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Al Pfadt lives in New York, USA. He was 69 when he was diagnosed in May, 2014. His initial PSA was 8.08 ng/ml, his Gleason Score was 9, and he was staged T2c. His initial treatment choice was Surgery (Robotic Laparoscopic Prostatectomy) and his current treatment choice is Other (). Here is his story.

THERE WAS NO RESPONSE TO AN UPDATE REMINDER IN 2021 SO THERE IS NO UPDATE.

My first PSA after surgery was .58 and it has been increasing exponentially ever since.

A curative attempt with salvage radiation therapy of the prostate bed was also unsuccessful. During the 4 months immediately after radiation my PSA doubling time was less than 3 months and its Specific Growth Rate was estimated to be .27 ng/mL/month, which was the same as it was before surgery.

Against this historical background, I am currently evaluating a trial with medical marijuana using a single subject research design that combines data analytic procedures derived from Statistical Process Control and Celeration Charting, both of which I used in my career as a research scientist to monitor health care outcomes associated with interventions that targeted specific biobehavioral processes - reductions in Body Mass Index, for example, in the case of one person with a genetic disorder (Prader Willi syndrome) who was treated with biosynthetic human growth hormone. In another case study, a person's life threatening self- injurious behavior was successfully treated pyschopharmacologically with a mood stabilizer after an attempt to suppress it with an opiate antagonist was unsuccessful. I hope to publish these results.

UPDATED

August 2016

To briefly recap, I am a 71 year old former research scientist with Gleason 9 (5+4) tumor diagnosed June 2014, which continued to grow aggressively after surgery (doubling time 3.2 months), as well as after salvage radiation therapy, completed in June 2015 (doubling time 2.5 months).

My oncologist wanted to enroll me in a clinical trial that offered the possibility to all participants that they would have a 1 in 3 chance of getting the promising combination of ADT plus Xtandi, what was not yet available directly.

I chose medical marijuana treatment and followed the Rick Simpson protocol by ingesting (via specially formulated suppositories) that delivered about 0.9 of a gram of a medicinal grade mixture consisting of 50% THC and CBD.

I will attempt to tell the rest of this story by publishing a picture of my graphed PSA data on this web site, but this is the wordy version.

My first round of medical marijuana treatment dramatically altered the progression of my PSA test results mentioned above. Across a 3 month interval my PSA test results actually decreased slightly. However, I temporarily discontinued treatment for almost 2 months, during which time the growth rate resumed again.

Three months ago, I started a new medical marijuana regimen that involves ingesting a tincture containing a preparation that delivers about 1.5 grams per week. The doubling time for that interval (from 5/13/16 when my PSA was 13.23 ng/mL) through 8/15/16, when my PSA was 12.71 ng/mL, is now a large negative value (it is projected to decrease to half its current value in 2.6 years).

Additional support for the therapeutic benefit of the medical marijuana regimen was provided by the results of imaging studies read by oncologist last week. My full body CT scan showed no bone metastases, but maybe even better news was the observation of the tumor in my iliac region that the technician called attention to it 6 months ago in his report, had now shrunk in size enough that the same technician looking at the newest scan results reported "no positive findings". When I mentioned to my oncologist (who doesn't support or approve of my medical marijuana trial) that we clearly saw a tumor 6 months ago, he re-examined the site and we were able to detect a tumor that was noticeably smaller than the previous one we had just looked at.

His recommendation is to delay any additional treatment until the PSA results start to rise dramatically again or if a scan in another six months indicates that the tumor has grown significantly.

He still refuses to accept medical marijuana as a reasonable explanation for these patterns in my test results. However, if this were a conventional treatment aimed at arresting tumor cell progression, he would be taking credit for it.

From my perspective as a research scientist, I recognize the inherent risk in trying to determine a clear cause ans effect relationship in graphs of single subject data.

However, the data are quite clear that something happened twice to arrest the progression of my prostate cancer.

It wasn't surgery or salvage radiation therapy. Both times the leveling off of the growth rate was associated with a medical marijuana trial.

I will continue my new regimen of ingesting between 1.5 and 2 grams of a medicinal grade preparation consisting of both THC and CBD and will update this site when the next results are available.

