T Nation

Mentality of My M.D.

A few days ago I had an appt regarding what I suspected was an enlarged prostate (weak urine flow, urgency.)
Bloodwork was done, including T.

I was pleased with my T numbers: total 806 (181-758)
free 22.0 (7.2-23.0)
I receive an email telling me to take one packet of Androgel instead of my usual 2 because my T is “slightly high.”

Right from the get go it was clearly understood between us that I wanted to shoot for the high end of the range, and he wants to reduce my dosage by half.

I am also to begin taking Avodart to shrink the prostate.
Avodart is an androgen inhibitor!
My limited research tells me it prevents conversion of T to DHT by 90%, thus gradually shrinking the prostate.

Anyone have knowledge on DHT? Will this cancel out my Androgel?

I know, I need a new Doc, this is ridiculous.

What was your Estradiol? That is what is making your prostate big.

Do not take Avodart. That will F you up.

You want DHT.

You’re right, get a new doc, preferably with “D.O.” instead of “M.D.”

[quote]bigdawg011 wrote:
You’re right, get a new doc, preferably with “D.O.” instead of “M.D.”[/quote]

I would have to say the exact opposite of this. I almost died because of a D.O. that had to be bailed out by some M.D.'s who knew what was wrong with me within a few minutes.

If someone referred me to a D.O., I wouldn’t show up for the appointment.

[quote]fedorov wrote:
A few days ago I had an appt regarding what I suspected was an enlarged prostate (weak urine flow, urgency.)
Bloodwork was done, including T.

I was pleased with my T numbers: total 806 (181-758)
free 22.0 (7.2-23.0)
I receive an email telling me to take one packet of Androgel instead of my usual 2 because my T is “slightly high.”

Right from the get go it was clearly understood between us that I wanted to shoot for the high end of the range, and he wants to reduce my dosage by half.

I am also to begin taking Avodart to shrink the prostate.
Avodart is an androgen inhibitor!
My limited research tells me it prevents conversion of T to DHT by 90%, thus gradually shrinking the prostate.

Anyone have knowledge on DHT? Will this cancel out my Androgel?

I know, I need a new Doc, this is ridiculous.[/quote]

Your doctor is doing the right thing!! You want your test levels to be in the normal range so you don’t have to worry about your prostate. If test has anything to do with prostate problems is for another thread.

Androgel is so weak that dropping it by half is not that much of a big thing. Before you drop your doc on the grounds that you know more then he does, which is what I get from your post, I suggest you do what he says and see if it doesn’t work first.

The big problem I see from what you have posted is there is no connection from your weak stream problem and your prostate. Have you had a digital exam? What is your PSA?? Just because you can’t pee like a race horse anymore doesn’t mean that you have an enlarged prostate.

If your doctor hasn’t done a digital exam before there is no way for him to tell if it has gotten bigger. And I understand why he wouldn’t have done one. Would you like sticking your finger up your ass every day?? No wait don’t answer that.

One of the big problems in medicine is thinking that because you are doing X it is causing Y. I’m not convinced, or even swayed, that your use of Androgel has anything to do with your weak stream.

On a personal note I have chronic pain. The pain meds I take dramatically affect my stream when I pee. This is not from an enlarged prostate it is from a weakening of the bladder wall. I’m also sure that your doc is responding to what you tell him. If you go in and say “Doc my prostate is causing my stream to be decreased” or anything like that he will start to think along those lines. He is only human after all.

So if I was you I would split the difference. Drop the andro in half, because we do know your test level are above max, and not take the Avodart, because we don’t know that there is a prostate problem, until you have at lest confirmed that you do have an enlarged prostate. Get your PSA score and have your doc get very familiar and stick his finger up your butt. Who knows maybe he will take you out to dinner first.

PS I hope you see that there is humor as well as solid advice in this post.

DHT is needed to support the sex organs and libido. Reducing DHT can cause some serious problems.

The biggest problem for the prostate is estrogen, not T or normal DHT levels that occur with TRT. Using an AI could create some serious improvements.

TT in the high normal range is not a concern for BPH. If cancer does exist, that may be a serious issue.

