RE: Mortality Spike was .....Swedish Study

[Guest guest]

Mike,

There is no right or wrong answer to

the question “What should I do?” So much depends on our individual

take on life, how we assess risk how we deal with risk.

My background and outlook on life is such that, after examining all

the information I could following my diagnosis – and I saw about thirteen

doctors on three Continents in the process, reading everything I could find, participating

in internet forums etc, I came to the conclusion that in my particular

circumstances and with my particular diagnosis it would be in my overall best interests

not to have invasive therapy. If you’re interested in more information I

wrote a piece “Why I did not choose surgery” which is at http://www.facebook.com/?sk=lf#!/topic.php?uid=2215342155 & topic=18237

There are very few men who would not have

chosen surgery with your diagnosis. Will that make a difference to your

survival in the long run? Yes, says the Swedish study, you have reduced the probability

of your dying from PCa. On the other hand, since the overall mortality

rate for men diagnosed with prostate cancer is not greatly different, the

chances are about equal that you may die of something else. To quote Dr

Whitmore again “Growing old is invariably fatal while prostate cancer is

only sometimes so.”

All the best

Prostate men need enlightening, not

frightening

Terry Herbert - diagnosed in 1996 and

still going strong

Read A Strange Place for unbiased information at http://www.yananow.org/StrangePlace/index.html

From: ProstateCancerSupport [mailto:ProstateCancerSupport ] On Behalf Of Clowes

Sent: Monday, 4 April 2011 10:52

AM

To: ProstateCancerSupport

Subject: Re:

Mortality Spike was .....Swedish Study

Thanks Terry. I guess I'm wondering if I was wrong

to have surgery (or any treatment) with my scores: PSA 4.95, Gleason 7 (3+4),

7 of 12 cores cancerous. If treatment doesn't add to life expectancy, why

bother.

Mike

Subject: Mortality Spike was .....Swedish Study [1

Attachment]

To: ProstateCancerSupport

Date: Sunday, April 3, 2011, 7:59 PM

[Attachment(s) from Terry Herbert

included below]

Mike,

In writing this piece I

want to acknowledge that I am no statistician. All I know about statistics

comes from many years of working in the insurance industry where I gained a

clear insight into how inaccurate statistics can be because of basic errors

or assumptions and how easily statistics can be manipulated by the adjustment

of assumptions. There is an old joke about the insurance manager looking for

an actuary. All applicants were presented with base data and asked to make a

series of projections. All were rejected until at last an applicant asked the

manager what result he wanted to see.

The figures that

demonstrate the significant rise in prostate cancer deaths after the

introduction come from the SEER (Surveillance, Epidemiology, and End Results

Program) statistics - http://seer.cancer.gov/ - which are accessible to

all of us. They are said to be the most accurate figures available but of

course there are, as is the case for all statistics, some issues in the

collection and compilation of the data which can affect the reported outcome

and estimates. Here are some of the basic points from my limited point of

view:

1. It is said that the

SEER data represents about 10% of the US population. National

statistics are extrapolated from this data. Clearly an error in the base data

will be significantly compounded when extrapolated to this extent.

2. The base data is

collected from a limited number of institutions and not from all institutions

in the US

.. A NCI pre4ss release in 2002 said in part <snip> Ten population-based

registries report this

information to the

NCI's Surveillance, Epidemiology, and End Results (SEER) Program.

<snip> Clearly they must be very large institutions if threes ten

represent 10% of the population. My

personal experiences tend to make me think that large institutions often

have built in error rates that may be higher than smaller institutions.

3. Calculations for

incidence rates and the like are made using the data from the Census.

Just which Census is used can make a significant difference in

projected, extrapolated data. For many years data from an old Census was used

(I think it was 1976?) This was then changed to a more modern Census with a

warning that it might make some figures not directly comparable.

It is important, when

looking at points 2 and 3 to realize that because of racially and or

economically differing incidence and mortality rates, there may be

significant discrepancies that develop if for example, there have been large

population movements or even if the reporting institutions change or move their

location. There is a good example of the kind of distortion that can be

introduced which was mentioned in a study in Britain

.. The incidence of prostate cancer was very much higher in an

institution in inner London where the inhabitants might be described as

economically disadvantaged compared with the more affluent area served by an

institution away from the city in what might be termed the ‘broker

belt. The study suggested that diet, living conditions, ability to seek good

advice, levels of service etc accounted for the difference. The point of this

is that if the inner city data were extrapolated into a national statistic,

there would be a very different set of rates than if the second

institution’s data was used.

4. There is a time lag

in reporting data which, incredibly, seems to have worsened despite the

advent of sophisticated computer based systems. The 2002 press release

referred to above (15-Oct-2002 Journal of the National

Cancer Institute) was issued because there was some puzzlement about the

apparent decline in prostate cancer incidence rates which curiously enough

occurred in the same time frame as the reduction in prostate cancer mortality

rates. This report stated in part <snip> The standard time between a

cancer diagnosis and its initial inclusion in cancer incidence statistics is

about 2 years………. They found that it would take 4 to 17

years for 99% or more of the cancer cases to be reported. <snip> This

raised the question of accuracy in my mind – bering in mind my views on

the way in which large institutions may operate.

I have tried on many

occasions to get an informed discussion going on the lock step rises and

falls of mortality and incidence rates following the introduction of PSA

testing in 1986. We know why the incidence rate rose – because more men

were biopsied and the more men you biopsy the more prostate cancer you will

find. As the 2004 study demonstrated so clearly if you biopsy men with a PSA

under 4.0 ng/ml you will find more cells currently defined as prostate

cancer than if you only biopsy men with a PSA higher than 4.0 ng/ml. But why

did the mortality rate rise. And why did the incidence rate AND the mortality

rate start to fall after 1991, five years later?

No one has ever come up

with a definitive answer. One of the leading activists has always dismissed

my desire for such a discussion as saying that the two items have nothing to

do with each other and doggedly repeats his mantra that the mortality rate

has fallen, as indeed it has, depending on where you measure it from. He no

longer responds to my postings.

My point

has always been that we need an explanation as to why both measures changed.

We have to understand that if we are to attribute the observed fall in

mortality rates from it’s all time high in 1991. From my limited

viewpoint, significant changes like these in a population statistical base

can come from a change in definition. Just what is a prostate cancer death?

How is it defined? Did all reporting institutions use the same definitions?

Did any definitions change? Those are the questions that no one can answer

for me. There have been some glimmers of light shone on the subject:

a. No less a person

than Dr Walsh (who was apparently at some conference discussing the

importance of screening in reducing mortality) was quoted last year as

being questioned as to why the mortality rates in Britain had fallen

when there was not the same emphasis or amount of screening in that country.

His response was that they had changed the definition of prostate cancer

related eeath to exclude pneumonia and this one factor had led to a reduction

in prostate cancer related deaths. On raising this point in a forum I was

told that this could not happen in the US . End of discussion.

b. Soon after I read of

Dr Walsh’s remarks, I came on a piece describing how the large European

study (ERSPC) had agreed to ‘standardize’ their definition of

prostate cancer to only include needle biopsy results that result in a

Gleason Score of 6 or higher – in other words anyone who had a

diagnosis of GS 5 would not be included in their data. This single change may

well have produced the discrepancy in the ERSPC reported results of

‘lives saved’ when compared with the US study that showed ‘no

lives saved’. Again I tried to discuss this change in definition

and wondered if this was a contributing fator in the decline in

reported deaths – after all if you are not diagnosed with PCa, you

cannot die of the disease. My

thoughts on the subject were ignored ar denied. Spurred on by this item I

then found that in practical terms, leading pathologists in the US had been

applying this criterion since about 2005 and in January this year the

proposal was formally adopted – see http://www.yananow.org/StrangePlace/forest.html#gleason

for a summary of the changes. This has led to a significant change in the

profile of diagnosed prostate cancer and the so-called

‘Migration” of Gleason Grades and Scores – see http://tinyurl.com/2jnpbu

In summary after what

many will have considered a long and boring post, in answer to your question

<snip> Your thoughts on the 30% increase and what it

means? <snip> I think that a number of changes

in diagnosis, definition, formulae and focus may have all resulted in the

changes observed in the population data.

All the best

Prostate men need

enlightening, not frightening

Terry Herbert -

diagnosed in 1996 and still going strong

Read A Strange Place for unbiased information at http://www.yananow.org/StrangePlace/index.html

Attachment(s) from

Terry Herbert

1 of 1 Photo(s)

StateCancerProfilesGraph-all ages.png

[Guest guest]

Mike,

I can't believe that any reasonable person would not have chosen some more aggressive treatment option then active surveillance given your numbers. That being said, I also can't believe that the treatment option that you chose will not add years of quality life to your story, regardless of what this or any study may suggest. Since my diagnosis and surgical removal in 2007 nothing has become more clear(to me at least) then the fact that there is nothing more unclear and muddy then this disease, it's treatment options and the treatment options of their subsequent side effects. There are no right or wrong choices when dealing with this disease. It comes down to a decision of what is right for the individual and what side effects of the treatment(or the side effects of no treatment)can you live with.

We all suffer the accumulative effects of the same disease "life", and hopefully, through the decisions we make along the way we can prolong the unavoidable end "death".

Good luck,

Rick

To: ProstateCancerSupport Sent: Sun, April 3, 2011 8:52:21 PMSubject: Re: Mortality Spike was .....Swedish Study

Thanks Terry. I guess I'm wondering if I was wrong to have surgery (or any treatment) with my scores: PSA 4.95, Gleason 7 (3+4), 7 of 12 cores cancerous. If treatment doesn't add to life expectancy, why bother.

Mike

Subject: Mortality Spike was .....Swedish Study [1 Attachment]To: ProstateCancerSupport Date: Sunday, April 3, 2011, 7:59 PM

[Attachment(s) from Terry Herbert included below]

Mike,

In writing this piece I want to acknowledge that I am no statistician. All I know about statistics comes from many years of working in the insurance industry where I gained a clear insight into how inaccurate statistics can be because of basic errors or assumptions and how easily statistics can be manipulated by the adjustment of assumptions. There is an old joke about the insurance manager looking for an actuary. All applicants were presented with base data and asked to make a series of projections. All were rejected until at last an applicant asked the manager what result he wanted to see. The figures that demonstrate the significant rise in prostate cancer deaths after the introduction come from the SEER (Surveillance, Epidemiology, and End Results Program) statistics - http://seer.cancer.gov/ - which are accessible to all of us. They are said to be the most accurate figures available but of course there are, as is the case for all statistics, some issues in the collection and compilation of the data which can affect the reported outcome and estimates. Here are some of the basic points from my limited point of view: 1. It is said that the SEER data represents about 10% of the US population. National statistics are extrapolated from this data. Clearly an error in the base data will be significantly compounded when extrapolated to this extent. 2. The base data is collected from a limited number of institutions and not from all institutions in the US . A NCI pre4ss release in 2002 said in part <snip> Ten population-based registries report this

information to the NCI's Surveillance, Epidemiology, and End Results (SEER) Program. <snip> Clearly they must be very large institutions if threes ten represent 10% of the population. My personal experiences tend to make me think that large institutions often have built in error rates that may be higher than smaller institutions. 3. Calculations for incidence rates and the like are made using the data from the Census. Just which Census is used can make a significant difference in projected, extrapolated data. For many years data from an old Census was used (I think it was 1976?) This was then changed to a more modern Census with a warning that it might make some figures not directly comparable. It is important, when looking at points 2 and 3 to realize that because of racially and or economically differing incidence and mortality rates, there may be significant discrepancies that develop if for example, there have been large population movements or even if the reporting institutions change or move their location. There is a good example of the kind of distortion that can be introduced which was mentioned in a study in Britain . The incidence of prostate cancer was very much higher in an institution in inner London where the inhabitants might be described as economically disadvantaged compared with the more affluent area served by an institution away from the city in what might be termed the ‘broker belt. The study suggested that diet, living conditions, ability to seek good advice, levels of service etc

