Florida Lifter's HRT Adventures

DrSkeptix · February 21, 2009, 9:48pm

[quote]Wise Guy wrote:
DrSkeptix wrote:

Sorry, WG: The remainder is wrong or unfounded or unnecessary.

Let’s debate then.

I say

His GH’s levels are low. Needs GHRT. Typical of nearly everyone over 40. GH levels begin to plummet by 50% every seven years after the age of 25.

His DHEA levels are low. Needs DHEA replacement. Typical of nearly everyone over 40. DHEA levels begin to plummet every year after the age of 25.

His estradiol levels are high, compared to his TT. I don’t see a FT range, but I would guess its around 200ish (NOT the age adjusted range, but the range for a 25 year old. His range given to him that he failed to list is bogus.)

I say he needs GHRT and DHEART.

Never did I say he needs TRT. He very well could see huge increases in Test with GHRT + DHEART + Substantial losses in body fat.

Dr might not precede my handle, but I’m no typical shlub you see on this forum
[/quote]

Oh…OK…then you must be right.

KSman · February 21, 2009, 10:30pm

PC: You exposure to estrogen is a bigger risk factor than T or DHT. TRT without an AI may increase your risks. TRT with an AI and E2 near 22pg/ml probably reduces PC risks significantly compared to men who are low on T and have relatively high E levels; they are estrogen dominant.

Bio identical T: When test cyp or eth are injected, they are not active hormones until one of a few bio processes strips off the ester group. The result is testosterone, the exact same testosterone molecule that is in the bio-identical trans dermal products. For make TRT, the bio-identical thing is more of a marketing campaign for transdermals. Injected testosterone esters are simply a delivery system for [bio-identical] testosterone.

Injections are also a time release delivery system. Not perfect, but when self injected twice a week the results are very excellent.

DrSkeptix · February 22, 2009, 12:05am

[quote]KSman wrote:
PC: You exposure to estrogen is a bigger risk factor than T or DHT. …[/quote]

This is one of those memes that float around here. Do you have a reference for this?

I doubt that it is proven true in intact men because:
–finasteride reduces pc risk by 25%. That is from a large trial in intact men. Finasteride, f course, is a selective inhibitor of T to DHT conversion, and if anything, leaves E2 stable or raises it very slightly
–Aromatase inhibitors in randomized trials do not lower the progression of BPH. That may be becauase they also raise T and DHT in most intact men.
–Aromatase inhibitors do not have a good track record in the therapy of prostate cancer (except with the co-administration of pharmacologic doses of glucocorticoids.) (This is a contentious issue lately)
–As a general statement, I will accept that in BPH, DHT may increase adenomatous hypertrophy and E may increase stromal hypertrophy. Is that where you are getting this bit about estrogen as a risk factor for PC?

Rapt · February 22, 2009, 1:47am

IGF is usually resulted from Somatomedin-C test which is NOT DIAGNOSTIC for igf it’s simply a screening test to see if you need the real test of which they are a couple. BTW mine was
IGF-I: 83 106-255 ng/mL
lol

sxracer · February 22, 2009, 2:05pm

[quote]Rapt wrote:
IGF is usually resulted from Somatomedin-C test which is NOT DIAGNOSTIC for igf it’s simply a screening test to see if you need the real test of which they are a couple. BTW mine was
IGF-I: 83 106-255 ng/mL
lol[/quote]

Here is a GREAT link for IGF-1 values.

Just tested mine … came back at 385
(I am on HGH therapy)

I feel pretty darn good : )

fedorov · February 22, 2009, 3:00pm

All of my research has not shown any concrete relationship between E2 and prostate cancer, or BPH as well. This is pure theory that is thrown around here as fact.

sxracer · February 22, 2009, 4:40pm

[quote]fedorov wrote:
All of my research has not shown any concrete relationship between E2 and prostate cancer, or BPH as well. This is pure theory that is thrown around here as fact.
[/quote]

You don’t look too hard…

http://www.drmirkin.com/archive/6731.html

http://tsangenterprise.com/news75.htm

That took 2 seconds … there are BETTER articles/studies out there that all say the same thing.

HIGH ESTROGEN IS BAD FOR MALE PROSTATE !

Rapt · February 22, 2009, 5:04pm

[quote]sxracer wrote:
Rapt wrote:
IGF is usually resulted from Somatomedin-C test which is NOT DIAGNOSTIC for igf it’s simply a screening test to see if you need the real test of which they are a couple. BTW mine was
IGF-I: 83 106-255 ng/mL
lol

Here is a GREAT link for IGF-1 values.

