possible remission?

califvader
califvader Member Posts: 108
edited March 2014 in Prostate Cancer #1
7 years ago i had a radical protatectomy. my psa at the time of surgery was 7.8. every six months since then i have had a psa check. it started out at .01 and has been steadily going up but very very slowly. my gleason score was 3+3=6 btw. however the last time i had it checked, my psa, the number went down. it was at 4.8 and decreased to 3.3. what do the members of this panel think?

Comments

  • bdhilton
    bdhilton Member Posts: 846 Member
    Interesting. If my PSA
    Interesting. If my PSA becomes detectable (greater than .01) then my oncologist would had given me radiation and if any rise continued after radiation then it would had been recommended that I have hormones, etc… These are all personal choices but based on what you state your PSA is you are not in remission as any reading means that your cancer is back… I would seek medical advice from an oncologist… Best to you
  • califvader
    califvader Member Posts: 108
    bdhilton said:

    Interesting. If my PSA
    Interesting. If my PSA becomes detectable (greater than .01) then my oncologist would had given me radiation and if any rise continued after radiation then it would had been recommended that I have hormones, etc… These are all personal choices but based on what you state your PSA is you are not in remission as any reading means that your cancer is back… I would seek medical advice from an oncologist… Best to you

    possible remission
    i agree with you. i am going to make an appointment with a oncologist monday. thank you.
  • mrspjd
    mrspjd Member Posts: 694 Member

    possible remission
    i agree with you. i am going to make an appointment with a oncologist monday. thank you.

    welcome back
    Calif,
    Welcome back. How have you been? Sorry that it doesn't sound like much has changed since your last posts in August: http://csn.cancer.org/node/199513 -- when you were considering ADT (Androgen Deprivation Therapy/Hormones) or maybe salvage RT. A 1.5 PSA decrease can be attibuted to many potential sources (better/healthier diet, different lab running the PSA blood sample, abstinence from physical/sexual activity 48 hrs prior to testing, etc.); however, IMHO, I would not call it "remission." Hopefully you will consider a 2nd opinion from a different urologist or an oncologist. Good luck.
  • tarhoosier
    tarhoosier Member Posts: 195 Member
    3+3=long time running
    I think you could go a long time before making a treatment decision. Longer still before this becomes a health risk (15-20 years)
  • VascodaGama
    VascodaGama Member Posts: 3,638 Member
    mrspjd said:

    welcome back
    Calif,
    Welcome back. How have you been? Sorry that it doesn't sound like much has changed since your last posts in August: http://csn.cancer.org/node/199513 -- when you were considering ADT (Androgen Deprivation Therapy/Hormones) or maybe salvage RT. A 1.5 PSA decrease can be attibuted to many potential sources (better/healthier diet, different lab running the PSA blood sample, abstinence from physical/sexual activity 48 hrs prior to testing, etc.); however, IMHO, I would not call it "remission." Hopefully you will consider a 2nd opinion from a different urologist or an oncologist. Good luck.

    Without a prostate in place
    Hi califvader,

    Without a prostate in place neither physical sexual activity nor a better diet would interfere with the levels of your PSA. A gap of 1.5 in PSA between labs is also difficult to accept as a reason, because of the big difference.
    After RP, biochemical recurrence (BR) is certain with a PSA=0.2 and clinical failure (CF) is declared when the PSA rises to 0.4. This is also the usual limit when we are told to start a salvage treatment. PSA of 3.3 is not taken as remission, it signals recurrence.
    Back in 2000 I experienced a similar case as yours. I was a Gleason score 5 (6 since the revised norms of 2005) and got to BR in 5 months after RP. The Walsh team considered my case as “Micro Metastasis” therefore recommending me AS (watchful waiting). RT was then not considered as a successful treatment for micro-mets cases, however, new concepts are now in place. I would suggest you taking a good list of question to your next appointment with your oncologist.

    Wishing you the best
    VGama
  • mrspjd
    mrspjd Member Posts: 694 Member

    Without a prostate in place
    Hi califvader,

    Without a prostate in place neither physical sexual activity nor a better diet would interfere with the levels of your PSA. A gap of 1.5 in PSA between labs is also difficult to accept as a reason, because of the big difference.
    After RP, biochemical recurrence (BR) is certain with a PSA=0.2 and clinical failure (CF) is declared when the PSA rises to 0.4. This is also the usual limit when we are told to start a salvage treatment. PSA of 3.3 is not taken as remission, it signals recurrence.
    Back in 2000 I experienced a similar case as yours. I was a Gleason score 5 (6 since the revised norms of 2005) and got to BR in 5 months after RP. The Walsh team considered my case as “Micro Metastasis” therefore recommending me AS (watchful waiting). RT was then not considered as a successful treatment for micro-mets cases, however, new concepts are now in place. I would suggest you taking a good list of question to your next appointment with your oncologist.

