Finasteride - HcG Monotherapy

Hi all,

I have been lurking around the forum for a very long time and learned precious info on the hypothalamic-pituitary-gonadal axis and TRT. After much research (and feeling very tired/low libido/depressed for quite some time) it became very clear to me that I might had low T. I went to my general practitioner and got my T level tested, which were very low (around 270 ng/dl at that time).

My doctor said it was most likely due to stress and to 10 years of Finasteride usage - I stopped taking the medication in March 2009 when suspecting that it might be the root of my health problems.

I started my quest to find a good doc in December 2008 and, after many failures, I finally found a decent endocrinologist in late 2009 (or so I thought…)

Here are my info and latest labs results:
Age: 31
Height: 6’2"
Weight: 200 Lbs
Waist size: 36
BF: 18% - Fat is mostly around mid section, also a little sign of gyno (sensitive nipples and some hard tissue behind)

Labs:
Total T: 285.71 ng/dl (290.5-995.9)
Bio Available T: 257.14 ng/dl (86.75 - 648.9)
SHBG: 9 nmol/ml (15-48)
Estradiol: 29 pg/mL (No reference Value on labs…)
Prolactin: 7.5 Ug/L (3 - 13)
LH: 4.9 Ui/L (2.0 - 12.0)
FSH: 3.5 Ui/L (1.0 - 18.0)
TSH: 1.84 mU/L (0.35-5.50 mUI/L)

I had a MRI on my pituitary and an osteodensitometry test, both came back normal.

Now, my doctor had me on HcG monotherapy (500 ui SC EOD) for 4 weeks and ran some tests.
Total T went up slightly (320 ng/dl), so she bumped my HcG to 1000 ui SC EOD to see if I would respond better. According to what I read 1000 ui of HcG EOD is quite high and could cause intratesticular E to rise up… so I’m a bit worried here. She told me that she would switch to T injections if things doesn’t get better with 1000 ui HcG EOD.

From what I read I’m not sure if this is a good way to kick start my own T production after my endocrine system was messed up by Finasteride and a most stressful life. Also it seems that my Endo wants to put me on HcG (or T) indefinitely… so I’m not sure if she’s tackling the problem correctly. I told her about Dr. Shippen’s book and brought the studies mentioned in the forum stickies but she’s still unsure about the T+HcG+Ai protocol.

Should I start looking for a new Endocrinologist?

Thanks for your help!

Small update:

Just got new results in after 4 weeks of HcG at 1000 ui SC EOD.

Total T: 320.23 ng/dl (290.5-995.9)
Bio Available T: 298.74 ng/dl (86.75 - 648.9)
SHBG: 9 nmol/ml (15-48)
Estradiol: 34 pg/mL (Still no reference value on labs…)
Prolactin: 8.9 Ug/L (3 - 13)
LH: 3.2 Ui/L (2.0 - 12.0)
FSH: 3.1 Ui/L (1.0 - 18.0)
TSH: 2.67 mU/L (0.35-5.50 mUI/L)
*Free T4 : 12.6 pmol/L (10.0-23.0)

I doesn’t seem to improve on this protocol and my physical condition is kinda worst. I feel much more lethargic since I began HcG monotherapy.

Any opinion on what my next steps should be?
Thanks!

Self inject T… you know the story
250iu hCG EOD long term
1.0mg anastrozole per week in divided EOD dosing

Retest after 6 weeks and adjust anastrozole accordingly

As you have read, liquid anastrozole allows for proper dose control

How are your testes hanging… any changes with hCG?
Size of testes changed with hCG?
How changed VS years ago?
How hairy are you?
Loss of hair below the knees?
Word searching?
lots of typos?
Noise really bothers you?
Short tempered?
Social avoidance or house bound?
What other long term Rx or OTC drug use?

PM with personal stuff if you want.

fish oil caps
6,000iu vit-D in 2,000 iu oil caps, double that for 2-4 weeks if not using any before.
50mg/day DHEA
Vit and mineral sups with zinc and lots of B vitamins

Later, test for DHEA-S and you want to be in the upper range.

Edit your posts above, use the edit button, and add lab ranges.

