Prostate

[edgarr]

Well I hate to bring this thread back up but there is very good info here and I want to give my 1 year update.

Unfortunatley it is not what I want to say. First, I have been completely off all HRT. No TEST or HGH. At first it sucked but after awhile I got use to it. Put on weight and still have all the symptons of low TEST. I never took any medications to fight any possible infection as my doc never prescribed any so I am still hopefull that it is an infection that never went away and I will request antibiotics this time. I got my bloodwork back and my PSA is 2.7. It went down to 1.3 and that is why the doc advised me to wait a year and re test. Funny thing is, my TEST came back at 337! That is triple what it was before I started HRT. So it seems like my natural TEST production came back, not sure how but it did. Bad thing is, seems like my rise in PSA is directly correlated with higher TEST levels. My doc wants to perfrom a digital exam and after those results, perhaps a bioposy, which scares me to death! I am so confused. I will be 41 in June, stay active and have no signs of an enlarged prostate, WTF? My appointment for the digital is next week and I will update this thread. Anyone familiar with a new anti biotic that is used for prostate infections that I should ask about? I found this on the web:

Antibiotics used to treat prostate infections include oral drugs like trimethoprim-sulfamethoxazole, fluoroquinolones and doxycycline. In some cases, doctors prescribe an injection of the antibiotic ceftriaxone followed by an oral antibiotic,

Thanks

[zaggahamma]

so he's saying since its at 2.7 that theres need of alarm and finger test and biopsy with 2.7 and no signs/problems?

[GotNoBlueMilk]

Those antibiotics aren't new. And unless you have an active bacterial infection they won't help.

[edgarr]

yes, feels that is too high for someone my age and since it has bounced around he thinks so.

[zaggahamma]

yes, feels that is too high for someone my age and since it has bounced around he thinks so.

my uncle is 66 and has had some urination issues but since resolved....i wish he would have got a copy(s) of his bloodwork(s) during all his tests so i could see his psa numbers as he's goin in for a biopsy tomorrow although there arent any symptoms....i just would hate for someone to go under the knife just to make these fvckers money

[edgarr]

well I go to the doc Tuesday. Will discuss antibiotics with him first. Will report back what he tells me. I am sure I am searching here but odly enough, I went back and checked and everytime I had bloodwork done and the results were high PSA number it was around the same time I was also being lasered to have some tattoos removed. Maybe my body is having an allergic reaction to the ink it is breaking up causing an infection ( I sound desperate).

[pat80flh]

Howdy to all, newbie here, not a body builder, 53 year old man. During my "turning 50 physical", found high PSa levels: 9.0 ; was biopsied, affirmative for cancer, surgical removal of gland recomended. Subsequent testing for any spread raised red flags, unknown lesions on ribs, more and more testing was inconclusive. Bottom line, they don't THINK the lesions are anything serious, let's cut that out of there and hope for the best. Long story short, I went on a "natural" prostate cure, vegan diet, quit drinking etc. drove PSA down to 5.0. Then divorce, job change, new house,taking in sick mother, slacked off the second year, started drinking again, eating poorly, gained weight, PSA slowly climbing, up to 14.0 last visit. But I am now in position to really attack this tumor, life has settled down, quit drinking at the new year, eating right, doing a little weight training, as well as meditation and excersize. Really feel like I can at least hold this at bay for the rest of my life.
My research found a school of thought that low testosterone can actually cause prostate cancer, and men with higher levels are less likely to get it. I started having free testosterone levels checked with PSA and they've been consistently low, 2.9 to 5.2. Of course the doctors think I'm nuts, my primary care phy. says it would be medical malpractice to write a scrip, urologist says why my prostate isn't in a jar by now he'll never know, but testosterone supplementation would be like throwing gas on a fire. I was a fairly typical 50 year old biker/partier/blue collar worker, overweight, high blood pressure etc. and had no symptoms other than a bit of urination frequency. My self cure has brought me from 240 lbs to 177, cured any blood pressure and cholesterol numbers and made me incredibly fit. I feel I am on the verge of kicking the shit out of this thing and am considering going off the grid and self administer some T. Anybody ever done it? I figure I'm still pretty safe and if worse comes to worse I can always cave in and get cut, but I'd really rather not. All I'm looking to do is make my prostate think it's attached to a young healthy male and give it some help in curing itself. Any thoughts?

[zaggahamma]

Howdy to all, newbie here, not a body builder, 53 year old man. During my "turning 50 physical", found high PSa levels: 9.0 ; was biopsied, affirmative for cancer, surgical removal of gland recomended. Subsequent testing for any spread raised red flags, unknown lesions on ribs, more and more testing was inconclusive. Bottom line, they don't THINK the lesions are anything serious, let's cut that out of there and hope for the best. Long story short, I went on a "natural" prostate cure, vegan diet, quit drinking etc. drove PSA down to 5.0. Then divorce, job change, new house,taking in sick mother, slacked off the second year, started drinking again, eating poorly, gained weight, PSA slowly climbing, up to 14.0 last visit. But I am now in position to really attack this tumor, life has settled down, quit drinking at the new year, eating right, doing a little weight training, as well as meditation and excersize. Really feel like I can at least hold this at bay for the rest of my life.
My research found a school of thought that low testosterone can actually cause prostate cancer, and men with higher levels are less likely to get it. I started having free testosterone levels checked with PSA and they've been consistently low, 2.9 to 5.2. Of course the doctors think I'm nuts, my primary care phy. says it would be medical malpractice to write a scrip, urologist says why my prostate isn't in a jar by now he'll never know, but testosterone supplementation would be like throwing gas on a fire. I was a fairly typical 50 year old biker/partier/blue collar worker, overweight, high blood pressure etc. and had no symptoms other than a bit of urination frequency. My self cure has brought me from 240 lbs to 177, cured any blood pressure and cholesterol numbers and made me incredibly fit. I feel I am on the verge of kicking the shit out of this thing and am considering going off the grid and self administer some T. Anybody ever done it? I figure I'm still pretty safe and if worse comes to worse I can always cave in and get cut, but I'd really rather not. All I'm looking to do is make my prostate think it's attached to a young healthy male and give it some help in curing itself. Any thoughts?

dude sorry to hear

glad you made your self better under all these f'd up conditions...from what all i've read the throwing gas on the fire comment you made is what i have came to believe as true...

i can google this but i like this format but what is the worse if you have it removed? ....

i'll be around

[THE-DET-OAK]

I would be cautious with my T dose, while new studies in the last year or so have affirmed that physiological TT levels actually reduce the risk of prostate cancer, everything changes when you get into the supraphysiological range.

On top of that PSA levels are a great indicator, it is not extremely un-common to still get P cancer with proper PSA's. men, especially when the get older, need to get the finger up the butt every once and a while, I know it sux to hear, but better safe than sorry.

[pittbulldad]

on a side note if you do have prostate cancer... testosterone feeds it and makes it grow faster...

in regards to PSA they have found that half of the men treated for Prostate cancer that was diagnosed via PSA in the previous 10 years didn't actually need any treatment that they received...

[zaggahamma]

on a side note if you do have prostate cancer... testosterone feeds it and makes it grow faster...

in regards to PSA they have found that half of the men treated for Prostate cancer that was diagnosed via PSA in the previous 10 years didn't actually need any treatment that they received...

who r "they" ?

and are you saying that the patients were told they had cancer and didnt actually have it?

