Why Do So Many Men Opt For Castration To Treat Prostate Cancer?

A PET-scan showing extent of bone metastases in a prostate cancer patient. Each dark area represents an agglomeration of actual prostate cancer cells, i.e. in the spine, pelvis, neck etc. If the spread and growth isn't stopped, bones will fracture, spinal discs compress and pain will be constant and excruciating.


Let's concede that once one joins a cancer support group, say for prostate cancer, there is a high probability he will learn about more horrors and fallout from the disease (and its treatments) than he'd normally care to process. Or accept! That also goes for one's wife, who may have to face the consequences of the disease and its treatments along with the patient.

In the support group to which I belong, I recently came across a post by a 68 -year old who bragged he'd added "15 years or so" to his life by resort to an orchiectomy.  On googling the term I learned it meant none other than surgical castration, i.e. the surgical removal of one's testicles leaving the scrotum full of mainly empty space. (Though we are informed "artificial plastic balls can be inserted if the patient desires to give a more natural sensation.")  When I read the guy's post I thought he had lost it: who would rather live life as a half-man, a eunuch basically, just to gain some extra time from prostate cancer? It turns out a lot of guys!

The relevant University of California At San Francisco  (UCSF) document on hormone therapy has billed  the orchiectomy "as the least expensive form of hormone treatment".  It effectively reduces testosterone - the main fuel for prostate cancer- by removing the testes a prime source. Specifically, the effect is almost immediate with testosterone levels plummeting to what is known as "castrate level" within 12 hours.

 The other alternative is chemical castration, which is used when a patient doesn't want to end up physically de-balled,, given it can have "devastating emotional consequences".  (Well, I will say it has to be enormously difficult walking around with an empty ball sack.)  Anyway, in chemical castration one is given one or more medications including casodex, flutamide and finestride.

The medical castration route takes advantage of the chemical-hormone pathways which begin in the hypothalamus with the secretion of luteinizing hormone-releasing hormone  (LHRH) which in turn stimulates the pituitary gland  to produce luteinizing hormone (LH) as well as follicle -stimulating hormone (FSH) . Then LH signals specialized cells in the testicles to secrete testosterone into the bloodstream. When testosterone reaches the prostrate it is converted into di-hydrotestosterone (DHT) a much more potent form of testosterone, via the action of an enzyme:5 -alpha reductase. The objective of medical castration then is to break this cycle, usually in one of two ways: 1) via  LHRH agonists or 2) LHRH antagonists.

In (1) the medication stops the testicles from making testosterone. This is achieved by inducing a continuous message from the brain to produce testosterone which over-stimulates the testes. They respond by being "overworked" so switch off.

In (2) the medication also induces the testes to stop producing testosterone but not by over stimulation (which can trigger a testosterone "flare"(or spike, including uncomfortable side effects) before the level subsides.

The differences between the assorted chemical castration agents and their effects are discussed here for those interested:

https://www.youtube.com/watch?v=KtIfsvQh2qI

In thirty percent or more of these administrations, one of the primary side effects is a condition called gynecomastia which is briefly outlined via one case in this issue of The New England Journal of Medicine. I warn all males, especially those now taking 'high T' supplements or shots, this may well be your future as I will show below!

http://www.nejm.org/doi/full/10.1056/NEJMicm1209166#t=article


Of course, there are sundry other side effects from either surgical or chemical castration, but this one stands out because....well....it's fucking humiliating to be walking around with a pair of man boobs! Also, that they may have to be treated at regular intervals using drugs like tamoxifen or procedures including liposuction (to extract extra glandular tissue) or partial mastectomy.  If you think I am kidding about this, do some googling on your own, starting with the phrase "gynecomastia and prostate cancer" or "gynecomastia and anti-androgen therapy".

The pain and/or sensitivity can be so pronounced that some medical centers which offer castration - surgical and chemical  - say like UCSF, advise patients to get "prophylactic" treatment before commencing hormone treatment. According to a UCSF document:

"This condition arises from a hormone imbalance resulting for a more dominant role for estrogen in a man's body once treatment begins. It occurs more commonly with anti-androgen drugs than with LHRH (luteinizing hormone-releasing hormone )  medications.

We recommend a single dose of radiation to both breasts at the start of treatment."

The dose of radiation is usually 8 Gy delivered by external beam to each nipple. Most guys complain about a "burned" sensation, and needless to say are in no mood for sex afterwards or anyone getting near their nipples or tweaking them. (Of course, the other general side effect of such therapies is to lower libido until when you're shown a Hustler honey in the nude, you have about as much reaction as to an old rocking chair.)