Digital exam showed enlargement. PSA indicated no cancer.
6 months on 1 mg adex.
Tried saw palmetto for the past twelve weeks, nothing.
Pissing 5 times a night doesn’t cut it. Something has to be done. WTF.

[quote]fedorov wrote:
Digital exam showed enlargement. PSA indicated no cancer.
6 months on 1 mg adex.
Tried saw palmetto for the past twelve weeks, nothing.
Pissing 5 times a night doesn’t cut it. Something has to be done. WTF.[/quote]

Getting E2 into the lower 20’s can be helpful. Note that tissue changes take some time. Coversely, elevated E makes things worse and can be a primary promoter of BHP.

My TT is over 1000 and my E2 is close to 20. My prostate is better now than before TRT over almost 2 years. During that period, one would expect BHP to progress.

The guess that T causes BHP is a persistant [non]fact in the medical community.

One thing that is true, is that T alone will raise E2 and that can make things worse. Given how many doctors do not understand the many issues with E2, the T-BHP connection is a truth under that level of ignorance.

My TT is over 1000 also and my E2 is mid 20’s. I NEVER have trouble peeing and my last digital was “perfect” and my PSA score is 1.0 w/a free% of 50%. It’s still small, happy and not enlarged.

I just started 1mg/day of finesteride to see if the “monkey butt” on the top/back of my head will go away, if it doesn’t show improvement in a month, I’ll stop taking it, and leave my prostate alone, as DHT is a good hormone to have. (Unless it takes away your hair.) Also on 60 drops (2.0mg) of liquid adex a week too.

[quote]fedorov wrote:
Digital exam showed enlargement. PSA indicated no cancer.
6 months on 1 mg adex.
Tried saw palmetto for the past twelve weeks, nothing.
Pissing 5 times a night doesn’t cut it. Something has to be done. WTF.[/quote]

For one thing do not trust the PSA test. Those can really be misleading. Do a little googling on PSA test and find articles on their accuracy. They are not that good. There is a new PSA test that is much more accurate, but many labs are still following the older (and cheaper) protocol. I would try to find out if the lab is doing the old or new. Also a urologist can do a ultrasound that is much better for finding mumps and malformations on the gland then having him digging for gold up you exhaust pipe.

You can have cancer and still have a good PSA number. There is only one way to know if you prostrate cancer and that is with the biopsy. If your prostrate is swollen and you are having problems, suck it up and do the biopsy. Yeah it does hurt, but think of the alternative. I had a prostrate cancer scare a couple of years ago. And went through it all. The peace of mind was well worth the short term picking and prodding.

1 Like

[quote]KNB wrote:
My TT is over 1000 also and my E2 is mid 20’s. I NEVER have trouble peeing and my last digital was “perfect” and my PSA score is 1.0 w/a free% of 50%. It’s still small, happy and not enlarged.

I just started 1mg/day of finesteride to see if the “monkey butt” on the top/back of my head will go away, if it doesn’t show improvement in a month, I’ll stop taking it, and leave my prostate alone, as DHT is a good hormone to have. (Unless it takes away your hair.) Also on 60 drops (2.0mg) of liquid adex a week too.
[/quote]

More on DHT:

A B2 blocker for stomach problems, cimedidine , is known to reduce libido. It was thought that it could be used to reduce prostate cancer risks, but research trials were not conclusive. What is known is that it interferes with DHT at the DHT receptors in the prostate… because they looked at prostate DHT receptors. But how does cimedidine affect DHT and other steroid receptors in the body? Unknown of course. But what is known is that taking cimedidine can reduce or kill one’s libido. There is a lesson in that.

Cimedidine is also a good anti-viral that can be of (off label) use with the flu. Many drugs have multiple effects and only one typically gets disclosed with drug marketing and labelling.

