Prostate ...

Prostate Cancer Canada: PSA Recommendation
http://www.prostatecancer.ca/getmed...SA-Position-Know-Your-Number-final_1.pdf.aspx

Prostate Cancer Canada’s (PCC) recommendation regarding the use of the PSA test for the early detection of prostate cancer in asymptomatic men has been reviewed given the release of recent national and international guidelines, as well as recent publications on the PSA test and prostate cancer mortality.

The purpose of this revised recommendation is to provide men and their primary care providers with information and guidance in making an informed decision regarding having a PSA test. The decision to undergo testing for prostate cancer is one that should be discussed with a man and his primary care provider as part of a shared decision making process and we hope that with this revised recommendation, men who have concerns regarding their future risk of developing prostate cancer will be encouraged to discuss the benefits and limitations of PSA testing.

PCC’s current recommendation regarding the use of the PSA test is to ‘encourage men over the age of 40, as part of their annual check-up, to initiate a conversation with their doctor about early detection (which may include PSA testing and a Digital Rectal Exam)’.

The development of our latest recommendations evolved from a comprehensive review of available scientific literature as well as listening to the views of our survivor stakeholders. Additionally, we have taken into account the views of national and international researchers and clinicians on the use of the PSA test for testing asymptomatic men.

Summary of Recommendation

Recommendation 1: Men should get a PSA test in their 40s to establish their baseline.

Recommendation 2: Men at high risk for prostate cancer should talk to their primary care provider before age 40 about prostate cancer.

Recommendation 3: At or over age 70, the decision to end PSA testing should be based on individual factors.
 
I went to a primary Jan 2012 and had a checkup done,he did a DRE and said my prostrate wasnt enlarged and was relieved.A week later after my blood work came back he told me my PSA was 7.7. I went to an endo in June 2012 and my bloodwork showed my PSA was 11.4 still no enlarged prostrate. he did a ultra sound and biopsy and it came back gleason 7 cancer. I was then scheduled for a CT scan of my mid section and a full bone scan.I was worried it might be spread to my bones or possibly other organs. It came back that it was confined to my prostrate and that was a big relief.I was treated and now my PSA was 0.1.since my sons are 39 and 40 i asked him if he has treated anyone in their 40s for PCA and he said he has...The only other PSA i had done was when i was 50 and it came back fine,my next was at 65 and i was 7.7,6 months later it was 11.4.
 
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Wibowo E, Wassersug RJ. The effect of estrogen on the sexual interest of castrated males: Implications to prostate cancer patients on androgen-deprivation therapy. Crit Rev Oncol Hematol 2013;87(3):224-38. Elsevier

Androgen deprivation therapy (ADT) for prostate cancer (PCa) treatment causes sexual dysfunction. We review here the effects of estrogen on the sexual performance of androgen-deprived males. The major findings are: We discuss the general benefits of estrogen therapy to quality of life of men on ADT, the potential risks of this treatment, and possible treatment regimes for estrogen therapy in males. Unless contraindicated, we propose that PCa patients on ADT would benefit from supplemental parenteral estrogen.
 
Evaluation of Genomic Applications in Practice and Prevention Working G. Recommendations from the EGAPP Working Group: does PCA3 testing for the diagnosis and management of prostate cancer improve patient health outcomes? Genet Med. Recommendations from the EGAPP Working Group: does PCA3 testing for the diagnosis and management of prostate cancer improve patient health outcomes? : Genetics in Medicine : Nature Publishing Group

The Evaluation of Genomic Applications in Practice and Prevention (EGAPP) Working Group found insufficient evidence to recommend prostate cancer antigen 3 (PCA3) testing to inform decisions for when to rebiopsy previously biopsy-negative patients for prostate cancer or to inform decisions to conduct initial biopsies for prostate cancer in at-risk men (e.g., previous elevated prostate-specific antigen test or suspicious digital rectal examination).

The EGAPP Working Group found insufficient evidence to recommend PCA3 testing in men with cancer-positive biopsies to determine if the disease is indolent or aggressive in order to develop an optimal treatment plan.

Based on the available evidence, the overall certainty of clinical validity to predict the diagnosis of prostate cancer using PCA3 is deemed “low.” The EGAPP Working Group discourages clinical use for diagnosis unless further evidence supports improved clinical validity.

Based on the available evidence, the overall certainty of net health benefit is deemed “low.” The EGAPP Working Group discourages clinical use unless further evidence supports improved clinical outcomes.
 
NOW THATS SUM FUKIN GREEK....

