THERE WAS NO RESPONSE TO AN UPDATE REMINDER IN 2016 SO THERE IS NO UPDATE.

I live with Lyn on a 20 hectare property near Cessnock in the Hunter Valley of New South Wales, two hours drive north of Sydney.

I had been having 6 monthly PSA tests for several years and these were relatively constant varying up and down between 4.0 and 4.5 and my free PSA was above 20%.

After my PSA increased to 5.2, I was 61 when referred for a biopsy and diagnosed in October, 2006. One core from six was positive, with a very small 0.5 mm diameter focus. Gleason' score was 3+3=6. My GP suggested I go down the brachytherapy path and referred me to a urologist in Sydney.

In May, 2007, I decided on brachytherapy as it seemed to offer the best outcome for my circumstances. As my prostate volume had been estimated by TRUS at the biopsy at 71 cc, I needed volume reduction, so in July, 2007, I had a 12 week Zoladex implant that was expected to reduce the prostate volume to a more manageable 45 to 50 cc.

In October, 2007, I had my pre-brachytherapy volume study, but alas, the prostate was still too large at 73 cc. How had 3 months of Zoladex caused my prostate to grow? The answer is simple, it was never 71 cc in the first place. An error had been made and my initial volume was really more like 93 cc, as revealed by another ultrasounds and a CT scans.

Brachytherapy was now not an option and the urologist instead suggested a radical prostatectomy. I felt uncomfortable with this advice and with my PSA now down to 4.4 due to the Zoladex hormones, I decided to take a deep breath and do nothing other than undertake much more of my own research, be more cautious about the advice I was given by the medical profession, and take charge of the situation myself. I subsequently changed to a different urologist.

A year and a half had passed since my diagnosis, and my new urologist recommended a repeat biopsy, but this time with 20 cores taken through the perineum. In June, 2008 I had the second biopsy, and this still showed only one positive core from 20, still with a small focus, and still scoring 3+3=6. The prostate volume was measured at this biopsy down to 60 cc, so there seemed to be a 9 months or more lag in the effects of the Zoladex. My PSA at this time was also down further to 4.0 ng/mL.

The new urologist, who was a leading Sydney robotic surgeon, suggested continuing with active surveillance, because my clinical data was no worse than 20 months earlier. I did a lot of reading on active surveillance and it sounded like a good idea, not just as an interim measure, but as a long term plan.

I also took a lot more interest in the effect of prostate volume on PSA test results. Work by Roehborn, Boyle, et al showed that for a benign prostate, there was a log-linear relationship between PSA and age, and another log-linear relationship between prostate volume and age. The research also gave PSA thresholds for 30 cc and 40 cc prostates for different decades of patient age. The information had not been plotted up, so I developed a chart with my own interpretation of the results. This chart shows the normal age related rate of prostate enlargement and the expected volume specific PSA as a function of both prostate volume and age. This means I could estimate how much of a man's total PSA could be linked just to the size of his prostate.

During the next 21 months I had nothing but 3 monthly PSA tests and free PSA as well. PSA increases averaging 0.3 ng/mL occurred for each 3 month period, but I expected that most of this was due to my prostate volume increasing again. Surprisingly my free PSA had gone up from 21% to 27%, which was better than going down.

In March, 2010, I had an ultrasound prostate volume of 94 cc and a PSA up to 6.4 ng/mL. Having researched the likely volume specific PSA (being distinct from the cancer specific PSA), I estimated that 4.6 of my total PSA was due to volume and 1.8 of the total PSA was due to cancer.

Active surveillance continues with me plotting PSA logarithmically against time so that a doubling time trend can be seen. I expect that the PSA increases for the last two years have been more to do with prostate volume increase, rather than cancer progression. Well, I hope so.

Now that my prostate volume is back up to where it was nearly three years ago pre-Zoladex, I am really expecting and hoping that the gradual PSA rise since June, 2008 will now flatten off and stabilise. Time will tell. Although I have a slight apprehension waiting for each PSA test result, I wouldn't describe it as PSA anxiety. I am fairly relaxed about it really.

As I write this, it is exactly two years to the day since I had my 20 core biopsy, and another was originally due this month (June 2010). However, I have postponed that for now and scheduled a PSA test for 18th June, then again in September and depending on these, a possible 20 core biopsy in October, 2010.