accounted for the difference. The point of this is that if the inner city data were extrapolated into a national statistic, there would be a very different set of rates than if the second institution’s data was used. 4. There is a time lag in reporting data which, incredibly, seems to have worsened despite the advent of sophisticated computer based systems. The 2002 press release referred to above (15-Oct-2002 Journal of the National Cancer Institute) was issued because there was some puzzlement about the apparent decline in prostate cancer incidence rates which curiously enough occurred in the same time frame as the reduction in prostate cancer mortality rates. This report stated in part <snip> The standard time between a cancer diagnosis and its initial inclusion in cancer incidence statistics is about 2 years………. They found that it would take 4 to 17 years for 99% or more of the cancer cases to be reported. <snip> This raised the question of accuracy in my mind – bering in mind my views on the way

in which large institutions may operate. I have tried on many occasions to get an informed discussion going on the lock step rises and falls of mortality and incidence rates following the introduction of PSA testing in 1986. We know why the incidence rate rose – because more men were biopsied and the more men you biopsy the more prostate cancer you will find. As the 2004 study demonstrated so clearly if you biopsy men with a PSA under 4.0 ng/ml you will find more cells currently defined as prostate cancer than if you only biopsy men with a PSA higher than 4.0 ng/ml. But why did the mortality rate rise. And why did the incidence rate AND the mortality rate start to fall after 1991, five years later? No one has ever come up with a definitive answer. One of the leading activists has always dismissed my desire for such a discussion as saying that the two items have nothing to do with each other and doggedly repeats his mantra that the mortality rate has fallen, as indeed it has, depending on where you measure it from. He no longer responds to my postings. My point has always been that we need an explanation as to why both measures changed. We have to understand that if we are to attribute the observed fall in mortality rates from it’s all time high in 1991. From my limited viewpoint, significant changes like these in a population statistical base can come from a change in definition. Just what is a prostate cancer death? How is it defined? Did all reporting institutions use the same definitions? Did any definitions change? Those are the questions that no one can answer for me. There have been some glimmers of light shone on the subject: a. No less a person than Dr Walsh (who was apparently at some conference discussing the importance of screening in reducing mortality) was quoted last year as being questioned as to why the mortality rates in Britain had fallen when there was not the same emphasis or amount of screening in that country. His response was that they had changed the definition of prostate cancer related eeath to exclude pneumonia and this one factor had led to a reduction in prostate cancer related deaths. On raising this point in a forum I was told that this could not happen in the US . End of discussion. b. Soon after I read of Dr Walsh’s remarks, I came on a piece describing how the large European study (ERSPC) had agreed to ‘standardize’ their definition of prostate cancer to only include needle biopsy results that result in a Gleason Score of 6 or higher – in other words anyone who had a diagnosis of GS 5 would not be included in their data. This single change may well have produced the discrepancy in the ERSPC reported results of ‘lives saved’ when compared with the US study that showed ‘no lives saved’. Again I tried to discuss this change in definition and wondered if this was a contributing fator in the decline in reported deaths – after all if you are not diagnosed with PCa, you cannot die of the disease. My thoughts on the subject were ignored ar denied. Spurred on by this item I then

found that in practical terms, leading pathologists in the US had been applying this criterion since about 2005 and in January this year the proposal was formally adopted – see http://www.yananow.org/StrangePlace/forest.html#gleason for a summary of the changes. This has led to a significant change in the profile of diagnosed prostate cancer and the so-called ‘Migration†of Gleason Grades and Scores – see http://tinyurl.com/2jnpbu

In summary after what many will have considered a long and boring post, in answer to your question <snip> Your thoughts on the 30% increase and what it means? <snip> I think that a number of changes in diagnosis, definition, formulae and focus may have all resulted in the changes observed in the population data.

All the best

Prostate men need enlightening, not frightening Terry Herbert - diagnosed in 1996 and still going strong Read A Strange Place for unbiased information at http://www.yananow.net/StrangePlace/index.html

Attachment(s) from Terry Herbert

1 of 1 Photo(s)

StateCancerProfilesGraph-all ages.png" src="http://xa.yimg.com/kq/groups/4926965/tn/1471474522">

StateCancerProfilesGraph-all ages.png

[Guest guest]

Thanks Rick. Good luck to you too. I guess all these studies make one second guess the decision at times.

Mike

Subject: Mortality Spike was .....Swedish Study [1 Attachment]To: ProstateCancerSupport Date: Sunday, April 3, 2011, 7:59 PM

[Attachment(s) from Terry Herbert included below]

Mike,

In writing this piece I want to acknowledge that I am no statistician. All I know about statistics comes from many years of working in the insurance industry where I gained a clear insight into how inaccurate statistics can be because of basic errors or assumptions and how easily statistics can be manipulated by the adjustment of assumptions. There is an old joke about the insurance manager looking for an actuary. All applicants were presented with base data and asked to make a series of projections. All were rejected until at last an applicant asked the manager what result he wanted to see. The figures that demonstrate the significant rise in prostate cancer deaths after the introduction come from the SEER (Surveillance, Epidemiology, and End Results Program) statistics - http://seer.cancer.gov/ - which are accessible to all of us. They are said to be the most accurate figures available but of course there are, as is the case for all statistics, some issues in the collection and compilation of the data which can affect the reported outcome and estimates. Here are some of the basic points from my limited point of view: 1. It is said that the SEER data represents about 10% of the US population. National statistics are extrapolated from this data. Clearly an error in the base data will be significantly compounded when extrapolated to this extent. 2. The base data is collected from a limited number of institutions and not from all institutions in the US . A NCI pre4ss release in 2002 said in part <snip> Ten population-based registries report this

information to the NCI's Surveillance, Epidemiology, and End Results (SEER) Program. <snip> Clearly they must be very large institutions if threes ten represent 10% of the population. My personal experiences tend to make me think that large institutions often have built in error rates that may be higher than smaller institutions. 3. Calculations for incidence rates and the like are made using the data from the Census. Just which Census is used can make a significant difference in projected, extrapolated data. For many years data from an old Census was used (I think it was 1976?) This was then changed to a more modern Census with a warning that it might make some figures not directly comparable. It is important, when looking at points 2 and 3 to realize that because of racially and or economically differing incidence and mortality rates, there may be significant discrepancies that develop if for example, there have been large population movements or even if the reporting institutions change or move their location. There is a good example of the kind of distortion that can be introduced which was mentioned in a study in Britain . The incidence of prostate cancer was very much higher in an institution in inner London where the inhabitants might be described as economically disadvantaged compared with the more affluent area served by an institution away from the city in what might be termed the ‘broker belt. The study suggested that diet, living conditions, ability to seek good advice, levels of service etc

accounted for the difference. The point of this is that if the inner city data were extrapolated into a national statistic, there would be a very different set of rates than if the second institution’s data was used. 4. There is a time lag in reporting data which, incredibly, seems to have worsened despite the advent of sophisticated computer based systems. The 2002 press release referred to above (15-Oct-2002 Journal of the National Cancer Institute) was issued because there was some puzzlement about the apparent decline in prostate cancer incidence rates which curiously enough occurred in the same time frame as the reduction in prostate cancer mortality rates. This report stated in part <snip> The standard time between a cancer diagnosis and its initial inclusion in cancer incidence statistics is about 2 years………. They found that it would take 4 to 17 years for 99% or more of the cancer cases to be reported. <snip> This raised the question of accuracy in my mind – bering in mind my views on the way

in which large institutions may operate. I have tried on many occasions to get an informed discussion going on the lock step rises and falls of mortality and incidence rates following the introduction of PSA testing in 1986. We know why the incidence rate rose – because more men were biopsied and the more men you biopsy the more prostate cancer you will find. As the 2004 study demonstrated so clearly if you biopsy men with a PSA under 4.0 ng/ml you will find more cells currently defined as prostate cancer than if you only biopsy men with a PSA higher than 4.0 ng/ml. But why did the mortality rate rise. And why did the incidence rate AND the mortality rate start to fall after 1991, five years later? No one has ever come up with a definitive answer. One of the leading activists has always dismissed my desire for such a discussion as saying that the two items have nothing to do with each other and doggedly repeats his mantra that the mortality rate has fallen, as indeed it has, depending on where you measure it from. He no longer responds to my postings. My point has always been that we need an explanation as to why both measures changed. We have to understand that if we are to attribute the observed fall in mortality rates from it’s all time high in 1991. From my limited viewpoint, significant changes like these in a population statistical base can come from a change in definition. Just what is a prostate cancer death? How is it defined? Did all reporting institutions use the same definitions? Did any definitions change? Those are the questions that no one can answer for me. There have been some glimmers of light shone on the subject: a. No less a person than Dr Walsh (who was apparently at some conference discussing the importance of screening in reducing mortality) was quoted last year as being questioned as to why the mortality rates in Britain had fallen when there was not the same emphasis or amount of screening in that country. His response was that they had changed the definition of prostate cancer related eeath to exclude pneumonia and this one factor had led to a reduction in prostate cancer related deaths. On raising this point in a forum I was told that this could not happen in the US . End of discussion. b. Soon after I read of Dr Walsh’s remarks, I came on a piece describing how the large European study (ERSPC) had agreed to ‘standardize’ their definition of prostate cancer to only include needle biopsy results that result in a Gleason Score of 6 or higher – in other words anyone who had a diagnosis of GS 5 would not be included in their data. This single change may well have produced the discrepancy in the ERSPC reported results of ‘lives saved’ when compared with the US study that showed ‘no lives saved’. Again I tried to discuss this change in definition and wondered if this was a contributing fator in the decline in reported deaths – after all if you are not diagnosed with PCa, you cannot die of the disease. My thoughts on the subject were ignored ar denied. Spurred on by this item I then

found that in practical terms, leading pathologists in the US had been applying this criterion since about 2005 and in January this year the proposal was formally adopted – see http://www.yananow.org/StrangePlace/forest.html#gleason for a summary of the changes. This has led to a significant change in the profile of diagnosed prostate cancer and the so-called ‘Migration†of Gleason Grades and Scores – see http://tinyurl.com/2jnpbu

In summary after what many will have considered a long and boring post, in answer to your question <snip> Your thoughts on the 30% increase and what it means? <snip> I think that a number of changes in diagnosis, definition, formulae and focus may have all resulted in the changes observed in the population data.

All the best

Prostate men need enlightening, not frightening Terry Herbert - diagnosed in 1996 and still going strong Read A Strange Place for unbiased information at http://www.yananow.net/StrangePlace/index.html

Attachment(s) from Terry Herbert

1 of 1 Photo(s)

StateCancerProfilesGraph-all ages.png" src="http://xa.yimg.com/kq/groups/4926965/tn/1471474522">

StateCancerProfilesGraph-all ages.png

[Guest guest]

Thanks Rick. Good luck to you too. I guess all these studies make one second guess the decision at times.

