expecting with HCG, then obviously, you could try dropping the aspirin to see if that helps, but, as you mention, you are taking a very small dose compared to the study dose so LIKELY the aspirin will not have an effect.
BTW, more likely than not your ASA 81mg protocol is doing more for your colon health than protecting you from plaque development in your arteries, BUT, at that dose, it shouldn't hurt. (We have studies showing that we react differently to different dosages of aspirin and in some cases aspirin use at too high a dose might be detrimental to the cardiovascular system).
 

blackebob

Member
Happy Easter Doc!

I switched to daily .1ml injections of Cyp from a cream compound at the end of December 2017. I also started HCG in mid January. I had good testical recovery from daily injections of 125ml HCG, but the bloat was pretty severe. I stopped taking the HCG four weeks ago, and the bloat has decreased. Is there a way to minimize the bloat for HCG, is there a time frame when it should resolve it self? If I am going to react to it, is there a minium dosage you have found to still activate the testicals?

Thank you for your time.
 
HI DR RAND ....thanks again for your answer about my test ai dosage...
-some MD speak about hemoglobin/hematocrit while on trt can be high without risk with a normal platelet count.THE BIG DANGER is high platelet count....is it true?
-does high estradiol make the cbc (hemoglobine hematocrit platelet count) goes higher?
-there is a famous trt doctor who said that 60 to 80mg/ week of testoterone is more than enough and higher dosage are not very recommended cause with the time goes on , the benefit of trt is reduced.My personnal experience is that low dose like 40 MG EVERY 3 DAYS i feel the effect on the libido but nothing special with the energy or capacity TO working out compare with 160 OR 200 MG /WEEK.
what is your your thought about this?

thank you very very much dr rand....

"Risk" with high H/H refers to what would be my first question. Risk of stroke? I have one patient with polycythemia rubra vera from an autoimmune disorder who has come in with a hemoglobin of 26 g/dL (I don't remember the hematocrit) and was and is doing fine constantly fighting to keep his levels down. I have other patients who either do not want to address their sleep apnea, submit to serial therapeutic phlebotomies, or (rarely) have a JAK2 gene mutation and have H/H assays above normal, and the worst symptoms I see are dizziness, lethargy, the "need" to take random deep breathes, and more pronounced post-prandial narcosis ("food coma"). The hematologists I have spoken with about this tell me that the issue is not about having this "thick blood" to which it is often referred, but whether you have a coagulation disorder (homologous for Leiden Factor V, eg) that could lead to "stickier" platelets and ultimately stroke. Yet, we also know that if one's blood gets more viscous, it makes it more difficult for the heart to pump which could lead to MI, stroke, hypertension or a venous thrombosis. So, I believe one consider all the avenues that might lead to these risks and address them intelligently.
I know of no mechanism by which estrogen leverages the production of RBC's (H/H increases).
Re T dosing, everyone is different. 60-80mg per week of testosterone (what form?) may work well for some and not for others, AND, it depends upon how we define "work" (eg, on libido, energy, anabolism, etc.). As for recommending more (or less), again, it depends upon for what purpose one is using T, but as for reducing benefit (as in some sort of accommodation taking place) I disagree. While androgen receptors can downregulate (or upregulate) to adjust to chronic T levels, the benefit of replacing T would not be diminished (one either needed it or did not and replacing either benefitted or did not). If more T than is necessary for replacement is used, then during a short period after which one stopped taking the exogenous T (for fertility, eg) then, yes, there is a short term reduction in benefit from HAVING TAKEN TRT because of downregulation of receptors (as well as there being less than "normal" (the original low T assay or less) T production temporarily until endogenous production resumes in its prior low but normal production) until these receptors upregulate to match the new level of T.
 
Dr. McClain
I realize that finasteride and dutasteride both block conversion of progesterone to 5-DHP, 5-isoprogesterone and 5-alloprogesterone, which are important neurohoromones. Can this effect of finasteride and dutasteride be offset or partially offset by taking pregnolone or progesterone in an effort to increase the available substrate to create 5-DHP, 5-isoP and 5-alloP?



