Lupron yeah or Lupron nay that is the question.

I would like to know how long is too long on Lupron and still be able to keep my quality of life. Cancer was found in one of 12 biopsies. went through 45 radiation treatments with no problem. was started on Lupron 2 weeks before my radiation and then a second shot 3 months later. I am leary about doing these shots for 18 months and still keep my quality of life. afraid my testosterone will not come back at all. cancer was not found anywhere else, it was caught real early.any input would be greatly appreciated

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I would like to know how long is too long on Lupron and still be able to keep my quality of life. Cancer was found in one of 12 biopsies. went through 45 radiation treatments with no problem. was started on Lupron 2 weeks before my radiation and then a second shot 3 months later. I am leary about doing these shots for 18 months and still keep my quality of life. afraid my testosterone will not come back at all. cancer was not found anywhere else, it was caught real early.any input would be greatly appreciated

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Diagnosed in late 18. PSA of 29, cancer in all biopsies. 24 months of Lupron [3 month shot] with 44 treatments of radiation. I am now 65. As you say, radiation is not the problem. Before being diagnosed, I could walk 18 holes and mow the yard the next day. Now fatigue takes its toll still with hot flashes and weight gain. Quality of life? I am still alive and grateful for that. I still do what I want to do in moderation. I have great support from family and friends. I heard that for as long as you are on Lupron, it will take that long after to get over side effects. Myself. I am looking forward to the end of this year.

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Here's my clinical history.

I was on Lupron for 18 months (see my clinical history in the attached chart).

Side Affects I experienced (keep in mind the Bell Curve...):

Hot Flashes.
Weight gain (10-15 pounds)
Fatigue
Muscle and joint stiffness.
Penis and testicle shrinkage.
I did not experience loss of libido nor depression.

As you can see from my clinical history, My T returned, interestingly, higher than when I started.

As others have said, loss of T does not results in all PCa cells dying.

Here's an explanation I found, why monotherapy only kicks the can down the road. For years, the medical community's thought process was monotherapy, try one treatment, when it fails, try the next, repeat, the end state was death when you ran out of treatments. Today, that dog won't hunt...Here's a quote from Alicia Morgan that I like and agree with:

“All signs clearly demonstrate that adding something (an androgen receptor signaling inhibitor (ARSI), or docetaxel chemotherapy, or both) to the traditional ADT backbone benefits patients in terms of disease control and quality of life outcomes. With more than a decade of experience using most of these agents, we can hardly say that we are not yet comfortable managing the side effect profiles that they confer. Further, it is disingenuous to suggest that a majority of the patients in our clinical practices have absolute contraindications to the use of an ARSI in combination with ADT. Why, then, have we as a field failed approximately half of our patients and not combined ADT with an ARSI or docetaxel (or a combination of both) in treating their mHSPC? Although I could identify a number of potential reasons, none seem sufficient to justify withholding these treatments from our patients. Rather than scratching our heads, pointing fingers, or debating further, it is time to come together as a group of clinicians, patients, and loved ones and stop the practice of using ADT alone. Our patients deserve combination treatment or a clear understanding of why this is not what will serve them best, and we owe it to them to achieve the outcomes that we know are possible. ADT alone is not enough, and it is time to act on the data and provide the care that every one of our patients deserves.”

In every prostate tumor, there are three different types of cells:
1 Fully androgen sensitive .
2 Partially androgen sensitive.
3 Fully Androgen resistant.
But the percentage of these three types of cells vary from man to man. One man can have 99% Androgen sensitive, 1/2% Partially resistant and 1/2 % Androgen resistant whereas another man can have 50% Androgen Sensitive 25% Partially Androgen sensitive and 25% Androgen resistant cells.
How do we find out what ratio one particular man has? A simple clue is Nadir PSA...meaning how low the PSA dropped in the first year of ADT. If it dropped say, 99.5% from top then, that man has most of his cancer cells as Androgen sensitive.
Coming to Chemotherapy...How does Chemo work...Chemo works by killing ALL cells which are growing...Chemo is an equal opportunity killer for all growing cells...whether Androgen sensitive or Androgen resistant.
Based on this, we can say Chemo will work well and needed early on in man who have high percentage of Androgen Resistant cells. The man with very high Androgen sensitive cells can always wait till way later for Chemo as ADT can keep his PCa controlled for a long time.
The use of early Chemo should be based on individual subtype and degree of Androgen Resistance.