[pittbulldad]

studies that have been done.. showed that about half of the men who had surgery or other treatments for prostate "cancer" due to elevated PSA's didn't actually need treatments... i don't have the acutal studies handy

[zaggahamma]

studies that have been done.. showed that about half of the men who had surgery or other treatments for prostate "cancer" due to elevated PSA's didn't actually need treatments... i don't have the acutal studies handy

this is very interesting

[THE-DET-OAK]

on a side note if you do have prostate cancer... testosterone feeds it and makes it grow faster...

in regards to PSA they have found that half of the men treated for Prostate cancer that was diagnosed via PSA in the previous 10 years didn't actually need any treatment that they received...

are you sure it was the testosterone???? I have seen some studies and I have always had the understanding that it was due to increase estrogen levels. Back in the day all they had to go on, for androgen therapy were studies of supraphysiological levels. This is why they screamed cancer. more recently, studies have been done on doses that keep TT in physiological range and the data changed, showing that TRT actually decreases risk of prostate cancer.

[zaggahamma]

are you sure it was the testosterone???? I have seen some studies and I have always had the understanding that it was due to increase estrogen levels. Back in the day all they had to go on, for androgen therapy were studies of supraphysiological levels. This is why they screamed cancer. more recently, studies have been done on doses that keep TT in physiological range and the data changed, showing that TRT actually decreases risk of prostate cancer.

yes i believe what you're saying is a poor estro to test ratio is shown in men with cancer but what's being said...IS...

IF...there is ALREADY cancer PRESENT.....THEN....testosterone is the fuel for the cancer...

and yes your last sentence is what i believe/read as well

[pittbulldad]

what jpkman says is correct.. if you already have prostate cancer testosterone feeds the cancer making it grow faster which is why they put men on estrogen therapy when they are diagnosed... although I think that type of therapy is not as common any more

[THE-DET-OAK]

testosterone DOES NOT FUEL PROSTATE CANCER, NOR DOES DHT. alot has changed in recent time about prostate cancer. Its the estrogen, in high amounts. all this stuff you read is old data. the reason it was believed to do so, like many other myths about TRT, is because for the longest time we had nothing to go except data on men taking bodybuilding doses, so as I said before, keeping TT levels within normal range is fine, even if you have prostate cancer, it may actually reduce studies have found, recently. for years docs wouldn't prescribe TRT because of this myth. same thing as diabetes. they are NOW finding TRT is not bad for diabetics, they are actually finding they need up to HALF the amount of insulin as they did before. TRT is rapidly changing, and is going to be HUGE! The health benefits are immeasurable!!!!!

Originally posted by Dr. Scally

“Dihydrotestosterone (DHT) treatment for 24 months does not affect prostate growth, but causes a decrease in spinal, but not hip, bone mineral density (BMD)," Australian researchers found after evaluating 114 men for two years. "Every six months, blood samples and questionnaires were collected, prostate volume was measured with ultrasonography, and BMD and body composition were measured with dual-energy x-ray absorptiometry," according to the paper in the Annals of Internal Medicine. "Compared with placebo, DHT reduced lumbar spine BMD (1.4%; 95% CI, 0.6% - 2.3%; P < .001) at 24 months but not hip BMD (P > .2) and increased serum aminoterminal propeptide of type I procollagen in the second year of the study."


Dihydrotestosterone May Not Affect Prostate Growth But May Reduce BMD
http://www.medscape.com/viewarticle/732585

November 16, 2010 — Dihydrotestosterone (DHT) treatment for 24 months does not affect prostate growth but causes a decrease in spinal, but not hip, bone mineral density (BMD), according to the results of a randomized, placebo-controlled, parallel-group trial reported in the November 16 issue of the Annals of Internal Medicine.

"Benign prostatic hypertrophy increases with age and can result in substantially decreased quality of life for older men," write Amanda Idan, BSc, MHSc, from Concord Hospital, ANZAC Research Institute, University of Sydney, Sydney, Australia, and colleagues. "Surgery is often required to control symptoms. It has been hypothesized that long-term administration of a nonamplifiable pure androgen might decrease prostate growth, thereby decreasing or delaying the need for surgical intervention."

At an ambulatory care research center, 114 healthy men older than 50 years without known prostate disease were randomly assigned to receive transdermal DHT (70 mg) or placebo gel daily for 2 years. Every 6 months, blood samples and questionnaires were collected, prostate volume was measured with ultrasonography, and BMD and body composition were measured with dual-energy x-ray absorptiometry. Data were analyzed by mixed-model analysis for repeated measures.

With time on study, there was an increase during 24 months in total prostate volume (29%; 95% confidence interval [CI], 23% - 34%), central prostate volume (75%; 95% CI, 64% - 86%; P < .01), and serum prostate–specific antigen level (PSA; 15%; 95% CI, 6% - 24%). However, DHT had no effect on these changes (P > .2).

Compared with placebo, DHT reduced lumbar spine BMD (1.4%; 95% CI, 0.6% - 2.3%; P < .001) at 24 months but not hip BMD (P > .2) and increased serum aminoterminal propeptide of type I procollagen in the second year of the study. In the DHT group, levels of serum DHT and its metabolites were increased, whereas serum testosterone, estradiol, luteinizing hormone, and follicle-stimulating hormone levels were suppressed. DHT increased hemoglobin levels (7%; 95% CI, 5% - 9%), serum creatinine levels (9%; 95% CI, 5% - 11%), and lean mass (2.4%; 95% CI, 1.6% - 3.1%) but reduced fat mass (5.2%; 95% CI, 2.6% - 7.7%; P < .001 for all).

DHT was not associated with any serious adverse effects but did cause some protocol-specific discontinuations. These were asymptomatic increased hematocrit levels in 8 patients, which resolved after treatment was stopped, and increased PSA levels in 3 patients, none of whom had prostate cancer.

"Negative findings on prostate growth cannot exclude adverse effects on the natural history of prostate cancer," the study authors write. "Dihydrotestosterone treatment for 24 months has no beneficial or adverse effect on prostate growth but causes a decrease in spinal but not hip BMD. These findings have important implications for the wider use of nonsteroidal pure androgens in older men."

In an accompanying editorial, Ronald S. Swerdloff, MD, from Harbor–University of California, Los Angeles, and Christina Wang, MD, from David Geffen School of Medicine at the University of California, Los Angeles, note that this study was not adequately powered to definitively answer the question of long-term safety of testosterone use.

"These data do show that a 10-fold increase in serum DHT levels had no significant effects on prostate size, serum DHT, and International Prostate Symptom Score, suggesting that the modest increases of serum DHT seen after testosterone treatment may not have a clinically significant effect on prostate health," Drs. Swerdloff and Wang write. "Idan and colleagues argue that their findings provide insight about the potential efficacy of future synthetic androgen receptor modulators that will likely share (with DHT) the anabolic effects on muscle and fat, as well as the sparing effects on the prostate. However, we caution that each synthetic androgen-receptor modulator could have a different target organ profile. We conclude that DHT acts as a hormone in tissues without high concentrations of 5α-reductase enzymes but mainly in an autocrine–paracrine manner in tissues like the prostate, in which 5α-reductase is abundant."

