Erectile Dysfunction and Inflammation

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Cytokines, are small secreted proteins released by cells have a specific effect on the interactions and communications between cells. Different cytokines are associated with different diseases or conditions(Zhang & An, 2007). One particular cytokine, TNF-α, has been shown to play an important role in ED as well as cardiovascular disease (CVD), due to the effect it has on the vascular system.  Patients with ED often show high levels of TNF-a, which is a cytokine that is often secreted by white blood cells in response to inflammatory stimuli.  In addition, the presence of a low-grade inflammatory process is associated with many cardiovascular diseases (CVD). Cytokines levels, such as TNF-α, are increased in response to inflammation and contribute to the changes in vascular reactivity observed in CVD (Carneiro et al., 2010). Two distinct surface receptors mediate the effects of TNF-α. These include TNFR-1, and TNFR-2.  Gene expression of TNFR-1 has been demonstrated in cavernosal tissue of the penis (Carneiro et al., 2010).  It has been pretty well established that this cytokine is an important contributor of many cardiovascular diseases related to endothelial dysfunction. Additionally, endothelial function is impaired in inflammatory conditions and conditions with increased oxidative stress.  In vivo laboratory administration of TNF-α demonstrates impairment of endothelium-dependent vasorelaxation in a variety of vascular beds and decreases the release of nitric oxide (NO), which is required for erectile function. TNF-α has the ability to increase arterial reactive oxygen species generation, which likely accounts for some of the reduction in NO levels.

So the question is, what is causing the TNF-α to be elevated?  I found the link to environmental toxins to be quite intriguing.  Could exposure to these toxins induce elevations in inflammatory cytokines, like TNF-α, that leads to downstream effects such as vascular dysfunction?  Some environmental toxins, such as endocrine disrupting chemicals (EDCs) interfere with the synthesis of cytokines, immunoglobulins, and inflammatory mediators, and they also affect the activation and survival of immune cells (Yang et al., 2014).  The dysfunction of the immune system caused by some EDCs may lead to immunity immunodeficiency against infection, or to hyperreactivity of immune responses, as seen in allergy and autoimmune disease (Yang et al., 2014).  Nonylphenol (NP), one of the alkylphenols, is the most important metabolite of a group of nonionic surfactants, is a common EDC that can bioaccumulate through the diet.  It is structurally similar to estrogen, which can feminize male animals and may be linked to infertility.  Some in vitro or ex vivo studies suggest that NP skews T cells towards Th2 responses through its influence on dendritic cells (DCs), resulting in increased expression of IL-6 and TNF-α, but not IL-10 and IL-12, in response to LPS stimulationNP increases the expression of TNF-α, but suppressed anti-inflammatory cytokine IL-10 production in a range of physiological doses, burning both ends of the candle.

Another interesting association with increased levels of TNF-α is associated with intestinal parasites such as Entamoeba histolytica.  Although TNF can be synthesized and secreted by many other cell types, such as neutrophils, eosinophils, and mast cells, the main source of TNF is activated macrophages.  Usually, TNF contributes to the control of parasitic and bacterial infection like in the case of Trypanosoma infection or by triggering an immune response. E. histolytica activates the inflammatory process by promoting TNF production, which is thought to be crucial for guiding E. histolytica towards TNF-producing cells of the host. One may speculate that this behavior is triggered by its need of nutrients that cannot be satisfied in the inflamed tissues. Inflammation causes change in the gastrointestinal microbiota, and these changes may provoke E. histolytica to search for alternative sources of nutrients.

Other intestinal parasites have been associated with HPA axis dysfunction, since the immune and neuroendocrine systems are interconnected by a network in which hormones, antigens, receptors, cytokines, antibodies and neuropeptides modulate immune response. This indicates that intestinal parasites can influence sex hormone production, such as testosterone.  Low testosterone levels often go hand in hand with erectile dysfunction, but that will be discussed in a future blog.

The bottom line; get to the bottom of the problem. Find the source of the inflammation that is ruining your sex life. Run functional labs such as a stool test to rule out intestinal parasites.  An HPA axis test, such as the Dutch Complete, can determine the hormone imbalance and potentially identify the root cause. An environmental toxin test can reveal if toxins are ruining contributing to your immune dysfunction.  Running these labs will allow you to get on a healing path so you can get off the purple pill and regain your life back. You should work with a practitioner who is knowledgeable about the tests and can work with you to find your path to wellness.

 

References

Ankri, S. (2015). Entamoeba histolytica – tumor necrosis factor: a fatal attraction. Microb Cell, 2(7), 216-218. doi:10.15698/mic2015.07.216

Carneiro, F. S., Webb, R. C., & Tostes, R. C. (2010). Emerging role for TNF-alpha in erectile dysfunction. J Sex Med, 7(12), 3823-3834. doi:10.1111/j.1743-6109.2010.01762.x

Yang, S. N., Hsieh, C. C., Kuo, H. F., Lee, M. S., Huang, M. Y., Kuo, C. H., & Hung, C. H. (2014). The effects of environmental toxins on allergic inflammation. Allergy Asthma Immunol Res, 6(6), 478-484. doi:10.4168/aair.2014.6.6.478

Zhang, J. M., & An, J. (2007). Cytokines, inflammation, and pain. Int Anesthesiol Clin, 45(2), 27-37. doi:10.1097/AIA.0b013e318034194e

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Author: naturalhealthachiever

I am a mom with 2 kids who has been suffering with IC and painful bladder syndrome for about 8 years. I am also a fitness and nutrition fanatic, and strive to ACHIEVE the best I can be, and that includes my health! I decided to start this blog to document my journey as I heal from this debilitating condition. I want to share the information I have learned with the world. Nobody should suffer from this condition. There is hope. We can ACHIEVE this together!

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