    Wishing you the best
    VGama

    I still adhere to the plausable reasons for PSA decrease cited in my previous post, with or without a prostate. Even with RP, portions of prostate can be left behind, which could have an effect on post RP PSA readings. As far as diet, making the argument (that diet may not have a potential effect on PSA) to some of the frequent post-RP CSN members here who believe in diet as one of the few areas they can control when it comes to PCa & PSA readings, would not go over too well. Just take a look at the posts on some recent threads on this subject--such as "Diet to bring down PSA." We are all entitled to our own opinions, and presenting those thoughts here is a good jumping off place to consider further research when making up your own mind about what to believe & what is personally right.
  • Kongo
    Kongo Member Posts: 1,166 Member

    3+3=long time running
    I think you could go a long time before making a treatment decision. Longer still before this becomes a health risk (15-20 years)

    Tarhoosier Question
    Tarhoosier,

    I don't understand what your suggestion here is saying...are you saying that recurrent prostate cancer with an original Gleason of 3+3=6 does not pose a health threat?

    There have been several studies that show that salvage radiation or radiation in conjunction with hormone therapy has a significantly higher positive impact on longevity than no treatment and that this was independent of the original Gleason scores.

    It seems clear that given the information califvader provided that he is experiencing biochemical recurrence under the definition most commonly accepted by urologists today which is a PSA of 0.2 ng/ml following RP. Most urologists and oncologists would, I believe, have urged him to start treatment long before he has reached the present levels he now exhibits as there really is no other explanation for a rise in PSA after RP other than that the cancer is growing and multiplying at distant points within the body.

    Unless the calculated PSA doubling time is insignificant, which does not appear to be the case here, I don't understand the logic of not making a treatment decision based on original Gleason scores. At this point, given that califvader still has PCA somewhere other than his prostate, it seems to me that the original Gleason score is irrelevant.
  • Kongo
    Kongo Member Posts: 1,166 Member
    mrspjd said:

    I still adhere to the plausable reasons for PSA decrease cited in my previous post, with or without a prostate. Even with RP, portions of prostate can be left behind, which could have an effect on post RP PSA readings. As far as diet, making the argument (that diet may not have a potential effect on PSA) to some of the frequent post-RP CSN members here who believe in diet as one of the few areas they can control when it comes to PCa & PSA readings, would not go over too well. Just take a look at the posts on some recent threads on this subject--such as "Diet to bring down PSA." We are all entitled to our own opinions, and presenting those thoughts here is a good jumping off place to consider further research when making up your own mind about what to believe & what is personally right.

    Agree with mrspjd
    Vasco, while sexual activity may not impact the PSA reading of men who have had their prostate removed (since the prostate gland is no longer there to spasm and release sperm at orgasm), I certainly agree with mrspjd that dietary choices can impact PSA. Since 1990 researchers at Stanford found that Insulin Growth Factors (IGFs) promote the growth of prostate cancer cells. For most of us, we get IGFs from dairy products. Removing dairy products from your diet has frequently been shown to reverse prostate cancer growth (as well as breast cancer growth) which can result in lowered PSA readings. In my own case, as well as others that I know of, eliminating dairy from my diet significantly lowered the PSA level.
  • hopeful and optimistic
    hopeful and optimistic Member Posts: 2,339 Member
    Kongo said:

    Agree with mrspjd
    Vasco, while sexual activity may not impact the PSA reading of men who have had their prostate removed (since the prostate gland is no longer there to spasm and release sperm at orgasm), I certainly agree with mrspjd that dietary choices can impact PSA. Since 1990 researchers at Stanford found that Insulin Growth Factors (IGFs) promote the growth of prostate cancer cells. For most of us, we get IGFs from dairy products. Removing dairy products from your diet has frequently been shown to reverse prostate cancer growth (as well as breast cancer growth) which can result in lowered PSA readings. In my own case, as well as others that I know of, eliminating dairy from my diet significantly lowered the PSA level.

    I wonder if you can site
    the study( that indicates that the intake of dairy products causes prostate cancer growth in humans.........not saying that consuming milk products is a good thing, especially high fat ones........but not consuming various food types such as milk, red meat, jelly bean soup, etc, etc is fairly radical, and involves great change for the majority of us, so I believe that these changes needs to be based on scientific data .

    I do agree for the most part that meat and high fat dairy is not heart healthy, and is not a good thing.........but...I'm wondering if there are any studies that show that it is bad for the prostate.