As to the length of time on ADT, well, there are medical folks who are stuck in the mud who simply say lifelong ADT and when you become castrate resistant, we'll try the next thing...

Many clinical trials have looked at this and as you might expect, the results are all over the map. I have seen a number that point to lifetime of ADT or until castrate resistance (which can be very soon or as others who have responded, a long time...) not useful in terms of progression free survival or overall survival.

For guys doing SRT, six months, for others, 18-24 months.

I think part of the answer lies in your response to ADT, how rapidly did your PSA respond, did your T drop to <20 and stay there, did your PSA become undetectable and stay there. If you stop, then have a plan o actively monitor...in my case I have labs and consult with my urologist every 2-4 months.

My T did return as the chart shows. Again, Bell Curve...Not all men are as fortunate. I have seen some data that may point to exercise playing a role...I work out 5-7 times a week, swim, ride my bike, elliptical, ski, hike in the mountains, yard work, walk our dog.

There has been a new oral ADT which may be used in place of Lupron. https://www.fda.gov/news-events/press-announcements/fda-approves-first-oral-hormone-therapy-treating-advanced-prostate-cancer#:~:text=FDA%20Approves%20First%20Oral%20Hormone%20Therapy%20for%20Treating%20Advanced%20Prostate%20Cancer,-Share&text=Today%2C%20the%20U.S.%20Food%20and,patients%20with%20advanced%20prostate%20cancer. It's advantage are:

Faster drop of T than Lupron, no flare.
Better cardiovascular side affect profile.
Faster return of T.

Again, as to the return of T, well, keep in mind the Bell Curve.

Jump to this post

Here's my clinical history.

I was on Lupron for 18 months (see my clinical history in the attached chart).

Side Affects I experienced (keep in mind the Bell Curve...):

Hot Flashes.
Weight gain (10-15 pounds)
Fatigue
Muscle and joint stiffness.
Penis and testicle shrinkage.
I did not experience loss of libido nor depression.

As you can see from my clinical history, My T returned, interestingly, higher than when I started.

As others have said, loss of T does not results in all PCa cells dying.

Here's an explanation I found, why monotherapy only kicks the can down the road. For years, the medical community's thought process was monotherapy, try one treatment, when it fails, try the next, repeat, the end state was death when you ran out of treatments. Today, that dog won't hunt...Here's a quote from Alicia Morgan that I like and agree with:

“All signs clearly demonstrate that adding something (an androgen receptor signaling inhibitor (ARSI), or docetaxel chemotherapy, or both) to the traditional ADT backbone benefits patients in terms of disease control and quality of life outcomes. With more than a decade of experience using most of these agents, we can hardly say that we are not yet comfortable managing the side effect profiles that they confer. Further, it is disingenuous to suggest that a majority of the patients in our clinical practices have absolute contraindications to the use of an ARSI in combination with ADT. Why, then, have we as a field failed approximately half of our patients and not combined ADT with an ARSI or docetaxel (or a combination of both) in treating their mHSPC? Although I could identify a number of potential reasons, none seem sufficient to justify withholding these treatments from our patients. Rather than scratching our heads, pointing fingers, or debating further, it is time to come together as a group of clinicians, patients, and loved ones and stop the practice of using ADT alone. Our patients deserve combination treatment or a clear understanding of why this is not what will serve them best, and we owe it to them to achieve the outcomes that we know are possible. ADT alone is not enough, and it is time to act on the data and provide the care that every one of our patients deserves.”