Are you thinking they said that in men who have had their prostate IRRADIATED due to cancer, and have replaced hormones with TRT, that the PSA has not risen..

1. not risen, But from what?
2. what is that? 13 or 16 subjects - I dont even recall.
3. I did note that all their TT levels seemed low at 178..?! And proposed interpreted as prior to radiation treatment as well as immediate post.
4. Where did they find Uro's with the balls or insanity to apply TRT to post radiological subjects with PC...???!!!!!
5. So the study speaks of the 2.5 year mark post INITIAL radiation therapy I can assume?
6. But if you note, they do not even discern whether or not THE SUBJECT IS STILL ALIVE....:rolleyes:
7. They TOTALLY discount the point that they are INFERRING as a RISE in serum TT is remarkably a GOOD thing.
8. The complete subject completely again omits the whole point the SERUM MEANS SQUAT... Sorry.. Just sayin...:drooling:
My PSA before seed implants and radiation therapy was 11.4,after treatments it was 0.1....I also had the ADT thearpy before treatments. Now i have to deal with a very low TT and FT 32 and 0.2..I have been to a endo and he will do nothing and told me to go back to my Uro who said i had 2 choices #1 a penile implant or #2 penile injections to keep it up. Im looking at option # 3 self imposed TRT.
 
This one is interesting to me as I recall seeing Grand dad's bone scan late into his PC and 5 years post diagnosis at the age of about 70. The scan was tore up with dark areas which I believe indicate Low Density areas as COMPROMISED by cancer of the skeletal system ensuing.

First it seems to me that I recall the skeletal system and bone specific is one of the body's tissues that metabolizes BOTH Androgens and Estrogens in somewhat balanced proportion?

In an attempt to understand "Sclerostin" as it pertains to this article, PC, and my genetic line...
FROM WIKI....:
"Sclerostin, the product of the SOST gene, located on chromosome 17q12–q21 in humans,[5] was originally believed to be a non-classical bone morphogenetic protein (BMP) antagonist"

"Mutations in the gene sclerostin are associated with disorders associated with high bone mass, sclerosteosis and van Buchem disease.[5] Sclerosteosis is an autosomal recessive disorder characterized by bone overgrowth."


BUT the long and short is the MORE Sclerostin ='s less bone growth (new bone AREA), in lieu of any disorders. Right?

** The whole thing rings home to me (to whatever degree I can understand it) but via some keywords in the primer. I have a genetic predisposition for some HEAVY ASS BONES which contribute about 20lbs (I speculate) of "invisible weight/I hide it well". Its the SAME frame Grand dad had with the same HIP osteoarthritis. He did do ADT Treatments for a year or two early on - but could not take it, don't recall why.

OFF TOPIC - I WONDER is Sclerostin the RESULTING Negative Feedback to Natural Bone Generation, AND HOW THIS RELATES to Testosterone (Androgens AND Estrogens), and with consideration for Estrogen Related "Fusing of Bone Growth Plates"...?(note: my underlying estrogen theme:D

FINAL POINTS:
- I wonder if the Sclerostin relationship has to do with estrogen imbalance/high E relative, and not necessarily T Diminishment OR Deprivation? Comparative studies should be done if they were/are still manually choppin off nutz as a PC Treatment. (thoughts on study oversight by "Preferential Hunted Prey Error")

- With consideration of being fully grown, bone plates fused, and Plenty-o-TEst in the body. I fractured my BIRD FINGER when a 75lb aluminum window sash slammed down on it from a foot up:eek:, and I think it healed in about 3 days. LOL Again, there would be no shortage of available T for Androgens, conversely, I have plenty of estrogens I KNOW. (Relative to the article citing More T ='s Less Sclerostin as well as no change in Bone Turnover Markers Observed)

- Perhaps the Denser the bones (genetically RELATIVE of course), the more the Sclerostin Activity? And as the reverse feedback.? But ALSO, as a RESULT of Estrogen Imbalance as due to lack of Androgen supply; OR High Estrogen turnover from healthy matured bones being a growth shutdown agent in normal conditions (noting no change in "turn over"/normal cell maintenance)....