Here are the approximate labs of a buddy of mine
Prior to TRT - T = 300; DHT = 20
TRT only - T = 1,300; DHT = 85
TRT and finasteride - T = 1,300; DHT = 30

He did not use finasteride prior to TRT, but if he had, I am sure his DHT would have been single digits. As you can see, his DHT on TRT with finasteride is higher than his DHT was when he had low T. So it seems that the DHT lowering effect of finasteride was more than offset by increasing the DHT substrate (Testosterone)

So, I am wondering if the progesterone-metabolite-lowering effect of finasteride could be offset by increasing the substrate of these metabolite, which in this case would be progesterone/pregnenolone


Great question and it concerns basic chemistry and stoichiometry. X + Y = Z. If you add more X, then you get more Z as long as Y is not a limiting factor is a very general interpretation. So, in your example, it is very possible that adding more progesterone/pregnenolone would lead to more 5-DHP, 5-isop and 5-allop. However, to what degree, AND with what OTHER effects from progesterone/pregnenolone converting to other metabolites as well? And, to what extent would you be "diluting" the 5-alpha reductase inhibition (from either dutasteride or finasteride) on testosterone into DHT?
I have not seen ANY studies of this, unfortunately.
 
Happy Easter Doc!

I switched to daily .1ml injections of Cyp from a cream compound at the end of December 2017. I also started HCG in mid January. I had good testical recovery from daily injections of 125ml HCG, but the bloat was pretty severe. I stopped taking the HCG four weeks ago, and the bloat has decreased. Is there a way to minimize the bloat for HCG, is there a time frame when it should resolve it self? If I am going to react to it, is there a minium dosage you have found to still activate the testicals?

Thank you for your time.

My first question is why did you switch from a daily topical to daily injectable? One of main ideas behind use of an esterified form of T is to avoid daily dosing, so I am always suspicious when I hear of daily injections.
As for the HCG and bloating, it is most likely secondary to excess estrogen being created while using the HCG. You could experiment with an AI (anastrozole or exemestane) or a blocker (tamoxifen or clomiphene citrate) to see which works best at countering this effect that HCG has on the Leydig cells and with consideration for how much estrogen is being made via aromatization outside of the testicle versus inside. Of course, you could also jigger your dose of the HCG to find minimum dose required to keep testicles functioning (that would be individually determined, but you are using a dose I would consider on the lower end).
 
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

Typically, your T levels will spike about 2.5 days after your injection of T Cyp, BUT, this average is wide, in my experience, meaning for some it is earlier and some later by a day or more. So, your DHT levels will spike in accordance with your T spikes because DHT is made from T and is fairly quickly. Reducing the height/degree of the spike is a useful tool in reducing conversion - I find the higher the spike, the higher the percentage of conversion - but then you begin dealing with the inconvenience of more frequent dosing and compliance with same. You could use a 5-alpha reductase inhibitor like finasteride (start with this one first because of the "commitment" to a much shorter half-life, in case you experience unwanted side effects from its use) to reduce the conversion of T into DHT either as a sole treatment or in conjunction with more frequent injections of a smaller dose of T. I would take your finasteride certainly on the same day as your T injection, so that as little as possible is made from any T injected from the moment it is injected, and every day thereafter if you want to maximize DHT minimization or for at least an additional next 1-2 days after T injection to maximize efficiency and effectiveness of a lesser dose.
 
Dr. McClain,
I would like to add to Lexer's question:
Would dutasteride be an acceptable alternative to finasteride, with out the unwanted effects the finasteride can have?
Thanks,

omi

No, dutasteride is "stronger" in that it works on all three receptors (rather than two as does finasteride) and has a much longer half-life (5 weeks!). So, if you have any unwanted SE's with finasteride, I would not use dutasteride. However, if you have know SE's with finasteride, but not enough result in terms of reducing the effects of DHT, then dutasteride is a good choice.
 

blackebob

Member
My first question is why did you switch from a daily topical to daily injectable? One of main ideas behind use of an esterified form of T is to avoid daily dosing, so I am always suspicious when I hear of daily injections.
).

I switched because after 18 months of building up my dose, I was finally at a dose of 7 clicks of 50mg compound T, and starting to feel well. A new DR, this time one I trusted.
Other protocols recommended by physicians based off of blood test and SHBG levels, and patient state of well being. As it was told to me the lower the SHBG the faster I am burning through my T dose, more frequent dosages split from original dosage. I am sure you have heard that before. You say X, other DR says Y next says Z, I just want to feel the best I can.

Thank you for your time I will take your answers to my next eval.
 

eudes

Member
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 !
 
Great question and it concerns basic chemistry and stoichiometry. X + Y = Z. If you add more X, then you get more Z as long as Y is not a limiting factor is a very general interpretation. So, in your example, it is very possible that adding more progesterone/pregnenolone would lead to more 5-DHP, 5-isop and 5-allop. However, to what degree, AND with what OTHER effects from progesterone/pregnenolone converting to other metabolites as well? And, to what extent would you be "diluting" the 5-alpha reductase inhibition (from either dutasteride or finasteride) on testosterone into DHT?
I have not seen ANY studies of this, unfortunately.

Man I love that response! Great post Rand!
 
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?
 

strum

New Member
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 .