Mike

Subject: Mortality Spike was .....Swedish Study [1 Attachment]To: ProstateCancerSupport Date: Sunday, April 3, 2011, 7:59 PM

[Attachment(s) from Terry Herbert included below]

Mike,

In writing this piece I want to acknowledge that I am no statistician. All I know about statistics comes from many years of working in the insurance industry where I gained a clear insight into how inaccurate statistics can be because of basic errors or assumptions and how easily statistics can be manipulated by the adjustment of assumptions. There is an old joke about the insurance manager looking for an actuary. All applicants were presented with base data and asked to make a series of projections. All were rejected until at last an applicant asked the manager what result he wanted to see. The figures that demonstrate the significant rise in prostate cancer deaths after the introduction come from the SEER (Surveillance, Epidemiology, and End Results Program) statistics - http://seer.cancer.gov/ - which are accessible to all of us. They are said to be the most accurate figures available but of course there are, as is the case for all statistics, some issues in the collection and compilation of the data which can affect the reported outcome and estimates. Here are some of the basic points from my limited point of view: 1. It is said that the SEER data represents about 10% of the US population. National statistics are extrapolated from this data. Clearly an error in the base data will be significantly compounded when extrapolated to this extent. 2. The base data is collected from a limited number of institutions and not from all institutions in the US . A NCI pre4ss release in 2002 said in part <snip> Ten population-based registries report this

information to the NCI's Surveillance, Epidemiology, and End Results (SEER) Program. <snip> Clearly they must be very large institutions if threes ten represent 10% of the population. My personal experiences tend to make me think that large institutions often have built in error rates that may be higher than smaller institutions. 3. Calculations for incidence rates and the like are made using the data from the Census. Just which Census is used can make a significant difference in projected, extrapolated data. For many years data from an old Census was used (I think it was 1976?) This was then changed to a more modern Census with a warning that it might make some figures not directly comparable. It is important, when looking at points 2 and 3 to realize that because of racially and or economically differing incidence and mortality rates, there may be significant discrepancies that develop if for example, there have been large population movements or even if the reporting institutions change or move their location. There is a good example of the kind of distortion that can be introduced which was mentioned in a study in Britain . The incidence of prostate cancer was very much higher in an institution in inner London where the inhabitants might be described as economically disadvantaged compared with the more affluent area served by an institution away from the city in what might be termed the ‘broker belt. The study suggested that diet, living conditions, ability to seek good advice, levels of service etc

accounted for the difference. The point of this is that if the inner city data were extrapolated into a national statistic, there would be a very different set of rates than if the second institution’s data was used. 4. There is a time lag in reporting data which, incredibly, seems to have worsened despite the advent of sophisticated computer based systems. The 2002 press release referred to above (15-Oct-2002 Journal of the National Cancer Institute) was issued because there was some puzzlement about the apparent decline in prostate cancer incidence rates which curiously enough occurred in the same time frame as the reduction in prostate cancer mortality rates. This report stated in part <snip> The standard time between a cancer diagnosis and its initial inclusion in cancer incidence statistics is about 2 years………. They found that it would take 4 to 17 years for 99% or more of the cancer cases to be reported. <snip> This raised the question of accuracy in my mind – bering in mind my views on the way

in which large institutions may operate. I have tried on many occasions to get an informed discussion going on the lock step rises and falls of mortality and incidence rates following the introduction of PSA testing in 1986. We know why the incidence rate rose – because more men were biopsied and the more men you biopsy the more prostate cancer you will find. As the 2004 study demonstrated so clearly if you biopsy men with a PSA under 4.0 ng/ml you will find more cells currently defined as prostate cancer than if you only biopsy men with a PSA higher than 4.0 ng/ml. But why did the mortality rate rise. And why did the incidence rate AND the mortality rate start to fall after 1991, five years later? No one has ever come up with a definitive answer. One of the leading activists has always dismissed my desire for such a discussion as saying that the two items have nothing to do with each other and doggedly repeats his mantra that the mortality rate has fallen, as indeed it has, depending on where you measure it from. He no longer responds to my postings. My point has always been that we need an explanation as to why both measures changed. We have to understand that if we are to attribute the observed fall in mortality rates from it’s all time high in 1991. From my limited viewpoint, significant changes like these in a population statistical base can come from a change in definition. Just what is a prostate cancer death? How is it defined? Did all reporting institutions use the same definitions? Did any definitions change? Those are the questions that no one can answer for me. There have been some glimmers of light shone on the subject: a. No less a person than Dr Walsh (who was apparently at some conference discussing the importance of screening in reducing mortality) was quoted last year as being questioned as to why the mortality rates in Britain had fallen when there was not the same emphasis or amount of screening in that country. His response was that they had changed the definition of prostate cancer related eeath to exclude pneumonia and this one factor had led to a reduction in prostate cancer related deaths. On raising this point in a forum I was told that this could not happen in the US . End of discussion. b. Soon after I read of Dr Walsh’s remarks, I came on a piece describing how the large European study (ERSPC) had agreed to ‘standardize’ their definition of prostate cancer to only include needle biopsy results that result in a Gleason Score of 6 or higher – in other words anyone who had a diagnosis of GS 5 would not be included in their data. This single change may well have produced the discrepancy in the ERSPC reported results of ‘lives saved’ when compared with the US study that showed ‘no lives saved’. Again I tried to discuss this change in definition and wondered if this was a contributing fator in the decline in reported deaths – after all if you are not diagnosed with PCa, you cannot die of the disease. My thoughts on the subject were ignored ar denied. Spurred on by this item I then

found that in practical terms, leading pathologists in the US had been applying this criterion since about 2005 and in January this year the proposal was formally adopted – see http://www.yananow.org/StrangePlace/forest.html#gleason for a summary of the changes. This has led to a significant change in the profile of diagnosed prostate cancer and the so-called ‘Migration†of Gleason Grades and Scores – see http://tinyurl.com/2jnpbu

In summary after what many will have considered a long and boring post, in answer to your question <snip> Your thoughts on the 30% increase and what it means? <snip> I think that a number of changes in diagnosis, definition, formulae and focus may have all resulted in the changes observed in the population data.

All the best

Prostate men need enlightening, not frightening Terry Herbert - diagnosed in 1996 and still going strong Read A Strange Place for unbiased information at http://www.yananow.net/StrangePlace/index.html

Attachment(s) from Terry Herbert

1 of 1 Photo(s)

StateCancerProfilesGraph-all ages.png" src="http://xa.yimg.com/kq/groups/4926965/tn/1471474522">

StateCancerProfilesGraph-all ages.png

[Guest guest]

Mike,

I am four years out and in my quite times I still wonder "what if". It seems the more I read and the more I learn about this dam disease the more cloudy things become. My main fear is for my two sons and their future in regards to this scourge. They are now 33 and 28 and I don't know if I should encourage them to be tested or tell them it's better not to know, there are valid points to make on both sides. I've read about many studies on the subject of heredity and the link between father and son,some say there is a link and others say not(more muddy water). So I just hope they never have to deal with this shit, and if they do, by then there is a better treatment option.

Rick

To: ProstateCancerSupport Sent: Mon, April 4, 2011 9:55:09 AMSubject: Re: Mortality Spike was .....Swedish Study

Thanks Rick. Good luck to you too. I guess all these studies make one second guess the decision at times.

Mike

Subject: Mortality Spike was .....Swedish Study [1 Attachment]To: ProstateCancerSupport Date: Sunday, April 3, 2011, 7:59 PM

[Attachment(s) from Terry Herbert included below]

Mike,

In writing this piece I want to acknowledge that I am no statistician. All I know about statistics comes from many years of working in the insurance industry where I gained a clear insight into how inaccurate statistics can be because of basic errors or assumptions and how easily statistics can be manipulated by the adjustment of assumptions. There is an old joke about the insurance manager looking for an actuary. All applicants were presented with base data and asked to make a series of projections. All were rejected until at last an applicant asked the manager what result he wanted to see. The figures that demonstrate the significant rise in prostate cancer deaths after the introduction come from the SEER (Surveillance, Epidemiology, and End Results Program) statistics - http://seer.cancer.gov/ - which are accessible to all of us. They are said to be the most accurate figures available but of course there are, as is the case for all statistics, some issues in the collection and compilation of the data which can affect the reported outcome and estimates. Here are some of the basic points from my limited point of view: 1. It is said that the SEER data represents about 10% of the US population. National statistics are extrapolated from this data. Clearly an error in the base data will be significantly compounded when extrapolated to this extent. 2. The base data is collected from a limited number of institutions and not from all institutions in the US . A NCI pre4ss release in 2002 said in part <snip> Ten population-based registries report this

information to the NCI's Surveillance, Epidemiology, and End Results (SEER) Program. <snip> Clearly they must be very large institutions if threes ten represent 10% of the population. My personal experiences tend to make me think that large institutions often have built in error rates that may be higher than smaller institutions. 3. Calculations for incidence rates and the like are made using the data from the Census. Just which Census is used can make a significant difference in projected, extrapolated data. For many years data from an old Census was used (I think it was 1976?) This was then changed to a more modern Census with a warning that it might make some figures not directly comparable. It is important, when looking at points 2 and 3 to realize that because of racially and or economically differing incidence and mortality rates, there may be significant discrepancies that develop if for example, there have been large population movements or even if the reporting institutions change or move their location. There is a good example of the kind of distortion that can be introduced which was mentioned in a study in Britain . The incidence of prostate cancer was very much higher in an institution in inner London where the inhabitants might be described as economically disadvantaged compared with the more affluent area served by an institution away from the city in what might be termed the ‘broker belt. The study suggested that diet, living conditions, ability to seek good advice, levels of service etc

accounted for the difference. The point of this is that if the inner city data were extrapolated into a national statistic, there would be a very different set of rates than if the second institution’s data was used. 4. There is a time lag in reporting data which, incredibly, seems to have worsened despite the advent of sophisticated computer based systems. The 2002 press release referred to above (15-Oct-2002 Journal of the National Cancer Institute) was issued because there was some puzzlement about the apparent decline in prostate cancer incidence rates which curiously enough occurred in the same time frame as the reduction in prostate cancer mortality rates. This report stated in part <snip> The standard time between a cancer diagnosis and its initial inclusion in cancer incidence statistics is about 2 years………. They found that it would take 4 to 17 years for 99% or more of the cancer cases to be reported. <snip> This raised the question of accuracy in my mind – bering in mind my views on the way

in which large institutions may operate. I have tried on many occasions to get an informed discussion going on the lock step rises and falls of mortality and incidence rates following the introduction of PSA testing in 1986. We know why the incidence rate rose – because more men were biopsied and the more men you biopsy the more prostate cancer you will find. As the 2004 study demonstrated so clearly if you biopsy men with a PSA under 4.0 ng/ml you will find more cells currently defined as prostate cancer than if you only biopsy men with a PSA higher than 4.0 ng/ml. But why did the mortality rate rise. And why did the incidence rate AND the mortality rate start to fall after 1991, five years later? No one has ever come up with a definitive answer. One of the leading activists has always dismissed my desire for such a discussion as saying that the two items have nothing to do with each other and doggedly repeats his mantra that the mortality rate has fallen, as indeed it has, depending on where you measure it from. He no longer responds to my postings. My point has always been that we need an explanation as to why both measures changed. We have to understand that if we are to attribute the observed fall in mortality rates from it’s all time high in 1991. From my limited viewpoint, significant changes like these in a population statistical base can come from a change in definition. Just what is a prostate cancer death? How is it defined? Did all reporting institutions use the same definitions? Did any definitions change? Those are the questions that no one can answer for me. There have been some glimmers of light shone on the subject: a. No less a person than Dr Walsh (who was apparently at some conference discussing the importance of screening in reducing mortality) was quoted last year as being questioned as to why the mortality rates in Britain had fallen when there was not the same emphasis or amount of screening in that country. His response was that they had changed the definition of prostate cancer related eeath to exclude pneumonia and this one factor had led to a reduction in prostate cancer related deaths. On raising this point in a forum I was told that this could not happen in the US . End of discussion. b. Soon after I read of Dr Walsh’s remarks, I came on a piece describing how the large European study (ERSPC) had agreed to ‘standardize’ their definition of prostate cancer to only include needle biopsy results that result in a Gleason Score of 6 or higher – in other words anyone who had a diagnosis of GS 5 would not be included in their data. This single change may well have produced the discrepancy in the ERSPC reported results of ‘lives saved’ when compared with the US study that showed ‘no lives saved’. Again I tried to discuss this change in definition and wondered if this was a contributing fator in the decline in reported deaths – after all if you are not diagnosed with PCa, you cannot die of the disease. My thoughts on the subject were ignored ar denied. Spurred on by this item I then

found that in practical terms, leading pathologists in the US had been applying this criterion since about 2005 and in January this year the proposal was formally adopted – see http://www.yananow.org/StrangePlace/forest.html#gleason for a summary of the changes. This has led to a significant change in the profile of diagnosed prostate cancer and the so-called ‘Migration†of Gleason Grades and Scores – see http://tinyurl.com/2jnpbu

In summary after what many will have considered a long and boring post, in answer to your question <snip> Your thoughts on the 30% increase and what it means? <snip> I think that a number of changes in diagnosis, definition, formulae and focus may have all resulted in the changes observed in the population data.

All the best

Prostate men need enlightening, not frightening Terry Herbert - diagnosed in 1996 and still going strong Read A Strange Place for unbiased information at http://www.yananow.net/StrangePlace/index.html

Attachment(s) from Terry Herbert

1 of 1 Photo(s)

StateCancerProfilesGraph-all ages.png" src="http://xa.yimg.com/kq/groups/4926965/tn/1471474522">

StateCancerProfilesGraph-all ages.png

[Guest guest]

I have two sons also, Rick, and I share the dilemma.

