This is a preliminary posting--to be edited.
for Life: Recharging Your Vitality, Sex Drive, Muscle Mass & Overall
Health! Abraham Morgentaler, M.D. Associate Clinical Prof. Harvard Medical School. McGraw Hill, 2009.
all my colleagues agree with me [treating low T]. But those same colleagues would not have
refrained from giving Shaun thyroid pills if he had thyroid deficiency.
What is the difference? … if treatment has
been shown to improve those symptoms, and if the treatment does not produce
risks that outweigh the benefits of improved symptoms, then why not give the
Morgentaler goes on to explain that for those with low testosterone
who have prostate cancer, such as those who have been chemically castrated, the giving these patients testosterone will accelerate
the cancers growth, assuming there is any left after excision. However, for those a normal level of testosterone, the
prostate is resistant to the uptake of more testosterone, thus the additional serum testosterone has no affect upon prostate
If the parallel with estradiol holds up in which the continuation of hormone replacement therapy
reduces the chance that the breast cancer will develop into (turn out to be) metastatic, at http://healthfully.org/fhr/id23.html
Breast tumors from HRT users were smaller (odds ratio, 0.47;
P=.005), had better histologic differentiation (P=.04), and had a lower
proliferation rate (S-phase fraction, P=.009) than tumors from nonusers.... . A subgroup analysis
showed that the tumor proliferation rates among HRT users were significantly
lower only if HRT had been used at the time of diagnosis (P=.001)... The association of HRT with lower proliferation
rate and smaller tumor size was exclusively caused by ER-positive tumors (P=.0001 and P=.0035 v P > .1, respectively).
and another article found for continued use: Abstract: Controversy exists
regarding the safety of hormone replacement therapy (HRT) after a diagnosis of
breast cancer... . The median
interval between diagnosis of breast cancer and initiation of HRT was 46 months
(range 0-401 months). The median
duration of HRT was 22 months (range 1-357 months). The
risk of death was
lower among the HRT survivors; odds ratio 0.28 (95% confidence interval
0.11-0.71). This analysis does not suggest that HRT after the treatment of
breast cancer is associated with an adverse outcome
has receptors in the brain which have been shown in animal study to control
sexual behavior. In the penis receptors
determine the percentage of muscle and adipose cells. Low T entails
accumulation of fat at the base which effects rigidity. T by control tissue
type governs blood flow to the penis.
The same phenomenon was confirmed in men. 29-33
T is associated with abdominal fat, and treatment with
On measuring T: “…variation in total
T can be as much 50-75
ng/dL” 70….there is general agreement that free T is more important, due to the possibility that high SHBG tends
to make total T appear normal…. For this reason I primarily use the free T test
result… In my practice, free
concentrations below 15 pg/mL are considered consistent with low T… For free T
determine by equilibrium analysis or calculated free T, values below 50 pg/mL are
considered to be low“71. “There
many blood tests to measures testosterone that it is no wonder most physicians
are confused about which ones to order and how to interpret them.
These tests include total testosterone and
free testosterone, which I’ve already mentioned, as well as bioavailable
testosterone, free androgen index, calculated free testosterone, free and
weakly bound testosterone, and percent free testosterone” 61.
“Testosterone is circulated in 3 primarly
forms: (1) attached to hormone-binding
globulin (SHBG) a glycoprotein, (2) attached to albumin, or (3) unattached
(free)” 62. SHGB is not available,
albumin is available as is free T. Only
1-2% of blood borne T is free. Total
testosterone has been the standard test for decades. “If a man has high SHBG levels, this will
tend to make his total T appear normal, even though he may truly have low
levels of bioavailable testosterone. This
is a shame, because free T is the best
test to determine if a man truly has low T”… The free T I recommend is called
the analog free T test (RIA test). 65-6.
Equilibrium dialysis is an
excellent laboratory technique, but it requires a lot of time and human labor…
it is not available to the average patient or his doctor. The Calculated free T is a measurement that
comes from knowing the value for total T, SHBD, and albumin.
