It evolves from love making with women who are in menopause, Dr. Albert Stuart Reece posits.
He contends that enlarged prostate, or benign prostatic hyperplasia (BPH), is a precancerous state caused by menopause-related changes in the bacterial mix in the female genital tract.
Reece is a clinical associate professor in the School of Psychiatry and Clinical Neurosciences at the University of Western Australia. The article he did on this subject is titled “Dying for love: Perimenopausal degeneration of vaginal microbiome drives the chronic inflammation-malignant transformation of benign prostatic hyperplasia to prostatic adenocarcinoma.” It was published in the journal Medical Hypotheses.
The article offers a string of circumstantial evidence linking BPH to menopause. The first slice is from the control arm of an American prostate cancer prevention trial. The study linked inflammation to prostate cancer development, and severe inflammation to a severe form of the cancer. It maintained that both inflammation and BPH are not normal health developments, but instead constitute a precancerous stage of prostate cancer.
Reece then argues that it is extraordinary that an enlarged prostate does not occur until the fifth decade of a man’s life, and that virtually no man is spared from the condition.
“It is also extraordinary that the condition goes from being almost unknown in the 50s to having a median age of onset at 66 years” — just 16 years later, Reece wrote. He was referring to the rapid increase in BPH rates in that time frame.
These facts indicate that chronic infections or other sources of inflammation — such as prostatic-duct or urinary-canal blockages — are behind the surge in BPH during those 16 years, he contends.
This idea is supported by studies that have found links between infections or inflammation and BPH.
From there, Reece makes what some will call an unwarranted leap in his argument by suggesting that menopause-related changes in female genital flora are what cause the infections.
He underscored that what he is offering is a theory, but he suggested ways of testing it. Studies that followed couples through the woman’s transition to menopause would be at the top of his list.
They would need to sample the genital environment, including prostate tissue and semen, for bacteria, he said. It would be particularly valuable to study couples with age differences, he said. This would allow researchers to make a connection between age and genital bacterial mix.
Reece’s theory about the connection between menopause and prostate cancer is sure to generate fireworks, but he opens himself to further criticism by proposing ways to prevent menopausal genital flora from causing enlarged prostate.
One suggestion is female genital probiotics. Another is using antiseptic douches to prevent the spread of infection. Critics are likely to pounce on that suggestion by saying that it indicates Reece is unfamiliar with a host of research that links vaginal douching to higher rates of infections and inflammatory conditions.
He is likely to be accused of compounding the error by going on to say that douching may harm male flora, so the practice could be a “double-edged sword.”
The risk to men could be reduced, he suggested, by using an antiseptic to clean the female genitalia, then washing it out with a salt solution.
Most studies link development of BPH to male health and lifestyle factors, including metabolic syndrome, obesity, cardiovascular disease, a poor diet, age, and low physical activity.
These are all factors that, unlike menopause, are steadily increasing in the population. The same factors are also all linked to more inflammation.
Reece’s article did not deal with how this wealth of research fits his menopause theory. Nor did he discuss the fact that many men with BPH are not sexually active.