Are you getting iodine from iodized salt at home? TSH might say that thyroid is ok, but one can have low TSH and low thyroid hormones at the same time. Test FT3 and FT4 after ensuring that iodine intake is adequate. You can find iodine or iodine rich supplements. You may need more than RDA amounts for a while.

Your doc is doing extended hCG challenge tests at this point. Whatever the outcome, you are not going to get normal that way.

You are very estrogen dominant right now. Without ant other changes you need low dose anastrozole. With TRT E2 could only go up from there if not using an AI.

Fasting cholesterol and serum glucose numbers?

We have seen severe damage from hair loss drugs before. DHT is important. A full head of hair and a limp dick is not. :slight_smile:

You need to do many thing to support vitality. If you get in TRT_AI_hCG you will have the energy to pursue other issues.

Another endo is not a good idea, as a group they are quite useless, all the more because they should have a superior grasp of these things. See if you can sell your current doc first. You can find and ask regional compounding pharmacies for referrals… they know the docs who know what to do.

Thanks for the very detailed reply KSman! It is very much appreciated.

[quote]KSman wrote:
Self inject T… you know the story
250iu hCG EOD long term
1.0mg anastrozole per week in divided EOD dosing

Retest after 6 weeks and adjust anastrozole accordingly

As you have read, liquid anastrozole allows for proper dose control[/quote]
I’ll definitely try to educate my Endo regarding this protocol :slight_smile:

No noticeable changes.

They seem a tad bigger and firmer but it can really vary from day to day.

Nothing major, size-wise they were always in the normal range.

I’m not very hairy; no hair on the back, little on the shoulders and chest.

Totally. In the last few years I always wondered why my calves are virtually hairless…

Yep. Since about 5 years after I started taking Finasteride I noticed some kind of “brainfog”. It will be soon 1 year since I stopped taking the medication and this issue is still very much present.

Yes. I always blamed it on stress and lack of sleep :wink:

Noise can be bothersome at time but I might say that very intense light is a lot worst. I have a lot of problems with my eyes but my ophtalmologist say my eyes are physicaly OK. He suspect a neurological/chemical issue due to my long term finasteride treatment.

My stress level is very high since I’m CEO of a videogame development studio, so I can say for sure that in the last few years I became quite short tempered. I’ve been working really hard on that but the results are not very good :frowning:

More than usual these days. Again I blame it on stress and very low energy…

Besides taking Finasteride in the past, I take some allergy medication (Aerius) during summer. I also take Nexium/Pantoloc when I have heartburns. Other than that I’m pretty much clean… I don’t drink and don’t use recreational drugs.

[quote]fish oil caps
6,000iu vit-D in 2,000 iu oil caps, double that for 2-4 weeks if not using any before.
50mg/day DHEA
Vit and mineral sups with zinc and lots of B vitamins[/quote]
I’m already taking 6,000iu vit-D3, 9 fish oil caps and 9 CLA caps a day. I also take Vit-E, Vit-C, Biotest creatine, ZMA, L-Leucine and glutamine everyday. Sadly DHEA is not available in Canada OTC. I’ll have to ask my doctor for a Rx.

I try to eat sushi and sea salt for iodine so I’ll definitely have a look at iodine supplements. As I edited in my last post, my FT4 is 12.6 (10-23), so I’m quite low… I’ll ask for FT3 next time I see my Endo.

[quote]Your doc is doing extended hCG challenge tests at this point. Whatever the outcome, you are not going to get normal that way.

You are very estrogen dominant right now. Without ant other changes you need low dose anastrozole. With TRT E2 could only go up from there if not using an AI.[/quote]
I already talked about anastrozole with my doc but she was not very keen to put me on it since its use is still very much experimental in men (in Canada). Is there a university study regarding AI uses in TRT? I already told her about Dr. Shippen and Crisler but I guess she won’t be convinced unless she sees something out of PubMed or AACE publications.

Results are all in the normal/healthy range.

[quote]We have seen severe damage from hair loss drugs before. DHT is important. A full head of hair and a limp dick is not. :slight_smile:

You need to do many thing to support vitality. If you get in TRT_AI_hCG you will have the energy to pursue other issues.