My quality of life at present is very good with no competing morbidities. And I want to keep it that way. I have lost 14 kg of weight since diagnosis, am eating healthier and exercising more. I am just a month off retirement and Lyn retires later this year. We have a lot of exciting plans for our retirement and that's why radical or definitive treatment will be my last resort, rather than the first course of action, as unfortunately it is for so many men.

I am really lucky that the brachytherapy was an aborted mission because it gave me the time to sit back, reflect, research and enjoy the quality of life that only the avoidance or postponement of radical therapy can give for someone like me with low risk cancer.

I have since reflected on the real meaning of life and now realise that the quality of living is much more important that the actual duration of life itself. Soon to be turning 65, I would rather clip a couple of years off my life expectancy than have a downturn in quality of life from now on.

Terry, thanks for all your work with YANA. It is an invaluable resource that doctors should direct all their patients to.

Since my last reported PSA of 6.4 in March, 2010, there was a small rise to 6.55 in June, 2010, and then to 6.83 in September, 2010.

Was originally intending to have a repeat biopsy in June, 2010, and revisit that question again in October, but despite the PSA increases (equivalent to a PSADT of 5 years) couldn't see any pressing need at that time.

October, 2010 was also the 4th anniversary of the original diagnosis and I felt relaxed about the role as my own case manager and pleased that active surveillance was my chosen path. The only difference to my regimen was having 180 ml of pomegranate juice daily and doing a bit more exercise.

I kept on reading and researching, and attended the Prostate Cancer Foundation of Australia conference at the Gold Coast in August (where Active Surveillance hardly received a mention). The highlight of the conference for me was attending a presentation by Mark Scholz and I subsequently read his new book, "Invasion of the Prostate Snatchers". I think that book should be required reading for all newly diagnosed men (and the women who love them).

Also around that time I stopped attending my local support group. Instead of it being supportive, I was becoming more annoyed at how the focus was on the "early detection and treatment while there is still time for a cure" message with hardly a mention of active surveillance, unless I mentioned it. I really think the YANA website is the best support group available and Terry Herbert is my hero.

Wind forward the clock to the present, and imagine how pleased I was yesterday to receive my latest PSA test result of 6.28, down from 6.83 four months ago. After four rises on a row, it was great to see a fall and although it may not have any great clinical significance, I'll take a drop in PSA any time. And with a PSA density of around 0.06, I have postponed the repeat biopsy again until at least September.

As my prostate volume has probably increased to back over 100 cc, recently I have been experiencing some urinary urgency and frequency issues, particularly at night. So I have decided to start on Avodart (actually a generic brand of dutasteride from India at a quarter of the price). I am hoping for a relief from my urinary problems and also the added bonus of a reduction in my DHT (dihydrotestosterone) to slow down cancer cell progression, and hopefully with no early onset of androgen independence.

Having all but retired (still tidying up a few loose ends), and with more time to enjoy life with Lyn who also has just retired from 34 years of school teaching, we are looking forward to two weeks in NZ in February and then our big seven week trip to USA and Canada in June and July. We will travel from San Francisco to Seattle, Vancouver, Canadian Rockies, Toronto, Montreal, Quebec, Prince Edward Island, Nova Scotia and home via Maine and Boston.

I used to think of active surveillance as something you did while waiting for the eventual reality of definitive treatment. But now I am more confident that it is something that can be followed with a reasonable expectation that radical treatment might never be required. Especially for someone like me with a PSA only about 1.1 above what it was at diagnosis more than four years ago.

My first year of retirement has gone well. The trip to NZ in February, 2011 and then our seven week Canada and USA trip in June and July were wonderful. And in between we have been busy around the house doing all the jobs that have been on hold for so long.

I am just coming up to the end of the first year on Avodart. PSA was 6.28 when I started the Avodart, then dropped as expected to 4.90 after 4 months, 4.21 after 8 months and 3.91 just before Christmas after 11 months. This means PSA down 38% , rather than the alleged normal 50% that everyone states. However, the 50% reduction should only be expected in men with little or no cancer present. It seems that the Avodart tends to reduce the PSA expressed by benign tissue by about 50%, but has little or no effect on PSA produced by cancer cells. Using these assertions, and my 38% reduction in PSA using Avodart, I have estimated that about 1.5 ng/mL of my PSA (for both the 6.28 a year ago and the 3.91 now) is due to PCa.