- And not really attempting to interpret how Osteo arthritis relates/involves with reference to "Bone caps"/Growth Plate activity standpoint. But thats where they seem to hurt as a result of something going on at the "Bone ends/Joints". Its my personal SUSPICION that MY Arthritis has a little bit to do with OVER-regeneration/excessive healing of the bones at the joints, thus EXCESS REGENERATION of the head of the Femur causing erratic "Rough" growth contributing to pelvic cup degeneration, and more-so scarring on the femur head preventing proper regeneration on that side, and plenty of "bone debris" in the joint area to further compound - As if 3M manufacturing headquarters are in my hips developing a new mechanical abrasion device... I have come to suspect this over the years due to the INTENSE Pain I get Erratically involving and uninvolving myself with high hip impact exercise, the pain that comes when I stop for a while then receding and the pain I get returning to action.. THe longer the period of layoff, the longer it is taking the pain to diminish on return and the greater the damage resulting - So it seems...

Finally, I must speculate/ask.. "Bone turnover marker "unchanged" relevance must indicate the Distinguishment of the observance of "Bone Growth" as NEW Cells/NEW Volume Created, VS. NORMAL Bone Synthesis/Re-GENESYS?

** THIS STUDY appears to be Unusually multi-faceted in that it BOTH infringes on/interjects some new concepts AS WELL as Serving an underlying motive, all as reviewing the skeletal related hormone action involved with cancer. I Suspect the underlying motive on this one is a simple plea (which we are all fine with pending source requesting - LOL) for more $ for cancer research which jack shit really is known as just status quo from any prospective Bias hunt.

Garcia-Fontana B, Morales-Santana S, Varsavsky M, et al. Sclerostin serum levels in prostate cancer patients and their relationship with sex steroids. Osteoporos Int. Sclerostin serum levels in prostate cancer patients and their relationship with sex steroids - Online First - Springer

The role of sclerostin on bone metabolism and its relation to sex steroids in patients with prostate cancer (PC) is not well known. We found that sclerostin levels are significantly increased in PC patients, particularly in those with androgen deprivation therapy (ADT), and there is an inverse relationship between sclerostin levels and testosterone.

INTRODUCTION: Recent studies have evaluated sclerostin levels in bone diseases as osteoporosis. However, there are few data in PC patients, particularly in patients with hypogonadism related to ADT. The aim of the present study was to compare serum sclerostin levels in ADT/non-ADT-treated PC patients and healthy controls and to evaluate their relationship with sex steroids and bone metabolism.

METHODS: We performed a cross-sectional study involving 81 subjects: 25 ADT-treated PC patients, 34 PC patients without ADT treatment, and 22 healthy controls. We measured serum sclerostin levels, bone turnover markers, bone mineral density (BMD) in all individuals, and sex steroids levels in PC patients.

RESULTS: Serum sclerostin levels were significantly higher in PC patients compared to those in control subjects. ADT-treated patients had significantly higher sclerostin levels than PC patients without ADT treatment: ADT 64.52 +/- 27.21 pmol/L, non-ADT 48.24 +/- 15.93 pmol/L, healthy controls 38.48 +/- 9.19 pmol/L, p < 0.05. In PC patients, we found a negative relationship between serum sclerostin levels and androgens after age adjustment (total testosterone: r = -0.309, p = 0.029; bioavailable testosterone: r = -0.280, p = 0.049; free testosterone: r = -0.299, p = 0.035). We did not observe any relationship between sclerostin levels and bone turnover markers or BMD in any group.

CONCLUSIONS: Circulating sclerostin levels are significantly increased in patients with PC and particularly in those receiving ADT. The inverse relationship between serum sclerostin and testosterone in these patients suggests that androgens are key regulators of bone metabolism in this population.
 
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So whats this article saying. I think they typo'd and mean Estrogen supplementation can maintain sexual interest in DEPRAVED MEN....:eek:[:o)]

Shit, whats the matter anyhow. The estrogen has already completed its mission and CAUSED the PC. Hell, whats more gonna hurt now anyway? LOL Perhaps they are of the mindset that since androgens well fuel the growth of PC already in place, lets go ahead and try to flood these tissue receptors with estrogens and see if we can "convert them from Beef eaters to Soy Bean Freaks" thus extinguishing the fire in place. In this case we should just all go on E supplementation and GET CANCER. Effectively there will be no growth of said and all's fine... LOL

Wibowo E, Wassersug RJ. The effect of estrogen on the sexual interest of castrated males: Implications to prostate cancer patients on androgen-deprivation therapy. Crit Rev Oncol Hematol 2013;87(3):224-38. Elsevier

Androgen deprivation therapy (ADT) for prostate cancer (PCa) treatment causes sexual dysfunction. We review here the effects of estrogen on the sexual performance of androgen-deprived males. The major findings are: We discuss the general benefits of estrogen therapy to quality of life of men on ADT, the potential risks of this treatment, and possible treatment regimes for estrogen therapy in males. Unless contraindicated, we propose that PCa patients on ADT would benefit from supplemental parenteral estrogen.
 