    Just examining this topic more closely..........(probably with no concrete answer, either way)
  • Kongo
    Kongo Member Posts: 1,166 Member

    I wonder if you can site
    the study( that indicates that the intake of dairy products causes prostate cancer growth in humans.........not saying that consuming milk products is a good thing, especially high fat ones........but not consuming various food types such as milk, red meat, jelly bean soup, etc, etc is fairly radical, and involves great change for the majority of us, so I believe that these changes needs to be based on scientific data .

    I do agree for the most part that meat and high fat dairy is not heart healthy, and is not a good thing.........but...I'm wondering if there are any studies that show that it is bad for the prostate.

    Just examining this topic more closely..........(probably with no concrete answer, either way)

    Citation
    Ira, here's the citation you asked for.

    This is from International Health News at www.yourhealthbase.com. The specific citation can be found at: http://www.yourhealthbase.com/milk_cancer.htm

    This was drawn from Professor Jane Plant's book, "Prostate Cancer" under Chapter 4: Is Milk A Four-Letter Word


    Milk and the Cancer Connection

    by Hans R. Larsen, MSc ChE


    On January 23, 1998 researchers at the Harvard Medical School released a major study providing conclusive evidence that IGF-1 is a potent risk factor for prostate cancer. Should you be concerned? Yes, you certainly should, particularly if you drink milk produced in the United States.

    IGF-1 or insulin-like growth factor 1 is an important hormone that is produced in the liver and body tissues. It is a polypeptide and consists of 70 amino acids linked together. All mammals produce IGF-1 molecules very similar in structure and human and bovine IGF-1 are completely identical. IGF-1 acquired its name because it has insulin-like activity in fat (adipose) tissue and has a structure that is very similar to that of proinsulin. The body's production of IGF-1 is regulated by the human growth hormone and peaks at puberty. IGF-1 production declines with age and is only about half the adult value at the age of 70 years. IGF-1 is a very powerful hormone that has profound effects even though its concentration in the blood serum is only about 200 ng/mL or 0.2 millionth of a gram per milliliter (1-4).

    IGF-1 and cancer
    IGF-1 is known to stimulate the growth of both normal and cancerous cells(2,5). In 1990 researchers at Stanford University reported that IGF-1 promotes the growth of prostate cells(2). This was followed by the discovery that IGF-1 accelerates the growth of breast cancer cells(6-8). In 1995 researchers at the National Institutes of Health reported that IGF-1 plays a central role in the progression of many childhood cancers and in the growth of tumours in breast cancer, small cell lung cancer, melanoma, and cancers of the pancreas and prostate(9). In September 1997 an international team of researchers reported the first epidemiological evidence that high IGF-1 concentrations are closely linked to an increased risk of prostate cancer(10). Other researchers provided evidence of IGF-1's link to breast and colon cancers(10,11).

    The January 1998 report by the Harvard researchers confirmed the link between IGF-1 levels in the blood and the risk of prostate cancer. The effects of IGF-1 concentrations on prostate cancer risk were found to be astoundingly large - much higher than for any other known risk factor. Men having an IGF-1 level between approximately 300 and 500 ng/mL were found to have more than four times the risk of developing prostate cancer than did men with a level between 100 and 185 ng/mL. The detrimental effect of high IGF-1 levels was particularly pronounced in men over 60 years of age. In this age group men with the highest levels of IGF-1 were eight times more likely to develop prostate cancer than men with low levels. The elevated IGF-1 levels were found to be present several years before an actual diagnosis of prostate cancer was made(12).

    The evidence of a strong link between cancer risk and a high level of IGF-1 is now indisputable. The question is why do some people have high levels while others do not? Is it all genetically ordained or could it be that diet or some other outside factor influences IGF-1 levels? Dr. Samuel Epstein of the University of Illinois is one scientist who strongly believes so. His 1996 article in the International Journal of Health Sciences clearly warned of the danger of high levels of IGF-1 contained in milk from cows injected with synthetic bovine growth hormone (rBGH). He postulated that IGF-1 in rBGH-milk could be a potential risk factor for breast and gastrointestinal cancers(13).

    The milk connection
    Bovine growth hormone was first synthesized in the early 1980s using genetic engineering techniques (recombinant DNA biotechnology). Small-scale industry-sponsored trials showed that it was effective in increasing milk yields by an average of 14 per cent if injected into cows every two weeks. In 1985 the Food and Drug Administration (FDA) in the United States approved the sale of milk from cows treated with rBGH (also known as BST) in large-scale veterinary trials and in 1993 approved commercial sale of milk from rBGH-injected cows(13-16). At the same time the FDA prohibited the special labeling of the milk so as to make it impossible for the consumer to decide whether or not to purchase it(13).