The latest take on hormone treatment is to recommend postponing it until prostate cancer metastases or "mets" appear in the bones. (See e.g.  Paller and Antonarakis: ' Management of Biochemically Recurrent Prostate Cancer After Local Therapy: Evolving Standards of Care and New Directions' ) 

 The reasons for such delay  take into account emergence of  "comorbidities" or hugely negative treatment outcomes, including not only gynecomastia but also a 50 percent higher risk of developing Type II diabetes because the therapy generates weight gain and with it, insulin resistance or metabolic syndrome. You can learn more from this youtube video about the need to treat especially once bone mets appear::

https://www.youtube.com/watch?v=GFHUCnwox7o

It is important to note from this how prostate cancer cells actually grow and develop inside bones and can lead to "skeletal events" that are catastrophic including fractures, and compression of the spinal cord..  The doctor here is referring to radio-pharmaceutical options but this is usually given in late advanced prostate cancer. For early AD treatment, i.e. after "mets" have first appeared, one would go with hormone therapy, anti-androgen therapy etc. See e.g.   https://www.youtube.com/watch?v=0aN0wrjS7_c

And:

https://www.youtube.com/watch?v=PGeFM9ofliA&list=PLu6CZL-_j8BbnvufjBIkBb2TH8f2QbZY4

Given that one absolutely doesn't want to become crippled or saddled with multiple fractures in his last days, i.e. via spread of bone mets, it looks as though I will have to choose some type of hormone therapy. This is assuming my MRI fusion biopsy shows Gleason scores and undifferentiation associated with the lesions detected in the MRI. This would likely not be commenced until bone mets appear, such as on a pet scan, CT-scan or MRI.

This choice would allow at least 10 years,  maybe longer,  for a relative quality of life until the end phase begins with castration resistance, meaning the testosterone plummets but the PSA continues to increase. In other words, hormone treatment ceases to be effective.  As Dr. Charles Ryan points out in the superb UCSF lecture which follows, the prostate cancer cells are capable of making their own testosterone, and hence driving the prostate specific antigens higher.. This "will to survive" marks the challenge of confronting all types of cancer.

To see the detailed UCSF lecture on treating prostate cancer with androgen deprivation and other hormone treatments go to:

https://www.youtube.com/watch?v=kQ4im2WQ75E


See also this basic discussion of how prostate cancer occurs.

https://www.youtube.com/watch?v=7_5MnsdQeQs

I do hope this blog post will be helpful for other guys facing this disease.

Younger Males Who Jerk off Too Much At Higher Risk of Prostate Cancer: Science Fact or Pseudo-science?

Four years ago the news erupted that those (mainly younger) males with stronger sex drives - inducing them to masturbate more than 1-2x a week are in for trouble later - with prostate cancer. See e.g.

http://www.telegraph.co.uk/health/healthnews/4352270/Sex-drive-linked-to-prostate-cancer-risk.html

Excerpt:

"Those who had regular sexual intercourse and masturbated frequently while they were in their 20s and 30s were most at risk, a new study has found. ........Dr Polyxeni Dimitropoulou, from the University of Cambridge, said: "We were keen to look at the links between sexual activity and younger men as a lot of prostate cancer studies focus on older men as the disease is more prevalent in men over 50.

"Hormones appear to play a key role in prostate cancer and it is very common to treat men with therapy to reduce the hormones thought to stimulate the cancer cells..... a man's sex drive is also regulated by his hormone levels, so this study examined the theory that having a high sex drive affects the risk of prostate cancer."

The researchers also found, get this, that masturbation has a "protective effect" after age 50. They base this on a hypothesis of "reverse causality" so imminent prostate cancer may be inducing the higher frequency then, while it is causing prostate cancer if done in the younger, high 'stud' years.

Can this be believed? First, what was the methodology? According to the paper (and assorted media reports on it) the study looked at the sexual behavior of more than 430 men who had been diagnosed with prostate cancer before age 60 and the behavior of another 409 men who didn't have the disease.  Incredibly,  the researchers concluded that most of the differences in behavior were linked to masturbation and not intercourse.

Why? They don't know and can't say. In basic human biology and sexuality one learns, however, that "an ejaculation is an ejaculation". "Mother Nature" doesn't distinguish between the two, so biologically there's no reason at all the effects should be different. The same hormones, physiological mechanism is the basis for each - which is why Viagra works irrespective of sexual activity. 