In every prostate tumor, there are three different types of cells:
1 Fully androgen sensitive .
2 Partially androgen sensitive.
3 Fully Androgen resistant.
But the percentage of these three types of cells vary from man to man. One man can have 99% Androgen sensitive, 1/2% Partially resistant and 1/2 % Androgen resistant whereas another man can have 50% Androgen Sensitive 25% Partially Androgen sensitive and 25% Androgen resistant cells.
How do we find out what ratio one particular man has? A simple clue is Nadir PSA...meaning how low the PSA dropped in the first year of ADT. If it dropped say, 99.5% from top then, that man has most of his cancer cells as Androgen sensitive.
Coming to Chemotherapy...How does Chemo work...Chemo works by killing ALL cells which are growing...Chemo is an equal opportunity killer for all growing cells...whether Androgen sensitive or Androgen resistant.
Based on this, we can say Chemo will work well and needed early on in man who have high percentage of Androgen Resistant cells. The man with very high Androgen sensitive cells can always wait till way later for Chemo as ADT can keep his PCa controlled for a long time.
The use of early Chemo should be based on individual subtype and degree of Androgen Resistance.

As to the length of time on ADT, well, there are medical folks who are stuck in the mud who simply say lifelong ADT and when you become castrate resistant, we'll try the next thing...

Many clinical trials have looked at this and as you might expect, the results are all over the map. I have seen a number that point to lifetime of ADT or until castrate resistance (which can be very soon or as others who have responded, a long time...) not useful in terms of progression free survival or overall survival.

For guys doing SRT, six months, for others, 18-24 months.

I think part of the answer lies in your response to ADT, how rapidly did your PSA respond, did your T drop to <20 and stay there, did your PSA become undetectable and stay there. If you stop, then have a plan o actively monitor...in my case I have labs and consult with my urologist every 2-4 months.

My T did return as the chart shows. Again, Bell Curve...Not all men are as fortunate. I have seen some data that may point to exercise playing a role...I work out 5-7 times a week, swim, ride my bike, elliptical, ski, hike in the mountains, yard work, walk our dog.

There has been a new oral ADT which may be used in place of Lupron. https://www.fda.gov/news-events/press-announcements/fda-approves-first-oral-hormone-therapy-treating-advanced-prostate-cancer#:~:text=FDA%20Approves%20First%20Oral%20Hormone%20Therapy%20for%20Treating%20Advanced%20Prostate%20Cancer,-Share&text=Today%2C%20the%20U.S.%20Food%20and,patients%20with%20advanced%20prostate%20cancer. It's advantage are:

Faster drop of T than Lupron, no flare.
Better cardiovascular side affect profile.
Faster return of T.

Again, as to the return of T, well, keep in mind the Bell Curve.

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Chris here from UK.
Agree with all of that.
My consultant adopted the same approach ie don't be passive get after the cancer with as many weapons as you can throw at it and look for a curative outcome rather than kicking the can down the road.
Like you I exercise regularly and have changed diet to whole food plant based. Reccomend reading the China Study which is eye opening.
My psa is <0.001 and T is 0.18 or thereabouts.
My consultant has repeatedly said to me don't underistmate the positive effect diet and exercise is having on my program.
In fact he regards it as an additional arm of treatment in its own right.
As well as Lupton injections I am on Enzalutimide tablets and have had chemo docytex and 20 rounds of radio to prostate and 2 lymph nodes in pelvis.
Got diagnosed last Sept with locally advanced Gleeson 10 PC.
Urologist originally said that he didn't think I could be cured, but when I went onto Oncology my new consultant said he wanted to get after it aggressively and a curative outcome was his objective.
Seems to me from my research that the more weapons you throw at it from the off which includes diet and exercise the better the outcome.

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My medical team has often said that they believe my diet, exercise and attitude have been a critical factor in the success I've enjoyed in my journey.

It was a video by Dr. Kwon that changed my approach where he talked about the failed linear and sequential approach destined to fail versus combining treatments and bring them forward in the treatment to overwhelm the disease when it was not in such an advanced state and the individual was not beaten down health wise from a variety of treatments.

Am I cured, probably not. However, coming up on four years off treatment is a pretty good response given my clinical history in January 2017.

I do believe we are entering a period where we live with this, much like diabetes snd AIDS.

The advances in treatments and imaging have been exponential since 2014 and I believe we are on the cusp of revolutionary advanced in genomic diagnosis and treatment where instead of population based decisions, we will be able to tailor it to an individual's specific disease.

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