To get the results it is necessary to find a
free T calculator on line. …
International society of the study of the Aging Male at issam.ch/freetesto.htm
Free Androgen Index (FAI) is a ration obtained by dividing the concentration of
total T by the concentration of SHBG….It has not shown any great clinical
usefulness. A diagnosis of
low T is
possible and requires clinical judgment if T is between 200 and 400 ng/dL, 71. [I would recommend this number for those 60,
and gradually reduce the hurdle with advancing years as an adjustment for
declining bioactivity of T. [He favors Androgel over compounded T, but
makes no mention of low does, and he thinks the FDA fulfills its inspection
obligation for Androgel, and that the manufacturer is required to go through
the clinical-trial approval process. 104-5, and makes no mention of the Chinese
source for Androgel]. Clomiphene
and anastrozole can stimulate the body to produce more of its own T.
They cause the pituitary to release more
luteinizing hormone, 107. He uses
to treat infertility. Regular T
Chorionic Gonadotropin (HCG) Injections:
requires 3 injections per week.
Stimulates the Leydig cells in the testicles to produce more T, 108. Supplemental therapies: As much as I want to support these
approaches, there is not a single shred of evidence that these treatments offer
any help to men with low T. [No
of below medicinal dose. The only
available over the counter with some plausible claim to affect male hormone
levels is dehydroepiandrosterone (DHEA), a precursor of T… no substantial affect
on T levels, 110. Injections are
less costly than Androgel, 111. T & Prostate Cancer: At the turn of the 20th century,
there were reports that castration was successful in treating some men with
server obstruction from BPH, and Huggins began experiment on the effects of
castration on BPH in dogs. Huggins
that after castration, dogs with these cancerous-appearing areas also
demonstrated shrinkage of their prostates.
Huggins and his coworkers then applied these dog results to humans. He took a group of men who had prostate
cancer that had already spread to their bones and lowered their testosterone
levels, either by removing the testicles or by administering estrogen.
A blood test called acid phosphatase was high
in men with metastatic prostate cancer.
Huggins and his coworkers showed that acid phosphatase dropped substantially
within days of lowering T. Huggins
reported that administration of T injections to men with prostate cancer caused
acid phosphatase to rise. They concluded
that reducing T levels cause prostate cancer to shrink and raising T levels caused
enhanced growth of prostate cancer. From
that point forward (in the 1940s) lowering T by castration or by estrogen
became the standard treatment. For advanced disease and remains a mainstay of
treatment to this day. Until recently,
this prevailing wisdom regarding prostate cancer and T had not been seriously
questioned, 117. A bunch of animal
studies years later with mice supported the role of T in the growth of prostate
cancer. First we fouind that men
low T did not seem to be protected against developing cancer.
Now, at the other extreme, we found that men
at high risk for prostate cancer did not seem to suffer any dramatic “explosion”
of cancer when treated for a year with T therapy. And when I look back at my extensive
experience of treating men with T therapy, many for ten years or longer,
precious few cases of cancer had developed.
For longitudinal studies (10 by 2008), ”not one had shown any direct
relationship between the level of
testosterone in a man’s blood and the subsequent likelihood that he will
develop prostate cancer… the men with the highest T values were at no greater
risk for later developing prostate cnacer than men with the lowest T values…
Our article appeared in the NEJM in 2004” 125-6. “Dr. Huggins had based his “enhanced
growth” conclusion on a single patient, suing a test-acid phosphatase-that has
since been abandoned because it provided such erratic results!128” At 129 he
shows how KOLs write abstracts and conclusions that don’t agree with the body
of the evidence, the devil is in the details.
Article detailing the experience of T administration to men with
metastatic disease from Memorial Sloan-Kettering Cancer Center, published in
1981 by the urologic giant of his day, Willet Whitmore, and his colleague,
Jackson Fowler. The short summary
paper was quite damning. Over a
of eighteen years, fifty-two men with metastatic disease had undergone
treatment with daily T injections… Of these fifty-two men, forty-five had
experie3nced an unfavorable response, most within the first month of treatment…
I discovered something equally shocking in the fine print of this article.