Another endo is not a good idea, as a group they are quite useless, all the more because they should have a superior grasp of these things. See if you can sell your current doc first. You can find and ask regional compounding pharmacies for referrals… they know the docs who know what to do.
[/quote]
I totally agree with you regarding Hair loss drug use… I was young and vanity was sadly the higher influence on my choice. Today I still have a head full of hair but my health was definitely not worth that. I really hope to be able to get back to my old self again one day.

Thanks again for your input and advices.
You truly live up to your reputation on this forum :slight_smile:

Aerius competes with estrogens for metabolization by liver P450 enzyme pathways. This can increase E levels which reduce T and increase SHBG that can reduce FT even further. Cimetidine is the worst and is an OTC [in USA] antihistamine that should be removed from the market.

The hair loss below the knee indicates a long term loss of T levels. Look at the legs of older guys and you will know something at a glance.

Anastrozole in smaller doses modulates estrogen levels by reducing T–>E aromatization rates. If a doc wants to lower estrogen levels, from a functional medicine point of view, this is a perfect drug, no side effects and the low dose of 1 mg/week means that there is very little chemical or metabolite loading on the body. When one reads about the side effects of Arimidex, these are not direct side effects but the effects of low estrogen. If E2 is reduced to optimal levels, the effects are only positive. For women using Arimidex to treat cancer, the goal is elimination of estrogen and the effect of that is a very sudden and deep menopausal condition. So the side effects of that include all of the problems of menopause. None of that applies to proper use in TRT. The goal is to maintain serum E2 near 22pg/ml. That is in normal range. The cannot be any medical reason for withholding this treatment based on inducing abnormal E2 levels. Your doc need to understand that E creates gene expression that counter acts the actions of T and also blocks T receptors which reduces the ability of existing T to dock into T receptors. Doc needs to know that elevated E levels, within normal range, can induce symptoms of hypogonadism even when TRT creates high levels of TT. To optimize FT level response to TRT dosing, E needs to be lower to prevent SHBG from increasing.

[quote]KSman wrote:
Aerius competes with estrogens for metabolization by liver P450 enzyme pathways. This can increase E levels which reduce T and increase SHBG that can reduce FT even further. Cimetidine is the worst and is an OTC [in USA] antihistamine that should be removed from the market.[/quote]
Interesting… I never thought desloratadine had that kind of effect on T and E. I’ll take something like Nasonex (nasal spray) instead.

[quote]The hair loss below the knee indicates a long term loss of T levels. Look at the legs of older guys and you will know something at a glance.

Anastrozole in smaller doses modulates estrogen levels by reducing T–>E aromatization rates. If a doc wants to lower estrogen levels, from a functional medicine point of view, this is a perfect drug, no side effects and the low dose of 1 mg/week means that there is very little chemical or metabolite loading on the body. When one reads about the side effects of Arimidex, these are not direct side effects but the effects of low estrogen. If E2 is reduced to optimal levels, the effects are only positive. For women using Arimidex to treat cancer, the goal is elimination of estrogen and the effect of that is a very sudden and deep menopausal condition. So the side effects of that include all of the problems of menopause. None of that applies to proper use in TRT. The goal is to maintain serum E2 near 22pg/ml. That is in normal range. The cannot be any medical reason for withholding this treatment based on inducing abnormal E2 levels. Your doc need to understand that E creates gene expression that counter acts the actions of T and also blocks T receptors which reduces the ability of existing T to dock into T receptors. Doc needs to know that elevated E levels, within normal range, can induce symptoms of hypogonadism even when TRT creates high levels of TT. To optimize FT level response to TRT dosing, E needs to be lower to prevent SHBG from increasing.[/quote]
This really make sense and I certainly hope my Endo will be willing to give me a Rx for Arimidex. Especially since I’ve started to have weird chest pain and a bit of hard tissue right below the nipple area on my left pectoral… I’m a bit worried since this started right after she upped my HcG dose to 1000iu EOD. I also noticed some fat gain in my midsection after the dosage increase…

Now, I was wondering if T+HcG+Ai is the best course of action in my case since what I ultimately want is to restore my hypothalamic-pituitary-gonadal axis to normal function if possible. I mean, if a treatment to “cure” this condition induced by Finasteride is possible (i.e.kickstart my natural T production), I would definitely prefer that to a life-long TRT process. Are you aware of some cases where idiopathic hypogonadotropic hypogonadism was reversed? Or once you are in the low T boat you are pretty much doomed to TRT?