Subject: Mortality Spike was .....Swedish Study [1 Attachment]To: ProstateCancerSupport Date: Sunday, April 3, 2011, 7:59 PM

[Attachment(s) from Terry Herbert included below]

Mike,

In writing this piece I want to acknowledge that I am no statistician. All I know about statistics comes from many years of working in the insurance industry where I gained a clear insight into how inaccurate statistics can be because of basic errors or assumptions and how easily statistics can be manipulated by the adjustment of assumptions. There is an old joke about the insurance manager looking for an actuary. All applicants were presented with base data and asked to make a series of projections. All were rejected until at last an applicant asked the manager what result he wanted to see. The figures that demonstrate the significant rise in prostate cancer deaths after the introduction come from the SEER (Surveillance, Epidemiology, and End Results Program) statistics - http://seer.cancer.gov/ - which are accessible to all of us. They are said to be the most accurate figures available but of course there are, as is the case for all statistics, some issues in the collection and compilation of the data which can affect the reported outcome and estimates. Here are some of the basic points from my limited point of view: 1. It is said that the SEER data represents about 10% of the US population. National statistics are extrapolated from this data. Clearly an error in the base data will be significantly compounded when extrapolated to this extent. 2. The base data is collected from a limited number of institutions and not from all institutions in the US . A NCI pre4ss release in 2002 said in part <snip> Ten population-based registries report this

information to the NCI's Surveillance, Epidemiology, and End Results (SEER) Program. <snip> Clearly they must be very large institutions if threes ten represent 10% of the population. My personal experiences tend to make me think that large institutions often have built in error rates that may be higher than smaller institutions. 3. Calculations for incidence rates and the like are made using the data from the Census. Just which Census is used can make a significant difference in projected, extrapolated data. For many years data from an old Census was used (I think it was 1976?) This was then changed to a more modern Census with a warning that it might make some figures not directly comparable. It is important, when looking at points 2 and 3 to realize that because of racially and or economically differing incidence and mortality rates, there may be significant discrepancies that develop if for example, there have been large population movements or even if the reporting institutions change or move their location. There is a good example of the kind of distortion that can be introduced which was mentioned in a study in Britain . The incidence of prostate cancer was very much higher in an institution in inner London where the inhabitants might be described as economically disadvantaged compared with the more affluent area served by an institution away from the city in what might be termed the ‘broker belt. The study suggested that diet, living conditions, ability to seek good advice, levels of service etc

accounted for the difference. The point of this is that if the inner city data were extrapolated into a national statistic, there would be a very different set of rates than if the second institution’s data was used. 4. There is a time lag in reporting data which, incredibly, seems to have worsened despite the advent of sophisticated computer based systems. The 2002 press release referred to above (15-Oct-2002 Journal of the National Cancer Institute) was issued because there was some puzzlement about the apparent decline in prostate cancer incidence rates which curiously enough occurred in the same time frame as the reduction in prostate cancer mortality rates. This report stated in part <snip> The standard time between a cancer diagnosis and its initial inclusion in cancer incidence statistics is about 2 years………. They found that it would take 4 to 17 years for 99% or more of the cancer cases to be reported. <snip> This raised the question of accuracy in my mind – bering in mind my views on the way

in which large institutions may operate. I have tried on many occasions to get an informed discussion going on the lock step rises and falls of mortality and incidence rates following the introduction of PSA testing in 1986. We know why the incidence rate rose – because more men were biopsied and the more men you biopsy the more prostate cancer you will find. As the 2004 study demonstrated so clearly if you biopsy men with a PSA under 4.0 ng/ml you will find more cells currently defined as prostate cancer than if you only biopsy men with a PSA higher than 4.0 ng/ml. But why did the mortality rate rise. And why did the incidence rate AND the mortality rate start to fall after 1991, five years later? No one has ever come up with a definitive answer. One of the leading activists has always dismissed my desire for such a discussion as saying that the two items have nothing to do with each other and doggedly repeats his mantra that the mortality rate has fallen, as indeed it has, depending on where you measure it from. He no longer responds to my postings. My point has always been that we need an explanation as to why both measures changed. We have to understand that if we are to attribute the observed fall in mortality rates from it’s all time high in 1991. From my limited viewpoint, significant changes like these in a population statistical base can come from a change in definition. Just what is a prostate cancer death? How is it defined? Did all reporting institutions use the same definitions? Did any definitions change? Those are the questions that no one can answer for me. There have been some glimmers of light shone on the subject: a. No less a person than Dr Walsh (who was apparently at some conference discussing the importance of screening in reducing mortality) was quoted last year as being questioned as to why the mortality rates in Britain had fallen when there was not the same emphasis or amount of screening in that country. His response was that they had changed the definition of prostate cancer related eeath to exclude pneumonia and this one factor had led to a reduction in prostate cancer related deaths. On raising this point in a forum I was told that this could not happen in the US . End of discussion. b. Soon after I read of Dr Walsh’s remarks, I came on a piece describing how the large European study (ERSPC) had agreed to ‘standardize’ their definition of prostate cancer to only include needle biopsy results that result in a Gleason Score of 6 or higher – in other words anyone who had a diagnosis of GS 5 would not be included in their data. This single change may well have produced the discrepancy in the ERSPC reported results of ‘lives saved’ when compared with the US study that showed ‘no lives saved’. Again I tried to discuss this change in definition and wondered if this was a contributing fator in the decline in reported deaths – after all if you are not diagnosed with PCa, you cannot die of the disease. My thoughts on the subject were ignored ar denied. Spurred on by this item I then

found that in practical terms, leading pathologists in the US had been applying this criterion since about 2005 and in January this year the proposal was formally adopted – see http://www.yananow.org/StrangePlace/forest.html#gleason for a summary of the changes. This has led to a significant change in the profile of diagnosed prostate cancer and the so-called ‘Migration†of Gleason Grades and Scores – see http://tinyurl.com/2jnpbu

In summary after what many will have considered a long and boring post, in answer to your question <snip> Your thoughts on the 30% increase and what it means? <snip> I think that a number of changes in diagnosis, definition, formulae and focus may have all resulted in the changes observed in the population data.

All the best

Prostate men need enlightening, not frightening Terry Herbert - diagnosed in 1996 and still going strong Read A Strange Place for unbiased information at http://www.yananow.net/StrangePlace/index.html

Attachment(s) from Terry Herbert

1 of 1 Photo(s)

StateCancerProfilesGraph-all ages.png" src="http://xa.yimg.com/kq/groups/4926965/tn/1471474522">

StateCancerProfilesGraph-all ages.png

[Guest guest]

I have two brothers. I gave them each a copy

of my booklet before they started having regular PSA tests so that they could

grasp some of the basics and the uncertainties of diagnosis, choices and

outcomes.

One brother – at 62 – had what

was termed an elevated PSA. We discussed this extensively (thanks to Skype

calls between Australia and South Africa

cost nothing!!) and he then rejected the urologist’s suggested biopsy. After

a spell of quarterly and then six monthly tests he has gone back to annual

tests. His PSA has dropped below the urologist’s trip line of 4.0 ng/ml. He

is aware of the study showing that 15% of men with a PSA less than 4.0

ng/ml would be diagnosed with PCa but he has not felt the need to have a biopsy.

My younger brother has had no elevated PSA (above 4.0 ng/ml) and,

again, although aware of the inaccuracy and vagaries of the PSA test, he has

not felt the need to have a biopsy.

Would this kind of approach be suitable

for your sons? Would you like me to send them a copy of my booklet, free of

charge so that they are informed ahead of any potential problems?

All the best

Prostate men need enlightening, not

frightening

Terry Herbert - diagnosed in 1996 and

still going strong

Read A Strange Place for unbiased information at http://www.yananow.org/StrangePlace/index.html

From: ProstateCancerSupport [mailto:ProstateCancerSupport ] On Behalf Of Clowes

Sent: Tuesday, 5 April 2011 10:57

AM

To: ProstateCancerSupport

Subject: Re:

Mortality Spike was .....Swedish Study

I have two sons also, Rick, and I share the dilemma.

Subject: Mortality Spike was .....Swedish Study

[1 Attachment]

To: ProstateCancerSupport

Date: Sunday, April 3, 2011, 7:59 PM

[Attachment(s)

from Terry Herbert included below]

Mike,

In writing this

piece I want to acknowledge that I am no statistician. All I know about

statistics comes from many years of working in the insurance industry

where I gained a clear insight into how inaccurate statistics can be

because of basic errors or assumptions and how easily statistics can be

manipulated by the adjustment of assumptions. There is an old joke about

the insurance manager looking for an actuary. All applicants were

presented with base data and asked to make a series of projections. All were

rejected until at last an applicant asked the manager what result he

wanted to see.

The figures that

demonstrate the significant rise in prostate cancer deaths after the

introduction come from the SEER (Surveillance, Epidemiology, and End

Results Program) statistics - http://seer.cancer.gov/ - which are

accessible to all of us. They are said to be the most accurate figures

available but of course there are, as is the case for all statistics,

some issues in the collection and compilation of the data which can

affect the reported outcome and estimates. Here are some of the basic

points from my limited point of view:

1. It is said that

the SEER data represents about 10% of the US population. National

statistics are extrapolated from this data. Clearly an error in the base

data will be significantly compounded when extrapolated to this extent.

2. The base data is

collected from a limited number of institutions and not from all

institutions in the US

.. A NCI pre4ss release in 2002 said in part <snip> Ten

population-based registries report this

information to the

NCI's Surveillance, Epidemiology, and End Results (SEER) Program.

<snip> Clearly they must be very large institutions if threes ten

represent 10% of the population. My

personal experiences tend to make me think that large institutions

often have built in error rates that may be higher than smaller

institutions.

3. Calculations for

incidence rates and the like are made using the data from the

Census. Just which Census is used can make a significant difference

in projected, extrapolated data. For many years data from an old Census

was used (I think it was 1976?) This was then changed to a more modern

Census with a warning that it might make some figures not directly

comparable.

It is important,

when looking at points 2 and 3 to realize that because of racially and or

economically differing incidence and mortality rates, there may be

significant discrepancies that develop if for example, there have been

large population movements or even if the reporting institutions change

or move their location. There is a good example of the kind of distortion

that can be introduced which was mentioned in a study in Britain . The incidence of prostate

cancer was very much higher in an institution in inner London where the

inhabitants might be described as economically disadvantaged compared

with the more affluent area served by an institution away from the city

in what might be termed the ‘broker belt. The study suggested that

diet, living conditions, ability to seek good advice, levels of service

etc accounted for the difference. The point of this is that if the inner

city data were extrapolated into a national statistic, there would be a

very different set of rates than if the second institution’s data

was used.

4. There is a time

lag in reporting data which, incredibly, seems to have worsened despite

the advent of sophisticated computer based systems. The 2002 press

release referred to above (15-Oct-2002 Journal of the

National Cancer Institute) was issued because there was some puzzlement

about the apparent decline in prostate cancer incidence rates which

curiously enough occurred in the same time frame as the reduction in

prostate cancer mortality rates. This report stated in part <snip>

The standard time between a cancer diagnosis and its initial inclusion in

cancer incidence statistics is about 2 years………. They

found that it would take 4 to 17 years for 99% or more of the cancer

cases to be reported. <snip> This raised the question of accuracy

in my mind – bering in mind my views on the way in which large

institutions may operate.

I have tried on

many occasions to get an informed discussion going on the lock step rises

and falls of mortality and incidence rates following the introduction of

PSA testing in 1986. We know why the incidence rate rose – because

more men were biopsied and the more men you biopsy the more prostate

cancer you will find. As the 2004 study demonstrated so clearly if you

biopsy men with a PSA under 4.0 ng/ml you will find more cells

currently defined as prostate cancer than if you only biopsy men with a

PSA higher than 4.0 ng/ml. But why did the mortality rate rise. And why

did the incidence rate AND the mortality rate start to fall after 1991,

five years later?

No one has ever

come up with a definitive answer. One of the leading activists has always

dismissed my desire for such a discussion as saying that the two items

have nothing to do with each other and doggedly repeats his mantra that

the mortality rate has fallen, as indeed it has, depending on where you

measure it from. He no longer responds to my postings.