I have seen some horror stories (rare) about finasteride and other 5 alpha reductase drugs, here and elsewhere. Permanent hormone system damage after ‘temporary’ DHT reduction. This drug was developed and the market established based on the premise that DHT causes BPH. Now it is known that E2 is the biggest thread to the prostate… but few in the medical community understand this. Some have been damaged using these drugs to combat hair loss. Loss of libido is a frequent result. Again, DHT is important for many reasons. Many aspects of DHTs actions are not well understood. With that ignorance, those who stand to profit by selling these drugs can hide safely behind what is not well understood, even though there are strong indications of adverse actions.

dogsoldier, good input. I have decided to get a second opinion with a urologist and continue to research PSA.

KSman, I appreciate the info. I will also continue to research DHT and try to get a better handle on this situation.

[quote]KSman wrote:
KNB wrote:

More on DHT:

I have seen some horror stories (rare) about finasteride and other 5 alpha reductase drugs, here and elsewhere. Permanent hormone system damage after ‘temporary’ DHT reduction. This drug was developed and the market established based on the premise that DHT causes BPH. Now it is known that E2 is the biggest thread to the prostate… but few in the medical community understand this. Some have been damaged using these drugs to combat hair loss. Loss of libido is a frequent result. Again, DHT is important for many reasons. Many aspects of DHTs actions are not well understood. With that ignorance, those who stand to profit by selling these drugs can hide safely behind what is not well understood, even though there are strong indications of adverse actions.[/quote]

I agree that DHT is important generally, and that estradiol is underappreciated as a contributor to BPH. But I offer a contradictory observation, just for laughs:

There is a single gene mutation which causes the deficiency of 5 alpha reductase. The result is “pseudohermaphroditism,” in which genotypic males have ambiguous genitalia. When they reach puberty, funny changes happen to their genitalia, inside and out. But they retain only a rudimentary prostate, even though they have high T, low or no DHT and high or uneffected estrogens. This “natural history” experiment suggest that DHT is the dominant cause of prostate stromal and cellular mainteneance or hyperplasia, and physiologic estrogen is much less important.

In another thread, I posted a couple articles—among many–that confirm that AIs reduce estrogen in men but do not effect BPH; perhaps T and DHT rise enough to “undo” the effect or estrogen isn’t that important.

Further, in and non-castrated men with prostate cancer, estrogen at high doses decreases prostate volume; whether this is due to a direct effect or T/DHT remains a mystery to me. But because estrogens and progesterones, in high doses, work in castrated men, there is a direct effect on prostate cancer and tissue to reduce prostate volume.

Re the Saw Palmetto. I recently heard an arguement that 'no one ever died of a lack of Saw Palmetto". That is correct, they call it Prostate Cancer. I have been taking a Life Plus Prostate Formula, and Proanthanol for 10+ years. I think anyone over 45 should spend the $22.00 a month, and will never “notice” anything. At 64 years my PSA is the lowest of any man my MD has as a patient. I get a blood test every 6 months. Staying healthy is a lot more fun that having fingers up your butt.

We work out to survive, to pass on our genes, and be healthy. Doing the stuff you are supposed to do works. I ride the bike 4 & 5 time a week for 45 minutes, full body workout 2@ wk, and fun lifting 1 or 2 days a week.

It sounds good to say we need to ‘research’ more of…I did the reading years ago, spend $45.50 @ month on the Proanthanols Bio Complex, and $22.00 each two months on the Prostrate Formula. That is about $60.00 @ month for a health status well beyond most men. Oh, that’s right, insurance does not cover them. Is it better to save $720.00 a year and die, or be unhealthy? And I do not sell this, I buy it.

phil, thanks for the response.

The “organic” preventitive measures you have taken have possibly worked, but then again pehaps you were never programmed hormonally to develop BPH.

My situation is not preventitive. I’ve got to reduce the size now.

Any readers ot there who have been through this?

Even though DHT reducing compounds in high dosage can be very bad for some, you might try the liquid version, using 1mg/day to possibly help the shrinkage. It’s possible after using adex for 1mg/week a low dose may help.
I still haven’t seen the results of your E2 test, and it’s possible being on gel T, 1mg/week of adex isn’t enough. My doc “puts everybody” on HRT on 2mg/week of adex. He does do the b/w obviously, so don’t misunderstand…
I have tried 1.5mg/week and the bacne is unbearable, so I am now at 50 drops a week instead of 60, and no zits, and no woodie issues either. I’ll stay at 50 until I get access to a lab that gives better results than >32.