I’ve found this study that point out in the direction that starting TRT and stopping after a few weeks could maybe reverse the situation:

High dose hCG is a bad idea. Needs to be short term. Better to use a SERM short term so the hypothalamus is driving the pituitary. You need a PCT exit and need to be keeping E2 controlled with an AI. AI needs to increase with increased hCG or use of a SERM. Do not use clomid.

hCG is the cause of your breast tissue problem.

[quote]Raoh wrote:
[… I mean, if a treatment to “cure” this condition induced by Finasteride is possible (i.e.kickstart my natural T production), I would definitely prefer that to a life-long TRT process. Are you aware of some cases where idiopathic hypogonadotropic hypogonadism was reversed?..

[/quote]

Well, yes.


Clomiphene increases free testosterone levels in men with both
secondary hypogonadism and erectile dysfunction: who does and
does not benefit?
AT Guay1*, J Jacobson2, JB Perez1, MB Hodge1 and E Velasquez1
1Center for Sexual Function (Endocrinology), Peabody, Massachusetts, USA; and 2Section of Medical Biostatistics,
Lahey Clinic Northshore, Peabody, Massachusetts, USA
Secondary hypogonadism is more common than primary gonadal failure and is seen in chronic and
acute illnesses. Although testosterone has a role in erections, its importance in erectile dysfunction
(ED) has been controversial. Hypogonadism produced by functional suppression of pituitary
gonadotropins has been shown to correct with clomiphene citrate, but with a modest effect on
sexual function. We wondered if longer treatment would produce improved results. A total of 178
men with secondary hypogonadism and ED received clomiphene citrate for 4 months. Sexual
function improved in 75%, with no change in 25%, while significant increases in luteinizing
hormone (Po0.001) and free testosterone (Po0.001) occurred in all patients. Multivariable analysis
showed that responses decreased significantly with aging (Po0.05). Decreased responses also
occurred in men with diabetes, hypertension, coronary artery disease, and multiple medication use.
Since these conditions are more prevalent with aging, chronic disease may be a more important
determinant of sexual dysfunction. Men with anxiety-related disorders responded better to
normalization of testosterone. Assessment of androgen status should be accomplished in all men
with ED. For those with lower than normal age-matched levels of testosterone treatment directed at
normalizing testosterone with clomiphene citrate is a viable alternative to giving androgen
supplements.
International Journal of Impotence Research (2003) 15, 156â??165. doi:10.1038/sj.ijir.3900981

Men with IHH can indeed regain normal pulsatile T secretion and it can be a sustained, medicine-free, remission.

That states that clomid is an alternative to “androgen supplements”. I do not see that there is long term ‘recovery’ after the clomid use is stopped. Other SERMs can do the same. Because clomid can have strong and adverse estrogen side effects, clomid should not be used. I can’t believe that they stated “viable alternative”.

“sustained, medicine-free, remission” does not follow from the abstract unless you think that clomid is not a medicine.

“responses decreased significantly with aging” is nothing really to do with clomid. It is simply aging testes that are less LH [and hCG responsive]. And libido recovery would be less also because there is more SHBG with age.

[quote]DrSkeptix wrote:

[quote]Raoh wrote:
[… I mean, if a treatment to “cure” this condition induced by Finasteride is possible (i.e.kickstart my natural T production), I would definitely prefer that to a life-long TRT process. Are you aware of some cases where idiopathic hypogonadotropic hypogonadism was reversed?..

[/quote]

Well, yes.