My

point has always been that we need an explanation as to why both measures

changed. We have to understand that if we are to attribute the observed

fall in mortality rates from it’s all time high in 1991. From my

limited viewpoint, significant changes like these in a population

statistical base can come from a change in definition. Just what is a

prostate cancer death? How is it defined? Did all reporting institutions

use the same definitions? Did any definitions change? Those are the

questions that no one can answer for me. There have been some glimmers of

light shone on the subject:

a. No less a person

than Dr Walsh (who was apparently at some conference discussing

the importance of screening in reducing mortality) was quoted last year

as being questioned as to why the mortality rates in Britain had

fallen when there was not the same emphasis or amount of screening in

that country. His response was that they had changed the definition of

prostate cancer related eeath to exclude pneumonia and this one factor

had led to a reduction in prostate cancer related deaths. On raising this

point in a forum I was told that this could not happen in the US . End

of discussion.

b. Soon after I

read of Dr Walsh’s remarks, I came on a piece describing how the

large European study (ERSPC) had agreed to ‘standardize’

their definition of prostate cancer to only include needle biopsy results

that result in a Gleason Score of 6 or higher – in other words

anyone who had a diagnosis of GS 5 would not be included in their data.

This single change may well have produced the discrepancy in the ERSPC

reported results of ‘lives saved’ when compared with the US study

that showed ‘no lives saved’. Again I tried to discuss this

change in definition and wondered if this was a contributing fator

in the decline in reported deaths – after all if you are not

diagnosed with PCa, you cannot die of the disease. My thoughts on the subject were ignored ar

denied. Spurred on by this item I then found that in practical terms,

leading pathologists in the US had been applying this criterion since

about 2005 and in January this year the proposal was formally adopted –

see http://www.yananow.org/StrangePlace/forest.html#gleason for a summary

of the changes. This has led to a significant change in the profile of

diagnosed prostate cancer and the so-called ‘Migration” of

Gleason Grades and Scores – see http://tinyurl.com/2jnpbu

In summary after

what many will have considered a long and boring post, in answer to your

question <snip> Your thoughts on the 30% increase and

what it means? <snip> I think that a number

of changes in diagnosis, definition, formulae and focus may have all

resulted in the changes observed in the population data.

All the best

Prostate men need

enlightening, not frightening

Terry Herbert -

diagnosed in 1996 and still going strong

Read A

Strange Place for unbiased information at

http://www.yananow.net/StrangePlace/index.html

Attachment(s)

from Terry Herbert

1 of 1 Photo(s)

StateCancerProfilesGraph-all

ages.png " src= " http://xa.yimg.com/kq/groups/4926965/tn/1471474522 " >

StateCancerProfilesGraph-all ages.png

[Guest guest]

Mike,

How old is Rick?

To: ProstateCancerSupport Sent: Mon, April 4, 2011 8:57:14 PMSubject: Re: Mortality Spike was .....Swedish Study

I have two sons also, Rick, and I share the dilemma.

Subject: Mortality Spike was .....Swedish Study [1 Attachment]To: ProstateCancerSupport Date: Sunday, April 3, 2011, 7:59 PM

[Attachment(s) from Terry Herbert included below]

Mike,

In writing this piece I want to acknowledge that I am no statistician. All I know about statistics comes from many years of working in the insurance industry where I gained a clear insight into how inaccurate statistics can be because of basic errors or assumptions and how easily statistics can be manipulated by the adjustment of assumptions. There is an old joke about the insurance manager looking for an actuary. All applicants were presented with base data and asked to make a series of projections. All were rejected until at last an applicant asked the manager what result he wanted to see. The figures that demonstrate the significant rise in prostate cancer deaths after the introduction come from the SEER (Surveillance, Epidemiology, and End Results Program) statistics - http://seer.cancer.gov/ - which are accessible to all of us. They are said to be the most accurate figures available but of course there are, as is the case for all statistics, some issues in the collection and compilation of the data which can affect the reported outcome and estimates. Here are some of the basic points from my limited point of view: 1. It is said that the SEER data represents about 10% of the US population. National statistics are extrapolated from this data. Clearly an error in the base data will be significantly compounded when extrapolated to this extent. 2. The base data is collected from a limited number of institutions and not from all institutions in the US . A NCI pre4ss release in 2002 said in part <snip> Ten population-based registries report this

information to the NCI's Surveillance, Epidemiology, and End Results (SEER) Program. <snip> Clearly they must be very large institutions if threes ten represent 10% of the population. My personal experiences tend to make me think that large institutions often have built in error rates that may be higher than smaller institutions. 3. Calculations for incidence rates and the like are made using the data from the Census. Just which Census is used can make a significant difference in projected, extrapolated data. For many years data from an old Census was used (I think it was 1976?) This was then changed to a more modern Census with a warning that it might make some figures not directly comparable. It is important, when looking at points 2 and 3 to realize that because of racially and or economically differing incidence and mortality rates, there may be significant discrepancies that develop if for example, there have been large population movements or even if the reporting institutions change or move their location. There is a good example of the kind of distortion that can be introduced which was mentioned in a study in Britain . The incidence of prostate cancer was very much higher in an institution in inner London where the inhabitants might be described as economically disadvantaged compared with the more affluent area served by an institution away from the city in what might be termed the ‘broker belt. The study suggested that diet, living conditions, ability to seek good advice, levels of service etc

accounted for the difference. The point of this is that if the inner city data were extrapolated into a national statistic, there would be a very different set of rates than if the second institution’s data was used. 4. There is a time lag in reporting data which, incredibly, seems to have worsened despite the advent of sophisticated computer based systems. The 2002 press release referred to above (15-Oct-2002 Journal of the National Cancer Institute) was issued because there was some puzzlement about the apparent decline in prostate cancer incidence rates which curiously enough occurred in the same time frame as the reduction in prostate cancer mortality rates. This report stated in part <snip> The standard time between a cancer diagnosis and its initial inclusion in cancer incidence statistics is about 2 years………. They found that it would take 4 to 17 years for 99% or more of the cancer cases to be reported. <snip> This raised the question of accuracy in my mind – bering in mind my views on the way

in which large institutions may operate. I have tried on many occasions to get an informed discussion going on the lock step rises and falls of mortality and incidence rates following the introduction of PSA testing in 1986. We know why the incidence rate rose – because more men were biopsied and the more men you biopsy the more prostate cancer you will find. As the 2004 study demonstrated so clearly if you biopsy men with a PSA under 4.0 ng/ml you will find more cells currently defined as prostate cancer than if you only biopsy men with a PSA higher than 4.0 ng/ml. But why did the mortality rate rise. And why did the incidence rate AND the mortality rate start to fall after 1991, five years later? No one has ever come up with a definitive answer. One of the leading activists has always dismissed my desire for such a discussion as saying that the two items have nothing to do with each other and doggedly repeats his mantra that the mortality rate has fallen, as indeed it has, depending on where you measure it from. He no longer responds to my postings. My point has always been that we need an explanation as to why both measures changed. We have to understand that if we are to attribute the observed fall in mortality rates from it’s all time high in 1991. From my limited viewpoint, significant changes like these in a population statistical base can come from a change in definition. Just what is a prostate cancer death? How is it defined? Did all reporting institutions use the same definitions? Did any definitions change? Those are the questions that no one can answer for me. There have been some glimmers of light shone on the subject: a. No less a person than Dr Walsh (who was apparently at some conference discussing the importance of screening in reducing mortality) was quoted last year as being questioned as to why the mortality rates in Britain had fallen when there was not the same emphasis or amount of screening in that country. His response was that they had changed the definition of prostate cancer related eeath to exclude pneumonia and this one factor had led to a reduction in prostate cancer related deaths. On raising this point in a forum I was told that this could not happen in the US . End of discussion. b. Soon after I read of Dr Walsh’s remarks, I came on a piece describing how the large European study (ERSPC) had agreed to ‘standardize’ their definition of prostate cancer to only include needle biopsy results that result in a Gleason Score of 6 or higher – in other words anyone who had a diagnosis of GS 5 would not be included in their data. This single change may well have produced the discrepancy in the ERSPC reported results of ‘lives saved’ when compared with the US study that showed ‘no lives saved’. Again I tried to discuss this change in definition and wondered if this was a contributing fator in the decline in reported deaths – after all if you are not diagnosed with PCa, you cannot die of the disease. My thoughts on the subject were ignored ar denied. Spurred on by this item I then

found that in practical terms, leading pathologists in the US had been applying this criterion since about 2005 and in January this year the proposal was formally adopted – see http://www.yananow.org/StrangePlace/forest.html#gleason for a summary of the changes. This has led to a significant change in the profile of diagnosed prostate cancer and the so-called ‘Migration†of Gleason Grades and Scores – see http://tinyurl.com/2jnpbu

In summary after what many will have considered a long and boring post, in answer to your question <snip> Your thoughts on the 30% increase and what it means? <snip> I think that a number of changes in diagnosis, definition, formulae and focus may have all resulted in the changes observed in the population data.

All the best

Prostate men need enlightening, not frightening Terry Herbert - diagnosed in 1996 and still going strong Read A Strange Place for unbiased information at http://www.yananow.net/StrangePlace/index.html

Attachment(s) from Terry Herbert

1 of 1 Photo(s)

StateCancerProfilesGraph-all ages.png" src="http://xa.yimg.com/kq/groups/4926965/tn/1471474522">

StateCancerProfilesGraph-all ages.png

[Guest guest]

Terry, That would be great. Although my boys are still young and not at an age where it would be time to get a baseline all the knowledge we could gather would be great.

Thanks,

Rick

To: ProstateCancerSupport Sent: Mon, April 4, 2011 9:18:22 PMSubject: RE: Mortality Spike was .....Swedish Study

I have two brothers. I gave them each a copy of my booklet before they started having regular PSA tests so that they could grasp some of the basics and the uncertainties of diagnosis, choices and outcomes.

One brother – at 62 – had what was termed an elevated PSA. We discussed this extensively (thanks to Skype calls between Australia and South Africa cost nothing!!) and he then rejected the urologist’s suggested biopsy. After a spell of quarterly and then six monthly tests he has gone back to annual tests. His PSA has dropped below the urologist’s trip line of 4.0 ng/ml. He is aware of the study showing that 15% of men with a PSA less than 4.0 ng/ml would be diagnosed with PCa but he has not felt the need to have a biopsy.

My younger brother has had no elevated PSA (above 4.0 ng/ml) and, again, although aware of the inaccuracy and vagaries of the PSA test, he has not felt the need to have a biopsy.

Would this kind of approach be suitable for your sons? Would you like me to send them a copy of my booklet, free of charge so that they are informed ahead of any potential problems?

All the best

Prostate men need enlightening, not frightening

Terry Herbert - diagnosed in 1996 and still going strong

Read A Strange Place for unbiased information at http://www.yananow.net/StrangePlace/index.html

From: ProstateCancerSupport [mailto: ProstateCancerSupport ] On Behalf Of ClowesSent: Tuesday, 5 April 2011 10:57 AMTo: ProstateCancerSupport Subject: Re: Mortality Spike was .....Swedish Study

I have two sons also, Rick, and I share the dilemma.

Subject: Mortality Spike was .....Swedish Study [1 Attachment]To: ProstateCancerSupport Date: Sunday, April 3, 2011, 7:59 PM

[Attachment(s) from Terry Herbert included below]

Mike,

In writing this piece I want to acknowledge that I am no statistician. All I know about statistics comes from many years of working in the insurance industry where I gained a clear insight into how inaccurate statistics can be because of basic errors or assumptions and how easily statistics can be manipulated by the adjustment of assumptions. There is an old joke about the insurance manager looking for an actuary. All applicants were presented with base data and asked to make a series of projections. All were rejected until at last an applicant asked the manager what result he wanted to see.

The figures that demonstrate the significant rise in prostate cancer deaths after the introduction come from the SEER (Surveillance, Epidemiology, and End Results Program) statistics - http://seer.cancer.gov/ - which are accessible to all of us. They are said to be the most accurate figures available but of course there are, as is the case for all statistics, some issues in the collection and compilation of the data which can affect the reported outcome and estimates. Here are some of the basic points from my limited point of view:

1. It is said that the SEER data represents about 10% of the US population. National statistics are extrapolated from this data. Clearly an error in the base data will be significantly compounded when extrapolated to this extent.