BHR Pharma supported this study. Some of the study authors have disclosed various financial relationships with BHR Pharma, Bayer Schering, Ascend/Besins, and/or Radius and Clarus Therapeutics. Drs. Swerdloff and Wang have disclosed no relevant financial relationships.



Idan A, Griffiths KA, Harwood DT, et al. Long-Term Effects of Dihydrotestosterone Treatment on Prostate Growth in Healthy, Middle-Aged Men Without Prostate Disease. Annals of Internal Medicine 2010;153(10):621-32. Long-Term Effects of Dihydrotestosterone Treatment on Prostate Growth in Healthy, Middle-Aged Men Without Prostate Disease — Ann Intern Med

Background: Benign prostatic hypertrophy increases with age and can result in substantially decreased quality of life for older men. Surgery is often required to control symptoms. It has been hypothesized that long-term administration of a nonamplifiable pure androgen might decrease prostate growth, thereby decreasing or delaying the need for surgical intervention.

Objective: To test the hypothesis that dihydrotestosterone (DHT), a nonamplifiable and nonaromatizable pure androgen, reduces late-life prostate growth in middle-aged men.

Design: Randomized, placebo-controlled, parallel-group trial. (Australian New Zealand Clinical Trials Registry number: ACTRN12605000358640)

Setting: Ambulatory care research center.

Participants: Healthy men (n = 114) older than 50 years without known prostate disease.

Intervention: Transdermal DHT (70 mg) or placebo gel daily for 2 years.

Measurements: Prostate volume was measured by ultrasonography; bone mineral density (BMD) and body composition were measured by dual-energy x-ray absorptiometry; and blood samples and questionnaires were collected every 6 months, with data analyzed by mixed-model analysis for repeated measures.

Results: Over 24 months, there was an increase in total (29% [95% CI, 23% to 34%]) and central (75% [CI, 64% to 86%]; P < 0.01) prostate volume and serum prostate-specific antigen level (15% [CI, 6% to 24%]) with time on study, but DHT had no effect (P > 0.2). Dihydrotestosterone treatment decreased spinal BMD (1.4% [CI, 0.6% to 2.3%]; P < 0.001) at 24 months but not hip BMD (P > 0.2) and increased serum aminoterminal propeptide of type I procollagen in the second year of the study compared with placebo. Dihydrotestosterone increased serum DHT levels and its metabolites (5α-androstane-3α,17β-diol and 5α-androstane-3β,17β-diol) and suppressed serum testosterone, estradiol, luteinizing hormone, and follicle-stimulating hormone levels. Dihydrotestosterone increased hemoglobin levels (7% [CI, 5% to 9%]), serum creatinine levels (9% [CI, 5% to 11%]), and lean mass (2.4% [CI, 1.6% to 3.1%) but decreased fat mass (5.2% [CI, 2.6% to 7.7%]) (P <0.001 for all). Protocol-specific discontinuations due to DHT were asymptomatic increased hematocrit (n = 8), which resolved after stopping treatment, and increased prostate-specific antigen levels (n = 3; none with prostate cancer) in the DHT group. No serious adverse effects due to DHT occurred.

Limitation: Negative findings on prostate growth cannot exclude adverse effects on the natural history of prostate cancer.

Conclusion: Dihydrotestosterone treatment for 24 months has no beneficial or adverse effect on prostate growth but causes a decrease in spinal but not hip BMD. These findings have important implications for the wider use of nonsteroidal pure androgens in older men.

Primary Funding Source: BHR Pharma.

[THE-DET-OAK]

Elsevier

Medical News: Revisiting Testosterone Tx in Prostate Ca - in Oncology, Prostate Cancer from MedPage Todayhttp://www.medpagetoday.com/Oncology...teCancer/26104

Purpose
A history of prostate cancer has been a longstanding contraindication to the use of testosterone therapy due to the belief that higher serum testosterone causes more rapid prostate cancer growth. Recent evidence has called this paradigm into question. In this study we investigate the effect of testosterone therapy in men with untreated prostate cancer.

Materials and Methods
We report the results of prostate biopsies, serum prostate specific antigen and prostate volume in symptomatic testosterone deficient cases receiving testosterone therapy while undergoing active surveillance for prostate cancer.

Results
A total of 13 symptomatic testosterone deficient men with untreated prostate cancer received testosterone therapy for a median of 2.5 years (range 1.0 to 8.1). Mean age was 58.8 years. Gleason score at initial biopsy was 6 in 12 men and 7 in 1. Mean serum concentration of total testosterone increased from 238 to 664 ng/dl (p <0.001). Mean prostate specific antigen did not change with testosterone therapy (5.5 ± 6.4 vs 3.6 ± 2.6 ng/ml, p = 0.29). Prostate volume was unchanged. Mean number of followup biopsies was 2. No cancer was found in 54% of followup biopsies. Biopsies in 2 men suggested upgrading, and subsequent biopsies in 1 and radical prostatectomy in another indicated no progression. No local prostate cancer progression or distant disease was observed.

Conclusions
Testosterone therapy in men with untreated prostate cancer was not associated with prostate cancer progression in the short to medium term. These results are consistent with the saturation model, ie maximal prostate cancer growth is achieved at low androgen concentrations. The longstanding prohibition against testosterone therapy in men with untreated or low risk prostate cancer or treated prostate cancer without evidence of metastatic or recurrent disease merits reevaluation.

http://www.healthnewstrack.com/health-news-2513.html

In an editorial in the journal Cancer, "Turning Conventional Wisdom Upside Down: Low Serum Testosterone and High-Risk Prostate Cancer Morgentaler wrote, "After seven decades of circumstantial evidence pointing us in the wrong direction, perhaps it is time to consider the once unthinkable -- conducting a testosterone therapy trial of sufficient size and duration to determine whether normalization of serum testosterone in older men may reduce the risk of prostate cancer, particularly high-risk prostate cancer."

please keep in mind I am not trying to "show off" this is info I had to learn too.

[zaggahamma]

no...appreciate...i will check this out bro

[pittbulldad]

Thats a pretty intersesting article.. I work in cancer therapy and haven't seen that before.. that is certainly a major change in philosphy but can't back down from evidence... however that being said.. looks like it was a small research group they will have to expand it and go outside of low to mid gleason scores to verify.

[THE-DET-OAK]

yes. well keep in mind that is not the only one. there are about 4 others I could put up with the same results. the thing is they were smaller studies with low to medium risk prostate cancer. so although they can be sure it does not increase the risk, to truly say it will reduce the risk they want to do a large scale study on high risk. the biggest most recent one was done in sept of last year, but i was having trouble finding it for some reason.

[edgarr]

I had to change my appointment, will have the digital exam on June 15th. I am hoping that it is an infection.

Not sure what this means but everytime my PSA is up so is my test levels. Funny thing is, how can anyone that is on TRT and been on it for sometime having any natural test levels? So my guess is that it is not the TEST fueling prostate cancer but the conversion to esto. Will update after my exam.

[zaggahamma]

I had to change my appointment, will have the digital exam on June 15th. I am hoping that it is an infection.

Not sure what this means but everytime my PSA is up so is my test levels. Funny thing is, how can anyone that is on TRT and been on it for sometime having any natural test levels? So my guess is that it is not the TEST fueling prostate cancer but the conversion to esto. Will update after my exam.