Clomiphene increases free testosterone levels in men with both
secondary hypogonadism and erectile dysfunction: who does and
does not benefit?
AT Guay1*, J Jacobson2, JB Perez1, MB Hodge1 and E Velasquez1
1Center for Sexual Function (Endocrinology), Peabody, Massachusetts, USA; and 2Section of Medical Biostatistics,
Lahey Clinic Northshore, Peabody, Massachusetts, USA
Secondary hypogonadism is more common than primary gonadal failure and is seen in chronic and
acute illnesses. Although testosterone has a role in erections, its importance in erectile dysfunction
(ED) has been controversial. Hypogonadism produced by functional suppression of pituitary
gonadotropins has been shown to correct with clomiphene citrate, but with a modest effect on
sexual function. We wondered if longer treatment would produce improved results. A total of 178
men with secondary hypogonadism and ED received clomiphene citrate for 4 months. Sexual
function improved in 75%, with no change in 25%, while significant increases in luteinizing
hormone (Po0.001) and free testosterone (Po0.001) occurred in all patients. Multivariable analysis
showed that responses decreased significantly with aging (Po0.05). Decreased responses also
occurred in men with diabetes, hypertension, coronary artery disease, and multiple medication use.
Since these conditions are more prevalent with aging, chronic disease may be a more important
determinant of sexual dysfunction. Men with anxiety-related disorders responded better to
normalization of testosterone. Assessment of androgen status should be accomplished in all men
with ED. For those with lower than normal age-matched levels of testosterone treatment directed at
normalizing testosterone with clomiphene citrate is a viable alternative to giving androgen
supplements.
International Journal of Impotence Research (2003) 15, 156â??165. doi:10.1038/sj.ijir.3900981

Men with IHH can indeed regain normal pulsatile T secretion and it can be a sustained, medicine-free, remission.[/quote]

Despite ksman’s objections, I answered Raoh’s question accurately.

  1. Yes, men with IHH can regain normal pulsatile T secretion, without being condemend to a life of needles, pills, expensive medicine and tests.

  2. Every man so treated had a rise in his natural LH production and measured testosterone levels; the “lower respone” rates referred to in the article are a lower frequency of remission of erectile dysfunction, not T production, among the sick , diabetic and older subjects. (i.e., correction of T levels is not sufficient to regain erectile function.)

  3. Most men with IHH can remit, and remain disease free, sithout androgen supplements. From the text of the article:
    We have found clinically that if the primary cause of the problem is corrected, clomiphene can occasionallybe tapered and stopped, and the testosterone level will remain normal (unpublished observations). The clomiphene effect on HH and ED total treatment rarely needs to be extended beyond 6months.

  4. Is clomiphene special in some way? Possibly, but probably not, and one might hypothesize that tamoxifen or AIs would be effective. But clomiphene has the most developed literature and trials in this area, and there is not one such trial for tamoxifen.

Clomid also has the many reports of messing up guys minds.

“can occasionally be tapered”
-----^^^^^^^^^^^^

Your claims might occasionally be correct. My BS meter is still going off.

I have dealt with a number of guys who had their docs try this and they did not have any progress. These were young men, typically 19-29 who had shutdown. In some cases, no known risk factors. One who did a single stupid deca only cycle, he is now doing well on T+AI+hCG and his wife is happy too. At least one other had used 5-alpha reductase inhibitors and lack of DHT seems to have made permanent changes.

5-alpha reductase inhibitors are steroid drugs, xeno steroids, that change gene expression. Possibly 5-alpha reductase inhibitors make a permanent change there that is not mediated by reduced DHT levels. When you introduce a foreign steroid into the nuclei there can be unexpected changes going on other than what is know to happen in most of the population. Which makes the risks of all of the bogus pro-hormone products severe. I have been contacted by a few who where damaged by the stuff, but they did not stay in contact so I do not know their outcomes. Genetic susceptibility does not need genomic changes, in some cases, differences will be from variation of methylation that exposes or hides genes from activation.

[quote]KSman wrote:
… My BS meter is still going off…

[/quote]

Clearly.

Thanks for the additional info!

I understand that a SERM could do the trick but Clomid is definitely out of the question… way too many horror stories related to it, especialy the permanent “eye floaters” issues.

I’ll ask my doctor about Nolvadex in order to kickstart my T production and lower my E2 (and fix that gyno problem at the same time).

BTW - I found this study to show my doc if I go with the Arimidex route :

http://www.nature.com/ijir/journal/v16/n1/full/3901154a.html

[quote]Raoh wrote:
Thanks for the additional info!

I understand that a SERM could do the trick but Clomid is definitely out of the question… way too many horror stories related to it, especialy the permanent “eye floaters” issues.

I’ll ask my doctor about Nolvadex in order to kickstart my T production and lower my E2 (and fix that gyno problem at the same time).

BTW - I found this study to show my doc if I go with the Arimidex route :

http://www.nature.com/ijir/journal/v16/n1/full/3901154a.html[/quote]

Well done!