2. The base data is collected from a limited number of institutions and not from all institutions in the US . A NCI pre4ss release in 2002 said in part <snip> Ten population-based registries report this

information to the NCI's Surveillance, Epidemiology, and End Results (SEER) Program. <snip> Clearly they must be very large institutions if threes ten represent 10% of the population. My personal experiences tend to make me think that large institutions often have built in error rates that may be higher than smaller institutions.

3. Calculations for incidence rates and the like are made using the data from the Census. Just which Census is used can make a significant difference in projected, extrapolated data. For many years data from an old Census was used (I think it was 1976?) This was then changed to a more modern Census with a warning that it might make some figures not directly comparable.

It is important, when looking at points 2 and 3 to realize that because of racially and or economically differing incidence and mortality rates, there may be significant discrepancies that develop if for example, there have been large population movements or even if the reporting institutions change or move their location. There is a good example of the kind of distortion that can be introduced which was mentioned in a study in Britain . The incidence of prostate cancer was very much higher in an institution in inner London where the inhabitants might be described as economically disadvantaged compared with the more affluent area served by an institution away from the city in what might be termed the ‘broker belt. The study suggested that diet, living conditions, ability to seek good advice, levels of service etc

accounted for the difference. The point of this is that if the inner city data were extrapolated into a national statistic, there would be a very different set of rates than if the second institution’s data was used.

4. There is a time lag in reporting data which, incredibly, seems to have worsened despite the advent of sophisticated computer based systems. The 2002 press release referred to above (15-Oct-2002 Journal of the National Cancer Institute) was issued because there was some puzzlement about the apparent decline in prostate cancer incidence rates which curiously enough occurred in the same time frame as the reduction in prostate cancer mortality rates. This report stated in part <snip> The standard time between a cancer diagnosis and its initial inclusion in cancer incidence statistics is about 2 years………. They found that it would take 4 to 17 years for 99% or more of the cancer cases to be reported. <snip> This raised the question of accuracy in my mind – bering in mind my views on the way

in which large institutions may operate.

I have tried on many occasions to get an informed discussion going on the lock step rises and falls of mortality and incidence rates following the introduction of PSA testing in 1986. We know why the incidence rate rose – because more men were biopsied and the more men you biopsy the more prostate cancer you will find. As the 2004 study demonstrated so clearly if you biopsy men with a PSA under 4.0 ng/ml you will find more cells currently defined as prostate cancer than if you only biopsy men with a PSA higher than 4.0 ng/ml. But why did the mortality rate rise. And why did the incidence rate AND the mortality rate start to fall after 1991, five years later?

No one has ever come up with a definitive answer. One of the leading activists has always dismissed my desire for such a discussion as saying that the two items have nothing to do with each other and doggedly repeats his mantra that the mortality rate has fallen, as indeed it has, depending on where you measure it from. He no longer responds to my postings.

My point has always been that we need an explanation as to why both measures changed. We have to understand that if we are to attribute the observed fall in mortality rates from it’s all time high in 1991. From my limited viewpoint, significant changes like these in a population statistical base can come from a change in definition. Just what is a prostate cancer death? How is it defined? Did all reporting institutions use the same definitions? Did any definitions change? Those are the questions that no one can answer for me. There have been some glimmers of light shone on the subject:

a. No less a person than Dr Walsh (who was apparently at some conference discussing the importance of screening in reducing mortality) was quoted last year as being questioned as to why the mortality rates in Britain had fallen when there was not the same emphasis or amount of screening in that country. His response was that they had changed the definition of prostate cancer related eeath to exclude pneumonia and this one factor had led to a reduction in prostate cancer related deaths. On raising this point in a forum I was told that this could not happen in the US . End of discussion.

b. Soon after I read of Dr Walsh’s remarks, I came on a piece describing how the large European study (ERSPC) had agreed to ‘standardize’ their definition of prostate cancer to only include needle biopsy results that result in a Gleason Score of 6 or higher – in other words anyone who had a diagnosis of GS 5 would not be included in their data. This single change may well have produced the discrepancy in the ERSPC reported results of ‘lives saved’ when compared with the US study that showed ‘no lives saved’. Again I tried to discuss this change in definition and wondered if this was a contributing fator in the decline in reported deaths – after all if you are not diagnosed with PCa, you cannot die of the disease. My thoughts on the subject were ignored ar denied. Spurred on by this item I then

found that in practical terms, leading pathologists in the US had been applying this criterion since about 2005 and in January this year the proposal was formally adopted – see http://www.yananow.org/StrangePlace/forest.html#gleason for a summary of the changes. This has led to a significant change in the profile of diagnosed prostate cancer and the so-called ‘Migration†of Gleason Grades and Scores – see http://tinyurl.com/2jnpbu

In summary after what many will have considered a long and boring post, in answer to your question <snip> Your thoughts on the 30% increase and what it means? <snip> I think that a number of changes in diagnosis, definition, formulae and focus may have all resulted in the changes observed in the population data.

All the best

Prostate men need enlightening, not frightening

Terry Herbert - diagnosed in 1996 and still going strong

Read A Strange Place for unbiased information at http://www.yananow.net/StrangePlace/index.html

Attachment(s) from Terry Herbert

1 of 1 Photo(s)

StateCancerProfilesGraph-all ages.png" src="http://xa.yimg.com/kq/groups/4926965/tn/1471474522">

StateCancerProfilesGraph-all ages.png

[Guest guest]

On 4/4/11, White wrote, in pertinent part:

> My main fear is for my two

> sons and their future in regards to this scourge. They are now 33

> and 28 and I don't know if I should encourage them to be tested

> or tell them it's better not to know, there are valid points to

> make on both sides.

I don't buy the idea of sitting around and waiting for the sky to

fall.

" Treatment or non-treatment decisions can be made once a cancer

is found but not

knowing about it in the first place surely burns bridges. "

--From " What Would You Do, Doctor? "

ph A, , Jr., Associate Editor

Journal of Urology Volume 182, Issue 2, Pages 421-422 (August 2009)

Regards,

Steve J

[Guest guest]

Since we are quoting doctors, here is Dr

Logothetis:

“One of the problems with prostate

cancer is definition. They label it as a cancer, and they force us all to

behave in a way that introduces us to a cascade of events that sends us to very

morbid therapy. It's sort of like once that cancer label is put on there we are

obligated to behave in a certain way, and its driven by physician beliefs and patient

beliefs and frequently they don't have anything to do with reality.”

Rick, mail me off line and give me your

postal address – same goes for anyone else who might find a copy useful.

All the best

Prostate men need enlightening, not

frightening

Terry Herbert - diagnosed in 1996 and

still going strong

Read A Strange Place for unbiased information at http://www.yananow.org/StrangePlace/index.html

From: ProstateCancerSupport [mailto:ProstateCancerSupport ] On Behalf Of Steve Jordan

Sent: Tuesday, 5 April 2011 11:26

AM

To: ProstateCancerSupport

Subject: Re:

Mortality Spike was .....Swedish Study

On

4/4/11, White wrote, in pertinent part:

> My main fear is for my two

> sons and their future in regards to this scourge. They are now 33

> and 28 and I don't know if I should encourage them to be tested

> or tell them it's better not to know, there are valid points to

> make on both sides.

I don't buy the idea of sitting around and waiting for the sky to

fall.

" Treatment or non-treatment decisions can be made once a cancer

is found but not

knowing about it in the first place surely burns bridges. "

--From " What Would You Do, Doctor? "

ph A, , Jr., Associate Editor

Journal of Urology Volume 182, Issue 2, Pages 421-422 (August 2009)

Regards,

Steve J

[Guest guest]



One thing on this is that technology and understanding evolve over the years.

What we assume to be true today maybe proved untrue in the future.

If your sons do become involved in our club (that no one wants to join), they could well have a different treatment regime.

It wasn't long ago that very little money was spent in the UK on independant research of PCa the ladies beat us by a mile on their bette noir. We still have a long way to go to catch up.

As has been pointed out the speed of growth of many PCas makes judging long term stats very difficult. Lots of other factors come into play, environment, diet, poverty, stress, impact of other illnesses. This results in nightmares for statisticians!

At the end of our thinking we must have hope, so we choose ways of feeling we are doing something about it. This might be anything from careful monitoring, through change of diet to more radical informed choices.

I'd still rather have 15 positive years of life than a decade and a half sitting worrying.

a. No less a person than Dr Walsh (who was apparently at some conference discussing the importance of screening in reducing mortality) was quoted last year as being questioned as to why the mortality rates in Britain had fallen when there was not the same emphasis or amount of screening in that country. His response was that they had changed the definition of prostate cancer related eeath to exclude pneumonia and this one factor had led to a reduction in prostate cancer related deaths. On raising this point in a forum I was told that this could not happen in the US . End of discussion. b. Soon after I read of Dr Walsh’s remarks, I came on a piece describing how the large European study (ERSPC) had agreed to ‘standardize’ their definition of prostate cancer to only include needle biopsy results that result in a Gleason Score of 6 or higher – in other words anyone who had a diagnosis of GS 5 would not be included in their data. This single change may well have produced the discrepancy in the ERSPC reported results of ‘lives saved’ when compared with the US study that showed ‘no lives saved’. Again I tried to discuss this change in definition and wondered if this was a contributing fator in the decline in reported deaths – after all if you are not diagnosed with PCa, you cannot die of the disease. My thoughts on the subject were ignored ar denied. Spurred on by this item I then found that in practical terms, leading pathologists in the US had been applying this criterion since about 2005 and in January this year the proposal was formally adopted – see http://www.yananow.org/StrangePlace/forest.html#gleason for a summary of the changes. This has led to a significant change in the profile of diagnosed prostate cancer and the so-called ‘Migration†of Gleason Grades and Scores – see http://tinyurl.com/2jnpbu

In summary after what many will have considered a long and boring post, in answer to your question <snip> Your thoughts on the 30% increase and what it means? <snip> I think that a number of changes in diagnosis, definition, formulae and focus may have all resulted in the changes observed in the population data.

All the best

Prostate men need enlightening, not frightening Terry Herbert - diagnosed in 1996 and still going strong Read A Strange Place for unbiased information at http://www.yananow.net/StrangePlace/index.html

Attachment(s) from Terry Herbert

1 of 1 Photo(s)

StateCancerProfilesGraph-all ages.png" src="http://xa.yimg.com/kq/groups/4926965/tn/1471474522">

StateCancerProfilesGraph-all ages.png

[Guest guest]

:

 

You wrote:

 

" At the end of our thinking we must have hope, so we choose ways of feeling we are doing something about it. This might be anything from careful monitoring, through change of diet to more radical informed choices.

 

I'd still rather have 15 positive years of life than a decade and a half sitting worrying. "

Thank you for writing this.  It succinctly summarizes how I arrived (finally) in being at peace with the fact that I have PCa, and why I am at peace with the decision I made to have surgery and to change my diet and lifestyle post surgery.

 

Next Monday, April 11th, will be the third anniversary of the day I was told I had a membership in the club no one one wants to join.  June 11th will be the third anniversary of my surgery.  So far, all is well with me.  PSA less than 0.01.  No need for follow up.  " Willy " is most definitely shorter than he was, but is functioning OK (as OK as it gets for a 58 year old).  I have been fortunate.

 

I fully realize that things can " so south " for me very quickly.  There are no guarantees.  But I like to think that I've kept my options open and there are other things that can be tried if need be.  I pray that they are never needed.

 

Thank you again for your words.  I can certainly relate to them.