MY belief was that it was the trt(exo test) that could fuel the cancer NOT NATTY TEST

[THE-DET-OAK]

there is really no diff between exogenous and endogenous test, some believe bio identical has less implications on things like hemo, but the evidence anecdotal.

There has never EVER been a casual link between testosterone and any type of cancer.

[pat80flh]

Great stuff guys especially DetOaks, thanks for quoting those studies.

Let me start by answering the question,"Why not just have it out?". Well first off, it's like giving in. Second, I was quoted 70% probability of complete cure. But never ejaculate again. Nor father a child. The ureter must be cut and reattached to the bladder. Possibility of diapers forever. Plus I was put on hold while 6 months worth of tests were run on my ribs. In the end," We don't know if you have bone cancer or not. We may as well take your prostate, just so we'll be doing something." During the interminable testing and retesting, was when I began to investigate alternative healing. They say prostate cancer is slow growing, what do I have to lose by trying?

Beacause my case was unique, I worked my way up the medical food chain, to larger and larger hospitals and every one made me feel like they were trying to sell me a used car. Glossy brochures with glowing reviews of their new DaVinci arthroscope/robot/joystick machine. Every uroligist has one now, they're only 1.7 million. When I asked my second uroligist how many of these surgeries had he done he stopped and said,"One every Thursday sometime two,and every other Tuesday, since I opened here 11 years ago." And he was in a smaller hospital. Tell you what, I'm a mechanic by trade, and if I buy a transmission fluid exchanger, know what I want to sell to every one I can? A nice fluid exchange. That's how I pay for that machine.

I think my problems stemmed from diet. As a matter of fact, I now believe that the current epidemic of diabetes, prostate/ovarian/breast cancers are a result of the food we eat. I'm not saying that meat is inherently bad , but that modern production of meat has made this food unhealthy. Junk food is designed to leave you hungry and buy more. They took whatever makes cocaine so addictive and put it in Diet Coke. So I'm not eating any meat, poultry,or seafood; trying to purge my body of whatever is stored in my fat. The plan is to starve the cancer out, give it nothing to eat, no sugar or fruit, honey, syrup. No dairy, butter, cheese. Whole grains, fresh vegetables,beans. Actually, there are several doctors out there promoting this diet, (not quite as strict) Dean Ornish is pretty well known. This diet can reverse heart disease. "The China Study", somebody Campbell, is a good book about this.

So I hit it hard at first, quit drinking, diet change, I lost 45 lbs in 60 days, 80 lbs in 6 months. PSA went from 9 down to 5.2. Then life kind of got in the way, quitting drinking spelled doom for my marriage to an alchoholic, less said about that the better. Started procedings, looking for houses, had an epiphany, saw that my old widowed mother was doing poorly, bought a wreck foreclosure cheap, carved out a downstairs bed and bath, moved her in. 6 months later she's got cancer, chemo, just getting over that, broke her hip. About a year into the change I went back to drinking, just a little at first, but while I dealt with this I started to slide, within my dietary limits, but poor choices, too much fat, too many processed foods, crackers, Fritos, coffee. PSA started rising again. And I put on 30 of the 80 pounds I lost.

I'm ready to get after this for real now, I'm off the booze as of the new year. Tightened up the diet. Lost almost 20 pounds since new years. Quit coffee 2 weeks ago. Somethings happening down there, hell I didn't have any symptoms before this started. I think that the reason they never gave you testosterone was because it enlarges the prostate, most men with prostate problems already have an enlarged prostate, when it's enlarged is when you have urinary problems. I figure I've got nothing to lose by trying a little testosterone supplementation, not go crazy, see how it feels, monitor my levels. I don't plan on getting cut any time soon, I'm 3 years in and it's time to shit or go blind.

I don't know why I'm telling you all this. Maybe it will help somebody. All I can say is a healthy body will have a healthy prostate. The human body was designed to kill cancer cells, it just needs to be adjusted right.

I stumbled in here in search of. I didn't find it here , but I found it all right. On the way, just got to get through customs. So we'll see.
Be well............

[THE-DET-OAK]

amen on the food, shits garbage. they give the animals shit food, they lose nutrients so do we. its a ****ing mess. you guys should read the warrior diet, you would be surprised how much you can control estrogen just with the foods you eat.

[lovbyts]

Pat80flh. It sounds like you make the right choice to wait and change your life. Yes it's easy to get back off track but it sounds like you know what you need to do to get back on. Life gets in the way for all/most of us and you have to just keep on doing what you know you should do. Keep up the good work and it will be easier the 2nd time.

[THE-DET-OAK]

More prostate info. If no one cares feel free to stop me. This was psoted by Scally.




Shifting The Paradigm Of Testosterone And Prostate Cancer: The Saturation Model And The Limits Of Androgen-Dependent Growth

For >65 yr, it has been widely accepted that prostate cancer (PCa) growth is dependent on serum testosterone (T) concentrations, based on experiments by Huggins et al, and that castration caused PCa regression, whereas T administration caused more rapid PCa growth. Yet recent studies have shown little or no relationship between serum T concentrations and PCa, making the long-held belief in a T-dependent model of PCa problematic, if not untenable, and. We present here a simple yet critical refinement to the traditional view of T and PCa, namely, that there is a limit to the ability of T to stimulate PCa growth. The Saturation Model presented below is founded on basic biochemical principles of androgen action within the prostate, and it provides a robust framework for understanding the seemingly contradictory sets of results seen with T manipulation.

Defining the relationship between T and PCa is of considerable importance. Not only is androgen deprivation a mainstay of treatment for advanced PCa, but there is also growing interest in T therapy for hypogonadism. Although T therapy has been shown to improve sexual function, bone density, and body composition, none of these benefits might be worthwhile if T therapy increased the risk of PCa.

The Saturation Model has been introduced previously; in this paper, we present the model in full, together with supporting evidence from human and laboratory studies. In brief, the Saturation Model accounts for the key observation that PCa growth is exquisitely sensitive to variation in serum T concentrations at or below the near-castrate range and is insensitive to T variations above this concentration. This model postulates that physiologic concentrations of T provide an excess of T and its intracellular prostatic metabolite, 5α-dihydrotestosterone (DHT), for optimal prostatic growth requirements. However, reducing T concentration below a critical concentration threshold (the Saturation Point) creates an intracellular milieu in which the availability of androgen becomes the rate-limiting step governing prostate tissue growth. This model is based on evidence that binding of androgen to the androgen receptor (AR) follows a similar saturation curve. We believe this simple model has important ramifications for clinical medicine and basic science research.


Morgentaler A, Traish AM. Shifting the paradigm of testosterone and prostate cancer: the saturation model and the limits of androgen-dependent growth. Eur Urol 2009;55(2):310-20. Shifting the Paradigm of Testosterone and Prostate Cancer: The Saturation Model and the Limits of Androgen-Dependent Growth - European Urology
http://www.europeanurology.com/artic...838(08)01124-X




CONTEXT: The traditional belief that prostate cancer (PCa) growth is dependent on serum testosterone (T) level has been challenged by recent negative studies in noncastrated men.

OBJECTIVE: To provide an improved framework for understanding the relationship of PCa to serum T level that is consistent with current evidence and is based on established biochemical principles of androgen action within the prostate.