[quote]fedorov wrote:
phil, thanks for the response.

The “organic” preventitive measures you have taken have possibly worked, but then again pehaps you were never programmed hormonally to develop BPH.

My situation is not preventitive. I’ve got to reduce the size now.

Any readers ot there who have been through this?[/quote]

Ok. I know I have no “street/blog” cred.
But I will say it anyway:

  1. Your doctor is not crazy.
  2. Randomized trials of saw palmetto and its extracts for BPH are repeatedly negative: no benefit better than placebo.
  3. Make sure that you do not have chronic prostatitis (which is much more likely in a young man than significant BPH). Antibiotics (cipro, bactrim, levaquin for 2 to 3 weeks) and ibuprofen can work wonders. (A trial of ibuprofen for you, if it works, will tell your doctor a lot.)
  4. Avodart works–a little–for BPH, but not chronic prostatitis. It is not poisonous. It can cause gyno or diminished libido. It will not turn you into a girl scout. It does not block T to an important degree. (In fact, because Avodart also blocks the skin reductase, your Androgel may become more effective.) I have found no information on permanent side effects.

[quote]DrSkeptix wrote:
KSman wrote:
KNB wrote:

More on DHT:

I have seen some horror stories (rare) about finasteride and other 5 alpha reductase drugs, here and elsewhere. Permanent hormone system damage after ‘temporary’ DHT reduction. This drug was developed and the market established based on the premise that DHT causes BPH. Now it is known that E2 is the biggest thread to the prostate… but few in the medical community understand this. Some have been damaged using these drugs to combat hair loss. Loss of libido is a frequent result. Again, DHT is important for many reasons. Many aspects of DHTs actions are not well understood. With that ignorance, those who stand to profit by selling these drugs can hide safely behind what is not well understood, even though there are strong indications of adverse actions.

I agree that DHT is important generally, and that estradiol is underappreciated as a contributor to BPH. But I offer a contradictory observation, just for laughs:

There is a single gene mutation which causes the deficiency of 5 alpha reductase. The result is “pseudohermaphroditism,” in which genotypic males have ambiguous genitalia. When they reach puberty, funny changes happen to their genitalia, inside and out. But they retain only a rudimentary prostate, even though they have high T, low or no DHT and high or uneffected estrogens. This “natural history” experiment suggest that DHT is the dominant cause of prostate stromal and cellular mainteneance or hyperplasia, and physiologic estrogen is much less important.

In another thread, I posted a couple articles—among many–that confirm that AIs reduce estrogen in men but do not effect BPH; perhaps T and DHT rise enough to “undo” the effect or estrogen isn’t that important.

Further, in and non-castrated men with prostate cancer, estrogen at high doses decreases prostate volume; whether this is due to a direct effect or T/DHT remains a mystery to me. But because estrogens and progesterones, in high doses, work in castrated men, there is a direct effect on prostate cancer and tissue to reduce prostate volume.

[/quote]

Shutting down the HPTA with estrogen or progesterone will reduce LH, T and DHT. This is useful for testosterone receptor positive prostate cancer. With HPTA shutdown, pregnenolone and DHEA levels probably fall as well.

I think the situation with men on TRT is quite different. They have higher levels of TT, FT and DHT. When an AI is used, the TT, FT and DHT levels will not change significantly, but E levels drop. There can be positive results for BPH.

Men with syndrome X or metabolic disorder have a much higher incidence of prostate problems. As a group they have low TT, FT, DHT and high or elevated levels of E2.

It would require a long term study to show that AI reduction of E would reduce BPH or reduce its progression. Such a study may need to address reduction of E to different levels and perhaps reduction would have to be to less that some number like 25mg/ml to so benefits.

Yes the prostate and other genitalia require DHT to develop. I think that your reach to E not been important is a bit of a reach.