    Concerns about the safety of milk from BST-treated cows were raised as early as 1988 by scientists in both England and the United States(14,15,17-22). One of the main concerns is the high levels of IGF-1 found in milk from treated cows; estimates vary from twice as high to 10 times higher than in normal cow's milk(13,14,23). There is also concern that the IGF-1 found in treated milk is much more potent than that found in regular milk because it seems to be bound less firmly to its accompanying proteins(13). Consultants paid by Monsanto, the major manufacturer of rBGH, vigorously attacked the concerns. In an article published in the Journal of the American Medical Association in August 1990 the consultants claimed that BST-milk was entirely safe for human consumption(16,24). They pointed out that BST-milk contains no more IGF-1 than does human breast milk - a somewhat curious argument as very few grown-ups continue to drink mother's milk throughout their adult life. They also claimed that IGF-1 would be completely broken down by digestive enzymes and therefore would have no biological activity in humans(16). Other researchers disagree with this claim and have warned that IGF-1 may not be totally digested and that some of it could indeed make its way into the colon and cross the intestinal wall into the bloodstream. This is of special concern in the case of very young infants and people who lack digestive enzymes or suffer from protein-related allergies(13,14,20,22,25).

    Researchers at the FDA reported in 1990 that IGF-1 is not destroyed by pasteurization and that pasteurization actually increases its concentration in BST-milk. They also confirmed that undigested protein could indeed cross the intestinal wall in humans and cited tests which showed that oral ingestion of IGF-1 produced a significant increase in the growth of a group of male rats - a finding dismissed earlier by the Monsanto scientists(25). The most important aspect of these experiments is that they show that IGF-1 can indeed enter the blood stream from the intestines - at least in rats.

    Unfortunately, essentially all the scientific data used by the FDA in the approval process was provided by the manufacturers of rBGH and much of it has since been questioned by independent scientists. The effect of IGF-1 in rBGH-milk on human health has never actually been tested and in March 1991 researchers at the National Institutes of Health admitted that it was not known whether IGF-1 in milk from treated cows could have a local effect on the esophagus, stomach or intestines(26,27).

    Whether IGF-1 in milk is digested and broken down into its constituent amino acids or whether it enters the intestine intact is a crucial factor. No human studies have been done on this, but recent research has shown that a very similar hormone, Epidermal Growth Factor, is protected against digestion when ingested in the presence of casein, a main component of milk(13,23,28). Thus there is a distinct possibility that IGF-1 in milk could also avoid digestion and make its way into the intestine where it could promote colon cancer(13,22). It is also conceivable that it could cross the intestinal wall in sufficient amounts to increase the blood level of IGF-1 significantly and thereby increase the risk of breast and prostate cancers(13,14).

    The bottom line
    Despite assurances from the FDA and industry-paid consultants there are now just too many serious questions surrounding the use of milk from cows treated with synthetic growth hormone to allow its continued sale. Bovine growth hormone is banned in Australia, New Zealand and Japan. The European Union has maintained its moratorium on the use of rBGH and milk products from BST-treated cows are not sold in countries within the Union. Canada has also so far resisted pressure from the United States and the biotechnology lobby to approve the use of rBGH commercially. In light of the serious concerns about the safety of human consumption of milk from BST-treated cows consumers must maintain their vigilance to ensure that European and Canadian governments continue to resist the pressure to approve rBGH and that the FDA in the United States moves immediately to ban rBGH-milk or at least allow its labeling so that consumers can protect themselves against the very real cancer risks posed by IGF-1.

    Note: The refrences can be seen in the original web posting.
  • VascodaGama
    VascodaGama Member Posts: 3,638 Member
    Kongo said:

    Tarhoosier Question
    Tarhoosier,

    I don't understand what your suggestion here is saying...are you saying that recurrent prostate cancer with an original Gleason of 3+3=6 does not pose a health threat?

    There have been several studies that show that salvage radiation or radiation in conjunction with hormone therapy has a significantly higher positive impact on longevity than no treatment and that this was independent of the original Gleason scores.

    It seems clear that given the information califvader provided that he is experiencing biochemical recurrence under the definition most commonly accepted by urologists today which is a PSA of 0.2 ng/ml following RP. Most urologists and oncologists would, I believe, have urged him to start treatment long before he has reached the present levels he now exhibits as there really is no other explanation for a rise in PSA after RP other than that the cancer is growing and multiplying at distant points within the body.

    Unless the calculated PSA doubling time is insignificant, which does not appear to be the case here, I don't understand the logic of not making a treatment decision based on original Gleason scores. At this point, given that califvader still has PCA somewhere other than his prostate, it seems to me that the original Gleason score is irrelevant.