EVIDENCE ACQUISITION: A literature search was performed of publications dating from 1941 to 2008 that addressed experimental and clinical effects of androgens on prostate growth. Review of studies investigating the prostatic effects of manipulation of androgen concentrations in human and animal studies, and in PCa cell lines.

EVIDENCE SYNTHESIS: Prostate growth is exquisitely sensitive to variations in androgen concentrations at very low concentrations, but becomes insensitive to changes in androgen concentrations at higher levels. This pattern is consistent with the observation that androgens exert their prostatic effects primarily via binding to the androgen receptor (AR), and that maximal androgen-AR binding is achieved at serum T concentrations well below the physiologic range. A Saturation Model is proposed that accounts for the seemingly contradictory results in human PCa studies. Changes in serum T concentrations below the point of maximal androgen-AR binding will elicit substantial changes in PCa growth, as seen with castration, or with T administration to previously castrated men. In contrast, once maximal androgen-AR binding is reached the presence of additional androgen produces little further effect.

CONCLUSIONS: The evidence clearly indicates that there is a limit to the ability of androgens to stimulate PCa growth. A Saturation Model based on androgen-AR binding provides a satisfactory conceptual framework to account for the dramatic effects seen with castration as well as the minor impact of T administration in noncastrated men.


Tombal B. Editorial comment on: Shifting the paradigm of testosterone and prostate cancer: the saturation model and the limits of androgen-dependent growth. Eur Urol 2009;55(2):321. Editorial Comment on: Shifting the Paradigm of Testosterone and Prostate Cancer: The Saturation Model and the Limits of Androgen-Dependent Growth - European Urology

http://www.europeanurology.com/artic...838(08)01129-9

In Roman mythology, Janus was the god of gates and doors. He was usually depicted with two heads looking in opposite directions and was frequently used to symbolize changes and transitions, such as the progression from one vision to another. This idea perfectly illustrates the saturation model proposed by Morgentaler and Traish in the current issue of European Urology.

Indeed, many of us still regard testosterone through Charles Huggins's eyes and consider it to be a key promoter of prostate cancer progression only because its abrupt suppression induces metastatic prostate cancer to shrink. But is this view enough to sustain our common-sense understanding that testosterone promotes or even causes prostate cancer?

Although urologists still diabolize testosterone, endocrinologists, rheumatologists, and cardiologists attract more and more of our attention to its virtues, especially with regard to metabolic and cardiovascular health.

This paradigm is an interesting one for the physician counseling a man who was successfully treated for localized prostate cancer and who suffers from late-onset hypogonadism. What puts him more at risk: a high-testosterone-promoting cancer or a low-testosterone-promoting cardiovascular disease? Considering the extensive use of hormone therapy in early prostate cancer, it seems that urologists have some difficulties seeing the man around the prostate, although they should be aware of the lack of efficacy in that setting.

Morgentaler and Traish's saturation model provides a nice rational background in which to move away from our unwarranted fear of testosterone in prostate cancer. This article should help urologists to understand that treating middle-age men with localized disease requires getting rid of those fears and developing a holistic view of men's health that encompasses balancing the risks and benefits of adjusting testosterone to normal values.

[THE-DET-OAK]

this is an article talking about the study Morgentaler did after his theory. also posted by Scally. I think the article is dated april 11th of this year.


Revisiting Testosterone Tx in Prostate Ca
Medical News: Revisiting Testosterone Tx in Prostate Ca - in Oncology, Prostate Cancer from MedPage Today

http://www.medpagetoday.com/PrimaryC...tiveCare/26104

Men with low-risk prostate cancer and symptomatic hypogonadism had no evidence of cancer progression during long-term testosterone therapy , results of a small clinical trial showed.

Neither the mean PSA level nor prostate volume changed significantly during testosterone treatment that continued for as long as eight years, according to Abraham Morgentaler, MD, of Beth Israel Deaconess Medical Center in Boston, and colleagues.

Cancer biopsies in two men suggested cancer upgrading, but subsequent biopsy in one patient and radical prostatectomy in the other showed no evidence of progression.

The findings support the saturation hypothesis, which postulates that maximal prostate cancer growth occurs with low-level androgen stimulation, and higher levels elicit little or no additional growth, the researchers wrote in the April issue of the Journal of Urology.

"There has been a scare about testosterone for about 70 years that somehow it is a fuel for the fire in prostate cancer," Morgentaler said in an interview. "It's clear that's not the case.

"This study, although it's small, is the first time anyone has ever bothered to give testosterone and see what's happening in a prostate that has cancer."

Testosterone therapy has several beneficial effects in men with testosterone deficiency, including improvement in fatigue, libido, and sexual function. However, concern about potential stimulatory effects on prostate cancer has limited use of the hormonal therapy, Morgentaler and co-authors noted in the introduction to their findings.

The concern has its origin in observations that androgen deprivation slows prostate cancer progression, as reflected in decreased serum PSA, and that normalization of testosterone in androgen-deprived men raises PSA levels.

Though modest and circumstantial, the evidence has supported a traditional ban on testosterone therapy in men with a history of prostate cancer. When asked to write a review of the issue several years ago, Morgentaler and his co-authors were stunned to find no published clinical data to support a prohibition of testosterone in men with prostate cancer.

Subsequently, Morgentaler found a single article, published in 1941 by future Nobel Prize winner Charles Huggins and colleague Clarence Hodges of the University of Chicago (Cancer Res. 1941; 1: 293-297). The article detailed the effects of various interventions on acid phosphatase levels in men with metastatic prostate cancer, including three men who received testosterone injections.

Huggins and Hodges reported data for two of the three men, one of whom had been surgically castrated before getting testosterone.

"The general idea -- that adding testosterone to an otherwise relatively normal guy with or without prostate cancer will make the cancer grow -- is based on one individual," said Morgentaler.

More recently, results from several small studies have called into question the traditional paradigm of testosterone prohibition in men with prostate cancer. The studies, which collectively involved about 100 men with definitively treated prostate cancer and testosterone deficiency, showed no evidence of biochemical recurrence during treatment with testosterone for as long as 12 years.

With that clinical and scientific background, Morgentaler and co-authors examined the effects of testosterone therapy in 13 men with untreated prostate cancer undergoing active surveillance. The men had a mean age of 59, mean PSA value of 5.5 ng/mL, mean testosterone concentration of 238 ng/mL, and all but one had a biopsy Gleason score of 6 (one patient with Gleason 7).

After a median treatment duration of 2.5 years, the group's testosterone values averaged 664 ng/dL (P<0.001).

Mean PSA level declined to 3.6 ng/mL, which did not differ significantly from baseline. Prostate volume also did not change.

The men had an average of two prostate biopsies during follow-up, and 54% of specimens had no evidence of cancer.

Limitations of the study included its small size, retrospective design, inclusion of some men who had prostate cancer diagnosed after the start of testosterone therapy, and lack of generalizability to those with higher grade or higher volume disease.

On the basis of the results, the longstanding prohibition against testosterone therapy in men with untreated or low-risk prostate cancer merits re-evaluation, the authors wrote in conclusion.

Use of testosterone therapy by prostate cancer patients should be guided by an individual patient's testosterone level and any associated symptoms, said Morgentaler.

