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Old 03-07-2012, 04:50 PM   #1
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REALLY IMPORTANT!! More on DHT...

Irv was at the gp's office to day and got a requisition to re-test his DHT, and to test his DHEA-S and Androstenedione. I do, however, imagine that the result is correct. We were at the prostate cancer support group last night and I was speaking to a man who was documenting the DHT levels of men on Avodart and there was a range from 300 to over 1800 or more pmol/l. As you know, Irv's DHT of over 1700 translate to about 49 ng/dl. It seems that many of these men have similar DHT results at the high end.

I found some recent abstracts on pubmed which I'm trying to understand. I don't know if the findings here cast any doubt on the validity of Avodart's ability to control the DHT which leads to castrate resistent PC. I hope some of you might be able to offer me some enlightenment on this.

Dihydrotestosterone synthesis from adrenal precursors does not involve testosterone in castration-resistant prostate cancer.

The 5α-androstanedione pathway to dihydrotestosterone in castration-resistant prostate cancer.

Dihydrotestosterone synthesis bypasses testosterone to drive castration-resistant prostate cancer.

I hope these don't indicate that Avodart may not have the same effect on cancer as we once thought.

I'm really interested in all responses to this.

Rhonda

 
Old 03-08-2012, 08:24 PM   #2
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Re: REALLY IMPORTANT!! More on DHT...

I'm wondering why I'm not getting any responses yet on my Avodart and DHT message threads. This is quite a concern for me....I'm feeling confused about the benefits of triple blockade....I so want to believe that Irv is going to beat this beast for a long time.

I hope to get some response soon...maybe with some enlightenment and renewed faith. I really wish Irv's DHT were down.

Rhonda

 
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Old 03-09-2012, 03:07 AM   #3
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Re: REALLY IMPORTANT!! More on DHT...

Quote:
Originally Posted by honda50 View Post
I'm wondering why I'm not getting any responses yet on my Avodart and DHT message threads. This is quite a concern for me....I'm feeling confused about the benefits of triple blockade....I so want to believe that Irv is going to beat this beast for a long time.

I hope to get some response soon...maybe with some enlightenment and renewed faith. I really wish Irv's DHT were down.

Rhonda
I would advice you of getting this question for your next meeting with Dr. Myers. Be sure on the units of the test results to avoid confusion.

 
Old 03-09-2012, 04:55 AM   #4
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Re: REALLY IMPORTANT!! More on DHT...

Hi Rhonda,

I'm going to need some time to look into what you have provided, including Irv's result and the studies. I hope I'll be able to do that soon.

Based on well-documented results with both finasteride and Avodart, we can be confident that these drugs are capable of supporting an anti-cancer effect. Have you taken a look at the Scholz, Lam, Strum and colleagues paper on adding finasteride to extend the vacation period? It was published in either Urology or the Journal of Urology several years ago.

Take care,

Jim

 
Old 03-09-2012, 02:41 PM   #5
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Re: REALLY IMPORTANT!! More on DHT...

Hi Rhonda (and all interested in DHT and its role in prostate cancer),

I have looked at the first study you listed ("Dihydrotestosterone synthesis from adrenal precursors does not involve testosterone in castration-resistant prostate cancer"), reading the abstract and discussion, looking at the graphic figures briefly, and glancing over some of the other parts. I also read the abstract of the study on which the study you cited was based. Thanks for calling attention to this interesting 2012 research that indicates that DHT, at least in castration resistant prostate cancer (CRPC), is mainly generated from an adrenal protein rather than more directly from testosterone. My bottom line impression is that the research underlines the importance of Avodart (dutasteride) as a way of combatting CRPC.

The paper indicates that 5-alpha reductase (5AR)is key to converting an adrenal protein to DHT. While DHT is also produced when testosterone is converted by 5AR, the research indicates that the alternate adrenal route is substantially more important. It seems clear to me that Avodart inhibits both pathways. I realize you and Irv are concerned about results that appear to indicate that his DHT has not been reduced despite Avodart, and I plan to give that more effort and thought.