    Kongo, Excellent post on IGF-1
    Kongo
    Excellent post on the potent risk factor for prostate cancer induced by IGF-1. I absolutely agree that we are what we eat, and that many factors induce cancer. However, in Califvader case do you think that by giving up with the milk or some other products, he managed to get a 30% reduction on cancer activity? How must time is it required to change a body biology through diet?
    It is hard to believe that his “new” diet is behind the lowering of PSA in such a short period of six months. If that is right, his comment of “Remission” is valid in 2-years time. Unless, of course, that he is taking some sort of food/supplements/herbs that includes compounds similar to hormonal drugs. I recall PS-Spes in 2000, claiming to be made of a combination of Chinese herbs, found later to include traces of estrogens.
  • Kongo
    Kongo Member Posts: 1,166 Member

    Kongo, Excellent post on IGF-1
    Kongo
    Excellent post on the potent risk factor for prostate cancer induced by IGF-1. I absolutely agree that we are what we eat, and that many factors induce cancer. However, in Califvader case do you think that by giving up with the milk or some other products, he managed to get a 30% reduction on cancer activity? How must time is it required to change a body biology through diet?
    It is hard to believe that his “new” diet is behind the lowering of PSA in such a short period of six months. If that is right, his comment of “Remission” is valid in 2-years time. Unless, of course, that he is taking some sort of food/supplements/herbs that includes compounds similar to hormonal drugs. I recall PS-Spes in 2000, claiming to be made of a combination of Chinese herbs, found later to include traces of estrogens.

    PSA Drop
    Vasco,

    Given the sparse information here and that Califvader has not mentioned a new diet I would agree with you that his diet is not responsible for such a PSA drop and that some other factor may be at play (although based on my own experience, I think a dietary change COULD have resulted in such a PSA drop...there just isn't any information here that would allow us to draw that conclusion) It's entirely possible that a lab error or something like it occurred. I would think that to fully determine the effect of diet, you would need a trend of PSA scores and it would be sketchy to draw a conclusion on a single reading.

    While many dietary changes may take years to have an effect, I know that in my own case, my PSA dropped from 4.3 to 2.8 in about a little less than two months time after I eliminated dairy. If you read Professor Jane Plant's book about her struggles with breast cancer, her tumors vanished after only about six weeks of eliminating diet. There are lots of other antecdotal instances of similar reversals (or apparent reversals) of cancer as a result of diet.

    I've read about the PC-Spes case and many people today still swear by the product, even with the traces of estrogen and there are conflicting reports about whether or not the artifical medications in the compound were really responsible for the decline in PSA readings or not.

    As I read Califvader's original post it seemed to me that he was seeking an opinion as to whether or not he had experienced BCR. My opinion is that his PSA reading (even the reduced one) was evidence of BCR and that he should discuss potential options with his medical team. Depending upon what the PSA velocity is post RP he may or may not wish to treat it at this time but there wasn't enough information to know what his PSA velocity or PSADT might be.

    In any event, I think that diet can definitely have an effect of lowering PSA, and sometimes in the short term, but we don't really know enough about Califvader's pathology to say one way or the other.
  • tarhoosier
    tarhoosier Member Posts: 195 Member
    Kongo said:

    Tarhoosier Question
    Tarhoosier,

    I don't understand what your suggestion here is saying...are you saying that recurrent prostate cancer with an original Gleason of 3+3=6 does not pose a health threat?

    There have been several studies that show that salvage radiation or radiation in conjunction with hormone therapy has a significantly higher positive impact on longevity than no treatment and that this was independent of the original Gleason scores.

    It seems clear that given the information califvader provided that he is experiencing biochemical recurrence under the definition most commonly accepted by urologists today which is a PSA of 0.2 ng/ml following RP. Most urologists and oncologists would, I believe, have urged him to start treatment long before he has reached the present levels he now exhibits as there really is no other explanation for a rise in PSA after RP other than that the cancer is growing and multiplying at distant points within the body.

    Unless the calculated PSA doubling time is insignificant, which does not appear to be the case here, I don't understand the logic of not making a treatment decision based on original Gleason scores. At this point, given that califvader still has PCA somewhere other than his prostate, it seems to me that the original Gleason score is irrelevant.