Perhaps they should develop a new PSA test. We'll coin it Active Aggravated Assessment. So take a 10" barbed spear and ram it around in there for a few minutes. The higher the spike in PSA, the more odds there is some other than a normal prostate going on.

FOR THAT MATTER. Does a cancer laiden fully affected PC cell even produce PSA from WITHIN ITS SELF. Or is it just its neighbors..!!!! In light of that though construct, it may very well be that physically manipulating a prostate as a method of intentionally creating a stimulus for PSA activity JUST MIGHT Evoke a DIMINISHED PSA Response (as compared to a healthy one) in a cancer laiden Prostate...!!! I wonder...:)

New PSA Test Recommendations: Clarifying or Confusing?
Over-treatment of prostate cancer is already a problem. Will this make it better or worse?
New PSA Test Recommendations: Clarifying or Confusing? - Cancer Research 101
 
Tomaszewski JJ, Richman EL, Sadetsky N, et al. Impact of Folate Intake on Prostate Cancer Recurrence Following Definitive Therapy: Data from CaPSURE. The Journal of Urology. Elsevier

Purpose - A randomized placebo-controlled clinical trial of folic acid supplementation for the chemoprevention of colorectal adenomas revealed an increased incidence of prostate cancer in the treatment group. Limited data exist on post-diagnostic folate/folic acid intake and risk of prostate cancer progression. We prospectively examined the association between post-diagnostic consumption of folate and the risk of prostate cancer recurrence following radical prostatectomy (RP), external beam radiation therapy (EBRT), and brachytherapy (BT).

Methods - This study was conducted among 1153 men treated with RP, EBRT, and BT with clinical stage T1-T2c prostate adenocarcinoma who participated in the Diet and Lifestyle sub-study of CaPSURE™ by completing a semi-quantitative food frequency questionnaire (FFQ) in 2004-2005. We utilized Cox proportional hazards regression to analyze the association between folate intake and prostate cancer progression.

Results - Overall, prostate cancer progression occurred in 101 (8.76%) men over a mean follow-up of 34 months. After multivariate adjustment, we observed no evidence of an association between intake of total folate, dietary folate, or dietary folate equivalents and prostate cancer recurrence. In a secondary analysis by treatment, patients in the lowest decile of dietary folate intake had a 2.6-fold increase in risk of recurrence (HR: 2.56; 95% CI: 1.23,5.29; p=0.01) following RP. In patients treated with EBRT and BT, we observed no evidence of an association between prostate cancer progression and increased intake of folate.

Conclusions - Our results suggest that the consumption of folate-containing foods and multivitamins is not associated with prostate cancer progression following definitive treatment.
 
Went to my uro to see if he would give me test since mine was low TT 137,he said no way.He did a new PSA test,my last one was 0.1, they called today and my new PSA was 0.09.....I have an appointment for Jan 3 and i am doing 100mg Test E every week and i will have him test my TT and PSA again then....will interesting to see if my PSA raises from the test E.
 
YES - It will... I am sure we are all interested in these results... As Clearly you are braving "New Frontier"!:)

What are you current stats? Plz?
1. Height -
2. Weight -
3. Estimated BMI -
4. Self described "fitness level" as - Toss in some workout stats like current bench and squat max'ez and current cardio routine.
5. Diet - Could you please describe current eating habits to some degree, and how they relate to past (as prior, during, and post diagnosis, during Treatment Periods, and Post "Final" or last significant treatment).

In short, obviously your avatar presents a fellow with some substantial workout and apparent competitive history. Meaning, how current is it - as I am trying to get an idea what your body is going to do with these exogenous hormones (for my own dementia:D)