Strum: I am not sure if I am breaking any rules in answering a question in this forum. I am an MD with a long term involvement with male hormone status. I have used tons of both finasteride (Proscar) and dutasteride (Avodart) in my practice and do not see any major hair growth. For men on testosterone replacement treatment (TRT) it is not unreasonable to check DHT levels and to use dutasteride to lower. Of course, monitoring PSA at intervals is very important.

* according to you ; the gynecomastia caused by finasteride is more due to the Low DHT or the high oestradiol ?
Strum: i have seen gynecomastia mostly due to elevations in estradiol, not low DHT. Many of my patients have suppressed DHT 2° dutasteride but do not have gynecomastia.

*IS there any interaction between an AI and a DHT blocker ?

Strum: none that I have seen.

*don't you think aromasin could be a better choice than arimidex ?

Strum: both are effective aromatase inhibitors. Even white button mushrooms are an AI. The proof of efficacy is the baseline E2 and what happens to it after initiating treatment.

* 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 ?

Strum: Tamoxifen is an anti-estrogen and is effective at reversing gynecomastia. I also use cabergoline as a prolactin inhibitor in very low dose such as 0.25 mg three times per week. But i monitor prolactin levels and aim to keep < 5.

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

Strum: your English is fine. Again, I hope I did not break any rules with my input here.
Stephen B. Strum, MD, FACP
Medical Oncologist
 

blackebob

Member
Thanks for stopping by doc. Someone more important than me will invite you to introduce yourself. If your going to stick around, PM Nelson for guidlines.

again welcome.
 

eudes

Member
Strum: your English is fine. Again, I hope I did not break any rules with my input here.
Stephen B. Strum, MD, FACP
Medical Oncologist

Thanks a lot for your answer doctor .
So according to you i could take dutasteride 0.5 mg daily and low dose aromasin ( 25 mg twice a week )
with no issue ?
Like this i will at least stop my hair loss and prevent the unwanted side caused by the high oestradiol .
 

eudes

Member
Thanks a lot for your answer doctor . this is really a great opportunity to talk with specialist .
Because here in france , doctors are not aware of testosterone replacement , or medications such as dutasteride / finasteride . they have really few knowledge about those drugs .

So according to you i could take dutasteride 0.5 mg daily and low dose aromasin ( 25 mg twice a week )
with no issue ?
Like this i will at least stop my hair loss and prevent the unwanted side caused by the high oestradiol .
You have many patient taking dutasteride with no gyecomastia issue ?
thanks
 

edvedder

New Member
Managing high Free T with low-normal SHBG

Hi Dr Rand, Thank you to both you and excelmale for providing this forum to interact with you. I was hoping you could provide some guidelines on optimizing FT/E2.

i've been on a hormonal roller coaster after having started TRT recently with T Cyp (80mg * 2x) & Hcg with no AI. After the initial honeymoon of 2 weeks, I ended up bloated and puffy after 8 weeks with very high E2. Was prescribed anastrazole, over did it and crashed e2 quickly. Then tried a short protocol of 70 mg twice a week with 0.25 mg anastrazole twice a week and no Hcg. This was for just 2 weeks as I wanted to measure shbg and sensitive E2 instead of ECLIA and Free T which I hadn't done earlier. This resulted in: T=1090 ng/dL, FT=31.8 pg/mL, E2 sensitive=25, Shbg=20.8 nmol/L.

I was told by a doc that the high Free T coupled with the low-normal Shbg means that I'm likely just peeing it out and that I should reduce T to 50mg 2x/wk with potentially no AI. I wanted to get another opinion before embarking on this new experiment as I do not 'feel' much when I go below a total of 130 mg/wk. Would you be able to offer some guidance on what a high Free T and low normal Shbg mean?

Thanks !
 

strum

New Member
Good morning Eudes,

Re the aromasin dose, I would use half tablet twice a week (abbreviated biw) and recheck the estradiol (E2) level and keep below the lower limit of normal (usually 40 but depends on the lab). If the level is still high, I would &#8593; the dose to three times a week (abbreviated as tiw) and again recheck the level. This is called TITRATION. This is an important concept in all of biology. Regarding hair loss and estrogen, I have not seen hair loss in men who are being treated with high dose DES (diethylstilbestrol) or with transdermal estrogen (TDE) patches for prostate cancer. If anything, it is the high doses of testosterone that may be a factor rather than the E2. Men who are on ADT (androgen deprivation therapy) to lower dramatically testosterone to castrate levels will lose body hair but some will sprout a full head of scalp hair. I would like to see any peer-reviewed literature citations relating to high E2 as a cause of alopecia (loss of scalp hair). I am here to share my experience but also to learn.
 

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