Eine neue Perspektive: Testosteron und Prostatakrebs verstehen

Zuletzt aktualisiert: August 16, 2026

• WordPress
• LinkedIn
• E-Mail

For decades the medical community operated under a single, frightening assumption: that testosterone is fuel for the fire when it comes to prostate cancer. If you were a man with a history of prostate cancer, testosterone therapy was strictly off the table. That absolute position has not held up, and the reasoning behind the change is worth understanding — along with the parts that are still genuinely uncertain.

During my time working with Professor Mohit Khera at Baylor College of Medicine, I had the opportunity to discuss his research on the saturation model. It offers a coherent explanation for why the old fear may have been misplaced. It is a model rather than a proven law, and this article tries to be honest about the difference.

The Old Guard: The Androgen Hypothesis

To understand where we are going, look at where we started. In the 1940s, Huggins and Hodges observed that depriving men of androgens improved the condition of those with metastatic prostate cancer, while administering testosterone appeared to cause rapid progression.

From these observations the androgen hypothesis was born: higher testosterone promotes prostate cancer, lower testosterone protects against it. For generations, medical students were taught that giving testosterone to a man with prostate cancer was like pouring petrol on a fire. That teaching created a culture of caution that persists — an international survey found prostate cancer risk remains the main concern for physicians considering testosterone therapy.

The Shift: The Saturation Model

The saturation model, developed by Dr. Abraham Morgentaler and studied by Dr. Khera among others, offers a more nuanced explanation of how the prostate interacts with hormones.

The core idea is simple: the prostate has a finite capacity to use testosterone. Think of a sponge. Once it is completely soaked, adding more water does not make it wetter. Similarly, the androgen receptors in the prostate appear to become saturated at relatively low levels of serum testosterone.

Key Mechanics of Saturation

• Threshold effect: prostate tissue is highly sensitive to changes in testosterone at very low concentrations.
• The saturation point: the receptors appear to be largely bound at levels in the region of 250 ng/dL (about 8 nmol/L). That figure is an estimate derived from a limited dataset rather than a precise physiological constant, and it should be read as approximate.
• Relative indifference above the threshold: beyond that point the prostate appears largely indifferent to further increases. This fits the observation that healthy men given high doses of testosterone do not show corresponding rises in PSA or prostate volume.

The model reconciles two observations that otherwise sit awkwardly together: prostate cancer clearly responds to testosterone at near-zero levels, which is why hormone deprivation therapy works, yet it does not appear to grow faster simply because a man has naturally high testosterone.

What the Evidence Does and Does Not Show

If the old hypothesis were straightforwardly true, men with high testosterone should get more cancer and men with low testosterone less. The data do not show that:

1. High testosterone is not an established risk. A large body of longitudinal work has found no relationship between naturally high serum testosterone and the risk of developing prostate cancer. This is the strongest part of the case, and it is the part I would defend most confidently.
2. Low testosterone is not protective. Several studies associate low testosterone with higher-grade tumours and worse prognosis. Worth reading carefully: this is an association, and part of it may reflect how disease is detected and who gets tested rather than testosterone itself doing the damage.
3. The PSA-to-testosterone ratio has been proposed as a better predictor than PSA alone in men with low testosterone. It is an interesting idea rather than standard practice.

Clinical Implications — and Their Limits

The recognition that testosterone may not feed the tumour above the saturation point opened a door for treating symptomatic men who were previously left without options. Men with testosterone deficiency suffer fatigue, low mood, bone density loss and sexual dysfunction, and for prostate cancer survivors the blanket refusal of treatment was a real cost to quality of life.

Testosterone Therapy After Treatment

Several small studies have followed men given testosterone therapy after radical prostatectomy or radiation. In one of the larger series, men who received testosterone after surgery had a lower rate of biochemical recurrence (4%) than a comparison group (16%). Post-radiation series have been similarly reassuring.

That 4%-versus-16% comparison needs reading with care, because it is the number most likely to be quoted back at me. These were not randomised trials. The men offered testosterone were selected — typically those with stable, undetectable PSA and lower-risk disease — and comparing them with men who were not offered it compares two different groups. The honest reading is that these series found no signal of harm, which is genuinely reassuring. They do not show that testosterone reduces recurrence, and nobody should be started on it for that reason.

Active Surveillance: The Most Provocative Area, and the Weakest Evidence

The most provocative research involves men on active surveillance — those with known, untreated, low-grade prostate cancer. In a study led by Dr. Morgentaler and colleagues, 13 men on active surveillance received testosterone therapy for an average of 2.5 years, with no definite cancer progression, and a proportion of follow-up biopsies showing no cancer.

Two things about that result deserve to be said plainly. Thirteen men, with no control group, is hypothesis-generating rather than practice-changing. And a repeat biopsy that finds no cancer in a man known to have cancer usually means the needle missed it — prostate biopsies sample a small fraction of the gland — rather than that the cancer has gone. Reporting that as cancer disappearing would be a misreading.

Testosterone therapy during active surveillance is not standard care. It remains an area of research, and a man in that situation should be having the conversation with the team managing his cancer, not acting on an article. The clinical use described below applies to men whose cancer has been treated.

Safety and Cautionary Criteria

The medical community remains appropriately cautious, and rightly so: we still lack large, long-term randomised trials. The criteria below are what responsible practice looks like in the meantime.