The case-controlled study also contradicts an earlier one reported in The Journal of the American Medical Association in 2004 in an article titled “Ejaculation frequency and risk of prostate cancer.” They looked at over 29,000 men who were part of a study of health professional’s health. High ejaculation frequency was reported to be associated with a lower incidence of prostate cancer. Averaged across a lifetime, those men with higher frequency of ejaculation (21 or more per month) had 2/3 the risk of developing prostate cancer as those with a lower frequency of ejaculation (4 to 7 per month).


The earlier study - note- had vastly more subjects included - more than a factor ten beyond the more recent "case study". It also did not distinguish ejaculation, or ages.   Another case-control study from Australia, reported in the British Journal of Urology International in 2003, titled Sexual factors and prostate cancer, found similar risks of prostate cancer incidence-  with those men who reported 5 ejaculations or more per week while in their 20s having 2/3 the risk of those who ejaculated less often.

Meanwhile, according to Dimitropoulou and her Nottingham researchers it’s not masturbation itself that’s increasing prostate cancer risk in young men. More masturbation just means more sex drive — and "more androgens bathing prostate tissues."     Yes, so why doesn't intercourse have the same effect, since androgens will also be released - unless one is impotent?

Dimitropoulou suggests that in older men, masturbation itself may actually be helpful, ridding the prostate gland of fluids that may contain cancer-causing substances. But then she is talking about "frequent masturbation" for older guys being no more than 1-2 times per week. Again, it's all relative.

According to her:

"In mature age, it may be more important that toxins get flushed out of the system. And because the masturbation frequency was not as high in the men’s 50s as it was in their 20s, even low levels of masturbation in the 50s has a protective effect.”

Still, a lot of it comes over as humbug, especially the "reverse causality" claim, e.g. that prostate cancer affected the men’s sexual activity, rather than the other way around.  A cynic or curmudgeon might wonder if her research was funded by the Roman Catholic Church which, of course, frowns on the solo act as "unnatural' like it frowns on artificial contraception - for the same reason.

A more objective take on the work appears in The Nursing Times, e.g.

http://www.nursingtimes.net/whats-new-in-nursing/masturbation-and-prostate-cancer-risks/1976459.article

The Nursing Times piece has the good sense to lay out the "limitations" of the most recent Nottingham study which are cited as (ibid.):

-  Asking men to recall their sexual activity and frequency across different decades of life from their 20s, 30s, 40s and 50s. This is obviously going to involve a lot of estimation inaccuracy.

-  Sexual activity is a highly personal matter. Some men may feel uncomfortable revealing such personal detail and may therefore have either over- or underestimated their activity, depending on their feeling to answering.

-  What constitutes a certain sexual activity to one person may not mean the same thing to another person.


 The NT article also adds other factors "to take into account" in assessing the work:

-  As with all studies of this type, an association between two factors does not necessarily mean that one causes the other. Other factors (confounders) that have not been adjusted for may be affecting the links found to masturbation.

-  The study involved a lot of statistical comparisons. As more tests and combinations are made, the more likely it is that a result that occurs by chance will appear to be significant.

-  There was a link found between cancer risk and frequency of masturbation, but no link was found to frequency of sexual intercourse. When both masturbation and intercourse were combined to give the variable of overall sexual activity, no link was found for any age group.

-  These are a specific group of people with prostate cancer who were all diagnosed with cancer prior to the age of 60. The men in this study are not typical of the vast majority of people with prostate cancer, who are generally diagnosed over the age of 65. Therefore there may be particular unknown characteristics of these people that makes them more predisposed to prostate cancer at a younger age. The results may also not be representative of what would be seen in men who develop prostate cancer later in life.

-  The study involved predominantly white men. Prostate cancer has been linked to ethnicity, with men of African-American origin believed to be at increased risk. Therefore a wider ethnic representation may have given different results.

 The omission (of black males)  is especially onerous and problematical and basically, to me, means the study is about as useful as the one of Michel Gauquelin some decades ago which found increasing UFO sightings to be correlated with Martian oppositions (close approaches to Earth).
Those younger males worried they may be overdoing a good thing, I suggest you chill out and get a bit of a laugh. Without a thorough confirmation, and with at least as many males as the earlier 2003-04 research (29,000) the work of Dimitropoulou  looks like one more incidence of "gimmick science"  - by which I mean research done to raise eyebrows, get publicity (and more funding)  and also because most other ground has already been well -covered.

The Nursing Times conclusion then is the one to pay attention to:

"Men should not be overly concerned by this research. Sexual functioning is a normal part of healthy adult life. The causes of prostate cancer are not known for certain. Increasing age is the most established risk factor and more research is needed."