IT SHOULD BE NOTED:
*** My journey with Testosterone began with "undertones of aging", and a REAL Perceived and REALIZED problems associated with, and pertaining to physical symptoms which were pretty clear. It all started simply as my involvement with "Health & Wellness" perspective with thoughts as "Fountains of Youth" via replacement of Age related Deficiencies. The Intended End Goal at the time (in my mind) was SUCCESS via SUPPLEMENTATION through "Now Available Modern Science". So, I am on my own somewhat "riskay venture", and placing some significant stock in Hormone Replacement as Potentially Viable as POSSIBLY being PREVENTATIVE of PC for me (and with a family history two dad's before me). THE "STOCK" which I am purchasing is that perhaps that the availability of TESTOSTERONE where as otherwise possibly NATURALLY Limited due to EITHER Excess Estrogen Factors limiting IMPEDING BASIC Androgen (production/availability) Activity, OR possibly even as AVOIDING genetically predisposed T production diminishment as a possible contributor to this family history of PC. I ALSO have personal hypotheses about receptor activity as it relates to these supplies with relation to TIME and HOW general Supply Availability may involve - With the Ultimate Premise being a Possible PREVENTION of "Negative" TISSUE RECEPTOR "REMODELING" over time (I only toss that in as I am currently out of shape with excess body fat for an extended period of years now). So my CONUNDRUM is ...:
(1) AM I EXPEDITING a Serious Problem ensuing via Genetic Predisposition;
(2) OR am I Successfully Intervening my Genetic Fate via "Natty Nutz Destined to FAIL"?[/B]
(3) MOST IMPORTANTLY - Will the excess available T PREVENT failures like PC and REGARDLESS of BMI? OR WILL IT KILL ME TWICE AS FAST considering family history!!?!?!?!??

Maybe you have some further thoughts for me? If you were in my shoes and now seriously training (which I suspect you have your whole life), would you invest in TRT (as I did in mid-thirties) if you had been afforded the foresight to see your PC diagnosis at the age which you were.??? I dont recall if you stated a family history? How early did you involve yourself with steroids, and did you involve a bunch of "bridging" over the years, as either SERM or CRUZING? Were there a lot of periods which you in between steroid usage, and NOT using any kind of med or exogenous supplementation (were you more of a "classic cycler" and what periods)???

Any thoughts appreciated...:)
TIA

Went to my uro to see if he would give me test since mine was low TT 137,he said no way.He did a new PSA test,my last one was 0.1, they called today and my new PSA was 0.09.....I have an appointment for Jan 3 and i am doing 100mg Test E every week and i will have him test my TT and PSA again then....will interesting to see if my PSA raises from the test E.
 
"YES - It will... I am sure we are all interested in these results... As Clearly you are braving "New Frontier"!


If you knew how really really terrible you feel with no test you would see why i am not going go that route......Im 67 years old now...how much longer can i expect to live?.Ive read a lot of studys the doc has posted and it seems theres only one way to find out what test will have on me now,i dont plan on using any more than what keeps me in the 500 range. Ive been BB off and on for about 30 years and health wise i dont have any medical issues at all except the PCa which was delt with. and im a little hypothyroid and taking 88mcg of T4 for that,but that seems to be pretty normal for older people.I will be seeing my primary for a check up the begining of every year and will do hormone and PSA levels.i will aslo be seeing my euro and Endo at least twice a year.Since my PCa was confined to my prostrate it makes it a little less risky.
 
I started doing steroids in 1980 after a couple years of serious BB training in a HARD CORE gym of BB and powerlifters. We knew nothing of PCT so we all just stopped taking steroids and let our systems return to normal on its own,i never had any issues doing it that way.I was 35 at the time i started.2008 to 2011 i did 2 or 3 8 week cycles a year all without PCT except for the last 2 when i learned how to do PCT but i always recovered and after my last cycle my TT was 502, and 440 6 months later when was biopsied and found grade 7 cancer.At that time i was put on ADT and was on that for 6 months,so i had 0 test. after all the treatments,seed implants and radiation the ADT was stopped and as of last month i hadnt recovered my test even with me doing HCG and a coulple cycles of Nolvadex and clomid.It was at 137 TT when my endo tested my Test and thyroid levels.I dont know if my father ever had PCa he died at 70 and i dont think he had it tested.I had my PSA done at 50 which was ok and at 65 when it was at 5.5 and then 11.4 6 months later.
 
Girard D, Marino FE, Cannon J. Evidence for reduced neuromuscular function in men with a history of androgen deprivation therapy for prostate cancer. Clin Physiol Funct Imaging. Evidence for reduced neuromuscular function in men with a history of androgen deprivation therapy for prostate cancer - Girard - 2013 - Clinical Physiology and Functional Imaging - Wiley Online Library

BACKGROUND: Indices of body composition and muscular strength were compared between men with prostate cancer (PCa) treated with androgen deprivation therapy (ADT) and asymptomatic matched men.