 

Coy

, Michigan USA

[Guest guest]

Well, it is so nice to hear some positive responses. But I cannot help but still let OUR voice be heard...to warn others, that my husband would rather now have his old life back, and to worry of what might or might not happen...than to NEVER be able to sit, and be in constant NERVE pain, where he has had to quit work, and all his most loved activities, duet to "unfortunate problems" after surgery. No one will say why it happened, or is interested in looking up statistics on how many this does happen to...and we know it has happened to others. But want others to know, a perfectly healthy, very well fit, very virile, 57 year old man (my husband) had RPP surgery over a year ago, Feb 15 2009, and still today "cannot sit". He is still on pain meds (oxycodone) besides Neurontin, and an antidepressant. He

was one the so called PC Club members, ... that had a fear of "living with cancer" and felt that the surgery seemed simple, straight forward, and a very slight possibility of long term impotence or incontinence for his age, status of cancer (PSA 2.3), and type of surgery (RPP) stats. Unfortunately, my hubby relied on the doctor's advise. Low and behold, the results were something that our doctor said he never dealt with before or heard of...(though we have found out differently of late). Our Urologist - said by many to be an EXPERT in this area in Mich. could not believe his outcome!My husband as of today, is still undergoing steroid injections to keep him out of pain!We are coming to terms with this way of living...slowly accepting this may be OUR WAY of life....for today, or for a while...or for ever! We continue to seek help, and do our own research, since no Doctor wants to. Our PC fellowship does not have much to

offer! But a few good men on this web site have given us some good research advice into helping us find someone who may be able to help. It seems to us, the doctors are all there for you BEFORE you undergo surgery...but after...if any problems that do not fall into the "norm"(impotence and incontinence)...you are an anomaly....and on your own. By the way, no incontinence for my spouse....but he is in so much pain, impotence is yet to be discovered...although psychologically, very present! Just for those who never hear the "other side of the story" that no one wants to keep record of...or maybe even HEAR about!!As we did not!mkTo: ProstateCancerSupport Sent: Tue, April 5, 2011 10:10:34 AMSubject: Re: Mortality Spike was .....Swedish Study : You wrote: "At the end of our thinking we must have hope, so we choose ways of feeling we are doing something about it. This

might be anything from careful monitoring, through change of diet to more radical informed choices. I'd still rather have 15 positive years of life than a decade and a half sitting worrying." Thank you for writing this. It succinctly summarizes how I arrived (finally) in being at peace with the fact that I have PCa, and why I am at peace with the decision I made to have surgery and to change my diet and lifestyle post surgery. Next Monday, April 11th, will be the third anniversary of the day I was told I had a membership in the club no one one wants to join. June 11th will be the third anniversary of my surgery. So far, all is well with me. PSA less than 0.01. No need for follow up. "Willy" is most definitely shorter than he

was, but is functioning OK (as OK as it gets for a 58 year old). I have been fortunate. I fully realize that things can "so south" for me very quickly. There are no guarantees. But I like to think that I've kept my options open and there are other things that can be tried if need be. I pray that they are never needed. Thank you again for your words. I can certainly relate to them. Coy , Michigan USA

[Guest guest]

I think readers should know that ’s husband had surgical removal of his prostate gland via the perineum.  Every extreme discomfort this man has experienced appears targeted to the pudendal nerve, and this appears as well a reasonable concern with the pudendal nerve transiting very closely to the perineum and significant pain associated with pudendal nerve damage.  Nothing else makes any sense to the continuing debilitating pain this man has been constantly experiencing; pain so severe that it has caused him to close his dental practice.  Yet, his original physician claims this isn’t likely and has provided no other avenues or resources to the continued care and concern of this prostate cancer patient.  I know that has performed volumes of research and that they have met with several physicians, but none seem to have any idea what to do about it other than prescribing pain medications.  In researching pudendal nerve damage/Pudendal Neuropathy, I found that this is a very difficult area to treat and provide long-term relief and surgery, even under experts, may cause more harm than good.  A major concern in this regard is that patients should be made aware that surgical removal via the perineum just might result in the terribly bad experience that this man has had to endure.  For :  Were you able to find any success in contact with one or more of the team of physicians in Houston, Texas I made note when I visited the website of The International Pudendal Nerve Association? If anyone reading this email has had similar experience, or knows of anyone experiencing Pudendal Neuropathy, or know of specialists in Pudendal Neuropathy, please email with such information. Chuck     Always as close as the other end of your computer to help address any prostate cancer concerns. " What you leave behind is not what is engraved in stone monuments, but what is woven into the lives of others. " (Chuck) Maack/Prostate Cancer Advocate/Mentor Wichita, Kansas Chapter, Us TOOBiography: http://www.ustoowichita.org/leaders.cfm?content=bio & id=1 Email: maack1@... Chapter Website " Observations " : http://www.ustoowichita.org/observations.cfm From: ProstateCancerSupport [mailto:ProstateCancerSupport ] On Behalf Of Sent: Tuesday, April 05, 2011 9:44 AMTo: ProstateCancerSupport Subject: Re: Mortality Spike was .....Swedish Study Well, it is so nice to hear some positive responses. But I cannot help but still let OUR voice be heard...to warn others, that my husband would rather now have his old life back, and to worry of what might or might not happen...than to NEVER be able to sit, and be in constant NERVE pain, where he has had to quit work, and all his most loved activities, duet to " unfortunate problems " after surgery. No one will say why it happened, or is interested in looking up statistics on how many this does happen to...and we know it has happened to others. But want others to know, a perfectly healthy, very well fit, very virile, 57 year old man (my husband) had RPP surgery over a year ago, Feb 15 2009, and still today " cannot sit " . He is still on pain meds (oxycodone) besides Neurontin, and an antidepressant. He was one the so called PC Club members, ... that had a fear of " living with cancer " and felt that the surgery seemed simple, straight forward, and a very slight possibility of long term impotence or incontinence for his age, status of cancer (PSA 2.3), and type of surgery (RPP) stats. Unfortunately, my hubby relied on the doctor's advise. Low and behold, the results were something that our doctor said he never dealt with before or heard of...(though we have found out differently of late). Our Urologist - said by many to be an EXPERT in this area in Mich. could not believe his outcome!My husband as of today, is still undergoing steroid injections to keep him out of pain!We are coming to terms with this way of living...slowly accepting this may be OUR WAY of life....for today, or for a while...or for ever! We continue to seek help, and do our own research, since no Doctor wants to. Our PC fellowship does not have much to offer! But a few good men on this web site have given us some good research advice into helping us find someone who may be able to help. It seems to us, the doctors are all there for you BEFORE you undergo surgery...but after...if any problems that do not fall into the " norm " (impotence and incontinence)...you are an anomaly....and on your own. By the way, no incontinence for my spouse....but he is in so much pain, impotence is yet to be discovered...although psychologically, very present! Just for those who never hear the " other side of the story " that no one wants to keep record of...or maybe even HEAR about!!As we did not!mk To: ProstateCancerSupport Sent: Tue, April 5, 2011 10:10:34 AMSubject: Re: Mortality Spike was .....Swedish Study : You wrote: " At the end of our thinking we must have hope, so we choose ways of feeling we are doing something about it. This might be anything from careful monitoring, through change of diet to more radical informed choices. I'd still rather have 15 positive years of life than a decade and a half sitting worrying. " Thank you for writing this. It succinctly summarizes how I arrived (finally) in being at peace with the fact that I have PCa, and why I am at peace with the decision I made to have surgery and to change my diet and lifestyle post surgery. Next Monday, April 11th, will be the third anniversary of the day I was told I had a membership in the club no one one wants to join. June 11th will be the third anniversary of my surgery. So far, all is well with me. PSA less than 0.01. No need for follow up. " Willy " is most definitely shorter than he was, but is functioning OK (as OK as it gets for a 58 year old). I have been fortunate. I fully realize that things can " so south " for me very quickly. There are no guarantees. But I like to think that I've kept my options open and there are other things that can be tried if need be. I pray that they are never needed. Thank you again for your words. I can certainly relate to them. Coy, Michigan USA

[Guest guest]

,

My number one hope for my sons goes without saying but, as you say, I'm sure there will be different(hopefully better)treatment regimes in the not to distant future. But my biggest hope for the future treatment of this disease is that they develop a better way of determining which ones need to be treated and which ones, without doubt, leave alone. I don't know if that's a realistic wish but that's mine.

Rick

To: ProstateCancerSupport Sent: Tue, April 5, 2011 6:10:59 AMSubject: Re: Mortality Spike was .....Swedish Study

 One thing on this is that technology and understanding evolve over the years.

What we assume to be true today maybe proved untrue in the future.

If your sons do become involved in our club (that no one wants to join), they could well have a different treatment regime.

It wasn't long ago that very little money was spent in the UK on independant research of PCa the ladies beat us by a mile on their bette noir. We still have a long way to go to catch up.

As has been pointed out the speed of growth of many PCas makes judging long term stats very difficult. Lots of other factors come into play, environment, diet, poverty, stress, impact of other illnesses. This results in nightmares for statisticians!

At the end of our thinking we must have hope, so we choose ways of feeling we are doing something about it. This might be anything from careful monitoring, through change of diet to more radical informed choices.

I'd still rather have 15 positive years of life than a decade and a half sitting worrying.

a. No less a person than Dr Walsh (who was apparently at some conference discussing the importance of screening in reducing mortality) was quoted last year as being questioned as to why the mortality rates in Britain had fallen when there was not the same emphasis or amount of screening in that country. His response was that they had changed the definition of prostate cancer related eeath to exclude pneumonia and this one factor had led to a reduction in prostate cancer related deaths. On raising this point in a forum I was told that this could not happen in the US . End of discussion.

b. Soon after I read of Dr Walsh’s remarks, I came on a piece describing how the large European study (ERSPC) had agreed to ‘standardize’ their definition of prostate cancer to only include needle biopsy results that result in a Gleason Score of 6 or higher – in other words anyone who had a diagnosis of GS 5 would not be included in their data. This single change may well have produced the discrepancy in the ERSPC reported results of ‘lives saved’ when compared with the US study that showed ‘no lives saved’. Again I tried to discuss this change in definition and wondered if this was a contributing fator in the decline in reported deaths – after all if you are not diagnosed with PCa, you cannot die of the disease. My thoughts on the subject were ignored ar denied. Spurred on by this item I then

found that in practical terms, leading pathologists in the US had been applying this criterion since about 2005 and in January this year the proposal was formally adopted – see http://www.yananow.org/StrangePlace/forest.html#gleason for a summary of the changes. This has led to a significant change in the profile of diagnosed prostate cancer and the so-called ‘Migration†of Gleason Grades and Scores – see http://tinyurl.com/2jnpbu

In summary after what many will have considered a long and boring post, in answer to your question <snip> Your thoughts on the 30% increase and what it means? <snip> I think that a number of changes in diagnosis, definition, formulae and focus may have all resulted in the changes observed in the population data.

All the best

Prostate men need enlightening, not frightening Terry Herbert - diagnosed in 1996 and still going strong Read A Strange Place for unbiased information at http://www.yananow.net/StrangePlace/index.html

Attachment(s) from Terry Herbert

1 of 1 Photo(s)

StateCancerProfilesGraph-all ages.png" src="http://xa.yimg.com/kq/groups/4926965/tn/1471474522">

StateCancerProfilesGraph-all ages.png

[Guest guest]



I'm in total agreement.

Celebrating 65 today and nearly 15 yrs since diagnosis

a. No less a person than Dr Walsh (who was apparently at some conference discussing the importance of screening in reducing mortality) was quoted last year as being questioned as to why the mortality rates in Britain had fallen when there was not the same emphasis or amount of screening in that country. His response was that they had changed the definition of prostate cancer related eeath to exclude pneumonia and this one factor had led to a reduction in prostate cancer related deaths. On raising this point in a forum I was told that this could not happen in the US . End of discussion.

b. Soon after I read of Dr Walsh’s remarks, I came on a piece describing how the large European study (ERSPC) had agreed to ‘standardize’ their definition of prostate cancer to only include needle biopsy results that result in a Gleason Score of 6 or higher – in other words anyone who had a diagnosis of GS 5 would not be included in their data. This single change may well have produced the discrepancy in the ERSPC reported results of ‘lives saved’ when compared with the US study that showed ‘no lives saved’. Again I tried to discuss this change in definition and wondered if this was a contributing fator in the decline in reported deaths – after all if you are not diagnosed with PCa, you cannot die of the disease. My thoughts on the subject were ignored ar denied. Spurred on by this item I then found that in practical terms, leading pathologists in the US had been applying this criterion since about 2005 and in January this year the proposal was formally adopted – see http://www.yananow.org/StrangePlace/forest.html#gleason for a summary of the changes. This has led to a significant change in the profile of diagnosed prostate cancer and the so-called ‘Migration†of Gleason Grades and Scores – see http://tinyurl.com/2jnpbu

In summary after what many will have considered a long and boring post, in answer to your question <snip> Your thoughts on the 30% increase and what it means? <snip> I think that a number of changes in diagnosis, definition, formulae and focus may have all resulted in the changes observed in the population data.