"To be a candidate for testosterone therapy, one needs to have symptoms and a low level of testosterone confirmed by blood testing," he said.

"In terms of giving it to men with a history of prostate cancer, the main impediment at this point is that there still are no large, long-term studies that can give us the bounds of safety data on this."

Before starting testosterone therapy, each of his patients must sign a consent form that spells out the unknown risks associated with the hormonal therapy, Morgentaler added.


Prognosis: Testosterone and Prostate Cancer
http://www.nytimes.com/2011/04/26/he...er=rss&emc=rss

By NICHOLAS BAKALAR

Doctors have long held that men with prostate cancer should not be given testosterone because the hormone might fuel tumor growth. But a small study adds to evidence that the fear may be overblown, at least in patients without evidence of recurrent or metastatic disease.

Researchers studied 13 men with scores of 6 or 7 on the 10-point Gleason scale, indicating mildly to moderately aggressive prostate cancer. They all initially chose watchful waiting rather than treatment for their cancers. All the men had low testosterone .

The men received testosterone therapy for an average of two and a half years, and had periodic prostate biopsies. None of their cancers progressed or spread to other organs. One subject whose score had increased to 7 from 6 had his prostate removed, but the final pathological exam found no aggressive disease.

The authors acknowledge that the study, published in the April issue The Journal of Urology, was small and retrospective. Still, it is the first to use biopsies to monitor the effects of testosterone in men with untreated, localized prostate cancer.

The lead author, Dr. Abraham Morgentaler, an associate clinical professor of surgery at Harvard, said that the findings of this and other recent studies suggest that the risks of testosterone therapy may have been exaggerated



I did find one that has a completely different view if you guys would like to see the other side of the story.

[zaggahamma]

thank you you are making my thread an even greater one...keeping it up current...hope youve made your peace in the aas forums cuz youve added a lot to the hrt forum

[THE-DET-OAK]

thanks bro, but i dont know if everyone likes me yet lol one day at a time i guess.

[Jupiter2]

Ok gang, been some time since I've been able to contribute here... life sometimes throws you curve balls, but I do still find the time to read the forums.

Regarding the matter of prostate cancer I would consider myself high risk since it runs quite strongly in my family. But all my research on the subject seems to provide evidence that Testosterone is not the culprit. As one authority on the subject put it: "How many males between the ages of 12 and 40 develop prostate cancer?" He feels, as do I at this point that higher testosterone levels provide a protective benefit to the body, and that declining levels give way to estrogen dominance which may be the real culprit.

Another school of thought puts DHT as being highly suspect which may be why saw palmetto (DHT blocker) has appeared to be beneficial in some studies. Recently, I've been looking into the possibility the Progesterone supplementation may be the miracle hormone that men are looking for with regard to this issue, and I encourage you folks who are staring prostate cancer in the face to do your own research regarding it.

One of the most interesting things I've ever read about prostate cancer was this: "Virtually every man by the time he is 80 has it, but he is far more likely to die from a cause other than that illness (ex. heart attack). As a matter of fact in many cases it will remain undiagnosed, but in those that are discovered advanced age means the risk of surgery is greater than the potential benefit provided given the general slow progression of the cancer." You can look at that statement any number of ways but in my mind, that is some lackey speaking on behalf of an insurance industry that has no interest in approving a surgery and a number of expensive followup visits for someone who may die of a heart attack (ie., natural causes) next week!

[THE-DET-OAK]

hey jupiter i alos thought about the DHT thing, well they believe that isnt it either, check this out:

and lastly the DHT theory. got all this info from Dr. Scally post's BTW.

“Dihydrotestosterone (DHT) treatment for 24 months does not affect prostate growth, but causes a decrease in spinal, but not hip, bone mineral density (BMD)," Australian researchers found after evaluating 114 men for two years. "Every six months, blood samples and questionnaires were collected, prostate volume was measured with ultrasonography, and BMD and body composition were measured with dual-energy x-ray absorptiometry," according to the paper in the Annals of Internal Medicine. "Compared with placebo, DHT reduced lumbar spine BMD (1.4%; 95% CI, 0.6% - 2.3%; P < .001) at 24 months but not hip BMD (P > .2) and increased serum aminoterminal propeptide of type I procollagen in the second year of the study."


Dihydrotestosterone May Not Affect Prostate Growth But May Reduce BMD
http://www.medscape.com/viewarticle/732585

November 16, 2010 — Dihydrotestosterone (DHT) treatment for 24 months does not affect prostate growth but causes a decrease in spinal, but not hip, bone mineral density (BMD), according to the results of a randomized, placebo-controlled, parallel-group trial reported in the November 16 issue of the Annals of Internal Medicine.

"Benign prostatic hypertrophy increases with age and can result in substantially decreased quality of life for older men," write Amanda Idan, BSc, MHSc, from Concord Hospital, ANZAC Research Institute, University of Sydney, Sydney, Australia, and colleagues. "Surgery is often required to control symptoms. It has been hypothesized that long-term administration of a nonamplifiable pure androgen might decrease prostate growth, thereby decreasing or delaying the need for surgical intervention."

At an ambulatory care research center, 114 healthy men older than 50 years without known prostate disease were randomly assigned to receive transdermal DHT (70 mg) or placebo gel daily for 2 years. Every 6 months, blood samples and questionnaires were collected, prostate volume was measured with ultrasonography, and BMD and body composition were measured with dual-energy x-ray absorptiometry. Data were analyzed by mixed-model analysis for repeated measures.

With time on study, there was an increase during 24 months in total prostate volume (29%; 95% confidence interval [CI], 23% - 34%), central prostate volume (75%; 95% CI, 64% - 86%; P < .01), and serum prostate–specific antigen level (PSA; 15%; 95% CI, 6% - 24%). However, DHT had no effect on these changes (P > .2).

Compared with placebo, DHT reduced lumbar spine BMD (1.4%; 95% CI, 0.6% - 2.3%; P < .001) at 24 months but not hip BMD (P > .2) and increased serum aminoterminal propeptide of type I procollagen in the second year of the study. In the DHT group, levels of serum DHT and its metabolites were increased, whereas serum testosterone , estradiol, luteinizing hormone, and follicle-stimulating hormone levels were suppressed. DHT increased hemoglobin levels (7%; 95% CI, 5% - 9%), serum creatinine levels (9%; 95% CI, 5% - 11%), and lean mass (2.4%; 95% CI, 1.6% - 3.1%) but reduced fat mass (5.2%; 95% CI, 2.6% - 7.7%; P < .001 for all).

DHT was not associated with any serious adverse effects but did cause some protocol-specific discontinuations. These were asymptomatic increased hematocrit levels in 8 patients, which resolved after treatment was stopped, and increased PSA levels in 3 patients, none of whom had prostate cancer.

"Negative findings on prostate growth cannot exclude adverse effects on the natural history of prostate cancer," the study authors write. "Dihydrotestosterone treatment for 24 months has no beneficial or adverse effect on prostate growth but causes a decrease in spinal but not hip BMD. These findings have important implications for the wider use of nonsteroidal pure androgens in older men."

In an accompanying editorial, Ronald S. Swerdloff, MD, from Harbor–University of California, Los Angeles, and Christina Wang, MD, from David Geffen School of Medicine at the University of California, Los Angeles, note that this study was not adequately powered to definitively answer the question of long-term safety of testosterone use.