METHODS: Nine subjects aged 63-83 years with PCa who received ADT (PCa+ADT; duration 6-180 months) and 11 asymptomatic aged-matched eugonadal men (HM) aged 59-80 years were assessed for prostate-specific antigen (PSA) and total testosterone (TT). Total body non-osseous lean mass (TBLM) and right thigh non-osseous fat-free mass (RTLM) were assessed using dual-energy X-ray absorptiometry. Peak torque of the right knee extensors at 0 degrees s-1 (ISO) and 60 degrees s-1 (CON), maximal handgrip strength of the dominant hand (MHS) and whole-body strength (WBS) were assessed. ISO and CON per unit mass of RTLM and MHS and WBS per unit mass of TBLM were calculated.

RESULTS: Age, height, mass, body mass index and prostate-specific antigen were comparable between groups (P>0.05), while TT was lower in PCa+ADT (P<0.01). RTLM was similar between groups (P>/=0.075). Absolute ISO and CON were lower for PCa+ADT (P<0.01) as were CON per unit of RTLM and ISO per unit of RTLM (P<0.05). Absolute MHS, WBS and MHS per unit of TBLM and WBS per unit of TBLM were lower for PCa+ADT (P<0.01; P<0.05).

CONCLUSIONS: Men with PCa who receive ADT experience significant losses in whole-body muscular strength compared with asymptomatic age-matched men, which may impair functional capacity. These losses in muscular strength appear to involve neuromuscular mechanisms that are yet to be identified.
 
No - I DEFINITELY KNOW how terrible it feels. I have quit once or twice. I also started TRT for a reason. I quit cold turkey for about 6 months straight. This was around 2 years ago. I watched my pecs start to sag, weigh fell off, and felt depressed in an apathetic kinda way. It was almost so disabling psychologically speaking, that i would have not had the mental capability to recognize this issue had I been any other. But I'm also the same person who identified the issue early on in mid thirties and went after it. I would do about what you are doing I AM SURE. YOU - - - Are braving the NEWEST FRONTIER. And Kudos bakacha.!!:)

"YES - It will... I am sure we are all interested in these results... As Clearly you are braving "New Frontier"!


If you knew how really really terrible you feel with no test you would see why i am not going go that route......Im 67 years old now...how much longer can i expect to live?.Ive read a lot of studys the doc has posted and it seems theres only one way to find out what test will have on me now,i dont plan on using any more than what keeps me in the 500 range. Ive been BB off and on for about 30 years and health wise i dont have any medical issues at all except the PCa which was delt with. and im a little hypothyroid and taking 88mcg of T4 for that,but that seems to be pretty normal for older people.I will be seeing my primary for a check up the begining of every year and will do hormone and PSA levels.i will aslo be seeing my euro and Endo at least twice a year.Since my PCa was confined to my prostrate it makes it a little less risky.
 
Girard D, Marino FE, Cannon J. Evidence for reduced neuromuscular function in men with a history of androgen deprivation therapy for prostate cancer. Clin Physiol Funct Imaging. Evidence for reduced neuromuscular function in men with a history of androgen deprivation therapy for prostate cancer - Girard - 2013 - Clinical Physiology and Functional Imaging - Wiley Online Library

BACKGROUND: Indices of body composition and muscular strength were compared between men with prostate cancer (PCa) treated with androgen deprivation therapy (ADT) and asymptomatic matched men.

METHODS: Nine subjects aged 63-83 years with PCa who received ADT (PCa+ADT; duration 6-180 months) and 11 asymptomatic aged-matched eugonadal men (HM) aged 59-80 years were assessed for prostate-specific antigen (PSA) and total testosterone (TT). Total body non-osseous lean mass (TBLM) and right thigh non-osseous fat-free mass (RTLM) were assessed using dual-energy X-ray absorptiometry. Peak torque of the right knee extensors at 0 degrees s-1 (ISO) and 60 degrees s-1 (CON), maximal handgrip strength of the dominant hand (MHS) and whole-body strength (WBS) were assessed. ISO and CON per unit mass of RTLM and MHS and WBS per unit mass of TBLM were calculated.

RESULTS: Age, height, mass, body mass index and prostate-specific antigen were comparable between groups (P>0.05), while TT was lower in PCa+ADT (P<0.01). RTLM was similar between groups (P>/=0.075). Absolute ISO and CON were lower for PCa+ADT (P<0.01) as were CON per unit of RTLM and ISO per unit of RTLM (P<0.05). Absolute MHS, WBS and MHS per unit of TBLM and WBS per unit of TBLM were lower for PCa+ADT (P<0.01; P<0.05).