[quote]KSman wrote:
DrSkeptix wrote:
KSman wrote:
KNB wrote:

More on DHT:

I have seen some horror stories (rare) about finasteride and other 5 alpha reductase drugs, here and elsewhere. Permanent hormone system damage after ‘temporary’ DHT reduction. This drug was developed and the market established based on the premise that DHT causes BPH. Now it is known that E2 is the biggest thread to the prostate… but few in the medical community understand this. Some have been damaged using these drugs to combat hair loss. Loss of libido is a frequent result. Again, DHT is important for many reasons. Many aspects of DHTs actions are not well understood. With that ignorance, those who stand to profit by selling these drugs can hide safely behind what is not well understood, even though there are strong indications of adverse actions.

I agree that DHT is important generally, and that estradiol is underappreciated as a contributor to BPH. But I offer a contradictory observation, just for laughs:

There is a single gene mutation which causes the deficiency of 5 alpha reductase. The result is “pseudohermaphroditism,” in which genotypic males have ambiguous genitalia. When they reach puberty, funny changes happen to their genitalia, inside and out. But they retain only a rudimentary prostate, even though they have high T, low or no DHT and high or uneffected estrogens. This “natural history” experiment suggest that DHT is the dominant cause of prostate stromal and cellular mainteneance or hyperplasia, and physiologic estrogen is much less important.

In another thread, I posted a couple articles—among many–that confirm that AIs reduce estrogen in men but do not effect BPH; perhaps T and DHT rise enough to “undo” the effect or estrogen isn’t that important.

Further, in and non-castrated men with prostate cancer, estrogen at high doses decreases prostate volume; whether this is due to a direct effect or T/DHT remains a mystery to me. But because estrogens and progesterones, in high doses, work in castrated men, there is a direct effect on prostate cancer and tissue to reduce prostate volume.

Shutting down the HPTA with estrogen or progesterone will reduce LH, T and DHT. This is useful for testosterone receptor positive prostate cancer. With HPTA shutdown, pregnenolone and DHEA levels probably fall as well.

I think the situation with men on TRT is quite different. They have higher levels of TT, FT and DHT. When an AI is used, the TT, FT and DHT levels will not change significantly, but E levels drop. There can be positive results for BPH.

Men with syndrome X or metabolic disorder have a much higher incidence of prostate problems. As a group they have low TT, FT, DHT and high or elevated levels of E2.

It would require a long term study to show that AI reduction of E would reduce BPH or reduce its progression. Such a study may need to address reduction of E to different levels and perhaps reduction would have to be to less that some number like 25mg/ml to so benefits.

Yes the prostate and other genitalia require DHT to develop. I think that your reach to E not been important is a bit of a reach.[/quote]

Thanks for your thoughts!

  1. I attempted, and failed, to make a distinction between physiologic estrogen and pharmacologic estrogen. Physiologic E levels seem to contribute something, but my point was how difficult it is to separate the effects of T/DHT from E in the intact man under trial with AIs. (Some studies are indeed long enough; a year and more). E and Progesterones work in previously castrated men with hormone-sensitive prostate cancer, so at pharmacologic levels, the effect on prostate tissue cannot be dependent on LH action on absent testes.
  2. The points about metabolic syndrome are well taken; and hypogonadism is both cause and effect of the syndrome, which is at root, a form of insulin resistance and hyperinsulinemia. Epidemiologic studies are divided on some points on cancer risk, but do support a higher risk for BPH. It is plausible that higher E:T ratio is responsible for BPH in this cohort—and that would be a fairly simple longitudinal study, but it hasn’t been published yet.
  3. I respect your thoughts, but to be practical, I also emphasize that specific inhibitors of 5 alpha reductase do work to decrease BPH (a little); so far, specific AIs or SERMs do not work in statistically valid trials. (Toremifene is under trial and won’t work where tamoxifen doesn’t work). One study I found addresses your comment about T replacement along with AI: the AI raised T by 40%, lowered E dramatically, but there was no reduction of BPH. (If you have a reference for a study of combined TRT and AI effect on BPH, I would be grateful.)

But all that does not argue against a contribution of E to prostate problems; it just provokes more analysis…

Do you think Anastrazole can increase DHT?