UPDATED

August 2016

While a picture is worth a thousand words, this is a very information-dense and technically sophisticated graphic format that I developed from my experiences as a research scientist to analyze changes in my PSA kinetics during the course of various treatments since my Gleason 9 (5+4) cancer was diagnosed in June 2014.

Notice that the horizontal, X-axis is used to plot time in a linear manner. That is the spaces between each numbered months is equal. This is technically not true- some months have 28 days, others 30 or 31. However, we can ignore these small differences and use equal intervals.

My PSA scores are plotted on the vertical, Y-axis, which looks different. This is called a "semi-log" chart and it reflects that cancer does not grow incrementally, by adding one cell at a time to the mass of cells already present.

Rather, when prostate cancer grows it does so geometrically in an exponential manner. Each cell sub-divides, and then those sub-divisions sub-divide.

This is why "doubling time" is a commonly accepted measure of a cancer's aggressiveness. It reflects the time it would take, based on previous growth patterns, for your tumor to double in size.

The graph displayed is a "3 cycle" semi-log chart.

there is no such thing as a zero value on a log axis- since this is a "base 10" or natural log axis, the scores run from 1-10. So what happens when your PSA test result goes from 10 to 11. This requires an additional cycle that goes from 10 to 100, again, cycles of 10. The same is true if your PSA drops below 1- you will need an additional cycle that goes from .1 to 1 ng/mL.

So the 3 cycles in my graph run from .1 to 1.0; from 1 to 10; and from 10 to 100 mg-mL.

Notice another interesting this about the semi- log scale.The distance on the scale from 1 to 10, is the same as from 10 to 100, and from .1 to 1.0.

Notice another interesting characteristic. The distance from .5 to 5 ng/mL on the Y-axis is the same as the distance from 5 to 50 ng/mL. Again, based on a scale of 1 to 10. This allows " doubling time" to be calculated from the graph, instead of relying on an internet based-algorithm. Like the one put out by MSKCC on their web site.

OK - take a deep breath. This same type of system is used to rate other natural phenomena like earthquakes and sound intensity. For our purposes, it is sufficient to remember that a change in one PSA unit from 1 to 2 ng/mL is not the same as a change from 8 to 9 ng/mL This is similar to earth quakes measured on the semi-log Richter scale. An earthquake at 5 on the Richter scale is much more than 2 times as strong as one which registers at 2.5. Likewise, a sound at 10 decibels is more than twice as strong as one registering at 5 decibels.

Back to the values plotted on the graph in the far left hand side of the graph. The values marked by a small box[], were recorded before my prostate cancer surgery on 8/19/14. From 2011 through 2013 my PSA values averaged 3.0 ng/mL, with a doubling time of about 1 year( 50 months). This means that if only my pre-cancer trends had continued, 3 years later in August 2016 my PSA value would be expected to be about 24 ng/mL, since there would have been 3 doubling cycles during that interval.

The second [] paints a more ominous picture however. The value of 9.8 ng/mL recorded just before my radical prostactectomy on 8/19/14 represented a doubling time of 2.8 months, based on the value of 8.2 ng/ mL recorded just 1 month earlier.

Looking at the next panel, which runs from 10/14 through 3/15 on the time axis, you can see that the rate of growth immediately after surgery was only slightly slower than before treatment, with a new doubling rate of 3.2 months.

The doubling rate rate after salvage radiation treatment was even shorter, only 2.5 months, indicating that neither conventional treatment had any significant impact on the underlying prostate cancer. As a result of those obvious treatment failures, my oncologist recommended that I enroll myself in a clinical protocol where I might have the best chance of getting the right combination of chemo and ADT that was not available anywhere else at that time.

Instead, I chose the option of medical marijuana treatment, following what is described as the "Rick Simpson protocol". This involves injesting over 62 grams of a high potency mixture medical marijuana consisting of a 50/50 mixture of THC and CBD during about 2 and 1/2 months.