Just tested mine … came back at 385
(I am on HGH therapy)

I feel pretty darn good : )[/quote]

Still doesn’t refute the fact the Somatomedin-C was never meant to diagnose but to screen people to see if they needed to be tested for low growth hormone. Alot of this stuff we take would make us feel better even if we didn’t have a problem.

fedorov · February 22, 2009, 5:25pm

Show clinical studies. Show abstracts. Not articles from the fringe element.

Wise_Guy · February 22, 2009, 6:55pm

[quote]DrSkeptix wrote:
Oh…OK…then you must be right.
[/quote]

Glad to see where on the same page here Dr.

Wise_Guy · February 22, 2009, 7:14pm

[quote]fedorov wrote:
Show clinical studies. Show abstracts. Not articles from the fringe element.[/quote]

LOL, proving E2 is responsible for prostate cancer is like proving the Earth rotates around the sun.

Perhaps you will find better company in the Get a Life portion of the forum

"esearchers discovered that when ?estradiol is added to testosterone treatment of rats, prostate cancer incidence is markedly increased and even a short course of estrogen treatment results in a high incidence of prostate cancer.

These scientists hypothesize that metabolites of estrogens can be converted to reactive intermediates that can adduct to DNA and cause generation of reactive oxygen species; thus, estradiol is a weak DNA-damaging carcinogen that causes DNA damage to prostate cell genes.

This kind of damage to DNA regulatory genes is what initiates prostate cancer. "

Bosland MC. Sex steroids and prostate carcinogenesis: integrated, multifactorial working hypothesis. Ann NY Acad Sci. 2006 Nov;1089:168-76.

DrSkeptix · February 22, 2009, 7:17pm

[quote]sxracer wrote:
fedorov wrote:
All of my research has not shown any concrete relationship between E2 and prostate cancer, or BPH as well. This is pure theory that is thrown around here as fact.

You don’t look too hard…

http://www.drmirkin.com/archive/6731.html

http://tsangenterprise.com/news75.htm

That took 2 seconds … there are BETTER articles/studies out there that all say the same thing.

HIGH ESTROGEN IS BAD FOR MALE PROSTATE ![/quote]

Both references are rubbish, including the Lancet article referred in the “drmirkin” site.

DrSkeptix · February 22, 2009, 7:33pm

[quote]Wise Guy wrote:
fedorov wrote:
Show clinical studies. Show abstracts. Not articles from the fringe element.

LOL, proving E2 is responsible for prostate cancer is like proving the Earth rotates around the sun.

Perhaps you will find better company in the Get a Life portion of the forum

"esearchers discovered that when ?estradiol is added to testosterone treatment of rats, prostate cancer incidence is markedly increased and even a short course of estrogen treatment results in a high incidence of prostate cancer.

These scientists hypothesize that metabolites of estrogens can be converted to reactive intermediates that can adduct to DNA and cause generation of reactive oxygen species; thus, estradiol is a weak DNA-damaging carcinogen that causes DNA damage to prostate cell genes.

This kind of damage to DNA regulatory genes is what initiates prostate cancer. "

Bosland MC. Sex steroids and prostate carcinogenesis: integrated, multifactorial working hypothesis. Ann NY Acad Sci. 2006 Nov;1089:168-76.[/quote]

You were able to find a single reference to a rat experiment, with a lengthy hypothesis not born out by the facts.

Note:
“Estradiol added to testosterone”

Now let’s see the improtant part of the abstract, skeptically:
[i]"Animal studies, however, demonstrate that [b] androgens are very strong tumor promotors for prostate carcinogenesis after tumor-initiating events.

Even treatment with low doses of testosterone alone can induce prostate cancer in rodents. [/b]Because testosterone can be converted to estradiol-17beta by the enzyme aromatase, expressed in human and rodent prostate, estrogen may be involved in prostate cancer induction by testosterone. [/b]When estradiol is added to testosterone treatment of rats, prostate cancer incidence is markedly increased and even a short course of estrogen treatment results in a high incidence of prostate cancer.[/b]

The active testosterone metabolite 5alpha-dihydrotestosterone cannot be aromatized to estrogen and hardly induces prostate cancer, supporting a critical role of estrogen in prostate carcinogenesis.

Estrogen receptors are expressed in the prostate and may mediate some or all of the effects of estrogen. However, there is also evidence that in the rodent and human prostate conversion occurs of estrogens to catecholestrogens.

These can be converted to reactive intermediates that can adduct to DNA and cause generation of reactive oxygen species, and thus estradiol can be a weak DNA damaging (genotoxic) carcinogen. In the rat prostate DNA damage can result from estrogen treatment; this occurs prior to cancer development and at exactly the same location. Inflammation may be associated with prostate cancer risk, but no environmental carcinogenic risk factors have been definitively identified.