"These data do show that a 10-fold increase in serum DHT levels had no significant effects on prostate size, serum DHT, and International Prostate Symptom Score, suggesting that the modest increases of serum DHT seen after testosterone treatment may not have a clinically significant effect on prostate health," Drs. Swerdloff and Wang write. "Idan and colleagues argue that their findings provide insight about the potential efficacy of future synthetic androgen receptor modulators that will likely share (with DHT) the anabolic effects on muscle and fat, as well as the sparing effects on the prostate. However, we caution that each synthetic androgen-receptor modulator could have a different target organ profile. We conclude that DHT acts as a hormone in tissues without high concentrations of 5α-reductase enzymes but mainly in an autocrine–paracrine manner in tissues like the prostate, in which 5α-reductase is abundant."

BHR Pharma supported this study. Some of the study authors have disclosed various financial relationships with BHR Pharma, Bayer Schering, Ascend/Besins, and/or Radius and Clarus Therapeutics. Drs. Swerdloff and Wang have disclosed no relevant financial relationships.



Idan A, Griffiths KA, Harwood DT, et al. Long-Term Effects of Dihydrotestosterone Treatment on Prostate Growth in Healthy, Middle-Aged Men Without Prostate Disease. Annals of Internal Medicine 2010;153(10):621-32. Long-Term Effects of Dihydrotestosterone Treatment on Prostate Growth in Healthy, Middle-Aged Men Without Prostate Disease — Ann Intern Med

Background: Benign prostatic hypertrophy increases with age and can result in substantially decreased quality of life for older men. Surgery is often required to control symptoms. It has been hypothesized that long-term administration of a nonamplifiable pure androgen might decrease prostate growth, thereby decreasing or delaying the need for surgical intervention.

Objective: To test the hypothesis that dihydrotestosterone (DHT), a nonamplifiable and nonaromatizable pure androgen, reduces late-life prostate growth in middle-aged men.

Design: Randomized, placebo-controlled, parallel-group trial. (Australian New Zealand Clinical Trials Registry number: ACTRN12605000358640)

Setting: Ambulatory care research center.

Participants: Healthy men (n = 114) older than 50 years without known prostate disease.

Intervention: Transdermal DHT (70 mg) or placebo gel daily for 2 years.

Measurements: Prostate volume was measured by ultrasonography; bone mineral density (BMD) and body composition were measured by dual-energy x-ray absorptiometry; and blood samples and questionnaires were collected every 6 months, with data analyzed by mixed-model analysis for repeated measures.

Results: Over 24 months, there was an increase in total (29% [95% CI, 23% to 34%]) and central (75% [CI, 64% to 86%]; P < 0.01) prostate volume and serum prostate-specific antigen level (15% [CI, 6% to 24%]) with time on study, but DHT had no effect (P > 0.2). Dihydrotestosterone treatment decreased spinal BMD (1.4% [CI, 0.6% to 2.3%]; P < 0.001) at 24 months but not hip BMD (P > 0.2) and increased serum aminoterminal propeptide of type I procollagen in the second year of the study compared with placebo. Dihydrotestosterone increased serum DHT levels and its metabolites (5α-androstane-3α,17β-diol and 5α-androstane-3β,17β-diol) and suppressed serum testosterone, estradiol, luteinizing hormone, and follicle-stimulating hormone levels. Dihydrotestosterone increased hemoglobin levels (7% [CI, 5% to 9%]), serum creatinine levels (9% [CI, 5% to 11%]), and lean mass (2.4% [CI, 1.6% to 3.1%) but decreased fat mass (5.2% [CI, 2.6% to 7.7%]) (P <0.001 for all). Protocol-specific discontinuations due to DHT were asymptomatic increased hematocrit (n = 8), which resolved after stopping treatment, and increased prostate-specific antigen levels (n = 3; none with prostate cancer) in the DHT group. No serious adverse effects due to DHT occurred.

Limitation: Negative findings on prostate growth cannot exclude adverse effects on the natural history of prostate cancer.

Conclusion: Dihydrotestosterone treatment for 24 months has no beneficial or adverse effect on prostate growth but causes a decrease in spinal but not hip BMD. These findings have important implications for the wider use of nonsteroidal pure androgens in older men.

Primary Funding Source: BHR Pharma.

[Jupiter2]

Det, thanks for the reply and the inclusion of strong supporting evidence. Definitely good news on the one hand, not so good on the other eh, lol. I guess most of the indications then are that estrogen is the real culprit which makes sense since declining testosterone and rising estrogen levels begin in mid-life, which is when coincidentally the risk of prostate cancer becomes an issue.

Curious to know what you come up with regarding progesterone and this subject since your research skills appear to be exemplary.

[THE-DET-OAK]

lol-thanks. I will def look into it, maybe you could expand a lil on how you think it would beneifit?? hopefully this will point me in the right direction.

[Jupiter2]

This just one of the many articles I've read concerning the issue. Grabbed it quickly as I'm on my way to work but it should provide you with some reference-able data. Dr. John Lee was the recognized authority. My understanding is that since his demise the research he conducted is being continued by other established medical authorities.

PROGESTERONE FOR PROSTATE HEALTH
By James South, M.A.

For middle-aged and older men, especially those over age 50, prostate problems are an unpleasant fact of life. It is estimated that half of men in the 50-plus age group suffer from benign prostatic hyperplasia (BPH), an abnormal enlargement of the prostate gland.1

This swelling of the prostate usually manifests as urinary problems: urinary frequency, urinary hesitation, reduced urinary flow, etc. The prostate gland is also the most common site for cancer to develop, with over 300,000 new cases in the U.S. in 1996.1 The medical establishment places the blame for these prostate problems on the male hormones testosterone (T) and dihydrotestosterone (DHT), yet this belief generates an obvious paradox. The highest levels of T/DHT occur in young men, and T/DHT levels drop with aging. Yet prostate problems are almost non-existent in young men, while they increase with age, affecting 90 percent of all men by age 85, when T/DHT levels are extremely low.2

The Estrogen Connection
An important determinant of male hormonal health is the testosterone/estrogen balance (T/E). Healthy male physiology depends on a high T:E ratio. Although testosterone is the “male hormone,” men naturally produce small amounts of estrogen from testosterone.3 With aging, the T:E ratio drops, often dramatically. An enzyme called “aromatase,” especially prevalent in fat cells, converts testosterone to estrogen.4 Since most men lose muscle and gain fat as they age, aromatase activity increases, reducing testosterone even as it increases estrogen. Many scientists have commented on the importance of estrogen and the T:E ratio in promoting prostate problems. M. Krieg and colleagues note “…numerous experiments indicate that estrogens might also be involved in the abnormal growth of the human prostate.”5 “The data in this communication show a clear-cut, direct biochemical effect of estrogens on the human prostate and provide a cellular mechanism by which estrogens may affect prostatic physiology [negatively].”2

In a review on benign prostatic hyperplasia (BPH) and estrogen, W. Farnsworth reports that “…the induction of BPH is shown to be determined by the androgen [T+DHT]/estrogen ratio….”6 S. Boehm and coworkers conclude that “… estrogen suppression may be considered an efficient pharmacotherapeutic strategy in the medical treatment of uncomplicated benign prostatic hyperplasia.”7

Progesterone to the Rescue
Most people think of progesterone as a “female hormone.” Yet men normally produce progesterone as well, in both their adrenal and testicular tissue.8 Unfortunately, male progesterone levels drop with aging, just as do male testosterone levels .4 Severe, prolonged stress also depletes progesterone, since the “state-of-siege” stress hormone cortisol is made from progesterone, as are testosterone, estrogen, aldosterone and other steroid hormones.8

And as researcher Ray Peat emphasizes, one of the most important roles for progesterone is to oppose the many toxic effects of excess estrogen.9 Progesterone expert Dr. John Lee noted multiple roles for progesterone in antagonizing estrogen and promoting prostate health.