One thing I noticed was that the authors of this paper were apparently not familiar with the wisdom of using two drug (LHRH-agonist + antiandrogen) and three drug hormonal blockade (LHRH-agonist + antiandrogen + 5AR inhibitor) in what they called CRPC. To those of us familiar with advanced hormonal blockade approaches, it's not really appropriate to call prostate cancer "castration resistant" (also known as "hormone refractory" or "hormone resistant") when only the LHRH-agonist drug has been used: how can you tell in that situation that it is resistant when only the front doors of the barn have been closed, but the back doors and windows are wide open? That said, I'm grateful for this thoughtful research and believe it improves our understanding of what is going on.

By the way, I just got my DHT result from last February 16, and the result was <5 with a reference range of 16 - 79 ng/dL. That's down from 5 a few months ago, with the decline probably due to more time on Avodart.

Take care,

Jim

Last edited by Administrator; 03-15-2012 at 06:17 PM.

 
Old 03-09-2012, 09:10 PM   #6
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Re: REALLY IMPORTANT!! More on DHT...

Thank you, Jim, for the time and attention you're giving this situation. I'm really happy for you that your DHT is so low, which makes me question, even more, what's going on with Irv's and the other men like him who are on Avodart.

Is there a specific time of day he should be taking it? Is there something he shouldn't be consuming when he takes it? I'd like to get to the bottom of why it isn't doing what it's supposed to be doing. Could it be that some men just produce more DHT naturally, and those are the ones who don't do as well on hormone therapy regardless of whether or not they are on triple blockade?

I'm glad that the information produced in the latest article supports the idea of taking Avodart. I just wish it would be working for Irv.

Regards, Rhonda

 
Old 03-11-2012, 03:00 AM   #7
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Re: REALLY IMPORTANT!! More on DHT...

Hi Rhonda
One of the cautions on Avodart reads

"Many drugs may affect the way that Avodart is metabolized ("broken down") in the body, leading to higher or lower than expected levels of the medication in the blood. Talk to your doctor and pharmacist before taking any prescription or over-the-counter medicines, including vitamins, minerals, and herbal products, during treatment with Avodart."



I talked to my pharmacist about what I was taking and he suggested taking in the evening. I was taking Casodex in the am and a couple of other drugs at the time. I take a number of supplements in the evening also, Omega 3, super Bio-Curcumin, Mega Lycopene and Vitamin D3 I have a hard time metabolizing the vit D so was advised to take the Lycopene by Dr Myers as it helps the absorption of the vit d. In any case it has helped my d levels. Not sure if it has any positive effect on Avodart but I have kept my level <5 ng/dl for some time.



If you are taking other supplements or drugs dutasteride you might want to review you regime with you pharmacist. I also noted that a generic dustasteride was available in Canada that would reduce the cost if Irv is staying on it.

Hope it works out.

John

 
Old 03-11-2012, 09:13 PM   #8
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Re: REALLY IMPORTANT!! More on DHT...

Thanks for your input, John. I just asked Irv and he said that he takes his Avodart at night before he goes to sleep with all his other supplements, much the same as you.

Rhonda

 
Old 03-12-2012, 12:00 PM   #9
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Re: REALLY IMPORTANT!! More on DHT...

Hi Rhonda-

You wrote:
Quote:
Originally Posted by honda50 View Post
I don't know if the findings here cast any doubt on the validity of Avodart's ability to control the DHT which leads to castrate resistent.
Just wanted to clear this up for you -- DHT does not lead to castrate resistance, nor does testosterone. It is the inhibition of these androgens with Lupron, Proscar, etc. that causes the cancer cells to adapt to the lack of androgens. That adaptation is known as castrate resistance. This is why you want vacations from androgen suppression -- to prevent that adaptation. I know you have decided to continue to suppress DHT during the vacation period, but it is not at all clear to me that this is a good idea. I haven't seen any comparative (one group on a 5ari during vacation, the other not) research that it lengthens the total time in which the cancer will remain androgen-sensitive. By suppressing the recovery of tumor-suppressing healthy cells, selecting for the viability of androgen-independent cancer cells, and preventing the androgen-induced differentiation of PC stem cells it may have the opposite effect. I don't think anyone really knows.