I am committed to the idea of taking Avodart for the rest of my life to maintain the best possible urinary function without the need for a prostate resection and the hope and expectation that it will also inhibit the growth of my small volume prostate cancer and keep it small.

It is now more than 5 years since my original diagnosis and three and a half years since my most recent 1 from 20, 3 + 3 biopsy in June, 2008. As for future biopsies, I don't think I will have any. The idea of Avodart changing the pathology and the resultant grading bias confounding the pathologist does not excite me. I think that now, at 66 and happily plodding along on active surveillance, I will just continue on with my (reasonably) healthy lifestyle, Avodart, pomegranate juice and 4 monthly PSA tests with the hope and expectation of never needing radical treatment.

Of course, if there is an otherwise unexplained dramatic spike in PSA that is confirmed on follow-up, a biopsy may be warranted, but a gradual rise (at maybe something like 10% per year) from the current Avodart inspired 3.91 baseline, will encourage me to postpone a biopsy indefinitely, even if that is not the recommendation of active surveillance protocols.

Just a brief update to note my latest Avodart inspired PSA is down further to 3.65 ng/mL, a lot lower than the 6.83 from 18 months ago.

Also I have added Tamsulosin to my daily Avodart (in the form of the combined drug Duodart) in an attempt to even further improve my night-time urination.

And even though it is nearly four years since my second (and last) biopsy, I still see no reason to ever have another one unless a compelling reason arises.

Have now been on Avodart (in the form of Duodart) for more than 18 months, and my PSA is down even further to 2.77 ng/mL. It is really amazing that my PSA has dropped by nearly 60% since September, 2010, more than the predicted 50% drop for those on Avodart. Just to summarise, these are my test results since then.

September, 2010 6.83
January, 2011 6.28
May, 2011 4.90
September, 2011 4.21
December, 2011 3.92
March, 2012 3.65
July, 2012 2.77

Needless to say, I will be doing nothing in the immediate future other than taking my daily Avodart and pomegranate juice. Although PSA is not necessarily entirely reliable as a sole monitoring tool, I am happy to rely on it and only have another biopsy if there is an unexplained and significant rise in PSA. I am still optimistic that I will never need radical treatment.

Nothing extraordinary has happened in the last year and a half.

It is now more than seven years since the original 3 + 3 prostate cancer diagnosis and five and a half years since my last "one positive from twenty cores" biopsy.

Still having daily pomegranate juice and Avodart. In fact it is exactly three years since I started the Avodart and it is treating me well. Libido still OK. PSA results since the last update.

July, 2012 2.77 (as previously reported)

December, 2012 2.65

May, 2013 2.23

October, 2013 2.65 (first rise for 9 PSA tests since September, 2010).

I am so pleased that I selected active surveillance. It has ensured the best possible quality of life for the last seven years. Radical treatment might be needed some day, but I will only embark on that course of action after very careful consideration.

After rises in PSA from an Avodart reduced 2.23 in May 2013 to 2.65 in October 2013 to 3.18 in March 2014, I decided it was time for another biopsy, but this time a 3T MRI fusion biopsy. After some procrastination, a month away on holidays and more procrastination, I had the biopsy in July 2014.

Imagine my amazement with a Gleasons 4+5=9 diagnosis. After seven years meandering along with a 3+3=6 small volume cancer, a spike in PSA heralded a new era, a high grade G9 result.

My surgeon Dr Philip Stricker from St. Vincents Hospital in Sydney did not like the diagnosis one bit, so scheduled a da Vinci surgery for inside three weeks. As a coincidence, the surgery was 6th August, 2014, the day my hero Terry Herbert finally succumbed to this nasty disease. All went to plan with negative margins and post surgery pathology confirming the G9 tumour. Continence was 99% after catheter removal and never needed pads - I was really pleased about that, especially after reading so many stories of misery from blokes still battling incontinence months and months later.

Now six months post surgery I can look back and say that I am glad of the Terry Herbert inspired seven years of active surveillance, but also glad to have been able to move quickly when a nasty G9 cancer was diagnosed.

As my story was essentially one of active surveillance, I have purposely not gone into much detail of the surgery, but despite my resolve to never have surgery, I am glad to say that it all worked out well in the end.

All the best from Brian.

Brian's e-mail address is: bltjwatts AT bigpond.com (replace "AT" with "@")

NOTE: Brian has not updated his story for more than 15 months, so you may not receive any response from him.