All the best

Prostate men need enlightening, not frightening Terry Herbert - diagnosed in 1996 and still going strong Read A Strange Place for unbiased information at http://www.yananow.net/StrangePlace/index.html

Attachment(s) from Terry Herbert

1 of 1 Photo(s)

StateCancerProfilesGraph-all ages.png" src="http://xa.yimg.com/kq/groups/4926965/tn/1471474522">

StateCancerProfilesGraph-all ages.png

[Guest guest]

,

Happy birthday and thanks for all you do.

Rick

To: ProstateCancerSupport Sent: Wed, April 6, 2011 6:11:16 AMSubject: Re: Mortality Spike was .....Swedish Study

 I'm in total agreement.

Celebrating 65 today and nearly 15 yrs since diagnosis

a. No less a person than Dr Walsh (who was apparently at some conference discussing the importance of screening in reducing mortality) was quoted last year as being questioned as to why the mortality rates in Britain had fallen when there was not the same emphasis or amount of screening in that country. His response was that they had changed the definition of prostate cancer related eeath to exclude pneumonia and this one factor had led to a reduction in prostate cancer related deaths. On raising this point in a forum I was told that this could not happen in the US . End of discussion.

b. Soon after I read of Dr Walsh’s remarks, I came on a piece describing how the large European study (ERSPC) had agreed to ‘standardize’ their definition of prostate cancer to only include needle biopsy results that result in a Gleason Score of 6 or higher – in other words anyone who had a diagnosis of GS 5 would not be included in their data. This single change may well have produced the discrepancy in the ERSPC reported results of ‘lives saved’ when compared with the US study that showed ‘no lives saved’. Again I tried to discuss this change in definition and wondered if this was a contributing fator in the decline in reported deaths – after all if you are not diagnosed with PCa, you cannot die of the disease. My thoughts on the subject were ignored ar denied. Spurred on by this item I then

found that in practical terms, leading pathologists in the US had been applying this criterion since about 2005 and in January this year the proposal was formally adopted – see http://www.yananow.org/StrangePlace/forest.html#gleason for a summary of the changes. This has led to a significant change in the profile of diagnosed prostate cancer and the so-called ‘Migration†of Gleason Grades and Scores – see http://tinyurl.com/2jnpbu

In summary after what many will have considered a long and boring post, in answer to your question <snip> Your thoughts on the 30% increase and what it means? <snip> I think that a number of changes in diagnosis, definition, formulae and focus may have all resulted in the changes observed in the population data.

All the best

Prostate men need enlightening, not frightening Terry Herbert - diagnosed in 1996 and still going strong Read A Strange Place for unbiased information at http://www.yananow.net/StrangePlace/index.html

Attachment(s) from Terry Herbert

1 of 1 Photo(s)

StateCancerProfilesGraph-all ages.png" src="http://xa.yimg.com/kq/groups/4926965/tn/1471474522">

StateCancerProfilesGraph-all ages.png

[Guest guest]



Thanks

It would be embarassing if everyone wished me happy birthday, I take it as read that you are all happy for me.

I do think the important message to newly diagnosed is that people like me and Terry are still battling after 15ish years. Cancer is not always an immediate death sentence!

a. No less a person than Dr Walsh (who was apparently at some conference discussing the importance of screening in reducing mortality) was quoted last year as being questioned as to why the mortality rates in Britain had fallen when there was not the same emphasis or amount of screening in that country. His response was that they had changed the definition of prostate cancer related eeath to exclude pneumonia and this one factor had led to a reduction in prostate cancer related deaths. On raising this point in a forum I was told that this could not happen in the US . End of discussion.

b. Soon after I read of Dr Walsh’s remarks, I came on a piece describing how the large European study (ERSPC) had agreed to ‘standardize’ their definition of prostate cancer to only include needle biopsy results that result in a Gleason Score of 6 or higher – in other words anyone who had a diagnosis of GS 5 would not be included in their data. This single change may well have produced the discrepancy in the ERSPC reported results of ‘lives saved’ when compared with the US study that showed ‘no lives saved’. Again I tried to discuss this change in definition and wondered if this was a contributing fator in the decline in reported deaths – after all if you are not diagnosed with PCa, you cannot die of the disease. My thoughts on the subject were ignored ar denied. Spurred on by this item I then found that in practical terms, leading pathologists in the US had been applying this criterion since about 2005 and in January this year the proposal was formally adopted – see http://www.yananow.org/StrangePlace/forest.html#gleason for a summary of the changes. This has led to a significant change in the profile of diagnosed prostate cancer and the so-called ‘Migration†of Gleason Grades and Scores – see http://tinyurl.com/2jnpbu

In summary after what many will have considered a long and boring post, in answer to your question <snip> Your thoughts on the 30% increase and what it means? <snip> I think that a number of changes in diagnosis, definition, formulae and focus may have all resulted in the changes observed in the population data.

All the best

Prostate men need enlightening, not frightening Terry Herbert - diagnosed in 1996 and still going strong Read A Strange Place for unbiased information at http://www.yananow.net/StrangePlace/index.html

Attachment(s) from Terry Herbert

1 of 1 Photo(s)

StateCancerProfilesGraph-all ages.png" src="http://xa.yimg.com/kq/groups/4926965/tn/1471474522">

StateCancerProfilesGraph-all ages.png

[Guest guest]

Dear Chuck,You can make my words so concise and better...and thank you again for "warning men" that some problems can occur. But like I have said to you before, my husband is not alone in these results, but for some reason...NO one will add this terrible outcome as a possible result.Not sure how many men have died form PC removal...due to the operation...that may be covered up too.As far as the Houston Doctors, my husband and I are trying to get a response back from Dr. Renney. It is very hard to get an actual phone call in to a real person. They put you through a Web site that you just do everything from email and await the call back. Very cold way to interact.We are still waiting a reply!In the meantime, I found another doctor in San Franciso California, Dr. Jerome Wiess. He

does work with Pudendal pain, and nerve damage, and the results of those patients who have undergone Pudendal nerve entrapment surgery, with not good results. Thought he may be a person we could try.However, my husband is still praying and hoping a Neurosurgeon in our area can help. He has started a series of steroid injections (again) every two weeks for 3 series. Ahg! I sure hope steroid overdose does not occur! I am a little frustrated to say the least. I want my husband to get out of this town to seek medical treatment...but he wants to exhaust all our chances here first, of getting help. We are thankful for this Neurosurgeon's trying to help, but I do not think he believes in PN. He thinks my husband has RSD! If it was my body...I'd be out of this state in a flash! But it is Pat's body...and he needs to follow his heart and mind, and I need to support him ... even if I think differently! I have Dr. Weiss'

phone number handy...to call when Pat is done with trying all the doctors here!My concern about Houston...is the fear of going to doctors that promote this surgery, get paid 10's of thousands of dollars to do this surgery, (which many med insurances do not cover) and then not really being able to see good statistics that it works. I feel my husband would be a research person for them. I still feel this is so "experimental" (as does Pat.)...that this would be our last resort. We would have to have way more diagnostic reason to do this. Getting proper diagnosis is our key...and why I would like to go to Houston! They can at least do more diagnosing for us, and then we can decide. ....but Dr. Jerome Weiss in California and can do this too. He promotes the book, "A Headache in the Pelvis".Thanks again...keep us in prayer...we so need it.maryTo: ProstateCancerSupport Sent: Tue, April 5, 2011 4:42:46 PMSubject: RE: Mortality Spike was .....Swedish Study

I think readers should know that ’s husband had surgical removal of his prostate gland via the perineum. Every extreme discomfort this man has experienced appears targeted to the pudendal nerve, and this appears as well a reasonable concern with the pudendal nerve transiting very closely to the perineum and significant pain associated with pudendal nerve damage. Nothing else makes any sense to the continuing debilitating pain this man has been constantly experiencing; pain so severe that it has caused him to close his dental practice. Yet, his original physician claims this isn’t likely and has provided no other avenues or resources to the continued care and concern of this prostate cancer patient. I know that has performed volumes of research and that they have met with several physicians, but none seem to have any idea what to

do about it other than prescribing pain medications. In researching pudendal nerve damage/Pudendal Neuropathy, I found that this is a very difficult area to treat and provide long-term relief and surgery, even under experts, may cause more harm than good. A major concern in this regard is that patients should be made aware that surgical removal via the perineum just might result in the terribly bad experience that this man has had to endure. For : Were you able to find any success in contact with one or more of the team of physicians in Houston, Texas I made note when I visited the website of The International Pudendal Nerve Association? If anyone reading this email

has had similar experience, or knows of anyone experiencing Pudendal Neuropathy, or know of specialists in Pudendal Neuropathy, please email with such information. Chuck Always as close as the other end of your computer to help address any prostate cancer concerns. "What you leave behind is not what is engraved in stone monuments, but what is woven into the lives of others." (Chuck) Maack/Prostate Cancer Advocate/Mentor Wichita, Kansas Chapter, Us TOOBiography: http://www.ustoowichita.org/leaders.cfm?content=bio & id=1 Email: maack1@... Chapter Website "Observations": http://www.ustoowichita.org/observations.cfm From: ProstateCancerSupport [mailto:ProstateCancerSupport ] On Behalf Of Sent: Tuesday, April 05, 2011 9:44 AMTo: ProstateCancerSupport Subject: Re: Mortality Spike was .....Swedish Study Well, it is so nice to hear some positive responses. But I cannot help but still let OUR voice be heard...to warn others, that my husband would rather now have his old life back, and to worry of what might or might not happen...than to NEVER be able to sit, and be in constant NERVE pain, where he has had to quit work, and

all his most loved activities, duet to "unfortunate problems" after surgery. No one will say why it happened, or is interested in looking up statistics on how many this does happen to...and we know it has happened to others. But want others to know, a perfectly healthy, very well fit, very virile, 57 year old man (my husband) had RPP surgery over a year ago, Feb 15 2009, and still today "cannot sit". He is still on pain meds (oxycodone) besides Neurontin, and an antidepressant. He was one the so called PC Club members, ... that had a fear of "living with cancer" and felt that the surgery seemed simple, straight forward, and a very slight possibility of long term impotence or incontinence for his age, status of cancer (PSA 2.3), and type of surgery (RPP) stats. Unfortunately, my hubby relied on the doctor's advise. Low and behold, the results were something that our doctor said he never dealt with before or heard of...(though we have

found out differently of late). Our Urologist - said by many to be an EXPERT in this area in Mich. could not believe his outcome!My husband as of today, is still undergoing steroid injections to keep him out of pain!We are coming to terms with this way of living...slowly accepting this may be OUR WAY of life....for today, or for a while...or for ever! We continue to seek help, and do our own research, since no Doctor wants to. Our PC fellowship does not have much to offer! But a few good men on this web site have given us some good research advice into helping us find someone who may be able to help. It seems to us, the doctors are all there for you BEFORE you undergo surgery...but after...if any problems that do not fall into the "norm"(impotence and incontinence)...you are an anomaly....and on your own. By the way, no incontinence for my spouse....but he is in so

much pain, impotence is yet to be discovered...although psychologically, very present! Just for those who never hear the "other side of the story" that no one wants to keep record of...or maybe even HEAR about!!As we did not!mk To: ProstateCancerSupport Sent: Tue, April 5, 2011 10:10:34 AMSubject: Re: Mortality Spike was .....Swedish

Study : You wrote: "At the end of our thinking we must have hope, so we choose ways of feeling we are doing something about it. This might be anything from careful monitoring, through change of diet to more radical informed choices. I'd still rather have 15 positive years of life than a decade and a half sitting worrying."Thank you for writing this. It succinctly summarizes how I arrived (finally) in being

at peace with the fact that I have PCa, and why I am at peace with the decision I made to have surgery and to change my diet and lifestyle post surgery. Next Monday, April 11th, will be the third anniversary of the day I was told I had a membership in the club no one one wants to join. June 11th will be the third anniversary of my surgery. So far, all is well with me. PSA less than 0.01. No need for follow up. "Willy" is most definitely shorter than he was, but is functioning OK (as OK as it gets for a 58 year old). I have been fortunate. I fully realize that things can "so south" for me very quickly. There are no guarantees. But I like to think

that I've kept my options open and there are other things that can be tried if need be. I pray that they are never needed. Thank you again for your words. I can certainly relate to them. Coy, Michigan USA