As for why his DHT remains normal even on Avodart ... DHT is made in a few places. Mostly from the prostate (which is out of the picture in Irv's case) and the testes and to a lesser extent in the adrenals and hair follicles. I really don't know why the Avodart is ineffective (I've seen the research you cited, but they don't apply here because he has testosterone during his vacation period and 5-a-reductase is still required). Maybe the renewed testosterone output is too much for the dose he's taking. Have you tried raising the dose?

- Allen

Last edited by Tall Allen; 03-12-2012 at 01:15 PM. Reason: forgot he's on a vacation period

 
Old 03-12-2012, 04:50 PM   #10
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Re: REALLY IMPORTANT!! More on DHT...

Hi Allen,

In one of the scientific abstracts that I read on pubmed, it explained that with Dutasteride, more testosterone is produced as compensation for the DHT block. They found that, for this reason, there's only a "modest clinical activity against CRPC".

Irv hasn't been off the hormone therapy long enough to see how much his testosterone level will jump and a double dose of Dutasteride was not considered. At the time it was checked, he was just coming off the Zoladex and Bicalutamide. His T level was at 1 which is still well below the normal range, but still slightly above castrate level.

From what I've read and understand, and I'll try to explain it simply and accurately, it's been found that the intratumoral synthesis of DHT in CRPC doesn't involve Testosterone as a precursor. (ie Androstenedione -->Testosterone -->DHT)

Instead, Prostate cancer becomes castrate resistent when DHT is generated intratumorally from the adrenal precursor steroids. The path to the generation of this DHT, (Androstenedione -->5α-dione -->DHT) requires the enzyme SRD5A1. That's when the cancer stops responding to the hormone therapy.

Avodart (Dutasteride), blocks the enzymes responsible for the synthesis of DHT, both from the Testosterone and from the Adrenal precursor steroids (ie DHEA-S). Since the transformation of Androstenedione -->5α-dione -->DHT by the SRD5A1 enzyme is required for the DHT synthesis and tumour progression, I can't see how Avodart, by blocking the SRD5A1(which increases with CRPC), CANNOT be beneficial to slow down the progression of the cancer, hopefully, BEFORE it becomes castrate resistent by blocking both pathways to DHT.

Unfortunately, nothing is perfect and the increased testosterone which is produced when the generation of the DHT is blocked will probably eventually drive the cancer. However, since DHT is considered to be the more potent of the two, I can't see it NOT being a benefit to take the Avodart in order to slow down the process.

Abiraterone, on the other hand, inhibits CYP17A1 which is required by the adrenal precursor steroid so, without that, the DHT can't be generated, thus suppressing the progression of the CRPC.

I hope this doesn't seem too technical and I hope I'm conveying the information correctly and haven't made a fool of myself by terrible misinterpretation. Nevertheless, it doesn't answer my question about Irv's DHT level being so high when he's been taking the Avodart. I can't make any sense of it at all.

 
Old 03-12-2012, 06:37 PM   #11
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Re: REALLY IMPORTANT!! More on DHT...

You have the associations right, but you have cause and effect reversed. Let me see if I can sort it out for you.

Quote:
Prostate cancer becomes castrate resistent when DHT is generated intratumorally from the adrenal precursor steroids.
This should read "When PC becomes castrate resistant, DHT is generated intratumorally..." Intratumoral DHT is not the cause of castrate resistance, it is merely one of the results of that happening.

Quote:
I can't see how Avodart, by blocking the SRD5A1(which increases with CRPC), CANNOT be beneficial to slow down the progression of the cancer, hopefully, BEFORE it becomes castrate resistent by blocking both pathways to DHT.
Castrate resistance is the result of blocking DHT and testosterone. If you never use ADT, the cancer might stay hormone-responsive. Of course, it's the androgens that spur the cancerous proliferation, so you would not want to do that.Testosterone and DHT seem to have important anti-proliferative roles to play in addition to their pro-proliferative roles. Intermittant ADT potentially finds a happy medium, alternating periods where you are blocking growth of the cancer with periods when you are preventing it from becoming castrate resistant.