Criterion	Requirement
Diagnosis	Clinical symptoms must match a confirmed diagnosis of testosterone deficiency — not a borderline number alone.
Consent	The patient understands that long-term safety data are limited and that this is a judgement made under uncertainty.
PSA stability	Undetectable or stable PSA before starting.
Shared decision	Made together with the oncology or radiotherapy team that treated the cancer, not by a urologist alone.
Monitoring	Rigorous PSA follow-up, particularly in the first year, is mandatory rather than advisable.
Exclusions	Not for men on androgen deprivation therapy, and not standard practice during active surveillance.

What to Report Between Appointments

A small early rise in PSA after starting therapy is expected as testosterone climbs from a very low level, and does not by itself mean recurrence. What should not wait for a scheduled visit: new bone or back pain, difficulty passing urine or an inability to pass urine at all, visible blood in the urine, or unexplained weight loss. And the general cautions of testosterone therapy apply here as they do to anyone — chest pain, sudden breathlessness, swelling in one calf or a sudden severe headache with weakness are emergencies, as set out in testosterone therapy today.

Conclusion: A Better Question Than a New Certainty

The shift from the androgen hypothesis to the saturation model is one of the more significant changes in modern urology. It moves us away from a one-size-fits-all prohibition toward individual assessment, where the whole patient is treated rather than a laboratory value.

What it does not do is replace an old certainty with a new one. The strongest claim the evidence supports is that the blanket ban was not justified — not that testosterone is proven safe for every man with a cancer history, and certainly not that it treats or prevents anything. For a man who survived prostate cancer and has spent years exhausted, low and without libido, being told his symptoms are the necessary price of survival is no longer the automatic answer. That is a meaningful change, and it is a different thing from a guarantee.

Applying this evidence safely depends on strict candidate selection and disciplined PSA follow-up. See how testosterone therapy with prostate monitoring is structured in practice, and how prostate cancer is assessed and followed.

If you are a prostate cancer survivor who has been told testosterone therapy is out of the question, it may be worth a discussion based on current evidence. Dr. Soarawee Weerasopone consults at Bangkok Hospital Hauptsitz and at Samitivej Sriracha Hospital, Chonburi — 088-022-1445.

Bangkok Hospital Telemedicine is available for patients who cannot attend in person, including international patients — arrange it in advance by email to the Urology department at bhquro@bdms.co.th. It suits reviewing PSA and hormone results and discussing whether the conversation is worth having; the assessment itself needs an in-person visit. Samitivej Sriracha is in-person only.

Frequently Asked Questions About Testosterone and Prostate Cancer

Does testosterone therapy cause prostate cancer?

Current evidence does not support the long-held belief that testosterone causes prostate cancer. A large body of longitudinal research has found no link between naturally high testosterone levels and prostate cancer risk. The saturation model explains why: prostate androgen receptors appear to be largely saturated at relatively low testosterone levels, so additional testosterone does not appear to stimulate further growth. This is the best-supported part of the argument.

Is it safe to take testosterone after prostate cancer surgery?

Several series suggest it can be, in carefully selected men. In one of the larger series, men who received testosterone after radical prostatectomy had a lower rate of biochemical recurrence (4%) than a comparison group (16%) — but these were not randomised trials, and the men offered treatment were selected for stable PSA and lower-risk disease. The honest reading is no signal of harm, not proof of benefit. Treatment requires undetectable or stable PSA, rigorous monitoring, and a decision made together with the team that treated the cancer.

What is the saturation model in simple terms?

Think of the prostate like a sponge. Once it is fully soaked with testosterone, adding more does not make it wetter. The androgen receptors appear to be largely saturated at relatively low testosterone levels, so beyond that point the prostate is largely indifferent to additional testosterone. It is a well-supported explanatory model rather than a proven physical law, and the commonly quoted threshold is an approximation.

Can I take testosterone while on active surveillance?

This is not standard care. The published experience is very small — a series of 13 men without a control group — and although no definite progression was seen, that is hypothesis-generating rather than practice-changing. Repeat biopsies that find no cancer usually reflect the needle missing it rather than the cancer resolving. If you are on active surveillance, this is a conversation to have with the team managing your cancer.

Is low testosterone protective against prostate cancer?

No, and the opposite may be true: several studies associate low testosterone with higher-grade tumours and worse prognosis. That is an association rather than a demonstrated cause, and some of it may reflect how and in whom disease is detected. It is enough to undermine the idea that low testosterone is protective; it is not enough to claim that raising testosterone protects anyone.

What should I report while on testosterone after prostate cancer?

A small early rise in PSA is expected as testosterone climbs from a very low level and does not by itself mean recurrence. New bone or back pain, difficulty or inability to pass urine, visible blood in the urine, or unexplained weight loss should be reported rather than waited on. The general emergencies of testosterone therapy also apply: chest pain, sudden breathlessness, swelling in one calf, or a sudden severe headache with weakness.

Haftungsausschluss: This content is written and reviewed by Dr. Soarawee Weerasopone, a board-certified urologist at Bangkok Hospital Headquarters. It is intended for educational purposes only and does not constitute medical advice. No advice, diagnosis or prescription is given through personal messaging channels or social media. Testosterone therapy after prostate cancer is a decision made with the team that treated the cancer, under monitoring. Always consult a qualified healthcare professional before starting or changing any medical treatment.