TRT vs. Prostate Cancer: New Data That Challenges the Dogma

Rene Caruso
Oct 10
4 min read

Every week I get notes like this:

“I’m a 61-year-old man with BPH. I’m on testosterone therapy and every 5–6 months my PSA jumps to 8–9, so I stop. Two biopsies have been negative. What peptides help BPH and high PSA?”

I see this all the time. Men chasing energy, drive, and vitality with TRT get spooked by PSA blips… hit the brakes… feel lousy again… and repeat. It’s time to update the narrative.

The 2025 Evidence, in Plain English

1) In carefully selected men with localized prostate cancer, TRT hasn’t shown worse cancer outcomes.A 2025 BJU International systematic review of observational studies in men with localized prostate cancer on TRT found no oncologic signal of harm (no increase in recurrence/progression). That’s a big deal because it directly tests the scenario everyone worries about. PubMed

2) TRAVERSE (NEJM 2023) — the largest modern safety trial — found TRT was cardiovascularly non-inferior to placebo and didn’t raise prostate events.More than 5,000 men with hypogonadism and high CV risk: no increase in major adverse cardiac events, and no prostate-safety penalty vs. placebo. PubMed

3) Men on active surveillance who used TRT weren’t more likely to “convert” to treatment or die from prostate cancer.A 2024 population-based analysis in European Urology Oncology showed no higher risk of leaving active surveillance, and no increase in prostate-cancer–specific mortality with TRT. PMC

4) Regulators moved in 2025.After TRAVERSE and post-market BP studies, the FDA required class-wide testosterone label changes: removal of boxed language suggesting increased CV risk, inclusion of TRAVERSE results, and a new blood-pressure warning. This doesn’t “green-light” recreational use — it clarifies risk. U.S. Food and Drug Administration+2Reuters+2

Why the Old Myth Lingers (and Why It’s Wrong)

The 1940s Huggins & Hodges work showed metastatic prostate cancer regresses when androgens are suppressed. That morphed into the simplistic idea that “more T = more cancer.” Modern data and the saturation model tell a different story:Prostate tissue is exquisitely sensitive at low T, but once androgen receptors are saturated, extra testosterone doesn’t keep pushing growth. PubMed+1

Corollary: chronic low T and hormonal volatility may actually correlate with worse biology at diagnosis in some cohorts — several studies link lower testosterone to more aggressive pathology. Association isn’t causation, but it fits the model. PMC+1

“My PSA Bumped — Do I Stop TRT?”

Not necessarily. Small, early PSA rises are common and often plateau as men move from a low-T state to the physiologic mid-range; that alone isn’t a reason to abandon therapy. What matters is pattern and magnitude, and sticking to a monitoring plan. PMC

Monitoring (align with your clinician):

Baseline PSA/DRE → recheck at 3–12 months after starting TRT → then follow age/risk-based screening thereafter. SAEDYN
Urology referral triggers (Endocrine Society): confirmed PSA rise >1.4 ng/mL in the first year, PSA >4.0 ng/mL at any time, or abnormal DRE. OUP Academic

Bottom line: Don’t yo-yo your hormones based on a single lab. Evaluate the trend, rule out prostatitis/BPH flares, and make changes with your urologist.

BPH, PSA, and Practical Tools

First-line symptom relief:

Tadalafil 5 mg once daily is guideline-supported for LUTS/BPH and often improves urinary flow and sexual function. Discuss contraindications and drug interactions with your clinician. American University Alumni Network+1

Other urology options (case-by-case): alpha-blockers; 5-alpha-reductase inhibitors (note they lower PSA ~50%, which complicates interpretation); minimally invasive procedures. (Your urologist will individualize.)

Where Peptides Might Fit (Adjuncts, Not Replacements)

Men ask about “peptides for PSA/BPH” constantly. Here’s the straight take:

KPV, TA-1 (Thymosin-alpha-1), and “bioregulator peptides” (e.g., Prostamax, Vesilute) are experimental for prostate indications. Quality, regulatory status, and clinical evidence vary; most data are preclinical or anecdotal. If used, they should be adjuncts inside a physician-supervised plan, not substitutes for urology care.
Focus first on the basics that move the needle: LUTS meds (e.g., tadalafil), ruling out infection/inflammation, sleep, visceral-fat loss, and keeping testosterone in the physiologic mid-range rather than oscillating.

(If you and your clinician trial peptides, use time-boxed protocols (8–12 weeks), track LUTS scores and PSA, and stop if no objective benefit.)

Is Low T Actually the Bigger Problem?

Living at chronically low testosterone leaves you on the steep, hyper-responsive part of the androgen curve. Small fluctuations can act like big signals. Restoring levels into the physiologic middle reaches the “plateau” where the prostate appears less reactive — which helps explain why physiologic TRT doesn’t show higher incidence, recurrence, or progression in contemporary cohorts. PubMed

The trick isn’t “more T forever.” It’s stable, optimized levels + standard monitoring — not yo-yo dosing that spikes and crashes.

Final Thoughts

For decades, men were told testosterone is “fuel” for prostate cancer. The modern picture is more nuanced and far more reassuring:

TRT didn’t worsen cancer outcomes in men with localized disease in observational cohorts. PubMed
TRAVERSE found no CV or prostate-safety penalty vs. placebo in hypogonadal men. PubMed
Active-surveillance men on TRT did not convert to treatment faster nor see worse cancer-specific survival. PMC
FDA labels were updated in 2025: no boxed warning for increased CV events; do watch blood pressure. U.S. Food and Drug Administration

So don’t fear physiologic testosterone — fear unmanaged symptoms, yo-yo hormones, and skipping real monitoring. With stable TRT, smart urology care, and lifestyle support, most men can protect prostate health and feel like themselves again.

René Caruso

METABOLIC RESTORATION + NUTRITION SPECIALIST + ANTI-AGING & LONGEVITY COACH