Hormone therapy is a very complex matter and probably won't proceed in the same way in any two people.

- Allen

 
Old 03-12-2012, 08:55 PM   #12
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Re: REALLY IMPORTANT!! More on DHT...

So how would one know if continuing with Avodart is a wise choice or not? I know a woman who went with her husband to see Dr. Myers and Dr. Myers told them that it would be foolish not to continue with the Avodart.

Also, how would you explain the findings that Avodart prolongs the time to further treatment for men on Active Surveillance?

Finally, how does one know the ideal time to remain on the hormone therapy before coming off in intermittent ADT?

Rhonda

Last edited by honda50; 03-12-2012 at 08:57 PM.

 
Old 03-12-2012, 09:42 PM   #13
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Re: REALLY IMPORTANT!! More on DHT...

The abstract explains that, with hormone therapy, eventually resistence to testosterone deprivation occurs with CRPC and is driven by the intratumoral synthesis of DHT.

So, keeping in mind what you're saying that DHT is generated when the PC becomes castrate resistent, how would you explain the above, specifically with the use of the word "driven"? If the synthesis of DHT drives the resistance to the testosterone, wouldn't that be the same as the synthesis of DHT drives the castrate resistant prostate cancer? That seems to make sense to me, afterall, it seems that the objective of both Avodart and Abiraterone**, in different ways is to block the generation of DHT which is considered to be a potent fuel for the cancer.
**(Abiraterone blocks CYP17A1 which is needed by the Adrenal Precursor steroids which generate DHT intratumorally in CRPC),

I understand that the point of intermittent therapy is two-fold, to rid the body of the harmful side effects, but also to .....hmmm....I'm thinking..."dumb-down" the pc so it doesn't have the chance to become resistent to the androgens (or grow independent of the androgens)....by putting the androgens back into the system so the cancer begins to rely on them again. Would that be a correct interpretation?

So, I guess the question would be whether or not it would be detrimental or beneficial to continually try to suppress DHT, while allowing the Testosterone to be brought back into the system during the "off" period. In other words, would the presence of testosterone alone have the same effect on "dumbing-down" (sorry...my impression...best way I can explain it) the PC and extending the time to CRPC?

According to the abstract I read on pubmed, it seems that there is only a "modest" clinical activity against CRPC with the Avodart. The reason for that is, when the DHT is suppressed, the Testosterone level is increased. PC relies on both Testosterone and DHT, with DHT being the more potent fuel. However, if Testosterone is increased, then that will partially compensate for the DHT. That being said, I think that this indicates a small benefit since DHT is the more potent fuel. This, of course, does not result in a life-time control of the cancer but, hopefully, will extend the time to castrate resistance.

With all of that in mind, I still don't know how this will translate in Irv's case as it seems his DHT has not been driven down, in spite of the Avodart. In fact, the DHT has not been driven down by the Zoladex or Bicalutamide either....while his PSA has been successfully dropped down to an undetectable level....Go figure. At any rate, Irv will be getting his blood taken on Wednesday to get his first PSA result after coming off Zoladex and Bicalutamide. My greatest hope and prayer is that his PSA doesn't rise too quickly. I'd like to see him have a decent break off the heavy meds...and if his PSA rises too quickly, my greatest concern will be that his time to castrate resistance could be reduced.

Rhonda

Last edited by honda50; 03-12-2012 at 09:53 PM.

 
Old 03-13-2012, 01:28 AM   #14
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Re: REALLY IMPORTANT!! More on DHT...

What it says is that the tumor is able to grow in spite of external testosterone (or external DHT) deprivation because the cancer cells make their own DHT internally. The internal DHT then "drives" the cancer cell growth while in this castrate-resistant state; i.e., it becomes self-sufficient. It goes on to say that abiraterone can block the internal synthesis of DHT, although even that doesn't last forever. I don't see how Avodart can prevent internal DHT synthesis -- how would it get inside the cell?

As for your other questions... I think anyone who tells you that they know what will happen is not being totally honest with you. I think many doctors (like your own, I think?) suspect 5aris may not be helpful and may even be harmful during the off periods. I certainly understand why they might believe that. Others, like Dr Myers, may suspect that it may be helpful. These are all suspicions, not based on any clinical trials I know of.