As you can see by inspecting the graph, I had completed most of the protocol by 1/15/16( by which time I had ingested over 57 grams of the mixture) and for the first time my PSA progression had stopped dramatically and I actually recorded the first decrease since my cancer was diagnosed over 2 years ago. However, this medical marijuana was too severe for me to tolerate its psychotropic side effects, so I drastically cut down and for actime eliminated the use of medical marijuana to allow me some time to recover my "normal" functioning.

Again, the graph reflects the accelerated growth rate for my PSA test results for the next 2 months until I resumed active treatment, following a new protocol that involved ingesting about 1.5 grams of a similar preparation per week.

Again, medical marijuana treatment is associated with a dramatic leveling off of the growth rate and for the second time I experienced a numerical decline in my PSA test result from one month to the next.

It is clear to me from inspecting this graph that something clearly happened on two occasions that were associated with medical marijuana treatment. It is not possible to identify the treatment as the causative factor but I am not aware of any alternative explanations. I did add 1000 mg og Metformin to my nutritional regimen 2 months ago, but this has not been increased since then and is similar to other nutritional changes I have made - less red meat, lots of green tea and Tumeric, etc.

If these were the results of conventional treatment, there would not be so much resistance to entertaining the possibility that medical marijuana produced the results.

Stay tuned, I will continue to present additional test results.

Based on my last 3 test results , the MSKCC nomogram predicts that my " doubling time" predicts a Reduction by 1/2 during the next 2.6 years.

Wouldn't that be great.

My last imaging study last week showed that the cancer tumor had shrunk to such an extent that the technician who read it suggested that no positive findings were present.

My oncologist and I were able to see signs of the previous tumor because we knew where to look. However, it definitely had shrunk in size, and he agreed that no additional treatment was indicated at this time.

Keeping my fingers crossed.

UPDATED

September 2017

I am preparing to enter my next active phase of treatment in November.

My PSA continues to rise exponentially following failed curative attempts by a robotic-assisted radical prostatectomy and salvage radiation within the past 3 years subsequent to my initial diagnosis with Gleason 9[5+4] cancer in June 2017.

As I indicated previously, a trial with medical marijuana following the Rick Simpson Oil protocol was the only intervention that successfully treated my prostate cancer, but I was not able to recapture the benefits after I stopped treatment. A recent trial with Casodex [150 mg per day] successfully reduced my PSA from over 52 to 3.5 in a three month period but I found the side effects to be excessive [severe gastritis, radical breast enlargement and severe nipple pain, gastritis, and worsening of my depression].

An Auximen enhanced PET scan identified 3 sites that were likely metastases but the verdict was not definitive. Since I am still not symptomatic, my oncologist and I agreed [with some prompting on my part] to redo the PET scan in November to determine if there are any identifiable sites that could be targets for focal treatment, before proceeding with ADT or another systemic treatment.

I am 72 and 1/2 am am enjoying relatively good health, except for the side effects of my previous treatments- severe impotence and incontinence, which has been relatively well managed by an artificial urinary sphincter implant.

By no means do I feel that I have exhausted my treatment options. However, I want to preserve what is left of the quality of my life as long as possible.

UPDATED

September 2018

Two months ago I started taking Erleda as a monotherapy. I had been taking Firmagon for about 7 months and my PSA levels plateaued at about 5 ng/ml, while my t levels were well below the castrate threshold- falling as low as 3 and coming in at 6 just before I started Erleda. Before I started Firmagon, I received treatment with Provenge as an immunotherapy. I wanted to wait for a longer time for Firmagon to "wash out" before I started Erleada but my oncologist suggested that I not do so since I might benefit from a synergistic effect. This meant confounding my long term experimental design by essentially manipulating multiple variables, my treatment history requires that I be able to find a treatment that works rather than trying to tease out why it works. My rationale for wanting to try Erleada as a monotherapy is that since Firmagon stopped working, I would be adding side effects on top of side effects without any evidence that I need to take both medications. i understand that a clinical trial is being planned to address just this question but I see no need to wait until it is completed when I can establish that for myself by continuing my own N=1 experiment.

After only two months the results have exceeded my wildest expectations. Not only has my PSA plunged to its lowest level (.14 ng/ ml) but my testosterone level has increased to over 400, almost double my pre-treatment levels.

