Oxytocin, Erectile Dysfunction, Stress, Frigidity, and Fear

August 22, 2012

Erectile dysfunction and reduced libido are usually related to stress, clinical depression, panic disorder, generalized anxiety, diabetes, vascular disease . . . Smoking, antidepressants and alcohol abuse can cause ED. Stress is a big one. A wide variety of chemical reactions occur under stress. Certain neurotransmitters are released in greater and greater amounts. Men are more vulnerable to ED due to stress and are more likely than women to develop aggressive behavior or drug and alcohol abuse. Pharmaceutical drugs like Beta blockers for heart patients and Tagamet for acid reflux can cause ED as well. Whatever the cause, reduced sexual function usually leads to insidiously anxious feelings which leads to even more performance anxiety, more dysfunction, more cortisol. It’s a slippery slope. Stress is like a muscle. If you keep using it will get bigger and stronger. Stressful neurons and axons grow just like muscles in the gym. Once in place they enable cortisol readiness, even in the absence of stress! Over time the good neurons and axons are further eroded and with them your sex life. 

Erection dysfunction, be it physical or psychological, is so closely tied to the male ego that it always triggers emotional consequences. Emotional stressors steal energy. Rather than fight stress fatigue and sexual apathy with stimulants: (cigarettes = dopamine, or coffee = caffeine, or soda = sugar + caffeine) or other drugs that numb or artificially “push” the endocrine system, the healthy way to go, the only way to go, is to cut off the head of the dragon. The cortisol dragon. And the way to do that is via greater oxytocin release. Oxytocin the most powerful antidote to cortisol that the body has.    

Viagra, Cialis and Levitra are very effective ED protocols. They physically stiffen the penal shaft by inhibiting the enzymes (phosphodiesterase-5 and 6) which constrict the circulatory system, effectively opening the flood gates to the groin. In terms of fundamental mechanics, this generation of ED pills is second to none. But, they are a strictly a mask, a targeted treatment protocol that does not address the underlying emotional or neuronal causes. They are concerned with a part of the body, rather than the whole of the body’s problem. 

Oxytocin’s approach to ED and frigidity is much more “endocrine interactive” in that oxytocin activates oxytocin throughout the entire hormonal system. For example, we generate oxytocin in our retina. Take exogenous nasal oxytocin and look someone in the eyes and even more oxytocin will be released via mutual eye contact. Touch triggers oxytocin release. Oxytocin is made in the testes, the ovaries, the adrenals, the pituitary, the pineal gland, the thymus, the pancreas, the uterus, the prostate . . . Team oxytocin! It is literally a case of more begets more. This capacity is completely unique to oxytocin. No other hormone acts in this way in our body. Administer exogenous testosterone or thyroid hormone and the body will mitigate its own production. Just ask any excessive steroid user where his testicles have gone. Or, any Synthroid user why she has to up her synthetic thyroid hormone every year. Yet MD’s blithely write more and more of these prescriptions. Keeping in mind that the endocrine system (the pituitary, pineal, pancreas, thymus, pancreas, adrenals . . . ) is the shock absorber of the body, dedicated to helping us to live optimally, doesn’t it makes sense to address the entire body, rather than just a part?  

The same goes for women. Stress can freeze the female endocrine system into anorgasmia (frigidity), tamper with menstrual cycles, exacerbate amenorrhea (low or absent menstruation), dysmenorrhea (uterine cramps during menstruation) and menorrhagia (heavy menstrual flow and cramps). Stress is emotionally and physically paralyzing. Ask any woman with a sexual issue and she will eventually admit to stress about something: work, boyfriend, husband issues  . . . Unfortunately, past sexual traumas are all too common.