We postulate that endogenous factors present in every man, sex steroids, are responsible for the high prevalence of prostate cancer in aging men, androgens acting as strong tumor promoters in the presence of a weak, but continuously present genotoxic carcinogen, estradiol-17beta."[/i]

One premise is of interest: estrogen can be an initiator (there is scant epigenetic evidence for this, too, out this month in a Swedish publication.)

The other premise is just wrong, that somehow, DHT cannot be a promotor. Why not? Did the author do a trial to specifically show this? No. All he showed was that estrogen is not necessary nor sufficient for prostate cancer induction in rats, and that the risk may rise with co-introduction of estrogen to testosterone.

Another hypothesis may be straightforward: estrogen initiates more conversion of T to DHT, and that may be an equally plausible explanation for his observation.
That other stuff about genotoxicity is groundless (insofar as this rat study goes.)

That does not in any way prove that in intact men, natural estrogen is a “more important” “cause” of prostate cancer than T or DHT. To the contrary!

And I still have all sorts of science and publication in men that show that reduction of DHT reduces the risk of prostate cancer overall, and of lower-grade prostate cancers speciifically. This rat study doesn’t change that paradigm.

My statements still stand.

KSman · February 22, 2009, 8:03pm

[quote]DrSkeptix wrote:
KSman wrote:
PC: You exposure to estrogen is a bigger risk factor than T or DHT. …

This is one of those memes that float around here. Do you have a reference for this?

I doubt that it is proven true in intact men because:
–finasteride reduces pc risk by 25%. That is from a large trial in intact men. Finasteride, f course, is a selective inhibitor of T to DHT conversion, and if anything, leaves E2 stable or raises it very slightly
–Aromatase inhibitors in randomized trials do not lower the progression of BPH. That may be becauase they also raise T and DHT in most intact men.

–Aromatase inhibitors do not have a good track record in the therapy of prostate cancer (except with the co-administration of pharmacologic doses of glucocorticoids.) (This is a contentious issue lately)

–As a general statement, I will accept that in BPH, DHT may increase adenomatous hypertrophy and E may increase stromal hypertrophy. Is that where you are getting this bit about estrogen as a risk factor for PC?

[/quote]

There is a lot of material. These just popped up in google and not meant to really make the case:
http://ajp.amjpathol.org/cgi/content/abstract/155/2/641

http://endo.endojournals.org/cgi/content/abstract/136/5/2309

I often see things like this: "Contrary to common perception, testosterone does not cause prostate cancer. Young men have high levels of testosterone and old men low levels. If testosterone were the cause of prostate cancer, young men would be dying of prostate cancer. Studies had shown that men with the highest level of testosterone have the least prostate enlargement.

Conversely, men with the highest level of estrogen have enlarged prostates. Declining testosterone from aging, together with increasing level of estrogen, is the most likely reason for prostate enlargement and cancer in men.

The prostate is embryologically the same as the uterus in the female. Research Studies (Listed at the end of this newsletter) have shown that when prostate cells are exposed to estrogen, the cells proliferate and become cancerous. When progesterone or testosterone was added, cancer cell dies.

During the aging process, progesterone level falls in men, especially after age 60. Progesterone is the chief inhibitor of an enzyme called 5-alpha reductase that is responsible for converting testosterone to dihydrotestosterone (DHT), a much more potent derivative that is linked to prostate cancer.

When the level of progesterone falls in men, the amount of conversion from testosterone to DHT increases. Unfortunately, DHT is not as powerful an inhibitor of cancer cell compared to testosterone.

When the level of testosterone decreases, the relative level of estradiol in men increases. Estradiol, turns on BCL2 oncogene (Onco means cancer) and increases the risk of prostate cancer if adequate amount of progesterone is not there to counteract its effect by stimulating the P53 cancer protection gene."

Men with estrogen dominance [metabolic disorder or syndrome X] have many problems. One significant issue is higher rates of BPH and cancer then those with more favorable T:E ratios. Just as E is blocks some T at T receptors, T blocks some E at E receptors.

While population wide studies will never happen, much is known about men with ED problems. If we allow ED to be a proxy for adverse T:E ratios - there is the observation that men with ED also have higher rates of prostate problems. Yes, some ED is the result of CAD.

The real issue is causes of BPH.

Another theory is that when T goes low and men are no longer ejaculating, is that seminal fluid becomes rancid and the resulting inflammation spreads to the prostate, which then leads to damaged cells.

DrSkeptix · February 23, 2009, 1:20am

[quote]KSman wrote:
DrSkeptix wrote:
KSman wrote:
PC: You exposure to estrogen is a bigger risk factor than T or DHT. …