    Question
    Based on the limited information provided by ca.vader he has been watchfully waiting on his psa. His G6 has, as is often the case, allowed a very slow rise. His psa doubling time is impossible to determine, though his most recent psa direction was actually negative, 4.8 to 3.3. If, as I assume, his psa has been moving over some years, then this means that he has some more years to go before addressing ADT. I also assume he is on no therapy at this time. A "threat to his health" would entail symptoms or side effects serious enough to cause further treatment. I believe he is still years away from that.
    It is crystal clear from his post that he is comfortable watching his psa and waiting to address the issue until some later time. Apparently his doctor(s) is (are) as well. I believe this is supported by the (few) facts he presents. I find no reason to encourage him to abandon his current course and to begin a systemic treatment.
  • Kongo
    Kongo Member Posts: 1,166 Member

    Question
    Based on the limited information provided by ca.vader he has been watchfully waiting on his psa. His G6 has, as is often the case, allowed a very slow rise. His psa doubling time is impossible to determine, though his most recent psa direction was actually negative, 4.8 to 3.3. If, as I assume, his psa has been moving over some years, then this means that he has some more years to go before addressing ADT. I also assume he is on no therapy at this time. A "threat to his health" would entail symptoms or side effects serious enough to cause further treatment. I believe he is still years away from that.
    It is crystal clear from his post that he is comfortable watching his psa and waiting to address the issue until some later time. Apparently his doctor(s) is (are) as well. I believe this is supported by the (few) facts he presents. I find no reason to encourage him to abandon his current course and to begin a systemic treatment.

    Understand you logic
    Tarhoosier, I understand your logic. From what I have read, a pre-surgical Gleason score cannot be accurately correlated to how PCa might progress in the event of recurrence.

    His present PSA readings, based on current guidelines, indicates that he has experienced BCR and my opinion is that he should discuss this with his medical team and consider if and when additional treatment should be initiated. I would hope that his doctors would calculate his PSA velocity and doubling time when laying out potential courses of action.

    We may have interpreted his postings differently. My impression was that he was not seeing an oncologist (or even a urologist) at the time of his original post.
  • hopeful and optimistic
    hopeful and optimistic Member Posts: 2,339 Member
    Kongo said:

    Citation
    Ira, here's the citation you asked for.

    This is from International Health News at www.yourhealthbase.com. The specific citation can be found at: http://www.yourhealthbase.com/milk_cancer.htm

    This was drawn from Professor Jane Plant's book, "Prostate Cancer" under Chapter 4: Is Milk A Four-Letter Word


    Milk and the Cancer Connection

    by Hans R. Larsen, MSc ChE


    On January 23, 1998 researchers at the Harvard Medical School released a major study providing conclusive evidence that IGF-1 is a potent risk factor for prostate cancer. Should you be concerned? Yes, you certainly should, particularly if you drink milk produced in the United States.

    IGF-1 or insulin-like growth factor 1 is an important hormone that is produced in the liver and body tissues. It is a polypeptide and consists of 70 amino acids linked together. All mammals produce IGF-1 molecules very similar in structure and human and bovine IGF-1 are completely identical. IGF-1 acquired its name because it has insulin-like activity in fat (adipose) tissue and has a structure that is very similar to that of proinsulin. The body's production of IGF-1 is regulated by the human growth hormone and peaks at puberty. IGF-1 production declines with age and is only about half the adult value at the age of 70 years. IGF-1 is a very powerful hormone that has profound effects even though its concentration in the blood serum is only about 200 ng/mL or 0.2 millionth of a gram per milliliter (1-4).

    IGF-1 and cancer
    IGF-1 is known to stimulate the growth of both normal and cancerous cells(2,5). In 1990 researchers at Stanford University reported that IGF-1 promotes the growth of prostate cells(2). This was followed by the discovery that IGF-1 accelerates the growth of breast cancer cells(6-8). In 1995 researchers at the National Institutes of Health reported that IGF-1 plays a central role in the progression of many childhood cancers and in the growth of tumours in breast cancer, small cell lung cancer, melanoma, and cancers of the pancreas and prostate(9). In September 1997 an international team of researchers reported the first epidemiological evidence that high IGF-1 concentrations are closely linked to an increased risk of prostate cancer(10). Other researchers provided evidence of IGF-1's link to breast and colon cancers(10,11).

    The January 1998 report by the Harvard researchers confirmed the link between IGF-1 levels in the blood and the risk of prostate cancer. The effects of IGF-1 concentrations on prostate cancer risk were found to be astoundingly large - much higher than for any other known risk factor. Men having an IGF-1 level between approximately 300 and 500 ng/mL were found to have more than four times the risk of developing prostate cancer than did men with a level between 100 and 185 ng/mL. The detrimental effect of high IGF-1 levels was particularly pronounced in men over 60 years of age. In this age group men with the highest levels of IGF-1 were eight times more likely to develop prostate cancer than men with low levels. The elevated IGF-1 levels were found to be present several years before an actual diagnosis of prostate cancer was made(12).