Tamoxifen may raise the T level but the Estradiol level is not entirely predictable.

But click on your citation above, and then go to reference #6.

The story there is complicated, and the authors are trying to make a point regarding estradiol potentiation of prolactin secretion from an active tumor. But they also offer an alternative explanation for how anastrazole–with or without exogenous testosterone–can correct hypogonadism:

An alternative explanation for the recovery of endogenous
testosterone production in this patient may relate to the
powerful effect of estradiol deficiency on stimulation of
GnRH neurons. Several recent studies have confirmed the
observation that lack of estradiol serves as a more potent
stimulator of gonadotropin secretion than testosterone deficiency
on a molar basis, at both the hypothalamic and
pituitary level (25â??29).

I like this; it supports the supposed mechanism of IHH, which is a (sometiimes temporary) hypersensitivity of the the hypothalamus to estradiol which impedes pulsatile GnRH production. SO…clomiphene works for (and in effect, defnes) IHH; AIs probably work ( I have reversed infertility with them, and there are other case reports as well), and tamoxifen may well work.

(Choose tamoxifen if you will, because it is so safe, but understand that its active metabolites are much different to clomiphene’s, and you should not take any suspect meds–2D6 inhibitors–at the same time.)

They nuked the subjects with 1mg/day adex and killed E2 levels. Breast tissue shrunk. Did they discuss the side effects? The only lesson is that Arimidex lowers E2 levels and that is not new information.

What you really need is a clinical paper about using adex to modulate E2 levels, target serum E2 levels and doses to achieve that. The dose in the paper is 7 times higher that what is typically needed.

[quote]Raoh wrote:
Thanks for the additional info!

I understand that a SERM could do the trick but Clomid is definitely out of the question… way too many horror stories related to it, especialy the permanent “eye floaters” issues.

I’ll ask my doctor about Nolvadex in order to kickstart my T production and lower my E2 (and fix that gyno problem at the same time).

BTW - I found this study to show my doc if I go with the Arimidex route :

http://www.nature.com/ijir/journal/v16/n1/full/3901154a.html[/quote]

[quote]KSman wrote:
They nuked the subjects with 1mg/day adex and killed E2 levels. Breast tissue shrunk. Did they discuss the side effects? The only lesson is that Arimidex lowers E2 levels and that is not new information.

What you really need is a clinical paper about using adex to modulate E2 levels, target serum E2 levels and doses to achieve that. The dose in the paper is 7 times higher that what is typically needed.
[/quote]

You are totally right about this… I did not pay proper attention to the dosage.
Back to square 1 in my search for the right clinical paper Mission impossible theme song playing in the background :wink:

Raoh, any update?

My story sounds a fair bit like yours (especially the cognitive issues) after 12 years on finasteride.

Hi all!

Here’s a little update on my current situation.

I finally succeeded to get an Arimidex RX last week! Quite a feat, especially in Canada.

Well, it’s a step in the right direction but it’s sad that it was because my E2 doubled the month I injected 1000ui EOD of HCG :frowning: Just got the labs 2 weeks ago.

(yup, it did exactly as KSMAN said and was the cause of the chest pain…)

So here I am now, with some arimidex and HcG in hand. I need to do labs tomorrow (I’ve been off HcG for 2 months now), then I’ll start HcG and Arimidex. No T for now though, my Endo want’s to try HcG 500ui EOD and Arimidex .5mg EOD (too high right??)

Hopefully I’ll feel better on this new protocol, because I’ve been feeling very tired and lethargic lately.

I’m also trying supplementing with Reservatrol, Alpha GPC and phosphatidylserine to combat the brainfog issue. So far, it seems to help a bit but nothing miraculous.

I’ll keep you guys posted on how things go.

What happened is predicable and repeatable.

The amount if anastrozole needed is proportional to the amount if T in your system. With injections, one knows where that is going to be most of the time. With hCG monotherapy, you do not know what your T levels are without testing, so the anastrozole requirements are not predictable.

Thanks KSman. So should I start with HcG alone for a few weeks, get some bloodwork done, THEN take the Arimidex according to the E2 Levels (and get some more bloodwork in a few weeks)?

BTW, I’m also taking some Calcium D-Glucarate to better eliminate bad estrogens.