Of the fifty-two men studied, all but four
had already been treated with castration or estrogen treatment to lower testosterone. And of these four previously untreated men,
one had an early unspecified unfavorable response, while
the remaining three men continued to receive daily T injections for 52, 55 and
310 days with apparent negative effects.
In fact, one of these men was reported to have a “favorable response” to
T administration… One had to read the article closely to learn the headline
applied only to men who had been previously not castrated… the authors in fact
clearly made the point that the worrisome effects of T administration did not
appear to occur in their small group of men without prior hormonal treatment.”
129-30 [Note in ordinary lingo, “prior hormonal treatment means” means the
castration either by knife or chemically with DES, the synthetic estrogen
commonly used. The castration treatment
the cancer worse.] . [Note:
“unfavorable response” is presumable continued growth of tumors and/or
spreading of the metastatic cancer; moreover, being unspecified entails different from the specified. The standard of journal articles and research
was often below that required for the top journals. Given the way the press and pharma used the
results, there is good reason to expect more tobacco science—jk.] As I read two
things became apparent. First, many
the bad outcomes attributed to testosterone flare occurred a month or more
after initiation of treatment. This
that those complications occurred not when AAT levels were high, but when T
levels had already dropped for some to castrate levels. Second out of the substantial literature on
LHRH agonists and prostate cancer, I could find only two articles that actually
measured the reported PSA levels during the time of the testosterone flare.
And here was the kicker: both articles showed
absolutely no changes in mean PSA value during the time of the T flare!
Curiously, neither article so much as
mentioned this result. PSA is an
excellent indicator of prostate cancer growth.
Even in men with metastatic disease, there was no evidence I could find
that raising T made prostate cancer grow more than it would have anyway.
Shockingly, the very publications cited so
regularly to demonstrate a dangerous relationship between testosterone and
prostate cancer contained evidence that is not true,” 130-131. [As I repeatedly
observed and stated, much of what is in print is funded by pharma for the
promotion of sales; this is what Dr. Morgentaler is alluding to, tobacco science.]
I too came to the same to the same conclusion that
does not promote prostate cancer but instead reduces risk. In my review HRT
men Testosterone Benefits
I published at http://healthfully.org/rc/id7.html
Prostate Cancer: Low levels
of TTT are associated with both higher
risk and disease progression. “In our study patients with prostate
cancer and low free TTT had more extensive disease, also, also. “This finding suggests
that low serum free TTT may be a marker for
more aggressive disease.” This evidence
calls to question chemical castration
for prostate cancer. The theory that TTT
regulates in later life the growth of the prostate organ is without support. Like
the penis, the window for growth closes
after puberty—neither organ grows with hormonal treatment later in life. Moreover,
TTT is only essential for prostatic
secretions, and not its growth in the mature man. Dr. Abraham Morgentaler, a
researcher, in his Testosterone for Life
reviews at length the articles commonly cited
in support of castration, and he finds the workings of Bad Pharma; namely no patient
benefit. This is consistent with Prof.
Ben Goldacre’s Bad Pharma;
viz. the evidence base is broken and
that positive bias is the norm,
and my analysis. I have uncovered a parallel treatment for
breast cancer with the chemical
castration of women. Two earlier clinical trials--before
pharma went after HRT--show that HRT after breast cancer greatly reduced the risk. Given this finding for estrogen, and the
positive risk reduction from higher TTT cited above, treatment with TTT, testosterone
to benefit those undergoing treatment for prostate cancer, just as it does
for breast cancer. A trial is needed
confirm a parallel with HRT—but pharma certainly won’t fund a scientific study.
TOTAL 12 lines
The consequence of this is that millions of men who
died of prostate cancer were given a treatment which made their cancer more aggressive. Moreover, instead of being limited to the
metastatic cancer, it is now normally applied to all who undergo prostate
cancer treatment. This is another
of the devil being in the details, and pharma following tobacco ethics.
I have uncovered the same pattern de-sexing for
women with breast or gentile cancers.--jk.
Luteinizing Hormone (LH): made in the pituitary
gland regulates the production of T.
Most men with low T will have a normal level of LH