Testosterone and prostate cancer. The story of a great and silent misunderstanding of modern medicine.
This year, it will be more than 80 years since Charles B. Huggins published the groundbreaking results of a study of patients treated with an experimental and, for those times, innovative hormone therapy.
It is impossible to describe the scale and pace of the progress that has been made in this period of time; we have landed on the moon, split the atom and regularly photograph the surface of Mars. What have we not yet achieved and what seems to be beyond the horizon of our possibilities?
Humility and the ability to put people’s health and lives before your own ambitions and dreams.
In this particular case, we can openly say that it was a mistake made a long time ago, the effects of which we are still feeling today, and there is no sign of that changing any time soon.
Testosterone and prostate cancer
If you have been wondering lately what is the reason for the progressive devaluation of the institution of the Noble Prize, this story will help you to broaden the historical outline of the phenomenon, and to understand the scepticism associated with it.
Charles B. Huggins in 1941 published a study that showed that in patients who had their testosterone levels lowered (by surgical or hormonal castration) prostate cancer cells stopped growing, while in patients who received exogenous testosterone, the cancer cells multiplied. The conclusion therefore pointed to testosterone as being responsible for and directly contributing to prostate cancer.
Where does the devil lie?
As usual, it is in the details. Digging into the methodology and documentation of the research itself, a sufficiently trained eye will see that …
The studies involved one and the same person! To be precise, we are talking about a situation where patient X was first given hormone therapy (with tumour regression) and then given external (exogenous) testosterone, which resulted in prostate cancer cells multiplying rapidly again.
An incredibly avant-garde methodology – a modern person would say.
But let us not forget that we are talking here about the wild 1960s. And that is not the end of the story. Charles B. Huggins was awarded the Noble Prize for his breakthrough discovery and since then the perception of testosterone’s role in prostate cancer development has remained virtually unchanged.
How wrong were we?
A 2016 meta-analysis1 of more than 20 studies from the period 1960-2010, single-mindedly concluded that none of the studies analysed showed a direct link between prostate cancer proliferation and testosteorn levels. A parallel and independent study2 showed that even when exogenous testosterone is administered to patients who already have the disease, it has no effect on the course of the disease, i.e. neither accelerates nor slows down the process of cancer cell growth.
Is HTZ (hormone replacement therapy) therefore safe?
This question remains open due to the disparity of research results on this issue. The element that makes it impossible to give a unanimous verdict is, as a standard, the multiplicity of factors responsible for the occurrence of cancer; and in this particular case, it concerns the personal predisposition to prostate cancer, and whether the said HTZ is to be used in a person who has already experienced prostate cancer, or is in a risk group. Seemingly contrary to what is stated above, it would seem that we are defending the position that there is no link between testosterone levels and the development of prostate cancer, however…. All the studies described above refer only to men with the disease, or undergoing treatment – that is, already with any focal cancerous lesions. They do not describe and analyse the cases of men who are ill/”expecting cancer”, because it is roughly impossible to carry out such studies, due to the huge number of men who would have to form a control group.
What causes prostate cancer?
This is a question we dare not answer unanimously, because the multitude of theories and the lack of solid foundations for each of them make them mere premises and not real indications; however objective the truth. However, let us post a short list of things whose elements seem to be universally consistent indicators of being in a risk group:
The risk of prostate cancer increases with age. The median age of diagnosis is 66, and a higher percentage of all prostate cancers detected are between the ages of 65-74. An alarming 28% are men over the age of 50, so we suggest not treating the age of 66 as any sort of sad point in the calendar, a forced examination. We suggest you don’t put your own luck to the test and go for a prostate examination even before you turn 40!
Family history of diseases
Prostate cancer appears to be strongly inoculated in the genes, i.e. the likelihood of developing the disease is proportional to the history of its occurrence in previous generations. According to various sources, an increased predisposition to the disease occurs not only in men with a history of prostate cancer itself, but with a history of cancer in general. Every case of cancer in the family should therefore be an additional alarming factor to be tested for it!
A high-carbohydrate, high-fat, highly-processed diet, or what we might collectively call a “diet of tragedy” may be a contributing factor in prostate cancer.
More specifically, a radically sedentary lifestyle, i.e. uninterrupted sedentary work for many hours combined with an acute aversion to any physical activity (other than sitting) is also a factor in the development of prostate cancer. We wish to point out here that such a lifestyle is likely to be detrimental to every single working organ, and therefore to the body in general. Developing a love of physical activity and your own health are two things we highly recommend and stipulate that it is really worth it!
What this article is and is not about
The purpose behind the above article was to attempt to knock testosteorn off the pillory on which it has been perched for so many years and still receives undue blows and insults. Leaving aside the discussion about whether testosterone is responsible for all the ills of the world, we would like to say that it is not – or not to the extent – responsible for the occurrence of prostate cancer, as we have unanimously and conveniently come to believe that it is.
This does not mean – and this part of the speech is addressed to some readers who appreciate elevated levels of testosterone – that long-term use and maintenance of its concentration x times above the norm will not result in premature or excessive growth of prostate cancer cells – this we do not know, because such studies simply do not conduct (they are incompatible with the widely understood ethics of human research); However, all practical reports indicate that testosterone in high doses administered for a sufficiently long time can initiate such changes, and certainly can cause overgrowth of the gland itself. The best evidence seems to be the widespread catheterisation of the Russian Olympic weightlifting team – a phenomena dating back to the 1960s-70s, when the only available form of testosterone was “free testosterone” – that is a single, free molecule without an attached ester. This most aggressive form of testosterone meant that 20-something athletes had to be catheterised due to prostate hypertrophy so severe that they were unable to urinate on their own.
Let’s research, educate ourselves and confront knowledge
Always and everywhere. For yourself and for posterity.