It is an open ended question as to whether or not my low PSA levels can be sustained in the face of these testosterone levels. However, I am now in a position to decide to take an additional medication with Erleada if it is necessary, not just because it is a regulatory guideline.

UPDATED

July 2019

since my last up-date, I have continued to take Erleada as a monotherapy. Initially the results immediate and impressive. The decline in my PSA continued to a nadir of .05 ng/ml and my testosterone levels stayed higher than my pre- cancer levels( about 450 ng/dL versus 250 or so). However, I experienced the side effects listed above and consulted with my oncologist about a dosage reduction from 240 to 120 mg daily. I had taken Provenge treatment at the same time that I started Firmagon and I wondered if the delayed effects of Provenge might compensate for a lower dose of Erleada. The first month on the lower dose saw no change in either PSA or t levels. However, by the second and 3rd months it was obvious that my PSA doubling time was back in the range of 2-3 months which is my characteristic response to treatment failure. Increasing the dose back to the original level has not leveled off the PSA progression as we hoped so now I am faced with a difficult choice.

My last PSA was .42 ng/ ml, still low but doubling rapidly. I have detectable metastatic cancer sites in my bones, primarily pelvic region, but these are relatively small and have not grown in the past 2 years. The logical choice would be to restart Firmagon and continue to take the Erleada with it. I tolerated the monthly Firmagon injections before they stopped working but since I have not been getting them I appreciate what a negative effect they had on my mental energy. I have completed three writing projects since I stopped taking Firmagon and have others I am working on. Readers can go to the Oncogen web site and download the paper I published there 3 months ago and since then, I have another under review in The Journal of Patient Experience. This work is my main source of satisfaction these days and I am reluctant to return to the foggy state I was in when I was taking Firmagon. On the other hand, I am also reluctant to subject myself to another rigorous medical marijuana trial, even though data in the article I referenced demonstrates that it was effective for a while.

My next oncology appointment is in 2 weeks and I will post an update when we decide on a course of treatment.

UPDATED

October 2019

Since my last entry, I completed my trial with Erleada as a monotherapy. After a spectacular start where my PSA plunged from about 5ng/ml where it plateaued while I was taking Firmagon and still had castrate T levels, my PSA started to rise after I cut the dose in half from 240 to 120mg per day. I did this to relieve the side effects I was experiencing (annoying sensory and motor neuropathy, very sensitive nipples and even more pronounced breast enlargement that when I was taking Firmagon, and pretty significant joint pain). I hoped that the previous round of Provenge treatment that took place at the same time that I started Firmagon would cover me while I took a lesser dose of Erleada. My PSA didn't change the first month after the dose reduction but by the second month it was clear from my graph of my data, using a semi- log charting format that tracks rate of acceleration very accurately, that my PSA was rapidly progression although it was still at a very low level. At its Nadir during the Erleada trial it reached .05 ng/ m and now it had doubled back to 0.1 in only two months. Gradually increasing the dose back to its original level did not slow down this rate of progression and I decided to take a drug holiday before returning to Firmagon. I spent one month without any medication but my oncologist was able to get me approved for a trial with Darulitamide, the new kid on the block, which is like a Erleada but doesn't cross the blood/brain barrier, so is expected to have fewer side effects. It is too early to tell if it is working but I haven't noticed any side effects. Imaging studies about a year ago detected several small metastatic sites in my pelvic area and we will eventually repeat the Augemin ( sp?) scan to see what if any changes have taken place. My current PSA level is 2.21 after having been as high as 161 after multiple treatment failures since my cancer was detected in June of 2014. Since then the little bugger has dodged two bullets meant to kill it( a radical prostatectomy and salvage radiation) as well as the other treatments I mentioned. Medical marijuana definitely stopped my PSA progression for over 3 months and during the time I was taking it my doubling time was 14 months, compared to doubling times of 3 and 2.5 months after surgery and radiation respectively. More later. But I never expected to be this healthy after all those failed treatments with a Gleason 9 (5+4) tiger that I have grabbed by the tail!

Al's e-mail address is: pfadtag AT gmail.com (replace "AT" with "@")

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


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