CONCLUSIONS: Men with PCa who receive ADT experience significant losses in whole-body muscular strength compared with asymptomatic age-matched men, which may impair functional capacity. These losses in muscular strength appear to involve neuromuscular mechanisms that are yet to be identified.

I can tell you from this experience that it is 100% true.I got extreamly weak and lost all my endurance ,also my joints ached to the point i had to quit working out.Ive been on 150mg test E for 2 weeks now and been working out again,making gains like i was on a cycle of test and another compound at high doses. most of my hurting joints have gone away,could be the test or possibly estrogen from conversion since im not using and AI or serm yet.I will get my dose adjusted to 100mg a week in the next month,dont know if im going to split the dose or just do 100mg a week.I go back to my eurologist Jan 3 to test my PSA and probably get him to do my test level also,i am hoping for a level in the 500 to 600 range.
 
PCa development is independent from endogenous serum T levels. TRT for symptomatic hypogonadism does not increase the risk of PCa development.

Data derived from the current literature indicate that TRT can be given to symptomatic hypogonadal patients who received radical prostatectomy, brachytherapy, or external beam radiotherapy for PCa with detailed discussion, obtaining written consent and with close and vigilant followup.

TRT can be started in first year after radical prostatectomy and with serum PSA level less than 1 ng/mL after external beam radiotherapy.

Atan A, Tuncel A, Yesil S, Balbay D. Serum Testosterone Level, Testosterone Replacement Treatment, and Prostate Cancer. Adv Urol. 2013:275945. Serum Testosterone Level, Testosterone Replacement Treatment, and Prostate Cancer

There has been an increase in the number of individuals seeking testosterone (T) replacement treatment (TRT) due to a decrease in their blood T levels. Prostate cancer (PCa) is also an important issue in the same age group. However, we, urologists, are anxious about PCa development after T treatment. This is because it has been assumed that T may cause PCa or exacerbate insidious PCa which is already present. In this paper, recent developments regarding the relationship between serum levels of sex hormone and prostate tissue, the causal relationship between T and development of PCa, the effect of TRT on the group of patients who are at high risk of developing PCa, the suitability of TRT for patients who have already been diagnosed with PCa, and the effect of TRT on serum prostate-specific antigen level are analyzed.
 
PCa development is independent from endogenous serum T levels. TRT for symptomatic hypogonadism does not increase the risk of PCa development.

Data derived from the current literature indicate that TRT can be given to symptomatic hypogonadal patients who received radical prostatectomy, brachytherapy, or external beam radiotherapy for PCa with detailed discussion, obtaining written consent and with close and vigilant followup.

TRT can be started in first year after radical prostatectomy and with serum PSA level less than 1 ng/mL after external beam radiotherapy.

Atan A, Tuncel A, Yesil S, Balbay D. Serum Testosterone Level, Testosterone Replacement Treatment, and Prostate Cancer. Adv Urol. 2013:275945. Serum Testosterone Level, Testosterone Replacement Treatment, and Prostate Cancer

There has been an increase in the number of individuals seeking testosterone (T) replacement treatment (TRT) due to a decrease in their blood T levels. Prostate cancer (PCa) is also an important issue in the same age group. However, we, urologists, are anxious about PCa development after T treatment. This is because it has been assumed that T may cause PCa or exacerbate insidious PCa which is already present. In this paper, recent developments regarding the relationship between serum levels of sex hormone and prostate tissue, the causal relationship between T and development of PCa, the effect of TRT on the group of patients who are at high risk of developing PCa, the suitability of TRT for patients who have already been diagnosed with PCa, and the effect of TRT on serum prostate-specific antigen level are analyzed.

Father-in-law is 71 and still works as a trial attorney for medical malpractice defense. He's sharp as a tack but man he has aged a lot in the past 5 years physically. I suggested he have his T checked and it came back tT 162. He had a radical prostatectomy 10 years ago with no issues....his doctors (plus many "expert" witnesses he's gotten to know over the years) all forbid him from going on TRT.

It's going to take time before this body of evidence filters down to your average doc in practice IMO. Meanwhile my FIL doesn't have all that much time left and I think would enjoy his last years much more on TRT...
 
