Last Updated on May 25, 2023 by Max
The question that arises is why we need to understand the mechanism of benign prostatic hyperplasia (BPH). The answer lies in the significance of the mechanism itself – it is the driving force behind everything. If we fail to identify the mechanism of a disease, we can liken ourselves to blind warriors attempting to fight an unseen enemy. We may observe the symptoms of the condition, but without understanding the causative process, our actions are somewhat misguided.
In this article, I aim to delve into the mechanism of BPH, first proposed a decade ago by Israeli scientists, and corroborated by numerous clinical studies since then.
Understanding the Paradox of Benign Prostatic Hyperplasia
A puzzling aspect of BPH is that, despite age-related declines in circulating testosterone levels, the prostate grows, contrary to expectations. Testosterone is instrumental in promoting the proliferation of muscle cells, including those in the prostate. Interestingly, while its concentration in the circulating blood is relatively low, intraprostatic testosterone and dihydrotestosterone levels, along with androgen receptor activities, remain consistently high.
The prostate, which contributes to about 30% of sperm ejaculate, operates under the control of androgens: free testosterone (FT) and dihydrotestosterone (DHT). The testes produce sperm and free testosterone, the latter of which, along with waste products, is drained into the body’s circulatory system via the internal spermatic veins. However, through venous and arterial circulations, FT is diluted, and most of it binds to albumin and sex hormone-binding globulin. Only about 2% of non-bound FT reaches the prostate via the prostate artery. Under normal conditions, FT takes a long journey from the testes through the body’s bloodstream to the prostate. Once there, the enzyme 5α‐reductase transforms approximately 90% of FT irreversibly into DHT, a more potent hormone that associates with the androgen receptors more readily. Numerous evidence-based studies have demonstrated DHT’s critical role in the pathology of BPH.
The Link Between Varicocele and Benign Prostatic Hyperplasia
Gat et al. found that the blood drainage of the reproductive system is not working correctly due to the damage of the one-way valves in the internal spermatic veins. Destruction of one‐way valves is a well-known vascular disease varicocele, progressing with age and reaching over 75% at the age of 70.
Several independent studies on hundreds of patients showed the presence of varicocele in all cases with BPH. Moreover, there is a high correlation between varicocele at the ages of 20-25 years and the development of BPH in men of 45 years.
Some speculate that this occurrence is the price we pay for the human’s advantageous erect posture. While our erect posture has allowed for greater hand function and creativity, it has also resulted in blood pressure-related diseases, back pain, varicocele, and BPH. Gat et al. have also linked the destruction of the testicular venous drainage system with almost 90% of male infertility cases.
Whether BPH is a normal consequence of an erect posture in aging men is debatable. Other significant factors such as sexual excesses, lifestyle choices, obesity, environmental pollution, and diet could trigger the process of varicocele. Additionally, this theory contradicts the findings of Jean D. and Wilson M.D., published in “The American Journal of Medicine”: “Development of prostatic hyperplasia is an almost universal feature of the aging man and dog, and in both species, the process develops only in males with intact testes.”
The Underlying Mechanism of Benign Prostatic Hyperplasia
With the one-way valves in the internal spermatic vein damaged, the vein can no longer effectively serve as a drainage system. Elevated hydrostatic pressure from a column of blood in the vein leads to:
- Persistent hypoxia in the testicular microcirculation results in degeneration in spermatogenesis and a decrease in sperm production.
- Redirection of undiluted FT flow straight from the testes into the prostate. The venous blood cannot flow upwards and is diverted into other channels common with the prostate. Hence, the prostate, in addition to receiving physiological FT from the arterial blood, becomes inundated with undiluted androgen, around 100 times above the normal level, from an unexpected source.
This sudden influx of undiluted androgen accelerates prostate cell production and prolongs cell lifespan, contributing to the development of BPH. These observations have been clinically proven in a large number of patients. A recent study (Goren M, Gat Y. 2018) observed bilateral varicocele in all 901 patients. Sclerotherapy of the spermatic vein led to a reduction in prostate volume in over 80% of men, with a significant improvement in prostate symptoms. This study establishes a clear pathophysiological link between bilateral varicocele and BPH.
This accelerates prostate cell production and prolongs cell lifespan, leading to the development of BPH.
Furthermore, these observations were clinically proven in a large number of patients. A recent study (Goren M, Gat Y. 2018 ) observed bilateral varicocele in all 901 patients. Sclerotherapy of the spermatic vein resulted in the reduction of the prostate volume in more than 80% of men, with prostate symptoms improved. A straightforward pathophysiologic connection exists between bilateral varicocele and BPH.
In the figure, the varicocele-affected spermatic vein is shown black, and the vessels common for testicles and prostate are shown red.
The Potential Medical Consequences
Reflecting on the possible medical implications of these scientific discoveries, the editor-in-chief of the “Andrology” journal, W. -B. Schill, stated: “The study by Gat et al. has several potentially powerful medical consequences. Firstly, the savings in hospitalizations, surgical, and indirect costs would be substantial. Secondly, if varicocele predisposes to later age prostatic pathology, the best strategy would be to establish criteria for preventive treatment by interventional radiology. Thirdly, their treatment restored circulating testosterone levels in aging men and could ‘naturally’ revive sexual function.”
Considering these findings, BPH should no longer be viewed as a paradoxical condition in aging men; rather, it should be expected. We now have a better understanding of the mechanism of benign prostatic hyperplasia, bringing us a step closer to defeating this common affliction.
For those concerned about their health and sexual well-being, I would strongly recommend consulting with a medical professional about the benefits and potential downsides of varicocele therapy. Once the main issue has been addressed, the focus can then be shifted toward maintaining prostate health through a balanced diet and healthy lifestyle choices.
- W. -B. Schill I. Ben‐Shlomo. Benign prostatic hyperplasia due to venous drainage malfunction in the male reproductive system: a price of erect posture in humans. Andrologia 2008 Volume 40, Issue 5 P: 272
- Y. Gat M. Goren. Benign Prostatic Hyperplasia: Long‐term follow‐up of prostate volume reduction after Sclerotherapy of the internal spermatic veins. Andrologia. 2018 Mar;50(2)
- Canales, Benjamin K. et al. Prevalence and effect of varicoceles in an elderly population.
Urology,2005 Volume 66,Issue 3,627 – 631
- Y. Gat M. Gornish M. Heiblum S. Joshua. Reversal of benign prostate hyperplasia by selective occlusion of impaired venous drainage in the male reproductive system: novel mechanism, new treatment. Andrologia 2008 Volume 40, Issue 5.
- Jean D.WilsonM.D. The pathogenesis of benign prostatic hyperplasia.The American Journal of Medicine. Volume 68, Issue 5, May 1980, Pages 745-756
- Goren M, Gat Y. Varicocele is the root cause of BPH: Destruction of the valves in the spermatic veins produces
elevatedpressure, which diverts undiluted testosterone directly from the testes to the prostate. Andrologia. 2018 Jun;50(5)