Progesterone inhibits the conversion of testosterone to DHT.4 DHT is a weaker androgen than testosterone, and thus lowers the androgen/estrogen ratio in favor of estrogen. In addition, DHT is a far more potent stimulant of prostate cell growth than testosterone.4 Both testosterone and progesterone stimulate the activity of a protective gene called “p53.”4 The products of this gene activation are anti-cancer, and promote healthy apoptosis.10 Apoptosis is a “programmed cell suicide” that plays a key role in preventing cellular overgrowth (e.g., BPH) and cancer.10 Estrogen, on the other hand, activates a gene called “bcl2.”4 Bcl2 products inhibit healthy apoptosis.10

Progesterone may even help with prostate cancer. V. Petrow et al reported results of their study with rats and prostate cancer in 1984. “Growth of the Dunning R 3327-H prostatic adenocarcinoma, implanted in the rat, is inhibited by 6-methylene progesterone. This compound is a potent inhibitor of rat prostatic 5-alpha-reductase [as is progesterone; 5-alpha-reductase is the enzyme that converts testosterone to DHT] and in-vivo produced marked involution [shrinkage] of the prostate. Thus, this tumor requires dihydrotestosterone and not testosterone for growth.”11 Andrews and colleagues also
note: “Another steroid hormone that interacts with the androgen receptor in LNCaP [prostate cancer] cells (progesterone) also promotes apoptosis of these cells.”12

Progesterone for Men
Dr. John Lee has recommended a dose of approximately 4 to 6 mg once or twice daily for men in their late forties or older.4,13 Approximately 6 mg can be achieved with one-eighth level teaspoon of a cream containing 900 to 1,000 mg progesterone per 2 ounces. The cream should be rubbed onto thin skin areas such as inner forearm, chest, neck or scrotum morning and/or evening. Do not exceed the recommended dose.

Progesterone therapy is especially relevant for obese men; those with a family history of prostate cancer; those with proven low androgen/low progesterone/high estrogen levels. Progesterone may reduce fertility in men,14 and it is to be avoided by men with nonalcoholic liver cirrhosis.15

References
1. Wright, J. and Lenard, L. Maximize Your Vitality and Potency, Petaluma, CA: SMART Publications™, 1999: 158.
2. Nakhla, A. et al. “Estradiol causes the rapid accumulation of cAMP in human prostate.” Proc Natl Acad Sci USA 1994, 91: 5402-05.
3. Kutsky, R. Handbook of Vitamins, Minerals and Hormones, NYC: Van Nostrand Reinhold, 1981: 418-19.
4. Lee, J. “Prostate disease and hormones.” The John R. Lee, M.D. Medical Letter Feb. 2002.
5. Krieg, M. et al. “Effect of aging on endogenous level of 5 a-dihydrotestosterone, testosterone, estradiol, and estrone in epithelium and stroma of normal and hyperplastic human prostate.” J Clin Endocrinol Metab 1993, 77: 375-81.
6. Farnsworth, W. “Estrogen in the etiopathogenesis of BPH.” Prostate, 1999, 41: 263-74.
7. Boehm, S. et al. “Estrogen suppression as a pharmacotherapeutic strategy in the medical treatment of benign prostatic hyperplasia: evidence for its efficacy from studies with mepartricin.” Wien Klin Wochenschr 1998, 110: 817-23.
8. Kutsky, op. cit. 427-28.
9. Peat, R. Progesterone in Orthomolecular Medicine Eugene, OR, 1993: 4-6.
10. Hetts, S. “To die or not to die: an overview of apoptosis and its role in disease.” JAMA 1998, 279: 300-07.
11. Petrow, V. “Endocrine dependence of prostatic cancer upon dihydrotestosterone and not upon testosterone.” J Pharmacol 1984, 36: 352-3.
12. Andrews, P. et al. “Dihydrotestosterone (DHT) modulates the ability of NSAIDs to induce apoptosis of prostate cancer cells.” Cancer Chemother Pharmacol 2002, 49: 179-86.
13. Mercola, J. “Progesterone cream can help prostate cancer.” 1998. www.mercola.com/fcgi/pf/1998/ archive/natural_progesterone2.htm.
14. deLarminat, M. and Blaquier, J. “Effect of in vivo administration of 5 alpha reductase inhibitors on epididymal function.” Acta Physiol Lat Am 1979, 29:1-6.
15. Farthing, M. et al. “Progesterone, prolactin, and gynecomastia in men with liver disease.” Gut 1982, 23: 276-79.

[zaggahamma]

Ok gang, been some time since I've been able to contribute here... life sometimes throws you curve balls, but I do still find the time to read the forums.

Regarding the matter of prostate cancer I would consider myself high risk since it runs quite strongly in my family. But all my research on the subject seems to provide evidence that Testosterone is not the culprit. As one authority on the subject put it: "How many males between the ages of 12 and 40 develop prostate cancer?" He feels, as do I at this point that higher testosterone levels provide a protective benefit to the body, and that declining levels give way to estrogen dominance which may be the real culprit.

Another school of thought puts DHT as being highly suspect which may be why saw palmetto (DHT blocker) has appeared to be beneficial in some studies. Recently, I've been looking into the possibility the Progesterone supplementation may be the miracle hormone that men are looking for with regard to this issue, and I encourage you folks who are staring prostate cancer in the face to do your own research regarding it.

One of the most interesting things I've ever read about prostate cancer was this: "Virtually every man by the time he is 80 has it, but he is far more likely to die from a cause other than that illness (ex. heart attack). As a matter of fact in many cases it will remain undiagnosed, but in those that are discovered advanced age means the risk of surgery is greater than the potential benefit provided given the general slow progression of the cancer." You can look at that statement any number of ways but in my mind, that is some lackey speaking on behalf of an insurance industry that has no interest in approving a surgery and a number of expensive followup visits for someone who may die of a heart attack (ie., natural causes) next week!

that is one of the things i read and never forgot regarding prostate

[THE-DET-OAK]

Study shows 6 cups of coffee a day may reduce your risk of prostate cancer.

http://www.cbn.com/cbnnews/healthsci...state-Cancer-/

having trouble finding current clinical data on progesterone treatment. newest drug I can find is one that directs your immune system to fight the cancer.

[JD250]

Good stuff, if drinking 6 cups of coffee a day reduces risk of prostate cancer by 60%.......shit man....I'm good to go. Of course I'll prolly end up with something else caused by those 6 cups a day.

Sorry for hijacking, been reading along and there is some great info here, thanks guys.

[THE-DET-OAK]

your actually right, there are some negatives to drinking that much coffe