    The evidence of a strong link between cancer risk and a high level of IGF-1 is now indisputable. The question is why do some people have high levels while others do not? Is it all genetically ordained or could it be that diet or some other outside factor influences IGF-1 levels? Dr. Samuel Epstein of the University of Illinois is one scientist who strongly believes so. His 1996 article in the International Journal of Health Sciences clearly warned of the danger of high levels of IGF-1 contained in milk from cows injected with synthetic bovine growth hormone (rBGH). He postulated that IGF-1 in rBGH-milk could be a potential risk factor for breast and gastrointestinal cancers(13).

    The milk connection
    Bovine growth hormone was first synthesized in the early 1980s using genetic engineering techniques (recombinant DNA biotechnology). Small-scale industry-sponsored trials showed that it was effective in increasing milk yields by an average of 14 per cent if injected into cows every two weeks. In 1985 the Food and Drug Administration (FDA) in the United States approved the sale of milk from cows treated with rBGH (also known as BST) in large-scale veterinary trials and in 1993 approved commercial sale of milk from rBGH-injected cows(13-16). At the same time the FDA prohibited the special labeling of the milk so as to make it impossible for the consumer to decide whether or not to purchase it(13).

    Concerns about the safety of milk from BST-treated cows were raised as early as 1988 by scientists in both England and the United States(14,15,17-22). One of the main concerns is the high levels of IGF-1 found in milk from treated cows; estimates vary from twice as high to 10 times higher than in normal cow's milk(13,14,23). There is also concern that the IGF-1 found in treated milk is much more potent than that found in regular milk because it seems to be bound less firmly to its accompanying proteins(13). Consultants paid by Monsanto, the major manufacturer of rBGH, vigorously attacked the concerns. In an article published in the Journal of the American Medical Association in August 1990 the consultants claimed that BST-milk was entirely safe for human consumption(16,24). They pointed out that BST-milk contains no more IGF-1 than does human breast milk - a somewhat curious argument as very few grown-ups continue to drink mother's milk throughout their adult life. They also claimed that IGF-1 would be completely broken down by digestive enzymes and therefore would have no biological activity in humans(16). Other researchers disagree with this claim and have warned that IGF-1 may not be totally digested and that some of it could indeed make its way into the colon and cross the intestinal wall into the bloodstream. This is of special concern in the case of very young infants and people who lack digestive enzymes or suffer from protein-related allergies(13,14,20,22,25).

    Researchers at the FDA reported in 1990 that IGF-1 is not destroyed by pasteurization and that pasteurization actually increases its concentration in BST-milk. They also confirmed that undigested protein could indeed cross the intestinal wall in humans and cited tests which showed that oral ingestion of IGF-1 produced a significant increase in the growth of a group of male rats - a finding dismissed earlier by the Monsanto scientists(25). The most important aspect of these experiments is that they show that IGF-1 can indeed enter the blood stream from the intestines - at least in rats.

    Unfortunately, essentially all the scientific data used by the FDA in the approval process was provided by the manufacturers of rBGH and much of it has since been questioned by independent scientists. The effect of IGF-1 in rBGH-milk on human health has never actually been tested and in March 1991 researchers at the National Institutes of Health admitted that it was not known whether IGF-1 in milk from treated cows could have a local effect on the esophagus, stomach or intestines(26,27).

    Whether IGF-1 in milk is digested and broken down into its constituent amino acids or whether it enters the intestine intact is a crucial factor. No human studies have been done on this, but recent research has shown that a very similar hormone, Epidermal Growth Factor, is protected against digestion when ingested in the presence of casein, a main component of milk(13,23,28). Thus there is a distinct possibility that IGF-1 in milk could also avoid digestion and make its way into the intestine where it could promote colon cancer(13,22). It is also conceivable that it could cross the intestinal wall in sufficient amounts to increase the blood level of IGF-1 significantly and thereby increase the risk of breast and prostate cancers(13,14).

    The bottom line
    Despite assurances from the FDA and industry-paid consultants there are now just too many serious questions surrounding the use of milk from cows treated with synthetic growth hormone to allow its continued sale. Bovine growth hormone is banned in Australia, New Zealand and Japan. The European Union has maintained its moratorium on the use of rBGH and milk products from BST-treated cows are not sold in countries within the Union. Canada has also so far resisted pressure from the United States and the biotechnology lobby to approve the use of rBGH commercially. In light of the serious concerns about the safety of human consumption of milk from BST-treated cows consumers must maintain their vigilance to ensure that European and Canadian governments continue to resist the pressure to approve rBGH and that the FDA in the United States moves immediately to ban rBGH-milk or at least allow its labeling so that consumers can protect themselves against the very real cancer risks posed by IGF-1.

