Scientists, at Kaiser Permanente in California, may have discovered a genetic risk factor for erectile dysfunction. Risk factors such as drinking, smoking and obesity are still risk factors, however, for many men, losing weight and quitting smoking and drinking does not resolve the problem. Finding a genetic link may help scientists identify new treatment options.
Erectile dysfunction (ED) is the persistent inability to achieve or maintain an erection sufficient for sexual activity. ED is a common disorder, affecting approximately 50% of men between the ages of 40 and 70. It can have a significant negative impact on the quality of life for both the sufferer and his partner. This new research proves there is a genetic connection and may mean future treatments that target specific genes to treat inherited erectile dysfunction.
Results of the study, which evaluated data on more than 250,000 men in the U.S. and the UK, were published in the Proceedings of National Academy of Sciences in June of 2018. Researchers split the data up into four groups that ranged from men who reported always being able to get and erection to men who reported never being able to get an erection. Men who reported problems with ED had higher odds of having a “T-risk allele” or a gene enhancer that affects a gene called SIM1.
The “T-risk allele” is not a gene but it affects a gene called SIM1. The SIM1 gene is part of the melanocortin system which has been linked to weight regulation and sexual function. The SIM1 gene regulates hormones critical for sexual function. It is not completely clear how the “T-risk allele” affects the SIM1 gene but men who had the allele were more likely to experience ED.
Currently the most common type of prescription medication used to treat ED is phosphodiesterase type 5 inhibitors which include; sildenafil, vardenafil, and tadalafil. These medications relax the penis tissue, allowing blood to enter the penis and cause and erection. But these medications only treat the symptoms and provide only a temporary solution. Patients that want to stay sexually active must use them for the rest of their lives. Gene therapy may be successful but it could take a long time for discovery and regulatory approval.
At the Stem Cells Transplant Institute we are proud to be providing stem cell therapy for the treatment of erectile dysfunction. The Stem Cells Transplant Institute uses adult autologous stem cells to successfully treat erectile dysfunction. Research has shown stem cell therapy in patients with erectile dysfunction resulted in:
- Improved rigidity
- Improved erections
- Continent and incontinent men recovered the ability to have and maintain an erection
- Improved erectile hardness scores
- Improved scored on the international index of erectile function
Cavernous smooth muscle cells and endothelial cells are thought to play a significant role in getting and maintaining an erection. Transplanted stem cells respond to the needs of the surrounding cells and the products secreted by the surrounding cells. Stem cells respond to the environment by differentiating into a variety of cell types and secreting cytokines, growth factors and extracellular matrix molecules that evoke specific responses from neighboring cells. For erectile dysfunction researchers believe the transplanted stem cells differentiate into cells including cavernous smooth muscle cells and endothelial cells as well as evoke responses from the existing cells.
Treatment at the Stem Cells Transplant Institute could help improve the symptoms of erectile dysfunction including:
- Difficulty getting an erection
- Difficulty keeping an erection
- Reduced sexual desire
- Depression
- Stress or anxiety
At the Stem Cells Transplant Institute, we want to provide you with the best regenerative medical strategy to improve your sexual health, overall health and quality of life. Contact us today and let us help you live your best life.
Reference:
Eric Jorgenson, Navneet Matharu, et al., Genetic variation in the SIM1 locus is associated with erectile dysfunction,PNAS published ahead of print October 8, 2018 http://www.pnas.org/content/early/2018/10/02/1809872115.full