This is very different from its use in active surveillance where the cancer is known to be indolent or minimally invasive. One does not suppress testosterone during AS and one does not have to worry about such cancers becoming androgen insensitive. In fact, testosterone may play a role in preventing the cancers from progressing, since it is well established that hypogonadal men experience more aggressive cancers.

Prostate cancers differ considerably from person to person. There are several different kinds of human PC that are grafted into mice for lab tests and they all behave differently. It is likely that different hormone strategies will work for different people.

As for the ideal timing, again, no one knows for sure, but I think the doctors who have developed the recent mathematical models I spoke of in another post will be the first to be able to answer that for the individual.

I know you are looking for black and white answers, but I fear you are not apt to find them anytime soon.

- Allen

 
Old 03-13-2012, 08:41 AM   #15
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Re: REALLY IMPORTANT!! More on DHT...

This newer “wave” of findings with regards to the intratumoral affairs of cancerous cells is revolutionizing the methods used in the hormonal treatment, and professionals will have to adjust and follow suit. After all, you have to feed the beast to keep him quiet.

In a past thread I have discussed with Jim about the importance of cells behaviour.
(http://www.healthboards.com/boards/cancer-prostate/833991-benefits-intermittent-modality-hormonal-treatment-2.html)

These human little parts are all prepared to adapt to newer environments to survive, and when threatened they will do what it is necessary even in activating their tinny androgen “factories” to produce their own food (intratumoral androgens).
The newer drugs have been conceived to address these activities and one should just hope that scientist lead their findings and purposes to success. The old ways in treatment may become obsolete.

It seems that Alpha Reductase Inhibitors in the hormonal context are important and not necessarily influencing the “behavioural adaption” of cancer cells, to consider any intratumoral production of androgens, even if one takes it continuously.
In any case, I have no doubts in the need of changing the traditional hormonal treatment to include the overall context of the treatment. Anecdotally speaking, I see the present setting like this;

Testes and Adrenal Glands produce androgens and cancer cells survive by feeding on androgens (mostly common referred as Testosterone and Dihydrotestosterone). HT therefore will try to “kill” or manage the cancer advancement by starving the cells cutting their feeding routes.

Using traditional HT drugs one can reach to castration levels of androgens (circulating in the body) of 95% with LHRH agonists. I say this just by comparing the testosterone proteins alone in their normal levels of 400 ng/dL against the castrate at 20 ng/dL.
The 5% in circulation is then considered the “culprit” of the problem for feeding the cancer which will allow it to survive.
Without any weapon (or possibility) to stop the “total production” of androgens (we need them for other system functions), specialists use tactics to prevent the androgens from being ingested by the cells, simply zipping their “mouths” (receptors), using the "sticky" antiandrogen drugs.

Still going further, they use 5-ARI drugs, to prevent “production” of dihydrotestosterone, which is considered tenfold more powerful than its sibling, the testosterone.
These tinny “super-calories” could provide the cells an extension in their surviving times ten “clocks” more than if they were fed on testosterone. This is a good reason why we should consider the drug in our protocols.

The overall is therefore what we know at present times as Total Blockade (or Total Androgen Deprivation Therapy), however that does not count with the intratumoral blockade.

In any case, the small percentage of androgens circulating in the body is being manufactured everyday and is consumed by the whole body, and by those cells that managed to unzip their “mouths” or strive through other means.

This situation is noticed when one has low levels of androgens in circulation but the cancer is active as expressed in a rising PSA. The case (patient) is then referred as Hormone Refractory Prostate Cancer (HRPC).
This is an ambiguous situation because it looks into refractory from the traditional hormonal drugs. It does not include the so called Intratumoral activities that have been taking place all along, probably in a dormant behaviour, which existence nobody knew.

The “antiandrogen withdrawal syndrome” is also a short lived phenomenon. At such times the intratumoral activity is taking the lead in the advancement of the disease with or without the ARI drugs.

Regards.

Baptista

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