    Note: The refrences can be seen in the original web posting.

    citation
    good post..thanks
  • tarhoosier
    tarhoosier Member Posts: 195 Member
    Kongo said:

    Understand you logic
    Tarhoosier, I understand your logic. From what I have read, a pre-surgical Gleason score cannot be accurately correlated to how PCa might progress in the event of recurrence.

    His present PSA readings, based on current guidelines, indicates that he has experienced BCR and my opinion is that he should discuss this with his medical team and consider if and when additional treatment should be initiated. I would hope that his doctors would calculate his PSA velocity and doubling time when laying out potential courses of action.

    We may have interpreted his postings differently. My impression was that he was not seeing an oncologist (or even a urologist) at the time of his original post.

    Califvader data
    I see Califvader that you posted in August about your psa at that time, the 4.+ reading. You were seeing your urologist. You appear to be on 3-month test schedule. Since have had surgery I assume any Gleason score discussed and shared is the post surgical pathology, which is definitive. Recurrence is obvious from psa. Further information from the pathology report will be helpful in assisting you to determine your course. Your data presented is the bare minimum. I hope you receive a full and thorough briefing at your next medical consultation.
  • califvader
    califvader Member Posts: 108
    bdhilton said:

    Interesting. If my PSA
    Interesting. If my PSA becomes detectable (greater than .01) then my oncologist would had given me radiation and if any rise continued after radiation then it would had been recommended that I have hormones, etc… These are all personal choices but based on what you state your PSA is you are not in remission as any reading means that your cancer is back… I would seek medical advice from an oncologist… Best to you

    drop in PSA
    my diet has remained the same. the only thing that has changed is my exercise level. i recently bought (in june) a eliptical trainer. i work out on it at least three times a week and also use some dumbells mixed in with the work out. i have been on a six month check up with the urologist. i have to admitt i am not thrilled with the prospect of hormonal therapy but of course i will do it if i have too. my next visit will be in feburary and this time i will see a oncologist. i have not seen one yet.
  • VascodaGama
    VascodaGama Member Posts: 3,638 Member

    drop in PSA
    my diet has remained the same. the only thing that has changed is my exercise level. i recently bought (in june) a eliptical trainer. i work out on it at least three times a week and also use some dumbells mixed in with the work out. i have been on a six month check up with the urologist. i have to admitt i am not thrilled with the prospect of hormonal therapy but of course i will do it if i have too. my next visit will be in feburary and this time i will see a oncologist. i have not seen one yet.

    Physical fitness will help
    Hi Califvader,
    No matter what you choose; AS, SRT or ADT, surely your elliptical trainer will be worth gold. The physical fitness will help you in minimizing the symptoms from the treatment's side effects.
    At the end of my AS period in 2006, I started a fitness program which includes an energetic walk of 5 to 8 km daily, except when I am travelling. I believe that it has helped me to combat the side effects from SRT (Nov 2006) and now from ADT (Nov 2010).
    Take care
    VGama
  • SRVR
    SRVR Member Posts: 11
    My next move would be
    My next move would be to schedule a consultation with proton beam provider. I know many men who have had proton salvage treatment after surgery has failed them. Depending on the severity of your situation, proton therapy alone, or combination therapies of proton, photon and hormone ablation can solve your problems. Specific treatment is up to an expert. Any proton facility will address all three possibilities.

    Last month I had a long conversation with a man who was in your situation ten years ago. He was healed with a combination of all 3 treatments at Loma Linda University. He is in great health today and his only worry is that there is always a small chance that any radiation treatment can lead to new cancer in nearby areas. No treatment is perfect, but you still have options with great chances of a long, good life.
  • califvader
    califvader Member Posts: 108

    Question
    Based on the limited information provided by ca.vader he has been watchfully waiting on his psa. His G6 has, as is often the case, allowed a very slow rise. His psa doubling time is impossible to determine, though his most recent psa direction was actually negative, 4.8 to 3.3. If, as I assume, his psa has been moving over some years, then this means that he has some more years to go before addressing ADT. I also assume he is on no therapy at this time. A "threat to his health" would entail symptoms or side effects serious enough to cause further treatment. I believe he is still years away from that.
    It is crystal clear from his post that he is comfortable watching his psa and waiting to address the issue until some later time. Apparently his doctor(s) is (are) as well. I believe this is supported by the (few) facts he presents. I find no reason to encourage him to abandon his current course and to begin a systemic treatment.

    you are correct tarhoosier.
    you are correct tarhoosier. i am stayin on top of this.