Testosterone seen unrelated to prostate cancer risk

Natural levels of a man’s testosterone do not affect his prostate cancer risk as some had thought, a finding that should spur scientists to rethink their approach to the disease, researchers said on Tuesday.

Nearly two dozen studies have examined a potential link between testosterone and prostate cancer risk but so far results have been inconclusive, said Andrew Roddam, an epidemiologist at the University of Oxford who led the study.

In the Journal of the National Cancer Institute, Roddam and colleagues said they found no such relationship after collecting worldwide data on hormone levels of 3,886 men who eventually developed prostate cancer and 6,438 men who did not.

Prostate cancer, which usually occurs in older men, is the second most common cause of cancer death among men after lung cancer. The prostate is a walnut-sized gland that makes fluid for semen.

“We looked at blood samples of men before they had cancer and men who didn’t develop cancer to see if their hormone levels were different,” Roddam said in a telephone interview.

“When you compare these two groups there is no substantial relationship between hormone levels and their risk of developing the disease.”

Testosterone is the primary “male” hormone that helps maintain muscle mass and strength, fat distribution, bone mass, sperm production, sex drive and potency. Women have testosterone too, but at lower levels.

The hormone’s role in men’s health is controversial, with the relationship between men’s natural testosterone levels and overall health not well understood, researchers say.

The reason scientists had believed it played a role in raising prostate cancer risk was because testosterone makes a tumor grow, and which is why some treatments seek to block the hormone.

A study last year also showed that higher naturally occurring levels of testosterone appeared to protect men from fatal heart attacks or strokes and death from several causes.

The latest findings, however, should prod researchers to shift the focus of their research into new risk factors for the disease, Paul Godley and colleagues at the University of North Carolina at Chapel Hill said in a commentary.

“The study obliges the scientific community to move past a seductive, clinically relevant, and biologically plausible hypothesis and get on with the difficult task of exploring, analyzing, and characterizing modifiable risk factors for prostate cancer,” they wrote.

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