This is a preliminary posting--to be edited.

Testosterone for Life:  Recharging Your Vitality, Sex Drive, Muscle Mass & Overall Health! Abraham Morgentaler, M.D. Associate Clinical Prof. Harvard Medical School.  McGraw Hill, 2009.

“Not 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 treatment?”

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 cancer. 

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   

Testosterone 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

Low 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 T 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 are so 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, to 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 citrate 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 them to treat infertility.  Regular T has more reliable benefit. 

Human 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 mention of below medicinal dose.  The only agen 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 much less costly than Androgel, 111.  T & Prostate Cancer:  At the turn of the 20^th 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 noticed 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 with 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 total 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 of the paper was quite damning.  Over a course 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 made 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 of the bad outcomes attributed to testosterone flare occurred a month or more after initiation of treatment.  This meant 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 T 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 leading 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  is likely 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.     

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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 case 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