I hear ya. I KNOW your dilemma. I have a buddy that is about 10 year older than me and in his early 50's. I advertised to him over the past 8 years which I have been involved with TRT VERY CAUTIOUSLY, but encouragingly, as I KNEW that I really dont know the implications of WHAT I MAY be doing to myself. And especially with a family PC history. Really, I wonder the sanity - but i continue to stick to my plan. WHICH IS - (as chicken or egg). Does the loss of hormone production with natural aging associate directly as "an unavoidable cost of aging" which CAN INDEED by circumvented by SIMPLY REPLACEMENT; and thus eliminating the development of cancer by supplementation of what otherwise lacked....? OR - Will the addition of hormones exogenously profoundly complicate and exacerbate the potentially INEVITABLE and/OR Unavoidable - as strict genetic CONSEQUENCE (meaning as not really yet scientifically overtable short of DNA manipulation, etc..)

SO - You are asking YOURSELF - WOULD I be sentencing my dad to a premature death sentence; OR would I be bolstering his life.?

My Thoughts:
1.) What is the REAL VALUE of TRT with regard to age and natural genetic specific progression. HOW Valuable COULD it be to him. Would he even notice it?
2.) WOULD IT POSSIBLY EVEN HELP HIM, and both psychologically as well as physically and ALL-ROUND even.? (Wouldn't it be funny if he started TRT and would up with the nursing home title - "The Aging Raging Bull"..?! LOL
3.) But what are the potential negatives? Cancers and more specifically - DNA perversions/failures ALREADY in place and action that could potentially be greatly increased. And PERHAPS even due to a failure of other systems that TRT cant influence, but NOW become a negative aspect of TRT. (Thyroid, Etc.., Could he even over exert himself and rupture a tendon due to increased muscular action that TRT wont necessarily bolster, or at least at the same rate.
4.) Would TRT just flat our prove pointless due to aged insulin activity, or other, and possibly even stretching that simply old pancrease to full blown diabetes now costing him an eye or a foot in three years. (as a scaled down example SHORT or progression of potential cancer in wait)
5.) The list goes on.. But the point is YOU REALLY CARE on this one. And MORE than just an objective patient - ITS YOUR DAD...!

Back of the subject of that buddy of mine who I hinted around to and even encouraged to look into it at times. He also had the common notion (as a negative in his head) that "injections = STEROIDS" thus further complicating his possible objectivity. THE OLD WITCH BURNING DEMONIZATION AGAIN STILL AFFECTING SOCIETY..!!!! The long and short - is that when I met him he was early forties and one of these guys NOT ONLY with a full head of hair, but young skin - the works. He was ten years older and could have passed for younger than me. So I always thought he would be 65 and passing for 40 still. BUT NO. I recently saw him and was shocked. He was half crippled and has essentially retired from his favorite past time of golf - due to same. Looking gray (never imagined possible). Most importantly kinda flabby, chubby, but not in healthy way. Also note this man was an INCREDIBLE athlete when young, and in top 5-10 percentile of population i suspect which could have played semi-pro out of school if he really wanted. I caught up with him again the other day. Even after toning it down to a minor, "man, you should just see a doc about a patch and test the water, back when we played that last round of golf a year ago - HE SIMPLY WOULD NOT EVEN RESPOND TO MY INQUIRY AS TO DID HE EVER TRY (in text comm.). So I have never pressed him, but always suggested AND ONLY BECAUSE HE DID INITIALLY EXPRESS INTEREST. I feel it would have helped him. But who knows, perhaps he would be dead of prostate cancer if he had. I JUST DONT KNOW. I'm really kinda glad he never did in the end, cause I would not have wanted to wonder if he did turn up ill in that time on, would I have caused by encouraging.. When still, it could have been a genetic development UNAVOIDABLE,,,, I would have to deal with the thought process, as there is simply not enough scientific evidence either way...

WE... Are the Beta group. Its almost like Bill Gates runs the medical science industry. As all microsoft final releases were really just the next beta now aren't they... LOL

I dont know. Like I said, I feel your dilemma. My dad had his prostate successfully removed 20 years ago at early fifties. I would not have told him to do it at any time in my experience over the last 8-9 years of research. I DONT speculate SPECIFICALLY WHY I would not. But I wont...

Hope that helps some..:)

Father-in-law is 71 and still works as a trial attorney for medical malpractice defense. He's sharp as a tack but man he has aged a lot in the past 5 years physically. I suggested he have his T checked and it came back tT 162. He had a radical prostatectomy 10 years ago with no issues....his doctors (plus many "expert" witnesses he's gotten to know over the years) all forbid him from going on TRT.

It's going to take time before this body of evidence filters down to your average doc in practice IMO. Meanwhile my FIL doesn't have all that much time left and I think would enjoy his last years much more on TRT...
 

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